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.
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.