Most choleliths in dogs and cats are clinically silent. Diagnosis of this disorder has increased subsequent to the increased use of abdominal ultrasound as a routine diagnostic modality. Choleliths are more common in middle-aged to older animals and incidence may be higher in small-breed dogs. Most choleliths in dogs and cats contain calcium carbonate and bilirubin pigments and are considered “pigment stones.” However, many do not contain enough mineral for detection on survey radiographs. Pigment gallstones are divided into 2 categories: “black-pigment” stones composed primarily of bilirubin polymers, reflect prolonged hyperbilirubinemia, while “brown-pigment” stones composed predominantly of calcium bilirubinate are associated with bacterial infections and biliary stasis. Mucin production, enhanced by local inflammation and prostaglandins, entangles calcium bilirubinate and bilirubin polymers into cholelith aggregates. This process is augmented by gallbladder dysmotility and bile stasis, creating a self-perpetuating process.

Clinical Findings and Diagnosis

Cholelithiasis may be associated with vomiting, anorexia, jaundice, fever, and abdominal pain. However, many animals remain asymptomatic. Laboratory features of cholelithiasis most commonly reflect related cholecystitis. In dogs with small duct lithiasis, clinicopathologic features reflect involvement of biliary structures (high AP and GGT activity). Jaundice is only directly related to cholelithiasis associated with EHBDO or sepsis; thus, many animals with cholelithiasis are not hyperbilirubinemic. Cholelithiasis may occur secondary to infection, or stones may promote infection. Mechanical trauma from choleliths may augment biliary tree infection. Consequently, high vigilance for signs of sepsis is warranted.

The hemogram may be normal or reflect inflammation or infection. A serum 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; skill and luck are needed to recognize stones lodged in segments of the common bile duct. For animals with small duct cholelithiasis, biopsy and culture of liver tissue is necessary to identify underlying disease processes and associated bacterial infections.

Treatment

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 should be performed followed by longterm monitoring for septic cholangitis. Chronic pulsatile antimicrobial administration may be needed to control retrograde infections of the biliary tree. Biopsy of involved biliary structures and liver is essential to determine if an underlying primary inflammatory, septic, or neoplastic disease predisposed 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 cholecystenteric 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.

Last full review/revision March 2012 by Sharon A. Center, DVM, DACVIM