Copd overview and update 2016
- 1. Presented by Dr. Ajay Kumar Agarwala Resident (Neurology) Bangabandhu Sheikh Mujib Medical University, Dhaka, Bangladesh. CHRONIC OBSTRUCTIVE PULMONARY DISEASE OVERVIEW & UPDATE
- 2. Key facts 90% of COPD deaths occur in low- and middle-income countries The primary cause of COPD is tobacco smoke The disease now affects men and women almost equally Not curable, but treatment can slow the progression 2 Chronic obstructive pulmonary disease (COPD)
- 3. 3rd leading cause death in developing world Prevalence in Bangladesh 21.25% (above 40 year age) Currently total burden about 6 million in BD (Worldwide 80 million) 3 Picture in Bangladesh Top 10 Causes of Death Cancer 13% Lower Respiratory Infections 7% Chronic Obstructive Pulmonary Disease 7% Ischemic Heart Disease 6% Stroke 5% Preterm Birth Complications 4% Tuberculosis 3% Neonatal Encephalopathy 3% Diabetes 3% Cirrhosis 3% Source: https://www.cdc.gov/globalhealth/countries/banglade sh/
- 4. It is characterized by Progressive air way limitation that is not fully reversible. Emphysema Chronic Bronchitis Small airway disease 4 What is COPD?
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- 7. Risk factors HOST FACTORS Genes Male sex Ethnicity (Caucasians) Airway hyper- responsiveness Poor lung development/ poor growth EXPOSURE FACTORS Tobacco smoke (Unusual if < 10 pack years) Occupational- dust/fumes/Smokes Air pollution Persistent Infections (adenovirus, HIV) Low Socioeconomic status 7
- 8. • Pink puffer Type A- Emphysema Predominant • Blue bloater Type B- Chronic Bronchitis Predominant Type C- Mixed (MOST COMMON) 8 Types
- 9. Abnormal permanent dilatation of airspaces distal to terminal bronchioles (resp. bronchioles, alveolar ducts and alveoli) Emphysema 9
- 10. 10 Pathology of emphysema Cigarette leads to inflammatory and immune cell recruitment within the terminal air spaces < 2mm Release elastolytic and other proteinases that damage the ECM Cell death (Endothelial and Epithelial) Ineffective repair of elastin and other ECM leads to airspace enlargement
- 11. Small Airways • Airway inflammation & edema, fibrosis, cellular infiltration and destruction of elastic fibers of respiratory bronchiole and alveolar ducts • Goblet metaplasia and mucus plugs • Reduce surfactant leads to airway narrowing and collapse • Smooth muscle hypertrophy • Increased airway resistance • Narrowing and drop out of small airway Lung Parenchymal Destruction • Loss of alveolar attachments • Perforated alveoli coalesce to form large air spaces • Decrease of elastic recoil Airway limitation Decrease pulmonary and chest wall compliance Airway hyperinflation Poor gas exchange Respiratory failure
- 12. Bronchitis is inflammation of the inner lining of the Bronchi ( Cough & Sputum for most of the days for 3 months for consecutive 2 years) Bronchitis Enlargement of mucus-secreting glands & goblet cells mainly in large airway Inflammatory cell infiltrate (Neutorphil elastase) Smooth muscle hypertrophy & bronchial hyper-responsiveness Increased sputum production and airway limitation
- 14. COPD Comorbidities Increased risk of: Cardiovascular diseases Cardioselective beta-blockers are not contraindicated in COPD Osteoporosis Respiratory infections Anxietyand Depression Diabetes Lung cancer These comorbid conditions may influence mortality and hospitalizations and should be looked for routinely, and treated appropriately.
- 15. HISTORY Dyspnoea Fatigue, Morning headache (hypercapnia) Cough, Sputum +/- Frequent respiratory infection Risk exposure (Smoke, pollution etc.) Family history 15 How to diagnose?
- 16. PHYSICAL EXAMINATION Pursed lip breathing and use of accessory respiratory muscles “ Paradoxical inward movement of the lower rib cage during inspiration: Hoovers sign” Rhonchi, Prolonged expiration, Crackles (if infection) Decreased intensity of breath and heart sound Polycythemia, Cyanosis, Digital clubbing (Malignancy), dependent pitting edema 16 Diagnosis…..(cont.)
- 17. Thin with a barrel chest Little or no cough or expectoration pursed lips and use of accessory respiratory muscles patients may adopt the tripod sitting position The chest may be hyper-resonant & wheezing may be heard Heart sounds are very distant Maintain normal PaC02 until late stage 17 Emphysema PINK PUFFER
- 18. Patients may be obese Frequent cough and expectoration are typical Coarse Ronchi and wheezing may be present Earlier hypercapnia so early secondary Polycythemia Patient may have edema and cyanosis 18 Chronic bronchitis BLUE BLOATER
- 19. 19 INVESTIGATION The global initiative for chronic obstructive lung disease (GOLD) used severity staging based on air flow limitation. stage I: MILD, FEV1 > 80% of normal stage II: MODERATE, FEV1 = 50-79% of normal stage III: SEVERE, FEV1 = 30-49% of normal stage IV: VERY SEVERE, FEV1 <30% of normal or <50% of normal with presence of chronic respiratory failure present The FEV1:FVC ratio should be <0.70 for all stages (Post-bronchodilator) Spirometry must to establish diagnosis
- 20. Spirometry: Normal Trace Showing FEV1 and FVC 1 2 3 4 5 6 1 2 3 4 Volume,liters Time, sec FVC5 1 FEV1 = 4L FVC = 5L FEV1/FVC = 0.8
- 21. Spirometry: Obstructive Disease Volume,liters Time, seconds 5 4 3 2 1 1 2 3 4 5 6 FEV1 = 1.8L FVC = 3.2L FEV1/FVC = 0.56 Normal Obstructive
- 22. Chest X ray HRCT Lung volumes 1. Helium dilution technique 2. Body plethysmography Arterial blood gas (ABG) 22 Investigation…(cont.) CBC Sputum examination ECG ECHO Alpha 1 Antitrypsin ( if Basal Emphysema)
- 23. 23 Emphysema
- 25. Centrilobular (centriacinar) primarily the upper lobes Occurs with loss of the respiratory bronchioles in the proximal portion of the acinus, with sparing of distal alveoli. This pattern is most typical for smokers 25
- 26. 26 Panlobular emphysema permanent destruction of the entire acinus distal to the respiratory bronchioles with no "obvious" associated fibrosis. Usually affect basal part. Common in patient with Alpha 1 AT deficiency.
- 27. Paraseptal Emphysema & sub pleural bullae 27
- 28. 1. Assessment of COPD 2. Relief of symptoms 3. Prevent frequency and severity of exacerbations 4. Improve quality of life 5. Reduce mortality 28 Goals of management
- 29. Modified MRC dyspnoea scale Six-minute walk test Exercise Oximetry COPD assessment test (CAT) 29 Assessment of COPD
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- 31. 31 Start pointTurnout point 100 feet/ 30m 100 feet/30m 6 minute walk test
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- 34. A B DC Gold stage Ⅰ Gold stage Ⅲ Gold stage Ⅳ Combined COPD Assessment (Airway limitation GOLD assessment + Exacerbation risk + breathlessness) ≥2 episode in last one 1 year or ≥1 episode leading to hosp admission ≤ 1episode not leading to hosp admission Gold stage Ⅱ mMRC 0-1 mMRC ≥ 2 Low risk, Less symptom High risk, More symptomHigh risk, Less symptom Low risk, More symptom
- 35. Patient Characteristic SpirometricClas sification Exacerbations per year mMRC CAT A Low Risk Less Symptoms GOLD 1-2 ≤ 1 0-1 < 10 B Low Risk More Symptoms GOLD 1-2 ≤ 1 >2 ≥ 10 C High Risk Less Symptoms GOLD 3-4 >2 0-1 < 10 D High Risk More Symptoms GOLD 3-4 >2 >2 ≥ 10 Combined Assessment of COPDWhen assessing risk, choose the highest risk according to GOLD grade or exacerbation history
- 36. Patient category First recommendation Alternative recomm. A Short acting anticholinergic or Short acting beta2 agonist as per need (pro re nata) -Long acting anticholinergic or -Long acting beta2 agonist or -Short acting anticholinergic and Short acting beta2 agonist B Long acting anticholinergic or Long acting beta2 agonist Long acting anticholinergic and Long acting beta2 agonist C Inhaled corticosterLong + Long acting anticholinergic or Long acting beta2 agonist -Long acting anticholinergic and Long acting beta2 agonist or -LAanticholinergic +PDE4 inhibitor or -LAbeta2agonist+ PDE4 inhibitor D Inhaled corticosteroid + Long acting anticholinergic and/or Long acting beta2 agonist LTOT /SURGERY Inhaled corticosteroid + Long acting anticholinergic and Long acting beta2 agonist or -LAanticholinergic +PDE4 inhibitor or -LAbeta2agonist+ PDE4 inhibitor 36 Pharmacotherapy
- 37. Oxygen Systemic steroid Antibiotic (According to C/S) Diuretics (If edema) Doxapram Parenteral Aminophylline Low dose benzodiazepines Morphine 37 Other drugs
- 38. Ultra short acting b2 agonist- Indacaterol Long acting muscarinic antagonist- Glycopyronium bromide Phosphodiesterase 4 inhibitor- Roflumilast and Cilomilast Newer generation phosphodiesterase inhibitors- Doxyphyllin Mucolytic and anti-oxidant agent- N acetylcysteine 38 Newer drugs
- 39. During exercise During exacerbation During air travel Category D disease (Severe) - LTOT 39 02 Therapy Temporary Need based
- 40. For continuous use at home in patients with chronic hypoxaemia 15 to 19 hours per day including sleeping periods 2-4 L/min For at least 30 days Goal: Increase baseline Pa02 > 60 mmHg Sa02 > 90% 40 Long term oxygen therapy (LTOT)
- 41. Indication 1. Chronic hypoxaemia: Pa02 < 55 mmHg + PaC02 rise Pa02 > 60 mmHg + {pulmonary hypertension/peripheral edema/ Nocturnal hypoxaemia} + PaC02 rise 1. Nocturnal Hypoventilation: (Obesity/ Neuromuscular disease/Obstructive Sleep apnoea) 2. Palliative use: Pulmonary malignancy or other causes of disabling dyspnoea. 41 Long term oxygen therapy (LTOT)
- 42. Category C and D disease In Category B if steroid shows responsiveness Severe exacerbation of COPD Frequent exacerbation Oral Steroid Trial Differentiation of COPD from Asthma of ACOS Can it predicts responsiveness to inhaled corticosteroid? 42 When to use inhaled steroid
- 43. Smoking cessation & Reduce exposure to noxious stimuli Vaccination (pneumococcal and Influenza vaccine) Exercise training & Breathing exercise Nutritional and Psychological counseling Palliation (Morphine for breathlessness and Addressing End of life issue) Pulmonary rehabilitation (A holistic multidisciplinary approach for patients with chronic respiratory impairment) 43 Other mode of management
- 44. Influenza vaccines can reduce serious illness. Pneumococcal polysaccharide vaccine is recommended for COPD patients 65 years and older and for COPD patients younger than age 65 with an FEV1< 40% predicted. vaccines
- 45. Brief Strategies to Help the Patient Willing to Quit Smoking ASSIST For the patient willing to make a quit ttempt, offer medication and provide or refer for counseling or additional treatment to help the patient quit. For patients unwilling to quit at the time, provide interventions designed to increase future quit attempts. ARRANGE For the patient willing to make a quit attempt, arrange for followup contacts,
- 47. Lung volume reduction surgery Bullectomy Lung transplantation 47 Surgery
- 49. Def: Acute change in baseline dyspnoea, cough and/or sputum that is beyond normal day to day variation Cause: 1. Infection 2. pollution 3. unknown (66% cases) Types: Type1: Mild exace. (Risk factor for poor outcome- ) (H. Influenzae, S. Pneumoniae, Chlamydia, Viruses) Type2: Moderate exace. (Risk factor for poor outcome +) (Type 1 plus Presence of resistant organism) Type3: Severe exace. (Risk factor for poor outcome +) (Type 2 plus P. aeruginose, Actinobactor) Exacerbations
- 50. 50 Exacerbations Investigation: Chest x ray, ECG, Pulse oximetry, ABG Sputum for gram stain and C/S CBC, B. Urea, S. Creatinine S. Electrolytes, B. Sugar Management: 1. Home-based 2. Hospital-based Controlled oxygen: at 24% or 28% should be used with the aim of PaO2above 60 mmHg or an SaO2 between 88% and 92% without worsening acidosis Systemic steroid: If baseline FEV1 is <50 % predicted….30-40 mg of prednisolone for 7-10 day (Nebulized budesonide if risk of hyperglycaemia or other steroid side effects) Antibiotic: Aminopenicillin or a Macrolide. Co-amoxiclav if β- lactamase-producing organisms are known to be common
- 51. Increased intensity or resting dyspnoea New sign appearance (cyanosis, edema, arrhythmia) Severe underlying disease Significant co-morbidities Frequent admission Diagnostic uncertainty Older age Inadequate home support 51 Indication for Hospital admission in exacerbation
- 52. Inadequate response to initial emergency therapy Change in mental status (lethargy, confusion, coma) Persistent of worsening parameters despite oxygen and Non-invasive ventilation Hypoxemia (Pa02) ….less than 40 mmHg Hypercapnia (PaC02)…..more than 60 mmHg Respiratory acidosis…..pH <7.35 Need for invasive ventilation Haemodynamic instability needing vasopressor 52 Indication for ICU admission
- 53. Able to use long acting bronchodilators Need for short acting b2 agonist not more than every 4 hour Patient can walk, eat and sleep without awakening by dyspnoea Clinically stable for 12-24 hours Fully understand the use of medication Good support at home Follow up plan home care arrangement completed 53 Discharge criteria
- 54. Maintenance pharmacotherapy regimen for home Inhaler technique Instruction regarding completion of steroid and antibiotic therapy Assess for long term oxygen therapy Provide management plan for Comorbidities Assurance of a follow up visit within 4-6 weeks 54 Assessment at time of discharge
- 55. Measurement of FEV1 Inhaler technique Ability to cope in usual environment Understanding recommended treatment regimen 55 Items to assess at F/U visit
- 56. Respiratory failure Pulmonary hypertension Arrhythmias Corpulmonale Secondary infection (Pneumonia) Osteoporosis Complications 56
- 57. Chronic hypoxia Pulmonary vasoconstriction Muscularization Intimal hyperplasia Fibrosis Obliteration Pulmonary hypertension Cor pulmonale Death Pulmonary Hypertension in COPD
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- 59. 59 Predictors of BAD prognosis 1) Increased age 2) Declined Post-bronchodilator FEV1 3) Weight loss (Cachexia) 4) Pulmonary hypertension
- 60. Body mass index Obstruction of airflow Dyspnoea measurement Exercise capacity 60 BODE index BODE score of 0-2 has a mortality rate of around 10% at 52 months, When BODE score 7-10 mortality rate around 80% at 52 months
- 61. 61 Distinguishing Asthma From COPD Lung function test: Airway hyper responsiveness (Methacholin challenge test) Arterial blood gas (Chronically abnormal in COPD) DLCO (reduced in COPD) PEFR (Diurnal variation less in COPD) Inflammatory Biomarkers: Skin prick tests for atopy, Ig E in blood, Blood eosinophilia, Suptum cell analysis Imaging : Chest X ray HRCT
- 62. Differential Diagnosis: COPD and Asthma COPD ASTHMA Onset in mid-life Symptoms slowly progressive Long smoking history Dyspnea during exercise Largely irreversible airflow limitation 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
- 64. Increased but not complete reversibility of the airway obstruction. 2 major and 2 minor required
- 66. 66 Beta Blockers in COPD
- 67. PLoS One. 2014 Nov 26;9(11):e113048. doi: 10.1371/journal.pone.0113048. eCollection 2014. Beta-blockers reduced the risk of mortality and exacerbation in patients with COPD: a meta-analysis of observational studies. Du Q1, Sun Y1, Ding N1, Lu L1, Chen Y1. An extensive search of the EMBASE, MEDLINE and Cochrane was performed to retrieve the studies of beta-blockers treatment in patients with COPD. The random effects model meta- analysis was used to evaluate effect on overall mortality and exacerbation of COPD. Fifteen original observational cohort studies with a follow-up time from 1 to 7.2 years were included. The results revealed that beta-blockers treatment significantly decreased the risk of overall mortality and exacerbation of COPD. The relative risk (RR) for overall mortality was 0.72 (0.63 to 0.83), and for exacerbation of COPD was 0.63 (0.57 to 0.71). In subgroup analysis of COPD patients with coronary heart disease or heart failure, the risk for overall mortality was 0.64 (0.54-0.76) and 0.74 (0.58-0.93), respectively. The findings of this meta-analysis confirmed that beta-blocker use in patients with COPD may not only decrease the risk of overall mortality but also reduce the risk of exacerbation of COPD. Beta-blocker prescription for cardiovascular diseases needs to improve in COPD patients. Beta-blocker use in patients with COPD may not only decrease the risk of overall mortality but also reduce the risk of exacerbation of COPD.
- 69. Abstract In order to clarify the possible role of N-acetylcysteine (NAC) in the treatment of patients with chronic bronchitis and chronic obstructive pulmonary disease (COPD), we have carried out a meta-analysis testing the available evidence that NAC treatment may be effective in preventing exacerbations of chronic bronchitis or COPD and evaluating whether there is a substantial difference between the responses induced by low (≤600 mg per day) and high (>600 mg per day) doses of NAC. The results of the present meta-analysis (13 studies, 4155 COPD patients, NAC n=1933; placebo or controls n=2222) showed that patients treated with NAC had significantly and consistently fewer exacerbations of chronic bronchitis or COPD (relative risk 0.75, 95% CI 0.66–0.84; p<0.01), although this protective effect was more apparent in patients without evidence of airway obstruction. However, high doses of NAC were also effective in patients suffering from COPD diagnosed using spirometric criteria (relative risk 0.75, 95% CI 0.68–0.82; p=0.04). NAC was well tolerated and the risk of adverse reactions was not dose-dependent (low doses relative risk 0.93, 95% CI 0.89–0.97; p=0.40; high doses relative risk 1.11, 95% CI 0.89–1.39; p=0.58). The strong signal that comes from this meta-analysis leads us to state that if a patient suffering from chronic bronchitis presents a documented airway obstruction, NAC should be administered at a dose of ≥1200 mg per day to prevent exacerbations, while if a patient suffers from chronic bronchitis, but is without airway obstruction, a regular treatment of 600 mg per day seems to be sufficient. 69 Influence of N-acetylcysteine on chronic bronchitis or COPD exacerbations: a meta-analysis Mario Cazzola1 , Luigino Calzetta1 , Clive Page2 , Josè Jardim3 , Alexander G. Chuchalin4 , Paola Rogliani1 and Maria Gabriella Matera5 patient suffering from chronic bronchitis with documented airway obstruction, NAC should be administered at a dose of ≥1200 mg per day to prevent exacerbations, while if a patient suffers from chronic bronchitis, but is without airway obstruction, a regular treatment of 600 mg per day seems to be sufficient.
- 71. Harrison's Principles of Internal Medicine .19th E Davidson's principles and practice of medicine. 22nd E National guideline on Asthma and COPD. 5th E 71 References
- 72. 72 THANK YOU!
- 73. 73 “We Rise by Lifting Others” Robert ingersoll