Part 88

Certain other factors must be taken into account. The inherited disposition to the production of fat which characterizes the improved breeds of butcher animals, and particular individuals of all breeds, mature age which predisposes to the deposit of fat in internal organs, old age which lessens the vitality of the cells, and hot, damp climates or stables, all operate more or less in determining the fatty change.

Lesions. In fatty degeneration the liver is enlarged, pale, bloodless, yellowish, its cut surface exudes an oily fluid which smears the knife, and it is so light that it floats on water. If scraped and the material drawn across a sheet of paper it forms a transparent oily stain. Under the microscope the liver cells are seen to be enlarged and to have their protoplasm and nuclei replaced by fat or oil. If due to obstruction in the heart or lungs the degeneration is greatest toward the centre of the acinus, if due to an infectious disease it is usually greatest towards its periphery. In infectious diseases too the liver is not pale yellow, but usually of a deep brownish or yellowish red. The degeneration may be local or general. McFadyean found a circumscribed lesion in an ox’s liver, of a bright ochreous color, and the cells completely transformed into fat cells, while the rest of the liver was sound. In the dog fatty areas, up to an inch in diameter, are not uncommon. The swollen cells pressing on the adjacent vessels, account for the bloodless condition, and favor the degenerative process.

Neyraud records a fatty liver of 28 ℔s. weight from the horse, and Kitt one of 10 ℔s. from the pig.

Symptoms. Like as in most chronic liver diseases the indications are uncertain. The conditions may, however, suggest fatty degeneration; if the patient is very obese; if it has had an abundant food, rich in hydrocarbons and carbohydrates, and little exercise; if it has received in food or water continuous doses of phosphorus, arsenic or antimony; if it has lived in a hot moist climate or stable; if there has been a tendency to costiveness and indigestion; if the patient is weak, easily fatigued and short-winded; if there is a slightly yellowish red tinge of the conjunctiva and if the urine is scanty and contains little urea. If the disease is more advanced and the animal emaciated, it may be possible in the smaller animals at least to manipulate the liver to make out its increase, its smooth surface, and its absence of tenderness.

Treatment. When met with in meat producing animals the best resort is to turn these over to the butcher. When in an animal which is mainly valuable for breeding purposes, or in horses or carnivora, something may be done to check the progress of the malady, and maintain at least the present condition. The value of this will of course depend on how far the disease has already progressed. Cows that have spent a winter in a hot swill stable are of little use afterward for breeding or dairy uses and advanced cases of fatty degeneration in the horse or dog hold out little hope of a satisfactory issue. For cases in the earlier stages, nothing can be better than a run at grass, where there is opportunity for shelter from the noonday sun. If the pasture is short and the animal has to exercise to secure a living, so much the better. If kept indoors the patient should have a clean, roomy airy box stall, with a moderate allowance of easily digested food, and laxatives and cholagogues daily such as Glauber salts, aloes, calomel, podophyllin or cream of tartar. Mineral acids, especially nitro-muriatic acid, and bitters may also be given. The preparations of iron are sometimes useful in maintaining the tone of the digestive organs and counteracting anæmia but they must be conjoined with diuretic doses of bicarbonate of soda.

There is great advantage in stimulating the skin, and active brushing, currying, hand-rubbing, and even cold douches may be resorted to.

AMYLOID DEGENERATION OF THE LIVER.

Degeneration of basement substance of connective tissue, swollen, transparent, homogeneous, colored mahogany brown by iodide. In wasting diseases, tubercle, cancer, malaria, dysentery, leukæmia, suppuration, ulceration, pleurisy, pericarditis, peritonitis, chronic catarrh, broncho-pneumonia, orchitis, biliary calculi, nephritis. Chronic. Lesions: Affected part swollen, sinks in water, bloodless, clear, smooth, homogeneous, yellowish or reddish gray, under compound solution of iodine becomes mahogany brown, under sulphuric acid dark violet. Extends from vessel walls to adjacent connective tissue. Symptoms: Of wasting diseases, but not diagnostic. Treatment: Unsatisfactory, directed to causative disease.

This is a condition in which the basement substance of the connective tissue, and especially of the walls of the vessels, becomes swollen and composed of a transparent, homogeneous substance, albuminous in character, and which stains of a deep mahogany brown on the application of a solution of iodine. The degeneration is usually associated with severe wasting diseases, in the human being with tuberculosis, syphilis, malignant tumors, malarial infection, dysentery, leukæmia, and chronic suppuration or ulceration, especially of the bones.

In the lower animals (horse, dog, ox, sheep, rabbit, poultry) it has been seen to attend or follow on similar cachectic conditions. In the horse it has been seen in connection with the effusions of pleurisy, pericarditis and peritonitis (Rabe), in chronic bronchial catarrh (Fischkin), in chronic broncho-pneumonia, and dilated right heart (Trasbot), in orchitis, phlebitis and cachectic states (Caparini), and in calculous obstruction of the biliary duct (Burgoin). In cattle it has accompanied chronic nephritis (Brückmüller), tuberculosis, leukæmia, etc. In lambs kept in confined stables, though well feed on oats (Werner). In long standing suppurations and in animals fed on distillery swill it has been observed.

It may last for months or years, and predispose to other disorders, functional and structural. It does not, however, interrupt secretion as bile continues to be formed.

Lesions. The affected part of the liver is enlarged, the entire organ in the horse may amount to 32 lbs. It is smooth and even, though thick and rounded at its inferior border, yet occasionally on the posterior aspect there may be hyperplasia and a rough irregular surface. The diseased liver is heavy and sinks in water, unlike the fatty liver. In the horse it is soft and friable or even pasty whereas in man it is firm and resistant. The cut surface is bloodless, smooth, clear, homogeneous and grayish, yellowish or reddish gray. When treated with a solution of iodine and potassium iodide it changes to a deep mahogany brown; if dilute sulphuric acid is then used it changes to a deep violet, almost black color. If the iodine solution is brushed over the smooth cut surface the mahogany color of the amyloid stands out in marked contrast with the bright yellow of the healthy hepatic tissue. The amyloid commences in the walls of the smallest arteries, in the media and intermediary layers of the intima, and thickens the walls so as to obstruct their lumen more or less completely and render the part comparatively exsanguine. It may extend to the connective tissue of the organ, but it is not certain that the hepatic cells are involved in the process. The cells are, however, pressed upon by the diseased vessels and stroma and undergo consequent fatty degeneration. The amyloid may be confined to but a small part of the liver or to its smaller blood-vessels or it may extend to the whole. In fowls it is always in multiple centres (Leisering). It may be found in other important organs, kidneys, spleen, lymphatic glands, intestinal mucosa, etc.

Symptoms are not diagnostic. If with an old standing, exhausting disease, paresis, weakness, emaciation and unfitness for work, there is loss of appetite, dryness of the mouth, congestion of the rectal mucosa, yellowish, whitish, or dark tarry fæces, and a slightly brownish or yellowish tinge of the visible mucous membranes (Rexante) it may be suspected. In fowls Leisering noticed, weakness, lameness, ruffling of the feathers and attacks of vertigo. Icterus, ascites and tenderness over the region of the liver may all be absent. In the absence of ascites, tympany, or an excess of fat in the smaller animals, manipulation may detect the considerable enlargement of the liver, and the characteristic smoothness, of its surface. In other cases some indication may, at times, be had from the increased area of dullness on percussion.

Treatment is essentially unsatisfactory even if a correct diagnosis can be made. The most hopeful course would be to correct the debilitating disease in which the amyloid seems to have originated. Diseased bones, ulcers, chronic suppurations, and catarrhs may be done away with, and at least any further advance of the degeneration arrested. Open air exercise and a green or otherwise laxative diet would be indicated. The amyloid in lambs fed on oats was corrected by a change of diet (Werner). As medication the alteratives, potassium iodide and potassium arseniate have been mainly resorted to. Bitters and iron may also be of use to build up the strength. The latter should be given with potassium bicarbonate.

BLACK PIGMENTATION OF THE HEPATIC CELLS. BROWN ATROPHY.

In horse. With melanoma and atrophy, or without, pigment granules fill hepatic cells, liver becomes brown or black. In calves. In sheep. Apart from melanosis, the real cause unknown.

The accumulation of granules of black pigment in the hepatic cells has been noticed in old and worn out horses (Louis Blanc, Cadeac, Bruckmüller), in calves (Degive, Cadeac), and in sheep (Siedamgrotzky, Barrier). In horses it has been found in connection with atrophy, or in other cases, with melanotic tumors in other parts. In atrophic cases the liver is small, puckered, brown and dull, with a leathery appearance on section, and with the hepatic cells charged with pigment granules so that each acinus has a stellate appearance from the radiating lines of cells. This constitutes brown atrophy.

The second form which may be called melanotic liver, is not associated with atrophy, but is characterized by the crowding of the hepatic cells with black pigment granules, which fill up the protoplasm and crowd the still pale nucleus to one side. The affected portions become of a deep black.

In calves the pigmentation may be confined to the superficial portion of the liver (Degive).

In sheep pigmentation may be in the peripheral cells only of the acinus (Cadeac) but is about equally distributed on the surface, and throughout the interior of the liver, and may extend to the stroma of the gland (Siedamgrotzky).

Apart from the general causes of melanosis, benignant or malignant, no definite reason for this pigmentation has been assigned. The development of melanæmia and tissue pigmentation in man from malarious microörganisms suggests that other germs and their products may have a similar effect in the lower animals but nothing certain is known as to the true cause.

Apart from melanosis, it is not known that this pigmentation of the hepatic cells is of any essential pathological importance. It is important however for the veterinarian to be acquainted with the condition, that he may intelligently deal with such lesions whether seen in ordinary post mortem examinations, or in the course of meat inspection.

DILATATION OF THE GALL BLADDER AND BILE DUCTS.

Causes: obstruction of common bile duct, distoma, round worms, tæmiæ, gall stones, encrustations, inflammations, tumors, cicatrices, hydatids. Congenital absence. Ducts stand out on liver. Symptoms of colic, icterus, bile poisoning, marasmus. Treat the causative conditions.

This may occur in all our domestic animals except solipeds in which latter there is no gall bladder.

Causes. Any serious obstruction to the discharge of the bile into the duodenum may cause it. The presence of trematodes, nematodes, or even tæniæ in the ducts, gall stones, incrustations, occlusion of the ducts by inflammatory swelling, tumors of the liver or adjacent parts, echinococcus, cysticercus, or cicatrices may be cited. Cadeac mentions a case of congenital atresia of the bile duct in the calf. Vigney records a case in the cow in which the greatly dilated gall bladder formed a hernial mass in the epigastric region which was, however, easily reduced by manipulation.

In all such cases the distended bile ducts stand out as white branching lines on the back of the liver converging toward the portal fissure. The walls of the ducts may be attenuated or thickened and it is alleged calcified. They are usually lined by a deposit of cretaceous consistency precipitated from the retained bile. The contents of the distended ducts and bladder are variable. They may have the color (yellow, green) and consistency of bile; they may be thick, dense and albuminous; they may be thin and serous from inflammatory or dropsical exudation; they may be granular, or purulent.

Though there is no gall bladder, in the soliped, a similar condition of the biliary ducts may be produced in the same way.