1853 Impaired Gastric Accommodation: A Key Player in Functional Dyspepsia

Abstract

INTRODUCTION: Poor gastric accommodation (GA) causes inadequate relaxation of the stomach during a meal. This leads to early satiety, fullness sensation, nausea, and vomiting. Poor GA is frequently seen in functional GI disorders and often coincided with anxiety and stress. It should be considered in the absence of metabolic disorders, eating disorders, and self-induced vomiting. Poor GA is quantified by the average increase of gastric volume after a meal over 1 hour. Poor GA is thought to be caused by altered neuro-modulatory pathways that affect accommodation time after a meal. CASE DESCRIPTION/METHODS: A 53-year-old woman with history of Type II Diabetes with Hba1c: 9.4%, complicated by diabetic neuropathy was admitted for treatment of UTI and Herpes Zoster. She also complained of new onset nausea, vomiting, and early satiety for 1 week. She could tolerate only thin liquids but no solids, due to persistent emesis within 10-20 min of food ingestion. An EGD was done and ruled out gastric outlet obstruction, but revealed candida esophagitis, which was treated with Fluconazole. The patient was then started empirically on Metoclopramide for presumptive Gastroparesis in the setting of poorly controlled Diabetes. The dose was gradually titrated up without favorable response. Her therapy was then escalated to Erythromycin along with Zofran and Benadryl, with no success. The patient was unable to complete a Gastric Emptying (GE) Study twice due to emesis following radiotracer ingestion. However, images from incomplete GE studies showed rapid movement of radiotracer from the fundus to the antrum. The patient was then switched to Buspirone 5 mg 30 minutes before lunch and dinner with remarkable improvement of her symptoms in 2 days. DISCUSSION: Early redistribution of radiotracer seen on scintigraphy is suggestive of impaired accommodation and is usually associated with early satiety, dyspepsia, nausea and vomiting. Rapid clinical improvement after 5-HT1a receptor agonist therapy not only implies anxiety and stress as contributing factors in this disorder, but also the role of presynaptic inhibitory 5-HT1a receptor activation in the gastric accommodation reflex. This allows for better stomach relaxation both in fasting and postprandial states. This therapy should be considered in patients with gastroparesis-like symptoms, but rapid gastric emptying seen on scintigraphy.