Respiratory emergencies

COPD exacerbation

Overview and approach

An exacerbation is worsening respiratory symptoms; exclude pneumonia, PE, pneumothorax and cardiac failure.

  • COPD-X defines an exacerbation as a change in baseline dyspnoea, cough and/or sputum beyond normal day-to-day variation, acute in onset, that may warrant a change in regular medication or admission. Early diagnosis and treatment may prevent admission and slow progression1.
  • Exacerbations become more frequent as COPD worsens. The best predictor of future exacerbations is a history of previous exacerbations. 12-month mortality is about 15% after hospitalisation versus 5% without1.
  • Triggers: bacterial infection in many episodes and viral infection in about a third; in 20-35% no trigger is found2.
  • People with moderate to severe COPD average one to three exacerbations a year, and quality of life tracks exacerbation frequency more closely than FEV12.
Assessment and clinical features

Work of breathing, cognition, saturation, sputum, haemodynamics and baseline CO2/oxygen history.

  • Increased breathlessness, cough, sputum volume or purulence, and fever. Sputum purulence and fever are the features that support antibiotics1.
  • Check baseline oxygen/CO2 history, home oxygen, previous NIV and the action plan.
  • History: how breathless they are with usual daily activities, fever, change in sputum, sick contacts, and how often and how badly they have flared before2.
  • Examination: degree of distress, tachycardia, tachypnoea, accessory muscle use, cyanosis, ability to speak in full sentences and mental state. Paradoxical inward movement of the abdomen on inspiration suggests diaphragm fatigue. Focal chest signs suggest pneumonia; asymmetry raises pneumothorax or large airway obstruction mimicking an exacerbation2.
  • Severity scoring: DECAF is a 30-day mortality score (extended MRC dyspnoea, eosinopenia, consolidation, acidaemia, atrial fibrillation)1.
Differentials and investigations

Blood gas when hypercapnia or severe illness is possible; chest imaging and targeted infection testing.

  • Other causes or mimics: left ventricular failure and pulmonary embolism. A systematic review found 16% of admitted COPD exacerbations undergoing CTPA had PE (range 3-29%)1.
  • Usual organisms colonising the airway: Haemophilus influenzae, Streptococcus pneumoniae, Moraxella catarrhalis; the role of bacterial infection is debated1.
  • Arterial or venous blood gas for hypercapnia and acidaemia; chest X-ray; ECG.
  • Chest X-ray is abnormal in about a quarter of people with severe COPD or marked distress, most often from pneumonia or heart failure2.
  • Reading the gas: pH falls by about 0.08 for each 10 mmHg acute rise in PaCO2, but only about 0.03 when the rise is chronic and compensated, which helps separate acute from acute-on-chronic hypercapnia2.
  • Unlike in asthma, spirometry or peak flow does not help diagnose or manage an exacerbation2.
  • Atypical organisms (Mycoplasma, Chlamydia) are found in about 5-10% of exacerbations2.
Management and follow-up

Controlled oxygen, bronchodilators, selected steroids/antibiotics and ventilatory support under local COPD-X-based pathway.

  • Bronchodilators: inhaled short-acting bronchodilators first line1.
  • Steroids: oral prednisolone 30-50 mg daily for 5 days1.
  • Antibiotics: amoxicillin or doxycycline for 5 days if features of infection (more or purulent sputum, fever)1.
  • Oxygen: for hypoxaemia, target SpO2 88-92% using controlled delivery (0.5-2 L/min). It improves survival1.
  • Non-invasive ventilation improves survival in acute hypercapnic respiratory failure1.
  • Recovery: refer to pulmonary rehabilitation (reduces readmissions), arrange comprehensive follow-up in primary care, use discharge bundles and review the action plan and inhaler technique1.
Red flags and clinical pearls

In hypoxaemic COPD exacerbations commonly target SpO2 88–92% with blood-gas reassessment. Acute hypercapnic respiratory failure may benefit from NIV; deterioration needs urgent escalation.

  • Readmission risk is highest in the first 3 months after discharge1.
  • Always repeat the blood gas after changing oxygen; rising CO2 or falling pH means escalation.
  • Consider PE if the exacerbation has no clear trigger or does not respond to treatment1.
  • Why oxygen can raise CO2: mainly because extra oxygen releases hypoxic vasoconstriction and worsens ventilation-perfusion matching, not because hypoxic drive is lost; minute ventilation usually stays the same. This is the reason for titrated targets, but needed oxygen should never be withheld2.
  • Hyperglycaemia is the commonest short-term problem with steroid treatment, so check glucose, especially in diabetes2.
  • Prognosis: hospital mortality is about 17-30% for those needing mechanical ventilation, and one-year mortality after ICU admission is about 60% in people over 652.
References
  1. COPD-X Plan 2025 (v2.78): X, Manage eXacerbations
  2. Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, editors. Harrison's Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012. Chapter 260, Chronic obstructive pulmonary disease.

Last updated from Sen’s notes on 22 October 2026.