Gastroparesis: Diagnosis & Care

Gastroparesis is delayed gastric emptying without mechanical obstruction. The most common etiologies are diabetic, idiopathic, and post-surgical — and increasingly, GLP-1 medication–related cases as Ozempic, Wegovy, and Mounjaro use has expanded.

Symptoms

• Nausea and vomiting (especially of undigested food hours after eating)
• Early satiety
• Postprandial fullness and bloating
• Upper abdominal pain
• Unintended weight loss
• Worsening glycemic control in diabetes

Causes

Diabetic gastroparesis

Long-standing type 1 or type 2 diabetes with autonomic neuropathy. Symptoms often correlate with poor glycemic control and can themselves worsen glucose variability.

Idiopathic gastroparesis

The most common category. No identifiable cause, often post-viral. Female predominance.

Post-surgical gastroparesis

After fundoplication, bariatric surgery, esophagectomy, or vagus nerve injury during foregut surgery.

GLP-1 receptor agonist–related delayed emptying

GLP-1 medications inherently slow gastric emptying as part of their mechanism. In some patients this becomes symptomatic gastroparesis, with persistent nausea, vomiting, bloating, and early satiety. Most cases improve when the medication is paused or the dose is reduced. Persistent symptoms after discontinuation warrant a gastric emptying study and full GI evaluation. See the GLP-1 GI page for procedural and pre-anesthesia considerations.

Other causes

Connective tissue disease (scleroderma), neurologic disease (Parkinson's), mesenteric ischemia, medication-related, and rarely paraneoplastic syndromes.

Diagnosis

• Upper endoscopy first — to exclude mechanical obstruction (stricture, tumor, ulcer)
• 4-hour gastric emptying scintigraphy (the standard) — using a radiolabeled solid meal; gastroparesis is defined as >10% retention at 4 hours (mild: 11–20%; moderate: 21–35%; severe: >35%)
• Wireless motility capsule — alternative when scintigraphy is not available
• 13C breath test — emerging non-radioactive option
• Stop opioids, anticholinergics, GLP-1 agonists for at least 48–72 hours before testing — these all slow gastric emptying and can falsely diagnose gastroparesis

Treatment

Dietary therapy (foundation of treatment)

• Small, frequent meals (5–6 per day)
• Low-fat (high fat slows emptying further)
• Low residue / low-insoluble-fiber (avoid raw vegetables, skins, seeds)
• Soft or pureed textures during flares
• Adequate hydration; carbohydrate-electrolyte beverages
• Walk after meals to promote emptying
• Sit upright during and after meals

Pharmacotherapy

• Metoclopramide — first-line prokinetic; FDA-approved but limited to 12 weeks due to risk of tardive dyskinesia
• Erythromycin — short-term prokinetic via motilin agonism; tachyphylaxis with chronic use
• Domperidone — accessible via expanded-access programs; QT prolongation requires monitoring
• Prucalopride — increasingly used off-label; better tolerated than metoclopramide
• Antiemetics — ondansetron, prochlorperazine, scopolamine for symptom control
• Tricyclic antidepressants — for refractory abdominal pain (use lowest effective dose)
• Optimization of glycemic control in diabetes — both HbA1c and post-prandial excursions
• Pause or reduce GLP-1 dose when GLP-1–related; coordinate with the prescribing physician

Procedural and surgical options for refractory cases

• Pyloric directed therapies — endoscopic pyloric balloon dilation, intra-pyloric botulinum toxin injection, and gastric peroral endoscopic myotomy (G-POEM)
• Gastric electrical stimulation — for refractory diabetic and idiopathic cases
• Surgical pyloroplasty or, rarely, gastrectomy in highly selected cases
• Enteral feeding tube (post-pyloric) for severely affected patients with malnutrition

Gastroparesis: Common Questions