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Gastroenterology
Endocrinology
General Medicine

Gastroparesis

High EvidenceUpdated: 2025-12-22

On This Page

Red Flags

  • Mechanical gastric outlet obstruction (must exclude)
  • Severe dehydration/malnutrition
  • Bezoar formation
  • Frequent hospitalisations
Overview

Gastroparesis

1. Clinical Overview

Summary

Gastroparesis is a syndrome of delayed gastric emptying in the absence of mechanical obstruction. The most common causes are diabetes mellitus (autonomic neuropathy), post-surgical (vagal injury), and idiopathic. Patients present with nausea, vomiting (often of undigested food hours after eating), early satiety, bloating, and abdominal pain. Diagnosis is confirmed by gastric emptying scintigraphy. Treatment involves dietary modification, prokinetic agents (metoclopramide, domperidone, erythromycin), and in refractory cases, gastric electrical stimulation or enteral feeding.

Key Facts

  • Definition: Delayed gastric emptying without mechanical obstruction
  • Major Causes: Diabetic (30%), Idiopathic (35%), Post-surgical (13%)
  • Symptoms: Nausea, vomiting (undigested food), early satiety, bloating
  • Diagnosis: Gastric emptying study (scintigraphy)
  • Treatment: Diet modification, Prokinetics (Metoclopramide, Domperidone, Erythromycin)
  • First Step: Exclude mechanical obstruction (OGD)

Clinical Pearls

"Exclude Obstruction First": Gastroparesis is a diagnosis of exclusion. Always perform upper GI endoscopy to rule out mechanical gastric outlet obstruction before diagnosing gastroparesis.

"Optimise Glucose Control": Hyperglycaemia directly impairs gastric motility. Excellent glycaemic control is a fundamental part of managing diabetic gastroparesis.

"Erythromycin Works Acutely, Tachyphylaxis Occurs": Erythromycin is a potent prokinetic (motilin agonist) but loses effectiveness within 4 weeks due to receptor downregulation.

"Diabetic Gastroparesis = Autonomic Neuropathy": If diabetic gastroparesis is present, look for other signs of autonomic neuropathy (postural hypotension, anhidrosis, erectile dysfunction).


2. Epidemiology

Incidence

  • Prevalence: 25-55 per 100,000 population
  • More common in women (4:1)

Demographics

  • Peak age: 20-50 years
  • More common in Type 1 diabetes than Type 2
  • Female predominance

Causes

CauseFrequencyNotes
Diabetic30%Autonomic neuropathy; correlates with duration and control
Idiopathic35%May follow viral illness; often young women
Post-surgical13%Vagotomy, fundoplication, bariatric surgery
Medications10%Opioids, anticholinergics, GLP-1 agonists
Connective tissueRareScleroderma, SLE
NeurologicalRareParkinson's, MS

3. Pathophysiology

Normal Gastric Emptying

  • Gastric accommodation and trituration
  • Antral contractions
  • Pyloric relaxation
  • Duodenal receptivity
  • Coordinated by vagus nerve and enteric nervous system

Mechanisms of Gastroparesis

MechanismCause
Vagal neuropathyDiabetes, surgery
Loss of ICC cellsInterstitial cells of Cajal (pacemaker cells)
Smooth muscle dysfunctionConnective tissue disease
Central dysregulationPost-viral, idiopathic

Diabetic Gastroparesis

  • Autonomic neuropathy (vagal damage)
  • Hyperglycaemia directly slows emptying (acute effect)
  • Loss of ICC cells
  • Associated with other diabetic complications

4. Clinical Presentation

Symptoms

FeatureNotes
NauseaMost common symptom (>0%)
VomitingUndigested food, hours after eating
Early satietyFeeling full after small amounts
BloatingPostprandial abdominal distension
Abdominal painUpper abdominal
Weight lossIf prolonged

Timing

Severity Grading (Abell Classification)

GradeSymptomsManagement
MildIntermittent, controlledDiet + PRN antiemetics
ModerateFrequent, medications neededRegular prokinetics
SevereRefractory, hospitalisationsIV fluids, enteral feeding, surgery

Symptoms typically worse postprandially
Common presentation.
Vomiting often hours after meals (vs immediately in obstruction)
Common presentation.
5. Clinical Examination

General

  • Weight loss / malnutrition (severe cases)
  • Dehydration (if vomiting significant)

Abdominal

  • Epigastric distension
  • Succussion splash (fluid in stomach when shaking)
  • No peritonism

Diabetic Complications

  • Signs of autonomic neuropathy
  • Retinopathy, peripheral neuropathy

6. Investigations

First-Line

TestPurpose
Upper GI Endoscopy (OGD)EXCLUDE mechanical obstruction (essential)
Blood testsGlucose (HbA1c), U&E, LFTs, nutritional markers

Diagnostic Test

  • Gastric Emptying Scintigraphy: Gold standard
    • Patient eats radiolabelled meal
    • Gastric retention measured at 2 and 4 hours
    • Abnormal: >60% at 2h or >10% at 4h

Alternative Tests

  • Wireless motility capsule: Measures gastric transit
  • 13C-breath test: Simpler, less validated

Exclude

  • Mechanical obstruction (OGD, CT)
  • Metabolic causes (hypothyroidism, adrenal insufficiency)
  • Drug causes (opioids, GLP-1 agonists)

7. Management

Management Approach

┌──────────────────────────────────────────────────────────┐
│   GASTROPARESIS MANAGEMENT                               │
├──────────────────────────────────────────────────────────┤
│                                                          │
│  STEP 1: EXCLUDE OBSTRUCTION (OGD)                        │
│                                                          │
│  STEP 2: TREAT UNDERLYING CAUSE                           │
│  • Optimise glycaemic control (diabetic)                 │
│  • Stop causative medications (opioids)                  │
│                                                          │
│  STEP 3: DIETARY MODIFICATION                             │
│  • Small, frequent meals                                 │
│  • Low fat, low fibre (easier to empty)                  │
│  • Liquid/pureed consistency if severe                   │
│  • Avoid carbonated drinks                               │
│                                                          │
│  STEP 4: PROKINETICS                                      │
│  • Metoclopramide 10mg TDS AC (risk: tardive dyskinesia) │
│  • Domperidone 10mg TDS AC (risk: QT prolongation)       │
│  • Erythromycin 40-250mg TDS AC (tachyphylaxis)          │
│                                                          │
│  STEP 5: ANTIEMETICS                                      │
│  • Ondansetron, Prochlorperazine                         │
│                                                          │
│  STEP 6: REFRACTORY CASES                                 │
│  • Gastric electrical stimulation (Enterra)              │
│  • NJ/PEG-J feeding if nutrition failing                 │
│  • Pyloroplasty / G-POEM                                 │
│  • Gastric resection (last resort)                       │
│                                                          │
└──────────────────────────────────────────────────────────┘

Prokinetic Agents

DrugDoseMechanismCautions
Metoclopramide10mg TDSD2 antagonist + 5HT4 agonistTardive dyskinesia (limit <12 weeks)
Domperidone10mg TDSD2 antagonist (peripheral)QTc prolongation, cardiac death
Erythromycin40-250mg TDSMotilin agonistTachyphylaxis by 4 weeks
Prucalopride1-2mg OD5HT4 agonistOff-label for gastroparesis

8. Complications

Of Gastroparesis

  • Malnutrition and weight loss
  • Dehydration
  • Bezoar formation (undigested food mass)
  • Poor glycaemic control (unpredictable absorption)
  • Frequent hospitalisations
  • Poor quality of life

Of Treatment

  • Metoclopramide: Tardive dyskinesia, extrapyramidal effects
  • Domperidone: QT prolongation, sudden cardiac death
  • Erythromycin: GI upset, drug interactions

9. Prognosis & Outcomes

Natural History

  • Chronic, relapsing condition
  • Post-viral idiopathic may improve
  • Diabetic gastroparesis often progressive

With Treatment

  • Many achieve symptom control with diet + prokinetics
  • 25-30% have refractory symptoms

Prognosis by Cause

CausePrognosis
Post-viralMay resolve spontaneously
DiabeticChronic, progressive
IdiopathicVariable
Post-surgicalMay improve over time

10. Evidence & Guidelines

Key Guidelines

  1. ACG Clinical Guideline: Management of Gastroparesis (2013)
  2. BSG Recommendations

Key Evidence

Prokinetics

  • Metoclopramide and domperidone have short-term efficacy
  • Long-term use limited by side effects

Gastric Electrical Stimulation

  • Reduces symptoms and hospitalisations in refractory cases
  • Limited evidence for improvement in gastric emptying

11. Patient/Layperson Explanation

What is Gastroparesis?

Gastroparesis means your stomach empties food more slowly than normal. It's like your stomach muscles aren't working properly, so food stays in your stomach for too long.

What Causes It?

  • Diabetes: Nerve damage from high blood sugars
  • After surgery: Especially stomach operations
  • Unknown: Sometimes no cause is found

What Are the Symptoms?

  • Feeling sick (nausea)
  • Vomiting, sometimes several hours after eating
  • Feeling full after only a few bites
  • Bloating
  • Tummy pain

How is it Diagnosed?

After ruling out blockages with a camera test (endoscopy), you may have a gastric emptying study - you eat a meal with a small amount of radioactive tracer, and a scanner measures how quickly your stomach empties.

How is it Treated?

  • Diet changes: Smaller, more frequent meals; low-fat, low-fibre foods
  • Medications: Tablets to help your stomach empty faster (metoclopramide, domperidone, erythromycin)
  • Good diabetes control: Essential if diabetic
  • In severe cases, special feeding tubes or surgery may be needed

12. References

Primary Guidelines

  1. Camilleri M, et al. Clinical Guideline: Management of Gastroparesis. Am J Gastroenterol. 2013;108(1):18-37. PMID: 23147521

Key Studies

  1. Parkman HP, et al. Gastroparesis and functional dyspepsia: excerpts from the AGA/ANMS review. Neurogastroenterol Motil. 2010;22(2):113-133. PMID: 20003077
  2. McCallum RW, et al. Gastric electrical stimulation with Enterra therapy improves symptoms from diabetic gastroparesis. J Gastrointest Surg. 2010;14(3):468-475. PMID: 20066545

Last updated: 2025-12-22

At a Glance

EvidenceHigh
Last Updated2025-12-22

Red Flags

  • Mechanical gastric outlet obstruction (must exclude)
  • Severe dehydration/malnutrition
  • Bezoar formation
  • Frequent hospitalisations

Clinical Pearls

  • **"Exclude Obstruction First"**: Gastroparesis is a diagnosis of exclusion. Always perform upper GI endoscopy to rule out mechanical gastric outlet obstruction before diagnosing gastroparesis.
  • **"Optimise Glucose Control"**: Hyperglycaemia directly impairs gastric motility. Excellent glycaemic control is a fundamental part of managing diabetic gastroparesis.
  • **"Erythromycin Works Acutely, Tachyphylaxis Occurs"**: Erythromycin is a potent prokinetic (motilin agonist) but loses effectiveness within 4 weeks due to receptor downregulation.
  • **"Diabetic Gastroparesis = Autonomic Neuropathy"**: If diabetic gastroparesis is present, look for other signs of autonomic neuropathy (postural hypotension, anhidrosis, erectile dysfunction).

Guidelines

  • NICE Guidelines
  • BTS Guidelines
  • RCUK Guidelines