Chapter 70: Chronic Obstructive Pulmonary Disease

INTRODUCTION AND EPIDEMIOLOGY

Chronic obstructive pulmonary disease (COPD) is characterized by persistent airflow limitation that is generally progressive and associated with an abnormal inflammatory response to noxious particles or gases.^1,2,3,4,5,6 COPD has two main forms: chronic bronchitis, defined in clinical terms, and emphysema, defined in terms of anatomic pathology. This traditional categorization is often indistinct, limiting the clinical utility of the definitions.^2,3,4,5,6 Chronic bronchitis is the presence of chronic productive cough for 3 months in each of 2 successive years, where other causes of chronic cough have been excluded.^2,3,4,5,6 Emphysema results from destruction of bronchioles and alveoli. The World Health Organization's Global Initiative for Chronic Obstructive Lung Disease definition of COPD encompasses chronic bronchitis, emphysema, bronchiectasis, and asthma, and acknowledges that most patients have a combination of the different diseases.

COPD accounted for 715,000 U.S. hospitalizations in 2010,⁷ with $49.9 billion estimated as the cost for care.⁷ The prevalence of COPD in women has doubled in the past few decades, and women now account for >50% of COPD-related deaths; the prevalence has remained stable in men.⁸ The prevalence of COPD is highest in those countries that have the greatest cigarette use.

CHRONICALLY COMPENSATED CHRONIC OBSTRUCTIVE PULMONARY DISEASE

PATHOPHYSIOLOGY

Although tobacco smoke is the major risk factor for developing COPD, only 15% of smokers will develop COPD. Occupational dust, chemical exposure, and air pollution are other risk factors for COPD. α₁-Antitrypsin deficiency accounts for <1% of COPD patients.

Irritants, notably tobacco smoke and air pollutants, trigger an increase in inflammatory cells in the airways, lung interstitium, and alveoli. Proteases eventually break down lung parenchyma and stimulate mucus secretion. Mucus-secreting cells replace cells that normally secrete surfactant and protease inhibitors. These changes result in a loss of elastic recoil, narrowing, and collapse of the smaller airways. Mucous stasis and bacterial colonization develop in the bronchi. The earliest objective changes in the evolution of COPD are clinically imperceptible; these early changes are small increases in peripheral airway resistance or lung compliance. Because dyspnea and hypersecretion often progress insidiously, it may take decades before COPD becomes clinically evident. The Global Initiative for Chronic Obstructive Lung Disease guidelines are helpful for the early diagnosis and treatment of COPD (Table 70-1),⁶ although there is only a weak correlation between forced expiratory volume in 1 second (FEV₁), symptoms, and health-related quality of life.⁶