Twentieth Century History of Findlay and Hancock County, Ohio, and Representative Citizens, Part 165

Author: Jacob Anthony Kimmell
Publication date: 1910
Publisher:
Number of Pages: 1189

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Microscopically. Within the lobules, usually at a distance from the portal spaces, are areas where the liver cells are clear and unstained with eosin in contrast to those about. With the high power the protoplasm is entirely unstained, but is slightly granu- lar. The cell body is somewhat swollen. The nucleus is smaller, somewhat irregular, and no longer vesicular, staining homogene- ously. In the center of one of these areas, a group of 10 to 12 cells whose protoplasm takes a conspicuous deep cosin stain is found. The nuclei are preserved; many polymorphonuclear leu- cocytes occur between these cells. (This case was reported by Opie in the JOHNS HOPKINS HOSPITAL BULLETIN, 1901, under the title, " The Etiology of Acute Hemorrhagic Pancreatitis ").

14. B. V., 1908-9, D. W. Died, February 19, 1908, 2.15 p. m. Autopsy, February 20, 1908, 11.30 a. m. Dr. Meloy.

Anatomical Diagnosis .- Infected ovarian cyst; multiple miliary abscesses (operation) ; acute and chronic peritonitis; chronic dif- fuse nephritis (large white kidney); infarct of spleen, zone of congestion of liver corresponding to distribution of occluded portal vein by thrombus; amyloidosis; chronic perihepatitis and perisplenitis; anemia; emaciation; polypoid œdematous tumors of bladder.

Unfortunately no other data concerning this case was avail- able. At the time of autopsy, however, the liver was practi- cally identical in appearance with that of Case 12. Micro- scopically, too, there was no evident change in the organ. It is probable that here also there were thrombi in the portal roots which only reached the intrahepatic branch after opera- tion.

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To briefly summarize, obstruction of the large branches of the portal vein may cause irregular wedge-shaped areas of congestion, and in rare instances of anemia, in the liver. These are not true infarcts since they show microscopically only a dilatation of the central veins and intralobular capil- laries, together with atrophy of the liver cells and no necrosis. Such an area may shrink considerably. This shrinkage is due to atrophy of the liver parenchyma, but to what extent pressure of the dilated capillaries, decreased nutrition, actual necrosis, or inactivity of the cells affects this atrophy is a problem inseparably associated with the still unsettled ques- tion of the atrophy of the liver occurring in chronic passive congestion due to general causes.

In all these cases the smallest branches of the portal vein in the congested zones were free of obstruction. The hepatic vein and artery were always unobstructed. The blood reached these zones through the inner portal vein radicals, but not in sufficient quantity to keep up the normal flow. This allowed a reflux from the larger hepatic vein which resulted in con- gestion. It must be repeated that occlusion of the portal vein alone may not necessarily be followed by congestion in zones supplied by the occluded vein. In order that these results should follow Köhler and Chiari consider that accessory circum- stances must exist, such as venous congestion, decreased cardiac activity, etc. The ultimate result of these areas of con- gestion is not known and the shortest time in any of the cases reported in which the area of congestion occurred following the thrombosis of the portal vein was three days in a case re- ported by Chiari. In Case 12 the time was less than 24 hours.

TRUE ANEMIC OR HEMORRHAGIC INFARCTS OF THE LIVER RE- SULTING FROM OCCLUSION OF SMALLEST INTERLOBULAR BRANCHES OF THE PORTAL VEIN.

True infarcts of the liver with necrosis occur as the result of occlusion of the smallest portal vein radicals, namely, the interlobular veins. Under these conditions the blood from the hepatic artery no longer can reach the capillaries of the lobule by its anastomosis with the interlobular veins. There is then a complete mechanical deficiency of the circulation leading often to complete local necrosis of the liver parenchyma which may be combined with hemorrhage.

Cohnheim and Litten " emphasized the fact that if the liver parenchyma is to remain free of secondary changes, the in- terlobular vein must not be involved by the occluding mass. Orth " also said that while there may be no effect from occlu- sion of big branches of the portal vein, if the interlobular branch is involved atrophy as well as necrosis results. To this type of necrosis belong the well-known necrosis of eclampsia as described by Schmorrl, Klebs, Lubarsch, etc. Chiari " in his discussion of these infarcts includes cases de- scribed by Rattone and Mondino, and Osler. Rattone and Mondino deny the occurrence of inner portal vein radicals, and consider the entrance of the branches of the hepatic

" Cohnheim and Litten: Loc. cit.

* Orth: Loc. cit.

" Chiari: Loc. cit.

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artery into the capillaries of the acini of the greatest in: ance. They describe two cases of infarction. In their # case the hepatic artery and portal vein were both och: the affected zone. This was also true in Osler's case. . liver was cirrhotic and showed a reddish-brown necrote; on the surface which extended through the liver tiser -;. triangle. The portal vein leading to this was thrombw. Osler considered the cirrhosis to have shut off the ! circulation.

Chiari then adds three cases. The first occurred in . . of tuberculosis. The liver was the seat of multip. .. tuberculous nodules. There were numerous thromli : mesenteric veins. leading from the colon. Mienne aside from the tuberculosis there were numerous interki. veins plugged by emboli, from the mesenteric thrombi. I .- were also small areas of coagulative necrosis of the live . which Chiari considered to be infarcts. The case is D: vincing.

In his second case following an operation (resection - pylorus of the stomach) there were thrombi in the and pancreatic veins. These fed small emboli to the : lobular portal branches and multiple small whitish x .: characterized by typical coagulative necrosis resulted.

As an instance of infarction of the liver resulting ! thrombosis of the interlobular veins he cites a va- eclampsia.

Ruczynski = adds two more cases of this type. Co case in which necrotic areas occurred in the liver thx ". of small emboli from thrombi in the portal roots and [ ... cope's case where there were yellow thrombi in the !. vein and smallest portal veins causing yellow, necrotie ir in the parts supplied by the portal vessel.

Versé also describes a case of chronic perityphilitie in 6. the surface of the liver showed numerous pale, brox :. pressed areas. On section these were dark red, soft and s. and showed microscopically dilated vessels and necrot .: cells. The portal vein was occluded by an old thrombus from the hilus, and near the infarct was a canalizel :" thrombus. This case is of further interest since the f. bosis of the large portal root was without effect, but it .. of the small branches brought about necrosis. The folk .. case belongs to this group :

15. G. L., colored male, 53 years. Autopsy No. 228. Anatomical Diagnosis .- Primary carcinoma of stomach: ondary in liver, lymph glands and pleura; chronic diffuse nept" nodular arteriosclerosis; thrombosis of minute portal ter softened hemorrhagic infarcts of liver.

Liver weighs 2600 grams. It is very large and contains E == ous rather soft, nodular masses which vary considerably i: 12 to 7 cm. These masses project slightly above the surface are flat and sometimes very slightly umbilicated. Some / nodules are exceedingly soft. On section a large amo .: bloody fluid escapes. This appears to come from smooth F: cavities. Some of these cavities are situated directly in the. tissue while others are surrounded by a small amount : tissue of the tumor. These spaces sometimes form large

25 Ruczynski: Loc. cit.

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the cavities from minute branches of the portal vein. On ter examination of these spaces in the liver they nearly all to be in relation to the tumors often running on one side ese. Some of the cavities are round, others very irregular, ed by numerous septa. Often the larger ones communicate. ches of both the portal and hepatic veins especially the latter De traced into them. On scraping the walls no epithelium found.

1 instance of peripheral zonal necrosis, similar to that ring in eclampsia, was found in an adult male in our osy series. This is of interest because peripheral zonal ›sis is considered by some to be the characteristic anatomi- icture of eclampsia.

OCCLUSION OF THE HEPATIC ARTERY.

le anatomy of the hepatic artery is such that firstly on int of its position at its origin from the coeliac axis it tle disposed to emboli and secondly on account of the anastomosis of its hepatic branches with the neighboring Is-inferior phrenic, internal mammary, superior adrenal, the arc of vessels on the lesser curvature of the stomach- sion of its branches is usually without effect.

:perimental ligation of the hepatic artery varies in its ts according to the animal which is used. In rabbits ses usually result, while in dogs there is very little effect

from a possible slight atrophy of the liver cells in the r of the lobule (Cohnheim, Litten, Whipple, etc.). schner ligated the hepatic artery in 26 rabbits and in one was there no necrosis. He says that the occlusion of epatic artery which is supposed only to nourish Glisson's ile causes degeneration of the walls of the portal vein 1 leads to thrombosis and infarct formation. In man ic infarcts resulting from occlusion of branches of the ic artery are extremely rare. To this type of infarction g a number of cases cited by Chiari; namely, those of nuller, Orth, Ogle, Kaufmann, two original contributions iari's, and two by Ruczynski who also cites cases by Bald- Heile and Bonome. Ruczynski's second case is particu- interesting for here despite thrombosis of both the ic artery and portal vein, the process had been so gradual 10 infarct, but only a local congestion with atrophy of the cells resulted.

iari emphasized the difference between these infarcts and resulting from occlusion of the smallest portal vein ils. In the arterial infarct there is also necrosis of the vessels and connective tissue which are nourished by epatic artery. There are no cases of this type in our :500 autopsies.

OCCLUSION OF HEPATIC VEIN.

Ich 26 cites a case reported by Arnold where a condition r to the " atrophic red infarct of Zahn " followed plug- of an hepatic vein by a retrograde embolus.

elch: Thrombosis and Embolism; Allbutt: System of Medi- .899, VII, 280.

have almost completely ligated an hepatic vein of a dog with- out marked effect. The lobe of the liver a few weeks after ligation is indistinguishable from the remainder of the organ macroscopically or microscopically. This is confirmed in the following post mortem record :

F. E., white male. Autopsy No. 769. Dr. Flexner.

Anatomical Diagnosis .- Amobic dysentery; amœbic abscess of liver penetrating into lung. Fibrino-purulent pleurisy; perfora- tion into inferior vena cava. Thrombosis of inferior vena cava extending into right auricle and hepatic veins.

The inferior vena cava beginning at a point just above the rupture (of liver, abscess into cava), contains an occluding de-

Max Brody 1161

Pulmonary embolus

Infarct ....

Thrombus in left renal vein

Portal embolus

> Small thrombi in mesentery

colorized, firm, adherent thrombus, which extends upwards and projects into the right auricle which it about one-third fills. Some of the hepatic veins are thrombosed in part of their extent. The thrombi in the upper part are decolorized, but deeper in the liver tissue they are red and soft.

CONCLUSIONS.

1. On account of the extensive anastomosis of the intra- hepatic branches of the portal vein and the hepatic artery, occlusion of either of them is usually without effect upon the liver parenchyma.

2. The portal vein may be completely occluded and the liver only appear slightly smaller and congested. In these cases an extensive collateral circulation usually establishes it- self in the hepato-duodenal ligament and the portal blood is in this way carried to the interlobular vessels.

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3. Following occlusion of the portal vein the entire liver, if it is the main branch, or only the part supplied by the oc- cluded vein may present a much more congested appearance. This is due to the insufficiency of arterial anastomosis which is enough to nourish the liver cells and prevent necrosis, but which allows the blood from the systemic veins to dam back into the liver capillaries. This picture is only produced when the general circulation is impaired.

4. When the smaller interlobular branches of the portal vein are occluded the anastomosis with the hepatic artery becomes ineffectual and there is a total mechanical obstruction of the circulation in the area. This is followed by infarct formation. There is necrosis of the liver cells often accompanied by hemor- rhage. The necrosis of eclampsia belongs to this group.

5. Occlusion of branches of the hepatic artery may result

in true infarct formation. This is rare, firstly, on an c' its peculiar position at the coeliac axis, and secondly Ing . of its abundant anastomoses.

6. Occlusion of both the portal vein and the hepatir e- results in infarct formation unless the process is very p.r.

7. Occlusion of the hepatic vein may bring about : gestion in the zone drained by it or may be absolutely a: . effect.

The accompanying illustrations, kindly made by Pr: Brödel, illustrate very well the course of the various in Case 12, and secondly the resultant wedge-shaped : congestion following the localization of the embolus inc: the large right branches of the portal vein.

THE TEACHING OF EXPERIMENTAL PATHOLOGY AND PATHOLOGY CAL PHYSIOLOGY TO LARGE CLASSES .*

By RICHARD M. PEARCE, M. D., Professor of Research Medicine and of Pathology, University of Pennsylvania.

The course in experimental pathology and pathological physiology here presented in outline, is an attempt to bring physiology into relation with morphology and symptoma- tology and thus to fill the gap which exists between the autopsy room and the laboratory of pathological histology on the one hand and the clinic on the other. Many teachers of pathology, following the lead of Cohnheim, have, it is true, introduced into their class work demonstrations illustrating some of the important problems of pathological physiology ; but these have usually been perfunctory demonstrations given in a fragmentary way before the entire class, and without, as a rule, the utilization of the methods of exact registration employed in physiology. Of an entirely different character is the method which was followed for several years by Dr. W. G. MacCallum at the Johns Hopkins Medical School and is continued there along similar lines by Dr. Whipple. In this course a class of eight students worked for a period of two to three months on one organ or a group of related or- gans, utilizing all the methods which experimental pathology could bring to bear on the problems under consideration. The value of such a course cannot be over estimated and it should have, as an elective, a place in the curriculum of every good medical school. It has, however, the disadvantage that it cannot be given, on account of the great detail of the work, to all the members of a large class and must remain essentially an elective course combining instruction and research for a small number of students.

For a long time, it has seemed to me desirable that a course in experimental pathology should be developed which, while including as far as possible valuable features of Mac- Callum's " small group " course, should at the same time be so arranged as to be available to all the members of a large * Read before the International Association of Medical Muse- April 13, 1911.

class. Amphitheatre demonstrations are not adrisate, only the few men close to the demonstration table : by such procedures. Likewise individual work by the sc." such as is now given in our better courses in experir .: pharmacology, is out of the question, for the present at" on account of the lack of equipment and space in most ! laboratories of pathology. The course which I have . during the latter half of the past academic year has compromise between these two methods, in that, althon? demonstration method has been used, the number of dz strations in one period has been sufficient to break : class into small groups. Thus a class of 90 men ha- divided into two sections, each section meeting, duriz: weeks, once a week for one hour. At these sessions si five demonstrations, each under the direction of a E :- of the department, have been presented simultaneously. each section of 45 men was subdivided into five groups men, and each of these had at least 12 minutes for a &s stration. The room in which the course was given wa- size sufficient to allow a wide space between the dems ** tion tables, and also to allow the passage of group- table to table, on signal, without confusion.

The general scope of the course was based in par Cohnheim's classical experiments, MacCallum's our Hopkins, Rous' course at Michigan, Longcope's course in " medical correlation " given last year at this : and the demonstration courses to physicians given for - years in the Medical Department of Columbia E'nin. and in part on an extensive personal acquaintance wit' methods of experimental pathology and their posi! The course is not to be considered as complete or !! or as in every way ideal, but rather as a tentative #5. of what has, in my hands, proved most satisfactor: " Digitized byinstruction of large classes. The possibilities of enlani:

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samazina will the frietflods of physi-

gy and chemistry as applied to experimental pathology. The following outline is a copy of the mimeographed sheets en each member of the class two days before the demon- itions :

EXERCISE I.

BLOOD DESTRUCTION AND JAUNDICE.

le I. (a) Rabbit which received, three days before demon- stration, 0.001 gm. rattlesnake venom in ear vein. Note hemo- globinuria, the result of the hemolytic action of snake venom.

(b) Dog which received, three days before demonstration, 0.2 cc. of hemolytic immune serum per kilo of body weight in saphenous vein. Note hemoglobinuria (and jaundice ?). le II. Experiments in vitro explaining phenomena seen above in vivo (hemagglutination and hemolysis).

le III. (a) Rabbit which received, 24 hours before demon- stration, 0.001 gm. cantharidin in acetic ether, subcutaneously. Result: Free blood in urine (hematuria), not hemoglobin- uria-equivalent to a hemorrhagic nephritis.

(b) Microscopic preparations showing the sediment of the urine of (1) hematuria (red blood corpuscles present) and (2) hemoglobinuria.

le IV. (a) Dog with jaundice, the result of the ligation of the common bile duct for three days. Note skin, conjunctiva and urine.

(b) Tests for bile in urine of Ib and IVa.

e V. (a) Test for albumin in urine of Ia, Ib, IIIa, IVa.

(b) Spectroscopic test of urine of Ib.

EXERCISE II.

DEGENERATION AND NECROSIS.

I. (a) Rabbit: Gross demonstration of cloudy swelling lue to repeated injections of cantharidin in ether.

(b) Microscopic preparations of liver and kidney treated vith salt solution and acetic acid.

, II. (a) Rabbit: Fatty changes due to poisoning by phos- horus.

(b) Microscopic preparations treated by acetic acid, Sudan II and osmic acid.

: III. (a) Dog: Necrosis from loss of blood supply. Liga- ion of superior mesenteric artery and one branch of renal rtery.

(b) Gangrene in guinea pig's leg secondary to ligation of emoral artery and vein.

IV. (a) Rabbit: Illustrating gas formation in emphyse- atous gangrene. Injection of B. aerogenes capsulatus in ar vein; animal then killed and placed in thermostat at 7.5° C. for 24 hours.

(b) Microscope with preparation of B. aerogenes capsulatus.

V. (a) Guinea pigs showing caseation of tuberculosis. our weeks after injection of bovine tubercle bacilli into eritoneal cavity.

(b) Microscope with preparation of B. tuberculosis.

EXERCISE III.

INFLAMMATION AND REPAIR.

I. (a) Ear of rabbit exposed to water at 56° C. for three inutes-condition after 24 hours.

(b) Ear of rabbit 24 hours after rubbing with croton oil. (c) Microscopic preparations illustrating histology of each.

to"pour lesion.

(b) Ditto due to injection of turpentine, 48-hour lesion. (c)

(d) Microscopes with exudate from (a)

(b)

Table III. (a) Rabbit: Multiple embolic abscesses resulting from injection of staphylococcus pyogenes aureus in ear vein, 48-hour lesion.

(b) Microscopic preparations illustrating lesion in kidney. Table IV. Dog: Repair of aseptic wound, 3 days. Table V. Dog: Repair of infected wound, 3 days. Compare carefully gross appearance of Ia and Ib. Compare carefully gross appearance of IV and V.

EXERCISE IV. THROMBOSIS, EMBOLISM, INFARCTION.

Table I. Rabbit: Multiple bland infarctions due to embolism produced by injection of foreign particles (tobacco seed). (Compare with multiple embolic abscesses due to injection of Staphylococcus pyogenes aureus, as seen in last weeks' ex- ercise.)

Table II. Dog: Air embolism with graphic registration of changes in blood pressure, heart action and respiration. Ether anesthesia. Autopsy showing method of demonstrating air in heart cavitles.

Table III. (a) Dog: Thrombus in jugular vein resulting from injury to intima caused by mechanical pressure.

(b) Thrombus formation in ligated artery (femoral).

Table IV. Sections of liver and spleen showing hyalin thrombi composed of agglutinated red blood corpuscles. From dog which received hemolytic (also hemagglutinative) serum (see Exercise I) and died after one hour; also sections from animals similarly treated, showing necrosis of the liver after twenty-four hours.

EXERCISE V. HEART.

(All experiments under ether anesthesia.)

Table I. Hydropericardium: Experimental condition produced by introducing a large amount of salt solution into the peri- cardial cavity. Graphic registration of effect on heart action and arterial and venous pressure. Artificial respiration.

Table II. Myocarditis: Production of myocardial insufficiency by injection of alcohol into heart substance. Graphic regis- tration of effect on heart action and blood pressure.

Table III. Valvular Insufficiency: Mechanical rupture of aortic valve by instrumentation through carotid artery. Graphic registration of effect on heart action and blood pressure.

EXERCISE VI. LUNGS.

(All experiments under ether anesthesia.)

Table I. Graphic registration showing effect of double Hydro- thorax on respiration, heart action and blood pressure. Hydrothorax produced by injection of salt solution.

Table II. Demonstration of the anatomical relations in the thorax under above conditions, Atelectasis.

Table III. Emphysema: The lungs of a guinea pig in the ex- perimental condition known as anaphylaxis. The gross ap- pearance of the lungs is similar to that of emphysema.

Table IV. (a) "Deglutition " pneumonia; due to foreign par- ticles in bronchi.

(b) Purulent pleuritis (empyema) due to Staphylococcus pyogenes aureus.

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JOHNS HOPKINS HOSPITAL BULLETIN.

Table V. Edema of lung; produced by infiltration of lung with salt solution. Graphic registration of effect on heart, blood pressure, and respiration.

EXERCISE VII. STOMACH AND INTESTINE.

Table I. Experimental Toxic gastritis, due to (a) carbolic acid and (b) corrosive sublimate.

Table II. Experimental Toxic gastritis, due to (a) sulphuric acid and (b) nitric acid.

Table III. Experimental Toxic gastritis, due to caustic alkali (sodium hydrate).

Table IV. Experimental Peptic ulcer, produced by injecting se- rum beneath mucosa and by excising small portion of mucosa. Table V. Intussusception and Volvulus of Intestine and internal hernia.

(All lesions produced under ether anesthesia followed by death from chloroform.)

EXERCISE VIII. PANCREAS.

Table I. Hog: Acute hemorrhagic and gangrenous pancreatitis and Fat necrosis following injection of bile into pancreatic duct. Lesions of twenty-four hours and forty-eight hours respectively.

Table II. Ligation of duct for period of two months; slight atrophy; no glycosuria.

Table III. Experimental Diabetes following extirpation of pan- creas.

Table IV. Phloridzin Diabetes.

Table V. Tests for sugar in the urine of all of above.

EXERCISE IX. LIVER.

Table I. Multiple focal necroses of liver due to the injection of hemolytic and hemagglutinative immune serum.

Table II. Necrosis of liver due to prolonged inhalation of chlo- roform.

Table III. Obstructive Jaundice.

Table IV. Demonstration of a "spontaneous" cirrhosis of the liver in the dog.

Table V. (a) Sections illustrating microscopic picture in above lesions.

(b) Tests illustrating changes in the urine in I, II, and III.

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Twentieth Century History of Findlay and Hancock County, Ohio, and Representative Citizens, Part 165

Author: Jacob Anthony Kimmell Publication date: 1910 Publisher: Number of Pages: 1189

Author: Jacob Anthony Kimmell
Publication date: 1910
Publisher:
Number of Pages: 1189