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Biliary Tree Rupture and Bile Peritonitis in Small Animals

By Sharon A. Center, BS, DVM, DACVIM, Department of Clinical Sciences, College of Veterinary Medicine, Cornell University

Rupture of the common bile duct, cystic duct, hepatic ducts, or gallbladder is most often associated with cholelithiasis, necrotizing choledochitis or cholecystitis, blunt abdominal trauma, or neoplasia. In dogs, necrotizing cholecystitis most often occurs as a result of a mature gallbladder mucocele that stretches the gallbladder wall to the extent of causing ischemic necrosis. Regardless of cause, rupture of any portion of the biliary tree can lead to bile peritonitis. Clinical signs may be minimal early in the disease process, consisting only of inappetence and vague abdominal discomfort. With chronicity, free bile initiates an inflammatory reaction (chemical peritonitis), an abdominal effusion accumulates, and vivid jaundice develops. Ultrasonography should guide collection of abdominal effusion as close to the biliary tree as possible, because this will increase detection of free and phagocytized bilirubin crystals and bacterial organisms. Abdominal adhesions develop with delay in diagnosis and complicate surgical remediation.

Surgical interventions are specific to the causal lesions and may involve biliary tree decompression, cholecystectomy, cholecystotomy, choledochotomy, biliary-enteric anastomosis, or bile duct stent insertion. A liver biopsy should be collected to identify antecedent or coexistent hepatobiliary disease. Portions of the ruptured structure, bile, and abdominal effusion should be sampled and cultured for aerobic and anaerobic bacteria. Affected tissue and adjacent and nonadjacent liver tissue should be biopsied. The abdominal cavity must be thoroughly lavaged with sterile warm saline to remove bile contamination. Antibiotic coverage against likely enteric opportunists (gram-negative bacteria) and anaerobic flora is recommended, eg, ticarcillin, piperacillin, third-generation cephalosporins, or enrofloxacin combined with metronidazole. Antimicrobial therapy should begin before surgery and, if sepsis is confirmed, continued for 4–8 wk. Antimicrobial selection should be guided initially by results of cytology and Gram staining, and adjusted based on results of culture and sensitivity. Animals with chronic jaundice should receive vitamin K1 (0.5–1.5 mg/kg, IM or SC, bid for up to three doses) before surgical intervention. Fresh frozen plasma may be necessary to abate bleeding tendencies during emergency surgery. Antiemetics are recommended if the animal is vomiting; H2-receptor antagonists are used if enteric bleeding is identified, because these act quickly. In animals with cholelithiasis and in dogs with gallbladder mucocele, hydrocholeresis (ursodeoxycholic acid and SAMe) and antioxidants (vitamin E and SAMe) are recommended postoperatively.