Fatty liver hemorrhagic syndrome (FLHS) is a metabolic condition that affects chickens worldwide. Sudden death of birds in full production is the most common complaint. Key findings are excessive fat in the liver, associated with varying degrees of hemorrhage. The condition is associated with high-energy diets and restricted exercise. It occurs most often in warm, summer months.
Etiology and Pathophysiology of Fatty Liver Hemorrhagic Syndrome in Poultry
Fatty liver hemorrhagic syndrome is associated with a surfeit of energy intake, regardless of the source, in birds whose exercise is limited. Additionally, this condition is observed primarily in females. With the initiation of egg production, the estrogen levels in the serum increase, as does the fat content in the liver. FLHS can be induced experimentally in layers and even male birds by administration of estrogen. This suggests that FLHS occurs more frequently in high-producing birds that presumably are producing more estrogen from active ovaries.
Clinical Findings of Fatty Liver Hemorrhagic Syndrome in Poultry
Affected birds are usually found dead without clinical signs. Layers with FLHS have increased blood levels of estrogen, osteocalcin, and leptin-like protein. There seems to be concomitant upregulation in bone turnover, which is significant in a laying hen that already relies on substantial daily flux of calcium in and out of the skeleton.
The liver is usually enlarged, putty colored, and friable, showing varying degrees of hemorrhage. The abdominal cavity often contains large amounts of oily, unsaturated fat. The ovary is usually active, at least in the early stages of FLHS, and the metabolic and physical stress associated with oviposition may be factors that induce the final, fatal hemorrhage. Affected birds often have pale combs, either due to reduced egg production or blood loss.
Diagnosis of Fatty Liver Hemorrhagic Syndrome in Poultry
Liver hemorrhage and fat engorgement in birds that have died suddenly
Fatty liver hemorrhagic syndrome is easy to recognize at necropsy because of the liver hemorrhage and because the liver is 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, although characteristic, is not always specific to FLHS. Normal layers fed appreciable quantities of yellow corn or high levels of xanthophyll pigments will also have a yellow-colored liver but without associated hemorrhages. A number of specific diet ingredients can induce liver hemorrhage but without concomitant accumulation of excess fat. Likewise, feeding rancid fat can cause liver hemorrhage, again without fat accumulation. In birds with FLHS, the liver dry matter is characteristically at least 40% fat.
The degree of FLHS can be described as a poultry liver hemorrhage score, which is usually based on a scale of 1–5:
1 = no hemorrhage
2 = 1–5 hemorrhages
3 = 6–15 hemorrhages
4 = 16–25 hemorrhages
5 = >25 hemorrhages, as well as a massive, usually fatal, hemorrhage
Fatty liver disorder also impairs calcium metabolism in the bird, thus affecting skeletal integrity and eggshell quality.
Control and Prevention of Fatty Liver Hemorrhagic Syndrome in Poultry
Monitor body weight and daily feed intake.
Substitute supplemental fat for carbohydrate, while keeping total energy stable.
On farms with a history of FLHS, diets should include at least 0.3 ppm selenium.
Because FLHS occurs more frequently when birds are in a positive energy balance, body weight and daily feed intake should be monitored. When potential problems are seen, remedial action to limit energy intake through the use of lower energy diets and/or change in feed management should be considered. Additionally, birds should be restricted from exposure to high temperatures, as these temperatures are more likely to result in a positive energy balance.
Experimentally, most attempts to prevent or treat the condition have been made 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 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 reduce the dietary energy level or necessitate using additional fat to maintain isoenergetic conditions, two factors known to influence FLHS. A wide energy:protein ratio in the diet will aggravate FLHS.
Various byproduct feeds such as distiller’s grains, fish meal, and alfalfa meal reduce the incidence of FLHS. Supplementation with selenium also has been shown to reduce FLHS, but the mode of action is unclear. When a farm has a history of FLHS, the diet should contain at least 0.3 ppm selenium, ideally as organic selenium, and up to 100 IU vitamin E/kg diet, with appropriate levels of an antioxidant such as ethoxyquin. There are reports of layers having greater incidence of fatty liver when fed chelated trace minerals versus conventional inorganic minerals. However, the relation between the increased organic minerals in layer diets and the incidence of FLHS is unknown. These various additives collectively help to limit the occurrence of tissue rancidity and thus hemorrhage of the excess fat in the liver.