A MANUAL OF PATHOLOGY. A MANUAL 
OF 
PATHOLOG Y. 
BY 
JOSEPH COATS, M.D., 
PATHOLOGIST TO THE WESTERN INFIRMARY AND THE SICK CHILDREN’S HOSPITAL, GLASGOW; 
LECTURER ON PATHOLOGY IN THE WESTERN INFIRMARY; EXAMINER IN PATHOLOGY 
IN THE UNIVERSITY OF GLASGOW; FORMERLY PATHOLOGIST TO THE ROYAL 
INFIRMARY, AND PRESIDENT OF THE PATHOLOGICAL AND 
CLINICAL SOCIETY OF GLASGOW. 
WITH THREE HUNDRED AND THIRTY NINE ILLUSTRATIONS. 
PHILADELPHIA: 
HENRY C. LEA’S SON & CO., 
1883. DORNAN, PRINTER, TO 
JOSEPH LISTER, M.B., F.R.S., 
WHOSE METHOD OF REGARDING PHYSIOLOGICAL AND PATHOLOGICAL 
PROCESSES AFFORDED TO THE AUTHOR, DURING THE 
EARLIER YEARS OF HIS CAREER, AN EXAMPLE OF 
SCIENTIFIC INSIGHT FOR WHICH HE HAS 
NEVER CEASED TO BE GRATEFUL, 
AND TO 
W. T. GARDNER, M.D., 
WHOSE ENTHUSIASM IN THE STUDY OF PATHOLOGY, IN THE POST-MORTEM 
ROOM AND AT THE BEDSIDE, HAS BEEN TO THE AUTHOR, 
DURING THESE FOURTEEN YEARS, A PERPETUAL 
STIMULUS, WHILE HIS GENEROUS FRIENDSHIP 
HAS BEEN A CONSTANT ENCOURAGEMENT, 
§his $jgork is, 
WITH GREAT RESPECT AND ESTEEM, 
DEDICATED. PREFACE. 
Tiie teaching of Pathology in the British schools of medicine 
has, of late years, assumed greatly enlarged proportions, while 
the publication of native text-books has by no means kept pace 
with it. Since the publication of Wilks and Moxon’s excellent 
work on Pathological Anatomy in 1875, no complete English 
work has appeared, Green’s “Introduction,” though improving 
both in scope and fulness with successive editions, laying no claim 
to be a complete systematic treatise. In the paucity of English 
works we have had several translations of foreign manuals. The 
Sydenham Society, in 1872, issued a translation of Rindfleisch’s 
Manual of Pathological Histology, and during the last few months 
we have had the first instalments of translations of Cornil and 
Ranvier’s “Manuel cTHistologie Pathologique,” and of Ziegler’s 
“ Lehrbuch der Pathologischen Anatomie und Pathogenese.” 
These two latter translations were announced after the author 
had undertaken the present work. 
v 
The want of a complete English text-book, felt by the author 
in the course of teaching, suggested this undertaking. It will be 
seen from the Contents that the scope of this work is somewhat 
more extensive than that of most works on the subject. These, 
for the most part, are limited either to Pathological Anatomy or 
General Pathology, while in this work an endeavor has been 
made to include both. It will be acknowledged that the whole 
aim of pathological anatomy is to elucidate the actual vital pro- 
cesses of disease, and it has been felt by the author in lecturing 
on Pathology that the subject gains in interest and intelligibility 
when the etiology, anatomy, and general pathology are all taken 
into account in forming a general conception of each morbid VIII 
PREFACE. 
condition. The author is conscious of many imperfections and 
omissions now that he contemplates his completed task; he can 
only ask for the indulgence of the reader, and he may be allowed 
to hope that an opportunity will be given of improving on the 
present work. 
It was in the plan of the author to indicate the literature of the 
various subjects treated of; this, however, has been necessarily 
left over. In the mean time it may be stated that the author has 
been much indebted to the works of Virchow, Wagner, Rind- 
fleisch, Cohniieim, Paget, Wilks and Moxon, Payne, Klebs, 
Cornil and Ranvier, Forster, Rokitansky, Birch-Hirschfeld, 
Billroth and Ziegler for general guidance in the preparation of 
the work. As the author for the last fourteen years has been 
constantly engaged as a practical Pathologist and in teaching 
large classes of students, the work in most of its departments 
rests upon his own observation and experience. 
In the preparation of the work for the press, and in arranging 
the index, the author has been under great obligation to Dr. Geo. 
S. Middleton and Dr. J. Lindsay Steven, the former of 'whom has 
also supplied, in the index, the derivations of words. 
Glasgow, March, 1883. CONTENTS. 
PART FIRST.—GENERAL DISEASES. 
INTRODUCTION. 
Pathology is the study of diseases in their essential nature, 17; The relation of 
morbid and healthy conditions, of Pathology and Physiology, 17 ; Pathology 
elucidated by means of Experimental Pathology, 18 ; Pathological Anatomy, 18 
(including Pathological Histology, 20) ; and Clinical Observation, 20. 
AFFECTIONS OF THE CIRCULATION AND OF THE BLOOD. 
Physiological Considerations.—Arrangements for regulating the distribution of 
the blood, 23; Tonicity of arteries, 24; Regulation of arteries by peripheral 
centres, 24. 
Hyperemia and Anaemia, 25; (1) General Hyperemia, Plethora an equivalent 
term, 25; Artificial Plethora produced by Transfusion, 25 ; Quantity of blood 
transfusible, 26 ; Disposal of excess, 26; Effects of blood containing free ferment, 
26 ; Effects of alien blood, 27. Plethora in man, 27. 
(2) General Anaemia.—A true general anaemia or oligaemia produced by 
hemorrhage, 27; the resulting conditions, Hydraemia, Leucocytosis, 27; Re- 
plenishment of the red corpuscles a slow process, 29. Spontaneous Anasmias. 
—Chlorosis, 29; Pernicious Anaemia, 30; Secondary anaemia, 31; Secondary 
organic changes in anaemia, 31. 
(3) Local Hyperemia.—Its two forms: («) Active Hyperemia or Active 
Congestion, 32 ; rarely from increase of blood-pressure, 32 ; collateral hyperaemia 
in relation to blood-pressure, 32. Dilatation of arteries the essential cause of 
active hyperaemia, 33; from application of warmth, from removal of pressure, 
from vaso-motor paralysis, 33 ; Results and signs, 34. (6) Passive Hyperemia 
produced by weakness of the heart with gravitation (hypostasis), 34; obstruction 
of arteries and veins, 35; and valvular disease, 35; Results are the consequence 
of increased blood-pressure, 35; chiefly hemorrhage by diapedesis, 36; and 
oedema, 36. 
(4) Local Anemia produced by obstruction of capillaries or arteries, 38 ; its 
results, 38. 
Thrombosis and Embolism.—Thrombosis is the coagulation of blood inside the 
vascular system, 39 ; Conditions of coagulation, 39; the part taken by the leuco- 
cytes, 39 ; red thrombi, 40; white and mixed, 40. The two main elements in 
thrombosis : stagnation of blood, 41 (illustrations, 41); injury to wall, 41 (illus- 
trations, 41). Growth of thrombi, 42. [Post-mortem coagula, 43.] Changes 
in thrombi: softening, 43 ; (vein stones, 44) ; organization, 44. Capillaries in 
relation to thrombosis, 45. Effects of thrombosis : Hyperaemia and oedema, 46 ; 
rarely gangrene, 46. X 
CONTENTS. 
Embolism.—In anastomosing arteries and capillaries, 46 ; in end-arteries, 47 ; Cohn- 
heim’s experiments, 47 ; the hemorrhagic infarction, 48. Illustrations in man : 
embolism in lungs, 49; spleen, 50; kidneys, 50; brain, 50; portal vein, 51. 
Peculiar case of the superior mesenteric artery, 52. Case of arteries rendered 
end-arteries, 53. Further consequences of embolism : necrosis, 53; absorption, 54. 
Oil embolism, 54. Air embolism, 54. 
Hemorrhage.—Hemorrhage by rupture or by diapedesis, 55 (illustrations, 56). 
Stilling of hemorrhage, 57 ; by thrombosis and other aids, 57 ; disposal of the 
extravasated blood, the fibrine and red corpuscles, 58; cells containing red cor- 
puscles, 59; pigmentation, 59. 
The Hematoma, of the scalp, 60; ear, 60; dura mater, heart, uterus, 60. 
(Edema and Dropsy.—The lymphatic circulation, 61. Causes of oedema and dropsy, 
61; obstruction of lymphatics, 61 ; increased transudation from capillaries, 63; 
the latter the essential cause, 63. Illustrations : venous hyperaemia, 63 ; hydraunia, 
64. The oedema of Bright’s disease and hydrasmic plethora, 64. 
Leukaemia.—Condition of the blood, an anaemia with increase of leucocytes, 66; 
nature of the change, 67. Association with lesions in supposed blood-forming 
organs: Spleen, 67; Bone-marrow, 68; Lymphatic glands, 68. Secondary 
changes in other organs: liver, kidney, 69; intestine, etc., 70; Pseudo-leu- 
kemia, 70. 
Mel anemia.—Solid pigment in blood after agues, 70; Its origin from red corpuscles, 
71; Deposition in spleen, liver, brain, kidneys, etc., 72. 
Uremia.—Supposed to be a poisoning with urinary constituents, 72 ; Various other 
views, 72 ; Reasons for adhering to original one, 73. 
Diabetes Mellitus.—The normal sugar in blood and urine has no relation to the 
food, 73; In diabetes the relation marked, 73 ; An excessive demand for sugar, 
74; The liver forms glycogen, not sugar, 74 ; Pathological conversion of glycogen 
into sugar, 75; Explanation of diabetes on this basis, 76; In artificial diabetes 
circulation in liver deranged, 76; also in some cases in man, 77. A hyperasmia 
of abdominal viscera generally, 78. Lesions in coeliac plexus, 78 ; in brain, 78. 
Etiology.—Irritants damage the tissues, 80. Internal inflammations also produced 
by irritants, 80. Relation of the nervous system, 81. Path of conduction of 
irritants, 82. 
The Principal Phenomena.—Experiment giving a summary view of these, 82. 
1. The State of the Vessels.—Dilatation of the arteries with active hyper- 
aemia (Determination of blood), 84. This a local process from paralysis of mus- 
cular coat, 85 ; irritants paralyze the tissues, 85; evidence from pigment cells of 
frog, etc., 85. Retardation of current and pavementing of veins from acquired 
adhesiveness of corpuscles, 86. Temperature of inflamed parts—the rise due to 
determination of blood, 87. 
2. The Inflammatory Exudation.—The exudation cells, their source in the 
blood, 89 ; emigration of leucocytes, 90; diapedesis of red corpuscles, 90. The 
serous exudation, shed from surface or causing oedema, 91 ; greatly increased 
transudation, 91. The fibrinous exudation, its manifestations, 91 ; not usually 
in serous spaces, 91. Mode of production of inflammatory exudation, 92; the 
damage to the vessels the cause of escape of corpuscles, 92; and increased trans- 
udation, 93; the formation of fibrine, 93. Mixed exudations—Variations as to 
site, etc., 94. Final disposal of exudation, 95. 
INFLAMMATION. CONTENTS. 
XI 
3. The Changes in the Tissues and New Formation.—At first retrograde 
changes, 95. New formation—Its type in the granulating wound, 95. 
Character of inflammations leading to granulation, 96. Two kinds of cells, 97. 
The formative cells and their changes, 97. New formation of bloodvessels, 98. 
The origin of the formative cells, 99. Connective tissue and the lymphatic 
system, 100. New formation of epithelium, 101. Other instances of new forma- 
tion, 101. New formation in connection with foreign bodies and dead tissue, 102. 
4. Individual Forms of inflammation: congestive, exudative, 103 ; infec- 
tive, phlegmonous, ulcerative, 104; degenerative, formative, 104. 
RETROGRADE METAMORPHOSES. 
Necrosis; Gangrene, 105. Conditions producing local death, 105; interference 
with circulation, 105; traumatic agents, 106 ; excessive heat or cold, 106 ; special 
case of senile gangrene, 107; senile softening of the brain, 107; ergotism, hos- 
pital gangrene, 107. Changes in the Dead Tissue give the character to the 
necrosis, so (1) Coagulation necrosis, 108; (2) Caseous necrosis, 111 ; (3) Desic- 
cation or mummification, 111; (4) Softening and moist gangrene, 112. Limita- 
tion of the necrosis, 112. Disposal of the dead tissue, 113. 
Simple Atrophy, 113. Physiological atrophy of hair, teeth, etc., a vital process, 
114. General emaciation, 114 ; local atrophies, 115; of muscles from disuse, 115; 
tropho-neuroses, 115. 
Albuminous Ineiltration, causes and appearances, 116. 
Fatty Degeneration, 118. The free and combined fat of the tissues, 118. Bauer’s 
experiments, 118. Fatty degeneration in anaemia, inflammation, etc., 118. 
Source of the fat, 119. The anatomical changes, 120 ; final disposal of the fat; 
absorption, 120; formation of cholestearine, 121; caseation (tuberculization), 122. 
Fatty Infiltration, 122. Obesity, 122. Infiltration in structures out of use, 122 ; 
in muscles, heart, disused glands, 122. Special case of fatty liver, 123. Appear- 
ance of the fat, 124. 
Pigmentary Infiltration, 124. Connection with hemorrhage, 124; in tumors, 
125; in lungs ; uterus; bronzing, etc., 125. 
Mucous and Colloid Degeneration, 126. The physiological mucus, 126; colloid 
ovarian cyst, 126; colloid goitre, etc., 127. Mucous degeneration of connective 
tissue, bone, cartilage, tumors, 127. 
Calcareous Infiltration, 128. Lime salts dissolved in tissues and juices, 128. 
Metastatic calcification, 128. Infiltration of dead or obsolete structures, 128 ; of 
parasites, inflammatory products, 129; of walls of arteries, etc., 129. 
Amyloid Degeneration, 131. The amyloid substance, 131. The disease affects 
connective tissue and walls of vessels, 132. Effects on structure and function, 
133. Localized amyloid degeneration, 134. Nature of the process, 134. Corpora 
amylacea, 135. 
HYPEPvTROPIIY, EEPAIE, AND REGENERATION. 
Hypertrophy, 137. Its type in normal growth, 137. Process of division of cells, 
137. Hypertrophy from excessive performance of a normal function, 138. (1) 
In muscle of bladder, heart, etc., 139 ; details of process, 139; hyperplasia, 140. 
(2) In epidermis, 140; from intermittent pressure, 140. Hypertrophy from in- 
creased blood-supply, 140; near inflammations, in hone, etc., 141. XII 
CONTENTS. 
Repair of Injuries and Restoration of Lost Parts, 141. Powers of restora- 
tion in lower animals, 142. Indication of law governing powers of restoration 
in adult animal, 142. Repair of injuries, 142. Healing of wounds: imme- 
diate union, 143; primary adhesion, 143; by second intention, 144. Regenera- 
tion of lost structures, 144; blood, 144 ; epidermis, 144; connective tissue, 145; 
bone (transplantation), 146; nerve fibres, 146 ; muscle, 146. 
Due to the action of viruses, 147. In structure analogous to inflammatory new forma- 
tions, and generally associated with inflammation, 147. 
Syphilis, 148. The primary chancre, 148. The secondary stage, in which the 
virus is in the blood, 149; blood and secretions contagious, 149. The tertiary 
stage characterized by unsymmetrical gummata, 150; structure and tendencies 
of gumma, 151; its relations to the virus, 152. Hereditary and congenital 
syphilis, 153. 
Tuberculosis.—(a) General Tuberculosis, 154. Case of Acute Miliary Tuber- 
culosis, 154; a virus in blood, 154; comparable to secondary stage of syphilis, 
154. The structure and tendencies of the miliary tubercle, 155. Connection of 
tuberculosis and inflammation, 157. (b) Local Tuberculosis, 157. Illustra- 
tions: tubercular peritonitis, 157 ; renal phthisis, 158. Tubercular ulcers, 158. 
Scrofulous tubercle of brain, 159. Artificial production of Tuberculosis ; 
by inoculation, 159 ; by inspired air, by food, 170. Nature of the tubercular 
virus, 150; the tubercular bacillus of Koch, 161. Scrofula, etc., included in 
tuberculosis, 162. Source of the tubercular virus ; in acute miliary tuber- 
culosis, 163 ; in local tuberculosis, 163. 
Bovine Tuberculosis or Perlsucht, 164. 
Lupus, 166. 
Leprosy, 166. 
Glanders and Farcy, 168. 
INFECTIVE TUMORS (GRANULATION-TISSUE TUMORS). 
TUMORS OR MORBID GROWTHS. 
Definition and general characters, 169. Homologous and heterologous, 169. Origin 
and development, 169 ; theory that tumors arise from embryonic tissue left over, 
170; applicability of this view to some tumors, 171. Growth and extension ; 
of simple tumors, 171; malignancy, local and general, 172; metastasis, 172; 
malignancy of tumors usually simple, 173. Secondary changes in tumors, 
173; cachexia, dyscrasia, etc., 174. Classification, 174. 
A.—Simple-tissue Tumors. 
(1) The connective-tissue tumor, or Fibroma, 176; including Elephantiasis 
arabum, 176 ; cutaneous outgrowth, 177 ; fibroma molluscum, 178 ; soft and hard 
fibromas, 178. (2) The fatty tumor or Lipoma, 178. (3) The mucous-tissue 
tumor or Myxoma, 180; including hydatid mole, 182 ; and mucous-tissue tumor 
proper, 182. (4) The cartilaginous tumor or Chondroma, 184. (5) The bony 
tumor or Osteoma, 185 ; including the spongy exostosis, 185 ; the ivory exostosis, 
186; and other osteomas, 187. (6) The muscular-tissue tumor or Myoma, 137; 
chiefly the smooth-celled form, 188. (7) The nervous-tissue tumor or Neuroma, 
190; the false and true neuromas, 191. The painful subcutaneous tumor, 191. 
(8) The vascular tumor or Angioma, 193. (9) The glandular tumor or Adenoma, 
194 ; including the mammary, prostatic, mucous, 194; thyroid and hepatic forms, 
196. (10) The glioma or tumor of nervous connective tissue, 196. (11) The 
brain sand-tumor or Psammoma, 198. CONTENTS. 
XIII 
B.—Compound-tissue Tumors. 
(1) The cystic tumor or Cystoma, 198; mode of formation of cysts, 198. 
(2) The papillary tumor or Papilloma, 202. (3) The Teratoma, 203; sacral 
tumors, 203; dermoid cysts of ovaries, etc., 204. 
C.—Cellular Tumors. 
(1) Sarcomas, 204; definition, structure, mode of growth, 204; relation to 
bloodvessels, 206; Varieties: the round-celled, 206; spindle-celled, 207; cystic, 
208; giant-celled, 208; osteoid, 209; melanoid, 209 ; alveolar, 210; and plexi- 
form, 210. (2) Cancer or Carcinoma, 210; definition and structure, 211. Origin 
of epithelium from preexisting epithelium, 212; illustrations, 212; mode of 
growth, 214; relation to lymphatics, 214; secondary changes, 215. Varieties: 
The epithelial cancers or epitheliomas, 215; the flat-celled, 215; and cylinder- 
celled, 217; Carcinoma proper, 217 ; including medullary, 218 ; scirrhous, 219 ; 
colloid, 221; melanotic, 222; and mucous cancers, 222. (3) The lymphatic 
tumor or lymphoma, including chiefly the lymphadenoma, 222; and lympho- 
sarcoma, 222. 
PARASITES. 
A.—Vegetable Parasites. 
Micro-organisms or Bacteria, 224 ; their occurrence in decomposing matter, 224; 
their source, in the air, etc., 224; their forms, 225; the cocco-hacteria, bacillus, 
spirillum, 226; methods of detection, 228. Influence of bacteria on the living 
tissues, 229. Case of putrefying or septic wounds, 230. Septicaemia, 231. Im- 
portance of distinguishing its two forms, 231. (1) Putrid or septic poisoning 
from the products of decomposition, 231. Wound fever, hectic, etc., 232. (2) 
Putrid or septic infection involving a self-propagating virus, 233; experiments 
of Kock and others, 233 ; septicaemia of mice, 234 ; and of rabbits, 235. Patho- 
genic bacteria, 236 ; cultivation of them, 236. Pyaemia a form of putrid in- 
fection, 237. Its phenomena, 237. Ulcerative endocarditis, 241. 
Pathogenic bacteria in acute specific diseases, 242. (1) The relation of 
micro-organisms to zymotic diseases, 242; splenic, 242; relapsing, 244; typhoid, 
245; and other fevers, 246; erysipelas, 246; ulcerative endocarditis, etc., 246. 
(2) Cultivation of pathogenic bacteria, 248; bacillus anthracis, 248; tubercular 
bacillus, etc., 249. (3) The question of immunity, 249; natural, 249; and ac- 
quired immunity, 251. Pasteur’s artificial production of a vaccine for anthrax 
and chicken cholera, 251. Explanation of immunity, 252. 
Sarcina Yentriculi, 253 ; development in blood outside the vessels, 254. 
Parasitic Fungi, 254. Outline of structure of fungi, 254. Fungi in the blood and 
tissues, 256. The madura foot, 257. Fungi in the ear, skin, 257; hair, 259; 
mucous membranes, etc., 259. Actinomycosis, 798. 
B.—Animal Parasites. 
(1) Trkmatoda or Flukes, 260. The distomahepaticum, 261; sinense, 261; 
lanceolatum and haematobium, etc., 262. 
(2) Cestoda or Tape-worms, 262. Their structure in general, 262. Taenia 
solium, 263 ; structure of strobila, 263; and cysticercus, 266 ; mode of propaga- 
tion, 268. Taenia mediocanellata, 268. Taenia echinococcus, 270. Formation 
of echinococci or hydatids, 270. Bothriocephalus latus, 273. Barer tape- 
worms, 274. XIV 
CONTENTS. 
(3) Nematoda or Round-worms. Trichina spiralis, 275; its appearance in 
muscle, 275; development and migration of embryos, 277. Ascaris lumbricoides, 
278. Oxyuris vermicularis, etc., 279. Filaria sanguinis, 279; its relations to 
chylous urine, 282 ; lymph-scrotum, etc., 282. Stages of development of filaria, 
283. 
Epizoa or External Parasites, 283. 
PART SECOND.—DISEASES OF THE SPECIAL ORGANS 
AND SYSTEMS. 
DISEASES OF THE ORGANS OF CIRCULATION. 
A.—The Heart and Pericardium. 
Malformations of the Heart, 285. Misplacements, 285. Malformations of the 
cavities and of their relation to the great vessels, 285 ; mainly dependent on 
stenosis of the pulmonary artery, 286; incomplete closure of septum ventricu- 
lorum, 286; of foramen ovale, 287; and of ductus arteriosus, 288.. Nature of 
foetal stenosis of pulmonary artery, 288. Irregularity of primary vessels, 289. 
Valvular malformations, 290. Fenestrated valves, 291. Cyanosis as a result of 
malformations, 392; duration of life, 293. 
Atrophy of the Heart, 294. 
Hypertrophy; its compensatory nature, 294; produced by increased force of con- 
tractions, in adherent pericardium, 295; in valvular disease, 296; in Bright’s 
disease, etc., 297. Forms of hypertrophy, 297 ; general, and of right or left ven- 
tricle, 297. Congestion of the heart, 299. 
Fatty Infiltration, 299. Fatty Degeneration, 300. Calcareous Infil- 
tration of the muscular substance, 302. Injuries and Eupture, 303. 
Inflammations of the heart.—(1) Myocarditis, 304; mostly interstitial, 304 ; fibroid 
myocarditis, 305; abscess of the heart, mostly septic, 305. (2) Endocarditis, 
306 ; acute, 306 ; characters and localization of lesions, 306; chronic, 308 ; effects 
on valvular structures, 308 ; relation in some cases to atheroma, 310. Ulcerative 
endocarditis, its specific characters, 310. (3) Pericarditis, 313; acute, 313 ; 
usual appearances, 313; and results, 315; adhesion of the pericardium, 315. 
Tubercular pericarditis, 316. White or milk spots, 316. 
Aneurisms.—(1) Of the heart, appearances and mode of formation, 317. (2) Of the 
valves, their relation to acute endocarditis, 318. 
Valvular Disease, 319. Insufficiency of mitral, 319; characters, 319 ; and effects, 
320. Stenosis of mitral, 321 ; the funnel-shaped malformation, 322; effects, 322. 
Aortic insufficiency, 323 ; conditions, 323 ; and effects, 324. Aortic stenosis, 325. 
Valvular diseases of the right heart, 326. 
Coagula in the Heart.—Simple clots, 327 ; thrombi, 327; warty, globular, poly- 
poid, 327. 
Tumors of the heart, 329. 
B.—The Bloodvessels. 
Inflammation, 330; acute, rare except as part of a septic process, 330. 
Chronic Endarteritis—Atheroma, 332; a disease of advanced life, 332. Ana- 
tomical changes, the patch, 332 ; the abscess, 334 ; the ulcer, 334 ; calcareous in- 
filtration, 334; changes in middle and external coats, 335. Effects on circula- 
tion, 335. CONTENTS. 
XV 
Endarteritis Obliterans, 337. Fatty degeneration of intima of arteries, 338. Cal- 
careous infiltration of arteries, 338. 
Syphilitic Disease of Arteries, 340. 
Aneurism, 342 ; forms, 342 ; causation—weakening of wall, 343 ; increase of blood- 
pressure, 344. Condition of the coats of the artery, middle, internal, and ex- 
ternal, 344. Thrombi in aneurisms, 346. Condition of branches arising at site 
of aneurism, 346. Effects on heart, 347; and on parts around, 347. Termina- 
tions, 348. Varieties of Aneurisms, 349; cirsoid and aneurism by anasto- 
mosis, 349; traumatic and spurious aneurism, 349; dissecting aneurism, 350; 
varicose aneurism and aneurismal varix, 351. 
Varix, 352 ; causation in increased blood-pressure, 352. Condition according to site: 
in lower extremities, 353; hemorrhoids, 354; varicocele, etc., 355. 
C.—The Lymphatic System, Spleen, and Bone-marrow. 
The Lymphatic Vessels, 355. Inflammation; lymphangeitis, 355; erysipelas, 
356. Dilatation of lymphatics, 356. 
The Lymphatic Glands.—Structure and function, 357. Pigmentation, 359. In- 
flammation, acute, 359 ; and chronic, 360. Scrofulous disease, a true tuberculosis, 
360. Syphilitic disease, 363. Degenerative changes, 363. Tumors, 363. 
The Spleen.—Structure, 364. Malformations, 365. Active congestion and inflam- 
mation : the acute splenic tumor, 365. Chronic inflammation, the chronic splenic 
tumor, 367. Passive hypersemia, 367. Embolic infarction, 368. Rupture of the 
spleen, 369. Amyloid disease, 369 ; the sago spleen, 369; the diffuse amyloid 
spleen, 370. Tuberculosis, etc., 371. 
The Bone-marrow, 371. 
Introductory, 372. The general plan of the nervous system, 372; lower and higher 
centres in cord, medulla, middle brain, 373 ; basal ganglia, cerebral convolutions, 
374. Lesions irritate or destroy, 374. Coarse and fine lesions, 374. 
DISEASES OF THE NERVOUS SYSTEM. 
A.—The Peripheral Nerves. 
Introductory Considerations as to structure and function, 375. 
Effects of Division of nerves, 377; degeneration and restoration, 377. Hyper- 
emia and ACUTE INFLAMMATION, 378. CHRONIC NEURITIS, 379. 
Tumors. Leprosy, neuroma, etc., 379. 
B.—The Spinal Cord and Medulla Oblongata. 
Introductory, 380. The gray substance, with its groups of ganglion cells, 380. 
The white substance, with its various tracts, 381. Separate development of 
fibres and centres, 382. Fibres and centres in medulla oblongata, 383. 
Secondary Degenerations of the Cord, 384. Characters of gray degeneration 
(sclerosis), 385. Descending degeneration, 386 ; its locality, 387 ; its relation to 
late rigidity, 387; and increased tendon reflex, 388. Ascending degeneration, 
388. Degeneration after amputation, 389. 
Inflammations of the Cord.—Transverse myelitis: acute, 390; chronic, 391. 
Systematic myelitis, 392. Reasons of systematization, 392. (1) Sclerosis of 
posterior columns, 393 ; special localization in these, 393; physiology of the 
disease, 394 ; trophic lesions, 396. Friedrich’s hereditary ataxia, 396. (2) Spon- 
taneous lateral sclerosis, 396. (3) Poliomyelitis anterior acuta, 397 ; anatomical 
condition, etc., 397; its occurrence in adults, 399. (4) Poliomyelitis anterior XVI 
CONTENTS. 
chronica, 399. (5) Progressive muscular atrophy, 400; changes in muscles, and 
in cord, 400. (6) Bulbar paralysis, 401; its locality and relation to nuclei of 
nerves, 402. (7) Pseudo-hypertrophic paralysis, 403 ; condition in muscles, 403 ; 
and cord, 403. 
Tumors of the Cord and Medulla, 406. 
C.—The Encephalon. 
Introductory.—Course of fibres and position of centres in basal parts, 406; in 
hemispheres, 409 ; and in cerebellum, 412. The arteries of the brain, 412. 
Secondar y Degeneration, chiefly of pyramidal tract, 414. 
Embolism and Thrombosis in cerebral vessels, 415. Causes and localities of em- 
bolism and thrombosis in arteries, 415. Effects of occlusion of arteries, 416. 
Embolism in chorea, 418. Thrombosis of the cerebral sinuses, 418; 
localities, effects, etc., 418. 
Cerebral Hemorrhage, 419. (1) From the larger cerebral arteries, 420; connec- 
tion with aneurisms, 420; atheroma, 421; increase of blood-pressure, 421. (2) 
From the nutritive arteries, 421; miliary aneurisms, 422. (3) From the capil- 
laries, 423. Appearances in the brain after hemorrhage, 423. Organization of 
the clot, 424. The apoplectic cyst, 424. 
Softening of the Brain, 425. Anatomical conditions and appearances, 426. 
Inflammations, 427. (1) Acute localized encephalitis, 427; usually traumatic, 
427; abscesses, 428. (2) Chronic localized encephalitis, 428; disseminated 
sclerosis, 429. (3) Diffused encephalitis, 429 ; delirium of fevers, 429 ; general 
paralysis of the insane, 430 ; (atrophy of the brain, 430 ;) hydrophobia, 432 ; 
lesions in nervous system and elsewhere, 433; tetanus, 434. 
Atrophy and Degenerations, 434. Congenital atrophy, 434. Atrophy of white 
substance, 435; and ganglion cells, 435. 
Syphilis of the Brain and its Membranes, 435. The gumma in brain and 
membranes, 435. Disease of the arteries, 437. Inflammations of the membranes, 
438. Localization in relation to symptoms, 438. 
Tumors of the Brain, 438. Solitary tubercle, 439 ; glioma, 439 ; sarcoma, etc., 440. 
Parasites, 440. 
D.—Membranes and Cavities of Brain and Cord. 
Introductory, 451. 
Meningeal Hemorrhage, 442. Ilsematoma of dura mater, 442; its relation to 
pachymeningitis, 442. Hemorrhage in the soft membranes, 443. 
Inflammations, 444. (1) Pachymeningitis, 444. (2) Simple acute meningitis, 
444. (3) Simple chronic meningitis, 444. (4) Epidemic cerehro-spinal menin- 
gitis, 445. (5) Tubercular meningitis, 445; appearances of brain, 446 ; situation 
of tubercles, 447. 
Accumulation of Cerebro-spinal Fluid, 447. Accumulations ex vacuo, 448. 
Hydrocephalus, 448 ; congenital and acquired, 448 ; chronic hydrocephalus, 449. 
Hydrencephalocele, 450. Spina bifida, 451 ; condition of cord, 452. 
Tumors of Meninges, 452. Parasites, 453. 
DISEASES OF THE ORGANS OF RESPIRATION. 
A.—The Air-passages. 
The Nasal Passages.—Congenital malformations, 454. Acute catarrh, 454; con- 
siderations as to its causes, 455; details of the process, 455. Chronic catarrh or 
coryza, 456. Tumors, especially mucous polypi, 456. CONTENTS. 
XVII 
Larynx and Trachea.—Malformations, 457. Croup and Diphtheria, 458. 
Catarrh, 460. (Edema glottidis, 460. Chronic catarrh, 461. Subglottic inflam- 
mation, 461. Perichondritis, 461. Syphilis, 462. Laryngeal phthisis, 463. 
Tumors, 464. 
The Bronchial Tubes.—Bronchiectasis, 465. Catarrh or bronchitis, 467. Fibrin- 
ous or plastic bronchitis, 469. 
General Considerations, 469. 
Malformations, 471. Atelectasis, 471; and collapse, 472. Hypertrophy of 
the lung, 473. 
Pulmonary Emphysema.—(1) Interlobular, 474. (2) Yesicular; its causes, 475; 
expiratory, 475; inspiratory or compensatory, 476; anatomical changes, 477; 
effects, 480. Senile emphysema, 480. 
Disorders op the Circulation.—Active hypersemia, 481; sometimes collateral, 
481. Passive hypersemia and oedema, 482 ; hypostatic engorgement, 482 ; mode 
of occurrence of oedema, 483 ; appearances, 483. Passive hypersemia from heart 
disease; brown induration, 484. The hemorrhagic infarction, 485. Embolism 
without infarction, 487 ; oil embolism, 487. Pulmonary hemorrhage, 488. 
Inflammations.—Acute Pneumonia, 489; stages of splenization, 490; red 
hepatization, 490 ; gray hepatization, 492 ; and purulent infiltration with resolu- 
tion, 493 ; occasional result in abscess, 493; gangrene, etc, 494; condition of 
pleura, 494. Chronic Pneumonia, 494; producing chiefly induration, 494. 
Acute Catarrhal Pneumonia, 496; related to capillary bronchitis, 496; its 
lobular arrangement, etc., 496 ; occasional interstitial pneumonia, 497. 
Gangrene of the Lungs, 498. 
Phthisis Pulmonalis, 499. Causes, 500; views as to its pathology, 500. Modern 
view of a local tuberculosis, 502. Conditions which predispose, 502; path of 
entrance of virus, 502; localization at apex, 502. Anatomical Changes, their 
complicated characters, 503. (1) Condition of bronchi, 503; catarrh, 504; 
peribronchitis, 504; acute with abscess, 505; or chronic with induration, 505. 
(2) Fibroid phthisis, 505; pigmentation of connective tissue; formation of 
connective tissue, peribronchitic, interlobular, and subpleural, 505; bronchiectatic 
cavities, 506; mode of occurrence of emphysema and cavities, 506. (3) 
Catarrhal or Caseous Phthisis, 507 ; the anatomical changes, 507; nature 
of the caseous necrosis, 509; formation of cavities, 509; general appearances of 
the lung, 510. Modes in which cavities form, 512. Sputa, 512. Hemorrhage 
in earlier and later periods, 512. Condition of pleura, 513 ; mode of occurrence 
of pneumothorax, 514. Condition of bronchial glands, 514; intestines, etc., 
514. 
Acute Miliary Tuberculosis, 515. Bovine tuberculosis, 515. 
Syphilitic Disease, 516. 
Tumors.—Barely primary, 516. Lympho-sarcomas, 516. Cancers, 517. 
Inhalation of Foreign Substances, 518; the ordinary pigmentation, 518; an- 
thracosis, 519; and other kinds of pigmentation, 520. 
B.—The Lungs. 
Pleurisy, 521; its causes, 521; anatomical changes, 522. Empyema, 222. Pleural 
adhesions, 523. Hydrothorax and pneumothorax, 523. Tumors, 524. 
C.—The Pleura. XVIII 
CONTENTS. 
DISEASES OF THE ALIMENTARY CANAL. 
A.—The Mouth. 
Inflammations.—Catarrh, 525; follicular stomatitis, 526 ; thrush, 526 ; gangrenous 
stomatitis, 527. Inflammation of the tongue, 528. 
Infective Tumors.—Syphilis, lupus, 528. 
Tumors, chiefly cancers, 529. Macroglossia, 530. Kanula, 530. 
The Teeth.—Caries, 531. Inflammations of pulp, cement, and structures around, 
532. Hypertrophy of cement, exostosis, 533. 
B.—Soft Palate, Pharynx, and Tonsils. 
Inflammations.—Acute catarrhal angina, 533 ; chronic catarrh, 534 ; acute phleg- 
monous inflammation of fauces (quinsy), 535; diphtheria, 536 ; tonsillitis, 536 ; 
and hypertrophy of the tonsils, 536. 
Syphilitic and tubercular diseases of the fauces, 537. 
C.—The (Esophagus. 
Dilatation, general and partial, 537; the diverticulum, 538. Obstruction, 538. 
Inflammations, 539. Perforating ulcer, 539. Tumors, especially epithelioma, 
540. 
D.—The Stomach. 
Introductory, as to structure and function, 541. Post-mortem changes, 542; in- 
cluding softening of the stomach, 543. 
Dilatation and Hypertrophy, 543. 
Inflammations, 545. Catarrh, acute, 545; and chronic, 546. 
Simple Perforating Ulcer, 546 ; its peculiarities, 547 ; effects, 547 ; and mode of 
origin, 448. 
Hemorrhage from the stomach, 549. 
Tumors.—Cancer in its epithelial, 550; medullary, 551; scirrhous, 552; and colloid 
forms, 552. Other tumors, 553. 
Introductory as to structure and function, 554. The movements of the contents, 
554. Post-mortem changes, 555. 
Malformations, 555. Meckel’s diverticulum, 556. 
Hernia, external and internal, 556. Mode of occurrence, 556. Forms of external, 
557 ; and internal hernia, 557. Contents of hernias, 558. Strangulation, 559. 
Twisting of the intestine, 560 , occurrence in sigmoid flexure and elsewhere, 561. 
Intussusception, 561. Prolapse of intestine, 563 ; two forms, 563. 
Simple Inflammations.—Catarrh, 563 ; ulcers: follicular catarrh and ulcers, 564. 
Localized inflammations; typhlitis and perityphlitis, 564; connection of these 
with vermiform appendage, 565 ; proctitis and periproctitis, 566. 
Specific Inflammations.—Dysentery, 567 ; acute and chronic, 567. Cholera, 568. 
Typhoid fever, 569 ; conditions of intestine, 570; and mesenteric glands, 571. 
Tuberculosis of intestine.—Formation of the tubercular ulcer, 572. 
Tumors.—Chronic epithelioma, 575; colloid cancer, 575. 
Obstruction of the intestine, 576 ; the various lesions producing it, 576. 
Effects of accumulation of contents, 576. 
E.—The Intestines. CONTENTS. 
XIX 
DISEASES OF THE LIVER, PANCREAS, AND PERITONEUM. 
A.—The Liver. 
Introductory.—As to structure and function, 578. 
Malformations and Misplacements, congenital and acquired—the female liver, 
579 ; folds in the liver, 580; changes in position, 580. 
Passive Hyperjsmia, 580. Thrombosis and Embolism of portal vein and hepatic 
artery, 582. Hypertrophy of the liver, 583. 
Retrograde Changes, chiefly fatty infiltration, 583 ; and amyloid degeneration, 585. 
Acute Yellow Atrophy, its probable nature, 586; characters of yellow and red 
tissue, 587. 
Inflammations of the liver, 587. The tropical abscess, 587; pysemic abscesses, 588. 
Chronic Interstitial Hepatitis or Cirrhosis, 589; nature of the process, 589; 
the new-formed connective tissue, 589; hypertrophic cirrhosis, 591; atrophy of 
hepatic tissue, 591; effects on circulation in the liver, 591. Perihepatitis, 650. 
Syphilitic Diseases of the liver: gummata and hepatitis, 594; congenital syphilis, 
595. 
Tuberculosis of liver, 595. 
Tumors, chiefly adenoma, 596; and cancer, primary and secondary, 598. 
Parasites, 600. 
Gall-stones, 601; single and multiple, 601; effects of their shifting, 602. 
Obstruction of ducts, causes, 602; results under different circumstances, 602. 
Tumors, 603. 
B.—The Bile-ducts and Gall-bladder. 
C.—The Pancreas. 
Hemorrhages, inflammations, 604; atrophy, fatty infiltration, tuberculosis, cancer, 
604; concretions and dilatation of pancreatic duct, 605. 
D.—The Peritoneum. 
Its relations and function, especially the power of absorption, 606. 
Disorders of the Circulation.—Active hyperaemia, 607 ; haematoma of the peri- 
toneum, 607. Ascites, 607. 
Inflammations.—Peritonitis, chiefly septic, 608. Chronic peritonitis, 610. 
Tuberculosis of the peritoneum—tubercular peritonitis, 610. Secondary tubercu- 
losis, rare, 611. 
Tumors, 612. 
The Secondary Extension of Cancers of the Abdominal Organs.—The 
secondary cancers of liver, 612; probable path of invasion, 612. Cancerous in- 
fection of the peritoneum, 614; relation to great omentum, diaphragm, etc., 615. 
DISEASES OF THE URINARY ORGANS. 
A.—The Kidneys and Ureters. 
Normal Structure and Function, 617. Arrangement of tubules, and blood- 
vessels, 617. Locality and conditions of secretion of urine, 618. 
Malformations and Misplacements, 620. Congenital malformations, including 
defect of one kidney, and horse-sboe kidney, 620. Movable kidney, 621. 
Compensatory Hypertrophy, 622. XX 
Disorders of the Circulation.—Active hyperasmia, 623; and passive, 623. 
Thrombosis, 623. Embolism, 624. 
Bright’s Disease, or Nephritis, 624. Caused by irritants brought by the blood, 
625; may attack specially one tissue, hence parenchymatous and interstitial 
nephritis, 626; acute nephritis from scarlet fever, cold, 626; chronic nephritis 
from gout, lead-poisoning, pregnancy, 626. Anatomical details. Glomerulo- 
nephritis, in acute nephritis, especially of scarlet fever, 626. Parenchymatous 
nephritis also chiefly acute, 627. Large white kidney, partly parenchymatous, 
partly interstitial, 631. Interstitial nephritis, usually chronic, 633; changes in 
glomeruli, 634; tubules, 634; formation of cysts, 635; bloodvessels, 636; the 
contracted kidney, 637. Albuminuria, 638; conditions of its occurrence, 639. 
Tube-casts, 639. Changes in heart and arteries and increased arterial tension, 
640; arterio-capillary fibrosis, 641 ; hypertrophy of middle coat, 641. Origin of 
increased tension from the kidney lesions, 641; its possible explanation from 
these, 643. 
Septic Inflammations, 645. Pysemic lesions, 645. Pyelonephritis, 647; path of 
entrance of septic organisms, 647; formation of abscesses, 648. Pyonephrosis, 
648. Pyelitis, 649. 
Retrograde Changes. Simple atrophy, parenchymatous infiltration, 649; fatty 
degeneration, 650. Amyloid degeneration, structures involved, 650; combination 
of amyloid and contracted kidney, 651. Concretions and calculi : biliary, 653; 
uric acid, etc., 653. 
Syphilis and Tuberculosis, 654. Renal phthisis a local tuberculosis, 654. 
Hydronephrosis, causes and mode of occurrence, 655. Occurrence of pyonephrosis, 
657 ; and independent cysts, 657. 
Tumors.—Simple cysts, 657. Cystoid degeneration, 658. Primary cancer, 659. 
Secondary cancers, 659. Sarcoma, etc., 659. 
Parasites.—Echinococcus, 660; filaria sanguinis, 660. 
CONTENTS. 
Congenital Malformations.—Extroversion, etc., 660. Rupture and perforation, 
661. Results of extravasation of urine, 661. Dilatation and hypertrophy, 
661 ; hypertrophy of muscular coat, 662 ; diverticula, 662. 
Disorders of the Circulation.—Passive hemorrhage, 662. Inflam- 
mations, chiefly from decomposition of urine, 663; character of urine, 664. 
Tuberculosis of the bladder, 664. Tumors, chiefly papilloma, cancer, cysts, 665. 
Parasites, 666. 
Concretions and Calculi.—Their chief constituents and causation, 666. Calculi 
composed of uric acid ; urates ; oxalate, 667 ; phosphates ; carbonate ; cystine ; 
xanthine, 668. 
Diseases of the Urethra.—Gonorrhoea, stricture, 668. 
B.—The Urinary Bladder and Urethra. 
DISEASES OF THE FEMALE GENERATIVE ORGANS. 
Malformations, including the various forms of Hermaphroditism, 670 ; and Pseudo- 
hermaphroditism, 671. Defect of uterus, etc., 672. Double uterus, 672; horned 
uterus, 673. 
A.—The Uterus and Vagina. 
Misplacements of the Uterus.—Arrangements for retention of the uterus in 
place, 674. Prolapse or descent, 674; procidentia, 675. Prolapse of vagina, 
675. Inversion of uterus, 675. Flexions and versions, 675. CONTENTS. 
XXI 
Atrophy, Hypertrophy, and Dilatation.—Atrophy and hypertrophy, 676; 
hypertrophy of cervix, 677. Dilatation from accumulation of contents, 677. 
Inflammations of Uterus and Appendages.—Endometritis, 678. Metritis, 678. 
Pelvi-peritonitis or perimetritis, 678. Pelvic cellulitis or parametritis, 679. 
Puerperal Fever, a septic disease, 679. The local lesions and their extension, 680. 
Phlegmasia dolens, 681. Periuterine hematocele, 681. 
Extrauterine Pregnancy, 682. 
Syphilis and Tuberculosis of Uterus, 683. 
Tumors.—Hsematoma, 684. Myoma, 685; suhserous; intraparietal; submucous 
forms, 685; structure and secondary changes, 686. Cancer, soft or medullary, 
688; epithelial; the cauliflower excrescence, 689 ; colloid, 690. Mucous polypi, 
sarcomas, etc., 690. 
Parasites, 691. 
B.—Ovaries, Fallopian Tubes, Ligaments. 
Ovarian Hernia, usually congenital, 691. 
Inflammations, of Fallopian tubes, 692; of ovaries, 692; chronic oophoritis, 692; 
formation of cysts, 693. Tuberculosis of the ovary and tubes, 693. 
Tumors.—Simple cysts, 694. Colloid ovarian cyst, or Cystoma, 695; origin and 
structure, 695: appearances, 697 ; secondary changes, 697; chiefly fatty degen- 
eration, hemorrhage, inflammation, 698; perforation, 698. Dermoid cysts, 698. 
Cancer, 699. Sarcoma, 700. Cysts of the broad ligaments, Parovarian, 700; 
their origin, 701; and connections, 701. Comparison of ovarian and parovarian 
cysts, 702. 
C.—The Mammary Gland. 
Malformations, 703. Inflammations, acute and chronic, 703. 
Tumors.—Adenoma, 704; adenoid sarcoma and sarcoma, 704; cysto-sarcoma, 706. 
Cancer, parenchymatous and duct cancers, 707 ; connection with Paget’s disease 
of the nipple, 708. Creighton’s views of cancers of breast, 708. Forms of cancer: 
scirrhus, 708; medullary, 710; acute scirrhus, 711; colloid, 711. Other 
tumors, 711. 
DISEASES OF THE MALE GENERATIVE ORGANS. 
A.—The Testicles. 
Malformations and Misplacements.—Imperfect descent; congenital hernia, 712. 
Inflammations, 712; acute and chronic orchitis, 713. Syphilitic disease, 713. 
Tuberculosis, 714. Tumors—Sarcoma and cysto-sarcoma, 714; cancer, 715; 
other tumors, 715. 
Hydrocele and hsematocele, 715. Congenital hydrocele, 716. Spermatocele or 
encysted hydrocele, 716. 
B.—The Penis and Scrotum. 
Ulcers or chancres, Condyloma, Cancer, 717. Lymph-scrotum, 717. Hypertrophy 
of prostate, 718. Concretions in prostate, 718. » XXII 
CONTENTS. 
DISEASES OF THE BONES AND JOINTS. 
A.—The Bones. 
Introduction.—Structure and growth of hone. Metaplasia, 719 
Rickets.—Its causes in malnutrition, 721; artificial production, 722. Normal 
ossification from cartilage and periosteum, 724. The ossifying cartilage in 
rickets, 724. The periosteal ossification, 726. Deformities of the hones in 
rickets, 726 ; of the long bones, chest, vertebrae, pelvis, head (craniotahes), 728. 
Recovery from rickets, 729. 
Osteomalacia, 729. Causes, 730. Forms of softening of the bones, 730. De- 
formities resulting, 731. 
Inflammations of Bone.—Changes chiefly in the soft structures, 731. Condensing 
and rarefying osteitis, 732 ; part taken by osteoblasts and osteoclasts, 732. Caries, 
733. Absorption of bone, 733 ; (Transplantation of bone, 734;) process of absorp- 
tion of dead, 734; and living bone, 734. Healing of fractures, 736; callus, 736. 
Periostitis ; chronic periostitis frequently secondary, 737 ; suppurative or malig- 
nant, and simple acute periostitis, 737. Osteomyelitis, 738. 
Necrosis of Bone.—Separation of dead from living, 738; formation of new bone, 
739. Phosphorus-necrosis, 739. 
Syphilitic Disease of Bones.—Gumma, with periostitis, 740. Hereditary syphilis, 
changes chiefly in long bones, 740. 
Tubercular Disease of Bones, 742. 
Spinal Curvatures.—The normal structure and curves of the spine, 743. Forms 
of curvature, 744. Pott’s disease, 744. Kyphosis, 745. Lordosis, 745. Lateral 
rotatory curvature, 746. 
Tumors of Bone.—Osseous tumors, related to inflammation, osteophytes, hyper- 
ostosis, exostosis, 748. Osteoid chondroma, 748. Sarcoma, 750; myelogenous, 
750; interstitial, 750; and periosteal, 751. Cancers, 751. Cysts, especially of 
the jaws, 752. 
B.—The Joints. 
Dislocations and Misplacements.—Congenital dislocations, 753. Talipes, con- 
genital and acquired, 753; its forms, 753. Traumatic dislocations, 754; mode 
of occurrence, 755; secondary changes, 755. Spontaneous dislocations, 755. 
Anchylosis, 755. 
Inflammations of Joints, 756. Simple acute arthritis, 756. Pysemic arthritis, 
757. Acute rheumatic arthritis, 757. Gouty arthritis, 758. Chronic rheumatic 
arthritis and arthritis deformans (morbus coxae senilis), 759. Scrofulous or 
tubercular arthritis, 760; changes in synovial membrane, ends of bones, carti- 
lage, etc., 760; caries, 761. 
Introduction.—Normal structure, 762. 
Hyperemia, Hemorrhage, and (Edema, 764. 
Retrograde Changes.—Simple atrophy of skin, 765; hairs (alopecia, canities), 
765 ; and nails, 766. 
Inflammations.—General subject illustrated by case of flea-bite, 766. Causation of 
cutaneous inflammations and connection with nervous system, 767. Forms of 
cutaneous inflammations. I. Symptomatic, in acute fevers, 768—smallpox 
DISEASES OF THE SKIN. XXIII 
CONTENTS. 
eruption a typical example, 768. II. Inflammatory skin eruptions, 770. (1) 
Erythema and roseola, 770. (2) Eczema in its various forms, 770. (3) Psoriasis, 
772. (4) Pityriasis rubra, 772. (5) Lichen ruber, 772. (6) Prurigo, 773. (7) 
Pemphigus, 773. (8) Acne, 773; its connection with comedo, 774; and milium, 
774; acne rosacea, 774. III. Traumatic and non-infective inflammations. 
(1) Burns and scalds, 774 ; in their three degrees, 775 ; collapse after burns, 775. 
(2) Frost-bite and chilblain, in three degrees, 776. (3) Boil and carbuncle, 776. 
(4) Wounds and excoriations, 777. (5) Ulcers, 777. IY. Infective inflamma- 
tions. (1) Lesions from cadaveric poisons, 778. (2) Erysipelas, 779. (3) Phleg- 
monous inflammations, 780; malignant oedema, 780. (4) Splenic fever or malig- 
nant pustule, 780. (5) Infective tumors, especially framboesia, 781. 
Syphilitic Skin Affections.—Chancre, 782; skin eruptions, 782; and gumma, 783. 
Tropho-neuroses.—(1) Herpes, its anatomical characters, 784 ; caused by lesions of 
nerves, spinal cord, brain (general herpes), 784. (2) Glossy skin, 785. (3) 
Morphoea and scleroderma, 785 (sclerema neonatorum, 786). (4) Acute bed- 
sore, 787. 
Hypertrophies and Tumors.—Callosity, 787 ; corn, 787; ichthyosis, 787. Wart 
and horn, 788. Keloid, true and false, 788. Soft warts and moles, 789. Mol- 
luscum eontagiosum, 789. Fibroma molluscum, 789. Xanthoma, 790. Ele- 
phantiasis, 790. Sarcoma, 790. Epithelioma in its infiltrating, 791; and flat 
forms, 793 (rodent ulcer, 793). Ordinary cancer, 794. 
Parasitic Affections.—Favus, 794; ringworm, 796; pityriasis versicolor, 796. 
Scabies, 797. Larvie of insects, 797. 
Addendum.—Actinomycosis, 798. LIST OF ILLUSTRATIONS. 
FIG. PAGE 
1. Blood in pernicious amemia . . . . . . .30 
2. Medulla of bone in pernicious amemia . . . . .30 
3. Endothelium in normal capillaries . . . . .37 
4. Capillaries in passive hypersemia . . . . . .37 
5. Crystals of hsematoidin from thrombus in vein . . . .44 
6. Organization of blood-clot . . . . . . .45 
7. Diagram of embolism of end-artery . . . . . .48 
8. Embolic infarction of kidney . . . . . . .51 
9. Infarction of kidney undergoing absorption . . . . .53 
10. Oil embolism of lung ........ 55 
11. Crystals of hasmatoidin from hemorrhage in brain . . . .58 
12. Crystals of haemin, prepared artificially . . . . .59 
13. Cells containing red-blood corpuscles . . . . .59 
14. Serous spaces and lymphatic capillaries . . . . .62 
15. Injection of capillary bloodvessels, serous spaces, and lymphatic capiliaries, . 63 
16. Charcot’s crystals in leukajmia . . . . . .67 
17. Bone-marrow in leukaemia . . . . . . .68 
18. Leukaemic formations in liver . . . . . .69 
19. Leucocytes of frog containing granules of vermilion . . .71 
20. Liver in melanaemia . . . . . . . .71 
21. Leucocyte showing amoeboid movement . . . . .84 
22. Inflamed human omentum . . . . . . .90 
23. Fibrinous exudation in pneumonia . . . . . .92 
24. Bloodvessels of granulating wound . . . . . .96 
25. Granulation cells in their various forms . . . . .97 
26. New formation of bloodvessels in a granulating wound . . .98 
27. Semidiagrammatic section of a granulating wound, .... 100 
28. Coagulation necrosis in muscle ...... 109 
29. Coagulation necrosis in muscle ...... 109 
30. Necrosis in pyajmic lesion in kidney . . • . . . .110 
31. Cloudy swelling in renal epithelium, . . . . . .117 
32. Fatty degeneration in vessels of brain . . . . .119 
33. Fatty degeneration in atheromatous aorta . . . . .120 
34. Fatty degeneration in cancer cells . . . . . .120 
35. Crystals of cholestearine ....... 121 
36. Fatty infiltration of voluntary muscle ..... 123 
37. Fatty infiltration of hepatic cells ...... 124 
38. Colloid degeneration in ovarian cyst ...... 127 
39. Calcareous infiltration in a tumor, ...... 129 
40. Calcareous infiltration of cysts of trichina . . . . .130 
41. Calcareous infiltration of middle coat of artery .... 130 
42. Amyloid disease of liver ....... 132 LIST OF ILLUSTRATIONS. 
XXVI 
FIG. PAGE 
43. Amyloid capillaries of liver ....... 133 
44. Corpora amylacea, ........ 135 
45. Division of cells . . . . . . . .138 
46. Elongation and curvature of tibia from hypersemia . . . .141 
47. Regeneration of epithelium in cornea of rabbit .... 145 
48. Section of hard chancre (syphilitic) . . . . . 148 
49. Gumma of kidney . . . . . . . .150 
50. Gumma of liver ........ 151 
51. Portions of same more highly magnified ..... 152 
52. Miliary tubercles in lung ....... 154 
53. Tubercle from a bronchial gland ...... 155 
54. Tubercle in artery of pia mater . . . . . .156 
55. Tubercular ulcer of intestine . . . . . . .159 
56. Tubercular bacillus ........ 161 
57. Lung in bovine tuberculosis ....... 165 
58. Appearance of face in leprosy ....... 167 
59. Elephantiasis of labia majora ....... 176 
60. Hyperostosis of bones of leg in elephantiasis . . . . .177 
61. Lipoma in wall of stomach ....... 179 
62. Pendulous lipoma of appendices epiploicae . . . . .180 
63. Portion of hydatid mole ....... 181 
64. Microscopic section of subcutaneous myxoma .... 182 
65. Myxoma of nerve stem ....... 183 
66. Multiple internal enchondromata of fingers . . . . .184 
67. Spongy exostosis of femur ....... 186 
68. Ivory exostosis of frontal bone (internal surface) .... 186 
69. Multiple exostoses of frontal bone ...... 187 
70. Microscopic section of myoma, stained ..... 188 
71. Isolated muscle cells from a myoma . . . . . .189 
72. Calcareous infiltration in a myoma ...... 190 
73. Amputation neuroma ........ 191 
74. Microscopic section of a neuroma ...... 192 
75. Section of painful subcutaneous tumor ..... 192 
76. Structure of same after maceration in nitric acid .... 193 
77. Section of skin in venous naevus ...... 193 
78. Cavernous angioma of liver . . . . . . .194 
79. Adenoma of mamma ........ 195 
80. Psammoma ......... 197 
81. Formation of mucous cysts ....... 199 
82. Hydronephrosis with granular atrophy of kidney .... 200 
83. Congenital cystic kidney ....... 201 
84. Dropsy of Graafian vesicles ....... 201 
85. Papilloma of larynx ........ 203 
86. Hair-follicle, etc., from dermoid cyst of ovary .... 204 
87. Round-celled sarcoma ........ 206 
88. Spindle-celled sarcoma ........ 207 
89. Large fungating spindle-celled sarcoma of foot .... 207 
90. Adenoid sarcoma of mamma ....... 208 
91. Giant-celled sarcoma ........ 208 
92. Stroma of soft cancer . . . . . . . .211 
93. Section of growing margin of an epithelioma .... 212 FIG. PAGE 
94. Tubule from margin of cancer of kidney ..... 213 
95. From epithelioma of skin, penetrating cylinders with signs of irritation . 214 
96. Cancer cells showing fatty degeneration ..... 215 
97. Structure of flat-celled epithelioma . . . . . .216 
98. Structure of cylinder-celled epithelioma . . . . .217 
99. From scirrhus of mamma showing cells and stroma . . . 219 
100. Cells from cancer of mamma ....... 219 
101. Colloid cancer ......... 220 
102. Colloid cancer, changes in cells ...... 220 
103. Colloid cancer, infiltrating muscle ...... 221 
104. Swarms of bacteria ........ 226 
105. Bacteria in pus-corpuscles ....... 226 
106. Two forms of bacilli ........ 227 
107. Tubercular bacillus . . . . . . . .227 
108. Blood in septicaemia of mice and in splenic fever .... 234 
109. Vein in septicaemia of mice ....... 235 
110. Pyaemic abscess in kidney ....... 239 
111. Micrococci in capillary of kidney in pyaemia, .... 240 
112. Bacillus anthracis and that of septicaemia of mice .... 243 
113. Villus of intestine in splenic fever ...... 243 
114. From same, more highly magnified ...... 244 
115. Spirillum Obermeieri ........ 245 
116. Typhoid bacillus ........ 245 
117. Micrococci in skin in erysipelas ...... 246 
118. Bacteria in capillary of kidney in scarlet fever .... 247 
119. Sarcinae ventriculi in vomited matter . . . , .254 
120. Aerial growth of penicilium ....... 255 
121. Formation of conidia in submerged portion of same . . . 255 
122. Fungous growth in kidney ....... 256 
123. Hair containing spores of fungus from ringworm .... 258 
124. Leptothrix buccalis ........ 259 
125. Oidium albicans in thrush ....... 260 
126. Distoma hepaticum ........ 261 
127. Distoma sinense ........ 262 
128. Taenia solium, head ........ 263 
129. Taenia solium, unripe proglottis ...... 263 
130. The globular body, or Mellis’s body ...... 264 
131. Taenia solium, branching of uterus ...... 264 
132. Taenia solium, fully developed uterus ..... 265 
133. Taenia solium, ova ........ 265 
134. Taenia solium, cysticerci in muscle ...... 266 
135. Taenia solium, head of cysticercus cellulosae ..... 266 
136. Taenia solium, development of cysticercus ..... 267 
137. Taenia solium, hooks of cysticercus ...... 267 
138. Hooks of echinococcus ....... 268 
139. Taenia solium, movements of head in intestine .... 268 
140. Taenia mediocanellata, head, extended and contracted . . . 269 
141. Taenia mediocanellata, unripe proglottis ..... 270 
142. Taenia mediocanellata, ripe proglottis ..... 270 
143. Taenia echinococcus, adult or strohila ..... 270 
144. Taenia echinococcus, diagram of development of brood-capsules . . 271 
LIST OF ILLUSTRATIONS. 
XXVII XXVIII 
FIG. PAGE 
145. Taenia echinococcus, brood-capsules ...... 272 
146. Taenia echinococcus, chitinous membrane of old hydatid cyst . . 273 
147. Bothriocephalus latus, natural size ...... 274 
148. Bothriocephalus latus, head and part of the body . . . .274 
149. Bothriocephalus latus, proglottis showing female organs . . .275 
150. Trichina spiralis in muscle . . . . . . .276 
151. Filaria sanguinis, embryo with sac ...... 280 
152. Filaria sanguinis as seen in drop of blood ..... 281 
153. Defect of inter-ventricular septum ...... 287 
154. Congenital adhesion of curtains of pulmonary valve . . . 288 
155. Congenital malformation of aortic valve, two curtains . . . 290 
156. Exaggerated fenestration of aortic valve, approach to condition of cuspid 
valve ......... 291 
157. Hypertrophy of left ventricle ...... 298 
158. Hypertrophy of right ventricle ...... 298 
159. Fatty degeneration of the heart, low power . . . . .301 
160. Fatty degeneration of the part, higher power .... 301 
161. Calcareous infiltration of muscular tissue of heart .... 302 
162. Calcareous infiltration of muscular tissue of heart, other form . . 303 
163. Aortic valve in acute endocarditis, warty vegetations . . . 307 
164. Mitral valve in chronic endocarditis ...... 309 
165. Ulcerative endocarditis, section of edge of valve .... 311 
166. Ulcerative endocarditis, lesion in kidney ..... 312 
167. Soldier’s spot on pericardium . . . . . .317 
168. Aneurism of valve, diagram of formation . . . . .318 
169. Diagram of funnel-shaped deformity of mitral valve . . . 322 
170. Diagram of aortic insufficiency ...... 323 
171. Globular thrombi in left ventricle ...... 328 
172. Longitudinal section of artery at seat of ligature .... 331 
173. Atheroma of aorta ........ 333 
174. Atheroma of femoral artery ....... 334 
175. Fatty degeneration of middle and internal coats in atheroma . . 335 
176. Atheroma of cerebral artery . . . . . . 336 
177. Normal cerebral artery ....... 336 
178. Endarteritis obliterans ....... 337 
179. Calcareous infiltration of middle coat of artery .... 339 
180. Calcareous infiltration of middle coat of artery .... 339 
181. Syphilitic arteritis, ........ 341 
182. Aneurism with tunnelled clots at openings of branches . . . 347 
183. Section of dissecting aneurism ...... 351 
184. Hemorrhoids of rectum ....... 354 
185. Section of normal lymphatic gland ...... 358 
186. Section of normal spleen ....... 364 
187. Section of sago spleen ........ 370 
188. Diffuse amyloid disease of spleen . . . . . .371 
189. Transverse section of a nerve ....... 375 
190. Medullated nerve fibres ....... 376 
191. Transverse section of a neuroma ...... 380 
192. Sections of spinal cord from cervical and lumbar swellings, showing groups 
of ganglion cells ........ 381 
193. Similar section from dorsal region ...... 382 
LIST OF ILLUSTRATIONS. FIG. PAGE 
194. Cervical.enlargement showing arrangement of fibres . . . 383 
195. Medulla oblongata at various levels ...... 384 
196. Gray degeneration or sclerosis of cord ..... 385 
197. Descending gray degeneration in medulla and cord .... 386 
198. Ascending and descending degeneration in cord .... 389 
199. Amyloid bodies from cord ....... 394 
200. Posterior sclerosis in early stage, limited extension .... 394 
201. Anterior poliomyelitis on one side ...... 398 
202. Cord in progressive muscular atrophy ..... 401 
203. Medulla oblongata at level of fourth ventricle .... 402 
204. Muscle in pseudo-hypertrophic paralysis ..... 403 
205. Cervical enlargement in pseudo-hypertrophic paralysis . . . 404 
206. Lumbar enlargement from the same ...... 405 
207. Section of pons varolii ....... 407 
208. Horizontal section of brain of child ...... 408 
209. Lateral aspect of cerebral hemisphere ..... 410 
210. Internal aspect of cerebral hemisphere ..... 412 
211. Arteries of brain showing cortical distribution .... 413 
212. Pons in descending gray degeneration . . . . .415 
213. Atheroma of small cerebral artery . . . . . .417 
214. Sacculated miliary aneurism of nutritive artery .... 422 
215. Fusiform miliary aneurism ....... 423 
216. Crystals of hsematoidin from cerebral hemorrhage .... 425 
217. Fatty degeneration ef vessels in cerebral softening .... 426 
218. Bloodvessel surrounded by leucocytes from medulla oblongata in hydro- 
phobia . . . . . . . . 432 
219. From parotid gland in hydrophobia . . . . . .433 
220. From a glioma of the brain ....... 440 
221. Arteries of the pia mater in tubercular meningitis .... 447 
222. Section of spina bifida ....... 451 
223. Papilloma of larynx ........ 464 
224. Section of lung in early stage of emphysema .... 478 
225. Perforation of alveolus in emphysema . . . . .479 
226. Lung alveolus from a hemorrhagic infarction .... 486 
227. Fat embolism of lung ........ 488 
228. Cast of infundibulum and air-vesicles in pneumonia . . . 490 
229. Alveolus filled with fibrine and a few leucocytes in pneumonia . . 491 
230. Lung in gray hepatization ....... 492 
231. Chronic pneumonia ........ 495 
232. Tubercular ulcer of bronchus. ...... 504 
233. Lung in caseous form of phthisis ...... 508 
234. Lung tissue from sputum in phthisis ..... 510 
235. Embolic cancer of lung ....... 517 
236. The same showing epithelial masses ...... 518 
237. Sputum with carbonaceous particles from anthracosis . . . 520 
238. Oidium albicans or thrush-fungus ...... 527 
239. Section of syphilitic chancre of lip . . . . . 529 
240. Section of tooth, showing caries and secondary dentine . . . 532 
241. Perforating ulcer of the oesophagus . . . . . . 539 
242. Large polypoid myoma of the oesophagus ..... 540 
243. Dilatation of the stomach ....... 544 
LIST OF ILLUSTRATIONS. 
XXIX XXX 
LIST OF ILLUSTRATIONS. 
FIG. PAGE 
244. Twisting of the intestine ....... 560 
245. Large cyst of vermiform appendage ...... 566 
246. Typhoid bacillus ........ 569 
247. Peyer’s patch in typhoid fever ...... 570 
248. Typhoid Peyer’s patch, diagrammatic representation . . . 571 
249. Tubercular ulcer of the intestine ...... 573 
250. Tubercular ulcer, microscopic section ..... 574 
251. Cylinder-celled epithelioma of rectum ..... 575 
252. Passive hyperaemia of the liver ...... 581 
253. Fatty infiltration of liver, general view ..... 584 
254. Fatty infiltration in isolated hepatic cells ..... 585 
255. Acute yellow atrophy of liver ...... 586 
256. Cirrhosis of livor, early stage ....... 590 
257. Advanced cirrhosis of liver . . . . . . . 592 
258. Gumma of liver ........ 595 
259. Miliary tubercle in liver ....... 596 
260. Cavernous angioma of liver ....... 597 
261. Secondary cancer of liver ....... 599 
262. Disseminated cancer of the peritoneum ..... 615 
263. Section of normal kidney ....... 618 
264. Diagram of course of uriniferous tubules ..... 619 
265. Horse-shoe kidney ........ 621 
266. Embolic infarction of kidney ...... 624 
267. Glomerulo-nephritis, exudation of leucocytes .... 628 
268. Glomerulo-nephritis, hemorrhage ...... 629 
269. Glomerulo-nephritis, increase of epithelium ..... 629 
270. Glomerulo-nephritis, great increase of epithelium .... 630 
271. Large white kidney, microscopic appearances .... 631 
272. Normal kidney for comparison ...... 632 
273. Interstitial nephritis, sclerosis of glomerulus .... 634 
274. Section of contracted kidney, showing contortion of structures . . 635 
275. Normal kidney, for comparison ...... 636 
276. Endarteritis obliterans in contracted kidney ..... 637 
277. Arteries of pia mater in chronic Bright’s disease and normal case . . 641 
278. Septic embolism of kidney ....... 646 
279. Micrococci in capillary of kidney in pyaemia .... 647 
280. Bacteria in capillary of kidney in scarlet fever .... 647 
281. Cloudy swelling of renal epithelium ...... 650 
282. Amyloid degeneration affecting basement membrane of uriniferous tubules . 651 
283. Amyloid and contracted kidney ...... 652 
284. Kidney in hydronephrosis ....... 656 
285. Cystoid degeneration of the kidney ...... 658 
286. Uriniferous tubule at border of advancing cancer . . . . 659 
287. Stratified chitinous membrane from hydatid cyst of kidney . . 660 
288. Large diverticulum of the urinary bladder ..... 663 
289. Tuberculosis of the bladder ....... 665 
290. Kudimentary uterus ........ 672 
291. Uterus hicornis . . . . . . . . 673 
292. Uterus unicornis ........ 673 
293. Polypoid hsematoma of the uterus ...... 684 
294. Section of myoma of uterus showing nuclei ..... 686 LIST OF ILLUSTRATIONS. 
XXXI 
FIG- PAGE 
295. Myoma with calcareous infiltration ...... 687 
296. Cancer of uterus, infiltrating muscular wall ..... 688 
297. Cancer of uterus and vagina, naked-eye appearance . . . 689 
298. Cauliflower cancer of uterus ....... 690 
299. Cystic formation in ovary from dilatation of Graafian vesicles . . 693 
300.. Tuberculosis of Fallopian tubes ...... 694 
301. Glandular tissue in wall of ovarian cyst ..... 695 
302. The same showing goblet cells ...... 695 
303. From wall of ovarian cyst, showing smaller cysts .... 696 
304. From wall of dermoid cyst, showing sebaceous glands . . . 699 
305. Hair and appendages from wall of dermoid cyst .... 699 
306. Diagrammatic view of uterus and appendages .... 701 
307. Section of adenoma of mamma ...... 704 
308. Adenoid sarcoma of mamma ....... 705 
309. Dilated glandular spaces, and intra-cystic growth in cysto-sarcoma of 
mamma ......... 706 
310. Cartilage from sarcoma of mamma ...... 707 
311. Section of scirrhus of mamma . . . . . .709 
312. Cells from scirrhus of mamma ...... 710 
313. Section of fractured rib, showing new-formed connective tissue, cartilage, 
and bone ......... 720 
314. From same, showing continuity of cartilage and bone . . . 721 
315. Normal ossification from cartilage ...... 722 
316. Longitudinal section of ossifying margin in rickets . • . . . 723 
317. Bone in osteomalacia . ... . . . . . 730 
318. New formation of hone in connection with inflammation . . . 733 
319. Bone in process of absorption showing Howship’s lacunae . . . 734 
320. From same, showing giant-cells (osteoclasts) and Howship’s lacunae . 735 
321. Hyperostosis of hones of leg in elephantiasis .... 737 
322. Rotation of vertebrae in lateral curvature ..... 746 
323. Section of chest in lateral curvature, compared with normal . . 747 
324. Multiple exostoses in hones of leg . . . . . .749 
325. Osteoid chondroma ........ 749 
326. Cyst of head of fibula . . . . . . .752 
327. Urate of sodium in the articular cartilage in gout .... 758 
328. Section of normal skin, epidermic layer and hair .... 763 
329. Section of smallpox pustule of skin ...... 769 
330. Section of smallpox eruption with necrosis ..... 770 
331. Micrococci in pus corpuscles from cadaveric pustule . . . 779 
332. Skin in erysipelas, micrococci in lymph-spaces .... 780 
333. Section of skin in frambcesia ....... 781 
334. Epithelioma with penetration of epidermis ..... 791 
335. Epithelioma showing laminated capsules, etc. .... 792 
336. Epithelioma, showing ingrowing processes and irritation of skin . . 793 
337. Achorion Schoenlenii from favus ...... 794 
338. Tricophyton tonsurans in a hair from ringworm .... 795 
339. Microsporon furfur from Pityriasis versicolor .... 796 A manual of pathology. 
INTRODUCTION. 
Pathology may be defined as the study of diseases not in 
their manifestations merely, but in their essential nature. There 
are various conditions met with from day to day which we name 
diseases. They produce certain alterations in the feelings of the 
person affected which induce him to say he is not well, and they 
in many cases lead to changes in the condition of the bodily frame 
which can be actually observed by the physician, and may enable 
him to come to a conclusion as to the actual disease which is 
present. These subjective phenomena and those objective signs 
are mere indications of the presence of something which we call 
the disease or morbid process; and it is surely incumbent on every 
one who undertakes to treat disease, not to content himself with 
a knowledge of its manifestations merely, but to satisfy himself 
as to its real nature. 
And here, at the very outset of our study of Pathology, it is to 
be remarked that we have to do with diseases, not disease in the 
abstract. There are certain definite conditions which the body 
presents, and which are recognized as morbid states, or conditions 
different from those of health, and our object is to find out what 
is the nature of these morbid states. Endless discussions might 
be raised as to the nature and causes of disease in the abstract; 
but we shall arrive at much more reliable conclusions if we study 
the individual states of disease and leave those more general dis- 
cussions aside. 
Without going into any general discussion as to the nature of 
disease as a whole, there is one subject which here calls for some 
consideration, namely, the relation of diseased to healthy con- 
ditions. Physiology is the study of the body and its actions in 
health/and it is not to be supposed that in disease these physio- 
logical processes suddenly cease. So far as the diseased condition 
is concerned, these processes are modified, and they must be 
studied under the altered circumstances; but in the study of each 
pathological condition the physiological must be taken as the basis. 
A knowledge of physiology is the necessary preliminary to the 
study of Pathology. It may be said, indeed, that the pathological 
processes are merely the physiological ones altered. In disease 18 
A MANUAL OF PATHOLOGY". 
there is something disturbing the natural processes, and there is 
an endeavor, as it were, on the part of the body to over the 
disturbance, and the phenomena of the disease are not infrequently 
the expression of the resistance which the natural processes present 
to the disturbing element. These normal processes must be taken 
into account, therefore, and, as we shall see further on, the physio- 
logical laws are really in essence identical with the pathological. 
We have to study the nature of diseases, and this will bring us 
into close connection with their causes. Much has been written 
concerning the causes of disease in general, and much that is 
valuable, but this study of itself would be almost sufficient to fill 
a volume. It will be enough here if we consider, as each disease 
comes under review, whether it is traceable to any definitely dis- 
tinguishable cause or causes. In some acute febrile diseases, we 
are able to predicate the existence of viruses, and even the nature 
of some of these viruses is to some extent known. Whatever is 
known as to the cause of diseases will assist in elucidating their 
nature. 
In the study of diseases in their nature, there are three main 
sources from which assistance is to be obtained; one may be desig- 
nated Experimental Pathology, another Pathological Anatomy, 
and the third Clinical Observation. John Hunter may be said 
to have laid the foundation of experimental pathology. So far as 
it can be prosecuted, this mode of study is calculated to afford us 
the most directly trustworthy information as to the nature of dis- 
eases, and much of the advance in modern pathology is due to this 
line of study. If we can actually induce a given disease in an 
animal, we have found out much as to its causation, and are in the 
way of finding out much as to its nature. In some cases we are 
able actually to observe the morbid processes in the living animal. 
Or, we can kill the animal at various periods after the onset of the 
disease, and observe the results at various stages. We can vary 
the experiment in different ways, so as to eliminate on one side 
and another the various elements, and so reduce the problem to its 
simple and necessary parts. Experimental pathology has carried 
us far towards understanding many of the conditions in disease. 
Reference need only be made to the reformations which this line 
of study has effected in our knowledge of Inflammation, Em- 
bolism, Tuberculosis. 
The study of morbid anatomy is not likely to effect such revolu- 
tions in Pathology as experimental pathology, but in the training 
of the individual medical student it is calculated to play an even 
more important part in giving him an understanding of the nature 
of the diseases he has to deal with. Morbid anatomy gives us the 
physical changes which disease produces in the body. These 
changes are, as it were, the expression of the pathological pro- 
cesses, and are only to be regarded as indications of the existence 
of these processes. It is probable that all morbid processes pro- 
duce changes in structure, although the changes may elude our 19 
INTRODUCTION. 
observation. For the most part, however, we are able to associate 
the change of structure with the morbid process, and the observed 
change leads us up to the actual nature of the disease. In fact, 
the nature of disease might be studied on the basis of the morbid 
structure, advantage being taken also of all information from the 
side of experimental pathology and clinical observation. 
Morbid Anatomy is the study of the structural changes in all 
periods and stages of the disease. It is sometimes objected to this 
mode of study that in observing the state of the tissues after death 
we see only the last stages of disease, and in some cases only the 
results. This, however, is not the case. Every clinical observer 
will admit that in the same disease the fatal issue occurs in different 
cases under the most diverse circumstances. Death ensues, as a 
rule, when by reason of defective nutrition, or a .deficiency in the 
supply of oxygenated blood mainly by interference with the respi- 
ration, the functions of the body can no longer be carried on. 
ilow there is in different individuals an infinite variety in the vigor 
of the vital processes, so that a condition which in one will very 
slightly affect the essential phenomena of life, will, in another, 
seriously compromise them. This is an experience of our every- 
day life. And so it happens that patients die in all stages of dis- 
ease. Even in the same case we are often able to study the various 
changes in their different stages. 
As an illustration of wdiat is meant, take the case of pneumonia 
or acute inflammation of the lungs. Patients die in this disease, 
as a rule, from failure of the heart and consequent cessation of the 
circulation; but the paralysis of the heart is not related solely to 
the condition of the lungs. It is often much more closely related 
to the elevation of temperature which is to be traced to changes 
in the nervous system, while the powers of resistance of the heart 
in each person are an important element in the matter. And so 
it happens that one man will die with a limited and advancing 
pneumonia, while another will survive through a very extensive 
condensation. The lung at death in the one case is in the same 
stage of disease as in the other at a certain date during life. We 
can study the nature of the disease in the former and we are surely 
warranted in assuming that in the patient who survived, the state 
of the lung is virtually identical with that of the patient who died. 
Again, in a carcinoma growing up to death, we have, at the 
growing margins of the tumor, changes which are the same as 
those by which the tumor has all along been extending, and we 
can study the methods of its growth as well as its relations to the 
structures in which it has been growing. 
Thus it is that, although morbid anatomy by itself may in some 
cases throw little light on the nature of the disease, yet, taken as 
an expression of the morbid process, it is of the highest value. 
It may be added that as similar processes must have similar 
changes as their correlatives, we may take these changes as a kind 
of test of the existence of the processes. 
In referring to processes and changes, it must be understood that 20 
A MANUAL of pathology. 
the finer structure of the body is taken into account. In Patho- 
logical Anatomy, we include Pathological Histology, and it may 
indeed be said that, as the coarser, naked-eye appearances are 
merely the expression of the finer structural details, so we shall 
not understand the former unless we are able to refer them to the 
latter. We can have no accurate idea of the proper structure of 
the normal liver by simply looking at it with the naked eye, and 
we can have little insight into its morbid conditions by the same 
method of observation. The morbid conditions, however, do gen- 
erally cause changes in the naked-eye appearances, and this is of 
great consequence as enabling us, when roughly examining an 
organ, to infer that its structure is changed. But these macro- 
scopic appearances are only useful when they are used to throw 
light on the microscopic changes or to direct attention to them. 
The really important processes are those which concern the finer 
elements of the tissues, and so it is to these that we shall chiefly 
attend in studying the various forms of disease. 
Clinical observation is of great importance in the study of 
pathology, and that in various ways. If what has been stated 
above be correct, then it is the processes occurring during life 
that are the real subject of study in pathology, and it is only by 
careful clinical observation that we are able to get, as it were, into 
close relations with these processes during their actual currency. 
Clinical Observation and Pathological Anatomy should thus be 
taken as mutually elucidating each other, and as working together 
towards just conceptions as to the nature of the conditions con- 
cerned. 
There is another aspect in which clinical observation is of im- 
portance in relation to pathology. The pathologist, if conversant 
only with morbid anatomy and experimental pathology, is apt to 
form a too mechanical and simple conception of the processes in- 
volved, and is likely to theorize on the basis of a too-limited view 
of the subject. Clinical Observation is a needed corrective to this, 
bringing the pathologist back to the practical aspects of the matter, 
and checking the tendency to theorize by the discipline of facts. 
In the systematic treatment of the various forms of disease, the 
plan adopted lias been to take up first the diseases in their general 
aspects, and afterwards the diseases of the special organs and 
systems. The work, therefore, divides itself naturally into a 
General Part and a Special Part. 
In the General Part will be taken up those diseases which are 
not confined to any organ or tissue; most of them, indeed, may 
affect any organ of the body. In this part are included the follow- 
ing subjects : The Affections of the Circulation and of the Blood, 
Inflammation, Retrograde Changes, Hypertrophy, Repair, and 
Regeneration, Infective Tumors, Tumors proper, and Parasites. 
In order to make this general part complete, the subject of Mal- 
formations should be included. With the general subject of 
Malformations, however, the author has little practical acquaint- INTRODUCTION. 
21 
ance, and he has thought it better to leave it to special works on 
that subject. 
In the Special Part, the diseases as they manifest themselves in 
the individual organs and tissues will be considered. It is clear 
that the diseases described in the General Part will again come 
under review in each division of the Special Part, and they will 
be taken up very much in the same order as in the General Part. 
But each disease presents various specialties according to its 
locality, and, from a practical point of view, it is important to 
understand the modifications thus occurring. The Special Part 
will be, in a certain sense, an expansion and amplified illustration 
of the general principles educed in the General Part. PART I 
GENERAL DISEASES. 
AFFECTIONS OF THE CIRCULATION AND OF 
THE BLOOD. 
We have here two somewhat diverse conditions to consider, 
namely, the abnormal variations in distribution of the blood, and 
the changes in its actual condition. In regard to distribution, 
we may have too much or too little blood in the vessels, or the 
blood or its constituents may get outside the vessels. On the 
other hand, the blood may undergo changes in its constitution, or 
it may change its condition by coagulating inside the vessels. 
In order to understand what is to follow it will be necessary, in 
the first place, to refer briefly to certain points in the physiology 
of the circulation. If we are to study alterations in the dis- 
tribution of the blood, then we must have in our minds clear 
ideas as to the arrangements by which the normal distribution is 
regulated. In the distribution of the blood the capillaries and 
veins may be regarded as virtually passive channels. They are 
able to accommodate more or less blood according to circum- 
stances, but of themselves they have probably little to do with the 
variations in the supply. It is obvious that the supply of blood 
to the tissues varies, chiefly according to their needs; the working 
brain or muscle requires and gets a fuller and more rapid supply 
of blood than when at rest. Although there may be some assist- 
ance to the circulation by the attraction to the tissues of needed 
material, yet essentially the supply is regulated by the arteries; 
when they dilate more blood passes into the capillaries and on to the 
veins, and when they contract less blood reaches the capillaries 
and veins. We may regard the arteries as regulating the supply 
of blood, the capillaries as distributing the blood, bringing it 
within reach of the elements of the tissues, and the veins and 
lymphatics as carrying it off. The amount of blood admitted by 
the arteries depends on the state of contraction or relaxation of 
the muscular fibres in the middle coat, and this, like all other 
muscular actions, is under the command of the nervous system. 
When the vaso-motor nerves are stimulated the muscular coat 
contracts, when these nerves are paralyzed it relaxes, and when a 24 
AFFECTIONS OF CIRCULATION AND BLOOD. 
moderate amount of stimulus is supplied, then we have that state 
of slight contraction to which the name of tonicity is applied. 
Much attention has been bestowed on the exact nervous rela- 
tions of the middle coat of arteries. There is no doubt that it is 
under the influence of centres situated in the cerebro-spinal axis, 
but there is reason to believe that there are, as well, in or near the 
walls of the arteries, peripheral ganglia, which are the immediate 
regulators of their calibre. The heart is often compared with 
arteries in its structure, and we know that it possesses intrinsic 
ganglia. By means of these ganglia it is able to persist in its 
contractions after separation from all higher centres or even when 
cut out of the body. We know, also, that the higher centres 
influence these ganglia in two ways, either by stimulating them 
(through the sympathetic) or by inhibiting them (through the 
vagus). In the arteries we see somewhat similar phenomena. 
When arteries are cut off from all central connections they are 
still capable of varying their calibre. If the sciatic nerve in a 
frog is divided the arteries indeed dilate, but after a time they 
resume, at least partially, their state of tonicity, and are capa- 
ble of still further variations. Again, an excess of carbonic acid 
in the blood will cause arteries to contract after all their central 
connections have been severed, and they may be made to dilate 
by means of chloral or atropine. It is well known that irritation 
of the vaso-motor nerves causes contraction of the arteries, and 
this is readily enough understood without supposing the existence 
of peripheral ganglia, but it has now been shown that the arteries 
may he caused to dilate by the stimulation of nerves passing to 
them, and this can only he by means of local ganglia. It is 
known, for instance, that dilatation of the arteries of the salivary 
gland may be produced by irritation of certain nerves passing to 
them, and so is it with the vessels of the penis. Lately, it has 
been shown that the arteries of the skin may be thus caused to 
dilate. In these cases the nervous influence paralyzes the local 
ganglia. In studying inflammation we shall see still further 
proof of the existence of these peripheral nerve-centres, the exist- 
ence of which Lister long ago inferred. 
Besides these local centres, there are higher and more general 
centres situated chiefly in the spinal cord and medulla oblongata. 
From these centres there seems to pass a continuous slight stimu- 
lation inducing that moderate contraction which we name tonicity. 
If the connection be severed, the tonicity ceases, the arteries dilate. 
There is a general centre for the whole vaso-motor system in the 
medulla oblongata. When this is stimulated all the arteries appear 
to contract. When it is destroyed all the arteries in the body 
dilate. But without being destroyed the centre may be paralyzed 
or inhibited. It is inhibited by the inhalation of nitrite of amyl, 
and the arteries dilate. It may also be inhibited by the stimula- 
tion of a nervous branch which passes upwards from the heart, 
the depressor nerve. This general centre, therefore, has nervous 
connections of a similar kind to the local ganglia. general hyperj MIA . 
25 
It may be added that each organ seems to have nervous arrange- 
ments of its own, by means of which, either reflexly through the 
spinal cord and sympathetic system, or more locally, it is in a 
position to regulate the contraction of its arteries and the supply 
of blood. 
HYPERAEMIA and anaemia. 
These physiological considerations would lead us directly to the 
consideration of the local variations in the distribution of the blood 
in the body. But prior to that, we have to consider alterations in 
the quantity of the blood as a whole. It is clear that with regard 
to both local and general variations the blood may be either 
excessive or deficient in quantity, and to express these the terms 
hyperemia and anaemia are used. It will, therefore, be possible 
to consider this subject under the four divisions of General Ily- 
peraemia, General Anaemia, Local Hyperaemia, and Local Anaemia. 
1. General Hyperemia.—This term designates the condition 
in which the total quantity of blood is in excess. The term 
Plethora is used in a similar sense. The first question that 
arises here is, whether the vascular system is capable of accom- 
modating more blood than it contains normally. There is no 
difficulty in answering this question in the affirmative. If the 
vessels as a whole could contain no more blood than they normally 
hold, then there could be no local variations, no blushing, no in- 
crease in the quantity of blood during activity of organs. The 
capillaries present great varieties in the amount of blood they 
contain at different times, and if we take the whole capillaries 
of the body into account, it will appear that in them there is a 
great reserve space, which may possibly on occasion be used for 
the accommodation of an excess of blood. This matter has been 
brought to the test of experiment, and as there are several points 
of interest in this regard, we shall refer more specially to the 
observations made. 
Transfusion of blood is the artificial introduction into the vas- 
cular system of blood from another animal. 
In the experiments of Worm Muller, which are chiefly of im- 
portance here, the defibrinated blood of dogs was injected, with 
precautions, into the vessels of animals of the same kind. It is 
not remarkable that the vascular system can accommodate a large 
additional quantity of blood, but it is remarkable that it should 
do so with little disturbance to the health of the animal. A 
quantity equal to one-half or three-fourths of the blood normally 
present in the animal may be injected without endangering the 
life of the animal, and the quantity needs to be double the normal, 
or over it, before the animal’s health is seriously impaired. It 
might be expected that when the vascular system is thus overfilled 
the blood-pressure would be greatly raised, but actual registration 26 
affections of circulation and blood. 
of the pressure, by a canula introduced into the carotid and con- 
necting with a kymographion, shows that though the 
actual operation there is a rise of pressure, yet it soon falls to 
within normal limits. If a quantity is injected beyond double 
the normal bulk of the blood, then the pressure begins to show 
remarkable elevations and depressions, and the animal usually dies 
in the course of the same day, or the next. Life is immediately 
endangered when one and a half times the normal bulk is injected. 
When blood is transfused, then, in large quantity it finds accom- 
modation chiefly in the capillaries and veins, the arteries being 
relaxed in order to admit of its passing into these, and the blood- 
pressure is not raised. It appears that the capillaries and veins of 
the abdominal organs form a great reservoir for the accommoda- 
tion of excessive blood, and that the blood lodges here chiefly 
after transfusion. 
The excess of blood thus supplied to an animal does not, how- 
ever, remain permanently as a part of its organism. There seem 
to be arrangements in the body for disposing of it. Worm Muller 
endeavored to determine what time it took to dispose of a large 
excess of blood. After the transfusion the animals were starved, 
and the blood and urine examined at intervals. It was concluded 
that the fluid of the blood is rapidly disposed of, being excreted by 
the urine. A few hours after transfusion much of the excess of 
liquor sanguinis had already gone, and even when sixty to eighty 
per cent, of the entire blood was injected, the whole excess had dis- 
appeared in the course of two or three days. The rapid disposal 
of the liquor sanguinis leaves the blood-corpuscles greatly in ex- 
cess, and the rate of disappearance was determined by counting 
them by means of Malassez’ method. If the quantity transfused 
is small, the corpuscles may be disposed of in a few days; but in 
the case of large transfusions it may take two or even three weeks. 
In this comparatively short period of time, however, the whole 
excess of blood, both plasma and corpuscles, is removed, and we 
may infer that there are arrangements in the body for the regula- 
tion of the amount of blood. 
These experiments all refer to the transfusion of defibrinated 
blood. If blood is injected when just about to coagulate, or if 
when it has just begun to coagulate some of the serum is pressed 
out and injected, then in some cases the animal dies rapidly with 
symptoms referrible to pulmonary embolism. The blood in the 
right side of the heart and pulmonary artery is found after death 
to be coagulated. The explanation of this is, that at the time of 
coagulation of the blood, the fibrinoplastic substance and the fer- 
ment, which Schmidt’s observations have shown to be so directly 
concerned in coagulation, are both set free. It appears that even 
a small quantity of these substances introduced in the free state 
into the blood of a living animal induces coagulation of it. The 
importance of these facts in regard to transfusion in human beings 
will not be overlooked. 
Hitherto the transfusion of blood from an animal of the same GENERAL hyperemia. 
27 
kind lias been referred to, dog's blood injected into a dog. But 
when blood from a different species of animal is used, there 
are frequently symptoms of poisoning developed. The urine is 
blood-colored, and it contains albumen and tube-casts; there is 
vomiting of bloody material, diarrhoea, etc. It is as if the foreign 
blood had acted as a poison, and we may inquire what is the nature 
of the poison. The observations of Ponfick (Virchow’s Archiv, 
vol. lxii.), and others, have thrown considerable light on this 
matter. It has been already mentioned that the urine is blood- 
colored, but microscopic examination shows that this is due, not 
to the presence of red blood-corpuscles, but to that of the coloring 
matter of the blood in solution. It is not a bloody, but a blood- 
colored urine, not a hsematuria but a hemoglobinuria. The fact 
seems to be that there is no poison in the foreign blood-plasma, 
but that the corpuscles are unable to survive in the alien blood; 
they dissolve, and their haemoglobin being dissolved in the plasma 
acts as a poison, and is eliminated by the kidneys. It seems to 
exercise its deleterious influence chiefly on the kidneys themselves, 
the tube-casts and albumen in the urine being evidences of the 
irritation of these organs. The general symptoms, in fact, are 
largely referrible to the irritation of the kidneys. 
If haemoglobin be introduced into the blood in other ways, it 
acts equally as a poison. The red corpuscles of animals may be 
destroyed by repeatedly freezing and thawing the blood, and when 
that has been done, the blood of the same kind of animal will 
produce symptoms such as those referred to. 
It is to be observed that all animals are not exactly in the same 
relation to each other in this respect. It is found, for instance, 
that a much smaller quantity of lamb’s blood than of hen’s blood 
produces luemoglobinuria in a dog. The importance of these facts 
in regard to transfusion in the human species will be apparent. 
In this place it may be mentioned that the blood transfused does 
not, according to Panum, act as food or take its place. If an 
animal is undergoing starvation, transfusion does not avert or delay 
the process of inanition; it rather hastens it by increasing the 
waste. In using transfusion as a means of treatment the object is 
to make up a deficiency of red corpuscles or blood-plasma. 
Having now seen that, by transfusion, an artificial plethora may 
be induced in animals, we may be prepared to admit the possibility 
of its existence in the human subject. It will presumably occur 
when the blood-forming organs are unduly active, and will mani- 
fest itself in an over-fulness of the capillaries and veins through- 
out the body, but especially in those of the abdominal viscera. 
Persons of vigorous digestion and active habits have often a florid 
appearance, as if the vessels, of the skin at least, were overfilled. 
The excess of blood is used, to a considerable extent, in the for- 
mation of fat, and we know that the subcutaneous adipose tissue 
and that of the abdomen are often much increased. But the ob- 
servations mentioned above show that any excess of blood is dis- 28 
affections of circulation and blood. 
posed of with considerable rapidity, and we rflay infer that in the 
human subject a moderate tendency to plethora will be overcome. 
It will develop when the formation of blood keeps in advance of 
its destruction by the arrangements provided for that purpose. 
2. General Anemia.—By this name is meant strictly a defect 
in the blood as a whole, a real want of blood, but the term is 
habitually used to designate conditions in which the blood is 
defective in any of its important constituents. 
A true antemia or want of blood, such as occurs in consequence 
of a severe hemorrhage, is designated Oligvemia, and this term 
may be regarded as virtually equivalent to Acute Traumatic 
Anaemia. When such a condition develops from a single large 
hemorrhage, the condition of simple reduction of the bulk of the 
blood does not long remain, but various processes occur which 
modify the state of the blood. We have now to consider what 
these processes are, and how they modify the condition of the blood. 
To begin with, the bulk of the blood does not long remain 
under the normal; it is rapidly made up, but not by a plasma of 
normal concentration. The blood is unduly watery, and so the 
oligsemia gives place to a Hydremia. The process by which this 
is brought about is not very obscure. As the hemorrhage pro- 
ceeds the arterial blood-pressure diminishes; in slight hemorrhages 
it soon recovers, but in severe cases the reduction continues for 
some time. The consequence of this must be a diminution in the 
transudation of the normal parenchymatous fluid from the capil- 
laries. If the reduction of pressure is considerable, there may 
even be a reverse current, the fluid from the tissues being absorbed 
into the blood. Again, the secretion of urine depends on the 
blood-pressure in the vessels of the Malpighian tufts in the kidneys, 
and the pressure here depends largely on the general arterial ten- 
sion. Any diminution of the general blood-pressure will therefore 
lessen the amount of urine secreted, and will diminish the loss of 
water by the blood. In this way, and by the absorption of water 
from the alimentary canal, the bulk of the blood is soon made up, 
but, as already mentioned, it is a watery blood. 
After such a hemorrhage also, there is an excess of leucocytes 
in the blood, especially as compared with the red corpuscles, which 
are much diminished. This condition of Leucocytosis is brought 
about in various ways. During the actual hemorrhage the white 
corpuscles being more adhesive pass less freely out of the ruptured 
vessels, and so fewer are lost than of the red corpuscles. But the 
principal cause of the leucocytosis is, that the white corpuscles are 
much sooner replenished than the red. The thoracic duct pours 
into the jugular vein lymph containing leucocytes both during 
and after the hemorrhage. Moreover, the organism seems to have 
a very great power of forming leucocytes. If we consider the 
excessive quantities of them which are formed during an active 
suppuration, we may have some idea of the rapidity with which 
they may be produced. 29 
The red.corpuscles are much more slowly regenerated. If the 
hemorrhage has been at all severe, it takes many weeks to make 
up their number. The number of corpuscles to a given bulk of 
blood can readily he estimated by the instruments devised for the 
enumeration of the corpuscles, of which one of the most conven- 
ient is that of Thoma, manufactured by Zeiss, of Jena. By this 
method it can he observed how the corpuscles are gradually re- 
plenished. 
The exact mode of formation of the red corpuscles, even the 
site of their formation, is very obscure. It has been generally 
believed that the spleen, lymphatic glands, and bone-marrow, have 
to do with the formation of these corpuscles. The observations of 
Neumann and others have caused great importance to be attached 
to the bone-marrow in this regard, and the fact that nucleated red 
corpuscles are to be found here, especially in young persons, has 
been regarded as an indication that this tissue is specially con- 
cerned in the formation of these bodies. It has generally been 
supposed that the red corpuscles develop out of the white, but 
considerable doubt has always existed as to this. Recently, it has 
been asserted that they arise by a process of budding from existing 
red corpuscles. 
It is not necessary to assume that the red corpuscles are replen- 
ished only by an excessive activity in the blood-forming organs. 
It may be, rather, that with an ordinary, or even reduced, activity, 
the corpuscles are made up by fewer of them being consumed than 
under ordinary circumstances. The coloring matters of the bile 
and of the urine are derived from the blood, and their existence 
implies that red corpuscles are destroyed in order to yield their 
coloring matter. In the case of the bile, this destruction probably 
takes place in the liver, but in the case of the urine, the coloring 
matter exists pre-formed in the blood, and the destruction of cor- 
puscles takes place elsewhere, perhaps in the spleen. After a 
severe hemorrhage, there is much less activity of all the functions 
of the body, and, presumably, less consumption of red corpuscles. 
In accordance with this the bile and urine are paler than normal; 
often very much so. It may be, then, that in the generally re- 
duced activity of the body, there is no increased formation of red 
corpuscles, but that their slow replenishment is really due to an 
economy of them. 
In the above, the case of a single considerable hemorrhage has 
been taken. Where there are frequent small hemorrhages, as from 
piles, bleeding from the uterus, etc., there will be a recurrent loss 
of blood, and a continuous hvdraemia. 
Spontaneous anaemia is a term used to designate conditions in 
which, without any loss of blood, there is a deficiency chiefly in 
the red corpuscles. There is generally an actual deficiency in the 
number of the corpuscles as determined by counting, but there are 
cases where, without any great reduction in number, there is a 
great deficiency of haemoglobin. The normal proportion of red 
GENERAL ANJ1MIA. 30 
AFFECTIONS OF CIRCULATION AND BLOOD. 
corpuscles to the plasma is thirteen per cent., and in spontaneous 
anaemia it has been found as low as six, five, and even four per cent. 
Various forms of spontaneous anaemia are met with, o*f which two 
call for special note, namely, Chlorosis and Pernicious Anaemia. 
Chlorosis occurs most frequently in young women about the age 
of puberty, and it is remarkably amenable to treatment by means of 
iron. There is reason to suppose that this condition may be due to 
a congenital defect in the organs for preparing the blood—they are 
unable to meet any extra strain on them, such as occurs at puberty. 
It is interesting, in this regard, that chlorosis lias been found in a 
certain number of cases to be associated with a visible defect in 
the circulatory system, which gives some corroboration to the 
supposition of a defect in the blood-preparing organs (Virchow). 
The most constant defect is narrowness and thinness of the aorta. 
There is also frequently an irregularity in the origin of the 
branches from the aorta, especially the intercostal ones. The 
narrowness of the aorta may lead to hypertrophy of the heart. 
It is sometimes stated that chlorosis is related to congenital defect 
of the organs of generation, but there is no sufficient evidence in 
support of this. 
There are certain anaemias of a very serious kind which come 
on without any apparent connection with other abnormal condi- 
Fig. 1. 
Fig. 2. 
Blood in pernicious anaemia. The larger 
bodies are the normal red corpuscles. The 
smaller are the round, more deeply colored 
ones usually found—so-called microcytes. 
(Eichhorst.) 
From red medulla of bone .in per- 
nicious anmmia.j a. Nucleated red 
corpuscles, c. A red corpuscle with 
granular nucleus, b. Large nucleated 
cells, forming the bulk of the altered 
marrow. X 350. 
tions. These are sometimes designated Essential Anjemias, of 
which the most important is Pernicious Anemia. This name is 
used to designate a disease in which, without apparent cause, the 
blood deteriorates, becoming deficient in red corpuscles. The de- 
terioration goes on progressively to a fatal issue, and nothing has 
been found to arrest it. In this disease there is a marked defici- 
ency in red corpuscles, but besides that, there are corpuscles pres- 
ent which are not represented at all in normal blood. These are 
red corpuscles of a much smaller size than the normal ones, as 
shown in Fig. 1. They are usually about half the size of the 
red ones; instead of being biconcave they are globular, and GENERAL anaemia. 
31 
they have a much deeper color than the ordinary red corpuscles. 
They are generally present in considerable abundance, and may 
even exceed in number the normal ones. It is asserted that these 
small corpuscles (microcytes) are present in all cases of this dis- 
ease. This is denied by some, but they are certainly present in a 
large proportion of cases. In addition, red corpuscles of larger 
size than normal and nucleated red corpuscles, have been met 
with in the blood in some cases of pernicious anaemia, and nucle- 
ated corpuscles may be found in the blood after death when exami- 
nation has failed to detect them during life. In some cases also 
of this disease, the medulla of bone is altered. Instead of the 
yellow adipose tissue, which is the normal structure in some parts 
of the medulla, a red semi-fluid marrow has been found, in the 
shaft of the femur for instance. Under the microscope, in these 
cases, the normal adipose tissue is found to be replaced by aggre- 
gations of cells, in the midst of which are found nucleated red 
corpuscles, while the non-nucleated corpuscles present great variety 
in size (Fig. 2). This change in the medulla, however, can 
hardly be regarded as distinctive of this form of anaemia. It has 
been found in ordinary forms of ansemia, and it is sometimes 
absent in pernicious anaemia. Probably it indicates an alteration 
in the organs having to do with the preparation of the blood, but 
nothing further can be definitely asserted. 
Besides these forms of anaemia already described in which there 
is an actual loss of blood or else a grave defect in the formation 
of the blood, there are some conditions in which the blood is 
impoverished in consequence of some other disease which either 
causes a waste of the constituents of the blood, or, by lowering 
the nutrition as a whole, leads to defect in the formation of the 
blood. This is called secondary anemia, and it may occur in all 
debilitating diseases such as malignant tumors, febrile conditions, 
albuminuria, etc. 
Anaemia, in its various forms, not unfrequently produces sec- 
ondary changes in various organs, and it will be proper briefly to 
refer to these. The foundation of all these changes is the deterio- 
ration of the blood, and we must be prepared to find functional 
activity reduced, and, above all, the nutrition of the tissues inter- 
fered with. A prominent result of this interference with the 
nutrition is the frequent occurrence of degenerative changes. 
Fatty degeneration of the muscular tissue of the heart is one of 
the commonest of these. Experiment on dogs shows that succes- 
sive large hemorrhages leading to inanition rapidly produce fatty 
degeneration of the muscle of the heart. The author has met 
with a case in which, after a single very severe hemorrhage from 
the stomach, with a fatal issue three weeks later, there wTas extreme 
fatty degeneration of the heart. Fatty degeneration also occurs 
in the epithelium of the uriniferous tubules of the kidney and in 
the hepatic cells of the liver. A fatty degeneration of the intima 32 
AFFECTION'S OF CIRCULATION AND BLOOD. 
of the aorta, producing a figured appearance in the wall of the 
vessel, has been seen in chlorosis and in other forms of anaemia 
(Virchow). This may he part of the defect of the vascular system 
in chlorosis already mentioned, hut more probably it is a secondary 
degeneration. The state of the medulla of bone in pernicious 
anaemia has been referred to, and it has been remarked that a 
similar red marrow has been seen in other forms. AVe meet with 
it in secondary anaemias, and, perhaps, especially in old persons. 
3. Local Hyperemia.—AVe have next to consider the local 
variations in the distribution of the blood. The term local 
hyperaemia is applied to conditions in which there is an excess of 
blood in the vessels of a particular part. It may be due to an ab- 
normal amount of blood being admitted by the arteries, and in that 
case the blood will generally be at a higher pressure and flow more 
quickly than normal; or to some interference with the passage of the 
blood away from the part by the veins, in which case the current 
will probably be unduly slow. In this way we distinguish two forms 
of local hyperaemia—an active or arterial and a passive or venous. 
Active Hyperaemia or Active Congestion.—This occurs when 
an excess of blood is admitted by the arteries into a part. The 
terms Atonic and Arterial Hyperaemia may be regarded as synony- 
mous with active hyperaemia, and also the expressions Fluxion and 
Determination of Blood. This condition will come about either 
when there is some increase of the blood-pressure forcing more 
blood in, or when the arteries are dilated so as to allow the blood 
freer access. 
Increase of blood-pressure-is not often local, and even when 
it is, a rapid accommodation is usually effected by which the press- 
ure is brought to an equilibrium. This accommodation is effected, 
as we have seen, by means of the arteries, their state of contrac- 
tion being subject to variation. There is one situation, however, 
in which arteries possess little tonicity, and hardly at all regulate 
the supply of blood except passively, and that is in the lungs. It 
is to be noted, therefore, that any increase of blood-pressure affect- 
ing the pulmonary circulation is apt to be followed by an active 
hyperaemia. In studying active hyperemia of the lungs, we 
shall see that increased activity of the heart may lead to active 
congestion in the lungs. 
There is a condition designated collateral hyperaemia, and it 
might be supposed that this is due essentially to increase of blood- 
pressure. It occurs when, on account of deficiency of blood in 
one part (local anaemia), there is excess of blood in another. If 
the blood is deficient in one part, it must be excessive in another 
or in the system in general. The local anaemia is due to some im- 
pediment to the circulation, chiefly obstruction of the arteries, and 
it may be supposed that the direct result of such obstruction will 
be to raise the blood-pressure iu the neighboring vessels and so 
lead to an active hyperaemia. As we shall see afterwards, this is active hyperemia. 
33 
probably the explanation of the congestion of the lungs which 
follows the drinking of large quantities of cold water. The cool- 
ing of the stomach causes contraction of the arteries in the ab- 
domen, and this increases the blood-pressure. But for the most 
part the bloodvessels are so fully under the control of the nervous 
system, and the mechanism for the regulation of the circulation is 
so well arranged, that when a local anaemia occurs the accommo- 
dation of the excess of blood is not left to mere accident, but is 
provided for according to the needs of the organism. Thus, if the 
carotid artery is obstructed, the dilatation and liyperaemia do not 
occur in the arteries of the arm, which are the nearest to the ob- 
structed artery, but in the other arteries passing to the brain. If 
one renal artery is obstructed, there is a collateral liyperaemia of 
the kidney opposite, and the secretion of urine is restored to the 
nprmal. Most collateral hyperaemias, therefore, are due rather to 
dilatation of the arteries, than to increase of blood-pressure. 
Turning to cases in which the liyperaemia is more directly due 
to dilatation of the arteries, a simple example is afforded by 
the congestion which follows the application of warmth to the 
skin in the form of poultices, etc. It is believed that this hyper- 
aernia causes a collateral anaemia in certain subjacent parts, and 
this, like collateral liyperaemia, has not a merely accidental dis- 
tribution. On this principle, as some suppose, poultices and 
fomentations are useful, although probably this is not the entire 
explanation of their action. 
But, again, the arteries dilate when an unusual pressure to 
which they have long been subject is suddenly removed. The 
arrangements for the regulation of the circulation are such that 
when arteries are subjected to pressure, as the arteries of the 
abdomen in ascites, the circular muscular fibres become less active, 
the external pressure causing narrowing of the arteries without 
their contraction. Should the pressure be suddenly removed, 
however, these vessels, taken as it were at a disadvantage, dilate, 
and an active hypersemia results. Hence, after removal of a large 
accumulation of ascitic fluid, it is usual to apply a supporting 
bandage which will partly take the place of the pressure removed, 
till the arteries accommodate themselves afresh to their new cir- 
cumstances. After removal of an ovarian tumor there may be a 
liyperaemia of the kidneys, which may even lead to a transitory 
albuminuria. 
Further, paralysis of the vaso-motor nerves may lead to relax- 
ation of the arteries. The author met with a case in which an 
accident caused a traumatic lesion of the medulla oblongata. The 
injury had apparently destroyed the vaso-motor centres of the 
kidneys. There was a most remarkable active liyperaemia of these 
organs, evidenced after death by an enormous overfilling of all the 
vessels with blood. During the few hours of life after the acci- 
dent, a very excessive quantity of watery urine was twice drawn 
off by the catheter, and after death the bladder was found highly 
distended. Division or injury to the spinal cord is likely to pro- 34 
affections of circulation and blood. 
duce hyperaemia in the parts supplied with, nerves by the cord 
beneath the point of injury. Nerve-stems may be interrupted in 
their continuity and dilatation of arteries so produced. Lastly, 
in neuralgias, we sometimes have dilatation of the arteries. 
Whether this is produced by the vaso-motor fibres being directly 
involved in the morbid process, or reflexly by stimulation of 
sensory fibres, it is impossible to say. 
As a result of the dilatation of the arteries, there is not simply 
an increased access of blood to the part, but the blood flows more 
quickly. The first effect of a sudden dilatation of a considerable 
number of arteries will be a reduction of the arterial blood- 
pressure. But, by contraction of arteries elsewhere, this will soon 
be restored unless the number of arteries dilated be very great. 
If the blood-pressure remain the same then, the blood will pass 
with less resistance through the dilated arteries, and will reach 
the capillaries and veins at a higher pressure than normal. As a 
matter of fact, the blood-current is accelerated and the pulse may 
be propagated through the capillaries into the veins. 
The most obvious signs of active hyperaemia are redness, slight 
swelling, and elevation of temperature. The swelling is due 
partly to the overfilling of the vessels, but also to an increased 
transudation from the vessels into the lymph-spaces. It has been 
found that if a canula is introduced into a lymphatic vessel in the 
leg of a dog, and the sciatic nerve cut, there is an increased flow 
of lymphatic fluid from the canula. If the hyperaemia continues 
long, and no other element occurs, there wfill probably be a hyper- 
trophy of the affected part. The vessels especially are liable to 
enlarge, and very insignificant ones may become of considerable 
size. 
It has been said that active hyperaemia may lead to hemorrhage, 
but experiment seems to prove that even a very great rise in the 
blood-pressure in the capillaries does not lead to hemorrhage 
unless the vessels are badly supported, or else defective in some 
way. By obstructing the respiration in a dog, you may raise the 
arterial pressure enormously, but there is no rupture of the capil- 
laries, or only in such delicate structures as the retina, brain, or 
conjunctiva. The increase in pressure in a pure active hyperaemia 
is, of course, greatly less than this. 
Passive Hyperemia or Passive Congestion is a condition in 
which the blood stagnates in the vessels; they are overfilled with 
blood, which, as it remains too long in the vessels, has a venous 
character, lienee passive hyperaemia is also called Venous Ilyper- 
aemia. 
This condition frequently occurs as a consequence of weakness 
of the heart. In the normal state the forces of the circulation 
have to overcome gravitation, in order to remove the blood from 
depending parts. The force of the heart propagated through 
arteries and capillaries to the veins is generally sufficient to do 35 
PASSIVE HYPEREMIA. 
this. But, if the heart is weak, the blood is apt to linger in 
depending parts, or in parts far removed from the centre. Weak- 
ening of the heart occurs in many forms of disease. It is often 
very marked in fevers, such as typhus and typhoid, or in long- 
continued debilitating diseases, which produce anaemia. In these 
cases the blood often stagnates in the dependent parts of the lung, 
where it produces the so-called hypostatic engorgement. It also 
stagnates frequently in depending parts of the skin, over the 
sacrum and shoulder-blades in persons lying on their backs, over 
the trochanters in persons lying on their sides. In these situations 
the weakness of the circulation, along with the mechanical effects 
of the weight of the body and irritation of decomposing material, 
leads frequently to sloughing of the skin and the formation of 
bed-sores. In fevers there may be hypersemia of the extremities 
of the fingers or toes, resulting even in necrosis or gangrene. 
Again, there may be difficulty in overcoming gravitation on 
account of the force of the heart being partly lost by reason of 
abnormal conditions in the aiiteries. If there be partial obstruc- 
tion in the arteries, as in atheroma, where there is thickening of 
the internal coat sometimes with a deposition of thrombi on the 
surface, the force of the heart may he lost in friction, and conse- 
quently the blood may stagnate in the parts supplied. 
Obstruction oe veins, however, is the most direct cause of 
passive hypersemia. This may be produced by pressure of tumors, 
exudations, bandages, the pregnant uterus, even hard masses of 
feces, by coagulation of blood within the veins, or by the bursting 
of tumors into veins, or their growth through their walls. 
Lastly, disease of the valves of the heart produces in a large 
proportion of cases a general venous hypersemia. 
We have now to consider the results of this engorgement of 
the vessels. Taking the simplest case, that of obstruction of a 
venous stem, the first result is an increase of blood-pressure in the 
veins behind the point of obstruction, and an accumulation of blood 
in the part. Considering the rapid manner in which increase of 
pressure in the arteries is compensated, it might be expected that 
the increase of pressure would soon be relieved, and the engorge- 
ment recovered from. If the vein have abundant anastomoses, 
then to a considerable extent the blood will find its way by other 
channels, and the normal conditions be restored. But, from the 
list of causes of passive hyperiemia, it will be seen that most of 
these involve sets of veins, or whole regions of the body; even in 
the case of thrombosis, the coagulation usually extends to a number 
of veins. Apart from relief by anastomosis, however, it might 
be supposed that, when obstruction in a vein occurs, the increase 
of pressure would, as in the case of obstruction of an artery, be 
compensated by changes in the state of contraction of the arteries. 
But a local relaxation of the arteries would only intensify the 
result by superinducing an active hyperremia; consequently the 
desired compensation could only be effected by a reduction of the 36 
AFFECTIONS OF CIRCULATION AND BLOOD. 
blood-pressure throughout the system, which will scarcely happen. 
The increase of pressure remains, and it affects not hnly the veins, 
hut, more particularly, the capillaries, the blood in which is, as it 
were, jammed between two pressures, the normal pressure from 
arteries and the abnormal from the veins. 
The further effects are to be traced to the excessive pressure in 
the capillaries. The blood accumulates in excessive quantity in 
these vessels and at an excessive pressure. In consequence of this, 
an increase in the natural transudation of fluid through the capil- 
laries occurs, and the blood-corpuscles, especially the red ones, 
escape from the vessels. Each of these phenomena merits more 
special consideration. 
The term Diapedesis, or hemorrhage by diapedesis, is applied 
to the escape of the red corpuscles from the bloodvessels when it 
occurs, as in the present case, without rupture of their wall. This 
process occurs mainly, if not entirely, in the capillaries, and it 
can be shown hy experiment that it does not involve rupture of 
these vessels. If the tongue of a frog is ligatured at its base so as 
to include all the veins, but excluding the artery, there will be the 
phenomena of hyperannia greatly intensified, and among these 
phenomena diapedesis. But, if the ligature be loosened within a 
moderate period, the circulation is restored, and the phenomena 
disappear. If the escape of blood-corpuscles had been by rupt- 
ure, it would have continued after resumption of the circulation. 
As to the manner in which the corpuscles escape, it is believed by 
some that they are pushed through the endothelial plates, but by 
others it is asserted, with more probability, that they pass between 
the endothelial cells. Fig. 3 shows the appearance of the endo- 
thelium of a capillary mapped out by treatment with nitrate of 
silver, and Fig. 4 shows capillaries similarly treated after passive 
liypersemia had existed. The latter illustration is taken from 
Arnold, who asserts that while in the normal condition there are 
minute apertures between the endothelial cells, chiefly at the 
angles where two or three meet, these are found much enlarged 
in passive hypersemia. The small apertures may be called stigmata, 
and the larger ones stomata. The excessive pressure in the capil- 
laries seems to he the chief agent in causing the escape of the 
corpuscles, as well as the increased transudation of fluid. 
That there is an increased transudation of fluid can he directly 
proved by experiment. The flow in the lymphatic vessels has 
been proved to be excessive. If the lymphatics are not capable 
of disposing of the entire excess, then the fluid accumulates in 
the serous spaces and cavities of the body, giving rise to (Edema 
and Dropsy, which are to be more fully considered afterwards. 
This accumulation will occur if, on the one hand, the transudation 
be too excessive for the lymphatics to dispose of it, or if, on the 
other, for some reason, the lymphatics do not take it up sufficiently. 
The current in the lymphatics depends on the blood-pressure, and 
we have just seen that the cause of the increased transudation is 
excess of blood-pressure, and so the same condition which deter- PASSIVE IIYPERA3MIA. 
37 
mines the increase will, to a certain extent, cause it to be more 
rapidly disposed of. Hence it is that a simple passive hypenemia 
from obstruction of a vein, let us say, is not usually associated 
with much oedema. When the hypenemia depends on weakness 
of the heart, then the attraction of gravity which prevents the 
return of blood will also interfere with the flow in the lymphatics, 
Pig. 3. 
Fig. 4. 
Normal capillary, with endo- 
thelium mapped out by treatment 
with nitrate of silver. 
Capillaries after passive hyperasmia. Apertures 
between the cells greatly enlarged; the so-called 
stomata. (Arnold.) 
and there will be no excessive blood-pressure to accelerate the 
flow. Hence, in these cases, oedema is more common and more 
serious. 
The exuded fluid, as may be inferred, contains red corpuscles, 
but it does so much less in actual pathological processes than 
might be supposed from experiments in animals. In the latter 
there is a sudden obstruction, with exaggerated results ; in actual 
disease in man the processes usually develop slowly, and there is 
some accommodation of the vessels. It should be added that the 
white corpuscles pass out of the vessels as well as the red, but not 
to such an extent, and that the corpuscles, both red and white, 
escape from the small veins as well as from the capillaries. 
When oedema does not occur, there is frequently developed some 
swelling of the connective tissue of the parts concerned. This is 
a true hypertrophy, and is not to be confounded with inflammatory 
increase of connective tissue which will afterwards come frequently 
before us. The increased transudation, by providing an increase 
of nutritious material, causes hypertrophy of the connective tissue, 38 
AFFECTION'S OF CIRCULATION AND BLOOD. 
which is swelled, and also denser. This increased density is often 
seen in the heart, when, from disease in its own there is a 
general venous engorgement in which the veins of the heart take 
part. We see it also very often in the kidney and in the lungs in 
cases of valvular disease. The tissue, as a whole, is rendered hard 
and resistant. 
The part which is the seat of passive hyperaemia will be unduly 
red, and the color will he dark or livid. It will be swollen, both 
from the overfilling of the vessels and from the oedema, and it will 
usually be lowered in temperature. 
4. Local Anaemia.—In this condition the vessels of a part are 
more or less deficient in blood. It may be due to various causes. 
The capillaries may be emptied by pressure on the part. For 
instance, an abscess approaching the surface may, by its pressure, 
prevent the blood reaching the capillaries of the skin, and a slough 
is the result. A cavity in the lung may, by undermining the 
pleura, cause sloughing of it. Tumors or clots of blood, etc., by 
their pressure, may cause anaemia of surrounding parts, and if 
the part thus rendered anaemic be a structure whose function is 
important to life, such as the brain, serious results may follow. 
Interference with the arteries will produce anaemia if the flow 
of blood through them be obstructed. There is such a thing as 
spasm of arteries—this, probably, produces the shivering which is 
so common at the outset of fevers, the arteries of the skin being 
spasmodically contracted. So also in some neuralgias a spasm of 
the arteries has been seen. The application of cold causes con- 
traction of the arteries—the ether spray causes complete anaemia 
by this means. Besides this, the arteries may be narrowed by 
disease of their coats. There is a rather common disease in small 
arteries which consists in a thickening of the internal coat and has 
somewhat the character of atheroma. This condition is often 
called endarteritis obliterans, and is in some cases a syphilitic 
manifestation. It is clear that, by reducing the calibre of arteries, 
it will produce anaemia. In arteries of the brain, atheroma pro- 
duces narrowing of the calibre which may be so considerable as 
to produce anaemia. More frequently, however, anaemia is pro- 
duced to a serious extent only when blood coagulates on the 
atheromatous patch and completely occludes the artery. Again, 
tumors, blood-clots, exudations may cause narrowing of arteries 
by pressure. Arteries also may be completely obstructed by 
ligature or by plugging. 
In considering the results of local anaemia, the case of complete 
closure of arteries will be here omitted, because it will come up for 
consideration under the head of embolism. In cases where there is 
incomplete obstruction, some blood will pass by the arteries, but the 
capillaries will be imperfectly filled. The part will be pale, reduced 
in temperature, flaccid. Its nutrition will be diminished, and its 
elements prone to undergo atrophy and degeneration, and even, as 
we have already seen, necrosis. The function will be interfered THROMBOSIS. 
39 
with if the nutrition is depreciated. If the anaemia affect an 
important organ, the results may be serious. Thus, obstruction 
of the coronary arteries may cause paralysis of the heart from this 
cause. Again, anaemia of the bloodvessels interferes so much with 
the nutrition of their own walls that, if after its suspension the 
circulation be renewed, the vessels may rupture and serious hem- 
orrhage result. Lastly, a local anaemia produces a hyperaemia 
elsewhere, but this has already been considered under collateral 
hyperaemia. 
THROMBOSIS AND EMBOLISM. 
These two conditions are often associated, but must be carefully 
distinguished. Thrombosis is the coagulation of blood within the 
vessels or heart. Embolism is the obstruction of a vessel by a plug 
brought from a distance. The coagulum which forms in throm- 
bosis is a thrombus, the plug which obstructs in embolism is an 
embolus. A thrombus detached from its place becomes an embolus, 
and an embolus, whether consisting of coagulum or not, may grow 
by successive deposition of clot or thrombosis. 
1. Thrombosis.—In considering the mode of occurrence of throm- 
bosis, it is necessary to refer to the conditions under which the 
blood coagulates. According to the views which are identified 
with the name of Alexander Schmidt, three agents are necessary 
for coagulation, the fibrinogen, the fibrino-plastic substance or 
paraglobulin, and the fibrin-ferment. The two former unite to 
form fibrine in the presence of the latter. The fibrinogen is dis- 
solved in the blood-plasma, the paraglobulin and ferment reside in 
the white corpuscles. It is only by destruction of the white cor- 
puscles that the paraglobulin and ferment are set free; so long as 
the white corpuscles circulate in the blood and remain alive, fibrine 
cannot form. Fibrine will form when the conditions are such that 
the white corpuscles are no longer preserved alive. Fibrine, it 
will thus be seen, is the result of a chemical combination, and the 
resulting albuminous substance, the fibrine, is not a vital structure 
but a dead chemical compound. In order to the preservation of 
the white corpuscles, they must not be exposed to the contact of 
dead matter. You may keep blood fluid for a long time if you 
simply ensure that it is in contact with living tissue. Lister long 
ago showed that if an artery be ligatured in two places, and cut 
out while full of blood, it may be hung up and the blood will 
remain fluid for some days. Within the body if a vessel is liga- 
tured carefully in two places, the middle portion remaining in con- 
nection with the living tissues, then the blood may be kept fluid 
from twelve to fifteen days. 
The main cause of coagulation, then, is the contact of the white 
corpuscles with dead matter or altered living tissue. In the living 
body anything which interferes with the integrity of the vessel-wall 
or the endocardium is likely to predispose to coagulation. Stagna- 
tion of the blood is often set down as a cause of coagulation, but 40 
affections of circulation and blood. 
this will act chiefly by altering the vessel-wall, and by keeping the 
white corpuscles removed from contact with the living tissue. As 
it is the endothelium of the vessels and endocardium which is in 
most immediate contact with the blood, it will he interferences 
with it that will conduce to coagulation. 
If a portion of blood inside a vessel be cut off from the circula- 
tion, then it will by and by coagulate just as it does outside the 
body, the main agent in the coagulation being the disintegrating 
white corpuscles. In this way a red thrombus is produced. But 
vessels are rarely so situated as to allow of a complete coagulation 
such as this; much more frequently the thrombus is formed from 
the blood which is still moving, although, it may be, slowly, and it 
is of gradual growth. The formation, of thrombi in the living 
vessels has been carefully studied by Zaiin (Virchow’s Archiv, 
vol. lxii.), whose experiments throw much light on the process. 
The mesentery of a frog is exposed and subjected to microscopic 
examination. A vessel of some size, an artery or vein, is chosen, 
and its wall in some way injured, as by twitching it slightly with 
the forceps, or placing a small crystal of common salt near it. 
Very soon white blood-corpuscles begin to adhere at the injured 
part. As the blood passes over it, successive layers of white cor- 
puscles adhere, and a growing clump of them is formed. Along 
with the white corpuscles a stray red one may be insinuated, or 
there may be several red ones. The clump so formed, be it wholly 
white or partly mixed with red corpuscles, may be carried off, in 
which case a new one begins to form; but the clump may remain 
fixed and be continuously enlarged by successive depositions of cor- 
puscles from the circulating blood. In course of time a change 
occurs in the appearance of the clump, the white corpuscles lose 
their individual outline to a great extent, and the clump gathers 
itself together into a gray granular mass in which neither by acetic 
acid nor by staining are the majority of the white corpuscles to be 
discovered. It has, indeed, very much the characters of flbrine 
which has been obtained by whipping the blood outside the body. 
The clump of white corpuscles, in fact, by the disintegration of the 
corpuscles and the attraction of the fibrinogen from the blood- 
plasma has converted itself into a fibrinous coagulum. All the 
white corpuscles, however, are not disintegrated, some are still 
recognizable in the mass. A similar mode of formation is observed 
when a vessel is injured by pricking with a needle, or by cutting 
it. The presence of foreign bodies if they are rough on the sur- 
face, produces adhesion of white corpuscles and their conversion 
into thrombi in similar fashion, but when smooth pieces of glass 
are introduced, there does not seem to be the same tendency to 
adhesion of the white corpuscles. It will be understood that 
thrombi formed in this way often contain a few red corpuscles. If 
by any alteration in position, or tearing of the clump, a channel is 
formed, then the red corpuscles will be wedged in and retained. 
The white thrombi and the mixed thrombi are therefore to be 
regarded as forming a single class. The red thrombi composed 
of the entire blood form another class. thrombosis. 
41 
Having learned so much as to the formation of thrombi, we may 
he prepared to consider the special circumstances under which 
they occur in actual cases. It may be said that in most cases of 
thrombosis there is either such a stagnation of the blood as to 
cause a serious deterioration of the endothelium, or else some pal- 
pable injury to the vessel compromising its endothelium, and 
the various thrombi may be studied according as they are formed 
in one of these ways or the other, while in some cases the action of 
both may he traced. As we have already seen, the stagnation is 
rarely complete, and accordingly the thrombi are mostly white or 
mixed, being formed in the way just described. 
Thrombi form in the heart from the blood stagnating in its 
chambers. This will occur when, from any cause, the cavities of 
the heart are imperfectly emptied, as from dilatation or weakness 
of the muscular substance. The coagulation will occur most 
readily in the parts of the cavities from which the blood is least 
likely to he emptied during the imperfect contractions. Hence 
we tind them near the apices of the ventricles and in the auricular 
appendages more frequently than elsewhere. So also they form 
most commonly behind the columnee carnese, and are frequently 
found peeping out between these muscular columns. These 
thrombi are frequently of a pearly-white color, and are never 
composed of the whole blood, although they may he brown from 
admixture of red corpuscles. As dilatation occurs more frequently 
in the right heart than in the left, these thrombi (which were called 
by Lrennec, globular vegetations), are more frequent in the right 
cavities than in the left, although by no means rare in the left 
ventricle. 
Weakness of the heart not infrequently produces thrombosis in 
the veins. In debilitating diseases, such as typhoid fever, phthisis, 
etc., the heart is weak, and the blood-current sluggish, especially 
in the veins. These thrombi are, at their commencement, usually 
related closely to the valves. In the sluggish state of the circula- 
tion the valves lie half closed, the force of the blood being insuffi- 
cient to press them back against the vessel-wall. Hence the blood 
will stagnate in the pouches of the valves and coagulation will 
begin there. Coagula so formed grow up the veins, but even 
when they have become continuous, they often present a knotted 
condition, from the parts corresponding with the valves being 
bulkier. In such cases the knotted character can often be detected 
through the skin. The coagulation occurs primarily in the larger 
veins, the femoral, jugular, sinuses of the dura mater, but accord- 
ing to Virchow, this is only due to certain local relations. 
In the cases hitherto mentioned, stagnation of blood has been 
the primary factor, but in the thrombosis sometimes occurring 
in the uterine veins after childbirth, we have this combined 
with a palpable injury to the vessel-wall. In some cases, after 
parturition, the uterus contracts imperfectly, and the blood, stag- 
nating in the uterine sinuses, is apt to coagulate. In this case the 
starting-point of the coagulation is often the open mouths of the 42 
AFFECTIONS OF CIRCULATION AND BLOOD. 
veins on the raw uterine surface, which in many respects resembles 
the surface of a wound. 
A more definite wound of a vessel may induce coagulation. 
The coagulation may occur at the ruptured edges, or a clot may 
form in the effused blood outside the vessel, and by successive 
deposition from the escaping blood grow through the gap into the 
vessel. In case of ligature of a vessel the internal and middle 
coats are ruptured, and coagulation occurs as in the case of a 
wounded vessel. If stagnation already exists in a vein, a very 
trivial wound may induce coagulation. Thus in cardiac disease 
where passive hypersemia has led to oedema, the punctures made to 
relieve the oedema or the ulcers which form spontaneously, not in- 
frequently lead to thrombosis in the veins. It is important to bear 
this in mind in connection with the general venous hypersemia of 
valvular disease of the heart. 
Diseases of the vessels and heart which interfere with the endo- 
thelium induce coagulation on the surface. Thus acute endo- 
carditis produces thrombosis on the valvular structures of the 
heart, and chronic endocarditis does so sometimes by the forma- 
tion of calcareous plates, which may, by and by, tear through and 
expose themselves in the current. Atheroma of arteries, by 
causing roughness and ulceration, or by producing calcareous 
plates, may lead to coagulation, which is more serious in such 
small arteries as those of the brain, where thrombi may completely 
obstruct, than in such a vessel as the aorta. The well-known 
coagulation of blood in Aneurism is susceptible of similar explana- 
tion. Here the internal wall is much altered, and usually deprived 
entirely of its endothelium. Another occasional cause of throm- 
bosis is the protrusion of tumors through the walls of vessels. It 
is very seldom that arteries are thus involved, and, as we shall 
afterwards see, thrombosis does not occur in the capillaries, hut 
veins are occasionally attacked by malignant tumors and their 
walls so altered as to induce coagulation. 
Thrombi which have once formed are liable to grow. The 
thrombus is composed of dead fibrine, and the surface is rough, so 
white corpuscles adhere and disintegrate, and coagulation occurs 
readily in successive layers. In the case of the veins the blood 
will be for the most part stagnant above and very often below the 
thrombus, and it is in these vessels particularly that they are apt 
to grow very extensively. Thus a coagulation starting in the 
uterus may travel along to the internal and common iliac veins, 
and thence pass into the veins of the legs. In a case observed by 
the author, coagulation had its origin in a cancer of the kidney, 
which involved the wall of the renal vein, and it extended thence 
to the inferior vena cava, and to the veins of both legs which were 
distended with old thrombi. 
In regard to the character of the thrombi formed under these 
various circumstances, it may be said that almost all are of the 
white or mixed character, as most of them form where the circu- 
lation, although it may be stagnant, is not absolutely at a stand- THROMBOSIS. 
43 
still. The more the blood is at rest, however, the more it is likely 
to contain red corpuscles. It is clear that thrombi forming at the 
edges of a wounded vessel as the escaping blood passes over them 
will be white thrombi, and, indeed, Zahn determined this in his 
experiments. Thrombi forming on the inflamed valves, on the 
diseased endocardium or intima of vessels, or in consequence of 
the projection of foreign bodies or tumors, will be white. The 
globular vegetations of the heart are also white or mixed—they 
are, indeed, often of a pearly whiteness, and even those occurring 
in veins from weakness of the heart are largely composed of white 
corpuscles. Growing thrombi will be mainly white or mixed, but 
as the blood above and beneath a growing thrombus is usually at 
a stand-still, or nearly so, we are apt in this case to have more 
nearly the entire blood entering into the constitution of the 
thrombus, and these are often redder than most. The stratified 
clots in an aneurism are white or mixed, aud it may almost be said 
that, except in the case of coagulation in an aneurism after ligature 
of the artery, it is seldom that the whole blood is concerned in the 
formation of a thrombus. 
It is important to distinguish thrombi which have formed during 
life from mere post-mortem coagula. It will be clear from what 
has gone before that the thrombi are mostly either white or gray, 
but being formed largely of white corpuscles, they are of a dead 
or opaque white or giTiy appearance. Post-mortem clots are some- 
times pale from the sinking of the red corpuscles or otherwise, but 
they are gelatinous and smooth on the surface and mostly trans- 
parent, whereas the thrombi are firmer, drier, more opaque, and 
granular on the surface. The thrombi also adhere to the wall to 
some extent, whereas the clots do not, although in the heart, from 
getting entangled among the columnse carneae, they may have an 
appearance of adhesion. Lastly, the thrombi are often stratified, 
indicating their deposition in successive layers. 
We have now to consider the changes avhich thrombi undergo 
after their formation. It is to be remembered that the coagulum 
is virtually a piece of dead matter, fibrine being merely a chemical 
compound, not a living structure. There are two indications, 
chiefly, in which thrombi are liable to change—the one is softening, 
and the other an apparent organization. 
Softening is a frequent result, especially in the coagula in the 
heart and veins. It should be said that the softening which occurs 
in connection with pyaemia is here left out of account, as the whole 
processes in connection with this disease will be studied afterwards. 
The globular vegetations in the heart frequently present very good 
examples of softening. It begins in the central parts of the 
thrombus, and the coagulum breaks down into a turbid brownish 
juice, the softening extending gradually outwards. 
The juice is often like a mixture of pus and blood, or in very 
white thrombi it may be like pure pus. It consists of the debris 44 
affections of circulation and blood. 
of the thrombus, and no well-preserved corpuscles are to he found 
in it. The softening may extend outwards till a niece rind of clot 
is left, and this may give way and cause the juice to be launched 
into the circulation. In veins, also, softening may take place, and 
here the coloring matter of the blood 
may be deposited in the form of 
hsematoidin crystals (see Fig. 5). Of 
course, where softening has occurred, 
there is much more probability of 
bits of the thrombi being torn away 
or carried forward so as to produce 
embolism. 
Thrombi, instead of softening, may 
dry in and shrivel. In such case we 
may have lime salts deposited, and 
even through time the formation of 
little stony masses—vein-stones or 
Phleboliths. 
The Organization of a thrombus 
is a process of some interest. As the ■ 
coagulum is dead, it is clear that it 
cannot take part in the process of 
organization. In studying inflamma- 
tion this subject will come up for fuller discussion, but it may here 
be stated that when a piece of dead animal substance is present 
among the living tissues, the first step towards its absorption is 
usually its replacement by an elementary tissue, the dead structure 
forming, as it were, a mould on which the new tissue forms itself. 
The constituents of the thrombus are, therefore, pushed aside or 
disintegrated by masses of round cells (as shown in Fig. 6, b); 
and at the same time bloodvessels springing from the vasa vasorum 
extend into the substance of the new-formed tissue. The thrombus 
is thus converted into, or replaced by, a vascular tissue, which 
subsequently develops into connective tissue. Like other new- 
formed connective tissue of this kind, this tissue tends to contract. 
The result of this sometimes is the drawing together of the walls 
of the vessel, and the permanent obliteration of its calibre. The 
vessel is thus converted into a solid cord. In other cases the con- 
traction acts on the walls of the proper vessels of the new-formed 
tissue, dragging them outwards. By this means the vessels are 
widened, and in time may come to assume a cavernous character. 
This may result in the reestablishment of the circulation, the 
wide spaces of the sponge-like tissue coming to communicate with 
the regular calibre of the vessel. A favorite place for the forma- 
tion of this cavernous tissue, is the place of union of the iliac 
veins to form the vena cava. Here, the vessels are sometimes 
found tilled with a spongy tissue through which the circulation is 
carried on. By a still further contraction of the new-formed tissue, 
the calibre of the vessel may be completely reestablished, the 
sinus-like blood-channels expanding into the calibre of the vessel. 
Fig. 5. 
Crystals of haematoidin found 
closely aggregated in the midst of an 
old thrombus in a vein. The crystals 
have a deep red color. X 350. THROMBOSIS. 
45 
Before leaving this subject of thrombosis, it may he well to con- 
sider WHETHER COAGULATION OCCURS IN THE LIVING CAPILLARIES. It 
is to be remembered that the deterioration of the endothelium is 
the proximate cause of the coagulation of the blood in the vessels. 
The capillary wall consists entirely of endothelium, and the dete- 
rioration of it means the deterioration of the entire capillary wall. 
Such an interference with the capillaries as to induce coagulation 
Pig. 6. 
Organization of blood-clot, a represents the clot little altered ; red corpuscles are chiefly 
seen, with a few solid round cells, which are like white corpuscles, but more numerous than 
in normal blood. In b the red corpuscles are entirely replaced by round cells. In c the 
round cells have given place to large spindle3. X 350. 
will only occur when actual necrosis takes place. Moreover, as 
the tissues depend on the capillaries for their nutrition, obstruction 
by thrombosis will involve the death of the tissues themselves. 
Hence thrombosis of the capillaries, or even complete stagnation 
in them, may be put out of the question except in connection with 
necrosis. The non-occurrence of thrombosis in the capillaries is 
of great practical consequence. If it were not so, the thrombi in 
veins, growing against the current as they so readily do, would 
grow into the capillaries, and through them into the arteries. The 
capillaries, not admitting of this, form a barrier to the extension 
of the coagulation. It thus happens that, after extensive coagula- 
tion in the veins, the circulation is largely maintained by arteries, 
capillaries, and lymphatics, and necrosis rarely occurs. It is 
worthy of note in connection with this matter that the blood found 
in the capillaries after death is nearly always fluid. 
In studying thrombosis, we have left out of account all cases of 46 
AFFECTIONS of circulation and blood. 
what is called septic thrombosis, where the coagulation arises in 
connection with the introduction of decomposing material into the 
veins. Such processes will receive consideration in another part. 
We have still to consider the effects of thrombosis. Apart 
from the occurrence of embolism, which may result from throm- 
bosis anywhere, it will be mostly thrombosis of the veins that is 
followed by serious results. The most direct effect of obstruction 
of veins by thrombi is, of course, passive hyperemia with its 
consequent cedema. The occurrence of serious oedema depends 
largety on the extent of the anastomosis of the obstructed vein, 
and also somewhat on the rapidity with which the thrombosis has 
occurred. If the thrombus forms slowly, the functions of the 
plugged veins may be largely taken up by the lymphatics and by 
other veins which remain unaffected. In the case already referred 
to, where a cancerous tumor in the kidney had burst into the renal 
veins, and thrombosis had extended to the vena cava and down 
the veins of both legs, there was comparatively little oedema at 
any time, although all the main venous trunks of both legs were 
plugged. One circumstance renders this compensation, especially 
by the lymphatics, the easier, the fact that the thrombosis 
does not extend into the capillaries, and consequently not into the 
arteries. The cause of this has been already explained, but it is 
clear that if the circulation is still maintained in the arteries and 
capillaries, the lymphatic circulation will not suffer. 
It is important to know that these secondary effects of throm- 
bosis, and especially cedema, will not usually show themselves for 
some time after the onset of the process. A coagulation begin- 
ning in a vein will take some time before it Completely obstructs 
it, and even when it has done so, it may be necessary for it to 
grow into other veins before any pronounced cedema will develop. 
Hence it is that a thrombosis may lead to embolism by detachment 
of portions of the thrombi before it has manifested its presence by 
hypersemia and cedema. 
Thrombosis in veins seldom leads to Gangrene, and in the few 
cases in which gangrene actually occurs some additional interfer- 
ence with the circulation will usually be discoverable. Weakening 
of the heart, in conjunction with thrombosis, may cause it, and so 
may disease of the arteries diminishing the force of the blood. 
2. Embolism.—This, as we have seen, is a process frequently 
associated with thrombosis. Embolism will affect arteries or 
capillaries, and, as the portal vein is distributed in the liver like 
an artery, it is also liable to embolism. The plug or embolus is 
most frequently a thrombus or a part of one. It may be a bit of 
tumor which has found its way into a vessel, or a foreign body 
which has obtained entrance. It may be a piece of cretaceous 
material from a degenerated valve or vessel. It may be a parasitic 
animal, as the echinococcus, which has found its way into the cir- 
culation. EMBOLISM. 
47 
Iii the case of many arteries the effects of embolism are very 
trivial. The anastomoses are so free that they readily compen- 
sate completely, and the circulation is restored almost at once. 
For the purposes of the tissues it is the capillary circulation which 
is of importance; and if the blood, by any route however circui- 
tous, reaches the capillaries, there is no serious result. 
When an artery with free anastomosis is obstructed by an em- 
bolus, there will be at once an increase of blood-pressure on the 
proximal side of the plug. The anastomosing branches by dilata- 
tion will reduce this excessive blood-pressure, but the excessive 
bloocl-pressure may itself assist in opening up the anastomosing 
channels. In this way the circulation is restored. At the seat of 
obstruction thrombosis occurs on each side of the embolus, and 
goes on upwards and downwards to the nearest branches. By the 
organization of the thrombus the calibre of the artery is destroyed 
and the vessel reduced to a solid cord. In this way a piece of 
artery is lost, and that is all the permanent result. 
It is similar with capillary embolism. The ultimate result is 
the loss of a piece of capillary between the two nearest communi- 
cations. At the time of its occurrence the embolus in a capillary 
will produce very little disturbance, as the communications are so 
free in the capillary system. It sometimes happens, however, that 
multiple embolisms cause more serious derangements of the circu- 
lation. 
It is very different in the case of arteries which have no anas- 
tomoses. There are parts of the body in which the arteries are 
distributed to a perfectly definite piece of tissue, and have no anas- 
tomotic connections. In the case of such arteries, to which Cohn- 
heim gives the name of End Arteries, the results of obstruction 
are very serious. The part is entirely deprived of its blood-supply 
through the arteries, and if any blood reaches it, it must be by 
the connection with neighboring capillaries or by the veins. The 
most direct result of obstruction of an end artery, therefore, is 
anaemia, and consequent death or necrosis of the tissue. But 
there are some cases in which an apparent exception to this occurs; 
there is the necrosis, but instead of anaemia, there is an excessive 
engorgement with blood. This is very well seen in the case of 
the lung, where embolism often produces the hemorrhagic infarc- 
tion. We have to consider how this is to be explained. 
Cohnheim’s experiments in elucidation of the pathology of em- 
bolism are of such importance in this regard that more particular 
reference to them may be here permitted. The subject of experi- 
ment was the tongue of the frog. The two main lateral arteries 
of the tongue are not end arteries, but their lateral branches are. 
Cohnheim introduced little blackened pellets of wax into the 
division of the aorta which communicates with the arteries of the 
tongue, and these were sometimes carried to the tongue, obstruct- 
ing the arteries there. Sometimes one pellet obstructed the anas- 
tomosing branch between the main arteries, while another stuck 48 
AFFECTION'S OF CIRCULATION AND BLOOD. 
in one of the main arteries, so that the latter was converted into 
an end artery. Whether a main artery thus conditioned or a 
plugged lateral branch was observed, the process was virtually the 
same. The blood was, immediately after the plugging, at a stand- 
still, in artery, vein, and capillaries. These vessels might be mod- 
erately full of blood or might contain only blood-plasma. Soon, 
however, a backward flow of the blood from the veins was observed 
(cliagrammatically shown in Fig. 7), and by and by this produced 
Fig. 7. 
Diagram of conditions following embolism of an end artery. In the figure to the left the 
state of anaemia after the embolism is shown. In the other figure the regurgitant current 
from the vein is indicated (after Cohnheim). 
an engorgement of the entire vessels, veins, capillaries, and arteries. 
After a time a remarkable diapedesis began to manifest itself 
through the capillaries into the surrounding tissue, which became 
engorged with blood. The portion of tissue concerned would, in 
accordance with the area of distribution of the artery, he wedge- 
shaped, and the result was a wedge-shaped, red, pulpy piece of 
tissue, not unlike a blood-clot—the Hemorrhagic infarction. If 
the frog survived, the piece of tissue by and by sloughed off. 
The explanation of these phenomena is not very difficult. The 
obstruction of the artery reduces the pressure in the vessels sup- 
plied by it to nothing. The veins are still in open communication 
with the veins of the part, in which, although the blood-pressure 
is low, it is still something. Accordingly, the backward flow 
occurs from the veins to the capillaries, and so to the obstructed 
artery. Thus the engorgement of the vessels is not difficult to 
explain. The diapedesis is to be referred to the fact that the 
capillaries, being deprived of blood, have the integrity of their 
walls impaired. .We have already seen that passive hypersemia 
produces diapedesis, owing to interference with the capillary wall. 
Much more serious is the nutritive deterioration in this case, and 
so the diapedesis is very great, leading to a marked infiltration of 
blood into the tissues around. The deprivation of fresh blood 
causes death of the tissue, which here, as it is an external part, 
sloughs. EMBOLISM. 
49 
In applying these facts to human pathology, we have to consider, 
in the tirst place, what arteries of the body are end-arteries. 
These are the renal and splenic arteries and their branches, the 
nutritive arteries of the brain, the central retinal artery, the pul- 
monary artery and its branches, to which we may add the portal 
vein, as in its relations an end-artery. We have not, in all of 
these, the typical hemorrhagic infarction, and it is necessary to 
consider each individual case separately, and endeavor to explain 
the divergencies which they present. 
Embolism in the lungs frequently presents the most typical 
hemorrhagic infarction, but it has been known since Virchow’s 
important researches that embolism of the pulmonary artery does 
not always lead to its formation. In the same lung you may have 
a number of obstructed arteries, in connection with some of which 
there is the hemorrhagic infarction, while in the case of others it 
is entirely absent. This apparent puzzle is explained when we 
come to consider more closely the relations of the circulation in 
the lungs. It has already been said that it is the circulation in the 
capillaries that is of consequence in considering the results of em- 
bolism, and we know that the capillaries everywhere anastomose 
freely with each other. It is conceivable, therefore, that the anas- 
tomosis of the capillaries might come to act like an arterial anas- 
tomosis, and that the circulation might be maintained through the 
capillaries. In the lung the capillaries of the pulmonary artery 
are wider than those of most other parts, and so the loss of force 
by friction will be less than elsewhere. There is, besides, less ten- 
dency to necrosis of the tissue here, as the connective tissue of the 
lung, the bronchi and the larger vessels, are supplied with blood 
by the bronchial arteries. In some cases, then, the circulation in 
the capillaries behind the plug is sufficient to maintain the capillary 
wall and prevent the formation of the hemorrhagic infarction, and, 
indeed, experiment seems to show that in normal animals embolism 
seldom results in the infarction. 
If we consider the usual situations of the hemorrhagic infarc- 
tions of the lung, we shall obtain still clearer views on the subject. 
If an artery is obstructed near the root of the lung, then the 
capillaries of the piece of tissue concerned will be in communica- 
tion on all sides with capillaries in which the circulation is still 
active. The piece of tissue is, as it were, buried in the spongy 
lung substance whose capillaries are tilled with actively moving 
blood. It is not surprising that, in this case, the capillary circula- 
tion in the affected piece of tissue, although rendered sluggish, is 
still maintained; the movements of respiration also assisting in 
maintaining the circulation. In accordance with these considera- 
tions the hemorrhagic infarction seldom occurs in the central parts 
of the lung. But if the obstructed artery has a peripheral distri- 
bution, if the piece of tissue is covered on one side by the pleura, 
or if, being situated at the edge of the lung, it has two sides 
covered by pleura, or even, being at the edge of a lobe as well as 
of the lung, it has three sides covered with pleura, then it will be 50 
AFFECTIONS OF CIRCULATION AND BLOOD. 
in a much less favorable position. On one, two, or three of its 
sides the capillaries are not in communication with other capillaries 
in which the circulation persists. It is not surprising, therefore, 
that the hemorrhagic infarction is nearly always peripheral, and 
that it frequently has its seat at the edge of the lung, or at the 
edge of a lobe. The infarction is wedge-shaped, and it is interest- 
ing, in relation to the points we are considering, to observe that 
the plug is usually not exactly at the apex of the wedge but a 
certain distance nearer the heart, so that sound tissue intervenes 
between the beginning of the plug and the infarction. The ex- 
planation of this is, that in the neighborhood of the plug, that is to 
say, at the apex of the conical piece of tissue supplied at the artery, 
the tissue is still surrounded on all sides by capillaries in which the 
circulation is active, and for a certain distance this is sufficient to 
carry on the circulation. It may even be said that all around the 
periphery of the infarction, so far as it is in connection with lung 
tissue, there will be a zone in which the surrounding capillaries 
keep up the circulation in the affected capillaries, and that the 
actual infarction is less in all these directions than the area of dis- 
tribution of the obstructed artery. 
It appears that if the heart is of normal strength, it, with the 
movements of respiration, is capable of maintaining the circula- 
tion in the capillaries, even when a peripheral branch is the seat of 
embolism, and it is mostly in cases of weakness of the heart, or 
when the pulmonary circulation is already in a state of engorge- 
ment, or where multiple embolisms obstruct numerous neighbor- 
ing trunks, that the infarction occurs. When embolism occurs in 
the pulmonary artery, there will always be stagnation of the blood, 
and even if the hemorrhagic infarction does not form, there will 
be great interference with the circulation. 
In the case of the spleen there are no such compensating con- 
ditions as in the lung, and here the hemorrhagic infarction seems 
to occur with great uniformity. 
In the kidney, embolism always produces necrosis of a wedge- 
shaped piece of tissue, but even in recent embolism this is not 
always engorged with blood. The very wideness and freeness of 
communication of the capillaries in the lung which so frequently 
prevents the formation of the hemorrhagic infarction, will ensure 
that when it does occur there will be a very great engorgement of 
the vessels and abundant diapedesis. In the case of the kidney, 
the capillaries are smaller, and their communications with the veins 
more circuitous, and so it often happens that necrosis occurs before 
the backward flow has been established. In that case the whole 
wedge-shaped piece of tissue coagulates into a solid mass (see 
Fig. 8). This is an instance of the so-called coagulation-necrosis, 
which we shall have a better opportunity of studying afterwards. 
We may have, therefore, a hard, solid, whitish wedge, instead of a 
hemorrhagic infarction. A true hemorrhagic infarction is some- 
times met with, especially when a small artery is obstructed. 
In the case of the brain, necrosis of the tissue occurs, and some- 51 
times so rapidly that the capillaries are rendered incapable of 
receiving the blood before the backward flow from the veins is 
sufficient to cause engorgement. The necrosis here does not result 
in coagulation of the tissue, but in its softening, so that as a result 
of embolism of the brain we have softening which may, or may 
not, be accompanied by hemorrhage, but is never associated with 
very considerable bleeding. Embolism of the retina is similar to 
that of the brain. 
We have still to consider the case of the portal vein, which, in 
its distribution, is comparable to an end-artery. The conditions 
EMBOLISM. 
Fig. 8. 
Embolic infarction of kidney, showing the wTedge-shaped piece of tissue affected 
(after Rayer). 
here, however, are peculiar, inasmuch as the liver is supplied with 
blood from the hepatic artery as well as from the portal vein. It 
has already been more than once noted that it is the condition of 
the capillaries which is of importance in relation to the hemor- 
rhagic infarction. A study of the circulation in the liver shows 
that when the portal vein is closed, blood still passes from the 
hepatic artery into the hepatic capillaries. The hepatic artery 
supplies blood to the connective tissue, the walls of the ducts and 
larger bloodvessels of the liver. The capillaries from these are 
collected into veins which open into the interlobular veins, which, 
of course, are the terminals of the portal vein. So that when the 
portal vein is obstructed, the blood from the hepatic artery passes 
into the interlobular veins, thence into the hepatic capillaries, and 
so on into the intralobular and hepatic veins. The capillaries of 
the portal system are thus kept supplied with blood, and their 
nutrition does not suffer. Experiment has even shown that when 
the entire portal vein is obstructed the secretion of bile is not 
entirely at a standstill; the blood of the hepatic artery affording 
material for a limited production. 
It has been said that the hemorrhagic infarction forms in the 
case of end-arteries, but there is an apparent exception to this in 52 
AFFECTIONS OF CIRCULATION" AND RLOOD. 
the case of the superior mesenteric artery. If the superior 
mesenteric artery or one of its larger branches be obstructed, 
hemorrhage occurs in the intestine and mesentery, and the portion 
of gut suffers necrosis, but it is well known that the anastomosis 
of the mesenteric arteries is tolerably free. The explanation of 
this apparent anomaly has been worked out by Cohnheim and his 
pupils in a very interesting manner. As a rule, it may be said 
that main stems have, in proportion to their size, much less con- 
siderable anastomotic communications than the smaller branches. 
Thus the anastomotic communications of the iliac or femoral artery 
are proportionally much less considerable than those of the tibial 
or of smaller arteries still, and the anastomoses of the superior 
mesenteric are much less voluminous in proportion than those of 
its branches nearer to the gut. If the main stem be obstructed, 
therefore, the restoration of the circulation occurs much more 
slowly than when a small stem is the seat of obstruction. Another 
illustration of this is afforded by embolism of the femoral artery. 
The temperature falls rapidly, the limb is numb and half-paralyzed, 
and this is doubtless due to insufficient supply of blood by the 
artery. It takes some days before the collateral vessels dilate suf- 
ficiently to restore the temperature and functions of the limb. 
The contrast is very great when a small stem is obstructed; in that 
case comparatively little inconvenience is suffered, and recovery is 
rapid, unless, indeed, several small stems are simultaneously 
affected, in which case, as we shall afterwards see, the results may 
be very serious. It is similar in the case of the superior mesen- 
teric and its larger branches. Obstruction here is slowly recovered 
from, and for a time the circulation is virtually at a standstill. 
But here a very important element comes into consideration. 
The vessels of all parts of the body are not equally resistant. 
Those of the skin and muscles (*and here it is of course the capil- 
laries and small veins that are concerned), are peculiarly resistant, 
and are able to stand a considerably prolonged deprivation of 
blood. It is different with those of the intestines. In order to 
test the vulnerability of the vessels of the intestine, the following 
experiment was made. A ligature was tied on the superior mesen- 
teric artery, and the precaution was taken of tying it over leather, 
so that it might not destroy the vessel, and thus admit of its being 
subsequently unloosed. It was found that if after two to two and 
a half hours the ligature was untied, hemorrhage occurred from 
the capillaries. The meaning of this is that within this period the 
deprivation of blood so seriously disorganizes the capillaries that 
they are no longer able to prevent the escape of blood at the 
normal pressure. A much longer time is required in order to the 
occurrence of hemorrhage at the pressure of the venous blood; a 
period of ten or twelve hours is needed. But it was found that 
for the establishment of the collateral circulation a period exceed- 
ing even this was required, namely, fourteen hours. Accordingly, 
before the anastomosis can be established, the backward flow from 
the veins has already begun, and even the diapedesis. The rees- EMBOLISM 
53 
tablishment of the circulation even increases the tendency to hem- 
orrhage, as it subjects the blood to a higher pressure than that of 
the venous blood. The experiments referred to showed that when 
the superior mesenteric artery is obstructed, the hemorrhagic 
infarction forms with a backward flow from the veins just as in 
other cases. 
It will be obvious that arteries possessing free anastomoses 
MAY BE REDUCED TO THE CONDITION OF END-ARTERIES if their aiiaS- 
tomoses are no longer available. If, as sometimes happens, an 
embolus passing to the leg breaks up, say, by being propelled 
against a bifurcation, and is scattered to a number of stems simul- 
taneously, then the circulation will be reestablished very slowly or 
not at all, and necrosis is liable to occur, especially if the circula- 
tion is already feeble. Thus, we may have gangrene of the toes 
occurring in this way. It is to be added that in old people ob- 
struction of a number of arteries sometimes occurs from throm- 
bosis as a result of atheroma, and this may likewise lead to necrosis. 
Hitherto we have considered only the more immediate results 
of embolism in end-arteries, we have still to pass under review the 
further consequences. We have seen that the regular result is 
necrosis of the piece of tissue concerned with or without the occur- 
Fig. 9. 
Infarction of kidney undergoing absorption. The infarction is white and depressed below 
the level while the tissue is puckered around it (after Rayer). 
rence of hemorrhage. In the case of the lungs there is a doubtful 
exception to the uniform necrosis of the piece of tissue. The lung 
tissue is nourished to a great extent by the bronchial artery, and 
obstruction of a branch of the pulmonary artery will not interfere 54 
AFFECTIONS OF CIRCULATION AND BLOOD. 
with the nutrition of the connective-tissue stroma and the bronchi, 
and it is probable that only a partial necrosis occurs. The air- 
vesicles, however, are nourished by the capillaries of the pulmonary 
artery, and it is to be expected that, for the most part, these at 
least will either necrose or atrophy. As a matter of fact, the 
whole infarction often undergoes necrosis, and in cases of liemor- 
hagic infarction of the lung which recover, symptoms like those 
of phthisis sometimes develop, and lung tissue has been known to 
be spit up. As the necrosed lung tissue is disposed of, a cicatrix 
will take its place. In the case of the spleen and kidney, the solid 
infarctions are gradually absorbed (see Fig. 9) like foreign animal 
matter in the living body generally, a preliminar}* decolorization 
first occurring. Their place is taken by cicatrices in the midst of 
which, even at a late date, little pieces of solid, cheesy-looking 
material may often be seen. The softened brain tissue is also ab- 
sorbed, and a cicatrix or a cyst takes its place. So is it with the 
retina; the piece of tissue is lost and absorbed. In the case of the 
superior mesenteric artery, the slough of the bowel and hemorrhage 
lead on mostly to a fatal result, but cases do occur in which, after 
the separation of a slough, an ulcer is left which may ultimately 
cicatrize. 
We have still to consider two rarer forms of embolism, namely, 
by oil and by air. Oil or fluid fat not unfrequently gets into the 
bloodvessels. It does so where, by fracture of a bone or injury 
to the subcutaneous adipose tissue, the fat cells in the bone mar- 
row, or adipose tissue are broken up so as to set free the oil, and, 
at the same time, the vessels, and especially the veins, are laid 
open so as to absorb the oil. Oil also occurs in the blood in cases 
of diabetes, and, as in Fig. 10, may produce embolism. The oil 
is carried, of course, to the right heart, and on into the lungs, 
where it sticks in the capillaries and the smallest arteries. If the 
capillaries are obstructed at considerable intervals, then no evil 
results, the anastomosis being so free that no serious disturbance 
occurs, and the oil itself does not irritate. But, if a considerable 
number of small arteries near each other be obstructed, or even a 
large number of capillaries, we may have a condition resembling 
the hemorrhagic infarction. It has been found on experiment 
that abundant fat embolisms in the ear of a rabbit, by obstructing 
numerous capillaries, may lead to necrosis. In some cases the oil 
may, to some extent, pass through the lung capillaries, and it is 
found mostly in the Malpighian tufts of the kidney, one or two 
loops being here and there tilled. There are a few rare cases on 
record in which extensive embolism has occurred in the smallest 
vessels of the brain, conjunctiva, skin, muscles, heart, intestines, 
liver, and kidneys, and has apparently been the cause of death. 
It is wrell known that the admission of a considerable quantity 
of air into veins near the heart often leads to a fatal result, and 
some have supposed that the embolism in the lungs is the cause. 
It need hardly be said that, as the pressure in the veins near the HEMORRHAGE. 
55 
heart is very low, and there is even a degree of suction during 
inspiration, there is great danger in opening such a vein as the 
jugular. In regard to the cause of death in these cases, it is im- 
portant to notice that a repeated admission of small quantities of 
air does not produce serious results, whereas a single large admis- 
sion is rapidly fatal. This hardly looks as if embolism were the 
cause, and, as a matter of fact, the air is found after death mainly 
in the right auricle and ventricle, which are usually enormously 
Fig. 10. 
Oil embolism of lung. The fat is seen in larger and smaller drops in branches of the pul- 
monary artery (a a) as well as in the capillaries. From an osmic acid preparation (Sanders 
and Hamilton). 
dilated. The fact seems to he that the right ventricle, in contract- 
ing, merely squeezes together the elastic air, which again expands 
during the diastole. The force of the heart is thus fruitlessly 
expended and the blood is not sent into the pulmonary artery. 
Moreover, the over-distention of the right auricle with air prevents 
the admission of blood from the verne caves. Thus the circulation 
is at a standstill, and death results. 
HEMORRHAGE. 
This is the escape of hloocl from the living vessels or the heart. 
It may take place in minute drops, perhaps frequently repeated, 56 
AFFECTIONS OF CIRCULATION AND BLOOD. 
or in larger quantities. The blood may pass outside the body or 
make a place for itself and form an extravasation inside the body, 
or it may infiltrate the tissues over a considerable area, forming 
an ecchymosis. 
From what has gone before, it will be understood that there are 
two forms of hemorrhage, which should be kept apart, namely, 
that by rupture of vessels, and that by diapedesis. The former 
may affect any size or kind of vessel, and when it occurs, there 
wili be an escape of the whole blood. The latter occurs only in 
the finest vessels, mainly the capillaries, and it is chiefly the red 
corpuscles which escape, and with them, of course, some fluid, but 
the fluid has not the constitution of the entire blood-plasma. These 
two forms of hemorrhage are different, not only in kind, but in 
the causes which lead to them, and yet in some cases it may be 
difficult to determine which is the form present. 
Taking first the case of hemorrhage by rupture, it is most 
obviously produced by some agent acting on the vessel from with- 
out, as in the case of a wound by a weapon or a piece of broken 
bone, etc. Then also ulceration may cause penetration of a vessel. 
Disease of the walls of vessels, or of the heart, may lead to rupture, 
as aneurism, atheroma, varix. It may here be said that new-formed 
vessels, whether in inflammations, or in tumors, are peculiarly 
prone to rupture, presumably from the thinness of their walls. 
There are further some cases of hemorrhage in which we have to 
assume some change in the vessels arising from an altered condi- 
tion of the blood, as the cause of hemorrhage, and in most of these 
cases it is doubtful whether the hemorrhage takes place by rupture 
or by diapedesis. In scurvy there is a deterioration of the blood 
which presumably has a direct effect on the structures comprising 
the vessel-wall. The hemorrhage here is probably by rupture, 
judging from the rapidity with which sometimes large extravasa- 
tions occur, but it is not impossible that it may be by diapedesis. 
In purpura hemorrhagica (or morbus maculosus Werlhofii), there 
is also hemorrhage traceable to weakening of the walls of the 
vessels from a change in the constitution of the blood. In anaemias 
and leukaemia, hemorrhages are very frequent, and doubtless the 
altered constitution of the blood has to do with it. In these the 
hemorrhage is probably by diapedesis. Alteration of the constitu- 
tion of the blood is also frequently a cause of hemorrhage in the 
acute specific fevers. The petechiae of typhus, and the frequent 
hemorrhages in smallpox are examples, the latter being often so 
marked as to warrant some cases being called hemorrhagic small- 
pox. 
In the hemorrhagic diathesis there is a peculiar fragility of the 
walls of the vessels, and this is doubtless congenital and often 
inherited. In such persons a slight injury produces rupture, and 
there is difficulty in getting the hemorrhage stopped. Even a 
temporary excess of pressure in the vessels may lead to hemor- 
rhage in these cases. 
In poisoning by phosphorus the vessels become fatty, and there HEMORRHAGE. 
57 
is a tendency to hemorrhage, hut whether by rupture or by diape- 
desis is unknown. 
Of hemorrhages undoubtedly by diapedesiswe have already con- 
sidered two good examples, in passive hypersemia and the hemor- 
rhagic infarction. In inflammation also there is escape of the 
blood-corpuscles by the same method. 
We have next to consider the stoppage of hemorrhage, and in 
regard to diapedesis it is clear that it will cease when its cause 
ceases to act. There is in this case no rupture of the vessel, and 
so soon as circumstances restore the vessel to its normal state of 
impermeability to the blood-corpuscles the hemorrhage will cease. 
In the case of hemorrhage by rupture, the problem is more com- 
plicated, and various elements enter into it. It is well known that 
such hemorrhages tend to cease spontaneously, and we have now to 
see how that result comes about. 
The direct means of stoppage is coagulation of blood, so that a 
thrombus obstructs the orifice. The thrombus may form at the 
ruptured edges, or the blood may coagulate outside the vessel, and 
the coagulum by successive deposition, grow in. The actual 
thrombus, as it is formed by flowing blood, will be a white or 
mixed one. The stilling of the hemorrhage being directly the 
result of thrombosis, it is to be added that various circumstances 
favor the formation of the thrombus, and aid in preventing its 
displacement. These circumstances are for the most part the 
direct results of the hemorrhage itself. In the first place, as a 
hemorrhage proceeds the white corpuscles become proportionately 
excessive, and this is itself favorable to the formation of thrombi. 
In the case of an artery again, the narrowing of the ruptured 
orifice by contraction of the muscular coat favors the stilling of 
the hemorrhage, and so does its retraction within its sheath, thus 
leaving a space in which the clot has room to form. This contrac- 
tion of the muscular coat is brought about in the first instance-by 
the stimulus of the agent which caused the rupture, and it will be 
kept up by the irritation of the blood on the exposed and torn 
structures. Then the bleeding as it progresses leads to anaemia, 
and this in two different ways assists in stilling the hemorrhage. 
It causes weakness of the heart, and so the arterial pressure is 
reduced and the thrombus is not so liable to be washed away. It 
also produces irritation of the vaso-motor centre in the medulla 
oblongata, and this leads to contraction of the finer arteries 
throughout the body. It is clear that in the case of an artery a 
longitudinal wound will be more difficult to close than a transverse 
one, as the contraction of the muscular fibre will only make it 
gape further. On this account it is customary when bleeding is 
serious from an artery thus wounded, to cut it right across in order 
to still the hemorrhage. 
We have now to study the further history of the blood which 
has escaped. Blood which has escaped by diapedesis is mostly 
carried off by the lymphatics, but there is no doubt that to some 58 
AFFECTIONS OF CIRCULATION AND BLOOD. 
extent it may also undergo partial transformations such as will be 
described immediately, and which result in pigmentation. 
In the case of hemorrhage by rupture the blood is sometimes 
entirely absorbed, and that with considerable rapidity, especially 
when it is infiltrated into the tissues, where it occupies the serous 
and lymphatic spaces, as in ecchymoses. In the case of larger 
hemorrhages the blood either accumulates in an existing cavity, or 
by tearing makes a cavity for itself. It may remain for some time 
as an independent mass, forming a kind of permanent tumor, the 
hsematoma, which is specially considered below. The blood may 
remain for some time fluid, but usually it coagulates by and by. 
After a longer or shorter period of time the blood is disposed 
of, and we have now to consider the manner of its disposal. It is 
easy to understand how the fibrine is dealt with, it disintegrates, 
and is through time absorbed. The red corpuscles undergo more 
considerable changes, and their history we have to trace. The 
coloring matter is frequently dissolved out of the red corpuscles, 
and in solution it is largely absorbed. The solution may stain the 
intercellular substance of the tissues, and possibly may lead to a 
more or less permanent pigmentation of them. In true pigmen- 
tations, however, the coloring matter is in cells, and it is doubtful 
whether living cells are capable of being simply stained by a solu- 
tion of coloring matter. The peculiar bright red color which one 
sees in the neighborhood of a hemorrhage in the brain, or the 
various colors seen in the skin after an effusion of blood into it, are 
due to staining of the tissues with the dissolved coloring matter of 
the blood, but neither of these is permanent. The coloring matter 
after being dissolved out of the corpuscles is often, after a time, 
deposited in the solid form, appearing as crystals of hsematoidin 
(see Fig. 11), or as granules. 
Fig. 11. 
Crystals of hmmatoidin from an old hemorrhage in the brain. Their color is reddish-brown. 
X 350. 
Again, the red blood-corpuscles may be taken into the substance 
of other cells, and so disposed of. The effused blood acts as an 
irritant in the tissues, producing inflammation around, and 
numbers of leucocytes collect in the neighborhood. These take 
into their substance red corpuscles, thus becoming blood-corpus- 
cle-holding cells (see Fig. 13), concerning which much has been HEMORRHAGE. 
59 
written. The leucocytes, as shown in the figure, may take up 
several red corpuscles, and of course they become greatly enlarged. 
Besides that, the giant-cells which we shall afterwards refer to in 
connection with inflammation, may take up red corpuscles. These 
cells pass in part into the lymphatics, and the red corpuscles are 
thus absorbed. But it appears that to some extent they remain 
Fig. 12. 
Fig. 13. 
Crystals of hasmin prepared artificially by adding 
glacial acetic acid to a drop of blood, heating and 
evaporating to dryness. X 350. 
Cells containing blood-corpuscles 
from the neighborhood of a hemor- 
rhage: a, with fresh corpuscles; b, 
with dark granules from disintegra- 
tion of red corpuscles. 
permanently, or else that the red corpuscles are taken up also by 
the fixed connective-tissue cells, and so a true pigmentation is 
brought about. In either case the red corpuscles within the cells 
shrink into reddish-brown irregularly shaped bodies (see Fig. 13, 6), 
which lie in the substance of the cell. Subsequently the pigment 
may break up and be dissolved out of the cell, and so the colora- 
tion will disappear. In the case of cliapedesis, a similar process of 
pigmentation may occur by the red corpuscles being taken up by 
cells. 
It has already been stated that the blood acts as a foreign body, 
and leads to inflammation around it. This inflammation some- 
times leads to what is called the organization of the blood-clot. 
In this case the process is very similar to that already referred to 
in the organization of the thrombus, and the result is usually the 
formation of a cicatrix. Sometimes a process in some respects 
similar to the formation of the cavernous tissue in place of a 
thrombus occurs, but instead of the meshes being filled with blood 
they are filled with serous fluid. Thus in the case of a hemor- 
rhage in the substance of the brain the new-formed connective 
tissue which replaces the effused blood, is unable, from the brittle 
nature of the brain tissue, to form a cicatrix by its contraction. 60 
AFFECTIONS OF CIRCULATION AND BLOOD. 
Instead of that, by its contraction it leaves spaces which are filled 
with serous fluid, and so we have the apoplectic cyst. 
An old clot which is not in a position to he readily disposed of 
in any of the ways described may dry in and finally become im- 
pregnated with lime salts. It need hardly be said that, when ex- 
posed to septic influences, a clot is liable—perhaps very liable—to 
undergo decomposition. 
Blood which has been effused occasionally takes up a somewhat 
permanent position in the body, and when masses of blood thus 
remain for a time they may assume the appearance of tumors. 
Sometimes a class of blood-tumors is distinguished under the 
name Hematoma, although they do not come under the strict 
definition of tumors. It will be proper here to enumerate the 
various conditions to which this name is given. 
The cephalhematoma is a condition sometimes met with in the 
child immediately after birth, and produced during delivery. In 
the act of delivery the pericranium is separated from the surface 
of the skull and vessels are ruptured. Blood collects between the 
pericranium and the skull, and is apt to remain long there, retain- 
ing its fluidity for an unusual time. The raised pericranium pro- 
duces new bone, and at first chiefly at its margins. There is thus 
a shell of new bone in the shape of a ring covering in the edges 
of the collection of blood. This produces the peculiar character 
that when the prominence is handled the impression is as if there 
were a gap in the skull. The shell of new bone is continuous 
with the cranium, and as the fingers pass inwards they suddenly 
dip into the gap, and it feels as if they dipped into the soft brain- 
substance. In some cakes there is also hemorrhage inside the 
skull. 
The Othsematoma, or hematoma auriculare or insane ear, is a 
condition in some respects comparable to the last mentioned. In 
it the perichondrium is raised from the cartilage of the ear, some- 
times bringing little bits of cartilage with it, and blood collects 
between cartilage and perichondrium. This occurs on the anterior 
surface of the concha, and the result is that the hollows are filled 
up and become prominences. It appear to be sometimes produced 
by violence, such as blows, but only in persons predisposed to it. 
It is met with almost alone in insane persons, and chiefly those 
suffering from general paralysis. As the blood is absorbed the ear 
does not recover, but shrivels up with great consequent deformity. 
The hematoma of the dura mater is also of most frequent 
occurrence in insane persons, though by no means confined to 
them. In persons dying with apoplectic symptoms there is some- 
times found a flat layer of blood on the internal surface of the 
dura mater, in some cases an inch or an inch and a half thick. 
On careful examination there is a thin false membrane on the 
surface of the clot, and the disease is usually the result of a chronic 
inflammation of the dura mater, pachymeningitis chronica hsemor- 
rhagica. (EDEMA AND DROPSY. 
61 
The hematoma of the heart is an interesting form. It some- 
times happens that large masses of fibrine are deposited on the 
valves or elsewhere, and these may come to form permanent pro- 
jections. In one case met with by the author there were immense 
festoons hanging from the mitral valve and tilling the greatly 
enlarged left ventricle. In some parts there was calcareous 
infiltration of the hard dry clot, but no proper organization had 
occurred. 
The uterine hematoma is a polypoid mass of blood, coagula- 
tion having occurred on a placental surface or retained placenta. 
It is sometimes called the fibrinous polypus. It projects into the 
cavity of the uterus and may simulate a polypoid myoma. 
Blood may collect in the peritoneal pouch behind the uterus, 
forming a kind of retro-uterine hematoma. 
(EDEMA AND DROPSY. 
In order to understand these conditions it is necessary to refer 
to certain points in the normal relations of tiie lymphatic circu- 
lation. The connective tissue throughout the body is, as it were, 
permeated with spaces of various shapes in which the connective- 
tissue corpuscles lie. These lacume or serous spaces are lined with 
endothelium like the blood and lymphatic vessels themselves. 
The serous spaces are provided (as shown in Fig. 14) with numer- 
ous anastomosing processes, and they Communicate on the one 
hand with the interior of the bloodvessels, and on the other with 
the lymphatics. Arnold and others (see Fig. 15) have succeeded 
in injecting the serous spaces from the bloodvessels, especially 
when, as in passive hypenemia, the channels of communication 
between the bloodvessels and spaces have been widened. We are 
to suppose that a circulation is continually proceeding from the 
capillary bloodvessels into these spaces, and so into the capillary 
lymphatics. The serous cavities of the body are to be regarded 
as large serous spaces. They are also lined with endothelium, 
and are continuous with the lymphatic capillaries. The serous 
spaces, therefore, and the serous cavities, are virtually the same in 
nature, and their pathology is similar. (Edema is overfilling of 
the serous spaces with fluid, dropsy is overfilling of the serous 
cavities, and so the two conditions are virtually identical. 
Anything which causes an excess of fluid in these spaces or 
cavities will produce oedema or dropsy, and the first condition 
which suggests itself is obstruction of the lymphatics. The force 
which carries on the lymphatic circulation is largely the blood- 
pressure propagated from the capillaries, and it may be expected 
that obstruction to a lymphatic stem would produce accumula- 
tion of fluid in the spaces. But it is to be remembered that the 
serous spaces are in as close relation to the blood capillaries as 
the}7 are to the lymph capillaries, and any obstruction to the 
lymphatics will probably have the effect of causing the transuded 62 
AFFECTIONS OF CIRCULATION AND BLOOD. 
fluid to return to the blood capillaries. The fluid flows from the 
bloodvessels because the pressure is higher in them than in the 
lymphatics, but an obstruction in the lymphatics will tend to 
equalize the pressure, and so prevent further transudation. At 
any rate, experiment has shown that the whole lymphatics of a 
Fig. 14. 
Serous spaces (cc) and lymphatic capillaries (dd) in pleural surface of diaphragm in prep- 
aration treated with nitrate of silver. The connection of the branched spaces with the 
commencing lymphatic vessels is shown. (Recklinghausen.) 
limb may be ligatured, or, what is equal to that, the entire 
lymphatic glands excised without producing oedema. The blood- 
vessels take up the functions till new lymphatic channels are 
formed. Even when the thoracic duct is obstructed there is not 
necessarily any oedema or dropsy. It is true that obstruction of 
the thoracic duct sometimes leads to distention, especially of the 
chyle vessels, and even the bursting of them so as to lead to a 
chylous ascites. It may even lead to an ordinary ascites. So far 
as human pathology is concerned, however, it must be exceedingly 
rare to find obstruction of the thoracic duct apart from other con- 
ditions which more directly lead to dropsy. We may say at least (EDEMA AND DROPSY. 
63 
that, with this possible exception, obstruction of lymphatics does 
not of itself lead to oedema, or dropsy, although it is clear that it 
Fig. 15. 
Capillary bloodvessels, serous spaces, and capillary lymphatics of the frog’s swimming 
web, filled with (blue) injection material thrown into the bloodvessels. (The black branched 
bodies are the normal pigment cells.) a, a, Capillary bloodvessels filled with injection 
material, b, b, Lymphatic capillaries also injected, but less full than the blood capillaries, 
c, e, Serous spaces injected from the bloodvessels. The injection was made after passive 
hypereemia had been produced by ligaturing the vein. (Arnold.) X 250. 
may aggravate an oedema whose cause is to he found in some other 
condition. 
Looking to these facts, it may he said that the conditions which 
lead to oedema and dropsy do so by causing increased transuda- 
tion from the capillaries into the serous spaces. A considerable 
increase may he compensated by the lymphatics and the blood- 
vessels carrying off an additional quantity7 of fluid, but when the 
limits of this are passed, the fluid will accumulate in the spaces 
and distend them, thus giving rise to oedema or dropsy. 
The most obvious cause of increased transudation is venous 
hyperemia. Here there is increased pressure in the capillaries 
and veins, and a greatly increased transudation. From what has 
gone before, it will appear probable that here the increase of 
pressure is not the only element in the case. The circumstances 
of the capillary wall are altered in such a way that we may pre- 
sume that it is rendered abnormally permeable. This view appears 
more probable when we find that active hyperaemia does not, if 
uncomplicated, produce oedema. In arterial hypercemia, it is true, 
the blood-pressure is not so much raised in the capillaries as it is 
in the venous form; still it is raised, but the transudation is never 
so much increased as to produce oedema, unless there is an inflam- 
matory element in the case.- In passive hyperaemia the fluid 
exuded will he a watery serum, and as there is diapedesis it will 64 
AFFECTIONS OF CIRCULATION AND BLOOD. 
contain red corpuscles in considerable numbers. The red corpus- 
cles will be taken up by the leucocytes as already described, and 
carried to the lymphatic glands, where they will disintegrate. It 
should be added that it requires considerable increase of pressure 
in the capillaries to produce an oedema by passive hypersemia when 
acting alone. It has even been stated that a simple passive hyper- 
Eemia, apart from vaso-motor paralysis (producing also active 
hypersemia), does not lead to oedema. It has been shown that if 
the iliac vein of a dog be ligatured, there is no oedema till the 
sciatic nerve is cut. The explanation of this, however, may be 
that this vein has such free anastomoses that its ligature does not 
raise the blood-pressure sufficiently to induce oedema, whereas a 
coincident vaso-motor paralysis producing dilatation of the arteries 
raises the blood-pressure sufficiently. Experiment proves that if a 
sufficient number of veins be obstructed oedema will result with- 
out vaso-motor paralysis. Sotnitchewsky, by introducing plaster 
of Paris into a peripheral vein of the leg of a dog while the thigh 
was constricted by an elastic band, succeeded in obstructing a 
number of veins by the gypsum hardening in them. In this case 
oedema followed without the induction of vaso-motor paralysis. 
In passive hyperaemia from thrombosis of veins there are usually 
many veins obstructed before oedema occurs. In the case of 
passive hyperaemia from heart-disease, it may well be supposed 
that the prolonged venous engorgement will produce a more than 
usual deterioration of the capillary wall, besides a depreciation of 
the blood itself. 
We now come to a question which is not so easy of answer as 
that we have just been discussing. It has been customary to say 
that a watery state of the blood, a hydremia, may induce (edema, 
and the case of the so-called cachectic oedemas is cited. This, 
however, has been rendered doubtful by a series of experiments 
by Colmheim and his assistants. A simple hydraemia, induced in 
a dog or other animal by repeated blood-lettings and the replace- 
ment of the blood withdrawn by a solution of common salt, does 
not lead to oedema. On the other hand, it may well happen that 
a prolonged hydraemia as opposed to this more acute form, such as 
we meet with in cases of chronic emaciating disease, may so depre- 
ciate the capillary wall as to give rise to oedema under compara- 
tively trivial circumstances. In such persons the heart is weak, 
and the blood has a tendency to stagnate in depending parts, as 
has already been described, and this comparatively slight increase 
in pressure may induce the occurrence of oedema. 
Next we have the frequent cedema of the skin in Bright’s 
disease to account for. There is undoubtedly here in many cases 
a hydrsemia, induced in two different ways. There is the loss of 
albumen, which renders the blood directly more watery. But in 
many cases there is also an abnormal retention of the water in the 
blood. In acute Bright’s disease, especially, there is great reduc- 
tion in the amount of urine secreted, and this implies an increase 
in the water of the blood. It is in these cases, it will be observed, (EDEMA AXD DROPSY. 
65 
that the occurrence of oedema is most frequent. These facts 
naturally suggest that if the oedema in Bright’s disease is not due 
simply to the hydrcemia, it may he due to this in conjunction with 
the increased bulk of the blood, to a hydremic plethora. This 
view has obtained much support. It has been supposed that, the 
entire bulk of the blood being increased, there will be increased 
pressure in the capillaries and increased transudation from the 
watery blood. But there are some objections to this view. We 
have already seen that plethora, even when suddenly induced, does 
not raise the blood-pressure. There is a form of Bright’s disease 
in which the arterial tension is raised, and the increased tension is 
related to hypertrophy of the left ventricle of the heart. But it is 
just in this form of Bright’s disease (the cirrhotic form) that 
oedema is least usual, and a case may proceed to a fatal issue with- 
out the occurrence of any oedema. Then there are cases of abso- 
lute suppression of urine, as in hysterical females, etc., in which we 
must presume an exaggerated hydrsemic plethora, but without a 
trace of oedema. 
In some experiments by Cohnheim and Liclitheim, a hydrremic 
plethora was induced by injecting a solution of common salt into 
the vessels of animals. Enormous quantities could be injected 
without seriously compromising the animal. We have seen that 
when blood is transfused in the dog, the limit consistent with the 
survival of the animal is one and a half times the bulk of the 
blood, but more salt solution than three times the bulk of the 
blood could be injected without killing the animal. From the pre- 
vious reference to transfusion, it will be understood that these 
injections did not produce any permanent rise in the blood- 
pressure. The most direct result was a great acceleration in the 
speed of the blood-current, presumably from the diminished fric- 
tion of the watery blood. There was also a greatly increased 
transudation and consequent increased flow of lymph. But this 
was remarkably localized. There was a greatly increased flow of 
lymph in the thoracic duct, showing that in the viscera the transu- 
dation was increased; while the lymphatics of the limbs showed 
no increase, indicating that in the skin and muscles the transuda- 
tion was not increased. There was also greatly increased secre- 
tion from the salivary glands, stomach and intestine, liver, 
lachrymal glands, and kidneys. In these organs an oedema was 
developed, that is to say, in the mucous membrane and submucous 
tissue of the stomach and intestines, in the lymphatic glands of 
the mesentery, in the pancreas, kidneys, gall-bladder, salivary 
glands; there was also ascites, but no oedema of the skin. The 
explanation suggested for this localization of the increased transu- 
dation and the oedema is, that these organs are all normally con- 
cerned in the removal of water from the blood, and that probably 
their bloodvessels are unusually permeable to water. The experi- 
ments produce a great increase in the water of the blood, and the 
vessels give ready passage to it. 
It will be observed that in these experiments the oedema was 66 
AFFECTIONS OF CIKCULATION AND BLOOD. 
present in parts where it is absent in Bright’s disease, and was not 
present at all in the skin. So that the oedema of Bright’s disease 
cannot be ascribed altogether to the hydnemic plethora, however 
much that may predispose to it. To explain the oedema of Bright’s 
disease, it seems necessary to suppose some alteration in the vessels 
of the skin rendering them unduly permeable. There are many 
facts indicating a relation between the skin and the kidneys in 
Bright’s disease, and it is very possible that the morbid agent 
which affects the kidney may also affect the skin. In scarlatina 
we have during the fever an inflammatory hypersemia of the skin, 
and it is natural to suppose that when subsequently a kidney affec- 
tion induces a hydrsemic plethora, the oedema will manifest itself 
in the previously damaged skin. In the experiments above re- 
ferred to, it was found that although the normal skin did not 
become oedematous, yet when it had been previously inflamed, as 
by pencilling with iodine solution, or by exposing to a strong sun, 
then oedema shows itself. It may hence be inferred that, although 
hydrsemic plethora is not by itself a cause of oedema of the skin, 
it is a strong predisposing element. 
We shall find in studying inflammation that the alteration in the 
vessels produced by this condition induces oedema, so that inflam- 
matory oedemas are of frequent occurrence. 
LEUKAEMIA. 
By this name is meant a condition in which the white blood- 
corpuscles are greatly increased, the name meaning literally white 
blood. This was the name applied by Virchow. Another name— 
Leucocythsemia—applied by Bennett, although literally more cor- 
rect, is cumbersome, and is now generally disused. The condition 
of the blood gives its name to the disease, and this will first 
engage our attention. 
The normal proportion of white corpuscles to red in the blood 
is stated as about one in three hundred to one in four hundred 
and fifty, but it may vary within normal limits. There is after 
hemorrhage, as we have seen, a slight increase in the proportion 
of white corpuscles, a leucocytosis, but it is of no special signifi- 
cance. In leukaemia the relative proportion of white to red cor- 
puscles is greatly altered. A case is not a very severe one in 
which the corpuscles are as one to ten, and they may be as one to 
two or even equal. This alteration in the proportion of white and 
red is not the only alteration in the blood. The white corpuscles 
are more varied in size than normal, some larger and some smaller, 
and they are sometimes more distinctly nucleated. Then the red 
corpuscles are not only proportionately few in number, but they 
are absolutely reduced, and that to a very high degree. Occasion- 
ally nucleated red corpuscles have been found in the blood, these 
corpuscles being of larger size than the normal red corpuscles. 
The specific gravity of the blood is considerably reduced; it may 
fall from 1055, which is the average normal, to 1040 or 1035. The LEUKAEMIA. 
67 
blood has thus the character of anaemia along with a great increase 
of the white blood-corpuscles. In leukaemic blood, after death, 
there are found small, colorless, glancing crystals of an octahedral 
shape, which are usually called from their discoverer Charcot’s 
crystals (see Fig. 16). There are also certain other abnormal 
chemical constituents, chiefly glutine and liypoxanthine. 
With regard to the probable explanation of this peculiar condi- 
tion of the blood, it must always be remembered that there is a 
very great diminution in the red corpuscles 
as well as a great' increase in the white. 
There must be either a greatly increased new 
formation of white corpuscles and destruction 
of red ones, or a serious interference with 
the conversion of the white into the red cor- 
puscles. This latter is the view originally 
taken by Virchow, and is the more probable. 
There may be an increased formation of 
white corpuscles, but the diminution in the 
number of the red is probably due to a re- 
duced conversion of white into red. The 
nucleated red corpuscles have been regarded 
by some as transition-forms, their presence 
indicating a delay in the conversion. 
The blood in persons affected with this dis- 
ease is unduly pale, but it has not a wuitery 
appearance. It is even a thicker fluid than 
usual and distinctly more opaque, resembling 
a mixture of pus and blood. 
The alteration in the constitution of the 
blood is associated with changes in certain organs which have 
generally been regarded as concerned in the preparation of the 
blood, namely, the spleen, the lymphatic glands, and the medulla 
of bone. In different cases of leukaemia these structures are vari- 
ously affected. The medulla of bone seems to be affected in all or 
nearly all cases, the spleen with the medulla in a considerable 
number, the lymphatic glands with the medulla in a smaller num- 
ber, and all three in many cases. 
The condition of the spleen in leukaemia will first concern us. 
In all stages of the disease it is enlarged. The enlargement in the 
earliest period appears to be due to an active congestion, and is 
accordingly of rapid development. Eindfleisch mentions a case 
which he saw at Virchow’s demonstrations in which the enlarge- 
ment had been so rapid as to cause a rupture of the capsule of the 
spleen. This enlargement is merely from overfilling of the vessels, 
but it is succeeded by, or develops into, a solid enlargement. The 
Malpighian bodies of the spleen have the structure of lymphatic 
follicles, and it is mainly by the enlargement of these that the 
permanent solid enlargement occurs, a great increase, therefore, 
of lymphoid tissue. But the new formation often occurs in the 
pulp as well as in the Malpighian follicles. The spleen thus be- 
Fig. 16. 
Charcot’s crystals from 
the blood in leukmmia after 
death. In b, the crystals 
are partly inside the white 
corpuscles. (Zbnicer.) 
X 500. 68 
AFFECTIONS OF CIRCULATION AND BLOOD. 
comes converted, into a hard, dense, bulky organ, sometimes like 
a piece of wood. It is also paler than normal, and we can often 
see the enlarged Malpighian bodies as whiter areas on the cut 
surface. In addition, there are frequently hemorrhages in the 
spleen, and these may take the form of the regular wedge-shaped 
infarction. 
In the medulla of bone the changes are very similar. There is 
a great new formation of round-cell tissue which occurs at the ex- 
pense of the adipose tissue and also of the 
bone. This new tissue consists mainly of 
cells as large as white blood-corpuscles, 
and has the structure of lymphatic tissue, 
showing the reticulum and round cells as 
in Fig. 17. Sometimes there are larger 
cells than these, and there may be also 
nucleated red corpuscles. There is thus a 
great new formation in the medulla and 
that mainly of lymphatic tissue. As the 
medulla of bone, especially the red medulla 
of spongy bone, normally contains lym- 
phatic tissue, the change in leukaemia may 
be regarded as a hypertrophy of this, and 
the amount of hypertrophy is sometimes 
very great. Thus, the whole yellow mar- 
row of the hollow shaft of the femur may 
be replaced by lymphatic tissue. The 
cavity of the shaft may also be widened at 
the expense of the bone, and many smaller trabeculae here and in 
the spongy bone may be destroyed. In this respect, as well as in 
intimate structure, the leukaemic bone-marrow differs from the red 
marrow of pernicious anaemia, as the latter does not cause a proper 
atrophy of the bony tissue. The occurrence of hemorrhages or 
even infarctions has been observed in the bone-marrow just as in 
the spleen. The appearance of the medulla is, of course, greatly 
altered. It has generally a grayish-red color without any of the 
normal greasy appearance, but it may be pale so as to look like 
solidified pus, or dark red, these differences depending on the de- 
gree of the new formation and the state of fulness of the vessels. 
It has, however, the character of a tolerably solid tissue, not a 
semi-fluid material as in anaemias. These changes may occur in 
all the bones in the body, and in both spongy and hollow bones, 
the affection being, however, variously distributed. 
The lesion in the lymphatic glands consists in an enlargement 
of them. This begins mostly in a particular set of glands usually 
situated externally, as in the axilla, groin, neck, etc., and spreads 
to other sets, generally first to those nearest. The enlarged glands 
may be three, five, or even ten times their normal size, but there 
is no tendency to any degeneration of their tissue. 
The relation of these organic changes in the spleen, bone- 
marrow, and lymphatic glands to the disease in its essence is ex- 
JFig. 17. 
Medulla of bone in leukaemia, 
from the cavity of the shaft of 
the femur. Adenoid reticulum 
and lymphoid cells are shown 
X 350. LEUKAEMIA. 
69 
ceedingly obscure. An attempt has been made to associate the 
disease in its origin with the bone-marrow, hut even this is by no 
means certain. There seems little reason to doubt, however, that 
the bone-marrow along with the lymphatic glands and spleen, and 
perhaps in a more important manner than they, is concerned in 
the formation of the blood-corpuscles. The discovery of nucleated 
colored cells in the normal red marrow of spongy bone seems to 
show that th,e red corpuscles are either formed or undergo impor- 
tant changes here. 
Besides these organs others are frequently attacked, but the 
lesions in them are of later manifestation, by no means uniformly 
present, and undoubtedly secondary. The liver is nearly always 
enlarged, and this enlargement may be due simply to parenchy- 
matous changes in the hepatic cells, but is often associated with a 
Fig. 18. 
Leuksemic formations in the liver. X 75. 
distinct new formation in tlie liver. This is in the form of minute 
collections of round cells occurring in myriads throughout the 
organ, as shown in Fig. 18. These are, at first sight, not unlike 
miliary tubercles, but they have no giant-cells and do not present 70 
AFFECTIONS OF CIRCULATION AND BLOOD. 
any tendency to degeneration, while they are much less definite in 
size and shape. Sometimes, instead of definite aggregations, there 
is an extensive infiltration of the connective-tissue stroma of the 
liver with round cells. The exact nature of these lesions is doubtful. 
They may be simple aggregations of white blood-corpuscles, hut 
they have usually too regular a form for this, and they have been 
regarded as small lymphatic formations. 
The kidney is affected not infrequently, and here the appearance 
to the naked eye very often is as if the organ were greatly enlarged 
by the presence of large pale tumors in the cortical substance. 
On microscopic examination, the lesion is seen to consist in an 
enormous infiltration of the stroma of the kidney with round cells, 
the proper secreting tissue remaining, but, of course, greatly 
pressed on. This infiltration occurs in definite areas, as if some 
agent had addressed itself to certain defined portions of the organ. 
The closed follicles of THE intestines, both the solitary ones 
and those aggregated in Peyer’s patches, may be enlarged, and as 
they are of lymphatic structure, their enlargement is a simple 
hyperplasia. This is not of frequent occurrence, and still less 
frequent is the formation of leukaemic tumors in the skin, these 
tumors consisting of infiltrations of round cells. 
The connective tissue in other regions may also he infiltrated. 
The author met with a case in which the connective tissue of the 
mediastinum was enormously infiltrated, so that the tissue formed 
a bulky tumor. The infiltration extended to the pericardium 
much in the fashion of a lympho-sarcoma. 
It is proper here to mention that there is a disease called 
variously Hodgkin’s disease and pseudo-leukemia, in which the 
organic lesions appear to be identical with those of leukaemia, but 
without the increase of white blood-corpuscles, the blood being 
simply anaemic. There may he great enlargement of the spleen 
and of the lymphatic glands, and the characters of the enlarge- 
ment may he essentially like those mentioned above. 
MEL ANAEMIA. 
By this name is meant, literally, black blood. It is used to 
designate a condition in which pigment occurs abnormally in the 
blood and is deposited in the tissues. The pigment is in the form 
of solid granules, and, although black in color, it is derived from 
the blood pigment, and contains iron. It is met with in cases of 
malarial fever, but not in every case, as a rule only in the more 
severe forms. The view usually entertained is that during the 
acute paroxysm of an ague, blood-corpuscles are destroyed in the 
spleen, and their pigment is set free in the granular form. Lately, 
Arnstein (Virchow’s Archiv, vol. lxi. p. 494) has brought forward 
the view that the destruction of blood-corpuscles occurs not in the 
spleen, but in the blood generally. Whether the spleen he the 
seat of its formation or not, it is certainly stored up there for MELANA1MIA. 
71 
years, and may pass into the blood by degrees, although it is more 
abundant immediately after the acute paroxysm. 
When the pigment gets into the blood it is rapidly taken up by 
the white blood-corpuscles, so that these appear in the blood as 
pigmented cells. These pigmented cells are often larger than the 
white corpuscles, being enlarged by their abnormal contents. It 
will thus be seen that very little free pigment will be present in 
the blood except immediately after the acute paroxysm, the white 
corpuscles picking up the solid granules just as they do when a 
solid pigment, such as vermilion, is artificially introduced into the 
blood of an animal (see Fig. 19). The white corpuscles containing 
Fig. 19. 
White blood-corpuscles of the frog, containing granules of vermilion, and showing 
amoeboid movement. (After Klein.) 
the pigment accumulate in certain organs, especially the spleen, 
liver, and bone-marrow. In the spleen and hone-marrow the 
pigmented cells appear to leave the capillaries readily, and pass 
Fig. 20. 
A lobule of the liver in melanmmia. The black pigment-granules are seen between the 
hepatic cells, being really in the capillaries. X 75. 
into the tissues, producing an actual pigmentation of them, but in 
the liver they linger longer in the capillaries, which may he seen 
with many such corpuscles in them (see Fig. 18), although here 
also the latter may pass out into the surrounding tissue. In very 72 
affections of circulation and blood. 
severe cases, other organs and tissues may bo pigmented in this 
way. The brain is very often pigmented, especially in cases where 
there has been much cerebral excitement. This will be in very 
acute cases, but it is doubtful whether the pigment has much to do 
with the cerebral symptoms, which may be merely a consequence 
of the acute attack. The kidneys are sometimes the seat of it as 
well as other tissues, such as pancreas, intestine, etc. 
This abnormal pigmentation of course produces changes in the 
color of the organs affected. The spleen is slaty-gray or almost 
black, the liver is steel-gray or blackish, the gray substance of the 
brain is of a dark chocolate or graphite color, and the kidneys 
present grayish spots. 
URAEMIA. 
This is a condition characterized by nervous symptoms, vomiting, 
sleepiness, headache, convulsions, coma, and it occurs in cases of 
kidney disease in which the secretion of urine is diminished. The 
result of the defect in the secretion of urine is accumulation in 
the blood or the constituents oe the urine, and it was natural 
to infer that these constituents, acting as poisons, produced the 
symptoms; hence the name uraemia. In animals, symptoms 
essentially similar may be produced by tying both ureters, and 
here also doubtless there is retention of urinary constituents. 
The urea is readily detected in the fluids and tissues in such 
animals, and it has been frequently detected clinically in cases of 
uraemia. 
And yet it is very difficult to be sure that the symptoms are 
due to poisoning by the urinary constituents. For one thing, the 
injection of urea, and even of filtered urine, into living animals 
does not produce uraemia, the only effect being an excessive secre- 
tion of urine. These facts have led to theories to account for the 
uraemic symptoms apart from the presence of urea in the blood. 
Frerichs’ theory at one time received great acceptance. He said 
that the symptoms were due, not to the urea or other urinary 
constituents, but to the products of their decomposition, and 
mainly carbonate of ammonia. It was asserted that carbonate of 
ammonia was to be found in the blood of uraemic patients, and 
that it was often to be detected in their breath. But there is a 
mistake here. More correct chemical investigation shows that 
there is no excess of carbonate of ammonia in the blood. Car- 
bonate of ammonia is to be found abundantly in the intestines, 
where it is the result of putrid decomposition. Moreover, the 
injection of carbonate of ammonia into animals does not produce 
uraemic symptoms, but symptoms of a different kind. 
Again Traube started a very ingenious theory, according to 
which the uraemic symptoms are due to cedema of the brain and 
its membranes, and consequent anaemia of that organ. It is 
known that oedemas occur sometimes very suddenly in Bright’s 
disease, and it was supposed that a sudden oedema of the brain DIABETES MELLITUS. 
73 
would produce sucli symptoms, the varying locality of the oedema 
determining the variations in the symptoms. But this theory is 
also scarcely tenable, because oedema of the brain is by no means 
constant in uraemia. 
It is rather probable that the original view is fundamentally 
the correct one. So long as there is a free outlet, the blood may 
contain a large quantity of urinary constituents, and so when 
urine is injected into the blood of animals it passes rapidly through 
the system and does little harm. But if the ureters be first liga- 
tured and then the urine injected, the uraemic symptoms will 
rapidly manifest themselves. It will he understood that the urea 
is not the only constituent concerned, hut that the other nitro- 
genous substances and salts probably take part in the production 
of the entire set of symptoms. 
It has already been said that in uraemia urea is present in excess 
in the blood and fluids of the body, and has frequently been 
detected during life, and it is in cases where the secretion of urine 
is diminished or suppressed that these symptoms occur. The 
secretion may he diminished in various ways—by obstruction in 
the outflow, by disease of the secreting tissue, by defect in the 
water of the blood so that the urinary constituents are not duly 
carried off, or even, as has been supposed in the case of eclampsia, 
by spasm of the renal arteries preventing the due passage of blood 
through the kidneys. In all these cases the one common element 
is a defective separation of the urinary constituents, and their con- 
sequent accumulation in the blood, and the presumption is that 
these constituents have a poisonous effect, although it may be 
impossible to say whether one or more of them is specially dele- 
terious. 
DIABETES MELLITUS. 
The pathology of diabetes is a subject of considerable difficulty, 
and it may be well at the outset to set forth the problem which 
requires solution. 
The BLOOD AND URINE CONTAIN NORMALLY A SMALL QUANTITY OF 
grape sugar, but in diabetes this undergoes an enormous increase. 
In the normal condition the sugar is at a constant minimum, un- 
affected by the amount or kind of food taken. In diabetes there 
is commonly a very obvious relation between the food taken 
and the sugar. There are some diabetics who cease to excrete 
any excess of sugar so long as they abstain from starch or sugar, 
but whenever they take any such food it is mostly converted into 
grape sugar and so excreted in the urine. On the other hand, 
there are diabetics who excrete an excess of sugar whatever the 
kind of food they take, and though the sugar may be diminished 
by the use of a mainly nitrogenous diet, yet it cannot be thus made 
to disappear. In that case it is obvious that sugar is formed not 
only from carbo-hydrates, but also from the albuminous principles 
of the food. According to Traube, diabetes is divided into a 74 
affections of circulation and blood. 
slighter and a more severe form according as the sugar is formed 
from the carbo-hydrates alone, or from nitrogenous principles as 
well, and it is probable that these forms represent an earlier and a 
later stage in the disease. Donkin, in view of the relation of the 
sugar production to the food, distinguishes three stages; first, that 
in which only the starch or sugar of the food furnishes the grape 
sugar; second, that in which fats as well as these are converted; 
and third, that in which albuminous foods, as well as starchy and 
oily, undergo conversion into grape sugar. 
It is obvious that in this latter stage there is a great consumption 
of albumen, and in the process of formation of the sugar urea is 
formed as a waste product in the chemical transformation. We 
find, therefore, that the urea is also greatly increased in the 
urine, amounting sometimes to two or three times the normal 
quantity in the twenty-four hours. In this stage of the disease 
there is no doubt that the fatty and albuminous constituents of 
the tissues are also used for the formation of sugar, and that the 
albuminous principles of the tissues, like the albumen of the food, 
furnish sugar and urea which appear in the urine. 
The problem which we have to face then is, that in diabetes there 
is, for some reason or other, an excessive demand for sugar in the 
organism. The greed for sugar seems to acquire intensity as the 
disease advances, so that while at first it is only the carbo-hydrates 
which fall a victim to it, there is ultimately a consumption of the 
nitrogenous foods and even of the nitrogenous tissues. We have 
to inquire what may be the meaning of this immense demand for 
sugar. Looking to the manner in which the processes of the body 
are arranged, we may take it for granted that there is some need 
to be supplied or else such an excess of material would not be 
furnished. 
Sugar is a crystallizable substance, and wherever it is formed it 
will readily be dissolved by the juices and find its way into the 
blood. Its occurrence in the blood and its excretion by the urine 
are therefore simply a result of the ready solubility and diffusibility 
of the substance. Its presence in these fluids throws no direct light 
on its place of origin. 
It is natural to look to the liver as the source of the sugar. It 
is well known that the liver is the place of formation of a substance 
nearly allied to sugar, namely glycogen. This substance, as its 
name implies, has a great tendency to become converted into sugar. 
It is true that in the living body the liver, apparently, contains 
glycogen and not sugar. If the liver of an animal be cut out 
immediately after death and without delay placed in boiling water 
after being cut into small pieces, then it will be chiefly glycogen 
that will be found, and any sugar that exists has probably formed 
after death by the transformation of the glycogen. It is difficult 
indeed to avoid the occurrence of traces of sugar in this experi- 
ment, and if the removal of the liver be delayed a large amount of 
sugar will be found. These facts show that glycogen is always 
just ready to be converted into sugar; its conversion is, as it were, 75 
diabetes mellitus. 
every moment imminent. During life this conversion does not 
take place to any considerable extent, and it is even doubtful 
whether the small amount of sugar existing normally in the body 
is due to a conversion of the glycogen in the liver, a comparison 
of the blood in the hepatic vein with that in the portal giving 
doubtful results. 
We have to consider, however, whether a pathological conver- 
sion of the glycogen into sugar may not occur in the liver, and 
in this regard the observations of Bock and Hoffmann are of great 
interest. These observers succeeded in the production of an arti- 
ficial diabetes mellitus by injecting into the blood of rabbits 
large quantities of a watery solution of common salt. The animals, 
soon after the injection was made, began to secrete a large quantity 
of urine, and this urine soon became saccharine. If the injection 
of salt solution was persisted in, the sugar by and by diminished 
in the urine and ultimately disappeared. 
The question now was as to the source of the sugar, and the 
condition of the liver was examined with this in view. It became 
abundantly clear that the sugar in the urine came from the liver 
and was caused by the conversion of the glycogen into sugar. In 
ail cases where the animal was killed after the diabetes had passed 
off, the liver was found free both of the glycogen which exists 
normally and of sugar. If, on the other hand, the animal was 
killed while the mellituria existed, then glycogen and sugar were 
both present in the liver. The inference from these observations 
is perfectly obvious. The abnormal condition of the blood causes 
the transformation of the liver glycogen into sugar, and the latter 
being a crystalloid and readily diffusible, it is at once washed out 
of the hepatic cells and passes into the circulation and on into the 
urine. The diabetes ceases because all the glycogen in the liver 
has undergone conversion into sugar and the source of supply is 
exhausted, the liver in these cases being found free of both gly- 
cogen and sugar. We may say, therefore, that a glycosuria may 
be produced by the conversion of the glycogen within the liver 
into sugar. 
It may be said that the diabetes thus produced is temporary and 
not comparable with the permanent disease in the human subject. 
Let us suppose, however, that diabetes is due to the conversion of 
the liver glycogen into sugar, then the problem with which we 
started will undergo a considerable modification. We saw that 
there is an excessive production of sugar, but in the view now 
brought forward this will resolve itself into an excessive produc- 
tion of glycogen which undergoes conversion into sugar. The 
problem therefore presents itself—Is there anything to account 
FOR THE EXCESSIVE FORMATION OF GLYCOGEN? 
It is to be presumed that glycogen has an important function in 
the animal body. Whether it be used in the production of 
muscular force, as many suppose, or otherwise, it seems clear that 
such an organ as the liver would not be engaged in its formation 
unless it had an important part to play. It is to be presumed then 76 
AFFECTIONS OF CIRCULATION AND BLOOD. 
that glycogen supplies some need in the organism, and that it is 
formed in the liver for that purpose. 
But if, as soon as it is formed in the liver, it is transformed into 
sugar, then the need in the organism will not be supplied. The 
sugar being a crystalloid will he washed out, and very little 
glycogen will get into the blood. In such circumstances the or- 
ganism will have, as it were, a hunger for glycogen, the liver will 
he stimulated to supply it, and will produce more glycogen. As 
soon as it is formed, however, the glycogen will be transformed 
into sugar, and the excessive demand for glycogen will only result 
in an excessive supply of sugar. In this case the liver will be 
stimulated to an ever-increasing formation of glycogen which will 
immediately pass into sugar. We can understand how in the 
earlier stages all foods which are near to glycogen in their chemical 
composition will be at once utilized, and liow as the disease goes 
on and the demand becomes more urgent, the other kinds of foods 
and even the tissues of the body will be used. 
So long, therefore, as the hepatic cells retain their activity we 
may presume that they will react to the hunger for glycogen, and 
the production of sugar will be the result. If the hepatic cells be 
destroyed or weakened, the probability is that the diabetes will 
diminish, the disease requiring that the hepatic cells retain their 
energy. 
It would appear from the above that diabetes is explainable on 
the supposition that the glycogen undergoes abnormally a trans- 
formation into sugar, and that this occurs in the liver itself. We 
have now to inquire whether any indication exists as to the cause 
OF THIS TRANSFORMATION OF THE GLYCOGEN. 
In the experiments of Bock and Hoffmann already alluded to it 
appears that a particular abnormal condition of the blood is capable 
of producing this transformation. An enormous dilution of the 
blood with salt solution seems capable of inducing the liver gly- 
cogen to pass into sugar. A temporary diabetes has been produced 
in a variety of other ways, and all of them are explicable on the 
ground of an abnormal condition of the circulation of the liver. 
The inhalation of nitrite of amyl induces a temporary glycosuria. 
We know that this agent produces a general vaso-motor paralysis, 
and a general dilatation of the systemic arteries. With the other 
arteries those of the abdomen will dilate, and the blood passing 
through the capillaries at an increased rate will reach the portal 
vein at a higher pressure than normal. The circulation in the 
liver will therefore be accelerated and the blood will be less venous 
in character, having passed rapidly through the capillaries of the 
intestines and other organs. 
The celebrated diabetic puncture of Bernard is made in the 
medulla oblongata, and we know that in this part of the nervous 
system are situated the principal vaso-motor centres of the body. 
There is, therefore, here also a paralysis of the arteries just as after 
the inhalation of nitrite of amyl. Injuries to the brain, spinal DIABETES mellitus. 
77 
cord, and sympathetic sometimes produce a temporary glycosuria, 
and they also may cause vaso-motor paralysis. 
The observations of Pavy are important in this regard. He pro- 
duced glycosuria by the injection of defibrinated arterial blood 
into the portal vein, and here again there is an excessive supply of 
blood to the liver. But then Pavy also produced glycosuria by 
ligaturing the portal vein, and so cutting off the blood-supply ex- 
cept through the hepatic artery, and at first this result seems a 
very contradictory one. 
The effect of that experiment would be to cause the liver to be 
supplied with arterial blood alone, and we may presume that the 
hepatic artery would dilate and so allow of an additional flow of 
blood. According to the researches of Cohnheim and Litten 
(Virchow’s Archiv, vol. lxvii.) the blood of the hepatic artery, after 
supplying the connective tissue, gall-ducts, and walls of the large 
bloodvessels, passes into the inter-lobular veins and on into the 
proper hepatic capillaries, so that the blood of the hepatic artery 
is finally distributed with that of the portal vein. When the portal 
vein is closed, the circulation in the liver will be kept up, but only 
by the blood of the hepatic artery. 
From these observations Pavy concluded that the cause of the 
glycosuria when the portal vein was ligatured was the circulation 
of arterial blood in the liver, and he proceeded to determine 
whether it was possible in animals to produce diabetes by super- 
saturating the whole blood with oxygen, so that the blood in the 
portal vein would be virtually arterial. He effected this in various 
ways: by causing the animals to inhale oxygen; by using artificial 
respiration till the fact that the animals ceased to make any spon- 
taneous respiratory movements showed a deficiency of carbonic 
acid; by causing the animals to inhale carbonic oxide. In all 
these ways glycosuria was produced. It would appear, therefore, 
that when diabetes is artificially produced in animals, the one 
essential condition is that the liver should be supplied with unduly 
oxygenated blood, such blood causing the glycogen to be trans- 
formed into sugar in the liver itself. 
We have now to consider the question whether this view will 
explain the occurrence of diabetes in the human subject. Is there 
any evidence of such an alteration of the circulation in the liver 
in cases of diabetes ? It is to be noted here that in order to an 
active hypersemia of the portal circulation there must be an active 
hypersemia in the parts to which the coeliac and mesenteric arteries 
are distributed. The circulation in the portal vein depends en- 
tirely on that in these vessels, and unless the blood passes in 
greater abundance and more rapidly than it does normally through 
the vessels of the abdominal viscera from which the portal blood 
comes, then it cannot pass more quickly through the portal vein. 
It is not, therefore, as is sometimes stated, a question directly of 
vaso-motor paralysis of the liver. Moreover, if diabetes depends 
on the blood in the portal vein being unduly oxygenated, then the 
only possible explanation of this will be that the blood passes so 78 
AFFECTIONS OF CIRCULATION AND BLOOD. 
quickly through the capillaries of the alimentary canal and other 
organs that it is imperfectly deoxygenated. The question to he 
answered then is, whether there is any evidence of diabetes being 
due to a vaso-motor paralysis inducing an active hypersemia of all 
these organs. 
Such a vaso-motor paralysis might arise by disease of the central 
nervous system, or of the local centres in the abdomen, mainly the 
cceliac plexus. In regard to the latter, some cases have been 
recorded (by Frerichs, Klebs, and Recklinghausen) in which dia- 
betes has coexisted with atrophy, formation of calculi, or cancer of 
the pancreas. In cases observed by Klebs there was, along with 
the atrophy of the pancreas, a very marked change in the coeliac 
plexus, consisting of a great destruction of ganglion cells. It 
seems very probable, considering the nearness of the pancreas to 
the cceliac plexus, that a cancer or the changes resulting from the 
formation of calculi in the ducts of the gland, might extend to the 
cceliac plexus, and Klebs accounts for the diabetes in his cases on 
the view that there was vaso-motor paralysis produced by the 
destruction of the ganglion cells of this plexus. In one of his 
cases, indeed, there was observed after death an extraordinary 
dilatation of the hepatic and splenic arteries and the gastric 
branches of the coeliac axis, the last-named branch attaining the 
size of a goose-quill and presenting a highly convoluted course. 
These facts seem to confirm the view that in man diabetes may be 
produced by paralysis of the arteries in the domain of the cceliac 
plexus. 
There have been also cases in which diabetes seemed to follow 
injury to the spinal cord or medulla oblongata, but these have 
been cases of temporary glycosuria comparable to that following 
Bernard’s diabetic puncture. On the other hand, there have been 
a few instances of softening of the brain and intra-cranial tumors 
in cases of diabetes, but these have been too rare to be regarded 
as of much importance in the pathology of diabetes. For the 
most part there is little or no alteration visible to the naked eye 
in the central nervous system. 
Recently Dickinson has described minute changes in the central 
nervous system, consisting mainly in excavations around the 
arteries, produced apparently by exudation from these vessels 
with disintegration of the brain substance around. In very recent 
cases there was even accumulation of leucocytes or hemorrhage 
around the arteries, but in the older cases a cribriform appearance, 
the arteries being surrounded by7 widened canals. These lesions 
are scattered through the brain, the largest and most striking 
being present in the corpora striata, optic thalami, pons, medulla 
oblongata, and cerebellum. They are less marked in the cord, 
where in addition there is usually7 great dilatation of the central 
canal. The white matter of the cerebral convolutions also fre- 
quently presents similar changes. 
These lesions are held by Dickinson to be primary and directly 
related to the cause of the disease. If this view be correct, then DIABETES MELLITUS. 
79 
we should have lesions of the central nervous system leading to 
diabetes, and doing so probably by vaso-motor paralysis of the 
arteries of the abdominal viscera. This view is open to the 
objection, however, that these lesions in the nervous system may 
possibly be secondary, due to a dilatation of the arteries, not to 
exudation from them, especially as we know that exudation occurs 
rather from capillaries and veins than arteries. 
Turning to the abdominal organs themselves, there have been in 
many cases indications of congestion observed. We have already 
referred to the enlargement of the arteries in one of the cases 
described by Ivlebs. The liver itself is generally described as 
congested, and in a few cases there has been thrombosis of the 
portal vein. 
The characteristic red tongue of advanced diabetes has been 
cited by Pavy as evidence of a progressive congestion of the 
alimentary canal. The congestion at first is confined to the ab- 
dominal organs, but in the later periods extends to the mouth, the 
vaso-motor paralysis being progressive. 
All the facts may be held as indicating that diabetes depends on 
the liver being supplied with blood of an abnormal character and 
at an accelerated rate of speed. The congestion of the liver de- 
pends on abnormal nervous arrangements, and these may be local, 
affecting the cceliac plexus, or possibly situated in the central 
nervous system. The observations of Dickinson would seem to 
point in the latter direction, but they stand in need of confirmation, 
and besides, the lesions may possibly be the effect rather than the 
cause of the affection. 
In regard to the other changes in diabetes mellitus, little has to 
be said. The tissues appear to be peculiarly vulnerable, wounds 
heal badly, inflammations are generally very severe, often going 
on to suppuration and gangrene, phthisis pulmonalis often closes 
the scene, and is frequently very acute. General emaciation is a 
striking feature in advanced cases. The kidneys may be found 
enlarged and their epithelium fatty, but this has no direct connec- 
tion with the essential pathology of the affection. INFLAMMATION. 
This is a subject whose importance in pathology can hardly he 
over-estimated. From the time of John Hunter its phenomena 
have been taken as the basis of various speculations on the nature 
of pathological phenomena in general. Following the course we 
have hitherto adopted, we have first to consider the conditions 
under which inflammation occurs. 
Etiology of Inflammation.—In many cases the causes of inflam- 
mation are obscure, and this applies mainly to internal organs 
whose actions are greatly hidden from our view. Inflammation is 
producible artificially, and if we study the modes of production 
we shall find that agents are used to which the general name of 
irritants is applied. The inflammation is produced, it is said, by 
irritating the part in some way. This name irritant is apt to be 
misleading, as it very readily gives rise to the conception of a 
stimulating action; whereas if we consider the nature of the so- 
called irritants we shall find that they are rather of a deadening 
than of a stimulating kind. They are agents which, when acting 
strongly, are calculated to kill the tissues, and acting less strongly 
they maybe supposed to damage it; it is in this case that they 
produce inflammation. A certain degree of heat or cold will kill, 
a less degree will lead, if sufficiently prolonged, to inflammation. 
Such agents as croton oil, nitrate of silver, chloride of zinc, have a 
damaging action on the tissues, and they are some of the com- 
monest in use when inflammation is to be produced. Again, trau- 
matic causes produce inflammation; a direct injury inflicted may 
kill, but acting less vigorously it may produce inflammation. 
It may be said, perhaps, that in inflammation of internal organs 
there is no such definite cause to be discovered. In pneumonia it 
might be supposed that there is no direct irritant or deleterious 
agent attacking the lung tissue. Hut even here there is reason to 
believe that there is some such agent at work. In one of the 
hospitals in Glasgow a medical man prescribed a tablespoonful of 
cough-mixture; the nurse gave a tablespoonful of carbolic acid 
instead. The result was an acute pneumonia presenting the usual 
physical signs and symptoms. In this case there was a deleterious 
agent introduced into the stomach and so into the circulation, and 
it acted on the tissue of the lungs (perhaps mainly on the blood- 
vessels), possibly during the process of excretion by these organs; 
the result was an acute inflammation. 
Again, when large blisters are applied, it sometimes happens ETIOLOGY OF INFLAMMATION. 
81 
that the active chemical principle is absorbed, and, passing into 
the blood, produces inflammation of the kidneys probably during 
the process of excretion. We have seen also that after transfusion 
of blood, the haemoglobin is sometimes dissolved out from the 
blood-corpuscle and produces inflammation of the kidneys. And 
so in all inflammations we are to infer the existence of some dele- 
terious agent, although it is very often difficult to tell whence it 
has come and what is its nature. 
At this point it may properly he inquired, whether the nervous 
system has anything to do with the causation of inflammation. 
There are not a few facts which suggest, at least, some connection. 
In some of the instances the connection is clearly an indirect one. 
For instance, when inflammation of the eye results from division 
of the fifth nerve, the inflammation is really traumatic in its origin. 
By the severance of the nerve, the reflex action of winking is 
abolished as well as the secretion of tears, and so the organ is ex- 
posed to injuries, and unable to get rid of foreign bodies. The 
inflammation is the result of irritation from without, and, if the 
eye be carefully preserved against such injuries, the inflammation 
does not occur. 
But there are cases where nervous action has a very important 
and apparently direct relation to the cause of the inflammation. 
A man with a stone impacted in his urethra will have an inflam- 
mation of the testicle. Or after the passage of a bougie through 
an urethra with a partially healed wound, there will be a rigor with 
immediate suppression of urine and an acute inflammation of the 
kidney. These results can only be effected by reflex action, and 
there are various ways in which we may suppose them to occur. 
Reflex irritation may produce, through the vaso-motor nerves, a 
contraction of the arteries of an organ, and in the case of the 
kidney this contraction may conceivably be sufficient virtually to 
bring the circulation to a standstill. The immediate suppression 
of urine resulting on the passage of a bougie can scarcely be 
accounted for, except on the supposition of such a spasmodic con- 
traction amounting almost to occlusion of the renal arteries. If 
such a stagnation of the blood continues long enough, the vessels 
will be so damaged that when the circulation is restored inflam- 
mation ihust result. 
But there are cases of internal inflammations which cannot he 
explained merely on the supposition of a reflex stimulation of the 
vaso-motor nerves. The manifest relief which many inflammations 
undergo in consequence of counter-irritation has been pointed out 
by Lister as indicating the influence of the nervous system in pro- 
ducing inflammation. The application of the actual cautery to 
the skin over an inflamed and painful joint will often relieve the 
pain and inflammation instantaneously. It is as if there was in 
the nerves of the part a state of over-action which affected in- 
juriously the tissues. This over-action being relieved by a still 
greater stimulation of nerves connected reflexly, the inflammation 
subsides. 82 
INFLAMMATION. 
It is probable that even in such cases nervous action alone is not 
sufficient to produce inflammation. It is more likely that under 
certain conditions of the local nervous arrangements the tissues 
are especially weak, and are liable to be damaged by agents which, 
under normal conditions, they would resist. It has been shown 
that a mild inflammation of the bone-marrow produced by caustics 
may be converted into an intense inflammation by causing the 
animal to eat putrid food. Here an existing damaged state makes 
the tissues unable to resist the attack of a further damaging agent, 
which normally they are able to withstand. It may be similar in 
the case of many internal inflammations produced apparently by 
exposure of the surface of the body to cold. Such exposure may 
produce, by reflex action, a state of the nervous system rendering 
the organ peculiarly liable to damage from conditions of the blood, 
which otherwise would not produce any such effect. In all these 
cases, also, it is to be borne in mind that the reflex action may 
affect specially the vascular system. 
It may be added that besides conditions brought about through 
the nervous system there may be individual peculiarities, hereditary 
or acquired, rendering different persons variously liable to the 
action of irritants, and even in the same person the various organs 
of the body may show different degrees of resistance. The char- 
acter of the inflammation also will, to some extent, be influenced 
not merely by the nature of the agent causing it, but also by the 
state of the individual. 
In studying individual cases of inflammation it will be impor- 
tant to consider by what path the irritant has reached the part 
which has become inflamed. In many cases it reaches it by the 
blood, and as the blood is distributed in every part of the organ, 
the inflammation will not probably show any special localization. 
And so, when we find two symmetrical organs, both of which are 
attacked in every region, we generally infer that the agent causing 
the inflammation has come by the blood or, at least, by a path 
common to both. Of course, there may be local differences in the 
organ itself of such a character that every part will not be equally 
susceptible to the action of an agent calculated to produce inflam- 
mation, and so the disease may develop more in one part of the 
organ than in another, although the general character of its distri- 
bution will generally still suggest the path by which the agent 
has come. 
THE PRINCIPAL PHENOMENA OF INFLAMMATION. 
The classical signs of inflammation are redness, swelling, heat, 
and pain, but in studying the nature of the process it will not be 
proper to follow this division. We have to investigate the exact 
nature of the processes occurring in the inflamed part, and in order 
to obtain a comprehensive view of the subject we shall, in the first 
instance, give an illustration which exhibits the main phenomena, THE PRINCIPAL PHENOMENA OF INFLAMMATION. 
83 
and afterwards consider the subject under headings suggested by 
that illustration. 
A simple experiment may be performed to illustrate the prin- 
cipal phenomena at the outset of an acute inflammation. If a frog 
be paralyzed with curare, the web of the foot may be spread out 
and observed under the microscope. With a pair of scissors a 
superficial longitudinal wound may be made, taking care to remove 
little more than the epithelium. By this operation the connective 
tissue of the web, with its vessels, is exposed; the action of the 
scissors in cutting, and the unusual exposure to the air, affect these 
structures, and the various phenomena of inflammation soon begin 
to manifest themselves, care being taken to keep a moist atmos- 
phere around the web so as to prevent the wound, deprived of its 
epidermis, from drying. At first the circulation goes on in the 
bottom of the wound as before, the area is merely more trans- 
parent from the absence of the epithelium. But very soon, if 
an artery is near or in the wound, it dilates, and there is an 
acceleration of the stream in the capillaries and veins. But this 
soon disappears, and the circulation, especially in the capillaries, 
becomes slower and slower, till here and there the blood-corpuscles 
now and then stand still for a moment or two. By and by a pecu- 
liar condition becomes visible in the veins, formally, the blood- 
corpuscles flow down the middle of the vein, and the peripheral 
zone contains plasma with a few white corpuseles rolling along. 
As the inflammation proceeds, the white corpuscles come to occupy 
this zone, and to adhere to the inner surface of the vessel. The 
individual corpuscles may not be all absolutely stagnant, they 
adhere for a time and then depart, but the result of the process is 
that there is a nearly complete filling up of the zone with white 
blood-corpuscles, so that the vein seems pavemented internally 
with these cells. This is seen not only in any vein which may 
happen to be in the bottom of the wound, but also in those for a 
short distance outside it. 
If the attention be now directed to the surface of the wound, it 
soon becomes manifest that certain peculiar bodies are appearing 
there. These are at first seen mostly towards the edge of the 
wound, and are especially numerous in the neighborhood of veins 
where the white corpuscles are adherent. They are of various 
shapes, and present a transparent gelatinous appearance. If ob- 
served carefully they are seen to be altering their shapes, presenting 
the well-known amoeboid movement, such as shown in Fig. 21. 
These cells gradually increase in numbers, and by their contractile 
power they move from the periphery towards the centre of the 
wound till they may come to cover it entirely. These bodies may 
be removed from the wound by placing the end of a capillary glass 
tube on the surface. A fluid runs up into the tube, and in this 
fluid are these free cells. The fluid may now be blown on to a 
glass slide and examined under a higher power of the microscope, 
when the slow amoeboid movement will be still more manifest. 
If, in the drop of fluid, these bodies are allowed to die or are 84 
INFLAMMATION. 
killed by the addition of a reagent, they become globular and 
granular, in fact, have the characters we recognize as those of 
white blood-corpuscles, lymph-corpuscles, pus-corpuscles—of leu- 
cocytes in general. The addition of acetic acid to the living cells 
will first cause them to assume the globular form, and then will 
bring out the nucleus or nuclei as in an ordinary white corpuscle. 
The fluid in which these corpuscles are found is coaguable, and if 
Fig. 21. 
A leucocyte from human blood showing amoeboid movement. (Klein.) 
it be kept till the corpuscles have died, strings of fibrine will be 
found in it. If this experiment be made in summer, the whole of 
these phenomena will manifest themselves in a few hours, and in 
five or six hours the entire wound may be plastered over with 
amoeboid cells. 
In the course of a few more hours the wound begins to be 
covered in with new-formed flat epithelium. This begins at the 
margins, and if the wound is small it may be wholly covered 
within twenty-four hours. The amoeboid cells are covered in, but 
they very soon disappear, and the connective tissue of the web 
remains with a thin transparent epithelium covering it. 
Without following out this experiment further, we may now 
proceed to consider the principal phenomena of inflammation, 
which have been partly illustrated. We shall consider, first, the 
state of the vessels ; secondly, the condition which is illustrated in 
this experiment by the fluid on the surface of the wound con- 
taining amoeboid cells; and lastly, the condition of the tissues in 
inflamed parts. 
i.—tiie state of the vessels in inflammation, 
When an irritant is applied to a transparent vascular tissue, such 
as the tongue or web of the frog, it produces effects which vary 
slightly, according to its nature. If croton oil be applied, there is 
first a slight contraction of the arteries, soon followed by a dilata- 
tion of them. If ammonia be used, there is dilatation without 
previous contraction. The dilatation of the arteries leads to an 
active hyperemia, the current is accelerated in the arteries, capil- 
laries, and veins, and these vessels are overfilled; there is a great 
excess in the quantity of blood passing through the vessels. The 
acceleration of the current does not persist, however, in the most 
affected parts; on the contrary the blood-corpuscles begin to lag, THE PRINCIPAL PHENOMENA OF INFLAMMATION. 
85 
especially in the capillaries and veins, although there is still accel- 
eration in the arteries, and in the capillaries and veins in the less 
inflamed parts. This stagnation in the capillaries and veins may 
assume a high degree, especially in the part most acted on by the 
irritant. Although the current is slow in these vessels they remain 
overfilled, a passive liypersemia supervenes on the active hyperaemia; 
at the same time the white corpuscles accumulate on the internal 
wall of the veins in the manner already described, and they also 
adhere at intervals in the capillaries. The circulation may come 
almost to a standstill in the capillaries of the parts most affected, 
while at various distances out from this there will be manifest a 
less and less amount of retardation till a zone is reached where the 
retardation disappears, and by and by gives place to acceleration. 
We have now to consider what may he the explanation of these 
various phenomena which the vessels manifest. The observations 
of Lister (Phil. Trans, for 1858, vol. 148) present us with a view of 
this subject which has been largely confirmed by other observers, 
and has only been corrected in one or two particulars. Saviotti 
has also published some very excellent researches (Virchow’s 
Archiv, vol. 1.) which are for the most part confirmatory of Lister’s 
views. 
Contraction of the vessels, which is in some cases the primary 
phenomenon, is probably reflex. It is frequently absent, and when 
it occurs is always very transitory. Irritation of sensory nerves is 
known to produce contraction of arteries by reflex action. If the 
web of the frog be observed under the microscope, and, at the same 
time, the skin irritated by tapping or by twitching with the forceps, 
the arteries will be seen to contract, and this contraction does not 
occur if the sciatic is first divided. In the case of inflammation, 
therefore, we may conclude that the primary contraction when it 
occurs is reflex, produced by the irritation of the sensory nerves. 
The dilatation of the arteries leading to acceleration of the 
stream, or active hyperemia (also called determination of blood), 
is not, like the contraction, of reflex origin. In order to enforce 
what follows, it is important here to recall the fact that irritants 
act injuriously on the tissues, and, in a certain sense, paralyze 
them. 
That the effect of irritants is to paralyze the tissues was long 
ago shown by Lister in his important researches on inflammation. 
The skin of the frog is supplied with pigment-cells. These cells 
are branching bodies (they are shown in Fig. 15, p. 63), and they 
possess the power of scattering the pigment into many branches, 
or of concentrating it more or less into the central parts of the 
cell. They are under the command of the nervous system, and by 
their means the animal is capable of changing its color, presenting 
a dark hue when the pigment is dispersed, and a lighter color 
according to the degree of concentration. Some irritants have the 
immediate effect of dispersing the pigment, and this itself is so far 
an evidence of paralysis as the dispersed condition seems to be the 86 
inflammation. 
state of rest of the cells; but whether the pigment is dispersed or 
not, the animal loses control of its pigment in the affected area, 
which does not change its color with the rest of the skin, and may 
be found dark while the animal is pale, etc. 
We have already had occasion to remark that, as Lister long ago 
inferred, that there are probably, in connection with the arteries, 
peripheral ganglia which are the immediate regulators of the state 
of contraction of these vessels. If these ganglia be paralyzed the 
arteries will dilate, and this is apparently the cause of the dilata- 
tion under consideration. That the dilatation is not reflex 
seems sufficiently proved by the fact that it occurs after all connec- 
tion with the central nervous organs has been severed. For 
instance, the sciatic nerve has been divided in a frog’s leg with 
resulting dilatation, but the application of an irritant to the web 
produces an increase of the dilatation. Again, the brain and 
spinal cord in the frog have been destroyed (Cohnheim), but the 
application of an irritant to the tongue still produces dilatation of 
its arteries. The acceleration of the blood-current in the arteries, 
capillaries, and veins, will be understood from what has gone 
before to be a direct result of the dilatation of the arteries; we 
have, in fact, an active hyperaemia. It will not be understood, 
however, that, apart from inflammation, active liypersemia is never 
produced by reflex action; it is frequently so, but inflammatory 
active hyperaemia is a local phenomenon. It is not impossible that 
an inflammatory may be associated with a reflex hyperaemia, and 
the problem may in this way be complicated. 
The cause of the retardation may not at first be apparent, but 
the researches of Lister afford an explanation of it. The cause of 
the retardation is an increased adhesiveness of the blood-corpus- 
cles. This is a matter of direct observation. The corpuscles in 
the inflamed area can be seen to move sluggishly along the wall as 
if attracted by it, and the pavementing of the veins with white 
corpuscles is clearly due to increased adhesiveness. It has been 
pointed out by Lister that, when the blood is removed from the 
vessels and comes in contact with dead matter, the blood-corpus- 
cles acquire an adhesiveness which they do not possess inside the 
normal vessels. The red corpuscles stick together by their flat 
surfaces and form the well-known rouleaux. The adhesiveness of 
the white corpuscles is not so obvious when a drop of blood is ex- 
amined outside the body, but we have reason to believe that it is 
even greater than that of the red. How inflammation damages 
the walls of the vessels, with the result that the corpuscles behave 
as if in the presence of dead matter—they become adhesive. 
This is excellently shown in an experiment of Lister’s. He 
ligatured the leg of a frog, producing thereby stagnation of the 
blood in the vessels, but on examining the web it could be seen 
that the corpuscles were able to move freely among one another— 
there was obviously no adhesiveness. But now, if a piece of 
mustard was applied to the web, this free movement ceased in the 
area affected; the corpuscles became adherent among themselves, 87 
THE STATE OF THE VESSELS IN INFLAMMATION. 
and to the wall of the vessels. The result of this was an accumu- 
lation of the corpuscles in the irritated area; any corpuscles which 
happened to glide into the area remained adherent there, and so, 
by degrees, the vessels became overfilled—a state of hyperremia 
superinduced on stagnation. If any corpuscles happened to escape 
from the affected area, it ceased to be adhesive, and moved freely 
about. 
We may therefore infer that the retardation of the current and 
the pavementing of the veins with white corpuscles are the result 
of the injury to the vessel-wall, and it may he added that, in con- 
nection with inflammations, all degrees of stagnation up to abso- 
lute stoppage or stasis may he produced, and are often manifested 
together in the same case. 
We may now sum up the conditions presented by the blood- 
vessels in the early periods of inflammation as follows: the arteries 
dilate by a relaxation of their muscular coats, due to a paralysis 
of the peripheral ganglia. In some cases this dilatation is pre- 
ceded by an evanescent contraction. The immediate result of the 
dilatation of the arteries is active hyperaemia, or determination of 
blood, involving overfilling of the arteries, capillaries, and veins, 
with acceleration of the current. This is followed by retardation 
of the current, the vessels remaining dilated and liypersemic, and 
this retardation may go on to almost complete stasis in the capilla- 
ries. The retardation is due to adhesiveness of the corpuscles, and 
to the same cause is to be traced the pavementing of the veins with 
white corpuscles. 
It is sometimes possible in acute inflammation of the skin, as in 
the case of a boil, to observe conditions directly traceable to the 
state of the vessels here indicated. Thus at the peripheral parts 
of such a focus of inflammation the skin presents a fiery-red ap- 
pearance due to determination of blood; the red color may be 
pressed away with the finger, but it immediately returns. Inside 
this zone there is an area in which the redness is not so vivid, and 
when the red color is pressed away it returns sluggishly; the 
corpuscles are here already adherent, and the current retarded. 
Then in the more central parts a dusky-red appearance is presented, 
and on pressure it may be impossible or very difficult to remove 
the redness; here a condition of extreme stagnation exists. 
In connection with the state of the vessels, we have to consider 
the temperature of inflamed parts. It is well known that heat 
is one of the so-called cardinal symptoms of inflammation, and in 
external parts a feeling of heat is almost universally complained 
of. The nerves of internal parts seem incapable of communicating 
the sense of differences in heat and cold. A hot potato swallowed 
gives an impression of pain, and it maj be argued that the pain in 
internal parts during inflammation is partly due to increase of 
temperature. We have to inquire whether there is an actual pro- 
duction of heat in inflamed external and internal parts. 
There is no doubt that the temperature of inflamed external 88 
INFLAMMATION. 
parts is increased in inflammation. John Hunter long ago deter- 
mined this by actual observation. He had a case of hydrocele 
to deal with, and undertook its treatment by the old operation of 
laying open the sac and inserting lint dipped in an irritating salve, 
with a view to producing inflammation. At the time of the opera- 
tion he found that the temperature in the tunica vaginalis was 92°, 
but next day, inflammation having been induced, the temperature 
had risen to 98f °. The question here arises whether this increase 
of temperature is due to an actual production of heat in the in- 
flamed part, or to an increased supply of hot blood, due to dilata- 
tion of the arteries. 
That there is a greatly increased supply of blood to inflamed 
external parts has been proved by experiment (Cohnheim). If the 
foreleg of a dog be inflamed by scalding or by painting with 
croton oil, or any other method, the quantity of blood coming 
from the limb may be compared with that on the sound side by 
introducing canulas into the corresponding veins on the posterior 
aspects of both legs. In a recent inflammation the amount of 
blood on the inflamed side may reach nearly the double of that on 
the sound side, and it may even be as great as when the arteries 
have been relaxed in a limb by dividing the axillary plexus of 
nerves. This extreme degree of difference may not continue long, 
but even for some days it is frequently very considerable. The 
relaxation of the arteries, it is clear, produces a determination of 
blood which extends beyond the immediate focus of the inflamma- 
tion, and is not counterbalanced by the retardation. 
John Hunter, having determined the great increase in tempera- 
ture above referred to, yet came to the conclusion that it was due 
to the determination of blood, for he found that the temperature 
of an inflamed external part never exceeded or even quite reached 
that of a normal internal part, or, in other words, of the blood in 
internal organs. Since Hunter’s time, Simon has thought to prove 
that there is some development of heat in inflamed parts. His 
experiments seemed to show that the arterial blood passing to an 
inflamed external part is not so warm as the focus of inflammation, 
and that the venous blood returning from the part is warmer than 
the arterial blood, although not so warm as the focus of inflamma- 
tion. But the experiments of Jacobsen, made with more exact 
instruments, entirely conflrm the views of Hunter. It appears 
that the most acute inflammation of the skin or muscle never 
causes an elevation of temperature sufficient to reach that of the 
rectum, vagina, or abdomen, the difference being generally 1° or 
2° C. Again, in artificial inflammations of internal parts, as in 
peritonitis or pleurisy, the temperature was never raised to that of 
the left ventricle, being always from .2° to .5° C. under it. This 
means that in these parts, the temperature being already near that 
of the blood in the left ventricle of the heart, inflammation, lead- 
ing to an increased supply of blood of a similar temperature, 
causes virtually no elevation above the normal heat. Again Cohn- 
heim has found that, when in one forepaw of a dog, a state of THE INFLAMMATORY EXUDATION. 
89 
acute inflammation is induced, while in the other active hypersemia 
is produced by dividing the axillary plexus of nerves, the tempera- 
ture in the inflamed foot is always slightly less than that in the 
other. We may safely infer, then, that in inflammation there is 
no local production of heat. 
In the experiment sketched at the outset the inflammatory 
exudation was the fluid which collected on the surface of the 
wound. We saw that this fluid contained amoeboid cells, and that 
it was coagulable. We may thus consider the inflammatory exuda- 
tion as consisting of cells, serous fluid, and fibrine, and we shall 
in the first place pass each of these under review. 
The Exudation-cells.—The resemblance of the cells met with 
in acute inflammations to the leucocytes in the blood long ago sug- 
gested the idea that they are white blood-corpuscles. In the year 
1846, Waller observed the pavementing of the internal coat of the 
veins with white blood-corpuscles in the inflamed tongue of the 
frog, and as he saw similar cells outside the vessel he inferred that 
the white corpuscles had got through the wall. It was, however, 
difficult to believe that the solid globular white corpuscles could 
pass through the intact wall of a bloodvessel, and Waller’s views, 
although supported by Wm. Addison, were lost sight of. By ancl 
by, however, Recklinghausen demonstrated that pus-corpuscles 
and white blood-corpuscles possess contractile power by virtue of 
which they are able to move from place to place, and to alter their 
shapes in the most diverse fashion. This paved the way for the 
actual observation of their passage through the walls of the vessels 
made by Colinheim. He made his observations on the mesentery 
of the frog. When this exceedingly delicate and transparent 
structure is drawn out of the body through a wound in the lateral 
aspect of the abdomen, the mere exposure to the air is sufficient 
to set up an acute inflammation, the phenomena of which can he 
readily observed under the microscope. Let us suppose that the 
pavementing of the veins has occurred, and that there is an occa- 
sional white corpuscle adherent in the capillaries, and the following 
surprising phenomena show themselves, as described by Cohnheim 
himself. “One sees, as a rule, first, in a vein which presents the 
pavementing with white corpuscles, but sometimes in a capillary, 
a pointed projection in the external contour of the vessel; it pushes 
itself farther and farther outwards, it increases in thickness, and 
the pointed projection develops into a colorless rounded knob; 
this increases in length and thickness, sends out fresh points, and 
draws itself gradually outwards from the vessel-wall, with which 
it comes to be connected only by a long thin stem. Finally, this 
also lets go the vessel, and there lies outside a colorless, dull, 
glancing, contractile corpuscle, with several short processes and a 
II.—THE INFLAMMATORY EXUDATION. 90 
INFLAMMATION. 
long one, of the size of a white blood-cell, with one or several 
nuclei; in a word, a white blood-corpuscle.” 
In the investigation of inflamed tissues in the usual way after 
death, there are often indications to be met with of this process of 
emigration of the white blood-corpuscles. The leucocytes in the 
tissues, for instance, are frequently aggregated especially around 
the bloodvessels. In the accompanying Fig. 22, the appearances 
in the human omentum are shown in a somewhat diagrammatic 
form, and the appearances there are sufficiently suggestive. 
There is no longer any doubt then that the white corpuscles of 
the blood wander out of the vessels, and they become the so-called 
exudation cells of recent inflammations. But, besides the leu- 
cocytes, the red corpuscles also pass out of the vessels, and this 
Fig. 22. 
Inflamed human omentum. The phenomena of inflammation are seen in the veins and 
capillaries, the condition being normal at the artery (c), where b represents endothelium 
covering the trabecula (a). In the vein (d) there are many white corpuscles along the wall. 
Some of these are emigrating (e); /, desquamated endothelium; g, extravasated red cor- 
puscles. (Ziegler.) 
they do by the process of diapedesis, of which we have already 
seen examples. The white corpuscles are active contractile cells, 
and they generally pass through the vessels to a larger extent than 
the red ones, but there are some inflammations in which these red 
corpuscles also pass through in large numbers. So far then as the 
cells which appear at the outset of an inflammation are concerned, 
they are doulitless, mainly, if not entirely, blood-corpuscles. THE INFLAMMATORY EXUDATION. 
91 
The Serous Exudation.—This has obviously its source in the 
blood. In inflammation there is a greatly increased transudation 
of the fluid of the blood from the vessels, and this passes primarily 
into the serous spaces. If these are, naturally or by reason of a 
wound, in communication with a surface, the fluid will appear 
on the surface. The inflammatory (edema indicates a greatly 
increased circulation in the serous spaces and lymphatics, and this 
can be proved by actual observation. If the leg of a dog be irri- 
tated with croton oil, the foot swells greatly, and if the lymphatics 
on the external aspect of the leg be then exposed they will be 
found greatly dilated; a canula being introduced, the lymphatic 
fluid will flow from it, drop rapidly following drop, whereas in the 
sound leg the circulation is very slow. If before setting up the 
inflammation a canula be introduced, and an inflammation set 
up by placing the foot in hot water, then it will be seen that almost 
immediately an increase in the flow of lymph occurs, while the 
oedema comes on later and is not followed by further increase in 
the flow. The meaning of this is that the oedema only develops 
when the increase of transudation is too great for the lymphatics 
to dispose of. 
But not only is the transudation increased, it is altered in 
quality. AVe have seen that in passive hyperemia the transudation 
is a watery fluid, more watery than the normal lymphatic fluid. 
In inflammation it is a concentrated fluid, containing a great deal 
more albumen and corpuscles, and on being shed, or even in the 
canula, it coagulates. 
The Fibrinous Exudation.—It is a familiar fact that after the 
infliction of a wound there occurs a glazing of the surface within 
a few hours, and this glazing is due to the coating of the surface 
with a layer of fibrine. In addition to this there is discharged 
from the surface a greater or smaller quantity of serous fluid. 
This deposition of fibrine on the surface of a wound may be 
taken as typical of the fibrinous exudation, but a similar deposition 
of fibrine occurs in many other inflammations, in acute inflam- 
mations of serous membranes as in pleurisy, in acute inflammation 
of the lungs, etc. The fibrinous exudation has all the characters 
of fibrine seen in a blood-clot. Figure 23, for instance, is taken 
from the lung in acute pneumonia, and it is seen that a lung 
alveolus is filled with a network of fine fibres. 
The fibrinous exudation, especially the yellow layer seen on 
serous membranes, is often called lymph, but this term is a some- 
what confusing one. It has its origin in the coagulable lymph of 
John Hunter, and has very interesting historical relations. As 
the term is used, however, to designate other structures besides 
the fibrinous exudation, and as it involves a theory as to the rela- 
tions of the exudation, its use had better be avoided. 
The fibrinous exudation, for reasons which will appear after- 
wards, is mostly met with on surfaces. It seldom forms in the 
serous spaces of the tissues unless the inflammation has been 92 
INFLAMMATION. 
severe enough to kill the tissue, as in the case of a boil or car- 
buncle where the slough which forms is composed, partly of dead 
tissue and partly of fibrine deposited in the meshes. 
Fig. 23. 
Lung alveolus in acute pneumonia. A plug of fibrine, with a few leucocytes in it, 
I fills the alveolus. X 350. 
Mode of Production of the Inflammatory Exudation.—As 
the constituents of the exudation come from the bloodvessels, it is 
natural to look to the state of their walls in order to account for 
the extraordinary passage of the constituents of the blood through 
them. 
We have seen reason to believe that the acquired adhesiveness 
of the white corpuscles in the veins and capillaries is due to a 
change in the walls of these vessels in the direction of dead matter. 
In the normal vessels the white corpuscles roll along in the plas- 
matic zone or in the capillaries, without presenting any independent 
movement, whereas outside the body they at once present amoeboid 
movement. It is very possible that the living tissues have a cer- 
tain power of restraining this amoeboid movement, or at least of 
preventing the amoeboid cells penetrating them. If a piece of 
dead tissue containing canals and cavities, such as the cornea, be 
placed in the peritoneal cavity, then the leucocytes in the cavity THE INFLAMMATORY EXUDATION. 
93 
penetrate into these cavities. In the state of inflammation the 
capillaries are altered, their walls have undergone a change which 
renders them more permeable, and, being more like ordinary 
matter, they may allow a freer contractility of the corpuscles. It 
is, therefore, the alteration of the wall of the vessel which is the 
principal agent. It has been supposed that an increase in pressure 
of the blood in the vessels may have something to do with the 
emigration of the white corpuscles. But we must be certain, to 
begin with, that there is an increase of pressure. As Cohnheim 
has pointed out, the conditions here are not such as to cause an 
increase of pressure. There is no obstruction in the veins; in 
fact, the circulation through them is unduly abundant, as has 
already been seen, and any stagnation which exists in the capil- 
laries has its origin in the adhesiveness of the blood-corpuscles. 
If this stagnation in the capillaries produces any increase of press- 
ure, it will do so not in the veins, where it will rather diminish 
pressure, but in the arteries. How there is no emigration from 
the arteries, but from the capillaries and veins alone, and so it can 
hardly depend on the increase of pressure. The same applies to 
the diapedesis of the red corpuscles. They pass through the ves- 
sels not because the pressure is increased, but because the capillary 
wall is so deteriorated that even at the existing pressure they are 
pressed through. We have already seen that in the case of the 
embolic infarction a diapedesis occurs under conditions in which 
the pressure is presumably less than the normal. It is to be re- 
marked that here as there the diapedesis of red corpuscles occurs 
in the capillaries alone, and not in the arteries and veins. 
The INCREASED TRANSUDATION OF THE BLOOD-PLASMA is to be 
accounted for on similar principles. Alteration in the vessel-wall 
is again the main condition; and seems in inflammation to be 
much more serious than in passive hypereemia, as a much greater 
amount of albumen and salts pass through. 
The formation of fibrine, as we have seen, is a prominent 
occurrence in many inflammations, and as the constituents of the 
fibrine come from the blood, it also is to be regarded as part of 
the inflammatory exudation. The fibrinogen is contained in the 
exuded blood-plasma. The white blood-corpuscles contain the 
paraglobulin and ferment, but in order to yield these, it is 
necessary, as we have already seen in studying thrombosis, that 
they should disintegrate. In the case of thrombosis, an alteration 
of the wall of the heart or bloodvessel is necessary in order to the 
disintegration of the white corpuscles. In the present case it is 
the tissues outside the vessels that are concerned, and these, as we 
have seen, are damaged as a necessary condition of the inflamma- 
tion. 
It has already been noted that firine forms usually on inflamed 
surfaces, and rarely in the substance of the inflamed tissues unless 
necrosis has occurred. This may be set alongside the fact that 
thrombosis does not occur in the capillaries unless they have 
undergone necrosis. The serous spaces in the tissues, like the 94 
INFLAMMATION. 
capillaries, are lined with endothelium; and these spaces, being 
small, the white corpuscles will hardly be sufficiently removed 
from the endothelium to allow of coagulation, so that this will not 
occur unless the endothelium be dead or shed. In some very 
acute inflammations of connective tissues (acute phlegmon) there 
is, however, not uncommonly a fibrinous exudation in the meshes 
of the tissue, forming a kind of fibrinous oedema. This may be 
seen not uncommonly in the skin in erysipelas. But where the 
exudation occurs on a surface and the white corpuscles are removed 
from immediate contact with the endothelium, then many of them 
perish and coagulation occurs. 
In this connection it may be remarked that the epithelium, like 
the endothelium, seems to have the power, and perhaps to a greater 
extent, of preventing the disintegration of the white corpuscles and 
the formation of fibrine. As a rule, a fibrinous exudation does not 
form on a mucous membrane, and when it does form it may be 
taken for granted that the epithelium has died or been shed. 
It will be understood that the inflammatory exudation presents 
various characters, under different circumstances, even apart 
from the question of coagulation. In some cases it is exceedingly 
watery, partaking chiefly of the characters of an ordinary transu- 
dation. This will be the case mainly in slight inflammations, and 
in those occurring in persons whose blood is watery. For instance, 
the inflammations which so frequently occur in Bright’s disease 
have usually a watery exudation. In such cases the exudation-cells 
will be also small in number. 
On the other hand, there are inflammations in which the exuda- 
tion-cells are exceedingly abundant, so abundant that the inflam- 
mation rapidly assumes a suppurative character. This is peculiarly 
the case with septic inflammations. For instance, in septic in- 
flammation of joints such as occurs in pyaemia, we have the exu- 
dation rapidly becoming purulent, the pus-corpuscles having all 
the characters of the ordinary exudation-cells, and being doubtless 
white blood-corpuscles. It will be observed that these suppurative 
inflammations are severe in character, and presumably imply 
serious alteration of the vessel-walls, such as to allow of the enor- 
mous emigration of the white corpuscles which is here presupposed. 
It may further be said regarding inflammatory exudations that 
they vary considerably according to their site and other rela- 
tions. We have already said that a serous exudation may flow 
from a surface, may accumulate in a cavity, or may lie in the serous 
spaces, causing oedema. We shall afterwards see that the serous 
fluid may be taken up by cells. Again, the exudation may be 
mixed with the secretion of a mucous membrane or gland. In the 
former case, the exudation will have more or less of the characters 
of the mucous secretion, variously modified according to the 
amount of the constituents; thus, we may have a mucous, sero- 
mucous, muco-purulent exudation, and in these exudations epi- 
thelium cells, ciliated and otherwise, will often be found. In the 95 
NEW FORMATIONS. 
case of the kidney, the exudation is to be found mixed with the 
urine, so that we have albuminuria. 
It may here be remarked that the exudation passes in the di- 
rection of least resistance, and will be found to accumulate or 
escape where it best can; thus, in the kidneys it passes largely into 
the uriniferous tubules, in the lungs it occupies the air-vesicles, in 
the connective tissue it fills the serous spaces, producing oedema. 
In some cases the oedema manifests itself mainly where the tissue 
is loosest; for instance, in inflammations of the larynx, oedema 
occurs mainly at the base of the epiglottis and the aryteno-epiglot- 
tidean folds, giving rise to so-called oedema glottidis. 
We have still to consider how inflammatory exudations are 
disposed of. In slight cases the exudation is carried off by the 
lymphatics, passing by that route back into the circulation, the 
exudation-cells being perhaps partly retained by the lymphatic 
glands. In more severe cases, and especially when the exudation 
is retained in cavities, its disposal is more difficult. The serous 
fluid will rapidly be absorbed, but the fibrine and the exudation- 
cells, where these are so abundant as to constitute a purulent in- 
flammation, or are entangled in the fibrine, are not got quit of so 
easily. Pus-corpuscles readily undergo fatty degeneration, and we 
shall afterwards see that structures which have undergone this 
change, by and by disintegrate, and the fat is absorbed. Some- 
times, however, the fat is too abundant, or the conditions are not 
suitable to absorption, in which case the pus may dry into a cheesy 
mass, which may afterwards be impregnated with lime-salts. 
Similarly the fibrine may disintegrate and be absorbed, or dry in 
and become calcareous. 
III.—CHANGES IN THE TISSUES AND THE INFLAMMATORY 
NEW FORMATION. 
We enter here on a somewhat debatable department, especially 
as under this heading will be included the subject of new formation 
in inflammation. 
It is undoubted that the tissues in inflammations sometimes 
undergo retrograde changes. The inflammation, if very severe, 
may kill the tissue, but short of that there are certain inflamma- 
tions which are characterized by the occurrence of fatty degenera- 
tion in the cells constituting the tissues. It may be said that in 
severe inflammations, and probably at the outset of all acute in- 
flammations, the tissues take no active part in the processes, and 
if affected in their structure at all, are affected for the worse. We 
have already seen that inflammations paralyze the tissues. But it 
may be presumed that when an inflammation has lasted for some 
time and has diminished in intensity, the tissues may recover, and 
it wrill not be surprising to find that they undergo changes of a 
kind different from the retrograde processes already mentioned. 96 
INFLAMMATION. 
This leads us up to the question of the new formation of tissue 
which is so characteristic of many inflammations. It may here be 
stated that two views are held as to the origin of such new forma- 
tions, the one being that the formative cells are the white blood- 
corpuscles, and the other that the existing tissues, and especially 
the connective tissues, supply the formative cells. AVe shall first 
mention certain facts connected with new formation and afterwards 
recur to this disputed point. It need hardly be said that by new 
formation is meant the production of a properly organized tissue, 
the form of tissue produced being for the most part connective 
tissue containing bloodvessels. 
A granulating wound, with the resulting cicatrix, may be taken 
as typical of the inflammatory new formation, and by considering 
the occurrences which present themselves there, we shall become 
acquainted with certain facts connected with the subject. Granu- 
lation-tissue is already an imperfectly organized but highly vascular 
tissue. In the accompanying woodcut (Fig. 24), the injected blood- 
vessels of a granulating wound are shown, and the degree of vascu- 
larity may be inferred. 
Fig. 24. 
Vessels of a granulating wound injected. (Billroth.) 
It is to be observed in the first place that in order to the produc- 
tion of granulations, the inflammation must be of some duration. 
If a wound close within the first few days, no granulations are 
formed. The damage done by the knife in inflicting the wound 
produces an inflammatory exudation in the form of a glaze of 
fibrine and a serous discharge. But if the wound be protected 
from further irritation it will not produce granulations even should 
it not heal by the first intention. Under antiseptic treatment, if 
the wound be protected from carbolic acid vapor and other sources 
of irritation, granulations do not form. Even in the case of a 
septic wound, after the preliminary glazing of the surface, there is 
what surgeons call “a pause” of two or three days before the 
granulation appear. There is in this case a prolongation of the 
inflammation for several days before the occurrence of new forma- 
tion. But, on the other hand, the inflammation must not be too 
severe, else the new formation will not occur. Inflammations 
which rapidly pass on to suppuration are not accompanied by new NEW FORMATION. 
97 
formation. Again, in order to new formation an abundant supply 
of blood is necessary, and in this connection it may be mentioned 
that the new formation of bloodvessels is one of the most marked, 
as it is frequently the earliest visible manifestation of this process. 
A granulating wound appears, at first sight, to be composed 
simply of round cells of nearly uniform size. But on more careful 
examination it is seen that, putting out of view the bloodvessels in 
the mean time, it consists of two kinds of cells (see Fig. 25). The 
Fig. 25. 
Granulation-cells, a and a, leucocytes; b, b, various formative cellsc, formative cell 
with two nuclei; «, with many nuclei; d, d, d, formative cells developing connective tissue; 
e, complete connective tissue. X 500, Picrocarmine preparation. (Ziegler.) 
one kind has the size and general appearance of the white blood- 
corpnsele, and gives with acetic acid a similar reaction (a and aj. 
The others (b, b) are about twice as large as these, and as they 
present a distinct outline and possess an oval nucleus, they have a 
considerable resemblance to epithelial cells, and are hence some- 
times called epithelioid cells. These cells may possess two nuclei 
(c). Sometimes there are still larger cells with multiple nuclei (ej, 
the so-called giant cells, but these are not uniformly present, and 
may be left out of sight in the further consideration of the subject. 
In the new formation of the tissue these epithelioid cells are mainly 
concerned, in so much that Zeigler, whose observations are here 
of very great value, has designated them formative cells. This 
author studied the new formation of tissue by introducing under 
the skin or periosteum, or into the peritoneum of animals, two 
pieces of glass cemented together in such a way that there was 
free access between them, while the distance apart was no more 
than a fraction of a line. One of the pieces of glass was a micro- 
scopic cover-glass, so that anything between the glasses could be 98 
INFLAMMATION. 
studied under the microscope afterwards. These foreign bodies 
set up inflammation, and through time vascular connective tissue 
formed around them, and penetrated between the plates of glass. 
In these ingenious experiments the formative cells did not appear 
till about the fifth day after the occurrence of the inflammation. 
These cells are, like pus-corpuscles, contractile, but they are much 
less active, and we shall see immediately that they subsequently 
assume the characters of fixed cells. 
By and by these formative epithelioid cells elongate, and send 
out processes (b, b), becoming stellate or spindle-shaped. After a 
time the processes grow out and become, with a certain part of the 
substance of the cell, converted into fine fibres (d). In this way it 
appears the fibres of the new-formed connective tissue are formed, 
the rest of the protoplasm of the cell remaining as the spindle- 
shaped, fixed, connective-tisue cell (e). The fibrillae, developed out 
of neighboring cells, communicate, and thus is formed the com- 
plete flbrillated connective tissue. 
This new formation of connective tissue is necessarily connected 
with new formation of BLOODVESSELS (see Fig. 26). If epithelioid 
Fig. 26. 
New formation of bloodvessels in a granulating wound. (After Arnold.) 
cells are formed in advance of the bloodvessels, they do not pro- 
ceed to the formation of tissue, blit undergo fatty degeneration. 
The formation of the bloodvessels always occurs in connection 
with the preexisting vessels, usually the capillaries, and by a 
process of budding apparently. An elongated process extends out 
from the wall of the capillary. It meets another process, and so is 
converted into an arch. The arch and buds increase in thickness, 
and, by and by, a tunnelling of them begins, and they are by 
degrees converted into vessels, the blood passing into them. It 
has been stated by some that in the formation of the bloodvessels 
from the buds and arches, the tunnelling takes place partly by a 
conversion of the substance of the solid arch or bud into red blood- 
corpuscles, in a manner similar to what occurs in the original for- 
mation of bloodvessels in the embryo. But this seems to be 
doubtful, and the probability is that no such new formation of NEW FORMATION. 
99 
blood-corpuscles takes place. The vessels formed are at first mere 
tubes, and the demarcation of endothelial plates seems to be of 
subsequent occurrence. The new-formed vessels are then regular 
capillaries, and by subsequent changes they may increase in size 
and thickness, and take on the characters of arteries and veins. It 
is marvellous how rapidly such new formation of vessels occurs 
not merely in inflammations, but also in the formation of tumors, 
and we may regard this as consistent with the wonderful adapta- 
bility which we have already seen the vascular system to show to 
the needs of the system. 
In the formation of the permanent tissue, we have referred to 
the important part played by the epithelioid cells, but we have not 
made any reference to the origin of these formative cells. 
Their origin is a matter of dispute. Ziegler asserts that they arise 
by the conjunction or coalescence of the exudation-cells, or leu- 
cocytes from the blood, while others assert that these cells which 
have to do with the actual building up of tissue have their origin 
in the fixed cells of the tissues. Many facts may be adduced in 
favor of this latter view. 
We have already seen reason to believe that in the early stages 
of inflammation the constituents of the tissues are mostly passive, 
and, if they undergo any change, it is in the direction of degener- 
ation. But when the tissues have had time to recover, it is not 
inconceivable that, being by the exuded fluid supplied with 
additional pabulum, they should undergo nutritive changes. Even 
in some forms of acute inflammation the exuded fluid finds its 
way into the cells. In parenchymatous inflammation of the kid- 
neys the renal epithelium enlarges and becomes cloudy, often 
undergoing degeneration subsequently. But if the inflammation 
subside to some extent, the epithelium cells may be found with 
double nuclei and showing other signs of germination. From the 
researches of Ivlein and others it is rendered evident that in 
certain inflammations of the peritoneum the endothelium shows 
active germination, and as a result of such active processes these 
cells may produce amoeboid leucocytes which are not to be distin- 
guished from white blood-corpuscles. It is even doubtful whether 
in the normal condition the endothelium does not take part in the 
formation of the white corpuscles. 
Looking to the fact that the connective tissue throughout the 
body is so intimately related to the lymphatic system we may 
possibly find here a means of reconciling divergent views. The 
endothelium cell and the connective-tissue corpuscle may be 
regarded as essentially similar structures. We have reason to re- 
gard the serous cavities as virtually the same as the serous spaces 
in the connective tissue. The endothelium of the peritoneum is 
normally beset with frequent aggregates of round cells which may 
be regarded as lymphatic follicles, and similar aggregates are fre- 
quent in the connective tissues, for instance, in that of the lung, as 
has been pointed out by Burdon Sanderson and recently confirmed 
by Arnold (Virchow’s Archiv, vol. 80). In view of all these facts 100 
INFLAMMATION. 
we may, perhaps, regard the connective tissue and the lymphatic 
system as a single system, and the lymphatic glands as simply 
larger developments corresponding with the smaller cellular 
aggregates which we meet with throughout the connective tissue. 
In this view the white blood-corpuscles themselves would be con- 
nective-tissue structures, and have their seat of origin not only in 
the lymphatic glands, spleen, and bone marrow, but in all parts of 
the connective tissue. 
At last we may say that in inflammations, when they have 
become chronic or subacute, the connective tissue or endothelium 
produces amoeboid cells which are not distinguishable from white 
blood-corpuscles. The epithelioid cells 
which are the immediate formative agents 
may take origin from the fixed connec- 
tive-tissue cells or from the amoeboid 
ones, and there is nothing inconsistent 
in the view that they may also take 
origin in white blood-corpuscles. 
To return now to the case of the gran- 
ulating wound, we may find in a section 
of it appearances confirmatory of what 
has been said above (see Fig. 27). In its 
superficial layers it is composed of round 
cells many of which have the size and 
appearance of leucocytes, while others 
have the characters of epithelioid cells. 
The leucocytes are probably in great 
part white corpuscles in process of migra- 
tion, but they may also be to some extent 
derived from the fixed connective tissue 
of the part. Some of them pass to the 
surface and appear in the discharge as 
pus-corpuscles. Others, however, will 
pass into the lympli-spaces or even into the capillary vessels, and 
in either case resume their position as white blood-corpuscles. As 
we pass deeper in the granulating wound there are evidences of 
the changes in the epithelioid cells described above. We find parts 
where large spindle-cells are abundant, forming sometimes an 
actual spindle-cell tissue. Still deeper, and at the base of the 
wound, wTe find new-formed connective tissue. 
Towards its base the granulating wound shows a striking ten- 
dency to contract, and we may account for this in two ways chiefly. 
The leucocytes, to a large extent, disappear when we pass a short 
distance beneath the surface; and at the same time the epithelioid 
cells, by becoming spindle-shaped and arranging themselves in 
parallel bundles, occupy less space than before. The new-formed 
connective tissue also shows a remarkable tendency to draw 
together, becoming more compact and drier. This shrinking of 
the connective tissue continues long after the wound lias healed, 
the cicatrix tending to become smaller and harder. By the con- 
Fig. 27. 
Semidiagrammatic section of a 
granulating wound. X 85. NEW FORMATION. 
101 
traction at the base of the wound its area is diminished as a whole. 
The bloodvessels also which form loops passing to the surface are 
partially constricted, and so the superficial granulations are less 
supplied with blood. We may suppose that another consequence 
of this will be a less considerable emigration of the white cor- 
puscles from the vessels. 
We have still to consider how the granulating wound becomes 
covered with epithelium. This process is one which it is rather 
difficult to observe, apparently because the new-formed epithelium 
is very delicate and transparent. The new epithelium always 
arises from that already existing. The epithelial cells at the 
margin of the wound enlarge and divide, and so provide fresh cells 
which gradually cover the surface and assume the place and char- 
acter of the usual flat epithelium. It is said that the young epithe- 
lium sometimes shows even a slight amoeboid movement. The 
formation of epithelium sometimes begins in the midst of the 
wound, but this only happens when some epithelial structures, such 
as hair-follicles or sebaceous glands, have escaped destruction when 
the wound wras made. It is known also that living epithelium may 
be transplanted from one part of the body to another or even from 
a different person. When grafting is performed in this way the 
epithelium germinates like that at the margin and covers the 
neighboring granulations. 
The processes which wre have sketched as occurring in the 
granulating wound are repeated with slight modifications in all 
other inflammatory new formations. For new formation to occur 
the inflammation must be prolonged for some time, and it must 
not be too severe. These are the characters of chronic inflamma- 
tions, and it is in connection with them especially that we have 
new formation occurring. In these chronic inflammations we have 
a tissue comparable to granulating tissue, consisting essentially of 
round cells, but in which when the process is active epithelioid 
cells may be distinguished. The round cells have the characters 
of leucocytes, and in some cases they pass outwards from the tissues 
and form pus. In most cases, however, they pass into the lym- 
phatics and disappear. 
If two surfaces in the condition of granulation come in contact 
they coalesce, and their vessels communicate so that they form a 
common layer. In that case when the inflammatory tissue de- 
velops into connective tissue the surfaces will be united by a 
permanent vascular connective tissue. In this way the flaps of a 
stump unite after granulating, and thus also permanent adhesion 
of the pleura and of the pericardium is often brought about. 
It should be noticed that the inflammatory new formation does 
not always develop into connective tissue, but that it may produce 
OTHER FORMS OF THE CONNECTIVE-TISSUE SERIES, AS BONE AND CAR- 
TILAGE. A chronic inflammation of the periosteum results in 
considerable new formation of bone, in which the formative cells 102 
inflammation. 
take part. The formation of callus round a broken bone is an 
instance of this. Then cartilage is sometimes formed in connec- 
tion with inflammations, though much less frequently. The callus 
formed after fractures in the lower animals has often cartilage in 
it, and it may be so also in man. 
Of considerable importance is the new formation of tissue 
around foreign bodies. If a foreign body be introduced among 
the living tissues, if not very virulent in its own nature, it sets 
up a mild chronic inflammation, with the result of producing a 
vascular, rudimentary, tissue-like granulation. If the foreign body 
he permeable by this tissue, then the granulations will grow into it 
and, as it were, devour it, replacing it first by their own rudi- 
mentary tissue, which afterwards gives place to connective tissue. 
As this connective tissue is comparatively small in bulk, and tends 
to contract more and more, the result of the whole process is an 
absorption of the foreign substance and the gradual disappearance 
of all trace both of it and of the tissue which has replaced it. 
But if the foreign body is not permeable, then the inflammation 
results in the production of a layer of connective tissue around it, 
and so the body becomes encapsuled. 
Many instances of this might be given. If a piece of dead animal 
tissue be introduced into the body, as, for instance, a piece of liver 
previously hardened in chromic acid solution, or a piece of prepared 
catgut used to ligature a vessel, then the dead tissue is tirst replaced 
by rudimentary tissue which gradually shrinks away. If a piece 
of the tissue of the body dies, and if severe inflammation is kept 
off, then its replacement by rudimentary tissue and absorption 
occur. In fractures of bones it often happens that a piece is en- 
tirely separated and dies. Such a piece of bone may lie exposed 
in the wound in a compound fracture, and it has frequently been 
seen how it has been eaten into by the granulations and absorbed 
by them. 
This tendency has been recently taken advantage of in a very 
ingenious manner by Hamilton, of Aberdeen, in the treatment of 
wounds. He finds that a a piece of sponge decalcified and placed 
on a granulating wound, becomes filled with granulations and 
replaced by them. By this means it is possible to encourage the 
growth of granulations and get them to fill spaces, etc. This pro- 
cess has been named sponge-grafting. 
The encapsuling of foreign bodies is frequentty seen. A parasite 
such as the trichina or echinococcus obtains a connective-tissue 
capsule. Dead material in the body which is not permeable by 
the granulations is similarly treated, such as dried-in inflammatory 
products, which have formed first a caseous and then a calcareous 
mass. We frequently find such calcareous material surrounded 
by a fibrous capsule in the lungs and elsewhere. 103 
INDIVIDUAL FORMS OF INFLAMMATION. 
IV.—INDIVIDUAL FORMS OF INFLAMMATION. 
We have already seen that all the phenomena of inflammation 
which we have been studying are not always present in the same 
case, and that they exist in varying proportions in different cases. 
The variations in this regard have been already to some extent 
indicated, but it may be well briefly to refer to some of them here. 
In almost all cases of inflammation hypersemia occurs, even in 
the more chronic. Some slight inflammations of an acute char- 
acter show little beyond hyperemia. The redness of the skin 
produced by exposure to the sun in a single day in summer is an 
instance of this. Doubtless there is along with the hyperremia 
increased transudation through the vessels, and the subsequent 
desquamation of the epidermis shows that it has been damaged, 
and, in fact, partly killed. It is similar with the cutaneous rashes 
in scarlet fever and measles. 
There is probably more or less exudation in all inflammations. 
The fluid constituents of the blood permeate the tissues and we 
frequently find them cedematous, and leucocytes are to be found in 
the tissues frequently in great abundance. In the examination of 
the tissues after death the presence of round cells is the most 
unequivocal sign of inflammation. These cells are found perme- 
ating the tissues generally in acute inflammations, but they are 
usually more localized in the chronic forms, and in that case they 
are associated with the new formation of tissue. In very acute 
inflammations they may be produced in such abundance as to 
break up the tissue and come together to form an abscess. In the 
formation of an abscess there is nearly always some destruction of 
tissue, not necessarily the death of considerable pieces of tissue so 
as to form sloughs, but the molecular disintegration of the tissue 
which breaks down before the crowding leucocytes. These two 
circumstances, namely, the great exudation of leucocytes and the 
necrosis of the tissue, imply that the irritant is a very severe one. 
In a large proportion of cases the irritant is of a septic nature, and 
we know that abscesses most frequently form in connection with 
septic wounds, etc. It may be said then, that where we find 
leucocytes in abnormal numbers in a part we conclude that in- 
flammation has been present, and if they be in very extraordinary 
numbers, we infer that the inflammation has been very acute. 
There are some cases which warrant the application of the term 
infective inflammation. This term infective is to be carefully 
distinguished from infectious, which involves the idea of a disease 
communicable from one person to another. By infective is meant 
a morbid condition which has a tendency to spread from its original 
seat to parts around or at a distance. An inflammation is infective 
when it is what is called “ spreading,” and it is to be inferred that 
in these cases the products of inflammation contain some irritating 
or phlogogenic material. The products of ordinary inflammations 
are not infective, and inflammations are not naturally “ spreading.” 104 
inflammation. 
When an inflammation has the infective characters there are always 
bacteria present in its products, and we may presume that these 
are related to this peculiarity. 
The term phlegmonous inflammation is used to designate an 
acute inflammation of the connective tissue of the hody, usually 
that beneath the skin. The inflammation is nearly always due to 
some specific infective material, as in erysipelas. There is rapid 
development of redness and oedematous swelling of the tissue, 
generally going on to suppuration, and frequently with some 
necrosis, evidenced by the formation of sloughs. 
Sometimes an inflammation of a surface is associated with pro- 
gressive destruction of tissue called ulceration. This means that 
the vitality of the tissue is being gradually destroyed and the 
structure breaking down, the process being well expressed by the 
designation molecular necrosis. Now, in order to this the presence 
of some very virulent irritant is necessary. Probably it does not 
occur except under the action of very specific forms of irritation, 
such as we shall have an opportunity of studying afterwards. 
Sometimes the ulceration progresses very rapidly, so that consider- 
able sloughing may combine with the molecular necrosis. IJlcers 
of this kind are sometimes called phagedenic. The irritation may 
be so intense and the necrosis so rapid that there is no time for 
much exudation of leucocytes. As a rule, however, profuse sup- 
puration exists along with ulceration, the intense irritation inducing 
a very abundant emigration of leucocytes. 
Again, an acute inflammation sometimes produces degeneration 
of tissues in a more pronounced manner than usual. This applies 
especially to cases in which the parenchyma of organs is engaged, 
as in inflammations of the kidney where the renal epithelium is 
specially involved. We have already seen that the inflammation 
produces cloudy swelling in this case, and this readily goes on to 
fatty degeneration. Fatty degeneration is also manifested in 
inflammations of the brain, where it is sometimes almost the only 
evidence post mortem of the existence of inflammation. 
We have already adduced a sufficient number of instances of 
new formation in inflammation. It is to be remembered that all 
such new formations have a striking tendency to contract and form 
a very dense connective tissue. When chronic inflammation exists 
in a organ such as the liver or kidney, this contraction frequently 
gives rise to considerable contortion of the normal tissue, which is 
often the seat of degeneration. This tissue, by the presence of the 
new-formed connective tissue, is pressed on, and, after degenera- 
tion, is absorbed. In this connection, we may speak of indura- 
tive inflammation, the strictures being rendered hard by the 
dense contracting connective tissue. RETROGRADE METAMORPHOSIS. 
Under this designation are included a number of conditions, all 
of which imply a degradation of the nutritive processes in the 
tissues. As the cells are concerned in the nutrition of the tissues, 
it is for the most part these which are at fault, although it may be 
that in some cases the most manifest visible changes are not in 
them. The most extreme case is, of course, where the nutrition 
ceases altogether, and the structure dies. Short of that, we have 
various forms of change manifesting themselves. Thus there is a 
simple diminution of the vitality, and the structures dwindle. 
Again, the chemical constituents of the structures change, split- 
ting up, it may be, into more elementary principles. Or the tissues 
are unable to prevent the deposition in them of extraneous ma- 
terial, which is thus infiltrated into them. These last are called 
infiltrations, whereas the conditions in which there is a degrada- 
tion of the normal constituents into lower chemical substances are 
designated degenerations. 
NECROSIS: GANGRENE. 
Under the designation necrosis are included conditions in which 
the vitalit}' of portions of the tissues entirely ceases; there is a 
local death. We have here to consider the conditions under which 
necrosis occurs, the appearances of and changes in the dead por- 
tions of tissue, and the effects on neighboring parts and on the 
organism as a whole. 
Causes of Necrosis.—The vitality of a part will be lost (1) if 
it be deprived of its supply of nutriment by interference with the 
circulation, or (2) if by some deleterious agent, or otherwise, the 
constituent elements, the cells, are so interfered with that they 
cannot carry on the vital processes. It is obvious that under vary- 
ing circumstances the tissues will have different powers of resist- 
ance, and that the tissues differ among themselves in this respect. 
The tissues of an old person will be less able to survive the attacks 
of certain agents than those of a young person, and any preceding 
degradation of a tissue, from whatever cause, will render it more 
susceptible to necrosis. 
Interference with the circulation causes necrosis, and here 
it is the capillary circulation we have to do with. If a tissue 
be of normal vigor, there must be complete stasis in the capillaries 
before necrosis occurs; any survival of the circulation in these 106 
EETROGRADE METAMORPHOSIS. 
vessels, however small, is sufficient to enable the capillaries and 
surrounding tissues to live on. We have already seen that ob- 
struction of an end-aktery, by embolism or otherwise, leads to 
this stasis in the capillaries and resulting necrosis of the tissues. 
A complete obstruction of the veins will have the same effect, but 
they anastomose so completely that this can occur but rarely. It 
does occur approximately when a piece of intestine is incarcerated 
in a sac with a narrow neck, and we know that under these cir- 
cumstances gangrene is very liable to occur. Even extensive 
thrombosis, especially when other conditions, such as weakness of 
the heart, conspire, may lead to gangrene, as in fevers. 
The obstruction of the capillaries may be directly produced. 
If a cavity approaches the surface of a lung, it may undermine 
the pleura, and, by obstructing the capillaries, cause a slough to 
form. Very often adhesion of the two layers of the pleura occurs, 
and vessels pass from the parietal to the pulmonary layer and 
nourish it; but where such adhesion does not take place, there is 
frequently sloughing, and pneumothorax may result from the 
partial separation of the slough. Similarly, an ulcer of the in- 
testine may undermine the peritoneal coat, and so cause sloughing 
and perforation. 
Less directly, weakness of the heart may so far interfere with 
the circulation in the capillaries, especially of distant and depen- 
dent parts, as to contribute to necrosis. It is obvious that this 
cause alone can never produce necrosis, but we shall see after- 
wards that this is a powerful predisposing cause. 
Turning next to cases where the necrosis is due to a direct 
action on the tissues, it may be said that the vitality of the cells 
of a tissue may be compromised by chemical agents acting on 
them, by direct traumatic agents, or by excessively high or low 
temperature. The chemical products of putrid decomposition 
are often peculiarly virulent. We have already seen that they 
frequently cause the most intense inflammation, and the inflamma- 
tion is commonly accompanied by necrosis. In fact, the infective 
inflammations, such as those of pysemia, are, for the most part, 
necrotic. When, in pyaemia, ulcerative endocarditis, etc., bacteria 
exist alive in the body, and form colonies in places to which they 
are carried, they produce necrosis of the immediately surrounding 
tissues, not probably bv their direct action, but by that of their 
products. We know also that decomposing urine in the tissues 
produces the most intense inflammation, generally along with ex- 
tensive sloughing. It is obvious that direct traumatic injuries 
may destroy the vitality of the tissues, either directly or else by in- 
terfering with the supply of blood. In cases of traumatic necrosis 
it is probable that, besides killing the tissues, the agent will so far 
interfere with surrounding parts as to induce inflammation. In 
fact, it can hardly fail to be seen that there is commonly a close con- 
nection between the causes of necrosis and those of inflammation. 
Excessive heat or cold is a cause of necrosis, the vitality of the 
cells being destroyed by excessively low or high temperatures. A necrosis: gangrene. 
107 
very short immersion of a living part in water heated to 130° to 
136° F., or in a freezing mixture reduced to 4° to 0° F., suffices to 
kill it. If the temperature be slightly less extreme, a short 
immersion produces a violent inflammation, and a long immersion 
may still result in necrosis. 
There are certain forms of necrosis still to be considered that 
depend on causes which cannot be absolutely brought under one 
or other of the categories already mentioned. One of the most 
interesting of these is senile gangrene. It is known that in 
certain cases a slight injury to the toe, such as cutting the nail too 
deeply or tearing oft' of a rag-nail, may lead to a necrosis which 
spreads from the seat of origin to the foot, or even to the lower 
part of the leg. Such a trivial injury in a healthy person would 
lead at most to a trifling inflammation, hut in these old persons 
gangrene is the result. The explanation is that, to begin with, the 
circulation is so seriously interfered with that the tissues are 
already, as it were, half dead, and a very slight cause suffices to 
suspend their vitality altogether. In addition to weakness of the 
heart, there is in these cases always atheroma of the arteries, and 
sometimes even thrombosis on the atheromatous patches. To this 
must be added the weakness of the tissues which may be presumed 
to exist in old age. 
Of somewhat similar significance is the softening of the brain 
which often occurs in old people from simple atheroma of the 
arteries, even without thrombosis. In a healthy person complete 
obstruction of an artery is necessary in order to softening of the 
brain-substance, but in old persons the mere lessening of the cali- 
bre of an artery by an atheromatous patch is often sufficient to 
cause softening. These softenings are very often on the surface of 
the brain, and lead as much to weakness of mind, etc., as to motor 
paralysis, whereas the softenings from embolism are much more 
frequently central, and lead to more definite loss of motion. 
In former days there used to be epidemics of what is now 
recognized as ergotism from eating bread made of grain mixed 
with ergot of rye. In these epidemics the symptoms frequently 
culminated in gangrene, usually beginning in the toes, but extend- 
ing thence, and sometimes attacking the ears, nose, etc. The 
gangrene is usually accounted for by the amemia due to the spas- 
modic contraction of the arteries from the action of the ergot. 
This explanation has been doubted, and the anaesthesia which is a 
concurrent symptom has been adduced as the cause. Possibly the 
interference with the circulation, the directly poisonous action of 
the agent, and the exposure to injury to which a part devoid of 
sensation is liable, may all have to do with the occurrence of gan- 
grene. 
In hospital gangrene there is a progressive necrosis of the 
tissue, beginning usually in a granulating wound, and resulting 
either in considerable sloughing or molecular necrosis. The gan- 
grene travels mostly along the connective tissue, and so may 
undermine the skin, or isolate muscles or bloodvessels. The dis- 108 
retrograde metamorphosis. 
ease is due to a specific virus, which spreads in the spaces of the 
loose connective tissue. 
Changes in the dead tissue.—‘When a tissue dies in the living 
body there is, at first, no obvious change in its anatomical charac- 
ters by which it could be distinguished after death from that which 
has survived. But the dead tissue is liable to undergo changes, 
chiefly chemical, by which its structure is altered, and it becomes 
obviously different from the remaining tissue. The different 
forms of necrosis, indeed, have been divided according to the 
character of the changes assumed by the dead tissue. It will 
he understood that, in the case of external parts, ordinary putre- 
factive decomposition will often occur and dominate all other 
changes, so that it is chiefly in internal parts that we find those 
which occur independently of decomposition. 
1. Coagulation-necrosis is a term which has recently come into 
use to designate a condition described very fully by Weigert (Vir- 
chow’s Archiv, vol. 79). The process is to be compared with the 
coagulation of the blood, the coagulated tissue being equivalent to 
the fibrine. In fact, the formation of a thrombus is a kind of co- 
agulation-necrosis implying the death of leucocytes, and the forma- 
tion of a dead structure, the fibrine. 
We have already seen that the coagulation of the blood is related 
to the death of white blood-corpuscles. In dying, these cells set 
free the paraglobulin, which is one of the principles that go to 
form fibrine. Now the active cells of the tissues generally con- 
tain paraglobulin, and if the fibrinogenetic substance be present, 
as it is present in the lymphatic fluid which bathes the tissues, 
then coagulation may take place if the cells die and yield their 
paraglobulin and ferment. In order to this coagulation the tissue 
must be a very cellular one, and an abundant supply of fluid con- 
taining the fibrinogenetic substance must be present. 
We meet with this change, chiefly in cases where death has 
occurred suddenly, in a limited piece of tissue, while the parts 
around remain vigorous. It is seen very typically in many cases 
as a result of embolism; the embolic infarction owes its dense 
character largely to the coagulation of the tissue. Sometimes this 
occurs without much hemorrhage, and, in the kidney for instance, 
we often find a pale, wedge-shaped infarction of almost cheesy 
consistence. But even when there is hemorrhage the tissue is 
commonly coagulated as well. 
Another example is sometimes afforded by muscle which under- 
goes a change to which the name colloid degeneration is some- 
times given, but which is perhaps better called waxy or hyaline 
degeneration. In typhoid fever, and, to a less extent, in acute 
tuberculosis, scarlet fever, smallpox, etc., this peculiar change is 
frequently observed in the muscles, chiefly the adductors of the 
arms, the rectus abdominis, diaphragm, etc. To the naked eye a 
portion of the muscle is seen to be pale and glassy-like, resembling 
the flesh of uncooked fish. This occurs in patches, and where COAGULATION-NECROSIS. 
109 
thus affected, the muscle appears to be more brittle, hemorrhages 
sometimes occurring in the patches. Under the microscope, the 
primary change is seen to be a disappearance of the transverse 
strife, and a greatly increased transparency of the muscular fibre. 
Fibres affected in this way may be seen close beside unaffected 
ones. The affected fibre is obviously unduly brittle, having a 
tendency to break transversely, and to crumble (see Fig. 28). By 
Fig. 28. 
Coagulation-necrosis or hyaline degeneration of muscle. X 75. 
this process it often happens that an oval piece of degenerated fibre 
gets isolated, the two tapering ends being irregularly crumbled 
(see Fig. 29) while the sarcolemma collapses on the ends of the 
oval piece. A similar glassy transformation occurs in the un- 
striated muscle in the acute diseases mentioned. 
Fig. 29. 
A coagulated clump of muscle more highly magnified. The sarcolemma surrounds it, 
drawing together at the ends. X 350. 
A somewhat similar condition is occasionally seen in paralyzed 
muscles, where it may exist side by side with ordinary atrophy and 
fatty infiltration. It has also been produced artificially in living 
animals by freezing the jnuscles. 110 
RETROGRADE METAMORPHOSIS. 
The process here is a coagulation of the contractile substance. 
This coagulation may even be brought about in the muscles after 
death if they be injured before the occurrence of the cadaveric 
rigidity, which may be regarded as the expression of the normal 
post-mortem coagulation of the sarcocele. In the case of typhoid 
fever it may be supposed that there is a premature death of in- 
dividual muscular fibres, induced by the phenomena of the disease, 
and, perhaps, assisted by traumatic causes. 
Another example of coagulation-necrosis is afforded by diph- 
theria. In this disease the exudation which appears on the fauces 
is, indeed, in part a true fibrinous exudation, but it is also in part 
composed of the coagulated superficial portions of the mucous 
membrane. 
The tube-casts of the kidney are also, to some extent, the result 
of coagulation of the epithelium of the uriniferous tubules, the 
Fig. 30. 
Formation of a pytemic abscess in the kidney. Section stained with aniline brown. The 
necrosed portion, a, shows no structure and is not stained. The surrounding inflamed area 
(6, b, b) is deeply stained. 
death of the epithelium occurring in connection with inflamma- 
tion of the organ. 
In all cases of coagulation-necrosis the tissue becomes more firm 
and solid. Sometimes the coagulum assumes a fibrillated character, DESICCATION and mummification. 
111 
but perhaps more frequently it is homogeneous, the structure of 
which the tissue is composed being obscured. 
It is characteristic of the process that the nuclei of the cells 
become obscured and are no longer brought into view by staining 
the tissue. Referring back to the formation of the white thrombus 
(p. 40) it will be remembered that the disappearance of the nucleus 
is there a characteristic occurrence, and in coagulation-necrosis it 
may be regarded as of similar significance, implying the death of 
the cell. This peculiarity may be used to distinguish the exist- 
ence of this process. If we stain a section of a tissue, as in the 
accompanying figure (Fig. 30), and find that a piece shows no 
nuclei, w’e may infer that necrosis has occurred. 
2. Caseous necrosis is a condition in many respects analogous 
to coagulation-necrosis. We have seen that the latter is an acute 
process, but caseous necrosis mostly occurs when the loss of vitality 
is brought about more gradually. It is met with mostly in tuber- 
culosis and syphilis, and in both of these we have a specific virus 
acting on the tissues. It may be a question how far the death of 
the tissue is due to the action of the virus or to the obstruction of 
the circulation. This form of necrosis also occurs occasionally in 
tumors and inflammatory products. 
The structures involved are cells, and so wTe have material for 
the resulting coagulum. But before the actual necrosis fatty de- 
generation occurs in the cells, so that the coagulum is furnished 
with tine fat-granules which give a very opaque appearance to it. 
To the naked eye the density of the tissue with its opaque appear- 
ance is suggestive of cheese, and hence the name. Under the 
microscope, the necrosed tissue presents the same obscuration 
of the nucleus as wTe find in coagulation-necrosis, but in addition 
all details of structure are completely obscured by the general 
opaque granular appearance presented by the caseous material. 
In fact, this general granular opacity frequently renders the orig- 
inal constitution of a structure exceedingly obscure. 
3. Desiccation and mummification is a simpler process than 
those we have been considering. The part dies, and instead of 
coagulating, it simply dries in and shrivels. An example of this 
on the large scale is afforded by some cases of extra-uterine preg- 
nancy, where the mother survives the death of the foetus. The 
latter may remain for years in the abdomen, simply drying up. 
Virchow found muscle, connective tissue, and vessels still quite 
recognizable after twenty years. In twin pregnancy, also, one of 
the foetuses may die at an early period, and be born as a flattened, 
shrivelled object with that which reached the full time. It will 
be obvious that cases of caseous metamorphosis and coagulation- 
necrosis may be brought under this heading, the resulting material 
having often a tendency to dry and contract. Calcareous infiltra- 
tion frequently overtakes such structures finally if they are not 
absorbed by the processes to be presently considered. 112 
RETROGRADE METAMORPHOSIS. 
But under certain circumstances an external part also undergoes 
desiccation, and the condition is called dry gangrene or mummi- 
fication. In some cases the drying-in will be facilitated by the 
part being at the time of death deficient in moisture, as where the 
gangrene has resulted from embolism or in senile gangrene. It 
will not probably occur if there has been much coincident inflam- 
mation. The part undergoes a gradual deepening of color; at 
first merely livid, it passes on into purple, deep blue, and even 
black. This is due to the blood-coloring matter being dissolved 
out and staining the tissues, which deepen in color as the pigment 
becomes concentrated by drying. The cuticle by and by gets 
raised by red fluid accumulating beneath it, and when it has 
separated evaporation goes on more rapidly, and the piece of 
tissue withers, shrinks, and is converted into a hard black mass, 
often with a mouldy smell. In the case of dry gangrene, the 
deficiency of fluid prevents the agents of decomposition obtaining 
a proper nidus. 
4. Softening or colliquefaction is seen typically in those ne- 
croses of the brain-substance which are so frequent in connection 
with embolism. The breaking down of the brain-substance is 
accompanied by fatty degeneration, so that a kind of fatty emul- 
sion is formed. 
When external parts die they very often undergo softening 
with decomposition. This occurs chiefly in cases where there has 
been considerable inflammation, so that the parts are saturated 
with fluid. An ordinary slough in an external wound is an in- 
stance of this. When a considerable portion of a limb is killed 
and separated by sloughing, then we speak of it as moist gan- 
grene. The appearances are well seen where a portion of a leg 
has died in consequence of a traumatic cause. The parts which 
were at first hot, red, and painful, become mottled with brown,' 
blue, and black, and may even present blisters. They become 
cold and darker, except at the margin where a dusky-red line of 
demarcating inflammation appears. The tissues get universally 
stained with blood-coloring matter, the cuticle gives way, and 
decomposition advances and causes breaking down of the tissues, 
which are separated as sloughs in all stages of softening, and 
exhaling a strong odor. The fluid which permeates the tissues 
contains fat, phosphates, and other salts, as well as extractives 
from the tissues. 
We have now to trace the further course of events in necrosis. 
In many cases the necrosis limits itself almost at once; the 
agent has been at work once for all, and has killed a certain por- 
tion of tissue, and it only remains, by processes which w7e shall 
now describe, to get rid of the dead piece. In other cases the 
agent acts also on surrounding parts, though, being less severe, it 
only produces inflammation, while necrosis may occur at a subse- 
quent period. This will happen the more readily if decomposition simple atrophy. 
113 
occurs in the gangrenous part. The juices of decomposition ex- 
tending to the inflamed parts may cause a further serious extension 
of the necrosis. Thus in traumatic gangrene it may be long before 
a proper line of demarcation forms, and the necrosis becomes 
definite. The importance in such cases of preventing decomposi- 
tion in the dead part will be obvious. But, again, in predisposed 
tissues, which are less able to resist than normal ones, as in old 
persons, or in persons the subject of diabetes, the gangrene may 
extend without there being any considerable inflammation or de- 
composition. 
The final disposal of the dead tissue.—In this, inflammation 
plays a most important part. We have seen that violent inflam- 
mation is often produced by the same cause as the necrosis, or 
may supervene on it. This will mostly be the case in external 
parts where decomposition often comes in to increase the inflam- 
mation. The inflammation is accompanied by exudation and 
hypereemia, like other inflammations, and commonly goes on to 
suppuration. A layer of pus comes thus to divide the dead tissue 
from the living, and the dead is cast off as a slough. There re- 
mains a suppurating wound or ulcer. This loss of tissue, whether 
molecular or as a massive slough, is the essential feature of an 
ulcer of whatever kind, and a suppurating surface will usually 
be left. 
In internal parts, if the necrosis be accompanied or followed by 
the production of irritating chemical substances, then a violent 
inflammation will be produced around. It is so in the case of 
pyiemia, where there is septic embolism. In this case the inflam- 
mation will usually be violent enough to produce suppuration, 
and the result will be the formation of an abscess. (See Fig. 30.) 
In the case of internal parts where there is no disturbing de- 
composition, or even in external parts which are protected from 
septic contamination, the inflammation is of a much milder char- 
acter. The necrosed portion now comes to act as a foreign body 
or dead piece of tissue, and is subject to the changes already 
described at p. 102. The dead tissue is often eaten into and 
replaced by vascular granulations, which finally contract and 
leave a small residue of connective tissue; or the dead piece is 
encapsuled and may lie quiescent. Not infrequently the encap- 
sulecl tissue undergoes infiltration with lime-salts, as we shall see 
afterwards. In the case of necrosis in bone the external capsule is 
frequently composed of new-formed bone. 
SIMPLE ATROPHY. 
There comes lip here for consideration, to begin with, what may 
he called physiological atrophy. At certain periods, for instance, 
the milk teeth drop off, and this is effected by an atrophy of the 
fang so that the crown is shed. At a still earlier period the thymus 114 
retrograde metamorphosis. 
gland atrophies. Then again throughout life there is a continual 
shedding of the hair, and if a cast-off hair from the eyelash, for 
instance, be examined under the microscope, it will be seen that 
its bulb is atrophied, and this is the cause of its being shed. In 
some persons the hair of the scalp is largely shed at a compara- 
tively early age, without being properly reproduced, there being 
here an atrophy of the liair-sheath and papilla. Then there is the 
normal atrophy of the tissues generally, which occurs in old age. 
The atrophy of old people may in many cases be due to some 
organic disease whose symptoms are not manifest; but we are all 
familiar with the healthy old person with shrivelled hands and 
face and plicated skin. 
In all these cases there is a kind of intention in the tissues, so 
to speak, according to which they live a certain period and then 
decay. As Paget has pointed out, such atrophies may almost be 
regarded as active processes. The fall of the leaf is due to an 
active absorption or atrophy of the libres uniting it to the stem; 
if the leaf dies before its time, or is killed, it remains hanging, but 
in the natural course it drops when its time is come. So with our 
tissues and the whole organism, there is a period to their activity. 
The period varies in different persons, and in this regard hereditary 
influences have an important bearing. Just as these largely deter- 
mine the period of growth of the body and its rapidity, so do they 
influence the duration of activity of the tissues. This is plainly 
seen in the case of the hair; baldness runs in families, just as lon- 
gevity does. 
Turning to more strictly pathological atrophies, we may distin- 
guish three forms: 1, those dependent on the supply of nutrition 
being defective; 2, those in which disuse of a structure causes its 
atrophy; and, 3, those in which the atrophy is related to some 
change in the nervous system. 
General emaciation is the most obvious example of the first 
class, occurring, as it does, either directly from interference with 
the supply of food, or from impoverishment of the blood by exces- 
sive waste. The food may be procured in insufficient quantity, 
or a stricture of the oesophagus may interfere with its passage to 
the stomach, or the stomach may reject it after it has been swal- 
lowed. On the other hand, there is frequently, in advanced 
phthisis or ulcerating cancers, a large consumption of the nutri- 
tious material available to the body, and the tissues sutler accord- 
ingly. In these and other cases of general atrophy, the tissues 
dwindle in different proportions, the fat most; next to it the spleen, 
testicles, liver, muscles, bones, and least of all the central nervous 
system. 
As belonging to this class also may be mentioned the atrophies 
of fevers, although perhaps the atrophy here is to some extent 
more of an active process. In fevers there is, with the high tem- 
perature, an increased combustion of the nitrogenous constituents 
of the tissues. If the supply of nutritious material were abundant, SIMPLE atrophy. 
115 
then this would not necessarily lead to atrophy, but the febrile 
patient eats little or nothing, and, besides, the constitution of the 
blood is altered, and so the structures atrophy, sometimes with 
great rapidity. 
To the same class belong local atrophies from local interference 
with the blood-supply. The overgrowth of connective tissue in 
interstitial inflammations of parenchymatous organs causes atrophy 
of the secreting structure of these organs, as in the case of the 
liver, kidney, testicles, etc. Growing tumors or aneurisms cause 
atrophy of the tissues around, etc. 
Of the second class, the most obvious are the atrophies of muscles 
from disuse. Paralysis or anchylosis of a limb results in its emaci- 
ation. In conjunction with the atrophy of the muscle, there is often 
an overgrowth of the adipose tissue between the muscular fibres. 
The retrograde changes which occur in the uterus after delivery 
may possibly be regarded as another example. 
As to the atrophies depending on nervous lesions, these are 
somewhat obscure in their essential pathology. It is true that 
after motor paralyses of all sorts, atrophy of the muscle occurs, 
after hemiplegia, for example; but the atrophy in this case may 
be from disuse of the muscle, just like atrophy after anchylosis of 
a joint. There are, however, some atrophies following nervous 
lesions which are rapid in their development, and appear to be due 
not directly to the paralysis, but rather to an interference with the 
nerve-centres concerned in the nutritive processes. It has been 
abundantly shown by experiments in animals that when a nerve- 
stem containing motor fibres is divided, there is a coagulation, dis- 
integration, and subsequent absorption of the medullary sheaths of 
the nerve-fibres in the stem. Erb states that the axis-cylinder per- 
sists, while others assert that it too atrophies. In any case, the 
muscles supplied by the nerves also atrophy. Even in the first 
week there is considerable wasting, and after a month the muscle 
has scarcely half its former thickness. This is a simple atrophy, 
the muscular fibres getting thinner, and presenting the nuclear 
change to be referred to afterwards. The atrophy which occurs 
in a common hemiplegia is not nearly so rapid as this, and is often 
scarcely perceptible after a month. In comparing the lesions in 
the nervous system in these two cases, the difference will at once 
appear; in the one the interruption to the motor fibres is high up 
above the spinal cord, while in the other it is low down, after the 
fibres have left the cord. 
But there are some forms of paralysis in which atrophy is a 
peculiarly pronounced feature. Infantile paralysis is one example; 
progressive muscular atrophy is another; and glosso-pharyngeal or 
bulbar paralysis a third. In these the atrophy is even more strik- 
ing than the paralysis, and in other forms of paralysis there is often 
a greater loss of function with much less atrophy. These forms 
of atrophy have been classed as tropho-neuroses, as it is evident 
that besides the mere paralysis there is some lesion of the structures 
which command the nutrition of the muscles. These structures 116 
RETROGRADE METAMORPHOSIS. 
are, presumably, trophic nervous centres situated in the spinal 
cord, and, as we shall see afterwards in connection with diseases of 
the nervous system, it is to he inferred that these trophic centres 
are near the motor centres, or are identical with them. Now the 
motor centres of the cord are in the anterior gray cornua, and the 
trophic centres are presumably there also, taking part in the de- 
struction which affects the cornua in this class of diseases. In 
infantile paralysis, for instance, there is an acute inflammation, 
with destruction of centres in the anterior cornua. 
Another case of a supposed tropho-neurosis is the atrophy with 
paralysis which occurs in lead-poisoning. Here the paralysis and 
atrophy affect the extensors of the arm, and the localization of 
these to a group of muscles has led to the view that here also the 
ganglion-cells of the anterior cornua are involved. This localiza- 
tion has not been made out, and there is no apparent reason why 
the lead should specifically attack this particular group of ganglion- 
cells. Still we know that poisons have frequently special afflnities, 
and the possibility is not to be excluded. 
In all these forms of muscular atrophy certain changes occur in 
the muscles. There is an increase in the nuclei of the muscular 
fibres, and sometimes an increase of the connective tissue, a con- 
dition which some have regarded as an interstitial inflammation. 
Sometimes also a great development of fat occurs in the connective 
tissue of the muscles. These changes are secondary; they are 
found in the muscles after division of nerves, and are therefore 
not to be regarded as the cause of the atrophy and paralysis. The 
muscular fibre itself becomes smaller, and is occasionally the seat 
of fatty degeneration. As the disease proceeds, the muscular fibre 
may altogether disappear. 
Among the troplio-neuroses is also commonly included that 
peculiar atrophy of half the face, of which a few cases have been 
published. This atrophy affects all the structures, bones, muscle, 
skin, etc., but is not accompanied by paralysis. It does not follow 
strictly the distribution of any nerve, although closely approxi- 
mating to that of the fifth. The pathology is obscure, but it is 
usually regarded as due to an affection of the trophic centres 
wherever they are. 
This is a term having a meaning equivalent to Cloudy Swelling 
as used by Virchow, and to Parenchymatous Degeneration. The 
condition has been incidentally referred to in considering inflam- 
mation. Its essential nature may be expressed by stating that in 
it cells increase in bulk, while the added material is not properly 
assimilated and so deposits in the cells in visible albuminous 
granules. The enlarged cells are therefore clouded (see Fig. 31), 
and the nuclei obscured. The condition implies a qualitative 
defect in the nutrition of the cells, while quantitatively there is 
ALBUMINOUS INFILTRATION. ALBUMINOUS INFILTRATION. 
117 
increase. The qualitative defect is very often still further mani- 
fested by the occurrence of fatty degeneration (as in the figure) 
along with the cloudy swelling, and these two conditions, in fact, 
frequently run into each other. 
Fig. 31. 
Cloudy swelling of renal epithelium with slight fatty degeneration. A portion of a tubule 
is shown, and some isolated cells. From a case of acute phthisis pulmonalis. X 350. 
The condition is brought about by causes which irritate cells 
and at the same time increase their supply of nutritious fluid. One 
of these is inflammation, and cloudy swelling is the most pro- 
nounced change in the earlier stages of the parenchymatous 
inflammations of organs, especially of the kidneys. Besides by 
inflammation, it is produced by nearly all febrile diseases, and 
seems to bear some relation to the elevation of temperature. It is 
met with in the acute specific fevers, in pneumonia, erysipelas, 
pyaemia, acute phthisis pulmonalis with high temperatures, etc. 
It is as if the blood, altered by the elevation of temperature and 
otherwise, acts as an irritant, producing a kind of sub-inflamma- 
tory condition. As the blood is carried throughout the body the 
parenchymatous change is not limited to any single organ, but is 
found in the liver, kidneys, muscular fibre of the heart, voluntary 
muscle, and elsewhere. 
The name cloudy swelling implies that the affected cells are 
enlarged. It is to be observed also that the cells concerned here 
are the proper cells of organs, that is to say, the structures which 
are concerned in their functions and make up the greater part of 
their bulk. Hence it arises that considerable enlargement of the 
organs as a whole may occur from this cause, and this is especially 
seen in the liver, which sometimes shows great increase in size 
and weight in acute fevers. The kidneys are also sometimes con- 
siderably enlarged from this cause. 118 
retrograde metamorphosis. 
FATTY DEGENERATION. 
In this condition, which affects the cells of tissues, we have a 
change in the chemical composition of the cell-contents; the albu- 
minous constituents split up and yield fat. Before going further 
it may he well to remember that fat exists in the tissues in two 
conditions; in the first place as free fat, and in the second place in 
such close chemical union with the albuminous constituents that it 
no longer responds to the ordinary reactions of fat. For instance, 
besides free fat in muscular fibre there is much combined fat, and 
in order to detect the latter, by extraction with ether for example, 
it is necessary in the first place to decompose the albuminous com- 
binations. When these combinations are decomposed the fat can 
be seen in the muscle as minute drops, and it can be extracted 
with ether. It may be well, in the first place, to take one or two 
typical examples of fatty degeneration, and endeavor to gather 
from them some conception of its pathology. 
The well-known experiments of Bauer on the effects of poisoning 
dogs with phosphorus afford an excellent example to begin with. 
This author deprived a dog of food for a period of twelve days, till 
it had consumed all its available store of fat, and the excretion of 
nitrogen in the urine had reached a constant minimum of eight 
grammes in the twenty-four hours. He then gave the animal 
small doses of phosphorus and found that the excretion of nitrogen 
markedly increased on to death, reaching treble its former amount, 
namely, 23.9 grammes. The phosphorus in the blood had in- 
duced a marked consumption of the albuminous tissues, manifested 
in a great increase in the urea excreted. But now when the 
animal was killed, an enormous increase in the free fat in the 
organs was found; the liver and muscles contained about three 
times their normal amount of fat, and other structures such as the 
renal epithelium, and the walls of the bloodvessels, presented 
marked fatty degeneration. Here was an agent circulating in the 
blood, whose effect was the decomposition of the albuminates and 
the formation of fats. 
Again, it has been mentioned above that in anemias there is 
often a marked fatty degeneration of the muscle of the heart, of 
the hepatic cells, and of the renal epithelium. In this case a de- 
terioration of the blood, and especially a defect in the haemoglobin, 
determines the occurrence of fatty degeneration. 
When an artery in the brain is occluded we have already 
seen that necrosis frequently occurs, accompanied by softening; 
but, along with this or preceding it, there is a pronounced fatty 
degeneration affecting the brain-substance and resulting in the 
formation of large cells filled with finely divided fat (the so-called 
compound granular corpuscles). A similar aggregation of fat 
occurs at intervals in the Avails of the capillaries (see Fig. 32). It 
is true that the fat here may be partly derived from the myelin of 
the disintegrated medullary sheath, but it is not probable that the FATTY DEGENERATION. 
119 
fat of the capillary nuclei can have this source. Here is a case in 
which a local deprivation of blood has the effect of inducing a 
fatty degeneration. 
We have also instances of fatty degeneration in inflammations, 
where the vitality of the cells is compromised, and in quickly 
Pig. 32. 
Patty degeneration in the cerebral vessels in softening of the brain. (Paget.) 
growing tumors, where, perhaps, the nutritive processes are sub- 
ordinated to the unduly active formative ones. 
We have now to endeavor to explain the occurrence of fatty 
degeneration in these various circumstances. There are some of 
them which we can account for on the same principles as we 
account for the fatty degeneration in phosphorus-poisoning. In 
acute yellow atrophy of the liver the hepatic cells break up, and 
present the characters of pronounced fatty degeneration; this is, 
presumably, due to the action of some poisonous agent, and it has 
even been supposed that phosphorus is the agent. Then, again, 
we have fatty degeneration frequently associated, as we have seen, 
with cloudy swelling in fevers, etc. In this case the fatty degen- 
eration may be due to the splitting up of the loosely combined 
fatty-albuminous principles. The same applies to some of the 
more local fatty degenerations. The mere degradation of the tissue 
may allow of these decompositions occurring, as when fatty de- 
generation occurs in yellow softening of the brain. 
But there are some cases in which more fat appears in the tissues 
than the mere breaking up of the normal combinations would 
account for. In these cases we must suppose a different mode of 
origin. 
It seems to he a function of most of the active cells in the body 
to form fat, which is oxidized or burnt either in the same place or 
elsewhere. The cells may form fat even from albuminous material. 
The mammary glands secrete milk just as abundantly when the 120 
RETROGRADE METAMORPHOSIS. 
animal feeds on meat free from fat as on a richly fatty diet. Mus- 
cular tissue contains fat loosely combined with the albumen, and 
probably it is continually forming fat, which is continually being 
oxidized. But something may interfere with its oxidation. The 
supply of blood may be insufficient, the quality of the blood may 
be altered, or the vitality of the cells may be so reduced as to ren- 
der the process of oxidation imperfect. It is possible, then, that 
there may be in these cases, not so much an increased decomposi- 
tion of the albumen as a decreased oxidation of the fat, and the 
latter will appear in the tissue as free fat, with all the appearances 
of fatty degeneration. 
We have now to consider the actual anatomical changes 
presented in fatty degeneration and visible under the microscope. 
The degeneration occurs mainly in the cells of the tissues. The 
fat, arising as it does by the chemical decomposition of the proto- 
plasm of the cell, appears in the form of fine drops or granules, 
which are strongly refracting. These granules are still separated 
from each other by the remains of the cell contents and are. there- 
fore isolated. It may happen in this way that, as in Fig. 33, a 
Fig. 33. 
Fig. 34 
Fatty degeneration in an atheromatous 
aorta. The shapes of the cells brought 
out by the fat; a, from internal coat; b, 
muscle-cells from middle coat. X 350. 
Fatty degeneration of cells in a cancer of 
the mamma ; or, slightly affected ; b, more 
so; c, completely fatty—the compound 
granular corpuscle. X 350. 
fatty degeneration occurring in a structure may render its con- 
stituent cells unusually distinct, their form being brought 
prominently out by the fat in them. As time goes on, the fat- 
granules increase till the whole cell is filled with fine refracting oil 
drops, which still remain isolated (see Fig. 34), being each 
surrounded by an albuminous envelope. The process is,"in fact, 
very much like what occurs in the cells of the mammary gland in 
the secretion of milk, the colostrum cells being like the fully 
degenerated cells, which are often described as compound granular 
corpuscles. 
When finely divided fat suspended in fluid is present in the living FATTY DEGENERATIOX. 
121 
tissues, it is very readily absorbed. We know bow readily tlie 
emulsionized fat in the alimentary canal is taken up by the epi- 
thelium, and passed on into the lacteals. When milk is injected 
into the abdominal cavity of a living animal, or even laid on the 
surface of the diaphragm after death, it very quickly passes into 
the lymphatics. In the case of fatty degeneration of cells, if fluid 
be present, the cells disintegrate, an emulsion is formed, and 
absorption occurs just as in the case of milk. 
But sometimes the fatty degeneration occurs in connection with 
structures not adapted to absorption, as in a hydrocele, where the 
tendency is rather to transudation, or in an ovarian tumor. In 
that case, the fat undergoes further changes, resulting usually in 
the production of crystals of cholestearine (Fig. 35). This sub- 
Fig. 35. 
Crystals of cholestearine; a, large ones from an old hydrocele; b, from stagnant bile in 
gall-bladder. X 350. 
stance occurs as a normal constituent of the central nervous tissue 
and bile, in which latter it is dissolved. Its crystals are rhombic 
tables whose angles measure 79° 30' and 100° 70'. On adding 
strong sulphuric acid to a crystal of eholestearine, letting it gradu- 
ally run in and act on it, the crystal appears to melt from the edge 
inwards, and take on a fatty appearance, and by and by it gathers 
into a brown drop. On adding iodine and sulphuric acid to a 
crystal, there is at first a beautiful display of colors. 
The changes mentioned above occur when there is abundant 
fluid in connection with the fatty debris, converting it into an 
emulsion, which either is absorbed or deposits crystals of cho- 
lestearine. But when the fluid is deficient, as when the vessels are 
few and the cells are heaped together closely, in that case the fatty 122 
retrograde metamorphosis. 
degeneration is often associated with necrosis, and there is a shrink- 
ing and drying-in of the structure, resulting in the formation of a 
cheesy-looking material. This process we have already considered 
under the designation caseous necrosis. The cheesy material used 
to be regarded as crude tubercle, and the metamorphosis was 
called tuberculization. We have already seen that although 
caseous necrosis is far more frequent in connection with tubercu- 
losis than any other condition, yet the name must not be monopo- 
lized by this process. 
FATTY INFILTRATION. 
By this term is meant the deposition of fat in the tissues. The 
normal fate of fat is, for the most part, to be burnt, thereby assist- 
ing in the maintenance of the animal temperature. But there 
may be too much fat formed or absorbed for the uses of the 
organism or for the purposes of particular parts, and it is then laid 
down, as it were, in store. 
In some persons digestion is active, and they assimilate more 
carbo-hydrates than their organism can oxidize. Such persons are 
often rather sluggish in their movements, and respiration is not 
very vigorous, and so the oxidation is less than normal. In that 
case the spare fat is deposited in the subcutaneous tissue and great 
omentum mainly. It is infiltrated into the connective-tissue cor- 
puscles, and it is well known that adipose tissue and connective 
tissue are to a certain extent mutually convertible. This general 
deposition is called obesity. 
Then there are local depositions that are more difficult to explain, 
which occur mainly in connection with structures that are in some 
way put out of use. A most typical example of this is afforded 
by muscles which have become fixed at their two ends by stiffen- 
ing of joints. The muscle can no longer produce any movement, 
and its fibres gradually atrophy as we have already seen. At the 
same time, in the connective tissue around the muscle and in that 
which supports it, there is a great infiltration of fat, so that adipose 
tissue appears between and around the fibres (see Fig. 36). Then, 
again, in pseudo-hypertrophic paralysis—a disease chiefly of chil- 
dren—there is a similar process. The muscular tissue atrophies, 
but there is at the same time an excessive transformation of the 
connective tissue into adipose tissue, so that the wasting of the 
muscle is more than counterbalanced by the excess of adipose 
tissue, and there is thus a pseudo-hypertrophy. 
A similar fatty infiltration occurs in the heart. Normally, there 
is a certain amount of adipose tissue beneath the pericardium. 
But sometimes this becomes excessive in quantity and extends into 
the muscular substance, between the muscular fibres, so that the 
wall of the ventricle may be largely composed of adipose tissue. 
If this fatty infiltration were primary, then we could understand 
how, in these cases, there should be great wasting of the proper FATTY INFILTRATION. 
123 
muscular fibre, and there are cases in which the over-loading of 
the heart seems to be part of a general obesity. But, more fre- 
quently, there is reason to believe that the weakening of the heart 
and the atrophy of the muscle are the primary occurrences, and 
the fatty infiltration secondary. 
Tig. 36. 
Fatty infiltration of muscle from a case of stiffening of the,nnkle by an epithelioma of the 
skin over it. The muscular fibres are narrowed, and adipose tissue appears between them. 
X 80. 
It is difficult to account for this local deposition of fat in con- 
nection with muscle. It may be that as normally fat is largely 
oxidized in muscle, or largely produced there in connection with 
the active process of contraction, when the demand is gone it is 
laid down by the vessels in the neighboring connective tissue. 
Fat is often deposited in excessive quantity around diseased and 
useless glands, especially the kidney. In hydronephrosis there is 
often an enormous increase of the fat which normally surrounds 
the kidney. This is also difficult to account for. 
The infiltration of fat into the liver, wffiich we meet with 
very frequently, is also difficult to explain. It is met with, in the 
first place, in persons addicted to the excessive use of alcohol, and 
in that case often goes along with an excess of fat in all the organs, 
probably due to the oxidation of the fat being interfered with by 
the alcohol. The fat, in these cases, is often very fluid, and the 
organs have a greasy appearance and feeling. But, in the second 
place, fat is often found in large quantities in the liver in cases 
where, in the subcutaneous tissue or elsewhere, there is an actual 
deficiency of it. The fat in the liver is in the peripheral parts of 
the lobules, and from this it is to be inferred that it has been 
brought by the portal blood. This fatty infiltration occurs fre- 
quently in phthisis pulmonalis, and in other cachectic diseases. 
Its accumulation under these circumstances may, in part, be ac- 
counted for by supposing that the fat which is normally used for 
the formation of the fatty acids and the cholestearine of the bile 
is not so used and is therefore stored in the hepatic cells. It is 
known that the secretion of bile is greatly diminished in such 124 
RETROGRADE METAMORPHOSIS. 
cases, and that the bile is watery. In that case the fatty infiltra- 
tion here would be like that in muscle, due to diminished activity 
of the organ. Another view, and one having some appearance of 
probability, is based on the theory that one of the functions of the 
liver is to prepare fat for oxidation. Xaumann (Reichert and Du 
Bois Reymond’s Archiv, 1871, p. 41) has shown that the liver fat 
is much more oxidizable than ordinary fat, and that in the verte- 
brata the size of the liver is in inverse proportion to the activity 
of the respiration, being largest in fishes and smallest in birds. It 
is, therefore, suggested that in phthisis and cachectic diseases the 
liver may produce an excess of easily oxidizable fat and store it up 
ready for use. Hence, perhaps, the utility of liver oils in cases of 
phthisis, etc. 
We have seen that in fatty degeneration the fat appears in the 
form of fine granules or drops, and that as these increase they re- 
main isolated. In fatty infiltration there are, of course, first fine 
fat-drops, but as more fat is added the drops grow in size. In the 
case of the conversion of connective tissue into adipose tissue, 
there is a single fat-drop in each cell, as in Fig. 36. In the case of 
fatty liver the fat-drops are of various sizes (see Fig. 37), but, as a 
Fig. 37. 
Fatty infiltration of the liver. Isolated hepatic cells with drops of fat of various sizes. 
X 350. 
rule, much larger than in fatty degeneration. The size is by no 
means an absolute criterion, but it is an important practical indica- 
tion. It is only in the liver that there can be much difficulty in 
distinguishing between fatty degeneration and fatty infiltration, 
and here the fact that in the latter the fat is deposited at first in 
the cells at the peripheral parts of the lobules, and always con- 
tinues more abundant there, is sufficiently distinctive. 
PIGMENTARY INFILTRATION. 
Iii studying hemorrhage we have already seen that a common 
result of the extravasation of blood is the pigmentation of the 
tissues around. This pigmentation may be brought about in 
various ways, and is of various degrees of permanence. In the 
first place, the blood-coloring matter may be dissolved out of PIGMEXTARY I XFILTR AT10X. 
125 
the corpuscles and stain the tissues, this being an evanescent pig- 
mentation. Then the dissolved coloring matter may be deposited 
in the solid form after a time. We may thus have crystals of 
hfematin in the form of oblique rhombic pillars, or simply amor- 
phous granules; the crystals occur mostly in large extravasations. 
Lastly, there is the pigmentation which results from the cells in the 
neighborhood of the hemorrhage taking up the red corpuscles and 
becoming pigmented by these. Probably much of the pigmen- 
tation which occurs as a consequence of chronic inflammation or 
passive hyperamiia is due to this last process, the hemorrhage here 
being by diapedesis. Chronic catarrhs of the stomach and intes- 
tinal canal are often distinguishable after death by the slaty color 
of the mucous membrane. In chronic passive hypersemia of the 
lungs from heart disease there is a brown pigmentation, frequently 
called brown induration. 
The pigmentation occurring in tumors, especially cancers and 
sarcomas, is often regarded as due to minute hemorrhages, 
and there are many facts which appear at least to connect it with 
the bloodvessels. Gussenbauer (Virchow’s Archiv, vol. lxiii. p. 
322) asserts that in melanotic tumors there is a thrombosis in the 
smaller vessels, and that the blood-coloring matter is dissolved out, 
and is taken up by the cells of the tumors. It is to be remarked 
that in pigmented tumors there is not a homogeneous distribution 
of the pigment, but the majority of the cells are unpigmented, and 
there is often an arrangement suggestive of local foci of origin. 
It is to be presumed that in these tumors there is some peculiarity 
of the bloodvessels which allows either of ready extravasation or 
thrombosis. It is to be added, however, that it is denied by some 
that the pigment in tumors is derived from the blood pigment, 
chiefly on the ground that it does not contain iron. 
Pigment is to be found in thrombi, and in the case of veins espe- 
cially it may be deposited in crystals as well as in granules (see p. 44). 
Pigmentation of the lungs may be regarded as a normal con- 
dition, although it is acquired after birth. It is due to inhalation 
of particles of dust which are carried into the lung-substance 
by amoeboid cells, and partly remain in the connective tissue of the 
lung, and partly are carried to the bronchial glands. Where this 
pigmentation is excessive, as in the case of miners, we have a rec- 
ognized morbid state designated Anthracosis. Other forms of 
pigmentation occur in the lungs from the inhalation of variously 
colored stuffs by workers exposed to them. 
Icterus is a yellow staining of the tissues with a coloring matter 
dissolved in the blood serum. This is usually the biliary coloring 
matter absorbed from the bile-ducts after its secretion. It implies 
an obstruction to the ducts in some part of their course. A similar 
staining may be a consequence of the destruction of red corpuscles, 
their coloring matter becoming dissolved in the blood—the so- 
called hrematogenous icterus. 
The bronze coloration or the skin in Addison’s disease is 
related to disease of the supra-renal capsules, in which there is a 126 
retrograde metamorphosis. 
caseous condition, a local tuberculosis. The solar plexus of nerves 
is probably affected along with the capsules, but the exact path- 
ology of the condition is not understood. 
Lastly, a tissue may be unduly deep in color simply from 
atrophy of the other constituents, and a concentration of the nor- 
mal pigment. Thus when emaciation occurs, and the fat is 
absorbed from the subcutaneous tissue, this often assumes an 
unusually dark yellow or brown hue. An emaciated heart 
presents in its muscular substance a very dark color from the 
diminution of the contractile substance and concentration of the 
pigment. 
MUCOUS AND COLLOID DEGENERATION. 
These two conditions present considerable similarity, and in 
individual cases it is often difficult to say which of them is actually 
present They are characterized by the abnormal occurrence in 
the tissues of two chemical principles, which are albuminates, and 
doubtless arise by transformation of the normal tissue-albumen. 
One of these substances is known as a definite chemical principle, 
and is named mucin; the other is not well known in its chemical 
relations, and is somewhat indefinitely named colloid material. 
Both have the peculiarity that in the presence of water they swell 
up and acquire a gelatinous consistence. With very similar 
physical characters, and arising under somewhat similar circum- 
stances, they are distinguished by their difference in chemical 
reaction. Mucin forms a somewhat membranous precipitate with 
acetic acid, and its solutions are also rendered turbid by alcohol 
and chromic acid. Colloid material is not obviously altered by 
these reagents. 
A physiological type of mucous and colloid degeneration is 
afforded by the normal secretion of mucus. Here it is known that 
the epithelial cells, whether of the surface of the mucous membrane 
or in the proper glands, become converted into goblet-cells, by the 
formation of mucus within them. The mucus is secreted by the 
rupture or disintegration of these cells, and the discharge of the 
material which has swelled them up. 
In certain pathological conditions this secretion of mucus is 
exaggerated, notably in the catarrhs of mucous membranes. But 
this can hardly be regarded as a proper mucous degeneration. 
In ovarian tumors a process is often visible which closely 
resembles the secretion of mucus. We shall see afterwards that 
the larger number of ovarian tumors originate in a glandular for- 
mation, and in this gland-tissue most characteristic goblet-cells are 
often to be seen (see Fig. 38), the gelatinous contents of the cysts 
formed being obviously secreted in this way. But then, the gelat- 
inous material does not usually give the reaction of mucin with 
acetic acid, and is clearly an albumen of a different kind, whose 
chemistry is not well known, lienee this would be included under MUCOUS AND COLLOID DEGENERATION. 
127 
colloid degeneration, although in histological details resembling 
the mucous form. 
Again, in the thyroid gland there are often, even normally, 
little gelatinous particles visible on dividing the gland, and in the 
commonest form of goitre (colloid goitre) there is a great increase 
of this clear gelatinous material. On microscopic examination it 
is clear that the gelatinous material arises by transformation of the 
epithelium lining the saccules which form the parenchyma of the 
Fig. 38. 
From internal surface of a colloid ovarian cyst. The lining epithelium is mostly in the 
form of goblet-cells, the superficial parts having clear, transparent contents. X 350. 
gland. The cells swell up and become filled with clear gelatinous 
material; by the discharge of this or the disintegration of the cells 
the colloid contents of the saccules are formed. But this material 
has not the reactions of mucus. 
In colloid cancers there is a similar transformation of the 
epithelium, so that the cellular masses are transformed into colloid 
masses, which fill the spaces in the stroma. This form of cancer 
is most frequent in the stomach and large intestine, and it may be 
thought that this colloid transformation, so closely resembling the 
normal secretion of mucus, is related to it, as the cancer takes 
origin in the mucous membrane. But colloid cancer occurs also 
in the mamma and even occasionally, to a partial extent, in epithe- 
lioma of the skin. 
In all the instances given hitherto, the mucous or colloid degen- 
eration has affected epithelial cells. But a mucous transformation 
sometimes occurs in the intercellular substance of connective 
tissue, including bone, cartilage, adipose tissue. The intercellular 
substance is converted into a gelatinous material, while the cells 
remain unaffected or undergo fatty degeneration. When this 
change occurs the tissue is softened, and this will produce a very 
striking result in the case of bone and cartilage. In these tissues 
it mostly takes place in old people. 128 
RETROGRADE METAMORPHOSIS. 
We shall see afterwards that there is a form of tumor which is 
characterized by the fact that its tissue contains mucin in its inter- 
cellular substance. This is not a case of mucous degeneration, but 
sometimes a portion of a tumor of a different kind will acquire 
these characters, and then we may use this designation. It is 
mostly in fatty tumors and sarcomas that this occurs. 
CALCAREOUS INFILTRATION. 
This is a condition of very frequent occurrence, and therefore 
deserving of very careful attention. By the designation is meant 
the deposition of lime-salts in abnormal fashion in the tissues. 
The lime-salts are for the most part the same as those which nor- 
mally take part in the structure of bone, namely phosphate and 
carbonate of calcium. 
There is a certain proportion of the salts of lime existing nor- 
mally in all the tissues and juices; these all leave an ash on 
burning, and lime-salts form part of this ash.. But the lime-salts 
here are dissolved in the juices, or form combinations with the 
albumen, so that they do not appear on microscopic examination. 
In calcareous infiltration there is a deposition of the lime in the 
form of insoluble carbonate and phosphate, and there is also an 
accumulation of these insoluble salts, so that the ash on burning 
the tissues is greatly increased. There is a precipitation of the 
lime, and as lime-salts in solution are continually being brought 
in along with the fluids of the tissue, they are continually pre- 
cipitated and thereby fixed. 
In considering the circumstances which induce this precipitation, 
we encounter what Virchow lias called metastatic calcification. 
In some cases where there is rapid destruction of bone, as by 
multiple caries, or by cancer or sarcoma advancing on bone, there 
has been found after death calcification of portions of the lung or 
digestive canal, the lime being deposited in the connective tissue 
in such a way as sometimes to make the tissue almost like pumice 
stone. In several of the cases disease of the kidney has coexisted, 
and there may have been therefore some interference with the due 
excretion of the absorbed lime-salts. In any case we may presume 
that the deposit is related to excess of lime-salts in the blood and 
fluids. There must, however, have been some cause determining 
the locality of the deposition, in the lung in some cases, in the in- 
testinal walls in others, but this is quite obscure. 
Turning to other cases of calcareous infiltration, we find that 
wherever there is a structure which has lost its vitality and yet is 
left as a kind of dead and foreign body in the midst of the tissues, 
there is apt to be deposition of lime in and around such structure. 
It may be said that obsolete or obsolescent structures are liable to 
be impregnated with lime. It has already been stated that lime is 
present in all the fluids and tissues of the body, and in the fluids 
it is probably kept in solution by the presence of an excess of car- CALCAREOUS INFILTRATION. 
129 
bonic acid. In the case of a structure which is obsolete the fluids 
will stagnate, will lie about in it, and it is not remarkable that 
their lime, which is so readily precipitated from solutions, should 
deposit. As the fluid is renewed, more and more lime is de- 
posited, and the structure may finally be converted into a stony 
mass. 
The lime-salts are deposited in the first instance in the form of 
fine globular granules, either in the protoplasm of cells or in the 
inter-cellular substance. The structure is as if dusted with re- 
fracting granules, and the appearances in many respects resemble 
those of fatty degeneration. (Fig. 39, a.) As the salts accumulate, 
Fig. 39. 
Calcareous degeneration in a tumor; a, cells of smooth muscle filled with lime granules: 
b, a bloodvessel converted into a solid rod. X 350. 
the appearance of granules is somewhat lost, and a more contin- 
uous petrifaction results. (Fig. 39, b.) The addition of a dilute 
mineral acid causes the salts to dissolve, and, as carbonates are 
nearly always present, solution occurs with evolution of gas. 
Examples of this process are very numerous. A minute parasite, 
the trichina spiralis, occurs in the embryo form in the muscle of 
man and animals; it lies there quiescent, coiled up spirally and 
surrounded by a capsule. It is virtually a foreign body, and the 
capsule is by degrees impregnated with lime, assuming an opaque 
appearance at its poles (Fig. 40). If the embryo itself dies, it also 
may become impregnated with lime (see Fig. 40, lower part). 
Sometimes an extra-uterine foetus dies and remains inside the ab- 
domen as a foreign body. It becomes surrounded by adhesions 
and partially encapsuled. The capsule and superficial parts of 130 
RETROGRADE METAMORPHOSIS. 
the foetus become through time encrusted with lime. Again, an 
inflammatory exudation in the pericardium may dry in and remain 
as a half-caseous material, which finally becomes impregnated with 
lime, and something like a shell may form around the heart. In 
phthisis pulmonalis, if healing occurs, the contents of cavities and 
Fig. 40. 
Trichina spiralis in muscle. The capsules infiltrated with lime, and in one case a dead 
worm shrivelled and impregnated with lime. 
inflammatory products may dry in and become surrounded by a 
capsule. Impregnation with lime results, leading to a pultaceous 
or mortary material, which may ultimately condense into a stony 
Fig. 41. 
Calcareous infiltration of the middle coat (b) of an artery. At the tapering borders of the 
patch the elongated shape of the opaque structures indicates that the muscular fibre-cells are 
specially affected. The internal coat (c) is thickened. X 60. 
mass. These stony masses are sometimes coughed up if the lung 
afterwards breaks down, but it is very common to meet with them 
in the midst of cicatrices at the apices of the lungs after death. 
Again, in valvular disease of the heart, due to chronic endocarditis, AMYLOID DEGENERATION. 
131 
the new-formed connective tissue, by its contraction, becomes hard 
and dry, and virtually obsolete, and deposition of lime-salts occurs. 
. In regard to the frequent deposition of lime-salts in the middle 
coat of arteries (Fig. 41) there seems to be little doubt that this 
is frequently associated with atheroma, which is a chronic inflam- 
mation of the internal coat, and we may suppose that the indura- 
tion of the internal coat affects the neighboring middle coat. This 
calcareous infiltration is peculiarly liable to occur in old persons, 
and we may believe that in them there is a defective vitality of 
the walls of the artery, perhaps specially affecting the more active 
middle coat. But there are cases, and some of them in not very 
old persons, where there is a remarkably extensive calcareous 
impregnation of the middle coat, so that the arteries are largely 
converted into rigid tubes. In these cases we nmy presume that, 
from some unknown cause, the middle coat is prematurely de- 
fective in vitality. 
In the cartilages of old people, especially those of the larynx and 
ribs, there is very commonly a deposition of lime-salts. But, in 
this case, there is not simply a calcareous impregnation, rather a 
true ossification occurs, and the process may be regarded as virtu- 
ally a physiological one, a late development of bone from cartilage. 
AMYLOID DEGENERATION. 
This name is applied to a condition in which the constituents of 
the tissues are converted into a substance whose chemical charac- 
ters are different to those of any normal principle in the body. 
The degeneration is also called waxy and lardaceous from the 
physical characters of the substance produced. This may be called 
for convenience amyloid substance, and, as the name suggests, it 
was originally supposed to be allied to starch. It has really no 
chemical relation to starch, being a nitrogenous substance and a 
modified form of albumen. It resembles starch, however, in re- 
spect that it gives a color reaction with iodine. When a solution 
of iodine in water1 is poured on the surface of an organ which 
presents amyloid degeneration, then the amyloid substance takes 
on a mahogany-red color. If, afterwards, a very dilute sulphuric 
acid be added, the color will sometimes assume a darker brown or 
bluish tint. More recently it has been found that amyloid sub- 
stance presents a peculiar reaction with methyl violet, one of the 
aniline dyes. Watery solutions of this dye color the normal tissues 
blue, but stain amyloid substance of a rose-pink color. Other 
aniline dyes show differences of tint with amyloid substance. 
The substance itself has a peculiar, bright, translucent, glancing 
appearance (see Fig. 42), and, as the structures in which it occurs 
are enlarged, they are often remarkably prominent under the 
1 A convenient solution is, iodine, ten grains ; iodide of potassium, twenty grains ; 
water, four ounces. For microscopic sections a solution half this strength is sufficient. 132 
RETROGRADE METAMORPHOSIS. 
microscope. It is a very dense, heavy material, and after death, 
at least, is somewhat brittle, so that the structures have often a 
kind of broken-up appearance. 
Fig. 42. 
Advanced amyloid disease of the liver. The arrangement of the transparent amyloid 
material suggests its formation in the capillaries. The round bodies at the peripheral parts 
of lobules are fat-drops, there being slight fatty infiltration. X 70. (Thierfelder.) 
Amyloid disease may affect any organ of the body, but it is 
particularly frequent in the spleen, liver, kidneys, intestine, and 
lymphatic glands. 
In all these organs it begins in the connective tissue or the 
walls of the bloodvessels, more especially the walls of the capil- 
laries and smaller arteries. As the disease is a progressive one 
and the amyloid substance accumulates in large quantity, it is im- 
portant to observe the condition in the very earliest stages. If a 
section of the liver be made at a time when the disease is not far 
advanced, and the section, after staining with iodine and sulphuric 
acid, or with methyl violet, he examined under the microscope, it 
will be seen that, besides the smaller arteries, the capillaries are 
the seat of degeneration (see Fig. 43). Their walls are swollen 
and translucent, and the calibre encroached upon. At the same 
time, the hepatic cells are compressed and are undergoing atrophy. 
In advanced stages, on the other hand, the whole tissue of the 
liver seems to be replaced by the amyloid substance, and it is diffi- 
cult to say in what structures the degeneration has originated, but 
even here there are often, as in Fig. 42, indications of its origin in 
the capillaries. In the spleen, as we shall see afterwards, there are 
two forms of amyloid disease, and in one form it seems to begin 
in the reticulum of the Malpighian bodies, methyl violet or iodine AMYLOID DEGENERA T ION. 
133 
revealing a fine network having an amyloid reaction in these 
bodies in the earliest stage. In the other form it affects the walls 
of the vascular sinuses of the pulp. In the kidney it is chiefly the 
vessels that are affected, but the basement membrane of the urin- 
iferous tubules is also sometimes involved. 
It would seem, therefore, that the amyloid substance first appears 
in the walls of the vessels and in the connective tissue in these 
three organs. It remains to be considered whether it passes 
beyond these to the other elements of the organs. In the case of 
Fig. 43. 
Amyloid disease of liver in early stage. The walls of the capillaries swollen and 
translucent. X 350. 
the liver there does not seem to be any undoubted evidence that 
it does so. In the earlier stages it is found in the vessels alone, 
and in the later stages there is such enlargement and contortion 
that the seat of origin is somewhat obscure. In the kidney, also, 
it seems to confine itself to the vessels and connective tissue of the 
organ. In the spleen it does not, according to the observations of 
the author, confine itself to the vessels and connective tissue 
proper. Even in very early stages he has generally found that 
here and there in the sago spleen the round cells of the lymphoid 
follicles are affected. These cells, from what has been said on a 
previous occasion, may be regarded, however, as belonging to the 
connective tissue. In the lymphatic glands, again, it is the blood- 
vessels and reticulum that are affected. In the intestine it is the 
capillaries and arteries, and to a less extent the muscular fibre-cells. 
From this it will appear that the view formerly held, according 
to which the disease might attack the epithelial cells of such organs 
as the liver, is erroneous, and that the degeneration is confined to 
the structures constituting the supporting framework of the tissues, 
including the vessels. 
We have now to consider the effects of amyloid degeneration. 
We have referred to the brittleness of the amyloid substance, but 
it is not to be inferred that this exists to any considerable extent 
during life, otherwise we should have frequent hemorrhages as a 134 
retrograde metamorphosis. 
result of amyloid disease. Hemorrhages rarely occur, and so we 
infer that the substance is tolerably elastic during life. In exam- 
ining amyloid organs after death, especially such organs as the 
intestine, great care should he taken in handling them lest de- 
struction of the amyloid structure should take place. 
It is clear from symptoms observed during life that the amyloid 
substance is very pervious to fluids, the prominent symptom of 
amyloid disease in the bowels being diarrhoea, and in the kidney 
excessive discharge of watery urine. 
It has already been said that the calibre of vessels is reduced 
when amyloid disease occurs in their walls. This will cause 
anaemia in the structures supplied; and atrophy, sometimes with 
fatty degeneration, is frequently the result. This we see in the 
kidney and in the liver, the atrophy of the proper secreting sub- 
stance of the liver being, however, to a great extent, the direct 
result of pressure by the swollen capillaries. 
The amyloid structures are greatly increased in bulk and weight, 
and this tells on the organ as a whole. The liver, spleen, and 
kidneys are often greatly enlarged, and they present a peculiar 
dense translucent appearance which has given rise to the names 
waxy and lardaceous disease, often applied to amyloid degeneration. 
Besides the generally diffused amyloid disease occurring in a 
number of organs, and present in every part of the individual 
organs affected, we sometimes meet with a localized amyloid 
degeneration. This mostly occurs in new-formed inflammatory 
tissue and cicatrices, especially when of syphilitic origin, and also 
in tumors. As jet this local amyloid degeneration has only been 
observed in pathological structures such as those mentioned. It 
has been seen in syphilitic cicatrices in the liver, in the tongue, 
and larynx, in degenerating cartilage, etc., and in some cases the 
amyloid piece of tissue is of considerable size, and as it differs in 
its hard translucent character from the tissues around, it may 
itself look like a tumor. 
We may now consider the nature of the process which has 
been described. Looking to the history of the cases in which it 
occurs, it is clear that it is to be referred primarily to an alteration 
in the blood, probably an impoverishment of it in albumen. The 
disease is not an independent one, but comes on in certain cachectic 
states due to chronic tuberculosis, syphilis, diseases of bone in- 
volving prolonged suppuration, chronic dysentery, chronic albu- 
minuria, etc. 
It is more difficult to determine the nature of the connection 
between the vice in the blood and the disease in the tissues. By 
some it is supposed that the amyloid substance arises in the blood 
by modification of the albumen, and is then infiltrated into the 
structures. But this view cannot be accepted, for various reasons. 
In the first place, the substance is eminently insoluble, and it is 
difficult to understand how it can be carried; besides this, it does 135 
AMYLOID DEGENERATION. 
not displace the normal structures simply, but replaces them, these 
structures being converted into the amyloid substance. It is more 
consistent to suppose that the tissues are reduced in vitality by the 
altered condition of the blood, and that the albumen received 
enters into combination with the protoplasm in such a way as to 
produce this peculiar substance. The process may perhaps be 
compared to the coagulation of the tissues, which, as we have 
seen, sometimes occurs when they undergo necrosis, the tissues 
entering apparently into a chemical union with the fibrinogen in 
the fluid exuded from the bloodvessels, so as to form fibrine or 
some substance allied to it. Amyloid substance has been often 
regarded as akin to fibrine, and fibrinous casts in the tubules of 
the kidney are sometimes converted into amyloid substance. The 
existence of localized amyloid disease is strongly confirmatory of 
some such view as this. Here abnormal structures enter into this 
peculiar chemical combination with the albumen of the blood, 
while normal structures do not. In this connection also, the fact 
that amyloid disease afiects the connective structures of the body 
is not to be forgotten. It is as if the chemical basis of these 
structures had a special relation to the amyloid substance. Amy- 
loid disease is therefore essentially a degeneration, although, in 
order to the formation of the amyloid substance, it is necessary to 
have added to the tissue material from without, and this adds 
greatly to the bulk and weight of the structures. 
We have still to refer to bodies occasionally met with, and des- 
ignated AMYLOID CONCRETIONS Or CORPORA AMYLACEA. Ill old ex- 
Fig. 44. 
Corpora amylacea: a, from the prostate; b, from a hemorrhagic infarction of the lung; 
c, from the spinal cord. X 400. (Ziegler.) 
travasations of blood we sometimes meet with round or oval 
stratified bodies of small size (see Fig. 44, 6), which give a typical 
amyloid reaction. Sometimes they contain in their central parts 136 
RETROGRADE METAMORPHOSIS. 
a foreign body, such as a blood-crystal. Again, in the prostate 
gland (a) we meet with concretions of considerable size, it may be 
visible, as brown granules, to the naked eye, with all the characters 
of stratified amyloid concretions. They are also met with in the 
tissues of the central nervous system (c), they are present in the 
normal brain, especially in the ependyma of the ventricles, but in 
cases of sclerosis they may be present in enormous numbers. 
The significance of these amyloid bodies is not usually very 
great in a directly practical point of view, but their presence under 
these various conditions seems to prove that the various albu- 
minous substances may undergo conversion into the so-called 
amyloid substance. HYPERTROPHY, REPAIR, AND REGENERATION. 
1. HYPERTROPHY. 
Hypertrophy, in its most literal sense, means overgrowth, or 
excessive growth, and it is so that we shall use it here. In order 
to understand overgrowth it will he necessary to make some ob- 
servations on the characteristics of normal growth. 
In the normal groavth of the bodj’ each tissue has the power of 
reproduction up to a certain point. By some hidden power the 
tissue grows and moulds itself into particular anatomical forms, 
and ceases growing when it has attained the proportions necessary 
for its function in the organism. We do not know what this 
power is, but we can say that it is inherited by the germ from its 
parents, and that in the variations which are presented in different 
individuals heredity plays a very important part. 
In order to this growth the new formation of bloodvessels is 
necessary, but here, as in pathological conditions, the formation 
of vessels is secondary, and takes place merely according to the 
needs of the organism. The amount of blood supplied and its 
distribution strictly follow the necessities of the growing tissues, 
and the vascular system shows a wonderful power of adaptation 
to the requirements of the tissues. It is true, as we shall see 
afterwards, that an excessive supply of blood may lead to increased 
growth, but such an excessive supply of blood never occurs nor- 
mally, is an accident, and as such may lead to morbid or excessive 
growth. 
When tissues cease to grow, it is not that the formative power 
inherent in them has ceased to exist, but simply that, being sub- 
ordinate to the general law of the organism they have attained 
the full size requisite for their intended uses. Should occasion 
occur for their renewed growth, then it will very often happen 
that a fresh start will be made. 
Looking to the details of normal growth, we find that it is the 
cells which are the essential factors in the process. It is by 
division of the cells, a process frequently designated proliferation, 
that growth is ultimately affected. Much careful observation has 
been bestowed on the process of division of cells. There are 
frequent indications that first the nucleus and afterwards the cell 
separate into two. Before the actual division begins the nucleus 
undergoes a transformation, the details of which may be studied 
in Fig. 45. In a the condition of an epithelial cell in its normal 
quiescent state is shown. By particular methods of staining it can 138 
HYPERTROPHY, REPAIR, AND REGENERATION. 
be shown that the nucleus contains a fine network of fibres, but 
here the substance of the nucleus as well as the fibres is stained. 
In b the condition preliminary to division is shown. The nucleus 
now contains a collection of convoluted tubes, and those alone are 
stained while the substance between does not take on the color. 
These fibres are apparently contractile and vary their position 
somewhat, but gradually tend to assume a radiating arrangement 
as in c and d. There now comes a separation in the middle, as at 
e, and the two sets of fibres retreat from one another towards the 
Fig. 45. 
)ivision of cells. Explanation in text. (After Flemming.) 
poles of the cells as in /. The division of the nucleus is thus 
effected, and that of the cell follows as in g. Subsequently the 
irregular bundle of fibres in each new cell assumes the shape of 
the regular nucleus and gets surrounded by a membrane. The 
fibres also give place to a fine network as in the original cell, and 
the substance of the nucleus between the fibres again takes on the 
staining as in i. 
This process of division has been observed in the fixed cells of 
many tissues, and it is probably the only one which occurs in the 
normal process of growth. In white blood-corpuscles, and 
probably also in the embryonic cells a more direct division of the 
nuclei appears to occur, but the details of that process are not very 
clear. 
Bearing in mind the facts mentioned as to normal growth we 
have now to consider the processes in overgrowth or hypertrophy, 
and the conditions under which it occurs. 
The simplest form of hypertrophy is that which arises from the 
necessity for the excessive performance of a normal function. 
We saw that growth ceases when the requirements of the organism H Yl'ERT R O PII Y . 
139 
are satisfied, but if increased requirements develop, then the 
tissues may take on a fresh growth to meet them. This is illus- 
trated chiefly by the muscular and epidermic tissues. 
Many instances of hypertrophy of muscle, from this cause, 
might be cited. If, in consequence of stricture of the urethra or 
obstruction at the neck of the bladder, the passage of urine is 
obstructed, and the muscular coat of the bladder must contract 
with more vigor to expel the urine, the muscle will undergo 
hypertrophy. In this way there may be a very remarkable thick- 
ening of the muscular coat. In like manner, we may have 
hypertrophy of the muscular coat of the intestine in connection 
with stricture of the rectum or colon. The muscular tissue of the 
heart also undergoes an exactly similar hypertrophy when, in order 
to expel the blood from its cavities, more forcible contractions are 
requisite. We know also that the voluntary muscles hypertrophy 
when they are repeatedly exercised in a forcible way. 
In all these cases of hypertrophy of muscle it is usually said 
that frequent exercise is the cause, but this is hardly a full descrip- 
tion of the circumstances. The exercise must not only be frequent , 
but the work to be done must require an unusually forcible 
exertion In the cases already cited it will be seen that the 
essential condition is the necessity for additional power, usually to 
expel the contents of a cavity through a narrowed orifice. The 
heart does not hypertrophy because its muscle undergoes frequent 
exercise, but only when additional force is required. It is so also 
in the case of voluntary muscles. Mere agility and rapidity of 
movement does not cause hypertrophy of muscle, whereas repeated 
severe exertion calls it forth. The muscles of the hand and arm 
do not hypertrophy in persons who use them frequently in writing, 
but they do in artisans who use great force in their occupations. 
It may be added that a muscular action which is ordinarily per- 
formed with moderate force may, from abnormal conditions, come 
to be performed frequently with excessive force, and so lead to 
hypertrophy. For example, the urinary bladder may be induced 
to contract frequently and with exaggerated force, although there 
is no obstruction, and this may induce hypertrophy. 
A question arises here as to the finer details of the hyper- 
trophy of muscle. In the case of involuntary muscle there can 
be no doubt that the hypertrophy occurs by division of the mus- 
cular fibre-cells by a process similar to that already described in 
referring to normal growth. But some question has been raised 
as to the exact nature of the process in striated muscle, and careful 
measurements have been made of the diameter of the muscular 
fibres in hypertrophy of the heart. It is stated by some that the 
diameter is increased and by others that it is not. It may be said, 
however, that the increase in thickness, if it occurs, is not so great 
as to account for the large additional bulk of the muscular sub- 
stance as a whole, and that there is, as well, a numerical increase 
in the muscular fibres effected by division. 
Enlargement of a tissue by such numerical increase has been 140 
HYPERTROPHY", REPAIR, ANJ) REGENERATION. 
designated by Yirchow hyperplasia, and this is sometimes distin- 
guished from true hypertrophy, in which there is merely an enlarge- 
ment of the elements of the tissue. This distinction, however, 
cannot be rigidly carried out, and the term hyperplasia will only 
be used here in order to indicate that the hypertrophy is by pro- 
liferation. 
The epidermis is the other tissue which frequently shows hyper- 
trophy when the necessities of the organism call for it. The func- 
tion of the epidermis is chiefly to protect the true skin from injury 
by friction against external objects, and, in its primary formation 
in the foetus, the epidermis is thicker or thinner according as the 
parts of the skin are liable after birth to be exposed to greater or 
lesser amounts of friction. But, if afterwards, certain portions of 
the skin are frequently exposed to friction, then an additional 
growth will occur in the epidermis, a hypertrophy. We liave< 
abundant instances of this in the horny hands of workmen. The 
thickening of the epidermis which results in the so-called corns is 
another instance of hypertrophy, in order to protect a portion of 
the sensitive skin from undue friction or pressure. 
In regard to these thickenings it is to be pointed out that they 
only occur when the friction or pressure is not constant, but 
recurs at frequent intervals. A constant pressure, as by a splint 
pressing on a part, causes atrophy, whereas a frequently repeated 
pressure results in hypertrophy, apparently by allowing the struct- 
ures to recover and afford time for increased nutrition. The same 
law applies to tissues in the interior of the body. When exposed 
to constant pressure they atrophy; when the pressure is intermit- 
tent they hypertrophy. It is here to be noted, however, that 
pressure from within (as by tumors, aneurisms, etc.) is usually con- 
stant, while that from without is mostly intermittent. Hence the 
original statement of John Hunter is justified, that pressure from 
without produces thickening, while that from within causes 
atrophy, although it is not to be taken without reservation. 
The hypertrophy of the epidermis in these cases is undoubtedly 
effected by division of the cells; it is a hyperplasia, and the process 
is similar to that already described. 
Hypertrophy from increased blood-supply.—In what has been 
already stated we have not exhausted the subject of hypertrophy, 
and, in order to appreciate what follows, it is necessary to refer 
again to normal growth. It was observed above that in ordinary 
growth of tissue the bloodvessels strictly follow the growing tissue, 
and are formed according to its needs. But if, from some acci- 
dental circumstance or by artificial interference, the blood-supply 
be greatly increased, then excessive growth may result. If the 
spur of the cock be removed from the leg and successfully trans- 
planted into the comb, it will grow with excessive vigor, forming 
a prominent horn-like structure. Here the excessive supply of 
blood, the comb having a much more active circulation than the THE REPAIR OF INJURIES. 
141 
leg, induces an excessive growth of the epidermis forming the 
spur. 
In human pathology we have numerous instances of hypertrophy 
analogous to this. Increased activity of the circulation will often 
lead to hypertrophies. We see it in the neighborhood of inflam- 
mations. We have already seen that determination of blood exists 
outside the immediately inflamed area, and if this is prolonged it 
may lead to overgrowth of the tissues. In 
this way we may account for the excessive 
growth of hair sometimes seen in the neigh- 
borhood of ulcers, near diseased joints, and 
at the ends of stumps which have remained 
long inflamed. 
A very striking instance of hypertrophy of 
this kind is sometimes afforded in bones. In 
the neighborhood of inflamed joints the sur- 
face of the bones is often nodulated, and the 
bones greatly thickened bv new formation 
from the periosteum. In cases of periostitis, 
the new formation of bone is perhaps more 
strictly to be regarded as a part of the inflam- 
matory process, as we shall see afterwards. 
There arc some curious instances of limited 
necrosis of bone occurring during the period 
of growth in which the bone, as a whole, has 
grown larger than the other. If a boy has a 
necrosis of the femur, the whole bone is 
probably more richly supplied with blood, and 
the normal gro\Vth is accelerated. The ne- 
crosis may be recovered from, and the person 
is left with a permanently elongated femur 
which may be as much as two inches longer 
than the other, and may lead to considerable 
lameness. The tibia is differently situated 
to the femur. Its two extremities, are tied 
to the ends of the fibula by firm ligaments, 
and so the bone cannot elongate.. If over- 
growth occurs, the bone must curve so as to 
accommodate itself. An example of this 
is shown in the accompanying Fig. 46, from 
a preparation in St. Bartholomew’s museum 
(quoted by Paget), in which the bone, measured over its curve, was 
two inches longer than the healthy one. 
Fig. 46. 
Elongation and cur- 
vature of tibia, the result 
of necrosis during period 
of growth. (Paget.) 
II. THE REPAIR OF INJURIES AND RESTORATION OF LOST PARTS. 
The term Regeneration is applied to the restoration of portions 
of the body which have been lost by injury or disease. The 
regeneration of a part is to be carefully distinguished from mere 
growth. A tissue may be able under suitable stimulation to 142 
hypertrophy, repair, and regeneration. 
reproduce its elements, and increase in size; but for the replace- 
ment of a lost part, if at all considerable, there must be, virtually, 
a renewal of the process of development. 
This reproduction of lost parts in their entirety occurs readily 
in some of the loavest forms of animals. In the hydra, if the 
creature be cut in two, each half will develop into a complete 
animal, and the process may be repeated indefinitely. This power 
of reproduction of the Avhole animal from a part seems confined 
to those creatures Avliicli can propagate by spontaneous fission or 
gemmation. When Ave come to animals higher in the scale the 
power of reproduction seems to be limited to the restoration of 
lost limbs, antennae, etc. 
Without going into details, Avliicli Avill be found by reference to 
Paget’s “Lectures on Surgical Pathology,” it may be said that 
there are indications which seem to shoAv that there is some kind 
of JjAAV according to which the reparative poAver in each perfect 
species is in inverse proportion to the amount of change which the 
animal has passed through in its development from the embryonic 
to the perfect state. It is as if, in the process of development, the 
formatiAre poAver as distinguished from mere growth Avere gradually 
exhausted, and the process of reproduction, which Ave have seen to 
be, as it were, a renewal of that of development, only occurs Avhen 
this power has been comparatively little expended. It appears, for 
instance, that in insects the power of reproducing antennae or 
limbs is limited to those species Avhich have attained the perfect 
state through a comparatively simple and direct course of develop- 
ment. It is consistent Avith this vieAv that in the larval state insects 
show a much greater poAver of reproduction than when perfect. 
The laiwa of one of the higher insects Avill be able to reproduce its 
limbs, Avliile the perfect insect is not. 
In man, and in the vertebrata in general, the long course of 
development seems largely to exhaust the reproductive poAver 
of the body, and, in the adult state at least, the poAver of restoration 
of lost parts is very small, and the processes concerned are almost 
as much related to growth of tissue as to development. In the 
embryonic state it is probable that the power of restoring lost parts 
is much greater than in the adult. Some children are born Avith a 
short arm, at the extremity of Avhich are imperfectly developed 
lingers; it is probable that in these cases amputation of the arm 
has occurred in utero, and an attempt at restoration has folloAved. 
In the adult it may be said that restoration of lost structures is 
almost confined to the blood and the epithelial and connective tissues. 
Along with the connective tissues Ave have, of course, bloodvessels 
Avhich are readily reproduced, and Ave may also, to a limited extent, 
include nerve-fibres, which, as we shall see after'wards, are some- 
times restored. 
While, therefore, the absolute restoration of complete and con- 
siderable portions of the body is scarcely possible in man, yet the 
body is by no means unprovided with poAvers by which injuries 
are repaired and loss of structures is made good. It may be said THE REPAIR OF INJURIES. 
143 
that the higher and more complex animals are endowed with 
greater ability to protect themselves from injury, and that their 
tissues possess the necessary powers of restoration in the case of 
those injuries to which they are specially liable. In the various 
processes here to be considered, it will be seen that wliat may be 
called the definite intention to attain a certain result which is shown 
in the process of development, is distinctly visible, and that the 
tissues have a remarkable power of meeting adverse conditions. 
Healing of wounds.—The power of repair is well seen in the 
various processes concerned in the healing of wounds. There are 
some wounds which heal by a process fitly designated immediate 
union. That is to say, the surfaces are brought together and 
coalesce without any new-formed material being produced to serve 
as a bond of union. This occurs mostly in clean-cut wounds, 
which, shortly after their infliction, are closed so as to bring the 
cut surfaces into close contact. It is necessary for this process 
that all inflammation be avoided either at the time of infliction of 
the wound or afterwards. The wound should therefore be clean- 
cut and made with a sharp instrument. We are to think of the 
living tissues not as mere mechanical pieces of texture, but as 
possessed, by virtue of their vitality, of wonderful powers of adapt- 
ability to circumstances. When two living surfaces are brought 
into contact and all disturbing conditions are averted, then the 
bloodvessels will form communications, the nerves will by and by 
unite and become continuous, and the connective tissue coalesce. 
In this way it frequently happens that a wound in the skin, or even 
in muscle, unites, and no trace of a bond of union or even of the 
line of union can be found after a few days. The epidermis 
probably does not unite so directly, and the wound is covered 
by new-formed epidermis. 
In union by primary adhesion we have a process of a more 
complicated kind. In it inflammation plays a part. When a 
wound is inflicted, the mere mechanical injury, or exposure after- 
wards, frequently leads to a trivial but acute inflammation, re- 
sulting, as we have seen, in the coating of the cut surface with a 
tibrinous exudation, the so-called glaze. If two surfaces thus 
coated with fibrine l)e brought in contact they unite, the fibrine 
acting as a glue or cement. But the fibrine does not form a per- 
manent bond of union, and if no attempt is made to effect union 
by other methods, then the wound will subsequently gape by the 
breaking down of the fibrine. In order to effect a permanent 
union we must have formative cells produced, such as we saw, 
when studying inflammation, to be necessary for the formation of 
connective tissue out of granulation tissue, and we must have a 
similar new formation of bloodvessels. The new formation of a 
uniting tissue here is very trivial in amount; there is no produc- 
tion of proper granulation tissue, but merely a limited production 
of formative cells which replace the thin layer of fibrine, and a 
budding of the bloodvessels till communications are formed be- 
tween the two surfaces. This whole process may occupy only a 144 
HYPERTROI’HY, REPAIR, AND REGENERATION. 
day or two, and the permanent new-formed tissue forming the 
cicatrix is usually very small in amount. This form of union is 
sometimes spokep of as union by the first intention, but that 
term is also applied sometimes, but not correctly, to immediate 
union, and so it is, perhaps, better to use the term primary adhe- 
sion for this form. 
In studying inflammation we have already considered the method 
of union by the second intention which occurs when two granu- 
lating surfaces come in contact. 
It is necessary now to refer more particularly to the processes of 
regeneration as manifested in the individual tissues of the body. 
In the first place we may regard the blood as a tissue, and we 
have already seen that after a severe hemorrhage its constituents 
are gradually regenerated, the fluid part most quickly, the white 
corpuscles comparatively soon, and the red corpuscles somewhat 
slowly. 
The epidermis and epithelium of the surface of the skin and 
mucous membranes are restored with considerable rapidity. In 
the case of the skin and mucous membranes there is normally a 
continuous shedding of the surface epithelium, and a new forma- 
tion in the deeper layers to replace that which is lost, a kind of 
physiological regeneration therefore. When, by accident or other- 
wise, a superficial portion of epithelium is shed before its time, it 
will be replaced by the normal growth of the deeper layers, prob- 
ably accelerated by the requirements of the body. When the 
whole thickness of the epithelium is destroyed, the gap is by de- 
grees filled by the proliferation of the epithelium at the edges of 
the wound, as we have already seen in the case of the cicatrization 
of a granulating wound. According to the observations of Klebs, 
the new-formed epithelium acquires a slight power of amoeboid 
movement, so that it can proceed to the spot which it is to occupy. 
The proliferation of the epithelium proceeds by a process similar 
to that already described in considering the normal division of 
cells. In the accompanying illustration (Fig. 47) from a paper by 
Eberth (Virchow’s Archiv, 67) the fibrous transformation of the 
nucleus and the other changes, as seen in the cornea of the rabbit, 
some days after a portion of the epithelium had been removed, are 
shown. In the normal cornea there are traces of a similar process 
by which, we may presume, the physiological regeneration occurs. 
It is here of interest to observe that the epidermic cells may be 
transported from their original seat and survive and proliferate on 
the surface of a wound, even in another individual. It is well 
known that advantage is taken of this fact in the process of graft- 
ing which surgeons resort to in order to accomplish the cicatriza- 
tion of large wounds. The whole thickness of the skin or mucous 
membrane may be transplanted from one place to another, or even 
from a different person; or the skin may be made to occupy the 
place of the mucous membrane, or vice versa. When the skin or 
mucous membrane is thus made to occupy a different position with REGENERATION. 
145 
different relations and duties, it by and by conforms itself to its 
new position and the epithelium acquires a structure like that in 
its neighborhood. 
In the case of the hairs and nails we have normally a process of 
desquamation and regeneration similar to that of the surface epi- 
dermis. If a hair be prematurely extracted or a nail torn off, it is 
restored by a strictly normal process. But if the hair-follicle be 
Fig. 47. 
Regeneration of epithelium in cornea of a rabbit, (a) Fibrous transformation of nucleus. 
(6) Partial separation of the fibres and hour-glass change of nucleus, (c) Complete division 
of nucleus. (d) Complete division of cell. (Eberth.) 
removed or the matrix of the nail destroyed, there is no restora- 
tion of the structure, the regeneration of such complex structures 
being beyond the powers of the ordinary epidermis. 
In some glands there is in health or disease a desquamation or 
destruction of the epithelium. Then, in the kidneys there is a 
form of inflammation in which the epithelium of the tubules is 
abundantly shed. In this case it is restored by a new formation, 
and we are sometimes able to observe the old epithelium in the 
lumen of the tubules, while the small, young epithelium lines 
them. In the liver there is great destruction of the secreting cells 
in acute yellow atrophy, and sometimes alongside the remains of 
the cells there are collections of new-formed cells, as if an attempt 
were being made at renovation of the tissue. 
The regeneration of connective tissue has been sufficiently 
illustrated in what has gone before. It is obvious that in the heal- 
ing of wounds, except by immediate union, there is a new forma- 
tion of connective tissue and bloodvessels. As connective tissue 
seems to be the simplest form of tissue, it is sometimes used to fill 
up gaps where more complex tissues have been lost. Thus a 146 
hypertrophy, repair, and regeneration. 
wound in a muscle is not restored by the formation of muscular 
but of connective tissue, and so is it with wounds of the liver, 
spleen, kidneys, etc. 
The regeneration of bone is frequently exemplified in the repair 
of fractures. In the various processes observable here we may see 
conditions analogous to those in healing by primary adhesion and 
by the second intention. In cases where the broken ends are kept 
closely together and at rest there may be very little inflammation, 
and the permanent uniting medium may be produced by the im- 
mediately neighboring tissue. As we shall see afterwards, although 
the periosteum usually supplies the new bone, yet it is not neces- 
sary to its formation, but the bone itself, perhaps rather the tissue 
occupying the Haversian canals, is capable, under certain conditions, 
of producing new bone. In other cases there is more considerable 
inflammation, it may be with suppuration, and granulation tissue 
is produced. This granulation tissue, arising largely from the 
periosteum, develops according to circumstances bone, cartilage, 
or connective tissue, forming the callus and ultimately supplying 
the permanent bond of union between the broken ends. 
It has recently been shown by the observations of Hr. Mace wen, 
of Glasgow, that bone may be transplanted. Pieces of bone have 
been taken from a person, and used to till up a gap in a bone, and 
they have both lived and grown larger in their new position. 
Nerve-fibres show a certain power of new formation when 
divided or when portions are excised. When a nerve is thus 
divided, even if the two ends are separated for some distance, 
there is often, after a time, a full reestablishment of the conduc- 
tion. It appears that from the central end pale fibres grow out. 
These pass to the peripheral end, and constitute the axis-cylinders, 
which afterwards acquire medullary sheaths and so become com- 
plete nerve-fibres. In this way a considerable length of nerve 
may apparently be restored. 
There is another form of regeneration sometimes described, but 
it is of a more doubtful nature. When a nerve is divided, the 
fibres in the peripheral portion, from its cut end downwards to its 
ultimate distribution, show a peculiar change, consisting mainly 
in degeneration of the medullary sheath. It is doubtful whether 
the axis-cylinder takes any part in this process. After the cut 
ends join, the nerve-fibres are restored, and this by a process which 
may be called regeneration of the medullary sheath. 
It has already been mentioned that when a muscle is wounded 
the gap is filled by connective tissue; there is no proper regenera- 
tion. But there may be loss of the contractile substance by de- 
generation, as in fatty degeneration of the heart. When such a 
process is intense, it seems impossible that the muscular fibres 
can be restored, and as the heart often recovers there must be a 
regeneration of the contractile substance. But in this case there 
is not a destruction of the muscular nuclei, and therefore not a 
regeneration of the muscular cell as a whole. In the case of 
unstriped muscle there is probably also an occasional degeneration 
and renewal of the contractile cells. INFECTIVE TUMORS (GRANULATION-TISSUE 
TUMORS). 
This class of tumors is taken u[> here chiefly because they show 
in their structure and general relations considerable analogies to 
inflammation on the one hand and tumors proper on the other. 
As indicated in a previous part, the expression infective means 
that the disease is “spreading,” that it depends on some virus 
which propagates itself, and tends to reproduce the same kind of 
lesion outside its original seat. In two forms of disease included 
here, the exact nature of the virus has been made out, namely, in 
tuberculosis and leprosy; and in both it is found to be a micro- 
organism in the form of a short rod-shaped bacillus. It may per- 
haps be legitimately inferred that in all the rest specific organisms 
are the infective agents. It may be added that several of these 
forms of disease are not only infective but infectious, communi- 
cable, that is to say, from person to person; some are capable of 
being inoculated into animals. 
The virus acts as an irritant, and the resulting lesions present 
strong analogies to inflammation. It is not to be inferred that the 
micro-organisms, where they are concerned, themselves irritate 
the tissues; it is more probable that the irritation is due to chemi- 
cal products resulting from their vital processes. The resulting 
lesions are in some cases indistinguishable from those of inflam- 
mation, and we shall see afterwards that we have to speak of 
syphilitic and tubercular inflammations. But the virus also takes 
usually a more local habitation, and concentrating its action on 
particular points, it gives rise to numerous lesions, having more 
or less the character of tumors. Even the tumors present great 
analogies to inflammation in their structure. They are formed of 
granulation tissue, and are often called granulation-tissue tumors 
or granulomas. 
But the tissue of the tumors presents certain differences from 
ordinary granulation tissue chiefly in its tendencies. The granu- 
lation cells tend to undergo fatty degeneration, and so the tissue 
may become caseous or break down. At the same time there is 
the more normal tendency to undergo development into connec- 
tive tissue, and this may go on in an imperfect way alongside the 
other change. Hence the tumors frequently present great varieties 
in structure, and it is sometimes difficult fully to unravel their 
relations. 148 
INFECTIVE TUMORS. 
SYPHILIS. 
In this section we have to consider the general relations of this 
disease. In what has gone before some of the grounds have been 
indicated for stating that a virus is concerned in its production. 
In addition the following may be mentioned; it is well known that 
the discharges from a syphilitic person are contagious; and it is 
also generally believed that in the secondary stage the blood, and 
even the milk, are infectious. In this connection it is to be remem- 
bered that an attack of syphilis generally confers immunity against 
a further attack, the analogy with the specific fevers being sug- 
gested by this. 
A virus is the cause of the disease, and as a general rule it is 
usually applied to some part of the organs of generation. It may 
be applied, however, to some other part, as to the finger (in the 
case of a surgeon examining a part), to the lip (as in the case from 
which Fig. 48 is taken), to the eyelids or other external part. The 
Fig. 48. 
Section of a hard chancre at its marginal part. The granulation tissue occupies the 
skin under the epidermis, gradually replacing the latter. X 75. 
result is the indurated or primary chancre. Tills consists of a 
raised hard structure generally with an ulcerated surface. Ex- 
amined microscopically, it is found that the epidermal covering of 
the skin is not necessarily lost, but that beneath it, and in the 
central part, it may be to some extent replacing it, there is an 
enormous formation of granulation tissue (Fig. 48). The true skin 
is entirely replaced by this granulation tissue, and instead of it 
there is a bulk}’ mass of round cells. This structure may be 
regarded as inflammatory, nut it may also be regarded as a kind 
of tumor, and may be taken as the type of the syphilitic tumor. 
In its less common seats it may very closely resemble another 
form of tumor. Thus a chancre of the lip may be mistaken for an 
epithelioma, and be excised under that impression. This actually 
occurred in the case from which Fig. 48 was taken. The tissue, SYPHILIS. 
149 
although like in structure to granulations, does not,'like them, 
readily form connective tissue, but remains long in the same rudi- 
mentary condition, and when it disappears leaves comparatively 
little of a cicatrix. On the other hand it sometimes becomes 
caseous, but this does not so readily occur here as in some other 
localities. 
The virus is carried from the indurated chancre by the lym- 
phatics, and in the first place lodges and is caught in the neigh- 
boring lymphatic glands, where it again produces similar results, 
namely a great production of ill-formed granulation tissue which 
has little tendency to develop into proper connective tissue, but 
readily undergoes an irregular caseous metamorphosis, and occa- 
sionally takes on the phagedsenic character. 
After an interval the virus passes into the blood. There is a 
period which may he regarded as a period of incubation, or self- 
propagation of the virus between its first introduction into the 
system and the evidences of its presence in the blood—the virus 
seems to take a certain time to reproduce itself in quantity, and it 
generally does so chiefly in the lymphatic glands. When an agent 
exists in the blood in a finely divided state it will be carried to all 
parts of the body, and if it produces lesions they will probably be 
symmetrical, as the corresponding parts in each lateral half of the 
body are for the most part in similar circumstances, and are 
similarly affected by any agent acting equally on them. The 
existence of symmetrical lesions is presumptive evidence that a 
disease is due to something in the blood. In the secondary stage 
of syphilis then we have the virus in the blood, and the' result is 
symmetrical lesions of the skin, mucous membranes, bones, etc. 
These secondary lesions are inflammatory in character, and have 
generally a resemblance to ordinary inflammations. They are 
most frequent in the skin, and so we have the syphilitic roseola, 
eczema, etc., but other parts may be affected, and we have syph- 
ilitic periostitis, pharyngitis, etc. It is a question to what extent 
inflammations occur in internal organs in this stage, but according 
to Hutchinson they are more frequent than is generally supposed, 
but are rarely seen because persons seldom die in the secondary 
stage. 
The secondary stage has been aptly compared with the eruptive 
stage of specific fevers, it is like a fever long drawn out. There is 
in both cases a virus in the blood, and in syphilis, as well as in 
the acute fevers, there is generally elevation of temperature. The 
analogy between the rash of secondary syphilis and those of 
measles, scarlet fever, smallpox, etc., is also suggestive, the skin 
affections in both classes of cases being inflammatory. 
During this stage then the virus is active in the blood, and it is 
generally held that the blood and secretions are contagious. The 
person is also in the position of transmitting the disease to his 
offspring, the virus apparently passing into the germ and sperm 
cells. Just as in the specific fevers, the virus dies out of the blood 150 
INFECTIVE TUMORS. 
spontaneously, and the various secondary lesions disappear. When 
the virus is no longer in the blood this fluid will cease to be con- 
tagious and the disease will no longer be transmissible to the 
offspring. But it is not to be inferred that the disappearance of 
the secondary lesions is absolute proof of the virus having died out 
of the blood, and it would not be safe to advise a patient that he 
could safely marry till at least two years after the subsidence of all 
secondary symptoms. 
In this secondary stage it is not common to meet with tumors 
like the indurated chancre. They are characteristic rather of the 
next stage, and when they do occur in this stage they are small 
and accompanied by more pronounced inflammatory manifesta- 
tions. 
The tertiary stage is chiefly characterized by the formation of 
tumors to which the name Gummata is applied. They are com- 
posed similarly to the indurated chancre, namely, of granulation 
tissue in the first instance, but in them this tissue has a much 
greater tendency to undergo caseous necrosis, although the trans- 
formation into connective tissue also occurs. Hence it happens 
that the gumma of the tertiary stage is very commonly more or 
less caseous in certain of its parts. 
Fig. 49. 
Gumma of kidney. The opaque central part (d) is caseous: around this there is fibrous 
and granulation tissue (c). X 20. (Cornil and Ranvier.) 
To the naked eye the tumor is a whitish or grayish body, com- 
monly with a yellow caseous appearance in its central parts, or 
irregularly distributed. It varies in size, sometimes as small as a 
millet seed, in which case it is usually multiple, but it is usually 
much larger, and may attain the size of an apple. The tumor is 
not generally sharply defined from neighboring structures, but its 
periphery merges in a firm connective tissue which usually extends SYPHILIS. 
151 
outwards into neighboring structures, so that the tumor appears 
planted in the midst of a cicatricial mass. 
Under the microscope the tumor will be found, as in Figs. 49 
and 50, to replace a certain portion of the normal tissue. The 
central caseous part will he opaque, as in c, Fig. 50. Externality 
Pig. 50. 
Gumma of liver. Explanation in text. X I*>. 
there is more transparent tissue (5), while around and in neigh- 
boring parts of the organ there is new-formed connective tissue, as 
at d in the figure. 
In Fig. 51 the appearances seen under a higher power are shown, 
the parts taken being from b and c in Fig. 50. it is seen that the 
peripheral portions (Fig. 51, a) of the tumor present innumerable 
round cells mixed with fibrous tissue, which latter is often very 
pronounced. The caseous parts are opaque and present fine fat 
granules with shrunken cells and nuclei (Fig. 51, b). 
The tumors are met with in almost all the tissues of the body, 
skin, mucous membranes, subcutaneous tissue, in the substance of 152 
INFECTIVE TUMORS. 
muscles (as in the tongue), periosteum, liver, dura mater, soft 
membranes of the brain, cerebral nerves, etc. The name gumma 
does not express their usual consistence, and is stated to have been 
first applied to the periosteal form. 
The caseous metamorphosis leads to various results, according 
to the situation and circumstances of the gumma. If the tumors 
have a superficial situation, then ulceration results, and we have 
Fig. 51 
From gumma of liver, same section as Fig. 50; «, taken from recent part (b, in other 
figure) ; b, from caseous (e). X 350. 
a deep excavated ulcer with swollen infiltrated walls, consisting of 
tissue like that of the gumma, and with the same tendency to 
degeneration, so that the ulceration extends. As the tumor in- 
volves neighboring structures which undergo necrosis along with 
the caseous process in the tumor, there may be great destruction 
of tissue brought about. In internal organs the caseous material 
may long lie apparently unaltered. The gumma may be virtually 
healed, its granulation tissue absorbed or converted into connec- 
tive tissue, while the caseous matter remains, and is finally left in 
the midst of a cicatrix where it may become calcified. 
It appears that the absorption of a gumma may be promoted by 
the administration of remedies. The exact process by which this 
is brought about is hardly known, but there seems to be a simple 
fatty degeneration with absorption, in the way indicated in the 
section on fatty degeneration. 
We have still to inquire what may be the relation of these ter- 
tiary lesions to the virus. The virus no longer exists in the blood, 
and in accordance with this the lesions are characteristically unsym- 
metrical. The most probable supposition is that, after the close of 
the secondary stage some of the virus has remained lying in a par- 
ticular part. Perhaps a small gumma lias formed, and the virus 
has lain in it quiescent but still surviving. It may be waked up 
by some accidental circumstance in the life of the patient, at any 
period afterwards, perhaps as long as twenty years. The virus TUBERCLE AND TUBERCULOSIS. 
153 
propagates itself, but its effects are local. It may produce a tumor 
of large size, but it does not pass into the blood, and does not pro- 
duce the lesions of the secondary stage. It has been matter of dis- 
pute whether a tertiary gumma is an infectious lesion, and the fact 
that the blood of the patient does not become infected might seem 
to answer the question in the negative. It is to be remembered, 
however, that the person already possesses an immunity by having 
passed through the secondary stage. The gumma is probably 
capable of producing syphilis in another person. 
The tertiary stage of syphilis is often in its later period associated 
with amyloid disease. This is not from the direct action of the 
virus, but is due to the condition of the blood induced by the 
serious organic lesions. 
Syphilis is often associated with a condition of the arteries 
which will come up for discussion further on. Wherever there is, 
as so frequently happens, a considerable formation of granulation 
tissue passing into connective tissue, the arteries take part in the 
inflammation, and we have especially thickening of the internal 
coat, sometimes going on to complete obliteration of the calibre of 
the vessel. This is sometimes very strikingly seen in the neigh- 
borhood of gummata, and by diminishing the blood supply, it may 
contribute to the degeneration of the gumma. It also predisposes 
to degenerations in parts around, as where softening of the brain 
occurs in connection with gummata. 
Hereditary Syphilis.—We have already seen that syphilis, in 
the secondary stage at least, may be transmitted to the offspring. 
In the acute period the children often die in utero, or they sicken 
soon after birth and die within a few weeks. But it often happens 
that the children do not show any evidence of syphilis for months 
or years. In this way we may distinguish cases of congenital 
syphilis from cases of simple hereditary syphilis, the former being 
born with syphilitic lesions, the latter only acquiring them after- 
wards. 
In congenital syphilis the most constant and unequivocal lesion 
is the affection of the bones, which will be considered afterwards. 
In this condition there is. the formation of a kind of gummatous 
tissue apparently, with inflammatory conditions. 
In the simple hereditary cases the lesions are, like those of the 
secondary stage, mainly inflammatory. There are inflammations 
of the skin, mucous membranes, cornea, etc. The characteristic 
malformation of the teeth which Hutchinson has pointed out seems 
related to the inflammation of the mucous membrane of the gums 
during the development of the teeth. 
TUBERCLE AND TUBERCULOSIS. 
We enter here on a somewhat debatable department of Pathology, 
but the investigations of experimental pathology have recently 
given a firmer basis to our knowledge of the subject. 154 
INFECTI V H T UMOKS. 
General Tuberculosis.—We have already seen in the case of 
syphilis that in the secondary stage there is a virus in the blood 
which produces secondary lesions in diverse organs. This secondary 
stage of syphilis has been sometimes compared to a long drawn- 
out fever, and we saw that the symmetrical character of the lesions 
was to be regarded as presumptive evidence that the virus is in the 
blood. 
Now in acute miliary tuberculosis we have a condition in 
which lesions appear in diverse organs and occur symmetrically, 
and it may be well to begin our study of tuberculosis with this 
disease. We have in it an undoubted tuberculosis, and the prin- 
ciples which we are able to establish in regard to this disease will 
afford us a criterion by which we may judge of the nature of other 
processes more doubtfully or less purely tubercular. The disease 
much more closely resembles an acute fever than secondary syphilis 
does, and is often mistaken for typhoid fever. In the course of a 
few weeks there spring up in the lungs, kidneys, liver, lymphatic 
glands, and frequently also in the soft membranes of the brain, 
substance of the heart, spleen, and elsewhere, a multitude of small 
lesions whose structure will be described presently. In the case 
of bilateral organs, such as the kidneys, the little lesions are 
Fig. 52. 
Miliary tubercles in lung. The opaque central parts are caseous. X 16. 
scattered through both, and are present in all parts of each organ. 
Looking at a case of acute miliary tuberculosis, the conclusion 
can hardly be avoided that there is here a virus which has been 
circulating in the blood, and sown wherever the blood has reached, 
although producing its effects only in organs affording a fitting 
nidus for it. tubercle and tuberculosis. 
155 
It may be well here at the outset to inquire what is the structure 
of these multitudinous lesions, each of which is a miliary tubercle. 
They present certain differences in their various situations, but 
there are certain points of agreement in all. If we take a very 
recent case and examine the lung, we shall find an immense num- 
ber of minute nearly globular bodies (Fig. 52), occupying the 
stroma of the lung, and very often either involving a bloodvessel 
or immediately bordering on one. These bodies are the tubercles, 
and whether in the lung or elsewhere, they present a structure 
which is virtually identical in every part. Fig. 53 shows a very 
Fig. 53. 
Tubercle in a bronchial gland. X 350. 
small tubercle from a lymphatic gland, considerably magnified. It 
is seen to be a defined, roundish body, presenting at its peripheral 
parts numbers of round cells like leucocytes; nearer the centre 
rather larger cells, like the formative cells of granulation tissue, 
and often called epithelioid cells; and in its more central parts one 
or more gigantic cells having numerous nuclei, the so-called giant- 
cells. These various structures are not to be distinguished in 
every one of the tubercles, as it depends on the section whether 
their central parts are shown, and, besides, they are liable to de- 
generation, which obscures their structure. 
We can hardly avoid calling these little bodies tumors, and to 
bodies of this kind we shall confine the name tubercles ; these are 
miliary tubercles. 
Their relation to the bloodvessels is often very well seen if the 
soft membranes of the brain are involved. In the adventitia of 
the fine arteries of the pia mater, there will be found aggregations 156 
I NT F E C TIV E T U M O li S . 
of cells, forming sometimes, as in Fig. 54, a prominence on the 
wall, or, if the vessel be small, a spindle-shaped sheath around it. 
The cells constituting the tubercles are prone to undergo caseous 
necrosis so that, as in Fig. 52, the central parts are often markedly 
opaque, and the structure completely obscured. The giant-cells 
are often dotted with fine fat granules, and fatty degeneration fre- 
quently overtakes the greater part of the tubercle. It should be 
Fig. 54. 
Tubercle on artery of pia mater. X 300. 
added that very frequently what appears to the naked eye to be a 
single tubercle often turns out, under the microscope, to he a group 
of two or more, and even when completely coalesced this may still 
be indicated by the caseous metamorphosis having two or more 
distinct centres joined at the periphery. The tubercles contain no 
bloodvessels, and this may partly explain their proneness to caseous 
metamorphosis. 
We have hitherto referred only to the caseous change which 
tubercles undergo, but it has to be added that they are liable also 
to a change which may be called fibrous transformation. We 
have already seen that tubercles contain the elements of inflamma- 
tory new formation, in their details having all the ultimate 
constituents of granulation tissue, except the bloodvessels. They 
may, like the tissue, present a tendency to organization, and be 
converted into masses of hard, solid, connective tissue. It is note- 
worthy that when this occurs the inflammatory products around 
commonly undergo similar changes, making, as a rule, common 
cause with the tubercles whether the change be caseous or fibrous. 
This form is less common than the caseous, and its occurrence is 
probably determined by peculiarities of the constitution or cir- 
cumstances of the individual. 157 
TUBERCLE AND TUBERCULOSIS. 
Connection of Tuberculosis and Inflammation.—In the above 
remarks the structure of the typical tubercle has been described, 
but it is not common to meet with tubercles entirely free from in- 
flammatory complication, although cases of acute miliary tubercu- 
losis do occur in children in which the tubercles are virtually pure. 
In the great majority of cases, however, there are evidences of in- 
flammation around them. In the case of the lung, for instance, 
the alveoli immediately bordering on the tubercle are tilled with 
large cells, the products of catarrhal inflammation, and the walls 
of the alveoli are infiltrated with round cells. These inflammatory 
products frequently make the tubercles appear to the naked eye 
much larger than they really are—the tubercle and inflamed lung 
tissue making a common mass. Throughout the lung also, and 
away from the immediate vicinity of the tubercles, there are often 
evidences of inflammation in the form of serous exudation and 
catarrhal cells in the alveoli. In the pia mater the inflamma- 
tory products are so abundant that they give their character to the 
disease called tubercular meningitis, and by their presence obscure 
the actual tubercles, which are often difficult to see. 
The inflammations which are of nearly constant occurrence in 
connection with tubercles may be accounted for in various ways. 
They may be due directly to the action of the virus, or to an irri- 
tation springing from the mere presence of the tubercles acting as 
foreign bodies. Looking to the case of syphilis where we have 
the virus producing both inflammations and gummata, the pre- 
sumption is that both tubercles and inflammation are to be traced 
to the virus. The tubercles themselves, in their structure, present, 
as we have seen, close analogies to inflammatory products, and to 
syphilitic gummata. We have the same round and epithelioid 
cells. And even the giant-cells are met with in luxuriant granu- 
lations. The new-formed cells in tubercles again are prone to de- 
generation just as those in gummata. The tubercles differ from 
gummata in their small size, a single tubercle being, as a rule, just 
visible to the naked eye; and in the regularity of their structure, 
which, with great uniformity, agrees with the description given 
above. It is interesting that in both these diseases there is such a 
tendency to inflammatory formations, and to the production of 
tumors, which in their structure show such analogies to inflam- 
mation. 
Local Tuberculosis.—We have seen that in acute miliary 
tuberculosis there is something analogous to the secondary stage 
of syphilis in which a virus exists in the blood, and we have now 
to inquire whether there is anything analogous to the tertiary 
stage in which the virus is localized, and the lesions are unsym- 
metrical. Doubtless tubercles, like gummata, may become obsolete, 
and possibly the virus may wear itself out, but it is not known 
that any patient has ever survived a general miliary tuberculosis, 
so that we have here nothing strictly analogous to the tertiary stage. 
But we have such a thing as a Local Tuberculosis, an unsym- 
metrical tubercular lesion. Many instances of this may be adduced, 158 
infective tumors. 
and in all of them there are evidences to be found of similar char- 
acters to those seen in acute general tuberculosis. The existence 
of a virus is indicated by the infective character of the lesions, 
that is to say, the tendency, when the disease has manifested itself 
in a part, to propagate itself in the neighborhood; as if there were 
a virus, which, reproducing itself in the original centre, was 
carried outwards and gave rise to similar lesions around. Again, 
in these local manifestations the tuberculosis is accompanied by 
inflammation, and here, also, the tubercles as well as the inflam- 
matory products tend to undergo changes the chief of which is 
caseous necrosis. 
As an example of this we may take tuberculosis of serous 
cavities, such as the peritoneum or pericardium. If the tubercular 
virus gets into the peritoneum it is carried up and down in it, and 
the result is the production of tubercles in every region of the 
cavity. The tuberculosis is accompanied by inflammation, so that 
tuberculosis of the peritoneum is known under the name of tuber- 
cular peritonitis. The peritoneum, being a lymphatic sac, is di- 
rectly related, as we shall see in connection with the spread of 
cancerous tumors, to the lymphatics in the diaphragm, and through 
the diaphragm with the pleural cavity, which is another lymphatic 
sac. The virus appears to be carried through the diaphragm in 
many cases of tuberculosis of the peritoneum, and produces an 
eruption of tubercles in the lower part of the pleural cavity. 
Take, again, local tuberculosis of the kidney, forming the dis- 
ease sometimes called renal phthisis. When this disease is fully 
developed there are, usually in one kidney, irregular cavities lined 
with ragged ulcers, and these cavities often replace the greater part 
of the kidney tissue. In this disease the course of events seems 
to be this: tubercles are formed at the apices of the pyramids of 
the kidney where they project into the calices, or else in the 
mucous membrane of the pelvis itself. These tubercles in the 
usual way undergo caseous necrosis, and being on a surface, they 
break down and form tubercular Ulcers. Meanwhile the virus 
has extended deeper into the kidney tissue, and a fresh crop of 
tubercles has arisen beyond the ulcer. These tubercles in succes- 
sion undergo caseous necrosis and break down, and at the same 
time fresh crops are formed, so that a progressive destruction of 
the kidney tissue results. (A similar process of ulceration is in- 
dicated in the accompanying illustration (Fig. 55) of a tubercular 
ulcer of the intestine.) But the virus is not only carried inwards 
into the kidney tissue, but also downwards into the pelvis of the 
kidney, and down the ureters. As it is borne along it seems to 
lodge on,these surfaces, and produce similar changes—tubercular 
ulceration of the pelvis, of the kidney, of the ureter, of the 
bladder, and sometimes also of the vesiculae seminales or vasa 
deferentia. From the bladder the ulceration may extend to the 
ureter of the opposite side, but usually it confines itself to the 
portion close to the vesical opening, hardly ascending against the 
current of the urine. tubercle and tuberculosis. 
159 
In the case of renal phthisis we see how the caseous necrosis 
leads to tubercular ulceration, the caseous material be removed, 
and leaving an ulcerated surface, and this case may be taken as 
typical of that process. But sometimes in the ureter the caseous 
material is not carried away, but remains as a dense consistent 
layer, lining the tube, it may be, in its entire length. There are 
cases again in which a local tuberculosis occurring in the midst of 
an organ leads to a considerable accumulation of caseous material. 
Fig. 55. 
Tubercular ulcer of intestine. The rounded form of the tubercles around the ulcer (a) is 
seen, some of them breaking up the muscular coat (ft): one (d) outside this coat, and be- 
neath the peritoneum. X U>. 
A typical instance of this is presented by the scrofulous 
tubercle of the brain. In the brain substance of children we 
sometimes meet with a considerable tumor composed of dense 
caseous material, surrounded by a zone of gray transparent tissue. 
The course of events has been, that a group of tubercles has first 
formed, let us say from the virus having lodged here. These have 
undergone caseous metamorphosis while a fresh crop has been pro- 
duced at their periphery. And so as time elapses there is ever 
fresh new formation of tubercles and their death and degeneration. 
In this way a caseous mass is formed of the remains of myriads of 
dead tubercles. The gray transparent zone at the periphery 
is composed of tubercles not yet degenerated, mixed with inflam- 
matory products. The existence of a virus is here shown by the 
tendency to extend by the successive formation of crops of fresh 
tubercles. 
Artificial Production of Tuberculosis.—In what has gone 
before it has been shown that in acute general tuberculosis there is 160 
infective tumors. 
a virus in the blood producing multitudinous tubercles in various 
organs, it has also appeared that in cases of local tuberculosis 
there is a virus producing tubercles by a process which may 
he called infective, inasmuch as the influence passes out from 
a centre and infects the neighboring tissues. We have now to 
inquire whether the virus can be conveyed from one animal 
to another by inoculation. 
Numerous experimenters since the time of Villemin have shown 
that in certain animals, especially guinea-pigs, it is possible to pro- 
duce a general tuberculosis by inoculation with certain products 
from the body of man. When pieces of a caseous tubercle 
or scrofulous lymphatic gland are inoculated under the skin or 
into the abdominal cavity of a guinea-pig, then the animal in six to 
ten weeks dies of general tuberculosis. Tubercles are found in 
the peritoneum, pleura, kidneys, liver, spleen, bone-marrow, etc. 
By the introduction of the material a virus has been introduced 
which gives rise to the regular tubercular manifestations. 
A local tuberculosis may also be produced by inoculation. In 
Cohnheim’s experiments, for instance, a piece of caseous material 
is introduced by an incision through the cornea into the anterior 
chamber of the eye of a rabbit or guinea-pig. If the substance has 
been so fresh as to contain none of the products of decomposition, 
the irritation produced by its introduction soon passes away, and 
the inoculated substance gets smaller and smaller and may even, 
after a time, disappear. For a time the eye appears quite clear 
and intact. Then suddenly there appears in the iris a larger or 
smaller number of fine gray nodules, which, just as in man, attain 
a certain size and then become caseous. In rabbits this eruption 
of tubercles generally occurs twenty-one days after inoculation, in 
guinea-pigs it is usually a week earlier, although even in rabbits it 
may take place in fourteen days. The tuberculosis may confine 
itself to the eye or it may extend to other organs. 
It is specially interesting that in this case the virus has appar- 
ently a period of incubation of fourteen or twenty-one days, in 
this respect conforming to the viruses of other forms of disease. 
Experiments have also been made in which animals have in- 
spired air containing the sputa of tubercular patients, with the 
result of inducing tuberculosis of the lungs and bronchial glands. 
Again, animals have been fed with tubercular matter, and have 
contracted tuberculosis of the intestines and mesenteric glands, 
and so on. These experiments prove undoubtedly that tubercular 
material contains a virus which is capable of transmission to other 
living animals just as the syphilitic virus is. 
Nature of the Tubercular Virus.—But now the question 
arises, Is this a specific virus only produced by itself, or may it 
arise in the body from other products? Opinions diverge on this 
point. Villemin, whose experiments are the earliest bearing on 
this subject, and Klebs have strongly expressed the view that the 
tubercular virus is specific, and can only be produced by self-prop- TUBERCLE AND TUBERCULOSIS. 
161 
agation. On the other hand, it is held by many that caseous 
material, whether the result of the degeneration of tubercular pro- 
ducts or of those of simple iniiammations, is capable of producing 
tuberculosis. In fact, in the experiments in which tubercular 
material is inoculated, these observers assert that it first produces 
a local inflammation, and that the finely divided material which 
results from the drying in of the inflammatory products is the 
cause of the tubercular eruption. In this connection it may he 
mentioned that acute miliary tuberculosis in man is often sup- 
posed to take its origin in some local mass of caseous material, 
and that local tuberculosis, say of the lung, is frequently, by such 
authors, referred to the products of caseous necrosis in the inflam- 
matory exudation of a simple catarrhal pneumonia. 
This matter we may now regard as finally set at rest by the 
recent discoveries of Koch, already confirmed by several others, 
that the virus of tuberculosis is essentially connected with a par- 
ticular form of micro-organism, a bacillus. These observations, 
establishing as they do the parasitic nature of tuberculosis, com- 
pletely corroborate and carry to their due conclusion the views 
expressed in the preceding pages. By a particular method of 
observation, Koch has succeeded in demonstrating the existence 
of a special bacterium (bacillus) in tubercles, whether occurring 
spontaneously in man and animals or induced by inoculation. 
Fig. 56. 
The bacilli are short rods, a quarter or half the length of a red 
blood-corpuscle (see Fig. 56), but occasionally a little longer. 
They are often in considerable aggregates, especially where the 
tubercular process is advancing, and they frequently exist inside 
the giant-cells. In many cases the rods contain spores, generally 
two to four in each bacillus. 
These organisms have been found in the following diseases— 
general miliary tuberculosis, phthisis pulmonalis, scrofulous tu- 
bercle of the brain, tuberculosis of the intestine, scrofulous disease 
Tubercular bacillus prepared from sputum in phthisis pulmonalis. X 1500. 162 
INFECTIVE TUMORS. 
of lymphatic glands, scrofulous synovitis. They have been found 
also, uniformly, in bovine tuberculosis, in the spontaneous tuber- 
culosis of guinea-pigs, rabbits, and monkeys. They are also 
present in the tubercles produced by inoculation in animals. 
But the bacillus has not only been discovered, it has been culti- 
vated outside the body. It grows in blood-serum, but very slowly, 
and only when the temperature is between 30° and 41° C. The 
organism has been cultivated through many generations, and from 
various forms of tuberculosis, and at the end it has been found to 
retain all its virulence. When introduced it takes about a week 
or ten days to produce any manifest change, but it ultimately gives 
rise to a regular tuberculosis in the internal organs. 
These observations, then, distinctly prove that tuberculosis is a 
specific infective disease. Considering that the bacillus is present 
abundantly in the sputum of phthisis, and gets dispersed every- 
where from that, there is no difficulty in understanding how the 
organism gets into the body. It is clear, however, that in order to 
its development there must be some existing condition of the body 
predisposing. It has already been mentioned that the bacillus is 
of slow growth, and when it is carried into the healthy tissues it 
probably gets eliminated before it undergoes considerable increase. 
In the case of weakly persons, however, the tissues may be less 
able to resist its inroads, and as different persons are variously con- 
stituted the locality of the development will vary. The lungs, 
however, are obviously the favorite seat of attack, and the organism 
is doubtless inhaled. 
According to the views already advanced, the relations of the 
tubercular process and the area covered by it are somewhat more 
extended than many have hitherto acknowledged. Hot only such 
definite tubercular conditions as the scrofulous tubercle of the 
brain, but also pulmonary phthisis, scrofulous disease of the glands, 
etc., are essentially tubercular in their nature. The virus is 
present in all such products, and they are capable of producing 
tuberculosis by inoculation. The domain of tuberculosis therefore 
covers that of scrofula. 
It is here proper to state that histological investigation seems to 
confirm this latter view. Scrofulous disease of the lymphatic 
glands is not a simple inflammatory swelling of them, but tubercles 
of typical structure are to be found in them from the earliest 
period, and the process is as much a tubercular one as the local 
tuberculosis of the brain. It is the same with phthisis pulmonalis. 
There are undoubted inflammatory phenomena here, but tubercles 
are found as well, and although it may be said that the tubercular 
formation is secondary to the degeneration of the inflammatory 
products, the constancy with which tubercles are to be found in the 
earliest periods rather contradicts this view. 
The so-called scrofulous diseases are characterized by a rich new 
formation of cells, apparently inflammatory, in the midst of which 
tubercles are to be found. Both tubercles and inflammatory 
products are prone to undergo caseous necrosis. Here the former TUBERCLE AND TUBERCULOSIS. 
163 
question comes up as to the relation of tlie inflammatory products 
to the specific tubercles. Looking to the fact that these pro- 
ducts undergo precisely the same changes as the tubercles it seems 
reasonable to infer that they are both due to the action of the same 
virus. This is only consistent with what we have seen in the case 
of syphilis where the same virus produces both the inflammatory 
manifestations and the gummata. 
Source of the Tubercular Virus.—There are still some ques- 
tions to be answered after all that has been stated above. If in 
acute miliary tuberculosis we have a virus in the blood, whence 
does it come ? If in local tuberculosis there is a virus, what is its 
source, and how does it reach its local habitation ? 
It has been stated that in acute miliary tuberculosis the virus is 
present in the blood, but this does not quite explain the whole. 
The virus is often present in the blood without producing this 
general tuberculosis. For instance, in phthisis pulmonalis there 
are often a few tubercles in the liver and kidneys, and the virus 
must have reached these organs by the blood. Then in local 
tuberculosis it is difficult to understand how the virus can have 
reached such organs as the kidneys or the joints except by the 
blood. We have already seen that the tubercular bacillus is slow 
of growth, and does not multiply with great rapidity, and the 
probability is that before acute miliary tuberculosis can be produced 
there must be a large accumulation of it in the blood. 
It is often stated that in acute general tuberculosis the source of 
the virus is to be found in some old caseous mass in the body, such 
as a scrofulous tubercle of the brain or a caseous gland. But the 
disease not infrequently occurs without any such caseous focus 
being discovered, and even when a caseous mass exists it is not 
clear how the virus is produced in such quantity as we are led to 
infer. In some cases tuberculosis of the thoracic duct, and in 
others of the branches of the pulmonary artery, has been found 
in acute miliary tuberculosis, and in these we have a sufficient 
source of virus in immediate connection with the blood. It may 
be that careful examination will reveal such sources of supply in 
most cases of this disease, but meanwhile we must wait. It is even 
possible that the virus may sometimes be introduced in a peculiarly 
virulent form. As Virchow long ago pointed out, epidemics of 
general tuberculosis occur, and tlie explanation may be found in 
this. 
In regard to local tuberculosis it is to be presumed that the virus 
is introduced in small quantity, and in order to its propagation two 
things are necessary. In the first place the virus must be allowed 
to tarry in the part, and in the second place it must find a fitting 
nidus. It seems as if the normal tissues had the power of destroy- 
ing small quantities of the virus. But if the tissues are defective 
in vitality, and especially if along with that the blood stagnates in 
them, then we may have the virus, if introduced, propagating 
itself and producing tuberculosis. 164 
INFECTIVE TUMORS. 
The source of the virus is not far to seek. If phthisis pulmon- 
alis is a tubercular disease, and if, as Ivoch and Ehrlich have 
shown, the sputum of such patients contains myriads of the spe- 
cific bacillus, then the air of towns must contain it in abundance, 
and everyone must inhale it. But it is only persons who have 
natural or acquired weaknesses that become the subjects of local 
tuberculosis. 
But the virus may be introduced by the food as well as the air, 
and in this connection it is important to note that the bacillus of 
bovine tuberculosis appears to be identical with that of human 
tuberculosis. There is reason to believe that the milk of tuber- 
cular cows contains the virus, which may thus find access to man. 
The virus then having been introduced by the air or in the food 
may lodge in the lungs or intestine, and, in persons predisposed, 
may develop tubercular disease at the seat of its entrance. But if 
the place of entrance does not afford a fitting nidus, the virus may 
be carried beyond. It will most readily be carried by the lym- 
phatics to the nearest lymphatic glands, and may thence pass into 
the blood. In children it seems as if the virus were peculiarly 
liable to lodge in the mesenteric glands after being taken in by 
the food. 
Again, the virus may get into the blood, but it does not develop 
unless it finds some part of the body fit for its reproduction. In 
many cases of scrofulous and tubercular disease, there has been, 
previous to their development, some injury or disease of the par- 
ticular part in which they have occurred. For instance, in scrofu- 
lous synovitis, there is very commonly some history of an injury 
as the starting-point of the disease, which is really a local tubercu- 
losis of the joint. 
BOVINE TUBERCULOSIS. 
This disease, perhaps better known by its German name of 
Perlsucht, is rather common among cattle. It is a general disease 
manifesting itself in a variety of organs like our own general 
tuberculosis, but running a much slower course. It is an infective 
disease, and has been communicated to the calf, lamb, goat, pig, 
and rabbit, by feeding these animals with milk from an affected 
cow, or with the actual pearl nodules. Like tuberculosis, it is due 
to a virus, which, as we have seen, is the same bacillus as that of 
ordinary tuberculosis; it is generally believed to be hereditary. 
The disease in the cow is characterized, like general tubercu- 
losis, by the formation of numerous isolated or conglomerated 
nodules. They occur chiefly on the serous membranes, in the 
lymphatic glands, and in the lungs. The nodules on the serous 
membranes are the most obvious and characteristic, and it is they 
which have given the disease its commonest name, Perlsucht or 
pearl disease. In the pleura and peritoneum appear vascular 
villous outgrowths in which the nodules ultimately develop (Fig. 
57). These nodules are of various dimensions, mostly about the BOVINE TUBERCULOSIS. 
165 
size of lentils, either sessile or stalked, and very often in the form 
of flat oval bodies crowded together on the surface like duckweed 
in a pool of water. They are liable to become caseous pr ulti- 
mately cretaceous. The lymphatic glands are simultaneously 
affected, especially the thoracic and abdominal ones, and they often 
grow to enormous dimensions, from the formation of nodules in 
them. They also are liable to caseous necrosis or calcareous depo- 
sition. The lungs rarely escape infection, and the nodules here 
frequently coalesce so as to form somewhat large masses, which 
Pig. 57. 
A piece of lung in bovine tuberculosis. On surface of lung many rounded tumors 
are seen, some pendulous. (Vim^iow.) 
tire most abundant towards the surface. These masses are often 
surrounded by distinct capsules, and if softening, which is of 
common occurrence, supervenes, we have cavities lined with a 
distinct connective-tissue membrane. Such cavities are regarded 
by very high authorities, and especially by Virchow, as due to 
dilatation of the bronchi by accumulated secretion. Besides in 
these organs, nodules may occur in the liver, intestine, joints, 
bones, genito-urinary organs, and udder, and in these situations 
they present similar characters to those already referred to. 
In its essential or minute structure the pearl nodule differs little, 
if at all, from the tubercular nodule of the human subject. It is 
made up of a congeries of minute bodies which may be called 
tubercles, consisting of rounded aggregations of cells, the most 
characteristic of which are the giant-cells, which are here even 
more abundant than in ordinary tubercles. It is therefore in its 
general features, and in the peculiar arrangement of its nodules, 
that this disease differs from tuberculosis in man. 
It has been indicated above that the virus of bovine tuberculosis, 
being the same as that in human tuberculosis, may produce the 166 
INFECTIVE TUMORS. 
latter when introduced into the bod}' of man. According to 
Creighton, the resulting lesions often resemble those of bovine 
tuberculosis rather than those of the human form. 
LUPUS. 
This is a disease of the skin, usually of the face, and occasionally 
of neighboring portions of the mucous membrane. It is character- 
ized by the formation of rounded prominences, generally of a 
brownish color, on the surface of which there is often desquama- 
tion of the epidermis. 
On microscopic examination of the rounded prominences (which 
are sometimes called tubercles, in the microscopic sense) they are 
found to consist essentially of granulation tissue. The cutis vera 
has been replaced by an abundantly cellular tissue, the cells mainly 
like leucocytes, but also epithelioid, and even giant-cells. The 
infiltration of the skin also is not homogeneous, but often in dis- 
tinct nodular aggregations resembling tubercles. 
As in the other forms of infective tumor, the cells here present 
a tendency to degeneration. It sometimes happens that the gran- 
ulation tissue is partially absorbed, and partially developed into 
connective tissue, so that a cicatrix results, but it is a cicatrix 
without previous ulceration (lupus non-exedens). In other cases 
the epidermis over the prominences gives way and an ulcer forms, 
the granulation tissue breaking down so as to cause a deep loss of 
substance. The mode of formation of these ulcers is like that of 
the syphilitic ulcer from the gumma, or the tubercular ulcer, and, 
like them, they tend to enlarge by successive new formation of 
lupus tissue at the periphery, and its destruction. In this way 
there may be extensive loss of substance of the skin (lupus 
exedens). There may be a partial healing of the ulcers at one 
part, and advance at another, so that considerable deformities 
result. 
As the disease is an infective one we may presume that it depends 
on a virus, but the nature of the virus is obscure. There are some 
cases in which the syphilitic virus seems to be the cause (syphilitic 
lupus), but these are a very small minority. It is believed by some 
that we have here a local tuberculosis of the skin, and it is possible 
that this view may turn out to be correct. There is, however, this 
objection to it, that it does not appear that the lymphatic glands in 
connection with the lupus become the seat of scrofulous disease. 
LEPROSY. 
This disease is also called Elephantiasis Graecorum. It was at 
one time spread all over Europe, but is now confined to Iceland, 
some parts of Norway and Russia, and the coast of the Mediter- 
ranean. LEPROSY. 
167 
The disease occurs in two forms which are designated lepra 
tuberculosa and lepra ansesthetica. In the first the new formation 
has its seat in the skin or mucous membrane; in the second it is 
the nerves which are affected. 
When it attacks the skin, it is mostly the face and hands which 
are affected, and the legs if they are exposed to the weather. There 
appear larger or smaller swellings, at first red or bluish in color, 
which become firmer and harder. These tubercles may reach the 
Fig. 58. 
Leprosy. The face shows nodular swellings, especially on nose, eyebrows, lips, chin, and 
ears. Patient had also a large ulcer on right leg, and a small one on left. (Virchow.) 
size of a hazel-nut or a walnut. They consist of granulation tissue 
in which cells of the size of leucocytes are most abundant. As in 
other granulation tumors, we often have ulceration, or, as in the 
case of lupus, there may be cicatrization without ulceration. By 
the formation of the swellings and cicatrization, great deformities 
frequently result, so that the patients have often a peculiarly 
hideous appearance, the face being knobbed and gnarled (Fig. 58). 
In the anaesthetic form the nerve-stems become the seat of gran- 
ulation tissue, forming spindle-shaped swellings, sometimes of con- 
siderable length. The granulation tissue here is in the interstitial 
connective tissue, so that the nerve-fibres are separated and com- 
pressed. In the anaesthetic parts it is not uncommon to find gan- 
grene occurring, so that fingers or toes drop off. 
In leprosy there are sometimes tumors formed in internal organs, 
but this is very rare. 
By the researches of Hansen and Heisser, it has been shown that 
leprosy is related to a micro-organism, which closely resembles the 
tubercular bacillus. The bacilli are always to be found in the 
granulation tissue forming the tumors. Their source, however, is 
not so clear. They are not acquired by contagion, and experi- 168 
INFECTIVE TUMORS. 
ment has hitherto failed to produce the disease by inoculation, 
although the possibility of inoculability is not to be denied. The 
fact that leprosy occurs at the present day only among fish-eating 
people may perhaps indicate that the organism has its origin in 
the decomposition of fish, and persons in a low state of health 
eating decomposing fish are liable to be affected by it. 
GLANDERS AND FARCY. 
This is a single disease, although the names to some extent are 
applied separately. It affects chiefly horses, and is called glanders 
when it has its chief seat in the nasal mucous membrane, and farcy 
when the skin is chiefly affected. It is eminently contagious, and 
communicated from animal to animal by inoculation. Occurring 
chiefly among horses and similar animals, it is met with also in 
some of the domestic animals, and is not infrequently communi- 
cated to man, especially to persons who work about horses. 
The disease in horses manifests itself first in the formation of 
swellings of the mucous membrane or skin, consisting of granu- 
lation tissue. The nasal mucous membrane is generally first 
attacked, and there is either a diffuse infiltration of it or else a 
more localized series of swellings like those of lupus. From this 
seat the disease spreads to neighboring lymphatic glands, also 
along the mucous membrane to the lungs and intestinal tract. 
The granulation tissue here, even more than in the other infec- 
tive tumors, tends to break down, so that, as a rule, ulcers soon 
form, which present a great tendency to spread. These ulcers 
arise by what is virtually a suppurative process, and if the tumors 
are situated deep in the skin or mucous membrane there may be 
actual abscesses, which, by bursting, form ulcers. If the ulcers 
heal, cicatrices are formed in the usual way. 
The manifestations in internal parts are largely inflammatory in 
character. The lymphatic glands of the neck are the seat of 
inflammatory swelling. In the lungs there are nodules either con- 
sisting of granulation tissue with caseous central parts, or more 
distinctly pneumonic. There are also in the mucous membrane 
of the intestinal canal nodules which are sometimes more solid, at 
other times breaking down into pus. 
It is to be added that the above description applies to the acute 
cases, which are the commoner, but that the disease is sometimes 
chronic in its course. Chronic cases have usually the nodules in 
the skin, and there are secondary tumors in the muscles, etc. 
In man, glanders is usually an acute, rapidly fatal disease. There 
are nodules and ulcers in the mucous membranes and the skin, and 
frequently phlegmonous inflammation of the skin with abscesses 
among the muscles, etc. In fact, in man the disease takes the 
inflammatory character more distinctly than in the horse. We may 
have in man also nodules, ulcers, and abscesses in internal organs. 
It is clear that we have in this disease a virulent agent, but the 
nature of it is unknown. TUMORS OR MORBID GROWTHS. 
Definition.—A tumor means literally a swelling, and formerly 
any swelling was called a tumor. Tumor, for example, is often 
named as one of the cardinal signs of inflammation, and it is still 
customary to speak of the inflammatory tumor. But now-a-days 
the use of the word has become limited' it is applied to a class of 
new formations of which it is difficult to give a strict definition. 
It may he said that tumors are pieces of tissue which have a life 
and growth of their own irrespective of the needs of the organism, 
and of the general local conditions around them. The structure 
of a tumor does not differ in any essential particular from that of 
normal tissues; in its elements it is wholly analogous to what may 
he found in the physiological tissues. It is nourished by the same 
blood, its bloodvessels being continuous with those of surrounding 
parts, its nerves are connected with neighboring nerve-stems, and 
its tissue, if not always similar to that near it, is frequently iden- 
tical. But it grows independently and without apparent object. 
Thus a fatty tumor goes on increasing in size irrespective of the 
adipose tissue in which it has its seat, and the person may be 
reduced to the greatest emaciation, most of the ordinary fat being 
absorbed, while little or no impression is made upon the fatty 
tumor. 
It may here be said that tumors usually arise in the midst of 
tissues of their own nature, and when they do so, they may be 
called homologous. But they not infrequently arise in the midst 
of tissue of a different kind, a tumor composed of muscular tissue, 
for instance, in the kidney, and they are then called heterologous. 
These words were at one time used to express the distinction, that 
in the one case the tissue corresponds to the tissue of the body and 
in the other is different from the tissue of the body. But as the 
tissues of tumors correspond in their structure to the physiological 
tissues, there is no such thing as heterolog}T in this sense. 
Origin and Development of Tumors.—In the definition given of 
tumors we have seen that they are composed of tissue which follows 
in its structure the normal tissues, but grows without reference to 
the needs of the organism. We have here to inquire how this piece 
of abnormally growing tissue takes origin. 
For the most part it may be asserted that it arises in tissue of its 
own nature, and that it grows by a process perfectly analogous to 
that of its own kind of tissue. Even in the case of heterologous 
tumors this is, at the outset, true. A muscular tumor, whatever 170 
TUMORS OR MORBID GROWTHS. 
its seat, must have had embryonic muscle as its primordial basis, 
and it grows by a process analogous to the growth of muscle. But 
most tumors in their primary position are strictly homologous, and 
their tissue presumably has its origin along with that of the tissue 
in which they have their seat. A fatty tumor has its seat among 
the adipose tissue, and is at the first a piece of fat indistinguishable 
from that which surrounds it. We have to inquire how it is that 
this particular piece of adipose tissue has taken upon itself this 
peculiar and unusual development. 
An explanation has been recently suggested by Cohnheim, and 
enforced by cogent arguments and ingenious experiments per- 
formed by him and his pupils. Let it be supposed that the pri- 
mordial tumor is a piece of tissue left over as it were from the 
embryonic state, and retaining unabated much of the embryonic 
power of growth and development, and much of the special phe- 
nomena of tumors will be explained. 
In the normal growth of the body the various tissues go on repro- 
ducing themselves up to a certain point, but they stop short when 
they have produced the proper amount of tissue for the needs 
of the organism. The finer details of this process are largely 
governed by heredity, but it is clear that there is a law in the 
organism regulating the growth of the tissues in relation to each 
other and to the organism as a whole. It may be presumed that 
the embryonic basis of each tissue starts with a great power of 
new formation, but this power is strictly under command of the 
organism as a whole. 
But if a piece of embryonic tissue be taken out of its normal 
relations and placed in a position favorable to its further growth, 
then it may perhaps grow on irrespective of the needs of the 
organism, and develop something in the nature of a tumor. We 
have already referred to a case in which a process like this occurs. 
When the spur of a cock is transplanted to the comb, it grows 
rapidly, and l3y and by forms a prominent tumor. Here is a piece 
of tissue removed from its proper relations into a position more 
favorable for its growth in respect to blood-supply, and it grows 
with a very special vigor. Again, Leopold has found that it is 
possible to transplant cartilage from a living animal into the 
anterior chamber of the eye, where it acquires vascular connec- 
tions with the iris. If foetal cartilage be used, it grows in its new 
position and may form a distinct tumor of some size, but if it be 
cartilage from an animal after birth it does not show the same 
vigor. It appears also that the earlier the period of development 
of the embryo from which the cartilage is taken, the more likely 
is there to be a vigorous growth in the new position. 
These facts would indicate that the normal tissues may under 
unusual circumstances, when they are disconnected from their 
normal relations, assume an independent growth, and the tissues 
of the embryo are more capable of this independent growth than 
those of the fully developed animal. 
But there are some facts in the pathology of tumors themselves 171 
GROWTH ANI) EXTENSION OF TUMORS. 
which indicate that in some cases, at least, they take origin in 
pieces of tissue left over, as it were, from the embryo. There are 
tumors which arise, as it is said, by inclusion. A very striking 
instance of this is the so-called sacral teratoma. In these tumors 
almost all the tissues of the body may be present, and sometimes 
there are parts as of a foetus. There seems no doubt that in this 
case, at an early period, a whole embryo has been included inside 
the foetus, and the person is born with an embryo included in his 
tissues. The various embryonic tissues grow in their abnormal 
position not altogether indiscriminately. 
Again, tumors of striped muscle have been found in the kidneys 
and other parts of the urino-genital system. The explanation of 
this seems to be that the Wolffian body from which the kidneys 
are developed is, in the embryo, close to the corneous and vertebral 
layers, and portions of these being included in the Wolffian body, 
in the embryonic state, they may afterwards develop into tumors. 
Again, it is not uncommon to find tumors developing in after- 
life from congenital moles or soft warts. These little outgrowths 
present throughout life a somewhat rudimentary structure, but 
they lie quiescent for many years, till suddenly, it may be, they 
present an extraordinary power of growth and develop tumors. 
It may then perhaps be presumed that in the case of many 
tumors they take origin in pieces of tissue left over from the em- 
bryo, and retaining largely their power of growth. 
But this does not apply to all tumors, and especially it does not 
apply to cancers. We shall afterwards see that these tumors do 
not grow from a single piece of tissue, but that in a considerable 
and extending area, the existing epithelial structures take on an 
unusual growth. At the marginal parts of an epithelioma of the 
tongue, for instance, it can nearly always be seen how the normal 
epithelium is extending and penetrating inwards; and again, a 
cancer of the kidney appears to arise and advance by transforma- 
tion of the existing tissue of the organ. It appears, therefore, that 
in this case the tumor arises from the existing normal structures, 
and that we must look for some abnormal impulse inducing it to 
grow outrageously. 
In the case of cancers and sarcomas the abnormal impulse is not 
infrequently related in some way to a traumatic cause. Many 
tumors are referred by patients to injuries received, although there 
must be some local peculiarity before a simple injury can produce 
such effects. 
Growth and Extension of Tumors.—For the most part, tumors 
enlarge by a new formation of tissue within themselves, just as 
the normal tissues increase during the period of growth. The 
tissue of the tumor is sometimes continuous with that of surround- 
ing parts, sometimes it is separated by a capsule composed of 
connective tissue; sometimes it begins by being continuous and 
afterwards gets separated. In any case the ordinary tumor simply 
grows by new formation of its own tissue. It often produces 172 
TUMORS OR MORBID GROWTHS. 
effects on neighboring parts, by pressure especially, but apart from 
these merely mechanical effects, it does not prejudice neighboring 
structures. Tumors possessing these characters are usually called 
SIMPLE OR INNOCENT growths. 
But then there are tumors of which this is not true. They have 
a tendency to grow into and infiltrate neighboring tissues, present- 
ing characters of what may be designated local malignancy. This 
is peculiarly the case with sarcomas and cancers.. In the case of 
sarcomas the tumor seems to penetrate into and develop, as it were, 
on the mould of the existing tissue—apparently very much in the 
style that a thrombus or a piece of catgut in the tissue is replaced 
by granulation-tissue which moulds itself on it. For instance, a 
sarcoma may penetrate through a bloodvessel, replacing and taking 
the shape of a thrombus in the vessel. In the case of cancers, on 
the other hand, their tissue, which is epithelial in character, pene- 
trates among the tissues, largely destroying them and producing 
inflammatory disturbances. 
There is another peculiarity which certain tumors show, and 
particularly the sarcomas and cancers, namely, metastasis or gen- 
eralization, which is another feature of malignancy. In the case 
of these tumors, secondary growths spring up in parts removed 
from the primary tumor. Doubtless something is carried from 
the original tumor to the remote part, and we have to inquire by 
what path this is carried, or what may be the nature of the material. 
In the case of cancers the epithelial processes penetrating into the 
tissues readily find their way into the lymphatic spaces. Around 
a cancer there are often indications under the microscope that the 
lymphatics are filled with epithelial masses. From these growths 
in the lymphatic spaces material may be carried off to distant parts 
of the lymphatic system and cause secondary tumors to form there. 
Thus, a cancerous tumor sometimes penetrates into the peritoneal 
cavity, which, of course, is a lymph-sac, and secondary tumors 
are sown uji and down the peritoneum. The lymph-sac of the 
peritoneum communicates with that of the pleura by lymphatic 
channels which pass through the diaphragm, and it is quite 
common to find the cancerous growth extending into these chan- 
nels, and through them into the pleura, producing secondary 
tumors there. In other cases the secondary tumors spring up in 
the lymphatic glands, and it is always those to which the lym- 
phatics around the tumor pass that are first involved, something 
passing off from the epithelial processes in the lymph-spaces and 
being conveyed to the lymphatic glands. 
While this is the course in cancers, we find that in sarcomas if 
metastasis occurs it is by the tumor penetrating through the walls 
of bloodvessels. The material from the tumor is therefore carried 
by the blood, and as it is mostly the thin-walled veins which are 
thus opened into, the metastasis is usually in this case to the lungs. 
As to the nature of the material which passes from the tumor, it 
must be either something dissolved in the juices, or else solid par- 
ticles of some kind. Looking to a secondary cancerous infection SECONDARY changes in tumors. 
173 
of the peritoneum, we can hardly escape the conclusion that it is a 
finely divided solid. The secondary tumors are not regularly dis- 
tributed over the peritoneal surface, but occur here and there or in 
groups, just as if solid particles had been carried and produced 
their effects where they got leave to lie. Then also it must be 
solid particles which are arrested by the lymphatic glands and give 
rise to the secondary tumors there, as it were, by embolism. The 
probability is that the actual cells of the tumor are carried oft' and 
deposited at a distance. Perhaps it is not the fully developed cells, 
but small rudimentary ones. 
In this connection it is important to note that the secondary 
tumor for the most part exactly reproduces the tissue of the 
original one, even to the smallest details, and it is natural under 
these circumstances to believe that pieces of the original tumor 
are actually transported. 
It has already been stated that sarcomas and cancers are the 
tumors which regularly present a malignant tendency, but on rare 
occasions other tumors also do so. Cartilaginous tumors are not 
infrequently malignant. Next to them mucous-tissue tumors most 
frequently become malignant, but even fibrous tumors have been ob- 
served to do so, and lately Cohnheim has recorded a case of colloid 
goitre in which secondary tumors occurred. So that malignancy 
is not confined to sarcomas and cancers. On the other hand, tumors 
having the structure of sarcomas may remain local to the end. 
It has been usual to believe that this malignancy is dependent 
on peculiarities of the tumor itself. And when a simple tumor, 
as sometimes happens, assumes malignant characters, it usually 
assumes the structure of a sarcoma or cancer. Lately Cohnheim 
has started another theory, according to which the peculiarity is 
not in the tumor but in the normal tissues. In the case of a 
simple tumor the normal tissues are able to prevent its tissue from 
penetrating into them, but in the case of malignant tumors the 
tissues have become weakened and are unable to form a barrier to 
their extension. When a simple tumor becomes sarcomatous, it 
is because the tissues around have assumed a peculiar weakness. 
When pieces of a tumor are transported to a distance, a struggle, 
as it were, occurs between the tendency of the tissue of the tumor 
to grow, and that of the normal tissues to prevent its growth. In 
the case of a simple tumor the tissues assume the upper hand, and 
cause the absorption of the tumor-tissue. In the case of malignant 
tumors, however, the tissues are too weak to accomplish this, and 
the secondary tumor develops. This theory is too strained, and 
all the facts are much better explained by supposing a special 
power of growth in the tumor. When a secondary infection of 
the peritoneum is examined, it is difficult to believe that there is 
anything but a peculiarly active agent and not any specialty in 
the peritoneal tissue. 
We have still to consider certain secondary changes to which 
tumors are liable. They are exposed to the same pathological pro- 174 
TUMORS OR MORBID GROWTHS. 
cesses as normal tissues, and in a higher degree. Thus we meet 
with fatty degeneration, which is common, especially in quickly 
growfing tumors; calcareous infiltration in structures which are 
obsolete; hemorrhages, principally in superficial rapidly growing 
tumors, when the bloodvessels are ill-formed; and necrosis mostly 
in tumors near the surface and thus exposed to mechanical irrita- 
tion, the consequences of such necrosis being ulceration with, it 
may be, suppuration, hemorrhage, decomposition. 
Conditions like those last named will seriously affect the or- 
ganism as a whole, and they will occur most frequently in the case 
of malignant tumors, which grow quickly, and rapidly come to 
the surface. Malignant tumors also affect the organism as a whole 
by the readiness with which they extend to or produce secondary 
tumors in important organs, and secondary cancers frequently also 
induce inflammations, as in the case of the peritoneum or pleura. 
It is clear therefore that malignant tumors, especially by bleed- 
ing, by ulcerating and sloughing, by invading important parts, by 
producing inflammations, etc., have a tendency to deteriorate the 
system, producing amemia and general weakness. If growing 
quickly, they also tend to emaciate by using up'the nutritive 
material of the body. A simple tumor, if it happens to be at the 
surface and exposed to mechanical violence, may also ulcerate and 
produce serious constitutional results, but it will be mainly in the 
case of malignant tumors that these results will follow. To these 
conditions of the body as a whole the name cachexia is often 
given. Sometimes also the term dyscrasia or diathesis is used 
with the meaning that there is some peculiar condition of the 
system preceding and inducing the formation of malignant tumors, 
but of this there is no evidence, and the changes in the general 
condition are always secondary. 
CLASSIFICATION. 
In considering the individual forms of tumors the simplest pos- 
sible method of classification will be adopted. In a work pro- 
fessedly on pathology it will be admitted that the structure of a 
tumor is the essential basis of classification and nomenclature, and 
in what follows terms will be used in what may be called their 
anatomical sense. It may be clinically convenient to designate 
tumors which present malignant properties as cancers, but it will 
not do here to group together in one class tumors of totally 
different structure. 
The various tumors will be divided into three groups. In the 
first will be included tumors whose tissue reproduces a single 
simple physiological tissue, such as adipose tissue, connective tissue, 
bone. In the second group are tumors into whose structure more 
than one simple tissue enters, such as tumors consisting of such 
complex structures as papillae, or even made up of a systematic 
formation of bone, skin, etc. In the last group we have tumors SECONDARY CHANGES IN TUMORS. 
175 
which are mainly composed of cells, or in which cells predominate. 
The individual cells are not different from those of the normal 
tissues, but there is an enormous new formation of them, with 
little tendency in them to develop into a proper physiological 
tissue. The first group may be called simple-tissue tumors, the 
second compound-tissue tumors, and the third cellular tumors. 
This classification, it may be remarked, is only used for conveni- 
ence, and does not lay claim to logical consistency. 
A very great advance has been made in our knowledge of tumors 
by the publication of Virchow’s classical work, Die krankhaften 
Geschwiilste. From this work many of the following illustrations 
are borrowed by the kindness of the author. A.—SIMPLE-TISSUE TUMORS. 
1. THE CONNECTIVE-TISSUE TUMOR OR FIBROMA. 
We have already abundantly seen that connective tissue is fre- 
quently produced in inflammations, and it is not surprising to find 
that one class of connective-tissue tumor lies on the borderland of 
inflammations and tumors. 
Fig. 59. 
Elephantiasis verrucosa from the labia majora. A tumor the size of a child’s head, withfa 
small base. The surface is lobulated, and each lobule presents warty projections, some fine 
and delicate, others thick and knobbed. The epidermis is everywhere somewhat thick. The 
internal parts are composed of thick, interlacing connective tissue, which is oedematous. 
(Virchow.) 
Elephantiasis arabum (E. grsecorum is leprosy) is a localized 
thickening of the skin, beginning in attacks resembling erysipelas, 
at first passing oft' and then recurring. There is finally a perma- 
nently progressive and apparently unaccountable new formation 
of connective tissue, and so the characters of a tumor are assumed. 
The tissue produced is a loose, succulent connective tissue, like 177 
CONNECTIVE-TISSUE TUMOR. 
that of the skin, but containing more cells, and so more like in- 
flammatory tissue. The epidermis is also thickened, so that the 
whole partakes of the character of an exaggerated hypertrophy of 
the skin (Fig. 59). The new formation 
may extend inwards to the fascire, the in- 
termuscular tissue, and even to the perios- 
teum, inducing thickening of the bones 
(Fig. 60). 
The conditions here present considerable 
analogies with those in the infective tumors. 
There is in both a spreading new formation 
of tissue like that produced in inflamma- 
tion, although in the present case the tissue 
does not remain so long in the granulation 
stage. To one of those forms of tumors, 
namely leprosy, there is the further resem- 
blance, that elephantiasis is endemic in 
certain localities. All these facts may be 
held as pointing to the inference that this 
disease is due to a virus of a similar nature 
to that of leprosy. The resemblance in 
pathology of the two diseases is further 
indicated by both having been designated 
by the same name, the disease under con- 
sideration being E. arabum, and leprosy E. 
graecorum. The disease is frequently re- 
garded as taking origin in obstruction of 
the lymphatics. This view is supported by 
the fact that the new-formed tissue is gen- 
erally very succulent, as if the spaces were 
overfilled with lymph, and there are some*- 
times dilated lymphatics visible in the 
hypertrophied skin. The obstruction pro- 
duced by filaria sanguinis (see section on 
Parasites) in the lymphatic glands has been 
assigned as the cause, as well as mere 
simple indurations of the glands. 
The commonest seat of elephantiasis is 
the leg, and here alone is the name prop- 
erly applicable; but it is also very frequent 
in the external generative organs. It occurs 
also not infrequently in a localized piece 
of skin, especially in the scrotum or labia 
pudendi, where a prominent outgrowth is 
the result. This may assume very large 
dimensions, becoming by and by pendulous. To such tumors 
Paget gives the name Cutaneous outgrowths, and they sometimes 
grow to enormous size, hanging down from the genital organs as 
far as the knee. The surface of the skin in these tumors, as well 
as in the more simple cases of elephantiasis, has a rough tuber- 
Fig. 60. 
Hyperostosis and synostosis 
of the bones of the leg and foot 
in elephantiasis. The bones 
present evei-ywhere flat or 
pointed projections. At +-+ 
the tibia and fibula are united, 
as they are also above the 
ankle-joint. The astragalus 
and os calcis are also united. 
(Virchow.) 178 
SIMPLE-TISSUE TUMORS. 
culated appearance, and sometimes a highly warty aspect, as in 
Fig. 59. 
Smaller tumors of similar structure sometimes occur in large 
numbers, and to these the name Molluscum fibrosum, or fibroma 
molluscum, or even elephantiasis mollusca is given. There are 
cases of elephantiasis having a certain resemblance to molluscum, 
inasmuch as there are multiple tumors outside the main one, and 
the growth seems to he increasing by the coalescence of these. 
These tumors at the margins are sometimes related to the seba- 
ceous glands, and appear to be formed around them. In the 
proper molluscum, however, w7e have multiple isolated tumors 
beginning as little growths of connective tissue in diverse regions 
of the skin, by and by growing out and becoming pendulous. 
Thus we may have hundreds of more or less pendulous tumors in 
various parts of the body. This purely fibrous molluscum must 
be carefully distinguished from molluscum contagiosum, a totally 
different disease, which will be considered in the section on Dis- 
eases of the Skin. 
In all the forms hitherto described the tumors have been con- 
tinuous with the skin. Tumors are sometimes met with, however, 
composed of a similar soft connective tissue, but enclosed in a 
capsule, so that they are separable from the skin. To these Paget 
gives the name Fibro-cellular tumors, and they are met with 
chiefly in the same regions (namely the external organs of genera- 
tion) as the fibro-cellular or cutaneous outgrowths with which 
they may be combined, the skin over the tumors being greatly 
thickened. 
Hard Fibromas or true Fibromas are exceedingly dense tumors 
composed of firm connective tissue tightly interlaced, and resem- 
bling tendon in its structure. On section they show a brilliant 
white surface, and often a concentric arrangement of the connec- 
tive-tissue bundles. We do not include here the uterine fibromas, 
which are really muscular tumors, and will be described as such. 
Fibromas are frequent in connection with periosteum and bone, 
especially on the jaws. Growing from the periosteum, they are 
sometimes intimately connected with the bone, which may be as if 
buried in the tumor. Sometimes the fibroma originates inside a 
bone. Fibromas also occur on fascias and membranes, as the dura 
mater, also rarely in the subcutaneous tissue and on nerve-stems. 
Just as dense connective tissue formed in chronic inflammation 
may become calcified, so may dense fibromas be partially infil- 
trated with lime-salts. 
2.—THE FATTY TUMOR OR LIPOMA, 
This form of tumor consists of adipose tissue exactly like that 
of the body, as for instance the subcutaneous adipose tissue. Adi- 
pose tissue contains bands of fibrous connective tissue which carry FATTY TUMOR OR LIPOMA. 
179 
the vessels and nerves, and so do lipomas, but in different tumors 
this is variously abundant, the hardness or softness of the tumor 
depending on this. If there is little connective tissue, the tumor 
will be soft, and may even feel fluctuant. If there is much, it will 
be hard, and we may even have an approach to the fibrous tumor, 
the fibro-lipoma. The fibrous character may be increased oy irri- 
tation, as where a tumor is exposed to friction, producing a kind 
of productive inflammation in the tumor. 
Fatty tumors are mostly surrounded by a distinct capsule, but 
sometimes they are continuous with the surrounding fat. Thus 
the fat around the mamma may undergo such an enlargement as 
to warrant the name of tumor (Lipoma capsulare). Billroth men- 
tions a lipoma which had grown in between the muscles of the 
thigh in such a way as that it could not be removed completely. 
Lipomas which are not definitely circumscribed may be called 
DIFFUSE LIPOMAS. 
Lipomas are of common occurrence. Their most frequent seat 
is under the skin, especially of the trunk. They are rare under 
mucous membranes, as that of the stomach (Fig. 61), were there 
Fig. 61. 
Lipoma in the wall of the stomach. It was the size of a hazel-nut, situated near the 
pylorus in the submucous tissue. Natural size. (Virchow.) 
is normally a small quantity of fat corresponding with the sub- 
cutaneous fat. They are occasionally met with in connection 
with serous and synovial membranes, in the appendices epiploicae 
of the intestines or the synovial fringes. Very rarely they occur 
where fat is not present normally, as in the kidneys, brain, etc. 
The author met with a case in which an elongated piece of fat lay 
on the upper surface of the corpus callosum. Lipomas are for the 
most part single, rarely multiple. 
Fatty tumors sometimes become pendulous. Those in the ap- 
pendices epiploicse (Fig. 62) are so from the first, and the neck of 
the polypoid tumor may get severed, the tumor becoming a loose 180 
SIMPLE-TISSUE TUMORS. 
body in the peritoneum; it is similar with the lipomas of the 
synovial fringes. But subcutaneous lipomas may become pendu- 
lous and polypoid, and may grow to great dimensions in this form. 
There is apt to be ulceration of the surface of such tumors, and 
even hemorrhage. Besides these changes we have the occasional 
Fig. 62. 
Pendulous lipoma of appendices epiploicm of colon. A pedunculated tumor (a) projects 
from the general mass of subserous adipose tissue (b). It is twisted twice on its axis, and 
the peduncle is very thin. (Virchow.) 
induration already mentioned, and sometimes calcareous infiltra- 
tion follows. Softening with the formation of a cyst inside the 
tumor is a rare occurrence. 
3.—THE MUCOUS-TISSUE TUMOE OE MYXOMA. 
This form of tumor is composed of mucous tissue, and as this 
is not one of the physiological tissues of the adult, it will be proper 
to refer more specially to its characters. The bloodvessels of the 
umbilical cord are padded and protected from pressure by a 
gelatinous substance called Wharton’s jelly. Under the micro- 
scope, this consists of variously shaped cells separated by a clear, 
transparent, intercellular substance. The intercellular substance 
is of gelatinous consistence, and owes this character to the fact 
that it consists of a watery solution of mucin. This substance is 
nearly allied to albumen, but has the physical characters that, 
when present in even small quantity in a solution, it gives it a 
sticky gelatinous character. Its chemical reactions also differ from 
those of albumen, in respect that though like it precipitated by 
alcohol, the precipitate is redissolved by water. Also, acetic acid 
and other organic acids precipitate mucin, but not usually albu- MUCOUS-TISSUE TUMOR OR MYXOMA. 
181 
men. The precipitate of mucin by alcohol or acetic acid is more 
membranous than that of albumen. The reaction with acetic acid 
can be readily brought out in Wharton’s jelly, a microscopic 
section showing, on adding acetic acid, a reticulated precipitate. 
These reactions can also be studied in the mucus from any mucous 
membrane, or in the bile, in which mucin is normally one of the 
dissolved constituents. 
Besides, in the umbilical cord, mucous tissue is present in the 
villi of the chorion of the fcetus, the villi consisting of a covering 
layer of epithelium with mucous tissue internally. In the foetus, 
it is also present in early stages in the subcutaneous tissue where 
Fig. 63. 
Portion of a hydatid m.ole showing the berry-like masses. Natural size. (Virchow.) 
it has the place of the subcutaneous adipose tissue, being, in fact, 
related to fat very much as the temporary cartilage is to hone. 
Some remains of this tissue may be met with in the adult. Thus, 
the vitreous humor of the eye is really composed of soft mucous 
tissue, and traces of it have been found in places where normally 
adipose tissue exists, as under the pericardium, at the hilus of the 
kidney, subcutaneously and in the medulla of bone. It appears 
that in these positions there is sometimes a partial recurrence to 182 
simple-tissue tumors. 
the foetal condition. The connective substance of the brain, the 
neuroglia, is allied to mucous tissue, and seems to present a prone- 
ness to return to that form. 
Of mucous-tissue tumors a very interesting form is the hydatid 
mole. Here the mucous tissue of the villi of the chorion under- 
goes great increase, and the result is the transformation of the villi 
into congeries of oval, cyst-like bodies which hang like grapes on 
a stalk, and often hang one on the other (Fig. 63). Thus a bulky 
mass often results, consisting of an enormous multitude of these 
berry-like cysts. If the change has begun early in foetal life, then 
the whole chorion is thus converted; if later, when the villi have 
become confined to the placental surface, then only one surface is 
affected. The dead and blighted foetus will be found inside the 
mass, generally in an early stage of development, but sometimes 
more advanced. 
Proper mucous-tissue tumors are met with principally in the 
subcutaneous tissue, where they may be regarded as perhaps due 
to a piece of embryonic tissue left over when the mucous tissue 
was converted into adipose, in this respect resembling the chon- 
dromas of bone. They form rounded or oval tumors generally 
soft, sometimes almost fluctuant in consistence and gelatinous in 
appearance. Examined under the microscope we have a very 
translucent tissue in the midst of which there are irregularly 
shaped cells. The tissue is intersected by more or less frequent 
bands of connective tissue (Fig. 64). The proportion of cells varies 
Fig. 64. 
Microscopic section of a myxoma of the subcutaneous tissue. Isolated cells and strands 
of fibres are shown. Between them a clear gelatinous material was present. X 350. 
considerably in different cases, and even in different parts of the 
same tumor. 
Myxomas are also of somewhat frequent occurrence in the brain 
as compared with other tumors in this organ. Here they some- 
times grow to considerable size, and are liable by softening to take MUCOUS-TISSUE TUMOR OR MYXOMA. 
183 
the form of cysts tilled with a mucous fluid. They are also met 
with oil peripheral nerves. They occur in the mamma, where not 
infrequently they appear to have the character of a diffuse forma- 
tion of mucous tissue between the glandular acini, so that the 
gland as a whole is converted into a tumor. In the salivary glands 
they occur, but are usually of mixed structure, being partly formed 
of other kinds of tissues. 
Considering the relations of adipose tissue and mucous tissue it 
is not remarkable that mixed forms occur in which apparently a 
Fig. 65. 
Malignant myxoma lipomatodes of the long saphenous nerve. A, Section. B, External 
appearance. The tumor measured 2\ X 13 inches. At A, the nerve-fibres are seen to be for 
the most part on the outside of the tumor, which, however, was completely covered by the neuri- 
lemma. Internally the tumor is lobulated, and it presented a gelatinous appearance, but 
somewhat opaque. A similar tumor was seated on the short saphenous nerve. (Virchow.) 
partial conversion of the myxoma into a lipoma is in progress, 
or conversely a metamorphosis of the lipoma. Then also the 
myxomas vary very greatly in the proportion of cells, the very 
cellular ones being called medullary myxomas, and frequently 
graduating into sarcomas. In fact, with pathologists who take the 
embryonic nature of the tissue as the criterion of sarcomas, the 
fact that mucous tissue is the embryonic precursor of adipose 184 
SIMPLE-TISSUE TUMORS. 
tissue induces them to class this form of tumor among the sar- 
comas. Consistently with these facts there are some myxomas 
which show malignant characters, either local or general. In a 
case recorded by Virchow (Fig. 65) there were tumors on the. 
nerves and in the dura mater of the cord and brain. 
4.—THE CARTILAGINOUS TUMOR OR CHONDROMA. 
This tumor is composed of cartilaginous tissue. The cartilage 
may be hyaline or fibrous, generally the latter. The tumor is also 
intersected with fibrous bands which carry bloodvessels that nourish 
the tissue. If a cartilaginous tumor grows in connection with and 
out from cartilage it is called an Ecciiondrosis, but if, as in the 
majority of cases, it grows in connection with other tissues, then 
it is called an Enchondroma. The term chondroma of course 
includes both. 
The ecchondroses are usually small unimportant outgrowths 
chiefly of the cartilages of the larynx and trachea and ribs. 
Virchow has described an interesting form of so-called ecclion- 
drosis at the basilar portion of the occipital and sphenoid bones. 
The basilar parts of these bones are formed from cartilage, and in 
adult life they are united, forming a single bone (os tribasilare). 
The junction takes place irregularly by a kind of toothed union. 
In this process a little bit of cartilage may be omitted, and this 
sometimes develops into a little tumor just under the basilar artery, 
to which it may be adherent. It will be seen that we have here 
an actual instance of a little piece of embryonic tissue left over to 
develop afterwards into a tumor. This little tumor sometimes 
undergoes a remarkable change; the 
cells swell up and become like those of 
the chorda dorsalis, but in other cases 
it ossifies. 
The cartilaginous loose bodies in 
joints are sometimes regarded as origi- 
nally outgrowths from the cartilages 
or synovial fringes which have been 
broken off and grown after their sepa- 
ration. 
Enchondromas are mostly met with in 
connection with Bones. As bones are 
developed out of cartilage for the most 
part, it may be supposed that little bits 
of the embryonic cartilage are left over 
and develop into tumors afterwards. 
The enchondromas of bone may be di- 
vided into central and peripheral, ac- 
cording as they originate in the medulla or at the surface. The 
former are the more common, and they are met with chiefly in 
early life, occurring especially in the fingers and toes, which may 
Fig. 66. 
Multiple internal enchondromata 
of fingers. (Cornil and Ranvier.) THE BONY TUMOR OR OSTEOMA. 
185 
he the seat of multiple tumors as in Fig. 66. These tumors 
begin inside the phalanges or metacarpal bones, or, less frequently, 
the analogous hones of the foot. Growing inside the hones they 
may he for a time unperceived, but afterwards swell up the hones 
and may even hurst through the external shell. These tumors 
often show a local malignancy, growing by the formation of new 
nodules in the tissue around. The peripheral chondromas are met 
with most frequently on the femur and pelvis, and most rarely on 
the bones of the face and skull. 
In soft parts chondromas are found occasionally, hut are com- 
monly mixed with fibrous, mucous, glandular, sarcomatous, or 
cancerous tissue. They are particularly frequent in glands, as the 
testes, ovaries, mammae, or salivary glands. In these situations 
they are occasionally found to follow chronic irritations. 
In their form chondromas are generally rounded tumors and 
distinctly encapsuled, but if large they are lobulated. 
It has already been said that the enchondromas are often mixed 
with other tissue, and it is to he added that secondary changes are 
not infrequent. They sometimes soften, and this is frequently due 
to partial transformation into mucous tissue. This is particularly 
the case with the glandular enchondromas. On the other hand, 
those of hone are liable to ossify. 
Lastly, chondromas are liable, as has already been said, to show 
a certain malignancy, forming secondary tumors, especially in the 
lungs. This is connected with the frequently mixed character of 
these tumors, and their association especially with sarcomas and 
cancers. 
5.—THE BONY TUMOR OR OSTEOMA 
In this class are included tumors composed of bone, not mere 
new formations due to inflammation, nor tumors in which bone 
exists as a subordinate element with other tissue. 
The immense majority of bony tumors grow from bone, and are 
hence called exostoses. In regard to their structure, some are 
like spongy hone with the interstices filled with ordinary hone- 
marrow, and some are composed of dense bone such as forms the 
shaft of a long hone, and are called ivory exostoses. There are 
even tumors which originate in the teeth. When these are com- 
posed of cement, they are called dental osteomas, hut when formed 
of dentine, odontomas. Several forms are to be distinguished. 
(1) The spongy exostosis, or the exostosis cartilaginea (Fig. 67). 
These tumors occur mostly at the epiphyses of the long bones, and 
are derived primarily from the epiphyseal cartilage. They grow 
during childhood, and, just as the cartilage from which they origi- 
nate ossifies, so do they, and the bony tumor formed is directly 
continuous with the bone beneath. The tumor begins as a small 
outgrowth, and so the first hone formed is a narrow piece. The 
cartilage as it goes on growing enlarges in every direction, and so 
overhangs its base, the tumor thus becoming larger as it grows 186 
SIMPLE-TISSUE TUMORS. 
outward, and consequently pedunculated. The tumor consists of 
spongy bone with a thin layer of cartilage on its surface. It is 
enough to snip through the base in order to remove the tumor. 
Pig. 67. 
Cartilaginous spongy exostosis of femur. (Virchow.) 
(2) The ivory exostosis is mostly met with on the bones of the 
head, but also on the pelvis, scapula, great toe, etc. The tumors 
Pig. 68. 
Internal ivory exostosis of the frontal bone. The surface is tuberculated, and the tumor has 
a narrow base. It was situated to the left of the falx (/). Natural size. (Virchow.) 
are usually rounded in form, and may be t.uberculated on the 
surface. In their favorite seat on the head they may grow from muscular-tissue tumor or myoma. 
187 
the external table and.project externally, or from the internal table 
and project internally (as in Fig. 68), in which case they may 
produce irritation of the brain substance beneath. It sometimes 
happens that an ivory exostosis grows from corresponding parts of 
both external and internal tables. These tumors are sometimes 
multiple, as in Fig. 69. 
Fig. 69. 
Multiple exostoses of the frontal bone. Natural size. (Virchow.) 
(3) Hyperostosis and periostosis are names applied to growths 
of bone which are not properly tumors. They are localized thick- 
enings of bones or portions of hones. This growth of particular 
parts of the bones of the head may become so independent in its 
manner that the characters of a tumor are simulated. 
Osteomas op other parts than bones are rather rare. It is 
remarkable, however, that bony masses occur sometimes in the 
central nervous system. They are met with in the arachnoid, 
where they used to be regarded as evidences of chronic irritation, 
and are hardly tumors. Actual tumors occur in the dura mater, 
and even in the brain substance. They are also met with in the 
eyeball, in the lungs, and, as little bony granules, in the skin. 
6. —THE MUSCULAR-TISSUE TUMOR OR MYOMA. 
These are tumors in which muscular tissue is the essential con- 
stituent, but just as all muscles have supporting connective tissue 
so have these, some more, some less. As there are two kinds of 
muscle, so are there two forms of muscular tumor, those composed 
of striated, and those of smooth muscle. 
The Myoma strio-cellulare or labdo-myoma is very rare. 
Tumors of this structure have been observed in the heart, where 
they are congenital. They have also been seen in the kidneys, 188 
ovaries, and testicles, where the tissue consists usually of spindle- 
shaped cells, which are transversely striated, and so the tumors are 
often called myo-sarcomas on account of their cellular character. 
The smooth-celled myoma (M. lfevi-cellulare or leiomyoma) is 
an exceedingly common form of tumor, and is met with in almost 
every part where smooth muscle exists normally. According to 
the amount and density of the interstitial connective tissue is the 
consistence of the myoma—it may be very dense and warrant the 
name fibro-myoma, or it may be so hard as to resemble cartilage. 
Myomas are often described as fibrous tumors, and in appear- 
ance they justify this designation. To the naked eye they appear 
fibrous on section, and even under the microscope they appear to 
be formed of fibres. On adding acetic acid to a microscopic section, 
or staining with carmine or other agent, the fibres are seen to be 
much more abundantly nucleated than ordinary connective tissue. 
In fact, rod-shaped nuclei (not spindles as in connective tissue) are* 
so closely set as at once to suggest a cellular tissue (see Fig. 70). 
SIMPLE-TISSUE TUMORS. 
Fig. 70. 
Section of a myoma of the uterus stained with carmine. The muscular nuclei are seen in 
longitudinal and transverse section. X 350. 
It may liere be remarked that in the unimpregnated uterus there 
is the same difficulty in distinguishing the individual spindle-cells. 
In both cases, however, the cells may be isolated by macerating 
the tissue for twenty-four hours in a 20 per cent, solution of nitric 
acid, or for twenty to thirty minutes in a 34 per cent, solution of MUSCULAR-TISSUE TUMOR OR MYOMA. 
189 
caustic potasli. This makes the tissue rotten, and separates the 
cells, which are recognized as spindles (as in Fig. 71). 
Myomas always arise where muscle already exists, and as smooth 
muscle is most frequent in the walls of mucous canals and cavities, 
it is there that they usually originate. The tumor may he con- 
tinuous with the muscular wall, forming an outgrowth from it, or 
it may be distinctly isolated and encapsuled. It niay remain in 
the substance of the muscular wall (intraparietal or intramural), 
or it may slip inwards so as to bulge under the mucous membrane 
Fig. 71. 
Muscular fibre-cells from a myoma isolated by steeping in nitric acid. X 350. 
(submucous), or it may pass outward and present under the serous 
coat (subserous). In the two latter cases the tumors often become 
polypoid. 
By far the most frequent seat of the myoma is the female organs 
of generation, most frequently the uterus, but also the ligaments 
and ovaries. The so-called uterine fibroids are myomas, and the 
most important of these are the submucous which so frequently 
become polypoid, and give rise to hemorrhage, sloughing, etc. In 
the prostate the hypertrophy frequently met with in old men is 
really from the formation of a muscular tumor, and the third lobe 
which forms a prominent bulging projection at the neck of the 
bladder is an outgrowth from the muscle of the prostate. Some- 
times there are even isolated muscular tumors in the midst of the 
prostate. This form of tumor is to be distinguished from the 
glandular tumor, which is a much rarer form of hypertrophy and 
occurs mostly in young men. Myomas of the stomach and intes- 
tine are infrequent, and are usually submucous. They have also 
been seen in the urinary bladder. Lastly, they are rarely met 190 
SIMPLE-TISSUE TUMORS. 
with in the skin, one or two cases in connection with the nipple 
and the scrotum have been observed. 
The myoma is of slow growth, but many go on as long as thirty 
or forty years, and many reach a very great weight, as much as 
sixty pounds. Retrograde changes may occur, such as fatty 
degeneration, resulting in shrinking or the formation of cysts. If 
induration occurs from formation of hard connective tissue, this 
may calcify, leaving the muscular tissue in the spaces between the 
calcified trabeculae. In some cases, from derangements of the cir- 
culation in large tumors, we may have an actual necrosis of a por- 
tion of the muscular substance, resulting sometimes in absorption 
and the formation of a cyst. In other cases, the dead structures 
become calcified as in Fig. 72, where muscular elements, connec- 
tive tissue, and walls of bloodvessels were all found impregnated 
Fig. 72. 
From a myoma, a portion of which had become calcified, a, muscular fibre-cells 
impregnated with lime-salts; b, a bloodvessel with wall incrusted. X 350. 
with lime. As the myomas so readily become polypoid, they are 
liable to be insufficiently nourished, as the neck gets thinner: 
sloughing may even occur, especially if they present on a mucous 
surface, and are exposed to injury. Such tumors are also liable 
to bleed, especially as the vessels in them sometimes undergo great 
dilatation. 
7.—THE NERVOUS-TISSUE TUMOR OR NEUROMA. 
By the name neuroma is often understood a tumor which grows 
on a nerve-stem, and this use of it may be convenient for surgical nervous-tissue tumor or neuroma. 
191 
purposes. Here we have to consider tumors according to their 
structure, and if a fatty, mucous, or iibrous tumor grows on a 
nerve, it is to be embraced in its own class. Tumors on nerves, 
but not of nervous structure, are designated false neuromas. 
But there are tumors composed essentially of nervous tissue. As 
there are two kinds of nerve-tissue, the central or ganglionic and 
the fibrous or fascicular, it might be expected that we should have 
two kinds of neuromas. But practically we have no such thing as 
a tumor composed of ganglionic nerve-tissue, although central 
nervous tissue does occasionally enter into the composition of a 
teratoma. 
The true neuroma is composed of nerve-fibres, which may be 
either medullated, as in the ordinary cerebro-spinal nerve, or non- 
medullated. One of the most striking 
forms is the so-called amputation-neuroma 
(Fig. 73). Sometimes after amputations 
the cut ends of the nerves produce little 
knots or knobs which have a hard consis- 
tence and to the naked eye look fibrous. 
Under the microscope medullated nerve- 
fibres are found running in bundles, but 
there are also many fine fibres which are 
probably non-medullated nerve-fibres. It 
is in this case as if the cut end of the 
nerve had made an attempt at regenera- 
tion of the lost portion. Allied to this 
form is the trauinatie neuroma, occurring 
as the result of injury in the course of a 
nerve. 
But neuromas occur in the course of 
nerves spontaneously, and they are often 
multiple, forming oval swellings, hard 
and fibrous in appearance. They contain 
much fibrous tissue, in the midst of which 
there are medullated nerve-fibres (see Fig. 
74) recognizable in the fresh state by the 
double contour, especially when the con- 
nective tissue has been rendered trans- 
parent by acetic acid or liquor potassse. 
But usually in addition to these medullated fibres, there are fine 
nucleated fibres which Virchow regards as non-medullated nerve- 
fibres. In some neuromas these are very abundant. 
The painful subcutaneous tumor, or Wood’s tumor, is a some- 
what difficult growth to classify. It occurs in the form of a small 
round tumor under the skin, and is commonly the seat of intense 
pain. The pain indicates some connection with the nerves, and it 
has been suggested that the tumor may even be a non-medullated 
neuroma. According to Virchow there are tumors of various 
Fig. 73. 
Amputation-neuroma. The 
nerves end in knobbed extremi- 
ties. The case was one of am- 
putation in the upper arm. 
Two-thirds of the natural size. 
(Virchow.) 192 
SIMPLE-TISSUE TUMORS. 
structure in this category, myomas, angiomas, neuromas. Re- 
cently Hoggan has described one which he believes to be an ade- 
noma of the sweat-glands, but which Virchow rather takes to be 
an angioma. In the case from which our figures are taken (Figs. 
Fig. 74. 
Transverse section of a neuroma. The medullated nerve-fibres are shown, the appearance 
being much like that of the section of a nerve. X 80. 
75 and 76) the tumor consisted of a dense interlacing network of 
fibres, very suggestive of the appearance of a myoma (Fig. 74). 
Fig. 75. 
Section of a painful subcutaneous tumor (Wood’s tumor). The appearance is somewhat 
like that of a myoma. X 80- 
On macerating portions in nitric acid the tissue broke up into large 
spindle-cells, as shown in Fig. 75. This tumor is probably a VASCULAR TUMOR OR ANGIOMA. 
193 
myoma of the skin, and several others examined by the author had 
a similar structure. 
Fig. 76. 
From same tumor as Fig. 75, after maceration in nitric acid. Large spindles are 
isolated, probably smooth muscle-cells. X 350. 
THE VASCULAR TUMOR OR ANGIOMA. 
We have here a tumor composed of blood or lymphatic vessels. 
Several forms are distinguished according to the kind of vessels 
which form the tumor. 
The commonest form is (1) the plexiform or capillary angioma. 
This includes most of the vascular nsevi, and consists of capillary 
Fig. 77. 
Section of skin in a case of diffuse venous nsevus. The large sinuses (shaded) are seen 
to lie superficially between the hair-follicles and glands. (Virchow.) 
and intermediate vessels forming a rich plexus. It is mostly a 
growth of the skin, and may be very small or cover a large area, 
forming a flat soft surface of dark or bright hue. It is nearly 194 
simple-tissue tumors. 
always congenital, although it may increase in size after birth. 
These capillary naevi graduate into those consisting of dilated 
veins, the venous or varicose nsevi (Fig. 77). They have similar 
situations to the capillary form and similar appearances. 
(2) The cavernous angioma consists of tissue like that of the 
corpus cavernosum of the penis or clitoris, namely a network with 
meshes which communicate freely and are filled with blood. When 
empty they are seen to be composed of a pale tissue, in its texture 
resembling a sponge, with variously thick trabeculae and variously 
wide spaces. These trabeculae are all accurately lined with endo- 
thelium, and consist of connective tissue with some muscular fibre- 
cells in them. These tumors are erectile and sometimes pulsatile. 
Sometimes the tumor merges into the neighboring vessels without 
distinct boundary, hut sometimes it has a distinct connective-tissue 
capsule, which, however, appears to be a secondary formation. 
Sometimes also they are indurated in the centre, and the indura- 
tion may gradually lead to the obliteration of the spaces and the 
destruction of the tumor. These tumors are not so usually con- 
genital as the former kind, but they come on in childhood at latest, 
and they may develop out of the other form. 
The skin is a frequent seat of the cavernous angioma, especially 
that of the face or head, but also sometimes of the trunk or limbs. 
They are also met with in the liver, not forming prominent tumors, 
hut simply replacing a piece of liver tissue by cavernous tisssue 
(see Fig. 78). 
Fig. 78. 
Cavernous angioma of liver. The fibrous septa are shown. The spaces between were 
occupied with blood during life. X 90. 
(3) Cavernous tumors communicating with the lymphatics and 
filled with lymphatic fluid have been described, and are designated 
cavernous lymphangiomas. 
9.—THE GLANDULAR TUMOR OR ADENOMA. 
As there are many glands of different structure, so are there 
various forms of adenoma. 
(1) The mammary glandular tumor is a form concerning which 
there is some difference of opinion. Glandular tissue is frequently GLANDULAR TUMOR OR ADENOMA. 
195 
present in sarcoma of the mamma, and this is expressed in the 
name adenoid sarcoma. Again, cancers of the mamma take origin 
in the glandular tissue, and it may sometimes be doubtful whether 
we have a cancer or an adenoma before us. But besides these, we 
meet with distinct isolated growths in the mamma whose tissue 
imitates that of the gland itself, except that there are no excretory 
ducts. The tumor occurs in, or over, or under the gland, some- 
times as if it were a supernumerary breast. It is markedly lobed 
and varies in consistence according to the predominance of gland 
tissue or connective tissue. Under the microscope we find lobes, 
consisting of groups of acini or terminal gland structures lined 
with glandular epithelium (Fig. 79). 
Fig. 79. 
Adenoma of mamma. Glandular structures are seen in the midst of fibrous tissue, but 
without proper ducts. X 90. 
(2) In the prostate gland we occasionally have a new formation 
of gland tissue, leading to enlargement of the gland, but this forms 
a very small proportion of the hypertrophies of the prostate. 
(3) Mucous polypi are very frequent forms of tumor, and are 
mostly composed of hypertrophied mucous glands. They form 
pendulous tumors, generally on mucous membranes which have 
been the seat of chronic inflammation. There are some polypi of 
mucous membranes which do not consist of gland tissue, especially 
those of the ear and of the female urethra (the urethral caruncles). 
Elsewhere, as in the nose, rectum, stomach, uterus, they are usually 
composed of masses of mucous gland tissue covered with epi- 
thelium of the kind existing in the mucous membrane where they 
grow, cylindrical in the stomach and rectum, ciliated in the nose. 
Very frequently from closure of their ducts, the mucous glands de- 
velop cysts. These polypi may generally be regarded as evidences of 
chronic catarrh of the mucous membrane in which they are found. 196 
SIMPLE-TISSUE TUMORS. 
(4) The thyroid adenomas form a large proportion of the 
goitres or bronchoceles. The thyroid gland consists of vesicles 
lined with epithelium, these vesicles being grouped into lobules. 
A goitre may consist in a simple enlargement of the whole gland, 
or of a single lobe of it, or it may be due to the formation of 
isolated tumors consisting of gland tissue. In the case of apparent 
simple enlargement the vesicles may be found greatly increased in 
size and many of them filled with colloid material. In the same 
case the various stages of colloid metamorphosis, as it affects the 
epithelium, may be observed. These colloid vesicles may coalesce 
and form considerable cysts. In other cases there is a distinct 
new formation of glandular tissue, the tumor consisting largely of 
vesicles of normal size. But the new-formed vesicles are also 
prone to undergo colloid degeneration. Where distinct isolated 
tumors exist, there is, of course, a great new formation of gland 
tissue, and here also there is often colloid change. In all the forms 
secondary changes are frequent. We have already seen that cysts 
form. Then blood may be extravasated into cysts or into the 
interstitial tissue, and though subsequently absorbed the pigment 
remains. Caseous degeneration may affect the extravasated blood 
or even the glandular tissue, and calcareous infiltration sometimes 
ensues, so that great changes may occur in the characters of the 
tumor. The relation of the colloid goitres to tumors is very dis- 
tinctly evidenced by the observation of a case by Cohnheim, in 
which secondary tumors developed by metastasis, the tumors occur- 
ring in the lungs, lymphatic glands, and elsewhere having the 
structure of the thyroid with colloid degeneration. 
(5) Adenomas are of occasional occurrence in the liver, con- 
sisting of liver tissue. There may be a single tumor or many, and 
the tumors may be distinctly encapsuled or not. They consist of 
liver tissue arranged in lobules, but the hepatic cells are larger 
than normal, and contain more nuclei. They usually show fatty 
metamorphosis. Similar multiple adenomas of the liver are of 
frequent occurrence in dogs. In addition to this form, we shall 
see in the section devoted to diseases of the liver that a form occurs 
sometimes designated adenoma, in which the tissue follows the 
type of tubular glands rather than that of the liver. 
Among the adenomas we might include tumors of lymphatic- 
gland tissue, but these will be more conveniently considered after- 
wards under the lymphomas. 
10.—THE GLIOMA. 
This is a tumor with the structure of the connective tissue of the 
central nervous system, the neuroglia. In examining a section of 
the brain substance, it is difficult to tell what is ’really nervous 
structure, and what the supporting connective substance, but when 
we examine the surfaces of the ventricles we find that the ganglion 
cells and nerve-fibres fall away, and just at the surface or ependyma THE GLIOMA. 
197 
we have what is presumably a purely connective substance. When 
hardened sections are examined, this is seen to consist of a finely 
reticulated network of fibres and round or slightly elongated cells. 
In the fresh state the fibres are not obvious, and we have a gran- 
ular material. This connective substance has some of the charac- 
ters of mucous tissue, and seems allied to it. 
The glioma as it occurs in the brain does not usually form an 
isolated tumor, but, being continuous with the brain substance, 
has more the appearance of a swelling of part of the brain. It is 
seen also that the different shades of color of different parts of the 
brain are lost when a glioma takes their place. Gliomas some- 
times occur as small granular or warty projections on the surface 
of the ventricles, hut the more important ones involve considerable 
portions of the brain substance. 
Under the microscope the glioma is seen to resemble the neu- 
roglia, but the cells are much more abundant. There is a well- 
developed fine or coarse network and in it cells with oval nuclei. 
The cells present considerable variety in size. Gliomas being soft 
and somewhat cellular tumors, are liable to secondary changes. 
Hemorrhage not infrequently occurs, and the blood causing 
pressure around, the case may end like one of hemorrhagic 
apoplexy. The tumor may also undergo fatty or caseous meta- 
morphosis, and if a limited hemorrhage has occurred the clot may 
change in a similar way. In this manner a tumor which had 
originally the appearance of brain substance may change con- 
siderably. 
Fig. 80. 
From a psammoma of the dura mater. Dark calcareous rods and masses are 
seen in a fibrous tissue. X 90. 
Gliomas occur also in the retina, forming soft tumors which 
till up the eyeball. The true glioma is an innocent tumor, but 
sometimes it assumes a sarcomatous character and malignancy is 
developed. 198 
COMPOUND-TISSUE TUMORS. 
11.—THE BRAIN SAND TUMOR OR PSAMMOMA. 
The pineal gland contains calcareous particles like grains of 
sand, and tumors are met with in which similar particles are 
present. It is necessary, of course, to distinguish these from 
tumors in which simply a secondary calcareous infiltration has 
occurred. The psammoma is composed of soft connective tissue 
in the midst of which there are calcareous masses in the form of 
irregular globes, rods or spines. (See Fig. 80.) The commonest 
form is the globe, which has rounded projections on its surface 
like a berry. The origin and significance of these masses is 
obscure. The tumors are met with in the pineal gland and choroid 
plexus—usually small. They also occur in the dura mater, where 
they form half globular tumors sometimes as large as a cherry 
and either smooth or irregular on the surface. 
B.—COMPOUKD-TISSUE TUMORS. 
1.—THE CYSTIC TUMOR OR CYSTOMA. 
A cyst is a cavity having well-defined walls and containing 
material which is more or less fluid. Some cysts are formed 
simply by the transformation of existing structures, and it is clear 
that according to our definition of tumors these do not come under 
that designation, as they are not pieces of tissue which grow inde- 
pendently without regard to the needs of the organism. There 
are other cysts, however, which do' owe their origin to the inde- 
pendent new formation of tissue, and therefore deserve the name 
of tumors. The two forms are so similar in appearance that it 
would be inconvenient to separate them rigidly, and without 
aiming at logical accuracy we shall here consider the cysts as a 
whole. If necessary, the name Cystoma may be reserved for 
strictly cystic tumors. 
Mode of Formation of Cysts.—As already indicated, cysts vary 
greatly in regard to their mode of origin. Some of them arise out 
of a preexisting cavity, very often by accumulation in it, in the 
first place, of its normal contents. Thus a gland will become a 
cyst by its duct becoming obstructed. Cysts arising thus are often 
designated retention cysts. But the other cysts arise simply by 
softening of existing tissue, the softened material being absorbed 
and fluid taking its place. This, as we have seen, often occurs in 
the brain, resulting in the apoplectic cyst. Again, we may have 
cysts arising by a distinct new formation; a preliminary tissue is 
formed, generally something like that of a gland, and this is after- 
wards transformed into a cyst somewhat in the fashion of the 
retention cyst. Instead of following out these modes of formation 
it will he more convenient to give some examples of cysts, and the cystic tumor or cystoma. 
199 
their mode of origin will come up for discussion as each is con- 
sidered. 
Cysts of the skin appear to arise in many cases from sebaceous 
glands. The duct becomes obstructed by inspissated secretion or 
adhesion of its walls, and the sebaceous material accumulates 
behind. Such a cyst may attain some size, and contains mainly 
fat, cholestearine, and epidermic scales. From the nature of their 
contents such cysts are often designated atheromatous. Their 
wall consists of connective tissue with a lining of epidermis, which 
may present papillary projections. They occur mostly on the 
head and face, and are often called wens. Besides these we some- 
times meet with more complex cysts in the skin, and these are 
congenital in their origin, probably arising by inclusion of a piece 
of embryonic skin. Their walls are like the skin, containing hairs 
with hair-follicles and sebaceous glands, and sometimes even sweat 
glands. These are called dermoid cysts, and they contain a less 
grumous material than the former ones, their contents consisting 
of cholestearine and epidermis often with loose hairs. 
Mucous cysts, or cysts with mucous contents, arise in situations 
where mucous glands are present, their chief sites being the nostrils 
and communicating cavities, the upper surface of the epiglottis, the 
larynx, the oesophagus, and in connection with the glands of 
Cowper and Bartolini. Of these a very typical form is the Ranula, 
whose origin and mode of formation have been carefully studied by 
Recklinghausen. 
It has long been taught that these cysts arise by obstruction of 
ducts and accumulation of the contents behind them, hut this 
Fig. 81. 
Formation of mucous cysts; a, the persistent mucous gland tissue; b, the 
dilated duct. X 300. (Recklinghausen.) 
scarcely explains the continuous enlargement of the cysts after 
they have been formed. It might be supposed that the epithelium 
lining the cysts would secrete mucus and so add to the contents, 200 
COMPOUND-TISSUE TUMORS. 
but there is the objection to this that the epithelium loses its gland- 
ular character, and there are no goblet cells to be found in it. The 
real state of matters appears to be that the cyst forms, not out of 
the gland, but from its duct, and, the gland persisting, its secre- 
tion is thrown into the cj'st. This is shown in Fig. 81, copied 
from Recklinghausen’s paper. It would thus appear that the per- 
sistence of the gland is an essential element in the formation of the 
cyst. In the enlargement of the cyst the power which mucin has 
of swelling up and absorbing water is of some consequence. A 
small amount of mucin formed by the gland and discharged into 
the cyst will swell up and add considerably to its contents. Before 
a regular cyst forms, the orifice of the duct is obstructed, usually 
by an inflammation around it. But on account of the peculiarity 
of mucin just noticed, a small temporary cyst may form without 
any considerable obstruction of the duct. If a quantity of mucin 
is discharged into the duct, it may swell so much as to be unable 
at once to escape from the orifice and so form a small cyst, which 
afterwards discharges. In this way cysts often form in the mucous 
membrane of the mouth. 
It has already been noted that cysts arise in mucous polypi, and 
they have a similar mode of formation to that just described. The 
obstruction of the orifices is here the more likely, as the polypus 
itself usually originates in connection with a chronic inflammation 
of the mucous membrane. 
Cysts of the thyroid gland have been already referred to as 
taking origin in the vesicles of the gland, but they may also have 
origin in softening of the tissue of the gland. Sometimes one or 
more cysts attain very large dimensions in the thyroid. 
In the kidney we have frequent cysts, most of which arise by 
obstruction, and are to be classed as retention cysts. By obstruc- 
Fig. 82. 
Hydronephrosis with granular atrophy of the kidney. The other kidney showed a 
marked compensatory hypertrophy. (Virchow.) 
tion of the ureter the condition of hydronephrosis is brought about, 
in which the whole kidney goes to form a cyst (Fig. 82). Obstruc- 201 
CYSTIC tumor or cystoma. 
tion of the uriniferous tubules by tube-casts, or more commonly by 
the contraction of new-formed connective tissue, produces cysts in 
the kidney substance which may be of microscopic size, or large 
enough to be seen by the naked eye. These cysts are multiple. We 
sometimes meet with a single cyst of 
large size, with a definite lining mem- 
brane, and obviously of old date. Such 
cysts are probably congenital, and owe 
their origin to foetal closure of one or 
more tubuli uriniferi. Again, the whole 
kidney may be converted into a con- 
geries of cysts large and small, filled 
with serous or bloody fluid, the outline 
of the organ being greatly enlarged 
(Fig. 83). These also are congenital in 
their origin, and probably arise by 
foetal closure of the tubuli uriniferi. 
In all these cases the cysts contain a 
serous fluid, although, in some of them 
at least, urine has been the primary 
contents; after a time, however, the 
urinary constituents are absorbed, and 
serous fluid alone remains. 
The gall-bladder may be converted 
into a cyst by obstruction of its duct. 
It is the secretion of the mucous glands 
—a mucous material—which accumu- 
lates and produces the distention; but 
after a time this gives way to a serous 
fluid, and the bladder is converted into 
a large thin sac full of a watery serum. 
There may be a formation of cysts in the substance of the liver 
by obstruction of the hepatic ducts in their finer ramifications. 
Obstruction of the common hepatic duct produces a distention of 
the ultimate terminations of the duct, but 
not a proper cystic formation. 
The vermiform appendage is sometimes 
converted into a cyst by obstruction of its 
orifice. At first mucus accumulates, and 
even when the cyst is of large size the con- 
tents may remain of a gelatinous consist- 
ence. But here also there is a tendency to 
simplification of the wall, involving atrophy 
of the mucous glands, so that there results 
a thin-walled cyst, consisting of connective 
tissue with merely a lining of epithelium, 
and the contents generally cease to have 
the mucous character. 
The ovaries are very frequently the seat of cysts. They may 
arise by simple accumulation of serous fluid in the Graafian 
Fig. 83. 
Congenital cystic kidney from a 
new-born child. Each kidney meas- 
ured 5£ inches long, 4 inches broad, 
and 3| inches thick. The entire 
kidney-tissue was replaced by cysts. 
(Virchow.) 
Fig. 84. 
Dropsy of Graafian vesicles 
in ovary of a girl ten years of 
age. (Virchow.) 202 
compound-tissue tumors. 
vesicles, a dropsy of these (Fig. 84), but in the great majority of 
cases a definite new formation precedes the cystic development. 
This consists in the production of tubular or gland-like structures 
out of which cysts develop apparently by closure of their orifices. 
In this way multitudes of cysts are formed, and as this tissue is 
continually being produced there is a progressive new formation 
of cysts. Very often one or more cysts become predominant, and 
they enlarge by coalescence of others, but there is always evidence 
in the walls of the cysts that new formation is progressing. These 
cysts contain originally a mucous or colloid material, which may 
be variously modified by fatty changes, hemorrhage, and inflam- 
mation. Similar cysts are occasionally, though very rarely, met 
with in the testicle. 
The ovaries are also the seat of cysts which will be referred to 
afterwards as teratomas. 
Cysts occur in tumors, and are particularly common in mam- 
mary tumors, especially the adenoid sarcomas. There is, in fact, 
a form of sarcoma designated cysto-sarcoma. The cysts here 
appear to originate from the glandular structures. The glandular 
acini dilate, much in the manner of retention cysts. When the 
cyst has formed, the sarcomatous tissue, apparently growing in the 
direction of least resistance, very often grows into the cyst, and 
may even fill it up with an intracystic growth. 
2.—THE PAPILLARY TUMOR OR PAPILLOMA. 
By this name is meant a tumor composed of a congeries of ex- 
aggerated papillae like those of the skin, or like the villi of mucous 
membranes. A papilla or villus consists of a basis of connective 
tissue in which there is a loop of capillary bloodvessel, and a 
covering of epithelium. The epithelium is like that of the surface 
concerned, and may be stratified or in a single layer. 
Their commonest situation is the skin, where they form the 
wart, which is an overgrowth of a group of existing papillae 
covered with hard epidermis. At the surface of the wart the 
papillae may be covered over with a continuous layer of epidermis, 
or the individual papillae may project independently. The horn 
is also formed on the basis of a group of papillae, but the hard, 
horny epidermis is greatly developed, and forms a consistent out- 
growth of considerable dimensions. The condyloma is a syphilitic 
outgrowth due to exaggeration of the papillae, with very soft epi- 
dermis. These occur near the genital organs mostly. 
On mucous membranes papillomas may be gathered into a local 
tumor, or cover a considerable surface, giving it a shaggy, villous 
appearance. In the larynx (Fig. 85) they often form localized 
prominent tumors, especially on the vocal cords. They are not 
uncommon in the rectum. In the urinary bladder they are of con- 
siderable importance on account of their tendency to hemorrhage. 
In this situation they may form distinct tumors with long-branched THE PAPILLARY TUMOR OR PAPILLOMA. 
203 
papillae, or there may be a large surface which is simply villous in 
appearance. The papillae are covered with delicate epithelium, 
and are liable to severe and frequent hemorrhage. 
The Pacchionian bodies of the encephalon are really papillary 
Fig. 85. 
Papilloma of larynx : e, epithelium; h, connective tissue; g, mucous glands; f, an atrophied 
gland. X 20. (Cornil and Ranvier.) 
formations, and Dr. Cleland has described large tumors of this 
region which seemed to arise by extreme hyperplasia of these 
papillae. 
3.—TERATOMA. 
This name has been applied by Virchow to tumors in which a 
number of very different tissues enter into the structure. The 
name is derived from repaq, a monster. The tumor contains various 
structures of the body as if from an ill-arranged foetus. Thus we 
may have in such tumors skin, hone, muscle, glands, nervous tissue. 
These tumors probably arise by the abnormal inclusion of a 
whole embryo or a portion of one. They are most frequently met 
with in positions where double monsters are usually attached to 
each other, namely, in the sacral region, or further up the hack, 
and the head and neck. They are also somewhat frequent in the 
ovary, where they may arise by a kind of equivocal generation, the 
germinal vesicle endeavoring to develop some of the perfect tissues 
of the body. 
The sacral teratomas and those of the head and neck are the 
more typical ones. They frequently contain pieces of hone which 
simulate the hones of the foetus, also brain substance and muscle. 
Considering that these tumors develop so frequently in the ordi- 
nary places of union of double monsters, they may safely he re- 204 
CELLULAR TUMORS. 
garded as representing twin pregnancies in which one of the 
foetuses has grown over and included the other. 
The teratomas of internal organs do not usually represent such 
complete systems or so many different 
tissues as the sacral. They are most 
frequent in the ovaries, but also occur 
in the peritoneum, testes, lungs, and 
so on. 
In these situations they occur in the 
form of cysts, approaching in structure 
to the dermoid cysts of the skin and 
often grouped along with them as 
dermoid cysts, hut having usually a 
more complex structure. These cysts, 
and especially those of the ovary, usu- 
ally present at some part of their wall 
a structure similar to that of the skin. 
There is corium with epidermis, and 
well-developed hair-follicles with hairs 
in them (Fig. 86). The sebaceous 
glands are often specially developed, so 
that a portion of the wall may present 
little more than open-mouthed glands. 
Then there is frequently bone in the 
wall, and in the bone there may be teeth. More rarely are muscle 
and nervous tissue represented. 
The contents of these cysts vary according to the structure of 
the wall. There is usually a great accumulation of fat secreted by 
the sebaceous glands, so that we may have masses like lumps of 
butter. These are often mixed with silky hairs, which are regu- 
larly shed from the liair-follicles just like the normal hairs of the 
skin. Then there are sometimes teeth mixed with the other con- 
tents, these being shed also at intervals. As many as three hun- 
dred teeth have thus been found free in such a cyst. 
Fig. 86. 
A hair-follicle with hair and 
sebaceous gland from the wall of 
a dermoid ovarian cyst. X 50. 
C.—CELLULAR TUMORS. 
1.—SAECOMA. 
Definition.—In its literal meaning this term simply mean 
fleshy tumor, and it was formerly applied in a very indefinite v 
In the hands of Virchow, however, it includes a group of turn 
which, though in certain respects differing in structure, yet pres 
such features in common that they form a consistent class by th 
selves. The sarcomas may he defined as tumors which in tl 
structure follow the type of one or other of the connective tissi 
but differ in respect of the great preponderance of the celh 
elements, and also in respect that the cells are more or less 
bryonic in their character. S A R C O M A . 
205 
Structure and Classification.—The structure of sarcomas has 
been somewhat aptly compared to that of inflammatory new forma- 
tions. We have already seen that the tendency of these, as exem- 
plified in the granulating wound, is to develop into connective 
tissue. The round cells pass into spindle-cells and then the con- 
nective tissue develops out of the latter. The round and spindle 
cells may thus be regarded as the preparatory, or in a certain 
sense embryonic stage of connective tissue. In sarcomas we have 
tumors composed of round cells and tumors composed of spindle 
cells without any tendency to further development, as if the em- 
bryonic form had been stereotyped for the whole life of the tumor. 
Besides these forms sarcomas sometimes contain giant-cells (myelo- 
plaques). We know that cells of this nature occur normally in 
growing bones where, as Wegener and Kolliker have shown, they 
exercise an important function (osteoclasts), and they are not un- 
known in granulation-tissue, even apart from bone. They also 
are to be regarded as connective-tissue structures, and as belonging 
to a developmental stage of connective tissue. 
In their mode of growth also it may be said that the sarcomas 
resemble inflammatory new formations. They very often form 
tumors of considerable size, and may even be encapsuled, as if the 
tissue simply increased like that of a simple tumor. But they 
present a peculiar tendency, which has been already mentioned, 
to incorporate neighboring structures. We have seen that in the 
disposal of dead animal tissue, such as a thrombus, or a catgut 
ligature, the inflammatory tissue advances, and, as it were, moulds 
itself in the first place on the dead structure, copying its general 
form. So an advancing sarcoma will incorporate the living tissues 
and mould itself on them, repeating their rougher anatomical de- 
tails in tissue of its own kind. 
In such cases it sometimes seems as if the sarcoma in advancing 
were inducing the neighboring tissues of themselves to become 
sarcomatous in structure, and *in the case of connective tissue 
which is present everywhere, we can easily suppose that by pro- 
liferation of its cells it might become sarcomatous. It is not 
impossible that this actually occurs, but it is more probable that 
the proper tissue of the tumor disposes of and displaces the exist- 
ing tissues. 
It has been said already that sarcomas follow in their type the 
various connective tissues of the body, and it might be possible to 
divide them according as one or other form is the type. So Vir- 
chow indicates the division into fibrosarcoma, myxosarcoma, glio- 
sarcoma, chondrosarcoma, osteosarcoma, melanosarcoma, to which 
some would add, myosarcoma and neurosarcoma, if muscle and 
nerve are regarded as connective tissues, and lymphosarcoma if 
lymphatic-gland tissue be taken as belonging to this group. It 
will be convenient to follow" a different arrangement, however, and 
we shall describe sarcomas according to their structure apart from 
any inferences as to the type which they follows It is to be added 
that the structure of the individual tumor is, as a rule, remarkably 206 
cellular tumors. 
homogeneous. We often find cells heaped on cells without any 
intersecting bands of connective tissue. In other tumors the 
bloodvessels are supported and the tumor intersected by a kind 
of stroma, equivalent to the interstitial connective tissue of muscles, 
glands, etc., but here there is rarely any fully developed connective 
tissue, and the bloodvessels are in immediate contact with the cells. 
Varieties.—(1) The round-cell sarcoma (Fig. 87) is also called 
the granulation sarcoma and the encephaloid sarcoma. It is com- 
Fig. 87. 
Section of a round-celled sarcoma of the brain. A thin-walled vein, with blood-corpuscles 
in it, divides the section. X 175. 
posed of round or slightly oval cells generally about the size of 
white blood-corpuscles, but sometimes much larger. It is an 
exceedingly soft tumor, often half *diffluent, and has usually a gray 
medullary appearance. Its bloodvessels are in the form mainly of 
large capillaries whose walls are embryonic in structure and often 
present varicose or aneurismal dilatations. The vessels are liable 
to rupture, and so these tumors often present interstitial hemor- 
rhage. Between the cells there may be some intercellular sub- 
stance. This is sometimes homogeneous and becomes opaque with 
acetic acid (myxosarcoma), or it may be somewhat fibrous or 
reticulated. 
This form of-sarcoma is met with in the skin, where it may origi- 
nate in a congenital soft wart or mole, in the subcutaneous tissue, 
in the bones—forming the majority of the so-called medullary 
cancers—in the muscles, in the glands, especially the mamma and 
testicle, in the brain and elsewhere. Being a soft tumor with 
delicate vessels, it more readily produces secondary tumors by 
metastasis than other sarcomas. It is also usually a tumor of 
rapid growth and commonly imperfectly delimited from the sur- 
rounding tissue. SARCOMA. 
207 
(2) The spindle-cell sarcoma (Fig. 88) is also called the fibro- 
sarcoma, and corresponds with Paget’s class of recurrent fibroids 
and Lebert’s group of fibroplastic tumors. The cells are spindle- 
shaped like those in the deeper layers of a granulating wound, 
and there is little or no intercellular substance, the tumor being 
Fig. 88. 
Large cells from a spindle-celled sarcoma. X 300. 
composed of masses of spindle-cells. They are arranged in bun- 
dles, which, to a certain extent, interlace like the bundles of fibre- 
cells in the myoma. There are great varieties in the size of the 
cells, some tumors being composed of very small cells, and these 
are usually soft, while at the opposite extreme are cases where the 
spindles are gigantic. When viewed in mass, the individual spin- 
dles may not be apparent, hut they are usually easily isolated, 
unlike the fibre-cells of the myoma. These tumors are usually 
Fig. 89. 
Large fungating spindle-celled sarcoma of the foot. (Virchow.) 
firmer than the round-cell sarcomas, except the small-celled forms, 
and may even approach the fibroma in hardness. 
The spindle-cell sarcoma occurs frequently in the periosteum, 
and in that case is firmly attached to the bone. It is also met with 
in or under the skin (see Fig. 89), in muscles, in the testicles, etc. 208 
CELLULAR TUMORS. 
It is a frequent tumor in the mamma, and here it not infrequently 
forms the adenoid sarcoma and the cystic sarcoma, the latter of 
which deserves more particular notice. 
In the cystic sarcoma there is, along with the proper sarco- 
matous tissue, a certain amount of glandular tissue (see Fig. 90). 
Fig. 90. 
Section of an adenoid sarcoma of the mamma. Glandular masses are seen with a very 
cellular interstitial tissue. X 90. 
In some cases the gland acini dilate and the sarcomatous tissue 
projects into the cysts thus formed. In this way the cyst, which 
has now solid contents, is sometimes enlarged by the intracystic 
growth. The ingrowing tissue is covered with epithelium which 
is usually more or less columnar. When these sarcomas recur the 
glandular tissue does not reappear, hut 
there is often an appearance of the sarco- 
matous tissue which suggests an arrange- 
ment like that around glandular structures. 
The spindle-cell sarcoma is sometimes a 
distinctly defined tumor, but often, as in 
the case of the periosteal form, its bound- 
aries are not defined, and it advances 
by incorporating neighboring structures. 
Although prone to return after removal, 
it has less tendency than the round-cell 
form to give rise to secondary tumors by 
metastasis. 
(3) Myeloid or giant-cell sarcoma 
(Fig. 91) is a tumor in which the giant- 
cell is characteristic, hut never forms the 
only sarcomatous element, there being 
generally spindle-cells and sometimes round-cells in great abund- 
ance. The giant-cells are in greater or smaller number in propor- 
tion to the others, and in the same tumor they may present various 
Fig. 91. 
Giant-cell sarcoma. X 175. SARCOMA. 
209 
proportions in different parts. The tumor tissue is soft and very 
often of a brown color. Cysts not infrequently develop. 
The myeloid sarcoma occurs in connection with hone, and most 
frequently grows from the medulla. This is especially the case 
with the long bones, where the tumors originate in the cancellated 
tissue at the extremity—the most usual situation being the lower 
end of femur or upper end of tibia. As the tumor grows it has 
a great power of destroying the bone before it, so that by and by 
it eats through the external layer, and may thus produce fracture 
of the bone. At the same time there is commonly new formation 
of bone so that a new external shell is formed continuous with the 
shaft, and internal septa representing a coarse, cancellated structure. 
The tumor tissue is thus frequently contained in bony loculi, and 
after maceration the shell of the tumor looks like a bulbous ex- 
pansion of the end of the bone with bony septa internally. 
Having broken through the external layer of the bone, the tumor 
may proceed into the muscular and other tissues, the tumor tissue 
being repeated, both the soft myeloid tissue and the bony septa. 
Myeloid sarcoma is also met with outside bones, growing from 
the periosteum, especially of the jaws. Many tumors, to which 
the name epulis is given, are myeloid sarcomas. 
(4) The osteoid sarcoma is a tumor which deserves special notice. 
It is the form which Paget has very skilfully described under the 
name of osteoid cancer. The disease occurs most frequently at the 
lower end of the femur, where it usually develops both within and 
without the shaft, but sometimes outside alone. The main mass is 
composed of bone which is usually very dense, but on the surface 
a tissue is found out of which the bone is being developed. This 
consists of dense fibres which are very abundantly nucleated. 
These dense fibres are really cells, and they present varieties of 
shape often tending to the stellate form. The new bone is devel- 
oped out of them, and is usually very irregular in structure, the 
bone-corpuscles often large and with no proper arrangement as in 
normal bone. The tumor, as it advances, often presents nodules 
slightly removed from the main mass, and it also forms secondary 
tumors in the lungs or in the lymphatic glands. These repeat the 
ossifying tissue. 
(5) Melanoid or pigmented sarcoma always originates in a situ- 
ation where pigment already exists, the eye or skin. The cells of 
which it is composed are usually spindle-shaped, but may be round, 
and from the first they tend to the aggregation of brown or black 
pigment in their substance. The pigment aggregates first around 
the nucleus, but is very irregular in its distribution. In a mela- 
notic tumor there may be bits unpigmented, and even in the pig- 
mented parts some cells are free from pigment. 
The melanotic sarcomas have a great tendency to metastasis, and 
as the material is conveyed by the blood there are pigmented tu- 
mors formed in a great variety of organs and tissues where they 
may grow to great dimensions, though the original tumor may be 
very small. 210 
cellular tumors. 
It is necessary to distinguish from these proper melanotic sar- 
comas those which become pigmented from blood. In the former 
the pigment is brown or black from the first, being obviously 
elaborated by the cells. In the latter the pigment is red or yellow, 
and the pigmentation may be related to a special weakness of the 
vessels allowing of hemorrhage. 
(6) Alveolae Sarcoma.—In this form we have round cells, as if 
packed in spaces or alveoli, and so the tissue resembles that of 
cancer. But when the structure is carefully examined, two distinct 
differences can be distinguished. The connective-tissue stroma is 
very directly related to the cells, and the masses of round-cells 
seem to he developing out of the connective-tissue stroma. Be- 
tween the cells there is sometimes a delicate reticulum, but this 
may be absent, and the tissue may be very like that of cancer. 
These tumors occur in connection with bone, skin, and muscle. 
(7) Plexiform sarcoma or cylindroma is a name applied to a 
form of tumor whose relations are somewhat obscure, and it 
probably includes more than one kind. The peculiarity of the 
tumor is the existence of cylinders and rounded structures having 
a hyaline character, and like mucous tissue. In the centre of the 
cylinder there is often a bloodvessel, so that the hyaline material 
clothes it like a mantle. Then, between the cylinders of hyaline 
material there are frequently masses of cells which may form long 
processes so as to give a close resemblance to cancer, to whose 
cells these may also conform in general appearance. 
The origin of these cylinders is not perfectly clear. In some 
cases it may be that we have a combination of sarcoma and 
myxoma, but this does not account for the peculiar form of the 
cylinders. A more probable explanation is that the cylinders arise 
by hyaline or mucous degeneration of the adventitia of the blood- 
vessels, and this is confirmed by the fact that they are often ar- 
ranged around the vessels. If this be the proper view, then, in 
the tumor, the formation of bloodvessels is an important element. 
In this way we should have a sarcoma in which a peculiar trans- 
formation occurs in the external coats of the vessels. It is in this 
view that the name plexiform angiosarcoma is applied to this form 
of tumor. 
The tumor as a whole is often of a gelatinous appearance, or it 
may be that the gelatinous material is seen to be in separate spaces 
throughout the tumor. It occurs in the orbit and its neighbor- 
hood, or the upper and lower jaws; it may form part of the con- 
stituents of tumors of the parotid, and it is also found in the brain 
and its membranes and the peritoneum, where it may grow to a 
large size. 
2.—CANCER OK CARCINOMA. 
We enter here on a class of tumors whose boundaries, when re- 
garded from a clinical point of view, are rather undefined. In its 
more general use, the term cancer is applied to any form of malig- CANCER OR CARCINOMA. 
211 
nant tumor, altogether irrespective of its finer structure, and in this 
sense would include most sarcomas. But in the study of Pathology 
such a general use of the word is not allowable; the structure must 
be taken into account, and it will be found that clinical facts are 
in essential accord with histological and anatomical relations. 
Definition. — As the sarcomas are tumors whose structure 
follows the type of the connective tissues, cancers may be defined 
as tumors whose structure follows the type of the epithelial tissues, 
but with an excessive production of cells. 
Structure.—It is well known that epithelial structures are non- 
vascular, and in order to the nourishment of any considerable mass 
of epithelium, it is necessary to have bloodvessels supported by 
connective tissue. This forms the stroma of cancers, and so it is 
always possible to distinguish in cancers a vascular connective- 
tissue basis, enclosing and supporting masses of epithelial cells. 
This stroma may be in whole or part the remains of the preexisting 
connective tissue of the part, generally giving evidence of the ex- 
istence of irritation in the presence of large numbers of round- 
cells, but very often it is as much a new formation as the epithe- 
lium, and may occur in the form of a delicate network with well- 
formed meshes (see Fig. 92). 
Where a cancer produces a well-formed stroma along with the 
epithelial masses, it will probably grow more readily into a dis- 
tinct tumor than where the epithelial masses depend for their 
Fig. 92. 
Stroma of a soft cancer of the mamma after the cells had been washed out. X 82. 
nourishment on the existing bloodvessels. In this latter case the 
cancer will commonly present more the characters of an infiltra- 
tion of the tissues with epithelial structures, and this infiltration 
may be associated with such irritation as to lead to considerable 
new formation of connective tissue, giving sometimes a consider- 
ably fibrous character to the structure, as in scirrhous cancer. 212 
CELLULAR TUMORS. 
An important question arises here as to the origin of the epi- 
thelium, which is the essential constituent of a carcinoma. One 
view is that the epithelium in some cases takes origin in the ex- 
isting epithelium, and in others develops out of the connective 
tissue, while another view is that it develops in all cases from the 
existing epithelium. We have seen in the study of inflammation 
that, as a precursor of the formation of organized tissue, there is 
always a rudimentary tissue, of which the granulating wound is a 
type. How in the development of tumors in general, the forma- 
tion of such rudimentary tissue precedes the formation of the ripe 
tissue, or, in other words, cells of all sorts, when young, have the 
form of round cells, which, from the fact that they are not distin- 
guishable from one another, may he called indifferent or em- 
bryonic cells. In the case of cancers it is supposed by some that 
indifferent cells may he formed from connective tissue, just as those 
of the granulating wound are presumed to be, and that these may 
afterwards develop into the epithelium of the cancerous tumor. 
In the case of inflammation we saw no reason to believe that 
epithelium is developed out of connective tissue. When epithelium 
forms on the surface of a granulating wound, it is always in direct 
Fig. 93. 
From the growing margin of an epithelioma of the skin. The interpapillary processes 
of epidermis penetrating inwards, a, a small laminated capsule. X 100. 
continuity with the existing epithelium. In the case of cancers 
there are certain facts which seem to indicate that here also epi- 
thelium can only develop from preexisting epithelium, or in other 
words, that when the differentiation of the tissues is completed, 
there is no recurrence to the embryonic form in which cells are CANCER OR CARCINOMA. 
213 
indifferent and have the power of developing this or that tissue 
according to circumstances. 
The first fact of importance in this regard is, that in some 
cancers we have the strongest indications that the epithelium of 
the cancer is actually developing from the existing epithelium. A 
section of an epithelioma of the skin shows this almost always if 
the growing marginal parts be examined (see Fig. 93). In the 
skin the epidermis forms a continuous layer on the surface, and 
the rete Malpighii, or deep layer, besides covering the papillae also 
lies between them, forming what may be called interpapillary pro- 
jections. At the margin of an epithelioma of the lip, we see an 
elongation of these interpapillary processes, and on passing more 
and more towards the tumor these processes pass deeper and deeper 
into the subjacent skin, forming penetrating cylinders. 
Again, in some cases of cancer of the kidney it can be seen that 
the tumor is arising as if by transformation of the kidney tissue. 
The primary cancer of the kidney is not a tumor added on to the 
kidney, but it is generally a portion of, or sometimes the whole 
kidney, which has undergone an enormous enlargement while 
keeping its general shape; it is in fact the kidney or portion of 
kidney transformed. And when we examine the marginal parts 
of such a tumor we find the epithelium of the uriniferous tubules in 
an active state of germination, the tubules getting distended with 
new-formed epithelium. The epithelium also is altering its shape 
in various ways, getting sometimes elongated and tailed (see 
Fig. 94). In fact the tumor is forming by proliferation of the 
Fig. 94. 
From a cancer of the kidney. A tubule is represented in which the epithelium is 
undergoing alterations in shape. X 300. 
epithelium, the stroma of the kidney forming the stroma of the 
tumor. 
Another fact of consequence in this matter is, that primary 
cancers in the vast majority of cases occur in situations where 
epithelium exists. There are some apparent exceptions to this, as 
where a cancer has been found growing into bone, hut these are 
of the rarest occurrence, and even they can he explained by sup- 
posing that there has been a connection with the surface which 
was undiscovered. It is not impossible also that some of these 
rare cases may be referrible to a foetal inclusion of a bit of em- 
bryonic epithelium. 
It is here to be remarked that in a growing cancer there is often 
great irritation of the connective tissue, so that, say in a case of 
epithelioma of the lip, the ingrowing processes are, at their deeper 
i 214 
cellular tumors. 
extremities, buried in a mass of inflammatory round-cells (I ig. 95). 
This may obscure the exact new formation ot the epithelium, but 
the fact that the new epithelium is always in connection with the 
old is of sutficient significance. 
Fig. 95. 
From an epithelioma of the skin. Cylinders of epithelium penetrating deeply and causing 
great irritation, as shown by the presence of abundant round cells. X 200. 
The growth of cancer happens in various ways. We have 
already seen that in some cases there is a transformation of existing 
tissues and in others a penetration of the epithelium into surround- 
ing structures. These modes are very common in primary cancers, 
and so we speak of cancerous infiltration very frequently. In 
some cases there is a distinct tumor, but even then at the marginal 
parts there is an infiltration of surrounding tissues, and the tumor 
is ill-defined. It is noteworthy that secondary tumors are fre- 
quently, or indeed commonly much larger and more independent 
in their growth than the primary ones. 
Cancers show peculiar relations to the lymphatics. For one 
thing, the alveoli or spaces containing the epithelial masses seem 
to be in direct communication with the lymphatics. If a cancerous 
tumor, before being opened, he punctured with the needle of a 
hypodermic syringe and a watery solution of Prussian blue, prop- 
erly prepared, be injected, the material first runs into the alveoli 
around the puncture, mapping out a series of cavities as it were, 
and then passes on into the lymphatics, issuing by their extremities 
divided during the removal of the tumor. Besides, it has been 
pointed out by Ivoster that in sending their processes into sur- CANCER OR CARCINOMA. 
215 
rounding parts the lymphatic spaces are often taken advantage of 
and are largely occupied. From these two circumstances we can 
understand how cancers so frequently present secondary tumors in 
lymphatic glands. 
The secondary tumors in the lymphatic glands reproduce the 
original tumor, but it has been pointed out by Cornil and Ranvier 
that at the first there is frequently 
a simple fibrous transformation of 
the gland as if the stroma was 
being formed in advance of the 
epithelium. 
It is further to be remarked that 
cancers are liable to secondary 
changes. The epithelium readily 
dies or undergoes fatty degenera- 
tion (Fig. 96), and the result may 
be either that the stroma becomes 
predominant from the absorption 
of the fat, or that the whole tissue 
softens and an ulcer forms. In 
fact, when a cancer is superficial 
it very commonly undergoes ulcer- 
ation. Sometimes, on the other hand, there is from the first a 
peculiar predominance of the stroma. The epithelial cells of 
cancers may undergo mucous or colloid metamorphosis, etc. 
Having entered so fully into general considerations as to cancers, 
we may be correspondingly brief in regard to the individual forms. 
(1) Epithelial Cancer or Epithelioma.—According to the 
description we have given of cancers, it might appear that all 
cancers are epithelial, but by custom the name has come to be 
used to designate tumors of the skin and mucous membranes, 
whose tissue reproduces in its characters to a large extent the sur- 
face epithelium of these regions. As there are two principal forms 
of epithelium, the flat and the cylindrical, so the epitheliomas may 
be divided into two forms, the flat-celled and the cylinder-celled. 
The flat-celled epithelioma occurs in situations where there 
is normally a flat epithelium, namely the skin, mouth, pharynx, 
(esophagus, larynx, vagina, and urinary bladder. Here there is an 
excessive growth of pavement epithelium, generally in the form, 
as we have seen, of more or less cylindrical processes. 
In some of the cases the epithelial processes tend to penetrate 
into the underlying structures so as to produce a more or less dif- 
fused infiltration and thickening of the part. In other cases the 
extension is more along the surface so as to form raised, very often 
circular tumors. The common epithelioma of the lip is a good 
example of the infiltrating form; the epithelioma of the skin else- 
where is usually of the extended flat form. The cylindrical pro- 
cesses of epithelium, as they grow, exercise pressure which, acting 
on their own cells, produces closely-compacted epidermic globes 
Fig. 96. 
Cells from a cancer, showing fatty 
degeneration. X 350. 216 
CELLULAR TUMORS. 
in the midst of them (see Fig. 97). These form very commonly a 
characteristic feature in epitheliomas, and are variously designated 
epidermic globes, laminated capsules, etc. 
Pig. 97. 
Flat-celled epithelioma : a, isolated cells; h, a cylinder with many laminated capsules; 
c, a laminate! capsule opened out so as to show the cells composing it. (Billroth.) 
Along with the production of epithelial processes penetrating 
inwards, there is very commonly the formation of papillae on the 
surface, and sometimes this is so marked as to give the surface a 
warty appearance. This is often seen in the flat extended epithe- 
liomas of the scrotum and other parts of the skin. It is also very 
pronounced sometimes in the vagino-uterine epitheliomas, giving 
rise to the cauliflower appearance. In the urinary bladder there 
is very frequently such a marked production of elongated villi that 
the surface is quite shaggy, while the mucous membrane presents 
infiltration with the epithelial processes. So much is this the case 
that the name villous cancer is often given to this form. Like 
the papilloma of the bladder, this tumor has a marked tendency 
to hemorrhage. 217 
CANCER OR CARCINOMA. 
The flat-celled epitheliomas are usually of slow growth, and are 
the least malignant of the cancers. They mostly have a tendency 
to ulcerate on the surface, especially the infiltrating ones. 
Cylinder-celled epithelioma.—This is a tumor of parts where 
cylindrical epithelium normally covers the surface, hence chiefly 
in the stomach and intestine, and more rarely in the uterus. 
The tumor takes origin in the mucous membrane, and the tissue 
has a glandular appearance, forming a congeries of tubes and cavi- 
ties, lined with cylindrical epithelium (see Fig. 98). Sometimes 
Fig. 98. 
From a cylinder-celled epithelioma of the rectum. 
the glandular appearance is strictly preserved, hut frequently the 
spaces enlarge, and as the epithelial cells accumulate they lose 
their cylindrical form, although the outer layer of cells next the 
stroma may still preserve their shape (see figure). The glandular 
elements are contained in a well-formed stroma, which is new- 
formed as well as the epithelial elements. 
In growing, the tumor infiltrates neighboring parts, insinuating 
itself among the muscular trabeculae very often, and extending 
further. It may form a considerable tumor, projecting from the 
surface, and is frequently ulcerated, as it occurs mostly in situa- 
tions where it is exposed to friction. 
From the strikingly glandular character of these tumors, many 
of them are included by some writers among the adenomas. 
(2) Ordinary cancer or carcinoma is divided into several forms 
in a somewhat arbitrary way. There are soft cancers and hard 
cancers; there are pigmented and colloid cancers, and even 
mucoid. 
The ordinary cancers consist of epithelial masses contained in 218 
CELLULAR TUMORS. 
meshes, hut the epithelium does not conform to that of the surface 
of the skin or mucous membranes, and is often characterized by 
great irregularity in form and size. It presents also little tendency 
to assume a glandular arrangement, and altogether shows less con- 
formity with normal structures than that of the epitheliomas. 
Soft cancers or medullary cancers are characterized by the 
existence of a very delicate stroma in which are abundant cells, 
usually of small size, and loosely packed in the alveoli with a good 
deal of fluid. They occur chiefly on mucous membranes, in the 
ovaries, testicles, kidneys, less commonly in the mamma. Being 
soft, they tend to bleed, and if originating on a surface or coming 
to it in their growth, they may undergo ulceration. Sometimes 
the softened, ulcerating, bleeding tissue projects in a very striking 
manner from a surface, forming the fungus h^ematodes. 
The cut surface of such tumors is gray in color, and a somewhat 
fluid juice can be scraped from it. In this juice will be found cells 
and free nuclei, the latter large and mainly oval in shape. Many 
of the cells contain fat-granules, and there may be some in an ad- 
vanced state of fatty degeneration. 
Cancers of this kind may grow to a considerable size, as those 
of the kidney, and they are often of very rapid growth. They 
are, as a rule, very malignant; the young cells, being loosely at- 
tached, readily pass away and lead to metastasis. 
Hard cancer or scirriius occurs most commonly in the mamma, 
but also in the stomach, the testicles, ovary, and kidney. It is 
characterized by the preponderance of connective tissue as com- 
pared with the epithelial structures. 
The cancers of this kind have usually a very infiltrating charac- 
ter, the epithelial processes penetrating among the surrounding 
structures, and it looks as if these processes, by their irritation, 
produced an excessive amount of connective tissue. This view is 
borne out by the fact that the connective tissue is not usually in 
the form of a well-developed stroma as if planned to support the 
epithelial structures, but is irregular and even impinges on and 
destroys the cells. The cells readily undergo fatty degeneration, 
and sometimes they to a large extent entirely disintegrate, the 
stroma assuming the upper hand. It therefore happens that dif- 
ferent parts of such tumors have often very different structures. 
The more recent parts will show well-marked epithelial masses 
with stroma (Fig. 99), while in the older parts the cells have 
almost disappeared, and there is nothing but dense connective 
tissue. 
As the scirrhus occurs more as an infiltration than a distinct 
tumor, the hardening and contraction of the connective tissue 
causes the organ in which it grows to be sometimes contracted 
rather than enlarged. It is frequently so in scirrhus of the mamma 
and of the stomach, its two most frequent seats. On cutting into 
the organ the tissue is felt to be dense and elastic. The cut surface 
is grayish and transparent, with opaque yellow markings indicating CAXCER OR CARCINOMA. 
219 
the existence of fatty degeneration in the cells. The juice to be 
obtained from the cut surface is scarce, and under the microscope 
Fig. 99. 
From a scirrhus of mamma, recent part showing stroma and epithelial cells. X 350. 
Fig. 100. 
Cells from a cancer of the mamma. Most of them contain several nuclei, and some 
daughter cells. X 200. 
it is seen to contain cells, often of large size, and free nuclei (see 
Fig. 100). The cells vary greatly in size and shape, and they 220 
CELLULAR TUMORS. 
often contain two nuclei, or even a fully formed cell inside (mother 
and daughter cells). 
Fig. 101. 
Colloid cancer. A finely reticulated stroma is seen with meshes full of colloid material, the 
cells having disappeared. X 90. 
These cancers are less malignant than the soft cancers, hut they 
produce somewhat readily secondary tumors in lymphatic glands. 
Fig. 102. 
Colloid cancer, m, n, stroma in whose meshes are cells undergoing colloid degeneration. 
X 300. (Cornil and Ranvier.) 
Between the hard and soft cancers there are cases presenting all 
shades of gradation; so that it might be possible to form a group cancer or carcinoma. 
221 
of simple or normal cancers. These have mostly a well-developed 
stroma with moderately sized cells which lie in the stroma in con- 
siderable spaces. The mamma presents these varieties, and they 
will be considered in the section devoted to the diseases of that 
organ. 
Colloid or alveolar cancer is a tumor characterized by the 
occurrence of colloid degeneration of epithelial cells. It is met 
with chiefly in the stomach and intestines, and in the mamma, 
more rarely elsewhere. 
There is here a definite new formation both of stroma and 
epithelial masses, and the stroma is often produced in the most 
beautiful and characteristic forms (see Fig. 101). As if it were 
in the plan of the growth, the cells regularly undergo colloid 
degeneration (Fig. 102), and finally the masses of cells become 
converted into masses of colloid material which fill the spaces. 
In the bulk of the tumor, therefore, there may he nothing visi- 
ble beyond the regularly formed stroma whose spaces are filled 
with clear, transparent material. Occasionally there may be in 
the centres of the alveoli some remains of the cells visible, while 
the peripheral cells are already completely converted. 
Fro. 103. 
Colloid cancer in wall of stomach, penetrating among and separating the muscular 
bundles. X 90. 
To the naked eye such tumors have a markedly gelatinous 
appearance, and as the fibrous stroma may in its coarser meshes he 
visible without the microscope, it may, even to the naked eye, look 
as if there were nothing but alveoli filled with gelatinous material, 
hence the name alveolar cancer. The tissue is frequently dense and 
hard to the feel. This arises apparently from the fact that the 222 
CELLULAR tumors. 
alveoli are tensely packed with the colloid material, and, the fibres 
being on the stretch, a dense resistance is ottered, just as a tightly 
blown-up bladder is hard. 
These tumors mostly occur as infiltrations, frequently penetrating 
among the constituents of the tissues (Fig. 103), and although 
they very often extend widely by continuity (as in the stomach), 
they show little tendency to metastasis; even when they attack 
the lymphatic glands secondarily they do not usually produce 
large tumors. 
Melanotic cancer is a rare form of tumor compared with the 
melanotic sarcoma. It occurs primarily in similar situations, 
namely, the skin and eyeball. It is really a soft cancer in which 
pigment is present in the cells and also sometimes in the stroma. 
It is usually a very malignant tumor, producing secondary growths 
by metastasis. 
Mucous cancer includes tumors in which the stroma of the 
cancer assumes the characters of mucous tissue. The cells of the 
cancer may undergo a similar degeneration. The tumor as a 
whole is very gelatinous in appearance, and resembles the colloid 
cancer. These tumors are of rare occurrence, being met with in 
similar situations to colloid cancer, but attaining the highest 
development in the ovary. 
3.—THE LYMPHATIC GROWTH OR LYMPHOMA. 
We have already seen that in leukemia there is sometimes an 
enlargement of the lymphatic glands, and that secondary tumors 
occasionally occur in the liver, kidneys, and elsewhere. We also 
saw that in Hodgkin’s disease, or adenia, there is an enlargement 
of the glands and other changes like those in leukaemia, without 
the peculiar condition of the blood which is the criterion of 
leukaemia. 
In typhoid eever we have an enlargement of the lymphatic 
glands of the mesentery, and sometimes secondary lymphatic 
growths occur in the liver and kidney similar to those in leukaemia. 
The names lymphadenoma and lymphosarcoma are given to 
tumors of the lymphatic glands, and it will be necessary to con- 
sider them more in detail. The lymphatic glands of the medias- 
tinum, for instance, sometimes undergo great enlargement, and 
get compacted into a bulky mass having the characters of a tumor, 
and to this condition the name of lymphadenoma has been given. 
The glands, although greatly enlarged and adherent by their cap- 
sules, are still individually distinct, and may be seen on section. 
The enlargement may now proceed to the glands of the neck, or 
it may originate there and pass downwards. The neck may be 
enormously enlarged and rendered somewhat rigid. These tumors 
are of slow growth, do not show any malignant tendencies, and are 
even amenable to treatment. 
But in the mediastinum tumors are not infrequent which consist 223 
THE LYMPHATIC GROWTH OR LYMPHOMA. 
of more than a simple enlargement of the glands. The glands do 
not remain distinct, and the new formation as it were passes 
through the capsule, and the whole mass becomes one, the indi- 
vidual glands being no longer distinguishable even on section. 
The new growth also tends to incorporate neighboring structures. 
It will envelop a bronchus, and gradually work through its wall, 
replacing its tissue with its own. It will incorporate the parietal 
pericardium, and afterwards pass on to the visceral layer, and 
replace even the wall of the heart by its tissue. It will surround 
a vein and work its wall up, gradually penetrating to its interior. 
Before this, thrombosis may have occurred, and the clot is Avorked 
up or replaced by the tumor tissue. Such tumors are fitly desig- 
nated lympho-sarcomas, and it will be seen that they possess a 
high degree of malignancy. They occur also in the mesentery, 
and may extend to the wall of the intestine, replacing its tube by 
lymphoid tissue, and forming a bulky tumor through which the 
calibre of the gut is maintained. They also sometimes develop 
secondary tumors by metastasis. PARASITES. 
Under this designation we include all forms of living creatures, 
whether vegetable or animal, which exist in or on the human body, 
and provide themselves with nourishment from the body or its 
juices. The parasites are beings of the most widely different kinds, 
and their relations to morbid processes in the body also differ 
greatly. In the description of parasites we shall begin with the 
lowest forms, these being the forms also around which most 
interest at the present moment centres. 
A.—VEGETABLE PARASITES. 
MICRO-ORGANISMS OR BACTERIA. 
If a fluid containing organic material, such as blood-serum or 
infusion of flesh, be exposed to the air, it soon becomes putrid, and 
everyone knows that in such putrid fluid minute forms of organized 
beings are to be found. All of these, however, are of very minute 
size, so that they may be classed as micro-organisms. To the entire 
series of such minute organisms, as we shall see afterwards, the 
name bacteria is often applied in a general sense, although various 
forms of such bacteria are distinguishable. With this simple every- 
day occurrence are connected questions of the highest importance 
and the greatest difficulty: Whence come these bacteria? What 
is their relation to the decomposition of the fluid? and many others 
of great importance. 
One of the most important of these questions, and one of the 
easiest to answer, is that which we have given first: Whence 
come the bacteria? To answer this, a very simple experiment is 
alone necessary. Let a boiled potato be cut in two, and one-lialf 
exposed with the cut surface uppermost in an inhabited room, 
while the other is kept under a bell-jar. After the exposure put 
the first half along with the other under the jar, and observe the 
condition of matters for the next few days. In the one which had 
been exposed, a number of little spots will appear in the course of 
a day or two, and these will increase in area in a more or less cir- 
cular manner. These little spots will very likely present consider- 
able differences in appearance, some yellowish, others whitish or 
pinkish in tint, and they have all the appearance of plants growing 
on the nutritious material supplied by the potato. It needs only micro-organisms or bacteria. 
225 
the most superficial microscopic investigation to prove that some 
of these spots are due to the growth of fungi, while others are the 
seat of myriads of bacteria, which are obviously multiplying at an 
extraordinary rate. It is no less obvious that these micro-organ- 
isms have arisen from something which has fallen on the potato 
from the air. The substance which has fallen from the air may 
be spores of the organism or simply the organisms themselves in a 
dried state, but we are warranted in inferring that the one or the 
other is floating in the air, and that the dust, which we know from 
other sources to be composed largely of organic matter, contains 
the germs of numerous living micro-organisms. It is only those 
which will grow on potato that will be rendered visible by their 
growth in the way mentioned. If different kinds of material suited 
to their growth be used, more varieties may be obtained. 
By thus exposing a proper soil to the air we may obtain a garden 
with several different plants in it. These plants we may propagate 
as much as we desire. We have only to transplant them with a 
needle or a knife, which has been recently heated in the flame of 
a lamp in order to destroy any organisms that may be adherent to 
it, and we obtain pnre cultivations of the various plants. By in- 
oculating several media we may find out the idiosyncrasies of the 
different organisms. Some will grow on potatoes, some need an 
animal diet, and for some a specially prepared soil is necessary. 
In this way we may cultivate the organisms through successive 
generations and in different media, and they retain their char- 
acteristics in every case. 
We may now consider what are the forms and characters of 
these bacteria. It is to be noted that all of these organisms are 
of very minute size, being scarcely visible with an ordinary low 
power of the microscope. It is their extraordinary number that 
renders them at all readily appreciable even with the microscope, 
and, it may be added, it is their extraordinary number that makes 
their existence of such importance. The extreme minuteness of 
the individual bacteria renders the classification of them very 
difficult. In the aggregate, when cultivated, say on the surface of 
the potato, they often show much more distinctive characters than 
when examined under the microscope. From this it will be under- 
stood how it is that considerable divergence exists in the nomen- 
clature of the bacteria, and differences of opinion as to their 
specific relations. 
Bacteria may be defined as minute plants of globular or oblong 
shape which increase by transverse fission. The whole group of 
bacteria is included in the family schizomycet,®. Individually 
they are for the most part only slightly colored, although in the 
aggregate they frequently show some shade of color, by which 
indeed they may be recognized. They present, like the cells of 
plants which possess a cellulose membrane, a remarkable resist- 
ance to the action of caustic alkalies and acids, although it seems 
that their wall is not actually composed of cellulose. 226 
PARASITES. 
According to Colin’s classification there are four forms of 
bacteria, namely, the spherical or globular, the small rod-shaped, 
the larger rod-shaped or thread-like, and the spiral. The first two 
are closely related, and we may even class them together as Klebs 
and Billroth do. In that case the globular bacteria and those 
which form short-beaded rods, as if from the imperfect separation 
of the globular cells, form one class, and the more definitely rod- 
shaped or thread-like form another. The first class may be called 
cocco-bacteria and the other bacilli. There remains the third 
class of spirilla, whose relations are rather obscure. 
The cocco-bacteria are very minute organisms, but they present 
the peculiarity that they have a great tendency to occur in great 
Fig. 104. 
Swarms of bacteria growing in a nutritive material. X 90. 
multitudes or swarms together. These swarms are united by a 
kind of viscous material apparently secreted by the bacteria. Ag- 
gregated thus in swarms they appear under the microscope as 
opaque cloudy masses such as those represented in Fig. 104. 
These are variously named colonies or 
zooglcea. When thus aggregated to- 
gether it is difficult to make out whether 
the bacteria are really globular or 
formed of fine rods. But if the colonies 
be flattened out, or if the edge be care- 
fully observed where the}7 are less thickly 
set, we may find out their actual struct- 
ure; they are probably most frequently 
formed of globular bacteria. The colo- 
nies often appear on the surface of de- 
composing fluids, forming the mem- 
branous-looking scum which we see so often in such situations. 
It should be mentioned that these globular bacteria are often called 
micrococci (Fig. 105), and that they have no power of spontaneous 
movement. 
Fig. 105. MICKO-ORGANISMS OR BACTERIA. 
227 
The minute rods, of which colonies are also sometimes formed, 
are believed by some to develop out of the globular bacteria. 
Klebs seems to believe that while colonies are often formed of 
globular bacteria, the peripheral ones frequently elongate into 
liner rods, and become free in the fluid. Whether this be the case 
or not, we meet with the fine rod-shaped forms free in fluids more 
frequently than the micrococci. It may be added that to this form 
of fine rods, which are so common in decomposing fluids, the term 
bacterium is sometimes applied in a more limited sense. 
The bacillus is a rod-shaped bacterium, but more elongated than 
those just referred to (Fig. 106). It has also the tendency to elon- 
gate so as to form threads of some length. Sometimes, as in the 
tubercular bacillus (Fig. 107) and in the very important bacillus 
anthracis, the threads produce spores inside themselves, which 
afterwards may become free. In regard to the cocco-bacteria, 
there seems no evidence that they bear spores of any kind, but 
they propagate merely by fission. 
The remaining form of bacterium is the spiral one or spikillum. 
This organism is in the form of a fine thread with a cork-screw 
twist in it. 
It has already been mentioned that the globular bacterium or 
micrococcus is incapable of spontaneous movement. In regard to 
Fig. 106. 
Fig. 107. 
Two forms of bacilli 
which were growing to- 
gether in the same nutri- 
tive material. One short 
and thick, the other long 
and thin. The short one 
was much more deeply 
stained than the long one. 
Methyl-violet prepara- 
tion. X 1500. 
Tubercular bacillus, consisting of threads beaded with 
spores. In the preparation the bacilli are red, and the 
other bodies (pus-corpuscles) are blue. X 1500. 
the others, some are motionless and some have locomotive powers. 
The rod-shaped forms have sometimes a wriggling movement 
which has caused them to receive sometimes the name of vibrios, 
although this name is often confined to the bacilli. The spirillar 
forms sometimes show a corkscrew movement and sometimes are 
quiescent. It may be said in general that bacteria which have 
power of motion become still at some period of their development, 
while others are motionless throughout. 228 
PARASITES. 
Methods of Detection.—It will be obvious that these minute 
organisms are often very difficult of detection, especially when 
they are mixed up with other structures or lie in the midst of the 
tissues. When they are in colonies their opaque clouded appear- 
ance and their frequent brown color make them often very prom- 
inent objects. But when more isolated, and even when in sparsely 
distributed colonies, it may be difficult to distinguish them from 
the mere granular debris of the tissues. In order to render them 
more easy of detection, various methods have been devised. The 
simplest is that originally suggested by Recklinghausen, which is 
based on the fact already mentioned, that these organisms present 
a much greater resistance to alkalies and acids than the animal 
tissues do. The addition of solution of caustic potash to an 
animal tissue renders it transparent and obscures the structure. 
If bacteria be present, they will be rendered more prominent than 
before. Dilute acetic acid, which as we know clears up the con- 
nective tissue especially, may be used in a similar way. This often 
succeeds in bringing into prominence the zoogloea of bacteria, but 
is not of much use in detecting isolated ones. 
Much advance has been made by the introduction of improved 
methods of staining bacteria devised by Weigert and improved by 
Koch. Bacteria absorb readily several kinds of dissolved pig- 
ments, but they show a peculiar tendency to become colored with 
aniline dyes. Many such dyes have been used, but the most 
suitable seem to be methyl-violet, Bismarck brown, and methyl- 
blue, of which the first two have been most used. Methyl-violet 
cannot be used with glycerine, as this agent extracts the color, and 
so a strong solution of acetate of potash in water (1 to 2) may be 
used. Preparations stained with Bismack brown may be mounted 
in glycerine or Canada balsam. 
As the observation of bacteria is now of considerable impor- 
tance, the more usual methods of investigation may be here briefly 
described. If bacteria be present in a putrid fluid, they can easily 
be seen by simply placing a drop under the microscope. But if it 
is desired to observe their characters more particularly, and to 
preserve them, the fluid may be subjected to the following treat- 
ment. A microscopic cover-glass is taken, and a small quantity 
of the fluid smeared on it in a thin layer, which is allowed to dry 
into a film on the cover-glass. To this film is added a drop of the 
methyl-yiolet or other aniline solution (prepared by adding a few 
drops of a strong spirituous solution of the dye to water). This 
solution should not be too weak, otherwise the viscid material 
which unites the colonies will be swelled up and the film loosened. 
The staining agent is allowed to act for a few seconds, and then 
run off from the cover-glass or sucked up with a pipette or blotting 
paper. If necessary, the stained film may be washed with a solu- 
tion of acetate of potash (1 to 10). After this a drop of strong 
acetate of potash solution is added to the film, and the cover-glass 
placed on a slide and examined. If aniline-brown be used, then 
glycerine may be substituted for solution of acetate of potash. In MICRO-ORGANISMS or bacteria. 
229 
some cases it is desirable to mount the specimen in Canada balsam, 
and in that case it is only necessary, after staining, to allow the 
film to dry and then add the balsam. 
It is sometimes desirable to examine blood or other fluid con- 
taining albumen in solution. When that is the case the film 
obtained by drying contains soluble albumen, and if it be treated 
as above, then the albumen is dissolved when the staining solution 
is added, and being afterwards precipitated in the granular form, 
obscures the appearances. It is necessary, therefore, to fix the 
albumen. This may be done by simplj’ leaving the film unstained 
for several days or weeks. It is more quickly done by immersing 
the cover-glass in spirits for a few days, but it is most quickly 
effected by exposing the film to a temperature of 120° to 130° C. 
If the cover-glass he placed for five or ten minutes in an air-bath 
raised to this temperature the further processes may generally 
proceed without difficulty, but sometimes it takes longer and some- 
times shorter, these exceptional cases being determined by experi- 
ment. A more rapid way of effecting the fixation of the albumen 
is to pass the cover-glass with the film three or four times through 
the flame of a spirit or Bunsen lamp. 
If the presence of bacteria be suspected in the tissues, then the 
process of preparation is more detailed. The tissue should be 
hardened in alcohol. Fine sections are then to be made, and these 
stained in the aniline solution in the usual way. They are next to 
be placed for a few seconds in diluted acetic acid, and they can 
afterwards be mounted in glycerine or acetate of potash solution, 
according to the staining agent used. If it be desired to mount 
them in Canada balsam they may be transferred direct from the 
staining solution to absolute alcohol, where they may be left for a 
time; they are then cleared up with oil of cloves, and mounted in 
balsam. Methyl-violet cannot usuall}- be used for this latter pur- 
pose, and Bismarck brown or gentian violet is perhaps the most 
useful dye. 
For the detection of bacteria in the tissues, Ivoch has introduced 
the use of a special form of illumination by means of Abbe’s con- 
denser. The use of this piece of apparatus is described in Koch’s 
work on Traumatic Infective Diseases, translated by the Sydenham 
- Society, and thus available to our readers. When sections stained 
as above are thus illuminated, the details of the tissues are obscure 
but all colored objects are rendered visible, and so the Dacteria, 
being the most definitely colored, may be prominently brought out. 
It is not to be inferred that all bacteria react equally to the 
aniline dyes. The more ordinary bacteria are stained by most of 
the colors, but the tubercular bacillus, as we have already seen, 
the typhoid bacillus, and others, have special affinities. 
Influence of Bacteria on the Living Tissues.—We have 
already seen that bacteria are present in fluids which are undergo- 
ing putrefactive decomposition, and it may now be regarded as 
demonstrated that the various forms of putrefaction are due to the 230 
PARASITES. 
action of these organisms. The details of these demonstrations 
need not detain us here, but it is important to consider whether 
the organisms or their products have any influence on the living 
body, or are the causes of disease. 
It is clear that many of these bacteria are perfectly innocuous 
when merely in contact with the surface of the body or the mucous 
membranes. The intestinal canal teems with bacteria, and the in- 
spired air, as we know, contains many kinds of them. These 
ordinary bacteria are incapable of penetrating the living tissues, 
but when death occurs they at once begin to swarm into them. 
Even when directly injected into the blood, few of these bacteria 
seem capable of surviving, although, as we shall see immediately, 
some of them undoubtedly are. 
Although ordinary bacteria and their products are incapable of 
penetrating into the healthy tissues, or at least work no mischief 
when they do, yet when they exist in wounds they find a more 
ready access to the tissues and the blood, and it will be proper 
here to consider the effects which occur in connection with putre- 
fying or septic wounds. It need hardly be stated that this subject 
is of vast importance in connection with the treatment of wounds, 
and that the antiseptic method of treatment is based on the view 
that the putrid wound is a source of mischief. 
Of great importance here are the observations of Ogston [British 
Medical Journal, March 12, 1881). These observations bear chiefly 
on the connection of micro-organisms with acute inflammations, 
especially where suppurations occur. The pus from a large 
number of abscesses was examined, and in all cases where the 
abscesses were acute, micrococci were found abundantly, whereas 
in the case of cold abscesses there were no such organisms. When 
pus containing these was injected under the skin of animals in 
small quantity it usually caused acute inflammation ending in 
abscess, and on examination the micrococci could be seen in the 
pus as well as invading the tissue around the abscess. A few 
organisms could also, in these animals, be detected in the blood, 
and the animal presented signs of general uneasiness. 
In suppurating -wounds also Ogston found micrococci, mixed 
here with bacteria of various kinds. The number and activity of 
growth of the organisms were proportionate to the intensity of the 
suppuration. 
It would appear therefore from these observations that the active 
agents in producing inflammations in the tissues are micrococci, 
while the ordinary bacteria of decomposition are not so distinctly 
concerned. From his further experiments Ogston inferred that 
micrococci grow best when not exposed to the air. He cultivated 
them by introducing a minute portion of pus into an egg, and pro- 
tecting the latter from the access of air. He found that the or- 
ganism grew vigorously when kept at the temperature of the 
body, but that they did not produce ordinary decomposition. The 
egg albumen in which the micrococci had grown produced ab- 
scesses when injected under the skin of animals. MICRO-ORGANISMS OR BACTERIA. 
231 
It may be held that these observations of Ogston prove that, of 
the organisms occurring in ordinary decomposing fluids, the mi- 
crococci are those which have the greatest power of resisting the 
living tissues, and propagating themselves inside the body. This 
is consistent with the fact that in pyremia, septic peritonitis, etc., 
it is micrococci that are found in connection with the inflammatory 
processes. It is not to be inferred, however, that in the case of 
external wounds where decomposition is going on, the chemical 
products evolved are not concerned in the production of inflam- 
mation. AYe know that these products are highly irritating, and 
they are, doubtless, capable of producing local inflammations as 
well as giving rise to general symptoms when absorbed into the 
blood. In the present state of our knowledge it is impossible to 
say whether there are many or few kinds of micrococci as of other 
bacteria, but it may be presumed that if there are not different 
species there are great differences in their state of activity at dif- 
ferent times. 
Septicemia.—The absorption of material from putrid wounds 
or, what is equivalent* to that, the injection of putrid material into 
the blood or under the skin, is followed by certain symptoms, of 
which the chief are fever, vomiting, and diarrhoea. In some cases 
there are such general symptoms alone, but in others there are 
in addition local internal inflammations which have a marked 
tendency to go rapidly on to suppuration ; the so-called metastatic 
abscesses. It has become customary to speak of cases where there is 
simply a general affection of the system, in which, in fact, there is a 
morbid condition of the blood, under the designation septicaemia, 
while those other cases in which there are metastatic inflamma- 
tions, doubtless due to embolism by septic material, are called 
cases of pyaemia. We shall speak first of conditions where there 
are no embolic phenomena, and which are generally included 
under the term Septicaemia. 
In considering the phenomena of septicaemia we have two pos- 
sible conditions to take into account. If putrid material be intro- 
duced into the blood it may produce symptoms due to the mere 
poisonous nature of the products of decomposition, namely, the 
volatile oils which give their odor of putrescence and other 
chemical principles. But on the other hand it may give rise to 
symptoms due to the bacteria which may live on in the blood and 
produce mischief there, multiplying as such organisms do with 
greater or lesser rapidity. We may thus distinguish a septicaemia 
due to chemical poisoning, and another due directly to the action 
of the organism. AVe shall first take up the former of these, and 
it will be convenient to refer to it as 'putrid or septic poisoning as dis- 
tinguished from pidrid or septic infection. (German writers use the 
expression intoxication as equivalent—it is so etymologically—to 
poisoning, hut this use is often rather confusing to English readers, 
especially when met with in translations.) 232 
p A k a s i t e s. 
(1) Septic Poisoning.—This is produced by the chemical products 
of decomposition entering the blood. It has been proved by many 
experiments that these products are capable of producing 
symptoms of poisoning, and as illustrative of such experiments 
we may cite those of Puky. 
The putrid yolk of egg containing free fat and active bacteria as 
well as the usual products of decomposition was injected into the 
jugular vein or under the skin. The result was the production of 
symptoms such as those already mentioned, but in most cases with- 
out any apparent new formation of organisms in the body. In 
these observations the organisms introduced may have had some- 
thing to do with the symptoms, but for the most part they seemed 
to be nullified by the blood, and the symptoms were due to the 
poisonous chemical products. That this was so was proved by 
boiling and filtering the putrid material before injecting it. The 
effect of boiling would be to kill the organisms, and the filtering 
would get rid of everything except the dissolved chemical products. 
'When the filtrate was used similar symptoms were produced, but 
it required a larger dose on account of some of the poison being 
carried down with the albumen. 
These experiments taken along with others seem to show that in 
putrid material there are chemical products which, if taken into 
the body in sufficient quantity, act as poisons, and may even prove 
fatal. These chemical products have not been separated as yet, 
but it appears from the observations of Panum (Virchow’s Archiv, 
vol. 60, p. 301) that they are soluble in water but not in alcohol. 
This observer evaporated the putrid material to dryness and ex- 
tracted first with alcohol and then with water. The latter solution 
produced the symptoms of poisoning, the former did not. 
There are, doubtless, in the human subject many cases in which 
the chemical products of decomposition are absorbed, the amount 
of absorption depending on the amount of the material present, 
and the capability of absorption of the surface exposed. Sub- 
stances introduced under the skin are very readily absorbed, as the 
material is introduced directly into the lymphatic channels. In a 
freshly made wound these channels are laid open, and any putrid 
material present is absorbed nearly as readily as if it were intro- 
duced under the skin. The wound fever which occurs so com- 
monly in septic cases within the first forty-eight, hours is doubtless 
due to septic poisoning, as is shown by its absence in aseptic cases. 
But, when the surfaces of a wound are covered up with granula- 
tions, the lymphatic spaces are shut off, and absorption is not so 
ready. The healthy granulations have a remarkable power of pre- 
venting absorption, as the most foul substances may be applied to 
them without any apparent absorption. 
But in some cases there is much more serious absorption of the 
products of decomposition in large or irregular wounds, such 
as those resulting from compound fractures of the bones of the 
limbs; or in the case of large suppurating and decomposing sur- 
faces such as those in an opened pleura, or peritoneum, or joint, or micro-organisms or bacteria. 
233 
chronic abscess. In these cases, the hectic fever so often leading- 
on with diarrhoea to a fatal termination, is no doubt due to septic 
poisoning. It is to be remarked that the peritoneum and the 
pleura, being lymphatic sacs, have a very high power of absorp- 
tion, and decomposing material in contact with them is very 
readily absorbed. Hence, probably, the rapid fatality of acute 
peritonitis, which, whether following on an operation, or due to per- 
foration of the intestines, is usually septic. 
On post-mortem examination in such cases, little that is definite 
can be discovered. The blood is dark in color and coagulates im- 
perfectly, and there are evidences of a tendency to liypersemia and 
capillary hemorrhage. The hemorrhage is mostly in the form of 
petechise beneath the pericardium, endocardium, and pleura, and 
the hypersemia is chiefly of the mucous membrane of the intestines, 
where it is sometimes very marked. 
It is a question whether the septic poison may not produce, 
especially in persons predisposed to it, inflammations in distant 
parts. The acute inflammation of the pleura, or pericardium, or 
even of joints, which sometimes occurs in connection with decom- 
posing wounds, may possibly be due to the septic poison, although 
more probably caused by organisms which have been absorbed. 
(2) Septic or Putrid Infection.—This condition differs from 
septic poisoning in respect that here we have to do with a virus or 
contagium capable of propagating itself, and multiplying in the 
body. In septic poisoning the effects, as in the case of other 
poisons, depend on the dose of the poison. In septic infection a 
small amount introduced will lead to the disease as well as a larger 
amount, although it may take a longer time. 
The term inoculation may be used to designate the application 
of minimum quantities of a virus to the living body. If we can 
induce putrid infection by inoculation in animals, we may expect 
that much light will be thrown on the nature of other diseases 
which are also capable of production by inoculation, and, indeed, 
on the nature of contagion in general. With this in view, as well 
as on account of its own inherent importance, it will be well to go 
more particularly into the subject here. 
The names of Coze, Feltz, Davaine, Pasteur, and Koch are asso- 
ciated with the investigation of putrid infection, and it may be said 
that Koch’s observations afford the most recent and strictly accu- 
rate information on this subject. We shall here, therefore, refer 
more in detail to his researches, especially those contained in his 
work on Traumatic Infective Diseases, and recent papers by himself 
and his assistants. 
If putrid material be injected under the skin of a mouse, the 
animal will die, as we have already seen, from septic poisoning, if 
the dose has been large enough. But if a small quantity be used, 
such as one or at most two drops, the symptoms of poisoning do 
not appear, and many of the mice recover. A certain number, 
however (about a third), of the animals become ill in about twenty- 
four hours, with certain symptoms which are quite constant, and 234 
PARASITES. 
they die in about fifty hours after the inoculation. If now a 
minute quantity of blood be taken from the body of the dead 
mouse and inoculated into a living mouse, the same symptoms 
occur, and the animal dies in about fifty hours. The disease may 
be propagated from animal to animal without fail for any number 
of generations, and an exceedingly minute quantity of blood is 
alone required in order to produce the disease. In this disease 
there are no metastatic abscesses, the only organic lesion being a 
considerable enlargement of the spleen, and so it is called by Koch 
SEPTICAEMIA OF MICE. 
When the blood of such mice is examined, whether the disease 
was produced by the primary inoculation of putrid material or by 
the inoculation of the blood of the animal which had died, it is 
found to contain myriads of minute bacilli. The accompanying- 
figure (Fig. 108, a) from Koch’s work, showing the appearances 
presented by a drop of blood stained with methyl-violet, dried, and 
mounted in Canada balsam, gives some idea of the appearance of 
these bacilli. Their size, as compared with that of the anthrax 
bacillus, is shown by contrast with the other figure (Fig. 108, b). 
Fig. 108. 
a, The blood in septicaemia of mice, showing blood-corpuscles and small bacilli. 6, Blood 
from splenic fever, showing blood-corpuscles and large bacilli. X 700. (Koch.) 
They can be shown also to be actually present in the bloodvessels 
in enormous numbers, as in Fig. 109, in which a vein from the 
diaphragm, is represented, prepared by Ivoch’s method. In this 
figure the relation of the bacilli to the white corpuscles is seen. 
They penetrate into them, multiply in their interior, and finally 
break them up. Many clusters of bacteria which might be taken 
for zooglcea have this origin. The bacilli are found not alone in 
the blood but their path of entrance is discoverable. In the sub- 
cutaneous tissue in the neighborhood of the inoculated spot they 
are very numerous, and they may extend widely in the loose con- 
nective tissue, but do not pass into the lymphatic vessels, although 
apparently finding access readily to the bloodvessels. 
The explanation of these facts is obvious. The putrid material 
originally used contains many forms of bacteria. Many of these 
are, in relation to mice, innocent, but there is a form usually 
present (apparently in small numbers) which is capable of multi- 
plying in the body of this animal. If bacteria of this kind be MICRO-ORGANISMS OR BACTERIA. 
235 
present in the fluid inoculated, they multiply in the subcutaneous 
tissue and pass into the bloodvessels, producing the disease which 
Koch calls septicaemia of mice. We shall not here follow the 
further facts in connection with this disease, as they will come up 
more suitably afterwards. 
A somewhat similar but even more virulent infective disease has 
been produced in rabbits, by the injection of putrid material. This 
Fig. 109. 
Vein of the diaphragm of a septicaemia mouse. The septicaemia bacilli are seen in great 
abundance, some of them attacking the white blood-corpuscles, which are occasionally 
reduced to masses of bacilli. X 700. (Koch.) 
disease has been more particularly studied by Coze and Feltz and 
Davaine. For the first infection a large quantity of putrid material 
is required, and it is to be remarked that while different kinds of 
fluid will produce the disease, such as putrid blood, or peritoneal 
fluid, or the slime of sewers, yet these materials often fail entirely. 
When the disease is produced, the animal begins to sicken in ten 
to twelve hours, and dies rapidly in about six or eight hours more. 
While it takes a considerable quantity of the original fluid to 236 
PARASITES. 
produce the disease, a much smaller quantity of blood from the 
animal killed by the disease suffices to produce it in a fresh animal. 
Yery striking statements have been made, on the ground of 
Davaine’s observations, as to the progressive virulence of this 
disease when propagated from one animal to another. It has been 
said that, as generation after generation is infected, a smaller dose 
is needed till the disease can be certainly produced by a trillionth 
part of a drop of blood. The observations of Koch, however, 
seem to show that these statements have arisen largely from mis- 
apprehension even of Davaine’s own observations. It is true that 
the propagated disease may be produced by such minute doses of 
blood, but it does not need to be propagated through several 
generations. In the first or at most the second generation it 
reaches its maximum of virulence, and a minimum dose is capable 
of producing the disease as in a later generation. 
Kow this septicaemia of rabbits is also produced by a bacillus, 
but one of larger size than that of the septicaemia of mice. Koch 
succeeded in obtaining a disease which he believes to be identical 
with Davaine’s putrid infection, and the bacteria were rods about 
one-half larger than those of the septicaemia of mice, and with a 
clear space in the middle, while the poles were opaque, giving a 
kind of figure-of-eight appearance. This disease was communi- 
cable to several other animals, and in the blood of these animals 
the parasite was found to have multiplied. 
It is clear from these observations that putrid material contains 
bacteria which may conveniently be classed into two groups in 
their relations to the living animal. The members of the one 
group produce, it may be, chemical matters which are poisonous 
to the living animal, but they themselves are innocuous, or at 
least the living tissues are able to resist their action and annul 
their virulent properties. The other class are able to propagate 
themselves in the animal body, and, probably by means of the 
chemical changes which they effect in the blood, they produce 
symptoms which are rapidly fatal. To the latter class of bacteria 
the adjective pathogenetic may be conveniently applied, and the 
class may be conveniently extended to include all bacteria which 
by propagating themselves inside the bod}7 produce morbid condi- 
tions in it. These pathogenetic organisms are of great importance 
not only in regard to septic infection, but, as we shall see after- 
wards, in relation to other diseases. 
In the case of the pathogenetic bacteria already mentioned efforts 
have been made to cultivate them in the pure state outside the 
body. In ordinary putrid fluid they are mixed up with other 
organisms and may be difficult to distinguish, but by using those 
developed in the blood of the animals a pure cultivation may be 
obtained. The bacillus of the septicaemia of mice has been found 
to grow best in an infusion of flesh to which has been added 1 per 
cent, of peptone, 0.6 per cent, of common salt, and enough phos- 
phate of soda to produce a weak alkaline reaction. This fluid MICRO-ORGANISMS OR BACTERIA. 
237 
may be rendered semi-solid by melting gelatine with it, and in 
this form it may be spread out on microscopic slides, and the 
blood containing bacteria sown on it. The bacteria cultivated 
in this way multiply vigorously, and they retain their pathogenetic 
character. Koch and his assistants have cultivated them through 
thirty-tive generations, and found them equally virulent through- 
out. The bacillus of the septicaemia of the rabbit has also been 
cultivated in liesh-infusion and peptone or blood-serum stiffened 
with gelatine. They also have been cultivated through nineteen 
generations and found perfectly infective at the end. 
We shall return afterwards to the subject of pathogenetic bacteria, 
and meanwhile the characters of those just described must be borne 
in mind. 
Pyemia.—We have hitherto considered those conditions con- 
nected with the absorption of putrid material in which the action 
of the virulent matter is mainly on the blood; we have still to 
consider those cases in which local inflammations result from the 
penetration of decomposing material. 
The name pyaemia is now commonly used to designate those 
conditions in which as a result of the absorption of putrid sub- 
stances multiple abscesses occur in the body. The occurrence of 
these multiple inflammations implies that a violent irritant is car- 
ried inwards and acts on the tissues. It may be said at once that 
these inflammations are always associated with the presence of 
bacteria, which may at first be carried to the part in small num- 
bers but afterwards grow into colonies. These organisms will 
primarily have their seat in the vessels, and the inflammations will 
therefore have an embolic origin. Sometimes considerable pieces 
of broken-down thrombi, arising as we shall afterwards see, are 
carried inwards and plug arteries; in other cases it is minute frag- 
ments which are conveyed, and they stick in the capillaries. As 
we have seen, however, the bacteria are self-propagating, and even 
a capillary embolism may set up a considerable inflammation. Let 
us now trace the course of events in an ordinary case of pyaemia. 
When putrid material is introduced into the blood from a wound, 
the active bacteria are usually destroyed by the living blood or 
vessels, and the result produced is, as we have already seen, a septic 
poisoning. But under certain circumstances, putrid material passes 
into the open mouths of veins, and the bacteria contained in the 
material survive and propagate. The first result produced is 
thrombosis in the veins. By and by the thrombi begin to soften, 
and they break down into a yellow material resembling pus. 
Hence the softening is sometimes called yellow or puriform 
softening. The material is not pus however, it is composed of the 
debris of the thrombus, along with the organisms which have been 
■the chief agents in the coagulation and in the subsequent softening. 
It is easy enough to determine the presence of these bacteria 
both here in their original seat and in the embolisms which are 
secondarily produced, but it is much more difficult to determine 238 
PARASITES. 
their exact nature and relations. It is clear that they are different 
from the ordinary bacteria of decomposition, the form called bac- 
terium termo. The fact that they survive within the body is evi- 
dence of this, but it is also evidenced by the communicability of 
the disease. Pysemia when it once occurs in a hospital ward is 
very apt to spread to other patients who have septic wounds. 
Puerperal fever, which is often a form of pyaemia, is known to be 
in the highest degree communicable. The probability is that we 
have here to do with a specially virulent form of bacterium which 
occasionally develops in putrid wounds. It does not, like the sep- 
ticaemia bacterium, propagate to any considerable extent in the 
circulating blood, but being carried along it fixes itself at partic- 
ular points and there forms colonies. It is even doubtful whether 
it is always the same bacterium which is concerned in pyaemia. 
The form in most, if not all, cases is that of the micrococcus. 
To return to the softened thrombus, it is clear that when the 
coagulum has broken down, the soft material and shreds of 
thrombus will pass up the vein and into the circulation, being 
carried to the right heart and the lungs. In passing up the veins 
it soon produces a second thrombosis, which for a time shuts off 
the vein with its softened contents from the rest of the circulation. 
The soft material at once proclaims its virulent character by setting 
up an acute inflammation in the walls of the vein, and this inflam- 
mation, like others produced by this virus, rapidly runs on to sup- 
puration, so that a suppurative phlebitis is the result. On post- 
mortem examination the vein or veins are often found full of pus, 
and this led earlier observers to infer that a phlebitis was the 
origin of the disease. The name pyaemia also is derived from the 
presence of pus in the veins, and its inferred entrance into the 
blood. 
It will be understood that successive coagulation and successive 
softenings of thrombi will occur, and that on each occasion a fresh 
series of embolisms will result. The products of the decomposi- 
tion will also be conveyed into the circulation, and so a septic 
poisoning will coexist. 
We have now to trace the effects which those emboli produce in 
distant organs, and it must be borne in mind that they are infective 
emboli, containing organisms which in some way produce an in- 
tense irritation leading to necrosis and inflammations with a ten- 
dency to develop suppuration very rapidly. The embolisms will 
occur primarily in the lungs, where we meet most constantly with 
the characteristic metastatic abscesses. Many times the emboli, 
especially when superficial, lead in the first place to hemorrhagic 
infarctions having the usual characters, but these soon break dod-n 
into collections of pus with the slough of lung tissue in the midst. 
If the embolism does not issue in the infarction, then the first re- 
sult of the inflammation is a condensation, the air-vesicles being 
filled up with inflammatory products, a grey hepatization, which 
rapidly gives way to a purulent inflammation with necrosis of lung 
tissue. These various stages may be visible side by side in the MICRO-ORGANISMS OR BACTERIA. 
239 
same lung. If an abscess be near the surface, the inflammation 
spreads to the pleura, and an acute pleurisy having the same sup- 
purative tendency results. 
Besides, in the lung we may have abscesses in various other 
organs. The infective material may pass through the lung capil- 
laries, or else thrombosis having occurred in the pulmonary veins in 
connection with the abscesses, pieces of the thrombi may be after- 
wards carried away. In this way abscesses not infrequently occur in 
the muscular substance of the heart, in the voluntary muscles, in the 
liver, kidney, etc. Moreover, suppurations occur not infrequently 
in the joints, and it may be in those far removed from the seat of 
the original wound. These secondary suppurations in the muscles 
and kidney are usually small but often very numerous, and we can 
understand this from the fact that the pieces of thrombus which 
pass the lung capillaries must be small, and will obstruct either 
small arteries or capillaries. 
In the accompanying figure (Fig. 110), the appearances of a 
Fig. 110. 
Pymmic abscess of kidney ; a, necrosed central part; b, area of inflammation, the tissue 
packed with pus-corpuscles; c, capillaries filled with micrococci; d, Malpighian glomeruli; 
e, uriniferous tubules. X 16. 
pysemic abscess of the kidney in process of formation are shown.. 
The preparation was stained with aniline-brown. The central part 
(a) is hardly at all colored; necrosis has occurred in it, and conse- 240 
PARASITES. 
quently the nuclei are no longer stained. In this area a high 
power showed numerous scattered bacteria. In the zone next the 
necrosis (b in figure) there are myriads of leucocytes produced 
by the inflammation. At c, c, c, are seen capillaries filled with 
bacteria. The artery whose obstruction was the primary lesion is 
not shown in this section, but many capillaries around are filled 
with organisms. 
A capillary containing the organism is shown in Fig. Ill, b, and 
this figure illustrates another fact. The figure was drawn from a 
Fig. 111. 
Capillary bloodvessel b in kidney filled with micrococci, from a case of pymmia. There is 
a tubule on either side (a, a), the nuclei of which are visible except in the neighborhood of 
the capillary. X 650. 
preparation stained with aniline-brown, and Abbe’s illuminating 
apparatus was used. As we have seen already, the effect of this 
is to bring into prominence all colored objects, while those which 
are unstained are scarcely visible. In this case the nuclei of the 
uriniferous tubules are stained as well as the bacteria, and they 
are represented in the figure at a, a. In the figure a tubule on 
either side of the capillary is shown, and it will be noticed that 
the nuclei on the sides of the tubule distal to the capillary are 
stained, while those next it are not. Here again we have evidence 
that the first effect of the bacteria is to cause necrosis, it is seen 
also that necrosis is produced at a certain distance from the 
bacteria in the uriniferous tubule while the bacteria are in the 
capillary. The organism here is a micrococcus. 
In the liver the abscesses are frequently large, and they may be 
present here while absent in the lungs. There are also not infre- 
quently considerable collections of pus in the joints. In these 
cases of the liver and joints it is probable that the phenomena are 
not so much embolic in the sense that distinct pieces of coagulum 
with bacteria are carried off, but rather that single bacteria or 
groups are conveyed by the blood, settle in the part, and propa- 
gate. The blood-current in the liver is so slow that bacteria may 
readily lodge in the capillaries, and there multiply. In the case 
of the joints also, if they once get admission to the interior, they MICRO-ORGANISMS OR BACTERIA. 
241 
are likely to multiply in tlie synovial fluid, and produce a general 
inflammation. 
Besides these embolic phenomena, the blood is altered. We 
have seen that it is poisoned with the products of decomposition, 
and it may be as a result of this that the red corpuscles are to some 
extent dissolved, their coloring matter staining the tissues and pro- 
ducing icterus, called haematogenous, as the coloring matter is 
directly derived from the blood. There is also an increase in the 
proportion of white corpuscles as compared with the red, a leu- 
cocytosis. 
Such is the ordinary course of events in pyaemia, but there are 
cases in which no thrombosis is discoverable in the veins. Putting 
aside cases in which thrombosis is present, but in such small veins 
that it is not discovered, there are undoubted cases in which 
abscesses occur in liver, kidney, spleen, and muscles, and suppura- 
tion in joints without any preceding thrombosis. These cases are 
to be accounted for on the supposition that the bacteria are intro- 
duced from the wound in such small numbers that they do not 
cause thrombosis in the veins, and consequently in these cases the 
probability is that they will pass through the lungs and over into 
the systemic circulation. The frequency of abscesses in the liver 
in such cases will be readily understood from what has gone before. 
To these we have to add a further class in which multiple ab- 
scesses occur without any external wound being discoverable. 
Some of these are associated with ulcerative endocarditis, in 
which, with an inflammation of the valvular structures, there is an 
aggregation of organisms, but there are cases in which no such 
connection can be found, and these are sometimes called cases of 
spontaneous pyemia. In this condition, as well as in ulcerative 
endocarditis, the mode of entrance of the bacteria is obscure. 
It is probable that in pyaemia, and in other diseases of a like 
nature, the bacteria do not of themselves produce the intense 
irritation manifested. It is the chemical products evolved by 
them that irritate. Hence the inflammation is frequently present 
for a considerable distance beyond the seat of the bacteria, the 
irritant passing out from them and acting on the tissues. 
Pathogenetic Bacteria in Acute Specific Diseases.—We have 
now to leave the diseases connected with putrid wounds, and con- 
sider the question whether pathogenetic bacteria exist apart from 
these. Much that has been already said will be of assistance here, 
and it will be necessary to make frequent reference to the facts 
already adduced. The diseases as they occur in man can only be 
made the subject of experimentation to a limited extent, and so 
recourse must be had to the similar diseases in animals. 
Bacteria have been found in the tissues in a large number of 
acute diseases in man. and most of these diseases belong to the 
class of zymotics. Among the diseases in which up to the present 242 
parasites. 
such organisms have been seen may be mentioned smallpox, scarlet 
fever, measles, diphtheria, acute rheumatism, erysipelas, typhoid 
fever, typhus fever, splenic fever, relapsing fever, pneumonia, 
leprosy, tuberculosis. All that is asserted in the meantime is that 
bacteria have been observed in these diseases; it is not meant that 
each of these diseases depends necessarily on a specific form of 
micro-organism. 
Most of these diseases have several things in common with the 
septicaemias of mice and rabbits, and it may he interesting to con- 
sider these points as well as some others, and to look at them in 
the light of ascertained facts. Most of them are communicable or 
infectious; that is to say, they are capable of being produced by 
the introduction of small quantities of their peculiar virus into the 
body. We have to inquire to what extent this virus is ascertained 
to he related to micro-organisms. Some of these diseases are appar- 
ently derived, not from persons already the subjects of them, but 
rather intermediately from foreign substances taken into the body. 
We have to inquire whether there is evidence that the micro- 
organisms of any of them are capable of cultivation outside the 
body, and in what kinds of media. Many of these diseases, when 
once they attack a person, create a complete or comparative im- 
munity against further attacks. We have to inquire what light 
can be thrown on this fact. Under these three headings, we shall 
consider this subject. 
(1) The Relation of Micro-organisms to Zymotic Diseases.— 
Although our information in regard to the causation of most of 
the specific fevers, and other infective diseases, is very imperfect, 
still there are several in which the evidence is tolerably clear that 
they are as closely related to bacteria as are the septicaemias of 
rabbits and mice. 
Of these, the most fully investigated is the disease now com- 
monly called splenic fever, but which has also the names anthrax, 
charbon, malignant pustule, etc. This is a disease exceedingly 
prevalent among our domestic animals, especially cattle, and it is 
sometimes propagated to man from these. The disease is an acute 
fever, in most cases beginning with shivering, and going on with 
elevation of temperature to a fatal issue. It sometimes has the 
characters of a local disease in the form of a malignant boil or 
pustule, and in many of these cases, as well as occasionally in 
cases of general infection, it does not prove fatal. Death, how- 
ever, generally occurs, both in animals and man, in from twenty- 
four to forty hours after the onset of the first symptoms. 
Uow, in this disease, there is present in the blood, and, if there 
is a local manifestation in the fluids of the part, a very definite 
form of bacterium which is called the bacillus anthracis. It is, 
as compared with most of these organisms, of a large size, as may 
be seen by comparing Fig. 112, a, in which it is represented, with 
Fig. 112,6, in which the bacillus of the septicaemia of mice is 
shown. In its distribution, the bacillus anthracis is very like the 
last-named form. It is present in quite enormous numbers in the MICRO-ORGANISMS OR BACTERIA. 
243 
blood of animals which have died of splenic fever. If an organ 
be hardened in alcohol, and fine sections stained with methyl- 
violet in the way already indicated, an appearance is presented 
Fig. 112. 
Bacillus anthracis, and of the septicaemia of mice. X 700. (Koch.) 
under a as if the capillaries were occupied by a blue 
injection material. The accompanying figure (Fig. 113) from 
Fig. 113. 
Villus of intestine in anthrax, the bacilli visible as minute threads. X 250. (Koch.) 
Koch’s work shows the appearance presented by the villus of the 
intestine in a rabbit. Under a high power this blue injection 
resolves into bacilli, as shown in Fig. 114, and it will he seen that 
these are present in enormous numbers. The bacilli are present 
in the capillaries, and hardly at all in the arteries and veins,' but 244 
PARASITES. 
as they exist in the capillaries apparently of every organ they 
must be in incredible numbers. The smallest quantity of blood 
from such an animal inoculated into a living animal, such as the 
mouse, produces the disease, and there is the same enormous 
reproduction of the organism in the blood. It is clear, therefore, 
that this disease stands in the same relation to this particular form 
of bacillus as do the septicaemias of rabbits and mice to theirs. 
Fig. 114. 
From same preparation as Fig. 113, more highly magnified. The bacilli visible as definite 
rods. X 700. (Koch.) 
In the next place, we have one of the acute fevers—relapsing 
fever—associated with the presence in the blood of a distinct 
micro-organism of a spiral form. This organism, which is shown 
in Fig. 115, belongs to the class spirillum, its specific name being 
Spirochseta Ohermeieri, from its discoverer Obermeier. Spiral 
organisms have been found in stagnant water, so that this form is 
not without its analogues in organisms met with outside the body. 
The spirilla are met with in the blood, and their detection is ren- 
dered the more easy from the lively movements which they ex- 
hibit, causing the blood-corpuscles to be moved about to some 
extent. That the disease depends on this organism seems to be 
established from the fact that it is always present in the blood 
during the acute stage of the disease, disappearing, however, in 
the interval of defervescence, but reappearing when the fever 
recurs. The disease had not, till recently, been conveyed to MICRO-ORGANISMS OR BACTERIA. 
245 
animals by inoculation of tlie blood, but now it has been com- 
municated to monkeys, and the spirillum has been found in these 
animals just as in that of man. Other animals seem, so far, to 
present an immunity against this 
form of organism. A full account 
of this organism is to be found in an 
excellent work, recently published 
by Vandyke Carter, on Spirillum 
Fever as seen in Western India. Dr. 
Carter was first to communicate the 
disease to monkeys by inoculating 
with the fresh blood of patients with 
relapsing fever. 
Typhoid fever is another disease 
in which a special form of bacillus 
has been observed. In this refer- 
ence the observations of Eberth 
(Virchow’s Arehiv, vols. 80 and 83) 
are the most important. He has 
found a bacillus in the lymphatic organs of the abdomen, namely, 
in the closed follicles of the intestine, in the mesenteric glands, 
and in the spleen (Fig. 116). This organism appears to stand 
Fig. 115. 
Blood from a case of relapsing fever, 
showing corpuscles and spirillum Ober- 
meieri. X 750. (Carter.) 
Fig. 116. 
Bacillus from lymphatic gland in a case of typhoid fever. X 1800. 
in definite relation to the duration of the disease. At the begin- 
ning of the disease, and at its height, before the sloughing of 
the intestines has occurred, it is present most abundantly, but 
as the disease becomes prolonged it diminishes and disappears. 
In the cases investigated it was found in a half, being absent in the 
more advanced cases. This bacillus does not stain so well as most 
forms, when sections have been made of organs hardened in 
alcohol, and it is most readily seen when it happens to be in 
colonies. But, if a lymphatic gland be laid open in the recent 
state, and a little of the juice from it spread on a cover-glass, and 
stained in the way already described after drying, then the rods 246 
parasites. 
will stain well, and we obtain an appearance like that shown in 
the figure. 
As somewhat less known, it may be mentioned that bacilli have 
been found in malarial fevers. Klebs and Tomasi Crudeli 
(Archiv f. Exjper. Path., vol. 11) have found in the air of malarial 
districts, in Italy, a bacillus which they were able to cultivate out 
of the body and inoculate in animals. They found a similar 
bacillus in the blood of men who had died of malarial fever. 
Klebs also states that in the blood in typhus fever there is a form 
of bacterium present. 
We have already seen that tuberculosis is to he added to the 
list of diseases due to a specific bacillus (see Fig. 54, p. 156). 
Hansen and Ueisser have described a bacillus as being univer- 
sally present in the nodules in the skin in leprosy. These bacilli 
lie partly in the round cells of the nodules. Klebs asserts that 
bacteria which can be cultivated are to be found in the syphilitic 
chancre, but these observations stand in need of confirmation. 
Erysipelas is another disease in which bacteria have been found 
by several observers. The bacteria occur in the lymphatics and 
lymph spaces, according to some also in the bloodvessels. In the 
milder cases the organisms, which are in the form of micrococci, 
are comparatively few in number, but in the more severe forms 
they fill out the lymph-spaces so as to give almost the appearance 
of an injection of them with finely granular material (see Fig. 117). 
Pig. 117. 
From the skin in a case of erysipelas. The upper drawing shows a lymphatic vessel at 
the border of a sebaceous gland filled with micrococci. The lower shows a straight vessel 
similarly filled. X 350. 
The organisms are to be found only at the advancing edge of the 
erysipelas; when the inflammation once becomes pronounced with 
rich exudation of leucocytes then the organisms disappear. 
Ulcerative endocarditis is a condition in which with acute 
inflammation of the valvular structures of the heart there is loss 
of substance by ulceration. On the inflamed surface there are 
colonies of bacteria, and these are evidently of a virulent kind, MICRO-ORGANISMS OR BACTERIA. 
247 
like, if not identical with, those in pyaemia. Pieces of the softened 
valvular structure with the bacteria are carried otf, and produce 
embolism in various organs. The disease occurs nearly always in 
the valves of the left side of the heart, mainly the aortic, and so 
the emboli are carried by the systemic arteries. Wherever they 
come to rest the emboli produce, like septic emboli, necrosis of the 
immediately neighboring tissue and acute inflammation, going on 
to suppuration around. Hence we have multiple abscesses, often 
with hemorrhage, in the kidneys, muscles, heart, skin, etc. In the 
midst of these abscesses the micrococci may be found even when 
the pus-corpuscles are crowded together. It may he added here 
that in ordinary acute endocarditis micrococci have been asserted 
by Koster to exist, not on the surface but in the substance of the 
altered valvular structure, and that by some, acute rheumatism 
which is the usual cause of acute endocarditis is regarded as due 
to the presence of bacteria in the blood. 
Without going further into particulars, it may be said that in a 
number of other diseases bacteria have been found in the blood or 
locally, although the question whether these are specific or are the 
generators of the disease must remain in abeyance. In diphtheria 
they have been found in the exudation on the mucous membranes, 
and, by some, in their substance. In scarlatina and diphtheria 
they have been found in the kidneys occupying the capillaries 
(Fig. 118), and uriniferous tubules. In smallpox they have been 
Fig. 118. 
From a section of the kidney in a case of scarlet fever. A capillary bloodvessel distended 
with bacteria is shown, with uriniferous tubules around. X 350. 
seen in the capillaries of the kidney and liver. In acute pneu- 
monia micrococci have been found occupying the lung alveoli at 
the advancing border of the disease, in this respect resembling 
those of erysipelas, and they have been seen also in the capillaries 
of the kidney. 
It is here to be stated that our knowledge of the organisms in 
the diseases mentioned in the preceding paragraph is at present 248 
PARASITES. 
exceedingly imperfect. It is remarkable that the organisms are 
found in the capillaries of the kidneys in so many cases. The 
explanation of this may be that at the time of death the bacteria 
are present there in very small numbers, and that after death they 
grow into considerable colonies. There is not usually evidence of 
considerable inflammation around the colonies, and so they can 
hardly have existed long before death. The mere fact of their 
presence, however, is important as connecting these diseases with 
micro-organisms. 
(2) Cultivation of Pathogenetic Organisms Outside the Body. 
—AVe have already seen that in the case of the septicemias of mice 
and rabbits the micro-organisms are capable of cultivation outside 
the living body, and, if this can be done in the case of the acute 
infective diseases of man then much light will be thrown on the 
origin and extension of these diseases. In the case of infective 
diseases arising from septic wounds, there is no difficulty in 
believing that the bacteria develop in the putrid exudations. In 
decomposing fluids there are numerous micro-organisms, and 
apparently a considerable variety of kinds. Certain of these seem 
adapted to one kind of animal and certain to others. But when 
we come to the acute fevers there are as yet few facts having any 
considerable degree of certainty. Concerning one disease, how- 
ever, our knowledge is tolerably complete, and on this account it 
will be treated of here in some detail. 
The bacillus anthracis exists, as we have seen, in the blood of 
animals affected with splenic fever, in the form of minute rods, as 
in Fig. 113. In the blood it seems incapable of existing in any 
other form, but it can be readily cultivated outside the body. 
AArhen placed in a proper medium and kept at a proper tempera- 
ture, the motionless rods elongate into threads, and if there be 
many bacilli present they form a network. After a short time there 
appear in the threads glancing oval bodies. By and by the threads 
disintegrate and leave these oval glancing bodies or spores free in 
the fluid. It has now been abundantly shown that, while the 
bacilli themselves do not survive long in the dry state, these spores 
are much more resistant and can be preserved for years in the dry 
condition. At the end they are as capable of producing the dis- 
ease as ever. These spores are therefore the fruit or seed of the 
anthrax bacillus, and may be the means of spreading the disease. 
This development of spores from the rods which exist in the 
blood can take place in a large number of media, both vegetable 
and animal. The bacilli grow and produce these spores very 
vigorously on the cut surface of boiled potatoes. They grow 
readily in hay infusion which has been rendered neutral or slightly 
alkaline, and in almost all kinds of vegetable infusions. They 
grow readily and form their spores in neutralized or weakly alka- 
line urine and in infusions of animal structures in general. It is 
quite clear that scattered over the surface of the earth there are 
abundant media for the propogation of this organism. If an animal 
with this disease is slaughtered, some of its blood is shed in the the question of immunity. 
249 
earth. If there is any piece of vegetable tissue lying there, and 
the conditions are such as to keep it moist and not too cold, and 
if it has not an acid reaction, then the bacilli will grow and pro- 
duce their spores. These spores may be carried hither and thither, 
and if by accident they get into the body of an animal they elongate 
into the regular rods, multiply with enormous rapidity, and lead 
to the symptoms of splenic fever. There is evidence to show that 
there are in certain parts areas of land which are regarded by the 
people as particularly dangerous as giving origin to anthrax. 
These are usually marsh}' places, and the disease is most likely to 
extend among cattle after inundations in which presumably the 
water has carried the infective material about. In these marshy 
places, especially if a chalky substratum keeps the earth more or 
less alkaline, there may be a continual growth of the bacillus and 
a continual danger of propagation. 
Another example of the propogation of a pathogenetic bacterium 
outside the body is afforded by Pasteur’s researches on chicken 
cholera. This disease of fowls is due to the existence in the 
blood of a minute bacterium constricted in the middle, so that at 
first it looks as if formed of two globular bodies. These organisms 
grow vigorously in chicken soup which has been neutralized and 
kept at a proper temperature. The organism may be propagated 
through several generations in the chicken soup, and is as capable 
of producing the disease as ever. It is interesting that this disease 
is propagated not only by inoculation. If a few drops of the fluid 
in which it has been cultivated be put on bread, and this given to 
fowls, the animals acquire the disease, the organisms passing in by 
the alimentary canal. This disease will occupy us again in con- 
sidering the question of immunity. 
It has been already mentioned that the tubercular bacillus has 
been cultivated outside the body through several generations, and 
has retained its virulence throughout. 
Regarding the existence of other pathogenetic organisms outside 
the body, very little is yet known. Most of these have been only 
recently discovered, and are even now being subjected to observa- 
tion. It may be said, however, that, as already mentioned, the 
malarial bacillus seems to exist in the air of malarial districts, and 
is probably propagated among the decayed vegetable substances 
there. A bacillus like that of typhoid fever has been described as 
having been found in the drinking water during an epidemic of 
typhoid fever. (Brautleclit, Virchow’s Archiv, vol. 84, p. 80.) 
(3) The question of immunity is the next subject with which 
we are concerned. We have to consider the fact that, under 
certain circumstances, an infective disease due to the existence of 
micro-organisms will certainly reproduce the disease in one animal, 
and will not produce it in another. There are different kinds of 
immunity. In some cases there is what may be called a natural 
immunity, and in others it is acquired or induced, as when an 
attack of smallpox confers immunity to a fresh attack of the disease. 
In regard to natural immunity, it seems that the same micro- 250 
PARASITES. 
organism will propagate itself and produce its special disease in 
one kind of animal and not in another. This has been brought 
out in a very striking way by Koch in his researches on the sep- 
ticaemia of mice. This disease which is so highly inoculable in 
the ordinary house mice is not at all inoculable in the nearly-allied 
field mouse. It is inoculable in the rabbit, but, as we shall see 
afterwards, it produces a local disease, and the bacillus does not 
propagate in the blood. The anthrax bacillus seems capable of 
propagation in every class of animal, and we have seen that it can 
be cultivated in a great variety of media. But yet, animals even 
of the same species show remarkable differences in the degree of 
certainty with which they can be inoculated. Chauveau (Comptes 
rendus, 1880, vol. 1. pp. 15-26) has shown that while ordinary sheep 
are highly susceptible, those from Algiers do not usually acquire 
the disease from a simple i noculation by a lancet. But when these 
animals are inoculated with larger quantities of the virus they do 
succumb. It seems as if they could resist a small number of the 
bacilli, but that a larger number were able to obtain the upper 
hand. Again, Pasteur has pointed out that while in ordinary 
fowls chicken cholera is highly inoculable, yet when inoculated in 
Cochin China fowls it produces for the most part merely a local 
inflammation resulting in abscess. The micro-organism which 
produces the disease is found in the pus, but the pyogenic mem- 
brane seems to limit the inroads of the organism. 
But even in the same species of animal there are some individ- 
uals which show the most remarkable resistance to the attacks of 
the various organisms. In nearly all the diseases of animals which 
have been proved to depend on micro-organisms, observation 
shows that, in the course of a considerable series of experiments, 
there are some which are proof against the disease, or at least do 
not acquire it from the same limited inoculation as the generality 
of their kind. 
It would seem from these observations that the organisms are 
not indifferent to the kind of animal which forms their hosts. 
One form will flourish in one kind of animal and not in another. 
Besides, there are individual peculiarities among the same species 
of animal so that one animal will offer much greater resistance to 
infection than another. 
These facts are perfectly consistent with what we know in regard 
to this class of diseases in the human subject. Among men there 
seem to be extreme differences in the degree of susceptibility to 
infective diseases, Anthrax itself forms sometimes in the human 
subject a local disease which is recovered from, while in other 
cases the bacillus enters the blood and produces a fatal general 
disease. In the former case the bacillus is found in the tissues 
which are the seat of local inflammation, in the latter it is present 
abundantly in the blood. We are familiar also with the fact that 
when several persons are equally exposed to the infection of small- 
pox, some may escape while others acquire the disease. It is 
known that among savage tribes measles may present an extraor- THE QUESTION OF IMMUNITY. 
251 
dinary malignancy; in this case it may indeed be that civilized 
nations have acquired a certain immunity rather than that the 
others have a special predisposition. A striking illustration of a 
similar fact is given by Grawitz (Virchow’s Archiv, vol. 84, p. 110). 
A troop of Esquimaux visited Berlin, and some were vaccinated 
with ordinary vaccine lymph. Immediately afterwards three died 
of an acute fever. Shortly afterwards the remainder were 
vaccinated in Paris, and they all perished of what the Parisian 
physicians called severe smallpox, Here again, it may be, that the 
European nations generally have acquired immunity from the 
vaccine virus. 
We have now to consider the question of acquired immunity, 
and from what has gone before it will appear that the line between 
natural and acquired immunity can hardly be rigidly drawn. In 
the case of measles it is well known that a degree of immunity is 
acquired by a single attack of the disease against further attacks, 
but then it appears that this immunity extends in some degree to 
the descendants of the person attacked, and so in countries where 
the disease is common there is not an immunity to the disease, hut 
certainly an immunity to the more severe forms of it. It is the 
same with vaccination. It confers a degree of immunity against 
smallpox, and even if this disease occurs it is in a milder form 
than usual. Without at present attempting any explanation 
of these facts we have to refer in the first place to certain observa- 
tions which bear on the question of immunity. 
In a practical point of view the protection afforded by vaccina- 
tion against the attacks of smallpox is the type of acquired im- 
munity. It is known that in the lymph of smallpox pustules as 
well as of those of vaccine there are fine globular bodies present, 
which may be called micrococci, and it has been proved by experi- 
ment that the virus resides in these solid particles, and not dissolved 
in the fluid (see Chauveau’s researches, confirmed by Burdon 
Sanderson); but the organisms have not been cultivated apart from 
the body, and it is even possible to suppose that they are not 
organisms at all. While our information in regard to smallpox is 
thus limited, some recent researches on other diseases by Pasteur 
and other French observers are of great interest as throwing light 
by analogy on vaccination. The aim in these researches was to 
obtain what may be called a vaccine of certain diseases, that is 
to say to obtain the virus in a form in which it would produce the 
disease in a mild form, and yet be a protection against the virulent 
form of the disease. 
Let us take Pasteur’sobservations on chicken cholera to begin 
with. By cultivating the bacteria of this disease in chicken soup 
with exposure to the atmospheric air he found that he could pro- 
duce what he calls an attenuation of the virus. That is to say by 
letting the organisms grow on in the same medium for several 
weeks or months before planting them in a fresh medium he found 
that each successive generation thus produced was less virulent 
when inoculated than its predecessor. In fact, by varying the ex- 252 
parasites. 
periment it was possible to procure viruses of varying degrees of 
intensity. The attenuated virus produces a local disorder rather 
than a general one, the bacteria being found in the locally affected 
parts. But the disease exhausts itself locally, the micro-organism 
being after a time nullified by the tissues. And now if animals 
which have been affected by the attenuated virus are inoculated 
with the virulent form they do not contract the disease, they have 
acquired an immunity which lasts at least a year. 
Next, in regard to anthrax, Pasteur has produced most striking 
results. Proceeding on the same principle as in the case of chicken 
cholera, his object was by prolonged cultivation of the bacillus with 
exposure to the oxygen of the air to obtain an attenuated condition 
of the virus. But here a difficulty occurred. We have already 
seen that when the bacillus anthracis is cultivated it develops 
threads and spores in the course of a comparatively short time. 
Pasteur desired, however, to cultivate the organism in the bacillus 
form. This was effected by cultivating it at a comparatively high 
temperature. It is not possible to grow it at all at 45° C., but 
coming down to 42° or 43° it does grow but yields no spores. 
Thus, the bacillus can be grown for days with exposure to oxygen, 
and as the period extends the virulence of the organism decreases. 
In this way an attenuated virus can be produced, and when this is 
inoculated in an animal the disease is acquired in a mild form, and 
the animal possesses immunity from the virulent form of it. 
Another instance of acquired immunity is afforded by the experi- 
ments of Koch. It has been already stated that the septicaemia of 
mice is not communicable to rabbits, but when the blood of such 
mice is inoculated into the skin of rabbits, it produces a disease 
like erysipelas; there is an extending inflammation of the skin, 
which, however, is recovered from. Similarly, the cornea of rab- 
bits may be inoculated, with the effect of producing a spreading 
inflammation, the inflammation in both cases being accompanied 
by the growth of the bacillus. But when the animal recovers it 
presents a condition of immunity against further inoculation. It 
is noteworthy that this immunity does not become complete all at 
once, but takes in some cases three or four weeks. 
We have now to endeavor to explain the different kinds of 
immunity. Here we are met with serious difficulties. Pasteur 
has suggested that for the growth of each micro-organism there 
is a certain substance in the blood necessary, and when this is 
exhausted the micro-organism dies, and till that substance is repro- 
duced there is no longer any possibility of its growth. There are 
obvious objections to this. For one thing, the organisms may be 
cultivated out of the body in the very blood in which they would 
not grow while it was in the living body. Then such a view will 
hardly explain the natural immunity which we have seen to be so 
closely allied to the acquired. We cannot suppose that those who 
are naturally indisposed to these diseases have blood which is 
defective in particular chemical principles. That this is not the SARCINA VENTRICULI. 
253 
case has been shown by Cliauveau, for he found that the Algerine 
sheep which are not affected by a small dose of anthrax virus do 
succumb to a larger dose. This points to an unusual degree of 
resistance to the virus; the bacillus is nullified by the tissues, and 
must attack in force before it surmounts the opposition. AVe may 
suppose that when an animal survives one of these diseases it has 
in its struggle with it acquired an increased power of resisting and 
destroying the organisms, and the power lasts a longer or shorter 
period. 
It should be stated here that by no means all of these diseases 
confer immunity by a single attack. Relapsing fever has been 
proved experimentally to be capable of repetition again and again 
in the same monkey, and it is well known that ague repeats itself 
frequently. There are even persons who are liable to repeated 
attacks of those fevers which usually confer immunity by a single 
attack. AVe find, for instance, persons who take scarlatina several 
times during a limited poriod. 
The question occurs here, how do these organisms produce 
their effects on the living bod}T? It is quite clear that some of 
them produce chemical principles which act injuriously on the 
living tissues. This is abundantly evident in the case of pyaemia. 
The organisms here produce a necrosis with inflammation around., 
But neither the necrosis nor the inflammation occurs in immediate 
proximity to the bacteria, and it is clear that some chemical pro- 
ducts passing off from the organisms act as violent irritants. It is 
so also in erysipelas. The organisms propagate themselves up the 
lymph spaces and leave behind products which lead to inflamma- 
tion. And we may suppose it to be the same when the organisms 
multiply in the blood. It is not they themselves, but the products 
evolved in the processes of multiplication and growth that are 
poisonous. Pasteur believes that the drowsiness which occurs 
in chicken cholera is due to the formation of a narcotic by the 
organism. 
SARCINA VENTRICULI. 
AVe have here to consider a form of parasite whose position in 
the vegetable kingdom is rather obscure. This organism occurs 
in the form of minute cubical bodies, each of which is partially 
divided by transverse grooves so as to make the cube somewhat 
like a parcel tied with crossing cord (see Fig. 119). It is as if the 
individual sarcina were made up by the coalescence of four smaller 
bodies, and by some methods of preparation the four smaller 
bodies assume a more nearly globular form, and so still more 
suggest such an origin. These bodies are found mostly in the 
stomach where processes of fermentation are proceeding. But 
they are met with in other situations besides. From the observa- 
tions of Lostorfer and Ferrier it appears that the sarcina appears 
spontaneously in the blood when it is kept free from contamina- 254 
PARASITES. 
tion at a certain temperature. If, for instance, blood be taken 
fresh from the vessels into a capillary tube, and preserved in a 
water-bath at a temperature near that of the body, in almost every 
case sarcinae will develop in the 
course of a few days (see Lostorfer, 
Wien. Med. Jahrbiicher, 1871, and 
Ferrier, Brit. Med. Jour., Jan. 27, 
1872). The sarcinae first appear 
as minute glancing globular 
bodies, and by and by they ag- 
gregate into the regular cubes. 
These cubes are much smaller 
than those of the sarcinae found 
in the stomach, but when placed 
in a proper nourishing fluid such 
as Pasteur’s solution, they grow 
to the size of these and assume 
their brownish color. 
It thus appears that, in the 
blood of man, and also, as ex- 
periment has shown, in that of 
animals, there are germs which 
have the capability of developing 
the sarcinae. Occurring in the 
stomach, the germs are probably derived from the blood, the 
stomach acting as a breeding oven. This explains the fact that 
sarcinae are met with elsewhere, as in urine, pus from cavities, 
gangrenous fluid, etc. 
The exact botanical relations of sarcinae are not determined. 
Some call them algae. The fact of their appearing in the blood 
first as minute globular bodies suggests that they may be allied to 
the bacteria. 
Fig. 119. 
Sarcinae ventrieuli (a), starch granules 
(6), and fungus spores (c), from vomited 
matter. X 350. 
PARASITIC FUNGI. 
The fungi are defined as consisting of cells devoid of chlorophyll, 
and occurring in the form of threads (hyphse) and round or oval 
bodies (spores and conidia). 
If the spores of ordinary penicillium fall into a fitting medium 
they soon begin to send out buds which become threads. By 
elongation and branching of these threads (hyphse) a network is 
formed, which is designated the mycelium, and is regarded gen- 
erally as the root structure of the fungus. Under favorable cir- 
cumstances upright stems (see Fig. 120) arise from this mycelium 
which bear the fructification of the fungus. These consist of elon- 
gated cells at the extremity of which rows of round or oval bodies 
develop in a pencil-like fashion, as seen in Fig. 120. This appear- 
ance has caused this form of common mould to be called peni- 
cillium. These round or oval bodies are spores, and each of them 
when carried off from the fungus is capable of giving rise to a fresh PARASITIC FUNGI. 
255 
plant. It is asserted that in addition to this mode of fructification 
which is non-sexual, there is, probably in the case of all fungi, a 
sexual fructification, and much speculation has arisen as to the 
powers of the spores thus variously produced. These speculations 
do not concern us here, but it may be observed that so long as the 
Fig. 120. 
Aerial growth of penicillium. 
sexual fructification is not determined the exact generic and specific 
relations of the individual fungi must remain obscure. 
The mode of production of spores figured above occurs when 
the fungus is able to send shoots up into the air; it is an aerial 
production as distinguished from the mycelium which is in the soil. 
But a process in some respects similar often takes place in the soil 
itself. This is shown in the case of the same fungus in Fig. 121, 
where it is seen that instead of forming elongated threads the cells 
Fig. 121. 
Formation of conidia in submerged portion of penicillium. 
are dividing into oval bodies. In many of these the liour-glass 
shape indicates the process of division actually in progress. In 
this way spores may be produced which are here called conidia. 
It is clear that this also is a non-sexual reproduction, and that it is 
strictly comparable with the aerial reproduction already mentioned. 
In fact the spores produced in the latter way are also frequently 
called conidia. 
It is to he remarked further that, with almost no attempt to 256 
PARASITES. 
produce threads, the spores or conidia may multiply in the medium 
which forms their soil, and so we may have masses of spores or 
conidia and little else. This is the condition of the yeast fungus, 
the torula cerevisise, and we often find multiplying spores of fungi 
in the contents of the stomach, as in Fig. 119. 
In their pathological relations, fungi are of much less conse- 
quence than the schizomycehe, and it does not appear that they 
are capable, to any considerable extent, of producing chemical 
principles that are seriously injurious to the animal tissues. There 
are some diseases in which the existence of fungi in the body is 
rather to be regarded as secondary, the primary diseased condition 
providing a titting soil for the growth of the fungus, but there are 
other conditions in which they act injuriously by their presence 
and growth. 
Fig. 122. 
Fungous growth in kidney. To the left of the figure the kidney-tissue has been cleared 
up by adding solution of soda so as to bring out the fungus (aspergillus). Fat-drops and 
crystals of tyrosin are present, but no spores. (Grawitz.) 
It may be well here to inquire whether fungi, like the bacteria, 
are divisible into pathogenetic and innocuous forms. In answer to 
this, it may be said that there appear to be no fungi capable of PARASITIC fungi. 
257 
actually multiplying in the body, but there are some which possess 
the capability of growing there. Most fungi, when the spores are 
injected into the blood, simply die and are destroyed, but, accord- 
ing to the researches of Grohe, Block, and Grawitz (Virchow’s 
Archiv, vols. 81 and 84), there are some which may survive and 
grow inside the body. When spores of such pathogenetic fungi are 
introduced into the blood, they pass to various parts of the body, 
where they bud out and grow, by their growth producing numerous 
local necroses which may cause death in three days, or an inflam- 
mation which may lead to the death of the fungus and the forma- 
tion of a capsule around it. In the illustrations to Grawitz’s paper, 
the condition presented to the naked eye by the kidneys is shown, 
and the resemblance of the multiple necroses to metastatic abscesses 
in pyaemia is very striking. In each of these a growing fungus is 
to be found, as shown in Fig. 122, but it does not go on to the 
formation of spores. If a piece of the tissue be used, however, 
the fungus may be cultivated outside the body in a suitable 
medium, and it goes on to the production of spores in the usual 
fashion. 
The question occurs here, Are there certain species of fungi 
which have this special character, or are the ordinary fungi capable 
of becoming pathogenetic 2 This question has been answered in the 
latter sense by Grawitz. He asserts that the ordinary mould fungi, 
by being cultivated through several generations in alkaline solu- 
tions of albumen, at a temperature of 38° to 40° C., acquire viru- 
lent properties as above. Considerable doubt has been thrown on 
these conclusions by the researches of Ivoch and his assistants. 
They have found that the spores of the aspergillus glaucus, without 
any cultivation in animal fluids, are always, pathogenetic, and they 
seem to assert that in the experiments of Grawitz there has been 
a contamination with the spores of this common fungus. We are 
to infer, therefore, that there are some fungi which are naturally 
able to resist the action of the living tissues, and grow in spite of 
them. 
The madura foot is a disease which occurs in the East, and 
whose relations to fungi have been investigated by ATandyke Carter. 
In this disease a fungus, called in honor of its discoverer Chionyphe 
-Carteri, penetrates into the substance of the foot, producing canals 
and cavities among the soft structures and the bones, and giving 
rise to severe inflammations. In the cavities and canals are masses 
of fungi of a blackish color, and forming frequent balls. The 
canals open externally, and discharge a fetid pus containing spores 
and threads of the fungus. There is great thickening and an 
appearance resembling that of scrofulous disease, and the condi- 
tion is a chronic one for which amputation must frequently be 
performed. 
In a considerable number of cases a fungus has been found in 
the ear. It has its seat in the external meatus and on the mem- 258 
PARASITES. 
brana tympani, where it is accompanied by desquamation of the 
epithelium and other signs of inflammation. It is noteworthy 
here, in connection with what has gone before, that the fungus 
met with seems always an aspergillus, although spores of peni- 
cillium are as abundant in the air, and the two fungi are usually 
associated in mould. Fungi have also been met with in cavities 
of the lungs, on ulcers of the skin, etc. 
Fungi are of frequent occurrence in the skin, and there are 
three forms of skin disease which are always associated with the 
Fig. 123. 
Hair from a case of ringworm, showing fungus penetrating and breaking up the shaft. X 350. 
presence of these parasites, namely, Ringworm, Pityriasis versi- 
color, and Favus. In all of these the fungus appears in the form 
of multiplying spores or conidia, with irregular production of 
mycelium, but thpre is no proper fructification, the nearest ap- 
proach to that being in the case of pityriasis versicolor. The 
consideration of these fungi will come up for more particular PARASITIC FUNGI. 
259 
study under the section on Diseases of the Skin. We have here 
to refer to the general conditions which they present. The fungus 
grows chiefly among the epidermic elements, spores and mycelium 
penetrating among the cells and displacing or breaking up the 
structures such as the hairs, etc. (Fig. 123). It is usual to describe 
the fungi of these three diseases as different, and they are named 
Achorion Schcenleinii (favus), Trichophyton tonsurans (ringworm), 
and Microsporon furfuri (pityriasis versicolor). Doubts have been 
raised, however, chiefly at the suggestion of Iiebra, whether the 
fungus is not identical in all the three, and whether it is not one 
of the common moulds occurring in a special form and locality. 
It might appear that such a question would be easy of answer by 
means of observation of the fungus and its cultivation. But there 
are two difficulties which are encountered here. In the first place, 
as the fungus only occurs in the form of multiplying spores and 
irregular threads, the fructification is not manifested, and the 
classification of fungi, as we know, is based on the fructification. 
Then, in the second place, the cultivation of the fungus has, in the 
hands of different observers, led to apparently contradictory results. 
Almost all the commoner moulds have been developed from the 
products of these diseases, and considering the wide prevalence of 
the spores of fungi in the air, and the probability that many such 
spores are continually falling on the skin, it is difficult to be certain 
that accidental contamination has not occurred. 
In the mouth, fungi are frequently to be found. The white 
material which lies in the angle between the teeth and the gums 
always contains multitudinous threads of a fungus or schizomyceta, 
called Leptothrix buccalis (see Fig. 124). This occurs in the form 
Fig. 124. 
Leptothrix buccalis from the gums at edges of teeth : a, the filaments separated; 
l, masses of filaments. X 350. 
of fine threads which often hang together in bunches. It has been 
asserted by Leber and Rottenstein that this organism, by pene- 
trating into the teeth produces caries; hut, considering its universal 
presence in contact with the teeth, this seems doubtful. There 260 
p a R a s IT E s. 
is one circumstance which, however, is in favor of this view, namely, 
that the organism seems to aggregate lime salts in its nutritive pro- 
cesses. It usually attracts the lime from the food, and forms with 
other matters the so-called “tartar” on the teeth, but it is con- 
ceivable that it may acquire lime from the teeth, and so produce 
softening of them and caries. 
There is a disease of the mouth called commonly thrush, de- 
pendent on a fungus, the Oidium albicans. Here, as in the case of 
the parasitic skin diseases, the fungus grows among the epithelial 
cells, detaching them from one another, but binding them together 
into a kind of soft membrane (Fig. 125). The so-called aphthous 
condition arising in this way does not develop in healthy persons, 
Fig. 125. 
Oidium albicans, from the mouth in a case of thrush. (Kuchenmeister.) 
but is met with chiefly in emaciated children, or in adults whose 
health has been depreciated by tuberculosis, typhus fever, etc. 
The fungus may extend to oesophagus, stomach, etc., producing 
the same aphthous patches. 
B.—ANIMAL PARASITES. 
The Animal Parasites are divisible into two groups according 
as they live inside the body (the entozoa), or on the surface (the 
epizoa). The entozoa are all included among the worms, and are 
met with in the alimentary canal and in the tissues. 
ENTOZOA OH INTERNAL PARASITES. 
(1) Trematoda.—We have here an order of flat-worms of a more 
or less oval form, and many of them somewhat in the form of a 261 
FLAT-WORMS. 
leaf. They possess, on the ventral surface, one or more sucking 
disks by which they attach themselves. They have only one 
opening of the alimentary canal, which is generally forked. These 
worms are commonly called flukes from the resemblance in shape 
of the commonest of them to the lisli of that name. 
The distoma hepaticum is the commonest worm of this order. 
As the name implies, it is met with in the liver, where it inhabits 
the bile-ducts. The liver fluke is generally about an inch in 
length (Fig. 126), and rather more than half an inch in greatest 
breadth. The body is very flat, and anteriorly it ends in an elon- 
gated process, forming a kind of head. This head bears the 
mouth, and a short distance behind it comes the sucking disk. 
Between these lies the opening of the sexual ap- 
paratus, of which both male and female organs 
exist in each individual. The uterus forms a con- 
voluted tube behind the sexual opening, and the 
seminal tubules lie still further back. This para- 
site is very common in certain of the lower 
animals, especially sheep. It occurs in enormous 
numbers in the bile-ducts, which are dilated by it 
but not otherwise strikingly altered. As many as 
1000 have been obtained from a single sheep. It 
produces in sheep the disease called commonly 
the rot, which in some years is very fatal. It is 
said that in 1830-31 between one and two million 
sheep perished from it. It occurs also in oxen, 
where it produces more considerable alterations of 
the ducts. These become greatly dilated, thick- 
ened by inflammation, and incrusted with lime. It sometimes 
happens that masses of inspissated bile and lime salts form in the 
liver where the flukes are present. It is probable that in these 
cases many of the parasites have died and become themselves the 
seat of incrustation. This fluke has also been met with in horses 
and asses, and in some rare cases in man. In man it has not been 
observed in large numbers, but it may produce serious obstruction 
of the bile-ducts. 
The eggs of this parasite are small oval bodies, which, in water, 
develop into embryos which swim about by the aid of cilia. 
Their further development is unknown, and also the form in which 
they pass into the animal which becomes the host of the adult. 
The distoma sinense is a parasite met with in the East, and de- 
scribed by M’Connell in the Lancet, in 1875, and independently 
by Macgregor in the Glasgow Medical Journal, in 1877. Although 
a much smaller worm it is of a more elongated shape than the 
distoma hepaticum, as will be seen from Fig. 127. It is rather 
more than half an inch in length, and about an eighth of an inch 
in greatest breadth. When seen in the bile in the fresh state, the 
edges show a beautiful, delicate, green color, tinged with yellow, 
while the centre is of a deep brown. In the accompanying figure 
Fig. 126. 
Distoma hepaticum. 
(Leuckakt.) 262 
the position and appearances of the various organs are indicated. 
The eggs are very small, and each animal possesses thousands. 
This parasite has only hitherto been observed in man, and is 
found in very large numbers—not less than 500, probably more— 
in the ducts of the liver and in the gall-bladder. 
In I)r. Macgregor’s cases the persons affected 
with the parasites were Chinese, and they were 
the victims of a peculiar paralysis of the legs 
and arms. Dr. M’Connell’s case was also in a 
Chinaman. 
The distoma lanceolatum is another form of 
fluke. It is less than three-eighths of an inch 
in length, and about the fifteenth of an inch in 
breadth. It is seldom seen in man, and occurs 
in comparatively small numbers in sheep and 
cattle, producing little disturbance. 
The distoma haematobium, also called the 
Bilharzia hfematobia, has the male and female 
organs in different individuals. The male is 
about half an inch in length, and flat, but rolled 
up at the edges, especially behind, so as to form 
a kind of gutter in which the female lodges. 
The female is about a half longer, but filiform. 
The eggs are small and furnished with a spine 
at the end or at the side. 
The parasite inhabits the bloodvessels of its 
host, chiefly the portal vein, the splenic and 
mesenteric veins, and those of the rectum and 
bladder. The penetration of the eggs in large 
numbers into the mucous membrane of the 
rectum and urinary bladder produces great 
irritation, and frequently hemorrhage. Similar 
irritation may be produced in the pelvis of 
the kidney and ureters. This parasite is met 
with almost solely in Egypt and Abyssinia, 
and it is said that in Egypt about half the 
natives are victims of it. 
(2) Cestoda or Tape-worms.—These are in the mature state 
long flat worms, without mouth or alimentary canal. Anteriorly 
there is a head furnished with some apparatus for attaching itself 
to the host. Behind the head and neck the worm forms a series 
of segments called proglottides, each of which develops a bi- 
sexual apparatus and is, so far, a complete individual. The adult 
worm or strobilus is therefore a colony of individuals. The worm 
inhabits the alimentary canal and apparently occurs only in verte- 
brate animals. Besides this adult form there is an intermediate 
immature form, called the scolex, which occurs in the tissues of 
animals. The scolex has a head like that of the mature worm, 
and generally possesses a sac or cyst into which it can retire. 
PARASITES. 
Fig. 127. 
Distoma sinense, a, 
oesophagus and stomach 
tubes ; b, uterus; c, yolk 
glands; d, ovary; e, 
testes; f, termination of 
water-vascular system. 
X 5. (After Mac- 
Gregor.) TAPE-WORMS. 
263 
There are representatives of two families of this parasite met 
with in man, namely, the Taenia and Bothriocephalus. 
The thsnia solium is of very common occurrence in this country. 
The strobilus or mature worm occurs in the alimentary canal, and 
the head is usually situated in the duodenum or upper part of the 
jejunum, while the rest of the animal extends downwards in the 
canal, attaining on an average a length of from ten to twelve feet. 
As already mentioned, this, like other tapeworms, has no ali- 
mentary canal, and supports itself by imbibition of nutritious 
material from the intestine. 
The head of the worm, which is represented in Fig. 128, is 
about the size of a pin’s head, and of a generally rounded form. 
In front it is prolonged so as to form a proboscis or rostellum, 
which is surounded b}7 a circle of twenty-six hooklets. The wide 
part of the head has four large sucking disks. On the head follows 
a narrow neck, which is so thin that it readily breaks when the 
worm is handled, rendering it difficult to obtain the small head. 
Fig. 128. 
Fig. 129 
Unripe proglottis of T. solium, showing sexual 
organs. The small vesicles scattered throughout 
are the male organs. The other structures shown 
are seminal tubes, vagina, globular body, yolk- 
body, ovaries, and unbranched uterus. X 10. 
(Leuckart.) 
Head of T. solium. X 45. (Leuckart.) 
The proper neck is about half an inch in length, and it gradually 
merges in the anterior part of the body, in which tine transverse 
lines begin to appear as the first indication of the formation of 
segments. On passing down, the worm increases in breadth, 
while the segments elongate and become more completely divided. 
At first the segments or proglottides are homogeneous in appear- 
ance, but by and by the sexual apparatus begins to appear. The 
total number of segments in a worm ten feet in length is about 
800. The sexual apparatus begins to appear about the 200th seg- 
ment from the front, and is mature about the 450th; it consists of 
the male and female organs which are present in each segment. 
The male organs consist of a large number of vesicles scattered 264 
PARASITES. 
throughout the segment, as shown in Fig. 129, but more abundant 
anteriorly, as the female organs occupy the space behind. The 
vesicles are connected with fine seminal tubules which are difficult 
to make out, and are shown in the figure as fine branching lines. 
These end in a slightly convoluted tube, the vas deferens which is 
generally very distinct, and this passes across the segment to the 
papilla, a slight projection at the side of the segment into which 
the male and female sexual organs open. At the papilla the vas 
deferens ends in a projectile penis which is capable of passing into 
the extremity of the female organ, the first part of which is called 
the vagina. 
Tlie vagina forms a canal which passes transversely across the 
segment towards the middle line and tends also backwards, to end 
in a somewhat globular dilatation, sometimes called the globular 
body. The connections of this body are difficult to make out, but 
they may be stated as follows, and understood by the annexed 
Figs. 129 and 130. In the posterior part of the segment, as shown 
in Fig. 129, are seen on either side the comparatively large ovaries, 
forming tree-like expansions, consisting of a congeries of closed 
tubes. The ovaries have ducts which pass into the globular body. 
Behind the ovaries and the globular body is the yolk-gland, which 
is of a somewhat pyramidal shape and spread out laterally. This 
also communicates with the globular body in front of it. Besides 
these communications the globular body, which is thus the central 
part of the female organs, communicates with the uterus in front. 
At this period of maturity the uterus consists of a simple tube 
extending longitudinally in the middle of the segment (see Fig. 
129). It will thus be observed (Fig. 130) that the globular body 
has communication with four distinct structures, a with the yolk- 
sac, b with the ovaries, c with the vagina, and d with the uterus. 
The eggs pass from the ovaries first into the globular body, where 
Fig. 130. 
-Fig. 131. 
The globular body, or Mellis’s body, and its 
connections. See text. X 30. (Leuckart.'I 
Proglottis of T. solium, showing branching of 
uterus. X 5. 
they receive a covering of yolk, are fertilized, and undergo the 
beginning of their development. Then they pass into the uterus, 
which they till up. As the ova accumulate in the uterus, this 
begins to throw out lateral branches to the number of seven to 
ten (see Fig. 131). The lateral branches often show considerable 
ramifications, in this respect and in their number contrasting with 
those of the next tapeworm. In the fully mature proglottis only TAPE-WORMS. 
265 
tlie uterus crowded with ova is visible, the remaining organs 
having disappeared (see Fig. 182). The prominent ova often make 
the position and .shape of the uterus very distinct, especially if 
the proglottis be spread out on a glass slide and allowed to dry. 
Besides the sexual organs the proglottides pos- 
sess muscular fibres, and a water-vascular system. 
The muscle is non-striated and consists of longi- 
tudinal and transverse bundles. The water-vas- 
cular or excretory system (shown in Figs. 129 
and 131) is in the form of tolerably wide channels, 
which begin at the head and are continued through 
the proglottides by two lateral channels right down 
to the last, where they open outwards. Xear the 
posterior extremity of each proglottis the tubes 
form transverse communications (see figures). It 
is possible to inject these tubes from above down- 
wards, but not from below upwards. In addition, 
the proglottides, as well as the head of the worm, 
possess numerous round or oval calcareous bodies, 
which are mainly in the superficial layers of the 
parenchyma. 
As the proglottides become mature they sever 
their connection with the worm and drop off from 
its lower extremity one by one. They pass down 
the alimentary canal, and are discharged with the 
feces, or else work their way out through the 
anus by virtue of their contractile power. For a 
short time after discharge they still show a writh- 
ing movement, b,ut they soon come to rest and die. By the decom- 
position of the proglottis the ova are set free and are ready under 
suitable circumstances to develop further. 
It is mostly in the bodies of swine that the taenia solium passes 
through the next phase of its development, although sometimes 
it occurs in man. It is exceedingly 
doubtful whether a man who is the 
host of a mature tape-worm can be 
affected from it with the form now to 
be described. 
The ova (Fig. 133) are surrounded 
by a dense shell of a brownish color. 
Inside the shell the egg develops an 
embryo which acquires six boring 
spines. When such ova get into the 
intestinal canal of the pig, the shell 
bursts, and the embryo with its spines 
escapes. It proceeds to bore its way outwards, and after piercing 
the alimentary canal it finds its way to the muscles of the animal 
where it finds a lodgement. 
Arrived in its desired seat, the embryo comes to a state of rest, 
and after a time develops into a vesicle or cyst, which afterwards 
Fig. 132. 
Two ripe proglot- 
tides of T. solium, 
with branches of 
uterus shown. X 2. 
(Leuckart.) 
Fig. 133. 
Ova of T. solium, a with yolk, b 
without yolk, as in mature seg- 
ments. The hard brown shell is 
indicated. (Leuckart.) 266 
PARASITES. 
forms the proper cysticercus. The appearance of these cysticerci 
in the muscular tissue is shown in Fig. 134, which is drawn of the 
natural size. The complete cysticercus or scolex has a head 
developed in connection with the vesicle, which closely resembles 
Fig. 134. 
Cysticerci of tenia solium in muscle. Natural size. (Leuckart.) 
the head of the mature worm (Fig. 135), and we have now to con- 
sider how this head forms. The observations of Leuckart and 
•others have thrown much light on this, as they are based on actual 
experiments in which swine were fed with the ova. 
Fig. 135. 
We have seen that in the muscle a vesicle or cyst is formed. 
After a time a slight thickening of the wall of the cyst appears. 
This grows inwards into the cyst, carrying with it, however, the 
external wall, so that the projection inwards is hollow with an 
internal canal continuous with the surface of the cyst, and so opens 
externally; this is shown in Fig. 136, where a portion of the wall 
of the cyst is preserved, and the projection is shown with its 
internal cavity communicating with the surface of the cyst. This 
projection enlarges, and by and by the peculiar structures of the 
Head of cysticercus cellulose found in substance of brain. X 90. TAPE-WORMS. 
267 
head, namely, the four sucking disks and the hooklets, show them- 
selves. But these are formed inside the canal, near its extremity, 
and they are in an inverted position as com- 
pared with that of the mature tape-worm. The 
head with its hooklets are thus at the bottom 
of the canal, and the four suckers, looking 
towards each other, follow. After a time 
the head acquires the power of inverting 
itself outwards, and thus projecting from the 
vesicle, or again withdrawing itself within 
the vesicle as before. This is effected by 
means of muscular fibres. For the comple- 
tion of this phase of development a period of 
from three to four months is required from 
the time of the ova being taken into the ali- 
mentary canal. 
It sometimes happens that this scolex of 
the teenia solium develops in the human sub- 
ject, and then it is often spoken of as the cysticercus cellulosje. 
It occurs chiefly in the brain, in the eyeball, and in muscle. 
It is to be remarked that in rare cases the scolex assumes in 
the brain a very peculiar character. The cyst, developing in the 
membranes on the surface of the brain, presents pouches and 
swellings which give it somewhat the character of a bunch of 
grapes, and so has given rise to the designation cysticercus race- 
mosus. The cysticercus is usually surrounded by a connective- 
tissue capsule which is produced from the surrounding tissue and 
encloses both cyst and head, but not infrequently, especially in 
the brain and eyeball, it is devoid of this secondary capsule. In 
Fig. 186. 
Cysticercus with begin- 
ning of development of 
head. A portion of the 
original cyst is shown with 
the projection inwards of 
a hollow process which 
communicates externally. 
X 25. (Leuckart.) 
Fig. 137. 
Hooks from head of cysticercus cellulose. X 350. 
that case the vesicle sometimes grows to considerable dimensions, 
and the head is able to protrude itself and move about in various 
directions, perhaps in the ventricle of the brain or the eyeball. In 
these parts the scolex may produce considerable disturbance. 268 
PARASITES. 
Although capable of a considerable duration of life, after a time 
the scolex usually dies, and then it shrinks and becomes, probably, 
incrusted with lime salts. The hooklets are the most resistant 
parts, and it is of some consequence to observe the size and general 
appearance of these. In Fig. 137 are represented the hooklets of 
this worm, magnified three hundred and fifty times. They are to 
be contrasted with those of the taenia echinococcus (Fig. 138), which 
are magnified to the same extent. 
It will be seen that in the taenia solium there are two sizes of 
hooklets, a larger and a smaller, and by comparison with Fig. 135 
it will be seen that these are arranged alternately around the 
rostellum. In this as in .other respects, the heads of the scolex 
and of the mature worm are identical. 
Fig. 138. 
Fig. 139. 
A single head of taenia solium before 
segmentation has begun. It shows 
movements of its suckers, etc. X 25. 
(LEtrCKAUT.) 
Hooks from taenia echinococcus. X 350. 
We have now to trace the further progress of development where 
living scolices are taken into the alimentary canal of man. In the 
first place, the vesicle and everything hut the head and neck are 
lost, and we have a small creature which has considerable power 
of elongating and moving about its suckers, as shown in Fig. 139. 
The head now fixes itself to the wall of the alimentary canal, and 
the body begins to develop from its posterior extremity. It takes 
eleven or twelve weeks for the worm to assume its full dimensions, 
and at the end of that time it begins to show proglottides. The 
worm is of tolerably long life, and may inhabit the intestine of its 
host for many years. It not infrequently happens that several 
coexist in the same person; as many as thirty or forty have been 
observed. 
The U3NIA mediocanellata may be dismissed much more shortly 
as the various stages in its development and its structure are, in 
most respects, essentially like those of the taenia solium. Leuckart 
calls this tapeworm the taenia saginata. 
The strobilus is a larger worm than the taenia solium, measuring 
from about thirteen feet in the contracted state to about twenty- 
four feet when extended. Fig. 140 shows the head and neck of 
this worm in the contracted apd relaxed conditions. The difference 
in length and breadth is very striking. The head has no rostellum TAPE-WORMS. 
269 
or circle of hooks, but it possesses four large sucking disks which 
are usually surrounded by a zone of pigment. The segments are 
in the most of the worm broader than they are long, attaining 
a breadth of about half an inch. But as we come to the fully 
Fig. 140. 
Head and neck of ti«nia mediocanellata ; a, in contracted, and b, uncontracted state. X 8* 
(Leuckart.) 
mature proglottides with embryos in the uterus, then they are 
considerably elongated and at the same time narrower. The 
number of segments is greater here than in the taenia solium, 
reaching as high a figure as thirteen hundred. There are generally 
about eight discharged from the posterior extremity daily, and 
these very often find their way outwards, through the anus, by 
their own movement. 
The sexual organs, except the uterus, are essentially the same 
as in the taenia solium. The uterus, however, presents in the 
mature proglottis a much larger number of lateral offsets, as many 
as twenty to thirty, and these mostly branch dicliotomously instead 
of ramifying (see Figs. 141 and 142). 
The individual segments, like the worm as a whole, possess 
muscular fibres, and are capable of elongating and contracting. 
The scolex form of this worm is found chiefly in cattle, and it 
inhabits mostly the muscles, but is also met with in other organs. 
The cysticercus measures about the third of an inch, and is of a 
roundish shape. 
This worm is nearly equal in frequency to the taenia solium in 270 
PARASITES. 
the human subject. Its cysticercus is not known to occur in man. 
The worm may live for many years, at least as long as eleven, 
and, as some assert, up to twenty or even thirty years. 
Pig. 141. 
Fig. 142. 
Immature proglottis of T. mediooanellata. 
X 5. (Leuckart.) 
Mature proglottis of T. medio- 
canellata. X 2. (Leuckart.) 
The taenia echinococcus in the strobilus form is a comparatively 
insignificant worm (Fig. 143). It inhabits the dog, and there are 
generally several individuals present at the same 
time. The total length of the worm is about an 
eighth of an inch, and it consists only of four seg- 
ments, including that which carries the head. In 
the fully developed state the last segment exceeds 
in length the rest of the worm altogether (see 
figure). The head is like that of the tamia solium 
in miniature, being very greatly less in size. It 
has a rostellum with thirty to forty hooklets, and 
four sucking disks. The last segment develops a 
large number of eggs, as many as 5000. 
These eggs develop the usual embryos with six 
spines, and, if they find their way into the intesti- 
nal canal of man, they pass out into the tissues. 
Settling in some organ of the body, they show the 
most extraordinary powers of development, pro- 
ducing the condition commonly called hydatids. 
It is proper to say here that hydatids occur in 
the form of large cysts, often of very complex 
arrangement, and they should be carefully dis- 
tinguished from the cysticerci, which form small 
cysts not more than half an inch in size. The 
hydatids occur in the majority of cases in the liver. Neisser has 
collected no less than 986 cases of hydatids in man, and he gives 
the scale of frequency in the different organs as follows : Liver, 
451; lungs and pleura, 84; kidneys, 80; muscle and subcutaneous 
tissue (including the orbit), 72; brain, 68; spinal cord, 13; female 
organs of generation (including the mamma), 44; male organs, 
Fig. 143. 
Adult tasnia ech- 
inococcus. X 12. 
(Leuckart.) TAPE-WORMS. 
271 
6; pelvis, 36; organs of circulation, 29; spleen and bones, 28; 
eye, 3. 
When the embryo reaches the liver or other resting place, it 
soon develops into a cyst which at tirst is of slow growth. The 
membrane of the cyst is of considerable thickness, and consists 
of an external cuticle in several layers and an internal parenchy- 
matous layer containing muscular fibre and a vascular system. 
Inside the original vesicle arise very frequently secondary vesicles, 
and inside these even tertiary ones, the successive vesicles being 
sometimes spoken of as daughter or granddaughter vesicles. It 
sometimes happens that the secondary vesicles project outwards, 
and form a series of external vesicles which may separate from 
their mother and attain an independent development alongside of 
her. This latter form is particularly common in the domestic 
animals, and it is variously designated exogenous hydatids, or 
echinococcus scolecipariens, or granulosus. There is a third form 
which has been met with in man, and always in the liver. The 
parasite develops a congeries of small vesicles, from the size of a 
grain of wheat to a pea. These are embedded in a gelatinous 
tissue and sometimes possess gelatinous contents. As the whole 
is surrounded by a firm fibrous capsule, the tumor is a somewhat 
solid one, and on section it presents a peculiar alveolar appearance. 
From this structure it is called the alveolar form, and it should be 
particularly'borne in mind, as this condition has been frequently 
mistaken for a tumor, especially before Virchow demonstrated its 
true nature. 
. Except in the case of the alveolar form, the vesicles, both pri- 
mary and secondary, enlarge very much and give rise to tumors 
of very large dimensions, so as sometimes to produce serious dis- 
turbance by their mere size. Those of the liver are usually the 
largest, and they may come to weigh as much as twelve, twenty, or 
even thirty pounds. The simple ves- 
icles, in which no daughters develop, 
attain the size of an orange or a fist. 
In all forms of hydatids the whole 
parasite is surrounded by a fibrous cap- 
sule, developed by the organ in which it 
has its seat. As the cysts enlarge, this 
also increases in size. 
We have now to consider the for- 
mation of the heads of the worms, 
which differs in certain respects from 
that of the other tsenias. In the walls of 
the vesicles, either primary or secondary, 
are to be seen when they are perfectly 
fresh, a number of small white points 
which have their seat in the internal wall. These are what arc 
called brood-capsules, and it is always in connection with them 
that the heads or scolices develop. The brood-capsules are little 
vesicles, in the walls of which the echinococcus head grows. The 
Fig. 144. 
Diagrammatical illustration of 
development of echinococcus heads 
in brood-capsules, a, Wall of cyst. 
b b, Brood-capsules, with heads in 
various stages of development. 
vLeuckaet.) 272 
PARASITES. 
heads begin (see Fig. 144, in which the development of heads in 
brood-capsules is shown) as projections outwards of the wall of 
the braod-capsule. The projection is hollow, and communicates 
with the interior of the brood-capsule. The head develops inside 
this projection, as in the vase of the taenia solium, and very soon 
acquires the power of inverting itself. When it does so, it projects 
into the brood-capsule, so that in this respect the brood-capsule is 
not like the cyst of the cysticercus as the scolex projects outwards 
from the latter. A single brood-capsule develops several heads, up 
to twelve, and they may be found either in the extended or inverted 
position. All the heads are contained in brood-capsules, but if 
after death or during removal the brood-capsule bursts, then an 
appearance may be produced as if the heads were attached to the 
wall of the cyst itself. If the capsule bursts, its remains may 
gather round its stalk and the heads stand up from this as in Fig. 
145, b b. Heads may also be found lying free if the capsules have 
Fig. 145. 
Brood-capsules in connection with wall of vesicle, a, A capsule in normal unruptured 
state, b b, Ruptured capsule. X 40. (Leuckart.) 
burst. It is to be added that sometimes the vesicles remain barren, 
neither brood-capsules nor heads developing in them. 
The heads are exactly like those of the mature worm. They 
are very minute objects, measuring about of an inch in long 
diameter, and just visible to the naked eye. They possess a pro- 
boscis with the ring of hooklets, and four suckers. They are also 
provided with a water-vascular system, and in their parenchyma 
abundant calcareous particles are to be found. 
The animal may die spontaneously, or be killed by the fluid 
which fills the vesicles being drawn off. In that case the vesicles 
shrink, and their contents become converted into a fatty debris, 
which afterwards may become infiltrated with lime salts. In this 
way the hydatid mass may be represented by a cyst filled with an 
atheromatous material. This may dry-in, and at last we may have 
nothing left but a stony or mortar-like mass, in which careful search 
may still discover the hooklets (Fig. 138). Besides the distinctive 
hooklets, or even without them, there are usually in these old cysts 
bits of the membrane of the cyst. The wall of the hydatid 
cyst consists of two layers, an external (called by Huxley the 
ectocyst) and an internal (the endocyst). The ectocyst consists of TAPE-WORMS. 
273 
a structureless stratified membrane, composed of a chitinous sub- 
stance, from which circumstance it is often called the cuticle. As 
this chitinous membrane is very resistant it may be found in the 
midst of the grumous contents and enable the structure to be rec- 
ognized. In the case from which Fig. 146 was taken the diagnosis 
Fig. 146. 
Transverse section of the chitinous membrane from an old hydatid cyst of the kidney, x 90. 
was made chiefly by flakes of this membrane being found, the 
search for hooklets being in vain. 
In regard to the distribution of the echinococcus, it is of pretty 
frequent occurrence in all known lands, hut is particularly common 
in Iceland where the men, living in close companionship with the 
dogs, are much exposed to infection. It is also said to be very 
common in Australia and neighboring colonies. 
The Bothriocephalus latus belongs to the family of Bothrio- 
cephalidse, and is the largest tape-worm which occurs in man. It 
attains a length of from 16 to 26 feet, and possesses from 3000 to 
4000 segments, which are mostly much broader than long, although 
the last ones (see Fig. 147) become longer and narrower, so as to 
assume more of a square shape. The breadth at the widest part is 
about half an inch. The worm is also thick and heavy. 
The head (Fig. 148) is oval, and about the twenty-fifth of an 
inch in breadth. It is blunt at the extremity, and possesses neither 
hooklets nor suckers, but fixes itself by means of a slit-like groove 
on either side of the head (see figure). 
The sexual organs, and especially the uterus, occupy the middle 
part of each segment, where they form a rather prominent knot or 
rosette (Fig. 149). The uterus is composed of a convoluted tube 
which gives the rosette-like appearance just mentioned. The 
sexual organs open in the middle line near the anterior extremity 
of the proglottis. The eggs are oval in form and are covered by a 
brown shell. 
The scolex form of the worm long eluded observation. It was 
known that a six-spined embryo formed in the eggs in the usual 274 
parasites. 
way, but the habitat of the cysticercus was unknown. Lately 
Braun has demonstrated its existence in the pike and turbot. It 
Fig. 147. 
Fig. 148. 
Head and portion of body of Bothriocephalus latus. 
X 8. (Leuckart.) 
was found in the muscles, sexual organs, 
liver, spleen, etc., of these fish. Braun 
proved that it was the scolex of this 
animal by feeding dogs with it. A tape- 
worm identical with the bothriocephalus 
developed. By this discovery all the 
tape-worms which occur in Europeans 
have been traced in their mature and 
cysticercus forms. 
This worm is of rather frequent occur- 
rence in Switzerland and north-east 
Europe, but it is not unknown in this 
country. The frequency of fresh-water 
lakes in Switzerland explains its fre- 
quent occurrence there from the use of 
the fish which form the hosts of the 
scolex form. Like the other tape-worms 
the mature worm occurs in the small 
intestines. 
Several other small and infrequent 
tape-worms have been met with in 
man. The Taenia nana has only been 
observed once, and in Egypt. It is very 
small, scarcely an inch in length, and about the fiftieth of an 
inch in breadth. It possesses a rostellum with hooklets and 
lour sucking disks. The Taenia flavo-puncta has also been ob- 
served but once, in America. It is about a foot in length, and 
about one-twentieth of an inch in breadth. The head of this 
worm is not known, but it is believed to possess hooklets. The 
Taenia madagascariensis has been found in an island on the Mada- 
gascar coast. It is about 3 inches long, and the head is not 
yet known. The Taenia ciicumerina is from 7 to 10 inches long. 
Its head possesses a rostellum with a quadruple circle of hooklets 
The Bothriocephalus latus. 
Natural size. (Leuckart.) 275 
ROUND-WORMS. 
to the number of about 60. The proglottides reach a breadth of 
about the twelfth of an inch. It occurs very frequently in dogs 
and cats, and is often present in large numbers, especially in 
dogs. It has been found in several cases in man, and it seems to 
be not infrequent in children. The scolex form has lately been 
found in the dog-louse (Tricliodectes canis), and it can be readily 
Fig. 149. 
Proglottis of Bothrioceplialus latus, showing female organs. X 12. (Leuckart.) 
understood how in the process of licking itself the dog often 
swallows its host and becomes itself the host of the strobilus. It 
may be conveyed to children from the tongue of the dog. The 
Taenia marginata is a tape-worm of large size, and of common oc- 
currence in the dog. Its usual length is about 5 feet, but it may 
be as long as 8 feet. It is very like the Tsenia solium, the head 
possessing a rostellum and booklets of about the same size but 
more numerous. On the whole, however, the worm is smaller, 
and so are the proglottides. The scolex form inhabits swine and 
the ruminants, and as it often develops a large vesicle or set of 
vesicles, it is liable to be confused with the Tsenia echinococcus. 
The scolex form is called the Cysticercus tenuicollis. Heither ma- 
ture worm nor cysticercus is met with in man. The dog also 
frequently contains two other tsenia, namely the T. serrata and 
T. ccenurus. These also resemble the Tsenia solium, and the latter 
is important, as its scolex form frequently attacks lambs, and, 
lodging in the brain, is the cause of the very fatal disease “ staggers.” 
(3) Nematoda or Round-worms.—The Trichina spiralis is met 
with in the muscular substance of man, and occurs there in im- 
mense numbers, producing the disease trichinosis. We shall see 
afterwards that this is not the mature form of the worm, but it is 
in this form alone that, for the most part, it is accessible to us, and 
it will be convenient to begin with its description here. 
The affected muscles, as seen with the naked eye, seem, for the 
most part, to be dusted throughout with fine white particles like 
sawdust. These are most abundant near the places where the 
muscular fibres are inserted into the tendons. As a rule the par- 
ticles are most abundant in the muscles of the trunk, the diaphragm, 
the intercostal muscles, and those of the abdominal wall, but they 276 
PARASITES. 
may extend to all the voluntary muscles of the body, even the most 
distant ones of the hands and feet. 
On microscopic examination of the fine particles, they are found 
to consist each of an oval cyst with a tolerably thick wall (see Fig. 
150), within which is a small worm coiled up in a spiral manner. 
Fig. 150. 
Trichina spiralis in muscle. The elongated shape of the cysts is due to the fact that these 
were near the insertion of the muscle into its tendon. In the lowest specimen the worm is 
dead and calcified. X 90. 
The cyst has very often abundant calcareous particles in its walls, 
especially at the poles, and, if the case is an old one, the impreg- 
nation with lime may be so great as to hide the parasite unless the 
salt be first dissolved out with an acid. When an acid, such as 
dilute hydrochloric, is used, the lime dissolves with some evolution 
of gas, and the whole structure becomes very transparent. Some- 
times the worm dies in its capsule, and in that case the wall 
thickens and the cyst collapses to some extent on the remains of 
the worm, which itself often becomes infiltrated with lime (see 
lower specimen in .figure). It may be said here that the worm in 
the muscle is in an immature state and quiescent, lying rolled up 
in this manner for years it may be. It may be present in immense 
numbers, even in millions, in the same person. 
We have now to inquire how these embryos get to the muscles. 
To begin with, it is to be said that the embryos exist in the mus- 
cles of swine just as in those of man. If, now, a piece of muscle 
containing them in their living state—that is to say, not killed by 
cooking tbe meat—be eaten, they undergo further development in 
the intestinal canal. The capsule is dissolved by the gastric juice, 
and the embryo set free. In the muscle, the embryo, if uncoiled, 
would measure about the twenty-fifth of an inch in length; but 
now it grows rapidly, and in the course of two and a half days it 
reaches the adult form, when the female is about one-eighth of an 277 
ROUND- WORMS. 
inch in length; and the male slightly less. The male possesses a 
testicle consisting of a convoluted tube. The female has an ovary, 
vagina, and uterus. The adult worms have an intestinal canal 
from end to end, which is divisible into oesophagus, stomach, and 
intestine. 
The impregnated ova pass into the uterus where they develop 
into living embryos of minute size. In six or seven days after 
the female has attained sexual maturity, that is, eight or nine days 
after the trichinous muscle has been eaten, the birth of living em- 
bryos begins. The female gives birth to large numbers, and 
probably continues to do so for some weeks, thus producing as 
many as 1000 to 1300. The adults do not live longer than five 
to eight weeks altogether. 
The minute embryos now begin to penetrate the intestinal 
canal, and they swarm outwards to the voluntary muscles. The 
route by which they reach the muscles is not absolutely certain. 
By most it is thought that they pass outwards into the peritoneal 
cavity, and thence into the connective tissue around, by which 
they travel to the muscles. By others it is thought that they pass 
into the submucous connective tissue, thence into the connective 
tissue of the mesentery, and so onwards. It is probable that they 
find their way by both these routes, but it is inconceivable that, as 
some suppose, they get into the bloodvessels, as the vessels avail- 
able to them are the portal radicles which would take them to the 
liver. 
Swarming outwards from the intestine they reach first the 
muscles of the trunk, where they are usually most abundant; they 
then pass to those of the neck and larynx; and, lastly, to those of 
the limbs. Arrived at the muscles they grow larger, and appar- 
ently wander about for a time. They penetrate inside the sarco- 
lemma of the primitive fibre of the muscle, and destroy the sarcous 
substance. In about fourteen days they have attained their full 
size, and begin to settle down. As they pass along inside the sar- 
colemma they are arrested at the insertion of the fibre into the 
tendon, hence they are particularly numerous near tendons, and 
here also the cysts, subsequently formed, are often much elongated 
(as in the figure). The sarcolemma collapses as the sarcous sub- 
stance is destroyed, and as the worm coils itself np spirally the 
sarcolemma forms for it an oval cyst. The worm itself seems also 
to add to the cyst a layer of its own. It is not uncommon to find 
two, or even more, in one cyst. In the muscles the worms assume 
a quiescent state, as already mentioned, and may remain so for 
years, the cyst being impregnated with lime. They produce con- 
siderable destruction by piercing the sarcolemma, and disintegrat- 
ing the sarcous substance, and there is often to be found a germi- 
nation of the muscle-nuclei around the worm. 
During the migration of the embryos considerable irritation is 
produced. There is in the first week intestinal catarrh (diarrhoea) 
with fever, and the case ma}7 be mistaken for typhoid fever. Later 
the muscles become stiff' and painful, and oedema of the skin, 278 
parasites. 
especially of the face, may develop. The symptoms are usually 
at their height in the fourth or fifth week, and death occasionally 
ensues. . 
Besides in man, trichinae have been found in the muscles of the 
pig, cat, rat, mouse, marmot, polecat, fox, marten, badger, hedge- 
hog, and raccoon. By some it is believed that the rat forms the 
permanent source of infection, as, when one of these animals dies, 
it is eaten by its neighbors, and so the infection spreads. From 
their habits, it will be understood how swine sometimes partake of 
dead rats. The parasite will be communicated to man by eating 
imperfectly cooked swine’s flesh. It is said that a temperature of 
50°-55° C. or 120° to 130° F., is enough to kill the embryos, 
but it is quite conceivable that when large pieces of flesh are 
cooked rapidly, some parts may escape the thorough penetration 
of the heat. 
The search for trichinae in the muscles of swine before the flesh 
is sold is compulsory in some countries. For the examination 
pieces of muscle (preferably from the diaphragm and larynx) are 
snipped oft'with scissors and spread out in water on a microscopic 
slide. Some liquor potassae may he added to make the prepara- 
tion more transparent. It is then to be examined with low 
magnifying powers and afterwards with higher. Several speci- 
mens should be prepared from each animal. 
The Ascaris lumbricoides or common round-worm is probably 
the commonest entozoon in the human subject. It is most common 
in children, and inhabits chiefly the small intestine. It resembles 
the common earth worm in its color and general appearance. It 
measures six to sixteen inches in length, is marked by transverse 
striae, and tapers to both ends. It possesses an intestinal canal 
from end to end. The female produces a large number of oval 
eggs which have a dense shell. 
The worm mostly occurs singly or in pairs, but is frequently 
present in considerable numbers up to one or two hundred. From 
the intestine it may pass into the stomach and be vomited, or may 
be discharged per anum. It has been known also to pass up the 
oesophagus and into the nostrils and sinuses of the head, or by the 
larynx into the bronchial tubes. Sometimes it penetrates into the 
bile-ducts, which it may obstruct, or through the intestinal wall 
into the peritoneal cavity. 
In the intestine they produce catarrh, and by reflex action they 
are supposed to lead to certain nervous symptoms. When present 
in large numbers, they have been observed rolled up in a ball, and 
so have obstructed the intestine. In cases where they have per- 
forated into the peritoneum they have given rise usually to/local 
abscesses pointing chiefly near the umbilicus or groin. More 
rarely they have led to general peritonitis. 
The Ascaris mystax is a small round worm which occurs in 
the cat, and is said to be always present in the intestine of that 
animal. ROUND-WORMS. 
279 
The Oxyuris vermicularis or thread-worm is an exceedingly 
common parasite. It is white in color, and the male measures 
about the eighth of an inch, and the female about three-eighths in 
length. It possesses an alimentary canal from end to end. The 
eggs are oval, and have a dense shell. The animal inhabits mostly 
the large intestine. It is stated by Zenker and Heller that the 
mature female is in the large intestine, the males and young being 
in the small. The worm often wanders, especially during the 
night, to the neighborhood of the anus, where it produces itching. 
Sometimes it passes over to the vagina, and up into it. It pro- 
duces catarrh of the bowel, and, as in the case of the ascaris, 
nervous symptoms are ascribed to it. 
The Trichocephalus dispar (the wliip-shaped worm) is of fre- 
quent occurrence in the caecum and neighboring parts of the in- 
testine. It measures one and a half to two inches in length, and 
has the peculiarity that the anterior portion is much thinner than 
the posterior, forming a long thread, like the lash of a whip, which 
is buried in the mucous membrane. The eggs possess a brown 
shell. The embryos have been traced in water and moist earth. 
The Strongylus duodenalis or Anchylostoma duodenale is not 
met with in this country, but occurs in Egypt, Italy, and tropical 
lands. It has been found frequently among the workers at the 
St. Gothard Tunnel in Switzerland. It is a third to half an inch 
in length, and it possesses a mouth armed with four strong teeth. 
By means of these it fixes itself on the mucous membrane, where it 
sucks the blood. When present in considerable numbers, as it 
often is among the valvulre conniventes, it may give rise to con- 
siderable loss of blood and serious anaemia. 
The Strongylus gigas is a large worm, reaching a length of 
over a yard, and a thickness of about three-eighths of an inch. It 
has been met with a few times in the pelvis of the kidney in man, 
and more frequently in the kidney, bladder, lungs, and liver of dogs. 
The Filaria or Dracunculus medinensis, or Guinea worm, is 
of frequent occurrence in tropical lands, where it is met with in 
the tissues of the foot and leg chiefly. The female is a long thin 
worm from twelve to forty inches in length, and it alone is known 
as a parasite. The male is much smaller. The worm wanders to 
some extent in the loose subcutaneous connective tissue, and may 
give rise to considerable irritation. When mature it presents its 
extremity at the surface, and a small pustule forms from which 
the extremity projects. The worm may then be removed gradually 
by rolling it gently round a quill from day to day as it becomes 
exposed, care being taken not to break it, in \vhich case the part 
left in may give rise to severe inflammation. 
Filaria Sanguinis Hominis.—This name was originally given 
to a minute thread-like worm which lias recently been found to be 280 
PARASITES. 
really the embryo of a larger worm. The embrj'O, as its name 
implies, has been found in the blood, although it has also been 
observed in chylous urine and elsewhere. The adult appears to 
live in lymphatic vessels, and so the name filaria sanguinis is not 
strictly applicable to it. Cobbold has given it the name filaria 
Bancrofti, from the observer who first discovered the adult. As 
it is inconvenient to give two different names to the adult and 
embryo forms of the same animal, we shall refer to them under 
the original designation of Filaria sanguinis. In some respects the 
two forms of this worm are comparable to those of the Trichina 
spiralis, which also obtains its name from the embryo form. 
The adult filaria has the sexes distinct, and as 'yet the female 
alone has been fully examined, only a small portion of a male 
having been discovered. The female is a long hair-like worm, 
three or four inches in length, and only inch in breadth. It 
has an opaline appearance, and, as described by Manson (Transac- 
tions of the Pathological Society of London, 1881), it looks like a 
delicate thread of catgut animated and wriggling as it lies in the 
tissues. By the observer just named it was found lying in a lym- 
phatic vessel while he was removing a scrotum which was affected 
in a way to be mentioned afterwards, and it appears that this is 
the usual habitat of the animal. The male is probably much 
smaller than the female, and they are supposed to live together in 
the same vessel. 
The female is believed to live for years in the same position, and 
gives birth almost continuously to large numbers of embryos. 
FTear the head is the vagina, and behind it the uterus with two 
Fig. 151. 
Filaria sanguinis (embryo) after preservation in weak spirit. The sac is seen at 
each end of the worm. X 300. (Lewis.) 
horns is found, stuffed with ova, and extending almost to the tail. 
MansOn states that the embryos can be seen escaping fully formed 
from the vagina, in exactly the same form as they are found in the 
blood. But the female sometimes gives birth to ova, as these 
have been found in the lymph and have been supposed to be the 
principal factors in producing certain local affections to be after- 
wards mentioned. 
The living embryo (Figs. 151 and 152) is about inch in length 
and inch in thickness; its breadth therefore nearly corre- 
sponds with that of a red blood-corpuscle. It is enclosed in a 
delicate sac, which is rather longer than itself, so that while ROUND -WORMS. 
281 
moving a portion of the sac extends beyond its extremity. The 
movements as seen in the blood and lymph are very active and 
snake-like in character. 
Fro. 152. 
Filaria sanguinis as they appear in the iiving state in the blood. From a case of 
chyluria. X 300. (Lewis.) 
This embryo is present in the hloocl of about ten per cent, of the 
natives where it is endemic, and most of these do not appear to 
sutfer in health from it. A very remarkable circumstance is that, 
during the day, the parasites are, unless in exceptional cases, absent 
from the blood, but about six or seven o’clock are so numerous 
that as many as a hundred may be counted in every drop of blood. 
As morning approaches they diminish in numbers, and by eight 
or nine o’clock they disappear entirely. This regular rhythm may 
apparently go on for years, but it does not appear to be understood 
what becomes of the embryos during the day. 
We have next to consider how the embryos find their way from 
the site of the parent worm in the lymphatics to the blood. It is 
probable that they travel by the way of the lymphatic fluid itself. 
Being not greater in breadth than a blood-corpuscle, and possess- 
ing powers of locomotion, they may be supposed to traverse the 
lymphatic glands with the lymph, and to reach the blood by the 
thoracic duct. It is also possible that they may get into the blood 
by penetrating through the bloodvessels. In the blood they will 
readily circulate with that fluid, and from their size they are 
capable of passing through the capillaries and repeating the circuit 
with the blood-corpuscles. They do not pass through any further 
stage of development in the blood, the embryos found there being 
exactly like those which escape from the mother. It is clear also 
that they do not, either by themselves or their products act in- 282 
PARASITES. 
juriously on the blood or tissues unless bv using the nutritious 
material. 
It lias been stated above that ova are sometimes discharged by 
the female, and it is probably in connection with this that various 
forms of disease are found to occur in connection with this parasite. 
The sac which has been mentioned as enclosing the embryo is 
really the chorional envelope of the ovum stretched and rendered 
elastic. But ova are sometimes born with the sac confining the 
embryos which are rolled up inside, and we have then an oval 
body tott inch to inch in length. This body is, of course, 
much thicker than the extended embryo, and when carried by the 
lymph to the glands it will be unable to traverse these. An in- 
farction of the fine afferent vessels of the gland will thus occur, 
and as the vessels leading from the part where the mother is 
situated are plugged one after another, there will by and by be a 
complete stasis of the lymph in the vessels of these parts. It is 
probable that dead embryos though extended will similarly plug 
the lymphatics. 
The effect of this complete plugging of all the lymphatic 
channels seems to be an accumulation of lymph in the vessel below 
the seat of obstruction. The lymph thus distending the vessels 
often escapes apparently by rupture. The locality of the parent 
will determine the exact nature of the resulting disease. If it be 
in the lymphatics of the pelvis or lumbar region, there may be 
distention of the lymphatics of the kidneys, ureters, or bladder. 
In that case chylous urine is found, and the embryos of the 
parasite have been observed in the urine. If the adult be in the 
lymphatics of the leg, there will be gradual plugging of the glands 
at the groin and accumulation of lymph in the legs and scrotum. 
The accumulation in the scrotum is of very frequent occurrence, 
giving rise to the lymph-scrotum, in which vesicles appear on the 
surface which occasionally discharge lymph. 
It is to be observed that the condition in these various situations 
is not a proper oedema, which we have already seen to consist in 
overfilling of the serous spaces, but rather an over-distention of 
the lymphatic vessels with occasional rupture of them. 
If the explanation given above be the correct one, then as the 
glands get plugged the embryos, even those born alive, will not 
get,to the blood, and it has actually been observed that in some 
cases no embryos were found in the blood although present in 
the urine or lymph from the scrotum. 
It has been asserted that Elephantiasis is one of the diseases 
dependent on this parasite, and is to be placed in the same category 
as lymph-scrotum and chyluria. But there are serious objections 
to this view. Elephantiasis has the features, as we have seen, 
rather of a specific inflammation, than a simple stagnation of 
lymph, and is more nearly allied to leprosy. It probably depends 
on a virus which has a much more active influence on the tissues 
than the embryo filaria lias. 
In what has gone before the adult and embryo filaria have been 283 
EPIZOA OR EXTERNAL PARASITES. 
described, hut the stages by which the embryo attains to the adult 
form have been omitted. The embryo in the human body does 
not pass beyond the stage which it had reached at birth, and in 
order to complete the cycle of its development it must pass into 
the body of another animal. The intermediate host has been 
found to be a species of mosquito (Manson). The female of this 
animal has a proboscis which she inserts into the skin and through 
which she sucks blood into the stomach. With the blood the 
embryos are taken in, and they have been found in the stomach 
even in larger proportional numbers than in the blood of the 
person from whom they were taken. In the stomach the embryo 
passes through certain stages of development occupying from four 
to six days. At this period the mosquito dies, and probably falls 
into the water, the parasite passing from the stomach. The further 
stages are not known as yet, but by the time the mosquito dies 
the parasite has already acquired a boring apparatus fitting it to 
penetrate the tissues. If it reaches the alimentary canal of man, 
it will then bore through the tissues till it finds its selected site in 
the lymphatics. It selects this site just as the trichina selects the 
muscles or the echinococcus the liver. In its new position it 
attains to sexual maturity, and being impregnated, gives birth to 
the embryos as we have seen. 
The species of mosquito here concerned is, like other mosquitoes, 
nocturnal in its habits, so that it attacks affected persons at the 
time when the parasite is present in the blood. The occurrence 
of the embryos in the blood at night has been regarded as a pro- 
vision of nature for the propagation of the species. 
EPIZOA OR EXTERNAL PARASITES. 
Tliese do not call for extended treatment here, as they are fully 
described in works on disease of the skin. Little more than an 
enumeration of them will he attempted. 
The Acarus scabiei, or Sarcoptes hominis, has an oval body 
just large enough to he visible to the naked eye, the female being 
one-fiftieth of an inch in length and the male about half that size. 
The anterior part has a head and four limbs, each of which has a 
sucker at its extremity. There are also four posteror limbs, all of 
which in the female have pointed extremities, but in the male two 
of them have suckers. The female burrows in the epidermis, 
forming long tunnels in which, as it proceeds, it deposits its eggs; 
it is usually to be found at the deepest end of the tunnel and the 
eggs at intervals. The eggs develop, and, as the epidermis des- 
quamates, they come to the surface by degrees, the young being 
born usually as they reach the surface. The irritation of the 
animal in the epidermis gives rise to a slight inflammation causing 
the formation of a papule. Usually there is great itching, and 
the scratching leads to further eruptions, especially in predisposed 
persons. 284 
ly a rasites. 
The Acarus folliculorum is a long narrow animal provided 
anteriorly with fonr pairs of short feet. It is found in the sebaceous 
follicles, especially of the external meatus of the ear and neighbor- 
hood of the nose. It seems to produce no special irritation. 
Pediculi or lice occur in three forms, the pediculus capitis, 
corporis, and pubis, which hardly require special description. 
The Pulex irritans, or common flea, is familiar to every one. 
The larvj3 of insects or maggots are occasionally found in the 
tissues of man. There are a few cases in which such larvte have, 
by migrating under the skin, produced considerable inflammation. 
There are also cases in which, deposited in neglected wounds, or 
even in the mouth and nostrils of excessively debilitated persons, 
they have actually produced considerable destruction by feeding 
on the tissues. In neglected military hospitals wounds are often 
abundantly tenanted by maggots. PART II. 
DISEASES OF THE SPECIAL ORGANS AND 
SYSTEMS. 
DISEASES OF THE ORGANS OF CIRCULATION. 
A.—THE HEART AND PERICARDIUM. 
MALFORMATIONS OF THE HEART. 
For a very full account of the malformations of the heart we 
are indebted to Dr. Peacock, whose work forms the basis of the 
remarks under this heading. 
Misplacements of the heart are of rare occurrence, and the more 
important of them are merely part of a general malformation of 
the body. The heart may be transposed, that is to say, placed in 
a position on the right side of the chest corresponding with that 
which it normally occupies on the left. With this there is usually 
transposition of the viscera, but it sometimes occurs alone. Again, 
the heart may occupy the middle line as it does in early foetal life. 
It may be placed outside the thorax altogether, but in this case 
there are other congenital malformations, and that of the heart 
only forms a part. 
Absence of the pericardium is a rare congenital malformation, 
and is mostly associated with misplacement of the heart. It is not 
to be confused with adhesion of the pericardium and consequent 
obliteration of the sac which is so frequent in after-life. 
True malformations of the heart and great vessels for the 
most part represent survivals of foetal conditions. In order to a 
comprehension of these conditions it will be necessary here to 
refer briefly to the state of the heart in early foetal life, and the 
changes which it subsequently undergoes. The heart at an early 
period consists of two cavities, an auricle and a ventricle. The 
simple auricle receives the two venae cavae, and the ventricle gives 
origin to the common arterial trunk. The ventricle, the auricle, 
and the common arterial trunk subsequently undergo subdivision 286 
DISEASES OF THE ORGANS OF CIRCULATION. 
each into two. This separation in the ventricle begins near the 
apex; the septum gradually rises towards the base, its completion 
at the base being delayed after the rest of the septum has been 
formed. The common arterial trunk begins to show signs of divi- 
sion by a septum about the time that the interventricular septum 
is approaching the base. A septum passing from both sides of the 
artery meets and divides the vessel into what are subsequently the 
pulmonary artery and the aorta. These are so adjusted as to con- 
nect with the right and left ventricles respectively. The division 
of the auricles does not begin till the ventricular septum is nearly 
completed, namely about the ninth week, and after being fully 
formed the septum remains partially open during the whole of 
intra-uterine life. 
Some of the malformations met with are survivals from a very 
early period of foetal life. The heart may consist of only two 
cavities, an auricle and a ventricle, with a single arterial trunk 
representing both aorta and pulmonary artery. Then there is the 
heart with three cavities, an imperfectly divided auricle with two 
auriculo-ventricular oritices, and a single ventricle with no septum, 
or a very rudimentary one. 
Leaving out of view these extreme cases, most instances of im- 
perfect closure of the septa are directly related to obstruction 
caused by disease of the pulmonary artery or aorta at or near their 
orifices. In a way to be presently explained such obstruction 
leads to imperfect closure and other malformations. It is to be 
remembered that the part at the base is the last part of the septum 
to close, and that it is at the base that the great vessels arise. 
Consequently an imperfect closure will cause both ventricles to 
communicate more or less with both great arteries, and if one of 
the latter be larger than the other it will, as it were, overlap the 
imperfeet septum and take origin partly from the other ventricle 
as well as its own. 
Let us consider the effect of stenosis of the pulmonary artery 
occurring at an early period, when the interventricular septum has 
not yet closed; or let us suppose that the common arterial trunk, 
instead of dividing into pulmonary artery and aorta, does so im- 
perfectly, and so there is a large aorta and a small pulmonary 
artery, or even an entire absence of the latter. In the case last 
mentioned the blood from the right ventricle, as well as that from 
the left, would pass into the aorta, and the constant recurrence of 
this passage of blood at each systole of the ventricle would pre- 
vent the closure of the septum at the base, and cause the aorta 
to take permanent origin from the right ventricle as well as from 
the left. The condition would in fact virtually be that of a heart 
with three cavities, and it is possible that some of the cases in 
which this is the form of malformation may have such an origin. 
Short of this complete atresia (or obliteration) of the pulmonary 
artery, obstruction may occur in varying degrees, and the results 
will vary correspondingly. The aorta will, in the more serious MALFORMATIONS OF THE HEART. 
287 
cases, take origin to a greater or lesser extent from the right ven- 
tricle, while in those which are less extreme there will simply be a 
gap in the septum. 
It has already been remarked that the last part of the septum 
to close in the foetus is the basal part, and there is, even in the 
adult, a small triangular space at the base of the septum, in which 
there is no muscular tissue, and which is composed only of the 
two layers of endocardium of the right and left ventricles and 
some loose connective tissue between. This space is called the 
undefined space, and in a considerable proportion of cases a 
minute aperture persists in adult life at this point. If the septum 
closes imperfectly the gap has its seat here (see Fig. 153). 
Fig. 153. 
Defect of interventricular septum. The gap is situated at the base, in the position of the 
undefended space in the normal heart. (Peacock.) 
We liave seen that imperfect closure of the septum and partial 
origin of the aorta from the right ventricle are the most direct 
results of stenosis or atresia of the pulmonary artery, hut there 
are other results which also follow. The septum is bulged to the 
left, and the right ventricle is generally greatly hypertrophied. 
This hypertrophy of the right ventricle is probably of the same 
nature as the hypertrophy of the ventricles in adult life, which 
occurs so frequently in connection with obstruction of orifices. 
It is due to the extra-powerful muscular efforts made by the right 
ventricle to overcome the obstruction of the pulmonary artery. 
In addition to imperfection of the interventricular septum, there 
is very often in these cases imperfect closure of the foramen 
ovale after birth. This will be a natural consequence of the 
enlargement of the right ventricle. The obstruction of the pul- 288 
DISEASES OF THE ORGANS OF CIRCULATION. 
monary artery keeps back the blood, as it were, in the right 
ventricle and auricle, and the blood, accumulating in the right 
auricle, continues to pass through the foramen ovale, and prevents 
its closure. This consequence, however, does not invariably follow. 
Another consequence of occasional occurrence is the permanent 
patency of the ductus arteriosus. If the pulmonary artery at 
its origin is so much obstructed as to prevent the passage of the 
blood in due amount to the lungs, then the aorta will after birth 
augment the supply by the ductus arteriosus, through which the 
blood will pass in the reverse direction to what is normal in the 
foetus. 
We have hitherto considered the case of obstruction of the 
pulmonary artery at a time when the interventricular septum is 
still incomplete, but it may occur after the completion of the 
septum. In that case the most direct result will be dilatation and 
hypertrophy of the right ventricle, and permanent patency of the 
foramen ovale. Patency of the foramen ovale will be a more 
constant result here than in the former case, as this oritice will 
afford the only means of relieving the excessive accumulation of 
blood in the right side, whereas in the case of imperfect inter- 
ventricular septum the excess is relieved by this communication. 
We have been considering the effects of obstruction of the 
pulmonary artery, but the aorta is sometimes, though by no 
means so frequently, the seat of obstruction. In that case the 
relation of matters is inverted. The septum of the ventricles is 
imperfect, but it is bulged to the right, and the pulmonary artery 
takes origin more or less from the left ventricle as well as from 
the right. The aorta beyond the obstruction often continues after 
birth to be supplied with blood from the pulmonary artery through 
the ductus arteriosus. The foramen ovale may remain open. 
It has been stated above that the pulmonary artery is much 
more frequently obstructed than the aorta during foetal life, and 
this leads us to consider what may be the cause 
of obstruction in these cases. The obstruction 
may he due to disease of the valves or to con- 
traction of the artery itself. We are familiar with 
malformation of the val ves from adhesion in adult 
life as a consequence of inflammation, and there 
is reason to believe that it is due to the same cause 
in the foetus. In the annexed figure (Fig. 154), a 
condition of the pulmonary valve is shown which 
is exactly similar to that which we so often see in 
the aortic valve in the adult. The three curtains 
are thickened and united by their margins so as 
to form a diaphragm instead of three mobile folds. 
In the adult, inflammation is immensely more 
common in the valves of the left side than in those 
of the right, and it is difficult to understand how it is exactly the 
reverse in the foetus. 
Fig. 154. 
Congenital adhe- 
sion of the curtains 
of the pulmonary 
valve. The valve is 
viewed from above. 
(Peacock.) 289 
malformations of the heart. 
The proclivity to disease shown by the valves of the left side in 
the adult is usually ascribed to the fact that these are exposed to 
greater strain than those of the right side. The blood-pressure in 
the systemic arteries is much higher, and is exposed to greater 
variations. But in the foetus, as Peacock has pointed out, a much 
larger proportion of the circulation is dependent on the right 
ventricle than in the adult, the descending aorta and the umbilical 
arteries being fed by this ventricle. The blood in the umbilical 
arteries must be exposed to considerable variations in pressure, 
from obstructions occurring in the umbilical cord and placenta, 
and these variations will be reflected to the pulmonary artery and 
right ventricle. On the other hand, the left ventricle and aorta in 
the foetus are related to a much smaller area of the circulation than 
in the adult, and the systemic arteries in the quiescent state of the 
foetus will be little exposed to variations in pressure. 
In the great majority of cases, the malformations hitherto 
referred to are connected with and due to obstruction of the 
pulmonary artery or aorta, but it is to be added that incomplete- 
ness of the septum and the partial misplacements of the great 
vessels which go along with it may occur without any such cause 
being apparent. The same applies to patency of the foramen 
ovale, but in a much higher degree. 
Mere patency of the foramen ovale is hardly to be regarded as 
a serious malformation, especially when we consider that in nearly 
a half of adult hearts there is a slight degree of incompleteness in 
the closure of this aperture. In these cases, however, there is no 
real mixing of the currents in the two auricles, as the remaining 
aperture is valved by folds in the septum. The imperfect closure 
becomes important when, through obstruction in the pulmonary 
artery, the blood-pressure in the right auricle is raised sufficiently 
to cause the blood to pass through the aperture. 
Before leaving this part of the subject it will be proper to refer 
to certain irregularities of the primary vessels. There are 
cases on record in which the aorta has arisen posteriorly from the 
right ventricle and the pulmonary artery anteriorly from the left. 
In this case, the blood from the systemic veins is sent into the 
systemic arteries without passing through the lungs. Such a con- 
dition seems hardly compatible with the prolongation of life after 
birth; yet several cases of survival are on record, in one case life 
being prolonged as long as three years. 
Another malformation is narrowness or obliteration of the 
isthmus of the aorta, or that portion between the giving off of the 
left subclavian and the insertion of the ductus arteriosus. In the 
foetus this portion is hardly in use, and it may be imperfectly de- 
veloped and form, after birth, an obstruction. In that case the 
pulmonary artery will usually supply the abdominal aorta, as in 
the foetus, the ductus arteriosus remaining patent. The ductus 
arteriosus may close, however, in which case the descending aorta 290 
DISEASES OF THE ORGANS OF CIRCULATION. 
must be replenished by circuitous anastomoses through the sub- 
clavian, mammary, intercostal, and epigastric arteries. 
In addition to these more serious malformations of the heart and 
its great vessels, there are certain congenital malformations of 
the valves which merit some attention. These malformations 
concern mainly the semilunar valves of the aorta and pulmonary 
artery. The valve may be in the form of a diaphragm in which 
there are merely indications of a tripartite formation. In this case 
the diaphragm is often protruded into the vessel in the form of a 
funnel. Again, we not unfrequently meet with some variety in 
the size or number of the semilunar folds. There may be only 
two curtains, usually a large and a normal one. The larger one 
commonly shows indications of a partial division (see Fig. 155). 
Fig. 155. 
Congenital malformation of aortic valve. There are two curtains, but the larger 
one shows a partial division. (Peacock.) 
Then with three curtains there may be two large segments and a 
small rudimentary one between. 
These malformations are probably to be referred to endocarditis 
occurring in the foetus. In adult life endocarditis often produces 
adhesion of the curtains, but there is also very great contortion of 
the valves. But, in the foetus, the plastic power and adaptability 
of the structures is much greater, and the three coalesced valves 
may form a well-shaped diaphragm, or the two a single larger 
semilunar fold. In either case there are still indications of the 
coalescence in the form of thickenings along the line of union. It 
is obvious that these malformations will frequently interfere with 
the functions of the valves. In the extreme cases of complete 
union of the three curtains (as in Fig. 154) there will be great 
obstruction as well as imperfect closure. When there are only 
two curtains the middle part, where coalescence has occurred, is 
thicker, and the curtain will be more rigid at this point. This, 
itself, will interfere with the curtains falling back against the 
aortic wall during the systole of the ventricle, and so there will be 
a certain degree of obstruction. But, again, during the process of 
growth, the thickened line of junction being unduly rigid will not 
probably expand sufficiently, and the middle of the curtain will 
thus be held back. During the closure of the valve there will thus MALFORMATIONS OF THE HEART. 
291 
be an aperture left, allowing of regurgitation. The tendency to 
regurgitation is increased by the imperfect support which the 
large curtain receives from the smaller one. During closure the 
edge of the large one must partially double up in order to adapt 
itself to the small one, and so a gap may occur. 
We have seen that these adhesions of the curtains are probably 
due to intra-uterine endocarditis, and there is apt to be a recur- 
rence of the disease after birth. It may be said that the previous 
existence of inflammation renders the structures liable to a recur- 
rence or possibly a prolongation from the foetal period. But, in 
addition, the imperfect adaptation of the valves will itself afford a 
certain irritation and predispose the structures to inflammation. 
So it happens that valves malformed in this way are peculiarly 
prone to disease in after-life, even though their function is not at 
first imperfect. 
Besides the variations already noted the curtains of the aortic 
and pulmonary valves are sometimes abnormally numerous, espe- 
cially those of the latter. There may be four curtains instead of 
three, and they may present all varieties of size relative to one 
another. 
The semilunar valves sometimes present a condition somewhat 
APPROACHING that of THE AURICULO-VENTRICULAR VALVES, which are 
of the cuspid form. It is to be noted that during the closure of a 
semilunar valve the curtains do not come in contact by their free 
margins, but that the line of contact is somewhat removed from 
Pig. 156. 
Fenestration of the marginal parts of the aortic valve. There is an appearance of chord® 
tendineas, and the bands from two proximal curtains are inserted into a projection from the 
aorta. 
the margin. During closure, therefore, when the artery is full, a 
certain portion of the curtain floats free in the blood. How the 
portion between the line of contact and the free margin is frequently 
the seat of apertures or fenestrations, and that without affecting the 
function of the valve. This fenestration may be very extreme and 
may graduate towards a condition in which (see Fig. 156), instead 292 
DISEASES OF THE ORGANS OF CIRCULATION. 
of a piece of tissue, there are merely a series of tendinous bands 
passing from the curtain, near the line of contact, to the wall of 
the vessel at the point of insertion of the curtain. These tendinous 
hands resemble the chordae tendinese of the cuspid valves, and the 
resemblance may be increased by the neighboring edges of the 
curtains being joined, and the tendinous bands from the adjacent 
borders of two curtains passing together to the wall of the vessel 
(see figure). There may be even on the wall of the vessel an 
elongated prominence into which the bands are inserted, and 
resembling a musculus papillaris. These bands may have a con- 
siderable free course from the middle of the curtain to the wall of 
the vessel. A certain indication of such conditions is very frequent 
in both the aortic and pulmonary valves. 
It may be asked, Does such a malformation interfere with the 
function of the valve ? Probably not much, but still to a certain 
extent. Bach form of valve is appropriate to its own place. The 
cuspid form is adapted to an aperture between two cavities, the 
semilunar to the orifice or course of a vessel. The latter takes up 
less room, and by reason of the complete separation of the curtains 
it falls back completely when the blood rushes past it. But if the 
valve approaches to the cuspid form, especially if the margins of 
the curtains are united, and the tendinous bands from two have a 
common insertion, then there can hardly be that complete falling 
back which occurs when the function is perfect. This will probably 
cause a trivial obstruction, and the curtains being unduly exposed 
to the force of the wave of blood may be specially liable to inflam- 
mation. 
Cyanosis.—Before leaving the subject of malformations of the 
heart, we have to consider this condition which is so often associated 
with certain forms. Children born with malformations of the 
heart are usually liable to symptoms connected with the respiration 
and circulation, which are in many respects comparable with those 
from valvular disease acquired in after-life, and consist chiefly in 
attacks of dyspnoea and lividity. These symptoms may occur at 
birth or soon after it, but they may be postponed even for years, 
and develop apparently by some extra stress laid on the circulation. 
Occurring at first intermittently the dyspnoea and lividity very 
often, to some extent, become permanent, and this is particularly 
true of the lividity. This generally becomes such a marked 
characteristic of such persons that they are visibly the subjects of 
Cyanosis or morbus (XERUleus. The lips and finger-nails are blue, 
and there is, perhaps, a deep lividity of hands, feet, and cheeks as 
well. 
Two explanations of this symptom have been ottered. The first 
is that, as in these cases, the septa of the heart are mostly imper- 
fect, the lividity results from the mixing of the currents, venous 
blood being mixed with the arterial in the systemic vessels. This 
looks a very likely explanation, but there are two serious objections 
to if. Cyanosis has been found in cases where the currents did not MALFORMATIONS OF THE HEART. 
293 
mix, and it has been absent where they undoubtedly did. Besides 
this, it is found that the degree of cyanosis is not at all propor- 
tionate to the mixing of the currents! The other explanation is 
that the cyanosis is due to venous engorgement, just as lividity oc- 
curring in valvular disease in the adult. In nearly all the cases 
there is obstruction of the pulmonary artery which we have seen 
to be at the basis of most malformations, and this has the effect of 
bringing about a general venous engorgement. During the early 
periods of life the bloodvessels are more yielding and plastic, and 
so the permanent congestion tells much more on them than it does 
in adult life. Cyanosis developed in after-life sometimes ap- 
proaches in intensity to that from malformation, but it rarely 
reaches it. 
It may be interesting to refer to the duration of life in persons 
affected with malformation of the heart. If there is merely slight 
imperfection of the septa, the defect is of little importance, and we 
have already seen that there is imperfect closure of the foramen 
ovale in a large proportion of the cases met with in the ordinary 
course of post-mortem examination. If there is moderate con- 
traction of the pulmonary artery while the heart is otherwise well 
formed, the right ventricle will probably hypertrophy, and this may 
almost completely compensate, so that life is scarcely shortened. 
If the foramen ovale is distinctly patent, this generally implies a 
greater degree of obstruction of the pulmonary artery, and life is 
usually abbreviated. Peacock has collected twenty cases of this 
kind, and only eleven of these lived to the age of 15 and upwards, 
but some lived as long as 34, 40, and 57. In three cases the 
ductus arteriosus was also open, and these died at the ages of 10 
months, 15 months, and 29 years. If the interventricular septum 
is imperfect, this implies an obstruction at an earlier period of 
foetal life, and the duration of life is shorter. Of sixty-four cases, 
only fourteen survived the age of 15, but still three lived as long 
as 25, and one to 39 years. Where the pulmonary artery is entirely 
impervious, the duration of life is still shorter; of twenty-eight 
such cases only seven lived over a year, and the longest duration 
was 12 years. Where there is still greater arrest of development, 
and the heart consists of but one ventricle, with one or two auricles, 
the period of survival is usually very limited, but it is interesting 
to find that four persons thus affected have lived to the ages of 11, 
16, 23, and 24 years. Transposition of the pulmonary artery and 
aorta might appear to be a malformation almost incompatible with 
life, and yet of twenty-one such cases, four lived between 2 and 3 
years. When the aorta is obstructed at its isthmus, and the 
descending aorta is supplied, wholly or partially, by the pulmonary 
artery, the duration of life is usually very limited. The lungs 
seem to be deprived of blood, because it passes to the abdominal 
aorta, and the children die with symptoms of dyspnoea and syncope. 
If the obstruction, however, be only slight, the person may 
survive to adult or middle life, even though the ductus arteriosus 294 
DISEASES OF THE ORGANS OF CIRCULATION. 
remains pervious; thus there are cases of survival to 24, 32, and 
43 years of age. If the constriction be so slight that the ductus 
arteriosus closes, it may yet become much more considerable after- 
Avards, or the aorta may even be obliterated at the point indicated. 
Yet such patients may suiwive long, as even with obliteration the 
ages of 45, 50, and 57 have been attained. 
ATROPHY OF THE HEART. 
This condition is one of comparatively frequent occurrence, but 
is for the most part merely a part of general atrophy, or emaciation 
of the body. In emaciating diseases such as phthisis pulmonalis, 
stricture of the oesophagus, cancer of the stomach, etc., where the 
muscular system as a whole has undergone great reduction in bulk, 
the heart is found to take part in the same .process. Taking the 
normal weight of the heart as nine ounces for the female, and ten 
or eleven ounces for the male, we may find it reduced to six or 
even five ounces. The heart as a whole is obviously smaller, and 
it has a darker color than normal, while the coronary arteries stand 
out unduly, often as somewhat prominent tubes. This change of 
color and the prominence of the arteries are largely due to the loss 
of the sub-pericardial fat, which normally covers the greater part 
of the surface and accompanies the coronary arteries, partially 
embedding them in the adipose tissue. The muscular tissue itself 
is darker in color, presenting a dirtv-brown hue instead of the 
normal robust red. It is also tougher and dryer. The deepening 
of the color is probably due to a concentration of the normal 
pigment from the diminution of the contractile substance without 
any loss of the pigment, just as red blood-corpuscles become much 
deeper in tint when they shrink by drying in. 
There is little doubt that the muscular fibres in this condition 
undergo an actual diminution in thickness, although from the 
great variety in diameter which the muscular fibres of the heart 
present this is very difficult to prove. The shrinking of the 
muscular fibres causes the connective tissue to be unduly promi- 
nent, and gives the muscle its undue toughness. 
HYPERTROPHY OF THE HEART. 
In entering on this subject it is necessary in the first place to 
consider under what circumstances such a condition may be 
brought about. It will be understood that the term is applied to 
hypertrophy of the muscular substance of the heart, giving rise 
according to circumstances to enlargement of particular ventricles 
or auricles, or of the heart as a whole. We have already seen 
that hypertrophy of muscle occurs as a result of repeated forcible 
contraction of the muscle, and apparently from no other cause, 
hence in each case of cardiac hypertrophy we have to look for IIYI’ERTEOPIIY OF THE HEART. 
295 
some cause producing increased vigor of the contractions of the 
cardiac muscle. The cardiac contractions are regulated by the 
wants of the system. When we lie quiet in bed they are com- 
paratively infrequent and deficient in force. When we exert 
ourselves by walking or climbing up a hill, they increase, it may 
be greatly, in frequency and force. The needs of the tissues assert 
themselves by the nervous connections of the body on the cardiac 
ganglia, and the contractions become more forcible. Within the 
limits of health, and without any increase of the volume of the 
cardiac muscle, there are great variations possible in the force of 
the cardiac contractions. But where the heart is for a prolonged 
period impelled to unusually violent exertion, it may become 
hypertrophied. Thus, in soldiers who have had to execute a series 
of long marches, hypertrophy has been found to develop; in such 
a case it is comparable with that of the muscles of a blacksmith’s 
arm, and is hardly pathological. How, anything which interferes 
with the due carrying on of the circulation will be likely to lead 
to increased vigor of the cardiac contractions, and, if prolonged, 
to hypertrophy. If the arteries are not duly filled at each systole, 
if the blood does not reach the capillaries with a sufficiently rapid 
current, then the heart replies to certain reflex impulses and con- 
tracts more vigorously. Conditions leading thus directly to im- 
poverishment of the circulation, may be situated in the heart itself 
or outside it, and it will be understood that the hypertrophy will 
be compensatory, and may be sufficient to overcome the difficulty. 
In many of these conditions there is a mechanical interference 
with the flow of the blood either in the heart itself or in the arteries, 
and as a consequence the heart is overloaded with blood. In such 
cases the cavities will be dilated and the dilatation may indeed be 
the primary condition, the hypertrophy occurring as a secondary 
consequence. It is usual, therefore, to consider dilatation and 
hypertrophy together, there being commonly some dilatation 
along with the hypertrophy, although it is rare to find dilatation 
without hypertrophy. 
For the sake of illustration we shall here consider some cases of 
cardiac hypertrophy. One of the commonest forms is that which 
occurs in adhesion of the pericardium. In this condition as we 
shall see afterwards, the sac of the pericardium is obliterated and 
the parietal pericardium has coalesced with the visceral. In some 
cases there is very little hypertrophy, but in others it is very great. 
It is to be remembered that adhesion of the pericardium takes 
origin in inflammation, and from this circumstance it results that 
in several ways the action of the heart is interfered with. During 
the acute stage of the inflammation there is fluid in the sac of the 
pericardium, and by the mere mechanical pressure of this fluid 
the cardiac contractions are interfered with; in order to overcome 
this obstacle the heart may hypertrophy, and if the effusion con- 
tinue long enough there may be hypertrophy from this cause alone. 
But again, the inflammation extends a certain distance into the 296 
DISEASES OF THE ORGANS OF CIRCULATION. 
muscular wall of the heart beneath the pericardium. A certain 
portion of muscle is thus interfered with in its action and more 
vigorous contraction is required of the rest. There may even be 
considerable thickening of the pericardium by development of 
connective tissue, and this extending some distance in the connec- 
tive tissue between the muscular fibres may seriously compromise 
them. But further, when adhesion is complete, the heart in con- 
tracting must drag in with it the parietal as well as the visceral 
pericardium. In the normal state the parietal pericardium lies 
against the visceral, and there is no cavity left, but then the two 
surfaces slide on one another, and the parietal layer accommodates 
itself to the movements of the heart. If there is adhesion, how- 
ever, unless the adhesion be very loose, there can be no such 
sliding, and there must be some loss of force in dragging the 
visceral layer inwards. But there is a further very important 
element in the problem. The inflammation of the pericardium 
does not coniine itself exactly to the sac, but extends somewhat 
outside it, so that when recovery occurs the visceral layer is united 
more firmly by new-formed connective tissue to parts around, to 
the ribs and intercostal spaces, the sternum, the pleura, and the 
roots of the lungs. This being the case, the heart will meet with 
greatly increased resistance in contracting, as it will have to drag 
in these adhesions in order to empty itself. In order, therefore, to 
send a normal amount of blood out of the ventricles, an excessive 
amount of muscular force will be required, and the continuance 
of this will lead to hypertrophy. It will be seen that these causes 
vary to a considerable extent, and the amount of hypertrophy 
varies in proportion. As the causes also act nearly uniformly on 
the heart, the hypertrophy is general, that is, it usually affects all 
the cavities of the heart. Such a hypertrophy may almost com- 
pletely compensate, so that a person with adherent pericardium 
and a very large heart may have no cardiac symptoms. 
As other illustrations of cardiac hypertrophy we might refer to 
cases of valvular disease of the heart. In these the force of 
the cardiac contractions is to some extent wasted, and the heart is 
spurred to increased exertion to supply the wants of the system. 
In studying the various forms of valvular disease we shall have 
sufficient illustration of this. 
Outside the heart itself there may be causes interfering with the 
circulation and leading to cardiac hypertrophy. These causes, 
like disease of the valves, will mostly act primarily on one cavity, 
and so we shall have partial hypertrophies. One of the most 
obvious illustrations of this is afforded by diseases in which the 
circulation in the lungs is obstructed. In emphysema there is great 
obliteration of the pulmonary vessels, and as the needs of the 
organism require a certain amount of blood to pass through the 
pulmonary vessels in a given time, the right ventricle is stirred to 
more vigorous contraction in order to force the due amount through 
the smaller number of vessels, and through time it hypertrophies. HYPERTROPHY OF THE HEART. 
297 
In the case of the systemic circulation, aneurisms and rigidity of 
the arteries are frequent causes of hypertrophy of the left ventricle. 
We come now to a form of hypertrophy of the left ventricle 
which it is somewhat difficult to explain, namely, that which occurs 
in Bright’s disease. It would carry us too far at the present 
stage were we fully to discuss the causes of this hypertrophy of 
the heart, which will be taken up again in considering the path- 
ology of affections of the kidney. In the mean time it may be 
noted that the hypertrophy is purely of the left ventricle, and its 
cause is to he looked for in something which increases the force of 
its contractions, or, in other words, some obstruction in the sys- 
temic arterial circulation. It is natural to look for this obstruction 
in the kidneys where, in chronic Bright’s disease, there is often 
great contraction and obstruction of the capillaries. There are 
serious objections to the acceptance of this view (which was that 
of Traube), at least in its simplest form, and we shall return to 
this point afterwards. In the mean time it may be stated that this 
form of Bright’s disease is associated with an increased blood- 
pressure (increased tension) in the systemic arteries, and that this 
is sufficient to account for the hypertrophy of the heart. An in- 
crease of the general blood-pressure is caused most effectually by 
a general narrowing of the smaller arteries throughout the body, 
and this would seriously stress the heart, if it had not sufficient 
force in its existing muscular fibre. In the case of Bright’s dis- 
ease increased arterial tension first develops, and this is followed 
by hypertrophy of the heart. 
Even when we have enumerated all the cases of hypertrophy of 
the heart, and especially of the left ventricle, in which a definite 
cause can be assigned, there still remains a residuum to which no 
mechanical explanation is discoverable. In these cases it may be 
presumed that there is some peripheral obstruction to the circula- 
tion, perhaps a habitual contraction of the arteries and consequent 
increased tension. Such persons are often liable to palpitation, 
and sometimes to other signs of heart disease, but without any val- 
vular lesion or other mechanical hindrance. 
Forms of Cardiac Hypertrophy.—From what has gone before, 
it will be apparent that hypertrophies of the heart vary greatly in 
amount and in the distribution of the enlargement. The total 
increase in weight is greatest in cases where both ventricles are 
enlarged, and the weight of the heart in such cases not uncom- 
monly reaches from twenty-seven to thirty ounces. It is least 
where the right ventricle alone is enlarged, because this ventricle, 
as a whole, weighs much less than the left, but in pure right ven- 
tricle hypertrophy a weight up to seventeen ounces is not infre- 
quent. In hypertrophy of the left ventricle, as in Bright’s disease, 
the weight is frequently over twenty ounces. 
In general hypertrophy the general shape of the heart is not 298 
diseases of the organs of circulation. 
much altered. The heart is enlarged in all its parts, the ven- 
tricles and auricles are increased in capacity, and their walls are 
thickened. The heart is like that of a bullock in size, so that the 
name cor bovis is often applied to it. 
When the right ventricle is mainly affected, the heart assumes 
a somewhat quadrilateral form (see Fig. 157). On examining the 
normal heart as it lies on its posterior surface, after removal from 
the body, the right ventricle is seen to occupy the greater part of 
the anterior aspect. The position of the septum, as shown in the 
accompanying figure, is slightly to the right of the left border, and 
it reaches the apex region slightly to the right of the true apex. 
In the heart the position of the septum is always indicated on the 
surface by the coronary artery which, with its padding of fat, 
occupies a groove corresponding with the anterior border of the 
Fig. 157. 
Fig. 158. 
Hypertrophy of right ventricle. The 
alteration in shape is indicated by the dot- 
ted line; «, superior vena cava; b, aorta: 
c, conus arteriosus ; d, right auricle; e, left 
auricle : f, left ventricle. (Rindfleisch.) 
Hypertrophy of left ventricle. The alter- 
ation in shape indicated by dotted line; g, 
the hypertrophied ventricle. (Rindfleisch.) 
septum. In hypertrophy of the right ventricle, as shown hv the 
dotted line in the figure, the apex is unduly obtuse, and it is often 
difficult to determine what is its exact seat. The septum is nearer 
the left border than usual, and it reaches the apex region rather to 
the left than the right of the most projecting point. The right 
ventricle also monopolizes the anterior aspect of the heart still 
more than in the normal condition. When the heart is laid open, 
the undue thickness of the right ventricle, as well as the enlarge- 
ment of its cavity, becomes apparent. 
In hypertrophy of the left ventricle the relations are very 
different, as shown in Fig. 158. The heart as a whole is more 
elongated and pointed than normal, and this is often very striking. 
The apex part especially appears greatly prolonged. When the 
heart is viewed on its anterior aspect the septum is seen to lie 
more to the right, and the true apex is much further to the left of FATTY INFILTRATION OF THE HEART. 
299 
the point at which the septum reaches the apex region. On laying 
open the heart, the thickening of the wall of the left ventricle is 
very obvious, and the septum is often greatly thickened. The 
septum belongs partly to the left and partly to the right ventricle, 
but as the left ventricle is much thicker than the right, the septum 
belongs more to the left. It will partake in the hypertrophy of 
either ventricle, and, in the case we are considering, the thickening 
is often very striking. The thickened septum frequently bulges 
into the right ventricle, sometimes diminishing its capacity greatly, 
and even producing actual obstruction of the conus arteriosus. 
The hypertrophied heart often presents a peculiarly firm condi- 
tion of its wall, and this has been ascribed by Sir William Jenner 
(Med.-Ch.ir. Trans., 1860, p. 199) to a passive congestion of the 
heakt. Cases of cardiac hypertrophy are very frequently such 
(as in the more common forms of valvular disease) as to lead to a 
general venous engorgement, in which the heart itself, being re- 
lated to the general venous system, partakes. How, prolonged 
venous hypercemia produces in organs, as we have seen already, a 
certain hypertrophy and increased density of the connective tissue. 
Some part of the hypertrophy in such cases may even be due to 
increase of the insterstitial connective tissue. Hence the result is 
that the walls of the heart are more rigid than normal, and when 
the cavities are laid open they do not collapse, but stand out with 
their outline retained, the walls having a tough leathery character. 
The muscular substance also is frequently of a very red color, this 
being largely due to the excess of blood in the vessels. 
FATTY INFILTRATION OF THE HEART. 
The normal heart is well known to present on its surface a cer- 
tain amount of adipose tissue. This fat is beneath the pericardium, 
lying between it and the muscular substance of the wall. It is 
normally most abundant along the course of the coronary arteries, 
along the inferior border of the right ventricle, at the apex and at 
the origins of the great vessels. In different individuals the 
amount of the adipose tissue and the extent to which it covers the 
muscular substance so as to conceal it from view, vary greatly, but 
it may be said generally that a considerable part of the surface of 
the right ventricle and the greater part of that of the left are 
usually free of fat. Sometimes this fat increases greatly, both in 
superficial area and in thickness. We know that adipose tissue in 
any part of the body is formed out of loose connective tissue by 
the infiltration of fat into its cells, and so the subpericardial con- 
nective tissue may become extensively converted into adipose tissue. 
In this way the entire right ventricle may be covered while a por- 
tion of the left is still free; or, the whole heart may be coated 
with a thick mantle of fat. 
The conversion does not always confine itself to the pericardium, 300 
DISEASES OF THE ORGANS OF CIRCULATION. 
but frequently extends into the connective tissue in the proper 
muscular wall of the heart, lying between the muscular fasciculi. 
In such cases if we make a section of the ventricle we find streaks 
of adipose tissue extending in from the surface. In this way the 
superficial layers of the muscular wall may be largely replaced by 
adipose tissue, which may even appear in isolated patches imme- 
diately beneath the endocardium, formally there is more fat on 
the surface of the right ventricle than on that of the left, and here 
also the pathological increase occurs to the greatest extent. It is 
not uncommon to find the proper muscular substance of the right 
ventricle largely replaced by adipose tissue, only a thin layer of 
red muscle appearing inside the thick layer of fat. Of course, in 
this case, there is great loss of the muscular power of the heart; 
the right ventricle is much more liable to this than the left. 
In some cases the increase of the external fat is merely part of 
a general obesity, in which the fat in all its various localities 
throughout the body takes part. But sometimes its significance 
is much more serious, and this applies especially to the cases in 
which adipose tissue forms between the muscular bundles. The 
space occupied by the fat must be obtained at the expense of the 
proper muscular substance, and the question arises whether the 
atrophy of the muscle is the primary condition or the fatty infil- 
tration. We are to take into consideration the fact that a fatty 
infiltration of an exactl}’ similar character occurs, as we have 
already seen, in voluntary muscle, and is there associated with loss 
of function of the muscle. The muscle may have lost its function 
by fixation of the joints which it has to move, or by reason of 
paralysis of a nervous origin. In either case the loss of function 
is the primary condition and the fatty infiltration is secondary. 
And so in the case of the heart, we meet with fatty infiltration in 
cases where there is no general obesity, often in old debilitated 
persons, or even in those who have been subject to some emaci- 
ating disease such as cancer. In that case we may infer that the 
weakening and atrophy of the muscle has been primary and the 
infiltration of fat secondary. 
FATTY DEGENERATI ON. 
From our former study of fatty degeneration as a whole, it will 
be understood that there is here meant an actual transformation of 
the muscular substance. This condition is of exceedingly frequent 
occurrence in the heart, especially in its minor degrees. Any dis- 
ease which causes a serious deterioration of the blood will produce 
it, and it is seen in its most pronounced form in the various kinds 
of amemia, in leukaemia, and in the acute fevers. It is also brought 
about in a very pronounced form in poisoning by phosphorus and 
arsenic. In a minor degree it is seen in debilitating diseases, and 
is often the more immediate cause of death in hypertrophy of the 
heart. FATTY DEGENERATION. 
301 
it is remarkable that, though the determining cause is a de- 
teriorated state of the blood, yet the fatty degeneration frequently 
shows itself in patches, so that the muscular tissue is seen to be, 
as it were, flecked with pale spots or streaks. This is best seen 
on examining the muscular tissue from within, as the endocardium 
generally produces but little obscuration of these markings, and 
they are most abundant in the inner layers of the muscular sub- 
stance. This flecked appearance is not always present, and it 
would be a mistake to infer the absence of fatty degeneration from 
its absence. The heart again is generally flabby, friable, and pale 
in color, but a very flabby heart may be very little fatty, and fatty 
degeneration may coexist with a comparatively firm muscular tissue. 
Microscopic examination should therefore always be resorted to. 
Under the microscope in those cases in which the degeneration 
is in patches, the transparent muscular tissue is seen with a low 
power to be interrupted by opaque patches, as in Fig. 159. The 
Fig. 159. 
Fatty degeneration of the heart. The occurrence of the lesion in patches is indicated by the 
dark appearance of the fibres. X 90. 
general outline of the muscular cylinders is preserved, but they 
are evidently replaced by some foreign material. Under a high 
power, as in Fig. 160, the individual fat-drops become apparent. 
Fig. 160. 
Fatty degeneration of the heart. A single fibre with oil-drops in it, as seen in the fresh 
state. X 350. 
These fat-granules are frequently seen to be in rows, representing 
the original muscular fibrillse, and the contractile substance is 
obviously lost or converted into oil. In minor degrees the de- 
generation is, as a rule, more uniformly distributed in the muscular 302 
DISEASES of the organs of circulation. 
substance, and we can see that the fat-granules generally appear 
first in the neighborhood of the nuclei of the muscular fibres, 
forming elongated collections extending from either pole of the 
nucleus. 
It is clear that muscular fibres which have undergone this trans- 
formation in its extreme form, are incapable of recovering their 
original condition. The sarcous substance has undergone trans- 
formation. It is to be inferred, therefore, that when such a heart 
recovers there is an absorption of the fat and an actual new forma- 
tion of muscular tissue. This process must be a comparatively 
frequent one when we consider how common fatty degeneration 
is in severe anaemias and in acute fevers. The fatty heart is usually 
a dilated one, even where there is no dilatation to begin with. On 
recovery the ventricles will resume their former dimensions. 
CALCAREOUS INFILTRATION OF THE MUSCULAR SUBSTANCE OF 
THE HEART. 
In this place we have to consider calcareous impregnation of the 
muscular substance of the heart, which is a somewhat rare occur- 
rence. But it is necessary, in the first place, to refer to certain 
other forms of calcareous impregnation in order to clear the 
ground for that more immediately before us. In connection with 
pericarditis it is not very uncommon to meet with calcareous in- 
filtration of old fibrine or dried-in pus which may remain on the 
surface. Again, where in the pericardium there has been great 
new formation of dense connective tissue from prolonged pericar- 
ditis, lime salts may be deposited in the hard tissue. In this way 
Fig. 161. 
Calcareous infiltration of the muscular tissue of the heart. The branching muscular 
cylinders are shown in a petrified condition with transverse fractures. From a case of 
pymmia. X 350. 
we may have the heart almost enclosed in a firm shell. But, 
further, in the muscular substance, old connective tissue may 
calcify, or an abscess may dry in and become impregnated with 
lime salts. In this way we may have stony masses developed in 
the muscular wall, these being actually in the connective tissue of 
the wall. 
But there is a true calcareous infiltration of the muscular tissue, INJURIES AND RUPTURE OF THE HEART. 
303 
and although recorded eases are few, the author is able to refer to 
two cases in which he has met with it, the condition, however, 
being somewhat different in each. In the one there were pale 
patches seen with the naked eye in the muscular substance, some- 
what like those of fatty degeneration, but larger and situated in 
the superficial layers just under the pericardium. These patches 
had, even to the naked eye, a streaked appearance, the streaks 
following the direction of the muscular fibres and indicating that 
the condition affected the muscular substance. On cutting into 
the patches a gritty feeling was experienced, and under the micro- 
scope the appearances shown in Fig. 161 were seen. The muscular 
fibres were converted into solid cylinders which had a markedly 
crystalline appearance. Many of the cylinders were fractured 
transversely. On adding hydrochloric acid to these patches, there 
was an abundant evolution of gas and a solution of the lime salts. 
After the lime salts were dissolved 
the muscular fibres were restored 
so far as their outline was con- 
cerned, but their transverse stride 
were gone. The case in which 
this occurred was one of pyeemia, 
and it is probable that the arteries 
in connection with these patches 
had been obstructed, causing a 
necrosis of the portion of tissue 
which subsequently became im- 
pregnated with lime salts. 
In the other case the condition 
was very different. A certain 
portion of the muscular sub- 
stance of the left ventricle was 
found of a pale color suggesting 
fatty degeneration, but the color 
was continuous, and it was the external layers that were affected, 
and that mainly towards the apex. On microscopic examination 
the muscular fibres were found clouded with fine granules not 
unlike fat-granules (Fig. 162). The granules, however, were dis- 
solved by hydrochloric acid, but without evolution of gas. Koster 
has met with a somewhat similar case, and he believes that the 
salt here is, in part at least, sulphate of lime. In this case the 
true pathology of the condition was obscure. 
Fig. 162. 
Calcareous infiltration of the muscular 
fibre of the heart. Fine granules occupy 
the muscular fibres. X 300. 
INJURIES AND RUPTURE OF THE HEART. 
Wounds of the heart are not by any means necessarily fatal, 
although, of course, commonly so. A needle or similar small in- 
strument may he passed into it without obvious injury. In most 
cases of penetrating wound of the heart there will be fatal hemor- 
rhage, but such wounds, especially if they do not divide the 304 
DISEASES OF THE ORGAN'S OF CIRCULATION. 
muscular fibres transversely, may heal, and be finally closed by 
connective tissue. There are even cases in which the point of a 
knife or a rifle-ball has lodged in the heart and become surrounded 
by a connective-tissue capsule. 
Spontaneous rupture of the heart is of* very rare occurrence, and 
the conditions which bring it about are by no means clear. It is 
natural to suppose that fatty degeneration, especially when asso- 
ciated with a lesion which increases the blood-pressure in the 
heart, as, for example, stenosis of the aortic orifice, will be the 
most frequent cause, but it is by no means fully proved that fatty 
degeneration is always present. The rupture mostly occurs in the 
left ventricle, and near the apex, or towards the aortic orifice. 
There is usually a large escape of blood into the sac of the peri- 
cardium, and the patient dies rapidly. 
Rupture of the heart may be the consequence of the bursting 
of an aneurism of the heart, but, as this subject comes up for 
consideration afterwards, it will not be further dwelt on here. 
MYOCARDITIS. 
It is to be understood that here we include inflammations occur- 
ring in the muscular substance of the heart, although not neces- 
sarily originating in the muscular tissue proper. It is doubtful 
whether a true inflammation of the muscular tissue of the heart 
occurs, a true parenchymatous myocarditis. Rindfleisch describes 
a case in which he supposes that this condition was the cause of 
sudden death. He found the muscular substance of a pale violet 
color, and with eccliymoses under the pericardium and endocar- 
dium. Under the microscope the muscular fibres presented a 
granular appearance, especially around the nuclei. We can well 
understand that an inflammation affecting the proper muscular 
fibre will destroy its function, and in the case of the heart cause 
death almost-immediately. The designation interstitial myocar- 
ditis is applied to inflammations which occur in the muscular 
substance, but affect the interstitial connective tissue. These in- 
flammations are mostly secondary, and are chiefly due either to 
propagation from the endocardium or pericardium, or to septic 
embolism. 
In the course of acute endocarditis the inflammation may spread 
into the muscular substance, causing, it may be, softening of it. 
This is particularly the case with ulcerative endocarditis, to be 
afterwards described. In this disease virulent bacteria are present 
in the endocardium, and these may invade the muscular substance, 
causing a suppurative inflammation of it, or a kind of abscess. 
As we shall afterwards see, there may, in ulcerative endocarditis, 
be abscesses in the substance of the heart from another cause. 
Again, chronic endocarditis not infrequently extends to the mus- 
cular substance. Like other forms of chronic inflammation, this 
is associated with great new formation of connective tissue. For MYOCARDITIS. 
305 
the most part it is the valvular structures which are involved, and 
they, as we shall afterwards see, are greatly thickened, but the 
inflammation frequently extends beyond the immediate valvular 
structures. This is most frequently seen in the case of the mitral 
valve. Here, along with 'thickening of the chordae tendinese, we 
often see a partial conversion of the musculi papillares into dense 
fibrous tissue; in fact, an interstitial inflammation with destruction 
of the muscular tissue. The muscular substance is not so imme- 
diately continuous with the aortic valve, but we sometimes see, 
just beneath the valve, a tendon-like thickening of the endocar- 
dium with extension to the muscular tissue beneath. But chronic 
endocarditis sometimes attacks the endocardium at a distance from 
the valves, and in that case it is very liable to extend to the 
muscular substance. This form occurs perhaps most frequently 
towards the apex of the left ventricle, where a considerable area 
may be converted into dense connective tissue. By the distention 
of this altered wall of the heart aneurisms of the heart may take 
origin. 
There has recently been described, especially by Fagge and 
Charlewood Turner, a more independent fibroid myocarditis. 
This may occur in patches, so that there are tendinous areas in 
the muscular substance in the midst of which the muscular fibres 
may be calcareous. But in other cases it is generalized, so that a 
condition is brought about in which the interstitial connective 
tissue is greatly increased, and the muscular fibres correspondingly 
separated from each other, a condition corresponding to cirrhosis 
of the liver or kidney. In the localized form the cause is prob- 
ably some interference with the circulation, perhaps an obstruction 
of the coronary arteries by atheroma or syphilis. In the more 
generalized form the cause must be one which affects the whole 
heart, and as it occurs mostly in dilated or hypertrophied hearts, 
the strain or over-distention may have to do with it. The hyper- 
trophy of the left ventricle in Bright’s disease is stated to be 
associated with this fibroid change, but the author has failed to 
convince himself that this is the case. It is possible that in some 
obscure oases of hypertrophy and dilatation of the heart this 
lesion may be the primary one. 
Abscess of the heart is a form of inflammation which probably 
occurs only by the transplantation of septic material in pyaemia, 
ulcerative endocarditis, etc. In about a third of the cases of 
pyaemia there are abscesses in the heart. In connection with 
these abscesses, colonies of micrococci are to be found in the 
midst of the pus in the abscess or in the fine arteries and capil- 
laries. These metastatic abscesses first appear as small pale yellow 
spots or streaks which rapidly soften and enlarge. The abscesses 
contain a brownish material composed of pus and the debris of 
muscular fibre. They are usually elongated in shape, and, while 
numerous, are individually of small size. If situated near the 
surface, they may burst into the pericardium, producing a septic 306 
DISEASES OF THE ORGANS OF CIRCULATION. 
pericarditis, but even without actual rupture they may, apparently 
by irritating material passing from them, give rise to pericarditis. 
When situated near the internal surface, they may communicate 
with one of the cavities, and it is said, that an aneurism of the 
heart may occur in this way, and may even lead to rupture of the 
heart. 
It will he understood that these abscesses rarely have the oppor- 
tunity of healing, as the patient dies from the general disease, but 
it is asserted that survival may occur, and the abscess dry-in to a 
caseous mass, which may afterwards calcify. 
ENDOCARDITIS. 
It will be necessary, in considering the subject of inflammation 
of the endocardium, to subdivide it. We shall consider in the 
first place simple acute endocarditis, then chronic endocarditis, 
and lastly the special form, ulcerative endocarditis. 
(a) Simple acute endocarditis is, in the great majority of cases, 
related to acute rheumatism, and, according to Bamberger, it 
occurs in twenty per cent, of the cases of that disease. Whatever 
view we fake of the origin and nature of acute articular rheuma- 
tism, it must be admitted that in it the hlood is in some way 
altered. The blood is in itself of an unusually irritating nature, 
or else it carries an irritant. The occurrence of acute inflam- 
mations in several joints often removed considerably from one 
another, and the frequent supervention of inflammation in the 
pericardium and endocardium, are sufficient evidence of this. The 
irritant, whatever be its nature, seems to act specially on connec- 
tive-tissue membranes, and on such as are exposed to friction of 
their surfaces. It affects the joints where the synovial membranes 
lie against each other, and in the movements of the joints are 
moved on one another. It attacks the pericardium where the 
movements of the heart cause continuous rubbing, and when it 
attacks the endocardium it affects exactly the localities where the 
surfaces come in contact. It is as if in addition to the irritant in 
the blood, the mechanical irritation of friction were necessary to 
the occurrence of inflammation, and it may be added that in the 
adult the inflammation is almost limited to the valves of the left 
side of the heart, where the higher tension of the blood and 
greater force of the heart make the mechanical force of friction 
greater than on the right side. We shall see afterwards how this 
fact bears on the localization of the endocarditis. 
The most characteristic effects produced in acute endocarditis 
are the so-called warty vegetations, which are irregular projections 
from the surface of the endocardium, generally of small size and 
somewhat shaggy in appearance. On their first occurrence these 
are limited to the parts of the valves which come against each 
other in the closure of the valves, and this localization continues 
more or less throughout. It is therefore important to know what 307 
are the lines of contact in the aortic and mitral valves, because it 
is there chiefly that we are to look for these endocarditic vegeta- 
tions. 
When after removal of the heart a stream of water is sent into 
the aorta cut transversely a short distance above the valve, we can 
look down on the valve closed by the force of the water. It will 
then be seen that the curtains are not in contact by their margins, 
but that the line of contact is slightly removed from their edges, 
and a certain portion of the valve floats free in the water, taking 
no direct part in the closure of the orifice. The line of contact is 
nearest the edge of the curtain at the middle of each segment or 
the corpus Arantii, and forms on either side of this a curved line 
with the convexity downwards. Between the line of contact and 
the edge of the curtain the valve is often perforated, and it may 
even, as we have seen before (p. 291, Fig. 156), be partially re- 
solved into tendinous cords, without interfering with the closure 
of the valve. It is by the modification of this portion that we may 
have the aortic valve showing approaches to the construction of a 
cuspid valve, as seen in considering malformations of the heart. 
In the mitral valve the line of contact is also removed from the 
edges of the curtains. In the case of the aortic valve the line of 
contact is of course on the ventricular side of the curtains, but in 
the mitral it is on the auricular side, and in order to see the vege- 
tation in acute endocarditis it is usually necessary to examine the 
orifice by looking in from the auricle. Acute endocarditis of the 
mitral often escapes notice from this not being done. 
In acute endocarditis the warty vegetations frequently demarcate 
very accurately the lines of contact of the aortic and mitral valves, 
and the appearances produced in the former case are indicated in 
Fig. 163. When the inflammation extends to the valves of the 
ENDOCARDITIS. 
Fig. 163. 
The aortic valve in acute endocarditis. The warty vegetations, occupying the line of 
contact, are shown. 
right side, the same principles apply. In the case of 
monary valve the vegetations appear along the line of contact on 
the ventricular aspect of the curtains, and in the tricuspid they 
are to he seen by looking down through the auricle. 308 
DISEASES OF THE ORGANS OF CIRCULATION. 
We now turn to the consideration of the actual changes and the 
structure of these warty vegetations. The inflammation affecting 
the connective tissue of the valve leads to formation of round cells 
or granulation tissue. The structures by this change are increased 
in bulk and rendered more friable, and in this way irregular pro- 
jections are produced. But the warty projections are not formed 
entirely or even chiefly by the granulation tissue. The blood de- 
posits fibrine on the inflamed irregular surface, and this covers up 
the granulation tissue and forms the principal part of the warty 
vegetations. Several authors have described micrococci as oc- 
curring in these vegetations, chiefly Iilebs, Roster, and Osier, and 
some are inclined to associate these organisms with the essential 
pathology of acute rheumatism. But these micrococci are not of 
the virulent sort found in ulcerative endocarditis, and they are 
probably of subordinate importance. 
The occurrence of these changes in the tissue renders it unduly 
brittle, and it is not surprising to find that bits of the vegetations 
are frequently broken off and carried by the arteries to distant 
parts, to produce embolism there. These broken-off pieces are 
mostly small, and, beyond the ordinary phenomena of embolism 
in small arteries and capillaries, they do not by their own nature 
produce much disturbance, in this respect contrasting with the 
emboli of ulcerative endocarditis." There is not usually any serious 
loss of substance of the valvular structures, but the softening of 
the tissue not uncommonly leads to the formation of valvular 
aneurisms, which we shall consider more fully further on. 
(b) Chronic endocarditis commonly follows on the acute form, 
and, like it, is related to acute rheumatism. It appears as if the 
irritation were prolonged in a less intense form, and the changes 
in the valvular structures extend beyond the localities which we 
have seen to be mainly affected in acute endocarditis. In the 
chronic form there is great new formation of connective tissue. 
The granulation tissue of the acute stage develops into connective 
tissue, and the process extends slowly to the remaining structures 
of the valves. In this way arise great thickenings of the valves 
(Fig. 164), and, as the connective tissue is of that dense nature 
common in chronic inflammations, the thickened valvular struct- 
ures are often exceedingly rigid. The new-formed tissue also 
contracts, and in this' way we may have great retractions of the 
valves leading to serious deformities, as we shall see in studying 
valvular diseases. Again, it frequently happens that two opposed 
inflamed surfaces coalesce, and we may have still further deformity 
from this. We have already seen that the inflammation may ex- 
tend from the endocardium to the muscular substance, leading to 
cicatricial transformation of it. 
In the great majority of cases, the endocarditis is limited to, or 
has its centre in, the valvular structures, but it sometimes happens 
that in other parts of the heart an apparently independent endo- 
carditis is set up. This may be along with valvular endocarditis, ENDOCARDITIS. 
309 
but separated from it by sound tissue, or it may be without any 
valvular lesion. We may find an isolated patch of thickening on 
the surface of the left ventricle, and we have already seen that the 
disease may penetrate into the muscular substance. 
The thickened and rigid connective tissue frequently becomes 
the seat of secondary changes. Fatty degeneration may occur. 
Fig. 164. 
Great thickening of the chordae tendinem of the mitral valve, the result of chronic 
endocarditis. 
But this is much less frequent than calcareous impregnation, which 
may he taken as evidence that the hard, dense, cicatricial connective 
tissue has, to a great extent, lost its vitality. This condition is of 
such frequent occurrence that it may be regarded as the normal 
termination of chronic endocarditis. It sometimes occurs with a 
very moderate degree of thickening, and its extent and the date of 
its occurrence are doubtless determined by individual peculiarities. 
It may occur in the form of a moderate calcification in the deeper 
parts of the thickened tissue, or the lime salts may be deposited in 
a more bulky form, so as to give the feeling of considerable stony 
masses. This occurrence is often of serious import. The valvular 
structures are rendered still more rigid, and there enters the new 
element of brittleness. The calcified portion of the valve is 
exposed very often to mechanical violence in the closure of the 
valve, and it is common to find that the valve has been broken and 
a piece of calcareous matter carried off. So far as the valve is con- 
cerned, this is not usually very serious, but as the piece carried off 
is usually of some size, the resulting embolism is frequently of 
great consequence. Embolism of the cerebral arteries leading to 
extensive softening is much more frequent in chronic than in acute 
endocarditis, and probably the same applies to aneurisms of the 
larger cerebral arteries, which, as we shall afterwards see, may 
have their origin in embolism. Embolism of the spleen and kid- 
neys is also a frequent result. The rough surface left by the 
breaking-off of the calcareous piece gets coated with fibrine, and 310 
DISEASES OF THE ORGANS OF CIRCULATION. 
here again it is said that micro-organisms may he present. The 
ffbrine may, by getting detached, form a fresh source of embolism. 
Besides the form of chronic endocarditis hitherto considered, 
which is the most frequent and most important in its results, there 
is a form which deserves some notice. This form is closely allied 
to the disease of arteries commonly designated atheroma, and it 
occurs most frequently in the aortic valve, being here continuous 
with atheroma of that vessel. In its causation, therefore, it has 
nothing to do with rheumatism, but is rather related to the degen- 
erative tendencies of old age. It produces thickenings and indu- 
rations of the endocardium, with fatty and calcareous changes just 
as in ordinary endocarditis, but the processes are more chronic, 
and produce less considerable deformity of the valvular structures, 
although from calcareous deposition there may be great rigidity. 
Besides this, and still more removed from inflammatory pro- 
cesses, we sometimes have simply opaque patches on the valves 
with very little thickening. In this case there is little more than 
a fatty degeneration of the endocardium. Such patches are not 
uncommon on the mitral valve, and are often erroneously regarded 
as due to endocarditis. 
(c) Ulcerative endocarditis, also called malignant and diph- 
theritic endocarditis, is regarded by some as merely a form of 
acute endocarditis, but it presents such differences that it seems 
necessary to place it in a class by itself. The special features in 
the disease are the activity of the destructive process in the heart, 
its connection with the existence of micrococci, and the virulence 
of the metastatic processes when emboli are carried to distant parts. 
In its local manifestations this form presents some resemblance 
to simple acute endocarditis. The disease affects, usually, the val- 
vular structures, and produces an enlargement and roughening of 
them. But there is not the same localization along the lines of 
contact, the process generally developing in a defined area, and 
sometimes removed from the valve. Again, the disease, as the 
name implies, is a much more destructive one. the parts concerned 
breaking down more readily. In this way perforation or aneurism 
of the valve may occur. Sometimes an actual suppuration mani- 
fests itself in the valvular structures, but the frequent passage of 
the blood prevents any considerable accumulation of pus. The 
ulceration sometimes passes to the muscular wall of the heart, 
especially when the patch of ulceration is away from the valves. 
The destructive process spreads rapidly in the myocardium, and a 
distinct abscess may be the result. In this way also an acute 
aneurism of the heart may supervene. 
In their more intimate characters, also, the conditions in ulcer- 
ative endocarditis differ from those in the ordinary simple form. 
As the accompanying figure shows, there is a very marked infiltra- 
tion of the valvular structures with round cells, almost a suppur- 
ative condition. This is immediately overlaid by a fibrinous 
coagulum, as in the case of simple endocarditis, but mixed with ENDOCARDITIS. 
311 
the fibrine there are colonies of micrococci which give quite a 
striking character to the layer. The appearances in distant parts 
are evidence that pieces are frequently carried off from the valves, 
Pig. 165. 
Portion of valve in ulcerative endocarditis, a, fibrine with colonies of micrococci; the 
colonies are indicated by the roundish clumps; b, endocardium becoming raised by inflam- 
matory infiltration; e, elastic layer of endocardium; c, round cells infiltrating endocardium, 
at d; passing into superficial layer of fibrine and micrococci. X 22. 
and looking to the soft character of the superficial parts we are not 
surprised at the occurrence of multiple embolism. 
Perhaps the most striking feature in this disease is the occurrence 
of metastatic abscesses in distant parts. These are found in the 
heart itself, in the spleen, in the kidneys, in the skin, etc. They 
are everywhere of small size, and usually in large numbers. These 
abscesses are obviously related to emboli carried off from the endo- 
cardial lesion, and lodged in the finer arteries or capillaries. The 
accompanying figure represents a small artery in the midst of an 
incipient abscess in the kidney. It is seen that its calibre is 
plugged by a material in which are occasional masses of micro- 
cocci. At the distal part the wall of the artery is obscure, appar- 
ently from necrosis, and the vessel is buried in an enormous 
aggregation of inflammation cells. The peculiar virulence of this 
process is surely to be associated with the presence of the micro- 
cocci, yet it seems to be not the micrococci themselves, but rather 
the chemical products evolved by them, which set up the intense 
inflammation. For, in the illustration given, the micrococci are 
confined to the calibre of the artery, yet there is necrosis of the 
wall, and an intense inflammation around. Then, again, the 
micrococci are frequent in the capillaries and Malpighian vessels, 
but not generally with obvious inflammation; apparently they are 
in that case of recent development, possibly to some extent post- 
mortem, and their products have not had time to produce inflam- 
mation. 
A very important question remains for consideration, namely, 
the origin of the micrococci which give such special characters to 312 
DISEASES OF THE ORGANS OF CIRCULATION. 
the disease. The disease has been observed to occur in the course 
of a number of acute febrile affections. It is met with in pyaemia, 
Fig. 166. 
From the kidney in ulcerative endocarditis. An artery is shown, plugged with a dark 
material containing micrococci. Around these are myriads of leucocytes which are infil- 
trating the necrosed wall of the vessel and the kidney tissue around. X 90. 
puerperal fever, acute rheumatism, smallpox, etc., and Osier has 
recently pointed out that in a large proportion of cases acute pneu- 
monia has been the primary disease. There are, however, cases 
in which no definite connection with any other disease can be 
traced. In the case of pyaemia and puerperal fever the source of 
the micro-organisms is not far to seek. For the rest we are hardly 
warranted in going further than merely calling attention to the 
occasional association of this apparently septic disease with these 
specific febrile conditions. It may be added that the micrococci 
removed from the valvular lesion soon after death have been found 
capable of propagation in the tissues of living animals, where 
they produce intense inflammation. Inoculated into the cornea 
of a rabbit they produced panophthalmitis with rapid growth of 
the organism. 
We have seen that the micrococci present, locally, an intensely 
irritating action, and that necrosis of the tissue attacked is a com- PERICARDITIS. 
313 
mon result. It is probable that they also produce changes in the 
constitution of the blood. Patients affected with this disease fre- 
quently present, like those in pysemia, a yellow color of the skin 
approaching to that of jaundice. The probable explanation of 
this is, that the blood-corpuscles undergo solution, and the coloring 
matter stains the skin. But, besides that, we often have little 
ecchymoses of the skin, and small hemorrhages in the pia mater, 
and even in the brain substance. These have been found asso- 
ciated with the presence of colonies of micrococci in the capillaries, 
and are to be ascribed to the action of these in weakening the wall, 
and allowing escape of blood. 
PERICARDITIS. 
The pericardium is comparable in its anatomical and path- 
ological relations to the serous sacs, and, to a certain extent, to the 
synovial. The pleura, peritoneum, and pericardium are to be re- 
garded, as we previously found in studying oedema and dropsy, as 
large lymphatic spaces. These sacs are composed of connective 
tissue, and lined with a single layer of flat endothelium. By 
means of numerous stomata they are in communication with the 
lymphatic vessels, and to some extent with one another. The 
pericardium is in less direct communication with the pleura and 
peritoneum than these are with each other, but by circuitous routes 
there is some communication, especially with the pleura. It is to 
be remembered also that through each serous cavity there is a 
certain circulation of serous fluid. This fluid does not accumulate 
in the sac, because it is carried off as quickly as it is transuded 
from the vessels, hut if the transudation increases greatly there 
may be an accumulation and consequent dropsy. 
(a) Acute Pericarditis.—In considering the causes of this 
disease it is of some consequence to note that the inflammation 
usually affects the whole surface at once. This seems to indicate 
that an irritant has found admission to the pericardial sac, and by 
the motions of the heart and the natural currents of the fluid in 
the sac, has been carried hither and thither throughout it. There 
are many cases in which the tubercular virus is the irritant; we 
flncl tubercles mixed up with the inflammatory products. The 
appearances in this case, however, are so peculiar, and the course 
of the disease differs to such an extent from that in ordinary cases 
that it will be proper afterwards to refer more particularly to 
tubercular pericarditis. The great majority of cases of pericarditis 
are associated with acute rheumatism. It is to be presumed that 
the irritant here is the same as that which produces the acute in- 
flammation of the joints of the endocardium. The irritant circu- 
lates in the blood, but we do not know its nature and form, nor 
why it settles in the pericardium and synovial sacs. The irritant, 
whatever it may be, having been conveyed to the sac by the blood 314 
DISEASES OF THE ORGANS OF CIRCULATION. 
is carried throughout the latter, and acts on its whole surface. 
There are some cases in which the disease appears tc be of spon- 
taneous origin; it is ascribed to cold. It is altogether obscure in 
what way such inflammations are brought about. 
We have now to consider the phenomena which manifest them- 
selves at the onset of an acute pericarditis. We may presume that 
the irritant induces the changes in the vessels which have been 
described in treating of inflammation in general, but opportunities 
are wanting for observing the consequent redness, as patients 
survive this early stage. Exudation from the vessels soon follows, 
and serous fluid begins to accumulate in the sac. As the inflam- 
mation affects the surface of the sac, the endothelial lining is very 
directly involved. The flat endothelial cells are to a considerable 
extent shed, being apparently killed by the irritant, but they may 
also be found showing signs of germination. The exudation con- 
sists primarily of exuded liquor sanguinis with contractile cells, 
but soon fibrine is deposited on the inflamed surface. The de- 
tachment of the endothelium seems to be the circumstance which 
determines the coagulation, on principles already explained. The 
deposition of fibrine occurs on both visceral and parietal layers of 
the sac, but it is usually thickest on the visceral surface, where it 
may present shaggy masses on the surface of the heart. It is 
whitish in color, and of soft, almost gelatinous consistence. The 
fibrinous layers on the opposed surfaces of the pericardium are 
usually separated by serous fluid which occupies the sac, but an 
appearance is often presented which suggests the application and 
withdrawal of the layers while still in a soft plastic condition. This 
appearance is variously described as the honeycomb or pine-apple 
condition, and it has been aptly compared to that presented when 
two pieces of bread thickly buttered are stuck loosely together 
and then separated. This honeycomb appearance, it will be 
understood, is most markedly present on those parts of the peri- 
cardium where the heart in its movement comes most frequently 
against the parietes. It will be most extensive and characteristic 
when there is little serous exudation, and may be taken roughly 
as an indication of the extent to which the soft fibrine of the op- 
posite layers has been able to come in contact. 
The exuded fibrine has the usual characters, as seen under the 
microscope, forming a fine reticulum; and in its meshes are leuco- 
cytes, and sometimes red corpuscles, whose origin we have already 
considered in studying inflammation in general. 
If the inflammation has been slight and transient, there may be 
little beyond a small serous and fibrinous exudation, which is 
gradually absorbed. But as a general rule further changes de- 
velop, and these are mainly in the connective tissue of the peri- 
cardial sac. This shows evidence of inflammation in the presence 
of innumerable cells, so that by degrees it is converted into what 
is equivalent to granulation tissue. This inflammatory transforma- 
tion does not confine itself to the superficial layers of the sac, but, 
according to the intensity of the irritation, penetrates more and PERICARDITIS. 
315 
more deeply, even extending frequently to the interstitial connective 
tissue in the muscular substance of the heart. A layer of granula- 
tions thus forms beneath the fibrinous exudation, and like other 
such layers, it is abundantly supplied by thin-walled bloodvessels. 
The formation of this granulation tissue implies here, as elsewhere, 
that the acuteness of the inflammation has somewhat subsided, or 
at least that a considerable interval has elapsed since its onset. 
The layer of granulations has the general tendencies as well as the 
structure of granulation tissue elsewhere, it tends to develop into 
connective tissue as soon as the inflammatory irritation becomes 
sufficiently mild. With the subsidence of the inflammation there 
will be a reduction of the serous exudation. The fibrine is also 
disposed of, partly undergoing fatty degeneration and so becoming 
absorbed, and partly eaten into from beneath by the granulation 
tissue. The result of this is that the granulations are, as it were, 
laid bare, and a vascular layer occupies the place of the former 
fibrinous deposit. 
Looking to this substitution of the fibrinous layer by the vas- 
cular granulations, it is easy to understand how the inference was 
formerly drawn that an actual transformation occurs. The fibrine 
was regarded as plastic lymph which had the power of developing 
into the vascular tissue, first granulations and then fibrous tissue. 
The soft fibrine is still sometimes called soft lymph, and the name 
is even applied to shreds of connective tissue which have been 
formed from the granulations. 
With the absorption of the exudation the two layers of the peri- 
cardium come in contact, and a coalescence of the granulating 
surfaces, more or less complete, occurs. The vessels intercom- 
municate, and the two layers so far as they are in contact become 
virtually one. As the granulation tissue passes on in its develop- 
ment into connective tissue the pericardial sac undergoes partial 
or complete obliteration, the uniting agent being vascular con- 
nective tissue. The connection will at first be delicate, and may 
be torn through, but as time goes on it gets firmer, and a condi- 
tion results in which the two layers are absolutely inseparable. 
Under certain circumstances the coalescence of the two layers is 
not complete, and there is only a partial adhesion; in that case the 
adhesions are sometimes greatly stretched by the movements of 
the heart so that tags or ligaments may unite the surface of the 
heart to the peripheral layer. 
This, which may be regarded as the normal course of pericar- 
ditis, is sometimes departed from, chiefly when the inflammation 
remains too intense to allow of the formation of proper connective 
tissue. Instead of progressing in this direction, suppuration oc- 
curs, and the serous exudation in the pericardium gives place to 
pus. The inflammation in that case is usually very prolonged, 
and even when it subsides there are obstacles to the adhesion of 
the layers. On the subsidence of the inflammation the pus dries 
in by the absorption of its fluid. The pus-corpuscles undergo fatty 
degeneration and die, but the surface not being well adapted for 316 
DISEASES OF THE ORGANS OF CIRCULATION. 
absorption, the debris remains as dead matter. In this way caseous 
material is produced, which subsequently gets infiltrated with lime 
salts. At first the lime forms a pultaceous layer on the surface of 
the heart, but it may afterwards become consolidated so as to form 
calcareous plates in the midst of thick adhesions. 
It is to be added that septic inflammations, such as those which 
occur in pysemia when an abscess in the substance of the heart ex- 
tends to the surface and bursts into the pericardium or gives off 
septic organisms, or in the rarer case of perforation of an ulcer of 
the stomach or oesophagus into the pericardium, are purulent from 
the outset. The septic irritant acts so intensely that leucocytes are 
at once exuded in such numbers as to give a purulent character to 
the exudation. 
In considering hypertrophy of the heart in a previous page, it 
was pointed out that this condition may be caused by complete 
synechia of the pericardium, and an endeavor was made to explain 
the mode of its production. It may here be stated that hyper- 
trophy may occur even in the stage of pericarditis associated with 
fibrinous and serous exudation, but these conditions must have 
persisted long in order to induce it; the mode in which they bring 
it about has been already explained. It should be borne in mind, 
however, that, as pericarditis is often associated with endocarditis, 
we may have hypertrophy from valvular disease associated with 
adherent pericardium, and it may be difficult sometimes to assign 
the exact proportion of one or other agent in bringing about the 
result. 
Tubercular pericarditis has commonly a subacute or chronic 
course. It is very often associated with tuberculosis of the pleura, 
and the conditions in that sac have similar characters. Occasion- 
ally we meet with an acute fibrinous pericarditis in which, when 
we remove the fib Fine, numerous small white fresh tubercles are 
to be seen on the pericardium. More frequently, however, the 
two layers of the pericardium are firmly united by connective 
tissue, and it is impossible to separate them. In the midst of the 
thickened layers are to be seen yellow caseous masses, sometimes 
of considerable size. These represent old tubercles, and the whole 
process is a more or less chronic one, even from the outset. Under 
the microscope there will be found large masses having the indefi- 
nite characters of caseous necrosis with occasional fresh tubercles, 
in the midst of tissue which presents in some parts evidences of 
recent inflammation and in others merely dense connective tissue. 
White spots, milk spots, or soldier’s spots, on the pericardium. 
—These are very common pathological conditions and warrant a 
passing notice. They occur in about half the cases examined post- 
mortem, and their frequency seems nearly in direct proportion to 
age. They are in the form of well-defined, whitish, opaque areas 
on the surface of the heart, of very various size, sometimes very 
small, at other times so large as almost to cover the anterior sur- ANEURISMS OF THE HEART AND VALVES. 
317 
face. Their edges are usually abrupt and well-defined, but they 
may merge gradually in the pericardium. They have often a bril- 
liant white tendinous appearance, but may be more dull. They 
are most frequently situated on the anterior surface of the right 
ventricle, and next on that of the left ventricle, especially near the 
apex. They are also met with on the posterior surface, especially 
near the base of the heart, and on the intra-pericardial portions of 
the great vessels. They are more uncommon on the parietal layer 
of the sac. 
These spots actually consist in a thickening of the pericardium, 
presenting merely dense connective tissue covered with endothelium 
(see Fig. 167). The thickening is due to a chronic irritation, and 
Fig. 167. 
Soldier’s spot on pericardium, b, muscular wall of heart; «, pericardium; c, thickening 
so as to form spot. X 25. 
the condition is really a chronic pericarditis. The cause of the ir- 
ritation is not at first very clear. We have here a circumscribed 
inflammation affecting by preference certain districts, and the cause 
must be a local one. It seems to be due to the irritation resulting 
from the projection of the heart against its surroundings. The 
commonest seat is where the anterior surface of the right ventricle 
comes against the sternum at the place where the edges of the 
lungs turn aside and expose the pericardium. The sternum is less 
yielding than most surrounding parts, and so the irritation is 
greater here. The spot where the left ventricle near the apex 
strikes against the fifth rib, is the next most frequent site. 
ANEURISMS OF THE HEART AND VALVES. 
Although these aneurisms are not usually of independent origin 
or significance, we give them here a special treatment because of 
their frequency and importance. 
By aneurisms of the heart are meant aneurisms which, in the 
form of sacs or diverticula, communicate with one of the cavities 
of the heart. These aneurisms are almost confined to the left 
ventricle, and they may be divided into two forms. In one form 
the aneurism projects out from the heart, so as to he visible 
externally as a protrusion; in the other form the aneurism burrows 318 
diseases of the organs of circulation. 
in the wall of the heart, and is not visible externally. The first 
form usually has its seat at the apex or the base, and in the latter 
case it may project up between the great vessels. These aneurisms 
mostly arise as a consequence of chronic endocarditis, or chronic 
myocarditis. The latter, especially when it produces a localized 
fibroid condition, or cirrhosis of the muscular wall, may allow of 
partial dilatation in the form of a pouch. In the second form, the 
dimensions and outline of the aneurism may be very complicated. 
The blood, getting into the muscular substance, may dissect a path 
for itself for a considerable distance from the original aperture. 
In this way it may almost form a girdle round the heart. Or it 
may undermine the pericardium, dissecting it largely from the sur- 
face of the heart, so as to form a kind of blood-filled sac around 
the heart. For the most part these aneurisms originate in soften- 
ing of the endocardium, admitting of penetration of the blood 
into the muscular substance. It need hardly be added that, in both 
forms, rupture of the aneurism is liable to occur, usually into the 
sac of the pericardium, and with fatal results. 
Aneurism of the valves is the condition in which a pouch 
exists, projecting from a valve and with a narrow neck. This 
form of aneurism results from acute endocarditis, either simple or 
ulcerative. With the aid of the accompanying diagram, the mode 
Fig. 168. 
Diagram of mode of formation of aneurism of aortic valve. The curtain (a) formed of two 
layers. At b, its outer layer roughened and softened. At c, the aneurism, which has burst 
at d, so as to perforate the valve. 
of formation of the aneurism may be illustrated in the case of the 
aortic valve, which is its most frequent seat. The semilunar 
curtains which form the valve are each composed of a double fold 
of endocardium, as represented at a. From what has already been 
stated, it will be known that in acute endocarditis it is the ven- 
tricular layer which is principally involved along the line of contact, 
as indicated at b. The aortic layer is usually smooth and unaltered 
to the naked eye. At the affected part of the ventricular layer the 
tissue is softened, and during the closure of the valve, the single 
aortic layer may he unable to support the full pressure of the blood. 
In this way it may he pushed towards the ventricle, carrying 
before it the softened ventricular layer, as at c. It will be apparent 
that, in the case of the aortic valve, the aneurism will always pro- 
ject into the ventricle. In the case of the mitral valve, on the VALVULAR DISEASE OF THE HEART. 
319 
other hand, the softened layer is on the auricular surface of 
the valve, and the pressure of the blood during closure of the valve 
will be exercised towards the auricle, and the aneurism consequently 
projects towards that cavity. 
As the aneurism owes its origin to acute endocarditis, its surface 
is usually covered with vegetations, which are often very abundant, 
and may so conceal the aneurism as to lead to its being overlooked. 
The aneurism, again, may rupture, and so produce a perforation 
of the valve. It is sometimes as if the bottom had been blown out 
of the aneurism and a short tube left, surrounded by shaggy vege- 
tations (as at d in figure). Even in that case, however, if the neck 
of the aneurism be examined, it is often found that the endocar- 
dium, as it passes into it, is smooth and unaltered. 
VALVULAR DISEASE OF THE HEART. 
In studying endocarditis, we have seen that the valves are fre- 
quently altered in their structure; we have now to consider these 
alterations more specifically, and their effects on the heart and cir- 
culation. It is not usual to designate anything as valvular disease 
unless it interferes with the function of a valve or orifice. The 
function of a valve is to close an orifice under certain circum- 
stances, and we speak of valvular disease when the alterations are 
such as either to obstruct the orifice or to interfere with its closure 
by the valve. Hence valvular lesions may be divided into two 
kinds, namely, narrowing or stenosis of the orifice, and insuffi- 
ciency of the valve. In referring to these same lesions, as they 
affect the current of blood in the heart, we speak of obstruction of 
an orifice and of regurgitation through the orifice or incompetency 
of the valve. Of course, it would be a very incorrect use of 
language to speak of obstruction of a valve, or insufficiency of an 
orifice. 
Valvular disease occurs much more frequently in the valves of 
the left side than in those of the right, and hence we have chiefly 
to do with the mitral and aortic valves. We have already seen 
that in the foetus it is the valves of the right side which are most 
frequently affected, and we have connected this with the fact that 
these valves are more liable to variations of pressure in the foetus 
than in the adult, 
Insufficiency or Incompetency of the Mitral Valve.—This is 
a condition in which, during the systole of the heart, some portion 
of the blood passes back into the left auricle instead of the whole 
being forced into the aorta. 
The actual physical conditions are somewhat various, but most 
of them are related to chronic endocarditis. The commonest is 
that in which the valvular structures are thickened by the new- 
formed connective tissue and retracted and shortened from its con- 
traction. This applies to the curtains themselves, but still more 320 
DISEASES OF THE ORGAXS OF CIRCULATION. 
to the chord* tendine*, which become thickened and shortened, 
and frequently grow together, so that they hold the curtains rigidly 
drawn down and do not allow them to go together during the sys- 
tole of the ventricle (see Fig. 164, p. 309). Again, much more 
rarely, in acute endocarditis, the valve may be perforated, as in the 
case of valvular aneurism, or the chord* tendine* torn so as to 
allow a portion of the valve to flap upwards through the oriflce. 
Lastly, without much alteration of the curtains, there may be a 
relative insufficiency of the valve. That is to say, the cavity of the 
ventricles sometimes enlarges greatly, and produces enlargement 
of the orifice, which the valve is no longer able to cover. There 
are some cases of permanent hypertrophy and dilatation of the left 
ventricle where this occurs, but it may be met with where the 
dilatation is temporary, as in the flabby fatty heart of typhus fever 
and an*mia. It is not to be supposed that the so-called an*mic 
murmurs are usually due to this cause, but there is in some cases 
an actual mitral regurgitation. When recovery occurs, and the 
heart resumes its former vigor, the valve will again cover the 
orifice. 
We have now to consider what results ensue from insufficient 
closure of the valve. At each ventricular systole blood regurgi- 
tates into the left auricle, and the most direct result is over-disten- 
tion of this auricle occurring at successive intervals. The wall of 
the auricle is weak, and does not offer much resistance to the dis- 
tensile force. There is another result which often follows, appar- 
ently from the unduly forcible impact of the blood against the 
endocardium, and the over-stretching of this membrane, namely, 
a thickening of the endocardium. We may find it generally 
thickened and opaque, or there may be patches of opacity. 
But the results do not confine themselves to the auricle—the 
abnormal blood-pressure is reflected to the pulmonary veins which 
feed the auricle, and they become distended. The distention is 
further reflected to the capillaries and the pulmonary arteries, and 
finally to the right ventricle. The right ventricle is overdistended, 
and unless it acts more vigorously than usual, so as to empty itself 
into the pulmonary artery at every systole with greater force, the 
overfilling is reflected to the systemic venous system. 
We have already seen, however, that when necessity arises the 
heart is stimulated to increased action. The rhythmical contrac- 
tions of the heart are referrible to its intrinsic ganglia, and the 
heart of a frog will beat for a time when empty of blood. But it 
beats much more vigorously when full, and the more its cavities 
are distended, up to a certain point, the more vigorous are its con- 
tractions. It is as if the stretching of the fibres supplied the reflex 
stimulus to increased vigor in the contraction of the muscle. In 
the case we are considering, the increase in the amount and 
pressure of the blood in the right ventricle, as well as the neces- 
sities of the pulmonary circulation, act as a spur to more vigorous 
contraction, and we have already seen that this increased action 
when prolonged leads to hypertrophy. Hypertrophy of the right VALVULAR DISEASE OF THE HEART. 
321 
ventricle is, therefore, a very constant result of the lesion we are 
considering. 
Returning now to the left side of the heart, it is clear that, as 
part of the blood in the left ventricle passes at each systole into 
the auricle, too little will go into the aorta, and the systemic cir- 
culation will be partially starved. But when the right ventricle 
acts with increased vigor, the blood passes into the left ventricle 
with increased force and in larger amount than normally. The 
result will be increased action and consequent hypertrophy of the 
left ventricle. We can see here again a double action such as we 
found in the case of the right ventricle. The systemic circulation, 
being starved, calls for increased supply of blood, and on the other 
hand the distention of the ventricle induces increase in the force 
of the contractions. The hypertrophy of the left ventricle is 
usually small in amount and quite subordinate to that of the right, 
which with the distention of the left auricle is the most prominent 
appearance. The heart presents the more globular or quadrilateral 
shape already referred to as characteristic of hypertrophy of the 
right ventricle. 
These changes may completely compensate for the incompetence 
of the valve, that is to say, the circulation may be restored to its 
normal efficiency ; hut it may not be so, or, even when established, 
the restored efficiency may be impaired from some further inter- 
ference with the pulmonary circulation or weakness of the heart. 
So there is apt, after a time, to be overdistention of the systemic 
venous circulation, and the train of changes which are usually 
more fully developed in mitral obstruction, and will be described 
under that heading. The pulmonary circulation suffers even more 
than the systemic from any insufficient compensation on the part 
of the right ventricle. The pulmonary vessels are permanently 
overdistended, and oedema and hemorrhage are frequent results. 
The hemorrhage is in the form of slight oozing from the pul- 
monary capillaries, so that the sputum is streaked with blood. 
It is not to be confused with that which occurs in consequence of 
embolism of the pulmonary artery, forming the hemorrhagic 
infarction, which is of frequent occurrence in disease of the mitral 
valve, but from a cause to be afterwards considered. 
Obstruction of the Mitral Orifice. Mitral Stenosis.— 
This name is applied to the condition in which the mitral orifice 
is not large enough to allow of the usual quantity of blood passing 
from the auricle to the ventricle. The normal width of the mitral 
orifice may be roughly estimated with the fingers ; in the adult it 
should allow the index and middle fingers to pass freely through 
as far as the first joint. The contraction may be very slight, or it 
may be to such an extent that hardly a crow-quill can be admitted 
into the orifice. In the case of stenosis of the mitral as well as 
in that of the aortic orifice, the obstruction is usually caused by 
the curtains of the valves becoming thickened and rigid, and 
especially by their coalescence. The thickened valves grow 322 
DISEASES OF THE ORGANS OF CIRCULATION. 
together by tlieir edges, and so the valve is converted into a 
funnel with its apex turned down into the ventricle. The normal 
orifice is at the base of the curtains. But when the valves coalesce, 
the orifice while becoming con- 
tracted is moved downwards, and 
comes to have its site at the apex of 
the funnel. This will be understood 
from the accompanying simple dia- 
gram (Fig. 169), in which black 
lines represent the orifice and cur- 
tains in their normal condition dur- 
ing the diastole of the ventricle, the 
curtains lying back against the wall 
of the ventricle, and the orifice at 
their base. The dotted lines repre- 
sent the coalesced, funnel-shaped 
valve; the contraction of the orifice 
and its removal downwards being 
shown. The chordae tendinese are 
commonly thickened and often 
partly incorporated in the funnel 
(see Fig. 164, p. 309). On laying- 
open the ventricle, this thick, rigid, 
funnel-shaped deformity is often 
strikingly prominent. These con- 
ditions result from chronic endo- 
carditis, and it will be readily understood that the rigid valve is 
frequent!}7 incompetent, so that this condition is often combined 
with the one before. There are also not infrequently changes in 
the aortic valve. 
It might be supposed that the vegetations occurring in acute en- 
docarditis would obstruct the orifice, but although these rough 
projections undoubtedly interrupt the even flow of blood, and may 
produce during life what is technically a murmur of mitral obstruc- 
tion, yet their actual influence on the function of the orifice must 
be very slight, and we are not to look for any definite evidences of 
their influence on the circulation. 
Obstruction is occasionally produced by thrombi growing on the 
valve, or having their seat in the auricle and projecting into the 
orifice. This is a rare cause of obstruction, and a still rarer is 
the presence of tumors growing in such a way as to obstruct the 
orifice. 
We have now to consider the results to the circulation of mitral 
obstruction. The most direct effect will be dilatation of the left 
auricle, as the blood is, to a certain extent, hindered in its passage 
into the ventricle. As a consequence, the whole pulmonary vessels 
will be loaded and the right ventricle distended with the accumu- 
lated blood. On the principles already laid down there will be 
increased action and consequent hypertrophy of the right ventricle, 
and this is commonly more extreme than in mitral insufficiency. 
Fig. 169. 
Diagram of funnel-shaped deformity 
of mitral valve. The dotted lines indi- 
cate the coalesced curtains forming a 
funnel projecting into the ventricle with 
a reduced aperture at the apex. VALVULAR DISEASE OF THE HEART. 
323 
Tlie contraction of the orifice interferes with the passage of blood 
into the left ventricle, which, in extreme cases, is, as it were, 
starved of blood. The increased force of the right ventricle may 
in great part make up for this deficiency, and sometimes there is 
also aortic insufficiency, so that the ventricle is fed from the aorta 
as well. According to these various circumstances will be the 
state of the left ventricle. It may be actually atrophied and 
appear as a small appendage to the enlarged right ventricle, or it 
may he normal in size or even hypertrophied. In any case the 
hypertrophy of the right ventricle is the predominating condition. 
The shape of the heart is more quadrilateral, the apex is blunt and 
formed by the right ventricle. During life, instead of the defined 
apex beat of the left ventricle, there is the more diffused heaving 
of the right. 
Passing from the heart, we have a permanent passive hypersemia 
of the pulmonary circulation, with consequent brown induration 
of the lungs. There will also be the tendency to slight hemor- 
rhages, showing itself in the sputa. (Edema of the lungs readily 
develops. The dilatation of the right ventricle, especially when 
followed by thrombosis, also frequently leads to embolism of the 
pulmonary artery and the hemorrhagic infarction. The hypersemia 
is reflected to the systemic venous circulation, especially if the 
dilatation of the right ventricle lead to relative insufficiency of 
the tricuspid valve, and we find evidences of passive hypersemia 
of the liver (nutmeg liver), kidneys and other organs. ISTot infre- 
quently serious oedema of the skin and dropsy of the serous cavities 
develop. Thrombosis in the veins of the legs often complicates 
the condition, and this again may be a source of pulmonary 
embolism. 
Insufficiency of the Aortic Yalve.—This is the condition in 
which, after the completion of the ventricular systole, a portion of 
the blood regurgitates into the left ventricle through the imper- 
Fig. 170. 
Diagram of aortic insufficiency, a, the normal valve closed, as seen from above: b, the 
valve with curtains shortened and leaving a triangular space. 
fectly closed semilunar valve. This condition is usually brought 
about by chronic endocarditis. The individual semilunar folds are 
thickened and shortened, the actual length of free margin being 
reduced. The consequence is that, during the closure of the valve, 324 
DISEASES OF THE ORGANS OF CIRCULATION. 
the edges have not sufficient length to meet perfectly and so a tri- 
angular aperture is left. This is illustrated diagrammatically in 
the accompanying figure. The contraction may reach such an extent 
as to leave only a nodulation on the wall of the aorta in place of 
the curtains. These changes are very commonly accompanied by 
adhesion of the adjacent folds of the curtains, and this necessarily 
causes contraction of the orifice; indeed, the curtains as such .may 
disappear, leaving only a diaphragm with a permanent aperture in 
its middle, the condition being similar to that illustrated in Figure 
154, p. 288. An unusual cause of aortic insufficiency is perforation 
of the curtains as a result of acute endocarditis or the bursting of 
a valvular aneurism. Of course, the perforation of the curtains 
beyond the line of contact already referred to is not to be mistaken 
for a pathological perforation. A rare cause of aortic insufficiency 
is the tearing of one of the curtains. During severe exertion the 
blood-pressure in the aorta may be so much raised as to rupture a 
curtain, and such a wound will hardly unite as it will be torn aside 
at each closure. 
It may be added here that aortic disease is often accompanied 
by mitral disease, chronic endocarditis, having its origin in rheu- 
matism, attacking both. Chronic endocarditis of the aortic valve 
again is often connected, as we have seen, with endarteritis or 
atheroma of the aorta, and in that case it is not so likely to be 
associated with mitral disease. 
It may be interesting here to observe that the origin of the 
endocarditis has an important bearing on the age at which these 
valvular lesions occur. Acute rheumatism is a disease of youth 
and manhood, and most cases of valvular disease take origin in it. 
Accordingly, diseases of the valves are most common, at least in 
their inception, between the ages of ten and thirty. But there 
are some cases of aortic disease which, as we have seen, stand in 
a different category. Chronic endarteritis or atheroma is a dis- 
ease mostly of advanced life, and so it is more common in old 
persons to meet with aortic disease than with mitral. 
We have now to consider the effect of this insufficiency of the 
aortic valve on the circulation. In the normal state during the 
diastole of the ventricle, the blood flows from the auricle into the 
ventricle. But just at the close of the diastole the auricle con- 
tracts and forces the blood more vigorously into the ventricle, so 
as to distend it, and perhaps give it the impulse to contract. 
When the ventricle contracts, the blood passes into the aorta, and 
the wave is propagated forwards, and at the same time partly 
distends that vessel. At the end of the systole the semilunar 
valve closes, and on the recoil of the distended aorta the blood is 
forced onwards in the systemic arteries. But now, suppose that 
the semilunar valve does not close completely, then the aorta in 
its recoil will force blood back into the ventricle as well as forward 
into the systemic arteries. This extra mass of blood driven with 
considerable force into the left ventricle will overfill it and forcibly 
distend it, while the systemic circulation will be proportionately VALVULAR DISEASE OF THE HEART. 
325 
starved. The left ventricle is called on to make increased exer- 
tions to get rid of the excess of blood and fulfil the wants of the 
system, and we may suppose that the stimulus to increased action 
is afforded by the stretching of the fibres by the excess of blood. 
The natural result is dilatation and hypertrophy of the left ven- 
tricle, which may almost completely compensate. In this disease, 
therefore, the primary and prominent fact is the enlargement of 
the left ventricle. As previously mentioned, the heart becomes 
more conical in shape; the septum takes part in the hypertrophy 
and bulges into the right ventricle. This may exist to such an 
extent that the right ventricle is seen on transverse section as a 
mere crescentic appendage of the left, and there may even be, to 
some extent, obstruction of the right auriculo-ventricular orifice 
by the bulging of the septum, inducing general venous hypenemia. 
As the ventricle propels a much larger amount of blood into the 
aorta, and with abnormal force, there is sometimes a resulting 
dilatation of the arch and great vessels. In this way there may 
even be an actual aneurism of the arch. 
It is to be added that, as hypertrophy of the left ventricle is 
associated with dilatation of that cavity, there is frequently a con- 
sequent widening of the mitral orifice. As a result of this, we 
may have a relative incompetency of the mitral valve, which is 
incapable of completely covering the dilated orifice. In this way, 
the consequences already considered of mitral insufficiency may 
be brought about; but they are usually much less pronounced, 
and of late occurrence. It is to be remembered, also, that mitral 
disease often coexists with aortic. 
Obstruction of the Aortic Orifice. Aortic Stenosis.—In this 
lesion the passage of blood from the left ventricle into the aorta is 
interfered with. It is, in the great majority of cases, caused by 
chronic endocarditis. The conditions already described as leading 
to insufficiency of the valve by causing rigidity of the curtains, 
mostly produce obstruction of the orifice, and this is all the more 
marked when calcareous infiltration ensues. Where the valve is, 
in the way already mentioned, converted into a rigid diaphragm, 
then there must be great obstruction of the orifice as well as insuf- 
ficiency of the valve. These two forms of lesion are, therefore, 
usually found associated. In acute endocarditis the roughening of 
the curtains may to some extent obstruct the flow of blood, but the 
interference is trivial, and will hardly lead to any of the secondary 
results of aortic stenosis. 
The obstruction at the orifice prevents the blood getting away 
fully during the systole of the ventricle, and there comes to be an 
overfilling of the ventricle. The ventricle, as in the previous case, 
is stimulated to increased exertion, and the distensile force of the 
blood may again be supposed to afford the necessary stimulus. 
Increased action induces hypertrophy as before, and so here, as in 
the previous case, the primary phenomenon is hypertrophy of the 
left ventricle. This may completely compensate for the obstruc- 326 
diseases of the organs of circulation. 
tion, and persons may go about comparatively well with an ob- 
structed oritice and enlarged left ventricle. But this is not so 
likely as in the previous case, and any extra need for exertion on 
the part of the heart, or weakness of its muscle, may lead to in- 
complete compensation. In such a case the ventricle will get 
abnormally dilated, and the auricle will not be able to empty itself 
fully into the dilated ventricle. The pulmonary circulation will 
become engorged and the right ventricle overloaded, and so we 
may have all the evil consequences of mitral disease. It will be 
observed, however, that, as the left ventricle is much more capable 
of undertaking additional work than the right, it succeeds much 
more frequently in bringing about a complete compensation. The 
hypertrophied left ventricle having to dispose of an increased mass 
of blood, generally does so slowly, and the pulse is consequently 
slow and regular. 
It will have become apparent that in many cases aortic disease is 
•associated with mitral, and that there is frequently combination and 
complication of the resulting changes in the heart and circulation. 
Valvular Disease of the Right Heart.—We have already seen 
that, except in the foetus, this form of disease is uncommon. In 
cases of acute or chronic endocarditis with well-marked lesions on 
the left side, however, there are very often slight indications of 
inflammation in the valves of the right heart. 
There is one condition of the tricuspid valve which, although 
secondary, is often of considerable consequence on account of the 
effects to which it leads, and that is relative insufficiency of 
the tricuspid valve. We have seen that in mitral disease the 
right ventricle usually dilates and hypertrophies, and with this 
change in the ventricle the oritice widens. The valve may thus 
be unable to cover the enlarged orifice, and become insufficient. 
In other forms of dilatation and hypertrophy of the left ventricle 
as in that due to obstruction to the pulmonary circulation, the 
same thing may occur. The tricuspid orifice normally admits 
readily three fingers up to the first joints, and when enlarged it is 
not uncommon to meet with cases in which it admits four, five, 
six, or even seven fingers. If the valve is thus incompetent to 
close the enlarged orifice the blood will, during the systole of the 
ventricle, regurgitate into the auricle. The wave will be propa- 
gated into the veins of the neck, and there will probably be an 
aggravation of existing congestion of the systemic veins. 
It need only be added that, if chronic endocarditis attacks the 
tricuspid or pulmonary valves, it may produce results similar to 
those effected in the mitral and aortic. The tissue here, however, 
is less substantial to begin with, and the inflammation is usually 
much less intense, and so the changes are rarely of any great 
consequence. COAGULA IX THE HEART. 
327 
COAGULA IX THE HEART. 
Simple Clots.—It is very common to meet with clots in the 
heart at post-mortem examinations, and very important to dis- 
tinguish those that are of pathological significance. In a great 
majority of cases we meet with soft gelatinous clots occupying 
auricles and ventricles, and sometimes extending from them into 
the aorta and pulmonary artery. These clots are produced just 
about the period of death. It cannot be said that they are always 
in the strictest sense post-mortem, because the fact that they are 
sometimes decolorized shows that the blood-corpuscles have been 
in these cases removed from them. Yet they are to all intents 
and purposes post-mortem. During the last minutes of life the 
heart may give irregular and imperfect contractions, not sufficient 
to forward the circulation, but having the effect of churning the 
blood. Coagula may thus be formed somewhat in the way that 
the ffbrine is separated in whipping blood. In that case the clot 
is apt to be stringy and slightly opaque in appearance. Again, 
the absence of the red corpuscles in a clot may be brought about 
in a different way. When blood is shed it coagulates quickly, 
and in human blood it is rare for the coagulation to be long 
enough delayed to allow of the sinking of the corpuscles so as to 
leave a buffy coat on the surface. In the heart, however, the 
coagulation, unless it be induced by the churning action just 
referred to, is delayed, because the tissue does not. immediately 
lose all vitality. Time is often thus afforded for the sinking of 
the red corpuscles, and so we may find some parts of the clot 
deeply red and others colorless or yellow. For practical purposes 
all this class of coagula may be designated simply clots, the term 
thrombi being applied to those occurring during life. 
The clots have more or less the shape of the cavity in which they 
are found. They sometimes extend into the great vessels, and show 
a constriction where they have taken the mould of the valve. They 
adhere very little to the endocardium, although they may have a 
deceptive appearance of adhesion from being entangled among the 
chords tendinese and musculi papillares. The gelatinous character, 
transparent appearance, and smooth surface of these clots are other 
indications. They are also as a rule much more bulky than thrombi. 
Thrombi are of various kinds and different significance, and it 
may be said that coagulation of blood within the heart during life 
is of frequent occurrence. We have already incidentally considered 
most of these forms of thrombi, and it will be necessary here to do 
little more than enumerate them. Thrombi are frequently desig- 
nated vegetations, but it is not advisable to use this word in place 
of the more accurate one thrombi. We may distinguish three 
forms of thrombi: warty, globular, and polypoid. 
Warty thrombi we have already seen to occur in acute endocar- 328 
DISEASES of the organs of circulation. 
ditis, owing to the coagulation of the fibrine on the inflamed and 
roughened surfaces. 
Globular thrombi have been described in the section on throm- 
bosis (see page 41) in the first part of this work, and are represented 
in Fig. 171. It is to be remembered that they are of frequent occur- 
Fig. 171. 
Globular thrombi near the apex of the left ventricle. Several of these are seen to 
project from between the musculi papillares. 
rence in dilated and hypertrophied hearts, and that they are prone 
to soften in the central parts and finally to break down, so that 
they may give rise to embolism. These thrombi are sometimes 
very loosely adherent to the endocardium and may be detached 
bodily and carried into the pulmonary artery or aorta—most fre- 
quently into the former, as they are more common in the right 
ventricle and auricle than in the left. 
The polypoid thrombi are much more uncommon than the other 
two forms. It sometimes happens that a thrombus is formed on a 
valve or on the internal surface of the heart and from this point 
grows out by successive deposition to a considerable size. The 
author has met with a case in which the left ventricle was filled 
with massive festoons thus formed, and great hypertrophy and 
dilatation had occurred. In this case also the coagula, had under- 
gone a partial impregnation with lime. He has also seen a case 
in which a thrombus, formed of firm fibrine and attached to the 
wall of the right auricle, hung free in the auricle and assumed a THE BLOODVESSELS. 
329 
nearly globular form. It was so placed as to hang down into the 
tricuspid orifice, which it greatly obstructed, like a ball-valve. 
TUMORS OF THE HEART. 
Primary tumors are exceedingly rare, but a primary sarcoma of 
the endocardium has been described, as also primary fibroma, 
myoma, and lipoma. 
Secondary tumors are not uncommon, and they are either 
malignant or infective tumors. Miliary tubercles are sometimes 
met with in cases of acute general tuberculosis, occupying the 
endocardium, or the pericardium, or even the muscular substance. 
Syphilitic gummata are occasionally met with in the muscular 
substance, and as usual they are accompanied by interstitial 
inflammation. The gumma has the usual indefinite and varied 
structure, in the more recent stage softer and more cellular, in the 
more advanced stage largely composed of dense connective tissue, 
with probably a caseous centre. There may be a single tumor 
replacing a portion of the wall, and surrounded by the cicatricial 
tissue of chronic inflammation, in which the endocardium or the 
pericardium maybe involved. In the latter case there is adhesion 
of the two layers of the sac. Or the gummata may be multiple, in 
which case there is a more diffused interstitial inflammation. 
Sarcomas occurring in the neighborhood may spread to the heart, 
and especially those of the mediastinum, involving first the parietal 
and then the visceral pericardium. Sometimes also a cancer of 
the oesophagus extends to the pericardium. Cancers when they 
become generalized very often occur in the heart, in the form of 
round pale tumors. 
Of parasites, the echinococcus and the cysticercus cellulosae 
have been found in the heart. 
B.—THE BLOODVESSELS. 
The bloodvessels are to be regarded as tubes of which the essen- 
tial constituent is the intima. According to circumstances the 
intima becomes clothed with external and middle coats, and so we 
have arteries and veins. We have already seen that, in nearly all 
new formations, bloodvessels are produced as well as the proper 
tissue, and it is first a tube composed of intima which is formed, 
or a capillary. This primary vessel is capable of enlargement and 
further complication in the way just indicated, so that a transfor- 
mation of the primary capillaries into arteries and veins may take 
place. This process of formation of vessels and their further de- 
velopment according to the requirements of the tissues is an ex- 
ceedingly common one, and may be regarded as equivalent to that 330 
DISEASES OF THE ORGANS OF CIRCULATION. 
which occurs in the formation of the tissues during the period of 
growth of the body as a whole. A process of a similar nature is 
sometimes seen when the obstruction of an artery causes the cur- 
rent to be in great part diverted into other channels. We know 
that in this case the anastomosing vessels enlarge, small arteries 
becoming converted into large ones, and perhaps even capillaries 
into arteries. The vascular system is thus an exceedingly plastic 
one, and possesses great powers of new formation and development 
according to the needs of the tissues. 
INFLAMMATION OF THE VESSELS. 
We have already seen that the bloodvessels bear an important, 
perhaps an essential, part in the inflammatory process, but apart 
from this we have to consider inflammations affecting the tissues 
composing the walls of the vessels, and some of these also have 
been already referred to incidentally. 
Acute Inflammation.—Considering the close analogy between 
the endocardium and the intima of bloodvessels it might be sup- 
posed that the latter would be prone to acute inflammation under 
similar circumstances to the former. But this is not the case, and 
an acute endarteritis scarcely ever occurs. Sometimes an acute 
endocarditis affecting the aortic valve extends to the neighboring 
portions of the aorta, resulting in the formation of irregular pro- 
jections, generally on the surface of a chronic thickening, but even 
this is rare. The acute inflammations of the vessels are nearly 
always secondary. 
A typical instance of acute inflammation is afforded by that 
which occurs in the veins in pyaemia (Phlebitis). The conditions 
here have been already considered, and we saw that the inflamma- 
tion depends on the action of a septic irritant. In the metastatic 
abscesses of pyaemia we have also a septic inflammation of the 
arteries. Vessels which communicate with wounds are liable to 
inflammations at their mouths, especially when the wounds are 
septic. The arteries and veins in stumps are thus often inflamed. 
In all cases of acute inflammation of bloodvessels, thrombi form 
in them, the blood coagulating on the inflamed surface. But the 
formation of thrombi may be the primary phenomenon, they by 
their presence inducing inflammation. This is sometimes because 
they are septic thrombi, as in the case we have already referred to 
of suppurative phlebitis in pyaemia; but a simple thrombus by its 
mere presence irritates the wall of the vessel, and induces inflam- 
mation. This is an essential factor in the organization of the 
thrombus itself, as we have already seen. 
Again, inflammation is induced in vessels by injury to them. 
When an artery is ligatured, for instance, the internal and middle 
coats, as shown in Fig. 172, are torn through, and the result of 
this injury as well as of the continued action of the ligature is to 
induce inflammation. INFLAMMATION OF THE VESSELS. 
331 
_ The condition of the coats of the inflamed vessel varies consider- 
ably, according to the nature of the case. In septic inflammations 
they are infiltrated with pus, softened and opened out, or even 
necrotic. Where the inflammation is less intense the coats are 
Pig. 172. 
Longitudinal section of an artery at seat of ligature, a, it, apertures in which the silk- 
ligature was found. The external coat is drawn in at this place, while the middle and in- 
ternal coats are absent, being absolutely disjoined. These coats are seen above at b and 
below at c. X 35. 
infiltrated with inflammatory cells, and so thickened and rendered 
more rigid than normal. In this way a vein may assume the 
appearance of an artery. If the inflammation be prolonged 
there will be a partial organization of the contained thrombus. 
A similar new formation of tissue occurs externally, and the 
thickened vessel is adherent to its sheath, and to parts around. 
In this way there is often considerable matting of the structures 
around the veins of the legs which are the seat of thrombosis. 
In the regular progress of the inflammation, the whole new- 
formed tissue, including that in the wall of the vessel, and that 
which replaces the thrombus, develops into connective tissue 332 
DISEASES OF THE ORGANS OF CIRCULATION. 
having the usual tendency to contraction. The common result is 
that the vessel and thrombus are replaced by a fibrous cord, but 
sometimes the contraction of the new-formed tissue causes, in the 
way already described at p. 44, the formation of a cavernous tissue 
through which the circulation may be restored. 
CHRONIC ENDARTERITIS—ATHEROMA. 
These names are applied to a disease of very frequent occurrence 
in arteries, the nature of which has been differently regarded at 
different times. Besides the common name atheroma, it is 
variously designated chronic endarteritis, sclerosis of arteries, etc. 
According to the former of these names the disease is an inflam- 
mation of the internal coat, and this view is so far a correct one; 
but degenerative processes play such an important part in the 
course of the disease that it would be a mistake to regard it as 
merely an ordinary chronic inflammation. The fact that the dis- 
ease is peculiarly one of advanced life is another indication of its 
degenerative nature, and it may almost be said that a weakness of 
the wall of the vessel must be regarded as one of the principal 
agents in the causation of the disease. While there is this predis- 
position the actual supervention of the disease is apparently caused 
by mechanical irritation. Its principal seat is the arch of the aorta, 
and this is doubtless due to the fact that this part is more exposed 
to the force of the wave of blood during the systole of the heart 
than any other portion of the arterial system. The disease is fre- 
quently met with in the arteries of the brain, and here it is more 
difficult to account for its occurrence on the theory of mechanical 
irritation, but the atheromatous patch is often situated just at a 
bifurcation, where, presumably, the vessel-wall is more exposed to 
the force of the current. Again, it is met with in the pulmonary 
artery in cases of hypertrophy of the right ventricle, the excessive 
impulse of the blood from the hypertrophied ventricle apparently 
determining its occurrence. As we shall see afterwards, syphilis 
produces a disease of arteries in many ways similar to atheroma, 
and it is matter of uncertainty how far ordinary atheroma may be 
due to syphilis. 
The disease consists in a more or less localized thickening of the 
internal coat. The thickening is nearly always distinctly limited 
in area, so that we speak of atheromatous patches. When we 
examine the aorta in the earlier stages we see elevated areas with 
tolerably abrupt edges, and usually of a dead-white color as com- 
pared with the surrounding intima. These patches are hard, and 
cut like cartilage. They have the appearance at first sight of 
deposits on the surface of the intima, and so they were long 
regarded, but on making a section through patch and vessel, it is 
seen that the intima is continuous with the raised patch. In the 
arteries of the brain the diseased parts are seen as white opaque 
patches, and the vessel is more rigid than normal, so that it does CHRONIC .ENDARTERITIS—ATHEROMA. 
333 
not collapse; the calibre also is diminished by the inward projec- 
tion of the patch. On cutting into the patch, either in the aorta 
or cerebral artery, there is often an opaque yellow color revealed 
in the deeper parts, and this is an indication of fatty degeneration. 
Very often, too, there is, especially in the aorta, calcareous infiltra- 
tion of the deeper parts of the patch, but these two conditions will 
be more fully discussed further on. 
In considering more particularly the details of the process, it is 
instructive to examine microscopic sections including the edge of 
the patch and the neighboring parts of the vessel (see Figs. 173, 
174, and 176). In well-preserved recent cases it can be seen that 
Fig. 173. 
Atheroma of aorta. The internal coat (a) is seen to be thickened. In its deeper layers 
there are darker markings indicating the commencement of fatty degeneration, b, middle, 
and c, external coat. X 22. 
the endothelium of the intima, is continued over the patch, and in 
nearly all cases there is little difficulty in observing that the patch 
is really a thickening of the internal coat, as shown in the figures. 
The thickened intima is composed of a dense connective tissue, 
which in the early stages contain many round, oval, and stellate 
cells. In a fully formed patch the structure is often exceedingly 
indefinite, and there are few cells that are at all prominent even 
when staining agents are used. The structure is indeed half 
obsolete, and, as already indicated, fatty degeneration readily 
occurs. The fatty degeneration begins usually in the deeper 
layers of the patch, so that on making a section one generally finds 
in the portion of the patch bordering on the middle coat an opaque 
yellow streak. (See also Fig. 173.) The fatty degeneration at first 
affects the cells of the intima, but as time goes on the intercellular 
substance gives way, and the tissue breaks down so that a cavity 
containing fatty debris and cholestearine is formed. From the 
character of this fatty debris the name atheroma is derived, and 
the cavity thus formed is sometimes called an atheromatous 334 
DISEASES OF THE ORGANS OF CIRCULATION. 
abscess. (See Fig. 174.) The tissue superficial to the cavity may 
ultimately give way, and so expose the cavity, thus forming an 
atheromatous ulcer. The ulcer sometimes presents calcareous 
masses in its walls, and in any case it may induce the deposition 
of fibrine on its surface. The fatty material may, on the other 
hand, be absorbed without forming an actual ulcer, and in that 
Fig. 174. 
Atheroma of femora! artery. The greatly thickened internal coat (a) is shown. In the 
midst of it, towards the right, are dark masses consisting mainly of fatty debris, and repre- 
senting the atheromatous abscess. At one part the middle coat (6) is considerably en- 
croached on from within. X 22. 
case there will be produced depressions and irregular foldings and 
puckerings of the internal coat. These depressions and foldings 
have often a kind of cicatricial appearance. 
Calcareous infiltration is a frequent result of the disease 
under consideration. It is generally stated that the calcareous 
salts are deposited in the fatty degenerated structure. But this is 
not always the case. The dense tissue of the patch may become 
infiltrated with lime salts without a preceding fatty degeneration, 
This is peculiarly the case when the tissue is very hard and dry. 
We shall see, in studying calcareous infiltration of the middle coat, 
that some individuals present a very great tendency to the deposi- 
tion of lime salts in the walls of their arteries, and there are cases 
of atheroma in which this tendency is very marked, so that with 
comparatively little atheromatous thickening there may be very 
extensive calcareous deposition. The peculiar tendency presented 
in some cases to the deposition of lime salts is a strong indication 
of the degenerative nature of the process. At first the salts are 
deposited in fine granules, and in the deeper layers of the patch, 
hut as time goes on these aggregate into consistent masses which, 
from the lateral extension of the affected parts, have the form of 
plates. Thus we have calcareous plates of various forms and 
sizes, sometimes attaining to a square inch in area. These plates, 
having abrupt edges, not infrequently tear through the remaining 
layers of the intima, and present an edge or angle inside the vessel. 
They may even become to a considerable extent separated, and CHRONIC ENDAETERITIS—ATHEEOMA. 
335 
hang into the calibre attached only by a strip of intima like a 
hinge. The rough calcareous edge very commonly induces a 
deposition of librine, and the thrombus thus formed may subse- 
quently get detached, and form an embolus. The determination 
of the preponderance of the fatty or calcareous change appears to 
depend on individual peculiarities. Both forms are very frequent 
in the aorta. The fatty change preponderates greatly in the 
cerebral arteries. 
It is to be noted here that there are some cases in which the 
atheroma has a much more distinctly inflammatory course than 
that described above. The thickened intima is infiltrated with 
round cells, and there is also inflammatory infiltration of the 
middle and external coats, the round cells aggregating specially 
around the bloodvessels, so that the whole wall of the vessel is 
affected. Such cases are perhaps hardly to be placed in the same 
category as ordinary atheroma, but as this condition occurs like 
the other, mainly in the aorta, and the result is a thickening of 
the internal coat in patches, it is difficult to draw a distinct line of 
demarcation between them. By some, this condition has been 
specially distinguished under the designation acute aortitis. 
It is important to consider what changes the atheromatous pro- 
cess produces in the middle and external coats. At first the 
middle coat is hardly at all affected, but if the process advances 
far, and especially if the degen- 
eration of the patch causes much 
deformity of the internal coat, 
then the middle coat becomes 
softened and loosened. It also 
becomes affected with fatty de- 
generation, the muscular fibre- 
cells being first involved (see Fig. 
175). In advanced cases, especi- 
ally in the cerebral arteries, we 
may even find, along with fat- 
granules, crystals of cholestearine 
and margarine and pigment, so 
that through time the middle coat 
may be considerably broken up. 
This process may be present in 
the middle coat while the hard 
thickening of the internal coat is 
still present, and we may find a localized dilatation of the vessel 
occurring, into which the thickened intima dips. The external 
coat is much less seriously affected than the middle; if at all in- 
volved it presents increased thickening and vascularization. 
We have now to consider the effect of atheroma on the circula- 
tion. There are three alterations which it produces, each of which 
may, according to circumstances, have important effects on the 
circulation. The disease causes narrowing of the calibre, loss of 
Fig. 175. 
Fatty degeneration in atheroma, a, from 
internal coat; b, muscle-cells from middle 
coat. X 350. 336 
DISEASES OF THE ORGANS OF CIRCULATION. 
elasticity and rigidity of the wall, and interference with the muscular 
contractility of the vessel. 
Fig. 176. 
Atheroma of cerebral artery. The greatly thickened internal coat is seen. In its sub- 
stance are dark masses (6) in which margarine crystals were found. On the surface is a 
paler layer (c) consisting of partially organized thrombus; (d) blood occupying the remain- 
ing calibre. X 34. 
The narrowing of the vessel will be of little consequence in such 
large arteries as the aorta, but in the case of the cerebral vessels 
Fig. 177. 
Transverse section of normal cerebral artery to contrast with Fig. 176. X 34. 
and those of the legs, the interference with the circulation may be 
considerable (see Fig. 176). This is somesimes peculiarly the case 337 
CHRONIC ENDARTERITIS —ATHEROMA. 
iii the coronary arteries of the heart, where an atheromatous patch, 
originating perhaps in the aorta, may cause very great narrowing 
and even complete obstruction. The disturbance of the circula- 
tion in the substance of the heart sometimes produces severe 
angina, and may lead to sudden death. If by reason of the rough- 
ness of the surface or the formation of the atheromatous ulcer 
fibrine is deposited, then the narrowing may be very serious, and 
may even amount to complete occlusion. 
The interference with the muscular contractility will also affect 
mainly the arteries of smaller dimensions, and in the case of the 
arteries of the brain, the absence of that control of the circulation 
which is afforded by their varying calibre may lead to serious 
consequences. 
But of all the consequences of atheroma the rigidity and weak- 
ening of the wall are the most important. These consequences 
are most serious in the aorta, where they are probably the chief 
factors in the causation of aneurism. The immediate consequence 
of rigidity of the aorta is that during the systole of the heart the 
vessel does not dilate, and at the end of the systole it does not re- 
coil, so that the force of the elastic recoil is lost to the circulation, 
and in distant parts there is apt to he more or less stagnation. As 
a result of this we have hypertrophy of the left ventricle, which 
is often very marked in cases where much calcareous infiltration 
exists. The hypertrophied ventricle sending the blood forcibly 
into the rigid aorta produces commonly a diffuse dilatation of the 
arch. The influence of atheroma in producing aneurism will be 
considered subsequently. 
The time of life at which atheroma is most frequent is a point of 
some importance in relation to 
the causation of aneurism. Ac- 
cording to Rokitansky, it is 
commonest between the ages of 
forty and sixty. It is still pretty 
frequent down to thirty years 
of age, hut rapidly diminishes 
in frequency from that age 
downwards. It is extremely 
rare under twenty years, and 
when it does occur it is mostly 
in connection with congenital 
anomalies of the great vessels 
or heart, such as stenosis of a 
stem with defect of the septum, 
etc. 
As an addendum to the sub- 
ject of atheroma, mention has 
to he made of a condition sometimes designated Endarteritis 
obliterans (Fig. 178). This is not an independent disease, but is 
frequently of considerable importance as a part of the phenomena 
Fig. 178. 
Endarteritis obliterans in arteries of kidney, 
a, thickened and fibrous internal coat; b, 
middle coat. 338 
DISEASES OF THE ORGANS OF CIRCULATION 
of other conditions. It affects the finer vessels of certain organs, 
and consists, like atheroma, in a thickening of the internal coat 
which, in these fine arteries, frequently leads to complete ob- 
literation. This form of lesion is seen especially in interstitial 
inflammations of organs, and is particularly frequent in chronic 
interstitial nephritis, where it will be again referred to. 
Fatty Degeneration of the Intima of Arteries.—This is a 
condition which Ave consider here because it is apt to be mistaken 
for atheroma. We frequently see, especially in the aorta, yellow 
markings on the internal surface. These markings are only 
slightly raised above the surface, and have the appearance of 
superficial figurings. They are to be found in the aorta, pul- 
monary artery, and other parts of the arterial system. If a portion 
of such a patch be examined under the microscope by removing a 
thin layer by a section parallel to the surface, it will be found that 
the condition consists in a fatty degeneration of the cells of the 
intima. The flat-1)ranched cells are demarcated by the presence in 
them of abundant fat-drops. If the fatty degeneration is much 
advanced then the intercellular substance becomes also the seat of 
fat-drops, and the cells are no longer demarcated. It sometimes 
happens that when the degeneration is very advanced the little 
patch softens and an erosion forms. This erosion is very super- 
ficial, and is not to be mistaken for the atheromatous ulcer. 
This condition is sometimes met with in the bodies of com- 
paratively healthy persons, but we have already seen that in 
anaemia and in emaciated persons it is frequent, and is to be classed 
in the same category as fatty degeneration of the muscular tissue 
of the heart. 
CALCAREOUS INFILTRATION OF ARTERIES. 
We have already seen that in atheroma there is very frequently 
a calcareous infiltration of the affected structures, and it has been 
stated that individual peculiarities appear to play an important 
part here. In some cases a more independent calcareous deposition 
occurs, and here individual peculiarities are of still greater con- 
sequence. Calcification of the middle coat is the most frequent 
and important form. This is very frequently associated with 
atheroma, but it is noteworthy that the atheroma and calcareous 
deposition very often affect different arteries or different parts of 
the same. We may have, for instance, an atheroma of the aorta 
and calcification of the middle coat in the femoral and smaller 
vessels; or there is atheroma as well as calcification in the femoral, 
but in their extreme degrees the two are present at separate parts 
of the artery. For instance, Figs. 174 and 180 are from the same 
femoral artery, and from parts near each other; but the one shows 
atheroma with fatty degeneration, while the other exhibits very 
advanced calcareous infiltration of the middle coat. It mav here CALCAREOUS INFILTRATION OF ARTERIES. 
339 
be remarked that calcitication affects by preference the arteries of 
medium and smaller size. It is often very pronounced in the 
femoral and brachial, and extends to those of smaller size, but not 
to the finest arteries. 
The deposition occurs primarily into the muscular fibre-cells of 
the middle coat, and at first marks these out by the presence of fine 
opaque granules (see Fig. 179). The granules flow together till a 
Fig. 179. 
Calcareous infiltration of the middle coat (b) in an artery, early stage, with atheroma (a). 
At the edges of the affected part, the general outline of the muscle fibre-cells can be made 
out. X 60. 
patch is formed of an opaque appearance, but confined to the 
middle coat. As the calcareous deposition increases, the patch 
sometimes assumes a crystalline appearance, and the material may 
become broken and irregular, as in Fig. 180. This condition 
Fig. 180. 
Calcareous infiltration of the middle coat in an artery. The lime salts have aggregated 
together so as to produce a crystalline appearance. This was taken from the same artery as 
Fig. 174. X 22. 
necessarily gives greatly increased rigidity to the walls of the 
arteries, and the feeling of rigidity so often felt in the radial and 
other small arteries is mostly due to this cause, and not to atheroma. 
The fact, however, that calcification of the middle coat is so often 
associated with atheroma renders this rigidity to some extent an 
indication of the existence of atheroma in the larger arteries. To 
the naked eye the calcified parts frequently manifest themselves by 340 
DISEASES OF THE ORGANS OF CIRCULATION. 
the appearance of a circular opaque striation, visible especially 
when the artery is laid open and viewed from within. The ap- 
pearance is better seen if the artery be allowed to dry partially, as 
then the normal tissue becomes more transparent and the chalky 
structures more prominent. In that case complete or partial rings 
are seen, not unlike the irregular cartilaginous rings of the bronchi, 
but smaller. Another method of rendering the calcification prom- 
inent is to tear off the internal coat, which is usually somewhat 
loosely attached. 
The calcareous infiltration of the middle coat renders the artery 
peculiarly rigid, and, when extensive, induces hypertrophy of the 
left ventricle just as rigidity of the aorta does. The rigid vessels 
are also liable to dilatation, as in the case of the aorta. But 
besides that, the calcified middle coat is brittle and affords a much 
less effective resistance to the distensile wave of blood. An addi- 
tional strain on the circulation, or some special movement of the 
body, may break the brittle coat and directly lead to aneurismal 
dilatation of the artery. It is not unlikely that peripheral aneu- 
risms are frequently induced in this way, and especially those of the 
popliteal region, where the artery is peculiarly liable to mechanical 
injury from the movements of the limb. 
A peculiar calcification of arteries has been described as a result 
of metastasis. We have already seen that when great destruction 
of bone is occurring the lime salts may be deposited in distant 
parts, the lungs and mucous membrane of the alimentary canal 
being the chief seats. Kuttner has described a case in which the 
incrustation occurred in the arteries. The deposition increased in 
amount the further the arteries were removed from the heart, and 
it was especially manifest where the current was permanently 
impeded, as where a small branch issued from a comparatively 
large stem. In this case it was the intima that was incrusted, and 
it was peculiar that the veins were not in the least affected. Apart 
from the incrustation, the arterial coats were apparently normal. 
The source of the lime salts was an acute caries of the vertebral 
column from the first dorsal to the last lumbar. In relation to the 
pathology of the case, it is to be added that there was a purulent 
interstitial nephritis, so that the excretion of lime salts was 
presumably obstructed. It is remarkable that in this case the 
metastasis was' to the arteries, and that the lungs and mucous 
membrane of the intestine were entirely free. 
SYPHILITIC DISEASE OF ARTERIES. 
The condition met with in syphilis in many respects resembles 
atheroma, and it is sometimes difficult to say definitely which of 
these processes is present. In fact it is not safe to call a lesion 
syphilitic unless there be other evidences of syphilis. The condi- 
tion has been most frequently seen in the arteries of the brain, but 
it has also been observed in the pulmonary artery, and it probably SYPHILITIC DISEASE OF ARTERIES. 
341 
occurs in other vessels. It is asserted by some that a large pro- 
portion of cases of atheroma of the aorta have a syphilitic origin, 
but this is exceedingly doubtful. Like atheroma it occurs in 
patches, but these are more frequently single and isolated than is 
the case in atheroma. Thickening .of the internal coat is the most 
characteristic appearance, and it may be so great as almost to close 
the artery. The patch is dense, almost cartilaginous or fibrous to 
the feeling. The thickening is sometimes not confined to the 
intima but extends to the other coats, and this is especially the case 
when the patch is in the neighborhood of a gumma or syphilitic 
inflammation. The disease begins with a cellular formation in the 
internal coat (Fig. 181), so that it comes to have the characteristics 
Fig. 181. 
Syphilitic arteritis. The internal coat («) thickened and infiltrated with cells. The 
external (d) and middle (c) coats also somewhat infiltrated. To the left the membrana 
fenestrata (b) is interrupted. X 150. vZiegler.) 
of granulation tissue, and this cellular character is most manifest 
when the lesion is in the neighborhood of a gumma. The new 
formation extends outwards as well as inwards, and very often the 
middle and external coats become involved. There is little ten- 
dency to fatty degeneration or calcareous infiltration in this disease. 
The new-formed tissue follows more commonly the regular course 
of granulation tissue. Capillaries by and by form in it, and the 
coats of the vessel may be, to a considerable extent, restored with 
some narrowing. On the other hand there may be great cicatricial 
contraction, the new-formed tissue developing into a dense fibrous 
tissue with great narrowing of the vessel, or even complete ob- 
struction if the vessel be a small one. It sometimes happens that 
a thrombus is formed on the patch, and the organization of this 
may aid or complete the obstruction of the vessel. 
As already indicated, the distinction of syphilitic disease from 
atheroma is sometimes difficult, and the main points of difference 342 
DISEASES OF THE ORGANS OF CIRCULATION. 
may be here indicated. Atheroma is a disease of advanced life, 
wdnle syphilis occurs mostly in comparatively young people. Both 
are very common in the cerebral arteries, hut in the case of athe- 
roma the aorta is usually simultaneously affected, whereas in the 
case of syphilis it has frequently been specially noted that the aorta 
was normal. In the syphilitic disease again the new formation is 
more cellular and tends more to extend to the other coats of the 
vessel. It has also been noticed that fatty degeneration and calci- 
fication are much less frequent. In spite of these differences there 
are many cases in which the distinction is impossible and the 
existence of syphilitic disease should never be absolutely concluded 
unless there are other evidences of the disease present. 
It is evident that syphilitic disease will induce secondary changes 
similar to those produced by atheroma. As it affects the arteries 
of the brain with peculiar frequency, and leads to obstruction of 
them, it may induce softening of the brain. The narrowing may 
also induce dilatation of the artery on the proximal side, and, in 
this reference, it is stated that aneurism of the cerebral vessels is 
not infrequently present in syphilitic persons. 
ANEURISMS. 
An aneurism is a localized dilatation of an artery. Taking this 
as the definition it will follow that in forming the aneurism the 
coats of the artery are stretched, and, to some extent, retained as 
the covering of it. We shall afterwards see that there are aneu- 
risms in which this is hardly the case, in which the coats rather 
give way and rupture. Such aneurisms are often designated 
spurious aneurisms, of which it will he necessary afterwards to 
describe several varieties. Even of the aneurisms which come 
under the above definition there are several varieties, but we have 
to consider here, in the first place, those which arise by a limited 
dilatation of an artery. The artery may be dilated in its whole 
circumference, thus forming a spindle-shaped or fusiform aneu- 
rism, or the dilatation may he at a limited point and we have then 
a SACCULATED ANEURISM. 
Causation of Aneurisms.—It may be said that permanent un- 
due dilatation of an artery can hardly occur unless the wall of the 
vessel he weakened. It is perhaps conceivable that the blood- 
pressure might he so increased as to dilate an artery unduly, hut 
such increased pressure would, in its extreme form, be temporary, 
and unless there were some weakness of the vessel-wall it would 
hardly produce a permanent dilatation. We shall see reason to 
believe that in the actual production of the ordinary aneurism, 
both of these conditions, namely, weakness of the wall and in- 
creased blood-pressure are nearly always to be traced. 
The more important of the two conditions is weakness of the 
wall of the artery. By far the most frequent cause of this weak- A XEUlilSMS. 
343 
ness is atheroma. We have already seen how atheroma with great 
calcareous deposition may lead to dilatation of the arch of the 
aorta. But aneurism is even more frequent in cases where the 
ordinary fatty change takes place in the patches, causing irregu- 
larity in the internal coat. By the formation of the atheromatous 
abscess and ulcer, or still more frequently by the absorption of the 
fat and consequent shrinking, depressions and furrows are formed 
in the internal coat. It is to be remembered also that the athero- 
matous part is rendered unduly rigid by the thickening of the in- 
ternal coat, and that any extra distending force will act specially 
on parts which have been weakened. Another element of equal 
importance is the weakening of the middle coat, which we have 
seen to be a frequent consequence of atheroma. Fatty degenera- 
tion is of frequent occurrence in the media under the atheroma- 
tous patch. In the case of the peripheral arteries calcareous 
infiltration of the media may occur with or without atheroma, and 
the calcification may be such as to render the media exceedingly 
brittle. It is true that, according to old experiments of John 
Hunter and Home, destruction of the external or even external 
and middle coats of arteries in animals is not sufficient to cause 
dilatation of these vessels, but with a seriously weakened middle 
coat any considerable increase of the blood-pressure may be suffi- 
cient to cause dilatation. 
While atheroma, especially when associated with weakening of 
the middle coat, is concerned in the causation of aneurisms, there 
are certain circumstances which indicate that this of itself is not 
a sufficient cause. One of these is the age at which aneurisms 
occur. We have seen that atheroma is a disease of advanced life, 
being most frequent after forty, although still very common be- 
tween thirty and forty. iSTow aneurisms are most common between 
the ages of thirty and forty. Another circumstance is the great 
preponderance of aneurisms in the male. It is true that atheroma 
is commonest in the male, but not to anything like the same ex- 
tent as aneurism. Bizot found in 189 cases of the latter, 171 in 
males and 18 in females, and Hodgson found in 63 cases, 56 in 
in males and 7 in females. It is noteworthy further that in some 
localities aneurisms are uncommon, while atheroma is by no means 
so rare. The great frequency of aneurism in the army as com- 
pared with civil life is another circumstance requiring explanation. 
All these circumstances are to be explained on the view that, in 
addition to weakening of the vessel-wall increase of blood-pressure 
is needed to produce aneurisms. In severe continued exertion we 
find the most frequent cause of increased blood-pressure. The 
engineer who has to manipulate a piece of hot iron while wielding 
a heavy hammer, or the soldier who has to perform long marches 
with heavy accoutrements, must put a strain on his heart and larger 
vessels which ordinary persons are not liable to. It will be apparent 
that men are much more exposed than women to such excessive 
stress on their vascular systems. It is again between the ages of 
twenty and forty that men are mostly exposed in this way. 344 
DISEASES OF THE ORGANS OF CIRCULATION. 
Between the ages of twenty and thirty atheroma is uncommon, but 
between thirty and forty it is tolerably frequent, and if it exists the 
liability to excessive stress will render the occurrence of aneurism 
more probable. On the same principle we explain the greater fre- 
quency of aneurism in some countries as compared with others. 
The excessive stress to which workmen in our engineering estab- 
lishments are frequently put in this country goes far to explain the 
frequency of aneurism here, besides the fact of the general greater 
vigor of the British workman in performing his appointed task. 
Another circumstance of importance in relation to the matter 
under discussion is the localization of aneurisms in different arteries. 
Nearly half the cases of aneurism occur in the aorta, and the great 
majority of these in the thoracic portion. We have seen that 
atheroma is most frequent in this vessel, but, in addition to that, 
the aorta is most exposed to the excessive pressure of the blood 
when the heart is stimulated to unduly forcible action. Next to 
the aorta the popliteal artery is most frequently the seat of 
aneurism. It has already been pointed out that this vessel is 
especially liable to injury from sudden flexures of the leg, especially 
when the middle coat is rendered brittle by calcareous infiltration. 
But besides that, the vessel is so situated as to be liable to localized 
increase of blood-pressure. As it issues from the popliteal space 
the artery passes between the two heads of the gastrocnemius, and 
is liable to constriction by the contraction of the muscle, On this 
principle has been explained the frequency of popliteal aneurism 
in flunkies whose principal occupation is to exercise their gastroc- 
nemii in standing. But apart from that, when a person makes a 
severe exertion in a standing posture, the gastrocnemii contract 
vigorously, thus producing a partial obstruction of the artery and 
an increase of pressure above the obstructed part, while the general 
blood-pressure is also increased. 
Before leaving the subject of the causation of aneurisms it should 
be mentioned that anything which weakens the wall of an artery 
will render it liable to dilatation. Thus a blow whose effects extend 
deeply enough to affect the arterial coats, a piece of fractured bone 
pushed against an artery, may be regarded as causes. Again it 
lias been pointed out by Ponflck that embolism is a frequent cause 
of aneurism in the cerebral vessels, the embolus injuring the walls 
of the artery. 
The Coats of the Artery in Aneurisms.—We have next to 
study the development and growth of aneurisms, and in connection 
with that the comportment of the various coats of the vessel. An 
aneurism begins in a little pouching of a limited portion of the 
artery. Even at this early stage the middle coat is already impaired, 
and it has probably been affected to begin with. Such pouches, 
into which one can put the tip of the finger, are often to be seen 
in an atheromatous aorta. The little pouch enlarges. It may 
enlarge laterally so as to comprehend more and more of the vessel 
in its length and circumference. In that case it forms a fusiform ANEURISMS. 
345 
or cylindrical aneurism. On the other hand the pouch may deepen, 
and while its opening remains small, it enlarges outwards in all 
directions into a distinct sac. The walls of the sac around the 
aperture often apply themselves to the external surface of the artery, 
and these may become mutually adherent. In that case the 
aperture has a sharp edge, and it appears as if the wall of 
the artery were folded over so as to form the wall of the aneurism. 
A sacculated aneurism sometimes develops out of a fusiform one; 
at a particular part of the wall a special dilatation begins and goes 
on increasing. 
The internal coat enters variously into the constitution of the 
aneurismal wall. In the case of a fusiform aneurism it is con- 
tinuous over the internal surface, and probably presents very 
marked atheromatous changes. In the sacculated form it is usually 
to he traced some little distance from the edge of the aperture on 
the wall of the aneurism, and even in the midst of the internal 
surface of the sac pieces of internal coat, greatly altered as a rule, 
may he discovered. 
The middle coat appears to he passively affected in the formation 
of the aneurism. Its fibres are loosened and stretched as dilatation 
occurs, and from the first are liable to degeneration. Even in fusi- 
form aneurisms it is often difficult to trace the middle coat far from 
the beginning of the dilatation. 
The external coat, on the other hand, may be regarded as form- 
ing the chief constituent of the sac. It is composed of connective 
tissue, and, as the aneurism grows, inflammatory processes occur 
and new connective tissue is formed, so that the sac does not 
necessarily undergo thinning as it enlarges. The connective tissue 
of the external coat usually makes common cause with that of 
neighboring structures, and so the aneurism acquires adhesions, 
and the surrounding structures come to form, to a certain extent, 
constituents of the sac. 
The connective-tissue formation in the external coat generally 
keeps pace with the enlargement of the sac, especially if it be slow 
of growth, but there are circumstances in which this is interfered 
with. If the aneurism comes to project against an osseous struct- 
ure like the vertebrae or the sternum, then the wall of the sac, 
being compressed by the recurrent wave of blood against the 
resisting tissue, atrophies, and the bare bone comes to be exposed 
and to form part of the sac, the proper connective-tissue wall being 
adherent to the bone around. Under circumstances like these the 
sac is apt to get loosened from the bone and hemorrhage is a fre- 
quent consequence. It is for this reason that hemorrhage is so fre- 
quent in aneurisms of the aorta which project against the vertebral 
column. Again, if the aneurism grows very quickly, or if the sac 
is imperfectly supported at any particular place, then the connec- 
tive-tissue covering may give way. The blood issuing may collect 
in the tissue around, forming a secondary sac for itself, and so we 
may have a spurious aneurism attached to a true one. Or the 346 
DISEASES OF THE ORGANS OF CIRCULATION. 
bleeding may be into a large cavity or canal, and lead, as we sliall 
see afterwards, to fatal results. 
Thrombi in Aneurisms.—It is well known that blood-clots are 
of nearly constant occurrence in aneurisms, and they may almost 
be regarded as constituents of the sac, as they doubtless aid to a 
great extent in preventing rupture. Coagula are most frequent 
and most important in sacculated aneurisms. We meet with them 
in the form of firm, dry layers, which present a distinct stratifica- 
tion generally parallel to the wall of the aneurism. The coagula 
often form a kind of sac inside the proper sac, and after removal 
retain the shape of the aneurism. The coagula are primarily 
white thrombi. The white blood-corpuscles adhere to the rough 
internal wall of the aneurism, and after they have accumulated to 
some extent coagulation occurs and a thrombus is formed. This 
process is repeated, and the formation of fibrine is thus in suc- 
cessive layers. Not infrequently the layers become partially sepa- 
rated, and the blood insinuates itself between them. A layer of 
whole blood is thus formed, and when it coagulates we have a red 
thrombus mixed with the white. As time goes on the clots 
become firmer, drier, and more stringy. The layers next the sac 
are often of a pearly whiteness, and may be taken for connective 
tissue. Under the microscope, however, they are seen to be devoid 
of definite structure, and acetic acid brings out no elongated nuclei 
as in the case of connective tissue. There seems little tendency 
to the organization of these coagula unless the whole aneurism 
becomes filled and its cavity obliterated by them. The continual 
distention of the cavity seems to interfere with the process of 
organization; but, if the cavity be obliterated by the formation of 
clots, then organization proceeds, and by and by the aneurism is 
converted into a connective-tissue nodule which contracts more 
and more. 
The condition of branches given off at the seat of an aneurism 
is a matter of great importance. These vessels are frequently 
obstructed, and there are various ways in which this may come 
about. The atheromatous process may occur to such an extent 
around the orifice of a branch as to narrow or even obliterate it. 
This is most frequent in small arteries like the intercostals, but is 
not uncommon in larger branches. Again, the coagula may come 
to overlie the aperture, already narrowed, it may be, by atheroma. 
Further, it will be apparent that, as an aneurism enlarges, espe- 
cially a sacculated one, it will often drag on and contort vessels 
whose apertures are in or near its walls. The aperture may thus 
be reduced to a fissure, and the edge may be so placed as to valve 
the aperture. This is particularly the case in the sacculated 
aneurisms of the arch of the aorta. Sometimes by the enlarge- 
ment of an aneurism the aperture of the branch is to be found at 
the summit of the aneurism. In that case the aperture may be 
obstructed in one of the ways already described, but it not infre- AXEUEISMS 
347 
quently remains at least partially free. The coagula may even be 
tunnelled in order to allow the current to flow into the branches 
(see Fig. 182). This channelling of the clots occurs mostly where 
the branch passes off' nearly in the axis of the artery; if it pass off* 
more at a right angle the clots are apt to close the aperture. 
Another mode of closure is by the pressure of the aneurism itself 
Fig. 182. 
Aneurism of the abdominal aorta with clots tunnelled so as to allow the blond to reach the 
branches. The general lie of the stratification of the clots is shown. The coeliac axis and 
superior mesenteric artery are seen to be narrowed at their orifices. The posterior wall of 
the aneurism is absent where it impinged against the vertebrae. Half the natural size. 
on the branch beyond the aperture. If a branch be closed in any 
of these ways it becomes the seat of a thrombus, and in the usual 
way becomes converted into a solid cord. In regard to the condi- 
tion of branches it is lastly to be observed that the aneurism may, 
as it were, be continued into the branch, the first part of the latter 
being dilated along with the aneurism. 
Effects on the Heart.—Aneurisms affect the heart somewhat 
variously. It is frequently depressed by the mere presence of the 
aneurism at its base. Room must be afforded for the increasing 
tumor, and as the position of the aorta forbids much movement 
upwards, the heart is pushed somewhat downwards. The extent 
of displacement will, of course, depend on the position and size of 
the aneurism. Besides this, the heart often undergoes enlarge- 
ment, especially of the left ventricle. It is clear that in distending 
the aneurism a considerable amount of the force of the left ven- 
tricle is wasted, and on principles already considered the ventricle 
must act more powerfully; the hypertrophy is therefore compen- 
satory. 
Effects on Parts Around.—The effects of the aneurism on 
other parts will depend on the amount of pressure exercised, and 
the nature of the structures involved. An aneurism often presses 
on nerves, causing primarily irritation of them, and sometimes 
ultimately interruption and consequent loss of function. Thus 
they often produce violent pains, and even symptoms of angina 348 
DISEASES OF THE ORGANS OF CIRCULATION. 
pectoris when the nerves of the heart are pressed on. By irrita- 
tion of the recurrent laryngeal nerve they may cause spasm of the 
laryngeal muscles, or by destroying the nerve lead to their paral- 
ysis. The various canals within the chest—the trachea, bronchi, 
oesophagus, venous stems—are often, narrowed or completely ob- 
structed, so that a great variety of symptoms are produced. When 
an aneurism meets with a firm structure, such as bone, it erodes 
it, as we have already seen. Cartilage resists more than bone; 
and in the case of an aneurism advancing to the front of the chest 
we majr find sternum and osseous ribs much eroded while the car- 
tilaginous ribs, almost isolated, are very little destroyed. 
Terminations.—Aneurisms have somewhat various termina- 
tions, much the commonest being unfortunate. Sometimes, 
although very rarely, a spontaneous cure occurs. It sometimes 
happens that the artery is pressed on by the bulging aneurism 
itself, and is obliterated. Or the aneurism having burst, the blood 
collecting outside, by its pressure, obliterates the aneurism. It is 
well known that obliteration of the artery is often effected by 
ligaturing it. If the artery is obliterated, the aneurism fills up 
with clot, and by and by organization occurs, and the aneurism is 
cured. 
But the majority of aneurisms are beyond the reach of surgical 
interference, and for the most part they continue enlarging till 
they lead to a fatal issue. This may be from the effects of pressure 
on parts around, so that death may result from hypenemia and 
oedema of the lungs, from general venous engorgement and 
oedema, from marasmus, and so on. But even more frequently 
the aneurism ends by rupture, which occurs in various directions 
according to the circumstances of the aneurism. It may here be 
said that the probability of rupture is by no means in proportion 
to the size of the aneurism. A large aneurism, by the amount of 
pressure it exercises, will probably, by its irritation, and by caus- 
ing counter-pressure from displaced organs, produce sufficient 
support, unless it conies actually to the surface of the body or 
bulges into a cavity. When rupture occurs it is into a cavity of 
the body, as the sac of the pericardium, the pleura, an auricle of 
the heart, etc.; or into a canal, as the trachea, bronchus, another 
artery or vein, such as the pulmonary artery; or into the substance 
of an organ as the lung or brain; or among the muscles or con- 
nective tissue of a part. The mode in which the rupture comes 
about varies somewhat. The aneurism may rupture into a cavity 
or on the surface of the body for want of support to its wall, a 
tear by and by occurring in the sac. Or the aneurism may under- 
mine a mucous membrane or the skin, and produce a necrosis, 
rupture occurring on the separation of the slough. Or the aneu- 
rism may induce inflammation of the mucous membrane, and the 
softened tissue may give way. We have already seen that in the 
case of an aneurism meeting an osseous structure a gap may occur 
in the wall of its proper sac, and the edge of the gap may become ANEURISMS. 
349 
detached from the bone, and so occasion a rupture. The rupture 
is not usually at the very first fatal; there is, to begin with, a slight 
leakage of blood through irregular apertures which get occasion- 
ally closed with blood-clot. But from some accidental increase of 
blood-pressure or other cause the aperture is enlarged, and a fatal 
hemorrhage is the result. Or death comes from exhaustion due to 
the prolonged drain and the interference with function that the 
aneurism otherwise produces. 
Varieties of Aneurisms.—There are certain lesions to which the 
name aneurism is commonly given, but which do not accord with 
the description given above, and these merit a brief description. 
The cirsoid aneurism and the aneurism by anastomosis are 
somewhat allied forms. The cirsoid aneurism is sometimes called 
varix arterialis, and the name is suggestive of the condition pre- 
sented. A portion of arterj7 with its branches becomes elongated 
and widened, and the vessels become convoluted like varicose 
veins. Sometimes the dilatation extends to the corresponding 
capillaries and veins. This form of aneurism occurs most fre- 
quently in the arteries of the scalp and face, especially the tem- 
poral and occipital, and the enlarged and tortuous vessels are to 
be felt under the skin. The aneurism by anastomosis is almost an 
arterial vascular tumor. There is enlargement and lengthening 
of a large number of small arteries, with probably new formation 
of arteries, and the mass of arteries can be felt like pulsating worms 
under the skin. The enlargement may extend to the capillaries. 
The affection forms a distinct growth of a bluish-red color, and 
with a somewhat granular surface. Its most frequent seat is the 
scalp. 
The traumatic aneurism arises in consequence of an injury to a 
vessel. An injury has been sustained, and after a longer or shorter 
period an aneurism appears. The mode in which such aneurisms 
arise varies in different cases. In some cases an artery ib wounded, 
and the blood makes a cavity for itself. The cavity remains in 
communication with the artery, and forms a kind of aneurismal 
sac. This is not a common result of wounds of arteries, as these 
usually close, but it does occur, and most readily when the wound 
has been an oblique or longitudinal one. It may result from a 
wound penetrating from the surface, but of such a form as to pre- 
vent the escape of the blood from the surface, or it may result 
from a broken bone tearing the coats. An aneurism arising in 
this way by direct rupture is called a spurious aneurism, as it 
does not arise from dilatation of the vessel. 
But there are some cases of traumatic aneurism which are more 
slow of formation and in which it is not probable that any distinct 
tear through the whole coats has occurred. In the fully developed 
aneurism it is impossible to trace the exact mode of origin, but it 
is probable that in many cases a fractured bone projected against 
a vessel injures or even ruptures the middle coat, and possibly the 350 
DISEASES OF THE ORGANS OF CIRCULATION. 
internal as well. We know that in applying a ligature these two 
coats give way, and we can conceive a violent force applied to the 
wall producing the same result. A simple blow may act in a 
similar way, but it will do so the more readily if the middle coat 
be already brittle from calcareous infiltration. Many of the 
aneurisms of the femoral and popliteal arteries are referred to 
blows and injuries; but these are not all to be regarded as pure 
traumatic aneurisms, as the arterial coats are frequently so altered 
by atheroma and calcareous infiltration as to make the injury 
merely the determining cause. 
Traumatic aneurisms, as appears from what has been said as to 
their origin, have usually less defined sacs than spontaneous ones. 
This is especially the case in those which arise directly from 
wounds. The blood makes an irregular cavity for itself. In the 
other case, where the coats are injured but the external coat is pre- 
served, the sac may be more distinct, but is likely to be thin. 
The dissecting aneurism is a somewhat interesting form, arising 
apparently by rupture of the internal coat, and partially of the 
middle. It sometimes arises from an injury, and is thus a trau- 
matic aneurism, but it occasionally occurs spontaneously, and 
there is no form of aneurism which is so frequently multiple as 
this. The author has met with a case in which there were four 
separate dissecting aneurisms on the aorta and its branches. It 
may be inferred from this fact that in these cases there is often an 
abnormal brittleness of the internal coat, apparently not due to 
atheroma or any other definite disease of the coat, but an inherited 
or acquired brittleness. The internal coat is torn through, and 
the blood passes among the fibres of the middle coat. It is not 
that the middle coat is dissected up from the internal coat, but the 
layers of the middle coat itself are separated, and the blood lies 
between an external and internal layer of the middle coat, as in 
Fig. 183. The splitting up of the middle coat may be carried a 
considerable distance, and after passing along in the wall of the 
vessel the blood may make another tear in the internal coat and 
pass back into the vessel. The aneurism may thus come to have 
two apertures, and a condition may occur as if the vessel were 
formed of a double tube, divided longitudinally by a septum com- 
posed of the internal and a part of the middle coat. The circula- 
tion may even be carried on to a great extent through the aneurism, 
the blood passing in at the original aperture and out at the sec- 
ondary one. In that case the proper calibre of the artery may 
become considerably narrowed. The approximation of such an 
aneurism in character to the regular channel is still further 
increased by the fact that the aneurism by and by acquires an 
internal lining resembling the internal coat. It is a homogeneous 
membrane of about the thickness of the internal coat, so that in a 
section it may be difficult, even under the microscope, to say 
whether a particular place is wall of vessel or wall of aneurism 
(see Fig. 183). In the case already referred to, one of the aneurisms A N E U R1S M 3 . 
351 
began in the thoracic aorta, and was continued down into the iliac 
arteries. There were two apertures, one in the thoracic, and the 
other far down in the abdominal aorta, and between these the 
aneurism had evidently carried on the circulation to a greater 
Pig. 183. 
section of portion of a dissecting aneurism of the aorta. At the left there is the entire wall 
of the artery, a being external, and b middle coat. The middle coat is split so as to form the 
aneurism. At d, d, a kind of internal coat is formed to the aneurism, but this is the seat of 
fatty degeneration at e. X 16. 
extent tlian the natural channel. Dissecting aneurisms being con- 
fined to the wall of the vessel will appear externally as thickenings 
or dilatations of the wall, and they may produce bulging or bag- 
ging of the vessel to a remarkable degree. Occasionally, a dis- 
secting aneurism tears through the remaining layers of the middle 
coat and the external coat, and so a spurious aneurism is attached 
to a dissecting one. 
Varicose Aneurism is a term applied to the case in which an 
artery and vein acquire a permanent abnormal communication. It 
may arise spontaneously or traumatically. This form used to be 
not uncommon at the bend of the elbow, when, in performing ven- 
esection, the lancet wounded artery and vein together. It occurs 
spontaneously when an aneurism ruptures into a vein. In some 
cases there is an actual aneurismal sac between artery and vein, 
and to this form the name ArARicosE aneurism is more properly 
applied. But the communication may be direct, and while the 
artery is little dilated the vein is enlarged, tortuous, and pulsating. 
To this form the name aneurismal varix is applied. The inter- 352 
DISEASES OF THE ORGANS OF CIRCULATION. 
ference with the venous current produced by the violent injection 
of the arterial blood, especially if it be suddenly produced, may 
lead to serious venous engorgement and oedema, which may even 
have a fatal issue. Spontaneous communications of this kind have 
been observed between the aorta and vense cavse, between the 
crural and popliteal arteries and the corresponding veins, between 
the splenic artery and azygos vein, and between the internal 
carotid and the sinus cavernosus. 
VARIX. 
Varix is dilatation of veins just as aneurism is dilatation of 
arteries. We saw that some weakening of the wall is always 
necessary to the occurrence of aneurism, but no such condition is 
required in the production of varicose veins. The walls of veins 
are already thin, and the blood-pressure within them is small. In 
the case of the veins of the skin wre are familiar with the fact that, 
as a rule, the blood-pressure is not sufficient to overcome the 
atmospheric pressure to any considerable extent and the veins are 
flattened or partially collapsed, a slow?- and wreak current passing 
through them. The circulation must be considerably excited, or 
the veins must be obstructed in order to make them stand out as 
cylinders under the skin. Such being the case it may be con- 
ceived that the thin-walled veins, accustomed to a slight blood- 
pressure, will readily dilate v-hen exposed to an increased blood- 
pressure. Varix then is always due to some cause which is calcu- 
lated to increase the blood-pressure within the veins, such as 
obstruction of the veins by thrombi, tumors, the gravid uterus, 
passive hypersemia from heart disease, and so on. It will be con- 
venient to refer more particularly to the casual conditions when 
we review the various localities in which varix occurs. Mean- 
while the mode in which the varicose condition develops will be 
considered. 
If the arm be grasped firmly above the elbowr so as to obstruct 
the superficial veins completely, the veins of the forearm wrill svTell 
up, and at certain points, especially where branches unite, there 
may be seen slight swellings like knots. These indicate the 
position of the valves, the knots being the slight dilatations which 
represent the sinuses of the valves. In the earlier stages of varix, 
as we have frequently an opportunity of seeing it in the legs, there 
is simply an exaggeration of this natural dilatation above the 
valves. When we stand erect the column of blood in the veins of 
the legs is, as it wrere, supported at each valve, and the downward 
pressure tells on the valve and the portion of the vessel forming 
the valvular sinus. Hence this part of the vessel is the first to 
dilate wffien the blood-pressure is increased, and the first sign of 
varix is an exaggeration of the knotted state of the vein. At the 
outset each valve forms a kind of fixed point, the dilatation occur- 
ring at its level, and diminishing as the valve next above is VARIX 
353 
approached. As the dilatation increases and extends up from the 
valve, the vein increases in length as well as in calibre, and in 
order to he accommodated it begins to form curves or convolutions. 
Thus begin those sinuosities which are so characteristic of varicose 
veins, and which tend to increase as time goes on. The dilatation 
of the vein has a tendency to render the valves incompetent, and 
this occurs all the sooner as the region of the valve is, as we have 
seen, the part where the pressure is most exercised. When the 
valves become incompetent the pressure tells much more on the 
walls of the veins as the column of blood is not now arrested at 
intervals. The pressure acts most on the dependent parts of the 
sinuosities, and will increase the projection of these. In this way 
we may have wide sinuses with their convexity downwards, and in 
some cases even diverticula or pouches projecting from the veins. 
In these exaggerated dilatations the blood stagnates greatly, and 
it is not uncommon for thrombosis to occur. The vein is obstructed 
more or less completely by the thrombus, which may organize. 
On the other hand, the latter often dries in and becomes impreg- 
nated with lime salts. In this way varicose veins frequently 
become the seat of vein stones or piileboliths. 
Of the various forms of varicose veins those of the lower ex- 
tremities are best known. As we have seen above, the cause of 
varicose veins is to be looked for in increase of the blood-pressure 
in these vessels, but various circumstances may lead to this increase 
of pressure. It may be the result of direct obstruction of the iliac 
veins by the pressure of tumors, etc., in the pelvis. It may be the 
consequence of prolonged assumption of the standing posture, 
especially in persons of tall stature. In persons who stand about 
much the muscles of the legs are frequently in a state of contrac- 
tion so that the blood is forced into the superficial veins. It is 
probable however that the intra-muscular veins are more frequently 
varicose than is generally supposed, and they may even be affected 
without the superficial ones being much dilated. Cramps of the 
muscles are frequent in cases of varicose veins, and these are to be 
referred to stagnation in the muscular veins. 
Inflammation of a chronic kind is common in the tissues around 
varicose veins wherever they may be, and so in the skin we often 
have very persistent eczema with a brown coloration of the skin 
which may be referred to hemorrhage by diapedesis from the 
hypersemic vessels. The skin is indurated and thickened, and 
ulceration is often induced. The ulcer is sometimes deep and 
sluggish and may persist for years. 
A varicose vein may burst. It ma}r be opened by the ulcerative 
process, or it may come to the surface and by its increasing dilata- 
tion at last rupture. In the case of the leg the results are some- 
times exceedingly serious. We have seen that one effect of the 
dilatation is to render the valves incompetent, and if the varicosity 
extends up into the thigh, the veins of the entire leg may be 
virtually devoid of valves. But the veins in the abdomen are 
normally devoid of valves, and so it may come about that from 354 
DISEASES OF THE ORGANS OF CIRCULATION. 
the lower leg up to the heart there may he a single column of 
blood without an arresting valve. If now a vein rupture in the 
leg, the whole system up to the heart may he, as it were, tapped, 
and if the person is in the erect posture a fatal hemorrhage may 
result. The hemorrhage will cease if the person lies down, but 
cases have been known in which an immense amount of blood has 
been shed into the boots without warning. 
Hemorrhoids are varicose veins of the lower rectum. At the 
lower part of the rectum a network of small veins surrounds the 
bowel, lying immediately under the mucous membrane. These 
veins communicate with the inferior mesenteric vein which is a 
tributary of the portal, and with the internal iliac which is a 
tributary of the vena cava. Any obstruction in the portal circula- 
tion (such as cirrhosis of the liver) or any abnormal pressure within 
the abdomen is apt to induce dilatation of this hsemorrhoidal 
plexus. The dilated veins push the mucous membrane before 
them and protrude as bluish flat nodules either immediately within 
or without the anus. They may assume considerable dimensions. 
The knots are composed originally of a congeries of small, con- 
voluted veins (Fig. 184, _B), which may communicate so as to form 
a kind of cavernous tissue, but sometimes there are large ones 
(Fig. 184, A). Through time the mucous membrane undergoes 
Fig. 184. 
Haemorrhoids of rectum, in section, natural size, r is internal surface of rectum, and m 
the mucous membrane continued over the haemorrhoid. At m' is represented the muscular 
coat, the dilated veins being in the submucous tissue. At A, the veins are few but much 
dilated, one especially so, just below the mucous membrane. At B, the dilated veins are 
more numerous, but smaller. Both occurred in the same case. (Virchow.) 
alterations. The piles at each movement of the bowels are exposed 
to mechanical irritation, and so the mucous membrane is almost 
constantly in a state of catarrh. Then at intervals when the blood- 
pressure is unusually great by reason of an attack of inflammation 
or otherwise, the veins rupture, and so there is bleeding both in 
the substance of the mucous membrane and on to the surface. 
The haemorrhoids thus get greatly altered. They become con- 
densed from inflammatory new formation of connective tissue. 
They sometimes become the seat of collections of blood, which 355 
inflammation of the lymphatics. 
may form blood-cysts. Phleboliths may also form in the veins. 
More severe inflammations sometimes occur, resulting in abscesses, 
fissures, fistulas, ulcers. 
Varicocele is a dilatation of the veins of the spermatic cord 
and the external scrotal veins. It affects in a greatly preponderat- 
ing proportion the left side, and the explanation of this seems to 
be that the left spermatic vein has a circuitous course, and enters 
the renal vein at a right angle, while the right opens into the 
lower vena cava. The varicosity generally begins at the external 
inguinal ring, and extends downwards as far as the testicle. There 
is not infrequently atrophy of the testicle, and sometimes hydro- 
cele or hsematocele. 
Varix may occur in other veins, such as those of the neck of the 
bladder and prostate. It is also met with in the female in the 
vesical plexus and veins of the vagina, and this may be combined 
with varix of the broad ligament. Varicosity also occurs in the 
veins of the dura mater. 
C.—DISEASES OF THE LYMPHATIC SYSTEM, SPLEEN, AND 
BONE-MARROW. 
THE LYMPHATIC VESSELS. 
We have already had occasion to observe that the lymphatic 
system is intimately related to the blood-vascular system, and may 
be regarded as a part of it. We have also seen that this system 
has close relations to the connective tissue, the spaces in the latter 
being lymph-spaces lined with endothelium and having direct 
connections with the lymphatic vessels. Wherever there is in- 
creased exudation from the bloodvessels the serous spaces and 
lymphatic vessels are distended, and the current through them in- 
creased. We have seen this to be the case in inflammations and 
oedemas. 
Inflammation of the Lymphatics. Lymphangeitis.—The lym- 
phatics are liable to inflammations of a more independent kind, 
and warranting the name lymphangeitis. In order to such in- 
flammation there must be in the vessels some irritant, and the 
irritant is similar to that which we find in the veins in suppurative 
phlebitis, namely, a septic poison. In connection with wounds 
which have been exposed to decomposing juices, such as dissecting 
wounds, we sometimes find the course of the lymphatic vessels 
marked by red streaks in the skin. These represent inflammation 
of the lymphatics and surrounding connective tissue. The in- 
flammation not infrequently goes on to suppuration, so that ab- 
scesses form at intervals in the course of the vessels or in the 
lymphatic glands. It is to be presumed that the material which 356 
diseases of the organs of circulation. 
passes into tlie vessels owes its irritating character to the existence 
in it of minute organisms, and that these propagate inside the 
vessels and so the inflammation extends onwards; in some cases 
minute organisms have been found in the dilated and inflamed 
lymphatics. Thus decomposing material may get into the uterine 
lymphatics after delivery, and we may have an inflammation ex- 
tending to the ligaments. This seems to be sometimes the primary 
lesion in puerperal fever. 
Erysipelas and other phlegmonous inflammations of the skin 
may be regarded as inflammations of the lymphatics, or at least of 
the serous spaces which form the radicles of the lymphatics. In 
these diseases, as we have seen, minute organisms extending, give 
rise to the inflammations (see Fig. 117, p. 246). The abundance 
of bacteria in the lymphatics of the skin in such cases may be 
such as to render the lymphatic vessels as well as the serous spaces 
peculiarly prominent, when the sections have been stained by 
aniline dyes. In that case the outlines of the serous spaces and 
even their relation to the lymphatic radicles may be brought out. 
The phlegmonous inflammation of the parotid which occasionally 
occurs in cases of septic wounds is probably of a similar nature. 
Epidemic parotitis (mumps) may perhaps be placed in the same 
category. 
We have already seen that elephantiasis frequently begins in 
recurrent attacks resembling erysipelas, in which the lymphatic 
vessels are obviously engaged. There are often red streaks pass- 
ing up the limb, and the lymphatic gland may be enlarged. The 
irritation here is slighter and more chronic. The inflammation 
results in great thickening of the connective tissue, but there is 
often along with it dilatation of the lymphatic vessels, so that 
when the part is cut into an abundant lymphatic fluid exudes 
which sometimes contains oil. 
Lymphangiectasis.—The lymphatic vessels are occasionally the 
seat of dilatation, but this is of comparatively rare occurrence. 
Obstruction of a lymphatic stem may produce a varicose dilatation 
of the vessels, and even their rupture. We have already seen this 
to be the case when the lymphatics are obstructed by the ova of 
the tilaria sanguinis, resulting in lympli-scrotum, chyluria, etc. 
In the enlargement of the tongue called macrogloss a, which is 
frequently congenital, there is commonly a great enlargement of 
the lymphatics which may form considerable cysts. The dilatation 
here appears to be due to obstruction of the lymphatics from in- 
terstitial inflammation of the connective tissue, although a different 
origin has been asserted. 
There is sometimes a localized dilatation of many lymphatics so 
as to form a distinct vascular tumor. These tumors are usually 
cavernous in structure and are classed as cavernous lymphan- 
giomas. 
We sometimes find lymphatic vessels dilated in the neighbor- 
hood of a cancerous tumor, the material in the vessels being de- the lymphatic glands. 
357 
rived from the tumor.. This occurs mostly in the case of cancers 
which are undergoing softening. It is most frequently seen in 
connection with mammary cancers, where the lymphatics may 
have the form of firm cylinders as large as quills, filled with white 
material. The same thing is seen in the case of secondary cancer 
of the lung, where there are nodules immediately under the pleura. 
The subpleural lymphatics around the nodule are found, as it were, 
injected with white material. So is it sometimes in the capsule of 
the liver when cancerous nodules are near the surface. These 
naked-eye appearances indicate how prone cancerous material is 
to pass into the lymphatics, and, under the microscope, at the 
margins of a growing cancer the lymph-spaces mav sometimes be 
found filled with the epithelial masses. 
THE LYMPHATIC GLANDS. 
It will be useful here, in the tirst place, to refer to some of the 
relations of lymphatic glands and to their structure. It is well 
known that all lymphatic vessels connect themselves directly with 
lymphatic glands so that no lymph passes into the circulation 
without first traversing a lymphatic gland. Dissolved substances 
introduced into the serous spaces of the skin and subcutaneous 
tissue are rapidly carried up the lymphatics and through the glands 
into the general circulation; this is matter of experience every 
day in the subcutaneous injection of medicinal agents. Granular 
material, however, does not pass through the glands, which form 
a filter for all solid particles. In the operation of tattooing 
granular pigment, such as Indian ink or vermilion, is introduced 
into the skin. Part of it remains permanently in the corium, but 
part is conveyed up the lymphatics and is caught by the glands, 
where it remains fixed. So is it in pathological conditions. The 
lymphatic glands are very frequently associated in morbid pro- 
cesses which are occurring in parts in which the vessels passing to 
the glands take origin. Dissolved and solid materials are thus 
conveyed to the glands, and according to the nature of the material 
will it affect the gland or not. We have seen that in septic in- 
flammations the infective material is often conveyed to the gland 
and produces inflammation there. As this material is presumably 
in the form of fine particles it is arrested at the gland, and the in- 
flammation makes a pause there only to proceed further, if the 
organisms propagate onwards. But even in the case of simple 
inflammations, although the products are for the most part dis- 
solved, still they are frequently of an irritating nature and the 
glands inflame. We have already seen that solid material from 
cancers is often conveyed along the lymphatic vessels and is caught 
at the glands. It is to be observed that in all these cases the 
material may produce no irritation in the lymphatic vessels along 
which it is being conveyed. If concentrated or very virulent it 
will do so, but it often does not, and it is only after lying in the 358 
DISEASES OF THE ORGANS OF CIRCULATION. 
glands for a time, and, it may be, increasing by self-propagation 
that it produces its results. In that case a wide interval of healthy 
structure intervenes between the primary disease and the lymphatic 
gland, and so it is common to speak of sympathy and metastasis 
in this connection. Most of the lesions to which the glands are 
liable are embraced among metastatic or sympathetic affections, 
but there are some which may be regarded as idiopathic. There 
are even some inflammations which cannot be traced to a peripheral 
cause, although it is sometimes difficult to be sure that no such 
cause exists. 
"The apparatus by which the filtration of the lymph is effected 
deserves a passing notice, and is illustrated in Fig. 185. When 
Fig. 185. 
Section of normal lymphatic gland: a, a, a, follicular or lymphoid cords; c, c, lyinph- 
sinuses; b, b, connective-tissue trabeculae: d, cl, bloodvessels. 
the afferent lymphatic vessel coming from the periphery reaches 
the gland, it first forms a plexus in the capsule. On the other 
hand the efferent vessel emerges from a plexus of vessels at the- 
hilus, and this plexus is connected with the medullary portion of 
the gland. In passing from the afferent to the efferent vessel, the 
lymph traverses a series of sinuses c, c, in figure. The sinuses are 
not clear spaces but contain a reticulum or mesh-work shown in 
the figure. These sinuses surround the proper glandular tissue 
which is in the form of rounded follicles or cords composed of 
densely packed lymph-cells (a, a, in figure). The lymph first 
passes from the afferent plexus into the sinuses of the cortex, then 359 
lymphadenitis. 
into those of the medullary part, where originate the radicles of 
the efferent vessel. The sinuses being occupied by the fine retic- 
ulum will catch solid particles brought to the gland, and such par- 
ticles will therefore be most readily caught at the cortical portion 
of the gland. 
Pigmentation of the Glands.—We have seen how pigment 
artificially introduced into the lymphatics, is arrested at the glands. 
Similarly, pigment is carried from the lungs and deposited in the 
bronchial glands. Again, in cases of extravasation of blood, or 
in inflammations with considerable hemorrhage, the altered pig- 
ment is conveyed to the lymphatic glands, and may produce con- 
siderable coloration there. 
The pigment is conveyed, in part at least, by the lymphoid cells, 
which are to be found in the lymphatic fluid. Arrived at the 
gland, the pigment is first caught by the stellate cells which form 
the reticulum in the sinuses of the cortex, and hence in the earlier 
stages we may have the sinuses marked out by the pigmentation. 
If it continues to arrive at the gland, it extends into the follicles 
and finally the whole gland may be deeply and uniformly colored. 
When present in such. quantity the pigment, although generally 
non-irritating, produces a chronic inflammation. There is increase 
of the connective tissue forming the trabeculae, and a corre- 
sponding atrophy of the glandular follicles. The affected gland in 
addition to the pigmentation is enlarged and hard. The gland in 
this state is probably to a large extent stuffed up by the pigment 
and rendered impervious. AYlien this is the case the lymph prob- 
ably passes by anastomosing vessels to other glands which in their 
turn become pigmented. In this way we may explain how pig- 
mentation sometimes extends from gland to gland in the central 
direction. Thus in anthracosis of the lungs we may have not only 
the bronchial glands but also those of the mediastinum, and even 
those at the porta of the liver pigmented. 
What has been said in regard to pigment applies also to other 
solid materials introduced similarly into the lymphatics. In stone- 
masons the particles of stone which get into the parenchyma of the 
lung are in part carried to the glands, where they produce similar 
changes to those mentioned, but even more readily, as from their 
mechanically irritating characters they are more apt to produce 
chronic inflammation. 
Acute Inflammation of Lymphatic Glands> Lymphadenitis.— 
As has already been said, this condition is nearly always a result 
of inflammation in the peripheral parts from which the vessels 
come to the gland. It has to be added, however, that in different 
persons there are great differences in the susceptibility to sympa- 
thetic inflammation, so that in some a slight catarrh of a mucous 
membrane may set up an inflammatory enlargement, which, how- 
ever, is not usually very acute. The greater number of the acute 
inflammations are infective. The inflammations following dis- 360 
DISEASES OF THE ORGANS OF CIRCULATION. 
secting wounds, those resulting from chancres, and the inflamma- 
tion of the mesentric glands in typhoid fever may be taken as 
examples. 
The inflamed gland is enlarged, its vessels hypersemic, and the 
tissue softened. The enlargement is due to a great increase of 
lymphoid cells which accumulate largely in the sinuses. The 
stellate cells forming the reticulum of the sinus also swell, and 
their nuclei divide. The exact source of the added lymphoid cells 
is difficult to determine with certainty. They may arise by division 
of the existing cells of the gland, and we know that the gland is 
normally occupied in cell formation; but they may have their 
origin in part in the emigration of white corpuscles from the 
vessels, and further, the primary inflammation of the periphery 
may send its contingent. The inflammation may subside and the 
gland return to its normal condition; the new-formed cells may 
possibly pass on into the efferent vessel and be disposed of in the 
circulation. Not infrequently suppuration occurs, the tissue of 
the gland breaks down and an abscess is the result. We have 
thus a suppurating bubo. The inflammation usually extends to 
the capsule and surrounding tissue which is involved in the sup- 
puration. In this way the abscess advances, and the pus is finally 
discharged at a surface. It is a common occurrence for such 
abscesses to discharge on the surface of the body, but they may 
burst into bronchi, into serous cavities, etc. If the inflammation 
be of an infective nature colonies of bacteria may be found in the 
pus. Organisms have been found, for instance, in the pus of 
inflamed glands in pyaemia and in splenic fever. It is to be added 
that some of these severe inflammations have a hemorrhagic and 
even a necrotic or gangrenous character. 
Chronic Lymphadenitis.—This term might be made to include 
a number of conditions which will be afterwards referred to as 
occurring in leukaemia, Hodgkin’s disease, etc., as well as scrofulous 
disease of the glands. Apart from these, we have a chronic inflam- 
mation in connection with prolonged irritation of the glands. We 
have seen this in the case of the introduction of foreign substances, 
where the solid particles are conveyed to the glands. It occurs 
also in connection with prolonged peripheral irritation, as where 
an eczema of the leg or the scalp produces an enlargement of the 
corresponding glands. The inflammation here results in increase 
of the entire elements of the gland, or else in a preponderating 
increase of the connective-tissue stroma such as we saw occur in 
the induration associated with pigmentation. 
Scrofulous Disease of the Lymphatic Glands.—This is a con- 
dition concerning which considerable difference of opinion has 
existed. The process is a very chronic one, and in many of its 
features it may be regarded as an inflammation, but it is an in- 
flammation presenting the peculiarity that caseous necrosis is of 
constant occurrence. There is no doubt that, if not at the very 361 
SCROFULOUS DISEASE OF THE LYMPHATIC GLANDS. 
outset, yet at a comparatively early stage in tlie process, tubercles 
occur in tlie scrofulous gland, that is to say nodules having one or 
more giant-cells in their centres and the remaining constituents 
arranged as in the miliary tubercle (see Fig. 53, p. 155). The 
observation of the tubercular bacillus in scrofulous glands is the 
culminating evidence that the disease is tubercular and is due to 
a specific virus. But this virus like many others acts on tissues 
which are predisposed. It is to be presumed that the virus is 
present in abundance around us, but it only finds a fitting nidus 
in certain persons. We may perhaps say that persons so predis- 
posed are of a scrofulous habit, and of such persons some are 
specially vulnerable in the lymphatic glands and some in other 
structures. 
Even in persons predisposed the disease generally begins in the 
glands in connection with a peripheral irritation. It is most 
common in the glands of the neck and may take its start in a 
catarrh of the pharynx. At first there is simple enlargement, and 
it may be difficult to say whether it is a true tubercular disease or 
not, all the more as many of these indolent enlargements by and 
by resolve completely. We may suppose that the tubercular virus 
is conveyed to the glands along with the products of the peripheral 
inflammation, but that it may not be abundant enough to produce 
a permanent tuberculosis, or else the glands are vigorous enough 
to prevent a permanent lodgement for the time being. The 
evidence that the disease is definitely scrofulous in its nature is the 
occurrence of caseous metamorphosis. 
As already indicated, the first change in the gland is enlarge- 
ment, due mainly to a great accumulation of round cells chiefly in 
the lymph-sinuses and follicles. These may accumulate to such an 
extent as to obscure the reticulum, and when the gland is cut into 
the follicles project as little softer prominences. The gland, as a 
whole, is softer than normal, and of a grayish-white color. Caseous 
necrosis soon occurs. It begins usually at a number of different 
centres nearly simultaneously, and it extends outward from them. 
The occurrence of tubercles precedes the caseous necrosis, and in 
the extension of that process the tubercles are inextricably united 
with the remaining tissue. The tubercles may be overlooked in 
the lymphatic gland on account of the cellular nature of the gland 
itself, but they have all the characters of tubercles elsewhere. 
The caseous necrosis, of course, stops all growth in the parts 
which it involves, but outside the caseous areas the gland may go 
on enlarging by increase of the glandular tissue and formation of 
tubercles. The caseous metamorphosis by its extension by and 
by comes to involve the greater part of the gland, which now has 
a very hard feeling, and on section presents a firm homogeneous 
yellow aspect which has been aptly compared to that of a raw 
potato. Sometimes a gray external zone can be seen outside the 
caseous material, and this represents the part where growth has 
been still going on. Under the microscope the caseous material 
has the usual homogeneously granular and opaque appearance, 3G2 DISEASES OE THE ORGANS OF CIRCULATION. 
and differences of structure are hardly to be made out, the whole 
tissue including the tubercles being involved in a common fate. 
Sometimes the outlines of the tubercles are vaguely visible, and 
scaly-looking objects may be discovered which represent the altered 
giant-cells. 
After the gland has become caseous it may, in process of time, 
undergo further changes. It might be supposed that in each 
caseous gland there would be a great laboratory for the tubercular 
virus which would thus be sown largely in the body. As compared 
with the great frequency of scrofulous disease, this occurrence, 
however, is one of great rarity. We do find general tuberculosis 
developing in connection with caseous glands, but it is by no 
means common. The change in the gland probably interrupts the 
flow of the lymph, and, just as in the case of cancer, the gland 
actually shuts off the general circulation from the infection. The 
caseous mass may then be regarded, as obsolete, but by its presence 
it is very frequently a source of irritation and consequent inflam- 
mation. The inflammation may be chronic and result in thicken- 
ing of the capsule and production of connective tissue around. 
In this way masses of caseous glands are sometimes united into 
firm packets; or the individual glands may be separately encap- 
suled. In either case one of two results may follow. The caseous 
mass may become infiltrated with lime salts, so as to form a 
mortary or putty-like mass, which may ultimately dry in and be- 
come like stone. This result we very often see in the mesenteric 
glands. Or the caseous material after a time may undergo soften- 
ing, and be converted into a yellow grumous fluid resembling pus, 
but containing debris instead of pus-corpuscles. This soft material 
often gives rise to an acute inflammation around the gland, so that 
a true abscess results in which pus is mixed with caseous debris. 
This process occurs mostly in subcutaneous glands, and the pus by 
and by finds its way to the surface and is discharged. The result- 
ing ulcer is apt to be a very chronic one, the skin and underlying 
tissue are swollen and converted into granulation tissue and 
tubercles may develop in them. This fact indicates that the caseous 
material does not readily lose its virulent properties, and it is well 
known that till the whole remains of the gland and unhealthy 
tissue are cleared out, sound granulations will hardly form. It 
sometimes occurs that, without undergoing softening, the caseous 
gland gives rise to acute inflammation around, with the formation 
of an abscess as already described. The suppuration in that case 
will follow much more rapidly on the enlargement, and the whole 
process will be a more acute one. 
Besides this scrofulous disease which may be regarded as a 
primary tuberculosis, the lymphatic glands are liable to several 
forms of secondary tuberculosis. They are very often the seat 
of tubercles in acute general tuberculosis. Here the tubercles are 
fresh and the enlarged glands are dotted with gray nodules. 
Again, in local tuberculosis of other organs we find the correspond- DEGENERATIVE CHANGES IN THE GLANDS. 
363 
ing lymphatic glands involved. This is commonest in the bron- 
chial glands as a consequence of phthisis pulmonalis and in the 
mesenteric glands in connection with tuberculosis of the intestine. 
The glands in most cases undergo changes similar to those of the 
scrofulous glands, but the enlargement is not generally so great. 
On the other hand the tubercles and gland tissue sometimes undergo 
the fibrous metamorphosis, so that the glands seem to be the seat 
of chronic indurative inflammation. 
Syphilitic disease of the glands partakes of the characters of a 
chronic inflammation in which the new-formed elements show the 
usual tendencies of the syphilitic new-formation partly to degen- 
erate and partly to form connective tissue. 
Degenerative changes in the glands are not of very common 
occurrence apart from scrofula and syphilis. Atrophy may occur 
just as in any other tissue in old age or emaciation. Amyloid dis- 
ease is the commonest form of degeneration, but it does not usually 
occur in a high degree, and it is only occasionally that the glands 
are enlarged and rendered firmer by the degeneration. For the 
most part it is detected only when the glands are examined micro- 
scopically with the aid of iodine or methyl-violet. The disease 
appears to attack mainly the reticulum of the gland, and one can 
sometimes make out the swollen hyaline network, or even detect 
how the normal reticulum swells out into the degenerated network. 
Recently a form of degeneration has been described under the name 
of colloid degeneration. It occurs in old persons and seems of no 
special significance. The gland shows a series of alveoli filled with 
colloid material, or the bloodvessels and trabeeulse of the gland 
become hyaline, the appearance resembling that in amyloid dis- 
ease but without the reaction. 
Tumors.—Of these the principal forms have been described 
already. There is the typhoid lymphoma, the leuksemic lymphoma, 
the lymph-adenoma and lympho-sarcoma. We have also seen that 
in Hodgkin’s disease we have an enlargement of the glands similar 
to that which occurs in leukaemia but without the alteration in the 
blood. In' that disease the spleen may also be affected as it is in 
leukaemia, and so the name of pseudo-leukaemia sometimes applied 
to it is warranted. Besides the lympho-sarcoma already described, 
sometimes meet with more ordinary sarcomas of the lymphatic 
glands, and these may be of the spindle-celled or round-celled 
kind. These tumors are not common, and, perhaps, their most 
frequent seat of origin is the retro-peritoneal glands near the head 
of the pancreas. Tumors arising here may grow to very large 
dimensions. Secondary sarcomas are very uncommon in the lym- 
phatic glands. On the other hand cancer very frequently develops 
secondarily here, and in all its forms. A few cases of srfpp°se(l 
primary epithelioma of the glands have been recorded. 364 
DISEASES OF THE ORGANS OF CIRCULATION. 
THE SPLEEN. 
The exact nature of the function of this organ is somewhat 
obscure. In order to understand the various changes which it 
undergoes, it will be necessary to bear in mind certain facts as to 
its structure. The splenic artery as it enters the organ is accom- 
panied by connective tissue which forms a continuous sheath 
around its branches. In this sheath there develop at intervals 
little masses of lymphoid tissue, forming the Malpighian bodies, 
which are therefore lymphatic follicles closely related to the 
arterial branches. The arteries break up into capillaries which 
are mostly distributed in the Malpighian bodies, where they form 
a somewhat wide-meshed network. At the periphery of the Mal- 
pighian bodies the capillaries open into the splenic pulp, which is, 
as it were, interposed between the capillaries and the veins. This 
consists of a honeycomb-like structure, with frequent trabeculae 
and meshes (see e, e, Fig. 186). The meshes contain blood, but 
Fig. 18G. 
structure of spleen. A, capsule; b, trabeculae; c, c, Malpighian bodies; in that to the 
right an artery, cut transversely, is seen ; d, cl, injected arteries, one running into a Mal- 
pighian body; e, honeycomb-like pulp. (Kollikeb.) 
also large cells and cells containing blood-corpuscles and pigment. 
The mesh-work of the pulp develops occasionally wider channels 
and sinuses which are virtually the radicles of the veins. The 
pulp has a brownish color both from its pigment and from the fact 
that it is full of blood. The Malpighian bodies being lymphoid in 
structure, and sparsely vascularized, are whitish in color. It is 
clear from this structure that the blood passing into the spleen by 
the arteries will linger long in the organ, and will especially stag- malformations of the spleen. 
365 
nate in the meslies of the pulp. It seems probable that in the 
pulp the red corpuscles are to some extent destroyed. The exist- 
ence in the normal spleen of cells containing red corpuscles and 
pigment seems to indicate this. The spleen also probably gives 
origin to white corpuscles, but it shares this function with the 
lymphatic glands, and the medulla of bone, as well as probably 
the widely diffused connective tissue throughout the body. Some 
have supposed that the spleen also forms red corpuscles, but this 
is exceedingly doubtful. 
From these remarks it will be understood that the amount of 
blood in the spleen will be subject to great variations according 
as the pulp is more or less distended. The pulp forms by far the 
greatest part of the substance of the spleen, and according as its 
honeycomb structure is more or less full of blood will the size of 
the organ vary. Accordingly there is no organ in the body which 
varies so much in size, even under physiological circumstances. 
During digestion there is an active hypenemia which causes en- 
largement of the organ. Again, the capsule and trabeculae of the 
spleen are abundantly supplied with smooth-muscle fibre-cells, 
and its size is influenced by the state of contraction of these. It 
is well known that by electric stimulation the size of the organ 
may be diminished, the muscular tissue contracting. 
Malformations.—In addition to the spleen in its-usual site, and 
of its ordinary size, there are very frequently small supernumerary 
spleens lying in its neighborhood. These are generally round in 
shape, and have the dark red or blue color and soft structure of 
the ordinary organ. There are sometimes several of these present, 
and although usually seated in the neighborhood of the spleen they 
may be away from it, having even been found embedded in the 
head of the pancreas. Cases have occurred in which there have 
been two spleens of nearly equal size. The spleen is also liable 
to variations in shape and position. These may be congenital, 
but alterations in position may occur during life, chiefly when the 
organ is enlarged and alters its position on account of its increased 
weight. Again, there may be an unusual length of the ligaments 
so as to allow of an undue mobility of the organ. This also may 
be congenital, or it may be due to a stretching of the ligaments 
from increased weight. 
Active or Congestive Hyperemia and Inflammation.—We 
have already seen that an active hypenemia of the spleen occurs 
physiologically during digestion ; it is met with as a distinctly 
pathological condition, and frequently in a very exaggerated form, 
in a variety of acute general diseases. In this country it is often 
seen in the highest degree in typhus fever, but it is found also in 
other acute fevers, in pyremia, in pneumonia, diphtheria, erysipelas. 
This hypenemia is generally to be regarded as inflammatoPy in its 
nature, the primary stage of an acute inflammation of the organ. 
In the group of diseases referred to, the blood is in a peculiarly 366 
DISEASES OF THE ORGANS OF CIRCULATION. 
irritating condition. We know that the various parenchymatous 
organs, the muscles, and so on, show evidences of inflammation in 
the presence of cloudy swelling, and this is to be traced to the 
irritating condition of the blood. In these organs there is doubtless 
dilatation of the vessels, but in the case of the spleen the hyperaemia 
produces much more marked results on account of the structure 
of the organ. The hyperaemic spleen is greatly enlarged, and the 
capsule stretched. In some cases of typhus and intermittent fever 
the enlargement has been so great and sudden as to rupture the 
capsule. The name acute splenic tumor is sometimes given to 
this hyperaemic enlargement. It will be inferred that in this con- 
dition the splenic tissue is exceedingly soft, sometimes almost 
diffluent, and the color of the cut surface is a dark red. 
But the condition does not continue as a pure hyperaemia. The 
cells forming the honeycomb structure of the pulp enlarge, the 
bloodvessels and the meshes of the pulp come to contain more 
round cells or white blood-corpuscles. These are all indications 
of inflammation, and a further indication is sometimes afforded 
by the deposition of fibrine on the capsule of the spleen. The 
Malpighian bodies sometimes undergo enlargement in this stage, 
but not in all the diseases named. This is most frequently seen 
in the later stages of typhoid fever and smallpox, and when it 
occurs the consistence of the organ is firmer than is usual in the 
acute splenic tumor. In this stage in which more definite inflam- 
matory processes are superadded to the congestion, the spleen is 
even larger than in the earlier stage, and it may reach two, three, 
or even four times the normal size. The organ is unduly soft, 
and on section may look half diffluent, although it is firmer than 
in the cases without enlargement of the Malpighian bodies. The 
color of the cut surface is considerably paler than in the earlier 
period, being more of a grayish or whitish red. On scraping the 
surface a thick juice is obtained which is not unlike pus mixed 
with blood. 
As a general rule the acute splenic tumor diminishes as the 
primary disease passes off', and the spleen may be left soft and 
loose with wrinkled capsule and unduly prominent trabeculae. 
Sometimes there results a chronic inflammation with thickening 
of the trabeculae, but this hardly occurs unless there have been 
repeated attacks of hyperaemia as in malarial fevers, and occasion- 
ally in typhoid fever. 
It is a very rare circumstance for suppuration to occur in the 
inflamed spleen, but this has been met with in intermittent fever. 
In such cases the pus appears in numerous little points which 
represent the Malpighian follicles, or there is a more diffuse sup- 
puration of the spleen. If the abscess bursts externally, a fatal 
peritonitis results. 
Among the cases of suppurative inflammation of the spleen 
should be mentioned those in which ulcerative endocarditis or 
pyaemia is the primary disease. In that case minute emboli are 
frequently carried to the spleen as to other structures, and being PASSIVE hyperemia. 
367 
of a septic nature they each form the focus of an acute inflamma- 
tion, which has at first a hemorrhagic character, and afterwards 
passes on to suppuration. The spleen as a whole is enlarged by 
active hypersemia. 
Chronic Inflammation.—In cases where the inflammatory 
enlargement is repeated frequently, or there is a more continuous 
irritation of the spleen, we have what may be called a chronic 
inflammation, causing the chronic splenic tumor. This is very 
common in malarious districts, and is regularly met with in persons 
who have been repeatedl}’ subject to attacks of ague. But in such 
districts it occurs even in persons who have had no apparent ague, 
so that almost every post-mortem examination reveals a chronic 
ague cake. As already mentioned, there may be a more or less 
permanent enlargement in prolonged typhoid fever. Syphilis in 
the acute stages produces an acute splenic tumor, which may 
result in the chronic form, but by no means constantly. Again, 
the chronic form may occur in congenital syphilis. 
The enlargement may depend on a general hypertrophy of the 
spleen, so that the consistence of the organ is nearly normal. 
There is, however, considerable increase of the lymphoid elements 
and the trabeculae are thickened. There is frequently also 
increased pigmentation. In other cases there is a marked new- 
formation of connective tissue in the trabeculpe, the pulp is firmer 
and the blood-spaces reduced in size. This condition warrants 
the designation fibrous induration of the spleen. The organ as 
a whole is not so much enlarged as in the other form, but it is 
much firmer and harder, so that the name ague cake is peculiarly 
applicable here. In extreme cases there is atrophy of the proper 
constituents of the spleen; the pulp is much encroached on, and 
the Malpighian follicles are greatly destroyed. There is usually 
also much deposition of pigment in the splenic tissue, especially in 
the pulp, but also to a slight extent in the Malpighian bodies, and 
in the thickened connective tissue around the vessels (see Mel- 
amemia). In both forms of chronic tumor of the spleen, the cap- 
sule is generally thickened. It is usually irregularly so, and we 
have tendon-like patches or loose shreddy connective tissue on the 
surface. Sometimes the capsule acquires adhesions to neighboring 
structures, and the spleen may be so buried in adhesions as to 
make it difficult to dissect it out. It is to be remembered, how- 
ever, that such adhesions are very frequent apart from any proper 
disease of the spleen at all, being due to inflammations in its 
neighborhood. In this latter case the spleen is usually small and 
firm in its texture. 
Passive Hyperemia.—This condition occurs in the spleen when 
there is any considerable obstruction of the portal circulation. 
Hence we meet with it in cirrhosis of the liver, and in cases of 
heart disease which have gone on to general venous engorgement, 
the hypenemia being, as it were, transmitted through the liver. It 368 
DISEASES OF THE ORGANS OF CIRCULATION. 
may, indeed, occur in consequence of any local or general obstruc- 
tion whose effects extend to the splenic vein. The organ is 
enlarged, but not to such an extent as in the congestive form. As 
in other cases of passive hyperaemia the connective tissue increases 
in firmness, and so the whole organ is denser than usual, while 
the tissue presents a deep red color. The thickening of the con- 
nective tissue affects the trabeculae and the sheaths of the blood- 
vessels. 
The Embolic Infarction.—This is probably of more frequent 
occurrence in the spleen than in any other organ, except perhaps 
the lungs. The explanation of this is probably the large size of 
the splenic artery. We have already seen that this artery and all 
its branches are end-arteries, and that obstruction of one of them 
can hardly fail to cause the hemorrhagic infarction. At first the 
infarction is of a deep red color, and has more or less the form of 
a wedge with its base at the capsule. On handling the organ it is 
to be detected by its density, forming a hard mass in the midst of 
the soft tissue. As a rule, there are several infarctions in the same 
spleen, and as the embolus in a larger trunk may break up and be 
distributed irregularly in various branches, we may have very 
complicated forms assumed by the infarction. For example, it is 
not uncommon to find the superficial parts of the spleen involved 
over a large area, while the infarction does not extend much 
beneath the surface, as if the emboli had been swept into a number 
of terminal branches near the surface. The spleen, as a whole, 
is enlarged, the obstruction of the arteries leading to a collateral 
hypersemia by dilatation of those remaining open. This enlarge- 
ment may reach considerable dimensions. On the capsular surface 
of the infarction there is often a deposition of fibrine, and it is 
interesting to know that during life the existence of this' has been 
sometimes diagnosed by the discovery of friction sound. 
From what has gone before, it will be understood that the piece 
of splenic tissue involved in the infarction is in a state of necrosis. 
At the very outset the elements of the spleen may be made out, 
the spaces in the pulp, the veins and venous sinuses being engorged 
with blood. After a time the tissues become less recognizable, 
they seem to undergo a coagulation, and at the same time fatty 
degeneration occurs in them. The blood-coloring matter is also 
dissolved out, being partly absorbed and partly deposited in solid 
granules throughout the infarction. The result is that the infarc- 
tion becomes gradually paler in color, and gains in consistence. 
Around the infarction a chronic inflammation occurs with the 
usual new-formation of connective tissue. As the infarction 
becomes absorbed this connective tissue draws together, the final 
result, as we have already seen, being a cicatrix in which some 
cheesy matter may be found representing the original infarction. 
During these processes the spleen gradually returns to its normal 
size and condition, with, it maybe, some thickening of the capsule. 
We frequently meet with one or more cicatrices in the spleen from 369 
THE SAGO SPLEEN. 
old embolism. These are always visible at the surface and pene- 
trate inwards, but often they have little depth. 
The condition of the spleen in leukaemia has been already de- 
scribed, and it is to be remembered that the spleen may be 
enormously increased in size, up to a weight of forty pounds. The 
condition in pseudo-leukaemia or Hodgkin’s disease is virtually 
the same. 
Rupture of the Spleen.—This occurs occasionally, as we have 
seen, in acute enlargements of the organ. But traumatic rupture 
is much more frequent. This is effected by blows or falls on the 
abdomen, and also by injuries to the chest by which the lower 
ribs are forced against the organ. There may be considerable 
rupture without any external marks of injury. It is important to 
remember that the enlarged and hard spleen is more liable to 
rupture than the normal one, both on account of its more brittle 
character and its size. This is important in a medico-legal aspect, 
especially in malarious districts. The rupture may lead to fatal 
hemorrhage, but bleeding is often associated with other injuries, 
and only plays a part in the result. On the other hand, the 
hemorrhage may be slight, and the wound may heal and leave a 
cicatrix. 
Degenerative Changes.—Of these, by far the most important 
is amyloid disease. It has already been mentioned that the spleen 
is more frequently the seat of this disease than any other, and that 
it appears in a majority of cases to be the organ primarily affected. 
There are two forms of amyloid disease, called respectively the 
sago form and the diffuse form. In the former the Malpighian 
bodies are mainly engaged; in the latter the pulp. We are 
entirely ignorant of the conditions which induce these differences 
in the situation of the degeneration, but there must be some im- 
portant diversity in the causes of the two forms. 
The Sago Spleen.—In this form the organ is moderately en- 
larged. On section we observe on the cut surface, instead of the 
normal small Malpighian bodies, transparent glancing areas which 
have been very aptly compared to grains of boiled sago. These 
are dotted over the surface in great profusion. On applying iodine 
solution the affected areas stand out as brown spots, which become 
of a deeper color on adding dilute sulphuric acid. Microscopic 
sections (see Fig. 187) show transparent hyaline areas of round 
shape and larger or smaller size, often so large that they are con- 
tinuous with one another at their peripheries. These areas repre- 
sent Malpighian bodies, which, when the disease is advanced, are 
entirely replaced by a nearly homogeneous transparent tissue. In 
the early stages, however, the addition of methyl-violet or iodine 
brings out a beautiful network in the Malpighian body, and it is 
obvious that the reticulum is first attacked. Even in the early 
stage it can be seen that the lymphoid corpuscles are also to some 370 
diseases of the organs of circulation. 
extent involved, and as the disease progresses they are more and 
more atfected, although to some extent they may be destroyed by 
the enlargement of the reticulum. The arteries whose lymphoid 
bodies are thus affected are often themselves degenerated, but they 
may remain unaffected. In advanced stages of the disease the 
Fig. 187. 
Section of a sago spleen. The enlarged and translucent Malpighian bodies are seen, 
In the middle an artery with amyloid walls. X 20. 
enormous enlargement of the Malpighian bodies causes atrophy of 
the pulp, and we may have the spleen presenting little beyond 
large round, sago-like bodies. The pulp may, however, itself take 
part in the amyloid disease at the periphery of the Malpighian 
bodies. 
The Diffuse Amyloid Spleen.—In this form the spleen under- 
goes much greater enlargement than in the sago form. It is in 
the highest degree hard and heavy, and the edges rounded. On 
section the tissue seems close and inelastic, and of a dark trans- 
parent appearance. The degeneration affects the greater part of 
the spleen, but there may be islands of normal pulp visible. The 
Malpighian bodies are hardly visible, and the cut surface has 
a smooth uniform appearance. The application of iodine pro- 
duces a general deep brown coloration of the tissue. Under the 
microscope (as shown in Fig. 188) it appears that the trabecula* 
of the pulp are involved, and the arrangement of these trabecula? 
is brought out in the early stages on the addition of methyl-violet 
or iodine. In the later stages the appearance is more uniform, 
but indications of the trabecular arrangement may still be visible. 
By the enlargement of the pulp the Malpighian bodies are greatly 
atrophied, but they may show traces of amyloid disease. In this 
form the walls of the arteries and veins are amyloid. TIIE BONE-MARROW. 
371 
Tuberculosis does not occur in the spleen as a primary disease, 
but in acute general tuberculosis we frequently find tubercles in 
great abundance. The tubercles are usually seated in the neighbor- 
hood of arteries, and are often diffi- 
cult to distinguish from the lymphoid 
Malpighian bodies which have a 
similar seat. The existence of the 
giant-cell structure and the tendency 
to caseous degeneration will assist in 
distinguishing them. Occasionally 
we meet with large caseous masses 
in the spleen, which may reach the 
size of walnuts. These occur mostly 
in children who are the subjects of 
scrofulous disease of the lymphatic 
glands. The general distribution of 
the nodules suggests that the infective 
material has been carried by the blood, 
and in some cases there may be a 
rupture of a softened gland into the 
splenic artery. Syphilitic gummata 
are very rare in the spleen, and have 
been met with chiefly in congenital 
cases. Other tumors are equally rare, 
but cases of fibroma, sarcoma, and 
one case of a pulsating cavernous 
angioma have been observed. Sar- 
comas occur secondarily in the spleen 
with greater frequency than any 
primary tumor, and this is especially 
true of melanotic sarcomas, which may possibly originate in the 
spleen. Secondary cancers only occur in cases where, from the 
general diffusion of such tumors, we may infer that the infective 
material has found its way into the blood. 
The Bone-marrow.—The medulla of bone is now generally 
regarded as forming a part of the circulatory system. The red 
medulla of the spongy bones is to some extent, in structure and 
in function, analogous to the lymphatic glands and spleen. In 
normal conditions this medulla contains nucleated cells of a 
yellowish tint which are probably red corpuscles in process of 
development. Most of the conditions described as occurring in 
the spleen have their analogues in the bone-marrow. We have 
already seen that in leukaemia there are changes corresponding to 
the lymphatic new-formation in the spleen. In acute fevers, and 
especially in relapsing fever and smallpox, but also in pyaemia, 
typhus, pneumonia, there has been found hyperaemia of the 
marrow and great accumulation of round cells. At present these 
facts must be regarded rather as indications of the direction in 
which investigation should go than as a solid basis of fact. 
Fig. 188. 
Diffuse amyloid spleen. The swollen 
and translucent tissue of the pulp (a) 
is shown. X 400. (After Kyber.) DISEASES OF THE NERVOUS SYSTEM. 
Introduction.—In studying the diseases of the nervous system 
it is very important to carry along with us some general concep- 
tion as to the anatomical and physiological relations. 
The simplest idea of a nervous system is that of a central gan- 
glion cell with an afferent or centripetal fibre, and an efferent or 
centrifugal one. An approach to this simplest form of nervous 
system is afforded us in the case of the heart. We have here in 
the substance of the organ certain groups of ganglion cells, which 
possess on the one hand centripetal fibres coming chiefly from the 
endocardium, and on the other hand centrifugal fibres passing to 
the muscular fibres of the heart. It is to be presumed that im- 
pressions conveyed from the endocardium induce the development 
of impulses which are conveyed by the centrifugal fibres to the 
muscle and bring about its contraction. 
But these intrinsic ganglia of the heart, although forming with 
their connections a complete nervous system, are not entirely 
isolated and independent. They are under the command of higher 
centres which control their action and through them effect the 
contractions of the heart. From these higher centres fibres reach 
the heart by two paths, by the vagus and by the sympathetic, and 
by means of these fibres the action of the intrinsic ganglia is re- 
strained or stimulated. 
Taking a general survey of the nervous system we find that 
among the innumerable centres there are grades or orders to be 
recognized, the lower or simpler being under the control of the 
higher and more complex. Leaving aside the peripheral centres 
and the sympathetic system we may fitly illustrate this in the case 
of the cerebro-spinal axis. 
In the spinal cord, as we shall see more particularly afterwards, 
there are, chiefly in the anterior cornua, groups of ganglion cells 
which form distinct individual centres. Many of these appear to 
be of the simplest and lowest kind, representing, as it were, single 
muscles or limited groups of muscles. The stimulation of such 
simple centres would produce no properly coordinated movement, 
but simply the contraction of a muscle or muscles. But in the 
cord itself there are centres of a higher order than this, represent- 
ing, not single muscles or very limited groups, but more consider- 
able groups of associated muscles, so that movements of some 
complexity are brought about by their stimulation. The lower 
order of centres are under the control of the higher, and it is to 373 
INTRODUCTION. 
be presumed that the higher in bringing about movements do not 
act directly on the muscles, but stimulate in the first instance the 
lower centres, which then act directly on the muscles. It is to be 
understood that even the hio-her centres in the cord are, as com- 
pared with those in the brain, of a very low order, and are only 
capable of effecting such simple actions as the extension of the 
toes, the drawing up of the leg, etc. 
The medulla oblongata may be regarded as simply an extension 
upwards of the spinal cord. Its centres are scarcely of a higher 
order than those of the cord, and the movements which may be 
effected by it alone are of the simplest character. In it are massed 
the great centres which have the control of the respiratory move- 
ments, and the contraction and dilatation of the bloodvessels. 
The muscles of the tongue, mouth, pharynx, etc., are represented 
here as are those of the legs and trunk in the spinal cord. 
Passing to the centres next in order above the cord and medulla 
oblongata we reach the so-called middle brain, including the 
centres in the pons varolii, the corpora quadrigemina, and as per- 
haps of a still higher order, the cerebellum. Many animals can 
go through very elaborate movements when deprived of all parts 
above this middle brain. A pigeon can fly, a frog can leap, and a 
rabbit can run. There is, however, a want of spontaniety in the 
movements, which present many of the characters of complex re- 
flex or automatic actions. A rabbit will remain quiet till its foot 
is pinched, and will then set about running. It is to be observed 
that the movements effected by means of the middle brain require 
the action of the same muscles as those in which the spinal cord 
alone is concerned, but the combinations are more complex and the 
grouping of the muscles more intricate. It is to be presumed that 
in effecting these more complex movements the higher centres act 
in the first place on the lower, and, through them, on the muscles, 
the lower centres in the cord being thus a necessary link in the 
chain. 
In man the middle brain appears to be much less independent 
than in the lower animals. In many animals, as we have seen, a 
stimulus coming from the periphery may induce such complex acts 
as flying, leaping, running, but it is not so in man. If the centres 
for such acts are situated in the middle brain in man, they are so 
dependent on the higher centres that when their connection with 
these is severed they are only able to act very imperfectly. A 
person may be completely paralyzed on one side by the connection 
being divided between the middle and upper brain, but when such 
a person yawns the paralyzed arm will often move in an ex- 
aggerated fashion entirely independent of the will. Yawning is 
an exaggerated inspiration, and in order to elevate the chest the 
arm is stretched upwards and backwards so as to bring the pecto- 
ralis into action on the chest-wall. When we have command of 
ourselves we can control these movements, but when the middle 
brain is severed, the paralyzed arm may act in an exaggerated 
fashion. 374 
diseases of the nervous system. 
Passing now to the basal ganglia of the cerebrum we find here 
a series of centres of a very high order. When such animals as 
the dog and cat are deprived of all centres higher than the corpus 
striatum, they are capable of running about, these movements 
being of course automatic. But in man, and also in monkeys, 
although the general movements of the body may be regarded as 
gathered together in these ganglia, they are not sufficient for the 
more complex acts of locomotion, etc. The movements of the 
body, although represented in a complex form in these ganglia, 
are represented higher up in a still more complex form, and, at the 
same time, the lower centres are less independent of these higher 
ones. 
In the convolutions of the cerebral hemispheres we have the 
highest order of centres, and in man the motor area may be taken 
to form the seat of all the centres which are concerned with the 
more complex voluntary acts. In the motor convolutions we have 
the movements of the body, as it were, written larger, occupying 
much more space than in the corpus striatum, and more indi- 
vidualized. 
In regard to sensation, we are not to look for a succession of 
centres such as we have' in the case of motion. There are 
peripheral organs of a highly specialized character, which are en- 
gaged in the transmission of the various special kinds of sensation. 
Between these and the highest centres there are virtually no others 
interposed, the intervening structures being only concerned in 
conduction, perhaps with arrangements for fortifying the impres- 
sions as they are conducted through greatly elongated paths. 
Besides the apparatus engaged in sensation there are afferent fibres 
which are related to reflex actions, and probably the same fibres 
to some extent subserve both functions. 
In studying the specific diseases of the nervous system it will be 
necessary to carry these physiological considerations along with 
us, and in the case of each disease it will be proper to take into 
account the effect which it will have on the physiological action. 
Lesions occurring in nervous structures may produce various 
effects. They may irritate the centres either directly or by 
means of their communicating fibres. If a motor centre be irri- 
tated there will be muscular movements, spasm, convulsion. If a 
sensory centre be irritated there will be subjective sensations as of 
sight, smell, touch, hearing, taste. If a mental centre be irritated 
there will be subjective mental phenomena, that is, mental phe- 
nomena which are beyond the control of the individual, peculiar 
thoughts, illusions, etc. On the other hand, lesions may destroy 
centres, in which case we shall have paralysis of motion, or loss of 
sensation (anaesthesia), or mental degeneracy. 
It may also be remarked, to begin with, that lesions which are 
large and palpable are often called coarse lesions, as where a 
tumor or a clot destroys or irritates, or does both. Coarse lesions 
are thus distinguished from those finer changes which are matter THE PERIPHERAL NERVES. 
375 
for microscopic observation. In some cases indeed the existence 
of actual physical changes is matter of inference, the anatomical 
demonstration of them being not yet furnished. 
A.—THE PERIPHERAL NERVES. 
Introductory Considerations.—A nerve-stem, whether met 
with embedded in the tissues of an organ or lying free, is com- 
posed of one or more bundles of nerve-fibres united together by 
connective tissue. The accompanying figure (Fig. 189) shows the 
Pig. 189. 
Transverse section of a nerve consisting of a single bundle; from a specimen stained and 
mounted by Clarke’s method, a, perineurium ; b, endoneurium. Inside the perineurium is 
the lymphatic space between it and the nerve-bundle. The nerve-fibres are represented by 
rings with a central dot—the axis-cylinder. X 120. (Klein.) 
general arrangement of this connective tissue in a stem composed 
of a single bundle of nerve-fibres. There is an external layer of 
connective tissue, the perineurium (a) binding the whole bundle 
together. But inside the bundle there is connective tissue binding 
the individual nerve-fibres together and forming the endoneurium 
(6), the nuclei of which are prominently seen in the figure. In a 
nerve-stem made up of several bundles these also are bound 
together by connective tissue, the epineurium or neurilemma. 
The nerve-fibres of such peripheral nerves are for the most part 
medullated, and when examined in the fresh state they present an 
opaque appearance and a double outline, as in Fig. 190, A. When 
examined in the fresh state, it is only this appearance that is visible, 
but by proper methods of preparation the constituent structures of 
the fibre can be shown as indicated in Fig. 190, B and C, and in 376 
DISEASES OF THE NERVOUS SYSTEM. 
Fig. 189. These are the axis-cylinder (3, Fig. 190), the medullary 
sheath or white substance of Schwann (2), and the primitive sheath 
(1). The axis-cylinder is the conducting part of the fibre, and 
runs continuously from end to end. The medullary sheath is com- 
Fig. 190. 
Medullated nerve-fibres. A, the natural appearance; B and G, diagrams showing the 
constituent structures as in text. (Quain.) 
posed of a fatty substance (myeline) and is prone to undergo a 
kind of coagulation which gives rise to the double contour. This 
substance is semi-fluid, and when the nerve-fibre is broken up, 
either during life or after death, it is apt to flow out and so we 
may have free drops of myeline which have a strongly refracting 
outline. The primitive sheath is a transparent membranous tube 
which covers the fibre and keeps the medullary sheath together. 
When transverse sections of a nerve which has been hardened and 
stained are examined these various constituents appear, as in Fig. 
189. The axis-cylinder is a colored point in the middle of each 
fibre. The medullary sheath around this is transparent and color- 
less. The primitive sheath forms a colored ring around the fibre. 
If a medullated nerve-fibre be examined after preparation with 
osmic acid, it will be seen that, as Ranvier has shown, the medul- 
lary sheath is not continuous, but is interrupted at intervals, the 
axis-cylinder and primitive sheath being alone present. These 
nodes divide the nerve-fibre into sections therefore, and each 
section receives a further individuality from the fact that about its 
middle an oval nucleus is present inside the primitive slieath, 
between it and the medullary sheath. 377 
EFFECTS OF DIVISION OF NERVE-STEMS. 
Hon-medullated or pale nerves have no medullary sheath, and 
consist essentially of axis-cylinders each covered with a primitive 
sheath in which nuclei occur at intervals. As the white appear- 
ance of ordinary nerves depends on the medullary sheath, non- 
medullated nerves are gray in color. Most nerves at their 
peripheral terminations lose the medullary sheath and become 
pale, but some are so throughout, chiefly the olfactory nerve and 
the sympathetic. 
Effects of Division of Herve-stems.—When a nerve is divided, 
there occurs motor and sensory paralysis in the peripheral parts 
dependent on it. But it frequently happens that conduction is 
after a time restored, the divided ends having reunited, and this 
sometimes so rapidly that immediate union has been supposed to 
occur. Most frequently, however, the restoration of function is 
tardy, and processes occur in the nerves which have been carefully 
studied by experimentation on animals. The changes which ensue 
on the division of a nerve occur mainly in the peripheral portion 
of it, and they consist in the first place in a degeneration, by 
which the structure is largely destroyed, and in the second place 
in a regeneration by which it is restored. 
Before describing the changes themselves, we have to refer to 
the probable explanation of the peculiar degeneration which is the 
primary occurrence. The nutrition of the nerve-fibres is under 
the command of certain ganglionic trophic centres, and when the 
fibres are cut off from these centres they suffer in their nutrition. 
For the sensory fibres the trophic centres are in the ganglia of the 
posterior or sensory roots. For the efferent nerves the centres are 
in the anterior cornua of the spinal cord. Most nerve-stems con- 
sist of both afferent and efferent fibres, but the division of the stem 
will cut the fibres off from their trophic centres, whether they be 
afferent or efferent. It is interesting to observe that when the 
posterior nerve-root is divided on the proximal side of the gan- 
glion, its fibres degenerate in the central direction, or towards the 
spinal cord. 
The degenerative process occurs in the whole peripheral distri- 
bution of the divided nerve, and almost simultaneously. The 
most obvious change is in the medullary sheath. It coagulates, 
breaks up into drops, and through time disappears by absorption. 
This disintegration of the medullary sheath occurs gradually, and 
the granular fat into which it breaks up is partly taken up by the 
nuclei of the nerve-fibre, but partly also finds its way out of the 
primitive sheath and is found in the surrounding connective tissue 
and the walls of the capillaries. There is some difference of 
opinion as to the part taken by the axis-cjlinder in the process. 
Erb asserts that it persists after the medullary sheath has been 
destroyed, but Ranvier states that it is broken up, its interruption 
corresponding with the abolition of electric conductivity in the 
nerve. Whether the axis-cylinder is destroyed or not, the nerve- 
fibre undergoes a great transformation by the loss of its medullary 378 
DISEASES OF THE NERVOUS SYSTEM. 
sheath, and it becomes converted into a pale fibre, interrupted at 
intervals by the nuclei or by some persisting clumps of myeline. 
It has been indicated above that these changes are degenerative 
in character, resulting from the severance of the nerve-fibre from 
its trophic centre. It is asserted by Ranvier, however, that the 
nuclei, which we have seen to exist inside the primitive sheath 
between every two nodes, take a more active part in the process. 
They enlarge and divide, and, by impinging on the medullary 
sheath, help to break it up. It is by them also, according to this 
author, that the axis-cylinder is interrupted. This enlargement 
and division of the nuclei is somewhat similar to that which occurs 
in muscle in certain lesions of the spinal cord to be considered 
afterwards, and it may be regarded as inflammatory in its nature. 
At the place of division of the nerve, as there is a wound, there 
are signs of inflammation. Leucocytes collect between and around 
the cut ends of the nerve, and even penetrate into the primitive 
sheath for some distance. These leucocytes, which are most 
abundant soon after the section, attack the medullary sheath, and 
assist in breaking it up; the myeline is taken up by the leucocytes 
so as to give them the appearance of compound granular corpus- 
cles. In the central end of the divided nerve, however, the 
destruction of the medullary sheath is limited, as the invasion of 
leucocytes generally stops short at the first node. 
After a time the inflammation subsides largely, and the wound, 
including skin and soft parts, is united by a cicatrix formed in the 
usual way. The divided ends of the nerves are united by a pale 
cicatricial band, which does not as yet contain any proper nervous 
elements, and does not effect a restoration of the conductivity. 
Conduction is restored by a process of Regeneration. Accord- 
ing to the researches of Ranvier, this occurs entirely by the axis- 
cylinders of the central end budding out and extending first into 
the cicatrix and then into the peripheral end. The axis-cylinder 
enlarges at its extremity, and becomes divided longitudinally into 
several fine fibres, which grow out into the cicatrix. Arrived at 
the cut end of the peripheral portion they penetrate into it and 
very frequently pass into the primitive sheath. In this way a 
number of new-formed axis-cylinders may be found inside an old 
nerve-tube, and there may be alongside of them some pieces of 
persisting myeline. These new axis-cylinders after a time acquire 
medullary sheaths, and the regeneration of the nerve is completed. 
It should be added that, according to Remak and others, the new 
fibres are not formed entirely by budding from the central end, 
but that they arise also from the remaining axis-cylinders of the 
peripheral end. 
Hyperemia and Acute Inflammation of Rerves.—These con- 
ditions are exceedingly common as secondary processes in the 
neighborhood of wounds and inflammations, but are rarely 
primary. Under such circumstances the vessels of the nerve may 
be highly engorged with blood, and there may even be capillary 379 
syphilitic gummata. 
hemorrhages. Leucocytes may he exuded, and may he found in 
the connective tissue between the nerve-fibres. It is very rare, 
however, to find a proper suppurative inflammation of a nerve. 
A stem may be bathed in pus and almost isolated by the suppura- 
tion around, and yet there may be almost no pus in the connective 
tissue of the nerve itself. This seems to indicate that the peri- 
neurium forms a barrier between the lymph-spaces of the nerve 
and those of surrounding parts. If a nerve be exposed and 
isolated, and the wound filled with water in which vermilion is 
suspended, the leucocytes which accumulate take up the vermilion 
and carry it in various directions but not into the nerve, showing 
that there is no open path into it. But if a nerve in a suppurating 
wound be itself wounded so as to lay open its internal structure, 
the suppuration will readily extend into it. 
Chronic Neuritis is, like acute, for the most part secondary. 
It may remain after an acute attack, but it may take origin in a 
prolonged inflammation of some peripheral organ. It may have 
its starting-point in an inflammation of a joint, in dysenteric in- 
flammation of the intestine, in inflammation around the kidney, 
and so on. It is very important to observe that inflammation 
originating thus may extend up the nerves. It is to be presumed 
that the irritant gradually finds its way along the lymph-spaces of 
the nerve, which we have seen to be somewhat independent of 
those around, and the resulting inflammation may even extend to 
the spinal cord and its membranes. Many cases which have been 
regarded as reflex paralysis have been due, according to Leyden, 
to this extension of chronic inflammation to the cord. There may 
also be an extension downwards to the muscles and a consequent 
interstitial myositis. 
The inflammation manifests itself in the connective tissue of the 
nerve, the perineurium and endoneurium presenting an excess of 
round cells and becoming gradually thickened. As a consequence 
of this the nerve-fibres atrophy, the medullary sheath being first 
destroyed. The nerve as a whole may be thickened and indurated, 
while there is actually an atrophy of the proper conducting fibres. 
These will be recognized as the general characteristics of chronic 
interstitial inflammations. 
Tumors. — Syphilitic gummata are very infrequent in the 
peripheral nerves, but they do occur, especially on the cranial 
nerves inside the skull, where they are probably propagated from 
the membranes of the brain. Leprosy, as we have already seen, 
sometimes manifests itself in the form of tumors of granulation 
tissue in the nerves. The neuroma is strictly a tumor consisting 
of nervous tissue, but as the name is applied to simple tumors of 
nerves in general, it is customary to refer to true and false neuro- 
mata. The true neuroma, as we have seen, and as Fig. 191 showrs, 
has a similar structure to a nerve-stem. It presents nerve-fibres 
embedded in connective tissue. The fibres are usually medullated, 380 
DISEASES OF THE NERVOUS SYSTEM. 
but cases of non-medullated neuromas have been described. The 
neuroma forms a hard tumor usually oval in shape and very often 
multiple. Of the false neuromas there have been cases of fibroma, 
myoma, myxoma. The painful subcutaneous tumor (tuberculum 
dolorosum) is apparently sometimes a fibroma, sometimes a myoma, 
Fig. 191. 
Transverse section of a neuroma, showing medullated nerve-fibres. X 80. 
or even a non-medullated neuroma. Sarcoma is very rare in 
nerves. Cancers do not occur as primary tumors, but nerves are 
often involved in the extension of such tumors. It often happens 
that a cancer or sarcoma grows around a nerve, which passes 
through its midst without becoming the seat of the tumor tissue. 
This is again to he associated with the apparent independence of 
the lymph-spaces in nerves. Sometimes, however, a cancer breaks 
into a nerve and grows in the lymph-spaces between the perineurim 
and the bundle of fibres. In such cases the nerve-fibres undergo 
degeneration. 
B.—THE SPINAL CORD AND MEDULLA OBLONGATA. 
Introduction.—In what has gone before a general view has been 
given of the functions of the central nervous system. Before begin- 
ning the description of the special diseases of the cord and medulla 
we have to see how these functions connect themselves with the 
anatomical details of these structures. 
The cord is made up of white and gray substance, the latter 
forming the ganglionic centres and consisting of ganglion cells in 
the midst of a fine network, the former consisting of medullated 
nerve-fibres having essentially the structure of those in the periph- 
eral nerves. 
The gray substance of the cord is arranged in the well-known 
form of an anterior and a posterior cornu on either side. The 
ganglionic centres have their seat chiefly in the anterior cornua, 
and form tolerably definite groups which may here be more par- 
ticularly indicated. SPINAL CORD AND MEDULLA OBLONGATA. 
381 
The description may be followed by reference to Fig. 192, which 
shows sections of the lumbar and cervical enlargements. The 
groups are named according to their situations. There are the 
lateral groups lying along the external parts of the horn and 
divided into an antero-lateral and a postero-lateral group (al and 
pi). Then in the front of the horn and inside the antero-lateral 
group is the anterior group (a), and inside it again and bordering 
on the white substance is the internal group (z). Towards the 
centre of the horn is the central group (c). There is further a 
group which is later in appearing in the development of the cord, 
and whose cells are generally smaller than those of the others. It 
occupies a place between the internal group on the one hand and 
the central and antero-lateral on the other, while the anterior 
group projects somewhat into it. This is the median group (m) 
which is much larger in the cervical than in other parts of the 
cord, and so causes the horn to be extended laterally much more 
here than elsewhere (see Fig. 192). Lastly, there is a group of 
Fig. 192. 
Sections of spinal cord from middle of lumbar and cervical enlargements, showing groups 
of ganglion cells ; a l and p l, antero-lateral and posterio-lateral, a, anterior, i, internal, c, 
central, m, median, groups. (Ross.) 
cells, generally called Clarke’s vesicular column, situated near the 
internal border of the posterior horns close to the posterior com- 
missure. The group is present only in the lower part of the cer- 
vical enlargement, in the dorsal region and in the upper part of 
the lumbar enlargement (see Fig. 193). 
The white substance, consisting of nerve-fibres, forms connec- 
tions in the first place with the various orders of centres in the 
cord itself and in the second place with the higher centres above 
the cord, in the brain. We may thus distinguish two sets of nerve- 
fibres, one forming connections within the cord and medulla and 382 
diseases of the nervous system. 
the other forming communications between the cord and the cere- 
bellum and cerebrum. These two sets of fibres will be divisible 
again into afferent and efferent. 
It is a fact of very peculiar interest, that the two sets of fibres 
distinguished above seem to be 
developed not only separately but 
at different periods, and so the aid 
of embryology has been sought to 
enable us to distinguish between 
them. The fibres which connect 
the different parts of the cord and 
medulla with each other may be 
regarded as the primary or funda- 
mental ones, and it is found that 
they are the first formed, while 
those forming higher connections 
are of subsequent development, 
As nerve-fibres are first developed 
without the medullary sheath, and 
recently formed tracts are therefore 
much paler than those which have 
acquired it, we have in this a means 
of distinguishing the fundamental 
from the secondary. What follows 
will be understood by reference to 
Fig. 194, which represents a trans- 
verse section of the cervical cord 
in the foetus of nine months. 
The first developed fibres imme- 
diately surround the gray matter, 
and are called the anterior and posterior root-zones. As they 
form communications between one part of the gray matter and 
another, the fibres are comparatively short and their number is 
generally in proportion to the amount of gray matter, or at least 
of ganglion cells in the horns. These fibres therefore do not 
diminish from above downwards as do the others. 
Of the fibres forming communications between the brain and 
cord, the best known are those which convey the motor impulses 
from the brain to the cord. These form the pyramidal tract. 
We shall afterwards trace them from the cortex of the brain down- 
wards, but at present we take them up at the medulla oblongata. 
Here they form the anterior pyramids and most of the fibres 
decussate so that in the cord they occupy the opposite side to that 
which they have in the brain. Some of them, however, do not 
decussate, but remain in the anterior parts of the cord, forming a 
small band on either side of the anterior longitudinal fissure, the 
columns of TuRCK(77in figure). The great mass of the fibres, 
having decussated, pass to the lateral column of the cord, where 
they occupy a definite position in its posterior parts (jpt in figure). 
The fibres in both these positions diminish in number from above 
Fig. 193. 
Section of dorsal region of cord. Let- 
ters same as in previous figure, with the 
addition that the antero-Iateral and 
postero-lateral groups are separated by a 
medio-lateral area (ml), and Clarke’s 
column (vc) is shown. (Ross.) SPINAL CORD AND MEDULLA OBLONGATA. 
383 
downwards, as they pass into the gray substance of the cord at 
successive levels in order to connect with the centres in the 
anterior cornua. 
The secondary centripetal fibres, or those which form sensory 
connections between the cord and brain, are represented by a tract 
in the posterior columns lying next the posterior longitudinal 
fissure, and occupying a position somewhat similar to that of the 
columns of Turck anteriorly. These are called the columns of 
Goll (Gin figure),and they also diminish from above downwards. 
Fig. 194. 
Cervical enlargement of cord in a foetus of nine months. A and P, anterior and posterior 
cornua; G, columns of Goll; T, columns of Tiirck ; ar and pr, anterior and posterior root- 
zones; pt, pyramidal tract; dc, direct cerebellar tract. (Ross.) 
Besides this there is a tract which forms communications between 
the cerebellum and the cord, hut which is not of late development. 
This is the so-called cerebellar tract (dc in figure), which lies in 
the lateral column outside the pyramidal tract, and as if flattened 
against the surface. The function of this tract is not known, but 
it is composed of centripetal fibres and diminishes from above 
downwards even more quickly than the pyramidal tract, so that 
by its disappearance the latter may come to the surface. 
In the medulla oblongata the gray and white substances of the 384 
DISEASES OF THE NERVOUS SYSTEM. 
cord may be traced upwards, but they undergo considerable dislo- 
cation. From the examination of Fig. 195 it will be seen that, as 
the central canal passes backwards and finally opens out in the 
fourth ventricle, the gray matter, departing from its arrangement 
into cornua hut still aggregated in 
the neighborhood of the central 
canal and ventricle, forms various 
masses in the posterior part of the 
medulla. These masses have special 
importance as being the nuclei of 
origin of certain nerves, and will 
he afterwards more particularly re- 
ferred to, in connection with bulbar 
paralysis. The white substance grad- 
ually comes to occupy the middle 
and anterior parts of the medulla, 
and the olivary body is intercalated 
in its midst. The pyramidal tract 
is easily recognized here, forming 
the anterior pyramids (p), which 
decussate at the lower part of the 
medulla (hi). The motor fibres hav- 
ing assumed a position in front re- 
main anterior to the sensory in the 
rest of their course upwards in the 
brain. 
SECONDARY DEGENERATIONS IN 
THE CORD. 
We have already seen that when 
a nerve-stem in an animal or in man 
is divided, the peripheral portion of 
the nerve degenerates. The most 
prominent changes are in the me- 
dullary sheath which coagulates, 
then breaks up, and is finally ab- 
sorbed. The degeneration occurs 
from the point of section towards 
the periphery, and we have seen 
that the explanation of this seems 
to be that the nerve-fibres are cut 
off from their trophic centres in the 
cord. 
In the central nervous system a 
somewhat similar secondary degeneration occurs when the fibres 
are interrupted, either by division, as in experiments on animals, 
or by coarse lesions in man. The degeneration is of the same 
character as in peripheral nerves, and results in the destruction of 
Pig. 195. 
Medulla oblongata at various levels, 
A, at decussation of pyramids (j»), the 
general shape of the cornua still re- 
tained. B, higher up, the gray matter 
passing backwards, and pyramids be- 
coming more isolated. C, in fourth 
ventricle, the nuclei in the floor of which 
are shown. (Qdain.) 385 
DESCENDING GRAY DEGENERATION. 
the medullary sheath. It is known that the opaque dead-white 
color of the white or fibrous nerve-substance is due to the medul- 
lary sheath, which is a highly refracting fatty substance. If this 
medullary sheath be lost then the white nerve-substance becomes 
gray, and so we speak of gray degeneration in all cases where the 
medullary sheath is lost, whether from the cause we are con- 
sidering or not. A tract of white nervous tissue affected with this 
degeneration will be like a tract of gray substance. Again, in pre- 
paring the tissue of the nervous system for microscopic examina- 
tion, some form of the method introduced by Lockhart Clarke is 
generally used. In this method staining by carmine or other dye 
is employed, and as the medullary sheath does not take on the 
staining at all, and as it is the most bulky constituent of the white 
substance, the normal white substance as a whole is less deeply 
stained than the gray substance. When secondary degeneration 
has occurred, the effect of staining is to make the altered white 
substance appear like the gray substance. In figures representing 
gray degeneration therefore the affected parts will be shaded like 
the gray substance. 
When a degenerated area is examined more particularly under 
the microscope the most marked change is the great reduction in 
the number of nerve-fibres, as shown in Fig. 196. The connective 
Fig. 196. 
Sclerosis or gray degeneration of cord. To the right is normal white substance. To the 
left the degenerated tissue shows a granular basis substance in which a few nerve-fibres are 
still visible. From a case of descending degeneration. X 80. 
substance is greatly increased, and the nerve-fibres appear only at 
intervals, a few surviving in the midst of the general destruction. 
There is sometimes also considerable shrinking of the degenerated 
area, but this is much more manifest in the medulla oblongata and 
parts above it than in the cord. 
In addition to simple degeneration there is sometimes a new 
formation of connective tissue, which some regard as inflammatory 
in character. The inflammatory character is little marked in 
secondary degeneration, but there are some forms of gray clegener- 386 
diseases of the nervous system. 
ation in which the inflammatory new-formation is perhaps the 
primary factor, and the degeneration of the nerve-fibres the result 
of it. Whether there he new-formed con- 
nective tissue or not, and whether the pro- 
cess be inflammatory or not, the absence 
of the soft medullary sheath causes a 
hardening of the tissue, and so the term 
sclerosis when applied to the white sub- 
stance is nearly equivalent to gray degen- 
eration. 
It has been said above that the degen- 
eration occurs in the fibres which are cut 
off from their trophic centres, and it 
seems that in the cord the trophic centres 
are at the lower termination of the cen- 
tripetal fibres and the upper termination 
of the centrifugal. Hence the degenera- 
tion follows the direction in which the 
nerve conducts, passing upwards from 
the seat of lesion in the case of centri- 
petal fibres and downwards in the case of 
centrifugal. So we speak of ascending 
and descending sclerosis. 
The degeneration takes some time to 
develop. According to experiments in 
dogs it begins fourteen days after the 
infliction of an injury, but it is many 
weeks before the appearances are fully 
established. 
Descending Gray Degeneration (de- 
scending sclerosis).—As we have just seen, 
this lesion afiects centrifugal or motor 
fibres, including the fibres of the anterior 
root-zone and the pyramidal tract. The 
former are short fibres, and when they 
are interrupted there is a descending 
degeneration extending only a short dis- 
tance downwards. But the fibres of the 
pyramidal tract are continuous from the 
brain downwards to the extremity of the 
cord, and wherever interrupted they show 
degeneration in all parts situated below 
the lesion. 
The degeneration of the pyramidal 
tract is most frequently brought about 
by a lesion of the brain, and in that case 
it exists in the parts of the tract above as 
well as in those below the medulla oblongata, where we shall trace 
it afterwards. We have here to consider it in the medulla and 
Pig. 197. 
Descending degeneration in 
medulla oblongata and cord, a, 
medulla at fourth ventricle, b, at 
decussation, c, d, e, f, cord in 
upper and lower cervical, dorsal, 
and lumbar regions. 387 
DESCENDING GRAY DEGENERATION. 
cord. In the medulla oblongata it occupies the anterior pyramid 
(see Fig. 197, a), where it frequently produces great shrinking. At 
the lower part of the medulla (b) the degenerated fibres decussate 
and the degeneration takes up its position at first at the side of the 
central canal (see figure), afterwards, in the cord, passing into the 
lateral columns in the regular position of the pyramidal tract (<?, d, 
e, /). In some cases it entirely decussates, but the columns of 
Tiirck in the anterior white columns are also affected in most 
cases. In its whole course the lesion diminishes from above down- 
wards, but is traceable down to the lumbar region. 
It will be understood that, if the pyramidal tract be interrupted 
in any part of its course, the degeneration follows in all succeeding 
parts. If the entire cord be divided there is, immediately beneath 
the point of section, a degeneration of the anterior root-zones 
which is continued but a short distance. There is also a degener- 
ation of the pyramidal tract continued downwards the whole length 
of the cord. The interruption either in the cord or brain may be 
incomplete, and in that case the degenerated fibres will be fewer 
in number and the area less distinctive in appearance. 
We have already seen that the pyramidal fibres end in the cord 
at successive levels, passing into the ganglionic centres. When 
the fibres are degenerated the ganglion cells will not be affected 
except that they are cut off from the higher centres and left more 
to themselves. They are still connected with the muscles, which 
retain their contractile power. Aroluntary motion is lost, but 
certain involuntary muscular phenomena may be even exaggerated. 
There are two symptoms generally supposed to be related to degen- 
eration of the lateral columns of the cord which it is proper here to 
consider with a view to their probable pathology, these are the so- 
called late rigidity and the exaggerated tendon reflex. 
Late rigidity, occurring in hemiplegia, comes on a considerable 
time after the onset of the paralysis, and may be regarded as coin- 
ciding in time with the full development of the sclerosis. There 
is here a more or less permanent contraction of some muscles with 
absence of contraction in others, producing sometimes fixation of 
the members of the body in special positions so as to have the 
appearance of deformity. This fixed condition, due to the mus- 
cular spasm, is often called contracture. It implies a continuous 
impulse to the contracted muscles originating in the cord or else- 
where. Charcot suggests that the inflammatory process which he 
supposes to be involved in the sclerosis may irritate the fibres 
passing to the anterior cornua and so result in the stimulation of 
the muscular centres there. But this view can hardly be accepted; 
there may be almost no signs of inflammation in the affected part 
and yet marked rigidity. Besides, it is difficult to understand how 
irritation of degenerated and virtually lost fibres should cause 
stimulation of the ganglion cells. A more probable explanation 
is suggested by Hitzig. Taking as an example the case of the arm 
in hemiplegia, it appears that the contraction occurs most readily 388 
DISEASES OF THE NERVOUS SYSTEM. 
in those muscles which are in a position to contract most easily. 
The hemiplegic generally lies in bed with his forearm across his 
chest, and even when walking about he supports it across his chest, 
and it is the biceps which becomes rigid. Then it has been shown 
that when the fingers are released from the action of the muscles 
and left to assume the position to which the hones and ligaments 
best accommodate themselves, they assume a semi-flexed position, 
such as we see in the dead body. It is obvious that the flexor 
muscles will most easily contract under these circumstances, and 
it is they which get rigid in hemiplegics. Take along with this 
the fact which Volkmann points out, that muscles can actively con- 
tract but cannot actively relax, and it is seen that any slight impulse 
is apt to be cumulative when there is no action of antagonistic 
muscles. The ganglion cells of the anterior cornua are still in 
connection with the muscles, and although cut off from the upper 
brain are still exposed to irregular and, as it were, accidental stim- 
ulation. There are reflex stimuli, and there are stimuli from 
above conveyed in a roundabout way through the still open com- 
munications in the cord. A multitude of slight stimulations will 
reach the ganglion cells and feeble impulses will be conveyed to 
the muscles. Those which from their position are stretched will 
not contract, but those which are so placed as to contract easily will 
do so, at first feebly but with cumulative force. This view is sup- 
ported by the fact that, in the early stages of late rigidity, there is 
often considerable relaxation of the muscles after prolonged rest as 
in sleep, so that a limb which was rigid at night is found in the 
morning soft and movable. The ganglion cells in sleep are pro- 
tected from external stimulation and they cease acting. 
The exaggerated tendon reflex may be regarded as due to the 
isolation of the muscular centres in the cord. When the control 
of higher centres is removed, lower centres usually act more 
readily. The skin reflex is frequently decreased, but the muscular 
centres seem to be more powerfully acted on by stimuli coming 
from the muscles. 
It may be added that these two symptoms are prominent in the 
spastic paralysis of Erb, where there is, as we shall see further on, 
a spontaneous sclerosis of the lateral columns. 
Ascending Gray Degeneration {ascending sclerosis).—This condi- 
tion occurs as a result of any cause which interrupts the ascending 
or sensory fibres of the cord. It may be the consequence of 
pressure by tumors, hemorrhages, abscesses, fractured or displaced 
vertebrae, inflammatory products, etc. It occurs in parts above the 
seat of interruption, and the degenerated fibres are centripetal. 
The degeneration affects the centripetal fibres, and these we 
have already seen to be of two kinds. There are the short fibres 
communicating between different segments of the cord, and form- 
ing the posterior root-zones, and there are the longer fibres com- 
municating between the cord and brain, and forming the columns ASCENDING GRAY DEGENERATION. 
389 
of Goll and the direct cerebellar tracts. Immediately above the 
lesion, both of these are affected so that the degeneration has 
considerable lateral extension involving the whole of the posterior 
columns and the direct cerebellar 
tracts. But the lesion soon limits 
itself to the columns of Goll and the 
direct cerebellar tract (see Fig. 198), 
and in these parts it can he traced up 
to the restiform body on the one hand, 
and the cerebellum on the other. 
According to Schiefferdecker, the de- 
generation in these two situations 
diminishes from below upwards, the 
diminution .occurring at intervals as if 
at definite levels fibres passed into the 
cord. 
Some cases have been recorded in 
which a tumor pressing on the cauda 
equina, or a severe traumatic lesion of 
the sciatic nerves, had led to ascending 
degeneration of the cord. In the lum- 
bar and lower dorsal regions the whole 
posterior white columns were degener- 
ated, but on passing upwards the degen- 
eration became limited to the columns 
of Goll and cerebellar fibres as above. 
It will be evident that a lesion which 
interrupts the cord will lead to an 
ascending degeneration above its seat 
and a descending degeneration below 
it, as in Fig. 198. The degeneration 
will diminish in both cases as we pass 
from the lesion, quickly at first, but 
afterwards more gradually. 
Degeneration in the cord after 
amputations lias been observed in a 
number of cases. The removal of a 
limb abolishes the function of the 
nervous structures concerned in the 
movements and other actions of the 
limb, and so these structures undergo 
atrophy from disuse. The posterior 
roots of the nerves are often slightly 
atrophied, but the white columns of 
the cord are not affected. The prin- 
cipal change is in the anterior cornua, 
where some of the ganglion cells com- 
pletely disappear, and others are shorn 
of their processes and atrophied. This 
Fig. 198. 
Transverse myelitis (e) with sec- 
ondary ascending and descending 
degeneration. At d, the ascending 
degeneration affects the posterior 
root-zones, the columns of Goll, and 
the direct cerebellar tracts, but above 
that it is confined to the two latter. 
At /to h, the columns of Tiirck and 
the pyramidal tracts are affected. 
(Erb.) 390 
DISEASES OF THE NERVOUS SYSTEM. 
occurs at a part of the cord corresponding with the amputated 
limb, and on the same side of the body. If the ampufation has 
been made comparatively late in life, there is usually little change 
in the cord; the earlier the age of the person at the time of the 
amputation the more likely are these changes to occur. 
In a case recorded by Edinger, in which intra-uterine amputa- 
tion of the forearm had occurred, and the person lived to the age 
of fifty-two, there was considerable atrophy of the nerves and of 
the corresponding half of the cord, especially of the gray matter. 
There was also some atrophy in the motor region of the convolu- 
tions in the brain. 
INFLAMMATIONS OF THE SPINAL CORD. 
In the widest acceptation, inflammation of the spinal cord, or 
myelitis, includes a large number of widely different conditions, 
each of which will be considered separately afterwards. The cases 
may for convenience he divided into two groups. In one of these 
the affection has a limited longitudinal extension, but involves the 
cord rather in its thickness. For this class of cases it is customary 
to use the expression transverse myelitis in order to distinguish 
from those in which a considerable length of cord is attacked, 
while the inflammation has a limited transverse extension. The 
former are usually due to a definite cause which acts on the cord 
at a particular level. In the second group the inflammation 
follows a particular physiological system in the cord, as for in- 
stance a tract of white substance, and extends in it for some 
distance from above downwards. Such inflammations may in- 
volve the white substance or the gray substance, and they are 
often distinguished by the names poliomyelitis (yoA<og — gray) and 
leucomyelitis (Aewcof — white). These inflammations have for the 
most, part no assignable cause, and are sometimes called sponta- 
neous. Closely allied to these systemic inflammations there is 
a form of spontaneous myelitis in which the distribution is some- 
what irregular, but still has a certain tendency to localize itself. 
We shall consider the two classes indicated above under separate 
headings. 
TRANSVERSE MYELITIS. 
1. Acute transverse myelitis, or simply Acute Myelitis.— 
Acute inflammation of the spinal cord is nearly always secondary 
to some other condition. It may be produced by fracture, disloca- 
tion, acute curvature of the vertebrae, direct injury to the cord. 
It may be caused by extension of inflammation, as when an abscess 
penetrates into the spinal canal, producing inflammation first of 
the meninges. A tumor may produce it by compression, but as 
the compression is usually gradual there is more frequently a 
chronic myelitis, and the same applies to most cases of curvature chronic transverse myelitis. 
391 
of the spine. Acute myelitis also occurs in consequence of ex- 
posure to cold, especially when the body has been overheated. It 
may be a complication or sequel of an acute specific fever, as 
typhus, and it is said to be not uncommon in syphilitic patients. 
The myelitis is limited in longitudinal extent, and as the usual 
result is softening of the cord, the expression acute softening of 
the cord is almost equivalent to myelitis. The softening is usually 
most manifest in the gray substance and may even be apparently 
confined to it, but it really involves the white substance as well, 
and usually the whole thickness of the cord. 
The softened nervous tissue presents, in different cases, consider- 
able variations in color, so that red, yellow, gray, white, and even 
green softening have been described. If much blood has escaped 
from the vessels, there will be red softening merging into yellow. 
The characteristic morbid changes are the breaking up of the 
nervous tissue and fatty degeneration of the other structures. In 
the white substance drops of myeline escaped from the medullary 
sheath are found, and the axis-cylinders are swollen. The fatty 
degeneration is manifested in the presence of abundant compound 
granular corpuscles, which, to a large extent, are probably leu- 
cocytes or neuroglia cells, which have picked up the disintegrated 
myeline; but there may be abundant leucocytes apart from these 
cells. There is also fatty degeneration of the walls of the blood- 
vessels, the fat here having a similar source. 
The myelitis rarely goes on to suppuration, but usually passes 
into a chronic stage. The fat both of the medullary sheath and 
of the compound granular corpuscles, is absorbed, and a condition 
of gray softening remains. As the inflammation becomes more 
chronic there is new formation of connective tissue of a cicatricial 
character. In this way the cord at the part affected may be re- 
placed by a cicatrix, or by a cyst, and its conduction completely 
interrupted. In some cases the interruption is not so complete, 
and there may even be a partial regeneration of the conducting 
fibres, and a partial recovery from the consequent paralysis. As 
a consequence of the interruption in the white substance, there 
is ascending and descending gray degeneration of the usual dis- 
tribution. 
2. Chronic Transverse Myelitis.—We have just seen that this 
condition may follow on an acute myelitis, but the inflammation 
may be chronic from the first, when it is produced by an irritant 
which acts gradually. It is most frequently the result of chronic 
compression of the cord, as in the case of curvature, or pressure 
by a tumor. It may also be propagated from the membranes, a 
spinal meningitis passing into a myelitis. We have already seen 
that it may arise by extension from a peripheral nerve, the inflam- 
mation travelling upwards to the cord. 
The changes produced are those common to chronic inflamma- 
tions. There is new formation of a dense connective tissue, de- 
veloping in the usual way from cells like those of granulations. 392 
DISEASES OF THE NERVOUS SYSTEM. 
The new-formed tissue causes compression of the proper nervous 
elements and their atrophy. In the white substance the nerve- 
fibres disappear, and in the gray substance the ganglion cells. 
With the growth of this dense tissue there is an induration of 
the cord, and the term sclerosis is applicable. In the wdiite sub- 
stance sclerosis, causing the disappearance of the nerve-fibres, 
brings about a gray condition, so that the appearances of gray de- 
generation are produced. There is also a degree of shrinking 
of the parts, and this is often especially manifest in the gray sub- 
stance. 
As the nervous structures are partially or completely destroyed 
there is a greater or less interruption of the cord, and this results 
in the usual secondary degenerations above and below the seat of 
the lesion. 
SYSTEMATIC MYELITIS. 
As already indicated, in the diseases included here the affection 
follows certain physiological systems, and we have, in the iirst 
place, to inquire whether any explanation of this can be suggested. 
In almost all the examples of inflammation studied in other 
parts of this work, the extension of the process is along definite 
paths. The irritant has been brought to an organ by the blood- 
vessels, or by some path of transit, such as a mucous canal, and it 
has extended, it may be, by the lymphatics or along a surface. In 
the lesions here to be considered, however, the problem is much 
more difficult. The localization of the disease bears no relation 
to the bloodvessels or lymphatic vessels, and if the irritant is 
brought by the blood there must be local peculiarities leading to 
differences in the susceptibility of different structures. 
In studying the various structures which constitute the cord we 
saw that in the development of the cord a certain difference is 
apparent. In the white substance there are certain fundamental 
structures constituting the root-zones, and certain accessory tracts 
which are separately developed, and mostly of later formation. In 
the gray substance also there are differences in the periods at 
which the groups of ganglion cells appear, so much so that some 
of them which appear later than the rest have been named acces- 
sory nuclei. These are chiefly the median and medio-lateral 
groups. It is hardly remarkable that these various tracts of white 
substance and groups of ganglion cells should have various powers 
of resistance, and that the more recently developed or accessory 
structures should be least resistant. It is even conceivable that 
some of these should be, from their origin, so unstable that without 
any exciting cause they may tend to degenerate. In this way the 
boundary line between actual inflammations and simple degenera- 
tions is reached. There are some of the diseases here to be con- 
sidered which have undoubtedly the characters of inflammation, 
and even of acute inflammation. But there are others in which 
the characters are rather those of a chronic degeneration or SCLEROSIS OF THE POSTERIOR COLUMNS. 
393 
atrophy of the structures concerned, with very little of an inflam- 
matory character. 
There are thus various degrees of susceptibility in the different 
structures of the cord and medulla oblongata, and when an irritant 
exists in the blood, developed perhaps in connection with exposure 
to cold or otherwise, there will he, according to circumstances, 
various manifestations. In this connection it will be understood 
how syphilis has frequently something to do with the causation of 
these diseases. 
1. Sclerosis op the Posterior Columns (Locomotor Ataxia., 
Tabes Dorsalis).—If the cord is examined in well-advanced cases 
of this disease, the posterior white columns are found gray and 
shrunken, and the posterior roots are also atrophied. There is 
often meningitis, the soft membranes being thickened and adherent 
to the cord beneath as well as to the dura mater on the surface. 
The meningitis corresponds in its extent to the degeneration, and 
is evidence of the inflammatory nature of the disease in the cord 
itself. In early stages of the disease the changes in the cord may 
be invisible to the naked eye, hut can be detected with the micro- 
scope. In advanced stages there may be similar changes in the 
optic nerve, the oculo-motor, the hypoglossal, etc. 
The lesion consists primarily in an inflammatory new-formation, 
round cells are first produced which may be seen most abundantly 
near the bloodvessels; afterwards there is the usual inflammatory 
new-formation of connective tissue, which may even be fibrillated. 
There is corresponding destruction of the nerve-fibres; in the 
earlier stages the fibres are still present, but separated by con- 
nective tissue; through time, however, very few nerve-fibres are 
left in the degenerated part. In earlier periods compound granular 
corpuscles may be met with, and in later stages there are commonly 
large numbers of amyloid bodies. These are round or oval bodies 
three or four times the size of blood-corpuscles, and presenting a 
peculiar bright glancing appearance (Fig. 199). They frequently 
present a concentric striation like grains of potato starch, and with 
iodine they take on a deep brown coloration. These bodies are 
sometimes present in such numbers as to form the most prominent 
feature under the microscope. 
The posterior columns are the parts affected, but Charcot has 
pointed out that the disease does not invade these columns uniformly. 
Its special seat is the outer parts of the posterior columns, those 
next to the posterior cornua (the posterior root-zones), and it is 
stated that these alone are affected in the earlier stages (see Fig. 
200). The columns of Goll are secondarily invaded, and probably 
as the result of an ascending sclerosis. That this is so appears 
from the actual examination of the cord at various levels. The 
disease begins, and is usually most advanced, in the lumbar region, 
but in the lowest part of that region the lateral parts of the pos- 
terior columns may be alone involved. On passing upwards the 
columns of Goll become also affected, so that in the upper half of 394 
DISEASES OF THE NERVOUS SYSTEM. 
the lumbar swelling the degeneration may be coextensive with 
the posterior columns. This continues in the dorsal region, but 
in the cervical the sclerosis begins to diminish laterally, and 
shades off'into the columns of Goll, in which it may be continued 
Fig. 199. 
Fig. 200. 
Amyloid bodies from cord. X 300. 
Posterior sclerosis in an early stage, 
confined to the external part of the 
posterior columns. (Pierret, quoted 
by Err.) 
up into the restiform body. The actual primary lesion is there- 
fore that in the lateral parts of the posterior columns, and the 
affection in the columns of Goll is really an ascending secondary 
degeneration, these columns being, as already stated, the principal 
seat of ascending sclerosis. 
Besides extending to the columns of Goll, the disease spreads 
commonly to the posterior roots, which are often much atrophied. 
It may also extend to the posterior gray cornua, in which case 
anaesthesia occurs, or to the lateral columns, in which case paralysis 
ensues; or it may even pass through to the anterior cornua, when 
muscular atrophy occurs in addition to paralysis. 
The physiology of this disease is a very difficult subject. It is 
known that the most prominent symptom is imperfect coordination 
of the muscular movements, and that this is usually associated in 
its early periods with violent pains, and sometimes in later stages 
with anaesthesia. There are two views as to the cause of the in- 
coordination. According to one, the connection between the 
cerebellum (which is the centre for coordination) and the cord is 
interrupted; and according to the other, it is centripetal or sensory 
fibres that are interrupted. The severe lightning pains of the 
earl}7 periods point to irritation of sensory fibres, and the region 
affected is one where centripetal fibres are undoubtedly in pre- 
ponderating numbers. The secondary extension to the columns 
of Goll also points to interruption of centripetal fibres, and on the 
whole there seems no escape from this view. It is no objection to 
it that amestliesia is absent in most cases, and is usually a late 
symptom, because sensory conduction appears to be by many 
paths, and interruption of one set of centripetal fibres does not 
abolish it. SCLEROSIS OF THE POSTERIOR COLUMNS. 
395 
Taking it for granted that the incoordination is due to interrup- 
tion of centripetal fibres, we have to inquire how it comes about. 
Lockhart Clarke has made a very suggestive observation in this 
regard. He notes that there is probably an interruption of the 
centripetal fibres which are concerned in the reflex function of the 
cord. We know that in locomotor ataxia the tendon reflex is 
abolished (according to Erb, whenever the ataxia is developed), 
and this seems to indicate that the reflex fibres from tendons and 
muscles are specially involved. Lockhart Clarke suggests that 
the normal tonicity of the muscles is due to the continuous stimu- 
lation of the ganglion cells of the anterior cornua by stimuli con- 
veyed from the cutaneous surface, is, in fact, a kind of permanent 
reflex action. The reflex fibres being interrupted, the tonicity is 
interfered with, and the contraction of the muscles starts, as it 
were, at a disadvantage, from an indeterminate state of relaxation. 
To this it may he objected, that the tonicity is probably as much 
due to accidental stimulation of the motor ganglia from above, 
and, besides, that ordinary reflex action may be well retained with 
advanced ataxia. It is here to be noted that in order to an etficient 
contraction of a muscle the centre producing the contraction must 
be in close communication with the muscle by centripetal fibres, 
in order that it may, as it were, start the contraction with a knowl- 
edge of the state of the muscle. Any interruption to this delicate 
adjustment between muscle and centre must seriously interfere 
with the efficiency of the contraction, and the incoordination may 
be accounted for on this ground. That there is such interruption 
is rendered evident by the loss of the tendon reflex, but short of 
absolute destruction of the connections, there may be such an in- 
terference with them as to render the contractions inefficient. The 
absence of this knowledge of the condition of the muscles previous 
to contraction may be partly compensated by using the eyes to 
direct the movements, the motor cells in the cord being, as it were, 
informed from above of the state of the muscles. 
The occasional supervention of anaesthesia in locomotor ataxia 
is to be held as indicating an extension of the disease to the gray 
matter of the cord. The occurrence of true paralysis indicates 
that the neighboring motor tracts in the lateral columns have be- 
come involved. 
The sclerosis not infrequently extends beyond the cord. Of very 
common occurrence is atrophy of the optic nerve from sclerosis, 
and there may be affections of the auditory and other cerebral 
nerves. There may be incoordination of the muscles of the eye- 
ball and of those of speech, indicating the extension of the disease 
to the medulla oblongata. 
In addition to the conditions already referred to, Charcot has 
called special attention to certain trophic lesions which occasion- 
ally occur in locomotor ataxia. These are of three kinds, namely, 
certain cutaneous eruptions, muscular atrophy, and affections of 
the joints. The cutaneous eruptions occur in the earlier periods, 396 
DISEASES OF THE NERVOUS SYSTEM. 
usually coinciding with the attacks of lightning pains, and they 
are in the form of local eruptions of herpes, lichen, pemphigus. 
As these occur in the earlier periods, and are coincident with the 
pains which are evidences of irritation of the centripetal fibres, 
we may infer that the trophic fibres of the skin are situated in the 
posterior roots, and that it is because these are involved in the in- 
flammatory process that the cutaneous eruptions occur. Muscular 
atrophy is not very common in locomotor ataxia, and is of later 
occurrence. The muscles may waste as a direct result of paralysis, 
hut this is a slow atrophy from disuse. In some cases, however, 
there are localized atrophies of special muscles similar to those in 
progressive muscular atrophy and in bulbar paralysis. In these 
cases the disease has extended to the anterior cornua in which are 
situated the trophic centres of the muscles, and there is destruction 
of the ganglion cells there, just as in progressive muscular atrophy. 
The affections of the joints consist in comparatively acute swell- 
ings, with exudation, followed by atrophy of the ends of the bones. 
Dislocations of the joints may occur in consequence. These 
trophic disturbances of the joints seem also to occur in cases 
where the disease extends to the anterior cornua, the trophic 
centres for the whole organs of locomotion having their seat there. 
The propagation of the disease to the anterior cornua, leading to 
muscular atrophy or trophic affections of the joints, seems to be 
not uncommon, and may occur at a comparatively early period. 
This can hardly be regarded as remarkable when we consider that 
there are, for purposes of reflex action, direct connections between 
the posterior root-zones and the anterior cornua. 
Freidrich’s Hereditary Ataxia.—A considerable number of 
cases have been described in which motor incoordination has 
appeared at an early age in several members of the same family. 
There is, in these cases, probably a congenital faulty development 
of the cord, and the ataxia is the consequence rather of a degenera- 
tive than an inflammatory process. Consistently with this there 
are seldom lightning pains, or any affection of sensation. There 
is also little tendency to transverse extension of the lesion in the 
cord, but, on the other hand, the longitudinal extension is very 
rapid, the disease attacking almost the whole extent of the cord 
at once. It also extends to the medulla oblongata, as evidenced 
by the occurrence of disturbance of speech and nystagmus. 
General Paralysis of the insane is often associated with ataxia, 
and the spinal cord presents sclerosis of the posterior columns 
similar to that in ordinary ataxia. 
2. Spontaneous Lateral Sclerosis (Erbs’ Spastic Paralysis).— 
In studying descending degeneration, we saw that the pyramidal 
tract is liable to secondary changes when interrupted in its course. 
In the disease now under consideration, we have an independent 
disease of the pyramidal tract, having a similar anatomical dis- 
tribution. It usually begins in the lumbar cord, and attacks POLIOMYELITIS ANTERIOR ACUTA. 
397 
simultaneously both pyramidal tracts. These cases are of some- 
what frequent occurrence, but seldom come to post-mortem ex- 
amination. In a case recorded by Dreschfeld, however, sclerosis 
was found in the lateral columns. 
The symptoms already referred to as characteristic of descending 
sclerosis are here very pronounced, namely, spasm of the muscles 
chiefly of the lower extremity, with exaggerated tendon reflex. 
There is also, of course, paralysis. 
The sclerosis appears to extend not infrequently from the pyram- 
idal tract to the anterior cornua of the gray substance. In that 
case there is muscular atrophy in addition to the other phenomena. 
To conditions of this kind, Charcot has given the name amyo- 
trophic LATERAL SCLEROSIS. 
3. Poliomyelitis Anterior Acuta (Infantile Paralysis, Acute 
Atrophic Spinal Paralysis).—This is a disease mostly of infancy and 
early childhood, but not by any means unknown in the adult. At 
the onset there are usually signs of acute inflammation (fever, 
sometimes convulsions), but these symptoms may be very slight, 
and the first thing noticed is the paralysis. Whether accompanied 
by fever or not, the paralysis develops suddenly, and generally 
attains its full extent almost at once. It may affect both arms and 
both legs, or the legs alone, or the arms alone, or the leg and arm 
on one side, or one leg or one arm alone. After some weeks, the 
paralysis begins to improve, and may go on improving for some 
time. Complete recovery rarely results, and generally the paralysis 
affects certain muscles permanently. The whole muscles of a limb 
may remain paralyzed, or the paralysis may be limited to a group 
or two of muscles. In the permanently paralyzed muscles a rapid 
atrophy occurs which becomes very extreme. The bones of the 
paralyzed part do not grow normally, and the articulations are 
imperfectly adjusted. Certain deformities ensue, the commonest 
and most prominent of which is clubfoot. Curvature of the spine 
is also a comparatively frequent result. All through the disease 
the patient may maintain good general health, and after recovery 
from the initial fever he may present nothing abnormal but the 
paralysis and atrophy. Through time he learns to use his remain- 
ing muscles to the best advantage, and may pass through a long 
life maimed by the infantile attack. 
In its anatomical aspects, the disease is an acute inflammation 
of the gray substance of the anterior cornua of the cord. There 
are no observations as to the changes at the very outset of the 
disease, but there can be little doubt that there is the usual inflam- 
matory hypersemia and oedema, causing by pressure interference 
with the ganglion cells of the anterior cornua. Some cases have 
also been observed in which there was hemorrhage in the anterior 
horns. The earliest cases examined had been already two months 
affected with the disease, and at this date little can be made out 
with the naked eye. Under the microscope, however, the anterior 
cornua are seen to be altered, not continuously, but in patches. 
They contain numerous round cells and compound granular cor- 398 
DISEASES OF THE NERVOUS SYSTEM. 
puscles. The ganglion cells in certain of the groups have disap- 
peared or have shrunk considerably. At the periphery of the 
affected patches round cells are aggregated and there is already 
some shrinking of the patches. The condition is most manifest 
in the lumbar and cervical enlargements. The anterior roots are 
also somewhat atrophied, and show evidences of degenerative 
changes. 
Many cases have been examined years after the onset of the 
disease, at intervals varying from seventeen to sixty-one years, 
and the changes have been very obvious even to the naked eye. 
These consist of sclerosis with shrinking, mainly of the anterior 
gray cornua, but also of the anterior and antero-lateral columns of 
white substance (see Fig. 201). These changes are very manifest 
when the cord has been hardened and fine transverse sections 
Fig. 201 
Anterior poliomyelitis. The left anterior cornu in the cervical region is shrunken, and 
there is atrophy of all the white columns on that side. From a woman, aged fifty, who was 
the subject of infantile paralysis of the right arm. (Charcot.) 
made. The shrinking of the horn affects certain of the groups of 
cells specially, and the shrunken part consists largely of connective 
tissue in which no ganglion cells are visible or only deformed and 
pigmented ones. There is connective tissue with abundant nuclei 
and enormous numbers of amyloid bodies. There is also sclerosis 
of the antero-lateral columns, the connective substance being in- 
creased and the nerve-fibres to some extent atrophied. The lesion 
in the anterior cornua is by no means homogeneous or symmetrical. 
One cornu may be atrophied and the other normal, and on ex- 
amining sections at different levels there is great variety in the 
longitudinal distribution. 
In the early periods of the disease the extensive paralysis seems 
due to pressure by the distended vessels and inflammatory exuda- poliomyelitis anterior chronica. 
399 
tion, and in some cases by extravasated blood. In this period 
some ganglion cells may be destroyed, but those not destroyed 
may recover as the acute inflammation passes oft’. In many parts 
the inflammation is slight and subsides completely, in others it is 
severe and goes on to sclerosis, and there is permanent destruction 
of the ganglion cells. Hence it is that a paralysis which has been 
at first almost universal may be recovered from almost completely. 
The improvement goes on till all the cells which are capable of it 
have recovered, and there is a residue which have been perma- 
nently lost and cannot be restored. These permanently lost cells 
represent single muscles and groups of muscles, and there is a 
corresponding localized paralysis. 
The centres which have the direct control of the contractions of 
the individual muscles are probably the centres which command 
the nutrition of the muscles and their nerves; or the trophic cen- 
tres, if separate, must at least lie alongside of the muscular centres. 
For the permanently paralyzed muscles soon undergo a marked 
and rapid atrophy, and the fibres of the anterior roots also degen- 
erate. The muscular atrophy is not simply from disuse, tor it is 
much greater and more rapid than in cases of paralysis where 
the anterior cornua are not affected. The muscles rapidly get soft 
and emaciated, and may entirely disappear. Besides the loss of 
substance there may be proliferation of the nuclei of the inter- 
stitial connective tissue, and sometimes there is infiltration of fat 
in the interstial tissue, so that the muscle may appear less atrophied 
than it really is. The defective development of the bones and 
joints may be partly from disuse, but also probably to some extent 
from destruction of trophic centres. 
Although most common in children a good many cases of this 
disease have now been recorded in adults. Here also it is ushered 
in by acute symptoms such as fever, pain in back and extremities, 
vomiting, headache. The paralysis develops mostly in a few 
hours, but it may be as long as a day or two. After a time re- 
covery begins, and is more frequently complete than in the case of 
children. It is frequently incomplete, and then we have paralytic 
deformities, which, however, as the bones are fully formed are not 
so striking as in the case of children. Here, also, there is rapid 
atrophy of the muscles, which is not so liable to be concealed by 
fatty infiltration as in the case of children. 
4. Poliomyelitis Anterior Chronica.—Some very interesting 
cases have been recorded in which, with little or no fever or dis- 
turbance of the general health, a motor paralysis has occurred, 
and in the course of a few days or weeks has extended to the 
entire lower limb and then rapidly to the upper. It rarely takes 
the opposite course. The muscles become slack and soft and lose 
their reflex irritability, and they rapidly atrophy. There have 
been few post-mortem examinations as yet, but they seem to show 
a chronic inflammation or sclerosis of the anterior cornua with 400 
DISEASES OF THE NERVOUS SYSTEM. 
loss of the ‘ganglion cells. The disease is frequently recovered 
from, but recovery is slow and complete restitution may take years. 
On the other hand, the disease may extend upwards and produce 
death. In this disease, also, it will be observed, centres for con- 
traction and trophic centres seem to be simultaneously affected. 
5. Progressive Muscular Atrophy.—This disease, although its 
name points to an affection of the muscles, is yet considered here, 
because there is every reason to believe that an affection of the 
spinal cord is the primary lesion, the muscular condition being 
secondary. 
In its clinical aspects the main feature is a gradually progressive 
atrophy and consequent paralysis of the muscles. It very com- 
monly begins in the muscles of the hand, but progresses from one 
muscle to another till the death of the patient. In its later stages 
it frequently becomes associated with a corresponding disease of 
the medulla oblongata, namely, bulbar paralysis, to be considered 
next. 
The change in the muscles consists in what may be regarded as 
a chronic iniiammation of them. The muscular nuclei increase in 
number, and as the contractile substance diminishes, the sarco- 
lemma may come to he tilled with cells, the result of this pro- 
liferation of the muscular nuclei. At the same time the interstitial 
connective tissue shows active changes, increase of nuclei, and 
new formation of connective tissue. In the muscular substance 
various forms of degeneration have been observed, chiefly fatty 
and waxy, or simple atrophy. In any case the muscular fibres are 
lost by degrees and the connective tissue increased, but not suffi- 
ciently to make up the bulk of the lost muscular substance. 
Sometimes a fatty infiltration of the connective tissue occurs, so 
that adipose tissue comes to occupy the place of the muscle to a 
large extent. This change, if it occurs, is only local, and pure 
atrophy may exist side by side with atrophy with formation of 
adipose tissue. This formation of adipose tissue is mostly a late, 
and by no means a characteristic, occurrence in this disease. 
Although these changes are very manifest in the muscles those 
in the spinal cord are doubtless the primary ones. There have 
been now not a few trustworthy observations in which the large 
ganglion cells in the anterior cornua have been found destroyed. 
Their destruction is variously described as due to chronic inflam- 
mation or atrophy, and at the best nothing can be found in the 
affected region but the shrivelled remains of these ganglion cells. 
This is probably an inflammation extending slowly along the cord 
and confining itself to the anterior gray cornua. 
As to the exact locality of the affected ganglion cells, it is, ac- 
cording to Ross, the central gray column (the gray substance on 
either side of the central canal) which is most affected, being 
traversed by large canals and fibrillated. In the annexed figure 
(Fig. 202) it is also seen that the cells of the median group have 
entirely disappeared, while the other groups of the anterior cornua bulbar paralysis. 
401 
are limited in size, the peripheral cells of the groups having dis- 
appeared, leaving only the more central ones. It very commonly 
happens that, short of absolute destruction of the ganglion cells, 
they are greatly atrophied and pigmented (;'pigmentary atrophy). 
It is to be added that Leyden has recorded a case of progressive 
muscular atrophy in which there was the peculiar condition of the 
cord designated syringomyelia; in this there are gaps of a longi- 
tudinal shape and tilled with fluid 
present in the cord. These cavities 
result probably from an inflamma- 
tory process, and there is along 
with their formation a destruction 
of ganglion cells, so that funda- 
mentally this case is not different 
from the others. 
In some cases there has been, in 
addition to disease of the anterior 
cornua, atrophy of the anterior 
roots of the nerves, hut this has 
not been observed in all cases. 
There has also been observed at 
the peripheral terminations of the 
nerves and in immediate connec- 
tion with the muscles a condition 
somewhat analogous to that of the 
muscles. There was thickening 
of the nerve-sheath with multi- 
plication of nuclei. Although gen- 
erally confined to the fine intra- 
muscular twigs these changes 
sometimes extend into the nerve- 
stems. 
It may be asked, How is the 
atrophy here such a remarkable 
feature, apparently preceding the paralysis ? It is difficult to 
answer this question, hut it looks as if the trophic ganglion cells 
and proper muscular ones were different and yet situated close to 
each other. The trophic are in this disease first affected seriously. 
6. Bulbar Paralysis, or Glosso-labio-laryngeal Paralysis. 
—This condition is called bulbar paralysis from the fact that the 
part affected is the medulla oblongata, which is frequently desig- 
nated the bulb. There is progressive atrophy and paralysis of 
muscles supplied from the medulla oblongata. The muscles are 
mainly those of the tongue, lips, arches of palate, pharynx and 
larynx, and in consequence there is progressive interference with 
articulation, chewing, swallowing, and even with the production 
of the voice. The disease may pass on later to affect the more 
important functions of the medulla oblongata, those concerned in 
respiration, etc. 
Fig. 202. 
Progressive muscular atrophy—section 
of cord in cervical region, from an ad- 
vanced case. The central portion of gray 
substance is fibrillated; the median group 
of cells has disappeared, and the other 
groups are atrophied. (Ross.) 402 
DISEASES OF THE NERVOUS SYSTEM. 
We have already seen in connection with the normal structure 
of the medulla oblongata that on passing from the cord the gray 
substance is dislocated backwards, and that in the posterior region 
of the medulla a set of gray nuclei appear, which, as the spinal 
canal opens up in the fourth ventricle, present themselves in the 
floor of that ventricle. These nuclei are mainly motor, corre- 
sponding with the anterior cornua, and they form the immediate 
centres for certain cerebral nerves (see Fig. 203). In the lower 
Fig. 203. 
Medulla oblongata at the level of the fourth ventricle, showing the position of the 
gray nuclei. (Quain.) 
half of the fourth ventricle we find the hypoglossal nucleus (xii') 
occupying the part next the middle line. Outside it there is the 
spinal accessory nucleus which begins in the cord, and does not 
extend far in the floor of the ventricle; it is not shown in figure, 
hut gives place to the nucleus of the pneumogastric or vagus (x'). 
Outside the vagus appears the glosso-pharyngeal, which partially 
divides the vagus nucleus into two. As we pass upwards the 
vagus nucleus gets smaller and the hypoglossal and glosso-pharyn- 
geal approximate to each other. Above that again come in the 
nucleus of the sixth (the abducens) in the middle line, and outside 
that the motor nucleus of the fifth and the facial. Outside these 
again are sensory nuclei, those of the acoustic and of the fifth. 
In bulbar paralysis there is atrophy of these gray nuclei. It is 
seldom that opportunity is afforded of examining the medulla in 
recent stages, but according to Benedikt, who had such an oppor- 
tunity, there are definite signs of inflammation, hypersemia, thick- 
ening of the walls of the vessels, and numerous round cells. In 
later periods increase of the connective tissue, with round cells 
and amyloid bodies, have been observed. These changes centre 
in the nucleus of the hypoglossal, and this nucleus is usually most 
seriously damaged, but they pass soon to the accessory and vagus, 
while the glosso-pharyngeal sometimes, but not usually, escapes. 
The nucleus of the facial is often attacked, and sometimes that of 
the motor branch of the fifth. The disease seldom extends to the 
abducens, and never attacks the sensory nuclei of the acoustic 
and fifth. 403 
PSEUDO-HYPERTROPHIC paralysis. 
The corresponding nerves usually show considerable atrophy, 
especially the hypoglossal, and next to it the accessory, vagus, aud 
glosso-pharyngeal. In them may be found a fatty degeneration 
involving destruction of the medullary sheath and subsequent over- 
growth of connective tissue. In this way the nerve-root may 
come to be almost nothing but a connective-tissue strand. 
In the affected muscles the change is exactly parallel to that in 
progressive muscular atrophy with which sooner or later this dis- 
ease is so frequently associated. There is increase of the muscular 
nuclei and connective tissue, with destruction of the proper con- 
tractile substance, and consequent atrophy of the muscle as a 
whole. Thus the tongue, palatine arches, lips, pharynx, and 
larynx may have their muscles intensely atrophied. Sometimes 
also the muscles of the neck, especially the trapezius (supplied by 
the spinal accessory), are affected. In some cases the atrophy is 
obscured, as in progressive muscular atrophy, by the interstitial 
tissue becoming adipose. 
7. Pseudo-hypertrophic Paralysis.—It is a disputed point 
whether this disease is primarily one of the muscles or of the cord, 
but it presents some features similar to those of the last two affec- 
tions we have considered, and deserves notice here. 
The disease consists in a great atrophy of the muscular substance 
proper, with a great new-formation of adipose tissue in the muscle. 
Fig. 204. 
Muscle in pseudo-hypertrophic paralysis. There is chiefly adipose tissue with a few 
atrophied muscular fibres. X 180. 
Gowers describes the appearance in a case where a post-mortem 
examination was procured as follows: “ On cutting into the gas- 
trocnemius it was difficult to believe that the section was that of 
muscle. Its appearance was precisely that of a fatty tumor—a 
yellow greasy mass of fat, in which no trace of muscular redness 404 
.LUDJliilDlbD KJ r injL IN L it V U U O DZ OTJilL. 
could he perceived. Under the microscope the resemblance to a 
fatty tumor was also strikingly close. Cells distended with homo- 
geneous fat covered the field. Passing among the fat-cells, how- 
ever, were narrow hands, which consisted of fibrous tissue and 
muscular fibres.” This is a very correct description of the ap- 
pearances in advanced cases. The muscular fibres which remain 
are of various sizes, and many of them in an advancing state of 
atrophy so as hardly to be recognized as muscular fibres, except 
by the transverse striae (Fig. 204). The primary process here is an 
increase of the connective tissue with atrophy of the muscle, the 
addition of fat and conversion into adipose tissue being secondarj'. 
DISEASES OF THE NERVOUS SYSTEM. 
Fig. 205. 
Cervical enlargement in a ease of pseudo-hypertrophic paralysis. 
This conversion takes place variously in different muscles. In the 
same individual you may find some muscles almost converted into 
fat and others in which there is very little adipose tissue, the con- 
dition in the latter case being virtually identical with that in pro- 
gressive muscular atrophy. 
In regard to the condition of the spinal cord in this disease, not PSEUDO-HYPERTROPHIC PARALYSIS. 
405 
many careful observations have been made, and some of these have 
afforded apparently negative results. In a case examined by 
Lockhart Clarke and Gowers there were obvious changes in the 
cord, consisting of sclerosis and consequent disintegration of white 
and gray substance in various regions. In a case examined by 
Ross there was very marked atrophy of certain groups of ganglion 
cells in the lumbar, dorsal, and cervical regions, the distribution 
of the atrophy varying in the different regions. 
Figs. 205 and 206 represent the cervical and lumbar enlarge- 
ments in a case examined by the author in conjunction with Dr. 
Alexander Robertson. The ganglion cells in the anterior and in- 
ternal groups in the cervical region, and in the internal group in 
Fig. 206. 
the lumbar, are deficient in number, but elsewhere they are 
abundant, and it could not be made out that there was any special 
shrinking or pigmentation of the ganglion cells of the various 
groups. 
Opinions are divided on the question whether this disease is 
primarily muscular or nervous, but the analogy with progressive 
muscular atrophy renders it probable that it is primarily a disease 
of the cord. 
Lumbar enlargement in a case of pseudo-hypertrophic paralysis, 406 
DISEASES OF THE NERVOUS SYSTEM. 
TUMORS OF THE CORD AND MEDULLA OBLONGATA. 
Tumors actually originating in the cord or medulla are exces- 
sively rare; tumors originating in the membranes or elsewhere 
outside the cord and pressing on the cord are rather more common. 
Cases of glioma and sarcoma, and also of fibroma of the cord and 
medulla oblongata, have been observed. 
Scrofulous tubercles similar to those which are so common in 
the brain, and will be described hereafter, have been met with in 
the cord, but are of very rare occurrence. They have been found 
most frequently in the lumbar region. 
Syphilitic gummata are also of occasional occurrence. Like 
those of the brain, they are mostly superficial and involve the 
membranes, where they probably originate. 
Cysts occur very rarely in connection with tumors. Apart from 
these, tubular cavities are sometimes met with (syringomyelia). 
Some of these are due to congenital dilatation of the central canal 
of the cord, but many of them are of independent origin. These 
latter are usually situated in the posterior columns, and in their 
deeper parts immediately behind the central canal. Cavities of 
this kind are caused by extensive loss of substance, but it is often 
obscure how this has come about, whether by inflammation or 
otherwise. In this connection, it is interesting to note that Eich- 
horst found in experiments on animals in which the cord had been 
divided or injured, that cavities formed frequently in the posterior 
columns, and sometimes extended into the central canal. When 
the syringomyelia is due to dilatation of the central canal the cysts 
are lined with ciliated epithelium, but even in the other forms this 
may be the case. 
C.—THE ENCEPHALON. 
ANATOMICAL INTRODUCTION. 
In the section introductory to diseases of the spinal cord and 
medulla oblongata the course of the respective tracts of nerve- 
fibres and their connection with the various ganglionic centres 
were traced. In the encephalon we shall adopt the same method, 
premising that the course of the fibres is here even more important, 
as they are liable to he interrupted in a more isolated fashion. It 
is of great importance that the pathologist should have an 
acquaintance with the general relations of parts so as to identify 
the position of lesions. In this section nothing more is attempted 
than to indicate these general relations, the more intricate par- 
ticulars being left to the special works on anatomy. In the actual 
work of post-mortem examination, it is important to note the 
exact locality of lesions on the spot. To assist in this, tracings THE ENCEPHALON—ANATOMICAL INTRODUCTION. 
407 
may be made of the figures which accompany this section, or of 
similar ones, the position of the lesions being entered in shading. 
In the medulla oblongata, as we have seen, the motor fibres 
which have been in the lateral columns of the cord come forward 
and form the anterior pyramids, in which they decussate. The 
sensory fibres are now behind, and they remain posterior to the 
motor in all the succeeding parts. In the pons varolii (Fig. 207) 
Fig. 207. 
Pons varolii. In lower half the transverse section of nerve-bundles continued upwards 
from the cord is seen, the pyramidal tract being in front (or lower in figure). The Roman 
numerals and letters indicate the nuclei of spinal nerves. (Quain.) 
the motor fibres are in front, forming bundles, as shown in lower 
half of figure, hut overlaid by the transverse fibres from the cere- 
bellum. Besides these fibres, which are mainly in the anterior 
half of the pons, there are gray nuclei (shown in figure) which 
continue up the series which lie in the floor of the fourth ventricle 
in the medulla oblongata. In the pons the principal nuclei are 
those of the sixth and facial, the motor and sensory roots of the 
fifth, and one of the nuclei of the auditory nerve. It is to be re- 
membered also that the fibres of these nerves in part at least 
traverse the pons, and are liable to be involved by a lesion, even 
when the nuclei are not reached. 
In the crura cerebri, or cerebral peduncles, the motor fibres 
are in front and internal, forming the greater part of the crusta. 
Sensory fibres occupy about the external fourth of the crusta. 
Behind the crusta is a locus niger, behind which again is the 
tegmentum, which contains a rather complex mass of fibres and 
gray matter. 
Above the crura the fibres are continued upwards, the motor 
still anterior and the sensory posterior in the mass of white sub- 
stance called the internal capsule. It is here necessary to be 
somewhat more minute in the description of the relation of the 
structures, as these relations are of great importance. When one 
of the lateral ventricles of the brain is opened, certain masses of 408 
DISEASES OF THE NERVOUS SYSTEM. 
gray nervous tissue*are seen in its floor. In front there is a long 
brown prominence, rounded anteriorly, and tailed behind. This 
is the nucleus eaudatus, which is often designated the corpus 
striatum, although really only one piece of it. Behind the nucleus 
eaudatus is the optic thalamus which is more bulky and rounded. 
It is to be remembered that in opening the lateral ventricle almost 
no nerve-fibres need to be cut except the commissural ones of the 
corpus callosum. The great mass of nerve-fibres passing upwards 
are as it were pushed outwards by the lateral ventricle, and we 
Fig. 208. 
Horizontal section of brain of a child nine months old, the right side at a somewhat lower 
level than the left. F, frontal; TS, temporo-sphenoidal; and 0, occipital lobes; Op, oper- 
culum ; In, island of Reil; CIs, claustrum ;f", third frontal convolution; Th, thalamus ; 
NC, nucleus eaudatus; NC', tail of same; LN, nucleus lenticularis; I, II, III, its first, 
second, and third divisions; IK, internal capsule, posterior division; IK', anterior division, 
and k, knee; ah and ph, anterior and posterior horns of left lateral ventricle; gee, knee of 
corpus callosum; sp, splenium; me, middle commissure; f, fornix; si, septum lucidum; 
a, cornu Ammonis. (Ross from Fi.echsig.) 
have to cut into its floor in order to reach them. From the 
accompanying figure, which represents a horizontal section of the the encephalon—anatomical introduction. 
409 
brain just below the floor of the lateral ventricle, the relations of 
parts may be gathered (Fig. 208). Beneath the outside the nucleus 
caudatus (NC), and continuous above and externally with the great 
central white substance of the hemispheres, the corona radiata, 
there is a mass of white substance. This is the internal capsule 
in which may be distinguished an anterior division IKa pos- 
terior division IK, and a middle part, the knee K To the outside 
of and beneath the internal capsule lies a mass of gray substance 
(IN), which on section has a triangular shape with the base turned 
outwards, and is seen to be divided into three pieces (shown on 
right side). This is the nucleus lenticularis, which is generally 
regarded as a part of the corpus striatum and motor in function. 
The nucleus lenticularis extends a considerable distance from 
before backwards, and in its posterior parts the internal capsule 
(IK') lies between it and the optic thalamus, which has now largely 
taken the place of the nucleus caudatus. Outside the nucleus 
lenticularis there is a narrow band of white substance (EK), called 
the external capsule, the capsules being named from their rela- 
tion to the nucleus lenticularis. Outside the external capsule again 
and close to the convolutions (here the Island of Beil) there is a 
narrow band of gray substance (Cls), which is fancifully compared 
to a tapeworm, and is called the nucleus tseniaeformis or elaustrum. 
The anterior parts of the internal capsule then contain motor fibres, 
and the posterior sensory; it is generally said that the anterior 
two-thirds are motor, and the posterior third sensory. 
It is to be remembered that the three nuclei we have referred 
to, the nucleus caudatus, nucleus lenticularis, and thalamus opticus, 
receive fibres from and give fibres to the internal capsule. There 
are fibres passing upwards to the convolutions and others down- 
wards to the lower centres. It hao been said by some that all the 
fibres from the convolutions pass into the basal ganglia, in which 
case all the fibres of the internal capsule would end or begin in 
these nuclei, but there is no proper foundation for this view. 
Passing upwards, the fibres of the internal capsule are continued 
into the corona radiata or centrum ovale, containing the white 
substance of the hemispheres, and it may be stated generally that 
in the corona radiata motor fibres are anterior and sensory pos- 
terior. But besides these fibres there are multitudes which form 
communications between one part of the convolutions and another, 
and altogether the connections here are very complicated. 
It will be necessary further to make some general remarks on 
the cerebral convolutions and their arrangement, which may be 
studied in Ecker’s work, in which the descriptions are very clear. 
If the lateral aspect of one of the cerebral hemispheres be ex- 
amined (see Fig. 209), two great landmarks should first be made 
out; these are the fissure of Sylvius (SSS), and the fissure of 
Rolando (BE). There is no difficulty with the fissure of Sylvius, 
of which the main or transverse arm is perfectly distinct, while its 
short ascending arm near the front is easy to make out. The 410 
diseases of the nervous system. 
fissure of Rolando passes obliquely forward from above downwards 
through the middle of the lateral aspect of the hemisphere, not 
reaching the longitudinal fissure above, or the fissure of Sylvius 
below. This fissure can usually be recognized by the fact that it 
is bounded by or lies between two convolutions which extend side 
Fig. 209. 
Left lateral aspect of cerebrum. Explanation in text. (Quain.) 
by side upwards and backwards from the fissure of Sylvius (A, A, 
A and B, B). 
Having distinguished these two fissures the various lobes of the 
brain may now be determined. All in front of the fissure of 
Rolando, and above the fissure of Sylvius, is frontal lobe. The 
parietal lobe lies behind the fissure of Rolando, and its posterior 
extremity is bounded by a fissure which is best seen on the inner 
face of the hemisphere, the parieto-occipital fissure. This fissure, 
beginning about the edge of the great median fissure, passes down- 
wards and forwards on the inner face of the hemisphere (par. occ. 
f., Fig. 210). Behind this is the occipital lobe. The remaining 
lobe is the temporo-spiienoidal which lies below the fissure of 
Sylvius and extends backwards to meet the occipital lobe, from 
which it is indefinitely distinguished. 
Turning now to the principal convolutions in these lobes, the 
easiest to determine are those bounding the fissure of Rolando, 
one of which is, of course, in the frontal and the other in the 
parietal lobe, and so they are called ascending frontal and 
ascending parietal convolutions respectively. In front of the 
ascending frontal, the frontal lobe presents three layers of convo- 
lutions (a, a', and a") which lie transversely and pass by their 
posterior extremities into the ascending frontal. These trans- 
verse frontal convolutions are distinguished as the first, second, 
and third, or superior, middle, and inferior. It is not to be 
supposed that these are single simple convolutions, they are rather 
layers or strata of convolutions. The inferior (a") is a very im- 
portant one, and it can generally be easily recognized as it curves THE ENCEPHALON—ANATOMICAL INTRODUCTION. 
411 
round the short ascending branch of the fissure of Sylvius (s). 
After curving round this branch it becomes continuous with the 
lower end of the ascending frontal. At this point the two convo- 
lutions form a somewhat triangular piece, and as this lies over 
and partially covers the island of Reil, it is often called the 
operculum (in the position of x A in Fig. 209). In addition to 
these we have still in the frontal lobe the supraorbital convolu- 
tions (a*) which have no arrangement that needs to be detailed. 
In the parietal lobe the ascending parietal convolution (J3, B) 
is already known. Another easily recognized one is that which 
lies immediately above the fissure of Sylvius and is called the 
supramarginal convolution. The posterior portion of this convo- 
lution curves round the upper end of the fissure of Sylvius, and 
as it turns thus round an angle it is often called the angular gyrus 
(■band is important, as Ferrier has supposed it to be the seat of 
the sense of sight. The rest of the parietal lobe is divided into 
an upper and a lower portion by a longitudinally placed fissure 
which is often not very distinct, the intra-parietal fissure, which 
arises close to the fissure of Sylvius behind the fissure of Rolando 
to which it at first lies parallel, and then passes backwards. The 
lobe is thus divided into the superior and inferior parietal 
lobules, the former being continuous in front with the ascending 
parietal convolution. 
In the occipital lobe, looking at the lateral aspect, three 
transverse layers of convolutions can be distinguished. These 
are named as in the frontal lobe, first, second, and third, or superior, 
middle, and inferior (d, dd"). On the under or basal surface 
there are two further layers which are continuous in front with 
those of the temporo-sphenoidal lobe and are named in common 
with them inferior occipito-temporal convolutions. 
The temporo-sphenoidal lobe presents on its lateral surface 
again three transverse convolutions, superior, middle, inferior 
(c, c', c"); the superior, bounding the fissure of Sylvius and also 
called infra-marginal, is continuous with the angular gyrus. 
The remaining two sets in the basal surface have been already 
mentioned as forming with those of the occipital lobe the inferior 
occipito-temporal convolutions. 
On examining the internal aspect of the cerebral hemisphere 
(Fig. 210) certain convolutions are to be distinguished. The 
superior frontal convolution and the ascending frontal and parietal 
convolutions are here partly visible. More distinctly on the 
internal surface we distinguish in front the marginal convolution 
(marg. c.) which is continuous with the superior frontal and lies 
along the superior longitudinal fissure. Immediately behind this 
convolution we come to the superior parietal lobule which, on its 
mesial surface, is called the precuneus or quadrate lobe (see 
figure). The parieto-occipital fissure is here very marked, and it 
is joined at an angle by the calcarine fissure (calc. /.) in such a way 
as to demarcate a triangular surface, the cuneus (cuneate l.). On 
this aspect also appear the inferior occipito-temporal convolutions 412 
diseases of the nervous system. 
(i. oc.-temp. c.). Within this external ring of convolutions we have 
now a deeper layer. Immediately bordering on the corpus 
callosum and following the fornix we trace from before backwards 
the gyrus fornicatus. Having skirted the corpus callosum from 
before backwards it turns round at its posterior extremity, and 
Fig. 210. 
passes downwards into the gyrus hippocampi. This gyrus is also 
continuous with the gyrus cunei and the median occipito-temporal. 
The gyrus hippocampi passes forward towards the anterior 
extremity of the temporo-sphenoidal lobe where it terminates in a 
liook-like curve, the gyrus uncinatus {line. c.). 
In the cornu Ammonis of the lateral ventricle there lies a con- 
volution whose surface is turned inwards and forms an elongated 
rounded projection in the cornu; this is the gyrus dentatus (d. c.). 
The Cerebellum.—There are only a few points which require 
notice here as to the general arrangements of the parts in the cere- 
bellum. Like the cerebrum it is divisible into two lateral hemi- 
spheres, the right and left lobes. These are united by a central 
piece, which is most marked on the under surface, called the vermi- 
form process. The cerebellum is divided by many fissures which 
run horizontally and leave narrow convolutions called the folia. 
One of these fissures, deeper than the rest, and called the great 
horizontal fissure, divides the cerebellum into an upper and a lower 
portion. In its internal structure it presents white matter which 
runs outwards from the peduncles diverging towards the folia and 
forming a tree-like expansion, the arbor In the midst of 
the white substance in each hemisphere there is a small gray 
nucleus, not unlike the olivary body, called the corpus dentatum. 
Arteries of the Brain.—With a view to the identification of 
the numerous lesions of the arteries in the brain, it will be proper 
here to refer briefly to the distribution of these vessels. The 
Internal aspect of right cerebral hemisphere. Explanation in text. (Quain.) THE ENCEPHALON ANATOMICAL INTRODUCTION. 
413 
circle of Willis gives oft' at the base three main arteries to the 
brain, the posterior, middle, and anterior cerebral. The posterior 
cerebral artery, besides giving certain central branches to be 
afterwards referred to, is distributed on the surface of the brain, 
supplying the greater part of the occipital and temporo-sphenoidal 
lobes with the exception of the upper temporo-sphenoidal convolu- 
tion. The middle cerebral artery, or the artery of the fissure of 
Sylvius, is of great importance as being much more frequently the 
seat of lesion than the others. Besides its central branches, after- 
wards considered, it supplies the middle district of the brain all 
round the fissure of Sylvius, including the parietal lobe, the poste- 
rior parts of the frontal lobe, and the superior convolution of the 
temporo-sphenoidal lobe. The anterior cerebral artery is dis- 
tributed to the anterior parts of the frontal lobe. These arteries, with 
the exception of their central branches, run in the sulci of the convo- 
lutions, and divide into successive orders of branches which lie in the 
pia mater. The larger branches anastomose sparely, but the finer 
twigs are end-arteries [Duret). All the arteries hitherto considered 
run on the surface of the brain in the soft membranes. The actual 
nutritive arteries are branches of these, and penetrate from them 
Fig. 211. 
I & 1 
Arteries of the brain showing cortical distribution. A, a tertiary branch of main artery. 
B, primary twig. C, C, G, secondary twigs. The nutritive arteries are seen to pass off from 
all these branches as fine hair-like offsets. (Ross, after Duret.) 
into the substance of the brain. We may thus distinguish [the 
larger arteries of the surface and the smaller or nutritive arteries. 
The nutritive arteries again are divisible into two groups, 
which may he designated the cortical and central systems. 
The nutritive arteries of the cortex pass off not merely from 
the finer twigs of the larger arteries, but also from the larger 
branches (see Fig. 211). They are fine thread-like vessels which 414 
DISEASES OF THE NERVOUS SYSTEM. 
pass down perpendicularly into the brain substance. Some of them 
are short and supply the gray substance of the convolutions, others 
are longer and reach the white substance, their territory here 
extending to the boundaries of that of the central arteries. In 
stripping the membranes from the surface of the brain these nutri- 
tive arteries are seen like fine hairs emerging from the brain sub- 
stance. If a portion of the soft membranes be nowr floated in 
water these fine vessels wall be seen like bristles passing from all 
the branches. All the nutritive arteries are end-arteries. 
The central nutritive arteries have a somewdiat different 
arrangement from those of the cortex. They are long vessels of 
larger calibre than the cortical ones, and they pass off' from the 
main arteries very near their origin. The most important are 
those vdiich come off' from the middle cerebral just outside its 
origin and pass through the anterior perforated space to the basal 
ganglia. Of these, three sets of branches have been distinguished: 
(1) short twigs lying internally vdiich pass to the internal parts of 
the lenticular nucleus, the lenticular branches; (2) a longer and 
larger vessel wdiich lies outside the first and supplies the outer 
parts of the lenticular nucleus with adjoining parts of the internal 
capsule and caudate nucleus. This branch, the lenticulo-striate 
branch, is the most important, as being most frequently the seat of 
hemorrhage; (3) the lenticulo-optic branch is posterior to the former 
and supplies the posterior part of the lenticular nucleus and the 
anterior part of the optic thalamus. The remaining central 
branches are supplied by the anterior and posterior cerebral 
arteries. The former sends branches which supply the anterior 
part of the caudate nucleus, and the latter sends tw?o sets, an 
internal and an external, to the optic thalamus. All these central 
arteries are end-arteries. 
The arteries of the pons and medulla oblongata are like the 
cortical arteries in their small size and like the central ones in 
respect that they come off from large stems, and pass directly into 
the substance of the part. 
SECONDARY DEGENERATION IN THE BRAIN. 
We have already seen in the case of the cord and medulla ob- 
longata that when the nerve-fibres are cut off from their trophic 
centres they undergo degeneration. In the brain it is only the 
pyramidal tract (see p. 407) that is the seat of this secondary 
change. The trophic centres of the pyramidal tract appear to he 
in the motor convolutions, and when the fibres are interrupted at 
any point below this, a secondary degeneration follows. The in- 
terruption is most commonly effected by hemorrhage or softening 
in the region of the corpus striatum, and it is the fibres which 
form the internal capsule which are here concerned. Destruction 
of the internal capsule at any part of its extent, except the poste- 
rior fourth or third (which contains sensory fibres), will cause a THROMBOSIS AND EMBOLISM OF CEREBRAL VESSELS. 
415 
descending degeneration in parts succeeding. If of long standing, 
there may be great shrinking of the portion of the pyramidal 
tract involved (see Fig. 212). It appears also that the fibres which 
form the internal capsule keep nearly the same arrangement from 
before backwards in the crura, pons, and medulla oblongata that 
they have in the capsule. The destruction may involve the whole 
Fig. 212. 
Pons in descending sclerosis. The pyramidal tract on the left side is seen to be 
shrunken and in a state of gray degeneration. 
internal capsule, or only a limited part of it, and the degeneration 
will be similar in extent. The posterior part of the internal cap- 
sule and the corresponding portions of the crura and pons being 
sensory, are not liable to descending degeneration. 
THROMBOSIS AND EMBOLISM OF THE CEREBRAL VESSELS. 
In considering the various conditions included here, it should be 
borne in mind that the arteries of the circle of Willis anastomose 
freely. The arteries in the meninges also anastomose, but much 
less freely, while the nutritive arteries, both those given off to the 
basal parts of the brain and those of the convolutions, are end- 
arteries. These facts are of great importance in relation to the 
effects of occlusion. 
Embolism in the arteries of the brain occurs in the great ma- 
jority of cases in connection with acute endocarditis or valvular 
disease of the heart from chronic endocarditis. In the former case 
the embolus is a piece of fibrine broken off from the inflamed 
aortic or mitral valve; in the latter cash it is mostly a piece of cal- 
careous matter from the indurated and calcified curtain. Besides, 
we may have globular thrombi in the left auricle or ventricle be- 
coming detached, or softening, and so giving rise to plugging. So 
also may thrombi in the aorta become detached and carried off. 
Much more rarely do emboli come from the lungs, but sometimes 
in gangrene of the lungs there is a thrombosis of the veins, and 416 
DISEASES OF THE NERVOUS SYSTEM. 
from bits of fibrine carried off we may have septic embolism of 
the brain. It is conceivable also that a cancer of the lungs may 
produce embolism by penetrating into the pulmonary vein. 
It is matter of general observation that in cerebral embolism the 
middle cerebral artery (or artery of the fissure of Sylvius) is the 
vessel plugged in the great majority of cases. It is also stated 
that the left middle cerebral is more frequently the seat of em- 
bolism than the right, but this has been doubted by competent 
observers. The frequency with which the middle cerebral is 
affected admits of easy explanation. As the vertebral artery 
arises from the subclavian nearly at a right angle, it is not com- 
mon for an embolus to pass into it. But the innominate and the 
carotid, being nearly in the direct line of the current from the 
aortic orifice, readily receive any fragment. Then again, the 
middle cerebral is the direct continuation of the internal carotid 
and an embolus will more readily sweep into it than diverge for- 
ward or backward. It is important here to bear in mind that the 
middle cerebral supplies the greater part of the basal ganglia, in- 
cluding nearly the whole of the corpus striatum and internal cap- 
sule and a part of the thalamus opticus. It also supplies the 
greater part of the motor convolutions. 
Thrombosis arises in consequence of some alteration of the 
walls of the arteries. It is predisposed to by weakness of the 
heart, but mere sluggishness of the circulation so induced will 
hardly cause thrombosis in a healthy artery, although it may do 
so in the venous sinuses of the dura mater, where the circulation 
is naturally so much slower. Thrombosis is mostly induced either 
by atheroma or by syphilitic disease of the arteries. In both 
cases the internal coat is thickened, and the surface is rough, 
while the calibre of the artery is already considerably encroached 
on, as Fig. 213 shows. Atheroma occurs mostly in old persons, 
and it is usually most pronounced in the larger arteries of the 
base, where there may be numerous yellow patches. But not in- 
frequently it extends to the finer ramifications, and it is in these 
that it most readily leads to occlusion by thrombosis. The artery 
from which the figure is taken, for instance, had an external 
diameter of the eleventh of an inch. Syphilitic disease of the 
arteries, on the other hand, occurs most frequently in younger 
people in connection with gummata, and these may occur at any 
part of the surface of the brain. 
Effects of Occlusion of Arteries in the Brain.—Here, as in 
other parts, the effects of occlusion depend chiefly on whether the 
arteries concerned are end-arteries or not. The arteries of the 
circle of Willis anastomose freely, and occlusion of them leads 
only to a very temporary derangement of the circulation. The 
larger branches anastomose sparely, and occlusion of them has 
much more serious effects. The nutritive arteries do not anasto- 
mose at all, and occlusion of them lias very evil results. 
The most direct result of occlusion of arteries is anaemia of the THROMBOSIS AND EMBOLISM OF CEREBRAL VESSELS. 
417 
part supplied. As the occlusion in the case of embolism is sudden, 
there is often a very abrupt interference with the cerebral functions. 
In the case of a large artery such as the main stem of the middle 
cerebral, there may be a very extensive amemia, leading to a fatal 
issue before the anastomosing circulation can be established. 
A more important result is softening of the brain substance. 
This, as we have previously seen, is really a necrosis with fatty 
Fig. 213. 
Atheroma of a small cerebral artery the eleventh of an inch in diameter, with thrombosis. 
b, atheromatous internal coat; c, thrombus on its surface partially organized. Between 
these two is an irregular clear space, which represents fresh blood which had been insinu- 
ated between patch and thrombus, d, remaining calibre filled with blood. X 34. 
degeneration of the nervous tissue, and it only occurs whenk the 
conditions are such that the circulation is brought absolutely to a 
standstill. This is the case when any of the nutritive arteries are 
obstructed, as these are end-arteries. The nutritive arteries which 
come off from the first part of the middle cerebral are the most 
exposed to obstruction from embolism, and hence softening of the 
central parts of the brain, especially in the region of the corpus 
striatum, is of somewhat common occurrence. It is important to 
notice that, for reasons to be afterwards considered, it is these 
arteries also which most frequently give rise to hemorrhage. But 
softening not infrequently occurs although the vessels occluded 
are not end-arteries. This is especially true where thrombosis is 
the cause of the occlusion. As we have already seen, thrombosis 
is common in connection with atheroma. ISTow this is a disease 
of old people, in whom the circulation is weak. Under these 418 
diseases of the nervous system. 
circumstances occlusion of a small peripheral artery may lead to 
softening, before the force of the blood has brought about an 
anastomosing circulation, all the more because many of the 
neighboring arteries are also partially obstructed by atheroma. 
Even in the case of embolism there may be considerable cortical 
softening if the embolus has broken up and plugged several vessels 
at the same time, so as to interfere with the establishment of the 
anastomosing circulation. 
Another occasional effect of the occlusion is hemorrhage. It is 
seldom that the proper hemorrhagic infarction is produced here, 
but it often happens that some blood is mixed with the softened 
brain substance, producing a yellow or red softening. 
Occlusion of Arteries in Chorea.—The frequent association of 
this disease with acute endocarditis has suggested the view that it 
may have its origin in embolism of the arteries and capillaries of 
the brain, multiple embolism with softening having been found in 
some cases, but not in all. According to the observations of 
Dickinson the most constant changes in chorea are dilatation of 
the arteries and veins throughout the substance of the brain and 
spinal cord, exudations or small hemorrhages, sometimes with 
blood-crystals around the vessels, and in chronic cases sclerosis in 
the neighborhood. These changes are most pronounced in the 
corpora striata and optic thalami, and in the gray substance of the 
spinal cord, especially near the junction of the posterior cornua 
with the central parts of the gray substance. They are most 
marked in the dorsal and cervical regions of the cord. 
It seems probable that in chorea there is an irritant present in 
the blood, and it may be the same irritant as that in acute rheu- 
matism. It attacks the nervous system, producing hypersemia and 
exudation from the vessels. While the whole central nervous 
system is more or less affected there are certain parts specially in- 
volved, these parts being what have been called the accessory 
portions of the nervous system. It may be supposed that the fun- 
damental and simpler parts of the brain and cord are more stable 
than the accessory parts, and that when attacked by an irritant the 
latter will give way first. The anatomical distribution of the 
lesions suggests that this is so, and the symptoms of chorea indicate 
disorder in “movements which are acquired, and which are 
probably only .learned by a long apprenticeship” (Hughlings 
Jackson). 
Thrombosis of the Cerebral Sinuses.—These venous channels 
are somewhat frequently the seat of thrombosis. The coagulation 
may have its starting-point in an inflammation propagated from a 
neighboring structure. The most frequent origin of such inflam- 
mations is caries of the temporal bone from disease in the ear, but 
it may follow on injury to the head, inflammations of the skin of 
the face and scalp, especially erysipelas, and of the bones. In all 
these cases the thrombosis usually has its starting-point towards CEREBRAL HEMORRHAGE. 
419 
the base of the skull, and especially in the lateral and petrosal 
sinuses. 
There is, however, another class of cases in which the throm- 
bosis has a more obscure origin, and seems sometimes even 
spontaneous. The blood simply coagulates in the sinus, and it is 
usually in the longitudinal sinus that the coagulation begins. In 
most of these cases the person is in a state of debility, and the 
thrombus may be regarded as marasmic in its origin. But there 
are cases in which there is no obvious weakness of the heart, and 
the coagulation has no apparent cause. The localization of the 
thrombosis suggests stagnation of the blood as its cause. The 
sinuses are rigid tubes incapable of narrowing when the circula- 
tion is slow, and they are intersected by bands of connective tissue. 
The longitudinal sinus also is so situated that, at its middle part at 
least, the blood passing from the cerebral veins flows upwards to it 
against the force of gravitation. 
The effects of thrombosis of the sinuses will vary according to 
the cause. If due to the propagation of inflammation from 
neighboring structures, then a suppurative phlebitis may result, 
with meningitis, and even abscess of the brain. There are, how- 
ever, cases of abscess of the brain without meningitis, in which 
the inflammation seems to have extended along the veins either in 
their interior or in their sheath. 
In the other form the results are usually much less serious. The 
veins which open into the sinus are greatly engorged, and the 
thrombosis may extend into them. It is here chiefly the longitu- 
dinal sinus that is concerned, and the veins which open into it are 
those of the cerebral hemispheres. These may stand out as 
prominent worm-like cords filled with dark coagula. In most 
cases the blood finds its way by other routes, and there may even, 
after a time, be a reestablishment of the circulation in the sinus. 
Sometimes, however, the obstruction in the veins is such as to 
lead to hemorrhage. This is usually in the form of numerous 
capillary hemorrhages, but sometimes there is along with this a 
large effusion of blood in the substance of the brain and under the 
soft membranes. The seat of such hemorrhages is usually the 
superficial and upper parts of the hemispheres, and they are fre- 
quently multiple. 
CEREBRAL HEMORRHAGE. 
By this term is meant bleeding in the substance of the brain. 
The blood may be large or small in quantity but it pushes aside 
the brain substance, tearing for itself a cavity where it coagulates. 
With the doubtful exception of certain diseases of the blood, 
where the hemorrhage may possibly he by diapedesis, there is 
always rupture of one or more vessels. 
In a previous page reference has been made to the two orders of 
cerebral arteries, and the difference in the circumstances of hemor- 420 
DISEASES OF THE NERVOUS SYSTEM 
rhages from these are such that we must consider them separately 
here. 
(1) Hemorrhage from the Larger Cerebral Arteries.—We 
have seen that these vessels run in the soft membranes, and it 
might be supposed that their rupture would give rise to meningeal 
rather than cerebral hemorrhage, and so it is usually stated. But 
this is not the case. The blood nearly always finds irs way into 
the brain substance, where it is found usually in much larger 
quantity than in the meninges, so that the case has much more the 
characters of cerebral than of meningeal hemorrhage. There is 
usually some blood in the meninges occupying the sulci between 
the convolutions, and it may even be considerable, extending to 
the base and perhaps covering the optic commissure; but usually 
the amount is small, and on account of the large cerebral hemor- 
rhage is apt to be overlooked. It is very rare indeed for the blood 
to escape towards the surface and appear in the cavity of the dura 
mater. Any appearance of blood in the meninges, however, should 
at once direct attention to the larger cerebral arteries as the prob- 
able source of the hemorrhage. 
The explanation of the extension of the blood into the brain sub- 
stance suggests itself when we consider the circumstances of the 
parts. When rupture of such an artery occurs the blood tears its 
way around; it passes into the loose connective tissue, and by and 
by reaches the surface of the brain. Here the tissue, being soft, 
tears readily, and the blood rapidly passes inwards. On the other 
hand the connective tissue on the surface is tough and the blood 
will tear it with difficulty. The blood may work its way from 
space to space in the connective tissue, but this takes time and 
probably needs considerable pressure. There is another circum- 
stance which probably has to do with the blood so constantly 
finding its way into the brain substance. As we shall see after- 
wards, a large number of the cases of hemorrhage in this situation 
are from rupture of aneurisms. How an aneurism will probably 
project more readily towards the surface of the brain where the 
substance is soft than in other directions, and when such an 
aneurism ruptures it may do so directly into the brain. 
The causes of the rupture of these larger arteries are to be sought 
for in disease of their walls and increase of the blood-pressure. 
The commonest cause is aneurism of these arteries, which is of 
remarkably frequent occurrence. The great majority of the cases 
of cerebral hemorrhage occurring before the age of fifty years is 
due to the rupture of aneurisms of these larger arteries. The 
aneurisms are mostly thin-walled and therefore prone to rupture. 
Their most frequent seat is on the middle cerebral artery or one of 
its branches in the fissure of Sylvius, but they may occur on any 
of the arteries of the brain and are not infrequently multiply. 
The frequent occurrence of these aneurisms and their serious 
import suggests an inquiry into the causes of their formation. In cerebral hemorrhage. 
421 
the first place the arteries are thin-walled and are placed in a loose 
tissue, so that they very readily undergo dilatation. Any local 
injury to the wall may he the starting-point to the dilatation. 
This is often produced by embolism. In a large proportion of cases 
the aneurism is associated with valvular disease of the heart, and 
an embolus imperfectly obstructing an artery, especially if it be a 
cretaceous piece broken off from a valve, may readily injure the 
wall so as to allow of dilatation. Ponfick has found that in a con- 
siderable proportion of cases of acute endocarditis there is embolism 
with either fully formed or incipient aneurisms. When they have 
an origin such as this the aneurisms will be specially thin-walled 
and partake of the characters of false aneurisms. This mode qf 
origin also goes far to explain the greater predominance of these 
aneurisms in the middle cerebral artery, which, as we have seen, 
is especially liable to embolism. Another occasional cause of 
cerebral aneurism is atheroma. This disease injures the vessel-wall 
and produces obstruction, and it may lead to aneurism on the one 
hand by weakening the wall, and on the other by locally increasing 
the blood-pressure on the peripheral side of the obstruction. 
Syphilitic disease is also assigned as a cause of aneurism. 
The subject of atheroma as a direct cause of cerebral hemor- 
rhage is a somewhat difficult one. This condition is undoubtedly 
in many cases associated with cerebral hemorrhage, but it is diffi- 
cult to believe that it can be the sole cause. Atheroma produces, 
as Fig. 213 shows, a thickening of the arterial wall. At the same 
time, however, it weakens the wall, and if the coats get separated 
and the blood penetrates behind the atheromatous patch, there 
may be serious risk of rupture. Besides this, atheroma will, as 
mentioned above, produce, by obstructing the vessel, an increase 
of blood-pressure on the proximal side of the patch and also in 
neighboring arteries. If there be extensive atheroma, the mere 
rigidity of the arteries may produce an increase of blood-pressure 
in the smaller arteries. But all these conditions seem scarcely 
capable by themselves of leading to hemorrhage, and it is in cases 
where atheroma is associated with a general increase of blood- 
pressure that this occurs, especially in chronic Bright’s disease. 
On the other hand increase of blood-pressure alone can hardly 
lead to hemorrhage. In chronic Bright’s disease there is fre- 
quently a constant increase in the arterial tension, and Irypertrophy 
of the left ventricle of the heart. This condition will conduce to 
hemorrhage in both orders of arteries in the brain, especially if 
this disease be associated with atheroma, or with fatty degenera- 
tion of the smaller arteries of the brain, which some assert to be 
common in Bright’s disease. 
(2) Hemorrhage frOxM the Nutritive Arteries.—As these 
vessels run in the substance of the brain the hemorrhage will be 
always cerebral and will rarely extend to the meninges. It might 
be supposed that as the nutritive vessels are small the hemorrhage 
from them would be small, and in many cases it is so; but when 422 
DISEASES OF THE NERVOUS SYSTEM. 
bleeding has once begun, the blood tearing the brain substance 
ruptures other vessels, and there is often a considerable effusion of 
blood. 
Hemorrhage rarely occurs from the cortical nutritive vessels, 
but is very common from the central ones. The circumstances of 
these latter go far to explain this. They arise from large stems, 
mainly from the middle cerebral immediately after its origin from 
the internal carotid. It is clear that the blood here will be at a 
pressure not much less than that of the aorta, and any variations 
of pressure will tell readily. On the other hand, the cortical 
vessels mostly arise from fine vessels in which the blood-pressure 
has been reduced by successive division and subdivision. 
As to the causes of hemorrhage in these arteries, aneurism 
again plays the most important part. As the arteries are small so 
are the aneurisms, but they are numerous in the same person. 
Such aneurisms have been called by Bouchard and Charcot 
miliary aneurisms. They occur in every region of the brain, 
but are most readily detected on the surface of the convolutions, 
where, on stripping off the pia mater from the convolutions, they 
may be seen as small red or brown spots. When examined under 
the microscope they have all the characters of ordinary aneurisms. 
Most of them are sacculated (Fig. 214), but some are fusiform 
Fig. 214. 
Sacculated miliary aneurism of a nutritive artery of the brain. The aneurism is about the 
twentieth of an inch in diameter. X 27. 
(Fig. 215). It is stated that the cause of their formation is a 
sclerosis of the walls of the arteries, involving first a formation of 
round cells in the external coat with subsequent fibrous trans- 
formation. There results an atrophy of the middle coat which 
seems to be the most direct cause of the dilatation. This diffused 
sclerosis of the nutritive arteries is mostly met with in old people; CEREBRAL HEMORRHAGE. 
423 
in persons above fifty cerebral hemorrhage is, in the larger pro- 
portion of cases, due to rupture of miliary aneurisms. 
Although the aneurisms are present in all regions of the brain, 
rupture seldom occurs except in those of the central arteries. The 
Fig. 215. 
Fusiform miliary aneurism. X 27. 
explanation of this has already been indicated, and it has been 
mentioned that the lenticulo-striate branch is preeminently that 
from which hemorrhage occurs. 
Atheroma, with increased blood-pressure, is occasionally a cause 
of hemorrhage from the nutritive arteries as from the larger ones. 
Atheroma is not common in small arteries, but as the central 
nutritive arteries are much larger than the cortical ones, atheroma 
is commoner in them, and hemorrhage from this cause is there- 
fore, for a double reason, more frequent in these. 
(3) Hemorrhage from the Capillaries.—A certain amount of 
capillary hemorrhage generally accompanies all larger bleedings. 
The explanation of this seems to be that the pressure of blood 
produces such obstruction of the vessels around that frequent 
leakage occurs from the capillaries. In the case of thrombosis of 
the sinuses and veins also, there is capillary hemorrhage. Again, 
embolism may cause a capillary hemorrhage, and, as we have 
seen, the blood is often mixed with the softened brain-tissue. 
Septic embolism as in ulcerative endocarditis, and pyaemia, leads 
to capillary hemorrhage. Lastly, we may have leakage from the 
capillaries in scurvy, purpura, and other morbid states of the blood. 
In capillary hemorrhages the collections of blood are generally 
small in size, forming a congeries of red puncta. But if very 
frequent and closely set they may run together and form a con- 
siderable effusion. 
Appearances of the Brain in Hemorrhage.—The appearances 
presented when a person dies soon after the occurrence of hemor- 
rhage are sufficiently characteristic. The effused blood increases 
the contents of the skull, and in order to its accommodation there 
must be some displacement and crushing of the remaining brain- 424 
DISEASES of the nervous system. 
substance. If the hemorrhage be at all extensive, we find on 
opening the skull that the corresponding hemisphere is bulged 
outwards and perhaps projects beyond the middle line. The con- 
volutions are more or less flattened, and there is a certain dryness 
and glazing of the surface which indicates that all available fluid 
has been absorbed to make room for the addition made to the 
contents of the skull. These are all indications of increased 
pressure within the skull, and during life this increase of pressure 
causes symptoms referrible to the brain as a whole or to parts 
removed from the seat of hemorrhage. It sometimes happens that 
the appearance of blood in the membranes suggests the existence 
of hemorrhage before the brain is laid open, and this will be 
especially the case when rupture of an aneurism, or thrombosis in 
the sinuses, has been the cause. On cutting into the brain-sub- 
stance the appearances will vary to some extent according to the 
cause and extent of the hemorrhage. If there are numerous small 
hemorrhages closely set there will be much softening of the brain, 
and the brain-substance will be mixed with blood. If the hemor- 
rhage be large the blood will be more pure. In any case the blood 
produces softening in the parts around, which may be stained with 
the blood-coloring matter. As already mentioned, there are usually 
red spots from capillary hemorrhage around the clot. The clot 
itself is mixed with the debris of brain-substance, and the internal 
wall of the cavity in which it lies has an irregular character. 
If the patient die almost immediately, the clot is exactly like an 
ordinary gelatinous coagulum. But if he survive a day or two, it 
has already drawn together somewhat and become firmer and 
more of a brown color. This is sometimes peculiarly manifest at 
the peripheral parts of the clot, so that a kind of capsule may be 
formed of condensed fibrine. 
Organization of the Clot. The apoplectic cyst.—The further 
organization of the coagulum is a slow process, and proceeds very 
much in the same way as organization of clots inside or outside of 
vessels. An inflammatory process is set up in the neighborhood, 
and this results in the production of connective tissue which by 
and by encapsules the clot. The clot in the mean while softens ; 
its pigment is dissolved out, and frequently deposited in the crystal- 
line (see Fig. 216) or granular form in the softened material or in 
the capsule, often giving the parts a rosy or rusty color. The 
blood being frequently mixed with brain-substance, and both these 
constituents being degenerated, various appearances are presented ; 
sometimes the capsule contains material of an atheromatous aspect. 
Through time, however, the contents tend more and more to 
absorption, and being replaced by clear fluid a cyst is the result, the 
so-called apoplectic cyst. This cyst is not merely a simple sac 
containing fluid, but it is generally intersected by connective-tissue 
trabeculae so as to appear to be filled with a network. Very often 
some crystalline or granular pigment is met with in the wall of 
the cyst. It is to be remarked that cysts which in their later SOFTENING OF THE BRAIN. 
425 
stages are indistinguishable from those now under consideration 
may have their origin in softening of the brain, especially as a 
result of embolism. It will be seen that the apoplectic cyst may 
be compared in its origin with a cicatrix; it arises by the forma- 
tion of connective tissue and fills the place of tissue lost, and it is 
Fig. 216. 
Crystals of hsematoidin from a cerebral hemorrhage. The crystals form oblique rhombic 
pillars of a reddish-brown color. X 350. 
only because, being situated in the midst of the brain-substance, 
it does not readily contract that we have a cyst rather than a 
cicatrix. If the hemorrhage has been near the surface of a ventricle 
or of the brain itself, we may have a cicatrix instead of a cyst; or 
a cyst by thickening of the trabeculae and gradual drawing together 
of the parts may be converted into a cicatrix. In the case of cica- 
trices occurring thus on the surface of the brain the soft mem- 
branes are depressed and puckered and firmly adherent to them. 
The cicatrices, like the cysts, often present some remains of blood- 
coloring matter. 
SOFTENING OF THE BRAIN (RAMOLISSEMENT). 
This subject has already been several times considered incident- 
ally. We have seen that localized softenings occur in connection 
with embolism and thrombosis of the cerebral arteries, and in 
addition to this there is softening in connection with inflammation, 
sometimes going on to the formation of abscess. Lastly, there is 
a softening to be referred to in studying tubercular meningitis. 
We have here to consider the character of the changes which 
occur in the brain substance in the simple softenings, apart from 
those of inflammation or tubercular meningitis. 
As these softenings occur mainly in connection with the occlu- 
sion of arteries, the affected piece of brain substance is limited to 
the distribution of the artery concerned. In the case of embolism 
it will nearly always be situated in the region supplied by the 
middle cerebral artery, and especially in the central parts, the 
more direct central nutritive arteries being much more frequently 
the seat of embolism than the cortical ones. 
Softenings have often been distinguished according to the color 426 
presented by the affected brain substance, so that white, yellow, 
and red softenings have been described. For the most part the 
color depends on the blood mixed with the nervous tissue, and 
the amount and condition of the former can hardly be regarded as 
a chief characteristic of the softening, and the color is therefore 
not of primary importance. 
We have already seen that softening of the brain substance is 
really due to a necrosis. The result of the death of the nervous 
structures is their disintegration. The nerve-fibres very rapidly 
break up; the myeline of the medullary sheath coagulates and 
escapes from the primitive sheath, and afterwards breaks up into 
fine fat-granules. The ganglion cells are more resistant, but they 
also become granular and gradually disappear. The cells of the 
neuroglia and the nuclei of the walls of the vessels undergo a 
change which appears at first sight to be a fatty degeneration, but 
which very probably has, to some extent, a different significance. 
These structures become filled with finely divided fat, so that the 
neuroglia cells are converted into characteristic compound gran- 
ular corpuscles and the nuclei of the vessels are converted into 
aggregates of fat-granules at intervals along the vessels (Fig. 217). 
DISEASES OF THE NERVOUS SYSTEM. 
Fig. 217. 
Fatty degeneration of the vessels in cerebral softening. (Paget.) 
So far as the neuroglia cells are concerned it is probable that they 
pick up the fat arising from the disintegrated myeline. It is not 
so clear that the nuclei of the bloodvessels do this, and there is 
here, more probably, a fatty degeneration of them. Besides the 
neuroglia cells there may be present in the part amoeboid cells, or 
these may pass into it after the occurrence of the necrosis, and 
these also take up the granular fat. In this way they are, fre- 
quently, large numbers of compound granular corpuscles which 
are very conspicuous when a piece of the softened tissue is 
examined in the fresh state under the microscope. 
In some cases, as already mentioned, the softened brain substance ACUTE LOCALIZED ENCEPHALITIS. 
427 
is largely mixed with blood, especially in embolic softening. At 
first the blood gives a red color to the softening. But as time 
goes on the coloring matter is dissolved out of the red corpuscles 
and diffused throughout the softened structures, as well as to some 
extent in the brain substance around. In that case the color 
becomes less intense and merges into yellow, or the color may be 
reddish-yellow from the outset. It will be seen from this that red 
and yellow softening run together, and that the latter is often 
merely a later stage of the former. At the time when the soften- 
ing occurs the vessels are often filled with blood, which soon 
coagulates. The fibrine disintegrates as the coloring matter is dis- 
solved out from the corpuscles. Sometimes the dissolved coloring 
matter is deposited in the granular or even in the crystalline form 
inside or outside the vessels. If there is very little blood in the 
vessels of the softened part, then the color is white or gray. This 
is mostly seen when death has occurred very soon after the occlu- 
sion of an artery. 
The ultimate disposal of the necrosed piece of brain-substance 
occurs on principles already considered. The softened brain-sub- 
stance has ultimately the characters of a fatty emulsion, which is 
gradually absorbed. A chronic inflammation occurs around, just 
as in the case of a hemorrhage, and in a similar fashion connective 
tissue is produced, taking the form of a cyst or a cicatrix, accord- 
ing to circumstances. The resulting cyst or cicatrix is not always 
to be distinguished from that of a cerebral hemorrhage. Usually 
the latter presents more distinct pigmentation, but the former may 
also present pigment-granules and crystals. 
INFLAMMATIONS OF THE BEAIN. 
These embrace a very extensive and varied set of conditions, 
some of which have little in common. Thus there are localized 
inflammations of an acute kind, going on sometimes to the forma- 
tion of abscesses; chronic localized inflammations; inflammations 
diffused throughout the brain; inflammations extending to the 
brain-substance from the membranes, etc. 
(1) Acute Localized Encephalitis.—We have already seen 
that, around and in the midst of hemorrhagic foci and cerebral 
softenings, there are inflammatory manifestations, evidenced by 
the presence of leucocytes, which take up fat-granules. The in- 
flammatory process does not go on to suppuration, but results in 
the formation of connective tissue, constituting a cyst or a cicatrix. 
When the brain is injured traumatically—lacerated, for example, 
by a blow on the head or directly wounded by a protruding piece 
of fractured bone—then there is usually a more intense inflamma- 
tion, which may go on to suppuration, especially when the brain 
communicates with an external wound. The brain may be con- 
siderably lacerated without any external wound or fracture of the 428 
DISEASES of the nervous system. 
skull, especially by falls on the head. In that case, when the head 
lights on the ground, the soft brain is, as it were, propelled against 
the dense skull which has been suddenly arrested, the laceration 
being brought about by contre coup. In all these cases the mere 
injury to the brain induces a certain amount of inflammation, re- 
sulting in an aggregation of leucocytes. Usually the ultimate 
result is the formation of a cicatrix or a sclerosis of the portion of 
brain-substance, but there may be suppuration, in which the mem- 
branes of the brain take part. 
Inflammation of the brain may result in abscess, but almost 
alone in septic cases. An injury to the brain communicating with 
a septic wound may have this result. More frequently the primary 
disease is caries of the bones of the skull, and especially of the 
temporal bone. The great majority of cases of abscess of the 
brain are connected with suppuration of the middle ear, very often 
of prolonged duration dating, it may be, from a scarlatina years 
before. There is most danger of abscess when caries exists in the 
petrous portion of the temporal bone; but even without caries an 
abscess may form. The abscess is due to a septic inflammation 
extending directly from the affected parts inwards. Some of the 
veins from the temporal bone pass inwards to the lateral sinus, 
and a septic process may be propagated along the sheath of these 
veins to the dura mater. This explains cases in which abscess of 
the brain is associated with inflammation of the dura mater, and 
is localized in the neighborhood of the temporal bone. But, in 
some cases, the path of propagation is more obscure, and an 
abscess is present in the midst of the brain-substance, separated 
from the temporal bone by sound tissue. Abscesses sometimes 
occur by propagation from the nose, the antrum of Highmore, and 
the orbit. 
In the early stages of abscess there is softening of the brain- 
substance, which is infiltrated with leucocytes. But the conditions 
hardly offer themselves to observation in this stage. The fully 
formed abscess is generally of old standing, and has been of slow 
growth. It contains thick, yellow pus, generally with a very offen- 
sive smell. The pus-corpuscles are usually cedematous and fatty, 
and altogether ill preserved. The abscess may be surrounded by 
softened brain-substance, but most usually there is a dense capsule 
surrounding it so that it can be enucleated by tearing away the 
capsule. The capsule is composed of inflammatory tissue, partly 
in the state of granulation tissue, but partly as connective tissue. 
This capsule, to a certain extent, represents sclerosed brain-sub- 
stance, but outside the capsule the brain-substance is frequently 
softened so as to allow of its enucleation. Abscesses may burst 
into the ventricles of the brain, or on to its surface. 
(2) Chronic Localized Encephalitis.—The processes of chronic 
inflammation here are similar to those in the spinal cord, and the 
result here, as there, is sclerosis. In the case of the brain there diffused encephalitis. 
429 
is hardly anything of the systematic sclerosis so frequent in the 
•cord. There is, however, one form of disease which affects both 
brain and spinal cord, and which presents some analogies with the 
systematic scleroses of the cord. 
Disseminated Sclerosis, or Sclerosis in Patches, is character- 
ized by the occurrence of patches of chronic inflammation scat- 
tered over the cord, or the brain, or both. These patches have 
all the characters of sclerosis; in the white substance they are 
gray, and in both white and gray substance they produce indura- 
tion and shrinking. Under the microscope the sclerosed white 
substance shows loss of the medullary sheaths of the fibres, while 
the axis-cylinders, according to Charcot, are largely retained. In 
the gray substance, the ganglion cells are shrunken sometimes 
with pigmentation. At the peripheral parts of the patch there 
may be evidences of more active inflammation, in the form of 
abundant round cells along with compound granular corpuscles. 
The distribution of the patches is somewhat irregular. They 
are found of various sizes in the cord, medulla oblongata, pons, 
peduncles, corona radiata, convolutions, cerebellum. In such 
various situations the sclerosis leads to very various functional dis- 
turbances. The great frequency of motor tremors, however, sug- 
gests some tendency to localization. Erb has pointed out that 
when tremors exist, patches are specially present on the pedun- 
cular parts (pons, medulla, peduncles). If patches are seated there, 
the motor impulses will be imperfectly conducted but not abso- 
lutely interrupted, as the axis-cylinders are preserved. 
(3) Diffused Encephalitis.—This term may be applied to con- 
ditions in which there is a general irritation of the brain, pre- 
sumably by some irritant circulating in the blood. It may be 
held to include a considerable number of varied conditions. As 
the irritant, being in the blood, will attack all parts equally, we 
may expect to find evidences of irritation in the spinal cord as 
well as in the brain. 
In the delirium of fevers it may be presumed that the brain is 
irritated by the morbid condition of the blood. According to 
Popoff, there are visible evidences of this in the case of typhoid 
fever in the presence of abundant leucocytes. These are stated 
to be particularly abundant around the vessels, and evidently 
spreading out from these. The leucocytes were frequently found 
in the spaces around the ganglion cells (pericellular lymph spaces), 
and even, in some cases, in the substance of the ganglion cells. 
These conditions indicate the presence of an irritation of the brain. 
Then Middleton has pointed out that in delirium tremens, tuber- 
cular meningitis, uraemia, fracture of the skull with injury to the 
brain, erysipelas, etc., the brain substance is overrun with leuco- 
cytes, the appearances being very similar to those which will be 
described as occurring in hydrophobia. In all cases where irrita- 
tion of the nervous centres is evidenced during life, these signs of 
irritation may be looked for in the brain after death. 430 
diseases of the nervous system. 
Condition of the Brain in General Paralysis of the Insane 
(.Dementia ■paralytica).—The condition of excitement with which, 
many cases of insanity begin, suggests irritation of the cerebral 
centres; but it is very difficult to determine the exact relation of 
the conditions here, especially as the cortex of the brain is very 
intricate in its structure and difficult to disentangle. In general 
paralysis the disease is usually in an advanced stage before the 
death of the patient, but it begins with acute symptoms, such as 
epileptic attacks and acute mania, and death sometimes occurs at 
this period. Meyer has recorded the results of observation in 
twenty cases of this kind, in which the disease began with head- 
ache and went on to maniacal outbreaks which he compares with 
the delirium of fever. lie asserts that death occurs more fre- 
quently in this stage than is generally supposed, but that the cases 
are very often not recognized as such. 
In these cases, after death there was the appearance of a general 
swelling of the brain, the convolutions being more voluminous, 
and the sulci smaller, while the gray substance presented a lively 
red appearance, frequently mottled and with multiple minute 
softenings. On microscopic examination the bloodvessels in the 
cortical substance were found engorged with blood, and around 
them leucocytes in abnormal quantity. Leucocytes were also 
abundantly present in parts removed from the vessels. This con- 
dition was seen mainly in the cortex, but also spreading to the 
white medullary substance. The vessels themselves had under- 
gone changes; in the most acute periods the principal change was 
fatty degeneration of the wall, visible chiefly in the capillaries. 
There were also minute hemorrhages, the blood often getting 
through the internal and middle coats, but accumulating inside 
the external so as to form a kind of dissecting aneurism. These 
minute dissecting aneurisms may be best detected (according to 
Rindfleisch) by carefully separating out the vessels from the surface 
iuwards under a stream of water. 
In the more chronic periods of the disease the appearances are 
those rather of degenerative than of active processes, but the 
degenerative are presumably secondary to the inflammatory, the 
disease having very much the characters of an interstitial cerebritis 
with loss of the proper nervous tissue as a consequence, a cirrhosis 
of the brain. 
The appearances of the brain as a whole are very suggestive of 
such a condition, especially if, as mostly happens, the case has 
been of some duration. The appearances are prominently those 
of atrophy of the brain. On removing the calvarium the dura 
mater is commonly found wrinkled over the frontal lobes, evidently 
from shrinking, but not necessarily of these lobes, because the 
position of the head causing the brain to gravitate backwards 
would probably make the shrinking tell anteriorly whatever its 
locality. On removing the dura mater a very manifest oedema of 
the membranes of the brain presents itself. There is also disten- 
tion of the ventricles, frequently very great, so that the brain sub- THE BRAIN IN GENERAL PARALYSIS. 
431 
stance lying between the fluid in the ventricles and the superficial 
oedema of the membranes is greatly shrunken. The oedema of the 
membranes is most visible in the sulci which gape and are filled 
up with oedematous connective tissue. The fluid is chiefly in the 
membranes over the parietal and occipital lobes, perhaps from 
gravitation. The surface of the ventricles is beset with little 
prominent granulations which are often very marked. It has been 
pointed out by Crichton Browne that the pia mater is adherent to 
the surface of the convolutions, so that on attempting to remove it 
bits of brain substance come away with it. These adhesions may 
be taken as indications of the inflammatory nature of the disease, 
and their locality affords some evidence of the localization of the 
lesions. Crichton Browne states that the adhesions occur mainly 
in the anterior three-fourths of the brain, affecting the frontal lobe 
chiefly in its anterior and posterior thirds, and the parietal in all 
its convolutions. 
The brain as a whole is greatly reduced in weight. Taking the 
normal weight of the brain, including membranes, etc., as fifty 
ounces for the adult male, and forty-five for the female, the weight 
in general paratysis often falls to thirty-five ounces. The loss of 
weight does not affect the brain uniformly; it is mainly the 
cerebral hemispheres that are affected, the basal ganglia and 
peduncular parts being much less so, and the cerebellum not at all. 
Besides these evidences of atrophy of the brain, the membranes 
show irregular thickenings. The pia mater presents milky 0£)ac- 
ities or more obvious patches of thickening. The dura mater is 
usually also affected, so frequently that at one time it was supposed 
to be the primary seat of the disease. It is commonly adherent to 
the calvarium, so that it is often difficult to remove the latter, and 
it is necessary to remove bone and dura mater together. That 
membrane presents patches of thickening, opacities, and even flat 
bony developments. Not infrequently there are extravasations of 
blood of smaller or larger size accompanied by appearances which 
we shall have to describe under pachymeningitis chronica hemor- 
rhagica. The calvarium itself sometimes presents thickening, 
which is usually diffuse, and may be chiefly due to the shrinking 
of the brain; sometimes there are also local prominences or actual 
exostoses. Sometimes also the diploe is converted into dense bone, 
so that the calvarium is much heavier than normal—so-called 
sclerosis of the bone. 
All these appearances are due to inflammation and shrinking of 
the brain substance, the dropsy of the ventricles and oedema of the 
membranes occurring in order to fill up the space formerly occu- 
pied by the brain, the cranium being a cavity of fixed size and the 
dropsy being ex vacuo. 
The appearances under the microscope are chiefly those of dif- 
fused sclerosis and atrophy of the brain substance. We have 
already seen that there is sclerosis of the posterior columns of the 
cord, and this may even be an early condition. In the brain there 
are often traces of the earlier acute condition in the form of little 432 
DISEASES OF THE NERVOUS SYSTEM 
clumps of pigment around the vessels, the remains of former 
extravasations. But the appearances are more those.of degenera- 
tion. The ganglion cells are shrunken and frequently pigmented; 
the bloodvessels show sometimes fatty degeneration, sometimes a 
homogeneous glancing appearance (colloid); and they are fre- 
quently obstructed by glancing masses which are partly calcareous 
and partly colloid. These appearances are not to be regarded as 
in any way peculiar to this disease, they are simply evidences of 
the profound atrophy of the brain, and may occur to a limited 
extent in old persons where there has been only a senile atrophy. 
Hydrophobia.—This is a disease in which there is every indica- 
tion of irritation of certain centres, and of a greatly increased 
reflex irritability. The centres irritated here are less those of the 
cerebral hemispheres than of the spinal cord and medulla oblongata, 
although delirium is also occasionally present. The symptoms 
point mainly to the medulla oblongata; there are various spasms 
of the muscles of deglutition and respiration which occur to some 
extent spontaneously, but are also evoked by slight sensory stimu- 
lation. The mere sight of water gives rise to the idea of swallowing 
Fig. 218. 
A bloodvessel from the medulla oblongata in a case of hydrophobia. Large numbers 
of round cells are seen in its sheath. X 350. 
it, and brings on a violent spasm of tlie muscles of deglutition. 
A breath of cold air on the surface of the body causes a violent 
respiratory spasm or gasp. The centres in the cord are also 433 
HYDKOPHOE1A. 
irritated, as shown by the tendency to spasm of the muscles 
generally. 
In this disease an irritating virus is present in the blood and 
induces these conditions of the nervous system. After death most 
manifest signs of irritation are visible on microscopic examination. 
They are to be found most characteristically in the medulla ob- 
longata and next to that in the spinal cord, but are not absent in 
the other parts of the nervous system. The most prominent con- 
dition is an accumulation of leucocytes around the vessels in the 
substance of the cord and medulla oblongata. There may be just 
a few leucocytes in the sheath, but from this there are all grada- 
tions up to a condition in which the vessel is clothed with a mantle 
consisting of many layers of leucocytes (Fig. 218). The leucocytes 
are also present elsewhere, and sometimes in such quantities as to 
have induced one observer to speak of the collections as miliary 
abscesses. This name is, however, objectionable, as there is no so- 
lution of the tissue such as is involved in the idea of an abscess. 
The leucocytes find their way into the pericellular spaces and are 
found keeping company with the ganglion cells in these situations. 
In the medulla oblongata the main nutritive vessels are towards 
the posterior part, and as the motor nuclei are in this region, it may 
be that the localization of the irritation here is partly determined 
by their proximity. In addition to these conditions minute hemor- 
rhages have been observed in the medulla and cord. 
Signs of irritation are present in other parts of the body besides 
the nervous system. The salivary glands have been found to pre- 
sent abundant leucocytes between the glandular elements (Fig. 219). 
Fig. 219. 
From the salivary gland in a case of hydrophobia. In the middle is portion of a duct; 
abundant round cells surround it as well as the glandular structures, shown in outline. 
X 350. 
In the kidneys also there are signs of irritation in the form of 
dilatation of vessels and hemorrhage. 
It is clear then that here an intense irritant is circulating in the 434 
diseases of the nervous system. 
blood, and the intensity of it may be judged from the fact that all 
these very marked appearances occur within two or three days of 
the onset of the nervous symptoms. 
Tetanus.—In this disease we have another example of an intense 
irritation of the spinal cord and medulla oblongata. There is here 
violent spasm of the muscles, but those under the control of the 
medulla oblongata are not so specially involved as in hydrophobia, 
although the person frequently dies from spasm of the muscles of 
respiration. 
Here again there are signs of irritation discoverable in the spinal 
cord and medulla oblongata, although they are very different from 
those in hydrophobia. In tetanus the most prominent and constant 
appearance suggests the exudation of fluid from the vessels. The 
fluid sometimes collects around the vessels, and, as in hardened 
specimens the albumen is coagulated, a granular appearance may 
be produced. In other cases it looks as if the fluid produced a 
disintegration of the neighboring nervous tissue, the appearance 
being that of the “ granular disintegration ” of Lockhart Clarke. 
The localization of the disintegration around the vessels suggests 
its origin in an exudation from them. 
The cause of the irritation in tetanus is not at all clear. It seems 
likely, however, that here also there is an irritant in the blood, 
just as there is in hydrophobia. In both of these diseases the 
temperature is elevated, and, especially in the case of tetanus, 
reaches sometimes a most startling height (110° F.). It is difficult 
to account for this extreme rise of temperature by the muscular 
spasm, though the possibility of this explanation is not to be abso- 
lutely denied. It seems more probable, however, that an irritant 
acting to some extent generally on the tissues is the cause of the 
elevation of temperature. This is the more likely because tetanus 
has been known to occur in epidemics, and because if a case 
survives eight days there is considerable probability of recovery, 
as if the poison ran its course in that period. 
ATROPHY AND DEGENERATIONS OF THE BRAIN. 
There are cases of congenital atrophy of the brain, which is 
very commonly partial. It may be of one cerebral hemisphere or 
of the cerebellum. An interesting case of the latter kind lias been 
recorded by Fraser in which there were striking symptoms of 
ataxia due to congenital smallness of the cerebellum. From the 
existence of similar symptoms in another member of the same 
family it was inferred that she also was the subject of a similar 
affection. 
The brain frequently atrophies in old age—senile atrophy. 
There is usually a general shrinking of the brain substance, but 
this may be greater in some parts than in others. The loss of 
substance is made up partly by thickening and oedema of the soft syphilis of the brain and its membranes. 
435 
membranes, such as have been already described as occurring in 
general paralysis, and partly by thickening of the skull. 
Of the more definite degenerative changes it is not necessary 
to give here a detailed account, as they have mostly been inci- 
dentally referred to. 
The white substance of the brain undergoes a process of atrophy 
under various circumstances—in softening of the brain, in sclerosis, 
etc. It also presents a condition which Lockhart Clarke has desig- 
nated granular disintegration. This occurs in the neighborhood 
of bloodvessels, and is probably due to exudation from them. The 
white substance degenerates into an indefinite granular material. 
The ganglion cells are frequently the seat of atrophy and de- 
generation. They may undergo a simple atrophy, shrinking and 
losing their processes. But very commonly the atrophy is accom- 
panied by pigmentation, and so a pigmentary degeneration is the 
result. Yirchow was the first to describe a calcification of the 
ganglion cells. This condition seems to be of frequent occurrence 
when these cells are suddenly deprived of vitality. It was found 
by Virchow originally in cases of commotio cerebri, but has since 
been seen in softening of the brain, in acute poliomyelitis anterior, 
etc. The ganglion cells, having died and having undergone coagu- 
lation-necrosis, become infiltrated with lime like other dead struct- 
ures. A hyaline or colloid degeneration of the ganglion cells 
has also been described, especially in cases of insanity. 
SYPHILIS OF THE BRAIN AND ITS MEMBRANES. 
Syphilitic lesions affecting the encephalon are of considerable 
frequency, and hence of great importance. For convenience of 
description we shall divide the lesions into three, although it is to 
be understood that these are often coincident in the same case. 
We shall consider, first, the syphilitic gumma; next, syphilitic 
disease of the cerebral arteries; and, lastly, syphilitic inflamma- 
tions. In this description the brain and its membranes will be 
considered together, inasmuch as the lesions, being almost entirely 
of the surface, frequently involve both brain substance and mem- 
branes. 
The gumma occurs either as a grayish tumor of soft consistence 
and transparent gelatinous appearance, or as a yellow mass of hard 
consistence and opaque cheesy appearance. These two forms are 
not absolutely separate in their occurrence, and it is probable that 
the cheesy form is due to metamorphosis of the gray transparent. 
In correspondence with this the gray form presents, under the 
microscope, masses of well-formed round cells, often with some 
admixture of the tissue in which the tumor is growing; in fact, 
the tumor consists of fresh granulation-tissue like other recent 
gummata. It is never distinctly circumscribed, but merges at its 
margins into the surrounding tissues, in which masses of round 436 
diseases of the nervous system. 
cells may be found for some distance outside the tumor. The 
gray tumor may be interspersed with 37ellow cheesy parts, which 
are clearly older. 
The yellow cheesy form is more frequently a defined tumor, and 
has commonty a peripheral zone of gray tissue. This form presents 
a very miscellaneous structure, the cheesy part consisting of 
shrunken cells, fatty debris, fat-crystals, masses of blood-pigment, 
with, it may be, some remains of the original tissue in the form 
of irregular fibres, etc. 
These tumors are met with chiefly in the dura mater or in the 
soft membranes. In the dura mater we sometimes see tumors of 
considerable size, as large as a pigeon’s or even a hen’s egg. The 
tumor grows in the substance of the dura mater, and is nearly 
always of the yellow caseous form; it is distinctly defined, and 
the dura mater around it is greatly thickened. These tumors 
occur in all regions of the dura mater, but they attain their largest 
size commonly in the duplicatures, such as the falx cerebri. They 
press on the brain within, and the skull without, but their chief 
effects are in the latter direction. They produce erosion of the 
internal surface of the skull, so-called dry caries. 
Of even greater importance than these are the gummata of the 
soft membranes, because they have a much greater effect on the 
brain itself. It may here be said that the great majority of gum- 
mata of the brain itself are at the surface, and really originate in 
the soft membranes, the pia mater, or the arachnoid. Tumors of 
this kind occurring on the convexity present the appearance of 
great matting and thickening of the entire membranes, the dura 
mater being adherent over the place so that it cannot be separated. 
In the midst of the matted tissue is found the tumor or tumors, 
recognized by their yellow cheesy appearance. The tumor is seen 
on section to involve the brain substance, which is partly replaced 
by its tissue. Around the tumor the brain substance is softened, 
and this softening may extend widely outside the growth. When 
seated over the convexity, the tumor will, of course, involve the 
gray substance of the surface of the convolutions. 
When the growth occurs at the base of the brain, the dura 
mater is less commonly affected, and we more frequently have the 
gray transparent form of gumma. The tumor is peculiarly prone 
to occur about the optic chiasma, the crura cerebri, and the pons. 
Here also it grows into the brain substance, working it up, and it 
may in like manner attack the cerebral nerves as they issue from 
the brain. The nerves most frequently affected are the optic, and 
those issuing from the peduncles and pons (the third, fourth, and 
fifth). 
It has been already stated that inflammation and thickening of 
the membranes occur around the gummata, but sometimes a con- 
dition exists which may be designated a gummatous meningitis. 
The gummatous tissue is formed more diffusely in the form of a 
gray gelatinous layer, covering a considerable surface at the base 
or on the convexity. In the former case, there may be some re- SYPHILITIC disease of the bloodvessels. 
437 
semblance to tubercular meningitis. In the latter, the whole 
membranes are thickened and matted together by gummatous 
tissue, and the brain substance beneath is softened. If under 
treatment, or otherwise, the proper gummatous tissue disappears, 
then the thickened membranes may present the appearance of an 
old simple inflammation. 
[Grummata of the brain substance proper are of the rarest occur- 
rence, if we exclude those which have some connection with the 
surface, and may have originated from the soft membranes. Of 
the very few cases recorded, there are even some where the con- 
ditions were ambiguous. 
Syphilitic disease of the bloodvessels, although not confined 
to those of the brain, is most frequent and most characteristic in 
them (see p. 840). The condition somewhat resembles atheroma, 
but presents certain distinct differences. The lesion may occur in 
the vessels near a gumma, but also independently and at a distance. 
It is noted that at a certain spot the vessel has become more opaque 
and grayish-white in color. Its wall in the affected part is firmer, 
so that instead of the vessel being flattened as usual it preserves a 
cylindrical shape. The part also feels hard and resistant. On 
section it is seen that the calibre of the vessel is greatly reduced 
by a new formation in its wall. This new formation has a grayish 
or whitish color, and is of dense, almost cartilaginous, consistence. 
The reduction of the calibre varies, but it may go on to nearly 
complete occlusion. The narrowed portion may become the seat 
of a thrombus which may complete the obstruction. The new 
formation has its seat in the internal coat of the artery, and (ac- 
cording to Heubner, whose description in Ziemssen’s Handbuch is 
here followed) especially between the elastic lamina and the endo- 
thelial layer. There is first a germination of the endothelial cells, 
which form a firm connective tissue containing spindle and stellate 
cells. There is also a formation of granulation-tissue in the wall, 
as in the gumma. This new formation extends along the vessel as 
well as inwards, and involves communicating branches. It is clear 
that this disease must often by narrowing, with or without throm- 
bosis, lead to complete, or nearly complete, occlusion of the artery, 
the natural result being softening of the brain in the region of 
distribution. Heubner has pointed out that the disease most fre- 
quently affects the carotid and its branches, especially the middle 
cerebral, so that this softening is most commonly in the same 
region as that from embolism. It has been noted above that soft- 
ening of the brain occurs around gummata, and in that case it is 
largely the result of this disease in the arteries. 
This form of disease of the arteries is to be distinguished from 
atheroma, chiefly from its occurrence in connection with other 
manifestations of syphilis. It also occurs in younger persons, and 
may be in single patches, while atheroma is prone to affect many 
vessels. 438 
diseases of the nervous system. 
Inflammation of the membranes in syphilis occurs mainly in 
connection with gummata. Oases have been recorded of inflam- 
mation without gummata and their occurrence is not to be denied, 
but there is often the possibility of gummata having previously 
existed, and been removed perhaps by treatment. 
In connection with the symptoms due to syphilitic lesions of the 
brain it is important to remember the localization of these 
lesions. The gummata and resulting inflammations of the con- 
vexity, occurring as they do on the surface, will, at first, irritate 
the surface of the convolutions. If a motor part be aftected then 
there will he muscular spasm, often progressing, and ending per- 
haps in general convulsions of a quasi-epileptic character. Any 
sort of local spasm may be produced according to the particular 
part irritated. If the lesion be over a sensory part, there will be 
subjective sensory impressions. We have already seen that the 
brain substance commonly gets involved in the gumma, and that 
outside it there is also softening of the brain. This destruction of 
brain substance involves loss of function, namely, paralysis or loss 
of sensation; but there will still be irritation of the marginal parts, 
and though paralyses and anaesthesias may develop, the signs of 
irritation generally remain prominent. At the base the gumma 
is very apt to involve motor tracts. The motor fibres of the pons 
and peduncles are anterior, and are therefore more exposed to the 
inroads of the tumor. But these paralyses are apt to be compli- 
cated by the lesion extending to the cerebral nerves which issue 
here, mainly the optic, third, fourth, and fifth, and so we have 
very complex conditions brought about, such as crossed paralysis, 
etc. Again, the syphilitic disease of the arteries occurs most fre- 
quently in the carotid and middle cerebral, and the resulting 
softening is usually most manifest in the region of the corpus 
striatum and motor convolutions. In this way a hemiplegia may 
be produced which imitates that from embolism. It will be seen 
that a great variety of symptoms may be produced from syphilitic 
lesions of the brain and its membranes. 
TUMORS OF TUP: BRAIN. 
Tumors are of very frequent occurrence in the brain substance, 
and are of great importance in a practical point of view. In ex- 
amination of the brain particular attention should be directed to 
the exact locality of the tumor, and the extent to which the brain 
substance is involved in it. 
A tumor nearly always induces inflammation of the brain sub- 
stance around it. If it be of rapid growth there is softening, but 
if slow in growth then there is sclerosis from chronic inflamma- 
tion. In the latter case the tumor will often at its margin merge 
gradually into condensed connective tissue. The tumors very 
often lead to the occurrence of hydrocephalus, which will come THE GLIOMA. 
439 
up for consideration afterwards. They also lead usually to optic 
neuritis when they have induced considerable increase of the in- 
tracranial pressure. The neuritis is localized in the intraocular 
termination of the nerve, where it gives rise to the characteristic 
“choked disk” or “engorged papilla.” 
The scrofulous tubercle is the commonest tumor of the brain. 
It occurs most frequently in young persons and is often multiple. 
We have seen that tubercles occur in the form of minute round 
tumors, hut here in the brain substance we have solid tumors of a 
size increasing up to that of a hen’s egg. These massive tumors 
are of course composed of myriads of tubercles, with the products 
of their degeneration. The greater part of the tumor is made up 
of a firm caseous mass, which resembles very closely in appearance 
a scrofulous gland. Sometimes the cheesy mass is directly con- 
tinuous with the brain substance, but usually there is a transparent 
gray zone outside it, and this gradually merges in the brain sub- 
stance around. This gray zone, when it exists, indicates that the 
tumor has been growing up till death, and is often distinctly com- 
posed of tubercles of characteristic form. Sometimes there are 
no rounded tubercles in it, and it forms simply a cellular zone. 
The gray tissue gradually merges in the brain substance, and both 
it and the brain substance show inflammatory conditions charac- 
terized by the presence of multitudes of round cells. The solitary 
tubercles are met with in all parts of the brain and spinal cord, 
but are peculiarly frequent in the cerebrum and cerebellum. In 
these they show a preference for the cortical substance, but in the 
case of the latter they ma}T grow to such a size as to replace almost 
the entire substance of one lobe. 
The glioma is also a somewhat frequent tumor. It sometimes 
grows to a large size and is usually of slow growth. In its general 
appearance it resembles brain substance, and as it commonly 
replaces a piece of brain and merges into the brain substance at its 
margin, it may be difficult to make out its limits accurately, and 
it may appear as an enlargement of a part of the brain. Two 
forms of glioma have been distinguished, a hard and a soft The 
variations in consistence depend largely on the character of the 
matrix of the tumor. It may be composed chiefly of stiff thick 
fibres (as in Fig. 220), in which case the consistence will be dense, 
or of a delicate network, when the tissue is soft. The cells are of 
small size and mostly round, and they present considerable varia- 
tions in abundance. In the softer forms the cells are generally 
numerous. Sometimes there is an excessive development of blood- 
vessels, in which case there is a tendency to hemorrhage. If death 
occur from the hemorrhage the appearances may resemble those 
of ordinary cerebral hemorrhage, the tumor broken up by the clot 
resembling the broken-up brain substance. The substance of the 
glioma not infrequently undergoes fatty degeneration and a cheesy 
appearance is produced. When hemorrhage occurs the clot may 440 
DISEASES OF THE NERVOUS SYSTEM. 
also assume a cheesy appearance. In this way very varied and 
peculiar appearances may be produced. 
Fig. 220 
From a glioma of the brain. The coarse fibrous structure with a few cells is shown. X 850. 
The myxoma occasionally occurs in the brain, but is more fre- 
quent on the peripheral nerves. It is a soft tumor of a trans- 
parent glancing appearance, and by still further softening may 
become cystic. 
Sarcomas are of considerable frequency, and are of various 
structure. There are sarcomas allied to the glioma and others to 
the myxoma, and so we have glio-sarcomas and myxo-sarcomas, 
the difference being mainty in the character of the intercellular sub- 
stance. In the myxo-sarcoma the cells are round, and the tumor 
very soft. In the glio-sarcoma the cells may be round or spindle- 
shaped, and the tumor soft or hard. 
Cancers will hardly occur in the brain, except by extension 
through the skull from the skin. 
Papilloma sometimes occurs as an outgrowth on the surface of 
the ventricles. 
Osteomas are very rare, but true bony tumors have been found, 
one occupying almost the entire cerebellum. 
The lipoma is. excessively rare. 
Cysts may arise from the myxoma, or may possibly originate 
more independently. Dermoid cysts have been observed. 
PARASITES. 
The cysticercus of the Taenia solium has occasionally its seat in 
the brain, mostly in the cortical portions, but it may he in any 
situation. membranes of brain and spinal cord. 
441 
It forms a small round structure enclosed in a connective-tissue 
capsule. Inside this the proper stratified membrane of the parasite, 
with the head and other structures, are to be found. Sometimes 
the parasite is dead and calcified. As a rule it produces little dis- 
turbance, and is often found by accident after death. If situated 
in the peduncular portions it may produce serious symptoms, but 
even here its slow growth and small size generally allow of accom- 
modation. Sometimes several cysticerci, as many as ten to twenty, 
have been found. 
The echinococcus sometimes develops in the brain, but has 
usually been found by accident on post-mortem examination. 
C.—THE MEMBRANES AND CAVITIES OF THE BRAIN 
AND SPINAL CORD. 
Introductory Considerations.—The dura mater is a dense con- 
nective-tissue membrane which is more intimately connected with 
the hone than with the brain and spinal cord, forming something 
like a periosteum to the hone. It is generally said that the dura 
mater is lined with arachnoid membrane, one layer of arachnoid 
covering the brain and cord and another the dura mater. It is 
thus customary to speak of the arachnoid sac as of the pleural sac, 
and of a visceral and a parietal layer. But these analogies are 
contradicted by pathological experience. There is no fine mem- 
brane lining the dura mater, and the arachnoid membrane covering 
the Drain has almost nothing in common with the dura mater in 
its diseases. We are accustomed to acute inflammations of the 
pleural and other serous sacs, in which the whole sac, including 
both visceral and parietal layers, takes part, but there is hardly 
such a thing as an arachnitis involving surface of brain and 
internal surface of dura mater. On the other hand the arachnoid 
and the pia mater go together in their inflammations, and it is 
better to speak of the dura mater as one membrane and the pia 
arachnoid as another. It will be proper also to speak of the 
arachnoid cavity as the cavity of the dura mater or subdural space, 
just as we speak of the subarachnoid space. 
The subarachnoid space contains the cerebro-spinal fluid, which 
appears to circulate somewhat freely on the surface of the brain 
and spinal cord. It is important to notice the connections of the 
subarachnoid space, as it, with its connections, forms a large com- 
municating system of lymph-spaces, and may be almost compared 
with a serous cavity. The subarachnoid space, lying between pia 
mater and arachnoid, is intersected by trabeculae. The pia mater 
and arachnoid become incorporated over the summits of the con- 
volutions, so that it is only in the sulci that there is any space. 
The pia mater is prolonged into the lateral ventricles, forming the 
supporting structure of the choroid plexus, and the subarachnoid 
tissue is also continued, so that the ventricles communicate here 442 
DISEASES OF THE NERVOUS SYSTEM. 
with the subarachnoid space. There is a still freer communication 
by means of the foramen of Majendie at the fourth ventricle. The 
subarachnoid space and the ventricles of the brain with the central 
canal of the spinal cord thus form a continuous system of lymph- 
spaces, and the cerebro-spinal fluid circulates in them. In addi- 
tion to this, the subarachnoid space communicates with lymph- 
spaces around the vessels and ganglion cells, the perivascular and 
periganglionic spaces. It is important to observe that the sub- 
arachnoid space does not communicate with the subdural space. 
MENINGEAL HEMORRHAGE. 
The hematoma of the dura mater is a condition concerning 
which considerable differences of opinion exist. It presents itself 
mostly in the form of a somewhat massive blood-clot covering the 
internal surface of the dura mater and compressing the brain sub- 
stance. When the clot is more particularly examined it is seen to 
be not exactly free on the surface of the dura mater, but covered 
with a delicate membrane, which is continued beyond the clot on 
the surface of the dura mater as a thin soft layer. This membrane 
generally has a brownish color, evidently from the blood-coloring 
matter, and it presents in its substance, as well as between the 
membrane and the dura mater, numerous smaller hemorrhages. 
This condition is of somewhat frequent occurrence, particularly 
among the insane. 
There are two views as to its true nature, and it is quite possible 
that there may be actually two diseases. According to one view, 
a hemorrhage into the cavity of the dura mater is the primary 
condition. It is undoubted that a hemorrhage may lead to a con- 
dition resembling that described. In a case of aneurism of one of 
the larger cerebral vessels, where bleeding had occurred into the 
subdural space some time before the fatal cerebral hemorrhage, 
the author found a layer of soft tissue covering the dura mater 
and having much of the character described above. In this and 
similar cases the coagulum on the surface of the dura mater 
becomes organized in the usual way, and the vessels pass from the 
dura mater into the rudimentary tissue thus produced. These 
thin-walled vessels are specially apt to bleed for reasons to be 
presently referred to, and so there is hemorrhage in the new- 
formed tissue and under it. 
But many cases have a more spontaneous origin, and agree with 
the description which Virchow has given of hemorrhagic pachy- 
meningitis. This disease begins in an inflammation of the dura 
mater, characterized by liypersemia. The inflammation being 
chronic, the result is the formation of a soft membrane on the 
internal surface of the dura mater, owing to an inflammatory trans- 
formation of its internal layer. In its structure this membrane 
somewhat resembles mucous tissue, containing stellate and spindle- 
shaped cells in a matrix which gives a precipitate with acetic acid. MENINGEAL HEMORRHAGE. 
443 
In it there are large thin-walled bloodvessels in large numbers. 
The false membrane is easily lifted from the dura mater with 
forceps, and as this is being done numerous red threads are seen 
to stretch from it to the dura mater; these are the bloodvessels. 
An explanation of the large size and tendency to rupture of these 
vessels has been suggested by Rindfleisch. To begin with, there 
is hypersemia of the dura mater with relaxation of the arteries. 
The normal capillaries being in a dense tissue will not dilate much, 
but the blood in them will be at a high pressure. The new-formed 
vessels, however, are delicate and lie in a soft tissue, and they com- 
municate with the capillaries of the dura mater in which the blood- 
pressure is excessive. They are therefore very liable to dilatation, 
and although they have the structure of capillaries they are mostly 
three or four times as wTide as ordinary ones. These vessels often 
rupture, so that there is frequent hemorrhage into the soft mem- 
brane. But sometimes a more considerable hemorrhage occurs, 
and the blood accumulating dissects up the membrane from the 
dura mater, rupturing fresh vessels as it advances. In this way a 
large flat clot as thick as the hand may be formed, the proper 
hsematoma. It will he observed that this clot is still covered wflth 
the membrane, and it is quite unusual to And the blood escaping 
into the cavity of the dura mater. 
If a fatal hemorrhage does not occur, the new-formed membrane 
undergoes organization in the way of other inflammatory structures. 
It becomes more cellular and finally develops into connective tissue 
which coalesces with that of the dura mater. The disease, howT- 
ever, is apt to recur, and a fresh soft layer is formed which goes 
through the same stages, so that there may be several layers in 
different stages of transformation on the surface of the dura mater, 
the innermost layer having the characters described above. 
This condition occurs chiefly over the convexity of the brain, 
and is stated to be mainly in the domain of the middle meningeal 
artery. An acute suppurative inflammation very rarely develops 
in connection with the hsematoma. 
Hemorrhage in the soft membranes is of comparatively trivial 
consequence. We have seen that in the case of rupture of 
aneurisms of the larger cerebral arteries blood passes into the 
subarachnoid space, but usually for a short distance only, the 
many septa apparently preventing the extension of the blood, 
which finds much freer access towards the brain. There may be 
hemorrhage also in consequence of injuries, wdiethqr accompanied 
by definite wounds or fractures, or only by violent shaking of the 
brain. Hemorrhages have also been observed in splenic fever 
and ulcerative endocarditis. 444 
DISEASES OF THE NERVOUS SYSTEM. 
INFLAMMATIONS OF THE MEMBRANES. 
The inflammations of the buka mater are not very important 
if we exclude the hemorrhagic form described above. Acute 
suppurative inflammation is always secondary, occurring in con- 
nection with wounds of the head, disease of the bones, especially 
caries, and thrombosis of the sinuses. The dura mater is softened 
and inliltrated with pus and portions of it often slough. 
Simple Acute Meningitis.—This name is applied to non-specific 
inflammations of the pia arachnoid. If it be desired to distinguish 
it from inflammation of the dura mater, it may be named lepto- 
meningitis. Some irritant obtains access to the membranes, and as 
it is carried by the circulating cerebro-spinal fluid the inflamma- 
tion is usually of a spreading character. The cases are frequently 
traumatic and the irritant is septic in nature; they may be due to 
extension from disease of the bones, and in these cases the men- 
ingitis may be associated with abscess of the brain. There are, 
however, cases in which the disease has its starting-point in a 
simple blow with commotio cerebri without any external wound, 
and there are even some in which no cause is discoverable, but 
these form rare exceptions. 
In the milder cases there may be simply a serous exudation in 
the subarachnoid space, constituting an inflammatory oedema. But 
in most instances the case goes on till pus, or pus with fibrine, is 
exuded. The first appearances are visible in the neighborhood of 
the veins, in the sulci between the convolutions. Very often there 
is a white or yellow band visible on either side of the vein, and 
this consists of accumulated leucocytes, it may be, with fibrine. 
As the exudation increases the vein£ become buried in it, and the 
whole subarachnoid space becomes filled. The spaces being filled 
out, the pia arachnoid forms a bulky, solid layer which may be 
separated from the surface of the brain, and form a mould of the 
convolutions on its under surface. The inflammation extends in 
some measure along the perivascular spaces into the superficial 
parts of the brain substance. This is important in relation to the 
symptoms, which are often those of irritation of the cortex of the 
brain. 
The inflammation usually begins in a particular locality, gener- 
ally some part of the convexity, and here the arachnoid and the 
dura mater are sometimes united by fibrinous exudation. It 
spreads from this, generally confining itself to the convexity, but 
sometimes it extends to the base, or to the spinal cord, or even 
into the ventricles. 
Simple chronic meningitis of the brain and spinal cord is usually 
secondary. There are thickenings and adhesions of these mem- 
branes in different forms of insanity, in diseases of the bones, in 
the various scleroses of the cord, especially posterior sclerosis. It tubercular meningitis. 
445 
is important to remember that a chronic inflammation of the mem- 
branes of the cord may be propagated from the peripheral nerves 
along their sheaths. 
Epidemic Cerebro-spinal Meningitis.—As the name implies, 
this is a disease which, like the acute fevers and hydrophobia, 
depends on a virus introduced into the body. The morbid poison 
shows a special affinity for the meninges of the brain and spinal 
cord, although other organs are also in a minor degree affected. 
The soft membranes present evidences of acute inflammation at 
first in the form of serous exudation with few leucocytes and red 
corpuscles. This condition is only seen in cases which have died 
very early after the onset of the disease, and soon the exudation 
takes on a purulent character as in simple meningitis. The 
exudation is here also in the subarachnoid space, and penetrates 
along the sheath of the nutritive arteries into the nervous tissue 
beneath. There is very seldom any exudation on the surface of 
the arachnoid, and the dura mater hardly ever takes part in the 
disease. The exudation is most marked in the sulci between the 
convolutions of the convexity, in the fissure of Sylvius, on the 
surface of the pons, and upper surface of the cerebellum. In the 
spinal cord it is most abundant in the lumbar region, and is almost 
confined to the posterior surface, where it often surrounds the 
posterior roots. 
The disease is fatal in over 50 per cent, of the cases, but, wThen 
recovery occurs, it is usually complete. Sometimes, however, 
there is permanent damage to the nervous structures, as evidenced 
by deafness, etc. 
Tubercular Meningitis [Basal meningitis, Hydrocephalus acutus). 
—This disease, as the name implies, depends on the presence in 
the meninges of the tubercular virus. In the large majority of 
cases the disease is simply part of a general tuberculosis, the 
virus being in the blood. There are disseminated tubercles in 
other organs, as the lungs, liver, kidneys, but the affection of the 
meninges produces such pronounced symptoms that it monopolizes 
the attention especially of the clinical observer. The meninges 
are affected more frequently in the general tuberculosis of children 
than in that of adults; it thus seems as if the soft membranes in 
children were more adapted to the growth of the virus. Hence 
water in the head is counted rather a disease of children. But 
tubercular meningitis is more frequent in the adult than is usually 
supposed, and many obscure head cases are found post-mortem to 
be cases of general tuberculosis with, it may be, a very limited 
meningitis. 
When not connected with general tuberculosis, tubercular men- 
ingitis is for the most part connected with solitary tubercles in the 
brain, although this is by no means a frequent association. 
The virus, reaching the meninges by the blood, lodges in the 
lymph-spaces of the membranes, and produces inflammation and 446 
diseases of the nervous system. 
tubercles in the walls of the finer arteries of the pia mater, and in 
the subarachnoid space. These conditions are peculiarly localized 
in the basal parts of the brain, although extending sometimes to 
the lateral aspects and to the spinal cord. It may be that this is 
related to the fact that the arteries are distributed from the base, 
or, more probably, that the cerebro-spinal fluid stagnates here 
more than elsewhere, and allows of the growth of the virus. 
The appearance of the brain on post-mortem examination is 
somewhat as follows. On removing the dura mater, the cerebral 
hemispheres are generally seen to be fuller than usual, and the 
surface of the arachnoid is somewhat dry and glazed. This is due 
to the pressure from the ventricles, which are distended with fluid, 
usually clear serum, but sometimes slightly turbid with pus. The 
amount of fluid is sometimes very great, and this prominent 
feature gave rise to the name acute hydrocephalus being applied 
to this disease. In the neighborhood of the lateral ventricles, and 
especially posteriorly, the brain substance is soft and almost 
diffluent (white softening). On exposing the base of the brain, the 
appearances of inflammation in the membranes are to be looked 
for. These are often somewhat obscure, and in appearance trivial. 
In the slighter cases they consist merely of a turbidity or opacity 
over the pons and optic chiasma. The subarachnoid space is 
occupied by a serous exudation with some pus, giving often a 
greenish color. But usually the exudation is much more abundant 
and covers the basal structures, extending to the surface of the 
cerebellum, and up the fissure of Sylvius, where it often reaches 
the lateral aspects of the hemispheres. The concentration of the 
exudation at the base is of great importance, and the covering-in 
of the optic chiasma is often the most direct and sometimes the 
only prominent sign of the existence of the disease. 
The evidences of inflammation are much more prominent to the 
naked eye than the tubercles. These are often only distinctly 
visible on microscopic examination, as they are so much buried in 
the exudation and attached to such small arteries. On opening 
up the fissure of Sylvius, however, where the exudation generally 
glues the opposed surfaces of the brain together, it is usually pos- 
sible to see the little white tubercles, often no larger than pins’ 
heads. If a piece of the soft membrane be removed, however, 
even from a part where the exudation is very abundant, and ex- 
amined with a low power under the microscope, the tubercles are 
readily seen as spindle-shaped prominences on the small arteries 
(see Fig. 221). These are seated in the adventitia, and are often 
somewhat ill-defined at their periphery on account of the inflamma- 
tory exudation. 
The exudation, and perhaps the tubercles also, extend along the 
sheaths of the nutritive vessels into the substance of the brain and 
spinal cord, as well as into the cerebral nerves. The superficial 
parts of the brain substance in particular are hypersemic, and not 
infrequently the seat of small hemorrhages. 
The dropsy of the ventricles, which is such a prominent feature accumulation of the cerebro-spinal fluid. 
447 
in this disease, will be considered afterwards in the section on 
hydrocephalus. The white softening of the parts around the 
ventricles has given rise to some discussion as to its cause. It may 
extend somewhat deeply into the brain substance, involving fornix, 
septum lucidum, corpus callosum, and even the thalamus opticus 
Fig. 221. 
Arteries of the pia mater in a case of tubercular meningitis. The frequent spindle- 
shaped swellings indicate the position of the tubercles. X 16. 
and corpus striatum, and it is sometimes so extreme as to reduce 
the tissue to the consistence of thick cream. It is clear from the 
comparative absence of symptoms that this extreme softening does 
not exist during life. Probably the fluid in the ventricles macerates 
and loosens out the brain tissue without interrupting the functions, 
and after death a more pronounced softening occurs. The condi- 
tion is not an inflammatory one, and it occurs mainly where the 
fluid gravitates, namely, in the brain substance around the posterior 
parts of the ventricle. 
ACCUMULATION OF THE CEREBRO-SPINAL FLUID IN THE 
MEMBRANES AND CAVITIES. 
It has been already pointed out that the subarachnoid space, 
with the ventricles and central canal of the spinal cord, form a 
single system of lymph-spaces which intercommunicate. The lymph 
in these spaces may accumulate, and so lead to various forms of 
oedema and dropsy of the brain. In this connection it is impor- 
tant to remember that the skull is a closed cavity, and any increase 448 
diseases of the nervous system. 
in tlie fluid in these spaces implies a decrease in the quantity of 
blood in the vessels or of the brain substance itself. 
There may be a general (edema of the membranes and spaces, 
perhaps including the perivascular spaces in the brain substance. 
This may take place in Bright’s disease, and may occur along with 
an oedema of other parts, or develop in a more isolated manner. 
The pressure of the fluid in this case has been supposed by some 
to be the cause of the symptoms usually called ursemic. 
Then there is an (EDExMA ex vacuo. When the brain shrinks, as 
we have seen in general paralysis, or when it undergoes a more 
simple atrophy as in senile atrophy, there is a serious loss of sub- 
stance. The latter condition may be extreme in very old persons, 
although the brain does not usually atrophy in proportion to other 
tissues. The loss of substance thus produced must be compensated, 
' and there are two ways in which this may be done, the one is by 
thickening of the cranium and the other by augmentation of the 
cerebro-spinal fluid. Thickening of the cranium takes place only 
to a limited extent, and the space is chiefly tilled up by fluid. The 
ventricles dilate greatly (,hydrocephalus), and the subarachnoid space 
is highly cedematous. It is to be particularly observed that there 
is seldom any excess of fluid in the subdural space, but that the 
soft membranes, especially between the atrophied convolutions, 
are highly cedematous. 
Hydrocephalus.—This name is applied to dropsy of the ven- 
tricles of the brain, and we have now to consider the condition as 
it occurs apart from oedema of the membranes. More strictly, 
dropsy of the ventricles is hydrocephalus internus, while a massive 
collection of fluid externally is hydrocephalus externus. But as 
the latter hardly occurs except as an oedema, the name hydro- 
cephalus is usually limited to the former. In a similar sense the 
term hydrorhachis is used for the spinal cord, liydrorhachis interna 
being a drops}’ of the central canal and hydrorhachis externa a 
dropsical accumulation in the subarachnoid spaces. We shall 
consider first some of the more easily explainable cases of hydro- 
cephalus. 
Acquired Hydrocephalus.—Apart from the form ex vacuo, 
hydrocephalus as met with in the adult is mostly related to a 
definite disturbance of the circulation in the brain. The ventricles 
are supplied with fluid chiefly through the choroid plexus, and any 
obstruction to the veins here is liable to lead, on principles already 
considered, to an excessive exudation. It seems also as if the 
choroid plexus, with its villi, acted as a drain to the ventricles, the 
fluid passing into its lymph-spaces, and so either into the veins or 
outwards to the subarachnoid space. If the veins are obstructed 
they can no longer aid in absorption, but on the contrary their 
obstruction causes, as we have just seen, excessive transudation 
from the capillaries. Again, if the lymphatic vessels and spaces 
are filled up, this will interfere with the absorption, so that dropsy 
may arise in this way. We have therefore two classes of cases, CHRONIC HYDROCEPHALUS. 
449 
one in which the veins, and another in which the lymph-spaces 
are obstructed. 
The veins of the choroid plexus gather themselves into the great 
veins oe Galen, which pass outwards between the corpus callosum 
and corpora quadrigemina to open into the straight sinuses. In 
cases of obstruction of these veins there may be a rapid accumula- 
tion of fluid in the ventricles, and death may even result from the 
sudden increase of intracranial pressure. These veins may he 
obstructed by pressure from without, especially by tumors of the 
cerebellum, or by thrombi occupying their calibre. In most cases 
the thrombus originates in the sinuses, and grows into the veins of 
Galen, but Newman has recorded a case in which these veins alone 
seemed to he the seat of thrombosis. 
In tubercular meningitis hydrocephalus is nearly constant, but 
it is rather difficult of explanation. Tubercles are generally found 
on the vessels of the choroid plexus, hut the exudation in the ven- 
tricles is rarely inflammatory in character, consisting of a clear 
pellucid fluid with little albumen, and a specific gravity of about 
1010. The explanation is probably to be found in the exudation 
outside the ventricles. This is generally abundant where the 
velum interpositum issues from the ventricles just in front of the 
cerebellum, and here, besides filling up the lymph-spaces, it is 
liable to cause pressure on the veins of Galen as they pass through 
the comparatively narrow isthmus. This is the more likely to 
produce hypersemia and exudation from the veins that the arteries 
reach the plexus by a different route, and are not so liable to be 
pressed on. 
Chronic Hydrocephalus.—This name is given to a condition 
which is very frequently congenital; if not congenital, it sets in 
at an early period after birth. The explanation of the enormous 
accumulation of fluid which occurs here is very obscure. As a 
rule, no mechanical cause is discoverable obstructing the venous 
circulation, although there are cases of solitary tubercle obstruct- 
ing veins in children and producing what is really an acquired 
hydrocephalus. It is said that chronic hydrocephalus often goes 
along with rickets, and it has been suggested that as a rickety skull 
is more yielding than a normal one, too little pressure is exercised 
on the brain, and the accumulation of fluid is allowed. This is 
not, however, a sufficient explanation, especially of the severe con- 
genital cases. The probability is that the disease depends on a 
congenital defect in the apparatus for the secretion and absorption 
of the cerebro-spiual fluid. 
The dropsy affects mainly the lateral ventricles, hut may extend 
to the others. Sometimes the ventricle of the septum lucidum is 
obviously distended as it lies between the twro lateral ventricles. 
The convolutions are flattened out, and as the accumulation in- 
creases they may be completely unfolded, the brain forming a 
smooth globe over the greatly distended ventricles. If the disease 
has begun early in foetal life, the brain may he deficient in some 450 
DISEASES OF THE NERVOUS SYSTEM. 
of its parts. The distention may be so great as to cause thinning 
of the covering brain substance to an extraordinary degree, leaving 
little between the pia mater and the fluid. The surface of the 
ventricles (ependyma) is usually somewhat thickened, giving a kind 
of leathery membranous lining to the cavity. In this respect the 
condition differs markedly from that in acute hydrocephalus, 
although in the chronic form there may be considerable softening 
of the brain substance outside the ependyma. In some very rare 
cases the corpus callosum and its pia arachnoid have given way, 
the fluid coming thus to the surface and filling the cavity of the 
dura mater. In that case the hemispheres are folded aside, and 
the central parts of the brain are exposed, the brain being as a 
whole pressed down towards the base. 
With this great enlargement of the ventricles the head is greatly 
enlarged, and as the bones are more yielding in some parts than 
others, an alteration in shape occurs. The fontanelles and sutures 
are enlarged and their closure greatly delayed. The frontal hone 
is pushed forward so that the forehead rises perpendicularly, or 
overhangs the eyebrows; the parietals bulge laterally, and the 
occipital bones are pushed backwards. The head in this way 
becomes greatly increased in circumference, while it is usually 
much flattened at the vertex. The bones of the face, even though 
they are of normal size, look dwarfed beside the enlarged cranium, 
and have a pinched look. The eyeballs are rendered prominent 
by the pressure on the roof of the orbit, and enlarged veins are 
generally seen beneath the thin skin of the head. 
Although there is this great thinning of the brain substance, it 
is remarkable how the functions may be retained. A child in this 
condition may remain very intelligent, and when recovery occurs 
may pass through life with no permanent defect in the functions 
of the brain. The yielding of the skull seems to prevent any such 
excess of pressure as to seriously damage the brain, which has a 
remarkable power of accommodating itself to alterations in posi- 
tion of its parts, If recovery takes place, the skull to some extent 
collapses, the fontanelles and sutures close, often with the forma- 
tion of additional centres of ossification, forming Wormian bones 
in the sutures. But the fontanelles are late in closing, and the 
cranium retains somewhat of the hydrocephalic shape during life. 
IIydrencephalocele.—This condition is somewhat allied to 
hydrocephalus. There is here, however, a congenital defect in the 
cranial bones, and the sac of fluid protrudes externally. It may 
be only the membranes that protrude in the form of a sac filled 
with fluid (meningocele), or there may be also a layer of brain 
substance. Sometimes the external sac becomes separated from 
the structures inside and forms an independent sac. The usual 
situations of these tumors are the root of the nose, the occipital 
region, and (more rarely) the sagittal suture. SPINA BIFIDA. 
451 
Spina Bifida.—This condition is associated with or depends on 
hydrorhachis, but there is in addition a congenital defect in the 
spinal column, by reason of which a sac containing cerebro-spinal 
fluid is protruded externally. It thus forms a rounded tumor in 
the middle line of the back, situated, in the great majority of cases, 
in the lumbar or lumbo-sacral region, but occasionally at other 
levels. 
The spina biflda seems to have its origin in a foetal hydro- 
rhachis. The cerebro-spinal fluid accumulates either in the cen- 
tral canal or in the subarachnoid 
space, and a protrusion of the drop- 
sical structures from the spinal canal 
takes place. It should be stated here 
that a hydrorhacis may occur after 
birth or even in the foetus, without 
spina bifida, the central canal being 
distended, and sometimes forming 
distinct cysts, or the subarachnoid 
space being in a dropsical condition. 
When spina biflda arises from 
a hydrorhachis interna, the spinal 
cord is usually split posteriorly, so 
that the central canal is laid open and 
communicates with the surface of the 
cord. Sometimes instead of this 
there is great thinning of the cord, 
which is spread over the dropsical 
cavity. The protruded sac in the 
case of hydrorhachis interna will 
consist of the pia arachnoid and the 
dura mater. In the other form, when 
the origin is in hydrorhachis externa, 
the pia mater will be absent from the 
sac. But the membranes are often 
so matted as to be unrecognizable, 
and, on the other hand, the dura 
mater is often thinned and perforated. 
The sac is generally protruded 
through the deficient arches of the 
vertebrae. But the arches, although 
completely formed, may not have 
united posteriorly, and there are even 
cases in which the protrusion is 
through the space between two 
arches. Outside the vertebrae the 
sac acquires a covering of skin, 
which is sometimes considerably 
thinned, so that rupture may occur. The external tumor is usually 
sessile, in which case it communicates by a rather large aperture 
Fig. 222. 
Section of a spina bifida of the lumbar 
region, a, b, cutis and subcutaneous 
tissue; e, fascia; d, spinous processes; 
e, dura mater, which passes into sac 
and becomes attached to the skin at e'; 
/, arachnoid, which passes into sac, 
forming its internal lining; g, spinal 
cord, which also enters the sac and be- 
comes attached to the skin g', where it 
had a small opening; the attachment 
forms a dimple in the sac; n, n, spinal 
nerves which pass from the cord round 
to the anterior aspect of the sac so as 
to reach their normal places of issue 
from the spinal canal. (Virchow.) 452 
DISEASES OF THE NERVOUS SYSTEM. 
with the spinal canal. In other cases there is a narrow neck, and 
the tumor may be pendulous. 
The condition of the cord is of great importance in these cases. 
When the protrusion is in the sacral region, the filum terminate 
is often attached inside the sac, giving it a central dimpling ex- 
ternally, and the spinal cord extends down into the sacrum as at 
the earlier months of foetal life, as if held down by its attachment 
externally. When dropsy of the central canal has been the primary 
condition, we have already seen that the cord is usually split, but 
it may be largely destroyed for some distance. Whatever the 
origin of the dropsy, the spinal cord is usually carried to some 
extent into the sac (Fig. 222), being apparently dragged inwards, 
either entirely or in some of its strands. The cord is mostly in 
that case firmly united to the wall of the sac. The nerves may issue 
from the cord within the sac, and in the case where the filum 
terminale is in the sac, the sacral nerves traverse the sac before 
passing to the intervertebral foramina. 
TUMORS OF THE MENINGES. 
Tumors of the membranes of the brain are of importance, 
especially when they press on the brain inside or on the nerves as 
they issue from the skull. They are of considerable variety. 
Fibromas have been found arising from the dura mater both of 
the brain and of the spinal cord. In the latter case they are liable 
to press on the cord and may even interrupt it. In a case observed 
by the author a hard fibroma the size of a marble produced serious 
mischief by pressing on the cervical cord. The chondroma has 
occasionally been observed, especially in the dura mater of the 
cord. In a dog observed by the author, paraplegia was produced 
by such a tumor in the dorsal region. The lipoma is a very rare 
form of tumor in the meninges; that already mentioned on the 
surface of the corpus callosum (p. 179) probably originated in the 
pia mater. Tlie psammoma occurs not infrequently in the dura 
mater, where it forms a rounded growth on its internal surface; 
sometimes it is multiple. The tumor is usually small, but may be 
as large as a walnut, and its surface is rough and tuberculated. 
This form of tumor is sometimes classified among the sarcomas, 
the calcareous particles being regarded as of insufficient impor- 
tance to give the name to the tumor; but the structure, apart from 
the lime deposits, is often that rather of a fibroma. The psammoma 
also occurs as a small soft tumor in the choroid plexus and in the 
pineal gland. In the latter case there may be a tumor of consider- 
able size, whose structure is like that of the normal gland, and so 
the condition is sometimes designated hyperplasia of the pineal 
gland. The osteoma hardly occurs in the membranes as a distinct 
tumor, but it is common to find flat pieces of bone in the dura 
mater, especially in the falx and tentorium, and even in the 
arachnoid. tumors of the meninges. 
453 
The Pacchionian bodies sometimes give origin to tumors which 
may grow to considerable dimensions. These bodies consist of 
papillae which spring from the arachnoid and project in various 
directions; some of them present towards the skull, where, after 
thinning the dura mater, they cause pits; others project into the 
longitudinal sinus. Cleland has described two tumors of a papil- 
lary character which grew from the dura mater and pressed on 
the brain substance. Although one of these was situated in the 
falx, which does not normally present Pacchionian bodies, yet the 
structure of the tumors conformed to that of these bodies. In that 
on the falx there were calcareous masses like those which charac- 
terize the psammoma. The tumors measured respectively two 
inches and one and a-half in diameter. 
Sarcomas are exceedingly important tumors, especially those of 
the dura mater. Most of these tumors are soft in consistence and 
contain chiefly round cells. Sometimes there is a distinct alveolar 
structure, and the cells have a distinct resemblance to epithelium, 
so that the tumors have been often described as cancers. There 
are even tumors remarkably like epitheliomas sometimes observed 
in the dura mater, but they are probably to be regarded rather as 
endotheliomas. The sarcomas generally present great malignancy. 
On the one hand they extend and involve neighboring parts of the 
dura mater as well as the soft membranes and the brain; and on 
the other hand they press outwards to the skull, and may, after 
destroying the bone, work through to the external surface. These 
tumors have mostly their seat at the base of the skull and often 
lead to serious nervous lesions. They may involve directly such 
structures as the pons or medulla oblongata, the sarcomatous 
tissue growing into and replacing the proper structure; they also 
grow into the cranial nerves. By involving the bone and enlarging 
it, they may impinge on the foramina by which the nerves take 
exit. As they are seated usually at the base, they generally, when 
they work through the skull, present at the pharynx or nares. 
Of the remaining tumors, the syphilitic have been already con- 
sidered (p. 436). Tubercular growths hardly ever occur except by 
propagation from disease of the vertebrie. Dermoid cysts of the 
dura mater have been observed in a few cases. 
The echinococcus sometimes develops in the neighborhood of 
the spinal canal, in the muscles, or in the vertebrie. By enlarging 
it may extend into the canal, pushing the dura mater before it and 
compressing the cord. It has even been found to have its seat 
inside the dura mater. A few cases of cystic ercus in the sub- 
arachnoid space have been described. DISEASES OF THE ORGANS OF RESPIRATION. 
A.—THE AIR-PASSAGES. 
We have here to study the diseases of the nasal passages, the 
larynx, trachea, and bronchi. As these parts have much that is 
common in structure, their lesions have much similarity. This 
applies especially to the larynx, trachea, and bronchi, which are 
of essentially similar structure. 
THE NASAL PASSAGES. 
Congenital Malformations.—Such deformities as absence of 
the nose and its cavities, stenosis, and so on, are usually parts of a 
general malformation, and are not of importance in a practical 
aspect. In clefts of the lip and palate, the nasal cavities are in 
communication to a greater or less extent with the mouth. This 
communication renders the mucous membrane of the nares liable 
to inflammation. Normally, the nasal passages are protected 
against any irritation except that of the air passing through them, 
and the mucous membrane is correspondingly sensitive. We 
know how the accidental passage of a piece of solid food into the 
nares causes great irritation, and we shall afterwards see that the 
existence of a foreign body in the nares is a frequent cause of 
prolonged catarrh. In cases of cleft palate the food and secretions 
of the mouth readily pass into the nares and, although a certain 
tolerance may be established, persons so affected are peculiarly 
liable to catarrh of the nares. 
Acute Catarrh.—This is by far the commonest disease of the 
nares, being usually called cold in the head. It is an inflammation 
of the nasal mucous membrane, but it is exceedingly difficult to be 
certain as to what the cause of the inflammation is. We shall see 
as we go on that the mucous membranes of the air-passages are 
much more liable to inflammations than those of the alimentary 
canal, and we can understand that an exposure to cold air which 
would not produce any catarrh of the mouth might do so in the 
nares. Moreover, the fact that the nares are the nearest part of 
the air-passages to the air, and are therefore most exposed to the 
action of the cold, is an indication that such exposure has probably 
something to do with it. But mere inhalation of cold air is not 
enough to produce catarrh, as every one who is liable to cold in ACUTE NASAL CATARRH. 
455 
the head will admit. There must be, as a predisposing cause, 
some peculiar sensitiveness of the mucous membrane. It is ex- 
ceedingly difficult to explain how, at one time, a person is able to 
brave any amount of exposure without any risk of catarrh, while 
at another time a bingle draught, or no perceptible exposure at all, 
will bring it on. Such circumstances as these, taken along with 
the fact that the catarrh has a definite course, usually of a week’s 
duration, has induced some to suppose that the disease is really 
due to specific organisms. In this view it is necessary to suppose 
that these organisms are abundantly present in the air, and that 
they take, as it were, advantage of the mucous membrane when, 
at any time, it is in a specially predisposed state. This predis- 
position may be induced by cold applied either directly to the 
mucous membrane or to some other part of the body, but other pre- 
disposing causes may exist. For instance, when a person is sitting 
before a warm fire the arteries of the skin and mucous membranes 
generally are relaxed, and there is an active hypersemia. At such 
a time a slight exposure to cold may induce catarrh, apparently 
by rendering the mucous membrane less able to resist. Much 
could be said in favor of this view of the causation of catarrh of the 
nares. There is apparent confirmation of it in the fact that nasal 
catarrh is known to occur as the result of irritation by known 
specific viruses. In measles the catarrh seems referrible to the 
specific virus. In hay asthma the irritation of the pollon of grasses 
is believed to be the cause of the catarrh. Again, it is commonly 
stated that nasal catarrh is communicable from person to person, 
and it is hardly conceivable that this could occur unless the disease 
had, as a part of its cause, some specific materies morbi. It will 
be seen that the causation of nasal catarrh offers many difficulties, 
and that no very settled result can be stated. 
The catarrh begins with an inflammatory hypersemia of the 
mucous membrane. This may, of itself, lead to swelling so great 
as partially to obstruct the passages, giving the feeling of a “ stuffed 
nose.” The inflammation soon passes on to exudation. This finds 
its way for the most part to the surface, but in its passage it 
increases the swelling of the mucous membrane. The exudation 
is the usual one of inflammation, namely, the blood-plasma with 
leucocytes. At first this is mixed with mucus, but as it increases 
in amount it rapidly assumes a serous character, and we know that 
a great abundance of serous fluid may be discharged from the 
nostrils. As time goes on the leucocytes increase in the exudation, 
and it may assume a semi-purulent character. Sometimes red cor- 
puscles are present, giving the discharge a greenish-yellow color. 
As the inflammation passes off the mucous character of the 
exudation returns and the leucocytes diminish. As a general rule 
the mucous membrane returns to its normal condition as the 
inflammation subsides. Sometimes a chronic catarrh remains, but 
this is seldom the case unless there be some permanent cause of 
irritation present. It is to be remembered that there are various 
cavities in direct communication with the nares, of which the 456 
DISEASES OF THE ORGANS OF RESPIRATION. 
principal are the frontal sinuses and the antrum of Highmore, 
and that these frequently take part in the acute catarrh. It will he 
observed that in all stages of the catarrh there is more or less 
swelling of the mucous membrane, and that this leads to the 
obstruction of the passages which is such a marked symptom. 
This swelling is temporary in the acute disease, but in chronic 
catarrh it is apt to give way to a more permanent thickening. 
Chronic Nasal Catarrh.—There is thickening of the mucous 
membrane and continuous exudation which is usually more or less 
purulent and may be strongly decomposing. In these cases there 
is nearly always a permanent source of irritation. It may be a 
foreign body in the nose, and this is always to be suspected, 
especially in children, when the one nostril is concerned. It is 
frequently a scrofulous (tubercular) or syphilitic manifestation, but 
in both of these conditions it is frequently associated with deeper 
lesions. 
Chronic catarrh frequently leads to ulceration of the mucous 
membrane. In ordinary cases the ulcers are superficial, and when 
the cause is removed (as a foreign body) the ulcers heal rapidly. 
In scrofulous and syphilitic cases the ulceration very often extends. 
It passes down through the mucous membrane to perichondrium 
or periosteum, and we are apt to have necrosis or caries as the 
result. In this way there may be considerable alteration of the 
nasal passages, abnormal communications with the mouth, falling 
in of the nose and so on. When the bones are affected, the dis- 
charge from them is added to that from the mucous membrane, 
and it is in such cases that a strong odor of decomposition is 
frequently developed (oz,ena). With or without ulceration, we 
commonly find thickening of the mucous membrane from the 
usual new-formation of connective tissue in chronic inflammation. 
In this way the nares are considerably obstructed. The finer 
ramifications of the olfactory nerve are injured by these tissue 
changes, and thus a chronic catarrh, even if recovered from, often 
leaves behind loss or impairment of the sense of smell. 
Tumors.—The most frequent tumors of the nares are the mucous 
polypi. Like other mucous polypi they occur very commonly as 
a result of chronic catarrh, but they appear occasionally without 
an}' such cause. They are usually in the form of rounded projec- 
tions, having a comparatively narrow base or neck, the growth 
becoming more pedunculated as it enlarges. They often produce 
much obstruction of the passages. In structure some of them 
present simply the constituents of the inflamed mucous membrane, 
connective tissue with rather wide serous spaces, and covered with 
cylindrical ciliated epithelium. (If the epithelium be examined in 
fluid immediately after removal, the ciliary motion will be seen.) 
The connective tissue is usually so infiltrated with serous fluid as 
to give an cedematous appearance to the polypus, and sometimes a 
more definite cystic formation occurs. In some cases there is in MALFORMATIONS. 
457 
the tumor great new-formation of mucous-gland tissue, so that the 
growth is truly a mucous adenoma. In such tumors again cysts 
may arise from dilatation of the glands with mucus. In the other 
form also cystic formation may occur from dilatation of normal 
glands contained in the tumor. The polypi are not infrequently 
multiple. Papillomata occur in the nares, and may he of con- 
siderable size. 
Other tumors are not common in the nares, but fibromas and 
sarcomas, originating mostly in the periosteum or perichondrium, 
may produce serious obstruction and deformities of the nasal struct- 
ures. The sarcomas especially often dislocate the nasal bones, and 
involve the neighboring structures in their substance. In this way 
they sometimes penetrate into the antrum, or involve the hard 
palate and alveoli. Cancers rarely occur in the nares as primary 
tumors, but may involve them by extension from neighboring 
parts. 
THE LARYNX AND TRACHEA, 
There are many disadvantages in dividing the subject of diseases 
of the respiratory passages, especially in separating the lesions of 
the bronchi from those of the trachea, because they are so often 
continuous. But the points in favor of such a division counter- 
balance its disadvantages, it being understood that the respective 
inflammatory conditions especially run into one another. 
Malformations.—Entire absence of the larynx and trachea 
occurs only in acephalic monsters which are incapable of living. 
There are, further, cases of communication between the trachea 
and (esophagus; generally in these cases the pharynx ends in a 
cul-de-sac and the oesophagus opens into the trachea. Then we 
meet with cases of imperfect closure of the original branchial 
arches. All that remains is usually a slight fissure in the skin, 
leading into a fistula which has mostly a blind end, hut sometimes 
opens by a small aperture into the pharynx or trachea. The aper- 
ture in the neck is small, and is situated about an inch above the 
sterno-clavicular articulation, usually on one or both sides, more 
rarely in the middle line. The aperture is usually slightly elevated, 
and sometimes it yields a drop of fluid. Again, individual car- 
tilages, as the epiglottis, or one or more of the rings of the 
trachea may he absent, or there may he one or more rings super- 
numerary. The trachea may divide into three main bronchi in- 
stead of two, and in that case two stems pass to the right lung and 
one to the left. Occasionally the larynx is congenitally narrow, 
or it may fail to undergo the usual changes at puberty, especially 
in cases of castration before puberty or of non-descent of the testes. 
Lastly, the trachea has been observed to the left of the oesophagus 
or even behind it. 458 
diseases of the organs of respiration. 
Croup and Diphtheria.—It is well known tliat much has been 
written on the question whether these two diseases are identical or 
not. Without in the mean time entering on that subject, it may- 
be said that in using the terms here it is intended to refer to the 
conditions which are designated clinically as croup and diphtheria, 
and that the distinction sometimes made between croupous and 
diphtheritic inflammation is not made use of. 
In diphtheria we have a disease which is undoubtedly infec- 
tious, its communicability from person to person being associated 
with the fact that it depends on the existence of micrococci in the 
mucous membrane. These organisms have been found not only 
in the mucous membrane, but, having penetrated into the blood, 
they have been observed in the bloodvessels and tubules of the 
kidneys. The organism is one of comparatively large size, and 
appears to be of an allied form to that which is to be found in 
decomposing animal juices. It occurs in the form of multitudes 
of minute globular bacteria aggregated into colonies, and capable 
of self-propagation in the tissues. ISTow this organism, either in 
itself or by its products, is an irritant to mucous membranes, and 
produces violent inflammations. 
The inflammations differ somewhat in the fauces and nares on 
the one hand, and the larynx and trachea on the other. In both 
cases a catarrh is the first sign of inflammation. The mucous 
membrane is hyperaemic, and there is increased mucous secretion. 
In the case of the fauces and n'ares, this is succeeded by the for- 
mation of a false membrane, which does not lie free on the surface, 
but involves the superficial layers of the mucous membrane as 
well. The irritant, in fact, has caused a partial necrosis of the 
mucous membrane which by and by sloughs and leaves an ulcer. 
The necrosis here may be regarded as an instance of coagulation- 
necrosis, the dead tissue undergoing the change already described 
and becoming converted into something like a fibrinous clot. It 
is probable that along with the coagulated tissue there is actually 
fibrine produced in the usual way in the meshes of the tissue. 
The false membrane is therefore composed of fibrine and necrosed 
and coagulated mucous membrane. When the slough separates, 
or is removed, there is apt to be a second formation of false mem- 
brane. 
While this is the process in the fauces and nares, that in the 
larynx and trachea is a somewhat different one. The disease 
usually begins in the former structures, its most frequent primary 
seat being the fauces, whence it occasionally extends into the 
nares, and more frequently into the pharynx and larynx. In the 
larynx, after the catarrhal stage, there is also the production of a 
false membrane, but this does not adhere to the mucous membrane, 
nor is there usually any necrosis. The false membrane is a whitish 
layer which is loosely connected with the mucous membrane, and 
is readily raised by the accumulation of mucus under it. There 
are undoubted inflammatory changes in the mucous membrane in 
the form of infiltration with round cells, but the only actual loss CROUP AND DIPHTHERIA. 
459 
of substance is the shedding of the epithelium of the surface. 
The epithelium always undergoes necrosis before the formation 
of the false membrane. 
Differences of opinion exist as to the nature of this false mem- 
brane in the larynx and trachea. By Wagner it has been asserted 
that it arises from the epithelium, being the product of what may 
be regarded as a coagulation-necrosis of it. It is not to be denied 
that the epithelium may undergo this process, but it does not seem 
possible that this can be the source of the whole membrane. We 
know that the membrane is often removed and reproduced, and 
that it may be produced in such quantity as to till up the larynx 
completely. The thin layer of epithelium is quite inadequate to 
such a result, and we must believe that fibrine is actually deposited 
on the inflamed surface. The removal of the epithelium leaves 
the surface incapable of preventing the disintegration of the leuco- 
cytes. The false membrane is therefore to be regarded as an 
inflammatory exudation, and in its histological characters it agrees 
with this. It consists of a fibrinous network, often very coarse 
in its texture, and with inflammatory cells in various abundance 
in it. 
Croup is a name given to membranous sore throats in which the 
exudation is mainly or entirely in the larynx and trachea. The 
name was first applied before the eminently contagious diphtheria 
was distinguished, and it was commonly understood to be a pecu- 
liarly violent inflammation of the air-passages. There seems to 
be no doubt that, nowadays at least, the great majority of cases of 
croup are really cases of diphtheria in which the disease is mainly 
or entirely in the larynx and trachea. 
We have seen that, in the larynx, diphtheria produces an inflam- 
mation in which, after the shedding of the epithelium, a fibrinous 
exudation occurs. It is asserted by some that the diphtheritic 
poison is the only agent capable of producing this form of inflam- 
mation. Looking at the matter from a purely pathological point 
of view apart from clinical experience, it certainly seems possible 
that other irritants may produce similar results. Croup has been 
produced artificially in rabbits by the injection of ammonia into 
the trachea (Weigert). In these cases the irritant first kills the 
epithelium, and then fibrine is deposited. If croup occurs in man 
apart from diphtheria, the irritant must be strong enough to 
destroy the surface epithelium. Apart from the action of minute 
organisms, such an irritant must be of rare occurrence, but the 
possibility of its existence is not to be denied. We shall see 
afterwards that, in rare cases, we meet with a bronchial croup 
where there can be no question of diphtheria, and so we may 
have laryngeal and tracheal croup of a simple inflammatory kind. 
In such cases there will be no signs of general disease, but all the 
symptoms will be referrible to the local inflammation and obstruc- 
tion of the larynx. It should be added that laryngeal croup has 
been met with in smallpox, measles, pyaemia, etc., but here it is 
to be ascribed to the action of organisms, as in diphtheria. 460 DISEASES OF THE ORGANS OF RESPIRATION. 
Catarrh of the Larynx and Trachea.—We have seen that 
acute catarrh forms the first stage in croup; it is the result of the 
action of the specific poison. Similarly we have acute catarrh in 
measles and smallpox, there being here a specific eruption similar 
to that on the skin, along with acute catarrh. In typhoid fever 
and other infectious diseases we may also have acute catarrh. It 
occurs also as an independent affection, just as nasal catarrh does, 
and in this case, although usually slight, it may assume a very 
severe character. Lastly, a catarrh may be set up by the inhala- 
tion of irritating chemical fumes. 
There are, as in other inflammations, liypersemia and exudation. 
The mucous membrane is red as seen during life, but on post- 
mortem examination the redness has usually disappeared entirely, 
the vessels emptying apparently by the shrinking of the tissue. 
The exudation is originally mucous in character, and is not gen- 
erally very abundant., After a time, as in the case of nasal catarrh, 
it usually assumes a more purulent character. The swelling of 
the mucous membrane is not usually great, and there is not com- 
monly any serious obstruction. On the other hand, in children a 
slight catarrh may bring on a sudden suffocative attack due not so 
much to the swelling as to spasm of the muscles. As an unusual 
complication of acute laryngitis may be mentioned oedema glottidis, 
the condition next to be described. 
(Edema Glottidis.—This name is applied to a comparatively 
sudden cedematous swelling, causing often a serious or even fatal 
obstruction of the larynx. The oedema is in most cases an inflam- 
matory exudation, but it occurs in Bright’s disease as part of a 
general oedema. It may be part of a simple inflammation of the 
larynx, or from diphtheria, or the pustular inflammation of small- 
pox. Or the inflammation may be propagated from the pharynx 
and fauces, or from the inflamed perichondrium. The condition 
is not an oedema of the mucous membrane itself; that would pro- 
duce a very moderate swelling, but it is an inflammation and 
oedema extending to the submucous tissue. Now, in most parts 
of the layrnx there is little or no submucous tissue, the mucous 
membrane being bound down to the perichondrium. There are 
some parts, however, where the tissue is looser, and these are 
chiefly the base of the epiglottis, and, to a less extent, the whole 
epiglottis, the ventricular bands, and most of all, the aryteno- 
epiglottic folds. The epiglottis is swollen, especially at its base; 
the aryteno-epiglottic folds are usually much tumefied, appearing 
as rounded tumors projecting backwards from the base of the 
epiglottis. These rounded swellings form, indeed, the most promi- 
nent appearances. The ligaments passing from the epiglottis to 
the tongue are also sometimes swollen. Examined from above, 
the tumefied aryteno-epiglottic folds conceal the parts beneath, but 
on laying open the larynx after death it is found that the ventricular 
bands (false cords) are tumefied, although the true cords are usually 
very little affected. The oedema may affect the submucous tissue 461 
inflammation of the perichondrium. 
in the trachea for some distance below the glottis. If the swollen 
parts be cut into a fluid exudes, which is usually sero-purulent and 
sometimes almost purulent. Occasionally there is blood in it. 
Chronic Catarrh.—This is a common result of repeated attacks 
of acute catarrh, but may occur spontaneously. It is chiefly char- 
acterized, like other chronic inflammations, by new formation of 
tissue; the mucous membrane is thickened, and its surface is 
irregular. The increase is mainly of connective tissue which, 
having the usual characters of that resulting from inflammation, 
gives rigidity to the parts. The movable structures of the larynx 
are thus rendered more or less stitf, and hoarseness is the result. 
IsTot infrequently flat superficial ulcers or erosions form, and these 
have their seats most commonly at the posterior commissure. The 
racemose glands of the larynx may undergo special enlargement 
so as to appear as rounded prominences. They sometimes ulcerate, 
and so give rise to small crater-shaped ulcers, which are chiefly to 
be seen on the epiglottis and aryteno-epiglottic ligaments. The 
thickening and contraction of the connective tissue are sometimes 
so great as to produce very great stenosis of the larynx, so that 
tracheotomy is needed to permit of respiration. Sometimes 
mucous polypi form on the surface, and add to the irregularity. 
Subglottic Inflammation.—This disease, which is not of very 
frequent occurrence, is an inflammation of the mucous membrane 
beneath the glottis. It may be acute in its onset but it generally 
passes into a chronic stage. It has been observed as a sequel to 
erysipelas and typhus fever, and may have origin apparently in in- 
flammation of the perichondrium. In acute cases there may be 
considerable oedematous swelling. In the chronic form there is 
thickening of the mucous membrane as in ordinary chronic laryn- 
gitis. The inflammation is often just beneath the cords and so 
may produce fixation of them, but it may occur further down, 
and is not infrequently in patches interrupted by normal mucous 
membrane. 
Inflammation of the Perichondrium.—This disease is rarely a 
primary one, being induced chiefly by syphilitic and tubercular in- 
flammations, especially when there is deep ulceration extending 
down to the perichondrium. It occurs occasionally as a sequel of 
typhoid and also probably of typhus fever. It has usually a some- 
what chronic course, but may be acute, and in either case it ends 
in the formation of pus under the perichondrium. The pus ac- 
cumulating under the perichondrium cuts oft* the cartilage from 
its source of nutrition, and just as in periostitis, this is usually 
followed by necrosis of the cartilage. The destruction of the 
cartilage may be a slow process and there may be a kind of caries 
followed by necrosis. The disease is generally confined to one 
cartilage at the outset, the cricoid being most frequently attacked, 
but it may extend to others. When suppuration has occurred the 462 
DISEASES OF THE OliGAXS OF 11ESPIR A TION, 
inflammation spreads to structures around, and we may have bur- 
rowing of the pus under the mucous membrane for some distance, 
or even outside the larynx among the structures of the neck. 
The pus, after a time, obtains an exit, usually by perforating the 
mucous membrane, but sometimes it flnds its way to the surface 
of the body. The necrosed cartilage is, by degrees, separated from 
the living and not infrequently it finds exit by the fistula which 
the pus has formed, it is usually discharged into the larynx, and 
cases have occurred in which the dead piece of cartilage has ob- 
structed the glottis. Or, after being discharged into the larynx, 
it may drop down into the trachea or bronchi to be afterwards 
coughed up. On the other hand, it is sometimes discharged 
through the skin. In connection with these processes, and often 
with the primary disease, there is usually great thickening and 
deformity of the larynx. If the patient survive the discharge of 
the cartilage, its loss leads to still greater deformity- The larynx 
may collapse, or, by a more chronic process, the inflammation may 
cause great contraction and obstruction of the larynx. When the 
cartilage is discharged it is generally found calcified or ossified, 
and it may be a question how far the calcification preceded the in- 
flammation. Dietrich has suggested that, in the case of the cricoid, 
ossification may sometimes be the primary condition, and that the 
inflammation may be induced by the pressure of the hardened 
cartilage against the vertebral column. 
Syphilis.—This disease produces very frequent and sometimes 
very serious lesions in the larynx. These lesions are almost 
entirely inflammatory, and they vary from a slight catarrh to a 
prolonged inflammation accompanied by great thickening with 
stenosis and deep ulceration. The slighter inflammations are 
earlier manifestations of syphilis, and like these in general they 
may entirely disappear. Those occurring later on are usually pro- 
longed and slow in their progress. The mucous membrane and 
submucous tissue are infiltrated and thickened, ulcers develop, 
first, as a general rule, in the epiglottis, but they are prone to 
extend deeply and widely so as to destroy large portions of the 
epiglottis or the whole of it. We have already seen that the 
ulceration may lead to perichondritis and necrosis of the cartilage 
with still wider results. With all this there is great new forma- 
tion of connective tissue with corresponding deformity, and if the 
ulcers heal the contraction of the cicatricial tissue leads to great 
deformity, and not infrequently to such obstruction of the glottis 
as to require tracheotomy. These inflammatory manifestations 
are not usually associated with the formation of proper gummata, 
although the granulation tissue may be produced at first in small 
nodules and is hardly of normal character, partaking of the ten- 
dency to regressive changes which the gummata show. Sometimes 
with the slighter inflammations there may be polypoid projections 
consisting of thickened mucous membrane and epithelium, form- 
ing the so-called condylomata. LARYNGEAL PHTHISIS. 
463 
Laryngeal Phthisis.—This is nearly always secondary to pul- 
monary phthisis, and is a true tubercular disease. It is not impos- 
sible that the tubercular virus may attack the laryngeal mucous 
membrane primarily, or it may attack it simultaneously with the 
lung, but as a matter of fact the lung is in almost every case dis- 
eased, and the probability is that in most cases the virus is carried 
from the diseased lung in the sputum. There are some cases in 
which the laryngeal symptoms are more pronounced than the pul- 
monary, and clinical observers describe them as cases of laryngeal 
rather than of pulmonary phthisis. The larynx has been found 
affected in about 30 per cent, of cases of pulmonary phthisis ex- 
amined after death. 
In cases of phthisis pulmonalis the mucous membrane is fre- 
quently pale from anaemia, but although this may be important as 
showing a tendency to laryngeal disease it is not to be regarded as 
really due to existing tuberculosis, especially as it occurs in 
ordinary anaemias. The first result of the actual tubercular dis- 
ease is thickening of the mucous membrane. This is due to 
chronic inflammation, and is caused chiefly by exudation of serous 
fluid and inflammatory cells with tubercles, so that it is mainly an 
cedematous thickening. It is most marked in the epiglottis and 
aryteno-epiglottic folds, these latter often showing themselves as 
rounded prominences. In this stage microscopic examination 
show's the presence of tubercles with their characteristic structure 
along with inflammatory cells. The tubercles are in the mucous 
membrane and the submucous tissue, the epithelium being as yet 
intact. 
To the thickening succeeds ulceration, the ulcers being at first 
small and superficial. These ulcers result from the caseation and 
softening of superficial tubercles. By coalescence larger ulcers form 
out of the smaller ones, and there is a continual tendency to 
spreading. As a rule there are many ulcers, and between them is 
thickened mucous membrane which at the borders of the ulcers 
sometimes presents irregular projections like papillary outgrowths. 
The ulcers are at first superficial,but as the disease progresses con- 
siderable destruction of tissue may result. The vocal cords are 
not infrequently destroyed, and so there is loss of voice, but the 
voice may be lost from the rigidity of the structures caused by 
thickening from chronic inflammation. Again, perichondritis not 
infrequently follows, with suppuration, and this causes still further 
i nflammatory manifestations. 
Ulceration not uncommonly exists in the trachea and bronchi as 
well as in the larynx. There are many ulcers, and it is not 
uncommon to find the cartilaginous rings of the trachea extensively 
exposed. With these ulcerations of the trachea there will be 
swelling of the remaining mucous membrane and sometimes a 
perichondritis with necrosis. 
The lymphatic glands in the neck are affected secondarily to the 
larynx, they are the seat of scrofulous processes such as we have 464 
DISEASES OF THE ORGANS OF RESPIRATION. 
already described, and their enlargement may, in some cases, aid 
in the exact diagnosis of the disease in the larynx. 
Tumors.—The most frequent form of tumor of the larynx is the 
Papilloma. This tumor is often preceded by catarrhal conditions, 
and is particularly common in persons who, from the nature of 
their profession, use the voice frequently. But it often occurs 
without either of these predisposing conditions. The tumors most 
frequently grow from the vocal cords, where the epithelium is flat. 
They consist, like other papillomas, of a basis of connective tissue 
forming numerous conical projections covered with epithelium (see 
Fig. 223. 
Papilloma*of larynx. e, e, greatly thickened epithelium; h, connective tissue; g, mucous 
glands; f, a gland at base of tumor atrophied by its pressure. X 20. (Cornil and 
Ranvier.) 
Fig. 223). The epithelium ma}7 be thick, and the connective tissue 
dense, so that the tumor is like a hard wart, or the epithelium may 
be thin and the connective tissue soft, sometimes richly intiltrated 
with round cells, and so the growth is soft like a soft wart or 
condyloma. The growth may occupy a small surface of the cord, 
being partially pedunculated, but it often has a considerable base, 
forming a shaggy, irregular outgrowth. Sometimes, after extirpa- 
tion, these tumors take on a sarcomatous character, or even develop 
a cancerous growth. 
A kind of false papilloma occurs, as we have already seen, in 
some cases of tubercular or syphilitic ulceration of the larynx. 
Sometimes, also, the surface of an epithelioma has a papillary 
character. 
Next to the papillomas the fibromas are the commonest tumors 
in the larynx. Morell Mackenzie has found in one hundred cases 
of non-malignant tumors, sixty-seven papillomas and sixteen 
fibromas. They are tumors of slow growth, mostly seated on the the bronchial tubes. 
465 
cords or at the base of the epiglottis. They consist of firm or 
soft connective tissue, those of firm consistence being the commoner. 
They are usually more or less pedunculated, and their surface is 
generally smooth, although it may he irregular or even furnished 
with papillae. They are usually small tumors, from the size of a 
split pea to that of an acorn. 
Mucous Polypi occasionally occur, taking origin in the mucous 
glands. They very commonly undergo transformation into cysts, 
and their most frequent seats are the epiglottis and the ventricles 
of Morgagni. 
Other forms of simple tumors are uncommon, but cases of 
lipoma, myxoma, and angioma have been met with. Cartila- 
ginous tumors formed by outgrowth from the normal cartilages 
have been found. They are usually multiple and sessile. They 
may project considerably into the larynx, and being covered with 
mucous membrane may be mistaken for one of the commoner 
tumors mentioned above. As these tumors are firmly connected 
with the cartilage beneath, they cannot be removed by forceps, 
and so it is important to distinguish them from the others. 
Sarcomas of the larynx are of occasional occurrence. They are 
usually of the spindle-celled form, but may be round-celled. They 
may grow to a considerable size, and are, of course, prone to recur 
unless the whole larynx be removed along with the tumor. 
Cancer of the larynx develops in the form of flat-celled epithe- 
lioma. It is not infrequently a primary tumor, growing usually 
from the ventricular bands, but also originating in other parts. 
An epithelioma may also extend from a neighboring part, particu- 
larly from the tongue. There is first an infiltration of a limited 
part which extends in area, involving more and more in an indis- 
criminate advance. Very commonly there is an abundant papillary 
growth on the surface, so that there is a resemblance to the cauli- 
flower cancer or to the papilloma. The central parts of the growth 
undergo ulceration while the disease is extending circumferentially. 
In this way great destruction of tissue may result, and the parts 
present great deformity. 
Tumors are of very rare occurrence in the trachea, but we may 
have similar growths to those in the larynx. 
THE BRONCHIAL TUBES. 
The diseases of the bronchi stand in close relation on the one 
hand to those of the larynx and trachea, and on the other to those 
of the lungs, and it is impossible to draw an absolute line of dis- 
tinction on either side. The affections of the larger and middle 
bronchi are essentially like those of the larynx and trachea, and 
this is consistent with the fact that in structure they are similar. 
As we pass down the bronchial tree, however, the structure 
changes considerably. The cartilaginous plates become irregular 
and smaller, and finally disappear; the elastic tissue becomes 466 
DISEASES OF THE ORGANS OF RESPIRATION. 
more completely incorporated with the mucous membrane, so as 
to form a single layer which becomes thinner as the tube diminishes 
in calibre; the bronchial glands altogether disappear in the liner 
tubes. The bronchial tube thus becomes more simple in structure, 
and approximates to that of the lung alveoli. So it happens that 
in their diseases the liner bronchi are more allied to the lungs, 
and are often involved with them. We shall afterwards see that 
in acute catarrhal inflammation of the lung the disease often 
begins in a capillary bronchitis, and is sometimes described under 
that name. 
Bronchiectasis.—By this name is meant dilatation of bronchial 
tubes, a condition of somewhat frequent occurrence, but depending 
on a considerable variety of circumstances. The normal bronchial 
tube oilers resistance to the dilating force of the air, chiefly by 
virtue of its elastic or dense walls, and the support which it receives 
from the pulmonary tissue around. If the walls be weakened or 
the support of the pulmonary parenchyma withdrawn, or if the 
distensile force of the air or other contents be considerably in- 
creased, then we may have bronchiectasis. It will be seen that 
one or other of these predisposing conditions may occur under 
very various circumstances. A prolonged catarrh may cause 
atrophy of the elastic tissue of the bronchial wall, and so reduce 
the resistance. On the other hand, obliteration of the liner 
bronchi and lung alveoli in a district will cause the pressure of 
the air in inspiration to act especially on the bronchial tubes, the 
dilatation being here similar in its origin to compensatory em- 
physema. Lastly, we may have the bronchi dilated from accumu- 
lation of secretion. This will occur chiefly when a small bronchus 
has been obstructed, and the condition may be compared to a re- 
tention cyst. 
The various forms of bronchiectasis may be divided into two, 
namely, cylindrical and sacculated dilatations. The former occurs 
mainly where the causal condition has been more or less of a 
general one, such as a prolonged bronchitis. The bronchi, 
especially the middle-sized ones, are unduly wide, and their walls 
are thinned. The dilatation may he quite regular, hut very often 
there are little bulgings or pouches. In the sacculated form there 
has usually been a more local agent at work. The most typical 
sacculated dilatations are found in fibroid phthisis, under which 
heading they will he treated of more fully. They may be pro- 
duced also by any cause which induces shrinking of the lung 
tissue. The wall of the bronchus is thinned, but it still presents 
a distinct membrane lining the sac. When cavities in the lung 
have a distinct lining membrane, they are generally of this origin, 
and they are especially so when the membrane is surrounded by 
lung tissue which approaches to the normal condition. As the 
secretion stagnates in the sacculated dilatation, and may decompose, 
there may be ulceration of its internal wall. BRONCHIAL CATARRH — BRONCHITIS. 
467 
Bronchial Catarrh or Ordinary Bronchitis. — This is an 
inflammation affecting the larger and middle-sized tubes, but not 
extending to any considerable degree into the finer ones. As to 
the conditions giving rise to it, much that has been said under 
nasal catarrh is again applicable here. It is to be added, however, 
that in many persons there is a special proclivity to recurrent 
attacks of bronchitis. This may be due to an inherited weakness 
in this direction, but is perhaps more frequently occasioned by an 
acute bronchitis which has left the bronchi considerably altered in 
structure, has rendered them, in fact, the least resistant part of the 
body. In such persons, cold may set up a bronchitis, or it may be 
set up by disorder of the stomach, or by some other trivial cause. 
Valvular disease of the heart frequently gives rise to bronchitis, 
but we shall consider this when the results of cardiac disease in 
regard to the lung are under review. 
In the slighter forms of bronchitis, the larger bronchi and the 
trachea are mainly affected. In fact, it frequently happens that 
along with a slight laryngitis there is a tracheitis and a bronchitis 
of the larger stems, without the name bronchitis being given. In 
the more definite cases of bronchial catarrh, it is the middle-sized 
tubes that are chiefly involved. 
In order to appreciate the changes which occur in bronchitis, it 
is necessary to refer to some points in the structure of the tubes. 
The mucous membrane is covered with epithelium whose super- 
ficial layer is cylindrical and ciliated. Beneath the epithelium 
there is a basement membrane which is separate from the proper 
mucosa under it. The mucosa is composed of connective tissue, 
and presents externally a muscular layer, chiefly of circular fibres, 
but with some longitudinal ones. Outside this we have the sub- 
mucosa or adventitia, which is continuous with and really forms a 
part of the general interstitial connective tissue of the lung. In 
this loose adventitia the cartilages are embedded, and there are 
abundant serous and lymphatic spaces, which are in communica- 
tion with those throughout the lung, the perivascular and others. 
According to the careful description of Hamilton, acute bron- 
chitis is accompanied first by great congestion, chiefly of the vessels 
in the proper mucosa. (Edema of the basement membrane follows, 
and this structure becomes greatly thickened. The superficial 
layer of columnar epithelium is shed, but vigorous germination of 
the deeper layers occurs, abundant embryonic cells being produced. 
At the same time there is great infiltration of the mucosa, muscular 
layer, and adventitia, with round cells of inflammation. This 
infiltration may be very great, and, as the adventitia communicates 
with the general interstitial tissue of the lungs, there may be a 
wide distribution of these cells, which pass on by the lymphatic 
channels to the lymphatic glands. 
If the disease becomes chronic, the inflammatory infiltration of 
the layers beneath the basement membrane continues, and there 
is the usual new formation of connective tissue producing an 
induration of the tissue. As in other productive inflammations, 468 
DISEASES OF THE ORGANS OF RESPIRATION. 
the new-formed tissue often causes atrophy of the proper structures. 
In many cases the muscular coat is to some extent atrophied, 
although sometimes it is hypertrophied. The mucous glands are 
often considerably destroyed, and even the cartilages may be 
partially atrophied. These alterations in the walls of the tubes 
no doubt weaken them, and, as they occur especially in long-con- 
tinued cases of bronchitis, we can understand how in such cases 
the bronchial tubes sometimes undergo dilatation. Dilatation of 
bronchial tubes is not, however, a very prominent feature of ordi- 
naiy bronchitis. 
The exudation in bronchitis is important, as it forms the sputum, 
and gives its characters to the latter. In the normal condition the 
mucous glands secrete enough mucus to keep the membrane moist, 
the secretion consisting of a glairy fluid containing a few leuco- 
cytes which are here called mucous corpuscles. The fluid owes 
its glairy or sticky character to the fact that it contains mucin, a 
chemical substance allied to albumen and secreted by the mucous 
glands. This normal secretion catches and holds the minute 
particles forming the dust which we inhale with the air, and the 
vibratile cilia of the epithelium acting towards the outlets carry 
mucus and dust outwards, to be swallowed or expectorated. In 
bronchitis there is at first very little increase of the secretion, and 
what there is is chiefly concentrated mucus, tough and scanty. 
As the disease progresses it becomes more abundant but less 
tough and less transparent, and this is brought about by the 
increase of the inflammatory exudation consisting of serous fluid 
and inflammatory cells. The degree of toughness depends on the 
proportion of mucin, and the degree of opacity on the quantity 
of cells. As the disease advances the leucocytes go on increasing, 
and so the fluid on the surface of the mucous membrane becomes 
more and more opaque. 
The sputum coctum, or ripe sputum met with at the acme of the 
disease, is yellowish-white or greenish and opaque. It is not 
homogeneous, but has more opaque and less opaque portions 
according as it has got mixed and coated with mucus from less 
affected parts of the tubes. The sputum as seen in a vessel appears 
at first sight like pus, but it is much more tenacious. Under the 
microscope it also resembles pus, the field being crowded with 
multitudes of leucocytes. But the tenacity of the fluid is often 
shown by the manner in which the plastic leucocytes are altered 
in shape, being drawn out into oval or more elongated forms 
according as the tough mucus is drawn out. On adding acetic 
acid the usual development of nuclei occurs in the cells, and the 
intermediate fluid becomes markedly opaque from the precipita- 
tion of the mucin which can be seen now in fine granules. With 
acetic acid the sputum assumes to the naked eye a whitish opaque, 
and almost membranous character. 
In chronic bronchitis the sputum is often very abundant, and is 
usually sero-mucous with comparatively few leucocytes, and hence DISEASES OF THE LUNGS. 
469 
transparent. There is a comparatively rich serous exudation with 
very little increase in the secretion of mucus. The sputum is not 
so tough as in more acute cases, and is often very frothy. In some 
very chronic cases there is a very abundant cellular exudation— 
the sputum is almost like pus and has not the toughness of the 
sputum coctum. Large quantities of pus may thus be expectorated. 
In these cases it may be supposed that leucocytes are present in 
the walls and outside the bronchi as well as in the expectoration, 
and it is in them that we may look especially for dilatation of the 
tubes. 
Fibrinous Bronchitis.—This name, as well as that of plastic 
bronchitis or bronchial croup, is given to a condition of very 
rare occurrence and of rather obscure pathology, but yet of great 
interest. We have seen that in laryngeal and tracheal croup the 
fibrinous exudation sometimes extends down into the bronchial 
tubes, and that casts of these are formed occasionally. Taking the 
other end of the bronchial tree we find that in acute pneumonia 
the fibrinous exudation which forms in the lung aveoli commonly 
extends some distance into the finer bronchi, and so we find casts 
in them. But there are cases in which fibrinous casts form in the 
bronchial tubes independently, without any disease of the trachea 
on the one hand, or of the lung proper on the other. These cases 
are somewhat chronic in character, and the expectoration of casts 
occurs at intervals during months or even years. The casts are 
of a whitish-gray color and represent the bronchi of, it may be, a 
single lobe, with their ramifications, as we can see very beautifully 
by floating them out in water. Sometimes the fine ends of the 
casts are swollen out as if they had come from the alveoli. The 
casts sometimes present on section a stratified arrangement as if 
the fibrine had been deposited in layers. They show under the 
microscope fibrine with leucocytes. 
The exact pathology and the source of this exudation are some- 
what obscure. In some cases, where death has occurred shortly 
after the expectoration of the casts, or where they have been found 
in situ, there lias been little preceptible alteration of the mucous 
membrane. This has led some to suppose that the fibrine comes 
from the lung alveoli, and in many cases the lung tissue is con- 
siderably altered, for there may be phthisis, or pneumonia, or 
collapse. But it is not apparent to what extent these may be 
secondary to the bronchitis. A possible indication of the pathol- 
ogy may be afforded by the fact that in a considerable proportion 
of the cases there has been hemorrhage from the lungs. 
B.—THE LUNGS. 
In examining the lungs after death we seldom meet with them 
in a perfectly normal condition. They may be abnormally ad- 
herent to the wall of the thorax, or unduly pigmented, or there 470 
DISEASES OF THE ORGANS OF RESPIRATION. 
may be cicatrices in them, or oedema, and so on. The explanation 
of this is, perhaps, that the lungs are peculiarly exposed to deleteri- 
ous influences in two directions. The air passing into them is apt 
to carry irritating materials with it, and the blood circulating so 
richly through their tissue is liable to variations in its constitution 
and degree of pressure. We have already seen, for instance, that 
organic disease of the heart has serious effects on the pulmonary 
circulation, but apart from that, simple weakness of the heart may, 
as we shall afterwards see, have important effects on the lung. It 
must not be forgotten also that there is no organ of the body 
whose tissue is so intimately related to its bloodvessels as the 
lungs. These organs are little more than a congeries of blood- 
vessels with a sufficient supporting stroma. Any deleterious sub- 
stance circulating in the blood, therefore, is very prone to affect 
the lungs, especially if there be any special weakness in this direc- 
tion. We have abundant illustrations of this in the frequency of 
lung complications in the acute fevers. 
There are one or two points in the anatomical relations of the 
lung which should be kept in mind. It is supplied with two 
different sets of bloodvessels, the pulmonary artery on the one 
hand, and the bronchial artery on the other. We should remember 
the distribution of these, and not confuse effects due to obstruction 
of the one with those due to obstruction of the other. Then we 
speak of diseases affecting the respiratory surface on the one hand, 
and the supporting structures on the other; that is to say, there 
are some diseases which affect the surfaces of the finer bronchi 
and of the alveoli, while others involve the walls of the alveoli 
and of the bronchi. It is true that these two are generally in- 
volved together, but in different cases the one or the other is 
primarily concerned, and usually retains the lead. It is obvious 
that to a certain extent the determining cause of the disease will 
have something to do with this. An agent which acts by being 
carried into the lungs with the air will mostly affect the surface 
of the alveoli and bronchi in the first place, whereas an agent 
arriving by the blood will be more apt to attack the walls. We 
shall see, however, that to this there are important exceptions, 
because, on the one hand, the capillary vessels have such a close 
relation to the surface of the alveoli, and, on the other hand, 
substances arriving from without very readily penetrate into the 
substance of the lung. A more important consideration arising 
from the anatomical relations has reference to the distribution of 
a lesion in larger or smaller districts of the lung. When a disease 
is caused by something arriving by the blood then we should expect 
it to be distributed over a large extent of lung tissue or over the 
whole ; the disease will occupy whole lobes. If it arrives by the 
bronchial tubes, we should expect it to extend to the proper lung 
tissue more irregularly, here and there an extension corresponding 
with a particular minute bronchus; the disease at first involves 
lobules. In this way we may distinguish roughly diseases which 471 
ATELECTASIS AND COLLAPSE OF THE LUNG. 
are lobar as due to alterations in the blood, and those that are 
lobular as related to the bronchial stem. 
MALFOKMATIONS OF THE LUNG. 
These are not frequent, and are of minor importance. Apart 
from absence or exceeding smallness of one or both lungs, which 
occurs as part of general malformations, there are cases where 
single lobes have been wanting, and their place taken by cicatricial 
tissue. These have probably their origin in obliteration of a 
bronchus in early foetal life. Again, the lungs may be normal in 
form, but very small in size. In such cases the whole body, and 
especially the circulatory system, will remain ill-developed. 
It is not uncommon to meet with abnormal lobulation of the 
lungs, the regular lobes being divided by the formation of deep 
fissures. Rokitansky has described a case in which an accessory 
lobe existed between the base of the left lung and the diaphragm, 
and quite separate from the lung. It had no bronchus, however. 
ATELECTASIS AND COLLAPSE OF THE LUNG. 
These names designate conditions in which the lung alveoli and 
finer bronchi contain no air, but are in a condition similar to that 
of the foetal lung before inflation, the internal surfaces of the alveoli 
being applied to each other. It may be a survival of the foetal 
state, or it may be subsequently produced by the alveoli being, in 
some way, emptied of their air. As this condition occurs under 
a considerable variety of circumstances we shall give no general 
description, but refer to the individual forms. 
Atelectasis is frequently found in new-born children, being, 
indeed, a survival of the foetal state. The lungs have to a greater 
or less extent remained uninflated. The non-inflation may be due 
to some obstruction in the bronchi, by meconium or mucus, hut 
in most cases it is merely due to the weakness of the respiratory 
efforts. The new-born child usually cries lustily, and in the deep 
inspiratory gasps between the cries the lungs are fully inflated. 
But if the child be weak or has not cried freely, certain parts of 
the lungs are apt to remain devoid of air. The atelectasis of the 
new-born is most frequent in the lower lobe, and in the posterior 
parts of this lobe. It may be only in small areas in the midst of 
the inflated lung tissue, or the greater part of a lobe, or the whole 
lobe may be affected. In any case the non-inflated part usually 
shows by its shape that it is the district supplied by one or more 
bronchi. The atelectasis shows itself by the smaller volume of 
the part. If it is in the midst of inflated lung it is depressed 
below the surface. Like the foetal lung, it is redder than the 
normal, firmer to the touch, and non-crepitant when handled. It 472 
DISEASES OF THE ORGANS OF RESPIRATION. 
is important to distinguish this condition from condensation of the 
lung, for which it is liable to be mistaken. In both the lung is 
devoid of air, but in the case of condensation it is so because the 
air-spaces are filled up with solid material, usually inflammatory 
exudation. The atelectatic portion is capable of inflation by 
blowing air into the lung by the bronchi, at least it is so at the 
outset, while the condensed part is not inflatable. 
There is no doubt that a lung which was partly atelectatic 
immediately after birth may subsequently become perfectly inflated. 
On the other hand there is reason to believe that, if the atelectasis 
presist long, the lung becomes incapable of inflation. If the child 
survive, the applied walls of the lung alveoli adhere and an actual 
obliteration of the latter occurs. The part gradually atrophies, 
and it has been supposed that cicatrices sometimes seen in the 
adult lung and without any obvious cause may have this origin. 
The question arises here whether, after inflation of the lung, 
portions or the whole may again collapse. We shall see immedi- 
ately that collapse occurs in the adult, and there is no reason to 
suppose that it does not occur in the new-born infant. There are 
undoubted cases of children who have lived over twenty-fours and 
have cried, in whose bodies the lungs have been found with only 
one island here and there of inflated lung. 
Collapse of the Lung is of frequent occurrence. In some cases 
it is due to direct compression of the lung; the air is simply 
squeezed out of it. Usually this arises from the presence of fluid 
or air in the pleural cavity. In that case the collapse is not 
unlikely to be only partial, that is to say, the air-vesicles are only 
partly emptied and readily recover. But if the exudation is great 
and remains long, then the lung may be pressed upwards and 
backwards and come to form merely a red fleshy layer flattened 
against the chest wall. This condition is often called carnifica- 
tion, and in it the tissue appears darkly pigmented, the absence of 
blood and the packing together of the lung tissue exaggerating 
the existing carbonaceous pigmentation. The cause mentioned 
above is by far the most frequent in producing collapse by pressure, 
but there are others. Curvature of the spine sometimes causes 
such a narrowing of a part of the chest that the lung is squeezed 
or collapsed. Aneurisms or tumors may also compress the lung, 
but they more frequently cause collapse by obstructing the bronchi. 
Even distention of the abdomen, by pressing the diaphragm 
upwards and limiting the chest space, may cause a partial collapse. 
A great distention of the pericardium may have a similar effect. 
A very important cause of collapse is obstruction of bronchi. 
To a limited extent collapse is exceedingly frequent in bronchitis, 
much more frequent than is usually supposed. The collapse very 
often appears in the form of small wedge-shaped depressions at the 
edges of the lungs, and may be almost concealed by neighboring 
emphysematous lung. But sometimes, especially in children, the 
collapse may he much more extensive. The mode in which this HYPERTROPHY of the lung. 
473 
collapse occurs has been well described by Gairdner. If a pellet 
of mucus obstructs a bronchus it generally does so at a bifurcation. 
The bronchus is partially obstructed, and the pellet of mucus being 
movable, acts to a certain extent like a valve; it is pushed out into 
the larger tube during expiration, and being drawn back against 
the bifurcation in inspiration stops the tube. In this way the 
escape of air during expiration is allowed, but the entrance of air 
during inspiration prevented. The respiratory movements will 
thus act, to a certain extent, like an air pump, and the portion of 
lung tissue concerned will be gradually emptied of air. 
There is another way in which collapse probably occurs when a 
bronchus is obstructed. It is to be remembered that the lung 
tissue is elastic, and that left to themselves the alveoli collapse 
and their walls apply themselves together. If a bronchus be 
obstructed, therefore, and communication with the external air 
withdrawn, the absorption of oxygen will soon reduce the bulk of 
the contained air, and cause a reduction of its elastic pressure. 
The elasticity of the lung tissue, again, will cause pressure to be 
exercised on the air, and absorption of the gases of the air will be 
thus promoted. It has been proved that such absorption actually 
occurs, first of the oxygen, then of the carbonic acid, the nitrogen 
being slowest of absorption. The lung of course collapses as the 
air is absorbed. 
ft has just been stated that collapse from bronchial obstruction 
is most common in the bronchitis of children, but it is necessary 
to observe that in children, in whom the form called capillary 
bronchitis is common, it is often accompanied by a condition which 
is apt to be mistaken for collapse, namely, lobular condensation. 
The catarrhal process in the bronchi readily passes in children to 
the lung alveoli, and the catarrhal products fill these up, causing 
condensation of a portion of the tissue which has a wedge-shaped 
configuration similar to that of the collapsed portion. Of course, 
these two conditions may coexist in the same lung, or we may 
even have a combination of them, the collapsed lung becoming the 
seat of catarrh, and so passing into the condition of condensation. 
HYPERTROPHY OF THE LUNG. 
A case occurred recently to the author which distinctly mani- 
fested the characters of compensatory hypertrophy of the lung. 
The left lung was of very small dimensions, especially the upper 
lobe, which appeared merely as a membranous structure in which 
dilated bronchi would be felt. There was no pigment in this lobe, 
and not a trace of lung parenchyma. The lower lobe contained 
the ordinary carbonaceous pigment in limited amount, but was 
greatly reduced in size. 
The right lung was of very unusual volume, extending across 
the middle line, so that its edge reached beyond the left nipple. 
The enlargement seemed to be due to an addition of lung tissue 474 
DISEASES OF THE ORGANS OF RESPIRATION. 
at the anterior parts. The supra-clavicular part of the apex of the 
lung had the normal form and size, and its anterior border indi- 
cated the position of the normal anterior margin. WThat should 
have been the anterior margin was indicated by this. Beyond 
this, however, a bulky piece of lung extended into the other half 
of the chest. This part of the lung had not the appearances of 
emphysema, at least in any considerable degree. The right ven- 
tricle of the heart was greatly enlarged, and the pulmonary artery 
showed a remarkable thickening of its wall, there being scarcely 
any difference between it and the aorta. 
The absence of pulmonary tissue in the upper lobe of the left 
lung indicated that the collapse had been of long standing, while 
the entire absence of pigment showed that, if not congenital, it 
had occurred in very early life. The enlargement of the right 
lung was thus compensatory, dating from a period when the organ 
was in a state of growth. The compensation seems to have been 
somewhat effective, as the person lived to the age of 46, and it was 
only during the later months of his life that he suffered from 
serious dyspnoea, followed by signs of venous engorgement. The 
remarkable thickening of the pulmonary artery without any ap- 
pearance of atheroma, also seems to point to a compensatory 
hypertrophy of the right ventricle during the period of growth, 
the vessel in its growth accommodating itself to the increased 
blood-pressure. It may be added that the left pulmonary artery 
had only about a third of the calibre of the right, but the main 
bronchus was of equal size on the two sides. 
PULMONARY EMPHYSEMA. 
This name includes two distinct lesions, in one of which air 
escapes into the connective tissue of the lungs and distends the 
connective-tissue spaces, while in the other the alveoli are over- 
distended and various other changes result, but the air does not 
escape from its natural chambers. It will he seen that the first 
form is comparable with surgical or cutaneous emphysema, while 
the second is essentially different. The one form is called inter- 
lobular or interstitial emphysema: the other, which‘is much com- 
moner, is named vesicular emphysema or simply emphysema. 
Interlobular Emphysema occurs when the air-vesicles are rup- 
tured and the air escapes into the interstitial tissue. The air- 
vesicles may be actually torn open by a broken rib coming against 
the lung, or by the lung being directly wounded. On the other 
hand, it occasionally happens that the air-vesicles rupture from 
acute over-disteution. We shall see afterwards that over-disten- 
tion usually produces the other form of emphysema, but, if very 
acute and very extreme, it may lead to an actual rupture of the 
air-vesicles. A sudden obstruction of a considerable bronchus, 
causing imperfect inflation of a portion of lung, may cause such VESICULAR EMPHYSEMA. 
475 
serious over-distentioo of other parts as to lead to actual rupture 
of the air-vesicles. More commonly it is the result of very violent 
expiratory efforts, generally with, but sometimes without, obstruc- 
tion of the air-passages. It has been met with in whooping-cough, 
in diphtheria, and in violent coughing from the inhalation of 
irritating material. The violent efforts with closed glottis cause 
such compression of the air in the alveoli, that at some place the 
vesicles rupture. As seen after death, the air appears in the form 
of minute rows of bead-like bubbles, visible through the pleura. 
These rows of beads demarcate the lobules. Occasionally there 
are larger bullse, which have been known to rupture externally, 
and so lead to pneumothorax. The air sometimes travels along 
the connective tissue for some distance, just as we find in the case 
of subcutaneous emphysema. It may pass to the root of the lung, 
and from there up along the trachea and out to the subcutaneous 
tissue of the neck, and so lead to a surgical emphysema. This 
has led in some cases to a mistake in diagnosis, as Virchow has 
pointed out. Interlobular emphysema sometimes occurs in diph- 
theria, and may lead to subcutaneous emphysema in the way just 
mentioned. But, if tracheotomy has been performed, it may be 
thought that the emphysema has taken origin in the wound. 
Vesicular Emphysema.—In this condition the air-vesicles are 
over-distended, and, by partial atrophy of their walls, to some 
extent coalesced, but without any actual tearing of them. It will 
be clear that the distention must be frequently repeated or per- 
manent, and we have to consider to what it may be due. Of 
course the distensile force is in the air within the air-vesicles, and 
it may be exercised either in inspiration or expiration. 
When the glottis is closed, and expiration violently performed, 
then the air in the vesicles will he at an increased pressure. The 
expiratory effort is produced by the muscles causing the movable 
walls of the chest to be pressed against the lung. The contraction 
of the abdominal muscles presses the diaphragm upwards, while 
the ribs are depressed. The lung is thus compressed, but at the 
same time it is supported by the structures which compress it, 
and the same force that increases the pressure helps the lung 
tissue to resist it by increasing the support. When the glottis is 
closed, the whole lung may be regarded as one cavity, and the 
pressure will be universally diffused. It may be expected, there- 
fore, that if any part of the lung be insufficiently supported, the 
distensile force will tell especially there. The question therefore 
arises, Are there any parts where the lung is not fully supported 
by the chest walls ? If a deep breath be taken, the glottis closed, 
and the act of expiration vigorously performed for a few seconds, 
we find in our own feelings indications that the lungs are over- 
clistencled, mainly at the anterior parts and the parts above the 
clavicles. We can easily understand how this should be. The 
anterior part of the chest, by reason of the flexibility of the costal 
cartilages, is more movable than the rest of it, and the anterior 476 
diseases of the organs of respiration. 
edges of the lungs, as we can see in an animal whose chest is laid 
open while artificial respiration is carried on, have very free play. 
Then, above the clavicle the lung is obviously less supported than 
where the chest has bony walls. We shall see afterwards that 
these, with one or two other parts, are those in which emphysema, 
when due to frequent expiratory efforts, occurs most typically. 
It will be obvious that if the lung tissue has lost in elastichy, 
the permanent dilatation of the air-vesicles will occur more easily, 
and will readily extend to parts more fully supported than those 
mentioned. In the form to be afterwards referred to under the 
name of Senile Emphysema, there is a loss of elasticity from the 
atrophy of old age. But there seems to be in some cases a general 
loss of elasticity, and it appears as if such a condition were heredi- 
tary to some extent. It is true that frequent over-distention will 
cause atrophy of the elastic tissue of itself, but it is quite apparent 
that in many individuals there is, to begin with, less elastic tissue, 
or it is less resistant, and so we have a predisposition to emphysema, 
sometimes inherited. 
We have still to inquire under what circumstances frequent or 
violent expiratory efforts are made with closed glottis. Coughing 
implies such efforts, and it is in diseases where coughing is a 
prominent feature that we are to look for emphysema from this 
cause. It is met with preeminently in bronchitis. It also occurs 
in whooping-cough, occasionally in croup, and even in the violent 
expiratory efforts of parturition, although in the last two cases 
interlobular emphysema is more likely to occur from the sudden 
and violent nature of the distention. As chronic bronchitis is 
peculiarly a disease of more advanced life, we may expect that a 
preliminary atrophy of the lung tissue, implying a loss of elastic 
tissue, plays an important part in the production of emphysema in 
a large number of cases. 
We turn now to cases in which the air-vesicles are over-distended 
during inspiration. A large number of cases of what is called 
compensatory or vicarious emphysema belong to this class. If 
a part of the lung does not distend fully in inspiration, there must 
either be a falling in of the chest to a corresponding extent, or else 
an over-distention of another part of the lung in order to fill up 
the space. To what extent one or other or both of these will 
occur is determined by circumstances, chiefly by the situation of 
the insufficiently distended part and the time occupied in the oc- 
currence of the lesion. There are many different circumstances 
under which compensatory emphysema may occur. If a portion 
of the lung is collapsed, the neighboring part often undergoes 
emphysematous distention. It occurs thus in bronchitis, and the 
wedges of collapse, already referred to, are often fringed with 
emphysema. We see it also around cicatrices in phthisis, or along 
with bronchiectasis in fibroid phthisis. Emphysema occurs some- 
times to a remarkable extent in connection with general adhesions 
of the lung, and the emphysema is often very marked at the VESICULAR EMPHYSEMA. 
477 
anterior parts. In order to explain this it is to be remembered 
that the lungs have a considerable play in the thorax. They come 
well forward in inspiration and retreat during expiration. We see 
this in the opened thorax during artificial respiration, but in the 
closed thorax the greater mobility of the anterior wall of the thorax 
and the elevation of the sternum produce a similar shifting of the 
lung. But now if one lung is bound down by firm general adhe- 
sions, this play of the lung is prevented, and the distention of the 
lung as a whole is hindered. There may be as a result deficient 
movement of that side of the chest as a whole. The sternum will 
continue to rise during inspiration, however, and, in order to fill 
up the space, one of two things will happen—either the other lung, 
if not also adherent, will be over-distended and project beyond the 
middle line, or else an emphysema will occur at the anterior parts 
of the adherent lung; this latter is very frequently seen. 
It is sometimes stated that emphysema occurs in cases of con- 
densation of the lungs, as in pneumonia and especially in phthisis. 
We have here to do with conditions in which the air-vesicles are 
filled up with solid material and air does not get in; the finer 
bronchi are at the same time plugged. The air-vesicles are not 
necessarily distended with the material, but, being plugged, they 
do not expand during inspiration. For this reason the chest in 
phthisis is often immobile in its upper part, and it may fall in 
somewhat even without the formation and collapse of a cavity. 
On the other hand, this deficient expansion may lead to a com- 
pensatory emphysema. 
There is still another way in which it is asserted emphysema 
occurs in the inspiratory phase. If the bronchi be partially 
obstructed, the more powerful inspiratory muscles may be able to 
overcome the obstruction, while the expiratory forces, which nor- 
mally depend mainly on the elasticity of the lung, may do so much 
less efiiciently. At each inspiration, therefore, the air-vesicles are 
over-distended, and are only partially relieved in expiration, so 
that there is an almost continuous condition of dilatation, which 
readily passes into emphysema. This applies chiefly to the case of 
bronchitis, and especially where the smaller bronchi are partially 
obstructed by swelling of the mucous membrane. This view does 
not now meet with very general acceptance, especially as in bron- 
chitis the coughing gives frequent violent expiratory acts. 
We have next to consider the anatomical changes which occur 
in the lung tissue in emphysema. We have to do with air-spaces 
of irregular shape and separated by partial partitions, and as the 
distensile force acts from within, its tendency is to distend equally 
and so render the spaces globular. The ultimate bronchial tubes 
terminate in the elongated passages called from their shape infun- 
dibula. From these passages open by wide apertures the air- 
vesicles, which therefore cluster around the infundibula and are 
mere pouches out from them. The distensile force will act first 
on the infundibulum with its system of air-vesicles, causing clisten- 478 
DISEASES OF THE ORGANS OF RESPIRATION. 
tion. The tendency will be to render the outline more globular 
and the cavity simpler. The partitions separating the alveoli 
atrophy, and the infundibulum expands into a simpler cavity (a a 
in Fig. 224). Thus while more space is occupied there is less res- 
Fig. 224. 
Section of the lung in emphysema, early stage. The infundibula, a, a, a, are 
dilated. X RIO- (Rinj>fi,eisch.) 
piratory surface. The infundibulum continues to expand and 
meets with other infundibula undergoing a similar process. By 
mutual pressure the adjoining tissue atrophies, and the two com- 
municate by such rounded apertures as are shown in Fig. 225. 
The larger cavity tends to become simpler by atrophy of all parti- 
tions and septa, and so the process goes on by coalescence of 
neighboring spaces and atrophy of the partitions. The enlarged 
air-spaces thus produced are of various sizes, up to considerable 
vesicles or bullse. With this atrophy there is great loss of tissue 
and of bloodvessels. Before the actual destruction of the blood- 
vessels the pressure seems to cause obstruction of them so that 
they are not able to be injected and appear as white cords. It is 
stated that this obstruction is effected by the formation of white 
thrombi. The epithelium for the most part persists in the dis- 
tended air-spaces, but it is frequently in a state of fatty degenera- 
tion. It may happen that, as in Fig. 225, the wall of the alveolus 
has atrophied except the epithelium, and the actual apertures are 
formed by its being shed. Of most importance is the atrophy of 
the elastic tissue, because on this account the lung tissue will be 
prevented from collapsing as it normally does. 
The changes in the lungs visible to the naked eye are in ac- 
cordance with these alterations in the finer structure. In the first 
place the changes described cause the affected lung tissue to take 479 
VESICULAR EMPHYSEMA. 
up more room, and there will, therefore, be enlargement of the 
lung varying in extent and situation according to circumstances. 
If the emphysema be at all extensive the lungs as a whole appear 
more bulky, and when the chest is laid open they may appear as if 
Tig. 225. 
Emphysema of lung, portion of the wall of an alveolus. There are several rounded 
apertures. In some parts, and especially at right-hand corner, an aperture seems to be 
forming by the separation of epithelium which has come to form the entire thickness of the 
alveolar wall. X <>00. (Thierfei.der.) 
bulging out at the aperture. This appearance is not altogether 
due to enlargement, but to a certain extent it is related to the fact 
that as the elastic tissue is largely lost the lungs do not retract in 
the normal fashion. The increase of bulk is usually most manifest 
at the anterior margins which, in bronchitis at least, are the most 
frequent seats of the lesion. The margins are unduly voluminous 
and the edges rounded. It not infrequently happens that certain 
portions of the anterior margins undergo special enlargement, a 
projecting piece of lung becoming by its increase in bulk partially 
isolated. The tongue-shaped projection at the edge of the left 
lung corresponding with the lower part of the heart, often presents 
considerable elongation and partial separation. 
Another locality where emphysema is often very manifest is the 
base. Here they are frequently rounded prominences projecting 
against the diaphragm, and the diaphragmatic surface of the lung 
as a whole may be convex instead of concave. This is especially 
the case in the left lung where the diaphragm is not supported by 
a solid organ as it is on the right side by the liver. Again the en- 
largement is very frequent at the apices. It has been pointed out 
by Jenner that the right lung often presents a special bulging pos- 
teriorly at a place corresponding to the space behind the trachea. 
The localization will be more various where the emphysema is 
compensatory, and in that case will depend greatly on the locality 
of the cause. Thus we see it around cicatrices or contracted 480 
DISEASES OF TIIE ORGANS OF RESPIRATION. 
pieces of lung, but in nearly all cases there is a tendency to affect 
especially the anterior parts. 
In all these places, with increase of bulk in general there is, even 
to the naked eye, a visible enlargement of the air-spaces, for- 
mally, the individual air-vesicles are scarcely visible, but in 
emphysema the abnormal air-spaces are plainly seen through the 
pleura, often giving a frothy appearance from the size of the vesi- 
cles and the delicacy of the partitions. Beyond this we may have 
all degrees of visible enlargement of the air-spaces up to consid- 
erable bladders as large as an egg. The emphysematous portion 
is unduly pale, and gives a soft downy feeling to the touch. On 
cutting into it there is often a creaking, crisp sound, and if the 
vesicles are large they collapse markedly. 
We have still to consider some of the effects of emphysema on 
other parts. The lungs are permanently increased in bulk, and 
the capacity of the chest is correspondingly increased. The chest 
is kept more or less in the condition of deep inspiration, the dia- 
phragm depressed and flattened, the shoulders elevated, the sternum 
pushed forwards and outwards, and the chest more or less barrel- 
shaped. The heart is depressed along with the diaphragm and 
placed more horizontally, while it is overlaid by the edges of the 
lung. The liver is pushed downwards by the flattened diaphragm. 
The emphysema has a serious effect on the circulation. We have 
seen that there is obstruction and destruction of the bloodvessels 
in the lung, and this reacting on the pulmonary artery causes 
engorgement of the right ventricle. The right ventricle is induced 
to hypertrophy by reason of the increased strain thrown on it, and 
by more vigorous efforts it may to a great extent compensate for 
the obstruction and send enough blood through the reduced 
channels. But the compensation may, as the disease advances, be 
insufficient, and so we have insufficient aeration of the blood and 
dilatation of the right ventricle without corresponding hypertrophy. 
On this follow all the serious results of venous engorgement already 
referred to. The dilatation of the heart is more apt to ensue 
if, from imperfect nutrition of the heart, the muscular ffbre under- 
goes fatty degeneration, and as a matter of fact the actual fatal 
result is often traceable to fatty degeneration allowing of very 
severe venous engorgement. 
Senile Emphysema is primarily an atrophy of the lung tissue 
along with atrophy of the other tissues of the body. The lung in 
this form does not become more voluminous, but rather retracts 
and becomes softer and more pliable. On opening the chest the 
lungs are found much reduced in bulk and collapsed against 
the posterior wall of the chest. The normal weight of the lungs 
is about 44J ounces in the male and 35 ounces in the female, but 
in senile emphysema they may be only two-thirds of this weight. 
The air-vesicles undergo changes similar in appearance to those in 
ordinary vesicular emphysema; their walls atrophy and the infun- ACTIVE HYPEREMIA OF THE LUNGS. 
481 
dibula coalesce so as to form larger cavities, but this is by a simple 
process of atrophy. On examining the lung the increased size of 
the air spaces may be invisible at first, but if the lung be distended, 
or if after laying it open by incision it be floated in water, the 
large vesicles become visible. Of course old people are subject to 
bronchitis, and senile atrophy may strongly predispose to the more 
ordinary form of emphysema. 
DISORDERS OF THE CIRCULATION IN THE LUNGS. 
It is to be remembered that the pulmonary arteries are thin- 
walled, and that their muscular coat is comparatively insufficient. 
Any increase of blood-pressure, therefore, will tell with full force 
on the pulmonary circulation. The capillaries are abundant and 
closely set, and are capable of great distention. Their dilatation 
will cause them to project into the air-vesicles, and it is not im- 
probable that they sometimes interfere seriously with the inflation 
of the air-vesicles. 
Active Hyperemia.—This is a condition which we have few 
opportunities of actually observing, but which is to be inferred as 
existing under certain circumstances. It has been a matter of 
question whether an increase in the strength of the cardiac con- 
tractions is capable by itself of producing active congestion of the 
lungs. But, to take a simple example, the feeling of breathlessness 
which one experiences in going up a hill, accompanied as it is with 
severe palpitation and a feeling of oppression in the chest, is 
probably due to an active hypersemia of the lungs from this cause. 
The exertion of the body sends more blood to the right ventricle 
and also stimulates the heart to increased exertion. A larger 
amount of blood is forced into the pulmonary artery, and at a 
greater pressure. Thus the feeling of oppression and breathless- 
ness may be due to the overloading of the vessels, and perhaps to 
some extent to the insufficient inflation of the alveoli. In some 
persons this condition is brought about by very slight exertion, 
their hearts being peculiarly excitable; or it may occur without 
any exertion at all. In persons with damaged hearts, in whom 
the pulmonary circulation is already somewhat engorged, a very 
slight increase in the force of the heart may bring on a further 
hypersemia such as to lead to severe dyspnoea. Thus we know that 
persons suffering from mitral disease find great difficulty even in 
ascending a stair. 
An acute hypersemia sometimes develops as a collateral hyper- 
emia. Cases have been recorded in which a person while heated 
has drunk large quantities of cold water, and has immediately been 
attacked by great dyspnoea, which has even been fatal. Hertz has 
related a case in which a workman, while much heated, went into 
a vault and drank a quantity of water which he had cooled with 
ice. He was immediately seized with the most intense dyspnoea, 482 
DISEASES OF THE ORGAN'S OF RESPIRATION. 
and soon began to expectorate a bright red sputum. In this case 
there was evidently an acute hypersemia, which would probably 
have proved fatal but for timely venesection. The exact mode of 
occurrence of such severe hypersemia has been made the subject 
of experimental investigation. Quantities of ice-cold water have 
been introduced into the stomach in animals, while the blood- 
pressure was registered by a kymograph connected with the 
carotid. The result was an immediate and very marked increase 
of blood-pressure. The cause of increase in pressure was not the 
absorption into the blood of an excess of fluid, because an equal 
quantity of warm water injected directly into the veins produced 
no such rise. The explanation is that the cold water reduces the 
temperature not only in the stomach but in the organs around. 
The result of this application of cold is contraction of arteries, and 
as in this neighborhood there are a large number of arteries—those 
of the stomach itself, the splenic, the hepatic, and the mesenteries, 
with their numerous tine ramifications in the mesentery and in- 
testine—their sudden contraction at once raises the blood-pressure, 
and this acts most readily backwards on the lungs. On similar 
grounds, we may explain the breathlessness which one experiences 
in plunging into cold water. Here the artefies of the skin contract, 
and the risk of pulmonary congestion is greater if the cutaneous 
arteries have been peculiarly relaxed, as when the person has been 
much heated beforehand. 
A simple active hypersemia of the lungs seldom gives rise to 
oedema. We have already seen this to be the case in regard to 
active hypersemia in general, and it especially applies here. In the 
case which we have cited from Hertz there was curvature of the 
spine, and some contraction of the thorax, and this may have had 
to do with the severity of the hypersemia and the occurrence of 
oedema as evidenced by the rales in the chest and the expectoration. 
Passive Hyperemia and Pulmonary (Edema.—Passive hyper- 
semia is of much more frequent occurrence than that just considered. 
In the regular course of post-mortem examinations, we very fre- 
quently find that the dependent parts of the lungs present a dark- 
blue color due to the vessels being overfilled with blood. This 
condition is commonly called hypostatic engorgement, and to a 
certain extent it is really of post-mortem occurrence, the blood 
gravitating to the dependent parts of the lungs. In many cases, 
however, it has existed, at least partly, during life, especially when 
it is associated, as it commonly is, with oedema. This condition 
arises most frequently in persons whose hearts are weakened by 
debilitating diseases, and it frequently develops not long before 
death. In a large number of cases of all kinds of debilitating 
diseases we find just before death the chest full of rales and the 
breathing much obstructed, and it is in these cases that we find 
hypersemia and oedema after death. Or the engorgement and 
oedema may occur in the midst of a debilitating disease, such as 
typhus fever, when they are regarded as of a very serious import. PASSIVE HYPEEJ1MIA AND PULMONARY (EDEMA. 
483 
Sometimes an oedema develops with remarkable suddenness, and 
seriously endangers life. 
It has been stated above that the hypersemia and oedema in 
these cases are connected with weakening of the heart, but it is 
not easy to see how this should produce such results, especially 
when they are of sudden occurrence. When the blood is already 
deteriorated, as in typhus fever, and when by reason of the 
weakness of the heart the circulation is very in the capil- 
laries of the lung, we can understand the occurrence of engorge- 
ment and oedema, just as in these diseases we may have gangrene 
of the toes. Here the absence of the proper renewal of the blood 
causes the vessels to lose their natural vigor and allow of transu- 
dation. In the more ordinary cases of hypostatic oedema occurring 
just before death, we have also, as a consequence of some debilitating 
disease, not only weakness of the heart, but the deterioration of 
the blood, and these together may account for the occurrence of 
the engorgement and oedema. 
But there are some cases in which oedema occurs suddenly, and 
without any previous anaemia or morbid condition of the blood. 
Some of these are cases of Bright’s disease, and the oedema here 
is of similar import to that of the skin in that disease. There are 
cases, however, chiefly of heart disease, in which a sudden oedema 
occurs and is sometimes fatal. These cases can hardly be accounted 
for by a simple weakening of the heart as a whole, or else we should 
have oedema in cases of syncope in which there is simple failure of 
the heart. An endeavor has been made to account for it by sup- 
posing increase of blood-pressure in the pulmonary circulation. 
It has been shown by Cohnheim, from experiments on animals, 
that in order to produce pulmonary oedema the blood-pressure 
must be enormously increased, much more than is ever likely to 
happen from simple mechanical interruption to the circulation in 
the ordinary way. This author has found, however, that if the 
left ventricle be paralyzed while the right keeps beating vigorously, 
we may have such an increase of blood-pressure as to cause oedema 
of the lungs. The weakened left ventricle does not empty itself, 
and acts as an obstruction to the return of blood from the lungs, 
and the obstruction is so great that the right ventricle cannot 
overcome it. It might be objected to this that if the left ventricle 
is thus paralyzed the systemic circulation will be at a standstill, 
and very little blood will find its way to the right ventricle. But 
we have to consider that in such patients there is urgent dyspnoea 
with violent inspiratory efforts which have the effect of sucking 
the blood into the chest. The diastole of the right heart also acts 
in the way of drawing blood towards it. These cases then of 
sudden oedema may be accounted for by weakening of the left 
ventricle while the right remains vigorous. Any special over- 
straining of the left ventricle may cause sudden paralysis of it. It 
is not improbable also that immediately before death the pulsations 
of the left ventricle may, in many cases, cease before those of the 484 
diseases of the organs of respiration 
right, and that the ordinary oedema at the end of debilitating 
diseases may have partly a similar origin. 
When the lungs are examined after death in cases of passive 
hypereemia, they present a dark-blue color which is often limited 
to the posterior parts and those towards the base. If oedema co- 
exists, as it so often does, the tissue is bulkier and more solid. If 
the lung be divided with the knife and the organ squeezed, a frothy 
fluid mixed with blood issues from the cut surface. If the oedema 
exists without much hypersemia the lung is pale, but bulky and 
heavy, and a watery fluid exudes from the cut surface. The con- 
dition of hypersemia with oedema is sometimes called splenization, 
because the tissue is like that of the spleen in its naked-eye 
characters. Examined minutely, it is found that the capillaries 
are distended and the air-vesicles filled with serous fluid in which 
leucocytes and red corpuscles are present. 
If this condition persists, it usually passes gradually into an in- 
flammatory condition. Fibrine is exuded into the air-vesicles, but 
it is mixed with serous fluid, and does not give that extreme solidi- 
fication to the lung which we find in acute pneumonia. The lung 
is more solid than in splenization, however, and the color is not so 
deep. In some cases we find a close approximation to actual 
hepatization, and there may even be breaking down of the inflam- 
matory products, as in the later stages of a pneumonia, so that on 
squeezing the lung a grumous fluid exudes from the cut surface. 
Passive Hyperjemia of the Lungs from Heart Disease.—This 
subject has to a large extent been treated of in previous para- 
graphs, hut some special points remain to be considered. In mitral 
disease especially, there is a constant obstruction to the return of 
blood from the lungs, which, in many cases, is largely compensated 
by hypertrophy of the right ventricle, but even when it is so the 
pulmonary circulation will be constantly at an increased pressure, 
and there will be, consequently, a more or less permanent passive 
hypersemia. This passive hypersemia has various secondary re- 
sults. The most prominent of these during life is bronchitis, a 
more or less persistent catarrh of the bronchial mucous membrane. 
Another result is the condition designated brown induration. In 
this, as in other cases of prolonged passive hypersemia, the con- 
nective tissue of the lung is thickened and increased in density, so 
much so that the condition was described by Rokitansky as an in- 
flammatory hypertrophy of the connective tissue. At the same 
time the capillaries are distended and rendered tortuous. This 
condition of the capillaries is rendered obvious by separating a 
piece of lung tissue by a ligature, placing it in nitric acid, and 
then in spirit. Sections will show the enlarged and varicose 
capillaries as a brownish-red network. The larger vessels are also 
dilated and their supporting connective tissue hypertrophied. 
The dilated capillaries are apt to allow of the leakage of blood- 
corpuscles into the interior of the alveoli, and these give the 
sputum a bloody appearance. Hemorrhage occurs also into the THE HEMORRHAGIC INFARCTION'. 
485 
connective tissue, and the result is a pigmentation, the coloring 
matter existing in the form of granules contained in the connec- 
tive-tissue corpuscles. The blood in some of the capillaries may 
stagnate altogether, and in that case the capillaries will come to be 
represented by a network of brown pigment. 
The general appearance of the lung corresponds to the finer 
characters. As a whole the lung is more consistent, and does not 
retract so fully as usual when the chest is laid open. The color is 
brownish, but it varies considerably both in different cases and 
in different parts of the same lung. There may be a general 
brownish color, or there may be lighter and darker pieces, accord- 
ing as local hemorrhages have occurred more or less recently. 
We must remember that the hemorrhagic infarction occurs 
mainly in cases of heart disease, but has a different origin as ap- 
pears in the next section. 
The Hemorrhagic Infarction.—This condition has already been 
the subject of study when treating of embolism at p. 49. We 
there saw that the pulmonary artery and its branches are end- 
arteries, and that obstruction of one of them is likely to produce 
the hemorrhagic infarction. We saw, however, that two circum- 
stances render this result less uniform in the lungs; in the first 
place, the wide capillaries may act as anastomosing vessels, and so 
the circulation may be kept up sufficiently to prevent diapedesis; 
and, in the second place, the bronchial artery keeps the lung tissue, 
to a certain extent, nourished. We saw that when the infarction 
occurs it is likely to form at the periphery of the lung, especially 
towards the edges where the lung substance is covered on more 
than one side with pleura. The infarction forms by the blood 
taking a backward course from the veins into the capillaries. The 
capillaries become engorged, and the red corpuscles pass through 
their walls into the lung alveoli, which they fill to the exclusion of 
the air. 
But the' hemorrhagic infarction appears to form sometimes as a 
result rather of thrombosis than of embolism of the pulmonary 
artery. In cases, especially of mitral disease, there may be, from 
the great obstruction of the circulation in the lungs, an actual 
stasis in the capillaries, and if the stasis extends backwards to the 
pulmonary artery, it may induce coagulation there. If thrombosis 
occurs in the pulmonary artery, then the blood in the correspond- 
ing veins will take a backward course as before, and the previous 
engorgement of the vessels from the mitral disease will render 
this all the more likely; the capillaries will be distended, and 
diapedesis will result. A hemorrhagic infarction occurring in this 
way will closely resemble one having an embolic origin, and the 
thrombus may be itself hardly distinguishable from an embolus. 
The infarction will, like the other, have a wedge-shape, with its 
blunt end towards the surface. It may be added that this mode 
of origin is much less common than the other, but that an embolus 486 
DISEASES OF THE ORGANS OF RESPIRATION. 
is often increased in size by thrombosis, and may not obstruct till 
added to by thrombosis. 
The appearances of the hemorrhagic infarction are such as result 
from distention of the air-spaces with blood. If quite recent, it is 
of a dark-blue color, dense to the feeling, and more or less wedge- 
shaped, with the apex inwards. It may present all varieties of size 
up to half the lung. As the infarction is mostly peripheral, it may 
be often recognized by the dark color seen through the pleura, but 
it is more easily discovered by handling the lung, when the solid 
mass is readily detected. At first it looks, on section, like a recent 
blood-clot, and has almost a similar smooth surface, but, as time 
goes on, the color merges into brown, and the appearance may 
come to resemble that of red hepatization. As blood fills the 
air-spaces, the piece of lung is more bulky than that surrounding 
it. The infarction, therefore, is often seen as a rounded bulging 
beneath the pleura, or, when the lung is divided, it stands at a 
Fig. 226. 
From a hemorrhagic infarction of the lung. The alveolus is filled with red blood-cor- 
puscles, with one or two large catarrhal cells. In the wall of the alveolus the capillaries are 
greatly distended with blood. X 350. 
higher level than the surrounding tissue. The pleura over the 
infarction is usually covered with a layer of fibrinous exudation 
of a yellow color, and the pleural cavity contains fluid, often in 
considerable quantity. embolism of the pulmonary artery. 
487 
Under the microscope, as shown in Figure 226, we have simply 
an enormous aggregation of red corpuscles in the lung alveoli 
and finer bronchial tubes, with distention of the pulmonary capil- 
laries. There is usually hardly a trace of fibrine to be seen, 
merely red corpuscles which have escaped by diapedesis, and 
perhaps a few catarrhal cells. 
If the patient live for some time after the occurrence of the 
infarction certain changes occur in it, but there are few actual 
observations bearing on this point. It is very probable that in 
some cases the infarction clears away; the blood is discharged by 
expectoration, and the circulation is reestablished, hut the portion 
of lung is unduly pigmented. In other cases the portion of lung 
gradually shrinks, and the ultimate result is a pigmented indura- 
tion. Indurations, probably of this origin, are not infrequently 
met with in cases of valvular disease. In still other cases the 
portion of lung tissue dies and sloughs, so that a cavity forms. 
This condition has probably been often mistaken for phthisis, 
especially as it has probably been preceded by haemoptysis. Some- 
times the slough decomposes, and we have all the features of gan- 
grene of the lungs. It may seem strange that necrosis, which is 
the regular result in other organs, is not of more constant occur- 
rence in the lungs. It is to be remembered, however, that the 
lung tissue in the midst of the infarction is still nourished by the 
bronchial artery, and that, while the capillaries and actual walls 
of the alveoli may die, the interlobular connective tissue may 
survive, and may even use the necrosed tissue as pabulum. 
Embolism of the Pulmonary Artery has been referred to in its 
relations to the hemorrhagic infarction, hut we have already seen 
that it by no means uniformly leads to that result. If the main 
artery of a lung be obstructed the infarction cannot occur, because 
by the obstruction of the artery the lung is deprived of blood. 
But even when smaller branches are occluded the infarction may 
he absent. Cases of sudden death after parturition occur from 
embolic obstruction of the lungs without any infarction. The 
suddenness of death in some of these cases seems to indicate that 
it is not due entirely to the obstruction in the lungs and consequent 
non-aeration of the blood. It seems rather due in great measure 
to the fact that, as the blood is prevented from reaching the left 
ventricle in sufficient amount, the brain and medulla oblongata 
are deprived of their proper nourishment. In such cases the 
right ventricle will be found dilated, while the lungs are pale and 
probably over-inflated by the violent but ineffectual respiratory 
efforts. These sudden deaths after confinement used to be ex- 
plained as cases of shock before Virchow pointed out their true 
significance. 
Reference has already been made to the special form of oil 
embolism. When the subcutaneous fat has been much torn by 
injury, or when in fracture of a bone the marrow is much broken 
up, then fat is apt to find its way into the veins, and this is espe- 488 
DISEASES OF THE ORGANS OF RESPIRATION. 
cially the case when the open mouths of the veins in the broken 
bone come in contact with the fluid fat rendered free by the 
tearing of the adipose tissue. The fat is carried by the veins to 
the right heart and thence to the lungs. It floats in the blood 
as larger or smaller drops, and it may obstruct branches of the 
pulmonary artery of not inconsiderable size, and frequently pro- 
duces extensive injection of the capillaries (see Fig. 227). If the 
Fig. 227. 
Oil or fat embolism of the lung. The fat occupies the smaller arteries and extends 
into the capillaries, which, towards the right, form a network injected with oil. X 90* 
(Thif.rfelder.) 
obstruction be extensive, even though the capillaries are the vessels 
mainly affected, and then serious results may follow. We mav 
have diapedesis and condensation, but in a scattered irregular 
form. When the lungs are laid open by incision, the fat drops 
may sometimes be detected with the naked eye by their glancing 
character as they have issued on the cut surface. 
Pulmonary Hemorrhage.—We have still to refer to certain 
forms besides the hemorrhagic infarction. The hemorrhage which 
occurs in heart disease, and which leads on to brown induration, 
has been considered already. That which so frequently occurs in 
phthisis will be taken up afterwards. Then there is hemorrhage 
in consequence of tearing of the lung by a broken rib or otherwise. 
It is asserted also that there may be rupture of a branch of the 
pulmonary artery from fatty degeneration of its walls, as we may 
have hemorrhage in the brain from atheroma, but this is excessively 
rare. 
In the case of tearing or rupture there is a massive hemorrhage, 489 
ACUTE PNEUMONIA. 
and the blood forms a cavity for itself just as it does in a cerebral 
hemorrhage. To such conditions some would apply the name 
pulmonary apoplexy, but as this is more frequently used to desig- 
nate the hemorrhagic infarction, it is perhaps better to discontinue 
its use. According to Rokitansky, blood thus effused may become 
encapsuled and subsequently become infiltrated with lime salts 
like a foreign body. 
When the hemorrhage is from the bronchial mucous membrane 
or the lung alveoli, then it appears in the sputum. To some 
extent, however, the blood remains in the air-passages, and if it be 
in considerable quantity it may even be carried in considerable 
quantity into the lung alveoli. The blood, in this case, is mixed 
with air, and there is no such condensation as that which occurs 
in the hemorrhagic infarction. In the lung alveoli the blood 
acting as a foreign body irritates the tissue and a catarrhal inflam- 
mation may result. In such cases large catarrhal cells may occupy 
the alveoli wherever the blood has penetrated, and these cells may 
be deeply stained with the coloring matter of the blood. 
It is stated that blood insufflated in large quantities may even 
cause necrosis of the lung tissue in which it lies, and so give rise 
to a condition like that of the infarction. This may, perhaps, 
occur when the lung is already seriously damaged, as in phthisis 
pulmonalis, but hardly in an otherwise healthy lung. It is also 
possible that blood may be drawn into cavities and form fibrinous 
plugs there. 
INFLAMMATIONS OF THE LUNGS. 
Acute Pneumonia.—This is a disease essentially of the lung 
alveoli, and as the most prominent feature is the exudation of 
fibrine into the alveoli, it is frequently called croupous pneumonia. 
Its causation is somewhat obscure. In considering the causation 
of inflammations in general, we have already referred to the fact 
that an irritant, such as carbolic acid, conveyed by the blood to 
the lungs may produce pneumonia. The fact that the disease 
affects whole lobes of the lung is also in favor of the view that the 
irritant is conveyed by the blood. Many physicians regard it as 
belonging to the group of zymotic diseases, and in favor of this is 
the fact that, while usually endemic, it sometimes assumes an 
epidemic prevalence. Lately Koch and others have asserted that 
a bacillus is present in the lung tissue. Koch finds it in the alveoli, 
but only in places where the disease is advancing, the condition in 
this respect resembling that in erysipelas. 
The disease is an acute inflammation, and as the lung alveoli 
possesses merely a single layer of pavement epithelium the inflam- 
mation resembles that of serous rather than of mucous membranes. 
As in the former we have here a fibrinous exudation, and though 
this occurs primarily and mainly in the alveoli, the fibrine, as wre 
shall see, generally extends to the finer bronchi, forming casts of 
them. 490 
DISEASES OF THE ORGANS OF RESPIRATION. 
Pneumonia has been divided into three stages, a preliminary 
one of engorgement, a second one of hepatization, which is divided 
into two divisions, red and gray hepatization, and lastly the stage 
of resolution. By separating the second stage into its two divisions 
we shall have four stages, under which arrangement it will he con- 
sidered here, namely, engorgement, red hepatization, gray hepati- 
zation, and finally purulent infiltration and resolution. 
In the first stage, that of engokgement, the lung-capillaries are 
highly injected, and there is an exudation of serious fluid into the 
air-vesicles. To the naked eye the affected portion of lung is of a 
dark-red color, to the touch it is inelastic, and the finger applied 
to the surface leaves a pit behind. On section a reddish serum 
flows out, and the tissue does not crepitate under the knife so 
much as in the natural state. Though heavier than usual, the dis- 
eased portion of lung still contains some air and therefore usually 
floats in water. This state, from the resemblance of the cut 
surface of the diseased lung to the spleen, has been called 
splenization. So far as the merely anatomical condition is con- 
cerned, the lung is very much in the same state as in passive 
hyperaemia and oedema, such as we see in the ordinary hypostatic 
engorgement, and we have seen that the same term splenization is 
applied there. In the present case, however, the splenization is 
not localized in the dependent parts as in the other, but it affects 
a definite region of lung, generally the lower lobe as a whole, 
along with, perhaps, a portion of the upper. The hyperaemia and 
oedema are, of course, inflammatory in character, and the serum 
is the inflammatory exudation. Like other 
inflammatory exudations, this fluid contains 
leucocytes and also red blood-corpuscles, some- 
times in large numbers. As the alveoli are 
filled with serous fluid, the air bubbling in and 
out among them during respiration produces 
the fine crepitation which is the characteristic 
auscultatory sign of this stage. 
In the second stage, that of red hepatiza- 
iion, we have fibrin e exuded from the over- 
filled capillary vessels. In consequence a 
coagulum (Fig. 228) comes to occupy the 
lumen of the vesicles and infundibula, instead 
of the mixture of serous fluid and air which is 
present in the first stage. But the coagulum 
is not entirely composed of the fibrine effused 
from the vessels; it contains, in addition, 
abundant leucocytes and red corpuscles which 
are often so abundant as almost to conceal the fibrine. The fibrine 
may be detected as a coarse network with interlacing fibres (Fig. 
229). The capillaries of the lung are in much the same state of 
over-distention as in the first stage, and the lung-parencliyma is 
likewise little altered. The red corpuscles are present in the 
alveoli in very varying proportion. They are never entirely absent, 
Fig. 228. 
Cast of small bronchus 
infundibula and air-vesi- 
cles in pneumonia. X 40. 
(Cornil and Ranvier.) ACUTE PNEUMONIA. 
491 
hut in general form the minority of the total cells present; in some 
cases they are equal to the white ones, in some more abundant. In 
very rare cases they are so abundant that the exudation has more 
the character of an ordinary clot than of a fibrinous exudation. In 
Fig. 229. 
Alveolus filled with fibrine and a few leucocytes, from a case of pneumonia in 
stage of red hepatization. X 350. 
these latter cases, which may he described as hemorrhagic pneu- 
monia, the lung itself has a deep-red color. These are mostly very 
severe cases, and imply a previous state of debility in the patient, 
very commonly referrible to alcoholic excess. In accordance with 
this exudation of red blood-corpuscles we have in this and in the 
preceding stage, the rusty tinge of the sputum which is character- 
istic of pneumonia. The appearance of the lung in this stage is 
somewhat different from that in the first. It retains its red color, 
both from the continuance of the congestion of the capillaries and 
from the red corpuscles in the exudation. But it is now much 
firmer and heavier—it does not crepitate under the knife or finger, 
and it sinks in water—no air being any longer contained in the 
vesicles. On section from a sound part into a hepatized part, it is 
observed that the latter remains on a level while the sound part 
sinks away so that the diseased part appears enlarged. Even on 492 
DISEASES OF THE ORGANS OF RESPIRATION. 
external examination the affected part of the lung looks bulky. 
On more close examination, the cut surface has not the homo- 
geneous velvety appearance of the lung in splenization, but a 
coarse granular appearance, and this will be more readily seen on 
tearing the tissue and examining the torn surface with a lens. The 
red granulations thus brought out are undoubtedly the plugs of 
fibrine with corpuscles which fill the air-vesicles. If you stroke a 
surface so cut with the blade of the knife, you may succeed in 
getting one or two casts of the vesicles and infundibula which, 
under the microscope, have the appearance shown in Fig. 228. If 
the bronchial tubes be cut open with scissors, the finer ones will 
generally be found to contain fine casts of soft fibrine, as if the 
exudation had overflowed from the alveoli into them. The appear- 
ance of a section of such a lung has been compared, from its solid 
character, granular surface and color, to that of the liver, hence 
the name hepatization applied to the second stage. The solidified 
lung is a much better conductor of sounds than that filled with 
air; hence, during life, we hear the sounds of the trachea and 
bronchi much more distinctly than usual; it is as if you put the 
stethoscope over the trachea itself. 
The third stage, that of gray hepatization, develops naturally 
out of the second (Fig. 2:10). In the earlier periods red corpuscles 
Pig. 230. 
Section of lung in gray hepatization. The alveoli filled with plugs in which are multitudes 
of round cells. In the stroma the usual carbonaceous pigmentation of the lung is seen at 
lower part of figure. X 90. 
are exuded largely, but except in cases of a hemorrhagic kind the 
white very much preponderate in the later periods. The leucocytes ACUTE PNEUMONIA. 
493 
swarming into the alveoli cover up the red corpuscles. The addi- 
tional material in the vesicles also causes pressure to be exercised 
on the capillaries, which are thereby emptied. In this way we 
have, instead of the previous hypersemia, an anaemia of the tissue. 
In accordance with the much less abundance of red blood, and the 
presence of an additional number of colorless cells, the color of the 
tissue is changed. It retains the firm character, and the granular 
appearance of the previous stage, but the color is gray. The pig- 
ipent of the lung intermixed with the white color of the multitu- 
dinous cells gives the appearance which has been aptly described 
as marbled. 
In the last stage, that of resolution and purulent infiltration, 
the lung returns to its normal condition. In some cases the cells 
and fibrine in the air-vesicles undergo fatty degeneration, and the 
plugs soften. The fat is partly absorbed, but to a large extent 
the degenerated corpuscles are expectorated. In other cases the 
leucocytes go on accumulating in the air-vesicles, and as the fibrine 
degenerates and softens the alveoli come to contain what is virtu- 
ally pus. The appearance of the lung in these two conditions is 
not very different, as the emulsion-like fatty material is not unlike 
pus. The lung is still solid, still sinks in water, but its firmness 
is gone, its surface is pale, yellowish, or grayish-red, it has lost the 
granular appearance, and a grajush, dirty fluid oozes out, which 
makes the surface so slippery that a small portion is with difficulty 
lifted or held in the fingers. The tissue is also extremely soft, and 
tears under the mere pressure of the fingers. In removing such 
a lung from the body, unless care is exercised, pressure of the 
fingers may rupture the tissue, and as the pus or emulsion flows 
into the cavity it may give rise to the appearance of abscesses in 
the midst of the lung. This stage may be looked on as the prepa- 
ration for the removal of the exudation, which takes place by the 
degeneration and absorption of the young cells, and by their ex- 
pectoration. The exudation must have very thoroughly softened 
before it can make its way through the narrow neck of the in- 
fundibulum into the bronchus. After the infundibula and vesicles 
are emptied the blood returns in full force into the capillaries. 
Instead of the anaemia we have indeed a liyperaemia, for the tissue 
has been weakened by the inflammation, and is less able to resist 
the blood-pressure than formerly. It should be remembered in 
practice that the lungs of a pneumonic patient take some time to 
recover from the effects of the inflammation, and great exertion 
during convalescence should be warned against, till the tissue has 
recovered its tone. 
While the above is the most common termination of pneumonia 
sometimes it does not issue so fortunately. The purulent infiltra- 
tion may involve the lung tissue, and by its sloughing an abscess 
may be formed. In this way we may have one or several abscesses 
of various sizes, or several ma}r coalesce into one of larger dimen- 
sions. In the wall of the abscess a consideraole vessel may rupture, 494 
diseases of the organs of respiration. 
and so we may have profuse hemorrhage. The abscess may sub- 
sequently hurst into a bronchus or the pleura, in the latter case 
producing empyema and perhaps pneumothorax. 
Another unfortunate result which sometimes occurs is gangrene 
of the lung. This is mostly met with in the hemorrhagic form 
and in drunkards, but it may occur where there is a bronchiectatic 
cavity with decomposing contents. 
There are some cases of pneumonia which end in phthisis 
pulmonalis, and that either in the indurative or caseous form. 
This outcome is rare, and only occurs in persons predisposed to 
phthisis. Another rare result is chronic pneumonia, whose de- 
scription follows below. It is more common than the termination 
in phthisis, and is probably mistaken for the latter not infrequently. 
The pleura always takes part more or less in the inflammation 
of the lung. The pleural surface of the inflamed portion of lung 
is coated with a white fibrinous exudation, which is sometimes of 
considerable thickness. There is rarely any considerable serous 
exudation in the pleura, probably because the lung is distended 
with the solid exudation, fills the cavity, and by its pressure pre- 
vents the accumulation of fluid. Sometimes the pleural exudation 
takes on a purulent character, and an empyema may remain after 
the resolution of the pneumonia. In some cases the inflammation 
extends to the pericardium, on the surface of which there may be 
a slight fibrinous exudation. 
Pneumonia is an acute febrile disease, and so produces secondary 
changes in the organs of the body, generally comparable with 
those in acute specific fevers. There is commonly, but not always, 
enlargement of the spleen. The liver is usually enlarged, and 
shows parenchymatous infiltration. 
Chronic Pneumonia.—This name is one whose significance is 
somewhat ambiguous, and it will be necessary in the first place to 
define the meaning attached to it here. We include those condi- 
tions in which the lung tissue is the seat of a simple chronic in- 
flammation, without anything of a tubercular or otherwise specific 
nature. The simplest cases are those in which an acute pneumonia, 
instead of resolving, passes into a chronic condition. In addition 
to that we may have a chronic inflammation set up by the inhala- 
tion of irritating particles, as among potters, stone-hewers, etc. 
In old persons ordinary pneumonia is apt to be chronic, and it 
may therefore be said that senile pneumonia is included under the 
present head. To a certain extent the same is true of pneumonia 
in drunkards, and in debilitated persons, especially when it affects 
the apex of the lung. 
The chronic inflammation here, as in other organs, is chiefly 
characterized by a new-formation of connective tissue, so that 
induration of the lung is the result. In this view of it the terms 
chronic interstitial pneumonia, cirrhosis, sclerosis, fibroid phthisis, 
are sometimes used as being virtually of the same meaning as CHROJSTIC PNEUMONIA. 
495 
chronic pneumonia. But here it is necessary to distinguish very 
carefully. We shall see afterwards that there is a form of phthisis 
pulmonalis in which a great new formation of connective tissue 
occurs, hut the inflammation in that case is due to the tubercular 
virus. In the disease at present under consideration there is no 
such irritant present, and the inflammation is simple. The proper 
tubercular fibroid phthisis is a much commoner condition than the 
simple chronic induration. 
The appearances presented by the lung in cases of acute pneu- 
monia which had a prolonged course and have become chronic 
are not unlike those of the lung in the stage of gray hepatization. 
The disease is generally confined to one lung, and may affect only 
a portion of it. The lung is bulky and dense, and feels solid to 
the touch. When cut into, the solid lung has usually a gray color, 
although sometimes with a tint of red, but it has a smoother cut 
surface than that in hepatization, and the tissue is also tougher. 
To this condition the name iron-gray induration may he aptly 
applied. 
Under the microscope the conditions are such as are indicated 
in Fig. 231. The walls of the alveoli are greatly thickened by 
fibrous tissue, which largely encroaches on the alveoli, the epi- 
Fig. 231 
Chronic pneumonia. The connective tissue is greatly increased, and the alveoli (a, a, a,) 
are represented by contracted spaces lined with well-formed epithelium. The epithelium 
here is much more distinct than in the normal alveoli. X 350. 
thelium of which is preserved, and sometimes occupies their 
interior. When it is considered that the lung as a whole is not 
reduced in bulk, and that the alveoli are in great part empty, then 
the overgrowth of connective tissue will be understood to he very 496 
DISEASES OF THE ORGANS OF RESPIRATION. 
great. Along with the interstitial new-formation there are 
commonly thickening and adhesion of the pleura. In the con- 
dition hitherto described, there is no considerable obliteration of 
the air-vesicles except in so far as they are encroached on from 
without. 
If the disease progresses, however, the new-formed connective 
tissue takes on a cicatricial character and by its contraction destroys 
and contorts the proper lung tissue. Just as in the case of cirrhosis 
of the liver, there is here an atrophy of the normal structure and 
a tendency in the organ to shrink. This leads to dilatation of the 
bronchi on principles already enunciated, so that bronchiectasis 
is a prominent feature in advanced cases of this kind. The 
bronchial secretion may stagnate in the dilated bronchi and de- 
compose ; the irritation of the decomposing juices sometimes 
causes ulceration, and ragged cavities may thus form, so that the 
condition closely resembles that of phthisis. 
Acute Catarrhal Pneumonia (.Broncho-pneumonia, Capillary 
Bronchitis).—This disease occurs most frequently in children, and 
is in them, as in adults, associated with catarrh of the liner bronchi. 
So close is the connection between the pulmonary catarrh and that 
of the bronchi that the disease may very properly be called broncho- 
pneumonia. The bronchi are first affected, and so it may be said 
that the pneumonia springs out of a capillary bronchitis, the 
tubes affected being those of the finest calibre. In a large pro- 
portion of cases the bronchitis originates in measles, or it may 
occur in diphtheria, or smallpox, or whooping-cough. In adults it 
may follow typhoid or other infectious fever, or it may be the 
result of the inhalation of irritating gases, or of the presence of 
decomposing material or foreign bodies. It is to be noted that an 
ordinary bronchial catarrh, such as was described in the section 
on bronchitis, seldom goes on to a catarrhal pneumonia, but that 
for the most part the latter is due to the existence of some special 
irritant such as the virus of measles or decomposing juices in the 
bronchial tubes. 
We have already seen that the presence of blood in the alveoli 
may cause it, and this is a good instance of the action of a foreign 
substance in its production. In this regard it is interesting that a 
catarrhal pneumonia may be produced in animals by division of 
the pneumogastric nerves. The pneumonia here seems due to 
stagnation of the secretion which is no longer expelled, and to the 
irritation which this produces. 
As the disease begins in the bronchial tubes and is propagated 
to the lung tissue, it follows in its distribution the arrangement of 
the bronchial tubes; that is to say, it occurs in a lobular form. 
Although the disease is thus primarily lobular, it is clear that it 
will often occur in several neighboring lobules, and so a considerable 
tract of lung may be involved. This will be more particularly the 
case when it is due to the insufflation of irritating substances, which 
may be distributed in almost all the lobules of the lung. ACUTE CATARRHAL PNEUMONIA. 
497 
As the disease begins in a catarrh of the finer bronchi, there is 
often collapse of the corresponding portion of lung before any 
actual inflammatory processes occur in it. The obstruction of the 
tubes with tough secretion sufficiently accounts for this collapse. 
It is a lobular collapse, and as seen from the surface areas of larger 
or smaller size are depressed and of a bluish-red color. These are 
mostly to be found in the first instance at the posterior and inferior 
parts of the lung. In other parts, and especially in .the upper 
lobes, we may have emphysema. "With or without a previous stage 
of collapse, the inflammation by and by extends to the lung alveoli. 
There is a rich production of catarrhal cells, which fill the 
alveoli and cause condensation of the lung. The affected pieces of 
lung tissue are firm and pale, and again present more or less of the 
lobular arrangement. This condensation of the lung tissue may 
he more or less extensive, and as it springs very often out of col- 
lapse there may be various gradations visible in the same lung. 
The inflammatory products in the air-vesicles may after a time 
undergo fatty degeneration, break down, and be discharged, some 
part of them being probably absorbed by the lymphatics. In 
some cases, however, the result is not in every part of the lung so 
fortunate. For one thing, the collapse may never go on to a proper 
condensation, and when recovery takes place the collapsed portion 
remains uninflated. Or, again, the catarrh may become chronic, 
and, being associated with an interstitial inflammation, result in a 
permanent induration, the alveoli being encroached on by the 
growing connective tissue, as in the case of chronic pneumonia. 
In this way, the person, though recovering, emerges from the disease 
with a damaged lung; according to the extent of the permanent 
damage will be the shrinking of the lung and possible displacement 
of organs. Again, phthisis pulmonalis may develop out of an acute 
catarrhal pneumonia, but this is fortunately an unusual result. 
The inflammatory products in this disease deserve particular 
notice. In the acute capillary bronchitis we have a muco-purulent 
material produced, and on section of the lung little yellow drops 
appear on the cut surface. In the alveoli themselves the secretion 
is more apt to contain large cells of epithelial origin and character, 
but here also pus-corpuscles or leucocytes often predominate 
largely. These leucocytes are very often not by any means 
confined to the surface of the mucous membrane and the alveoli, 
but are often present abundantly in the connective tissue around 
the bronchi and between the lobules. In fact the lung tissue may 
be largely over-run by leucocytes, and the characters of an acute 
interstitial pneumonia may be added to those of catarrhal 
inflammation. 
It has already been mentioned that the disease begins in the 
bronchi, and it has been asserted by Buhl that, throughout, the 
inflammation remains confined to the bronchi, the inflammatory 
products found in the alveoli being simply insufflated from the 
bronchi. This view, however, can hardly be maintained, as 498 
DISEASES OF THE ORGANS OF RESPIRATION. 
evidence of acute changes can actually be observed in the epithe- 
lium of the alveoli. 
GANGRENE OF THE LUNGS. 
Iii this condition necrosis of a definite piece of lung tissue 
occurs. The necrosis is always accompanied or followed by de- 
composition, and the irritating character of the decomposing 
material plays an important part in the processes concerned. The 
gangrene may itself arise by the action of decomposing material. 
If a foreign substance, such as a piece of solid food, gets into the 
bronchi, it may induce a bronchitis with putrescence of the secretion, 
and the irritation of the putrid juices may induce gangrene of the 
lung. Similarly, putrid juices inspired from ulcers and wounds of 
the mouth and air-passages, or perforation of abscesses or ulcers 
into the trachea or bronchi may set it up. Again, the juices in 
cavities, especially in those arising by dilatation of bronchi, may 
stagnate and decompose, and lead to gangrene. Wounds and con- 
tusions may cause necrosis directly. Sometimes the lung tissue 
dies in severe cases of typhoid fever or other zymotic diseases. 
We have also seen that gangrene may occasionally follow the 
hemorrhagic infarction or acute pneumonia, and that it is a constant 
feature of the metastatic abscess. Lastly, there are some cases in 
which the cause of the gangrene is obscure, but these cases, as well 
as those with more definite cause, are somewhat common in persons 
given to alcoholic excess. 
It is customary to divide gangrene of the lung into a circum- 
scribed and a diffuse form. In both the lung tissue dies and 
decomposes, ultimately becoming separated, if the patient survive, 
as a shreddy slough, which occupies the cavity formed by the loss 
of tissue. In the diffuse form there are gangrenous patches 
throughout the lung, or a considerable portion of it, and there is 
much less probability of the effects becoming limited by reactive 
inflammation in the neighborhood. The diffuse form not infre- 
quently develops from the circumscribed, the decomposing juices 
from the slough causing still further necrosis. 
The various changes which occur around a gangrenous piece of 
lung, and in more distant parts of the organ, are related to the 
irritating character of the slough. These changes are mainly in- 
flammatory. The immediately neighboring lung tissue is acutely 
inflamed, and there is thus a zone of condensation around having 
the usual features of acute pneumonia, often with a specially 
hemorrhagic character. In this inflammatory zone the gangrene 
may advance. On the other hand the slough may be detached by 
the inflammatory process, and through time, a more chronic in- 
flammation having occurred, the slough may be separated from 
the lung tissue by a layer of granulation tissue which produces 
pus abundantly into the interior of the cavity. If the slough be 
small enough the cavity may, after the discharge of the slough, PHTHISIS PULMONALIS. 
499 
ultimately contract and form a cicatrix, but in the case of larger 
sloughs a suppurating cavity may long remain. 
The effect on the bronchial mucous membrane is of importance. 
The decomposing juices from the slough and from the inflamed 
lung tissue find their way into the bronchial tubes, where they set 
up an acute inflammation of a highly suppurative character. A 
rich secretion of putrid pus is the result. This secretion carried 
to the bronchi in other parts of the lung may set up gangrene in 
numerous small isolated patches, and in this way multiple small 
abscesses may occur. If the gangrene be near the surface an acute 
pleurisy is the result with fibrinous exudation. Sometimes the 
cavity opens into the pleura, and we have a suppurative pleurisy, 
perhaps with pneumothorax. An occasional complication of gan- 
grene is hemorrhage. As the slough separates from the living 
tissue the more resistant tissues retain their connection longest. 
The bronchi and larger vessels sometimes remain as rigid trabeculae 
in the midst of the soft slough. The arteries remain longest in 
connection, but they are usually filled with thrombi and ob- 
literated. Occasionally, however, the gangrene advances around 
an artery which is still pervious, and in that case hemorrhage of 
a serious or even fatal character may result. Sometimes the gan- 
grene leads to a definite septicaemia, or metastatic inflammations 
result, having their seats especially in the brain. In these cases 
the decomposing material gets into the pulmonary veins, having 
first caused thrombosis of them. 
A peculiar feature in gangrene of the lung is the very abundant 
and highly putrid sputum. The decomposing juices from the 
slough set up, wherever they are carried, acute suppurative in- 
flammations, and the abundant inflammatory products also undergo 
decomposition. The bronchial tubes being weakened by the severe 
inflammation often undergo dilatation, and the material stagnates 
in them all the more, and decomposes. So it happens that in the 
cavity itself, and in the dilated bronchi there are usually large 
quantities of putrid secretion. This is expectorated at intervals, 
and sometimes so abundantly that it pours out of the nose and 
mouth. The sputum is extraordinarily fetid, and if allowed to 
stand deposits triple phosphates, crystals of margarin, etc. It also 
contains abundant pus-corpuscles, many of them broken down by 
decomposition, pieces of lung tissue, and bacteria isolated and in 
colonies. Sometimes the sputum contains also spirilla. 
PHTHISIS PULMONALIS. 
Under this designation are included conditions in which there 
is disease of the lungs, accompanied by destruction of the lung 
tissue and wasting of the body. The disease is usually progressive, 
hut it presents all degrees of acuteness and the greatest variety in 
its duration. When we look at the lung removed from a case of 
phthisis, and observe the various appearances, the cavities, the 500 
DISEASES OF THE ORGANS OF RESPIRATION. 
solidifications, the indurations, the yellow caseous appearances, 
and so on, we seem to see nothing but inextricable confusion. 
And when we subject the phthisical lung to microscopic examina- 
tion, the confusion is hardly reduced. We see evidences of inflam- 
mation affecting bronchi, alveoli, and interstitial tissue; we see the 
inflammatory products undergoing processes of degeneration and 
organization; we see tubercles, also variously modified ; but the 
interrelation of the various conditions is by no means apparent. 
It is clear that there is some serious disturbing cause present, but 
the connection of the various phenomena with this cause is not 
clear. 
In accordance with our usual method it will be proper here to 
inquire what is the cause of phthisis pulmonalis. We shall put 
aside in the mean time the true tubercles which are of almost 
constant occurrence in most forms of phthisis, and, looking merely 
at the anatomical changes in the lung tissue, we shall find them 
comprised under the two processes—namely, inflammation and 
necrosis. The inflammation manifests itself in the interstitial 
connective tissue, in the alveoli, and in the bronchi; and the 
necrosis involves inflammatory products and lung tissue. We 
shall see afterwards that in different cases the different structures 
of the lungs are involved to a varying degree, but in a large pro- 
portion we have both catarrhal and interstitial inflammations to 
some extent. Now, we have seen that inflammations arise as the 
result of the action of some irritant, and that necrosis frequently 
goes along with inflammation if the irritant be a severe one. We 
have to inquire here what may be the nature of the irritant, and 
what may be the cause of the necrosis which is such a frequent 
concurrent. 
There are some cases of phthisis which owe their origin to 
syphilis. The syphilitic virus here, as in other organs, gives rise 
mainly to an interstitial inflammation. Along with this we find, 
in some cases, at intervals that more pronounced new formation 
of granulation-tissue which is designated the gumma. In the 
gumma we have caseous necrosis, so that in this disease we may 
have, as in ordinary phthisis, the combination of inflammation 
and necrosis. But syphilitic phthisis is a rare disease, and in 
the vast majority of cases of phthisis, syphilis has nothing to do 
with it. 
There can now be little doubt that in the ordinary forms of 
phthisis there is a virus present, and that this is related to the 
micro-organism already referred to and described at p. 161. It is 
not to be asserted that the existence of this organism explains 
everything. We must presume a previous state of susceptibility 
in the individual, but when this exists the virus takes possession, 
and all the progressive lesions are apt to follow. 
It may be well here to refer briefly to the various phases 
through which the views as to the pathology of phthisis have 
gone since the time of Liennec, especially as many of the terms PHTHISIS PULMONALIS. 
501 
in common use in connection with the disease are related to some 
of these views. 
Lsennec believed that there was a particular tubercular matter 
which was liable to be deposited in the lungs or elsewhere. It 
might be deposited in isolated places, forming miliary tubercles, 
or infiltrated into a considerable portion of lung, forming infil- 
trated tubercle. In both cases the deposit usually begins as a gray, 
transparent structure, which, however, is prone to change into a 
yellow or whitish material which is drier and harder. This yellow 
material was called yellow or crude tubercle, whether occurring 
in the isolated or in the infiltrated form. All cases were regarded 
as tubercular in which there were either isolated nodules or exten- 
sive infiltrations, whether these were gray or yellow. 
By and by it came to be seen, however, that many of the con- 
ditions in phthisis are simply inflammatory. The minute histo- 
logical characters of what we now call the tubercle were discrimi- 
nated, and the essentially inflammatory processes were sought to 
be separated from the tubercular. It was shown that the existence 
of caseous material is no evidence of tuberculosis, since the ordi- 
nary products of inflammation and other new formations, such as 
tumors, may undergo this change, which, in its essence, is really 
a necrosis with degeneration of the structures concerned. In 
phthisis, then, the process is largely an inflammatory one, with 
the special tendency in the products of inflammation to undergo 
a caseous metamorphosis. In this way arose Virchow’s designation 
caseous pneumonia—namely, an inflammation with a caseous ten- 
dency in its products, just as scrofulous disease of the glands is an 
adenitis with a similar tendency. 
When the lungs in phthisis were more particularly examined, 
however, it was found that the condition is not such a purely 
inflammatory one as Virchow’s position would indicate. In all 
stages of the disease, tubercles are to be found alongside the 
inflammatory products. The tubercles undergo changes similar 
to these, and it is often difficult to discriminate between the two, 
especially when caseous metamorphosis has occurred. But in 
nearly all cases where the disease is advancing proper tubercles 
are to be found along with the inflammatory conditions. 
The more modern position brings us back more nearly to that 
of Lsennec. Again we regard phthisis as a tubercular disease, 
but not merely in the general sense of Leennec. We are to ob- 
serve carefully the inflammatory processes and distinguish their 
effects on the lung tissue. Our position differs also from Lsen- 
nec’s in respect that he regarded a particular state of the constitu- 
tion as the essential cause of the tuberculosis. It is not to be 
denied that the lungs must be in a state of susceptibility before 
they can be affected by the tubercular virus, but the same may be 
said concerning any form of tuberculosis, and, indeed, concerning 
ordinary inflammatory processes. We know that different per- 
sons, or the same person at different times, are very variously sus- 
ceptible to catarrhs, and to inflammations of all sorts. 502 
diseases of the organs of respiration. 
We are to regard phthisis pulmonalis as a local tuberculosis, 
in which chronic inflammatory processes and the actual formation 
of tubercles play their parts, and both lead on to necrosis and 
ulceration. 
It is necessary here to observe that phthisis pulmonalis has 
nothing to do with acute miliary tuberculosis of the lungs. This 
condition is merely part of a general tuberculosis in which the 
virus is in the blood. Phthisis may indeed give origin to general 
tuberculosis by the virus getting into the blood in sufficient 
quantity, but it does so very rarely, and the great majority of cases 
of general tuberculosis are not even associated with phthisis pul- 
monalis. 
We have still to consider the conditions of the lungs which 
predispose to the occurrence of phthisis, and the path by which 
the tubercular virus finds access to the lungs. All authors seem 
agreed that phthisis is in many cases hereditary. That is to say, 
persons are born with a condition of lungs which renders them 
peculiarly susceptible to the changes which are to be described 
below. Taking the view that these changes are due to the tuber- 
cular virus it seems that persons are horn with constitutions 
peculiarly incapable of resisting the action of the virus. It need 
hardly he said that this is perfectly consistent with what w7e know 
concerning other diseases. There are families in which diphtheria 
and scarlet fever make the most serious ravages, and there are 
others which they never attack. There are persons who are 
attacked by every form of fever in turn, there are others equally 
exposed who take none. But, besides an inherited liability, there 
is an acquired tendency to phthisis. This occurs principally in 
persons placed in circumstances in which the general health is 
reduced, and where especially the respiratory functions do not get 
justice. Persons living in close dwellings, especially when at their 
work, in factories and otherwise, are in the habit of breathing 
vitiated air, in which, it may be, finely divided dust is abundantly 
suspended, and thus frequently acquire a tendency to phthisis 
although originally free from it. 
We have now to inquire as to the path of entrance of the irri- 
tant to the lungs. In the study of the lesions met with we shall 
find that they all start at the finer bronchi. A catarrh of the finest 
bronchial tubes, usually occurring in a number of these simultane- 
ously, is the starting-point of a variety of lesions, which, however, 
for a considerable time remain related to the bronchi in their dis- 
tribution. This is a sufficient indication that the agent finds access 
to the lungs by the inspired air. 
Before leaving the etiology of phthisis, we may consider its 
almost uniform localization at the apex of the lungs, at least at 
the outset. The cause of this localization is generally regarded as 
obscure, but as has been hinted it has probably to do with the fact 
that the apices of the lungs are the least expansile portions. The 
first rib even in women is very little raised in inspiration, and in PHTHISIS PULMOXALIS. 
503 
persons with weak respiratory movements the air is apt to stagnate 
at the apex. This view receives some confirmation from the fact 
that phthisis so frequently improves when the patients go to reside 
in high altitudes where the rarefied air requires more vigorous 
respiratory efforts. In such persons the size of the chest as a 
whole generally undergoes an increase. If the localization of the 
disease at the apices is due to imperfect expansion of the lungs, 
then this will fall in perfectly with the view that the disease 
orginates in a virus inhaled from without. If the air stagnates 
the virus will remain lying in the lung, and will have time to 
develop and begin its disastrous effects. Koch found that the 
bacillus is of slow development, at least at first, so that the absence 
of disturbance will greatly favor its growth. 
Anatomical Changes in Phthisis.—In studying the changes in 
the lung it will be necessary to give descriptions of the various 
processes separately, and to a certain extent these processes are 
separable, but at the same time it will be understood that many 
of them go together and by their simultaneous occurrence fre- 
quently mask each other. It may be said in general that the 
disease, beginning in the finer bronchi, tends to spread in one of 
two directions, or in both of them at once, namely, from the 
bronchus to the surrounding connective tissue and on into the 
general connective tissue of the lungs, or else along the bronchus 
to the lung alveoli. In both cases we find tubercles developed in 
all stages of the process, and in both there is inflammation, but of 
different kinds according to the structures involved. In the case 
of the connective tissue the inflammation produces new formation 
of connective tissue and consequent induration. In the case of 
the alveoli it is a catarrh, although the alveolar wall may be at the 
same time involved. It is exceedingly difficult to say what de- 
termines the one or the other mode of extension, but it is probable 
that it depends on individual peculiarities. Some persons are 
peculiarly liable to catarrh of the alveoli, and some are not. It is 
important to observe that the tubercles which occur in both cases 
partake, to a considerable extent, of the peculiarities of the in- 
flammations. In the case of extension to the connective tissue the 
tubercles tend to undergo fibrous transformation. In the other 
case they are liable rather to caseous metamorphosis. As the 
morbid changes begin in the bronchial tubes we shall begin our 
description by the processes met with there. 
Condition of the Bronchi.—The most constant primary change 
is catarrh, but it is a much more chronic catarrh than that of 
ordinary bronchitis. Whether catarrh occurs without the forma- 
tion of tubercles or not, it is impossible to say, but certainly 
tubercles are to be found at a comparatively early period. The 
catarrhal products sometimes dry in and become caseous, especially 
when the phthisis passes on to catarrh of the alveoli. This change 
may also occur in the other form of extension, and we may find a 504 
DISEASES OF THE ORGANS OF RESPIRATION. 
bronchus plugged with a white mass and surrounded by indurated 
connective tissue. The catarrh is not infrequently accompanied 
by ulceration of the bronchial mucous membrane, and little cavities 
frequently arise in this way, the cavity appearing to the naked eye 
to form a sacculated dilatation of a small bronchial tube. These 
ulcers are surrounded by inflamed and indurated connective tissue, 
in the midst of which numerous tubercles are to be found (see 
Fig. 232). The ulcer here is essentially like the tubercular ulcer 
Fig. 232. 
Tubercular ulcer of bronchus; a, mucous membrane; b, muscular coat. At d there is a 
small ulcer on the summit of a swelling. In the latter are several tubercles indicated by the 
concentric shading. The muscular coat is broken up by the tubercles. X 60. (Rinofleisch.) 
of the intestine or the urino-genital canals. AVe shall next consider 
the appearances presented when the irritation extends from the 
bronchi to the surrounding connective tissue, in which case the re- 
sulting inflammation may be designated peribronchitis. 
Acute Peribronchitis.—In some very rapid cases the peribron- 
chitis is acute, and may even be purulent. Suppuration occurs in 
the bronchial wall as well as in the surrounding tissue, and, these 
structures being broken up, a kind of acute abscess is formed. 
Some of these abscesses may be near the surface and by rapidly 
undermining the pleura cause it to slough. By the separation of 
the sloughs the cavity of the abscess may come to communicate 
with the pleural cavity and so pneumothorax may result. The 
peribronchitis, however, is very rarely the only prominent condition. 
Along with it there is inflammation of the alveoli, but here too it 
is an acute inflammation, and the products are small round cells 
rather than the larger epithelioid elements of catarrhal inflamma- 
tion. This inflammatory condition of the alveoli existing in the 
neighborhood of the suppurating bronchi assists in the formation 
of the abscesses. Sometimes there is even a gangrenous condition 
developed, and actual sloughing of pieces of lung tissue occurs. 
Acute cases such as these bespeak a peculiar virulence of the 
morbid agent or a peculiar susceptibility of the patient. They 
usually pass rapidly on to a fatal issue with high fever. In some 
cases recovery takes place, the pus dries in or is discharged, and PHTHISIS PULMONALIS. 
505 
the abscesses become surrounded by indurated connective tissue 
and contract. 
Fibrous Peribbonchitis. Fibroid Phthisis.—This is a chronic 
process, and is more common than the acute condition just de- 
scribed. In an early stage of this disease the lung, especially in 
the upper lobes, may he found dotted over with hard masses, often 
nearly black in color. These are small in size and isolated. On 
examination they are found to consist each of a small bronchus 
surrounded by indurated and pigmented connective tissue in which 
tubercles are to be found. The disease has begun in a set of bronchi 
of nearly the same size and has produced similar results in all. 
The appearances of inflammation here are similar to those in other 
parts. The mucous membrane and the connective tissue outside 
are infiltrated with round cells, which as usual develop dense con- 
nective tissue. Sometimes there are tubercular ulcers of the 
bronchi having the characters already described. It has been 
stated above that these nodules are often nearly black in color. 
This coloration is derived from the blood-pigment, and may be an 
indication of the existence of minute hemorrhages, or else of 
occlusion of the vessels by the contracting tissue and staining 
of the tissue with the coloring matter dissolved out from the blood 
left in the obstructed vessels. It is to he noted that in this stage 
considerable hemorrhage may take place into the bronchi. The 
hemorrhage from each spot may be trifling, but from many 
together a severe haemoptysis may occur. Some cases of haemop- 
tysis before any clinical signs of phthisis have manifested them- 
selves are of this kind. The blood may to some extent come from 
the tubercular ulcers, but apparently this is not necessary. In 
many cases this tendency to pigmentation is manifest throughout 
the disease, and the extensive formations of connective tissue which 
occur are frequently of a slaty color. 
The new formation of connective tissue may limit itself for a 
considerable time to the neighborhood of the bronchial tubes, and 
the nodules may enlarge. But as a rule it slowly extends outwards 
to the interstitial tissue of the lungs generally. An extensive new 
formation of dense connective tissue thus occurs throughout the 
lungs. The normal connective tissue of the lungs lies mainly 
around the bronchi and vessels, and between the lobules, and it 
forms one system with the subpleural layer, the tissue in these 
three situations being in intimate connection by means of the lym- 
phatics. Hamilton has pointed out very instructively how foreign 
material, such as dust, when inhaled and conveyed into the lung 
tissue is carried about the lung and deposited in these three situa- 
tions. In similar fashion the irritant in the condition under con- 
sideration seems to he conveyed and produces inflammatory indura- 
tion everywhere. The new-formed connective tissue may be found 
in different stages of development, according to the particular part 
examined. We may find mainly round cells, spindle cells, or a 
dense tissue like that of the cicatrix, in which only small spindle 506 
diseases of the organs of respiration. 
cells are to be found. In all these stages tubercles can be seen, 
and they also, as they undergo fibroid transformation, present 
various appearances. In the latter stage the tubercles are repre- 
sented merely by a concentric arrangement of the dense connec- 
tive tissue at intervals, this concentric appearance being sometimes 
emphasized by the existence of pigment. 
If the lung be examined when this disease is fully developed, 
there will be found, to begin with, a very firm adhesion of the 
pleura over the diseased part. The pleura often undergoes a very 
remarkable thickening reaching sometimes half an inch, and the 
thickened portion may form a kind of hard cap at the apex of the 
lung. When cut into there are trabeculae of firm tissue traversing 
the lung, and frequently retaining something of the interlobular 
arrangement'in respect that the trabeculae tend to pass towards the 
root of the lung. The lung tissue which remains in the midst of 
these masses of connective tissue is often emphysematous, hut the 
dilated alveoli present also thickening of their walls. 
Besides all this there are commonly cavities, and sometimes 
these are of very large dimensions. The cavities have as a rule 
the characters of bronchiectasis. The broncliiectatic cavity has a 
distinct lining membrane which may limit it from surrounding 
lung tissue. This lining membrane is sometimes directly con- 
tinuous with the bronchial membrane, and the cavity may be 
obviously continuous with the bronchus, having sometimes an 
elongated shape with sacculated dilatations. But the cavities are 
often much more than mere dilatations of the bronchi. We may 
find almost the entire upper lobe forming one cavity with a dis- 
tinct lining membrane, and with partial septa radiating from the 
neighborhood of the root of the lung. 
The occurrence of emphysema and cavities in this form of 
phthisis merits more particular consideration. The emphysema is 
largely compensatory. By the formation and contraction of the 
connective tissue large numbers of alveoli are destroyed and the 
remaining ones dilate to fill up the space. The cavities are 
obviously formed in connection with the bronchial tubes. To a 
certain extent the dilatation is compensatory like the emphysema, 
and the inflammatory infiltration of the wall may allow more 
readily of dilatation. It is to be remembered also that tubercular 
ulceration often accompanies the process, and where this exists 
dilatation will more readily occur; besides that, a gap caused by 
ulceration may, as we have seen, have much the appearance of a 
dilatation. There is another way in which dilatation of the 
bronchi occurs, and this has been well described by Hamilton. 
There are agents at work which may directly pull out the bronchial 
wall. We have seen that there is usually thickening and adhesion 
of the pleura on the one hand, and the peribronchial induration on 
the other. Between these there is the indurated interlobular con- 
nective tissue, which by its contraction tends to approximate the 
two. As the pleura is fixed to the chest wall by firm adhesions 
there is a dragging in of this wall, producing the flattening of the PHTHISIS PULMONALIS. 
507 
apex which is sometimes so very marked in this disease. But the 
bronchial wall is also drawn outwards, at tirst unequally, so that 
the cavity is an irregular one. 
There is still another method by which cavities form in this 
disease; it has been already referred to and compared to that of 
the formation of the retention-cyst. The peribronchial connective 
tissue may contract concentrically and obstruct small bronchial 
tubes, or the obstruction may be assisted by the drying-in of the 
catarrhal products in the lumen of the tube. If a small tube be 
thus obstructed, the secretion may accumulate behind and cause 
dilatation of the tube, this occurring the more readily that these 
tine tubes are thin-walled. In this way we may have sacculated 
dilatations of the tubes, and the communications with the bronchi 
from which they took origin may even be obscured or cut off. 
In cavities thus formed the lining membrane is very commonly 
directly in contact with sound lung tissue, and although the wall 
is composed largely of round-celled tissue of an inflammatory 
kind, yet here, as in other bronchiectatic cavities, ciliated epi- 
thelial cells are usually to be found. The cavity frequently con- 
tains pus, and if it be near the surface and of rapid formation it 
may so undermine the pleura as to cause necrosis and render 
pneumothorax imminent. 
It is to be remembered that, although these processes may occur 
by themselves, and in their aggravated form warrant the special 
designation of fibroid phthisis or cirrhosis of the lung, yet many 
of them occur along with the changes next to be described. This 
applies especially to the peribronchitis and the induration of the 
connective tissue around the individual lobules, as distinguished 
from an induration of the general connective tissue of the lungs. 
Catarrhal or Caseous Form.—We have now to consider the 
other mode of extension, namely, from the finer bronchi along to 
the alveoli. In studying acute catarrhal pneumonia we have seen 
that the disease begins with a capillary bronchitis which runs into 
a proper pneumonia. In the present case there is a similar ex- 
tension, so that the condition is sometimes called chronic catar- 
rhal pneumonia, or broncho pneumonia. But there are certain 
important differences which from the first should be borne in 
mind. In the first place the affection of the finer bronchi is not a 
simple catarrh, but is accompanied by the formation of tubercles. 
These tubercles form most readily, according to Bindfleisch, just 
where the bronchial tubes pass into the lung alveoli, attacking the 
projecting angles at the points where bronchi give place to in- 
fundibula. Another distinction is that, as the tubercles are in the 
connective tissue forming the bronchial wall, so there is always 
some inflammatory infiltration of the wall with more or less peri- 
bronchitis. In like manner, when the disease passes into the 
alveoli it does not, like the acute catarrhal pneumonia, confine 
itself to the surface, but here again we have it extending into the 
alveolar wall and producing thickening and induration there. 508 
DISEASES OF THE ORGANS OF RESPIRATION. 
Lastly, there is a marked tendency for the products of inflamma- 
tion to undergo caseous necrosis. This process occurs not only 
in the material accumulated in the alveoli, but also in the alveolar 
wall and the wall of the bronchus. So characteristic is this con- 
dition in many cases that 
as we have seen the name 
CASEOUS PNEUMONIA lias 
been sometimes applied. 
The disease beginning 
in a catarrh with infiltra- 
tion of the bronchus passes 
on to catarrh of the alveoli. 
The inflammation leads to 
the filling up of the alveoli 
with cells which are mostly 
of the large epithelioid 
character, such as are 
shown in Fig. 233. With 
these may he mingled small 
round cells such as exist in 
ordinary acute pneumonia, 
but there is rarely a filling 
up of the alveoli with small 
round cells and fibrine such 
as we see in hepatization, 
although in very acute 
cases this may occur. The 
alveolar wall, as has already 
been noticed, is infiltrated 
with inflammatory round 
cells, and it is very often 
difficult to distinguish the 
exact boundaries of the 
alveoli, the swollen wall 
being ill-defined from the 
products inside. The re- 
sult of all this is a conden 
sation of the lung tissue, 
and according to the extent 
of the affected areas will 
there be larger or smaller 
solidifications of the lung. 
These will always in their 
distribution hear a relation 
to the bronchial stems, 
having usually in this early 
stage a distinctly lobular 
arrangement, like bunches 
of fruit in clusters. 
These condensations will 
Fig. 233. 
Lung in caseous form of phthisis ; the capillaries 
injected (shown black). At A there are catarrhal 
cells (6) in alveoli, and the capillaries are well filled. 
At B, the capillaries are less injected. At C, caseous 
necrosis has begun; and at D, it is complete, the 
structure being here quite obscured in a general 
granular opacity. X 350. (Hamilton.) PHTHISIS PUL MON A LIS. 
509 
have a gray color, hut soon caseous necrosis occurs, and it is rare 
to find many of them purely gray. The caseous necrosis has been 
ascribed to the infiltration of the alveolar wall, causing compression 
of the bloodvessels, and consequent aneemia, resulting in degenera- 
tion and death. It is true that in a caseating condensation the 
vessels do become obstructed, as may be proved by injection (see 
Fig. 233), but this is just as likely to be the result of the necrosis 
as the cause. In the swelling and induration of connective tissue 
produced in ordinary inflammations we never have such obstruction 
of the vessels or a caseous process. Moreover, the inflammatory 
infiltration is derived from the blood, and it seems strange that 
the bloodvessels should yield material to such an extent as to cause 
their own obstruction. The process of caseation so characteristic 
of the condition we are describing must be set down to a different 
cause. It is analogous to the caseation of syphilitic and tubercular 
formations, and due to the virulence of the agent which produces 
the primary changes. In the present case the caseous necrosis 
attacks indiscriminately the whole structures concerned. Begin- 
ning in the central parts of each small condensation, it involves 
the products within the alveoli, the altered alveolar wall, the 
tubercles, and the fine bronchus. The caseous area presents 
under the microscope a finely granular homogeneous appearance 
as in Fig. 233, D, in which it is very often impossible to recognize 
any structure at all. Sometimes the outlines of the alveoli can be 
made out, but even these may be obscured. As seen with the 
naked eye, the caseous condition is recognized by the opaque 
yellow or white appearance presented, this usually beginning in 
the central parts of the gray condensations. 
As confirmatory of the view that the caseous necrosis is due 
directly to the action of the original irritant, it is to be noted that 
in very acute cases necrosis may occur almost directly and without 
caseation. An acute condensation takes place not unlike that of 
pneumonia but with the lobular distribution, and goes straight on 
to sloughing of the lung tissue, perhaps with a purulent peri- 
bronchitis. 
The caseous material is of course dead, and in any further 
changes it is merely passive. In some cases, which unfortunately 
are not very common, the disease makes pauses. The caseous 
mass becomes encapsuled and dries in more and more. By and 
by it becomes infiltrated with lime salts* and may thus be converted 
into a putty-like material, or condensed into a stony mass, which 
may lie for years in the lung tissue. 
More frequently the caseous material softens and partially 
liquefies, so that a cavity forms. It may be that, as Hamilton 
suggests, this may be due to a chemical change analogous to that 
which occurs in the ripening of cheese, in which, according to 
M. Duclaux, certain insoluble albuminates become soluble in 
water. The softening affects the whole caseous material, and the 
piece of lung concerned breaks down and liquefies, so that a small 
cavity results. The broken-down caseous material forms a grumous 510 
DISEASES OF THE ORGANS OF RESPIRATION. 
turbid fluid, in which the more resisting elastic tissue of the lung 
may be found still retaining to some extent the form of the alveoli. 
This elastic tissue may be frequently recognized in the sputum of 
such patients by proper methods of search (see Fig. 234). At first 
the cavity formed is small, but by extension of the process and 
Fig. 234. 
Lung tissue from the sputum in phthisis. The sputum was digested in caustic soda according 
to Fenwick’s method, and then subjected to microscopic examination. X 350. 
coalescence of neighboring softenings, larger cavities result. 
These cavities are very irregular, and their walls at first ragged 
and ill-defined. After all the caseous material has been cleared 
out there may be a smoothing of the walls of the cavities by the 
formation of connective tissue, but there is not the regular lining 
membrane of the bronchiectatic cavity, nor the same relation to 
the bronchi. The cavity sooner or later opens into one or more 
bronchi, and its contents are discharged. When the caseous 
material is cleared out the wall assumes an inflammatory character 
and secretes pus more or less abundantly. In the walls of such 
cavities, and in the mucous membrane of the bronchi with which 
they are in communication, tubercular ulcers may usually be dis- 
tinguished. 
It may be well here to consider the general appearances pre- 
sented by the lung on post-mortem examination of an advanced 
case of the kind we are considering. The lung will be found 
firmly adherent over the upper lobe or more extensively. There 
will not, however, be the same thickening of the pleura as is met 
with so commonly in the indurative form. In removing the lung, 
it will generally be found that there are cavities at the apices, often PHTHISIS PULMONALIS. 
511 
of very large size, and in separating the lung from the pleura 
there is great risk of opening into some of these cavities. If the 
lung after removal be divided from apex to base, various appear- 
ances will be presented, many of which are sometimes difficult of 
interpretation. There are cavities tilled mostly with a grumous 
yellow material. These are exceedingly irregular in shape, and 
traversed by partial septa or by completely isolated trabeculae. 
These trabeculae represent branches of the pulmonary artery which 
have survived the general necrosis, and although the arteries are 
mostly obstructed, some of them remain partially pervious, and 
we may find aneurismal dilatations on these. The cavities have 
frequently no proper lining membrane, but if they are large and 
of some duration there is a red layer having the appearance of 
granulation tissue. Looking away from the cavities, the lung 
tissue is found condensed and frequently caseous. In the imme- 
diate neighborhood of the cavities the condensation is probably 
continuous, and is frequently accompanied with great induration 
of the lung tissue. But farther off, and especially in the lower 
lobe, there are usually more isolated patches of condensation. 
These on section very commonly have a circular form, or they 
present the appearance already mentioned of clusters of fruit. By 
the coalescence of these we may have more continuous condensa- 
tions, but at the marginal parts there are usually indications of the 
lobular extension of the lesion. The condensed portions are 
usually very firm, and in each we find the opaque appearance of 
the caseous necrosis. In the central parts there may be softening 
and incipient cavities. After examining the cut surface, the 
bronchial tubes may be opened up with the scissors. Those which 
pass towards the cavities are nearly always the seat of tubercular 
ulceration. The mucous membrane is irregularly destroyed, and 
the ulcers have commonly a rather ragged appearance, but are 
usually superficial. The ulceration is very often prolonged into 
the main bronchus of the affected lung, and even to the lower part 
of the trachea. In the larynx there is also frequently ulceration 
as already described, but it is not usually continuous with that in 
the bronchi or lower trachea, there being mostly an interval be- 
tween in which the mucous membrane of the trachea is normal or 
only red from inflammation. 
It is to be understood that these appearances will vary greatly 
according to circumstances, the chief cause of variation being the 
different degrees in which, along with the caseous catarrhal pneu- 
monia, there is induration of the connective tissue of the lung. 
We have seen how this induration so often starts from the bronchi, 
but after the extension of the catarrh to the alveoli we may have 
a very pronounced inflammation of the connective tissue, causing 
induration of the alveolar wall and extending to the general con- 
nective tissue. This will cause the condensation to have a much 
firmer character to begin with, and if the induration predominate 
over the caseous catarrh we may have the features of fibrous 
phthisis becoming pronounced in the older parts of the lesion, 512 
diseases of the organs of respiration. 
while the more recent parts show rather those of lobular broncho- 
pneumonia. 
It may be useful here, before leaving the subject, to refer to the 
various modes in .which cavities form and extend. We have 
seen that in the indurative form of fibrous phthisis, cavities form 
by dilatation of the bronchial tubes, tubercular ulceration often 
playing an important part in the process. Then we have cavities 
formed by the softening of the caseous material. Around such 
softening there is frequently a reactive inflammation, resulting in 
the formation of granulation tissue which finally forms the lining 
of the cavities, J'mch cavities commonly enlarge by the coales- 
cence of neighboring softenings, and in their walls also tubercular 
ulceration often progresses. Then there is the more direct destruc- 
tion of the lung tissue occurring in very acute cases, associated, 
as we have seen, with purulent peribronchitis, acute inflammation 
of the alveoli, and such a rapid necrosis of the tissue as to approach 
to the characters of gangrene of the lung. 
The sputum in phthisis pulmonalis is variously composed. In 
the earlier stages the expectoration has the usual characters of that 
in catarrh, consisting of mucus, with more or less abundant leuco- 
cytes. In the sputum in this early stage are often found large 
epithelioid cells with one or more nuclei such as wre find in the 
lung alveoli in the catarrhal form of phthisis. These cells fre- 
quently present fatty degeneration. Considerable weight has 
sometimes been attached to the presence of such cells as evidence 
of the existence of the disease in its early stage, and their discovery 
may be useful in this regard; but as they may exist in simple 
catarrhs their diagnostic value may be overrated. The sputum in 
phthisis often contains elastic tissue from the breaking down of 
the lung. In very rapid cases we may find this by a simple exam- 
ination of the sputum, but the search is often a difficult one because 
the thick mucus and pus hold the pieces of lung tissue suspended 
and isolated. By Fenwick’s method of digestion in soda solution, 
pieces of lung tissue, such as that shown in Fig. 284, will frequently 
be found in the deposit. This method is also applicable to the 
sputum in gangrene of the lungs. The tubercular bacillus is 
usually to be found in the sputum, especially in advanced cases. 
The characters are shown in Fig. 56, p. 161, and have been 
already described. 
The sputum often contains blood in phthisis, and it will be 
proper here to inquire as to the source of hemorrhage. Bleeding 
sometimes occurs in early stages before cavities have formed, 
arising from the mucous membrane of the finer bronchial tubes. 
We have already seen that this frequently occurs in the early 
stages of the indurative form of phthisis, and we saw reason to 
believe that it is sometimes related to tubercular ulceration of 
these bronchi, although the hyperpemia coincident with the process PHTHISIS PULMONALIS. 
513 
probably plays the principal part. In the other form of phthisis 
the liner bronchi are also the source of the early hemorrhage, and 
here, too, the inflammatory hypersemia appears to be the principal 
cause, although it may be complicated with tubercular ulceration 
as well. In late stages after cavities have formed hemorrhage may 
occur from their walls. In the process of extension of cavities, 
whether by caseous necrosis or tubercular ulceration, the more 
resisting walls of the pulmonary arteries are able to persist longer 
than the rest of the tissues, and these form prominent elongated 
projections on the walls of the cavities or isolated cylindrical trabe- 
culae traversing them. The calibre of the artery is frequently 
obliterated, and the structure consists of granulation tissue in 
which some remains of elastic tissue may be found. But some- 
times the calibre persists, at least partially. At the same time the 
wall is infiltrated and consists essentially of soft granulation tissue. 
This soft tissue frequently allows of dilatation of the artery, and 
we have aneurisms whose walls are similarly soft and friable. 
Rupture of the softened wall of the artery or aneurism would 
occur more readily were it not that the blood-pressure is already 
reduced by the narrowing of the calibre, but it does occur not 
infrequently, and it appears that in a large proportion of cases the 
blood comes from aneurisms. The resulting hemorrhage is com- 
monly very severe, and often fatal, either by obstruction of the air- 
passages with the blood or from the general collapse resulting from 
loss of blood. 
The condition of the pleura in phthisis has already several times 
been incidentally referred to. As the pulmonary layer of the 
pleura or at least the subpleural tissue is part of the system of 
the interstitial connective tissue, it takes part in the inflammatory 
new-formation in the indurative form of phthisis, and we have seen 
that it is sometimes greatly thickened. In the other form of 
phthisis when the disease approaches the pleura there is always 
inflammation with new-formation of connective tissue, and adhe- 
sion of the two layers. This adhesion occurs in the way that will 
be described in considering the diseases of the pleura, and consists 
of an actual coalescence of the two layers with communication of 
the bloodvessels. The adhesion is often so firm that it is easier to 
strip off the parietal pleura from the internal surface of the thorax 
than to separate the layers. Sometimes it happens that the inflam- 
matory condition extends beyond the parietal pleura and causes 
adhesion of this layer to the periosteum of the ribs and intercostal 
tissue. In that case the separation of the lung from the chest-wall 
is very difficult, and sometimes cannot be accomplished without 
cutting. 
Cavities in the lung very often come close up to the pleura and 
undermine it. If the cavity be at all large, it cuts off a portion of 
pleura from its vascular supply from the lung. But, as a general 
rule, adhesion has already taken place between the two layers of 
pleura, and, the vessels being in communication, the portion over 514 
DISEASES OF THE ORGANS OF RESPIRATION. 
the cavity is kept supplied with blood from the parietal layer. We 
may even suppose that the blood passing from the branches of the 
bronchial artery out into the parietal pleura may be conveyed 
along over the cavity and return in part to nourish the visceral 
layer. But if a cavity comes to the surface at a place where vas- 
cular adhesion has not taken place, then necrosis of the pleura 
will probably result. The portion of pleura is of a dead-white 
color, and by and by it becomes abruptly demarcated from the 
neighboring parts. The line of demarcation becomes more and 
more distinct, and an actual separation often occurs, the result of 
which is communication between the cavity and the pleural sac, 
leading to pneumothorax. This is nearly always the manner in 
which pneumothorax occurs. It will happen mostly in acute 
cases, where the cavities form rapidly without affording time for 
the formation of vascular adhesions. More especially is this the 
case where cavities form by purulent peribronchitis with or with- 
out sloughing of the lung tissue. It will be seen that the occur- 
rence of the pneumothorax depends on the absence of adhesions, 
hence it happens that it so frequently occurs in the lung which is 
least advanced in the disease, because in that lung adhesions are 
less likely to be present. The pneumothorax, being associated 
with the passage into the sac of foreign material from the pulmo- 
nary cavity, generally results in an acute pleurisy, so that the 
layers of the pleura may be glued together by recent fibrinous 
exudation. It very frequently happens in a case of pneumothorax 
that there are several places in which necrosis of the pleura exists, 
one of these having given way, but the others being in a condition 
in which they might readily have done so. 
The bronchial glands are nearly always more or less effected 
in phthisis. They are frequently enlarged and caseous, exactly 
like scrofulous glands. Like them, they contain tubercles. These 
caseous glands are sometimes found in a state of softening. ISTot 
infrequently the caseous material becomes impregnated with lime 
salts, and we may find the gland represented by a capsule filled 
with a material like mortar, or more nearly of a stony consistence. 
In the indurative form of phthisis, the tubercles in the glands 
undergo fibrous transformation like those in the lung tissue, and 
we meet with dense, hard, pigmented glands with an almost cica- 
tricial appearance. 
We have already noted the existence of tubercular ulceration of 
the mucous membrane of the bronchi, and of the trachea and 
larynx. These are to be explained by the passage of the virulent 
material from the broken-down lung substance, over the struct- 
ures concerned and its action on them. Of similar import is the 
ulceration of the intestines, which occurs in the later stages of 
about two-thirds of the cases of phthisis. The material from the 
cavities is partly swallowed, and, containing the virus, it produces 
a tuberculosis in the parts of the intestine which afford a fitting ACUTE MILIARY TUBERCULOSIS. 
515 
soil. These ulcers are most common in the easeating form of 
phthisis, and we may associate this with the fact that the debris 
of the lung is much greater in that form. 
Besides the tuberculosis of the bronchial glands and intestine, 
we find sometimes a tuberculosis of the urino-genital organs, 
but this is comparatively rare. Then we sometimes find miliary 
tubercles in the liver and kidneys, scattered through these organs 
as in acute general tuberculosis. There are usually, however, but 
few tubercles compared with what we find in the latter disease. 
When tubercles exist scattered throughout the liver or in the 
kidney, we must regard that as evidence that the virus has got 
into the blood, although present only in small quantity there. 
ACUTE MILIARY TUBERCULOSIS. 
This condition we have already seen to be that in which the 
tubercular virus is contained in the blood, apparently in consider- 
able abundance, giving origin to miliary tubercles in many organs. 
The lungs are affected in almost all cases. Acute miliary tuber- 
culosis is very common in children, being nearly always the fund- 
amental condition in acute hydrocephalus, but it also occurs in 
adults. If the patient die in the earlier stages, the lungs are found 
beset from apex to base with minute tubercles which are often 
very closely placed. The tubercles may be so small as to be only 
distinguishable as such with the microscope, but they present the 
typical structure of miliary tubercles. In the early stages this, 
with general hypercemia of the lungs, is all that can be seen. But 
if the case be one of rather longer duration, we find around the 
individual tubercles processes which can be strictly compared with 
those in phthisis pulmonalis. The air-vesicles are filled with 
catarrhal cells, and the alveolar walls infiltrated with inflammatory 
round cells. The tubercles appear larger, but this is because each 
of them is surrounded by a zone of condensed lung tissue which 
cannot with the naked eye be distinguished from the tubercle. 
By and by caseous necrosis occurs, beginning in the centres of the 
tubercles. As in the case of phthisis, the caseous process extends 
to the lung tissue and inflammatory products, and the whole is 
involved in an indiscriminate necrosis. The caseous material may 
also soften, and numerous minute cavities form, but the patient 
rarely survives till this has occurred to any considerable extent. 
The disease of animals, called by the Germans perlsucht, pre- 
sents many analogies to tuberculosis, and, according to the obser- 
vations of Koch, it depends on the same form of organism. This 
relation is expressed in the term bovine tuberculosis which is 
sometimes applied to it. We have already seen that cases of what 
looks like general tuberculosis occur which are probably actual 
cases of bovine tuberculosis transmitted to the human subject. 
There are also cases in which the lung is the seat of a more local 516 
DISEASES OF THE ORGANS OF RESPIRATION. 
destructive process which may be mistaken for ordinary phthisis, 
especially as there may be considerable cavities produced. This 
subject has received notice, however, at an earlier part of this 
work (see p. 164). 
SYPHILITIC DISEASE OF THE LUNGS. 
This is somewhat rare, at least in the adult, although more fre- 
quent in the newly-born. We have here similar lesions to those 
in other organs, consisting of inflammatory changes with the occa-- 
sional formation of gummata. The inflammation affects mainly, 
but not alone, the connective tissue, so that a condition sometimes 
ensues like that of fibrous phthisis. In syphilis, however, the Virus 
coming by the blood is more generally diffused, and we have not 
that relation to the bronchi which we saw in ordinary phthisis. 
An extensive tract of lung is involved, and we liavq,a rich forma- 
tion of connective tissue so that the alveoli are compressed, while 
they also contain catarrhal products. In this way is produced 
what is called a white pneumonia. If gummata occur, they are as 
usual surrounded by a connective-tissue formation, so that cicatri- 
cial depressions and corresponding deformities of the lung may 
result. The gummata are often distinguishable by the caseous 
necrosis which they present, and if the caseous material soften we 
may have cavities resembling those in ordinary phthisis. 
TUMORS OF THE LUNGS. 
Tumors of the lungs are much more frequently secondary than 
primary growths, but there are some forms of primary tumor. 
Little pieces of bone have been met with in the interstitial connec- 
tive tissue, also little cartilaginous tumors in connection with the 
cartilages of the bronchi. 
Secondary tumors of various kinds are met with. We have 
most frequently lympho-sarcomas originating in the bronchial 
glands and extending into the lung. The new-formation follows 
the connective tissue of the lung, and we find it penetrating in a 
radiating manner from the root, often burying the bronchial tubes 
in a sheath of new-formed tissue and partially or completely 
obstructing them. Other forms of sarcoma originating in the 
mediastinum may spread in a similar fashion. Secondary tumors 
may arise by embolism, the tumor having its origin in something 
conveyed to the lungs by the pulmonary artery, and being thus 
metastatic. 
Sarcomas, as we know, sometimes penetrate directly into the 
veins, and portions being carried to the right heart are caught 
in the branches of the pulmonary artery or capillaries. The 
secondary tumors in the lung are multiple and they repeat exactly 
the structure of the primary one. Thus we have giant-celled, TUMORS OF THE LUNGS. 
517 
round-celled, and spindle-celled sarcomas. A tolerably frequent 
form is the pigmented sarcoma. The enchondroma also not infre- 
quently undergoes secondary development, like the sarcoma, by 
penetrating into veins, and the embolic origin of these secondary 
tumors has been directly demonstrated. 
Cancers, as we have seen, do not readily penetrate into the veins 
directly. Finding an easier path by the lymphatics, they nearly 
always first develop in the lymphatic glands. After a time the 
cancerous tissue may penetrate from the lymphatic sinuses in the 
gland into the veins, or they may possibly in a few cases penetrate 
Fig. 235. 
Embolic cancer of lung. Two branches of the pulmonary artery (a, a) are obstructed. 
Around them are various spaces (6, 6) filled with epithelial cells, c, c, normal lung alveoli. 
X 16. 
directly into the latter, and the material is carried on to the lungs. 
As the cancer is usually arrested for a considerable time at the 
lymphatic glands, it happens that in all forms of cancer secondary 
tumors in the lungs are of late development. As the secondary 
tumors are in the lymphatic glands, we may regard these in the 
lungs as of a tertiary order. Further, the material which produces 
these tumors often passes to some extent through the wide capil- 
laries of the lung and on into the systemic arteries, so that we 
may have tertiary tumors occurring at the same time in a variety 
of organs. The tumors in the lung are multiple, and they repeat 
the structure of the primary tumor whatever be the variety of 
cancer which has formed it. 
That these tertiary cancers form by embolism was readily seen 
in a case which occurred to the author, and which may here he 518 
DISEASES OF THE. ORGANS OF RESPIRATION. 
briefly related. It illustrates as well the tendency, which tumors 
even of this order showy of the cancerous masses to penetrate into 
existing spaces and canals. The primary tumor was a cancer of 
the stomach, and secondary growdhs had occurred in the preverte- 
bral glands. One of these glands was adherent to the vena cava, 
and several radicles of this vein emerged from the midst of can- 
cerous glands. Actual cancerous thrombi of some of these veins 
were detected by the naked eye, and under the microscope it was 
seen that the cancerous masses had partially penetrated into the 
venous radicles in the glands. In the lungs the finer branches of 
Fig. 236. 
Embolic cancer of lung. One of the spaces filled with epithelial cells (b in preceding 
figure) under a high power. There is a larger space with two branches into which the 
epithelial cells have extended. X 90. 
the pulmonary artery were found frequently obstructed (see Fig. 
235). The obstructing material was not entirely cancerous in 
structure. There was often a round-cell formation with now and 
again a distinctly cancerous appearance. In most cases the ob- 
struction was complete. Outside the obstructed arteries there 
were spaces and canals filled with cancerous growths, as shown in 
Figs. 235 and 236. These were obviously the lymphatic channels 
of the sheath of the vessels into which the cancerous formation 
had penetrated. 
INHALATION OF FOREIGN SUBSTANCES. 
The lungs of all adults have more or less of a gray color from 
the existence of a black pigment in the lung tissue. This pigment 
is absent from the lungs of children, and is undoubtedly the dust 
of the air inhaled with the respired air. It need hardly he said 
that the air of all confined spaces, such as rooms, is loaded with 
finely divided particles. This is particularly the case in cities ANTHRACOSIS. 
519 
where coal is burnt extensively, and it attains its maximum in the 
black fogs of such cities as London and Glasgow. The particles 
of dust inhaled with the air are for the most part caught by the 
mucus with which the surface of the bronchial tubes is moistened, 
and, as the ciliated epithelium plays in the direction towards the 
larynx, the dust-laden mucus is carried upwards to the larynx, 
where it is either expectorated or swallowed. ]STo doubt when the 
air is unusually laden with dust the mucous secretion is increased, 
and those who live in cities know that, when the weather is thick, 
a considerable mass of black mucus is brought up from the larynx 
in the morning, the busy cilia having swept it thither during the 
hours of sleep. But some of the dust penetrates beyond the reach 
of those scavengers and passes into the lung alveoli, where it 
lodges. From the lung alveoli it penetrates into the lung tissue. 
It is to be remembered that the structure of the alveolus is some- 
what like that of a serous membrane. There is a single layer of 
epithelium, and some have even described stomata or pseudo- 
stomata as existing. At any rate, the dust particles penetrate 
through or between the epithelial cells, and emerge into the 
lymph-spaces of the alveolar wall. Having entered the lymphatic 
system of the lung, the dust is carried into all the communi- 
cating channels of that system, and is partially deposited and 
retained as it goes by the connective-tissue cells. In this way a 
kind of pigmentation of the entire lymphatic system of the lung 
is obtained which for demonstration may serve the purposes of 
an injection of that system. In this conveyance of the dust par- 
ticles the leucocytes which are always present in the lymphatic 
spaces probably play an important part. The parts pigmented 
are, the walls of the alveoli, the interstitial connective tissue, 
especially that around the pulmonary artery and the bronchi, and 
the subpleural tissue, which is often definitely demarcated from 
the pleura proper by the pigmentation. The pigment is also 
'carried to the bronchial glands at the root of the lung, which are 
more or less blackened. This pigment is a carbonaceous material 
consisting mostly of round particles, and is to a great extent the 
soot of coal. 
Persons who live in a very dusty atmosphere are liable to a very 
excessive pigmentation of the lungs, to which the name anthracosis 
is applied. This is seen most typically in the coal-miner’s lung. 
Here the path by which the dust gets in, and its permanent locality, 
are the same as those indicated above, but the amount is greatly 
increased. The material also is essentially the same. It is some- 
times asserted that in the coal-miner’s lung the pigment consists 
of coal dust, each minute particle having the irregular crystalline 
character of a piece of broken coal. But this is not entirely the 
case. The particles are largely spherical and smooth, and these 
consist of the soot from the lamps that are burnt in the mines 
with imperfect combustion. The pigment in this case, as in the 
ordinary pigmentation of the lungs, is in the lymphatics and 520 
DISEASES OF THE ORGANS OF RESPIRATION. 
follows the distribution of the connective tissue. It is often seen 
in excessive quantity around the branches of the pulmonary artery, 
where it occupies the perivascular lymphatic spaces. It is not 
present in the proper walls of the bronchi, but exists to some 
extent in the lymphatic spaces of their adventitia. The inter- 
lobular and subpleural connective tissue is deeply pigmented. 
The inhaled dust seems a comparatively innocuous substance. 
In the bronchial tubes and in the alveoli it may induce, or be 
associated with, a catarrh, and in that case the inflammatory pro- 
ducts contain abundant pigment, giving rise 
to the well-known black spit of miners. 
The pigment is found abundantly in cells 
as in Fig. 237. 
But in the lung tissue itself there is usu- 
ally little disturbance, and even in severe 
cases of anthracosis there may be merely a 
moderate induration of the connective tissue. 
It is to be noted that in persons whose lungs 
are the seat of excessive pigment, a catarrh 
is often associated with a recurrence of the 
“black spit,” although thepersons may have 
left the pit for years. In that case the black 
spit will not occur unless the inflammation 
involves the connective tissue as well as the 
epithelial layers of the bronchi and alveoli, 
and it is to be presumed that the pigment 
passes out of the lungs in the same way as it has passed into them, 
namely, from the connective tissue into the alveoli and thence 
outwards. As mentioned above, there is no pigmentation of the 
bronchial mucous membrane, and it does not seem probable that 
pigment will penetrate from without through the bronchial wall 
into the interior of the tube. This indicates that in catarrhs the 
connective tissue is active, and that the pigment is conveyed by 
leucocytes into the alveoli or bronchi. 
There are some persons exposed to the inhalation of particles of 
a more irritating nature. It has long been known that masons 
are peculiarly liable to bronchitis and phthisis. The particles of 
sandstone are inhaled just as are the particles of dust. From 
their shape and the sharp angles which the particles of rock 
crystal present, they are much more irritating than the dust par- 
ticles. They irritate the bronchial mucous membrane. When 
they pass into the interstitial tissue of the lungs they irritate it, 
and in this case there is frequently a very marked induration of 
the connective tissue. This induration, along with the bronchitis, 
may go on to the formation of cavities by bronchiectasis. The 
indurations in this disease often have special centres of greatest 
intensity in the form of hard nodules, in the centres of which a 
collection of glistening particles may be found. 
Other kinds of dust may be inhaled, and give rise to inflamma- 
Pig. 237. 
Part of the contents of a 
lung alveolus in anthracosis. 
Black particles are seen, 
some angular, and others 
rounded. The large catar- 
rhal cells contain many par- 
ticles. X 350. 521 
PLEURISY. 
tory conditions in the lungs. They seem to irritate more or less 
according to the mechanical qualities of the particles. Particles 
which are hard, heavy, and angular, like the siliceous particles of 
sandstone, or like the steel dust to which file-cutters are exposed, 
irritate more than those which are light and rounded like those in 
the miner’s lung. The color of the inhaled dust communicates 
itself to the lungs, and so we have various pigmentations, but in 
all the forms there is a tendency to the occurrence of black pig- 
ment along with the other colored substances. 
C.—THE PLEURA. 
Pleurisy.—Tlie pleural sac in its structure and in many of its 
relations is comparable to the pericardial and peritoneal sacs, and 
much that has already been stated above regarding inflammation 
of the pericardium is applicable to inflammation of the pleura. 
There are two circumstances, however, that place the pleura in its 
pathological relations in a somewhat different position from the 
pericardium, and these are its connections with the lung on the 
one hand, and with the peritoneum on the other. In studying 
diseases of the lung, we have seen that whenever any form of 
inflammation comes to the surface of the lung it causes inflam- 
matory changes in the pleura; there is acute pleurisy in acute 
pneumonia, and chronic pleurisy is a nearly constant accompani- 
ment of phthisis pulmonalis. On the other hand, the pleura seems 
to have intimate connections with the peritoneum, as there are 
lymphatic channels passing through the diaphragm which form 
communications between the two sacs. These channels are doubt- 
less intricate and narrow, so that the diaphragm acts to a certain 
extent as a barrier between the two sacs, but it is not sufficient 
to prevent the passage, for instance, of the tubercular virus from 
the one to the other. A tubercular peritonitis is nearly always 
accompanied by a tubercular pleurisy, perhaps limited to the lower 
parts of the sac. Similarly a septic peritonitis has usually a de- 
pendent pleurisy. Tumors of the peritoneum also frequently lead 
to similar formations in the pleura. 
In the above cases the pleurisy is secondary to inflammation in 
some other part, but there are also cases of primary pleurisy. 
Persons take pleurisy from catching cold, as it is said, whatever 
be the exact mode in which the cold produces its effects. There 
is very often a localized pleurisy occurring in a limited area, just 
where the pleura is most directly exposed to the effects of cold, 
namely, in the left lower lateral region. In this position the chest 
is not covered by any considerable mass of muscles, as the fleshy 
masses of the latissimus dorsi and pectoralis major passing upwards 
to the arm leave, as it were, an unprotected space covered by the 
comparatively thin origins of the serratus magnus and external 
oblique muscle of the abdomen. This part is also removed from 522 
DISEASES OF THE ORGANS OF RESPIRATION. 
the centre of heat in the heart, and on the left side instead of the 
liver there is the hollow stomach. On the right side the liver is a 
source of heat, and renders the corresponding part on this side less 
exposed to cold than that on the left, but still more exposed than 
most other parts of the chest. It is probable that, in these locali- 
ties especially, cold, acting directly on the chest wall, may cause 
an inflammation of the pleura by depressing the temperature. 
But cold may produce a general pleurisy just as it is said to pro- 
duce a general pneumonia, the fact of the general character of the 
inflammation indicating that some irritant is present in the fluid 
which exists in the pleural sac. 
It is here proper to state that a considerable number of cases 
appearing to be simple pleurisy are really cases of tubercular 
pleurisy. The tubercular virus sometimes finds its way into the 
pleura independently of neighboring organs, being apparently 
carried by the blood to the pleural sac. The lymphatic system of 
the lungs is not in direct communication with that of the pleura, 
and so it does not usually happen that a tubercular pleurisy de- 
velops from phthisis pulmonalis except in its later stages. The 
true tubercular pleurisy develops independently of lung disease, 
although it may be present along with tuberculosis of the lungs in 
acute miliary tuberculosis, where the virus is undoubtedly con- 
veyed by the blood. Tubercular pleurisy is usually an acute dis- 
ease, and is often associated with tubercular pericarditis, or, more 
rarely, with tubercular peritonitis. 
In its anatomical details, acute pleurisy is closely analogous to 
acute pericarditis. There is hypersemia, soon followed by a thin, 
fibrinous deposit. This fibrinous exudation, forming a soft, yellow 
layer, often attains to a considerable thickness, forming shaggy 
projections from the pleural surface, especially in the region of the 
lower lobe. Serous fluid is also exuded, sometimes in considerable 
abundance. If the fluid in the pleura is not too abundant, the 
two surfaces of the membrane come in contact, and there is adhe- 
sion of the two layers of fibrine. This adhesion prevents further 
deposition of fibrine, which is often very thin over the upper lobe. 
If the inflammation goes on, there is a new formation of vascular 
granulation tissue which may come to replace the fibrine. If two 
such surfaces are in contact, by absorption of the serous fluid or 
otherwise, coalescence occurs and complete union of the surfaces, 
the granulation tissue afterwards developing into connective tissue. 
We have already seen that the fluid accumulated in the pleural sac 
frequently compresses the lung great!}7, producing collapse of it. 
An ordinary pleurisy may go on to suppuration (empyema) if the 
inflammation be very acute, or it may be suppurative from the 
outset. In the latter case there has usually been some specially 
virulent irritant present in the pleura, as where a metastatic ab- 
scess in the lung has approached the pleura, or where the pleurisy 
is one of the phenomena of septicfemia. In these cases the disease pneumothorax. 
523 
is generally rapidly fatal, and we may find remains of the fibrinous 
exudation mixed with abundant pus. Where the suppuration has 
come on in the course of a simple pleurisy the disease is often 
greatly prolonged, and the pleura undergoes great thickening, 
being converted into a bulky layer of granulation tissue like the 
wall of an abscess. The granulation tissue may undergo partial 
transformations into connective tissue with occasional adhesion, 
and as the lung has been compressed by the exudation we may 
have drawing together of the chest to an extreme degree should 
the pus be discharged or partially absorbed. 
Reference has already been made to tubercular pleurisy. The 
tubercles occur in the form of comparatively small white nodules 
which are present in the substance of the pleura, but near the 
surface. They are very commonly hidden by fibrinous exudation, 
and are therefore most easily seen on separating the lobes, the 
contact of which has prevented any thick fibrinous deposit. The 
pleurisy is usually prolonged, and we have at once fibrinons 
exudation with a certain amount of serum and chronic thickening 
of the membrane. 
Pleural Adhesions.—We have already seen that an acute 
pleurisy may result in adhesion of the sac, the process of adhesion 
resulting from coalescence of the surfaces which have become like 
granulation tissue from the inflammation. Such adhesion will not 
occur so long as fibrine is present on the surface, and is to be care- 
fully distinguished from the mere gluing which may occur in the 
earlier stages from the adhesion of the fibrinous exudation on 
opposed surfaces. But we have also seen that in the frequent 
chronic pleurisy of phthisis a similar adhesion occurs, and the 
method of its occurrence is similar. Without any fibrinous or 
serous exudation (hence called dry pleurisy) the surfaces come to 
have the characters of granulation tissue and coalescence with 
vascular communication occurs. 
Hydrothorax is a dropsy of the pleural sac. The serous exuda- 
tion of acute pleurisy is not to be placed in this category, which 
only includes cases in which the transudation is increased without 
inflammation. Most frequently it is part of a general dropsy, as 
in Bright’s disease, cardiac disease, or antemia. Malignant tumors, 
especially secondary cancers, produce hydrothorax just as they 
produce accumulation in the peritoneal sac. As cancers spread 
along the lymphatic spaces it may possibly be that the dropsy 
results from obstruction of these. 
Pneumothorax has been referred to in connection with phthisis 
pulmonalis, and the mode of origin there indicated is that in the 
great majority of cases. Of the remainder there are some in which 
it is due to empyema—the visceral pleura has softened and the 
lung has become ulcerated so as to communicate with the pleura, 
or to gangrene of the lung, or to metastatic abscesses, or to the 524 
DISEASES OF THE ORGANS OF RESPIRATION 
bursting of emphysematous vesicles, or to a traumatic cause. The 
air in the pleural cavity is usually at a high pressure and the cavity 
is much distended, so that when the chest is opened the air rushes 
out with some force. The pleural cavity as exposed presents a 
remarkably empty appearance, the lung being compressed except 
where there are adhesions, which may form tense bridges across 
from parietal to visceral layer or may limit the pneumothorax con- 
siderably. If the patient live there is nearly always an acute 
suppurative pleurisy, so that the condition may be designated pyo- 
pneumothorax. 
Experimental observation seems to show that the air may be 
absorbed, and this is confirmed by actual clinical observation. In 
the great majority of cases, however, the pneumothorax being 
followed by suppurative pleurisy, the aperture does not close and 
the condition persists till death, which is not generally long de- 
layed. 
Tumors of the pleura are rarely primary, but osteomas and 
lipomas have been seen. Cases have also been described of 
primary cancer of the pleura in which the tumor appeared to take 
origin in the endothelium of the sac or of its lymphatics. 
Secondary tumors are not infrequent. A sarcoma of the medi- 
astinum, originating in the bronchial glands, may result in an erup- 
tion of secondary tumors in the pleura, or a cancer originating in 
connection with the bronchi at the root of the lung may have a 
similar consequence. In cancer of the mamma the secondary 
tumors sometimes involve the chest-wall and are propagated to 
the pleura, where they produce an eruption, and may pass on to the 
lungs. Cancers of the peritoneum also frequently cause cancer of 
the pleura. In all these cases the tumors form pale soft masses 
which are usually flat and sessile, but may show considerable 
prominence. As already mentioned, the cancers are usually asso- 
ciated with dropsical exudation. DISEASES OF THE ALIMENTARY CANAL. 
INTRODUCTORY OBSERVATIONS. 
In studying the diseases of the alimentary canal certain facts as 
to its structure and functions are to be borne in mind. The canal 
is lined throughout by a mucous membrane, which consists of 
loose connective tissue covered with epithelium in one or several 
layers. In the mucous membrane and to some extent beneath it 
are glands which in different parts have different structures, hut 
everywhere secrete materials that pass into the calibre of the canal. 
In addition to these there are in many parts closed follicles of a 
lymphatic structure which usually lie near the surface and fre- 
quently take part in changes going on there. Beneath the mucous 
membrane is the submucous tissue which, for the most part, is 
loose, and so allows the mucous membrane to go into folds or be 
stretched out flat according to the state of dilatation or contraction 
of the canal. Outside this there is a muscular coat, generally in 
two layers, by means of which movements and variations in calibre 
are effected. In most parts of the intestinal canal there is a serous 
coat outside of all. 
In the diseases of the alimentary canal it is chiefly the mucous 
membrane that we have to deal with, the subjacent structures 
being usually subordinate to and affected secondarily to it. The 
serous coat, it is true, is often affected independently; its diseases, 
however, do not belong specially to the alimentary canal, but to 
the peritoneum as a whole. The mucous membrane on account 
of its exposure to a variety of influences derived from the varying 
contents of the canal is specially liable to inflammations, and the 
great majority of the diseases to be considered here are inflam- 
matory ones. 
It will be necessary for convenience to subdivide the alimentary 
canal into different sections and to consider each of these separately. 
A.—THE MOUTH. 
As the mouth is exposed in an especial manner to external 
influences, so its mucous membrane possesses an epithelium in 
many layers, and it is not nearly so liable to inflammations as most 
other parts of the alimentary canal. 526 
DISEASES OF THE ALIMENTARY .CANAL. 
INFLAMMATIONS OF THE MOUTH. 
Catarrh.—If we leave out of view the catarrhs of the fauces 
and pharynx which we consider afterwards, simple catarrh of the 
mouth is exceedingly rare as a primary disease. It is not infre- 
quent, however, as a secondary affection, arising from the irritation 
of carious teeth, from the use of mercury, the presence of ulcers, 
etc. It is also of frequent occurrence in the acute fevers, especially 
typhus, scarlet fever, smallpox and measles. In these fevers there 
is also a catarrh of the stomach, and the inflammation in both seems 
due to the action of the poison in the blood. 
The mucous membrane is swollen and red and there is greatly 
increased desquamation of the epithelium, especially inside the 
cheeks and on the tongue. The desquamated epithelium is mixed 
with leucocytes, serous exudation, and mucus in varying proportions, 
and on that account it has varying characters. On the tongue 
there is usually much epithelium which lies on the surface, and so 
a tolerably thick layer is formed mostly of a whitish or yellowish 
color (furred tongue). On the cheeks and gums there is more fluid 
and less epithelium. In the midst of the epithelium and leucocytes 
bacteria and leptothrix threads are to be found. If the patient is 
feverish and lies with the mouth open, the catarrhal products dry 
in and form a dirty brownish coating of the tongue and gums 
which goes under the name of sordes. 
Sometimes the inflammation centres especially around the 
mucous glands, and they may form prominent nodules or vesicles. 
To this form the name follicular stomatitis has been given, and 
it is frequently seen in children during dentition or after measles, 
and is often associated with catarrh of the stomach or intestine. 
The vesicles or small prominences frequently burst and leave 
multiple small ulcers covered by a dirty exudation. 
Catarrh of the mouth rarely assumes a phlegmonous character, 
in this respect contrasting with inflammation of the fauces. 
Thrush or Aphthous Stomatitis or Soor.—This condition has 
already been mentioned as connected with the presence of a fungus. 
It occurs in the mouths of young unhealthy children, but is also 
occasionally seen in emaciated adults, as in diabetes. The normal 
secretion of the mouth is alkaline, but in this disease it becomes 
acid, which may perhaps be the reason that the fungus develops. 
If the mouth be examined it will be found beset with small white 
spots, which look like little bits of white curd on the surface of 
the mucous membrane. These patches are, however, adherent, 
and in removing them the mucous membrane beneath will be 
found red and bleeding. The white patch consists of epithelium 
united into a membrane by a fungus, the oidium albicans (Fig. 238). 
It consists of branching threads composed of elongated cells 
placed end to end and sometimes losing themselves in masses gangrenous stomatitis. 
527 
of spores. The aphthous patches frequently extend from the 
mouth downwards to the pharynx and oesophagus. 
The condition of the mucous membrane in certain special 
forms of inflammation deserves particular mention. In smallpox, 
besides a general catarrh there are vesicles or pustules analogous to 
those on the skin. We have first whitish patches consisting 
of raised and desquamating epithelium. The epithelium is soon 
Fig. 238. 
Oidium albicans or thrush-fungus. The constituents of the fungus are associated 
with flat epithelium, X 450. (Kuchenmeister.) 
discharged and superficial ulcers result. In scurvy there is great 
swelling and oedema of the mucous membrane of the gums around 
the teeth. The gums bleed and, apparently as a consequence of 
this, ulcers form at the edges of the teeth and may extend down to 
the bone, which may undergo necrosis. Very often the teeth are 
loosened. As a consequence of the use of mercury we sometimes 
have a considerable stomatitis. It occurs after the medicinal use 
of mercury and also among workmen who employ it in their occu- 
pations. The mucous membrane is swollen, especially that of the 
gums and cheeks, and there is severe salivation. Ulcers frequently 
form, especially on the internal surface of the cheeks and lips, and 
on the edges of the tongue. They may he in the form of flat 
excoriations or deeper ulcers with a membranous covering. 
Gangrenous Stomatitis or Cancrum Oris or Homa.—This dis- 
ease, which is fortunately a rare one, occurs in badly nourished 
children, particularly when reduced by severe illness such as 
scarlet fever or measles. It presents itself first as a diffuse swelling 
of the cheek which is seen to be tense, red, and glistening, with 
one spot in the centre usually redder than the rest. On examining 
the inside of the mouth there is already an excavated ulcer oppo- 528 
DISEASES OF THE ALIMENTARY CANAL. 
site the red spot on the cheek, and the gums opposite may also be 
ulcerated. As the disease progresses, more and more of the 
mucous membrane of the mouth is ulcerated away. At the same 
time the red spot on the cheek gets black in the centre, and after- 
wards extends in area. By and by a slough of various sizes sepa- 
rates and a communication forms through the cheek with the 
inside of the mouth. If the patient survive still further destruction 
occurs, the necrosis passing on to the surrounding skin of the jaws, 
even to the ear and eyelids. There may be necrosis of the jaws. 
Not infrequently this disease is associated with a gangrenous pneu- 
monia and there are general symptoms of septic poisoning. 
The exact nature of this disease is not known, but it must be 
suspected from the rapid necrosis that a specific virus has to do 
with it. 
Inflammation of the tongue deserves a brief special notice. We 
have seen that the tongue takes part in most of the inflammations 
of the mucous membrane, but sometimes it becomes the seat of a 
special inflammation of its substance, a true glossitis. This may 
occur as a result of wounds or irritations from without, or in the 
course of such diseases as erysipelas and smallpox. The tongue 
swells greatly in consequence of the inflammatory infiltration of 
the interstitial connective tissue, and this sometimes, though 
rarely, goes on to the formation of abscesses. The muscular fibres 
are swollen, pale and brittle. Usually the inflammation ends in 
resolution, but sometimes it becomes chronic, and there may be 
great increase of connective tissue with permanent induration of 
the tongue. 
INFECTIVE TUMORS OF THE MOUTH. 
Syphilis.—We have various syphilitic lesions in the mouth, from 
slight inflammation to deep ulceration. It is not uncommon to 
meet with a primary chancre on the lips. In that case there is a 
prominent tumor which has, in more than one case, been taken 
for an epithelioma. On microscopic examination the tumor is 
found to consist of immense aggregations of round cells (Fig. 239). 
The catarrh which accompanies the secondary stage is often very 
slight, but it may be accompanied by superficial ulceration of con- 
siderable extent. Flat condylomata are particularly frequent in 
the mouth, and they often break down and form superficial ulcers, 
especially on the lower lip and angle of the mouth. The deeper 
ulcers arise in connection with gummata, which form in the sub- 
stance of the mucous membrane, and may lead to very serious loss 
of substance. If healing occurs a cicatrix forms, but cicatrices 
sometimes occur without ulceration having taken place, the 
gumma itself giving place to a cicatrix. The gummata not infre- 
quently have their seat deep in the substance of the tongue, and 
the resulting cicatrices, with or without ulceration, may produce 
very marked deformity of this organ. TUMORS OF THE MOUTH. 
529 
Lupus not infrequently extends from the neighboring skin into 
the mouth and may produce considerable destruction. Leprosy 
also affects the mucous membrane of the mouth sometimes. 
Fig. 239. 
Section of a chancre of the lip which was excised under the belief that it was an epithe- 
lioma. There are multitudes of round cells beneath the epithelium, which is encroached on 
towards the left. X 90. 
Glanders occasionally manifests itself here. Tubercular ulcers 
are exceedingly rare. 
TUMORS OF THE MOUTH. 
These are of somewhat frequent occurrence and considerable 
variety. We rarely meet with fibromas, lipomas, and erichon- 
dromas. Iiather more common are .adenoid tumors of the lips. 
These take origin in the mucous glands of the lips, and frequently 
become converted into mucous or colloid cysts. They form promi- 
nent rounded tumors sometimes as large as a hazel-nut, and are 
readily enucleated. Vascular tumors, mostly congenital nsevi, 
are not infrequent on the lips, forming either fiat elevations or, 
more rarely, prominent tumors with limited base. Vascular tumors 
are also met with on the tongue. Warts occur on the lips, espe- 
cially at the edges. In that situation they are mostly hard, while 
those on the proper mucous membrane are soft. Vot infrequently 
the wart ulcerates, and, it is said, may give origin to a cancerous 
tumor. Warty outgrowths also occur on the tongue. The papillse 
of the tongue sometimes undergo great elongation, especially their 
epithelial layers, and we may have a condition as of hairs on the 
tongue. 
Sarcomas rarely develop in the mouth itself, although they have 
been met with in the tongue. On the other hand, it is not uncom- 
mon to find a sarcoma of the jaws growing from the periosteum 
and projecting into the mouth. This applies especially to the form 
of tumor called epulis. This name is given generally to tumors 530 
DISEASES OF THE ALIMENTARY CANAL. 
which arise from the alveolar processes of the jaws, growing mainly 
from the periosteum. These are mostly sarcomas, and composed 
of spindle-cells, hut they nearly always contain giant-cells, and 
sometimes these are in large numbers. Osseous trabeculae pass 
into them frequently from the bone beneath. As these tumors 
grow they push the mucous membrane of the gums before them, 
and so form red prominences of a rounded form, behind, in front 
of, or between the teeth, and generally hard to the feel. The teeth 
are often considerably displaced by them as they grow, especially 
when they assume large dimensions as sometimes happens. 
Cancers of the mouth are nearly all of the epithelial variety. 
They are of very frequent occurrence on the lips and are also 
common on the tongue. On the lips epithelioma is almost con- 
fined to the male sex, and has its seat in the great majority of 
cases in the lower lip. This is frequently ascribed to the fact that 
in men the lip is more frequently exposed to irritation by smoking 
short pipes and in shaving. On the tongue the epithelioma usually 
forms at the edge, and it is often said that the irritation of the 
sharp edge of a carious tooth has been the starting-point. The 
epithelioma begins in a limited infiltration of the lip or tongue, 
but as a rule ulceration soon occurs, and the tumor presents itself 
as a flat or excavated ulcer with infiltrated edges. By ulceration 
great destruction may take place of the lips and skin around, or 
of the tongue. Secondary epitheliomatous formation frequently 
occurs in the submaxillary lymphatic glands, and may extend to 
the glands of the neck. 
Macroglossia is a condition in which the tongue is greatly in- 
creased in bulk, the enlargement being nearly always congenital. 
Even at birth the tongue may be too large for the mouth and 
project beyond the lips. Afterwards it may increase still more, 
and as the child grows it may displace the alveolar processes 
considerably. For the most part there is no hypertrophy here 
except of the interstitial connective tissue, but evidences of new 
formation of muscular tissue have been observed. As a rule, the 
lymph-spaces of the hypertrophied connective tissue are greatly 
enlarged, and there is even a formation of cavernous tissue, the 
spaces in which are filled with lymph. In this way we may speak 
of lymphangioma cavernosum as taking part in the condition. It 
will be observed that the condition here somewhat resembles that 
in elephantiasis, there being in both cases a great new formation 
of succulent connective tissue with wide lymph-spaces. The re- 
semblance is further indicated in the fact that the lips frequently 
hypertrophy as well. 
Banula is a name applied to cysts which form beneath the 
tongue. These mostly arise as retention cysts from closure of 
‘Wharton’s duct (duct of the submaxillary gland) or the duct of 
the sublingual gland, but they may take origin in the mucous affections of the teeth. 
531 
glands. Before the occurrence of the cyst there is usually some 
infiammation of the floor of the mouth very often connected with 
affections of the teeth. According to the observations of Reck- 
linghausen, referred to at p. 199, the cyst arises by dilatation of 
the duct, while the gland structure persists and furnishes the ma- 
terial by whose accumulation the cyst forms (see Fig. 81, p. 199). 
AFFECTIONS OF THE TEETH. 
In studying tlie diseases of the teeth, we have to remember 
what are their constituent and related structures. The hard part 
of the tooth consists of enamel, dentine, and cement. The enamel, 
containing very little organic matter (only about two or three 
per cent.), is for the most part passive, and even presents great 
mechanical resistance to destructive processes. In its original 
formation it is a superadded structure, and for this reason also it 
takes little part in the morbid changes which occur in the teeth. 
The dentine, consisting of tubules with a hard matrix, possesses 
a much larger proportion of organic matter (twenty-eight per 
cent.), and is much more directly involved in morbid processes. 
The cement, which covers those parts of the tooth which are 
devoid of enamel, consists of true hone, and is liable to changes 
of a similar nature to those of hone. 
Turning to the soft parts, the pulp tills the cavity of the tooth 
and has an outline parallel to that of the tooth as a whole. The 
pulp is a soft, highly vascular tissue, and is concerned in the nutri- 
tion of the dentine. It is also richly supplied with nerves whose 
filaments pass in part into the dentinal tubules. The pulp is so 
sensitive that in popular language it is called “the nerve.” In the 
original formation of the tooth the dentine is produced by the 
structure which is afterwards represented by the pulp, and through 
life the latter retains to a considerable extent its formative power. 
As we shall see afterwards, it is concerned in the formation of the 
secondary dentine. 
The tooth is fitted accurately into the alveolus by means of the 
cement on the one hand and the dental periosteum or periodontal 
membrane on the other. This membrane, lying between the 
cement and the bone of the jaw, forms a kind of double periosteum, 
and is, from its position, very liable to the action of mechanical 
forces, being placed between two rigid structures, one of which 
(the tooth) is peculiarly exposed to mechanical interference. It is 
continuous at the apex of the root with the pulp, and at the neck 
with the mucous membrane of the gums on the one hand and the 
periosteum of the jaw on the other. We shall see afterwards that 
inflammations are apt to extend from the pulp to the dental peri- 
osteum, and from the latter to the gums and maxillary periosteum. 
Caries.—This name is applied to a condition which is not quite 
analogous to caries of bone, except in so far as in both there is 532 
DISEASES OF THE ALIMENTARY CANAL. 
destruction of the dense calcified structure. Caries of bone is 
related to inflammatory processes, but caries of the teeth lias no 
such origin. It consists of a softening usually progressive, of the 
enamel and dentine and their subsequent disintegration. The pro- 
cess appears to begin very commonly in places where the enamel 
shows normally rather deep furrows, and is therefore thinner and 
more easily destroyed than elsewhere. When the caries reaches 
the dentine it advances more freely, so that the enamel may to some 
extent be undermined. The lime salts are first absorbed, and then 
the organic basis is broken down. The caries advances in the 
direction of the dentinal tubules, as shown in Fig. 240. 
Various views have been held as to the nature of the process. 
At one time it was regarded as inflammatory, but this view may be 
set aside, chiefly on the ground that a process 
exactly similar occurs in teeth which have been 
drawn and reinserted, as well as in artificial 
teeth made of the ivory of the hippopotamus. 
The caries consists, in fact, of a gradual solution 
of the lime salts, and for this solution we must 
infer the existence of an acid. The secretion of 
the mouth is naturally alkaline, but in carious 
teeth an acid reaction has been detected. The 
acidity is often connected with derangements of 
the stomach, but it may have a more local origin, 
as when the secretion of the gums is abnormal, 
or perhaps when food is undergoing acid fermen- 
tation in contact with the teeth. It may be that 
before the teeth yield to an undue acidity they 
have already an abnormally weak power of 
resistance, and this may he related to personal 
peculiarities, inherited or otherwise. 
At the advancing margin of the caries a 
widening of the dentinal tubes is visible, and in 
these widened tubes, as well as in the carious 
cavity, bacteria and leptothrix threads are to be 
found. By some the process has been ascribed 
to the action of these organisms, and especially 
by Klebs, but these views stand in need of con- 
firmation. 
Inflammation frequently follows on caries, and 
the pulp is usually involved. It is almost cer- 
tainly attacked if the caries causes penetration 
into the pulp, but even before this takes place 
there is frequently some inflammation. This 
sometimes expresses itself in a new formation of 
sf.condary dentine inside the tooth around the 
point to which the caries is advancing (see Fig. 240). In this way 
the carious cavity may be shut off from the cavity of the pulp, and 
so a more serious inflammation warded off. Very frequently, 
Eig. 240. 
Section of tooth with 
caries. There are two 
cavities, one on each 
side, and in the pulp- 
cavity a new formation 
of secondary dentine. 
The secondary dentine 
is not exactly on the 
same level as the cavi- 
ties, but at the ex- 
tremities of the denti- 
nal tubules leading 
from these. (After 
Salter.) THE SOFT PALATE, PHARYNX, AND TONSILS. 
533 
however, a more acute inflammation of the pulp occurs, with 
redness, swelling, great pain, not infrequently also with complete 
necrosis of the pulp, and, in consequence, of the whole tooth. 
The inflammation often extends to structures around the tooth. 
The root-membrane or dental periosteum, which covers the root 
portion of the tooth, is the structure most directly attacked. This 
membrane is, as we have seen, intimately connected towards the 
neck of the tooth with the submucous tissue of the gums, and the 
periosteum of the alveolar process of the jaw. Inflammations of 
these structures, especially of the gums, very frequently ensue, 
resulting in the well-known gum-boil, which often goes on to sup- 
puration and abscess, forming the so-called parulis. The abscess 
usually bursts into the mouth, but it may produce extensive swell- 
ing of the gum, and lead even to penetration outwards, resulting 
in a fistulous opening in the skin. 
The result may be even more serious if the periosteum of the 
jaw becomes inflamed, resulting, it may be, in suppuration which 
is apt to be chronic. With the periostitis there is usually new 
formation of bone, causing thickening of the jaw. 
It is to be added that these inflammations of the root-membrane 
and periosteum of the jaw sometimes occur apart from caries, as a 
result, for instance, of poisoning with phosphorus or mercury, and 
in scurvy. In that case the inflammation is not limited to the 
neighborhood of one tooth, but extends probably to a series. 
The cement, which, it must be remembered, is composed of 
bony tissue, sometimes undergoes a hypertrophy to which the 
name exostosis or osteoma is often given. This is scarcely a true 
bony tumor, but originates rather in a chronic inflammation of the 
cement, leading to a considerable new formation of bony tissue. 
In this way are formed prominent tuberous outgrowths from the 
roots of the teeth, which may be localized in one part of the fang, 
or cover a considerable portion of it, or even the whole root por- 
tion of the tooth. In the latter case it is as if the root was enlarged 
by rough accretions on its surface. These so-called exostoses 
sometimes otter serious resistance to the extraction of the teeth. 
Another form of tumor connected with the teeth is that which 
Virchow has called the odontoma. This tumor arises in connec- 
tion with teeth retained in the alveoli by faulty development. 
The tumors are composed of dentine and enamel, and are of small 
size and rare occurrence. 
B.—THE SOFT PALATE, PHARYNX, AND TONSILS. 
Introductory Observations.—In studying the diseases of these 
parts there are two circumstances to be taken into account very 
carefully: the one concerns the structure of the mucous membrane, 
and the other the circumstances as to its exposure to influences 
from without. 534 
DISEASES of the alimentary canal. 
The mucous membrane here differs from that of the mouth 
proper chiefly in respect that in addition to the ordinary mucous 
glands there are numerous lymphatic follicles. The distinction 
between these two is not always correctly appreciated. The 
mucous glands are racemose glands with proper ducts, opening on 
the surface of the mucous membrane. The follicular glands, as 
they are often called in rather a confusing way, are strictly com- 
parable with the closed follicles of the intestine. In the pharynx, 
soft palate, and root of the tongue they occur in the form of 
isolated rounded masses of lymphatic tissue, like the solitary 
follicles of the intestine. In the tonsils we have aggregations of 
these follicles not unlike Peyer’s patches. The prominence of 
these follicles in the tonsils causes the mucous membrane to be 
thrown into folds, and so wre have comparatively deep recesses, 
which are sometimes called crypts, and in which secretions may 
accumulate, especially if their depth is exaggerated by diseased 
conditions. 
The other circumstance alluded to is that from their exposed 
condition these parts are peculiarly prone to irritation from agents 
coming to them by the inspired air. The mucous membrane of 
the mouth generally seems peculiarly resistant to external irrita- 
tions, but here, where there is the transition, as it were, from the 
mucous membrane exposed to external influences to that protected 
from them these inflammatory manifestations occur with peculiar 
frequency. Almost all the diseases we have to treat of here are 
forms of inflammation, and it is usual to describe these under the 
general designation of Angina. 
INFLAMMATIONS OF THE FAUCES. 
Acute Catarrhal Angina.—This forms the most ordinary sore 
throat, and occurs either from “cold,” especially at seasons of the 
year when sudden changes of temperature are prevalent, or as a 
local symptom of a general disease, such as measles, scarlet fever, 
smallpox. It may be said regarding scarlet fever, smallpox, and 
diphtheria that the throat affection in them begins with an acute 
catarrh, hut that, especially in scarlet fever and diphtheria, it 
nearly always goes on to something more serious. In the simple 
catarrh there are redness and swelling of the mucous membrane 
with a mucous exudation which covers the surface and may have 
a tough consistence. Sometimes vesicles form on the mucous 
membrane. 
Chronic catarrh very frequently follows on the acute form, 
especially when there have been repeated attacks. The conditions 
are somewhat different in different cases, and rather complicated 
classifications have been introduced. As in other chronic inflam- 
mations, there is here, for the most part, thickening of the mucous 
membrane, but there are different ways in which this may, to some INFLAMMATION OF THE FAUCES. 
535 
extent, localize itself. There may be a general hypertrophy of the 
superficial layers of the mucous membrane, and, as the bloodvessels 
remain congested, it is a rather succulent swelling. This causes 
what is called the relaxed throat. The appearances are most pro- 
nounced in the case of the uvula, which becomes elongated, some- 
times to a very marked extent. At other times the swelling is 
not so uniform, but with some general thickening there is an 
occasional localized prominence, causing the mucous membrane to 
assume a granular appearance. This form occurs mostly among 
clergymen, singers, actors and others whose occupation requires 
them to use their voices for prolonged periods with a loud tone. 
It is not by any means certain what the exact structure of the 
prominent granulations in this disease- is, but it seems likely that 
there are really two conditions included under the name. In one 
of them, the mucous glands are involved and may be seen dis- 
charging a milky fluid. In the other, the enlargement is not 
connected with the mucous glands, but is usually supposed to 
depend on enlargement of the closed follicles, although Stoerk has 
recently stated that it really consists of a hypertrophy of the epi- 
thelium. The condition is often called follicular pharyngitis from 
the view that the closed follicles are mainly concerned. Ulcers 
may form in connection with these swellings, and they are called 
follicular ulcers. 
Acute phlegmonous inflammation of the fauces frequently 
results in the formation of abscesses. It is a condition of some- 
what common occurrence. Here there is not merely a surface 
catarrh, but the mucous membrane and submucous tissue are 
involved in an acute inflammation of a very intense kind which 
usually goes on to suppuration. The disease very commonly 
begins on one side and frequently involves the tonsil, sometimes 
extending thence to the posterior wall of the pharynx. The 
swelling and redness are very great from liypersemia and oedema 
of the whole structures, and the patient may have difficulty in 
opening the mouth. If it goes on to suppuration, the pus often 
collects and forms an abscess which bursts into the throat. In 
some cases the acute inflammation extends downwards to the base 
of the epiglottis, and the case becomes dangerous because of the 
possible supervention of oedema glottidis. It should be added 
that the name quinsy is applied to this disease as well as to a more 
local inflammation of the tonsils alone. 
The causes of the inflammation are frequently obscure. It 
seems as if some intense irritant were acting on the fauces, and 
the fact that severe sore throats often occur in a number of per- 
sons about the same time would point to the existence of a virus 
of some kind. The occurrence of a similar inflammation in scarlet 
fever is also confirmatory of the supposition that the disease owes 
its origin to a virus. It sometimes happens that the inflammation, 
after attacking one side, passes round and involves the other, and 
this looks like an irritant which propagates itself. 536 
DISEASES OF THE ALIMENTARY CANAL. 
Diphtheria.—The changes which occur in this disease have 
already been referred to in considering its manifestations in the 
air-passages. It usually begins in the fauces and has its centre 
there. The characteristic phenomenon here is the formation of 
a fibrinous exudation. In order to that there must he necrosis 
of the epithelium on the surface. As we have seen, there is 
usually in the fauces a deeper necrosis involving the mucous 
membrane to a greater or less depth. Besides the exudation and 
necrosis there are other signs of inflammation, chiefly in the pres- 
ence of leucocytes infiltrating the mucous membrane and passing 
into the exudation. 
It sometimes happens that the mucous membrane is not in- 
volved in the exudation, so that when the exudation is removed 
there is no loss of substance. As a rule, however, there is necrosis 
of the mucous membrane, and this in all degrees till we come to 
the so-called gangrenous form. In this form, as the exudation 
separates, if carries with it portions of tissue, and as these only by 
degrees become detached from the living tissue, it looks as if 
exudation and dead tissue were together sloughs of the mucous 
membrane. These sloughs frequently look more serious than they 
are, but there may be considerable loss of substance, and ulcers of 
some depth and size may be left. 
The disposition of the patches of exudation is very various. 
Sometimes they are mainly on the tonsils, sometimes on the soft 
palate and uvula. Extension to the posterior nares on the one 
hand and to the larynx on the other is very frequent, the latter, as 
we have seen, being particularly common. 
Acute Tonsillitis is, as we have seen, occasionally a part of a 
general phlegmonous inflammation of the fauces. Occurring 
more independently it is accompanied by considerable swelling, 
consisting of an inflammatory infiltration of the lymphatic follicles 
of the tonsils. Sometimes it goes on to suppuration, but rarely 
does so when the tonsils alone are affected. The swelling in many 
cases does not fully subside, and gives rise to a more or less per- 
manent enlargement such as we have next to consider. 
Chronic Tonsillitis mainly shows itself in the form of hyper- 
trophy of the tonsils. Certain persons, especially in \outh, are 
prone to repeated subacute inflammations of the tonsils, and as these 
recur the tonsils acquire a permanent enlargement. This consists 
anatomically in a true hypertrophy of the lymphatic follicles, 
although there is sometimes also an increase of the interstitial con- 
nective tissue. For this reason the tonsils are rarely much indu- 
rated, the soft lymphatic tissue existing so abundantly as to make 
the structure as a whole somewhat soft. The hypertrophy appears 
to be not always the result of chronic inflammation, or at least it 
is frequently altogether out of proportion in amount to the inflam- 
mation. The greatest degree of hypertrophy is met with in 
children, and they are not so liable to acute tonsillitis as youths. DILATATION OF THE (ESOPHAGUS. 
537 
There are cases even of congenital hypertrophy of the tonsils, and 
there are still more frequent cases of a gradual enlargement with- 
out any apparent attacks of inflammation. In this way the tonsils 
may acquire very large dimensions, reaching the size of a hen’s 
egg on some occasions. 
Syphilitic Disease of the Fauces.—This manifests itself in 
multifarious ways. A persistent catarrh having the ordinary 
characters of subacute simple catarrh is very common. Mucous 
tubercles or condylomata are tolerably frequent, especially in the 
pillars of the fauces and in the soft palate. In the tertiary stage, 
with or without the formation of gummata, there may be ulcer- 
ation of the mucous membrane. Not infrequently the ulceration 
extends very deeply and causes destruction of the uvula and palate. 
It may extend to the epiglottis and no further. It is frequently 
accompanied by considerable thickening and cicatricial contraction, 
so that it may lead to great deformity and sometimes to stenosis of 
the pharynx. 
Tubercular Ulcers.—These are of very rare occurrence here, 
although so common in the larynx. The disease is associated with 
phthisis pulmonalis, and is really due to an extension upwards of 
tubercular ulceration of the larynx. It occurs in the form 
of superficial ulcers, originally of a circular form. 
The Tumors of the Fauces are not so different from those of 
the mouth as to call for very special remark, and they are altogether 
of much less frequent occurrence. We meet with papillary 
excrescences, cysts, sarcomas, and epitheliomas. 
C.—THE (ESOPHAGUS. 
The diseases of this part of the alimentary canal are important 
from a practical point of view, chiefly because of the natural narrow- 
ness of the tube. The mucous membrane of the oesophagus is 
covered by a thick layer of stratified flat epithelium, and the 
mucous glands are comparatively few. 
Dilatation of the (Esophagus.—Of this somewhat frequent 
condition two forms may be distinguished. Besides a local dilata- 
tion about to be mentioned, we have a general dilatation of the 
tube as a result of obstruction at any part of its course. The 
obstruction is mostly low down in the oesophagus and may be even 
at the cardiac end of the stomach; or the stomach and oesophagus 
may be simultaneously dilated by obstruction of the pyloric end of 
the stomach. With the dilatation in these cases there may be con- 
siderable thickening of the muscular coat, although this is not 
always present. 538 
diseases of the alimentary canal. 
Contrasted with this general dilatation is the partial dilatation 
or diverticulum. The mode of origin of these diverticula is 
sometimes obscure. There are some which seem to owe their 
origin to an imperfect closure of the communication between the 
(esophagus and the trachea during foetal life. If this closure be 
delayed, then the wall of the oesophagus may remain bulged out 
in front and from this beginning a larger diverticulum may arise. 
More commonly, however, the diverticula form on the posterior 
wall at the lower part of the pharynx or upper part of the oesoph- 
agus. It is probable that for the most part these originate by a 
piece of hard food lodging in a fold of the mucous membrane, and 
being gradually pushed outwards, carrying the wall of the tube 
with it. As the sac enlarges, it hangs downwards with its mouth 
presenting upwards, and so it is always ready to receive the food 
in its passage downwards. It is probable that in most of these 
cases there is a separation of the fibres of the muscular coat of the 
oesophagus or pharynx, and that the mucous membrane is pushed, 
as it were, through the muscular coat. It is consistent with this 
view that the diverticula are most common at the junction of 
pharynx and oesophagus, where the circular muscular coat is 
thinnest. If the sac is of any consideraole size and filled with 
food, it will press on the oesophagus below its mouth, and of itself 
produce an obstruction. In this way the food is prevented passing 
down the oesophagus and goes readily into the sac. We have, 
therefore, for the most part, a continually increasing enlargement 
of the diverticulum which may reach the dimensions of a child’s 
head or larger. It contains the remains of the decomposing food, 
with more or less mucus, which is sometimes present in consider- 
able masses. If the diverticulum is moderate in size its wall may 
still contain some muscular fibre, although, from what has been 
already mentioned, it will appear that the muscular coat is mostly 
absent except just at the neck. 
Besides the two modes of origin already mentioned a third has 
been distinguished. The lymphatic glands at the root of the lung 
sometimes, after enlarging, undergo softening and cicatricial con- 
traction. If a gland, under these circumstances, has acquired 
adhesion to the oesophagus, it may in its contraction drag the wall 
of the latter outwards. In this way the oesophagus may acquire a 
funnel-shaped pouch which is liable to enlargement by the food 
being pushed against it. As it is mostly the bronchial glands that 
are concerned here, such diverticula are usually found near the 
bifurcation of the trachea, and they sometimes perforate into the 
trachea, forming fistulous openings. They have also been observed 
to perforate into neighboring cavities such as the pericardium or 
pleura, producing serious inflammations of these. 
Obstruction op the (Esophagus.—This condition may arise as a 
consequence of pressure from without, by tumors, aneurisms, 
abscesses. But it is much more frequent from disease in the tube 
itself. Ulcers of various kinds, by the cicatricial contraction PERFORATING ULCERS OF THE (ESOPHAGUS. 
539 
incident to attempts at healing, may induce obstruction, as, for 
example, ulcers from swallowing strong acids, syphilitic ulcers, etc. 
Still more frequent are obstructions from tumors of the oesophagus, 
and especially cancers, which we shall have to refer to immediately. 
As we have already seen, obstructions of the oesophagus frequently 
give rise to dilatations with hypertrophy of the muscular coat 
above the seat of constriction. Sometimes the dilatation becomes 
more partial, so that with a general dilatation there is a partial 
diverticulum. 
Inflammations of the oesophagus are of comparatively little 
moment. The mucous membrane is formed so as to resist the 
action of irritants, and unless the action be peculiarly strong we 
have not considerable inflammation. When strong acids or 
alkalies, or substances at a high temperature, are swallowed, they 
may cause superficial necrosis and considerable inflammation of 
the mucous membrane. The small- 
pox eruption may extend into the 
oesophagus, producing inflammation 
there. 
Strong acids or alkalies when swal- 
lowed usually produce much more 
serious results in the stomach than 
in the oesophagus, as they pass rap- 
idly over the surface of the latter. 
Acids produce whitish, yellowish, or 
brownish sloughs of the epithelium, 
sometimes penetrating to the mucous 
membrane itself. Caustic alkalies, 
on the other hand, dissolve the 
epithelium, producing a grayish gel- 
atinous material which lies on the 
surface. If they penetrate to the 
mucous membrane they reduce it to 
a soft, brownish, half-diffluent sub- 
stance. If recovery occurs, there 
are at first ulcers with more or less 
violent inflammation, and afterwards 
healing with contraction of the ulcers 
and possibly considerable narrowing 
of the tube. 
Smallpox pustules in the oesoph- 
agus are very similar to those in the mouth, and, like them, they 
readily lose their epithelial covering and become converted into 
ulcers. They are accompanied by signs of inflammation of the 
mucous membrane generally. 
Perforating Ulcers of the (Esophagus.—A few cases have 
been observed of round ulcers in the lower part of the oesophagus 
similar to those which will be described as of common occurrence 
Fig. 241. 
Perforating ulcer in lower part of 
oesophagus. The ulcer penetrated the 
main bronchus of the left lung. 540 
DISEASES OF THE ALIMENTARY CANAL. 
iii the stomach. Fig;. 241 represents an nicer of this kind which 
perforated into the left main bronchus, causing gangrene of the 
lung on account of the food passing in. There have been cases 
also in which the ulcer has penetrated into the aorta. 
Tumors of the (Esophagus.—Simple tissue tumors are rare. We 
meet with lipomas and fibromas, and the author has described a 
case of myoma (Fig. 242) in which a 
tumor four and three-quarter inches long 
and two inches in thickness was attached 
by a comparatively narrow neck, and 
produced death by obstructing the tube. 
Polypoid tumors of a similar form are 
met with having a fibrous structure. 
Cancer of the oesophagus is by far the 
most important form of tumor met with. 
The cancer is nearly always in the form 
of flat-celled epithelioma, and in its his- 
tological details closety conforms to 
cancer of the lip. The masses of epi- 
thelial cells infiltrate the spaces in the 
underlying connective tissue, and the 
tumor also projects somewhat into the 
calibre of the tube. Here also there is 
a great tendency to ulceration, the me- 
chanical action of the food in swallowing 
doubtless contributing to this result. 
The tumor begins at a limited part of 
the mucous membrane, but it has a 
special tendency to extend round the 
tube in the form of a ring. There has 
been considerable discussion as to the 
most common situation of the tumor, 
and the result of the comparison of 
various statistics seems to be that the 
most frequent seat is the lower third. 
Scarcely less frequent than this is the 
middle third, and especially the place 
corresponding with the bifurcation of the treacliea. In the upper 
third epithelioma is comparatively infrequent. 
This form of tumor frequently leads to obstruction of the 
oesophagus, and it produces this result in more ways than one. On 
examining the oesophagus after death the seat of the tumor is often 
indicated externally by a narrowing of the tube, which is also more 
rigid here than elsewhere. The infiltration of the walls of the 
oesophagus, by irritating the connective tissue, causes a chronic 
inflammation with the usual new-formatiou of connective tissue, 
which contracts and narrows the tube. Besides this, the mere 
rigidity of the tube preventing its dilatation when the morsel is 
being swallowed, may produce during life a feeling of obstruction 
Fig. 242. 
Polypoid myoma of oesophagus 
in section, and semi-diagram- 
matie. The tumor was attached 
by a band-like pedicle a. It 
caused considerable distention of 
the oesophagus, and obstructed 
the tube. b cardiac orifice of 
stomach. Half the natural size. THE STOMACH — INTRODUCTORY. 
541 
at the point concerned. The projection of the tumor into the 
calibre is another element, which tells especially in the earlier 
periods. But as ulceration occurs, this projection of the tumor 
usually becomes inconsiderable, and there may even be a temporary 
relief to the stricture by partial destruction of the tumor. The 
ulceration itself, however, by inducing still further cicatricial con- 
traction, may ultimately confirm the obstruction. 
The tumor sometimes extends from the oesophagus to neigh- 
boring lymphatic glands, or to surrounding structures, and so we 
may have the trachea, bronchi, or lungs involved in it. Some- 
times it extends to the diaphragm, pericardium, vertebrae, etc. 
D.—THE STOMACH. 
Introductory.—In considering the diseases of the stomach, it is 
necessary to bear in mind certain points in regard to its structure 
and functions. The innumerable glands which exist in the 
mucous membrane are regularly engaged in the formation of the 
gastric juice for the purposes of digestion. The diseases of the 
stomach very readily interfere with the function of these glands, 
so that the secretion of gastric juice is insufficient in quantity or 
deteriorated in quality. In that case the food is apt to lie in the 
stomach undigested, and it very commonly undergoes various 
forms of decomposition. The products of decomposition acting 
on the mucous membrane still further interfere with the process 
of secretion, and by their irritative action keep up or induce a con- 
dition of catarrh of the stomach. Gases also develop in the process 
of decomposition, and these, by distending the organ, interfere 
with its proper peristaltic movements, and so hinder the passage 
of the food through the pylorus. 
But it is not merely local diseases, such as inflammations and 
tumors, which interfere with the secretion of the gastric juice. 
Changes characterized by cloudy swelling and fatty degeneration 
are met with in the glandular epithelium in numerous infective 
diseases, smallpox, typhus, septicaemia, as also in poisoning with 
phosphorus, etc. In these cases the secretion of the gastric juice 
may be almost at a standstill, and if food be introduced it is apt 
to lie in the stomach; by its mere presence, and by the action of 
the products of decomposition, it may produce still further struc- 
tural changes. 
The forms of decomposition which the food undergoes when it 
lies undigested in the stomach are various, hut the chief are those 
characterized by the development of acetic, lactic, and butyric 
acids. The agents in these changes are micro-organisms which 
are introduced in abundance with the food and propagate in the 
stomach, unless their multiplication is hindered by the action of 
the gastric juice. In the contents of the stomach, when at any 
time they are discharged during life, swarms of bacteria are found, 542 
DISEASES OF THE ALIMENTARY CANAL. 
and in addition there are nearly always proliferating spores of 
fungi and sometimes large numbers of sarcinse. 
It has been mentioned that the products of decomposition irritate 
the mucous membrane, but in addition to that the organisms have 
been found in some cases to enter the glands and mucous mem- 
brane. In cases observed the action of such organisms has- pro- 
duced little pustules in the mucous membrane, or even larger 
prominences with necrosis and ulceration. It may be inferred that 
it is organisms of a special kind or in a peculiar state of activity 
which thus penetrate into the mucous membrane. 
Stagnation of the food in the stomach and its decomposition 
will occur, as we have already mentioned, when anything interferes 
with proper digestion. But it will occur still more when by 
stricture of the pylorus there is a mechanical obstacle to the pass- 
age from the stomach. In such cases the gastric juice may be 
secreted nearly in the normal way, or it may not, and so according 
to circumstances there will be greater or less decomposition of the 
food. 
Besides the mere local effects induced by the products of decom- 
position, it is to be remembered that the mucous membrane of the 
stomach is actively engaged in absorption, and that these products 
may to some extent be taken into the blood. It is probable that 
much of the headache and other nervous symptoms occurring in 
dyspepsia is due to the existence in the blood of small quantities 
of these poisonous agents and their action on the nervous system. 
Some of these symptoms may be reflex, but to a certain extent 
they are more probably direct. 
When the food remains in the stomach and accumulates there, 
it is usually got rid of after a time by vomiting. This action is 
produced by irritation of a centre in the medulla oblongata, and 
the muscles emploj-ed are mainly those used in respiration, but in 
different combinations. The centre may be irritated directly, as 
by introducing apomorphia or tartar emetic into the blood, or by 
disease of the brain itself. But in the case we are considering it 
is irritated by reflex stimulation, the stimulation taking origin in 
centripetal fibres in the stomach itself. The occurrence of vomit- 
ing is dependent on the nature and amount of the irritation ap- 
plied, and on the sensitiveness of the centre in the individual. 
Post-mortem Changes.—After death any remains of food lying 
in the stomach are apt to decompose rapidly, especially as the 
gastric juice in most cases is not secreted in the normal way up to 
the period of death, and so the decomposition is not interfered 
with. The decomposing juices therefore act readily on the mucous 
membrane, and the decomposition may even extend to the latter. 
The principal changes produced are alterations in color, result- 
ing from chemical changes in the coloring matter of the blood. 
The coloring matter may become diffused out of the bloodvessels 
and stain the mucous membrane of a generally red hue, the color 
being specially pronounced in the neighborhood of the larger DILATATION AND HYPERTROPHY OF THE STOMACH. 
543 
vessels. There is often a greenish color developed by the decom- 
position of the blood. Lastly, the color may be almost black or 
slaty, hut in many cases this deep color is not altogether post- 
mortem, depending rather on a true pigmentation from chronic 
catarrh of the mucous membrane. 
Softening of the stomach is also a post-mortem change. It is 
really a digestion of the coats of the stomach by the gastric juice. 
As a rule, in persons near death the gastric juice is not secreted 
normally, but if the person die somewhat suddenly then there 
may be a considerable amount of active gastric juice in the 
stomach at the time of death. When the mucous membrane of 
the stomach dies, the gastric juice in such cases begins to digest it, 
and so a softening occurs which may extend beyond the mucous 
membrane. As already hinted, this condition occurs mostly in 
persons who die suddenly, especially if the body is kept in a warm 
place, and it is more frequent in children than in adults. In the 
slightest degree the mucous membrane alone is softened, and it 
can be removed from the surface of the muscular coat with the 
linger as a soft paste. Penetrating deeper, the muscular coat and 
even the serous coat may be half liquefied, so that on handling the 
stomach it may be perforated. The stomach may even rupture in 
the body, and the contents pass outwards producing softening in 
neighboring parts. In some cases the diaphragm has been softened 
in this way, and the stomach contents have passed partly into the 
pleural cavity. 
These changes, both the ordinary alterations from decomposition 
and the softening of the coats by digestion, occur in those parts of 
the stomach where the contents have been lying after death. 
This is generally the neighborhood of the fundus. As the contents 
are usually fluid, it is often seen that the changes stop short at a 
definite level and the unaltered mucous membrane rapidly emerges 
from the altered part. The pyloric portion of the stomach, as it 
usually lies highest, is least frequently affected, and this is im- 
portant, as that part of the stomach is the most frequent seat of 
disease. 
It will be understood that mail}7 of the pathological changes of 
the stomach will be obscured by the occurrence of these post- 
mortem changes. 
DILATATION AND HYPERTROPHY OP THE STOMACH. 
These conditions mostly result from obstruction to the passage 
of food through the pylorus from contraction of that orifice. It is 
also stated that sometimes a simple weakness of the muscular 
coat allows of passive distention. Obstruction of the pylorus 
causing an accumulation of the stomach contents leads in the first 
instance to a simple distention of the organ. The distention tells 
chiefly on the parts which are free to swell out. The lesser curva- 
ture is fixed by its attachments, and it usually retains nearly its 544 
DISEASES OF THE ALIMENTARY CANAL. 
normal position except that its middle part is somewhat dragged 
downwards (see Fig. 243). The greater curvature, on the other 
hand, is carried downwards, and the stomach may virtually till the 
entire abdomen, reaching as far as the symphysis pubis in some 
Fig. 243. 
Dilatation of the stomach, shown diagrainmatically. The stomach is shaded, a being 
cardiac, and b pyloric orifice. The greater curvature is much depressed, while the lesser 
curvature fixed at its two extremities forms a sharp curve, in the bend of which are visible 
the first loop of the jejunum (e), and the region of the pancreas (rf); f /, transverse colon 
depressed; in the midst of it the position of the umbilicus is indicated. (After Penzoldt.) 
cases. Sometimes the pylorus is depressed and the duodenum 
correspondingly displaced. 
It may he anticipated that when there is obstruction of the 
pylorus there will he an effort on the part of the muscular coat to 
overcome it, just as in the hypertrophy of the heart from obstruc- 
tion of the aortic orifice, or the similar hypertrophy of the urinary 
bladder. But the muscular coat of the stomach has a somewhat 
different function to that of the heart or bladder. In the latter 
there is a simultaneous contraction of the entire muscle with a 
view to the emptying of the viscus. In the stomach, however, the 
contraction is vermicular, and its object is as much to move the 
contents about inside the stomach as to empty them into the 
duodenum. In the actual propulsion of the contents into the 
duodenum it is the pyloric portion of the stomach that is engaged, 
and here also the material is carried forward by a vermicular move- 
ment. Hence the hypertrophy of the muscular coat in obstruction 
of the pylorus does not occur uniformly in the stomach, but INFLAMMATIONS OF THE STOMACH — GASTRITIS. 
545 
localizes itself in the pyloric portion, sometimes even with a special 
thickening just at the orifice, forming a tight sphincter. In these 
cases, when the wall of the stomach is divided the progressive 
thickening of the rigid muscular coat can often be distinguished 
as the pylorus is approached. Along with hypertrophy of the 
muscle there is very often thickening of the connective tissue in 
the mucous membrane and submucous tissue, as well as of that 
between the muscular bundles. 
INFLAMMATIONS OF THE STOMACH.—GASTRITIS. 
Acute inflammations may be produced by tlie action of irritant 
poisons which have been swallowed, the inflammation here being- 
accompanied by sloughing. Acute spontaneous inflammation is 
rare except in the milder forms which constitute catarrh, and we 
have very rarely, in the stomach, conditions comparable with the 
phlegmonous angina of the fauces, or the dysenteric inflammation 
of the intestine. Such phlegmonous inflammations are met with 
occasionally in severe infective diseases, and particularly in puer- 
peral fever. There is great swelling and redness of the mucous 
membrane, terminating in a diffuse purulent infiltration of the 
wall of the stomach. Sometimes abscesses have been formed in 
the wall of the stomach which have burst into its cavity. 
Catarrh of the Stomach, on the other hand, is a condition of 
very frequent occurrence, and is met with in the acute and chronic 
forms. 
Acute Catarrh. — This is induced for the most part by the 
direct action of irritants on the mucous membrane, mainly by the 
use of irritating foods or drinks. We have already seen that, 
when food remains in the stomach undigested, it undergoes de- 
composition, and the irritating products may induce an acute 
catarrh. The mere prolonged stay of food in the stomach prob- 
ably induces it, as when by exposure to cold the secretion of the 
gastric juice and the peristaltic action necessary to the process of 
digestion are interfered with. 
It is seldom that the stomach can be examined after death in 
this condition, but from observations of Beaumont on his patient 
with a gastric fistula, as well as from experiments on animals, the 
appearances of the mucous membrane have been tolerably well 
made out. There is intense redness with swelling of the mucous 
membrane, which is covered by a layer of mucus or muco-pus, 
sometimes slightly mixed with blood. The appearances are most 
marked towards the pylorus, and sometimes confined to that 
region. 
Under the microscope the bloodvessels in the mucous mem- 
brane, and especially in the submucous tissue, are found enor- 
mously distended, and the epithelial cells, both those of the surface 
and of the glands, enlarged and granular. 546 
DISEASES OF THE ALIMENTARY CANAL. 
Chronic Catarrh.—This often remains after one or more attacks 
of the acute form. It is also present in cases of passive hypercemia 
of the stomach, which so frequently occurs in consequence of dis- 
ease of the heart and liver. Cancer of the stomach is also accom- 
panied by chronic catarrh in most cases. 
If the catarrh is prolonged, there usually occurs a considerable 
new-formation of connective tissue, as in other chronic inflamma- 
tions. There is thus a thickening which affects mucosa, sub- 
mucosa, and muscular coat, and causes the surface of the mucous 
membrane to assume an irregularly folded or warty appearance, 
which has given rise to the designation etat mamelonne. The 
mucous membrane also presents, in many cases, dark spots or a 
general deep color from the presence of pigment granules in the 
tissue. The pigment is derived from the blood, and indicates the 
occurrence of hemorrhages, probably by diapedesis. The increase 
of the connective tissue produces atrophy of the glands, which are 
also considerably distorted. 
It sometimes happens that the increase of connective tissue is 
specially great, and the wall of the stomach may be converted 
into a thick, hard, resistant structure. As all these processes occur 
mainly in the pyloric portion of the stomach, considerable narrow- 
ing of the orifice may result. The rigidity of the wall and the 
narrowing of the orifice induce more forcible muscular contrac- 
tions, and the muscular coat therefore hypertrophies. In the 
interstitial tissue of the muscular coat there is also thickening, 
and the fleshy muscular bundles are separated by trabeculae of 
connective tissue. The resulting appearance is often very charac- 
teristic, the hypertrophied connective tissue dividing the hyper- 
trophied muscular bundles into divisions, which on section are 
somewhat like the pieces of a fan. This thickened and indurated 
condition may closely resemble scirrlius of the stomach, especially 
as a similar' appearance is presented by the muscular coat in that 
disease. 
Occasionally mucous polypi develop in connection with chronic 
catarrh, and these may develop into mucous cysts. 
THE SIMPLE PERFORATING ULCER. 
This peculiar form of ulcer is met with only in the stomach, 
first part of the duodenum, and lower part of oesophagus. It is 
also called sometimes the round and the chronic ulcer. It is 
clear from the localities in which it occurs that its peculiarities are 
due to the action of the gastric juice, but the more detailed con- 
sideration of its mode of origin will be better taken up after the 
appearances of the ulcer have been described. 
The ulcer is usually round or oval in shape, and presents the 
appearance as if a conical piece of the wall of the stomach had 
been punched out from within, its edges being perfectly defined 
without any considerable thickening of the neighboring mucous THE SIMPLE PERFORATING ULCER. 
547 
membrane, and the floor of the ulcer perfectly clean (see Fig. 242, 
in which an ulcer of the oesophagus having all the characters of 
that of the stomach is represented). The superficial extent and 
depth of the ulcer vary considerably. The commonest size is 
about that of a shilling, but this may be exceeded considerably, 
and Cruveilhier has described an ulcer which was 6J inches long 
and 3J inches broad. In the smaller ulcers the floor is formed of 
the coats of the stomach, probably with some new-formed con- 
nective tissue. In the larger and deeper ones the tissue of neigh- 
boring organs may be exposed, such as the pancreas or liver. 
The floor of the ulcer does not present any of the usual appear- 
ances of a granulating wound, but is clean and smooth, the actual 
tissue of the part being exposed, perhaps with some induration 
from new formation of connective tissue. 
The situation of the ulcer is mostly in the neighborhood of the 
lesser curvature, and nearer the pyloric than the cardiac orifice. 
It is more frequent on the posterior than the anterior wall. It is 
not uncommon to find more than one ulcer present in the same 
case. Though the ulcer is much more common in the stomach, 
yet the duodenal situation has been observed in a considerable 
number of cases, the oesophagus being, however, exceedingly rare. 
The ulcer in these situations has exactly the same characters as 
that in the stomach. 
The ulcer presents a tendency to penetrate more and more 
deeply, from which circumstance it is named the perforating 
ulcer. It does not appear to extend laterally to any considerable 
degree; it is probable that at the very first the ulcer assumes its 
full superficial dimensions. Eating into the wall of the stomach, 
it may penetrate through the entire coats, and sundry accidents 
are liable to ensue. 
One of the commonest of these accidents is hemorrhage. The 
ulcer penetrates one or more vessels at its base. The vessels may 
be small and the hemorrhage not very considerable, but sometimes 
a considerable artery is laid open, and a serious, even a fatal, 
hemorrhage results. From the commoner situations of the ulcers 
the arteries most frequently penetrated are these—the coronary 
artery or one of its branches, the gastro-epiploic, the pancreatic, 
and the splenic. Sometimes the open mouth of the vessel can be 
seen after death in the floor of the ulcer. 
Perforation is another result of the penetration of the ulcer, 
but a much less frequent one than hemorrhage. For the most 
part, by the time the ulcer has eaten through the wall of the 
stomach, the latter has already acquired adhesion to some neigh- 
boring structure, and so actual rupture of the stomach and escape 
of its contents into the peritoneal cavity is not common. The 
adhesion may be to the liver or pancreas, or, more rarely, to the 
spleen, diaphragm, colon, abdominal wall. By the extension of 
the ulcer, these structures may be eaten into and their tissue 
exposed. The tissue when first exposed has its normal appear- 
ance, but it usually becomes condensed and cicatricial. Some- 548 
diseases of tile alimentary canal. 
times the irritation of the gastric juice produces suppuration and 
the formation of abscess, especially in the case of penetration into 
the liver. But if adhesion does not occur, then the ulcer is likely 
to cause rupture of the stomach. This will happen most readily 
where the wall of the stomach is most liable to shift about during 
the regular peristaltic movements, and also where there is no solid 
viscus to which it may readily adhere. Both these conditions are 
fulfilled in the case of ulcers of the anterior wall, and so it hap- 
pens that rupture most frequently occurs in this situation. The 
ulcers which lead to perforation are frequently very small, and the 
aperture in the serous coat may be as large as the ulcer itself. The 
result of the perforation is acute and fatal peritonitis. 
Healing of the perforating ulcer is by no means an unusual 
occurrence. In the experiments to he referred to presently, in 
which ulcers were produced artificially in animals, they healed 
very readily. In man, also, they are frequently recovered from, 
and we often meet with cicatrices in the stomach. They may 
indeed heal without leaving a very obvious cicatrix at all. The 
author met with a case in which three weeks after a very severe 
hemorrhage, presumably from an ulcer of the stomach, only an 
obscure cicatrix could he found. 
We have now to consider the mode of origin of these ulcers, 
and this is a matter of some difficulty. It is obvious from the 
shape and appearance of the ulcer that it has arisen by the necrosis 
and subsequent digestion of a piece of the wall of the stomach. 
The question arises as to the cause of the necrosis. The funnel- 
shaped outline of the ulcer suggested to Virchow that the necrosis 
occurred by obstruction of or interference with an arterial branch, 
and he observed as confirmatory of this that the ulcers most fre- 
quently had their seat at the point of entrance of arterial branches 
into the wall of the stomach. 
The experiments of Panum and Cohnheim confirm this view in 
so far as they show that ulcers may be produced by embolism of 
the arteries of the stomach. In ColmheinTs experiments, if the 
animals were killed a day or two after embolism had been pro- 
duced there wTere found large ulcers with abrupt edges and perfectly 
clean floors. The difficulty of the case is, however, that the per- 
forating ulcer is not met with specially in cases of embolism or 
thrombosis of the arteries of the stomach, but in the immense 
majority of instances in cases where no such disturbance of the 
circulation exists. It has been suggested again that a venous 
hyperemia, by causing stagnation and even hemorrhage (see after- 
wards) in defined areas of the mucous membrane, may produce 
such weakening of the tissue as to induce necrosis and digestion 
of it. 
In most cases of gastric ulcer there is serious and usually 
prolonged dyspepsia, and the persons are frequently anaemic. This 
seems to indicate that the condition of the gastric juice has an 
important relation to the gastric ulcer. It is also important in this HEMORRHAGE FROM THE STOMACH. 
549 
connection that, while ordinary ulcers of the stomach such as are 
produced by wounds or the action of caustics, or by such experi- 
ments as those already referred to, heal readily, this form of ulcer 
is peculiarly chronic and shows a tendency rather to extend deeply 
than to heal. Some abnormal condition of the gastric juice by 
virtue of which it is peculiarly irritating to the mucous membrane 
seems to be the essential factor, while a weakened condition of the 
mucous membrane is also of consequence. In most cases the gas- 
tric juice is abnormally acid, and it has been thought that by 
neutralizing the natural alkalinity of the tissues it may lead to their 
necrosis. 
On the whole it seems probable that an acrid gastric juice, 
taking advantage of any accidental stagnation in a defined area of 
the mucous membrane, may lead to its necrosis and the formation 
of the ulcer. 
It has been already stated that while ordinary ulcers heal readily 
this form is peculiarly persistent. But if the condition of the 
gastric juice be improved, and especially if its excessive acidity be 
corrected while solid food is prevented acting on the surface of the 
ulcer, the ulcer often heals readily, leaving a cicatrix which is 
sometimes very obscure, but may be more distinct and with some 
puckering. 
The frequency of ulcer of the stomach may be judged from the 
fact that according to the results of post-mortem examinations it 
is said that there are ulcers or cicatrices in about one in twenty of 
the cases examined after death. 
HEMORRHAGE FROM THE STOMACH. 
Besides the hemorrhage which occasionally supervenes in the 
case of the perforating ulcer, and that which is occasionally a 
feature in cancer of the stomach, we have certain other forms which 
call for notice here. 
The vessels are apt to rupture when the pressure of the blood in 
them is considerably raised above the normal. This will occur 
especially with disturbances of the vascular system involving 
hypenemia of the portal system. In diseases of the heart leading 
to general venous engorgement, we have passive congestion of the 
liver reflected to the portal vein. In this case there are signs of 
general venous engorgement probably including dropsy of the 
limbs, etc. But disease of the liver itself, especially cirrhosis and 
cancer, may cause obstruction to the portal circulation. In these 
cases there is a general engorgement of the portal vessels, and 
hemorrhage from the stomach frequently occurs. 
The blood mostly escapes from the superficial vessels of the 
mucous membrane, which are least supported, and it passes into 
the cavity of the stomach. In some cases it is from a large 
number of small superficial vessels, and the exact source is not 550 
DISEASES OF THE ALIMENTARY CANAL. 
apparent. At other times the blood passes to some extent into the 
superficial layers of the mucous membrane, infiltrating it. The 
mucous membrane infiltrated with blood is acted on by the gastric 
juice and digested by it, so that small flat superficial ulcers are 
formed, the so-called hemorrhagic erosions. These are generally 
present in considerable numbers, chiefly in the pyloric region. In 
the erosions there may be still some remains of blackened blood, 
and alongside them there are little areas of mucous membrane 
infiltrated with blood. In these cases also the mucous membrane 
is often generally red from the passive hyperaemia, and possibly 
thickened by catarrh. 
The blood is generally mixed with the contents of the stomach, 
and blackened by the gastric juice. If the hemorrhage be very 
severe, as from an ulcer perforating a considerable artery, the 
blood may be vomited nearly in the fresh state, but usually it is 
tarry or like coffee-grounds. The altered blood may also pass into 
the duodenum and onwards. 
TUMORS OF THE STOMACH. 
Cancer.—This is the only form of tumor which is of much prac- 
tical importance, and it is of exceedingly frequent occurrence. 
From the statistics of a considerable number of observers it ap- 
pears that cancer occurs more frequently in the stomach than in 
any other situation in the body, the uterus being the next most 
frequent site. 
The great frequency of cancer in the stomach is probably re- 
lated to the fact that the epithelial structures of this organ are 
more exposed to various irritations than those of any other part of 
the body. Not only are there varieties of irritating foods, but the 
foods are liable, as we have seen, to decomposition, the products 
of which produce irritation. In cases of cancer there is very com- 
monly a history of prolonged dyspepsia, perhaps from youth. 
In this regard the simple ulcer may be again referred to. There 
have been cases observed in which cancer seemed to originate in 
the simple ulcer; but the simple ulcer is a disease mostly of youth, 
whereas cancer is a disease of middle life, the average age being 
fifty years. It is almost as if similar causes produced the simple 
ulcer in youth, and cancer in middle life. 
In its structure cancer of the stomach is like cancer elsewhere. 
There are epithelial masses which tend to insinuate themselves 
among the neighboring tissue elements, and there is a connective- 
tissue stroma. The epithelial elements also originate in the ex- 
isting epithelium, chiefly that of the glands. But in the mode of 
growth of the epithelium and its relation to the stroma there are 
considerable differences presented, and although not rigidly to be 
distinguished from each other it is possible to divide the cases into 
four forms. cancer of the stomach. 
551 
Ill epithelial cancer there is a tolerably definite gland-like 
new-formation, as we have in other cases of cylinder-celled epithe- 
lioma. There are ducts and acini lined with cylindrical epithelium, 
but very often this regular arrangement is lost in great part, and,' 
except in the more recently formed part, we have more irregular 
masses. The glandular structures are limited by a distinct stroma, 
which is well formed. As in all cancers of the stomach, the new 
formation of epithelium begins in the glands, and at first the tumor 
grows in the mucous membrane. But the growth extends into the 
submucous tissue, and insinuates itself among the other coats of the 
stomach, passing into the muscular coat, and even outside it into 
the serous coat. From the glandular character of the tissue in 
this tumor it is sometimes called adenoma. 
The tumor is a slowly growing one, and it generally involves a 
considerable portion of the stomach before the death of the patient. 
It usually begins in the pyloric region, frequently forming a ring 
around the stomach, but it extends inwards from this, it may be 
for some distance. The surface is nearly always ulcerated, and 
may be considerably excavated. There are sometimes papillae on 
the surface of the tumor, especially at the marginal parts, which 
give the surface a warty appearance. The advancing tumor infil- 
trates and thickens the mucous membrane and the subjacent coats, 
and so while the greater part of the tumor may be rough and 
warty and somewhat excavated, the edges are usually prominent, 
and sometimes rather abrupt. 
The epithelioma of the stomach is not a very frequent form of 
tumor, and it does not so readily extend beyond the neighboring 
lymphatic glands to the liver as the next form. 
Medullary or Soft Cancer of the stomach is probably the most 
frequent of all forms of tumor. In it the epithelial growth does 
not arrange itself in proper glandular structures, but there are 
large masses of comparatively loose epithelium in a sparse and 
delicate stroma. Hence the tissue is very soft. The epithelial 
masses tend to infiltrate the subjacent structures as well as to ex- 
tend laterally. 
The tumor is usually seated near the pylorus, forming, in some 
cases, a ring or a defined circular tumor. The tissue being soft it 
is specially liable to bleed and to ulcerate. The latter condition 
is so frequent and characteristic that the tumor often presents 
itself as a round, shaggy ulcer with prominent edges. Doubtless 
the gastric juice and the food acting on the surface of the tumor 
break down its tissue and lead to the ulceration. At the margins 
the cancer is infiltrating the mucous membrane, and so the edges 
are raised and somewhat abrupt. 
This form of tumor is exceedingly malignant, the soft and loose 
cancerous elements readily finding their way into the lymphatic 
channels. Hence cancerous formations in the lymphatic glands 
around the stomach and in the other glands of the abdomen are 
very frequent. The liver also is very often the seat of numerous 552 
DISEASES OF THE ALIMENTARY CANAL. 
and large cancerous tumors, and a large proportion of the cases 
which clinically have the characters of cancer of the liver are 
primarily cases of this disease. The enormous secondary growths 
in the liver may contrast very markedly with the insignificant 
primary lesion, sometimes little more than a comparatively small 
round ulcer with irregular surface and prominent margins. 
The tendency to bleed which this tumor presents is to be borne in 
mind. The bleeding may be slight but frequent, and the blood 
carried off into the intestines. Or it may be more considerable, 
and even fatal. 
Scirrhus is a somewhat frequent form of cancer of the stomach. 
Here, the new formation of epithelial cells is not very rapid or 
vigorous, and it is accompanied by an excessive formation of con- 
nective tissue in the form of stroma. Originating in the glandular 
epithelium, long processes composed of rows of cells, often with 
few abreast, are produced, and they grow not only into the mucous 
membrane, but also into the muscular coat separating its trabeculae, 
and even into the peritoneal coat. These processes seem to be 
peculiarly irritating, as they give rise to the production of dense 
connective tissue which is much more manifest than the proper 
epithelial elements. These elements may, in fact, degenerate, and 
leave little besides condensed hard connective tissue. 
The cancer mostly begins in the pyloric region, but extends 
inwards till, in some cases, it has involved the entire wall of the 
stomach, except the fundus. The wall of the stomach is con- 
verted into a stiff hard mass which may be, in some places, an inch 
in thickness. This dense structure has replaced the mucous mem- 
brane, and, to a certain extent, the other coats which, however, are 
usually separately distinguishable. The muscular coat is much 
hypertrophied by the new formation both of muscle and of hard 
connective tissue, and a section of it presents the peculiar fan-like 
appearance already mentioned. The surface of the affected por- 
tion of the stomach is irregular, with rounded prominences, and 
there are sometimes ulcers present, but there is not a general 
ulceration as in the case of the epithelial and medullary forms. 
The stomach is often greatly contracted in this disease. The edges 
of the cancerous portion are not well defined, but shade off 
gradually into the normal mucous membrane. 
Extension of the cancer to the liver does not readily occur, 
although neighboring lymphatic glands may be involved. 
Colloid Cancer is not a frequent form as compared with the 
medullary, but is met with in a considerable number of cases. 
The other forms and especially the epithelioma, occasionally 
undergo a partial colloid degeneration. In the colloid form as in 
the others the epithelial elements take origin in the glandular cells, 
and after infiltrating the mucous membrane these epithelial masses 
insinuate themselves among the muscular trabeculae (Fig. 102, p. 
220), and even into the serous coat. The stroma consists of a CAXCER OF THE STOMACH. 
553 
somewhat abundant well-developed network of connective tissue. 
The peculiarity of this form is that the cells have a special tendency 
to undergo colloid metamorphosis. They seem from their first 
formation to present a regular intention in this direction, and even 
in the more recent parts there is often already a considerable 
advance in the degeneration. The outlines of the cells disappear 
as the protoplasm becomes transformed into colloid material, and 
as the nuclei resist the degeneration longer, we sometimes see the 
peculiar appearance of oval nuclei as if floating in a clear trans- 
parent material. Finally, the whole epithelial elements are 
converted into colloid material, and the structure presented is a 
beautiful reticulated network with spaces filled with a transparent 
colorless jelly (Fig. 101, p. 220). 
As the colloid material occupies more space than the original 
cells, the spaces of the alveoli are, as it were, tightly packed with 
the jelly, and the fibres of the stroma rendered tense and rigid. 
Hence, it happens that although the structure is composed mainly 
of a soft jelly, yet it is to the feeling hard and rigid, just as a 
tensely filled bladder may be. 
The tumor, like other cancers, usually begins towards the 
pyloris, but it extends gradually till it comes to involve a large 
area, sometimes even as much as three-fourths of the entire extent 
of the viscus. The wall of the stomach is converted into a trans- 
parent glancing tissue, and in the more advanced parts it is 
impossible any longer to distinguish the different coats, all being 
homogeneously replaced by the cancerous tissue. The wall of the 
stomach is considerably thickened, and the internal surface may 
present an irregular aspect with prominences; but there is little 
tendency to ulceration. As the thickened wall is tense and hard, 
the stomach when cut into does not generally collapse but keeps 
its shape. There is no tendency to contraction of the stomach as 
in scirrhus, but, on the contrary, the organ may be considerably 
enlarged. 
This form has a very marked tendency to extend continuously 
both along the stomach, and also through the stomach to the 
peritoneum. Hence it produces secondary tumors in the perito- 
neum itself much more readily than in the lymphatic glands and 
liver. 
It will appear from what has been mentioned above that cancers 
Of the stomach frequently lead to the formation of secondary 
tumors elsewhere. In this respect the cancers of the intestine 
resemble those of the stomach, and as the modes of extension 
present certain points of interest and practical importance, a special 
section will afterwards be devoted to this subject in general. 
The remaining tumors of the stomach are of trivial consequence. 
We have already seen that mucous polypi and cysts occur in 
chronic catarrh. Lipomas and myomas have been met with, as 
also fibromas and sarcomas, but they are very rare. 554 
DISEASES OF THE ALIMENTARY CANAL. 
E.—THE INTESTINES. 
Introductory.—The diseases of the intestines resemble in many 
respects those of the stomach, hut there are important differences. 
In structure, the intestine differs from the stomach in several 
respects. We no longer have the specific glands peculiar to the 
stomach, but, on the other hand, the intestine presents numerous 
closed lymphatic follicles in its mucous membrane, and these are 
only present to a very slight extent in the stomach. These 
lymphatic follicles are solitary or collected into groups, in the 
latter case forming the well-known Beyer’s patches. 
Of considerable importance in regard to the diseases of the 
intestine are the time which the intestinal contents stay in the 
different parts of the canal, and the changes they undergo there. 
After leaving the stomach, the food appears to pass rapidly through 
the upper part of the small intestine, occupying on an average from 
two and a half to three hours in doing so, and it is at the same time 
rendered alkaline and partially protected from further decomposi- 
tion by the pancreatic fluid and the bile. 
The movement of the intestinal contents is effected by the peri- 
staltic contraction of the bowel, and the rapid passage of the con- 
tents through the small intestine indicates that here the peristalsis 
is peculiarly active, whereas, in the large intestine, it is slow. 
When the feces reach the large intestine they are still fluid, and 
the chief function of the colon seems to be to complete the absorp- 
tion of the fluid, and allow the feces to become thicker. But if 
the peristaltic action of the large intestine be increased, then there 
will be no time for the feces to become thick, and fluid evacuations 
will be the result. This will be still more the case should the 
movement of the small intestine be increased, and the contents 
carried even more quickly than usual through them. 
It will be seen that diarrhoea results from increased peristaltic 
movement, and that the evacuations will be more fluid the higher 
up the increased movement begins. It is well known that certain 
medicinal agents produce fluid motions, and these seem all to act 
by increasing the peristalsis, their relative vigor depending greatly 
on the part of the intestine at which they begin to produce their 
effects. Irritating articles of food produce a like increase of the 
peristalsis and diarrhoea, and so may ulcers and inflammations of 
the intestine itself. 
In the stools of diarrhoea we may expect to find chemical con- 
stituents which normally are present in higher parts of the intes- 
tine, but absorbed before reaching the rectum. If the diarrhoea 
arises from increased peristalsis of the colon, then we shall find 
material which is normal in the csecum, such as undecomposed 
bile, leucin, chloride of sodium, peptones, and sugar, some of 
which are present in appreciable quantity in normal feces. But 
if the diarrhoea has involved the small intestine, then we shall MALFORMATIONS OF THE INTESTINE. 
555 
find these constituents much more abundantly, and also remains 
of undigested food. 
We have already seen in the case of the stomach that many of 
its diseases are connected with the fact that the food stagnates and 
decomposes in that viscus. It will be seen from what has gone 
before that the intestinal contents stagnate chiefly in the large 
intestine, and next to that in the lower part of the small intestine. 
It is probably due to this that we find the jejunum peculiarly free 
from all forms of disease; in this, respect it contrasts with the 
lower part of the small intestine, the ileum, but still more with 
the large intestine. Hence it is that the diseases of the large 
intestine resemble those of the stomach much more than those of 
the small intestine do. This is especially true in regard to simple 
inflammations, which very often concentrate themselves in those 
parts where the intestinal contents most readily stagnate, namely, 
the ceecum and the rectum. It is true also of cancer, which is 
very rare in the small intestine hut common in the large, especially 
in the caecum and rectum. 
It is to he remembered, further, that the intestine is a compara- 
tively narrow tube, and is subject to obstruction in various ways. 
Post-mortem Changes.—These are not so important as those of 
the stomach. After death the blood is apt to gravitate towards 
the more dependent parts of the wall of the intestine, and the 
coloring matter being dissolved out and staining the mucous 
membrane, it may give rise to a deceptive appearance of inflam- 
mation. Similarly the intestine may be stained with the biliary 
coloring matter in the neighborhood of the gall-bladder. 
MALFORMATIONS OF THE INTESTINE. 
Congenital malformations of tlie intestine are of considerable 
frequency. The most important are those in which, from a fault 
of development, a part of the intestine is wanting. The colon or 
the rectum may be entirely absent at birth, being represented by 
a solid cord; or the rectum may be partially occluded, in some 
cases in its middle part, in others at its lower extremity. All 
these cases present the characters of imperforate anus, but of 
course in view of possible surgical interference their gravity varies, 
ths most hopeful being those in which only the extreme lower part 
of the rectum is defective, and the gut is separated from the anus 
only by a membrane. 
There occur also narrowness and defect of the small intestine, 
especially in the duodenum and lower end of the ileum. The 
whole intestine is sometimes deficient in length, having something 
like the form of the letter S instead of the usual convolutions. In 
such cases the absorption and digestion of food must be defective, 
but the persons may live on to old age. 556 
DISEASES OF THE ALIMENTARY CANAL. 
The commonest malformation is Meckel’s diverticulum. This 
consists in a finger-like projection from the intestine. It occurs 
in the ileum, about three or four feet above the ileo-csecal valve in 
the adult, and about a foot above it in the new-born; it projects 
from the free convex border of the gut. It is from one to six 
inches long, possessing the same structure as the intestine, and 
communicates with the latter: it is narrower in its calibre, being 
of a diameter rather more than that of the linger. The diver- 
ticulum arises by the imperfect closure of the omphalo-mesenteric 
duct, and sometimes it is united to the umbilicus by a cord. Very 
rarely the diverticulum is continued to the umbilicus, and opens 
there by a fistula at the surface. 
HERNIA OR RUPTURE. 
True hernia consists in a protrusion of the intestine, omentum, 
or other abdominal organ into a sac formed by a prolongation of 
the peritoneum. The sac may project externally, or it may be 
contained within the abdomen, and so we may distinguish ex- 
ternal and internal hernias. The hernias, especially the ex- 
ternal ones, are of so much importance in a surgical point of view 
that full descriptions are given in the surgical text-books, and 
need not be repeated here, except in outline. 
For the most part the sac is an entirely abnormal projection of 
the peritoneum, and seems to be protruded before the contents. 
An exception to this occurs in the case of congenital inguinal 
hernia, in which the sac is formed by the persistence of a foetal 
condition. There is a partial exception also in the case of most 
internal hernias, where the sac usually arises by the exaggeration 
of an existing normal pouch. 
In the production of hernias, we have to account for the ab- 
normal protrusion of the viscera. This is usually due to the 
abdominal contents being subjected to undue pressure. In severe 
muscular efforts, such as are involved in lifting heavy weights, the 
glottis is closed, and the muscles of expiration fix the chest and 
abdomen, the contents of the abdomen being subjected to severe 
pressure by the contraction of the muscles of the abdominal wall. 
If there is any part of the wall which is unduly weak a bulging 
outwards may occur here, and so give the starting-point for the 
hernial protrusion. In this connection the greater frequency of 
hernia on the right side may be noted. In violent exertions the 
right arm is usually more used than the left, and as the chest is 
bent over to the left side to counterbalance the strain on the right, 
the lower surface of the diaphragm faces more to the right and 
presses the viscera towards that side. It is clear that straining at 
stool or otherwise will also increase the pressure on the abdominal 
contents, and any excess will predispose to hernia. 
It has been said that the protrusion takes place where there is 
any weakness of the abdominal wall, and it is well known that the hernia or rupture. 
557 
external hernias occur at specially unsupported parts of the wall, 
while the internal ones have usually a pouch ready made as a 
starting-point. The abdominal wall from its anatomical conforma- 
tion is weak at certain points in every person, hut there may be 
congenitally a special weakness, which in some cases seems to be 
hereditary. Or the weakness may be induced by stretching of the 
abdominal parietes by increase in their contents (ascites, tumors, 
pregnancy, etc.), or more directly by injury to a particular part. 
In protruding, the viscera nearly always push the peritoneum 
before them, and the proper sac is formed by the peritoneum, 
which shows a remarkable power of stretching. But there are 
cases of protrusion in which the aperture has been produced by 
actual rupture of the wall, and in these cases the hernia may be 
devoid of a proper sac. These cases, however, of what may be 
called false hernia, are exceedingly rare, as an injury, although 
tearing the muscular wall and other tissues, will very often leave 
the elastic peritoneum uninjured and capable of protrusion. 
The hernial sac acquires for the most part adhesion to the 
structures among which it is protruded, and it does so by a chronic 
inflammation. It very often happens also that the contents of the 
sac become adherent to its internal surface by inflammation, and 
in that case the hernia is irreducible. 
It is not necessary to enter fully into the individual forms of 
hernia, and of the external ones little more than an enumeration 
will suffice. 
The external hernias are, (1) Inguinal hernia in the congenital 
and acquired forms, or, as otherwise divided, direct and oblique. 
(2) Femoral hernia. These two are by far the commonest forms. 
Of comparatively rare occurrence are, (3) Hernia of the sciatic 
notch; (4) Perineal hernia, protruded between the fibres of the 
levator ani; (5) Vaginal hernia; (6) Hernia of the foramen ovale; 
(7) Umbilical hernia which is congenital or acquired, in the former 
case arising by protrusion into the dilated umbilical cord; (8) Ab- 
dominal hernia occurring in various parts of the abdomen, chiefly 
towards the edges of muscles, and arising by tearing of tendons 
or muscular fibres, hence, frequently, traumatic. Its commonest 
situation is near the linea alba. 
Internal hernia comes less frequently into sight, and the possi- 
bility of its existence is apt to be forgotten. 
(1) Diaphragmatic hernia is perhaps the commonest. There is 
a congenital form in which a sac is protruded through one of the 
normal apertures, or through a part of the diaphragm which by 
reason of defective development has given way. The protrusion 
is into the chest, and the sac may contain intestine, spleen, liver, 
stomach. There is also an acquired form, due nearly always to 
some injury to the diaphragm, and the hernia is frequently devoid 
of a proper peritoneal sac. From a case recorded by Dr. Adams, 558 
diseases of the alimentary canal. 
it appears that a tumor growing against the diaphragm (in his case 
from the capsule of the spleen) may so weaken it as to lead to her- 
nial protrusion. In diaphragmatic hernias from rupture, a large 
portion of the abdominal viscera may be protruded. 
(2) Retroperitoneal hernia includes cases in which the intes' 
tine passes into a preexisting pouch in the peritoneum, greatly 
enlarging and filling it. The hernial sac hence lies behind the 
peritoneum of which it is an offset. There are three pouches in 
the peritoneum which are capable of giving rise to such hernias. 
The JEJUNO-DUODENAL pouch is the most important. It exists 
just where the jejunum arises from the duodenum, and lies be- 
tween the last part of the duodenum, which bounds it on the right, 
and the aorta, which bounds it on the left. The pouch was present, 
according to Waldeyer, in about 70 per cent, of the bodies which 
he has examined, and is generally large enough to admit the 
terminal phalanx of the thumb. It is best seen when the jejunum 
and small intestine generally are raised and carried to the right, so 
that the origin of the mesentery may be exposed. The little pouch, 
if present, is then seen lying in the posterior wall of the abdomen 
with sharp sickle-like margins. Sometimes a fold of the jejunum 
passes into this pouch, constituting a hernia. The pouch may be 
greatly enlarged by the protrusion of further portions of the in- 
testine into it, and cases have been recorded in which the entire 
intestine has passed into the greatly distended sac. 
Another pouch of the peritoneum is the sub-cjecal, which has 
its seat between the folds of the meso-colon ascendens. Into this 
pouch the intestine is very rarely protruded, and the pouch itself 
only occurred in about 30 per cent, of the bodies examined by 
Waldeyer. 
The fossa intersigmoidea is a pouch in the mesentery, lying 
between the two folds near the beginning of the sigmoid flexure. 
The aperture is in the underlayer. This is the commonest of these 
pouches, occurring in about 80 per cent, of the bodies, but from its 
position it does not appear ever to become the seat of hernia. 
The contents of hernias are usually the intestine, and, for the 
most part, the more movable small intestine. Sometimes also the 
great omentum is carried into the sac. The large intestine pos- 
sesses for the most part no free mesentery, being only partially 
covered with peritoneum, so that it is hardly possible for it to pass 
into a sac unless it be dragged down with considerable force. 
The method of descent of the large intestine merits a more 
special notice. The process may in some respects be compared to 
the descent of the testis in the foetus. Before its descent the testis 
is only partially covered with peritoneum, being free of it at its 
posterior aspect. As it descends it remains with only a partial 
peritoneal covering, and even in the tunica vaginalis, after the sac 
has separated from the general peritoneum, the testis lies behind 
with its posterior aspect free of peritoneum. And so in a hernial 
sac, the csecum may be carried down, but in its new position it HERNIA OR RUPTURE. 
559 
remains only partially covered with peritoneum, and really forms 
as it were a part of the wall of the sac. This will only occur in 
very large hernias as a rule, hut when it does occur the piece of 
intestine will he irreducible. 
A still more peculiar condition sometimes occurs. The intestine 
may be protruded mainly at the part where it is uncovered by peri- 
toneum, and instead of pushing a peritoneal sac before it, it may 
as it were drag it after. As the gut is protruded it may even get 
more and more stripped of peritoneum, so that the hernia may be 
much more extensive than the sac. This, however, is an exceed- 
ingly exceptional occurrence, and it is more common to find that 
as an ordinary hernia advances it drags the colon into it, so that 
besides free loops of small intestine there may he, fixed in the wall 
and only partly covered by peritoneum, a piece of the caecum, or 
the sigmoid flexure, or even the fundus of the bladder. 
In a similar fashion to that just described, the ovary may be 
protruded. A large majority of cases of ovarian hernia are con- 
genital, and they appear to arise by a fault of development by 
which the ovary descends as the testis does normally. The ovary 
passes through the inguinal ring and takes a sac with it, but just 
like the testis it is itself attached to the wall. The sac remains 
open like the tunica vaginalis in a congenital inguinal hernia. 
The ovary in that case will be irreducible, unless, as sometimes 
happens, the broad ligament is so long as to allow the ovary to 
pass back through the neck. In this case, however, the ovary will 
still have its fixed attachment in the sac. Apart from this con- 
genital inguinal form, ovarian hernias may he acquired, and these 
may be either inguinal or femoral. 
The strangulation of hernias is of great importance. By this 
expression is meant the condition in which the neck of the sac is 
so tightly impacted that not only is the return of the contents pre- 
vented, but even the bloodvessels are obstructed by the pressure 
of the ring. This mostly occurs when, on account of some pecu- 
liarity in the situation of the intestine as it issues from the sac, 
there is, to begin with, a partial obstruction. If the intestine at 
its entrance into the sac be free, while at its exit it makes a sudden 
bend so as to cause a partial obstruction, then the feces will pass 
readily in, but will accumulate inside as they do not find free exit. 
The mere loading with feces may cause irreducibility, and if the 
feces decompose the development of gas may still further increase 
the bulk of the contents. In this way the sac will become too full, 
and as the neck is narrow there will be special constriction here. 
Again, the intestine already in the sac by its peristaltic movement 
may drag more and more of the gut after it, till stopped by the 
intestine becoming too tight for the neck. 
In any case the neck of the sac constricts the portion of intestine 
concerned, and the most direct effect is obstruction of its veins. 
This itself, by producing hypersemia, and, it may be, oedema of the 560 
DISEASES OF THE ALIMENTARY CANAL. 
mucous membrane, leads to swelling and further constriction. 
The whole protruded piece becomes of a dark color from venous 
engorgement and hemorrhage. Finally the pressure may be 
enough to close even the arteries. 
The venous obstruction alone seems sufficient, if complete, to 
cause necrosis of the intestine, and so gangrene is an occasional 
result, If the arteries are also obstructed there is still greater 
probability of the occurrence of gangrene. 
But sometimes the obstruction is relieved before gangrene has 
occurred, and yet in some of these cases a severe inflammation 
results after the intestine has been returned to the abdomen, 
leading on, it may be, ultimately to gangrene of the affected piece 
of gut. The probable explanation of this is that during the incar- 
ceration the arteries have been obstructed, and during this period 
the bloodvessels have been so damaged that on the restoration of 
the circulation they are no longer able to recover. It has been 
shown by experiment (in the ear of the rabbit) that if, by liga- 
turing the main arteries, the vessels of the part are deprived of 
blood for a time, and then the circulation restored by loosening the 
ligature, the result is, active hypersemia, acute inflammation, or 
the hemorrhagic infarction, according to the time during vrhich the 
ligature has acted. So in the case before us, the release of the 
constriction, by allowing of the reestablishment of the circulation 
in vessels seriously compromised, may lead to inflammation or 
gangrene. 
TWISTING OF THE INTESTINE. 
This is a condition probably of frequent occurrence, but one 
which is perhaps too little borne in mind as a cause of obstruction. 
It occurs in the great majority of cases at the 
sigmoid flexure of the colon, and the reason 
of this will appear from the anatomical re- 
lations of that part of the gut. The ascend- 
ing colon above the flexure, and the rectum 
below it, have virtually no mesentery, being 
fixed to the abdominal wall. The flexure 
therefore is fixed at its two extremities and 
these are near one another, while the loop 
forming the flexure is movable. It is as if 
the loop were attached by its two ends to a 
fixed point, and it is easy to understand how 
it should sometimes twist round this as an 
axis. The twist is, as it were, in two half 
turns (see Fig, 244), and it is usually the 
upper limb of the loop which turns round 
the lower at its neck. 
It is clear that the twisting will cause 
some obstruction of the intestine, but this 
will not usually be complete. The lower limb is narrowed at its 
neck by being grasped by the upper limb twisted round it, while 
Fig. 244. 
Twisting of the sigmoid 
flexure. The upper limb 
has a much sharper turn 
than the lower, so that a 
flexible tube could be passed 
up from the rectum. INTUSSUSCEPTION OR INVAGINATION. 
561 
the upper limb is narrowed by the sudden curve which it makes. 
Feces still pass into the flexure, however, and they may ac- 
cumulate in enormous quantity. This partial obstruction with 
accumulation of feces may persist for months and lead to extreme 
dilatation of the flexure, so that it may fill the abdomen and reach 
up to the diaphragm. As the upper limb is twisted over the lower 
and the latter is straight, a tube may he passed from the anus up 
into the enormously dilated flexure. The walls of the intestine in 
these prolonged cases may be greatly thickened, especially the 
muscular coat. In some cases twisting may exist without any 
obstruction of consequence. 
While twisting is most common in the sigmoid flexure, it is 
liable to occur also when other parts of the intestine assume 
similar relations, that is to say, when a free loop of small intestine 
becomes fixed at its extremities, and these extremities are near 
each other. This will happen most frequently when one extremity 
is already fixed, as is the case at the upper and lower ends of the 
small intestine, where, on the one hand, the duodenum, and on 
the other, the colon, is fixed to the abdominal wall and holds the 
intestine down. If, by inflammation or otherwise, an abnormal 
adhesion is acquired, so that the gut is fixed at a point near the 
situation of the natural fixation, then twisting is apt to occur, and 
probably more readily here than in the sigmoid flexure, as the 
small intestine is naturally more mobile. 
INTUSSUSCEPTION OR INVAGINATION. 
In this condition a portion of the intestine passes into a succeed- 
ing portion. In order that one piece may slip inside the other, 
the one must present active peristaltic contractions, while the 
other is relaxed. The portion narrowed, by the violent peristalsis 
passes inside of the relaxed part. 
These conditions are most frequently found at the junction of 
the small and large intestines. The large intestine is naturally 
wide, and its peristaltic movements sluggish. If then the ileum 
at its last part presents peculiarly violent peristaltic contractions it 
may pass into the large intestine. This may explain the fact that 
the most frequent seat of invagination is in this situation. 
The invagination, however, is not usually a simple inversion of 
the ileum into the colon; in most cases the ileo-csecal valve is 
carried before the advancing ileum and forms the apex of the in- 
truded piece. This implies that the caecum itself is carried inwards 
and inverted, and the orifice of the vermiform appendage is some- 
times to be found near the apex of the invagination. The in- 
vagination is not infrequently very extreme, so that in children (in 
whom it most commonly occurs) the invaginated part may be 
carried right on to the rectum, so that the apex may be felt per 
anum. 
Besides this form we also meet with invagination of the large 562 
DISEASES OF THE ALIMENTARY CANAL. 
intestine itself, one part into a succeeding. It occurs but rarely in 
the small intestine. 
It has been stated above that invagination is peculiarly frequent 
in children, especially that form in which the large intestine is in- 
volved, and this is probably due to the much greater mobility of 
the colon in children than in adults. In the bodies of children 
also we frequently meet with a form of invagination which has 
produced no symptoms during life, and has really occurred just at 
the time of death. It is usually present in the small intestine, 
where a small inversion of one part into a succeeding one is found. 
The invagination is easily reduced by slight dragging, and there 
are none of the secondary changes visible, such as are to be men- 
tioned immediately as following invagination. Just at death, or 
immediately after it (as may be frequently seen in animals), the 
intestine commonly shows violent peristaltic movements, but these 
are irregular, and it readily happens that a much contracted part 
passes inside a relaxed portion. This form of invagination is, 
therefore, either post-mortem or occurs just at the agony. 
When a piece of intestine is invaginated, there are three tubes, 
the outside one in its natural position, forming the sheath, the 
internal one, which, although abnormal in position, runs in the 
usual direction, and the middle one joining the other two, and 
with its mucous surface directed outwards. It sometimes happens 
that a second invagination occurs, and then there are live tubes, 
or a third, in which case there are seven. The mesentery is 
carried in with the intestine, and by dragging on it at one side, it 
may give the gut a somewhat oblique direction. 
The packing of intestine into the interior of succeeding portions 
causes considerable interference with the circulation, and this is 
increased by the mesentery being partly included and its vessels 
pressed on. In this way there usually occurs an acute inflamma- 
tion, with swelling and hemorrhage of the mucous membrane, and 
flbrinous exudation on the peritoneal surface. The inflammation 
may lead on to a general peritonitis with fatal issue. Again, the 
obstruction of the vessels may be such as, with the added inflam- 
mation, to lead to gangrene of the gut, and this by the slough 
separating and causing perforation may produce a fatal peritonitis. 
On the other hand, permanent adhesion may occur between the 
sheath and the upper end of the included part at the proximal 
extremity of the invagination, and, the inner and middle tubes 
becoming gangrenous, they may come away in whole or in part, 
as a slough, and the continuity of the intestine be restored with 
the loss of a piece. 
It is not usual for complete gangrene of the included tubes to 
occur, but what remains becomes adherent to the sheath, and, by 
contraction, gradually accommodates itself, and so the calibre is 
fully restored. simple inflammations of the intestine. 
563 
PROLAPSE OF THE INTESTINE. 
This condition connects itself naturally with invagination. It is 
the protrusion of the intestine outside the body through the anus 
or through an artificial anus. The commonest form is the ordinary 
prolapsus ani. This only occurs when the sphincter is greatly 
relaxed by catarrh or by violent pressing at stool, but when it has 
frequently happened the sphincter atrophies and the prolapse 
occurs very readily. 
There are, strictly speaking, two forms of prolapsus ani. In the 
one little more than the mucous membrane is protruded, and it is 
seen to be continuous with the skin at the anus. In the other 
form there is really an invagination as well as a protrusion. The 
lower part of the rectum is so fixed that the whole wall cannot be 
protruded, but only its mucous membrane as in the form just con- 
sidered. But the upper more movable part may be invaginated 
into the lower part and then protruded. This mostly occurs as a 
consequence of violent peristaltic contraction of the rectum in 
cases of severe diarrhoea with tenesmus. 
In both forms the exposed mucous membrane becomes inflamed 
and liable to bleeding. The inflammation sometimes causes 
through time adhesion and fixation of the bowel in its abnormal 
position. 
SIMPLE INFLAMMATIONS OF THE INTESTINE. 
We have already seen that the mucous membrane is frequently 
irritated by the contents being of an obnoxious nature by reason 
of decomposition or otherwise. In addition to that, inflammation 
may be produced by the action of specific morbid poisons, chiefly 
those of dysentery, typhoid fever, and cholera. We have there- 
fore in the first place to consider the simple inflammations and 
afterwards these others. The term enteritis is often used to 
designate inflammations of the intestine of all kinds. 
Phlegmonous inflammations of the intestine sometimes occur 
as the result of peculiarly irritating contents. We shall see that 
in dysentery we have an inflammation of this kind, but there are 
what may be called dysenteric inflammations without the special 
dysenteric poison, the anatomical changes being virtually the same, 
although as a rule much less intense. 
Catarrh of the Intestine.—As already indicated, this occurs 
chiefly in connection with the presence of irritating contents, but 
exposure to cold may also lead to it. Perhaps this latter cause 
produces its effects by means of the former. That is to say, the 
exposure of the surface to cold may interfere with digestion and 
absorption, and so leave the contents to decompose and become 
irritating. 
The influence of the intestinal contents in producing catarrhs is 564 
diseases of the alimentary canal. 
shown by the localities at which inflammations are most common. 
The large intestine is much more frequently affected than the small, 
and in the large intestine the caecum, with the vermiform appen- 
dage, is the most frequent seat, and next to that the rectum, appar- 
ently because the contents stagnate especially in these parts rather 
than in the much more movable transverse colon. 
The catarrh is characterized by hyperaemia and swelling of the 
mucous membrane, with exudation of serous fluid and leucocytes. 
There is also increased secretion of mucus, which in the case of 
the colon may be very excessive. The exudation is usually 
mucous in character, but in the more acute inflammation it may 
assume more or less of a purulent character. If this be the case, 
the mucous membrane is liable to be infiltrated with inflammatory 
cells, and after a time to undergo ulceration. This occurs with 
peculiar frequency in the caecum, and next to it in the rectum. 
Catarrhal ulcers are usually of considerable area and compara- 
tively superficial. Neighboring ulcers may coalesce so as to 
produce extensive, variously shaped losses of substance, in the 
midst of which the remaining mucous membrane appears as 
raised patches with irregular outline. Sometimes the floor of the 
ulcer is so smooth, and the remaining mucous membrane so 
irregular from inflammatory infiltration, that it looks as if the ulcer 
were the normal mucous membrane and the patches of persisting 
mucous membrane adventitious. 
In the course of catarrhs, ulcers also arise from the closed 
follicles. There are indeed some catarrhs in which the latter are 
mainly affected, appearing as rounded prominences and flat eleva- 
tions, corresponding to the solitary follicles and Peyer’s patches. 
This form is called follicular catarrh, or follicular enteritis. 
But without the inflammation preponderating in the follicles they 
are often enlarged, and may be so infiltrated with inflammatory 
products as to form virtually small abscesses resulting in crater- 
shaped ulcers which may afterwards enlarge. In this way arise 
the so-called follicular ulcers. 
The ulcers of ordinary catarrh are superficial, and unless 
exposed to continued irritation, as by the prolonged presence of 
hard feces, they do not tend to perforation, and readily heal when 
the cause of catarrh is removed. 
If the catarrh be moderate—not so intense as to lead to 
ulceration—then, if long continued, it will give rise to hypertrophy 
of the mucous membrane such as we find so frequently in the case 
of the stomach. Here also there may be mucous polypi and cysts 
as in the stomach. They are most frequent in the large intestine, 
and if seated in the rectum they may project through the anus. 
Localized Inflammations.—It has already been indicated that 
certain localities are more liable to inflammation than others, and 
as the inflammations of certain of these regions present special 
points of importance they have received special names, and require 
more particular attention. SIMPLE INFLAMMATION'S OF THE INTESTINE. 
565 
Duodenitis is usually an extension of a catarrh of the stomach, 
and it would not warrant any special reference except from the fact 
that the common bile-duct often takes part in the catarrh, and we 
have obstruction and icterus sometimes resulting from this simple 
cause. 
Typhlitis and Perityphlitis designate conditions which require 
very special notice. These two terms mean respectively inflam- 
mation in and around the caecum, but they are frequently used so 
as to include inflammations in connection with the vermiform 
appendage, and, in fact, Ziegler seems to limit the designations to 
these latter inflammations. 
In some cases the caecum is very seriously inflamed and ulcer- 
ated, especially when large masses of hard feces lodge in it. 
Under these circumstances the ulcers may increase in depth, and 
extend, in the posterior part of the wall where the gut is not 
covered by peritoneum, through the entire thickness of the' intes- 
tine so as to penetrate into the retroperitoneal connective tissue. 
The result is acute inflammation in this region, often going on to 
the formation of abscess. It will be inferred that this condition is 
that designated perityphlitis. 
The vermiform appendage much more frequently gives rise to 
acute inflammations around the ciecum than the caecum itself does, 
so that, although the term typhlitis is not applicable, yet perity- 
phlitis is. 
It may here be mentioned in the first place that the appendage 
sometimes undergoes peculiar transformations on account of the 
closure of its orifice, with or even without inflammation of its 
mucous membrane. If, as a result of inflammation or otherwise, 
the orifice be closed, the secretion, along with the catarrhal 
exudation, accumulates in the appendage and distends it, so as to 
convert it into a large retention cyst (Fig. 245). The contents 
usually become serous, so as to constitute a dropsy of the vermi- 
form appendage, but they may continue mucous in character and 
form a thickish jelly. The dilated appendage may acquire con- 
siderable dimensions, as in the case from which the accompanying 
figure is taken. 
But of more importance are the inflammations due to the 
presence of foreign bodies in the appendage. Any hard substance 
lying in the caecum may, if small enough, pass into the vermiform 
appendage. In this way apple, grape, cherry, or orange seeds are 
said to get into it. But much more frequently pieces of hardened 
feces are met with, and as these dry and frequently assume the 
shape and appearance of cherry or orange stones, they are fre- 
quently mistaken for them. This occurs all the more because the 
inspissated feces are often coated with phosphates which form 
a kind of rind. 
The presence of the foreign body causes inflammation of the 
mucous membrane, and this, from the continued pressure and con- 
fined space, readily results in ulceration. The ulcers frequently 566 
DISEASES OF THE ALIMENTARY CANAL. 
penetrate through the appendage and lead to peritonitis. As a 
general rule the appendage has acquired adhesions before actual 
perforation occurs, and so the peritonitis is limited by the adhe- 
sions. But the inflammation is apt to recur, and not infrequently 
Fig. 245. 
Cyst of vermiform appendage. The appendage is converted into a bulky 
cyst which was filled with gelatinous material. 
results in the formation of recurring abscesses. The bursting of 
one of these into the cavity of the peritoneum often leads to fatal 
peritonitis. From the accounts in the newspapers, the death of 
M. Gambetta seems to have been due to this cause. 
From the relation of the parts it will be seen that a perityphlitis 
arising from the caecum will usually be in the subperitoneal tissue, 
whereas that from the vermiform appendage will be in the perito- 
neum, as the appendage is completely surrounded by peritoneum 
and has a mesentery. It follows that the latter is much the more 
dangerous as it is also the more frequent form. It is, indeed, 
much more frequently a cause of death than is usually supposed. 
Proctitis and Periproctitis are inflammations in the rectum 
and around it, of an equivalent character to those in and around 
the ctecum. If the ulceration leads to perforation and the forma- 
tion of abscess, then the disease may have a very chronic course 
with flstuke discharging into the rectum. Sometimes these burst 
externally, or into the vagina, and they may retain their communi- DYSENTERY. 
567 
cation with the rectum, so forming false passages for the feces and 
flatus, or the internal aperture may close, leaving merely an ex- 
ternal fistula. 
SPECIFIC INFLAMMATIONS OF THE INTESTINE. 
Dysentery.—This inflammation is determined by the action of 
a specific morbid poison. As already indicated, similar lesions 
sometimes occur in connection with other diseases, such as typhoid 
fever, cholera, acute rheumatism, but in these also, although the 
virus is not the same, we may presume that a violent irritant is 
present. It is difficult to say whether the poison acts on the 
mucous membrane by being present in the intestinal contents, or 
because it is carried by the blood. At any rate, the locality of the 
disease is evidently determined by the stagnation of the intestinal 
contents. It is always most marked in the large intestine, and 
especially in the flexures, these being the parts where the feces 
tarry longest. It usually decreases in intensity, from the rectum 
upwards, but not uniformly, there being more affected and less 
affected parts, the former corresponding usually with the flexures. 
In severe cases the whole colon is affected, and sometimes even 
the lower part of the ileum. 
The disease manifests itself as an acute inflammation, which, in 
the milder cases, may present the characters of a severe catarrh, 
but is apt to go on to phlegmonous inflammation with sloughing 
of the mucous membrane. In the earlier stages the mucous mem- 
brane is swollen by serous exudation, soft and juicy, and it is 
thrown into folds on the summits of which it is peculiarly hy- 
persemic. The surface is covered by a mucous or grumous ma- 
terial, consisting of shed epithelium with mucus and inflammatory 
exudation. The mucous membrane and submucous tissue are in- 
filtrated with serous fluid and leucocytes in great abundance. 
In higher degrees the mucous membrane is still more thickened 
and thrown into still more prominent folds. There is also con- 
siderable hemorrhage in its substance occasionally. The summits 
of the folds being specially exposed to mechanical irritation, very 
commonly undergo necrosis, and the sloughs are generally dis- 
tinguishable by the brown color which they assume from becoming 
stained with the bile pigment. The necrosis involves the mucous 
membrane to varying depths, sometimes very superficially, some- 
times through its whole thickness, and, if the slough surrounds 
the gut, we may have a ring of necrosed tissue ultimately dis- 
charged by the anus. 
Of course, these sloughs leave ulcers behind, whose walls present 
great infiltration of leucocytes. But ulcers form also by processes 
similar to those in catarrh, namely, by inflammatory infiltration 
and molecular destruction of the mucous membrane, and by sup- 
puration of the closed follicles. 
The contents of the intestine are in severe cases formed of dark 568 
DISEASES of THE ALIMENTARY" canal. 
decomposing material, mixed with blood. The mesenteric glands 
are always secondarily affected, being enlarged and hyperasmic. 
If the patient survives the acute attack, the disease very com- 
monly passes into chronic dysentery. The ulcers formed in the 
various ways described above show little tendency to heal, but 
remain as open, discharging sores. Sometimes they penetrate more 
deeply, and lead to abscesses in the surrounding tissue, especially 
of the rectum (periproctitis). The remaining mucous membrane 
is swollen and in a state of catarrh. The whole intestinal wall is 
thickened, except where the ulcers exist, and it is irregularly 
drawn in and adherent to the surrounding parts. 
In some cases a tendency to healing manifests itself. If the 
attack has been slight and the ulceration only superficial, there 
may be a complete restoration of the mucous membrane, with 
insignificant cicatrices. But for the most part the ulceration has 
been considerable, and the cicatrices are of considerable superficial 
extent, perhaps surrounding the gut. When such cicatrices, in 
the usual fashion, contract, they cause narrowing of the intestine, 
which, in some cases, is very considerable. Alternating with the 
narrowing, there is very commonly dilatation of the more healthy 
parts, so that a very remarkable pouching of the colon may result, 
the narrowed parts being probably adherent to the tissues around. 
The obstruction produced in this way is all the greater because the 
contraction often throws the remaining mucous membrane into 
folds which may act as valves to the constricted part. 
Cholera.—This disease, which occurs in an epidemic form, de- 
pends on the action of a specific virus. In addition to the epidemic 
disease known as Asiatic cholera, there is a condition known as 
British cholera, in which the poison does not appear to be a 
specific one, but in which the anatomical changes are identical 
with those in the epidemic form. From an individual case, there- 
fore, it would be impossible to say which form is present; this 
must be judged from circumstances, bearing in mind especially 
that the Asiatic form is preeminently epidemic, and spreads by 
the extension of a specific virulent poison. The exact form of the 
virus is unknown, although there is room to believe that it is a 
micro-organism. 
In both forms it is clear that a very violent irritation of the 
mucous membrane of the intestine is produced. During life, the 
disease is characterized by the discharge of extremely fluid stools, 
which, from the intermixture of finely divided material, give the 
characteristic rice-water appearance. Sometimes a patient dies 
without the bowels having been moved, but in that case they are 
found distended with the rice-water discharge. 
It is obvious that there is here an enormous transudation from 
the vessels of the intestine. The chemical character of the dis- 
charge, however, seems to indicate that it is not a mere inflamma- 
tory exudation from the vessels, but rather a secretion of the 
glands. Its specific gravity is low, 1006 to 1013. There is very TYPHOID FEVER. 
569 
little albumen present, and the discharge contains a ferment which 
has the power of converting starch into sugar. 
It is commonly stated that the flakes which give their character 
to the rice-water evacuations are composed of desquamated epi- 
thelium. Investigations have shown, however, that this is not the 
case; they are little masses of mucus containing leucocytes. After 
death the epithelium may be found loose in the intestine, but this 
appears to be from post-mortem maceration, for, if examined suf- 
ficiently early, the epithelium is found present and apparently 
normal. 
The most marked post-mortem appearance in the intestine is a 
remarkable rosy injection of the vessels of all its coats, so that a 
red appearance is visible even in the serous coat whenever the 
body is opened. The mucous membrane is swollen and the closed 
follicles prominent. Occasionally there is a decidedly inflam- 
matory condition present, which may be even of a dysenteric 
character. 
The condition of other parts of the body is directly referrible to 
the enormous withdrawal of water from the blood. The blood 
itself is thick, dark, and imperfectly coagulated. The skin, serous 
membranes, and all the soft tissues are shrunken, and dry, and 
parchment-like. The membranes of the brain are frequently in- 
jected. The kidneys present the characters of a slight parenchy- 
matous inflammation. 
Typhoid Fever.—This disease is also due to the action of a 
specific poison. In the affected parts of the intestine, bacilli have 
Fig. 246. 
Bacillus from mesenteric gland in a case of typhoid fever. The rods are shown. The large 
bodies beside them are blood-corpuscles, the paler ones the red, the darker ones the white. 
Preparation stained with methyl-violet. X 1800. 
been found, and exactly similar bacilli have been found in the 
mesenteric glands (see Fig. 246) and in the spleen. It may be in- 
ferred that the virus is present in the blood, and from this produces 
the general symptoms of the disease, while locally it produces the 570 
DISEASES OF THE ALIMENTARY CANAL. 
changes to be presently described. It is very probable that it finds 
entrance by the intestine and produces irritation of the follicles 
and mesenteric glands in its passage. 
The affection in the intestine consists of an inflammatory swell- 
ing of the closed follicles and of the mucous membrane in their 
neighborhood, the inflammation often going on to necrosis and 
sloughing. The disease has usually its point of greatest intensity 
at the lower extremity of the ileum, and it is often possible to see 
various stages of the process in proceeding from above downwards 
through the small intestine till it culminates close to the ileo-ciecal 
valve. 
In the normal state, especially in the adult, the Pe}Ter’s patches 
and the solitary follicles are very slightly prominent. The patch 
Fig. 247. 
Portion of a Peyer’s patch in an early period of typhoid fever; a, mucous membrane which 
becomes raised when the swollen patch is reached; h, internal layer, and c, external layer of 
muscular coat; d, swollen patch composed of round cells with dilated bloodvessels. At the 
right of the section the round cells are invading the submucous tissue and approaching the 
muscular coat. X 16. 
viewed from the surface shows a congeries of shallow depressions 
separated by slightly elevated ridges, which run in from the 
general mucous membrane, and form a kind of network. It is in 
the depressions that the follicles are placed. In typhoid fever there 
is at first a general swelling of the patch; it is an inflammatory 
swelling accompanied by abundant infiltration of leucocytes which 
occupy both the closed follicles and the mucous membrane. The 
patch is obviously raised and its margins somewhat abrupt (Fig. 
248, a). Viewed from the surface there is at this early stage 
simply an exaggeration of the normal appearance. The ridges of 
mucous membrane are swollen so that the depressions are more TYPHOID FEVER. 
571 
hidden, and an appearance is produced which has heen compared to 
that of the convolutions of the brain in miniature. The swollen 
patch has a pinkish or whitish color. At the same time the solitary 
follicles show themselves as elevations at intervals. 
As time goes on the whole tissue gets more and more infiltrated 
with leucocytes (Fig. 247), and the raised patch gets more solid 
and its surface more homogeneous. The invasion of round cells 
extends to the submucous and muscular coats, even to the serous, 
and passes to some extent beyond the patch. A similar condition 
occurs in the solitary follicles; they also present a marked increase 
in size, and are less defined, by reason of the infiltration around 
them. 
On this condition follows necrosis (Fig. 248, b). The infiltrated 
and altered patch or solitary follicle forms a slough, of larger or 
smaller size. This slough remains ad- 
herent for a time, and like all sloughs 
in the intestine it becomes brown or 
yellow from the biliary coloring matter, 
which stains dead tissue, while the living 
structures are able to resist it. Generally 
there is a single slough on a Peyer’s patch, 
not involving the whole patch, but of con- 
siderable superficial extent (see figure). 
Sometimes there are several sloughs cor- 
responding to some of the closed follicles 
of which the patch is made up. 
After a time the slough separates and 
an ulcer is left with infiltrated base and 
margins (Fig. 248, c). The ulcers are 
confined to the patches and solitary fol- 
licles, so that they repeat their shape and 
locality. The walls are succulent and 
vascular, and considerable hemorrhage 
may occur from them. The ulceration 
may extend more deeply than the mucous membrane, involving a 
necrosis of the muscular and even of the serous coat, so that per- 
foration may result. Perforation may occur in one of two ways. 
In the first place an ulcer may extend in depth till it penetrates 
through the muscular and serous coats. In this case the process 
is somewhat- gradual, and there is generally a sufficiently acute 
inflammation of the peritoneum to cause adhesion and prevent the 
intestinal contents passing into the abdominal cavity. In the 
second place, perforation sometimes occurs in a manner com- 
parable to the perforation of the pleura in phthisis pulmonalis 
which leads to pneumothorax. The serous coat is undermined by 
the ulcer, and as its nutrition is cut off' it undergoes necrosis. In 
such cases the brown slough may he visible on viewing the in- 
testine externally. A partial separation of the slough may allow 
perforation, and as this form is more acute and not so likely to be 
accompanied by considerable adhesions, the contents of the in- 
Fig. 248. 
Diagrammatic representation 
of Peyer’s patches in typhoid 
fever, a, early stage with swell- 
ing of the patch; b, later stage 
with sloughing; c, ulcer with in- 
filtrated walls. (Thierfelder.) 572 
DISEASES OF THE ALIMENTARY CANAL. 
testine are more apt to escape into the peritoneal cavity and pro- 
duce fatal peritonitis. 
When recovery takes place from the fever, the process in the 
intestine retrogrades. According to the stage reached will be the 
exact process of resolution. If, in any part, ulceration has not yet 
occurred, then there is a gradual diminution of the patch and a 
return to the normal. If ulceration exists, the ulcer fills up and 
cicatrizes. The cicatrix, however, remains long, often with a slaty 
color, but not usually with much puckering. 
In the lymphatic glands of the mesentery processes occur which 
are quite parallel to those in the follicles of the intestine. The 
glands enlarge, and present on section a red injected appearance 
and soft consistence. There may be necrosis here aLo, giving rise 
to an opaque grayish condition in the midst of the gland. When 
recovery takes place the glands return to the normal, and the 
sloughs are usually absorbed, although they may become caseous 
and subsequently calcareous. 
It is to be remembered also that the spleen is enlarged, and 
there is here more than in typhus fever a swelling of the Malpighian 
follicles, which are lymphatic in structure, and so the spleen is 
firmer and paler on section. 
TUBERCULOSIS OF THE INTESTINE. 
In the great majority of cases this condition is secondary to 
pulmonary phthisis, and it occurs in about three-fourtlis of the 
cases of that disease examined after death. It may be doubted 
whether it ever occurs as a primary disease. We have already 
seen that tubercular ulceration is very common in the mucous 
membrane of the bronchial tubes in connection with pulmonary 
cavities, and that it is also frequent in the tracheal and laryngeal 
mucous membranes. The tubercular lesions are doubtless due to 
the direct action of the virus carried from the lungs. The tuber- 
cular disease in the intestine is to be accounted for by the sputa 
being partly swallowed, and the virus applying itself to the in- 
testine directly. 
The virus here attacks the same structures as in typhoid fever, 
namely the closed follicles and Peyer’s patches, and at first it pro- 
duces a change of a somewhat similar kind. There is an enlarge- 
ment of the closed follicles by reason of a great new-formation of 
cells which infiltrate the neighboring mucous membrane as well 
as the follicles. This primary enlargement is, however, much less 
uniform than in typhoid fever. On the whole, it is greatest 
towards the lower part of the ileum, but it presents great irregu- 
larities. Even on the Peyer’s patch it generally affects a few 
closed follicles, and not the whole, so that there are rounded 
prominences dotted over the patch. Moreover, it is not simply an 
inflammatory infiltration which occurs; there are tubercles present 
of characteristic structure. TUBERCULOSIS OF THE INTESTINE. 
573 
The enlarged follicles undergo caseous necrosis, so that very 
soon they are seen to have an opaque yellow kernel, while the 
epithelium still covers them. In the next place softening occurs, 
and the caseous mass is discharged, leaving an ulcer. The ulcer 
is crater-shaped with overhanging edges, which are infiltrated with 
leucocytes and contain miliary tubercles (see Figs. 249 and 250). 
There may be at first several such ulcers on a Peyer’s patch, and 
Fig. 249. 
Tubercular ulcer of the intestine. Naked-eye appearance. The swollen overhanging 
edges are indicated. 
other solitary ones in other parts. They extend by fresh infiltration 
of the neighborhood and fresh necrosis, while at the same time 
miliary tubercles are visible in the midst of the inflammatory in- 
filtration. The infiltration very commonly involves the muscular 
coat, and even the serous (see Fig. 250), but the ulcer rarely 
extends in depth beyond the mucous and submucous coats. On 
the other hand tubercles are often to be seen almost free of inflam- 
matory infiltration at a distance from the ulcers in the midst of the 
muscular coat, or even outside it and in the peritoneum. 
The ulcer extends much more laterally than deeply, involving 
ever increasing portions of the mucous membrane. In its extension 
it does not in the least respect the boundaries of the Peyer’s patches 
or solitary follicles, but extends beyond them, generally advancing 
more across the gut than longitudinally. In this way ulcers are, 
not infrequently, much elongated in a direction transverse to the 
intestine, and may even form a ring around it. As they begin 
largely in the Peyer’s patches, the ulcers have usually their centres 
at the part of the gut opposite the mesenteric attachment, the 
patches having their seats along this free portion. 
The position of the ulcers is often indicated before opening the 
intestine by the appearance of the peritoneal surface. If the ulcer 
be of any considerable size there is some inflammation of the 
peritoneum, evinced by redness and, very often, elongated pro- 574 
DISEASES OF THE ALIMENTARY CANAL. 
jections of vascular connective tissue. But above all we can 
generally see in the peritoneum groups of little white nodules, 
which are tubercles in or under the serous coat. The existence 
of these tubercles is sometimes even useful in determining whether 
an ulcer is a tubercular one or not. It is very rare indeed that the 
Fig. 250. 
Section of a small tubercular ulcer. In the middle there is a crater-shaped ulcer (a) with 
overhanging edges. The mucous membrane around is infiltrated with round cells in the 
midst of which a few tubercles are indicated. Beneath the ulcer the muscular coat is in- 
filtrated. At d there is a small sub-serous tubercle. X 16. 
ulcer penetrates through the peritoneal coat, and if it does, it is 
usually protected by adhesion to neighboring loops of intestine. 
As a general rule the tubercular ulceration is most marked in 
the ileum, but not infrequently the colon is attacked, and there 
may be ulcers of very large size there. 
The process is for the most part a chronic one, and the ulcers 
advance slowly. Sometimes, however, and usually in connection 
with acute phthisis, there is a rapid swelling of the follicles, and 
ulceration occurs by softening without preliminary caseous necrosis. 
In these cases perforation is much more liable to occur. 
TUMORS OF THE INTESTINE. 
Cancer.—This is by far the most frequent and important form 
of tumor. Cancers are almost confined to the large intestine; we 
have already connected this with the fact that this portion is most 
exposed to the irritation of the stagnant feces. This is the more 
evident as the most frequent localities are the rectum, the flexures, TUMORS OF THE INTESTINE—CANCERS. 
575 
and the ciecum. At the same time, cancers are not unknown in 
the small intestine. 
The commonest form of cancer is a very chronic epithelioma 
with gland-like masses of cylinder cells (Fig. 251). The tumor is 
very frequently ring-shaped, and, as ulceration readily occurs, 
there may be little more than an ulcer with infiltrated edges. 
Even the infiltration of the edges may be very slight, and it may 
Pig. 251. 
Cylinder-celled epithelioma of rectum. There are gland-like spaces containing epithelium, 
which at the periphery is characteristically cylindrical. 
be difficult to be sure that the disease is cancerous. The ulceration 
is accompanied by new formation of connective tissue in all the 
coats of the intestine, and, while adhesion occurs to parts around, 
there is great contraction of the intestine. In this way strictures 
arise, and the occlusion of the calibre may be increased by the 
mucous membrane at the edges of the ulcer being thrown into 
folds. In fact, if we except hernias, this is probably the most 
frequent cause of intestinal obstruction. 
It has been already noted that the proper cancerous structure is 
often to a large extent destroyed by ulceration, but at the edges 
we may distinguish masses of epithelial cells with a glandular 
arrangement. In the adhesions around the affected part of the 
intestine enlarged glands may be found with cancerous tissue. 
Next to the epithelial, the most common is colloid cancer. 
This forms a much more prominent tumor, which may involve a 
considerable length of the gut, and incorporate the entire coats. 
This form may produce obstruction by its mere bulk, although it 
also is liable to ulceration, and the consequent contraction of the 
gut, added to the bulk of the tumor, frequently effects obstruction. 
It does not so readily affect the lymphatic glands, but more usually 
extends through the wall into the peritoneum. 576 
DISEASES OF THE ALIMENTARY CANAL. 
Soft cancer is much less common here than in the stomach, and 
it resembles the same form of tumor there. It extends to the 
lymphatic glands and frequently also to the liver. 
The remaining tumors of the intestine are of little importance. 
Fibromas, lipomas, myomas, and sarcomas occur, and they are all 
apt to pass into the interior of the intestine and assume the form 
of submucous polypi. It is said that these polypi, by being dragged 
on in the peristaltic movements ot the intestine, may produce in- 
vagination. Mucous polypi are also to be mentioned as occurring, 
especially in the rectum in catarrh. 
OBSTRUCTION TO THE CALIBRE OF TIIE INTESTINE. 
This condition lias been incidentally mentioned as occasioned 
by several o‘f the lesions already described. It may be well here 
to sum up the various forms of intestinal obstruction and to 
describe the effects produced when the calibre of the intestine is 
interrupted. 
Next to hernia, the most frequent cause of obstruction is the 
contraction of cicatrices resulting from ulceration, and in the 
great majority of cases the ulcers are malignant, that is to say, 
they arise by the breaking down of cancers. It is to be remem- 
bered that, in contractions of the calibre such as these, the direct 
cause of the final obstruction may be the folding of the mucous 
membrane above the stricture, this acting like a valve to the 
narrowed part. Tumors also obstruct sometimes by their bulk. 
Similarly, gall-stones, masses of feces, collections of round worms 
may occlude the calibre. Invagination is the commonest cause in 
children. There is also twisting or torsion. Lastly, we have 
obstruction by incarceration, the intestine passing into a position 
where a loop is caught at the neck and strangled. Hernias form 
the commonest examples of this kind, but there are a number of 
cases in which the intestine slips under a bridge or ligament and 
gets, as it were, pinioned and compressed. 
This last cause of obstruction occurs so obviously to the mind 
that its frequency is apt to be thought much greater than it is. In 
reality it forms a small proportion of the entire cases. The ab- 
normal band may be formed by the adhesion of structures to 
various parts of the abdomen so as to form bridges. Thus the 
vermiform appendage may adhere by its tip and form a bridge; or 
a Meckel’s diverticulum may similarly adhere; or the omentum 
may be tied down in such a way as to form a narrow bridle. But 
sometimes the band is itself distinctly of new formation; there 
has been a local peritonitis, and two opposing surfaces have be- 
come adherent in the usual way of inflammatory adhesion, by vas- 
cular connective tissue; by the movements of the intestine the 
connective tissue has been dragged upon and elongated till it forms 
a band or ligament, which may afterwards tie down a loop of in- 
testine. obstruction to the calibre of the intestine. 
577 
A very unusual form of incarceration is that in which there is 
an aperture in the mesentery through which the intestine passes. 
This may be produced by a tear in the mesentery. But in a case 
observed by the author, there was a large round gap about 5 
inches in diameter with rounded edges, and obviously of long 
standing, perhaps congenital. The greater part of the small in- 
testine had become impacted in a complicated fashion into the 
aperture, and obstruction had finally resulted. 
When obstruction occurs the intestinal contents accumulate in 
the parts of the intestine above. The bowel may be greatly dis- 
tended and its muscular tissue paralyzed by the internal pressure; 
the stagnating feces decompose, and the contents of the small in- 
testine may acquire the characters of those of the large. This 
decomposition of the intestinal contents leads to several important 
results. In the first place there may be great formation of gas 
which still further distends and may produce the condition of ex- 
aggerated inflation called meteorism. Then a return of the feces 
in the reverse direction may occur, and if the decomposition is 
sufficiently advanced there may be a vomiting of matter having 
the characters of feces. This alarming phenomenon of stercora- 
ceous vomiting is sometimes referred to the reverse current ex- 
tending from the colon. We can hardly suppose, however, that 
the feces are able to pass the ileo-csecal valve, and for the most 
part the vomited matters are really the stagnant contents of the 
small intestine which have undergone the fecal decomposition. 
Of course there is a reverse current, else the intestinal contents 
would not reach the stomach. But this does not necessarily imply 
a vermicular movement in the reverse direction. If the intestine 
is distended, and is interrupted at a particular point, then the 
vermicular movement in the usual direction will carry the external 
layer of contents downwards to the point of obstruction. But in 
order to accommodate this fresh arrival there must be a return 
current upwards in the centre of the tube. There is a similar 
condition to what exists normally in the stomach where the con- 
tents are carried to the pylorus, and meeting the obstructing 
sphincter return for the most part down the centre of the cavity 
towards the fundus. 
Again, the products of decomposition may be absorbed to an 
abnormal extent and appear in the urine. There are two sub- 
stances resulting from the decomposition of albuminous substances 
which are normally present to a limited extent in the urine, 
namely, indican and carbolic acid. In cases of obstruction these 
substances, or one of them, are increased in quantity sometimes 
to a very striking extent. This increase does not occur unless the 
stagnation extends to the small intestine where the albuminoids 
are present. It does not occur therefore in ordinary constipation 
which affects the large intestine alone, apparently because the al- 
buminoids are absorbed before the}" reach the large intestine. DISEASES OF THE LIVER, PANCREAS, 
AND PERITONEUM. 
A.—THE LIVER. 
Introductory.—The liver is the largest gland in the body, its 
weight being on an average from 48 to 58 ounces in the adult male 
and 40 to 50 ounces in the female. From this alone it may be 
inferred that its diseases are of great importance. 
When we come to consider the functions of the liver we are met 
with serious difficulties from the pathological point of view. 
Diseases may largely destroy or render inactive the proper paren- 
chyma without seriously interfering with the general health of the 
patient unless, by interfering with the bloodvessels in the liver, 
they produce secondary effects in the portal circulation. Even 
the suspension of the biliary secretion may be without serious 
effect on the nutrition of the body. In considering the subject of 
diabetes mellitus (p. 74) the glycogenic function of the liver has 
been sufficiently referred to, and it only remains to be said here 
that, practically, nothing is known of the influence on this function 
of lesions which destroy the liver tissue. The influence may be 
very great and important, but no facts are known in regard to it. 
It is not to be inferred, however, that the liver is unimportant to 
the organism, but merely that the organism seems to have a 
remarkable power of compensation when its tissue is diseased. 
In considering the diseases of the liver the arrangements of the 
circulation must be borne in mind. It is well known that most of 
the blood comes to the liver by the portal vein, and the proper 
hepatic tissue is arranged in relation to the ultimate ramifications 
of that vessel. The interlobular veins form these ultimate ramifi- 
cations, and these are in immediate connection with the hepatic 
lobules. The hepatic lobule is a group of hepatic cells with blood- 
vessels, having in man a polygonal or somewhat globular shape; 
it measures about the twentieth of an inch in diameter. The 
interlobular vein lying outside the lobule sends multitudinous 
capillaries into it, and these seeking the centre of the lobule open 
into the central or intralobular vein which is the radicle of the 
hepatic vein. Blood is also brought to the liver by the hepatic 
artery which supplies the connective tissue and walls of the blood- 
vessels chiefly. Its capillaries terminate in veins which open into 
the interlobular veins (according to Cohnheim and Bitten), so that malformations and deformities of the liver. 
579 
this blood also finds its way into the hepatic capillaries and on into 
the hepatic vein. 
The connective tissue of the liver is often described as if it 
formed a special covering to the portal vein, being called Glisson’s 
capsule. It really forms a supporting stroma which holds the 
portal vein, the hepatic artery, and the hepatic duct, which all lie 
side by side. The lymphatic channels are also contained in it. In 
some animals the connective tissue surrounds each lobule and 
defines it distinctly from its neighbor, but in man it stops short at 
the interlobular vein, and except where this vein is, the lobules at 
their margins merge into each other, and their capillaries are in 
common. Examination of Fig. 254, in which the lobules are 
demarcated by fatty infiltration, will show how they run into one 
another at their peripheries. Although no proper fibrillated con- 
nective tissue is present inside the lobules, yet a fine recticulum 
accompanies and supports the capillaries. 
The lobules are large enough to be visible to the naked eye, yet 
unless there is some abnormal condition present, they are not indi- 
vidually distinguishable. On the other hand, it is they which give 
the liver when torn that granular appearance with which we are 
familiar. 
It is important to remember that the circulation in the portal 
vein, and especially in the capillaries of the liver must be unusually 
slow. The blood before it reaches the liver has passed through 
one set of capillaries, and here it passes through a second set; it 
has, therefore, lost very largely the force derived from the contrac- 
tion of the heart. It is probably for this reason that the liver is 
so very frequently the seat of secondary diseases, such as tubercu- 
losis, abscesses, cancers, etc. We may suppose that as the blood 
moves so slowly there will be time for any infective material 
to settle down and produce its special effects. We know that when 
vermilion is injected into the blood it is found largely in the 
capillaries of the liver. Similarly the abnormal pigment present 
in the blood in melanremia is found largely in these capillaries. 
MALFORMATIONS AND DEFORMITIES OF THE LIVER. 
Congenital malformations of the liver are not common. There 
are cases of absence of the liver, and of defect of one of the lobes, 
or irregularity in the lobes. What may be called supernumerary 
livers have also been found in the form of isolated pieces of liver 
tissue in the suspensory ligament. Of more importance is con- 
genital absence of the gall-bladder, along with which there is 
usually a dilatation of the bile-ducts. 
The liver is sometimes transposed along with a general trans- 
position of the viscera. In a case recorded by Fraser, there was 
not only a transposition, but an occasional dislocation of the liver, 
which came down into the left inguinal region. 
An acquired deformity is very frequently met with in females, 580 
diseases of liver, pancreas, and peritoneum 
and is to be associated with the method in which the clothes are 
worn. This deformity is usually stated to be due to tight lacing, 
but, although doubtless greatly aggravated by this, it is also in- 
duced by the ordinary methods of suspending the garments used 
by females. These are held up by being drawn tight at the waist 
above the crest of the ilium, the projection of this bone preventing 
them slipping down. By this tight band, often of considerable 
breadth, the abdominal organs are compressed and the lower ribs 
are held down and pressed inwards. This is greatly aggravated 
by the wearing of stays, even although they be not tightly laced, 
as by them the lower ribs are kept compressed inwards. The 
effect on the liver is that it is greatly flattened, while a transverse 
shallow depression forms along the upper surface, affecting chiefly 
the right lobe. In this groove the capsule is thickened, and there 
is obviously considerable loss of liver tissue. Sometimes the 
atrophy along this groove is such that the liver is, as it were, 
divided by it, and the two portions can be folded together. With 
the flattening there is great displacement of the liver, whose lower 
edge may extend as far down as the umbilicus. More or less of 
this deformity is to be found in nearly all female bodies, and is 
even found in the bodies of men who have been in the habit of 
wearing tight belts round their waist. 
Sometimes the upper surface of the right lobe of the liver pre- 
sents elongated depressions passing from behind forwards, which 
are really folds of the liver, and are produced chiefly when there 
is some obstruction to expiration. In that case the diaphragm is 
depressed by the dilated lung, and at the same time the lower ribs 
are drawn down in violent expiratory movements by the abdominal 
muscles, ana pressed against the liver, which is supported below 
by the contraction of the abdominal muscles. 
The liver is very liable to changes of position. Tumors or fluid 
in the abdomen carry it upwards. Depressions of the diaphragm 
press it downwards. The suspensory ligament may be elongated 
so that the organ is unduly movable, and may undergo displace- 
ment downwards. 
PASSIVE HYPEREMIA OF THE LIVER. 
The names nutmeg liver and red atrophy are sometimes given 
in cases of prolonged passive hypersemia, these names indicating 
certain appearances presented by the tissue, and to he referred to 
afterwards. Passive hypersemia occurs when any obstruction exists 
in the circulation of such a nature as to interfere with the return 
of blood from the inferior vena cava to the right* side of the heart. 
The commonest cause is valvular disease of the heart, especially 
mitral disease, but it also results from obstruction to the pulmonary 
circulation as in bronchitis and emphysema, etc. In these cases 
there is a general engorgement of the systemic venous circulation, PASSIVE HYPEREMIA — NUTMEG LIVER. 
581 
with increase of blood-pressure in the veins. We have already 
seen that in the capillaries of the liver, and consequently in the 
hepatic veins, the normal circulation is unusually slow, and the 
blood-pressure low. Any increase in the blood-pressure in the 
general venous circulation will, consequently, tell particularly on 
the vessels of the liver, and we may even suppose that the blood 
passing up the inferior cava may in such cases regurgitate into the 
hepatic vein. 
The result of this is a very great distention of the hepatic vein 
and its radicles—the central or intralobular veins. The distention 
extends to the capillaries, which, as in Fig. 252, are sometimes 
Fig. 252. 
Passive hypermmia of the liver. One lobule and parts of other two are shown. In the 
central parts of the lobules there is almost nothing but dilated capillaries containing blood- 
corpuscles only; a few atrophied and pigmented hepatic cells being visible. At the 
peripheral parts of the lobules the hepatic cells are seen, many of them pigmented. X 90. 
found enormously dilated. The dilated capillaries by pressure 
cause atrophy of the hepatic cells, and it often happens that the 
central parts of the lobules are entirely occupied by enormously 
dilated capillaries, while the hepatic cells are hardly visible (see 
figure). The remains of the hepatic cells frequently contain brown 
pigment-granules. The atrophy of the hepatic cells in these regions 
may be complete, only a few pigment-masses representing them. 
Sometimes, in addition to these changes, there is hypertrophy 582 
DISEASES OF LIVER, PANCREAS, AND PERITONEUM 
of the connective tissue surrounding the lobules, but this is usually 
inconsiderable, and it is a mistaken view that a cirrhosis of the 
liver arises out of passive hypersemia. 
The naked-eye appearances may be directly connected with 
these minute changes. At first there is a general enlargement of 
the organ, which, on section, appears unduly red. On closer 
examination it is seen that there are minute areas of a deep-red 
color corresponding with the central parts of the lobules, and 
these are surrounded by zones of a gray or yellowish color. The 
result is that the lobules are, as it were, mapped out by these con- 
trasting colors, and are for the most part individually visible to 
the naked eye. Sometimes several adjacent lobules are almost 
completely occupied by dilated vessels, and there is a narrower 
ring of normal tissue around each, so that the part of the liver as 
a whole has an almost cavernous structure, and presents a deeper 
red color on section. It is these variations in color and figuring 
which give the cut surface the appearance of the section of a 
nutmeg. 
In parts where there has been great loss of the proper tissue, 
the liver may appear to the naked eye after death partially 
atrophied. During life the dilated veins and capillaries are dis- 
tended with blood, but after death, the blood-pressure being 
removed, these may, to some extent, collapse. In this way the 
surface has sometimes an irregular appearance, which may be 
mistaken for that of cirrhosis, but it will be noticed that the 
depressed or atrophied parts have a deep-red color. 
THROMBOSIS AND EMBOLISM IN THE LIVER. 
Thrombosis of the portal vein is of somewhat frequent occur- 
rence, especially as a result of cirrhosis. It also occurs sometimes 
by propagation of a thrombosis from the radicles of the vein, or 
by embolism from them. The embolus may be a septic one, and 
there will be a phlebitis with the thrombosis. The coagulum in 
the vein, if not of a septic character, leads to a chronic inflamma- 
tion with adhesion in its neighborhood. The consequences to the 
liver itself, even of complete closure of the portal vein, are not so 
important as might be looked for. It is stated by some that it 
may lead to cirrhosis of the liver, but there is no proper founda- 
tion for this statement, and cirrhosis is much more frequently the 
cause than the result of thrombosis. It has also been asserted 
that diabetes mellitus may occur as a result of thrombosis of the 
portal vein. The consequences outside the liver are much more 
important. There is dilatation of the radicles of the portal vein 
in the abdominal viscera, with ascites, which is generally very 
extreme. The results in this regard are essentially similar to 
those which occur in cirrhosis, and are referred to more particu- 
larly below under that heading. 
Thrombosis and embolism of the hepatic artery are not of RETROGRADE CHANGES IN THE LIVER. 
583 
consequence unless the plug be of a septic nature. The hepatic 
artery is not an end-artery, and, if some of its branches be ob- 
structed, the anastomosing communications restore the circulation. 
If the main branch of the artery be obstructed, then we may have 
necrosis of the liver, but such an obstruction is scarcely liable to 
occur in man, and its effects have only been studied in experi- 
ments in animals. 
HYPERTROPHY OF THE LIVER. 
When considerable portions of the liver are destroyed, there is 
liable to be a compensatory hypertrophy of remaining parts. The 
loss of liver substance may be congenital, as in a case observed by 
the author in which, probably from some injury early in foetal life, 
the right kidney and the greater part of the right lobe of the liver 
were wanting. In that case the left lobe was greatly increased 
in size, and the liver as a whole was of the normal weight. There 
may be a similar compensatory hypertrophy from destruction of 
liver tissue in after-life. The destruction may be by pressure of 
hydatid cysts, syphilitic gummata, and cicatrices, or even by cir- 
rhosis. The region of the atrophy will determine that of the hy- 
pertrophy, but sometimes the left lobe or the lobus Spigelii under- 
goes great enlargement. 
Hypertrophy of the liver has been described as occurring in 
diabetes. Undoubtedly the liver is frequently enlarged in this 
disease. Some of the enlargement is due to hypersemia, and some 
to swelling of the hepatic cells. This latter is probably a true hy- 
pertrophy of the liver tissue. 
RETROGRADE CHANGES IN THE LIVER. 
Atrophy of the Liver.—We have already referred to the 
atrophy which occurs in passive hypersemia. In the preceding 
section also we have seen that pressure, as by a hydatid cyst, pro- 
duces atrophy. In old persons we meet with a senile atrophy, the 
organ as a whole being reduced in size, and more deeply colored 
than normal. 
Parenchymatous Infiltration of the liver occurs, as we have 
previously seen, in connection with many acute diseases. It is this 
which causes the enlargement of the liver in the acute fevers, 
pneumonia, erysipelas, etc. The hepatic cells are highly granular, 
and if the albuminous granules be destroyed by liquor potassse it 
will be seen that there are numerous tine fat-granules, the cloudy 
swelling passing into fatty degeneration. 
Fatty Degeneration is not common except as a further stage of 
the condition just mentioned, and as occurring in acute yellow 
atrophy to be presently described. 584 
DISEASES OF LIVER, PANCREAS, AND PERITONEUM 
Fatty Infiltration was referred to in a former part of this 
work, and its pathology considered (see p. 123). In this place we 
have to consider the locality of the fat and the changes it effects. 
In the normal liver there is very little free fat in the hepatic 
cells. In fatty infiltration fat is brought in quantity by the portal 
vessels and deposited in the hepatic cells. It is first deposited in 
those nearest the terminals of the portal vein, that is to say, in the 
peripheral parts of the lobules (see Fig. 253), so that at first each 
Fig. 253. 
Fatty infiltrations of the liver, osmic acid preparation as seen with a very low power. The 
peripheral parts of the lobules are demarcated by the fatty infiltration. X 16. 
lobule lias a peripheral zone of fatty infiltration. This is still more 
strikingly seen when a microscopic section is treated with osmic 
acid. The fatty peripheral parts become of a blackish color, and 
the section assumes a very striking figured appearance, as shown 
in the figure. As the condition advances, more and more of the 
lobule is affected, and the infiltration may overtake its whole ex- 
tent. Even in extreme cases, however, it usually preponderates at 
the peripheral parts. The fat is present in larger and smaller 
drops inside the hepatic cells, but the tendency is for the drops to 
assume a considerable size (as in Fig. 254). The protoplasm of 
the cells is pushed aside by the fat, but probably its function is not 
greatly interfered with. 
The fatty liver presents usually distinct appearances to the naked 
eye. According to the extent of the infiltration is the organ in- 
creased in weight, but in extreme cases it may be double the 
normal. The enlargement is general, the thickness especially AMYLOID DEGENERATION OF THE LIVER. 
585 
being much increased. The consistence is unduly soft, and the 
color more or less opaque yellow. If the infiltration be not ex- 
treme, so that the whole lobule is not infiltrated, then with the 
naked eye we can see on the cut surface the indications of its 
presence. The lobules are, in fact, mapped out in the most char- 
acteristic figured manner, so that, on looking closely, we can dis- 
tinguish each with perfect accuracy. The appearance presents a 
Fig. 254. 
Fatty infiltration of liver. The cells are isolated, and they contain larger and smaller 
drops of oil. X 350. 
considerable resemblance to that of the nutmeg liver, where also 
the lobules are mapped out; but in the fatty liver it is by unduly 
pale tissue at the peripheral parts of the lobules, which contrasts 
with the normal central parts; while in the other case it is the 
normal which is at the periphery, and it contrasts with the red 
central parts, and the whole cut surface is unduly red. 
Amyloid degeneration of the liver has already been considered 
in its general aspects (see p. 132). The degeneration appears first 
in* the arteries and capillaries, the appearance in the latter being as 
if, at intervals, the wall were swollen with a translucent material. 
In these earlier stages there is no difficulty in making out that 
inside the lobules it is the capillaries which are affected. The 
general arrangement of the capillaries is beautifully shown by the 
rose-pink color of the amyloid ones in a section stained with 
methyl-violet, the appearance being almost that of an injected 
specimen. Even in the earlier periods considerable atrophy of the 
hepatic cells can be observed as a result of pressure from the 
swollen capillaries, and the atrophic cells frequently contain fat. 
In advanced stages, however, the cells are very greatly destroyed, 
so that the liver tissue is replaced by amyloid substance. 
It is remarkable that with this great loss of the secreting sub- 
stance there is actual increase in size and weight of the liver. It 
is not uncommon to find the liver weighing two or three times the 
normal. The increase in size is not proportionate to that in 
weight, as the amyloid substance is of greater density than the 
liver tissue. The edges of the organ are rounded and its consist- 
ence elastic and resistant. The surface, and especially the cut 
surface, presents a peculiar translucent waxy appearance, which in 
advanced stages is highly characteristic. 586 
DISEASES OF LIVER, PANCREAS, AND PERITONEUM. 
We have already seen that amyloid degeneration of the liver is 
part of a general condition, and that it is associated with a similar 
condition in other organs, especially the spleen, kidneys, and in- 
testine. We also know that the amyloid disease is very often the 
result of a chronic tuberculosis, and it not infrequently happens 
that miliary tubercles are to be found in the amyloid liver. 
ACUTE YELLOW ATROPHY. 
This is a disease whose exact pathology is somewhat obscure. 
It is characterized by a rapid destruction of the hepatic cells, but 
the exact cause of this destruction is doubtful. It is obviously due 
to the action of a morbid poison circulating in the blood, because 
changes of a somewhat similar nature are met with in the epithe- 
lium of the kidneys, and in the muscular fibre of the heart, and 
elsewhere. This view also receives some confirmation from the 
fact that in acute poisoning with phosphorus changes occur in the 
liver and other organs very like those in the disease under con- 
sideration. In this regard also it is interesting to observe that two 
writers, "Waldeyer and Zander, have described colonies of bacteria 
as existing in the liver in cases of this disease. 
When the liver is examined after death it is generally found 
smaller than normal, and its tissue is soft and flabby. In some 
Fig. 255. 
From liver in acute yellow atrophy. The hepatic cells form irregular clumps. There are 
numerous pigment-crystals of similar shape to the crystals of hcematoidin (Figs. 5 and 11), 
and of a similar deep-red color, but smaller. X 350. 
cases it is of the normal size, and it is stated that in the earlier 
stages it is even enlarged, although the disease is not fatal during 
these periods. The capsule is often wrinkled from the atrophy of 
the substance of the organ, and the organ flattens out by its own inflammations of the liver. 
587 
weight, its thickness being greatly diminished. The diminution 
in size sometimes affects the left lobe especially. On cutting into 
the organ the section shows usually different shades of color. The 
predominating tint is yellow, varying from the color of gamboge 
to a dark yellowish-brown. Mixed with this, however, there is a 
red color forming the red substance of Zenker. Where the color 
is yellow the tissue is softest, but the red parts are the most 
atrophied, the red substance arising by the absorption of the 
degenerated hepatic cells. 
On examining the yellow tissue under the microscope, it will 
hardly be recognizable as that of the liver (see Fig. 255). There 
are no proper hepatic cells, but instead, larger and smaller fat- 
drops, with granular debris, and here and there rhombic crystals 
of a reddish-brown color (see figure). Sometimes leucine is found 
in opaque clumps, white in color and generally stratified. Acicular 
crystals of tyrosine are also found. The crystals of pigment, 
which resemble those found in old blood-clots in the brain, may 
be really formed from the biliary coloring matter. 
The red substance does not present the abundant fatty debris; 
that has been cleared away, and there is now a fibrous material 
visible, merely sprinkled with fat-granules. In some cases glan- 
dular-looking processes have been observed, and have been taken 
to indicate an attempt at regeneration of the lost hepatic substance, 
beginning in the capillary network of the hepatic ducts. 
INFLAMMATIONS OF THE LIVER. 
1. Purulent Hepatitis.—Abscess of the liver occurs in two 
forms, the tropical and the pysemic or metastatic abscess. 
(a) The tropical abscess is not met with in this country, except 
in persons who have been in hot climates, especially in India. 
Much doubt exists as to the cause of the inflammation which gives 
rise to the abscess. In a large proportion of cases it is associated 
with dysentery, and it is believed by many that the abscess in the 
liver arises by material being carried from the ulcerated intestine 
to the liver. This material presumably contains minute organisms, 
and the abscesses would be septic. This view, however, is not 
beyond question, and post-mortem examination shows that the 
tropical abscess is by no means uniformly associated with dysen- 
tery. While, therefore, we may admit that bacteria probably 
have to do with the causation of the tropical abscess, yet it is not 
unlikely that certain states of the liver predispose to their develop- 
ment, and that they may find entrance to the body by other paths 
than the intestine. 
The abscess is mostly solitary, and it may grow to large dimen- 
sions, causing great enlargement of the liver. Having approached 
the surface, it sometimes causes a marked projection from the 
liver. The capsule, being undermined, may undergo necrosis, 
and the abscess rupture by the separation of the slough. In this 588 
DISEASES OF LIVER, PANCREAS, AND PERITONEUM. 
case, the abscess may rupture into the peritoneum and cause fatal 
peritonitis. Or the capsule may adhere to the abdominal wall, 
and the abscess by and by find its way to the surface of the body, 
there to discharge. It also occasionally bursts in other directions, 
as through the diaphragm into the pleural cavity, or even the 
lung; into the colon or other part of the intestine; or into the 
gall-bladder from which the pus is carried into the duodenum. In 
these various ways the pus may be disposed, of and perhaps re- 
covery occur, but more probably a wasting discharge from the 
cavity of the abscess remains. 
In other cases the abscess does not enlarge, but rather dries in. 
A thick connective-tissue capsule forms around it like the wall of 
a cyst, and the pus thickens to a cheesy consistence. Afterwards 
the contents may become calcareous and the disease virtually ob- 
solete. 
(b) abscesses are much more definitely understood in 
their causation and mode of formation. They are undoubtedly 
produced by bacteria being carried by the blood to the liver and 
propagating themselves there. Sometimes the abscesses in the 
liver are secondary to those in the lungs, the organisms being 
carried on by the blood after having developed there. But there 
are cases where abscesses occur in the liver alone, and these also 
arise in connection with putrid external wounds. 
So long as it was supposed that, in order to the formation of 
such abscesses, an obstruction of an artery with an embolus was 
necessary, the occurrence of such abscesses in the liver was obscure. 
We know, however, that micro-organisms may be conveyed by 
the bloodvessels, and, after passing the pulmonary capillaries, be 
carried to the liver by the hepatic artery, or even, after traversing 
the intestinal capillaries, by the portal vein. We have already 
seen that the circulation in the capillaries of the liver is peculiarly 
slow, and it is probably for this reason that the bacteria so readily 
lodge there and propagate. 
Abscesses may also be induced in cases where there is stagna- 
tion of bile, and where decomposition occurs in the bile, extend- 
ing upwards from the intestine. Such abscesses will be referred 
to afterwards. 
The bacteria multiply and form zooglcea in the capillaries and 
interlobular veins, passing into the central veins. Wherever the 
colonies of bacteria extend, the liver tissue undergoes necrosis, the 
cells lose their nuclei, and become individually indistinguishable. 
We have already seen that this arises, not from the direct action 
of the bacteria, but by the chemical products which are given off. 
These irritating stuffs also produce inflammation around, and there 
is here, as elsewhere under similar circumstances, an acute sup- 
purative inflammation. The round cells accumulate around the 
necrosed portion, and gradually infiltrate‘it and break it down, so 
that an abscess forms. 
The abscess may be primarily a small or a large one according 
as the capillaries over a smaller or larger area are invaded, but INFLAMMATIONS OF THE LIVER. 
589 
several abscesses may ultimately coalesce, and so we have them 
sometimes of very considerable dimensions. 
The abscesses in this form are always multiple. In accordance 
with what has been stated the actual abscess is preceded by a gray 
or yellowish discoloration indicating the existence of necrosis of 
the tissue. There will be probably a group of such areas corre- 
sponding to necrosed hepatic lobules. Ultimately these break 
down and form a common abscess. 
2. Chronic Interstitial Hepatitis or Cirrhosis.—This is, for 
practical purposes, the most important affection of the liver, at 
least in this country. We have to do here with a chronic inflam- 
mation of the interstitial connective tissue of the organ. 
As in the case of other inflammations, we have to consider here 
the nature of the irritant which induces the inflammation. Leaving 
aside in the mean time the case of syphilis, which will be taken up 
afterwards, it may be said that, as the disease occurs for the most 
part homogeneously throughout this organ, the irritant is contained 
in the blood circulating in the liver. The name “ gin-drinker’s 
liver,” frequently applied to this disease, involves the view that 
alcohol is commonly the irritant. Alcohol taken frequently in 
the form of undiluted spirits is believed to cause the disease, while 
beer and wine do not. This is probably in most cases the cause, 
but the disease may originate from other kinds of irritation whose 
nature is obscure. This is evident from the fact that it has been 
met with in young children, and the author has recorded a case 
in which a typical cirrhosis with the usual secondary phenomena 
occurred in a cat. The fact that it was a butcher’s cat may indi- 
cate that it indulged in excess of eating rather than of drinking. 
It has been asserted of recent years that obstruction of the bile- 
ducts is a cause of cirrhosis, and a special form of “ biliary 
cirrhosis ” has been distinguished. The frequent occurrence of 
obstruction by gall-stones and otherwise without any of the ap- 
pearances of cirrhosis, however, rather contradicts this view. It 
is also stated that tuberculosis may induce cirrhosis, and there are 
some facts which seem to support this view. 
In cirrhosis we have chronic inflammation of the connective 
tissue of the liver, resulting in new formation of a similar tissue, 
which, like such inflammatory new-formation, has a special 
tendency to shrink. It will be proper to consider the distribution 
of this new formation and its effects on the hepatic tissue on the 
one hand and the bloodvessels and ducts on the other. 
The interstitial connective tissue of the liver follows, as we have 
seen, the portal vessels, forming a frame-work in which are sup- 
ported the portal vein and its branches, the hepatic artery and 
hepatic duct. The new formation occurs in the great majority of 
cases only in these regions, that is to say, outside the lobules. 
Cases have been described, however, in which the new formation 
has extended into the interior of the lobules (so-called intercellular 590 
DISEASES OF LIVER, PANCREAS, AND PERITONEUM. 
cirrhosis), but this is exceedingly rare; it is stated to occur in 
cases of syphilis of the new-born. As a rule the new formation 
occurs in such a way as to surround groups of lobules, so that as 
the disease progresses the liver is subdivided into larger and 
smaller areas, each representing a set of lobules surrounded by 
new-formed connective tissue (so-called multilobular cirrhosis). 
In other cases the new formation, although not extending into the 
interior of the lobules, is homogeneous in its distribution, occurring 
wherever there is fibrillated connective tissue, and so present at the 
peripheries of all the lobules (so-called unilobular cirrhosis). 
In the earlier stages the affected connective tissue is abundantly 
cellular, like granulation tissue, and the process of new formation 
is evidently similar in its details to that in other chronic inflam- 
mations (see Fig. 256). Along with these changes, however, there 
are appearances, which have received various interpretations. In 
Fig. 256. 
Cirrhosis of liver in early stage. The connective tissue is occupied by numerous round- 
cells which are involving the peripheral parts of the lobules, the hepatic cells being here 
frequently isolated in the midst of the round-cells. X 75. 
many cases there are elongated gland-like processes in the midst 
of the tissue which look like new-formed ducts. Some suppose 
them to be ducts in process of formation from the existing bile- 
ducts. Certain French observers regard this condition as a special 
feature of “ biliary cirrhosis,” and take the changes in the ducts 
as well as the other changes to be the result of obstruction. 
Hamilton has stated that these duct-like processes are really com- 
posed of hepatic cells which are in process of forming connective INFLAMMATIONS OF THE LIVER. 
591 
tissue. The most probable explanation is that they are really 
capillary ducts which have undergone enlargement, and so have 
become prominent. The normal capillary ducts are seated inside 
the lobules between the rows of hepatic cells. We shall see after- 
wards that the hepatic cells undergo great destruction in cirrhosis, 
but the capillary ducts may survive, and their epithelium may 
enlarge so as to give them the appearance of new-formed ducts. 
This appearance is only observed when the disease is in active 
progress, and the connective tissue shows a cellular character. 
If there were nothing more than the new formation of con- 
nective tissue hitherto mentioned, then the liver would be enlarged 
in this disease. In the earlier stages there is such enlargement, 
but the existence of the disease is not generally distinguished in 
these stages. On the other hand, Charcot and others have de- 
scribed a special form of hypertrophic cirrhosis in which very 
great enlargement of the organs occurs. In this condition the 
distribution of the new formation is unilobular, and the appear- 
ance of new formation in the ducts referred to above is manifest. 
It will be seen that the names biliary, unilobular, and hypertrophic 
cirrhosis are used to designate a condition whose pathological 
bearings can hardly be said to be fully established. 
As a general rule, the new-formed tissue undergoes develop- 
ment into dense connective tissue which has a tendency to shrink. 
By its shrinking it causes atrophy of the proper hepatic tissue. 
As the cirrhosis is usually multilobular, the contracting tissue 
isolates groups of lobules of larger or smaller size, and these, 
consisting of soft tissue, stand out somewhat when the liver is 
divided, or present themselves prominently at the surface. There 
are thus areas of remaining hepatic tissue which are being grad- 
ually encroached on by the connective tissue. The atrophy of the 
hepatic tissue takes place by the supply of blood being cut off. 
By the contraction of the new-formed tissue the portal vessels are 
narrowed, and there is in addition, according to Ziegler, thicken- 
ing of the internal coat of the portal vein, an endophlebitis oblit- 
erans, similar to the endarteritis obliterans which exists in cirrhosis 
of the kidney. This will increase the obstruction of the portal 
vessels. The hepatic artery is not much affected by the contract- 
ing tissue, and it is generally possible to inject it with considerable 
success. As it is the portal vessels which supply the proper 
hepatic capillaries, the hepatic cells will by these processes be 
deprived of their nutrition, while, as the hepatic artery supplies 
the connective tissue, the latter will be well nourished. 
The consequence of this is great destruction of the hepatic cells. 
To a large extent this takes place by fatty degeneration, and one 
can often see, in the midst of connective tissue, islands of remain- 
ing hepatic tissue consisting of little more than collections of oil- 
drops (see Fig. 257). The hepatic tissue is also commonly stained 
with bile-pigment of a yellow or brown color, and this we may 
associate with obstruction of the bile-ducts by the contracting 
connective tissue. For the most part the pigment is biliary, but 592 
DISEASES OF LIVER, PANCREAS, AND PERITONEUM. 
it is also to some extent blood-pigment arising from the obstruction 
to the circulation. The connective tissue is also commonly stained, 
and to the naked eye the cut surface has a yellow color, sometimes 
with here and there quite an orange tint. The name of the dis- 
ease, cirrhosis, was originally applied from the color of the altered 
organ. 
The gall-ducts are for the most part structurally unaltered. They 
are partially obstructed by the new-formed tissue, and, on account 
Fig. 257. 
Cirrhosis of liver in an advanced stage, shown with a very low power. There are great 
areas of fibrous connective tissue, in the midst of which are islands of hepatic tissue having 
an opaque appearance from the presence of fat in the cells. X 20. 
of reabsorption of the bile, there may be staining of the tissues 
and icterus. In some cases, as we have seen, and especially in 
hypertrophic cirrhosis, there is the appearance of new-formed bile- 
ducts, already referred to. 
The result of all these changes is not only atrophy, but distortion 
of the liver. The connective tissue contracts, and, as it is irregu- 
larly distributed, the contraction is irregular. The surface of the 
organ presents larger or smaller projections consisting of the less 
affected hepatic tissue between the cicatricial depressions. These 
projections may be comparatively large, forming the hob-nail 
appearance of the surface, or they may be smaller, giving a 
generally granular appearance. They are usually yellow or brown 
and opaque, being fatty and stained with pigment. Sometimes 
there is special shrinking of the left lobe, and generally there is INFLAMMATIONS OF THE LIVER. 
593 
dragging in of the edges, so that the liver assumes more of a 
compacted form, being perhaps even thicker than usual, but re- 
duced in superficies. It is dense to the feeling, and more tough 
to cut than normal. On the cut surface it may he possible with 
the naked eye to make out the gray connective tissue, with islands 
of opaque or pigmented hepatic tissue in it. 
In hypertrophic cirrhosis the liver is not only enlarged, hut 
smooth on the surface. Sometimes it is adherent to surrounding 
parts, and there may even be a fibrinous exudation on the surface. 
On section, also, the cut surface is much more homogeneous both 
in color and otherwise. 
Outside the liver the principal changes depend on obstruction 
of the portal circulation, which, it is obvious, must be very great. 
There is a chronic passive hyperremia in all the radicles of this 
vein, in the peritoneum, in the mucous membrane of the stomach 
and intestine, in the spleen, and so on. The most frequent conse- 
quence is ascites, but we also meet with hemorrhages from the 
mucous membrane, especially of the stomach and large intestine, 
as well as catarrh of these. The spleen is also enlarged. 
The obstruction of the portal vein often leads to widening of 
the venous channels which form communications between the 
portal radicles and the systemic veins. In this way we may have 
great dilatation of the internal hemorrhoidal veins (leading to 
piles) and of the hypogastric. The cutaneous branches of the 
latter often stand out prominently on the abdominal wall. The 
hemorrhoidal veins also communicate with the vesical, and these 
latter may undergo dilatation. There may also be widening of 
communications with the veins of the diaphragm and oesophagus, 
which have sometimes been found highly varicose. Another 
channel occasionally met with is a small vein which runs from the 
portal vein to the umbilicus. In some cases this is so much en- 
larged as to approach the size of the portal vein itself. 
The patient generally dies from the disorders due to the con- 
tinuous passive hypersemia—the persistent catarrh of the alimen- 
tary canal, perhaps with hemorrhages, the ascites, etc. There is 
great emaciation, and sometimes icterus. It is not clear that the 
mere loss of the function of the liver bears an important part in 
the fatal result. 
3. Perihepatitis.—This condition is an inflammation of the 
capsule of the liver, and it is always secondary to some other 
lesion. A chronic pleurisy of the right side often extends through 
the diaphragm, and causes inflammation of the subjacent perito- 
neum, including the under surface of diaphragm and upper sur- 
face of liver, so that firm adhesion is the result. This is often 
the case in phthisis pulmonalis. A general chronic or acute peri- 
tonitis usually involves the capsule of the liver as well as other 
parts of the peritoneum. Sometimes cirrhosis or syphilitic disease 
of the liver extends to the capsule. 594 
DISEASES OF LIVER, PANCREAS, AND PERITONEUM. 
The inflammation is in most cases chronic, and results in a 
thickening of the capsule. Sometimes there are shaggy papilliform 
projections from the capsule, which have been compared to the 
Pacchionian bodies of the dura mater. There is frequently also 
adhesion to the parts around, especially to the diaphragm. The 
thickened capsule undergoes contraction like the new-formed 
connective tissue in other inflammations, and the result frequently 
is considerable deformity of the liver. This is most marked when 
there is a general inflammation of the capsule as in cases of chronic 
peritonitis. The capsule contracting all round the liver doubles 
in its sharp anterior edge, and causes the organ to assume an ap- 
proach to the globular shape. The contraction causes also atrophy 
of the liver tissue, and seriously interferes with the circulation in 
the organ. This deformity of the organ may be compared with 
that of the lung which occurs in consequence of the contraction 
of the pleura in chronic pleurisy, especially with empyema. 
SYPHILITIC DISEASE OF THE LIVER. 
Syphilis manifests itself for the most part as an indurative in- 
terstitial inflammation, with or without the formation of gummata. 
There may be a cirrhosis indistinguishable from the ordinary forms 
of this disease, and only judged to be syphilitic from other circum- 
stances. Sometimes in the midst of the general new-formation of 
connective tissue there are numerous small gummata, distinguished 
especially by their caseous condition. 
For the most part, however, the disease is localized. To the 
naked eye the liver is seen to present one or several cicatrices 
which often make deep indentations in its surface. These cica- 
trices are most frequent in the neighborhood of the suspensory 
ligament. On cutting into the middle of the cicatrix a gumma- 
tous tumor is usually divided with its caseous central part. The 
periphery of the gumma is not distinctly demarcated from the 
surrounding connective tissue which extends outwards into the 
hepatic tissue. Other gummata may be found more deeply in the 
liver tissue, and these also are surrounded by cicatricial tissue. 
The cicatrix is composed of fibrous tissue, and the gumma itself 
frequently presents irregular strands of connective tissue, but 
giving place to round-cell tissue. The central caseous portion 
contains merely granular debris (see Fig. 258). Sometimes at the 
periphery of the gumma there is great dilatation of bloodvessels, 
giving almost a cavernous appearance. 
When there are a considerable number of gummata, the cirrhosis 
may be nearly continuous, but with special cicatricial contraction 
at intervals corresponding to the gummata. The liver in this way 
may assume a very striking appearance, as if subdivided into 
manifold small lobes. Be the cicatrices large or small in number, 
the lobed and subdivided condition is characteristic of the syphilitic 
liver. TUBERCULOSIS OF THE LIVER. 
595 
The liver is sometimes found affected in infants who are the 
subjects of congenital syphilis. It may be a general induration 
forming a cirrhosis, usually of the hypertrophic form, with perhaps 
numerous small gummata; or the induration maybe more localized, 
but never with that cicatricial condition which we find in acquired 
Fig. 258. 
Gumma of liver, a, normal hepatic lobules; l, recent tissue of gumma with dilated blood- 
vessels; c, caseous part of gumma; d, d, d, connective tissue outside gumma extending into 
the hepatic tissue. X 16. 
syphilis. The connective-tissue formation in this case does not 
confine itself to the neighborhood of the portal vessels, but extends 
into the lobules, so that between the cells and around the capillaries 
there is connective tissue. 
TUBERCULOSIS OF THE LIVER. 
In acute miliary tuberculosis the liver is almost without excep- 
tion the seat of myriads of minute tubercles which are usually 596 
DISEASES OF LIVER, PANCREAS, AND PERITONEUM. 
invisible to the naked eye. In phthisis pulmonalis examination 
very often shows the presence of tubercles in the liver, but much 
more sparsely distributed, and often associated with fatty infiltration. 
The tubercles are situated in the connective tissue, and are there- 
fore outside the lobules. They present (Fig. 259) the usual con- 
Fig. 259. 
Tubercle of liver from a case of acute miliary tuberculosis. The tubercle is of a rounded 
form, and presents chiefly round cells with three giant-cells in the midst of these. X 75. 
stituents; round cells with large giant-cells in their more central 
parts. Very often the central parts are already caseous, or in more 
acute cases they may he affected by a more ordinary fatty degener- 
ation with distinct refracting oil-drops. 
Along with the eruption of tubercles there is some interstitial 
inflammation affecting the connective tissue, and evidenced by the 
presence of round cells, hut in acute miliary tuberculosis this is 
not usually considerable. 
Besides this form of tuberculosis we sometimes meet with a con- 
dition in which numerous larger caseous tubercles are present, and 
are associated with a much greater indurative inflammation. The 
nodules are distinctly visible to the naked eye and sometimes are 
as large' as peas. The larger ones may soften in the central parts 
and so small cavities may result. Cases have also been described 
in which large solitary caseous tubercles have occurred, like the 
scrofulous tubercles of the brain, but all these forms are exceed- 
ingly rare. 
TUMORS OF THE LIVER. 
Primary tumors of the liver are not very common, hut secondary 
forms, especially cancers, are frequent. 
Cavernous Angioma of the liver is the commonest form of 
primary tumor. Its structure has already been described (see p. TUMORS OF THE LIVER. 
597 
194). It develops apparently by dilatation of the existing capil- 
laries and atrophy of the intervening hepatic cells. Subsequently 
the walls of the capillaries become thickened by new-formation of 
connective tissue and converted into the trabeculae of the cavernous 
tumor (Fig. 260). Hence it is that the tumor replaces a certain 
Fig. 260. 
Aogioma of liver. X 90. 
portion of hepatic tissue. When seated immediately under the 
capsule the tumors are visible as red blotches, and on section they 
have a red color and collapsed appearance, and usually it is only 
after the blood is washed out that the white trabeculie become 
visible. The tumors present great varieties of size and may be as 
large as the fist. 
A case has been described by Ziegler of multiple Fibroneuroma 
in the liver on the fibres of the sympathetic, there being similar 
tumors on the various nerves of the body except the olfactory and 
optic. 
Concerning Adenoma of tlie liver there is considerable variety in 
statement and opinion, mainly because on the one hand this form 
of tumor is rare, and on the other there are tumors concerning 
which it is difficult to say whether they should be called cancers or 
adenomas. There is one form of adenoma about which there is 
not much doubt; it is that already mentioned in the general 
section. It is sometimes designated nodular hyperplasia, and 
occurs as solitary or multiple tumors which, while perfectly defined, 
have the same structure as the proper hepatic tissue, the cells being 
usually larger and some having double nuclei. If single, they may 
reach the size of a cherry or larger; if multiple, they are smaller. 
The larger ones are sometimes surrounded by a connective-tissue 
capsule. These tumors are of no practical consequence and are 
met with accidentally. They are not uncommon in the liver of 
the dog. 
Another form sometimes called tubular adenoma is described, 
in which, while the individual cells are like those of the liver, they 
are arranged not in groups like the acini of the liver, but rather in 
gland-like masses, which have been compared to the convoluted 598 
DISEASES OP LIVER, PANCREAS, AND PERITONEUM. 
tubules of the kidney. It is clear from the epithelial character of 
these glandular masses that the structure approximates to that of 
cancer, and indeed some of these cases can hardly be distinguished 
from cases of cancer. The adenoma may grow to a considerable 
size, while secondary tumors develop in the hepatic tissue around. 
This latter fact again suggests cancer, and an observation by Pro- 
fessor Greenfield in which tumors formed by metastasis in the 
lungs is still more suggestive. According to some the glandular 
processes grow from the liver cells, while others hold that they 
sprout out from the bile-ducts. 
Primary Cancer of the liver is of rare occurrence, and yet 
several varieties are described. The cancer may be in the form ot 
several small tumors, or a large growth infiltrating a considerable 
portion of the liver. The structure resembles that of tubular 
glands but less regularly formed than in the case of the adenoma, 
and more interpenetrating among the proper hepatic tissue. 
Another form has been described in which the cancer originates 
in the bile-ducts, and the cancerous processes have at first their 
seat in the connective tissue accompanying the portal vessels, etc. 
There are in this form numerous tumors which follow the portal 
distribution. They may cause obstruction of the ducts and the 
formation of cysts with bile-stained contents. 
Secondary Cancer is exceedingly frequent in connection with 
primary cancer of the stomach, pancreas, and large intestine, but 
it occurs also in cancers of the uterus, the oesophagus, and mamma. 
In the case of these last-mentioned localities the metastasis is pro- 
duced by the way of the hepatic artery, while in the other case it 
is by the portal vein. We shall afterwards discuss in a separate 
section the subject of the secondary extension of cancers of the 
abdomen. 
In the great majority of cases the primary seat of the cancer is 
the stomach, and next to that it is the large intestine, and the 
secondary tumors arise by pieces of active cancerous tissue being 
carried to the liver by the portal vein. We shall see afterwards 
that there is reason to believe that, in some cases at least, the 
cancerous material does not come directly from the primary 
tumor. As the cancer is sown in every part of the liver, the con- 
sequence is the development of numerous tumors which may be 
found in all stages of growth. 
It is usual to find a large number of isolated tumors of circular 
form and pale color (see Fig. 261). They are seated in the liver- 
tissue, but those near the surface produce rounded elevations of it 
which can often be felt through the abdominal parietes during life. 
Even to the naked eye the tumors show evidences of fatty degener- 
ation in the appearance of opaque yellow coloration. The absorp- 
tion of the degenerated cells is also indicated by the partial con- 
traction of the larger tumors in their central parts, producing in 
the superficial ones a dimpling or umbilication of the rounded TUMORS OF THE LIVER. 
599 
projections. The liver, as a whole, is sometimes enormously 
enlarged, weighing not infrequently as much as ten or twelve 
pounds. 
In some cases the new-formation is not so much in the form of 
individual tumors as a general cancerous infiltration, as if almost 
Fig. 261. 
Pieces of liver with secondary cancerous tumors in it. A larger one, a, is viewed from the 
surface. Another large one, b, in section. There are several smaller tumors, c, c. cl, a vein 
in section. (Virchow.) 
throughout the liver a simultaneous development had occurred, 
and the cancerous tissue had grown vigorously, displacing the 
proper hepatic tissue. 
In structure the tumors follow the primary ones. For the most 
part it is soft cancers of the stomach that form the original tumors, 
and we have a well-formed stroma with irregular masses of epithe- 
lial cells. But sometimes the primary tumor is an epithelioma, 
and in that case the tumors in the liver are usually fewer in 
number, firmer and more distinctly defined. When the primary 
tumor is in such a position that the cancer reaches the liver by the 
hepatic artery, the tumors are usually smaller in size and the liver 
not so much enlarged. This was at least very strikingly true in a 
case seen by the author where the primary tumor was in the 
mamma. 
The cancerous material, as it is brought by the bloodvessels, 
develops inside them, and particularly in the portal vessels. It 
seems also that the tumor to a large extent develops by growing 
inside the capillaries, although also in the spaces in the connective 
tissue. The consequence of this great new-formation in the vessels 
is atrophy of the hepatic cells. These are often to be seen at the 
peripheral parts of the tumors arranged in concentric layers as the 
pressure is exercised, and they undergo atrophy. It is asserted by 600 
DISEASES OF LIVER, PANCREAS, AND PERITONEUM. 
several authors that the cancerous tissue sometimes develops di- 
rectly from the tissue of the liver, arising largely by a transforma- 
tion of the latter. This is supposed to be effected by the influence 
of some infective material brought from the primary tumor, which 
induces the hepatic tissue to undergo this peculiar change. This 
view, however, stands in need of confirmation. 
The hepatic cells are often deeply stained with bile, and it is 
clinically of importance that the whole white structures of the 
body are usually jaundiced. This implies that the ducts are ob- 
structed, and the biliary coloring matter absorbed into the circu- 
lation. The numerous developing tumors press on the bile-ducts 
and obstruct them, and this occurs all the more as the growths 
arise by embolism of the portal vessels, and are, in the first place, 
related to them. As the ducts are in the immediate neighborhood 
of these vessels, they are liable to be pressed on very soon. The 
hepatic cells are frequently of a greenish color, and the biliary 
pigment is sometimes extensively deposited in them as brown 
granules. 
The portal vessels suffer obstruction, not only by the pressure 
of the tumors, but as being the seat of their primary growth, and 
hence we meet with ascites as a common result. 
Sarcoma is of occasional occurrence in the liver in the spindle- 
celled and pigmented forms. Some cases of melano-sarcoma have 
been described as primary tumors, but secondary tumors following 
melanotic sarcomas of the eye are more common. The liver may 
be largely occupied by these black tumors, and greatly enlarged. 
Here also the growth appears to occur in the bloodvessels and 
results in destruction of the hepatic tissue proper. 
PARASITES OF THE LIVER. 
These have already been somewhat fully described. The most 
important constitute the hydatids of the liver arising from the 
taenia echinococcus. When the liver is examined after death there 
is found a sac or sacs of very various size, up to that of a man’s 
head. The larger ones produce necessarily great enlargement of 
the liver as a whole, and atrophy of the hepatic tissue around 
them. They present first a connective-tissue capsule, inside which 
the proper wall of the cyst appears. As the vesicles are some- 
times much broken down, and it may even be difficult to find 
hooklets, it is important to remember that the proper cuticula of 
the cyst is lamellated (Fig. 146, p. 273). Sometimes the contents 
of the cyst, after the death of the parasite, form a fatty athero- 
matous or mortary material, in the midst of which pieces of this 
chitinous membrane may be found with its characteristic lamella- 
tion. The multilocular and exogenous forms of hydatids are to 
be remembered, the former resembling colloid cancer in its general THE BILE-DUCTS AND GALL-BLADDER. 
601 
appearance. Flukes do not frequently occur in the human liver, 
yet they have been observed (see p. 261). 
B.—THE BILE-DUCTS AND GALL-BLADDER. 
Gall-stones.—As gall-stones not infrequently form the primary 
cause of further disease of the bile-ducts, we may begin our de- 
scription with them. They are of very frequent occurrence, espe- 
cially in people past middle life, and they are often found in the 
gall-bladder after death without their existence having been sus- 
pected during life. 
The cause of their formation is very obscure. They are formed 
in the gall-bladder by the deposition of the constituents of the bile, 
chiefly cholestearine, and next to that bile-pigments, hut also lime 
and magnesia salts in varying proportions. Probably stagnation 
of the bile in the gall-bladder at least predisposes to their forma- 
tion, and this is rendered the more probable from their more 
frequent occurrence in old people where the actions are sluggish. 
In the centre of gall-stones there is frequently a nucleus composed 
of remains of epithelium or mucus. 
Gall-stones occur singly or in numbers. The single gall-stones 
are commonly composed almost purely of cholestearine, of which 
there may be over ninety-eight per cent. They are oval in shape, 
somewhat nodulated on the surface, and have a glistening appear- 
ance, altogether not unlike that of a sugar-plum. When divided 
or broken they present a characteristic radiating appearance from 
the centre, and also sometimes a concentric stratification. The 
broken surface has the same glistening appearance as the outer 
surface, and distinct scales can be separated. The stone is very 
light in weight, floats in water, and has a soft almost soapy feeling. 
Multiple Gall-stones are more frequent, and although some- 
times nearly pure, they are more frequently composed of choles- 
tearine mixed with bile-pigment and lime salts. There may be 
two or three, hut they may be present in large numbers, fifty, a 
hundred, or several hundreds. If few they may he comparatively 
large, but if numerous they are small, the bladder sometimes 
having the appearance of a bag filled with peas. The multiple 
stones are always facetted, taking their shape according as there is 
room, and fitting into each other. In appearance they have been 
compared to the macerated carpal bones, having somewhat similar 
facets, and often presenting a similar grayish color, although some- 
times yellow, brown, or even black. They are very light in weight, 
and on section present little of the glistening appearance or radi- 
ating arrangements of the single ones, being rather stratified, more 
deeply pigmented strata alternating with less. 
Gall-stones are sometimes met with which are composed almost 
entirely of bile-pigment. They are small and nearly black, and 
occur in considerable numbers at a time. They are very rare. 602 
DISEASES OF LIVER, PANCREAS, AND PERITONEUM. 
Sometimes there are stones composed mainly of lime salts, espe- 
cially the carbonate, but these also are very rare. 
The calculi may remain long in the gall-bladder, which may be 
found full of them, and with no bile in it. Its mucous membrane 
may he inflamed, and the calculi surrounded by an abundant 
mucous secretion. 
On the other hand a gall-stone often passes into the cystic duct, 
where it may remain for a time and obstruct it. After a time it 
often passes on into the ductus choledochus. The last part of this 
duct is narrow, and, if the stone is of any considerable size, it 
usually sticks here, at least for a time. By dilating the duct it 
may get into the duodenum, but very commonly it does not find 
its way through without ulceration, and sometimes it ulcerates into 
the peritoneum, producing inflammation of this serous membrane. 
Lying at the mouth of the ductus communis it obstructs the out- 
flow of bile and produces the results to be presently described. 
When it gets into the duodenum it usually passes off with the 
feces, but if large, it may produce obstruction of the intestine at 
some point. This is of rare occurrence, and only in the case of 
large stones, chiefly of the solitary kind. 
Obstruction of tiie Bile-ducts and its Results.—Obstruction 
occurs from various causes, of which the commonest is that just 
considered, namely, gall-stones. Inflammation of the ducts 
sometimes produces obstruction, the inflammation being nearly 
always secondary. It occurs most frequently at the terminal por- 
tion of the ductus communis from prolongation of catarrh from the 
stomach and duodenum. As the duct here is narrow a trivial 
inflammatory swelling may produce an obstruction, which the bile, 
possessing a low pressure, is unable to overcome. Then gall- 
stones themselves may produce inflammation, leading to a more 
or less prolonged closure of the ducts. We shall see afterwards 
that inflammation is not infrequently a consequence of obstruction, 
and these two should not be confounded. Tumors and inflamma- 
tions around the duct may cause obstruction. This is not infre- 
quently the case with cancers where the head of the pancreas or 
the lymphatic glands in the portal region of the liver are engaged. 
We have already seen that an obstruction of the hepatic ducts in the 
substance of the liver occurs in cancer of the liver, in cirrhosis, etc. 
The results of obstruction vary according to the site of the 
obstruction. 
If the cystic duct alone be obstructed, then the consequence is 
that no bile can get into the gall-bladder. In that case the bladder 
may shrink, and any mucus in it dry in and perhaps afterwards 
become chalky. In many cases, however, there is an abundant 
secretion of mucus, and the bladder gets filled with it. The mucus 
often after a time gives way to a more fluid secretion, and the 
bladder may be converted into a tliin-walled cyst, which may be 
as large as the fist, with clear fluid contents. When the gall- 
bladder is thus cut off and no longer available as a store for the THE BILE-DUCTS AND GALL-BLADDER. 
603 
bile, there sometimes occurs a dilatation of the larger bile-ducts, 
so that the bile may lie here instead of in the gall-bladder, and 
pass into the duodenum during digestion. This constitutes an 
imperfect compensation for the loss of the gall-bladder. 
In the case of obstruction of the ductus ciioledochus, there is 
of course stagnation both in the gall-bladder and in the whole 
system of bile-ducts. The stagnation tells first on the gall-bladder, 
which dilates readily and stores up the bile. There may even be 
rupture of the gall-bladder from excessive dilatation. If the ob- 
struction be prolonged, great dilatation occurs throughout the 
whole system, and serious changes frequently result in the liver 
itself. 
Next to the gall-bladder, the ductus choledochus and the larger 
bile-ducts, which are not supported by the firm liver tissue, are 
most liable to dilate. This dilatation may be very extreme, these 
ducts becoming sometimes as great in external size as the thumb, 
and sometimes even going on to rupture. 
In the liver itself the dilatation is not generally so great, at least 
at first, but if prolonged it may lead to serious dilatation after- 
wards. The first result on the proper hepatic tissue is staining of 
it with the bile-pigment. The hepatic cells assume a deep yellow 
color, most marked at the peripheral parts of the lobules, being 
the parts nearest the bile-ducts. In these the bile-pigment is often 
deposited in the granular form, as green or brown masses. The 
pigment, which is at first brown, may, after the tissue has heen in 
alcohol or other fluid, become green. These conditions indicate 
the reabsorption of the bile, and this is also manifested in the 
staining of all the tissues of the body, forming a general jaundice. 
The absorbed biliary coloring matter is often deposited in the 
uriniferous tubules of the kidney, presumably in the process of 
excretion. 
Sometimes considerable atrophy of the proper tissue of the liver 
occurs, and we have the smaller bile-ducts dilated and forming 
numerous cavities or cysts througout the liver. This probably 
does not occur without inflammation of the ducts, and may be 
accompanied by ulceration, so that the cysts are cavities like those 
occurring in the lung from dilatation of bronchi : they contain 
inflammatory products as well as bile. 
There is sometimes even a more definite acute inflammation of 
the bile-ducts apparently from decomposition of the bile, and this 
may lead to what may be called biliary abscesses, which contain 
a mixture of pus and bile. These abscesses may contain gall- 
stones deposited by the stagnant bile, and the irritation set up by 
these may have been concerned in causing the inflammation. 
According to Charcot and others, as previously mentioned, the 
stagnation sometimes leads to inflammation of the connective tissue 
of the liver, producing cirrhosis of the hypertrophic kind. 
Tumors of the Bile-ducts and Gall-bladder.—Of these the 
most important are the cancers. We sometimes meet with pri- 604 
DISEASES OF LIVER, PANCREAS, AND PERITONEUM. 
mary cancer of the gall-bladder resembling in structure cancer of 
the stomach and intestine. By extension it may largely involve 
the liver tissue. We have already seen that some of the cancers of 
the liver probably take origin in the finer bile-ducts in its substance. 
C.—THE PANCREAS. 
In some aspects the diseases of the pancreas are not of very 
great practical importance. Although the secretion of the gland 
is known to have important functions in the digestion of food, the 
starches, albuminates, and fats being all affected by it, yet lesions 
of the gland which destroy its functions seem to be compensated 
by the other secretions of the alimentary canal. On the other 
hand, the diseases of this organ, and especially cancers, may affect 
neighboring structures, and cause serious disturbances around. 
The pancreas has the structure of a salivary gland, consisting 
of glandular acini whose ducts communicate with a main duct 
lying in the centre of the gland (Wirsung’s duct) and opening 
into the duodenum in common with the ductus choledochus. 
The pancreas is occasionally the seat of hemorrhages into its 
substance. These may be the result of injuries to the abdominal 
wall or the consequence of passive hyperaemia in diseases of the 
heart, lungs, or liver. Some cases of sudden death have been 
recorded by Zenker, Hooper, and Klebs, in which the most obvious 
lesion was hemorrhage into the substance of this gland. It is 
supposed that the lesion caused pressure on the neighboring coeliac 
plexus and semilunar ganglion and a consequent reflex paralysis 
of the heart, just as paralysis of the heart is producible by blows 
on the abdomen (Goltz’s experiment). 
Inflammations of the pancreas are of various kinds. We have 
suppurative pancreatitis like suppurative parotitis, resulting in 
abscesses; also indurative interstitial inflammation with loss of 
gland tissue, this condition being sometimes of syphilitic origin. 
Atrophy of the pancreas is observed often as a part of general 
emaciation, hut it has been found in a good many cases of diabetes 
mellitus. It can hardly be held that the destruction of the function 
of the pancreas is the cause of the diabetes, and the probability is 
that, as Klebs suggests, the primary condition is disease of the 
coeliac plexus causing vaso-motor paralysis (see p. 78). 
Fatty Infiltration of the pancreas is one of the commonest 
lesions of this gland. There is normally some adipose tissue in 
the midst of the gland, and this sometimes undergoes considerable 
increase, the proper glandular substance becoming atrophied, and 
adipose tissue taking its place, the shape and general appearance 
of the gland being preserved. The condition may be part of a 
general obesity, or it may occur in old age, and, in this latter case, the pancreas. 
605 
it may be presumed that atrophy of the glandular tissue is the 
first condition, the adipose tissue developing afterwards, as in 
fatty infiltration of voluntary muscle. 
The glandular structure sometimes undergoes cloudy swelling 
in common with that of the liver and other organs in the acute 
fevers. Fatty degeneration is also met with. 
Tuberculosis is not common in the pancreas, hut we meet with 
caseous masses having the characters of a local tuberculosis. 
More frequently the pancreas is involved secondarily in a tubercu- 
losis arising in neighboring lymphatic glands. 
Of the tumors of the pancreas, cancer is by far the most im- 
portant. It occurs most frequently in the head, rarely in the body 
or tail. It is mostly a dense tumor of fibrous appearance (scirrlius), 
but cases of soft and of colloid cancer have been seen. The cancer 
often produces obstruction of Wirsung’s duct, or produces still 
more serious results by obstructing the ductus choledochus. It 
may even by its retraction cause a partial obstruction of the 
duodenum. There may arise in this way considerable disturbances 
from the continuous extension of the tumor. We may also have 
secondary tumors in lymphatic glands, liver, or peritoneum. It is 
to be added that cancer of the stomach or duodenum may extend 
to the pancreas, and that the gland may be the seat of metastatic 
tumors when the disease becomes generalized. 
The Pancreatic Duct (Wirsung’s) is liable to certain changes. 
Concretions occur in it, comparable to those of the salivary glands. 
They are mostly round or oval, and white or grayish-white. In 
size they have been met with as large as a hazel-nut or larger, but 
they are usually small like grains of sand. They are composed 
chiefly of carbonate and phosphate of lime. They very often arise 
in dilated ducts, but if large may cause dilatation by obstructing 
the duct. 
Obstruction and dilatation of Wirsung’s canal may arise, as 
w7e have seen, from calculi, cancers of the head of the pancreas, or 
from tumors in the neighborhood. Dilatation also occurs second- 
arily to atrophy of the gland. The dilated duct forms a series of 
pouches, or else there is a more definitely localized dilatation so 
that actual cysts are formed. This latter will occur vdien the 
orifice is completely obstructed; the cysts may reach the size of 
the fist or that of a child’s head, and these are sometimes desig- 
nated ranula pancreatica. The contents of the dilated duct may 
be simply the fluid secretion, but sometimes there is thickening of 
the contents and even hemorrhage. In this way wre may have 
coagula causing the cysts to look like aneurisms, all the more as 
the lining of the cyst may become the seat of calcareous plates 
like the internal coat of an artery in aneurism. 606 
DISEASES OF LIVER, PANCREAS, AND PERITONEUM. 
D.—THE PERITONEUM. 
Introductory.—The peritoneum which is stretched over so 
many different organs, and has so many recesses and pouches, is 
very liable to he affected by diseases having their source outside 
itself. 
It is necessary here to make some reference to the general rela- 
tions of the peritoneal sac. It is a large lymph-sac and fluid is 
continuously circulating through it. The surface of the membrane 
is covered with endothelium, and there are innumerable apertures 
or stomata by which it communicates with lymphatic vessels 
beneath. It is proved by experiment that finely divided solid 
material introduced into the peritoneal cavity is very readily ab- 
sorbed and carried into the lymphatics. The transudation fluid 
which normally passes out of the bloodvessels is doubtless absorbed 
by the stomata throughout the peritoneum, but there are two 
localities in which its absorption presents points of peculiar interest. 
From certain facts to be afterwards referred to in connection 
with tuberculosis and cancer of the peritoneum, it may be inferred 
that the great omentum is specially concerned in the process of 
absorption. This double layer of peritoneum lying free in the 
cavity may be regarded as a drain by means of which the fluid is 
drawn off*. 
The relation of the diaphragm to the process of absorption is 
also important, and has already been referred to in considering the 
subject of acute pleurisy. The lymphatics of the diaphragm com- 
municate on the one hand with the peritoneal sac and on the other 
with the pleura, so that fluid and finely divided solids may be 
carried through from one to the other. It is probable that the 
general course of the current is from peritoneum to pleura, 
although it may be reversed. 
It is very important to bear in mind this great power of absorp- 
tion possessed by the peritoneum, especially in relation to septic 
processes. The products of septic decomposition as well as the 
organisms which produce these changes may be absorbed, and that 
sometimes in such quantity as to produce fatal results before they 
have had time to induce any considerable local effects. Hence it 
is that septic processes in the peritoneum are so serious and lead 
so commonly to septicaemia. 
The fluid in the peritoneal sac is not at rest, but circulates, and 
the movements of the intestines doubtless have to do with its trans- 
portation from place to place. This fact is also of great impor- 
tance, because we shall find that when any pathogenetic agent is 
introduced into the peritoneal cavity it is generally carried to every 
part of the sac and produces its effects in every region. Abundant 
examples of this are afforded by tuberculosis of the peritoneum, 
inflammations, and so on. 607 
THE PERITONEUM. 
DISORDERS OF THE CIRCULATION IN THE PERITONEUM. 
Active Hyperemia of the peritoneum is not a condition of much 
practical importance. It is produced when from any cause a 
general relaxation of the arteries in the sac occurs. Leaving 
inflammation out of account, this will hardly occur except as a 
result of sudden removal of extra pressure from these vessels. If 
a large ovarian tumor be removed from the abdomen, or ascitic 
fluid drawn off, the arteries, which have previously accommodated 
themselves to the undue pressure on their walls, will relax, and a 
hypersemia result. The hypersemia may result in the occurrence 
of a peculiar form of chronic hemorrhagic peritonitis, compar- 
able with hemorrhagic pachymeningitis (see p. 442), the effused 
blood being here also sometimes a prominent feature (hematoma 
of the peritoneum). As in the other case it may be a question 
whether there is an inflammation preliminary to the hemorrhage, 
or whether the hypersemia induces bleeding, the succeeding organ- 
ization of the clot leading to the formation of a membranous layer 
on its surface. Where ascitic fluid has been drawn off many times, 
there may be several layers of soft membrane on the surface of the 
peritoneum, the innermost being the most delicate and the newest. 
Passive Hyperemia occurs as a result of obstruction to the 
portal circulation either alone or as a part of a general venous 
hypersemia. It is chiefly important in relation to ascites, of which 
it is the most frequent cause. 
Ascites.—This name is given to dropsy of the peritoneal cavity, 
and it occurs as the result either of excessive transudation of fluid 
from the bloodvessels, or diminished absorption by the lymphatics. 
It is sometimes merely a part of a general oedema, occurring in 
diseases of the heart and lungs, in Bright’s disease, and in anaemic 
states. But it is peculiarly prone to occur when the portal circu- 
lation is specially obstructed. This may happen by the portal 
vein being the seat of thrombosis, or pressed on from without, but 
more frequently it is by some lesion in the liver itself, such as cir- 
rhosis or cancer, which obstructs the portal vessels, as it were, in 
detail. 
In these cases 1he ascites is from increased transudation, and it 
is much less common to have it occurring from interference with 
absorption. This may have something to do with it, however, in 
cases of cancer of the peritoneum, where the numerous cancerous 
tumors originate from material carried into the lymphatic channels 
and growing there. These tumors will necessarily obstruct the 
lymphatics to a large extent in detail, although they may also 
produce by their irritation a hypersemia of the peritoneal vessels. 
In a similar way the dropsy of tuberculosis of the peritoneum, 
although mainly inflammatory, may to some extent be referred to 
obstruction of the paths of absorption. 
Ascites is of occasional occurrence in connection with obstruc- 608 
diseases of liver, pancreas, and peritoneum. 
tion of the thoracic duct by tumors, aneurisms, thrombosis, etc., 
interfering with the duct or with the vein into which the duct 
opens. If the obstruction be complete, there is great distention of 
the duct and its radicles below the seat of obstruction. Occasion- 
ally an actual rupture occurs, and the chylous fluid passes into the 
pleural or the peritoneal cavity. The fluid is in this case a whitish 
milky material, and we have the conditions named respectively, 
chylous hydrothorax and chylous ascites. The fluid contains 
abundant leucocytes in which are fat-granules. 
The fluid in ascites is contained in the general sac of the peri- 
toneum, hut where adhesions have previously existed it may be 
confined to particular parts, and sacculated. Sometimes also, in 
children, there is a dropsy between the folds of the omentum. 
The character of the fluid in ascites is that of ordinary transuda- 
tions, a clear, slightly yellow, limpid fluid of low specific gravity. 
After it has stood for a time it often deposits a very gelatinous 
coagulum of fibrine. In some cases the fluid is slightly milky 
(chylous ascites). 
In prolonged ascites the peritoneum is apt to get somewhat 
thickened, especially when puncture has been frequently per- 
formed. The great omentum is not infrequently gathered up so 
as to be thicker and shorter than usual, and in that case it will act 
less efficiently as a drain. 
INFLAMMATIONS OF THE PERITONEUM.—PERITONITIS. 
Inflammation of the peritoneum is very seldom spontaneous in 
its origin. It seems remarkable that, compared with the pleura or 
pericardium, this membrane is so seldom the seat of independent 
inflammation as a result, for instance, of the. irritation of the blood 
in acute rheumatism, or of the more vague causes of irritation 
designated as cold. 
The peritoneum is, however, peculiarly liable to inflammation 
of a secondary character, the irritant proceeding either from 
without, as in wounds of the abdomen, or from one of the organs 
lying beneath the membrane. 
Mere exposure to the air or the entrance of air into the ab- 
dominal cavity does not induce peritonitis, and even a somewhat 
prolonged cooling of the membrane, as during an operation, does 
not seem to lead to inflammation. 
Most of the inflammations of the peritoneum are septic, that 
is to say, they are due to the presence and propagation of bacteria, 
usually in the form of micrococci, and the irritating chemical pro- 
ducts which result. Those who are familiar with the manner in 
which bacteria propagate in suitable fluids will not be astonished 
that a limited inoculation of septic material produces a very rapid 
propagation in the peritoneum. The conditions are here pecu- 
liarly favorable to this. The movements of the intestine and the INFLAMMATIONS OF PERITONEUM — PERITONITIS. 
609 
normal circulation of the peritoneal fluid carry the septic particles 
hither and thither, so that they are sown over an extensive surface, 
and supplied with nutritive material. The warmth of the cavity 
also favors their propagation. So it happens that in comparatively 
few hours we may have an intense inflammation, or we may have, 
as already stated, such an absorption as to cause death by septi- 
caemia before considerable inflammation can develop. 
The septic inoculation may take place by a wound in the ab- 
domen, made by accident or by an operation. More frequently 
the source is an underlying organ, as the stomach, or intestine, or 
the uterus after delivery. In regard to the last-mentioned source, 
acute peritonitis is often a special feature in puerperal fever, and 
as this disease occurs in epidemics and is highly contagious, we 
must infer that there is something specific in the organism which 
causes it. 
The septic inflammations partake of the character of similar 
inflammations in the pericardium and pleura. They are pre- 
eminently acute, and tend rapidly towards suppuration. At first 
there is hypersemia and a serous and fibrinous exudation. The 
exuded fibrine is visible on free surfaces as a soft yellow layer, and 
is often present in the fluid as yellow flakes. It glues together 
surfaces which are in contact, such as the loops of the intestine, 
but the adhesions are not firm; they can be readily separated, and 
the gluing material is seen to have a soft gelatinous character. As 
the inflammation goes on, the fibrinous exudation, which from the 
first contains very numerous leucocytes and is correspondingly 
soft, becomes still more infiltrated with these, and assumes the 
characters of pus. Pus may be found in some parts, while in 
others there is still the soft fibrinous exudation. Thus pus may 
be found in the neighborhood of the original source of the inflam- 
mation, as around the vermiform appendage, the inflammation 
being here more intense or of longer standing. The pus, and even 
any free fibrine that may exist, commonly gravitate to dependent 
parts, and we may find a collection of yellow pus in the pelvis, 
and especially in Douglas’s pouch. 
The peritoneum presents in its finer details changes similar to 
those in septic pleurisy and pericarditis. The endothelial cells are 
separated, and the connective tissue opened out by serous fluid 
and leucocytes. The underlying tissues are also altered, especially 
the wall of the intestine. The subserous, muscular, and mucous 
coats are often cedematous and thickened. There is not infre- 
quently considerable tympanitic distention of the intestine from 
paralysis of its muscular coat. This meteorism is sometimes a 
peculiarly distressing feature in puerperal fever. 
It will be inferred that septic peritonitis, if general, is almost 
necessarily fatal. Sometimes it is localized by adhesions, and even 
after the occurrence of suppuration may subside and give place to. 
chronic inflammation. 610 
diseases of liver, pancreas, and peritoneum. 
Chronic peritonitis, whether developing out of the acute form 
or occurring in connection with disease in an underlying organ, is 
characterized by new formation of connective tissue, frequently 
with adhesion of opposing surfaces. The details of this process 
are similar to those in chronic pleurisy, etc.; it remains here to 
specify some of the more common occasions of the affection. 
A diffuse chronic peritonitis sometimes develops in the course 
of Bright’s disease. There is also commonly, in cases of secondary 
cancer of the peritoneum, a general chronic peritonitis. 
Local thickenings of the capsule of the liver and spleen are of 
frequent occurrence in connection with diseases in these organs or 
their neighborhood. Sometimes the connective tissue is hard, 
almost like cartilage. Very commonly there is adhesion to the 
parts around, especially to the diaphragm. On the other hand, 
the diaphragm may be adherent by reason of the extension of an 
inflammation from the pleura, the irritant having passed down- 
wards in a direction contrary to that of the usual circulation. 
The peritoneum around the female generative organs is liable 
to very frequent local chronic inflammations (perimetritis), re- 
sulting in complex adhesions and mattings of the pelvic organs. 
The contraction of the new-formed connective tissue may cause 
considerable distortion of these organs. 
TUBERCULOSIS OF THE PERITONEUM. 
Tubercular Peritonitis.—This disease is usually a primary and 
independent one, due to the existence of the tubercular virus in 
the peritoneal cavity. It may seem at first sight remarkable that 
tubercular ulcers of the intestine hardly ever give rise to a general 
tuberculosis of the peritoneum. We have seen that in connection 
with these ulcers tubercles are formed in the muscular coat and 
very commonly beneath or in the peritoneum, and it might seem 
probable that the virus would get readily into the peritoneal cavity. 
Put it is to be remembered that the lymph circulation is from the 
surface of the peritoneal cavity into the substance of the mem- 
brane, and that the normal currents will not carry the virus into 
the sac. Whether this be the true explanation or not, it is rare 
for tubercular ulcers to produce tuberculosis. 
In tubercular peritonitis the virus gets into the sac, and is car- 
ried hither and thither throughout it by the regular circulation. 
The consequence is the formation of innumerable tubercular 
nodules and an inflammation of the peritoneum. It is not clear, 
however, in most cases, how the virus gets into the peritoneum. 
In a few cases the tuberculosis of the peritoneum has obviously 
had its origin in a local tuberculosis of the testis and vas deferens, 
and has begun in the inguinal region where the vas deferens 
approaches the peritoneum. But in the majority of cases no such 
source of infection can be found, and although commonly the 
person is in a state of ill health before the tuberculosis begins to TUBERCULOSIS OF THE PERITONEUM. 
611 
manifest itself, and may have scrofulous tubercular manifestations 
elsewhere, yet the disease may supervene in persons apparently 
healthy and robust. We can only say that the formation of 
tubercles in every part of the peritoneum, and the fact that by 
reason of the communications through the diaphragm they also 
spring up in the pleura, are sufficient evidences of the existence 
of an iulective material in the peritoneal cavity. 
When a case of tubercular peritonitis is examined post mortem, 
we find evidences of chronic inflammation in the form of thicken- 
ing of the peritoneum and multiplied vascular adhesions in every 
part. The loops of the intestine are adherent to each other, and 
the superficial ones to the anterior wall of the abdomen, the 
omentum is adherent to the intestine, the liver to the diaphragm, 
and so on. In the midst of these adhesions are numerous yellow 
masses of very various sizes, some as large as split-peas, and usually 
flat. These caseous masses are composed of groups of tubercles 
which have very much the character of those found in tubercular 
pericarditis. The caseous tubercles have developed in the usual 
way out of gray miliary tubercles, and examination will usually 
show examples in the various intermediate stages. 
The condition of the omentum is worthy of special mention. 
It is drawn together and thickened, and closely adherent to the 
intestine and wall of the abdomen, while in its substance numerous 
tubercular masses are to be found. 
All these conditions indicate a chronic inflammation, accom- 
panied as usual by the new formation of vascular connective tissue 
with consequent adhesion. The yellow caseous masses are col- 
lections of tubercles mostly obsolete, just as the caseous tubercles 
of the brain are; and here, as there, we may find recent tubercles 
at the margins of the caseous masses. 
While this is the usual condition found after death there is 
reason to believe that the inflammation in the earlier stages is 
more acute. There is often at first considerable accumulation of 
serous exudation in the abdomen. This is by and by for the most 
part absorbed, giving place to adhesive inflammation, but often 
there is serous fluid among the adhesions, and during life the hand 
on the abdomen may sometimes enable one to detect the move- 
ment of fluid from space to space among the adhesions. The dis- 
ease may be recovered from in these earlier stages, the virus being 
apparently overcome by the reinvigorated forces of the body. On 
the other hand the inflammation produced is sometimes more acute 
.than usual, and in rare cases may be fibrinous and suppurative. 
It has already been • mentioned that tubercular pleurisy often 
develops in association with tubercular peritonitis. There is in the 
pleura for the most part a serous exudation, and as the eruption is 
usually recent the tubercles are in the form of small white or gray 
nodules. They are commonly grouped mainly in the lower part 
of the pleural cavity, in this way indicating the source of the 
infective material. 612 
DISEASES OF LIVER, PANCREAS, AND PERITONEUM. 
Tuberculosis of the peritoneum is sometimes met with in acute 
miliary tuberculosis, but it is not frequent, and the appearances 
are altogether different from those of tubercular peritonitis. In the 
case of general tuberculosis the virus is in the blood, and the 
tubercles develop in connection with the bloodvessels and not 
specially on the surface. Besides, the disease proves fatal so soon 
that there is not time for the occurrence of adhesive inflammation 
or the development of groups of tubercles. The tubercles are very 
small gray nodules hardly visible to the naked eye and specially 
abundant in the upper part of the abdomen and omentum. 
TUMORS OF THE PERITONEUM. 
These are rarely primary. Several cases of retroperitoneal 
sarcoma have been described in which a tumor of very large size 
has formed and distended the abdominal cavity. 
Sometimes we meet with bulky gelatinous tumors in the abdo- 
men, and the recognition of the exact nature of some of them is 
matter of considerable difficulty. Colloid cancer of the stomach 
and intestine not infrequently, as we shall see afterwards, passes 
on till it reaches the peritoneum, and may result in the formation 
of bulky gelatinous masses there. But, besides that, there are 
primary tumors of the peritoneum which belong to the class of 
cylindroma or plexieorm angiosarcoma. In these cases there is 
a new formation of bloodvessels in whose adventitia is produced a 
peculiar gelatinous tissue. These tumors may attain a large size, 
weighing as much as forty pounds. 
Secondary cancer of the peritoneum will be considered in the 
next section more fully and need not be taken up here. 
Lympiio-sarcoma is not such a common tumor here as in the 
mediastinum, but it sometimes originates in the lymphatic glands 
of the mesentery and involves all the neighboring structures. We 
may thus have bulky tumors occupying the place of a portion of 
the mesentery and intestine, and repeating roughly the anatomical 
relations of these. 
THE SECONDARY EXTENSION OF CANCERS OF THE 
ABDOMINAL ORGANS. 
We have seen in the study of the diseases of the stomach and 
intestine that the cancers of these organs very often lead to 
secondary tumors in the liver and peritoneum, and it may be well 
to consider here more systematically what paths the infective 
material follows in passing from the primary tumor to the seat of 
the secondary growths. 
The Secondary Growths in the Liver, in the case of cancers of 
the organs mentioned, form in connection with the portal vessels, SECONDARY EXTENSION OF CANCERS. 
613 
and there is no doubt that the material is brought to the liver 
through the portal vein from its radicles. But the question remains, 
how does the cancerous material find its way into the radicles of 
the portal vein? We know that, as a rule, in external cancers 
the secondary tumors occur uniformly in the lymphatic glands, 
and it is only after these have been long involved that the 
cancerous material reaches the blood. We have to inquire whether 
the alimentary canal is in this regard placed in any different posi- 
tion to external organs or whether any other explanation may be 
practicable. 
For one thing, we find in almost all cases of cancer of the 
stomach the lymphatic glands near it involved. They are the seat 
of cancerous growth, although perhaps not very large. This raises 
the question whether, after all, the real course of events in the 
abdomen is not, first, metastasis to the lymphatic glands and then 
from the glands into the radicles of the portal vein. In that case 
the formation of tumors in the liver would be an occurrence com- 
parable to the generalization of external cancers, where the blood 
becomes the vehicle of infection and tumors spring up all over the 
body, the material being carried by the systemic arteries. The 
tumors in the lymphatic glands would thus he the secondary and 
those in the liver really tertiary. 
Supposing this view to he correct, then it follows that if a cancer 
of the stomach or intestine causes secondary growths in lymphatic 
glands whose veins are not radicles of the portal, the tumors of 
the tertiary order would not be in the liver but in the lungs, or 
beyond the lungs, in organs fed by the systemic arteries. 
The author met with a case of cancer of the stomach in which, 
instead of the glands immediately outside its wall, as is usually 
the case, the prevertebral glands were enlarged and cancerous. 
One of these was adherent to the wall of the inferior vena cava, 
and on opening this vein a little white thrombus was seen peeping 
out of a small branch which emerged from the enlarged gland into 
the vein. There were cancerous thrombi in other veins within 
these glands, and on microscopic examination it was found that 
the cancerous tissue in the glands had largely broken up the veins, 
and epithelial cells were found in them along with the blood. In 
this case there were innumerable cancerous embolisms in the 
lungs. Fig. 235, p. 517, shows a section of the lung with two 
arteries completely occluded with solid material, and with a high 
power cancer cells could be seen in these vessels. As shown in 
the figure, and the one following it, there were outside the arteries 
well-formed epithelial processes apparently inside the tymphatic 
spaces. 
This case would seem to indicate that cancers in lymphatic 
glands may, by breaking up the gland, penetrate into the venous 
radicles in the gland, and so pass into the general circulation. It 
seems a legitimate inference from this exceptional case that when 
the liver becomes involved in cancer of the alimentary canal, it 614 DISEASES OF LIVER, PANCREAS, AND PERITONEUM. 
does so by the portal blood becoming infected through the lym- 
phatic glands. 
There remains one possible difficulty in the way of accepting 
this view. In external cancers it is exceptional for the general 
circulation to become infected. The disease generally ends by in- 
fecting the lymphatic glands, whereas in cancers of the abdominal 
organs the liver is affected in a large proportion of the cases. 
But this difficulty also is hardly insurmountable. A person with 
a cancer of the mamma, let us say, very commonly dies from the 
ulceration of the primary or secondary growth, or of both. The 
lymphatic glands of the axilla being situated externally, are liable 
to ulceration, and the patient usually dies before the infection has 
reached the general circulation. In the case of abdominal cancers, 
however, the organs themselves, and especially the lymphatic 
glands, are protected by their position, and the cancers are not so 
apt to interfere with the general health as external -cancers are. 
If the history of even an extensively ulcerating cancer of the 
stomach be compared with that of a cancer of the mamma, the 
difference will be very apparent. If the cancer of the stomach 
does not produce vomiting or stricture of the pylorus, there may 
be for a long period very little disturbance of the general health, 
and little more than symptoms of dyspepsia. It seems probable, 
from the history of some eases, that a cancer of the stomach may 
go on for many years without causing death. The abdominal 
lymphatic glands are still more protected. They practically never 
ulcerate, and in relation to direct injury to health cancer in them 
is of little account. 
It seems probable, then, that in cases where the liver is affected 
the disease is of much longer duration in its primary seat than is 
often suspected. Cases of multiple cancer of the liver are often 
examined after death, in which no suspicion has existed during 
life of the existence of a primary tumor in the stomach, and this 
tumor may possibly have been going on for a period whose dura- 
tion cannot in any way be gathered. 
It is not to be inferred that the portal blood is infected only in 
the way indicated. It is possible that a cancer may make its way 
through the walls of the veins directly, just as an external cancer 
sometimes penetrates a vein. 
We have now to consider the case of cancerous infection of 
the peritoneum by extension of cancer from the abdominal organs. 
The seat of the cancer may be any of the abdominal organs; the 
peritoneum becomes infected when the cancerous material finds its 
way into the cavity. 
There are some cancers which have comparatively little tendency 
to extend along the lymphatics to the glands, but prefer to in- 
sinuate themselves among neighboring structures, and advance by 
continuity of tissue. This applies especially to colloid cancer, 
which often grows through the wall of the stomach or intestine, CANCEROUS INFECTION OF THE PERITONEUM. 
615 
while the glands are hardly at all affected. We can understand 
that a cancer with such a rigid stroma as this form has, and with 
cells which so readily swell up and become transformed, will not 
readily allow of transportation of its elements. But this form of 
cancer very readily, after growing through the wall of the stomach 
or intestine, infects the peritoneum, and there is no form of cancer 
which, in such a large proportion of cases, produces secondary 
tumors there. 
The cancers of the ovary being already very close to the peri- 
toneum, readily produce cancerous infection, and do so in almost 
every form of cancer. Cancers of the pancreas also frequently 
have a similar course for the same reason. The ordinary cancers 
of the alimentary canal more rarely pass through the walls and 
infect the peritoneum, but they sometimes do. It is besides not 
uncommon to meet with secondary cancers of the liver which have 
produced an infection of the peritoneum, some of the tumors of 
the liver having reached the surface and extended through the 
capsule. 
When the cancerous material gets into the peritoneum it is 
carried throughout it by the circulating fluid, aided by the move- 
ments of the intestine, and secondary cancerous tumors commonly 
spring up in the most diverse regions (Fig. 262). It is to be 
Fig. 262. 
Disseminated cancer of the peritoneum, from cancer of the stomach. (Virchow.) 
remembered that in the peritoneum there are innumerable open 
stomata ready to absorb any finely divided solid matter that may 
be suspended in the peritoneal fluid. The infective material will 
therefore be carried from the surface into the substance of the 
peritoneum, or into the subperitoneal tissue, and the resulting 
tumors may even be subperitoneal. They form usually flat growths 
with smooth surface, the general surface of the peritoneum being 
perhaps unbroken. Not infrequently the tumors are continuous 
with one another in some parts of the abdominal wall, a layer of 
cancerous tissue appearing like a subperitoneal thickening. 
The great omentum is somewhat peculiarly situated in this 616 
DISEASES OF LIVER, PANCREAS, ANI) PERITONEUM. 
regard. We have seen that it probably acts as a kind of drain in 
the peritoneal cavity, and if this be the case it will specially absorb 
any material which gets into the cavity. In accordance with this 
there is usually in cancer of the peritoneum great new-formation 
in the omentum. In colloid cancer it sometimes assumes the form 
of a bulky heavy mass, and in other forms we have it gathered up 
and converted into a solid tumor lying transversely in the abdomen. 
We may venture the statement that this fact is too little known 
among physicians, and that a great omentum thus altered is fre- 
quently taken during life for an enlargement of the liver, or a 
primary tumor of some obscure kind. 
The relation of peritoneal cancers to the diaphragm presents 
some points of interest. We have seen that the diaphragmatic 
lymphatics communicate with the peritoneal sac on the one hand, 
and the pleural sac on the other. In peritoneal cancers the dia- 
phragm is usually permeated with cancerous growths, and these 
are often in the form of cords as if following the course of the 
lymphatics. Through time they extend to the pleural surface, and 
tumors may appear there. If there are no pleural adhesions in 
this region the infective material passes into the pleural cavity, 
and numerous tumors are often found, especially in the lower 
parts of the pleura. A preexisting adhesion of the diaphragm to 
the lung prevents this extension of the cancer. DISEASES OF THE URINARY ORGANS. 
A.—THE KIDNEYS AND URETERS. 
Normal Structure and Function.—III studying the diseases of 
the kidneys, it is necessary to bear constantly in mind the general 
facts as to their structure, otherwise the examination of the organs 
will lead to confusion. The functions of the kidney must also be 
understood in their outlines in order to a compi’ehension of the 
changes wrought by disease. 
When a microscopic section of the kidney, made so as to include 
both the cortical and pyramidal substance, is examined, the con- 
trast between these two regions is sufficiently striking in respect 
that in the cortical substance the uriniferous tubules have a 
markedly irregular and convoluted course. If attention be now 
confined to the cortex alone, as in Fig. 263, it will be seen 
that convoluted tubules are not the only kind present. There are 
straight tubules prolonged up from the pyramids in the form of 
tapering bundles (a) between which lie convoluted tubules (b). 
These tapering bundles, called medullary rays, or pyramids of 
Ferrein, do not reach the surface, the most superficial part of the 
cortex presenting a continuous layer of convoluted tubules. In 
this way the deeper parts of the cortex present a regular division 
into alternating areas of straight tubules or medullary rays, and 
convoluted tubules. 
Among the convoluted tubules lie the Malpighian capsules (e in 
figure). These occur somewhat frequently, and at tolerably reg- 
ular intervals. 
In addition to these arrangements of the tubules, the blood- 
vessels must receive attention. The larger arteries, as shown (d 
in figure), run between pyramids and cortex, and send up stems 
given off at right angles into the coi'tex. These pass at intervals 
into the region of convoluted tubules, and as they ascend they 
give off lateral branches to the Malpighian tufts. It will thus 
appear that the areas of convoluted tubules are also the areas of 
the ascending arteries (which are also called interlobular arteries) 
and Malpighian tufts. In the Malpighian capsule the afferent 
vessel breaks up into a congeries of capillary vessels, called the 
tuft. These gather together to form the efferent vessel, which 
again breaks up into capillaries which surround the tubules with a 
rich network. 
We have seen that the large arteries which run between the 
pyramids and the cortex give off the ascending or interlobular 618 
DISEASES OF THE URINARY ORGANS. 
arteries to the cortex. They also give off arterial branches down- 
wards to the pyramids. These arteries break up into bunches of 
straight arterioles (arterise rectse, c in figure) which are increased 
by branches coming down from the afferent vessels in the deeper 
Fig. 263. 
Section of normal kidney, including cortex and base of pyramid, with a very low magni- 
fying power, a, medullary rays; b, convoluted tubules; c, region of arterim rectse in 
pyramids; d, larger vessels running between pyramid and cortex; e, Malpighian tufts; 
/, capsule. X 12. 
parts of the cortex. These bunches of arterioles taper as they 
pass down the pyramids, so that they form small pyramids with 
their bases towards the cortex. They correspond in position with 
the areas of convoluted tubules, which areas they, as it were, pro- 
long down into the pyramids. 
In the normal kidney all these arrangements are very regular, 
and as in disease there is apt to be dislocation of the various 
structures in a high degree, it is important to become familiar with THE KIDNEYS AND URETER 
619 
the normal appearances. Even with the naked eye the various 
regions indicated above may usually be made out to some extent 
in the normal kidney. There is. first the distinction of pyramids 
and cortex, and, normally, the bases of the pyramids are strictly 
demarcated from the cortical 
substance. Then a more care- 
ful examination brings out in 
the cortex the medullary rays, 
as prolongations upwards of 
the pyramids. Alternating 
with these are the more irreg- 
ular areas of convoluted tu- 
bules in which the Malpighian 
tufts may be visible as red 
dots. Then in the pyramids 
we may notice that as we fol- 
low the medullary rays down- 
wards there are, alternating 
with them, red streaks which 
represent the bunches of arte- 
rise rectte. 
In studying the function of 
the kidney, we have to remem- 
ber in the first place the course 
of each uriniferous tubule, 
which may be followed in the 
annexed diagram. It begins 
in the Malpighian capsule (i). 
Issuing thence the tubule be- 
comes convoluted (u),and then 
it dips down in a long loop 
(Henle’s loop) whose bend (h) 
is usually in the pyramidal 
portion. Turning upwards 
(iv), the loop comes back to 
the cortex, again becomes con- 
voluted (v), and then opens, 
sometimes at an acute angle, 
into a straight tubule (vi) which passes directly downwards, joined 
by other tubules (vn), till it opens at the apex of the pyramid (ix) 
into one of the calices. 
So far as the water of the urine is concerned, it is generally 
agreed that it passes from the blood at the Malpighian tufts; it 
filters, in fact, from the capillaries into the ends of the tubules. 
According to Ludwig, the whole constituents of the urine filter 
through into the Malpighian capsules, but along with an excess of 
water. In travelling through the long course of the tubules, the 
water is to a considerable extent absorbed, and the urine concen- 
trated. According to Bowman’s views, on the other hand, it is 
mainly the water which passes through at the Malpighian capsules, 
Fig. 264. 
Diagram of course of uriniferous tubules 
from Malpighian capsule (I) to pyramid (IX). 
See text. (Quain.) 620 
DISEASES OF THE URINARY ORGANS. 
the urea, urates, etc., being secreted from the blood by the large 
granular epithelium which lines the convoluted tubules. 
Without insisting on one or other of these views, it is important 
for our purpose to observe that the actual amount of urine secreted 
will depend on the blood-pressure in the Malpighian vessels, or on 
the speed with which the blood passes through the vessels, these 
two, as a rule, strictly corresponding with each other. The amount 
secreted will be increased by increase of pressure in the Malpighian 
vessels, as, for instance, by relaxation of the renal arteries, and it 
will be diminished by any cause which diminishes the pressure in 
these vessels. Considering the close relationship of the renal 
vessels to the systemic arteries and veins, it is clear that the blood 
in the former will be liable to considerable variations in pressure 
and in the speed of the current from circumstances affecting the 
general circulation, such as disease of the heart and lungs, preg- 
nancy, and so on. 
We shall see afterwards that serious results may follow from 
the action of deleterious agents brought to the kidneys by the 
blood, and it is important to consider at the outset how lesions 
brought about in this way will be distributed. In the first place, 
such diseases will probably affect both kidneys at the same time. 
But, further, considering that it is in the cortical portion of the 
kidney that the secretion of the urine takes place, it is not remark- 
able that these lesions occur mainly in connection with the Mal- 
pighian tufts and the convoluted tubules of the cortex. 
MALFORMATIONS AND MISPLACEMENTS OF THE KIDNEY. 
Congenital Malformations.—These are frequently such as to 
present comparatively little interference with the function of the 
organs. This does not apply to the extreme cases where both 
organs are absent or extremely small, but as this only occurs with 
serious malformations of the foetus as a whole, the child does not 
survive. 
Defect of One Kidney is not infrequently met with in well- 
formed adults without any of the signs of disease of the kidneys. 
It is mostly the left kidney that is defective, and it may be entirely 
absent, its vessels and a diminutive ureter ending in a piece of con- 
nective tissue. The other kidney in these cases undergoes a com- 
pensatory hypertrophy, as we shall see immediately. 
The kidney also not infrequently shows some trace of the 
original lobulation which exists in the foetus and is retained 
throughout life in some animals. 
Coalescence of the Two Kidneys across the middle line is one 
of the most frequent malformations. Various degrees of it are 
presented. It may be a simple elongation of the inferior extremi- 
ties of the kidneys which are united by a fibrous band passing 
across the vertebrae. Or there may be a proper isthmus of renal malformations and misplacements of kidney. 
621 
tissue uniting the two kidneys into one and forming the well- 
known horseshoe kidney (Fig. 265). From this we have various 
grades on to complete coalescence of the kidneys into an elongated 
or square body across the vertebrae. In almost every case there 
are the regular two ureters or they may even be increased in 
number, and they pass down in front of the isthmus. This form 
Fig. 265. 
Outline sketch of horseshoe kidney. (Roberts.) 
of kidney is often depressed in position, even coming as low in 
some cases as the hollow of the sacrum. When depressed the 
arteries usually have abnormal origins, as from the common iliac, 
hypogastric, etc. 
Variations of Position.—These maybe congenital or acquired. 
In the former case and in some of the latter the kidney is fixed in 
its unusual situation. In congenital malposition it is generally 
the left kidney which is concerned. It may be depressed so as to 
lie as low as the brim or even the cavity of the pelvis. It is not 
infrequently seated opposite the sacro-iliac synchondrosis. Such 
kidneys have usually the hilus presenting forward and are flat- 
tened, while their vessels are branches of the lower end of the 
aorta and the iliac veins or even entirely the iliac vessels. The 
kidney may also lie nearer the middle line than normal or in the 
middle line. 
The malposition, may be acquired by the pressure of tumors or 
of the liver, by the dragging of a hernial sac, and so on. In a 
case observed by the author the kidney was fixed near the middle 
line, apparently on account of the abnormal shortness of the renal 
vein. 
Of great interest here is the movable or floating kidney. In 
connection with the etiology of this condition it is very important 
to remember that it occurs in the great majority of cases in 
females (according to Roberts in forty-six out of fifty-one cases) 
and mostly on the right side. This connects the lesion with dis- 
placement and malformation of the liver caused by wearing stays, 
and perhaps also with the displacements of the organs generally, 622 
DISEASES OF THE URINARY ORGANS. 
incident to the rise of the uterus in pregnancy. In the case of the 
movable kidney the organ is so loosely bound down by the peri- 
toneum that it can pass forward out of its position, carrying the 
peritoneum before it till it lies at the edge of the liver. It is said 
in some cases to possess a kind of mesentery. During life it is 
often to be detected at the border of the liver, although it is not 
constantly there. 
The movable kidney is not very liable to secondary changes, 
although sometimes the abnormal position interferes with the flow 
through the ureter, and leads to hydronephrosis, or even inflam- 
mation of the pelvis. Of more importance is the fact that by 
dragging there may be serious nervous disturbances, in the form 
of excruciating cramps, often of very obscure origin during life. 
The kidney may, however, be movable without any such nervous 
symptoms presenting themselves. 
COMPENSATORY HYPERTROPHY OF THE KIDNEY. 
This condition develops sometimes when one kidney is lost or 
congenitally defective. In the case of congenital absence of one 
kidney the other will be found homogeneously enlarged, and 
probably weighing nearly the same as the two normal kidneys 
together. The different regions of the kidney bear the same rela- 
tions to each other, each being enlarged in its due proportion. 
The function of the kidneys is also completely carried out by the 
single one. 
It has been determined by experiments in animals that compen- 
satory hypertrophy develops after excision in full-grown animals, 
although it is more complete when the operation is done in the 
new-born. It is remarkable how soon after such excision com- 
plete restoration of the renal functions occurs, the secretion of 
urea reaching its normal in one case about two days after the 
operation, and the animals remaining from the first apparently 
unaffected in health. This would indicate that the kidney does 
not, like a gland, secrete the urinary constituents, but that these 
come to it performed and are simply excreted by it. 
Measurements have been made of the structures in the kidney 
to determine whether there is in compensatory hypertrophy an 
actual new formation of glomeruli and tubules' or merely an en- 
largement of these. The results are by no means conclusive, and 
some observers hold to one view and some to the other. Gudden, 
on the basis of observations, in which he excised one kidney in 
new-born rabbits and examined the remaining hypertrophied one 
when the animals were full grown, concludes that there is no 
actual new formation of glomeruli, but a simple enlargement of 
them. In relation to what follows it may here be noted that 
hypertrophy of the heart does not usually follow extirpation of 
one kidney. DISORDERS OF THE CIRCULATION IN THE KIDNEYS. 
623 
DISORDERS OF THE CIRCULATION IN THE KIDNEYS. 
Active Hyperemia is caused by dilatation of the renal arteries. 
This may be from traumatic injury to the vaso-motor centre in the 
medulla oblongata. In a case observed by the author of this kind 
there was the most intense hypersemia with enlargement of both 
kidneys, the injection affecting all the vessels. During the few 
hours that the patient survived, large quantities of urine were 
twice removed by the catheter, and after death the bladder was 
again found distended by a watery urine. Again, we may have an 
active hypersemia from removal of pressure, as after excision of 
large tumors from the abdomen or the removal of ascitic fluid, or 
even the removal of pleuritic iiuid. Under these circumstances 
there is often for a day or two excessive secretion of urine lasting 
till the renal vessels resume their normal state of contraction. 
The hypersem-ia which follows on the administration of certain 
poisons, such as cantharides, arsenic, and carbolic acid, is to be 
regarded as really inflammatory. 
Passive Hyperemia results from obstruction to the venous cir- 
culation, and is most frequently met with in valvular disease of 
the heart and in diseases of the lungs, in which the circulation is 
seriously interrupted, as in severe emphysema. 
The naked-ey.e appearances of the kidney are usually very sug- 
gestive of over-tilling of the vessels. There is a general redness, 
but this is generally most manifest in the pyramids where the 
arteriee rectae often show very special dilatation indicated by ex- 
aggeration of the red streaks which pass from the bases of the 
pyramids in the direction of the apices. The Malpighian tufts are 
also visible in the cortex as small red spots. 
When hyperaemia has subsisted for a considerable time, as in so 
many cases of heart disease, a more definite change occurs in the 
kidney. The connective tissue here, as in other organs (see passive 
congestion of the heart, p. 299), becomes hypertrophied, and the 
organ assumes a distinct increase in density. The organ, while 
harder to the feel, is sometimes slightly enlarged, and the capsule 
can be peeled from the surface even more easily than normal. 
Sometimes there is fatty degeneration of the epithelium, and this 
may result in collapse of some of the tubules, leading to slight de- 
pressions of the surface. 
Under the microscope, the kidney shows overfilling of the 
vessels, the epithelium presenting little alteration, at most some 
fatty degeneration. The hypertrophy of the connective tissue is 
not accompanied by any considerable formation of round cells; it 
is simply seen that the interstitial tissue is more prominent and 
perhaps more definitely fibrous than normal. 
Thrombosis of the renal veins is sometimes a result of passive 
liypersemia, but it usually occurs just before death and when the 
patient is very much debilitated. 624 
DISEASES OF THE URINARY ORGANS. 
Embolism of the kidney has been already referred to with some 
degree of fulness (see p. 50). llemembering that the renal arteries 
are strictly end-arteries, it will be understood that when an artery 
is obstructed the infarction always occurs. The arteries of the 
kidney being distributed primarily to the cortex, the infarction is 
Fig. 266. 
Embolic infarction of kidney. The white appearance and wedge-shape of the infarction 
is represented. (After Rayer.) 
more or less wedge-shaped (Fig. 266), with the base of the wedge 
at the surface. If the wedge be of larger size it will extend also 
into the pyramids. 
As a rule, the infarction is of a pale color and of dense consist- 
ence, the tissue having undergone coagulation necrosis. In some 
cases, and especially in small infarctions, hemorrhage occurs, and 
we may have the regular hemorrhagic infarction, or a partial red 
coloration. Around the infarction, whether red or pale, there is 
commonly a zone of liyperamiia. 
As already seen, the infarction gradually undergoes absorption, 
and is replaced by a cicatrix. In this way deep depressions of the 
kidney may occur, and if there are several of them the kidney 
may assume a lobed appearance. In cases of old mitral or aortic 
disease it is very common to find deep cicatrices, indicating that 
probably at the time of acute endocarditis, embolism of the 
kidney had occurred. 
The kidney is not infrequently the seat of septic embolism in 
pyaemia, ulcerative endocarditis, etc. The result is the formation 
of miliary abscesses, which will come up for consideration hereafter. 
BRIGHT’S DISEASE, OR NEPHRITIS. 
This is a subject of great complexity and difficulty, and one con 
cerning many points in which differences of opinion exist. bright’s disease, or nephritis. 
625 
General Considerations.—At the outset it may be said that we 
include here cases in which there are undoubted inflammatory 
manifestations in the kidneys, but we exclude those in which there 
are no such manifestations present. The domain of Bright’s 
disease, therefore, is not coextensive with that of albuminuria, as 
the latter may include such conditions as amyloid degeneration 
and passive hypersemia. 
In studying the causes of Bright's disease, we have to look for 
an irritant, and it is here important to observe in the flrst place 
that the inflammatory manifestations occur in both kidneys, and 
although, on examining the kidneys in detail, these manifestations 
will be found to present themselves in innumerable minute foci, 
and to confine themselves for the most part to the cortex, yet they 
do not affect a few definite areas, but are diffused over the length 
and breadth of the organ. These facts indicate that the irritant is 
carried to the kidneys by the blood, and is distributed with the 
blood homogeneously over them. As the blood is primarily 
distributed to the cortex, and as the cortex contains the more 
active secreting tissue of the organ, it so happens that the inflam- 
matory manifestations occur almost exclusively there. 
In the various cases of Bright’s disease we do not find the 
various constituents of the kidney tissue equally engaged, and it is 
necessary, in studying the causation, to refer to this matter. In 
the kidney we have, as the main constituents, the bloodvessels, the 
secreting tissue (consisting of the glomeruli and the tubules with 
their epithelium), and the connective tissue. 
It is not impossible that an irritant brought to the kidneys by 
the blood may show a predilection for the renal epithelium on the 
one hand or the connective tissue on the other. But it seems more 
likely that in the majority of cases it will act on both at the same 
time. We have already had several opportunities of observing 
that chronic inflammations very commonly produce inflammatory 
new formation in the connective tissue, and the kidney forms no 
exception in this respect. It may be said, therefore, that for the 
most part irritants which act through a long period and with little 
intensity produce a chronic inflammation mainly of the connective 
tissue. On the other hand, irritants which act intensely so as to 
produce acute inflammation, while they produce the usual changes 
in the bloodvessels which we have seen occur in acute inflam- 
mations, affect mainly the epithelium of the uriniferous tubules. 
It may, therefore, be said that acute inflammations are mostly 
parenchymatous, while chronic inflammations are mostly inter- 
stitial. 
This distinction, however, cannot be rigidly carried out. There 
are some acute inflammations which affect the interstitial connec- 
tive tissue even more than the secreting epithelium, and in all 
acute inflammations which are somewhat prolonged the connective 
tissue is involved. On the other hand, inflammations which 
begin acutely frequently become chronic or subacute, and in them, 626 
DISEASES OF THE URINARY ORGANS. 
while the epithelium continues to show marked changes, the 
interstitial tissue always shows distinct inflammatory proliferation. 
After these observations, we are now in a position to consider 
what may be the nature of the irritants which produce Bright's 
disease. In the first place, as to acute nephritis, a very common 
cause, and indeed in children the commonest, is the specific poison 
of scarlet fever. It may also be produced by the poison of 
measles and other specific febrile diseases. In adults the disease is 
mostly ascribed to cold, and we have to consider how exposure to 
cold should give rise to an irritant of such a nature as to cause 
acute inflammation of the kidneys. It is of interest in this regard 
that, as Dickinson so well points out, cold mostly produces these 
effects when the person is exhausted or asleep, and when the 
exposure has occurred immediately after profuse perspiration. It 
is as if, the functions of the skin being suspended, some deleterious 
material accumulated in the blood and irritated the kidneys. It 
appears that nephritis hardly occurs in persons exposed to cold in 
the arctic regions, probably because, the respiration being more 
vigorous, the deleterious material is carried off by way of the 
lungs. In warm climates also nephritis is uncommon, probably 
because the body is less liable to sudden exposure to cold than in 
temperate regions. 
Turning to the causes of chronic nephritis, it sometimes remains 
after an acute attack. For the most part, however, when the dis- 
ease begins as acute nephritis it remains subacute with repeated 
exacerbations, and the anatomical condition is a combination of 
that seen in acute Bright’s disease and chronic, or, in other words, 
of parenchymatous and interstitial nephritis. Sometimes, however, 
the disease, even after scarlet fever, becomes definitely chronic, and 
the anatomical features are those of interstitial nephritis, although 
the changes in the tubules may still be such as to suggest an earlier, 
mainly parenchymatous, inflammation. 
On the other hand, in a large proportion of cases, the disease is 
chronic from the outset, and is to be ascribed to a cause which has 
been acting with slight intensity for a long period. Of all these 
causes the most definitely determined is gout. The pathology of 
this disease is not very apparent, but there is an obvious alteration 
in the blood in consequence of which salts of uric acid are deposited 
in certain joints, generally with signs of acute inflammation. The 
same condition of the blood frequently induces chronic nephritis, 
and it is remarkable that when it attacks the kidneys it is less 
likely to affect the joints, and vice versa. Among the working 
classes gout largely arises from chronic lead-poisoning (see stat- 
istics in Dickinson’s work on Albuminuria), and in these cases the 
disease is particularly liable to attack the kidney, so much so that 
a large proportion of painters and others who work with lead die 
of chronic nephritis. Where the gout is due to the constant use 
of alcohol the disease is more liable to attack the joints. 
Chronic nephritis is also sometimes induced by the poison of bright’s disease, or nephritis. 
627 
syphilis. In this ease it is apt to be associated with amyloid dis- 
ease, but may also occur as a simple inflammation. 
Pregnancy not infrequently leads to a chronic nephritis, in all 
probability by obstructing the vessels of the kidney by the pressure 
of the uterus. In recent cases there is extreme hypersemia of the 
kidney, which, with repetition of the cause, may go on to assume 
the regular characters of chronic nephritis. 
Lastly, there are cases in which there is no special cause apparent, 
and we can only say that the person has been exposed to some 
influence whose nature we do not know. In many cases the dis- 
ease has been very prolonged, and all through, the actual active 
disease at any particular time has been very slight. With this 
very insidious march, there may be the most serious permanent 
changes in the kidneys before any prominent symptoms have 
called attention to these organs. Among the causes which are some- 
times mentioned, it is proper to refer to prolonged mental disturb- 
ance. It is not impossible that the deterioration of the body, and the 
defective condition of the alimentary functions in such cases, may 
render the kidneys peculiarly liable to chronic inflammation. 
The Anatomical and Histological Conditions in Bright’s Dis- 
ease.—We shall consider these changes under three heads, namely, 
inflammation mainly affecting the Malpighian bodies, or glome- 
rulo-nephritis, that in which the tubules are chiefly concerned, 
parenchymatous nephritis, and that which affects chiefly the con- 
nective tissue, interstitial nephritis. We have already seen that 
no absolute line of distinction can be drawn between these, and 
especially that when parenchymatous nephritis becomes chronic, 
the interstitial tissue is more and more involved. 
The term glomerulo-nephritis has been applied by Klebs to a 
condition in which the Malpighian tufts show the chief signs of 
inflammation. This he describes as being present in the kidneys 
of persons who have had scarlatina, and have died in consequence 
of the post-scarlatinal nephritis. 
It seems strange that the actual pathological condition in the 
nephritis of scarlatina has been so little determined till of late 
years. It has been customary to state that the condition is a par- 
enchymatous nephritis. Recent observations, however, have shown 
that in the earliest stage of scarlatinal nephritis there is an accumu- 
lation of round cells in the glomeruli and connective tissue around. 
This observation, originally brought into prominence by Klebs, 
has been confirmed by the author, Klein, Charcot, and others, and 
may now be generally accepted. 
Looking on scarlatinal nephritis as a typical acute inflammation 
of the kidney, we are not surprised to find that the occurrence of 
leucocytes in the Malpighian tufts is the most prominent appear- 
ance at the outset, and it is this condition apparently which is 
specially designated glomerulo-nephritis. The exudation is not 
usually confined to the glomeruli, but exists around them, and 628 
DISEASES OF THE URINARY ORGANS. 
may extend to the general connective tissue. In the case of the 
author, in which the patient died on the ninth day from the outset 
of the fever, there was an enormous infiltration of the interstitial 
tissue, as well as the glomeruli, with leucocytes (Fig. 267). It is 
Fig. 2G7. 
Glomerulo nephritis from a case of scarlet fever. The Malpighian tuft in the middle of 
the figure is crowded with round cells, which are also present very abundantly in the inter- 
stitial substance between the tubules, whose epithelium is granular. X 300. 
stated by Rosen stein that, in the nephritis caused artificially in 
animals by cantharides, there is a similar appearance of leucocytes 
around the glomeruli and elsewhere. 
Besides these changes, there is very commonly, in the acute 
stage of scarlatinal nephritis, blood in the uriniferous tubules. 
The blood is in the convoluted tubules, and it is sometimes seen 
also inside the glomerulus. In a favorable section an appearance 
such as that shown in Fig. 268 may be found. There is seen to 
be blood (b) in the glomerulus, between the tuft of vessels (a) and 
the capsule, and there is also blood in a tubule (c), which is so 
related to the glomerulus as to be evidently its prolongation, 
although the section did not happen to be made so as to show the 
actual communication. 
Sometimes the changes in the kidney do not consist so much of 
exudation of leucocytes or extravasation of the whole blood, but 
rather in alterations in the epithelium. In scarlatina the changes 
in the epithelium also centre in the glomeruli. The epithelium 
lining the glomerulus is distinctly enlarged (Fig. 269), and whereas 
normally this epithelium is hardly visible, it may become remark- 
ably prominent, as in the figure. It sometimes increases very 
greatly, as in Fig. 270, accumulating inside the glomerulus in such 
a way as to crush the tuft. In the case from which this figure was 
taken there were many tufts very seriously encroached on by the 
growing epithelium. Similar changes occur in the epithelium of 
the tubules, but there is a remarkable concentration of the lesion 
in that of the glomeruli. bright’s disease, or nephritis. 
629 
In eases where there is little more than a glomerulo-nephritis, 
such as we have described above, there are sometimes severe 
Fig. 268. 
Hemorrhage from a Malpighian tuft in a case of scarlet fever, a, tuft; b, blood between 
tuft and capsule; c, blood in uriniferous tubule extending from tuft. X 350. 
Fig. 269. 
Glomerulo-nephritis in scarlet fever. The epithelium lining the capsule is unduly large 
and abundant. X 350. 
uraemic symptoms leading, rapidly it may be, to death. It is to be 
remembered in this connection that the urine is secreted essentially 
by the glomeruli, and if in many of these the vessels are suddenly 630 
DISEASES OF THE URINARY ORGANS. 
obstructed by the pressure of leucocytes, as in Fig. 267, or of epi- 
thelium, as in Fig. 270, or even by blood inside the capsule, then 
the secretion of urine may be much reduced. Under these cir- 
Fig. 270. 
Glomerulo-nephritis in scarlet fever. The epithelium lining: the capsule is greatly increased 
so as to crush the tuft. X 350. 
cumstances suppression of urine and uraemia are not very extra- 
ordinary occurrences. 
The kidneys in these cases may be very little changed to the 
naked eye; they are sometimes enlarged with considerable injec- 
tion of the vessels. The glomeruli may be visible as red points, 
and there may he on the surface and on section red streaks and 
spots, indicating the intratubular hemorrhage. Sometimes, on the 
other hand, the exudation of leucocytes may he sufficient to pro- 
duce great enlargement, and the kidney (as in the author’s case, 
from which Fig. 267 is taken) has all the appearance of the large 
white kidney. 
Parenchymatous nephritis is characterized by the occurrence 
of changes in the renal epithelium. From what lias been already 
stated it will be understood that these changes hardly ever occur 
without coincident signs of inflammation in the interstitial con- 
nective tissue. 
The changes consist in the first place mainly in cloudy swelling 
of the epithelium, with a tendency for the cells to become loosened 
and to discharge. The tubules are often found greatly distended, 
and as if choked with desquamated epithelium. Fatty degenera- 
tion occurs in the epithelium, and is often present in a high degree, 
not uniformly, but usually in a considerable stretch of tubule at a 
time. In the tubules, besides desquamated and frequently fatty 
epithelium, there may be blood, in the form of brown granular 
matter or fresh red blood. Tube-casts are also to be found, often BRIGHT’S DISEASE, OR NEPHRITIS. 
631 
in great abundance. The tube-casts lie in the calibre of the tubules 
as transparent hyaline cylinders, and they may be traced for a con- 
siderable distance. The changes in the epithelium are almost 
entirely confined to the convoluted tubules of the cortex, although 
the disintegrated epithelium may be carried downwards into the 
loops of Henle and the straight tubules. The tube-casts are found 
in the straight tubules as well as in the convoluted. 
The kidney as a whole is considerably enlarged, and it may reach 
twice its normal weight. The bloodvessels are intensely injected, 
so that the surface presents a red color after removal of the capsule, 
which comes oft' easily. On section the cut surface is also seen to 
be red, and blood flows freely from it; the mucous membrane of 
the pelvis is injected. If the cut surface be washed so as to re- 
move the blood, it may appear as if the tissue, apart from the 
bloodvessels, were unduly pale, and there may even be opaque 
streaks if fatty degeneration is considerable. The enlargement of 
the organ is seen to be mainly due to increase of the cortex, which 
may be very much thickened, and it is in the cortex that the paler 
color mentioned above appears. 
It is not common for death to occur in this exceedingly acute 
stage, and as the inflammation subsides into a subacute or chronic 
Fig. 271. 
Section of large white kidney in a child of seven. The tubules contain irregular epi- 
thelium, and are distorted; in one a tube-cast is present. The interstitial tissue is greatly 
increased and contains abundant round cells. (Dickinson.) 
condition we have developed the large white kidney. It is neces- 
sary here to mention that amyloid degeneration produces enlarge- 632 
DISEASES OF THE URINARY ORGANS. 
ment and paleness of the kidney, and confusion has no doubt 
frequently occurred between that condition and the one now under 
consideration. 
In the large white kidney the tubules are still distended with 
epithelium, which is enlarged and desquamated (Fig. 271). There 
is here usually considerable fatt}7 degeneratian of the epithelium. 
The epithelium, and debris resulting from its disintegration, are 
often packed to a considerable extent into the straight tubules. 
Tube-casts are present usually in large numbers, and present the 
hyaline appearance already described, or else contain debris of 
epithelium and fat. 
The changes in the tubules are so prominent that they are apt 
to obscure the condition of the connective tissue. In every case 
probably there are round cells in the tissue, and sometimes they 
are present in great abundance. In the accompanying woodcut 
(Fig. 271), taken from Dr. Dickinson’s work, the condition of the 
interstitial tissue is shown in the case of a child seven years of 
age, in which each kidney weighed four and a quarter ounces. 
An illustration of the appearances of a similar section from a 
healthy child is given along with it for comparison (Fig. 272). It 
Fig. 272. 
Section of normal kidney for comparison with preceding. (Dickinson.) 
is seen that in addition to the changes in the epithelium, already 
described, there are numerous round cells in the interstitial tissue. 
The longer the case lasts the more pronounced is the change in 
the interstitial connective tissue. As time goes on also the disten- 
tion of the tubules with epithelium becomes less. The disinteg- 
rated epithelium is discharged and there is less reproduction. In 
this way the condition shades towards that of interstitial nephritis, 
and may pass into that of the contracted kidney. A case which rrigiit’s disease, or nephritis. 
633 
has begun acutely, however, generally even in the later stages pre- 
sents traces of the epithelium being specially involved. We shall 
see afterwards that in the typical chronic interstitial nephritis the 
epithelium is also involved, but the connective tissue in this case 
is increased to such an extent that the alteration of the tubules is 
apparently secondary. 
To the naked eye the enlargement and paleness of the kidney 
are the striking features in this condition. The weight of the 
organs is often double the normal or more. The increase in bulk 
is almost altogether in the cortex, and its exceedingly pale color 
contrasts with that of the pyramids, which are often unduly red. 
The color of the cortex is opaque white or buff, and it is often 
possible with the naked eye to distinguish yellow streaks and spots 
on the surface of the kidney after removal of the capsule or on 
the cut surface, indicating fatty degeneration of the epithelium. 
It will be clear that from the large white kidney to the contracted 
form there are all gradations, and a kidney which is normal in 
size, but which presents paleness and irregularity of the cortex, 
will show under the microscope already a very marked increase of 
the connective tissue. 
Interstitial nephritis is the name applied to intlammation of 
the connective tissue of the kidney. From what has gone before 
it will be understood that this scarcely occurs independently of 
inflammation of the epithelium of the tubules, and that in almost 
all cases the intlammation is really diffuse. We have even seen 
that in acute nephritis there may be such an exudation of leuco- 
cytes as to give the appearance of an intense interstitial inflam- 
mation. 
Even subacute nephritis is sometimes mainly interstitial, that is 
to say there is a persistence of the exudation of leucocytes which 
infiltrate the entire connective tissue of the cortex, and find their 
way also into the uriniferous tubules. In such cases leucocytes 
appear in the urine in considerable abundance, and they may even 
be so numerous as to give rise to the supposition that pus is present 
in the urine. 
It is, however, in very chronic cases that we find the most typical 
interstitial changes, resulting in the so-called granular contracted 
kidney, or cirrhosis of the kidney. 
The disease begins with a formation of round cells in the cortical 
part of the kidney, so that a kind of granulation tissue is formed. 
These cells, as in the other chronic inflammations, go on to the 
formation of connective tissue, so that there is-a great increase in 
the interstitial tissue of the organ. This connective tissue tends 
more and more to assume a fibrous condition, and to contract, so 
that by its cicatricial shrinking it seriously interferes with the 
secreting tissue and the bloodvessels. 
The formation of round cells does not take place homogeneously 
in the cortex. There are frequent areas in which it is present 
alternating with areas in which it is absent. It is usually most 634 
DISEASES OF THE URINARY ORGANS. 
apparent at first near the surface of the cortex, and the cells often 
accumulate specially round the Malpighian glomeruli. 
As time goes on, the increase of dense fibrous tissue produces 
very marked secondary results. The capsules of many of the 
glomeruli undergo a marked thickening, as shown in Fig. 273 a, 
Fig. 273. 
Interstitial nephritis. Sclerosis of glomerulus. a, thickene 1 capsule; !/, condensed vessels 
of tuft; d, abundant round cells in interstitial tissue; c, dwarfed tubules remaining. X 350. 
and the tuft of vessels (b) solidities into a dense homogeneous 
nodule. In this way the glomerulus is greatly contracted (com- 
pare with normal glomerulus in Fig. 272, which is magnified a 
third less) reduced often to less than half its normal size, and com- 
posed of white glancing connective tissue, in which can still be 
recognized as a rule the thickened capsule presenting a concentric 
fibrous arrangement (see figure), and the more homogeneous cen- 
tral part composed of the condensed and impervious vessels. This 
sclerosis of the tufts is often very striking, as the small glancing 
bodies attract the eye. 
The uriniferous tubules undergo still more striking changes. 
In the midst of the new-formed tissue they are to a great extent 
destroyed, so that large districts of cellular connective tissue may 
be found with no tubules at all (d in Fig. 273). When they per- 
sist in the midst of the new-formed tissue the}* are greatly atro- 
phied (c in figure), and their epithelium is rudimentary in appear- 
ance. This great destruction of tubules in conjunction with the 
contraction of the connective tissue causes the remaining struct- 
ures to he drawn together, and the altered glomeruli are often 
crowded together in a very extraordinary way (see Fig. 274). 
Where the tubules are not directly destroyed by the contracting 
tissue, their epithelium presents alterations somewhat similar to 
those mentioned as characteristic of subacute parenchymatous 
nephritis. There is accumulation of epithelium and debris, often 
with great distention and distortion of the tubules (b in Fig. 274), 
and the epithelium frequently presents fatty degeneration. It will bright’s disease, or nephritis. 
635 
thus occur that parts where nothing but the merest traces of tu- 
bules are present will alternate with parts where they are greatly 
distended. As there is a general shrinking of the cortex the dis- 
tended tubules are gathered together into folds as if crowded to- 
wards the bases of the pyramids. 
Fig. 274. 
Section of contracted kidney with a very low magnifying power. (This figure should be 
compared with the next, which is similarly magnified.) a, medullary rays; b, convoluted 
tubules crushed together and dilated; c, region of arteriae rectae and loops of Henle, the 
latter dilated and forming cysts; d, large artery between pyramid and cortex, showing en- 
darteritis obliterans: the space between this and surface represents the cortex, and may be 
compared with similar space in next figure; e, glomeruli, closely set and contracted, they 
also present a white homogeneous appearance ; /, capsule. X 12. 
Cysts form not infrequently in the contracted kidney. There 
may be some visible to the naked eye, yet in most cases they are 
to be distinguished mainly by microscopic examination. They are 
round or oval in shape, and often lie in rows, especially in the 
pyramidal portion where they probably originate from the loops 
of Henle (see Fig. 274, c). These small cysts are thin-walled and 
contain clear fluid. They arise by obstruction of the tubules from 
the contraction of the interstitial tissue, which constricts them and 
causes the urine to accumulate and distend the tubules. The 
glomeruli may give origin to cysts of a similar nature, the fluid 
accumulating in the capsule and separating the tuft of vessels from 
the capsule. Cj’sts in the kidney sometimes contain a colloid 
material as if from degeneration of the epithelium in the tubules 636 
DISEASES OF THE URINARY ORGANS. 
which have been cut oft* by the constriction of the connective tissue. 
The great alteration and dislocation which the structures of the 
kidney undergo in advanced cases may be gathered from Fig. 274, 
which was drawn under the camera lucida with the same apparatus 
as that used in Fig. 275, with which it should be compared, the 
lettering indicating similar structures in each. 
Fig. 275. 
Section of normal kidney for comparison with preceding figure. The letters indicate 
similar regions, and the magnifying power is the same. X 12. 
The bloodvessels are often much affected in the contracting 
kidney. The vessels of the glomeruli are greatly obstructed and 
destroyed by the sclerosis already mentioned, and when the kidney 
is injected many remain empty or only show a very slight injection. 
The capillaries also, which normally form such an abundant net- 
work around the tubules, are greatly destroyed by the new-forma- 
tion, as appears abundantly when a colored injection of gelatine bright’s disease, or nephritis. 
637 
with carmine is thrown into the renal artery. It is clear that the 
interference with the tufts and the capillaries must seriously 
obstruct the circulation in the kidney, and experiments by Thoma 
show that when a solution of gelatine and common salt is injected 
Fig. 276, 
Endarteritis obliterans from a contracted kidney. Two arteries seen in transverse section, 
and one in longitudinal, a, thickened and fibrous internal coat j b, middle coat. X 350. 
into the renal artery at a fixed pressure the outflow from the veins 
is greatly diminished in the contracted kidney as compared with 
the normal. 
Besides this, however, the branches of the renal artery frequently 
show considerable alterations. There is thickening of the muscular 
coat probably in all cases of interstitial inflammation. But in 
addition to that there is, in many cases, though not at all, a 
marked thickening of the internal coat. This is sometimes very 
striking, as shown in Fig. 276, almost resulting in obliteration of 
the smaller arteries (endarteritis obliterans). It would even appear 
that this endarteritis may be an early lesion in some cases, occur- 
ring before the definite onset of the interstitial changes. 
We have still to refer to the naked-eye appearances which are 
to be connected with the minute changes already described. The 
most definite change is loss of bulk. If the disease has begun 
with enlargement, then the reduction in bulk may only bring the 
kidney back to the normal size. But in ordinary chronic cases it 
is greatly reduced in size, so that it may weigh only 3 ounces or 
less. The capsule is adherent to the surface, strikingly so in the 
very chronic cases, so that in attempting to remove it pieces 
of kidney tissue come with it, and it may be thickened and opaque. 
The proper surface of the kidney is markedly uneven, being 
studded with small rounded granulations. The prominent granu- 
lations are often somewhat pale in color, representing the parts 
where the tubulos are to some extent preserved, while the inter- 
vening depressions have a reddish color. Very often the general 
color is red with only a pale mottling from the granulations. 
Cysts are often visible on the surface and on section. On section 638 
DISEASES OF THE URINARY ORGANS. 
the cortex is very manifestly changed. It is much less regularly 
defined from the bases of the pyramids than normal, and the 
regular markings which we see in the cortex indicating the medul- 
lary rays are greatly obscured. Its color is gray or buff, and its 
texture is much more dense and tough than normal. It is also 
greatly thinned, sometimes so that it forms merely a thin rind, 
perhaps only a twelfth of an inch in thickness between the bases of 
the pyramids and the surface. The great loss of cortex may be 
inferred from the comparison of Fig. 274 with Fig. 175; the 
arteries which run between cortex and pyramids (c c) are seen to be 
very little removed from the surface in the former figure as 
compared with the latter. 
We have now to consider certain very important points in the 
pathology of Bright’s disease, in regard to which it is necessary to 
bear in mind the anatomical conditions already described. These 
points are (1) the causation of albuminuria, (2) the formation 
of tube-casts, and (3) the condition of the heart and other arteries 
throughout the body in Bright’s disease, chiefly in relation to the 
increased arterial tension which is so important a result of chronic 
Bright’s disease. 
Albuminuria is well known to be the most important clinical 
sign of Bright’s disease. By the term is meant escape of albumen 
from the blood serum along with the urine. It is probable that the 
albumen undergoes slight modifications in its chemical reactions 
(Kirk), but its source is undoubtedly the serum albumen. We 
have to consider under what circumstances albumen makes its 
escape. 
It may perhaps be a necessary preliminary to inquire why it 
does not make its escape under ordinary circumstances, why the 
urine is not normally albuminous. We know that the other 
transudations from the blood contain albumen, and it seems at first 
sight strange that the urine does not. Some have even supposed 
that the urine as it is separated from the blood at the glomeruli is 
normally albuminous, and that in its subsequent passage through 
the tubules the albumen is absorbed by the epithelium just as the 
water is taken up and the urine concentrated. But this view is 
completely opposed to known facts. We have already seen that in 
chronic Bright’s disease there is great destruction of the secreting 
epithelium, so that the glomeruli are, as it were, more near to the 
outlets of the tubules than normal; the urine secreted in these 
cases is very watery, and has, in fact, characters which are pre- 
sumably those of the urine as it is separated at the glomeruli. 
But it is exactly in this class of cases that albumen is frequently 
absent from the urine. Again, in acute Bright’s disease the renal 
epithelium is unduly active, and might be supposed to be peculiarly 
ready to absorb albumen as nourishment, but it is in these cases in 
which the quantity of urine is small that albumen is peculiarly apt 
to be present. *■ bright’s disease, or nephritis. 
639 
It might be supposed that increased blood-pressure in the vessels 
of the glomeruli might lead to albuminuria, but this also does not 
seem to be the case. We shall afterwards see that in chronic 
nephritis the blood is at an excessive pressure, the excess of urine 
being partly due to this, but here albumen is frequently absent. 
Then in active hypersemia there is increased pressure in the vessels 
of the glomeruli, but the urine although excessive in quantity 
contains no albumen. 
The occurrence of albumen seems, in fact, definitely related to 
the structural changes in the kidney. We have seen that the 
inflammation in its acute form affects the glomeruli primarily, and 
it is probably because the structure of the glomerulus is altered 
that the albumen escapes. In this view of it we infer that it is due 
to the structure of the glomerulus that the albumen does not get 
through in the normal kidney, and when this structure, especially 
the epithelium, is tampered with then albumen passes through as 
in ordinary transudations. It is to be presumed that other causes 
besides inflammation may interfere with the epithelium of the 
glomeruli. In acute febrile diseases it may partake in the general 
parenchymatous degeneration of the organs generally, and so 
allow of the passage of albumen. In passive hypersemia also its 
nutrition will suffer and we may have albuminuria. 
Tube-casts.—In cases of Bright’s disease these are usually vis- 
ible in all parts of the tubules, in the convoluted tubules of the 
cortex, the loops of Henle, and the straight tubules, and they are 
sometimes present in very large numbers. Those in the convo- 
luted tubules and in the straight tubules of the pyramids are of 
larger dimensions than in the loops of Henle. For the most part 
the casts are translucent and homogeneous in appearance, forming 
hyaline casts. But there may be epithelium or fatty debris in- 
closed in them, and so we have epithelial and fatty casts. Very 
frequently, as it lies in the tubule, a cast presents a transverse 
fracture, as if by shrinking it had parted in the middle. 
In regard to the origin of these casts, they are probably for the 
most part of the nature of fibrinous exudations. They are mostly 
present in the more acute forms of Bright’s disease, and in these 
forms we have the conditions requisite for the formation of fibrine 
(see p. 93). The albumen in the urine indicates an exudation of 
blood-plasma containing fibrinogen, and there are also leucocytes 
exuded in these acute cases. The coagulation will occur the more 
readily if the tubules have already lost their epithelium. But, 
besides this origin, tube-casts may apparently be composed of 
altered epithelium. Epithelium may be broken down and dis- 
charged from the convoluted tubules and impacted into the loops 
of Henle, where it may form cylinders. The epithelium may also, 
as we have formerly seen, undergo coagulation necrosis, and even 
hyaline cylinders may have this origin. It will be observed, how- 
ever, that such casts are hardly different from the proper fibrinous 
ones, the fibrinogen has the same source, while the epithelium 640 
DISEASES OF THE URINARY ORGANS. 
furnishes the fibrino-plastic substance and ferment instead of the 
leucocytes. 
It is well known that tube-casts are of common occurrence in 
the urine, being washed out of the tubules. In this connection 
it is to be remembered that they are composed of a soft plastic 
substance, and will be readily floated along, accommodating them- 
selves to the various bends of the tubules. Looking to the large 
size of the convoluted tubules as compared with the loops of lLenle 
which immediately succeed them, it has been supposed that tube- 
casts often become impacted in the latter and cause obstruction to 
the exit of the urine. It is very doubtful, however, whether this 
takes place to any considerable extent, the casts are so soft and 
compressible that they probably pass these smaller tubules very 
readily. It seems likely that tube-casts are often present in much 
larger numbers in the kidneys after death than they have usually 
been during life. Just before death the blood-pressure is generally 
low, and the secretion of urine diminished, so that the casts are 
not washed out as they are during the more vigorous period of 
life. 
We have next to consider the changes in the heart and arte- 
ries which are frequent concomitants of Bright’s disease. Of the 
structural changes, the most important are hypertrophy of the 
left ventricle of the heart and of the walls of the vessels, while 
the increased tension in the arteries is the most important func- 
tional alteration. 
We have already referred to the hypertrophy of the left ven- 
tricle of the heart, and ascribed it to increase of the arterial ten- 
sion. It has been held that the hypertrophy of the heart is itself 
the cause of the increased arterial tension, or at least that it is a 
concomitant, but it is now generally acknowledged that the in- 
crease of the muscular tissue of the heart is due to an effort to 
overcome an excessive resistance in the peripheral bloodvessels. 
There are several diflicult questions which here come up for con- 
sideration. One of these is whether the lesions in the kidney are 
sufficient of themselves to produce increased blood-pressure in the 
general systemic arterial system. If this question be answered in 
the negative, then it has to be decided whether the changes in the 
arteries throughout the body are consequent on the kidney disease, 
or coincident phenomena due to the irritant which produces the 
lesions in the kidney. 
Here, at the outset, it is important to remark that in these dis- 
cussions we have to do with chronic Bright’s disease, that is to 
say, with cases in which interstitial changes have occurred. The 
changes occur most typically with the pronounced cirrhotic kidney, 
but they are also present with the large white kidney if the inter- 
stitial change be at all considerable. The hypertrophy of the heart 
does not occur unless the general health of the patient be suffi- 
ciently good to allow of the muscular substance of the heart being 
well nourished. Hence it is absent»in cases where the presence of bright’s disease, or nephritis. 
641 
amyloid disease indicates that the blood is deteriorated. It is also 
absent in cases where a profuse albuminuria has rendered the 
blood highly watery. 
Of late years there has been a tendency to regard the increased 
arterial tension as due to changes in the smaller arteries through- 
out the body, the changes in the kidney being merely a part of a 
genera] vascular lesion. This view has received its most systematic 
formulation in the descriptions by Gull and Sutton of the so-called 
arterio-capillary fibrosis. Their view is that in the finer arte- 
ries and capillaries a development of fibrous tissue occurs, and 
that, though this may begin in the kidneys, it may also take origin 
in other organs. The contraction and atrophy of the kidneys, in 
this view, are but part and parcel of the general morbid change. 
We have here, then, represented a general disease of the vessels 
as the essential basis of chronic Bright’s disease. Still more lately, 
Mahomed has asserted the existence of increased arterial tension 
with hypertrophy of the left ventricle without any considerable 
disease of the kidney, and he even speaks of a stage of “ chronic 
Bright’s disease without nephritis.” 
As to the arterio-capillary fibrosis of Gull and Sutton, there are 
many very competent observers who, after careful investigation, 
have denied its existence altogether. The arteries usually chosen 
for investigation are those of the pia mpfer, and while hypertrophy 
of the muscular coat is generally acknowledged to be present, the 
thickening of the external coat is much more doubtful. It may 
be acknowledged that the walls of the arteries are thickened, how- 
ever, and the degree of thickening may be inferred from the 
accompanying figures (Fig. 277) from Dr. Dickinson’s work on 
Fia. 277. 
Gi'cixv.JL. 
7vccHthif 
Gritiv.H. 
(in/G&j&cruie) /'80 dicun s. 
Arteries of the pia mater in case of granular kidney and in health. In the former the 
middle coat and, to some extent, the external are thickened. (Dickinson.) 
Albuminuria. It may quite well be, however, that these condi- 
tions are really the result of increased tension. If the blood is 
present in the finer arteries at an increased pressure, then in order 
to prevent a permanent active hypersemia the muscular coat must 
contract more vigorously, and this will produce a hypertrophy of 
it. The thickening of the external coat will fortify the middle 
coat and assist in keeping the circulation in proper condition. 
This raises the important question whether there is any proof 642 
DISEASES OF THE URINARY ORGANS. 
that lesions of undoubted renal origin ever produce increased 
arterial tension and hypertrophy of the heart. In order to answer 
this question it is necessary to leave out of account all cases in 
which the origin of the kidney disease is obscure, because it may 
he said that in these cases arterial changes have occurred simul- 
taneously elsewhere, and had a similar cause. 
In answer to this question various facts may he adduced. Dick- 
inson refers to cases in which distention of the pelvis of the kidney 
from stone has led to the contracted kidney with all the vascular 
and cardiac lesions. Then there are on record a considerable 
number of cases of double hydronephrosis in which extreme hyper- 
trophy of the left ventricle has been present. Decently Gravitz 
and Israel have produced nephritis in animals by ligaturing the 
renal artery on one side for one and a half to two hours, and then 
letting the ligature loose. The consequence was similar to that 
already referred to in regard to ligature of the arteries in the ear 
of the rabbit, namely, an acute inflammation. If the animal sur- 
vived long enough the inflammation resulted in contraction of the 
kidney, and in many cases there was hypertrophy of the left ven- 
tricle of the heart. Here is an undoubted case in which disease 
artiflcially induced in one kidney has resulted in hypertrophy of 
the left ventricle. 
When we consider that hypertrophy of the left ventricle results 
not only from the ordinary chronic nephritis, but also in cases 
which have begun acutely after scarlet fever, and where the con- 
dition presented is that of the large white kidney; when we see 
also that a disease such as double hydronephrosis which obstructs 
the circulation in the two kidneys, as well as a shrinking of the 
kidney artificially produced, are followed by hypertrophy of the 
heart, then we seem forced to the conclusion that the increased 
arterial tension and hypertrophy are really due to the disease in 
the kidneys. The general statement may indeed be made that, 
given a disease which seriously obstructs the capillaries and 
smaller arteries of both kidneys, you will have hypertrophy of the 
left ventricle, provided the person is in a tolerably vigorous state 
of health. 
That there is a serious obstruction of the capillaries and small 
arteries of the kidney in interstitial nephritis does not admit of 
question. The mere anatomical details indicate this. We have 
seen that the uriniferous tubules, with their surrounding capilla- 
ries, are greatly destroyed, and the glomeruli to a large extent 
reduced to solid clumps. In addition to this the result of injection 
with colored material shows that there is great impermeability of 
the capillaries and of the vessels of the glomeruli. This has been 
proved in a different way by some important observations of 
Thoma. He has injected at a constant pressure dilute solutions of 
common salt and gelatine into the renal artery in normal and con- 
tracted kidneys, and observed the amount which flowed out by the 
veins in a given time. In the case of the contracted kidney the bright’s disease, or nephritis. 
643 
outflow per minute was considerably reduced, evidently pointing 
to an obstruction in the finer vessels. 
We have now to point out that the effect of this obstruction in 
the capillaries and glomeruli will be to increase the blood-pressure 
in the remaining arteries of the kidney, provided there is no 
serious obstruction in them. The endarteritis which we saw to 
exist in interstitial nephritis narrows the calibre to some extent, 
but careful measurements by Thoma show that on the average the 
size of the arteries is but very slightly diminished, and that in 
comparison with the weight of the kidney the arteries are greatly 
larger than the normal. Under these circumstances, with a normal 
pressure in the aorta, there will be an excessive pressure in the 
general renal arteries and this pressure will tell on the vessels of 
the glomeruli which remain unobstructed. 
There are several facts which indicate that the pressure, in the 
vessels of the glomeruli which remain pervious, is very excessive. 
The author, in a paper published in 1875, recorded some observa- 
tions on injections of the kidneys in Bright’s disease. When a 
solution of gelatine colored with carmine was injected into the 
renal artery, in cases of chronic Bright’s disease, it was found that 
while the capillaries were largely uninjected, the mass ran to a 
considerable extent from the glomeruli into the convoluted tubules. 
This would indicate an excessive pressure in the vessels of the 
glomeruli. Then the occurrence of blood-corpuscles in the tu- 
bules in interstitial nephritis is not infrequent, the blood being 
present in the first part of the tubules and obviously coming from 
the glomeruli. 
The excessive pressure in the glomeruli is also indicated during 
life by the large amount of urine secreted by the contracted 
kidney. The increase in the general arterial tension, with the 
hypertrophy of the heart, doubtless has to do with this increased 
flow of urine, but when we consider that in cases of contracted 
kidney there are frequently only a few glomeruli still pervious, 
we may infer that a very excessive pressure must exist in their 
vessels in order to produce this exceedingly abundant flow. 
One of Thoma’s observations is of considerable importance 
here. In his various experiments, in which gelatine and salt solu- 
tion were injected into the renal artery, he used a constant pressure. 
He desired to obtain the pressure in the renal artery, and in order 
to obtain this approximately, he connected the eanula inserted 
into that artery with a manometer. He found that while in the 
normal kidney the pressure was 14.5, in the contracted kidney it 
amounted to from 15 to 15.7 cm. of mercury. There was thus, 
even in the main renal artery, an abnormally high pressure in the 
contracted kidney, and in the finer arteries the excess of pressure 
must have been still greater. 
We have now to consider what bearing these facts have on the 
question of increase of the general arterial tension. It is clear 
that, though the obstruction in the renal circulation is sufficient to 
raise the pressure in the renal arteries, it alone is not enough to 644 
DISEASES OF THE URINARY ORGANS. 
raise it in the general systemic arteries, considering that there are 
such means of varying the tension in the arteries by relaxing or 
contracting the muscular coat. Ligature of the renal artery or 
extirpation of the kidney has not been found as a rule to raise the 
tension, and even ligature of the aorta at its bifurcation does not 
raise it for any considerable time. Even the view of Cohnheim 
cannot meet with general acceptance, at least in its original form. 
According to this view ansemia of an organ must be compensated 
either by hypersemia in another organ or else by loss of a corre- 
sponding amount of blood, otherwise a rise in the blood-pressure 
occurs. When one kidney is excised or its artery ligatured a col- 
lateral hypersemia occurs in the other kidney and it undergoes 
compensatory hypertrophy. But when both kidneys are simul- 
taneously diseased, as in Bright’s disease, there is no organ to 
compensate, and if the arteries of the kidney are to admit as much 
blood as normal there must be a rise of blood-pressure in them. 
Looking now at the matter more closely, we have seen that, in 
the case of the contracted kidney, with a normal pressure in the 
general arterial system there is a greatly increased pressure in the 
finer renal arteries, and a considerable increase even in the main 
renal artery. This increase will be communicated to the general 
systemic circulation, as the renal arteries are in communication 
with the aorta. Let us suppose that it is at once compensated by 
a relaxation of many arteries throughout the body, and the pressure 
falls to normal. But even at the normal pressure there is a com- 
parative increase of pressure in the renal arteries which is again 
communicated to the general circulation. So that as soon as there 
is a fall of pressure there will be a fresh renewal of the excessive 
pressure from the renal arteries, and it will be again raised. But 
if the rise of pressure is not immediately compensated by relaxa- 
tion of the peripheral arteries throughout the body, then the blood 
passing into the renal arteries at an excessive pressure will, in the 
arteries of the kidney, be raised to a pressure still further above 
the normal for these vessels. 
We have seen that the arteries proximal to the glomeruli are 
hardly at all reduced in calibre, and with the great obstruction 
ahead we may suppose these arteries distended and their walls re- 
acting against the excessive pressure of the blood. It is as if at a 
part of the arterial system there were the continuous action of an 
apparatus engaged in raising the general pressure within this 
system. 
On these principles we can even understand how, under certain 
circumstances, excision of one kidney may produce permanent in- 
crease of tension. After excision of one kidney the arteries of 
the other undergo a considerable relaxation and there is a collateral 
hypersemia. An excessive amount of blood reaches the glomeruli, 
and it is conceivable that these and the capillaries may be unable 
to allow of the passage of this excessive blood quite freely. There 
will be thus a comparative obstruction in the glomeruli and capil- 
laries with increased pressure in the arteries. As a rule, this is septic inflammations of the kidney. 
645 
not sufficient to affect the general circulation, hut according to the 
experiments of Gravitz and Israel extirpation of one kidney does 
lead to hypertrophy of the heart when the other does not fully 
compensate. 
By some it may he supposed that, considering the small capacity 
of the renal arteries as compared with that of the entire arterial 
system, the effects of such a local increase of pressure must be 
very limited and insufficient to account for the general rise in 
pressure. If this argument be well founded then we have to look 
for some permanent obstruction in the systemic circulation, either 
in the arteries or in the capillaries, to explain the increased tension. 
From what has gone before it is manifest that such changes, if 
they exist, must be secondary to the lesions in the kidney, and are 
to be probably referred to changes in the constitution of the blood 
causing morbid effects in the arteries and capillaries. We may 
even suppose that the altered blood has greater difficulty in pass- 
ing through the capillaries generally than normal, and this would 
produce increase of tension in the arteries. 
SEPTIC INFLAMMATIONS OF THE KIDNEY. 
These are such as are induced by the presence in the organ of 
septic organisms. There are two important classes of cases; in 
one the source of the organisms is outside the urinary organs, the 
septic material being brought by the blood; in the other the source 
of the organisms is decomposition of the urine in the bladder, and 
they are propagated up from the latter. 
We have already seen that in pyaemia and ulcerative endo- 
carditis pieces of librine or other material may he carried to the 
kidneys and produce embolism there. In this way arise meta- 
static abscesses. For the most part the emboli are small and are 
carried to the ascending arteries or the glomeruli before they 
stick. Hence the abscesses are mostly in the cortical substance, 
although they are not infrequently seen in the pyramids along 
the course of the arterise rectse, and there may even he large ones 
taking in portions both of pyramids and cortex. The abscesses 
are usually elongated in the direction of the arteries, and they 
often project slightly from the surface when the capsule is removed. 
They are frequently present in considerable numbers in both 
kidneys. 
Under the microscope it can be seen that the abscesses arise by 
obstruction of the arteries (see Fig. 278). Where the embolism 
has been recent, the wall of the vessel and the tissue in the imme- 
diate neighborhood of the embolus present evidences of necrosis, 
while around there are multitudes of leucocytes occupying the 
interstitial tissue. In the embolus there are colonies of bacteria 
in the midst of remains of the transported fibrine. When the 
abscess has fully formed, these characters may he lost in the great 
multiplication of leucocytes. Besides in the arteries, colonies of 646 
DISEASES OF THE URINARY ORGANS. 
bacteria are to be found in the vessels of the glomeruli, sometimes 
filling many of them out with a dark, granular mass, and also in 
the capillaries. It is sometimes to be seen that these colonies are 
present in the glomeruli and capillaries without signs of inflam- 
mation around. In such cases they are of recent growth and have 
Fig. 278. 
From a section of the kidney in ulcerative endocarditis. An artery is plugged with dark 
material which contains micrococci. In the neighborhood of the plug the wall of the artery 
is necrosed. Leucocytes are infiltrating the tissue around, and extending through the vessel 
wall. X 90. 
not liad time to produce inflammation by giving off irritating 
products. To some extent the bacteria may multiply in the glom- 
eruli and capillaries after death. 
The bacteria found in these cases, as probably in all septic 
inflammations, are micrococci (see Fig. 279). 
In cases of scarlet fever colonies of bacteria are sometimes to 
be seen in the capillaries and uriniferous tubules of the kidney 
(Fig. 280). They are not evidently accompanied by local inflam- 
mation, and it is not improbable that we have here to do with the 
specific organisms of the fever, which have been sparsely present 
in the kidney at the time of death—perhaps in process of excretion 
—and have multiplied into colonies after death. septic inflammations of the kidney. 
647 
Pyelonephritis.—The other kind of septic inflammation arises 
in connection with inflammation in the bladder, ureter and pelvis 
of the kidney. As the inflammation of pelvis and kidney is con- 
tinuous, the condition is often designated pyelonephritis, which 
means a combined inflammation of these two. The inflammation 
Fig. 279. 
Micrococci in a capillary (6) of the kidney from a case of pyaemia. There is a tubule on 
either side, the nuclei of whose epithelium (a, a) are visible except in the neighborhood of 
the micrococci, where they seem to be destroyed. X 650. 
in all these parts is septic, due to the action of bacteria producing 
decomposition of the urine. We shall have to study afterwards 
the condition of the bladder, ureters, and pelvis in these cases, but 
meanwhile we have to note that the organisms may propagate 
themselves into the kidney tissue. For the most part they enter 
the tubules from the pelvis of the kidney, and are to be found 
Fig. 280. 
Bacteria distending a capillary bloodvessel in a case of scarlet fever. X 350. 
forming the usual colonies inside the tubules, although sometimes 
the alterations in the tissue are such that it is difficult to determine 
whether the organisms are in the tubules or in capillary bloodves- 
sels, especially as the epithelium is often necrosed and overwhelmed 
with bacteria. 648 
DISEASES OF THE URINARY ORGANS. 
Besides this regular path of entrance, the organisms may pene- 
trate from the ureter or bladder into the loose connective tissue 
around, and as this is continuous with that around the kidney, 
they may propagate up to the capsule of the kidney, producing 
abscesses there (perinephric abscesses), as well as penetrating into 
the kidney from the surface, and forming abscesses in it. This 
mode of travel has been followed out by Dr. Steven in a case 
which came under observation here. 
The septic material in the tubules affects the renal epithelium 
most directly, causing necrosis and disintegration of it. But the 
dissolved products extend beyond the tubules and set up an acute 
inflammation of the kidney substance. The inflammation may be 
tolerably homogeneous, the leucocytes infiltrating the whole inter- 
stitial tissue, and appearing also in the uriniferous tubules. But, 
as a rule, there are special foci, in which it goes on to suppuration, 
resulting in the formation of small abscesses. When the abscesses 
have formed, it is usually difficult any longer to find the bacteria. 
The appearance of the kidneys in such cases is usually suffi- 
ciently distinctive. It often happens that only one kidney is 
affected, the septic process having extended up one ureter and not 
the other. In this respect this disease differs from the preceding 
one, where the metastatic abscesses are always present in both 
kidneys. The kidney is greatly enlarged, and, generally with 
signs of inflammation of the pelvis, there are numerous small 
yellow points and abscesses in the kidney tissue. The abscesses 
are in the form of elongated streaks in the direction from pelvis 
to surface, and they are present as well in the pyramids as the 
cortex. They are sometimes in groups, and we may have such 
groups visible, projecting from the surface, when the capsule is 
removed. 
As a general rule the patient dies with these miliary abscesses 
in the kidney, but if only one kidney is involved he may survive 
and the process assume a further development. The abscess, by 
fresh invasion of bacteria, may multiply and coalesce. In this 
way abscesses of large size may form, finally, perhaps, involving 
the entire kidney out to its capsule. The abscess ma}7 even 
increase in size after the whole kidney is destroyed, and form a 
bulky tumor. The suppuration may extend beyond the kidney 
and lead to perinephric abscess. Perforation sometimes occurs 
externally, or into a neighboring loop of intestine. 
Sometimes these abscesses have no communication with the 
pelvis throughout their course. But not infrequently they are 
associated with and originate in suppuration in the pelvis. In 
that case the destruction of the renal tissue proceeds in a more 
regular manner out from the pelvis, following the arrangement of 
the calices to a large extent. In this way the abscess may be 
divided by partial septa, and the kidney may come to have an 
appearance like that in hydronephrosis, but in this case pus fills 
the cyst—pyonephrosis. 
With this great production of pus, or after it has attained its 649 
retrograde changes in the kidneys. 
height, there may be production of cicatricial connective tissue, 
limiting the abscesses, and by its contraction producing sometimes 
considerable deformity. If the production of pus ceases the 
abscesses may dry in, and we may have the cavities filled with a 
pultaceous material from fatty and calcareous deposition. Some- 
times the cavities of the abscesses contract greatly, and there may 
remain simply a shrunken kidney with some cavities in which are 
pieces of chalky substance or pultaceous material. It will be 
understood that these abscesses very often do not communicate 
with the pelvis, and that when they do the shape of the kidney is 
much better retained. In the shrunken kidneys there is often 
considerable obliteration of the pelvis from inflammatory adhesion. 
Pyelitis.—This name is given to inflammation of the pelvis of 
the kidney, and it is very frequently associated with inflammation 
of the kidney itself. Even in acute Bright’s disease there is often 
some inflammatory congestion of the pelvis of the kidney, and 
inflammations originating in the pelvis frequently spread to the 
kidney proper. Inflammation of the pelvis is very frequently 
septic, and in that case, as we have seen, it may associate itself 
with a septic inflammation of the kidney, and go on to pyelone- 
phritis. Sometimes the inflammation of the pelvis is particularly 
violent, so as to assume a necrotic character, going rapidly on to 
suppurative nephritis, and perinephritis. 
Pyelitis is sometimes set up by the irritation of calculi in the 
pelvis. It is here for the most part a chronic inflammation. 
Chronic inflammation may also occur as the result of stagnation 
of urine from obstruction in the urinary passages. The mucous 
membrane is thickened, sometimes showing even irregular pro- 
jections, and is not infrequently incrusted with phosphates from 
the stagnating urine. In this way calculi may form, and it may 
be difficult to say whether an existing calculus is the cause or the 
effect of the inflammation. 
RETROGRADE CHANGES IN THE KIDNEYS. 
Some of these occur, as we have seen, in the renal epithelium in 
Bright’s disease, chiefly cloudy swelling and fatty degeneration, 
but we have here to do with such as are met with more inde- 
pendently. 
Simple atrophy occurs mostly as one of the phenomena of old 
age. The wdiole structures of the kidneys undergo diminution in 
size, but very often this affects especially the secreting epithelium 
of the convoluted tubules. If this be the case there may be a 
special shrinking of the cortex, and the kidneys may he like those 
of chronic Bright’s disease. Sometimes also the surface is granular 
and the capsule adherent. 
Parenchymatous infiltration, or cloudy swelling, must be 
remembered as liable to occur in acute febrile diseases. There is 650 
diseases of the urinary organs. 
a general enlargement of the renal epithelium with infiltration of 
fine granules in the midst of which fine fat-drops are scattered. 
(Fig. 281.) The pyramidal tubules as well as those of the cortex 
Fig. 281. 
Cloudy swelling of renal epithelium. The cells are enlarged and filled with fine granules, 
in addition to which there are occasional minute oil-drops. X 350. 
are involved, the affection being usually homogeneous. It is 
important to note that this condition may produce considerable 
enlargement of the kidney without obvious change in its structure 
to the naked eye. 
Fatty degeneration of the renal epithelium is not infrequently 
present in cachectic conditions such as advanced phthisis pul- 
monalis, in which, however, it is often associated with amyloid 
disease or interstitial nephritis. In severe anaemias it is also met 
with along with fatty degeneration of the muscular substance of 
the heart. It occurs, too, in acute yellow atrophy of the liver. 
Amyloid degeneration of the kidney develops, as we have 
already seen, along with amyloid disease in other organs in conse- 
quence of certain altered states of the blood. As in other situa- 
tions, so here it is chiefly the walls of the bloodvessels which are 
affected. 
Even in very early cases, in which the amount of amyloid dis- 
ease is slight we usually find it in two distinct and separate 
structures, namely, the Malpighian tufts and the arteries rectee of 
the pyramids. The vessels of the tufts, generally along with the 
arteries leading to them, are swelled up and hyaline. The rose 
color developed with methyl-violet is so striking that in sections 
stained with this dye it often looks as if the tufts were injected. 
They are also considerably enlarged, and even without the addition 
of iodine or methyl-violet they form very prominent, transparent 
and glancing clumps in the cortex. The arterise rectse run, as we 
have seen, in hunches, and their appearance with methyl-violet is AMYLOID DISEASE OF THE KIDNEYS. 
651 
that of a series of rose-colored tubes. They are also sufliciently 
pronounced, as a rule, without any reagent, appearing as pearly 
glancing tubes. 
While these structures are first and chiefly involved, others 
usually follow. There is amyloid disease extensively present in 
the arteries of the cortex, the ascending and afferent arteries. 
Very often there is here and there a capillary of the cortex affected, 
and sometimes these are extensively so even in comparatively slight 
cases. Lastly the basement membrane of the tubules may become 
amyloid, chiefly in the cortical substance. (See Fig. 282.) 
Fig. 282. 
Amyloid degeneration of the basement membrane of uriniferous tubules. The thickened and 
translucent basement membrane is shown with the renal epithelium inside. X 350. 
Along with the amyloid disease of the vessel there is usually 
fatty degeneration of the epithelium of the tubules, apparently the 
result of anaemia from the obstruction of the vessels. 
There is also very often interstitial inflammation present, and it 
is frequently so great as to present a combination of the amyloid 
and contracted kidney. Fig. 283 shows a microscopic section of 
such a kidney in which the amyloid glomeruli are brought close 
together by contraction and destruction of the tubules. 
This combination of contracted and amyloid kidney is some- 
times met with in syphilis, the virus of which may be the cause of 
the interstitial inflammation. Again in phthisis pulmonalis, and 
in extensive suppurations from diseased bone, there may readily 
occur an absorption of irritating materials which are capable of 
settingup inflammation. The contracted amyloid kidney is not 
accompanied by hypertrophy of the heart, the reason apparently 
being that, as the blood is deteriorated, the compensatory growth 
of muscular tissue can scarcely occur. 652 
DISEASES OF THE URINARY ORGANS. 
In regard to the naked-eye appearances, the simple amyloid 
kidney is enlarged, and sometimes greatly enlarged, so that the 
organ weighs nine or ten ounces. The surface is pale and the 
capsule comes oft* easily. On section, the cortex is seen to be 
thickened and pale in color. The general appearance, therefore, 
resembles that of the large white kidney, and doubtless many 
cases have been mistaken for that. But the organ in amyloid dis- 
ease has a firm elastic feeling and a transparent bacony appearance 
on section, which is distinctive enough. The thick pale trans- 
parent cortex usually contrasts with the redder but still tolerably 
Fig. 283. 
Amyloid and contracted kidney. The highly amyloid and therefore greatly enlarged 
Malpighian tufts are shown, their capsules being somewhat thickened. The tufts are very 
unduly close together, owing to contraction of the intervening tissue. Between them there 
is round-cell tissue with remains of tubules. X 85. 
firm pyramidal substance, and the appearance has been somewhat 
aptly compared to the section of bacon ham. The name larda- 
ceous kidney is often applied from the transparent appearance of 
the tissue. In the midst of the transparent basis, opaque yellow 
streaks are often visible, from the fatty degeneration of the epi- 
thelium. The addition of a solution of iodine to the cut surface 
of such a kidney brings out the affected glomeruli as brown dots, 
and the arterise rectse as brown streaks. If the kidney be con- 
tracted, the granulations on the surface show the usual transparent 
waxy appearance of the amyloid kidney, and on section the cortex, 
though greatly thinned, shows a similar condition. 
The amyloid substance apparently allows fluid to pass through 
it more readily than ordinary albuminous structures. Injection of 
the amyloid kidney shows that the vessels of the glomeruli and the 
arteries of the cortex are largely obstructed. It may well be that 
this leads to increased blood-pressure in the remaining arteries, 
but with the general narrowing of the smaller arteries this can 
hardly tell with much force on the glomeruli which remain per- 
vious. The excessive secretion of urine, like the diarrhoea which 653 
CONCRETIONS AND CALCULI IN THE KIDNEY. 
is a prominent symptom in amyloid disease of the intestine, is 
probably to be accounted for by a greatly increased transudability 
of the vessels. 
CONCRETIONS AND CALCULI IN THE KIDNEY. 
Two very interesting forms of deposition in the tubules are 
met with in new-bobn ciiildben. In the common icterus of the 
new-born the biliary coloring matter (bilirubin) is excreted, as 
in the adult, by the kidneys, but in the new-born it very readily 
passes into the crystalline form, so that round or rhombic orange- 
colored crystals are found in the pyramidal tubules, sometimes in 
such numbers as to warrant the designation bilirubin-infarction. 
Similar crystals are found in the blood and tissues of the body. 
Uric acid is found in the tubules of new-born children, in about 
half the cases of those which die within the first few weeks. It 
is mostly in children who have breathed that the crystals are met 
with, but they have been observed in still-born children, although 
very rarely. The concretions consist of salts of uric acid (mostly 
urate of ammonia), and they are deposited mainly in the tubules 
near the apices of the pyramids, giving the appearance of opaque 
yellow or reddish streaks, converging to the apex of the pyramid. 
Under the microscope, amorphous urates are seen in the tubules, 
and when acetic acid is applied these dissolve and form crystals of 
uric acid. 
Urates are also deposited in the substance of the kidney in 
gout. In that disease, salts of uric acid (urate of soda) are de- 
posited, as we have seen, in the fibrous and cartilaginous structures 
in the joints, but they may also appear in crystalline masses in 
the kidney. These lie in the thickened connective tissue of the 
contracted kidney. 
Lime salts are sometimes deposited in the straight tubules of 
the pyramids, especially in cases where from disease of bone there 
is excessive absorption of lime salts and excretion of them by the 
urine. The appearance presented is that of white streaks usually 
near the apices of the pyramids. It is to be observed, however, 
that a deposition of urates occurring after death in the straight 
tubules may produce a somewhat similar appearance. 
Calculi are of frequent occurrence in the pelvis of the kidney. 
As we have seen, they nray originate from chronic pyelitis, espe- 
cially with stagnation of urine, but they may apparently originate 
in the uriniferous tubules, and having passed into the pelvis 
grow larger there. They sometimes attain very large dimensions, 
moulding themselves into the shape of the pelvis and calices, so 
that we may have branches extending out into elongated recesses 
formed by dilated calices. By obstructing the flow of urine these 
calculi may lead to the occurrence of hydronephrosis, and as the 
cavity of the pelvis and calices enlarges so may the calculus. A 654 
diseases of the urinary organs. 
small calculus will often pass into the ureter and obstruct it, in 
this way leading to hydronephrosis. 
SYPHILIS AND TUBERCULOSIS OF THE KIDNEY. 
Syphilitic Disease is rare in the kidney, unless it be that some 
cases of contracted kidney from interstitial nephritis are due to 
this cause. Gummata have been found in a very few cases. 
Tuberculosis occurs as part of a general tuberculosis or as a 
local disease. In acute miliary tuberculosis there are usually 
numerous tubercles scattered throughout the kidney. These 
mostly occur in groups visible to the naked eye, and they may 
even assume considerable dimensions. They are most abundant 
in the cortex, and they are prone to become caseous. 
Local Tuberculosis gives rise to the condition frequently called 
renal phthisis. The tuberculosis here is often propagated from 
the bladder and ureter, and may even originate in the passages of 
the organs of generation, as the vas deferens and vesiculse semi- 
nales. On the other hand, it very often originates in the kidney, 
and extends down the ureter. The disease is usually of one kid- 
ney, or at least involves one much more than the other. 
It may begin in the pelvis of the kidney, in the calices, or at 
the apices of the papillae, and there are the usual phenomena of 
tubercular ulceration. Tubercles are formed which become case- 
ous and break down so as to form an ulcer. Fresh tubercles form 
outside the ulcer which undergo the same process and produce an 
extension of the ulcer. There is thus a continually extending 
ulceration, and a continually growing irregular cavity. But the 
extension of the ulcers occurs mainly into the kidney tissue, ad- 
vancing here apparently by reason of the less resistance of the 
tissue. We have already seen that the papillae are often attacked 
at the very first, and the ulceration extends into the pyramids, 
sometimes eating its wray a considerable distance in. If several 
papilhe have been attacked, then we may have several ragged 
pouches extending out from the pelvis like prolongations of the 
calices, or even the whole kidney may be converted into an irreg- 
ular cavity divided by partial septa. This condition is to be dis- 
tinguished from pyelonephrosis, chiefly by the irregular ulcerated 
surface and the presence of broken-down caseous material. 
Under the microscope, the kidney tissue around the ulcer will 
be found infiltrated with round cells, in the midst of which tuber- 
cles in various stages of alteration will be discovered. The proper 
secreting tissue within this area will be pushed aside and greatly 
destroyed. 
The tubercular ulceration affects the pelvis of the kidney, and 
usually the ureter. Their walls are thickened and infiltrated. In 
the case of the ureter, the caseous material, instead of softening 
and discharging, may remain as a dense yellow layer lining the HYDRONEPHROSIS. 
655 
greatly thickened tube. The wTall of the tube showys multitudes 
of inflammatory round cells in the midst of which tubercles appear, 
but their outlines are frequently obscured by the round cells. The 
existence of giant-cells at intervals may indicate their presence. 
HYDRONEPHROSIS. 
In this condition there is a dilatation of the pelvis and the caliees 
of the kidney, as a result of obstruction of the ureter or urethra. 
The obstruction occurs in a considerable variety of ways. It may 
he congenital, and is then usually in the urethra, in which case 
there is dilatation of bladder, ureters, and pelves. Acquired 
stricture of the urethra is a less frequent cause, as it tends rather 
to produce dilatation and hypertrophy of the urinary bladder. A 
very frequent cause is obstruction of the ureter, and this itself is 
brought about very variously; as by a calculus descending from 
the pelvis, a tumor pressing on the ureter in some part of its course, 
a hydatid cyst bursting into the pelvis of the kidney, even a renal 
artery taking an abnormal course and crossing in front of the 
ureter below the pelvis. Sometimes the ureter does not, as in the 
normal condition, form a continuation of the pelvis, but starts 
from it at an acute angle, passing obliquely through its wall, very 
much as the lower end of the ureter passes into the bladder. In 
that case, distention of the pelvis valves the upper orifice, and the 
valve may be only relieved when great dilatation is reached. This 
obstruction will be intermittent. Again, an abrupt bend in the 
ureter sometimes causes obstruction; this may be from a congen- 
ital convolution in its course, or the ureter may turn more abruptly 
than usual over the brim of the bony pelvis, if the edge here be 
unusually sharp. Such a sharp edge may be formed by the iliac 
arteries at the brim of the pelvis, when the tissues which naturally 
pad them are atrophied, as in cases of general emaciation. It 
appears from this last instance that a comparatively small external 
pressure may obstruct the ureter, and that the urine in the pelvis 
and ureter is at such a low pressure as to be incapable of over- 
coming a comparatively slight resistance. 
As already seen, the result of the obstruction is dilatation of 
the pelvis and calices (Fig. 284), but, in addition, there is frequently 
a considerable destruction of renal tissue. That is to say, the 
calices in dilating cause atrophy, first of the papillae which project 
into them, and then of the pyramidal portion of the kidney, ad- 
vancing into the deeper parts of the organ. We thus sometimes 
find the pyramids as if cut abruptly across transversely. But the 
condition frequently advances still further. The dilated calices 
increase in volume till, in the most extreme case, the kidney is 
replaced by a cyst which represents dilated pelvis and calices, 
partitions existing in it corresponding to the divisions between 
the calices. When this has occurred, the cyst may go on enlarg- 
ing so as to form a tumor of great bulk. The ureter is also 656 
DISEASES OF THE URINARY ORGANS. 
dilated, often very greatly, so as to look like a piece of small 
intestine. It sometimes becomes convoluted in its course as well. 
It is not in every case quite apparent what circumstances deter- 
mine the degree of hydronephrosis. With complete obstruction 
we may have a moderate dilatation, and with an apparently trivial 
obstruction it may be much more 
considerable. In order to under- 
stand how this may be, it will be 
necessary to. refer to the course of 
events when the ureter is obstructed. 
The ureter has been ligatured in 
animals and the processes observed. 
The first result is dilatation of the 
pelvis and of the ureter above the 
ligature. The tension of the urine 
in the ureter also rises up to a cer- 
tain point, which, however, is far 
below the blood-pressure. When 
this point is reached, the full extent 
of the distensile force .derived from 
the secretion of the urine is attained. 
The secretion of urine, consisting 
in the transudation of a watery 
fluid through the vessels of the 
glomeruli, is due to the difference 
in pressure between the blood in 
the tufts and the fluid in the 
tubules, and, when the pressure in the tubules is raised, the secre- 
tion of urine ceases as soon as a state of equilibrium is brought 
about. 
There are, however, two elements in the problem still to be 
considered. In cases where the ureter has been ligatured in 
animals, the actual dilatation of the pelvis and calices has been 
comparatively slight, the state of equilibrium of tension being 
easily reached. In cases met with in the human subject, it appears 
also that, where the obstruction is complete, the hydronephrosis is 
generally much less considerable than where the obstruction is 
incomplete or is relieved at intervals. The extreme dilatation 
which constitutes a complete hydronephrosis may be met with, for 
instance, in cases where the ureter has an abnormal insertion into 
the pelvis, and the urine only gets out when the dilatation has 
reached a certain point, or where the ureter has a sudden bend in 
it, and the obstruction is overcome when the dilatation is sufficient, 
as it were, to round out the bend; or, again, where the pressure 
of a tumor causes an occasional obstruction. The explanation of 
this seems to be that, when the obstruction is complete, the press- 
ure of the fluid in the dilated pelvis soon causes considerable 
obstruction of the renal vessels, and the power of secretion is 
reduced. But if at times an outlet is formed for the urine, and 
the pressure is suddenly reduced, there will be a relief of the 
Fig. 284. 
Kidney in hydronephrosis. The 
pelvis and calices are greatly dilated, 
and the renal tissue reduced to a thin 
layer. (Virchow.) TUMORS OF THE KIDNEY. 
657 
vessels in the kidney and a violent hypercemia leading to an ex- 
cessive secretion of urine. As a matter of fact, the sudden relief 
of an obstruction of the ureter has been found to be followed by 
an excessive secretion of urine which contained albumen. Where 
then there are such repeated sudden collapses and dilatations the 
advance of the hydronephrosis is much more complete. 
At first the dilated pelvis and calices contain urine, but as the 
condition gets fully established the urinary constituents become 
absorbed, and a watery, albuminous fluid is found. Sometimes 
the dilatation is due to a calculus in the pelvis of the kidney, and 
in that case there may be inflammation, possibly with suppuration. 
If pus tills the cyst, then the condition is designated pyonephrosis. 
It sometimes happens that, where a prolonged obstruction has 
existed, the external fatty capsule of the kidney is greatly thick- 
ened, while only a moderate hydronephrosis exists, the external 
outline of the organ being not at all increased. It is not unlikely 
that an oedema of the capsule following the obstruction of the 
ureter may be the cause of this great new formation of fat by 
affording an extra supply of nourishing fluid, or perhaps by acting 
as a prolonged irritant. 
We sometimes meet with cases resembling hydronephrosis, but 
in which some of the cysts, representing dilated calices, do not 
communicate with the pelvis, but form independent cysts. This 
occurs when from inflammation there has been partial or complete 
obliteration of the pelvis. The inflammation may be caused by 
the presence of calculi in the pelvis, and some of the cysts may 
contain calculi. Again, an inflammation of the pelvis may extend 
to a dilated calyx, which, with others, is afterwards shut off by 
adhesion and obliteration of the pelvis. In that case we may have 
a cyst full of pus, or of the pultaceous material which we have 
seen to result from changes in the pus in pyonephrosis, and such 
cysts may be alongside others which have serous contents, these 
latter having been shut off before inflammation has extended to 
them. 
TUMORS OF THE KIDNEY. 
Cysts are of peculiarly frequent occurrence and of several 
kinds. We have already seen that in the contracted kidney it is 
common to meet with small cysts which are the result of dilatation 
of the uriniferous tubules and Malpighian capsules from obstruc- 
tion of the tubules. 
Simple Cysts are frequently met with in kidneys which are 
otherwise perfectly normal, and the cysts themselves do not, as a 
rule, seriously interfere with the functions of the organ. They 
are larger or smaller well-formed cysts, which not infrequently 
project from the surface of the organ. They contain usually a 
clear fluid, but the fluid is sometimes colloid in character. The 
wall of the cyst is composed of connective tissue lined with a 
proper tessellated epithelium. These cysts sometimes grow to a 658 
DISEASES OF THE URINARY ORGANS. 
large size, and may push aside the renal tissue to a large extent. 
It is probable that they are of congenital origin, arising l)}7 foetal 
obstruction of one or more uriniferous tubules. The obstruction 
and the beginning of the cyst are congenital, as those formed in 
after-life do not apparently form such perfect cysts. 
Cystoid Degeneration of the kidneys is also a condition of 
congenital origin, at least in many cases, and probably in all. 
The whole kidney is converted into a 
congeries of cysts of larger and smaller 
size. The cysts form rounded promi- 
nences from the surface, and on section 
(Fig. 285) the}7 are seen to replace the 
renal tissue. The wall of the cyst is 
composed of tunica propria with well- 
formed tessellated epithelium lining it. 
It contains usually a clear fluid, but 
the fluid may be brownish or even 
hemorrhagic, and it is noteworthy that 
it contains the constituents of the 
urine, often with albumen, and some- 
times throws down a granular precipi- 
tate of uric acid. Between the cysts 
there is very little space, but there are 
traces of remaining renal tissue, and 
the pelvis and ureter are present. The 
outline of the organ is greatly enlarged, 
measuring sometimes in the new-born 
child as much as eight inches by four. 
Kidneys of this kind have been fre- 
quently met with in new-born children, 
and from their size they may seriously 
interfere with parturition, even requir- 
ing evisceration before delivery can be 
effected. It is of importance to note that this condition often 
coexists with other congenital defects, such as hydrocephalus, 
defective urinary bladder, and liorse-slioe kidney. But cystoid 
degeneration is also met with in the adult, and it is remarkable 
that the functions of the organs may he preserved for a long time, 
although both kidneys are composed of a congeries of cysts. The 
author met with a case in which the patient died at the age of 
forty-three. For eighteen years before his death there had been 
recurring attacks of lisematuria, and he at last died with urgemic 
symptoms. The kidneys were much enlarged and cystic, but with 
some renal tissue remaining between the cysts. 
The cystoid degeneration in all probability arises by obstruction 
of the uriniferous tubules. Virchow has found in some cases an 
obstruction of the papillae apparently from a foetal inflammation. 
The fact that these cysts contain the urinary constituents is also 
much in favor of the view that they arise by obstruction of the 
tubules. Those met with in the adult are also most probably of 
Fig. 285. 
Cystic degeneration of kidney. 
The organ is shown in section, and 
is made up of a congeries of cysts 
of various sizes. (Virchow.) secondary cancer. 
659 
congenital origin, although they may have grown on into adult life. 
In the author’s case there was a congenital malformation of the 
aortic valve, indicating perhaps a proclivity to malformations. 
Primary Cancer.—This is not of very frequent occurrence, and 
is usually unilateral, although there have been cases of bilateral 
cancer. The tumor is virtually a cancerous degeneration of the 
organ. The kidney may be completely converted into a tumor 
which sometimes attains a very large size, retaining the general 
shape of the organ and covered by its capsule. But in some cases 
only a part of the kidney is involved, and in that case, while the 
affected part retains the general shape of the organ, although 
enlarged, the remaining piece of kidney has quite its normal 
appearance. To the naked eye, it is as if a portion of kidney 
were transformed; and with the microscope it can be seen, at the 
margin of normal and pathological, that the tumor is advancing 
by a conversion of the proper kidney tissue. The epithelium of 
Fig. 286. 
A uriniferous tubule at the border of an advancing cancer. The epithelium is undergoing 
transformation. X 300. 
the tubules is multiplying so as to form the cancerous epithelium, 
and is becoming irregular in form (Fig. 286), while the cancerous 
stroma is being formed of the connective tissue of the organ. 
These tumors are usually very soft, but may be firmer. They 
present a remarkable tendency to break down the walls of the 
pelvis of the kidney and of the renal veins, so as to project in a 
fungating fashion into these. Hence arise hsematuria on the one 
hand and thrombosis of the veins on the other. The thrombosis 
may be very extensive, the clot propagating itself in various 
directions. Pulmonary embolism may result, and cancerous 
elements may be present in the obstructing material. In a case 
observed by the author cancer cells were found in coagula in the 
pulmonary artery, and in the heart. 
Secondary Cancers occur not infrequently when the cancerous 
elements have got into the systemic circulation. They form 
multiple tumors. 
Sarcoma, as a primary tumor, is rare in the kidney, but sec- 
ondary tumors of this kind are tolerably common. Of the 
primary sarcomas reference has already been made to the myo- 
sarcoma, which is usually a small tumor not larger than a pea, 
but may be of large dimensions. The lymphosarcoma sometimes 
forms bulky infiltrations of the kidney, and leukeemic lymphoid 
infiltrations may be very similar. 660 
diseases of the urinary organs. 
Fibromas of small size are common in the kidney, and some 
have occurred of large size. Lipomas have also been met with. 
PARASITES. 
The echinococcus is of occasional occurrence, sometimes along 
with a simultaneous hydatid cyst of the liver. There is here, as 
in the liver, a large mother-cyst surrounded by a distinct connec- 
tive-tissue capsule, and containing the usual daughter-cysts and 
broad-capsules. The cyst not infrequently bursts into the pelvis 
of the kidney, and the daughter-cysts and heads may be evacuated 
by the urine; or rupture may occur into the pleura. Sometimes 
the parasite dies, and the cyst comes to be occupied by a pultaceous 
material in which the remains of the chitinous membranes are 
found (Fig. 287). The stratified character of this membrane is 
here, as in the case of the liver, of assistance in distinguishing the 
Fig. 287. 
Section of a stratified chitinous membrane from an old hydatid cyst of kidney. X 90. 
nature of the cyst, especially as all other trace of the parasite, even 
the hooklets, may have disappeared. The kidney tissue may be 
considerably opened up and pushed aside by this parasite. 
The filaria sanguinis occurs probably in the adult form in the 
lymphatic vessels of the kidney. The embryos have been met 
with in the parenchyma of the kidney and in the chylous urine 
which seems to be the result of the presence of the parasite. 
B.—THE URINARY BLADDER AND URETHRA. 
Congenital Malformations.—These are chiefly represented by 
extroversion of the bladder. In this the anterior wall of the 
bladder and the corresponding portion of the abdominal wall are 
wanting, so that the posterior wall of the bladder fills the gap, and 
is continuous at its margins with the skin. The symphysis pubis 
is also usually incomplete, the rami ending in rounded lateral the urinary bladder and urethra. 
661 
prominences; the urethra is also laid open on its superior aspect, 
the bladder being continued in the form of a gutter into the 
urethra. There are also generally other coincident defects in the 
organs of generation. The abdominal viscera bulge out the wall 
of the bladder which forms a red convex surface in the lower part 
of the abdomen. On this exposed surface the openings of the 
ureters may be seen with the urine trickling from them. The 
mucous membrane is usually inflamed and bleeds readily, and 
as the urine escapes involuntarily the skin around is irritated and 
frequently excoriated. 
Occasionally the urachus remains open, generally from obstruc- 
tion in the urethra. If the patency be complete, the urine will 
come away from its aperture at the umbilicus. 
Perforation and Rupture of the Bladder.—Rupture may be 
produced in various ways. It may be by a direct wound, by 
fracture of the pelvis, by injuries during parturition. Then ulcera- 
tion not infrequently produces perforation, ulceration from stone 
on rare occasions, but most frequently the ulceration of a cancer. 
Lastly, the bladder may be ruptured by a blow, or by a catheter 
being pushed through its wall, but this will hardly occur unless its 
wall has already been greatly thinned by dilatation or ulceration. 
These conditions are important chiefly in their consequences, 
leading as they commonly do either (1) to extravasation of urine 
in the surrounding tissue, or (2) to the formation of fistulous com- 
munications with the surface or neighboring canals. 
Simple extravasation of urine is not in itself serious. The 
normal urine is a bland fluid, and it may flow from a severed 
ureter or a ruptured bladder into the peritoneal cavity without 
producing any peritonitis, the urine being absorbed by the perito- 
neum and again excreted by the kidney. It is when the extrava- 
sated urine undergoes alkaline decomposition that it acquires 
excessively irritating characters. The urine being an exceedingly 
decomposable fluid, and being kept at the temperature of the 
body, it rapidly decomposes if the proper organisms find access to 
it. The products of decomposition lead to the usual violent septic 
inflammations associated with necrosis and suppuration. 
Fistulous openings from rupture of the bladder may be into the 
uterus or vagina, into the rectum, or on to the surface of the skin. 
From these flstulse the urine passes involuntarily as it reaches the 
bladder, there being no sphincter to retain it. They occur also as 
a result of perforation of the bladder from without, especially 
from the uterus and vagina, the cause of perforation being some- 
times cancer of these parts, sometimes sloughing from injury 
during parturition. 
Dilatation and Hypertrophy of the Bladder.—A simple 
dilatation may occur from a sudden obstruction to the urethra, 
or from paralysis of the muscles concerned in emptying the 
bladder. In this way a very extreme general dilatation may result. 662 
diseases of the urinary organs. 
Hypertrophy of the muscular coat is of very frequent occur- 
rence as a result of some obstruction either at the neck of the 
bladder or in the urethra. The commonest cause is enlargement 
of the prostate leading to the prominence of the so-called middle 
lobe at the internal orifice of the urethra. The muscular coat of 
the bladder is in the form of bundles of muscular fibre-cells which 
run in special directions. The muscular coat is therefore not a 
homogeneous layer, but more like a network of interlacing bands. 
It is so at least when the bladder is distended, the bands coming 
closer together as the bladder contracts. "When hypertrophy 
occurs these bundles increase greatly in size, and the internal ones 
raise the mucous membrane into elongated prominences. As the 
bundles interlace, the result is that the internal surface of the 
bladder presents a network of prominent trabeculse which suggest 
the appearance of the internal surface of a ventricle of the heart. 
As these trabeculae interlace, little spaces are left between them 
in the form of small pouches. Sometimes these pouches undergo 
considerable enlargement, and we may have diverticula formed 
in this way, which sometimes attain to a considerable size. The 
diverticulum is originally formed of the mucous membrane pushed 
out between the thickened muscular trabeculae. When small it 
will be contained in the thickened wall of the bladder and emptied 
during micturition. But as it deepens and projects outside the 
wall of the bladder it becomes free of the muscular coat, and as 
it possesses no muscular coat of its own the effect of contraction 
of the bladder during micturition will be to force the urine into it, 
just as it is forced into the urethra. The diverticulum is liable in 
this case to periodical dilatation. The urine also will stagnate in 
it, and if decomposition occurs, then there will be inflammatory 
disturbances in the wall of the diverticulum. Hew formation* of 
connective tissue occurs, and as this tissue is at first soft the recur- 
ring dilatation during micturition causes it to yield so that a con- 
tinuous enlargement goes on. In this way we sometimes meet 
with a large sac, usually behind the bladder and communicating 
with it by a narrow neck (Fig. 288). The sac may be larger than 
the bladder itself, and it presents a somewhat thick fibrous wall 
with signs of recent inflammation internally. 
In diverticula of moderate or large size calculi are liable to form 
from the stagnation of the urine. Or a calculus may slip into such 
a pouch and escape detection with the sound. 
Disturbances of the Circulation in the Bladder.—Passive 
IIyperjemia occurs in consequence of obstruction in the veins by 
tumors or otherwise. Sometimes in such cases the veins of the 
mucous membrane undergo great dilatation and become varicose, 
especially in the floor of the bladder, giving rise to vesical iijemor- 
rhoids. The dilated veins may even obstruct the orifice of the 
urethra, and there is sometimes hemorrhage from them. 
Hemorrhage from the bladder may occur also in consequence 
of the irritation of calculi, from tubercular ulcers, from papillary INFLAMMATION OF THE BLADDER. 
663 
and cancerous tumors. There may be hemorrhages from the 
mucous membrane in scurvy, hemorrhagic smallpox, etc. If the 
bleeding into the bladder be considerable the blood may coagulate, 
Fig. 288. 
Large diverticulum of urinary bladder; a, bladder with greatly thickened wall; e, 
prostate and prostatic urethra; b, diverticulum with fibrous wall; c, aperture between 
bladder and diverticulum; d, rectum. 
and may be discharged with some difficulty. Or it may mix itself 
with the urine, and no consistent coagulum be formed. 
Inflammation of the Bladder.—This occurs as a consequence 
of various kinds of irritation. Stone may produce it, and the ex- 
tension of gonorrhoea, but by far the most frequent cause of it is 
alkaline decomposition of the urine. 
This decomposition of the urine is due to the growth of bacteria, 
and we have to consider how the bacteria find entrance. They 
are introduced from without, and mostly by the passage of the 
catheter, which, as it were, inoculates the contained urine with 
the micro-organisms. The question still remains, however, how 
it is that in the great majority of cases, although the catheter be 
used without taking the precaution of rendering it free of bacteria, 
no decomposition results. The answer to this question will be 
found in the kind of cases in which decomposition does occur in 
consequence of passing the catheter. It very readily occurs in 
cases of paraplegia in which the urinary bladder is paralyzed, also, 
’ although much less readily, in persons with dilatation of the 
bladder in consequence of enlargement of the prostate gland, or 
obstruction of the urethra. It occurs also readily when any 
amount of inflammation already exists, as from the irritation of a 
stone. In these cases the mucous membrane of the bladder is 
abnormal. In the case of spinal paralysis its muscle is paralyzed, 
and probably the mucous membrane is affected in its nutrition. 
In cases of dilatation the mucous membrane is stretched, and in 
inflammation it is directly altered. We may infer, therefore, that 664 
DISEASES OF THE URINARY ORGANS. 
while the normal mucous membrane is able to prevent the multi- 
plication of bacteria, like other living tissues, the altered mucous 
membrane is less able to do so. In addition to this, in most of 
the cases there is stagnation of the urine, and the organisms get 
leave to multiply, whereas normally they are carried out at the 
first micturition. Besides being carried in by the catheter, the 
bacteria may find other means of entrance, as by fistulous openings. 
It is not impossible that in the case of the short female urethra 
they may propagate along that passage from the vagina. 
The products of decomposition produce the usual inflammatory 
manifestations with various degrees of violence. In very acute 
cases there is great swelling of the mucous membrane, it may be 
with superficial or deep sloughing. In more chronic cases the 
mucous membrane gets thickened and very frequently becomes 
the seat of ulceration, so that with thickening and ulceration there 
is very great irregularity of the surface, sometimes with polypoid 
projections. The surface is occasionally incrusted with phosphates 
deposited by the alkaline urine. The muscular coat is often 
thickened, especially when there is at the same time obstruction 
to the passage of the urine, and there is the usual trabecular ap- 
pearance, but obscured by the thickening of the mucous mem- 
brane. The bladder may undergo great contraction in conse- 
quence of this chronic inflammation, the new-formed tissue in 
the mucous membrane shrinking. 
The urine contains the inflammatory exudation as well as the 
products of decomposition. In acute cases there may be con- 
siderable quantities of pus. In more chronic cases the urine is 
thick and gelatinous like a mucous secretion. The toughness does 
not, however, depend on the presence of mucin, but is occasioned 
by the albumen of the inflammatory exudation being acted on by 
the alkaline salts in the urine. It is well known that the presence 
of pus in the urine may be detected by adding an alkali; the urine 
assumes a gelatinous character. The pus and other inflammatory 
products in the bladder are similarly acted on when the urine be- 
comes alkaline, and we have the viscid character referred to. 
Under the microscope the urine presents abundant pus-corpuscles 
and epithelium, with immense numbers of bacteria and crystals of 
phosphates. 
Tuberculosis of the Bladder.—This condition is usually only 
a part of much more extensive tuberculosis. There is often a 
coincident tuberculosis of the kidney and ureter, the disease having 
originated there and extended downwards to the bladder, or more 
rarely it has begun in the bladder and passed upwards. Then the 
vesiculse seminales, vas deferens, and testicle are not infrequently 
affected, and the bladder affection may be due to propagation from 
an organ as far off as the testicle. 
The tuberculosis is in the form of ulcers of the mucous mem- 
brane which at first are circular, but acquire various shapes by 
coalescence (Fig. 289). The ulcers are mostly superficial and their TUMORS OF THE BLADDER. 
665 
edges very slightly raised, the latter having a pale color, so that the 
ulcer is surrounded by a whitish zone. The disease begins by the 
formation of tubercles in the mucous membrane. These break 
down and form ulcers, which continuously extend by the infiltra- 
tion of their walls and the breaking down of the infiltration. The 
Fig. 289. 
Tuberculosis of the bladder. Many round or serpiginous ulcers are shown. These are 
superficial, but are defined by their white edges which represent recent tubercles. There 
are several white spots indicating tubercles which have not yet ulcerated. (Virchow.) 
general appearances of these ulcers are very well shown in the 
annexed figure from Virchow’s work on tumors. Their super- 
ficial character renders them liable to be overlooked. 
Tumors of the Bladder.—A few cases of fibroma and myoma 
have been described, but they are rare. A much commoner form 
is the papilloma. This is met with for the most part in the inferior 
parts of the bladder, and forms either a prominent mass with pro- 
jecting papillae or else a surface covered by villi. The tendency 
of these villi to bleed is an important fact. Sometimes the villi 
break down and an ulcer forms. In any case they discharge 
abundant epithelium, which is to be found in the urine, and is not 
to be taken as evidence of the existence of cancer. 
Cancer of the bladder is mostly met with in the form of villous 
cancer, the wall of the bladder beneath the villi being infiltrated 
with the cancerous structures. In some cases the structure gives 
way and a cancerous ulcer with raised edges is the result. There 
are also cancers without any villous projections of the surface. 666 
DISEASES OF THE URINARY ORGANS. 
The cancer may extend to neighboring structures, but it is much 
more common for a cancer originating in the uterus or rectum to 
extend into the bladder than for the reverse process to occur. We 
have already seen that fistulous communications occur in this way. 
Cysts have been found, especially in the posterior wall of the 
bladder. 
Parasites.—If we except the bacteria already referred to, para- 
sites in the bladder are of secondary importance. We have already 
seen that the echinococcus may burst into the pelvis of the kidney, 
and portions of the parasite will pass into the bladder. Ascarides 
and oxyurides have been found to wander into the bladder. The 
distoma hrematobium, as we have seen, by the penetration of its 
ova may produce considerable irritation and hemorrhage. The 
filaria sanguinis is also found in the bladder as in the kidney and 
its pelvis. 
Sarcime have been found in the urine by no means infrequently. 
From what has already been stated as to their development from 
the blood, their occurrence here will be understood. They are 
met with in cases of inflammation of the bladder. 
CONCRETIONS AND CALCULI IN THE BLADDER. 
These consist of the urinary constituents, normal or abnormal, 
deposited in bulk so as to form distinct smaller or larger stones. 
We have to consider what determines this abnormal precipitation 
of the urinary constituents, and we may begin by considering how 
these same constituents come to be precipitated in the urine after 
evacuation. 
The most frequent constituents of urinary calculi are phosphates, 
uric acid, and oxalate of lime. Phosphates are precipitated from 
alkaline urine, uric acid and oxalate of lime from acid urine. The 
phosphates are deposited abundantly when the urine undergoes its 
usual alkaline decomposition, uric acid and oxalates are thrown 
down in crystals when the urine, at the time of evacuation or 
afterwards, becomes unduly acid, the deposition of oxalates occur- 
ring usually some time after the urine has been passed, so that this 
precipitate often, as it were, powders the surface of other deposits. 
Inside the bladder or the pelvis of the kidney, phosphates may 
be deposited because of undue alkalinity, especially in the case of 
alkaline decomposition of the urine. These often form an external 
coating on other stones when, from decomposition, the urine has 
become alkaline. Phosphates are also frequently deposited on 
foreign bodies which have found their way into the bladder, such 
as broken bits of catheters. 
In the case of uric acid and oxalate of lime it seems that some- 
times their precipitation is due to an excess of them in the urine. 
This applies especially to the oxalates, and there are undoubtedly 
cases in which there is almost continually an excess of oxalate of CONCRETIONS AND CALCULI IN THE BLADDER. 
667 
lime in the urine (oxalic acid diathesis). But in both cases the 
substances are deposited from an acid urine, and in the case of 
uric acid it must be strongly acid. The cause of this abnormal 
acidity is not always clear. In some cases it may be due to 
excessive development of acid in the stomach. 
The formation of calculi of uric acid and oxalate seems always 
to begin in the kidney, and even in some cases in the uriniferous 
tubules. In these and in the pelvis it is very common to find 
small concretions of uric acid, forming the so-called sand and 
gravel, composed of aggregates of uric acid crystals, usually 
rounded in shape and of a brownish-red color. There may even 
be large concretions of uric acid in the pelvis of the kidney. In 
connection with the formation of the uric acid and oxalate calculi 
it is interesting to observe that the two bodies are often combined 
in one calculus, the mulberry stone especially having frequently a 
nucleus of uric acid, and perhaps layers of it alternating with the 
oxalate. 
It may now be convenient to give a brief description of the 
different forms of calculi, with an indication of the chemical 
methods for determining their constitution. As a rule it is con- 
venient to have the calculus sawn through the middle with a 
lapidary’s saw, so that the arrangement of its layers may be seen 
and the character of its nucleus. 
The uric acid calculus is the most frequent. It is usually a 
small oval stone with small rounded prominences regularly dis- 
tributed over the surface. The color varies from a light fawn to a 
deep brick-red. It is heavy for its size, and of hard consistence. 
Uric acid is insoluble in water and dilute acids, hut very soluble 
in caustic alkalies and weak solutions of alkaline carbonates. A 
convenient test is the murexid reaction. A fragment of the calculus 
is treated with a drop of strong nitric acid and heated. Effer- 
vescence occurs, and the heat is continued till a dry yellowish-reel 
residue remains. When caustic ammonia is added a bright violet- 
red hue is developed. 
Calculi formed of urates are rare, the salts being urates of 
ammonia and magnesia. They are small soft concretions formed 
in the kidney, and are distinguished by their solubility in boiling 
water. They hardly deserve to he reckoned among the vesical 
calculi. 
The oxalate of lime or mulberry calculus is a very important 
form. Sometimes small stones are discharged as gravel, forming 
smooth, round, grayish balls like hemp seeds. The calculus proper 
is mostly of an irregularly spherical shape, tuberculated on the 
surface like a mulberry, and of a grayish or nearly black color. 
On section it is seen to be in layers, some of them generally com- 
posed of uric aid, which usually forms the nucleus. The calculus 
contains abundant organic material which holds the coloring 
matter, so that when the oxalate is dissolved out the organic basis 
often retains the shape of the calculus. Oxalate of lime is insoluble 668 
diseases of the ueixary organs. 
in the alkaline carbonates and organic acids, but soluble in nitric 
and hydrochloric acids. If a fragment be heated on a piece of 
platinum before the blow-pipe it becomes black, swells up, and 
leaves a bulky white ash of caustic lime which renders litmus blue. 
Calculi of basic phosphate of lime alone are very rare. They 
form comparatively small yellowish or grayish-white stones, rather 
hard and smooth on the surface. 
The mixed or tribasic PHOSPHATic calculus is very common, at 
least many calculi are partly formed of these salts, although few 
are so entirely. The phosphates are deposited from alkaline urine 
as a light, bulky, white substance, which is commonly very brittle. 
The salts are insoluble in water and alkalies, but are very soluble 
in acids. When a fragment is heated in the blow-pipe flame, the 
salts melt and form a hard enamel; hence this form is often called 
the FUSIBLE CALCULUS. 
The carbonate of lime calculus is rare. It forms small, round, 
soft stones. The salt dissolves with effervescence on adding an 
acid, leaving an organic matrix of the shape of the stone. 
Cystine forms calculi in persons who are subjects of cystinuria. 
It appears as if by a congenital derangement of the nutritive pro- 
cesses such persons form cystine, to a certain extent probably in 
place of uric acid; and this peculiarity occurs frequently in several 
members of the same family. The urine, continuously or fre- 
quently, contains flat hexagonal crystals of cystine, and these may 
be already present in the urine at the time of evacuation, or may 
be deposited after the urine has stood for a time. The cystine 
may begin to be deposited in the uriniferous tubules so that calculi 
are formed in the pelvis of the kidney, or it may be deposited in 
the bladder. The stones are oval in shape and have a waxy con- 
sistence. The surface is brownish or greenish-yellow in color, and 
crystals can often be separated from it. The stone may be buried 
in a shell of phosphates. Cystine is soluble in alkalies, mineral 
acids, and oxalic acid. 
Xanthine calculi are exceedingly rare. The substance is allied 
to uric acid, and the stones are like those of uric acid but of a 
redder color. On applying the murexid test to a fragment of such 
a stone, it is found to dissolve in nitric acid but without effer- 
vescence ; the addition of ammonia gives an orange color. 
DISEASES OF THE URETHRA. 
Of these the most important are the inflammations. 
Gonorrhcea is a specific inflammation accompanied by redness 
and swelling of the mucous membrane with purulent exudation, 
sometimes mixed with blood. The inflammation is thus at first 
acute, and it may result in suppuration around the urethra, in the 
prostate or in the testicle, the virus in the last-mentioned case 
probably propagating itself along the vas deferens. There may be 669 
DISEASES OF THE URETHRA 
an ulceration of the mucous membrane as a consequence of the 
inflammation. 
If the acute stage subside there often remains a chronic inflam- 
mation, characterized mainly by a persistent mucous or muco- 
purulent discharge. As in other chronic catarrhs there is new 
formation of connective tissue, and in the male urethra this fre- 
quently leads to stricture. The new-formed connective tissue 
contracting narrows the tube, and sometimes quite a hard cicatri- 
cial tissue occupies the mucous membrane and submucous tissue. 
Or the thickening may be mainly in the mucous membrane which 
bulges inwards and forms folds which obstruct the calibre in the 
male urethra, or form projecting or prolapsed folds in the female. 
Besides gonorrhoea we may have inflammations produced by 
other causes. A simple catarrh may arise, especially in the female 
urethra, sometimes from propagation of an inflammation from 
neighboring parts. DISEASES OF THE FEMALE GENERATIVE ORGANS. 
Introductory.—It is hardly necessary to state that these organs 
are specially liable to disease from their functional relations. At 
the times of menstruation and pregnancy very extraordinary 
changes occur, some of which, although strictly physiological, 
border on the pathological. The anatomical relations of the 
internal organs of generation in the female have also to be taken 
carefully into account in connection with the changes in position 
to which the uterus is especially liable. It will be necessary to 
take up the individual portions of the organs of generation sepa- 
rately, but for purposes of convenience the malformations of the 
whole set of organs will be taken together. 
MALFORMATIONS OF THE FEMALE ORGANS. 
Ill treating of this subject it is necessary to bear in mind that 
the internal and external organs have no connection with each 
other in their origins, and so the malformations of the one are 
not necessarily connected with the malformations of the other. 
Hermaphroditism.—This name implies the union of the two 
sexes in the same individual. So far as the internal organs are 
concerned, such a condition is rendered possible by the fact that 
in every foetus the embryonic structures for both sexes are present 
at a certain period of development; the Wolffian ducts go to form 
the male organs, and the Mullerian ducts go to form the female 
organs. It is by the subsequent retrogression of one of these and 
the preponderance of the other that the sex of the child is deter- 
mined. It is well known that in the adult the testicle is repre- 
sented in the female by the parovarium, and the ovary is repre- 
sented in the male by the hydatid of Morgagni, which lies beside 
the epidydimis, while the vesicula prostatica represents the uterus. 
These facts indicate that we may have a true hermaphroditism, 
in which ovary and testicle are both represented. Cases have 
been recorded in which, on both sides, both of these glands have 
been present, one of them, however, generally ill-developed. This 
would form a true bilateral hermaphroditism. On the other 
hand, there may be a testicle on one side and an ovary on the 
other, forming a true lateral hermaphroditism. It is necessary, 
however, in such cases to be careful, and not to conclude that an MALFORMATIONS OF THE FEMALE ORGANS. 
671 
organ is testis or ovary from its mere position, but to subject it to 
microscopic examination. 
It is clear that the sex of an individual is determined by the 
existence of the testicle on the one hand or the ovary on the other, 
and no case is truly bisexual unless both these glands are present. 
But there are cases in which, with the sex determined by the pres- 
ence of ovaries or testicles, the other parts present the structures 
belonging to different sexes. In such cases the designation pseudo- 
hermaphroditism is used, and, according as the ovaries or the 
testicles are the glands present, they are male or female. 
In cases of male pseudo-hermaphroditism, three different com- 
binations may be recognized, but in all there are testicles present. 
(1) Internal. In this case the external organs are those of the male 
and the testes are present, but from the prostatic urethra a canal 
arises which represents an elementary vagina with a uterus at its 
extremity, sometimes with Fallopian tubes. The uterus may be 
of the regular form but small, or it may be two-horned, or with 
one horn and a Fallopian tube. We have already seen that the 
vesicula prostatica is the representative in the male of the vagina 
and uterus, and the condition we are now considering is an exag- 
geration of that pouch due to an unusual persistence of the lower 
part of Muller’s ducts. There may be all degrees of this persist- 
ence, but the case is not one of pseudo-hermapliroditism unless 
there is something that can be called a vagina and uterus, even if 
very rudimentary. (2) Complete male pseudo-hermapliroditism is the 
condition in which, while the glands are the testes, all the remain- 
ing organs, both internal and external, approach to those of the 
female. This arises by a persistence of Muller’s ducts and an 
imperfect closure of the urethra. It may here be remarked that, 
as the external generative organs arise from the same foetal struct- 
ures in both sexes, they cannot really represent both the female 
and the male sexes in the same person. But as the male organs 
present, as it were, a further development, chiefly consisting in 
enlargement of the clitoris and closing in of the urinary passage 
to form a urethra, we may have, by arrest of development, more 
or less approach to the condition of the female organs. (3) Ex- 
ternal male pseudo-hermaphroditism is characterized by the external 
organs presenting the characters of those of the female, while the 
entire internal organs are those of the male. The cases are to be 
excluded in which there is simply an opening up of the urethra 
(hypospadias) from arrest of development. There must, in addi- 
tion, be an approach in the form of the organs to those of the 
female. At the same time the general form of the body is that 
of the female. Several such cases have been married as females, 
and the true sex only discovered on post-mortem examination. 
Female pseudo-hermaphroditism is of much more rare occur- 
rence than male and is susceptible of similar division. In all these 
forms there are ovaries, and the variations are in the other organs. 
There is (1) the internal in which with well-developed female organs, 672 
DISEASES OF THE FEMALE GENERATIVE ORGANS. 
both external and internal, there are male organs present in the 
persistence of the Wolffian ducts, tubes passing from the par- 
ovarium to the uterus or vagina. This condition is excessively 
rare, although in ruminating animals it is a normal condition. 
(2) Complete female pseudo-hermaphroditism presents the male form of 
the external organs as well as a portion of the male internal organs, 
while the ovaries are the glands present. In one case the male 
organs were complete as far as the prostate, but from this sprang 
vagina, uterus, and Fallopian tubes. (3) In external female pseudo- 
hermaphroditism the external parts have the characters of the male 
while the internal have those of the female. It will be understood 
that an elongation of the clitoris will cause the parts to approach 
to those of the male, and some cases present nothing more than 
this. The name hermaphrodite can hardly be applied unless there 
is as well a type of body approaching that of the male. A case is 
recorded in which the real sex was only suspected when the person 
became pregnant. 
Other Malformations of the Female Organs. — We have 
defect of various parts and in various forms. The ovaries may 
be wanting or may remain rudimentary. The uterus may be 
wanting, and with it the Fallopian tubes; or it may be quite 
rudimentary (Fig. 290), presenting perhaps a solid rudiment, or 
merely two diverging horns. With this the vagina is often de- 
Fig. 290. 
Rudimentary uterus. (Graily Hewitt, from Ivussmaul.) 
fective. Then the uterus may remain in the adult of the foetal or 
infantile form. Again, the uterus or vagina may be imperforate, 
or the hymen imperforate. There are also various defects of the 
external organs, as absence of the vulva, the vagina and urethra 
opening by a small aperture in the region which the vulva should 
occupy. The hymen may be absent, or it may present fimbriated 
processes sometimes so large as to project externally. 
A very interesting and important malformation is the double 
uterus. This arises by reason of the two Muller’s ducts uniting 
imperfectly, and there may be several varieties. We may have 673 
MALFORMATIONS OF THE FEMALE ORGANS. 
the uterus forming two distinct diverging horns, and each with a 
separate vagina. Or the two horns may unite below to a greater 
or lesser extent (Fig. 291), the cavities remaining separate, and 
Fig. 291. 
Uterus bicornis. The two horns, which are distinct above, are coalesced in the lower 
part. The cavities, however, are separate, and there are two vaginas, as shown in figure. 
(Graily Hewitt, from Ivussmaul.) 
with the vagina single or' double. Or the two horns may be so 
united that the cavity of the neck or even a portion of the body is 
single. 
Fig. 292. 
Uterus unicornis. The parts are viewed from behind, and the distended bladder occupies 
the background. The right horn is large and runs into the Fallopian tube whose fimbriated 
extremity is shown. There is no proper left horn, the Fallopian tube and round ligament 
springing from the base of the right horn. (Gkaily Hewitt from, Kussmattl.) 
There are cases, again, in which, without any indication of 
separate cornua, the uterus is divided up the middle by a septum, 
each half with a separate cervix and sometimes a separate vagina. 674 
DISEASES OF THE FEMALE GENERATIVE ORGANS. 
Or the division may be only partial, the body of the uterus having 
usually a septum, while the cervix has none. 
The uterus unicornis occurs when one Muller’s duct is unde- 
veloped. This uterus is a long thin structure which curves to one 
side, while the other horn is absent or rudimentary (Fig. 292). 
Pregnancy may occur in all these forms of malformation, the 
foetus developing in one half of the uterus. Even the single horn 
in the case of uterus unicornis, although usually imperfectly 
formed, may be the seat of a developing foetus, which, however, 
usually causes rupture of the ill-developed organ in the third to 
the sixth month. 
A.—THE UTERUS AND VAGINA. 
MISPLACEMENTS OF THE UTERUS. 
The arrangements by which the uterus is supported are of im- 
portance to the understanding of the misplacements of the organ. 
In the virgin the vagina forms a tolerably solid column, on the 
summit of which the uterus is supported and so prevented from 
descending. The vagina is also attached, by means of the pelvic 
fascia, to the bladder in front and the rectum behind. The uterus 
is further supported by its ligaments, and these assist in preventing 
its descent, although not so directly as the vagina. By the liga- 
ments passing off from its lateral aspects, the uterus is kept from 
inclining to one side or the other. While capable of very limited 
movement from above downwards and from side to side, the body 
of the uterus is very movable, within certain limits, from before 
backwards. When the bladder and rectum are full the uterus will 
be tolerably erect. When the bladder is empty it will be inclined 
forward, and a certain amount of anteversion may be regarded as 
the normal condition with an empty bladder. 
Prolapse or Descent of the Uterus.—This occurs for the most 
part as a result of the loosening of the attachments of the organ, 
combined frequently with increased weight from chronic inflam- 
mation. It may also be produced suddenly by a severe exertion, 
as in raising a heavy weight. In this case the abdomen is fixed in 
the expiratory position, and by the pressure of the abdominal 
muscles and diaphragm the viscera are forced downwards and so 
may carry the uterus down, although here also there may have 
been some preliminary looseness of vagina and ligaments. Besides 
increased weight of the organ itself, a tumor by its weight may 
assist in dragging it downwards. It will be apparent that preg- 
nancy, with its various circumstances, will have great effect in 
loosening the attachments of the uterus, and prolapse is conse- 
quently much more frequent in married women than in virgins. 
The degree of descent is very various; it may simply amount to misplacements of the uterus. 
675 
a lowering of the position of the uterus an inch or so, or it may 
be to any extent up to the presentation of it in the vulva or out- 
side, this latter condition being designated procidentia. The 
vaginia must be inverted in proportion to the descent of the uterus, 
and in cases where it is completely procident the vagina will form 
an external covering continuous with the skin around. 
As the uterus descends, it is held more by the posterior attach- 
ments to the rectum than by the anterior ones to the bladder, and 
there is accordingly a certain amount of retroversion along with 
the prolapse. 
The mucous membrane of the uterus is mostly in a state of 
catarrh in prolapse, with a profuse mucous discharge, and the 
organ itself is enlarged. There is often a special enlargement of 
the cervix which may be so elongated as to present externally 
without much misplacement of the body of the uterus. The 
mucous membrane of the inverted vagina is thickened, and its 
epithelium, where exposed, acquires characters like those of the 
epidermis. 
Prolapse of the Vagina.—This occurs mostly in connection 
with pregnancy, and seems to be caused by the walls remaining 
hypertrophied when they ought to undergo the regular involution. 
The thickened and loose vagina is thrown into folds, and these 
may project outside the vulva. As a consequence there may be 
prolapse of the uterus. Again, looking to the close connections 
of the vagina with the rectum and bladder, it is not surprising 
that prolapse of the former causes dragging on these latter struct- 
ures. The connection of the vagina with the neck of the bladder 
and trigonum is much more intimate than with the rectum, and so 
we have more frequently descent of the former than of the latter. 
In this way cystocele and rectocele occur, pouches or diverticula, 
from these organs respectively, passing downwards with the pro- 
lapsed vagina. 
I 
Inversion of the Uterus.—This is of very rare occurrence. It 
can only happen when the uterus is somewhat enlarged, or when, 
either by its own contraction or by the exercise of traction on its 
fundus, the organ is turned outside in. These conditions are best 
fulfilled during or after parturition, especially when the umbilical 
cord is pulled on while the placenta is adherent. It may also 
occur in connection with a tumor growing inside the uterus and 
attached to its internal wall. The inverted uterus projects from 
the vulva as a bleeding mass, the hemorrhage being frequently so 
severe as rapidly to cause death. If the patient survives, and the 
organ is not restored, inflammation results, and the uterus acquires 
attachments in its new situation, so that resort has sometimes to 
be had to amputation. 
Anteflexion and Retroflexion.—By these names are desig- 
nated the bending of the uterus on itself, the lower part forming 676 
DISEASES OF THE FEMALE GENERATIVE ORGANS. 
an open angle with the upper. The flexion takes place at a point 
corresponding with the internal os, and the explanation of this 
seems to be that the portion of the uterus corresponding with the 
cervix is, in front at least, closely attached to the wall of the 
bladder, the pouch of peritoneum between bladder and uterus not 
reaching below the level of the internal os. The cervix therefore 
being comparatively flxed, the rest of the uterus may be bent 
either forwards or backwards. Abnormal looseness of the texture 
of the uterus, occurring especially after delivery, renders it more 
liable to bend, and the flexion is always at this place. But again, 
if the fundus or body of the uterus acquires adhesions to the 
parts in front or behind, then these adhesions will tend to give it 
a permanent bend in their direction. There is another circum- 
stance which tends to make the flexions permanent; the uterine 
tissue is apt to waste in the concavity of the bend, and so there is 
all the more tendency to doubling up. 
All that has been stated applies equally to anteflexion and retro- 
flexion, and they are both of frequent occurrence, the former being 
usually regarded as the common form. 
Anteversion and Retroversion.—In these conditions there is 
displacement of the entire organ forwards or backwards. The 
organ comes to lie more horizontally than usual, and the cervix 
and os will be displaced backwards or forwards in the opposite 
direction to the fundus. These changes in position occur for the 
most part as a result of pregnancy, the uterus remaining loose 
and unable to support itself properly in some cases. Anteversion 
and retroversion rarely occur without a certain amount of the 
corresponding flexions. 
These flexions and versions sometimes produce serious results 
in the uterus itself. We have already seen that, in the concavity 
of the bend, the uterine tissue frequently wastes and becomes less 
able to retain the uterus in the upright position. Then the bend, 
if at all sudden, compresses the vessel, and may lead to a chronic 
congestion, by and by resulting in hypertrophy. Again, the curve 
may obstruct the canal of the cervix, thus leading to dysmenor- 
rhcea. The flexions and versions not infrequently predispose to 
prolapse. The fundus of the uterus projected backwards or for- 
wards is apt to irritate the bladder or rectum, and so induce re- 
peated straining efforts which tend to force the uterus down. 
ATROPHY, HYPERTROPHY, AND DILATATION OF THE UTERUS. 
Atrophy.—We have already seen that the uterus may retain in 
adult life the undeveloped condition of that of the child. On the 
other hand the organ becomes smaller at the close of the period of 
sexual activity, a kind of physiological atrophy. There may be, 
however, a premature atrophy, in some cases ascribed to long-con- 
tinued catarrh, frequent pregnancies, pressure of tumors, etc. INFLAMMATIONS OF UTERUS AND ITS APPENDAGES. 
677 
Hypertrophy.—This sometimes occurs as a result of imperfect 
involution after the physiological enlargement of pregnancy, and 
in this case the increase in size is from excess in the muscular 
substance mainly. Hypertrophy of a similar kind occurs, though 
very rarely, without apparent cause. There may he hypertrophy 
from congestion and chronic inflammation however caused. 
A special hypertrophy of the cervix has been observed in 
many cases. It occurs as a result of imperfect involution after 
pregnancy, hut also as a consequence of prolapse of the vagina, the 
cervix being dragged down and greatly elongated. With very 
little descent of the uterus the cervix may be so elongated as to 
present externally. 
Dilatation.—This occurs in consequence of the retention and 
accumulation of material in the cavity of the uterus. It results, 
therefore, from obstruction of the vagina or of one of the orifices 
of the uterus. There may be congenital closure of the external or 
internal os (generally the external) or imperforate hymen. 
When the period of puberty is reached and menstruation begins 
the blood accumulates in the uterus, and there may be enormous 
distention, the contents having a tarry or pulpy character. This 
condition is designated The uterus may assume 
the size of the pregnant organ, and there is thickening of its walls, 
which, however, are loose. If escape is not provided artificially 
the uterus may actually rupture, not usually into the peritoneum, 
but, after the formation of adhesions, into some neighboring organ. 
The rupture is by a process of ulceration from within, unless 
external violence bursts the distended organ. 
There may be an acquired obstruction of the os uteri as from 
chronic catarrh, or even from inflammation occurring after deliv- 
ery. In such cases also we may have dilatation with the menstrual 
blood. It is more common, however, to have such closure after 
menstruation has permanently ceased, and as a result of chronic 
catarrh. In that case the catarrhal secretion may accumulate and 
distend the uterus. After a time the contents, which are at first 
mucous in character, become serous. This condition is sometimes 
Called HYDROMETRA. 
Lastly, the organ is sometimes distended with gas. This may be 
the result of decomposition of the accumulated fluid in hydrometra, 
or from decomposition of retained clots, etc.; but cases have 
occurred in which the cavity has been dilated with gas and 
assumed considerable proportions without apparent cause. 
INFLAMMATIONS OF THE UTERUS AND ITS APPENDAGES. 
These are somewhat various, and they are differently named 
according to the locality specially affected. In this way we have 
to consider endometritis, metritis, parametritis, amd perimetritis. 
The condition of the uterus and vagina after delivery lays them 
open to the occurrence of septic inflammations, and many of the 
conditions here have often this origin. 678 
DISEASES OF THE FEMALE GENERATIVE ORGANS. 
(1) Endometritis.—This is an inflammation of the mucous 
lining of the uterus. We may have an acute inflammation set up 
by catching cold at a menstrual period, or by the extension of a 
gonorrhoeal inflammation from the vagina, or in the course of an 
acute fever. The inflammation may go on to suppuration or even 
to sloughing of the mucous membrane and the formation of ulcers. 
Chronic Endometritis or chronic catarrh is a very frequent 
disease, and as a whitish discharge is a characteristic feature the 
condition is often called leucorrhcea. Apart from the excessive 
secretion the mucous membrane is apt to become thickened, and 
it may he thrown into folds or give origin to mucous polypi. The 
cervix especially is often thickened, and the os may present ulcer- 
ations. These ulcerations are for the most part little more than 
superficial excoriations, and are important chiefly as indicating the 
existence of catarrh of the cervix and interior of the uterus. 
Chronic catarrh sometimes arises without any apparent exciting 
cause except a general anaemia, which may he related to scrofula 
or chlorosis. During pregnancy inflammations sometimes arise 
giving occasion to abortions, adhesions of the placenta, and other 
lesions. The catarrh may also have its origin in a tumor, a flexion, 
or a version of the uterus. 
(2) Metritis.—This name is given to inflammation of the wall 
of the uterus, but it hardly occurs as an independent affection, 
being commonly the result of extension of inflammation from the 
mucous membrane. Acute inflammation, even with infiltration 
of the muscular substance with blood, may follow gonorrhoea. 
We may have also, from various causes, a chronic inflammation 
leading to induration, it may be with enlargement of the uterus. 
This is sometimes related to imperfect involution of the uterus 
after parturition, or to the various causes which bring about 
endometritis. 
The terms Perimetritis and Parametritis are used to designate in- 
flammations occurring in the peritoneum around the uterus (peri- 
metritis), and in the connective tissue around the organ between 
it and the peritoneum (parametritis). As, however, the whole of 
the peritoneum of the pelvis is apt to be involved in the one and 
the whole of the connective tissue of the pelvis in the other, the 
names pelvic peritonitis and pelvic cellulitis are at least equally appro- 
priate terms. It will be understood also that with inflammation 
of the pelvic peritoneum, there will frequently be an inflammation 
of the sub-peritoneal connective tissue, so that these two conditions 
frequently go together. 
(3) Pelvic Peritonitis or Perimetritis includes inflammations 
produced by all sorts of causes. Most frequently it is an inflam- 
mation of the uterus occurring after delivery or from gonorrhoea, 
which extends through the substance of the organ to its serous 
coat. Or it may be inflammation in the neighboring intestine or PUERPERAL FEVER. 
679 
bladder that has led to it. Or a tumor in the uterus or outside it 
may so far irritate as to cause a chronic inflammation. 
In some of these cases the inflammation is acute and there is 
danger of a general peritonitis, but even when acute or subacute 
it may be circumscribed by adhesions, and an abscess may form 
which remains confined to the pelvis. Such an abscess may after- 
wards burst into the rectum, or vagina, or externally. When the 
inflammation is more chronic the result is adhesion of the pelvic 
organs, the adhesion being effected here as in the pleura, peri- 
cardium, etc., by new-formed vascular connective tissue. The 
adhesion and contraction sometimes lead to great matting together 
of the pelvic tissues and considerable fixity of the uterus, frequently 
with misplacement and deformity. 
(!) Pelvic Cellulitis or Parametritis.—This consists in a sub- 
acute inflammation of the pelvic connective tissue, generally oc- 
curring after delivery, but also sometimes as a result of operations 
on the uterus, the introduction of pessaries, the uterine sound, etc. 
The inflammation is no doubt septic, being propagated through 
the uterine wall, being in this respect comparable with erysipelas 
and phlegmonous inflammations generally. The inflammation 
extends from the uterus, finding its way apparently by the lym- 
phatic spaces. There are the usual results of inflammation, but 
the exudation is here the most important. The spaces of the con- 
nective tissue get filled up with a serous exudation which may be 
partly fibrinous. There is in this way a great tumefaction of the 
subperitoneal tissue, especially of the broad ligament, but also that 
in front of and behind the uterus and in the pelvis as a whole. 
The uterus is thus, as it were, fixed in the midst of tumefied con- 
nective tissue, which may be felt as a firm swelling on examination 
per vaginam. 
Suppuration generally ensues, but it may do so very gradually, 
so that it may be long after parturition before it occurs. The pus 
sometimes extends a considerable distance from the neighborhood 
of the uterus. In this way the inflammation may extend and the 
suppuration follow into the iliac or even into the lumbar region. 
The abscesses which result open in very various localities, into the 
vagina, the rectum or the bladder, or at the surface in the iliac or 
inguinal region. In these latter cases the condition may simulate 
that of lumbar abscess, and mistake is the more likely as the sup- 
puration has perhaps occurred long after the originating cause. 
The pus discharged has usually the characters as of having been 
long retained, the corpuscles are largely fatty, and there is usually 
a feculent odor due to the proximity of the abscess to the rectum. 
PUERPERAL FEVER. 
We have in this case not merely .a local inflammation but a 
general affection of the system. The disease is really a septic in- 
fection with or without pysemic abscesses. 680 
DISEASES OF THE FEMALE GENERATIVE ORGANS. 
We have here to deal with the entrance into the body of patho- 
genic bacteria. From what has gone before, especially in studying 
pyaemia, it will be apparent that it is probably a special kind of 
bacterium which is concerned. It is not necessary to suppose that 
the organism is so special as that which causes splenic fever, or in 
tact that it is always the same organism. But it must be a patho- 
genic form capable of living and multiplying inside the body. 
There are probably organisms of this kind in many putrid fluids, 
but they are greatly multiplied in the body of a person infected 
with them, and are much more likely to be carried to another 
person from such a one. The infective material of other diseases, 
especially erysipelas, may be the cause of puerperal fever. Hence, 
although puerperal fever is not to be ranked as one of the specific 
fevers, we can understand how it is highly communicable, and 
how it occurs in groups of cases so as to simulate the epidemic 
form. In regard to the form of the organism, it is here as in 
other septic diseases a micrococcus, and in the peritonitis which is 
a frequent feature of a puerperal fever, there may be myriads of 
these organisms in the peritoneal cavity. 
The disease occurs in connection with the puerperal state, and 
in most cases there has been some wounding of the soft parts by 
the passage of the child. The protecting epithelium being re- 
moved, the bacteria may penetrate into the submucous tissue. 
The result is usually a very violent local inflammation, generally 
with a distinctly gangrenous tendency. The inflammation, with 
sloughing and suppuration, extends over the internal surface of 
the uterus, and extensive ulceration may occur. The fibrinous 
exudation, covering and involving the mucous membrane, may 
have the appearance of the diphtheritic exudation in the fauces. 
Sometimes, however, the local inflammation is not very consider- 
able. 
From its local seat the process extends, and results in a more 
general infection. The path of extension and the resulting con- 
ditions are various. The septic inflammation may extend along 
the Fallopian tubes, and septic pus find its way into the peritoneum. 
The resulting peritonitis is rarely localized, but we have rather a 
general septic peritonitis with resulting absorption of the products, 
and septic poisoning. In other cases the organisms get into the 
uterine veins, and by the ordinary process of thrombosis, etc., we 
may have a pyaemia having the usual characters, with suppuration 
in the joints and miliary abscesses in the lungs and elsewhere. 
The thrombosis here nearly always starts from the veins of the 
placental part of the uterus. In some cases there appears to be a 
septic infection of the blood without any local abscesses from 
embolism. In other cases the inflammation extends to the con- 
nective tissue of the pelvis. We have a violent parametritis with 
acute suppuration. The inflammation extends by and by to the 
peritoneum, and there is a violent septic peritonitis, just as when 
the extension is by the Fallopian tubes. The inflammation may 
extend through the diaphragm, and lead to a pleurisy. 681 
PERIUTERINE HiEMATOCELE. 
It will be seen that in all these cases there is a vigorous multi- 
plication of the micrococci, and that there must consequently be 
a great formation of chemical products. An acute septic poison- 
ing is the result, and it is probably this which leads to the more 
pronounced symptoms of puerperal fever. 
PHLEGMASIA DOLENS. 
This is an affection in which great oedema occurs in one or both 
legs, usually as a sequel to the puerperal state. There is throm- 
bosis of the uterine veins, the thrombi growing, as we have seen 
thrombi readily do, into the iliac veins, and onwards into the 
femoral and its branches. The starting-point of the thrombosis 
is the placental surface of the uterus, and it is most apt to occur 
when, through imperfect contraction of the uterus, the veins are 
left with gaping mouths. It may be a question whether the intro- 
duction of septic material induces the coagulation, hut in the usual 
absence of the general symptoms of septic poisoning, it may he 
doubted whether this has to do at least with the extension of the 
coagulation. The thrombosis may also have its starting-point 
apart from the puerperal state, as in tumors of the uterus, dysen- 
tery, disease of the rectum, typhoid fever, etc., but as causes these 
are exceedingly rare. 
We have already seen that there may be extensive thrombosis 
in the veins of the leg without oedema, and so in this case oedema 
is by no means coincident in its occurrence with the thrombosis. 
As, however, the femoral vein takes by far the greater part of 
the blood from the leg, and as the other veins of the leg also join 
the iliac, and are consequently liable to thrombosis as well, there 
is often ultimately a very complete plugging of the veins of the 
leg. This results in a very marked oedema. It is not improbable 
that the lymphatics may he also to some extent obstructed. We 
have formerly seen that thrombosis of a vein induces a chronic 
inflammation in its wall and around it (phlebitis and periphlebitis), 
so that there is often considerable adhesion of the vein to its sheath 
and of the sheath to the parts around. The lymphatic vessels may 
be affected by this adhesion and partially obstructed. The disease 
occurs most frequently in the left leg, and this is ascribed by some 
to the fact that the parts on the left side of the pelvis are more 
liable to bruising during delivery than those on the right. 
PERIUTERINE HEMATOCELE. 
This name is given to the condition in which blood accumulates 
around the uterus, usually in Douglas’s space. The bleeding 
occurs nearly always at a menstrual period, and it is natural to 
look for the source of the .blood in the processes occurring then, 
namely the bursting of the Graafian vesicle and bleeding from the 
uterine mucous membrane. If there is an obstruction to the exit 682 
DISEASES OF THE FEMALE GENERATIVE ORGANS. 
of blood from the uterus it may pass backwards by the Fallopian 
tubes into the peritoneum. This is probably the commoner source 
of the hemorrhage, which also occurs from rupture of one of the 
veins of the uterine plexus, especially if these be varicose. At the 
menstrual period there is hyperaemia of these veins, as of the whole 
vascular system of the uterus, and they may rupture. There may 
also be hemorrhage by rupture in extra-uterine pregnancy, but 
this falls to be considered afterwards. It is also stated that rupture 
of the vessels forming adhesions in perimetritis may cause the 
hemorrhage. 
For the most part the blood falls by gravitation into Douglas’s 
space behind the uterus, where, as the serum is pressed out by the 
contracting clot and absorbed, the coagulum becomes condensed 
and assumes a kind of permanent position, from which the desig- 
nations hematoma and 11 hematocele have been given. The uterus 
is pushed forward by the tumor which can be felt filling Douglas’s 
space on vaginal examination. 
But the blood is probably not in every case within the perito- 
neum, although in most cases it is so. When the blood escapes 
from a ruptured vein it may accumulate either in the peritoneum, 
or else in the subperitoneal connective tissue, thus forming a 
parametric or extra-peritoneal hematocele. It must be said, 
however, that as the blood when in the peritoneum sets up inflam- 
mation with multiform adhesions, it may be difficult in some cases 
to say whether it has been originally intra or extra-peritoneal. 
The blood acting as a foreign body sets up a chronic inflamma- 
tion. Connective tissue is produced around it forming adhesions 
of the neighboring loops of intestines and the ligaments of the 
uterus. The blood thus becomes inclosed in a capsule, and it may 
be slowly encroached on by the connective tissue and undergo a 
gradual absorption. After absorption there will usually remain 
more or less serious adhesions causing misplacement and deformity 
of the uterus, tubes, or ovaries. In some cases the inflammation 
is more acute, and suppuration occurs in and around the blood. 
Thus an abscess may form which bursts into the vagina, rectum, 
or bladder, or even into the peritoneal cavity with probably a fatal 
issue. 
EXTRA-UTERIXE PREGNAXC 
In this condition the foetus does not develop in the uterus, as 
usual. It is not necessary to describe particularly the various 
forms here, as these are taken up in works on midwifery. The 
ovum may be impregnated in the ovary itself, and, probably after 
the rupture of the Graafian vesicle, may remain in the ovary and 
develop further. In this case we have an ovarian pregnancy, 
which, is exceedingly rare. Or the ovum may drop into the peri- 
toneal cavity, and having been impregnated either before or after 
its escape from the ovary, it may develop in the abdomen, forming 
an abdominal pregnancy. Or it may fail to reach the uterus, only 683 
SYPHILIS AND TUBERCULOSIS OF THE UTERUS. 
travelling a certain distance along the tube—lodging at any part 
of the tube—tubal pregnancy—which is the commonest form. 
Sometimes it is in the last part of the tube so close to the uterus 
as to be imbedded in the substance of the organ—interstitial 
PREGNANCY. 
In all these situations the foetus develops and is surrounded by 
its regular membranes, the whole being usually inclosed in a cap- 
sule formed of connective tissue from the parts around. The 
placenta forms and attaches itself to some of the parts around, 
although cases occur in which the placenta is in the uterus, while 
the foetus is in the tube or even in the abdomen. After developing 
for a time the cyst usually ruptures, this occurring earliest, as a 
rule, in the tubal cases. The result is profuse and generally fatal 
hemorrhage. If the hemorrhage does not cause death, peritonitis 
usually develops and proves fatal. But the person may even 
survive this, and in that case, as a general rule, the foetus softens 
and an abscess forms, which by and by bursts externally, dis- 
charging the more solid parts which have escaped the process of 
softening. In some cases, however, after rupture of the cyst the 
foetus may produce little inflammation and become quietly encap- 
suled, or even without rupture it may die and lie quiescent as a 
foreign body. In these cases the foetus shrivels and becomes 
mummified, being surrounded by a capsule formed of connective 
tissue and adherent to surrounding organs. In the mummified 
foetus the various tissues may be recognized years after. The cap- 
sule usually becomes infiltrated with lime salts, so that a kind of 
shell forms around the foetus. 
In cases of extra-uterine pregnancy the uterus enlarges, usually 
becoming two or three times as large as in the unimpregnated 
condition. 
SYPHILIS AND TUBERCULOSIS OF THE UTERUS. 
Syphilis manifests itself in the vagina and vulva in the form of 
the hard chancre, which may even occur at the os uteri. It does 
not present in these situations any peculiarities distinguishing it 
from chancre of the skin elsewhere. Condylomata of consider- 
able size also occur in the vulva and vagina, often forming warty 
projections. 
Tuberculosis hardly occurs in the vagina; it is met with in the 
uterus, but is probably always secondary, being propagated from 
the Fallopian tubes (see p. 693). It may produce extensive de- 
struction of the uterus, ulcers forming, on the surface of which 
there may be considerable caseous masses. Tubercular nodules 
form outside the ulcers in the mucous membrane and muscular 
substance, and the ulcers enlarge by caseous necrosis and breaking 
down of these tubercles. The ulcers thus enlarge in depth and 
superficies, and may involve the whole interior of the uterus, 
whose surface is exceedingly irregular. There is nearly always  diseases of the female generative organs. 
associated tuberculosis of the tubes, and sometimes of the ovaries 
and peritoneum. 
TUMORS OF THE UTERUS AND VAGINA. 
Polypoid ILematoma of the Uterus.—This form of tumor con- 
sists of coagulated and condensed blood, and strictly speaking is 
not a proper tumor. It is of importance, however, as it consider- 
ably resembles the much commoner myoma of the uterus. It is 
sometimes designated the fibrinous uterine polypus. It consists 
Fig. 293. 
Polypoid hmmatoma of uterus after an abortion in the second month; a, projecting part 
of maternal placenta and wall of uterus; b, remains of foetal placenta; c, stratified coagula 
around the foetal placenta. Natural size. (Virchow.) 
of a mass of blood-clot which by shrinking has become dense and 
hard. It may attain considerable dimensions, hanging it may be 
into the vagina. Consisting of blood-clot, it has originated in 
hemorrhage, but there must be some reason for the adhesion of 
the clot to the uterine wall. This is mostly afforded by the pla- 
centa which has been retained after delivery or abortion. The 
whole placenta may be retained, as in Fig. 293, or it may be only tumors of the uterus and vagina. 
685 
a portion. On the other hand, the rough surface, after removal 
of the placenta, may induce the coagulation of blood, which, if 
retained, may grow by fresh coagulation. As the hsematoma 
originates in hemorrhage, it is usually associated with it through- 
out its course. The blood mostly escapes into the vagina, but 
some of it may coagulate and increase the size of the polypus. 
Myoma of the Uterus.—This is an exceedingly frequent form of 
tumor; it is said to occur in about every tenth woman. Nothing 
can be said definitely as to the cause of the formation of these 
tumors, but as they grow for the most part in the form of isolated 
pieces of muscular tissue, it may be supposed that in the foetus 
there have been bits of the embryonic muscular tissue left over in 
the formation of the organ. 
The structure of the myoma has already been sufficiently de- 
scribed in the part devoted to this form of tumor in general (see 
p. 188, and Figs. 70 and 71), and we have here mainly to do with 
certain local peculiarities. The tumor is very often multiple, and 
there may be as many as fifty attached to the same uterus. We 
may have a* single small tumor no larger than a pea, or a large 
growth weighing as much as fifty pounds, or a group of tumors 
surrounding the uterus and burying it. 
The subserous myoma, originating in the external layers of the 
uterus, passes outwards as it grows, and pushes the peritoneal coat 
before it. In this way it frequently becomes pedunculated. The 
subserous form is often multiple, and as from its situation it is pro- 
tected, the tumor may grow for many years undisturbed, and 
reach very large dimensions. Such large myomas may be mistaken 
for ovarian tumors and excised as such, and this is the more likely 
to occur as the formation of cysts, to be referred to presently, not 
infrequently occurs in them. A subserous myoma has been known 
to part company with the uterus and become attached to a neigh- 
boring part of the peritoneum where it has grown. Of course the 
separation and the acquirement of new attachments would be 
gradual. 
The interstitial or intraparietal myoma arises in the middle 
layers of the uterus. In its growth it involves the wall of the 
uterus, and may cause enormous enlargement of the organ. This 
form develops mostly at the fundus. The tumor and greatly 
enlarged uterus may form together a very bulky mass, which as 
a whole is liable to be mistaken for an ovarian or other tumor. 
The author has met with several cases in which the tumor and 
uterus were excised under this belief. In one of these the tumors 
seemed to be multiple and the uterine wall could not be distin- 
guished from tumors, the greatly enlarged cavity of the uterus 
being surrounded by irregularly lobulated masses of muscular 
tissue. In this case it looked as if the uterus as a whole had un- 
dergone an irregular hypertrophy, or had grown into a massive 
tumor. 
The submucous myoma is the form which most frequently comes 686 
DISEASES OF THE FEMALE GENERATIVE ORGANS. 
under the notice of the practitioner. Arising in the internal la} ers 
of the uterus, it readily passes inwards, pushing the mucous mem- 
brane before it, and from the action of gravity it tends to become 
pendulous. The submucous myoma, therefore, very often presents 
itself as a polypus (the so-called fibroid polypus), and it may have 
a very narrow neck. It very often arises at the fundus, and may 
grow to such dimensions as to fill the uterus, and hang down 
through the cervix into the vagina. The mucous membrane 
covering the tumor is subject to irritation, and there is frequently 
hemorrhage and ulceration, even with sloughing in some cases. 
The myomas present considerable varieties in the details of their 
structure. They vary in the proportion of muscular to fibrous 
tissue, as we have already seen, but the muscular bundles always 
occupy such a preponderating relation that when attention is paid 
to the arrangement of the nuclei (Fig. 294) there can never be any 
doubt as to the nature of the tumor. It is true that the hardness 
Fig. 294. 
Section of a myoma of uterus stained with carmine so as to show the multiple nuclei. X 350. 
of many myomas, and the glistening character of the cut surface, 
as well as the concentric arrangement of the trabeculae as seen 
with the naked eye, suggest the characters of a fibrous tumor. 
But even in the hardest of them the muscular elements are perfectly 
pronounced, and the name uterine fibroid is misapplied. There is 
always a certain amount of connective tissue in myomas, as in all TUMORS OF THE UTERUS AND VAGINA. 
687 
tumors, this tissue accompanying and supporting the bloodvessels 
just as in other tumors. It sometimes undergoes increase and 
causes induration of the tumor, but the hardness of myomas is by 
no means always in proportion to the amount of connective tissue 
which they contain. 
(Edema occurs in myomas, especially when they are polypoid, 
and have a narrow neck. The oedema consists in a distention of 
the lymphatic spaces with fluid, and it causes the tumor to be re- 
markably soft, so as even in some cases to resemble a mucous 
polypus. The formation of cysts may be a further development 
of the oedema, but it also occurs by breaking down of the tumor 
tissue. This occurs for the most part in large subserous myomas. 
The cysts are very irregular in form, and have no proper layer of 
epithelium lining them. Their origin in connection with the 
lymphatics is often indicated by the fact that the fluid, when with- 
drawn, frequently coagulates spontaneously. 
Fig. 295. 
Calcareous infiltration of a myoma of the uterus. The muscular fibre-cells and a bloodvessel 
are infiltrated. X 350. 
Dilatation of the bloodvessels occurs not infrequently, and 
especially in the uterine polypi. This dilatation, occurring at the 
expense of the muscular tissue, may lead to a cavernous condition 
of the tumor, there being large irregular spaces filled with blood. 
In that case there may be considerable hemorrhage in the sub- 
stance of the tumor, as well as externally. 
As we have already seen, the connective tissue of the tumor 
may undergo calcareous infiltration, so that the tumor has 
externally a hard shell, and is divided internally by septa, between 
which there lies the muscular tissue. The muscular tissue itself 688 
diseases of the female generative organs. 
also sometimes undergoes calcification, as we have seen, and as 
Fig. 295 shows. 
Cancers of the Uterus and Vagina.—In the great majority of 
cases the cancer begins just about the junction of the uterus and 
vagina, and involves both as it extends. The disease scarcely 
occurs before the age of thirty, and is most prevalent between 
forty and fifty. It appears also from the statistics of West that, 
contrary to what is sometimes stated, it occurs much more fre- 
quently in women who have borne children than in those who 
have not, and most frequently in those who have had more than 
the usual number of pregnancies; as if the disease developed most 
readily when the uterus is deteriorated by repeated conceptions. 
Fig. 296. 
Section of cancer of uterus under a very low power, showing mode of advance into wall of 
uterus; a, muscular substance of uterus, interrupted frequently (as at b) by masses of can- 
cerous structure. At lower part of figure (at c) the muscular substance is still more frequently 
interrupted, and the tissue has quite an alveolar appearance, the muscle partly forming the 
stroma. X 22. 
There are various appearances presented by cancer of the uterus, 
hut the commonest form is that usually described as soft or medul- 
lary cancer. The individual elements are not essentially different 
to those in what is called epithelial cancer, but this form tends 
much more to infiltrate deeply, while the epithelioma is more 
superficial in its mode of growth. The medullary cancer begins 
as an infiltration of a limited part of the portio vaginalis of the TUMORS OF THE UTERUS AND VAGINA. 
689 
cervix, and thus extends more or less round the external os. By 
and by the whole portio vaginalis is converted into a hard, irreg- 
ularly prominent tumor. At first the infiltration is confined to 
the mucous membrane and submucous tissue, but by degrees it 
spreads both deeply and laterally. It insinuates itself into the 
muscular substance of the uterus, separating and breaking up the 
muscular trabeculae, which come to form a kind of rough stroma 
for it (see Fig. 296). It also passes into the vagina, infiltrating its 
wall. Yery soon ulceration of the surface sets in, and in the 
subsequent progress there is a progressive ulceration and infiltra- 
tion, the former following the latter. The infiltration passes into 
the body of the uterus, but does not usually reach the fundus 
before the death of the patient. If 
the parts be now examined post- 
mortem (Fig. 297), it will be seen 
that an irregularly excavated ulcer 
occupies the adjacent parts of the 
uterus and vagina, rendering their 
respective limits inappreciable. Then 
outside this there is the whitish can- 
cerous tissue, which extends into the 
uterine substance some lines beyond 
the ulcer. 
This disease affects neighboring 
structures. There are cancerous 
masses usually in the ligaments and 
under the peritoneum. The bladder 
is frequently adherent to the uterine 
cancer, and its mucous membrane 
red and irregular, or else it presents 
cancerous nodules. The ulceration 
even extends sometimes into the 
bladder, which forms thus a com- 
munication with the vagina. The 
rectum is much less closely related 
to the cervix uteri than the bladder, 
and it is less frequently involved. Those parts of the uterus which 
are not engaged in the cancerous disease are inflamed, and adhe- 
sions are formed to the rectum and urinary bladder. Although 
thus extending locally, the cancer tends very little to form secon- 
dary tumors in the lymphatic glands, and still more seldom does 
it become generalized. 
It sometimes happens that the new formation of cancerous tissue 
is more vigorous than the ulceration, and in that case we may have 
prominent ragged masses hanging into the vagina. 
The microscopic examination of this form of cancer shows 
masses of epithelial cells, usually of considerable size, arranged 
irregularly in alveoli, the stroma being largely formed by the re- 
mains of the structures into which it has infiltrated. 
Epithelial Cancer is hardly to be distinctly delimited from the 
Fig. 297. 
Cancer of uterus, the parts shown in 
section. To the right is the urinary- 
bladder. To the left are vagina and 
uterus, both of them to a large extent 
converted into irregular cancerous 
masses. (Graily Hewitt, from Mar- 
tin.) 690 
DISEASES OF THE FEMALE GENERATIVE ORGANS. 
former, but is characterized by a more superficial outgrowth of 
prominent warty projections, while the deeper infiltration is slower 
and less in degree. The disease begins, as in the other case, in the 
portio vaginalis, and at first there is little more than a prominent 
warty outgrowth. But the warty growth increases while the base 
becomes infiltrated till a bulky prominence results, whose surface, 
consisting of masses of papilliform projections, gives the character 
of the CAULIFLOWER EXCRESCENCE (Fig. 298). 
Fig. 298. 
Cauliflower cancer of posterior lip of os uteri. A probe is passed through the os, and the 
anterior lip in front of it is seen to be normal, while a cauliflower growth projects from the 
posterior. (Simpson.) 
This form of-tumor is also liable to ulceration, and there may he 
a combination of ulceration with papilliform projections, although, 
after a time, the papillae may be destined and the appearances 
approximate to those of the other form of cancer. 
Under the microscope the structure here is more that of flat- 
celled epithelioma. The prominent papillae are covered with pave- 
ment epithelium, and the deeper infiltration consists of masses of 
flat cells. 
A few cases have been observed in which colloid cancer has 
been the form occurring in the uterus, the situation being the same 
as in the other more common forms. In rare cases also a cancer 
may arise from the fundus uteri. 
Mucous Polypi of the Uterus.—These are met with mainly as 
the result of chronic inflammation of the mucous membrane, and 
may spring from the body of the uterus or the cervix. Sometimes 
there is a general irregular prominence of the mucous membrane, 
but usually there are definite polypoid outgrowths. The mucous 691 
OVARIAN HERNIA. 
polypus may consist of a limited hypertrophy of the mucous mem- 
brane, the tumor being a tolerably firm one unless, as sometimes 
happens, it becomes soft by oedema or by the excessive develop- 
ment of its vessels. In this latter case we may have a tumor ap- 
proaching to the cavernous character. Or polypi may consist 
largely of glandular structures, mucous glands being apparently 
new formed so as to provide the tissue of the tumor. These polypi 
are comparatively soft, and may grow to a considerable size, 
especially when they become cystic. We have already seen that 
tumors consisting of glandular tissue are peculiarly apt to become 
cystic, and these form no exceptions. These larger polypi may 
somewhat distend the uterus. 
Other Tumors are seldom met with. Sarcomas are of rare 
occurrence, and of those recorded the majority have been spindle- 
celled sarcomas, although the round-celled form has also been seen. 
The sarcoma may develop in a myoma, or a muscular tumor in its 
rapid growth, soft consistence, and looser structure may assume 
the characters of a myosarcoma. Papillomas are also met with 
at the portio vaginalis, and may resemble cauliflower cancers. 
Parasites are rare in the uterus and vagina. Thread worms 
may pass over from the rectum. Bacteria are frequently met with 
in the vaginal secretion, and the fibres of leptothrix also occur 
frequently. The oiclium albicans is found in connection with 
thrush. The cysticercus cellulosse has been doubtfully seen in the 
uterus, and the echinococcus with exceeding rarity. 
B.—OVARIES, FALLOPIAN TUBES, AND LIGAMENTS. 
OVARIAN HERNIA. 
In this condition one or both ovaries descend into a regular sac. 
The ovary sometimes forms part of the contents of an ordinary 
hernial sac, but there are cases in which the ovary alone is present, 
and its descent constitutes the primary condition. These cases are 
mostly inguinal and have a congenital origin, and there seems 
reason to infer with Englisch that they are produced by a descent 
of the ovary comparable with the normal descent of the testicle. 
When the testicle has descended, the sac forms the tunica vaginalis, 
and is shut off from the peritoneum except in the case of congenital 
inguinal hernia when the sac remains open. In ovarian hernia 
the sac remains open also, so that it is like congenital inguinal 
hernia in the male, but generally without the presence of intestine 
in the sac. The sac usually appears in the upper inguinal region, 
but may pass into the labium majus. Like the testicle, the ovary 
is fixed in the wall of the sac except in so far as its ligaments allow 
of a certain mobility. Hence it is usually irreducible, although, 692 
DISEASES OF THE FEMALE GENERATIVE ORGANS. 
if the ligaments are long, they may allow of the ovary passing 
into the abdomen while still attached to the bottom of the sac. 
The ovary in its abnormal position undergoes the usual changes 
at the menstrual periods, and being in a confined position its en- 
largement may cause pain. Sometimes the condition is discovered 
by attention being directed to it by pain and inconvenience during 
menstruation. The ovary may also become the seat of tumors 
while in the sac or may be inflamed. Sometimes it has given rise 
to such inconvenience in its abnormal situation that excision has 
been resorted to. 
Besides these cases of inguinal hernia the ovary may enter a 
crural or an abdominal hernia, but these are not congenital and 
are not in the same relation to the descent of the testicle as the 
case just considered. 
INFLAMMATIONS OF THE OVARIES AND TUBES. 
The Fallopian Tubes sometimes inflame when the uterus is the 
seat of acute inflammation, but they and the ovaries are most 
frequently affected with acute inflammation in connection with the 
puerperal conditions already considered. An acute perimetritis or 
a puerperal fever is very often accompanied by suppurative inflam- 
mation of the tubes, which may be distended with pus so as to 
form abscesses, their apertures having become obstructed. In 
addition to that the tubes are often adherent and distorted by 
chronic inflammations of the uterine peritoneum and of the 
ovaries. These chronic inflammations, by contorting and obstruct- 
ing the tubes, often lead to dilatation by the secretion being 
retained. 
Acute Oophoritis, or acute inflammation of the ovaries, occurs 
also as a sequel of the puerperal state. It may be a part of a peri- 
metritis, or a pelvic abscess may be associated with abscesses in the 
ovaries, and as these conditions rarely occur apart from pregnancy 
so is it with the ovarian inflammation. The ovary becomes swollen 
and hypersemic and suppuration usually ensues. The pus at first 
forms in elongated streaks from the hilus to the periphery, but 
after a time there are more distinct abscesses. The Graafian 
vesicles also frequently become filled with pus. The peritoneal 
surface will also be inflamed and probably coated with a fibrinous 
or semi-purulent exudation. 
Chronic Oophoritis is a condition concerning which consider- 
able variety of opinion is held. We know that at each menstrual 
period the ovaries undergo changes which present many analogies 
with inflammation. They become hypenemic and enlarged, and 
a Graafian vesicle bursts, leaving a wound which has tolieal by 
granulation. At these periods then it seems likely that a chronic 
inflammation may be readily set up by exposure to cold, cold baths, TUBERCULOSIS OF THE OVARY AND TUBES. 
693 
or sexual excitement. But it is not to be inferred in all cases 
where ovarian disturbances are thus produced that there are 
present the actual anatomical phenomena of inflammation. 
Chronic inflammation is manifested by an interstitial new forma- 
tion of connective tissue, and is comparable to cirrhosis of the 
liver or kidney, and like these accompanied by shrinking of the 
organ. The capsule is thickened, and the contracting tissue in 
the organ produces irregular depressions of the surface. The 
thickening is often peculiarly manifest around the Graafian vesicles, 
and this with the thickening of the capsule may prevent the vesi- 
cles bursting. Sometimes a ripe vesicle instead of bursting ex- 
ternally ruptures into the substance of the 
ovary, and so produces further inflamma- 
tory disturbance. With these changes in 
the ovary itself there is usually adhesion 
of the capsule to the parts around, the 
chronic inflammation causing the forma- 
tion of vascular connective tissue which 
unites opposed surfaces. In this way there 
may be displacement of the ovaries. 
If the Graafian vesicles are prevented 
from bursting, the fluid which naturally 
exists in them may become augmented, 
and the vesicles thus be converted into 
cysts (Fig. 299). A limited number of 
small cysts may thus be formed, and it is not impossible that cysts 
having this origin may grow to some size, having always the 
character of simple cysts with serous contents. 
It is to be remembered that in old age the ovaries are often 
shrunk and the capsules thickened, but this is not to be set down 
as the result of chronic inflammation. 
Fig. 299. 
Cystic formation in ovary 
from dilatation of Graafian 
vesicles. (Virchow.) 
TUBERCULOSIS OF THE OYAEY AND TUBES. 
This affection occurs with exceeding rarity in the ovaries, in the 
form of caseous masses. It is more common in the tubes, and 
here the appearances are very like those in tuberculosis of the 
ureters. The tube is enlarged, sometimes very greatly so, and it 
forms varicose sausage-like convolutions (Fig. 300). Internally 
there is a caseous layer with, it may be, some accumulation of pus, 
mucus, and debris. The caseous layer is somewhat consistent, 
forming a continuous lining to the tube. Outside this the wall is 
greatly thickened, mainly by inflammatory new formation in which 
tubercles are to be found. 
Along with the tuberculosis of the tubes and the very rare 
tuberculosis of the ovaries there is usually similar disease else- 
where, such as phthisis pulmonalis, tuberculosis of the urinary 
organs, or tuberculosis of the peritoneum. The disease commonly 
affects both tubes, generally beginning near the abdominal ex- 694 
DISEASES OF THE FEMALE GENERATIVE ORGANS. 
tremity, and often extending the whole length of the tube even 
into the uterus. 
Fig. 300 
Tuberculosis of Fallopian tubes seen from behind, a, uterus; b, b, fimbriated extremities 
of the tubes; c, right ovary. The right tube is seen to be very greatly dilated and con- 
voluted. The dilatation disappears just before the uterine termination of the tube. The 
left tube is much less affected, being most dilated at its distal part. There was also tuber- 
culosis of the lungs and mesenteric glands. 
TUMORS OF THE OVARY. 
Tumors of the ovary have the peculiarity that they commonly 
grow to large dimensions. We may perhaps associate this with 
the functions of the organ, which imply, at least in the Graafian 
vesicles, a remarkable formative power. The cysts are the most 
frequent and important forms, and they are here taken first. 
Simple Cysts occur which are in many respects comparable with 
the simple cysts which are so frequent in the kidney, and like 
them have no very special significance. They are produced, as 
already indicated, by dropsy of the Graafian vesicles, as was 
proved by the discovery by Rokitansky of an ovum in such a cyst. 
Simple cysts may be of congenital origin, having been observed in 
new-born children. As a general rule there are several cysts 
simultaneously developed, usually from ten to twenty, but one or 
a few may attain a preponderating size. The cysts have a distinct 
smooth lining membrane, with a single layer of epithelium. The 
contents are mostly clear serum, hut from hemorrhage they may 
be dark, or from inflammation turbid. The enlargement of the 
ovary is not generally great in this form of cystic disease; it rarely 
reaches the size of the fist, and still more rarely that of the head. 
If there are several cysts, they take shape by mutual pressure. TUMORS OF THE OVARY. 
695 
Colloid Ovarian Cysts.—These are of much more frequent 
occurrence and vastly more important. To this class of cysts the 
name cystoma is properly applied, because they arise by a distinct 
new-formation, there being first produced a preparatory tissue, 
which goes right on to the formation of the cysts. 
These cysts form very bulky tumors, and while the tumor itself 
is formed of a number of larger and smaller cysts, there is always 
Fig. 301. 
Section of tissue in wall of an ovarian cyst. There is a congeries of glandular 
structures lined with cylindrical epithelium. X 150. 
in the walls of these more or less solid material which shows 
various stages in the process of cystic formation. It is to be noted 
also that the tumor, sometimes of enormous size, represents the 
ovary as a whole, and is not merely something added to it, the 
external covering of the cyst being strictly analogous to the surface 
of the ovary. 
Fig. 302. 
Portion of wall of colloid ovarian cyst. The lining epithelium is mostly in the 
form of goblet-cells. X 350. 
It has been said that in the wall of the cysts there is solid tissue 
which showrs the various stages in the process. If this he examined 
microscopically, there will be found a glandular structure (see 
Fig. 301) in the form of tubular canals lined with cylindrical epi- 
thelium. These gland-like structures often project into cysts in a 696 
DISEASES OF THE FEMALE GENERATIVE ORGANS. 
somewhat papilliform manner, and altogether they show a very 
striking power of new-formation. We have in this way glandular 
tubes on the one hand, and villous or papillary outgrowths on the 
other. The transformation into cysts is readily seen in many cases. 
The glandular tubes become constricted at their necks, or, the villi 
being pressed together, unite at their apices. The cylindrical epi- 
thelium presents very markedly the goblet form seen in mucous 
glands (Fig. 302), and it secretes a colloid material, which accumu- 
lates in the cavity and distends it more and more into a globular 
cyst. We have therefore in the walls of the cysts, very commonly 
large numbers of smaller cysts which take their shape by mutual 
pressure as in Fig. 303. Cysts formed in this way project into the 
Fig. 303. 
Section of portion of a projection on internal surface of ovarian cyst. It consists 
of a congeries of variously sized smaller cysts. X 20. 
already existing cysts as they grow, and may afterwards burst and 
become flattened out on the wall of the older cyst. As all the 
cysts have had a similar origin, they are lined with epithelium, 
whose function it is to secrete a colloid or mucoid fluid, and so the 
cysts, once formed, have an almost continuous tendency to increase. tumors of the ovary. 
697 
There arises here the question as to the origin and significance 
of this glandular tissue, and in order to understand this we must 
go back to the original development of the ovary. The primordial 
ovary consists of a layer of epithelium on the surface of a connec- 
tive-tissue projection. The ova form by the penetration or redu- 
plication inwards of this superficial epithelium, which at first 
forms a series of communicating channels, which Waldeyer com- 
pares to a cavernous tissue. By the constriction of these canals 
the ova are formed, it being doubtful whether the cells of the 
membrana granulosa which line the Graafian vesicle are derived 
from this epithelium or from the connective-tissue stroma. The 
glandular formation in ovarian cystoma may be regarded as a 
pathological and exaggerated recurrence of the foetal condition. It 
may he that some of the glandular structure which originally forms 
the ova is left over from the foetal state, or else that even in adult 
life there may be a fresh development of the glandular structures, 
originating in the Graafian vesicles. The probability is that the 
real origin is in a persistence of the original glandular tubules. 
Having studied the mode of formation of the cysts, it now 
remains to consider the appearances of the tumors as a whole. 
The tumor represents an ovary, and its outer covering is the outer 
covering of the ovary with its layer of endothelium. The surface 
is usually smooth and very often free from adhesion to neigh- 
boring structures. In shape the tumor is more or less globular, 
and its external configuration may not suggest that it is com- 
posed of many cysts. The size of the tumor may be very 
great in some cases, much larger than that of the uterus at 
full time. On cutting into it there escapes from the cysts a 
sticky brownish or yellow fluid, which is tolerably clear unless 
some of the secondary changes to be presently described have 
occurred in it. There may be one cyst or a few of greatly pre- 
ponderating size, but even when at first sight there is only one 
larger cyst, examination will show the existence of others. These 
may be flattened out in the wall, or they may be collected here 
and there in clusters. Generally towards the base of the tumor, 
but in many cases at various places, there are solid or semi-solid 
masses in which cysts are in process of development in the way 
already described. Sometimes the glandular tissue presents a 
tendency to form papilliform projections into the cysts, and we 
may have in this way dentritic or shaggy projections in the internal 
wall. If, as is usually the case, there are many cysts, they take 
shape by mutual pressure against each other, while the general 
globular outline of the tumor as a whole is preserved. 
The cysts are liable to undergo certain changes which concern 
chiefly their contents. It seems almost a normal condition in 
large cysts that the internal wall should present collections of cells 
in a state of fatty degeneration, these cells being often in many 
layers. The cells also pass into the fluid, so that in all ovarian 
fluids cells are to be found of round shape and with oil-drops in 698 
DISEASES OF THE FEMALE GENERATIVE ORGANS. 
them. So universally are these present in the fluid from ovarian 
cysts that Dr. Drysdale has insisted on their discovery as an im- 
portant diagnostic indication. In addition to small cells having 
a few minute oil-granules in them there are usually larger ones 
with more oil-drops, up to large cells having the regular characters 
of compound granular corpuscles. 
The number of these fatty cells maybe greatly increased, and as 
many of them in that case break down we may have a fluid which 
is turbid from the presence of numerous fatty cells and free oil. 
The fluid is also pale like a fatty emulsion, and in many cases it 
resembles pus in its physical characters. The change is most 
likely to occur in old and large cysts, but it is not infrequent in 
younger and smaller ones, and it is important to bear this in mind 
because this condition is apt to be mistaken for actual suppuration 
of the cysts, a much more rare occurrence. 
The free fat if long retained is very apt to form crystals of 
cholestearine, and in fact these crystals are frequently found in 
the fluid of cysts which otherwise are not strikingly altered. 
Hemorrhage occasionally occurs into the cysts, especially when 
there are papilliform projections. This will cause the fluid to be 
turbid and deep brown or red in color. There may also be masses 
of softened fibrine in the cavity. Sometimes, however, the fluid 
has a dark-brown color without hemorrhage. 
Inflammation of the cyst-wall is not of very frequent occurrence. 
There may be an acute suppurative inflammation, so that the con- 
tents become mixed with pus and assume more and more of the 
purulent character. With this there is generally an acute inflam- 
mation of the surface with fibrinous exudation and adhesion to 
neighboring structures. If the suppuration continue, there is apt 
to be perforation of the pus into the abdominal cavity with re- 
sulting fatal peritonitis. A chronic inflammation is more common, 
causing adhesion of the cyst to neighboring parts, and these ad- 
hesions may be very extensive and firm. 
Perforation of the cyst-wall is usually the result of suppuration 
or gangrene, but may be a consequence of the papillary growths 
impinging against the wall and causing atrophy. A case is men- 
tioned by Ivlebs in which the cyst had opened into the rectum in 
this way. The result is usually peritonitis, but if there has been 
no inflammation or gangrene, then the simple existence of the 
fluid in the abdominal cavity need not cause peritonitis. 
It is here to be remarked that the colloid ovarian cyst sometimes 
occurs in combination with the dermoid cyst on the one hand and 
cancer on the other. 
Dermoid Cysts.—These have already been referred to in de- 
scribing the teratoma. They are of comparatively frequent occur- 
rence in the ovary, and considering the function of this organ it 
may perhaps be inferred that they arise from the ova by a kind of 
equivocal generation. The cysts are usually single, but there may 
be several in the same ovary. They grow slowly and form globular TUMORS OF THE OVARY. 
699 
tumors with a dense connective-tissue capsule. Internally there 
is an epithelial lining which, in some parts, develops a more 
Fig. 304. 
Section of wall of dermoid cyst of ovary. A congeries of sebaceous glands with open 
mouths (a, a, a) occupy the wall. The cyst contained large masses of buttery material with 
hairs. X 20. 
complex structure. We have already 
mentioned how sebaceous glands (Fig. 
304), hairs (Fig. 305), bones and even 
teeth may enter into the constitution of 
the wall, and a buttery material with 
hairs and sometimes teeth form the 
contents. 
These cysts not infrequently inflame 
and may rupture, most frequently into 
the bladder and rectum, their peculiar 
contents being discharged and so re- 
vealing the nature of the case. 
Cancer of the Ovary occurs mostly 
as a cyst wTith cancerous growths in its 
walls. There may be a combination 
of the colloid cyst with cancer, or a 
partial transformation of the former into 
the latter ; considering the glandular 
Fio. 305. 
Hair in its follicle with sebaceous 
gland, from wall of same cyst as 
the former figure. X 20. 700 
DISEASES OF THE FEMALE GENERATIVE ORGANS. 
character of the structures forming the colloid cyst, this cannot 
be regarded as very remarkable. In the ordinary colloid cyst the 
epithelium has a regular and normal arrangement, and we may 
call the tumor in that aspect an adenoma; in the cancer the 
epithelium is distinctly abnormal in its arrangement, being aggre- 
gated into indefinite masses. It may even happen that in the 
midst of the cancer the epithelium is undergoing metamorphosis, 
so that cysts are developing from it as from the more regular 
glandular tissue. 
Besides these cancerous cysts we may have a solid cancerous 
tumor in the ovary, presenting the usual characters, but like the 
ovarian tumors showing a very excessive growth. 
Sarcoma is a rare tumor in the ovary. Spindle-celled sarcoma 
is the more usual form, but round-celled sarcomas also occur. 
These tumors may also assume very large proportions reaching 
the size of the head sometimes, and the3T are not infrequently 
bilateral. Cysts are frequently present in the midst of them, and 
these may he simple serous cysts or they may have colloid 
contents. These latter may arise from glandular structures, and 
the disease may form a combination of the colloid cystoma and 
the sarcoma, or they may originate in a softening of the sarcoma- 
tous tissue. 
For the rest, fibromas and enchondromas have been met with in 
the ovaries on rare occasions. 
CYSTS OF THE BROAD LIGAMENTS—PAROVARIAN CYSTS. 
These cysts deserve special mention, especially from a practical 
point of view, in relation to their diagnosis from ovarian cysts. 
The probability is that most of the cysts of the broad ligament 
develop in connection with the remains of the Wolffian body, 
commonly called the parovarium. The exact relations of this 
body are of importance in regard to the relations of the resulting 
cyst, and the principal points will be gathered from the accom- 
panying figure (Fig. 306). 
The parovarium lies between the two folds of the peritoneum 
constituting the broad ligament, and under the arch of the Fallopian 
tube, between the latter and the ovary. When the broad ligament 
is held up against the light by catching the Fallopian tube, the 
parovarium can be seen as a series of tubules, converging towards 
the ovary. In the figure a little tube with a knob at its end (h) 
represents a frequently occurring so-called hydatid, which is one 
of the tubules with a cystic dilatation at its extremity. This cyst 
may undergo slight enlargement, but it does not come practically 
into account as forming the proper parovarian cyst; probably if it 
enlarges much its very narrow neck is apt to get broken or twisted 
and the cyst will then shrink. In connection with the anatomical 
details it is to be further noted that a firm ligament unites the CYSTS OF BROAD LIGAMENTS. 
701 
ovary to the upper angle of the uterus just below the origin of the 
Fallopian tube (see figure). The ovary is also united (see figure) 
to the fimbriated extremity of the Fallopian tube, so that the par- 
ovarium is as it were surrounded by a girdle of structures, Fallopian 
tube above, and continuous with it the ligament passing to the 
ovary, the ovary itself and the proper ovarian ligament. 
Fig. 300. 
Diagrammatic view of uterus and appendages, po, parovarium; od, Fallopian tube; ji, 
its fimbriated extremity; o, ovary, with a ligament to the right proceeding to the fimbriated 
extremity, and one to the left to the uterus near the origin of the Fallopian tube. (Quain.) 
One or more of the tubes of the parovarium sometimes undergo 
great enlargement and constitute the parovarian cyst, Whether 
originating in one tube, or in more than one, the cyst is nearly 
always a single one, and it assumes a typically globular form. 
From the anatomical relations just referred to, it comes about that 
the cyst as it enlarges stretches the structures named as forming a 
girdle round it. There is frequently great elongation and dilata- 
tion of the Fallopian tube, which may be fourteen or fifteen inches 
in length, and arches over the convexity of the cyst, its fimbriated 
extremity being spread out on the surface, considerably exagger- 
ated and drawn out. One part of the fimbriated mouth is drawn 
downwards towards the ovary, which again is found flattened and 
greatly elongated on the under surface of the cyst. The ligament 
of the ovary is also elongated and thickened. 
The cyst itself is a perfectly homogeneous bladder, consisting 
of a connective-tissue wall, lined with epithelium. Besides this 
proper cyst-wall there is an external coat of peritoneum, which is 
quite distinct from the proper cyst-wall. So loose is the connec- 
tion between the two that the peritoneal coat can usually be 
stripped from the cyst-wall, so that two globular cysts can be 
separated, like the external and internal layers of a football. As 
the parovarium is covered on both sides with peritoneum, forming 
the folds of the broad ligament, we can understand how in en- 
larging the cyst retains a distinct peritoneal coat. The elasticity 702 
DISEASES OF THE FEMALE GENERATIVE ORGANS. 
of the peritoneum doubtless allows of its distention, but there 
must also be some increase of peritoneal tissue, as the coat is not 
thinner than the ordinary peritoneum. 
The contents of the cyst are a clear, limpid fluid, of low specific 
gravity, sometimes as low as 1003, and not exceeding 1008. It is 
very rare to find any considerable secondary alteration of the cyst- 
wall or its contents, but inflammation may occur. 
By rupture or perforation (paracentesis), the cyst, being a 
single one, will be completely emptied, and it is noteworthy that 
there does not seem to be much tendency to refilling. In one 
examined by the author with Dr. Gairdner, the cyst, to judge from 
the symptoms, had been of large size, and ruptured sixteen months 
before death. It was found lying in the abdomen collapsed and 
flattened, and a cicatrix represented the point of rupture. The 
cyst could be blown up to the size of a child’s head, but the cor- 
rugated appearance of the internal wall showed that it had been 
much larger. Here the peritoneal coat, which could be easily 
stripped, had contracted to suit the diminished size, and was 
smooth on the surface, while the proper cyst-wall, being devoid of 
elasticity, was thrown into ridges. 
It may be useful here to compare the parovarian with the ovarian 
cyst. The former is a single cyst, the latter never really single, 
although it may simulate the unilocular character; accordingly, 
the former is completely emptied by tapping, the latter only par- 
tially. The parovarian fluid is limpid, and its specific gravity 
never above 1008, while the fluid of the ovarian cyst is mostly 
more or less glutinous, usually brownish in color, and of a specific 
gravity over 1020. It is important also that the parovarian cyst, 
after being emptied, may not refill, while in the case of the ovarian 
cyst, if that which has been emptied does not refill, others grow to 
take its place. When the cyst itself is examined, the stretching 
and enormous elongation of the Fallopian tube are usually very 
characteristic in the parovarian cyst, although it may happen that 
an ovarian cyst will grow mainly from the upper part of the ovary, 
and so cause stretching of the tube. Then there is, in the case of 
the parovarian cyst, the ready separation of the peritoneal coat, 
whereas in the ovarian cyst there is no such isolable layer. This 
arises from the fact that the peritoneum over the ovary is only 
represented by a layer of endothelium, and not by a membrane 
distinct from the capsule. The ovarian cyst being the ovary itself 
with cystic development, it has its external covering formed simply 
of the exaggerated ovarian capsule. One can sometimes tear this 
capsule into layers for a certain distance, but no continuous sepa- 
ration of the coats is possible. There is, lastly, the fact that the 
parovarian cyst is a single simple bladder, whereas even in the 
case of dropsy of the Graafian vesicles there are several cysts, and 
in the common colloid cyst there are multitudes of developing 
cysts and solid glandular tissue. the mammary gland. 
703 
C.—THE MAMMARY GLAND. 
Malformations of the Breast.—One or both mammae may be 
absent. It is more frequent, however, to have supernumerary 
breasts or nipples, sometimes three, four, or even five, instead of 
two. The supernumerary breasts are usually situated near the 
axillae, or under the normal ones. But there are cases in which 
they have had a very abnormal situation, as in the inguinal region, 
on the thigh, or even on the back. They are usually small in size, 
but in some cases they have produced milk during lactation. It 
may be noted that the occurrence of additional mammae is not 
altogether extraordinary, considering that in the lower animals 
the mammae are usually more in number than in man. 
Inflammation of the Mamma.—This rarely occurs except in con- 
nection with lactation. During this process, and especially at its 
commencement, the structures in the mamma are the seat of very 
active processes; there are hyperaemia and an active secretion of 
milk. Under these circumstances inflammation is more readily 
induced than usual. It may happen that contraction of the arteries 
from accidental circumstances, such as exposure to cold, may 
induce inflammation. We know that an inflammation may be 
induced in animals by ligaturing an artery for a time and then 
loosening it, and we may believe that partial contractions of the 
arteries may act in this way. Even a general irritation of the 
vaso-motor centre by reflex action, when the skin is exposed to 
cold, may, in the case of the highly excited vascular system of the 
mamma at the commencement of lactation, induce inflammation. 
Again, disease of the nipples, such as cracks and * ulcers, often 
induces inflammation in the breasts. We may believe that here 
the irritant which has caused the lesion in the nipple may extend 
along the tubes and cause inflammation in the mamma. At the 
time of puberty, the female breast undergoes a special develop- 
ment, and is also in an active state, and at this period inflamma- 
tions are also apt to be induced. 
The inflammation is usually an exceedingly acute one, and is 
accompanied by exudation, the interstitial tissue being packed 
with leucocytes and the breast hardened. This hardening is often 
local, as the inflammation is usually to some extent limited to 
certain parts of the breast. But very often the exudation of leuco- 
cytes goes on to actual suppuration and the formation of abscess, 
sometimes with sloughing of the tissue. The abscess so formed 
may have extensive ramifications in the mamma, especially if the 
pus does not get vent externally. After evacuation the cavity fills 
with granulation cells, and finally closes, and a cicatrix is formed. 
A chronic inflammation resulting, after the usual manner of 
interstitial inflammation, in induration of the organ, has been 
described, but is not of frequent occurrence. 704 
DISEASES of the female generative organs. 
TUMORS OF THE MAMMA. 
Adenoma of the Mamma.—This form of tumor is of somewhat 
common occurrence. It is met with chiefly as an isolated tumor, 
either in the midst of the gland or in its neighborhood. There is 
preserved in the museum of the Western Infirmary a tumor the 
Fig. 307. 
Section of an adenoma of mamma. Glandular structures of well-formed outline 
are shown in the midst of fibrous tissue. X 90. 
situation of which was behind the gland, which had to be cut 
through in order to remove it. The tumor was thus almost like a 
supernumerary mamma. Tumors of this kind are surrounded by 
a distinct connective-tissue capsule which isolates them from the 
gland or from the neighboring tissue. 
Under the microscope the tumor (see Fig. 307) presents a per- 
fectly regular glandular structure, with acini and ducts, but of 
course without any external communication. Between the gland- 
ular elements there is connective tissue which is sparsely nucleated 
like that of the normal gland. 
Adenoid Sarcoma and Sarcoma.—The adenoid sarcoma is a 
form of tumor in which there is glandular tissue with sarcoma- 
tous tissue between the glandular structures. Doubts have been 
expressed as to the actual new-formation of gland-tissue in tumors 
presenting sarcomatous elements, but as we meet with tumors pre- 
senting all gradations between the simple adenomas and the 
typical sarcomas, we can hardly refuse to believe that glandular 
new-formation does take place in the cases under consideration. 
When much glandular tissue is present, as in Fig. 308, the tumor 
is usually isolated, and partially separated from the surrounding TUMORS OF THE MAMMA. 
705 
mammary tissue, and there is sometimes more than one distinct 
tumor present. 
The glandular structures are as in the adenoma, acini and smaller 
tubules, hut they do not conform so strictly in their arrangement 
to the type of the normal mamma. The sarcomatous tissue 
evidently arises from the interstitial tissue, and is usually spindle- 
Fig. 308 
Section of an adenoid sarcoma of the mamma. G-laudular structures are shown 
with spindle-cell tissue between. X 90. 
celled. In regard to this tissue great varieties are presented. The 
cells may be comparatively limited in number, so that the tissue is 
a connective tissue with an excess of spindle-cells. From this we 
have all gradations up to a complete spindle-celled tissue separating 
the glandular elements. 
From cases in which there is a new7 formation both of glandular 
and sarcomatous tissue, it is difficult to distinguish those in which 
the new formation is entirely sarcomatous, and any glandular 
tissue is simply the remains of the normal mammary structure. 
Tumors are of frequent occurrence in the mamma, in which it may 
he said at least that the glandular element is very subordinate, and 
these tumors warrant the designation of true sarcoma. 
Such tumors are not usually isolated or defined from the neigh- 
boring mammary tissue. They sometimes involve a limited part 
of the mamma, that portion undergoing what may almost be called 
a sarcomatous degeneration. That is to say, its interstitial tissue 
becomes converted into spindle or round-celled tissue, while its 
glandular structures are variously contorted. But not infrequently 
the disease affects the whole mamma; there is a diffuse sarcoma- 
tous growth. In that case the mamma is greatly enlarged, and 
may attain a weight of ten or twenty pounds. The tumor may 
involve the skin and ulceration may occur. There may thus be a 
deep ulcer in the midst of a massive tumor. 706 
DISEASES OF THE FEMALE GENERATIVE ORGANS 
Under the microscope the sarcomatous elements are seen most 
prominently, wrhile the glandular elements are somevrhat sparse or 
entirely absent; but here and there a duct lined wfith epithelium 
or a misshapen acinus may be found. For the most part the 
glandular structures seem to be drawm out, so that tubes are much 
more frequent than acini. 
In these sarcomas cysts are very frequent, and sometimes the 
cystic formation is so marked that the name cystosarcoma is given. 
The cysts take origin in the glandular structures. Perhaps because 
of obstruction of the latter they may dilate and form distinct cavi- 
ties in the midst of the sarcomatous tissue. A minor degree of 
this is very common, glandular structure being represented by 
elongated spaces lined with epithelium, which is mostly cylindrical 
(see Fig. 309). Even in these incipient cysts we can often see that 
Fig. 309. 
Semidiagrammatic view of dilated glandular spaces in a cystosarcoma of the mamma. The 
spaces are lined with cylindrical epithelium. The tendency to intracystic growth is shown, 
especially in the upper one. These were drawn under the camera lucida, so that the outlines 
are correct. X 62. 
the sarcomatous tissue is, as it were, pushing its way into them 
(see figure), a kind of papillary growth presenting itself in the wall 
of the space, the growth being covered with epithelium like that 
lining the space. Sometimes this intracystic growth is very 
marked, and we may have large cysts filled with ingrowing masses 
of sarcoma. In fact, it sometimes appears as if the main growth of 
the tumor were into greatly dilated gland-ducts. 
It need hardly be added that the sarcomas and adenoid sarcomas 
present malignant characters, chiefly in the form of a tendency to 
local recurrence. If an adenoid sarcoma is excised, it will prob- TUMORS OF THE MAMMA. 
707 
ably recur as a pure sarcoma, but the author has seen, in a case ot 
recurrence, an arrangement of the spindle-cells as if around dis- 
tinct centres, which suggested glandular structure. These tumors, 
on recurrence, also become softer, and the cells more loose. 
There are also sarcomas in the mamma which are not related to 
the glandular structure either directly or indirectly. These are 
Fig. 310. 
Section of cartilaginous part of a tumor of mamma which contained besides 
spindle-celled and fibrous tissue. X 200. 
usually spindle-celled sarcomas, but they may be considerably 
mixed, cartilage even occurring as part of their structure, as in the 
case from which Fig. 310 was taken. 
Cancer of the Mamma.—According to what has been stated in 
the general section of this work, we have in cancer an aberrant 
growth of epithelium as the foundation process, and in the first 
place we may consider the finer details of the overgrowth. In the 
more ordinary form of cancer of the breast the process begins in 
the glandular acini. As a rule, it is a chronic process, and, along 
with new formation of epithelium in the acini, there is formation 
of round cells in the connective tissue around. The epithelium of 
the acini grows through the basement membrane, forming pene- 
trating processes, and the round cells develop connective tissue 
which frequently causes great contraction of the tumor (Scirrhus). 
It is as if the epithelium, growing outwards, acted as an irritant, 
causing inflammatory new-formation in the interstitial tissue of the 
gland. Where the case is very chronic, the connective-tissue for- 
mation may be very pronounced, but when more acute the epithe- 
lial elements preponderate. Cancers which take origin in the 
glandular acini may be called parenchymatous cancers. 
But cancers may take origin rather in the ducts of the gland, 
forming a class called duct cancers (Thin). These very often 
begin in the large ducts in or near the nipple. In this case the 
growing epithelium often distends the ducts, forming cavities 
which are sometimes lined with cylindrical epithelium, with more 
irregular epithelium inside. Such dilated ducts may even have 
the appearance of cysts, so that the tumor may appear cystic. 
This process in the ducts is also associated with irritation of the 708 
DISEASES OF THE FEMALE GENERATIVE ORGANS. 
surrounding connective tissue, so that there are round cells and 
new-formed connective tissue. The special characters of duct 
cancer are usually most manifest in the parts near the nipple, 
where it generally begins. On passing into the substance of the 
gland the appearances are more like those of the other form. 
Duct cancer is sometimes associated with the condition known 
as Paget’s disease or eczema of the nipple. Eczema, as indicated 
in the section on Diseases of the Skin, is an inflammation of the 
skin, in which both the epidermis and the superficial layers of the 
cutis are engaged. In case of duct cancer, the affection of the ducts 
seems to induce an inflammation of the skin of the nipple and parts 
around, characterized by the usual formation of round-cell tissue. 
The superficial or papillary region of the skin may then be replaced 
almost entirely by round cells with nests of epithelium in their 
midst, and the condition is somewhat like that of a granulating 
wound. The epithelium of the surface takes little part in the 
process, and it may be lost, so that the granulation tissue is exposed. 
As the cancerous process begins commonly in the nipple, this con- 
dition of eczema may be a very early one, and may precede, it 
may be for many months, the actual appearance of a tumor in the 
mamma. It is to be remembered also that a simple eczema may 
occur in the nipple, due to an ordinary irritant. 
In connection with this subject, the views recently enunciated 
by Creighton deserve notice. According to the observations of 
this author, there is, during the process of evolution of the gland 
preparatory to lactation, a great new formation of glandular 
epithelium, which gradually, after a number of generations, 
assumes the condition in which it forms milk. In the involution 
after lactation there is a reverse process, successive generations of 
epithelium being produced till it assumes the resting state. All 
these stages between the resting state and the milk-producing 
state are characterized by the production of epithelium which is 
in itself useless, and has to be disposed of. It is disposed of by 
the lymphatic system, into which the cells pass, and are carried to 
the lymphatic glands. Creighton regards cancer as the exaggera- 
tion of a condition comparable to one or other of the stages of 
evolution or involution, and therefore primarily a disorder of 
function. There is an excessive production of epithelium, which 
bursts through the basement membrane and is grouped outside 
the acini. In like manner the cells pass to the lymphatic glands, 
where they give rise to secondary tumors, not bv themselves 
growing and proliferating, but by inducing the lymphatic gland- 
ular tissue to assume the characters of cancerous tissue. These 
views are somewhat theoretical, and stand in need of confirmation. 
We have now to consider cancer of the mamma according to 
the more ordinary division into its several forms. 
The commonest form of cancer is scirrhus. The description 
of scirrhous cancer in the general part of this work is chiefly based 
on scirrhus of the mamma, and need not be repeated here. It TUMORS OF THE MAMMA. 
709 
will be remembered that the epithelial masses often form elongated 
processes (Fig. 311) in the midst of an excessive stroma composed 
of dense contracting fibrous tissue. The cells are often atrophied, 
so that in some parts of the tumor there is little beyond dense 
connective tissue. The cancer commonly forms rather a limited 
infiltration of a part of the gland than a proper tumor, and as the 
tissue contracts there is commonly an actual diminution of bulk 
with great induration. The gland is distorted and puckered 
towards the affected part. Very often the disease is continuous 
with the nipple, and by the dragging of the tissue the nipple is 
Fig. 311. 
Section of cancer of mamma from a recent nodule. Epithelial cells in spaces formed by 
connective tissue; these are sometimes in single rows, and by multiplication form larger 
masses. X 200. (Cornil and Ranvier.) 
drawn in, sometimes even forming an umbilicated depression. 
The tumor is very irregular in its extension in the gland, and it 
very often happens that in the midst of hard scirrhous tissue some 
adipose tissue appears, being the remains of some of the fat 
which normally surrounds the gland. In like manner, pieces of 
the gland-tissue may crop up amidst the contracting tumor. Not 
infrequently scirrhus goes on to ulceration of the skin, which 
usually occurs about the site of the nipple and areola. The ulcer 
is crater-shaped, with dense prominent walls. Sometimes after 
formation of the ulcer the growth of the cancer becomes more 
rapid. 710 
DISEASES OF THE FEMALE GENERATIVE ORGANS. 
When a mamma which is the seat of scirrhous cancer is cut 
into, either the whole gland or a portion of it is seen to be occu- 
pied by a hard mass of a grayish color on the cut surface. It is 
very hard to cut, and the cut surface is commonly concave, the 
elasticity of the dense connective tissue producing retraction. In 
the general gray basis there are various whitish or yellowish pieces 
which represent the remains of mammary or adipose tissue, or 
the cancerous epithelium in a state of fatty degeneration. If the 
cut surface be scraped a tliickish juice is obtained, which micro- 
scopic examination shows to be composed of epithelial cells and 
their debris. Many of the cells are large and well formed, while 
some may contain secondary cells within them or double nuclei 
(see Fig. 312). There are also free nuclei which have escaped 
Fig. 312, 
Cells in the juice scraped from a scirrhus of mamma. They are of very irregular shape, 
Most of them contain several nuclei and some daughter-cells. X 200. 
from cells as a result of the mechanical interference in the process 
of preparing the specimen. Many of the cells contain fatty de- 
generation—in fact, very often nearly all contain fatty granules— 
and there are some completely degenerated, showing nothing but 
an aggregation of fat-drops like the compound granular corpuscle. 
The lymphatic glands commonly become secondarily affected in 
scirrhus of the mamma, and the tumor produced here is also a 
hard cancer with excessive development of the stroma. It is to 
be observed, however, that in the glands the stroma usually forms 
a more distinct meshwork than in the mamma, and the epithelial 
cells form more definite groups. 
Medullary Cancer forms the opposite extreme to scirrhus, and 
there are all intervening grades. In the medullary cancer we have 
a bulky tumor of soft consistence and rapid growth. There is a 
well-formed alveolar stroma, and the cells are somewhat loosely 
contained in it. The tumor involves neighboring tissues, very 
readily infiltrating the skin, subjacent muscle, and even the osseous 
ribs and the pleura. This form is not uncommonly present simul- 
taneously in both breasts. On section the tumor presents a gray 
brain-like appearance. The juice furnishes numerous cells, mostly TUMORS OF THE MAMMA. 
711 
small in size but with prominent oval nuclei, also abundant free 
nuclei which have escaped from the delicate cells. As the tumor 
commonly extends to the skin, we may have ulcers with fungating 
prominence of the tissue. The lymphatic glands are early affected 
and they also may ulcerate. 
Many large tumors of the mamma of comparatively rapid growth 
do not correspond with the description either of the medullary 
cancer or the scirrhus. In their minute structure they are more 
like the scirrhus, and perhaps may be designated acute scirrhus. 
They have a remarkably tirm fibrous stroma, but it forms distinct 
meshes in which the epithelial masses are contained with consid- 
erable regularity. The cancer cells are also large and essentially 
like those in scirrhus. The tumor as a whole also is hard, this 
depending on the abundance and density of the stroma. 
Colloid Cancer is, as compared with scirrhus, an exceedingly 
rare form of tumor, but it- does occur not infrequently. The col- 
loid degeneration may affect the cells of an ordinary cancer, pro- 
ducing a partial metamorphosis. Or the cancer as a whole may 
present, from the first, a tendency in this direction, and the whole 
tumor have the characters of colloid cancer. The entire mamma 
is commonly affected, and it is greatly enlarged, while it presents 
a hard feeling like that of acute scirrhus. On section the tumor 
presents a flickering gelatinous appearance. Under the micro- 
scope there is the usual pronounced stroma with colloid material 
in the meshes. In the midst of the colloid masses there are often 
seen groups of cells, the remains of the epithelium. 
It is to be added that sometimes cancers occur having a close re- 
semblance to colloid cancers, but in which the metamorphosis is in 
the stroma, which is the seat of mucous degeneration. We may 
thus have a large gelatinous tumor which, on microscopic examina- 
tion, shows epithelial masses embedded in a gelatinous flickering 
stroma. To this form may be applied the term mucous cancer. 
Other Tumors of the breast are of uncommon occurrence. We 
may have an excessive growth of the adipose tissue around the 
mamma, forming a lipomatosis or lipoma capsulare. Even iso- 
lated lipomas have been met with. Isolated fibromas have also 
been seen. Myxoma of the mamma has been observed in a con- 
siderable number of cases. It forms a tumor of considerable size, 
the interstitial tissue of the mamma generally being converted 
into mucous tissue, while the glandular structures have atrophied; 
this form of tumor is apt to be mistaken for colloid or mucous 
cancer. 
The Myoma has been met with in the nipple. DISEASES OF THE MALE GENERATIVE ORGANS. 
A.—THE TESTICLES. 
Malformations and Misplacements of the Testicle.—The 
testicle may he absent on one or both sides, while the vesiculse 
seminales and vasa deferentia are perfect. Or the vas deferens 
may be deficient while the testis is well developed. 
Imperfect descent of the testis, or cryptorchismus, is a very 
frequent and important condition. The descent of the testis occurs 
normally before birth, but in a considerable number of cases the 
organ has not yet appeared externally at birth. In the majority of 
such cases it comes down within the first week, but it is sometimes 
delayed for months or a year, or even till puberty. When thus 
delayed the descent is very often imperfect, so that the gland 
remains in the inguinal canal or at the ring. On the other hand, 
the testis may be retained throughout life in the abdomen. The 
testicle retained in the abdomen or on the way down is usually 
imperfectly developed, and although apparently of normal size, it 
does not generally contain spermatozoa in its tubules. It is also 
more prone to inflammation and the formation of tumors than the 
normally placed testis, especially when in the inguinal canal where 
it is exposed to external violence. When it is late in descending 
the accompanying pouch of peritoneum, which forms the tunica 
vaginalis, is apt to remain open and so to induce a congenital 
hernia. 
Besides these congenital misplacements, we may have the testis 
descending into the crural canal, or into the perineum. 
Inflammation of the Testicle.—This condition presents itself 
under a considerable variety of forms, certain of which are difficult 
altogether to separate from syphilis and tuberculosis. It is to be 
remembered that the testicle is bounded externally by a dense 
fibrous capsule, the tunica albuginea, and that the products of 
inflammation are apt to be closely confined within this. 
Acute Orchitis is mostly secondary, although occasionally 
resulting from a blow or other injury. It occurs as a secondary 
result in gonorrhoea, the specific irritant being apparently prop- 
agated along the vas deferens; also in cases of irritation of the 
urethra by calculi, the passage of instruments, etc., the inflamma- 
tion in such cases being called sympathetic, and probably brought the testicles. 
713 
about by reflex irritation of the vaso-motor centres. In mumps 
there is also, in a certain proportion of cases, orchitis as a secondary 
result, the specific irritant attacking the testicles as well as the 
parotid gland. 
The inflammation very often begins in the epididymis, and may 
remain confined to that region or pass on to the testis. There are 
hyperaemia and serous exudation producing great swelling, so that 
the tunica albuginea is tightly stretched, and the organ feels hard 
and tense. At the same time there is often serous fluid in the 
tunica vaginalis. There may be resolution without suppuration, 
the testis returning to the normal condition, or the disease may 
become chronic, or suppuration may occur. In the latter case an 
abscess or abscesses form in the testicle, and these may burst exter- 
nally. In that case the tense albuginea often forces the tissue of 
the testicle through the opening, so that it projects in a fungating 
form. This, which forms the benign fungus, and is not to be mis- 
taken for cancer, has a red color and looks like protruding 
granulations. But it really contains the seminal tubules, and after 
the subsidence of the inflammation these may be replaced and 
resume their function. On the other hand, the abscess may dry in 
and form a caseous mass, which becomes surrounded by a fibrous 
capsule. This mass may ultimately become calcareous. 
Chronic orchitis may arise out of an acute attack, remaining 
after the formation of abscess, or else supervening without that. 
There is also a spontaneous chronic orchitis which in most cases is 
either syphilitic or tubercular. The ordinary chronic orchitis 
is characterized by new formation of connective tissue in the 
stroma of the organ, and consequent induration of it. The tubules 
atrophy and the whole organ is reduced in bulk and hardened. 
Generally on section it can be seen that the albuginea and the septa 
which proceed towards the mediastinum, are greatly thickened. 
At the same time there is frequently adhesion of the tunica 
vaginalis which may obliterate the sac. 
The other form of chronic orchitis which is described is char- 
acterized by the occurrence of yellow caseous masses. Such 
masses may arise from the drying in of abscesses, or in connection 
with syphilis or tuberculosis, and probably have no independent 
origin. 
Syphilitic disease of the testicle sometimes occurs as a gen- 
eral induration, having the usual characters of chronic orchitis. 
The albuginea is thickened and the trabeculae are enlarged as they 
converge.towards the mediastinum. These thickened structures 
may be largely composed of granulation tissue, and we may have 
in addition definite gummata. The gummata may undergo caseous 
necrosis, and by coalescence of neighboring tumors we may have 
considerable masses of caseous material. In the midst of this 
caseous material the outlines of the seminal tubules can sometimes 
be made out, indicating that the necrosis has overtaken the proper 
tissue as well as the new formed. 714 
diseases of the male generative organs. 
Tuberculosis of the testicle is characterized by the formation 
of caseous masses, sometimes of considerable size, and these are 
surrounded by a gray inflammatory tissue in which tubercles are 
to be found. The tuberculosis is very often associated with similar 
disease in the prostate and vesiculse seminales, and this coincidence 
points to propagation from the one to the other. The starting- 
point may be at the testis or at the other extremity of the vas 
deferens. There is also, not infrequently, tuberculosis elsewhere, 
as in the form of scrofulous glands or phthisis pulmonalis. 
As a general rule, the tuberculosis begins in the epididymis, 
mostly in its tubules. The result is great thickening and the 
formation of a caseous mass, enclosed very often in a firm fibrous 
capsule. Thus a firm elongated tumor may form behind the 
testicle. In the testicle also caseous masses form, at first isolated, 
but afterwards running together into considerable conglomerates. 
The caseous masses are very dense, but after a time they generally 
break down, and having burst externally, tedious fistulae are the 
consequence. 
When the testicle is examined in section the caseous structure 
is seen to be surrounded by a transparent gray tissue, in which, as 
already mentioned, tubercles are present. This inflammatory and 
tubercular structure by its pressure destroys the tubules for the 
most part, but not altogether, as bits of tubules are sometimes ex- 
pelled along with the softened caseous material. 
Tumors of the Testicle.—These are mostly somewhat malig- 
nant in their characters, and there is a peculiar tendency to a 
mixed structure. 
Sarcomas occur frequently mixed with tissue of other tumors, as 
the myxoma, enchondroma, etc. Even when the tumor is a pure 
sarcoma there may be combined the structures of various forms 
of this tumor, spindle cells, round cells, and mucous tissue. There 
may, however, be a simple round-celled sarcoma. The sarcomas 
form usually large tumors of soft consistence and rapid growth. 
They occur in comparatively young persons, and are prone to 
metastasis, the secondary tumors occurring mainly in the lungs. 
The relation of the sarcomas to the seminal tubules deserves 
special consideration. The tissue of the tumor, like that of other 
sarcomas, originates in the interstitial tissue. In many cases the 
glandular structures undergo atrophy; but in others, changes occur 
comparable with those we have already considered in sarcomas of 
the mamma. Cysts are thus of frequent occurrence, and they are 
so characteristic in some cases that the name cystosarcoma is 
given. These cysts often contain a gelatinous material, although 
in the larger ones the contents are usually serous. Sometimes the 
contents undergo fatty degeneration, and we may have choles- 
tearine in the fluid, or even an atheromatous substance. As in the 
mamma, there may be a papillary ingrowth of the sarcoma into 
the cyst, forming peculiar intracystic projections. It appears also 
that there is sometimes an actual new formation of glandular tissue 715 
THE TESTICLES. 
along with the sarcomatous, in this respect resembling the adenoid 
sarcoma of the mamma. 
Cancer of the testicle connects itself with the cystic and 
adenoid sarcomas. It appears that not infrequently the glandular 
tissue in these tumors has more of the irregular atypical cancerous 
character than of the strictly glandular, and in particular the epi- 
thelial masses do not possess a membrana propria. These char- 
acters are also expressed in the fact that sometimes these tumors 
extend to the neighboring lymphatic glands, while others penetrate 
more readily into the veins. 
Proper cancer of the testes is mostly a large, quickly growing, 
soft tumor—medullary cancer. It involves the whole organ as 
well as the epididymis, converting them together into a massive 
tumor. It may also extend along the vas deferens, and on to the 
lymphatic glands, inguinal, lumbar, and prevertebral. From these 
glands it may extend to the radicles of the portal vein and so pro- 
duce tumors in the liver, or more frequently to the radicles of the 
vena cava, producing tumors in the lungs. In the midst of the 
tumor we may have cysts formed by mucous or fatty degeneration. 
The cancerous tissue is derived from the epithelium of the 
seminal tubules, and the stroma from the interstitial tissue. It is 
necessary, however, to mention that tumors may arise in connec- 
tion with the bloodvessels which have a resemblance in their 
structure to cancers, but which are properly plexif'orm angio- 
sarcomas. 
Other tumors of the testicle are uncommon. We meet with 
cysts, but the chief of them, the spermatocele, will be described 
afterwards. The testis is also sometimes the seat of the dermoid 
cyst. It may be a simple dermoid in the midst of the gland, 
arising apparently by inclusion of a piece of embryonic skin. But 
sometimes there is a more complex cyst, like that of the ovary, 
and deserving the name of teratoma. Such tumors probably owe 
their origin to the inclusion of a whole foetus. For the rest, the 
occasional occurrence of fibromas, lipomas, enchondromas, myomas 
of the striated variety and even osteomas, has been observed. 
Hydrocele.—By this name is meant the accumulation of fluid 
in the tunica vaginalis. The fluid is serous and the cause of its 
accumulation is inflammation. It is not properly a dropsy of the 
tunica; a general dropsy, affecting the skin of the scrotum very 
greatly, causes little fluid to accumulate in the tunica vaginalis. 
The inflammation may be acute, in which case there is fibrine de- 
posited on the surface as well as serous fluid in the sac. More 
commonly it is chronic, and there is a gradual accumulation of 
serum. 
The fluid distends the sac, and so a bulky tumor is formed which 
is pear-shaped with its blunt end downwards. The fluid is usually 
a clear serum, but sometimes it is slightly opalescent. In the true 
hydrocele this is not from the presence of spermatozoa, but from 
the existence of tine fat-drops, resulting from degeneration of the 716 
DISEASES OF THE MALE GENERATIVE ORGANS. 
leucocytes floating in the fluid. There may even be cholestearine 
crystals formed in this way. 
Not infrequently hemorrhage occurs, most commonly as the 
result of a blow or other injury, and the hydrocele becomes a 
hematocele. The blood mostly coagulates, and the coagulum 
through time undergoes various changes, softening into a brown 
pultaceous material or into a brown turbid fluid, in which are 
enormous numbers of cholestearine crystals. The blood seems to 
act as an irritant to the tunica vaginalis, causing often a very great 
thickening of it. The interior also is rough and sometimes presents 
considerable projections. The thickened cyst may contract some- 
what so that the tumor is reduced in size. This thickening of the 
wall, even when the contents are fluid, may cause the haematocele 
to be mistaken for a solid tumor, and castration has often been 
performed under this belief. 
A hydrocele or hsematocele may be cured by the fluid being 
absorbed, the result usualty being adhesion of the opposed surfaces 
of the tunica vaginalis and obliteration of the sac. 
In the condition named congenital hydrocele the tunica vagin- 
alis retains its communication with the peritoneal cavity. The 
fluid may come from the peritoneal cavity, or may originate as in 
an ordinary hydrocele. It can be pressed into the peritoneum 
through the neck. It will be understood that a congenital hernia 
may occur along with or alternate with this form of hydrocele. 
Spermatocele. Encysted Hydrocele.—In this affection there 
is a cyst having in many cases much the exterhal appearance of 
hydrocele, but containing a fluid in which spermatozoa are abund- 
antly present. In other respects also the condition differs from 
that in hydrocele, for we have here not merely an accumulation 
in an existing sac, but a proper new-formed cyst. Hence the name 
Encysted Hydrocele is often used as equivalent to spermatocele. 
The cyst arises in connection with the epididymis for the most 
part, and probably takes origin in one or more aberrant tubules 
which have formed blind diverticula from the seminal tubules. 
They usually arise near the upper end of the epididymis, but it 
may be at the lower end or from the rete testis. The cysts grow 
often to a large size, and they sometimes push themselves into the 
sac of the tunica vaginalis, inverting one layer of the wall against 
the other. As a rule, the tunica vaginalis is found below and in 
front of the cyst, this position being connected with the origin of 
the cyst in the neighborhood of the testis. 
The fluid from these cysts has a peculiar opalescent appearance, 
which is due to the presence of multitudes of lively spermatozoa. 
The existence of these shows that the cyst has retained its con- 
nection with the seminal tubules. The cyst is usually lined with 
a ciliated epithelium, but in large ones the pressure of the fluid 
may cause it to assume the pavemented form. 
It will be observed that these spermatic cysts are comparable in 
their origin to the parovarian cysts. THE PENIS AND SCROTUM. 
717 
Other forms of hydrocele have been described, but they re- 
quire only a passing notice. There may be an encysted hydrocele 
without spermatozoa in the fluid. Then there is encysted hydro- 
cele of the cord, sometimes arising by a portion of the communi- 
cation between the tunica vaginalis and the peritoneum remaining 
unobliterated and becoming the seat of an accumulation of fluid. 
There is also diffuse hydrocele of the cord, in which there is an 
cedematous condition of the connective tissue around the spermatic 
cord. There may even be a hydrocele from a hernial sac, which 
has got emptied of its contents, and shut off' from the peritoneum 
by adhesion of the neck. 
B.—THE PENIS AND SCROTUM. 
In the penis, the ulcers or chancres are the commonest forms 
of disease. The simple chancre is an ulcer which has its usual 
seat on the glans or frenum. Sometimes we meet with a deeply 
penetrating or phagedenic ulcer. The hard chancre is the primary 
syphilitic sore, and as such we have already considered it. 
Another syphilitic manifestation is the condyloma, which forms 
warty outgrowths sometimes of considerable size. There may be 
large groups of papillae forming a cauliflower-like tumor. 
Cancer of the penis occurs in the form of epithelioma. It 
begins usually in the glans, and the tumor is often covered with 
prominent papillae, which give it a highly characteristic warty 
appearance, like the cauliflower excrescence. It may remain long 
without ulceration, but usually sooner or later breaks down, and 
there are sometimes deep ulcerating Assures or fistulae between 
the groups of papillae. 
In the scrotum, cancer is somewhat common, and it is so often 
chimney-sweepers who are affected that the disease is often called 
chimney-sweepers’ cancer. In Glasgow it has been found that 
workers in paraftin refineries are also liable to this disease. It 
generally forms a flat tumor from whose surface prominent papillae 
protrude. Through time ulceration occurs, and the testicle may 
be exposed. 
Elephantiasis of the scrotum has been sufficiently treated of in 
the general part of this work. 
Lymph scrotum has already been referred to in connection with 
the filaria sanguinis. In it there is a varicose condition of the 
lymphatic vessels of the scrotum with the formation of vesicles in 
the skin. These frequently burst and discharge a fluid in which 
the embryo filaria is usually to be found. In some such cases the 
filaria is also present in the blood, but sometimes not. The lym- 
phatic glands of the groin are indurated, and the dilatation of the 
lymphatics seems to be due to the obstruction of these vessels in 
the glands by the embryo filarise. According to Manson, elephan- 
tiasis sometimes develops from lymph scrotum, and depends on 718 
DISEASES OF THE MALE GENERATIVE ORGANS. 
the same parasite, but this view can hardly be accepted on the 
present evidence. In lymph scrotum, the adult female filaria, and 
probably the male also, inhabits a lymphatic vessel in the groin, 
and their embryos or ova pass off' and stick in the glands, thus 
obstructing the lymphatics. 
The prostate, as we have already seen, is subject to hyper- 
trophy. The common enlargement of old age is due to increase 
of the muscular substance. This enlargement exists in about 
thirty per cent, of men above sixty years of age. It develops 
slowly without any apparent cause, and in this respect has the 
characters of a tumor. Sometimes the whole prostate enlarges, 
and it may reach the size of the fist. But sometimes there is a 
more partial hypertrophy, forming the so-called third lobe of the 
prostate, which projects inwards at the neck of the bladder, and 
is sometimes so large as to act like a valve to the orifice of the 
urethra. The effect of enlargement of the prostate on the urethra 
is to be noted. If there is a general enlargement, the urethra is 
necessarily elongated in its prostatic portion, and whereas normally 
this portion measures one and a half inches in length it may come 
to be four inches. At the same time the tube may be narrowed 
and even distorted. If, for instance, the central part of the pros- 
tate is specially hypertrophied, then the urethra, being pushed 
upwards, has on section a crescentic shape with the convexity 
upwards; or if one side is larger than the other, there will be a 
convexity towards the opposite side. 
Besides this muscular hypertrophy, the much .rarer hypertrophy 
of the glandular structure is to be mentioned. The glandular 
structure does not commonly increase with the muscular, but 
sometimes enlarges by itself, so that we have an adenoma of the 
prostate. 
Cancer of the prostate is not of frequent occurrence. The 
gland enlarges, and the disease is apt to extend to neighboring 
structures. 
Tubercle occurs not infrequently in the prostate and vesiculre 
seminales in conjunction with similar disease in other parts of the 
urino-genital passages. There is caseous necrosis with ulceration 
as usual, and this may cause even perforation into the rectum or 
bladder. 
Concretions are of frequent occurrence in the prostate in old 
persons. They are formed in the gland ducts, and are of various 
sizes, from very minute to the size of a grain of corn. When 
small, they are colorless, but as they enlarge they frequently be- 
come blackish or reddish-brown in color. They are round or oval 
in form, and frequently present concentric stratification (Fig. 44, 
p. 135). They have usually a central cavity. Very commonly 
these bodies present the character of amyloid bodies, giving a 
bluish or mahogany-red color with iodine. Sometimes the}’ con- 
tain lime salts in their substance. They may pass into the urethra 
and escape with the urine. While in the prostate they do not 
appear to produce much disturbance. DISEASES OF THE BONES AND JOINTS. 
A.—THE BONES. 
Introduction.—In considering the diseases of the bones, it is 
necessary to bear in mind certain matters regarding their structure 
and life. It is to be remembered that bone grows, not like ordi- 
nary tissues by interstitial expansion, but by addition of new tissue 
to the old. An attempt has indeed been made, on the basis of the 
architecture of the fine lamellae of the spongy bone at the ends of 
the long bones, to show that growth occurs by interstitial expan- 
sion ; but this attempt is not generally accepted as successful, and 
it may be said that in the growth of bone, deposition and absorp- 
tion go on simultaneously, so as to* preserve the architecture while 
the size is increased. Bone is therefore to be regarded as a solid, 
comparatively unalterable structure. When hypertrophy of bone 
occurs, this takes place by the action not of the bone itself, but of 
the periosteum or endosteum. For the most part also, when 
destruction of bone takes place, it is by agents acting from with- 
out. It is to be noted, however, that the bone corpuscles are not 
altogether inactive cells. They doubtless look after the nutrition 
of the bone, and although they do not, in pathological processes, 
as a rule, present any great increase in activity, they are certainly 
capable of degeneration, in which case they induce changes in the 
solid intercellular matrix. 
In studying the diseases of bone, and more especially in regard 
to rickets and inflammations, it is important to bear in mind certain 
facts as to the relation of osseous tissue to cartilage and connective 
tissue. These three tissues appear to be fundamentally one, and 
they are to some extent mutually convertible. This fact is some- 
times expressed in the term metaplasia, and may be illustrated by 
the accompanying figures (313 and 314), from a case of fracture of 
a rib. 
As we shall see afterwards, an inflammatory process is concerned 
in the healing of fractures, the so-called callus being an inflamma- 
tory new-formation. As a rule in the human subject, this callus 
is formed of bone, but in animals cartilage enters into its constitu- 
tion, and in the section of which the figures are representations, 
the callus was variously composed of bone, cartilage, and fibrous 
tissue, the existence of one or other being apparently determined 720 
DISEASES OF THE BONES AND JOINTS. 
by circumstances. In some parts, as at b, b, in Fig. 313, cartilage 
and bone exist side by side, and it is sometimes even difficult to ' 
Longitudinal section of a fractured rib, showing callus, etc.; the section is imperfect at the upper part, a, a, a, a, a, the broken 
extremities of the rib dove-tailing into each other; b, b, b, now-formed cartilage constituting part of the callus; c, c, c, new-formed bone 
constituting the external layers of the callus; d, d, d,d, new-formed connective tissue constituting the more immediate bond of union 
between the broken ends. X 11. 
Fig. 313. 
say which is actually present, there being obviously transition 
forms. In this as in other inflammations, the new-formed tissue RICKETS OR RACHITIS. 
721 
has originally the structure of granulations, and the granulation 
tissue may develop bone, or cartilage, or fibrous tissue. 
Fig. 314. 
From same section as Fig. 313, showing continuity of cartilage and bone in the callus. At 
a there are cartilage-cells, and at b bone-corpuscles, the matrix being continuous and appar- 
ently of the same structure. X 350. 
RICKETS OR RACHITIS. 
This disease occurs in children during the earlier periods of 
growth, and so far as the bones are concerned it is a disease of de- 
velopment, the normal process of ossification being interfered with. 
Cases have been observed of congenital rickets, but these are rare, 
and in the majority of cases it begins in the first or second year, 
its commencement being very rarely delayed beyond the fourth or 
fifth year. In a large proportion of cases its onset seems to be in 
the latter half of the first year or the first half of the second. 
An endeavor has been made lately to make out that rickets is 
merely a manifestation of hereditary syphilis. This view has not 
received acceptance in this country. It has been pointed out again 
and again that rickets is very common in cities where syphilis is 
uncommon. In the city of Glasgow, for instance, rickets is very 
common among the poorer classes, but syphilis is very uncommon. 
It is so also in Aberdeen, Edinburgh, Belfast, and elsewhere. We 722 
DISEASES OF THE BOXES AXD JOINTS. 
shall see afterwards that syphilis produces changes in the bones in 
some respects analogous to rickets, and atrophy of the cranial 
bones, sometimes designated craniotabes, although formerly re- 
garded as rachitic, is probably in most cases syphilitic; the two dis- 
eases, however, are essentially separate. 
Rickets occurs amongst children who are injudiciously fed and 
badly housed, and the disease in the bones is to be regarded as part 
of a general loss of health. The 
body is weakened, and, besides 
the bones, there are other parts 
that suffer. The state of malnu- 
trition may be the effect of an un- 
healthy state of the mother during 
utero-gestation, or it may be pro- 
duced by unhygienic conditions 
after birth. According to Mac- 
ewen, it supervenes in a considera- 
ble number of cases on an attack 
of one of the acute fevers, such as 
measles or scarlet fever, such an 
attack leaving the child in an ill- 
nourished condition. There are 
usually symptoms of indigestion 
and intestinal catarrh, sometimes 
with fever, and in a certain pro- 
portion of cases there is enlarge- 
ment of the spleen and sometimes 
also of the liver and lymphatic 
glands. The bones, being per- 
haps the most actively growing 
parts at this period of life, may be 
specially affected when the general 
nutrition suffers. 
Rickets has been produced arti- 
ficially in growing animals by feed- 
ing them with small doses of phos- 
phorus, or by giving them lactic 
acid, by the mouth or subcutane- 
ously. In both cases the diet must 
be deficient in lime salts. In the 
latter case it has been supposed 
that the lactic acid, being a ready 
solvent of lime, prevents its depo- 
sition in the bones, and it has been 
inferred that in the human subject 
the gastric derangement causes the 
formation of an excess of lactic 
acid, which is the cause of the dis- 
ease in the bones. There is, how- 
ever, the objection to this view, 
Fig. 315, 
Longitudinal section of bone ossifying 
from cartilage : a, commencement of pro- 
liferation of cartilage-cells; b, cells ar- 
ranged in longitudinal groups; c, matrix 
of cartilage impregnated with lime, this 
calcified matrix is continued beyond the 
ossifying border (c on right side); d, me- 
dullary spaces containing round cells re- 
placing cartilage-cells; e, e, formation of 
bone at borders of calcified matrix, the os- 
teoblasts each forming a piece of bone and 
remaining as the bone-corpuscle. X 90. 
(After Thierfelder.) RICKETS OR RACHITIS. 
723 
that rickets is not always accompanied by any considerable gastric 
disorder, and such a view does not explain its occasional occurrence 
in the foetus. Besides, the disease is clearly an error in develop- 
Longitudinal section of ossifying margin of a long bone in rickets, a, proliferating cartilage-cells, the area of these very greatly extended and 
the arrangement quite irregular; b, b, calcification of the cartilaginous matrix at different levels, but not followed by formation of medullary 
cavities. The formation of medullary cavities (e, e) and of bone is occurring quite irregularly, the level being higher at the right (c) than at the 
left (c). Ate? the osteoblasts are forming bone. In various places, especially at d, pieces of cartilage are seen in the midst of bone, and an ap- 
parent transition of the one into the other is seen. X 90- (Thierfelder.) 
Fig. 816. 724 
DISEASES OF THE BONES AND JOINTS. 
ment, and were it due merely to absence of the lime salts, we 
should expect the bony matrix to be formed without the lime salts. 
The very opposite frequently occurs; we have often an impregna- 
tion of the cartilage with lime salts, a calcification of the cartilage 
(see Fig. 316, b, b), while true ossification lingers. Rickets can in 
most cases be cured by supplying sufficient food and proper lodging, 
and this points to its origin in the opposite of these. 
In order to comprehend the processes presented to us in rickets 
it is necessary to bear in mind the main points in normal ossifi- 
cation. If in a growing child a long bone be divided longitudin- 
ally, and the cartilage and ossifying border examined, it will be 
seen that the transition from cartilage to bone with medullary 
spaces, occurs somewhat suddenly. With the naked eye it can be 
seen that, the deepest layer of the cartilage has a bluish color, this 
zone being very narrow. It is succeeded by a still narrower yellow 
zone which is scarcely more than a line in breadth. On micro- 
scopic examination of a longitudinal section the conditions can be 
made out as shown in Fig. 316. At the upper part of the figure 
(a) is the normal appearance of hyaline cartilage. As the ossify- 
ing margin is approached the cells multiply, and at first they form 
irregular groups, as at b. Still nearer the margin the multiplying 
cells become arranged in rows parallel to the long axis of the bone, 
the elongated groups being separated by narrower elongated pieces 
of hyaline matrix. The beginning and end of this zone of multi- 
plying cartilage-cells are quite abrupt, and form nearly straight 
transverse lines. This zone is that which, to the naked eye, is 
blue. Next occurs an infiltration with lime salts of the hyaline 
matrix between the groups, the matrix becoming opaque and 
granular, c in figure. This forms the yellow zone as seen with 
the naked eye. This zone is also suddenly interrupted, and at a 
definite level the groups of cartilage-cells give place to cavities 
filled with foetal marrow, consisting of round cells and bloodves- 
sels (d). These cavities are still bounded by the calcified carti- 
laginous matrix. Some of the marrow cells are osteoblasts, and 
these fix themselves on to the surface of the calcified matrix and 
begin to develop the' bony matrix around them. Each osteoblast 
forms a piece of bone around it (e in figure), retaining a cavity for 
itself, which is the lacuna. In this way the cartilaginous matrix 
is encroached on and destroyed by the new-formed bone, while, at 
the same time, it is partly destroyed without the new formation of 
bone so as to make the medullary cavities larger. 
On the surface of the bone we have beneath the periosteum a 
layer of cells similar to those in the medullary cavities. Here also 
the osteoblasts form bone around them and add to the thickness of 
the bone. 
Turning now to rickets, the condition of the ossification from 
cartilage may be studied with the assistance of the accompanying 
excellent figure copied from Thierfelders atlas. The most pro- 725 
RICKETS OR RACHITIS. 
nounced difference from the normal is the enormous exaggeration 
of the zone of multiplication of the cartilage-cells (a, a). These 
seem to be proliferating without any purpose and without the 
regular arrangement. There are groups of cells as in the normal 
case, but they are in much larger numbers and occupy a much 
greater space; at the same time they have not always the normal 
arrangement in rows parallel to the long axis of the bone. The 
cells of the groups also vary considerably in size. In the normal 
bone the cells in the deepest part of this zone are large, but in 
rickets while some are large, as at b, there are others even at the 
same level, or deeper, of small size. 
Next, in regard to the zone in which the cartilaginous matrix 
becomes calcified, this also is represented here in the most irregular 
fashion. Calcification of the matrix occurs, and calcification of 
the cartilage-cells (as at b on left), but this occurs quite indiscrim- 
inately. There will be calcification of the cartilage high up, as at 
b, while there are numerous groups lower than that uncalcified. 
In many cases also, whether calcified or not, the cartilage-cells lose 
to a considerable extent their grouping into rows (as below b on 
left). 
Then as to the formation of medullary cavities and development 
of bone, the figure shows how irregularly this occurs. Blood- 
vessels appear with considerable frequency in the midst of the 
cartilage, and towards the deeper parts there are medullary spaces 
with osteoblasts in them. These may even be seen forming new 
bone, as at d. But the medullary cavities do not occur with any 
greater regularity than the other stages in the process, and it is not 
always apparent that they have always to do with the formation of 
the bone. It will be seen in the figure that at a certain somewhat 
indefinite level, which is lower at the left side than the right, bony 
trabeculae appear (e, c). But it will also be seen that the bone is 
directly continuous with cartilage, the difference in the two being 
signalized chiefly by the difference in the cells. It appears also 
that in the cartilage, which is thus immediately continuous with 
the bone, the individual cartilage-cells are separated by a matrix 
just as the bone corpuscles are (see figure). In fact it looks very 
much as if a conversion of cartilage into bone were occurring, and 
there are even appearances suggestive of the gradual transformation 
of cartilage-cells into bone-corpuscles. The examination of such 
sections as that figured can leave hardly any doubt that an actual 
transformation of this kind occurs, this being consistent with what 
has been stated above in regard to metaplasia. 
It will be seen in various places, but especially at d, that pieces of 
cartilage survive in the midst of the new-formed bone. The carti- 
lage may be calcified or not. 
To the naked eye the changes described above are indicated in a 
longitudinal section of a rickety long bone. The blue zone which 
forms a straight narrow transverse line in the normal bone is here 
greatly increased and its boundaries are irregular. The yellow 
zone of calcification of the cartilage is still more irregular, and 726 
diseases of the bones and joints. 
yellow pieces crop up in the midst of the blue zone. Bloodvessels 
appear also at different levels. In the area of the blue zone the 
cartilage is greatly swollen, as the enormously multiplying cells 
take more space than normal. 
Under the Periosteum we have a process which may, like that 
in the cartilage, be described as an enormous preparation for 
ossification while the process of ossification lags behind. The thin 
layer of osteoblasts is increased till it forms a layer of considerable 
thickness. By this layer bone is formed to a very limited extent 
and very imperfectly. Instead of a proper dense bone, such 
as should be formed on the surface of the shaft, there is a loose 
irregular spongy bone. But even the trabeculae of this spongy 
bone are not properly formed. Immediately under the thick 
subperiosteal layer the new-formed bone does not show in its 
matrix the homogeneous character of the matrix of bone ; it is 
granular, and the lime is obviously deposited without combining 
with the matrix in the normal manner. It is a calcification rather 
than an ossification, and the trabeculae are rather osteoid than 
osseous. On passing inwards the tissue becomes more strictly 
osseous however, although hardly acquiring the regular arrange- 
ment of the dense bone of the shaft. 
Corresponding with the structure described are the naked-eye 
characters. The subperiosteal layer is seen in the form of a red 
vascular layer of some thickness. This is so obvious in some cases 
that, at one time, it was described as if a blood-clot were formed 
under the periosteum. Beneath this the spongy character of the 
bone can be seen, while the shaft is considerably thicker than nor- 
mal and obviously more easily bent. 
Deformities of the Bones due to Rickets.—In considering the 
deformities so often produced by rickets, it is to be remembered 
that the two chief changes in the bones are, in the first place, 
enlargement and softening of the epiphyseal extremities of the 
bones from the affection of the cartilages, and, in the second place, 
thickening with loss of resistance of the shafts from the periosteal 
lesion. These conditions do not always go strictly parallel, one or 
other being frequently the more prominent in a particular bone. 
The various bones of the body also present very commonly 
different degrees of rickets although the disease is a general one, 
and usually affects many bones. Even in bones affected to a 
similar extent, however, the resulting deformities present very 
great variations; the deformities consist largely of curvatures of 
the bones from the application of external forces, and the bones 
are differently placed in relation to such forces. 
Deformities of the Long Bones.—The most obvious change at 
the outset is swelling of the cartilaginous ends of the long bones, 
giving a clubbed or knobbed appearance to the limbs. This is 
common to all the long bones, and is the condition generallv taken rickets or rachitis. 
727 
iii practice as evidence of the existence of tlie disease. The bones 
are also arrested in their growth, so that they are stunted while 
at the same time they are unduly thick. 
The remaining deformities occur in the majority of cases in the 
lower limbs, and are the result of the weight of the body acting on 
the bones in their weakened condition. Similar deformities are 
met with in the bones of the arms in cases where external force is 
frequently applied to them, as where a child in creeping leans on 
the arms, or where a nurse frequently lifts a child by one arm 
(Macewen). The deformities consist mainly of curvatures of the 
shafts of the bones, along with shifting of the epiphyses in some 
cases. In regard to the latter, the extended blue zone at the car- 
tilaginous border being soft allows the epiphysis to change its 
position according to the direction of pressure, and so at the ankle, 
the epiphysis is sometimes displaced inwards, and, as it were, 
overhangs the joint on its internal aspect. The same may occur 
at the knee-joint, and the internal condyle may exceed in length 
the external even after the disease has been cured. 
The familiar curvatures of rickets are due mainly to the weight 
of the body acting on the softened shafts, and as the pressure acts 
mainly on the lower limbs the two principal forms are genu valgum 
and genu varum. 
Genu valgum, or knock-knee, is a condition in which the thigh 
and leg form an angle at the knee opening outwards. This 
deformity depends usually on several alterations. There is gener- 
ally a curve of the lower third of the femur, with its convexity 
inwards, the effect of this being that the internal condyle is lower 
and the external higher than normal. Along with this there is 
usually the lengthening of the internal condyle already referred 
to. As a rule the tibia is not bent, the two conditions named 
taking the chief part in producing the deformity, but sometimes 
the shaft of the tibia is at an angle with the epiphysis, as if the 
latter were to some extent overhanging the former. In addition 
the femur or tibia sometimes shows an anterior curvature, which 
of course does not increase the valgum condition. 
Genu varum, or bow-legs, is the converse condition to genu 
valgum. The shafts of the femur and tibia are curved, with the 
convexity outwards, but these bones take part in the deformity in 
very different degrees, the tibial curve being more frequent and 
usually more pronounced than that of the femur. 
The lono; bones beino; soft and flexible are not so liable as normal 
bones to complete fractures, but they are specially liable to partial 
fractures or infractions. If the bone is suddenly bent it does 
not break across, but is partially torn as when an attempt is made 
to break a green stick. In this case the concave surface of the 
bent bone gives way and the convex surface does not. The marrow 
is torn by the broken concave portion, and the broken edges may 
be projected through the marrow to the opposite internal wall. 
This kind of fracture has been aptly compared by Virchow to 
the breaking of a quill. These infractions occur most frequently 728 
DISEASES OF THE BONES AND JOINTS. 
at the lower part of the tibia,.also in the pelvis and ribs, and less 
frequently in the bones of the arm. 
Deformities of the Chest.—The junction of the cartilaginous 
and bony ribs is analogous to the ossifying cartilage of a long bone, 
and undergoes a similar thickening in rickets. These parts of the 
ribs are therefore knobbed, and there is thus a row of knobs on 
each side of the chest—the so-called rachitic rosary. The chest 
is also liable to deformity from the flexibility of the ribs. During 
inspiration the lateral aspects of the ribs are drawn inwards from 
being unable to withstand the atmospheric pressure, so that instead 
of the natural arch with the convexity outwards, these lateral por- 
tions are flattened or even rendered concave. As the ribs take 
thus a straighter course the sternum is pushed forward, and the 
characteristic pigeon-breast is produced. It may even be some- 
times seen how, in inspiration, the lateral wall of the chest is 
visibly carried inwards. 
Deformities of the Vertebrae.—The vertebrae very often escape 
in the milder forms of rickets, but in many cases they also are com- 
posed of abnormally spongy bone, and allow of the occurrence of 
curvature. Such curvatures are mostly exaggerations of the 
normal antero-posterior curves, but lateral curvature also occurs. 
Any considerable curvature will cause narrowing of the chest, and 
if this be associated with the pigeon-breast the interference with 
the circulation and respiration may be serious. 
Derfomities of the Pelvis.—These are of great importance in 
the female in relation to the possible occurrence of pregnancy in 
after-life. The chief deformity is produced by the weight of the 
body acting through the vertebral column on the sacrum. This 
hone is pushed forward and the pelvis undergoes a corresponding 
displacement of its parts, the antero-posterior diameter being 
diminished. The growth of the bones here also is stunted, and 
the pelvis therefore remains unduly small. 
The.bones of the head frequently undergo very marked deform- 
ities. The bones of the face, like the other hones generally, are 
stunted in their growth, so that the face is small. It is also stated 
that the jaws by the action of the muscles undergo changes in 
shape by which the lower jaw is shortened and the upper jaw 
lengthened, so that the teeth of the latter overlap very much those 
of the former. While these are the conditions in the face, the 
hones of the cranium present striking peculiarities. The flat 
bones ossify from membrane, and in rickets we have the ossifi- 
cation lingering behind, so that at their borders these bones pre- 
sent somewhat broad areas in which there is soft tissue like that 
under the periosteum. The effect of this is to cause an apparent 
widening of the sutures and extension of the fontanelles. The 
closure of the fontanelles is also delayed. The cranium is enlarged 
in rickets, at least its circumference is greater, and at the same 
time it is commonly flattened on the summit. The enlargement 
of the cranium, with the stunted condition of the face, causes the 
well-known overhanging of the brows so often seen. OSTEOMALACIA. 
729 
Another occasional consequence of rickets is the condition 
designated craniotabes. As we shall see afterwards, this is 
probably most frequently a consequence of syphilitic disease of 
the bones, but it occurs also in rickets. The bone in rickets is 
soft, possessing less power of resistance than normal bone. If 
the child be lying constantly on one spot, or if the contents of 
the skull be increased, as in chronic hydrocephalus, then the 
pressure on the bone may cause it to waste. This occurs most 
frequently when both these conditions are present, and the bone 
is, as it were, between two pressures. In this way may occur 
thinning and actual perforation of the skull, so that in the midst 
of the bones there will be holes, where the brain is covered by the 
soft parts alone. From the nature of the case it will be under- 
stood that these apertures are mostly in the occipital or the parietal 
bone, according as the child lies mostly with the back or side of 
the head downwards. 
t Recovery takes place in rickets by the removal of the insani- 
tary conditions, or by the termination of the period of growth. 
The ossification advances in the cartilage and under the periosteum. 
The spongy bone produced under the periosteum becomes dense, 
and so the bone may be unduly heavy and thick, while it is stunted. 
The deformities having occurred in a rigid structure are rendered 
even more fixed by the completion of the ossification. There is, 
however, in the course of time, an effort on the part of nature to 
restore the normal architecture of the bones; where they are 
bent, absorption occurs on the convex surfaces, and increased 
new formation on the concave ; there may be considerable restor- 
ation of the proper shape in the long bones, but usually much 
less in the pelvis, head, and thorax. 
OSTEOMALACIA AND MOLLITIES OSSIUM. 
This disease contrasts with rickets in respect that it affects the 
hones after their complete ossification. Like rickets, it produces 
a softening of the bones, hut it is a softening which supervenes 
after they have acquired the normal resistance of fully formed 
bone. It rarely occurs in children, although at least one case has 
been reported by Dr. Rehn, in which it was present without a 
trace of rickets. 
It is to be stated at the outset that several distinct conditions 
are often included under the designation osteomalacia. We must, 
in the first place, eliminate cases of mere senile atrophy, or others 
of a similar kind. It often happens in old persons that the medul- 
lary spaces increase in size at the expense of the bone, and the 
bone becomes in consequence less resistant. But the remaining 
bone is not softer than normal; it often contains even more lime 
salts than it should do, and is therefore abnormally brittle. Put- 
ting aside such cases, however, there are two distinct forms of 730 
DISEASES OF THE BONES AND JOINTS. 
mollities ossium in which the calcareous constituents of the hone 
are reduced. It is not possible to separate these two absolutely 
in their causation, but it may be said that both forms are rare in 
this country, and that one of them, while it is sometimes met 
with here, seems hardly to occur on the Continent. 
The disease seems to be caused for the most part by defective 
nutrition, but there are two conditions which specially predispose 
to it, namely, pregnancy and insanity. It not infrequently comes 
on during pregnancy, and runs a rapid course. It has also been 
frequently observed in insane persons, and here the softness of 
the bones may lead to fractures under comparatively slight 
violence. 
Turning now to the different forms of the disease, there is one 
which appears to occur most frequently in England, and the class- 
ical description of which is that given by John Hunter. It appears 
to consist in a fatty degeneration of the bone-corpuscles with soft- 
ening of the matrix. The condition, so far as the naked eye is 
FlG. 317. 
A fragment of bone from a case of osteomalacia. The central part shows the usual ap- 
pearance of bone, while the marginal parts are transparent, being devoid of lime salts, 
although still showing bone-corpuscle. X 90. 
concerned, is thus described by Hunter: “ The component parts 
of the bone were totally altered, the structure being very different 
from other bones, and wholly compos’ed of a new substance re- 
sembling a species of fatty tumor, and giving the appearance of 
a spongy bone deprived of earth and soaked in soft fat.” In 
these cases the medulla forms a bright yellow, pink, or deep INFLAMMATIONS OF BONE. 
731 
crimson material, anti, when examined microscopically, presents 
free oil in great quantity with crystals of margarine as well as 
ordinary adipose tissue. 
The other form of the disease is that described by writers on the 
Continent as osteomalacia, but it is not so infrequent in this 
country as has been supposed, the mollities ossium of insanity 
being probably always of this form. In this form, as shown in 
Fig. 317, there is a direct absorption of the lime salts from the 
bone. The solution of the lime salts occurs primarily in the por- 
tions of the bone next the medullary spaces and Haversian canals, 
so that, if the bone be examined, the central parts of the trabeculee 
are seen to be opaque like normal bone, while the peripheral parts 
are transparent because deprived of their lime salts. The condi- 
tion of these parts is like that of bone which has been decalcified 
by steeping in an acid, the bone-corpuscles are preserved, and the 
matrix has a homogeneous or fibrous appearance. As the disease 
. advances, the decalcified matrix is encroached upon by the medulla, 
and the decalcification advances further. The medulla itself is 
altered; the adipose tissue is largely replaced by round cells some- 
times with several nuclei. 
The effect of these changes is, of course, to make the bones 
much softer and more flexible, so that they can often be cut with 
a knife, or crushed with the fingers. And so in the living body 
the bones are often bent or crushed. The disease has a particular 
tendency in some cases to attack the pelvis and vertebrge, but the 
long bones are also affected. Serious deformities result, especially 
in the pelvis and vertebral column. The pelvis is narrowed by the 
acetabula being pushed in on either side, so that the pubes are 
pointed and prominent. The vertebral column is curved. The 
sternum sometimes undergoes sharp bendings, and the ribs may 
be fractured. 
INFLAMMATIONS OF BONE. 
AVe have already seen that the proper bony tissue is somewhat 
inert, and for the most part conducts itself passively in patho- 
logical processes. On the other hand, in its development and 
nutrition it is intimately connected with the periosteum on its 
surface, and with the tissue lining its various cavities and canals, 
whether forming proper medullary cavities or narrower canals 
(Haversian) and spaces. The periosteum, endosteum, and contents 
of the various spaces in bone, form thus integral parts of the 
osseous tissue, and in studying inflammation our principal concern 
will be with the changes in these structures, and their inter-rela- 
tions with the proper bony tissue. 
In most cases the inflammations of bone are propagated from 
neighboring structures. Many of them originate in connection 
with disease of the joints, and many from inflammation of the 
periosteum. If the inflammation be acute there may be suppura- 
tion, but whether acute or chronic; so far as the bone is concerned 732 
diseases of the bones and joints. 
the most important result is the formation of granulation tissue 
which, coming into relation with the osseous substance produces 
various changes there. This granulation tissue replaces the proper 
medulla of bone, and is often in great abundance under the peri- 
osteum, as we shall see in studying periostitis and the healing of 
fractures, and its effect on the bony tissue is either to destroy it, 
or to add to it by the new formation of fresh hone. It is possible, 
in theory to separate these two processes, and to speak of a rare- 
fying or destructive, and a formative or condensing osteitis, 
but the processes so frequently go on together that it will be better 
to consider them in connection. 
In order to understand these processes it is necessary to refer to 
the state of matters in the original formation and growth of bone. 
We find in a growing bone that (as already mentioned at p. 724) 
the medullary spaces are occupied by cells, and that cells of a 
similar character are present under the periosteum. Many of 
these cells are evidently busy forming the new bone. They are to 
be found applied to the surface of the existing bone, and gradually 
becoming buried in a bony matrix which is apparently formed 
around them, while they take up the position of bone-corpuscles. 
The cells thus engaged in the formation of bone are properly 
designated osteoblasts. But in order to preserve the architecture 
of the growing bone, there must be at some parts destruction of 
the already formed tissue. It used to be supposed that this de- 
struction occurred by the bone-corpuscles enlarging and causing 
the surrounding tissue to melt down, but it has now been shown 
that a special form of cell is engaged in the destruction of the bone, 
and these cells are properly called osteoclasts. They are very 
large cells with a granular protoplasm and many nuclei, or in other 
words, they are giant-cells or myeloplaques (see Fig. 320, p. 735). 
Wherever absorption of bone is going on these cells are to be 
found, and they appear to adhere to the surface of the bone and 
cause absorption of the matrix. In this way they dig themselves 
into the bone and form gaps, in which they are often to be found 
lying. These rounded gaps in the bone have long heen known, 
and they are usually designated Howship’s lacuna. 
In the granulation tissue of an inflamed bone both osteoblasts 
and osteoclasts are frequently present. By the action of the osteo- 
clasts in the Haversian canals and medullary spaces, the bone 
becomes opened out and dense bone is made spongy or spongy 
bone more open. At the same time the osteoblasts are often at 
work, and perhaps under the periosteum there are spiculse of new- 
formed bone, at the marginal parts of which processes exactly 
similar to those beneath the periosteum of a growing bone can be 
seen (see Fig. 318). It happens not infrequently that after the 
bone has been opened out by the rarefying process, the osteoblasts 
subsequently set to work, and the bone is restored, or even con- 
siderably condensed as compared with its original condition. 733 
ABSORPTION OF BONE. 
It is to be added that besides the rarefaction of the bone by the 
process already described, it appears that the bone sometimes gets 
channelled for the accommodation of nevr-formed bloodvessels. 
We know that the bone-corpuscles, with the canaliculi, convey 
nutritious fluid through the dense bone, and according to require- 
ments these may expand into bloodvessels apparently by the lacunae 
enlarging and running together. This, however, as compared 
with the other, is an insignificant factor. 
Fig. 318. 
New formation of bone in connection with inflammation. The osteoblasts are getting 
surrounded by bony matrix and becoming bone-corpuscles. X 85. 
Caries.—This subject may be conveniently considered here, 
especially in connection with rarefying osteitis. We have seen 
that in this latter condition the hone is encroached upon by the 
osteoclasts, and the lamellae are thinned, How, this process may 
go on to the complete destruction of the bony lamellae, so as to 
produce, in fact, a progressive destruction of the bone. This con- 
dition is usually associated with either a very acute inflammation 
or one which has an infective character (tuberculosis, syphilis). 
As the place of the bone is taken by soft inflammatory tissue, this 
structure is not able to resist the mechanical wear to which bone 
is naturally exposed, and so there is an ulceration of the soft tissue 
generally associated with suppuration. As the soft tissue gives 
way, the invasion of the bone advances, and so, beyond the actual 
ulcerating and suppurating surface, the bony lamellae are greatly 
thinned and ready to break down. In the majority of cases the 
caries is connected with disease of the joints, as we shall see after- 
wards, but a periosteal inflammation, especially when connected 
with syphilis, may lead to it. 
Before leaving the general subject of osteitis, it will be proper 
to make some observations on the absorption of bone. We have 
already seen in the case of rarefying osteitis and caries that ab- 
sorption of bone takes place by means of the osteoclasts or giant- 
cells, and it appears further that whenever hone is absorbed, 734 
DISEASES OF THE BONES AND JOINTS. 
whether it be dead bone or living, the same agents are at work. 
When, in a simple fracture, a considerable piece of bone is 
separated from all its attachments and all its bloodvessels torn 
across, then it will probably die. Necrosis does not occur in every 
case, as the observations of Macewen on transplantation of bone 
show that pieces of bone removed from one person to another may 
survive and become incorporated in their new position. But in 
order to their survival, the pieces must be small, so as to allow of 
ready penetration of bloodvessels into their medullary spaces. 
When pieces of considerable size are broken off they do not 
survive. Similarly in compound fractures pieces of bone are 
frequently separated from all their vascular connections and may 
be seen lying in the wound, with a dead white color and a hard 
feeling when touched, being evidently dead. Or again, at the end 
of stumps necrosis of a piece of the bone may occur from osteo- 
myelitis or otherwise. Or, as we shall see afterwards, periostitis 
may lead to extensive necrosis. 
Fig. 319. 
Section of a piece of necrosed bone which had been undergoing absorption. The margins 
of the bone at the medullary spaces and Haversian canals have an eaten-out appearance 
from the presence of Howship’s lacunrn. X 85. 
Now, in all these cases, if acute suppurative inflammation be 
averted, and especially if septic inflammation be kept oft', the dead 
bone may be absorbed. This is sometimes seen very plainly in 
cases of compound fracture where a piece of dead bone may be- 
come visibly eaten into and replaced by vascular granulations. 
It must occur frequently in simple fractures and at" the ends of 
stumps. It is also not uncommon in necrosis from periostitis, but 
it will not occur unless the inflammation be moderate in intensity, 
just as new formation occurs only in chronic inflammations. ABSORPTION AND TRANSPLANTATION OF BONE. 
735 
The absorption is effected by the osteoclasts. If a piece of dead 
bone which has been partially absorbed be examined, its surface 
will be seen to have a worm-eaten appearance, and under the 
microscope this is found to be due to the existence of innumerable 
Howship’s lacunae (see Fig. 319). In these lacunae, or lying beside 
them, giant-cells are to be seen, and sometimes a regular row of 
such cells is visible as if feeding on the bone. Sometimes they 
are nearly buried in flask-shaped spaces (see Fig. 320). 
Fig. 320. 
Howship’s lacunae with giant-cells (osteoclasts) in them, and free giant-cells; from same 
piece of necrosed bone as preceding figure. X 350. 
The process of absorption occurs not only in pieces of bone 
which have died in the body, but in pieces of ivory or bone intro- 
duced for therapeutic purposes, as in ivory pegs for ununited 
fracture, bone drainage-tubes, etc. Here also the bone or ivory 
is eaten into, and Howship’s lacunae with osteoclasts are visible. 
Such pieces of dead and macerated bone may thus be completely 
absorbed. 
By a similar process living bone is absorbed. Where an 
aneurism advances against a bone, as the sternum or vertebrae, 
and erodes it, the destruction of the bone is produced, as in the 
other case, by osteoclasts. So it is also when a tumor advances 
against a bone and erodes it, although it is necessary to exclude 
from the category the case of certain turners which, as we shall 
see afterwards, may originate in the bone itself, and cause destruc- 
tion of the bone by softening occurring around the bone-corpuscles 
which give origin to the tissue of the tumor. 
It is necessary to add to all this that although osteoclasts in the 
form of giant-cells appear to be the chief agents in the destruction 
of bone, both dead and living, and both in the physiological growth 
of bone and under the command of pathological processes, yet that 
absorption may be produced by other agents. We have seen how 736 
DISEASES OF THE RONES AND JOINTS. 
in osteomalcia there is destruction without giant-cells, and we have 
also seen how by canalization there may be rarefaction of the bone 
without giant-cells. 
We may now enter more specifically on the individual Forms 
of Inflammation in which the bone is involved, and it will perhaps 
illustrate the matter if we take up first the processes concerned in 
the healing of fractures. 
Healing of Simple Fractures.—As we have seen, this occurs 
mainly by the formation of callus, and we have to consider how 
this callus is formed. At the time of fracture the periosteum is 
torn and, to some extent, raised from the surface. The marrow 
is also torn across. Blood is effused, but it generally gets diffused, 
and if it exercises any influence on the further course of events it 
is by keeping the parts separate and interfering with the healing 
process. The blood, however, usually offers little obstacle, and is 
either absorbed or displaced by the new-formed tissue. The peri- 
osteum around the broken ends becomes vascular and swollen, 
and by an inflammatory process is converted into granulation 
tissue. A similar process occurs in the medulla, and here too the 
tissue is replaced by inflammatory structures. More slowly, a 
rarefying osteitis causes the enlargement of the Haversian canals 
and medullary spaces, and these also are filled with granulation 
tissue. 
The next process is the new formation of mature tissue, and the 
amount of tissue formed and its kind are determined by circum- 
stances. If the bones are kept very fixed then there is compara- 
tively little inflammation, and the amount of granulation tissue 
produced is small. The granulation tissue under these circum- 
stances forms new bone, in the way already described (formative 
osteitis). In the periosteum, in the marrow, and between ends of 
the bone, the osteoblasts set to work and produce bone. This 
bone is at first in the form of narrow trabeculae, and the callus 
thus formed consists of soft tissue in which are narrow trabeculae 
of bone. According to its situation the callus is called external, 
internal, or intermediary. The external callus encloses the 
broken ends in a sheath, the internal forms a rod uniting them, 
the intermediary, formed in the widened canals and spaces of the 
bone itself, passes from one broken end to the other and so unites 
them in detail. If the bone has not been kept rigidly fixed, the 
amount of granulation tissue and of callus is large, and especially 
the external callus, in which a large number of narrow trabeculse 
of bone are formed. When the rigidity is very imperfectly pre- 
served, then, instead of the granulation tissue forming bone, it 
develops into fibrous tissue and cartilage. This occurs almost 
uniformly in the fractures of animals, but is sometimes seen also 
in man, especially in fractures of the ribs where it is difficult to 
prevent a certain amount of movement. Fig. 313, p. 720, was 
taken from a case of multiple fractures in an insane person, in periostitis. 
737 
whom the existence of the fractures was unknown, and no attempt 
made to keep the bones at rest. We have already seen that carti- 
lage, connective tissue, and bony trabeculae are all represented. 
When the bone has become fully united the parts of the callus 
not necessary for the preservation of the continuity of the bone 
are disposed of. The intermediary callus becomes, for the most 
part, the permanent bond of union, while 
the external and internal disappear except 
in so far as they are needed to fill up gaps 
where the bones have not been exactly in 
apposition. Sometimes the bones are con- 
siderably out of position, and a large amount 
of new bone remains permanently as the 
bond of union. 
Periostitis.—The periosteum is inflamed 
under somewhat various circumstances. 
Chronic periostitis is a frequent circum- 
stance of inflammation in joints and of 
necrosis of bone; it occasionally results 
even from ulcers of the skin when situated 
immediately over a bone which has little 
more than the skin covering it, as, for in- 
stance, the tibia. The periosteum is the 
seat of granulation tissue which, as time 
goes on, is developed into mature tissue. 
In some cases, and especially in old rheu- 
matic affections of the joints and under 
ulcers of the skin, the new tissue formed is 
cicatricial connective tissue, so that the bone 
is covered with a dense hypertrophied peri- 
osteum. In the majority of cases, however, 
and this applies to most inflammations of 
the joints, the inflamed periosteum pro- 
duces new bone and the osteoblasts add 
irregular outgrowths of bone to the surface. 
In this way we have localized thickenings 
of the bone which are sometimes designated 
hyperostoses, or periostoses (see Fig. 321). 
The new formation of bone may even 
extend out a considerable distance from the 
bone, and we may have the joint locked 
by projecting bony outgrowths, which sometimes coalesce, forming 
a synostosis. 
Suppurative Periostitis occurs in two forms. There is a rare 
form in which a rapid suppuration occurs with gangrene of the 
periosteum and acute inflammation around. With this malignant 
periostitis there are sometimes associated pysemic lesions in the 
lungs and elsewhere. In this disease micrococci are found in the 
pus which forms beneath and around the periosteum, as well as in 
Fig. 321. 
Hyperostosis in the bones 
of the leg and foot in ele- 
phantiasis. (Virchow.) 738 
DISEASES OF THE BONES AND JOINTS. 
the bloodvessels in the metastatic inflammations. The disease is 
thus an infective one, although the mode of entrance of the 
organisms is just as obscure as in the case of ulcerative endo- 
carditis. 
Simple Acute Periostitis occurs mostly in weakly children as 
the result of a blow or other injury, and it takes place most fre- 
quently in the bone which is most exposed to such injuries, namely, 
the tibia. The inflammation affects the subperiosteal layer and 
the subjacent bone chiefly. At first there is swelling from inflam- 
matory infiltration of the periosteum, and, if the inflammation does 
not resolve, then suppuration ensues. The pus collects between 
the periosteum and the bone and raises the former over a certain 
area. The bone thus denuded of its periosteum dies, as the 
nutrient vessels passing into the bone are severed. The sub- 
sequent events connect themselves with the necrosis of the bone, 
and will be considered afterwards under that heading. 
Osteomyelitis.—This name is given to inflammation of the 
bone-marrow, and it occurs very rarely as a spontaneous or in- 
dependent disease. There are cases of malignant osteomyelitis 
which are strictly comparable to malignant periostitis, and in 
which also micrococci have been found. A general pyaemic con- 
dition may develop also in this disease. Traumatic osteomyelitis 
arises as a septic inflammation in connection with compound 
fractures and amputations. The marrow becomes swollen from 
inflammatory hyperaemia and infiltration, and ultimately abscesses 
may form. This disease is of importance for two reasons. The 
suppurating marrow may induce necrosis of the bone, or it may 
be the starting-point of a pyaemia, the infective organisms getting 
into the open-mouthed veins of the bone and extending inwards. 
NECROSIS OF BONE. 
This name implies the death of a portion of hone, and we have 
already considered some of the ways in which it may be brought’ 
about. It may be by periostitis or osteomyelitis, or by direct 
violence. We have seen also how in some cases the piece of dead 
bone is absorbed. But in many cases absorption does not occur, 
chiefly where an acute inflammation exists around. Whether ab- 
sorption occurs or not, the first occurrence is the separation of 
the dead bone from the living, and this is effected by an inflam- 
matory process. The dead bone by its mere mechanical presence 
sets up an inflammation around it. By means of a rarefying 
osteitis the Haversian canals and medullary spaces enlarge, and 
the bone immediately around the dead piece being replaced by 
granulation tissue, the necrosed portion becomes a sequestrum. 
The process of absorption may, as we have seen, proceed to attack 
the dead piece, which may completely disappear. But this pre- 
sumes that the sequestrum is itself non-irritating, and that the 739 
NECROSIS OF BONE. 
granulation tissue is not stimulated to suppuration. In many 
cases these conditions are not fulfilled. The acute inflammation 
which caused the necrosis may continue, or a septic inflammation 
may extend from a wound communicating with the dead piece of 
bone, it may be after the opening of an abscess in periostitis or 
otherwise; in either case suppuration may occur in the granula- 
tions around the sequestrum, and this is fatal to the absorption of 
the dead bone. 
In these cases we have a considerable area of inflammation 
around the sequestrum, and in this area of inflammation we have 
both new-formation and destruction of bone. The surrounding 
bone is opened out by rarefying osteitis. At the same time the 
periosteum or endosteum produces new bone, so that the bone as 
a whole is thickened and the sequestrum is covered in by a mass 
of soft bone like callus. The commonest cause of necrosis is peri- 
ostitis, and the sequestrum in that case is on the surface of the 
bone, and the periosteum is raised in the original suppuration. 
This raised periosteum produces a shell of new bone as just 
mentioned, and if the necrosis be considerable this shell of new 
bone may exercise the function of support instead of the bone. 
In this shell there are very commonly apertures through which 
the pus of the original suppuration has passed, and through 
which the pus of the existing suppuration finds exit. Such an 
aperture is called a cloaca, and it is usually by enlarging the 
existing cloacae that the sequestrum is removed. 
Phosphorus-necrosis.—This condition occurs chiefly in persons 
who are employed in workshops where lucifer matches are manu- 
factured, and who are thus exposed to the vapor of phosphorus. 
The vapor acts locally, on the jaws chiefly, and it is said that 
persons with carious teeth are particularly liable to be affected. 
The phosphorus produces an inflammation mainly of the perios- 
teum, resulting in a great new-formation of cancellated bone on 
the surface of the jaw. This bone may afterwards become con- 
densed by the ossification encroaching on the medullary spaces. 
After a time the inflammation leads to suppuration, and the pus 
forms between the new-formed bone and the original bone of the 
jaw. From this results a necrosis of the jaw which may involve 
the entire bone, and be accompanied also by necrosis of the new- 
formed bone. The resulting suppuration is usually fatal in their 
results, but after removal of the sequestrum healing may occur. 
From the observations of Wegner it appears that phosphorus 
acts as a general stimulant to the structures concerned in the for- 
mation of bone. The phosphorus vapor acting directly stimulates 
so violently as to produce the inflammation and necrosis just 
described, and this result has been produced also in rabbits 
exposed to the vapor of phosphorus. When given in small doses 
internally, phosphorus produces in growing animals a distinct 
stimulation of the process of formation of bone. In such cases the 
bone produced at the ossifying border of the cartilage is not a 
spongy bone, but a dense layer, and there is also an unusually 740 
DISEASES OF THE BONES AND JOINTS. 
dense bone produced beneath the periosteum. It is noteworthy 
that in growing animals to whom small doses of phosphorus were 
given, while insufficient quantities of lime were supplied, there 
was a great production of osteoid tissue, somewhat like that pro- 
duced in rickets. 
SYPHILITIC AFFECTIONS OF BONE. 
These lesions have nearly always their seat of origin in the peri- 
osteum, although the subjacent bone may be simultaneously 
involved. The condition may be briefly described by stating that 
gummata are-produced, while inflammation occurs around. The 
existence of the gummata is sufficient indication that the lesions 
are of the tertiary stage. 
Gummata of the usual structure are produced in the internal 
layers of the periosteum, and there is thickening of the periosteum 
around. This membrane being tightly stretched over the tumor, 
the swelling is hard to the feeling, but often with a certain elastic 
resistance. The gumma undergoes caseous metamorphosis in its 
central parts, but advances peripherally, and as it advances against 
the bone it causes erosion of it. The advance is in the first instance 
along the vessels, and as erosion occurs around them a worm-eaten 
appearance is produced in the bone. Beneath the gumma, which 
has most frequently its seat on the bones of the skull, especially 
the frontal bone, there may be thus considerable loss of substance, 
so that even the entire thickness of the skull may be penetrated. 
The caseous material often undergoes softening and suppuration 
ensues. If great care is not taken in evacuating the abscess at an 
early date, there may be very obstinate and even extending ulcers 
produced. Without ulceration the gumma may undergo resolu- 
tion, and a cicatricial depression result, or after ulceration healing 
may occur. 
Along with these processes immediately related to the gumma, 
there are in the neighborhood conditions referable to inflammation. 
The bone around is condensed by new-formation filling up the 
medullary spaces, and there is sometimes a thickening of the bone 
by inflammation of the periosteum. This is much less common in 
the skull than in the long bones, especially those of the legs, where 
it sometimes leads to a very striking hypertrophy of the bone, whose 
surface is exceedingly rough from the loss of substance in some 
parts, and the irregular new-formation in others. The bone around 
the syphilitic defect or ulcer is dense bone, and in this respect con- 
trasts very markedly with that around the ulceration in caries. 
Hereditary syphilis leads to certain important changes in the 
bones which have been described chiefly by Wegner. These 
changes consist mainly in a stimulation of the ossifying structures 
of the bone, while the proper process of ossification is imperfectly 
effected. In certain respects, therefore, they show some analogy SYPHILITIC AFFECTION'S OF BONE. 
741 
to the changes in rickets, but differ from them, as we shall see, in 
detail. They also differ in respect that the principal changes in 
syphilis are congenital, and are to he seen in their typical form in 
the long bones of still-born syphilitic foetuses. These changes 
may even be used to diagnose the existence of congenital syphilis. 
In the cranial bones there are frequently changes, mainly 
affecting the periosteum, hut they are by no means constant, and 
are to be distinguished from those in the long bones, which are 
more distinctive of syphilis. These changes in the periosteum 
consist in slight inflammatory processes, leading to thickenings 
with softening of the bone. They are of importance as being 
probably the cause of craniotabes, which appears to be a frequent 
concomitant of hereditary syphilis. This condition is brought 
about when a child with bones affected as above is in the habit of 
lying with one part of its head resting on a support; in that case 
the bone is apt to give way, and the brain to be covered merely by 
soft parts. 
In the long bones the changes occur at the ossifying margin of 
the cartilage. We have already seen that in the normal bone the 
border of ossification is a narrow line, the transition zone occupying 
little space and forming a straight transvere line. In congenital 
syphilis this is altered, and for convenience of description Wegner 
distinguishes three stages; these may be followed in the bones 
divided longitudinally, so as to show cartilage, ossifying border, 
and bone, in section. 
In the first stage the ossifying border is not linear, but forms a 
zone about the twelfth of an inch in breadth, and of a whitish or 
reddish-white glancing appearance. In this zone microscopic 
examination shows an excessive proliferation of the cartilage-cells, 
which, with the matrix, have become calcified as if in preparation 
for ossification, but this process has not been completed. 
In the second stage the zone is about twice the breadth of that 
in the first stage, being occupied as before by calcified and prolif- 
erated cartilage. The boundaries of this zone in both directions 
are very irregular, the calcified cartilage on the one hand sending 
papillary-like projections into the hyaline cartilage above, and 
being encroached upon by the irregularly ossifying margin below. 
Bloodvessels occur in the midst of the cartilage, and these are 
often surrounded by fibrous tissue instead of the proper foetal 
marrow. In this dense tissue a direct ossification may occur, 
a formation of bone without the agency of the foetal medulla. 
In the third stage wTe have again the calcified zone, which, 
however, is more brittle than formerly. Above it the cartilage is 
swollen and blue as in rickets, and beneath it there is a zone not 
represented in the previous stages. It has a grayish-red or yellow 
appearance, resembling granulation tissue or pus, and is exceed- 
ingly soft so as almost to dissolve the continuity of the bone. 
This zone actually consists of granulation tissue, and appears to be 
tlie result of a reactive inflammation induced by the condition 
of the zone above. This, the calcified zone, shows no longer well- 742 
DISEASES OF THE BONES AND JOINTS. 
formed cartilage-cells; these have shrunken and become ill-shaped 
like the cells in caseous material. It appears, indeed, as if the 
calcified cartilage had become necrosed, and by its irritation had 
set up the inflammation in the medulla beneath. This condition 
has suggested the question, whether the separation of the epi- 
physes, which is sometimes met w7ith in young children, may not 
be due to congenital syphilis. 
It is to be noted that, so far as known, these affections of the 
bones have their origin during intra-uterine life, although they 
may continue and perhaps develop further after birth. It is even 
possible that future observation may show that they can originate 
after birth. 
In regard to the bones affected, the order of frequency given by 
Wegner is, lower end of femur, lower ends of bones of leg 
and forearm and upper end of tibia, upper ends of femur and 
fibula much more seldom than upper end of radius and ulna; and 
most rarely the lower end of the humerus. It may be inferred 
that the disease is usually multiple, being present in several bones 
simultaneously; and the various stages may be seen in the same 
person, the disease being variously advanced in different parts. 
TUBERCULAR OR SCROFULOUS DISEASE OF BONE. 
This connects itself in a majority of cases with similar diseases 
of joints, under which heading it will again be considered. But 
apart from the joints we may find it in the bodies of the vertebrae, 
in the bones of the carpus and tarsus, etc. The disease manifests 
itself as a rarefying osteitis with caseous necrosis. The opened- 
out spongy tissue is filled with granulation tissue, and in the midst 
of this tissue tubercles of regular structure are to be found. The 
tubercles in the midst of the granulation tissue indicate the true 
nature of the disease, and it is therefore proper to recur to the 
older designation, tuberculosis of bone, rather than to use the term 
scrofulous disease. 
In many cases the disease goes on to suppuration, but it is a 
chronic process, and the abscesses which result are cold abscesses; 
these, in the case of the vertebrae, may attain a considerable size. 
The destruction of the bone and substitution of soft granulation 
tissue cause the structure to lose greatly its power of bearing 
pressure. As the bodies of the vertebrae are exposed to consider- 
able pressure, they very often become in this disease crushed 
together, and an acute curvature (antero-posterior) is the result. 
Although the disease is tubercular, it is capable of healing, and in 
that case the granulation tissue forms new bone, often dense, so 
that the structure is firmer and heavier than it was originally. If 
collapse of the vertebrae has occurred, then the healing will make 
permanent the loss of substance, and confirm the curvature. SPINAL CURVATURES. 
743 
SPINAL CURYLATURES. 
Introductory.—The spinal column is composed of vertebrae 
whose bodies are separated by elastic fibro-cartilages. The ver- 
tebra articulate with each other at four other points, two on the 
upper and two on the lower surface of the arch. The vertebrae 
are also bound together by firm ligaments in front of and behind 
their bodies. The effect of these various connections is that, even 
when the spine is separated from all its attachihents except the 
ligaments, it retains its form to a large extent, and its natural con- 
formation may be studied after its removal from the body. 
When seen in profile the spine presents the well-known antero- 
posterior curves, the convexity being forwards in the cervical and 
lumbar regions, and backwards in the dorsal. These curves are 
capable of considerable variation in the movements of the body. 
The whole of the curves may be obliterated and converted into a 
general convexity backwards by stooping forwards, as when, with 
the arms extended and the legs straight, an attempt is made to 
touch the toes with the tips of the fingers. By arching the body 
backwards the dorsal curve may be partially obliterated, and a 
general convexity forwards be produced. It appears, therefore, 
that the spine is capable of considerable antero-posterior move- 
ment. These antero-posterior movements imply a considerable 
degree of compressibility of the intervertebral cartilages. The 
combined cartilages occupy about a fifth of the entire length of 
the spinal column, and their compressibility may be inferred from 
the fact that during the retention of the erect posture the entire 
length of the column gradually diminishes, so that the stature is 
usually from half an inch to three-quarters less at night than in 
the morning. This is believed to be due chiefly to the compres- 
sion of the cartilages, which recover at night when the recumbent 
posture is assumed. The antero-posterior movement of the spine 
is freest in the cervical and lumbar regions, and most limited in 
the dorsal. 
The spine is capable to a much more limited extent of lateral 
movement. The articulating processes, being situated on either 
side of the arches, prevent any considerable lateral deviation, as 
they become locked against each other when that occurs. If the 
surfaces of these processes were horizontal, facing one another 
above and below, then they might allow of freer lateral movement, 
but the more they assume the perpendicular position, and the 
more they face inwards and outwards, the greater is the impedi- 
ment to lateral movement. It will be found that on passing from 
above downwards the articulating surfaces assume more and more 
of a perpendicular position. In the cervical region they are 
oblique, and face slightly inwards and outwards; in the dorsal 
they are more perpendicular and face nearly forwards and back- 
wards, while in the lumbar region they are nearly perpendicular, 
and face each other nearly inwards and outwards. In this way it 744 
diseases of the bones and joints. 
occurs that while lateral movement is limited in all regions it is 
almost impossible in the lumbar region. 
For a similar reason, twisting of the spine on its axis is possible 
to a very limited extent. 
The question of the existence of a natural lateral curvature has 
been matter of dispute. It is generally stated that there is a slight 
lateral deviation to the right in the upper dorsal region, and this 
is usually ascribed to the more frequent and forcible exertion made 
with the right arm; but the existence of this curve has been 
seriously questioned (Adams). The late Dr. Foul is, in one hundred 
and ten post-mortem examinations, found lateral deviation in no 
less than fifty-eight cases. He did not observe it specially in the 
upper dorsal region or towards the right, and concluded that it 
was due to the positions habitually assumed by the persons at 
their various trades. We may perhaps conclude that normally 
there is no lateral curvature, but that a very slight permanent 
deviation is often assumed when a frequently repeated position of 
the body predisposes to it. 
Forms of Spinal Curvature.—The function of the spine is to 
support the structures attached to it, and to hold the head erect, 
the latter function being in man the more prominent one. Any 
single curvature of the spine will have the tendency to remove the 
head from the erect position, and tilt it backwards or forwards or 
to one side, and in order to preserve the erect position there 
is required a curvature in the opposite direction. The natural 
antero-posterior curves are in this sense mutually compensatory, 
the lumbar restores the position lost by the sacral curve, and the 
cervical that of the dorsal. When abnormal curvatures occur 
there is a tendency to a similar compensation, so that the 
curvatures may be divided into primary and secondary. It will 
not be necessary to consider in detail the secondary curvatures; 
their amount and direction may be inferred from those of the 
primary ones. It may be stated, however, that there are, fre- 
quently, several secondary or compensating curves, the spine 
presenting several sinuosities in order to reach the stable position 
for the head. 
1. Antero-posterior Curvature.—There are two quite distinct 
forms of antero-posterior curvature, the curve in the one form 
being rounded, and mainly an exaggeration of the natural curva- 
ture, and in the other sharp or angular. 
(a) Angular Curvature, or Pott’s Disease of the Spine.—This 
depends on disease of the bodies of the vertebrae. For the most 
part it is a local tuberculosis of one or more of the bodies with 
the caseous necrosis and caries described above. The result 
is usually a slow suppuration with psoas, lumbar, or other abscess. 
The softened bodies of the vertebrae give way under the superin- 
cumbent weight, and the spine is bent at a sharp angle, the spinous 
processes becoming unduly prominent behind. The affection of spinal curvatures. 
745 
the bodies may be unsymmetrical, and if collapse be more at one 
side than the other the angular curvature will not be exactly 
antero-posterior. This form of curvature is more rarely due to 
traumatic causes, as crushing of the bodies by heavy weights 
falling on the head or back, or by a fall from a height. This may 
lead immediately to an angular curvature, or may be the starting- 
point of a necrosis and suppurative inflammation. Even tuber- 
cular disease of the bodies seems often to have its starting-point in 
an injury, such as a fall or twist of the spine, such injury leading 
to this result only in predisposed persons. In the majority of 
cases Pott’s disease occurs in children, tuberculosis of bone being 
commonest in early life. 
If healing of the disease of the bodies occurs, the carious bone 
becomes firm, but the loss of substance by the collapse of the 
bodies is not recovered, and the bone is fixed permanently in its 
abnormal position. The new-formed bone may be even firmer 
than the old, and if several bodies have been diseased there may be 
anchylosis of them, so that a piece of the spine is absolutely fixed. 
It is worthy of special notice that angular curvature is much 
more obvious in the dorsal region than elsewhere, as it here 
increases the natural posterior curvature. In the cervical and 
lumbar regions, where the natural convexity is forwards, there may 
be a rounded posterior curvature produced, or even with extensive 
disease, there may be very little posterior curvature visible 
externally. 
The spinal cord is not generally injured by angular curvature, 
but in some cases it is crushed and interrupted. It may be so even 
during the process of healing, the sclerosis or condensation of the 
vertebrae sometimes causing further shrinking and increase of 
the curvature. 
(b) Kyphosis or Posterior Curvature.—This is mainly an 
exaggeration of the normal curvature with the convexity back- 
wards in the dorsal region, and is due chiefly to muscular 
weakness or a habit of stooping. It is most frequent in children 
and old people, leading in its most exaggerated form to hump- 
back, and in a lesser degree to round shoulders. 
(c) Lordosis or Anterior Curvature.—In this condition the 
of the curve is forwards, and the tendency of it is 
to throw the head backwards. It is most common in the lumbar 
region, and in the majority of cases is due to rickets. Rickets 
when it affects the pelvis causes the sacrum fo assume a more 
horizontal position than normal, and in order to retain the erect 
position the lumbar anterior curve is exaggerated. It may also be 
produced by congenital dislocation of the hip-joint (stated by 
Adams to be of considerable frequency), and anchylosis of the hip. 
There may be also, but rarely, a direct lordosis in the lumbar 
region from rickets, the natural curvature being increased by 
reason of the softness of the bones. In the dorsal and cervical 
regions lordosis is very uncommon. 746 
DISEASES OF THE BONES AND JOINTS. 
2. Lateral Curvature or Rotatory Curvature.—In the intro- 
ductory section we have seen that the mechanism of the spine 
allows of exceedingly limited lateral deviation. But it often hap- 
pens that from habitual faulty positions at work or otherwise there 
is a frequently repeated tendency to lateral deviation. In that 
case, as a direct displacement is not possible, there may be, espe- 
cially in persons constitutionally weak, a deviation with partial 
rotation of the vertebrae. The faulty position may be merely the 
result of a bad habit, of standing on one leg for instance, so as to 
cause obliquity of the pelvis; or it may be from sitting in a con- 
strained position at study or manual labor, so that either the pelvis 
is oblique or the arms are used in one particular direction so as to 
displace the centre of gravity to one side; or there may be a hys- 
terical contraction of the muscles of the scapula lasting for a long 
period and altering the centre of gravity; or there may be an ob- 
liquity of the pelvis from one leg being shorter than the other, as 
sometimes in rickets. There is also softening of the bones in 
rickets, and very severe curvature may occur when this is asso- 
ciated with obliquity of the pelvis. 
Fig. 322. 
Diagram showing rotation of vertebra in lateral curvature. The various lines show the 
positions of the body and transverse processes in the different degrees of rotation. The 
axis of rotation is behind the tip of the spinous process, where the three lines meet. (Adams.) 
The mechanism of this rotation will be understood from the ac- 
companying diagram (Fig. 322). The dark outline indicates the 
natural position of the vertebra, the dark straight lines indicating 
the natural axis and the direction of the transverse processes. 
When rotation occurs the body moves round so as to present to 
one side in the direction of the lines aa and aa, while the spinous 
process deviates very little. In the figure the centre of rotation is 
just behind the tip of the spine, and there is a slight deviation of 
it; but the centre of rotation may be at the tip of the spine, and LATERAL OR ROTATORY CURVATURE. 
747 
with very marked rotation of the vertebrae, there may be no devia- 
tion of the spines. 
Lateral rotatory curvature is met with chiefly in the dorsal and 
lumbar regions, being, as a rule, much more extreme in the former, 
probably from the greater mobility there. There is usually curva- 
ture in both these regions, the two curves being in opposite direc- 
tions, and one of them in a certain sense secondary. It is not 
possible, however, to distinguish rigidly between primary and 
secondary curves, as the two form nearly pari jmssu; a slight de- 
viation to one side will result in a similar curve to the opposite 
side, and they will increase together. 
AVe have seen above in connection with Fig. 322 that the plane 
of the transverse processes is altered by the rotation of the verte- 
brae. An examination of that figure will show that the transverse 
process on the side of the convexity is considerably displaced back- 
wards, and in actual cases it may be felt projecting under the skin. 
If the curve be in the dorsal region the rib will be similarly dis- 
placed, and its angle especially will project. As showm in Fig. 323, 
the rib in that case commonly makes a sharp curve at its angle, so 
Fig. 323, 
Diagrammatic section of normal chest and that with rotatory curvature. In the latter it 
is seen that the body of the vertebra is rotated into the right side of the chest, the rib on 
this side turning at an unduly sharp angle. The prominence of the transverse process on 
this side and of the breast on the opposite side is shown. (Adams.) 
that it is greatly flattened laterally; The figure also shows that, 
in such a case, the capacity of the corresponding side of the chest 
is greatly diminished. The body is rotated into that side of the 
chest and the ribs are flattened towards the vertebrae, these condi- 
tions sometimes attaining to such a degree that the bodies of the 
vertebrae approach the internal surfaces of the ribs. There is con- 
sequently great reduction in the capacity of this side of the chest, 
the lung being correspondingly compressed and curtailed in its 
movements. It will be seen also that posteriorly there is prom- 
inence of the angles of the ribs on the side corresponding with 
the convexity of the curve, while anteriorly the breast on the op- 
posite side is prominent. 748 
DISEASES OF THE BONES AND JOINTS. 
TUMORS OF BONE. 
Osseous Tumors.—In view of the fact already illustrated on 
more than one occasion that inflammatory processes in and around 
bone lead frequently to new formation of osseous tissue, it is not 
remarkable that there are certain bony growths which stand, as 
it were, on the border-land between tumors and inflammatory 
growths. Some of these have been mentioned at p. 187, under 
the designations hyperostosis and periostosis. In these cases there 
is always some form’of irritation inducing the new formation, and 
the new bone takes origin from the periosteum, so that it is applied 
to the surface of the existing bone, forming outgrowths from it. 
The irritation may have its origin in an inflammation of the bone, 
of the periosteum, or of the joints, and we shall see afterwards 
that diseases of joints, especially chronic rheumatic inflammations, 
are frequently accompanied by new growth of bone. 
A'arious names have been applied, according to the circum- 
stances of these bony outgrowths due to irritation of the peri- 
osteum. The name osteophyte is given when there are numerous 
small elevations of the surface without any considerable thickening 
of the bone; these may have a figured appearance on the surface, 
and they are sometimes loosely adherent to the bone, coming off 
with the periosteum when it is removed. Hyperostosis is a gen- 
eral enlargement of a whole bone, or a considerable part of it, 
with roughness and tuberculation of the surface, such as occurs 
sometimes in a long bone in consequence of syphilis or elephan- 
tiasis (see Fig. 321, p. 737). Such a hypertrophy of a long bone 
has hardl}T the characters of a tumor, but when a small bone is 
thus enlarged, it acquires much more of the appearance of an 
independent separate growth. 
Exostosis is a more definite tumor of bone, an outgrowth with 
a limited basis, but even some of these have intimate relations to 
irritations of bone. This applies especially to multiple exostoses, 
which are of occasional occurrence. In the case from which Fig. 
324 is taken (Virchow), the patient, a boy ten years of age, had 
suffered, during the course of three years, from repeated attacks 
of rheumatism affecting the joints and muscles. The result was 
the formation of sixty-five exostoses on various bones of the body. 
Exostoses also occur not infrequently at the insertion of tendons, 
growing into the latter and sometimes even separate from the 
bones. These are connected in their origin with the contraction 
of powerful muscles, occurring chiefly where such muscles are 
inserted, and sometimes induced by specially violent exercises of 
the muscles. 
The more simple exostoses have been already considered at 
p. 185. 
The name osteoid chondroma has been given by Virchow to a 
form of tumor which merits a more special description. The TUMORS OF BONE. 
749 
Fig. 324. 
Fig. 325. 
Fig. 325.—Osteoid chondroma of the tibia, divided ob- 
liquely. At the upper extremity the tumor has surrounded 
the cartilages of the knee, and new-formed cartilages have 
been produced. Internally the bone is condensed by the 
new formation of bony masses. From a boy 13 years of 
age. (Virchow.) 
Fig. 324.—Multiple exostoses of femur, tibia, and fibula. These are grouped towards the 
ends of the diaphyses. At its lower end the fibula is flattened by the exostoses growing out 
from the tibia. From a boy 10 years of age. One-third the natural size. (Virchow.) 750 
DISEASES OF THE BOXES AND JOINTS. 
tumor is composed essentially of tissue such as we iind in the 
deep layer of the periosteum of a growing bone, or in callus, its 
main constituents being osteoblasts. The cells are smaller than 
oartilage-cells and mostly round, but they do not possess a capsule. 
There is a dense intercellular substance which has a somewhat 
fibrous appearance. In the midst of the tissue bits of true car- 
tilage may be found. Being formed of tissue analogous to that 
which is preliminary to ossification, it frequently undergoes calci- 
fication, and even true conversion into hone. The tumors form, 
mostly, under the periosteum of the long bones, and their seat of 
election is the lower end of the femur or the upper end of the 
tibia, originating probably in the layer of osteoblasts there, and 
they may grow to large dimensions. They thus form club-shaped 
expansions of the long hones (Fig. 325). On section, the tissue is 
found to be dense, and it is found to be osseous or calcareous on 
passing deeply, where it is incorporated with the bone. The 
medullary cavity of the hone is often filled with new-formed bone. 
This form of tumor sometimes presents a tendency to become 
sarcomatous, and even without that it may recur after removal. 
Sarcomas in connection with bone are a very important group 
of tumors. As the sarcomas are of a connective-tissue structure, 
so they originate from connective tissue. The marrow and the 
periosteum being connective-tissue structures, we may have sar- 
comas originating from them, but the bone also is a connective 
tissue, and there seems no reason to doubt that it may also give 
origin to sarcomas. We may, therefore, distinguish sarcomas 
according as they have a central (myelogenous), interstitial (osse- 
ous), or peripheral (periosteal) origin. 
Of the myelogenous sarcomas the most characteristic is the 
myeloid or giant-celled sarcoma, already sufficiently considered. 
But we also meet with central round-celled sarcomas, or even 
spindle-celled sarcomas. The central sarcomas originating in the 
medulla of the cancellated tissue or in that of the shaft of a bone, 
usually destroy the external shell of bone as they grow. In this 
way they frequently reach the surface and may even work them- 
selves into surrounding tissue. In some tumors which are usually 
regarded as central, it is not certain that the destruction of the 
bone occurs entirely by the tumor acting on it. Considering that 
the bone-corpuscles are but modified medullary cells, it is not 
unlikely that they also take part in the tumor-formation. As we 
have already seen in the case of the myeloid tumor, there may be 
a new formation of bone at the same time as the destruction, and 
so the tumor may acquire a bony shell after the destruction of the 
proper external shell of the bone. 
The sarcomas of interstitial growth do not form such a 
definite group. It has been customary to regard sarcomas of 
bone as originating either in the medulla or periosteum, but 
Ziegler has shown that the tissue of a sarcoma may take origin 
directly from the bone-corpuscles. Tumors taking origin in this TUMORS of bone. 
751 
way will in the first instance replace the bone, and they may grow 
to a considerable size, simply occupying the place of the bone. In 
a preparation in the museum of the Western Infirmary the entire 
humerus of both arms is replaced by a soft sarcoma, which occu- 
pies the place of the bone, although larger than it in circum- 
ference. It is only at the extremities that any of the bone remains, 
and here the appearance is not as if the bone were being destroyed 
by a myelogenous tumor, but as if it were actually expanding into 
the tumor. A tumor of soft tissue replacing the bone will readily 
lead to fracture, and in the case referred to the first indication of 
any disease of the bone was a spontaneous fracture. These sar- 
comas are usually soft tumors whose cells are mostly round and 
generally small. 
The periosteal sarcoma is usually composed of spindle cells, 
and such tumors may grow around a bone, extending outwards 
for a considerable distance. We have seen also that sometimes a 
myeloid tumor takes origin in the periosteum of the jaw, forming 
an epulis. Of peculiar interest here is the tumor named the 
osteoid sarcoma. This tumor is that which by Paget and others 
has been well described as osteoid cancer. It shows some relation 
to the osteoid chondroma in respect that its cells are like those of 
the ossifying layer of the periosteum. In the osteoid sarcoma, 
however, the cells are more abundant and less regular, and they 
produce bone more uniformly. The tumor, in fact, usually pre- 
sents the appearance of a dense mass of bone of ivory hardness, 
on the surface of which there is a layer of fibrous-looking tissue. 
This layer is often comparatively thin, and on microscopic exami- 
nation it presents spindle cells or round cells which are so closely 
adherent to each other that they are with difficulty isolated. The 
bone is formed by the direct transformation of these cells, and one 
has sometimes the opportunity of observing remarkable transition 
forms. The tumor, like the osteoid chondroma, mostly originates 
at the end of one of the long bones, and forms a bulbous swelling 
there, the end of the bone, with its medullary spaces, being com- 
pletely transformed into a hard, heavy, osseous tissue. The tumor 
enlarges by incorporating neighboring parts, and it not infrequently 
extends by metastasis. 
Primary cancer is very rare in bone, but tumors of a glandular 
or epithelial structure have been met with, destroying the bone in 
their growth. In some cases this is really a penetration of a cancer 
into bone, but there seem to be actual cases in which a cancer has 
originated in bone. Secondary cancer is much more frequent. 
There are some cancers which, when they become generalized by 
the cancerous material getting into the blood, have a special pro- 
clivity to develop their metastatic tumors in the bone marrow. 
We may thus in a great number of bones have a cancerous trans- 
formation of the medulla, and as the tumor grows the bone is de- 
stroyed. A condition sometimes develops in this way not unlike 
osteomalacia in the manner in which the bone becomes softened. 
We may thus have cancerous softening of the bodies of the verte- 752 
diseases of the bones and joints. 
brse, of the ribs or of the long bones, the tumors being in large 
numbers, and everywhere growing from the medulla. 
The bones are sometimes the seat of cysts. These mostly occur 
in the jaws, where they may greatly distend the bone, but in the 
case represented in Fig. 426, the 
fibula was at its end distended into 
a bulky cyst which contained merely 
a serous fluid. 
The cysts of the jaws, originating 
as they do for the most part near the 
alveolar processes, are probably re- 
lated to the teeth. Some of them 
are single, unilocular cysts, and 
have their origin in teeth which have 
not undergone the usual eruption. 
A tooth or pieces of hard substance 
(dentine) are usually present in the 
wall of the cyst. Others are multi- 
locular and develop out of a gland- 
like tissue, the cells of which un- 
dergo colloid degeneration, and in 
this way form cysts. In its original 
structure the tumor might be called 
an adenoma, and a considerable por- 
tion of it is sometimes composed of 
solid glandular or epithelial tissue. 
According to Eve the tumor arises 
by penetration downwards of the 
epithelium of the gums, and he re- 
lates this to the normal penetration 
of this epithelium in the foetus in 
order to form the enamel organ. 
These multilocular cysts are mostly 
innocent, but sometimes the epithe- 
lium is less regularly arranged, and 
they approach in structure and ten- 
dencies to the cancers. Both forms 
of cysts originate in the interior of 
the jaws and distend them; those in the upper jaw have a special 
tendency to pass into the antrum, which they may fill out. 
Fibromas have been occasionally observed growing from the 
periosteum in the neighborhood of the mouth and nose, and they 
sometimes project inwards into the nares or mouth as fibrous polypi. 
The myxoma is a very rare form of tumor. 
Parasites are very rare in bone. The cysticercus cellulose has 
been observed, but the echinococcus more frequently. The hydatid 
cyst has mostly been met with in the bones of the pelvis or in the 
tibia. After growing and distending the bone it may burst through 
it and develop further in the soft parts around. 
Fig. 326. 
Cyst of upper end of fibula. The 
upper part of the bone is expanded 
into a cyst which contained a reddish 
serous fluid. 753 
DISLOCATIONS AND MISPLACEMENTS. 
B.—THE JOINTS. 
DISLOCATIONS AND MISPLACEMENTS. 
Congenital Dislocations.—Children are sometimes born with 
the joints in faulty positions, some of these being really traumatic 
and others of more obscure origin. The traumatic cases arise for 
the most part during parturition, either from the natural forces 
engaged in delivery, or by dragging on the part of attendants. 
The hip-joint is not infrequently dislocated in this way, and usually 
the displacement is on both sides at once. The head of the bone 
is usually displaced upwards so as to rest on the dorsum of the 
ileum above and behind the acetabulum. Through time the head 
makes for itself a new joint, and the acetabulum tills up. Con- 
genital dislocations of other joints are exceedingly rare. 
Talipes or Club-foot.—These names are applied to distortions 
of the feet, or more rarely of the hands; the bones assume certain 
abnormal positions in which they are retained by the contraction 
of muscles. A certain proportion are congenital, and these seem 
to arise in utero by a faulty distribution of the impulses by which 
the muscles are made to contract. One or more muscles are kept 
in a continuous state of more or less rigid contraction, while the 
others are not, and the consequence is that the foot is held in a 
distorted position. 
The non-congenital forms are, in the great majority of cases, 
due to infantile paralysis. In this disease, as we have seen, some 
muscles are paralyzed, while others are not. It has been generally 
stated that the deformities are due to contraction of the unpara- 
lyzed muscles which are not opposed in the normal manner by the 
paralyzed ones. This appears to be the explanation in some cases, 
but it does not account for the occurrence of talipes in cases where 
nearly all the muscles of the foot are paralyzed. Such cases indi- 
cate that the faulty position may arise to some extent because the 
muscles are not able to keep the foot in its proper position, so that 
it tends to fall into the attitude it would assume if there were no 
muscles. These positions are also variously modified by the use 
made of the foot in walking, the parts being brought against the 
ground in the position most suitable to stability in the maimed 
condition of the limb. In a similar way club-foot may occur in 
pseudo-hypertrophic paralysis. 
Besides paralysis, it seems that spasm may lead to talipes, al- 
though the explanation of the local spasm is often very obscure. 
It is stated that mimicry sometimes leads to it, or disease of the 
nervous centres or reflex irritation. It is undoubted that children 
sometimes acquire a talipes after a convulsive attack. 
The forms of talipes do not call for detailed description here. 
There are four principal forms, some of which may be combined. 
In talipes varus the toes are inverted, and the inner margin of 754 
diseases of the bones and joints. 
the foot is raised upwards; the tibiales anticus and posticus are 
the muscles which are chiefly contracted. In talipes valgus, 
which is one of the rarer forms, the foot is turned outwards, and 
the outer border is raised, there is usually also some elevation of 
the heel; the peronei, extensor longus digitorum and gastrocne- 
mius are the muscles chiefly engaged. In talipes equinus the 
heel is raised and the foot extended, so that the person walks on 
the distal extremities of the metatarsal bones; the gastrocnemius 
is the muscle contracted. In talipes calcaneus the heel is de- 
pressed and the foot flexed at the ankle, this deformity being the 
reverse of the preceding one; the contracted muscles are chiefly 
the tibialis posticus, the peronei, and the extensors. 
By long retention of the fixed position the bones become variously 
modified in shape, undergoing atrophy where exposed to prolonged 
pressure. Where the cartilage is no longer used in the movements 
of the joints it also atrophies. The bones frequently acquire ad- 
hesions in their new positions, and the ligaments, by elongating or 
shortening, accommodate themselves to the new position. £\ew 
ligamentous attachments are sometimes formed, and the bones may 
become joined together by anchylosis. 
Traumatic Dislocations.—We have here to do with cases in 
which the bone is pushed out of its place by some external force 
acting on it. The bones are kept in their places mainly by the 
ligaments of the joints, but no inconsiderable aid in this regard is 
given by the muscles which act on the bones. As a general rule 
when external pressure is exercised on a bone at a joint, the mus- 
cles are so braced as to enable the bone to retain its place in spite 
of the external force. But if unexpectedly, or when the muscles 
are generally relaxed, as by alcoholic stupor, a force is exercised on 
a bone, then it may be displaced, although the force under ordi- 
nary circumstances would be insufficient to produce this effect. 
The bone may even be displaced by the action of the muscles 
themselves, where a certain group acts very vigorously while their 
antagonists are relaxed. There are indeed persons who can vol- 
untarily produce dislocation of almost all the more movable joints, 
and that by mere muscular efforts. In order to this we must sup- 
pose a certain laxness of the ligaments, but there is also a power 
acquired by education of strongly contracting certain muscles, 
while others which usually contract along with them are relaxed. 
We know that for the most part the muscles in their contractions 
are coordinated, and most people are unable to contract individual 
muscles apart from their coordinates, but there are exceptional 
persons who possess this power, some in a limited degree and 
others very remarkably. Many persons, for instance, cannot shut 
one eye without the other, and most persons when they shut one 
require to make an active effort at opening the other, in order to 
prevent it shutting too. But there are persons who can close the 
eyelids of one eye as easily as they can close the fingers of one 
hand. ANCHYLOSIS. 
755 
In traumatic dislocation there is usually tearing of the ligaments 
to some extent, and in the case of some joints much laceration is 
necessary before dislocation can occur. 
When the bone is dislocated, the same contraction of the muscles 
which normally aids in preventing dislocation, generally offers 
serious obstacles to the return of the bone to its normal place. If 
restoration does not occur soon, then the bone acquires adhesions 
in its abnormal situation, the adhesions being the result of chronic 
inflammation set up by the irritation of the bone. The displaced 
bone generally comes to press with its head against a neighboring 
part of the bone with which it formerly articulated, and the ad- 
hesions attach it to the periosteum in its new position. Friction 
by degrees wears down to some extent the opposed piece of bone, 
and as new bone is produced around by the irritation there may 
be a kind of hollow joint formed. By the wearing of the bone 
the cancellated tissue would be exposed, were it not that dense 
bone is produced on the surface so as to cover in the spongy tissue. 
A smooth hollow surface may thus be produced, and a tolerably 
perfect joint, although cartilage is not formed to cover it, but only 
a layer of smooth polished bone. The head of the displaced bone 
also loses its cartilage, and may even get worn away considerably. 
If the bone remains permanently displaced the old hollow of the 
joint becomes filled up, bone growing when the friction of the 
opposing bone is no longer exercised. 
Spontaneous dislocations are mostly due to inflammatory 
changes in the joints or their ligaments, or to the contraction of 
cicatrices in the neighborhood. It will be understood also from 
what has gone before, that the sudden contraction of one set of 
muscles while the rest are relaxed may cause dislocation. If 
spontaneous dislocations are unreduced there may be changes in 
the joints similar to those in traumatic cases, but there are fre- 
quently primary inflammatory changes, which are more prominent 
than those secondary changes. 
ANCHYLOSIS. 
By this name is meant fixation of a joint by union of the op- 
posing hones by means of firm adhesions. The expression “false 
anchylosis” is sometimes used to designate the condition in which 
the joint is fixed, not by adhesion between the bones, but by 
rigidity and shortening of the surrounding soft parts. 
For the most part anchylosis is the result of inflammations of 
joints, where the cartilage has been destroyed and healing has 
subsequently occurred. In the process of healing the inflammatory 
tissue on the opposing surfaces develops into connective tissue, and 
as the two surfaces have to a considerable extent coalesced, fibrous 
tissue unites them permanently. In this fibrous bond of union 
there are often bony plates, and occasionally the union is effected 756 
DISEASES of the bones and joints. 
by bone itself. This, however, is a very unusual occurrence, as 
even slight movement of the joint is sufficient to prevent the 
formation of bone. The fixation of the joint, however, is often so 
firm as to resemble an actual coalescence of the bones. 
An interesting discovery was made by Meier, of Zurich, in 
regard to the architecture of the cancellated tissue of bones. 
The bony trabeculae of the spongy tissue do not form an irregular 
network, as they seem at first sight to do, but they are arranged 
according to a definite architectural plan. They form, in fact, 
pillars, which are directed towards the surfaces on which pressure 
is exercised in the various movements of the joints. Each bone 
has its own architectural structure, and the structure corresponds 
exactly with what mathematicians make out as to the direction of 
pressure in the various bones. When anchylosis occurs, or after 
the healing of fractures, the lines of pressure may be changed. If 
these occur in growing bones, the architecture readily undergoes 
a corresponding change. But even in adults, by thickening of 
the lamellae in some parts and absorption at others, there is a 
gradual adaptation of the structure to the changed circumstances. 
INFLAMMATION OF JOINTS—ARTHRITIS. 
This is a somewhat extensive subject, and includes the great 
bulk of the diseases to which the joints are liable, especially if we 
include scrofulous or tubercular disease of the joints. 
In most cases of arthritis the inflammation affects, more or less, 
all the structures which enter into the construction of the joint. 
The irritant is usually present in the joint itself, and is distributed 
over it with the synovial fluid by the movements of the joint. We 
may expect, therefore, that the synovial membrane and the carti- 
lage, as they cover the surface, will in most cases be primarily 
affected. The cartilage, being non-vascular, is less liable to in- 
flammatory changes than the synovial membrane, which in most 
cases is primarily and chiefly engaged, especially in acute in- 
flammations. But in chronic cases the irritation extends beyond 
these structures to the ends of the bones, to the neighboring peri- 
osteum, and even to the ligaments. 
Simple Acute Arthritis.—This condition is produced most 
directly by the opening of joints and the occurrence of septic de- 
composition in their fluids. But it also occurs sometimes by ex- 
posure to cold, from injuries, and from the extension of plileg- 
monous inflammations from surrounding parts. 
The inflammation resembles closely that of the pleura and peri- 
cardium in its anatomical details. The synovial membrane and 
cartilages are covered with fibrinous exudation, and the cavity con- 
tains serous fluid in which flakes of fibrine are visible. This fluid 
is sometimes very considerable and distends the joint. In this 
stage the disease may resolve and the joint return to its normal 757 
inflammation of joints—arthritis. 
condition. On the other hand, especially if the joint has been laid 
open and exposed to decomposition, the inflammation goes on to 
suppuration. The synovial membrane becomes swollen and dull, 
being infiltrated with inflammatory cells, and gradually converted 
into granulation tissue. If the inflammation is very acute, we may 
have suppuration by the mere exudation of leucocytes without 
much change in the synovial membrane. When the disease has 
gone on to the formation of granulation tissue it is now in a sub- 
acute condition and is apt to he prolonged. The inflammation 
also extends beyond the synovial membrane. In the cartilage the 
cells undergo active proliferation, and the matrix breaks down; 
thus softening occurs, and ulcers form. There is inflammation of 
the bone, a rarefying osteitis with caries. The ligaments also take 
part in the inflammation, they are softened and, with the synovial 
membrane, take part in the formation of granulation tissue. The 
periosteum is inflamed and new bone is formed, so that irregular 
projections occur near the ends of the bones. With all this there 
is, of course, usually an abundant purulent discharge from the 
joint, which may weaken the patient and prove fatal, perhaps with 
amyloid disease. 
If the inflammation subsides, the various masses of granulation 
tissue develop into connective tissue, and, by the contraction of 
this, great rigidity of the joint may be produced. The granulation 
tissue lining the joint does also to a great extent coalesce, and the 
result is a partial or complete obliteration of the joint. The bones 
thus become finally united by fibrous or osseous adhesions, and a 
permanent anchylosis is the result. 
Pyemic arthritis has already been partly considered. In this 
disease a virus is deposited in the joint and spread over the surface 
by the synovial fluid. The result is an acute inflammation with 
fibrinous exudation, but generally going rapidly on to suppuration. 
It is remarkable that when the joint is full of pus there is some- 
times very little structural change in the synovial membrane, the 
whole condition being almost confined to the bloodvessels from 
which an excessive exudation has occurred. The inflammation 
usually affects several joints simultaneously. It is to be added 
that occasionally in typhus, dysentery, diphtheria, scarlet fever, 
etc., a similar acute arthritis occurs. 
Acute rheumatic arthritis is, like pysemic arthritis, due to an 
irritant which is present primarily in the blood and aflects the 
structures of the joints like other connective-tissue structures. 
The result is an acute inflammation accompanied by serous and 
fibrinous exudation into the joint. The synovial membrane is in- 
jected and swollen, and if the inflammation is of sufficient inten- 
sity and duration the cartilage, and even the bone, take part in it. 
The cartilage cells undergo proliferation, and may burst into the 
cavity of the joint. The bones show inflammatory proliferation 
in the medulla in the usual fashion. As a rule these changes do 758 
DISEASES OF THE BONES AND JOINTS. 
not reach an extreme degree, and suppuration is hardly known to 
occur. 
Gouty Arthritis.—In this disease uric acid, in the form of urate 
of sodium, is deposited in the tissues of the joints. It is first de- 
posited in the cartilage, and, according to Charcot, always, to begin 
with, at the middle of the articulating surface, that being the point 
furthest removed from the bloodvessels. The urate is sometimes 
in the form of stellate crystals (Fig. 327), the cartilage cells forming 
the middle points of the bunches of crystals. But the salt is also 
deposited in the matrix and often in the form of irregular needles. 
It is also frequently deposited in the synovial membrane, and in 
the bones, ligaments, and soft parts around the joints. Sometimes 
the salts are deposited even under the skin, forming visible projec- 
tions (the so-called tophi or chalk-stones). 
This deposition seems to lead to an acute irritation of the 
structures of the joint, chiefly an intense hyperaemia, often with 
serous exudation. It never goes on to 
suppuration, however. When recovery 
takes place it frequently leaves a chronic 
inflammation, resulting in changes 
analogous to those in chronic articular 
rheumatism. 
Chronic Rheumatic Arthritis.— 
As a rule, this disease affects many 
joints, but as the changes are virtually 
the same as in arthritis deformans, 
and the two conditions run into one 
another, we may describe them together. 
In arthritis deformans the disease is 
partial, being confined perhaps to a 
single joint, and the lesions attain a 
much greater development than in 
general articular rheumatism. It is 
also much more a disease of old people, 
and is met with chiefly among the poor. 
In both these diseases the nature of the 
irritant is entirely obscure. 
The inflammatory phenomena appear 
first in the synovial membrane and the 
cartilages. The synovial fringes enlarge by a slow process of 
inflammation, and the villous projections increase in number and 
become more prominent. Rot uncommonly pieces of cartilage 
develop in the fringes, originating in the cartilage cells which 
exist normally there, and these pieces of cartilage, being usually 
pedunculated, act very much like free bodies in the joint and may 
become loose. The cartilage also sometimes undergoes ossification 
in whole or in part. At the same time there is an increase of the 
synovial fluid, but without any formation of fibrine or pus. 
Fig. 327. 
Vertical section of an articular 
cartilage infiltrated by urate of 
soda, from a gouty patient, p. 
Articular surface of the cartilages. 
v, n. Amorphous and crystallized 
urate of soda. o. Capsules and 
cartilage cells. X 200. (Cornil 
and Ranvier.) chronic rheumatic arthritis. 
759 
The cartilage cells undergo proliferation and the matrix presents 
a peculiar fibrillation, so that the cartilage assumes a soft, velvety 
condition, and readily undergoes destruction from the friction of 
the opposing surfaces. It is stated by Rindfleisch that the fibrillae 
of the matrix undergo mucous degeneration, and that mucus may 
be found in the synovial fluid. 
The bone beneath the cartilage also undergoes considerable 
alteration, especially when the cartilage gets worn away. To pre- 
vent the cancellated tissue from being opened, there is formed, as 
the cartilage is destroyed, a layer of dense bone, wThicli is smooth 
and polished, and takes the place of the cartilage. This forms a 
much less efficient covering, and the ends of the bones work 
roughly against each other. This layer of bone may also be worn 
down, and so considerable atrophy of the head of the bone may 
result, a layer of dense, smooth bone being always reproduced. 
At the borders of the articular surface there is often consider- 
able new formation of bone, the result of the inflammation where 
the parts are not exposed to friction. It appears from the obser- 
vations of Ranvier that the bone here develops largely from car- 
tilage. The synovial membrane, at the edge of the joint, covers 
in some of the marginal portions of the cartilage, and, being thus 
protected, the cells may proliferate so as to lead to new formation 
of cartilage, which may ossify. The periosteum may also produce 
new bone, and even the ligaments attached to the periosteum may 
be the seat of bony processes. 
With all this there is considerable thickening of the ligaments 
by inflammatory new formation of connective tissue, and often 
fibrous union between opposing parts of the joints. Indeed, if 
the joints are kept at rest, there may be a complete union of the 
parts around the joints opposite each other, leading to anchylosis. 
Without anchylosis there is stiffness of the joints, whose move- 
ments are greatly curtailed. There is frequently great deformity 
from the thickening of the tissues and new formation of bone. 
An extreme degree of arthritis deformans is sometimes seen in 
the hip-joint, when it gets the special name of morbus coxiE 
senilis. Here the wearing down of the head of the bone is some- 
times very extreme, so that ultimately the articulating surface may 
lie between the trochanters. As new formation of bone occurs 
simultaneously at the borders of the articular surface, a kind of 
artificial head is produced, and the appearance is presented as if 
the neck were atrophied and the head displaced. In like manner, 
an apparent widening of the acetabulum may occur. The original 
articular surface is worn away, but, by the formation of new bone 
by the periosteum around, a wall is formed, giving the appearance 
of the borders of a widened acetabulum. 
Syphilis does not frequently attack the joints, but rheumatic 
attacks in syphilitic persons may have some relation to the specific 
virus. According to Lancereaux, there may he in the secondary 
stage an inflammation like that of acute or subacute rheumatic 760 
diseases of the bones and joints. 
arthritis, and, in the tertiary stage, manifestations like those of 
chronic arthritis. 
Scrofulous or Tubercular Arthritis.—Besides these names, 
this disease is often called strumous synovitis, gelatinous degen- 
eration of the joint, tumor albus, fungous caries, etc. The 
disease occurs mostly in delicate children, but as it is associated 
with the formation of definite tubercles we must regard it as 
taking origin in the specific tubercular virus. It is sometimes 
said that the tubercular formation is secondary, and that there is 
first a chronic inflammation of a scrofulous kind going on to 
caseous degeneration, and so leading to the formation of tubercles. 
A case observed by the author is quite opposed to such a view. 
There was in this case a great thickening of the synovial mem- 
brane, which was converted into a bulky, soft, gray tissue, which 
overlapped the cartilage, and was so prominent that when the 
joint was opened for the purpose of excision the idea of a tumor 
was suggested. There was not a trace here of caseous material or 
of pus, and yet the thickened synovial membrane consisted essen- 
tially of an immense aggregate of tubercles with inflammatory 
tissue around them. The tubercles were of typical form, with 
large giant-cells. 
The disease begins usually in the synovial membrane, and 
consists in a formation of tubercles and a chronic inflammation 
with great production of granulation tissue. The soft, pulpy 
granulation tissue gives the synovial membrane a gelatinous ap- 
pearance, from which one of the names of the disease is taken. 
There is also a slow enlargement of the joint from the increased 
bulk of the synovial membrane. 
The ends of the bones constituting the joint are affected simul- 
taneously or soon after, and here the characters presented are those 
of a rarefying osteitis. The medullar}' spaces become filled with 
granulation tissue and enlarged by destruction of the bony lamellae. 
In this granulation tissue there are also tubercles. In this way 
there is, as it were, a pad of granulations under the articular 
cartilage. 
The cartilage also at the sides is partly encroached on and over- 
lapped by the altered synovial membrane which advances over it. 
In this way it is partly enclosed between two layers of granulation 
tissue, and it gradually becomes eaten into. The granulations, 
chiefly those of the medulla, extend into the cartilage, and their 
encroachment is assisted by proliferation of the cartilage corpuscles, 
which enlarge and cause softening of the matrix around. 
By the absorption of the cartilage the whole joint may be con- 
verted into a cavity lined with granulation tissue, and the liga- 
ments also are frequently transformed in a similar way. 
Generally suppuration results, and the joint becomes filled with 
pus. Abscesses also not uncommonly form around the joints. 
Through time the pus generally finds its way outwards, and is 
discharged by an aperture in the skin. A fistulous canal is the CHRONIC RHEUMATIC ARTHRITIS. 
761 
result, forming a communication between the cavity of the joint 
and the surface, and this canal is also lined with exuberant granu- 
lations, which pout out at the opening at the skin. Among the 
granulations here, as elsewhere, tubercles are found. 
The rubbing of the two ends of the bones, wdiich are now covered 
by granulations, leads to an ulcerative destruction of these soft 
structures. The inflammation extends more deeply in the bone 
as the superficial parts are ulcerated, and so we have progressive 
caries. For some distance beneath the surface the medullary 
spaces are filled with granulations and the bony trabeculae thinned. 
It will be understood from this how the disease is apt to recur 
unless the whole carious portion be removed, for tubercles are 
present in the granulation tissue filling the medullary spaces, and 
unless they be removed a fresh extension may occur. 
In an early period of the disease, before suppuration has oc- 
curred, there may be recovery; but after the occurrence of sup- 
puration, there is seldom a spontaneous restoration, which at best 
is a slow process. If recovery takes place the granulating surfaces 
unite more or less, and the joint being partly or completely ob- 
literated, a fibrous union may come about, leading, it may be, to 
anchylosis. DISEASES OF THE SKIN AND ITS APPENDAGES. 
INTRODUCTION. 
Tiie diseases of the skin are exceedingly manifold, and the 
names applied to them somewhat complicated. In the present 
section no attempt will be made to give a complete description of 
the appearances presented in each affection. So far as the naked- 
eye appearances are concerned, these are sufficiently described in 
the text-books on the practice of medicine or on diseases of the 
skin. We shall endeavor here to summarize the pathological 
conditions and group together the various diseases according to 
the nature of the lesion. It will be necessary first to refer to the 
normal structure of the skin. 
Normal Structure.—The corium or true skin is a very vas- 
cular dense membrane composed of interlacing fibres of connective 
tissue, with numerous elastic fibres. It is richly supplied with 
nerves, and possesses bundles of smooth muscles. It has also a 
rich system of lymphatic vessels. In the corium we may distin- 
guish a superficial or papillary layer and a deeper one. Many of 
the diseases affect the papillary layer especially. 
The epidermis on the surface of the corium is in several layers 
(Fig. 328). Most superficial is the horny layer (a) composed of flat 
cells, which are little more than scales, and have lost their nuclei.. 
Next comes the stratum lucidum (b) composed of flat transparent 
cells. This is followed by the stratum granulosum, also composed 
of flat cells which are granular. Most deeply situated is the 
stratum mucosum or rete Malpigliii, composed of cells which, in 
the deepest layer, are cylindrical, but towards the surface become 
polygonal and flattened. In the deeper layers the cells are serrated 
at the margins, so as to give the appearance of prickles by which 
the cells fit into each other. The stratum lucidum and stratum 
granulosum are thin, and for practical purposes the epidermis may 
be divided into the horny and Malpighian layers. The Malpighian 
layer extends between the papillae of the corium, forming inter- 
papillary processes. 
The sebaceous glands may be regarded as modified prolonga- 
tions of the Malpighian layer. They are mostly connected with 
hair-follicles, into which they open, but sometimes large glands 
are connected with small hairs, and small glands with large hairs, 
while there are glands not connected with hairs at all. The 
sudoriparous glands are usually situated beneath the skin, their INTRODUCTION. 
763 
ducts passing through corium and epidermis, having a spiral course 
in the latter. The hairs are composed of horny epidermis, and 
are placed in follicles. In the latter, two layers of epidermis can 
be distinguished (Fig. 328), the outer root-sheath corresponding 
Fig. 328. 
Section of epidermic layer of skin with a hair and its follicle, a, horny layer; b, stratum 
lucidum; c, Malpighian layer with (cl) the deepest layer of cylindrical cells; e, hair, whose 
sheath presents two layers, one continuous with the horny and the other with the Malpighian 
layer. X 350. 
with the Malpighian layer, and the inner root-sheath corresponding 
with the horny layer. At the bottom of the follicle is a papilla 
continuous with the corium, and on this is set the bulb of the hair. 
The nails are composed of compressed horny epidermis. Beneath 
the nail are still two layers of epidermis, a horny layer of loose 
cells, and a Malpighian layer covering well-formed papillae. 
The exposed position of the skin renders it very liable to the in- 
fluence of agents acting from without. It is also liable to be in- 
fluenced by irritants circulating in the blood, in which case the 
skin affection will probably be an insignificant part of a general 
condition. The skin again is liable to be affected by states of the 
nervous system. From these remarks it will be inferred that the 
inflammations of the skin are the most important morbid condi- 
tions, and these will call most largely for description. 764 
DISEASES OF THE SKIN AND ITS APPENDAGES. 
HYPEREMIA, HEMORRHAGE, (EDEMA OF THE SKIN. 
The skin is very liable to variations of its blood supply. An 
active hyperemia hardly occurs as a pathological condition except 
as part of an inflammation. Passive hypersemia, on the other 
hand, is exceedingly common as a result of general venous en- 
gorgement, especially in disease of the heart, where it leads fre- 
quently to CYANOSIS. 
Hemorrhages are frequent and of various kinds. As to their 
causes little need be added to what is stated at p. 56. The skin is 
liable to hemorrhage by traumatic rupture of its vessels, but still 
more, perhaps, by alterations in the state of the blood affecting its 
vessels. In scurvy, in purpura, in smallpox, in typhus, etc., the 
skin is the seat of hemorrhage much more frequently than any 
other structure. 
The blood escaping from the vessels collects in the serous spaces 
of the corium for the most part, but may pass to the subcutaneous 
tissue, where the fat is sometimes considerably infiltrated. When 
the blood has escaped from a small vessel and infiltrates a limited 
area so that a bluish spot is seen on viewing the surface, the term 
petechia is given. As these small hemorrhages depend on the 
state of the blood the petechias are nearly always multiple. When 
the blood infiltrates a larger area, then the term ecchymosis is used. 
Sometimes the blood collects between corium and epidermis, and 
then a hemorrhagic vesicle is the result; but this can only happen 
if the deeper layers of the epidermis have been killed so as to al- 
low of their separation from the corium. When there are numer- 
ous small hemorrhages forming a large number of petecliiae, then 
it is customary to use the term purpura, or to speak of a purpuric 
condition. 
The blood effused in the skin undergoes changes like those 
already described at p. 58. The affected area is first dark blue, 
and the color does not disappear on pressure. After a time, as the 
blood-coloring matter is dissolved, the color gets fainter and 
changes in hue, while the discoloration becomes more extended. 
If blood has collected between the layers of epidermis, it comes to 
the surface and is disposed of as the epidermis is shed. 
(Edema of the skin, apart from inflammation, is chiefly related 
to disease of the heart and kidneys. Its general pathology has 
been considered at pp. 63 and 64. The exuded fluid collects in 
the lymph-spaces and is carried off by the lymphatics. A condi- 
tion of the skin has been recently described under the name 
myxcedema. It appears to occur in connection with Bright’s dis- 
ease, and differs from ordinary oedema in respect that the fluid oc- 
cupying the spaces contains a considerable amount of mucine. 
The oedematous parts are much firmer than in ordinary oedema 
and do not pit on pressure. ATROPHIC CHANGES IN THE SKIN. 
765 
ATROPHIC CHANGES IN THE SKIN. 
Simple Atrophy is not uncommon in the skin. The most fre- 
quent example of it is afforded by senile atrophy, resulting in the 
wrinkled skin of old people. In this case the connective tissue of 
the cutis loses in bulk, especially the papillary layer. Very often 
the remaining fibres have a strikingly granular appearance under 
the microscope, but there are sometimes patches in which the 
fibres have assumed a glassy or colloid character, so as to give rise 
to the designation colloid or hyaline degeneration. The epidermis 
is also thinner and dry, and there is often desquamation in the 
form of dry scales or larger membranous pieces. The hairs are 
atrophied, as their papillae have taken part in the general atrophy 
of the papillee of the skin. The hair-follicles are shortened and 
the sebaceous glands on this account may be brought close to the 
surface, almost opening directly on it. The secretion may ac- 
cumulate in the sebaceous glands so as to form small or large 
CYSTS. 
A general atrophy also occurs in emaciated persons, and it may 
closely resemble the condition in senile atrophy. 
There are further conditions variously named parchment skin, 
xeroderma, general atrophy, hide-bound skin, which are of rare 
occurrence, and are not very well understood in their exact rela- 
tions. The skin is thinned and hardened, especially the epidermis, 
so that the body seems covered with stiff parchment, which often 
looks as if too small for the surface to be covered, so that the 
movements of the limbs are impeded. It is sometimes mottled 
with pigmented spots, sometimes white. The disease generally 
begins in early life and extends gradually over the skin. This con- 
dition will be considered subsequently under the tropho-neuroses. 
Of the local atrophies, the most familiar is that which occurs 
after pregnancy. It is well known that white lines are found in 
the abdomens of persons who have been pregnant. Similar lines 
occur in persons whose abdomens have been distended by tumors, 
by ascites, or even by accumulation of fat. The white lines have 
a cicatricial appearance, and they seem to owe their origin to the 
connective-tissue fibres of the cutis being dissociated by the stretch- 
ing. Somewhat similar white lines or striase sometimes occur 
idiopathically, especially over the buttocks, trochanters, pelvis, 
and thighs. 
The hairs are liable to atrophy, and two forms may be distin- 
guished according as either the hair itself or its pigment dimin- 
ishes. Alopecia or baldness is atrophy of the hair itself. All 
through life a continuous falling out of hair is occurring, and is 
due, as we have seen before, to an atrophy chiefly of the bulb. 
But the papilla remains, and a healthy new hair is produced on 
the site of the old one. In old people, however, the new hairs 
are not usually reproduced of normal size, and they become grad- 766 
DISEASES OF THE SKIN AND ITS APPENDAGES. 
ually finer and finer, till there are only the finest woolly hairs on 
the bald part, or even none at all. It is well known that this 
condition frequently occurs in comparatively early life—premature 
alopecia. The cause seems to he an atrophy of the papilla, and 
sometimes of the skin itself. Besides being produced in this way, 
baldness may be secondary to syphilis, to inflammations, and to 
certain parasitic diseases; in these cases it depends on interference 
with the nutrition of the sheath and papilla. 
Special attention has been paid to alopecia areata, in which 
baldness occurs in circular patches. These patches are not entirely 
bald, but are covered with fine woolly hairs, and the papillse are 
not destroyed. The nature of this disease must still be regarded 
as obscure. Some regard it as of parasitic origin, and Eichhorst 
states that, as the fungus is mainly in the liair-sheath, it is usually 
left behind when the hair is extracted, and so is overlooked. 
Others assert that it is due to changes in the nerves which com- 
mand the nutrition of the skin, and is a tropho-neurosis. 
Canities or grayness of the hair is also for the most part a 
natural atrophy of old age. But it also sometimes comes on pre- 
maturely. It depends for the most part on a deficiency of pigment 
in the individual hairs at their original formation, so that the 
pigment granules between the cells in the cortical layers of the 
hair are diminished. But there may be a temporary blanching of 
the hair from air getting infiltrated among the cells of the cortex. 
Cases of sudden permanent blanching have received no satisfac- 
tory explanation. 
The nails are liable to atrophy, which may be congenital or 
acquired. In the course of acute illnesses, such as fevers or 
maniacal attacks, the formation of the nails is often diminished, 
and the illness is marked for a time by a transverse depression, 
which, with the growth of the nail, proceeds from the root out- 
wards, and disappears in due course. The nails also atrophy 
sometimes in consequence of various parasitic or inflammatory 
skin diseases. The nail substance may be simply thinner and 
more delicate than normal, or it may be brittle and split or 
crumble readily. 
INFLAMMATIONS OF THE SKIN. 
These include a very great variety of disease, and the nomencla- 
ture is exceedingly complicated. In the skin, as elsewhere, in- 
flammation is produced by the action of irritants, and the form of 
the inflammation will depend greatly on the nature and source of 
the irritant. But it depends perhaps just as much on the nature 
and condition of the skin itself, the same irritant producing very 
different effects in different persons. 
As illustrative of many points in the pathology of inflammation inflammations of the skin. 
767 
of the skin, we shall refer to the very simple case of the results of 
a flea-bite. The results are not the same in every person, because 
different persons are variously susceptible to the irritant. When 
a flea penetrates the epidermis, it introduces an irritant, which has 
an immediate effect on the sensory nerves. This is followed in 
certain persons by an oedema of the superficial layers of the skin, 
leading to the formation of a flat elevation called a wheal. By 
rubbing, the poison is dispersed in the serous spaces around the 
puncture, and the wheal is enlarged up to a certain point. The 
wheal is preceded by a slight hypersemia, and at its periphery there 
is still some redness of the skin, but this is generally insignificant. 
After a short time, all trace of the irritation subsides; the inflam- 
mation has been very slight and transient. But the irritant still 
remains, and next day more permanent changes show themselves. 
At the place of the puncture there is a conical elevation, which at 
first is solid, forming a papule, but after a time presents a clear 
cavity containing fluid, a vesicle. Both of these conditions are 
again due to inflammatory exudation. The exudation is from the 
vessels of the papillary layer of the skin, and it consists of serous 
fluid, with leucocytes. This may confine itself to the papillae, or 
it may pass among the epidermic cells, loosening them out, in 
either case forming a solid elevation or papule. But it may so 
dissociate the epidermic cells as to form a cavity in which it 
collects, thus producing a vesicle. The vesicle does not form, as 
might be supposed, between the epidermis and cutis, but among 
the deeper layers of the epidermis itself, the softer cells of the 
Malpighian layer becoming separated, so as to leave a space. 
According to Ziegler, this is always by necrosis and destruction 
of some of these cells. 
The papules and vesicles thus formed are often very persistent, 
remaining with trivial alterations for days or even weeks. As a 
rule, the vesicles dry in, and only papules are left, but the vesicles 
are sometimes renewed at intervals. The elevations ultimately 
subside, but a piece of epidermis is discharged from the surface, a 
desquamation, and the skin is restored to its normal condition. 
Causation of Cutaneous Inflammations.—From what has gone 
before, it will be apparent that in the case of all inflammations we 
have to look for an irritant. But the illustration just given shows 
that the same irritant produces very different effects in different 
persons. We have seen that in some persons a flea-bite produces 
an exudation leading to the formation of a wheal, but in many 
persons it does not. In some persons a wheal may be produced by 
a very trivial irritation. A simple scratch with the finger-nail will, 
in some, cause a raised line such as in others is produced by the 
lash of a whip. Then it is remarkable that in the same person at 
one time a wheal will be produced by a simple scratch and at 
others it will not. These differences apparently depend on varia- 
tions in the state of the nervous system at different times and in 
different persons. In urticaria there is a formation of wheals in 768 
DISEASES OF THE SKIN AND ITS APPENDAGES. 
various parts of the body without any special external irritant. 
Such attacks are usually brought on by eating shell-fish, walnuts, 
or other special forms of food. These substances appear to produce 
their effects through the nervous system, inducing, by reflex action, 
a peculiarly sensitive state of the skin. The wheals occur espe- 
cially in parts of the skin which are irritated by rubbing or by the 
contact of the clothes, and there may be very striking oedema of 
the eyelids, for instance, where the feeling of itchiness has induced 
the person to rub them more than other parts. 
In almost all forms of inflammation the state of the nervous 
system and individual peculiarities have a most important bearing 
on the form and intensity of the process. But there are some forms 
of inflammation in which the condition of the nervous system has 
even a more direct bearing on the causation. Where the trophic 
centres of parts of the skin are interfered with, a trivial irritation 
may lead to necrosis or severe inflammation. 
Inflammations owe their immediate origin to direct or indirect 
irritation of the skin. The irritant may be circulating in the 
blood and carried to the skin as to other structures. This applies 
to the cutaneous eruptions in the acute specific fevers and in 
syphilis; in these cases we may designate the eruptions as symp- 
tomatic. On the other hand, the irritant may come from without, 
as in the case of erysipelas, scalding, etc., and the inflammation is 
localized according to the extent of the irritation. 
FORMS OF CUTANEOUS INFLAMMATIONS. 
It is somewhat difficult to classify the various inflammations of 
the skin, but for convenience we shall consider them in four 
groups: (1) Symptomatic Inflammations ; (2) Inflammatory Skin 
Eruptions; (3) Traumatic and Ison-infective Inflammations; (4) 
Septic and Infective Inflammations. 
SYMPTOMATIC INFLAMMATIONS. 
This class embraces the inflammations occurring in the acute 
fevers. Of the former, some are very trivial so far as the actual 
lesion in the skin is concerned. Thus the eruptions in measles, 
scarlatina, typhoid and typhus fevers consist of little more than an 
inflammatory hypersemia, with slight exudation. The action of 
the irritant on the epidermis is evidenced in many cases by the 
subsequent occurrence of desquamation, which implies that the 
cells have been so injured as to lead to their premature necrosis 
and discharge. 
In smallpox there is a much more severe inflammation. As 
the changes here afford an excellent example of the more pro- 769 
SYMPTOMATIC INFLAMMATIONS OF THE SKIN. 
nounced inflammatory lesions of the skin, and may be regarded 
as typical of the anatomical conditions in inflammatory skin erup- 
tions in general, they merit a more careful study. In this case 
the virus evidently lodges in the skin and multiplies there, leading 
to pronounced local changes. The fine particles, which we saw 
in a previous page to be the direct vehicles of the virus, are pres- 
ent in the smallpox eruption, especially in the earlier stages of the 
process, and it is evidently the products of their action that irritate 
the skin. 
The effects of the irritant are seen mainly in the epidermis, 
which show changes chiefly in the more plastic Malpighian layer. 
Many of the cells undergo a kind of coagulation-necrosis, their 
nuclei being lost and their substance converted into a hyaline 
material. These necrosed epidermic cells allow of spaces being 
formed among their layers, in which exuded fluid collects. In this 
way a vesicle is formed, but it does not consist of a single cavity. 
As shown in Fig. 329, the epidermic cells or their remains form a 
Fig. 329. 
Section of a smallpox vesicle. Superficially there is a network formed of the altered 
epidermis. In the meshes of this (b, b) are pus-corpuscles. For the most part the Mal- 
pighian layer in its deepest cells (c) is preserved, hut at some points, as at d, it is broken 
through, and the pus is infiltrating the skin, a, umbilication of the vesicle, due to a sweat- 
gland, the coils of which are distinguishable. X HO- (After Rindfleisch.) 
network of fibres and partitions which divide the vesicle into com- 
partments or loculi (b in figure), in which a serous fluid containing 
the fine particles already referred to is contained. As the inflam- 
mation increases in intensity leucocytes are exuded, and these 
accumulate, as seen in the figure, both in the superficial layers of 
the cutis (d) and in the loculi of the vesicle. By the aggregation 
of these the vesicle becomes a pustule. In the figure it is seen 
that while the papillary layer of the skin (d) is somewhat infiltrated 
with leucocytes, yet it is not destroyed, and the interpapillary pro- 
cesses of the Malpighian layer of the epidermis (c) still persist. 770 
DISEASES OF THE SKIN AND ITS APPENDAGES. 
Sometimes no further destruction occurs than this; the pustule 
dries in and a crust is formed, and under it the Malpighian layer 
forms new epidermis, so that when the crust is shed healing occurs 
without any loss of substance. But more commonly the action of 
the virus causes death of the superficial layers of the cutis as well 
as of the epidermis. This is shown in Fig. 330, where an injection 
Fig. 330. 
Smallpox eruption with necrosis, from an injected specimen. The normal skin at either 
side (a, a) has its vessels fully injected, while the necrosed part (b) is uninjected and homo- 
geneous. X 50. v®'INDFLEISCH0 
thrown into the arteries runs into the surrounding skin (a, <z), but 
does not penetrate into the slough (b). In this case, when the 
crusts are torn, little sloughs infiltrated with pus are revealed, on 
the removal of which ulcers appear. By the healing of the flat 
ulcers we have the depressed reticulated cicatrices characteristic 
of smallpox (the so-called pitting of smallpox). 
2. INFLAMMATORY SKIN ERUPTIONS. 
We include here all simple inflammations of the skin which do 
not depend on any traumatic or infective cause. 
(1) Erythema and Roseola.—These names are applied to mild 
inflammatory conditions in which the chief, and sometimes the 
only apparent, change is hypersemia. The inflammatory nature 
of the condition is, however, often indicated by the existence of 
more or less swelling, due to oedema of the superficial layers of 
the skin (erythema nodosum and papulosum). The attacks are 
frequently evanescent, hut are often followed by desquamation, 
which also evidences the inflammatory nature of the condition. 
These very mild inflammations are frequently somewhat gen- 
eralized, and appear in many cases to be, like urticaria, related to 
special conditions of the nervous system, especially, perhaps, of 
the vaso-motor nerves. They may also be produced by external 
irritants, especially in susceptible persons. 
(2) Eczema.—This name is applied to localized inflammations 
of the skin, usually of a subacute or chronic character. The mere ECZEMA. 
771 
fact of their local nature would indicate that the irritant here comes 
from without; but external irritation is hardly ever the entire ex- 
planation of the attacks. In no other disease do individual pecu- 
liarities and special states of the organism play a more important 
part. The external irritant may he very various, such as medicinal 
ointments, stuffs used by the patient in his occupation, as in dyeing, 
parasites which induce scratching, etc. The intensity of the in- 
flammation depends on the susceptibility of the patient and the 
character of the irritant. The various degrees of intensity are, to 
a great extent, distinguished by the characters of the eruption, so 
that we have papules, vesicles, pustules, etc., characterizing dif- 
ferent cases of eczema. 
If the irritation be very mild there is little beyond a patch of 
redness, with raised papules, depending on infiltration of the 
papillary layer of the skin—eczema papulosum. 
In cases where the irritation is more violent, there is partial 
necrosis of the epidermis, and vesicles form in the manner already 
described—eczema vesiculosum. 
A greater degree of inflammation will convert the vesicles into 
pustules—ECZEMA PUSTULOSUM. 
In the two forms last mentioned crusts are often formed, and 
sometimes, without any considerable formation of vesicles, scales 
and crusts form, so that the eczema is nearly dry and the surface 
scaly—eczema squamosum. On the other hand the vesicles may 
break, and as fresh exudation passes to the surface there may be a 
continual discharge—eczema madidaxs. The surface thus exposed 
is often very red and infiltrated, so the name eczema rubrum is 
given. 
These forms are not to be rigidly distinguished, and several of 
them may be present in the same case, there being papules, 
vesicles, pustules, crusts, and a weeping surface represented on 
the same patch. 
In what has gone before the conditions referred to have been 
chiefly those in subacute eczema. When the disease becomes 
chronic there are more permanent changes which may be compared 
to those in catarrh of mucous membranes. The inflamed surface 
usually keeps on discharging serous fluid, not always to the same 
extent. The epidermis is softened, and, to a considerable extent, 
lost, so that the cutis is exposed or covered with irregular crusts. 
The cutis itself is red and it is thickened both by the serous ex- 
udation and by accumulation of round cells. The skin, in fact, 
shows more or less the characters of a chronic inflammation with 
the usual new formation of connective tissue. 
When the inflammation subsides, there is, in the milder forms, 
a complete restoration. But where considerable infiltration of the 
skin has occurred there may be a very imperfect restoration of the 
papillse, the skin, as a whole, having somewhat of a cicatricial 
character. Hence the smooth homogeneous appearance some- 
times presented. The part is also not infrequently the seat of 
pigmentation. 772 
DISEASES of the skin and its appendages. 
(3) Psoriasis.—The nature of the irritant is in this case quite 
unknown, but it is probably to be found in some special condition 
of the blood. We know, at least, that remedies introduced into 
the blood (arsenic, and, according to Napier, chrysophanic acid 
administered internally) frequently cure the disease. 
The lesion is mainly of the epidermis, and especially of its 
Malpighian layer. The papillary layer of the cutis is hypersemic 
and partly infiltrated with leucocytes; the papillae are also described 
as enlarged, but these alterations are comparatively trifling, as, 
after death, very little indication of them is to be found. During 
life the hypersemia gives the corium a red color. In the middle 
regions of the Malpighian layer of the epidermis there is an 
abundant new formation of epidermic cells. This new formation 
is so great that there is no time for the cells to become horny 
before they pass to the surface. Hence the epidermis on the 
patch is entirely composed of Malpighian layer, and, these cells 
being soft, they adhere, as they dry much more readily into con- 
siderable scales than do the horny cells. For a similar reason, as 
they dry they shrink much more than the horny cells, and air 
insinuates itself in interstices between them. It is the finely di- 
vided air which gives the scales‘the peculiar silvery appearance 
characteristic of this disease (Rindfleisch). When the scales are 
removed the papillary layer of the skin is seen to be red and readily 
bleeds. 
(4) Pityriasis Rubra.—In this disease we have a more or less 
general affection, and it is not improbable that it depends on 
a lesion of the trophic centres of the skin. It is characterized by 
an excessive discharge of scales consisting of masses of epidermic 
cells. These scales pass off from slightly raised and reddened 
surfaces, which in the earlier periods are limited in size, but 
often extend till they cover nearly the entire body. In the earlier 
periods the cutis presents little more than hypersemia with excess of 
leucocytes in its papillary layer, but when the disease has lasted 
for some time there is thinning of it with flattening of the papillse. 
The sebaceous glands and hairs as well as the sweat-glands, are 
usually atrophied. There is often a very excessive discharge of 
epidermis, and the disease may lead by debility and marasmus to a 
fatal issue. 
(5) Lichen Ruber.—The designation lichen is frequently used 
to denote a simple papular eruption, and in this sense lichen 
simplex is nothing but eczema papulosum. Lichen ruber, on the 
other hand, is a diffused papular eruption, depending like pityriasis 
rubra on some obscure general cause. There is an inflammation of 
the skin, generally begining in patches, but sometimes extending 
till nearly the entire body is covered. There are individual red 
papules on a red basis. As the disease goes on, the skin gets 
infiltrated and thickened, so that the movements of the joints are 
hindered, and fissures are formed at the folds of the skin. On the ACNE 
773 
face the lines of expression are obliterated. The nails are usually 
thickened. In its details the disease seems to consist in an inflam- 
matory infiltration of the papillary layer of the cutis and the 
Malpighian layer of the epidermis. The cells of the rete Malpighii 
are enlarged and increased in number, and the interpapillary pro- 
cesses are enlarged. The papillae show abundant accumulation of 
round cells, especially around the vessels. There is often accumu- 
lation of epidermic cells in the hair-follicles. 
(6) Prurigo.—This also is a diffused affection of the skin, which 
somewhat resembles urticaria, except that it is more permanent. 
Like urticaria, it seems to depend on some condition of the nervous 
system, induced, especially among children, by neglect of sanitary 
conditions and defective nutrition. Numerous small papules 
appear on the skin, and they are intensely itchy. The papules are 
due to an inflammatory thickening of the papillae and rete 
Malpighii. There are round cells and a serous fluid exuded, so 
that when the head of the papule is removed by scratching a drop 
of fluid appears. The papules are often induced to bleed by 
scratching, and it is probably from this that they frequently leave 
a brown stain. The irritation produced by scratching may also 
lead to eczema. 
(7) Pemphigus.—This condition is characterized by the forma- 
tion of large vesicles or bullae filled with fluid, which is at first 
clear, but usually becomes more or less purulent. As the bullae 
usually occur at intervals over a considerable surface, the disease 
is to be ascribed to some general cause, and in some acute cases the 
existence of an irritant in the blood is suspected. There arise at 
first patches of a red color and slightly raised. The epidermis is 
then separated from the cutis by fluid accumulating beneath it. 
There is not here, as in smallpox, an exudation among the cells of 
the Malpighian layer, hut for the most part the whole epidermis is 
raised, and the bleb is not divided by septa into loculi. If the bleb 
remain unruptured, a layer of epidermis forms on the surface of 
the cutis. But if it burst, then the exposed cutis discharges for a 
time; by and by, however, a crust forms, under which the epider- 
mis grows. In some cases the blebs are imperfectly formed and 
neighboring ones coalesce, so that a considerable surface is affected. 
When these blebs burst there is little tendency to new formation 
of epidermis, and the skin continues discharging fluid as well as 
crusts produced by the fluid drying in. This form is designated 
PEMPHIGUS FOLIACEUS. 
(8) Acne.—This name is applied to inflammations of the seba- 
ceous glands and their neighborhood, chiefly in connection with 
accumulation of the secretion in the gland. There are two forms 
in which the accumulation of sebum occurs, named respectively 
comedo and milium, but it is chiefly in connection with the former 
that acne occurs. 774 
DISEASES OF THE SKIN AND ITS APPENDAGES. 
In comedo a sebaceous follicle is filled with secretion, which 
forms a solid plug in the gland. The end of the plug presents at 
the surface, and has a black or dark-blue color. It has been 
usually supposed that this color is simply due to dirt, but Unna 
has asserted that there is a true pigment concerned, whose compo- 
sition is allied to that of ultramarine, and whose color is destroyed 
by aqua regia. The plug can be readily pressed out by squeezing 
the skin around the gland; it emerges as a worm-like structure 
with a dark head. The plug consists of shed epidermis and sebum, 
with occasionally a small parasite, the acarus folliculorum. 
In milium there is an accumulation of the secretion with closure 
of the orifice of the gland. The accumulated secretion forms a 
rounded solid globe, which can be felt in the substance of the skin, 
but over which the epidermis passes unbroken. It is, in fact, a 
small retention cyst, and it contains the secretion of the gland 
mixed with epidermis, so that on cutting into it a whitish globular 
body is discharged. The cause of the closure of the duct is ob- 
scure. 
In acne there is a more or less acute inflammation of the sebace- 
ous glands, usually in connection with comedo. There are redness 
and swelling around, and pus is usually formed, and mingles with 
the substance of the comedo. Sometimes there is not a proper 
suppuration, but the substance of the plug is softened by the in- 
flammatory exudation. The inflammation is due to the irritation 
of the plug, especially when by long stagnation it has become foul. 
The name acne mentagra, or sycosis, is given to cases where 
there is inflammation of the sebaceous glands in connection with 
the hairs of the beard. There is a sycosis of parasitic origin, but 
in the simple form there is suppuration in and around the hair- 
follicles of the nature of acne. 
A more chronic inflammation of the sebaceous glands of the 
face, with special hypersemia of the vessels around, has received 
the name acne rosacea. There is very little tendency to suppura- 
tion, but great thickening of the skin occurs, so that sometimes 
there are large lobulated and red protuberances, especially on the 
nose, on the surface of which many comedones are seen. This 
disease is not uncommon in women, especially about puberty and 
at the climacteric period. In men it is often associated with dissi- 
pated habits. 
3. TRAUMATIC AND NON-INFECTIVE INFLAMMATIONS. 
(1) Burns and Scalds.—We include here the lesions produced 
by the application of excessive heat to the skin, whether the heated 
substance applied be in the solid, liquid, or gaseous form. The 
heat acting as an irritant damages or kills the tissue, and so we 
have signs of inflammation frequently associated with necrosis. 
Burns have been distinguished into three degrees, according to 
their intensity, and we have to consider the exact condition of the BURNS and scalds. 
775 
skill in each. The three degrees are characterized by these three 
phenomena—hyperaemia, vesication, sloughing. 
In the fir>t degree the heat is only sufficient to produce a hy- 
peraemia of the skin. Exposure to the rays of the sun, or to hot 
water of a temperature of 100° F. and upwards, causes such a re- 
laxation of the arteries as to induce congestion. The inflamma- 
tory nature of this hyperaemia is shown by its continuance for 
some time after removal of the cause, and by the occasional occur- 
rence of some cedematous swelling of the skin. After a time there 
may be desquamation. 
The second degree is produced by the action of a temperature 
of 140° to 185° F., or by the evanescent action of a still higher 
temperature. The effect is to cause a necrosis with swelling of 
the epidermic cells of the Malpighian layer, and an inflammatory 
exudation from the papillary layer of the skin. The changes in 
the rete Malpighii are similar to those already described as occur- 
ring in the formation of the smallpox vesicle, but they are more 
rapidly produced and the layer of cells is more homogeneously 
affected. The exudation, passing out from the papillae, separates 
the epidermic cells from the surface of the papillae, and a vesicle 
is thus formed. Usualty the interpapillary cells of the rete Mal- 
pighii escape destruction, but when the action is more intense they 
also may be killed. The inflammation soon subsides, and from 
the remaining cells of the rete Malpighii new epidermis is repro- 
duced; there may be already a complete coating of new epidermis 
before the vesicle bursts. But sometimes the vesicle bursts early, 
and the inflamed surface of the skin is exposed; or nearly the 
whole of the rete Malpighii may have been destroyed, even the 
interpapillary processes. In these cases the covering over of the 
surface with epidermis may be delayed, and the surface may even 
become like a granulating wound, discharging pus. 
In the third degree there is necrosis not only of the epidermis, 
but of the true skin to a greater or less depth. The temperature 
is over 140° F., and if very high may have acted for a very short 
time. As a general rule the necrosed tissue lies as a dry crust on 
the surface. An inflammatory process occurs around it, with exu- 
dation, going on usually to suppuration. In this way the slough 
is separated, and a granulating wound is left, which heals in the 
usual way, leaving a cicatrix, the character of which varies with 
the depth of the slough. 
Severe burns sometimes lead rapidly to death with symptoms 
of collapse. The explanation of this is not easy, but there are two 
conditions which affect the body in general which probably are 
the chief agents. When a part of the skin is exposed to a high 
temperature, the red corpuscles in the vessels perish, and they do 
so even in parts where the circulation persists. If the heat has 
acted for some time, then the blood in the vessels may have been 
frequently renewed and large numbers of corpuscles may have 
been destroyed. The red corpuscles yield their haemoglobin, 
which, as we have seen at p. 27, acts as a poison. Besides this, 776 
diseases of the skin and its appendages. 
the mere destruction of large numbers of corpuscles may seriously 
interfere with the respiratory functions. Again, the vessels of the 
skin are dilated after the occurrence of the burning. If the surface 
affected be large there may be, as a result of this, a serious loss of 
heat and reduction of temperature in the body as a whole. At the 
same time the dilatation of so many arteries may reduce the blood- 
pressure to a considerable extent. The combined action of these 
conditions seems to bring about the collapse after burns. 
If the person survives for some time after the burning, there 
are frequently found inflammations of internal organs, the lungs, 
kidneys, serous membranes; also fatty degeneration of the heart 
and of the liver. These are to be ascribed with great probability 
to the alteration of the blood. 
It is much more difficult to account for the occurrence of the 
duodenal ulcer after burns. When several weeks elapse before 
death, there is found in about twenty per cent, of the cases one or 
more ulcers, usually situated in the duodenum near the pylorus, 
but sometimes in the pyloric region of the stomach. It may be a 
superficial hemorrhagic erosion or a deeply penetrating ulcer. 
(2) Frostbite and Chilblain.—These conditions are produced 
by the action of excessively low temperatures. We can distinguish 
three degrees here also. 
The common chilblain is an example of the first degree. If 
portions of the body are exposed to a low temperature and then 
heated, a chronic or subacute inflammation is induced. This 
occurs especially in the Angers and toes. There is passive hy- 
persemia sometimes amounting almost to stasis, so that the part 
lias a livid hue. There is also serous exudation, so that the part 
is swollen and oedematous ; there may be red corpuscles as well as 
leucocytes in the exudation. Sometimes ulceration occurs. 
The second degree includes the less severe cases of frostbite. 
The skin has been frozen and too rapidly thawed, the result being 
such an injury to the tissue as to cause an acute inflammation. 
The epidermis is raised in blisters, which often contain a bloody 
serum. There may even be sloughing of the superficial layers of the 
cutis, and by the separation of the slough an indolent ulcer forms. 
In the third degree, forming the more severe cases of frost- 
bite, there has been prolonged exposure to very intense cold. 
The consequence is the complete freezing of part of the body, 
especially in regions removed from the heart, as the fingers and 
toes. The tissues are stiffened by freezing, and the blood coagu- 
lated, so that sometimes parts can be broken off like glass. When 
the parts are thawed gangrene sets in. The whole frozen part 
does not die, but there is partial recover}7 with inflammation. 
The gangrenous part is separated in the usual way, generally with 
decomposition (moist gangrene). 
(3) Boil and Carbuncle.—These names are applied to localized 
acute inflammations of the skin with partial necrosis. The boil or ULCERS. 
777 
furunculus occurs for the most part in persons who are debilitated 
or exhausted, but in addition to this we have to look for some local 
irritant. The fact that it begins in the neighborhood of a hair- 
follicle or sebaceous gland seems to suggest that accumulation of 
secretion may afford the irritant. The boil would thus be related 
to the acne pustule, the more intense inflammation in the former 
being related to the state of the patient. The inflammation 
manifests itself in hyperiemia and exudation, so that a localized 
redness and swelling are the result. A piece of skin in the very 
centre of the inflamed area dies, and a small abscess having formed, 
the slough is by degrees discharged along with the pus. 
The carbuncle or anthrax is similar in its general characters to 
the boil, but a much larger piece of skin is involved. The slough 
is therefore of much larger extent. It sometimes happens that the 
whole piece of skin in its entire thickness dies and is separated as a 
dry leathery slough. More frequently the necrosis is less extensive 
in the superficial layers, but more extensive in the deeper parts, 
and the slough is discharged through numerous small apertures. 
(4) Wounds and Excoriations.—The phenomona connected 
with the healing of wounds and the formation of granulations 
have been considered in previous pages. When merely a portion 
of the epidermis is removed by an injury, forming an excoriation, 
it is restored with remarkable celerity. The cells at the margin, 
and those of the deeper layers, divide and form new cells, which 
fill in the gap. In the case of a deeper wound, the epidermis also 
shows great vigor, and it sometimes advances beyond the line of 
the other healing processes. Dr. Macewen has pointed out to the 
author that the new-formed epidermis may advance over a blood- 
clot filling up a wound. The epidermis here has a remarkably 
transparent hyaline appearance, and is continuous, not with the 
Malpighian layer, but with the layers superficial to that. The 
character of the cells here and their transparency suggest that 
they may be derived from the stratum lucidum. It may, indeed, 
be suggested that this layer in the normal skin is composed of 
young epidermis, and that the loss on the surface is supplied by 
new formation here, and not in the Malpighian layer. 
(5) Ulcers.—By this name we understand losses of substance in 
the skin which are mostly in process of enlargement. The margin 
of the ulcer is inflamed and infiltrated with inflammatory products. 
The enlargement takes place by a gradual molecular necrosis of 
the inflamed structures, and it implies the continuous action of an 
irritant. The irritant is mostly an infective virus, and the majority 
of the ulcers will be again referred to under the next heading. 
The varicose ulcer, however, does not belong to this category. 
The original lesion here is a prolonged venous hypersemia, leading 
to oedema and infiltration of the skin. The nutrition of the skin 
is seriously compromised, and a trivial external injury may cause 
the epidermis to give way. The exposed and inflamed skin forms 778 
DISEASES OF THE SKIN AND ITS APPENDAGES. 
granulations, but these also, from the persistent venous engorge- 
ment, are readily destroyed by slight injuries, and the ulcer 
advances, while the inflammatory infiltration of the skin outside 
extends. The granulations will only proceed to healing in the 
usual way when the venous hypersemia is removed. 
In the case of infective ulcers there is also usually a granulating 
surface, which is gradually destroyed by the action of the virus. 
When the virus has been destroyed, the ulcer proceeds to heal 
like a granulating wound. 
4. INFECTIVE INFLAMMATIONS. 
We include here those forms of inflammation of the skin which 
can he traced to the action of specitic viruses. The syphilitic 
inflammations might be considered here, hut they will be taken 
up afterwards by themselves. 
(1) Lesions from Cadaveric Poisons.—In the juices of the dead 
body, when in process of decomposition, there are innumerable 
bacteria of different kinds. Some of these may attack the skin of 
the dissector or pathologist, and find a lodgement there. The 
organisms themselves are of very various degrees of virulence. 
If the subject has died of a septic disease, then the organisms 
which have during the life of the patient been active factors in the 
production of the disease may remain specially virulent after death. 
The fluid in the abdomen after septic peritonitis, such as that which 
occurs in one form of puerperal fever, teems with micrococci, and 
this fluid is peculiarly virulent when applied to the skin. So is it 
also with septic pleurisy, etc. 
Besides degrees of activity in the virus, there are various degrees 
in the susceptibility of different persons, and of the same person 
at different times. The frequent exposure to the cadaveric viruses 
creates a certain immunity, so that a person will be more secure 
against them when frequently engaged in post-mortem work than 
when making only an occasional examination. A. state of exhaus- 
tion of the body renders one much more susceptible, and makes 
the inroads of the virus when once implanted more vigorous than 
when in ordinary health. The inference from this is that the best 
treatment for this condition is to leave off’ work and at once seek 
rest and fresh air. 
The virus very often finds access to the skin without any breach 
of surface. When a wound is made during dissection it is usually 
washed thoroughly and sucked, while bleeding is encouraged; in 
this way the virus may be washed away. But if it gets into the 
hair-follicles or sweat-glands, it may lodge and multiply undis- 
turbed. 
The immediate effects are usually an acute localized inflamma- 
tion of the skin, resulting in the formation of a small pustule. 
The virus may have attacked at several points, and there is a crop 
of pustules, usually on the back of the hand or forearm where the ERYSIPELAS. 
779 
epidermis is thin, the left hand being more frequently affected 
than the right, as it is most frequently exposed in separating and 
holding the organs. In many cases nothing more than the pus- 
tules is produced, and in the case of the regular pathologist a crop 
of pustules in the spring may be his 
annual experience. The pus contains 
micrococci, some of them free, but some 
in the substance of the pus-corpuscles 
(see Fig. 331). 
Sometimes, however, there are more 
severe local effects, and sometimes the 
virus travels further inwards. Instead 
of dying away, the pustule, after par- 
tially disappearing, sometimes leads to 
an acute inflammation in a larger area 
around, so that a boil is the result. The inflammation is often so 
acute as to lead to a necrosis of a piece of skin, so that suppura- 
tion is set up and a slough is ultimately discharged. In this case 
there is a cicatrix left when healing occurs. In other cases it is 
what has been called a blind boil which develops after the pustule. 
There is a more chronic inflammation of the skin with considerable 
thickening and elevation. The surface of these elevations is often 
irregular and somewhat warty in appearance—the pathological 
wart. These, however, not infrequently develop without a pre- 
vious pustule, the virus acting slightly but continuously from the 
first. In all these cases the forces of the tissues seem sufficient to 
keep the virus local, although there may be some general disturb- 
ance of the body, perhaps from the absorption of the products. 
In some cases, however, the virus propagates itself upwards to- 
wards the trunk. It may he that an erysipelas starts from the 
local inflammation, extending upwards along the lymph-spaces of 
the skin. In other cases, the axillary glands become inflamed 
without any intervening lesions, the virus passing up the vessels, 
and only producing mischief after lodging in the glands. Here 
suppuration is common. An inflammation of the skin resembling 
erysipelas may spread from the glands, as the virus, checked in its 
upward course towards the trunk by the gland, passes outwards to 
the lymph-spaces around. This course of events is shown in the 
exquisite account which Paget has given of his own case in his 
Clinical Lectures and Essays. The inflammation may travel along 
the connective tissue of the skin and subcutaneous tissue, and may 
even reach the pleura. In the skin its effects may be very severe, 
resulting in sloughing and profuse suppuration like that in ery- 
sipelas. It may even lead to septic infection or pyaemia. 
Fig. 331. 
Pus-corpuscles with micrococci 
in them, from a cadaveric pustule. 
X 1500. 
(2) Erysipelas.—This is an acute infective inflammation of the 
skin. The virus depends on bacteria in the form of micrococci 
which extend more or less abundantly in the lymph-spaces and 
vessels of the skin (see Fig. 332) and subcutaneous tissue. The 
result is a more or less severe inflammation. At first there is an 780 
DISEASES OF THE SKIN AND ITS APPENDAGES. 
inflammatory hyperaemia, which advances as the virus propagates 
along the lymph-spaces. This, with a moderate exudation of fluid 
and leucocytes, may be all the phenomena. But sometimes there 
is much more intense inflammation. The skin is infiltrated with 
leucocytes to such an extent that it is softened and opened out 
Fig. 332. 
From the skin in a case of erysipelas. The upper illustration shows a lymphatic vessel at 
the border of a sebaceous gland, filled with micrococci. The lower shows a straight vessel 
similarly filled. X 350. 
with pus. The epidermis is raised by exudation, so that vesicles or 
pustules are formed. Sometimes the lymph-spaces are occupied 
with fibrine. Besides suppuration, there is often necrosis of por- 
tions of the skin, so that sloughs are separated with the pus. 
(3) Phlegmonous Inflammations.—These have very much the 
character of the severer forms of erysipelas, for which, indeed, the 
name phlegmonous erysipelas is used. The term phlegmonous is 
applied to inflammations of the skin of a very acute character, 
associated with sloughing. Such inflammations may be produced 
directly by the presence of virulent decomposing material in the 
skin and subcutaneous tissue, as where urine is extravasated and 
decomposed. But the condition may be more directly allied to 
erysipelas, depending on the gradual extension of micrococci in 
the lymph-spaces. This occurs mostly around septic wounds, and 
may be followed by abscesses at some distance from the wounds. 
Sometimes the virus is of such an intense nature that gangrene 
rapidly develops, being preceded only by an oedema. To this 
condition the name malignant cedema is sometimes given. 
(4) Splenic Fever or Anthrax.—This disease, as we have seen, 
depends on a special bacillus. There is usually a local affection 
to begin with, arid the disease may remain local. The local affec- 
tion has the characters of a phlegmonous inflammation of the skin 
and subcutaneous tissue. Sometimes the appearances of malignant INFECTIVE TUMORS. 
781 
(Edema are produced. From these local manifestations the condi- 
tion is sometimes called malignant pustule. As a general rule, 
the bacillus penetrates to the blood, and the patient dies from the 
general specific fever. 
(5) Infective Tumors.—Of these lupus, leprosy, and glanders 
have been sufficiently described in the general part of this work. 
Syphilitic diseases will receive special description in the next 
section. 
The name frambcesia is given to a disease which evidently 
depends on a virus which acts on the skin. There are prominent 
irregular swellings produced which have the general appearance 
Fig. 333. 
Section of skin in framboesia, from a part where the disease was not very far advanced. 
The papillary layer of the cutis is seen to be replaced by granulation tissue while the epi- 
dermis is preserved on the surface. X 75. 
of exuberant granulations. These have been compared in appear- 
ance to strawberries and raspberries. The local names yaws 
(African for raspberry) and pian (mulberry) also suggest these re- 
semblances. The disease is endemic in. the West Indies and 
Africa; it also occurs in Peru, where it is called verruga. It is 782 
DISEASES OF THE SKIN AND ITS APPENDAGES. 
contagious, and in many respects so much resembles syphilis that 
some authors have regarded it as the same disease. 
It begins as a small raised spot, usually on the face, on the 
upper or lower extremities, or near the organs of generation. The 
spot enlarges and gradually assumes the red irregular appearance 
which has suggested its names. It may continue for months or 
years, and, neighboring areas coalescing, it may affect a large 
portion of the cutaneous surface. 
The structure of these growths closely resembles that of the 
syphilitic chancre, as may be seen by comparing Fig. 833 with 
Fig. 48, p. 148. The cutis is converted into granulation tissue, 
whose bulky masses form the irregular prominences characteristic 
of the disease. The epidermis may be continuous over even the 
most prominent of these masses (see figure), and may even be ex- 
aggerated; but the horny layer is lost and the soft Malpighian 
layer alone remains. The epidermis may give way, and an ulcer 
form, from which a thin fluid is discharged, not usually a true pus. 
SYPHILITIC LESIONS OF THE SKIN. 
In the first part of this work it has been sufficiently indicated 
that syphilis depends on a virus, and that the various manifesta- 
tions in the skin are the results of the action of this virus. In 
regard to these lesions it has been stated that they are either simply 
infiammatory, or that they have the characters of the gumma, form- 
ing in the latter case more or less definite tumors composed of 
granulation tissue. Even the purely inflammatory lesions have a 
tendency, when they have persisted long, to present considerable 
new formation of granulation tissue. The syphilitic lesions of the 
skin may be divided into the primary, secondary, and tertiary. 
1. The hard chancre lias been already sufficiently considered 
at p. 148, and its structure is illustrated in Fig. 48, p. 148. 
2. Syphilitic Skin Eruptions.—We may, under this heading, 
group together the various secondary manifestations. It is to be 
remembered that here the virus is in the blood, and that, as a rule, 
the manifestations occur over the skin as a whole, although cir- 
cumstances may determine a certain local selection. The eruptions 
are for the most part symmetrical, and they present a peculiar 
tendency to occur in round patches. These patches by healing in 
the centres and extending at the periphery, frequently assume a 
circular or serpiginous shape. 
The syphilitic eruptions of the secondary stage are somewhat 
similar in character to the simple inflammatory eruptions, and they 
are commonly designated by similar names. There is, however, 
more tendency in the syphilides to the development of granulation 
tissue in the skin, and hence the papular forms of eruption are 
more frequent. The syphilitic eruptions present very various 
characters, and there is no form which is constantly present at a 783 
syphilitic lesions. 
particular stage. In the earliest periods there is usually a gen- 
eralized hypersemia of the skin (syphilitic erythema or roseola). 
A more local development of elevated papules, generally in groups, 
constitutes the syphilitic lichen. In these papules, the corium, 
especially its superficial layers, and to a certain extent the epi- 
dermis, are infiltrated with round cells; generally there is des- 
quamation of epidermis, and this is sometimes very prominent. 
Occurring in the palms of the hands and soles of the feet this 
desquamation is so characteristic as to give rise to the designation 
syphilitic psoriasis, the papules after a time coalescing and so 
merely producing a generally raised surface. 
The Condyloma (plaque muqueuse, mucous tubercle) is a further 
development of the papule. It occurs usually in situations where 
two surfaces of the skin are in contact and are thus kept moist, as 
in the neighborhood of the genital organs, in the axilla, beneath 
the mamma, etc. We have here a very marked and extensive in- 
filtration of the papillary layer of the skin with round cells, so 
that an elevated surface is formed. Sometimes there is a special 
elongation of the papillie, so that a warty surface is produced, 
giving rise to the pointed condyloma. Sometimes the condyloma 
breaks down on the surface and an ulcer forms. 
The syphilitic papules sometimes develop into pustules or 
vesicles. The pustule forms by the epidermis being raised from 
the surface, while a fluid inflammatory exudation occurs between 
it and the corium, which latter remains infiltrated with round cells. 
The pustule or vesicle and its infiltrated basis may enlarge so as to 
produce a broad bleb on a red raised base (syphilitic pemphigus). 
The blebs often dry in and form raised crusts (rupia). In these 
cases the pustules are as if on the surface of condylomata. This 
is still more the case in pemphigus neonatorum, which is one of 
the manifestations of hereditary syphilis. Here the corium is 
affected somewhat as in the condyloma, but the infiltration has 
more the characters of granulation tissue. In the condyloma the 
structure of the skin remains to a great extent, but it is infiltrated 
with round cells which are mostly leucocytes. In pemphigus 
neonatorum, however, the tissue is replaced by a vascular tissue in 
which are many large cells, the condition approaching to that of 
the gumma. On the surface of this the epidermis is raised, form- 
ing a vesicle or pustule. 
The Gumma.—This is not of very common occurrence, and is, 
as we have seen, a special tertiary manifestation. It begins as a 
hard swelling in the cutis. It increases in size and raises the sur- 
face, sometimes forming a tumor of considerable dimensions. It 
is peculiarly prone to ulcerate, and after ulceration has occurred it 
may go on extending, the infiltrated edges gradually giving way. 
The structure of the gumma has been described and illustrated at 
p. 150. 784 
DISEASES OF THE SKIN AND ITS APPENDAGES. 
TROPHO-NEUROSES OF THE SKIN. 
We include under this heading lesions of the skin in which, by 
reason of disease of the nervous system, such changes occur in 
the nutritive processes as to lead to definite anatomical results. 
The existence of separate trophic nerves for the skin has not been 
anatomically demonstrated. But there are evidences, especially in 
pathological processes, that trophic centres exist, and that fibres 
convey impulses of this kind to the cutaneous surface. The 
ganglia of the posterior roots of the spinal nerves and the similar 
Gasserian ganglion seem to contain trophic centres, and the trophic 
fibres are either identical with the sensory ones or run along with 
them. 
(1) Herpes.—This disease is typically of nervous origin. It is 
commonly accompanied by neuralgia, and in its site it nearly 
always follow's the distribution of a single nerve-stem. It appears, 
for instance, in the course of an intercostal nerve, or occupies one 
side of the face in the area of distribution of the fifth. 
The eruption in the skin is in the form of vesicles which some- 
what rapidly pass through a series of changes. There is first a 
group of slight elevations occupying a reddened patch of skin, and 
each of these rapidly develops a vesicle; in a few days the vesicle 
dries up into a crust, under which fresh epidermis is formed. In 
its details the eruption is inflammatory. There are hypenemia and 
oedema of the papillary layer of the skin. The serous exudation 
collects in the Malpighian layer of the epidermis, separating its cells 
just as in the case of the smallpox eruption. The vesicle is divided 
by a network composed of the elongated and contorted epidermic 
cells, which often present clear spaces or vacuoles in their sub- 
stance. In the serous contents of the vesicles there are leucocytes, 
and these may accumulate till the fluid approaches to the nature 
of pus. The papillary layer is also frequently the seat of infiltra- 
tion with round cells. Occasionally there is hemorrhage, and the 
papillary layer of the skin may be destroyed, so that when healing 
occurs by granulation a cicatrix may be the result. 
The nervous origin of herpes has been abundantly established. 
Direct injury to a nerve, as by a gunshot or other wound, may 
cause it. It is to be presumed that, in this case, the inflammatory 
process in the wound irritates the nerve, and the cutaneous in- 
flammation may be regarded as due to the irritation of trophic 
fibres. Spontaneous herpes, and especially herpes zoster, has 
been found associated with inflammations of the intervertebral or 
Gasserian ganglia, but it has been questioned whether the trophic 
centres have actually their seat there. 
The herpetic eruption may arise from disease of the spinal cord 
and brain. In the case of the cord it is chiefly in locomotor ataxia 
that we meet with herpes, and the eruption is accompanied by the 
severe pains characteristic of that disease. We know that in loco- 
motor ataxia it is the posterior columns of the cord that are MORPHCEA AND SCLERODERMA. 
785 
affected, and this would indicate that the cutaneous trophic centres 
or fibres run in these parts, while the coincidence of neuralgic 
pains also indicates a sensory locality. It is here again to he pre- 
sumed that the lesion producing the herpes is an irritative one, as 
indicated by the violent coincident pains. 
But we may have herpetic eruptions from disease in the brain. 
There are cases recorded in which one-half of the body was 
affected, and in some of these there was a hemiplegia due to a 
coarse lesion in the brain. It is clear that there must be trophic 
fibres and centres in the brain as well as in the cord, and their 
irritation may lead to herpes. There are also a few cases on 
record of universal or nearly universal herpes, as if a general 
centre for the whole body were irritated. 
(2) Glossy Skin.—This name was applied by Paget to a condi- 
tion which he observed in connection with injuries or wounds of 
the nerves. There is here again indication of irritation of the 
nerves, as there is always neuralgic pain, described by Mitchell as 
burning pain. The condition also occurs sometimes after an attack 
of herpes (Paget), and it may be associated with eczema. It may 
also follow disease of the spinal cord (Mitchell). 
The disease occurs mainly in the hand, and especially in the 
fingers. The affected fingers “are usually tapering, smooth, hair- 
less, almost devoid of wrinkles, glossy, pink or ruddy, or blotched 
as if with permanent chilblains” (Paget). The most striking pecu- 
liarity is the shining, glossy appearance of the surface, as if it had 
been varnished. The comparison to chilblains is usually applicable, 
but sometimes the appearance is rather that of highly polished 
scars, and the condition resembles that in morphcea. In the affected 
part the hairs mostly disappear, and the nails undergo peculiar 
changes. The latter become greatly curved, much more than in 
cases of phthisis, while the skin at the root of the nail becomes 
retracted, leaving the sensitive matrix partly exposed. The dis- 
ease affects mainly the fingers and toes, but it may extend to the 
palm of the hand or the dorsum of the foot. The histological 
details in this condition are unknown. 
(3) Morphcea and Scleroderma.—These names are applied to 
denote conditions which are sometimes regarded as of a different 
nature, but the presumption is that they are virtually the same 
disease. 
The nervous origin of the disease has been brought prominently 
forward by Hutchinson on the ground that it usually occurs in 
defined patches, often distinctly following the distribution of par- 
ticular nerves. But sometimes the disease is more extensive, and 
it may be almost universal. The same may be said, however, as 
regards herpes, and it does not invalidate the supposition of its 
nervous origin. 
When the disease is in the form of patches it is often described 
as morphcea or Addison’s keloid. The patches have the char- 786 
DISEASES OF THE SKIN AND ITS APPENDAGES. 
acters of induration and stiffening of the skin; they are mostly 
white and ivory-like, hut may have a yellowish or mottled appear- 
ance. The greatest peculiarity is the hardness, as if the skin were 
frozen. The skin is sometimes bound down to the parts beneath, 
the induration extending to the subcutaneous tissue, and even 
deeper, and in that case there may he considerable interference 
with motion and even deformity of limbs from contraction of the 
skin. 
In the more diffuse form of scleroderma proper, extensive 
tracts of skin are sometimes involved, such as the greater part of 
the face, the arms, etc. In a ease observed by the author, the 
face, chest, and both forearms and hands were affected, and dry 
gangrene had occurred in the fingers, which had a stiff black 
appearance. 
In its anatomical details the skin presents characters which may 
be summarized as atrophy with chronic inflammation. The pa- 
pillae are mostly flattened, and the cutis thinner than normal, but 
it is composed of more homogeneous connective tissue than usual, 
having somewhat the characters of cicatricial tissue, and less 
fibrous than that of the normal skin. This condition extends 
somewhat to the subcutaneous tissue, where the fat is to a con- 
siderable extent atrophied, apparently by the encroachment of the 
connective tissue. The hairs are also atrophied in the affected 
areas, and there is said to be alopecia when the patches extend to 
the hairy scalp. The evidence of chronic inflammation is the 
existence of abundant nuclei in the altered skin. These are usu- 
ally aggregated around the bloodvessels, but they are also seen 
around sebaceous glands and under the rete Malpighii. 
It will be seen from the above that the changes here are to a 
great extent comparable to those which occur in muscle after 
destruction of its trophic centres; there is atrophy with chronic 
inflammation. 
An endeavor has been made to associate this disease with stasis 
of lymph, and relate it to elephantiasis. Some also regard it as 
allied to leprosy. We have already seen that both elephantiasis 
and leprosy are diseases probably dependent on specific irritants, 
and that they are endemic in particular localities, whereas this is 
in no sense true in regard to scleroderma. 
Allied to scleroderma in the general characters of the lesion in 
the skin is the condition commonly designated sclerema neona- 
torum. In this disease the skin, usually of the lower extremities, 
is hard and swollen, so that movement of the limbs is curtailed. 
When it persists for some time the skin may be like parchment. 
In the earlier stages the skin is oedematous, while in the later 
there is thickening from new formation of connective tissue. The 
disease occurs, as the name implies, in new-born children, being 
sometimes congenital. The children are weakly and usually die 
in a few days. ICHTHYOSIS. 
787 
(4) Bedsores.—Besides the ordinary bedsores which occur in 
persons who lie long in one position, especially when cleanliness 
is not attended to, there are some which are obviously related to 
nervous lesions. The acute decubitus is met with in connection 
with lesions of the spinal cord or brain, usually in severe cases, 
such as cerebral hemorrhage or injury to the cord. The appear- 
ances presented in the skin are those of an acute phlegmonous 
inflammation with sloughing. At first there are simple oedema and 
hyperaemia, but vesication follows and deep ulceration. The 
sloughing may extend to the muscles, tendons, etc., sometimes 
laying bare the bones. These acute bedsores imply a grave lesion 
of the trophic fibres, and there are indications that these follow 
the course of the sensory fibres. .Bedsores have been observed, 
for instance, in unilateral lesions of the cord where there were 
paralysis of motion on one side and anaesthesia on the other; in 
that case the bedsores are on the anaesthetic side. 
HYPERTROPHIES AND TUMORS OF TPIE SKIN. 
The Callosity is an exaggeration of the horny epidermis occur- 
ring where the parts are exposed to unusual friction. It is a true 
hypertrophy, being a direct provision of nature to protect the true 
skin from the excessive friction to which it is exposed. The best 
example of the callosity is in the horny hands of workmen, but it 
is often seen in the feet, at points which are much exposed to 
pressure. 
The corn (clavus) is closely related to the callosity. Here, also, 
there is friction, but it is associated with compression. It occurs 
chiefly in the foot, where there is a concentric pressure from ill- 
fitting boots, and friction against either the boot or a neighboring 
toe. There is, as in the former case, an excessive new formation 
of horny epidermis, but, by the concentric pressure, the layers of 
epidermis have their directions changed, and growing against each 
other are projected inward towards the cutis. There is thus an 
ingrowing kernel of hard horn}7 epidermis which has given rise to 
the name of corn. The cutis is irritated and undergoes atrophy. 
Around the kernel the epidermis is always thickened, the condi- 
tion being like that of the callosity. 
Ichthyosis.—This is a disease which apparently owes its origin 
to a congenital defect in the structure of the skin. The disease 
itself is sometimes manifest at birth, but if not it begins in the 
earlier years of life, gradually extends over the whole body, and 
continues during life. 
It consists, anatomically, in an exaggeration of the horny layer 
of the epidermis, which is sometimes greatly thickened. The 
thickened horny layer forms scales of larger or smaller size, some- 
times producing merely a furfuraceous exfoliation, but in more 788 
DISEASES of the skin and its appendages. 
severe cases giving rise to large plates like fisli-scales. From this 
latter appearance the name of the disease is derived. The scales 
do not consist entirely of epidermis, but contain sebaceous material, 
which is sometimes so abundant as to give the scales a polished 
appearance like mother-of-pearl. The large scales may be fixed in 
their peripheral or middle parts, and project considerably at their 
edges, so as to give an imbricated appearance. The milder forms 
of the disease, in which there is little more than an excessive 
scaliness of the surface, are often included under the designation 
ichthyosis simplex or xeroderma, while the more severe forms, in 
which there are prominent scales, are distinguished by the name 
ichthyosis cornea or ichthyosis hystrix. 
In the milder forms the cutis is not markedly affected, but in 
some cases the papillae are greatly elongated. The substance of 
the corium is often atrophied, and the subcutaneous fat deficient. 
The common wart may be variously regarded either as a tumor 
or a hypertrophy of the skin. There are warts which have dis- 
tinctly the characters of tumors, presenting specialties of structure 
and growth which entitle them to that designation. But the 
common wart, consisting for the most part of local exaggeration 
of the normal structures and occurring in numbers in the same 
person, has more doubtfully the characters which we ascribe to a 
morbid growth. A group of papillae are elongated, and the epi- 
dermis over them thickened, so that the characters are those of a 
hard papilloma. The horn is of similar structure to the wrart, but 
the papillae are usually more elongated, while the horny layer of 
the epidermis forms a more consistent mass which grows into a 
prominent outgrowth. 
The true Keloid is an elevation of the skin which has in its 
marginal parts branching processes extending out. There are 
evidently considerable contraction and dragging on the part of the 
central tumor and of the radiating processes, so that the skin is 
puckered around as in the case of a contracting cicatrix. The 
lesion has many of the characters of a definite tumor. It is com- 
posed in the fully developed state of dense connective tissue which 
may be unduly cellular. The new formation has its seat in the 
deeper layers of the cutis, and it is stated that the papillary layer 
is intact. In the earlier stages it consists mainly of spindle cells, 
and Virchow therefore regarded it as a sarcoma. The analogy to 
the sarcomas is supported by the fact that the tumor recurs on re- 
moval. The most common site of keloid is the front or back of 
the chest, but it is found in other parts. 
The name false keloid is sometimes used to designate a condi- 
tion which occurs in scars. A localized thickening, usually in the 
midst of a large cicatrix, as from a burn or an ulcer, presents 
itself, and there are raised processes passing out from it as in the 
true keloid. FIBROMA MOLLUSCUM. 
789 
Soft Warts and Pigmented Moles (ncevi pigmentosi).—These are 
very often congenital, or they occur very early in life, and usually 
remain stationary throughout life. They are smaller or larger 
elevations of the skin, either colorless or pigmented, and frequently 
beset with hairs. They present a somewhat peculiar structure, 
especially considering that they exist unchanged for many years. 
They are covered by epidermis which shows little difference from 
the normal. But instead of the normal tissue of the cutis beneath 
the epidermis, there are masses of cells separated by connective 
tissue. The cells in these nests are usually large and resemble 
epithelial cells or large sarcomatous cells. The presumption is 
that these structures are really survivals of the foetal condition, 
and their importance in relation to tumors has already been 
referred to at p. 171. In their structure it will be observed that 
these warts are much more like tumors than the ordinary warts, 
and that their tissue conforms to that of the cellular tumors, prob- 
ably the sarcomas. 
Molluscum Contagiosum.—This name is applied to little growths 
of the skin, occurring chiefly on the face and showing a preference 
for the eyelids, but sometimes extending so as to be almost uni- 
versal over the body. It will be inferred that the growths are 
multiple. The individual ones have been compared to pearl 
buttons, which they resemble in their circular shape and central 
depression, but they are usually pink in color. There is consider- 
able elevation of the little growth, and, although generally sessile, 
it sometimes becomes pedunculated and may even drop off. 
In the centre of the elevation a depression is visible which is the 
oriflce of a sebaceous gland, and the tumor consists of an enlarged 
sebaceous gland. A section of the growth shows the exaggerated 
lobules of the gland, while within there is an irregular cavity con- 
taining white sebaceous material which sends prolongations into 
the gland lobules. The lobules of the gland consist of epithelium, 
the peripheral cells of which are cylindrical. In the midst of the 
sebaceous material are found peculiar glancing bodies, compared to 
swollen starch-granules. 
The disease depends on some virus, and, as the name implies, it 
is contagious. It generally occurs in groups in the same person, 
as if spreading, and several members of the same family, or several 
persons living together, are usually affected simultaneously. It is 
usually seen in children, but occurs also in adults. 
Fibroma Molluscum.—This condition is to be carefully distin- 
guished from that just mentioned. We have here also multiple 
growths, but they are definite fibrous tumors having their seat of 
origin in the cutis. When small they may lie embedded in the 
cutis, but as they increase in size they become prominent, and 
may finally assume a pendulous condition. They are sometimes 
present in enormous numbers, the individual growths varying in 790 
DISEASES OF THE SKIN AND ITS APPENDAGES. 
size from very small tumors up to those having even the bulk of 
a man’s head. 
The epidermis is usually unchanged on the surface of the tumor. 
The tumor consists of connective tissue in which there may he an 
excess of small spindle-shaped cells. To the naked eye all the 
characters of a hard fibroma are presented. 
It appears from the observations of Recklinghausen that these 
multiple fibromas of the skin are often associated with multiple 
fibromas of the nerves. The structure in the two cases is the 
same, namely, a soft connective tissue, rather more cellular than 
normal. The fibromas of the nerves are often described as neu- 
romas, but, as they contain no new-formed nerve-tissue, they are 
false neuromas. From these observations there seems reason to 
suspect that the tumors in the skin have their origin in the nerves 
of the skin, and that they also are primarily false neuromas. 
Looking to this probable origin of these tumors, they may, per- 
haps, along with those of the nerves, be grouped as multiple 
neurofibromas. In several cases of this kind a distinct hereditary 
tendency has been observed, and some of the tumors are often 
congenital. 
Elephantiasis.—This condition has been already described at 
p. 176. It may be added here that a condition somewhat resem- 
bling elephantiasis, and designated lymph-scrotum, is sometimes 
brought about by obstruction of the lymphatics. There are dilata- 
tion of the lymphatics and formation of vesicles, and there may 
be, after a time, a thickening of the skin, hut without the attacks 
of acute inflammation characteristic of elephantiasis. This con- 
dition (which has been named elephantiasis lymphangiectodes) is 
usually the result of the filaria in the lymphatics, and has already 
been referred to (see p. 282). 
Xanthoma, or Xanthelasma.—This name is applied to slight 
elevations of the skin of a yellowish color. They occur mostly 
on the eyelids, where they appear as firm yellow patches, which 
are usually quite flat, but may be slightly tuberculated. They 
consist of firm connective tissue in which finely divided fat-gran- 
ules are abundantly present. The latter give the opaque yellow 
character to the lesion. 
Of the remaining simple-tissue tumors, the lipoma is common, 
originating in the subcutaneous tissue. The myxoma is not infre- 
quent, and- the enchondroma and osteoma very unusual. The 
angioma of the skin is common as the congenital naevus (see 
p. 193). 
Sarcoma.—This form of tumor is of somewhat frequent occur- 
rence, and we may have round-celled or spindle-celled growths, 
which sometimes assume considerable dimensions. We have 
already seen that sarcomas sometimes originate from soft warts or CANCERS. 
791 
moles, and, when they do so, they frequently present a similar 
structure to that described above, namely, masses of large round 
cells in a stroma. To this form the name alveolar sarcoma is 
applicable. Sarcomas originating from moles are peculiarly apt 
to be pigmented. 
Sarcomas rarely occur as secondary tumors in the skin, but a 
case is known to the author where multiple tumors composed of 
round-celled tissue formed at intervals in the subcutaneous tissue 
and some of them disappeared. These were either round-celled 
sarcomas or lymphosarcomas. 
Cancers.—The epithelioma of the skin forms the majority of 
the flat-celled epitheliomas, and it has been already referred to at 
p. 215. 
In the skin, two forms of epithelioma have been distinguished, 
one in which the cancer cylinders tend to penetrate deeply into 
subjacent structures, and the other in which there is rather a 
tendency to extend along the surface. The one form is sometimes 
called infiltrating cancer, the other flat cancer. 
The infiltrating epithelial cancer has its most familiar seat in 
the lower lip. Beginning as a slight thickening, it gradually 
Fig. 844. 
Section of an epithelioma at its marginal part. The epidermis is seen to be penetrating 
inwards into the cutis. At a a small laminated capsule is indicated. X 100. 
extends, producing a knotted, thick appearance. The surface 
ulcerates, and a scab forms. On making a section through such 
a tumor an appearance is presented as of a wart growing inwards, 792 
DISEASES OF THE SKIN AND ITS APPENDAGES. 
and the material of which it is composed has a brittle, crumbling 
appearance. Under the microscope, it is seen at the margin that 
the epidermis is growing downwards, the growing cells having the 
characters of those of the rete mucosum (see Fig. 334). The 
growth is in cylinders, and as it progresses there seems to be a 
mutual pressure of the cylinders, causing great compression of 
the central cells. To this cause, and perhaps also to a tendency 
to degeneration on the part of the cells, is due the formation of 
the peculiar glistening epithelial globes, or laminated capsules, 
which are so prominent in many cases (Fig. 335). These globes 
Fig. 335. 
Parts from an epithelioma, a, isolated epithelial cells; b, a cylinder composed of epi- 
dermis, and with many laminated capsules; c, a laminated capsule opened out so as to show 
the cells composing it. From a fresh preparation with the addition of dilute acetic acid. 
X 400. (Billroth.) 
consist of epidermic cells wrapped round a common centre, and, 
when they are disintegrated, the cells may retain their curved 
shapes. The epithelial cylinders may penetrate very deeply, and CANCERS. 
793 
usually cause great irritation, evidenced by the presence of round 
cells in the tissue, as in Fig. 386. 
In the scrotum the cancer is very much as it is in the lips, having 
the infiltrating character. It is met with principally in chimney- 
sweepers, but also in Glasgow among workers in paraffin refineries. 
Fig. 336. 
Portions of three cylinders of an epithelioma, embedded in round cells produced 
as a result of irritation of the cutis. X 200. 
At the edges of the scrotal cancers there is often some enlargement 
of the papillae. 
In other parts of the skin it is generally the flat form which is 
met with. The epithelioma tends to spread laterally rather than 
deeply, so that it may come to cover a considerable surface, which 
is often circular in form, with raised warty-looking edges. On 
examining these edges under the microscope it is often seen that 
there are series of elongated papillae. The central parts are 
ulcerated, hut even here there is an appearance as if papillae had 
been cut otf at their bases. Sometimes these flat cancers appear to 
take origin in the sebaceous glands, and to grow rather by an 
exaggeration of them than of the surface epithelium. All flat 
cancers of the skin grow slowly, and sometimes they cicatrize in 
their central parts while slowly extending at their edges. 
In the flat form ulceration very often overtakes to a large extent 
the new formation, so that the lesion presents itself as an ulcer 
with infiltrated margins, and is often called rodent ulcer. Some- 
times healing occurs in the central parts, a cicatrix forming, while 
the ulcer extends peripherally. At other times the ulcer goes on 794 
DISEASES OF THE SKIN AND ITS APPENDAGES. 
extending. In these cases with the ulceration there is a great new 
formation of inflammatory tissue, and this may greatly obscure the 
epithelial elements, which, however, are to be found in nests of 
large flat cells. The flat ulcerating form occurs mostly in old 
people, and does not usually lead to secondary tumors in the lym- 
phatic glands. The rodent ulcer occurs on the face, especially on 
the eyelids and side of nose. 
Ordinary cancer is of rare occurrence in the skin, but cases 
have been observed to which the names scirrhus and soft cancer 
have been given. Pigmented cancers are of occasional occurrence, 
and they are of importance on account of their tendency to form 
secondary tumors, first in the lymphatic glands and then through- 
out the body. They are, however, much less frequent than 
melanotic sarcomas, with which they are apt to be confused. 
PARASITIC DISEASES OF THE SKIN. 
We have already seen that certain forms of inflammation are 
associated with the presence of micro-organisms, especially the 
infective inflammations. We saw also that leprosy depends on a 
specific bacillus. These do not require further treatment here. 
Fungi are present in three forms in the skin. It has already 
been indicated that many are of opinion that the same fungus 
is at the basis of all three forms, and that this fungus is the o'idium 
lactis. But if this be the case it seems strange that the three 
varieties keep perfectly distinct, and that when the diseases are 
communicated from person to person they do not interchange. 
1. Tinea Favosa or Favus.—This is a disease chiefly of the 
hairy scalp, although it occurs on other parts of the skin and also 
Fig. 337. 
The fungus in favus. Short threads are shown. X 350. 
in tlie nails. On the scalp it forms crusts which at first are isolated 
and about the size of split-peas. They are circular in shape, pale- TINEA TONSURANS. 
795 
yellow in color, and dimpled in the centre through which a hair or 
hairs generally pass. When removed the crusts are usually seen 
to he somewhat cup-sliaped, the convexity of the cup being next 
the skin, the latter presenting a corresponding depression. If the 
cups be divided with a knife they are seen to have a porous 
appearance, the interstices being tilled with air, and they are 
brittle, so that they can be easily broken down in water. 
The crusts are formed of fungus along with epidermic scales 
and their debris. The fungus is the aciiorion Sciioenleinii, in the 
form for the most part of short tubes (Fig. 337) with rows of 
conidia spores.- The proper mycelium is not jointed, but the 
receptacula are. The fungus appears to begin its growth in the 
hair-follicles, enveloping the hair and passing into it. It also 
Fig. 388. 
Hair from tinea tonsurans. The shaft is penetrated and broken up by spores. X 350. 
passes into the hair-sheath and epidermis around, separating the 
eells and destroying them. It has its seat thus in the first instance 
beneath the horny layer, which may be continuous over it. It 796 
diseases of the skin" and its appendages. 
does not invade the true skin, but the crust may cause inflamma- 
tion around it which may go on to suppuration and ulceration. 
As a rule, however, it only affects the epidermic structures, the 
hairs being largely destroyed where the crusts are developed. 
When it attacks the nail, it forms a yellow crust, the tissue of 
the nail being opened out and softened by the fungus penetrating 
between the horny cells. 
2. Tinea Tonsurans.—This is also a disease chiefly of the scalp, 
but the same fungus attacks the beard and the parts of the body 
devoid of hair. The disease is therefore divisible into three forms, 
TINEA TONSURANS PROPER, TINEA SYCOSIS, and TINEA MARGINATA. 
In tinea tonsurans, or ringworm, there are circular patches on 
the scalp, in which the hairs are short and small, as if the hair 
had been badly cut. The fungus, called the trichophyton ton- 
surans, is here chiefly in the form of spores (see Fig. 338) which 
infiltrate the hair and its sheath, as well as, to a less extent, the 
epidermis around. The mycelium is only represented by short 
threads. The hair-shaft is greatly penetrated by the spores, which 
break it up. 
In tinea sycosis, or ringworm of the beard, the fungus is again 
chiefly in the form of spores in the hairs and hair-follicles, but 
here it produces great irritation, so that pustules and papules 
form. 
In tinea marginata, or ringworm of the body, there are patches 
generally more or less circular or crescentic in shape, and consist- 
ing of vesicles on a raised surface, or simply scaly elevations. In 
this form the fungus develops mycelium abundantly, whose threads 
pass among the epidermic cells. The spores are much less abun- 
dant than in the other two forms. The name eczema marginatum 
has been given to what is really a severe form of the condition 
which we are now considering. 
Fig. 339. 
Fungus in pityriasis versicolor. Threads are seen with groups of spores. X 500, 
(Duhring.) 
3. Pityriasis Versicolor.—In this disease there are patches of 
a yellowish or dark-brown color with a scaly surface, and occur- SCABIES. 
797 
ring chiefly oil the trunk in adults. If the surface he scraped, 
and the scaly products examined under the microscope (best with 
the addition of liquor potassie, both in this case and the others), 
there will be found epidermic cells with the elements of a fungus, 
the microsporon furfur. There are usually abundant mycelium 
threads, and the spores are in rounded masses which have been 
compared to bunches of grapes (see Fig. 339). 
Of the lesions due to animal parasites, the most important is 
scabies. 
Scabies.—This disease is characterized by the formation of 
papules, vesicles, pustules, and other signs of inflammation due 
to the effects of the acarus scabiei or sarcoptes hominis. The 
female of this insect penetrates into the substance of the epidermis. 
It forms a tunnel for itself as it penetrates, and in this it deposits 
ova and feces, the latter in the form of brown granules. It usually 
passes through the horny layer into the rete Malpighii, sometimes 
approaching the surface of the papillae. It opens up the epidermis 
and causes irritation, evidenced by intense itching. 
The inflammatory conditions are the result partly of the irrita- 
tion of the acarus and its embryos, which, as they develop from 
the ova, begin to travel along the tunnels, and partly the effect of 
the scratching induced by the itching. The primary lesion is a 
papule on which a minute furrow is visible to the naked eye. The 
papule is produced by the opening up of the epidermis and swell- 
ing of the papillary layer, which is infiltrated with serous fluid 
and round cells. Vesicles and pustules are produced when the in- 
flammation is more severe, and are met with chiefly in children 
and persons with delicate skins. 
The acarus folliculorum is an insect sometimes met with in 
comedones. 
The LARViE of insects are occasionally met with in the skin. 
The ova are deposited in the skin, and the larvse having developed, 
may traverse the skin and subcutaneous tissue for a considerable 
distance till they present at some part and are squeezed out or ex- 
tracted. They may produce considerable inflammations in the 
form of boils or swellings. ADDENDUM. 
ACTINOMYCOSIS. 
This disease should have been considered under the heading of 
parasitic fungi, but was overlooked. 
The disease occurs chiefly in cattle, and occasionally in pigs, hut 
it has been met with in a certain number of cases in man. It 
depends on the existence of a fungus whose exact botanical posi- 
tion is unknown. The fungus is in the form of short threads 
which are clubbed at their extremities. These threads, which are 
perhaps conidia, are arranged in a radiating fashion, many spring- 
ing from a common centre, with their clubbed extremities out- 
wards. They thus form peculiar radiating groups of a globular 
or oval form, which, being made up of club- or wedge-shaped 
pieces, present a peculiar glandular or knobbed surface, like that 
of a mulberry. The club-shaped fibres are united in the centre 
by a matted mass of fibres, which may be the mycelium. It is 
from these radiating structures that the fungus has received its 
name of Ray-fungus or Actinomyces (anrig, a ray), and the disease 
that of Actinomycosis. 
The radiating clumps are individually of very small size, like 
grains of dust, but the}7 are usually united into larger masses as 
the heads in a cauliflower (Ponfick). These larger masses are the 
characteristic indications of the disease, appearing to the naked 
eye as yello\v, sulphur-colored granules in the midst of the 
structures about to be described. 
The disease was first described and named by Bollinger, in 
1877, lie having distinguished it in cattle, in which it seems some- 
what common in certain localities. Its occurrence in the human 
subject has been established, chiefly by the observations of Israel 
and Ponfick. 
In cattle it mostly appears as a tumor-like swelling of the jaw, 
most commonly the lower jaw7. It growrs outwards to considerable 
dimensions, forming a simple or lobulated tumor. After a time 
the skin gives way, and a prominent projecting mass protrudes, 
which discharges a thick pus with pieces of slough. In this dis- 
charge are visible little sulphur-yellow granules, which are some- 
what firm in consistence, and have a greasy feeling. These are 
the fungous masses already described. The new formation may 
extend from the jaw7 to the tongue, pharynx, larynx, oesophagus, 
stomach, and intestinal wTall. ACTINOMYCOSIS. 
799 
The disease is communicable by inoculation from one animal to 
another. The rabbit and dog seem to be incapable of inoculation, 
but cattle are highly susceptible. It may be produced by inocula- 
tion into the subcutaneous or intermuscular tissue, and produces 
its effects in a very striking manner when inoculated into the 
peritoneal cavity. When introduced into the blood it produces 
typical new formations in the lungs. 
In man the disease is induced apparently by accidental inocula- 
tion, usually by a wound in the mucous membrane of the mouth 
(as from extraction of a tooth) or pharynx, but possibly by a wound 
in the skin. When so induced it produces swellings, as in cattle, 
but these do not usually grow to such bulky tumors, as they break 
down more readily so as to form abscess-like cavities which open 
externally and give rise to-fistulre. The disease may remain local, 
affecting, it may be, the jaws and surrounding parts. On the other 
hand, it may extend slowly till it involves the bodies of the verte- 
brae or the pleura. In such cases the introduction is probably by 
the pharynx. In these internal parts it produces a slow inflam- 
matory process with exuberant granulations and chronic suppura- 
tion. When it affects the vertebrae, which it seems to do with 
peculiar frequency, these become carious, and a chronic abscess 
forms which may gradually extend to the surface and open in the 
lumbar region or the groin. In these cases the person becomes 
slowly emaciated, and dies after months or years from exhaustion, 
sometimes with amyloid disease. In some cases there has been a 
metastasis, so that abscess-like formations have occurred in various 
organs, and the case has been like one of pyaemia. In all these 
situations the sulphur-yellow granules are found, and they are to 
be recognized in the pus of the abscesses, etc. 
Looking more closely at the anatomical details in this disease, 
it is clear that we have to do with a specific irritant. The most 
direct effect of the action of this irritant is the formation of 
granulation tissue. In cattle this is so abundant that a bulky 
tumor is produced, which, from its structure, might be taken for 
a round-celled sarcoma. In man the granulation tissue is not so 
exuberant, although produced abundantly, and when the abscesses 
find their way to the surface the granulations pout at the opening 
like those of a sinus leading from a scrofulous joint. Looking at 
this great new formation of granulation tissue and at its tendency 
to break down, Ponfick has suggested that the disease should be 
placed among the infective tumors. The granulation tissue here 
resembles that in the infective tumors, not only in its exuberance 
and tendency to break down, but also in its tendency to form con- 
nective tissue in an irregular way. In the midst of the masses of 
granulations there may be strands of coarse connective tissue. IN D E X. 
A BSCESS of brain, 428 
x\. Acarus folliculorum, 284, 797 (anapi, 
a mite) 
scabiei, 283, 797 
Achorion Schoenleinii, 259 (axuPi scurf) 
Acne, cinvr], the highest point, the bloom), 
773 
mentagra (mentum, the chin, and 
ay pa, a taking or affection), or 
sycosis (<rvkov, a fig), 774 
rosacea, 774 
Actinomyces or ray-fungus, 798 (aurlg, a 
ray, and pvuT/g, a mushroom) 
Actinomycosis, 798 
Acute miliary tuberculosis, 154 
lungs in, 515 
Acute yellow atrophy of liver, 586 
Addison’s disease, bronzing of skin in, 125 
Adenoma, 194 (adgv, a gland) 
mammary glandular tumor, 194 
mucous polypi, 195 
of liver, 195, 597 
of prostate, 195 
of thyroid, 196 
Ague cake, 367 
Air-embolism, 54 
Albuminous infiltration, 116 
Albuminuria, 638 (albumen, white of egg, 
and ovpov, urine) 
Alimentary canal, introduction to diseases 
of, 525 
Alopecia, 766 (d/lu7n;f, a fox) 
areata, 766 
Alveolar cancer, 221 
Amyloid concretions, 135 
Amyloid degeneration, 131 (a/ivAov, fine 
meal, and eidog, likeness). See also 
under individual organs 
Amyloid degeneration, connective tissue 
and bloodvessels affected in, 132 
Amyloid degeneration, effects of, 133 
localized, 134 
nature of the process, 134 
substance, characters of, 131 
tests of, 131 
Amemia, essential, 30 (a, priv., and alpa, 
blood) 
fatty degeneration, 118 
fatty heart, etc., in, 31 
general, 28 
local, 38 
secondary, 31 
spontaneous, 29 
Anchylosis of joints, 755 (ayicvhuoig, a stif- 
fening of joints, from ayicvfaig, crooked) 
Aneurism, by anastomosis, 349 (avevpvapa, 
from avevpvvu, I dilate) 
causation of, 342 
cirsoid, 349 {mpaog, enlargement of a 
vein, and eldog, like) 
condition of coats of vessels in, 344 
condition of branches at seat of, 346 
dissecting, 350 
effects on heart, 347 
effects on surrounding parts, 347 
fusiform and sacculated, 342 
localization of, 344 
miliary in brain, 422 
of cerebral vessels a cause of hemor- 
rhage, 420, 421 
of heart and valves, 317 
spurious, 349 
terminations of, 348 
thrombi in, 346 
traumatic, 349 
varicose, 351 
varieties of, 349 
Angina, acute catarrhal, 534 (angina, the 
quinsy, from ango, I cause pain) 
Angioma, 193 (ayyog, a vessel) 
cavernous, 194 
of liver, 596 
lymphatic, 194 
plexiform or capillary, 193 
venous or varicose naevi, 194 
Angiosarcoma, plexiform, 210 (ayyog, a 
vessel, oap!-, flesh, and plexus, a plait- 
ing) 
Angular curvature of the spine, 744 
Animal parasites, 260 
Anthracosis, or coal-miner’s lung, 519 
coal) 
Anthrax, 242 (avOpa%, a coal, a carbuncle). 
See splenic fever 
Aortic insufficiency, 323 
Aortic obstruction or stenosis, 325 
Apoplectic cyst of brain, 424 
Arterial tension, cause of increase in 
Bright’s disease, 640, 644 
Arteries, atheromatous patches in, 332 
calcareous infiltration of, 338 
condition in Bright’s disease, 640 
effects of ligature, 330 
fatty degeneration of intima, 338 
syphilitic diseases of, 340 
Arteritis, acute, 330 (aprtjpia, an artery) 802 
INDEX 
Arthritis, 756 (apdpov, a joint) 
acute rheumatic, 757 
chronic rheumatic, or deformans, 758 
gouty, 758 
pyaemic, 757 
simple acute, 756 
scrofulous or tubercular, 760 
Ascaris lumbricoides, 278 (aonapig, an in- 
testinal worm) 
mystax, 278 
Ascites, 697 (der/edf, a hag) 
chylous, 608 
Ataxia, hereditary, 396 (a, priv., and raftf, 
order) 
Atelectasis, 471 (are/lsfc, incomplete, and 
EKracug, expansion) 
to be distinguished from condensation 
of lung, 472 
Atheroma, 332 (adijpupa, a tumor full of 
gruel-like matter, from aOypr/, fine 
meal) 
a cause of gangrene, 107 
calcareous plates in, 334 
changes in middle and external coats, 
335 
effect on circulation of, 335 
in cerebral vessels, a cause of hemor- 
rhage, 421, 423 
Atheromatous abscess and ulcer, 334 
Atrophy, 113 (a, priv., and rpeipu, I 
nourish) 
from deficient nutrition, 114 
from disuse, 114 
from fever, 114 
from nervous lesions, 115 
of brain in general paralysis, 430 
of brain in hydrocephalus, 448 
of half the face, 116 
physiological, 113 
pACILLUS, 227 (bacillus, a little staff) 
_D antliracis, 242 
cultivation of, 248 
Pasteur’s observations, 252 
tuberculosis, 161 
Bacteria, 224 (fiaicTi/pia, a rod) 
detection of, 228 
forms and characters, 225 
influence on the living tissues, 229 
in putrefying or septic wounds, 230 
origin, 224 
Baldness, 765 
Bedsores, 787 
acute, 787 
Bile-ducts, obstruction of, 602 
results of obstruction, 602 
tumors of, 603 
Biliary abscesses, 603 
Bladder, urinary, calculi and concretions 
in, 666 
dilatation of, 661 
diseases of, 660 
diverticulum of, 662 
extroversion of, 660 
hemorrhage from, 662 
Bladder, hypertrophy of the muscular coat, 
662 
inflammation of, 663 
parasites in, 666 
passive hyperamiia of, 662 
perforation and rupture of, 661 
tuberculosis of, 664 
tumors of, 665 
Blood-corpuscle-holding cells, 59 
Blood in leukaemia, 66 
Bloodvessels, acute inflammation of, 330 
chronic endarteritis, atheroma, 332 
diseases of, 329 
Boil or furunculus, 776 
Bone, absorption of, 732 
cancer of, 751 
cysts of, 752 
deformities of, due to rickets, 726 
formation of sequestrum (Lat., some- 
thing separated) in necrosis, 738 
formation of cloaca (Lat , a drain) in 
necrosis, 739 
gummata in, 740 
healing of simple fractures, 736 
inflammations of, 731 
introduction to diseases of, 719 
metaplasia, 719 
necrosis of, 738 
necrosis from phosphorus, 739 
normal ossification, 724 
osteoblasts, osteoclasts, myeloplaques, 
and Howship’s lacunae in, 732 
parasites of, 752 
partial fractures in rickets, 727 
regeneration of, 146 
results of hereditary syphilis in, 740 
rickets or rachitis, 721 
sarcoma of, 750 
senile atrophy of, 729 
syphilitic affections of, 740 
transplantation of, 146, 734 
tubercular or scrofulous disease of, 742 
tumors of, 748 
Bone and cartilage, new-formation in in- 
flammation, 101 
Bone-marrow, affections of, 371 
in leukaemia, 68 
Bony tumor. See Osteoma 
Bovine tuberculosis, 164, 515 
Bothriocephalus latus, 273 (fioOplov, a little 
pit, and K£<j>a?iy, the head) 
Brain, abscess of, 428 
anatomical introduction to diseases 
of, 406 
convolutions, 409 
corona radiata, 409 
crura, 407 
external capsule, 409 
internal capsule, 407 
nucleus lenticularis, 409 
pons Yarolii, 407 
arteries of, 412 
atrophy, congenital and senile, 434 
degenerative changes in, 435 
delirium of fevers, 429 
disseminated sclerosis, 429 Brain, embolism, 50 
general odema of, 448 
general paralysis of the insane, 430 
hemorrhage, 419. See cerebral hem- 
orrhage 
inflammations of. See encephalitis 
localization of syphilitic lesions, 438 
nutritive arteries, 413 
occlusion of arteries, 416 
in chorea, 418 
oedema ex vacuo, 448 
parasites in, 440 
scrofulous tubercle of, 159, 439 
secondary degeneration in, 414 
softening (ramolissement), white 
yellow, and red, 425 
syphilitic disease of the vessels, 437 
thrombosis and embolism of the 
vessels, 415 
thrombosis of the sinuses, 418 
tumors of, 438 
Brain and membranes, syphilis of, 435 
Bright’s disease of the kidneys, 624 
albuminuria in, 638 
anatomical and histological 
changes in, 627 
arterio-capillary fibrosis, 641 
(apTT/pia, an artery, capillus, a 
hair, andfibra, a fibre) 
causes of, 625 
changes in heart and arteries, 640 
distinction into parenchymatous 
and interstitial nephritis, 625 
general introductory considera- 
tions, 625 
glomerulo-nephritis, 627 
hemorrhages in, 628 
uraemic symptoms in, 629 
interstitial nephritis, cysts in, 635 
sclerosis of glomeruli in, 634 
state of bloodvessels in, 636 
state of tubules in, 635 
increased arterial tension in, 641, 
644 
oedema from, 64 
relation to cold, 626 
gout, 626 
lead-poisoning, 626 
pregnancy, 627 
scarlet fever, 626 
syphilis, 627 
tube-casts in, 639 
Bronchial croup, 469 
Bronchial tubes, aftections of, 465 
catarrh, 467 
Bronchiectasis, 466 the wind- 
pipe, and EKTaoig, expansion) 
in chronic pneumonia, 494 
in fibroid phthisis, 506 
Bronchitis, 467 the windpipe) 
capillary, 496 
exudation (sputum) in, 468 
fibrinous or plastic, 469 
Bronchocele, 196 the windpipe, 
and K>/ATj: a tumor) 
Broncho-pneumonia, 496 
INDEX 
Bulbar paralysis, 401 (bulbe, French name 
for medulla and pons) 
Burns, 774 
Bubo, suppurating, 360 ([3ov(3uv, the groin) 
CACHEXIA, 174 (Kandg, bad, etjig, habit) 
Cadaveric poisons, effects of, 778 
Calcareous infiltration, 128 
anatomical characters of, 129 
of arteries, 338 
of cartilage, 131 
of dead tissues and foreign bodies, 
128 
of middle coat of arteries, 131 
Calculus in kidneys of new-born children, 
653 (calculus, dim. of calx, a stone, 
or limestone) 
in pelvis of kidneys, 653 
vesical, carbonate of lime, 668 
cystine, 668 
oxalate of lime, mulberry, 667 
tribasic phosphiitic, 668 
uric acid, 667 
xanthine, 668 
Callosity of skin, 787 
Callus, external, internal, and inter- 
mediary, 736 (callus, a hard skin) 
Cancer, forms of. See Carcinoma 
of abdominal organs, secondary ex- 
tension of, 612 
of the intestine, 574 
of kidney, 659 
of liver, ■698 
secondary growths in, 612 
of lung, 517 
of mamma, 707 
of oesophagus, 540 
of ovary, 699 
of stomach, 550 
of urinary bladder, 665 
Cancerous infiltration, 214 
Cancrum oris, 527 
Canities, 766 (canus, gray) 
Capillary bronchitis, 496 
Carbuncle (anthrax), 777 
Carcinoma, 210 (napnivog, a cancer) 
colloid or alveolar, 221 
definition of, 211 
growth of, 224 
hard, or scirrhous, 218 
inflammatory round-cells at the 
margin of, 224 
melanotic, 222 
mucous, 222 
ordinary, 217 
origin of the epithelium in, 212 
relations to the lymphatics, 214 
secondary changes in, 215 
soft or medullary cancer, 218 
structure of, 211 
villous, 216 
Caries, 733 (Lat., rottenness, decay) 
fungous, 760 
Cartilaginous tumor. See Chondroma 
I Caseous necrosis, 111 
803 804 
INDEX 
Casts (fibrinous) of bronchial tubes, 468 
in kidney. See tube-casts 
Catarrh of nasal passages, 454 (aara, down, 
and peo>, I flow) 
Cauliflower excrescence of the uterus, 
690 
Cause of disease, 18 
Cell division, 137 
Cellular tumors, 204 
Cephalhasmatoma, 60 the head, 
and alpa, blood) 
Cerebellum, anatomy of, 412 
atrophy of, 434 
Cerebral hemorrhage, 419 
appearances of brain in, 423 
causes of, 422 
causes of rupture of large vessels, 
aneurism, atheroma, etc., 420 
from the capillaries, 423 
from the larger arteries, 420 
from nutritive arteries, 421 
organization of the clot, 424 
membranes, hemorrhage from, 442 
inflammations of, 444 
sinuses, thrombosis of, 418 
vessels, embolism of, 415 
thrombosis of, 416 
Cerebro-spinal fluid, accumulation of, in 
cerebral membranes and cavities, 447 
Cestoda, 262 (/cftxrd?, a girdle, and eldog, 
likeness) 
Bothriocephalus latus, 273 
Tajnia echinococcus, 270 
mediocanellata, 268 
solium, 263 
other varieties, 274 
Chancre, indurated, primary, 148 
Charbon, 242 
Charcot’s crystals in leukaemia, 67 
Chest, rachitic deformity of, 728 
Chicken cholera, cultivation of the organ- 
ism, 249 
Pasteur’s observations, 251 
Chilblain, 776 
Chionyphe Carteri, 257 
Chlorosis, 30 (jAwpdf, green) 
Cholera, condition of intestine, 568 
from x°Mi bile) 
Cholestearine in fatty degeneration, 121 
Chondroma 184 (xbvtipog, giistle) 
ecchondrosis, 184 
enchondroma, 184 
malignancy of, 173 
osteoid, 748 
Chorea, occlusion of cerebral arteries in, 
418 (xopeia, a dance) 
Chylous urine, 282 
ascites, 607 
Circulation and blood, affections of, 23 
physiology of, 23 
Cirrhosis of the liver, 589 (mppog, tawny) 
Clinical observation, relation to pathology, 
20 
Cloudy swelling, 116 
Club foot, 753 
Coagulation in capillaries, 45 
Coagulation, theory of, 38 
necrosis, 108 
characters of the tisssue in, 110 
from embolic infarction, 108 
in diphtheria, 110 
Cocco-hacteria, 226 (wfc/cof, a kernel, and 
jianTT/pia, a rod) 
Colliquification, a form of gangrene, 112 
Colloid cancer, 221 
Colloid degeneration, 126 (k6/lAa, glue, 
fiSog, like) 
in cancer, 127 
Colloid or hvaline degeneration of muscle, 
108 
Colloid ovarian cysts, 695 
Comedo, 774 (comedo, I consume) 
Compound granular corpuscles, 120 
in cerebral softening, 426 
Compound-tissue tumors, 198 
Condyloma, 202 (novdv?Mpa, a knob) 
in larynx, 462 
in skin, 783 
Connective-tissue tumor,'176 
regeneration of, 145 
Corn (clavus) 787 
Corpora amylacea, 135 (corpus, a body, 
and a/nvlov, fine meal) 
Craniotabes, 729 (/cpavwv, the skull, and 
tabes, wasting) 
Croup, 459 
Cryptorchismus, 712 (Kpurrrdg, hidden, and 
opxig, a testicle) 
Cutaneous outgrowths, 177 
Cyanosis, 292, 764 (xvavog, blue) 
Cystic duct, obstruction of, 603 
Cysticercus, 266 (avarig, a bladder, and 
nepnog, a tail) 
Cystic sarcoma, 208 
Cystic tumor. See cystoma and cyst 
Cystinuria, 668 (cystine, from Kvang, a 
bladder, and ovpov, urine) 
Cystitis, 662 (uvang, a bladder) 
Cystoma, 198 (/cwmf, a bladder) 
dermoid cysts, 199 
mucous cysts, 199 
of the thyroid gland, 200 
of the ovary, 695 
Cysts, apoplectic, 198 
in tumors, 202 
mode of formation of, 198 
of gall-bladder, liver, and vermiform 
appendage, 201 
of the jaws, 752 
of the kidney, 200 
of the mamma, and intracystic 
growths of, 706 
of the ovaries, 201, 694 
of the parovarium, 700 
of the skin (atheromatous), 199 
retention, 198 
DEAD or obsolete structures, calcareous 
infiltration into, 128 
Dead or obsolete structures, disposal of, 
I 102,113 INDEX 
805 
Decubitus, acute, 787 
Delirium of fevers, condition of brain in, 
429 
Dermoid cysts, 204 
Desiccation a form of gangrene, 111 
Diabetes mellitus, 73 (dia, through, fiaivu, 
I flow, and peXi, honey) 
artificial production of, 75, 76 
effects of hyper-oxygenation of 
the blood, 77 
liver circulation in, 77 
pathological anatomy, 79 
relation of food to sugar in urine, 
73 
relations of the glycogen, 74 
state of the circulation in, 76 
urea excretion in, 70 
Diapedesis, 36, 56 (dia, through, and 
irydycug, a bursting or oozing) 
in inflammation, 89 
Diaphragm, its relation to peritoneal 
cancer, 616 
Diathesis, 174 (dia, through, and ridypi, I 
arrange) 
Diphtheria (di<j>depa, a skin, or leather), 458 
coagulation necrosis in, 110 
of fauces, 536 
nature of the membrane in larynx 
and trachea, 459 
Dislocations of joints, congenital, 753 
spontaneous, 755 
traumatic, 754 
Dissection wounds, 777 
Distoma (dig, twice, and aropa, the mouth) 
haematobium, 262 
hepaticum, 261 
lanceolatum, 262 
sinense, 261 
Diverticulum of the intestine, 556 (diverto, 
I turn aside) 
Division of cells, 137 
Dracunculus medinensis,' 279 (dracun- 
culas, a little dragon) 
Dry gangrene, 112 
Ductus choledochus, results of obstruction 
of, 603 
Duodenitis, 565 (duodenum, from duodeni, 
twelve) 
Dura mater, acute suppurative inflamma- 
tion of, 444 
gummata of, 436 
haematoma of, 442 
Dyscrasia, 174 (dvg, difficult or bad, and 
Kpaoig, a mixture) 
Dysentery, condition of intestine, 567 (dvg, 
with difficulty, and evrepov, the guts) 
EAR, fungi in, 257 
Ecchondrosis, 184 (en, out of, %dvdpog, 
gristle) 
Ecchymosis, 764 (hi, out of, and jvyof, 
juice) 
Eczema, 770 from enC,tu, I boil over) 
Elephantiasis, 356, 790 (ete<j>ag, an ele- 
phant) 
Elephantiasis, Arabum, 176 
Graecorum. See leprosy 
Emaciation, 114. 
Embolic infarction, coagulation necrosis 
in, 108 
its ultimate fate, 53 
Embolism, 46 (ep[5o?iog, a plug) 
Cohnheim’s experiments, 47 
in arteries with anastomosis, 47 
in arteries with anastomosis plugged, 
52 
in brain, 50 
in capillaries, 47 
in cerebral vessels, 415 
in end-arteries, 47 
in lungs, 49 
in kidney, 50 
in portal vein, 51 
in retina, 51 
in superior mesenteric artery, 52 
oil and air, 54, 487 
Emphysema (pulmonary) (eptyvoijpa, in- 
flation, from epcjivcdu, 1 blow 
in), anatomical changes in, 477 
compensatory, 476 
effects of, on other parts, 480 
expiration a cause of, 475 
inspiration a cause of, 476 
interlobular, 474 
senile, 476, 480 
vesicular, 475 
Empyema, 522 (epnvypa, a gathering, 
from ev, in, and ttvov, pus) 
Encephalitis, acute localized, 427 (eynetya- 
Aog, the brain) 
chronic localized, 428 
diffused, 429 
Enchondroma, 184 (ev, in, and %ovdpog, 
gristle) 
End-arteries, 47 
Endarteritis, chronic, 332 (evdov, within, 
aprypia, an artery) 
obliterans, 337 
Endocarditis, 306 (evdov, within, and 
napdia, the heart) 
chronic, 308 
simple acute, 306 
ulcerative, 310 
Endocardium, atheroma and opaque 
patches of, 310 
Endometritis, acute, 678 (evdov, within, 
and pyrpa, the womb) 
chronic, 678 
Enteritis, 563 (evrepov, a piece of gut, from 
evrog, within) 
Entozoa or internal parasites, 260 (evrdg, 
within, and £uov, an animal) 
cestoda or tapeworms, 262 
trematoda, 260 
Epidermis, hypertrophy of, 140 
regeneration of, 144 
Epithelial cancer, 215. See epithelioma 
Epithelioma, 215 
cylinder-celled, 217 
fiat-celled, 215 
of larynx, 465 806 
INDEX 
Epithelioma, of skin, forms of, 791 
of stomach, 550 
Epithelium, new-formation in granulating 
wound, 101 
regeneration of, 144 
Epizoa, 283 {ini, upon, and £uov, an 
animal) 
Epulis, 529 (eTTi, upon, and ov?a>v, the 
gum) 
Ergot, a cause of gangrene, 107 
Erysipelas {kpva'nre/iag, redness of the skin, 
from root of epvdp6g, red, and ttI/Jm, 
skin), 356, 779 
bacteria in, 246 
Erythema, 770 {ipvdaivu, I dye red, from 
epvOpdg, red) 
Excoriation of the skin, 777 
Exostosis, 185 (rfw, out of, barkov, a bone) 
multiple, 748 
Experimental pathology, relation to path- 
ology, 18 
17ALLOPIAN tubes, inflammation of, 
1 692 
tuberculosis of, 693 
Farcy, 168 
Fatty degeneration, 117 
anatomical changes in, 120 
in anasmia, 118 
in inflammations, 119 
of the brain substance, 118 
theories as to mode of occurrence 
of, 119 
Fatty infiltration, 122 
anatomical changes in, 123 
from disuse, 122 
around diseased and useless 
glands, 123 
of the liver, 123 
of muscle, 122 
Fatty tumor. See lipoma 
Fauces, acute catarrhal angina, 534 
acute phlegmonous inflammation of, 
535 
chronic catarrh of, 534 
diphtheria, 636 
inflammations of, 534 
syphilitic disease of, 537 
tubercular ulcers of, 537 
tumors of, 537 
Favus, 258, 794 {favus, a honeycomb) 
Fibrine, formation in inflammations, 93 
Fibrinous exudation, 91 
Fibro-cellular tumors, 178 
Fibroid phthisis, 505 
formation of cavities in, 506, 512 
Fibroma, 176 (fibra, a fibre) 
hard,178 
molluscum, 789 
of larynx, 464 
soft, 177 
Filiria medinensis, 279 {filum, a thread) 
Filaria sanguinis, 279 
relations to lymph-scrotum, 282 
relations to elephantiasis, 282 
Floating kidney, 621 
Foreign bodies, calcareous inliltration of, 
128 
inflammatory new-formation 
around, 101 
Foreign or dead tissue, absorption of, 102 
Formative cells in inflammation, 97 
Fractures, healing of, 736 
Framboesia, 781 (framboise, a raspberry) 
Frostbite, 776 
Fungi, characters and development of, 254 
in the ear, 257 
in the mouth, 259 
in the skin, 258 
madura foot, 257 
parasitic, 254 
pathogenic and innocuous forms, 256 
Fungus haematodes, 218 (fungus, a mush- 
room, and blood, and e'uhg, like) 
GALEN, veins of, obstruction in hydro- 
cephalus, 449 
Gall-bladder, tumors of, 603 
Gall-stones, 601 
single and multiple, 601 
Ganglion cells, calcification, 435 
hyaline or colloid degeneration, 
435 
simple and pigmentary atrophy, 
435 
Gangrene, causes, 105 (yayypaiva, an eat- 
ing sore) 
changes in the dead tissue, 108 
from thrombosis, 46 
of lungs, 498 
of lung, after acute pneumonia, 494 
senile, 107 
weakness of heart a cause of, 106 
Gastritis, 545 {yaargp, the belly, the 
stomach) 
General paralysis, state of brain in, 430 
General tuberculosis, 154 
Generative organs, female, defective de- 
velopment of, 672 
introduction to diseases of 
670 
male, 712 
malformations, 670 
Genu valgum, 727 {genu, the knee ; valgus, 
bow-legged) 
varum, 727 {genu, the knee; varus, 
bow-legged) 
Glanders, 168 
Glandular tumor. See Adenoma 
Glioma, 196, 439 {y?da, glue) 
cerebral, 439 
Glomerulo-nephritis {glomerulus, dim. of 
glomus, a clue of thread, and vecfipdg, the 
kidney). See Bright’s disease 
Glossitis, 528 {y/Mooa, the tongue) 
Glosso-labio-laryngeal paralysis {y/.uaaa, 
the tongue; labium, the lip), 402 
Glossy skin, 785 
Glycogen, conversion into sugar in dia- 
betes, 75 807 
INDEX 
Goitre, 196 (French, goitre; from Lat. 
guttur, the throat) 
Gonorrhoea, 668 [y6vog, seed, and piu, I 
flow) 
Graafian vesicles, conversion into cysts, 
693 
Granular disintegration of brain substance, 
435 
Granulating wound, as type of inflamma- 
tory new-formation, 96 
Granulation-tissue tumors, 147 
Gravel, 667 
Gray degeneration, ascending, 388 
of cord, characters of, 385 
Gum-boil, 533 
Gumma, 150 
structure of, 151 (gummi, gum) 
of the dura mater and soft membranes 
of brain, 436 
of the liver, 594 
Hematocele, 716 (aipa, blood, and 
Kifkr}, a tumor) 
periuterine, 681 
parametric, 682 
Htematoidin crystals, from hemorrhage, 58 
in thrombi, 44 
Hsematoma, 60 [alpa, blood) 
of scalp, 60 
of ear, 60 
of dura mater, 60, 442 
of heart, 61 
of uterus, 61 
of the peritoneum, 606 
polypoid of uterus, 684 
Hiematometra, 677 [alpa, blood, and pr/rpa, 
the womb) 
ILemin-crystals, 59 
Haemoglobin, its poisonous characters, 27 
Htemoglobinuria, 27 
Hair, atrophy of, 765 
grayness of, 766 
Head, rachitic deformity of the bones, 
728 
Healing of wounds, 143 
immediate union, 143 
primary adhesion, 143 
union by first intention, 144 
union by second intention, 144 
Health and disease, 18 
Heart, abscess of, 305 
aneurisms of, 317 
atrophy of, 294 
calcareous infiltration of, 302 
causes of foetal obstruction of pul- 
monary artery, 288 
coagula in, 327 
congenital malformation of the valves, 
290 
diseases of, 285 
endocarditis, 306 
fatty degeneration of, 300 
fatty infiltration of, 122, 299 
forms of cardiac hypertrophy, 297 
hypertrophy of, 294 
Heart, hypertrophy of, compensatory, 295 
from adherent pericardium, 295 
from Bright’s disease, 297 
from valvular disease, 296 
of left ventricle, 298 
of right ventricle, 298 
partial hypertrophies, 296 
imperfect closure of interventricular 
septum, 286 
in Bright’s disease, 640 
injuries and rupture of, 303 
irregularities of the primary vessels, 
289 
malformations of, 285 
duration of life in, 293 
misplacements of, 285 
myocarditis, 304 
passive congestion of, 299 
patency of foramen ovale, and ductus 
arteriosus, 287 
rupture, 304 
semilunar valves simulating auriculo- 
ventricular, 291 
thrombi in, 327 
tumors of, 329 
valvular disease of, 319 
of right side, 326 
Hemorrhage, 55 [aipoppayla, bleeding; 
from alpa, blood; and the root of 
pr/pywpc, I burst through) 
causes, 56 
disposal of escaped blood, 57 
from the stomach, 549 
in brain. See cerebral hemorrhage 
in phthisis pulmonalis, 512 
pigmentary infiltration from, 124 
pulmonary, 488 
stoppage of, 57 
Hemorrhagic infarction, 48 
in lungs, 49 
Hemorrhoids, 354 [alpa, blood, and peu, 
I flow) 
Hepatitis [r/nap, the liver), chronic inter- 
stitial, 589 
purulent, 587 
Hepatization of lung, 490 [girarifa, to be 
like the liver, from i/nap, the liver) 
Hereditary syphilis, 153 
Hermaphroditism, 670 ('Eppgq, Mercury, 
and ’A<j>po<Vi.TT], Venus). See also pseudo- 
hermaphroditism 
Hernia, contents of, 558 (hernia, a rupture) 
diaphragmatic, 557 
external and internal, 557 
external, enumeration of, 557 
false, 557 
mode of production, 556 
ovarian, 559, 691 
retroperitoneal (jejuno-duodenal, sub- 
ccecal, and into fossa intersig- 
moidea), 558 
strangulation of, 559 
Herpes, 784 [kpiru, I creep) 
Histology, pathological, relation to path- 
ology, 20 
Hodgkin’s disease, 70 808 
INDEX 
Homologous and heterologous tumors, 169 
(op6g, the same, and Myog, word, pro- 
portion), (krepog, other, and ?Py6g) 
Horn, 202 
Horse-shoe kidney, 621 
Hospital gangrene, 107 
Howship’s lacunae, 732 (lacuna, a cavity 
or gap) 
Hyaline degeneration in muscle, 108 
Hydatid mole, 182 (vSarig, a drop of water) 
Hydatids, 270. See taenia echinococcus 
Hydraemia, 28 (vbup, water, and alpa, 
blood) 
oedema from, 64 
Hydraemic plethora in Bright’s disease, 64 
Hydrencephalocele, 450 (iibup, water, 
kyuktyalog, the brain, and ay Ay, a tumor) 
Hydrocele, 715 (v6up, water, and nk/ky, a 
tumor) 
congenital, 716 
encysted, 716 
rarer forms of, 717 
Hydrocephalus, 448 (vSup, water, Ketpaky, 
the head) 
acquired, 448 
acute, 445 
chronic, or congenital, 449 
in atrophy of brain, 448 
in tubercular meningitis, 449 
Ilydrometra, 676 (vbup, water, and pyrpa, 
the womb) 
Hydronephrosis, 655 (vdup, water, and 
VE<j>p6g, the kidney) 
Hydrophobia, lesions in brain, etc., in, 
432 (vdup, water, and <po(3ku, I fear) 
Hydrorhachis, foetal, a cause of spina 
bifida, 451 (vSup, water, and paxty, the 
hack) 
Hydrothorax, 523 (vSup, water, and 06pa£, 
the breast) 
Hyperaemia (vnkp, over, and alua, blood) 
and anaemia, 25 
active, of the lungs, 481 
general, 25 
collateral, 32 
from dilatation of arteries, 33 
of the lungs, 482 
local, 32 
active, 32 
passive, 34 
oedema from, 63 
passive, from thrombosis, 46 
Hyperostosis, 748 (vnkp, over or excessive, 
and oarkov, bone) 
Hyperplasia, 140 (vnkp, over, and nlamg, 
a moulding; from nXaaau, I mould) 
Hypertrophy, 137 (vnkp, over, and rpk<j>u, 
I nourish) 
from excessive performance of a 
normal function, 138 
from frequently recurring pressure, 
140 
from increased blood supply, 140 
in bones, 141 
in epidermis, 139 
in muscle, 139 
Hypertrophy, in neighborhood of inflam- 
mations, 141 
Hypostatic engorgement of lungs, 482 
(vTrooTaTucdg, from ixpiorapai, 1 stand 
under) 
TCHTHYOSIS, 787 (1*%, a fish) 
x Icterus, 125 (bcTepog, jaundice) 
Immediate union, 143 
Immunity, acquired, 251 
natural, 249 
in zymotic diseases, theories of, 252 
Indurated chancre, 148 
Infantile paralysis, 397 
Infarction from embolism, 48 (infarcio, I 
cram in) 
hemorrhagic, of lungs, 485 
Infective inflammation, 103 
tumors, 147 
Inflammation (inflammo, I set on fire), 80 
active hyperamia in, 84 
artificial production of, 80 
changes in the tissues and new forma- 
tion, 95 
characters of the inflammatory ex- 
udation, 94 
disposal of exudations, 95 
emigration and diapedesis in, 90 
etiology of, 80 
exudation cells, 89 (exsudo, I sweat 
out) 
fibrinous exudation, 91 
formative cells, origin of, 99 
formation of fibrine in, 93 
individual forms of, 103 
inflammatory exudation, 89 
internal pavementing of veins, 86 
its mode of occurrence, 91 
nervous system, its influence in causa- 
tion of, 81 
new formation of bloodvessels, 98 
new formation of bone and cartilage, 
101 
paralysis of tissues in, 85 
path of entrance of irritants, 82 
principal phenomena, 82 
processes observed in wounded web 
of frog, 83 
produced by irritants, 81 
retardation and stasis of blood-current, 
86 
retrograde changes, 95 
the serous exudation—inflammatory 
oedema, 91 
state of the vessels in, 84 
syphilitic, 149 
temperature of inflamed parts, 87 
Insane ear, 60 
Intestine, catarrh of, 563 
catarrhal ulcers of, 664 
condition in dysentery, 567 
cholera, 568 
typhoid fever, 569 
cysts of, 564 
follicular ulcers of, 564 INDEX 
809 
Intestine, hernia or rupture, 556 
introduction to diseases of, 554 
intussusception or invagination of, 
561 
in leukaemia, 70 
malformations of, 555 
mucous polpi of, 564 
obstruction to calibre of, 576 
post-mortem changes in, 555 
prolapse of, 563 
results of obstruction of, 577 
simple inflammations of, 563 
specific inflammations of, 567 
tuberculosis of, 572 
secondary to phthisis pulmonalis, 
515 
tumors of, 574, 576 
twisting of, 560 
Introduction, 17 
Intussusception of the intestine, 561 (intus, 
within, and suscipio, I receive) 
Iodine as a test in amyloid degeneration, 
131 
Irritants, their nature, 80 
TOINTS, anchylosis of, 755 
f) dislocations and misplacements of, 753 
inflammations of. See arthritis 
syphilis of, 759 
KELOID, true and false, 788 a 
spot) 
Kidneys, active hyperaemia of, 623 
acute miliary tuberculosis, 654 
amyloid degeneration of, 650 
Bright’s disease of, 624 
calculi and concretions in, 653 
coalescence of (horse-shoe kidney), 
621 
compensatory hypertrophy of, 622 
cirrhosis of, 633 
cystoid degeneration of, 658 
cysts of, 635 
embolism, 50, 624 
tatty degeneration of epithelium, 650 
granular contracted, 633 
hydronephrosis, 655 
independent cysts of, resembling hy- 
dronephrosis, 657 
in leukaemia, 70 
in scarlet fever, 646 
lardaceous, 652 
local tuberculosis of, 654 
malformations and misplacements of, 
620 
metastatic abscesses in, 645 
micrococci in, 646 
movable or floating, 621 
normal structure and functions of, 
615 
parasites in, 660 
parenchymatous infiltration of, 649 
passive hyperaemia of, 623 
perinephric abscess, 648 
Kidneys, primary cancer of, 659 
retrograde changes in, 649 
septic inflammations of, 645 
simple atrophy of, 649 
simple cysts of, 657 
syphilis of, 654 
thrombosis of veins, 623 
tubercular ulceration of, 158 
tumors of, 657 
Kyphosis, 745 (Kvipdg, bent forwards) 
T AKDACEOUS degeneration, 131 
lu Large white kidney, 631 
Larvae of insects in the skin, 797 
in the tissues, 284 
Laryngeal phthisis, 463 
Larynx and trachea, acute catarrh of, 460 
diphtheria and croup, 458 
diseases of, 457 
Larynx, condylomata of, 462 
chronic catarrh of, 461 
inflammation of the perichondrium, 
461 
malformations of, 457 
oedema glottidis, 460 
phthisis of, 463 
subglottic inflammation, 461 
syphilis of, 462 
tumors of, 464 
Late rigidity in descending sclerosis, 387 
Lead poisoning, atrophy with paralysis 
in, 116 
Lepra anaesthetica, 167 (/xirp/jg, scaly) 
tuberculosa, 167 
Leprosy, 166 (Aeirpdg, scaly) 
bacillus in, 167, 246 
nerves in, 379 
Leptomeningitis, 444 (AerrTdg, fine, pijvi-yt;, 
a membrane) 
Leptothrix buccalis, 259 (XeirrSg, slender, 
Qpttj, a hair, and bucca, the cheek) 
Leucocytosis, 28 (Tievnog, white, and avrog, 
a hollow, a cell) 
Leucomyelitis, 390 (fevn6g, white, and 
pveXSg, marrow) 
Leukaemia, 66 (Aevnog, white, and aipa, 
blood) 
Charcot’s crystals, 67 
intestines in, 70 
kidney in, 70 
liver in, 70 
skin in, 70 
lymphatic glands in, 68 
medulla of bone in, 68 
relations to lymphoma, 222 
spleen in, 67 
Lichen ruber, 772 (Aeixyv, a tree-moss, a 
scab, and ruber, red) 
Lipoma, 178 (Awrof, fat) 
diffuse, 179 
pendulous, 179 
Liver, acute yellow atrophy of, 586 
acquired deformities of, 679 
adenoma, 597 
amyloid degeneration of, 585 810 
Liver, atrophy of, 583 
atrophy of cells in passive hyperaemia, 
580 
cancer of, 598 
cirrhosis of 589 
congenital syphilitic disease of, 594 
deformity in females, 579 
embolism in, 582 
fatty degeneration of, 583 
fatty infiltration of, 123, 584 
folds of, 580 
hypertrophic cirrhosis of, 591 
hypertrophy of, 583 
inflammations of, 587 
introduction to diseases of, 578 
in leukaemia, 70 
malformations of, 579 
nutmeg, 580 
parasites of, 600 
passive hyperaemia of, 580 
parenchymatous infiltratiort of, 583 
perihepatitis, 593 
pyaemic abscesses of, 588 
red atrophy of, 580 
retrograde changes in, 583 
syphilitic disease of, 594 
thrombosis and embolism in, 582 
tropical abscess of, 587 
tuberculosis of, 595 
tumors of, 596 
Locomotor ataxia, 393 {locus, a place; 
moveo, I move; a, priv., and 
rat;ig, order) 
lesion in, 393 
physiology of, 394 
trophic lesions of skin, muscles, 
and joints, 395 
Lordosis, 745 (Aopdog, bent supinely) 
Lungs, active hyperaemia of, 481 
acute pneumonia, 489 
anthracosis, 519 
atelectasis, 471 
brown induration of, 484 
cancer of, 517 
carnification of, 472 
collapse of, 472 
causes of collapse, 472 
collateral hyperaemia of, 481 
diseases of, 469 
disorders of the circulation in, 481 
embolism of the pulmonary artery, 
487 
emphysema of, 474 
gangrene of, 498 
hemorrhage from, 488 
hemorrhagic infarction of, 485 
hypertrophy (compensatory) of, 473 
induration of. See pneumonia, 
chronic 
inflammations of, 489 
inhalation of foreign substances, 518 
malformations of, 471 
oil embolism in, 487 
passive hyperaemia and oedema of, 482 
passive hyperaemia from heart disease, 
INDEX 
Lungs, phthisis pulmonalis, 500 
pigmentation of, 125, 518 
syphilitic disease of, 516 
tumors of, 516 
Lung-tissue in sputum in phthisis, 509 
Lupus, 166 (lupus , a wolf) 
exedens, 166 
non-exedens, 166 (non, not, and exedo, 
I devour) 
Lymphadenitis, acute, 359 (lypmpha, 
water, and adijv, a gland) 
chronic, 360 
Lymphadenoma, 222 (lympha, water, and 
afir/v, a gland) 
Lymphangeitis, 355 (lympha, water, and 
ayyelov, a vessel) 
Lymphangiectasis, 356 (lympha, water ; 
ayyelov, a vessel; and enracug, expansion) 
Lymphangioma, cavernous, 356 (lympha, 
water, and ayyelov, a vessel) 
Lymphatic circulation, 61 
glands, acute inflammation of, 359 
diseases of, 357 
in leukaemia, 68 
pigmentation of, 359 
scrofulous disease of, 162, 360 
secondary tuberculosis of, 362 
in syphilis, 149 
syphilitic disease, degenerative 
changes, and tumors of, 363 
growth. See lymphoma 
vessels, obstruction of, 61 
inflammation of, 355 
Lymphoma, 222 (lympha, water) 
Lympho-sarcoma, 222 
of mediastinum and mesentery, 
222 
of lung, 516 
Lymph-scrotum, 282, 790 
MACROGLOSSIA, 356, 530 (ya/cp<k, 
large, and y'Auaoa, the tongue) 
Madura foot, 257 
Malarial fevers, bacilli in, 246 
Malformations. See the individual organs 
Malignant pustule. See splenic fever 
Mamma, acute scirrhus of, 711 
adenoid sarcoma of, 704 
adenoma of, 704 
cancer of, 707 
colloid cancer of, 711 
cysts and cysto-sarcoma of, 706 
duct cancers, 707 
/ inflammation of, 703 
malformations of, 703 
medullary cancer of, 710 
mucous cancer of, 711 
parenchymatous cancer of, 707 
rarer tumors of, 711 
sarcoma of, 705 
scirrhus of, 708 
Meckel’s diverticulum, 556 
Medulla oblongata, bulbar paralysis, 401 
introduction to diseases of, 380 
tumors of, 406 INDEX 
811 
Melanaemia, 70 (pelag, black, and a\pa, 
blood) 
Melanotic cancer, 222 (peTiag, black) 
Membranes and cavities of brain and cord, 
introduction to diseases of, 441 
Membranes of brain, hemorrhage from, 
443 
syphilitic disease of, 435, 438 
tumors of, 452 
Meningeal hemorrhage, 442 
Meningitis, epidemic cerebro-spinal, 445 
a membrane) 
gummatous, 436 
simple acute, 444 
simple chronic, 444 
tubercular, 445 
Meninges, tumors of, 452 
Mercury, effects on mouth, 527 
Mesentery, aperture in, causing obstruc- 
tion, 577 
lympli-sarcoma of, 222 
Metaplasia, 719 (perdniiaoig, transforma- 
tion, from pera, indicating change, and 
Tvhaaau, I mould) 
Metastasis, 172 (peOloTtjpt, I change place) 
Metastatic calcification, 128 
Meteorism, 577, 609 I elevate) 
Methyl-violet, as a test, in amyloid de- 
generation, 131 
Metritis, 678 (pr/rpa, the womb) 
Micrococci, 226 (pispog, small, and KUKuog, 
a kernel) 
in kidney, 646 
Micro-organisms, 224 
Microsporon furfur, 259, 797 
Milium, 774 (Lat., millet) 
Mitral insufficiency or incompetency, 319 
obstruction or stenosis, 321 (orevog, 
narrow) 
Moles, pigmented, 789 
Mollities ossium, 730 (Lat., softness of 
bones) 
Molluscum contagiosum, 789 (molluscum, 
a fungus, from mollis, soft) 
Molluscum fibrosum, 178 
Morbid anatomy, relation to pathology, 
18 
Morbus coxae senilis, 759 (Lat., disease of 
the hip in the aged) 
Morpha3a, 785 
Mouth, catarrh of, 526 
effects of scurvy, 527 
of mercury, 527 
epithelioma of, 530 
follicular stomatitis, 526 
infective tumors of (syphilis, etc.), 
528 
smallpox eruption in 527 
syphilis of, 528 
thrush or aphthous stomatitis, 526 
tumors of, 529 
Mucous and colloid degeneration, physio- 
logical type of, 126 
in ovarian tumors, 126 
in thyroid gland, 127 
in cancers, 127 
Mucous cancer, 222 
degeneration, 125 
of intercellular substance, 127 
tissue tumor. See myxoma 
Mummification, 111 
Muscle, fatty infiltration of, 122 
hypertrophy of, 139 
regeneration of, 146 
Muscular-tissue tumor. See myoma 
Myelitis, transverse acute, 390 (pvelog, 
marrow) 
transverse chronic, 391 
Myeloplaques, 732 (pveXog, marrow, and 
7r/laf, a flat surface) 
Myocarditis, 304 (pvg, a muscle, and 
/capJla, the heart) 
interstitial, 304 
Myoma, 187 (pvg, a muscle) 
of female generative organs, 189 
of nipple, 711 
of uterus. See uterus 
retrograde changes of, 190 
situations of, 189 
smooth-celled, 188 
strio-cellulare, 187 
Myxcedema, 764 (fivt-a, mucous, and oUrjpa, 
a swelling) 
Myxoma, 180 (/iv%a, mucus) 
characters of mucous tissue, 181 
hydatid mole, 182 
situation and characters of, 183 
N.2EVI, vascular (naevus, a mole). See 
angioma 
Nails, atrophy of, 766 
Nasal passages, acute catarrh of, 454 
chronic catarrh of, 456 
congenital malformations of, 454 
tumors of, 456 
Necrosis, caseous, 111 (veKpuoig, state of 
death, from venp6g, a dead body) 
disposal of the dead tissue in, 113 
its causes, 105 
limitation of, 112 
of bone, 738 
Nematoda, or round worms, 275 (vi/pa, a 
thread, eidog, likeness) 
Nephritis (vetypdg, the kidney). See 
Bright’s disease 
Nerves, chronic neuritis, 379 
diseases of, introductory considera- 
tions, 375 
effects of division of, 377 
hypersemia and acute inflammation 
of, 378 
regeneration after division of, 146, 378 
tumors of, 379 
Nervous system, diseases of, introduction, 
372 
Nervous-tissue tumor. See neuroma 
Neuritis, acute, 378 (vevpov, a nerve) 
chronic, 379 
Neuroma, 190 (vevpov, a nerve) 
false, 191 
painful subcutaneous tumor, 191 812 
INDEX 
Neuroma, relation to multiple fibromata of 
skin, 790 
true, structure of, 191 
Nipple, Paget’s disease of, 708 
Noma, 527 (vbpu, I devour) 
Normal growth, 137 
ABESITY, 122 
V (Edema and dropsy, 61 (otrfrw, I swell, 
vdponp, dropsy; from v6up, 
water) 
in passive hypericinia, 36 
from hydrfemia, 64 
from thrombosis, 46 
from venous liyperaimia, 63 
glottidis, 460 
in Bright’s disease, 64 
inflammatory, 91 
of the brain, 448 
of the lungs, 482 
(Esophagus, diseases of, 537 
general dilatation of, 537 
inflammations of, 539 
obstruction of, 538 
partial dilatation (diverticulum) of, 
538 
perforating ulcers of, 539 
tumors of, 540 
Oidium albicans, 260, 527 
Oil-embolism, 54 
Oligaemia, 28 (oAiyog, small, and alpa, 
blood) 
Omentum, condition of, in tubercular peri- 
tonitis, 611 
its relations to cancer of peritoneum, 
616 
Oophoritis, acute, 692 (tpcxpdpog, bearing 
eggs, or roe, from udv, an egg, and 
<popfu, I bear) 
chronic, 692 
Orchitis, acute, 712 (opxig, the testicle) 
chronic, 713 
Organization of thrombi, 44 
Organs of respiration, diseases of, 454 
Osseous tumors, 748 
Ossification, normal, 724 
in rickets, 724 
Osteitis, rarefying or destructive and 
formative or condensing, 732 (oarbov, 
bone) 
Osteoblasts, 732 [ogteov, bone, and (ilacrog, 
a sprout) 
Osteoclasts, 732 (oarkov, bone, and K?aioT6g, 
broken in pieces) 
Osteoid chondroma, 748 [ogteov, bone, and 
eidog, likeness) 
Osteoma, 185 (ogteov, bone) 
hyperostosis and periostosis, 187 (virip, 
over, and ogteov, bone), (7r spi, 
around, and ooteov , bone) 
ivory exostosis, 186 
spongy exostosis, 185 
unconnected with bone, 187 
Osteomalacia, 729 [ogteov, a bone, and 
paTuiKia, softness, from pdkaKog, soft) 
Osteomalacia, different forms of, 731 
simulated by cancer, 751 
Osteomyelitis, malignant, and traumatic, 
738 (ogteov, bone, and pve'Abg, marrow) 
Osteophytes, 748 (ootPov, bone, and <pvr6v, 
a plant) 
Ovarian cysts, 693 
appearances of, 697 
changes in, 697 
characters of fluid in, 702 
origin and significance of the 
glandular tissue in, 697 
Ovarian tumors, colloid degeneration in, 
126 
Ovaries and tubes, inflammations of, 
692 
Ovary, cancer of, 699 
colloid cysts of, 695 
cysts of, 201. See also ovarian cysts 
dermoid cysts (teratoma) of, 698 
hernia of, 691 
sarcoma of, 700 
simple cysts, 694 
tuberculosis of, 693 
tumors of, 694 
Oxyuris vermicularis, 279 (otjvg, sharp, 
and ovpa, the tail) 
PACCHIONIAN bodies, 203 
tumors from, 453 
Pachymeningitis hemorrhagica, 442 
(naxvg, thick, pijviyt;, a membrane) 
Paget’s disease of the nipple, 708 
Painful subcutaneous tumor, 191 
Pancreas, atrophy of, 604 
cancer of, 605 
fatty infiltration and degeneration of, 
605 
hemorrhages of, 604 
inflammations of, 604 
tuberculosis of, 605 
Pancreatic duct, obstruction and dilatation 
of, 605 
Papilloma of larynx, 464 (papilla, a 
nipple) 
of mucous membrane, 202 
of the skin, 202 
of urinary bladder, 202, 665 
Parametritis, 679 (napd, beside, and pyrpa, 
the womb) 
Parasites, animal, 260 
vegetable, 224 
Parasitic fungi, 254 
Parenchymatous nephritis, 630 (irapiyxvpa, 
anything poured in beside, from irapd, 
beside, and I pour in. A name 
early applied to the peculiar substance 
of lungs, liver, kidney, and spleen) 
Parovarian cysts, anatomical and other 
characters of, 701 
characters of fluid in, 702 
perforation or rupture of, 702 
Parulis, 533 (Trapa, beside, and ov'/mv, the 
gum) 
Passive hyperamiia, 34 INDEX 
813 
Pathogenic bacteria, 236 {nddog, suffering, 
and yewau, I give rise to) 
attenuation of the virus, 252 
cultivation of, outside the body, 
248 
immunity from, 249, 252 
in acute specific diseases, 241 
mode of producing effects, 253 
relation to zymotic diseases, 242 
Pathological wart, 779 
Pediculi, 284 (Latin, lice) 
Pelvic cellulitis, 679 
peritonitis, 678 
Pelvis, rachitic deformity of, 728 
Pemphigus, 773 {nkp<j>i%, a bubble) 
syphilitic, 783 
Penis, affections of, 717 
Peribronchitis, 505 {izepl, around, and 
(3p6yx°g, the windpipe) 
Pericarditis, 313 {ivept, around, and aapdia, 
the heart) 
acute, 313 
cardiac hypertrophy in, 316 
septic, 316 
tubercular, 316 
Pericardium, absence of, 285 
adherent, hypertrophy of heart in, 
295 
white spots on, 316 
Perihepatitis, 593 {irepl, around, and r/rnip, 
the liver) 
Perimetritis, 610, 678 {irepl, around, and 
pijrpa, the womb) 
Periostitis, chronic, 737 {irepl, around, and 
ooteov, bone) 
simple acute, 738 
suppurative malignant, 737 
Periproctitis, 566 {ireplt around, and irpua- 
r6g, the anus) 
Peritoneum, active hyperaemia of, 607 
cancerous infection of, 614 
condition of in acute miliary tubercu- 
losis, 612 
inflammations of, 608 
introduction to diseases of, 606 
passive hyperaemia of, 607 
tuberculosis of, 610 
tumors of, 612 
Peritonitis, 608 (irepirdvacov, the stretched- 
out membrane, from irepl, around, 
and tecvu, I stretch) 
chronic, 610 
chronic hemorrhagic, 607 
tubercular, 610 
Perityphlitis, 565 {irepl, around, and 
rvtpXdv, the caecum) 
Perlsucht, 164, 515 (German, Perl, a pearl, 
and Sucht, sickness) 
Pernicious anaemia, 30 
Petechia, 764 (Italian, pettechies, flea- 
bites, probably from petigo, an eruption) 
Pharynx, soft palate, and tonsils, diseases 
of, 533 
Phlebitis, 330 (<pteip, a vein) 
Plileboliths, 353 a vein, and Xl<bog, 
a stone) 
Phlegmasia dolens, 681 from 
<p?Leygaivu, I inflame, and dolens, painful) 
Phlegmonous inflammation, 104 (tylEypovq, 
fiery heat, from </>Xeyu, I burn) 
Phosphorus necrosis of hone, 739 
poisoning and fatty degeneration, 118 
Phthisis pulmonalis, 499 (tyOlvu, I waste, 
and pulmo, the lung) 
acute peribronchitis in, 504 
anatomical changes in, 503 
aneurism in cavities of, 513 
caseous pneumonia, 501 
caseous formation of cavities in, 
509, 512 
catarrhal or caseous form, 507 
causes of, 500 
condition of bronchi in, 503 
condition of lungs predisposing 
to, 502 
condition of pleura in, 513 
fibrous peribronchitis in, 505 
fibroid, 505 
general appearances of lung in, 
510 
localization at apex, 502 
local tuberculosis, 501 
path of entrance of the irritant, 
502 
pneumothorax in, 514 
source of hemorrhage in, 512 
sputum in, 512 
state of bronchial glands in, 514 
ulceration of intestines in, 514 
views as to pathology of, 500 
Physiology, relation to pathology, 18 
Pian, 781 
Pigmentary infiltration, 124 
from hemorrhage, 59, 124 
in tumors, 125 
Pigmentation from atrophy and concen- 
tration, 126 
of the lungs, 125 
Pityriasis versicolor, 258, 796 (nhvpov, 
bran, versicolor, of changing color) 
rubra, 772 {richer, red) 
Plethora, 25 {nXi/dupr/, fulness) 
Pleura, affections of, 513 
condition of, in phthisis pulmonalis, 
513 
tumors of, 524 
Pleural adhesions, 523 
Pleurisy, 521 {nlevpa, the side) 
anatomical details of, 522 
tubercular, 523 
Plexiform angiosarcoma, 210 
Pneumonia, acute, 489 {pvevpuv, the lung) 
abscesses in, 493 
engorgement or splenization in, 
490 
gangrene in,494 
gray hepatization, 492 
occasional results of, 494 
purulent infiltration or resolu- 
tion, 493 
red hepatization, 490 
state of pleura in, 494 814 
INDEX 
Pneumonia, acute catarrhal, 496 
collapse of lung in, 497 
interstitial, 497 
caseous, a form of phthisis, 508 
chronic, 494 
bronchiectasis in, 496 
induration of lung in, 494 
white, 516 
Pneumothorax, 523 (nvEvpa, air, dupatj, the 
chest) 
in phthisis pulmonalis, 514 
Poliomyelitis, 390 (no?u6g, gray, and pvEA/k, 
marrow) 
anterior acuta, 397 
chronica, 399 
Polypi, mucous, 195 (noTivnovg, the sea- 
polypus) 
Portal vein, embolism, 51 
Pott’s disease of the spine, 744 
Pregnancy, extra-uterine, 682 
relation to Bright’s disease, 627 
Primary adhesion, 143 
chancre, 148 
Proctitis, 566 (npuKTdg, the anus) 
Progressive muscular atrophy, 400 
Prolapsus ani, 563 ( prolabor•, I fall down) 
Prostate, cancer of, 718 
concretions in, 718 
hypertrophy of, 718 
tubercle, 718 
Prurigo, 773 (prurio, I itch) 
Psammoma, 198 (tpdppog, sand) 
Pseudo-hermaphroditism, 671 (ipEvdr/g, 
false, 'Epprjg, Mercury, and ’Agipodlrt/, 
Venus) 
female, 671 
male, 671 
Pseudo-hypertrophic paralysis, 122, 403 
(ipsvtif/g, false; vnip, over ; and rplfu, I 
nourish) 
Pseudo-leukasmia, 70 (ipEtrdS/g, false, and 
leukannia) 
Psoriasis, 772 (1pupa, the scab) 
Puerperal fever, 679 
Pulex irritans, 284 (Latin, a flea) 
Pulmonary artery, embolism of, 487 
stenosis of, 286 
Pulmonary emphysema, 474 
hemorrhage, 488 
Pyagmia, 237 (nvov, pus, and alpa, blood) 
condition of kidneys in, 645 
embolic multiple abscess in, 237 
spontaneous, 241 
Pyelitis, 649 (nvEkog, an oblong vessel or 
basin) 
Pyelonephritis, 649 (irvE/Mg, an oblong 
vessel, and vE<pp6g, the kidney) 
Pyonephrosis, 648, 659 (nvov, pus, and 
vs<pp6g, the kidney) 
Pyo-p11eumothora 524 (nvov, pus, ttvev/m, 
air, and dupa£, the breast) 
QUINSY, 535 (through French csr/ui- 
nancie, from awaya?/, dog-quinsy, or 
sore throat, from kvuv, a dog, and 
ayxui I strangle) 
Rachitic rosary, 728 
Rachitis. See rickets, (paxig, the 
spine) 
Eanula, 530 (dim. of rana, a frog) 
Red corpuscles, replenishment of, 29 
Regeneration, 141 
of blood, 144 
after loss, 144 
of bone, 146 
of connective tissue, 145 
of epidermis and epithelium, 144 
of muscle, 147 
of nerve fibres, 147 
Relapsing fever, 244 
Renal phthisis, 158, 654 
Repair of injuries and restoration of lost 
parts, 141 
Reproduction of lost parts, law of, 142 
Retrograde metamorphosis, 105 
Ehabdo-myoma, 187 (pafidog, a stripe, and 
pvg, a muscle) 
Rickets, 795 
deformities of hones in, 726 
of chest in, 728 
of head in, 728 
of long bones in, 726 
mode of ossification in, 724 
partial fractures in, 727 
shifting of the epiphyses in, 727 
Ringworm, 258 
Rodent ulcer, 793 
Round worms. See Nematoda 
O AND tumor, 198 
U Sarcina ventriculi, 253 (sarcina, a 
bundle, and ventriculus, the 
stomach) 
in blood, 254 
Sarcoma, definition of, 204 (crapf, flesh) 
division of, according to type, 205 
mode of growth, 205 
of lung, 516 
of membranes of brain, 453 
retroperitoneal, 612 
structure and classification of, 205 
varieties of, round-celled, 206 
alveolar, 210 
cystic, 208 
melanoid or pigmented, 209 
myeloid or giant-celled, 208 
osteoid, 209 
plexiform or cylindroma, 210 
spindle-celled, 207 
Sarcoptes hominis, 797 
Scabies, 797 (Latin, the itch) 
Scalds, 774 
Scarlet fever, state of kidneys in, 646 
Sehizomycetae, 225 I split, and 
pvKt/g, a mushroom) 
Scirrhus, 218 (cnappdg, hard) 
of the mamma, 708 
of the stomach, 552 
Sclerema neonatorum, 786 (anb/pog, hard, 
veog, new, and natus, born) 
Scleroderma, 786 (akfo/pog, hard, and dep/m, 
the skin) INDEX 
815 
Sclerosis, disseminated or in patches, 429 
(oKlrjpog, hard) 
of spinal cord, 386 
Scolex, 266 (midiXr/t;, a worm) 
Scrofula, its relation to tuberculosis, 162 
(scrofa, a sow) 
Scrofulous tubercle of the brain, 159 
Scrotum, cancer of, 717 
lymph-scrotum, 717 
Scurvy, condition of mouth, 527 
Senile emphysema, 480 
gangrene, 107 
Septicaemia, 231 (ot/tvtihoc, putrefying, and 
alpa, blood) 
cff mice (Koch), 234 
of rabbits, 235 
pathogenic bacteria in, 236 
septic poisoning, 232 
septic or putrid infection, 233 
Septic poisoning, 232 
infection, 233 
thrombosis, 46 
Simple-tissue tumors, 176 
Skin, cancer (epithelioma) of, 791 
causes of cutaneous inflammation, 767 
cysts in, 765 
eruptions in fevers, 768 
eruption of smallpox, 768 
fibroma molluscum, 789 
fibro-neuromata of, 790 
forms of cutaneous inflammations, 768 
“glossy skin,” 785 
gumma of, 783 
hemorrhages of, 764 
hyperaemia of, 764 
hypertrophies and tumors of, 787 
infective inflammations of, 778 
infective tumors of, .781 
inflammatory skin eruptions, 770 
introduction to diseases of, 763 
lesions of, due to cadaveric poisons, 
778 
leukaemia, lesion in, 70 
local atrophy of, in pregnancy, 765 
molluscum contagiosum, 789 
multiple fibromata of, 790 
normal structure of, 762 
cedema of, 764 
parasitic affections of, 794 
parchment skin, 765 
phlegmonous inflammations of, 780 
pigmented cancer of, 794 
sarcoma of, 790 
simple and senile atrophy of, 765 
symptomatic inflammations, 768 
syphilitic lesions of, 782 
traumatic and non-infective inflam- 
mations, 774 
tropho-neuroses of, 784 
tumors of, 787 
Smallpox eruption in mouth, 527 
on skin, 768 
Softening of the brain, 425 
in the aged, 107 
Softening with decomposition in gangrene, 
112 
Soor, 526 
Spastic paralysis (Erb), 396 (anaariKog, 
stretching, from Girdu, I draw, napd, 
beside, and lvo>, I loosen) 
Spermatocele, 716 (oneppa, seed, and nrf/jj, 
a tumor) 
Spina bifida, 451 
condition of cord in, 452 
Spinal cord, acute softening of, 391 
amyotrophic lateral sclerosis, 397 
(a, priv , pvg, a muscle, and 
rptyo, I nourish) 
anterior and posterior root zones, 
382 
arrangement of gray substance, 
380 
of white substance, 381 
ascending gray degeneration, 388 
degeneration of, after amputa- 
tions, 389 
descending gray degeneration, 
386 
descending sclerosis, 386 
inflammations of, 390 
introduction to diseases of, 380 
poliomyelitis anterior acuta, 397 
poliomyelitis anterior chronica, 
399 
progressive muscular atrophy, 
400 
pseudo-hypertrophic paralysis, 
403 
pyramidal and cerebellar tracts, 
columns of Turck and Gull, 
382 
sclerosis of the posterior columns, 
393 
secondary degenerations of, 384 
spontaneous lateral sclerosis, 396 
tumors of, 406 
Spinal curvatures, antero-posterior, 744 
forms of, 744 
introductory considerations, 743 
lateral or rotatory, 746 
Spirillum, 226 (dim. of spira, a coil) 
Spirochseta Obermeieri, 244 
Spleen, active hyperaemia and inflamma- 
tion of, 365 
acute splenic tumor, 366 
amyloid disease, 369 
chronic inflammation of, 367 
chronic splenic tumor, 367 
diseases of, 364 
embolic infarction, 368 
general hypertrophy and fibrous in- 
duration of, 367 
in leukaemia, 67, 369 
malformations of, and supernumerary 
spleens, 365 
passive hyperaemia of, 367 
rupture of, 369 
sago spleen and diffuse amyloid spleen, 
369 
tuberculosis, syphilis, tumors, 371 
Splenic fever, 242, 780 
Sponge grafting, 102 816 
Sputum coctum of bronchitis, 468 (spuo, 
I spit, and coquo, I cook) 
Stasis, 87 (orders, a standing, from iorri/u, 
I stand) 
Stercoraceous vomiting, 577 (stercus, ex- 
crement) 
Stomach, acute catarrh of, 545 
acute and phlegmonous inflamma- 
tions of, 545 
cancer of, 551 
chronic catarrh of, 546 
colloid cancer of, 552 
dilatation and hypertrophy of, 543 
epithelial cancer of, 70 
hemorrhage from, 549 
in ulcer, 547 
inflammations of (gastritis), 545 
introduction to diseases of, 541 
medullary or soft cancer of, 551 
mode of origin of ulcers, 548 
perforation of, 547 
post-mortem changes of, 542 
scirrhus of, 552 
simple perforating ulcer of, 546 
tumors of, 550 
Stomatitis, aphthous, 526 (orofia, the 
mouth, a<j>0a, an eruption) 
follicular, 526 
gangrenous, 527 
Strobilus, 263 {cTpdfiilog, a fir cone) 
Strongylus duodenalis, 279 
gigas, 279 
Superior mesenteric artery, embolism, 52 
Synovitis, strumous, 760 {aiv, with, and 
<f)6v, an egg) 
Syphilis, 148 
amyloid disease in, 153 
arteries in, 153 
chancre, 148 
congenital, 153 
due to a virus, 148 
effects on mouth, 529 
hereditary, 153 
affection of the bones in, 741 
incubation period, 149 
inflammations in, 149 
lymphatic glands in, 149 
of the brain and its membranes, 435 
of the larynx, 462 
secondary lesions, 149 
symmetrical lesions in, 149 
skin eruptions in, 782 
tertiary stage of gummata, 150 
ulceration in, 152 
Syphilitic disease of cerebral bloodvessels, 
437 
Syringomyelia, 406 (crvpiyt;, tube, and 
pvt:Mg, the marrow) 
TABES dorsalis, 393 (tabeo, I waste, and 
dorsum, the back) 
Tamia echinococcus, 270 (tcenia, a ribbon; 
£X'v<K, a hedgehog ; and noKKog, 
a kernel) 
brood capsules of, 271 
INDEX 
Taenia echinococcus, characters of cyst 
wall, 275 
development of cysts, 271 
mediocanellata, or saginata, 268 
solium, habitat and characters of, 263 
sexual apparatus, 263, 
water vascular system, and de- 
velopment of, 265 
Talipes, its various forms, 753 (talus, the 
ankle, and pes, the foot) 
Tapeworms. See cestoda and taenia 
Teeth, caries of, 531 
constituents of, 531 
inflammations of, 532 
osteoma of, 533 
tumors of, 533 
Temperature of inflamed parts, 87 
Tendon reflex, exaggeration of, 388 
Teratoma of internal organs, 203 (repag, a 
monster) 
of ovary. See dermoid cysts 
sacral, 203 
situations and structure of, 203 
Testicle, benign fungus of, 713 
haematocele, 716 
hydrocele, 715 
imperfect descent of, 712 
inflammation of, 712 
malformations and misplacements of, 
712 
syphilitic disease of, 713 
tuberculosis of, 714 
tumors of, 714 
Tetanus, lesions in, 434 (reravog, stretch- 
ing, tension) 
Threadworm, 279 
Thrombi distinguished from clots, 43 
('0p6fi[3og, a lump or clot) 
in heart, 41, 327 
in veins, 41 
liable to grow, 42 
organization, 44 
red, 40 
softening, 43 
white and mixed, 40 
Thrombosis and embolism, 39 
Thrombosis, hypersemia, oedema, gangrene 
from, 46 
of cerebral sinuses, 418 
vessels, 415 
Thrush, 260, 526 
Thvroid gland, colloid degeneration of, 
127 
Tinea favosa, 794 {tinea, a worm, and 
favus, a honeycomb) 
tonsurans, 796 (tonsura, a shaving) 
Tongue, inflammation of, 528 
Tonsillitis, acute, 536 (tonsillce, the 
tonsils) 
chronic (hypertrophy), 536 
Trachea, malformations of, 457 
Transfusion of blood, 25 
of alien blood, 26 
of blood about to coagulate, 26 
Transplantation of bone, 146 
Transverse myelitis, 390 INDEX 
817 
Trematoda, 260 [Tpr/parudr/g, perforated) 
Trichina spiralis, site and characters of, 
275 [rpixivog, of hair) 
impregnation of capsule with 
lime, 129 
Trichocephalus dispar, 279 
Trichophyton, 259 (dpif, a hair, and <pvr6v, 
a plant) 
tonsurans, 796 
Tricuspid valve, relative insufficiency of, 
326 
Tropho-neuroses, 115 [rpeipu, I nourish, 
vevpov, a nerve) 
of skin, 784 
Tube casts, 639 
from coagulation necrosis, 110 
Tubercle and tuberculosis, 153 [tubercu- 
lum, a little lump) 
caseous necrosis of, 156 
fibrous transformation of, 156 
miliary, its structure, 155 
Tubercles, their relation to bloodvessels, 
155 
Tubercular bacillus, characters of, 161 
meningitis, 445 
appearance of brain in, 446 
white softening around ventricles, 
447 
peritonitis, 610 
ulcer, 158 
ulcer of intestine, 573 
virus, nature of, 160 
source, 163 
Tuberculization and fatty degeneration, 
122 
Tuberculosis, acute miliary, 154 
and inflammation, 157 
artificial production of, 159 
bacillus in, 246 
by inoculation, 160 
from inspired air, 160 
general, 154 
local, 157 
of serous cavities, 158 
relations to scrofula, 162 
Tumor albus, 760 (Lat., white swelling) 
Tumors, 169 
classification of, 174 
Cohnheim’s theory of malignancy, 
173 
cysts in, 202 
definition of, 169 
growth and extension of, 171 
local malignancy, 172 
metastasis or generalization of, 172 
origin and development of, 169 
origin from embryonic remains, 170 
secondary changes of, 173 
simple or innocent, 172 
Twisting of intestine, 560 
Typhlitis, 565 (rv(j>16v, the ccecum or blind 
gut) 
Typhoid fever, 569 [rixpog, smoke, and 
etdof, likeness) 
lymphoma in, 222 
Typhoid fever, bacillus (Eberth’s) in, 245 
condition of intestine in, 571 
mesenteric lymphatic glands in, 
572 
characters of, 571 
ITLCElt, perforating of, stomach. See 
J stomach 
Ulceration, 104 (ulcus, a sore) 
syphilitic, 152 
Ulcerative endocarditis, 241, 310 
kidneys in, 645 
organisms in, 246 
Ulcers of the skin, 777 
Union by first intention, 144 
by second intention, 144 
Uraemia, 72 (ovpov, urine, and, «!//«, blood) 
Urachus, patency of, 661 
Urethra, diseases of, 668 
Urinary organs, diseases of, 617 
Uterus, anteflexion, 675 
anteversion, 676 
atrophy of, 676 
dilatation of, 677 
distention of by gas, 677 
double, 673 
epithelial cancer of, 689 
fibrinous polypus, 684 
hypertrophy of, 676 
cervix, 677 
inflammations of, 677 
inversion of, 675 
malformations of, 674 
mucous polypi of, 690 
myoma, 685 
cysts, dilatation of bloodvessels, 
and calcareous infiltration in, 
687 
induration and oedema of, 687 
prolapse of, 674 
parasites of, 691 
retroflexion, 675 
retroversion, 676 
soft or medullary cancer of, 688 
syphilis of, 683 
tuberculosis of, 683 
tumors of, 684 
less frequent forms of, 691 
unicornis, 674 
TTAGINA, cancer of, 688 
V prolapse of, 675 
tumors of, 684 
Valvular disease of heart, 319 
Varicocele, 355 (varix, a dilated vein, and 
lif/lri, a tumor) 
Varicose ulcer, 777 
Varix, 354 [varix, a dilated vein) 
results of, 353 
Vascular tumor. See angioma 
Vegetable parasites, 224 
Vein-stones, 44 
Vermiform appendix, foreign bodies in, 565 818 
INDEX 
Vermiform appendix, retention cyst of, 565 
Vertebra1, rachitic deformity of, 728 
WART, common, 202, 788 
pathological, 779 
soft, 789 
Waxy degeneration, 131 
White pneumonia, 516 
Wood’s tumor, 191 
Wounds. See healing of wounds 
bacteria in, 230 
Wounds of the skin, 777 
Wound fever, 232 
V ANTHOMA, xanthelasma, 790 (gavdog, 
iV yellow, and Duwfia, a plate) 
Xeroderma, 704, 788 (fjjp6g, dry, and Stppxi, 
the skin) 
i yAWS, 781 pLINT’S PRACTICE—A Treatise on the Principles and Practice 
of Medicine. Designed for the use of Students and Practitioners of Medicine. 
By Austin Flint, M.D., Professor of the Principles and Practice of Medicine and of 
Clinical Medicine in Bellevue Hospital Medical College, N. Y. Fifth ediiion, entirely 
rewritten and much improved. In one large and closely-printed octavo volume of 1150 
pages. Cloth, $5.50; leather, $6.50; very handsome half Russia, raised bands, $7.00. 
""pHIS volume is certainly one of the standard text- 
books on medicine; and we may safely affirm 
that, taken al ogether, it exhibits a fuller and wider 
acquaintance with recent patholrgical inquiry than 
any similar work with which we are acquainted, 
whilst at the same time it shows its author to be 
possessed of the rare faculties of clear exposition, 
thoughtful discrimination, and sound judgment.— 
London Lancet, July 23, 1881. 
pLINT’S AUSCULTATION AND PERCUSSION—A Manual of 
Auscultation and Percussion; Of the Physical Diagnosis of Diseases of the 
Lungs and Pleart, and of Thoracic Aneurism. By Austin Flint, M.D., Professor of 
the Principles and Practice of Medicine in the Bellevue Hosp. Med. Coll., N. Y. Third 
edition. In one handsome royal i2mo. volume of 240 pages. Cloth, $1.63. Just ready. 
JT is safe to say that there is not in the English or j 
any other language the equal amount of clear, 
exact, and comprehensible information touching the 
physical exploration of the chest in an equal number 
of woids. Professor Flint’s language is precise and 
simple, conveying, without dubiety, the results of 
his careful study and ample experience.—American 
Practitioner, June, 1883. 
JQRISTOWE’S PRACTICE—A Treatise on the Practice of Medi- 
cine. By John Syer Bristowe, M.D., F.R.C.P., Physician and Joint Lecturer 
on Medicine at St. Thomas’ Hospital. Second American edition, specially revised by 
the Author. Edited, with additions, by James H. Hutchinson, M.D., physician to the 
Pennsylvania Hospital. In one handsome octavo volume of 1085 pages, with illustra- 
tions. Cloth, $5.00; leather, $6.00; very handsome half Russia, raised bands, $6.50. 
'J’HE reader will find every conceivable subject j 
connected with the practice of medicine ably 
presented, in a style at once clear, interesting and 
concise. The additions made by Dr. Hutchinson 
are appropriate and practical, and greatly add to 
its usefulness to American readers.—Buffalo Medi- 
cal and Surgical Journal, March, 1880. 
H YDE ON THE SKIN—A Practical Treatise on Diseases of the 
Skin. For the Use of Students and Practitioners. By J. Nevins Hydf, M.D., 
Professor of Dermatology and Venereal Diseases in Rush Medical College, Chicago. 
In one handsome octavo volume of 570 pages, with 66 beautiful and elaborate illustrations. 
Cloth, $4.25; leather, $5.25. Just Ready. 
TDROF. HYDE has given to the profession a valu- 
able and comprehensive work upon this special 
subject, exposing the etiology, symptomatology, and 
treatment of diseases of the skin in a concise and 
thorough manner. The book is a valuable one for 
the student and practitioner, containing all the latest 
progress made in dermatology, and will, without 
doubt, attain the end expected by its author—to 
make the general practitioner thoroughly informed 
in regard to the treatment Of cutaneous diseases. 
It will prove a valuable book of reference to the 
specialist. — N. O. Medical and Surgical Journal, 
April, 1883. 
JgRYANT’S SURGERY—The Practice of Surgery. By Thomas 
Bryant, F.R.C.S., Surgeon to Guy’s Hospital, London. Third American from 
the third and revised English edition. Thoroughly revised and much improved, by 
John B. Roberts, A.M., M.D. In one large and very handsome imperial octavo volume 
of 1009 pages, with 735 illustrations. Cloth, $6.50; leather, $7.50; very handsome half 
Russia, raised bands, $8.00. 
~\\TITHOUT freighting his book with multiplied 
details and wearying descriptions of allied 
methods of procedure, he is ample enough for refer- 
ence on all the departments of surgery, not omitting 
such strict specialties as dental, ophthalmic, mili- 
tary, orthopedic and gynecological surgery. Some 
of these chapters are written by specialists in their 
respective branches. The labors of the American 
editor deserve unqualified praise. His additions to 
the author’s text are numerous, judicious and ger- 
mane —Medical and Surgical Reporter, Feb. 12, 
1881. 
HENRY C. LEAS SON & CO., Philadelphia.  SURGERY—A System of Surgery: Pathological, Diag- 
nostic, Therapeutic and Opeiative. By S. D. Gross, M.D., LL.D., D.C.L. Oxon., 
LL.D. Cantab., Emeritus Professor of Surgery in the Jefferson Medical College of Phila- 
delphia. Sixth edition, thoroughly revised and greatly improved by the Author and 
Samuel W. Gross, A.M., M.D., Professor of the Principles of Surgery and of Clinical 
Surgery in the Jefferson Medical College. In two large and beautifully-printed imperial 
octavo volumes containing 2382 pages, illustrated by 1623 engravings. Strongly bound 
in leather, raised bands, #15.00; half Russia, raised bands, #16.00. Just ready. 
w E have purposely abstained from comment or j 
criticism of the book before us. It has for- 
merly been noticed more than once in our columns, 
and it is enough now to remark that the present 1 
edition fully maintains the reputation the work has 
acquired The several parts have been extended, 
elaborated and amplified, till it has become a com- 
plete and systematic book of reference alike for the 
student and the practitioner.— The London Lancet, 
Jan. 27, 1883. 
ON IMPOTENCE—A Practical Treatise on Impotence, 
Sterility, and Allied Disorders of the Male Sexual Organs. By Samuel 
W. Gross, A.M., M.D., Professor of the Principles of Surgery and of Clinical Surgery 
in the Jefferson Medical College. Second edition, thoroughly revised. In one very 
handsome octavo volume of 168 pages, with 16 illustrations. Cloth, $1.50. Just ready. 
'J'HE book is the outcome of intelligent clinical 
observation and extensive experience. The 
arrangement and classification leave nothing to be 
desired in the way of clearness; and practitioners j 
who may be called upon to treat these cases will 
find the directions both for diagnosis and treatment 
very perspicuous and sound—Liverpool Medico- 
Chirurgical Journal, July, 1882. 
gTIMSON ON FRACTURES—A Practical Treatise on Fractures. 
By Lewis A. Stimson, B.A., M.D. Professor of Pathological Anatomy at the 
University of the City of New York, Surgeon and Curator to Bellevue Hospital, Surgeon 
to the Presbyterian Hospital, New York, etc. In one very handsome octavo volume of 
598 pages, with 360 beautiful illustrations. Cloth, $4.75 ; leather, $5.75. Just Ready. 
THE author has given to the medical profession in 
this treatise on fractures what is likely to be- 
come a standard work on the subject It is certainly 
not surpassed by any work written in the English, 
or, for that matter, any other language. There is 
nothing scanty or superficial about it, as in most 
other treatises ; on the contrary, everything is thor- 
ough. His mode of treatment of the different frac- 
tures is eminently sound and practical. We con- 
sider this work one of the best on fractures ; and it 
will be welcomed not only as a text-book, but also 
by the surgeon in full practice.—New Orleans Med- 
ical and Surgical Journal, March, 1883. 
ANATOMY—A System of Human Anatomy, Including 
Its Medical and Surgical Relations. For the Use of Practitioners and 
Students of Medicine. By Harrison Allen, M.D., Professor of Physiology in the 
University of Pennsylvania. With an Introductory Chapter on Histology, by E. O. 
Shakespeare, M.D., Ophthalmologist to the Philadelphia Hospital. In one large and 
handsome quarto volume of about 600 double-columned pages, with 380 illustrations on 
109 lithographic plates, many of which are in colors, and about 100 engravings in the text. 
In six Sections, each in a portfolio. Section I. Histology {Just Ready). Section II. 
Bones and Joints {Just Ready). Section III. Muscles and Fascia (Just Ready). 
Section IV. Arteries, Veins and Lymphatics {Just Ready). Section V. Nervous 
System {Shortly). Section VI. Organs of Sense, of Digestion, and Genito-Urinary 
Organs {In Press). Price per Section, $3.50. For sale by subscription only. 
THE appearance of the book marks an epoch in 
medical literature. It is the first important 
work on human anatomy that has appeared in 
America ; and, more than this, its scope is new and 
original. It is intended to be both descriptive and 
topographical, scientific and practical, so that while 
satisfying the anatomist, it will be of value to the 
practising physician As the author points out, 
such a work as he has undertaken is necessarily 
encyclopedic, and the result shows that he has 
brought to it a mind well prepared for the task by 
extensive reading, critical judgment, and literary 
ability. We can cordially recommend the work to 
the profession, believing that it is suited not only to 
those of scientific tastes, but that it will be of use to 
the practising physician.—Boston Medical and Sur- 
gical Journal—January n, 1883. 
HENRY C. ERA'S SON & CO., Philadelphia.  ■ 
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LEA BROTHERS S CO.’S 
CLASSIFIED CATALOGUE 
MEDICAL AND SURGICAL 
Publications. 
In asking the attention of the profession to the works advertised in the following pages, 
the publishers would state that no pains are spared to secure a continuance of the confi- 
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LEA BROTHERS & CO. 
Nos. 706 and 708 Sansom St., Philadelphia, July, 1891. 
Practical Medical Periodicals. 
THE AMERICAN JOURNAL OF THE MEDICAL 
SCIENCES, Monthly, $4.00 per annum. 
THE MEDICAL NEWS, Weekly, $4.00 per annum. 
To one address, 
post-paid, 
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per annum. 
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With either or both above periodicals, in advance, 75c. 
THE YEAR-BOOK OF TREATMENT (see page 17), $1.50. With either 
JOURNAL or NEWS, or both, 75c. Or JOURNAL, NEWS, VISIT- 
ING LIST and YEAR-BOOK, $8.50, in advance. 
Subscription Price Reduced to $4.00 Per Annum. 
THE MEDICAL NEWS. 
THAT The News fulfils the wants of men in active practice is made clear by the 
steady growth of its subscription list. This increase of readers has rendered possi- 
ble a reduction in the price of The News to Four Dollars per year, so that it is now 
by far the cheapest as well as the best large weekly journal published in America. 
By means of The Medical News every physician is now able at a minimum outlay 
to insure his own receipt of the earliest and most authoritative information on all subjects 
(Continued on next page.) 2 
Lea Brothers & Co.’s Periodicals—Am. Journal, Medical News. 
THE MEDICAL NEWS—Continued. 
of interest to the great medical world. The foremost writers, teachers and practitioners 
of the day furnish original articles, clinical lectures and notes on practical advances; 
the latest methods in leading hospitals are promptly reported; a condensed summary of 
progress is gleaned each week from a large exchange list, comprising the best journals 
at home and abroad; a special department is assigned to abstracts requiring full treat- 
ment for proper presentation ; editorial articles are secured from writers able to deal 
instructively with questions of the day; books are carefully reviewed; society proceedings 
are represented by the pith alone; regular correspondence is furnished by gentlemen in 
position to know all occurrences of importance in the district surrounding important 
medical centres, and minor matters of interest are grouped each week under news items. 
Everything is presented with such brevity as is compatible with clearness, and in the 
most attractive manner. In a word The Medical News is a crisp, fresh, weekly news- 
paper and as such occupies a well-marked sphere of usefulness, distinct and comple- 
mentary to the ideal monthly magazine, The American Journal of the Medical 
Sciences. 
The American journal of tie Medical $cienceg 
Published Monthly, at Four Dollars Per Annum 
Enters upon its seventy-second year (1891) with assurances of increased usefulness. Encour- 
aged by the emphatic endorsement of the profession, as indicated by a growth in its subscrip- 
tion list of fifty per cent, since its appearance as a monthly at a reduced price, those in charge 
will spare no effort to maintain its place as the leader of medical periodical literature- 
Being the medium chosen by the best minds of the profession during the past seventy 
years for the presentation of their ablest papers, The American Journal has well 
earned the praise accorded it by an unquestioned authority—“from this file alone, were 
all other publications of the press for the last fifty years destroyed, it would be possible to 
reproduce the great majority of the real contributions of the world to medical science 
during that period.” Original Articles, Reviews and Progress, the three main departments 
into which the contents of The Journal are divided, will be found to possess still greater 
interest than in the past. The brightest talent on both sides of the Atlantic is enlisted in 
its behalf and no effort will be spared to make The Journal more than ever worthy of 
its position as the representative of the highest form of medical thought. 
COMMUTATION RATE. 
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and afford their readers the assurance that nothing of value in the progress of medical 
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SPECIAL OFFERS. 
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News, Visiting List and Year-Book, $8.50. 
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annually), and for The News (one annually), free by mail, by remitting Ten Cents for The 
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LEA BROTHERS & CO., 706 & 708 Sansom Street, Philadelphia. Lea Brothers & Co.’s Publications—Period., Manuals. 
3 
THE MEDICAL NEWS VISITING LIST FOR 1891 
Is published in four styles, Weekly (dated for 30 patients); Monthly (undated, for 120 
patients per month) ; Perpetual (undated, for 30 patients weekly per year) ; and Per- 
petual (undated, for 60 patients weekly per year). The 60-patient Perpetual is a nov- 
elty for 1891, and consists of 256 pages of assorted blanks. The first three styles 
contain 32 pages of important data and 17 6 pages of assorted blanks. Each style is in 
one wallet-shaped book, leather-bound, with pocket, pencil, rubber, erasable tablet and 
catheter-scale. Price, each, $1.25. 
The Amer. Journal ($4) with Visiting List ($1.25), or Year-Book ($1.50), for $4.75 
The Medical News ($4) “ “ “ “ “ “ “ “ 4.75 
The Journal and News ($7.50) “ “ “ “ “ “ “ 8.25 
The Journal, News, Visiting List and Year-Book (see page 17), . . 8.50 
SPECIAL COMBINATIONS WITH VISITING LIST. 
This list is all that could be desired. It con- 
tains a vast amount of useful information, especi- 
ally for emergencies, and gives good table of doses 
and therapeutics.—Canadian Practitioner. 
It is a masterpiece. Some of the features are 
peculiar to “ The Medical News Visiting List,” 
notably the Therapeutic Table, prepared from Dr. 
T. Lauder Brunton’s book, which contains the 
list of diseases arranged alphabetically, giving 
under each a list of the prominent drugs em- 
ployed in the treatment. When ordered, a Ready 
Reference Thumb-letter Index is furnished. This 
is a feature peculiar to this Visiting List.—Physi- 
cian ami Surgeon, December. 
For convenience and elegance it is noi surpass- 
able.—Obstetric Gazette, November. 
THE 3LEDICAL NEWS PHYSICIANS9 LEDGER. 
Containing 300 pages of fine linen “ ledger ” paper, ruled so that all the accounts of a 
large practice may be conveniently kept in it, either by single or double entry, for a long 
period. Strongly bound in leather, with cloth sides, and with a patent flexible back, 
which permits it to lie perfectly flat when opened at any place. Price, $4.00. 
HAIiTSnoilNE, HENRY, A. 31, M. I)., LL. D., 
Lately Professor of Hygiene in the University of Pennsylvania. 
A Conspectus of the Medical Sciences; Containing Handbooks on Anatomy, 
Physiology, Chemistry, Materia Medica, Practice of Medicine, Surgery and Obstetrics. 
Second edition, thoroughly revised and greatly improved. In one large royal 12mo. 
volume of 1028 pages, with 477 illustrations. Cloth, $4.25; leather, $5.00. 
The object of this manual is to afford a conven- 
ient work of reference to students during the brief 
moments at their command while in attendance 
upon medical lectures. It is a favorable sign that 
it has been found necessary, in a short space of 
time, to issue a new and carefully revised edition. 
The illustrations are very numerous and unusu- 
ally clear, and each part seems to have received 
its due share of attention. We can conceive such 
a work to be useful, not only to students, but to 
practitioners as well. It reflects credit upon the 
industry and energy of its able editor.—Boston 
Medical and Surgical Journal, Sept. 3.1874. 
We can say with the strictest truth that it is the 
best work of the kind with which we are ac- 
quainted. It embodies in a condensed form all 
recent contributions to practical medicine, and is 
therefore useful to everybusy practitioner through- 
out our country, besides being admirably adapted 
to the use of students of medicine. The book is 
faithfully and ably executed.—Charleston Medical 
Journal, April, 1875. 
NEILL, JOHN, 31. D., and SMITH, F. G., M. D., 
Late Surgeon to the Penna. Hospital. Prof, of the Institutes of Med. in the Univ. oj Penna. 
An Analytical Compendium of the Various Branches of Medical 
Science, for the use and examination of Students. A new edition, revised and improved. 
In one large royal 12mo. volume of 974 pages, with 374 woodcuts. Cloth, $4; leather, $4.75. 
LUDLOW, J. L., 31. D., 
Consulting Physician to the Philadelphia Hospital, etc. 
A Manual of Examinations upon Anatomy, Physiology, Surgery, Practice of 
Medicine, Obstetrics, Materia Medica, Chemistry, Pharmacy and Therapeutics. To which 
is added a Medical Formulary. Third edition, thoroughly revised, and greatly enlarged. In 
one 12mo. volume of 816 pages, with 370 illustrations. Cloth, $3.25; leather, $3.75. 
The arrangement of this volume in the form of question and answer renders it espe- 
cially suitable for the office examination of students, and for those preparing for graduation 
HOBLYN, RICHARD D., M. D. 
A Dictionary of the Terms Used in Medicine and the Collateral 
Sciences. Revised, with numerous additions, by Isaac Hays, M. D., late editor of 
The American Journal of the Medical Sciences. In one large royal 12mo. volume of 520 
double-columned pages. Cloth, $1.50; leather, $2.00. 
It is the best book of definitions we have, and ought always to be upon the student’s table.—Southern 
Medical and Surgical Journal. 4 
Lea Brothers & Co.’s Publications—Dictionaries. 
JUST READY. 
THE 
IlftTionsL U2gdi(£al Dictiodary 
INCLUDING 
English, French, German, Italian and Latin Technical Terms used in Medicine and 
the Collateral Sciences, and a Series of Tables of Useful Data. 
BY 
John SJ.D., LL.D,, Edig. and Hanv., D.C.L., Op. 
Member of the National Academy of Sciences, Surgeon U. S. A., etc. 
WITH THE COLLABORATION OF 
Prof. W. O. ATWATER. JAMES M. FLINT, M. D., WASHINGTON MATTHEWS, M. D., 
FRANK BAKER, M. D., J. H. KIDDER, M. D., C. S. MINOT, M.D. 
S. M. BURNETT, M. D., WILLIAM LEE, M.D., H. C. YARROW, M. D., 
W. T. COUNCILMAN, M. D., R. LORINI, M.D., 
In two very handsome royal octavo volumes containing 1574 pages, 
with two colored plates. 
Per Volume—Cloth, $6; Leather, $7; Half Morocco, Marbled Edges, $8.50. For Sale 
by Subscription only. Specimen pages on application. Address the Publishers. 
The publishers have great pleasure in presenting to the profession a new practical 
working dictionary embracing in one alphabet all current terms used in every depart- 
ment of medicine in the five great languages constituting modern medical literature. 
For the vast and complex labor involved in such an undertaking no one better quali- 
fied than Dr. Billings could have been selected. He has planned the work, chosen the 
most accomplished men to assist him in special departments, and personally supervised 
and combined their work into a consistent and uniform whole. 
Special care has been taken to render the definitions clear, sharp and concise. 
They are given in English, with synonyms in French, German and Italian of the more 
important words in English and Latin. 
Regarded as a dictionary, therefore, this standard work supplies the physician, 
surgeon and specialist with all information concerning medical words, simple and com- 
pound, found in English, giving correct spelling, clear, sharp definitions and accentua- 
tion, and furthermore it enables him to consult foreign works and to understand the large 
and increasing number of foreign words used in medical English. It is especially full 
in phrases comprising two, three or more words used in special senses in the various 
departments of medicine. 
The work is, however, far more than a dictionary, and partakes of the nature of an 
encyclopaedia, as it gives in its body a large amount of valuable therapeutical and chemi- 
carinformation, and groups in its tables, in a condensed and convenient form, a vast 
amount of important data which will be consulted daily by all in active practice. 
The completeness of the work is made evident by the fact that it defines 84,844 
separate words and phrases. 
The type has been most carefully selected for boldness and clearness, and everything 
has been done to secure ease, rapidity and durability in use. 
Its scope is one which will at once satisfy the 
student and meet all the requirements of the med- 
ical practitioner. Clear and comprehensive defi- 
nitions of words should form the prime feature of 
any dictionary, and in this one the chief aim 
seems to be to give the exact signification and the 
different meanings of terms in use in medicine 
and the collateral sciences in language as terse as 
is compatible with lucidity. The utmost brevity 
and conciseness have been kept in view. The work 
is remarkable, too, for its fulness. The enumera- 
tions and subdivisions under each word-heading 
are strikingly complete, as regards alike the Eng- 
lish tongue and the languages chiefly employed 
by ancient and modern science. It is impossible 
to do justice to the dictionary by any casual illus 
tration. It presents to the English reader a 
thoroughly scientific mode of acquiring a rich 
vocabulary and offers an accurate and ready means 
of reference in consulting works in any of the 
three modern continental languages which are 
richest in medical literature. To add to its use- 
fulness as a work of reference some valuable 
tables are given. Another feature of the work is 
t he accuracy of its definitions, all of which have 
been checked by comparison with many other 
standard works in the different languages it deals 
with. Apart from the boundless stores of informa- 
tion which may be gained by the study of a good 
dictionary, one is enabled by the work under notice 
to read intelligently any technical treatise in any 
of the four chief modern languages. There can- 
not be two opinions as to the great value and use- 
fulness of this dictionary as a Dook of ready refer- 
ence for all sorts and conditions of medical men. 
So far as we have been able to see, no subject has 
been omitted, and in respect of completeness it will 
be found distinctly superiorto any medical lexicon 
yet published.— The London Lancet, April 5,1890. Lea Brothers & Co.’s Publications—Anatomy. 
5 
GRAY, HENRY, F. R. S., 
Lecturer on Anatomy at St. George's Hospital, London. 
Anatomy, Descriptive and Surgical. Edited by T. Pickering Pick, 
F. R. C. S., Surgeon to and Lecturer on Anatomy at St. George’s Hospital, London, 
Examiner in Anatomy, Royal College of Surgeons of England. A new American from 
the eleventh enlarged and improved London edition, thoroughly revised and re-edited 
by William W. Keen, M. D., Professor of Surgery in the Jefferson Medical College of 
Philadelphia. To which is added the second American from the latest English edition of 
Landmarks, Medical and Surgical, by Luther Holden, F. R. C. S. In one imperial 
octavo volume of 1098 pages, with 6S5 large and elaborate engravings on wood. Price of 
edition in black: Cloth, $6; leather, $7; half Russia, $7.50. Price of edition in colors 
(see below): Cloth, $7.25; leather, $8.25; half Russia, $8.75. 
This work covers a more extended range of subjects than is customary in the ordinary 
text-books, giving not only the details necessary for the student, but also the application to 
those details to the practice of medicine and surgery. It thus forms both a guide for the 
learner and an admirable work of reference for the active practitioner. The engraving 
form a special feature in the work, many of them being the size of nature, nearly all 
original, and having the names of the various parts printed on the body of the cut, in 
place of figures of reference with descriptions at the foot. In this edition a new departure 
has been taken by the issue of the work with the arteries, veins and nerves distinguished 
by different colors. The engravings thus form a complete and splendid series, which will 
greatly assist the student in forming a clear idea of Anatomy, anu will also serve to refresh 
the memory of those who may find in the exigencies of practice the necessity of recall- 
ing the details of the dissecting-room. Combining, as it does, a complete Atlas of 
Anatomy with a thorough treatise on systematic, descriptive and applied Anatomy, 
the work will be found of great service to all physicians who receive students in their 
offices, relieving both preceptor and pupil of much labor in laying the groundwork of a 
thorough medical education. 
For the convenience of those who prefer not to pay the slight increase in cost necessi- 
tated by the use of colors, the volume is published also in black alone, and maintained 
in this style at the price of former editions, notwithstanding its largely increased size. 
Landmarks, Medical and Surgical, by the distinguished Anatomist, Mr. Luther Holden, 
has been appended to the present edition as it was to the previous one. This work gives 
in a clear, condensed and systematic way all the information by which the practitioner can 
determine from the external surface of the body the position of internal parts. Thus 
complete, the work will furnish all the assistance that can be rendered by type and 
illustration in anatomical study. 
The most popular work on anatomy ever written. 
It is sufficient to say of it that this edition, thanks 
to its American editor, surpasses all other edi- 
tions —Jour, of the Amer. Med. Ass'n, Dec. 31, 1887. 
A work which for more than twenty years has 
had the lead of all other text-books on anatomy 
throughout the civilized world comes to hand in 
such beauty of execution and accuracy of text 
and illustration as more than to make good the 
large promise of the prospectus. It would be in- 
deed difficult to name a feature wherein the pres- 
ent American edition of Gray could be mended 
or bettered, and it needs no prophet to see that 
the royal work is destined for many years to come 
to hold the first place among anatomical text- 
books. The work is published with black and 
colored plates. It is a marvel of book-making.— 
American Practitioner and News, Jan. 21,1888. 
Gray’s Anatomy is the most magnificent work 
upon anatomy which has ever been published in 
the English or any other language.—Cincinnati 
Medical News, Nov. 1887. 
As the book now goes to the purchaser he is re- 
ceiving the best work on anatomy that is published 
in any language.— Virginia Med. Monthly, Dec. 1887. 
Gray’s standard Anatomy has been and will be 
for years the text-book for students. The book 
needs only to be examined to be perfectly under- 
stood.—Medical Press of Western New York, Jan. 
1888. 
Also for sale separate— 
HOLDEJY, LTJTHER, F. R. C. S., 
Surgeon to St. Bartholomew's and the Foundling Hospitals, London. 
Landmarks, Medical and Surgical. Second American from the latest revised 
English edition, with additions by W. W. Keen, M. D., Professor of Artistic Anatomy in 
the Penna. Academy of Fine Arts. In one 12mo. volume of 148 pages. Cloth, $1.00. 
DUNGLISON, ROBLFY, M. I)., 
Late Professor of Institutes of Medicine in the Jefferson Medical College of Philadelphia. 
MEDICAL LEXICON; A Dictionary of Medical Science: Containing 
a concise Explanation of the various Subjects and Terms of Anatomy, Physiology, Pathol- 
ogy, Hygiene, Therapeutics, Pharmacology, Pharmacy, Surgery, Obstetrics, Medical Juris- 
prudence and Dentistry, Notices of Climate and of Mineral Waters, Formulae for Officinal, 
Empirical and Dietetic Preparations, with the Accentuation and Etymology of the Terms, 
and the French and other Synonymes, so as to constitute a French as well as an English 
Medical Lexicon. Edited by Richard J. Dunglison, M. D. In one very large and 
handsome royal octavo volume of 1139 pages. Cloth, $6.50; leather, raised bands, $7.50; 
very handsome half Russia, raised bands, $8. 
It has the rare merit that it certainly has no rival in the English language for accuracy 
and extent of references.—London Medical Gazette. 6 
Lea Brothers & Co.’s Publications—Anatomy. 
ALLEN, HARRISON, M. D., 
Professor of Physiology in the University of Pennsylvania. 
A System of Human Anatomy, Including Its Medical and Surgical 
Relations. For the use of Practitioners and Students of Medicine. With an Intro- 
ductory Section on Histology. By E. O. Shakespeare, M. D., Ophthalmologist to 
the Philadelphia Hospital. Comprising 813 double-columned quarto pages, with 380 
illustrations on 109 full page lithographic plates, many of which are in colors, and 241 
engravings in the text. In six Sections, each in a portfolio. Section I. Histology. 
Section II. Bones and Joints. Section III. Muscles and Fascia. Section IV. 
Arteries, Veins and Lymphatics. Section V. Nervous System. Section VI. 
Organs of Sense, of Digestion and Genito-Urinary Organs, Embryology, 
Development, Teratology, Superficial Anatomy, Post-Mortem Examinations, 
and General and Clinical Indexes. Price per Section, $3.50; also bound in one 
volume, cloth, $23.00; very handsome half Russia, raised bands and open back, $25.00. 
For sale by subscription only. Apply to the Publishers. 
It is to be considered a study of applied anatomy 
in its widest sense—a systematic presentation of 
such anatomical facts as can be applied to the 
practice of medicine as well as of surgery. Our 
author is concise, accurate and practical in his 
statements, and succeeds admirably in infusing 
an interest into the study of what is generally con- 
sidered a dry subject. The department of Histol- 
ogy is treated in a masterly manner, and the 
ground is travelled over by one thoroughly famil- 
iar with it. The illustrations are made with great 
care, and are simply superb. There is as much 
of practical application of anatomical points to 
the every-day wants of the medical clinician as 
to those of the operating surgeon. In fact, few 
general practitioners will read the work without a 
feeling of surprised gratification that so many 
points, concerning which they may never have 
thought before are so well presented for their con- 
sideration. It is a work which is destined to be 
the best of' its kind in any language.—Medical 
Record, Nov. 25,1882. 
CLARKE, W. B.,F.R.C.S. & LOCKWOOD,C. B., F.R.C.S. 
Demonstrators of Anatomy at St. Bartholomew's Hospital Medical School, London. 
The Dissector’s Manual. In one pocket-size 12mo. volume of 396 pages, with 
49 illustrations. Limp cloth, red edges, $1.50. See Students’ Series of Manuals, page 31. 
Messrs.Clarke and Lockwood have written abook 
that can hardly be rivalled as a practical aid to the 
dissector. Their purpose,whicn is “how to de- 
scribe the best way to display the anatomical 
structure,” has been fully attained. They excel in 
a lucidity of demonstration and graphic terseness 
of expression, which only a long training and 
intimate association with students could have 
given. With such a guide as this, accompanied 
by so attractive a commentary as Treves’ Surgical 
Applied Anatomy (same series), no student could 
fail to be deeply and absorbingly interested in the 
study of anatomy.—New Oi'leans Medical and Sur- 
gical Journal, April, 1884. 
HIRST, BARTON C., M.D., & PIERSOL, GEO. A., M.D. 
Professor of Obstetrics in the University Professor of Anatomy and Embryology in 
of Pennsylvania. 'the University of Pennsylvania.' 
Human Monstrosities. Magnificent folio, containing about 120 pages of text, 
illustrated with engravings, and many photographic plates from nature. In four parts, 
price, each, $5. Limited edition, for sale by subscription only. Address the Publishers. 
TREVES, FREDERICK, F. R. C. S., 
Senior Demonstrator of Anatomy and Assistant Surgeon at the London Hospital. 
Surgical Applied Anatomy. In one pocket-size 12mo. volume of 540 pages, 
with 61 illustrations. Limp cloth, red edges, $2.00. See Students’ Series of Manuals, 
page 31. 
BELLAMY, EDWARD, F. Jt. C. S., 
Senior Assistant-Surgeon to the Charing-Cross Hospital, London. 
The Student’s Guide to Surgical Anatomy: Being a Description of the 
most Important Surgical Begions of the Human Body, and intended as an Introduction to 
operative Surgery. In one 12mo. volume of 300 pages, with 50 illustrations. Cloth, $2.25. 
WILSON, Fit ASM US, F. It. S. 
A System of Human Anatomy, General and Special. Edited by W. H. 
Gobrecht, M. D., Professor of General and Surgical Anatomy in the Medical College of 
Ohio. In one large and handsome octavo volume of 616 pages, with 397 illustrations. 
Cloth, $4.00; leather, $5.00. 
CLELAND, JOHN, M. D., F. R. S., 
Professor of Anatomy and Physiology in Queen’s College, Galway. 
A Directory for the Dissection of the Human Body. In one 12mo. 
volume of 178 pages. Cloth, $1.25. 
HARTSHORNE’S HANDBOOK OF ANATOMY 
AND PHYSIOLOGY. Second edition, revised. 
In one royal 12mo. volume of 310 pages, with 220 
woodcuts. Cloth, $1.75. 
HORNER'S SPECIAL ANATOMY AND HISTOL- 
OGY. Eighth edition, extensively revised and 
1 modified. In two octavo volumes of 1007 pages, 
j with 320 woodcuts. Cloth, $6.00. Lea Brothers & Co.’s Publications—Physics, Pliysiol., Anat. 
7 
BRAPER, JOHN C., M. B., LL. B., 
Professor of Chemistry in the University of the City of New York. 
Medical Physics. A Text-book for Students and Practitioners of Medicine. In 
one octavo volume of 734 pages, with 376 woodcuts, mostly original. Cloth, $4. 
FROM THE PREFACE. 
The fact that a knowledge of Physics is indispensable to a thorough understanding of 
Medicine has not been as fully realized in this country as in Europe, where the admirable 
works of Desplats and Gariel, of Robertson and of numerous German writers constitute a 
branch of educational literature to which we can show no parallel. A full appreciation 
of this the author trusts will be sufficient justification for placing in book form the sub- 
stance of his lectures on this department of science, delivered during many years at the 
University of the City of New York. 
Broadly speaking, this work aims to impart a knowledge of the relations existing 
between Physics and Medicine in their latest state of development, and to embody in the 
pursuit of this object whatever experience the author has gained during a long period of 
teaching this special branch of applied science. 
While all enlightened physicians will agree that 
a knowledge of physics is desirable for the medi- 
cal student, only those actually engaged in the 
teaching of the primary subjects can be fully 
aware of the difficulties encountered by students 
who attempt the study of these subjects without 
a knowledge of either physics or chemistry. 
These are especially felt by the teacher of physi- 
ology. 
It is, however, impossible for him to impart a 
knowledge of the main facts of his subject and 
establish them by reasons and experimental dem- 
onstration, and at the same time undertake to 
teach ah initio the principles of chemistry or phys- 
ics. Hence the desirability, we may say the 
necessity, for some such work as the present one. 
No man in America was better fitted than Dr. 
Draper for the task he undertook, and he has pro- 
vided the student and practitioner of medicine 
with a volume at once readable and thorough. 
Even to the student who has some knowledge of 
physics this book is useful, as it shows him its 
applications to the profession that he has chosen. 
Dr. Draper, as an old teacher, knew well the diffi- 
culties to be encountered in bringing his subject 
within the grasp of the average student, and that 
he has succeeded so well proves once more that 
the man to write for and examine students is the 
one who has taught and is teaching them. The 
book is well printed and fully illustrated, and in 
every way deserves grateful recognition.— The 
Montreal Medical Journal, July, 1890. 
ROBERTSON, J. McGREGOR, 31. A., M. B., 
Muirhead Demonstrator of Physiology, University of Glasgow. 
Physiological Physics. In one 12mo. volume of 537 pages, with 219 illustra- 
tions. Limp cloth, $2.00. See Students’ Series of Manuals, page 31. 
The title of this work sufficiently explains the 
nature of its contents. It is designed as a man- 
ual for the student of medicine, an auxiliary to 
his text-book in physiology, and it would be particu- 
larly useful as a guide to his laboratory experi- 
: ments. It will be found of great value to the 
practitioner. It is a carefully prepared book of 
reference, concise and accurate, and as such we 
heartily recommend it.—Journal of the Amerncan 
Medical Association, Dec. 6, 1884. 
BARTON, JOHN C., M. B., 
Professor Emeritus of Physiology in the College of Physicians and Surgeons, New York. 
Doctrines of the Circulation of the Blood. A History of Physiological 
Opinion and Discovery in regard to the Circulation of the Blood. In one handsome 
12mo. volume of 293 pages. Cloth, $2. 
Dr. Dalton’s work is the fruit of the deep research 
of a cultured mind, and to the busy practitioner it 
cannot fail to be a source of instruction. It will 
inspire him with a feeling of gratitude and admir- 
ation for those plodding workers of olden times, 
who laid the foundation of the magnificent temple 
of medical science as it now stands.—New Orleans 
Medical and Surgical Journal, Aug. 1885. 
In the progress of physiological study no fact 
was of greater moment, none more completely 
revolutionized the theories of teachers, than the 
discovery of the circulation of the blood. This 
explains the extraordinary interest it has to all 
medical historians. The volume before us is one 
of three or four which have been written within a 
few years by American physicians. It is in several 
respects the most complete. The volume, though 
small in size, is one of the most creditable con- 
tributions from an American pen to medical history 
that has appeared.—Med. & Surg. Rep., Dec. 6,1884. 
BELL, F. JEFFREY, M. A., 
Professor of Comparative Anatomy at King's College, London. 
Comparative Physiology and Anatomy. In one 12mo. volume of 561 pages, 
with 229 illustrations. Limp cloth, $2.00. See Students’ Series of Manuals, page 31. 
The manual is preeminently a student’s book— 
clear and simple in language and arrangement. 
It is well and abundantly illustrated, and is read- 
able and interesting. On the whole we consider 
it the best work in existence in the English 
language to place in the hands of the medical 
student.—Bristol Medico-Chirurgical Journal, Mar. 
1886. 
ELLIS, GEORGE VINER, 
Emeritus Professor of Anatomy in University College, London. 
Demonstrations of Anatomy. Being a Guide to the Knowledge of the 
Human Body by Dissection. From the eighth and revised London edition. In one very 
handsome octavo volume of 716 pages, with 249 illustrations. Cloth, $4.25; leather, $5.25. 
ROBERTS, JOHN B., A. M., M. B., 
Lecturer in Anatomy in the University of Pennsylvania. 
The Compend of Anatomy. For use in the dissecting-room and in preparing 
for examinations. In one 16mo. volume of 196 pages. Limp cloth, 75 cents. 8 
Lea Brothers & Co.’s Publications—Physiology, Chemistry. 
CHAPMAN, HENRY C., M. D., 
Professor of Institutes of Medicine and Medical Juris, in the Jefferson Med. Coll, of Philadelphia. 
A Treatise on Human Physiology. In one handsome octavo volume of 
925 pages, with 605 fine engravings. Cloth, $5.50; leather, $6.50. 
It represents very fully the existing state of 
physiology. The present work has a special value 
to the student and practitioner as devoted more 
to the practical application of well-known truths 
which the advance of science has given to the 
profession in this department, which may be con- 
sidered the foundation of rational medicine.—Buf- 
falo Medical and Surgical Journal, Dec. 1887. 
Matters which have a practical bearing on the 
practice of medicine are lucidly expressed; tech- 
nical matters are given in minute detail; elabo- 
rate directions are stated for the guidance of stu- 
dents in the laboratory. In every respect the 
work fulfils its promise, whether as a complete 
treatise for the student or for the physician ; for 
the former it is so complete that he need look no 
farther, and the latter will find entertainment and 
instruction in an admirable book of reference.— 
North Carolina Medical Journal, Nov. 1887. 
The work certainly commends itself to both 
student and practitioner. What is most demanded 
by the progressive physician of to-day is an adap- 
tation of physiology to practical therapeutics, and 
this work is a decided improvement in this respect 
over other works in the market. It will certainly 
take place among the most valuable text-books.— 
Medical Age, Nov. 25, 1887. 
It is the production of an authof delighted with 
his work, and able to inspire students with an en- 
thusiasm akin to his own —American Practitioner 
and News, Nov. 12,1887. 
DALTON, JOHN C., M. D., 
Professor of Physiology in the College of Physicians and Surgeons, New York, etc. 
A Treatise on Human Physiology. Designed for the use of Students and 
Practitioners of Medicine. Seventh edition, thoroughly revised and rewritten. In one 
very handsome octavo volume of 722 pages, with 252 beautiful engravings on wood. Cloth, 
$5.00; leather, $6.00. 
From the first appearance of the book it has 
been a favorite, owing as well to the author’s 
renown as an oral teacher as to the charm of 
simplicity with which, as a writer, he always 
succeeds in investing even intricate subjects. 
It must be gratifying to him to observe the fre- 
quency with which his work, written for students 
and practitioners, is quoted by other writers on 
physiology. This fact attests its value, and, in 
great measure, its originality. It now needs no 
such seal of approbation, however, for the thou- 
sands who have studied it in its various editions 
have never been in any doubt as to its sterling 
worth.—N. Y. Medical Journal, Oct. 1882. 
Professor Dalton’s well-known and deservedly- 
appreciated work has long passed the stage at 
which it could be reviewed in the ordinary sense. 
The work is eminently one for the medical prac- 
titioner, since it treats most fully of those branches 
of physiology which have a direct bearing on the 
diagnosis and treatment of disease. The work is 
one which we can highly recommend to all our 
readers.—Dublin Journal of Medical Science, Feb.’S3. 
FOSTER, MICHAEL, M. I)., E. R. S., 
Prelector in Physiology and Fellow of Trinity College, Cambridge, England. 
Text-Book of Physiology. New (fourth) and enlarged American from the 
fifth and revised English edition, with notes and additions. In one handsome octavo vol- 
ume of about 900 pages, with about 300 illustrations. In press. 
A REVIEW OF THE FIFTH ENGLISH EDITION IS APPENDED. 
It is delightful to meet a book which deserves 
only unqualified praise. Such a book is now before 
us. It is in all respects an ideal text-book. With a 
complete, accurate and detailed knowledge of his 
subject, the author has succeeded in giving a 
thoroughly consecutive and philosophic account 
of the science. A student’s attention is kept 
throughout fixed on the great and salient ques- 
tions, and his energies are not frittered away and 
degenerated on petty and trivial details. Review- 
ing this volume as a'whole we are justified in say- 
ing that it is the only thoroughly good text-book 
of physiology in the English language, and that it 
is probably the best text-book in any language. 
—Edinburgh Medical Journal, December 1889. 
POWER, HENRY, M. B., F. R. C. S., 
Examiner in Physiology, Royal College of Surgeons of England. 
Human Physiology. Second edition. In one handsome pocket-size 12mo. vol- 
ume of 509 pp., with 68 illustrations. Cloth, $1.50. See Students’ Series of Manuals, p. 31. 
SIMON, W., Ph. I)., M. D., 
Professor of Chemistry and Toxicology in the College of Physicians and Surgeons, Baltimore, and 
Professor of Chemistry m the Maryland College of Pharmacy. 
Manual of Chemistry. A Guide to Lectures and Laboratory work for Beginners 
in Chemistry. A Text-book, specially adapted for Students of Pharmacy and Medicine. 
New (second) edition. In one 8vo. vol. of 478 pp., with 44 woodcuts and 7 colored plates 
illustrating 56 of the most important chemical tests. Cloth, $3.25. 
In this book the author has endeavored to meet 
the wants of the student of medicine or pharmacy 
in regard to his chemical studies, and he has suc- 
ceeded in presenting his subject so clearly that no 
one who really wishes to acquire a fair knowledge 
of chemistry can fail to do so with the help of this 
work. The largest section of the book is naturally 
that devoted to the consideration of the carbon 
compounds, or organic chemistry. An excellent 
feature is the introduction of a number of plates 
showing the various colors of the most important 
chemical reactions of the metallic salts, of some 
of the alkaloids, and of the urinary tests. In the 
part treating of physiological chemistry the section 
on analysis of the urine will be found very practi- 
cal, and well suited to the needs of the practitioner 
of medicine.— The Medical Record, May 25, 1889. 
Wohler’s Outlines of Organic Chemistry. Edited by Fittig. Translated 
bv Ira Remsen, M. D., Ph. D. In one 12mo. volume of 550 pages. Cloth, $3. 
LEHMANN’S MANUAL OF CHEMICAL PHYS- 
IOLOGY. In one octavo volume of 327 pages, 
with 41 illustrations. Cloth, 82.25. 
CARPENTER’S HUMAN PHYSIOLOGY. Edited 
by Henby Power. In one octavo volume. 
CARPENTER’S PRIZE ESSAY ON THE USE AND 
Abuse of Alcoholic Liquors in Health and Dis- 
ease. With explanations of scientific words. Small 
12mo. 178 pages. Cloth, 60 cents. Lea Brothers & Co.’s Publications—Chemistry. 
9 
FRANKLAND, E., JD. C. L., F.R.S., &JAEE, F. R., F. I. C., 
Inorganic Chemistry. In one handsome octavo volume of 677 pages with 51 
woodcuts and 2 plates. Cloth, $3.75 ; leather, $4.75. 
Professor of Chemistry in the Normal School 
of Science, London. 
Assist. Prof, of Chemistry in the Normal 
School of Science, London. 
This work should supersede other works of its 
class in the medical colleges. Itis certainly better 
adapted than any work upon chemistry,with which 
we are acquainted, to impart that clear and full 
knowledge of the science which students of med- 
icine should have. Physicians who feel that their 
chemical knowledge is behind the times, would 
do well to devote some of their leisure time to the 
study of this work. The descriptions and demon- 
strations are made so plain that there is no diffi- 
culty in understanding them.—Cincinnati Medical 
News, January, 1886. 
This excellent treatise will not fail to take its 
place as one of the very best on the subject of 
which it treats. We have been much pleased 
with the comprehensive and lucid manner in 
which the difficulties of chemical notation and 
nomenclature have been cleared up by the writers. 
It shows on every page that the problem of 
rendering the obscurities of this science easy 
of comprehension has long and successfully 
engaged the attention of the authors.—Medical 
ana Surgical Reporter, October 31,1885. 
FOWNES, GEORGE, Eh. I). 
A Manual of Elementary Chemistry; Theoretical and Practical. Em- 
bodying Watts’ Physical and Inorganic Chemistry. New American, from the twelfth English 
edition. In one large royal 12mo. volume of 1061 pages, with 168 illustrations on wood 
and a colored plate. Cloth, $2.75; leather, $3.25. 
Fownes' Chemistry has been a standard text- 
book upon chemistry for many years. Its merits 
are very fully known by chemists and physicians 
everywhere in this country and in England. As 
the science has advanced by the making of new 
discoveries, the work has been revised so as to 
keep it abreast of the times. It has steadily 
maintained its position as a text-book with medi- 
cal students. In this work are treated fully: Heat, 
Light and Electricity, including Magnetism. The 
influence exerted by these forces in chemical 
action upon health and disease, etc., is of the most 
important kind, and should be familiar to every 
medical practitioner. We can commend the 
work as one of the very best text-books upon 
chemistry extant.—Cincinnati Med. News, Oct. ’85. 
Of all the works on chemistry intended for the 
use of medical students, Fownes’ Chemistry is 
perhaps the most widely used. Its popularity is 
based upon its excellence. This last edition con- 
tains all of the material found in the previous, 
and it is also enriched by the addition of Watts’ 
Physical and Inorganic Chemistry. All of the mat- 
ter is brought to the present standpoint of chemi- 
cal knowledge. We may safely predict for this 
work a continuance of the fame and favor it enjoys 
among medical students.—New Orleans Medical 
and Surgical Journal, March, 1886. 
ATTEIELI), JOHN, M. A., Eh. I)., F. I. C., F. R. S., Etc. 
Professor of Practical Chemistry to the Pharmaceutical Society of Great Britain, etc. 
Chemistry, General, Medical and Pharmaceutical; Including the Chem- 
istry of the U. S. Pharmacopoeia. A Manual of the General Principles of the Science, 
and their Application to Medicine and Pharmacy. A new American, from the twelfth 
English edition, specially revised by the Author for America. In one handsome royal 
12mo. volume of 782 pages, with 88 illustrations. Cloth, $2.75; leather, $3.25. 
D.f F. I. CF. R. S., Etc. 
Attfield’s Chemistry is the most popular book 
among students of medicine and pharmacy. This 
popularity has a good, substantial basis. It rests 
upon real merits. Attfield’s work combines in the 
happiest manner a clear exposition of the theory 
of chemistry with the practical application of this 
knowledge to the everyday dealings of the phy- 
sician and pharmacist. His discernment is shown 
not only in what he puts into his work, but also in 
what he leaves out. His book is precisely what 
the title claims for it. The admirable arrangement 
of the text enables a reader to get a good idea of 
chemistry without the aid of experiments, and 
again it is a good laboratory guide, and finally it 
contains such a mass of well-arranged information 
that it will always serve as a handy book of refer- 
ence. He does not allow any unutilizable knowl- 
edge to slip into his book; his long years of 
experience have produced a work which is both 
scientific and practical, and which shuts out 
everything in the nature of a superfluity, and 
therein lies the secret of its success. This last 
edition shows the marks of the latest progress 
made in chemistry and chemical teaching.—New 
Orleans Medical and Surgical Journal, Nov. 1889. 
BLOXAM, CHARLES L., 
Professor of Chemistry in King's College, London. 
Chemistry, Inorganic and Organic. New American from the fifth Lon- 
don edition, thoroughly revised and much improved. In one very handsome octavo 
volume of 727 pages, with 292 illustrations. Cloth, $2.00; leather, $3.00. 
Comment from us on this standard work is al- 
most superfluous. It differs widely in scope and 
aim from that of Attfield, and in its way is equally 
beyond criticism. It adopts the most direct meth- 
ods in stating the principles, hypotheses and facts 
of the science. Its language is so terse and lucid, 
and its arrangement ot matter so logical in se- 
quence that the student never has occasion to 
complain that chemistry is a hard study. Much 
attention is paid to experimental illustrations of 
chemical principles and phenomena, and the 
mode of conducting these experiments. The book 
maintains the position it has always held as one of 
the best manuals of general chemistry tn the Eng- 
lish language.—Detroit Lancet, Feb. 1884. 
We know of no treatise on chemistry which 
contains so much practical information in the 
same number of pages. The book can be readily 
adapted not only to the needs of those who desire 
a tolerably complete course of chemistry, but also 
to the needs of those who desire only a general 
knowledge of the subject. We take pleasure in 
recommending this work both as a satisfactory 
text-book, and as a useful book of reference.— Bos- 
ton Medical and Surgical Journal, June 19,1884. 
GREENE, WILLIAM II., M. 1)., 
Demonstrator of Chemistry in the Medical Department of the University of Pennsylvania. 
A Manual of Medical Chemistry. For the use of Students. Based upon Bow- 
man’s Medical Chemistry. In one 12mo. volume of 310 pages, with 74 illus. Cloth, $1.75. 
It is a concise manual of three hundred pages, 
giving an excellent summary of the best methods 
of analyzing the liquids and solids of the body, both 
or the estimation of their normal constituent and 
the recognition of compounds due to pathological 
conditions. The detection of poisons is treated 
with sufficient fulness for the purpose of the stu- 
dent or practitioner.—Boston Jl. of Chem. June, ’80. 10 
Lea Brothers & Co.’s Publications—Chemistry. 
RE3ISEN, IRA, 31. I)., Fh. I)., 
Professor of Chemistry in the Johns Hopkins University, Baltimore. 
Principles of Theoretical Chemistry, with special reference to the Constitu- 
tion of Chemical Compounds. New (third) and thoroughly revised edition. In one hand- 
some royal 12mo. volume of 316 pages. Cloth, $2.00 
This work of Dr. Remsen is the very text-book 
needed, and the medical student who has it at 
his fingers’ ends, so to speak, can, if he chooses, 
make himself familiar with any branch of chem- 
istry which he may desire to pursue. It would be 
difficult indeed to find a more lucid, full, and at 
the same time compact explication of the philos- 
ophy of chemistry, than the book before us, and 
we recommend it to the careful and impartial 
examination of college faculties as the text-book of 
chemical instruction.—St. Louis Medical and Sur- 
gical Journal, January, 1888. 
It is a healthful sign when we see a demand for 
a third edition of such a book as this. This edi- 
tion is larger than the last by about seventy-five 
pages, and much of it has been rewritten, thus 
j bringing it fully abreast of the latest investiga- 
! tions.—N. Y. Medical Journal, Dec. 31, 1887. 
CHARLES, T. CRANSTOVN, 31. D., F. C. S., 31. S., 
Formerly Asst. Prof, and Denwnst. of Chemistry and Chemical Physics, Queen's College, Belfast. 
The Elements of Physiological and Pathological Chemistry. A 
Handbook for Medical Students and Practitioners. Containing a general account of 
Nutrition, Foods and Digestion, and the Chemistry of the Tissues, Organs, Secretions and 
Excretions of the Body in Health and in Disease. Together with the methods for pre- 
paring or separating their chief constituents, as also for their examination in detail, and 
an outline syllabus of a practical course of instruction for students. In one handsome octavo 
volume of 463 pages, with 38 woodcuts and 1 colored plate. Cloth, $3.50. 
Dr. Charles is fully impressed with the impor- 
tance and practical reach of his subject, and he 
has treated it in a competent and instructive man- 
ner. We cannot recommend a better book than 
the present. In fact, it fills a gap in medical text- 
books, and that is a thing which can rarely be said 
nowadays. Dr. Charles has devoted much space 
to the elucidation of urinary mysteries. He does 
this with much detail, and yet in a practical and 
intelligible manner. In fact, the author has filled 
his book with many practical hints.—Medical Rec- 
ord, December 20, 1884. 
HOFF3IANN, F., A.3I., Fh.D., & LOWER, F.B., Fli.D., 
Public Analyst to the State of New York. Prof, of Anal. Chem. in the Phil. Coll, of Pharmacy. 
A Manual of Chemical Analysis, as applied to the Examination of Medicinal 
Chemicals and their Preparations. Being a Guide for the Determination of their Identity 
and Quality, and for the Detection of Impurities and Adulterations. For the use of 
Pharmacists, Physicians, Druggists and Manufacturing Chemists, and Pharmaceutical and 
Medical Students. Third edition, entirely rewritten and much enlarged. In one very 
handsome octavo volume of 621 pages, with 179 illustrations. Cloth, $4.25. 
We congratulate the author on the appearance 
of the third edition of this work, published for the 
first time in this country also. It is admirable and 
the information it undertakes to supply is both 
extensive and trustworthy. The selection of pro- 
cesses for determining the purity of the substan- 
ces of which it treats is excellent and the descrip- 
tion of them singularly explicit. Moreover, it is 
exceptionally free from typographical errors. We 
have no hesitation in recommending it to those 
who are engaged either in the manufacture or the 
testing of medicinal chemicals.—London Pharma•* 
ceutical Journal and Transactions, 1883. 
CLOWES, FRANK, D. Sc., London, 
Senior Science-Master at the High School, Newcastle-under-Lyme, etc. 
An Elementary Treatise on Practical Chemistry and Qualitative 
Inorganic Analysis. Specially adapted for use in the Laboratories of Schools and 
Colleges and by Beginners. Third American from the fourth and revised English edition. 
In one very handsome royal 12mo. volume of 387 pages, with 55 illustrations. Cloth, 
$2.50. 
This work has long been a favorite with labora- 
tory instructors on account of its systematic plan, 
carrying the student step by step from the simplest 
questions of chemical analysis, to the more recon- 
dite problems. Features quite as commendable 
are the regularity and system demanded of the 
student in the performance of each analysis. 
These characteristics are preserved in the present 
edition, which we can heartily recommend as a sat- 
isfactory guide for the student of inorganic chem- 
ical analysis.—New York Medical Journal, Oct. 9, 
1886. 
RALFE, CHARLES II., 31. I)., F. R. C. F., 
Assistant Physician at the London Hospital. 
Clinical Chemistry. In one pocket-size 12mo. volume of 314 pages, with 16 
illustrations. Limp cloth, red edges, $1.50. 
This is one of the most instructive little works 
that we have met with in a long time. The author 
is a physician and physiologist, as well as a chem- 
ist, consequently the book is unqualifiedly prac- 
tical, telling the physician just what he ought to 
know, of the applications of chemistry in medi- 
See Students' Series of Manuals, page 31. 
cine. Dr. Ralfe is thoroughly acquainted with the 
latest contributions to his science, and it is quite 
refreshing to find the subject dealt with so clearly 
and simply, yet in such evident harmony with the 
modern scientific methods and spirit.—Medical 
Record, February 2,1884. 
CLASSEN, ALEXANDER, 
Professor in the Royal Polytechnic School, Aix-la-Chapelle. 
Elementary Quantitative Analysis. Translated, with notes and additions, by 
Edgar F. Smith, Ph. D., Assistant Professor of Chemistry in the Towne Scientific School, 
University of Penna. In one 12mo. volume of 324 pages, with 36 illus. Cloth, $2.00. 
It is probably the best manual of an elementary j 
nature extant, insomuch as its methods are the j 
best. It teaches by examples, commencing with ] 
single determinations, followed by separations, j 
and then advancing to the analysis of minerals and 
such products as are met with in applied chemis- 
try. It is an indispensable book for students in 
chemistry.—Boston Journal of Chemistry, Oct. 1878. Lea Brothers & Co.’s Publications—Pliarm., Mat. Med., Tlierap. 
11 
DARE, HOBART AMORY, B. Sc., M. I)., 
Professor of Materia Medica and Therapeutics in the Jefferson Medical College of Philadelphia; 
Secretary of the Convention for the Revision of the United States Pharmacopceai of 1890. 
A Text-Book of Practical Therapeutics; With Especial Reference to the 
Application of Remedial Measures to Disease and their Employment upon a Rational 
Basis. With special chapters by Drs. G. E. de Schweinitz, Edward Martin, 
J. Howard Reeves and Barton C. Hirst. New (2d) and revised edition. In one 
handsome octavo volume of 650 pages. Cloth, $3.50; leather, $4.75. Just ready. 
The fact that the first edition of this book was exhausted within six months of its 
publication, and adopted as a text-book in a number of medical schools during that time, 
has encouraged the author in his efforts to make the work more serviceable than before. 
A number of new drugs are discussed which have been tried with sufficiently good results 
to warrant their introduction into a text-book and work of reference, and the latest 
information regarding the more familiar medicaments has been added. The method of 
employing the rest-cure, and the use of suspension in the treatment of locomotor ataxia 
and allied affections are given, and a large number of new prescriptions have been inserted 
to illustrate still further the best means of applying remedies for the cure of disease. 
FROM THE PREFACE TO THE SECOND EDITION. 
BR UNION, T. LAUDER, M l)., D.Sc., E.R.S., E.R.C.P., 
Lecturen' on Materia Medica and Therapeutics at St. Bartholomew's Hospital, London, etc. 
A Text-Book of Pharmacology, Therapeutics and Materia Medica; 
Including the Pharmacy, the Physiological Action and the Therapeutical Uses of Drugs. 
Third edition. Octavo, 1305 pages, 230 illustrations. Cloth, $5*50; leather, $6.50. 
No words of praise are needed for this work, for 
it has already spoken for itself in former editions. 
It was by unanimous consent placed among the 
foremost Dooks on the subject ever published in 
any language, and the better it is known and studied 
the more highly it is appreciated. The present 
edition contains much new matter, the insertion 
of which has been necessitated by the advances 
made in various directions in the art of therapeu- 
tics, and it now stands unrivalled in its thoroughly 
scientific presentation of the modes of drug action. 
No one who wishes to be fully up to the times in 
this science can afford to neglect the study of Dr. 
Brunton’s work. The indexes are excellent, and 
add not a little to the practical value of the book. 
—Medical Record, May 25, 1889. 
MAISCH, JOHN M., Phar. I)., 
Professor of Materia Medica and Botany in the Philadelphia College of Pharmacy. 
A Manual of Organic Materia Medica; Being a Guide to Materia Medica of 
the Vegetable and Animal Kingdoms. For the use of Students, Druggists, Pharmacists 
and Physicians. New 14th) edition, thoroughly revised. In one handsome royal 12mo. 
volume of 529 pages, with 258 illustrations. Cloth, $3. 
For everyone interested in materia medica, 
Maisch’s Manual, first published in 1882, and now 
in its fourth edition, is an indispensable book. 
For the American pharmaceutical student it is 
the work which will give him the necessary knowl- 
edge in the easiest way, partly because the text is 
brief, concise, and free from unnecessary matter, 
and partly because of the numerous illustrations, 
whicn bring facts worth knowing immediately be- 
fore his eyes. That it answers its purposes in this 
respect the rapid succession of editions is the best 
evidence. It is the favorite book of the American 
student even outside of Maisch’s several hundred 
personal students. The arrangement of its con- 
tents shows the practical tendency of the book. 
Maisch’s system of classification is easy and com- 
prehensive.—Pharmaceutische Zeitung, Germany, 
1890. 
PARRISH, EDWARD, 
Late Professor of the Theory and Practice of Pharmacy in the Philadelphia College of Pharmacy. 
A Treatise on Pharmacy: Designed as a Text-book for the Student, and as a 
Guide for the Physician and Pharmaceutist. With many Formulae and Prescriptions. 
Fifth edition, thoroughly revised, by Thomas S. Wiegand, Ph. G. In one handsome 
octavo volume of 1093 pages, with 256 illustrations. Cloth, $5; leather, $6. 
No thorough-going pharmacist will fail to possess 
himself of so useful a guide to practice, and no 
physician who properly estimates the value of an 
accurate knowledge of the remedial agents em- 
ployed by him in daily practice, so far as their 
miscibility, compatibility and most effective meth- 
ods of combination are concerned, can afford to 
leave this work out of the list of their works of 
reference. The country practitioner, who must 
always be in a measure his own pharmacist, will 
find it indispensable.—Louisville Medical News, 
March 29,1884. 
HERMANN, Dr. L., 
Professor of Physiology in the University of Zurich. 
Experimental Pharmacology. A Handbook of Methods for Determining the 
Physiological Actions of Drugs. Translated, with the Author’s permission, and with 
extensive additions, by Robert Meade Smith, M. D., Demonstrator of Physiology in the 
University of Pennsylvania. 12mo., 199 pages, with 32 illustrations Cloth, $1.50. 
STILL E, ALFRED, M. D., LL. D., 
Professor of Theory and Practice of Med. and of Clinical Med. in the Univ. of Penna. 
Therapeutics and Materia Medica. A Systematic Treatise on the Action and 
Uses of Medicinal Agents, including their Description and History. Fourth edition, 
revised and enlarged. In two large and handsome octavo volumes, containing 1936 pages. 
Cloth, $10.00; leather, $12.00. 12 
Lea Brothers & Co.’s Publications—Mat. Med., Tlierap. 
STILLEf A., M.D.,LL.D., & MAISCH, J. M.9Phar.D.f 
Professor Emeritus of the Theory and Prac- 
tice of Medicine and of Clinical Medicine 
in the University of Pennsylvania. 
Prof, of Mat. Med. and Botany in Phila 
College of Pharmacy, Sec'y to the Ameri 
can Pharmaceutical Association. 
The National Dispensatory. 
CONTAINING THE NATURAL HISTORY, CHEMISTRY, PHARMACY, ACTIONS AND USES OF 
MEDICINES, INCLUDING THOSE RECOGNIZED IN THE PHARMACOPEIAS OF THE 
UNITED STATES, GREAT BRITAIN AND GERMANY, WITH NUMEROUS 
REFERENCES TO THE FRENCH CODEX. 
Fourth edition revised, and covering the new British Pharmacopoeia. In one mag- 
nificent imperial octavo volume of 1794 pages, with 311 elaborate engravings. Price 
in cloth, $7.25 ; leather, raised bands, $8.00. ***This work will be furnished with Patent 
Ready Reference Thumb-letter Index for $1.00 in addition to the price in any style of binding. 
In this new edition of The National Dispensatory, all important changes in the 
recent British Pharmacopoeia have been incorporated throughout the volume, while in 
the Addenda will be found, grouped in a convenient section of 24 pages, all therapeutical 
novelties which have been established in professional favor since the publication of the 
third edition two years ago. Since its first publication, The National Dispensatory 
has been the most accurate work of its kind, and in this edition, as always before, it may 
be said to be the representative of the most recent state of American, English, German 
and French Pharmacology, Therapeutics and Materia Medica. 
It is with much pleasure that the fourth edition 
of this magnificent work is received. The authors 
and publishers have reason to feel proud of this, 
the most comprehensive, elaborate and accurate 
work of the kind ever printed in this country. It 
is no wonder that it has become the standard au- 
thority for both the medical and pharmaceutical 
profession, and that four editions have been re- 
quired to supply the constant and increasing 
demand since its first appearance in 1879. The 
entire field has been gone over and the various 
articles revised in accordance with the latest 
developments regarding the attributes and thera- 
peutical action of drugs. The remedies of recent 
discovery have received due attention.—Kansas 
Citv Medical Index, Nov. 1887. 
We think it a matter for congratulation that the 
profession of medicine and that of pharmacy have 
shown such appreciation of this great work as to call 
for four editions within the comparatively brief 
period of eight years. The matters with which it 
deals are of so practical a nature that neither the 
physician nor the pharmacist can do without the 
latest text-books on them, especially those that are 
so accurate and comprehensive as this one. The 
book is in every way creditable both to the authors 
and to the publishers.—New York Medical Journal, 
May 21, 1887. 
FARQVHARSON, ROBERT, M. D., F. R. C. I\, LL. I)., 
Lecturer on Materia Medica at St. Mary's Hospital Medical School, London. 
A Guide to Therapeutics and Materia Medica. New (fourth) American, 
from the fourth English edition. Enlarged and adapted to the U. S. Pharmacopoeia. By 
Frank Woodbury, M. D., Professor of Materia Medica and Therapeutics and Clinical 
Medicine in the Medico-Chirurgical College of Philadelphia. In one handsome 12mo. 
volume of 581 pages. Cloth, $2.50. 
It may correctly be regarded as the most modern 
work of its kind. It is concise, yet complete. 
Containing an account of all remedies that have 
a place in the British and United States Pharma- 
copoeias, as well as considering all non-official but 
important new drugs, it becomes in fact a miniature 
dispensatory.—Pacific Medical Journal, June, 1889. 
An especially attractive feature is an arrange- 
ment by which the physiological and therapeutical 
actions of various remedies are shown in parallel 
columns. This aids greatly in fixing attention and 
facilitates study. The American editor has en- 
larged the work so as to make it include all the 
remedies and preparations in the U. S. Pharma- 
copoeia. The book is a most valuable addition to 
the list of treatises on this most important subject. 
—American Practitioner and News, Nov. 9th, 1889. 
EDES, ROBERT T., M. 1)., 
Jackson Professor of Clinical Medicine in Harvard University, Medical Department. 
A Text-Book of Therapeutics and Materia Medica. Intended for the 
Use of Students and Practitioners. Octavo, 544 pages. Cloth, $3.50; leather, $4.50. 
The present work seems destined to take apromi- 
nent place as a text-book on the subjects of which 
it treats. It possesses all the essentials which we 
expect in a book of its kind, such as conciseness, 
clearness, a judicious classification, and a reason- 
able degree of dogmatism. All the newest drugs 
of promise are treated of. The clinical index at 
the end will be found very useful. We heartily 
commend the book ancfc congratulate the author 
on having produced so good a one.—N. Y. Medical 
Journal, Feb. 18, 1888. 
Dr. Edes’ book represents better than any older 
book the practical therapeutics of the present 
day. The book is a thoroughly practical one. The 
classification of remedies has reference to their 
therapeutic action.—Pharmaceutical Era, Jan. 1888. 
BRICE, J. MITCHELL, M. IX, F. R. C. P., 
Physician and Lecturer on Materia Medica and Therapeutics at Charing Cross Hospital, London. 
Materia Medica and Therapeutics. An Introduction to Rational Trc atment. 
Fourth edition. 12mo., 591 pages. Cloth, $1.50. See Students’ Series of Manuals,j age 31. 
GRIFFITH, ROBERT EGLESFIELD, M. D. 
A Universal Formulary, containing the Methods of Preparing and Adminis- 
tering Officinal and other Medicines. The whole adapted to Physicians and Pharmaceut- 
ists. Third edition, thoroughly revised, with numerous additions, by John M. Maisch, 
Pliar. D., Professor of Materia Medica and Botany in the Philadelphia College of Pharmacy. 
In one octavo volume of 775 pages, with 38 illustrations Cloth, $4.50; leather, $5.50. Lea Brothers & Co.’s Publications—Pathol., Histol. 
13 
GIBBES, HENEAGE, 31. I)., 
Professor of Pathology in the University of Michigan, Medical Department. 
Practical Pathology and Morbid Histology. In one very handsome octavo 
volume of 314 pages, with 60 illustrations, mostly photographic. Cloth, $2.75. Just ready. 
FROM THE PREFACE. 
This work is intended to cover the essential points with which the student must be- 
come familiar in the work of a pathological laboratory. Such instructions are given as 
will enable him to transfer a specimen of any morbid change directly to his microscope in 
an unaltered condition, and to recognize it unerringly. Of the practical importance of 
such ability and the daily growing appreciation of its value, nothing need be said. In 
the section on Practical Bacteriology the student will find all the instruction he needs to 
enable him to study by the microscope the different forms of micro-organisms in their 
growth, their action on animals by inoculation, and their morphology. 
SENN, NICHOLAS, 31. D., Ph. l)., 
Professor of Surgery in Rush Medical College, Chicago. 
Surgical Bacteriology. New (second) edition. In one handsome octavo of 
268 pages, with 13 plates, of which 10 are colored, and 9 engravings. Cloth, $2. Just ready. 
A very thorough and exhaustive review of cur- 
rent literature of that part of bacteriology relating 
to surgery. Such books as this are of incalcula- 
ble benefit to the general practitioner, as they 
bring before him in a condensed and orderly man- 
ner all the literature of a subject, thus saving 
much time. We cordially commend this book to 
all physicians desirous of keeping pace with mod- 
ern investigations.—Cincinnati Lancet-Clinic, May 
| 30,1891. 
GBEEN, T. HEN BY, 31. I)., 
Lecturer on Pathology and Morbid Anatomy at Charing-Cross Hospital Medical School, London. 
Pathology and Morbid Anatomy. New (sixth) American from the seventh 
revised English edition. Octavo, 539 pp., with 167 engravings. Cloth, $2.75. Just ready. 
The Pathology and Morbid Anatomy oY Dr. 
Green is too well known by members of the medi- 
cal profession to need any commendation. There 
is scarcely an intelligent physician anywhere who 
has not the work in his library, for it is almost an 
essential. In fact it is better adapted to the wants 
of general practitioners than any work of the kind 
with which we are acquainted. The works of 
German authors upon pathology, which have been 
translated into English, are too abstruse for the 
physician. Dr. Green’s work precisely meets his 
wishes. The cuts exhibit the appearances of 
pathological structures just as they are seen 
through the microscope. The fact that it is so 
generally employed as a text-book by medical stu- 
dents is evidence that we have not spoken too 
much in its favor.—Cincinnati Medical News, Oct. 
1889. 
PAYNE, JOSEPH F., 31. I)., F. B. C. P., 
Senior Assistant Physician and Lecturer on Pathological Anatomy, St. Thomas' Hospital, London. 
A Manual of General Pathology. Designed as an Introduction to the Prac- 
tice of Medicine. Octavo of 524 pages, with 152 illus. and a colored plate. Cloth, $3.50. 
Knowing, as a teacher and examiner, the exact 
needs of medical students, the author has in the 
work before us prepared for their especial use 
what we do not hesitate to say is the best introduc- 
tion to general pathology that we have yet ex- 
amined. A departure which our author has 
taken is the greater attention paid to the causa- 
tion of disease, and more especially to the etiologi- 
cal factors in those diseases now with reasonable 
certainty ascribed to pathogenetic microbes. In 
this department he has been very full and explicit, 
not only in a descriptive manner, but in the tech- 
nique of investigation. The Appendix, giving 
methods of research, is alone worth the price of the 
book, several times over, to every student of 
pathology.—St. Louis Med. and Surg. Jour., Jam.'89. 
COATS, JOSEPH, M. H., F. F. P. S., 
Pathologist to the Glasgow Western Infirmary. 
A Treatise on Pathology. In one very handsome octavo volume of 829 pages, 
with 339 beautiful illustrations. Cloth, $5.50; leather, $6.50. 
Medical students as well as physicians, who 
desire a work for study or reference, that treats 
the subjects in the various departments in a very 
thorough manner, but without prolixity, will cer- 
tainly give this one the preference to any with 
which we are acquainted. It sets forth the most 
recent discoveries, exhibits, in an interesting 
manner, the changes from a normal condition 
effected in structures by disease, and points out 
the characteristics of various morbid agencies, 
so that they can be easily recognized. But, not 
limited to morbid anatomy, it explains fully how 
the functions of organs are disturbed by abnormal 
conditions.—Cincinnati Medical News, Oct. 1883. 
SCHAFEB, EDWABD A., F. B. S., 
Jodrell Professor of Physiology in University College, London. 
The Essentials of Histology. In one octavo volume of 246 pages, with 
281 illustrations. Cloth, $2.25. 
KLEIN, E., 31. I)., F. B. S., 
Joint Lecturer on General Anat. and Phys. in the Med. School of St. Bat tholomew's Eosp., London. 
Elements of Histology. Fourth edition. In one 12mo. volume of 376 pages, 
with 194 illus. Limp cloth, $1.75. See Students’ Series of Manuals, page 31. 
WOODHEAD’S PRACTICAL PATHOLOGY. A I 
Manual for Students and Practitioners. In one j 
beautiful octavo volume of 497 pages, with 136 
exquisitely colored illustrations. Cloth, $6.00. | 
PEPPER’S SURGICAL PATHOLOGY. In one 
pockeLsize 12mo. volume of 511 pages, with 81 
illustrations. Limp cloth, red edges, $2.00. See 
Students,' Series of Manuals, page 31. 14 
Lea Brothers & Co.’s Publications—Practice of Med. 
FLINT, AUSTIN, M. D., LL. D., 
Prof, of the Principles and Practice of Med. and of Clin. Med. in Bellevue Hospital Medical College, N. Y. 
A Treatise on the Principles and Practice of Medicine. Designed for 
the use of Students and Practitioners of Medicine. New (sixth) edition, thoroughly re- 
vised and rewritten by the Author, assisted by William H. Welch, M. D., Professor of 
Pathology, Johns Hopkins University, Baltimore, and Austin Flint, Jr., M. D., LL. D., 
Professor of Physiology, Bellevue Hospital Medical College, N. Y. In one very handsome 
octavo volume of 1160 pages, with illustrations. Cloth, $5.50; leather, $6.50. 
No text-book on the principles and practice of 
medicine has ever met in this country with such 
general approval by medical students and practi- 
tioners as the work of Professor Flint. In all the 
medical colleges of the United States it is the fa- 
vorite work upon Practice; and, as we have stated 
before in alluding to it, there is no other medical 
work that can be so generally found in the libra- 
ries of physicians. In every state and territory 
of this vast country the book that will be most likely 
to be found in the office of a medical man, whether 
in city, town, village, or at some cross-roads, is 
Flint’s Practice. We make this statement to a 
considerable extent from personal observation, and 
it is the testimony also of others. An examina- 
tion shows that very considerable changes have 
been made in the sixth edition. The work may un- 
doubtedly be regarded as fairly representing the 
present state of the science of medicine, and as 
reflecting the views of those who exemplify in 
their practice the present stage of progress of med- 
ical art.—Cincinnati Medical News, Oct. 1886. 
BRISTOWE, JOHN SYER, M. I)., LL. D., F. R. S., 
Senior Physician to and Lecturer on Medicine at St. Thomas' Hospital, London. 
A Treatise on the Science and Practice of Seventh edi- 
tion. In one large octavo volume of 1325 pages. Cloth, $6.50; leather, $/.50. Just ready. 
physician who has every claim to be considered 
an authority, and composed in a style which at- 
tracts the practitioner as much as the student. No 
one can say that this book has obtained a success 
which was undeserved, and we trust that its author 
will long continue to supervise the production of 
fresh editions for the advantage of the coming 
generation of medical students.— The Lancet, July 
12,1890. 
Dr. Bristowe’s now famous treatise appears in 
its seventh edition. It has long passed the stage 
in which it requires critical examination or com- 
mendation, and has thoroughly established itself 
as among the most complete and useful of text- 
books.—British Medical Journal, September 27,1890. 
The remarkable regularity with which new edi- 
tions of this text-book make their appearance is 
striking testimony to its excellence and value. 
This, too, in spite of the numerous rivals for the 
favor of the student which have been put forth 
within the sixteen years since Bristowe’s “Medi- 
cine ” first appeared. Nor can it be said that the 
author himself has failed to keep his manual 
abreast of advancing knowledge, arduous as that 
task must prove. So long as there is shown such 
care and circumspection in the inclusion of all 
new matter that has stood the test of criticism, so 
long will this work retain the favor which it has 
always met. For it is a work that is built on a 
stable foundation, systematic, scientific and prac- 
tical, containing the matured experience of a 
HARTSIJORNE, HENR Y, M. I)., LI. D., 
Lately Professor of Hygiene in the University of Pennsylvania. 
Essentials of the Principles and Practice of Medicine. A Handbook 
for Students and Practitioners. Fifth edition, thoroughly revised and rewritten. In one 
royal 12mo. volume of 669 pages, with 144 illustrations. Cloth, $2.75; half bound, $3.00. 
Within the compass of 600 pages it treats of the j 
history of medicine, general pathology, general 
symptomatology, and physical diagnosis (including 
laryngoscope, ophthalmoscope, etc.), general ther- 
apeutics, nosology, and special pathology and prac- 
tice. There is a wonderful amount of information 
contained in this work, and it is one of the best 
of its kind that we have seen .—Glasgow Medical 
Journal, Nov. 1882. 
An indispensable book. No work ever exhibited 
a better average of actual practical treatment than 
this one; and probably not one writer in our day 
had a better opportunity than Dr. Hartshorne for 
condensing all the views of eminent practitioners 
into a 12mo. The numerous illustrations will be 
very useful to students especially. These essen- 
tials, as the name suggests, are not intended to 
i supersede the text-books of Flint and Bartholow, 
but they are the most valuable in affording the 
means to see at a glance the whole literature of any 
disease, and the most valuable treatment.—Chicago 
; Medical Journal and Examiner, April, 1882. 
REYNOLDS, J. BUSSELL, M. I)., 
Professor of the Principles and Practice of Medicine in University College, London. 
A System of Medicine. With notes and additions by Henry Hartshorne, 
A. M., M. D., late Professor cf Hygiene in the University of Pennsylvania. . In three large 
and handsome octavo volumes, containing 3056 double-columned pages, with 317 illustra- 
tions. Price per volume, cloth, $5.00; sheep, $6.00; very handsome half Russia, raised bands, 
$6.50. Per set, cloth, $15; leather, $18. Sold only by subscription. 
STILLE, ALFRED, M. JD., LI. />., 
Professor Emeritus of the Theory and Practice of Med. and of Clinical Med. in the Univ. of Penna. 
cholera: Its Origin, History, Causation, Symptoms, Lesions, Prevention and Treat- 
ment. In one handsome 12mo. volume of 163 pages, with a chart. Cloth, $1.25. 
WATSON, SIB THOMAS, M. H., 
Late Physician in Ordinary to the Queen. 
Lectures on the Principles and Practice of Physic. A new American 
from the fifth English edition. Edited, with additions, and 190 illustrations, by Henry 
Hartshorne, A. M., M. D., late Professor of Hygiene in the University of Pennsylvania. 
In two large octavo volumes of 1840 pages. Cloth, $9.00 ; leather, $11.00. Lea Brothers & Co.’s Publications—System of Med. 
15 
For Sale by Subscription Only. 
A System of Practical Medicine. 
BY AMERICAN AUTHORS. 
Edited by WILLIAM PEPPER, M. D., LL. D., 
PRO YOST AND PROFESSOR OF THE THEORY AND PRACTICE OF MEDICINE AND OF 
CLINICAL MEDICINE IN THE UNIVERSITY OF PENNSYLVANIA, 
Assisted by Louis Starr, M. I)., Clinical Professor of the Diseases of Children in the 
Hospital of the University of Pennsylvania. 
The complete work, in five volumes, containing 5573 pages, with 198 illustrations, is now ready. 
Price per volume, cloth, $5; leather, $6 ; half Russia, raised bands and open back, $7. 
In this great work American medicine is for the first time reflected by its worthiest 
teachers, and presented in the full development of the practical utility which is its pre- 
eminent characteristic. The most able men—from the East and the West, from the 
North and the South, from all the prominent centres of education, and from all the 
hospitals which afford special opportunities for study and practice—have united in 
generous rivalry to bring together this vast aggregate of specialized experience. 
The distinguished editor has so apportioned the work that to each author has been 
assigned the subject which he is peculiarly fitted to discuss, and in which his views 
will be accepted as the latest expression of scientific and practical knowledge. The 
practitioner will therefore find these volumes a complete, authoritative and unfailing work 
of reference, to which he may at all times turn with full certainty of finding what he needs 
in its most recent aspect, whether he seeks information on the general principles of medi- 
cine, or minute guidance in the treatment of special disease. So wide is the scope of the 
work that, with the exception of midwifery and matters strictly surgical, it embraces the 
whole domain of medicine, including the departments for which the physician is accustomed 
to rely on special treatises, such as diseases of women and children, of the genito-urinary 
organs, of the skin, of the nerves, hygiene and sanitary science, and medical ophthalmology 
and otology. Moreover, authors have inserted the formulas which they have found most 
efficient in the treatment of the various affections. It may thus be truly regarded as a 
Complete Library of Practical Medicine, and the general practitioner possessing it 
may feel secure that he will require little else in the daily round of professional duties. 
In spite of every effort to condense the vast amount of practical information fur- 
nished, it has been impossible to present it in less than 5 large octavo volumes, containing 
about 5600 beautifully printed pages, and embodying the matter of about 15 ordinary 
octavos. Illustrations are introduced wherever requisite to elucidate the text. 
A detailed prospectus will be sent to any address on application to the publishers. 
These two volumes bring this admirable work | 
to a close, and fully sustain the high standard 
reached by the earlier volumes; we have only 
therefore to echo the eulogium pronounceu upon 
them. We would warmly congratulate the editor 
and his collaborators at the conclusion of their 
laborious task on the admirable manner in which, 
from first to last, they have performed their several 
duties. They have succeeded in producing a 
work which will long remain a standard work ot 
reference, to which practitioners will look for 
fuidance, and authors will resort for facts. 
'rom a literary point of view, the work is without 
any serious blemish, and in respect of production, 
it has the beautiful finish that Americans always 
give their works.—Edinburgh Medical Journal, Jan. 
1887. 
* * The greatest distinctively American work on 
the practice of medicine, and, indeed, the super- 
lative adjective would not bo inappropriate were 
even all other productions placed in comparison. 
An examination of the five volumes is sufficient 
to convince one of the magnitude of the enter- 
prise, and of the success which has attended its 
fulfilment.— The Medical Age, July 26,1886. 
This huge volume forms a fitting close to the 
great system of medicine which in so short a time 
nas won so high a place in medical literature, and 
has done such credit to the profession in this 
country. Among the twenty-three contributors 
are the names of the leading neurologists in 
America, and most of the work in the volume is of 
the highest order.—Boston Medical and Surgical 
Journal, July 21,1887. 
We consider it one of the grandest works on 
Practical Medicine in the English language. It is 
a work of which the profession of this country can 
feel proud. Written exclusively by American 
I physicians who are acquainted with all the varie 
ties of climate in the United States, the character 
of the soil, the manners and customs of the peo- 
ple, etc., it is peculiarly adapted to the wants 
of American practitioners of medicine, and it 
seems to us that every one of them would desire 
to have it. It has been truly called a “Complete 
Library of Practical Medicine,” and the general 
i practitioner will require little else in his round 
1 of professional duties.—Cincinnati Medical News, 
; March, 1886. 
Each of the volumes is provided with a most 
copious index, and the work altogether promises 
to be one which will add much to the medical 
literature of the present century, and reflect great 
credit upon the scholarship and practical acumen 
of its authors.— The London Lancet, Oct. 3, 1885. 
| The feeling of proud satisfaction with which the 
American profession sees this, its representative 
system of practical medicine issued to the medi- 
cal world, is fully justified by the character of the 
j work. The entire caste of the system is in keep- 
ing with the best thoughts of the leaders and fol- 
lowers of our home school of medicine, and the 
combination of the scientific study of disease and 
the practical application of exact and experimen- 
tal knowledge to the treatment of human mal- 
adies, makes every one of us share in the pride 
j that has welcomed Dr. Pepper’s labors. Sheared 
of the prolixity that wearies the readers of the 
[ German school, the articles glean these same 
| fields for all that is valuable. It is the outcome 
of American brains, and is marked throughout 
by much of the sturdy independence of thought 
and originality that is a national characteristic. 
Yet nowhere is there lack of study of the most 
advanced views of the day.—North Carolina Medi- 
I cal Journal, Sept. 1886. 16 
Lea Brothers & Co.’s Publications—Clinical Med., etc. 
FOTHERGILL, J. 31., M. I)., Edin., M. R. C. F., Bond., 
Physician to the City of London Hospital fo* Diseases of the Chest. 
The Practitioner’s Handbook of Treatment; Or, The Principles of Thera- 
peutics. New (third) edition. In one 8vo. vol. of 661 pages. Cloth, $3.75; leather, $4.75. 
To have a description of the normal physiologi- 
cal processes of an organ and of the methods of 
treatment of its morbid conditions brought 
together in a single chapter, and the relations 
between the two clearly stated, cannot fail to prove 
a great convenience to many thoughtful but busy 
physicians. The practical value of the volume is 
greatly increased by the introduction of many 
prescriptions. That the profession appreciates 
that the author has undertaken an important work 
and has accomplished it is shown by the demand 
for this third edition.—N. F. Med. Jour., June 11,’87. 
This is a wonderful book. If there be such a 
thing as “ medicine made easy,” this is the work to 
accomplish this result.— Va. Med. Month., June,’87. 
It is an excellent, practical work on therapeutics, 
well arranged and clearly expressed, useful to the 
student and young practitioner, perhaps even to 
the old.—Dublin Journal of Medical Science, March, 
1888. 
We do not know a more readable, practical and 
useful work on the treatment of disease than the 
one we have now before us.—Pacific Medical and 
Surgical Journal, October, 1887. 
VATJGHAN, VICTOR C., JPh. H., M. 1)., 
Prof, of Phys. and Path. Chem. and Assoc. Prof, of Therap. and Mat. Med. in the Univ. of Mich. 
and NOVY, FREDERICK G., 31. H. 
Instructor in Hygiene and Phys. Chem. in the Univ. of Mich. 
Ptomaines and Leucomaines, or Putrefactive and Physiological 
Alkaloids. New edition. In one handsome 12mo. vol. of about 300 pages. In press. 
FINLAYSON, JAMES, 31. J)., Editor, 
Physician and Lecturer on Clinical Medicine in the Glasgow Western Infirmary, etc. 
Clinical Manual for the Study of Medical Cases. With Chapters 
by Prof. Gairdner on the Physiognomy of Disease; Prof. Stephenson on Diseases of 
the Female Organs; Dr. Robertson on Insanity; Dr. Gemmell on Physical Diagnosis; 
Dr. Coats on Laryngoscopy and Post-Mortem Examinations, and by the Editor on Case- 
taking, Family History and Symptoms of Disorder in the Various Systems. New edition. 
In one 12mo. volume of 682 pages, with 158 illustrations. Cloth, $2.50. 
The profession cannot but welcome the second 
edition of this very valuable work of Finlayson 
and his collaborators. The size of the book has 
been increased and the number of illustrations 
nearly doubled. The manner in which the subject 
is treated is a most practical one. Symptoms 
alone and their diagnostic indications form the 
basis of discussion. The text explains clearly and 
fully the methods of examinations and the con- 
clusions to be drawn from the physical signs.— 
The Medical News, April 23, 1887. 
We are pleased to see a second edition of this 
admirable book. It is essentially a practical 
treatise on medical diagnosis, in which every sign 
and symptom of disease is carefully analyzed, and 
their relative significance in the different affec- 
tions in which they occur pointed out. From their 
synthesis the student can accurately determine 
the disease with which he has to deal. The book 
has no competitor, nor is it likely to have as long 
as future editions maintain its present standard of 
excellence. The general practitioner will find 
many practical hints in its pages, while a careful 
study of the work will save him from many pitfalls 
in diagnosis.—Liverpool Medico-Chirurgical Jour- 
nal, January, 1887. 
BROAHBENT, W. II., M. 1)., F. R. C. P., 
Physician to and Lecturer on Medicine at St. Mary's Hospital, London. 
The Pulse. In one 12mo. volume of 312 pages. Cloth, $1.75. See Series of Clin- 
ical Manuals, page 31. 
This little book probably represents the best 
Iiractical thought on this subject in the English 
anguage. A correct interpretation of the pulse, 
with its almost infinite modifications, brought 
about by almost unlimited bodily variations, can 
only be achieved by experience, and, as an aid 
toward attaining this goal, nothing will be of more 
service than this brochure on the study of the 
pulse.—The American Journal of Medical Sciences, 
September, 1890. 
HABERSHON, S. O., M. H., 
Senior Physician to and late Lect. on Principles and Practice of Med. at Guy's Hospital, London. 
On the Diseases of the Abdomen; Comprising those of the Stomach, and 
other parts of the Alimentary Canal, (Esophagus, Caecum, Intestines and Peritoneum. Second 
American from third enlarged and revised English edition. In one handsome octavo 
volume of 554 pages, with illustrations. Cloth, $3.50. 
This valuable treatise on diseases of the stomach 
and abdomen will be found a cyclopaedia of infor- 
mation, systematically arranged, on all diseases of 
the alimentary tract, from the mouth to the 
rectum. A fair proportion of each chapter is 
devoted to symptoms, pathology, and therapeutics. 
The present edition is fuller than former ones in 
many particulars, and has been thoroughly revised 
and amended by the author. Several new chap- 
ters have been added, bringing the work fully up 
to the times, and making it a volume of interest to 
the practitioner in every field of medicine and 
surgery. Perverted nutrition is in some form 
associated with all diseases we have to combat, 
and we need all the light that can be obtained on 
a subject so broad ana general. Dr. Habershon’s 
work is one that every practitioner should read 
and study for himself.—N. F. Medical Journal, 
April, 1879. 
TANNER, THOMAS HAWKES, M. H. 
A Manual of Clinical Medicine and Physical Diagnosis. Third American 
from the second London edition. Revised and enlarged by Tilbury Fox, M. D. 
In one small 12mo. volume of 362 pages, with illustrations. Cloth, $1.50. 
LECTURES ON THE STUDY OF FEVER. By 
A. Hudson, M. D., M. R. I. A. In one octavo 
volume of 308 pages. Cloth, $2.50. 
A TREATISE ON FEVER. By Robert D. Lyons, 
K. C. C. In one 8vo. vol. of 354 pp. Cloth, $2.25. 
LA ROCHE ON YELLOW FEVER, considered in 
its Historical, Pathological, Etiological and 
Therapeutical Relations. In two large and hand- 
some octavo volumes of 1468 pp. Cloth, $7.00. Lea Brothers & Co.’s Publications—Hygiene, Electr., Pract. 
17 
BARTHOLOW, ROBERTS, A. M., M. I)., LL. I)., 
Prof, of Materia Medica and General Therapeutics in the Jefferson Med. Coll, of Phila., etc. 
Medical Electricity. A Practical Treatise on the Applications of Electricity 
to Medicine and Surgery. New (third) edition. In one very handsome octavo volume of 
308 pages, with 110 illustrations. Cloth, $2.50. 
The fact that this work has reached its third edi- 
tion in six years, and that it has been kept fully 
abreast with the increasing use and knowledge of 
electricity,demonstrates its claim to be considered 
a practical treatise of tried value to the profession. 
The matter added to the present edition embraces 
the most recent advances in electrical treatment. 
The illustrations are abundant and clear, and the 
work constitutes a full, clear and concise manual 
well adapted to the needs of both student and 
practitioner.— The Medical News, May 14,1887. 
YEO, I. BURNEY, M. JD., F. R. C. P., 
Professor of Clinical Therapeutics in King's College, London, and Physician to King's College 
Hospital. 
Food in Health and Disease. In one 12mo. volume of 590 pages. Cloth, $2. 
See Series of Clinical dlanuals, page 31. 
7 I O 
Dr.Yeo supplies in a compact form nearly all that 
the practitioner requires to know on the subject of 
diet. The work is divided into two parts—food in 
health and food in disease. Dr. Yeo has gathered 
together from all quarters an immense amount of 
useful information within a comparatively small 
compass, and he has arranged and digested his 
materials with skill for the use of the practitioner. 
We have seldom seen a book which more thor- 
oughly realizes the object for which it was written 
than this little work of Dr. Yeo.—British Medical 
Journal, Feb. 8, 1890. 
RI CHARD SON, B. W., M.H., XL. 11., F.R.S., 
Fellow 0/ the Royal College of Physicians, London. 
Preventive Medicine. In one octavo volume ot 729 pages. Cloth, $4; leather. $5. 
Dr. Richardson has succeeded in producing a 
work which is elevated in conception, comprehen- 
sive in scope, scientific in character, systematic in 
arrangement, and which is written in a clear, con- 
cise and pleasant manner. He evinces the happy 
faculty of extracting the pith of what is known on 
the subject, and of presenting it in a most simple, 
intelligent and practical form. There is perhaps 
no similar work written for the general public 
thatcontains such acomplete, reliable and instruc- 
tive collection of data upon the diseases common 
to the race, their origins, causes, and the measures 
for their prevention. The descriptions of diseases 
are clear, chaste and scholarly; the discussion of 
the question of disease is comprehensive, masterly 
and fully abreast with the latest and best knowl- 
edge on the subject, and the preventive measures 
advised are accurate, explicit and reliable.—The 
American Journal of the Medical Sciences, April, 1884. 
T11E YEAR-BOOK OF TREATMENT FOR 1891. 
A Comprehensive and Critical Review for Practitioners of Medi- 
cine. In one 12mo. volume of 485 pages. Cloth, $1.50. Just ready. 
*** For special commutations with periodicals see pages 1 and 2. 
The present issue, the seventh, has been in- 
creased by more than one hundred and fifty pages, 
but the original plan of the book is not altered. 
It still remains a concise epitome of the chief 
articles of the past year—articles selected and 
epitomised by a staff of contributors which in- 
cludes many of the best-known and ablest spe- 
cialists, and these gentlemen have wisely kept in 
mind that the Year Book is for practitioners, and 
they have given what actual practice requires— 
useful, workable information. We have no hesi- 
tancy in recommending the present volume, which 
we consider to be superior to any of its predeces- 
sors; more practical, more generally useful to 
practitioners. The sectional editors have confined 
their attention to fulfilling the object of the book’s 
existence—the providing of an epitome of the 
most practical and useful of the medical articles, 
of the past year, for the use of men whose prac- 
tice does not allow time for the study of a large 
number of home and foreign medical journals.— 
The Dublin Journal of Medical Science, May, 1891. 
THE YEAR- BOOKS of TREATMENT for9 86,9 87 and 990 
Similar to above. 12mo., 320-341 pages. Limp cloth, $1.25 each. 
SCHREIBER, JOSEPH, M. 1). 
A Manual of Treatment by Massage and Methodical Muscle Ex- 
ercise. Translated by Walter Mendelson, M. D., of New York. In one handsome 
octavo volume of 274 pages, with 117 fine engravings. Cloth, $2.75. 
STURGES’ INTRODUCTION TO THE STUDY 
OF CLINICAL MEDICINE. Being a Guide to 
the Investigation of Disease. In one handsome 
12mo. volume of 127 pages. Cloth, $1.25. 
DAVIS’ CLINICAL LECTURES ON VARIOUS 
IMPORTANT DISEASES. By N. S. Davis, 
M. D. Edited by Fbank H. Davis, M. D. Second 
edition. 12mo. 287 pages. Cloth, $1.75. 
TODD’S CLINICAL LECTURES ON CERTAIN 
ACUTE DISEASES. In one octavo volume of 
320 pages. Cloth, $2.50. 
PAVY’S TREATISE ON THE FUNCTION OF DI- 
GESTION; its Disorders and their Treatment. 
From the second London edition. In one octavo 
volume of 238 pages. Cloth, $«.00. 
BARLOW’S MANUAL OF THE PRACTICE OF 
MEDICINE. With additions by D. F. Condie, 
M. D. 1 vol. 8vo., pp. 603. Cloth, $2.50. 
CHAMBERS’ MANUAL OF DIET AND REGIMEN 
IN HEALTH AND SICKNESS. In one hand 
some octavo volume of 302 pp. Cloth, $2.75. 
HOLLAND’S MEDICAL NOTES AND REFLEC- 
TIONS. 1 vol. 8vo., pp. 493. Cloth, $3.50. 
FULLER ON DISEASES OF THE LUNGS AND 
AIR-PASSAGES. Their Pathology, Physical Di- 
agnosis, Symptoms and Treatment. From the 
second and revised English edition. In one 
octavo volume of 475 pages. Cloth, $3.50. 
WALSHE ON THE DISEASES OF THE HEART 
AND GREAT VESSELS. Third American edi- 
tion. In 1 vol. 8vo., 416 pp. Cloth, $3.00. 
SLADE ON DIPHTHERIA; its Nature and Treat- 
ment, with an account of the History of its Pre- 
valence in various Countries. Second and revised 
edition. In one 12mo. vol., 158 pp. Cloth, $1.25. 
SMITH ON CONSUMPTION; its Early and Reme- 
diable Stages. 1 vol. 8vo., 253 pp. Cloth, $2.25. 
LA ROCHE ON PNEUMONIA. 1 vol. 8vo. of 490 
pages. Cloth, $3.00. 
WILLIAMS ON PULMONARY CONSUMPTION; 
its Nature, Varieties and Treatment. With an 
analysis of one thousand cases to exemplify its 
duration. In one 8vo. vol. of 303 pp. Cloth, $2.50 18 
Lea Brothers & Co.’s Publications—Throat, Lungs, Heart, Nerves. 
FLINT, A US TIN, M. 13., LI. 13., 
Pi'ofessor of the Principles and Practice of Medicine in Bellevue Hospital Medical College, N. T. 
A Manual of Auscultation and Percussion; Of the Physical Diagnosis of 
Diseases of the Lungs and Heart, and of Thoracic Aneurism. New (fifth) edition. 
Edited by James C. Wilson, M. D., Lecturer on Physical Diagnosis in the Jefferson 
Medical College, Philadelphia. In one handsome royal 12mo. volume of 274 pages, with 
12 illustrations. Cloth, $1.75. Just ready. 
This little book through its various editions has 
probably done more to advance the science of 
physical exploration of the chest than any other 
dissertation upon the subject, and now in its fifth 
edition it is as near perfect as it can be. The 
rapidity with which previous editions were sold 
shows how the profession appreciated the thor- 
oughness of Prof. Flint’s investigations. For stu- 
dents it is excellent. Its value is shown both in 
the arrangement of the material and in the clear, 
concise style of expression. For the practitioner 
it is a ready manual for reference.—North Ameri- 
can Practitioner, January, 1891. 
B T THE SAME A UTHOR. 
A Practical Treatise on the Physical Exploration of the Chest and 
the Diagnosis of Diseases Affecting the Respiratory Organs. Second and 
revised edition. In one handsome octavo volume of 591 pages. Cloth, $4.50. 
Phthisis: Its Morbid Anatomy, Etiology, Symptomatic Events and 
Complications, Fatality and Prognosis, Treatment and Physical Diag- 
nosis ; In a series of Clinical Studies. In one octavo volume of 442 pages. Cloth, $3.50. 
A Practical Treatise on the Diagnosis, Pathology and Treatment of 
Diseases of the Heart. Second revised and enlarged edition. In one octavo volume 
of 550 pages, with a plate. Cloth, $4. 
Essays on Conservative Medicine and Kindred Topics. In one very hand- 
some royal 12mo. volume of 210 pages. Cloth, $1.38. 
BROWNE, LENNOX, F. R. C. S., E., 
Senior Physician to the Central London Throat and Ear Hospital. 
A Practical Guide to Diseases of the Throat and Nose, including 
Associated Affections of the Ear. New (third) and enlarged edition. In one 
imperial octavo volume of 734 pages, with 120 illustrations in color, and 235 engravings 
on wood. Cloth, $6.50. 
The third edition of Mr. Lennox Browne’s in- 
structive and artistic work on “ The Throat and 
Its Diseases” appears under the title of “The 
Throat and Nose and Their Diseases.” This 
change has been rendered desirable by the ad- 
vances male during the last decade in rhinology. 
The nasal sections, which extend to upwards of 
100 pages, give in a short space the best account 
of the present position of rhinology with which 
we are acquainted. The engravings'in this hand- 
some volume are of the same high order as here- 
tofore, and more numerous than ever; they can- 
not fail to be of the greatest assistance to senior stu- 
dents and practitioners. The instruments, either 
figured or described, are those which, as the result 
of experience, Mr. Browne has found to be of the 
greatest utility in diagnosis and treatment; they are 
most simple, inexpensive and easily kept aseptic- 
points of much importance. We have on a former 
occasion eulogised the beautiful and typical col- 
ored plates drawn on stone by the author-artist 
himself, and forming in themselves a valuable 
and instructive atlas, the equal of which is not to 
be found in any modern work, treating Of these 
subjects. Mr. Lennox Browne is to congratulated 
on having produced the best practical text-book 
on diseases of the throat and nose extant. We 
are glad to learn that it is being translated into 
French and German.— The Provincial Medical 
Journal, August 1,1890. 
BY THE SAME A UTHOR. 
Koch’s Remedy in Relation to Throat Consumption. In one octavo 
volume of 121 pages, with 45 illustrations, 4 of which are colored, and 17 charts. 
Cloth, $1.50. Just ready. 
SEILER, CARL, 31. I)., 
Lecturer on Laryngoscopy in the University of Pennsylvania. 
A Handbook of Diagnosis and Treatment of Diseases of the Throat, 
Nose and Naso-Pharynx. Third edition. In one handsome royal 12mo. volume 
of 373 pages, with 101 illustrations and 2 colored plates. Cloth, $2.25. 
Few medical writers surpass this author in 
ability to make his meaning perfectly clear in a 
few words, and in discriminat.on in selection, both 
of topics and methods. The book deserves a large 
sale, especially among general practitioners—Chi- 
cago Medical Journal and Examiner, April, 1889. 
COHEN, J. SOLIS, M. I)., 
Lecturer on Laryngoscopy and Diseases of the Throat and Chest in the Jefferson Medical College. 
Diseases of the Throat and Nasal Passages. A Guide to the Diagnosis and 
Treatment of Affections of the Pharynx, (Esophagus, Trachea, Larynx and Nares. Third 
edition, thoroughly revised and rewritten, with a large number of new illustrations. In 
one very handsome octavo volume. Preparing. 
GROSS, S. JO., 31.13., LL.JD., I3.C.L. Oxon., LL.I3. Cantab. 
A Practical Treatise on Foreign Bodies in the Air-passages. In one 
octavo volume of 452 pages, with 59 illustrations. Cloth, $2.75. Lea Brothers & Co.’s Publications—Nerv. and Ment. Dis., etc. 
19 
ROSS, JAMBS, M. I)., F. R. C. P., LL. I)., 
Senior Assistant Physician to the Manchester Royal Infirmary. 
A Handbook on Diseases of the Nervous System. In one octavo 
volume of 725 pages, with 184 illustrations. Cloth, $4.50; leather, $5.50. 
The book before us is entitled to the highest 
consideration; it is painstaking, scientific and 
exceedingly comprehensive.—New York Medical 
Journal, July 10, 1886. 
The author has rendered a great service to the 
profession by condensing into one volume the 
principal facts pertaining to neurology and nerv- 
ous diseases as understood at the present time, 
and he has succeeded in producing a work at once 
brief and practical yet scientific, without entering 
into the discussion of theorists, or burdening the 
mind with mooted questions.—Pacific Medical and 
Surgical Journal ana Western Lancet, May, 1886. 
This admirable work is intended for students of 
medicine and for such medical men as have no time 
for lengthy treatises. In the present instance the 
duty of arranging the vast store of material at the 
disposal of the author, and of abridging the de- 
scription of the different aspects of nervous dis- 
eases, has been performed with singular skill, and 
the result is a concise and philosophical guide to 
the department of medicine of which it treats. 
Dr. Ross holds such a high scientific position that 
any writings which bear his name are naturally 
expected to have the impress of a powerful intel- 
lect. In every part this handbook merits the 
highest praise, and will no doubt be found ol the 
greatest value to the student as well as to the prac- 
titioner.—Edinburgh Medical Journal, Jan. 1887. 
HAMILTON, ALLAN McLANE, M. I)., 
Attending Physician at the Hospital for Epileptics and Paralytics, Blackwell's Island, N. Y. 
Nervous Diseases; Their Description and Treatment. Second edition, thoroughly 
revised and rewritten. In one octavo volume of 598 pages, with 72 illustrations. Cloth, $4. 
When the first edition of this good book appeared 
we gave it our emphatic endorsement, and the 
present edition enhances our appreciation of the 
book and its author as a safe guide to students of 
clinical neurology. One of the best and most 
critical of English neurological journals, Brain, has 
characterized this book as the best of its kind in 
any language, which is a handsome endorsement 
from an exalted source. The improvements in the 
new edition, and the additions to it, will justify its 
purchase even by those who possess the old.— 
Alienist and Neurologist, April, 1882. 
TTJKE, HANIEL HACK, M. J)., 
Joint Author of The Manual of Psychological Medicine, etc. 
Illustrations of the Influence of the Mind upon the Body in Health 
and Disease. Designed to elucidate the Action of the Imagination. New edition. 
Thoroughly revised and rewritten. In one 8vo. vol. of 467 pp., with 2 col. plates. Cloth, $3. 
It is impossible to peruse these interesting chap- 
ters without being convinced of the author’s per- 
feet sincerity, impartiality, and thorough mental 
grasp. Dr. Tuke has exhibited the requisite 
amount of scientific address on all occasions, and 
the more intricate the phenomena the more firmly 
has he adhered to a physiological and rational 
method of interpretation. Guided by an enlight- 
ened deduction, the author has reclaimed for 
science a most interesting domain in psychology, 
previously abandoned to charlatans and empirics. 
This book, well conceived and well written, must 
eommend itself to every thoughtful understand- 
ing.—New York Medical Journal, September 6,1884. 
GRAY, LAND ON CARTER, M.E>., 
Professor of Diseases of the Mind and Nervous System in the New York Polyclinic. 
A Practical Treatise on Diseases of the Nervous System. Preparing. 
CLOUS TOY, THOMAS S., M. I)., F. R. C. P., L. R. C. S., 
Lecturer on Mental Diseases in the University of Edinburgh. 
Clinical Lecttires on Mental Diseases. With an Appendix, containing an 
Abstract of the Statutes of the United States and of the Several States and Territories re- 
lating to the Custody of the Insane. By Charles F. Folsom, M. D., Assistant Professor 
of Mental Diseases, Med. Dep. of Harvard Univ. In one handsome octavo volume of 541 
pages, with eight lithographic plates, four of which are beautifully colored. Cloth, $4. 
The practitioner as well as the student will ac- 
cept the plain, practical teaching of the author as a 
forward step in the literature of insanity. It is 
refreshing to find a physician of Dr. (Houston's 
experience and high reputation giving the bed- 
side notes upon which nis experience has been 
founded and his mature judgment established. 
Such clinical observations cannot but be useful to 
the general practitioner in guiding him to a diag- 
nosis and indicating the treatment, especially in 
many obscure and doubtful cases of mental dis- 
ease. To the American reader Dr. Folsom’s Ap- 
pendix adds greatly to the value of the work, and 
will mike it a desirable addition to every library. 
—American Psychological Journal, July, 1884. 
fta?*Dr. Folsom’s Abstract may also be obtained separately in one octavo volume ot 
108 pages. Cloth, $1.50. 
SAVAGF, GEORGE EE., M. H., 
Lecturer on Mental Diseases at Guy's Hospital, London. 
Insanity and Allied Neuroses, Practical and Clinical. In one 12mo. vol. 
of 551 naves, with 18 illus. Cloth, $2.00. See Senes of Clinical Manuals, page 31. 
As a handbook, a guide to the practitioner and 
student, the book fulfils an admirable purpose. 
The many forms of insanity are described with 
characteristic clearness, the illustrative cases are 
carefully selected, and as regards treatment sound 
; common sense is everywhere apparent. Dr. Sav- 
age has written an excellent manual for the prac- 
| titioner and student.—Amer. Jour, of Insan., Apr.’85. 
PLAYFAIR, W. S., M. D., F. R. C. P. 
The Systematic Treatment of Nerve Prostration and Hysteria. In 
one handsome small 12mo. volume of 97 pages. Cloth, $1.00. 
BLANDFORD ON INSANITY AND ITS TREAT- 
MENT. Lectures on the Treatment, Medical 
and Legal, of Insane Patients. In one very hand- 
some octavo volume. 
JONES’ CLINICAL OBSERVATIONS ON FUNC- 
TIONAL NERVOUS DISORDERS. Second 
American Edition. In one handsome octavo 
volume of 340 pages. Cloth, $3.25. 20 
Lea Brothers & Co.’s Publications—Surgery. 
BOBEBTS, JOHN B., M. I)., 
Professor of Anatomy and Surgery in the Philadelphia Polyclinic. Professor of the Principles and 
Practice of Surgery in the Woman's Medical College of Pennsylvania. Lecturer in Anatomy in the Univer- 
sity of Pennsylvania. 
The Principles and Practice of 
and Practitioners of Medicine and Surgery, 
pages, with 501 illustrations. Cloth, $4.50; 
In this work the author has endeavored to give 
to the profession in a condensed form the doctrines 
and procedures of Modern Surgery. He has made 
it a work devoted more especially to the practice 
than to the theory of surgery. His own large 
experience has added many valuable features to 
the work. It contains many practical points in 
diagnosis, which render it the more valuable to 
the practitioner; and the systematization which 
pervades the whole work, together with its 
perspicuity, enhance its value as a student’s 
manual. The fact that this work is eminently 
practical cannot be too strongly emphasized. It 
is modern, and as its teaching is that generally 
accepted and such that affords little opportunity 
for discussion, it will be lasting. It is clear and 
concise, yet full. The book is entitled to a place 
Modern Surgery. For the use of Students 
In one very handsome octavo volume of 780 
leather, $5.50. Just ready. 
in modern surgical literature.—Annate of Surgery, 
Jan. 1891. 
This work is a very comprehensive manual upon 
general surgery, and will doubtless meet with a 
i favorable reception by the profession. It has a 
i thoroughly practical character, the subjects are 
treated with rare judgment, its conclusions are in 
' accord with those of the leading practitioners of 
the art, and its literature is fully up to all the ad- 
vanced doctrines and methods of practice of the 
present day. Its general arrangement follows 
this rule, and the author in his desire to be con- 
; cise and practical is at times almost dogmatic, but 
this is entirely excusable considering the admira- 
ble manner in which he has thus increased the 
usefulness of his work.—Medical Record, Jan. 17, 
1891. 
ASIIIIUBST, JOHN, Jr., M. B., 
Barton Prof, of Surgery and Clin. Surgery in Univ. of Penna., Surgeon to the Penna. Hosp., etc. 
The Principles and Practice of Surgery. New (fifth) edition, enlarged 
and thoroughly revised. In one large and handsome octavo volume of 1144 pages, with 
642 illustrations. Cloth, $6; leather, $7. 
A complete and most excellent work on surgery. 
It is only necessary to examine it to see at once 
its excellence and real merit either as text-book 
for the student or a guide for the general practi- 
tioner. It fully considers in detail every surgical 
injury and disease to which the body is liable, and 
every advance in surgery worth noting is to be 
found in its proper place. It is unquestionably the 
best and most complete single volume on surgery, 
in the English language, and cannot but receive 
that continued appreciation which its merits justly 
demand.—Southern Practitioner, Feb. 1890. 
This is one of the most popular and useful of 
the many well-known treatises on general surgery. 
It furnishes in a concise manner a clear and 
comprehensive description of the modes of prac- 
tice now generally employed in the treatment of 
surgical affections, with a plain exposition of the 
principles on which those modes of practice are 
based. The entire work has been carefully revised, 
and a number of new illustrations introduced 
that greatly enhance the value of the book.— 
Cincinnati Lancet-Clinic, Dec. 14, 1889. 
B BUILT, BOBEBT, M. B. C. S., etc. 
Manual of Modern Surgery. Twelfth edition, thoroughly revised by Stan- 
ley Boyd, M. B., B. S., F. R. C. S. In one 8vo. volume of 965 pages, with 373 illustra- 
tions. Cloth, $4: leather, $5. 
It is essentially a new book, rewritten from be- 
ginning to end. The editor has brought his work 
up to the latest date, and nearly every subject on 
which the student and practitioner would desire 
to consult a surgical volume, has found its place 
here. The volume closes with about twenty pages 
of formulae covering a broad range of practical 
therapeutics. The student will find that the new 
Druitt is to this generation what the old one was 
to the former, and no higher praise need be 
accorded to any volume.—North Carolina Medical 
Journal, October, 1887. 
Druitt’s Surgery has been an exceedingly popu- 
lar work in the profession. It is stated that 50,000 
copies have been sold in England, while in the 
United States, ever since its first issue, it has been 
used as a text-book to a very large extent. Dur- 
ing the late war in this country It was so highly 
appreciated that a copy was issued by the Govern- 
ment to each surgeon. The present edition, while 
it has the same features peculiar to the work at 
first, embodies all recent discoveries in surgery, 
and is fully up to the times.—Cincinnati Medical 
News, September, 1887. 
GAFT, FBEBEBICK JAMES, F. B. C. S., 
Senior Surgeon to the Royal Free Hospital, London. 
The Student’s Surgery. A Multum in Parvo. In one square octavo volume 
of 848 pages, with 159 engravings. Cloth, $3.75. 
GBOSS, S. B., M. B., LL. B., B. C. L. Oxon., LL. B. 
Cantab., 
Emeritus Professor of Surgery in the Jefferson Medical College of Philadelphia. 
A System of Surgery: Pathological, Diagnostic, Therapeutic and Operative. 
Sixth edition, thoroughly revised and greatly improved. In two large and beautifully 
printed imperial octavo volumes containing 2382 pages, illustrated by 1623 engravings. 
Strongly bound in leather, raised bands, $15. 
BALL, CHABLFS B., M. Ch., Bub., F. B. C. S., E., 
Surgeon and Teacher at Sir P. Dun's Hospital, Dublin. 
Diseases of the Rectum and Anus. In one 12mo. volume of 417 pp., 
with 54 cuts, and 4 colored plates. Cloth, $2.25. See Series of Clinical Manuals 31. 
GIBNFY, V. F., M. B., 
Surgeon to the Orthopcedic Hospital, Neio York, etc. 
Orthopaedic Surgery. For the use of Practitioners and Students. In one hand- 
some octavo volume, profusely illustrated. Preparing. Lea Brothers & Co.’s Publications—Surgery. 
21 
ERICHSEN, JOHN E., F. R. S., F. R. C. S., 
Professor of Surgery in University College, London, etc. 
The'Science and Art of Surgery; Being a Treatise on Surgical Injuries, Dis- 
eases and Operations. From the eighth and enlarged English edition. In two large and 
beautiful octavo volumes of 2316 pages, illustrated with 984 engravings on wood. 
Cloth, $9; leather, raised bands, $11. 
We have always regarded “The Science and 
Art of Surgery” as one of the best surgical text- 
books in the English language, and this eighth 
edition only confirms our previous opinion. We 
take great pleasure in cordially commending it to 
our readers.— The Medical News, April 11, 1885. 
For many years this classic work has been 
made by preference of teachers the principal 
text-book on surgery for medical students, while 
through translations into the leading continental 
languages it may be said to guide the surgical 
teachings of the civilized world. No excellence 
of the former edition has been dropped and no 
discovery, device or improvement which has 
marked the progress of surgery during the last 
decade has been omitted. The illustrations are 
many and executed in the highest style of art. 
—Louisville Medical News, Feb. 14, 1885. 
BRYAJYT, THOMAS, F. R. C. S., 
Surgeon and Lecturer on Surgery at Guy's Hospital, London. 
The Practice of Surgery. Fourth American from the fourth and revised Eng- 
lish edition. In one large and very handsome imperial octavo volume of 1040 pages, with 
727 illustrations. Cloth, $6.50; leather, $7.50. 
The fourth edition of this work is fully abreast 
of the times. The author handles his subjects 
with that degree of judgment and skill which is 
attained by years of patient toil and varied ex- 
perience. The present edition is a thorough re- 
vision of those which preceded it, with much new 
matter added. His diction is so graceful and 
logical, and his explanations are so lucid, as to 
place the work among the highest order of text- 
books for the medical student. Almost every 
topic in surgery is presented in such a form as to 
enable the busy practitioner to review any subject 
in every-day practice in a short time. No time is 
lost with useless theories or superfluous verbiage. 
In short, the work is eminently clear, logical and 
practical.—Chicago Medical Journal and Examiner, 
April, 1886. 
This book is essentially what it purports to be, 
viz.: a manual for the practice of surgery. It is 
peculiarly well fitted for the student or busy general 
practitioner.—The Medical News, August 15,1885. 
TREVES, FREDERICK, / . R. C. S., 
Hunterian Professor at the Royal College of Surgeons of England. 
A Manual of Surgery.. In Treatises by Various Authors. In three 12mo. 
volumes, containing 1866 pages, with 213 engravings. Price per volume, cloth, $2. See 
Students’ Series of Manuals, page 31. 
We have here the opinions of thirty-three 
authors, in an encyclopedic form for easy and 
ready reference. The three volumes embrace 
every variety of surgical affections likely to be 
met with, the paragraphs are short and pithy, and 
the salient points and the beginnings of new sub- 
jects are always printed in extra-heavy type, so 
that a person may find whatever information he 
may be in need of at a moment’s glance.—Cin- 
cinnati Lancet-Clinic, August 21, 1886. 
HOLMES, TIMOTHY, M. A., 
Surgeon and Lecturer on Surgery at St. George's Hospital, London. 
A System of Surgery; Theoretical and Practical. IN TREATISES BY 
VARIOUS AUTHORS. American edition, thoroughly revised and re-edited 
by John H. Packard, M. D., Surgeon to the Episcopal and St. Joseph’s Hospitals, 
Philadelphia, assisted by a corps of thirty-three of the most eminent American surgeons. 
In three large imperial octavo volumes containing 3137 double-columned pages, with 
979 illustrations on wood and 13 lithographic plates, beautifully colored. Price per 
set, cloth, $18.00; leather, $21.00. Sold only by subscription. 
WHARTON, HENRY R., M. D., 
Demonstrator of Surgery and Lecturer on Surgical Diseases of Children in the Univ. of Penna. 
Minor Surgery and Bandaging. In one very handsome 12mo. volume of 
about 500 pages, with about 450 engravings, many being photographic. In press. 
MARSH, HOWARD, E. R. C. S., 
Senior Assistant Surgeon to and Lecturer on Anatomy at St. Bartholomew's Hospital, London. 
Diseases of the Joints. In one 12mo. volume of 468 pages, with 64 woodcuts 
and a colored plate. Cloth, $2.00. See Series of Clinical Manuals, page 31. 
B UTLIN, HEAR Y T., F. R. C. S., 
Assistant Surgeon to St. Bartholomew's Hospital, London. 
Diseases of the Tongue. In one 12mo. volume of 456 pages, with 8 colored 
plates and 3 woodcuts. Cloth, $3.50. See Series of Clinical Manuals, page 31. 
TREVES, FREDERICK, E. It. C. S., 
Surgeon to and Lecturer on Surgery at the London Hospital. 
Intestinal Obstruction. In one pocket-size 12mo. volume of 522 pages, with 60 
illustrations. Limp cloth, blue edges, $2.00. See Series of Clinical Manuals, page 31. 
GOULD, A. PEARCE, M. S., M. B., E. R. C. S„ 
Assistant Surgeon to Middlesex Hospital. 
Elements of Surgical Diagnosis. In one pocket-size 12mo. volume of 589 
paaes. Cloth, $2.00. See Students’ Series of Manuals, page 31. 
PIRRIE’S PRINCIPLES AND PRACTICE OF 
SURGERY. Edited by John Neill, M. D. In 
one 8vo. vol. of 784 pp. with 316 illus. Cloth, $3.75. 
MILLER’S PRINCIPLES OF SURGERY. Fourth 
American from the third Edinburgh edition. In 
one 8yo. vol. of 638 pages, with 340 illustrations. 
Cloth, $3.76. 
MILLER’S PRACTICE OF SURGERY. Fourth 
and revised American edition. In one large 8vo. 
I vol. of 682 pp., with 364 illustrations. Cloth ,$3.75. 22 
Lea Brothers & Co.’s Publications—Surgery, Frac., Disloc. 
SMITH, STEPHEN, M. I)., 
Professor of Clinical Surgery in the University of the City of New York. 
The Principles and Practice of Operative Surgery. New (second) and 
thoroughly revised edition. In one very handsome octavo volume of 892 pages, with 
1005 illustrations. Cloth, $4 00; leather, $5.00. 
This excellent and very valuable book is one of 
the most satisfactory works on modern operative 
surgery yet published. Its author and publisher 
have spared no pains to make it as far as possible 
an ideal, and their efforts have given it a position 
prominent among the recent works in this depart- 
ment of surgery. The book is a compendium for 
the modern surgeon. The present, the only revised 
edition since 1879, presents many changes from 
the original manual. The volume is much en 
larged, and the text has been thoroughly revised, 
so as to give the most improved methods in asep- 
tic surgery, and the latest instruments known for 
operative work. It can be truly said that as a hand- 
book for the student, a com panion for the surgeon, 
and even as a book of reference for the physician 
not especially engaged in the practice or surgery, 
this volume will long hold a most conspicuous 
place, and seldom will its readers, no matter how 
unusual the subject, consult its pages in vain. Its 
compact form, excellent print, numerous illustra- 
tions, and especially its decidedly practical char- 
acter, all combine to commend it.—Boston Medical 
and Surgical Journal, May 10, 1888. 
HOLMES, TIMOTHY, M. A,, 
Surgeon and Lecturer on Surgery at St. George's Hospital, London. 
A Treatise on Surgery; Its Principles and Practice. New American 
from the fifth English edition, edited by T. Pickering Pick, F. R. C. S., Surgeon and 
Lecturer on Surgery at St. George’s Hospital, London. In one octavo volume of 997 
pages, with 428 illustrations. Cloth, $6; leather, $7. 
To the younger members of the profession and 
to others not acquainted with the book and its 
merits, we take pleasure in recommending it as a 
surgery complete, thorough, well-written, fully 
illustrated, modern, a work sufficiently volumi- 
nous for the surgeon specialist, adequately concise 
for the general practitioner, teaching those things 
that are necessary to be known for the successful 
prosecution of the physician’s career, imparting 
nothing that in our present knowledge is consid- 
ered unsafe, unscientific or inexpedient.—Pacific 
Medical Journal, July, 1889. 
HAMILTON, FRANK II,, M, I)., LL, 2>., 
Surgeon to Bellevue Hospital, New York. 
A Practical Treatise on Fractures and Dislocations. New (8th) edi- 
tion, revised and edited by Stephen Smith, A. M., M. D., Professor of Clinical Surgery 
in the University of the City of New York. In one very handsome octavo volume of 832 
pages, with 507 illustrations. Cloth, $5.50; leather, $6.50. Just ready. 
It has received the highest endorsement that a 
work upon a department of surgery can possibly 
receive. It is used as a text-book in every medi 
cal college of this country, and the publishers 
have been called upon to print eight editions of it. 
What more can be said in commendation of it? 
It has been said w;th truth that it is doubtful if 
any surgical work has appeared during the last 
half century which more completely filled the 
place for which it was designed. As Dr. Smith 
says, its great merits appear most conspicuously 
in its clear, concise, and yet comprehensive state- 
ment of principles, which renders it an admirable 
text-book for teacher and pupil, and in its wealth 
of clinical materials, which adapts it to the daily 
necessities of the practitioner. Fractures and 
dislocations are injuries which the general practi- 
tioner, in his character as a surgeon, is most called 
upon to treat. They form a part of surgery that 
he cannot avoid taking charge of. Under the 
circumstances, therefore, he needs all the aid he 
can secure. But what better assistance can he 
seek than a work that is devoted exclusively to 
treating fractures and dislocations, and conse- 
quently contains full information, in plain lan- 
guage, for the management cf every emergency 
that is likely to be met with in such injuries? 
The country is filled with railroads and manufac- 
tories where accidents are constantly occurring, 
and to which general practitioners, and not dis- 
tinguished surgeons, are constantly liable to be 
called. We consider that the work before us 
should be in the library of every practitioner.— 
Cincinnati Medical News, February, 1891. 
STIMSON, LEWIS A,, B. A., M. 2>., 
Surgeon to the Presbyterian and Bellevue Hospitals, Professor of Clinical Surgery in the Medical 
Faculty of Univ. of City of N. Y., Corresponding Member of the Societe de Chirurgie of Paris. 
A Manual of Operative Surgery. New (second) edition. In one very hand- 
some royal 12mo. volume of 503 pages, with 342 illustrations. Cloth, $2.50. 
There is always room for a good book, so that 
while many works on operative surgery must be 
considered superfluous, that of Dr. Stimson has 
held its own. The author knows the difficult art 
of condensation. Thus the manual serves as a 
work of reference, and at the same time as a 
handy guide. It teaches what it professes, the 
steps of operations. In this edition Dr. Stimson 
has sought to indicate the changes that have been 
effected in operative methods and procedures by 
the antiseptic system, and has added an account 
of many new operations and variations in the 
steps of older operations. We do not desire to 
extol this manual above many excellent standard 
British publications of the same class, still we be- 
lieve that it contains much that is worthy of imi- 
tation.—British Medical Journal, Jan. 22, 1887. 
By the same Author. 
A Treatise on Fractures and Dislocations. In two handsome octavo vol- 
umes. Vol. I., Fractures, 582 pages, 360 beautiful illustrations. Vol. II., Disloca- 
tions, 540 pages, with 163 illustrations. Complete work, cloth, $5.50; leather, $7.50. 
Either volume separately, cloth, $3.00; leather, $4.00. 
The appearance of the second volume marks the 
completion of the author’s original plan of prepar- 
ing a work which should present in the fullest 
manner all that is known on the cognate subjects 
of Fractures and Dislocations. The volume on 
Fractures assumed at once the position of authority 
on the subject, and its companion on Dislocations 
will no doubt be similarly received. The closing 
volume of Dr. Stimson’s work exhibits the surgery 
of Dislocations as it is taught and practised by the 
most eminent surgeons of the present time. Con- 
taiaing the results of such extended researches it 
must for a long time be regarded as an authority 
on all subjects pertaining to dislocations. Every 
Eractitioner of surgery will feel it incumbent on 
im to have it for constant reference.—Cincinnati 
Medical News, May, 1888. 
PICK, T, PICKERING, F. R. C. S., 
Surgeon to and Lecturer on Surgery at St. George's Hospital, London. 
Fractures and Dislocations. In one 12mo. volume of 530 pages, with 93 
illustrations. Limp cloth, $2.00. See Series of Clinical Manuals, page 31. Lea Brothers & Co.’s Publications—Otol., Ophtlial. 
23 
BURNETT, CHARLES 11., A. 31., M. E., 
Professor of Otology in the Philadelphia Polyclinic; President of the American Otological Society. 
The Ear, Its Anatomy, Physiology and Diseases. A Practical Treatise 
for the use of Medical Students and Practitioners. Second edition. In one handsome 
octavo volume of 580 pages, with 107 illustrations. Cloth, $4.00; leather, $5.00. 
We note with pleasure the appearance of a second 
edition of this valuable work. When it first came 
out it was accepted by the profession as one of 
the standard works on modern aural surgery in 
the English language; and in his second edition 
Dr. Burnett has fully maintained his reputation, 
for the book is replete with valuable information 
and suggestions. The revision has been carefully . 
carried out, and much new matter added. Dr. 
Burnett’s work must be regarded as a very valua- 
ble contribution to aural surgery, not only on 
account of its comprehensiveness, but because it 
contains the results of the careful personal observa- 
tion and experience of this eminent aural surgeon. 
—London Lancet, Feb. 21, 1885. 
BERRY, GEORGE A., M. B., F. R. C. S., Ed., 
Ophthalmic Surgeon, Edinburgh Royal Infirmary. 
Diseases of the Eye. A Practical Treatise for Students of Ophthalmology. In 
one octavo volume of 683 pages, with 144 illustrations, 62 of which are beautifully 
colored. Cloth, $7.50. 
This newest candidate for favor among ophthal- 
mological students is designed to be purely clinical 
in character and the plan is well adhered to. We 
have been forcibly struck by the rare good taste 
in the selection of what is essential which per- 
vades the book. The author seems to have the 
uncommon faculty of viewing his subject as a 
whole and seizing the salient points and not con- 
fusing his reader—presumably a student and a 
novice—with a mass of details with no key to their 
unravelling. It is apparent that the literature of 
each subject has been gone over in a very thor- 
ough manner. The fact that he was writing a 
clinical treatise for beginners and not an encyclo- 
paedia has always been present with the author. 
The number and excellence of the colored illus- 
trations in the text deserve more than a passing 
notice.—Archives of Ophthalmology, Sept. 1889. 
NETTLESHIP, EE WARE, F. R. C. S., 
Ophthalmic Surgeon at St. Thomas' Hospital, London. Surgeon to the Royal London (Moorfields) 
Ophthalmic Hospital. 
Diseases of the Eye. New (fourth) American from the fifth English edition, 
thoroughly revised. With a Supplement on the Detection of Color Blindness, by Wil- 
liam Thomson, M. D., Professor of Ophthalmology in the Jefferson Medical College. 
In one 12mo. volume of 500 pages, with 164 illustrations, selections from Snellen’s test- 
types and formulae, and a colored plate. Cloth, $2.00. Just ready. 
This is a well-known and a valuable worn. It 
was primarily intended for the use of students, 
and supplies their needs admirably, but it is as 
useful lor the practitioner, or indeed more so. It 
does not presuppose the large amount of recondite 
knowledge to be present which seems to be as- 
sumed in some of our larger works, is not tedious 
from over-conciseness, and yet covers the more 
important parts of clinical ophthalmology. A 
supplement is made to the present edition on the 
practical examination of railroad employes as to 
color-blindness and acuteness of vision and hear- 
ing. This is well written, and contains good 
suggestions for those who may be called on to 
make such examinations.—JSew York Medical 
Journal, December 13, 1890. 
JULER, HENRY E., F. R. C. S., 
Senior Ass't Surgeon, Royal Westminster Ophthalmic Hosp.; late Clinical Ass't, Moorfields, London. 
A Handbook of Ophthalmic Science and Practice. Handsome 8 vo. vol- 
ume of 460 pages, with 125 woodcuts, 27 colored plates, selections from Test-types of 
Jaeger and Snellen, and Holmgren’s Color-blindness Test. Cloth, $4.50; leather, $5.50. 
It presents to the student concise descriptions 
and typical illustrations of all important eye affec- 
tions, placed in juxtaposition, so as to be grasped 
at a glance. Beyond a doubt it is the best illus- 
trated handbook of ophthalmic science which has 
ever appeared. Then, what is still better, these 
illustrations are nearly all original. We have ex- 
amined this entire work with great care, and it 
represents the commonly accepted views of ad- 
vanced ophthalmologists. We can most heartily 
commend this book to all medical students, prac- 
titioners and specialists.—Detroit Lancet, Jan. ’85. 
NORRIS, JVM. F., M. I)., and OLIVER, CHAS. A., M. E. 
Clin. Prof, of Ophthalmology in Univ. of Pa. 
A Text-Book of Ophthalmology. In one octavo volume of about 500 pages, 
with illustrations. Preparing. 
CARTER, R. BRUEENELL, & FROST, W. A DAMS, 
F. R. C. S., F. R. C. S., 
Ophthalmic Surgeon to and Led. on Ophthal- Ass't Ophthalmic Surgeon and Joint Led. 
mic Surgery at St. George's Hospital, London. on Oph. Sur., St. George's Hosp., London. 
Ophthalmic Surgery. In one 12mo. volume of 559 pages, with 91 woodcuts, 
color-blindness test, test-types and dots and appendix of formulae. Cloth, $2.25. See 
Series of Clinical Manuals, page 31. 
WELLS ON THE EYE. In one octavo volume, i 
LAURENCE AND MOON’S HANDY BOOK OF! 
OPHTHALMIC SURGERY, for the use of Prac- 
titioners. Second edition. In one octavo vol- 
ume of 227 pages, with 66 illus. Cloth, $2.75. 
LAWSON ON INJURIES TO THE EYE, ORBIT 
AND EYELIDS: Their Immediate and Remote 
Effects. In one octavo volume of 404 pages, with 
92 illustrations. Cloth, $3.50. 24 
Lea Brothers & Co.’s Publications—Urin. Dis., Dentistry, etc. 
ROBERTS, SIR WILLIAM, M. D., 
Lecturer on Medicine in the Manchester School of Medicine, etc. 
A Practical Treatise on Urinary and Renal Diseases, including Uri- 
nary Deposits. Fourth American from the fourth London edition. In one hand- 
some octavo volume of 609 pages, with 81 illustrations. Cloth, $3.50. 
It may be said to be the best book in print on the 
subject of which it treats.— The American Journal 
of the Medical Sciences, Jan. 1886. 
The peculiar value and finish of the book are in 
a measure derived from its resolute maintenance 
of a clinical and practical character. It is an un- 
rivalled exposition of everything which relates 
directly or indirectly to the diagnosis, prognosis 
and treatment of urinary diseases, and possesses 
a completeness not found elsewhere in our lan- 
guage in its account of the different affections.— 
The Manchester Medical Chronicle, July, 1885. 
The value of this treatise as a guide book to the 
physician in daily practice can hardly be over- 
estimated. That it is fully up to the level of our 
present knowledge is a fact reflecting great credit 
upon Dr. Roberts, who has a wide reputation as a 
busy practitioner.—Medical Record, July 31, 1886. 
By the Same Author. 
Diet and Digestion. In one handsome 12mo. volume of 270 pages. Cloth, $1.50. 
Just ready. 
PURDY, CHARLES W., M. D., Chicago. 
Bright’s Disease and Allied Affections of the Kidneys. In one octavo 
volume of 288 pages, with illustrations. Cloth, $2. 
The object of this work is to “furnish a system- 
atic, practical and concise description of the 
pathology and treatment of the chief organic 
diseases of the kidney associated with albuminu- 
ria, which shall represent the most recent ad- 
vances in our knowledge on these subjects and 
this definition of the object is a fair description of 
the book. The work is a useful one, giving in a 
short space the theories, facts and treatments, and 
going more fully into their later developments. 
On treatment the writer is particularly strong, 
steering clear of generalities, and seldom omit- 
ting, what text-books usually do, the unimportant 
items which are all important to the general prac- 
titioner.— The Manchester Medical Chronicle, Oct. 
1886. 
MORRIS, HENRY, M. B., F. R. C. S., 
Surgeon to and lecturer on Surgery at Middlesex Hospital, London. 
Surgical Diseases of the Kidney. In one 12mo. volume of 554 pages, with 40 
woodcuts, and 6 colored plates. Limp cloth, $2.25. See Series of Clinical Manuals, page 31. 
In this manual we have a distinct addition to 
surgical literature, which gives information not 
elsewhere to be met with in a single work. Such 
a book was distinctly required, and Mr. Morris 
has very diligently and ably performed the task 
he took in hand. It is a full and trustworthy 
book of reference, both for students and prac- 
titioners in search of guidance. The illustrations 
in the text and the chromo-lithographs are beau- 
tifully executed.— The London Lancet, Feb. 26,1886. 
LUCAS, CLEMENT, M. B., B. S., F. R. C. S., 
Senior Assistant Surgeon to Quy's Hospital, London. 
Diseases of the Urethra. Ill one 12mo. volume. Preparing. See Series 
of Clinical Manuals, page 4. 
THOMPSON, SIR HENRY, 
Surgeon and Professor of Clinical Surgery to University College Hospital, London. 
Lectures on Diseases of the Urinary Organs. Second American from the 
third English edition. In one 8vo. volume of 203 pp., with 25 illustrations. Cloth, $2.25. 
By the Same Author. 
On the Pathology and Treatment of Stricture of the Urethra and 
Urinary Fistulse. From the third English edition. In one octavo volume of 359 
pages, with 47 cuts and 3 plates. Cloth, $3.50. 
THE AMERICAN SYSTEM OF DENTISTRY. 
In Treatises by Various Authors. Edited by Wilbur F. Litch, M. D., 
D. D. S., Professor of Prosthetic Dentistry, Materia Medica and Therapeutics in the 
Pennsylvania College of Dental Surgery. In three very handsome octavo volumes con- 
taining 3160 pages, with 1863 illustrations and 9 full-page plates. Per volume, cloth, $6 ; 
leather, $7; half Morocco, gilt top, $8. The complete work is now ready. For sale by 
subsd'iption only. 
As an encyclopaedia of Dentistry it has no su- 
perior. It should form a part of every dentist’s 
library, as the information it contains is of the 
greatest value to all engaged in the practice of 
dentistry.—American Jour. Dent. Sci., Sept. 1886. 
A grand system, big enough and good enough 
and handsome enough for a monument (which 
doubtless it is), to mark an epoch in the history of 
dentistry. Dentists will be satisfied with it and 
proud of it—they must. It is sure to be precisely 
what the student needs to put him and keep him 
in the right track, while the profession at large 
will receive incalculable benefit from it.—Odonto- 
graphic Journal, Jan. 1887. 
COLEMAN, A., L. R. C. P., F. R. C. S., Exam. L. D. S., 
Senior Dent. Surg. and Lect. on Dent. Surg. at St. Bartholomew's Hosp. and the Dent. Hosp., London. 
A Manual of Dental Surgery and Pathology. Thoroughly revised and 
adapted to the use of American Students, by Thomas C. Stellwagen, M. A., M. D., 
D. D. S., Prof, of Physiology in the Philadelphia Dental College. In one handsome octavo 
volume of 412 pages, with 331 illustrations. Cloth, $3.25. 
It should be in the possession of every practi- 
tioner in this country. The part devoted to first 
and second dentition and irregularities in the per- 
manent teeth is fully worth the price. In fact, 
price should not be considered in purchasing such 
a work. If the money put into some of our so- 
called standard textrbooks could be converted into 
such publications as this, much good would result. 
—Southern Dental Journal, May, 1882. 
BASHAM ON RENAL DISEASES: A Clinical 
Guide to their Diagnosis and Treatment. In 
one 12mo. vol. of 304 pages, with 21 illustrations. 
Cloth, S2.00. Lea Brothers & Co.’s Publications—Venereal, Impotence. 
25 
GROSS, SAMUEL W., A. M., M. I)., LL. D., 
Professor of the Principles of Surgery and of Clinical Surgery in the Jefferson Medical College of Phila. • 
A Practical Treatise on Impotence, Sterility, and Allied Disorders 
of the Male Sexual Organs. New (4th) edition, thoroughly revised by F. R. 
Sturgis, M. D., Prof, of Diseases of the Genito-Urinary Organs and of Venereal Diseases, 
N. Y. Post Grad. Med. School. In one very handsome octavo volume of 165 pages, 
with 18 illustrations. Cloth, $1.50. 
Three editions of Professor Gross’ valuable book 
have been exhausted, and still the demand is 
unsupplied. Dr. Sturgis has revised and added 
to the previous editions, and the new one appears 
more complete and more valuable than before. 
Four important and generally misunderstood sub- 
jects are treated—impotence," sterility, spermator- 
rhoea, and prostatorrhcea. The book is a practical 
one and in addition to the scientific and very in- 
teresting discussions on etiology, symptoms, etc., 
there are lines of treatment laid down that any 
practitioner can follow and which have met with 
success in the hands of author and editor.—Medi- 
cal Record, Feb. 25, 1891. 
It has been the aim of the author to supply in a 
compact form, practical and strictly scientific 
information especially adapted to the wants of the 
general practitioner in regard to a class of common 
and grave disorders. The work contains very 
j many facts in regard to the sexual disorders of 
men, of the most interesting character. We com- 
mend the study of it to every professional man, 
and especially to those engaged in the general 
practice of medicine.—Cincinnati Medical News, 
Jan. 1891. 
The work before us has become a standard text- 
book on the subjects of which it treats. In the 
i present edition the author’s work has been con- 
| siderably augmented by Dr. Sturgis, whose con- 
tributions and views are to be teen everywhere. 
They contain many valuable suggestions and are 
the fruit of a ripe experience which cannot but 
enhance the original text. The profession is 
quick to appreciate succinct treatises which are 
full and complete, more especially when the 
authors are known to be worthy of respect and 
confidence.—St. Louis Medical ana Surgical Journal, 
Feb. 1891. 
TAYLOR, R. W., A. if., if. JD., 
Clinical Professor of Genito-Urinary Diseases in the College of Physicians and Surgeons, New York, 
Prof, of Venereal and Skin Diseases in the University of Vermont, 
The Pathology and Treatment of Venereal Diseases. Including the 
results of recent investigations upon the subject. Being the sixth edition of Bumstead 
and Taylor. Entirely rewritten by Dr. Taylor. Large 8vo. volume, about 900 pages, 
with about 150 engravings, as well as numerous chromo-lithographs. In active preparation. 
A few notices of the previous edition are appended. 
It is a splendid record of honest labor, wide 
research, just comparison, careful scrutiny and 
original experience, which will always be held as 
a high credit to American medical literature. This 
is not only the best work in the English language 
upon the subjects of which it treats, but also one 
which has no equal in other tongues for its clear, 
comprehensive and practical handling of its 
tnemes.—Am. Jour, of the Med. Sciences, Jan. 1884. 
The character of this standard work is so well 
known that it would be superfluous here to pass in 
review its general or special points of excellence. 
The verdict of the profession nas been passed; it 
has been accepted as the most thorough and com- 
plete exposition of the pathology and treatment of 
venereal diseases in the language. Admirable as a 
model of clear description, an exponent of sound 
pathological doctrine, and a guide for rational and 
successful treatment, it is an ornament to the medi- 
cal literature of this country. The additions made 
to the present edition are eminently judicious, 
from the standpoint of practical utility.—Journal of 
\ Cutaneous and Venereal Diseases, Jan. 1884. 
1 
CORNU, V., 
Professor to the Faculty of Medicine of Paris, and Physician to the Lourcine Hospital. 
Syphilis, its Morbid Anatomy, Diagnosis and Treatment. Specially 
revised by the Author, and translated with notes and additions by J. Henry C. Simes, 
M. D., Demonstrator of Pathological Histology in the Univ. of Pa., and J. William 
White, M. D., Lecturer on Venereal Diseases, Univ. of Pa. In one handsome octavo 
volume of 461 pages, with 84 very beautiful illustrations. Cloth, $3.75. 
The anatomy, the histology, the pathology and 
the clinical features of syphilis are represented in 
this work in their best, most practical and most 
instructive form, and no one will rise from its 
perusal without the feeling that his grasp of the 
wide and important subject on which it treats is 
a stronger and surer one.— The London Practi- 
tioner, Jan. 1882. 
HUTCHINSON, JONATHAN, F. It. S., F. B. C. S., 
Consulting Surgeon to the London Hospital. 
Syphilis. In one 12mo. volume of 542 pages, with 8 chromo-lithograplis. Cloth, 
$2.25. See Series of Clinical Manuals, page 31. 
Those who have seen most of the disease and 
those who have felt the real difficulties of diagno- 
sis and treatment will most highly appreciate the 
facts and suggestions which abound in these 
pages. It is a worthy and valuable record, not 
only of Mr. Hutchinson’s very large experience 
and power of observation, but of his patience and 
assiduity in taking notes of his cases and keep- 
ing them in a form available for such excellent 
use as he has put them to in this volume.—London 
Medical Record, Nov. 12, 1887. 
GROSS, S. JD., M. JD., LL. D., JD. C. L., etc. 
A Practical Treatise on the Diseases, Injuries and Malformations 
of the Urinary Bladder, the Prostate Gland and the Urethra. Third 
edition, thoroughly revised by Samuel W. Gross, M. D. In one octavo volume of 574 
pages, with 170 illustrations. Cloth, $4.50. 
CULLERIER, A., & B UMSTEAH, F. J., M.D., LL.H., 
Surgeon to the H&pital du Midi. Late Professor of Venereal Diseases in the College of Physicians 
and Surgeons, New York. 
An Atlas of Venereal Diseases. Translated and edited by Freeman J. Bum- 
stead, M. D. In one imperial 4to. volume of 328 pages, double-columns, with 26 plates, 
containing about 150 figures, beautifully colored, many of them the size of life. Strongly 
bound in cloth, $17.00. A specimen of the plates and text sent by mail, on receipt of 25 cts. 
HILL ON SYPHILIS AND LOCAL CONTAGIOUS 
DISORDERS. In one 8vo vol. of479 p. Cloth, $3.25. 
LEE’S LECTURES ON SYPHILIS AND SOME 
FORMS OF LOCAL DISEASE AFFECTING 
PRINCIPALLY THE ORGANS OF GENERA- 
TION. In one 8vo. vol. of 246 pages. Cloth, $2.25. 26 
Lea Brothers & Co.’s Publications—Venereal, Skin. 
TAYLOR, ROBERT TV., A. 31., 31. B., 
Clinical Professor of Qeni'o Urinary Diseases in the College of Physicians and Surgeons, New York ; 
Surgeon to the Department of Venereal and Skin Diseases of the New York Hospital; Presi- 
dent of the American Dermatological Association. 
A Clinical Atlas of Venereal and Skin Diseases: Including Diagnosis, 
Prognosis and Treatment. In eight large folio parts, measuring 14 x 18 inches, and 
comprising 58 beautifully-colored plates with 213 figures, and 431 pages of text with 85 
engravings. Complete work just ready. Price per part, $2.50. Bound in one volume, 
half Russia, $27 ; half Turkey Morocco, $28. For sale, by subscription only. Specimen 
plates sent on receipt of 10 cents. A full prospectus sent to any address on application. 
The completion of this monumental work is a 
subject of congratulation, not only to the author 
and publishers, but to the profession at large; 
indeed it is to the latter that it directly appeals as 
a wonderlully clear exposition of a confessedly 
difficult branch of medicine Good literature has 
joined hands with good art with highly satisfac- 
tory results for both. There are altogether 213 
figures, many of which are life size, and represent 
the highest perfection of the chromo-litho- 
graphic art, and scattered throughout the text are 
innumerable engravings. Quite a proportion of 
these illustrations are from the author’s own 
collection, while on the other hand the best 
atlases of the world have been drawn upon for 
the most typical and successful pictures of the 
many different types of venereal and skin dis 
ease. We think we may say without undue 
exaggeration that the reproductions, both in color 
and in black and white, are almost invariably 
successful. The text is practical, full of thera- 
peutical suggestions, and the clinical accounts of 
disease are clear and incisive. Dr. Taylor is, 
happily, an eminent authority in both departments, 
and we find as a consequence that the two divis- 
ions of this work possess an equal scientific and 
literary merit. We have already passed the limits 
allotted to a notice of this kind, and while we 
have nothing but praise for this admirable atlas, 
it must be said in justification that it is more than 
warranted by the merits of the work itself.— 
The Medical News, Dec. 14,1889. 
It would be hard to use words which would per- 
spicuously enough convey to the reader the great 
value of this Clinical Atlas. This Atlas is more 
complete even than an ordinary course of clinical 
lectures, for in no one college or hospital course 
is it at all probable that all of the diseases herein 
represented would be seen. It is also more ser- 
viceable to the majority of students than attend- 
ance upon clinical lectures, for most of the 
students who sit on remote seats in the lecture 
hall cannot see the subject as well as the office 
student can examine these true to-life chromo-lith- 
ographs. Comparing the text to a lecturer,’it is 
more satisfactory in exactness and fulness than 
he would be likely to be in lecturing over a single 
case. Indeed, this Atlas is invaluable to the gen- 
eral practitioner, for it enables the eye of the 
physician to make diagnosis of a given case of 
skin manifestation by comparing the case with 
the picture in the Atlas, where will be found also 
the text of diagnosis, pathology, and full sections 
on treatment.— Virginia Medical Monthly, Dec. 1889. 
HYDE, J. XEVIXS, A. M., M. D., 
Professor of Dermatology and Venereal Diseases in Rush Medical College, Chicago. 
A Practical Treatise on Diseases of the Skin. For the use of Students and 
Practitioners. New (second) edition. In one handsome octavo volume of 676 pages, 
with 2 colored plates and 85 beautiful and elaborate illustrations. Cloth, $4.50; leather, $5.50. 
We can heartily commend it, not only as an 
admirable text-book for teacher and student, but 
in its clear and comprehensive rules for diagnosis, 
its sound and independent doctrines in pathology, 
and its minute and judicious directions for the 
treatment of disease, as a most satisfactory and 
complete practical guide for the physician.—Ameri- 
can Journal of the Medical Sciences, July, 1888. 
A useful glossary descriptive of terms is given. 
The descriptive portions of this work are plain 
and easily understood, and above all are very 
accurate. The therapeutical part is abundantly 
supplied with excellent recommendations. The 
picture part is well done. The value of the work 
to practitioners is great because of the excellence 
of the descriptions, the suggestiveness of the 
advice, and the correctness of the details and the 
principles of therapeutics impressed upon the 
reader.— Virginia Med. Monthly, May, 1888. 
The second edition of his treatise is like his 
clinical instruction, admirably arranged, attractive 
in diction, and strikingly practical throughout. 
The chapter on general symptomatology is a model 
in its way; no clearer description of the various 
primary and consecutive lesions of the skin is to 
be met"with anywhere. Those on general diagno- 
sis and therapeutics are also worthy of careful 
study. Dr. Hyde has shown himself a compre- 
hensive reader of the latest literature, and has in- 
corporated into his book all the best of that which 
the past years have brought forth. The prescrip- 
tions and formulae are given in both common and 
metric systems. Text'and illustrations are good, 
and colored plates of rare cases lend additional 
attractions. Altogether it is a work exactly fitted 
to the needs of a general practitioner, and no one 
will make a mistake in purchasing it.—Medical 
Press of Western New York, June, 1888. 
FOX, T., M. JD., F.R. C. F., and FOX, T. C., B.A., 3I.R. C.S., 
Physician to the Department for Skin Diseases, Physician for Diseases of the Skin to the 
University College Hospital, London. Westminster Hospital, London. 
An Epitome of Skin Diseases. With Formulae. For Students and Prac- 
titioners. Third edition, revised and enlarged. In one 12mo. vol. of 238 pp. Cloth, $1.25. 
The third edition of this convenient handbook 
calls for notice owing to the revision and expansion 
which it has undergone. The arrangement of skin 
diseases in alphabetical order, which is the method 
of classification adopted in this work, becomes a 
positive advantage to the student. The book is 
one which we can strongly recommend, not only 
to students but also to practitioners who require "a 
compendious summary of the present state of 
dermatology.—British Medical Journal, July 2,1883. 
We cordially recommend Fox’s Epitome to those 
whose time is limited and who wish a handy 
manual to lie upon the table for instant reference. 
Its alphabetical arrangement is suited to this use, 
for all one has to know is the name of the disease, 
and here are its description and the appropriate 
treatment at hand and ready for instant applica- 
tion. The present edition has been very carefully 
revised and a number of new diseases are de- 
scribed, while most of the recent additions to 
dermal therapeutics find mention, and the formu 
lary at the end of the book has been considerably 
augmented.—The Medical News, December, 1883. 
WILSOX, ERASMUS, F.R.S. 
The Student’s Book of Cutaneous Medicine and Diseases of the Skin. 
In one handsome small octavo volume of 535 pages. Cloth, $3.50. 
HILLIER’S HANDBOOK OF SKIN DISEASES; 
for Students and Practitioners. Second Ameri- 
can edition. In one 12mo. volume of 353 pages, 
witli plates. Cloth, $2.25. Lea Brothers & Co.’s Publications—I>is. of Women. 
27 
The American Systems of Gynecology and Obstetrics. 
Systems of Gynecology and Obstetrics, in Treatises by American 
Authors. Gynecology edited by Matthew D. Mann, A. M., M. D., Professor of Obstetrics 
and Gynecology in the Medical Department of the University of Buffalo; and Obstet- 
rics edited by Barton Cooke Hirst, M. D., Associate Professor of Obstetrics in the 
University of Pennsylvania, Philadelphia. In four very handsome octavo volumes, con- 
taining 3612 pages, 1092 engravings and 8 plates. Complete work just ready. Per vol- 
ume: Cloth, $5.00; leather, $6.00; half Russia, $7.00. For sale by subscription only. 
Address the Publishers. Full descriptive circular free on application. 
WILLIAM H. BAKER, M. D., 
ROBERT BATTEY, M. D., 
SAMUEL C. BUSEY, M. D., 
JAMES C. CAMERON, M. D., 
HENRY C. COE, A. M„ M. D., 
EDWARD P. DAVIS, M. D., 
G. E. De SCHWEINITZ, M. D., 
E. C. DUDLEY, A. B., M. D., 
B. McE. EMMET, M. D., 
GEORGE J. ENGELMANN, M. D., 
HENRY J. GARRIGUES, A. M., M. D., 
WILLIAM GOODELL, A. M., M. D.. 
EGBERT H. GRANDIN, A. M., M. D., 
SAMUEL W. GROSS, M. D., 
ROBERT P. HARRIS, M. D., 
GEORGE T. HARRISON, M. D., 
BARTON C. HIRST, M. D. 
STEPHEN Y. HOWELL, M. D., 
A. REEVES JACKSON, A. M., M. D., 
W. W. JAGGARD, M. D., 
EDWARD W. JENKS, M. D., LL. D., 
HOWARD A. KELLY, M. D., 
LIST OF CONTRIBUTORS. 
CHARLES CARROLL LEE, M. D., 
WILLIAM T. LUSK, M. D., LL. D., 
J. HENDRIE LLOYD, M. D., 
MATTHEW D. MANN, A. M., M. D., 
H. NEWELL MARTIN, F. R. S., M. D., 
D. Sc., M.A., 
RICHARD B. MAURY, M. D., 
C. D. PALMER, M. D., 
ROSWELL PARK, M. D., 
THEOPHILUS PARVIN, M. D., LL. D., 
R. A. F. PENROSE, M. I)., LL. D., 
THADDEUS A. REAMY, A. M., M. D., 
J. C. REEVE, M. D., 
A. I). ROCKWELL, A. M., M. D., 
ALEXANDER J. C. SKENE, M. D., 
J. LEWIS SMITH, M. D., 
STEPHEN SMITH, M. D., 
R. STANSBURY SUTTON, A. M., M. D., 
LL. D., 
T. GAILLARD THOMAS, M. D., LL. D., 
ELY VAN DE WARKER, M. D., 
W. GILL WYLIE, M. D. 
These volumes are the contributions of the most 
eminent gentlemen of this country in these de- 
partments of the profession. Each contributor 
presents a monograph upon his special topic, 
apparently without restriction in space, so that 
everything in the way of history, theory, methods, 
and results is presented to our fullest need. The 
work will long remain as a monument of great in- 
dustry and good judgment. As a work of general 
reference, it will be found remarkably full and in- 
structive in every direction of inquiry.— The Ob- 
stetric Gazette, September, 1889. 
There can be but little doubt that this work will 
find the same favor with the profession that has 
been accorded to the “ System of Medicine by 
American Authors,” and the “System of Gynecol- 
ogy byAmerican Authors.” One is at a loss to know 
wnat to say of this volume, for fear that just and 
merited praise may be mistaken for flattery. The 
papers of Drs. Engelmann, Martin, Hirst, Jaggard 
and Reeve are incomparably beyond anytning that 
can be found in obstetrical works. Certainly the 
Editor may be congratulated for having made such 
a wise selection of his contributors.—Journal of 
the American Medical Association, Sept. 8, 1888. 
In our notice of the “System of Practical Medi- 
cine by American Authors,” we made the follow- 
ing statement:—“It is a work of which the pro- 
fession in this country can feel proud. Written 
exclusively by American physicians who are ac- 
quainted with all the varieties of climate in the 
United States, the character of the soil, the man- 
ners and customs of the people, etc., it is pecul- 
iarly adapted to the wants of American practition- 
ers of medicine, and it seems to us that every one 
of them would desire to have it.” Every word 
thus expressed in regard to the “American Sys- 
tem of Practical Medicine” is applicable to the 
“System of Gynecology by American Authors,” 
which we desire now to bring to the attention of 
our readers. It, like the other, has been written 
exclusively by American physicians who are 
acquainted with all the characteristics of American 
people, who are well informed in regard to the 
peculiarities of American women, their manners, 
customs, modes of living, etc. As every practis- 
ing physician is called upon to treat diseases of 
females, and as they constitute a class to which 
the family physician must give attention, and 
cannot pass over to a specialist, we do not know of 
a work in any department of medicine that we 
should so strongly recommend medical men gen- 
erally purchasing.—Cincinnati Med. News, July,1887. 
TH03IAS, T. GAILLARI), and 3IUNDF, RAUL F., 
31. I)., LR. R>., 31. 13., 
Professor of Diseases of Women in the College Professor of Gynecology in the New York 
of Physicians and Surgeons, N. Y. ' Polyclinic. 
A Practical Treatise on the Diseases of Women. New (sixth) edition, 
thoroughly revised and rewritten by Dr. Munde. In one large and handsome octavo 
volume of about 900 pages, with over 300 illustrations. In press. 
In this revision Dr. Munde has undertaken to preserve the practical nature of the 
work which has rendered it so useful to the student and physician, and also to bring it 
fully abreast with the best gynecological practice of the present day. 
FI) IS, ARTHUR W., M. I)., Roncl., F.R. C.R., 31. R. C.S., 
Assist. Obstetric Physician to Middlesex Hospital, late Physician to British Lying-in Hospital. 
The Diseases of Women. Including their Pathology, Causation, Symptoms, 
Diagnosis and Treatment. A Manual for Students and Practitioners. In one handsome 
octavo volume of 576 pages, with 148 illustrations. Cloth, $3.00; leather, $4.00. 
It is a pleasure to read a book so thoroughly 
good as this one. The special qualities which are 
conspicuous are thoroughness in covering the 
whole ground, clearness of description and con- 
ciseness of statement. Another marked feature of 
the book is the attention paid to the details of 
many minor surgical operations and procedures, 
as, for instance, the use of tents, application of 
leeches, and use of hot water injections. These 
are among the more common methods of treat- 
ment, and yet very little is said about them in 
many of the text-books. The book is one to be 
warmly recommended especially to students and 
general practitioners, who need a concise but com- 
plete r'esumi of the whole subject. Specialists, too, 
will find many useful hints in its pages.—Boston 
Med. and Surg. Journ., March 2, 1882. 28 
Lea Brothers & Co.’s Publications—Dis. of Women, Midwfy. 
EMMET, THOMAS ADDIS, M. D., LL. D., 
Surgeon to the Woman's Hospital, New York, etc. 
The Principles and Practice of Gynaecology; For the use of Students and 
Practitioners of Medicine. New (third) edition, thoroughly revised. In one large and very 
handsome octavo volume of 880 pages, with 150 illustrations. Cloth, $5; leather, $6; 
very handsome half Russia, raised bands, $6.50. 
We are in doubt whether to congratulate the 
author more than the profession upon the appear- 
ance of the third edition of this well-known work. 
Embodying, as it does, the life-long experience of 
one who has conspicuously distinguished himself 
as a bold and successful operator, and who has 
devoted so much attention to the specialty, we 
feel sure the profession will not fail to appreciate 
the privilege thus offered them of perusing the 
views and practice of the author. His earnestness 
of purpose and conscientiousness are manifest. 
He gives not only his individual experience but 
endeavors to represent the actual state of gynae- 
cological science and art.—British Medical Jour- 
nal, May 16, 1885. 
TAIT, LAWSOX, F.B. C. S., 
Professor of Gynaecology in Queen's College, Birmingham; late President of the British Gyne- 
cological Society; Fellow American Gynecological Society. 
Diseases of Women and Abdominal Surgery. In two very handsome 
octavo volumes. Volume I., 554 pages, 62 engravings and 3 plates. Cloth, $3. Now 
ready. Volume II., preparing. 
The plan of the work does not indicate the regu- 
lar system of a text book, and yet nearly every- 
thing of disease pertaining to the various organs 
receives a fair consideration. The description of 
diseased conditions is exceedingly clear, and the 
treatment, medical or surgical, is very satisfactory. 
Much of the text is abundantly illustrated with 
cases, which add value in showing the results of 
the suggested plans of treatment. We feel con- 
fident that few gynecologists of the country will 
fail to place the work in their libraries.— The 
Obstetric Gazette, March, 1890. 
DAVEXPOBT, F. II., M. I)., 
Assistant in Gynaecology in the Medical Department of Harvard University, Boston. 
Diseases of Women, a Manual of Non-Surgical Gynaecology. De- 
signed especially for the Use of Students and General Practitioners. In one handsome 
12mo. volume of 317 pages, with 105 illustrations. Cloth, $1.50. Just ready. 
We agree with the many reviewers whose no- 
tices we have read in other j ournals congratulating 
Dr. Davenport on the success which he has 
attained. He has tried to write a book for the 
student and general practitioner which would 
tell them just what they ought to know without 
distracting their attention with a lot of compila- 
tions for which they could have no possible use. 
In this he has been eminently successful. There 
is not even a paragraph of useless matter. 
' Everything is of the newest, freshest and most 
practical, so much so that we have recommended 
it to our class of gynecology students. What the 
author advises in the way of treatment has all 
been practically tested by himself, and each 
method receives only so much commendation as he 
has found*that it deserves. We are sure that 
these good qualities will command for it a large 
sale.—Canada Medical Record, Dec. 1889. 
MAY, CHABLES II., M. I)., 
Late House Surgeon to Mount Sinai Hospital, New York. 
A Manual of theDiseases of Women. Being a concise and systematic expo- 
sition of the theory and practice of gynecology. New (2d) edition, edited by L. S. Rau, 
M. D., Attending Gynecologist at the Harlem Hospital, N. Y. In one 12mo. volume of 
360 pages, with 31 illustrations. Cloth, $1.75. Just ready. 
This is a manual of gynecology in a very con- 
densed form, and the fact that a second edition 
has been called for indicates that it has met with 
a favorable reception. It is intended, the author 
tells us, to aid the student who after having care- 
fully perused larger works desires to review the 
subject, and he adds that it may be useful to the 
practitioner who wishes to refresh his memory 
rapidly but has not the time to consult larger 
works. We are much struck with the readiness 
and convenience with which one can refer to any 
subject contained in this volume. Carefully com- 
piled indexes and ample illustrations also enrich 
the work. This manual will be found to fulfil its 
purposes very satisfactorily.—The Physician and 
Surgeon, June, 1890. 
I) UNO AX, J. MATTHEWS, M I)., LL. I)., F. B. S. E., etc. 
Clinical Lectures on the Diseases of Women; Delivered in Saint Bar- 
tholomew’s Hospital. In one handsome octavo volume of 175 pages. Cloth, $1.50. 
They are in every way worthy of their author ; 
indeed, we look upon them as among the most 
valuable of his contributions. They are all upon 
matters of great interest to the general practitioner. 
Some of them deal with subjects that are not, as a 
rule, adequately handled in the text-books; others 
of them, while hearing upon topics that are usually 
treated of at length in such works, yet bear such a 
stamp of individuality that they deserve to be 
widely read.—N. Y. Medical Journal, March, 1880. 
HODGE ON DISEASES PECULIAR TO WOMEN. 
Including Displacements of the Uterus. Second 
edition, revised and enlarged. In one beauti- 
fully printed octavo volume of 519 pages, with 
original illustrations. Cloth, $4.60. 
RAMSBOTHAM’S PRINCIPLES AND PRAC- 
TICE OF OBSTETRIC MEDICINE AND 
SURGERY. In reference to the Process of 
Parturition. A new and enlarged edition, thor- 
oughly revised by the Author. With additions 
by W. V. Keating, M. D., Professor of Obstetrics, 
etc., in the Jefferson Medical College of Phila- 
delphia. In one large and handsome imperial 
octavo volume of 640 pages, with 64 full page 
plates and 43 woodcuts in the text, containingln 
all nearly 200 beautiful figures. Strongly bound 
in leather, with raised bands, $7. 
WEST’S LECTURES ON THE DISEASES OF 
WOMEN Third American from the third Lon- 
don edition. In one octavo volume of 543 pages. 
Cloth, $3.75; leather, $4.75. Lea Brothers & Co.’s Publications—Midwifery. 
29 
PARVIN, HIEOPIIILLS, 31. 1)., LL. B., 
Pof. of Obstetrics and the Diseases of Women and Children in Jefferson Med. Coll., Phila. 
The Science and Art of Obstetrics. New (2d) edition, In one handsome 
8vo. volume of 701 pages, with 239 engravings and a colored plate. Cloth, $1.25; leather, 
$5.25. Just ready. 
The second edition of this work is fully up to the 
present state of advancement of the obstetric art. 
The author has succeeded exceedingly well in 
incorporating new matter without apparently in- 
creasing the size of his work or interfering with 
the smoothness and grace of its literary construc- 
tion. He is very felicitous in his descriptions of 
conditions, and proves himself in this respect a 
scholar and a master. Rarely in the range of 
obstetric literature can be found a work which is 
so comprehensive and yet compact and practical. 
In such respect it is essentially a text book of the 
first merit. The treatment of the subjects gives a 
real value to the work—the individualities of a 
practical teacher, a skilful obstetrician, a close 
thinker and a ripe scholar.—Medical Record, Jan. 
17, 1891. 
PLAYFAIR, W. S., 31. B., F. R. C. P., 
Professor of Obstetric Medicine in King’s College, London, etc. 
A Treatise on the Science and Practice of Midwifery. New (fifth) 
American, from the seventh English edition. Edited, with additions, by Robert P. Har- 
ris, M. D. In one handsome octavo volume of 664 pages, with 207 engravings and 5 
plates. Cloth, $4.00; leather, $5.00. 
Truly a wonderful book; an epitome of all ob- 
stetrical knowledge, full, clear and concise. In 
thirteen years it has reached seven editions. It 
is perhaps the most popular work of its kind ever 
presented to the profession. Beginning with the 
anatomy and physiology of the organs concerned, 
nothing is left unwritten that the practical ac- 
coueheur should know. It seems that every 
conceivable physiological or pathological condi- 
I tion from the moment of conception to the time 
I of complete involution has had the author’s 
patient attention. The plates and illustrations, 
carefully studied, will teach the science of mid- 
wifery. The reader of this book will have before 
him the very latest and best of obstetric practice, 
and also of all the coincident troubles connected 
therewith.—Southern Practitioner, Dec., 1889. 
KING, A. F. A., 31. I)., 
Professor of Obstetrics and Diseases of Women in the Medical Department of the Columbian Univer- 
sity, Washington, D. C., and in the University of Vermont, etc. 
A Manual of Obstetrics. New (fourth) edition. In one very handsome 12mo. 
volume of 432 pages, with 140 illustrations. 
Dr. King, in the preface to the first edition of 
this manual, modestly states that “its purpose is 
to furnish a good groundwork to student at 
the beginning of his obstetric studies. ’ Its pur- 
pose is attained; it will furnish a good ground- 
work to the student who carefully reads it; and 
further, the busy practitioner should not scorn the 
volume because written for students, as it con- 
tains much valuable obstetric knowledge, some 
of which is not found in more elaborate text- 
books. The chapters on the anatomy of the 
female generative organs, menstruation, fecunda- 
tion, the signs of pregnancy, and the diseases of 
pregnancy, are all excellent and clear; but it is in 
Cloth, $2.50. 
the description of labor, both normal and abnor- 
mal, that Dr. King is at his best. Here his style 
is so concise, and the illustrations are so good, 
that the veriest tyro could not fail to receive a clear 
conception of labor, its complications and treat- 
ment. Of the 141 illustrations it may be safely 
said that they all illustrate, and that the engraver’s 
work is excellent. The name of the publishers 
is a sufficient guarantee that the work is pre- 
sented in an attractive form, and from every 
standpoint we can most heartily recommend the 
book both to practitioner and student.— The Medi- 
cal News, Dec. 7, 1889. 
B All NFS, ROBERT, 31. JD., and EANCOURT, 31. B., 
Phys. to the General Lying-in Hosp., Lond. Obstetric Phys. to St. Thomas’ Hosp., Lond. 
A System of Obstetric Medicine and Surgery, Theoretical and Clin- 
ical. For the Student and the Practitioner. The Section on Embryology by Prof. Milnes 
Marshall. In one 8vo. volume of 872 pp., with 231 illustrations. Cloth, $5; leather, $6. 
The immediate purpose of the work is to furnish 
a handbook of obstetric medicine and surgery 
for the use of the student and practitioner. It is 
not an exaggeration to say of the book that it is 
the best treatise in the English language yet 
published, and this will not be a surprise to those 
who are acquainted with the work of the elder 
Barnes. Every practitioner who desires to have 
the best obstetrical opinions of the time in a 
readily accessible and condensed form, ought to 
own a copy of the book.—Journal of the American 
Medical Association, June 12,1886. 
The Authors have made a text-book which is in 
every way quite worthy to take a place beside the 
best treatises of the period.—New York Medical 
Journal, July 2, 1887. 
WINCKFL, F. 
A Complete Treatise on the Pathology and Treatment of Childbed, 
For Students and Practitioners. Translated, with the consent of the Author, from the 
second German edition, by J. E. Chadwick, M. D. Octavo 484 pages. Cloth, $4.00. 
ASHWELL’S PRACTICAL TREATISE ON THE 
DISEASES PECULIAR TO WOMEN. Third 
American from the third and revised London 
edition. In one 8vo. vol., pp. 520. Cloth, $3.50. 
PARRY ON EXTRA-UTERINE PREGNANCY: 
Its Clinical History, Diagnosis, Prognosis and 
Treatment. Octavo, 272 pages. Cloth, 82.50. 
TANNER ON PREGNANCY. Octavo, 490 pages, 
colored plates, 16 cuts. Cloth, 84.25. 
CHURCHILL ON THE PUERPERAL FEVER 
AND OTHER DISEASES PECULIAR TO WO- 
MEN. In one 8vo. vol. of 464 pages. Cloth, 82.50. 
MEIGS ON THE NATURE, SIGNS AND TREAT- 
MENT OF CHILDBED FEVER. In one 8vo. 
volume of 346 pages. Cloth, 82.00. 30 
Lea Brothers & Co.’s Publications—Midvvfy., Dis. Childn. 
SMITH, J. LEWIS, M. D., 
Clinical Professor of Diseases of Children in the Bellevue Hospital Medical College, N. Y, 
A Treatise on the Diseases of Infancy and Childhood. New (seventh) 
edition, thoroughly revised and rewritten. In one handsome octavo volume of 881 
pages, with 51 illustrations. Cloth, $4.50; leather, $5.50. Just ready. 
Notwithstanding the many excellent volumes 
that have been issued recently on diseases of 
children, the work of Dr. J. Lewis Smith easily 
holds a front plaie. Its several editions have all 
been thoroughly revised. In the present one we 
notice that many of the chapters have been en- 
tirely rewritten. Full notice is taken of all the 
recent advances that have been made. As its 
author states in the preface, the necessary revision 
has virtually produced anew work. Inthe amount 
of information presented the work may properly 
be considered to have doubled in size, but by 
condensation and the exclusion of all obsolete 
material the volume has not been rendered incon- 
veniently large. Many diseases not previously 
treated of have received special chapters. The 
work is a very practical one. Especial care has 
been taken that the directions for treatment shall 
be particular and full. In no other work are such 
I cartful instructions given in the details of infant 
hygiene and the artificial feeding of infants.— 
Montreal Medical Journal, Feb. 1891. 
Every department shows that it has been thor- 
oughly revised, and that every advantage has been 
taken of recent advance in knowledge to bring it 
completely up to the times What makes the work 
of Dr. Smith of especial value is the attention paid 
to diagnosis and the careful detail of treatment. 
It is undoubtedly one of the best treatises on 
children’s diseases, and as a text book for students 
and guide for young practitioners it is unsurpassed. 
—Buffalo Medical and Surgical Journal, Jan. 1891. 
All the important peitinent facts that modern 
research has brought to light are embodied in the 
present volume, thus bringing it up to date and 
giving it the dignity of ultimate authority upon 
the subjects of which it treats.—New York Medical 
Journal, Dec. 6, 1890. 
LEISHMAN, WILLIAM, M. D., 
Regius Professor of Midwifery in the University of Glasgow, etc. 
A System of Midwifery, Including the Diseases of Pregnancy and the 
Puerperal State. Fourth edition. Octavo. 
LANDIS, HENRY G., A. M., M. D., 
Professor of Obstetrics and the Diseases of Women in Starling Medical College, Columbus, O. 
The Management of Labor, and of the Lying-in Period. In one 
handsome 12mo. volume of 334 pages, with 28 illustrations. Cloth, $1.75. 
The author has designed t® place in the hands 
of the young practitioner a book in which he can 
find necessary information in an instant. As far 
as we can see, nothing is omitted. The advice is 
sound, and the procedures are safe and practical. 
Centralblatt fur Gynakologie, December 4, 1886. 
This is a book we can heartily recommend, 
the author goes much more practically into the 
details of the management of labor than most 
text-books, and is so readable throughout as to 
tempt any one who should happen to commence 
the book to read it through. The author pre- 
supposes a theoretical knowledge of obstetrics, 
and has consistently excluded from this little 
work everything that is not of practical use in the 
lying-in room. We think that if it is as widely 
read as it deserves, it will do much to improve 
obstetric practice in general.—New Orleans Medi- 
cal and Surgical Journal, Mar. 1886. 
• 
OWEN, EDMUND, M. B., E. R. C. S., 
Surgeon to the Children's Hospital, Great Ormond St., London. 
Surgical Diseases of Children. In one 12mo. volume of 525 pages, with 4 
chromo-lithograpliic plates and 85 woodcuts. Cloth, $2. See Series of Clinical Manuals, 
page 31. 
One is immediately struck on reading this book 
with its agreeable style and the evidence it every- 
where presents of the practical familiarity of its 
author with his subject. The book may be 
honestly recommended to both students and 
practitioners. It is full of sound information, 
pleasantly given.—Annals of Surgery, May, 1886. 
STUDENTS’ SERIES OF MANUA LS. 
A Series of Fifteen Manuals, for the use of Students and Practitioners of Medicine and Surgery, 
written by eminent Teachers or Examiners, and issued in pocket-size 12mo volumes of 300-540 pages, 
richly illustrated and at a low price. The following volumes are now ready: Treves’ Manual of Sur- 
gery, by various writers, in three volumes, each, $2; Bell’s Comparative Physiology and Anatomy, $2; 
Gould’s Surgical Diagnosis. 92; Robestson’s Physiological Physics, $2; Bruce’s Materia Medicaand Thera- 
peutics (4th edition), $1.50; Power’s Human Physiology (2d edition), $1.50; Clarke and Lockwood’s 
Dissectors' Manual, $1.50; Ralfe’s Clinical Chcm’stry, $!.50; Treves’ Surgical Applied Anatomy, $2; 
Pepper’s Surgical Pathology, $2; and Klein’s Elements of Histology (4th edition), $1.75. The following 
is in press : Pepper’s Forensic Medicine. For separate notices see index on last page. 
SERIES OF CLINICAL MANUALS. 
In arranging for this Series it has been the design of the publishers to provide the profession with 
a collection of authoritative monographs on important clinical subjects in a cheap and portable form. 
The volumes will contain about 550 pages and will be freely illustrated by chromo-lithographs and wood- 
cuts. The following volumes are now ready : Yeo on Food in Health and Disease, $2; Broadbent on 
the Pulse, $1.75; Carter <fc Frost’s Ophthalmic Surgery, $2.25; Hutchinson on Syphilis, $2.25; Ball on 
the Rectum and Anus, $2.25; Marsh on the Joints, $2; Owen on Surgical Diseases of Children, $2; 
Morris on Surgical Diseases of the Kidney, $2.25; Pick on Fractures and Dislocations, $2; Bctlin on 
the Tongue, $1.60; Treves on Intestinal Obstruction, $2; and Savage on Insanity and Allied Neuroses, $2. 
The following is in active preparation: Lucas on Diseases of the Urethra. For separate notices see 
index on last page. 
CONDIE’S PRACTICAL TREATISE ON THE I 
DISEASES OF CHILDREN. Sixth edition, re- | 
vised and augmented. In one octavo volume of I 
779 pages. Cloth, $5.25; leather, $6.26. 
WEST ON SOME DISORDERS OF THE NERV- 
OUS SYSTEM IN CHILDHOOD. In one small 
12mo. volume of 127 pages. Cloth, $1.00. Lea Brothers & Co.’s Publications—Med. Juris., 31iscel. 
31 
TIDY, CHARLES MEYMOTT, M. B., F. C. S., 
Professor of Chemistry and of Forensic Medicine and Public Health at the London Hospital, etc. 
Legal Medicine. Volume II. Legitimacy and Paternity, Pregnancy, Abor- 
tion, Rape, Indecent Exposure, Sodomy, Bestiality, Live Birth, Infanticide, Asphyxia, 
Drowning, Hanging, Strangulation, Suffocation. Making a very handsome imperial oc- 
tavo volume of 529 pages. Cloth, $6.00; leather, $7.00. 
Volume I. Containing 664 imperial octavo pages, with two beautiful colored 
plates. Cloth, $6.00; leather, $7.00. 
The satisfaction expressed with the first portion 
of this work is in no wise lessened by a perusal of 
the second volume. We find it characterized by 
the same fulness of detail and clearness of ex- 
pression which we had occasion so highly to com- 
mend in our former notice, and which render it so 
valuable to the medical jurist. The copious 
tables of cases appended to each division of the 
subject must have cost the author a prodigious 
amount of labor and research, but they constitute 
one of the most valuable features of the book, 
especially for reference in medico-legal trials.— 
American Journal of the Medical Sciences, April, 1884. 
TAYLOR, ALFRED S., M. D., 
Lecturer on Medical Jurisprudence and Chemistry in Ouy's Hospital, London. . 
Poisons in Relation to Medical Jurisprudence and Medicine. Third 
American, from the third and revised English edition. In one large octavo volume of 788 
pages. Cloth, $5.50; leather, $6.50. 
By the Same Author. 
A Manual of Medical Jurisprudence. Eighth American from the tenth Lon- 
don edition, thoroughly revised and rewritten. Edited by John J. Reese, M. D. In one 
large octavo volume. 
PEPPER, AUGUSTUS J., M. S., M. B., F. R. C. S., 
Examiner in Forensic Medicine at the University of London. 
Forensic Medicine. In one pocket-size 12mo. volume. Preparing. See Students’ 
Series of Manuals, below. 
LJEA, HE NR Y C., LL. D. 
Chapters from the Religious History of Spain.—Censorship of the 
Press.—Mystics and Illuminati.—The Endemoniadas.—El Santo Nino 
de la Guardia.—Brianda de Bardaxi. In one 12mo. volume of 522 pages. 
Cloth, $2.50. Just ready. 
The width, depth and thoroughnesst>f research 
which have earned Dr. Lea a high European place 
as the ablest historian the Inquisition has yet 
found are here applied to some side-issues of that 
great subject. We have only to say of this volume 
that it worthily complements the author’s earlier 
studies in ecclesiastical history. His extensive 
and minute learning, much of it from inedited 
manuscripts in Mexico, appears on every page.— 
London Antiquary, Jan. 1891. 
After attentively reading the work one does not 
know whether the author is a Catholic, a Protestant 
or a free-thinker. This moderation deprives the 
indictment of none of its force. The facts and 
the documents, of which the number and novelty 
attest a patient erudition, are grouped in luminous 
order and produce on the reader an effect all the 
more powerful in that it seems the less designed. 
When we add that the style is in every way excel- 
lent, that it is clear, sober and precise, we do full 
justice to a work which reflects the highest honor 
on the talents of the writer and on the method of 
the modern school of history.—Revue Critique 
d'Histoire et de Litterature, Paris, Jan. 1891. 
By the same Author. 
Superstition and Force: Essays on The Wager of Law, The Wager of 
Battle, The Ordeal and Torture. Third revised and enlarged edition. In one 
handsome royal 12mo. volume of 552 pages. Cloth, $2.50. 
Mr. Lea’s curious historical monographs, of 
which one of the most important is here produced 
in an enlarged form, have given him a unique 
position among English and American scholars. 
He is distinguished for his recondite and affluent 
learning, his power of exhaustive historical analy- 
sis, the breadth and accuracy of his researches 
among the rarer sources of knowledge, the gravity 
and temperance of his statements, combined with 
singular earnestness of conviction, and his warm 
attachment to the cause of freedom and intellect- 
ual progress.—N. Y. Tribune, August 9, 1878. 
By the Same Author. 
Studies in Church History. The Rise of the Temporal Power—Ben- 
efit of Clergy—Excommunication—The Early Church and Slavery. Sec- 
ond and revised edition. In one royal octavo volume of 605 pages. Cloth, $2.50. 
The author is preeminently a scholar; he takes 
up every topic allied with the leading theme and 
traces it out to the minutest detail with a wealth 
of knowledge and impartiality of treatment that 
compel adm’ration. The amount of information 
compressed into the book is extraordinary, and 
the profuse citation of authorities and references 
makes the work particularly valuable to the student 
who desires an exhaustive review from original 
sources. In no other single volume is the develop- 
ment of the primitive church traced with so much 
clearness and with so definite a perception of 
complex or conflicting forces.—Boston Traveller. 
Mr. Lea is facile prinr.eps among American 
scholars in the history of the Middle Ages, and, 
indeed, we know of no European writer who has 
shown such research, accuracy and grasp in 
investigating important and out-of-the-way topics 
connected with the history of Europe' in the Mid- 
dle Ages.—N. Y. Times. 
It is some years since we read the first edition 
of this work by Mr. Lea, and the impression made 
by it on us at the time is confirmed by reperusal 
of it in this enlarged and improved form; namely, 
that it is a book of great research and accuracy, 
full of varied information on very interesting 
phases of church life and history. It discusses 
each subject with a rare fulness of dates and in- 
stances, and a curious conscientiousness of veri- 
fication and citation of authorities.—Edinburgh 
Scotsman. Allen’s Anatomy ..... 6 
American Journal of the Medical Sciences . 3 
American Systems of Gynecology and Obstetrics 27 
American System of Practical Medicine. . 15 
American System of Dentistry 24 
Ashhurst’s Surgery . . . . .20 
Ashwell on Diseases of Women . . .29 
Attfield’s Chemistry . .... 9 
Ball on the Rectum and Anus . . . 20, 30 
Barlow’s Practice of Medicine ... 17 
Barnes’ System of Obstetric Medicine . . 29 
Bartholow on Electricity .... 17 
Basham on Renal Diseases .... 24 
Bell’s Comparative Physiology and Anatomy . 7, 30 
Bellamy’s Surgical Anatomy ... 6 
Berry on the Eye ..... 23 
Billings’ National Medical Dictionary . . 4 
Blandford on Insanity . . . .19 
Bloxam’s Chemistry ..... 9 
Bristowe’s Practice of Medicine . . .14 
Broadbent on the Pulse . . . . 16,30 
Browne on Koch’s Remedy . ... 18 
Browne on the Throat, Nose and Ear . . 18 
Bruce’s Materia Medica and Therapeutics . 12,30 
Brunton’s Materia Medica and Therapeutics . 11 
Bryant’s Practice of Surgery . . . .21 
Bumstead and Taylor on Venereal. See Taylor. 25 
Burnett on the Ear ..... 23 
Butlin on the Tongue . . . . .21,30 
Carpenter on the Use and Abuse of Alcohol . 8 
Carpenter’s Human Physiology . . . S 
Carter & Frost’s Ophthalmic Surgery . .23,30 
Chambers on Diet and Regimen ... 17 
Chapman’s Human Physiology ... 8 
Charles’ Physiological and Pathological Chem. 10 
Churchill on Puerperal Fever . . .29 
Clarke and Lockwood’s Dissectors’Manual . 6,30 
Classen’s Quantitative Analysis ... 10 
Cleland’s Dissector ..... 6 
Clouston on Insanity . ... 19 
Clowes’ Practical Chemistry . . . io 
Coats’ Pathology . . , . .13 
Cohen on the Throat . . . . .18 
Coleman’s Dental Surgery . . . .24 
Condie on Diseases of Children . . .30 
Cornil on Syphilis ..... 25 
Dalton on the Circulation .... 7 
Dalton’s HumanPhysiology ... 8 
Davenport on Diseases of Women . . . 28 
Davis’ Clinical Lectures ... 17 
Draper’s Medical Physics .' . . . 7 
Druitt’s Modern Surgery .... 20 
Duncan on Diseases of Women . . .28 
Dunglison’s Medical Dictionary ... 5 
Edes’ Materia Medica and Therapeutics . 12 
Edis on Diseases of Women .... 27 
Ellis’ Demonstrations of Anatomy . . 7 
Emmet’s Gynaecology . . . 28 
Erichsen’s System of Surgery . . .21 
Farquharson’s Therapeutics and Mat. Med. . 12 
Finlayson’s Clinical Diagnosis . . .16 
Flint on Auscultation and Percussion . . 18 
Flint on Phthisis ..... 18 
Flint on Respiratory Organs ... 18 
Flint on the Heart ..... 18 
Flint’s Essays . .... 18 
Flint’s Practice of Medicine . . .14 
Folsom’s Laws of U. S. on Custody of Insane . 19 
Foster’s Physiology ..... 8 
Fothergill’s Handbook of Treatment . . 16 
Fownes’ Elementary Chemistry ... 9 
Fox on Diseases of the Skin . ... 26 
Frankland and Japp’s Inorganic Chemistry . 9 
Fuller on the Lungs and Air Passages . . 17 
Gant’s Student’s Surgery . . . .20 
Gibbes’ Practical Pathology . . .13 
Gibney’s Orthopaedic Surgery . . .20 
Gould’s Surgical Diagnosis . . . .21,30 
Gray’s Anatomy . . . . . .5 
Gray on Nervous Diseases . . . .19 
Greene’s Medical Chemistry .... 9 
Green’s Pathology and Morbid Anatomy . 13 
Griffith’s Universal Formulary ... 12 
Gross on Foreign Bodies in Air-Passages . IS 
Gross on Impotence and Sterility ... 25 
Gross on Urinary Organs . . . 25 
Gross System of Surgery . . . 20 
Habershon on the Abdomen . . . 16 
Hamilton on Fractures and Dislocations . 22 
Hamilton on Nervous Diseases ... 19 
Hare’s Practical Therapeutics ... 11 
Hartshorne’s Anatomy and Physiology . . 6 
Hartshorne’s Conspectus of the Med. Sciences . 3 
Hartshorne’s Essentials of Medicine . . 14 
Hermann’s Experimental Pharmacology . 11 
Hill on Syphilis ...... 25 
Hillier’s Handbook of Skin Diseases . . 26 
Hirst & Piersol on Human Monstrosities . 6 
Hoblyn’s Medical Dictionary ... 3 
Hodge on Women .... 28 
Hoffmann and Power’s Chemical Analysis . 10 
Holden’s Landmarks ..... 5 
Holland’s Medical Notes and Reflections . 17 
Holmes’ Principles and Practice of Surgery . 22 
Holmes’ System of Surgery . . .21 
Horner’s Anatomy and Histology . . 6 
Hudson on Fever . ... 16 
Hutchinson on Syphilis . . . . 25,30 
Hyde on the Diseases of the Skin . . .26 
Jones (C. Handfield) on Nervous Disorders . 19 
Juler’s Ophthalmic Science and Practice . 23 
King’s Manual of Obstetrics .... 29 
Klein’s Histology . . . . . 13,30 
Landis on Labor ..... 30 
La Roche on Pneumonia, Malaria, etc. . . 17 
La Roche on Yellow Fever .... 16 
Laurence and Moon’s Ophthalmic Surgery . 23 
Lawson on the Eye, Orbit and Eyelid . . 23 
Lea’s Chapters from Religious History ot Spain 31 
Lea’s Studies in Church History . . .31 
Lea’s Superstition and Force . . 31 
Lee on Syphilis . ..... 25 
Lehmann's Chemical Physiology ... 8 
Leishman’s Midwifery .... 30 
Lucas on Diseases of the Urethra . . .24,30 
Ludlow’s Manual of Examinations . . 3 
Lyons on Fev er ...... 16 
Maisch’s Organic Materia Medica ... 11 
Marsh on the Joints . . ,21,30 
May on Diseases of Women . . . .28 
Medical News ...... 1 
Medical News Visiting List .... 3 
Medical News Physicians’ Ledger ... 8 
Meigs on Childbed Fever . . . •. 29 
Miller’s Practice of Surgery .... 21 
Miller’s Principles of Surgery . . .21 
Morris on Diseases of the Kidney . . .24,30 
National Dispensatory .... 12 
National Medical Dictionary . . 4 
Neill and Smith’s Compendium of Med. Sci. . 3 
Nettleship on Diseases of the Eye . . .23 
Norris and Oliver on the Eye . . .23 
Owen on Diseases of Children . . .30 
Parrish’s Practical Pharmacy . . .11 
Parry on Extra-Uterine Pregnancy . . 29 
Parvin’s Midwifery . .... 29 
Pavy on Digestion and its Disorders . . 17 
Payne’s General Pathology .... 13 
Pepper’s System of Medicine ... 15 
Pepper’s Forensic Medicine . . . . 30,31 
Pepper's Surgical Pathology . . .13,30 
Pick on Fractures and Dislocations . . 22,30 
Pirrie’s System of Surgery . ... 21 
Playfair on Nerve Prostration and Hysteria . 19 
Playfair’s Midwifery ..... 29 
Power’s Human Physiology . . . . 8.30 
Purdy on Bright’s Disease and Allied Affections 24 
Ralfe’s Clinical Chemistry . . . 10,30 
Ramsbotham on Parturition . . .28 
Remsen’s Theoretical Chemistry . . .10 
Reynolds’ System of Medicine ... 14 
Richardson’s Preventive Medicine . . 17 
Roberts on Diet and Digestion . . .24 
Roberts on Urinary Diseases . . .24 
Roberts’ Compend of Anatomy ... 7 
Roberts’ Surgery . .... 20 
Robertson’s Physiological Physics . . 7,30 
Ross on Nervous Diseases .... 19 
Savage on Insanity, including Hysteria . . 19,30 
Schafer’s Essentials of Histology, . . 13 
Schreiber on Massage . ... 17 
Seiler on the Throat. Nose and Naso-Pharynx 18 
Senn’s Surgical Bacteriology . . 13 
Series ot Clinical Manuals .... 4 
Simon’s Manual of Chemistry ... 8 
Slade on Diphtheria . .... 17 
Smith (Edward) on Consumption ... 17 
Smith (J. Lewis) on Children . . .30 
Smith’s Operative Surgery .... 22 
Stille on Cholera . . . . .14 
StillS & Maisch’s National Dispensatory . 12 
StillS’s Therapeutics and Materia Medica . 11 
Stimson on Fractures and Dislocations . 22 
Stimson’s Operative Surgery . . .22 
Students’ Senes of Manuals .... 4 
Sturges’ Clinical Medicine .... 17 
Tait's Diseases of Women and Abdom. Surgery 28 
Tanner on Signs and Diseases of Pregnancy . 29 
Tanner's Manual of Clinical Medicine . . 16 
Taylor’s Atlas of Venereal and Skin Diseases 26 
Taylor on Venereal Diseases . . . 25 
Taylor on Poisons . .... 31 
Taylor’s Medical Jurisprudence ... 31 
Thomas on Diseases ot Women . . .27 
Thompson on Stricture . ... 24 
Thompson on Urinary Organs . . .24 
Tidy’s Legal Medicine. .... 31 
Todd on Acute Diseases . ... 17 
Treves’Manual of Surgery . . . .21,30 
Treves’Surgical Applied Anatomy . .6,30 
Treves on Intestinal Obstruction . . . 21,30 
Tuke on the Influence of Mind on the Body . 19 
Vaughan & Novy’s Ptomaines and Leucomaines 16 
Visiting List, The Medical News ... 3 
Walshe on the Heart . . . . .17 
Watson’s Practice of Physic . . . .14 
Wells on the Eye . . . . .23 
Weston Diseases of Women . . .28 
West on Nervous Disorders in Childhood . 30 
Wharton’s Minor Surgery and Bandaging . 21 
Williams on Consumption . . . .17 
Wilson's Handbook of Cutaneous Medicine . 26 
Wilson’s Human Anatomy .... 6 
Winckel on Pathol, and Treatment of Childbed 29 
WOhler’s Organic Chemistry ... 8 
Woodhead’s Practical Pathology . .13 
Year-Books of Treatment for 1886, ’87, ’89 and ’90 17 
Yeo on Food in Health and Disease . . 17,30 
LEA BROTHERS & CO., Philadelphia.