1257 Pancreatic Pseudocyst-Portal Vein Fistula: A Rare Life-Threatening Complication of Pancreatitis

Abstract

INTRODUCTION: Pancreatitis is an acute inflammatory process that can results in activation of systemic inflammatory cascade. The pancreas is encased by vasculature which can be directly and indirectly affected. The aim of this case is to provide insight into a rare complication of pancreatitis. CASE DESCRIPTION/METHODS: 35-year-old male with history of alcohol abuse presented to the emergency room with three days of severe epigastric pain. Denied symptoms of overt gastrointestinal bleeding. On admission, vital signs were temperature of 99.2°F, heart rate 115 beats/min, blood pressure of 120/72 mmHg. Initial laboratory evaluation demonstrated hemoglobin of 6.6 g/dL, lipase of 1,910 U/L, alanine transaminase 152 U/L and aspartate transaminase 167 U/L, alkaline phosphatase 681 U/L and direct hyperbilirubinemia 9.2 mg/dL. A computed tomography (CT) of the abdomen showed a large well-circumscribed cystic lesion with hypodense fluid in the peripancreatic C-loop with linear hyperdensity in the center, suggestive of a clot, and with direct communication to a dilated non-opacifying portal vein along with cavernous transformation. These findings were suggestive of a hemorrhagic pancreatic pseudocyst with fistulization of the main portal vein and portal vein thrombosis. The cystic lesion was compressing the common bile duct, measuring 1.1 cm, leading to hyperbilirubinemia. Portovenography did not show active opacification of the cystic lesion and, therefore, the cyst was percutaneously aspirated and 25 cc of light brown fluid removed. Fluid analysis revealed an amylase of 10,196 U/L. Given persistent hyperbilirubinemia, patient was taken for ERCP with biliary stent placement resulting in resolution of jaundice. His clinical course was further complicated by development of ascites and secondary peritonitis which was managed with antibiotics. DISCUSSION: Pancreatic pseudocyst with portal vein fistulization is an extremely rare complication of pancreatitis. The proposed mechanism of fistulization is believed to be due to high pancreatic enzyme contents of the pseudocyst eroding into adjacent structure. The release of digestive enzymes into a patent portal vein may directly cause intravascular thrombosis. Alternatively, it is hypothesized that fistulization usually occurs after portal vein thrombosis. No clear consensus exists on management with high mortality and morbidity secondary to hemorrhage, septic shock, and lipolysis. Our patient improved with conservative management of the pseudocyst with a decrease in cyst size.