Management of AECB/COPD includes supportive adjuvant treatment and pharmacologic therapy. Begin by determining the etiology of the exacerbation, which could lead to removal of environmental triggers and cessation of smoking if contributory, use of a flutter valve to assist with sputum expectoration, supplemental oxygen therapy for patients with oxygen saturations <90%, hydration, pulmonary rehabilitation, improved nutrition, and appropriate vaccinations.1,2
The goal of pharmacologic therapy in chronic bronchitis/COPD is to prevent and control symptoms, reduce exacerbations, and improve exercise tolerance. However, none of the current medications slows the rate of decline in lung function. Pharmacologic management of chronic bronchitis/COPD is twofold: outpatient therapy during stable disease periods with medications tailored to disease severity and therapy during acute exacerbations. Combining different agents improves spirometry and symptoms more than single agents alone.1,2
Treatment of AECB/COPD includes the same medications as used in stable disease, with addition of systemic corticosteroids and appropriate antibiotic therapy. The 10-year combined mortality for patients with chronic bronchitis and AECB resulting in hypoxemic respiratory failure is 50%.5
Bronchodilators (BDs): These medications are the mainstay of management in stable COPD and during exacerbations. Classes of BDs include both short and long-acting ß-agonists, short and long-acting anticholinergics, and theophylline. Therapy begins with “as needed” short-acting agents and escalates with increasing disease severity, adding long-acting BDs, corticosteroids, and even long-term oxygen therapy. The most significant effect of BD therapy is change in lung volumes and ability to exhale with a reduction in residual volume. This decreases dyspnea and improves exercise tolerance and occurs even if there is minimal change in FEV1. Combining both short-acting BD agents (ß and anticholinergic) produces a greater change in FEV1 than either agent alone. Combining a long-acting ß-agonist with a short-acting anticholinergic agent (ipratropium) results in fewer exacerbations than either drug alone. Tiotropium, a long-acting anticholinergic, improves health status and reduces exacerbations when compared with scheduled ipratropium. Regular therapy with long-acting BD is more effective than with scheduled short-acting agents; combination therapy of a short-acting and long-acting agent also produces greater improvement.1 Although theophylline is a BD and has anti-inflammatory properties, it has a high side-effect profile and is not routinely recommended.
Corticosteroids: The effect of inhaled corticosteroid (IC) treatment is much less than that observed in asthma. Maintenance ICs are recommended only for patients with severe baseline COPD (FEV1 <50%, predicted) or with more than three exacerbations per year.1,2 In this group of patients, adding steroids decreases the frequency of exacerbations and improves health status. Short-term treatment with combined long-acting ß-agonists and ICs results in greater improvement in symptoms than combined bronchodilator therapy. In order to ascertain the effectiveness of ICs when there is minimal change in symptoms, the agent can be withdrawn. If there is a recurrence of symptoms, the ICs should be restarted and maintained. Oral steroids are not recommended except with an exacerbation.
Systemic steroids are beneficial in the management of acute exacerbations of COPD in patients with baseline FEV1 <50% predicted or when bronchodilator therapy has failed in patients with less severe disease. Systemic steroids shorten recovery time. Oral prednisone may be given for 10-14 days. If the patient is unable to tolerate oral therapy, IV steroids may be given.2
Antibiotic therapy: Studies have demonstrated a small beneficial effect on lung function with antibiotic therapy. Although staging of AECB has not been well validated, patients with dyspnea, increased sputum volume, and purulence were shown to benefit the most from antibiotic therapy.1 Antibiotics are also recommended in patients who have two of the three symptoms, if one symptom is increased purulence, and in patients requiring ventilatory support.1 The choice of antibiotic should be tailored to local resistance patterns and culture results. Empiric antibiotic regimens should cover S. pneumoniae, H. influenzae, and M. catarrhalis with second-generation macrolides or second- or third-generation cephalosporins. If the patient has been recently hospitalized or received recent antibiotics, respiratory fluoroquinolones may be more appropriate.
Dr. Hardin is assistant professor of internal medicine, Division of Pulmonary and Critical Care Medicine, University of California, Davis, School of Medicine, in Sacramento.
- Pauwels RA, Buist AS, Calverley PM, et al. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. NHLBI/WHO Global Initiative for Chronic Obstructive Lung Disease (GOLD) Workshop summary. Am J Respir Crit Care Med. 2001;163:1256-1276; The Global Strategy for the Diagnosis, Management and Prevention of COPD. 2001.
- Celli BR, MacNee W; ATS/ERS Task Force. Standards for the diagnosis and treatment of patients with COPD: a summary of the ATS/ERS position paper. Eur Respir J. 2004;23:932-946.
- Sandford AJ, Weir TD, Pare PD. Genetic risk for chronic obstructive pulmonary disease. Eur Respir J. 1997;10:1380-1391.
- Celli BR, Cote CG, Marin JM, et al. The body-mass index, airflow obstruction, dyspnea, exercise capacity index in chronic obstructive pulmonary disease. N Engl J Med. 2004;350:1005-1012.
- Turato G, Di Stefano A, Maestrelli P, et al. Effect of smoking cessation on airway inflammation in chronic bronchitis. Am J Respir Crit Care Med. 1995;152(4 Pt 1):1262-1267.