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Show SECTION VII] DISEASES OF THE LIVER, SPLEEX, AND LYMI'IIATIC" TABLE III. FIG. 1.- Uriah/ms of {/u' Lo'rr. (C'o)‘s71:c/l.) (A A), bection of a number of globular tumors, varying from an eighth of an inch to an inch and a half in diameter, of a deep brown or black color, honmgeneous aspect, uniform texture, of soft consistence, and lying in immediate contact with the substance of the liver. (B). Similar tumors but smaller in size. (C (l, 1)) represent appear- anees which sometimes are, seen to precede the tbrmation of such tumors. At (1)) the dark-brown substance is contained in the minute veins, and presents, when closely e amined, a ramiform distribution. The appea 'ance. shown at (D) also illnst *ates the fact of melanotic matter being contained in the blood of the venous ciqfillarics prior to its deposition in the molecular structure of the liver. (The dark substance is reduced hzeinoglobin and bilirubin.) (Ref) Fro. 2,-(‘r/rcoiemu/011s JIM/owes. The 3arcinomatous alte 'ation is recognized byits pale and yellowish-white color, the melanotie by its dark-brown tinge. Both give the structures of the live ‘ a tula-ritorm ar *angement. (A A), inelanotic portions; (B), earcinomatous, degenerated tissue. The organic structures are still conspicuous from the form and ar‘augcment of the. (Icon, but the color of these bodies has disap- peared and their volume increased by neoplastic deposits. At ((‘) J) in the interacinous portion of the organ, readilv noticed at (I) D). Flos. 3;, 4. :3, o‘ represent different forms of caiicinomatous altera~ tions in the liver. Fig. 3, a tumor (A) removed from within the liver substance, with a munber of small veins (B B) adhering to it. These yessels passed through the tumor, and contained the. same bram»l1ke substanc . as the tumor. Two of the vessels ((7 C) communicated with a large venous trunk (1)) also thus affected. Fig. 4, carcinomatous matter in a larger venous trunk, from a tlunor 1B), being a large branch of the portal vein (III); at ((‘) the vein passes from the tumor and receives a superficial branch (It). Into this branch three smaller branches of veins (1‘)) terminate (F). The whole venous trunk is divided to show its careinomatous contents (G) and its communicatitin with the chief division of the portal vein (II). Fig '3 shows the compressed state of a vein produced by carcinomatous infiltration of its own walls and perivaseular structures, causing venous stasis and subsequent dropsy in the abdomen. etc. (A), it large-sized branch of the portal vein laid open; (B B), tumors projecting into it (C C) without l'wrtorating the vessel; (it), partly obliterated cavity of the vein. Fig. 6, lardaceous tumors of different sizes in the liver (\ A). They are of ag 'ayish vellow color, with a central depression from which fiber-like darker structures project in a radiary manner. The. tumors contain quite a quantitv of b ‘ain- like carcinomatous infiltrate. Minute vessels ramifv in them, from a. quantity of carcinomatous structure is zu-cunmlated, and seems to the circumference to the center. be increasing in bulk by the aggregation of the neighboring (mm, which form an irregular border along the inner side of the principal mass. The melanotic substances seem to be principally deposited lary cancer form, some containing very many miliary lnemorrhages; (A U), the vaseularity is very conspicuous; (l) 1)), tumors on the surface of the organ, visible through the peritoneal covering. organ. In partial atrophy recovery usually takes place when the inciting cause is removed, for the blood vessels are under such circumstances but little affected, and the destroyed cells are r‘adily tissue. Along with the invasion is going on an intense inflammation, beginning in the portal and central veins, ending in enormous infiltration of the tissues with lymphoid cells and serous exudate. Farther increase of the infiltrate colliquates the decaying tissue, and an abscess results. The suppurative inflammation varies according to the manner in which the infection is propagated in the organ. \Vhen the connective tissue is the seat of the primary infection, then a number of lobnlcs become gangrenous, and the abscess is formed secondarily. In wounds of the liver sumuiration may begin the second day after the injury and abscess follow soon after. I'rimary abscesses are formed in consequence of wounds, pylephlebi'tis, peri- replaced, when free circulation is re-established. Even under normal circumstances does the liver contain about 11 per cent, of fat in the fresh state, and about 32 per cent. ex- t ‘aeted with ether. After every in ad there is an increase of fat in the organ, varying in quantity according to more or less fat in food and drink taken. Great quantities of fat accumulate in the organ in many infectious diseases and in high-graded fevers. The greatest quantity is found in livers of patients down with pucrpe 'al fever, poisoning with alcohol or phosphorous. Amemia from compression of the vessels by the fat only takes place in lizZI/lx-[pw/wl fat livers; ordinarily anaemia, in livers is due to other causes. Accumulation of fat. in the organ is either due to infilt 'ation or fatty metamorphosis: 1. \Vhen theidcstruction of fat formed in the liver from albmninates, normally taking place, is prevented by introduction into the organ of great quantities of carbo-hydrates (sugar, amyloids, etc.) 2. \Vhen fat formed in the liver does not become oxidized (as in typhus. inanition, pulmonary tuberculosis.) 3. \Vhen enormous quantities of fat formation take place in the liver, but inadequately destroyed (as in poisoning with phosphorous, acute yellow atrophy, etc.) Many causes often combine to produce accumulation of fat; in the liver. It is often impossible to determine between accumulation of fat by infiltration and fat metamorphosis. . I/iflmnmaz‘irm of (/«c Liver. Fairway/mamas z'nflumnmlz'om-IVhen the liver is moderately enlarged in all its dimensions, and is of a yellowish-gray color, amemie. and of an inelastic doughy consistence, smooth on the surface, and dry on a cut surface, like smoked in alt, it an be set down that there was morbid alteration of the liver cells, which Tire iou‘ designated as liar/iii], swelling, and forms the essential basis of the 1mrenchymatous inflammation. This morbid process consists of enlargement of the cells by very numerous protoplastie g'anules. Sometimes these granules are in enormous quantities, and hide the nuclei of the cells of the liver. The lobules are then enlarged, and the interlobular connective tissue infiltrated with serum. Between the lobular cells spaces are formed and their otherwise. regular roWs disarranged. The serous infilt'ation likely extends between the cell-rows. Diffuse pareuchymatous infialnmation, of a light grade, is found in many infectious diseases, in many acute eruptive diseases, in septic and other poisonings, puerperal fever, etc. As a rule, this form of inflammation terminates in recovery. I'rowlcnt Inflammation. Abscess in tire Lirrr. Such inflammation takes place when the morbific agency, either introduced from without or derived from any part of the body, is *apable. of producing pus. Modern research has proveu that only schizomyeetes, and the products of their activities, are able to form pus. The ways by which such mieroparasites penetrate into the liver may differ, yet are easily conceived. Any pertorating abdominal wound may afford them entrance, or an adjacent organ may be in a suppu ‘ative. state of inflannnation, and the infection may be d0~ rived from those, either direct or by the lymph-current. l'arasitory infections are oftenest carried into the liver by the portal vein and hepatic artery. very seldom by the hepatic vein. In newdmrn babes they are conveyed bythe umbilical veins. Especially is this the case when in the. region of distribution of the respective vessels-the portal vein in the intestine, the hepatic; in the lungs; brain-there exists already a suppurating focus. Idiopathic abscess of the liver is very rare in temperate zones, but frequent in hot climates. The biliary ducts are often the ways of communicatit>11 ofthe infection with the liver, when there is stagnation of bile in the ducts and formation of biliary conerements. \Vhen the 'no'crococms septic/is, for instance, enters into the liver vast colonies are soon developed in the 'apillaries and in the veins. The zooglxea and the colonies soon obstruct and eventually close the vascular cavities. At first the pareuehyma is unaffected, but finally the lobular cells become infilt‘ated with them and become granular. lose their nucleus, and are broken up into fragments. Successively the fungi invade greater numbers of vessels until the 'apillaries, the gland cells, etc., are filled with them, and carry in their track the work of destruction of the (A B) are near y all of the medul- pylephlebitis, obstruction or total closure of the larger biliary duets, with subsequent inflammation ofthe. interlobular connective tissue. The liver-in pyrrmir abscess-is usually of normal size, ‘ather anzemic; in the tissues as well as under the peritoneal covering are scattered a number of abscesses of about Zcentimctcrs diameter, surrounded byhype ‘almie tissue. A quantity ofyellm 'and brownish matter, tinged with some blood, is found in the abscess. Here and there-near the large ‘ abscesses chiefly-are goodsizcd portions of the tissue in a state of partial degene ‘acy and infiltration with fat. They are g ‘ayish yellow and show g ‘adual softening and formation of abscesses. In abscess from pyltqihlebitis and compression of the liver cells there is found thrombosis of the portal vein and suppurative inflammation of the interlobular connective tissue, near the veins; great dilatation of some biliary ducts, innume 'able miliary absces es in the liver, inflammation of the spleni - and mesenteric veins, abscesses in the brain, seropurulent peritonitis, swelling ofthe intestinal walls and follicular *atarrh, ulcers in the duodenum and rectum, swelling of the mesenteric glands, tumors of the spleen, emphysema of both lungs. Fatty degene ‘ation of the biliary ducts sometimes produces abscesses in the liver and are followed by per- forating abscesses into other cavities, chiefly into the thoracic or abdominal cavity and formation of filn'o-purulent, peritonitis, peris carditis, or pleuritis. Besides transitory dilatations of the hepatic vessels there may be formed permanent vascular dilatation in consequence of inflammation of the parenchyma of the liver or from ha'lnostasis either in the cardio-pulnmnie circulation or in the gene ‘al circulation of the body. Occasionally the 'ascular lesion is confined to a limited part ofthe organ. The affected portions are remarkable by the dark color in the widened veins, or by palcness of the tissue. which is partly compressed. There is usually but little histological alteration to be noticed in this disease. Dgflimr C7o'on/c Im/«owl/rr Jar/annnr/Hon. Ah‘up/u'e (on! IIyprrtroy/Hie (,llil‘l'lroxiis‘ of? Mr Jilit't'i'. Chronic indurative inflammation is tlv'ays insidious and slowly progressive. Very seldom is it the sequel of an acute process. The first stages consist of considerable infiltration of lymphoid cells in the interstitial tissue. The periportal connective tissue is chiefly, and the most early. involved part. Gradually the indurative prtn-ess passes into the lobular parenehyma. As a rule the lesion is formed in spots; very seldom is it ditfused over the whole organ. Subsequent to the infilt‘ation is formation of connective tissue produced from large fibroblasts, that is, cells with very t'ansparent nuclei. Steadily the disease progresses by accumulating lymphoid and fibroblast cells in the capillaries and eventually formed con neetive tissue. \Vitb this intravascular infiltrate are associated extra 'aseular developments of connective tissue round the capillaries and between the lobular cell rows, which they at first compress and at last replace. I'ndcr such circumstances great quantities of parenehymatons cells are destroyed. The destruction ofthe cells is followed by pigmentation of the remaining tissue, from thedebris of the blood in the destroyed capillaries. A portion of the pigment is derived from the bile. which stagnates in the obstructed biliary ducts. After the indurative process has been going on for some months the connective tissue becomes hyperplastic. which also is first found in the periportal connective tissue, to which it is sometimes permanently eonfined, or from which the hyperplasm progresses toward and into the lobular structures. The cellular groups are driven apart and separated from thead'iacent capillaries. Some are destroyed. some remain and form wide biliary ‘anals comThe biliary municating with the still preserved biliary ducts. |