COPD Management in Primary Care
Chronic obstructive pulmonary disease is a progressive, largely irreversible airway disease characterised by airflow obstruction, affecting 1.2 million diagnosed and an estimated 2 million undiagnosed in the UK, managed with smoking cessation, inhaled therapy, pulmonary rehabilitation, and exacerbation prevention.
Key Facts
COPD affects 1.2 million diagnosed and an estimated 2 million undiagnosed in the UK; third leading cause of death worldwide Smoking is the cause in >85% of cases; NICE NG115 diagnostic criteria: post-bronchodilator FEV1/FVC <0.7 Smoking cessation is the ONLY intervention proven to alter the rate of FEV1 decline (Fletcher-Peto curve; Lung Health Study) NICE NG115 inhaler pathway: SABA/SAMA PRN → if asthmatic features/higher eosinophils: LABA+ICS; if no asthmatic features: LABA+LAMA Pulmonary rehabilitation: 6-12 week supervised exercise programme; NNT 4 to prevent one hospital admission; most effective non-pharmacological intervention LTOT (long-term oxygen therapy): for PaO2 ≤7.3kPa or ≤8kPa with secondary polycythaemia/cor pulmonale; use ≥15 hours/day (MRC LTOT trial) Acute exacerbation: oral prednisolone 30mg OD for 5 days + antibiotic if purulent sputum (amoxicillin 500mg TDS or doxycycline 200mg stat then 100mg OD) Annual influenza and pneumococcal vaccination recommended for all COPD patients
Overview
Key Facts
COPD is a common, preventable, and treatable disease characterised by persistent respiratory symptoms and airflow limitation due to airway and/or alveolar abnormalities, usually caused by significant exposure to noxious particles or gases, most commonly tobacco smoke.
Epidemiology
- 1.2 million diagnosed, estimated 3 million total (including undiagnosed) in the UK
- Third leading cause of death worldwide (WHO)
- Approximately 30,000 deaths/year in the UK
- Prevalence: 2% overall; >10% in smokers >40 years
- Significant health inequality: 3-5× more prevalent in most deprived quintile
Aetiology
- Smoking: >85% of cases; risk proportional to pack-years
- Alpha-1 antitrypsin deficiency: 1-2% of cases; suspect if young onset, non-smoker, lower lobe emphysema
- Occupational exposure: coal dust, silica, cadmium, grain dust
- Air pollution: indoor (biomass fuel) and outdoor
- Childhood lung infections: severe childhood pneumonia
Pathophysiology
- Chronic bronchitis: mucus hypersecretion, goblet cell metaplasia, squamous metaplasia of bronchial epithelium
- Emphysema: destruction of alveolar walls distal to terminal bronchioles; loss of elastic recoil; air trapping
- Small airway disease: inflammation and fibrosis of small airways (<2mm)
- Neutrophilic inflammation (unlike asthma's eosinophilic predominance)
- Progressive, largely irreversible airflow limitation
- Systemic effects: skeletal muscle wasting, cardiovascular disease, osteoporosis, depression, lung cancer risk
Clinical Presentation
Typical Presentation
- Exertional dyspnoea (progressive over years)
- Chronic productive cough (particularly morning)
- Wheeze
- History of smoking (typically >10 pack-years)
- Age typically >35 years
- Reduced exercise tolerance
Examination
- Hyperinflation (barrel chest, reduced cricosternal distance)
- Pursed lip breathing
- Use of accessory muscles
- Wheeze and reduced air entry on auscultation
- Cyanosis (if hypoxic)
- Peripheral oedema (cor pulmonale)
Red Flags
- Rapidly progressive dyspnoea (exclude PE, pneumothorax, heart failure)
- Haemoptysis (exclude lung cancer)
- Significant weight loss (exclude lung cancer, TB)
- Young onset without smoking history (alpha-1 antitrypsin deficiency)
- Cor pulmonale (peripheral oedema, raised JVP)
Differential Diagnosis
| Diagnosis | Key Features | Investigation |
|---|---|---|
| Asthma | Variable symptoms, atopy, reversible obstruction, eosinophilic | Spirometry (reversibility), FeNO |
| Heart failure | Orthopnoea, PND, bibasal crackles, raised BNP | BNP, CXR, echocardiography |
| Bronchiectasis | Chronic productive cough, recurrent infections, clubbing | HRCT chest |
| Lung cancer | Haemoptysis, weight loss, smoker | CXR, CT chest |
| Pulmonary fibrosis | Bibasal fine inspiratory crackles, clubbing, restrictive pattern | HRCT, spirometry (restrictive) |
| TB | Chronic cough, haemoptysis, weight loss, night sweats, endemic exposure | CXR, sputum AFB |
Diagnosis / Investigation
Diagnostic
- Post-bronchodilator spirometry: FEV1/FVC <0.7 confirms airflow obstruction
- Mild: FEV1 ≥80% predicted
- Moderate: FEV1 50-79%
- Severe: FEV1 30-49%
- Very severe: FEV1 <30%
- Reversibility testing: limited reversibility (<12% or <200ml) — distinguishes from asthma
Baseline
- CXR: hyperinflation, flat diaphragms, bullae; exclude other pathology
- FBC: polycythaemia (chronic hypoxia), anaemia
- BMI: track nutritional status
- Pulse oximetry: SpO2 <92% → refer for ABG and LTOT assessment
- Alpha-1 antitrypsin level: in all patients (one-time test)
Monitoring
- Spirometry annually
- MRC dyspnoea scale (grade 1-5)
- Exacerbation frequency
- BMI
- CAT score (COPD Assessment Test)
Special Tests
- ABG: for LTOT assessment (PaO2 ≤7.3kPa)
- TLCO (transfer factor): reduced in emphysema
- HRCT: if bronchiectasis or alternative diagnosis suspected
- Echocardiography: if cor pulmonale or concurrent heart failure suspected
Management
Non-pharmacological
- Smoking cessation: single most important intervention; offer NRT, varenicline (1mg BD for 12 weeks), or cytisine
- Pulmonary rehabilitation: 6-12 week supervised exercise + education programme; offer to all MRC grade ≥3; NNT 4 to prevent hospitalisation
- Annual influenza vaccination + pneumococcal vaccination
- Self-management plan: recognising and managing exacerbations
- Nutritional support (if BMI <20)
- Psychological support (anxiety, depression common)
Pharmacological — NICE NG115 Inhaler Pathway
- Initial: SABA (salbutamol) or SAMA (ipratropium) PRN
- If persistent symptoms/exacerbations:
- No asthmatic features/lower eosinophils: LABA (formoterol/salmeterol) + LAMA (tiotropium/glycopyrronium) — e.g. Ultibro Breezhaler
- Asthmatic features/higher eosinophils (≥300): LABA + ICS — e.g. Symbicort, Seretide
- If still uncontrolled: Triple therapy — LABA + LAMA + ICS (e.g. Trimbow, Trelegy Ellipta)
- Mucolytics: carbocisteine 750mg TDS if chronic productive cough
- Oral theophylline: consider after inhaler optimisation (narrow therapeutic index — monitor levels)
- Prophylactic antibiotics: azithromycin 250mg 3×/week for patients with ≥3 exacerbations/year (specialist initiation; check ECG/QTc, LFTs, sputum culture for NTM)
Long-Term Oxygen Therapy (LTOT)
- Indications: PaO2 ≤7.3kPa on two ABGs 3 weeks apart (stable), or PaO2 ≤8kPa with secondary polycythaemia, pulmonary hypertension, or peripheral oedema
- Use for ≥15 hours/day (MRC LTOT trial: improved survival)
- Target SpO2 88-92% in exacerbation
- NEVER prescribe LTOT without confirming smoking cessation (fire/explosion risk)
Acute Exacerbation Management
- Controlled oxygen: 24-28% Venturi mask, target SpO2 88-92%
- Nebulised bronchodilators: salbutamol 2.5-5mg + ipratropium 500mcg
- Prednisolone 30mg OD for 5 days (no need to taper)
- Antibiotics: if purulent sputum — amoxicillin 500mg TDS 5 days, doxycycline 200mg stat then 100mg OD, or clarithromycin 500mg BD
- NIV (BiPAP): for acute hypercapnic respiratory failure (pH 7.25-7.35) despite initial treatment
Referral Criteria
- Respiratory specialist: diagnostic uncertainty, FEV1 <30%, frequent exacerbations (≥3/year), LTOT assessment, alpha-1 antitrypsin deficiency, lung volume reduction surgery consideration
- Palliative care: severe COPD with significant symptom burden
Prognosis
- COPD is a progressive disease; FEV1 decline can be slowed by smoking cessation but not reversed
- Smoking cessation: reduces rate of FEV1 decline from 60ml/year to ~30ml/year (Lung Health Study)
- BODE index (BMI, Obstruction, Dyspnoea, Exercise capacity) predicts mortality
- Median survival with FEV1 <30%: approximately 3-4 years
- Acute exacerbation requiring hospitalisation: 10% in-hospital mortality, 25% 1-year mortality
- LTOT improves survival in hypoxic patients (MRC LTOT trial: reduced mortality by ~50% at 5 years)
- Pulmonary rehabilitation improves exercise capacity and quality of life but does not alter FEV1
- Lung cancer risk is significantly increased in COPD (independent of smoking)
Other Relevant Information
MRC Dyspnoea Scale
| Grade | Description |
|---|---|
| 1 | Breathless only with strenuous exercise |
| 2 | Short of breath when hurrying on level ground or walking up a slight hill |
| 3 | Walks slower than contemporaries on level ground or stops after 15 minutes |
| 4 | Stops for breath after ~100m or a few minutes on level ground |
| 5 | Too breathless to leave the house or breathless when dressing/undressing |
NICE NG115 Inhaler Selection Summary
| Feature | Pathway |
|---|---|
| No asthmatic features, eosinophils <300 | SABA → LABA+LAMA → LABA+LAMA+ICS |
| Asthmatic features or eosinophils ≥300 | SABA → LABA+ICS → LABA+LAMA+ICS |
GOLD ABCD Assessment Tool
| Group | Exacerbations | Symptoms (CAT/mMRC) | Initial Therapy |
|---|---|---|---|
| A | 0-1 (no hospital) | Low (CAT <10) | Bronchodilator |
| B | 0-1 (no hospital) | High (CAT ≥10) | LABA or LAMA |
| C | ≥2 or ≥1 hospital | Low | LAMA |
| D | ≥2 or ≥1 hospital | High | LAMA ± LABA ± ICS |