We present a case of spontaneous duodenal fistulization in a 43-year-old man with acute necrotizing pancreatitis demonstrating an unusual temporal sequence, raising questions about the etiopathogenesis of the fistulous connection. The patient presented with severe epigastric pain and was diagnosed with acute pancreatitis based on elevated lipase (579 U/L) and characteristic imaging. By day 6, the disease progressed to necrotizing pancreatitis with extensive peripancreatic collections. However, the patient was tolerating low fat diet. Following discharge, he was re-admitted one week later due to worsening pain and anorexia. Repeat imaging (day 13) demonstrated progression of necrotizing pancreatitis with retroperitoneal fluid collections. On day 16, he developed sudden severe pain with imaging revealing active hemorrhage from a gastroduodenal artery branch, necessitating emergency embolization of the superior pancreaticoduodenal artery. Following embolization, he developed persistent fevers and ileus requiring nasogastric decompression. Imaging on day 24 revealed the pancreatic necrotic collection had dramatically decreased from 7.7 × 12.3 cm to 5.5 × 9.6 cm with copious internal gas, and gas appeared within a hepatic subcapsular collection. Gastrografin study confirmed fistulous communication between the second duodenal portion and the peripancreatic collection. Endoscopy confirmed a fistulous opening extruding necrotic material – this was cleared and a double pigtail catheter was placed for drainage, leading to clinical improvement.

This case highlights a potentially under-recognized mechanism of fistula formation. Gastrointestinal fistulas in acute necrotizing pancreatitis are well-established complications driven by infected necrosis, local anatomical factors, and pancreatic duct disruption.[1] In this patient, spontaneous fistulization can be attributed to infected pancreatic necrosis, pressure from substantial necrotic mass, and direct enzymatic and inflammatory damage to the nearby duodenal wall. [2,3] The temporal relationship with arterial embolization warrants consideration. While iatrogenic factors such as percutaneous drainage or surgical intervention can contribute to external fistula formation, IR-guided arterial embolization has not been reported to predispose to enteric fistulization. Prior studies demonstrate IR-guided embolization to be safe and effective without enteric fistulization as a recognized complication.[4] However, duodenal ischemia following embolization of gastroduodenal artery branches has rarely been reported.[5] The temporal sequence in our patient—arterial embolization on day 16 followed by fistula evidence on day 24 suggests possible association. We hypothesize that IR-guided arterial embolization, particularly of gastroduodenal artery branches, may have contributed to duodenal ischemia that, when superimposed on pre-existing infected necrosis and inflammatory injury, compromised duodenal wall integrity sufficiently to facilitate fistulization. This potential iatrogenic mechanism warrants clinical investigation.