Lucan · Conditions

Chronic obstructive pulmonary disease

Australian guidance: COPD-X Handbook (Lung Foundation / TSANZ)

1. Definition and epidemiology

Chronic obstructive pulmonary disease (COPD) is characterised by persistent, largely irreversible airflow limitation resulting from a combination of small airways disease (obstructive bronchiolitis) and alveolar destruction (emphysema), driven by an abnormal inflammatory response to inhaled noxious particles or gases. In Australia, COPD is substantially under-recognised and under-treated, representing a major public health burden with immense opportunity to improve outcomes through standardised evidence-based care. Tobacco smoking is the single most important risk factor, with approximately half of all smokers developing some degree of airflow limitation and 15 to 20% developing clinically significant disability.

2. Pathophysiology

Per Robbins Ch 15, COPD encompasses two overlapping patterns of injury. In centriacinar emphysema, the predominant form in smokers, destruction of respiratory bronchioles creates enlarged airspaces in the central portions of the acinus while sparing distal alveoli; this pattern is most pronounced in the upper lobes. In panacinar emphysema, seen with alpha-1 antitrypsin (A1AT) deficiency, destruction involves the entire acinus uniformly and predominates in the lower lobes. Both patterns share a common mechanism: chronic inhalation of cigarette smoke activates macrophages and neutrophils, releasing proteases (elastase, matrix metalloproteinases) that degrade elastin and collagen. Physiologically this produces loss of elastic recoil, dynamic airway collapse on exhalation, gas trapping with hyperinflation, ventilation-perfusion mismatch, and progressive hypoxaemia. Chronic bronchitis, defined clinically as productive cough on most days for at least 3 months per year for 2 consecutive years, reflects goblet cell hyperplasia and submucosal gland hypertrophy in large airways, distinct from but often coexisting with emphysema.

3. Clinical presentation and diagnostic criteria

COPD typically presents in patients older than 35 years with relevant risk factor exposure. The cardinal symptoms are progressive exertional dyspnoea, chronic cough, sputum production, recurrent respiratory tract infections, and wheeze. Dyspnoea often develops insidiously over years, initially occurring only on moderate exertion before limiting activities of daily living. Examination findings in advanced disease include hyperinflated chest with increased anteroposterior diameter, reduced chest expansion, prolonged expiratory phase, quiet breath sounds, and expiratory wheeze. Peripheral oedema and raised jugular venous pressure suggest cor pulmonale. COPD cannot be diagnosed on clinical grounds alone; spirometry confirming a postbronchodilator forced expiratory volume in 1 second to forced vital capacity ratio (FEV1/FVC) below 0.7 is required to establish the diagnosis. Alpha-1 antitrypsin deficiency should be considered in patients presenting before age 40, particularly with a family history of premature COPD or emphysema.

4. Investigations and AU-specific cutoffs

Spirometry is mandatory for diagnosis: a postbronchodilator FEV1/FVC ratio below 0.7 is diagnostic. Severity is staged by FEV1 percent predicted: mild 60 to 80%, moderate 40 to 59%, severe below 40%. These spirometric thresholds are acknowledged as somewhat arbitrary in the COPD-X guidance and must be interpreted alongside symptom burden using the COPD Assessment Test (CAT) and modified Medical Research Council (mMRC) dyspnoea scale. A chest X-ray is useful to exclude alternative diagnoses such as lung cancer or heart failure. CT chest is not required for routine diagnosis but can characterise emphysema distribution and identify bronchiectasis. Full lung function testing with plethysmographic lung volumes demonstrates gas trapping (increased residual volume) and a diffusion defect (reduced diffusing capacity for carbon monoxide). Arterial blood gas analysis on room air is required in patients with oxygen saturation measured by pulse oximetry (SpO2) at or below 90% to assess eligibility for long-term domiciliary oxygen therapy; assessment must occur when stable and not within 4 weeks of an exacerbation. Serum A1AT level and phenotype should be measured in patients presenting below age 40.

5. Management

Management follows a stepwise escalation model anchored to the COPD-X framework (Lung Foundation Australia / TSANZ), with initial emphasis on non-pharmacological measures applicable to all patients regardless of severity. Smoking cessation is the only intervention proven to slow the natural history of COPD and reduce mortality, and it remains the single most important therapeutic act at any disease stage. Pulmonary rehabilitation is effective at all severity levels, improving exercise capacity and quality of life and reducing hospitalisation frequency; programs typically run for at least 8 weeks with sessions on 2 or 3 days per week. All patients should receive annual influenza vaccination and up-to-date pneumococcal vaccination. Pharmacological therapy is introduced when symptoms persist despite these measures. For mild or infrequent symptoms a short-acting beta-2 agonist (SABA) such as salbutamol 100 to 200 micrograms via pressurised metered-dose inhaler with spacer is used as required. When symptoms persist, long-acting bronchodilator monotherapy is added: either a long-acting muscarinic antagonist (LAMA) or a long-acting beta-2 agonist (LABA). LAMAs are preferred over LABAs for reducing exacerbations per meta-analysis evidence. If symptoms and exacerbations continue despite monotherapy, dual LABA plus LAMA therapy is added. Inhaled corticosteroid (ICS) is reserved for patients who have experienced a severe exacerbation requiring hospitalisation or at least two moderate exacerbations in the prior 12 months and who remain symptomatic on dual bronchodilator therapy; triple LABA plus LAMA plus ICS therapy should be assessed after 3 to 6 months and referred to a respiratory physician if the patient remains uncontrolled. Theophylline is not recommended in Australia. Inhaler technique should be checked at every review, as up to 90% of patients use devices incorrectly. A written COPD action plan, developed with the patient, should be provided and include guidance on escalating bronchodilators, initiating a short course of oral corticosteroids for worsening dyspnoea, and considering antibiotics for suspected infective exacerbation.

6. Pharmacology and AU PBS notes

Short-acting rescue therapy: salbutamol (Ventolin, Asmol, Airomir) 100 micrograms per actuation via pressurised metered-dose inhaler, 1 to 2 puffs as required; terbutaline (Bricanyl) 500 micrograms via dry powder inhaler (Turbuhaler), 1 inhalation as required. Ipratropium is contraindicated in patients already using a LAMA and carries an increased cardiovascular risk.

LAMA monotherapy (PBS available): tiotropium (Spiriva, Braltus) 18 micrograms via Handihaler or 13 micrograms via Zonda device, 1 inhalation daily; tiotropium 5 micrograms via Respimat mist inhaler, 2 inhalations daily; glycopyrronium (Seebri) 50 micrograms via Breezehaler, 1 inhalation daily; aclidinium (Bretaris) 322 micrograms via Genuair, 1 inhalation twice daily; umeclidinium (Incruse) 62.5 micrograms via Ellipta, 1 inhalation daily.

LABA monotherapy (PBS): indacaterol (Onbrez) 150 micrograms via Breezehaler, 1 to 2 inhalations daily, is the only LABA listed on the Pharmaceutical Benefits Scheme (PBS) as COPD monotherapy.

Fixed-dose LABA plus LAMA combinations available on the PBS include indacaterol plus glycopyrronium (Ultibro) 110 plus 50 micrograms via Breezehaler once daily, vilanterol plus umeclidinium (Anoro) 25 plus 62.5 micrograms via Ellipta once daily, and olodaterol plus tiotropium (Spiolto) via Respimat once daily.

Triple therapy single-inhaler options include fluticasone furoate plus umeclidinium plus vilanterol (Trelegy) 100 plus 62.5 plus 25 micrograms via Ellipta once daily, and budesonide plus glycopyrronium plus formoterol (Breztri) via pressurised metered-dose inhaler twice daily. ICS monotherapy inhalers are not PBS-listed for COPD; ICS must be prescribed as combination products. Oral corticosteroids should be limited to short courses for exacerbations due to adverse effects including bone density loss and increased diabetes risk, particularly relevant given COPD's frequent coexistence with type 2 diabetes.

7. Complications and monitoring

Key complications include acute exacerbations (the most common cause of hospitalisation and an independent predictor of mortality), cor pulmonale (right heart failure driven by hypoxic pulmonary vasoconstriction), pulmonary hypertension, respiratory failure with hypercapnia, secondary polycythaemia, pneumothorax, and lung cancer. Common comorbidities requiring active surveillance are ischaemic heart disease, heart failure, atrial fibrillation, depression, anxiety, osteoporosis, and type 2 diabetes; these often share risk factors and mutually worsen prognosis. Domiciliary oxygen therapy is indicated when arterial oxygen tension (PaO2) is at or below 55 mmHg on two occasions at least 3 weeks apart while stable, or 55 to 59 mmHg with evidence of pulmonary hypertension or polycythaemia; it must be used for at least 16 to 18 hours per day to confer mortality benefit.

Monitoring schedule: mild to moderate COPD requires review at least annually with spirometry, CAT score, mMRC score, BMI, inhaler technique, and vaccination status. Severe COPD requires review at least twice per year, adding arterial blood gas analysis if SpO2 is below 90%, and assessment for cor pulmonale, nutritional status, and end-of-life planning. Indications for referral to a respiratory physician include diagnostic uncertainty, frequent exacerbations despite optimised therapy, haemoptysis, rapid FEV1 decline, and COPD onset before age 40.

Written for Australian practice and grounded in the guidance named above. Study material only — not medical advice. Always check against current guidelines.