Acute Severe Asthma | Jindal chest clinic

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

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

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 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

4. 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

5. Management: Recommendations Confirm the diagnosis Evaluate and treat confounding or exacerbating factors 3. Manage acute exacerbation 4 . Optimize the “standard” asthma pharmacotherapy 5. Prevent future exacerbations

6. Physician’s assessment Is the diagnosis correct? Does any other disease, drug or trigger complicate the problem? Is the anti asthma treatment adequate and appropriate? What about patient compliance and inhaler technique? Environmental control measures? Any pharmacokinetic abnormality of the pt ? Are the drugs being used reliable,…..?

7. Wrong Diagnosis Chronic Obstructive Pulmonary Disease Cardiac asthma Upper airway obstruction Vocal cord dysfunction Sleep apnoea Local obstruction by tumours /foreign body Hypersensitivity pneumonias Infections/Bronchiectasis Pulmonary embolism

8. Asthma - triggers Home environment Aero allergens House dust (mites/others) Tobacco smoke (ETS) Solid fuel smoke Infections Outdoor exposures: SO 2 , Ozone Occupational exposures Psychological stresses Drugs: aspirin, betablockers , ACE inhibitors

9. Aggravating Factors (GER) Old age Autonomic dysfunction – lowering of LESP Increased pressure gradient between esophagus and stomach Medication: Nicotine, Caffiene , calcium channel blockers, atropine, theophylline, nitroglycerine etc.

10. Managing Aggravating Factors Tmt of sinusitis and polyps Managing GE reflux Weight reduction Sleep disorder evaluation Tmt of psychological stress Management of VCD if any Reducing allergen load, dust, smoke/ETS , pets, others.

11. 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

12. 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

13. 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 epinephrin e If no improvement Confusion, coma, bradycardia , hypotension, paradoxical respiratory movement Endotracheal intubation and invasive mechanical ventilation

14. Pharmacotherapy High dose/high potency ICS Oral CS at the lowest possible dose Additional 1 to 3 controllers PEF monitoring (daily) “Asthma action plan” – rescue steps Frequent clinic visits/advice

15. 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

16. 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 Favors IV Favors inhaled Travers et al Cochrane Database Syst Rev 2001

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

18. 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

19. 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

20. 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

21. 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

22. 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

23. 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

24. 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

25. 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

26. 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

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

28. 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

29. 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

30. 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

31. 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

32. 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

33. Conclusions Life-threatening medical emergency Treatment- hospital-based/ED Repetitive rapid-acting inhaled β 2 -agonist Early introduction of systemic steroids Oxygen supplementation Prevention of subsequent asthma attacks On discharge- educated to use the aerosol devices, given instructions in self-assessment 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

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