3231 Gastric Outlet Obstruction in a Patient After Hip Surgery

Abstract

INTRODUCTION: Until the 1970s, peptic ulcer disease was the most prevalent cause for gastric outlet obstructions (GOO) and accounted for 90 percent of all cases. However, with the introduction of proton pump inhibitors (PPI) and the treatment of H. pylori infections, the etiology of GOO changed rapidly. Today, only around two percent of all peptic ulcers lead to GOO. Here we report the case of a woman with nausea, abdominal pain and coffee ground emesis, found to have a GOO, whose symptoms completely subsided under PPI treatment of a 12 mm large peptic ulcer (Forrest III) in the duodenal bulb. CASE DESCRIPTION/METHODS: A 62-year-old female patient with a history of hypothyroidism, recent left hip fracture repair and subsequent pulmonary embolism, presented with nausea, hematemesis, melena, epigastric pain, decreased appetite and weight loss. She was treated with daily aspirin 325 mg and apixaban, and denied any drug abuse. PPI prophylaxis was not administered. Her physical examination was unremarkable. Initial blood tests included blood count, electrolytes and coagulation monitoring, and were unremarkable except for mild anemia (hemoglobin 9.9 g/dL). Contrast CTs of the abdomen and pelvis with PO/IV contrast showed marked gastric distension with luminal narrowing at the level of the duodenal bulb. Small and large bowel appeared normal in caliber and neither obstructions nor wall thickenings could be found. Accordingly, an esophagogastroduodenoscopy was performed showing a non-bleeding, cratered ulcer with a clean ulcer base (Forrest III) in the duodenal bulb. The lesion was 12 mm in largest dimension and surrounded by edema and erythema, resulting in a complete luminal obstruction. Upon gastric decompression with a nasogastric tube and PPI treatment, the patient recovered quickly and was discharged after four days. DISCUSSION: Due to an increase in PPI administration and H. pylori eradication in the last decades, peptic ulcers are nowadays treated early on, and gastric outlet obstruction has become a rare complication of peptic ulcer disease. In this case, we report on a 62-year-old patient who developed an obstructive peptic ulcer following extensive hip surgery and anticoagulation with aspirin and apixaban. We hereby want to highlight the importance of a timely PPI prophylaxis for peptic ulcer disease in severely ill patients with chronic NSAID intake. Conservative measures can moreover suffice to resolve the issue.