S2999 Not Your Typical Abdominal Pain

Abstract

INTRODUCTION: We present a unique case of a 43 year old male with acute epigastric pain who rapidly decompensated emphasizing the importance for prompt recognition due to potential for increased morbidity. CASE DESCRIPTION/METHODS: Patient presented with acute, dull epigastric pain three days prior to admission with non-bloody emesis. His past medical history was significant for GERD. On presentation he was hemodynamically stable and tender in the epigastric area to palpation without guarding. Initial evaluation of CBC, CMP, and lactate were unremarkable. CT demonstrated diffuse thickening of the gastric wall. PPI therapy was initiated. The subsequent day patient developed altered mental status. He was tachycardic, hypotensive and had a pH of 7.09 with a lactic acid of 11.0. He was transferred to the ICU for aggressive resuscitation. Physical exam was consistent with an acute abdomen. A repeat CT demonstrated marked thickening of the gastric wall, duodenum and jejunum. Patient had an emergent exploratory laparotomy with findings of a partial necrotic stomach resulting in a partial gastrectomy. Post operatively he was febrile and required vasopressor support. He required multiple abdominal washouts. Group A streptococcus grew from both peritoneal fluid culture and gastric pathology. Empiric antibiotics were started and adjusted based on susceptibilities. He continued to decompensate and required a subtotal gastrectomy and omentectomy due to further necrosis. In addition, he developed LV systolic dysfunction and acute gangrene with a right below knee amputation. DISCUSSION: We present a rare cause of acute epigastric pain in a patient ultimately diagnosed with Acute Phlegmonous Gastritis (APG) complicated by septic emboli and below knee amputation. APG is a rare (average about 1 case per year) rapidly progressive bacterial infection of the gastric wall. Early diagnosis, prompt antibiotic treatment, and surgical intervention are crucial in survival benefit of this fatal disease. APG is most commonly caused by β-hemolytic-group A which is resistant to gastric acid. Known risk factors include chronic gastritis, diabetes mellitus and recent upper endoscopy. Despite these risk factors, approximately 50% of patients with APG are without any risk factors. APG is a diagnostic challenge as symptoms are non specific and may rapidly progress to an acute abdomen. Thus, APG should be considered in patients with epigastric abdominal pain who rapidly decompensate to an acute abdomen to avoid delay in diagnosis.