Figure 13-29 Ultrasound image (A) just proximal to the biliary confluence demonstrates mild dilatation of the right and left hepatic ducts. The distal common bile duct could not be visualized. Magnetic resonance cholangiopancreatography performed to evaluate this finding (B) confirmed choledocholithiasis. The stones were successfully managed endoscopically.
CHAPTER 13 Gallbladder and Bile Ducts
Disorders of the biliary tree and gallbladder commonly require imaging evaluation for diagnosis and management, although imaging findings are often nonspecific when patients present with suspected biliary disease. For example, gallbladder wall thickening may be entirely incidental and benign (adenomyomatosis), life-threatening (gallbladder cancer), or unrelated to primary gallbladder disease (congestive heart failure). When interpreting nonspecific imaging findings, it is helpful to interpret them within the appropriate clinical context. For this reason, we briefly discuss clinical presentations of common diseases of the gallbladder and biliary tract.
Acute cholecystitis usually begins with colicky pain that localizes to the right upper quadrant, occasionally radiating to the right scapula. Nausea and vomiting are often present, and pain can be exacerbated by deep inspiration. The gallbladder can be palpable and tender, and involuntary guarding eventually develops. A positive Murphy sign is said to be present when severe pain and guarding occur with palpation of the right upper quadrant during deep inspiration. Once gangrenous cholecystitis develops, the Murphy sign may be absent. High fever, rebound tenderness, and ileus are associated with gangrene or perforation. Leukocytosis in the range of 10,000 to 15,000 cells/mm3 is usually present with acute cholecystitis, and serum transaminase and alkaline phosphatase levels are often slightly increased. Sonography is the preferred imaging modality for the initial evaluation of patients with suspected acute cholecystitis.
When there is marked hyperbilirubinemia, one should suspect common bile duct stones, although a mild increase of serum bilirubin level (e.g., 4 mg/dl) can occur in the absence of choledocholithiasis. Increased serum amylase and lipase levels usually indicate associated pancreatitis.
The patient with common bile duct stones classically presents with jaundice and abdominal pain, although symptoms may be transient and intermittent. The presence of fever and chills suggests cholangitis or coexistent acute cholecystitis. The serum bilirubin level tends to be increased more with choledocholithiasis than with acute cholecystitis but usually does not exceed 15 mg/dl. A normal bilirubin level does not exclude the diagnosis of choledocholithiasis. Increased levels of alkaline phosphatase, 5′-nucleotidase, and leucine aminopeptidase are typical of choledocholithiasis, although increased levels of these substances may occur with bile duct obstruction from any cause. Transaminases are usually mildly increased (two to three times normal) but may occasionally be high, particularly in the setting of acute cholangitis.
Acute cholangitis is generally diagnosed clinically and requires urgent medical therapy. Left untreated, acute cholangitis can progress to hepatic abscess formation and septicemia. Most cases result from ascending infection from bowel or bacterial seeding via the portal venous system. Gram-negative enteric bacteria are the typical offending organisms. Risk factors for the development of acute cholangitis include choledocholithiasis, biliary-enteric anastomosis, biliary stricture or obstruction, and recent biliary procedure (e.g., endoscopic retrograde cholangiopancreatogram [ERCP]). The Charcot triad of fever, jaundice, and right upper quadrant pain represents the classic presentation, although one or more feature may be absent in any given patient. Patients with acute cholangitis typically experience less pain than patients with acute cholecystitis. Laboratory studies often reveal leukocytosis, increased serum alkaline phosphatase level, and hyperbilirubinemia (so-called cholestatic pattern). A mild transaminitis may develop. Up to a third of blood cultures will be positive in the setting of acute cholangitis.
Recurrent pyogenic cholangitis (RPC) is characterized by recurrent bouts of cholangitis associated with intrahepatic stones and biliary strictures. This disorder is predominantly found in Asia (and was previously called oriental cholangiohepatitis), although Asian immigrants elsewhere in the world can present with RPC. Symptoms include right upper quadrant pain, fever, and mild jaundice. Leukocytosis and a cholestatic pattern of liver function tests are often present. If left unchecked, cirrhosis or liver failure may ensue. Additional complications of RPC include choledochoduodenal fistula, stone-related pancreatitis, and cholangiocarcinoma.
This biliary disorder affects human immunodeficiency virus (HIV)–positive patients and is most often associated with secondary Cryptosporidium or cytomegalovirus infection. Patients can present with severe right upper quadrant pain. Alkaline phosphatase level will often be increased in the presence of a normal serum bilirubin concentration. CD4 cell count is usually less than 100 cells per microliter and often less than 50 cells per microliter in patients with acquired immune deficiency syndrome (AIDS) cholangitis.
Primary sclerosing cholangitis (PSC) occurs most commonly in patients with inflammatory bowel disease. Average age at diagnosis is 40 years, and the disease is more prevalent in men. Ulcerative colitis is more closely associated with PSC than other forms of inflammatory bowel disease. However, fewer than 10% of patients with ulcerative colitis will experience development of PSC. Symptoms can include fatigue, pruritus, and jaundice, although patients are often asymptomatic early in course of the disease. The serum alkaline phosphatase level is typically increased, and increase of serum bilirubin is variably present. Unlike primary biliary cirrhosis (PBC), the mitochondrial antibody test is negative in PSC. Up to 15% of patients (or approximately 1% per year) eventually experience development of cholangiocarcinoma. The progression of PSC is highly variable, with some patients remaining asymptomatic for many years and others progressing rapidly to cirrhosis and portal hypertension. Carcinoembryonic antigen (CEA) or CA 19-9 levels, or both, may be increased in the setting of cholangiocarcinoma.
Patients with cholangiocarcinoma often have painless jaundice. Serum bilirubin levels are frequently greater than 10 mg/dl, and alkaline phosphatase is usually markedly increased. CEA or CA 19-9 levels may also be increased at presentation but are not specific for cholangiocarcinoma. Making a definitive diagnosis of cholangiocarcinoma is often frustrating and challenging. Bile cytology, bile duct brushings, transluminal biopsy, and even percutaneous fine-needle aspiration all have relatively low sensitivity for cholangiocarcinoma, rendering a negative result unreliable.
The right-sided intrahepatic bile ducts draining their respective hepatic segments converge to form the right anterior segment duct (draining segments V and VIII) and right posterior segment duct (draining segments VI and VII). These ducts join to form the relatively short right hepatic duct. The right hepatic duct joins the left hepatic duct formed from the segmental ducts draining the left lobe of the liver (segments II, III, and IV) to form the common hepatic duct. This biliary confluence is typically extrahepatic and anterior to the portal vein bifurcation. The caudate lobe (segment I) duct can drain into either the right or left system. The common hepatic duct joins with the cystic duct to form the common bile duct. The common bile duct travels in the hepatoduodenal ligament and drains into the duodenum at the ampulla (of Vater). The pancreatic duct can join the bile duct before the duodenal wall (long common channel) or within the duodenal wall. The pancreatic and common bile ducts can also drain into the duodenum through separate ostia.
Variations in biliary anatomy are common; less than two thirds of individuals exhibit standard bile duct anatomy (one of the authors has a right posterior segment duct draining into his left hepatic duct). The most common biliary anatomic variants involve aberrant confluence of the right posterior segment duct (Figs. 13-1 to 13-3). Variations in bile duct anatomy do not necessarily parallel variations in portal venous anatomy. Variations of the cystic duct include a long parallel course with low insertion into the common duct, insertion into the left side of the common duct, and drainage into a right hepatic duct. Rarely, an accessory hepatic duct may enter the gallbladder. Agenesis, duplication, and ectopic location of the gallbladder may also rarely occur.
The gallbladder is divided into a fundus, body, infundibulum, and neck. The cystic duct joins with the common hepatic duct to drain the gallbladder. The site of union of the cystic duct with the common hepatic duct is variable, but usually the cystic duct joins with the common hepatic duct at an acute angle on the right side.
Several anatomic structures are in close proximity to the gallbladder. The gallbladder neck is intimately associated with the lateral proximal duodenum, and the gallbladder fundus resides near the hepatic flexure of the colon. The body and fundus of the gallbladder are also immediately adjacent to segments IVb and V of the liver. Veins drain directly into adjacent liver from the body and fundus of the gallbladder.
The normal intrahepatic bile ducts course along with the portal veins and appear as thin structures that may be visible on either side of the accompanying vein on imaging studies. The right and left hepatic ducts are usually less than 3 mm in diameter. With improvements in imaging techniques, intrahepatic ducts are routinely visible with a variety of imaging modalities. The common bile duct usually measures less than 6 mm in diameter, although larger ducts are occasionally visible in patients without bile duct obstruction. There is significant variability in the literature regarding the location from which extrahepatic bile-duct measurements are taken. With ultrasound (US), the bile duct is typically measured at the level of the right hepatic artery, although the maximum duct diameter may be a more useful measurement. Advanced age has been associated in some studies with increased common duct diameter, although most elderly patients have a common bile duct diameter less than 6 mm. Likewise, several studies have linked prior cholecystectomy with increased bile duct diameter, although several other studies have failed to confirm a clinically relevant effect of cholecystectomy on common bile duct diameter. When the common bile duct is dilated from choledocholithiasis, the bile duct will return to normal in three fourths of patients after choledochostomy.
For better or worse, many radiologists have adopted 6 mm as the common bile duct diameter threshold beyond which further evaluation is indicated, particularly when clinical evidence for pancreaticobiliary disease exists. Many radiologists will also accept a common bile duct diameter of 8 or even 10 mm in an elderly patient in the absence of other radiological or clinical evidence for pancreaticobiliary disease. Be aware that the effect of age and prior cholecystectomy on bile duct diameter is a subject of controversy
With US, intrahepatic bile ducts appear as thin, anechoic tubes, although usually only the first- (right and left hepatic ducts) and second-order bile ducts are readily visible with US. The ducts usually appear on the ventral side of the portal vein with US, although color Doppler or spectral analysis may be necessary to distinguish between blood vessels and bile ducts. Harmonic imaging may improve conspicuity of the bile duct and its contents.
With computed tomography (CT), the intrahepatic ducts are thin structures with nearly imperceptible walls that parallel the portal veins. The bile within the ducts normally measures fluid attenuation and appears homogeneous. On magnetic resonance (MR) images, the normal bile ducts parallel simple fluid on all pulse sequences. The signal intensity of the gallbladder contents varies on T1-weighted images but usually appears relatively bright on T2-weighted images.
Gallstones are common, particularly in the Western hemisphere. They can be associated with biliary colic, acute or chronic cholecystitis, bile duct obstruction, cholecystenteric fistula formation, and gallbladder carcinoma.
Abdominal radiographs show gallstones as rounded densities in the right upper quadrant. However, radiographs may miss up to 85% of gallstones. Occasionally, gas within gallstones is visible on radiographs. Signs of rare complications of cholelithiasis such as pneumobilia, gallstone ileus, or emphysematous cholecystitis can occasionally be detected with abdominal radiographs.
Transabdominal US is highly sensitive for the diagnosis of uncomplicated cholelithiasis. Larger (>5 mm) stones appear as echogenic foci with strong posterior acoustic shadowing (Fig. 13-4). The color comet tail artifact (“twinkle artifact”) can be helpful for confirming the presence of a stone, and the intensity of this artifact is related to the surface characteristics of the stone. Isolated stones smaller than 5 mm may not demonstrate acoustic shadowing but can be differentiated from polyps by their mobility. In general, when echogenic foci are detected with sonography, one should image in several different patient positions to confirm mobility of the abnormality (Fig. 13-5). Large stones or collections of smaller stones may completely fill the gallbladder, making the gallbladder difficult to identify. The WES (wall-echo-shadow) complex has been described as a means of differentiating gallstones filling the gallbladder from other abnormalities such as emphysematous cholecystitis or porcelain gallbladder, or structures such as the colon (Fig. 13-6). Before invoking the WES complex, one must ensure that the wall is seen as a distinct entity. When air or calcium is present in the gallbladder wall, a normal wall is not visualized. Instead, only an echogenic line and posterior shadow are seen. Stones impacted within the neck or cystic duct of the gallbladder may not be outlined by anechoic bile and can be missed. Therefore, it is always important to examine the neck region and cystic duct to detect evidence of posterior acoustic shadowing and color comet tail artifact. Cystic duct stones, in particular, are a relatively frequent cause of false-negative US results for cholelithiasis.
Pitfall: Stones impacted within the neck or cystic duct of the gallbladder may not be outlined by anechoic bile and can be missed. Therefore, it is always important to examine the neck region and cystic duct to detect evidence of posterior acoustic shadowing and color comet tail artifact.
CT is considerably less sensitive than US but more sensitive than radiographs for detection of gallstones. CT is primarily used in patients with abdominal pain when acute cholecystitis is not the prime consideration and should not be relied on to exclude the presence of gallstones. On CT, gallstones range from hypodense (pure cholesterol stones) to hyperdense and may occasionally contain gas. It is not unusual for even large stones to be missed on technically excellent CT images (Fig. 13-7).
Figure 13-7 Enhanced axial computed tomographic (CT) (A) and T2-weighted magnetic resonance (B) images through the upper abdomen of a patient with cholelithiasis. The single large stone within the gallbladder was not appreciated on the CT examination.
Although MRI is rarely performed as the primary means of diagnosing cholelithiasis, MRI is highly sensitive for the detection of gallstones, particularly when motion-insensitive T2-weighted images are performed. Gallstones are typically very low signal intensity on T2-weighted images and variable (very dark to very bright) signal intensity on T1-weighted images.
Occasionally, dropped gallstones will be encountered on imaging examinations after cholecystectomy (usually laparoscopic cholecystectomy). These most often accumulate in the subhepatic space but may be found as far away as the pelvis (Fig. 13-8). The most frequent complication of dropped gallstones is abscess formation. Abscesses related to dropped gallstones can present months to years after cholecystectomy.
Sludge consists of precipitated material within the bile that cannot be resolved into individual particles on imaging studies. With sonography, sludge appears as dependent, low-level echoes within the gallbladder lumen (Fig. 13-9). Sludge is usually amorphous, lacks internal vascularity, does not shadow, and slowly changes shape and position with patient movement. When sludge fills the entire gallbladder lumen, it produces echogenicity similar to liver. This observation led the expression “hepatization of the gallbladder.” Occasionally, sludge can take on a rounded, masslike appearance mimicking a gallbladder polyp or cancer (tumefactive sludge). Tumefactive sludge will change appearance between serial US examinations. About half of patients with gallbladder sludge will experience spontaneous resolution, whereas at most 15% of patients will progress to cholelithiasis.
Milk of calcium bile is occasionally detected with abdominal radiography or CT. Milk of calcium bile appears as dependently layering high-attenuation (>150 HU) material within the gallbladder. Milk of calcium bile can cause signal loss in the dependent part of the gallbladder on T2-weighted MRI scans. With US, milk of calcium bile appears echogenic and can exhibit posterior acoustic shadowing.
Vicarious excretion of iodinated intravenous contrast material will also appear as high-density material within the gallbladder with radiography and CT. A history of recent intravenous contrast administration is helpful in differentiating this phenomenon from other causes of dense bile. Imaging with MRI during the hepatobiliary phase after administration of gadobenate dimeglumine or gadoxetate disodium will often reveal accumulation of these contrast media in the gallbladder.
Blood within the gallbladder typically has a density greater than 30 HU but does not appear as dense as typical cases of milk of calcium or vicarious excretion of iodinated contrast material (Fig. 13-10). Hemorrhage appears as echogenic material within the gallbladder lumen with US.
Diffuse thickening of the gallbladder wall is one of the most common abnormalities seen on an US examination of the right upper quadrant. This is due to the myriad of processes that result in gallbladder wall thickening. Many of the causes of gallbladder wall thickening are listed in Table 13-1.
|Cause||Diagnostic Clues (Variably Present)|
|Adenomyomatosis (Fig. 13-11)|
|Carcinoma (Fig. 13-12)|
|Cholangiopathy/cholangitis (e.g., acquired immune deficiency syndrome cholangiopathy, sclerosing cholangitis)|
|Cholecystitis (Fig. 13-13)|
|Congestive heart failure (Fig. 13-14)|
|Gallbladder torsion (Fig. 13-15)|
|Hepatitis (Fig. 13-16)|
|Varices (Fig. 13-17)|
Figure 13-15 Enhanced axial computed tomographic image (A) and coronal T2-weighted magnetic resonance (MR) image (B) through the gallbladder of an elderly woman with acute onset of right upper quadrant pain. The diagnosis of gallbladder torsion was made with MR imaging and confirmed at surgery.
Chronic cholecystitis results from chronic irritation or repeated episodes of acute inflammation leading to mural fibrosis. Chronic cholecystitis can be asymptomatic, is usually associated with gallstones, and is commonly found in cholecystectomy specimens after surgery for symptomatic cholelithiasis. When sufficiently severe, it can manifest on imaging studies as gallbladder wall thickening in the presence of gallstones. Features present with acute cholecystitis, such as pericholecystic fluid, gallbladder distention, Murphy sign, and hyperemia are absent in chronic cholecystitis, although acute and chronic cholecystitis may coexist.
Cholescintigraphy is often normal in the setting of chronic cholecystitis, although delayed (>1 hour) filling of the gallbladder is seen in some patients. Patients with symptomatic chronic cholecystitis may demonstrate a low gallbladder ejection fraction.