Definition. Increase of connective tissue, decrease of gland parenchyma. Causes: in man, alcoholism; in animals, chronic heart disease, chronic recurrent perihepatitis, biliary obstruction, toxins. In horses: age, emphysema, unwholesome fodders, vegetable alkaloids, infection. Symptoms: prostration, hebetude, impaired appetite, colics, constipation, later diarrhœa, unthriftiness, emaciation, dropsy, icterus, ascites, intestinal catarrh, tender hypochondrium, early fatigue. Lesions: increase of connective tissue, compression and absorption of parenchymatous tissue, greatest around portal vessels, thickening of fibrous stroma between capillaries of acini, shrunken, granular, pigmented liver cells. Treatment: salines, Glauber salts, diuretics, sodium carbonate, or iodide, or salicylate, derivatives, mineral acids, bitters, open air, laxative food, pure water. In cattle: obstruction to circulation or the flow of bile; advances from the vessels, causes absorption, caseated foci, adhesions, enlarged liver. Symptoms: jaundice, yellow, red, albuminous urine, chronic indigestion, tends to fatal though slow advance. Treatment: green food, open air life, saline laxatives, alkalies. In dog: common following heart disease, parasites, bacteria. Lesions: Congested brownish red liver, fibroid increase from Glisson’s capsule, compression of acini, their elevation above surface, fatty and pigmentary degeneration of hepatic cells, increasing sclerosis. Symptoms: as in parenchymatous hepatitis with slower advance, in time tender loins, brownish or reddish urine, ascites, intestinal catarrh, it may be icterus. Treatment: Correct cardiac troubles, digitalis, strophanthus, and intestinal, careful diet, mineral acids, bitters, pure water, saline laxatives, antiseptics, alkaline diuretics. Potassium iodide. Derivatives. Draw off liquid. Laxative non-stimulating diet.
Definition. An interstitial inflammation of the liver characterized by a great increase of the connective tissue and compression, atrophy and degeneration of the glandular elements.
The same final result may undoubtedly originate in various different primary morbid processes.
In man cirrhosis is looked upon as almost always the result of abuse of alcohol. In animals this cannot be the case, apart from a few kept in connection with breweries or distilleries.
In heart disease a long continued mechanical congestion of the liver causes compression and degeneration of the secreting cells in the centre of the acini (around the intralobular veins), while the peripheral portions undergo cell proliferation and increase of connective tissue.
In chronic or recurrent perihepatitis, a whole lobe may be compressed by the hyperplasia of the investing connective tissue, and the hepatic cells are degenerated and absorbed.
Overdistension of the biliary ducts from obstruction to the flow of bile (gall stone, catarrhal inflammation, constipation), leads to proliferation and hyperplasia in the walls of the biliary radicals throughout the entire liver.
The presence in the liver of toxic agents, ingested, or generated from microbian fermentation in the intestinal canal or liver is another recognized cause of connective tissue hyperplasia.
Cirrhosis of venous origin has been observed mainly in old horses, while hypertrophic cirrhosis from biliary obstruction occurs rather in the young (Cadeac). Bruckmüller records a case of the first kind in a horse with extreme pulmonary emphysema. Walley gives a bad condition of fodders as the main cause, virtually implying, in many cases, infective catarrh and obstruction of the biliary ducts.
A form of the disease prevails at Schweinsberg in Hesse, and has been variously attributed to spoiled fodders (Nicklas), to vegetable alkaloids and other poisons in the food (Friedberger and Fröhner), to clover, to telluric poisons (Redner), to infection (Meminger), and to heredity (Neidhardt). It is a suggestive fact that it is confined to the valleys of the Ohm, Glon, and Zusam where the land is peaty or swampy and subject to inundations, while it is unknown on the dry table lands (Friedberger and Fröhner). This strongly suggests intoxication with microbes or their deleterious products. The gastric catarrh that frequently attends the disease may point in the same direction.
Symptoms. These are too often general rather than diagnostic. Dullness, prostration, hebetude, yawning, hot, sticky mouth, lost, irregular or depraved appetite, colics, constipation or diarrhœa, dry, harsh coat, emaciation, weakness, œdema of the limbs, vertigo and drowsiness may be among the symptoms. More characteristic are icterus, abdominal distension from ascites, or congestion of the liver, yellow or high colored urine, intestinal catarrh, indigestion, and tenderness in the region of the liver. The mucosæ are usually pale at first and not always icteric later. On exertion the horse shows early fatigue, tumultuous heart beats and oppressed breathing.
The Schweinsberg disease often lasts for months, with alternate improvements and exacerbations, but almost invariably ends in death, and sometimes completely depopulates a stable.
Lesions. These consist primarily in the great increase of the connective tissue and the relative decrease of the hepatic tissue. This is usually mostly around the divisions of the portal vein and the periphery of the acini, but also in the end around the hepatic veins as well. When it has formed around the biliary canals there is a great increase of the liver (often doubled) and its edges have become rounded. Within the acini the increase of the fibrous stroma is seen between the radiating capillaries, and the hepatic cells are contracted, granular, pigmented, and comparatively destitute of protoplasm around the still persistent nucleus.
Treatment. Glauber salts to clear the bowels of offensive matter, and deplete from liver and portal vein, bicarbonate of soda or iodide of potassium to eliminate the poisons through the kidneys and to lessen the induration, and finally salicylate of soda as a liver stimulant and intestinal antiseptic are suggestive of the line of treatment that may be pursued. The saline laxatives and diuretics, and antiseptics may be changed for others according to special indications, and bitters and mineral acids may be resorted to. Counter-irritants to the right hypochondrium should not be neglected in case of local tenderness. In the otherwise fatal Schweinsberg disease, Imminger, Künke and Stenert had a remarkable success from the free use of potassium iodide, which suggests a cryptogamic origin, as this agent is so valuable in polyuria which results from musty fodder. In all cases, gentle exercise in the open air and a moderate ration of laxative food (green) are of great value. Above all the old suspected diet should be carefully avoided, also any impure water supply.