IN THE NAME OF GOD
COPD Dr.O.Paknejad Pulmonologist Shariati Hospital TUMS
Definition of COPD* COPD is a preventable and treatable chronic lung disease characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lung. * Adapted from the Global Initiative for Chronic Obstructive Lung Disease 2007
Epidemiology of COPD COPD is a leading cause of mortality worldwide and projected to increase in the next several decades. COPD mortality trends generally track several decades behind smoking trends. In the US and Canada, COPD mortality for both men and women have been increasing. In the US in 2000, the number of COPD deaths was greater among women than men.
Percent Change from 1965 in Age- Adjusted Death Rates, U.S., 1965-1998 3.0 2.5 2.5 2.0 2.0 Coronary Heart Disease Stroke Other CVD COPD All Other Causes 1.5 1.5 1.0 1.0 0.5 0.5 0.0 0 59% 64% 35% +163% 7% 1965-1998 1965-1998 1965-1998 1965-1998 1965-1998 Source: NHLBI/NIH/DHHS
Number Deaths x 1000 COPD Mortality by Gender, U.S., 1980-2000 70 60 50 40 30 Men Women 20 10 0 1980 1985 1990 1995 2000 Source: US Centers for Disease Control and Prevention, 2002 cited in GOLD 2007
Risk Factors for COPD Nutrition Infections Socio-economic status Aging Populations 7
Pathophysiology of COPD Chronic inflammation, bronchial wall edema, mucous secretion, hyperinflation and air trapping Increase in proteinases compared to antiproteinases and in free radicals leading to parenchymal destruction Changes in pulmonary vasculature leading to ventilation-perfusion mismatching, pulmonary hypertension, cor pulmonale
Cigarette smoke Biomass particles Particulates Pathogenesis of COPD Host factors Amplifying mechanisms Anti-oxidants LUNG INFLAMMATION Anti-proteinases Oxidative stress Proteinases Repair mechanisms COPD PATHOLOGY Source: GOLD 2007
Changes in Small Airways in COPD Patients Inflammatory exudate in lumen Disrupted alveolar attachments Thickened wall with inflammatory cells - macrophages, CD8 + cells, fibroblasts Lymphoid follicle Peribronchial fibrosis Source: COLD 2007
Changes in Lung Parenchyma in COPD Alveolar wall destruction Loss of elasticity Destruction of pulmonary capillary bed Inflammatory cells macrophages, CD8 + lymphocytes Source: GOLD 2007
How Does COPD Affect Breathing?
Pulmonary Hypertension in COPD Chronic hypoxia Pulmonary vasoconstriction Pulmonary hypertension Cor pulmonale Muscularization Intimal hyperplasia Fibrosis Obliteration Death Edema Source: GOLD 2007
PATHOPHYSIOLOGY AIRWAY OBSTRUCTION: DECREASE OF FEV1 & DECREASE FEV1/FVC HYPERINFLATION GASEXCHANGE:DECREASE PO2:FEV1<50% INCREASE PCO2:FEV1<%25 INCREASE PAP&CORPULMONALE:FEV1<25% & PO2<55
Reversible Causes of Airflow Limitation Accumulation of inflammatory cells, mucus, and plasma exudate in bronchi Smooth muscle contraction in peripheral and central airways Dynamic hyperinflation during exercise
Irreversible Causes of Airflow Limitation Fibrosis and narrowing of the airways Loss of elastic recoil due to alveolar destruction Destruction of alveolar support that maintains patency of small airways
NATURAL HISTORY SEVERITY OF EXPOSURE DURATION OF EXPOTURE BASALE LUNG VOLUME
Diagnosis and Assessment of COPD
CLINIC NL EXPIRATORY TIME>4 SEC HYPERINFLATION ACCESSORY MUSCLE USE CYANOSE:PINK PUFFER& BLUE BLOATER DECREASE BMI RT HEART FAILURE CLUBBING_
Patient A 54 year old man with a 80+ pack-year smoking history, presents with dyspnea while climbing stairs and an occasional, non-productive cough What would you look for/expect on exam?
Patient A: Examination Diminished breath sounds on auscultation Forced expiratory time of >6 seconds Decreased I/E ratio Increased thoracic circumference and decreased change with respiration Increased resonance to percussion
Patient A: Test Results CXR Hyperinflation and increased lucency FEV1/FEV=.55 FEV1=40%
Patient B 62 year woman with 40 p-yr history presents with chronic cough for 3 months, productive of clear to light yellow phlegm What would you look for/expect on exam?
Patient B Rhonchus breath sounds 1+ ankle edema
Patient B: Test Results CXR peribronchial thickening FEV1/FEV=.60 FEV1=55%
Diagnosis and Assessment 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 FEV 1 /FVC < 0.70 confirms the presence of airflow limitation that is not fully reversible. 27
0 1 2 Spirometry: Normal and COPD FEV 1 Normal COPD FEV 1 4.150 5.200 80 % 2.350 FVC 3.900 FEV 1 / FVC 60 % Liter 3 4 FEV 1 COPD FVC 5 Normal FVC 1 2 3 4 5 6 Seconds
Classification of COPD Severity by Spirometry post Bronchodilator* 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 * Adapted from the Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2007
Differential Diagnosis: COPD and Asthma COPD Onset in mid-life Symptoms slowly progressive Long smoking history Dyspnea during exercise Largely irreversible airflow limitation ASTHMA Onset early in life (often childhood) Symptoms vary from day to day Symptoms at night/early morning Allergy, rhinitis, and/or eczema also present Family history of asthma Largely reversible airflow limitation
Management of COPD
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 32
General Points Only smoking cessation and O2 therapy (when indicated) have been shown to prolong survival Other therapies aimed at relieving symptoms, improving quality of life, reducing exacerbations and need for hospitalizations
Risk Factor Reduction Smoking cessation (prolongs survival) Avoid exposure to second hand cigarette smoke Reduction of exposure to indoor and outdoor pollution Influenza vaccine Pneumococcal vaccines
ASK Brief Strategies to Help the Patient Willing to Quit Smoking Systematically identify all tobacco users at every visit. ADVISE Strongly urge all tobacco users to quit. (even a brief (3-minute) period of counseling to quit results in smoking cessation in 5-10% of patients.) ASSESS Determine willingness to make a quit attempt (stages of change). ASSIST Aid the patient in quitting. ARRANGE Schedule follow-up contact.
Therapy at Each Stage of COPD I: Mild II: Moderate III: Severe IV: Very Severe FEV 1 /FVC < 70% FEV 1 /FVC < 70% FEV 1 > 80% predicted FEV 1 /FVC < 70% 50% < FEV 1 < 80% predicted FEV 1 /FVC < 70% 30% < FEV 1 < 50% predicted FEV 1 < 30% predicted or FEV 1 < 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
Treatment of Stable COPD: 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 ß 2 - agonists and anticholinergics used singly or in combination Regular treatment with long-acting bronchodilators is more effective and convenient than treatment with short-acting bronchodilators 37
Treatment of Stable COPD: Inhaled Glucocorticoids Consider adding regular treatment with inhaled glucocorticosteroids to bronchodilator treatment is for symptomatic COPD patients with an FEV1 < 50% predicted (Stage III and IV) and repeated exacerbations (Evidence A). An inhaled glucocorticosteroid combined with a long-acting ß2-agonist is more effective than the individual components (Evidence A). 38
Treatment of Stable COPD Other Medications Chronic oral Prednisone Use in chronic COPD is controversial. No effect on survival. May improve symptoms and reduce hospitalizations in some patients already at maximum treatment Mucolytics & Expectorants (SSKI, guafenesin) Relives symptoms from copious, viscous secretions Oral Theophylline If inhalers not sufficient Side effects common
Treatment of Stable COPD: Home Oxygen Therapy > 15 hours/day reduces mortality Criteria for O2 therapy Pa O2 < 55 mm Hg (O2 saturation < 88%) at rest or during exercise or sleep or Pa O2 < 60 mm Hg and hematocrit >52% Bipap when sleeping may provide additional improvement
Treatment of Stable COPD: Pulmonary Rehabilitation and Patient Education Typically includes exercise, education and psychological support Shown to improve symptoms, exercise capacity, reduce use of medical care, reduce anxiety and depression
Treatment of Stable COPD: Surgery Primarily for patients with emphysema Few RCTs, no evidence for improvement in mortality but can relieve symptoms Improves QOL and exercise capacity in patients with primarily upper lobe disease, low exercise capacity, and FEV1 between 20 and 30% Lung transplantation
Treatment of Acute Exacerbations of COPD
Acute Exacerbations of COPD 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. 44
Outpatient Treatment of Acute Exacerbations: Bronchodilators Inhaled bronchodilators (particularly inhaled ß2-agonists with or without anticholinergics) are effective treatment for exacerbations of COPD (LOE: A). 45
Outpatient Treatment of Acute Exacerbations: Prednisone Oral prednisone is effective treatment for exacerbations of COPD (LOE: A). 46
Outpatient Treatment of COPD Exacerbation: Antibiotics Surprisingly little evidence of efficacy Typically use in patients with purulent sputum or other signs of infection Amoxicillin, doxycycline, azithromycin, trimethoprim-sulfa are reasonable first line choices
Indications for Hospital Admission of Patient with Acute Exacerbation Resting dyspnea after initial treatment Lack of response to initial treatment Significant co-morbid conditions) Severe underlying COPD/prior ICU ventilation for exacerbations New physical signs (e.g., new peripheral edema) Diagnostic uncertainty Insufficient home support
Inpatient Treatment of Acute Exacerbations Oxygen to keep O2 sat >90% Nebulizer treatments with bronchodilators Steroids (LOE A) (40 to 60 mg daily for 7 to 14 days, IV or PO) Antibiotics (LOE B) Typically ceftriaxzone (1 gram IV q 24 h) + doxycycline (100 mg po q 12 h) at SFGH Fluids
The End Thank you