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Metallic biliary endoprosthesis causing duodenal perforation and acute upper gastrointestinal bleeding

1994; Elsevier BV; Volume: 40; Issue: 2 Linguagem: Inglês

10.1016/s0016-5107(94)70188-1

1097-6779

Benjamin J. Marano, Charles A. Bonanno,

Esophageal and GI Pathology

We describe a patient with a duodenal perforation and a biliary-duodenal fistula presenting with acute UGI bleeding as a complication of a self-expanding metallic biliary endoprosthesis. A 76-year-old man with a long history of smoking presented with recent onset of weight loss and jaundice. Physical examination was remarkable for hepatomegaly. Laboratory values revealed a total bilirubin of 7.7 mg/dl. CT of the abdomen revealed a liver mass, liver metastases, dilated intrahepatic bile ducts but a normal caliber common bile duct. A percutaneous trans-hepatic cholangiogram identified a mass at the level of the common hepatic duct (Klatskin tumor). A plastic stent was placed through the obstructing lesion, and an external drain provided initial decompression. Total bilirubin improved to 3.5 mg/dl. A repeat percutaneous trans-hepatic cholangiogram with biopsy confirmed the diagnosis of well-differentiated cholangiocarcinoma. The patient received iridium (Ir-192) implants delivered by a radiologically guided introducer to the site of the lesion. The implants were removed 48 hours later when treatment was complete. Internal drainage was believed to provide the best palliation and quality of life for this patient with malignant bile duct obstruction. A self-expanding metallic biliary endoprosthesis (Schneider Wallstent; Wallstent, Schneider/Pfizer, Minneapolis, Minn.) was inserted by a trans-hepatic route. Two 42-mm-long stents were required to bridge the common hepatic duct malignancy. The stents were expanded to the full 10 mm diameter. Excellent internal drainage was achieved, and total bilirubin returned to normal range. He was discharged to receive a course of external radiation therapy. The patient did well at home for 6 months but then returned to the hospital with pneumonia and pneumococcal sepsis. The metallic endoprosthesis was functioning well, and the total bilirubin remained in the normal range. During recovery ascites developed. Ultrasound examination revealed progression of metastatic lesions in the liver parenchyma but no biliary obstruction. Paracentesis revealed a low protein level and a high WBC count consistent with spontaneous bacterial peritonitis. Cultures grew Enterobacter cloacae. The spontaneous bacterial peritonitis resolved with intravenous antibiotics, and the ascites was controlled with diuretics. The patient did well for 1 month when hematemesis developed and a drop in his hematocrit occurred. Upper endoscopy revealed small non-bleeding esophageal varices and a large ulcer on the posterior wall of the duodenal bulb. The mesh of the lateral aspect of the metal biliary endoprosthesis was clearly visible perforating through the ulcer base (Fig. 1, Fig. 1). Endoscopic biopsy specimens of the ulcer were free of malignant cells. Bleeding stopped spontaneously, and no further episodes were noted. CT of the abdomen confirmed position of the endoprosthesis in the biliary system. UGI series also documented endoprosthesis position and demonstrated a fistula from the bile duct to the posterior wall of the duodenum (Fig. 2). Fig. 2UGI series with barium contrast demonstrating the stomach and duodenal sweep with metallic biliary endoprosthesis in place and biliary-duodenal fistula (arrow).View Large Image Figure ViewerDownload (PPT)The metallic biliary endoprosthesis remained patent and continued to drain well, providing de-compression of the biliary system. The patient recovered and was discharged. He remained at home for 6 weeks when he experienced hematemasis. Upper endoscopy again documented the metallic endoprosthesis perforating the duodenal wall and the biliary duodenal fistula. Bleeding stopped spontaneously. During the admission the metastatic liver disease progressed. Hepatorenal syndrome developed and the patient expired approximately 1 year after his initial diagnosis of cholangiocarcinoma. Duodenal perforation is a rare complication of plastic biliary endoprosthesis.1Lammer J Neumayer K Biliary drainage endoprosthesis: experience with 202 placements.Radiology. 1986; 159: 625-629Crossref PubMed Scopus (130) Google Scholar, 2Dooley JS Dick P George RM et al.Percutaneous transhepatic endoprosthesis for bile duct obstruction: complications and results.Gastroenterology. 1984; 86: 905-909PubMed Google Scholar, 3Cohen ME Goldberg RI Barkin JS et al.Bile duct perforation: a complication of large caliber endoprosthesis.Gastrointest Endosc. 1989; 35: 456-458Abstract Full Text PDF PubMed Scopus (3) Google Scholar, 4Gould J Train JS Dan SJ et al.Duodenal perforation as a delayed complication of placement of a biliary endoprosthesis.Radiology. 1988; 167: 467-469Crossref PubMed Scopus (46) Google Scholar Duodenal ulcer from a metallic endoprosthesis protruding through the papilla has been reported.5Lameris JS Stoker J Nijis HGT et al.Malignant biliary obstruction: percutaneous use of self-expandable stents.Radiology. 1991; 179: 703-707Crossref PubMed Scopus (160) Google Scholar We now describe a perforation of the posterior duodenal wall, a biliary-duodenal fistula, and acute UGI bleeding as a complication of a metallic biliary endoprosthesis. The underlying mechanism of these complications is not completely clear. This patient had cholangiocarcinoma. It is possible that malignancy in the bile duct or duodenal wall contributed to weakness of these structures with subsequent perforation and fistula formation. Evaluation of the CT scan and endoscopic biopsy specimens do not demonstrate malignancy in this area. Our patient also received both radioactive implants and external radiation therapy. It is possible that radiation injury to the bile duct or duodenal wall pre-disposed these structures to perforation and fistula formation. Finally, the metallic endoprosthesis may have exerted force on the lateral bile duct wall causing pressure necrosis that resulted in duodenal perforation and biliary-duodenal fistula. We believe the last explanation is the most likely in this specific case.