The initial images (axial FIESTA fat saturated) demonstrate mild intrahepatic ductal dilatation. The proximal common hepatic duct is dilated. A stone is noted centrally in the region of the porta hepatis (3rd axial image). At this stage it is difficult to identify exactly where this stone is, however, a small tubular structure is noted anterior to this stone. Further images more inferiorly demonstrate that the common bile duct and pancreatic ducts are decompressed. There are gallstones in the gallbladder with some wall thickening.
Coronal thin section SSFSE sequences and demonstrate the biliary tree beautifully. These show that there is dilatation of the left hepatic ductal system extending into the common hepatic duct (first image). The second image demonstrates the stone visible on the axial images demonstrates that this stone is actually within the cystic duct. The common bile duct distal and anterior to this on the axial images is compressed at this level and decompressed beyond it. Is also confirmed on the 3-D radial ray thick slab projection demonstrating compression of the common bile duct by a stone in the cystic duct. These findings are typical of Mirizzi syndrome.
Mirizzi syndrome is easy to confuse for cholecystitis or choledocholithiasis and has similar clinical presentation. However, at ERCP the gastroenterologist is often concerned as to the absence of identification of the common bile duct stone identified at ultrasound or MRCP. Typically the syndrome is the result of a stone in the distal cystic duct compressing the common hepatic duct/common bile duct confluence, however, can also occur due to chronic cholecystitis with secondary inflammatory fibrosis affecting the duct at this level.
A fistula may develop from the cystic duct or gallbladder to the more distal biliary tree or small bowel. Such cholecystocholedochal or cholecystoenteric fistulae are part of the syndrome of Mirizzi and are classified as Type II-IV as opposed to Type I for CBD obstruction without fistula. The precise classfication is not so important and is in evolution. IA implies the cystic duct is still present, IB that it is no longer seen, Type II-IV relate to progessive destruction of the CBD). However, it is important to realise that nearly 90% of cholecystoduodenal fistulae are associated with Mirizzi syndrome and therefore this should be sought in circumstances suggesting gallstone ileus.
Surgery, particularly the laparoscopic approach, is complicated in patients with concomitant fistula by an increased risk of CBD injury due to chronic inflammatory effacement of the triangle of Calot. The triangle of Calot is the cystohepatic triangle defined by the common hepatic duct medially, the cystic duct inferolaterally on the inferior aspect of the liver superiorly. In these patients is subtotal cholecystectomy and/or Roux-en-Y surgical approach may be required.
Coronal thin section SSFSE sequences and demonstrate the biliary tree beautifully. These show that there is dilatation of the left hepatic ductal system extending into the common hepatic duct (first image). The second image demonstrates the stone visible on the axial images demonstrates that this stone is actually within the cystic duct. The common bile duct distal and anterior to this on the axial images is compressed at this level and decompressed beyond it. Is also confirmed on the 3-D radial ray thick slab projection demonstrating compression of the common bile duct by a stone in the cystic duct. These findings are typical of Mirizzi syndrome.
Mirizzi syndrome is easy to confuse for cholecystitis or choledocholithiasis and has similar clinical presentation. However, at ERCP the gastroenterologist is often concerned as to the absence of identification of the common bile duct stone identified at ultrasound or MRCP. Typically the syndrome is the result of a stone in the distal cystic duct compressing the common hepatic duct/common bile duct confluence, however, can also occur due to chronic cholecystitis with secondary inflammatory fibrosis affecting the duct at this level.
A fistula may develop from the cystic duct or gallbladder to the more distal biliary tree or small bowel. Such cholecystocholedochal or cholecystoenteric fistulae are part of the syndrome of Mirizzi and are classified as Type II-IV as opposed to Type I for CBD obstruction without fistula. The precise classfication is not so important and is in evolution. IA implies the cystic duct is still present, IB that it is no longer seen, Type II-IV relate to progessive destruction of the CBD). However, it is important to realise that nearly 90% of cholecystoduodenal fistulae are associated with Mirizzi syndrome and therefore this should be sought in circumstances suggesting gallstone ileus.
Surgery, particularly the laparoscopic approach, is complicated in patients with concomitant fistula by an increased risk of CBD injury due to chronic inflammatory effacement of the triangle of Calot. The triangle of Calot is the cystohepatic triangle defined by the common hepatic duct medially, the cystic duct inferolaterally on the inferior aspect of the liver superiorly. In these patients is subtotal cholecystectomy and/or Roux-en-Y surgical approach may be required.
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