TextbookGeneral PracticeCOPD Management in Primary Care

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

DiagnosisKey FeaturesInvestigation
AsthmaVariable symptoms, atopy, reversible obstruction, eosinophilicSpirometry (reversibility), FeNO
Heart failureOrthopnoea, PND, bibasal crackles, raised BNPBNP, CXR, echocardiography
BronchiectasisChronic productive cough, recurrent infections, clubbingHRCT chest
Lung cancerHaemoptysis, weight loss, smokerCXR, CT chest
Pulmonary fibrosisBibasal fine inspiratory crackles, clubbing, restrictive patternHRCT, spirometry (restrictive)
TBChronic cough, haemoptysis, weight loss, night sweats, endemic exposureCXR, 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

GradeDescription
1Breathless only with strenuous exercise
2Short of breath when hurrying on level ground or walking up a slight hill
3Walks slower than contemporaries on level ground or stops after 15 minutes
4Stops for breath after ~100m or a few minutes on level ground
5Too breathless to leave the house or breathless when dressing/undressing

NICE NG115 Inhaler Selection Summary

FeaturePathway
No asthmatic features, eosinophils <300SABA → LABA+LAMA → LABA+LAMA+ICS
Asthmatic features or eosinophils ≥300SABA → LABA+ICS → LABA+LAMA+ICS

GOLD ABCD Assessment Tool

GroupExacerbationsSymptoms (CAT/mMRC)Initial Therapy
A0-1 (no hospital)Low (CAT <10)Bronchodilator
B0-1 (no hospital)High (CAT ≥10)LABA or LAMA
C≥2 or ≥1 hospitalLowLAMA
D≥2 or ≥1 hospitalHighLAMA ± LABA ± ICS