Part 86

INFECTED HEPATITIS. NODULAR NECROBIOSIS OF THE LIVER.

In ox, sheep, pig, dog, horse. Necrotic areas projecting on surface of liver. Causes: bacteria, toxins, from bowels, womb, navel. Lesions: In cattle dirty gray nodules in brownish red liver, nodules firm, granular, necrotic, elements do not stain, later leucocytes and fibro-plastic growth in periphery. In lambs the nodules are white, common to the lungs and pleura, pathogenic to rabbit. In pigs nutmeg liver, cells without nuclei, fatty, granular, pathogenic to rabbits, guinea pigs, rats and young pigs. In dog, nutmeg liver, with violet areas, and white spots, 1–2 lines, having granular, fatty cells without nuclei. Symptoms: fever, constant lying, tarry fæces, icterus, tender right hypochondrium, and those of the primary disease. Treatment: antisepsis of primary seat, and bowels, elimination by kidneys, general antisepsis, stimulants, etc. Case usually hopeless. Prevention.

This has been observed particularly in cattle, but also in sheep, pig, dog and horse. It is characterized by the formation of circumscribed areas of gangrene, becoming hard, dry, yellowish and usually slightly projecting beyond the adjacent surface. Its infected character is shown by the presence in the lesion and adjacent parts of the hepatic tissue of an abundance of bacteria, which, from the varied description, appear to differ in different cases. The cause may however be safely stated as one of the bacteria of gangrene. It is alleged with some show of reason, that the lesion may be determined by the action of toxins and ptomaines produced by bacteria in the alimentary canal and carried to the liver with the portal blood (Cadeac). The bacteria themselves commonly come from the same source, (Stubbe), but also from the uterus (Berndt), the mammæ (LeBlanc), and above all from the suppurating or septic umbilicus. McFadyean in five cases found a long slender bacillus, Hamilton in a single case in the horse found cocci, Rivolta in an infectious hepatitis in sheep found bacterium subtilis agnorum, and Semmer found the same condition in young pigs from micrococci introduced through the diseased umbilicus.

Lesions. In cattle the liver has a general brownish red, or greenish white color, and shows projecting, hard nodules of a dirty gray color more or less tinged with yellowish brown. The margins of these hard nodules are very sharply defined, and on section show a homogeneous granular surface, devoid of areas of softening or of connective tissue, and formed of the hepatic parenchyma in a state of necrobiosis. The granules and nuclear elements do not stain like those of healthy liver. As the disease advances the periphery of the nodule may be invaded by leucocytes and become the seat of a fibro-plastic hypertrophy (McFadyean) with the ultimate formation of cicatricial tissue (Stubbe).

In lambs Rivolta found the necrosed nodules standing out as white patches under the capsule of the liver, but similar lesions were met with in the lungs and pleuræ, an observation which has been confirmed by Hanbold. The affection was conveyed by inoculation to the rabbit.

In pigs Semmer found nutmeg liver, deep red or grayish yellow, hypertrophied, the hepatic cells swollen and divested of nuclei but containing fatty and pigmentary granules. It was inoculable on rabbits, guinea pigs, white rats and on young pigs.

In the dog, Courmont and Doyon found congested liver (portal congestion) with projecting patches of a deep violet color and sharply defined borders, and one to two lines in diameter, also salient white spots with distinct outlines. In the white spots the hepatic cells had lost their nuclei and were charged with fatty granules.

Symptoms. These are indications of hepatic disease. In parturient cows, Berndt noted fever (102° to 104°), anorexia, stiffness, cough, labored breathing, intense thirst, constant decubitus, and constipation followed by lowering temperature, tarry fæces and icterus. The region of the liver was very sensitive to pressure or percussion. In the other animals the symptoms appear to be largely over-shadowed by those of the primary disease, but the same general indications of jaundice, hepatic tenderness and digestive disorder are superadded.

Treatment when it can be intelligently adopted, consists largely in evacuation and antisepsis of the seat of primary infection, and of the prima viœ, and in maintaining elimination by the kidneys. In this way, as in congestion and hepatitis, the concentration of the poison is as far as possible counteracted, and an opportunity may sometimes be furnished for the recuperation of the liver cells. As a rule, however, the case is hopeless, and thus preventive measures, by cleanliness, disinfection and antisepsis of the ascertained sources of the infection are indicated.

PERIHEPATITIS.

Inflammation of capsule of liver (external and Glisson’s). Causes: Traumas, infective diseases, phlebitis of the portal vein, chill, distomatosis. Lesions: Peritonitis and inflammation of the capsule in patches, yellowish gray exudate, fibroid thickening or pus. Adhesions to adjacent objects. Thickening of trabeculæ. Symptoms, tardy respiration and circulation, tender hypochondrium, colics, diarrhœa, painful defecation, moan with expiration. Slight cases recover. Sequelæ: compression of portal vein or bile duct, gastric catarrh, piles, etc. Treatment: Salines, alkaline diuretics, mineral tonics, bitters.

This is inflammation of the external capsule of the liver and Glisson’s capsule. It may arise from direct mechanical injury, or by extension of inflammation from adjacent structures, such as the peritoneum. It may also complicate contagious pneumonia in the horse, tuberculosis in the ox, pneumoenteritis in pigs, and also phlebitis of the vena portæ (Cadeac, Morot). It may follow a chill, or distomatosis.

Lesions. These are essentially peritonitis circumscribed by the liver, and extending to the proper capsule, and its vaginal investments of the hepatic vessels. It is usually limited to certain spots which become the seats of a yellowish gray exudation, with a tendency to fibroid development and thickening, but sometimes degenerating into pus. The deposits on the outer side of the hepatic peritoneum may develop false membranes and fibrous adhesions to surrounding objects, the diaphragm, omentum, stomach or intestine. The deposits under the peritoneum lead to similar fibrous development with hypertrophy or thickening of the capsule, the trabeculæ extending thence into the liver and the vaginal sheaths of the vessels. Such areas of thickening are revealed as depressed spots or patches of a white color, and showing a firm fibrous, pearly appearance when incised. Such lesions are not uncommon in the livers of horses, cattle and swine. In the pig they may have a violet, or brownish red color, but with spots of other colors—grayish or brownish (Kitt).

Symptoms. Dopheïde, who has studied the disease in cows and to a less extent in horses, found a reduction in pulsations (26 per minute) and respirations (6 per minute) in connection with a mild peritonitis, intestinal catarrh, colicy pains and diarrhœa. The conjunctiva is pale, the pulse compressible, the respirations unequal and accompanied by a moan, and the appetite impaired or lost.

If confined to mere spots on the liver, a restoration to apparently vigorous health may take place, but if extensive it may lead to compression and obstruction of the portal vein or bile duct, or to compression and atrophy of the liver, with corresponding symptoms.

Treatment. As in other congestions of the liver, the use of salines to deplete the portal system, and of alkaline diuretics are especially indicated, to be followed by bitters and mineral acids. Sinapisms and other counter-irritants to the region of the liver are of great service. If not complicated with abscess, or microbian infection, cases of this kind will often do well.

CIRRHOSIS OF THE LIVER. FIBROID DEGENERATION.

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 IN THE HORSE.

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.