Cholelithiasis in Small Animals

• Laboratory testing

• Ultrasonography

Cholelithiasis may be associated with vomiting, anorexia, jaundice, fever, and abdominal pain. However, many animals remain clinically normal or show signs of 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 alkaline phosphatase and gamma-glutamyl transferase activities).

Jaundice is directly related only to cholelithiasis associated with extrahepatic bile duct obstruction or sepsis; thus, many animals with cholelithiasis are not hyperbilirubinemic. Cholelithiasis may develop secondary to infection, or stones may promote infection secondary to a mechanical trauma derived from choleliths.

Animals with ductal plate malformations (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 are necessary to identify underlying disease processes and associated bacterial infections.

• Antimicrobial treatment

• Choleretics

• Cholecystectomy

Medical treatment of cholelithiasis includes broad-spectrum antimicrobials and a choleretic regimen of ursodeoxycholic acid at a daily dose of 15–25 mg/kg, PO, divided every 12 hours and given with food, and S-adenosylmethionine (SAMe) at 20–40 mg/kg, PO on an empty stomach, every 24 hours. Liver biopsy determines whether immunomodulatory treatment is appropriate. Vitamin E at 10 U/kg, PO, every 24 hours 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.