Obstruction of the common bile duct is associated with a number of diverse primary conditions, including inflammation (eg, pancreatitis, duodenitis, etc), cholelithiasis, gallbladder mucocele, choledochitis/cholecystitis, neoplasia, malformations, parasitic infection, extrinsic compression, fibrosis, and strictures. Hepatomegaly and distention of intrahepatic bile ducts promptly follow EHBDO. If obstruction is resolved within a few weeks, resolution of fibrosis and bile duct distention can follow. However, obstruction for >6 wk results in biliary cirrhosis, portal hypertension, and APSS.
Complete obstruction may result in white bile when bilirubin pigments cannot enter the distal “stagnant loop” of the ductal system. Increased ductal mucin contributes to duct distention. In some cases, the biliary tree is colonized by bacteria, which are not cleared owing to failed mechanical expulsion of bile and inadequate antibiotic penetration into bile.
Clinical Findings and Diagnosis
Acute complete EHBDO leads to lethargy, cyclic fever, and prompt development of jaundice; the total bilirubin concentration increases within 4 hr. Vomiting may be episodic. Some animals are intermittently inappetent while others become polyphagic, reflecting fat maldigestion due to the lack of enteric bile acids. Hepatomegaly, acholic feces, and the absence of urine urobilinogen usually develop within the first week. Bleeding tendencies may be notable within 2–3 wk and are more common in cats. GI ulceration at the pyloricduodenal junction is common and can lead to considerable blood loss. Even with miniscule enteric bleeding, bilirubin pigments gain access to the bowel, allowing feces to become brown (stercobilin formation) and urine to test positive for urobilinogen.
The hemogram may reveal a nonregenerative anemia with chronic obstruction or a strongly regenerative anemia in animals with substantive enteric bleeding. A neutrophilic leukocytosis with or without a left shift is common. As bile stagnates in the biliary tree, serum ALT and AST increase. Serum AP and GGT activity increase within 8–12 hr of obstruction and are substantial within a few days. Parenchymal necrosis, periportal inflammation, and cholestasis sustain serum transaminase and cholestatic enzyme activity. In cats, the magnitude of AP and GGT are less dramatic than in dogs but are useful indicators of biliary tree obstruction, injury, and inflammation. Hypercholesterolemia develops within 2 wk of complete obstruction, reflecting impaired cholesterol elimination and increased hepatic cholesterol biosynthesis. With chronic obstruction and development of biliary cirrhosis, serum cholesterol declines, reflecting impaired cholesterol synthesis and portosystemic shunting. Coagulopathies associated with vitamin K deficiency may develop within 2–3 wk. Response to vitamin K1 administration is usually dramatic. Confirmation of EHBDO is made with ultrasonographic imaging and exploratory laparotomy.
Surgical inspection of the liver and biliary structures and appropriate biliary decompression are requisites of optimal therapy. Gross inspection of the gallbladder and common bile duct usually reveals the site and cause of obstruction; duct palpation is essential to identify intramural mass lesions. Gentle gallbladder compression is used to verify obstruction and the site of restricted bile flow. A grossly distended, tortuous common bile duct makes the diagnosis apparent. The most difficult obstructions to confirm and resolve involve hepatic ducts. A duodenotomy, cholecystotomy, or choledochotomy may be necessary for passage of a flexible catheter into the common bile duct to verify the site of obstruction and to allow removal of inspissated biliary sludge or choleliths. Successful treatment of biliary tract sepsis requires mechanical removal of biliary debris and infectious material and a decompressive surgical correction. Animals tend to become hypotensive and are susceptible to endotoxic shock during surgery and anesthesia. Liver biopsy by percutaneous needle or laparoscopic methods does not allow safe biliary decompression and may lacerate distended bile ducts leading to bile peritonitis.
Controversy exists regarding the need for biliary tree decompression in animals with EHBDO secondary to pancreatitis. In most dogs, obstruction resolves spontaneously over several weeks as the inflammation resolves. In animals in which obstruction persists beyond 2–3 wk, temporary or permanent decompression of the biliary tree should be considered. The risk of mortality in dogs with pancreatitis undergoing extrahepatic biliary surgery may be as high as 50%.
Last full review/revision March 2012 by Sharon A. Center, DVM, DACVIM