Emergent Care / Stabilization:
Assess for signs of severe dehydration and electrolyte disturbances. Obtain point-of-care glucose and intravenous (IV) access.

Diagnosis Overview:
Gastroparesis is a chronic gastric motility disorder that results in delayed gastric emptying without evidence of mechanical obstruction. Patients present with upper gastrointestinal (GI) symptoms including nausea, vomiting, postprandial satiety, bloating, belching, and often epigastric pain. Gastroparesis itself is not an emergency; however, complications of the disease include severe electrolyte derangements that must be identified and addressed quickly to prevent further complications.

The prevalence of gastroparesis has been difficult to quantify, largely due to lack of confirmatory studies in those with suspected symptoms. The estimated prevalence in the general population ranges from 13.8 to 267.7 per 100 000 adults annually. There is a notable female predominance, with women affected nearly 4 times as often as men. Unfortunately, gastroparesis is associated with high frequencies of hospital admissions and visits to the emergency department. The considerable morbidity related to this condition can greatly affect patients' quality of life, often leading to frequent work absenteeism that further increases the socioeconomic burden.

The etiology of gastroparesis varies widely; however, 30%-50% of cases have been labeled as idiopathic. Diabetes and poor glycemic control have been classically associated with gastroparesis. It is estimated that approximately 25%-55% of patients with type 1 diabetes have gastroparesis, and symptoms often persist regardless of subsequent improvements in glycemic control. Certain medications such as proton pump inhibitors (PPIs), glucagon-like-peptide-1 (GLP-1) agonists, narcotics, and CB1 receptor agonists are frequently associated with the development of gastroparesis. PPIs may impair peptide digestion, thus delaying gastric emptying of solids, while GLP-1 agonists, narcotics, and CB1 receptor agonists are all known to slow gastric emptying. Other etiologies include surgical procedures (specifically abdominal surgeries or complications like vagal nerve injury), neurologic diseases (Parkinson disease, multiple sclerosis), connective tissue diseases, and viral infections.

The pathophysiology of gastroparesis is still not well understood, and it is likely that there are multiple contributing factors. Some of the proposed mechanisms include denervation of the vagal nerve, loss of nitric oxide synthase in enteric nerves, and loss of interstitial cells of Cajal, which ultimately leads to delayed gastric emptying. The role of progesterone in promoting relaxation of the smooth muscles of the gut, leading to hypomotility, may contribute to the difference in gender prevalence.