Management of COPD & Asthma in Anaesthesia.pptx

Management of COPD & Asthma in Anaesthesia

1. Status asthmaticus and copd MANAGEMENT By : Dr Riya Sharma Moderator : Dr Reena Singhal

2. Definition: Status asthmaticus is a medical emergency, an extreme form of asthma exacerbation characterized by hypoxemia, hypercarbia, and secondary respiratory failure. All patients with bronchial asthma are at risk of developing an acute episode with a progressive severity that is poorly responsive to standard therapeutic measures, regardless of disease severity or phenotypic variant. This is also known as status asthmaticus.

3. etiology

4. types The time course of progression and the severity of airway obstruction follow two distinct patterns. If appropriately documented, one subgroup shows a slow subacute worsening of peak expiratory flow rate (PEFR) over days, known as "slow onset asthma exacerbation." This patient subgroup usually has intrinsic patient-induced predisposition factors, including inadequate inhaler regimen, suboptimal compliance, and psychological stressor. (Ref: The other phenotype, known as "sudden onset asthma exacerbation," presents with severe deterioration within hours. They often correlate with sudden massive exposure to external triggers like predisposed allergens, food articles, sulfites, among others.

5. pathophysiology At a physiological level, premature airway closure during exhalation causes an increase in functional residual capacity and air trapping. Heterogeneous distribution of air trapping results in ventilation-perfusion mismatch and hypoxemia- triggering anaerobic metabolism and lactic acidosis. It is offset initially by respiratory alkalosis and is compounded once respiratory fatigue and respiratory acidosis ensue. Pathophysiology

6. Severity Assessment:

7. Clinical findings:

8. Examination finding Hyperresonance on percussion Bilateral diffuse wheezing Bilateral crepitations secondary to pulmonary oedema Pulses paradoxus sIGNS

9. Xray findings: Air-trapping on expiratory scans most common finding Bronchial wall thickening (50-90%) Decreased lung attenuation (50%) Mosaic lung attenuation Degree of mosaic attenuation correlates with degree of asthma Peri bronchial cuffing

10. Xray findings:

11. Mosaic attenuation on ct chest :

12. Management Beta-agonist Short-acting inhaled beta-agonists are the drug of the first choice in acute asthma Initial treatment consists of 2.5 mg of albuterol (0.5 mL of a 0.5% solution in 2.5 mL normal saline) by nebulization every 20 minutes for 60 minutes (three doses) followed by treatments hourly during the first several hours of therapy.

13. Management Corticosteroids In a meta-analysis of 30 randomized clinical trials (RCT), concluded that the use of steroids in the emergency department significantly reduces rates of admission and the number of future relapses in subsequent 7 to 10 days due to their anti inflamatory effect. Currently available data support the approach of 60 to 125 mg methylprednisolone intravenously every 6 hours for the initial 24 hours of treatment of status asthmaticus. Oral steroids are usually required for the next 10 to 14 days.

14. management Anticholinergics 0.25 mg of ipratropium bromide with 5 mg of albuterol by nebulizer resulted in greater improvement in FEV1 than albuterol alone. The response time was also much faster than corticosteroids, with a detectable change in FEV1 within 19 minutes.

15. management Magnesium Sulphate Magnesium inhibits calcium-mediated smooth muscle constriction, decreases acetylcholine release in the neuromuscular junction, and affects respiratory muscle force generation. Commonly used dose of 2 gm intravenously (IV) in 2 separate doses over 20 minutes

16. management Heliox and Oxygen Heliox is a mixture of 70:30 or 60:40 helium: oxygen decreases airway resistance and turbulence and reduces work of breathing and inspiratory muscle fatigue.

17. management Indications of Intubation: Coma  Respiratory arrest Deterioration of arterial blood gas tensions despite optimal therapy:  PaO2 < 8 kPa (60 mmHg) and falling PaCO2 > 6 kPa (45 mmHg) and rising pH low and falling (H+ high and rising)  Exhaustion, delirium, drowsiness

18. COPD COPD, a common preventable and treatable disease, is characterized by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases. © Global Initiative for Chronic Obstructive Lung Disease

19. COPD includes 1) Chronic Bronchitis 2) Emphysema

20. CHRONIC BRONCHITIS Defined as a chronic productive cough for three months in each of two successive years in a patient in whom other causes of chronic cough have been excluded

21. Emphysema Abnormal and permanent enlargement of the airspaces distal to the terminal bronchioles that is accompanied by destruction of the airspace walls, without obvious fibrosis

22. Airways Chronic inflammation Increased numbers of goblet cells Mucus gland hyperplasia Fibrosis Narrowing and reduction in the number of small airways Airway collapse due to the loss of tethering caused by alveolar wall destruction in emphysema

23. Lung Parenchyma Emphysema affects the structures distal to the terminal bronchiole, consisting of the respiratory bronchiole, alveolar ducts, alveolar sacs, and alveoli, known collectively as the acinus .

24. Emphysema Paraseptal Distal acinar - the alveolar ducts are predominantly affected Panacinar Refers to enlargement or destruction of all parts of the acinus. Seen in alpha-1 antitrypsin deficiency and in smokers Centrilobular/Proximal Abnormal dilation or destruction of the respiratory bronchiole , the central portion of the acinus. It is commonly associated with cigarette smoking ,

25. Risk Factors for COPD Genes Infections Socio-economic status Aging Populations © 2015 Global Initiative for Chronic Obstructive Lung Disease

26. Genetics Alpha 1-antitrypsin deficiency is a genetic condition that is responsible for about 2% of cases of COPD. In this condition, the body does not make enough of a protein, alpha 1-antitrypsin. Alpha 1-antitrypsin protects the lungs from damage caused by protease enzymes, such as elastase and trypsin , that can be released as a result of an inflammatory response to tobacco smoke.

27. Modified MRC ( mMRC ) Questionnaire © 2015 Global Initiative for Chronic Obstructive Lung Disease

28. Barrel-shaped chest Accessory respiratory muscle participate Prolonged expiration during quiet breathing Expiration through pursed lips Paradoxical retraction of the lower interspaces during inspiration ( i.e , Hoover's sign) Tripod Position signs

29. Tripod Position Patients with end-stage COPD may adopt positions that relieve dyspnea , such as leaning forward with arms outstretched and weight supported on the palms or elbows.

30. Palpation: Decreased fremitus vocalis Percussion : Hyperresonant Depressed diaphragm, Dimination of the area of absolute cardiac dullness. Auscultation: Prolonged expiration ； Reduced breath sounds; The presence of wheezing during quiet breathing Crackle can be heard if infection exist. Clinical Manifestation

31. The presence of a post-bronchodilator FEV1/FVC < 0.70 confirms the presence of persistent airflow limitation and thus of COPD. © 2015 Global Initiative for Chronic Obstructive Lung Disease In patients with FEV 1 /FVC < 0.70: GOLD 1: Mild FEV 1 > 80% predicted GOLD 2: Moderate 50% < FEV 1 < 80% predicted GOLD 3: Severe 30% < FEV 1 < 50% predicted GOLD 4: Very Severe FEV 1 < 30% predicted *Based on Post-Bronchodilator FEV 1 DIAGNOSIS

32. Chest x-ray-Chronic bronchitis No apparent abnormality Or thickened and increased lung markings are noted.

33. Chest X-Ray - emphysema Marked over inflation is noted with flattend and low diaphragm Intercostal space becomes widen A horizontal pattern of ribs A long thin heart shadow Decreased markings of lung peripheral vessels

34. CT(Computed tomography) Greater sensitivity and specificity for emphysema For evaluation of bullous disease

35. ARTERIAL BLOOD GAS MEASUREMENTS PaO 2 < 8.0 kPa with or without PaCO 2 > 6.7 kPa when breathing room air indicates respiratory failure.

36. Management Based on the principles of Prevention of further progress of disease Preservation and enhancement of pulmonary functional capacity Avoidance of exacerbations in order to improve the quality of life.

37. Bronchodilators Bronchodilators are central to the symptomatic management of COPD. Improve emptying of the lungs,reduce dynamic hyperinflation and improve exercise performance . Three major classes of bronchodilators: β2 - agonists: Short acting: salbutamol & terbutaline Long acting :Salmeterol & formoterol Anticholinergic agents: Ipratropium, tiotropium Theophylline : (a weak bronchodilator, which may have some anti-inflammatory properties)

38. Glucocorticoids Regular treatment with inhaled glucocorticoids is appropriate for symptomatic patients with an FEV1<50%pred and repeated exacerbations. Chronic treatment with systemic glucocorticoids should be avoided because of an unfavorable benefit-to-risk ratio.

39. COMBINATION THERAPY Combination therapy of long acting ß2-agonists and inhaled corticosteroids show a significant additional effect on pulmonary function and a reduction in symptoms. Mainly in patients with an FEV1<50%pred

40. OTHERS Antioxidant agents Mucolytic PDE 4 inhibitors : Roflumilast 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.

41. Oxygen Therapy Oxygen -- > 15 h /d Long-term oxygen therapy (LTOT) improves survival,exercise,sleep and cognitive performance in patients with respiratory failure. The therapeutic goal is to maintain SaO2 ≥ 90% and PaO2 ≥ 60mmHg at sea level and rest .

42. Pulmonary rehabilitation Nutrition Surgery: Bullectomy Lung volume reduction surgery Lung transplantation Other Treatments

43. Smoking cessation has the greatest capacity to influence the natural history of COPD Pharmacotherapy and nicotine replacement reliably increase long-term smoking abstinence rates. Nicotine replacement therapy (nicotine gum, inhaler, nasal spray, transdermal patch, sublingual tablet, or lozenge) as well as pharmacotherapy with varenicline, bupropion, and nortriptyline reliably increases long-term smoking abstinence rates and are significantly more effective than placebo. © 2015 Global Initiative for Chronic Obstructive Lung Disease Smoking cessation

44. Asthma-COPD overlap syndrome "characterized by persistent airflow limitation with several features usually associated with asthma and several features usually associated with COPD. ACOS is therefore identified in clinical practice by the features that it shares with both asthma and COPD."

45. Thank you