A text-book of general pathological anatomy and pathogenesis

Front matter

Em si

The original of this book is in the Cornell University Library.

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Preface To Part H

The very rapid sale of Professor Ziegler's text-book in Germany has led to an unforeseen delay in the completion of the Second Part. Two editions of the sections already published having been exhausted, the Professor has been obliged to give to the preparation of a third edition of these the time he hoped to spend in completing the remaining sections. My own purpose was that the second volume of this English version should conclude the book, but in view of the requests which reach me from every side I have thought it better to bring out the first eight sections as an instalment than to put off the publication of the whole for another year. The third and concluding volume is already in hand, and will be of about the same size as the present. It will contain the sections on the Kidney, the Lungs, and the Nervous System, together with general indexes to the whole work.

In the third German edition the arrangement of the articles has been recast, and other changes of form have been made but in order to preserve the continuity of the English version I shall follow throughout the plan of the first volume. This plan has been generally approved, and it appears to be the most convenient for English students.

My renewed acknowledgments are due, and are very heartily rendered, to Professor Klein and Professor Greenfield, who have read and commented on each sheet as it passed through the press. Dr. George Thin has in like manner done me the kindness of reading the chapters on the Skin. Professor Ziegler has given me his ready help on many

PEBFACE.

points, and has enabled me to utilize his additions to the text of the later sections. Dr. Sims Woodhead courteously placed at my disposal the drawing of Acbmomyces from which Fig. 174 B was engraved.

In view of the generous aid I have thus received I am encouraged to hope that little in recent Pathology has been overlooked which is likely to be of value to English students.

DONALD MACALISTEB

Section I. Blood And Lymph

PASS

CHAP. I. Functions of blood and lymph (Art. 251) . 5

II. Intravascular coagulation or Thrombosis (Arts. 252-258) 7

III. Changes in the quantity and composition op the blood

IV. Changes in the blood-corpuscles (Arts. 260-262) . . 21

V. Solid impurities in the blood (Arts. 263-268) . . 27

VI. Changes in the lymph (Art. 269) . . . .33

Section II. The Vascular Mechanism

VII. Malformations and malpositions of the Heart (Arts.

270-272) 37

VIII. Atrophy and Degeneration of the Heart (Arts. 273-

277) 42

IX. Hypertrophy and Dilatation of the Heart (Arts. 278-

279) 48

X. Endocarditis and Myocarditis (Arts. 280-284) . . 51

XI. Infective granulomata, Tumors, and Parasites of the

XII. Hypoplasia and Degeneration of the Vessels (Art. 286-

288) 58

XIII. Hypertrophy and Hyperplasia of the Vessels (Art. 289) 62

XIV. Inflammations of the Vessels (Arts. 290-296) . . 63

XV. Sclerosis and Atheroma (Arts. 297-300) . . .70

XVI. Changes in the calibre of the Vessels (Arts. 301-307) 74

XVII. EUPTURE OF THE COATS OF THE VESSELS (Arts. 308-312) . 80

XVIII. The Lymphatics (Arts. 313-316) . . . .83

VI CONTENTS. >

Section III. The Spleen And The Lymphatic Glands

XIX. Structure and functions of the spleen (Arts 317-318) . 89

XX. Disorders of circulation and inflammations of the

XXI. Degenerations and injuries of the Spleen (Arts. 325-

326) . . . . . . .97

XXII. Infective gkanulomata of the Spleen (Art. 327) . 99 XXXIII. Hyperplasias and Tumors of the Spleen (Arts.

XXIV. Atrophy and Degeneration of the Lymphatic glands

[XXV. and XXVI. omitted by misnumbering.]

XXVII. Foreign substances in the Lymphatic glands (Arts.

334-335) . . . . . . .107

XXVIII. Inflammations of Lymphatic glands (Arts. 336-342) 109

XXIX. Tumors of Lymphatic glands (Arts. 343-347) . . 116-

Section IV. The Serous Membranes

XXX. Development of the serous cavities (Art. 348) . 123 :

XXXI. Effects due to disorders of the Circulation (Arts.

349-350) 125

XXXII. Inflammations of serous membranes (Arts. 351-354) 128

XXXIII. Tuberculosis of serous membranes (Arts. 355-357) 134

XXXIV. Tumors and Parasites of serous membranes (Art.

358) 137

Section V. The Skin

XXXV. Introductory (Art. 359) ..... 141

XXXVI. Disorders of circulation (Arts. 360-361) . , 143

XXXVII. Discoloration and Atrophy of the skin (Arts. 362-

365 ) • • . • . .146

CONTENTS. Vil

XXXVIII. Inflammations of the skin.

a. Transitory eruptions with slight exudation: erythema, papulae, b. Eruptions with considerable exudation: tubercula, squamce, vesi-

c. Eruptions ending in necrosis, suppuration, ulceration, or granula-

XXXIX. Inflammatory hypertrophies of the skin (Arts. 393-

396) . . . . . .182

XL. Non-inflammatory hypertrophies and Tumors (Arts.

397-502) . . , . . . . 186

XLI. Affections of the Sebaceous Glands, Hair, and Nails

XLII. Parasitic affections (Arts. 409-413) . . . 201

Section VI. The Mucous Membranes

XLIII. Structure and Functions (Art. 414) . . . 209

XLIV. Hyperemia and Hemorrhage (Arts. 415-416) . . 211

XLV. Degeneration, Atrophy, and Hypertrophy (Arts. 417-

418) 213

XL VI. Inflammatory affections (Arts. 419-427) . . 215

XLVII. Infective granulomata and Tumors (Arts. 428-431) 225

Section VII. The Alimentary Tract

XLVIII. General considerations (Art. 432) . . . 233

XLIX. The Mouth.

Inflammatory affections: stomatitis (Arts. 433-435) . . . 234

Parasitic affections (Art. 436) ...... 238

Hypertrophy and Atrophy (Art. 437) ..... 240

Changes affecting the teeth (Arts. 440-441) . . . . .244

LI. The Salivary glands (Arts. 447-448) . . .251

LII. The Oesophagus (Arts. 449-451) . . . .253

LIII. The Stomach (Arts. 452-462) . . . .258

LIV. The Intestine (Arts. 463-479) .... 273

VU1 CONTENTS.

Section VIII. The Liver And Panceeas

LV. Pigmentary infiltration of the Liver (Arts. 480-481) . 299 LVI. Malformations and malpositions of the Liter (Art.

482) 304

LVII. Disorders of the Hepatic circulation (Arts. 483-484) 306 LVTII. Atrophy and Degeneration of the Liver (Arts. 485-

491) 309

LIX. Hypertrophy and Eegeneration of Liver-tissde (Art.

492) .317

LX. Inflammations of the Liver.

Purulent hepatis and Hepatic abscess (Arts. 493-495) . . . 319

Chronic indurative hepatitis and Cirrhosis (Arts. 496-498) . . 322

Syphilitic hepatitis (Arts. 499-500) . . . . . .329

Tuberculosis of the liver (Art. 501) . ..... 332

LXI. Tumors and Parasites of the Liver.

Secondary tumors (Arts. 505-506) ...... 338

Animal parasites (Art. 507) ....... 340

LXII. The Gall-bladder and biliary ducts (Arts. 508-512) . 341 LXIII. The Pancreas (Arts. 513-515) . . . .345

Index of authors cited ...... 349

INDEX OF FIGURES.

ITO. PAGE.

118. Thrombus in process of organization 12

119. Diagrammatic section of a ligatured vessel 13

120. Section through a degenerating patch from the brain .... 33

121. Brown atrophy of the muscles of the heart 42

122. Fatty degeneration of the muscles of the heart 43

123. Fatty endocardium 43

124. Myomalacia cordis 46

125. Endocarditic vegetation 52

126. Sclerosis resulting from myocarditis 55

127. Fatty degeneration of the aorta and of a cerebral capillary ... 59

128. Calcification of the aorta 61

129. Acute aortitis 64

130. Syphilitic arteritis 68

131. Atheromatous cerebral artery 71

132. Dilated capillaries from the brain 77

133. Amyloid swelling of the adenoid reticulum 104

134. Chalky concretions 106

135. Lymphatic gland containing pigment-granule cells .... 107

136. Slate-colored bronchial gland , . . 108

137. Large-celled hyperplasia of a lymphatic gland 112

138. Fibrous hyperplasia of a lymphatic gland 113

139. Tuberculosis of a lymphatic gland 114

140. Inflamed omentum 138

141. Adhesive pericarditis 131

142. Tuberculosis of the omentum 135

143. Senile atrophy of the skin 148

144. Syphilitic mucous patch ......... 153

145. Blister due to a burn 155

146. Skin in erysipelas bullosum 156

147. Vesicle of herpes zoster 157

148. "Vesicle of small-pox 158

149. Blister from a burn in process of healing ...... 160

150. Skin in erysipelas bullosum 161

151. Syphilitic mucous patch 165

152. Infantile syphilitic pemphigus 171

153. Vesicle of small-pox becoming pustular ...... 173

154. Lupus vulgaris 180

155. Venereal wart 183

156. Ichthyosis hystrix 187

157. Papillae from a cutaneous wart 188

158. Section through a soft wart 189

159. Fibroma (neurofibroma) molluscum 190

X INDEX OF FIG0EE8.

BACH.

160. Pustule of acne j-J*

161. Fungi from a favus patch 202

162. Cup or scutulum of favus 202

163. Hair affected with favus 203

164. Skin in scabies 205

165. Atrophy of the intestine 214

166. Catarrhal secretions . • • 216

167. Colon in dysentery 218

168. Glandular atrophy and fibrous hyperplasia of the stomach . . 219

169. Croupous membrane from the trachea 220

170. Uvula in diphtheritis faucium 221

171. Uvula in diphtheritis faucium 222

172. Tuberculosis of the bronchial mucous membrane . 225

173. Tuberculosis of the large intestine 226

174. A Destructive adenoma of the stomach 228

174. B Actinomyces from the tongue of a cow 239

175. Fibroid fold (etat mamelonne) of the stomach ..... 264

176. Gastric polypus 264

177. Colon in dysentery 285

178. Peyer's patch in typhoid 287

179. Tuberculosis of the large intestine 290

180. Pigmentary infiltration of the liver 300

181. Infiltrated liver-cells in pernicious anaamia 302

182. Simple atrophy of the liver 310

183. Atrophied liver-cells ........*• 311

184. Fatty liver-cells 311

185. Amyloid lobular capillaries 315

186. Micrococcus septicus in hepatic capillaries 320

187. Hepatic abscess: first stage 321

188. Recent interstitial hepatitis 323

189. Extravascular development of fibrous tissue 323

190. Intravascular development of fibrous tissue 323

191. Granular atrophic cirrhosis of the liver 324

192. Atrophic cirrhosis of the liver 327

193. Gumma of the liver 329

194. Syphilitic scar and gumma of the liver ...... 330

195. Diffuse fibroid induration of the liver from congenital syphilis . . 331

196. Miliary tuberculosis of the liver 333

197. Carcinoma of the bile-ducts ; . 336

198. Cavernous angioma of the liver .... .... 837

199. Cancerous embolus of a liver-capillary 839

200. Metastatic growth of cancer in the liver 339

SPECIAL PATHOLOGICAL ANATOMY.

Chapter I. Functions Of Blood And Lymph

251. Blood and lymph are the essential juices of the body. They stand in the closest relation to the vital processes which go on in the tissues. By means of the blood, the constituent elements of the body are supplied with the nutrient substances and the oxygen which they require. By the blood and the lymph are conveyed away the waste and surplus matters which have ceased to be useful to the tissues.

The nutrient substances and the oxygen are derived from without. The former usually enter the body from the alimentary canal, the latter usually through the lungs. But most parts of the body are under certain conditions capable of directly assimilating both nutriment and oxygen. The channels of entrance are in such cases the smaller blood-vessels and lymphatics.

The matters which have to be removed from the tissues are partly surplus nutriment, partly the products of tissue-waste and metabolism. These matters are carried off either to be utilized elsewhere within the system, or to be ejected altogether.

Under normal conditions, the incomings and outgoings balance each other in amount.

The channels by which the normal constituents gain access to the blood and lymph may also serve to admit matters which are noxious or at least abnormal. These matters may be either wholly extraneous, or produced within the body itself in virtue of some morbid or abnormal metabolism. The result of their admission is a more or less enduring pollution of the blood and lymph. In many cases, the blood is able to eliminate them harmlessly and speedily, chiefly by means of the kidneys and the liver; but in other cases, the pollution is more permanent. The composition of the blood often suffers in consequence, and its renovation may not be effected until some of the tissues or organs have been more or less injured by malnutrition.

The abnormal matters which gain access to the blood may be in very various states of aggregation. Most commonly they are in the form of gases or liquids; but the blood is likewise not infrequently polluted by the admission of solid corpuscular matters. These latter have by far the greatest interest to the pathologist, for they are demonstrable by means of the microscrope.

BLOOD AND LYMPH.

We cannot regard the blood as a liquid whose chemical composition is variable or indefinite. Experiment shows that the proportions of albuminoids, salts, iron, etc., which it contains are constant within narrow limits, and that its composition is maintained by nicely-adjusted assimilation and elimination of material. We must therefore look upon any serious variation from the normal in the composition of the blood as a pathological phenomenon.

The blood is in fact a definite living tissue.

Although the changes that occur in the composition of the blood are by no means so important as were formerly believed, though we no longer consider the juices and " humors " to be \he seat of all diseases, yet we should be in error if we regarded the blood as nothing more than a solution of various chemical substances. The blood always contains living cells, and these fulfil definite vital functions. And even if the red corpuscles are so transformed from the ordinary cell-type that some deny their right to the title of living cells, the life and activity of the white blood-cells is unmistakable, and they are an essential constituent of the blood.

In disease, too, the blood comports itself as a living tissue. We may have localized death or necrosis in a solid tissue, and we may likewise have a localized death of the blood. The retrogressive and formative changes in cells and intercellular substance, which we have recognized as the manifestation of diseased function in the solid tissues, have their analogues in the elements of the blood. Many of the morbid processes afEecting the blood are thus manifested not merely by changes in its chemical composition, but by simultaneous changes in the form and quantity of its morphological elements; and in many diseases the morbid activity of the white blood-cells plays a highly important part.

CHAPTEE II.

INTRAVASCULAR COAGULATION OR THROMBOSIS.

252. We have already seen (Art. 35) that when blood dies it usually coagulates, that is to say — solid masses of fibrin are formed in the plasma, the masses consisting of granules or granular fibrils or homogeneous flakes. When coagulation occurs within the vessels during life the process is called thrombosis, and the coagulum is called a thrombus.

On Schmidt's hypothesis the coagulation of the blood depends on the union of two albuminoid bodies, fibrinogen and fibrinoplastin (or paraglobulin), in presence of a third factor or ferment (Art. 35). Taking the fibrinogen as furnished by the plasma, and the other factors as furnished by the colorless elements of the blood, coagulation is evidence of the death of the latter in whole or in part.

Coagulation may take place in blood which is at rest, or in blood which is in motion; and the appearance of the thrombus is different in the two cases. In blood at rest coagulation takes place throughout the entire mass simultaneously. The thrombus is thus dark-red or brown in color, and consists of granular and fibrous clots of fibrin containing multitudes of red corpuscles and a few white corpuscles. Red thrombi of this kind are most commonly formed in occluded or highly engorged vessels. When recent they are soft and full of serum. Afterwards they become firmer, tougher, and drier, the fibrin contracting and squeezing out the serum. They become at the same time paler and grayer; the decolorization proceeds in fact by the same steps as in extravasated blood (Art. 68).

When coagulation begins in blood which is still flowing, the entire mass does not coagulate at once; minute flakes separate out, consisting chiefly (according to Zahn) of white blood-cells with a varying number of red blood-cells. According to the number and arrangement of these latter the thrombus may be white or gray, or pale reddish, or mottled and stratified.

In the case of pure white thrombi, only the colorless elements of the blood separate out. When the necessary local conditions for coagulation are set up at any spot (on the intima of the heart or of a vessel) the clots adhere to the surface, and gradually increase in size by successive additions. At first the cellular elements of the mass are distinguishable; but in twenty-four hours the outlines of the cells disappear,

BLOOD AND LYMPH.

and the mass is transformed into homogeneous or finely-granular fibrin.

The thrombus grows by the addition of colorless elements like those in which it began. If red corpuscles are entangled with the others, it may gradually become more and more tinged with red. If the red corpuscles are precipitated per saltum or intermittently, the thrombus will exhibit strata of red and white. This alternate precipitation, which leads to the formation of mottled thrombi, is most likely to happen if the blood is alternately at rest and in motion at the site of the deposit.

The fundamental investigations on the subject of thrombosis are those of Vibchow (Qesamm. Abhandl. 1856, Sand d. spec. Path. I.), who made out by experiment the conditions of intravascular coagulation and its effects on the circulation. Zahn has shown (Virch. Arch. vol. 62, and Rev. mid. de la Suisse rom. 1881) that the formation of a thrombus in the blood-vessel of a frog may be directly observed under the microscope; one has only to injure the vessel mechanically or place on it a crystal of common salt; and coagulation at once begins. In this way the behavior of the white corpuscles has chiefly been made out. Quite recently Bizzozero (Centralb. f. d. med. Wiss. 1882, Arch. ital. de biologiei., and Virch. Arch. vol. 90) has observed in living blood certain small colorless disc-like bodies, about half the size of the ordinary white corpuscles.. These he calls " Blutpldttchen" or blood-plates, and regards as identical with Hayem's haematoblasts (Art. 35). In blood taken from the vessels in the usual way they break up into the knots of granules described by Max Schultze and others. According to Bizzozero coagulation takes place when the blood-plates begin to break up in a liquid containing fibrinogen; and he maintains that they form the essential constituent of white and mottled thrombi. Ratjschenbach, a pupil of Schmidt's, has criticised these statements in a recent inaugural dissertation (Dorpat 1882). See also Wooldridge, Du Bois-Beymond's Arch. 1883.

1 253. Thrombosis depends upon two factors; one is the morbid alteration of the vessel-wall, the other the retardation or stoppage of the blood-current. In most cases the two factors are in action simultaneously.

[ In normal conditions coagulation is prevented by the ever-renewed contact of the blood with the living endothelium of the vessel-wall (Beuckb). If the endothelium die in consequence of disease of the inner coat of the vessel, or if the blood is in part prevented from fresh contact with the endothelium by stagnation or cessation of the current, the influences which inhibit coagulation are interfered with. In accordance with this view we find that thrombosis is commonest where there is degeneration or inflammation of the lining membrane of the vessels or the heart, or where the circulation is impeded by such causes as compression or occlusion or dilatation of the vessels, fatty change in the heart, etc. Direct injury of the vessel-wall, if it extend to the intima, likewise leads to thrombosis. If a vessel be perforated by a small opening, the wound is quickly closed by white corpuscles which deposit themselves around and over the opening, while a white thrombus gradually forms and projects into the lumen of the vessel.

LNTBAVASCirLAB COAGULATION OE THROMBOSIS. 365

The various forms of thrombus are distinguished according to their relation to the lumen of the vessel. Parietal thrombi are seated on the walls, valvular thrombi on the valves of the heart or of the veins. If the thrombus occludes the vessel it is called obliterating. The first deposit is spoken of as primary or autochthonous, the accretions superimposed on it as secondary or induced. By such accretions a parietal thrombus may grow into an obliterating one. In this way, too, it not seldom happens that a thrombus originally white or mottled is covered over with a red thrombus: the first deposit takes place in blood which is still moving, this by degrees occludes the vessel, the current is stayed, and the blood then coagulates as a whole. The reverse occurs when an obliterating red thrombus contracts, and leaves the channel partly free again. Both cases are illustrated in the niarasmic thrombosis of cachectic anaemic patients; in them the vascular system seems too capacious for the diminished quantity of blood in circulation, and in consequence the current is here and there abnormally slow or ceases altogether.

Thrombosis may occur in any part of the vascular system. Cardiac thrombosis usually begins in the auricles, or in the crevices between the trabeculse carneas. In both sites the thrombi start from the deeper folds and involutions of the endocardium, -but by continued apposition of fibrin they may grow into large polypoid masses projecting into the cavity, and are then spoken of as cardiac polypi. Coagula form in like manner upon the surfaces of inflamed valves. Both the parietal and the valvular forms of cardiac thrombi may grow to a very large size, and fill out the greater part of the auriculo-ventricular cavity.

Thrombosis of the larger arteries may occur in the most various situations. In marasmic patients with highly degenerate arteries parietal thrombi, both white and mottled, may be formed in the aorta and adhere firmly to the inner coat. In the veins thrombi are most commonly formed in the pockets of the valves; whence they grow out and become obliterating thrombi. Or a thrombus primarily formed in a small tributary vein may grow out into the lumen of a larger vein. For example, thrombosis originating in a small vein of the lower limb may ultimately extend continuously till it reaches the vena cava inferior or even the heart itself. Thrombosis of the smallest vessels is usually the result of some disorder of the tissues, chiefly of the nature of inflammation or necrosis.

Post-mortem clots. Thrombi which have been formed during life are in general easily distinguished from clots formed in articulo mortis or post-mortem. After death the blood usually coagulates in such a way that the red corpuscles are entangled and included in the clots; on post-mortem examination we find the vessels containing soft dark-red gory masses. Sometimes however the corpuscles have time to separate from the plasma before the fibrin is formed; in such cases the clots are soft, moist, somewhat elastic, yellowish, and faintly opalescent. From these somewhat bacon-like clots the true white or mottled thrombi are distinguished by their grayish and more opaque appearance, and by their more or less marked stratification. They are moreover firmer, drier, akd less elastic;

when torn across the surface is corrugated or step-like; and finally they adhere to the wall of the vessel and generally distend it (Humphrey), while the post-mortem clots are free. Under the microscope the thrombi are seen to contain a larger proportion of white blood-cells than the post-mortem clots.

It is less easy to distinguish red thrombi from red post mortem clots. The chief characters of the former are their greater firmness and dryness, and their adhesion to the vessel-wall. In less recent thrombi signs of decolorization appear, by which the dark-red of freshly coagulated blood passes into a lighter and brownish-red. Not uncommonly we may find true thrombi overlaid and concealed by post-mortem coagulations.

With regard to the effects of thrombosis upon the circulation see Arts. 23-25 and 30.

254. Issues of thrombosis. The fully-developed thrombus is a somewhat firm and dry mass adhering to the lining membrane of a vessel or of the heart, its color and structure varying as we have described. The comparatively small quantity of liquid it encloses is explained by the fact that the fibrin after its separation always shrinks, and so squeezes out the liquid from its meshes. This shrinking, when it occurs in an obliterating thrombus, may leave the channel of the vessel open once more. In many instances the contraction due to shrinking is very considerable. The fibrin is transformed into a dense mass, which may persist unchanged for a long time and ultimately becomes calcified. It is thus that the chalky concretions called phleboliths are formed in the veins. In the same way thrombi which are seated on roughened surfaces in the aorta or valves of the heart may become calcified; and may become sheltered from secondary deposits by the growth of an endothelial covering over them.

Contraction with calcification is what we may call a favorable issue of thrombosis. The very common issue of thrombosis in softening is much less favorable. Softening is distinguished as simple or red softening, and puriform or yellow softening. In simple or red softening the central parts of the thrombus are first of all changed into a grayish or reddish pulp, consisting of broken-down and shrunken red corpuscles, pigment granules, and colorless granular detritus. If the softening then extends to the surface layers, and if the blood-current is still flowing over the thrombus, the products of disintegration may be carried into the general circulation. This occurs both in the case of cardiac polypi and in venous thrombosis, especially when the tip of a thrombus projects from the orifice of a small vein into the channel of a larger in which the blood is still flowing. The result is the formation of emboli (Arts. 30 and 37, and 257).

The most unfavorable issue of all is the puriform or yellow softening of the thrombus. In this case the thrombus is transformed into a dirty or reddish yellow, foetid, pus-like cream or pulp. This contains a multitude of pus-corpuscles and a large proportion of a finely-granular matter, which consists in part of fatty and albuminous detritus and

INTRAVASCULAR COAGULATION OR THROMBOSIS. 367

in part of micrococci. The latter frequently form groups or colonies, and are probably to be regarded as the exciting cause of the softening process. Such puriform thrombi act destructively on the surrounding tissues and set up inflammation. The intima of the vessel becomes turbid or opaque ; and suppurative inflammation begins in the tnnica media and tunica adventitia, extending to the tissue inclosing the vessel. Soon the entire thickness of the vessel-wall is infiltrated, «td takes on a dirty-yellowish or grayish appearance. Ultimately the tissues undergo putrid disintegration (Art. 291). If the puriform matters are carried by the blood-current to distant spots, they there produce necrotic and putrefactive changes in the tissues, and set up suppurative inflammation.

The entire process, in which puriform softening of a venous thrombus is associated with suppurative inflammation of the vessel-wall, is described as purulent thrombophlebitis. It is due in the first instance to the causes which lead to thrombosis, and in the second, to the access of micrococci to the thrombus. In other cases, the inflammation of the vessel-wall is primary, and the thrombosis a secondary effect. The purulent form is most commonly met with in the neighborhood of septic wounds and ulcers. ,

255. The most favorable issue of thrombosis is in organization of the thrombus. By this'is meant the replacement of the fibrin and corpuscles by vascularized fibrous tissue.

The new fibrous tissue is mainly the product of an inflammatory process; it is developed from migrated white blood-cells. Regenerative multiplication of the endothelial cells plays but a subordinate part or none at all. The thrombus itself takes no active share in the process ; it is a lifeless mass, a foreign body, and as such sets up inflammation in its neighborhood. The inflammation runs the same course as other constructive or plastic inflammations. The histological changes follow • exactly on the lines of those described in the Arts. 108-111; and the behavior of the tissues towards the foreign body (the thrombus) is identical with that described in Arts. 112-116. The process by which a thrombus is organized resembles most closely the plastic inflammation of a serous membrane. A blood-vessel has indeed a certain anatomical analogy to the serous cavities, being mainly distinguished by its particular configuration and by the special structure of its walls.

In the first stages of the organizing process we observe that the vessel-wall is here and there infiltrated with small leucocytes, the infiltration appearing in the outer and middle coats (Fig. 118 e), as well as in the inner coat (/). Presently migratory cells begin to accumulate, partly within the lumen of the vessel (g), partly within the substance of the thrombus, and partly between the latter and the vessel-wall. The first cells which migrate are small and round, and their nuclei are strongly stained by coloring reagents. Presently larger cells appear, with clear

BLOOD AND LYMPH.

vesicular nuclei (h); these have been developed out of the migratory cells. They are of various forms, rounded, elongated, or ramified (h). These larger cells are the formative or fibroplastic cells. When they have multiplied sufficiently, so that they become contiguous, they are gradually transformed into fibrous tissue. New blood-vessels are simultaneously developed, and at length the new-formed tissue is vascularized throughout.

This is the general course of the process, but considerable variation may take place in details. Thus, if the thrombus result from ligature, in a young and healthy patient, the accumulation of leucocytes will be

Fig. 118.— Section of a thrombus in process of organization.

(Prom the femoral artery of an aged man three weeks after ligature : hcematoxyUn staining : X 350.)

a, tunica media.

b, fenestrated elastic membrane.

c, intima thickened by previous inflamma-

tion.

d, coagulated blood.

e, cells infiltrating the media. /, cells infiltrating the intima. g, leucocytes, partly within the thrombus,

partly between it and the Intima. h, various kinds of formative cells.

much more marked than in such a case as is represented in Fig. 118 : in this case the patient was old, and his arteries had already undergone a certain amount of morbid change. The accumulation of leucocytes may become so great as to give the thrombus the appearance of a mass of granulation tissue. The duration of the process also varies greatly. By operating on one of the lower animals, we can be sure of finding the thrombus completely vascularized in twelve days. In the case figured above, the first formative cells are developing three weeks after the ligature.