Fatty liver hemorrhagic syndrome is a metabolic disorder of chickens typically causing sudden death of birds fed high-energy diets with limited exercise. Diagnosis is based on finding liver hemorrhage and enlarged, pale liver with fat at necropsy. The disorder can be controlled by monitoring feed intake and body weight when birds are in a positive energy balance. Changing the balance of carbohydrates and fat in the diet and supplementing with selenium may also help.
Fatty liver hemorrhagic syndrome (FLHS) is an economically important disease in the poultry industry, frequently occurring in caged high-production hens. Additionally, it is a leading noninfectious cause of death in backyard chickens (1).
Etiology and Pathophysiology of Fatty Liver Hemorrhagic Syndrome
Fatty liver hemorrhagic syndrome is a metabolic condition of chickens. The pathogenesis remains incompletely elucidated but likely involves nutritional, environmental, and hormonal factors.
FLHS is associated with a surfeit of energy intake, regardless of the source, in birds whose exercise is limited.
With the initiation of egg production, the estrogen concentrations in the serum increase, as does the fat content in the liver. Therefore, this condition is observed primarily in females.
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.
Epidemiology of Fatty Liver Hemorrhagic Syndrome
Fatty liver hemorrhagic syndrome affects chickens worldwide.
Risk factors associated with fatty liver hemorrhagic syndrome include female sex, high-energy diets, and restricted exercise. It occurs most often in warm summer months.
Clinical Findings of Fatty Liver Hemorrhagic Syndrome
Birds with fatty liver hemorrhagic syndrome are usually found dead without premonitory signs. Birds are found dead with pale comb and wattles (due to blood loss).
In addition to sudden death, FLHS is associated with decreased egg production.
Layers with FLHS have increased blood concentrations of estrogen, osteocalcin, and leptinlike protein. There seems to be concomitant upregulation in bone turnover, which is noteworthy in a laying hen that already relies on substantial daily flux of calcium in and out of the skeleton.
Lesions
Courtesy of Dr. Rocio Crespo.
The liver is usually enlarged, putty colored, and friable, showing varying amounts of hemorrhage (see Fatty liver hemorrhagic syndrome, chicken). 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.
Pallor (pale head, wattles, comb, or skin) is attributable to hypovolemic anemia.
Diagnosis of Fatty Liver Hemorrhagic Syndrome
Postmortem examination
In birds that have died suddenly, fatty liver hemorrhagic syndrome is recognizable at necropsy because of 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 extent 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
Controlled energy intake
Vitamin and mineral supplementation
Because sudden death is typical, treatment options for fatty liver hemorrhagic syndrome are limited. Therefore, control and prevention are key.
Control of disease can be achieved by monitoring body weight and daily feed intake. Energy intake should be limited; alternatively, supplemental fat can be substituted for carbohydrate, while keeping total energy stable.
On farms with a history of FLHS, diets should include appropriate concentrations or selenium (at least 0.3 mcg/g of feed) and vitamin E (up to 100 IU/kg of feed) or appropriate concentrations of an antioxidant such as L-tryptophan (1000 mg/kg of feed).
Key Points
FLHS is a metabolic disorder associated with high-energy diets and limited exercise that can result in sudden death in chickens.
The disease is characterized by a large amount of clotted blood in the abdomen, pale and friable liver, and abundant abdominal fat.
Reference
Trott KA, Giannitti F, Rimoldi G, et al. Fatty liver hemorrhagic syndrome in the backyard chicken: a retrospective histopathologic case series. Vet Pathol. 2014;51(4):787-795. doi:10.1177/0300985813503569
