Dilated Bile Duct and Pneumobilia

Defining Dilated Bile Ducts

There is no consensus definition for what constitutes a dilated bile duct. Rather, it is important to understand that the definition is contextual and depends on the site of measurement, the imaging modality used, and the clinical scenario. Even with parameters such as these, definitions can vary widely based on individual patient characteristics and imaging study characteristics. Dilation may be present in isolated intrahepatic ducts, diffusely in the intrahepatic ducts, in the extrahepatic duct, or combinations thereof. If dilation is secondary to obstruction in the distal duct, diffuse dilation of intrahepatic and extrahepatic bile ducts will usually be seen. If obstruction is at a more proximal site, focal intrahepatic dilation will usually be observed. Normal intrahepatic ducts as small as 1 to 2 mm are seen as scattered and nonconfluent biliary branches on abdominal computed tomography (CT) or ultrasonography, and become confluent and more easily imaged as they move centrally, with diameters exceeding 2 mm ( Fig. 36.1 ). Abnormally dilated intrahepatic ducts are present when duct diameter exceeds 40% of the diameter of the adjacent intrahepatic portal vein and when the ducts appear as parallel tubes coursing together. An increase in diameter of the extrahepatic bile ducts, in particular the common hepatic duct (CHD) or common bile duct (CBD), is most often what is referred to as biliary dilation. The normal size of the duct varies at different levels, varies from person to person, and may even vary in estimation based on time of day, respiration, or patient positioning.

The imaging modality used to evaluate the biliary system can influence the reported duct diameter. Transabdominal ultrasonography (TUS) measures the internal diameter of the duct ( Fig. 36.2 ). Measurements of the CHD are typically obtained at the level of the hepatic artery in the porta hepatis, anterior to the main or right portal vein; measurements of the CBD are obtained more proximal to this site. Using TUS, most studies have placed the upper limit of normal for the diameter of the CBD at 6 to 8 mm and that of the CHD at 6 mm. However, a study using ultrasonography to measure CBD diameters in asymptomatic patients recorded normal values up to 8 to 10 mm. This may reflect variation among operators obtaining the measurements and among interpreters of these imaging modalities. By CT, values of 8 to 10 mm are more commonly accepted as normal for the CBD ( Fig. 36.3 ). This difference is in part attributable to measurements performed at different locations along the duct. Unlike ultrasonography, CT can more easily image the midportion to distal portion of the CBD, which are often larger in diameter. It also more readily identifies the fat around the duct, and measurements by CT generally include the duct wall. Evaluation of the biliary system with cholangiography, by either endoscopic retrograde cholangiopancreatography (ERCP) or percutaneous transhepatic cholangiography (PTC), may also yield results different from those with other imaging techniques. A study of 135 patients who underwent imaging of the extrahepatic bile ducts with ultrasonography and ERCP or PTC demonstrated normal duct size of up to 4 mm by ultrasonography compared with 10.4 and 10.6 mm by ERCP and PTC, respectively. This was likely a result of radiographic magnification of the cholangiogram and may also reflect distension from contrast injection.

Patient characteristics can affect measurement of duct size. Some studies have shown that CBD diameters increase in older individuals, prompting authors to suggest adding 0.4 mm to the upper limit of normal for duct size for each decade of life or 1 mm per decade of life after age 60 years. However, results from a large TUS study of 1018 asymptomatic adults showed a slight trend toward an increase in duct size with age but not as large as previously reported, with a mean diameter of 3.6 mm at age 60 and 4 mm at age 85. In this study, 99% of patients had a CBD diameter less than 7 mm. Since Oddi first predicted the phenomenon of ductal dilation after cholecystectomy in 1887, some studies have found no dilation, whereas others have found a slight trend. In a study of 234 patients undergoing cholecystectomy, the CBD increased 1 to 2 mm after surgery from a mean of 5.9 mm before cholecystectomy to 6.1 mm at an average of 393 days after cholecystectomy. Although most patients have minimal, if any, dilation after cholecystectomy, there are those who clearly manifest profound asymptomatic ductal dilation.

Given all possible circumstances that may affect the measurement of the extrahepatic biliary system, it is difficult to define an absolute measurement that will by itself yield satisfactory predictive values for pathologic dilation of the bile duct. Instead, duct diameter should be interpreted in the context of potential causes of obstructive or nonobstructive biliary dilation so that any pertinent findings from the clinical presentation or biochemical tests may be considered in the decision to pursue further diagnostic evaluation ( Fig. 36.4 ).

Etiology

Dilated bile ducts may be secondary to obstructive lesions (neoplastic or benign; Table 36.1 ) or to nonobstructive lesions. Benign etiologies of bile duct dilation include choledocholithiasis and, uncommonly in the United States, infections such as parasitic diseases. In one study, endoscopic ultrasonography (EUS) was used in the evaluation of a dilated biliary tree in 90 patients with a nondiagnostic TUS, and the study found that 40 patients had choledocholithiasis, 13 malignancy, 8 benign stricture, 2 choledochal cysts, and 1 ascariasis, and in 24 there was no evidence of an obstructing lesion. Other studies have confirmed common causes of biliary obstruction leading to ductal dilation, in order of decreasing prevalence: choledocholithiasis, pancreatic cancer, ampullary carcinoma, and cholangiocarcinoma.

Clinical Evaluation

A thorough history should be obtained, including history of malignancy and the presence or absence of symptoms such as abdominal pain, fever, weight loss, jaundice, pruritus, acholic stools, dark urine, or steatorrhea. The physical examination may be limited in its utility, but special attention should be paid to the presence of abdominal tenderness or mass, hepatomegaly, jaundice, or lymphadenopathy. A positive history or physical examination may serve to lower the threshold for further diagnostic evaluation in those patients with an equivocal duct size on initial imaging.

Biochemical Evaluation

Integral to the biochemical evaluation of obstruction are serum bilirubin and liver-associated enzymes (LAEs) (alkaline phosphatase [AP], alanine aminotransferase [ALT], and aspartate aminotransferase [AST]). The principal markers of cholestasis are elevated bilirubin and AP. The total bilirubin present in the serum represents a balance between input from production and output from hepatobiliary clearance. In obstructive jaundice the serum bilirubin is principally conjugated (water soluble). Transient elevations of AST/ALT within 1 to 2 days with levels into the thousands may occur in acute CBD obstruction, from trauma, or more typically in the presence of choledocholithiasis with subsequent rapidly declining levels. Aminotransferase levels may also rise from other subacute or chronic obstructions but typically remain less than 500 IU/dL. Hepatobiliary AP is present on the apical membrane of the hepatocyte and in the luminal bile duct epithelium. Increases in AP result from increased synthesis and release into the serum. As a result, levels may not rise until 1 to 2 days after biliary obstruction occurs. In addition, the enzyme has a half-life of 1 week and may therefore remain elevated for several days after the resolution of biliary obstruction. Levels of AP up to three times normal are relatively nonspecific and occur in a variety of liver diseases. However, higher elevations are more specific for biliary obstruction (intrahepatic or extrahepatic) and infiltrating liver diseases. As AP can be produced in sources outside the liver, it may be necessary in certain instances to use other biochemical tests such as the AP isoenzymes, gamma-glutamyl transpeptidase, or 5′-nucleotidase to confirm a hepatobiliary etiology of an elevated AP.

In general, there is an increased likelihood of choledocholithiasis with abnormalities in bilirubin, AP, and transaminase levels. It would be unusual for a lesion to cause biliary obstruction and dilation without any clinical or biochemical abnormality. However, this is not universal, and there have been case reports of patients with normal LAEs in the presence of dilated ducts and choledocholithiasis. In the era of laparoscopic cholecystectomy, models of clinical features in addition to biochemical values have been developed to predict choledocholithiasis before surgery. More recently, the American Society for Gastrointestinal Endoscopy has adopted guidelines for the evaluation of suspected choledocholithiasis, grouping presenting factors as being very strong (CBD stone on abdominal ultrasonography, clinical ascending cholangitis, bilirubin >4 mg/dL), strong (dilated CBD on abdominal ultrasonography >6 mm, bilirubin 1.8 to 4 mg/dL), and moderate (abnormal liver biochemical tests, age older than 55 years, clinical gallstone pancreatitis ). The presence of very strong predictors or strong predictors should trigger further evaluation with ERCP.

Imaging

Imaging of the biliary tract continues to evolve with the enhancement of noninvasive techniques for cross-sectional evaluation and with biliary reconstruction techniques. Each technique has strengths and limitations in the common goal of confirming the presence of an obstruction and defining its location, extent, and etiology.