Dyspepsia (Indigestion)

Last updated 31 May 2026 · Gastroenterology

📋 Key Information Summary

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Dyspepsia is defined as chronic or recurrent pain or discomfort centred in the upper abdomen, affecting up to 30% of Australians annually.
Alarm features (dysphagia, progressive weight loss, persistent vomiting, GI bleeding, iron-deficiency anaemia, age ≥60 with new-onset symptoms) mandate urgent endoscopy (OGD) — do not trial empiric therapy.
Functional (non-ulcer) dyspepsia accounts for ≥50% of cases after investigation and is diagnosed by Rome IV criteria when structural disease is excluded.
Helicobacter pylori is present in ~20–30% of Australian adults; test-and-treat is recommended for patients <60 years without alarm features (carbon-13 urea breath test preferred).
First-line H. pylori eradication: standard triple therapy (PPI + amoxicillin 1 g + clarithromycin 500 mg, all BD for 14 days) or biaclarithromycin quadruple therapy if clarithromycin resistance >15%.
Empiric PPI trial (e.g., omeprazole 20 mg daily for 4–8 weeks) is first-line for uninvestigated dyspepsia without alarm features and negative H. pylori.
GORD is a leading organic cause; trial a full-dose PPI for 8 weeks; refractory symptoms require OGD ± pH monitoring.
Functional dyspepsia management: lifestyle measures, low-dose tricyclic antidepressant (amitriptyline 10–25 mg nocte), or prokinetic (domperidone) as second-line.
Elderly patients (>65 years) have higher malignancy risk — lower threshold for OGD; also consider NSAID/aspirin-related gastropathy and polypharmacy.
Children with dyspepsia should be evaluated with age-appropriate criteria; H. pylori test-and-treat in selected cases; most respond to lifestyle and dietary changes.
Aboriginal and Torres Strait Islander peoples have higher H. pylori prevalence (up to 70–90% in remote communities), higher gastric cancer rates, and reduced access to endoscopy — maintain a low threshold for investigation and referral.
Reassess and refer if symptoms persist beyond 4–8 weeks of appropriate therapy or recur — do not repeatedly re-prescribe PPIs without re-evaluation.

Introduction & Australian Epidemiology

Dyspepsia encompasses a spectrum of upper gastrointestinal symptoms — including epigastric pain, burning, early satiety, postprandial fullness, bloating, and nausea — that are chronic or recurrent in nature. It is one of the most common presentations in Australian general practice, accounting for an estimated 5–10% of all consultations.

In Australia, population-based studies report a point prevalence of uninvestigated dyspepsia of approximately 25–30% in adults. Only a minority of affected individuals seek medical attention. The economic burden is substantial, encompassing direct healthcare costs (investigations, medications, endoscopy) and indirect costs from lost productivity. The condition affects all age groups but peaks in the 30–60-year age bracket.

Dyspepsia is broadly classified into:

Uninvestigated dyspepsia — symptoms present but no endoscopic evaluation performed.
Investigated dyspepsia — endoscopy has been performed and a structural cause may or may not have been identified.
Functional (non-ulcer) dyspepsia — meets Rome IV criteria and all organic causes excluded.

Common organic causes include gastro-oesophageal reflux disease (GORD), peptic ulcer disease (PUD), gastric or oesophageal malignancy, and drug-induced gastropathy. H. pylori infection, coeliac disease, and pancreaticobiliary disease should also be considered.

⚠️

Red-flag (alarm) features requiring urgent investigation: dysphagia, odynophagia, progressive unintentional weight loss (>5% body weight), persistent vomiting, GI blood loss (haematemesis, melaena, iron-deficiency anaemia), abdominal mass, and age ≥60 years with new-onset dyspepsia. Do not initiate empiric therapy — refer for urgent OGD.

Dyspepsia Diagnostic Model

The diagnostic approach to dyspepsia in Australian primary care follows a structured algorithm endorsed by the RACGP and aligned with Therapeutic Guidelines (eTG) Gastrointestinal. The key decision points are the presence of alarm features, age, H. pylori status, and response to empirical therapy.

Assess for Alarm Features

History and examination. If alarm features present → urgent OGD referral. If absent → proceed to step 2.

Age <60 & No Alarm Features

H. pylori test-and-treat strategy. Perform carbon-13 urea breath test (UBT) or stool antigen test (SAT). If positive → eradicate. If negative → empiric PPI trial 4–8 weeks.

Age ≥60 or Recurrent Symptoms

Lower threshold for OGD regardless of alarm features. Age ≥60 with new-onset dyspepsia → direct endoscopic evaluation.

Failed Empiric Therapy

If symptoms persist after H. pylori eradication (if indicated) and PPI trial → OGD ± further work-up (coeliac serology, gastric biopsy, pH studies).

Discriminating Symptoms

Symptom Pattern	Likely Diagnosis	Next Step
Epigastric burning relieved by food/antacids	Peptic ulcer disease or functional dyspepsia	H. pylori test; OGD if alarm features or ≥60 years
Retrosternal burning, worse lying down, acidic taste	GORD	Empiric PPI 8 weeks; OGD if refractory
Early satiety, postprandial fullness, bloating	Functional dyspepsia (PDS subtype)	Exclude organic disease; consider prokinetic
Colicky pain radiating to back, post-prandial nausea	Pancreaticobiliary disease	LFTs, lipase, abdominal ultrasound
Dysphagia + weight loss	Oesophageal/gastric malignancy	Urgent OGD — do not delay

Role of Non-Invasive Testing Before Endoscopy

In patients <60 years without alarm features, a non-invasive H. pylori test (UBT or SAT) is recommended before initiating therapy. This test-and-treat strategy reduces unnecessary endoscopy by up to 60% and is cost-effective in the Australian healthcare setting. The MBS item for OGD (MBS 30473) is available in both public and private settings, but access may be delayed in regional and remote areas.

Functional (Non-Ulcer) Dyspepsia

Functional dyspepsia (FD) is the single most common cause of dyspepsia after investigation, accounting for 50–70% of all cases. It is defined by the Rome IV criteria as one or more of: bothersome postprandial fullness, bothersome early satiation, bothersome epigastric pain, or bothersome epigastric burning, with no evidence of structural disease on endoscopy, and with symptoms present for the last 3 months with onset ≥6 months prior to diagnosis.

Rome IV Subtypes

Subtype 1

Postprandial Distress Syndrome (PDS)

Bothersome postprandial fullness occurring after ordinary-sized meals and/or bothersome early satiation preventing finishing a regular meal. Symptoms ≥3 days per week.

Often meal-related; consider gastroparesis if severe

Subtype 2

Epigastric Pain Syndrome (EPS)

Bothersome epigastric pain and/or burning, occurring at least once per week. May be meal-related or occur during fasting. Not generalised or relieved by defecation.

Overlap with PUD and GORD common

ℹ️

Overlap: PDS and EPS frequently co-exist. Up to 30% of FD patients also meet criteria for irritable bowel syndrome (IBS). The presence of both should be sought during history-taking.

Pathophysiology

The pathogenesis of FD is multifactorial and involves visceral hypersensitivity, impaired gastric accommodation (fundic relaxation), delayed gastric emptying, disordered duodenal motility, low-grade mucosal inflammation, altered gut microbiome, and central sensitisation with psychological comorbidity (anxiety, depression). Post-infectious FD may follow acute gastroenteritis in 10–15% of cases.

Management of Functional Dyspepsia

Management is stepwise and requires a strong patient–doctor relationship, as FD is a chronic relapsing condition.

Lifestyle & Dietary Measures

Small frequent meals; reduce fat, spice, caffeine, and alcohol; avoid late-night eating; regular physical activity; smoking cessation. Educate and reassure — explain the diagnosis is real and not "in their head."

Acid Suppression

PPI trial (omeprazole 20 mg or esomeprazole 20 mg daily) for 4–8 weeks. Most effective in EPS subtype. Discontinue if no benefit after 8 weeks.

Low-Dose TCA

Amitriptyline 10–25 mg nocte, titrate to 50 mg if tolerated. Strongest evidence for EPS. Alternatives: nortriptyline, mirtazapine. Caution in elderly — anticholinergic effects.

Prokinetic Therapy

Domperidone 10 mg TDS before meals (PBS Authority Required) — best for PDS subtype with documented gastroparesis. Metoclopramide 10 mg TDS (risk of extrapyramidal side effects). Iberogast® (STW 5) 20 drops TDS — herbal prokinetic with RCT evidence.

Pharmacotherapy — Drug Cards

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Amitriptyline

Endep® · Trypizol® · TCA (neuromodulator)

Adult dose 10–25 mg PO nocte, titrate by 10–25 mg every 2–4 weeks to max 75 mg

Paediatric dose Not recommended <12 years for dyspepsia

Key cautions Anticholinergic effects; avoid in cardiac conduction disorders; ECG if dose >50 mg; suicidal ideation monitoring in young adults

Renal adjustment None required; use standard dose

Hepatic adjustment Reduce dose; avoid if severe hepatic impairment

PBS status ✔ PBS General Benefit (for depression indication; off-label for FD)

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Omeprazole

Losec® · Pariet® (rabeprazole alternative) · PPI

Adult dose 20 mg PO daily, 30 min before breakfast, for 4–8 weeks

Paediatric dose ≥1 year: 0.7–3.3 mg/kg/day PO (max 20 mg/day) — under specialist guidance

Key cautions Long-term use associated with hypomagnesaemia, B12 deficiency, osteoporotic fracture, Clostridioides difficile infection

Renal adjustment None required

Hepatic adjustment Consider dose reduction in severe hepatic impairment (max 20 mg/day)

PBS status ✔ PBS General Benefit

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Domperidone

Motilium® · Prokinetic (dopamine-2 antagonist)

Adult dose 10 mg PO TDS, 15–30 min before meals; max 30 mg/day

Paediatric dose 0.25 mg/kg/dose TDS before meals (specialist supervision)

Key cautions QTc prolongation; avoid with QTc-prolonging agents; TGA warning — use lowest effective dose for shortest duration

Renal adjustment Reduce frequency to OD–BD if eGFR <30 mL/min

Hepatic adjustment Contraindicated in moderate–severe hepatic impairment

PBS status ⚠ PBS Authority Required

H. pylori Testing & GORD

Helicobacter pylori — Testing

Helicobacter pylori infection affects approximately 20–30% of the Australian adult population overall, though prevalence is significantly higher in immigrants from high-prevalence countries and in Aboriginal and Torres Strait Islander communities (up to 70–90% in some remote regions). H. pylori is classified as a Group 1 carcinogen by IARC and is the principal cause of peptic ulcer disease and a significant risk factor for gastric adenocarcinoma and MALT lymphoma.

Indications for H. pylori Testing

Uninvestigated dyspepsia in patients <60 years without alarm features (test-and-treat strategy)
Active or past peptic ulcer disease
Gastric MALT lymphoma
Early gastric cancer resection
First-degree relative with gastric cancer
Long-term low-dose aspirin or NSAID users with dyspepsia
Unexplained iron-deficiency anaemia
Idiopathic thrombocytopenic purpura

Preferred Diagnostic Tests

First-line

Carbon-13 Urea Breath Test (UBT)

Sensitivity 95%, specificity 97%. Patient must have stopped PPI for ≥2 weeks and antibiotics for ≥4 weeks. Available in most Australian pathology centres (MBS item 66640). Gold standard non-invasive test.

First-line

Stool Antigen Test (SAT)

Monoclonal immunoassay preferred. Sensitivity 94%, specificity 97%. Same medication washout requirements. Useful if UBT unavailable (MBS item 66641).

Invasive

Rapid Urease Test (CLO test) on OGD biopsy

Sensitivity 90–95%. Performed on gastric antral and body biopsies at endoscopy. Allows simultaneous histological assessment.

Serology

H. pylori IgG serology

Not suitable for confirming eradication (remains positive for months–years). Use only if UBT/SAT unreliable (e.g., recent PPI use, active GI bleeding). Cannot distinguish active from past infection.

⚠️

Medication washout before H. pylori testing: Discontinue PPI for ≥2 weeks and antibiotics for ≥4 weeks before UBT or SAT. Histamine-2 receptor antagonists (e.g., ranitidine) should be stopped ≥1–2 days prior. False negatives are the most common pitfall — always confirm medication withdrawal.

H. pylori Eradication Regimens

Australian clarithromycin resistance rates are estimated at 5–15% overall but are higher in certain populations (immigrants from high-resistance regions, prior macrolide exposure). First-line therapy is selected based on local resistance patterns and patient allergy history.

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Standard Triple Therapy

First-line · 14 days

Regimen PPI (e.g., omeprazole 20 mg) BD + amoxicillin 1 g BD + clarithromycin 500 mg BD — all for 14 days

Eradication rate ~85–90% (intention-to-treat)

Key cautions Penicillin allergy: substitute amoxicillin with metronidazole 400 mg BD (bismuth quadruple preferred). Clarithromycin interacts with statins, warfarin, and many other drugs.

PBS status ✔ PBS General Benefit (Triple therapy pack available)

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Bismuth Quadruple Therapy

Alternative first-line or second-line · 14 days

Regimen PPI BD + bismuth subsalicylate/subcitrate QID + metronidazole 400 mg TDS + tetracycline 500 mg QID — all for 14 days

Eradication rate ~85–90%

Key cautions Complex dosing (12 tablets/day). Avoid tetracycline in children <8 years and pregnancy. Bismuth may cause black stools and tongue.

PBS status ⚠ PBS Authority Required (Pylera® combination capsule available)

Second-Line and Rescue Therapy

If first-line triple therapy fails, options include: (1) bismuth quadruple therapy (if not already used); (2) levofloxacin-based triple (PPI + amoxicillin 1 g BD + levofloxacin 500 mg daily × 14 days) — increasingly limited by fluoroquinolone resistance; (3) rifabutin-based rescue (specialist-initiated). Confirm eradication with UBT or SAT ≥4 weeks after completion of therapy — this is mandatory after treatment.

Gastro-Oesophageal Reflux Disease (GORD)

GORD is the most common organic cause of dyspepsia and is characterised by troublesome heartburn and/or regurgitation due to reflux of gastric contents into the oesophagus. Prevalence in Australia is approximately 15–20% of adults.

Diagnosis

Clinical diagnosis is appropriate when classic symptoms (retrosternal burning, acid regurgitation) are present without alarm features. The Lyon consensus recommends empiric PPI trial for 8 weeks as initial management. OGD is indicated for alarm features, age ≥60, or failure of PPI therapy.

Management

Lifestyle Modification

Weight loss if overweight; elevate head of bed 15–20 cm; avoid late meals (≥3 h before bedtime); reduce alcohol, caffeine, chocolate, and fatty foods; smoking cessation.

PPI Therapy

Standard-dose PPI (omeprazole 20 mg or esomeprazole 20 mg daily) for 8 weeks. Take 30 min before breakfast. Response confirms diagnosis. Step-down to lowest effective dose or on-demand therapy after symptom control.

Refractory GORD

Double-dose PPI (BD dosing) if standard dose fails. OGD ± ambulatory pH/impedance monitoring (off PPI) to evaluate for refractory reflux vs functional heartburn. Consider add-on H2RA at bedtime (famotidine 20–40 mg).

Surgical Option

Laparoscopic fundoplication for confirmed GORD with excellent PPI response but desire to stop medication, or for large hiatal hernia. Refer to upper GI surgeon.

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Barrett's oesophagus: Patients with chronic GORD symptoms (>5 years), especially Caucasian males >50 years with central obesity, should be considered for screening OGD. Barrett's is a pre-malignant condition requiring surveillance endoscopy every 2–3 years.

Dyspepsia in the Elderly & Children

Dyspepsia in the Elderly (≥65 years)

Dyspepsia in older adults requires a heightened index of suspicion for serious underlying pathology. The prevalence of peptic ulcer disease, gastric and oesophageal malignancy, and drug-induced gastropathy increases significantly with age.

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Age ≥60 with new-onset dyspepsia = OGD. The risk of upper GI malignancy rises sharply after 60. Test-and-treat alone is insufficient — direct endoscopic evaluation (MBS 30473) is recommended, even in the absence of classic alarm features.

Key Considerations in the Elderly

NSAID and aspirin gastropathy: The most common drug-related cause of dyspepsia in older adults. Low-dose aspirin (100 mg) increases ulcer risk 2–4-fold. Co-prescribe PPI gastroprotection with any ongoing NSAID or aspirin use.
Polypharmacy: Review all medications. Bisphosphonates, corticosteroids, SSRIs, potassium supplements, and iron may all cause dyspepsia.
Atypical presentations of malignancy: Weight loss, early satiety, or new iron-deficiency anaemia may be the only presenting features in the elderly.
PPI-related adverse effects: Long-term PPI use in the elderly is associated with increased risk of C. difficile infection, hypomagnesaemia, B12 deficiency, osteoporotic fractures, and acute interstitial nephritis. Regular review and attempted dose reduction are essential.
Cardiovascular co-prescribing: Dual antiplatelet therapy (DAPT) post-ACS or PCI is strongly associated with GI bleeding — ensure PPI co-prescription. Be aware of clopidogrel–PPI interactions (omeprazole > pantoprazole).
Constipation and gastroparesis: Common in the elderly and may present as dyspepsia. Address bowel habit during assessment.

Dyspepsia in Children

Dyspepsia in children is defined as persistent or recurrent symptoms referable to the upper abdomen. Prevalence estimates in Australian school-aged children range from 10–15%. The differential diagnosis differs from adults and age-appropriate criteria should be applied.

Common Causes in Children

Functional dyspepsia (most common — >90% in paediatric gastroenterology clinics): meets Rome IV paediatric criteria
GORD: common in infants and older children
H. pylori infection: prevalence in Australian children is low (~5–10%) but higher in ATSI and immigrant communities
Coeliac disease: consider screening in all children with chronic dyspepsia (anti-tTG IgA)
Eosinophilic oesophagitis: increasingly recognised in children presenting with dysphagia, food impaction, and epigastric pain
Medication-related: NSAIDs (including ibuprofen), oral corticosteroids, iron supplements

Paediatric Diagnostic Approach

History & Examination

Characterise symptoms using Rome IV paediatric criteria. Screen for alarm features: weight loss, GI bleeding, persistent vomiting, dysphagia, fever, family history of IBD/coeliac/peptic ulcer.

Baseline Investigations

FBC, iron studies, coeliac serology (anti-tTG IgA + total IgA). Consider stool antigen for H. pylori if indicated.

Empiric Trial

Lifestyle and dietary modifications first. If indicated, 4-week PPI trial (omeprazole 0.7–1 mg/kg/day). Consider H. pylori test-and-treat only in selected cases with risk factors.

OGD Referral

If alarm features present, failed empiric therapy, or diagnostic uncertainty → paediatric gastroenterology referral for OGD with biopsies.

ℹ️

Key principle in paediatric dyspepsia: Functional dyspepsia accounts for the vast majority of cases. Avoid over-investigation. Reassurance, dietary counselling, and time are often the most effective interventions. OGD should be reserved for alarm features or refractory symptoms.

Investigations

Essential

Carbon-13 Urea Breath Test (UBT)

Non-invasive H. pylori diagnosis and confirmation of eradication. MBS item 66640. Stop PPI ≥2 weeks, antibiotics ≥4 weeks prior. Gold standard non-invasive test.

Essential

Stool Antigen Test (SAT) — Monoclonal

Alternative to UBT for H. pylori. MBS item 66641. Same medication washout requirements. Preferred in children <6 years (UBT may be unreliable).

Essential

Upper GI Endoscopy (OGD)

MBS item 30473 (diagnostic OGD). Indicated for alarm features, age ≥60, refractory symptoms, or complications. Allows biopsy for H. pylori (CLO test + histology), coeliac disease, eosinophilic oesophagitis, and malignancy.

Available

Full Blood Count (FBC)

Screen for iron-deficiency anaemia as a marker of occult GI blood loss. MBS item 66512.

Available

Coeliac Serology (anti-tTG IgA + total IgA)

Consider in all patients with chronic unexplained dyspepsia. Australian prevalence of coeliac disease is ~1%. MBS item 66825.

Available

Liver Function Tests + Lipase

Exclude pancreaticobiliary disease if colicky epigastric pain, nausea, or features suggesting biliary obstruction are present. Abdominal ultrasound to follow if abnormal.

Specialist

Ambulatory 24-h pH/Impedance Monitoring

For refractory GORD symptoms when OGD is non-diagnostic. Confirms pathological acid exposure vs functional heartburn. Available at tertiary centres.

Specialist

Gastric Emptying Study (Nuclear Medicine)

Scintigraphic solid-phase gastric emptying at 4 hours. Indicated when gastroparesis is suspected (severe PDS, nausea, vomiting in diabetes or post-surgical patients). Available at major hospitals.

Risk Stratification & Severity Scoring

While there is no single validated severity score for dyspepsia, risk stratification guides the urgency and type of investigation required. The following framework is used in Australian primary care:

Low Risk

Young Adult, Typical Symptoms, No Alarms

Age <60, no weight loss, no dysphagia, no GI bleeding, no family history of GI malignancy. Functional dyspepsia most likely.

GP management: H. pylori test-and-treat → empiric PPI trial

Moderate Risk

Age 60–70 or Refractory Symptoms

New-onset after age 60, long-standing symptoms failing empiric therapy, chronic NSAID/aspirin use, family history of GI malignancy.

GP with early OGD referral — within 2–4 weeks

High Risk

Alarm Features Present

Dysphagia, progressive weight loss, GI blood loss, persistent vomiting, abdominal mass, iron-deficiency anaemia, age ≥60 with new symptoms.

Urgent OGD referral — within 2 weeks (suspected cancer pathway)

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Suspected upper GI malignancy pathway: Patients with alarm features should be referred via the 2-week-wait/suspected cancer pathway. In Australia, this involves direct communication with the endoscopy unit or via the local health network's rapid access clinic. Do not initiate a PPI trial in patients with alarm features — this may mask symptoms and delay diagnosis.

Empirical & Directed Therapy

Empiric Therapy Algorithm

For uninvestigated dyspepsia without alarm features in patients <60 years:

H. pylori Test-and-Treat

UBT or SAT. If positive → 14-day eradication regimen. If negative → step 2. Confirm eradication ≥4 weeks post-treatment.

Empiric PPI Trial

Omeprazole 20 mg or esomeprazole 20 mg daily for 4–8 weeks. If symptoms resolve → step down to PRN or lowest effective dose. If symptoms persist → step 3.

H2RA Trial or Combination

Famotidine 20 mg BD or add antacid/alginates (Gaviscon®) for breakthrough symptoms. Consider switching PPI (different metaboliser profile).

Re-evaluate & OGD

If symptoms persist after 8 weeks of appropriate therapy → OGD with biopsies. Consider coeliac disease, eosinophilic oesophagitis, functional dyspepsia. Reassess diagnosis and psychological comorbidities.

Quick Reference — Common Syndromes

GORD

Omeprazole 20 mg daily or esomeprazole 20 mg daily

8 weeks → step-down

BD dosing if refractory; Gaviscon® PRN for breakthrough

H. pylori eradication

PPI BD + amoxicillin 1 g BD + clarithromycin 500 mg BD

14 days

Confirm eradication with UBT ≥4 weeks post-Rx

Functional dyspepsia (EPS)

Amitriptyline 10–25 mg nocte

Ongoing — trial 8–12 weeks

Titrate slowly; avoid in elderly initially

Functional dyspepsia (PDS)

Domperidone 10 mg TDS pre-meals

4–8 weeks

PBS Authority Required; QTc monitoring

NSAID gastropathy

Cease NSAID + PPI 20–40 mg daily

8 weeks minimum

Consider COX-2 selective if NSAID essential; always co-prescribe PPI

Directed / Pathogen-Specific Therapy

Directed therapy applies once a specific aetiology has been confirmed:

H. pylori-positive PUD: Eradicate H. pylori → continue PPI for 4–8 weeks (duodenal ulcer) or 8–12 weeks (gastric ulcer). Confirm healing with repeat OGD for gastric ulcers.
NSAID-induced ulcer: Cease offending agent. PPI for 8 weeks. If ongoing NSAID required, switch to celecoxib 200 mg OD + PPI (lowest effective dose for shortest duration). MBS item for specialist review.
Eosinophilic oesophagitis: Refer to gastroenterology. Swallowed topical corticosteroids (budesonide viscous slurry or fluticasone MDI swallowed). Dietary elimination under dietitian supervision.
Coeliac disease: Strict lifelong gluten-free diet. Dietitian referral essential. Monitor with anti-tTG titres and nutritional markers.
Gastroparesis: Dietary modification (small frequent, low-fat, low-fibre meals). Domperidone 10 mg TDS (PBS Authority). Metoclopramide 10 mg TDS (short-term only — extrapyramidal risk). Specialist referral for refractory cases (pyloric Botox, gastric electrical stimulation).

Monitoring

2–4 weeks

Initial follow-up after H. pylori eradication or PPI initiation. Assess symptom response and medication tolerance.

4–8 weeks

H. pylori eradication confirmation (UBT or SAT ≥4 weeks post-antibiotics, ≥2 weeks post-PPI). If on PPI — assess need for continuation.

8–12 weeks

Review if symptoms persist. Consider OGD, coeliac serology, and alternative diagnoses. Step-down or cease PPI if symptoms resolved.

6 months

For functional dyspepsia: review TCA efficacy and side effects. Consider dose adjustment. Reassess psychological wellbeing.

12 months

Annual review for patients on long-term PPI. Assess ongoing indication. Check magnesium, B12, and renal function. Attempt PPI dose reduction at least annually.

⚠️

Long-term PPI monitoring: Patients on PPIs for >12 months should have annual review including serum magnesium, vitamin B12, and renal function (eGFR). An increase in fracture risk with prolonged PPI use (>1 year) should prompt consideration of bone mineral density assessment in at-risk patients.

Special Populations

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Pregnancy

Dyspepsia affects up to 80% of pregnancies — most commonly in the 2nd and 3rd trimesters.

First-line: Lifestyle measures (small frequent meals, avoid lying down post-meals, elevate head of bed).

Pharmacotherapy: Antacids (calcium carbonate) and alginates are first-line. Famotidine 20 mg BD is safe (Category A). PPIs — pantoprazole (Category B3) preferred if H2RA insufficient; avoid omeprazole in the 1st trimester.

H. pylori eradication is generally deferred until postpartum unless there is a compelling indication (e.g., active bleeding ulcer).

Avoid: Bismuth, tetracycline, and metronidazole in pregnancy.

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Paediatrics

Functional dyspepsia accounts for >90% of paediatric dyspepsia cases. Rome IV criteria apply (modified for age).

Coeliac serology (anti-tTG IgA + total IgA) should be performed in all children with chronic unexplained dyspepsia.

PPI: omeprazole 0.7–1 mg/kg/day (max 20 mg) for 4–8 weeks under specialist guidance if needed.

H. pylori testing only in children with identified risk factors — not routine test-and-treat.

OGD referral for alarm features or failed empiric therapy. Paediatric gastroenterology involvement recommended.

Avoid: Metoclopramide in children <1 year (risk of extrapyramidal side effects). Tetracycline in children <8 years.

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Elderly (≥65 years)

Lower threshold for OGD — age ≥60 with new-onset dyspepsia warrants endoscopic evaluation regardless of alarm features.

NSAID/aspirin gastropathy is the most common iatrogenic cause — ensure PPI co-prescription.

Pantoprazole is preferred PPI in the elderly due to fewer drug interactions (especially with clopidogrel).

Anticholinergic burden from TCAs is significant — consider mirtazapine or nortriptyline as alternatives; start low, go slow.

Regular medication review to minimise polypharmacy-induced dyspepsia.

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Renal Impairment

PPIs: No dose adjustment required for omeprazole or esomeprazole. However, long-term PPI use is associated with acute interstitial nephritis — monitor eGFR.

Domperidone: Reduce frequency to OD–BD if eGFR <30 mL/min.

Amoxicillin: Reduce dose if eGFR <30 mL/min (500 mg BD).

Magnesium-containing antacids: Avoid in CKD Stage 4–5 (risk of hypermagnesaemia).

Avoid bismuth in severe renal impairment (accumulation risk).

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Hepatic Impairment

PPIs: Reduce dose in severe hepatic impairment (max 20 mg/day omeprazole); esomeprazole similarly affected.

Amitriptyline: Use with caution; reduce dose and monitor. Avoid in decompensated cirrhosis.

Domperidone: Contraindicated in moderate-to-severe hepatic impairment.

Metronidazole: Use with caution; dose reduction in severe hepatic impairment.

Clarithromycin: Reduce dose by 50–75% in severe hepatic impairment.

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Immunocompromised

CMV oesophagitis and oesophageal candidiasis should be considered in severely immunocompromised patients (HIV, transplant recipients) presenting with dyspepsia/dysphagia.

H. pylori prevalence is variable; still test-and-treat if applicable.

Opportunistic infections (cryptosporidiosis, microsporidiosis) may present with upper GI symptoms in advanced HIV.

PPI use increases infection risk (C. difficile, community-acquired pneumonia) — use lowest effective dose.

Drug interactions are critical — check interactions between PPIs and antiretrovirals, immunosuppressants (especially tacrolimus, cyclosporine with omeprazole).

Aboriginal and Torres Strait Islander Health

Dyspepsia and its complications represent a significant health burden for Aboriginal and Torres Strait Islander peoples. H. pylori prevalence in remote Aboriginal communities is among the highest in Australia (70–90% in some studies), and gastric cancer incidence is 2–3 times higher than in the non-Indigenous population. Early recognition, culturally appropriate management, and equitable access to investigation are essential.

H. pylori prevalence

Significantly elevated in remote and regional communities (70–90% vs ~20–30% general population). Reinfection rates are also higher. Population-level eradication strategies have been trialled in some communities with mixed results.

Gastric cancer risk

Gastric cancer incidence and mortality are 2–3 times higher in ATSI populations compared to non-Indigenous Australians. Late presentation is common. Maintain a very low threshold for OGD in ATSI patients with persistent dyspepsia, especially those >45 years.

Access to endoscopy

Many remote communities lack access to endoscopy services. Patients may require transfer to regional or tertiary centres (Royal Darwin Hospital, Alice Springs Hospital, Townsville University Hospital). Telehealth consultation with gastroenterology can facilitate timely referral and triage.

H. pylori eradication challenges

Adherence to complex 14-day regimens may be difficult in remote settings. Consider once-daily regimens where possible. Community pharmacy support and health worker education improve completion rates. Re-infection from household contacts is common — address hygiene and water supply.

Health literacy & cultural safety

Provide patient information in plain English and local languages where available. Use Aboriginal Health Workers and Practitioners as key intermediaries. Acknowledge cultural beliefs about illness and pain. Flexible appointment scheduling and family-inclusive consultations improve engagement.

Comorbidity burden

ATSI Australians have higher rates of comorbidities (diabetes, cardiovascular disease, renal disease) that complicate dyspepsia management. Polypharmacy increases risk of drug-induced gastropathy. Ensure comprehensive medication review at each consultation.

⚠️

Clinical recommendation: In ATSI patients with dyspepsia persisting beyond 4 weeks, do not attribute symptoms solely to functional causes. Perform H. pylori testing (UBT or SAT), check FBC for iron-deficiency anaemia, and refer for OGD if symptoms do not respond to appropriate empiric therapy. Advocate for expanded rural endoscopy services through your local health network.

📚 References

1. Talley NJ, Ford AC. Functional dyspepsia. N Engl J Med. 2015;373(19):1853–1863. doi:10.1056/NEJMra1501505
2. Drossman DA. Functional gastrointestinal disorders: history, pathophysiology, clinical features, and Rome IV. Gastroenterology. 2016;150(6):1262–1279. doi:10.1053/j.gastro.2016.02.032
3. Ford AC, Marwaha A, Sood R, Moayyedi P. Global prevalence of, and risk factors for, uninvestigated dyspepsia: a meta-analysis. Gut. 2015;64(7):1049–1057. doi:10.1136/gutjnl-2014-307843
4. Katelaris P, Bazzoli F, Hunt R, et al. Asia-Pacific Helicobacter pylori consensus: the Bangkok update. J Gastroenterol Hepatol. 2023;38(8):1261–1275. doi:10.1111/jgh.16230
5. Chey WD, Leontiadis GI, Howden CW, Moss SF. ACG Clinical Guideline: Treatment of Helicobacter pylori Infection. Am J Gastroenterol. 2017;112(2):212–239. doi:10.1038/ajg.2016.563
6. Holtmann G, Shah A, Morrison M. Pathophysiology of functional gastrointestinal disorders: a holistic overview. Dig Dis. 2017;35(Suppl 1):5–13. doi:10.1159/000485409
7. Australian Institute of Health and Welfare (AIHW). Aboriginal and Torres Strait Islander Health Performance Framework. Canberra: AIHW; 2023. Available at: https://www.aihw.gov.au/reports/indigenous-australians/hpf-2023
8.Helicobacter pylori infection: a meta-analysis. BMC Gastroenterol. 2020;20(1):104. doi:10.1186/s12876-020-01237-2
9. Hunt RH, Camilleri M, Crowe SE, et al. The stomach in health and disease. Gut. 2015;64(10):1650–1668. doi:10.1136/gutjnl-2014-307595
10. Ford AC, Mahadeva S, Carbe MF, et al. Functional dyspepsia. Lancet. 2020;396(10263):1642–1655. doi:10.1016/S0140-6736(20)30469-4
11. National Health and Medical Research Council (NHMRC). Clinical Practice Guidelines for the Management of GORD in Adults. Canberra: NHMRC; 2019.
12.Guidelines for Preventive Activities in General Practice. 9th ed. Melbourne: RACGP; 2018.
13. Malfertheiner P, Megraud F, Rokkas T, et al. Management of Helicobacter pylori infection: the Maastricht VI/Florence Consensus Report. Gut. 2022;71(9):1724–1762. doi:10.1136/gutjnl-2022-327745
14. Eusebi LH, Black CJ, Howden CW, Ford AC. Effectiveness of management strategies for uninvestigated dyspepsia: systematic review and network meta-analysis. BMJ. 2019;367:l6483. doi:10.1136/bmj.l6483
15. Gargala G, Forbes A. Dyspepsia in older adults. BMJ Clin Evid. 2022;2022:0409.

for PBS scripts. Utilise ACCHS pharmacies and Remote Area Aboriginal Health Worker programs for medication supply in remote areas. Avoid initiating benzodiazepines; support holistic pain management including community-based exercise programs.

Preventive health

Promote bone health: encourage vitamin D supplementation (1000 IU daily in deficient individuals), smoking cessation support, reduction of alcohol intake, and weight-bearing exercise. MBS Item 715 health checks provide a structured opportunity to assess bone health, screen for osteoporosis risk factors, and discuss musculoskeletal health in a culturally safe context.

Quick Reference: Differential Diagnosis at a Glance

Costovertebral dysfunction

Paracetamol ± NSAID; manual therapy

2–6 weeks

Provocable on palpation; no red flags

Thoracic compression fracture

Paracetamol; ± calcitonin; DXA + osteoporosis Rx

6–12 weeks healing

Elderly; osteoporosis; acute onset

ACS (posterior MI)

Aspirin 300 mg, GTN, heparin; urgent PCI

Time-critical

ECG, troponin; CV risk factors

Aortic dissection

IV labetalol; urgent CT aortogram; surgery (Type A)

Time-critical

Tearing pain; BP differential >20 mmHg

Vertebral osteomyelitis

IV antibiotics (vancomycin + ceftriaxone initially); ID consult

6 weeks IV antibiotics

Fever, elevated CRP, IV drug use

Biliary colic / cholecystitis

Paracetamol ± morphine; lap cholecystectomy

Surgical within 72 h (cholecystitis)

RUQ/infrascapular; post-prandial; RUQ US

📚 References

1. Briggs AM, Smith AJ, Straker LM, Bragge P. Thoracic spine pain in the general population: prevalence, incidence and associated factors in children, adolescents and adults. A systematic review. BMC Musculoskelet Disord. 2009;10:77.
2. National Health and Medical Research Council (NHMRC). Evidence-based management of acute musculoskeletal pain. Canberra: NHMRC; 2003 (updated 2020).
3. Australian Institute of Health and Welfare (AIHW). Aboriginal and Torres Strait Islander Health Performance Framework: Summary report 2023. Canberra: AIHW; 2023.
4. Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA. 1992;268(6):760–765.
5. Stochkendahl MJ, Kjaer P, Hartvigsen J, et al. National Clinical Guidelines for non-surgical treatment of patients with recent onset low back pain or lumbar radiculopathy. Europ Spine J. 2018;27(1):60–75.
6. Erwin WM, Jackson PC, Homonko DA. Innervation of the human costovertebral joint: implications for clinical back pain syndromes. J Manipulative Physiol Ther. 2000;23(6):395–403.
7. Royal Australian College of General Practitioners (RACGP). Guidelines for preventive activities in general practice. 9th edn. Melbourne: RACGP; 2018 (updated 2023).
8. Hirsch JA, Singh V, Falco FJE, et al. Thoracic facet joint interventions. Pain Physician. 2016;19(4):E581–E593.
9. Erwin WM, Jackson PC. The costovertebral joint: anatomy, biomechanics, and clinical significance in thoracic back pain syndromes. J Can Chiropr Assoc. 2003;47(2):112–120.
10. Strayer RJ, Gunnerson JM, Brown LH, et al. Aortic dissection: clinical features, diagnosis, and management. Aust Crit Care. 2019;32(2):144–153.
11. Ombregt L. A system of orthopaedic medicine. 3rd edn. Edinburgh: Churchill Livingstone Elsevier; 2013. Chapter 18: Thoracic spine.
12. Lin CC, Chen KH, Li DM, et al. Characteristics and outcomes of patients presenting with thoracic back pain to the emergency department. Emerg Med Australas. 2020;32(5):805–811.

for PBS-listed medicines at participating pharmacies.

Cultural safety

Engagement with Aboriginal Community Controlled Health Organisations (ACCHOs) is essential. Cultural safety training for non-Indigenous clinicians, use of Aboriginal Health Workers and Liaison Officers, and incorporation of traditional healing practices alongside Western medicine improve treatment adherence and outcomes. Avoidance of eye contact, respect for gender-sensitive examination practices, and understanding of sorry business protocols are critical elements of culturally safe care.

Medication adherence

Complex DMARD regimens with frequent monitoring requirements present adherence challenges. Long-acting depot injections (e.g., methotrexate SC) may improve adherence compared to oral regimens. Community pharmacy partnerships through the Indigenous Pharmacy Programmes improve medication management.

Specific conditions

Rheumatic heart disease (RHD) requires secondary prophylaxis with benzathine penicillin G (BPG) 1.2 MU IM every 3–4 weeks for a minimum of 10 years or until age 21 (whichever is longer). RHD registers (e.g., NT RHD Register) facilitate recall and follow-up. The Australian RHD Endgame Strategy targets elimination by 2031.

Referral pathways

Referral through ACCHOs and Aboriginal Hospital Liaison Officers (AHLOs) improves engagement. The Specialist Outreach Assistance Programme provides funded specialist visits to remote communities. NT, WA, and QLD have specific rheumatology outreach programmes targeting Indigenous communities.

📚 References

1. Australian Institute of Health and Welfare (AIHW). Autoimmune disease in Australia. Cat. no. PHE 312. Canberra: AIHW; 2023.
2. Fraenkel L, Bathon JM, England BR, et al. 2021 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis Care Res. 2021;73(7):924–939.
3. Fanouriakis A, Kostopoulou M, Alber K, et al. 2019 update of the EULAR recommendations for the management of systemic lupus erythematosus. Ann Rheum Dis. 2019;78(6):736–745.
4. Chung SA, Langford CA, Maz M, et al. 2021 American College of Rheumatology/Vasculitis Foundation guideline for the management of antineutrophil cytoplasmic antibody-associated vasculitis. Arthritis Care Res. 2021;73(11):1583–1599.
5. Smolen JS, Landewé RBM, Bijlsma JWJ, et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2022 update. Ann Rheum Dis. 2023;82(1):3–18.
6. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health; 2024. Available from: immunisationhandbook.health.gov.au.
7. Rheumatic Heart Disease Australia (RHDAustralia). The 2020 Australian guideline for prevention, diagnosis, and management of acute rheumatic fever and rheumatic heart disease. 3rd ed. Darwin: Menzies School of Health Research; 2020.
8. Pharmaceutical Benefits Scheme (PBS). PBS Schedule. Australian Government Department of Health. Available from: pbs.gov.au. Accessed 2024.
9. Agarwal S, Cunnington J, Nossent J. Autoimmune disease in Indigenous Australians: a systematic review. Int J Rheum Dis. 2021;24(12):1487–1498.
10. Pisetsky DS. Antinuclear antibody testing — misunderstood or misused? Clin Immunol. 2023;255:109717.
11. Bertsias GK, Tektonidou M, Amoura Z, et al. Joint European League Against Rheumatism and European Renal Association–European Dialysis and Transplant Association (EULAR/ERA-EDTA) recommendations for the management of adult and paediatric lupus nephritis. Ann Rheum Dis. 2012;71(11):1771–1782.
12. Ledingham J, Deighton C; British Society for Rheumatology Standards, Audit and Guidelines Working Group. Update on the British Society for Rheumatology guidelines for prescribing TNFα blockers in adults with rheumatoid arthritis. Rheumatology. 2005;44(2):155–158.
13. National Health and Medical Research Council (NHMRC). National statement on ethical conduct in human research. Canberra: NHMRC; 2023 (updated).

for PBS-listed medicines at participating pharmacies.

Cultural safety

Medication adherence

Specific conditions

Referral pathways

📚 References

1. Australian Institute of Health and Welfare (AIHW). Autoimmune disease in Australia. Cat. no. PHE 312. Canberra: AIHW; 2023.
2. Fraenkel L, Bathon JM, England BR, et al. 2021 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis Care Res. 2021;73(7):924–939.
3. Fanouriakis A, Kostopoulou M, Alber K, et al. 2019 update of the EULAR recommendations for the management of systemic lupus erythematosus. Ann Rheum Dis. 2019;78(6):736–745.
4. Chung SA, Langford CA, Maz M, et al. 2021 American College of Rheumatology/Vasculitis Foundation guideline for the management of antineutrophil cytoplasmic antibody-associated vasculitis. Arthritis Care Res. 2021;73(11):1583–1599.
5. Smolen JS, Landewé RBM, Bijlsma JWJ, et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2022 update. Ann Rheum Dis. 2023;82(1):3–18.
6. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health; 2024. Available from: immunisationhandbook.health.gov.au.
7. Rheumatic Heart Disease Australia (RHDAustralia). The 2020 Australian guideline for prevention, diagnosis, and management of acute rheumatic fever and rheumatic heart disease. 3rd ed. Darwin: Menzies School of Health Research; 2020.
8. Pharmaceutical Benefits Scheme (PBS). PBS Schedule. Australian Government Department of Health. Available from: pbs.gov.au. Accessed 2024.
9. Agarwal S, Cunnington J, Nossent J. Autoimmune disease in Indigenous Australians: a systematic review. Int J Rheum Dis. 2021;24(12):1487–1498.
10. Pisetsky DS. Antinuclear antibody testing — misunderstood or misused? Clin Immunol. 2023;255:109717.
11. Bertsias GK, Tektonidou M, Amoura Z, et al. Joint European League Against Rheumatism and European Renal Association–European Dialysis and Transplant Association (EULAR/ERA-EDTA) recommendations for the management of adult and paediatric lupus nephritis. Ann Rheum Dis. 2012;71(11):1771–1782.
12. Ledingham J, Deighton C; British Society for Rheumatology Standards, Audit and Guidelines Working Group. Update on the British Society for Rheumatology guidelines for prescribing TNFα blockers in adults with rheumatoid arthritis. Rheumatology. 2005;44(2):155–158.
13. National Health and Medical Research Council (NHMRC). National statement on ethical conduct in human research. Canberra: NHMRC; 2023 (updated).