Part 84

CONGESTION OF THE LIVER IN THE DOG.

Active congestion is very rare excepting in over-fed and indolent family pets. Passive congestion induced by diseases of the lungs and heart is however far from uncommon.

Lesions. True to their origin these usually appear as the spotted nutmeg liver with the deep congestion in the centre of the acini. For the same reason the fibroid degenerations shown in chronic cases, show the firm fibroid neoplasm chiefly around the hepatic veins. Granular, fatty and pigmentary degeneration of the cells are found as in the solipeds.

Symptoms. These are as obscure as in the horse. There is always a history of a sluggish, gourmandizing life, and in the early stages, a manifestation of embonpoint which suggests a torpid liver. Further suggestions may also be obtained from coexisting diseases of the lungs, or heart, from gastro-intestinal catarrh, from piles, or ascites. Then there is at times a slight icterus of the conjunctiva and urine. Finally tenderness on percussion on the right hypochondrium, decubitus on the left side, and an increased area of dullness on percussion may afford useful hints for diagnosis.

Treatment. In the rare cases due to infection from the intestine, an active saline purgative followed by antiseptics (salol, naphthalin, naphthol, etc.,) daily will be of value. It is also desirable to keep up the action of the bowels by morning doses of salines. In cases consequent on chest disease attention must be given to such primary trouble. In all cases a restricted laxative diet, and graduated but increasing exercise in the open air are demanded.

HEPATIC HÆMORRHAGE OR RUPTURE.

Causes: Mechanical injuries, falls, blows, kicks, degenerations, amyloid, fatty, granular, congestion, neoplasms, glanders, tuberculous, myomatous, microbian infection. In the horse, disease of liver, heart, lungs, hepatic artery, portal vein, degenerations following overfeeding, idleness, foreign bodies, arsenic, phosphorus, parasites, violent movements in colic, running, draught, leaping. In the dog, pampering and traumatism. In cattle forced feeding, emaciation, microbian infection. In birds, tubercle, tæniasis, microbian infection. Lesions: extravasation, intracapsular, or through capsule into the peritoneal cavity. The extravasation bulges of a deep black, covering a dark softened, pulpy, hepatic tissue, with light colored fatty tissue around. Clots may be stratified from successive bleedings. Liver usually enlarged. Symptoms: onset sudden, or preceded by stiffness, soreness and other signs of hepatic trouble. Extensive rupture, entails weakness, unsteady gait, perspiration, pallor of mucosæ, small weak rapid pulse, palpitations, dilated pupils, rolling eyes, amaurosis, tremors, convulsion in case of survival, coldness, œdemas. Death in five hours to five days. Risk of relapse in recovering cases. Treatment: rather hopeless, rest, laxative, ergot, ferric chloride, tannic acid, witch hazel, cold water, snow or ice to right side. In meat producing animals fatten.

Causes. Hemorrhage and rupture of the liver are closely correlated to each other, the accumulation of extravasated blood in the parenchyma in the one case leading to over distension of the capsule, and the laceration of this capsule and of the adjacent substance of the liver occurring in the other as a mere extension of the first. They usually occur as the direct result of mechanical injury (falls, blows, kicks) acting on a liver already softened and friable through disease. These predisposing degenerations may be amyloid (Caparini, Johne, Rabe), fatty (Julien, Gowing, Adam, Siedamgrotzky), granular softening, hepatitis or congestion (Zundel), glander neoplasms (Mathis), tubercles, angiomata (Trasbot), microbian infection (Stubbe), tumors (Brückmüller).

In the horse predisposing conditions may be found in diseases of the liver, heart or lungs, in embolism of the hepatic artery (Wright), in obstruction of the portal vein (Pierre), in infarction of the liver, in degeneration with softening, in sarcomatous, melanotic, glanderous or cancerous deposits in its substance, in degenerations consequent on over feeding, idleness, congestions, on the penetration of husks of grains into the liver substance, on arsenical or phosphorus poisoning. The presence of flukes, echinococci and other parasites may also cause congestion and softening. To the immediate or traumatic causes above named may be added the violent movements attendant on a severe attack of colic, and violent exertions in running, draught, leaping, etc. (Friend).

In the =dog= we must recognize all the pampering conditions which predispose to congestion and degeneration, together with more direct operation of kicks, blows, falls, fights, over exertion, etc.

In =cattle= a forcing regimen is especially predisposing, and yet the loss of vigor resulting from a diametrically opposite treatment, must be accepted as an occasional cause. Stubbe found in emaciated cows miliary hemorrhagic infarcts of a dark red color which gradually extended to an inch or more in diameter. These he traced to microbian infection coming by way of the chronic intestinal lesions which are common in old cows. The final result of such infarctions was loss of hepatic substance and the formation of cicatricial tissue with a marked depression on the surface of the organ.

In =birds= fatal hepatic hemorrhages occur in connection with local tubercle (Cadiot), tæniasis of the liver, or microbian infection.

Lesions. The hemorrhage may take place into the substance of the liver only, or the capsule may be lacerated so that the blood escapes into the peritoneal cavity in considerable quantity.

In the horse it usually occurs in the right or middle lobe, rarely in the left. There may be one or more hemorrhagic effusions varying in size from a cherry to a duck’s egg, or even an infants’ head (Lorge). This projects from the surface of the organ and its deep black contrasts strongly with the white of the adjacent capsule. When laid open the hepatic tissue is seen to be softened and pulpy, and its dark color forms a striking contrast with any surrounding fatty liver. Any form of degeneration may be revealed on microscopic or chemical examination. Not unfrequently small clots of blood form under the capsule raising it in the form of little sacs. Such clots are usually stratified indicating a succession of small hemorrhages.

When the capsule is torn, the lesion may extend from one surface of the organ to the other, and the edges, smooth, uneven or fringed, are united together by a blood clot.

In case of hemorrhagic infarcts the lesion usually has a distinctly conical outline corresponding to the vascular distribution. These are especially characteristic of cases supervening on heart disease.

The volume of the liver is usually increased and the weight may reach 30 lbs. (Schmeltz), 34 lbs. (Lorge), or even 66 lbs. (Trasbot).

In other domestic animals analogous lesions are found modified largely according to the size of the subject.

Symptoms. These may develop instantaneously without any marked premonitory indication. In other cases tenderness on percussion over the liver, stiffness or groaning under sudden movements or turning, arching of the back, hanging of the head, slowness in rising, costiveness, slight transient colics, and even icterus may have been detected on close observation. The symptoms of actual rupture are essentially those of internal hemorrhage. The animal becomes weak, or unsteady upon its limbs, perspires, arches the back, and shows a marked pallor of the visible mucosæ. The pulse is small, thready, weak and accelerated, and the heart beats violent or palpitating. The percussion dullness over the liver is extended (Weber), the loins become insensible to pinching, and there may be some distension of the abdomen. Dilatation of the pupils, retraction or rolling of the eyes, amaurosis, tremors of the muscles of the neck, lying down, or falling, and general convulsions may precede death. This may occur in a few hours or it may be delayed if the lesions are restricted. In case of survival, coldness and œdema of the extremities and sheath have been observed. The lesser hemorrhages may terminate in recovery if there is no attendant incurable disease. In anthrax, glanders, cancer, tuberculosis, septicæmia, etc., a favorable issue is not to be looked for.

Duration. Termination. In severe cases a fatal issue may be expected in from five hours to five days. In the milder cases which make a temporary recovery there is great danger of a second hemorrhage from the new vessels in the tissue undergoing organization or from the adjacent degenerate liver tissue. The course of the affection may be altered by such complications as arthritis (Dieckerhoff), pneumonia, pulmonary thrombosis (Leblanc), enteritis or peritonitis (Cadeac).

Treatment is usually of no avail. Rest, and the administration of laxatives and hæmostatics, have been especially recommended. Of the latter, ergot by the mouth or ergotin subcutem, tends to contraction of the blood-vessels and to check the flow. Ferric chloride is also used, though apt to interfere with hepatic function. Tannic acid, hamamelis, and other astringents may be used instead. Cold water, snow or ice applied to the right hypochondrium may act as a check to the hemorrhage. Unless in purely traumatic cases in an otherwise healthy liver, a recovery is at best temporary, and the already degenerate liver is liable to relapse at any moment. In horses and dogs, therefore, recovery is by no means an unmixed good. Meat producing animals that recover should be prepared for the butcher.

HEPATITIS.

Forms of hepatitis: Parenchymatous hepatitis. Definition: Degeneration of hepatic cells. Relation to enteritis and nephritis. In horse—causes:—as in congestion, pampering, spoiled fodder, malt, inundated meadows, chill, overfeeding, hot moist climate, hæmoglobinæmia, infection. In cattle—causes:—forcing ration, hot weather, overwork, infection. In dog—causes:—infection from alimentary canal. Lesions: Enlarged, softened liver, round edges, a week later yellow atrophy, granular on section, bloodless. Acini with indefinite margins, cells granular, nuclei lost. In dog centres of softening. Symptoms:—in horse: Attack sudden, rigor, fever, dullness, prostration, yellowish red mucosæ, unsteady gait, slight colic, anorexia, urine decreased, glairy, brownish red, groaning in defecation, excited circulation and breathing, increased icterus by third day, fœtid, colorless diarrhœa. Diagnosis: Coincidence of fever, prostration, icterus, painful defecation, fœtid diarrhœa, light color of stools, tenderness and flatness on percussing hepatic area. From influenza by absence of watering eyes and contagion. Prognosis in horse: Very grave unless urine is free. Treatment in horse: Portal depletion, calomel, ipecacuan, salines, diuretics, fomentation of loins, antiseptics, derivatives, mineral acids, bitters. Careful laxative diet in convalescence. Symptoms in cattle: Slower onset, anorexia, dullness, depression, drivelling saliva, grinding teeth, icterus, constipation, later fœtid diarrhœa, pale colored stools, recumbency, groans on rising, arching back, tender right hypochondrium, fever. Prognosis grave. Death in five to six days. Treatment as in horse: Only saline laxatives. Symptoms in dog: Muscular tremors, staring coat, hyperthermia, icterus, fœtid breath, ventral decubitus, extreme prostration, anorexia, tender right hypochondrium, diminished urine, death in two or three days. Treatment in dog: Calomel and jalap, diuretics, laxatives, derivatives, germicides, in convalescence, mineral acids, bitters, careful diet.

The different forms of inflammation of the liver are distinguished according as they affect, especially the hepatic cells and tissue of the acini (parenchymatous), as they result in suppuration (suppurative, catarrhal, abscess), as they cause necrobiosis in nodular masses (infectious or necrotic), as they lead to fibroid thickening under the peritoneum and proper capsule (perihepatitis); or as they cause general fibroid induration of the organ by increase of its connective tissue (cirrhosis).

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).