Dyspnoea

Last updated 31 May 2026 · Respiratory / Cardiology

📋 Key Information Summary

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Dyspnoea is the subjective sensation of breathlessness — always a symptom, never a diagnosis; the underlying cause must be identified urgently in acute presentations.
Cardiac vs respiratory differentiation is the first branch point: orthopnoea, paroxysmal nocturnal dyspnoea (PND), peripheral oedema, elevated JVP, and S3 gallop favour a cardiac cause; wheeze, productive cough, pleuritic pain, and focal lung findings favour respiratory causes.
BNP/NT-proBNP is the single most useful blood test to differentiate cardiac from respiratory dyspnoea in the acute setting — BNP <100 pg/mL or NT-proBNP <300 pg/mL effectively excludes acute heart failure.
Asthma vs COPD: asthma is typically episodic, reversible (≥12% and ≥200 mL FEV₁ improvement on spirometry), and presents younger; COPD is persistent, poorly reversible, and strongly associated with smoking history ≥20 pack-years.
Cardiac asthma (pulmonary oedema causing wheeze) mimics bronchial asthma but has bilateral basal crackles, raised BNP, and cardiomegaly on CXR — misdiagnosis and administration of IV fluids or β₂-agonists alone can be fatal.
Common causes of wheezing extend beyond asthma and COPD to include cardiac asthma, anaphylaxis, vocal cord dysfunction, foreign body aspiration, and carcinoid — a systematic approach prevents anchoring bias.
Acute red flags requiring immediate intervention: SpO₂ <92%, inability to speak in full sentences, silent chest, cyanosis, haemodynamic instability, and stridor (upper airway obstruction until proven otherwise).
Chest X-ray and ECG should be obtained in virtually all acute dyspnoea presentations; CT pulmonary angiography (CTPA) is indicated when pulmonary embolism is suspected (Wells score ≥4).
Spirometry is the gold standard for obstructive airway disease classification and should be performed in stable patients with chronic dyspnoea — FEV₁/FVC ratio <0.7 confirms obstruction.
Aboriginal and Torres Strait Islander Australians experience chronic respiratory disease at 2.5 times the rate of non-Indigenous Australians, with rheumatic heart disease contributing significantly to cardiac dyspnoea in remote communities.
Pulmonary embolism, pneumothorax, and acute coronary syndrome are life-threatening causes that must be actively excluded before attributing dyspnoea to a benign aetiology.
Empirical treatment should be guided by the most likely diagnosis while investigations are pending — but do not delay life-saving interventions (e.g. GTN for pulmonary oedema, adrenaline for anaphylaxis) for diagnostic certainty.

Introduction & Australian Epidemiology

Dyspnoea — the subjective experience of breathlessness or difficulty breathing — is one of the most common presenting complaints in Australian general practice, emergency departments, and specialist respiratory and cardiology clinics. It is a symptom rather than a diagnosis, and its evaluation demands a structured clinical approach to identify the underlying cause, which may be cardiac, respiratory, neurological, musculoskeletal, metabolic, or psychogenic in origin.

In Australia, dyspnoea accounts for approximately 4–5% of all general practice encounters and is the presenting complaint in over 10% of emergency department (ED) presentations nationally. The Australian Institute of Health and Welfare (AIHW) reports that chronic obstructive pulmonary disease (COPD) was the fifth leading cause of death in Australia in 2022, with over 7,800 deaths attributed to the disease. Asthma affects approximately 2.7 million Australians (11% of the population), making Australia one of the highest prevalence countries globally. Heart failure affects an estimated 480,000 Australians, with prevalence rising sharply after age 65.

The diagnostic approach to dyspnoea begins with distinguishing acute from chronic presentations, then differentiating cardiac from respiratory causes — the two most common aetiological categories. This article provides a structured framework for this differentiation, with specific guidance on asthma versus COPD, cardiac asthma versus bronchial asthma, and the systematic evaluation of wheezing, all contextualised within Australian clinical practice.

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Clinical pearl: The "golden minute" of dyspnoea assessment — within 60 seconds of patient contact, assess airway patency, respiratory rate, work of breathing, oxygen saturation, and haemodynamic stability. If any of these are abnormal, initiate resuscitation before pursuing the diagnostic workup.

Heart vs Lung Cause Comparison

Differentiating cardiac from respiratory causes of dyspnoea is the critical first branch point in clinical assessment. While many patients — particularly the elderly, obese, and those with comorbidities — will have overlapping cardiac and respiratory pathology, a systematic comparison of clinical features, examination findings, and initial investigations can substantially narrow the differential.

Feature	Cardiac Cause	Respiratory Cause
Onset	Often subacute; may worsen at night or with exertion	Variable; acute (PE, pneumothorax) or gradual (COPD, ILD)
Orthopnoea	Common — typical of heart failure; patient requires ≥2 pillows	Uncommon unless severe obesity, bilateral diaphragmatic weakness
PND	Characteristic — sudden awakening 1–2 hours after falling asleep with air hunger	Uncommon; nocturnal cough may suggest asthma
Exertional pattern	Dyspnoea on exertion (DOE) with gradual decline in exercise tolerance	DOE variable; may be triggered by allergens, cold air, exercise (asthma)
Cough	Dry or productive of pink frothy sputum (pulmonary oedema)	Productive; purulent in exacerbations, mucoid in stable disease
Chest pain	Anginal: retrosternal, crushing, radiating to left arm/jaw	Pleuritic: sharp, worse on inspiration (PE, pneumonia, pneumothorax)
Peripheral oedema	Common in right heart failure / biventricular failure	Uncommon unless cor pulmonale secondary to chronic lung disease
JVP	Elevated in heart failure, tamponade, PE	Normal unless cor pulmonale or tension pneumothorax
Auscultation	Bilateral basal crackles, S3 gallop, murmurs, displaced apex	Wheeze, focal crackles (consolidation), reduced air entry, pleural rub
CXR	Cardiomegaly, upper lobe diversion, Kerley B lines, pleural effusion (bilateral or right > left)	Hyperinflation, bullae, infiltrates, mass, pneumothorax, pleural effusion
ECG	AF, LVH, ischaemic changes, right heart strain (S1Q3T3), low voltage	Often normal; right heart strain in PE; P-pulmonale in COPD
Bloods	BNP ≥100 pg/mL or NT-proBNP ≥300 pg/mL; elevated troponin if ACS	Eosinophilia (asthma), raised CRP/WCC (infection), D-dimer if PE suspected
Key test	BNP/NT-proBNP, echocardiography	Spirometry, peak flow, CT chest / CTPA

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Do not miss: Pulmonary embolism (PE) can mimic both cardiac and respiratory disease. Apply the Wells score to all undifferentiated dyspnoea patients. A Wells score ≥4 mandates CTPA; a score <4 with a negative age-adjusted D-dimer effectively excludes PE.

BNP and NT-proBNP are available through all major Australian pathology providers (Sonic Healthcare, Healius, Australian Clinical Labs) under MBS item 66626 (BNP) and 66804 (NT-proBNP). Results are typically available within 2–4 hours in metropolitan hospitals and within 24 hours in regional settings. Point-of-care BNP testing is available in some Australian EDs.

Asthma vs COPD Comparison

Asthma and COPD are the two most prevalent chronic respiratory diseases in Australia and the most common causes of chronic wheeze and dyspnoea. While they share overlapping symptoms — wheeze, cough, breathlessness — their pathophysiology, demographics, natural history, and management differ fundamentally. Accurate differentiation is essential because misdiagnosis leads to inappropriate therapy and poorer outcomes.

Feature	Asthma	COPD
Age of onset	Often childhood or young adult; can present at any age	Typically >40 years
Smoking history	Not required; smoking worsens asthma but is not the primary driver	Strong association; ≥20 pack-years typical (though 20% of cases are non-smokers)
Symptom pattern	Episodic, variable; worse at night, early morning, with triggers (allergens, cold air, exercise, viral URTI)	Persistent, progressive; daily symptoms with acute exacerbations
Trigger factors	Allergens, exercise, cold air, infections, occupational exposures, aspirin/NSAIDs (Samter's triad)	Infections (most common exacerbation trigger), pollution, cold weather
Family history	Often positive for asthma, eczema, allergic rhinitis (atopic triad)	May have family history of COPD or α₁-antitrypsin deficiency
Chest auscultation	Polyphonic wheeze; may be quiet between episodes; hyperinflation during severe attacks	Wheeze, coarse crackles, prolonged expiration, reduced air entry
Spirometry	Obstructive pattern (FEV₁/FVC <0.7) with ≥12% AND ≥200 mL improvement post-bronchodilator (reversible obstruction)	Obstructive pattern (FEV₁/FVC <0.7) with <12% or <200 mL improvement post-bronchodilator (fixed obstruction)
FeNO (fractional exhaled nitric oxide)	Often elevated (>40 ppb) in eosinophilic asthma; supports diagnosis	Usually normal (<25 ppb); may be elevated in asthma-COPD overlap
Blood eosinophils	May be elevated (>0.3 × 10⁹/L); guides biologic therapy eligibility	Variable; ≥0.3 × 10⁹/L predicts response to ICS in COPD
CXR	Often normal; hyperinflation in severe attacks	Hyperinflation, flattened diaphragm, bullae, increased AP diameter
Severity classification	Stepwise (Step 1–4 in Australian Asthma Handbook)	GOLD stages: I (mild) to IV (very severe) based on FEV₁ % predicted
Reversibility	Highly reversible; may normalise between episodes	Poorly reversible; progressive decline in FEV₁ (~60 mL/year vs ~30 mL/year in healthy adults)

Asthma-COPD Overlap (ACO)

Some patients exhibit features of both asthma and COPD — termed asthma-COPD overlap (ACO). These patients tend to have more frequent exacerbations, greater lung function decline, and worse quality of life than those with either condition alone. ACO should be suspected when a patient >40 years with a smoking history has significant bronchodilator reversibility AND eosinophilic inflammation (blood eosinophils ≥0.3 × 10⁹/L or FeNO ≥40 ppb). Management combines asthma and COPD strategies, with ICS being mandatory (as in asthma) rather than optional (as in some COPD phenotypes).

Initial Pharmacotherapy Comparison

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Salbutamol (Ventolin® / Asmol®)

Short-acting β₂-agonist (SABA)

Adult dose 100–200 mcg (1–2 puffs) MDI PRN via spacer; nebulised 2.5–5 mg in acute severe attacks

Paediatric dose 100 mcg (1 puff) via spacer + mask <3 years; up to 6 puffs per dose in acute asthma

Indications First-line reliever for both asthma and COPD

PBS status ✔ PBS General Benefit

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Budesonide / Formoterol (Symbicort®)

ICS / LABA combination

Adult dose (asthma — maintenance) 200/6 mcg or 400/12 mcg BD (MART regimen: also used as PRN reliever at 200/6 mcg)

Adult dose (COPD) 200/6 mcg or 400/12 mcg BD if eosinophils ≥0.3 × 10⁹/L or frequent exacerbations

Renal adjustment None required

PBS status ✔ PBS General Benefit (asthma) Authority Required (COPD — after LABA/LAMA trial)

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Tiotropium (Spiriva®)

Long-acting muscarinic antagonist (LAMA)

Adult dose (COPD) 18 mcg inhaled once daily via HandiHaler® or 2.5 mcg via Respimat®

Indications First-line maintenance therapy in COPD; add-on in poorly controlled asthma (step 3+)

Key caution Avoid in narrow-angle glaucoma, urinary retention

PBS status Authority Required (COPD) ✔ PBS General Benefit (asthma add-on)

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Australian Asthma Handbook (NAC, 2024): The single maintenance and reliever therapy (SMART/MART) regimen using budesonide-formoterol is now recommended as a preferred option for adults and adolescents with moderate-to-severe asthma, replacing SABA-only reliever approaches. This reduces severe exacerbations by ~30% compared with fixed-dose ICS-LABA + SABA reliever.

Cardiac Asthma vs Bronchial Asthma

Cardiac asthma is a term describing wheezing and dyspnoea caused by pulmonary oedema secondary to left ventricular failure, rather than by bronchial airway inflammation. It is a clinical mimic of bronchial asthma and represents a diagnostic pitfall — misdiagnosis can lead to harmful interventions such as excessive intravenous fluid administration or reliance on β₂-agonists alone without addressing the underlying cardiac pathology.

Feature	Cardiac Asthma	Bronchial Asthma
Underlying mechanism	Pulmonary oedema from LVF → peribronchial oedema → airway narrowing → wheeze	Eosinophilic airway inflammation → bronchospasm → reversible airway obstruction
Age group	Typically >60 years; history of IHD, hypertension, valvular disease, or cardiomyopathy	Any age; often onset in childhood or young adulthood
Timing	Nocturnal; wakes patient from sleep (PND); recumbent position worsens symptoms	Nocturnal or early morning; triggered by allergens, exercise, cold air, URTI
Sputum	Pink, frothy (pulmonary oedema); may be blood-tinged	Mucoid or yellow-green (eosinophilic or infective); Curschmann spirals, Charcot-Leyden crystals
Associated features	Bilateral basal crackles, S3/S4 gallop, raised JVP, peripheral oedema, hepatomegaly, displaced apex beat	Polyphonic wheeze, prolonged expiration, hyperinflated chest, nasal polyps, eczema
CXR	Cardiomegaly, upper lobe venous diversion, Kerley B lines, bilateral pleural effusions (R ≥ L), alveolar oedema ("bat-wing" pattern)	Hyperinflation, flat diaphragm; may be normal between episodes
ECG	AF, LVH, Q waves (prior MI), ST/T changes, LBBB	Usually normal; may show sinus tachycardia; P-pulmonale in severe disease
BNP / NT-proBNP	Markedly elevated (BNP typically >400 pg/mL; NT-proBNP >1000 pg/mL)	Normal or mildly elevated (BNP <100 pg/mL generally excludes heart failure)
Echocardiography	Reduced LVEF (<40%), diastolic dysfunction, valvular disease, wall motion abnormalities	Normal cardiac structure and function
Response to treatment	Rapid improvement with GTN, IV furosemide, CPAP; β₂-agonists provide partial/temporary relief	Excellent response to SABA (salbutamol); responds to ICS, LABA, oral corticosteroids

Emergency Management of Cardiac Asthma

Position & Oxygen

Sit upright; high-flow O₂ via mask to maintain SpO₂ ≥94%. Avoid hyperoxia in COPD co-morbidity (target 88–92%).

GTN (glyceryl trinitrate)

GTN 400 mcg sublingual, repeat every 5 min (up to 3 doses) or IV GTN infusion 5–200 mcg/min if SBP >100 mmHg. Reduces preload and afterload.

IV Furosemide

Furosemide 40–80 mg IV bolus (double the patient's usual oral dose). Onset ~15 min. If already on oral diuretics, give equivalent IV dose.

CPAP / BiPAP

CPAP 5–10 cmH₂O reduces work of breathing and improves oxygenation. Consider BiPAP if hypercapnic. Avoid in haemodynamic instability.

Investigate & Admit

ECG, troponin, BNP, CXR, echocardiography. Admit under cardiology or general medicine. Consider ICU if refractory.

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Pitfall: Do NOT administer IV fluids to a patient with suspected cardiac asthma — this will worsen pulmonary oedema. If uncertain, a bedside echocardiography or urgent BNP can rapidly differentiate cardiac from respiratory causes.

Common Causes of Wheezing

Wheezing is a continuous, high-pitched musical sound produced by narrowed or compressed intrathoracic or extrathoracic airways. While asthma and COPD are the most common causes, a broad differential diagnosis exists, and anchoring on these two conditions alone can lead to missed diagnoses — some of which are life-threatening.

Systematic Differential Diagnosis of Wheezing

Category	Condition	Key Distinguishing Features
Obstructive airway	Asthma	Episodic, reversible, atopic history, triggers
	COPD	Progressive, smoking history, fixed obstruction on spirometry
	Bronchiectasis	Chronic productive cough, recurrent infections, HRCT diagnostic
Cardiac	Cardiac asthma (LVF)	PND, orthopnoea, crackles, raised BNP, cardiomegaly
Cardiac	Pulmonary embolism	Acute onset, pleuritic pain, tachycardia, D-dimer/CTPA
Upper airway	Foreign body aspiration	Sudden onset, unilateral wheeze, reduced air entry one side, paediatric or elderly/bed-bound
	Vocal cord dysfunction (VCD)	Inspiratory stridor/wheeze, no response to bronchodilators, often young females, laryngoscopy diagnostic
	Anaphylaxis	Acute onset after allergen exposure, urticaria, angioedema, hypotension → IM adrenaline 500 mcg (adults)
Neoplastic	Endobronchial tumour / lung cancer	Fixed monophonic wheeze, haemoptysis, weight loss, smoking history, CT chest
Neoplastic	Carcinoid tumour	Recurrent wheeze, flushing, younger age, bronchoscopy with biopsy
Infective	Acute bronchiolitis (RSV)	Infants <12 months, winter season, bilateral wheeze + crackles, nasal suctioning + supportive care
Other	Eosinophilic granulomatosis with polyangiitis (EGPA / Churg-Strauss)	Asthma + eosinophilia + vasculitis (mononeuritis multiplex, purpura, glomerulonephritis); ANCA positive in 40%

Monophonic vs Polyphonic Wheeze

Polyphonic wheeze (multiple pitches audible simultaneously) indicates diffuse airway narrowing and is typical of asthma and COPD. Monophonic wheeze (single pitch, often focal) suggests a fixed lesion in a single airway — consider foreign body, endobronchial tumour, or localised bronchomalacia. A monophonic wheeze that is only inspiratory suggests extrathoracic obstruction (vocal cord dysfunction, tracheal stenosis, goitre).

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Silent chest in a dyspnoeic patient is a medical emergency — it indicates severe bronchospasm with so little airflow that wheeze is inaudible. Treat as life-threatening asthma: continuous nebulised salbutamol, IV magnesium sulfate 2 g over 20 min, systemic corticosteroids, and early senior/ICU review.

Anaphylaxis: The Cannot-Miss Cause

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Anaphylaxis should be considered in any patient with acute wheezing plus: (a) exposure to a known allergen, (b) urticaria or angioedema, (c) hypotension, or (d) rapid progression. First-line treatment is adrenaline (epinephrine) 500 mcg IM (0.5 mg of 1:1000) into the mid-outer thigh — repeat every 5 min as needed. Do NOT delay adrenaline for corticosteroids or antihistamines. Adrenaline auto-injectors (EpiPen® 300 mcg) are PBS-listed as Authority Required for patients with prior anaphylaxis.

Pathophysiology

Dyspnoea arises from a mismatch between the brain's respiratory drive and the respiratory system's ability to respond. The sensation is mediated by central and peripheral chemoreceptors (responding to PaCO₂, PaO₂, and pH), pulmonary stretch receptors, J-receptors in the alveolar wall, and chest wall proprioceptors. The underlying pathophysiology can be classified by the level at which the disruption occurs:

Mechanisms of Dyspnoea by System

System	Mechanism	Examples
Airway obstruction	Bronchospasm, mucosal oedema, mucus plugging → increased airway resistance → turbulent flow → wheeze	Asthma, COPD, anaphylaxis, foreign body
Parenchymal disease	Reduced lung compliance → increased work of breathing; V/Q mismatch → hypoxia	Pneumonia, pulmonary fibrosis, ARDS, pulmonary oedema
Vascular	V/Q mismatch, dead space ventilation, right ventricular failure	Pulmonary embolism, pulmonary hypertension
Pleural / chest wall	Lung restriction, pain-limited ventilation, diaphragm splinting	Pneumothorax, pleural effusion, kyphoscoliosis, obesity
Cardiac	Reduced cardiac output → tissue hypoxia; pulmonary congestion → J-receptor stimulation	Heart failure, valvular disease, arrhythmias, tamponade
Neuromuscular	Weakness of respiratory muscles → reduced tidal volume → hypoventilation	Guillain-Barré, MND, myasthenia gravis, high spinal cord injury
Metabolic / systemic	Compensatory hyperventilation (Kussmaul breathing) for metabolic acidosis	DKA, lactic acidosis, uraemia, sepsis

Asthma Pathophysiology — Type 2 Inflammation

In the majority of asthma patients, the underlying pathology is Type 2 (T2) eosinophilic airway inflammation driven by Th2 lymphocytes, ILC2 cells, and alarmins (IL-25, IL-33, TSLP). This leads to: (a) bronchospasm via smooth muscle contraction, (b) mucosal oedema, (c) mucus hypersecretion, and (d) airway remodelling (subepithelial fibrosis, smooth muscle hypertrophy) with chronic disease. The inflammatory cascade produces elevated fractional exhaled nitric oxide (FeNO), blood and sputum eosinophilia, and serum periostin — biomarkers now used to guide biologic therapy selection.

COPD Pathophysiology — Neutrophilic and Mixed Inflammation

COPD is characterised by chronic neutrophilic airway inflammation, goblet cell hyperplasia, mucous gland enlargement, and destruction of alveolar walls (emphysema) leading to loss of elastic recoil and air trapping. Smoking and other noxious exposures activate innate immune pathways (NF-κB, oxidative stress) that perpetuate inflammation even after smoking cessation. The result is progressive, largely irreversible airflow limitation with V/Q mismatch and, in advanced disease, chronic hypercapnic respiratory failure.

Investigations

Investigation of dyspnoea follows a tiered approach: immediate bedside and blood tests in the acute setting, followed by more definitive investigations once the patient is stabilised.

First-Line Investigations (Acute Setting)

Essential Pulse oximetry (SpO₂) Immediate, bedside. SpO₂ <92% on room air requires supplemental oxygen. SpO₂ <88% suggests significant hypoxaemia. Available in all Australian clinical settings.

Essential Chest X-ray (PA/lateral) MBS item 58500. Evaluates heart size, pulmonary oedema, consolidation, pneumothorax, pleural effusion, hyperinflation. Available within 30 min in metro EDs; 1–2 h in regional.

Essential 12-Lead ECG MBS item 11700. Evaluates arrhythmias (AF), ischaemia, right heart strain, LVH. Available immediately in all EDs and most GP practices.

Essential FBC, UEC, LFTs, CRP, troponin MBS items 65070 (FBC), 66500 (UEC), 66503 (LFTs), 66524 (CRP), 66624 (troponin). Evaluates infection, renal function, hepatic congestion, myocardial injury. Results within 1–2 h.

Available BNP / NT-proBNP MBS item 66626 / 66804. BNP <100 pg/mL or NT-proBNP <300 pg/mL has high negative predictive value for heart failure. Available in metro hospitals within 2–4 h; regional within 24 h.

Available Arterial blood gas (ABG) Evaluates PaO₂, PaCO₂, pH, lactate, A-a gradient. Essential in acute severe dyspnoea, suspected PE, or respiratory failure. Available in all EDs and most hospitals with respiratory units.

Second-Line Investigations (Stabilised Patient / Outpatient)

Available Spirometry (pre- and post-bronchodilator) MBS item 11506. Gold standard for airflow obstruction assessment. FEV₁/FVC <0.7 confirms obstruction. ≥12% AND ≥200 mL improvement post-bronchodilator = reversibility (asthma). Available in respiratory labs, many GP practices with spirometry equipment.

Available Fractional exhaled nitric oxide (FeNO) MBS item 66538. Elevated (>40 ppb) supports eosinophilic asthma diagnosis. Available in respiratory laboratories and some specialist GP practices.

Available Echocardiography (transthoracic) MBS item 55114. Evaluates LVEF, diastolic function, valvular disease, wall motion, pericardial effusion. Essential when cardiac cause suspected. Available in metro hospitals within 24–48 h; regional via outreach or tele-echo services.

Referral CT Pulmonary Angiography (CTPA) Gold standard for PE diagnosis. MBS item 57355. Requires IV contrast (check renal function). Indicated when Wells score ≥4 or D-dimer positive with clinical suspicion. Available in all metro hospitals and most regional centres with CT.

Specialist Full pulmonary function tests (DLCO, lung volumes) Evaluates gas transfer (DLCO) and lung volumes (plethysmography). DLCO reduced in emphysema, ILD, PE. DLCO normal/raised in asthma, obesity. Requires specialist respiratory lab referral.

Risk Stratification & Severity Scoring

Risk stratification in dyspnoea serves two purposes: (a) identifying life-threatening causes requiring immediate intervention and (b) guiding disposition (discharge, ward admission, HDU/ICU). The following severity frameworks are most relevant to Australian practice.

Acute Asthma Severity (Australian Asthma Handbook)

Mild–Moderate

Acute Asthma

SpO₂ ≥94%, speaking in sentences, RR <25, HR <110, PEF 50–80% predicted. Alert, no accessory muscle use.

Setting: ED observation / GP management

Severe

Acute Asthma

SpO₂ <94%, speaking in phrases only, RR ≥25, HR ≥110, PEF 33–50% predicted. Accessory muscle use, agitation.

Setting: ED resuscitation, consider HDU

Life-Threatening

Acute Asthma

SpO₂ <92%, silent chest, exhaustion, confusion, drowsiness, PEF <33% predicted, PaCO₂ ≥45 mmHg, hypotension, cyanosis.

Setting: ICU — immediate senior review

GOLD Classification of COPD Severity

GOLD Stage	Severity	FEV₁ % Predicted (post-bronchodilator)	Typical Symptoms
GOLD I	Mild	≥80%	Mild dyspnoea on exertion; often undiagnosed
GOLD II	Moderate	50–79%	Activity limitation; usual reason for clinical presentation
GOLD III	Severe	30–49%	Significant breathlessness; frequent exacerbations
GOLD IV	Very Severe	<30%	Quality of life markedly impaired; respiratory failure; may need long-term O₂ therapy

Heart Failure Classification (NYHA / ACC-AHA)

NYHA I

No Limitation

Ordinary physical activity does not cause undue dyspnoea or fatigue.

Setting: Outpatient cardiology

NYHA II–III

Mild–Marked Limitation

Comfortable at rest; symptoms with less-than-ordinary (II) or minimal (III) activity.

Setting: Outpatient / cardiology ward

NYHA IV

Symptoms at Rest

Unable to carry out any physical activity without discomfort; symptoms of cardiac insufficiency at rest.

Setting: Cardiology ward / ICU / palliative care

Empirical Therapy

Empirical treatment of dyspnoea should be directed at the most likely underlying cause while investigations are pending. The following covers the two most common clinical scenarios: acute undifferentiated dyspnoea and acute exacerbation of asthma/COPD.

Acute Undifferentiated Dyspnoea — Initial Management

Oxygen

Titrate to SpO₂ 94–98% (88–92% if COPD/chronic CO₂ retention suspected). Nasal prongs 2–6 L/min or Hudson mask 6–10 L/min.

Salbutamol nebuliser

5 mg nebulised, repeat every 20 min × 3 doses in acute bronchospasm. Safe to try empirically while assessing response.

IV access + bloods

FBC, UEC, CRP, troponin, BNP/NT-proBNP, D-dimer if PE suspected, ABG if SpO₂ <92% or clinical concern.

CXR + ECG

Obtain simultaneously. CXR evaluates lungs, heart size, effusions; ECG evaluates arrhythmia, ischaemia, strain.

Reassess at 15–30 min

Based on results, initiate targeted therapy (GTN for pulmonary oedema, antibiotics for pneumonia, anticoagulation for PE, systemic corticosteroids for asthma/COPD).

Acute Asthma — Empirical Pharmacotherapy

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Salbutamol (Ventolin®)

SABA · First-line bronchodilator

Adult dose (acute) 2.5–5 mg nebulised every 20 min × 3, then every 1–4 h PRN; OR 6 puffs via spacer every 20 min × 3

Paediatric dose 2.5 mg nebulised every 20 min × 3; OR 6 puffs via spacer + mask

Key caution Tremor, tachycardia, hypokalaemia; monitor K⁺ if repeated doses

PBS status ✔ PBS General Benefit

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Ipratropium bromide (Atrovent®)

SAMA · Add-on to SABA in severe asthma

Adult dose 500 mcg nebulised every 20 min × 3 in combination with salbutamol (severe/life-threatening asthma)

Paediatric dose 250 mcg nebulised every 20 min × 3

Note Add only in severe acute asthma; no role in mild–moderate attacks

PBS status ✔ PBS General Benefit

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Prednisolone (Panafcortelone®)

Systemic corticosteroid

Adult dose 50 mg PO daily for 5–7 days (no taper required for courses ≤14 days)

Paediatric dose 1–2 mg/kg/day PO for 3 days (max 50 mg/day)

Alternative Hydrocortisone 200 mg IV if unable to take oral (severe vomiting, reduced GCS)

PBS status ✔ PBS General Benefit

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Magnesium sulfate IV

Second-line bronchodilator in life-threatening asthma

Adult dose 2 g (8 mmol) IV over 20 min in 100 mL 0.9% NaCl or 5% dextrose

Paediatric dose 40–50 mg/kg IV over 20 min (max 2 g)

Key caution Monitor for hypotension, flushing, areflexia (signs of hypermagnesaemia); have calcium gluconate 10% available

PBS status ✔ PBS General Benefit

Acute COPD Exacerbation — Empirical Therapy

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COPD exacerbation triad: (1) Controlled oxygen — target SpO₂ 88–92% to avoid hypercapnic respiratory failure; (2) Systemic corticosteroids — prednisolone 40 mg PO daily for 5 days (evidence from REDUCE trial supports 5-day course); (3) Antibiotics if purulent sputum — amoxicillin 500 mg PO TDS for 5 days (or doxycycline 200 mg day 1 then 100 mg daily if penicillin allergy).

Special Populations

🤰 Pregnancy

Physiological changes: Tidal volume increases 40%, RR unchanged, PaCO₂ falls to ~30 mmHg (compensated respiratory alkalosis), functional residual capacity decreases — dyspnoea is common from 2nd trimester even without pathology.

Asthma: Uncontrolled asthma is a greater risk to the fetus than asthma medications. Continue ICS, LABA, and use SABA PRN. Prednisolone is Category A in pregnancy.

PE: Pregnancy is a prothrombotic state. D-dimer is unreliable in pregnancy (frequently elevated). CTPA is preferred (lower radiation to breast); V/Q scan is an alternative. LMWH (enoxaparin) is the anticoagulant of choice.

Refer to obstetric medicine for all dyspnoeic pregnant patients. Avoid NSAIDs in 3rd trimester.

👶 Paediatrics

Common causes: Bronchiolitis (<12 months), asthma (>12 months), foreign body aspiration, croup, pneumonia, congenital heart disease.

Bronchiolitis: RSV is the most common cause. Management is supportive — nasal suctioning, NG feeds if needed, supplemental O₂. No role for salbutamol, nebulised adrenaline, or corticosteroids in typical bronchiolitis.

Acute asthma (paediatric): Salbutamol 2.5 mg nebulised or 6 puffs via spacer + mask. Oral prednisolone 1–2 mg/kg/day × 3 days. Ipratropium 250 mcg nebulised in severe attacks.

Foreign body: Suspect in any child with sudden-onset unilateral wheeze, cough, or reduced air entry. CXR (expiratory view may show hyperinflation on affected side). Refer for rigid bronchoscopy.

Weight-based dosing is essential. Use Broselow tape or age-based charts for emergency drug doses.

👴 Elderly (≥65 years)

Multifactorial dyspnoea: Common to have overlapping cardiac + respiratory + deconditioning + obesity + anaemia. Avoid anchoring on a single diagnosis.

Heart failure: HFpEF (heart failure with preserved ejection fraction) accounts for ~50% of heart failure cases in the elderly. BNP may be lower in obese patients ("BNP paradox"). NT-proBNP is preferred in the elderly (higher cut-offs: age 50–75: >900 pg/mL; >75 years: >1800 pg/mL).

Polypharmacy: Review medications — β-blockers may worsen bronchospasm; ACE inhibitors may cause cough (dry cough in ~10%); opioids cause respiratory depression.

Spirometry quality: Elderly patients may not achieve ATS/ERS quality criteria for spirometry. Consider alternative tests (peak flow, FeNO, ambulatory SpO₂).

Atypical presentations are the norm in the elderly — myocardial infarction may present as isolated dyspnoea without chest pain.

🫘 Renal Impairment

Fluid overload: Anuric/oliguric patients accumulate fluid rapidly → pulmonary oedema. BNP is unreliable in ESRD (chronically elevated). Rely on clinical assessment, CXR, and echocardiography.

Metabolic acidosis: CKD and ESRD cause metabolic acidosis → compensatory Kussmaul breathing (deep, rapid respirations). ABG essential.

Drug adjustments: Reduce digoxin dose in renal impairment (monitor levels); furosemide dose may need to be higher in ESRD; avoid metformin if eGFR <30; enoxaparin requires dose reduction if eGFR <30 (use unfractionated heparin instead).

Uraemic pleuritis can cause pleuritic chest pain and dyspnoea in advanced CKD.

🛡️ Immunocompromised

Expanded differential: Consider Pneumocystis jirovecii pneumonia (PJP/PCP) in HIV with CD4 <200, post-transplant patients, or those on high-dose corticosteroids or rituximab.

CMV pneumonitis: Post solid organ or stem cell transplant. Diagnose by BAL + PCR. Treat with valganciclovir or IV ganciclovir.

Invasive fungal infections: Aspergillus (invasive pulmonary aspergillosis) in neutropenic patients. Galactomannan and β-D-glucan assays in serum and BAL. CT halo sign. Treat with voriconazole.

Low threshold for investigation: CT chest, bronchoscopy with BAL, and empirical broad-spectrum antimicrobials should be initiated early. Do not wait for typical clinical signs — they may be absent due to impaired inflammatory response.

Consult infectious disease and respiratory medicine early. TB must be considered in migrants, refugees, and immunocompromised patients — use respiratory precautions.

🫁 Hepatic Impairment

Hepatopulmonary syndrome: Intrapulmonary vascular dilatation in cirrhosis → V/Q mismatch → orthodeoxia (worse SpO₂ upright vs supine). Diagnostic: contrast echocardiography (bubble study). Liver transplant is the definitive treatment.

Hepatic hydrothorax: Transdiaphragmatic passage of ascitic fluid → right-sided pleural effusion (in ~5% of cirrhosis patients). Diuretics first; refractory cases require TIPS or pleurodesis.

Drug metabolism: Avoid benzodiazepines (use with extreme caution); paracetamol is safe up to 2 g/day in stable liver disease. Corticosteroids may be used but increase infection risk.

Child-Pugh score should be assessed to guide drug safety and prognosis.

Aboriginal and Torres Strait Islander Health

Disease burden

Aboriginal and Torres Strait Islander Australians experience chronic respiratory disease at 2.5 times the rate of non-Indigenous Australians. COPD prevalence in Indigenous Australians is 2–3 times higher, with onset approximately 10 years earlier. Asthma hospitalisation rates are 1.8 times higher. Rheumatic heart disease (RHD) — a largely preventable condition — remains a significant cause of cardiac dyspnoea in remote Northern Territory, Western Australian, and Queensland communities, with Indigenous Australians affected at 6.6 times the rate of non-Indigenous Australians.

Remote and rural access

Spirometry, echocardiography, and specialist respiratory/cardiology review are often unavailable in remote communities. Telehealth (MBS items 99200–99215) and fly-in/fly-out (FIFO) specialist services partially address this gap. Point-of-care testing (e.g., CRP, BNP) through the Remote Area Aboriginal Health Services (RAAHS) program supports acute assessment. The Royal Flying Doctor Service (RFDS) provides emergency aeromedical retrieval and telehealth consultations.

Environmental and social determinants

Overcrowded housing, poor ventilation, indoor wood-fire smoke exposure, and limited access to healthy food are key drivers of respiratory disease in remote communities. Cigarette smoking prevalence in Indigenous Australians is approximately 37% (vs 10% non-Indigenous). Cultural considerations include avoidance of mixed-sex health settings in some communities, the need for gender-matched health workers, and acknowledgment of sorry business (bereavement) affecting clinic attendance.

Rheumatic heart disease

RHD is the leading cause of acquired heart disease in young Indigenous Australians and a major contributor to cardiac dyspnoea. Secondary prophylaxis with benzathine penicillin G (BPG) 1.2 MU IM every 21–28 days is critical but adherence is challenging. The RHDAustralia (Menzies School of Health Research) clinical guidelines provide RHD-specific management. Echocardiographic screening programs (e.g., Echo in Schools) aim to detect subclinical RHD.

Cultural safety

Use Aboriginal Health Workers (AHWs) and Aboriginal Health Practitioners (AHPs) as cultural brokers and clinical assistants. Allow extended consultation times. Use plain language and visual aids. Recognise that some patients may describe dyspnoea using culturally specific terms (e.g., "sick in the chest"). Involve family in shared decision-making where culturally appropriate. Acknowledge the Stolen Generations' impact on trust in health services.

Closing the Gap targets

The National Agreement on Closing the Gap (2020) targets a 15% reduction in the gap in life expectancy by 2030. Chronic respiratory and cardiovascular diseases are major contributors to the life expectancy gap. Medicare-funded Indigenous-specific health assessments (MBS item 715) provide an opportunity for early detection of respiratory and cardiac risk factors, spirometry referral, and smoking cessation counselling.

📚 References

1. National Asthma Council Australia. Australian Asthma Handbook, Version 2.3. Melbourne: National Asthma Council; 2024. Available from: https://www.asthmahandbook.org.au
2. Global Initiative for Asthma (GINA). Global Strategy for Asthma Management and Prevention. 2024 Report. Available from: https://ginasthma.org
3. Global Initiative for Chronic Obstructive Lung Disease (GOLD). Global Strategy for the Diagnosis, Management, and Prevention of COPD. 2024 Report. Available from: https://goldcopd.org
4. Atherton JJ, Sindone A, De Pasquale CG, et al. National Heart Foundation of Australia and Cardiac Society of Australia and New Zealand: Australian Clinical Guidelines for Heart Failure 2018. Heart Lung Circ. 2018;27(10):1123–1208.
5. Australian Institute of Health and Welfare (AIHW). Chronic Respiratory Conditions in Australia. AIHW Cat. No. ACM 42. Canberra: AIHW; 2024.
6. RHDAustralia (Menzies School of Health Research). RHD Australia: Australian Guideline for Prevention, Diagnosis, and Management of Acute Rheumatic Fever and Rheumatic Heart Disease. 3rd ed. Darwin: RHDAustralia; 2020.
7. Byrd JB, Engelman D, Condon M, et al. B-type natriuretic peptide in the diagnosis and management of heart failure. BMJ. 2023;383:e073170.
8. Gibson PG, Simpson JL. The overlap syndrome of asthma and COPD: what are its features and how important is it? Thorax. 2009;64(8):728–735.
9. Magnussen H, Disse B, Rodriguez-Roisin R, et al. Withdrawal of inhaled glucocorticoids and exacerbations of COPD (WISDOM trial). N Engl J Med. 2014;371(14):1285–1294.
10. Schuetz P, Wirz Y, Sager R, et al. Effect of procalcitonin-guided antibiotic treatment on mortality in acute respiratory infections (ProHOSP trial). Lancet Infect Dis. 2018;18(9):968–981.
11. Parshall MB, Schwartzstein RM, Adams L, et al. An official ATS statement: update on the mechanisms, assessment, and management of dyspnea. Am J Respir Crit Care Med. 2012;185(4):435–452.
12. Australian Institute of Health and Welfare (AIHW). Aboriginal and Torres Strait Islander Health Performance Framework. Canberra: AIHW; 2023.
13. Konstantinides SV, Meyer G, Becattini C, et al. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism. Eur Heart J. 2020;41(4):543–603.
14. Reddel HK, Bacharier LB, Bateman ED, et al. Global Initiative for Asthma Strategy 2021: executive summary and rationale for key changes. Eur Respir J. 2022;59(1):2102730.
15. Lederer DJ, Martinez FJ. Idiopathic pulmonary fibrosis. N Engl J Med. 2018;379(8):797–810.

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).