Chronic obstructive pulmonary disease (COPD) is mostly caused by smoking, which leads to progressive irreversible airflow limitation. Optimal drug treatment can reduce exacerbations and improve quality of life.

Use spirometry to diagnose COPD early

Consider a diagnosis of COPDfor any current or ex-smokerover the age of 35 years [1,2]

In early COPD, airflow limitation is often asymptomatic.[1,2] Patients usually seek medical help at a stage of dyspnoea when airflow limitation may already be moderate to severe.[1,2]

Consider a diagnosis for patients with other smoking-related conditions; there is a high prevalence of COPD in patients with vascular disease and smokingrelated carcinomas.[1]

Spirometry is needed to confirm the diagnosis [1,2]

Spirometry demonstrates airflow limitation. Physical examination or peak expiratory flow measurements alone are not diagnostic.[1,2] Airflow limitation is not fully reversible when, after administering a bronchodilator:

• FEV1 (forced expiratory volume in one second) is < 80% predicted, and
• FEV1 to FVC (forced vital capacity) ratio is < 70%.[1,2]

Consider asthma if there are reversible components

Spirometry also identifies patients at risk; an early indicator of COPD is when FEV1 is > 80% but FEV1/FVC is < 70%.[1]

A clinically significant response to a bronchodilator is an increase in FEV1 > 200 mL and > 12% above pre-bronchodilator level.[1,2] Consider referral to a respiratory physician to exclude other diagnoses or complications.[1]

Stopping smoking is the most important intervention

Brief intervention by a healthcare professional helps smokers to quit

Provide brief counselling (3–5 minutes) on smoking cessation by using the 5As approach:

• Ask and identify smokers at every visit
• Advise about the risks of smoking and benefits of quitting
• Assess the motivation to quit
• Assist cessation
• Arrange follow-up within a week of the quit date and one month after.[1–3]

Offer intensive intervention and/or pharmacotherapy

Telephone counselling (e.g. Quitline), group behavioural therapy, or counselling by a smoking cessation specialist can help smokers to quit.[3]

Use nicotine replacement therapy with brief or intensive interventions 

Consider adding pharmacotherapy to counselling and support if patients smoke more than 10 cigarettes/day: cessation rates after 6–12 month srange from 5–15% with placebo and 10–30% with either nicotinereplacement therapy or bupropion (Zyban SR).[3–7]

Choose one nicotine product (gum, tablets or lozenges, patches or inhaler) and continue for up to 12 weeks.[8] Heavy smokers may benefit from using a higher dose.[3,8] 

Only use bupropion with intensive intervention

Bupropion* only has evidence for an effect in conjunction with intensive counselling and support.[3,6] Start bupropion at least 7 days before the quit date and continue for 7–9 weeks.[8]

Combine therapies for smokers who relapse

Offer a combination of nicotine products (e.g. patches and gum) and/or intensify counselling and support, if one nicotine product is ineffective alone.[3,8] Add bupropion if a further relapse occurs.[3,5]

Introduce stepwise drug treatment in stable COPD

Drug treatments improve symptoms and quality of life

Monitor patients for changes in symptoms, daily activities and exercise capacity; improvements can occur without changes in FEV1.[1,2,9,10] For patients with COPD and asthma, treat as for asthma.[1]

Start with inhaled shortacting bronchodilators

Use a short-acting beta2 agonist (salbutamol [Airomir, Asmol, Epaq] or terbutaline [Bricanyl]) or anticholinergic (ipratropium [Atrovent]) asneeded.[1,2,9,10] Start regular treatment if symptoms worsen.[10] Ipratropiumis suitable for regular use because it has a relatively long duration of action.[1,10] If needed, combine salbutamol or terbutaline with ipratropium† to improve symptom control and limit adverse effects.[1,10]

Step up to a long-acting bronchodilator if needed 

Use a long-acting anticholinergic (tiotropium [Spiriva]) or long-acting beta2 agonist (eformoterol [Foradile, Oxis] or salmeterol [Serevent])† if symptoms are not controlled by short-acting bronchodilators.[1,9,10] If symptoms persist, try a different long-acting bronchodilator or combine a long-acting anticholinergic and beta2 agonist.[9]

Tiotropium may be of more benefit than ipratropium to patients with frequent exacerbations

Tiotropium reduces exacerbations in patients with moderate to severeCOPD — treating 14 patients with tiotropium for 1 year, instead of ipratropium or placebo, prevents 1 exacerbation.[11] Tiotropium is more likely than ipratropium to cause anticholinergic side-effects, particularly dry mouth; it may be unsuitable for patients intolerant of ipratropium.[8,11]

Reassess response to long-acting beta2 agonists if patients report no improvement 

The effects of long-acting beta2 agonists are generally small and
inconsistent between studies.[12–24] Patients with the greatest response to long-acting beta2 agonists have some reversible airflow limitation.[13–17]

Stop salmeterol or eformoterol if there is no change after 4 weeks.[9,10,25] Restart if symptoms worsen; consider adding tiotropium to improve symptom control.[9,10]

Consider inhaled corticosteroids in moderate to severe COPD (FEV1 ≤ 50%)

Start an inhaled corticosteroid, with or without a long-acting beta2 agonist†, for patients with:

• a documented response to a short course (2 weeks) of oral corticosteroid, or
• 2 or more exacerbations per year requiring treatment with antibiotics or oral corticosteroids.[1,2,9,10]

Oral corticosteroids do not predict the response to inhaled corticosteroids and should not be used to identify patients for such treatment.[1,9,10] Assess response to inhaled corticosteroids by monitoring FEV1 and symptoms every 2 weeks; stop if there is no improvement after 6 weeks.[10] Inhaled corticosteroids reduce exacerbations compared with placebo (relative risk reduction 30%, 95% CI 16% to 42%).[26] This has been shown in patients with reversible or irreversible airflow limitation, but only with high doses and only in moderate to severe COPD.[26–28]

Combining an inhaled corticosteroid and a long-acting beta2 agonist improves symptoms and health-related quality of life, compared with inhaled corticosteroids alone.[22–24,29]

Minimise systemic absorption of inhaled corticosteroids

Instruct patients to rinse their throat and mouth with water, and spit out, after inhalation.[8,10] Advise patients who use a metered-dose inhaler (MDI) that a spacer reduces the risk of dysphonia.[8,10]

Inhaled corticosteroids at high doses can increase the risk of osteoporosis, especially in patients with COPD; bruising and cataracts may also occur.[1,8,10]

Consider theophylline if symptoms persist despite inhaled bronchodilators

Use theophylline for patients who do not respond to short-acting and/or long-acting bronchodilators, or who cannot use inhaled therapy.[1,9,10] Only slow-release preparations have shown benefit in COPD.[1,2] For further guidance on stepwise drug treatment for stable COPD see NPS News 45.

Check inhaler technique regularly

Optimal technique can be achieved with an MDI, breath-activated inhaler (e.g. Autohaler) or dry powder inhaler (DPI); however, ability to use varies and can decline within 2 months of first instruction.[9,10,30] Where possible, minimise the different types of inhaler that the patient needs to use.

Nebulisers do not improve lung function

Use a spacer if the patient has difficulty with inhaler devices.[8,9] Reserve nebulisers for symptoms which persist despite maximum inhaled therapy — nebulisers do not improve lung function compared with an MDI (with or without spacer) or DPI.[9,10,30]

Complete a COPD action plan for acute exacerbations

Detect and manage exacerbations early to prevent deterioration and hospital admission[1]

Give a COPD action plan to patients and/or their carers (available from the Australian Lung Foundation, www.lungnet.org.au). Consider supplying oral corticosteroids and/or antibiotics as part of the patient’s management plan, to assist early treatment. Instruct patients to start treatment if there is an increase in 1 or more symptoms of: cough, wheeze or breathlessness;
sputum purulence and/or volume; or fever.[1,2,9,10]

Increase use of short-acting bronchodilators [1,10] 

Only use a nebuliser for exacerbations if symptoms persist using a spacer; if bronchodilators are needed more than 3 hourly, tell the patient to get medical attention.[1,10] Step down treatment when symptoms resolve and review management.

Start a short course of oral corticosteroid

Use oral prednisolone 30–50 mg daily for 7–14 days then stop without taper; where continuous treatment is needed use the lowest dose.[1,9,10] Oral corticosteroids prevent hospital re-admission or changes to therapy, restore lung function and improve dyspnoea in patients with acute exacerbations.[31]

Use antibiotics only if sputum purulence is present with increased sputum volume and/or dyspnoea[10]

Prescribe amoxycillin or doxycycline for 5–10 days; only use a macrolide antibiotic (e.g. erythromycin, roxithromycin), cephalosporin or amoxycillin plus clavulanic acid if there is no response to these and only use a macrolide if Haemophilus influenzae has been excluded.[1,2,10] There is no evidence for
antibiotic prophylaxis.[1,2]

Influenza vaccinations reduce the relative risk of exacerbations, hospitalisation and death by 50%.1,2 Pneumococcal vaccination is also recommended.[1,2,10]

Expert reviewers

Assoc Prof David McKenzie, Head of Department,
Respiratory and Sleep Medicine,
Prince of Wales Hospital, Randwick

References 

1. Australian Lung Foundation and Thoracic Society of Australia and New Zealand. The COPD-X Plan:Australian and New Zealand guidelines for the management of chronic obstructive pulmonary
disease. Australian Lung Foundation, 2005.

2. Global Initiative for Chronic Obstructive Lung Disease
(GOLD COPD). Global strategy for the diagnosis,management, and prevention of chronic obstructive pulmonary disease. GOLD COPD, 2005.

3. Miller M,Wood L. Smoking cessation interventions:review of evidence and implications for best practice in health care settings. Canberra: Australian Government Department of Health and Ageing, 2002.

4. The Royal Australian College of General Practitioners (RACGP). Smoking, Nutrition, Alcohol and Physical activity (SNAP). A population health guide to behavioural risk factors in general practice. Melbourne: RACGP, 2004.

5 Jorenby DE, et al. N Engl J Med 1999;340:685–91.

6. Woolacott NF, et al. Health Technol Assess 2002;6(16).

7. Tashkin D, et al. Lancet 2001;357:1571–5.

8. Australian Medicines Handbook 2006.

9. National Institute for Clinical Excellence (NICE). Chronic obstructive pulmonary disease: management of chronic obstructive pulmonary disease in adults in primary and secondary care. London: NICE, 2004.

10. Therapeutic Guidelines. Respiratory, 2005.

11. Barr R, et al. Cochrane Database Syst Rev 2005;(2):CD002876.

12. Brusasco V, et al. Thorax 2003;58:399–404.

13. Aalbers R, et al. Eur Resp J 2002;19:936–43.

14. Mahler DA, et al. Chest 1999;115:957–65.

15. Appleton S, et al. Cochrane Database Syst Rev 2001;(4):CD001104.

16. Rossi A, et al. Chest 2002;121:1058–69.

17. Hanania NA, et al. Chest 2003;124:834–43.

18. Donohue JF, et al. Chest 2002;122:47–55.

19. Shukla V, et al. Long-acting beta-2-agonists for maintenance therapy of stable chronic obstructive pulmonary disease: a systematic review. Ottawa:
Canadian Coordinating Office for Health Technology Assessment, 2002.

20. Wadbo M, et al. Eur Resp J 2002;20:1138–46.

21. Boyd G, et al. Eur Resp J 1997;10:815–21.

22. Szafranski W, et al. Eur Resp J 2003;21:74–81.

23. Calverley P, et al. Lancet 2003;361:449–56.

24. Calverley PM, et al. Eur Resp J 2003;22:912–9.

25. Institute for Clinical Systems Improvement (ICSI). Chronic Obstructive Pulmonary Disease. Health Care Guideline. Bloomington: ICSI, 2005.

26. Alsaeedi A, et al. Am J Med 2002;113:59–65.

27. Burge PS, et al. BMJ 2000;320:1297–303.

28. Vestbo J, et al. Lancet 1999;353:1819–23.

29. Nannini L, et al. Cochrane Database Syst Rev2004;(3):CD003794.

30. Brocklebank D, et al. Health Technol Assess 2001;5(26).

31. Wood-Baker R, et al. Cochrane Database Syst Rev 2005;(1):CD001288.