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Canine Gallbladder Mucocele


This canine disorder is characterized by progressive accumulation of tenacious mucin-laden bile, which may extend into the cystic, hepatic, and common bile ducts, resulting in variable degrees of bile duct obstruction. Progressive expansion of a biliary mucocele leads to gallbladder ischemia and necrosis, bile peritonitis, and sometimes opportunistic infection. A gallbladder mucocele should be considered when sequential ultrasonographic examinations fail to indicate a reduction in gallbladder size or content after feeding, and confirm lack of movement of luminal “sludge.” Gallbladder stasis, perhaps reflecting dysmotility, and distention predispose to cholecystitis.

Affected dogs are 3–14 yr old; there is no gender predisposition but incidence is increased in Shetland Sheepdogs, Miniature Schnauzers, and Cocker Spaniels.

Factors predisposing to gallbladder mucocele formation include middle to older age, hyperlipidemia or hypercholesterolemia, gallbladder dysmotility, and cystic hyperplasia of the gallbladder mucosa. The inciting cause of mucus hypersecretion is unknown and may be multifactorial. Decreased gallbladder motility leads to luminal bile stasis and enhanced absorption of electrolytes and fluid, promoting biliary sludge formation. Dogs with risk factors may rapidly mature a developing mucocele after beginning glucocorticoid therapy or a high-fat diet (eg, some diets for renal disease or hepatic insufficiency). Because concurrent VH is common, associated underlying disorders should be investigated.

Symptomatic illness averages ~5 days, although some dogs have vague episodic signs (ie, inappetence, vomiting, vague abdominal pain) for months. In decreasing order of frequency, clinical signs include vomiting, abdominal pain, anorexia, jaundice, tachypnea, tachycardia, PU/PD, fever, diarrhea, and abdominal distention. Dogs progressing to gallbladder rupture demonstrate abdominal pain, jaundice, tachycardia and tachypnea, and fever. Clinicopathologic indicators include leukocytosis with a mature neutrophilia and monocytosis; high liver enzymes including AP, GGT, ALT, and AST; and hyperbilirubinemia. Aerobic bacteria may be cultured from bile or gallbladder wall, with a number of enteric organisms identified including, Escherichia coli, Enterobacter spp, Enterococcus spp, Staphylococcus spp, Micrococcus spp, and Streptococcus spp. Ultrasonographic-guided cholecystocentesis should not be performed if a gallbladder mucocele is apparent. Ultrasonography may detect hepatomegaly and either a heterogeneous or hyperechoic hepatic parenchyma. Hypoechoic “nodules” correspond to a severe VH with formation of reticulin defined nodules and regenerative repair. After gallbladder removal, sequential hepatic ultrasonographic evaluations are necessary to determine if parenchymal lesions resolve.

Histologically, cystic mucosal hyperplasia of the gallbladder wall is a common finding. All dogs have thick biliary debris, some components may be profoundly viscous and mucin laden, others more liquid; some dark green to black, some with white bile; some contain gritty black material, and some contain a firm, organized gelatinous matrix. Transmural ischemic necrosis may develop leading to necrotizing cholecystitis and gallbladder rupture. Liver biopsies may disclose a VH or mild to moderate portal hepatitis or fibrosis; the later changes reflect associated cholangitis or transient biliary tree occlusion. Some dogs lack concurrent hepatic lesions.

Dogs without signs of mucocele leakage or biliary tree obstruction at the time of initial diagnosis may benefit from hydrocholeresis induced by administration of ursodeoxycholic acid (15–25 mg/kg, PO, divided bid and given with food), SAMe (20–40 mg/kg/day, PO, after an overnight fast; food should also be withheld for 2 hr after dosing), and antimicrobial coverage. Biochemical and ultrasonographic evaluations every 6 wk are useful to monitor treatment response or syndrome progression. Rarely, an apparent gallbladder mucocele may resolve with medical treatment only. Progression in any parameter indicates poor control and the need for surgical intervention.

Cholecystectomy is the best course of treatment and is essential for most dogs with clinical signs and clinicopathologic findings consistent with biliary tree inflammation or rupture. Because bile stasis predisposes to infection, broad-spectrum antimicrobials should be initiated before surgical manipulation of the biliary structures. Examination and staining of cytologic preparations of the bile and imprints of liver and biliary tree biopsies may be invaluable if antibiotic coverage interferes with submitted culture specimens. Evidence of bacteria in cytologic samples or histologic confirmation of suppurative cholecystitis or cholangitis indicates a need for chronic postoperative antimicrobial therapy. The resected gallbladder should be submitted for histopathology, and a liver biopsy collected distant to the site of surgery. Perioperative mortality is high for symptomatic dogs with a ruptured gallbladder complicated by sepsis. If bile peritonitis is present, the peritoneal cavity must be extensively cleansed with sterile warm polyionic fluids to remove debris, bacteria, and injurious bile salts. Abdominal drains may be necessary. Antibiotics should be administered for 4–6 wk.

Cholecystotomy for removal of gallbladder contents without cholecystectomy is not advised because gallbladder muco-celes usually recur. Furthermore, necrosis of the gallbladder wall may not be grossly evident at surgery, leading to postoperative gallbladder rupture. After gallbladder resection, chronic choleretic therapy is recommended. Underlying causes of hyperlipidemia or endocrine disorders should be identified and managed appropriately. Clinicopathologic abnormalities (high AP usually) normalize after gallbladder removal in most dogs, except those with associated suppurative cholangiohepatitis, unresolved endocrinopathies, or persistent hyperlipidemia. Feeding a protein-restricted, high-fat diet to hyperlipidemic animals may be detrimental.

Last full review/revision March 2012 by Sharon A. Center, DVM, DACVIM

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