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Digestive System
Hepatic Disease in Small Animals
Biliary Tree Rupture and Bile Peritonitis in Small Animals
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  • Cholecystocentesis in Hepatic Disease in Small Animals
  • Liver Cytology in Small Animals
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  • Pathologic Changes in Bile in Small Animals
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  • Fulminant Hepatic Failure in Small Animals
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  • Hepatocutaneous Syndrome in Small Animals
  • Nodular Hyperplasia in Small Animals
  • Hepatic Neoplasia in Small Animals
  • Miscellaneous Liver Diseases in Small Animals
  • Diseases of the Gallbladder and Extrahepatic Biliary System in Small Animals
  • Cholecystitis in Small Animals
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  • Extrahepatic Bile Duct Obstruction in Small Animals
  • Cholelithiasis in Small Animals
  • Biliary Tree Rupture and Bile Peritonitis in Small Animals
  • Feline Cholangitis/Cholangiohepatitis Syndrome
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Biliary Tree Rupture and Bile Peritonitis in Small Animals

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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 biliary mucocele that stretches the gallbladder wall, 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 as 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. 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, continue 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 3 doses) before surgical intervention. Fresh frozen plasma may be necessary to abate bleeding tendencies during emergency surgery. Antiemetics are recommended if the patient is vomiting; H2-receptor antagonists are used if enteric bleeding is identified. In animals with cholelithiasis and in dogs with gallbladder mucocele, hydrocholeresis (ursodeoxycholic acid and SAMe) and antioxidants (vitamin E and SAMe) are recommended postoperatively.

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

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