C: Case finding and confirm diagnosis

Case finding and confirm diagnosis

Evidence level




III - 3



Smoking is the most important risk factor in the development of COPD (Fletcher 1977, Burrows 1977) [evidence level I].

Chronic Obstructive Pulmonary Disease (COPD) is a preventable and treatable disease with some significant extrapulmonary effects that may contribute to the severity in individual patients. Its pulmonary component is characterised by airflow limitation which is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases (Global Initiative for Chronic Obstructive Lung Disease 2017). In clinical practice, diagnosis is usually based on:

  • A history of smoking, or exposure to other noxious agents
  • FEV1/FVC<0.7 post-bronchodilator

Small-airway narrowing (with or without chronic bronchi­tis) and emphysema caused by smoking are the common conditions resulting in COPD. Chronic bronchitis is daily sputum production for at least three months of two or more consecutive years. Emphysema is a pathological diagnosis, and consists of alveolar dilatation and destruction. Breath­lessness with exertion, chest tightness and wheeze are the results of airway narrowing and impaired gas exchange. The loss of lung elastic tissue in emphysema may result in airway wall collapse during expiration, leading to dynamic hyper­inflation and consequent increased work of breathing.

The irreversible component of airflow limitation is the end result of inflammation, fibrosis and remodelling of periph­eral airways. Airflow limitation leads to non-homogeneous ventilation, while alveolar wall destruction and changes in pulmonary vessels reduce the surface area available for gas exchange. In advanced COPD there is a severe mismatching of ventilation and perfusion leading to hypoxaemia. Hypercapnia is a late manifestation and is caused by a reduction in ventilatory drive. Pulmonary hypertension and cor pulmo­nale are also late manifestations, and reflect pulmonary vasoconstriction due to hypoxia in poorly ventilated lung, vasoconstrictor peptides produced by inflammatory cells and vascular remodelling (Global Initiative for Chronic Obstructive Lung Disease 2017). The clinical features and patho­physiology of COPD can overlap with asthma, as most COPD patients have some reversibility of airflow limitation with bronchodilators. The follow up of a cohort of children aged 10 to 16 initially recruited in 1964 demonstrated that childhood participants who had wheezy bronchitis (n=53) and asthma (n=38) had an increased risk (OR 1.81 and 6.37 respectively) of COPD by mean age of 61, compared to cohort controls (n=239). Multivariate analysis details of adjustment for smoking were not provided (Tagiyeva 2016). By contrast, some non-smokers with chronic asthma develop irreversible airway narrowing. The overlap between chronic bronchitis, emphysema and asthma and their relationship to airflow obstruction and COPD are illustrated in Figure 1. This proportional Venn diagram presents data from the Wellington Respiratory Survey which recruited subjects over the age of 50 and invited them to have detailed lung function testing and chest CT scans (Marsh 2008). It can be seen that almost all patients with both chronic bronchitis and emphysema meet the GOLD definition of COPD, as do most with both chronic bronchitis and asthma . Patients with chronic bronchiolitis, bronchiectasis and cystic fibrosis may also present with similar symptoms and partially reversible airflow limitation.

Figure 1: COPD Phenotypes


The diagram (reproduced from Thorax 2008;63:761-7 with permission from the BMJ Publishing Group and corrected in Thorax 2015;70:905 to now include the clear circle in the middle of the emphysema circle) presents the different phenotypes within the Wellington Respiratory Survey study population. The large black rectangle represents the full study group. The clear circles within each coloured area represent the proportion of subjects with COPD (post-bronchodilator forced expiratory volume in 1 s/forced vital capacity (FEV1/FVC) ,0.7). The isolated clear circle represents subjects with COPD who did not have an additional defined phenotype of asthma, chronic bronchitis or emphysema.

In recent years there has been a focus on the prevalence and implications of the co-existence of asthma and COPD. A systematic review and meta-analysis of 19 studies found that the prevalence of co-existing asthma in patients with COPD was 27% in population based studies and 28% in hospital based studies (Alshabanat 2015). Both this review and systematic reviews by Gibson (Gibson 2015) and Nielsen (Nielsen 2015) found an increased frequency of exacerbations in patients with features of both asthma and COPD compared to those with COPD alone.