Section 1: Epidemiology and aetiology
COPD is a chronic inflammatory condition of the airways and lung parenchyma, characterised by persistent airflow obstruction that is usually irreversible and progressive.1
In contrast, asthma is characterised by variable airflow obstruction that is usually reversible and rarely progressive in severity.
COPD consists of a variable mixture of pathological lung lesions: emphysema with destruction of the alveolar walls and development of airspaces; airways inflammation; mucous gland hyperplasia in larger airways; and fibrosis mainly in smaller airways.
COPD is also associated with extra-pulmonary systemic effects, which may contribute to the severity of disease in individual patients.2
The global economic and social burden of COPD is enormous. By 2020, COPD is expected to increase from the sixth to the third most common cause of death worldwide and become the third most common cause of morbidity.
It has been estimated approximately 2 per cent of the UK population has COPD, but this figure represents the 'tip of the iceberg' as many patients remain undiagnosed.3,4
The single most important risk factor for the development of COPD is cigarette smoking, which causes 80-90 per cent of all cases.
Noxious particles and gases in cigarette smoke cause an irritant immunological and inflammatory response in the airways and lung parenchyma. However, there is large individual susceptibility to the effects of cigarette smoking, as demonstrated by the many smokers ((approx)75 per cent) who never develop significant airflow obstruction and COPD.
Other risk factors include environmental air pollution, occupational exposures (coal and gold mining, cement and cotton industries, cadmium workers), genetics (e.g. alpha-1 antitrypsin deficiency), childhood respiratory illness (predisposes to chronic adult disease), recurrent bronchopulmonary infections, low socioeconomic status, poor diet and chronic asthma.
The burning of indoor biomass cooking fuels represents a significant risk factor in developing countries.
Section 2: Diagnosis
A combination of medical history, risk factor assessment, physical examination and confirmation of airflow obstruction on spirometry are required to make a diagnosis.
COPD should be considered in patients over the age of 35 years who have a risk factor (usually smoking) and who report progressive exertional dyspnoea, chronic cough, regular sputum production and/or wheeze.
It is important to enquire about weight loss and haemoptysis (underlying carcinoma), nocturnal wakening (sleep-related disorder) and ankle oedema or chest pain (concomitant cardiac pathology).
Documentation of exercise tolerance using the MRC dyspnoea scale (see box below) with activities of daily living and quality of life should be recorded and how these have changed over the past months/years.
|Medical Research Council (MRC) Dyspnoea Scale|
Grade Degree of patient's breathlessness
1. Not troubled by breathlessness except on strenuous exercise.
2. Short of breath when hurrying or walking up a slight hill.
3. Walks slower than contemporaries on the level because of breathlessness, or has to stop for breath when walking at own pace.
4. Stops for breath after about 100m or after a few minutes on the level.
5. Too breathless to leave the house, or breathless when dressing or undressing.
Estimate smokers' 'pack-years' (one pack year = 20 cigarettes a day for one year).
Signs of nicotine-stained fingernails, anaemia, clubbing and lymphadenopathy, bounding pulse (CO2 retention seen in type-2 respiratory failure), raised jugular venous pressure (pulmonary hypertension) and ankle oedema (right ventricular failure) should be looked for.
Signs of hyperinflated lungs may be suggested by a 'barrel chest', indrawing of the intercostal muscles and a hyper-resonant percussion note. In this situation, breath sounds may sometimes be difficult to hear.
A full assessment of a patient with COPD must include spirometry. Airflow obstruction is defined as an FEV1 <80 per cent predicted and an 'obstructive' FEV1/FVC ratio of <70 per cent (where FVC is forced vital capacity).
An obstructive spirometry is compatible with a diagnosis of both COPD and asthma. However, in COPD, unlike asthma, there is usually poor bronchodilator reversibility, which is defined as FEV1 <15 per cent reversibility (or increase <200ml) 20 minutes after inhaled short-acting beta-2 agonist compared with baseline value.
Reversibility to oral corticosteroids (30mg daily prednisolone for two weeks) is often helpful to exclude patients with underlying asthma.
In primary care, newly diagnosed patients should have a BMI calculation (review weight loss), chest radiography (exclude other pathology), FBC to assess anaemia or polycythaemia (secondary to hypoxaemia) and biochemistry for alpha-1 anti-trypsin deficiency, especially in young people (<50 years) with a minimal smoking history.
Patients who produce sputum on a regular basis should have samples assessed for microscopy, culture and sensitivities.
Where the degree of breathlessness is out of proportion to the spirometry results or there is uncertainty in the diagnosis, referral may be necessary.
Pulse oximetry may be useful in general practice to monitor stable patients, assess acute respiratory exacerbations, as a screening tool for patients requiring long-term oxygen therapy (LTOT) and assess the need for a fitness-to-fly test.5
Oxygen saturations ≤ 92 per cent at rest should warrant an outpatient hospital assessment for oxygen therapy.
Section 3: Management
The aims of treatment are to relieve symptoms, improve exercise/functional capacity, optimise lung function and prevent exacerbations and long-term complications.
Smoking cessation advice should be given to all COPD patients who smoke at every opportunity, irrespective of disease severity.6
Smoking cessation programmes usually combine pharmacotherapy, including NRT, bupropion and varenicline, with psychosocial support.
Small airways bronchoconstriction contributes to the expiratory airflow limitation in COPD patients and bronchodilators (beta-2 agonists, antimuscarinics and oral methylxanthines) form the mainstay of drug therapy. Combining drugs with different mechanisms of action may result in additional bronchodilation.
Inhaled corticosteroid (ICS) monotherapy does not appear to affect the rate of decline in lung function. However, recent randomised trials have shown that ICS in combination with long acting beta-agonists (LABA) reduce the number and severity of exacerbations and improve health status.7
NICE guidelines recommend ICS-LABA inhalers are used in patients with FEV1 <50 per cent predicted and with more than two exacerbations per year.6
Due to their systemic side-effects, oral corticosteroids should be reserved for exacerbations, where they have been shown to improve lung function and gas exchange.
The use of LTOT for >15 hours a day has been shown to increase survival and reduce the morbidity of COPD patients with chronic respiratory failure.
LTOT is recommended for patients with stable disease who have a PaO2 <7.3kPa corresponding to arterial oxygen saturations SaO2 <88 per cent. Patients with cor pulmonale with a PaO2 between 7.3-7.8kPa at rest may also benefit from LTOT.
Some patients experience arterial desaturation during exercise or episodic breathlessness and supplemental ambulatory oxygen may be provided in these circumstances. Short-burst oxygen therapy may help some patients with end-stage COPD.
Commercial air travel presents a special situation where COPD patients can experience significant in-flight desaturations. Patients with an FEV1 <50 per cent predicted, resting oxygen saturation of <92 per cent at rest, known bullae on imaging or those already receiving LTOT should be assessed.
NICE recommends the use of non-invasive ventilation (NIV) as the treatment of choice for persistent hypercapnic ventilatory failure during hospital exacerbations, despite optimal medical therapy.6 In this scenario, NIV has been shown to improve survival and reduce the need for mechanical ventilation.8
NIV can also be used as a bridge to lung transplantation.
Pulmonary rehabilitation programmes involve physical training, disease education, nutritional and psychosocial support, and have been demonstrated to provide improvements.9
Pulmonary rehabilitation should be offered to COPD patients who are MRC grade 3 (see box above) and prior to consideration for surgical intervention.
Pneumococcal and annual influenza vaccination should be offered to all patients with COPD. The antiviral zanamivir should be used with caution in patients with COPD because of the risk of bronchospasm.
Anxiety and depression can co-exist in patients with COPD and may exacerbate their perception of breathlessness. Simple validated assessment tools (e.g. Hospital Anxiety and Depression score) may help to screen such patients in general practice in addition to a directed clinical history.
Patients should be referred to a dietitian if their BMI is low, in addition to being given nutritional supplements to increase their daily intake of calories.
Diuretics may often be helpful in controlling peripheral ankle oedema in patients with cor pulmonale.
Mucous hypersecretion and retention in the airways often contribute to the symptoms of COPD. Effective therapy to aid mucus clearance may provide benefit. However, few data support the use of regular mucolytic treatments in COPD.
In contrast, antitussive therapy, such as codeine and dextromethorphan, should be avoided in the management of stable COPD, particularly because opiates may depress the respiratory drive. Opiates may be helpful, however, as part of the palliative care of breathlessness in end-stage COPD.
Surgery may benefit carefully selected patients with severe COPD with or without large hyperinflated lungs. Options include bullectomy, lung volume reduction surgery and lung transplantation in very severe cases.
Section 4: Prognosis and care in the community
It is important to assess if there is an obvious cause for deterioration, e.g. a bacterial infection, with a sputum assessment prior to treating with antibiotics.
Inhaled bronchodilators should be used, in addition to a short course of oral corticosteroids (30mg prednisolone daily for 7-14 days maximum).
Clinical conditions that may mimic a COPD exacerbation include pneumothorax, pneumonia, pulmonary oedema, pulmonary embolus, lung cancer and pleural effusion.
The only interventions that have been shown to reduce mortality are smoking cessation, LTOT in chronic respiratory failure and lung-volume reduction surgery in selected patients.
It is important to note that CVD (MI, cerebrovascular and thromboembolic disease) remain the leading cause of death in patients with COPD (not respiratory failure), thought to be due to systemic inflammation resulting from COPD.2
A recent study has shown that the addition of tiotropium reduces the rate of serious cardiac events in patients with COPD.10
Prognosis is dependent upon disease severity and rate of decline in lung function: the lower the lung function and the greater the rate of decline, the higher the mortality.
Patients with severe COPD who present with cor pulmonale have a poor prognosis.
Loss of fat free mass and low BMI have also been shown to correlate with increased mortality. The BODE index, which uses BMI, airflow obstruction, dyspnoea and exercise capacity, is a better indicator of prognosis than lung function or BMI alone.11
Hospital-at-home schemes have been shown to be safe and effective. A multidisciplinary team is required: respiratory nurse specialists, physiotherapists, occupational therapist and a respiratory physician to oversee the service.
Emergency oxygen and nebulisers may need to be provided, IV antibiotics may need to be initially administered under guidance and social services input may be required.
Patients with COPD may benefit from patient support network groups such as local community 'Breathe Easy' groups. These provide a supportive atmosphere for local residents living with chronic lung conditions and their carers.
It is vital that all patients with end-stage COPD have access to palliative care services. It is important to make end-of-life decisions with the patient, for example, regarding mechanical ventilation in the event of further deterioration.
Palliation of breathlessness in terminal illness is extremely important and specialist palliative care doctors and nurses can provide invaluable help.
- 18 November is World COPD day. For more information visit www.goldcopd.com
1. Global Initiative for Chronic Obstructive Pulmonary Disease (GOLD). Global strategy for the diagnosis, management, and prevention of COPD. NHLBI/WHO Workshop Report November 2006. www.goldcopd.com (Accessed 7 August 2009).
2. Barnes PJ, Celli BR. Systemic manifestations and comorbidities of COPD. Eur Respir J 2009; 33: 1165-85.
3. Sichletidis L, Chloros D, Spyratos D et al. The validity of the diagnosis of chronic obstructive pulmonary disease in general practice. Prim Care Respir J 2007; 16: 82-8.
4. Frank TL, Hazell ML, Linehan MF et al. The estimated prevalence of chronic obstructive pulmonary disease in a general practice population. Prim Care Respir J 2007; 16: 169-73.
5. Ingram G, Munro N. The use (or otherwise) of pulse oximetry in general practice. Br J Gen Pract 2005; 55: 501-2.
6. NICE. Guideline on management of chronic obstructive pulmonary disease in adults in primary and secondary care. www.nice.org.uk/guidance/CG12 (Accessed 7 August 2009).
7. Macedo P, Usmani OS. Inhaled drug therapy in for Chronic Obstructive Pulmonary Disease. Clin Pulm Med 2008; 15: 239-47.
8. McEvoy RD, Pierce RJ, Hillman D et al. Nocturnal non-invasive ventilation in stable COPD: a randomised controlled trial. Thorax 2009; 64: 561-6.
9. Morgan M. Pulmonary rehabilitation for COPD. NHS Evidence. www.library.nhs.uk/respiratory (Accessed 7 August 2009).
10. Tashkin DP, Celli B, Senn S et al. A 4-year trial of tiotropium in chronic obstructive pulmonary disease. N Eng J Med 2008; 359: 1543-54.
11. Celli BR, Cote CG, Marin JM et al. The body-mass index, airflow obstruction, dyspnoea, and exercise capacity index in COPD. N Eng J Med 2004; 350: 1005-12.
- British Thoracic Society www.brit-thoracic.org.uk
- British Lung Foundation www.lunguk.org
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