Gastro-oesophageal reflux disease

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

The antireflux barrier comprises the lower oesophageal sphincter, diaphragmatic crura and gastro-oesophageal junction anatomy. Transient sphincter relaxations, hiatus hernia, impaired clearance and raised abdominal pressure can increase exposure, while mucosal sensitivity explains why symptom intensity and acid burden are not tightly linked. GORD phenotypes include erosive disease, non-erosive reflux with abnormal acid exposure, reflux hypersensitivity with normal exposure but symptom association, and functional heartburn without supportive reflux evidence.

Most adults with typical symptoms and no alarm feature can begin empirical management without endoscopy. The consultation should still review cardiac risk, medicines, dysphagia, bleeding, weight, anaemia, vomiting and family history. Persistent symptoms may reflect incorrect PPI use, weakly acidic or volume reflux, rumination, supragastric belching, eosinophilic oesophagitis, achalasia, functional chest pain or an unrelated cardiopulmonary disorder. Repeatedly doubling acid suppression without revisiting the phenotype creates risk without diagnostic progress.

Long-term therapy is justified by ongoing symptom benefit or complications such as severe erosive disease, but should be reviewed rather than stopped reflexively or continued automatically. Explain that rebound acid symptoms can occur after withdrawal. Surgery is an option for selected people with confirmed reflux who prefer it or cannot tolerate effective medication; manometry and objective reflux monitoring follow the BSG pathway. Endoscopic or implant procedures are governed by specific NICE and local commissioning arrangements.

Key points

GORD occurs when reflux of gastric contents causes troublesome symptoms or complications; heartburn alone is neither necessary nor sufficient for a conclusive diagnosis.
Typical symptoms are burning retrosternal discomfort and acid regurgitation, often meal-related or worse supine, but chest pain must first be risk-assessed for cardiac disease.
Dysphagia, weight loss, bleeding, iron-deficiency anaemia, persistent vomiting and an abnormal examination override empirical treatment and prompt urgent investigation.
For uncomplicated suspected GORD, NICE supports a four- or eight-week course of a full-dose proton pump inhibitor, followed by the lowest dose that controls symptoms.
Check adherence and timing before declaring PPI failure; a gastro-resistant PPI is generally taken before food according to its product instructions.
Endoscopy detects erosive oesophagitis, stricture, Barrett mucosa and malignancy, but a normal endoscopy does not exclude reflux disease.
Ambulatory pH or pH-impedance monitoring distinguishes persistent reflux from reflux hypersensitivity and functional heartburn when the answer will change management.
High-resolution manometry is not a reflux test; it excludes achalasia or a major motor disorder and locates the lower sphincter before selected reflux testing or surgery.
Lifestyle advice should be individualised: weight reduction when overweight and avoiding personally reproducible late meals or triggers is more credible than a universal prohibition list.
Antireflux surgery requires objectively supported GORD, appropriate physiology, informed consent and specialist follow-up because dysphagia, gas-bloat and recurrent reflux can occur.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Junction barrier failure

Transient lower sphincter relaxations, hypotensive sphincter function and sliding hiatus hernia permit gastric contents to reflux into the oesophagus.

Pressure and clearance factors

Central obesity, pregnancy, delayed gastric emptying and impaired oesophageal clearance increase exposure, particularly after meals or when supine.

Medicine and behavioural modifiers

Smoking, alcohol, late meals and medicines that reduce sphincter tone may aggravate individual symptoms, though triggers vary and blanket restriction is unnecessary.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Reflux events
Failure of the antireflux barrier allows acidic or weakly acidic gastric contents to enter the oesophageal lumen.
2
Prolonged mucosal exposure
Poor peristaltic clearance and reduced salivary neutralisation lengthen contact time, provoking symptoms and epithelial injury in the distal oesophagus.
3
Inflammation and remodelling
Repeated injury can cause erosive oesophagitis, ulceration, fibrosis or replacement of squamous mucosa by Barrett metaplasia.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Typical reflux syndrome

Burning behind the sternum and sour or bitter regurgitation recur after meals, bending or lying down and may improve with acid suppression, without progressive swallowing difficulty.

Erosive or peptic complicationRed flag

Odynophagia, bleeding, anaemia or dysphagia can reflect severe oesophagitis, ulcer or peptic stricture and requires endoscopic assessment rather than indefinite empirical treatment.

Possible oesophageal cancerRed flag

Progressive dysphagia, weight loss, early satiety, haematemesis, iron-deficiency anaemia or persistent vomiting enters the current NICE suspected-cancer pathway according to age and symptom combination.

Extra-oesophageal symptoms

Chronic cough, throat clearing, hoarseness, wheeze or dental erosion may coexist with reflux, but are multifactorial and should not be labelled reflux-related solely from a PPI trial.

Refractory symptom phenotype

Symptoms persist despite correctly taken therapy and may represent ongoing acid or non-acid reflux, hypersensitivity, functional heartburn, rumination or an alternative structural or motility disorder.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Clinical assessment and full blood countFirst step
Why
Separate uncomplicated reflux from urgent structural or systemic disease.
Interpretation and limitations
Document dysphagia, odynophagia, bleeding, weight trajectory, vomiting and cardiac features. Anaemia strengthens the need for source investigation but a normal count does not exclude cancer.
02
Upper gastrointestinal endoscopy
Why
Identify mucosal injury, narrowing, Barrett change or malignancy.
Interpretation and limitations
Grade erosive oesophagitis, describe the gastro-oesophageal junction and biopsy visible abnormality or suspected EoE appropriately. Normal mucosa does not rule out pathological reflux.
03
Ambulatory pH monitoring
Why
Confirm abnormal acid exposure when endoscopy is non-diagnostic and objective proof is required.
Interpretation and limitations
Testing off acid suppression is generally used when GORD is unproven; protocol and medication washout follow the physiology service. Symptom association supplements, but does not replace, acid-exposure interpretation.
04
Combined pH-impedance monitoring
Why
Assess acid and non-acid reflux during persistent symptoms in selected patients.
Interpretation and limitations
BSG supports impedance-pH assessment for refractory symptoms and particular pre-surgical scenarios. Low event counts and inaccurate symptom pressing can limit inference.
05
High-resolution oesophageal manometry
Why
Exclude major motor disease and guide catheter or surgical planning.
Interpretation and limitations
Manometry can identify achalasia, absent contractility or outflow obstruction but cannot prove GORD. Minor abnormalities alone do not necessarily explain symptoms.
06
Barium swallow
Why
Define anatomy or bolus hold-up when dysphagia or a large hernia is suspected.
Interpretation and limitations
It complements rather than replaces endoscopy and manometry. Free reflux during a brief study is neither sufficiently sensitive nor specific for a GORD diagnosis.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Cardiac chest pain

Exertional pressure, breathlessness, autonomic symptoms or cardiovascular risk requires cardiac assessment before discomfort is labelled reflux.

Functional heartburn or dyspepsia

Persistent symptoms with normal endoscopy and physiological reflux testing suggest altered sensitivity rather than pathological acid exposure.

Eosinophilic or motor disease

Dysphagia, impaction, retained food or abnormal biopsies and manometry support EoE, achalasia or another motility disorder.

Additional chapter-specific clues

Cardiac chest-pain mimicRed flag

Pressure-like discomfort with exertion, breathlessness, sweating, radiation or cardiovascular risk must be assessed urgently for myocardial ischaemia even if reflux has occurred before.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Initial careTreat uncomplicated probable GORDFirst stepTypical heartburn or regurgitation occurs without alarm features or a dangerous chest-pain phenotype.

1Review alarm features, cardiac risk, pregnancy, medicines and symptom pattern; arrange urgent investigation instead of empirical therapy when the assessment is concerning.
2Offer individual weight and meal advice, then use a full-dose PPI for four or eight weeks according to NICE and the selected product instructions.
3Review response, adherence and timing; if controlled, step down to the lowest effective dose or on-demand use when clinically appropriate.
4If symptoms recur frequently or complications exist, agree a longer-term plan with periodic indication, adverse-effect and deprescribing review.

02Persistent symptomsRe-phenotype before escalatingEscalationSymptoms continue despite an adequately taken initial PPI course.

1AlternativeConfirm the correct medicine, dose, pre-meal timing and adherence, and reassess dysphagia, cardiac features, weight, bleeding and alternative medicines or diagnoses.
2Optimise acid suppression within NICE and BNF limits or consider an H2-receptor antagonist response, while avoiding unsupervised indefinite dose multiplication.
3Refer for endoscopy or physiology when the diagnosis is uncertain, symptoms are troublesome or invasive treatment is considered; choose on- or off-treatment reflux testing to answer the stated question.
4If physiological testing is normal, explain reflux hypersensitivity or functional heartburn and use the appropriate specialist gut-brain pathway rather than continuing ineffective acid suppression.

03Procedural treatmentSelect antireflux surgery safelyA patient with important symptoms is considering an operation or commissioned intervention.

1DefinitiveConfirm objective GORD and ensure the reported symptoms are plausibly reflux-mediated; response to PPI alone is helpful but not definitive.
2Perform high-resolution manometry and the indicated pH or pH-impedance study, and define hiatus anatomy through the specialist service.
3Discuss fundoplication or another commissioned option with an upper-GI MDT, including durability, dysphagia, gas-bloat, inability to belch or vomit, recurrence and possible medication use.
4After treatment, investigate rather than assume the cause of recurrent chest pain, dysphagia or reflux symptoms, and record long-term outcome.

Key medicines and prescribing safety2 treatments · regimens, roles and cautions

Suppresses acid to relieve typical symptoms and heal acid-mediated oesophagitis; maintenance uses the lowest effective dose.

Omeprazole

For symptomatic GORD, a common licensed adult regimen is 20 mg orally once daily; reflux oesophagitis is usually treated for four to eight weeks, with 40 mg daily used for severe disease under current product guidance.

Check alarm features before prescribing and review long-term indication. Consider interactions, hepatic impairment, enteric infection, hypomagnesaemia, fracture and vitamin or mineral issues in context; do not stop abruptly without warning about rebound symptoms.

Provides short-term relief of post-prandial breakthrough heartburn or regurgitation and can supplement rather than replace cause-directed care.

Alginate-antacid preparation

Use the licensed product-specific adult dose after meals and at bedtime when needed, separating it from interacting medicines in accordance with the current BNF or package instructions.

Sodium, calcium or potassium content matters in renal, cardiac or salt-restricted patients. Frequent use can mask an alarm presentation, and antacids impair absorption of several oral medicines if taken together.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Erosive oesophagitis and bleeding

Acid-related mucosal breaks can ulcerate, bleed and cause odynophagia or iron deficiency, particularly with antithrombotic exposure.

Peptic stricture

Repeated inflammation heals with fibrosis and luminal narrowing, producing progressive solid-food dysphagia that requires structural assessment.

Barrett oesophagus

Chronic reflux can produce intestinal metaplasia, which carries a small but important dysplasia and adenocarcinoma risk requiring evidence-based surveillance.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Review symptom frequency, nocturnal disturbance, regurgitation, swallowing and treatment adherence after the initial four- or eight-week course.
Ask specifically about progressive dysphagia, bleeding, vomiting, weight loss and anaemia at every review of persistent or changing symptoms.
For continued PPI treatment, document the indication and lowest effective dose, and perform targeted magnesium, renal, blood or nutrient testing only when risk or symptoms justify it.
After antireflux surgery, track dysphagia, gas-bloat, recurrent reflux, nutritional effect and continuing medicine use through the surgical pathway.
Reassess the diagnosis when symptoms do not correlate with objective reflux; avoid using repeated empirical prescriptions as a substitute for physiology or cardiac evaluation.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

PPI response is supportive

Placebo response and spontaneous variation are common, while some proven reflux persists despite PPIs. Improvement alone cannot conclusively diagnose GORD.

Normal endoscopy is common

Non-erosive reflux may have abnormal acid exposure despite normal mucosa; conversely, symptoms with normal exposure can reflect hypersensitivity or functional heartburn.

Manometry answers another question

It assesses motor function and locates the sphincter. It is essential before surgery but cannot replace ambulatory reflux monitoring when reflux evidence is needed.

Throat symptoms are multifactorial

Hoarseness and cough should prompt respiratory, ENT, medicine and behavioural assessment; a label of laryngopharyngeal reflux from symptoms alone is unreliable.

Surgery trades one burden for another

Well-selected patients can gain excellent reflux control, yet postoperative dysphagia, gas-bloat and recurrent symptoms belong in shared consent rather than being treated as surprises.

11Common pitfallsFrequent interpretation and management errors.

01
Calling exertional chest pain reflux because it improved after an antacid and failing to assess acute coronary syndrome.
02
Renewing a PPI indefinitely without checking adherence, dose timing, indication or alarm symptoms.
03
Using a normal gastroscopy to claim that all reflux disease has been excluded.
04
Attributing cough or hoarseness to reflux solely from an empirical treatment response.
05
Referring for fundoplication without objective reflux evidence and high-resolution manometry.
06
Doubling acid suppression repeatedly when physiology instead supports functional heartburn or rumination.