Overview

• Chemical peritonitis due to release of free bile into the abdominal cavity.
• Can involve focal or diffuse peritoneal inflammation depending on chronicity and causal factors, and omental adhesions.

Signalment

• More common in dog than in cat
• No age, breed, or sex predilection

Signs

Causes & Risk Factors

• Limited arterial perfusion (cystic artery) to GB fundus predisposes to ischemic necrosis and GB rupture.
• Trauma to biliary structures-auto-mobile injuries, surgical, animal bites, gunshot wounds, cystic artery laceration during cholecystocentesis.
• Common bile duct (CBD): common site of rupture with blunt trauma.
• Cholecystitis/choledochitis-may derive from GB mucocele (GBM); sepsis more common with necrotizing cholecystitis.
• EHBDO-may derive from neoplasia, cholelithiasis, pancreatitis, duct stricture.
• Focal, small-volume, bile peritonitis-associated with cholecystitis; may reflect omental entrapment of bile or transmural bile leakage without rupture.
• Chemical peritonitis due to bile-predisposes to septic peritonitis.

Differential Diagnosis

• Conditions promoting inflammation/devitalization of biliary structures, e.g., cholecystitis, choledochitis, neoplasia, GBM, neoplasia, blunt trauma.
• Conditions causing EHBDO, e.g., neoplasia, choleliths, pancreatitis, duct stricture/fibrosis.
• Sepsis or endotoxemia.
• Ascites: in jaundiced cirrhotic patient.
• Non-hepatic conditions causing abdominal effusion and jaundice.

CBC/Biochemistry/Urinalysis

Other Laboratory Tests

Coagulation tests-abnormal if sepsis syndrome, DIC, or chronic EHBDO.

Imaging

• Abdominal radiography-reduced abdominal detail, generalized or focal in GB area; cranial abdominal mass effect; rare mineralized cholelith or biliary gas (emphysematous cholecystitis).
• Thoracic radiography-rare bicavity effusion (pleural effusion), signs of trauma (e.g., fractured rib, hernia).
• Abdominal ultrasonography-effusion; EHBDO-distended GB or CBD; cholecystitis /choledochitis-thick GB or duct wall; necrotizing cholecystitis-segmental GB wall hyperechogenicity, laminated wall (represents necrosis); pericholecystic fluid; hepatic /pancreatic mass effect: common with bile peritonitis; choleliths or GBM (“kiwifruit sign”); gas in GB or bile ducts (emphysematous inflammation, implicates gas-forming organisms) casting acoustic shadow; ruptured GB may be difficult to image; liver size usually normal; variable parenchymal echogenicity reflects hepatic pathology (e.g., ascending cholangitis, CCHS).

Diagnostic Procedures

• Abdominocentesis-physicochemical, cytologic, and culture evaluations; ultra-sound guidance optimizes sampling; sample close to biliary structures but avoid structure penetration.
• Cytology-impression smears of GB, liver, and bile (with particulate material) used for immediate detection of infection and neoplasia; modified transudate or exudate, phagocytized/free bile and bilirubin.
• Acellular mucinous material reflects biliary mucin production; GBM material may be free within abdominal cavity.
• Ratio of bilirubin in effusion:serum usually 2–3:1.
• Bacterial aerobic/anaerobic culture and sensitivity-effusion, GB wall, liver, GB contents; Gram-negative enteric opportunists and anaerobes most common; polymicrobial infection possible.
• Exploratory laparotomy-appropriate for definitive diagnosis and treatment; permits cholecystectomy, cholecysto-enterostomy, duct or GB repair.
• Liver biopsy-important, evaluates for antecedent or coexistent disease, sample distant to the GB to avoid artifacts.

Pathologic Findings

Depend on cause and site of rupture

Drug(s)

• Antimicrobials-in all patients, initiate broad-spectrum antimicrobials before surgical intervention; enteric Gram-negative and anaerobic organisms most common opportunists (good initial choices: ticarcillin, piperacillin, or third-generation cephalosporins, with enro-floxacin and metronidazole); customized antimicrobial treatment, thereafter based on cultures; continue antimicrobials 4–8 weeks if signs of infection confirmed by culture or on cytology.
• Vitamin K₁ (0.5–1.5 mg/kg IM or SC q12h for up to 3 doses)-all jaundiced patients before surgery.
• Prepare for blood component ± synthetic colloid therapy.
• Antiemetics if patient is vomiting-metoclopramide (0.2–0.5 mg/kg PO, SC q6–8h or 1–2 mg/kg/24h IV by CRI); ondansetron (0.5–1.0 mg/kg q12h, IV or PO, 30 minutes before feeding); maropitant (1.0 mg/kg/day IV, SC, PO, maximum of 5 days).
• H₂-receptor antagonists if gastric bleeding-famotidine (0.5–2.0 mg/kg PO, IV, SC q12–24h); sucralfate (0.25–1.0 g PO q8–12h).
• Ursodeoxycholic acid as choleretic and hepatoprotectant if GBM, choleliths, CCHS, or chronic hepatitis-may administer chronically if GBM or cholelithiasis: 10–15 mg/kg PO daily, divided, with food for best bioavailability.
• Antioxidants-Vitamin E (10 IU/kg/24h); S-adenosylmethionine (SAMe, with proven bioavailability and efficacy; (20 mg/kg PO daily 2h before feeding) until enzymes normalize, indefinitely if chronic hepatitis or CCHS, GBM, inspissated bile syndrome; choleretic influence requires higher dose (40 mg/kg/day).

Patient Monitoring

• Sequential hematologic, biochemical, and imaging tests.
• Repeat abdominocentesis to assess continued infection and/or bile leakage as indicated.

Possible Complications

• Cholangitis/cholangiohepatitis
• Pancreatitis
• Recurrent bacterial cholangitis if biliary-enteric anastomosis required

Expected Course and Prognosis

• High survival rate for dogs with sterile bile peritonitis, if successful surgery, depending on underlying cause.
• Higher mortality in septic bile peritonitis (up to 73%).
• Anticipate slow clinical recovery and normalization of liver enzymes but rapid resolution of hyperbilirubinemia with successful surgery.

See Also

• Cholecystitis
• Cholelithiasis
• Gallbladder Mucocele
• Hepatitis, Chronic

Abbreviations

• ALP = alkaline phosphatase
• CCHS = cholangitis/cholangiohepatitis
• CMD = common bile duct
• CRI = constant rate infusion
• EHBDO = extrahepatic bile duct obstruction
• GB = gallbladder
• GBM = GB mucocele