In non-necrotizing cholecystitis, inflammation of the gallbladder may involve nonsuppurative or suppurative inflammation; 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 more commonly affects middle-aged to older adult dogs and may develop secondary to thromboembolism, blunt abdominal trauma, bacterial infection, EHBDO (cystic duct obstruction or distal duct obstruction by choleliths, stricture, or neoplasia), or a mature gallbladder mucocele (causing tense gallbladder distention). 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.
Necrotizing cholecystitis requires prompt surgical intervention (cholecystectomy and potential biliary diversion). Clinical signs usually develop acutely and include abdominal pain, fever, and increased liver enzyme activity. However, signs may remain vague and episodic, and hyperbilirubinemia is inconsistent.
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 ALP 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 before surgical intervention. 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.
Diagnosis is based on clinical signs, clinicopathologic features, and ultrasonographic imaging. 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. Because necrotizing cholecystitis is often associated with gallbladder mucocele in dogs, early intervention by prophylactic cholecystectomy may reduce need for emergency surgery.
Management of cholecystitis 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 (plasma preferred to colloids). Because EHBDO is a differential diagnosis, vitamin K1 should be administered (0.5–1.5 mg/kg, IM or SC, three doses at 12-hr intervals) before surgery to avert 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 during surgery. Patency of the cystic and common bile ducts must be determined, and viability of the gallbladder ascertained as surgical assessments are made.
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 because of the high rate of complications, especially in cats. Cats with EHBDO secondary to pancreatitis demonstrate greater morbidity associated with this technique than dogs. In one case series of seven cats with EHBDO secondary to pancreatitis, after stent insertion, two cats reobstructed within 1 wk, one cat developed ascending cholangitis, two cats suffered chronic intermittent vomiting, and two cats died during the perioperative period.
Samples of bile, gallbladder wall, choleliths, and liver tissue should be submitted for aerobic and anaerobic culture. Cytologic evaluations of tissue imprints and bile help initial selection of antimicrobials (based on bacterial 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 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 because of reduced sodium and water 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 with increased formation of secondary bile acids.
Animals undergoing biliary tree decompression by biliary enteric anastomoses are thereafter 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 hemogram and liver enzymes should be monitored quarterly. Chronic or intermittent antimicrobial administration may be needed to control ascending cholangitis. Fortunately, illness is usually transient and responsive to antibiotics. Longterm survival with good quality of life is expected in the absence of neoplasia. Owners should be instructed to monitor the rectal temperature of animals with cyclic illness to detect episodes of septic cholangitis to enable institution of at-home antimicrobial therapy.
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 the 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.