PARENCHYMATOUS HEPATITIS, ACUTE YELLOW ATROPHY OE THE LIVER.

The characteristic morbid lesion in this disease is the degeneration of the liver cells, loss of their protoplasm and nuclei and of their normal functions. It may be circumscribed to limited areas, or may affect the liver, generally. As the hepatic functions, are so intimately related to those of the bowels and kidney, the affection is usually accompanied by inflammations of these organs as well.

Causes in horses. The same general causes which produce congestion, may also determine the further morbid stage of inflammation. Cadeac mentions a case which developed in a horse kept alone and idle in the stable. He makes no mention of condition, food, cleanliness nor ventilation. Haubner and Franzen have traced it to a diet of malt or of hay harvested from inundated meadows. Zundel records a case following exposure to extreme cold. More commonly the disease is secondary to the overtaxing of the liver, by heavy feeding in warm moist climates, or in hæmoglobinæmia, or to the arrest of the micro-organisms of the food, or of infectious diseases.

Causes in Cattle. These suffer rarely, but from essentially the same conditions. It has followed aphthous fever (Eletti), and arisen under a forcing ration, in hot weather (Callot, Cruzel), or under overwork (Cruzel).

Causes in Dogs. Most cases result from infection by way of the stomach and intestines, or by the transfer to the liver of the ptomaines and toxins of such infections. It is thus related in its origin to catarrhal jaundice and hyperæmia.

Lesions. In the earliest stage with albuminoid exudation into its substance the liver may be greatly enlarged, its sharp edges rounded, and its consistency softened. After a week’s illness atrophy may have set in and the organ appears shrunken and of ocherous yellow. In the early stages there may be sanguineous engorgement, the cut surface may bleed freely, and small extravasations may show throughout the liver substance, later the clay yellow hue, the granular aspect and the absence of blood on the cut surface are characteristic. The margins of the adjacent acini are indefinite or lost, and under the microscope the hepatic cells are charged with granules (albuminoid, fatty and pigmentary), while the nuclei are no longer demonstrable.

In cattle the liver may be double the normal size and at first of a deep purple red, which may change later to the earthy yellow.

In dogs the liver is tumid and yellow, and marked by small pea-like centres of softening. There is marked softening and the microscope reveals the characteristic degeneration of the hepatic cells.

Symptoms in the Horse. These resemble those of congestion rendered more intense and therefore somewhat less obscure. The attack is usually sudden, there may be rigor followed by hyperthermia, dullness, pendent head, drooping eyelids, injected conjunctiva with a yellowish tinge, unsteady gait and slight indications of colic. There is anorexia, partial suppression of urine, and what is passed is thick, glairy and brownish red, fæces are passed with pain, and groaning, probably from compression of the liver, the heart beats violently, while the pulse is small, breathing accelerated and perspiration abundant. The temperature rises (101° to 106°) and remains high throughout unless lowered through biliary intoxication. Percussion over the liver and especially on the right side shows increased area of dullness and marked tenderness. On the second or third day the icterus usually increases, and a slight fœtid diarrhœa may set in with marked fœtor of the pale or colorless discharges. The jaundice is not, however, a criterion of the danger, as it may become less marked or entirely disappear because of the extensive degeneration of the hepatic cells and the arrest of the formation of bile.

Diagnosis in the horse. The disease is recognized by the coincidence of fever, with great depression, icterus, painful defecation, constipation followed by a fœtid diarrhœa with lack of color in the stools and by increased area of dullness and tenderness in the region of the liver and especially on the right side. From influenza which it resembles in many respects, it is distinguished by the absence of watery discharge from the eyes, and by the entire absence of all indication of contagion. The cases occur one at a time.

Prognosis in the horse. The disease is exceedingly fatal. When the kidneys remain active, the poisons are eliminated and there may be hope of recovery, but when urine is suppressed an early death by poisoning is to be expected.

Treatment in the horse. A most important indication is to secure depletion from the portal system. Calomel 1 dr., aloes 4 drs., ipecacuan 1 dr. may be given in bolus, and followed by small daily doses of sulphate and nitrate of soda with bitters, with or without the ipecacuan. Action on the kidneys is essential to secure elimination of the poisons which threaten a fatal poisoning if retained. To favor the same action fomentations may be applied to the loins. The frequent presence of pathogenic microörganisms either in the bowels or liver suggests the use of germicides (salol, salicylic acid, salicylate of soda, naphthalin, naphthol, beta-naphthol, etc.) as in catarrhal jaundice. Sinapisms or blisters applied to the right side of the chest and over the short ribs may be useful, and after the subsidence of the more violent symptoms, dilute mineral acids and especially nitro-muriatic acid may be resorted to in combination with diuretics and bitters.

When appetite returns succulent, laxative, non-stimulating food in small quantity should be given. Wheat bran mashes, carrots, turnips, potatoes, apples, fresh grass, ensilage may be adduced as examples. Throughout the disease the ingestion of an abundance of pure water should be encouraged.

Symptoms in the ox. These may appear more tardily than in the horse, loss of appetite, staring coat, dullness, pendent head and ears, unsteady movements, rigors, drivelling of saliva from the mouth and grinding the teeth are usually noted. To these are added the more diagnostic symptoms of slight (or severe) jaundice, constipation followed by a fœtid light colored diarrhœa, a strong disposition to remain recumbent, marked suffering attendant on rising, arching of the back when up, and tenderness on percussion over the right hypochondrium. The temperature gradually rises, though more slowly than in the horse, and may again descend under a profound poisoning.

Course. The disease reaches its acme in four to six days, and generally has a fatal issue.

Treatment, is on the same lines as for the horse only as a purgative, sulphate of soda may advantageously replace the aloes.

Symptoms in the dog. The symptoms are those of congestion in an exaggerated form. There are muscular tremors, erection of the hair, followed by rising temperature up to 105° or 106°, an icteric hue of the mucosæ, the pulse is accelerated, strong, irregular, respiration rapid, panting, fœtid breath, ventral decubitus, and prostration extreme. Appetite is completely lost, the bowels become relaxed, the stools fœtid, the right hypochondrium painful on pressure or percussion, and the urine greatly reduced and icteric or suppressed. This feature of urinary suppression, determines a rapid poisoning and death in two or three days.

Treatment must follow the same lines as in other animals, a purgative of calomel and jalap, followed by diuretics, laxatives, derivatives, and above all germicides. In case of survival mineral acids, aqua regia, bitters, and a carefully regulated diet will be in order.