Treatment of status asthmaticus

1. Treatment of status asthmaticus ???

3. Status asthmaticus Severe attacks of asthma poorly responsive to adrenergic agents and associated with signs or symptoms of potential respiratory failure

4. Treatment Administration of oxygen �2-agonists (by continuous or repetitive nebulisation) Systemic corticosteroids Subcutaneous administration of epinephrine or terbutaline should be considered in patients not responding adequately to continuous nebulisation, unable to cooperate, Intubated patients not responding to inhaled therapy. Intubated and mechanically ventilated based mainly on clinical judgment should not be delayed once it is deemed necessary should be appropriately sedated Permissive hypercapnia, increase in expiratory time, and promotion of patient-ventilator synchronism

5. Inhaled �2-agonists Continuous or repetitive nebulisation of short-acting �2-agonists the most effective means of reversing airflow obstruction More effective and induces less hypokalaemia when delivered by the inhaled route Salbutamol (albuterol) is the most frequently used agent because of its potency, duration of action (four to six hours) and �2-selectivity 2.5 mg (0.5 ml) in 2.5 ml normal saline by nebulisation continuously or every 15�20 min until a significant clinical response is achieved or serious side effects appear Intravenous administration should be considered in patients who have not responded to inhaled or subcutaneous treatment, in whom respiratory arrest is imminent

6. Corticosteroids Should begin much earlier, at the first sign of loss of asthma control Early treatment with adequate doses of corticosteroid improves outcome Reduce mortality Controversy about the optimal dose of corticosteroid No particular advantage of the intravenous over the oral route provided there is reliable gastrointestinal absorption

7. Ipratropium Ipratropium bromide has a mild additional bronchodilating effect when added to � agonists that may only be significant in severe asthma Ipratropium bromide 0.5 mg by nebulisation every 1�4 hours, combined with salbutamol

8. Aminophylline The addition of aminophylline does not add to the bronchodilating effect of optimal doses of � agonists Not recommended as a first line drug in acute asthma management Its inclusion as a second line agent is still debated

9. Subcutaneous epinephrine and terbutaline Should be considered in patients not responding adequately to continuous nebulised salbutamol unable to cooperate intubated patients not responding to inhaled therapy 0.3�0.4 ml of a 1:1000 solution subcutaneously every 20 min for 3 doses

10. Mechanical ventilation Cardiopulmonary arrest and deteriorating consciousness are absolute indications for intubation and assisted ventilation Hypercapnia, acidosis, and clinical signs of severe disease at presentation may not require immediate intubation before an aggressive trial of conventional bronchodilator therapy Conversely, progressive deterioration with increasing distress or physical exhaustion may warrant intubation and mechanical ventilation without the presence of hypercapnia

11. Mechanical ventilation Correction of the hypoxemia is one of the first priorities To avoid further significant increase of lung hyperinflation Decrease of VE Increase of expiratory time Decrease of resistance Controlled hypoventilation (Permissive hypercapnia (PaCO2 does not exceed 90 mmHg) with an associated acidosis (pH 7.2�7.15) ) Decreasing either the tidal volume or the respiratory frequency, or both The recommended strategy to reduce lung hyperinflation Pressure-controlled ventilation seems more appropriate to maintain airway pressure especially in status asthmaticus

12. Mechanical ventilationInitial ventilator settings

13. Mechanical ventilationSedation

14. Mechanical ventilationNeuromuscular-blocking agents Lessens the patient -ventilator asynchronism Lowers the risk for barotrauma Reduce oxygen consumption and dioxide production, and reduces lactate accumulation Disadvantages: myopathy, excessive airways secretions, histamine release (atracurium), and tachycardia and hypotension (pancuronium). Currently the use of paralytics is usually recommended only in those patients who cannot adequately be controlled with sedation alone

15. THERAPEUTIC OPTIONS IN THE NON-RESPONDING PATIENT Manual compression Mucolytics Inhalational anaesthetic agents Helium Magnesium sulphate Leukotriene inhibitors Platelet activating factor (PAF) inhibitors Nitric oxide (NO)

16. Manual compression Hyperinflation is relieved by manual compression of the chest wall during expiration Has not been fully evaluated by a controlled clinical study in humans

17. Mucolytics Chest physiotherapy and mucolytics have no proven benefit Bronchoscopic lavage with locally applied acetylcysteine may be used to help clear impacted secretions in selected refractory patients but its routine use is not advocated

18. Inhalational anaesthetic agents Halothane, isoflurane, and sevoflurane are potent bronchodilators in asthmatic patients receiving mechanical ventilation who have failed to respond to conventional � adrenergic agents Sevoflurane, a halogenated ether, is largely devoid of cardiorespiratory side effects and may be the preferred agent

19. Helium A mixture of helium and oxygen (heliox) may reduce the work of breathing and improve gas exchange because of its low density that reduces airway resistance and hyperinflation However, the benefits are marginal and the concentration of inspired oxygen is consequently decreased The use of heliox to prevent intubation has not been studied But dyspnoea scores were improved in one study, possibly by reducing the work of breathing

20. Magnesium sulphate Early anecdotal reports suggested benefit from intravenous magnesium sulphate, which has been inconsistently supported by randomised studies A significant benefit was recently observed in children receiving intravenous magnesium sulphate (40 mg/kg) during acute asthma attacks

21. Leukotriene inhibitors relatively minor role Platelet activating factor (PAF) inhibitors attenuate the late response in asthma but have limited clinical efficacy Nitric oxide (NO): weak bronchodilator effect. It dilates pulmonary arteries When inhaled, may improve ventilation/perfusion matching