A defining feature of chronic obstructive pulmonary diseases (COPD) is the irreversible airflow limitation measured during forced expiration (1), caused by either an increase in the resistance of the small conducting airways (2,3), an increase in lung compliance due to emphysematous lung destruction (4) or both (5). Patients with acute exacerbation of COPD (AECB) typically present with increased cough, changes in sputum volume and purulence, and greater breathlessness, wheezing, and chest tightness (6). In a longitudinal study of patients with moderate to severe COPD, significant decreases in the peak-expiratory flow rates (PEFR), forced expiratory volume in one second (FEV1), and forced vital capacity (FVC) were observed during exacerbations. The recovery time was related to the extent of the decreases, and a reduction in PEFR was greater in patients with increased dyspnoea (7). A purulent exacerbation is usually an indication for a bacterial etiology and should be treated appropriately (8).