Gastroparesis consists of abnormally delayed emptying of stomach contents into the small bowel, usually as a result of damage to the nerves or smooth muscle involved in gastric emptying.
Gastroparesis can result from chronic disorders (diabetes mellitus, scleroderma, intestinal pseudo-obstruction, previous gastric surgery) or, less frequently, from acute metabolic derangements (hypokalemia, hypercalcemia, hypocalcemia, hyperglycemia) or medications (narcotic analgesics, anticholinergic agents,
Mechanical obstruction should always be excluded
Symptoms include nausea, bloating, and vomiting, usually hours after a meal.
A gastric-emptying study consisting of gamma camera scanning after a radiolabeled meal can help with the diagnosis.
Endoscopic evidence of retained food debris in the stomach after an overnight fast may be an indirect indicator of delayed gastric emptying.
Underlying metabolic derangements should be corrected.
Patients should avoid high-fat, high-fiber meals.
High-calorie liquid iso-osmotic meals may be beneficial in refractory situations.
Prokinetic agents have been used with varying degrees of success.
Metoclopramide (10 mg PO qid half an hour before meals) has variable efficacy, and side effects (drowsiness, tardive dyskinesia, parkinsonism) may be limiting.
Erythromycin (250 mg PO tid or 200 mg IV) also stimulates gastric motility.
Tegaserod, a 5-HT4 agonist with prokinetic properties, is being studied for use in gastroparesis