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 biliary system) has been reported in horses with chronic active liver disease. Mild behavior changes, weight loss, variable colic, icterus, and alterations in hepatic enzyme activity may be seen in affected horses. Treatment consists of longterm antimicrobial and supportive therapy as indicated.

Hepatic failure in neonatal foals may follow septicemia (especially Actinobacillus equuli), endotoxemia, perinatal asphyxia, Leptospira Pomona infection, equine herpesvirus 1, hepatic duct obstruction secondary to gastroduodenal obstruction, biliary atresia, and iron toxicity. 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. Administration of total parenteral nutrition may cause cholestasis and concurrent hepatic disease.

Biliary atresia (extrahepatic) has been reported in foals and in a neonatal lamb. Affected foals presented for anorexia, depression, lethargy, poor growth, colic, polydipsia, polyuria, pyrexia, and icterus at 1 mo of age. Markedly increased serum γ-glutamyl transpeptidase or transferase (GGT) and bilirubin with mildly increased sorbitol dehydrogenase (SDH) supported a diagnosis of biliary obstruction. 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 people, Mynah birds, Salers cattle, and horses.

The right lobe of the liver is the largest lobe in young horses but frequently atrophies in older animals and becomes fibrous. Right hepatic lobe atrophy was previously considered an incidental postmortem finding, but some consider it to be a pathologic condition.

Right hepatic lobe atrophy has been proposed to result from chronic compression of this portion of the liver by the right dorsal colon and base of the cecum. Feeding horses high-concentrate, low-fiber diets may contribute to atony of the right dorsal colon with resultant distention; this compresses the right hepatic lobe against the visceral surface of the diaphragm. Although there is no morphologic evidence of direct vascular impairment to the right hepatic lobe, vascular compromise may result secondary to compression. 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 be seen. Some horses may have signs not related to the GI tract.

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

Amyloidosis refers to disease characterized by the extracellular deposition of amyloid, a proteinaceous fibril 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. (Also see Amyloidoses.)

In a retrospective study of the records from the University of Berne, Institute of Animal Pathology, 30 Swiss Freiberger foals with pathologic lesions compatible with congenital hepatic fibrosis were identified. Affected foals were 1–12 mo old (average 3.7 mo). Most showed signs and had clinicopathologic changes reflecting severe liver damage. Pedigree analysis traced the disease back to one stallion. Results suggest that congenital hepatic fibrosis in Swiss Freiberger horses is a recessively inherited autosomal genetic defect. A similar condition has been reported in a calf.

In this syndrome of hyperammonemia, blindness and severe neurologic signs are seen in adult horses. The etiology is unknown, but a primary intestinal problem with overgrowth of urease-producing bacteria within the intestine is suspected.

The syndrome 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 hr. Laboratory abnormalities include increased blood ammonia concentrations (200–400 μm/L), severe metabolic acidosis, low plasma bicarbonate (≤12 mEq/L) concentration, and profound hyperglycemia (250–400 mg/dL). Serum concentrations of liver enzymes, total bile acids, and bilirubin are normal.

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

Portosystemic shunts are seen 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 degree of hepatic involvement is seen in Morgan foals. Affected foals have been related, but the cause of the syndrome is undetermined. Clinical signs are usually first seen around weaning time. Encephalopathy may temporarily improve with aggressive supportive therapy but 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.