Medicine chapters
Gastro-oesophageal reflux disease (including Barrett oesophagus)
Why acid refluxes into the oesophagus, how heartburn is told apart from cardiac pain, when to scope, how PPIs and surgery are used, and how Barrett oesophagus is diagnosed and followed up.
- GORD is caused mainly by transient relaxations of the lower oesophageal sphincter; the key symptom is heartburn, worse on bending and lying down and relieved by antacids.
- Patients without alarm features can be treated empirically with lifestyle change and a PPI; endoscopy is for alarm features or poor response, and 24-hour pH monitoring is the gold standard to prove reflux.
- Barrett oesophagus (columnar metaplasia) is a complication of chronic GORD and the precursor of oesophageal adenocarcinoma.
On this page
Overview
Gastro-oesophageal reflux disease (GORD) means reflux of stomach contents (acid, pepsin, bile) into the oesophagus causing troublesome symptoms or damage. It is one of the most common gut problems, affecting roughly 10–20% of adults in Western countries, and is common in Pakistan too.
Most patients have heartburn and do well on a proton pump inhibitor (PPI). The important exam points are the alarm features that need endoscopy, the tests that prove reflux, and the complications, especially Barrett oesophagus and adenocarcinoma.
Causes and pathophysiology
Normal anti-reflux barrier
- Lower oesophageal sphincter (LOS): tonically closed between swallows.
- Crural diaphragm acting as a pinch-cock around the LOS.
- Intra-abdominal segment of the oesophagus acting as a flap valve.
- Clearance of any refluxed acid by secondary peristalsis, gravity and swallowed salivary bicarbonate.
What goes wrong
- Transient LOS relaxations (TLESRs): brief relaxations not triggered by a swallow, especially after meals. They cause most reflux episodes, in normal people and in most GORD patients.
- Low resting LOS pressure.
- Hiatus hernia, which removes the crural pinch-cock and holds an acid pocket above the diaphragm.
- Raised intra-abdominal pressure: pregnancy, obesity.
- Poor oesophageal clearance or slow gastric emptying.
Risk factors
- Obesity, pregnancy, large meals, fatty food, chocolate, coffee, alcohol, smoking.
- Drugs: anticholinergics, calcium-channel blockers, nitrates, theophylline.
- Systemic sclerosis (weak LOS), previous treatment for achalasia, hiatus hernia.
Hiatus hernia
| Type | What happens | Clinical point |
|---|---|---|
| Sliding (most common) | Gastro-oesophageal junction slides up into the chest | Very common over 50; symptoms come from reflux |
| Rolling (para-oesophageal) | Part of the fundus rolls up beside the oesophagus; the junction stays below the diaphragm | LOS stays competent; risk of volvulus or strangulation |
Clinical features
Typical symptoms
- Heartburn: burning retrosternal pain, worse on bending, stooping and lying down, after large or spicy meals, hot drinks or alcohol; relieved by antacids.
- Regurgitation of acid or food into the mouth, often at night.
- Water brash: sudden filling of the mouth with saliva.
- Odynophagia with severe oesophagitis.
Atypical (extra-oesophageal) symptoms
- Chronic cough, asthma that is hard to control, hoarse voice, sore throat and throat clearing (laryngopharyngeal reflux).
- Dental erosion.
- Non-cardiac chest pain.
Heartburn versus cardiac pain
| Feature | Reflux pain | Cardiac ischaemic pain |
|---|---|---|
| Character | Burning | Gripping, crushing, heavy |
| Provoked by | Bending, lying flat, meals | Exertion |
| Radiation | Seldom to the arms | Neck, jaw, left arm |
| Relief | Antacids | Rest, nitrates |
| Associated | Regurgitation, sour taste | Breathlessness, sweating |
Nitrates can relieve oesophageal spasm as well as angina, so relief with GTN does not prove cardiac pain. Always exclude a cardiac cause in chest pain first.
Alarm (red flag) features
- Dysphagia (the most important).
- Weight loss, anorexia.
- Persistent vomiting.
- Haematemesis or melaena, iron deficiency anaemia.
- Epigastric mass.
- New symptoms in an older patient, or failure to respond to treatment.
Investigations
Most young patients without alarm features need no tests; treat empirically.
Upper GI endoscopy
Done for alarm features, failure of treatment, or long-standing symptoms. It may show:
- Reflux oesophagitis, graded by the Los Angeles classification:
| LA grade | Endoscopic finding |
|---|---|
| A | Mucosal break(s) 5 mm or less, confined to the folds |
| B | At least one break over 5 mm, not joining between folds |
| C | Breaks continuous between folds but less than 75% of the circumference |
| D | Breaks involving at least 75% of the circumference |
- Hiatus hernia, peptic stricture, Barrett oesophagus.
- A normal endoscopy does not exclude GORD: many patients have non-erosive reflux disease (NERD).
Dysphagia in a patient with reflux means stricture or cancer until shown otherwise and needs endoscopy.
24-hour ambulatory pH monitoring (± impedance)
- Gold standard to prove abnormal acid reflux.
- A probe near the LOS (nasal catheter, or wireless Bravo capsule clipped to the oesophagus) records the time the oesophagus spends at pH below 4, and links reflux episodes to symptoms.
- A composite DeMeester score above 14.72 indicates pathological reflux.
- Impedance adds detection of non-acid (weakly acidic) reflux.
- Indicated when endoscopy is normal and symptoms continue on PPI, when symptoms are atypical, and always before anti-reflux surgery.
Oesophageal manometry
Used before surgery to exclude achalasia and poor peristalsis (which would make a tight wrap dangerous), and to position the pH probe.
Endoscopy shows damage; pH monitoring proves reflux; manometry assesses motility.
Management
1. Lifestyle
- Lose weight, stop smoking, cut down alcohol and caffeine.
- Avoid large late meals and trigger foods; do not lie down soon after eating.
- Raise the head of the bed.
- Review causative drugs.
2. Drugs
| Drug | Use |
|---|---|
| Antacids and alginates (e.g. 10 mL three times daily) | Mild symptoms; alginate forms a raft on the stomach contents |
| H2-receptor antagonists (famotidine, cimetidine) | Milder disease or add-on at night |
| Proton pump inhibitors (omeprazole, lansoprazole, pantoprazole, esomeprazole) | Drug of choice for all but mild GORD; block the H+/K+-ATPase and cut acid output by up to 90% |
| Prokinetics (metoclopramide, domperidone) | Limited role; domperidone restricted because of cardiac effects |
- Start a standard-dose PPI once daily; about 60% are symptom-controlled after 4 weeks.
- Severe cases may need twice-daily PPI.
- Step down to the lowest effective dose (for example omeprazole 20 mg daily) or on-demand use.
- Long-term PPI use has been linked with osteoporosis and C. difficile and other enteric infections; these are uncommon.
3. Surgery
Laparoscopic Nissen fundoplication: the fundus is wrapped completely (total fundoplication) around the lower oesophagus, the junction is returned to the abdomen and the crura are closed.
- Indications: proven reflux with good PPI response but intolerance of, or unwillingness to take, lifelong drugs; persistent volume regurgitation; complications.
- Best results in patients with typical symptoms, documented acid reflux and a good PPI response.
- Never operate for a hiatus hernia alone.
- Side-effects: dysphagia, gas-bloat (inability to belch or vomit). The commonest cause of mechanical failure is a recurrent hiatus hernia.
- Endoscopic options and the LINX magnetic sphincter device are newer alternatives.
Complications
- Reflux oesophagitis, ulceration and bleeding (iron deficiency anaemia).
- Peptic stricture: older patients; slowly worsening dysphagia for solids; treat with endoscopic dilatation plus long-term PPI.
- Barrett oesophagus.
- Oesophageal adenocarcinoma.
- Aspiration, chronic cough, asthma, dental erosion.
Barrett oesophagus
Definition
Part of the normal stratified squamous lining of the lower oesophagus is replaced by metaplastic columnar epithelium (a "columnar-lined oesophagus"), seen as salmon-pink mucosa extending at least 1 cm above the gastro-oesophageal junction and confirmed on biopsy.
- Intestinal metaplasia with goblet cells (which stain with Alcian blue) carries the cancer risk; American guidelines require it for the diagnosis, British guidelines do not.
- It is an adaptation to chronic acid and bile reflux; a hiatus hernia is nearly always present.
Who gets it
- Typically middle-aged, obese white men with long-standing reflux; central obesity strongly increases risk.
- Short-segment (under 3 cm) and long-segment (3 cm or more) forms.
- Many patients have few symptoms, which is why routine population screening is not advised.
Cancer risk
Barrett progresses in a minority through low-grade dysplasia → high-grade dysplasia → adenocarcinoma. The annual risk of cancer is low (roughly 0.12–0.5% per year), but much higher than in the general population.
Recording the extent: Prague C and M
C = length of the circumferential segment; M = maximum length including tongues, both measured from the top of the gastric folds.
Top of gastric folds (GOJ) at 40 cm from the incisors
Top of circumferential Barrett at 37 cm → C = 40 − 37 = 3 cm
Tip of longest tongue at 35 cm → M = 40 − 35 = 5 cm
Report: C3M5 (long-segment Barrett, as M is 3 cm or more)
Surveillance and treatment (British guidance)
| Finding | Plan |
|---|---|
| Under 3 cm, intestinal metaplasia, no dysplasia | Endoscopy every 3–5 years |
| 3 cm or longer, no dysplasia | Endoscopy every 2–3 years |
| Under 3 cm, gastric metaplasia only | Consider discharge |
| Low-grade dysplasia | High-dose PPI and repeat endoscopy within 6 months; ablation if it persists |
| High-grade dysplasia or early cancer | Endoscopic mucosal resection of visible lesions, then radiofrequency ablation |
At surveillance endoscopy, biopsies are taken from each quadrant at 1–2 cm intervals, plus any visible lesion.
- All patients take a PPI to control reflux.
- Radiofrequency ablation has replaced photodynamic therapy; oesophagectomy is now rarely needed for high-grade dysplasia.
Barrett oesophagus is columnar metaplasia, a premalignant change for adenocarcinoma, not squamous carcinoma.
Endoscopy + biopsy confirms Barrett. Columnar lining with goblet cells = intestinal metaplasia. Do not confuse it with squamous dysplasia, the precursor of SCC.
"Barrett Becomes Adenocarcinoma" (Barrett → glandular → adeno).
Pakistan note
PPIs and H2 blockers are widely available over the counter, so many patients self-treat for years. Ask about dysphagia, weight loss and anaemia before repeating a prescription, and check local and national guidance on endoscopy access, which can change.
Expect: transient LOS relaxation as the main mechanism, risk factors and drugs that lower LOS pressure, sliding versus rolling hiatus hernia, reflux versus cardiac pain, alarm features, the role of endoscopy, 24-hour pH monitoring as the gold standard (pH under 4, DeMeester), manometry before surgery, PPIs as drugs of choice, Nissen fundoplication and its side-effects, peptic stricture, and Barrett oesophagus (columnar metaplasia, goblet cells, adenocarcinoma risk, surveillance and ablation).
Quick revision
- Mechanism: transient LOS relaxations; hiatus hernia and obesity worsen it.
- Heartburn worse lying and bending, relieved by antacids.
- No alarm features and young: treat empirically with lifestyle + PPI.
- Alarm features (dysphagia, weight loss, bleeding, anaemia, vomiting): endoscopy.
- Gold standard to prove reflux: 24-hour pH ± impedance (pH under 4).
- Before fundoplication: pH study and manometry.
- Nissen = total wrap; side-effects dysphagia and gas-bloat.
- Barrett = columnar metaplasia over 1 cm; goblet cells; risk of adenocarcinoma.
- Barrett with high-grade dysplasia: EMR then radiofrequency ablation.
Written by The House Job from standard references (Kumar and Clark's Clinical Medicine; Bailey & Love's Short Practice of Surgery).
FAQ
What is the most common mechanism of reflux in GORD?
Transient relaxations of the lower oesophageal sphincter that happen without a swallow, mostly after meals.
Does a normal endoscopy rule out reflux disease?
No. Many patients have non-erosive reflux disease; 24-hour pH or pH-impedance monitoring is used to prove reflux when endoscopy is normal.
What is Barrett oesophagus?
Replacement of the normal squamous lining of the lower oesophagus by columnar epithelium, usually with intestinal metaplasia, caused by chronic reflux and predisposing to adenocarcinoma.
When is anti-reflux surgery considered?
In patients with proven reflux who respond to PPIs but cannot or will not take them long term, or who have persistent regurgitation; surgery is never done for a hiatus hernia alone.