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Chronic obstructive pulmonary disease COPD
- 1.
- 2. Burden The 4thleading cause of death worldwide 2.7 million people across the globe die of COPD 12.36 million Indians suffer from COPD
- 3. Definition A preventableand treatable disease state characterized by persistent airflow limitation that is not fully reversible. The airflow limitation is usually progressive and is associated with an abnormal chronic inflammatory response of the lungs and airways to noxious particles or gases, primarily caused by cigarette smoking. Although COPD affects the lungs, it also produces significant systemic consequences.
- 4. preventable andtreatable: COPD can be prevented if the risk factors, especially cigarette smoke are avoided and it is treatable with the new treatments available not fully reversible: there is some reversibility, which can be treated with bronchodilators progressive: with each exacerbation causing a further deterioration in the lung functions, which never come back to what it was prior to the exacerbation. Also the elastin that is present in the alveolar walls, once destroyed by the enzymes will never be synthesized again
- 5. COPD Spectrum COPD isa spectrum of diseases that includes: Chronic bronchitis Emphysema Small airway disease Long-standing asthma that has become unresponsive to treatment
- 7. Clinical observations ledto suggestions that there were two distinct type of patients TYPE-A fighter is pink and puffing. Although the person is breathless, arterial tensions of oxygen and carbon dioxide are normal and there is no cor pulmonale. These individuals were thought to be suffering predominantly from emphysema. TYPE-B non-fighter, on the other hand, is blue and bloated. The person does not appear to be breathless but has marked arterial hypoxemia, carbon dioxide retention, secondary polycythemia and cor pulmonale. These patients were thought to be suffering predominantly from chronic bronchitis
- 8. Causes of COPD COPD is usually related to a history of tobacco smoking, cigarette smoking, pipe & cigar smoke. Breathing in air pollution and chemical fumes or dust from the environment or workplace also can contribute to COPD. In rare cases a genetic condition called alpha1-antitrypsin deficiency may play a role in causing COPD Non-Smoker Smoker Smoking causes 80-90% of COPD. 50% of smokers develop chronic bronchitis 15-20% of smokers develop clinical airflow obstruction
- 9. Pathogenesis of COPD Noxiousparticles and gases Lung inflammation Host factors COPD pathology Proteinases Oxidative stress Anti-proteinases Anti-oxidants Repair mechanisms
- 10.
- 11. Pathophysiological Features ofCOPD INFLAMMATION IN COPD Small airway disease Airway inflammation Airway remodeling Parenchymal destruction Loss of alveolar attachments Decrease of elastic recoil AIRFLOW LIMITATION
- 12. Bronchoconstriction Mucus hyper secretion Lossof elastic recoil Airway narrowing Dynamic hyperinflation during exercise Oxidative stress Neutrophils Macrophages CD8+ lymphocytes IL-8 and TNF- Protease/antiprotease imbalance Alveolar destruction Glandular hypertrophy Airway fibrosis Blood vessels Airflow Limitation Inflammation Structural Changes normal small airway COPD small airway
- 13. Differential Diagnosis: COPDand Asthma
- 14.
- 15. Spirometry in COPD Early,accurate diagnosis More sensitive than peak flow or CXR Document change in lung function over time Having a “number” may benefit the patient Helpful in stratifying the degree of disease Normal FEV1 > 80% of predicted value Predicted value varies with age, height and sex Normal FEV1% > 70% Consider spirometry in past and present smokers over age 45, and patients with chronic cough, dyspnea or wheezing
- 16. In COPD Spirometryshould be done for : Diagnosis of the disease Assessment of severity of the disease Follow the progress of the disease Spirometry may detect the presence of mild airflow obstruction 5-10 years before the disease starts to cause symptoms. Spirometry: Normal and Patients with COPD
- 17. Factors determining severityof Chronic COPD Severity of Symptom Severity of airway limitation Frequency of severity of exacerbations Presence of complications of COPD Presence of respiratory insufficiency Comorbidity General health status Number of medications needed to manage disease
- 18.
- 19. The GOLD Initiative2011 A Change of Paradigm
- 20. The change 2010 Assessing impact ofthe disease on lung function (FEV1) 2011 Assessing impact of the disease on FEV1; Symptoms & health status; the risk of future events (exacerbations & mortality) A move beyond the “One size fits all” approach
- 21. Why the change? FEV1- ‘gold standard’ for the diagnosis and assessment of COPD severity But alone, it is an unreliable marker of severity of breathlessness exercise limitation health status impairment exacerbation frequency What do we have today? Easy to use questionnaires for symptoms (mMRC) & health assessment (CAT) available Hence, a new approach to • Assessment • Management (one that matches assessment to treatment objectives) FEV1 alone does not completely capture the heterogeneity that exists among patients with COPD
- 22. The New Combinedassessment Assess symptoms (Less symptoms/more symptoms) - Use the COPD Assessment Test (CAT) OR - mMRC Breathlessness scale Assess degree of airflow limitation using spirometry Assess risk of exacerbations (low risk/high risk) - High risk: 2 exacerbations or more in the last year OR - FEV1 <50% predicted (GOLD 3 & 4)
- 23. Grade Description ofBreathlessness Group 0 I only get breathless with strenuous exercise. A or C 1 I get short of breath when hurrying on level ground or walking up a slight hill. A or C 2 On level ground, I walk slower than people of the same age because of breathlessness, or have to stop for breath when walking at my own pace. B or D 3 I stop for breath after walking about 100 yards or after a few minutes on level ground. B or D 4 I am too breathless to leave the house or I am breathless when dressing. B or D The Modified Medical Research Council Dyspnea Scale, or MMRC, uses a simple grading system to assess a patient's level of dyspnea -- shortness of breath. The MMRC is used to help calculate BODE Index, a tool for predicting life expectancy of someone with COPD. MMRC Dyspnea Scale
- 24. COPD Assessment Test(CAT) 8 item unidimensional measure of health status impairment in COPD. Score 0-40 0 to 9 – less symptoms- Group A or C > 10 - More symptoms- Group B or D
- 25. Less symptoms Moresymptoms High risk Low risk Risk (GOLD Classification of Airflow Limitation) Risk (Exacerbation history) > 2 1 0 (C) (Less symptoms, high risk) mMRC 0-1 CAT < 10 4 3 2 1 mMRC > 2 CAT > 10 Symptoms (mMRC or CAT score) The A, B, C and D of COPD (A) (Less symptoms, low risk) (B) (More symptoms, low risk) (D) (More symptoms, high risk)
- 27. Management of StableCOPD The problems of the COPD patient that should be treated are as follows: 1. Breathlessness & exercise limitation 2. Frequent exacerbations 3. Respiratory failure 4. Cor pulmonale 5. Under nutrition 6. Chronic productive cough 7. Anxiety & depression
- 28. The clinicalgoals in the treatment of COPD 1. Prevent or reverse disease progression 2. Relieve symptoms 3. Improve health status 4. Increase exercise tolerance 5. Prevent and treat exacerbations 6. Prevent and treat complications 7. Decrease mortality and/or prolong survival 8. Minimize treatment side e ects ff
- 30. Main components inthe management of COPD Pharmacotherapy Non pharmacological management
- 31. Non- Pharmacotherapy Component Smokingcessation Pulmonary rehabilitation Pneumococcal and influenza vaccination Long-term oxygen therapy Non-invasive positive pressure ventilation Surgery
- 32. Smoking cessation Strategy- ASK ADVISE ASSESS ASSIST ARRANGE Pharmacotherapy- NRT – Nicotine gum, patch, lozenges, inhaler, nasal spray Varenicline Bupriopion Nortriptyline
- 33.
- 34. Patient First choice (Evidencebased) Second choice (Clinical judgment) Alternative choices (cost issues and availability) A (Less sympto ms, low risk) mMRC 0-1 GOLD1,2 Exacerbati on 0-1 SAMA or SABA LAMA or LABA or SABA and SAMA Theophylline B (More sympto ms, low risk) mMRC >2 GOLD1,2 Exacerbati on 0-1 LAMA or LABA LAMA and LABA SABA and/or SAMA Theophylline C (Less sympto ms, high risk) mMRC 0-1 GOLD3,4 Exacerbati on ≥ 2 ICS + LABA or LAMA LAMA and LABA PDE4-inh. SABA and/or SAMA Theophylline D (More sympto ms, high risk) mMRC >2 GOLD3,4 Exacerbati on ≥ 2 ICS + LABA or LAMA ICS and LAMA or ICS + LABA and LAMA or ICS+LABA and PDE4-inh. or LAMA and LABA or LAMA and PDE4-inh. Carbocysteine SABA and/or SAMA Theophylline New approach to management
- 35. Long-term oxygen therapy(LTOT) > 15 Hrs/day Indications PaO2 ≤ 55 mm Hg or SaO2 ≤ 88% ± hypercapnia PaO2 55-60 mm Hg or SaO2 88% if there is e/o PHT, CCF or Polycythemia (PCV> 55%)
- 36. Surgical treatments LVRS(Lung Volume Reduction Surgery) parts of lung resected to ↓ hyperinflation, ↑ elastic recoil -in severe predominantly upper lobe emphysema - low post rehabilitation exercise capacity BLVR (Bronchoscopic Lung Volume Reduction) - in severe heterogenous emphysema ( on CT scan) and hyperinflation ( TLC> 100% and RV> 150% predicted)
- 37. Surgical treatments LungTransplantation in COPD with BODE index > 5 and at least one of the following- H/o exacerbation with acute hypercapnia ( > 50 mm Hg) Pulmonary HTN or corpulmonale or both despite O2 therpy FEV1 < 20% predicted with either < 20% predicted or homogenous emphysema Bullectomy for large bulla
- 38. COPD EXACERBATION Aprominent feature of the natural history of COPD episodes of increased dyspnea and cough and change in the amount and character of sputum. Viral respiratory infections are present in approximately one-third of COPD exacerbations. Bacteria frequently implicated in COPD exacerbations include Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis.
- 39. MANAGEMENT OF EXACERBATION Bronchodilators Nebulized inhaled beta 2 agonist anticholinergic agent. methylxanthines (such as theophylline). If added, serum levels should be monitored in an attempt to minimize toxicity. Antibiotics Glucocorticoids 30–40 mg of oral prednisolone for a period of 10– 14 days
- 40. Oxygen keep arterialsaturations around 90% Mechanical Ventilatory Support The initiation of noninvasive positive-pressure ventilation (NIPPV) in patients with respiratory failure, defined as PaCO2 >45 mmHg, results in a significant reduction in mortality rate, need for intubation, complications of therapy, and hospital length of stay.
- 41. Invasive (conventional)mechanical ventilation via an endotracheal tube is indicated for patients with severe respiratory distress despite initial therapy, life-threatening hypoxemia, severe hypercarbia and/or acidosis, markedly impaired mental status, respiratory arrest, hemodynamic instability, or other complications.
Editor's Notes
- #19 The Global Initiative for Chronic Obstructive Lung Disease (GOLD) committee has recently released a new, extensively revised version of its existing guidelines on Chronic Obstructive Pulmonary Disease. It builds on the strengths of its original recommendations and incorporates newer scientific knowledge and evidence. The revised report brings in a more individualized approach to COPD classification and, based on this, a new paradigm for management of stable disease.
- #20 In previous GOLD documents, recommendations for management of COPD were based solely on spirometric category. However, there is considerable evidence that the level of FEV1 is a poor descriptor of disease status and for this reason the management of stable COPD based on a strategy considering both disease impact (determined mainly by symptom burden and activity limitation) and future risk of disease progression (especially of exacerbations) is recommended.
- #21 In previous GOLD documents, recommendations for management of COPD were based solely on spirometric category. However, there is considerable evidence that the level of FEV1 is a poor descriptor of disease status and for this reason the management of stable COPD based on a strategy considering both disease impact (determined mainly by symptom burden and activity limitation) and future risk of disease progression (especially of exacerbations) is recommended.
- #22 In previous GOLD documents, recommendations for management of COPD were based solely on spirometric category. However, there is considerable evidence that the level of FEV1 is a poor descriptor of disease status and for this reason the management of stable COPD based on a strategy considering both disease impact (determined mainly by symptom burden and activity limitation) and future risk of disease progression (especially of exacerbations) is recommended. Assessment of COPD is now based on the patient’s symptoms, risk of exacerbations, the severity of the spirometric abnormality, and the identification of comorbidities.
- #25 You need to assess the symptoms first (as per the COPD Assessment Test (CAT) or mMRC Breathlessness scale), followed by the risk of exacerbations (looking at the FEV1 and history of exacerbations (two or more exacerbations within the last year or an FEV1 < 50 % of predicted value are indicators of high risk). Based on this combined assessment, the GOLD report divides patients into four groups: A (less symptoms, low risk of exacerbations and other negative events); B (more symptoms, low risk); C (less symptoms, high risk); and D (more symptoms, high risk).
- #34 The classes of medications commonly used in treating COPD are shown in the table below. The choice within each class depends on the availability and cost of medication and the patient’s response. Each treatment regimen needs to be patient-specific as the relationship between severity of symptoms, airflow limitation, and severity of exacerbations will differ between patients.