Overview
Gastroparesis
1. Clinical Overview
Summary
Gastroparesis is a chronic motility disorder characterised by delayed gastric emptying in the absence of mechanical obstruction. It results from impaired gastric neuromuscular function. The cardinal symptoms are nausea, vomiting (often of undigested food hours after eating), early satiety, bloating, and abdominal pain. The most common causes are Diabetic Neuropathy (especially in long-standing, poorly controlled T1DM), Idiopathic, and Post-surgical (e.g., after vagal injury). Diagnosis is confirmed by Gastric Emptying Scintigraphy (GES). Management is challenging, focusing on dietary modification, prokinetics (Metoclopramide, Domperidone), and managing complications. [1,2]
Clinical Pearls
Diabetic Gastroparesis: Strongly associated with long-standing Type 1 Diabetes (often >10 years) and the presence of other neuropathies (peripheral, autonomic). Hyperglycaemia itself acutely slows gastric emptying.
Exclude Mechanical Obstruction First: Always perform an OGD (Upper GI Endoscopy) to rule out GOO (Gastric Outlet Obstruction - e.g., Peptic Stricture, Malignancy) before diagnosing gastroparesis.
Drug-Induced Gastroparesis: Many drugs slow gastric emptying (Opioids, Anticholinergics, GLP-1 agonists). Stop offending agents if possible.
Bezoars: Undigested food (Phytobezoar) or hair (Trichobezoar) can accumulate in the stomach, worsening obstruction.
2. Epidemiology
Demographics
- Prevalence: ~10-40 per 100,000 population.
- Sex: More common in Women (4:1).
- Age: Can occur at any age; often diagnosed 30-50 years.
- Association: 30-50% of patients with long-standing T1DM have some degree of delayed emptying.
Aetiologies
| Category | Details |
|---|---|
| Diabetic | ~30-40%. Long-standing T1DM > T2DM. Associated with other neuropathies. |
| Idiopathic | ~30-40%. Often post-viral (cytokine-mediated damage to ICC). |
| Post-Surgical | Vagotomy (historical), Fundoplication, Roux-en-Y, Bariatric surgery. |
| Neurological | Parkinson's Disease, Multiple Sclerosis. |
| Connective Tissue Disease | Systemic Sclerosis (Scleroderma), Amyloidosis. |
| Drug-Induced | Opioids, Anticholinergics, GLP-1 Agonists (Semaglutide can unmask it). |
3. Pathophysiology
Mechanism
- Interstitial Cells of Cajal (ICC): These are the "pacemaker" cells of the gut. They generate slow waves that coordinate gastric peristalsis.
- Damage to ICC or Vagus Nerve: In diabetic gastroparesis, hyperglycaemia-induced oxidative stress causes loss of ICCs and vagal neuropathy.
- Antral Hypomotility: The antrum fails to grind food and propel it through the pylorus.
- Pyloric Dysfunction: Pyloric spasm (Pylorospasm) may also impede emptying.
- Fundic Relaxation Impairment: The fundus fails to relax normally to accommodate food ("Impaired Accommodation").
- Result: Solid food is retained in the stomach for prolonged periods, causing symptoms.
Gastric Emptying Physiology
- Liquids: Empty by gravity and fundic pressure. Usually less affected.
- Solids: Require antral grinding and coordinated pyloric opening. More affected in gastroparesis.
4. Differential Diagnosis (Nausea/Vomiting/Bloating)
| Condition | Key Features |
|---|---|
| Gastric Outlet Obstruction (Peptic Stricture, Malignancy) | Mechanical blockage. May have mass on endoscopy. |
| Peptic Ulcer Disease | Epigastric pain. H. pylori or NSAID use. |
| Superior Mesenteric Artery Syndrome | Rare. Compression of third part of duodenum. Weight loss, lean habitus. |
| Functional Dyspepsia | Symptoms without objective delayed emptying. |
| Cyclic Vomiting Syndrome | Episodic pattern. Often associated with migraine or cannabis use. |
| Rumination Syndrome | Effortless regurgitation of recently ingested food. Behavioural. |
5. Clinical Presentation
Symptoms
Signs
Nausea (>90%)
Often constant and debilitating.
Vomiting (60-80%)
Vomitus contains undigested food, sometimes hours after a meal.
Early Satiety
Feeling full after a few bites.
Postprandial Fullness / Bloating.
Common presentation.
Abdominal Pain (20-50%)
Epigastric. Can be difficult to manage.
Weight Loss / Malnutrition
In severe cases.
6. Investigations
Essential First Steps
- Upper GI Endoscopy (OGD): Mandatory. Excludes mechanical obstruction (Stricture, Malignancy). May show retained food/bezoar.
Gastric Emptying Study (Diagnostic)
- Gastric Emptying Scintigraphy (GES): Gold Standard.
- Patient eats a radiolabelled solid meal (egg sandwich).
- Serial scans measure % retained at 1, 2, and 4 hours.
- Diagnosis: >10% retained at 4 hours is abnormal (mild). >35% at 4 hours is severe.
- Note: Stop prokinetics/opioids before test.
Other Tests
- Gastric Emptying Breath Test (GEBT): Non-radioactive alternative using 13C-Spirulina.
- Wireless Motility Capsule (SmartPill): Measures transit through entire GI tract.
- Electrogastrography: Research tool. Measures gastric slow waves.
Assess Underlying Cause
- Blood Glucose / HbA1c: Diabetic control.
- TFTs: Hypothyroidism.
- Autoantibodies (if CTD suspected).
- Neurological Assessment (if Parkinson's etc.).
7. Management
Management Algorithm
GASTROPARESIS DIAGNOSED
(Delayed Emptying on GES, No Obstruction)
↓
IDENTIFY & TREAT CAUSE
(Optimise Glucose Control)
(Stop Offending Drugs)
↓
┌─────────┴─────────┐
MILD/MODERATE SEVERE / REFRACTORY
↓ ↓
DIETARY ADVANCED THERAPIES
MODIFICATION - Jejunostomy (J-tube)
- Small, frequent feeding
meals - Gastric Electrical
- Low fat, low fibre Stimulation (GES)
- Avoid carbonated - Per-Oral Endoscopic
drinks Pyloromyotomy (G-POEM)
↓ - TPN (Last resort)
PROKINETICS
- Metoclopramide
(Max 5 days UK)
- Domperidone
(Use lowest dose)
- Erythromycin
(Short-term only)
↓
ANTIEMETICS
- Ondansetron
- Prochlorperazine
1. Dietary Modification (First Line for All)
- Small, Frequent Meals: 4-6 small meals per day (Reduces volume load on stomach).
- Low Fat: Fat delays gastric emptying.
- Low Fibre: Fibre can form bezoars.
- Liquid / Blenderised Foods: Solids are harder to empty.
- Avoid Carbonated Drinks: Cause bloating.
2. Glycaemic Control (Diabetic Gastroparesis)
- Optimise blood glucose. Hyperglycaemia acutely worsens gastric emptying.
3. Prokinetics
- Metoclopramide: D2 antagonist + 5-HT4 agonist. First-line in many regions.
- UK Restriction: Use for max 5 days due to risk of Tardive Dyskinesia.
- S/E: Extrapyramidal symptoms, Depression, Hyperprolactinaemia.
- Domperidone: D2 antagonist. Does not cross BBB (less CNS S/E).
- Warning: QT prolongation. Use lowest effective dose. Check ECG.
- Erythromycin: Motilin receptor agonist. Potent prokinetic.
- Problem: Tachyphylaxis (tolerance) develops rapidly. Used short-term only.
- Prucalopride: 5-HT4 agonist. Off-label use. May be considered.
4. Antiemetics (Symptomatic)
- 5-HT3 Antagonists (Ondansetron): For nausea.
- Phenothiazines (Prochlorperazine).
- Tricyclic Antidepressants (Amitriptyline): Low dose. For pain and nausea.
5. Advanced / Refractory Therapies
- Gastric Electrical Stimulation (Enterra): Implanted device delivers high-frequency electrical pulses. Improves symptoms (especially nausea/vomiting) more than emptying.
- Per-Oral Endoscopic Pyloromyotomy (G-POEM): Endoscopic cutting of pyloric muscle. Promising results.
- Jejunostomy (J-Tube): Bypasses the stomach for enteral nutrition. For severe malnutrition.
- Botulinum Toxin Injection: Injected into pylorus. Mixed/disappointing results.
- Total Parenteral Nutrition (TPN): Last resort.
8. Complications
- Malnutrition / Weight Loss.
- Dehydration / Electrolyte Disturbances (Hypokalaemia from vomiting).
- Bezoar Formation: Masses of undigested material. May cause complete obstruction.
- Erratic Blood Glucose Control: In diabetics, unpredictable absorption leads to swings.
- Poor Quality of Life: Often severely impacts daily functioning.
9. Prognosis and Outcomes
- Idiopathic / Post-Viral: Some patients may spontaneously improve over 1-2 years.
- Diabetic: Chronic and progressive. Correlates with overall disease control and neuropathy.
- Response to Treatment: Many patients have refractory symptoms despite optimal therapy.
- Mortality: Increased in diabetic gastroparesis, largely related to underlying diabetes complications.
10. Evidence and Guidelines
Key Guidelines
| Guideline | Organisation | Key Recommendations |
|---|---|---|
| Gastroparesis | ACG (2022) | GES is gold standard. Dietary first. Metoclopramide/Domperidone cautiously. G-POEM is emerging. |
| Motility Disorders | AGA | Similar recommendations. |
Landmark Evidence
1. Gastric Electrical Stimulation (GEMS Trial)
- Showed symptom improvement (nausea, vomiting) with Enterra device.
- Impact: FDA HDE approval for GES.
2. G-POEM Meta-analyses (2020s)
- Demonstrated significant improvement in symptoms and objective emptying.
- Impact: Increasing adoption as minimally invasive treatment.
11. Patient and Layperson Explanation
What is Gastroparesis?
Your stomach is like a mixer and pump. It normally churns food and empties it into the small intestine. In gastroparesis, the stomach's muscles don't work properly, so food stays in the stomach for too long. This causes nausea, vomiting, bloating, and feeling full very quickly.
What causes it?
The most common causes are:
- Diabetes: Long-term high blood sugar damages the nerves controlling the stomach.
- Unknown (Idiopathic): Sometimes it happens after a viral illness.
- After surgery: Operations near the stomach or oesophagus can damage the nerve (Vagus nerve).
How is it treated?
- Diet: Eat smaller meals more often. Avoid fatty and high-fibre foods. Soft or liquid foods empty more easily.
- Medication: We can use tablets to help the stomach squeeze food through (Metoclopramide, Domperidone) and anti-sickness tablets.
- If severe: We may consider a feeding tube that bypasses the stomach, or a special pacemaker for the stomach.
12. References
Primary Sources
- Camilleri M, et al. ACG Clinical Guideline: Gastroparesis. Am J Gastroenterol. 2022.
- Parkman HP, et al. American Gastroenterological Association medical position statement: diagnosis and treatment of gastroparesis. Gastroenterology. 2004.
13. Examination Focus
Common Exam Questions
- Diagnosis: "Gold standard investigation?"
- Answer: Gastric Emptying Scintigraphy (4-hour solid-meal study).
- Pharmacology: "Mechanism of Metoclopramide?"
- Answer: Dopamine D2 Antagonist + 5-HT4 Agonist. Increases antral contractions.
- Side Effect: "Why limit Metoclopramide duration?"
- Answer: Risk of Tardive Dyskinesia (Extrapyramidal side effects).
- Clinical Sign: "Succussion Splash present 4 hours after eating?"
- Answer: Suggests gastroparesis or gastric outlet obstruction.
Viva Points
- Motilin: Explain that Erythromycin acts on Motilin receptors to stimulate gastric emptying, and why tachyphylaxis limits its use.
- G-POEM: Describe the emerging endoscopic treatment of cutting the pyloric muscle.
Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists.