Management of Delayed Gastric Emptying

31-year-old woman with a 20-year history of insulin-dependent diabetes mellitus presents for the evaluation of nausea, vomiting, postprandial fullness, and discomfort for 6 months. There has been a loss of approximately 10% of her body weight during the same time period. On examination she has a body mass index of 20 (normal, 21–25 kg/m 2 ). Orthostatic hypotension is present on standing. The abdomen is mildly tender in the epigastric region without distention. Stool is negative for occult blood. Fasting blood glucose is 160 mg/dL, and the hemoglobin A1C value is 8.9%. Abdominal ultrasound, complete blood count, thyroid function tests, aminotransferases, and lipase are normal. Upper endoscopy after an overnight fast demonstrates a small amount of retained solid food; however, the mucosa appears normal, and a rapid urease test for Helicobacter pylori is negative. A gastric emptying test with a meal consisting of scrambled eggs radiolabeled with 99m Tc sulfur colloid demonstrates 64% retention at 2 hours (normal, 50%) and 26% retention at 4 hours (normal, 10%). How should this patient with delayed gastric emptying be managed? The Problem Gastroparesis, or delayed gastric emptying, is a common cause of chronic nausea and vomiting. In referral clinics, up to 40% of patients with long-standing type 1 diabetes have delayed gastric emptying primarily as a complication of vagal nerve dysfunction. Symptom exacerbation is frequently associated with poor glycemic control. Acute hyperglycemia may impair gastric emptying. In addition to nausea and vomiting, symptoms of gastroparesis might include early satiety and postprandial fullness. Postprandial and nocturnal abdominal pain can be particularly bothersome in up to 60% of patients and is often recalcitrant to treatment. However, in contrast to functional dyspepsia, pain is usually not the predominant complaint in patients with diabetic gastroparesis. Patients with diabetic gastroparesis frequently have evidence of autonomic neuropathy involving other portions of the gastrointestinal tract including dysphagia, diarrhea, and constipation. Orthostatic hypotension and tachycardia might also be present. Physiologic changes that might explain symptoms in patients with diabetic gastroparesis include impaired fundic relaxation in response to a meal, abnormal antral contractile activity during phase III of the migratory motor complex, gastric dysrhythmias, and pylorospasm. All of these abnormalities might improve with control of hyperglycemia. In patients with gastroparesis, liquid emptying remains relatively normal until the late stages of disease. Delayed gastric emptying of solids is commonly documented scintigraphically by using a radioisotope-labeled meal (Figure 1). Most centers use a 99m Tc sulfur colloid– labeled egg sandwich as a test meal. Scintigraphic images are obtained at baseline, 30 minutes, and then 1 and 2 hours after ingestion, and the results are expressed as percent gastric retention. It has been proposed that extension of the test to 4 hours improves accuracy, but this is not commonly done at most centers. It might be useful to know how much is retained at 4 hours to plan the frequency, consistency, and size of meals.