Gastro-oesophageal reflux disease (GORD)

Synonyms: GORD or GERD; reflux oesophagitis

See also separate articles Childhood Gastro-oesophageal Reflux Disease and Dyspepsia.

A certain amount of gastro-oesophageal reflux of acid is normal and there is a natural protective mechanism of the lower oesophagus.
If reflux is prolonged or excessive it may cause breakdown of this protection with inflammation of the oesophagus (oesophagitis).


Reflux is two to three times more common in men than in women.
Population-based studies have shown that between 21% and 40% of people report suffering from "heartburn" in any 6- to 12-month period.1

  • There is a spectrum of disorders ranging from the most common endoscopy-negative gastro-oesophageal reflux disease (GORD) to oesophageal mucosal damage, which can progress to ulceration and stricture formation, although only about 8% will have moderate or severe oesophagitis.
    Reflux oesophagitis
  • Abnormalities of the lower oesophageal sphincter may facilitate excessive reflux of gastric contents including acid and sometimes bile from the stomach into the oesophagus.
  • Bile is particularly caustic and reflux of duodenal contents is more troublesome than reflux of gastric contents alone.2 There is little correlation between severity of symptoms and findings on endoscopy.
  • Sometimes drugs that have not been taken with an adequate amount of water stick in the oesophagus and are slowly released causing oesophagitis. Non-steroidal anti-inflammatory drugs (NSAIDs) and doxycycline are especially notorious and must be taken with adequate water. Bisphosphonates can be extremely troublesome. Oesophageal reflux is recognised as a risk factor for oesophageal cancer.


Factors that predispose to reflux include:

  • Increased intra-abdominal pressure.
  • Inadequate cardiac sphincter for anatomical reasons or factors that reduce tone, and also poor oesophageal peristalsis.
  • Smoking, alcohol, fat, coffee.
  • Pregnancy.
  • Obesity.
  • Tight clothes.
  • Big meals.
  • Surgery in achalasia of the cardia.
  • Systemic sclerosis.
  • Hiatus hernia.
  • Drugs including tricyclic antidepressants, anticholinergics, nitrates and calcium-channel blockers.

Most of these predisposing factors increase intra-abdominal pressure and a fatty meal delays gastric emptying but the listed drugs and smoking relax the tone of the cardiac sphincter.

NB: there is no relationship between Helicobacter pylori infection and GORD.

There are three phases in the secretion of gastric acid:

  1. The cephalic phase: 30% of the total gastric acid secretions to be produced is stimulated by anticipation of eating and the smell or taste of food.
  2. The gastric phase: 60% of the acid secreted is stimulated by the distention of the stomach with food. Plus, digestion produces proteins, causing even more gastrin production.
  3. The intestinal phase: The remaining 10% of acid is secreted when chyme enters the small intestine, and is stimulated by small intestine distention.

Treatments used for GORD act on the mechanisms controlling acid secretion. Protein pump inhibitors (PPIs), such as omeprazole and lansoprazole, act on the proton pump - number 5 in the diagram above.


  • Heartburn is a burning feeling, rising from the stomach or lower chest up towards the neck, that is related to meals, lying down, stooping and straining. It is relieved by antacids.
  • Retrosternal discomfort, acid brash - regurgitation of acid or bile.
  • Water brash - this is excessive salivation.
  • Odynophagia (pain on swallowing) may be due to severe oesophagitis or stricture.

Atypical symptoms3

These include chest pain, epigastric pain, and bloating.

  • Non-cardiac chest pain caused by GORD has been found in up to 50% of patients with chest pain and normal coronary angiography. Usually there is no relationship to exercise and this helps to differentiate most cases of reflux-induced chest pain from true angina.
  • Respiratory symptoms include chronic hoarseness (the Cherry-Donner syndrome), chronic cough, and asthmatic symptoms like wheezing and shortness of breath. Episodic or chronic aspiration can cause pneumonia, lung abscess, and interstitial pulmonary fibrosis. In 6% to 10% of patients with chronic cough, GORD is the underlying cause.


  • Endoscopy is the investigation of choice.
  • Perform FBC to exclude significant anaemia.
  • Barium swallow may show hiatus hernia (fluid level on CXR does not prove oesophagitis).
  • Oesophageal pH monitoring to assess if symptoms coincide with acid in the oesophagus. This can be done with:
    • Naso-oesophageal pH catheter (24-hour study).
    • Wireless pH capsule (Bravo®).4
    • Oesophageal impedance and pH via nasal catheter (can give quantitative information about amount of fluid refluxed).

Endoscopic grading of oesophagitis

The Savary-Miller grading system is commonly used.5

  • Grade 1: single or multiple erosions on a single fold. Erosions may be exudative or erythematous.
  • Grade 2: multiple erosions affecting multiple folds. Erosions may be confluent.
  • Grade 3: multiple circumferential erosions.
  • Grade 4: ulcer, stenosis or oesophageal shortening.
  • Grade 5: Barrett's epithelium. Columnar metaplasia in the form of circular or non-circular (islands or tongues) extensions.

The more recent and more objective Los Angeles grades A to D classification is also used:

  • Grade A: one or more mucosal breaks no longer than 5 mm, none of which extends between the tops of the mucosal folds.
  • Grade B: one or more mucosal breaks more than 5 mm long, none of which extends between the tops of two mucosal folds.
  • Grade C: mucosal breaks that extend between the tops of two or more mucosal folds, but which involve <75% of the mucosal circumference.
  • Grade D: mucosal breaks which involve ≥75% of the mucosal circumference.

Differential diagnosis


The UK National Institute for Health and Clinical Excellence (NICE) has published guidelines on the management of dyspepsia (including reflux symptoms) that impact on clinical practice.7

Department of Health guidelines for urgent referral for suspected upper GI cancer8

  • Dysphagia - food sticking on swallowing, at any age.
  • Dyspepsia at any age combined with one or more of the following 'alarm' symptoms:
    • Weight loss.
    • Proven anaemia.
    • Vomiting.
  • Dyspepsia in a patient aged 55 years or more with at least one of the following 'high-risk' features:
    • Onset of dyspepsia <1 year ago.
    • Continuous symptoms since onset.
  • Dyspepsia combined with at least one of the following known 'risk factors':
    • Family history of upper GI cancer in more than two first-degree relatives.
    • Barrett's oesophagitis.
    • Pernicious anaemia.
    • Peptic ulcer surgery over 20 years previously.
    • Known dysplasia, atrophic gastritis, intestinal metaplasia.
    • Jaundice.
    • Upper abdominal mass.

In a prospective observational study the prevalence of gastric cancer was 4% (and serious benign disease 13%) in a cohort of patients referred urgently for alarm symptoms.9 Referral for dysphagia or major weight loss at any age, together with those older than 55 years with alarm symptoms, would have detected 92% of the cancers found in the cohort.

In contrast, the presence of typical reflux symptoms was less likely to indicate the presence of malignancy.9Routine endoscopic investigation of dyspepsia is not necessary for patients (of any age) without alarm symptoms.

Pharmacological treatment

Patients with reflux symptoms, but no alarm symptoms, should receive initial treatment with full-dose PPIs for one month.

  • In cases of uninvestigated dyspepsia, eradication therapy for H. pylori can also be provided if infection is evident on serology or urea breath test. Where there is known GORD (i.e. post-gastroscopy), H. pylori eradication is not recommended.
  • If symptoms return after treatment, and long-term acid suppression is required, a step-down strategy to the lowest dose of PPI that provides effective relief of symptoms is more cost-effective than the step-up approach.7 Start acid suppression at a healing dose for 1 to 2 months. Then either step up a level if still symptomatic, or step down, once symptoms have improved, to the lowest level that provides effective symptom control. All patients should have a treatment plan and should be told if they can stop if symptom-free.

Referral for endoscopy

It may become appropriate to refer some patients with an inadequate response to therapy, or new emergent symptoms, to a specialist for a second opinion.

  • Review medications for possible causes of dyspepsia; for example, calcium antagonists, nitrates, theophyllines, bisphosphonates, steroids and NSAIDs. Patients undergoing endoscopy should be free from medication with either a PPI or an H2-receptor antagonist (H2RA) for a minimum of two weeks.
  • Consider the possibility of cardiac or biliary disease as part of the differential diagnosis.


  • If endoscopy is carried out and oesophagitis is present, a healing dose of PPI should be prescribed for two months.
  • In such patients, symptoms usually relapse when treatment is withdrawn, and maintenance PPI therapy is usually required.

Systematic reviews for the Cochrane Collaboration10 have confirmed that PPIs are more effective than H2RAs, e.g. ranitidine, at healing oesophagitis and maintaining remission from mucosal injury and symptoms.

Long-term management with PPIs for over 10 years has been shown to be safe and effective, although the dose requirement may increase over time.11


Unfortunately, most patients do not respond to lifestyle advice and require further therapy.12 However, the following are recommended:

  • Reduce weight.
  • Stop smoking.
  • Reduce alcohol intake.
  • Raise the head of the bed at night.
  • Take small, regular meals.
  • Avoid hot drinks, alcohol, and eating within three hours of going to bed.
  • Avoid drugs that affect oesophageal motility (nitrates, anticholinergics, tricyclic antidepressants) or damage the mucosa (NSAIDs, potassium salts, alendronate).

Management problems

A minority of patients have persistent symptoms despite PPI therapy and this group remains a challenge to treat.

Some evidence suggests that once patients develop the disease, severity is determined early and patients seem to continue with that phenotype long-term.12

Therapeutic options include:

  • Doubling the dose of PPI therapy.
  • Adding an H2RA at bedtime.
  • Extending the length of treatment.

Prokinetic drugs, such as metoclopramide 10 mg tds, may occasionally help symptoms by promoting gastric emptying and increasing the tone in the cardiac sphincter.

Specific groups should be given continuous, rather than intermittent, therapy:

  • Patients with a documented NSAID-induced ulcer, who must unavoidably continue with NSAIDs (e.g. severe rheumatoid arthritis), should remain on maintenance doses of PPIs.
  • Patients with severe reflux oesophagitis should remain on maintenance doses of PPI to prevent its recurrence.
  • Patients with complicated reflux disease (stricture, ulcer, haemorrhage) should be left on 'full-dose' PPI.

The cheapest effective PPI should be used.

NB: sudden or progressive worsening of symptoms if over 55 years old, or the development of dysphagia, anaemia, persistent vomiting or weight loss at any age, merits urgent referral for endoscopy (two-week rule - as per local guidelines).


  • Oesophagitis/ulcer
  • Anaemia
  • Oesophageal stricture
  • Barrett's oesophagus:
    • This is premalignant ectopic gastric mucosa.
    • Patients with chronic GORD are at increased risk of developing the changes of Barrett's oesophagus.
    • The risk increases with longer duration and increased frequency of gastro-oesophageal symptoms.

Document references

  1. Ruth M, Mansson I, Sandberg N; The prevalence of symptoms suggestive of esophageal disorders. Scand J Gastroenterol. 1991 Jan;26(1):73 [abstract]
  2. Kauer WK, Peters JH, DeMeester TR, et al; Mixed reflux of gastric and duodenal juices is more harmful to the esophagus than gastric juice alone. The need for surgical therapy re-emphasised. Ann Surg. 1995 Oct;222(4):525. [abstract]
  3. Lord RVN, Demeester TR. Reflux disease and hiatus hernia; OTS 2e Section 22.2.1
  4. Gillies RS, Stratford JM, Booth MI, et al; Oesophageal pH monitoring using the Bravo catheter-free radio capsule. Eur J Gastroenterol Hepatol. 2007 Jan;19(1):57-63. [abstract]
  5. Kinnear M, Ghosh S, Hudson S. GORD. Pharmaceutical Journal; August 1999.
  6. Fox M, Forgacs I. Gastro-oesophageal reflux disease. BMJ; January 2006.
  7. Dyspepsia: Managing dyspepsia in adults in primary care, NICE Clinical Guideline (2004)
  8. Referral for suspected cancer, NICE Clinical Guideline (2005)
  9. Kapoor N, Bassi A, Sturgess R, et al; Predictive value of alarm features in a rapid access upper gastrointestinal cancer service. Gut. 2005 Jan;54(1):40. [abstract]
  10. Leontiadis GI, Sharma VK, Howden CW; Proton pump inhibitor treatment for acute peptic ulcer bleeding. The Cochrane library. 2006.
  11. Klinkenberg, Nelis F, Dent J, et al; Long-term omeprazole treatment in resistant gastroesophageal reflux disease: efficacy, safety, and influence on gastric mucosa. Gastroenterology. 2000 Apr; 118(4):661-9. [abstract]
  12. Moayyedi P, Talley NJ; Gastro-oesophageal reflux disease Lancet. 2006 Jun 24;367(9528):2086 [abstract]

Internet and further reading


EMIS is grateful to Dr Hayley Willacy for writing this article. The final copy has passed scrutiny by the independent Mentor GP reviewing team. ©EMIS 2010.
Document ID: 325
Document Version: 3
Document Reference: bgp844
Last Updated: 12 Jan 2010
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