The Management of COPD

Summarized by Robert W. Griffith, MD
December 19, 2001 (Reviewed: December 5, 2003)

Introduction

The reduction in smoking by certain sections of the population has had little effect on the problem presented by chronic obstructive pulmonary disease (COPD). This condition is the 4th leading cause of death in the USA, with an incidence of approximately 20% in US adults. Of course, absence of a standardized definition of the disease leads to misleading numbers. A good working definition is that it's a progressive chronic obstruction of airflow due to chronic bronchitis, emphysema, or both. Asthma, which also features airflow obstruction, differs from COPD by having reversible pulmonary dysfunction.

The course of COPD is chronic disability with intermittent acute exacerbations, which are commoner in the winter. Treatment of the stable phase is largely directed at preventing these acute exacerbations. A review of the management of COPD has recently been published in American Family Physician, and forms the basis for this summary.

Etiology, pathophysiology, prognosis

Cigarette smoking is incriminated in 90% of cases. Other inhaled irritants (e.g. 'smog') and episodic infections can also be partially responsible. Chronic inflammation of the bronchial lining epithelium leads to hypertrophy, edema, excess mucus production, and impaired ciliary function. There is a chronic productive cough, wheezing, dyspnea, and secondary bacterial colonization. Diverticulae are formed in the bronchial tree, with coalescence and, finally, formation of emphysematous bullae.

Exacerbations are usually caused by bacterial or viral infections, although respiratory irritants or heart failure can be responsible. Streptococcus pneumoniae, Haemophilus influenzae, or Moraxella catarrhalis are to blame for about 60% of exacerbations.

The long-term prognosis of patients with COPD is poor -- a 60-year-old smoker with chronic bronchitis has a 60% 10-year mortality risk, four-times that of a non-smoking asthmatic. The most relevant predictor (apart from continuing to smoke) is a decreasing forced expiratory volume per second (FEV-1). In younger COPD patients, a deficiency of alpha1-antitrypsin is an indicator of a rare genetic abnormality in which there is panlobular emphysema.

Management of chronic stable COPD

A healthy lifestyle is key -- no smoking, regular exercise, good nutrition. Obese patients -- labelled "blue bloaters" -- must lose weight, while very thin patients -- "pink puffers" -- may require nutritional supplements. Pulmonary physical therapy may be useful. Patients should be kept up-to-date with their influenza and pneumococcal vaccinations.

Are medications required? Mild symptoms may be adequately managed using a beta-2 agonist given by a pressurized metered dose inhaler (MDI). These may be short-acting (e.g. salbutamol, terbutaline) or long-acting (e.g. formoterol, salmeterol). For more moderate continual symptoms, an inhaled anticholinergic (e.g. ipratropium) can be substituted for, or added to, the beta-2 agonist. Failure to control symptoms in a stable patient may necessitate the addition of an oral corticosteroid. Continued problems mean that the patient will probably require multidisciplinary pulmonary rehabilitation.

Supplemental oxygen therapy reduces mortality in patients with COPD. It should be given to all those with a PaO2 of 55 mm Hg or less at rest, or an oxygen saturation of 88% or less while sleeping. Oxygen can be delivered through nasal cannulae, or using continuous positive airway pressure (CPAP).

Management of exacerbations

Hospitalisation may be necessary, in order to treat exacerbations promptly and adequately. As most exacerbations are caused by, or accompanied by, infections, mild to moderate instances should be treated with broad-spectrum antibiotics (e.g. doxocycline, trimethoprim-sulfamethoxazole, amoxicillin-clavulanate). More severe exacerbations warrant a cephalosporin, a fluorquinalone, or aminoglucoside. Hospitalised patient should receive intravenous antibiotics, as determined by bacterial sensitivity patterns.

Oxygen treatment using external devises or mechanical ventilation may be required to keep oxygen saturation at 90% or above. Nasal cannulae, a positive pressure mask, or CPAP should be used, as necessary.

Inhaled beta-2 agonists must be started at once, by nebulizer, or by MDI if the patient is able to use one properly. Formoterol and salmeterol are long-acting beta-2 agonists that are effective in exacerbations of COPD; the former has a fast onset of action. ¹

Inhaled anticholinergics, such as ipratropium, provide similar, or greater, bronchodilation. They can be given by nebulizer or MDI, and can be added on to beta-2 agonists.

Should corticosteroids be used? There have been several studies showing benefits of short courses of systemic steroids in acute exacerbations of COPD. Hospital stays are shortened, and FEV-1 values increased. ²,³ There is no apparent advantage in extending steroid treatment beyond two weeks. Intravenous methylprednisone is usually given initially, changed after 2-3 days to oral prednisone for up to 2 weeks, which is then tapered off gradually over 2 weeks.

Methylxanthine treatment?

The use of methylxanthines such as theophylline and aminophylline in COPD is controversial. In exacerbations, they may help in patients who don't respond to other bronchodilators (beta-2 agonists or anticholinergics). However, side effects are not inconsiderable -- rarely, there can be cardiac arrhythmias, seizures, or extreme dyspnea. Methylxanthines may also be used in stable patients who have difficulty in operating an MDI, or when other bronchodilators produce unacceptable side effects.

Surgical procedures

Lung transplantation is beneficial in selected cases. Lung volume reduction procedures are sometimes done, to reduce hyperinflation of one or both lungs. An increase in FEV1 is produced, accompanied by improved exercise tolerance; however, peri-operative mortality is somewhat high -- as much as 10% has been reported.

Source

• COPD: Management of acute exacerbations and chronic stable disease. MH. Hunter, DA. King, Am Fam Physician, 2001, vol. 64, pp. 603--612

Footnotes
1. Rapid onset of bronchodilation in COPD: a placebo-controlled study comparing formoterol (Foradil Aerolizer) with salbutamol (Ventodisk). D. Benhamou, A. Cuvelier, JF. Muir,  et al., Respir Med, 2001, vol. 95, pp. 821--917
2. Oral corticosteroids in patients admitted to hospital with exacerbations of chronic obstructive pulmonary disease: a prospective randomized controlled trial. L. Davies, RM. Angus, PMA. Calverley, Lancet, 1999, vol. 354, pp. 456--460
3. Effect of systemic glucocorticoids on exacerbations of chronic obstructive pulmonary disease. Department of Veterans Affairs Cooperative Study Group. DE. Niewoehner, ML. Erbland, RH. Deupree,  et al., N Engl J Med , 1999, vol. 340, pp. 1941--1947

Related Links
Steroid Use in COPD
The Stop Smoking Center

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