Diagnostic considerations when COPD is a possibility
Consider the possibility of COPD as an alternative diagnosis or asthma–COPD overlap in patients with respiratory symptoms and any of the following risk factors:
- current smoking or history of smoking and age 35 years and over
- exposure to environmental tobacco smoke or other smoke
- age 55 years and over
- longstanding asthma.
If spirometry before and after bronchodilator demonstrates airflow limitation that is not completely reversible in an adult with risk factors for COPD, consider the possibility of COPD, even if the person has never smoked.
- How this recommendation was developed
Based on clinical experience and expert opinion (informed by evidence, where available), with particular reference to the following source(s):
- Abramson et al. 20123
If an adult has risk factors for COPD, spirometry before and after bronchodilator demonstrates airflow limitation that is not completely reversible, and other diagnostic tests do not confirm asthma, start a treatment trial with an inhaled corticosteroid and repeat spirometry 6–8 weeks later.
After the trial of inhaled corticosteroid treatment, the diagnosis of asthma is supported if pre-bronchodilator spirometry shows that airflow limitation has resolved, or if spirometry before and after bronchodilator demonstrates airflow limitation that is fully reversible.
- How this recommendation was developed
Based on clinical experience and expert opinion (informed by evidence, where available)
Identify patients with characteristics strongly favouring either asthma or COPD. If several features of both are present and neither is strongly favoured, manage according to recommendations for asthma–COPD overlap. If the diagnosis is unclear, consider referral to a specialist respiratory physician.
Note: It is clinically important to identify asthma features because, in patients with features of both asthma and COPD, (1) treatment should always include an inhaled corticosteroid to reduce risk of flare-ups and asthma-related death, and (2) the use of long-acting beta2 agonist or long-acting muscarinic antagonist without concomitant inhaled corticosteroid should be avoided to reduce the risk of flare-ups and asthma-related death.
- How this recommendation was developed
Based on clinical experience and expert opinion (informed by evidence, where available).
- Risk factors for COPD
Smoking is the most important risk factor for COPD.4 Current national COPD guidelines recommend that COPD should be considered in all smokers and ex-smokers over 35 years, and in all patients with other smoking-related diseases.4
- exposure to environmental tobacco smoke
- occupational exposure to dusts and fumes
- exposure to biological dust, diesel exhaust
- exposure to smoke from biomass fuels
- genetic predisposition (alpha1 antitrypsin deficiency) interacting with environment (e.g. smoking)
Other risk factors for fixed (irreversible or incompletely reversible) airflow limitation include:1
- inadequate maximal lung function achieved in early life (e.g. due to untreated asthma or severe asthma in early childhood, premature birth, or bronchopulmonary dysplasia)
- longstanding asthma.
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- Diagnosis of COPD
The main symptoms of COPD are:4
- sputum production.
Patients often attribute breathlessness to ageing or poor cardiopulmonary fitness. A persistent cough, typically worse in the mornings with mucoid sputum, is common in smokers.
Other common symptoms of COPD include chest tightness, wheezing, fatigue and airway irritability.4
- a history of smoking or exposure to other noxious agents
- post-bronchodilator FEV1/FVC < 0.7 (or < lower limit of normal).
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- Asthma–COPD overlap
Distinguishing between typical allergic asthma (childhood-onset allergic asthma) and typical COPD (emphysema in a heavy smoker) is straightforward.6 However, it can be difficult to distinguish COPD from asthma in adults who have features of both conditions.7, 8These people are described as having asthma–COPD overlap.7, 6, 9
Asthma–COPD overlap is not a single, well-defined disease entity, but includes a range of airway disease phenotypes with different causal mechanisms.7, 10 Features of both asthma and COPD have been described in:9, 11, 12, 13
- people with current asthma (allergic or non-allergic) who have had significant exposure to tobacco smoke
- people with longstanding asthma or late-onset asthma who have become persistently short of breath over time
- people significant smoking history and symptoms consistent with COPD who also have a history of childhood asthma
- people who present in middle age or later with shortness of breath, with a history of childhood asthma but no or few symptoms in between, and little smoking history.
Figure. Development of asthma, COPD and asthma–COPD overlap Please view and print this figure separately: http://www.asthmahandbook.org.au/figure/show/108
- high need for healthcare services
- worse quality of life, more wheezing, dyspnoea, cough and sputum production, and more frequent and severe respiratory exacerbations and hospitalisations, than people with COPD or asthma alone
- worse lung function demonstrated by spirometry than those with COPD alone, despite lower average exposure to tobacco smoke.
Features of asthma, COPD and asthma–COPD overlap
If several features of both asthma and COPD are present and neither condition is strongly favoured, respiratory disease should be managed according to recommendations for asthma–COPD overlap.
Treatment for patients with asthma–COPD overlap
Most patients also need treatment with a long-acting bronchodilator (either long-acting beta2 agonist or long-acting muscarinic antagonist) in addition to an inhaled corticosteroid. Long-acting beta2 agonists and long-acting muscarinic antagonists should not be used by people with asthma or asthma–COPD overlap unless they are also taking an inhaled corticosteroid (either in combination or separately).
Management should also include smoking cessation, treatment of comorbid conditions, physical activity, pulmonary rehabilitation, vaccinations, self-management (including a regularly updated action plan) and regular follow-up.7
Respiratory tract infections should be monitored carefully because people with asthma–COPD overlap have high morbidity rates and because ICS treatment is associated with increased risk of non-fatal pneumonia in people with COPD.19 Most of the available evidence is from patients treated with fluticasone propionate, particularly at higher doses. Increased pneumonia rates have also been observed in studies of patients with COPD using fluticasone furoate/vilanterol. The higher dose of fluticasone furoate/vilanterol (Breo Ellipta 200/25 microg) is not approved for patients with COPD, so it should also not be used in patients with asthma–COPD overlap.
Specialist referral should be considered for patients with atypical symptoms or symptoms that suggest an alternative diagnosis, persistent symptoms or flare-ups despite treatment, or complex comorbidities.
For information on diagnosis and management of COPD, refer to the COPD-X Concise Guide for Primary Care.20
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- Definition of variable expiratory airflow limitation
Most of the tests for variable expiratory airflow limitation are based on showing variability in FEV1. While reduced FEV1 may be seen with many other lung diseases (or due to poor spirometric technique), a reduced ratio of FEV1 to FVC indicates airflow limitation.21 Normal FEV1/FVC values derived from population studies vary,22, 23 but are usually greater than:22
- 0.85 in people aged up to 19 years
- 0.80 in people aged 20–39 years
- 0.75 in people aged 40–59 years
- 0.70 in people aged 60–80 years.
In children, it is less useful to define expiratory airflow limitation according to a specific cut-off for FEV1/FVC ratio, because normal values in children change considerably with age.23
Some spirometers provide predicted normal values specific to age group. If these are available, a FEV1/FVC ratio less than the lower limit of normal (i.e. less than the 5th percentile of normal population) indicates airflow limitation.
Variable expiratory airflow limitation (beyond the range seen in healthy populations) can be documented if any of the following are recorded:
- a clinically important increase in FEV1 (change in FEV1 of at least 200 mL and 12% from baseline for adults, or at least 12% from baseline for children) 10–15 minutes after administration of bronchodilator
- clinically important variation in lung function (at least 20% change in FEV1) when measured repeatedly over time (e.g. spirometry on separate visits)
- a clinically important reduction in lung function (decrease in FEV1 of at least 200 mL and 12% from baseline on spirometry, or decrease in peak expiratory flow rate by at least 20%) after exercise (formal laboratory-based exercise challenge testing uses different criteria for exercise-induced bronchoconstriction)
- a clinically important increase in lung function (at least 200 mL and 12% from baseline) after a trial of 4 or more weeks of treatment with an inhaled corticosteroid
- clinically important variation in peak expiratory flow (diurnal variability of more than 10%)
- a clinically important reduction in lung function (15–20%, depending on the test) during a test for airway hyperresponsiveness (exercise challenge test or bronchial provocation test) measured by a respiratory function laboratory.
Patients referred to a respiratory function laboratory may be asked not to take certain medicines within a few hours to days before a spirometry visit.
A clinically important increase or decrease in lung function is defined as a change in FEV1 of at least 200 mL and 12% from baseline for adults, or at least 12% from baseline for children, or a change in peak expiratory flow rate of at least 20% on the same meter.24, 21 A clinically important increase in FVC after administering bronchodilator may also indicate reversible airflow limitation, but FVC is a less reliable measure in primary care because FVC may vary due to factors such as variation in inspiratory volume or expiratory time.
The finding of ‘normal’ lung function during symptoms reduces the probability that a patient has asthma, but a clinically important improvement in response to bronchodilator or inhaled corticosteroid can occur in patients whose baseline value is within the predicted normal range.
The greater the variation in lung function, the more certain is the diagnosis of asthma. However, people with longstanding asthma may develop fixed airflow limitation.
Reversibility in airflow limitation may not be detected if the person is already taking a long-acting beta2 agonist or inhaled corticosteroid.
Airflow limitation can be transient and does not necessarily mean that the person has asthma (e.g. when recorded during a severe acute infection of the respiratory tract). Ideally, airflow limitation should be confirmed when the patient does not have a respiratory tract infection. Reduction in lung function during a respiratory tract infection with improvement in lung function after its resolution, commonly occurs in people with asthma, but can also be seen in patients with COPD or in healthy people without either asthma or COPD.25,26Close
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- Guerra S. Asthma and chronic obstructive pulmonary disease. Curr Opin Allergy Clin Immunol. 2009; 9: 409-16. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2832909/
- Abramson MJ, Crockett AJ, Dabscheck E, et al. The COPD-X Plan: Australian and New Zealand guidelines for the management of chronic obstructive pulmonary disease. Version 2.34. The Australian Lung Foundation and The Thoracic Society of Australia and New Zealand, 2012. Available from: http://www.copdx.org.au/
- Abramson, M, Frith, P, Yang, I, et al. COPD-X concise guide for primary care. Lung Foundation Australia, Brisbane, 2017.
- Yousef, E., Hossain, J., Mannan, S., et al. Early intervention with high-dose inhaled corticosteroids for control of acute asthma exacerbations at home and improved outcomes: a randomized controlled trial. Allergy Asthma Proc. 2012; 33: 508-13. Available from: https://www.ncbi.nlm.nih.gov/pubmed/23394509
- Knorr, B, Matz, J, Bernstein, JA, et al. Montelukast for chronic asthma in 6- to 14-year-old children: a randomized, double-blind trial. Pediatric Montelukast Study Group. JAMA. 1998; 279: 1181-1186. Available from: https://www.ncbi.nlm.nih.gov/pubmed/9555757
- Zeiger, RS, Szefler, SJ, Phillips, BR, et al. Response profiles to fluticasone and montelukast in mild-to-moderate persistent childhood asthma. J Allergy Clin Immunol. 2006; 117: 45-52. Available from: https://www.ncbi.nlm.nih.gov/pubmed/16387583
- Becker, A, Swern, A, Tozzi, C A, et al. Montelukast in asthmatic patients 6 years-14 years old with an FEV1 > 75%. Curr Med Res Opin. 2004; 20: 1651-1659. Available from: https://www.ncbi.nlm.nih.gov/pubmed/15462699
- Gibson PG, Simpson JS. The overlap syndrome of asthma and COPD: what are its features and how important is it?. Thorax. 2009; 64: 728-735. Available from: http://thorax.bmj.com/content/64/8/728.full
- Stempel, D. A., Szefler, S. J., Pedersen, S., et al. Safety of adding salmeterol to fluticasone propionate in children with asthma. N Engl J Med. 2016; 375: 840-9. Available from: https://www.ncbi.nlm.nih.gov/pubmed/27579634
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- Reed CE. Asthma in the elderly: diagnosis and management. J Allergy Clin Immunol. 2010; 126: 681-7; quiz 688-9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20673985
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