Biliary Tract Obstruction

Also known as:	Extra-hepatic Biliary Tract Obstruction EHBO
See also:	Biliary Tract - Rupture

Description

The biliary tract comprises the gall bladder, hepatic duct, common bile duct and the duodenal papilla 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).
  • Aberrant migration of intestinal helminths may cause an obstruction if they enter the common bile duct. This has been reported with Ascaris suum in pigs and Parascaris equorum in horses and it may occur after these animals have been treated with an anthelmintic that causes spasticity of the parasite muscles.
• 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.

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

Vomiting and anorexia are the most common signs of biliary obstruction.

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.

Biliary obstruction results in a reduction in the normal function of the hepatic monocyte-phagocyte system (chiefly composed of Kupffer cells) and the absence of bile salts allows intestinal bacteria to proliferate. Affected animals are not able to remove bacteria from the portal blood with normal efficiency and they may suffer systemic bacterial infection, causing sepsis, polyarthritis, endocarditis, meningitis or uveitis.

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.

Laboratory Tests

Cholestasis causes damage to the cells of the biliary tract and these may release the biliary tract enzymes ALP and GGT which can be measured in serum. Levels of hepatocellular enzymes (such as ALT) may also become elevated if intra-hepatic cholestasis occur. Hyperbilirubinaemia and hypercholesterolaemia may also be detected.

If it can be assayed, urobilinogen will be absent from the urine in cases of complete biliary tract obstruction. Bilirubin may be present in urine but this is not abnormal as it has a low renal threshold.

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 and gall bladder mucocoeles may resemble kiwi fruit.

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, including mucocoeles which have a striped appearance.

Treatment

The appropriate treatment depends on the cause of the obstruction. In cases where biliary obstruction is thought to be secondary to pancreatitis, medical management of this condition is indicated. In advanced cases, fibrosis and abscesses may form and surgical intervention may be warranted to re-establish bile flow. A temporary cholecystostomy tube may be used in cases that are not sufficiently stable to undergo abdominal surgery. The tube may be placed laparoscopically through the right body wall. As with a gastrostomy or cystostomy tube, ten days should elapse before the tube is removed to allow fibrous tissue to form around the tube tract, preventing subsequent leakage of bile.

Intraluminal obstructions such as choleliths can be removed surgically via a cholecystotomy (incision into the gall bladder) but, if stone is within the common bile duct and this is very dilated, a choledochotomy can be performed. Alternatively, the duodenal papilla can be catheterised and the cholelith can be flushed back into the gall bladder. If the duct is not dilated, strictures may occur if a choledochotomy is performed and the procedure is associated with higher rates of mortality in humans. The abdomen is entered via a midline coeliotomy and the gall bladder is exposed in its normal position between the quadrate and right medial lobes of the liver. A needle is inserted to aspirate bile (using a syringe or suction) and stay sutures are placed in the infundibulum and fundus of the gall bladder. The incision is made between these sutures and, after removal of any obstruction, it is closed with an inverting suture pattern. In cases of recurrent cholelithiasis, cholecystectomy is recommended. This involves mobilisation of the gall bladder from its fossa and ligation of the cystic duct and cystic artery with transfixing ligatures.

Palliative surgical intervention may be undertaken in cases with large masses the involve the biliary tract. In these cases, biliary re-routing procedures such as cholecystoduodenostomy or cholcystojejunostomy may be considered, where a stoma is created directly between the gall bladder and duodenum or jejunum, respectively. Cholejejunostomy is easier to perform as a loop of jejunum may be brought to the gall bladder but this results in discharge of bile further down the gastro-intestinal tract. It is highly advisable to refer animals to a specialist centre for any biliary tract surgery.

Prognosis

The prognosis depends on the cause of the obstruction but affected animals are often very ill.

References

• Ettinger, S.J, Feldman, E.C. (2005) Textbook of Veterinary Internal Medicine (6th edition, volume 2) Elsevier Saunders
• Fossum, T. W. et. al. (2007) Small Animal Surgery (Third Edition) Mosby Elsevier