Severe Acute-on-Chronic Hypercapnic Respiratory Failure in Long-Standing Bronchiectasis: A Case Report

Introduction

Bronchiectasis is a chronic and progressive airway disorder characterised by irreversible bronchial dilatation caused by recurrent airway inflammation and infection. The disease is associated with impaired mucociliary clearance, chronic sputum production, repeated pulmonary infections, and progressive airflow limitation. 1 Acute infective exacerbations are major contributors to morbidity and mortality, frequently resulting in hospitalisation and respiratory compromise.

In advanced bronchiectasis, chronic hypoventilation and ventilation–perfusion mismatch may culminate in hypercapnic (Type II) respiratory failure. Although moderate carbon dioxide (CO 2) retention is commonly observed in chronic respiratory disorders, extremely elevated partial pressure of carbon dioxide in arterial blood (PaCO 2) levels above 150 mmHg are rarely documented in the literature and may lead to altered sensorium, cardiovascular instability, and respiratory arrest. 2

Non-invasive ventilation (NIV) has become an established therapeutic intervention for acute hypercapnic respiratory failure by improving alveolar ventilation, reducing the work of breathing, and decreasing the requirement for invasive mechanical ventilation. 3 We present a case of severe acute-on-chronic hypercapnic respiratory failure in a patient with long-standing bronchiectasis, successfully managed with early NIV and supportive care.

Case Report

A 71-year-old male with a seven-year history of bronchiectasis presented with sudden worsening of breathlessness over the past day, associated with fever and increased productive cough over the preceding 5–6 days. The patient had been receiving long-term lowflow oxygen therapy at home (1 L/min) and intermittent bilevel positive airway pressure (BiPAP) support. On admission, the patient was tachypnoeic with reduced oxygen saturation on room air. Bilateral diffuse rhonchi and basal crackles were noted on chest auscultation. Cardiovascular examination was unremarkable, and peripheral oedema was absent.

Investigations

Arterial blood gas (ABG) analysis demonstrated severe respiratory acidosis with progressive hypercapnia. Initial ABG showed a pH of 7.17, PaCO 2 of 100 mmHg, partial pressure of arterial oxygen (PaO 2) of 35 mmHg, and bicarbonate (HCO 3) of 35 mmol/L. Subsequent monitoring revealed transient improvement followed by worsening hypercapnia, with peak PaCO 2 reaching 156 mmHg and bicarbonate 55 mmol/L, consistent with acute-on-chronic ventilatory failure.

Laboratory evaluation revealed haemoglobin of 13.5 g/dL, total leucocyte count of 10.6 × 10⁹/L with neutrophilic predominance (86%), and elevated inflammatory markers, suggestive of an infective exacerbation. Renal function remained preserved despite a mild elevation in blood urea levels. Chest radiography demonstrated bilateral lower-zone fibrotic changes with patchy opacities suggestive of superimposed infection (Figure 1).

Diagnosis

Acute infective exacerbation of bronchiectasis complicated by severe acute-on-chronic hypercapnic respiratory failure.

Management

The patient was managed in the Intensive Care Unit (ICU) with carefully titrated oxygen therapy targeting oxygen saturation between 88% and 92%. NIV was initiated promptly using BiPAP support. Additional treatment included broad-spectrum intravenous (IV) antibiotics, inhaled bronchodilators, nebulisation, airway clearance therapy, and intensive chest physiotherapy. Serial ABG monitoring was performed to assess the therapeutic response. Endotracheal intubation was avoided due to gradual clinical and biochemical improvement.

Outcome

Over subsequent days, progressive reduction in PaCO2 levels and correction of respiratory acidosis were observed. Respiratory distress improved, oxygen requirements decreased, and the patient was successfully transferred out of the ICU after stabilisation.

Discussion

Bronchiectasis predisposes patients to recurrent respiratory infections, mucus retention, and chronic airflow obstruction, all of which contribute to progressive ventilatory impairment. 4 Long-standing disease may lead to chronic CO 2 retention with renal metabolic compensation. However, acute infective exacerbations can precipitate sudden ventilatory decompensation and severe hypercapnic respiratory failure.

Extreme hypercapnia is associated with significant physiological consequences, including cerebral vasodilation, altered mental status, increased intracranial pressure, and cardiovascular compromise. 5 The successful outcome in this case highlights the importance of early recognition and prompt intervention.Current evidence supports the use of NIV as first-line therapy in acute hypercapnic respiratory failure because it improves gas exchange, reduces respiratory muscle fatigue, shortens the duration of ICU stay, and decreases mortality.6

Careful oxygen titration is equally important because uncontrolled oxygen administration may worsen hypercapnia through increased ventilation–perfusion mismatch and reduced hypoxic respiratory drive. 7 In the present case, timely institution of NIV, controlled oxygen therapy, antimicrobial treatment, and chest physiotherapy contributed to rapid stabilisation and the avoidance of invasive mechanical ventilation.