Miscellaneous Hepatic Disorders in Large Animals

Diseases of the gallbladder are rare in ruminants. Obstruction may be associated with liver fluke infestation, foreign bodies, abscesses, neoplasia, suppurative cholecystitis, or abdominal fat necrosis. Rupture of the gallbladder has been reported in a cow. Cholangitis (inflammation of the bile ducts) may occur in horses as an acute disease or as an acute exacerbation of chronic progressive hepatitis. Fever, depression, anorexia, weight loss, variable colic, icterus, and alterations in hepatic enzyme activity may be evident in affected horses. Treatment consists of longterm antimicrobial and supportive care as indicated.

Hepatic failure in neonatal foals may follow septicemia (especially septicemia due to Actinobacillus equuli), endotoxemia, perinatal asphyxia, Leptospira pomona infection, equine herpesvirus 1 infection, hepatic duct obstruction secondary to gastroduodenal obstruction, biliary atresia, and iron toxicosis. Gastric ulcers and duodenitis in foals can cause strictures of the duodenum and subsequent cholangiohepatitis due to bile stasis. Neonatal isoerythrolysis and hemolysis may cause hypoxic and cholestatic hepatic disease.

Biliary atresia (extrahepatic) is a rare congenital defect; it has been described in individual case reports of foals and in a neonatal lamb. Affected foals presented for anorexia, depression, lethargy, poor growth, colic, polydipsia, polyuria, pyrexia, and icterus at 1 month of age. Markedly increased plasma gamma-glutamyl transferase (GGT) and bilirubin with mildly increased sorbitol dehydrogenase (SDH) supported a diagnosis of biliary obstruction. A diagnosis of biliary atresia was confirmed at necropsy.

Hemochromatosis is an iron storage disease in which hemosiderin is deposited in the parenchymal cells, causing damage and dysfunction of the liver and other tissues. The disease is either primary (idiopathic) or secondary. It is reported in humans, Mynah birds, Salers cattle, and horses.

In Salers cattle, hemochromatosis appears to be a homozygous recessive condition with inappropriate intestinal absorption of iron, excessive hepatic storage, and eventual loss of hepatic function. In horses and cattle, increased iron is deposited in the liver.

In cattle, clinical signs include decreased weight gain, poor body condition, dull hair coat, and diarrhea. In both horses and cattle, plasma GGT, alkaline phosphatase (AP), AST, SDH and total bile acids are increased. Serum iron, total iron binding capacity (TIBC), and percentage saturation of the TIBC are usually normal. Iron content of the liver tissue is greatly increased in horses (normal 100–300 ppm) and cattle (normal 84–100 ppm).

Diagnosis of hemochromatosis is based on history, clinical signs, and laboratory findings. Differential diagnoses include iron toxicosis from exogenous sources, and diseases causing chronic weight loss and hepatic dysfunction or disease.

Phlebotomy to remove blood and decrease the iron stores has been used in the treatment of humans with hemochromatosis, but it is not effective in large animals.

Right hepatic lobe atrophy in older horses has been proposed to result from chronic compression of this portion of the liver by the right dorsal colon and base of the cecum. With chronicity, the portal circulation to the right lobe is impaired, resulting in hepatic anoxia, deprivation of nutrients, and gradual atrophy of the right lobe of the liver. No evidence of biliary tract disease has been noted. Colic may occur. Some horses may have clinical signs not related to the GI tract.

Hepatic lobe torsion can be a rare cause of colic in horses. Liver enzymes and fibrinogen are increased; abdominal fluid analysis varies. Bacteria, including Clostridium spp, may be found in the necrotic portion of the liver. Exploratory celiotomy is required for a definitive diagnosis.

Hepatic amyloidosis is characterized by the extracellular deposition of amyloid, a proteinaceous fibrillar substance, in the tissue. Deposition of amyloid within an organ distorts normal tissue architecture and possibly function. In horses, the liver and spleen are the most common organs affected by systemic amyloidosis. Reactive or secondary systemic amyloidosis with deposition of amyloid A (AA) fibrils in the liver has been associated with severe parasitism and chronic infection or inflammation in horses.

Congenital hepatic fibrosis is a rare condition that has been identified as a recessively inherited autosomal genetic defect in Swiss Freiberger horses.(1) A similar condition has been reported in a calf.

In primary hyperammonemia of adult horses, blindness and severe neurologic signs are observed. The etiology of this syndrome is unknown, but a primary intestinal problem with overgrowth of urease-producing bacteria within the intestine is suspected. Excessive ammonia production is believed to ensue, overwhelming the liver's ability to metabolize it through the urea cycle.

Primary hyperammonemia is nearly always associated with enteric disease, diarrhea, or colic. Diarrhea and, in some cases, protein-losing enteropathy may persist for several days. In most cases, diarrhea or colic precedes the neurologic signs by 24–48 hours. Laboratory abnormalities include increased blood ammonia concentrations (200–400 mcmol/L), severe metabolic acidosis, and profound hyperglycemia (250–400 mg/dL). Plasma concentrations of liver enzymes, total bile acids, and bilirubin are normal.

In most horses, neurologic signs resolve within 2–3 days with supportive care (intravenous fluids, potassium chloride, glucose, sodium bicarbonate) and administration of drugs (eg, lactulose, neomycin) to decrease ammonia absorption.

Portosystemic shunts occur rarely in foals and calves. Hyperammonemia and neurologic signs result from liver dysfunction with little laboratory or microscopic evidence of liver disease.

A syndrome of depression, ill thrift, and hyperammonemia with a variable extent of hepatic involvement occurs in Morgan foals. Affected foals are often related, but a genetic cause has not been determined. Clinical signs are usually first observed around weaning time. Encephalopathy may temporarily improve with aggressive supportive care, but it recurs after withdrawal of treatment. Liver enzymes and blood ammonia concentrations are increased. Bilirubin concentration is often normal. Pathologic hepatic lesions include portal and bridging fibrosis, bile duct hyperplasia, karyomegaly, and cytomegaly. The disease is fatal.