Issues

Gallbladder Mucocele

 

Gallbladder Mucocele is an accumulation of tenacious, thick, mucoid bile conglomerate in the gallbladder (GB), obstructing storage capacity and function.

Inspissated biliary sludge expands the GB, leading to necrotizing cholecystitis.

A canine syndrome, rare in cats.

 

SIGNALMENT

Dog

• Middle-aged to older adults.
• No sex predilection.
• Associated with endocrinopathies.

 

SIGNS

General Comments

• Symptomatic or asymptomatic
• Asymptomatic discovered on abdominal ultrasonography for other health concerns

 

Historical Findings: symptomatic

• Episodic abdominal discomfort
• Anorexia
• Vomiting
• Polyuria/polydipsia
• Lethargy
• Collapse: vasovagal or bile peritonitis

 

Physical Examination Findings

• May show no physical signs early in syndrome
• Lethargy
• Cranial abdominal discomfort
• Jaundice late in syndrome
• Dehydration
• Fever

 

CAUSES & RISK FACTORS

Inborn errors of lipid metabolism may increase risk: miniature schnauzer, Shetland sheepdogs.

Medical conditions associated with hypercholesterolemia or promoting dyslipidemias: hypothyroidism, typical or atypical (sex hormone) adrenal hyperplasia, glucocorticoid therapy, diabetes mellitus, recurrent pancreatitis, feeding high fat diet to dog with a predisposing disorder.

GB dysmotility—may play a causal role.

Cystic hypertrophy of mucus-producing GB mucosa—common in older dogs; may play a causal or facilitatory role.

 

DIAGNOSIS

DIFFERENTIAL DIAGNOSIS

Conditions causing bile stasis—GB dysmotility; neoplasia; choleliths; pancreatitis

 

CBC/BIOCHEMISTRY/URINALYSIS

CBC

• Inflammatory leukogram—variable
• non-regenerative anemia—if chronic inflammation or hypothyroidism
• Biochemistry
• High liver enzymes—the only sign of illness in some dogs or may be noted on acute presentation; ALP, GGT, ALT, ± AST.
• High ALP: early in syndrome development may indicate an underlying glycogen-type vacuolar hepatopathy (VH) and endocrinopathy (adrenal-related).
• Variable hyperbilirubinemia.
• Low albumin if a ruptured biliary tree and bile peritonitis.
• Prerenal azotemia if ruptured GB, sepsis, or dehydration from postprandial vomiting.
• Electrolyte abnormalities with fluid and acid-base disturbances—reflecting bile peritonitis or extensive vomiting.
• Urinalysis
• No specific features

 

OTHER LABORATORY TESTS

Triglyceride concentrations—high if an inborn error of lipid metabolism: certain breeds, endocrinopathies, diabetes mellitus, hypothyroidism, or pancreatitis.

Coagulation tests—normal, unless chronic EHBDO, GB rupture, bile peritonitis, sepsis, or DIC.

 

IMAGING

• Abdominal radiography—normal or large liver; loss of detail in the cranial abdomen if focal peritonitis (necrotizing cholecystitis, GB rupture); intrahepatic gas indicates septic inflammation with gas-producing bacteria (rare).
• Abdominal ultrasonography—liver may be large, with rounded margins; diffuse to multifocal hyperechoic hepatic parenchyma common (associated with VH); typical US image is a GB lumen filled with amorphous echogenic debris appearing as a stellate or finely striated pattern, resembling a sliced kiwi fruit (“kiwi sign”); distended GB and sometimes distended common bile duct and cystic duct if EHBDO; fluid interface surrounding GB enhances wall image and suggests cholecystitis or GB rupture; diffusely thick GB wall with segmental hyperechogenicity and double-rimmed or laminated wall if necrotizing cholecystitis; edema may enhance GB wall imaging: may occur with hepatitis, cholangiohepatitis, or third-space fluid dispersal (hypoproteinemia, right heart failure, renal failure, pyelonephritis, abdominal effusion, iatrogenic fluid overload); GB rupture associated with discontinuous GB wall, or a difficult to image GB; GB mucocele (GBM) may be released into the abdominal cavity where a discrete free floating “mass” may be discovered; pericholecystic fluid or generalized effusion, and hyperechogenicity of surrounding tissues may indicate focal peritonitis and bile leakage; intrahepatic bile ducts may be difficult to visualize or may appear prominent (ascending cholangitis) or distended (EHBDO).
• GB motility study—indicated if impending GBM is recognized serendipitously and GB volume ≥ 1.2 mL/kg body weight; sequential GB volume measurements after meal ingestion (100 g), may include 1 mg/kg erythromycin as motilin agonist provoking GB contraction. Normal GB contracts ≥ 25% initial volume on one or more postprandial images: image GB at 0, 15, 30, 45, 60, 90, 120 minutes after feeding.

 

DIAGNOSTIC PROCEDURES

• Aspiration sampling—fluid adjacent to biliary structures or free in the abdominal cavity; clarifies GB rupture and infection; caution: do not perform cholecystocentesis on a suspected GBM as this may cause bile peritonitis; GBM contents are usually difficult to sample owing to their thick, tenacious character.
• Laparotomy—for diagnosis, cholecystectomy, and perhaps cholecystenterostomy.
• Laparoscopy: only if technical excellence is achieved for cholecystectomy by this method.
• Liver biopsy—evaluates for coexistent or antecedent hepatobiliary disorders. Collect biopsy distant to the GB to avoid sampling peribiliary glands.
• Bacterial culture /sensitivity—effusion, GB wall and contents, and liver; aerobic and anaerobic bacteria.
• Cytology—impression smears of GB, liver, and bile for immediate determination of suppurative septic inflammation and neoplasia. Make smears of bile particulates where bacteria are “tangled.”

PATHOLOGIC FINDINGS

• Gross—GB distended, the wall may be erythematous or hemorrhagic with focal areas of necrosis; focal peritonitis may be evident; liver and extrahepatic biliary structures usually appear normal; GB contents: dark green-black, tenacious, firm, or organized solid yellow-green on the cut surface with a rubbery texture. Proliferative lesions on GB mucosa usually represent cystic mucosal hyperplasia or papillary proliferations.
• Microscopic—variable mixed inflammatory infiltrate and fibrosis (chronic) in lamina propria of GB wall, focal areas of necrosis if necrotizing cholecystitis; GB mucosal hyperplasia—common; ascending cholangitis and cholangiohepatitis may develop as secondary complications; hepatocytes may demonstrate VH (glycogen and/or lipid inclusions) if underlying endocrinopathy (see associated conditions). Asymptomatic GBM removed preemptively may only demonstrate cystic mucosal hyperplasia.

 

TREATMENT

• Outpatient management with ursodeoxycholic acid and S-adenosylmethionine (SAMe) to induce choleresis and provide hepatoprotection—medical therapy is not advised to resolve a GBM. Has resolved syndrome in some dogs but patients are subject to GBM recurrence. Naïve treatment with choleretics may result in GB rupture.
• Inpatient—treatment depends on whether the patient presents with severe acute necrotizing cholecystitis or syndrome determined incidentally on ultrasound examination.
• If the patient is hyperlipidemic, investigate the cause and restrict dietary fat (food, medications).
• Symptomatic patients require exploratory surgery for cholecystectomy and evaluation/treatment for potential bile peritonitis.
• Cholecystotomy and mucocele removal with GB retention may lead to GBM recurrence and bile peritonitis.
• Fluid therapy—balanced polyionic solutions to correct hydration and electrolytes.
• Be prepared for blood component therapy.
• Abdominal lavage—at the surgery if bile peritonitis is confirmed.

 

MEDICATIONS

DRUG(S)

Antimicrobials

Initiate broad-spectrum antimicrobials before surgery: enteric Gram-negative and anaerobic organisms most likely opportunists; continue treatment 4–8 weeks if septic complications; adjust drugs based on culture and sensitivity test reports.

 

Vitamin K1

0.5–1.5 mg/kg IM or SC q12h for three doses—if jaundiced; the oral route may be ineffective if EHBDO: fat-soluble vitamin malabsorption.

 

Antiemetics/Antacids/Gastroprotectants

Metoclopramide 0.2–0.5 mg/kg PO, IV, or SC q6–8h or 1–2 mg/kg/day by CRI.

Ondasetron 0.5–1.0 mg/kg PO 30 min before feeding, maximum q8h or 0.1–0.2 mg/kg slow IV push q6–12h—if vomiting.

H2-receptor antagonists: famotidine 0.5 mg/kg PO, IV, SC q12–24h; may need to increase the dose for efficacy.

Omeprazole or pantoprazole may induce p450 cytochrome-associated drug interactions; 24–48 h delay onset of action.

Sucralfate 0.25–1.0 g PO q8–12h)—for upper gastrointestinal bleeding.

Choleresis

Maintain hydration status.

Ursodeoxycholic acid: choleretic, hepatoprotectant, anti-inflammatory, anti-endotoxic effects: (10–15 mg/kg PO divided BID daily with food), tablets provide the best bioavailability); treat indefinitely

S-adenosyl-methionine (SAMe) provides GSH-dependent choleretic effect, the dose may be higher than that used as an antioxidant (see below); choleresis with 40 mg/kg PO per day.

Antioxidants

Vitamin E: α-tocopherol 10 IU/kg PO daily with food); antioxidant, anti-inflammatory, antifibrotic effects.

S-adenosylmethionine (SAMe): 20 mg/kg PO daily 2h before feeding, use SAMe with proven bioavailability; give until liver enzymes normalize or indefinitely if chronic hepatitis.

 

FOLLOW-UP

PATIENT MONITORING

• Repeat sequential hematology, biochemistry, and imaging to monitor response.
• Persistent clinicopathologic features may implicate underlying endocrinopathy requiring documentation and treatment, or an intrahepatic cholangiopathy.

 

POSSIBLE COMPLICATIONS

• Cholangitis or cholangiohepatitis
• Bile peritonitis
• EHBDO

 

EXPECTED COURSE AND PROGNOSIS

Good with successful surgery, chronic choleretic therapy, correction or management of comorbid conditions, diet modification.

Anticipate a protracted clinical course with ruptured biliary tract or peritonitis.

Recrudescence may occur even if mucocele removed and GB retained, with or without chronic medical therapy.

 

ABBREVIATIONS

ALP = alkaline phosphatase

ALT = alanine aminotransferase

AST = aspartate aminotransferase

BUN = blood urea nitrogen

CRI = constant rate infusion

DIC = disseminated intravascular coagulation

EHBDO = extrahepatic bile duct obstruction

GB = gallbladder

GBM = gallbladder mucocele

GGT = γ–glutamyltransferase

GSH = glutathione

VH = vacuolar hepatopathy

 

Visit your veterinarian as early recognition, diagnosis, and treatment are essential.

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