Gastroparesis
Delayed emptying of the stomach without a physical blockage, causing severe nausea, vomiting, and early fullness, most commonly linked to diabetes.
Emergency Management: Severe hypokalemia leading to cardiac arrhythmias, or acute Mallory-Weiss tear from intractable vomiting requiring endoscopic intervention.
Gastroparesis is a chronic, symptomatic disorder of the stomach characterized by delayed gastric emptying in the absence of mechanical obstruction. It leads to debilitating nausea, vomiting, early satiety, and upper abdominal pain.
Detailed Overview
Normal gastric emptying requires the coordinated action of the enteric nervous system (specifically the interstitial cells of Cajal), vagus nerve, and gastric smooth muscle. In gastroparesis, neuromuscular dysfunction prevents the stomach from contracting adequately to grind food and empty it into the duodenum. The most common identifiable causes are diabetes mellitus (due to autonomic neuropathy) and post-surgical states, though many cases remain idiopathic. It significantly impairs quality of life and complicates glycemic control in diabetics.
Epidemiology & Demographics
More common in women (approximately 4:1 female-to-male ratio). Prevalence is about 40 per 100,000 in the general population, but much higher among patients with long-standing type 1 or type 2 diabetes.
Etiological Mechanism
Idiopathic (most common, ~50%), Diabetic (associated with poor glycemic control over years, ~30%), Post-surgical (accidental injury to the vagus nerve during fundoplication, bariatric, or peptic ulcer surgery, ~10%), and medication-induced (GLP-1 agonists, opioids, anticholinergics).
Primary Causes
["Diabetic Autonomic Neuropathy.", "Vagal Nerve Injury (iatrogenic).", "Viral Infections (post-viral gastroparesis, e.g., after Norovirus)."]
The intrinsic pacemaker of the stomach (interstitial cells of Cajal) and the extrinsic vagal innervation are damaged. This loss of innervation and pacemaker function results in loss of fundic accommodation, antral hypomotility, and pylorospasm. Solid foods remain in the stomach for prolonged periods, causing distension, nausea, and vomiting. In severe cases, undigested food can coalesce into a solid mass called a bezoar.
Diagnostic Criteria & Guidelines
Requires 1) presence of characteristic symptoms, 2) upper endoscopy ruling out mechanical obstruction, and 3) objective evidence of delayed gastric emptying via scintigraphy.
Dietary modification: small, frequent meals low in fat and insoluble fiber, favoring liquids/purees. Glycemic control in diabetics. Pharmacotherapy includes prokinetics: Metoclopramide (first-line FDA approved, 5-10 mg PO/IV AC and HS - caveat: black box warning for tardive dyskinesia) and antiemetics like Ondansetron (4-8 mg PO/IV q8h) or Promethazine.
Second-Line & Adjunctive Therapy
Off-label prokinetics: Domperidone (10 mg PO TID - requires special FDA IND program due to QT prolongation) or Erythromycin (250 mg PO TID AC - rapid tachyphylaxis occurs). Tricyclic antidepressants (e.g., Nortriptyline) for symptom control of nausea/pain (though they can slow motility).
Surgical & Procedural Management
For refractory, severe cases: Gastric electrical stimulation (Enterra device), pyloromyotomy (G-POEM), or placement of a feeding jejunostomy tube (J-tube) to bypass the stomach for nutrition.
Patient Counseling & Advice
Warn patients on Metoclopramide about the risks of tardive dyskinesia (involuntary facial movements) and to stop the drug immediately if they occur. Emphasize that dietary modification is the cornerstone of management.
Follow-Up & Monitoring Schedule
Regular nutritional assessments, monitoring of HbA1c, and monitoring for side effects of prokinetic drugs (ECG for QT prolongation if on Domperidone/Erythromycin).
Preventive Strategies
Strict, long-term blood glucose control in patients with diabetes to prevent autonomic neuropathy.
Chronic and uncurable in most cases (except some post-viral cases which may resolve). Many patients endure long-term symptoms that fluctuate in severity.