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Managing disorders of the gallbladder in dogs (Proceedings)

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Aug 01, 2010

Basic Gallbladder Anatomy and Physiology

The gallbladder is a small, pear-shaped organ located in the cranial abdomen between the right medial and quadrate liver lobes.1 Bile is synthesized by hepatocytes and collects within canaliculi and is sequentially drained from into bile ductules, interlobular, lobar and hepatic ducts. 1,2 Hepatic ducts coalesce and join the cystic duct (extends from the neck of the gallbladder) to form the common bile duct 3. In the dog, the common bile duct empties into the duodenum at the major duodenal papilla. Bile is composed of water, bile acids, bilirubin, cholesterol and electrolytes1,3. The physiologic functions of bile are to: (1) Enhance fat digestion by emulsifying fat into smaller particles that are more susceptible to the actions of pancreatic lipase; (2) Enhance ileal absorption of digested fats; (3) Aid in the excretion of cholesterol1,3. Within the gallbladder bile is acidified and concentrated via the absorption of water, lipids, proteins and electrolytes2,3. Glands within the gallbladder mucosa secrete mucin into the gallbladder lumen to protect the organ from the cytotoxic effects of bile acids2. Gallbladder contraction is stimulated by cholecystokinin; a gastrointestinal peptide released from enterocytes in response to fat and proteins entering the small intestine1,3.

Extrahepatic Biliary Obstruction (EHBO):

Obstruction of bile flow through the common bile duct can occur secondary to gallbladder mucocele, cholelithiasis, pancreatitis, neoplasia (biliary, hepatic, pancreatic, intestinal, surrounding structures) and stricture, among other causes2,4. Regardless of the underlying cause, surgical exploration of the abdomen, focusing on the biliary tree and liver, is generally required. As such, prompt diagnosis of EHBO is important. Clinical signs of acute EHBO can include lethargy, vomiting, fever and rapid development of icterus2. Although gradual obstruction of the common bile duct is most common, most patients will present acutely when clinical icterus develops4. Additional clinical signs include lethargy, anorexia, vomiting and cranial abdominal pain. Occasionally, clinical signs may wax and wane for several weeks4. Icterus of post-hepatic origin is characterized by hyperbilirubinemia, bilirubinuria, increased serum activities of cholestatic (ALP and GGT) +/- hepatocellular leakage (ALT, AST) enzymes, +/- hypercholesterolemia and consistent diagnostic imaging findings. Hematocrit is expected to be normal or near normal except in cases with concurrent hemorrhage (often due to gastrointestinal ulceration) or if the icterus is of pre-hepatic origin (i.e. hemolytic anemia). Abdominal ultrasound is an important tool is assessing the hepatobiliary system. Distension of the gallbladder and common bile duct is evident ultrasonographically within 24-48 hours of complete EHBO, while distension of the intra-hepatic bile ducts is evident after 5-7 days2,5. Bile duct diameter cannot be used to determine the chronicity or severity of obstruction2. Treatment generally requires surgical exploration of the hepatobiliary system and biliary decompression, cholecystectomy or cholecystoenterostomy, depending on the site and cause of the obstruction. If the common bile duct can be catheterized across the obstructive lesion, choledochal biliary stenting may be an appropriate option2,6.