

A 68-year-old retired factory worker with a six-year history of chronic obstructive pulmonary disease (COPD) presented with worsening breathlessness, cough and increased sputum production over three days. He had a significant 40 pack-year smoking history and was still smoking. His sputum had become yellowish-green, and he had required his rescue inhaler more frequently over the preceding two days. On assessment, he was hypoxaemic with increased work of breathing and respiratory acidosis, consistent with an acute exacerbation of COPD with acute-on-chronic hypercapnic respiratory failure.
The patient presented with an acute increase in shortness of breath, cough, and sputum production over three days. The sputum had become yellowish-green.
He normally used an inhaled bronchodilator but reported increased use of his rescue inhaler during the previous two days.
There was no history of chest pain, haemoptysis or leg swelling.
On examination, the patient showed signs of respiratory distress and increased work of breathing.
Accessory muscle use was present. Air entry was decreased bilaterally, with diffuse expiratory wheezing. There were no clinical signs of focal consolidation.
The initial investigations were performed to assess the severity of the exacerbation, identify a possible precipitating factor and evaluate for complications.
Investigation | Result |
Haemoglobin | 15.1 g/dL |
WBC count | 13,800/µL |
CRP | Elevated |
Creatinine | 1.0 mg/dL |
Chest X-ray | Hyperinflated lungs; no focal consolidation |
ECG | Sinus tachycardia |
ABG | pH 7.32, PaCO₂ 58 mmHg, PaO₂ 52 mmHg |
Previous spirometry | FEV₁ 45% predicted |
The arterial blood gas demonstrated respiratory acidosis with hypercapnia and hypoxaemia, supporting the diagnosis of acute-on-chronic hypercapnic respiratory failure.
The patient was diagnosed with:
Acute exacerbation of COPD (AECOPD) with acute-on-chronic hypercapnic respiratory failure.
The exacerbation was considered likely to have been triggered by a respiratory infection, given the acute increase in sputum production and purulence.
Controlled oxygen supplementation was initiated because of significant hypoxaemia.
In patients at risk of hypercapnic respiratory failure, oxygen therapy is carefully titrated, with a target SpO₂ of 88–92%. Arterial blood gas monitoring is important to assess carbon dioxide retention and acid-base status.
Short-acting inhaled bronchodilators were administered to relieve airflow obstruction.
Nebulised therapy can be used when clinically appropriate, particularly when the patient’s respiratory distress makes conventional inhaler use difficult.
A short course of systemic corticosteroid therapy was initiated to reduce airway inflammation and support recovery from the exacerbation.
Antibiotic treatment was considered appropriate because of the increased sputum purulence and increased respiratory symptoms, with a possible bacterial respiratory infection contributing to the exacerbation.
Antibiotics are particularly considered when bacterial infection is suspected or when ventilatory support is required.
The patient’s ABG showed respiratory acidosis, with a pH of 7.32 and elevated PaCO₂ of 58 mmHg. Non-invasive ventilation (NIV), such as BiPAP, was therefore considered and initiated because of persistent hypercapnia and respiratory acidosis.
NIV can help improve ventilation and reduce the need for invasive mechanical ventilation in appropriately selected patients.
Other potentially serious causes of acute respiratory deterioration were considered and evaluated, including:
The absence of focal consolidation on chest X-ray helped make pneumonia less evident radiographically, although the clinical picture remained suggestive of a respiratory infection.
The patient was admitted for close monitoring and treatment. He received controlled oxygen therapy, nebulised bronchodilators, systemic corticosteroids and antibiotics.
NIV was initiated because of persistent hypercapnia and respiratory acidosis.
After 48 hours of treatment, his respiratory status improved:
With clinical improvement, he was gradually weaned from NIV and subsequently discharged on optimised inhaled maintenance therapy.
Long-term management focused on reducing the risk of future exacerbations and improving overall COPD control.
The discharge plan included:
Smoking cessation was particularly important in this patient because of his ongoing tobacco exposure and established COPD.
This case demonstrates a significant acute exacerbation of COPD complicated by acute-on-chronic hypercapnic respiratory failure. The combination of worsening respiratory symptoms, hypoxaemia, hypercapnia and respiratory acidosis required prompt assessment and hospital-based management.
Controlled oxygen therapy, bronchodilators, systemic corticosteroids, appropriate antibiotics and NIV contributed to clinical improvement. Following stabilisation, optimisation of maintenance inhaled therapy and preventive measures were important to reduce the risk of future exacerbations.
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Medical Note: This case study is intended for educational purposes only. Diagnosis and treatment should be based on an individual assessment by a qualified healthcare professional.
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