Obstruction of the common bile duct is associated with a number of diverse primary conditions, including inflammation (eg, pancreatitis, duodenitis, duodenal foreign body, etc), cholelithiasis, gallbladder mucocele, choledochitis/cholecystitis, neoplasia, bile duct malformations, parasitic infection, extrinsic compression, fibrosis, and bile duct stricture. Hepatomegaly and distention of intrahepatic bile ducts promptly follow EHBDO. If obstruction resolves within a few weeks, resolution of fibrosis and bile duct distention can follow. However, obstruction for >6 wk results in persistent peribiliary fibrosis, connective tissue bridging between portal tracts, remodeling of the liver consistent with biliary cirrhosis, portal hypertension, and formation of APSSs.
Complete EHBDO may result in development of white bile within the bile duct or gallbladder, reflecting the absence of bilirubin pigments in bile; ie, bile cannot enter the distal “stagnant loop” of the ductal system or gallbladder (cystic duct occlusion). Increased ductal mucin contributes to duct distention and the color of luminal contents. In some cases, the biliary tree becomes colonized by bacteria, which are not cleared because of failed mechanical expulsion of bile and inadequate antibiotic penetration into bile.
Acute complete EHBDO leads to lethargy, cyclic fever, and prompt development of jaundice; total bilirubin concentration increases within 4 hr. Vomiting may be episodic. Some animals are intermittently inappetent, whereas others become polyphagic, reflecting fat maldigestion due to the lack of enteric bile acids and consequent fat malabsorption. Hepatomegaly, acholic feces, and the absence of urine urobilinogen (inconsistent) usually develop within the first week. Bleeding tendencies may be notable within 2–3 wk and are more common in cats and develop earlier. GI ulceration at the pyloric-duodenal 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, negating the reliability of finding acholic feces and negative urine urobilinogen for EHBDO diagnosis.
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 activities increase. Serum ALP and GGT activities increase within 8–12 hr of obstruction and are substantial within a few days. Parenchymal necrosis, periductal inflammation, and cholestasis sustain serum transaminase and cholestatic enzyme activity. In cats, the magnitude of ALP and GGT are less dramatic than in dogs but nevertheless are useful indicators of biliary tree obstruction, injury, and inflammation. Hypercholesterolemia develops within 10–14 days of complete obstruction, reflecting impaired cholesterol elimination and possibly increased hepatic cholesterol biosynthesis. With chronic obstruction and development of biliary cirrhosis, serum cholesterol declines, reflecting impaired cholesterol synthesis and APSSs. Coagulopathies associated with vitamin K deficiency may develop within 2–3 wk in dogs and earlier (within 1 wk) in cats. Response to vitamin K1 administration is usually dramatic. EHBDO is confirmed with ultrasonographic imaging and exploratory laparotomy.
Surgical inspection of the liver and biliary structures and appropriate biliary decompression are requisites for 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. A grossly distended, tortuous common bile duct makes the diagnosis apparent. Gentle gallbladder compression is used to verify obstruction and the site of restricted bile flow. 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 maneuver often involving a surgical correction. Animals with biliary tree infections tend to become hypotensive and are susceptible to endotoxic shock during surgery and anesthesia, especially cats. Liver biopsy by percutaneous needle or laparoscopic methods does not allow safe biliary decompression and may lacerate distended bile ducts, leading to bile peritonitis; thus, laparotomy is the optimal managerial and assessment approach.
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 with obstruction persisting beyond 2–3 wk, temporary (stenting of the bile duct at the sphincter of Oddi) or permanent decompression of the biliary tree is usually considered. The risk of mortality in dogs with pancreatitis undergoing extrahepatic biliary surgery may be as high as 50%. Transhepatic ultrasound-guided aspiration of the gallbladder as a decompressive approach has been successfully completed in some affected animals but has high risk of focal or more generalized bile peritonitis.