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TREATMENT OF ACUTE EXACERBATIONS OF COPD

TREATMENT OF ACUTE EXACERBATIONS OF COPD

Acute exacerbation of COPD (AECOPD) represents an acute worsening of the patient's baseline condition, generally characterized by worsened dyspnea and increased volume and purulence of sputum. Depending on the severity of baseline COPD, additional derangements may become manifest, such as hypoxemia, worsening hypercapnia, cor pulmonale with worsening lower extremity edema, or altered mental status. The main goals of treating AECOPD are to restore the individual to his or her previous stable baseline and to prevent or reduce the likelihood of recurrence. This requires identification of the precipitating factor or condition and its reversal or amelioration while optimizing gas exchange and improving the individual patient's symptoms. Treatment modalities similar to the ones used in stable COPD are used in managing acute exacerbations. These include oxygen therapy, bronchodilators, antibiotics, corticosteroids, mechanical ventilation, and others.

Recommendations by Professional Societies for Management of Acute Exacerbations of COPD
American Thoracic Society, European Respiratory Society, British Thoracic Society, Global Initiative for Chronic Obstructive Lung Disease.

Bronchodilators
Recommended: ß 2 agonists ± anticholinergics; IV aminophylline if inadequate response
Recommended: ß 2 agonists ± anticholinergics; methylxanthines if needed as second-line therapy in severe exacerbations
Recommended: ß 2 agonists ± anticholinergics; IV aminophylline if inadequate response
Recommended: ß 2 agonist dose increase ± anticholinergics ± IV aminophylline depending on disease severity

Corticosteroids
Oral or systemic
Oral or systemic empirically
7-14 days of systemic steroids
Systemic steroids

Antibiotics
Narrow-spectrum antibiotic; broad spectrum if no response
Inexpensive antibiotic empirically for 7-14 days; if ineffective, choice guided by sputum culture
Common oral antibiotics usually adequate Broader spectrum if no response or if more severe exacerbation Empirically with increased sputum volume and purulence based on local sensitivity patterns to usual pathogens

Oxygen Therapy
Raise PaO2 >60 mm Hg
Keep SaO2 >90% and/or PaO2 ≥60 mm Hg. Avoid PaCO2 rise by >10 mm Hg or pH drop to <7.25
Raise PaO2 to ≥50 mm Hg while avoiding pH <7.26
Keep SaO2 >90% and PaO2 >60 mm Hg

Ventilatory Support
NIPPV or invasive mechanical ventilation based on criteria
NIPPV in appropriate patients
NIPPV or invasive mechanical ventilation if pH <7.26 with rising PaCO2 despite controlled oxygen therapy
NIPPV or invasive mechanical ventilation based on selection and exclusion criteria.

Chest Physiotherapy
If sputum volume is >25 mL/day
Help in clearance of secretions
Not recommended
May be beneficial in certain circumstances

Oxygen Therapy
The role of oxygen therapy is to correct the hypoxemia that usually accompanies the AECOPD. The end point is to maintain oxygen tension at approximately 60 to 65 mm Hg, thereby assuring near-maximal hemoglobin saturation while minimizing the potential for deleterious hypercapnia. Hypercapnia complicating supplemental oxygen is mainly a result of ventilation-perfusion mismatch, with generally smaller contributions of depression of the respiratory drive and the Haldane effect.

Bronchodilators
Bronchodilators are widely used in AECOPD, and β-adrenergic agonists and anticholinergics are first-line therapies. As in stable COPD, both can improve airflow in AECOPD, and although recommendations vary, combined therapy is often recommended. β-adrenergic agonists have a quicker onset of action, whereas anticholinergics have a more favorable side-effect profile. Because of their potential side effects, as well as their limited benefit, methylxanthines are used mostly as second-line therapy.

Antibiotics
Antibiotics play a favorable role in treating AECOPD, especially in the setting of increased volume and purulence of phlegm. A narrow-spectrum antibiotic (e.g., amoxicillin, trimethoprim-sulfamethoxazole, doxycycline, etc.) is often recommended as first-line therapy, although use of a beta-lactam/beta-lactamase combination has been recommended in patients with severe AECOPD, and fluoroquinolones have been recorded in individuals suspected to be colonized with Pseudomonas aeruginosa. 8 The optimal duration of treatment is still unclear, although most guidelines recommend treating for between 7 and 14 days.

Corticosteroids
Randomized clinical trials generally support the use of systemic corticosteroids to enhance airflow and to lessen treatment failure in AECOPD. Prolonged therapy beyond 2 weeks confers no additional benefits, with 5 to 10 days being the likeliest optimal duration. 66–68

Noninvasive Positive Pressure Ventilation and Mechanical Ventilation
Noninvasive positive pressure ventilation (NIPPV) is emerging as a preferred method of ventilation in adequately selected patients with acute respiratory acidemia. This mode is currently used in the treatment of acute respiratory failure of many causes, including COPD. Appropriate patient selection is critical to assure the success of NIPPV. Poor candidates are those with acute respiratory arrest, altered mental status with agitation or lack of cooperation, distorted facial anatomy preventing adequate mask application, cardiovascular instability, or excessive secretions, or both. NIPPV improves symptomatic and physiologic variables, reduces the need for intubation, hospital stay, and mortality, and does not use additional resources.

For patients who do not qualify for NIPPV and/or show evidence of worsening respiratory failure and life-threatening acidemia despite NIPPV, intubation and mechanical ventilation are indicated. This method of ventilation carries numerous risks and complications, including ventilator-acquired pneumonia and barotrauma. Adequate ventilator management is necessary, and every effort should be undertaken to minimize the duration of mechanical ventilation.

Others
Mucolytics, expectorants, and chest physiotherapy have not been shown to improve the outcome and are not recommended.

Conclusion
Overall, COPD poses a common and significant clinical challenge for patients and clinicians alike. Clinicians' expert knowledge regarding diagnosis and management can enhance patients' longevity and quality of life.

Summary
 Chronic obstructive pulmonary disease is emerging as a major cause of morbidity and mortality in the United States. COPD currently is the fourth leading cause of death among Americans.
 Chronic obstructive pulmonary disease is under-recognized overall, as is alpha-1 antitrypsin deficiency, a genetic predisposition to COPD.
 Among the available therapies for COPD, many can improve symptoms (e.g., bronchodilators, pulmonary rehabilitation). Three treatments—smoking cessation, supplemental oxygen used for 24 hours a day, and lung volume reduction surgery—have been shown to prolong life in appropriately selected COPD individuals.

Suggested Readings
 AACP/AACVPR Pulmonary Rehabilitation Guidelines Panel. Pulmonary rehabilitation: Joint ACCP/AACVPR evidence-based guidelines. Chest. 112: 1997; 1363-1396.
 American Thoracic Society. Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease.
 American Thoracic Society/European Respiratory Society Statement. Standards for the diagnosis and management of individuals with alpha-1 antitrypsin deficiency. Am J Respir Crit Care Med. 168: 2003; 818-900.
 Anthonisen NR, Connett JE, Murray RP. Smoking and lung function of Lung Health Study participants after 11 years. The Lung Health Study Research Group. Am J Respir Crit Care Med. 166: 2002; 675-679.
 Maurer JR, Frost AE, Estenne M. International guidelines for the selection of lung transplant candidates. The International Society for Heart and Lung Transplantation, the American Thoracic Society, the American Society of Transplant Physicians, the European Respiratory Society. Transplantation. 66: 1998; 951-956.
 National Emphysema Treatment Trial Research Group. A randomized trial comparing lung-volume-reduction surgery with medical therapy for severe emphysema. N Engl J Med. 348: 2003; 2059-2073.
 Pauwels RA, Buist AS, Calverley PM. GOLD Scientific Committee. 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. 163: 2001; 1256-1276.
 Pauwels RA, Lofdahl CG , Laitinen LA. Long-term treatment with inhaled budesonide in persons with mild chronic obstructive pulmonary disease who continue smoking. European Respiratory Society Study on Chronic Obstructive Pulmonary Disease. N Engl J Med. 340: 1999; 1948-1953.
 Sutherland ER, Cherniack RM. Management of chronic obstructive pulmonary disease. N Engl J Med. 350: 2004; 2689-2697.
 The Lung Health Study Research Group . Effect of inhaled triamcinolone on the decline in pulmonary function in chronic obstructive pulmonary disease. N Engl J Med. 343: 2000; 1902-1909.

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