S3352 The Impostor Within: Contained Gastric Perforation Mimicking Pancreatic Walled-Off Necrosis

Introduction: The Atlanta classification defines walled-off necrosis (WON) as a mature, encapsulated collection of necrotic tissue that develops at least 4 weeks after necrotizing pancreatitis. Although imaging and clinical context guide diagnosis, overlapping features may obscure alternative etiologies. We present a case of presumed early walled-off pancreatic necrosis (WOPN) that was instead a contained gastric ulcer perforation with rapid wall formation. Case Description/Methods: A 59-year-old obese man with history of alcohol use disorder and recurrent pancreatitis presented with sharp epigastric pain and a lipase >2000 U/L, consistent with acute pancreatitis. A computed tomography scan on hospital day 2 revealed an acute peripancreatic necrotic fluid collection without wall formation. For peritoneal signs on day 3, repeat computed tomography demonstrated interval enlargement of the peripancreatic fluid collection with early wall formation, presumed to be WOPN. Esophagogastroduodenoscopy (EGD) with endoscopic ultrasound (EUS) revealed a >10 cm × 10 cm walled-off necrosis, drained via EUS-guided cystogastrostomy using 2 lumen-apposing metal stents in the proximal and distal gastric body (multiple transluminal gateway technique). A total of 3 necrosectomies were performed. During the second, a large gastric body ulcer was discovered. Given the ulcer’s proximity to the necrotic cavity with rapid wall formation within 13 days of pancreatitis, a contained gastric perforation was suspected to be the true etiology, not WOPN. The patient was ultimately discharged in stable condition to rehab with outpatient monitoring. Discussion: This case illustrates the importance of challenging diagnostic assumptions. Given the history of alcohol use disorder, the patient’s fluid collection was initially attributed to his presentation with pancreatitis. However, the timeline was not consistent with typical WOPN. Radiographic and endoscopic findings concluded that the peripancreatic fluid collection was instead a result of a contained gastric ulcer perforation with rapid wall formation. The enlarging fluid collection was likely due to intraluminal hemorrhage with clot formation and necrotic cavity expansion adjacent to the stomach. This case underscores the risk of anchoring bias in pancreatic pathology and highlights the diagnostic value of endoscopy when imaging is non-specific. Early recognition of contained gastric perforation can guide timely intervention and avoid unnecessary or mistimed procedures.