A 42-year-old man was evaluated by our hospital with a 3-week history of epigastric abdominal pain and melena. He described the abdominal pain as intermittent, dull, 4/10 in intensity, non-radiating, and with no aggravating or relieving factors. He also reported 2–3 episodes of melena daily for 3 weeks, nausea and non-bloody emesis, unrelated to eating. He had been admitted 1 year previously with severe alcohol-related necrotizing pancreatitis. Though he had quit alcohol for several months after this first admission, he had relapsed and reported drinking 1 pint of whiskey up to 3 days prior to admission. He also reported falling while skiing 1 month prior and said that he was taking ibuprofen 600 mg up to twice a day for aches in his extremities. The only other medication he reported taking was omeprazole 20 mg once a day for heartburn. Aside from melena on rectal examination, his physical examination and vital signs were unremarkable. Nevertheless, laboratory evaluation revealed a hemoglobin of 8.8 g/dL (13.8–17.2 g/dL), reduced from 13.3 g/dL 1 year ago, with MCV 98 fl (81–101 fl), RDW 13.3% (11–14.5%). His liver enzymes were unremarkable. Computed tomographic (CT) scan of the abdomen showed changes of acute pancreatitis with focal necrosis involving the distal pancreatic body and tail, as well as an incidental finding of partial thrombosis of the splenic vein. Given the presentation of melena, a fall in hemoglobin concentration, and a history of using ibuprofen, a peptic ulcer was suspected as the cause of bleeding. On the second hospital day, esophagogastroduodenoscopy (EGD) was performed; this revealed no source of bleeding in the esophagus or stomach, but in the duodenum active extravasation of blood from the duodenal papilla was observed. Upon close examination, it appeared that there was also an intermittent flow of clear bile, suggesting that the pancreas, and not the liver, was the bleeding source, i.e., the presence of hemosuccus pancreaticus. Given the history of pancreatitis, a ruptured pseudoaneurysm was suspected. At CT angiography, the ruptured vessel was identified as the pancreaticoduodenal artery (PDA) where it arose from the gastroduodenal artery (GDA) (Fig. 1). Using selective angiography, an interventional radiologist treated the area of bleeding by embolizing coils to the pancreaticoduodenal and gastroduodenal arteries (Figs. 2, 3). Two days later, CT angiography showed no evidence of a pseudoaneurysm, vascular lesion, or continuing hemorrhage. Six months after embolization and discharge from hospital, the patient remains well.
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