Cholelithiasis, Choledocholithiasis, and Hepatolithiasis in Large Animals
Cholelithiasis in horses may cause biliary obstruction and concurrent liver disease or may be an incidental finding at necropsy. It most commonly affects middle-aged (6–15 yr old) horses with no sex or breed predilection. Solitary or multiple calculi may be present in the common bile duct (choledocholithiasis), intrahepatic bile ducts (hepatolithiasis), or bile duct or gallbladder in ruminants (cholelithiasis). In large animals, choledocholithiasis is the most common cause of biliary obstruction, with horses more frequently affected. The cause of cholelith formation in horses is not known. Ascending biliary tract inflammation (cholangiohepatitis), intestinal bacterial infection resulting in bile stasis, and a change in bile composition or cholesterol concentration have been proposed. Choleliths formed around a foreign body or parasites may occlude the common bile duct. Cholelithiasis and hepatolithiasis reportedly are not well recognized as a clinical problem in sheep and goats. Incidence in camelids is unknown.
Clinical signs commonly seen in horses with choleliths or cholangiohepatitis include weight loss, abdominal pain, icterus, depression, and intermittent fever. Signs of hepatic failure, including encephalopathy, photosensitivity, and coagulopathy, occur less frequently. Clinical signs are often intermittent. Complete obstruction of the common bile duct often is accompanied by persistent abdominal pain. Laboratory abnormalities include hyperbilirubinemia with increased direct (conjugated) bilirubin, a marked increase in serum γ-glutamyl transpeptidase or transferase (GGT) activity, and increased serum total bile acid concentration. Sorbitol dehydrogenase (SDH) and AST activities are increased but to a lesser degree. BUN, glucose, and potassium concentrations may be decreased. Metabolic tests indicate reduced hepatic function. Activated partial thromboplastin time and one-stage prothrombin time may be prolonged. Leukocytosis, anemia of chronic disease, hyperproteinemia, hyperglobulinemia, and hyperfibrinogenemia are often present due to inflammation. Histologic changes include periportal and intralobular fibrosis, moderate bile duct dilatation and proliferation, and cholestasis. Culture of the liver may reveal a bacterial infection.
Cholelithiasis should be considered in horses with a history of fever, icterus, and recurrent abdominal pain. Other signs of hepatic failure (encephalopathy, photodermatitis, weight loss) are less consistently seen with cholelithiasis. A marked increase in serum GGT with hyperbilirubinemia (direct bilirubin >25%) is supportive. Increases in SDH, AST, and alkaline phosphatase are often also present, but when absent despite an increased serum GGT make the presumptive diagnosis of biliary stasis more justified. Neutrophilic leukocytosis with inconsistent increase in globulin and fibrinogen concentrations are noted on leukograms. Ultrasonographic examination may reveal hepatomegaly with increased echogenicity of the liver, thickened distended bile ducts, and hyperechoic regions suggestive of choleliths. Choleliths in horses are most often visualized in the most cranioventral portion of the right lobe of the liver, especially in the sixth to eighth intercostal spaces. Choleliths may be hyperechoic, casting an acoustic shadow, or sonolucent. Stones may be seen as discrete calculi or less discrete sludge deposits within the biliary tract. The thickened distended bile ducts may appear as dilated channels adjacent to portal veins. Because of the large lung field of horses, choleliths may be missed on ultrasound examination.
Although biliary obstruction in horses is often fatal, choledocholithotripsy and choledocholithotomy have been performed successfully. Prognosis in cases requiring choledocholithotomy depends on the severity of concurrent cholangiohepatitis and on the size of the horse. The procedure is difficult because of limited exposure and poor visibility of the common hepatic duct. Complications include bile contamination, bile peritonitis, dehiscence, bile duct stricture, cholelith reformation, and enterocolitis (eg, stress-induced, salmonellosis). The prognosis is better if the obstruction is corrected by choledocholithotripsy.
When small calculi or less discrete sludge deposits are present, resolution by medical therapy may be successful. In addition, dissolution of bilirubinate stones, which are common in horses, may be facilitated by concurrent administration of IV dimethyl sulfoxide (<20% solution at 0.5–1 mg/kg). Dimethyl sulfoxide should be used cautiously or avoided in horses with coagulopathies or signs of hemolysis. Anti-inflammatory agents are administered to reduce inflammation and provide analgesia. Because cholangitis is often present, longterm broad-spectrum antimicrobial therapy is indicated. Antimicrobial choice is best guided by culture and sensitivity of the bacteria from a liver biopsy, bile duct aspirate, or from the cholelith. Supportive care is provided to manage any degree of accompanying hepatic insufficiency.