S1834 Spontaneous Bacterial Peritonitis in a Postpartum Female Secondary to Necrotizing Pancreatitis

Abstract

Introduction: SBP is an infection of the fluid that accumulates in the abdomen caused by translocation of bacteria without an obvious source, such as bowel perforation. Typically, this translocation represents a failure in defensive factors to contain pathogens to the bowel and can lead to seeding other extra-intestinal sites. Our patient is unique in that her SBP was characterized in the setting of a recent pregnancy. Her course was complicated by pre-eclampsia resulting in emergent c-section, further complicated by hypertriglyceridemia-induced pancreatitis. After significant intervention, necrotizing pancreatitis leading to retroperitoneal fat saponification and abscess formation was the likely etiology for SBP. Case Description/Methods: A 27-year-old female presented with diffuse abdominal pain, nausea, vomiting, and diarrhea. Past medical history is significant for recent emergency c-section due to pre-eclampsia complicated by hypertriglyceridemia-induced pancreatitis. On admission, she was hypotensive, tachycardic, tachypneic and febrile, with significant bilious emesis. CT revealed large volume ascites, peri-pancreatic fluid, small volume fluid and gas within the endometrial cavity. Peritoneal fluid analysis presented an SBP picture. Abdominal drains were placed to mitigate peritoneal fluid collection, which settled in the retro-peritoneal space. Cultures resulted in pan-sensitive E.coli growth and the patient was started on appropriate therapy. However, the patient continued to have persistent fevers and severe abdominal pain while on medical management. At this point, exploratory abdominal surgery was indicated revealing significant amounts of retroperitoneal saponified fat secondary to necrotizing pancreatitis, and extensive communicating abscesses which were subsequently drained. Discussion: SBP is an infection of fluid that accumulates within the abdomen, typically seen in patient's with chronic liver disease and can be managed with medical therapy. In our patient's case, there was no know history of liver disease. Our patient presented febrile, with diffuse abdominal pain. Imaging revealed significant ascites and cultures resulted in pan-sensitive E.coli. Multiple differentials were assessed including recurrent pancreatitis, C.difficile infection leading to bowel perforation and/or protein-losing enteropathy, endometritis given recent c-section amongst others. After surgical assessment, our likely diagnosis was necrotizing pancreatitis seeding pancreatic enzymes into the retroperitoneal cavity.