Gastro-Oesophageal Reflux Disease (GORD)

Meet the patient

A 52-year-old overweight man arrives with retrosternal burning that woke him at 2am after a late curry, eased when he sat up and drank milk, and melted away with a Gaviscon from the bedside drawer. He has had it on and off for years, never told a doctor, and tonight — for the first time — he wonders if his heart is the problem.[1]

Two questions now run the rest of this page, and every GORD consult: is that chest pain cardiac? (you exclude it before you reach for the antacid) and do I scope him, or trial a PPI? (the alarm features decide). Hold those two and the management ladder writes itself.[1]

What GORD is — troublesome reflux, not a single heartburn

GORD is reflux severe enough to trouble the patient, or to cause complications — that is the whole Montreal definition, and it is symptom-based on purpose. "Troublesome" means mild symptoms on two or more days a week, or moderate-to-severe symptoms on one or more days a week.[1]

A normal endoscopy does not exclude GORD — six in ten sufferers have a pristine mucosa (NERD), and the disease lives in the symptom and the acid exposure, not in the break. That is why a PPI trial is both diagnostic and therapeutic, and why pH-impedance — not the OGD — is the objective arbiter.[2]

Montreal sorts GORD into oesophageal syndromes (chest-pain, oesophagitis, stricture, Barrett, adenocarcinoma — a clean symptom-to-cancer ladder) and extra-oesophageal syndromes (cough, laryngitis, asthma, dental erosion). The extra-oesophageal links are associations until you prove pathological reflux, because a hoarse voice and a cough belong to fifty other causes.[1]

One spectrum, two faces — and the Lyon line

The single exam-relevant split is erosive versus non-erosive. Roughly 30 to 40 percent of symptomatic patients have erosive reflux disease (ERD) — visible breaks graded Los Angeles A to D; the other 60 to 70 percent have non-erosive reflux disease (NERD) with normal mucosa but real reflux. Barrett is the complication-grade third phenotype.[1]

[1]

The Los Angeles grades — one named line and you never forget them:[1]

• A under 5 mm — a mucosal break no more than 5 mm long, within one fold.
• B over 5 mm — a break more than 5 mm long, not bridging adjacent folds.
• C Continuous — breaks bridging the tops of two or more adjacent folds.
• D Done it all — circumferential, at least three-quarters of the oesophageal circumference.

[1]

C and D plus typical reflux symptoms equal conclusive GORD (Lyon Consensus 2.0) and carry the heaviest Barrett, stricture and cancer risk. A and B are common but non-specific — pill, infectious and peptic injury overlap.[2]

The 6/4 number rule — when reflux is "conclusive"

Acid exposure time is the objective arbiter, and the Lyon Consensus 2.0 thresholds are the numbers examiners quote. On ambulatory pH or pH-impedance monitoring done off PPI, the percent of time oesophageal pH sits under 4 divides cleanly:[2]

• AET over 6 percent — conclusive GORD.
• AET under 4 percent with a negative symptom association — GORD excluded.
• AET 4 to 6 percent — inconclusive (adjudicate with the number of reflux episodes and symptom-association indices).

[2]

Over 40 reflux episodes a day, or over 80 on prolonged monitoring, supports pathological reflux; a symptom association probability over 95 percent or a symptom index over 50 percent ties symptoms to events in the grey band.[2]

[1] [2]

How common, who, and why the sphincter fails

GORD is the commonest diagnosis in the gastroenterology outpatient clinic — 10 to 20 percent of Western adults, and rising fast across Asia as obesity, westernised diet and H. pylori eradication (which restores acid secretion) spread. Prevalence peaks in the fifth to seventh decades; severe erosive disease and Barrett cluster in white males, smokers and the obese.[1]

The barrier at the gastro-oesophageal junction is a composite — LES tone, the diaphragmatic crural pinch (the right crus is an external sphincter that augments the LES on straining), the acute angle of His (a flap-valve), and the mucosal rosette. Reflux happens whenever that barrier is overcome. The resting LES is a 2 to 4 cm pressure zone of 10 to 30 mmHg; under 10 mmHg it is abnormal and refluxes freely.[1]

Five mechanisms, five clinical hooks — name them in this order:[1]

1. Transient LES relaxations (TLESRs) — the dominant mechanism in NERD and most ERD. A vagally-mediated LES relaxation without a swallow, triggered by gastric distension — above all by the acid pocket, the unbuffered layer of gastric juice that floats on a meal for up to an hour. TLESRs drive 50 to 80 percent of reflux in NERD. This is the mechanism baclofen 5 to 10 mg tds (a GABA-B agonist) is built for — it cuts TLESR frequency by 40 to 60 percent and earns its place in refractory disease, CNS side-effects permitting.
2. Weak or hypotensive LES — under 10 mmHg from scleroderma/CREST, myotonic dystrophy, ageing or drugs. Reflux on any ordinary strain.
3. Hiatus hernia — over half of LA C/D patients have one; it disrupts the crural diaphragm, shortens the LES, enlarges the acid pocket and re-refluxes from its sac. Paraoesophageal hernias add volvulus and strangulation and warrant repair even when reflux is mild.
4. Impaired clearance — ineffective peristalsis (the elderly, scleroderma), dry mouth (Sjogren, anticholinergics, smoking, radiation), or the hernia sac. Longer contact, worse injury.
5. Delayed gastric emptying — diabetes, opioids, GLP-1 agonists, amyloidosis. Bigger post-prandial volume, more TLESRs.

[1]

The injury cascade is acid, pepsin and bile on a three-tier defence. Pre-epithelial (mucus-bicarbonate film from saliva), epithelial (tight junctions, intracellular buffers), post-epithelial (mucosal blood flow). When the refluxate wins, acid and bile drive cytokine release, intercellular-space dilation (the earliest change — and the pain in NERD with no visible break), then erosion, ulcer, and finally metaplasia as a maladaptive but premalignant repair.[1]

Who refluxes — the risk-factor face-off

Most risk factors converge on one of two levers: they raise intra-abdominal pressure, or they drop LES tone. Name the lever and the mechanism follows.[1]

[1]

The chest pain that is not GORD — until you have excluded the heart

Always exclude acute coronary syndrome first. GORD is the commonest cause of non-cardiac chest pain, but "non-cardiac" is a label you earn only after the ECG and troponin are back. Post-prandial burning that radiates to the arm or jaw can be oesophageal, and it can be an inferior MI sent home as gastritis. The first test in retrosternal pain is the ECG, not the antacid.[1]

The cardiac and reflux histories overlap deliberately — both can be central, both can radiate, both can ease with something. The discriminator is the pattern, not the relief: cardiac pain is exertional, crushing, with autonomic features and ECG or troponin change; reflux pain is post-prandial, postural, burning, eased by antacid. When the picture is mixed, you exclude the heart and then you treat the reflux.[1]

Beyond the heart, name the killers and the mimics. Aortic dissection (tearing pain to the back, a pulse or BP differential — never anticoagulate), pulmonary embolism, Boerhaave rupture after vomiting. Then the oesophageal mimics that change management completely:[1]

• Achalasia — progressive solid and liquid dysphagia, regurgitation of undigested non-acidic food, weight loss; bird's-beak on barium swallow, raised integrated relaxation pressure with aperistalsis on manometry. Often mislabelled refractory GORD; PPIs do not help and fundoplication without excluding it is a disaster.
• Eosinophilic oesophagitis — solid-food dysphagia and food impaction in an atopic young adult; rings, furrows, white plaques on OGD; over 15 eosinophils per high-power field on biopsy. Treat with swallowed topical steroid or dupilumab, not a PPI escalation.
• Peptic ulcer disease — epigastric pain, nocturnal burning, H. pylori-linked; diagnosis on OGD.
• Functional heartburn — burning not explained by reflux, normal OGD and pH; Rome IV. A neuromodulator (TCA or SSRI), not a PPI, is the treatment.
• Rumination and supragastric belching — behavioural mimics of refractory reflux; pH-impedance shows the pattern; treat with diaphragmatic breathing, not drugs.

[1]

Chronic cough over 8 weeks runs the cough triad — GORD, asthma, post-nasal drip. Attribute reflux only after objective reflux is confirmed, because a PPI for a non-reflux cough does nothing but add a long-term-PPI risk.[1]

When to scope, when to trial — the alarm line

GORD is a clinical diagnosis in the patient with typical symptoms and no alarm features — most need no test at all. Take the history (relation to meals, posture, sleep; triggers; PPI response; LES-lowering drugs), screen for alarm features, and feel for complications and mimics at the bedside. GORD has no specific physical sign; the exam exists to find anaemia, epigastric tenderness, scleroderma facies, wheeze and dental erosion.[1]

The diagnostic hierarchy is short, and the order matters. A 4 to 8 week PPI trial is first-line and both diagnostic and therapeutic; OGD is for alarm features, age over 55 at onset, persistent symptoms on PPI, or pre-surgery; pH-impedance is the objective arbiter for refractory or pre-operative cases; manometry is mandatory before any fundoplication to exclude achalasia and to choose a complete versus partial wrap.[1]

Symptom scores earn easy marks. GerdQ (six items, past week; a score over 8 predicts GORD) and the Reflux Symptom Index (nine laryngeal items; over 13 suggests supraoesophageal reflux) triage primary care and the ENT referral.[1]

[1]

The stepwise ladder — omeprazole is the centre of gravity

Treatment climbs a six-rung ladder, escalating only on failure. Lifestyle is the foundation for everyone; omeprazole is the workhorse; surgery is the last rung and only for confirmed objective reflux. Memorise the doses — they are viva-critical.[1]

[1]

[1]

Long-term PPI — the risks you must name before you sign the repeat

A PPI is safe for a course and not free for a decade. Before you sign the repeat prescription, name the long-term risks and deprescribe to the lowest effective dose.[1]

• Osteoporotic fracture (hip and spine) — modest risk; check calcium and vitamin D; review the indication.
• Hypomagnesaemia (and secondary hypocalcaemia) — check magnesium, especially with diuretics or digoxin.
• Vitamin B12 deficiency — food-cobalamin malabsorption on years of use.
• Enteric infection — C. difficile, Salmonella, Campylobacter; acid loss removes the microbial kill.
• Acute interstitial nephritis — idiosyncratic; check creatinine for unexplained renal injury.
• Rebound acid hypersecretion on abrupt cessation — taper, do not stop dead.

[1]

The classic trap: reflex long-term PPI without an indication and no deprescribing plan. Six weeks of omeprazole for a clear-cut reflux flare is good medicine; six years without a review date is a medication error in slow motion.[1]

The cutters and the cure — surgery only after you confirm

Never operate on symptom-only GORD. The single rule that protects the fundoplication patient: confirm objective reflux (a positive pH study or LA C/D oesophagitis) and normal manometry excluding achalasia before the surgeon picks up the laparoscope. Operating on symptoms alone is the commonest cause of a failed fundoplication.[1]

Laparoscopic Nissen fundoplication (a 360 degree wrap) is the gold standard. It restores LES competence and recreates the angle of His; at 5 years it is equivalent to chronic esomeprazole for heartburn and superior for regurgitation (LOTUS). The price is dysphagia, gas-bloat, paraoesophageal herniation and a 10 to 20 percent recurrence at 10 years.[4]

[1] [4]

In the morbidly obese (BMI over 35), Roux-en-Y gastric bypass beats fundoplication — it loses weight, relieves reflux and diverts bile away from the refluxate in one operation. Scleroderma patients with a patulous aperistaltic oesophagus are the ones fundoplication fails — poor motility guarantees postoperative dysphagia; treat them with lifelong high-dose PPI instead.[1]

[4]

Barrett — the metaplasia that earns surveillance

Barrett oesophagus is the distal squamous epithelium replaced by specialised intestinal metaplasia with goblet cells — an adaptive response to chronic acid-bile injury that resists acid better than squamous mucosa but is prone to cancer. It is the gateway lesion for oesophageal adenocarcinoma.[3]

Diagnosis needs both endoscopy and histology. Endoscopically, salmon-pink velvety tongues of columnar mucosa extend above the GE junction; histologically, biopsy must show intestinal metaplasia with goblet cells (Alcian-blue-positive acidic mucin). A regional delta examiners like: US guidelines require goblet cells for the label, whereas UK (BSG) guidelines accept columnar metaplasia of any length.[1]

Extent is recorded in Prague C and M — Circumferential and Maximum extent in centimetres above the gastric folds. C2M4 means 2 cm circumferential with tongues reaching 4 cm; long-segment (over 3 cm) carries more cancer risk than short-segment (under 3 cm).[1]

The pathology ladder is metaplasia to dysplasia to carcinoma — one biopsy step at a time: intestinal metaplasia, indefinite for dysplasia, low-grade dysplasia, high-grade dysplasia, intramucosal carcinoma, invasive adenocarcinoma. Each step is confirmed by two specialist GI pathologists, because inter-observer agreement on dysplasia is the weak link. The sequence unfolds over years — which is exactly what makes surveillance and eradication work.[3]

Cancer risk scales with dysplasia — memorise the gradient: non-dysplastic Barrett about 0.5 percent per year, low-grade dysplasia about 0.7 to 1 percent per year, high-grade dysplasia 5 to 10 percent per year with a real short-term risk. The gradient is the whole rationale for the surveillance ladder below.[1]

[1]

The endoscopic eradication ladder — resect the nodule, ablate the flat mucosa.[1]

• Endoscopic mucosal resection (EMR) — first, for any visible lesion (nodule, plaque, ulcer) in Barrett; it gives a histological specimen and stages the depth of invasion. Ablation destroys tissue, so always resect a visible lesion before you ablate.
• Radiofrequency ablation (RFA, HALO) — first-line for flat dysplastic Barrett; thermal ablation to squamous re-epithelialisation; complete eradication of intestinal metaplasia in over 90 percent.
• Endoscopic submucosal dissection (ESD) — en-bloc resection of larger or suspicious lesions (over 15 mm, poorly lifting) for deeper histology; technically demanding.
• Cryotherapy — an alternative for RFA failure or awkward anatomy.
• Oesophagectomy — reserved for refractory or multifocal high-grade dysplasia, or confirmed submucosal invasion where lymph-node risk warrants surgical staging; mortality 1 to 2 percent in high-volume centres.

[3]

The classic traps — five ways to hurt a reflux patient

Trap 1 — the "refractory GORD" that is achalasia. A tight LES that cannot relax looks like food sticking and regurgitation; a PPI changes nothing and a fundoplication on top of an unrecognised achalasia is a dysphagia disaster. Manometry before any wrap.[1]

Trap 2 — missing malignancy by skipping the OGD. Anaemia, dysphagia, weight loss or new reflux over 55 are alarm features; they earn an OGD, not a PPI trial. Treating the symptom and missing the cancer is the mistake the alarm mnemonic exists to prevent.[1]

Trap 3 — reflex long-term PPI with no indication and no plan to stop. Good for a course, not free for a decade. Deprescribe to the lowest effective dose, counsel on the risks, taper rather than stop dead.[1]

Trap 4 — operating on symptoms alone. A fundoplication without confirmed objective reflux (positive pH study or LA C/D) is the commonest cause of a failed wrap. Confirm before you cut.[1]

Trap 5 — escalating the PPI in functional heartburn. Burning with a normal OGD and normal acid exposure is reflux hypersensitivity or functional heartburn; the treatment is a neuromodulator (TCA or SSRI) and cognitive-behavioural therapy, not a higher PPI dose.[1]

Special populations — pregnancy, the elderly, the child, the scleroderma patient

Pregnancy: heartburn is near-universal — progesterone relaxes the LES and the third trimester compresses the stomach. Climb the same ladder, gently: lifestyle and alginate first; H2RA second (ranitidine is withdrawn — use famotidine); omeprazole or lansoprazole for severe refractory disease (low-risk in pregnancy), avoiding the first trimester where possible. Skip prokinetics and misoprostol.[1]

The elderly: blunted symptom perception hides severe disease. A pristine history does not spare them the OGD — keep a low threshold for scoping (silent severe oesophagitis, Cameron erosions, malignancy). PPI doses are unchanged; watch magnesium, B12 and bone health, and prefer pantoprazole over omeprazole in the elderly on dual antiplatelet therapy (the CYP2C19-clopidogrel interaction).[1]

The obese: weight loss first; in morbid obesity (BMI over 35) Roux-en-Y gastric bypass is preferred over fundoplication because it treats reflux, weight and bile in one operation.[1]

The child and infant: the thriving happy spitter needs no treatment. Reflux plus failure to thrive, oesophagitis, recurrent pneumonia or apnoea is GORD — thicken feeds, alginate, H2RA, then omeprazole 0.7 to 1.4 mg/kg/day for severe disease; reserve Nissen for refractory neurological impairment.[1]

Scleroderma and CREST: a patulous, aperistaltic oesophagus produces severe silent reflux with high stricture risk. Lifelong high-dose PPI; fundoplication usually fails because the motility cannot push through a wrap.[1]

The bleeding emergency: haematemesis or melaena from erosive oesophagitis, Cameron erosions or a Mallory-Weiss tear — ABCDE, two large-bore cannulae, transfuse to Hb over 70 g/L (over 80 g/L if comorbid), IV PPI (pantoprazole 40 mg bolus then infusion, or omeprazole 80 mg bolus then 8 mg/h), and urgent OGD; risk-stratify with the Glasgow-Blatchford score.[1]

Regional deltas — same spine, different thresholds

Two open controversies to name calmly: the PPI-clopidogrel interaction (omeprazole inhibits CYP2C19 — prefer pantoprazole in dual antiplatelet therapy, though the clinical impact is debated) and the cost-effectiveness of routine Barrett surveillance in elderly, comorbid patients with short-segment non-dysplastic disease.[1]

Prognosis is excellent for the majority. NERD rarely progresses; most patients live well on intermittent or on-demand PPI and never develop complications. The cancer-risk burden sits with ERD, especially LA C/D, and with Barrett — which is exactly who you scope and surveil. Fundoplication controls symptoms in 80 to 90 percent at 5 years, equivalent to PPI for heartburn and better for regurgitation, with 10 to 20 percent recurring over a decade.[4]

The mantra, and the mnemonic

The mantra: Trial the PPI, scope the alarmed, confirm before you cut.[1]

Ward-round test — three stems, thirty seconds each

Stem 1 — the 'refractory GORD' that is not (answer)

A 48-year-old man has "failed two PPIs" for heartburn and regurgitation; food sticks in his chest and he brings back undigested, non-acidic material at night. The surgical registrar has offered a Nissen. What is the next investigation, and why does it change the operation? Model: This is achalasia, not refractory GORD — the regurgitation is undigested and non-acidic, and the dysphagia is for solids and liquids. The next test is high-resolution manometry, which will show a raised integrated relaxation pressure with aperistalsis; a barium swallow shows the bird's-beak. Fundoplication here, without outflow correction, guarantees intractable dysphagia — the wrap sits on a LES that cannot relax. Confirm objective reflux on pH-impedance first (achalasia often has low acid exposure), and direct the patient toward myotomy or pneumatic dilation, not a Nissen.[1]

Stem 2 — the anaemic elderly woman with a hiatus hernia (answer)

A 76-year-old woman is referred for iron-deficiency anaemia; she denies heartburn. OGD shows a sliding hiatus hernia with linear erosions at the hiatus and no mass. What are the erosions, and what is the management? Model: These are Cameron erosions — linear mucosal breaks within a hiatus hernia sac, a classic cause of iron-deficiency anaemia in the elderly who report no heartburn because of blunted symptom perception. Biopsy to exclude malignancy, then a full course of PPI (omeprazole 20 to 40 mg daily for 8 weeks), iron replacement, and repeat OGD to confirm healing. The lesson: in the elderly, keep a low threshold for OGD — silent severe disease is the rule, not the exception.[1]

Stem 3 — the Barrett with a visible nodule (answer)

A 62-year-old man under Barrett surveillance has a new 12 mm nodule within flat Barrett mucosa; biopsies report high-grade dysplasia. The endoscopist plans radiofrequency ablation. What is missing, and why? Model: Resect the nodule by EMR before any ablation. RFA destroys tissue, and a nodule may harbour submucosal invasion that only a histological specimen can stage; ablating it blind buries the cancer. EMR provides the T-stage; if invasion is confined to mucosa, proceed to RFA of the remaining flat Barrett to achieve complete eradication of intestinal metaplasia. Reserve oesophagectomy for confirmed submucosal invasion (sm2/sm3) or refractory multifocal disease.[3]

References

1. [1]Katz PO, Dunbar KB, Schnoll-Sussman FH, et al. ACG Clinical Guideline for the Diagnosis and Management of Gastroesophageal Reflux Disease Am J Gastroenterol, 2022.PMID 34807007
2. [2]Gyawali CP, Kahrilas PJ, Savarino E, et al. Modern diagnosis of GERD: the Lyon Consensus Gut, 2018.PMID 29437910
3. [3]Spechler SJ, Souza RF. Barrett's esophagus N Engl J Med, 2014.PMID 25162890
4. [4]Hatlebakk JG, Zerbib F, Bruley des Varannes S, et al. Gastroesophageal Acid Reflux Control 5 Years After Antireflux Surgery, Compared With Long-term Esomeprazole Therapy Clin Gastroenterol Hepatol, 2016.PMID 26226096