Gallbladder Mucoceles…… more common than you think
A remainder of hepatic physiology:
Bile is continuously produced by hepatocytes and is mainly composed of water, bile acids, bilirubin, phospholipids, cholesterol and electrolytes. Bile is initially collected in the hepatic canaliculi, and then travels through the biliary tree until it reaches the common bile duct. Although some bile flows directly into the small intestine from the liver, most of it is kept in the gallbladder prior to release into the duodenum. So the gallbladder acts as storage vessel for bile. While in the gallbladder, bile undergoes substantial modification with the addition of bicarbonate-rich mucin by the gallbladder epithelial cells, being particularly important.
Formation of gallbladder mucoceles (GBM):
A GBM is a collection of gelatinous material that causes distension of the gallbladder. It is unclear what causes GBM’s to form, but it is generally accepted that factors that impede gallbladder emptying and/or stimulate mucus production or a change in its composition, are likely to predispose to GBM formation.
In recent veterinary literature several breeds show a predisposition to GBM formation, suggesting that genetics may play a role (i.e. Shetlands Sheepdogs), in addition numerous dogs with GBM’s have concurrent endocrinopathies, including hyperadrenocorticism, hypothyroidism and diabetes mellitus.
History and signalment: most patients with mucoceles are older (average age of 9 years). There is no sex predisposition. Small to medium-sized dogs are most commonly affected and Shetland sheepdogs, miniature schnauzers and cocker spaniels are overrepresented.
Clinical signs: Many dogs with GBM’s are asymptomatic (incidental finding on the abdominal ultrasound), whilst others will present with chronic waxing and waning clinical signs, which include anorexia, lethargy, abdominal discomfort, polyuria, polydipsia, jaundice, vomiting and diarrhoea. Acute signs may also occur, especially if the mucocele leads to GB rupture or if it is associated with acute cholecystitis.
On haematology a stress leukogram (neutrophilia, lymphopaenia, monocytosis, and eosinopaenia) may be seen. If concurrent cholecystitis is present, a neutrophilic leucocytosis with a left shift can also be seen.
On serum biochemistry there can be marked hyperbilirubinemia and increased liver transaminase activity (ALKP, ALT, GGT, AST). Hypercholesterolemia and fasting hypertriglyceridemia may be seen.
Bile culture (cholecystocentesis sample) from affected dogs has yielded positive results in many cases. Bacterial isolates include enteric organisms like Escherichia coli, Streptococcus spp. and Enterococcus spp. and in some occasions anaerobic bacteria like Clostridium perfringens.
Abdominal ultrasound findings: The classic description of the ultrasonographic appearance of a GBM is "kiwi-like" or "stellate patterned". A GBM can be distinguished from biliary sludge by its immobility (sludge will be gravity dependent) and by its appearance (sludge is more uniformly hyperechoic, and lacks from the striated appearance). Gallbladder rupture and associated peritonitis can also be seen.
Treatment: surgical vs medical
The management of GBM has not been investigated in any controlled trials. Surgery (cholecystectomy) is normally recommended if there are moderate clinical signs associated with the presence of the GBM or if there is a suspicion of gallbladder rupture (many of these patients have necrosis of the gall bladder wall and will eventually rupture causing peritonitis). Although prognosis is good, surgery has a mortality rate of 15-30% and it is not always necessary in all dogs with GBM.
Medical therapy appears to be appropriate for asymptomatic dogs found to have a mucocele as an incidental finding, or in the early stages of GBM formation. Such dogs should be tested for concurrent endocrinopathies (hyperadrenocorticism and hypothyroidism) and treated accordingly. Medical therapy for GBM includes:
Low fat diets: A low fat diet may improve biliary flow. The diet would be specially indicated in patients with confirmed hypertriglyceridaemia.
Ursodeoxycholic acid/ursodiol: Ursodiol is a naturally occurring bile acid that has choleretic properties by reducing the cholesterol saturation in the bile and thinning biliary secretions by producing bicarbonate-rich enhanced bile flow. Ursodiol also has hepatoprotective effects. It is important to mention that ursodiol is contraindicated in extrahepatic biliary duct obstruction.
S-adenosylmethionine: SAMe increases hepatic glutathione levels, which is a potent antioxidant that protects hepatocytes from toxins and death.
Broad spectrum antibiotics: If bacteria are isolated, a 6-8-week´s course of antibiotics is recommended, based on the culture and sensitivity panel. In cases in which ultrasound-guided cholecystocentesis is not feasible, empirical antibiotic therapy with broad spectrum antibiotics (i.e. potentiated amoxicillin) should be started.
The owner should be warned of the potential risk of gallbladder rupture and consequent bile peritonitis. Patients should be closely monitored and repeat examinations, blood tests and abdominal ultrasound are recommended (at 2, 4 and 8 weeks and then every 6-8 weeks). If no signs of resolution or improvement are noticed after 4-6 months of treatment, surgery should be recommended.