Hassnain Syed, MD, Abrar Arshad, MD, Tage Haase, MD, Suman Shekar, MD, Avinash Aravantagi, MD; University of Kentucky, Bowling Green, KY
Introduction: Endoscopic biliary stenting plays a major role in the management of pancreaticobiliary disease. Unfortunately, even this novel idea comes with complications. Some of these risks include stent occlusion, cholangitis, and pancreatitis. Stent migration, although rare, has also been described, with more cases associated with plastic stents as compared to metal stents. More unlikely still is resultant perforation, as most dislodged stents remain in the bowel without causing clinical symptoms until ultimately excreted in the stool. This case report aims to discuss the first example of rectal perforation caused by a migrated biliary stent.
Methods: Our patient is a 77-year old female who presented to the emergency room for abdominal pain. She has a significant history of recurrent pancreatitis complicated by bile duct stricture requiring multiple visits for common bile duct stent placement. The patient was admitted two months prior for acute pancreatitis. At that time, an ERCP revealed rapid tapering of the bile duct at the level of the ampulla with subsequent intervention via placement of a 10-French 7-cm plastic stent. During this visit, a CT scan of the abdomen revealed migration of the previously placed stent to the rectosigmoid colon, along with diverticulosis. Specifically, the proximal portion was seen located in the wall of the left lateral sigmoid colon and distal portion of the stent had perforated the right aspect of the rectal vault. A flexible sigmoidoscopy was performed with successful extraction through the anus. Discussion: The most common site of perforation by a biliary stent is the duodenum. The most likely reason for this is that the duodenum is largely retroperitoneal, and therefore fixed. Furthermore, anatomic proximity also plays a part as the major papilla is located in the second part of the duodenum. Bowel fixation in a hernial sac, presence of adhesions, and diverticular disease all seem to be associated with increasing risk of perforation due to the impedance of peristalsis. Our case is unique as the stent perforated the distal rectum, which is anatomically extra-peritoneal. Extra-peritoneal organs are embedded in connective tissue hence making them fixed-thus increasing risk of perforation. It was most probably her diverticular disease which predisposed her to the rectal wall perforation. The diverticulum acted as an anchor, essentially trapping the stent proximally. The distal end was free to poke and prod, eventually perforating the rectal wall.
Disclosures: Hassnain Syed indicated no relevant financial relationships. Abrar Arshad indicated no relevant financial relationships. Tage Haase indicated no relevant financial relationships. Suman Shekar indicated no relevant financial relationships. Avinash Aravantagi indicated no relevant financial relationships.