INTRODUCTION:
Chronic obstructive pulmonary disease (COPD) is a preventable and treatable disease characterized by persistent progressive airflow limitation associated with chronic inflammation in response to noxious particles or gases. Related diagnoses include chronic bronchitis (cough and sputum on most days for at least 3 mths, in 2 consecutive yrs) and emphysema (abnormal permanent enlargement of the distal air spaces, with destruction of alveolar walls).
Extrapulmonary manifestations include weight loss and skeletal muscle dysfunction, and COPD is associated with cardiovascular disease, cerebrovascular disease, the metabolic syndrome, osteoporosis and depression.
The prevalence of COPD is related to the prevalence of tobacco smoking and, in low- and middle income countries, exposure to biomass fuel smoke. Approximately 80 million people worldwide suffer from moderate to severe disease. In 2005, COPD contributed to over 3 million (5%) deaths globally but it is forecast to become the third most important cause of death worldwide by 2020. This rise will be greatest in Asian and African countries because of increasing tobacco consumption there. Not all smokers develop COPD, and it is unusual in smokers of < 10 pack yrs (1 pack yr = 20 cigarettes/day
for 1 yr). Other risk factors include air pollution (especially biomass fuels), occupational exposure (coal dust, silica) and inherited deficiency of α1-antitrypsin.
CLINICAL FEATURES:
COPD should be suspected in any patient over the age of 40 yrs with persistent cough and sputum and/or breathlessness. The level of breathlessness should be quantified (e.g. MRC dyspnoea scale). In advanced disease there may be oedema or morning headaches (hypercapnia). Physical signs may help to indicate disease severity.
Two classical phenotypes have been described:
● ‘Pink puffers’: thin and breathless, and maintain a normal PaCO2.
● ‘Blue bloaters’: develop hypercapnia, oedema and secondary polycythaemia.
In practice, these phenotypes often overlap.
INVESTIGATIONS:
● CXR: may reveal hyperinflation, bullae or other complications of smoking (lung cancer).
● FBC: may demonstrate polycythaemia.
● α1-antitrypsin level: should be checked in younger patients with emphysema.
● Spirometry (% of predicted value): used to classify disease severity (e.g. UK NICE guidelines):
Stage 1 (mild) – FEV1 > 80%, FEV1/FVC < 0.7 plus symptoms;
Stage II (moderate) – FEV1 50–79%, FEV1/FVC < 0.7;
Stage III (severe) – FEV1 30–49%, FEV1/FVC < 0.7;
Stage IV (very severe) – FEV1 < 30%, FEV1/FVC < 0.7.
● Lung volume measurements: quantify hyperinflation.
● Carbon monoxide transfer factor: low in emphysema.
● Exercise tests: an objective assessment of exercise tolerance.
● Pulse oximetry: may prompt referral for a domiciliary oxygen assessment if < 93%.
● CT: likely to play an increasing role in the assessment of COPD, as it allows the detection, characterisation and quantification of emphysema.
MANAGEMENT:
Pessimism is unjustified, as it is usually possible to improve breathlessness, reduce the frequency and severity of exacerbations, and improve health status and prognosis.
Reduce smoke exposure: Always offer the patient help to stop smoking, combining pharmacotherapy with appropriate support as part of a programme. Cessation is proven to decelerate the decline in FEV1. Smokeless alternatives to biofuels should be promoted wherever possible.
Bronchodilators: Short-acting bronchodilators are given for mild disease (β2-agonist or anticholinergic). Longer-acting bronchodilators are more appropriate for patients with moderate to severe disease. From the wide range available, select a device that the patient can use effectively. Significant improvements in breathlessness may be reported despite minimal changes in FEV1,probably reflecting reduced hyperinflation. Theophylline preparations improve breathlessness but use is limited by side-effects.
Oral β2-agonists and selective phosphodiesterase inhibitors have a limited role.
Inhaled corticosteroids: These reduce the frequency and severity of exacerbations; they are recommended in patients with severe disease (FEV1 < 50%) who report ≥ 2 exacerbations/yr requiring antibiotics or oral steroids. Regular use leads to a small improvement in FEV1 but no change in the rate of decline of lung function.
ICS/LABA combinations produce further improvements in breathlessness and exacerbation rate. Oral corticosteroids are useful during exacerbations, but maintenance therapy contributes to osteoporosis and impaired muscle function and should be avoided.
Pulmonary rehabilitation: Encourage exercise. Multidisciplinary programmes (usually 6–12 wks’ duration) incorporating physical training, education and nutritional counselling reduce symptoms, improve health status and enhance confidence.
Oxygen therapy: Long-term domiciliary oxygen therapy (LTOT) improves survival in selected patients with COPD and hypoxia (PaO2 < 7.3kPa (55 mmHg)). A minimum of 15 hrs/day is recommended, keeping PaO2 > 8 kPa (60 mmHg) or SaO2 > 90%. Ambulatory oxygen should be considered in patients who desaturate on exercise and show objective improved exercise capacity and/or dyspnoea with oxygen. Short-burst oxygen therapy is of no benefit and should be avoided.
Surgical intervention: In highly selected patients, lung volume reduction surgery (removing non-functioning emphysematous lung tissue) reduces hyperinflation and decreases work of breathing. Bullectomy is occasionally performed for large bullae that compress surrounding lung tissue. Lung transplantation may benefit selected patients.
Other measures: Give influenza vaccination and pneumococcal vaccination; treat depression and cachexia.
COPD has a variable natural history. Prognosis is inversely related to age and directly related to FEV1. Poor prognostic indicators include weight loss and pulmonary hypertension.
Acute exacerbations of COPD
These are characterised by an increase in symptoms and deterioration in lung function. They are more common in severe disease and may be caused by bacteria, viruses or a change in air quality.
Respiratory failure and/or fluid retention may be present. Many patients can be managed at home with the use of increased bronchodilator therapy, a short course of oral corticosteroids and, if appropriate, antibiotics. Cyanosis, peripheral oedema or altered conscious level should prompt hospital referral.
Oxygen therapy: High concentrations of oxygen may cause respiratory depression and worsening acidosis. Controlled oxygen at 24% or 28% should be used, aiming for PaO2 > 8 kPa (60 mmHg) (or SaO2 88–92%) without worsening acidosis.
Bronchodilators: Nebulised short-acting β2-agonists and anticholinergics are used. If concern exists regarding oxygen sensitivity, nebulisers may be driven by compressed air.
Corticosteroids: Oral prednisolone (usually 30 mg for 5–10 days) reduces symptoms, improves lung function and shortens hospital stay. Prophylaxis against osteoporosis should be considered if frequent courses are needed.
Antibiotics: These are recommended for an increase in sputum purulence, sputum volume or breathlessness. An aminopenicillin or a macrolide should be used. Co-amoxiclav is only required in regions where β-lactamase-producing organisms are known to be common.
Ventilatory support: In patients with persistent tachypnoea and respiratory acidosis (H+ ≥ 45 nmol/L (pH < 7.35)), NIV is associated with reduced need for intubation and reduced mortality. Consider intubation and ventilation where there is a reversible cause for deterioration (e.g. pneumonia); the evidence for NIV with pneumonia is much weaker.
Additional therapy: Evidence for IV aminophylline is limited and there is a risk of arrhythmias and drug interactions. The respiratory stimulant doxapram has been superseded by NIV. Diuretics should be administered if peripheral oedema has developed.
THOSE ABOVE ARE COLLECTED FROM SOME BOOKS AND
WEBSITES..
(DAVIDSON’S ESSENTIALS OF MEDICINE)
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