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Status Asthmaticus

Status Asthmaticus. PICU Resident Lecture Series Lucile Packard Children’s Hospital (Updated: June 2014). Objectives. General principals Pathophysiology Pharmacologic Therapies Respiratory Management. Relevance.

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Status Asthmaticus

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  1. Status Asthmaticus PICU Resident Lecture Series Lucile Packard Children’s Hospital (Updated: June 2014)

  2. Objectives General principals Pathophysiology Pharmacologic Therapies Respiratory Management

  3. Relevance • Asthma affects 6 million children in the United States, making it the most common chronic disease of childhood.1,2 • Up to 10 % have severe disease unresponsive to typical therapeutic interventions. • Annually, childhood asthma accounts for 4 million outpatient visits, 600,000 emergency department visits, 150,000 hospitalizations, and 75 deaths.3

  4. Pathophysiology • Primary pathophysiology • Airway inflammation & hyper-reactivity • Smooth muscle spasm • Mucosal edema & plugging • Status asthmaticus • Reversible • Recurrent • Diffuse • Obstructive

  5. Pathophysiology Pathologic changes in the airway airflow obstruction premature airway closure on expiration dynamic hyperinflation  hypercarbia Dynamic hyperinflation or “air-trapping” also leads to ventilation / perfusion (V/Q) mismatching causing hypoxemia PaO2 = FiO2(Patm – PH2o) – paCO2/0.8

  6. Pathophysiology Hypersecretion Epithelial damage with exposed nerve endings Epithelium Hypertrophy of goblet cells and mucus glands Interstium Equals airway obstruction and resultant air trapping

  7. Pharmacologic Targets • Relaxation of bronchial smooth muscles • B2 receptors • M1 receptors • Improving oxygen delivery • Attenuating underlying inflammation • Instituting vigorous pulmonary toilet

  8. Pharmacologic Therapies Albuterol Atrovent Methylprednisone/Decadron Magnesium Sulfate Terbutaline Aminophylline Heliox Ketamine Oxygen Epineprhine

  9. Albuterol • MOA: • Inhaled B2 agonist • B2 receptor  activates adenylatecyclase  increases cAMP  activates protein kinase A  inhibits of myosin-light chain phosphorylation and decreases intracellular Ca2+ • Dosing: Continuous nebulization – 10–20 mg/hr with an O2flow rate of 10–12 L/min • Superior to intermittent nebulization  Rapid improvement, cost effective, patient friendly 4,5 • Advantages: rapid acting, rapidly administered, easily titrated • Disadvantages: tachycardia (B2 effects on heart), hyperglycemia (glycogenolysis & gluconeogenesis), hypokalemia (intracellular shunting).

  10. Ipratroprium Bromide • MOA: • Muscarinic agonist (anticholinergic) • M1 receptor  decrease cGMP  decreases intracellular Ca2+ • Dosing: 0.25–0.5 mg nebulized q 4h • Advantages: no systemic anticholinergic action • Disadvantages: unilateral pupillary dilation can occur with local medication entry

  11. Corticosteroids • MOA: • Systemically reduce inflammation, decrease mucus production, and enhance the effects of B2-agonists.2 • Prevents the sustained inflammatory phase which occurs 6-8 hours after allergen exposure • Dosing: • Methylprednisone: 0.5–1 mg/kg IV q 6h (2-4 mg/kg/day), duration 5-7 days • Decadron6: 0.3–0.6 mg/kg IM x 1 • Steroids should be administered IV to assure adequate drug delivery in a timely manner

  12. Magnesium Sulfate • MOA: • Inhibits Ca2+ influx into cytosol  smooth muscle relaxant • Increases B2 agonist affinity for its receptor, thereby potentiating its effect • Inhibits histamine release from mast cells • Dosing: 50 mg/kg IV over 20 min with max of 2 gm • Advantages: has been shown to be effective in “severe” (FEV1<25% predicted) asthma • Disadvantages: rarely noted: hypotension, respiratory depression & muscle weakness can be treated with IV Calcium Gluconate • Respiratory depression & muscle weakness are noted at levels >12 mg/dL. (normal Mg levels are 1.5-2 mg/dL and minimal increase in level is noted with a single dose)

  13. Terbutaline • MAO: • IV B2 agonist • B2 receptor  activates adenylatecyclase  increases cAMP  activates protein kinase A  inhibits of myosin-light chain phosphorylation and decreases intracellular Ca2+ • Dosing: • Loading dose: 5–10 mcg/kg IV over 10 min • Continuous infusion: 0.4–4 mcg/kg/min IV (incr by 0.4 mcg/kg/min q 30 mins) • Advantages: effectively reaches areas of lung by IV infusion that Albuterol does not due to airway obstruction • Disadvantages / side effects: tachycardia, hyperglycemia, hypokalemia, (rhabdomyolysis & cardiac ischemia – rarely)

  14. Aminophylline • MAO: • Xanthine derivative • competitive nonselective phosphodiesterase inhibitor  increase cAMP (by preventing its degradation)  activates PKA inhibits myosin-light chain kinase and decreases intracellular Ca2+ • Inhibits TNF-alpha and leukotriene synthesis • Dosing: • Loading dose: 6 mg/kg over 20 min IV • Continuous infusion: 0.6–1 mg/kg/min IV • Advantages: may prove very effective in patients resistant to above treatments given the different MOA • Disadvantages / side effects: N/V, agitation, arrhythmias, seizures • Level q8hr after drug initiation and then every morning. • Therapeutic levels are 10 – 20 mcg/ml.

  15. Heliox • MOA: • Low-density gas that increases laminar flow of oxygen and decreases turbulent flow. • Dosing: 60%/40% or 80%/20% helium/O2 • Advantages: has no systemic side effects • Other: Data suggests prevents intubation. In intubated patients, heliox has been shown to decrease the PIP requirements.

  16. Ketamine • MAO: • “Dissociative” anesthetic • Bronchodilatesby intrinsic catecholamine release • Decreases airway resistance and maintains laryngeal tone & reflexes • Dosing: 0.5–1 mg/kg IV, 1 time doses or continuous infusion. • Advantages: Ketamine should be the drug of choice for intubation induction. • Other: it can be considered in SA patients with severe agitation, but be prepared to intubate the patient should it cause hypoxia. Be cautious of agitation however since it often precedes respiratory failure.

  17. ABG • ABG’s generally not indicated in an asthmatic • Early status asthmaticus: hypoxemia, hypocarbia • Late status asthmaticus: hypercarbia • Decision to intubate should not depend on ABG, but on clinical assessment. • Frequent ABGs are crucial in the ventilated asthmatic.

  18. Management The use of mechanical ventilation during an asthma exacerbation is associated with significant morbidity and increased risk of death. The decision to intubate a patient should not be delayed until respiratory failure is imminent. If progressing toward respiratory muscle fatigue, NPPV may avoid intubation by easing WOB while awaiting maximal therapeutic effects of pharmacotherapy.9

  19. Intubation • The two primary indications to intubate an SA patient are: • Severe hypoxia & Depressed level of consciousness • Other potential indications for mechanical ventilation include: • Obvious life-threatening respiratory distress not responding to bronchodilator therapy • Impending respiratory failure • Hemodynamic compromise, including bradycardia, severe pulsusparadoxus • Lactic acidosis associated with increased work of breathing • Apnea or near-apnea • Peak flows <40% of predicted

  20. Intubation • General guidelines for mechanical ventilation management: • Start with low tidal volume, permissive hypercapnia strategy. • Tidal volume 4-7 ml/kg (prevents barotrauma / volutrauma, minimize lung distension) • Goal pH>7.25 (may require HCO3) • Low ventilatory rate 10-14 breaths per minute • I:E ratio 1:4 to 1:6 (avoid air trapping by allowing for complete exhalation) • PEEP match intrinsic • Peak pressures <30-35 (prevent barotrauma) • Keep well sedated – consider ketamine and versed infusions. • As the patient is on steroids, limit use of paralytics (to avoid myopathy)

  21. References National Asthma Education and Prevention Program. Expert panel report 3 (EPR-3): Guidelines for the diagnosis and management of asthma-summary report 2007. J Allergy ClinImmunol. 2007;120(suppl 5): S94–S138 ScarfoneRJ, Friedlaender E. Corticosteroids in acute asthma: past, present, and future. Pediatr Emerg Care. 2003;19(5):355–361 Akinbamiet al. Pediatrics. 2009;123(suppl 3):S131–S145. Papo MC. Crit Care Med 1993;21:1479-86 Ackerman AD. Crit Care Med 1993;21:1422-4 Keeney et al. Pediatrics. 2014;133(3):493-499. http://peds.stanford.edu/Rotations/picu/pdfs/14_status_asthmaticus.pdf Howell J. Acute severe asthma exacerbations in children: Intensive care unit management, www.uptodate.com Manselet al. Mechanical ventilation in patients with acute severe asthma, Am J Med. 1990;89(1):42-8

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