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Diseases of the Gallbladder and Extrahepatic Biliary Ducts

Ben Harris, MA, VetMB, CertSAM, MRCVS

Northwest Veterinary Specialists, Sutton Weaver, Cheshire, UK

The gallbladder is a bladder‐like organ possessing a thin, America and Asia, with clinical disease ranging from
mucosa‐lined wall with a muscular layer and an outer asymptomatic to severe obstructive cholangitis or subse­
serosal layer. Its function is to store, modify, and secrete quent neoplastic transformation to cholangiocarcinoma.
bile, which is synthesized in the hepatocytes and reaches Mucosal resistance to the extreme chemical nature of
the gallbladder via bile canaliculi, lobar bile ducts, and bile is afforded by secretion of mucin from mucous
eventually the cystic bile duct. During its time stored in glands within the biliary tract. Hypersecretion, possibly
the gallbladder, bile becomes concentrated (up to 10 as a result of inflammatory stimuli or transporter defects
times) and mildly acidified. Gallbladder contraction pro­ (ABCB4 phosphatidylcholine translocator mutation in
pels bile into the common bile duct (CBD) and then via Shetland sheepdogs), may result in accumulation of
the sphincter of Oddi into the proximal duodenum at the mucin within the gallbladder in dogs, leading to the for­
major duodenal papilla. Gallbladder contraction is stim­ mation of a biliary mucocele (Figure 67.1). Untreated
ulated by cholecystokinin, gastrin, and motilin, which in biliary mucoceles may rupture, as the gallbladder wall
turn are released in response to fatty acids, peptides, and becomes necrotic under pressure from the accumulating
amino acids in the stomach and duodenum. concretion of mucus. Bile is a highly irritating substance,
In cats, the CBD joins the pancreatic duct, sharing a so leakage into the abdomen results in a chemical perito­
common opening into the duodenum at the duodenal nitis (“bile peritonitis”). Cholecystocentesis is contrain­
papilla. In dogs, the pancreatic and CBD meet only at the dicated in biliary mucocele patients because of the risk of
papilla; in many dogs, an additional separate pancreatic gallbladder rupture.
duct enters the duodenum more distal to the papilla. Biliary obstruction may be either intrinsic to the bil­
iary tract or outside it. Blockage of biliary flow results in
posthepatic jaundice. One of the more common causes
Etiology/Pathophysiology of biliary obstruction is acute pancreatitis. This occurs
due to the intimate association of the body of the pan­
Disorders of the canine and feline biliary tract are more creas with the CBD near the duodenal papilla – the point
frequently acquired than congenital, although congenital of entry of the CBD into the small intestine. Pancreatic
biliary cysts, malformations, and biliary atresia have carcinoma or biliary carcinoma similarly may result in
been reported. The flow of bile from the gallbladder to complete bile duct obstruction. Inflammation or neo­
the duodenal papilla, as well as the chemical character of plastic infiltration of and around the duodenal papilla
bile and the mucosal immunity (secretory IgA and (e.g., duodenal lymphoma, carcinoma) is an occasional
mucosal mononuclear cells), serves to reduce the risk of cause of jaundice.
biliary bacterial infection. In vivo studies and molecular Choleliths are uncommon in cats and dogs but may
techniques have detected transitory bacteria in bile of cause bile duct obstruction or rupture. Most canine and
normal dogs. Interruption or obstruction to flow may feline choleliths contain some bile pigments, rather than
allow these transitory bacteria to colonize the tract, being pure cholesterol liths such as those commonly
causing bacterial cholangitis. found in humans. A predisposition to cholelithiasis may
Trematode infections (Platynosomum fastosum and occur due to gallbladder motility disorders, endocrine
other Platynosomum spp.) of the biliary tract are found disease, cholestasis, cholangitis or supersaturation of the
occasionally in cats in the southern USA, in South components of bile (cholesterol, pigments).

Clinical Small Animal Internal Medicine Volume I, First Edition. Edited by David S. Bruyette.
© 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.
Companion website: www.wiley.com/go/bruyette/clinical