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Canine Gallbladder Mucocele

By Sharon A. Center, BS, DVM, DACVIM, Department of Clinical Sciences, College of Veterinary Medicine, Cornell University

Canine gallbladder mucocele (GBM) is characterized by progressive accumulation of tenacious, pale yellow to dark green, 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 GBM leads to gallbladder ischemia and necrosis, bile peritonitis, and sometimes opportunistic infection. Gallbladder stasis, perhaps reflecting dysmotility, and distention predispose to cholecystitis. A GBM should be considered when sequential ultrasonographic examinations fail to indicate a reduction in gallbladder volume after feeding, confirming lack of movement of luminal “sludge.” Feeding a dog (100 g of food) and recording gallbladder dimensions at 0, 15, 30, 45, 60, 90, and 120 min, recorded in cm ([width × height × length] × 0.52) yields the gallbladder volume in mL. Failure to reduce baseline gallbladder volume by at least 25% suggests dysmotility. Erythromycin (0.5–1 mg/kg, PO, one dose) combined with a small meal also may stimulate initiation of gallbladder motility; however, in healthy dogs studied, neither feeding with or without erythromycin was consistently superior to initiate contraction.

Dogs with GBM range in age from 3–14 yr old with no gender predisposition. Incidence is increased in Shetland Sheepdogs, Miniature Schnauzers, and Cocker Spaniels. A genetic mutation in the ABCB4 (MDR3) phospholipase flippase transporter was demonstrated in Shetland Sheepdogs and other dogs with GBM. All affected dogs were heterozygous for this mutation.

Factors predisposing to GBM formation include middle to older age, endocrinopathies (typical and atypical hyperadrenocorticism, hypothyroidism, diabetes mellitus), hyperlipidemia or hypercholesterolemia (idiopathic, nephrotic syndrome, feeding of a high-fat diet, pancreatitis), gallbladder dysmotility, and cystic hyperplasia of the gallbladder mucosa (shown to be inducible by progestins in dogs). The inciting cause of mucus hypersecretion or accumulation is unproved and may be multifactorial. Nevertheless, mucin imparts important viscoelastic properties to bile and likely importantly contributes to GBM formation. 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.

Clinical Findings and Diagnosis:

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 discomfort, anorexia or hyporexia, jaundice, tachypnea, tachycardia, PU/PD, fever, diarrhea, and abdominal distention. Dogs progressing to gallbladder rupture usually demonstrate abdominal pain, jaundice, tachycardia, tachypnea, and fever. However, occasionally, ruptured GBMs asymptomatic with a free-moving congealed mucocele have been imaged in the peritoneal cavity. Typical clinicopathologic indicators include leukocytosis with a mature neutrophilia and monocytosis and sometimes a left shift, high liver enzyme activities (ALP, GGT, ALT, and AST), hyperbilirubinemia, and inconsistent hypercholesterolemia. Aerobic bacteria may be cultured from bile or the gallbladder wall, with a number of enteric organisms identified, including Escherichia coli, Enterobacter spp, Enterococcus spp, Staphylococcus spp, Micrococcus spp, and Streptococcus spp. Transhepatic ultrasound--guided cholecystocentesis should not be performed if a GBM is suspected. 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 whether parenchymal lesions resolve. A liver biopsy should be collected from a liver lobe distant to the gallbladder to evaluate for underlying or coexisting disorders; sections collected adjacent to the gallbladder contain peribiliary glands and numerous ductal elements that may result in erroneous assessments.

Histologically, cystic mucosal hyperplasia of the gallbladder wall is common. 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 and lead to necrotizing cholecystitis and gallbladder rupture. Liver biopsies may disclose a VH or mild to moderate portal hepatitis or periductal fibrosis; the later changes reflect associated cholangitis or transient biliary tree occlusion. Some dogs lack concurrent hepatic lesions, especially when cholecystectomy is done preemptively (before GBM maturation).


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 evolving GBM may resolve with medical treatment. However, progression in any clinical, clinicopathologic, or imaging parameter indicates poor control and 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, obstruction, or rupture. Because bile stasis predisposes to infection, broad-spectrum antimicrobials should be initiated before surgical intervention. Examination and staining of cytologic preparations of bile and imprints of liver and biliary tree biopsies may be invaluable if antibiotic coverage interferes with submitted cultures. Evidence of bacteria in cytologic samples or histologic confirmation of suppurative cholecystitis or cholangitis indicates a need for chronic postoperative antimicrobial administration. The resected gallbladder should be submitted for histopathology (sectioned before fixation to allow formalin penetration), 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 after surgery.

Cholecystotomy for removal of gallbladder contents without cholecystectomy is not advised, because GBMs 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, especially for Shetland Sheepdogs in which a genetic risk is surmised for sludged bile. Underlying causes of hyperlipidemia or endocrine disorders should be identified and managed appropriately. Clinicopathologic abnormalities (high ALP usually) normalize after gallbladder removal in most dogs, except those with associated suppurative cholangiohepatitis, unresolved endocrinopathies, persistent hyperlipidemia, or surgical complications of cholecystectomy. Feeding a protein-restricted, high-fat diet to hyperlipidemic animals may be detrimental and is not recommended.