GORD / PUD

See h-pylori.md for H. pylori testing/eradication detail. Barrett’s oesophagus (a GORD complication) is covered below.

GORD

Reflux of gastric contents into the oesophagus is a normal physiological process — it becomes a disease when symptomatic (usually ≥2×/week, or impairing quality of life) or when complications develop (oesophagitis, Barrett’s, adenocarcinoma, stricture). Acid and pepsin are the main irritants; mainly due to transient lower oesophageal sphincter relaxation, sometimes hiatus hernia. Dietary triggers: fat, chocolate, caffeine, alcohol, smoking, some medications.

Demographics: common (10–20% of adults have weekly symptoms); risk factors — obesity (BMI>30), >7 standard drinks/week, first-degree relative with heartburn; associated with scleroderma, asthma, cystic fibrosis, institutionalisation/ intellectual disability.

History

• Heartburn (cardinal symptom — burning retrosternal pain), regurgitation (often re-swallowed, sometimes mistaken for vomiting), “waterbrash” (reflex salivation ± nausea).
• Atypical: angina-like chest pain, voice change, cough, nausea.
• Complication symptoms: dysphagia (inflammation, dysmotility, stricture), odynophagia (usually severe oesophagitis), haematemesis (rare, usually mild).

Alarm symptoms (indication for endoscopy): dysphagia, odynophagia, haematemesis/melaena, weight loss, vomiting, anaemia — plus new symptoms in an older patient, changing symptoms, severe/frequent symptoms, or inadequate treatment response.

Investigation

• A therapeutic trial of high-dose PPI for 2–4 weeks is comparable to pH monitoring and better than endoscopy for diagnosis in typical, uncomplicated presentations.
• Endoscopy is not for everyone — young patients with mild typical symptoms don’t need it; it’s specific but not sensitive (2/3 of patients with GORD have a normal endoscopy). Reserve for alarm symptoms, diagnostic uncertainty, new symptoms in an older patient, changing/severe/refractory symptoms, or concern about infective/drug-induced oesophagitis, malignancy, or gastroduodenal disease.
• Barium swallow (stricture/hiatus hernia) and 24h pH monitoring are uncommonly used.

Management

Lifestyle (all severities): elevate the head of the bed, smaller meals, drink fluids between rather than with meals, avoid lying down after eating or eating/ exercising within 2–3h of bedtime, stop smoking, weight loss (particularly abdominal adiposity), avoid known trigger foods (high-fat meals, alcohol, coffee, chocolate, citrus, tomato, spicy food, carbonated drinks) — but don’t unnecessarily restrict foods; re-introduce if not helping.

Mild-intermittent symptoms (≤1 episode/week): diet/lifestyle first; then on-demand antacid/alginate or Mg/Al-hydroxide liquid; then an H2-antagonist (famotidine 20mg once–twice daily, nizatidine 150mg once–twice daily as required — ranitidine is no longer available, withdrawn by the TGA 2020–2024 due to NDMA contamination); then standard-dose PPI as required, taken 30–60 minutes before a meal.

Frequent/severe symptoms (≥2 episodes/week or impairing quality of life): PPIs are preferred over H2-antagonists — standard dose daily for 4–8 weeks (before breakfast if daytime-predominant symptoms, before the evening meal if night-predominant). If well controlled, step down to maintenance (halve the dose, alternate-day dosing, or on-demand use — stopping abruptly can cause rebound acid hypersecretion; ~30% of patients remain in remission after stopping). If poorly controlled, confirm adherence then arrange endoscopy; if standard dosing at twice daily is needed, this is more effective than a once-daily double dose.

Endoscopy-guided therapy: no/mild (LA grade A/B) oesophagitis — treat per symptoms as above. Grade C/D oesophagitis or ulceration: high-dose PPI (standard dose twice daily) for 8 weeks, managed with gastroenterology input; step down after 8 weeks to the lowest effective dose but do not stop if strictures or scleroderma are present (high relapse risk).

Long-term PPI risks: interstitial nephritis, hypomagnesaemia, increased pneumonia and C. difficile risk, impaired B12/iron absorption, increased fracture risk, and a small increase in cardiac events reported in some studies. Weigh against benefit in patients on long-term therapy without a clear ongoing indication — see the deprescribing approach below.

Surgical (fundoplication): for “volume reflux” not controlled by drug therapy, or symptoms from a large hiatus hernia.

Pregnancy: diet/lifestyle first; H2-antagonists are safe; PPI (omeprazole has the most clinical experience) if inadequate control.

Deprescribing long-term PPI therapy

Most patients on a PPI can trial deprescribing once mucosal healing is likely. PPI use beyond 8 weeks is rarely indicated outside a defined long-term list: Barrett’s oesophagus, Zollinger-Ellison syndrome, clinically significant severe erosive oesophagitis (LA grade C/D), peptic stricture, oesophageal scleroderma, eosinophilic oesophagitis, gastroprotection in patients at high NSAID/aspirin bleed risk, or prevention of pulmonary fibrosis progression. Everyone else is a candidate for deprescribing.

• Two evidence-based approaches: gradual dose tapering to the lowest dose for a defined period before stopping, or stopping and switching to PRN use. Switching to an H2-antagonist instead is an option but has a higher rate of symptom recurrence than either of the above.
• ~80% of patients remain symptom-free after gradual tapering or discontinuation. Abrupt cessation can cause rebound acid hypersecretion in 10–50% (can mimic symptom return, even in people without GI disease) — minimise this with gradual tapering or alternate-day low-dose PPI before stopping, and manage any rebound with PRN PPI or antacids/H2-antagonists.
• Frame it to the patient as “a trial of deprescribing” — it can always be restarted. Document the intended review/re-prescribing plan.

Barrett’s oesophagus

A premalignant condition in which metaplastic columnar epithelium replaces the stratified squamous epithelium that normally lines the lower oesophagus — caused by chronic oesophageal injury from gastro-oesophageal reflux in susceptible people. Associated with a significant increase in the risk of adenocarcinoma of the lower oesophagus. Risk is greatest in Caucasian males older than 50 with central obesity and a long segment of Barrett’s oesophagus.

Management: detection of Barrett’s oesophagus (confirmed on biopsy) should lead to a discussion with the patient about whether a surveillance program (regular biopsies to detect dysplasia or early malignancy, plus specialist follow-up) is appropriate — endoscopic surveillance is the current standard of care.

Therapy aims to control symptoms and reduce the risk of complications. PPI therapy is effective for oesophagitis and reflux symptoms in patients with Barrett’s oesophagus.

GORD in children

Common in infants, improves by 12 months. A mild degree (“possetting”) is normal. Associated signs needing assessment: failure to thrive, oesophagitis, stricture, feeding refusal, recurrent pneumonia, anaemia, dental erosions, apnoea, apparent life-threatening events. Thriving infants with uncomplicated reflux need no drug therapy — try smaller/more frequent feeds, thickened feeds, elevating the head of the cot.

May be a presenting feature of cow’s milk (or soy) protein allergy — irritability, diarrhoea, feeding difficulty; trial a 2–4 week extensively hydrolysed (Alfaré, Pepti-Junior Gold) or elemental (Neocate, EleCare) formula, or a maternal dairy (± egg) exclusion diet if breastfed. Older children: diet/lifestyle first, then a 4–8 week PPI trial if needed (esomeprazole 0.7mg/kg up to 20mg, lansoprazole 1mg/kg up to 30mg, omeprazole 0.7mg/kg up to 20mg, or pantoprazole 1mg/kg up to 40mg, once daily).

Peptic ulcer disease (PUD)

Causes: H. pylori (most duodenal ulcers, ~2/3 of gastric ulcers — DU:GU ratio ~4:1); NSAIDs (most of the remainder); rare — Zollinger-Ellison syndrome, Crohn’s disease, viruses.

Risk factors: family history, NSAID use, male sex, smoking (also delays healing), stress, blood group O; H. pylori risk factors (older age, low SES, migrant from a high-prevalence country). Without H. pylori and without NSAIDs, peptic ulcers essentially don’t occur.

History: epigastric pain/discomfort 1–2h post-meals, relieved by food or antacids, ± nausea/vomiting/heartburn, relapsing-remitting course, nocturnal epigastric pain. Examination is often unhelpful.

Diagnosis: endoscopy (biopsies for histology/rapid urease test identify H. pylori and exclude malignancy); urea breath test; faecal antigen (less accurate than UBT but better than serology); serology only if PPI can’t be stopped. Recent antibiotics (4wks) or PPI (2wks) reduce biopsy/UBT/faecal-antigen accuracy (H2-antagonists don’t). Consider serum gastrin if multiple ulcers.

Management

Uncomplicated duodenal ulcer: H. pylori eradication therapy alone is usually sufficient (see h-pylori.md).

Complicated ulcers, large gastric ulcers, high-risk patients, or NSAID-induced ulcers: ongoing PPI therapy for ~8 weeks in addition.

Bleeding peptic ulcer (upper GI haemorrhage): urgent endoscopy + IV PPI (pantoprazole typically).

Follow-up endoscopy is usually not needed after treatment except for gastric ulcers and some complicated duodenal ulcers. Maintenance acid suppression is usually unnecessary after successful H. pylori eradication for an H. pylori-associated ulcer. If eradication is unsuccessful/impracticable, or an NSAID is still required, standard-dose PPI markedly reduces ulcer recurrence risk.

NSAID-induced ulcers

15–30% of NSAID users have an ulcer at endoscopy (many asymptomatic until bleeding, anaemia, or perforation occurs); ~half of NSAID users report upper abdominal discomfort. Long-term low-dose aspirin causes ulcers in ~10% (mostly asymptomatic). The combination of H. pylori + NSAID use increases ulcer risk 60-fold and bleeding risk ~6-fold over neither risk factor alone.

Risk factors: older age, previous upper GI bleed or PUD, H. pylori, smoking, concomitant anticoagulants/antiplatelets/SSRIs/SNRIs/corticosteroids (in roughly that order of added risk).

Management:

• High-risk patients needing ongoing NSAIDs: prophylactic standard-dose PPI. COX-2-selective NSAIDs (e.g. celecoxib) reduce but don’t eliminate ulcer/ complication risk.
• Previous PUD: co-prescribe a PPI and consider H. pylori screening/treatment before starting the NSAID.
• Established NSAID-induced ulcer: stop the NSAID if possible; PPI for 8–12 weeks.
• After a bleeding ulcer where NSAID therapy must continue: H. pylori eradication (if positive) plus ongoing PPI — for aspirin specifically, PPI ± H. pylori eradication reduces recurrent bleeding risk; a COX-2-selective NSAID + PPI combination gives the most protection if NSAID choice can be changed, but avoiding NSAIDs altogether is preferred wherever possible in this group.

Autoimmune gastritis

Parietal cell and intrinsic factor antibodies; typically >40yrs. Usually asymptomatic until iron or B12 deficiency develops (pernicious anaemia) — often found incidentally during work-up for these deficiencies. Investigate with parietal cell/intrinsic factor antibodies, B12/iron studies; confirm on endoscopic histology. Refer to gastroenterology for consideration of endoscopy (and subsequent gastric cancer surveillance, given the associated inflammation risk); supplement iron/B12.