Cholecystitis in Small Animals

• Abdominal radiography

• Abdominal ultrasonography

• Comparison of total bilirubin concentration in effusion versus serum

Clinical signs of acute cholecystitis include abdominal pain (may only be postprandial), fever, vomiting, ileus, and mild to moderate jaundice. Some animals develop 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 alkaline phosphatase (ALP) and gamma-glutamyl transferase (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 antimicrobial 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 decrease need for emergency surgery.

Management of cholecystitis focuses on restoration of fluid and electrolyte status, treatment with broad-spectrum antimicrobials 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-hour 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 re-obstructed within 1 week, 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 antimicrobial treatment 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 decreased 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 antimicrobials. 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 treatment.