Abstract

Purpose: Acute pancreatitis is a common diagnosis with approximately 210,000 new cases annually in the United States. Of these new cases, 80% are interstitial and 20% are necrotizing. Necrotizing pancreatitis is associated with both increased mortality and multiple complications including multi-organ failure, shock and fistulization with massive GI bleed. A 60-year-old AAM with a mechanical aortic valve on chronic anticoagulation and a history of alcohol abuse initially presented 2 months prior with acute necrotizing pancreatitis secondary to alcohol abuse. He was treated conservatively with aggressive hydration, pain control and antibiotics and had an uneventful hospitalization. He represented with the acute onset of shortness of breath, nausea, emesis and epigastric pain. Routine labs on admission were notable for an elevated lipase of 417, wbc of 10.7, ALT of 20, AST of 27 and hemoglobin 13.7 g/dL. Hypoxia developed requiring mechanical ventilation along with atrial fibrillation with rapid ventricular response necessitating ICU transfer. He was hemodynamically stabilized and treated aggressive for acute pancreatitis with IVF and narcotic pain medications. Upon transfer from the ICU, he developed worsening epigastric and RUQ pain and melena with a notable decrease in hemoglobin to 6.7 g/dL in the setting of a supratherpeutic INR. A CT pancreas protocol was performed which demonstrated a large pseudocyst measuring 7.3 x 11.4 cm with a large hemorrhagic component, mass effect on the gastric antrum and air present in the head of pancreas without evidence of pseudoaneurysm. His underlying coagulopathy was corrected and an upper endoscopy was performed which found hematin through the stomach and a large fistula in the duodenal bulb with blood/mucin exuding through the tract. A pancreaticoduodenal fistula with associated massive hemorrhage was suspected as the source to his GI bleed. Gastroenterology and pancreaticobiliary surgery were consulted and conservative management was recommended. Pancreaticoduodenal fistula is a rare complication of necrotizing pancreatitis and is associated with massive GI bleeding in 30% of cases. Pancreatic fistulas tend to develop late in the clinical course of severe pancreatitis either from decompression of a pseudocyst or as a complication of phlegmonous pancreatitis. Fistulous communication allows bowel enterokinases to activate pancreatic trypsinogen. Trypsin and other pancreatic enzymes may ultimately result in erosion into nearby vasculature resulting in massive hemorrhage. Treatment is usually conservative. Pancreaticoduodenal fistula should be considered in all patients with recent severe/necrotizing pancreatitis and upper GI bleed.

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