Chronic Obstructive Pulmonary Disease

1. Chronic Obstructive Pulmonary Disease E. Sevda Özdoğan MD Chest diseases

2. COPD • COPD is a disease state characterized by airflow limitation that is not fully reversible. The airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases.

3. Terminology • Chronic Bronchitis Defined as the presence of cough and sputum production for at least 3 months in each of 2 consecutive years, is not necessarily associated with airflow limitation. • Emphsema Irreversibl dilatation and destruction of the airways distal to terminal bronchie (without fibrosis) • Centrlobular emphysema (respiratory bronchioles) • Panlobular emphsema (resp. Br+alv ductus and alveolus)

4. Environmental Smoking (active, passive) Responsible from 80-90% of COPD) RR for Chronic bronchitis among smokers is 50 %, COPD 15-20 % Occupational exposures Miners (kadmiyum,silica) bakers, construction, wood workers Grain dust Wool Air pollution Social factors Dietary factors Low Antioxidans and vitamin (A,C,E;Mg) High salt Host related Genetic factors (%1) Alfa-1 antitripsin deficiency (otozomal recessive) Family history Age Childhood viral infections (RSV,Adenovirüs) Bronchial hyperreactivity Atophy Low birth weight RİSK FACTORS İN COPD

5. Pathophysiological Mechanisms • Inflammation • Protease-antiprotease imbalance • Oxydative stress

6. CELLULAR MECHANISMS OF COPD Cigarette smoke Alveolar macrophage ? CD8+ MCP-1 lymphocyte Neutrophil chemotactic factors Cytokines (IL-8) Mediators (LTB4) 4 ) ) Neutrophil PROTEASE INHIBITORS Neutrophil elastase - PROTEASES Cathepsins Matrix metalloproteinases Alveolar wall destruction Mucus hypersecretion (Emphysema) (Chronic bronchitis)

8. Diagnosis of COPD EXPOSURE TO RISK FACTORS SYMPTOMS cough tobacco sputum occupation dyspnea indoor/outdoor pollution è

9. Physical examination • Prolonged expiration (>6 sec), • Barrel chest • Accesory muscle activity, pursed lip respiration • Cyanosis • Wheesing, ronchus silent chest • Corpulmonale signs • Flapping tremor

10. Diagnosis of COPD EXPOSURE TO RISK FACTORS SYMPTOMS cough tobacco sputum occupation dyspnea indoor/outdoor pollution è SPIROMETRY

11. FEV1/FVC<%70 • FEV1 is used for the classification of severity • Decreased FEF 25-75 (MMFR)

12. Decreased DLCO and DLCO/VA in emphysema • Air trapping

13. Reversibility test (-) • Chestradiology • Normal • Emphysema • Pulmonaryhypertension • Blood gas Measurement of arterial blood gas tension should be considered in all patients with FEV1 < 40% predicted or clinical signs suggestive of respiratory failure or right heart failure.

19. Routine blood tests: • Polistemia • Liver function abnormality • Renal function abnormalities • ECG: • Axis changes due to diafragmatic flattening or right ventricular hypertrophy • P pulmonale • Right bundle block • İmpaired R progression

20. Alfa-1 antitripsin deficiency tests: • COPD before the age of 45 • Family history • Nonsmokers • Panlobular emphysema in the lower lobes

21. Pulmonary Hypertension in COPD • Decreased pulmonary vascularity • Hypoxemia-pulmonary vasoconstruction • Polistemia and increased blood viscosity • Pulmonary thrombosis • Hypoxemia- decreased renal blood supply-fluid retantion

22. Physical signs of Corpulmonale • Cyanosis • Peripheral edema (Pretibial) • Enlarged liver • Venous enlargement on the neck • Conjunctival hyperemia

23. Radiologic signs of corpulmonale • Cardiomegaly • Increased vascular arborization • Enlarged pulmonary artery of right hilum (over 14-16 mm) • Enlargement in main pulmonary artery • Costophrenic dullness- pleural effusion

26. Objectives of COPD Management • Prevent disease progression • Relieve symptoms • Improve exercise tolerance • Improve health status • Prevent and treat exacerbations • Prevent and treat complications • Reduce mortality • Minimize side effects from treatment

28. 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 cessationis the single most effective-and cost-effective- intervention to reduce the risk of developing COPD and stop its progression

29. Vaccines: • Influenza vaccines reduce serious illness and death in COPD patients by 50%. Give once (in Autumn) each year. • Pneumococcal vaccine

30. Pharmacologic treatment • Can improve and prevent symptoms, • Reduce the frequency and severity of exacerbations, • Improve health status, • Improve exercise tolerance.

31. Bronchodilators • These medications are central to symptom management in COPD. • Short acting beta agonists • LABA • Anticholinergics (long and short acting) • Theophyline

32. Regular treatment with long-acting bronchodilators is more effective and convenient than treatment with short-acting bronchodilators, but more expensive. • Combining drugs with different mechanisms and durations of action may increase the degree of bronchodilation for equivalent or lesser side effects. • Theophylline is effective in COPD, but due to its potential toxicity inhaled bronchodilators are preferred when available.

33. Regular treatment with inhaled glucocorticosteroids is not always necessary only appropriate for patients with: • symptomatic improvement and a documented spirometric response to inhaled glucocorticosteroids or • If FEV1 < 50% predicted and repeated exacerbations (for example, 3 in the last three years).

34. Antibiotics: Not recommended except for treatment of infectious exacerbations and other bacterial infections. • Mucolytic (Mucokinetic, Mucoregulator) Agents: Patients with viscous sputum may benefit from mucolytics, but overall benefits are very small. • Antitussives: Regular use contraindicated in stable COPD.

35. If Corpulmonale is formed: • Diuretics • Anticoagulation • Flebotomy (if Htc>55)

36. Manage Exacerbations • Exacerbations: • Increased dyspnea • Increased cough and sputum • Purulance in sputum (Sometimes drowsiness, high fever etc) • The most common causes of an exacerbation are infection of the tracheobronchial tree (80%) and; s pneumonia; h influensae; m catarrhalis; are the most common pathogens (viruses less common)

37. Tracheobronchial infections Air pollution Pneumonia Pulmonary embolism Pneumothorax Thorax trauma Code fractures Beta blockers narcotic use Arhytmia Cardiac failure Main Causes of exacerbations

38. Manage Exacerbations in the Emergency Department • Oxygen (cautious) • Short acting beta agonist and/or anticholinergic inhalation (Spacer or nebulisation) • Iv Teophyline (5-6 mg/kg in 20 min, 0.5 mg/kg/hr infusion) • Iv steroid in severe attack

40. Antibiotics (iv, oral) • Check fluid imbalance, nutrition • Treat concomitant disease (Corpulmonale, px etc) • Prophylactic anticoagulation • Noninvasive (BİPAP) and invasive mechanic ventilation

41. Noninvasive intermittent positive pressure ventilation (NIIPPV) in acute exacerbations improves blood gases and pH, reduces in-hospital mortality, decreases the need for invasive mechanical ventilation and intubation, and decreases the length of hospital stay

42. Severe Exacerbation • Cyanosis • RR>25 • HR>110/dk • Somnolence • Severe deteoriation in PFT • Pneumonia, pneumotorax • Confusion, coma, arrest • PO2<50, PCO2>70, pH<7.35 Intensive care indication

43. Hospitalization Indications • Severe attack • No response to 4-6 hours of treatment • İmpared sleep and feeding due to dyspnea • İnsufficient care at home • >3 attack with hospitalization in one year • Concomitant severe disease • Deteoriated mental functions • Increased hypoxemia or hypercapnia

44. Non-Pharmacologic Treatment • Rehabilitation • Oxygen therapy • Surgical interventions

45. Rehabilitation programs should include, at a minimum: • Exercise training • Nutrition counseling • Education. • The goals of pulmonary rehabilitation are to reduce symptoms, improve quality of life, and increase participation in everyday activities.

47. Oxygen Therapy • The long-term administration of oxygen (>15 hours per day) to patients with chronic respiratory failure increases survival and has a beneficial impact on pulmonary arterial pressure, polycythemia (hematocrit > 55%), exercise capacity, lung mechanics, and mental state. • The goal of long-term oxygen therapy is to increase the baseline PaO2 at rest to at least 60 mm Hg at sea level, and/or produce SaO2 at least 90%, which will preserve vital organ function by ensuring an adequate delivery of oxygen. • Low flow rates 2-3lt/min should be given

48. Surgical Treatments • Bullectomy, lung volume reduction surgery (LVRS) and lung transplantation may be considered in carefully selected patients with Stage IV: Very Severe COPD.

49. COPD IS NOT ASTHMA ! • Different causes • Different inflammatory cells • Different mediators • Different inflammatory consequences • Different response to treatment

50. http://www.youtube.com/watch?v=aktIMBQSXMo