Is ‘GOLD’ standard for the management of COPD in clinical practice?

Introduction Chronic obstructive pulmonary disease (COPD) is a preventable and treatable but usually progressive obstructive lung disease most often associated with tobacco smoking in ‘developed’ countries and accentuated by exposure to biomass fuel smoke in ‘developing’ countries [1]. COPD affects more than 200 million people worldwide. It is the third leading cause of mortality in the USA [2], and is predicted to become the third most common cause of death worldwide by 2030 [3]. COPD is the ‘umbrella’ term for emphysema and chronic bronchitis. Emphysema is the abnormal permanent enlargement and destruction of the airspaces distal to the terminal bronchioles, and is a pathologic description that is often recognized by imaging. Chronic bronchitis is a syndrome defined as a chronic productive cough for 3 months in each of 2 successive years in a patient in whom other causes of chronic cough have been excluded. COPD is characterized by alveolar destruction, loss of alveolar attachments, loss of elastic recoil and increased airway resistance. This leads to limitations in expiratory flow and inadequate lung emptying upon expiration, resulting in lung hyperinflation [4]. Static hyperinflation occurs at rest and dynamic hyperinflation occurs with increased ventilation, such as during exercise [5]. Hyperinflation is usually experienced as dyspnea, and dynamic hyperinflation as dyspnea upon exertion. Patients with COPD often experience a chronic productive cough as well as significant and progressive deteriorations in lung function, peripheral muscle function, exercise capacity, activity level and quality of life (QoL) [1]. COPD is associated with several important comorbidities. These include osteoporosis, anxiety, muscle wasting and weight loss, depression, coronary artery disease (CAD), congestive heart failure, cancer (especially that of the lung) and pulmonary vascular disease [6]. Some of the morbidities are associated with smoking and coexist with COPD, whereas others (e.g. muscle wasting, weight loss and depression) may be associated with the pathophysiology and impact of COPD itself [7, 8]. A significant proportion of COPD patients die from non-respiratory causes [1]. The progressive airflow limitation in COPD is due, in large part, to fibrosis and inflammation-induced narrowing in the small airways [8]. Destruction of the lung parenchyma, edema, secretions, smooth-muscle contraction and decrements in lung elastic recoil also play a part in limiting expiratory airflow. However, airflow limitation is not the only pathophysiologic mechanism at play. Abnormalities in gas exchange, primarily due to emphysema [9], are also characteristic of COPD, and can cause hypoxemia and hypercapnia. Respiratory pathogens (e.g. bacteria, atypical bacteria, viruses and fungi) are common in the lungs of patients with COPD even in the absence of respiratory symptoms, in contrast with the sterile lung environment seen in healthy lungs [8]. COPD is accompanied by inflammation in the lower airways and lung parenchyma. This inflammation is associated with abnormally high counts of neutrophils, activated macrophages, activated T lymphocytes and, sometimes, eosinophils [1, 9]. COPD begins with a localized inflammatory response to environmental stimuli, but it is now understood to be a systemic inflammatory disease that extends beyond the lungs. The precise mechanisms of the inflammatory processes in COPD are incompletely understood. The systemic inflammation seen in COPD may result from a ‘spillover’ of inflammatory mediators from the airways or from independent pathways, which may include physical inactivity in