Presentation on theme: "CHRONIC OBSTRUCTIVE PULMONARY DISEASE"— Presentation transcript:
1 CHRONIC OBSTRUCTIVE PULMONARY DISEASE By Dr Aguilera
2 DefinitionIn 2001, the Global Initiative for Chronic Obstructive Lung Disease (GOLD) report was developed to define COPD by an expert panel which includes the National Heart, Lung and Blood Institute and the World Health Organization.COPD is “A disease state characterized by airflow limitation that is not fully reversible; it is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases.”
3 Definition Cont’dPrevious Guidelines and Definitions included Chronic bronchitis and emphysema, but these are not included in the current definition.The GOLD report’s definition of COPD regards chronic bronchitis, emphysema and asthma as different aspects of the disease that are not mutually exclusive.
4 Definition Cont’d Chronic Bronchitis Emphysema Asthma Defined by the presence of chronic productive cough for three months in each of two successive years in a patient in whom other causes of cough are excludedEmphysemaIs a pathological term describing the abnormal permanent enlargement of airspaces distal to the terminal bronchioles, accompanied by destruction of their walls without obvious fibrosis.AsthmaChronic inflammatory disease of the airways with bronchial hyper-responsiveness, reversible airway obstruction, and respiratory symptoms. (See previous lecture)
5 Pathophysiology Bronchial inflammation Caused by inflammatory cells (macrophages, neutrophils and CD8 cytotoxic T cells) in a response to noxious stimulirelease of enzymes (proteases)these cause destruction of connective tissue in the airways and alveolar walls.Also stimulate mucus production by goblet cellsDifferent than what we see in Asthma (CD4 and eosinophils)Ciliary damage occurs directly by noxious stimuli (tobacco, occupational dusts and chemicals, and air pollution)
6 Pathophysiology Cont’d Variability of Response to Noxious StimuliGeneticsimbalance of antiproteasesMay explain why only approximately 15% of smokers develop COPDAlpha-1-antitrypsin deficiencyAs a result, air trapping, collapse of alveoli and inability to clear debris from the airways occur, which manifest clinically as the COPD syndrome.
8 Epidemiology Approx 16 million people in U.S. have COPD 5th leading cause of death4th in people > 45 yrsMost deaths occur in people > 65 yearsIn 2000: ED visits = 1.5 millionHospitalizations = 726,000Deaths = 119,000Health care costs approx 15 billion/yearTobacco smoking accounts for 80-90% of casesOnly 15% of smokers develop COPDWomen are affected more than men with same tobacco exposureAlpha-1-antitrypsin accounts for <.1% of casesHomozygous (.02%) < Heterozygous (2-3%) - whitesWhen to test for serum levels? In pts with COPD at young age, particularly in those with (+) FHx and no exposure to tobaccoReplace with alpha-1-proteinase inhibitor (Prolastin)
9 DiagnosisHistoryPatients with COPD usually have been smoking at least 20 pack years before symptoms develop.Cough usually is the first symptom. This is followed by sputum production and then shortness of breath which worsen over time and may get worse with exacerbations.Wheezing may be presentExposure to risk factors: tobacco, occupational dusts and chemicals, air pollution
10 Diagnosis Cont’d Physical Examination Usually normal early in the course of the diseaseFindings are variable as the disease progressesChest SignsProlonged expiration with/out wheeze; decreased breath sounds; Crackles especially with exacerbations; Increased anteroposterior diameter due to hyperinflationDistant heart soundsExtrathoracic SignsLeaning forward to relieve dyspnea; weight loss, cyanosisManifestations of Cor PulmonalePoor Px
11 Diagnosis cont’d Pulmonary Function Test (PFT)/Spirometry Gold standard for diagnosis COPDFEV1/FVC ratio of < 70% defines the presence of obstructive disease.Cannot determine difference between COPD, chronic bronchitis or emphysemaFEV1 is used to determine severity of diseasePeak Expiratory Flow Rate (PEFR) is used to monitor response to therapyLung function should be measured with bronchodilator evaluation. The absence of a significant response (>15% increase in FEV1) on one test should not be the reason to hold bronchodilator therapy.If improvement >20% and FEV1 becomes normal = AsthmaIf FEV1 increases but is still below normal = Mixed Asthma/COPD
12 Diagnosis Cont’d Chest X-Ray (CXR) Arterial Blood Gas (ABG) Radiological changes don’t usually occur until COPD is advanced (overdistention, bullae formationDone to identify co-existing conditionsArterial Blood Gas (ABG)Used in most cases to determine if a patient requires oxygen maintenance based on level of hypoxiaUsually done when FEV1 < 40%, and in those with signs of respiratory failure (PO2<60 or PCO2>45) or right heart failureCan also give information regarding CO2 levelsComplete Blood Count (CBC)Can identify erythrocytosis/polycythemia as a result of chronic hypoxemia and should be done in patients being considered for O2 supplementation
13 Classification of COPD (Remember FEV1/FVC is used in the Dx COPD!) % Predicted FEV11995 ATS % Predicted FEV12001 GOLD Report % Predicted FEV1SymptomsStage 0: At risk, but PFT’s are normalFEV1/FVC > 70%Cough and sputum production may be present80-100%Stage I: Mild> 80% predicted50-80%50-80% predictedStage IIA: ModerateCough and sputum and dyspnea may be present0-50%Stage II: Moderate35-50% predictedStage IIB: Moderate30-50% predictedCough, sputum and dyspnea with more exacerbationsStage III: Severe<35% predicted< 30% predicted or resp failure or RHFCough, sputum and dyspnea with frequent exacerbations
14 Overall Treatment of COPD 1st Step is to establish a diagnosisSpirometry in patients with Sx or RFCXR to exclude other conditions2nd Step is to Classify the stage of diseaseUsed to guide therapyFor example, Stage II requires smoking cessation, an ABG, pharmacotx and consultation with a pulmonologist3rd Step is to educate your patientsThis is the key componentMain goals of treatment are to improve quality of life and decrease mortalityOnly 2 interventions decrease mortality: smoking cessation and long term O2 supplementation
15 Overall Treatment Cont’d 4th Step is to begin PharmacotherapyInhaled BronchodilatorsImprove symptoms and decrease airflow limitationAlbuterol 2 puffs Q6hrs/PRNIpratropiumUsually first line therapyStart with 2 puffs QID and may increase to 6 puffs TIDCommon problemsInadequate education regarding meds and techniqueSuboptimal dosingInadequate monitoring of response to treatmentThe use of long acting beta agonists (Salmeterol and Formoterol) in COPD is still in evolution.
16 Overall Treatment Cont’d Inhaled SteroidsDo not affect the decline in FEV1, thus the severityIn mod-severe disease these meds showed a significant decrease in the frequency of symptoms and exacerbationsTheophyllineGOLD report recommends against its use due to availability of other drugs, high Sfx profile and drug interactions.Does work for some patientsKeep levels between 8-12 mcg/mlMonitor regularlyBe aware of drug interactions
17 Overall Treatment Cont’d Oral SteroidsLong term use is not recommendedA beneficial response to a short course of an oral steroid does not predict benefit from the chronic use of oral steroids.Long term disease effects are unknown.Studies failed to show a difference in the # of exacerbations, symptoms or spirometry results when continuation vs withdrawal of prednisone was comparedIf considering long term oral steroids for a patient with severe disease, then use smallest dose possible. Usually done in conjunction with pulmonologist.
18 Overall Treatment Cont’d 5th step is to prevent and treat complicationsChronic HypoxiaConsequences include dyspnea, impaired cognition, ischemic CM, ploycythemia/ erythrocytosis with hyperviscosity syndromes, and pulmonary HTNSupplemental O2 can improve symptoms and prevent some of these complications. In fact, life expectancy increases.ABG evaluation at appropriate timesMediCare guidelinesPaO2 < 55mmHg; POx < 88% for any patientPaO mmHg; POx = 89% for those with chronic hypoxic complications as listed above
19 Overall Treatment Cont’d ImmunizationsAnnual influenza shotsPolyvalent pneumococcal vaccine at time of diagnosis and again in 5 years or at age 65, whichever comes later.Consultation with a specialistPulmonologistStage IIB and IIISurgeonWhen considering lung volume reduction surgery or transplantation