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CHRONIC OBSTRUCTIVE PULOMONARY DISEASE RON BARAC, DO INTERNAL MEDICINE LECTURE SERIES FEBRUARY 13, 2008 COPD STATISTICS An estimated 16 million Americans are diagnosed with COPD It is likely that an additional 14 are undiagnosed True prevalence of COPD may be as high as 30 million cases COPD is the fourth leading cause of death in the United States for people ages 65 to 84, and it is the fifth leading cause of death for people ages 45 to 64 and those age 85 and older The annual cost to the nation for COPD is approximately $30.4 billion COPD accounts for: 13.4 million yearly office visits 634,000 yearly hospitalizations Percent Change in Age-Adjusted Death Rates, U.S., 1965-1998 3.0 3.0 2.5 2.5 Coronary Heart Disease Stroke Other CVD COPD All Other Causes –59% –64% –35% +163% –7% 2.0 2.0 1.5 1.5 1.0 1.0 0.5 0.5 0.0 0 1965 - 1998 1965 - 1998 1965 - 1998 1965 - 1998 1965 - 1998 Source: NHLBI/NIH/DHHS Of the six leading causes of death in the United States, only COPD has been increasing steadily since 1970 Source: Jemal A. et al. JAMA 2005 4 COPD Mortality by Gender, Number Deaths x 1000 U.S., 1980-2000 70 60 Men 50 40 Women 30 20 10 0 1980 1985 1990 1995 2000 Source: US Centers for Disease Control and Prevention, 2002 COPD RISK FACTORS Smoking is the primary risk factor: -80-90% of all COPD deaths are related to smoking -Female smokers are 13 times more likely to die of COPD than female non- smokers -Male smokers are 12 times more likely to die than male nonsmokers Second hand smoke Alpha-1-antitrypsin deficiency Air pollution Occupational exposures (involved in 19% of total COPD cases, 31% of nonsmokers diagnosed with COPD) History of childhood respiratory infections Heredity Atopic dermatitis patients Risk Factors for COPD Nutrition Infections Socio-economic status Aging Populations 7 Cigarette smoke Biomass particles Particulates Pathogenesis of COPD Host factors Amplifying mechanisms LUNG INFLAMMATION Anti-oxidants Oxidative stress Anti-proteinases Proteinases Repair mechanisms COPD PATHOLOGY Source: Peter J. Barnes, MD Changes in Lung Parenchyma in COPD Alveolar wall destruction Loss of elasticity Destruction of pulmonary capillary bed ↑ Inflammatory cells macrophages, CD8+ lymphocytes Source: Peter J. Barnes, MD EMPHYSEMA EMPHYSEMA CXR & CT CHRONIC BRONCHTIS COPD A clinical diagnosis of COPD should be considered in any patient who has dyspnea, chronic cough or sputum production, and/or a history of exposure to risk factors for the disease. The diagnosis should be confirmed by spirometry. A post-bronchodilator FEV1/FVC < 0.70 confirms the presence of airflow limitation that is not fully reversible. 17 Diagnosis of COPD SYMPTOMS cough sputum shortness of breath EXPOSURE TO RISK FACTORS tobacco occupation indoor/outdoor pollution SPIROMETRY COPD: Spirometry Spirometry should be performed after the administration of an adequate dose of a shortacting inhaled bronchodilator to minimize variability. A post-bronchodilator FEV1/FVC < 0.70 confirms the presence of airflow limitation that is not fully reversible. Where possible, values should be compared to age-related normal values to avoid overdiagnosis of COPD in the elderly. 19 Spirometry: Normal and Patients with COPD Classification of COPD Severity by Spirometry Stage I: Mild FEV1/FVC < 0.70 FEV1 > 80% predicted Stage II: Moderate FEV1/FVC < 0.70 50% < FEV1 < 80% predicted Stage III: Severe FEV1/FVC < 0.70 30% < FEV1 < 50% predicted Stage IV: Very Severe FEV1/FVC < 0.70 FEV1 < 30% predicted or FEV1 < 50% predicted plus chronic respiratory failure Differential Diagnosis: COPD and Asthma COPD • Onset in mid-life • Symptoms slowly progressive ASTHMA • Onset early in life (often childhood) • Symptoms vary from day to day • • Long smoking history • Dyspnea during exercise • • Largely irreversible airflow • limitation • Symptoms at night/early morning Allergy, rhinitis, and/or eczema also present Family history of asthma Largely reversible airflow limitation COPD ASTHMA Cigarette smoke Allergens Ep cells Mast cell CD4+ cell (Th2) Eosinophil Bronchoconstriction AHR Reversible Alv macrophage Ep cells CD8+ cell (Tc1) Neutrophil Small airway narrowing Alveolar destruction Airflow Limitation Irreversible Source: Peter J. Barnes, MD COPD and Co-Morbidities COPD patients are at increased risk for: • Myocardial infarction, angina • Osteoporosis • Respiratory infection • Depression • Diabetes • Lung cancer COPD and Co-Morbidities COPD has significant extrapulmonary (systemic) effects including: • Weight loss • Nutritional abnormalities • Skeletal muscle dysfunction GOALS of COPD MANAGEMENT • • • • • • • Relieve symptoms Prevent disease progression Improve exercise tolerance Improve health status Prevent and treat complications Prevent and treat exacerbations Reduce mortality 26 Reduce Risk Factors Reduction of total personal exposure to tobacco smoke, occupational dusts and chemicals, and indoor and outdoor air pollutants are important goals to prevent the onset and progression of COPD. Smoking cessation is the single most effective and cost effective intervention in most people to reduce the risk of developing COPD and stop its progression (Evidence A). 27 Pharmacotherapy: Bronchodilators Bronchodilator medications are central to the symptomatic management of COPD (Evidence A). They are given on an as-needed basis or on a regular basis to prevent or reduce symptoms and exacerbations. The principal bronchodilator treatments are ß2- agonists, anticholinergics, and methylxanthines used singly or in combination (Evidence A). Regular treatment with long-acting bronchodilators is more effective and convenient than treatment with short-acting bronchodilators (Evidence A). 28 Pharmacotherapy: Glucocorticosteroids The addition of regular treatment with inhaled glucocorticosteroids to bronchodilator treatment is appropriate for symptomatic COPD patients with an FEV1 < 50% predicted (Stage III: Severe COPD and Stage IV: Very Severe COPD) and repeated exacerbations (Evidence A). An inhaled glucocorticosteroid combined with a long-acting ß2-agonist is more effective than the individual components (Evidence A). 29 Pharmacotherapy: Glucocorticosteroids The dose-response relationships and longterm safety of inhaled glucocorticosteroids in COPD are not known. Chronic treatment with systemic glucocorticosteroids should be avoided because of an unfavorable benefit-to-risk ratio (Evidence A). 30 Pharmacotherapy: Vaccines In COPD patients influenza vaccines can reduce serious illness (Evidence A). Pneumococcal polysaccharide vaccine is recommended for COPD patients 65 years and older and for COPD patients younger than age 65 with an FEV1 < 40% predicted (Evidence B). 31 Therapy at Each Stage of COPD I: Mild II: Moderate III: Severe IV: Very Severe FEV1/FVC < 70% FEV1/FVC < 70% FEV1 > 80% predicted FEV1/FVC < 70% 50% < FEV1 < 80% predicted FEV1/FVC < 70% 30% < FEV1 < 50% predicted FEV1 < 30% predicted or FEV1 < 50% predicted plus chronic respiratory failure Active reduction of risk factor(s); influenza vaccination Add short-acting bronchodilator (when needed) Add regular treatment with one or more long-acting bronchodilators (when needed); Add rehabilitation Add inhaled glucocorticosteroids if repeated exacerbations Add long term oxygen if chronic respiratory failure. Consider surgical treatments Other Pharmacologic Treatments Antibiotics: Only used to treat infectious exacerbations of COPD Antioxidant agents: No effect of n- acetylcysteine on frequency of exacerbations, except in patients not treated with inhaled glucocorticosteroids Mucolytic agents, Antitussives, Vasodilators: Not recommended in stable COPD 33 Non-Pharmacologic Treatments Rehabilitation: All COPD patients benefit from exercise training programs, improving with respect to both exercise tolerance and symptoms of dyspnea and fatigue (Evidence A). Oxygen Therapy: The long-term administration of oxygen (> 15 hours per day) to patients with chronic respiratory failure has been shown to increase survival (Evidence A). 34 Key Points An exacerbation of COPD is defined as: “An event in the natural course of the disease characterized by a change in the patient’s baseline dyspnea, cough, and/or sputum that is beyond normal day-to-day variations, is acute in onset, and may warrant a change in regular medication in a patient with underlying COPD.” 35 Key Points The most common causes of an exacerbation are infection of the tracheobronchial tree and air pollution, but the cause of about one-third of severe exacerbations cannot be identified (Evidence B). Patients experiencing COPD exacerbations with clinical signs of airway infection (e.g., increased sputum purulence) may benefit from antibiotic treatment (Evidence B). 36