Part 87

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.

CIRRHOSIS IN CATTLE.

This has been recorded by different observers and usually as the result of some obstacle to the circulation, or of catarrh and obstruction of the biliary passages. Morot saw it in young calves, which showed greatly enlarged liver (in one case 24 lbs.) and kidneys, the former containing numerous cysts and marked sclerous thickening around the vessels. This advancing thickening of the connective tissue, causes increasing firmness of the liver and absorption, distortion and diminution of the lobules. Albrecht describes a chronic interstitial hepatitis with caseated centres (nontuberculous) many of them an inch in diameter. The liver is brown or grayish with whiter callosities which extend into its substance and make points of attachment to the diaphragm or other adjacent organ. The contrast between the fibrous layers and the hepatic tissue has been likened to a checker board (Höhmann). The enlarged liver may weigh 30 lbs.; in one remarkable case it weighed 300 lbs. (Adam). The bile is of a light color and mixed with mucus.

Symptoms. The symptoms are indefinite: a gradually increasing jaundice, the passage of yellowish red urine becoming more and more red and albuminous, and finally coagulating on the walls of the urethra or on the litter, chronic indigestion, salivation (Schäffer), weakness, breathlessness and more or less fever may give indications of the disorder. Höhmann failed to find tenderness of the right hypochondrium. The disease is liable to go on to a fatal issue, so that it is often sought to prepare the animal for the butcher.

Treatment will follow the same line as in the horse. Green food, pasturage, open air life, saline laxatives, and alkalies with a free use of potassium iodide to check the sclerosis will be indicated.

CIRRHOSIS IN THE DOG.

In the dog, cirrhosis is much more common than in the larger animals, in connection with idle pampered habits, the frequency of diseased heart and consequent disturbance of the circulation, and the presence of parasites in the liver or biliary ducts. Bacteria intoxication and infection are also common.

Lesions. The liver is at first tumefied, with hard consistency and rounded edges, and a deep brownish red color, but this is modified by the grayish fibroid hyperplasia which is especially abundant in and around the vaginal sheaths of the capsule of Glisson. In cases arising from diseased right heart or lungs the induration is rather concentrated around the hepatic veins. The contraction and shrinking of the fibroid hyperplasia as the disease advances causes the projection of the hepatic tissue in minute rounded elevations which give a peculiar uneven appearance to the surface of the organ. The fibroid growth gives a remarkable hardness to the liver which resists even the edge of a knife. The hepatic cells are the seat of fatty and pigmentary degeneration. Inflammation and tumefaction of the kidneys, and ascites are common features of the malady.

Symptoms. The general symptoms are as in parenchymatous hepatitis with a more tardy development. There are impaired or irregular appetite, dullness, sluggishness, in an obese animal short-windedness or palpitations on slight exertion, symptoms of disease of the heart, lungs or digestive organs, a spasmodic cough, constipation followed by relaxation of the bowels, nausea and vomiting. As the disease advances tenderness of the loins, the passage of brownish or reddish, albuminous urine, the formation of ascites and of gastro-intestinal catarrh may be noticed. Icterus may be entirely absent, but, with a flaccid abdomen, enlarged liver and spleen may be detected.

Treatment. The indications are to first combat the causes. Irregularities in the heart’s action may be met by digitalis or strophanthus; gastro-intestinal catarrh by a carefully regulated diet, with mineral acids and bitters; portal congestion by a free use of water and other diluents and by saline laxatives; intestinal fermentations by antiferments (salol, naphthol) and toxic matters in the blood by alkaline diuretics. For the liver hyperplasia, potassium iodide may be freely used. Blisters to the right side will occasionally prove useful. The ascitic fluid must be drawn off when it accumulates. A diet of milk, bread and milk, buttermilk and mush, or one in which albuminoid elements are in minimum amount and the action of which is laxative is to be preferred. Out door exercise is desirable.

CHRONIC ATROPHY OF THE LIVER.

Chronic Atrophy: In old horses: in right and spigelian lobes; others show hypertrophy. In ruminants, omnivora and carnivora: in areas compressed by tumors or parasites. Perihepatitis. Sclerosis. Remedy causes if possible. Fatty Degeneration: Oil globules in liver cells, pathological when they destroy the protoplasm. In ducks and geese on forced feeding. Causes: poisoning by phosphorus, arsenic, antimony, lead, phenol, iodoform, alcohol; excess of fat in food, spoiled fodders, colchicum autumnale, yellow lupins, bacteria, hemorrhages, inflammations, tumors, parasites; improved meat producing breeds, old animals, hot stables. Lesions: liver enlarged, pale, yellow, bloodless, knife in cutting is smeared with fat, oily stain on paper, liver cells enlarged, protoplasm replaced by fat or oil; may be circumscribed. Symptoms: obesity, over-fed in fats and starches, of fattening breed, kept in confinement, in hot moist environment, if fed certain poisons, with costiveness and indigestion, no endurance, short winded, slight icterus, scanty urine, little urea, later, emaciation, palpation of enlarged liver. Treatment: send to butcher, pampered horses, cows from swill stable, a run at grass, with shade trees, a poor pasture, salines, cholagogues, mineral acids, bitters, iron with alkalies, currying, massage, douches.

Acute yellow atrophy has been referred to under parenchymatous hepatitis but a chronic atrophy is also met with in all domestic animals.

In old horses it affects, by preference the right and spigelian lobes, the portal circulation of which is less direct because of the veins of supply leaving the parent trunk at right angles (Leblanc), and because these lobes are more exposed to compression by solid accumulations in the double colon (Kitt). In such cases a compensatory hypertrophy of the left and middle lobes is often observed.

In ruminants the lesion is often circumscribed to the areas that have undergone compression by tumors or parasites (echinococcus, actinomycosis), and there may be compensatory increase elsewhere in the organ.

In swine, dogs and cats the same conditions are operative. In all alike perihepatitis may be a causative factor, and sclerosis (cirrhosis), with contraction of the fibrous hyperplasia may also operate.

Symptoms are very obscure and treatment unsatisfactory unless the active causes can be recognized and arrested.

HEPATIC STEATOSIS. FATTY LIVER. FATTY DEGENERATION.

The presence of oil globules in the liver cells is normal and physiological, the liver acting to a certain extent as a store-house for fat. This is always a marked feature, in healthy animals on high rations, and taking little or no work, but so long as the protoplasm and nuclei of the cells retain the normal characters and functions the condition is not a morbid one. It may, however, become excessive, with great enlargement of the liver, and with the substitution of fatty granules for the protoplasm of the cells as in ducks and geese subjected to forced feeding, and the condition becomes a distinctly pathological one.

In true fatty degeneration the protoplasm of the hepatic cells is destroyed and replaced by fatty granules, the resulting condition being a permanent destruction of the cell for physiological uses.

Causes. The liver cells undergo fatty degeneration under the action of certain poisons like phosphorus, arsenic, antimony, lead, phenol, iodoform and alcohol. According to Neyraud oxide of antimony is given daily to fattening geese to hasten the development of fatty liver.

An excess of fatty elements in the food leads to the same result as shown first by Majendie in dogs, in which not only did the liver undergo this degeneration but the sebaceous glands of the skin secreted an excess of volatile fatty acids.

The cryptogams and their products on musty fodders determine a gastro-enteritis in herbivora, accompanied by fatty degeneration of the liver.

Colchicum Autumnale, and poisonous yellow lupin both determine this degeneration.

The products of a number of pathogenic bacteria have a similar effect. This has been noticed in the cat with bacillus pyocyaneus (Charrin), the cholera spirillum, pyæmic and septicæmic infection, contagious pneumonia of the horse, strangles, and ulcerative endocarditis. It has been long noticed to be a complication of pulmonary tuberculosis, the result in this as in other affections of the lungs having been attributed to lessened oxidation in the tissues. It occurs also in hæmorrhages, ruptures and inflammations of the liver and in passive congestions of the organ, the impairment of the normal functions (in the altered conditions of nutrition, or under the influence of poisons,) proving an important factor in the process. The same remark may apply to the fatty degeneration which complicates most other liver diseases, cirrhosis, catarrh of the bile ducts, distomatosis, echinococcus, carcinoma, and epithelioma.