Gastroparesis

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Gastroparesis is characterized by delayed gastric emptying in the absence of mechanical obstruction. Common etiologies include diabetes mellitus, postsurgical complications, and medication side effects, although many cases are idiopathic. Patients typically present with nausea, vomiting, bloating, upper abdominal pain, and early satiety. Diagnosis requires ruling out mechanical obstruction via esophagogastroduodenoscopy (EGD) and confirming delayed emptying with a 4-hour gastric emptying study. Underlying causes and factors (e.g., diabetes mellitus, medications) should be identified and addressed. Initial management involves dietary modifications, such as consuming small, frequent, low-fat meals, and adjusting medication that delays gastric emptying. Pharmacotherapy includes prokinetics like metoclopramide and erythromycin, and antiemetics for symptom relief. Refractory cases may require procedural interventions, such as gastric peroral endoscopic pyloromyotomy, or enteral nutrition via jejunostomy. Significant complications include malnutrition, electrolyte imbalances, and postprandial hypoglycemia in patients with diabetes.

• Prevalence: 21.5 per 100,000 persons in the general population ^[2]
• Incidence (10-year cumulative) ^[3]
  • 0.2% of patients without diabetes mellitus
  • 1.0% of patients with type 2 diabetes
  • 5.2% of patients with type 1 diabetes

Epidemiological data refers to the US, unless otherwise specified.

Causes of gastroparesis ^[2][4][5]

• Idiopathic (most common)
• Diabetes mellitus with poor glycemic control (diabetic gastroparesis)
• Postsurgical (e.g., following bariatric or other foregut surgery)
• Neurological disorders (e.g., Parkinson disease, multiple sclerosis)
• Infiltrative disorders (e.g., amyloidosis)
• Connective tissue disorders (e.g., scleroderma)

Factors associated with delayed gastric emptying ^[2][6]

• Medications
  • Opioids
  • Tricyclic antidepressants
  • Calcium channel blockers
  • Clonidine
  • Dopamine agonists
  • Lithium
  • Progesterone
  • GLP-1 receptor agonists ^[7]
  • Pramlintide ^[8]
• Recreational substances (e.g., cannabis, nicotine, heavy alcohol use) ^[9][10]
• Acute hyperglycemia
• Hypothyroidism
• Acute gastrointestinal infection

The pathophysiology of gastroparesis is complex; contributing factors include disordered: ^[11]

• Gastric accommodation
• Nerve conduction (e.g., electrical dysrhythmias, vagal nerve injury)
• Antroduodenal coordination
• Pyloric function
• Visceral sensation

Chronic hyperglycemia in patients with diabetes leads to vagal and interstitial cell of Cajal dysfunction, resulting in a loss of gastric electrical rhythm and pyloric coordination. This breakdown in neuromuscular control manifests as delayed gastric emptying (gastroparesis), typically presenting with postprandial fullness and the vomiting of undigested food. ^[3][12]

• Common symptoms ^[4]
  • Nausea and/or vomiting
  • Bloating
  • Upper abdominal pain
  • Loss of appetite
  • Early satiety
  • Postprandial fullness
• Examination findings ^[13][14]
  • Abdominal distension
  • Epigastric tenderness
  • Succussion splash

• Rule out alternative causes of gastrointestinal symptoms.
• Obtain EGD to exclude mechanical gastric outlet obstruction. ^[4]
• Refer to gastroenterology for one of the following 4-hour studies to confirm delayed gastric emptying: ^[4]
  • Gastric emptying scintigraphy (preferred): positive if > 10% gastric retention after 4 hours ^[4][15]
  • Stable isotope breath test: Results are reported as normal, delayed, or accelerated gastric emptying. ^[16]
• Investigate for underlying causes of gastroparesis (e.g., screening for diabetes mellitus, diagnostics of hypothyroidism).

Whenever possible, stop medications that affect gastric emptying at least 48 hours before a gastric emptying study to improve the accuracy of the results. ^[15]

• Gastric outlet obstruction
• Gastroesophageal reflux disease
• Acute pancreatitis or chronic pancreatitis
• Malignancy (e.g., gastric cancer)
• Eating disorders (e.g., avoidant restrictive food intake disorder) ^[15]
• Cyclic vomiting syndrome
• Cannabinoid hyperemesis syndrome ^[15]
• Functional dyspepsia ^[17]
• See also "Differential diagnoses of abdominal pain."

The differential diagnoses listed here are not exhaustive.

Approach ^[4]

• Address factors associated with delayed gastric emptying (e.g., review medications, counsel on substance use).
• Initiate dietary modifications in consultation with a nutritionist. ^[6][15][18]
  • Small, frequent meals
  • Low in fat and fiber
  • Small particle size ^[19]
• Consider pharmacotherapy if symptoms persist.
• Manage underlying causes of gastroparesis (e.g., diabetes mellitus).
• Refer patients with refractory gastroparesis to gastroenterology for potential procedural interventions.

Pharmacotherapy ^[4]

Assess treatment efficacy and tolerance of pharmacotherapy every 4–8 weeks to determine if therapy should be continued or adjusted. ^[4]

Prokinetics

Prokinetics are used to improve symptoms and gastric emptying.

• First line
  • Metoclopramide (off-label) ^[4]
    • Inform patients about the risk of tardive dyskinesia with long-term use.
    • Use shared decision-making.
  • Low-dose erythromycin (off-label) ^[4]
    • Consider structured treatment interruptions to avoid tachyphylaxis. ^[4]
    • Azithromycin has similar gastric prokinetic effects (motilin agonism) and may be used as an alternative.
• Alternatives
  • Prucalopride
  • Buspirone
  • Domperidone ^[4]
  • Low-dose nortriptyline

Antiemetics

These agents reduce nausea and vomiting without affecting gastric emptying and include:

• 5-HT3 antagonists (e.g., ondansetron)
• Histamine H1 antagonists (e.g., promethazine)
• Dopamine D2 antagonists (e.g., prochlorperazine)
• NK1 receptors antagonists (e.g., aprepitant)

Management of diabetic gastroparesis ^[4][15]

Management is similar to that of other gastroparesis etiologies. In addition:

• Optimize glycemic control to achieve glycemic targets for diabetes.
• Prefer DPP-4 inhibitors over GLP-1 receptor agonists and pramlintide.
• Acupuncture may improve gastric emptying and symptoms.

Avoid or discontinue GLP-1 receptor agonists and pramlintide in patients with gastroparesis; these agents significantly delay gastric emptying and exacerbate symptoms.

Management of refractory gastroparesis ^[4]

Refractory gastroparesis refers to persistent symptoms with confirmed delayed gastric emptying and inadequate response to ≥ 2 medical therapies (including prokinetics and antiemetics) after alternative causes have been excluded.

• Use a multidisciplinary team approach, e.g., primary care, gastroenterology, registered dietician, and endocrinology.
• Evaluate the accuracy of the diagnosis.
• Ensure adequate nutritional support.
  • Prioritize oral nutrition as tolerated.
  • Use enteral nutrition (e.g., via jejunostomy) if necessary.
  • Avoid parenteral nutrition when possible due to its high risk of complications (e.g., infection, thrombosis).
• Consider procedural interventions based on shared decision making.
  • Venting gastrostomy: may be used for symptom relief (e.g., bloating, vomiting) ^[15][20]
  • Pyloric botulinum toxin injection every 3 months
  • Gastric peroral endoscopic pyloromyotomy: indicated for confirmed ≥ 20% retention at 4 hours, with symptoms persisting for 6–12 months ^[4]
  • Gastric electric stimulation: targets nausea and vomiting; generally ineffective for abdominal pain

• Electrolyte imbalances
• Malnutrition
• Increased risk of postprandial hypoglycemia in patients with diabetes mellitus
• Bezoar formation

We list the most important complications. The selection is not exhaustive.