In non-necrotizing cholecystitis, inflammation of the gallbladder may involve nonsuppurative or suppurative processes; may be associated with infectious agents, systemic disease, or neoplasia; or may reflect blunt abdominal trauma or gallbladder obstruction by occlusion of the cystic duct (eg, cholelithiasis, neoplasia, or choledochitis). Cystic duct occlusion incites gallbladder inflammation secondary to bile stasis; this process is augmented by mechanical irritation of a cholelith. The gallbladder wall thickens, and the lumen distends with a white, viscid, mucin-laden bile (white bile).
Necrotizing cholecystitis requires prompt surgical intervention (cholecystectomy and potential biliary diversion). Clinical signs develop acutely and include abdominal pain, fever, and increased liver enzymes. However, signs may remain vague and episodic, and hyperbilirubinemia is inconsistent. Middle-aged to older adult dogs are more commonly affected. Ultrasonographic detection of a thickened gallbladder wall or cystic bile duct and tenderness during the imaging procedure or on deep abdominal palpation may be the only evidence of illness.
Necrotizing cholecystitis may develop secondary to thromboembolism, blunt abdominal trauma, bacterial infection, EHBDO, cystic duct obstruction (choleliths, neoplasia), or a gallbladder mucocele. Extension of an inflammatory or neoplastic process from adjacent hepatic tissue also may be an underlying cause. Necrotizing cholecystitis can present with or without gallbladder rupture, or as a chronic syndrome associated with adhesions between the gallbladder, omentum, and adjacent viscera. Bacteria are commonly cultured from the gallbladder wall.
Diagnosis is based on clinical signs, clinicopathologic features, and ultrasonographic imaging. Because necrotizing cholecystitis is often associated with gallbladder mucocele in dogs, early intervention by prophylactic cholecystectomy may reduce need for emergency surgery.
Emphysematous cholecystitis/choledochitis is an uncommon condition associated with gas within the wall or lumen of the gallbladder or segments of the biliary tree. In dogs, it has been associated with diabetes mellitus, acute cholecystitis with or without cholecystolithiasis, traumatic ischemia, mature gallbladder mucocele formation, and neoplasia. Gas within biliary structure indicates serious septic inflammation associated with a gas-forming bacteria such as Escherichia coli or Clostridium spp. Treatment requires cholecystectomy and antimicrobial therapy based on culture and sensitivity of bile and involved biliary tissues. Broad-spectrum antibiotic coverage should be initiated before surgical exploration. Use of a β-lactamase resistant penicillin, with enrofloxacin and metronidazole, is initially indicated until culture and sensitivity results are available.
Signs of acute cholecystitis include abdominal pain (may only be postprandial), fever, vomiting, ileus, and mild to moderate jaundice. Some animals present in endotoxic shock. The hemogram discloses variable leukocytosis, with or without toxic neutrophils or a left shift. Hyperbilirubinemia and development of jaundice depend on chronicity, involvement of extrahepatic biliary structures, presence or extent of biliary tree occlusion, bile peritonitis, and endotoxemia. Liver enzyme activity is variable, but AP and GGT are usually moderately to markedly increased. Gallbladder rupture leads to pericholecystic abscess formation (localized by the omentum) or focal or generalized bile peritonitis. Abdominal radiography may reveal indistinct detail in the cranial abdomen consistent with focal peritonitis; a sentinel intestinal loop may implicate focal ileus. Rarely, the gallbladder wall may become radiodense due to dystrophic mineralization secondary to chronic inflammation. Choleliths may be found on ultrasonography. Detection of gas within the biliary tree or gallbladder heralds an emphysematous process associated with sepsis and should prompt antibiotic administration. Consideration of triage for emergency cholecystectomy is appropriate in some cases. Pericholecystic fluid can be sampled using ultrasonographic guidance to confirm bile leakage and infection. Comparison of total bilirubin concentration in effusion versus serum helps confirm bile leakage.
Treatment and Prognosis
Management focuses on restoration of fluid and electrolyte status, treatment with broad-spectrum antibiotics effective against enteric opportunists, and prompt surgical intervention. In some cases, colloids and plasma transfusion are necessary. Because EHBDO is a differential diagnosis, vitamin K1 should be administered (0.5–1.5 mg/kg, IM or SC, 3 doses at 12-hr intervals) before surgery to avoid hemorrhagic complications. If emergency surgery is necessary, fresh frozen plasma should be given judiciously based on coagulation tests and a buccal mucosal bleeding time. Careful exploration of all biliary structures is warranted. Patency of the cystic and common bile ducts must be determined and viability of the gallbladder ascertained.
A cholecystectomy is the treatment of choice in most cases. However, some animals benefit from a cholecystoenterostomy or choledochoenterostomy to circumvent a permanently occluded distal common bile duct. Placement of a temporary biliary stent may be appropriate but should be carefully considered first because of the high rate of complications, especially in cats. Samples of bile, gallbladder wall, choleliths, and liver tissue should be submitted for aerobic and anaerobic culture. Cytologic evaluations of tissue imprints and bile assist in initial antimicrobial selection (morphology and Gram staining). A combination of metronidazole, ampicillin clavulanate, and enrofloxacin provides broad protection against commonly encountered enteric opportunists. If only the gallbladder is involved, simple cholecystectomy may be curative. If the common bile, cystic, or hepatic ducts are involved, a more guarded prognosis is warranted, and longterm antibiotic therapy is recommended.
There are few adverse consequences of cholecystectomy, although episodic abdominal pain and diarrhea associated with fat malabsorption have been described. Cholecystectomy results in loss of the absorptive and pressure-regulating function of the gallbladder and the fasting reservoir where bile is concentrated. After cholecystectomy, the volume of bile increases due to reduced sodium resorption that normally occurs in the gallbladder, the size of the bile acid pool diminishes, and the enterohepatic circulation of bile becomes continuous. Bile composition shifts because of the increased exposure of bile acids to enteric flora and increased formation of secondary bile acids.
Animals that undergo biliary tree decompression by biliary enteric-anastomoses are susceptible to retrograde septic cholangitis and choledochitis. Dogs tolerate this procedure with fewer clinical signs than cats. Animals should be monitored for fever, inappetence, vomiting, and signs of cyclic illness. A CBC and liver enzyme measurement should be done quarterly. Chronic or intermittent antimicrobial administration may be needed to control ascending infection in biliary structures. However, illness is usually transient and responsive to antibiotics. Longterm survival with good quality of life is expected in the absence of neoplasia.
Last full review/revision March 2012 by Sharon A. Center, DVM, DACVIM