COPD seminar presentation by resident year 3

COPD seminar presentation by resident year 3

1. CHRONIC OBSTRUCTIVE PULMONARY DISEASE Presenter – Dr. Taddese L.( IMR2 ) Moderator- Dr. Amsalu Bekele (consultant internist & PCCM specialist)

2. OUTLINE Introduction Epidemiology Risk factor pathogenesis Clinical feature Diagnosis and initial assessment Management of stable COPD and exacerbations 2 7/5/2024

3. Introduction Definition COPD - Heterogeneous lung condition characterized by chronic respiratory symptoms (dyspnea, cough, expectoration, exacerbations) due to abnormalities of the airway (bronchitis, bronchiolitis) and/or alveoli (emphysema) that cause persistent , often progressive, airflow obstruction . Spirometry post-bronchodilator- FEV1/FVC ratio < 0.7 3 7/5/2024

4. Emphysema -enlargement of the airspaces distal to the terminal bronchioles that is accompanied by destruction of the airspace walls Chronic bronchitis -defined by “cough and sputum production for at least 3 months per year for 2 consecutive years” (in the absence of another cause 7/5/2024 4

5. Cont’d Pre-COPD -individuals may present with structural lung lesions ( e.g.,emphysema ) and/or physiological abnormalities (including low-normal FEV1, gas trapping, hyperinflation, reduced lung diffusing capacity and/or rapid FEV1 decline ) without airflow obstruction (FEV1/FVC ≥ 0.7 post bronchodilation). PRISm (Preserved Ratio Impaired Spirometry ) -those with normal ratio but abnormal spirometry. Young COPD- in patients aged 20–50 years 5 7/5/2024

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7. Epidemiology Estimated global prevalence is 10.3 % LMIC contribute about 85% global burden the third leading cause of death worldwide, causing 3.23 million death Nearly 90% of COPD deaths in LMIC Tobacco smoking accounts for over 70% of COPD cases in high-income countries. In LMIC tobacco smoking accounts for 30–40% of COPD cases, and household air pollution is a major risk factor. 7 7/5/2024

8. 8 Int J Chron Obstruct Pulmon Dis.  2021; 16: 2953–2962 The Prevalence of Spirometry Diagnosed COPD is 10.6%

9. BMC Pulmonary Medicine   volume 19 , Article number: 181 (2019)   9 The Prevalence of COPD is 17.8%

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11. Causes and risk factors COPD results from Gene( G )-Environment( E ) interactions occurring over the lifetime( T ) of the individual ( GETomics ) -- damage the lungs and/or alter their normal development/aging processes . Tobacco smoking (cigarette ,pipe cigar, water pipe ETS,)..70%...high in come countries and 30% to 40% in LMICs . Gene SERPINA 1 mutation,,,,,ɑ -1 AT deficiency 11 7/5/2024

12. Etiotypes for COPD 12 7/5/2024

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15. Pathology Large airway Mucus gland enlargement Goblet cell hyperplasia Squamous metaplasia of bonchi Smooth muscle hypertrophy and hyper reactivity Small airway The major site of increased resistance Goblet cell metaplasia Luminal narrowing Reduced surfactant Inflammation Vessels Increased medial thickness Concentric intimal fibrosis Lung parenchyma Destruction of gas-exchanging air spaces Neutrophils and T lymphocytes, particularly CD8+ cells and macrophages are also increased in the alveolar space of smokers 15 7/5/2024

16. Pathophysiology Small airways may become narrowed by cells ( hyperplasia and accumulation), mucus, and fibrosis, followed by extensive small airway destruction has been demonstrated to be a hallmark of COPD. Hyperinflation Air trapping with increased RV and RV/TLC ratio Late stage progressive hyperinflation (increased TLC) Airflow obstruction Persistent and does not show large response to bronchodilator unlike asthma 16 7/5/2024

17. cont’d Gas exchange Non uniform ventilation and VQ mismatch Pao2 usually near normal until the FEV1 is < 50% of predicted Paco2 is not expected to increase until the FEV1 is <25% of predicted Cor pulmonale and pulmonary HTN-FEV1<25% and PaO2< 55mmhg 17 7/5/2024

18. Emphysema Proximal acinar (Centrilobular emphysema) Commonly associated with cigarette smoking T he central portion of the acinus is affected Also seen in coal workers pneumoconiosis The most common emphysema subtype seen in patients with COPD 18 7/5/2024

19. Panacinar – destruction of all parts of the acinus Diffuse panacinar emphysema is seen in A1AT deficiency 19 7/5/2024 Flattened diaphragms hyperinflated Thin appearance to heart (tiny cardio-thoracic ratio) Variability in the density of vessels in the lungs

20. Distal acinar ( paraseptal ) predominantly alveolar ducts are affected when it occurs alone is usually associated with spontaneous pneumothorax 20 7/5/2024

21. Clinical features Symptoms Variable over time and more worse in the morning Exertional Dyspnea Chronic cough Sputum production Fatigue Wheezing Weight loss History of smoking or other risk factors Comorbid diseases Lung ca, bronchiectasis, CVD, depression Family history 21 7/5/2024

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23. Diagnosis 23 7/5/2024

24. Lung function test S pirometry required to establish the diagnosis of COPD Irreversible or partially reversible air flow limitation with bronchodilator post-bronchodilator FEV1/FVC < 0.70 Lung volumes and diffusing capacity -Increased RV with increased RV/TLC later increased TLC Measurement of DLCO (functional impact of emphysema in COPD) -Done for patients with hypoxemia, breathlessness out of proportion to airflow limitation and evaluation for LVRS Exercise testing and assessment of physical activity Oximetry and arterial blood gas measurement 24 7/5/2024

25. Other investigations Alpha-1 antitrypsin deficiency (AATD) screening For young, non smoker, predominant basilar changes on CXR and family history ,ANCA < 100mg/dl or < 20% of normal CBC BNP, N-terminal pro-BNP Elevated serum bicarbonate level may suggest chronic hypercapnia Workup for alternative diagnosis including OFT and electrolytes 25 7/5/2024

26. Chest x-ray look for alternative parenchymal processes and assess pulmonary comorbidities. H ave a poor sensitivity for detecting COPD (50 %) Rapidly tapering vascular shadows, increased radiolucency of the lung, a flat diaphragm,bullae and a long, narrow heart shadow on a frontal radiograph. prominent hilar vascular shadows(pulmonary HTN and cor pulmonale)  26 7/5/2024

27. Chest CT Detection of bronchiectasis Lung cancer risk assessment Concomitant disease assessment Complication assessment Lung volume reduction surgery eligibility assessment For patients being evaluated for lung transplantation 27 7/5/2024

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30. Assessment of severity and staging GOLD staging Combined COPD assessment tool BODE index 30 7/5/2024

31. GOLD Classification 31 7/5/2024

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35. BODE INDEX-SURVIVAL PREDICTION 35 7/5/2024

36. Celli et al NEJM 2004 36

37. COMORBID DISEASES Lung cancer  -COPD increases the risk of lung cancer by 6-13x Bronchiectasis 20-69% of COPD patients Cardiovascular disease Coronary heart disease  -Patients with COPD have 2-5x risk of IHD Heart failure  – both ( HFpEF ) and ( HFrEF ) . Arrhythmias  -Atrial fibrillation Peripheral artery disease Hypertension Sleep-related breathing disorders (SRBD) Metabolic syndrome and diabetes mellitus  -30%of patients with COPD  Osteoporosis  — Osteopenia, osteoporosis, and osteoporotic fractures (especially vertebral) are common in COPD patients  Renal insufficiency GERD Depression and anxiety Cognition impairment   37 7/5/2024

38. Management of stable COPD 38 7/5/2024

39. Management Identify and reduce risk factors Non pharmacological treatment Pharmacological treatment Management of exacerbations Monitoring and follow up 39 7/5/2024

40. Identify and reduce risk factors Smoking cessation Approximately 40% of COPD patients are current smokers long term quit success rate is up to 25% Reduces the rate of decline in lung function(FEV1) and improves survival Nicotine replacement therapy( nicotine gum ,inhaler, transdermal patch , sublingual tablet) 40 7/5/2024

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43. Long term Oxygen therapy 43 7/5/2024

44. Long term Oxygen therapy 7/5/2024 44 MRT trial NOTT trial

45. In patients with stable COPD and – Moderate resting hypoxemia (SpO2 89-93%) Moderate exercise-induced desaturation (6MWT SpO2 ≥80% for ≥5 minutes and <90 for >10 second NOT oxygen did not have benefit 7/5/2024 45 LOTT trial enrolled 738 adults

46. Ventilatory support NIV is the standard of care for decreasing morbidity and mortality in patients hospitalized with an exacerbation of COPD and acute respiratory failure NIV may be considered in pts with pronounced daytime hypercapnia and recent hospitalization CPAP is Indicated for patients with both COPD and obstructive sleep 46 7/5/2024

47. NPPV in stable Hypercapnic COPD improves survival 7/5/2024 47 Kohnlein Lancet Respir.Med 2014

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49. Pulmonary rehabilitation 49 7/5/2024

50. Pharmacological therapy in Stable COPD Choices depend on Severity of symptoms and air flow obstruction Cost and availability of drug Adverse effect of drugs Bronchodilators Anti inflammatory agents Mucolytics Antibiotics 50 7/5/2024

51. Bronchodilators Mechanism of action and benefits Adverse effects B2agonists(LABA) Relax air way smooth muscle by increasing CAMP Improve FEV1and lung volumes, symptoms ,no of exacerbation and hospitalization No effect on MR or rate of lung fuction decline Sinus tachycardia, tremor hypokalemia Antimuscarinic drugs Block bronchoconstrictor effect of acetylcholine via M3 receptor on air way smooth muscle Improve symptoms ( esp cough and sputum production) no of exacerbation(>LABA), hospitalization , effectiveness of pulmonary rehabilitation Dry mouth Bitter metallic test and small increase in cardiovascular events( ipratropium) Glaucoma ( use of solution with facemask ) UR methylxanthines Non selective PDE inhibitors Modest bronchodilator effect, improve FEV1, SOB , enhanced inspiratory muscle function Arrythmia GTCS heart burn insomnia 51 7/5/2024

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53. RESCUE BRONCHODILATOR THERAPY FOR ALL PATIENTS Short-acting bronchodilator to use as needed for relief of episodic dyspnea and early treatment of exacerbations Patient On LAMA –SABA will be rescue therapy on PRN base .if Patients requiring frequent use should transition to LABA Not on LAMA –SABA-SAMA can be used as rescue therapy b/c of increased bronchodilator effect Dose –SAMA (ipratropium ) in MDI 2 inhalation 4-6x/ day Nebulized 0.5mg/2.5ml TID/QID combination of ipratropium-albuterol (20 mcg/100 mcg per actuation) in a soft mist inhaler (SMI) can be administered one inhalation every four to six hours as needed SABA can be given as we do for asthma exacerbation 7/5/2024 53

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55. Anti inflammatory Corticosteroid Alone no effect on long term FEV1 decline In combination with LABA it improves lung function and reduce exacerbation no effect on mortality Side effect oral candidiasis ,skin bruising, hoarseness of voice, pneumonia,decreased bone density & fracture 55 7/5/2024

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58. 58 7/5/2024 The step up in triple therapy can occur by various approaches and has been shown to improve lung function, patient reported outcomes and reduce exacerbations when compared to LAMA alone , LABA/LAMA and LABA/ICS

59. 7/5/2024 59 Triple therapy resulted in a lower rate of moderate or severe COPD exacerbation and lower rate of Hospitalization compared to LABA-LAMA or LABA-ICS

60. . NEJM 2016; 374:2222 60

61. Mucolytics Regular treatment with mucolytics such as carbocysteine and N-acetylcysteine may reduce exacerbations and modestly improve health status Phosphodiesterse 4 inhibitors( Roflumilast ) No bronchodilator effect Reduce inflammation by inhibiting breakdown of intracellular C-AMP Considered in patients with an FEV1 < 50% predicted and chronic bronchitis particularly if they have experienced at least one hospitalization for an exacerbation in the previous year Side effect diarrhea ,nausea loss of appetite, sleep disturbance, headache 61 7/5/2024

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65. Candidates for LVRS Age <75 Ex –smokers>6month Dyspnea despite maximal medical Rx FEV1<45% of Predicted DLCO not <20% of predicted Lung volume = air trapping RV>150 of predicted TLC> 100% of predicted increased RV/TLC ratio Chest CT heterogeneous predominantly upper lobe 6 minute walk test >140m 65 7/5/2024

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67. COPD Exacerbation Definition An event characterized by worsening of dyspnea and/or cough and sputum production in < 14 days accompanied by tachypnea and or tachycardia and increased local and systemic inflammation caused by infection, pollution or other insult to air ways. 67 7/5/2024

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69. Risk factors Prior exacerbation Advanced age Longer duration of COPD History of antibiotic therapy COPD related hospitalization in the past year Chronic mucus hyper secretion One or more co morbidity Triggers Viral infection(rhino virus , infuenza para infuenza bacterial infection H.influenza Moraxella catarrhalis S.pneumoniae P.aeruginosa Fungal ; invasive aspergillosis rare 1.3-3.9% Risk factors sever obs , recent antibiotic,steroid use hypalbuminemia Environmental pollution PTE Unknown etiology 69 7/5/2024

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71. Indications for hospitalization Acute respiratory failure Severe symptoms including confusion ,drowsiness, SOB Onset of new physical sign including arrhythmia, edema cyanosis Comorbid illness Failure to respond to initial medical mg’t Insufficient home support Criteria for ICU admission Patients with high risk co morbidities Continued need for NIV or invasive ventilation Persistent hypoxemia Pao2< 40mmhg acidosis PH<7.25 despite NIV Hemodynamic instability Need for frequent monitoring and nebulizer treatment Change in mentation 71 7/5/2024

72. Treatment General measure Smoking cessation Nutritional support Thromboprophylaxis Oxygen therapy Target SpO2 88-92% or Pao2- 60-70mmHg 72 7/5/2024

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74. Pharmacologic treatment Bronchodilators SABA with or without SAMA are recommended Its recommended to start long acting bronchodilators as soon as possible Magnesium sulfate  — For patients not responding to short-acting inhaled bronchodilators, intravenous administration of a single dose of magnesium sulfate is recommend  74 7/5/2024

75. Glucocorticoids I t improves lung function( FEV1),shortens recovery time , improves oxygenation ,risk of relapse, treatment failure, and length of hospitalization. Prednisone 40mg po daily for 5 days is recommended Po equally effective with IV and nebulization Adverse effect pneumonia,  hyperglycemia, sepsis, venous thromboembolism,  75 7/5/2024

76. Antibiotics E mpiric antibiotic treatment in patients with a COPD exacerbation and ≥2 of 3 cardinal symptoms: (increased dyspnea, increased sputum volume/viscosity, or increased sputum purulence ) or  a COPD exacerbation requiring hospitalization and/or ventilatory support (either invasive or noninvasive). Risk stratification to guide antibiotic selection  –   categorize patients based on treatment setting ( eg , outpatient versus inpatient), risk for poor clinical outcomes and risk for infection with  Pseudomonas. 76 7/5/2024

77. Risk stratification to guide antibiotic selection  77 7/5/2024

78. Antibiotics cont’d…. For outpatients who do not have risk factors for poor outcomes or Pseudomonas infection a macrolide or  a second- or third-generation cephalosporin For outpatients who have risk factors for poor outcomes (but no increased risk for Pseudomonas infection)   amoxicillin-clavulanate  or a respiratory fluoroquinolone ( ie ,  levofloxacin  or  moxifloxacin ). 78 7/5/2024

79. Antibiotics cont’d…. For most inpatients without risk factors for Pseudomonas infection a respiratory fluoroquinolone or a third-generation cephalosporin For most inpatients with risk factors for Pseudomonas infection - select one of the following:  cefepime ,  ceftazidime , or  piperacillin-tazobactam . For those who cannot tolerate these agents ciprofloxacin ,  aztreonam , certain carbapenems ( eg ,  meropenem ,  imipenem ), and aminoglycosides. 79 7/5/2024

80. Hospital discharge and follow up Care bundle at hospital discharge Education optimization of medication Supervision and correction of inhaler technique Assessment and optimal management of comorbidities Early rehabilitation(<4weeks) Early follow up within 4 weeks 80 7/5/2024

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82. References Harrisons 21 st edition GOLD 2024 update Up-to-date online 82 7/5/2024

83. Thank you 83 7/5/2024