3239 Gastric Outlet Obstruction in Setting of Acute Cholecystitis With Duodenal Lipoma

Abstract

INTRODUCTION: Gastric outlet obstruction (GOO) overall incidence has declined after improved treatment of its benign etiologies. The only remote association between GOO and acute cholecystitis is through Bouveret syndrome, which is characterized by a gallstone ileus in setting of a bilioenteric fistula. Duodenal lipomas are very rare, and literature review reveals only 39 cases reported specifically in the second portion of the duodenum. This is the first reported case of GOO occurring in setting of severe acute cholecystitis and duodenal lipomas, with complete resolution after treatment of the acute cholecystitis. CASE DESCRIPTION/METHODS: A 71 year-old male presented for an unrestrained motor vehicle crash with multiple fractures including left femur fracture requiring surgical intervention. CT on admission showed mild gastric distention, 1.2 cm calcified cholelith. One week postoperatively, he complained of new onset right upper quadrant pain, with subsequent nausea and non bloody emesis. His physical exam was positive for Murphy's sign. His vitals showed tachycardia. His labwork revealed increasing leukocytosis from 13K to 43K with concerns for sepsis. Liver chemistries were WNL, except elevated alkaline phosphatase 171. Repeat imaging demonstrated new findings of acute cholecystitis, duodenal wall thickening, duodenal lipomas, and gastric distention with fluid suggesting gastric outlet obstruction, presumably secondary to the inflammatory process. The patient had nasogastric tube decompression with 2.6 liter output, followed by emergent percutaneous cholecystostomy tube. The patient gastrointestinal symptoms, gastric distention, and leukocytosis significantly improved. Then two days later, EGD was notable for LA Grade D esophagitis and two large duodenal lipomas the in second portion. DISCUSSION: To our knowledge this is the first documented case of GOO associated with acute cholecystitis in the setting of duodenal lipoma. With our case we concluded the GOO pathophysiology was dependent on the degree of inflammation from cholecystitis causing worsening intraluminal narrowing in relation to the specific location of the lipoma. Given the entities have varying presentations, clinical suspicion should remain high, and diagnosis relies on successful imaging and endoscopic evaluation. Treatment of the underlying acute cholecystitis should be urgent with either percutaneous cholecystostomy tube or cholecystectomy, if feasible. The excision of the benign duodenal lipoma can be made on a case-by-case basis.