Chronic Obstructive Pulmonary Disease E. Sevda Özdoğan MD Chest diseases
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. http://www.youtube.com/watch?v=aktIMBQSXMo
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)
RİSK FACTORS İN COPD 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
Pathophysiological Mechanisms • Inflammation • Protease-antiprotease imbalance • Oxydative stress
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)
Diagnosis of COPD EXPOSURE TO RISK FACTORS SYMPTOMS cough tobacco sputum occupation dyspnea indoor/outdoor pollution è
Physical examination • Prolonged expiration (>6 sec), • Barrel chest • Accesory muscle activity, pursed lip respiration • Cyanosis • Wheesing, ronchus silent chest • Corpulmonale signs • Flapping tremor
Diagnosis of COPD EXPOSURE TO RISK FACTORS SYMPTOMS cough tobacco sputum occupation dyspnea indoor/outdoor pollution è SPIROMETRY
FEV1/FVC<%70 • FEV1 is used for the classification of severity • Decreased FEF 25-75 (MMFR)
Decreased DLCO and DLCO/VA in emphysema • Air trapping
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.
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
Alfa-1 antitripsin deficiency tests: • COPD before the age of 45 • Family history • Nonsmokers • Panlobular emphysema in the lower lobes
Pulmonary Hypertension in COPD • Decreased pulmonary vascularity • Hypoxemia-pulmonary vasoconstruction • Polistemia and increased blood viscosity • Pulmonary thrombosis • Hypoxemia- decreased renal blood supply-fluid retantion
Physical signs of Corpulmonale • Cyanosis • Peripheral edema (Pretibial) • Enlarged liver • Venous enlargement on the neck • Conjunctival hyperemia
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
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
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
Vaccines: Influenza vaccines reduce serious illness and death in COPD patients by 50%. Give once (in Autumn) each year. There is no evidence for recommending the general use of pneumococcal vaccine for COPD.
Pharmacologic treatment • Can improve and prevent symptoms, • Reduce the frequency and severity of exacerbations, • Improve health status, • Improve exercise tolerance.
Bronchodilators • These medications are central to symptom management in COPD. • Short acting beta agonists • LABA • Anticholinergics (long and short acting) • Theophyline
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.
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).
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.
If Corpulmonale is formed: • Diuretics • Anticoagulation • Flebotomy (if Htc>55)
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)
Main Causes of exacerbations • Tracheobronchial infections • Air pollution • Pneumonia • Pulmonary embolism • Pneumothorax • Thorax trauma • Code fractures • Beta blockers narcotic use • Arhytmia • Cardiac failure
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
Antibiotics (iv, oral) • Check fluid imbalance, nutrition • Treat concomitant disease (Corpulmonale, px etc) • Prophylactic anticoagulation • Noninvasive (BİPAP) and invasive mechanic ventilation
Noninvasive intermittent positive pressure ventilation (NIIPPV, NIMV) 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 IMV
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
Hospitalization Indications • Severe attack • No response to 4-6 hours of treatment • İmpared sleep and feeding due to dyspnea • İnsufficient care at home • >1 attack with hospitalization in one year • Concomitant severe disease • Deteoriated mental functions • Increased hypoxemia or hypercapnia
Non-Pharmacologic Treatment • Rehabilitation • Oxygen therapy • Surgical interventions
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.
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
Surgical Treatments • Bullectomy, lung volume reduction surgery (LVRS) and lung transplantation may be considered in carefully selected patients with Stage IV: Very Severe COPD.
COPD IS NOT ASTHMA ! • Different causes • Different inflammatory cells • Different mediators • Different inflammatory consequences • Different response to treatment