Managing gallbladder mucoceles (Proceedings)

A gallbladder mucocele is an enlarged gallbladder that contains an excessive amount of mucus. Histologically, the gallbladder mucosa is characterized by cystic mucosal hyperplasia, with or without inflammation or necrosis. Dogs with gallbladder mucoceles can be asymptomatic early in the course of disease. Clinical and biochemical abnormalities occur when mucoceles are complicated by secondary bacterial infection, extrahepatic biliary obstruction (from bile-laden mucus accumulation in the cystic, hepatic or common bile ducts), or marked distention of the gallbladder leading to ischemic necrosis, gallbladder rupture, and bile peritonitis. Gallbladder rupture is a common life-threatening complication. The incidence of gallbladder mucocele appears to be increasing and it is one of the most common causes of extrahepatic biliary tract disease in dogs.

The cause of gallbladder mucocele formation in dogs is unknown. Hyperlipidemia/hypercholesterolemia appears to be a risk factor and may be idiopathic (Shetland sheepdog, Miniature schnauzer) or secondary to pancreatitis, nephrotic syndrome, endocrinopathies (hyperadrenocorticism, hypothyroidism) or feeding a high fat diet. Administration of corticosteroids may be a contributing factor. A primary or secondary motility disorder of the gallbladder has also been proposed. In humans, gallbladder mucoceles form secondary to functional or mechanical biliary obstruction associated with cholecystitis, cholangitits, or cholelithiasis. However, predisposing disorders causing mechanical biliary obstruction (infiltrative disease of cystic duct, cholelithiasia) are not typically identified in dogs. A primary bacterial or inflammatory disorder of the gallbladder and biliary tract appear unlikely, since aerobic and anaerobic cultures are frequently negative and gallbladder inflammation is inconsistent. A recent report suggests that affected dogs (Shetland sheepdogs and other breeds with gallbladder mucocele) may have a disorder of gallbladder mucin secretion associated with a mutation in canine ABCB4 (phospholipid translocator protein). A dominant inheritance with incomplete penetrance is suspected. Genotyping for the ABCB4 mutation could allow early identification of at risk individuals, allowing for monitoring and early medical, dietary, or surgical intervention.

Gallbladder mucocele appears to be more likely in older (median age of 10 years) small to medium size dogs. No sex predilection is apparent. Shetland Sheepdogs, Cocker spaniels, and Miniature schnauzers appear to be at increased risk. Common clinical signs include anorexia, lethargy, vomiting, icterus, diarrhea, weight loss, PU/PD, abdominal discomfort, and abdominal distention. Signs are usually acute to subacute and less than three weeks in duration. Physical examination findings include depression, weakness, lethargy, abdominal pain, icterus, fever, hepatomegaly, tachypnea, and tachycardia. Most dogs with gallbladder rupture have abdominal pain. Some dogs with gallbladder mucocele are clinically (and biochemically) normal.

Common hematologic findings in symptomatic dogs include leukocytosis (mature neutrophilia or neutrophilic with left shift), and increased liver enzyme activity (ALP, ALT, AST, and GGT). Findings of hyperbilirubinemia, hypercholesterolemia, and hypertriglyceridemia are less consistent. Biochemical findings may be normal in some dogs with early gallbladder mucocele formation detected ultrasonographically. The ultrasonographic appearance of a gallbladder mucocele is characteristic. The gallbladder bile is echogenic and organized in a stellate or finely striated ("kiwi") pattern. As opposed to billiary sludge, a gallbladder mucocele is not gravity dependent. Ultrasonographic findings suggestive of secondary gallbladder rupture include loss of gallbladder wall continuity, hyperechoic fat or fluid around the gallbladder, free abdominal fluid, and striated or stellate echogenic material outside the gallbladder. Additional findings may include extrahepatic biliary obstruction and pancreatitis.

Medical management: When gallbladder mucocele is diagnosed in an asymptomatic dog and concurrent systemic disorders or risk of anesthesia precludes surgery, antibiotic therapy (amoxicillin 20 mg/kg PO q 12 hours or amoxicillin/clavulanate 12.5 mg/kg PO q 12 hours) to control secondary bacterial infections is recommended. Asymptomatic dogs may also benefit from treatment with ursodeoxycholic acid (UDCA) 20 mg/kg/day PO divided q 12 hours with food. The role of choleretics such as UCDA to prevent progression of mucocele formation is unclear. In addition to the general beneficial effects UDCA on the liver, it may reduce mucin secretagogue activity of gallbladder bile and may improve gallbladder motility. UDCA is contraindicated if biliary obstruction is present. S-adenosylmethionine (Denosyl/Nutramax Laboratory) 20 - 40 mg/kg PO once a day on an empty stomach may also be beneficial. Additional therapy is directed at identified risk factors and may include treatment of endocrinopathies (hyperadrenocorticism, hypothyroidism), low fat diet for idiopathic hyperlipidemia, and discontinuing corticosteroid therapy (if possible). The patient should be monitored biochemically and ultrasonographically every 4-6 weeks to assess response. If no improvement (or deterioration) is noted, surgical intervention is warranted. Resolution of gallbladder mucoceles with medical management has been described, but appears to occur infrequently. Further knowledge regarding underlying mechanisms and risks factors for gallbladder mucocele may improve results of medical management.

Surgical management: Cholecystectomy is indicated when a gallbladder mucocele is diagnosed ultrasonographically in a dog with clinical and biochemical evidence of hepatobiliary disease. If gallbladder rupture is suspected, emergency surgery is warranted. Cholecystectomy is also currently recommended for treatment of gallbladder mucocele in dogs (especially Shetland Sheepdogs) without clinical and biochemical abnormalities, since gallbladder rupture is a life-threatening and unpredictable complication. Pre-operative stabilization with fluid therapy and antibiotics is recommended. Broad-spectrum antibiotic therapy (amoxicillin combined with enrofloxacin) is commonly used to treat secondary bacterial infections of the biliary tract or if gallbladder rupture is suspected. Antibiotic therapy should be based on results of culture and sensitivity testing of bile or peritoneal fluid (rupture) when possible. If a coagulopathy is detected, vitamin K1 (0.5-1.5 mg/kg SC q 12 hours for 3 doses) is given for 24-48 hours prior to surgery. At surgery, the gallbladder is often markedly distended and firm, with dark serosal discoloration. The gallbladder contents appear as a shiny, greenish black to brown gelatinous material that often has a striated pattern. Cholecystectomy (rather than cholecystotomy) is recommended. The bile ducts should be flushed to remove any residual gelatinous material. If gallbladder rupture has occurred, abdominal contamination with mucocele contents is present. The abdominal cavity should be thoroughly flushed. Abdominal drains may be necessary if septic peritonitits is present. The excised gallbladder should be submitted for histopathologic examination. A liver biopsy and aerobic and anaerobic bacterial cultures of bile should be routinely performed. Liver biopsy findings are non-specific and include mild to moderate portal hepatitis and fibrosis with bile duct proliferation and vacuolar hepatopathy. Antibiotics should be continued for 4 to 6 weeks. Acute pancreatitis may be a concurrent finding or a post-operative complication of gallbladder mucocele surgery.

The longterm prognosis after cholecystectomy appears to be excellent, if the dog survives the post-operative period. Post-operative complications include sepsis and biliary infection, leakage at the surgery site with bile peritonitis, obstruction of the common bile duct by residual mucus, and acute pancreatitis. Mortality rates are similar in dogs with gallbladder rupture and prompt surgical intervention compared to dogs without gallbladder rupture. Although a dramatic decrease in liver enzymes and bilirubin occurs after surgery, some dogs have mild persistent liver enzyme elevations that may be due to a concurrent chronic inflammatory hepatopathy.

Suggested Reading: Center SA. Vet Clin North Am 39:543-598, 2009; Mealey KL. Proceedings of the ACVIM Forum 2010:452-453; Walter R et al. JAVMA 232:1688-1693, 2008; Aguirre AL et al. JAVMA 231:79-88, 2007; Crews LJ et al. JAVMA 234:359-366, 2009.