etal. 1973), many researchers began to support this theory. Abnormal pancreaticobiliary duct conuence is a congeni­tal developmental abnormality, in which the pancreatico­biliary duct ows far from the intestinal wall outside the sphincter of the duodenal papilla. According to the differ­ent parts of the conuence, it can be divided into (a) muco­sal or submucosal conuence; (b) external conuence of the intrinsic muscular layer. In the latter case, the pancreati­cobiliary ducts conuence in the pancreatic parenchyma outside the proper muscular layer of the duodenum, and then form a common duct opening to the Vater papilla, which is the theory of abnormal pancreaticobiliary duct conuence. The anatomical basis of this theory is the con­uence of the pancreaticobiliary duct outside the sphincter, the conuent tube is long, and the junction is obtuse. When the distal ampullary sphincter acts, the two tubes can com­municate freely, and the pancreatic juice is often counter­current to the bile duct because of high pressure in the pancreatic duct. The pathological changes of biliary tract caused by pancreatic juice ow into the bile duct were related to the degree of the activation of pancreatic enzyme: (a) there were no pathological changes in the biliary tract if the pancreatic enzyme was not activated; (b) mild or slow activation of the pancreatic enzyme caused hyperplasia of the mucous membrane of the bile duct, metaplasia of the mucosa, and chronic bacterial infection. Mucosal epithelial metaplasia easily leads to complications such as cholecys­titis, biliary calculi, and gallbladder cancer carcinoma; (c) intense activation of the pancreatic enzyme leads to patho­logical changes such as the exfoliation of the mucous mem­brane, rupture of elastic ber in the muscle layer, stricture of the end of the bile duct, and acute bacterial infection. The laceration of elastic bers in the muscular layer of the bile duct is more likely to cause complications such as per­foration of the bile duct and dilatation of the common bile duct. Bile ow into the pancreatic duct mainly causes acute pancreatitis or acute necrotizing pancreatitis.

pancreas can be displayed; from which the degree and range of the dilatation of the intrahepatic and extrahepatic bile ducts can be determined. US has become the currently pre­ferred imaging method. Todani classication: type II biliary cysts and Caroli’s disease are apparent by ultrasound imag­ing. The typical US show “cysts” in the common bile duct, most of which are spherical, oval, or fusiform, and can extend to the hilar of the liver or the head of the pancreas, presenting with a clearly bounded cystic anechoic area. This area is connected to the common bile duct, associated with no or slight dilatation of the proximal bile duct. The cyst is distributed along the main branch of the bile duct and merged with the hepatic portal. The cyst presents a round or fusiform non-echoic area; those which present as “lotus root gan­glion” located in the ventral side of the portal vein and the intrahepatic bile duct with bead dilatation are the manifesta­tion of Caroli’s disease. When complicated with calculi, strong echoic masses are seen in the anechoic area of the bile duct, accompanied by an acoustic shadow, and the position of the bile duct can be moved. When malignant change occurs in the choledochal cyst, it can be seen that the cyst protrudes from the cystic wall to the cystic lumen, presenting an irregular hyperechoic mass or local thickening of the cys­tic wall. Real-time dynamic observation of the changes of the bile duct wall is of great value for early detection of car­cinogenesis. Choledochal cyst and extrahepatic cystadenoma

improved in terms of spatial and temporal resolution. Through MRCT, the size, shape, and extent of cysts can be displayed clearly; also, the relationship between the cysts and their surrounding structures, as well as the complications and signs conducive to the diagnosis of this disease can be well displayed. For example, “central dot” sign: small dotted soft tissue shadow in cystic shadow, whose density is lower or equal to that of liver parenchyma on the plain scan. This “central dot” is the imaging of the intrahepatic portal vein branch, which was previously considered to be a specic sign for the diagnosis of Caroli’s disease; however, some scholars believe that this sign can also be seen in the dilated bile duct after obstruction. Therefore, the diagnosis should be combined with other comprehensive analyses. The “bead­ing sign,” or “tadpole sign”: intrahepatic biliary cysts appear as multiple circular water-like density lesions, with mildly dilated bile ducts and saccular lesions intermingling with each other or on their margins. This disproportionate dilation and its characteristics with normal bile ducts are the keys to differentiate biliary cysts from obstructive biliary dilatation, which is manifested as a gradual thinning ratio from the cen­ter to the periphery. The “beading sign,” or “tadpole sign” is valuable in the diagnosis of Caroli’s disease (Park et al.

able information for the selection of treatment schemes. If there is a communication between the cyst and the bile duct, the resolution of CT is sufcient to show the accumulation of contrast media in the cyst, thus making a denite diagno­sis of the choledochal cyst. However, the display of cholan­giography needs a contrast agent to be discharged into the bile duct. The results of the MSCT can be affected when BD is complicated with obstructive jaundice and cholangitis. Stockberger etal. (Yu etal. 2004) found that the develop­ment rate of the bile duct was only 25% when the level of serum bilirubin was higher than 34μmol/L; while the devel­opment rate of the bile duct was 93% when the level was less than 34μmol/L.At the same time, the incapability of CT to clearly display the detailed characteristics of the dis­tal common bile duct and pancreaticobiliary duct conu­ence brought certain difculties to the formulation of the operation plan.