Fatty liver syndrome was first described in the 1950s as excessive fat in the liver associated with varying degress of hemorrhage. The condition is almost universally confined to caged birds fed high-energy diets, and is most often seen in summer months. The liver is usually enlarged, yellow or putty colored, and very friable. The abdominal cavity contains large amounts of fat. Fatty liver syndrome without excessive body fat is thought to be associated with mycotoxins (eg, aflatoxins) in feed. See mycotoxicoses, Mycotoxicoses: Introduction . The affected birds may also have pale combs. The ovary is usually active and the metabolic and physical stress associated with oviposition may be factors that induce the fatal hemorrhage, although mortality generally is <5%Because fatty liver syndrome seems to occur only when birds are in a positive energy balance, the monitoring of body weight is a good diagnostic tool. Through force-feeding techniques, it has been shown that fatty liver syndrome is caused by an oversupply of energy rather than by an excess of any specific nutrient, such as fat or carbohydrate. The condition can be induced experimentally in layers and even male birds by the administration of estrogen, reinforcing the concept that it occurs more frequently in high-producing birds that presumably are producing estrogen from very active ovaries.

The condition is easy to recognize at necropsy due to the liver hemorrhage and also the fact that the liver is often enlarged and engorged with fat. This makes the liver friable, and it is difficult to remove each lobe in one piece. The pale yellow color of the liver, while characteristic, is not always specific to this condition. Normal layers fed appreciable quantities of yellow corn will also have a yellow liver. Also, liver color may be indicative of dietary xanthophylls rather than fatty liver syndrome, because the condition can be induced by force-feeding semi-purified diets devoid of pigment; these birds lack the characteristic yellow liver. Birds with fatty liver syndrome have 40-70% fat in the liver dry matter. In many studies, the degree of fatty liver syndrome is described via a liver hemorrhage score, which is usually based on a scale from 1-5, in which 1 = no hemorrhage, 2 = 1-5 hemorrhages, 3 = 6-15 hemorrhages, 4 = 16-25 hemorrhages, and 5 = >25 hemorrhages, including a massive, usually fatal, hemorrhage.

Attempts have been made to prevent or treat the condition through diet modification. Substituting carbohydrate with supplemental fat, while not increasing the energy content of the dietary, seems to be beneficial. Presumably such modification means that the liver needs to synthesize less fat for yolk. Replacement of corn with other cereals, such as wheat and barley, is often beneficial. However, this substitution may involve a reduction in dietary energy level or may necessitate the use of additional fat to maintain isoenergetic conditions, and these 2 factors are known to influence fatty liver syndrome. The syndrome has reportedly been reduced through the use of various byproduct feeds such as distiller’s grains and solubles, fish meal, and alfalfa meal. Although the mode of action is unclear, unintentional supplementation of selenium may be involved. Addition of 6% oat hulls to the feed has been successful at times. Fatty liver syndrome is best prevented by not allowing an excessive positive energy balance in older birds. Body weight can be monitored and when potential problems are seen, remedial action taken to limit energy intake through the use of lower energy diets and/or change in feed management. A wide energy:protein ratio in the diet will aggravate fatty liver syndrome. On farms with history of fatty liver syndrome, the diet should be supplemented with 0.3 ppm selenium, up to 100 IU vitamin E/kg diet, and appropriate levels of an antioxidant such as ethoxyquin.