Abstract
Presenter: Prakash Jayanthi MD | Michigan State University College of Human Medicine Background: Mirizzi’s Syndrome is rare, with < 1% incidence in developed countries. No best treatment algorithm is available. Correct preoperative identification and planning is associated with less morbidity, with operative preference based on surgeon experience. The greater the degree of inflammation/erosion, the more complex the treatment - Csendes Type 1 Mirizzi patients benefit from cholecystectomy alone; Types 2-4 may require subtotal cholecystectomy/choledochoplasty versus biliary-enteric reconstruction; Type 5 usually requires fistula takedown/reconstruction. Methods: A 74-year old female presented with severe RUQ pain. CECT Abd/Pelvis: pneumobilia with air in gallbladder fossa. Perforated, gangrenous cholecystitis was suspected. MRI/MRCP: 3.5 cm gallstone impacted in the gallbladder neck, proximal hepatic duct dilatation, likely adjacent abscess. Bilioenteric fistula was suspected due to pneumobilia. Open cholecystectomy was planned for a diagnosis of Csendes Type V - fistula with complete bile duct wall erosion. Normally, fistula takedown with bilio-enteric reconstruction is preferred; however, the fistula ruptured, with resultant severe inflammation making bilio-enteric reconstruction hazardous. Hence, choledochoplasty using a well-vascularized pedicle of gallbladder neck was performed. Results: Intraoperatively, severe inflammation obscured normal anatomy. The gallbladder was taken dome-down. A broad neck of the gallbladder was attached to the CHD, consistent with Mirizzi’s Syndrome. Subtotal cholecystectomy was performed, leaving a remnant cuff vascularized via cystic artery. Frozen sections were sent, with no evidence of cancer. A pericholecystic abscess, likely from a ruptured bilioenteric fistula, was debrided. A 3.5cm gallstone caused near complete erosion of anterior bile duct - Csendes Type V. The back wall of the duct was identified, with proximal channel towards the liver and distal channel towards duodenum. Choledochoscopy demonstrated no obstruction or lesions. Extensive xanthogranulomatous inflammation precluded biliary-enteric reconstruction, with further dissection concerning for possible Right Hepatic artery compromise. The gallbladder flap approximated easily- therefore choledochoplasty was decided upon. Proximal/distal bile duct was cannulated by 18Fr T-tube; choledochoplasty was performed over it, using interrupted 3-0 Maxon suture without narrowing luminal diameter, re-creating an anterior wall for the bile duct common channel. Pressurized saline through T-tube showed no leak. T-tube cholangiogram confirmed patency and absence of stenosis/obstruction. Several weeks later, a T-tube cholangiogram showed satisfactory repair, with appropriate passage of contrast. Hence, the tube was then removed. The patient did not have any complications. Conclusion: Although rare, Mirizzi’s Syndrome is well-known and historically classified into Type 1 - Gallstone compression of bile duct; Type 2 - Common hepatic/bile duct erosion. Csendes et al. (1989) classified Mirizzi syndrome based on degree of erosion of duct wall into 4 types. Type 5 including cholecystoenteric fistula +/- gallstone ileus was added in 2007. Preoperative suspicion is paramount as bile duct injury approaches 17% incidence, with preoperative diagnosis only made in 62% of patients. Open repair is the gold standard. Cholecystectomy should be sufficient in type 1; any duct wall erosion makes a total cholecystectomy potentially unsafe. Bilioenteric reconstruction, e.g. choledochoplasty or hepaticojejunostomy, may be required for continuity. Choledochoscopy is used to confirm patency, as are cholangiograms in patients with T-tube. This case highlights this disease's unpredictable nature, and the need for familiarity with options for repair.
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