Chronic obstructive pulmonary disease (COPD) is a disease characterized by progressive, persistent, expiratory airflow limitation that is not fully reversible.^1,2 In the United States, COPD annually accounts for $29.5 billion in direct health care costs,³ 750,000 hospitalizations, and 1.5 million emergency visits.⁴ Globally it is now ranked as the fifth leading cause of death.^1,3,4 COPD is generally described as a progressive disease; however, there is considerable variability among patients.⁵ Exacerbations are often the cause of morbidity and mortality in COPD patients.^1,2,6 An exacerbation of COPD is characterized by an acute worsening of a patient’s respiratory symptoms that results in change in treatment and increased utilization of health care resources. Most exacerbations can be managed in the outpatient setting; however, patients with more severe underlying disease or exacerbation may require hospitalization. Acute exacerbations in patients with moderate to severe COPD can cause respiratory failure and a possible need for ventilatory support. Patients with acute exacerbation of COPD causing acute respiratory failure with severe hypoxia or persistent or severe respiratory acidosis, altered mental status, or hemodynamic instability require admission to an intensive care unit (ICU) for management.

COPD is a preventable and treatable disease. COPD is preventable because the majority of cases are the result of cigarette smoking. It is treatable because maintenance with long-term bronchodilators has been shown to improve lung function and reduce the frequency of exacerbations. The expiratory airflow limitation that characterizes COPD is usually progressive and is associated with an abnormal inflammatory response of the lungs to noxious particles or gases, mainly cigarette smoking. Diagnosis of COPD should be considered in any patient with chronic cough or sputum production, dyspnea, and/or a history of exposure to risk factors for the disease. Physical examination in a patient with COPD may be normal, especially in mild stages of the disease. Diminished breath sounds with prolonged expiratory phase (>4 seconds) are usually found in patients with symptomatic disease. Rhonchi and wheezes indicate bronchospasm and may be heard on lung auscultation but are not consistent findings. They are more likely to be heard with exacerbations. In severe disease, characteristic physical signs such as increased accessory muscle use, pursed lip breathing to facilitate exhalation, and signs of pulmonary hypertension and right heart failure may be apparent. Although COPD affects the lungs, it also produces significant extrapulmonary effects such as cor pulmonale, osteoporosis, skeletal muscle dysfunction, weight loss, and depression. Systemic comorbidities of COPD include myocardial infarction, congestive heart failure (CHF), arrhythmia, and venous thromboembolism (VTE).⁷

The diagnosis of COPD is made by spirometry, demonstrating the presence of airflow limitation that is not fully reversible with a post-bronchodilator FEV1/FVC (forced expiratory volume in 1 second over the forced vital capacity) ratio less than 0.70.^1,2 Diffusion capacity may be decreased in COPD due to destruction of alveoli and loss of alveolar capillary basement membrane. Due to loss of elastic recoil of the lung, hyperinflation occurs with an increase in total lung capacity (TLC). Increase in residual volume (RV) may also be seen and reflects air trapping. Spirometric classification is useful in guiding care and monitoring the progression of disease.

While the presence of airway obstruction is determined by a ratio of FEV₁ to forced vital capacity of less than 0.07, the severity of COPD is based on the post-bronchodilator FEV₁ (forced expiratory volume in 1 second) as follows^1,2,8:

Treatment of COPD is aimed at (1) improving airflow obstruction, (2) providing symptomatic relief, (3) modifying or preventing exacerbations, and (4) altering disease progression. Treatment modalities of stable COPD are shown in Box 1.

Bronchodilators are used in COPD for prevention of symptoms (maintenance therapy) as well as to acutely relieve symptoms (rescue inhalers). Bronchodilators act by altering the bronchial smooth muscle tone and reducing dynamic hyperinflation (air trapping) at rest and with exertion. Maintenance medications include long-acting β₂-agonists such as salmeterol and formoterol and long-acting anticholinergics such as tiotropium for prevention of symptoms. Short-acting bronchodilators are used for the acute relief of symptoms, including the β₂-agonist albuterol and anticholinergics such as ipratropium. The preferred mode of administration of these bronchodilators is by metered dose inhaler (MDI) or dry powder inhaler (DPI).^1,2

Inhaled corticosteroids provide anti-inflammatory therapy. Because patients with COPD often have an underlying inflammatory process, inhaled corticosteroids are sometimes used to stabilize the inflammatory process as well as to reduce the frequency of exacerbations.

Supplemental oxygen therapy is indicated in patients with COPD with resting P_ao₂ of 55 mm Hg or lower on room air or P_ao₂ of 56 mm Hg or greater and 59 mm Hg or lower in conjunction with cor pulmonale or erythocytocis (hematocrit >55%).^1,2 A decrease in oxygen saturation (Sao₂) to less than 88% with normal walking is an indication for supplemental O₂ with activity.¹ Pulmonary rehabilitation has become an established mode of treatment to improve functional capacity and reduce symptoms of dyspnea in patients with COPD.^1,2

Treatment for a hospitalized patient with acute exacerbation of COPD includes bronchodilator therapy with short-acting β₂-agonist (albuterol, salbutamol) and/or ipratropium, administered via spacer or nebulizer as needed.^14,15 Corticosteroids therapy should be started in these patients: oral prednisone 30 to 40 mg/day or intravenous equivalent dose if the patient cannot tolerate oral intake with subsequent transition to oral. Steroids should be tapered over 10 to 14 days.^16,17 Supplemental oxygen should be administered for O₂ saturation of less than 90%. Antibiotics^18,19 should be initiated in patients who have a change in their sputum characteristics (purulence and/or increased volume) or obvious radiographic or microbiological evidence of respiratory tract infection. Choice of antibiotic should be based on local bacteria resistance patterns. Per the American Thoracic Society/European Respiratory Society (ATS/ERS) guidelines, macrolides, amoxicillin/clavulanate, or respiratory fluoroquinolones may be options for use in an acute exacerbation.^1,2 If infection with Pseudomonas and/or other Enterobacteriaceae species is suspected, combination therapy should be considered.