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Chronic obstructive pulmonary disease (COPD) is a term used to describe a group of airways diseases that are not fully reversible. COPD accounts for a large amount of morbidity and mortality and is expected to become the third leading cause of death worldwide by 2030.
The symptoms of COPD include breathlessness, chronic cough and regular sputum production. Diagnosis should take these symptoms into account, in addition to exposure to risk factors such as cigarette smoke. The severity of COPD can be assessed using spirometry. Mortality may be better predicted using other measures.
The term chronic obstructive pulmonary disease (COPD) was first coined by William Briscoe in 1965.1 It is an umbrella term used to describe a group of airways diseases that are not fully reversible, are predominantly caused by smoking and affect patients over 35 years of age.2 COPD is a progressive, life-threatening condition that affects millions of people within the UK and worldwide. An understanding of the risk factors, symptoms and diagnostic measures are required to be able to manage this progressive disease effectively. Details of the pathophysiology of COPD can be found in Box 1.
COPD is often undiagnosed — it is estimated that only 900,000 out of three million people who have COPD in England have been diagnosed.3 Globally, COPD is currently the fourth leading cause of death and the World Health Organization estimates that, by 2030, COPD will become the third leading cause of death.4,5
In England and Wales, one person dies every 20 minutes as a result of COPD. It accounts for 1.4 million GP consultations and over 30,000 deaths in the UK each year.5 COPD is the second most common cause of emergency admissions to hospital and the fifth largest cause of readmissions into hospital.6 COPD results in over one million hospital bed days in England.6 In the UK, direct care costs associated with COPD amount to £3bn per year, and the overall cost is £6.6bn annually.6
The risk factors for COPD are not completely understood — epidemiological studies have identified associations rather than cause and effect relationships.
It is hypothesised that the risk of developing COPD is due to an interaction between “host factors” (such as genetics and gender) and “environmental factors” (such as smoking and occupational exposure).2,7
Tobacco smoke has been implicated in the development of chronic bronchitis and emphysema since the 1960s.8 Tobacco smoke has numerous pulmonary effects, which include the release of destructive proteolytic enzymes from inflammatory cells in the lung, oxidative stress and inactivation of α1-antitrypsin (see Box 1).
Although it has been estimated that 15–20% of smokers develop COPD, recent evidence suggests that the actual proportion is 50%.9 The risk of COPD developing in smokers is dose related and is affected by the age at which smoking started and the total pack-years smoked:
Environmental exposure to tobacco smoke is also associated with reduced lung function. Maternal smoking has been shown to affect lung development in utero and is linked with reduced lung function among offspring in adulthood.10,11 Passive smoking is also associated with reduced lung function, although this association is not as strong. The effect of smoking and smoking cessation on lung function is illustrated in Figure 1.
Occupational dusts and chemicals
Occupational dusts and chemicals have been recognised as co-factors for developing COPD and there is a relationship between the degree of lung impairment and the intensity and duration of exposure. Examples of implicated substances include organic and inorganic dusts, chemicals and fumes.2,12 A survey involving almost 10,000 adult patients showed that occupational exposure caused 19.2% of COPD cases, with 31.1% having never smoked.13 This is consistent with American Thoracic Society estimates of occupational exposure accounting for 10–20% of all COPD cases.14,15
Indoor air pollution
The burning of open fires of wood, animal dung, coal and agricultural residues (eg, for cooking and heating) can lead to high levels of indoor air pollution in poorly ventilated dwellings. The global population at risk of this form of COPD is three billion, with women in parts of the Middle East, Africa and Asia at particular risk.16 This COPD risk factor currently causes 10–20% of all cases worldwide and results in two million deaths each year.17
The best documented “host factor” for the development of COPD is the recessive, hereditary deficiency of α1-antitrypsin (Box 1). Predominantly affecting people of northern European origin, α1-antitrypsin deficiency results in the early and accelerated development of panlobular emphysema in smokers and non-smokers, with the risk in smokers increasing exponentially.18 Worldwide, α1-antitrypsin deficiency accounts for only a small number COPD cases.2,19
Other risk factors
Other risk factors for the development of COPD include:
- Lung growth and development: a meta-analysis has shown a positive correlation between birth weight and forced expiratory volume in one second (FEV1) (see “Diagnosis” below) in adulthood7,20
- Gender: the role of gender in the development of COPD is unclear, although some studies have suggested that women are more susceptible to the effects of tobacco smoke than men. Previous studies had shown a greater prevalence and mortality among men than women; however more recent studies show that in developed countries the prevalence is now similar, probably as a result of women living longer and their changing patterns of smoking2
- Infection: a history of tuberculosis and childhood infections have both been associated with reduced lung function and airflow obstruction that predisposes to COPD in later life.7,21 The development of pneumonia before two years of age has been shown to result in a mean loss in FEV1 of 0.65L in males, and twice that figure when associated with lifelong smoking22
- Socioeconomic status: the risk of developing COPD is inversely associated with affluence.23 Reasons are multifactorial and include greater smoking prevalence, poorer housing and poorer nutrition23
- Nutrition: a diet rich in fruit and vegetables is associated with a reduced risk of COPD24
- Asthma: the presence of asthma in adults results in a 12-fold increased risk of developing COPD.25 Approximately 20% of asthmatics develop signs of irreversible airway limitation26
COPD is characterised primarily by the presence breathlessness, chronic cough and sputum production. However, the early stages of COPD are often asymptomatic and it is not until patients experience significant limitation that they seek medical advice.
For patients, breathlessness (dyspnoea) is often the most concerning early symptom of COPD. It is persistent and progressive, and is usually worse with physical exertion. As the disease progresses, breathlessness becomes more problematic, even with minimal exertion or at rest.
The Medical Research Council dyspnoea scale (see Box 2), can be used to establish the extent of a patient’s exertional breathlessness and can help to predict mortality in COPD.2,27
In addition to defining the degree of dyspnoea-related disability associated with COPD, the MRC dyspnoea scale can also be used to determine at which stage pulmonary rehabilitation would be costeffective and indicated (see p393 of accompanying article). Pulmonary rehabilitation is indicated for patients admitted to hospital following a COPD exacerbation or for patients with an MRC score of 3 or higher.
Chronic cough is one of the earliest symptoms of COPD. Cough can be productive or unproductive and initially occurs intermittently, becoming more frequent as the disease progresses. Unlike breathlessness, chronic cough usually occurs at the earliest stage of COPD and is often discounted by patients as a sign of ageing or lack of physical fitness.
Regular production of sputum in three or more months over two consecutive years defines the presence of chronic bronchitis.2 However, sputum purulence in COPD patients varies considerably (in terms of quantity and colour, which may depend on the underlying causes of COPD) and is difficult to evaluate accurately due to differing patient habits with sputum (some patients will swallow rather than expectorate). A change in colour or volume of sputum may signify the early signs of an exacerbation of COPD.
Wheeze and chest tightness can occur at any stage of COPD, but usually occurs in severe COPD.2 More frequent “winter colds” or “winter bronchitis” and fatigue are also common among those with COPD.
A diagnosis of COPD should be considered in patients over the age of 35 years who have a risk factor such as smoking and who display one or more of the symptoms described above.28 The diagnosis should take into account the patient’s medical history and previous exposure to risk factors for the disease. Airflow obstruction can be measured accurately using spirometry, and this should be performed at the time of diagnosis, with specific reference to the following measures:2,28
- FEV1: volume of air that the patient is able to expel in the first second (expressed in litres and as a percentage of the predicted value)
- Forced vital capacity (FVC): total volume of air that the patient can forcibly exhale in one breath (expressed in litres and as a percentage of the predicted value)
- FEV1/FVC: the ratio of FEV1 to FVC
A post-bronchodilator FEV1/FVC ratio <0.7 confirms the presence of COPD.2,28 If the FEV1 is ≥80% of predicted, a diagnosis of COPD should only be made in the presence of other respiratory symptoms such as breathlessness or chronic cough.28
Similarities with asthma
COPD and asthma may have some overlapping symptoms but can be distinguished based on the patient’s history, exposure to risk factors and spirometry results. Box 3 shows the clinical features differentiating COPD and asthma. It is worth noting that, in patients with chronic asthma, the distinction with COPD is sometimes difficult to make and it is assumed that asthma and COPD can co-exist in such patients.2
If COPD diagnosis is in doubt, reversibility testing can help to distinguish the presence of COPD or another underlying respiratory disease such as asthma. Since COPD is characterised by airflow obstruction that is not fully reversible,28 reversibility testing using an inhaled bronchodilator (eg, salbutamol) can be used to distinguish between COPD and asthma. Minor degrees of reversibility have no prognostic value, but a marked post-bronchodilator response greater than 400ml suggests the presence of asthma.28
The severity of COPD can be classified according to the patient’s FEV1 compared with predicted values (see below). However, it should be borne in mind that severity based on FEV1 may not always correspond to the degree of symptom control and exacerbation rates.
Disease severity is an indicator of prognosis. The five-year survival of patients with mild COPD is 78% for men and 72% for women.29 This reduces to 30% and 24%, respectively, for patients with severe disease.29
Unsurprisingly, the economic impact of COPD also correlates with severity, with the annual cost for a patient with mild COPD estimated at £120 compared with over £3,000 for a patient with severe COPD.5
According to the National Institute for Health and Clinical Excellence and the Global Initiative for Chronic Obstructive Lung Disease, patients with a postbronchodilator FEV1/FVC ratio below 0.7 can be classified as follows:2,28
- FEV1 ≥80%: stage 1 (mild)
- FEV1 50–79%: stage 2 (moderate)
- FEV1 30–49%: stage 3 (severe)
- FEV1 <30%: stage 4 (very severe)
Some studies have found that an index known as “BODE” is a better predictor of exacerbations, hospital admission and mortality than FEV1.30–32 BODE is an acronym for:
- Body mass index
- Obstruction (degree of airway obstruction): measured as a percentage of predicted FEV1
- Dyspnoea: measured using a modified MRC dyspnoea scale
- Exercise tolerance: measured with a six-minute walk test
The BODE index is a 10-point scoring system, with a higher score corresponding with a higher likelihood for poor patient outcomes. (Box 4 shows how points on the BODE index are allocated.) The updated NICE guidelines suggest that the BODE index should be used to assess the prognosis of all patients. The BODE index can be modified to a “BOD” index if there is difficulty carrying out an exercise tolerance test.
The severity of COPD will also guide treatment (see accompanying article, p390).
- 1 Petty TL. The history of COPD. International Journal of COPD 2006:1;3–14.
- Global Initiative for Chronic Obstructive Lung Disease. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. 2008. www.goldcopd.com (accessed 29 October 2010).
- World Health Organization. Chronic respiratory diseases. www.who.int/ respiratory/copd/burden/en/index.html (accessed 29 October 2010).
- Hospital Episodes Statistics. Met Office health forecasts for COPD patients. www.hesonline.nhs.uk (accessed 29 October 2010).
- Department of Health. On the state of the public health: annual report of the chief medical officer 2004. July 2005. www.dh.gov.uk (accessed 29 October 2010).
- British Thoracic Society. The burden of lung disease. June 2006. www.brit-thoracic.org.uk (accessed 29 October 2010).
- Chapman KR, Mannino DM, Soriano JB, et al. Epidemiology and costs of chronic obstructive pulmonary disease. European Respiratory Journal 2006;27:188–207.
- Hoogendoorn M, Rutten-van Mölken MP, Hoogenveen RT, et al. A dynamic population model of disease progression in chronic obstructive pulmonary disease. European Respiratory Journal 2005;26:223–33.
- Lundbäck B, Lindberg A, Lindström M, et al. Not 15 but 50% of smokers develop COPD? Report from the obstructive lung disease in Northern Sweden studies. Respiratory Medicine 2003;97:115–22.
- Barker DJP. Chronic bronchitis. In: Mothers, babies and disease in later life. London: BMJ Publishing Group, 1994; pp94–105.
- Tager IB, Ngo L, Hanrahan JP. Maternal smoking during pregnancy. Effects on lung function during the first 18 months of life. American Journal of Respiratory and Critical Care Medicine 1995;152:977–83.
- Isoaho R, Puoluoki H, Huhti E, et al. Prevalence of chronic obstructive pulmonary disease in elderly Finns. Respiratory Medicine 1994;88:571–80.
- Hnizdo E, Sullivan PA, Bang KM, et al. Association between chronic obstructive pulmonary disease and employment by industry and occupation in the US population: a study of data from the Third National Health and Nutrition Examination Survey. American Journal of Epidemiology 2002;156:738–46.
- Trupin L, Earnest G, San Pedro M, et al. The occupational burden of chronic obstructive pulmonary disease. European Respiratory Journal 2003;22:462–9.
- Balmes J, Becklake M, Blanc P, et al. American Thoracic Society statement: occupational contribution to the burden of airway disease. American Journal of Respiratory and Critical Care Medicine 2003;167:787–97.
- Chan-Yeung M, Ait-Khaled N, White N, et al. The burden and impact of COPD in Asia and Africa. International Journal of Tuberculosis and Lung Disease 2004;8:2–14.
- Smith K. Pollution management in focus. Washington DC: The World Bank; 1999.
- Blanco I, de Serres FJ, Fernandez-Bustillo E, et al. Estimated numbers and prevalence of PIS and PIZ alleles of alpha1-antitrypsin deficiency in European countries. European Respiratory Journal 2006;27:77–84.
- Sandford AJ, Weir TD, Paré PD. Genetic risk factors for chronic obstructive pulmonary disease. European Respiratory Journal 1997;10:1380–91.
- Lawlor DA, Ebrahim S, Davey Smith G. Association of birth weight with adult lung function: findings from the British Women’s Heart and Health Study and a meta-analysis. Thorax 2005;60:851–8.
- Menezes AM, Hallal PC, Perez-Padilla R, et al. Tuberculosis and airflow obstruction: evidence from the PLATINO study in Latin America. European Respiratory Journal 2007;(6):1180–5.
- Shaheen SO, Barker DJP, Shiell AW, et al. The relationship between pneumonia in early childhood and impaired lung function in late adult life. American Journal of Respiratory Critical Care Medicine 1994;149:616–9.
- Prescott E, Lange P, Vestbo J. Socioeconomic status, lung function and admission to hospital for COPD: results from the Copenhagen City Heart Study. European Respiratory Journal 1999;13:1109–14.
- Watson L, Margetts B, Howarth P, et al. The association between diet and chronic obstructive pulmonary disease in subjects selected from general practice. European Respiratory Journal 2002;20:313–8.
- Silva GE, Sherrill DL, Guerra S, et al. Asthma as a risk factor for COPD in a longitudinal study. Chest 2004;126:5965.
- Vonk JM, Jongepier H, Panhuysen CI, et al. Risk factors associated with the presence of irreversible airflow limitation and reduced transfer coefficient in patients with asthma after 26 years of follow up. Thorax 2003;58:322–7.
- Bestall JC, Paul EA, Garrod R, et al. Usefulness of the Medical Research Council (MRC) dyspnoea scale as a measure of disability in patients with chronic obstructive pulmonary disease. Thorax 1999;54:581–6.
- National Institute for Health and Clinical Excellence. Management of chronic obstructive pulmonary disease in adults in primary and secondary care. June 2010. www.nice.org.uk/cg101 (accessed 29 October 2010).
- Soriano JB, Maier WC, Egger P, et al. Recent trends in physician diagnosed COPD in women and men in the UK. Thorax 2000;55:789–94.
- Ong KC, Earnest A, Lu SJ. A multidimensional grading system (BODE index) as predictor of hospitalization for COPD. Chest 2005;128:3810–6.
- Marin JM, Carrizo SJ, Casanova C, et al. Prediction of risk of COPD exacerbations by the BODE index. Respiratory Medicine 2009;103:373–8.
- Celli BR, Cote CG, Marin JM, et al. The body-mass index, airflow obstruction, dyspnea, and exercise capacity index in chronic obstructive pulmonary disease. New England Journal of Medicine 2004;350:1005–12.