Gastroparesis: A Practical Approach to Diagnosis and Treatment: JAMA | 2026
Introduction:
Gastroparesis is defined by delayed gastric emptying without mechanical gastric outlet obstruction, typically presenting with nausea, vomiting, early satiety, bloating, and abdominal discomfort. Diabetes remains the leading cause, but postsurgical, medication-induced, and idiopathic gastroparesis are also common.
Why is this topic important?
Symptoms overlap considerably with functional dyspepsia and other upper GI disorders.
Diagnosis requires objective evidence of delayed gastric emptying—not symptoms alone.
Several commonly used medications, including opioids, cannabis, anticholinergics, and GLP-1 receptor agonists, can delay gastric emptying.
Treatment should be individualised according to symptom severity, nutritional status, and underlying cause.
G-POEM has expanded treatment options for severe refractory disease.
Major Clinical Messages:
4-hour gastric emptying scintigraphy remains the diagnostic standard; >10% gastric retention at 4 hours supports gastroparesis after mechanical obstruction has been excluded.
The FDA-approved 13C-spirulina gastric emptying breath test provides a nonradioactive alternative.
Gastric retention at 4 hours can be classified as mild 10–15%, moderate 16–35%, and severe >35%.
Common causes include type 2 diabetes, postsurgical gastroparesis, medications, idiopathic disease, and type 1 diabetes.
Review and discontinue, when feasible, drugs that impair gastric emptying—particularly opioids, anticholinergics, cannabis, and GLP-1 receptor agonists.
A small-particle diet low in fat and nondigestible fibre is an important first-line nutritional intervention.
Antiemetics provide symptom control, while metoclopramide and short-term erythromycin can improve gastric motility in appropriate patients.
Severe disease with inadequate oral nutrition may require a liquid diet or jejunal enteral feeding.
G-POEM and gastric electrical stimulation are options for carefully selected patients with severe refractory gastroparesis.
Future Direction:
Better patient phenotyping and identification of pyloric dysfunction, impaired gastric accommodation, and neuromuscular abnormalities may allow more targeted treatment rather than relying solely on gastric emptying severity.
Clinical Impact:
Clinicians should confirm objective delayed gastric emptying, exclude obstruction, identify reversible causes, and optimise diet and medications before considering invasive therapies.
Bottom Line:
Gastroparesis requires symptoms plus objectively delayed gastric emptying without obstruction. Management begins with correcting reversible causes, dietary modification, antiemetics and prokinetics, while G-POEM or other interventions are reserved for severe refractory disease.