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By Elfateh Seedahmed, Consultant in Pulmonary/Critical Care, Flint, MI

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  • It is likely that these statistics underestimate the prevalence of COPD by as much as 50%, as many patients underreport their symptoms and remain undiagnosed.
  • The dawn of the 21st century brings another guideline, the GOLD initiative sponsored by the World Health Organization and the National Heart, Lung, and Blood Institute (NHLBI) . presents an evidenced-based approach that can be followed by all health-care systems throughout the world.
  • Last point:leads to the development of emphysema
  • including abdominal obesity, elevated triglyceride levels, elevated high-density lipoprotein cholesterol levels, elevated BP, and high fasting blood glucose levels
  • It is believed that weight loss, and particularly skeletal muscle mass loss, is associated with a systemic inflammatory response in malnourished patients with COPD as the levels of proinflammatory cytokines IL-6 and TNF-have been shown to be elevated
  • COPD

    1. 1. COPD Elfateh Seedahmed, M.D.Assistant Professor of Medicine (Clinical) Department of Medicine College of Human Medicine Michigan State University
    2. 2. Disclosures None
    3. 3. Definition and Epidemiology Disease state characterized by chronic airflow limitation due to  Emphysema  Chronic bronchitis
    4. 4. Chronic Bronchitis Defined in clinical terms as,“ the presence of chronic productive cough for ≥3 consecutive months in 2 consecutive years” Other causes of chronic productive cough must been ruled out
    5. 5. Emphysema“An abnormal enlargement of the air spaces distal to the terminal bronchioles accompanied by destruction of their walls”
    6. 6. Definition and Epidemiology COPD ranks as the 12th largest disease burden in the world, and some project that it will rank number 5 by the year 2020 In the US more than 16 million people are afflicted with COPD The 4th cause of death in USA  The leading cause of death worldwide by 2050 (WHO prediction)
    7. 7. Definition and Epidemiology In 1996, COPD was listed as the 8th leading cause of disability-adjusted life-years in men and the 7th leading cause of disability-adjusted life- years in women In 1998, nearly 2% of all hospitalizations were attributed to COPD, and 7% of hospitalizations had COPD as a contributing cause
    8. 8. Definition and Epidemiology Nearly 20% of all hospitalizations in patients >65 years had COPD as a primary or contributing cause Mortality rates associated with cardiovascular disease and stroke were declining Mortality rate for COPD was rising at an alarming rate
    9. 9. GOLD new Definition “A disease state characterized by airflow obstruction that is no longer fully reversible and is usually progressive” Caused by an interaction between noxious inhaled agents e.g. cigarette smoke, industrial and environmental pollutants, and host factors (genetic, respiratory infections, etc.) leading to chronic inflammation in the walls and lumen of the airways
    10. 10. Biomass for cooking
    11. 11. Genetic Risk Factors for COPD α1-Antitrypsin Deficiency:  Accounts for <1% of COPD in the US  AAT is a serum protein made in the liver  Inhibits activity of specific proteolytic enzymes such as trypsin, chymotrypsin, and neutrophil elastase  Neutrophil elastase destroys lung connective tissue, particularly elastin
    12. 12. α1-Antitrypsin Deficiency Asians and African Americans are rarely affected Cigarette smoking is the most important risk factor for the development of COPD in patients with AAT deficiency Symptoms begin early in adult life (usually by 40 years of age)
    13. 13. Natural History of COPD Preclinical period of approximately 20-40 years During this asymptomatic period, lung function deteriorates Nonsmokers without respiratory disease lose 25- 30 mL/yr of lung function after age 35 years
    14. 14. Natural History of COPD Susceptible smokers, have a decline in lung function of ≥ 60 mL/yr This ultimately causes exertional dyspnea when the FEV1 is between 40-59% of its predicted value When FEV1 falls below 1 L, the 5-year mortality rate is approximately 50%
    15. 15. Natural History of COPD Smoking cessation in susceptible smoker will not result in recovery of lost FEV1 but will slow the rate of decline to normal 1 to 2 exacerbations per year will often develop in patients with milder stages of COPD Exacerbations cause a decrease in lung function for up to 90 days
    16. 16. Pathology and Pathophysiology Pathologic changes are found in large and small ( 2 mm) airways and in the lung parenchyma In advanced stages, there are changes in the pulmonary circulation, the heart, and the respiratory muscles
    17. 17. Pathology and Pathophysiology Alveolar hypoxia causes medial hypertrophy of vascular smooth muscle Intimal hyperplasia also occurs in advanced stages leading to pulmonary hypertension With advanced COPD, there is atrophy of diaphragmatic muscle, loss of skeletal muscle, and wasting of limb muscles
    18. 18. Emphysema Is a destructive process that occurs gas- exchanging airspaces:  Respiratory bronchioles  Alveolar ducts  Alveoli There is permanent enlargement of the gas- exchanging units of the lungs (acini)
    19. 19. Panacinar (panlobular) emphysema
    20. 20. Systemic Inflammation and COPD There is growing evidence that the inflammatory response of COPD is not limited to the lungs Significantly raised blood levels of C-reactive protein (CRP), fibrinogen, TNF-α, endothelin-1, IL-6, and circulating leukocytes compared with healthy subjects
    21. 21. CRP and prognosis in COPD Dahl et al, Am J Respir Crit Care Med 2007
    22. 22. Chest 2011; 139(3):648-657
    23. 23. Systemic Inflammation and COPD Airflow obstruction doubles the risk of CV mortality, irrespective of current smoking status For every 10% decrease in FEV1, cardiovascular mortality ↑ by ~ 28%, and non-fatal coronary event ↑ by ~ 20% in mild to moderate COPD Anthonisen et al, Am J Respir Crit Care Med 2002
    24. 24. Systemic Inflammation and COPD Nearly half of all COPD patients in a pulmonary rehabilitation program were shown to have 3 or more features of the metabolic syndrome
    25. 25. Clinical Features & Diagnosis Symptoms usually not present till patient has been smoking a pack/day for at least 20 years Presentation usually in the 5th decade with chronic cough The second major symptom is dyspnea Dynamic hyperinflation during exercise causes exercise limitation
    26. 26. Physical Examination Slow and prolonged expiration Wheezing Chest wall hyperinflation Limited diaphragmatic motion Distant breath and heart sounds Coarse early inspiratory crackles
    27. 27. Physical Examination Accessory muscles of respiration may be in use, as pursed-lip breathing Signs of cor pulmonale include pedal edema, a tender congested liver, and neck vein distention Cyanosis and asterixis (associated with severe hypercapnia)
    28. 28. Low flat diaphragm, an increased retrosternal airspace, and a teardrop shaped heart
    29. 29. Diagnosis PFT is important in the diagnosis and staging of COPD FEV1/VC ratio below the 5th percentile of the predicted value, identifies obstruction Severity of airway obstruction is according to reduction of FEV1 FEV1 correlate with morbidity and mortality
    30. 30. ExpirationInspiration
    31. 31. Predictors of mortality other than FEV1
    32. 32. N Eng J Med 2004;350:1005-12
    33. 33. Better than the FEV1 at predicting the risk of death from any cause and from respiratory causes among patients with COPD Score 0-2 Score 3-4 Score 5-6 Score 7-10 N Eng J Med 2004;350:1005-12
    34. 34. Management Pharmacologic intervention is offered according to  Disease severity  Patient’s tolerance for specific drugs Goals of therapy are to induce:  Bronchodilation  ↓ Airway inflammation
    35. 35. Management Smoking cessation Preventive therapy with a pneumococcal vaccine and a yearly influenza vaccine is recommended Flu vaccination has been shown to result in 52% fewer hospitalizations for pneumonia and influenza Vaccinated patients also have fewer outpatient visits for respiratory symptoms
    36. 36. Smoking Cessation Cigarette smoking compromises airway function by:  Damaging airway epithelial cells  ↑ Mucous viscosity  Slowing mucociliary clearance  ↑ Greater bacterial adherence to oropharyngeal epithelial cells
    37. 37. Smoking Cessation Physician-delivered smoking cessation interventions significantly increase smoking abstinence rates Smoking cessation interventions:  Set a quit date  Group smoking cessation clinics  Pharmacologic therapy with nicotine replacement
    38. 38. Treatment Pharmacologic Therapy Non-pharmacologic Therapy Short-Acting β2-Agonists  Oxygen Therapy  Pulmonary Rehabilitation Long-Acting β2-Agonists  Nutrition Anticholinergic Therapy  Noninvasive Positive- β2-Agonists Plus Anticholinergic Drugs Pressure Ventilation  LVRS Systemic Corticosteroids Inhaled Corticosteroids Mucolytic Drugs Antibiotics
    39. 39. Short-Acting β2-Agonists Rapid onset of action with duration of 4-6 h Improve symptoms and exercise capacity MDI use is safe three or four times daily Higher doses may cause hypokalemia, cardiac arrhythmias, and reduced arterial oxygen tension
    40. 40. Long-Acting β2-Agonists Longer duration of action (12 h) e.g. salmeterol and formoterol Improved symptoms and quality of life No tachyphylaxis Occasional tremor that improves after several days of use
    41. 41. Anticholinergic Therapy Short-acting agents (ipratropium) afford bronchodilation and relief of symptoms for 4 to 6 h Long-acting anticholinergic tiotropium offers improved bronchodilation for 24 h No tachyphylaxis Tiotropium has been shown to reduce exacerbation rates and hospitalizations Side effects are mild (occasional dry mouth)
    42. 42. β2-Agonists Plus Anticholinergic Drugs Small additional benefit to the use of either drug alone No additional side effects from combination therapy
    43. 43. Systemic Corticosteroids 20 to 30% of patients with chronic COPD improve with oral steroid therapy Responders have more eosinophils in sputum and bronchial biopsy specimens, and likely have concomitant asthma Long-term treatment is not recommended
    44. 44. Systemic Corticosteroids Treatment of hospitalized patients with high doses results in  Fewer treatment failures  Shorter hospital stays  2 weeks of therapy is sufficient Complications include cataracts, osteoporosis, secondary infection, diabetes, and skin damage
    45. 45. Inhaled Corticosteroids No significant benefit in long-term decline in FEV1 Studies demonstrated fewer exacerbations Improved quality of life indexes Benefits enhanced when coupled with long- acting β-agonist Guidelines recommend when FEV1<50% predicted and frequent exacerbations
    46. 46. Mucolytic Drugs RCTs suggest that they are ineffective at shortening the course or improving the outcomes of patients with acute exacerbations
    47. 47. Antibiotics Trials favor the use of antibiotics for acute exacerbations with  Worsening dyspnea  Increased sputum volume  Sputum purulence No evidence supporting prophylactic use
    48. 48. Oxygen Therapy When used for at least 15 h/d led to significant fall in pulmonary artery pressures and an increase in cardiac output Should be given when  PaO2 < 55 mm Hg or  Arterial oxygen saturation is < 88%; or  PaO2 is 56 to 59 mm Hg with,  ECG evidence of P pulmonale  Pedal edema, and/or  Secondary erythrocytosis
    49. 49. Oxygen Therapy Long-term therapy does not improve survival in patients with  Moderate hypoxemia (PaO2 56 to 65 mm Hg) or  Patients with only nocturnal hypoxemia
    50. 50. Refractory Disease Theophylline PDE-4 inhibitors
    51. 51. Theophylline Small changes in FEV1 with long-term use Improve symptoms and exercise capacity Adverse effects (e.g., nausea, diarrhea, headache, and irritability) Seizures and cardiac arrhythmias are common (10 to 15 times) in elderly patients with toxic blood levels
    52. 52. PDE-4 Inhibitors ↓ Inflammation and promotes airway smooth muscle relaxation  Cilomilast  Roflumilast (FDA approved 3/2011)
    53. 53. 1. The magnitude of benefit on COPD exacerbations and lung function is modest2. Back pain; decreased appetite; diarrhea; dizziness; flu-likesymptoms; headache; weight loss; nausea.
    54. 54. Pulmonary Rehabilitation Multidisciplinary program that attempts to return the patient to the highest functional capacity possible lower-extremity exercise training improves exercise tolerance Improves dyspnea, quality-of-life scores, and reduces number of hospitalizations and days spent in the hospital The effects on survival are not definite
    55. 55. Nutrition Malnutrition occurs in one quarter to one third of patients with moderate-to-severe COPD Malnutrition is an independent risk factor for mortality Both fat mass and fat-free mass are depleted
    56. 56. Nutrition Nutritional supplements alone do not reverse the loss Results with anabolic steroids, growth hormone, and the progestational agent megestrol acetate show some effect on appetite and body weight
    57. 57. Noninvasive Positive-Pressure Ventilation COPD patients have a high prevalence of  Sleep apnea  Hypoxemia at night  Hypercarbia at night  Less REM sleep  Shorter sleep times No definite conclusion regarding the effects of NIPPV in COPD patients
    58. 58. Lung Volume Reduction Surgery (LVRS) Resection of functionless emphysematous lung to improve lung elastic recoil, lung, and chest wall hyperinflation  Upper lobe emphysema  Low exercise capacity
    59. 59. Lung Volume Reduction Surgery (LVRS)  Marked increase in early mortality in patients with:  FEV1 <20 percent predicted  DLCO <20 percent predicted  Homogeneous changes on chest CT
    60. 60. Lung Transplantation BODE index >5 Post-bronchodilator FEV1 <25 percent of predicted Resting hypoxemia, defined as PaO2 <55 to 60 mmHg Hypercapnia Secondary pulmonary hypertension Accelerated decline in FEV1
    61. 61. Thank You