Hard masses of necrotic fat are occasionally identified in the peritoneal cavity of mature cattle, especially the Channel Island breeds, Japanese Black cattle, and beef cattle grazing fescue for long periods. The disease has also been seen in goats and some species of deer maintained on pastures consisting primarily of tall fescue. The masses are commonly mistaken for a developing fetus on palpation per rectum because they feel like “floating corks” similar to cotyledons. The masses of necrotic fat usually do not cause clinical signs but in advanced cases can create an extraluminal obstruction that results in episodes of moderate abdominal pain, distention of intestine proximal to the fat, and the passage of small amounts of feces.
The composition of the deposits in cattle with fat necrosis is identical to that of fat of healthy cows. The abnormal fat deposition is confined to abdominal fat and is consistent with current understanding that abdominal fat is controlled in a different manner than fat deposits elsewhere in the body. Fat necrosis has historically been termed lipomatosis, but this term is now considered inappropriate because the masses are not neoplastic or hyperplastic.
The etiology is unknown, but one proposed cause is consumption of feeds containing high concentrations of long-chain, saturated fatty acids. Fat necrosis is most commonly seen in beef cattle ≥2 yr old after prolonged grazing of tall fescue infected with the endophyte Neotyphodium (Acremonium) coenophialum (also see Fescue Poisoning); fat necrosis is associated with endophyte infection rates of ≥65%. Fat necrosis is seen throughout the southeastern USA where tall fescue is the primary pasture plant for grazing.
Hard masses of necrotic fat form in the omentum, mesentery, and perirenal fat. The masses may cause clinical disease 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 may 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 localized masses appearing to float in an excess of peritoneal fluid. Hyperechoic masses adjacent to intestine may be associated with luminal constriction. A presumptive diagnosis of abdominal fat necrosis can be made using ultrasound-guided biopsy of the echogenic masses or by direct biopsy during right flank exploratory laparotomy. Less commonly, isolated fat masses may be found freely floating in the peritoneal fluid at surgery. The size of the masses usually slowly increases, but spontaneous resolution can occur. Removal of cattle from fescue pastures or dilution of fescue intake by supplying legume or other grass pasture can promote the slow reduction in the size of masses. Isoprothiolone (50 mg/kg/day, PO, for 8 wk) effectively decreases the size of fat necrosis lesions in Japanese Black cattle.
In affected deer herds, 90% of the females may be affected with fat necrosis. Clinical signs include slow development of anorexia, depression, and uremia associated with large masses of necrotic abdominal fat constricting the ureters, causing hydroureter and hydronephrosis.
A second form of abdominal fat necrosis in domestic animals, less well defined, appears to be related to pancreatitis. Although not associated with a clinical syndrome, the lesions (discrete or confluent masses of necrotic adipose tissue) are usually confined to peripancreatic fat. However, fat necrosis lesions may also be found throughout the abdomen.
A third form, a focal necrosis of abdominal and retroperitoneal fat (steatitis or yellow-fat disease), is seen most often in sheep but also in pigs, horses, cats, and other species. Little information is available about the condition in these species, but abdominal radiography or ultrasonography may help identify focal necrosis in cats.
Last full review/revision May 2014 by Peter D. Constable, BVSc (Hons), MS, PhD, DACVIM