CT and MRI of the Whole Body, 2-Volume Set, 6e, Volume II PDF
Preview CT and MRI of the Whole Body, 2-Volume Set, 6e, Volume II
CHAPTER 41 Chest Imaging in the Pediatric Patient 1189 160. Taylor GA, Atalabi OM, Estroff JA: Imaging of congenital 172. Weinberg PM: Aortic arch anomalies. J Cardiovasc Magn Reson diaphragmatic hernias. Pediatr Radiol 39(1):1–16, 2009. 8(4):633–643, 2006. 161. Terheggen-Lagro SW, Arets HG, van der Laag J, et al: Radiological and 173. Weisbrod GL, Chamberlain DW, Tao LC: Pulmonary blastoma, report functional changes over 3 years in young children with cystic fibrosis. of three cases and a review of the literature. Can Assoc Radiol J Eur Respir J 30(2):279–285, 2007. 39(2):130–136, 1988. 162. Terheggen-Lagro S, Truijens N, van Poppel N, et al: Correlation of six 174. Wells TR, Gwinn JL, Landing BH, et al: Reconsideration of the anatomy different cystic fibrosis chest radiograph scoring systems with clinical of sling left pulmonary artery: The association of one form with parameters. Pediatr Pulmonol 35(6):441–445, 2003. bridging bronchus and imperforate anus. Anatomic and diagnostic 163. Tiddens HA: Chest computed tomography scans should be considered aspects. J Pediatr Surg 23(10):892–898, 1988. as a routine investigation in cystic fibrosis. Paediatr Respir Rev 175. White RI, Pollak JS: Pulmonary arteriovenous malformations: 7(3):202–208, 2006. Diagnosis with three-dimensional helical CT—A breakthrough without 164. Van Dyke JA, Sagel SS: Calcified pulmonary sequestration: CT contrast media. Radiology 191(3):613–614, 1994. demonstration. J Comput Assist Tomogr 9(2):372–374, 1985. 176. Wick MR, Ritter JH, Humphrey PA: Sarcomatoid carcinomas of the 165. Van Meurs KP, Newman KD, Anderson KD, et al: Effect of lung: A clinicopathologic review. Am J Clin Pathol 108(1):40–53, extracorporeal membrane oxygenation on survival of infants with 1997. congenital diaphragmatic hernia. J Pediatr 117(6):954–960, 1990. 177. Wielpütz MO, Eichinger M, Puderbach M: Magnetic resonance imaging 166. Veenma DC, de Klein A, Tibboel D: Developmental and genetic aspects of cysti fibrosis lung disease. J Thorac Imaging 28(3):151–159, 2013. of congenital diaphragmatic hernia. Pediatr Pulmonol 47(6):534–545, 178. Williams AJ, Schuster SR: Bronchial atresia associated with a 2012. bronchogenic cyst. Evidence of early appearance of atretic segments. 167. Vu L, Tsao K, Lee H, et al: Characteristics of congenital cystic Chest 87(3):396–398, 1985. adenomatoid malformations associated with nonimmune hydrops and 179. Wilson RD, Hedrick HL, Liechty KW, et al: Cystic adenomatoid outcome. J Pediatr Surg 42(8):1351–1356, 2007. malformation of the lung: Review of genetics, prenatal diagnosis, and 168. Vult von Steyern K, Björkman-Burtscher IM, Geijer M: Radiography, in utero treatment. Am J Med Genet A 140(2):151–155, 2006. tomosynthesis, CT and MRI in the evaluation of pulmonary cystic 180. Winters WD, Effmann EL: Congenital masses of the lung: Prenatal and fibrosis: An untangling review of the multitude of scoring systems. postnatal imaging evaluation. J Thorac Imaging 16(4):196–206, 2001. Insights Imaging 4(6):787–798, 2013. 181. Wootton-Gorges SL, Stein-Wexler R, Walton JW, et al: Comparison of 169. Wagner AL, Szabunio M, Hazlett KS, et al: Radiologic manifestations of computed tomography and chest radiography in the detection of rib round pneumonia in adults. AJR Am J Roentgenol 170(3):723–726, fractures in abused infants. Child Abuse Negl 32(6):659–663, 2008. 1998. 182. Yano Y, Mori M, Kagami S, et al: Inflammatory pseudotumor of the 170. Wan YL, Kuo HP, Tsai YH, et al: Eight cases of severe acute respiratory lung with rapid growth. Intern Med 48(15):1279–1282, 2009. syndrome presenting as round pneumonia. AJR Am J Roentgenol 183. Yasufuku M, Maeda K, Takano Y: Thymopharyngeal duct cyst: An 182(6):1567–1570, 2004. unusual cause of respiratory compromise. Pediatr Surg Int 25(9):807– 171. Weber SA, Ferrari GF: Incidence and evolution of nasal polyps in 809, 2009. children and adolescents with cystic fibrosis. Braz J Otorhinolaryngol 184. Yi E, Aubry MC: Pulmonary pseudoneoplasms. Arch Pathol Lab Med 74(1):16–20, 2008. 134(3):417–426, 2010. 42 Biliary Tract and Gallbladder Jae Hoon Lim, Kyoung Won Kim, and Dong-il Choi tography (ERCP), the ampullary segment is usually not visualized BILIARY TRACT because of the contraction of the sphincter of Oddi (Fig. 42-2). The ampulla of Vater is also responsible for the potential reflux of pancre- NORMAL ANATOMY AND VARIANTS atic juice into the CBD. On high-resolution computed tomography (CT), normal intrahepatic bile ducts (IHDs) appear as linear water-density structures accompa- CONGENITAL BILIARY ANOMALIES nying the portal vein branches.177 Normal IHDs measure less than Biliary Atresia 3 mm. They appear to be randomly scattered throughout the liver but are confluent toward the hilum. The IHDs from each lobe unite to In biliary atresia, ultrasonography (US), CT, and a DISIDA (diisopro- form the right and left main hepatic ducts, which are located anterior pyl iminodiacetic acid) scan are the initial imaging studies to evaluate to the portal veins (Fig. 42-1). Periportal lymphedema can mimic a the biliary tree. In more than 10% of patients with biliary atresia, other dilated IHD but shows a low-density area completely surrounding the anomalies are present, such as polysplenia, bilateral bilobed lungs, portal vein.306 azygos continuation of the inferior vena cava, intestinal malrotation, A common anomaly is an aberrant IHD that drains a circumscribed and situs inversus.76 CT can identify the development of cirrhosis, portion of the liver, such as an anterior or posterior segment right lobe varices, splenomegaly, and ascites and plays an important role in the duct that drains into the left rather than the right main hepatic duct. evaluation of such patients before liver transplantation. Surgical difficulties may arise when the cystic duct enters the right Anomalous Pancreaticobiliary Ductal Junction main hepatic duct before joining the left main hepatic duct. The right and left main hepatic ducts unite in the hilum to form the common Anomalous pancreaticobiliary ductal junction is an uncommon con- hepatic duct (CHD). The CHD usually courses along a 45-degree genital anomaly in which the main pancreatic duct and CBD are joined oblique plane with reference to the midline sagittal plane, which lies outside the duodenal wall and form a long common channel (usually to the right and lateral to the proper hepatic artery. The right hepatic >15 mm).181,322 Although this anomaly is found in almost all patients artery typically branches off the proper hepatic artery and passes with congenital choledochal cyst, it is also observed in patients without between the CHD and the main portal vein in about 80% of choledochal cyst.181 Because an anomalous pancreaticobiliary ductal subjects.342 junction is frequently associated with cholangiocarcinoma, early diag- The common bile duct (CBD) forms when the cystic duct joins the nosis is important.181 ERCP is the most reliable method for detecting CHD. This union occurs at varying levels, from high in the porta anomalous pancreaticobiliary ductal junction, but it is an invasive hepatis to near the ampulla of Vater. Because the union is usually not procedure (Fig. 42-3A). Recently magnetic resonance (MR) cholangio- demonstrated on CT, the term common duct is used when the CHD pancreatography (MRCP) and multidetector CT (MDCT) with mul- and CBD cannot be differentiated. Duplications of the CBD and cystic tiplanar reconstruction of images have been used to diagnose this duct are rarely observed. anomaly (see Fig. 42-3B and C).146,237 On CT the CHD usually measures 3 to 6 mm in short-axis diam- eter, and the CBD measures up to 8 mm.12 The diameter should be Choledochal Cyst measured in the short axis because the duct often courses obliquely Choledochal cyst involves congenital cystic dilatation of any portion through the transverse image.96 In postcholecystectomy patients and of the extrahepatic bile ducts, most commonly the main portion of the some older adults, the CBD may measure up to 10 mm without CBD.70,80,108,187,357 It is classified based on the spectrum of morphologic obstruction.12 The wall of the CHD and CBD can normally be dem- changes in the bile ducts. The most common classification scheme is onstrated and measures less than 1.5 mm.298 The wall may enhance the Todani modification of the Alonso-Lej classification326: normally and be brighter than the adjacent pancreas on contrast- Type I: single cystic dilatation of the CBD, CHD, or both (80%-90% enhanced CT. The CBD enters the pancreas and typically lies along the of cases) (Fig. 42-4) posterior and lateral aspect of the pancreatic head. The distal CBD and Type II: true diverticulum of the CBD (3%) main pancreatic duct come into contact on the medial side of the Type III: choledochocele (5%) descending part of the duodenum. The two ducts pass separately Type IV: any combination of cysts, which may include intrahepatic through the wall of the duodenum and unite to form a short dilated cystic dilatation (10%). Type IV-A involves multiple cysts of the tube—the ampulla of Vater. The sphincter of Oddi is the circular common duct and IHDs, and type IV-B involves multiple cysts muscle complex around the CBD, pancreatic duct, and ampulla of of the common duct. Vater; it consists of the sphincter choledochus, sphincter pancreaticus, Type V: cystic dilatation of only the IHDs—so-called Caroli’s and sphincter ampullae. On endoscopic retrograde cholangiopancrea- disease (rare) 1192 CHAPTER 42 Biliary Tract and Gallbladder 1193 A B FIG 42-1 A, High-resolution CT shows normal intrahepatic bile ducts (IHDs) (arrows) as linear water-density structures accompanying the portal vein branches. B, T1-weighted MRI after administration of gadobenate dimeglumine demonstrates IHDs (arrows) with biliary excretion of contrast material located anterior to the portal veins. detecting cystic dilatation of the bile duct on cross-sectional imaging. CT and magnetic resonance imaging (MRI) can make the diagnosis if direct communication with the cyst and the biliary tree is demon- strated (see Figs. 42-3 and 42-4). Cholangiography can confirm the diagnosis. Mild secondary dilatation of IHDs, stones, or sludge may be found as well (Fig. 42-5). Complications of choledochal cysts in adults include rupture with bile peritonitis, stone formation, cholangitis, hemorrhage, portal vein thrombosis, biliary cirrhosis, liver abscess, pancreatitis, and cholangio- carcinoma.108,284 An increased incidence (4%-28%) of malignancy involving the hepatobiliary system has been reported in patients with choledochal cysts, compared with normal subjects.188,325-327,354 Malig- nancy developing in patients with choledochal cyst may be caused by chronic mucosal irritation; it usually occurs in the choledochal cyst but can develop anywhere in the biliary tree, including the gallbladder354 (Fig. 42-6). Cholangiocarcinoma arising in a choledochal cyst appears as a soft tissue–density mass or irregular thickening of the cyst wall. The principal management of choledochal cysts is surgery, with exci- sion of all cyst tissue and reconstruction of continuity between the liver and the gut.284,325 FIG 42-2 Normal ERCP image shows the bile ducts, gallbladder, and main pancreatic duct. The distal part of the common bile duct (arrow) Choledochocele is not seen owing to contraction of the sphincter of Oddi. Choledochocele is a rare anatomic anomaly of unknown cause. It is a protrusion of a dilated intramural segment of the distal CBD into the duodenum, analogous to a ureterocele.61,296,361 On CT a round water- Among these five types, types III and V are not cystic dilatation of the density structure is found in or medial to the pancreatic head or CBD and thus are not considered true choledochal cysts. occasionally within the lumen of the duodenum. Differential diagnos- The cause of this condition is not clear, but it may be multifactorial. tic considerations include an intraluminal duodenal diverticulum, It has been suggested that choledochal cyst, biliary atresia, and neonatal small pseudocyst, duodenal duplication cyst, or small cystic neoplasm hepatitis are part of the same spectrum of disease.194 This condition is of the pancreas. Cholangiography shows smooth saccular dilatation of also associated with an increased incidence of gallbladder anomalies the intramural segment of the CBD (Fig. 42-7). Stones and sludge are and congenital hepatic fibrosis. It may result from an anomalous pan- common, and patients sometimes have episodes of biliary colic, inter- creaticobiliary ductal junction, with free reflux of pancreatic enzymes mittent jaundice, and pancreatitis as well.61,296 into the CBD. Caroli’s Disease Choledochal cysts are more common in females. Although they can present from birth to old age, about 60% of choledochal cysts are Caroli’s disease is also known as communicating cavernous ectasia of the found before adolescence. Newborns and infants present with obstruc- IHDs. The uncommon pure form of this entity involves congenital tive jaundice; older children and adults may have right upper quadrant saccular dilatation of only the IHDs. The more common classic form pain, mass, and intermittent jaundice. The diagnosis is easily made by consists of saccular dilatation of the IHDs with congenital hepatic C A B C FIG 42-3 Anomalous pancreaticobiliary ductal junction. A, ERCP shows a long common channel measuring more than 15 mm (arrowheads). B, MRCP demonstrates an anomalous pancreatico- biliary ductal junction (arrow) and a choledochal cyst (C). Note the long common channel (arrowheads). C, Coronal MDCT with mul- C tiplanar reconstruction demonstrates a long common channel (arrowheads) and choledochal cyst (C). C C FIG 42-4 Choledochal cyst (C). MRCP demonstrates a markedly dilated common bile duct (choledochal cyst) and aberrant insertion of the common duct into the pancreatic duct (arrow). FIG 42-5 Choledochal cyst (C) with a small stone (arrow) on MRCP. CHAPTER 42 Biliary Tract and Gallbladder 1195 C A B FIG 42-6 Gallbladder cancer associated with choledochal cyst (C). A, MRCP shows a lobulated filling-defect lesion (arrows) in the gallbladder. B, T2-weighted transverse MRI demonstrates gallbladder cancer (arrows). C A B C FIG 42-7 Choledochocele. A, MRCP shows a choledochal cyst (C) and choledochocele (arrow). T2-weighted transverse MRI (B) and MDCT (C) show a small cholangiocarcinoma (arrow) within the choledochocele. 1196 PART II CT and MR Imaging of the Whole Body FIG 42-8 Caroli’s disease. MDCT shows cystic dilatation of the intra- FIG 42-9 Three small stones in the gallbladder and one stone in the hepatic bile ducts with stones (white arrows). The black arrow indicates common bile duct, which migrated from the gallbladder. the so-called central dot sign. fibrosis.56,234,314 The common association of congenital CBD dilatation suggests that Caroli’s disease may be part of the spectrum of chole- dochal cyst. In addition this disease is frequently associated with renal tubular ectasia and other renal cystic disease.234 Clinically Caroli’s disease usually manifests in adulthood; however, it can be observed in newborns and infants. Adult patients generally present with recurrent attacks of cholangitis. Infants and children may present with hemateme- sis caused by hepatic fibrosis and portal hypertension.77,158,234 On CT the saccular dilatation of the IHDs may mimic multiple hepatic cysts. The cystic areas of Caroli’s disease can be shown to com- municate directly with the IHDs.12 The distribution of cystic dilatation is often segmental (Fig. 42-8). CT may also show tiny dots with strong contrast enhancement within dilated IHDs—the so-called central dot sign. These dots represent the enhancing portal veins.56 Caroli’s disease is best demonstrated by cholangiography, which shows saccular dilata- tions of the IHDs. Complications of Caroli’s disease include stone formation, cholan- FIG 42-10 A small stone (arrow) in the common bile duct originated gitis, hepatic abscess, hepatic amyloidosis, pancreatitis, and biliary in the gallbladder. The wall of the gallbladder is thickened and enhanced, malignancy.133,222 suggesting acute cholecystitis. PATHOLOGIC CONDITIONS In Asia, pigment stones account for more than 50% of stones, and Choledocholithiasis (Bile Duct Stones) they are formed primarily in the bile ducts6 (Fig. 42-11). Unlike cho- Stones in the extrahepatic duct may originate from the gallbladder or lesterol stones, pigment stones can crumble or crush easily.6 Some primarily from within the bile ducts. Primary stones are formed pri- stones are very friable or muddy, like earth, floating in the bile as marily in the extrahepatic bile ducts. Clearly, stones in the extrahepatic debris. The formation of pigment stones is related to a high prevalence ducts in patients with cholecystectomy or congenital absence of the of recurrent pyogenic cholangitis. Infection of the biliary tract, such gallbladder are primary.27 Extrahepatic duct stones that originate in the as with Escherichia coli, Clonorchis sinensis, Opisthorchis viverrini, or gallbladder and later pass through the cystic duct into the CBD are Ascaris lumbricoides, increases the likelihood of pigment stone forma- called secondary stones.27 tion by increasing the concentration of insoluble calcium salts of In Western countries, stones in the CBD are composed of choles- unconjugated bilirubin.239 terol in about 80% of cases and calcium bilirubinate in 20%. Choles- terol stones arise exclusively in the gallbladder; these stones contain Intrahepatic Stones. Intrahepatic biliary stones, which are formed more than 50% crystalline cholesterol monohydrate.6 Calcium biliru- primarily within the IHDs, are rare in Western countries.183 These binate stones are composed predominantly of bilirubin calcium stones occur in patients with underlying biliary anomalies such as salt; these fragile stones are also called pigment stones.6 About 95% of Caroli’s disease, biliary atresia, or cystic fibrosis or previous biliary patients with choledocholithiasis in Western countries also have gall- surgery.92 In some parts of Asia, intrahepatic stones are common in bladder stones228 (Fig. 42-9); when they do not, the gallbladder may patients with recurrent pyogenic cholangitis. The stones are found show acute or chronic inflammatory changes, suggesting that it previ- mostly in the large-caliber ducts, such as the left hepatic lobe (Fig. ously contained stones27 (Fig. 42-10). 42-12) or the posterior segment of the right hepatic lobe. The stones CHAPTER 42 Biliary Tract and Gallbladder 1197 migrate downward to the CBD or reside in the liver when there is a a stone obstructs the bile duct in the absence of infected bile, asymp- stricture. The bile duct wall shows chronic proliferative cholangitis, tomatic fluctuating jaundice often ensues. When a stone obstructs the suppurative cholangitis, and chronic granulomatous cholangitis, CBD and the bile becomes infected, acute suppurative cholangitis resulting in severe fibrosis and inflammatory cell infiltration.183 ensues (Fig. 42-15). The classic triad of symptoms is fever with chills, pain, and jaundice. Natural History. The natural history of choledocholithiasis is unpre- In patients with recurrent pyogenic cholangitis, stones are continu- dictable. Small stones may pass spontaneously into the duodenum ally formed in the bile ducts and repeatedly pass through the ampulla without causing symptoms. Clinical and autopsy series suggest that of Vater and duodenal papillary orifice; this can cause papillary steno- nearly half of stones do not produce clinical manifestations such as sis, presenting with recurrent bile duct obstruction and cholangitis.272 cholangitis or jaundice.359 Spontaneous resolution of jaundice occurs Typically patients experience one or two attacks of acute suppurative as the stones pass through the duodenal papilla or if the stones float cholangitis a year. back up to the proximal bile duct away from the narrow distal end.27 Passage of a large stone through the narrow duodenal papilla can Imaging Findings. The detectability of a bile duct stone on CT induce papillitis or papillary stenosis and incomplete bile duct obstruc- depends on the calcium content. Although many stones are cholesterol tion254 (Fig. 42-13). stones, some have sufficient bilirubinate and calcium to exhibit high Stones that do not pass and reside in the bile duct may induce attenuation on CT images6 (Fig. 42-16). About 20% of stones are obstructive jaundice and cholangitis or pancreatitis (Fig. 42-14). When homogeneously calcified and easily seen; in others the calcium content is variable.14 Depending on the composition, stones may show soft tissue attenuation, near-water attenuation, or fat or air attenuation, with peripheral calcification around the stone.14 Precontrast CT is FIG 42-11 Multiple stones formed in the common bile duct. There is a tight stricture at the confluence of the bile ducts (arrow). This patient underwent cholecystectomy 10 years ago, so the stones formed in the FIG 42-12 Multiple calcified intrahepatic stones formed in the liver in common bile duct. a patient with recurrent pyogenic cholangitis. A B FIG 42-13 Duodenal papillitis due to a passed stone. The duodenal papilla is swollen (arrow) on CT (A) and cholangiogram (B), and the bile ducts are dilated. 1198 PART II CT and MR Imaging of the Whole Body necessary to visualize calcified stones because postcontrast CT masks them264 (Fig. 42-17). Some stones with mixed composition are isoat- tenuating to bile or adjacent soft tissue and are therefore difficult to detect on CT (Fig. 42-18). Pure cholesterol stones are rare but exhibit low attenuation resembling that of soft tissue (Fig. 42-19) or bile (Fig. 42-20). Stones containing fat or air can be detected because of the difference in attenuation from bile (Fig. 42-21). For more accurate detection of intrahepatic ductal stones, thin section with narrow collimation (<2.5 mm) is necessary. The presence of bile around a stone results in a ring (bull’s-eye or target sign) or a crescent of water attenuation between the stone and the bile duct wall11,14 (Fig. 42-22). A concentrically thickened bile duct wall with enhancement may be seen around a stone, representing inflamma- tion and fibrosis due to irritation by the stone. On cholangiograms or MR cholangiograms, stones are depicted as single or multiple filling defects (Fig. 42-23). Muddy stones, small fragments of stones, and FIG 42-14 Gallstone pancreatitis. The pancreas is enlarged and there gravel are difficult to visualize on CT (see Fig. 42-20), MR, or even is a peripancreatic fluid collection. The common bile duct (arrow) is dilated and the wall is thick. Note the tiny stones in the gallbladder and cholangiography. the thickened gallbladder wall. Bile ducts may not be dilated despite the presence of stones in the common duct in 24% to 36% of cases12,65 (Fig. 42-24). In acute obstruc- tion due to stone impaction, the bile duct does not become dilated until some time has passed. Bile ducts remain dilated after passage of FIG 42-15 Suppurative cholangitis caused by gallbladder stone migra- tion into the common bile duct. Coronal CT shows slightly dilated bile ducts with severe thickening of the walls of the extrahepatic duct and gallbladder. FIG 42-16 Calcified stone (arrow) in the distal common bile duct. A B FIG 42-17 A, Heavily calcified left intrahepatic stones (arrows) are seen on precontrast CT. B, The stones are not clearly delineated on postcontrast CT because the adjacent liver parenchyma enhances. CHAPTER 42 Biliary Tract and Gallbladder 1199 A A B B FIG 42-18 Innumerable small intrahepatic stones in a patient with recurrent pyogenic cholangitis. Because attenuation of the stones and FIG 42-20 Common bile duct stone (arrow) with water attenuation on liver is similar, CT (A) shows several weakly calcified intrahepatic stones CT (A) and cholangiogram (B). (arrows), whereas many stones are visible on cholangiogram (B). FIG 42-19 Common bile duct stone with soft tissue attenuation (arrow). FIG 42-21 Common bile duct stone (arrow) containing air presenting with the “Mercedes-Benz” sign. 1200 PART II CT and MR Imaging of the Whole Body a stone through the papilla of Vater because the duodenal papillary Sometimes a stone that is not detected by one imaging modality is orifice becomes tight owing to papillitis and papillary edema (see demonstrated by another (Fig. 42-25; see Fig. 42-24). Thus two or Fig. 42-13). more imaging methods may be necessary for the diagnosis of bile duct Small stones and gravel repeatedly passing through the duodenal stones. papillary orifice can cause papillitis and eventually papillary steno- sis.92,359 CT or MRI demonstrates a dilated and thickened bile duct and Cholangitis an enlarged duodenal papilla164,275 (see Fig. 42-13) but no actual stone Suppurative Cholangitis. Acute suppurative cholangitis is a bacte- in the bile duct. rial infection of the bile ducts occurring mostly in patients with biliary The ability to detect a biliary stone by imaging varies depending on obstruction caused by either stones or a tumor. Most stones originate the size, location, and components of the stone.90,142,164,209,275,282 Each from the gallbladder (Fig. 42-26). The tumor may be a carcinoma of modality has advantages and disadvantages. With CT, detection the bile ducts, head of the pancreas, or ampulla of Vater or (uncom- depends on the stone’s calcium content and bile duct dilatation. Detec- monly) a benign tumor. tion of stones by MRI is hampered by artifacts caused by pulsation of The bile ducts may be normal or dilated, depending on the cause, the adjacent vessels. During cholangiography, the technique of can- duration, and degree of obstruction. In acute obstruction caused by a nulation and bile duct opacification must be optimal for visualization stone, the bile ducts may not be dilated for some time, whereas in of small stones. obstruction caused by cancer, the bile ducts are usually dilated. FIG 42-23 Small stone (arrows) in the common bile duct on MR FIG 42-22 Common bile duct stone with rim calcification (arrow) mim- cholangiogram. icking a bull’s-eye. A B FIG 42-24 Small stone in the common bile duct. Intraductal sonogram discloses a stone (A), but there is no stone visible on cholangiogram (B).
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