Biliary Tract Obstruction

Description

The biliary tract comprises the gall bladder, hepatic duct, common bile duct and the duodenal papillae onto which it opens. If any part of this tract is obstructed, the normal flow of bile is interrupted resulting in cholestasis and post-hepatic jaundice. If the obstruction is not relieved, the biliary tract may rupture to produce a chemical bile peritonitis.

The causes of biliary tract obstruction may be intraluminal or extraluminal:

• Intraluminal obstructions:
  • Choleliths ('gall stones') are much less common in animals than they are in humans. They are usually composed of bilirubin salts in dogs and calcium carbonate in cats, although they are very rare in the latter species.
  • Gall bladder mucocoeles produce a kiwi sign on radiographs and may be a sequel to cystic mucinous hyperplasia of the gall bladder mucosa.
  • Biliary neoplasia, most commonly cholangiocellular cystadenoma (in cats) or carcinoma (in dogs).
• Extraluminal obstructions:
  • Pancreatitis is the most common cause of obstruction in dogs. Pancreatic abcesses or neoplasia may also obstruct the flow of bile.
  • Biliary tract rupture
  • Pyloric or duodenal mass
  • Diaphragmatic rupture with herniation of parts of the liver may result in exertion of pressure on the biliary tract.
  • Biliary pseudocysts are a rare cause of obstruction.

Animals suffering from extra-hepatic biliary obstruction (EHBO) are often profoundly unwell. The reduced flow of bile salts into the gastro-intestinal (GI) tract allows GI bacteria to proliferate and eventually translocate across the intestinal wall. In addition, biliary stasis reduces the function of Kupffer cells within the liver, reducing their ability to remove and neutralise translocated bacteria from the portal blood. These animals should be stabilised adequately before any surgical repair is attempted.

Diagnosis

The signs of biliary obstruction relate to the failure of bile to move into the small intestine and to the reduction in function of the hepatic monocyte-phagocyte system.

Clinical Signs

The failure to excrete bilirubin results in an increase in the blood concentration of conjugated bilirubin. Beyond a certain level, this bilirubin stains tissues causing jaundice which may be visible on the mucous membranes or sclera. Since bilirubin has a low renal threshold, high concentrations are found in urine, although bilirubinuria is not necessarily an abnormal finding in healthy animals. In a complete biliary obstruction, urobilinogen will also be absent from the urine.

The absence of bile salts in the gut results in fat maldigestion and steatorrhoea. Small intestinal bacterial overgrowth (SIBO) may develop over time as bacteria metabolise the additional substrate in the intestinal lumen. Bacteria convert fatty acids to hydroxy fatty acids that irritate the colonic mucosa and may cause diarrhoea. The failure to absorb fat may lead to deficiencies in the fat soluble vitamins (K, E, D and A) and in very severe cases, this may result in a coagulopathy due to poor production of vitamin K-dependent clotting factors..

Diagnostic Imaging

Plain radiographs of the abdomen may show soft tissue masses associated with the region of the biliary tract or pancreas. Signs of pancreatitis (such as a ground glass appearance in the cranial abdomen and a 'hockey stick' duodenum) may also be evident. Choleliths may be visible as radio-opaque structures within the gall bladder.

Ultrasonography is a very useful technique in the diagnosis of EHBO as the distention of different parts of the biliary tract can be traced easily. Initially, only the gall bladder is distended (seen as a loss of an evident neck) but the hepatic duct may be seen to dilate after outflow has been obstructed for 3 days and the intrahepatic bile ducts after 7 days. The bile ducts may be dilated in Caroli Disease without obstruction but this is extremely rare. Many of the processes that might cause EHBO can also be diagnosed with ultrasound.