Treatment recommendations for gastroparesis Gastroparesis is defined as delayed gastric emptying due to non-mechanical obstruction, with upper gastrointestinal symptoms such as nausea, vomiting, early satiety, postprandial fullness and abdominal pain. Patients with gastroparesis present frequently to the emergency room and require hospitalization, and may present with malnutrition and metabolic disorders. Most patients with gastroparesis are idiopathic, but many of them have diabetes mellitus. Another important cause of gastroparesis is vagotomy, which is often thought to be an accidental or medical cause of vagus nerve damage. The gold standard for the diagnosis of gastric emptying is that a definitive diagnosis is made by retention of isotopically labeled solid food in the stomach that remains above 10% after 4 hours. Treatment of gastroparesis is based on relieving symptoms (mainly nausea and vomiting), accelerating gastric emptying, and correcting nutritional disorders, while searching for the primary cause. When patients present with symptoms of gastroparesis, the first step is to rule out reversible causes, using upper gastrointestinal endoscopy and imaging including whole small bowel imaging to rule out structural lesions of the gastrointestinal tract, small bowel abnormalities or superior mesenteric artery syndrome. Reversible causes of gastroparesis include: (1) pharmacologic effects, such as anticholinergics, calcium channel blockers, exenatide, pramlintide, lithium preparations, octreotide, narcotics, and side effects of medical or recreational marijuana. (2) Anatomical abnormalities, e.g., median arcuate ligament syndrome. Metabolic disorders, such as optic neuromyelitis optica, neurogenic appetite deficiency, bulimia nervosa. (3) Endocrine disorders, e.g. hypothyroidism, hypoadrenalism. (4) Central nervous system disorders, such as multiple sclerosis, Parkinson’s disease. (5) Tumor concomitant syndromes. When the above etiologies and vagal nerve damage are excluded, patients with gastroparesis are classified as either idiopathic or diabetic gastroparesis depending on the history of diabetes (type 1 and type 2) and glycated hemoglobin data. The current treatment for gastroparesis is based on the severity of gastroparesis at the time of presentation: (1) Mild gastroparesis, where the symptoms of gastroparesis do not occur on a non-daily basis and do not interfere with daily life, with less than 25% isotopically labeled solid food residue in the stomach. (2) Moderate gastroparesis, in which the symptoms of gastroparesis occur daily but do not persist, and daily life can be taken care of by oneself, with occasional emergency visits and isotope-labeled solid food residue of 25% to 35% in the stomach. (3) Severe gastroparesis, in which the symptoms of gastroparesis persist and daily life cannot be taken care of, requiring frequent hospitalization, and isotope-labeled solid food residue in the stomach is greater than 35%. Initial treatment is mainly dietary modification, including small, frequent meals, fluid diet, low dietary fiber and low fat diet. Energy and protein supplementation (e.g., Ensure) is used to maintain body weight, with emphasis on glycemic control in diabetic patients. Interventional pharmacotherapy depends on the severity of symptoms in patients with gastroparesis. Pharmacologic treatment for gastroparesis begins with antiemetics (e.g., ipecac, 5HT3 antagonists, and scopolamine patches) and prokinetics (e.g., metoclopramide at a maximum dose of 10 mg four times daily). Domperidone (10-30 mg orally 4 times daily), the most effective prokinetic and antiemetic agent for the treatment of gastroparesis, is not currently available for clinical treatment in the United States, but can be submitted to the FDA for access through an investigational new drug (IND) application. Erythromycin (50 to 250 mg orally before meals or 3 mg/kg intravenously every 8 hours in hospitalized patients) helps to accelerate gastric emptying. Patients who do not respond to these treatments may be considered for pyridostigmine (Mestinon; 60 to 240 mg daily in divided doses). Central nervous system modulators, such as tricyclic antidepressants (e.g., amitriptyline) and selective 5HT reuptake inhibitors (e.g., duloxetine), may also be used for the treatment of nausea and vomiting in patients with gastroparesis with symptoms of abdominal pain. However, up to 25% of patients have poor outcomes or are intolerant to these medications, referred to as “drug refractory”. In these cases, a surgical intervention of gastric electrical nerve stimulator insertion (Enterra device) accompanied by pyloroplasty is highly effective in resolving all symptoms. In patients with severe symptomatic gastroparesis, a temporary placement of a J-tube to provide nutritional support therapy is possible. In contrast, the ultimate treatment for those patients who do not respond to neurostimulation and pyloroplasty, and those who have been treated with Billroth type I or II surgery in the past, as well as those who do not respond to pharmacological treatment, is total gastrectomy.