THE CHICAGO MEDICAL RECORDER PRIZE ESSAY FOR 1895. CHYLOUS AND ADIPOSE ASCITES ; A CLINICAL, HISTOR- TORICAL AND EXPERIMENTAL STUDY. BY ARTHUR R. EDWARDS, A. M,, M. D. PATHOLOGIST AND PHYSICIAN TO COOK COUNTY HOSPITAL ; INSTRUCTOR IN MEDICINE AND PHYSICAL DIAGNOSIS, NORTHWESTERN UNIVERSITY MEDICAL SCHOOL. Reprinted from The Chicago Medical Recorder, April, 1895. PRESS OF The MoCluer Printing Company, 300 DEARBORN ST., CHICAGO. CHYLOUS AND ADIPOSE ASCITES; A CLINICAL, HIS- TORICAL AND EXPERIMENTAL STUDY. By ARTHUR R. EDWARDS, A. M., M. D. PATHOLOGIST AND PHYSICIAN TO COOK COUNTY HOSPITAL; INSTRUCTOR IN MEDICINE AND PHYSICAL DIAGNOSIS, NORTHWESTERN UNIVERSITY MEDICAL SCHOOL. AWARDED THE MEDICAL RECORDER PRIZE OF $100 BY THE CHICAGO MEDICAL SOCIETY. Medical literature of the sixteenth and seventeenth centuries abounds in instances of traumatic lymphorrhagia and lymphorrhea especially after venesection1. Reviewing the records, we cannot avoid the conclusion that a large number of these cases were chronic pyogenic or tubercular infection. Nuck2 and Fractions3 have recorded, 1695, cases of milky saliva, and Rommel one in which a milk-like fluid exuded from the exterior surface of the abdomen. Milk-like discharges recorded in puerperal women are probably pyemic processes. Dilated lymph vessels, lymphatic varices, have been observed in serous membranes, the heart, lungs, small intestines, liver, spleen, conjunctiva and tunica vaginalis. The causes are filaria, adenitis, periorchitis hemorrhagica, Kocher, lymphatic obstruction and possibly also lymphangitis gonorrhoica. Lymphocele is increasing in frequency both abroad and in this country4. Chylo-pericardium is extremely rare. Hasebroeck18 reports a case in which albumin 7.0, cholesterin 0.3, lecithin 0.1, fat 1.0, alcoholic extractives 0.2, aqueous extractives 0.2, and salt 0-9 per cent were found. Chylo-thorax is more frequent about twenty cases being recorded. Some sixteen22*10 resulted from direct trauma 2 to the thoracic duct. Rupture of the thoracic duct is uncommon on account of its protected location, and it heals readily because of low pressure there, although it has been stated that recovery never follows rupture. Other causes of chylo-thorax are chylous effu- sions, Quinke, altered pus, Gudneau de Mussey, and chyliform fluids distinct from serous, purulent and serofibrinous effusions, Debove. The peritoneal cavity more frequently than any other serous sac, is the seat of those unusual exudates and transudates known as chylous, chyliform, lactiform, oily, or adipose ascites. The first authentic case is Poncy's, 1699, but during the last two centuries only ninety-seven cases, including the spurious, have been published. Rigid analysis reduces the number to ninety-two, while the definite total confirmed by autopsy or operation, falls to nearly sixty. The established facts warrant the following clinical and pathological minutiae: John Shoemaker; single, colored, twenty years old, American born. Under observation nineteen days in Cook County Hospital. Family history: Mother died of renal carcinoma, father alive. Per- sonal history: Printer, always lived in Chicago. Previous diseases: No venereal history admitted, two years ago had ascites, causing great dyspnea, his feet never swelled, measles, pharyngitis. Pres- ent affection: For a number of weeks has felt weak and sleepless. Physical examination: Patient fairly well nourished. Central and peripheral nervous system entirely negative; no cough, no sputum, no T. B.; skin moist; no eruption; no edema. Scalp, calvarium; eyes, ears and throat negative. Bones and joints are negative; spinal column negative. Lungs. Normal resonance; vesicular breathing; borders normal; few diffuse bilateral moist mucous rales; respiratory excur- sion of lungs over heart, liver and spleen entirely absent. Heart. Apex, normal; outlines normal; heart tones pure; no murmurs; no accentuated sounds. Liver. Fourth rib in vertical mammary line; sixth, anterior axillary line, seventh intercostal space, post axillary line, to costal arch; edge not palpable; organ not tender; no respiratory excur- sion for either upper or lower border. Spleen. Could not be outlined on account of persistent tym- pany; universal typmpanitis; diffuse but slight abdominal tender- ness; percussion gave a tympanitic note everywhere except in right inguinal and lumbar regions; dullness did not change with varying position. Urine negative. Stools soft but otherwise negative. 3 Blood. A series of stained coverslips showed no increase of leucocytes nor any abnormal constituents. The pulse ranged from 70° to 140° temperature from 97° to 104° F., being very irregular and respiration numbered 28 to 50. Rectal examination revealed high up on either side an indis- tinct nodular resistance, too distant, however, for accurate demar- cation. External genitalia negative. Lymph glands in left axilla large, hard, conglomerate, nodular. To the left of the navel, in the transverse umbilical line is a tumor over which tympany on super- ficial percussion and flatness on deep percussion is obtained. The tumor is painless, somewhat tender, hard and nodular. It does not exhibit respiratory excursion nor does it vary with change of patient's position. A retroperitoneal lymphatic tumor was diag- nosed. The further clinical course was almost uneventful. The emaciation and tympanites became more pronounced. Euphoria was complete, the patient asking on the day of his death for his discharge. The patient went into collapse daily during the last five days of his life, and a single convulsion of one minute's duration is recorded. Diarrhea increased during the final ten days. Treat- ment: Free stimulation, supporting diet, whisky, creosote and strychnia. The clinical diagnosis was obliterative pleuritis and general lymphatic tuberculosis. Autopsy. Emaciation; rigor mortis well marked; head could not be examined; pericardium negative; heart firmly contracted and every cavity entirely empty, 290 grams in weight. Myocardium homogeneous, firm, yellow-brown; endocardium negative; aortic and pulmonary valves competent by hydrostatic test. Mitral admits three and tricuspid valve four finger tips. Left ventricle 8 cm. long and 1.3 cm. thick; right ventricle 6 cm. long and 0.3 cm. thick. Both pleural cavities obliterated by ad- hesions, some organized, others recent; no tubercles present, even in deeper layers of exudate. Lungs thickly studded with miliary tubercles, pin head in size, the smaller being pale, the larger yel- low and granular. Lungs float, crepitate and yield frothy fluid on pressure. Pharynx, larynx, trachea, esophagus, thoracic duct, aorta, cavae, and thyroid gland negative. Lungs, liver, stomach, diaphragm, pancreas, spleen, colon, small gut, thoracic and abdom- inal parietes firmly adherent. The peritoneal adhesions were fibrous and careful examination between the viscera found no tubercles. Liver, 26 x 22 x 15 x 7 x 2 cm., somewhat pale, perihepa- tetic scars; numerous discrete miliary tubercles, the smallest 4 the size of a pin head and pale; some somewhat larger and yel- low. Spleen 12x9x6 cm. In the perisplenic adhesions are oal- carious nodules which are entirely extra splenic. Consistence in- creased. Through the pulp are nodules varying in diameter from miliary to 1 cm., soft, dry, on removal breaking into multiple minute granules. At hilus is a supernumerary spleen measuring 9 cm. long, whose pulp contains nodules the same as contained in spleen. At hilus several small soft caseated lymph glands in whose substance punctate hemorrhages have occurred. Left kidney, 12.5 x 6.5 x 6 x 4 cm.; capsule nonadherent. Cor- tex is to medulla as one is to two and one-half. Miliary tubercles similar to those seen in liver and lungs, surrounded by a narrow hemorrhagic zone. Cortex somewhat pale, increased in size, and markings somewhat blurred. Right kidney the same. Pelvis of each kidney, ureters, bladder, genitalia negative. The peritoneal cavity is entirely obliterated in its upper three-quarters. Below and above pubes, as well as in the right inguinal and lumbar regions, is a cavity, evidently formed by the retraction upward of the small intestines, mesentery and omentum, and communicating with smaller cavities constituted of folds of small intestines, inter- adherent by thin friable fibrous membranes. There exist also other small cavities which are quite separate from each other, the relics of the general cavum peritonei. The large cavity is filled with a liter of an opaque, foul smelling, milky fluid and separation of the loops of small intestines evacuates successively smaller quantities of the same fluid. The parietal peritoneum shows sev- eral nodules as large as and the shape of the distal phalanx of the index finger, projecting into the cavity containing caseated and fatty material, with a thin fibrous investment and in one instance with incomplete calcification. The cul-de-sac of Douglas is filled with a similar firmer, sausage shaped caseated mass with a thin fibrous membrane between it and the peritoneal space. Cervical, inguinal and cubital lymph glands negative. Bronchial glands show various changes, anthracosis with increase of connective tissue, coagula- tion necrosis, caseation, calcification, but no actual hyperplasia. The abdominal lymph glands show constant enlargement but diverse characters. The mesenteric glands show caseation, coag- ulation necrosis, here and there calcification, obviously tubercular. The iliac and axillary glands resemble the mesenteric. The re- troperitoneal glands are distinctly hard, nodular, varying in color from green to yellow and the size of a walnut. On section the ma- jority are perfectly homogeneous : no fluid can be scraped from the 5 surface ; a few show punctate hemorrhages ; in no instance do the glands transcend their capsules nor would their lateral distribution suggest material compression of the chyle system. The mesen- tary is retracted, indurated but contains no dilated lymph vessels. Microscopical Examination : Tubercle bacilli found in lungs, liver, spleen, kidney and broncial glands. The retroperitoneal glands revealed an increase in the trabeculae and reticulum, while the adenoid structures were normal. No follicles could be recog- nized in the glands. The green pigment was not detected since the sections had been placed in absolute alcohol for bacteriologi- cal examination. No bacilli tuberculosis were found, hence the diagnosis of lymphoma, possibly chloroma was made. Analysis of fluid: Specific gravity 1,012; alkaline; albumin by weight 2.7 percent; fat 6.0 per cent; no diastatic ferment present; Fehling's solution not reduced. On standing, fat rises to surface, forming a yellow upper stratum but separation into distinct layers is not observed. Microscopical examination ; long bacilli and cocci in abundance, post-mortem made three days after death ; very few endothelial cells which were slightly granular ; many amor- phous granules which refract light strongly; large globules of fat ; no tendency to coagulate. Ether alone without potassium hydrate did not dissolve the fat. Pathogenesis. Letulle5 holds that chylous or adipose effu- sions are always formed by peritonitis, independently of any open- ing or connection with the lacteal vessels. He espouses the view of Gueneau de Mussy that products of purulent or serous inflam- mation are slowly transformed by leucocytes into a granulo-fatty emulsion. All cases of chylous ascites, according to Letulle, are instances of mere chronic tubercular, cancerous and neo-membran- ous peritonitis. On comparison of pus, chylous effusions and as- cites, he finds that chylous extravasations and pus are quite similar as regards the percentage of albumen, amount of salts and total solids, and he concludes that chylous fluids are residual, occupying a position intermediate between ascitesand pyo-peritoneum. The amount of fat is not sufficient to cause the opacity which he refers rather to the regressive process. In one of Mdhu's cases there was only .48 gm. of fat per mille, yet the fluid was opague. Lais- saigne6 and Robin, Traitd des humeurs, claim that fat is pre- sent in the fibrin of serous exudations, as in chronic pleurisy. Cullen7 and Gendrin6 remarked the lactiform appearance of chronic inflammatory serositis. Broussais described a lactiform 6 effusion with a thickened peritoneum and De Laharpe mentions the occurrence of a milky fluid whose opalescence was due to particles of fat. M£hu10 says that fat, and often cholesterin, was found in ovarian cysts, hydrocele tunicae vaginalis, ascites, old cysts and very old hematoceles. Letulle thinks that this quota- tion solves the entire problem. Gudneau de Mussy also explains fatty pleurisy by fatty degeneration of endothelial cells11. Veil agrees with Letulle and Sainton with Debove12, claims that rup- tures in the chyle system found by others were made by post-mor- tem violence. The symptoms of chylous effusions are not those of suppurative pleurisy or peritonitis and he therefore excludes pyo- genic processes from the etiology. These effusions are then a special variety of exudate of whose genesis and pathology we re- main ignorant. Perde and Secrdtan deny the possibility of lacteal rupture. French writers have hesitated to admit that the effusions were chylous, yet Littrd early in the eighteenth century published the third case in our record. Depoix admits the possibility of rupture. Rokitansky and Oppolzer, 1861, in Austria described cases, but until twenty years ago chylous and adipose ascites were regarded in Germany as mythical. Less skepticism has been felt in America and in England where the first case was recorded. Etiology. Excluding unruptured chyle cysts,16 and mythical puerperal cases, 64 cases of chylous and 28 of adipose ascites remain. They occur from birth to the sixty-fifth year, and sex, race, occupation and social status apparently play no causal role. It is striking that fully one-third of the entire series has occurred within the last decade, and two-thirds since 1870. They may, as to etiology, be summarized thus : Etiology of chylous ascites. I. Indisputable cases. 1. Ma- croscopical rupture, 17 cases. 2. Microscopical wounds, 4 cases. 3. Sugar present, 10 cases. II. Uncertain cases, 34. III. Very uncertain cases, 3. Rupture may occur in any part of the lymphatic system : in the thoracic duct 3 cases, receptaculum 2, lacteal vessels 6, lymph gland 4 and chylous cysts 3. Various regions are obstructed: lymph glands 5, lymph vessels 5, thoracic duct 6, left subclavian vein 4, calculus in receptaculum 1, embolism of pulmonary artery 1, compression from without of lymphatic tract 10. Other causes : exertion 5, violence 1, liver disease 5, syphilis 2, nontubercular peritonitis 10, filaria 3, carcinoma 9, malignant lymphoma 2, calcarious mesentery 1, hereditary tendency to angio- 7 lymphatic disease 1, disproportion between the size of the chyle channels and its supply 1, heart disease 3, tubercular peritonitis 1, nephritis 2, carcinoma of thoracic duct 2. Chyle may extravasate into a serous effusion by mural alteration in the lymphatic vessels, or by violent contraction of the abdominal muscles, the diaphragm or indeed by intestinal peristalsis. Busey17 has written upon the relation of obstructed cardiac action to lymph stasis, while Niemeyer19 and Hertz20 have also recognized its importance. Etiology of ascites chyliformis or adiposus. Twenty- seven cases in all. Gumma of liver 1 case, tuberculosis 15, lungs, peritoneum, etc., nephritis 1, cirrhosis liver 3, nontubercular chronic peritonitis 3, carcinoma of various abdominal viscera 4, sarcoma of abdominal viscera 3, primary degeneration of peri- toneal endothelium 1, heart disease 3, lipemia 1, uterine fibroma 1. Busey insists that all abnormalities in the entire lymphatic system must be absent in adipose ascites. " Ascites chyliformis s. adiposus is that variety of milky ascites in which the lymph and chyle vessels, lymph glands, lacteals, mesentery are intact and free from disease, pressure, distention or obstruction and are normal in structure, size and position. We must exclude the effusion of chyle or lymph by transudation or es- cape by solution of continuity in any part of the lymph system. The milky, fatty, chyle like fluid must necessarily be a morbid product. " Busey. Senator's formula includes as possible sources, fatty degenera- tion of cellular and other formed elements in effusions, chiefly from endothelial cells, carcinomata and seldom also from pus cells, fibrin and inflammatory products. Definition of Terms. Much confusion has arisen from in- accurate nomenclature. Chylous ascites properly designates an effusion of chyle. Adipose ascites includes fluids containing a large percentage of fat and with no chylous mixture. Some authors use the terms "adipose " and " chyliform " as interchange- able. Boulengier24 prefers the terms " chyliform, " or " lacti- form " to " chylous, " on the ground that the fluid is rarely chyle. While his statement is too sweeping, yet the distinction is well made where the nature of the fluid is sub judice. Chyliform ascites is a chyle like fluid in which lymph or chyle may be mixed with exudates or even transudates. It is often impossible to differ- entiate sharply, for two varieties may co-exist or transition forms may intervene. Nature of Fluids. Strauss' case is the clearest example of 8 chylous ascites. Chemically typical chyle extravasated through two fistulae. Ingested butter was recognized in the fluid with- drawn by paracentesis from the abdominal cavity. Chylous ascites contains sugar, which fact is a diagnostic datum when diabetes is excluded. Senator, who thinks sugar one of the most constant criterion for the recognition of chyle, admits however, that its absence is not equally significant. Sugar when primarily present, may disappear later, Whitla's case. Its pres- ence is as rare as suggestive, having been detected not more than a dozen times. A small amount of fat speaks for chyle. Landois estimates the percentage of fat in chyle at nine-tenths of 1 per cent. Chylous ascites also is rich in solids, especially mineral salts and albumin. Albumin and fat occur conjointly in small punctiform granules susceptible of differentiation by chemical tests. Microscopic examination may differentiate between chylous and adipose fluids by the size of the fat globules, or fat and albu- min granules. Adipose ascites is characterized by the absence of sugar and the higher percentage of fat. The degree of opacity is no index to the amount of fat, since the turbidity may be due to the pres- ence of emulsionized albumin. Fat occurs in all cases. Its maxi- mum percentage is 5.25 per cent and 6.4 in our case, but it may be diluted by venous stasis or inflammation. It is recognized by the osmic acid, the alkanna stain and solu- bility tests. The granules of albumin and fat are much coarser in adipose than on chylous ascites. Hydropic and fatty carcinoma cells may, if numerous, cause a creamy layer and their microscopic detection favor a diagnosis of hydrops adiposus. Inflammatory products may obscure the pathogenesis and hence conclusions cannot be dogmatized from every analysis. Again, the fluid changes with time, the blood absorbing parts of the original fluid, in cachexia for example. Lymph or chyle may escape into serous exudate or a serous transudate of earlier origin- The fluid of whatever kind usually clears with ether and caustic potash. It is said to resist decomposition on account of the emulsion of fat and a supernatant fatty layer, to which propo- sitions our own case is an exception. The reaction is usually neu- tral or alkaline, although it was once recorded as acid. The fluid is opalescent from suspended molecular fat and emulsionized albumin. Some fluids coagulate spontaneously, others do not. 9 Poncy noted the odor of ingested food, while Wickerson pro- nounced the taste in his case cadaveric. A specimen standing ten days, Quinke, became acid, due to the formation of fatty acids. Specific gravity varies from 1.007 to 1.026, the average being 1.016. Reaction and specific gravity do not differentiate between the various forms. Macroscopically nothing is seen except oil globules. Microscopically, fine point like granules of fat are visi- ble which often have molecular movement and are soluble in ether. Large fatty cells, lymphoid, endothelia, carcinoma and sar- coma cells are observable. Red blood disks occur as well do also fibrin, seven times, filaria, Winkel, casein, Stiaus and Omerod, mucin, sodium, alkali, albuminate, Oppolzer, bile, Omerod, ace- tone, hydropsin, peptone, five times, lecithin twice, cholesterin three times, fibrinogen twice, a diastatic ferment twice, various in- organic compounds of calcium, sodium, sulphur, phosphorus, po- tassium and chlorine. Urea has been recorded three times, Quinke, R6mond, Foot. Tubercle bacilli have never been found. The highest percentage of albumin is 6.086 per cent. Ballmann. Symptomatology and Diagnosis. The symptoms possible with such a varied etiology are not limited in number or charac- ter. The primary disease does not indicate the character of the ascites, for ascites adiposus s. chylosus is no morbid entity. In conjunction with chylo-peritoneum chylous fluid may be vomited, Sprague, Pellitier, Foot, Nickerson, or discharged per anum, Pelli- tier, Nickerson. The association of the ascites with chylo- thorax is suggestive even before abdominal paracentesis. The only conceivable etiological hints relate to diseased lymphatic glands and vessels, affections of the thoracic duct or left subclavian vein, i. e., compression, or chyluria. "The chylous nature of an ascites may be suspected when as- sociated with sudden anorexia, acute anemia and emaciation" (?). Rapid recurrence may indicate chyle fistulae. Temperature is neither frequent nor significant. If transudation through lymph vessel walls be the cause, the clinical course is less stormy in onset and less rapidly progressive than is observed with antecedent rup- ture. A diagnosis has never been made prior to puncture. The blood varies, of course, with the fundamental disease; lipemia was observed once, Popham. The local signs and symptoms do not differ from those of serous ascites. It is probable that many cases diagnosed as the vulgar ascites, healing without treatment, are in- stances of chylous hydrops. The increasing frequency of the disease is best explained thereby. 10 Prognosis. Reference to the appended table shows that 67 per cent died, 21 per cent were not followed, 12 per cent recovered. Considering only those in which the ultimate issue is known, 84.41 per cent died and 15.584per cent recovered. Bianchi says that the prognosis is better in any rupture than in cases of chylous transudation. The rupture is more likely to heal when it is due to trauma than when caused by mural disease, since thrombosis occurs more readily in trauma. Weischer22, reviewing sixteen cases of chylo-thorax from rupture of the thoracic duct, concludes that rupture is almost invariably fatal. It is noteworthy that seven cases of ascites chylosus complicated with chylo-thorax died. Case 40 is the only exception. Rupture of the lymph vessels or receptaculum chyli may be compatible with life by the formation of thrombi and establishment of a collateral circulation27. Monro stabbed the receptaculum of a pig but effusion was prevented by thrombosis. If there be no communication left between the blood vascular and the lymph vascular system, progressive inanition and death are inevitable. A chylous fistula increases the gravity of the prog- nosis, as copious and continuous chylous discharge is invariably fatal. I believe the immediate prognosis is better in adipose ascites. Extensive obstruction to the lymph stream is always serious. The prognosis is impressed by causative or concomitant visceral lesions. A close analysis of reported recoveries to deter- mine favorable prognostic characters demonstrates that three cases were puerperal, and therefore fabulous: One was chlorosis, three were ruptured lymph vessels, three were ruptured chyle cysts; one was tubercular peritonitis, one was chronic recurrent peritonitis, possibly tubercular. Only the last two cases were adipose, while the first ten were chylous hydrops. Therefore the ultimate prog- nosis is better in chylous effusions, the converse being true of adi- pose accumulations. Laparotomy improves the prognosis. Treatment. Analysis vindicates surgical interference under two restrictions. First, laparotomy is indicated as prophylaxis against possible chylous rupture with consequent constitutional depletion; second, laparotomy for tubercular peritonitis. Para- centesis should be avoided as far as possible save first, as a pre- liminary diagnostic resort, and, second, as an ultimate resort against compression of the thoracic viscera. Otherwise, puncture depletes the organism especially in the genuine chylous form. The peritoneum should be allowed to resorb all it can of the chylous transudate. A diet readily digestible and absorbable by 11 the stomach is advised, P. J. Murphy, to permit healing by throm- bosis of ruptured lymph vessels. The use of water should be re- stricted. For filariosis, Lancereaux recommends mercurial in- unctions and local injections into the diseased lymph glands. remarks that there is no hope beyond the death of the adult worm. Other than mercurial parasiticides are probably use- less. The therapy in other directions is absolutely symptomatic. Experimental Consideration. Considering the elements in the etiological analysis seriatim, two main classes of cases are distin- guished. First, chylous resulting from change in the absorbent sys- tem between the intestinal villi and the subclavian vein. Previous consideration has been given to the individual factors, and in my experimental work, I have not paid special attention to obstruction in the chyle stream. The sequence in this class is sufficiently obvious, obstruction of the vessel, stasis, proximal ectasia, parie- tal attenuation, rupture extravasation, chylous ascites or chylo- thorax. Cooper, Morton and Dupuytren have shown that interrup- tion of the flow of chyle is distention, if there is not a speedy collateral circulation. Experiments on anitnals in which the ductus thoracicus is ligated cause no lymph stasis, owing to the prompt collateral compensation. Schmidt-Miilheim ligated the duct with no effect upon the metabolism, since the blood vessels assume the functions of the chyliferous vessels. V. literature, ref. 22 and 27. Experiments I and 2. Ligated in each instance all the veins 14 in the left side of a dog's neck deep below the clavicle. No chyle stasis resulted. Boegehold11 has shown that there are great anomalies in the terminus of the thoracic duct. This seems especially true as to dogs. Second, adipose ascites, in which the entire lymph chylous system is intact. To this variety the following experiments have been directed. The possible causative factors are tuberculosis or carcinoma peritonei, simple fatty degeneration of the endo- thelial cells of the peritoneum, and finally the constituents of exu- dation, pus cells or fibrin, or metamorphoses in transudates. Car- cinoma was not considered as the cancer juice and fatty cellular degeneration are sufficiently obvious explanations. The altera- tions to which ancient cellular exudates are liable have not, to my knowledge, been tested experimentally. The first series of experi- ments was made upon the portal vein, to produce an ascites in which, once produced, I hoped to produce secondary changes by pyogenic infection. Experiments 3 and 5. Ligated the portal vein but not com- 12 pletely, hoping the current would be sufficiently slowed to produce thrombosis. Animals well after three months. Experiment 4.. Ligated portal vein somewhat tighter than in Experiments 3 and 5. Shock like death in one and one-half hours. Autopsy showed great distention in the abdominal veins. Portal vein just admitted probe end. Otherwise autopsy was negative. Experiment 6. Ligated vena cava just below liver. Death in 24 hours. Animal did not rally from operation. Autopsy showed all abdominal veins greatly distended. No peritonitis; death from cardiac failure. Experiment 7. Ligated as in Experiment 6. Recovered without edema or ascites. Experiment 8. To produce thrombosis by injury to the endo- thelial coat, the portal vein was pressed firmly between the fingers, and one side rubbed upon the other. Then the vein was lifted by a silk ligature which was seesawed beneath the vein. Finally the vein was clamped for five minutes in artery forceps guarded by gauze. A ligature was next applied so that there was marked dis- tal venous stasis. These manipulations upon the vein occupied forty minutes, but the animal being killed after a month, showed the intima intact. No symptoms occurred. Experiment 9. Subject of Experiment No. 3 again operated upon. The ligature was covered with a few bands of thickened connective tissue. Portal vein distended behind the ligature, but intestinal veins not larger than normal. Portal vein was patent. On that side of the vein nearest the gut unguarded artery forceps were applied for four minutes. On removal, ridges and depres- sions were left upon the vein. In one hour the dog was running about; no thrombosis in eight days when the abdomen was opened. Experiment 10. Practically the same operation, clamping the portal vein firmly for 10 minutes. The animal well after three weeks. Experiments 11, 12 and 13. The basis of these three experi- ments was the inducement of trauma in the portal vein and slow- ing the blood current. The vein was ligated rather tightly to reduce the current, which reduction was proved by slight visible intestinal hyperemia. Then the vein was punctured and a double silk ligature drawn through the vein from side to side by a cambric needle, 1, to produce trauma and 2, to introduce a foreign body to aid coagulation. This experiment is analogous to the influence which the trabeculae in the cerebral sinuses exercise upon sinus 13 thrombosis. Death resulted in two hours, twelve hours and twenty-six hours. The cause in each case was thrombotic portal occlusion, with peripheral venous ectasia, and the inevitable sequence of shock. Experiment 14. Same operation. Animal lived seventeen days. Killed him and found only an inconsiderable parietal thrombus. No ascites. Experiments 15 and 16. Tied off, as shown by autopsy, 50 per cent of the portal vein tributaries. Gut greatly injected before sewing up abdomen. Lived four and twelve days respectively. Some free serous peritoneal fluid found in one case. Cause of death not ascertained. Experiment 17. Tied off seventy-five per cent of portal tribu- taries, as shown by autopsy. Death in three days, with no obvious cause. From the above experiments I conclude that ligature of the portal vein firmly enough to produce abdominal stasis, usually produces venous hyperemia, so that the animal dies of shock before ascites occurs. These experiments show that the same result may ensue from ligation of the vena cava below the liver. Lower,15 1669-1680, claims to have produced ascites if the vena cava were ligatured above the diaphragm. A priori, this seemed impossible in the light of the portal vein experiments, because of the consecutive stasis produced, which must be far more than closure of the portal vein alone. Experiments 18 and 19. Opened the right pleural cavity and ligated the inferior cava just above the diaphragm. Before the li- gation was complete, the animal was practically dead from right pneumothorax and dislocation of the heart and compression of the left lung, the very thin tissue between the two pleurae offering no resistance to atmospheric pressure in the right side. These con- siderations make Lower's claim questionable, to say the least. Experiment 20. An attempt was made to reach' the cava in- ferior within the pericardial sac, but without opening pleurae it was impossible, as the pericardium lies at some distance beneath the thorax wall. Pneumothorax, death. Experiment 21. Attempted to ligate the cava below diaphragm and between it and the convex surface of the liver by pulling liver down. The vein was ruptured by the needle and by the tension. Packed with gauze. Recovery. Killed animal after two months. Few thrombi in hepatic vein but none in the portal. Experiment 22. Ligature cava between the liver and the dia- 14 phragm. Death occurred in ten minutes with symptoms of shock and great intestinal engorgement, but on autopsy the cava was partly pervious. Experiments 23 and 24.. Same as 22. Death in thirty minutes, and in two hours from shock. Experiment 23. With the aim to produce thrombosis of the portal vein by injecting foreign bodies into its tributaries 10 cc. of a sterilized absolute alcohol solution of shellac was injected into an omental vein. Marked delirium. Snapped and groaned constantly. Death in two days. Autopsy showed that most of the ultimate portal radicles were occluded by a granular substance proven by solubility tests to be shellac. The liver showed innu- merable hemorrhagic infarcts, some very minute and some three inches in size. Experiments 26 and 27. With shellac injections. Same result, death within two days, with delirium. Experiments 28 and 29. Injected sterilized sand in oil. Same result. Experiments 30, 31 and 33. Attention was next directed to the heart. Measuring the distance on the dog cadaver from the right jugular vein to the tricuspid valve, a probe was thrust down into the heart and the heart lacerated. No ill effects observed. After two months, during which no clinical symptoms appeared, the hearts were examined, only a few white connective tissue bands being found in the tricuspid valve in one case, and in the ventricle wall in the other two. Experiment 32. Same operation, with gradually increasing ascites. Aspiration proved it serous. Injected sterilized shellac in alcoholic solution into the abdominal cavity. In three weeks the ascitic fluid became slightly turbid and showed microscopically numbers of granule bearing leucocytes. In three months fluid was distinctly opaque, milky, 10.15 specific gravity, alkaline, con- tained 1.9 per cent albumin, no free fat globules but leucocytes which gave dark points on treating with osmic acid. Opacity cleared with ether and caustic potash solution. No sugar was present. In all, eight aspirations were made. Animal was killed in five months. Heart showed tricuspid insufficiency with deform- ity of one valve. The body was negative except that the peri- toneum was somewhat thickened and contained a chyle-like fluid. Negative as these experiments seem, I have proven by No. 32 that a transudate can undergo metamorphosis from serous to cellular and come to contain fat. This places the pure hypotheses 15 of the French observers upon a somewhat firmer basis and may elucidate the pathology of some of the cases reported. A chronic peritonitis may therefore result in an ascites chyliformis s. adipo- sus. In eight out of the ninety-ssven cases, the fluid at first serous became opaque later. It is too much to say that pus infec- tion was the cause in all instances. Three cases, 24, 75, 90, were circulatory disturbances, three were hepatic disease chiefly cirrho- sis, 96, 89, 54, and two were peritonitis, 75, 92. I wish here to thank my friends, Dr. T. J. Williams, of the resident staff of Cook County Hospital, and Messrs. W. S. Har- pole and W. T. Kirby, of Northwestern University Medical School, for valuable assistance. 'Busey, Am. Jour. Med. Sci., 1889, p. 563. 2Sialographia et Ductuum Aquosorum, Anat. Nova Lugduni Batavorrum, 1695, p. 49. 3Ephemerides Germaniae decur. ii., ann. viii. 4Manson, Lewis, Sonsino, Mastin, Sr. and Jr., Guiteras. "Revue de Medecine, No. 11, November, 1885, p. 960. 6Journ. de Chem. Med., 1825, T. I. Cit. Gendrin, Histoire anat. des. inflam. T, ii. p. 548. 7Medicine pratique, Edit. 1787 and II., De 1'ascite en note p. 580. 8Broussais, Histoire des phlegmasies ou inflammations chromique T III, ch. iv. De 1'inflammation du peritoine, Paris, 1831. "Arch. gen. de medicine, T XIV., p. 358, 1842. '"Gjorgevic, Langenbeck's Archiv., Bd. XII, 1890, s. 653. ''Clinique Medicale, t. T. p. 658. Mem. de la Soc. Med. des hopiteaux de Paris, 1881, p. 49. '"Etude sur une variete latente et Benigne d'empyeme. Paris, These, 1881. 13Quinke, Ueber Ascites, Dent. Arch. f. klin. med., 1882, 30, p. 569, 587. 14Boegehold, Arch, fur Chirurgie, Bd. 32. ''Lower Tractatus de corde, 1669. 16Chyle cysts. Excellent summary in Virch Arch. 134 Bd. Heft 1 S-118 by Leydhecker who also gives exhaustive review of entire pathology of thoracic duct. Weichselbaum (see table) Ziegler, Orth. Gusserow, Charite Annalen, 1890, XV., 613. "Am. Jour. Med. Sci., Vol. XC., p. 373. '"Hasebroeck Zeitsch f. Physiol Chenie, XII. p. 289, 1888. '"Niemeyer Handb. Pathol, u. Therap. Bd. I. S. 120. ""Hertz, Ziemssen's Handbuch der Pathol, u. Therap. Bd. V. s. 382. "'Literature of Galactocele ref. 1, 4 and 25. Literature of Lymphorrhagia, ref. 1. ""Weischer, Zur casuistik der Verletzung des Ducts. Thoracicus, Deut. Zeits. f. Chirurg, Bd- 38, Heft 4, 5. 23Peree, Etude sur les 'epanchments Chyliforms des cavities sereuses These de Paris, 1881, No. 382. BIBLIOGRAPHY. 16 24Boulengier Contrib. & 1'dtude des epanch. chylifs. Presse Med. Beige. Brux. 1890, xlii., No. 3, p. 33, and No. 4, p. 49. 25Debove Epanchements Chylif. des cavsereuses, Mem. Soc. Med. hop, 1881, p. 49. 26Depoix, Contribut, & 1'etude des epanch. chyl. du peribsine. These de Paris, 1889. 27Experiments of Monro, Lower, Cooper, Dupuytren, Schmit-Millheim, Teichmann, Leuret. Lassaigne, Colin, Flandrin, Magendie, Noeckher-Rogers. 2818 Indiana Avenue.