Anatomy and physiology
The biliary tract starts at the hepatocyte canaliculi, which empty into biliary ductules. Larger ducts join the right and left hepatic ducts, which drain into the common hepatic duct at the porta hepatis. When the cystic duct from the gallbladder joins the common hepatic duct, the common bile duct is formed.
The common bile duct is usually 8 cm long and 0.5 to 0.9 cm in diameter. It passes behind the first portion of the duodenum, through a groove in the head of the pancreas, and empties into the second portion of the duodenum at the ampulla of Vater. Distally the pancreatic duct may join the common bile duct before it also empties into the ampulla.
The gallbladder, a pear-shaped distensible organ, 4 x 8 cm in size with a normal capacity of 30 to 50 mL, lies in a fossa on the visceral surface of the liver on a line separating the right and left hepatic lobes. When distended with acute inflammation, the fundus comes in close contact with the anterior abdominal wall in the right upper quadrant near the ninth and tenth costal cartilages, giving rise to the Murphy’s sign. Posteriorly, it abuts the first and second portion of the duodenum and the hepatic flexure of the colon. Thus, extension of the inflammation of the gallbladder may lead to spontaneous fistulas into these hollow organs.
Bile, formed by the hepatocytes (600 mL per day), consists of water, electrolytes, bile salts, cholesterol, phospholipids, bilirubin, and other organic solutes. The gallbladder stores and concentrates bile during fasting. Approximately 90% of the water and the electrolytes are resorbed by the gallbladder epithelium, resulting in bile rich in organic constituents. The stratification of this bile into a density gradient is thought to play a role in gallstone formation.
Obstructive cholangitis is an inflammation of the bile ducts associated with enteric bacterial infection in the setting of biliary obstruction. Obstruction may be secondary to common bile duct stones, biliary strictures, choledochal cysts, biliary fistulas, stenosis of biliary-enteric anastomoses, and occasionally malignancy. Mechanical manipulation of the biliary ducts (i.e., during percutaneous transhepatic cholangiography, endoscopic retrograde cholangiopancreatography, or T-tube studies) may also result in cholangitis.
The most common organisms found in the bile in cholangitis are E. coli, Klebsiella, Proteus, Enterobacter, Pseudomonas, Streptococcus fecalis, and Clostridium. The spillage of the bacteria into the bloodstream often gives rise to bacteremia and sepsis. When infection is severe, invasion of the liver parenchyma may occur, resulting in abscess formation. Recurrent infection and inflammation of the bile ducts may result in strictures, areas of dilatation, and intraductular calcium bilirubinate stone formation. Secondary biliary cirrhosis and portal hypertension may be late sequelae.
Patients usually present with intermittent abdominal pain, fever, chills, and jaundice. Dark urine and pale stools suggest the presence of biliary obstruction.
Leukocytosis with a shift to the left and elevation of serum alkaline phosphatase and bilirubin levels are common. Serum alanine aminotransferase, aspartate aminotransferase, and amylase levels are usually elevated.
When cholangitis is suspected, prompt diagnosis and relief of the obstruction is essential. Patients should be given intravenous antibiotics for enteric organisms to prevent sepsis.
Ultrasonography, endoscopic retrograde cholangiopancreatography, percutaneous transhepatic cholangiography, and abdominal computed tomography scan may be necessary to diagnose the extent, nature, and location of the obstruction. The choice of definitive treatment for relief of the obstruction depends on the findings. Surgery or other less invasive techniques such as percutaneous transhepatic cholangiography or endoscopic retrograde cholangiopancreatography may be required.