An update on gallbladder mucoceles in dogs
The gallbladder musculature contracts in response to cholecystokinin; this hormone is released from enterocytes after the ingestion of a fatty meal. In particular, proteoses, peptones, and long-chain fatty acids stimulate cholecystokinin release. Cholecystokinin concentrations peak about 20 minutes after a meal and may remain elevated for almost two hours. Once the gallbladder contracts, its contents are emptied into the duodenum within about 60 minutes.3 Cholecystokinin also causes relaxation of the sphincter of Oddi and the release of pancreatic digestive enzymes.
Other factors that contribute to gallbladder contraction include parasympathetic stimulation by the vagus nerve, sympathetic inhibition of the splanchnic nerve, neurotensin, and substance P.6-8Gallbladder relaxation
The gallbladder relaxes in response to somatostatin, vasoactive intestinal polypeptide, nitric oxide, and pancreatic polypeptide.3,6,9 The relaxation phase is associated with bile storage and modification. During this period, the sphincter of Oddi is closed.
GALLBLADDER MUCOCELE PATHOPHYSIOLOGY
Predisposition to mucoceles may be associated with dyslipidemias in particular breeds such as Shetland sheepdogs.12 While extrahepatic biliary duct obstruction is a recognized cause of mucocele formation in people, prospective studies in dogs do not support this finding.13 Conversely, it appears that extrahepatic biliary duct obstruction is secondary to mucocele formation.14 Other suggested causes of canine mucocele formation include progestational therapy or progestational compounds, cholecystitis, and glucocorticoid excess.4,15,16 To date, none of these theories has been widely supported.
It has been proposed that mucocele formation is the result of progressive biliary sludging.17 As biliary sludge forms and progresses, gallbladder motility may be decreased, resulting in biliary stasis and increased water absorption. As the gallbladder continues to absorb water, its contents become more solid and immobile.
The most widely supported theory of canine mucocele formation implicates mucus-secreting cell proliferation and dysfunction.18 In this condition, cystic mucinous hyperplasia of the gallbladder epithelium occurs, and the gallbladder epithelial cells secrete excessive mucus into the gallbladder lumen. This condition may be a primary defect (an inherent disorder of the mucous cells) or a secondary defect (exposure to excessive bile salts).19
DIAGNOSING GALLBLADDER MUCOCELES
History and signalment
Most patients with mucoceles are older (average age of 9 years), and no sex predilection has been established.11 Mucoceles are usually reported in small or medium-sized dogs, and Shetland sheepdogs and cocker spaniels are overrepresented.20 In one study, 66% of Shetland sheepdogs with gallbladder disease had confirmed mucoceles.12
About 77% of patients with mucoceles are clinically ill, often with an acute onset of signs.21 Vomiting, anorexia, lethargy, polyuria, polydipsia, and diarrhea are most often reported.21 Cumulatively, studies have shown that almost one-quarter of patients with mucoceles were asymptomatic.10,14,17,18,22