Chronic Obstructive Pulmonary Disease

1. Chronic Obstructive Pulmonary Disease Chief’s Conference: Kevin L. Gilliam II, M.D. April 16, 2009 Emory Family Medicine

2. What is COPD? • It is a syndrome of progressive airflow limitation caused by chronic inflammation of the airways and lung parenchyma. • The terms chronic bronchitis and emphysema are no longer included in the formal definition of COPD, although they are still used clinically • Emphysema: pathologic term used to describe destruction of the alveolar capillary membrane • Chronic Bronchitis: clinical term used to describe the presence of cough or sputum production for at least a three month duration during two consecutive years

3. Who gets COPD? • Smokers • Smokers • Smokers • More than 80 percent of deaths from the disease are directly attributable to smoking, and persons who smoke are 12 to 13 times more likely to die from COPD than nonsmokers. • The absolute risk of COPD among active, continuous smokers is at least 25 percent

4. Who else is at risk for getting COPD? • People of advancing age • Those exposed to secondhand smoke • Chronic exposure to environmental or occupational pollutants • Alpha1-antitrypsin deficiency (typically early) • Childhoodhistory of recurrent respiratory infections • Family history of COPD

5. What’s the Physiology? • Related to chronic airway irritation, mucus production, and pulmonary scarring. • Irritation from environmental pollutants (most commonly cigarette smoke) or a genetic predisposition leads to airway inflammation, which causes increased mucus production and decreased mucociliary function • The combination of increased mucus and decreased mucociliary clearance leads to the hallmark COPD symptoms of coughing and sputum production

6. A Little More Physiology • Continued airway irritation and inflammation causes scarring within the airways leading to airway obstruction and dyspnea • Irritation, inflammation, mucus production, and scarring also predispose patients to respiratory infections which leads them to seek medical attention • Without symptoms many patients will not seek medical attention and therefore disease can progress before diagnosis or treatment

8. Epidemiologically Speaking • 10 million adults in the United States have been diagnosed with COPD • National Health and Nutrition Examination Survey (NHANES) suggests that roughly 10 percent of the adult U.S. population has evidence of impaired lung function consistent with COPD • 26 million • Underdiagnosed and Underrecognized

9. Some more Epidemiology • More common in women • More fatal in Women • Secondary to differences in lung size and mechanics, women’s airways are more hyper-responsive to exogenous irritants • Although the diagnosis of COPD is often overlooked in both populations, it is diagnosed even less in women than in men

10. How is it Diagnosed? • Clinical suspicion in patients presenting with any of the hallmark symptoms which is then confirmed by spirometry. • Cough, ↑’ed sputum production, and dyspnea • Especially in patients with a smoking history • Since symptoms may not occur until lung function is substantially reduced, early detection is enhanced by spirometric evaluation of FEV and FVC. • The National Heart, Lung, and Blood Institute recommends spirometry for all smokers 45 years or older, particularly those who present with shortness of breath, coughing, wheezing, or persistent sputum production

11. More on Diagnosis • Physical examination findings are not sensitive for the initial diagnosis of COPD • Many patients have normal examination findings • Features of lung hyperinflation include a widened anteroposterior chest diameter, hyperresonance on percussion, and diminished breath sounds

12. Some More on Diagnosis • Persistent pulmonary damage can lead to increased right-sided heart pressure causing right sided heart failure (cor pulmonale) • Which can give an accentuated second heart sound, peripheral edema, jugular venous distension, and hepatomegaly. • Signs of increased work of breathing include the use of accessory respiratory muscles, paradoxical abdominal movement, increased expiratory time, and pursed lip breathing; auscultatory wheezing is variable. • Other physical findings are occasionally cyanosis and cachexia • Weight loss is an independent predictor of mortality therefore BMI should be followed

13. A Little More on Diagnosis • The stage of the disease suggests the prognosis, and follow-up data from longitudinal studies indicate that moderate and severe stages of the disease are associated with higher mortality • Joint guidelines from the American Thoracic Society (ATS) and the European Respiratory Society (ERS) recommend screening for alpha1-antitrypsin deficiency in symptomatic adults with persistent obstruction on pft’s and asymptomatic adults with history of smoking or occupational exposure

14. Just a Smidge More Diagnosis

15. Then What? • Evidence suggests that dyspnea is a better predictor of mortality than spirometry in patients with COPD • MRC dyspnea index has also been combined with BMI, FEV1, and exercise capacity (six-minute maximum walking distance) into the 10-point BODE index. • Used to predict disease severity, risk of hospitalization, and all-cause mortality

17. How to Manage Chronic Disease? • The major goals of therapy include: • smoking cessation • symptom relief • improvement in physiological function and limitation of complications • i.e. abnormal gas exchange and exacerbations of the disease

20. 0: Avoidance of Risk Factor; Immunizations 1: PRN short acting bronchodilator 2: Reg treatment with one or more long acting bronchodilators, add Rehab 3: Inhaled steroids if repeated exacerbations 4: Oxygen, consider surgery How to advance therapy

21. More on Management • Spirometry should be performed at least annually, and more frequently if needed, to assess clinical status or the response to therapy • Abstinence from smoking results in a sustained 50 percent reduction in the rate of lung-function decline in patients with COPD, and smoking cessation is the only intervention known to be so effective in modifying the disease • Annual Influenza Vaccination • Pneumococcal Vaccination

22. What meds to use • Inhaled bronchodilators are the foundation of pharmacotherapy for COPD because of their capacity alleviate symptoms, decrease exacerbations of disease, and improve the quality of life • Albuterol and ipratropium are equally effective with regard to bronchodilation, symptom scores, and the rates of treatment failure and can be used interchangeably for mild disease as the first step in a series of measures for treating patients with COPD

23. More on Mgmt • Most patients have at least moderate airflow limitation when first evaluated, they are likely to require regularly scheduled bronchodilation and to derive benefit from a long-acting bronchodilator as initial therapy • Treatment may be initiated with either a long-acting anticholinergic agent or a b-agonist, since there is little evidence to suggest clinically significant differences between pharmacologic classes • Not appropriate for acute exacerbations

24. Mgmt Cont’d • The combination of albuterol and ipratropium provides greater bronchodilation than either drug used alone, and similar benefits are obtained by combining long-acting b-agonists with ipratropium

25. More on Mgmt • The appropriate role of inhaled corticosteroids in COPD is controversial • Trials have demonstrated that treatment with inhaled corticosteroids alleviates patients’ symptoms, reduces the frequency of exacerbations, and improves health status • Patient oriented evidence • Exacerbations appear to accelerate the rate of lung function decline in COPD • Optimize bronchodilator therapy prior to initiation of corticosteroids

26. Supplemental Therapies • Pulmonary rehabilitation improves patients’ exercise capacity, reduces dyspnea, improve the quality of life, and reduces the number and duration of hospitalizations related to respiratory disease • Hypoxemia develops as a result of a worsening ventilation–perfusion mismatch, and aggressive testing for hypoxemia is critical • Studies illustrate mortality is reduced by treatment with supplemental oxygen for 15 or more hours per day

27. Therapy cont’d • Medicare guidelines suggest that oxygen therapy should be initiated if the resting partial pressure of arterial oxygen is 55 mm Hg or lower or if the oxygen saturation is 88 percent or less • These limitations may not identify all patients who would benefit from supplemental oxygen. • For example, supplemental oxygen substantially improves training intensity and exercise tolerance even in patients in whom desaturation does not occur during exercise • As always treat the patient and not the numbers • Worsening hypoxemia during air travel must be considered, and a general recommendation is that patients requiring oxygen should increase their oxygen flow rate by 2 liters per minute during flight

28. If nothing else is working • Lung-volume–reduction surgery can reduce hyperinflation and should be considered in patients with severe upper-lobe emphysema and reduced exercise tolerance who are not faring well with medical therapy alone • Overall improvement in exercise tolerance but not resultant decrease in mortality • Single-lung transplantation is an alternative surgical option for patients with end-stage emphysema who have an FEV1 that is less than 25 percent • No significant improvement in survival

30. Management of Acute Exacerbations • Typically manifest as increased sputum production, more purulent sputum and worsening of dyspnea. Although infectious etiologies account for most exacerbations, exposure to allergens, pollutants, or inhaled irritants • Use the same medications that are used in chronic mgmt to include beta2 agonists and anticholinergics (or an increase in their dosage), the intravenous administration of corticosteroids, antibiotic therapy when indicated, and the intravenous administration of methylxanthines. • Hospitalization may be necessary to provide antibiotic therapy, appropriate supportive care and monitoring of oxygen status.

32. And that’s all folks