Cholelithiasis in Small Animals

Cholelithiasis may be associated with vomiting, anorexia, jaundice, fever, and abdominal pain. However, many animals remain asymptomatic or display postprandial discomfort (eg, stretching, position of relief, changing postures, wandering, pacing). Laboratory features of cholelithiasis most commonly reflect related cholecystitis or choledochitis, or cholangitis (intrahepatic choleliths or hepatolithiasis). In animals with small duct lithiasis, clinicopathologic features reflect involvement of biliary structures (high ALP and GGT activities). Jaundice is only directly related to cholelithiasis associated with EHBDO or sepsis; thus, many animals with cholelithiasis are not hyperbilirubinemic. Cholelithiasis may develop secondary to infection, or stones may promote infection secondary to amechanical trauma derived from choleliths. Animals with DPMs, especially Caroli malformation (sacculation of large intrahepatic bile ducts) are predisposed to intrahepatic cholelithiasis and infection. High vigilance for signs of sepsis is warranted in any animal with cholelithiasis.

The hemogram may be normal or reflect inflammation or infection. A serum biochemical profile may be normal or reveal high cholestatic enzyme activity or evidence of obstructive jaundice. Ultrasonography can detect stones >2 mm in diameter in the gallbladder; however, both skill and luck are needed to recognize stones lodged in segments of the common bile duct or in the hepatic bile ducts. For animals with small duct cholelithiasis, biopsy and culture of liver tissue is necessary to identify underlying disease processes and associated bacterial infections.

Medical treatment of cholelithiasis includes broad-spectrum antibiotics and a choleretic regimen of ursodeoxycholic acid at 15–25 mg/kg, PO, divided bid and given with food, and SAMe at 20–40 mg/kg/day, PO, on an empty stomach. Liver biopsy determines whether immunomodulatory therapy is appropriate. Vitamin E at 10 U/kg/day can be used for its antioxidant and anti-inflammatory effects.

Surgical intervention is necessary if choleliths are associated with cholecystitis, are causing cystic duct obstruction, or are occluding the common bile duct. Successful treatment of cholecystitis and cystic duct occlusion requires cholecystectomy and lavage of the common bile duct. The causal factors of cholelith formation must be carefully considered; retaining a diseased or dysmotile gallbladder imposes risk of recurrent lithiasis or necrotizing cholecystitis. In cases in which obstruction of the common bile duct is irresolvable, a cholecystoenterostomy is necessary, followed by longterm monitoring for septic cholangitis. Chronic pulsatile antimicrobial administration may be needed to control retrograde infections of the biliary tree thereafter. Biopsy of involved biliary structures and liver is essential to determine whether an underlying primary inflammatory, septic, or neoplastic disease is present and predisposing to cholelith formation. Tissue (liver, bile duct, gallbladder), bile, and cholelith nidus should be submitted for aerobic and anaerobic bacterial cultures.

Cholecystoduodenostomy and cholecystojejunostomy are the most common surgical procedures for biliary bypass in small animals. Cystoenteric anastomosis to the proximal duodenum is most physiologic, because it allows bile to enter the duodenum in a position that closely maintains normal physiologic responses in the proximal bowel to allow coordinated mixing of bile acids and pancreatic enzymes necessary for digestion and assimilation.