TextbookRespiratory MedicineAcute Exacerbation of COPD

Acute Exacerbation of COPD

Sustained worsening of COPD symptoms beyond normal day-to-day variation, requiring a change in treatment. Commonly triggered by viral/bacterial infection.

Key Facts

Definition: acute sustained worsening of dyspnoea, cough, and/or sputum beyond normal variation Triggers: viral (50-70%), bacterial (30-50% — H. influenzae, S. pneumoniae, M. catarrhalis), environmental pollutants Immediate management: controlled O₂ (target SpO₂ 88-92%), nebulised bronchodilators, prednisolone 30mg OD for 5 days, antibiotics if purulent sputum Controlled oxygen: 24-28% Venturi mask initially; avoid high-flow O₂ which may worsen hypercapnia NIV (BiPAP): for persistent respiratory acidosis (pH 7.25-7.35) despite optimal medical therapy Antibiotics: amoxicillin 500mg TDS, doxycycline 200mg then 100mg OD, or clarithromycin 500mg BD for 5 days Frequent exacerbations (≥2/year) are a distinct phenotype associated with accelerated FEV₁ decline In-hospital mortality: ~5-10%; 90-day mortality: ~15%

Overview

Key Facts

An acute exacerbation of COPD (AECOPD) is defined as a sustained worsening of the patient's symptoms from their usual stable state which is beyond normal day-to-day variations and is acute in onset, commonly requiring a change in regular medication.

Epidemiology

  • Average 1-3 exacerbations per year per COPD patient
  • ~115,000 COPD admissions per year in England
  • Leading cause of emergency medical admission in the UK
  • Winter predominance (viral triggers)
  • 30-day readmission rate ~25%

Aetiology

  • Viral infections (~50-70%): rhinovirus, influenza, parainfluenza, RSV, adenovirus
  • Bacterial infections (~30-50%): Haemophilus influenzae, Streptococcus pneumoniae, Moraxella catarrhalis, Pseudomonas (if severe COPD/bronchiectasis)
  • Environmental: air pollution, cold weather, allergens
  • Non-infectious: PE (~25% of AECOPD admissions may have concurrent PE), pneumothorax, heart failure, non-adherence

Pathophysiology

  • Infection or irritant triggers enhanced airway inflammation (neutrophilic)
  • Increased mucus production and bronchospasm worsen airflow obstruction
  • Dynamic hyperinflation increases work of breathing
  • V/Q mismatch worsens causing hypoxaemia
  • In severe cases, type 2 respiratory failure (hypoxia + hypercapnia) develops due to respiratory muscle fatigue

Clinical Presentation

Typical Presentation

  • Increased breathlessness beyond usual level
  • Increased sputum volume and/or purulence
  • Increased cough
  • Wheeze
  • Chest tightness
  • Reduced exercise tolerance
  • May have fever, confusion (hypercapnia), or ankle swelling (cor pulmonale)

Severity Assessment

  • Mild: managed with increased bronchodilator use alone
  • Moderate: requires systemic corticosteroids and/or antibiotics
  • Severe: requires hospitalisation or ED attendance

Red Flags

  • Confusion or reduced consciousness (CO₂ narcosis)
  • SpO₂ <88% on air
  • Respiratory rate >30/min
  • Use of accessory muscles, paradoxical abdominal movement
  • Cyanosis
  • Peripheral oedema (acute cor pulmonale)
  • Unable to speak in full sentences
  • Failure to respond to initial treatment
  • pH <7.35 (respiratory acidosis)
  • Significant comorbidities (heart failure, pneumonia)

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
PneumoniaFever, consolidation signs, productive coughCXR, CRP, blood cultures
Pulmonary embolismPleuritic pain, haemoptysis, unilateral leg swelling, risk factorsCTPA, D-dimer
PneumothoraxSudden onset, unilateral absent breath soundsCXR
Acute heart failureOrthopnoea, bilateral crackles, raised JVP, oedemaBNP, CXR, echo
Acute asthmaAtopy, reversible obstruction, younger ageSpirometry, FeNO
Lung cancerHaemoptysis, weight loss, non-resolving symptomsCXR, CT
Pleural effusionStony dull percussion, reduced breath soundsCXR, USS
Upper airway obstructionStridor, acute onsetFlexible nasendoscopy

Diagnosis / Investigation

Bedside

  • ABG: essential if SpO₂ <92% or severe exacerbation — assess pH, PaCO₂, PaO₂, HCO₃⁻, lactate
  • Pulse oximetry: continuous; target SpO₂ 88-92%
  • ECG: arrhythmia, right heart strain, exclude ACS
  • Sputum colour chart: green/purulent suggests bacterial infection

Bloods

  • FBC: WCC (infection), eosinophils, haemoglobin
  • CRP: elevated in infective exacerbation
  • U&Es: renal function, electrolytes
  • Blood cultures: if pyrexial or severe sepsis
  • BNP/NT-proBNP: if heart failure suspected
  • Theophylline level: if on maintenance theophylline
  • Procalcitonin: may help guide antibiotic decisions (reducing unnecessary antibiotics)

Imaging

  • Chest X-ray: exclude pneumonia, pneumothorax, pleural effusion, pulmonary oedema
  • CTPA: if PE suspected (25% of severe AECOPD have concurrent PE)

Special Tests

  • Sputum MC&S: if frequent exacerbations, failure to respond to empirical antibiotics, or bronchiectasis
  • Spirometry: NOT performed during acute exacerbation; reassess 4-6 weeks after recovery

Management

Non-pharmacological

  • Controlled oxygen therapy: 24% or 28% Venturi mask initially (target SpO₂ 88-92%)
  • Titrate oxygen based on repeat ABG at 30-60 minutes
  • Sit patient upright
  • Chest physiotherapy for sputum clearance

Pharmacological

Bronchodilators:

  • Nebulised salbutamol 2.5-5mg QDS (driven by compressed air in hypercapnic patients, with nasal O₂ at 2L/min)
  • Nebulised ipratropium bromide 500mcg QDS

Corticosteroids:

  • Prednisolone 30mg OD for 5 days (REDUCE trial showed 5 days equivalent to 14 days)
  • IV hydrocortisone 100mg if unable to swallow

Antibiotics (if purulent sputum or consolidation):

  • Amoxicillin 500mg TDS for 5 days (first-line)
  • Doxycycline 200mg loading then 100mg OD or clarithromycin 500mg BD if penicillin allergic
  • Co-amoxiclav 625mg TDS or piperacillin-tazobactam if Pseudomonas risk or severe

NIV (BiPAP):

  • Indicated for persistent respiratory acidosis (pH 7.25-7.35, PaCO₂ >6 kPa) despite 1 hour of optimal medical therapy
  • Typical settings: IPAP 12-20 cmH₂O, EPAP 4-6 cmH₂O, back-up rate 12-15
  • If pH <7.25 or failure to improve — consider ITU referral for invasive ventilation

Other:

  • VTE prophylaxis: LMWH (enoxaparin 40mg SC OD) unless contraindicated
  • IV aminophylline: rarely used; consider if poor response (loading 5mg/kg over 20 min)

Surgical/Interventional

  • Intubation and mechanical ventilation if NIV fails or pH <7.25
  • Chest drain if pneumothorax

Referral Criteria

  • ICU referral if pH <7.25 or failing NIV
  • Respiratory team review for all admitted AECOPD patients
  • Pulmonary rehabilitation referral within 4 weeks of discharge
  • Specialist review if frequent exacerbations (≥2/year) or diagnostic uncertainty

Prognosis

  • In-hospital mortality: ~5-10%
  • 30-day mortality: ~10%
  • 90-day mortality: ~15%
  • 30-day readmission rate: ~25%
  • 1-year mortality after hospitalised AECOPD: ~25%
  • Each exacerbation associated with ~5-8% decline in FEV₁
  • Frequent exacerbations (≥2/year) are an independent predictor of mortality
  • Post-exacerbation pulmonary rehabilitation reduces readmissions by 30-50%
  • NIV reduces mortality by ~50% in acidotic AECOPD (vs standard care)

Other Relevant Information

DECAF Score (Hospital Mortality Predictor)

VariablePoints
Dyspnoea (eMRCD 5a=1, 5b=2)0-2
Eosinopenia (<0.05×10⁹/L)1
Consolidation on CXR1
Acidaemia (pH <7.3)1
Atrial Fibrillation1
Score 0-1: low risk (~1-2% mortality)
Score 2: intermediate risk (~10%)
Score ≥3: high risk (~30%)

NIV Settings Summary

ParameterInitial Setting
IPAP12-15 cmH₂O (titrate to 20)
EPAP4-6 cmH₂O
Back-up rate12-15 breaths/min
Target SpO₂88-92%
Review ABG1 hour post-NIV