Gastro-Oesophageal Reflux Disease
Common condition caused by reflux of gastric contents into the oesophagus, causing heartburn and regurgitation. Affects ~20% of the UK adult population. First-line treatment is PPI therapy.
Key Facts
Prevalence: ~20% of UK adults experience weekly GORD symptoms NICE CG184: step-down approach — full-dose PPI for 4-8 weeks then lowest effective dose; consider H. pylori test-and-treat Alarm features (NICE NG12): dysphagia, odynophagia, weight loss, persistent vomiting, GI bleeding, anaemia → urgent 2-week wait OGD if ≥55 years Complications: oesophageal stricture, Barrett oesophagus (3-5% of GORD patients), oesophageal adenocarcinoma PPI therapy: omeprazole 20 mg OD or lansoprazole 30 mg OD for 4-8 weeks; long-term risks include C. difficile, hypomagnesaemia, osteoporosis, B12 deficiency Lifestyle measures: weight loss, elevate head of bed, avoid late meals, reduce caffeine/alcohol/fatty foods, smoking cessation
Overview
Key Facts
Gastro-oesophageal reflux disease (GORD) occurs when reflux of gastric contents causes troublesome symptoms or complications. It is one of the most common conditions in primary care and accounts for significant healthcare expenditure.
Epidemiology
GORD affects approximately 10-20% of the Western population. In the UK, ~20% of adults report weekly heartburn. Prevalence increases with age and BMI. Male:female ratio is approximately equal for symptoms, but males predominate in complications (Barrett oesophagus 3:1, adenocarcinoma 7:1).
Aetiology
- Lower oesophageal sphincter (LOS) dysfunction: transient LOS relaxations (most common mechanism), reduced basal LOS tone
- Hiatus hernia: sliding (type I — 90%) disrupts the anti-reflux barrier; present in >80% of severe GORD
- Obesity: increased intra-abdominal pressure, mechanical disruption of gastro-oesophageal junction
- Medications: CCBs, nitrates, anticholinergics, bisphosphonates, NSAIDs
- Pregnancy: hormonal (progesterone) + mechanical factors
- Delayed gastric emptying: gastroparesis, pyloric stenosis
Pathophysiology
Reflux of acidic gastric contents (pH <4) causes mucosal damage to the oesophageal squamous epithelium, which lacks the protective mucus barrier of the stomach. Chronic acid exposure causes oesophagitis, which may progress to ulceration, stricture formation, or metaplastic change (Barrett oesophagus). Transient LOS relaxations are the primary mechanism — vagally mediated relaxations unrelated to swallowing that allow retrograde flow. Hiatus hernia impairs the crural diaphragm's contribution to the anti-reflux barrier and creates an acid pocket above the diaphragm.
Clinical Presentation
Typical Symptoms
- Heartburn: retrosternal burning, worse after meals and on lying flat
- Regurgitation: acid/food reflux into mouth
- Dyspepsia: epigastric discomfort
Atypical/Extra-oesophageal Symptoms
- Chronic cough (especially nocturnal)
- Laryngitis/hoarseness (laryngopharyngeal reflux)
- Dental erosion
- Asthma exacerbation
- Non-cardiac chest pain
Red Flags
- Dysphagia (progressive — stricture or malignancy)
- Odynophagia (severe oesophagitis, ulceration)
- Weight loss (malignancy)
- GI bleeding/melaena/haematemesis (ulceration, malignancy)
- Iron deficiency anaemia (chronic blood loss)
- Persistent vomiting (obstruction)
- Age ≥55 with new/unexplained dyspepsia → urgent 2WW OGD (NICE NG12)
Differential Diagnosis
| Diagnosis | Key Features | Investigation |
|---|---|---|
| Peptic ulcer disease | Epigastric pain, relieved/worsened by food, H. pylori | OGD, H. pylori testing |
| Oesophageal cancer | Progressive dysphagia, weight loss, age >55 | OGD + biopsy, CT staging |
| Cardiac chest pain | Exertional, radiation to arm/jaw, risk factors | ECG, troponin, stress test |
| Eosinophilic oesophagitis | Young male, food bolus obstruction, atopy | OGD + biopsies (≥15 eos/hpf) |
| Achalasia | Dysphagia to solids AND liquids, regurgitation | Barium swallow, manometry |
| Gastroparesis | Nausea, vomiting, early satiety, diabetic | Gastric emptying study |
| Functional dyspepsia | Chronic symptoms, normal OGD | Rome IV criteria, exclusion diagnosis |
Diagnosis / Investigation
Bedside
- Clinical diagnosis: typical symptoms responding to PPI often sufficient — no investigation needed in <55 years without alarm features
- BMI: obesity assessment
Bloods
- FBC: iron deficiency anaemia (chronic blood loss, Barrett, malignancy)
- H. pylori: urea breath test (first-line) or stool antigen test — stop PPI for ≥2 weeks before testing
Imaging
- OGD (oesophagogastroduodenoscopy): indicated for alarm features, age ≥55 with new dyspepsia, failure of PPI therapy, Barrett surveillance
- Los Angeles classification of oesophagitis: Grade A-D
- Barium swallow: if dysphagia and OGD normal; shows hiatus hernia, stricture, motility disorders
Special Tests
- 24-hour oesophageal pH/impedance monitoring: gold standard for quantifying reflux; indicated when symptoms persist despite PPI, pre-operative workup for fundoplication, or diagnostic uncertainty
- High-resolution oesophageal manometry: excludes motility disorders (achalasia); mandatory pre-fundoplication
- Bravo wireless pH capsule: alternative to catheter-based pH monitoring (better tolerated)
Management
Non-pharmacological
- Lifestyle modifications: weight loss (most evidence-based), elevate head of bed 15-20 cm, avoid eating within 3 hours of bedtime, reduce portion size
- Dietary: reduce caffeine, alcohol, fatty/spicy foods, chocolate, citrus
- Smoking cessation: reduces LOS tone
- Medication review: stop/switch drugs that worsen reflux (CCBs, nitrates, NSAIDs)
Pharmacological
- Step 1 — full-dose PPI: omeprazole 20 mg OD or lansoprazole 30 mg OD for 4-8 weeks (NICE CG184)
- Step 2: step down to lowest effective PPI dose or PRN use; consider H2RA (ranitidine withdrawn — famotidine 20 mg BD or cimetidine 400 mg BD as alternative)
- Antacids/alginates: Gaviscon Advance (sodium alginate) for mild/intermittent symptoms; can be used as adjunct
- Prokinetics: metoclopramide 10 mg TDS (short-term only due to extrapyramidal risk); domperidone 10 mg TDS (QT prolongation risk — MHRA restriction)
- Long-term PPI risks: review annually; lowest dose for shortest time; monitor Mg²⁺, B12, bone health
Surgical/Interventional
- Laparoscopic fundoplication (Nissen — 360° or Toupet — 270°): for confirmed GORD refractory to PPI, PPI-intolerant, or patient preference; requires pre-operative pH study and manometry
- LINX magnetic sphincter augmentation: alternative to fundoplication for selected patients
- Endoscopic treatments: TIF (transoral incisionless fundoplication), Stretta — limited evidence
Referral Criteria
- 2-week wait OGD: alarm features in any age, or new dyspepsia ≥55 years (NICE NG12)
- Gastroenterology referral: symptoms refractory to 8 weeks PPI, suspected Barrett oesophagus, recurrent strictures
- Surgical referral: confirmed GORD not controlled by PPI, large symptomatic hiatus hernia
Prognosis
GORD is typically a chronic relapsing condition. ~80% of patients relapse within 6 months of stopping PPI. Long-term PPI therapy controls symptoms in >90%. Barrett oesophagus develops in 3-5% of GORD patients; annual progression to adenocarcinoma is 0.3-0.5% per year. Oesophageal stricture occurs in ~5% of untreated severe GORD. Fundoplication provides long-term reflux control in ~85% but 10-20% require revision or PPI resumption.
Other Relevant Information
Los Angeles Classification of Erosive Oesophagitis
| Grade | Description |
|---|---|
| A | Mucosal break(s) ≤5 mm, not extending between mucosal fold tops |
| B | Mucosal break(s) >5 mm, not extending between mucosal fold tops |
| C | Mucosal break(s) extending between ≥2 mucosal fold tops, <75% circumference |
| D | Mucosal break(s) involving ≥75% of oesophageal circumference |
NICE CG184 — Step-Down PPI Approach
| Step | Action |
|---|---|
| 1 | Full-dose PPI for 4-8 weeks |
| 2 | Step down to half-dose PPI |
| 3 | Use lowest effective dose or PRN |
| 4 | Trial off PPI (with antacid/alginate as needed) |
| 5 | Re-start PPI at previous effective dose if relapse |