Acute Asthma Exacerbations | Jindal Chest Clinic

Presentation on "Acute Asthma Exacerbations" by Dr. S.K Jindal

1. Surinder K. Jindal www.jindalchest.com Acute Asthma Exacerbations

2. Acute severe asthma A chronic inflammatory disorder of the airways characterized by recurrent episodes of wheezing, breathlessness, chest tightness and cough that is often reversible either spontaneously or with treatment Exacerbations - worsening of symptoms with increase in dyspnea , cough and wheeze Indian Guidelines for asthma 2005

3. Acute severe asthma Worldwide (200 million) 10 to 11 million - acute exacerbations- 13.9 million outpatient visits, 2 million requests for urgent care, and 423,000 hospitalizations India (~ 20 million) 1 million - acute exacerbations- 1.4 million outpatient visits, 2 lakh requests for urgent care, and 50000 hospitalizations McFadden ER et al Am J Respir Crit Care Med 2003

4. Acute severe asthma Unable to complete a sentence in one breath RR > 30/minute Use of accessory muscles of respiration HR > 120/minute Pulsus paradoxus > 25 mm Hg Extensive inspiratory and expiratory wheeze PEFR < 50% personal best PaO2 < 60 mm Hg, PaCO2 > 45 mm Hg GINA 2004

5. Acute severe asthma Silent chest Alteration in sensorium Bradycardia or hypotension Respiratory fatigue as indicated by a paradoxical respiratory motion Requires mechanical ventilation GINA 2004

6. Goals of Management Relieve respiratory distress and hypoxia Maintain adequate hydration 3. Treat bronchospasm Treat mucosal inflammation & edema Handle triggers – infection (etc)

7. Algorithmic management Good Response Observe for at least 1 hour If Stable, Discharge to Home Initial Assessment History, Physical Examination, PEF or FEV 1 Initial Therapy Bronchodilators; O 2 if needed Incomplete/Poor Response Add Systemic Glucocorticosteroids Good Response Discharge Poor Response Admit to Hospital Respiratory Failure Admit to ICU GINA 2004

8. Managing Severe exacerbations Life-threatening medical emergency Treatment- hospital-based/ED Primary therapy for exacerbations Repetitive administration of rapid-acting inhaled β 2 -agonist Early introduction of systemic steroids Oxygen supplementation Closely monitor response to treatment (Clinical, serial measures of lung function)

9. Rapid-acting bronchodilators Salbutamol or its equivalent- initial treatment of choice If sustained improvement- patient can be discharged from the ED Ipratropium and salbutamol combination improves outcomes- substantial reduction in hospital admissions (30 to 60%, NNT 5- 11) and improvement in lung function Rodrigo et al Chest 2002

10. Route of delivery Intravenous route no benefits Potential for increased adverse effects Inhaled route preferred mode Easy, safe, faster onset of action More effective than parenteral routes Travers et al Cochrane Database Syst Rev 2001

11. Chamber better Nebulizer better Cates et al Cochrane Database Syst Rev 2003

12. Continuous vs. intermittent β2 agonists in acute asthma Use of continuous β-agonists (defined as continuous aerosol delivery using large-volume nebulizer or medication delivery that was effectively continuous i.e. 1 nebulisation every 15 minutes or 4 / hour) Improves pulmonary functions and reduces hospitalization Favors intermittent Favors continuous Camargo et al Cochrane Database Syst Review 2000

13. Dose of Salbutamol in Acute Asthma GINA- 2.5 to 7.5 mg every 20 minutes for the first hour Salbutamol 2.5 mg every 20 min vs. 7.5 mg every 20 minutes - no difference in FEV1 values or admission rates Emerman CL et al Chest 1999 Cydulka R et al Chest 2002 Stein et al Acad Emerg Med 2003

14. Systemic Steroids in ASA Mainstay of management Require 6-24 hours to bring about maximal benefit Use within 1 h of presentation to an ED reduces hospital admission No advantage of parenteral over oral No advantage of a particular preparation Prednisolone 40-60 mg/d x 5-10 days Rowe et al Cochrane Database Syst Rev 2001 Manser et al Cochrane Database Syst Rev 2001

15. Inhaled Steroids in ASA Controversial Causes mucosal vasoconstriction -↓ edema formation and plasma exudation Two conflicting meta-analysis (1 for & against) 3 recent studies- high dose ICS in addition to oral steroids decrease relapse rates Rodrigo et al Chest 1998 Rowe et al JAMA 1999 Edmonds et al Chest 2002 Edmonds et al Cochrane Database Syst Review 2003 Rodrigo et al Am J Respir Crit Care Med 2003

16. Theophyllines in asthma No additional bronchodilation compared to inhaled beta-agonists Frequency of adverse effects is higher Used only if the patient not able to cooperate for any form of inhaled therapy, or if inhaled therapy ineffective Parameswaran et al Cochrane Database Syst Rev 2001

17. Magnesium in asthma First reported as a treatment for ASA in 1936 Large RCT- IV Mg 2 gm at admission improved pulmonary function but not hospitalization (FEV 1 less than 25% predicted) Recent RCT- isotonic nebulized Mg 2.5 mg- enhanced bronchodilator response (FEV 1 < 30%) Silverman et al Chest 2002 Hughes et al Lancet 2003

18. LTRA in asthma Block cysteinyl LT1 receptors and thus action of LTC4, D4, and E4 Two recent studies have shown that addition of LTRAs improve pulmonary function and dyspnea scores Silverman et al Ann Emerg Med 2000 Camargo et al Am J Respir Crit Care Med 2003

19. Heliox in asthma Airflow - laminar In ASA – turbulent Heliox -mixture of helium and oxygen- lower density and higher viscosity than oxygen-nitrogen mixture Reduces the Reynolds number - converts turbulent flow to laminar flow - improves decrease dynamic hyperinflation

20. Heliox in asthma Clinical results- not favorable Recent meta-analyses- heliox did not improve pulmonary function, airway resistance and hospital admission Favors heliox Favors control Rodrigo et al Cochrane Database Syst Rev 2001

21. Other therapies… Inhaled frusemide Inhaled lignocaine Intravenous glucagon Inhalational anesthetics Inhaled mucolytics - no role, worsen bronchospasm Antibiotics- fever, purulent sputum, leucocytosis or radiographic infiltrate

22. Pathophysiology of ASA Airway obstruction Expiratory airflow limitation High respiratory rates AutoPEEP Decreases preload during expiration Exaggerated inspiratory effort increases preload Exaggerated inspiratory workload Compresses coronary and pulmonary vessels Diaphragm dysfunction Hypoxemia Hypotension Myocardial ischemia Pulmonary hypertension Increased work of breathing V/Q mismatch NIV

23. Extrinsic PEEP in asthma… Auto PEEP with dynamic hyperinflation and airflow limitation:- airway obstruction- delay in alveolar emptying - air trapping Auto PEEP with dynamic hyperinflation without airflow limitation:- decrease expiratory times- high minute ventilatory requirements Auto PEEP without dynamic hyperinflation:- active contraction of expiratory muscles

24. Extrinsic PEEP in asthma… Auto PEEP with dynamic hyperinflation with airflow limitation “Equal pressure point” - extramural pressure > airway opening pressure PEEP (less than auto PEEP)-shifts the EPP mouthward - dilates the collapsed or severely narrowed airways All the 3 mechanisms operate and low levels of PEEP in ASA does benefit

25. NIV in asthma IPAP will decrease inspiratory work of breathing EPAP will counteract PEEPi - decrease the adverse hemodynamic effects of large swings in pleural pressures Nebulized drugs are delivered better with NIV

26. NIV vs. conventional therapy One prospective RCT (30 patients)- improved lung function and decreased hospitalization in patients with ASA Another RCT (35 patients)- no significant advantages of NIV in patients with ASA

27. Lung function in patients who received NIV vis-à-vis none

28. Outcomes in patients who received NIV vis-à-vis none

29. NIV in asthma- consensus No guidelines Reasonable approach - use NIV in patients who do not respond to initial medical therapy Word of caution… recognize failure of NIV - facilities for immediate endotracheal intubation and ventilation being readily available

30. Invasive ventilation in ASA… Transient rest to respiratory muscles Adequate oxygenation (PaO2 ≥ 60 mm Hg or SpO2 ≥ 92%) Prolongation of expiratory times -allow alveolar emptying Prevention of barotrauma - controlled hypoventilation - permissive hypercapnia strategy

31. Invasive ventilation in ASA… Not the mode but the settings- important Mode- V-ACMV fR - 8-12/minute, V T 4-6 mL /kg PBW, PEEP- ≤ 5 cm H 2 O I: E ratio- 1:4 and higher (avoid plateau) Inspiratory flow- 100-120 L/minute FiO 2- PaO 2 ≥ 60 mm Hg or SpO 2 ≥ 89% Plateau pressure- < 30 cm H 2 O pH ≥ 7.1 in young adults, ≥ 7.2 in elderly

32. Invasive ventilation in ASA… Post-intubation hypotension - excessive ‘bagging’ the AMBU - dynamic hyperinflation and auto PEEP with decreased cardiac preload- disconnect the patient from the AMBU and administer IV fluids Sudden high plateau pressures - pneumothorax , ET tube block, lobar collapse

33. Invasive ventilation in ASA… Permissive hypercapnia - Normoxic hypercarbia not harmful- PaCO2 of ~ 200 mm Hg for 10 hours has been recorded with no immediate or late consequence Maintain pH ≥ 7.1 in young adults, ≥ 7.2 in elderly Avoid sodium bicarbonate- worsen the hypercapnia and associated acidosis in these patients

34. Acute severe asthma Unable to complete a sentence in one breath, RR > 30/minute, use of accessory muscles of respiration, HR > 120/minute, pulsus paradoxus > 25 mm Hg, extensive wheeze, PEFR < 50%, PaO2 < 60 mm Hg, PaCO2 > 45 mm Hg Salbutamol 2.5 mg q 15 minutes + Ipratropium 250 mcg q 15 minutes + PO prednisolone 40-60 mg/day Sustained improvement after 1 hour- discharge on oral steroids and bronchodilators No improvement- ADMISSION IN HOSPITAL OR ICU

35. Continue inhaled salbutamol and ipratropium IV magnesium sulfate- 2 gm over 10 minutes Consider noninvasive ventilation/ heliox If no improvement IV aminophylline , PO montelukast , SC epinephrine If no improvement Confusion, coma, bradycardia , hypotension, paradoxical respiratory movement Endotracheal intubation and invasive mechanical ventilation

36. Conclusions Prevention of subsequent asthma attacks On discharge- educated to use the aerosol devices, given instructions in self-assessment (PEF measurements, symptoms diary), follow-up, instructions for managing recurrences Access to health care services, compliance with treatment, avoidance of triggers, socioeconomic and psychosocial factors also need to be addressed

37. Inhaled drugs in mechanically ventilated patient MMAD- 1 and 5 μm Factors decrease delivery- humidification, high inspiratory flow Increase V T , decrease insp flow, switch off the humidifier MDI with spacer as effective as jet nebulizer Rrs = ( Ppeak–Pplat )/Peak inspiratory flow

38. Extrinsic PEEP in asthma… Auto PEEP with dynamic hyperinflation but no airflow limitation- decreasing minute ventilatory requirements (sedation or paralysis) If spontaneously triggering- PEEP (80% of autoPEEP ) - ↓ work of breathing - ↓ insp threshold to trigger ventilator Auto PEEP -10 cm H 2 O, trigger -1 cm H 2 O patient - 11 cm H 2 O

39. Extrinsic PEEP in asthma… Auto PEEP-10 cm H 2 O, trigger -1 cm H 2 O- If extrinsic PEEP- 8 cm H 2 O Patient has to generate only 3 cm H 2 O to trigger the ventilator This mechanism holds true only if the patient is spontaneously breathing No value in paralyzed patients where it increases end-expiratory lung volume and can be detrimental

40. Experience of NIV in asthma… Meduri et al. Prospective observational study- 17 asthmatic patients Only two required intubation - associated with ↓ in PaCO 2 , improvement in dyspnea Fernandez et al. Retrospective analysis - 33 asthmatic patients Only three patients eventually required endotracheal intubation Meduri et al Chest 1996 Fernandez et al. Intensive Care Med 2001

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