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Acute Exacerbation of Chronic Obstructive Pulmonary Disease
1.. Chronic obstructive pulmonary disease (COPD) refers to fixed airflow obstruction caused by chronic bronchitis (productive cough for at least 3 months of the year for at least 2 consecutive years) or emphysema (destruction of alveoli). 2.. Tobacco smoking accounts for almost all cases of COPD. 3....
Formato: | Online Artículo Texto |
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Lenguaje: | English |
Publicado: |
2007
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7152152/ http://dx.doi.org/10.1016/B978-141603203-8.10015-4 |
Sumario: | 1.. Chronic obstructive pulmonary disease (COPD) refers to fixed airflow obstruction caused by chronic bronchitis (productive cough for at least 3 months of the year for at least 2 consecutive years) or emphysema (destruction of alveoli). 2.. Tobacco smoking accounts for almost all cases of COPD. 3.. Precipitants of COPD exacerbations include viral upper respiratory tract infections, bacterial infections (most commonly Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis), pollution, heart failure, pulmonary embolism, and medications (beta‐blockers, narcotics, sedatives). 4.. There is no universally accepted definition of an acute exacerbation of COPD. The most commonly used definition is worsening dyspnea, an increase in sputum purulence, or an increase in sputum volume in a patient with COPD. 5.. Symptoms and signs of COPD exacerbations include wheezing, distant breath sounds, tachypnea, tachycardia, accessory muscle use, cyanosis, agitation, confusion, and stupor. 6.. Initial testing should include pulse oximetry, chest x‐ray, and an electrocardiogram. Other possible tests include arterial blood gas (if the patient's distress or somnolence raises concern for acute respiratory acidosis) and sputum Gram stain and culture (most appropriate for patients who fail to respond to empiric therapy). 7.. Administer supplemental oxygen if there is hypoxemia. The goal oxygen saturation is 90% to 92% with a corresponding partial pressure of arterial oxygen of 60 to 65 mmHg. Higher oxygen saturations may cause hypercarbia by reducing the respiratory drive and promoting ventilation–perfusion mismatching. 8.. Beta‐agonists and anticholinergic agents are equally efficacious at improving airflow during a COPD exacerbation. Combination therapy is typically used in clinical practice, but does not appear to confer substantial benefit over monotherapy with either agent alone. 9.. The role of aminophylline (methylxanthine bronchodilator) in the setting of a COPD exacerbation is controversial because this medication has uncertain efficacy and potential toxicity. 10.. Systemic glucocorticoids improve FEV(1) and reduce treatment failure rates and length of hospitalization for a COPD exacerbation. The optimal dose, route, and duration of therapy are unknown. 11.. Patients with a severe COPD exacerbation are the ones most likely to benefit from antibiotics, although the effect of antibiotics on the duration and severity of the exacerbation appears minimal. There are no definitive data regarding optimal duration of therapy. 12.. Mucolytic agents and mechanical chest percussion are probably not beneficial in patients with a COPD exacerbation. 13.. Many patients do not use metered‐dose inhalers correctly. We recommend spacers to all patients, especially when inhaled glucocorticoids are prescribed. 14.. Smoking cessation should be discussed. The pneumonia and influenza vaccines should be administered at the follow‐up clinic visit, if applicable. |
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