Fatty liver hemorrhagic syndrome (FLHS) was first described in the 1950s as excessive fat in the liver associated with varying degrees 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, putty colored, and very friable, and it contains varying degrees of hemorrhage. The abdominal cavity often contains large amounts of oily fat. Affected birds may have pale combs, likely as a consequence of reduced egg production. The ovary is usually active, at least in the early stages, and the metabolic and physical stress associated with oviposition may be factors that induce the fatal hemorrhage.

Because FLHS 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 FLHS is caused by a surfeit of energy rather than an excess of any particular nutrient, such as fat or carbohydrate. The condition can be induced experimentally in layers and even male birds by the administration of estrogen. This supports the concept that FLHS occurs more frequently in high-producing birds that presumably are producing estrogen from very active ovaries. Injecting immature pullets with testosterone also causes increased feed intake and liver fat accumulation, although without any major incidence of fatty liver.

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 FLHS. Normal layers that are fed appreciable quantities of yellow corn will have a yellow-colored liver. In birds with FLHS, the liver dry matter is at least 40% fat. The degree of FLHS can be described as a liver hemorrhage score, which is usually based on a scale of 1–5, where 1 = no hemorrhage; 2 = 1–5 hemorrhages; 3 = 6–15 hemorrhages; 4 = 16–25 hemorrhages; and 5 = >25 hemorrhages, as well as a massive, usually fatal, hemorrhage.

Attempts have been made to prevent or treat the condition through dietary modification. Substituting carbohydrate with supplemental fat, while not increasing the energy content of the diet, 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 FLHS. FLHS 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. There are reports of layers having greater incidence of fatty liver when fed chelated trace minerals compared to conventional inorganic minerals. However, the use of inorganic minerals in layer diets is increasing, and FLHS is not usually reported. There are also reports of association with Mycoplasma infection.

FLHS 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 FLHS. When a farm has a history of FLHS, the diet should contain at least 0.3 ppm selenium, up to 150 IU vitamin E/kg diet, and appropriate levels of an antioxidant such as ethoxyquin.

Last full review/revision March 2012 by Steven Leeson, PhD