Abdominal Fat Necrosis in Large Animals

Hard masses of necrotic fat are occasionally identified in the peritoneal cavity of mature cattle, especially the Channel Island breeds (Jersey, Guernsey), Japanese Black cattle, and beef cattle grazing fescue for long periods. Abdominal fat necrosis also occurs in goats and some species of deer maintained on pastures consisting primarily of tall fescue.

The fat masses are commonly mistaken for a developing fetus on palpation per rectum because they feel like “floating corks,” similar to cotyledons. Clinical signs are uncommon; however, in cases in which many masses are present, an extraluminal intestinal obstruction can result in episodes of moderate abdominal pain, distention of the proximal intestine, and decreased fecal production. A 2025 outbreak of abdominal fat necrosis affecting reproductive tissues in cattle has also been reported (1).

The specific etiology of abdominal fat necrosis in cattle is unknown; one proposed cause is consumption of feeds containing high concentrations of long-chain saturated fatty acids. Fat necrosis most commonly occurs in beef cattle ≥ 2 years old after prolonged grazing of tall fescue infected with the endophyte Epichloë coenophialum. Fat necrosis occurs throughout the southeastern US, where tall fescue is the primary pasture plant for grazing.

Overconditioning, genetic factors, and lack of exercise may be associated with fat necrosis in cattle. Steatitis can precede abdominal fat necrosis in cattle; however, this term is not generally used to describe lesions in this species.

Hard masses of necrotic fat form in the omentum, mesentery, and perirenal fat. The masses are usually flat and rarely pedunculated and can cause clinical signs when they compress the abomasum, small intestine, and spiral colon; obstruct the birth canal; or, more rarely, compress the ureters.

Palpation per rectum is useful in diagnosis and in determining prevalence in a cattle herd. Advanced cases in aged dairy cows can be detected by abdominal ballottement with the identification of large firm masses in the abdomen. Ultrasonographic examination of the abdomen reveals the presence of hyperechoic masses of variable size in the omentum, with free or localized masses appearing to float in excessive peritoneal fluid. Hyperechoic masses adjacent to intestines can be associated with luminal constriction.

A presumptive diagnosis of abdominal fat necrosis can be made by means of ultrasound-guided biopsy of the echogenic masses or by direct biopsy during right flank exploratory laparotomy. Less commonly, isolated fat masses can be found freely floating in the peritoneal fluid at surgery.

The size of the masses usually slowly increases; however, spontaneous resolution can occur. Removal of cattle from fescue pastures or dilution of fescue intake by supplying legume or other grass pastures can slowly decrease the size of masses. Isoprothiolane (50 mg/kg every 24 hours, PO, for 8 weeks) increases lipolysis of adipose tissues and inhibits lipid deposition into adipocytes, reportedly decreasing the size of fat necrosis lesions in Japanese Black cattle (2). This treatment is not permitted in the US.

In affected deer herds, 90% of females can be affected with fat necrosis. Clinical signs include gradual onset of anorexia, depression, and uremia due to large masses of necrotic abdominal fat obstructing the ureters, causing hydroureter and hydronephrosis.

Abdominal fat necrosis in companion animals is less well defined and appears to be related to pancreatitis. Although not associated with specific clinical signs, the lesions (discrete or confluent masses of necrotic adipose tissue) are usually confined to peripancreatic fat. However, fat necrosis lesions can also be found throughout the abdomen. One small study found histopathological pancreatitis in the majority of Japanese Black cattle with abdominal fat necrosis and a correlation between pancreatic fibrosis and abdominal fat necrosis (3).

Steatitis, or inflammation of adipose tissue, affects many species, including sheep, pigs, horses, and cats. This condition, which is relatively rare, can progress to overt fat necrosis and formation of discrete necrotic masses.

There are several case reports of steatitis in yearling or younger horses, with occasional reports in older animals (4, 5, 6, 7). In affected animals, vitamin E deficiency and diets high in polyunsaturated fatty acids are risk factors. Horses with diffuse steatitis develop clinical signs of systemic inflammation, and reported mortality rates vary from 25% to 100%; reported comorbidities include laminitis and fat embolism (4, 5, 6, 7).

Steroids have been reported as treatment for steatitis in horses; however, they should be used judiciously, according to risk of laminitis. Steatitis localized to the cutaneous fat is called panniculitis and is associated with firm masses of cutaneous fat inflammation that can lead to necrosis. Steatitis is also called yellow fat disease; affected adipose tissue develops a yellow discoloration as a result of oxidative damage and lipofuscin accumulation.