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Status Asthmaticus In Children

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Status Asthmaticus In Children

  1. 1. Status Asthmaticus in Children Heinrich Werner Pediatric Critical Care University of Kentucky Children’s Hospital
  2. 2. Objectives <ul><li>The participant will increase his/her </li></ul><ul><li>Awareness of rising morbidity/mortality of severe asthma in children </li></ul><ul><li>Ability to define who is at risk for dying </li></ul><ul><li>Understanding of the pathologic, metabolic and biomechanical events </li></ul><ul><li>Ability to predict respiratory failure and to determine the need for early transfer </li></ul><ul><li>Ability to tailor the therapeutic regimen according to severity and progression of status asthmaticus </li></ul>
  3. 3. Status Asthmaticus in Children <ul><li>Epidemiology </li></ul><ul><li>Pathophysiology </li></ul><ul><li>Presentation and Assessment </li></ul><ul><li>Treatment </li></ul>
  4. 4. Status Asthmaticus in Children <ul><li>Epidemiology </li></ul><ul><ul><li>Prevalence </li></ul></ul><ul><ul><li>Morbidity </li></ul></ul><ul><ul><li>Mortality </li></ul></ul><ul><ul><li>Risk factors </li></ul></ul><ul><li>Pathophysiology </li></ul><ul><li>Presentation and assessment </li></ul><ul><li>Treatment </li></ul>
  5. 5. Prevalence <ul><li>The prevalence of pediatric asthma in the US is increasing </li></ul>Rate of self-reported asthma/1,000 population Mannino DM. MMWR 1998;47(1):1-27 : Epidemiology
  6. 6. Morbidity <ul><li>The morbidity of pediatric asthma in the US is increasing </li></ul>Hospital discharge rates for asthma MMWR 1996;45(17):350-3 : Epidemiology
  7. 7. Mortality <ul><li>The mortality of pediatric asthma in the US is increasing </li></ul>Rates of death in children from asthma Mannino. MMWR 1998;47(1):1-27 : Epidemiology
  8. 8. Risk factors for fatal asthma <ul><li>Medical </li></ul><ul><ul><li>Previous attack with rapid/severe deterioration or respiratory failure or seizure/loss of consciousness </li></ul></ul><ul><li>Psychosocial </li></ul><ul><ul><li>Denial, non-compliance </li></ul></ul><ul><ul><li>Depression or other psychiatric disorder </li></ul></ul><ul><ul><li>Dysfunctional family </li></ul></ul><ul><ul><li>Inner city resident </li></ul></ul><ul><li>Ethnic </li></ul><ul><ul><li>Non-white child </li></ul></ul>: Epidemiology
  9. 9. Status Asthmaticus in Children <ul><li>Epidemiology </li></ul><ul><li>Pathophysiology </li></ul><ul><ul><li>Cytokines </li></ul></ul><ul><ul><li>Airway pathology </li></ul></ul><ul><ul><li>Autonomic nervous system </li></ul></ul><ul><ul><li>Pulmonary mechanics </li></ul></ul><ul><ul><li>Cardiopulmonary interactions </li></ul></ul><ul><ul><li>Metabolism </li></ul></ul><ul><li>Presentation and assessment </li></ul><ul><li>Treatment </li></ul>
  10. 10. Pathophysiology <ul><li>Asthma is primarily an inflammatory disease </li></ul>Mucous plugging Smooth muscle spasm Airway edema : Pathophysiology
  11. 11. Inflammatory cytokines <ul><li>Activated mast cells and lymphocytes produce pro-inflammatory cytokines (histamine, leukotrienes, PAF), which are increased in asthmatics’ airways and bloodstream </li></ul>: Pathophysiology
  12. 12. Irritable and damaged airway Hypersecretion Epithelial damage with exposed nerve endings Hypertrophy of goblet cells and mucus glands : Pathophysiology
  13. 13. Airway <ul><li>The irritable and inflamed airway is susceptible to obstruction triggered by </li></ul><ul><ul><li>Allergens </li></ul></ul><ul><ul><li>Infections </li></ul></ul><ul><ul><li>Irritants including smoke </li></ul></ul><ul><ul><li>Exercise </li></ul></ul><ul><ul><li>Emotional stress </li></ul></ul><ul><ul><li>GE reflux </li></ul></ul><ul><ul><li>Drugs </li></ul></ul><ul><ul><li>Other factors </li></ul></ul>: Pathophysiology
  14. 14. Autonomic nervous system Bronchodilation Bronchoconstriction Sympathetic Circulating catecholamines stimulate ß-receptors - Parasympathetic <ul><ul><li>Vagal signals stimulate bronchodilating M 2 - receptors </li></ul></ul><ul><ul><li>Vagal signals stimulate bronchoconstricting M 3 -receptors </li></ul></ul>Nonadrenergic-noncholinergic (NANC) Release of bronchodilating neurotransmitters (VIP, NO) <ul><ul><li>Release of tachykinins (substance P, neurokinin A) </li></ul></ul>: Pathophysiology
  15. 15. Lung mechanics <ul><li>Hyperinflation </li></ul><ul><ul><li>Obstructed small airways cause premature airway closure, leading to air trapping and hyperinflation </li></ul></ul><ul><li>Hypoxemia </li></ul><ul><ul><li>Inhomogeneous distribution of affected areas results in V/Q mismatch, mostly shunt </li></ul></ul>: Pathophysiology
  16. 16. Severe airflow obstruction Incomplete exhalation Increased lung volume Increased elastic recoil pressure Increased expiratory flow Expanded small airways Decreased expiratory resistance Compensated: Hyperinflation, normocapnia Decreased expiratory resistance Decompensated: Severe hyperinflation, hypercapnia Worsening airflow obstruction From text in : Tuxen. Am Rev Respir Dis 1992;146:1136 : Pathophysiology
  17. 17. Cardiopulmonary interactions <ul><li>Left ventricular load </li></ul><ul><ul><li>Spontaneously breathing children with severe asthma have negative intrapleural pressure (as low as -35 cmH 2 O) during almost the entire respiratory cycle </li></ul></ul><ul><li>Stalcup S. N Engl J Med 1977;297:592-6 </li></ul><ul><ul><li>Negative intrapleural pressure causes increased left ventricular afterload, resulting in risk for pulmonary edema </li></ul></ul><ul><ul><li>Buda AJ. N Engl J Med 1979;301(9):453-9 </li></ul></ul>: Pathophysiology
  18. 18. Cardiopulmonary interactions <ul><li>Right ventricular load </li></ul><ul><ul><li>Hypoxic pulmonary vasoconstriction and lung hyperinflation lead to increased right ventricular afterload </li></ul></ul>Dawson CA. J Appl Physiol 1979;47(3):532-6 : Pathophysiology
  19. 19. Cardiopulmonary interactions <ul><li>Pulsus paradoxus </li></ul><ul><ul><li>P. paradoxus is the clinical correlate of cardiopulmonary interaction during asthma. It is defined as exaggeration of the normal inspiratory drop in systolic BP : normally < 5 mmHg, but > 10 mmHg in pulsus paradoxus. </li></ul></ul>Expir Inspir Nl P. paradoxus Inspir Expir : Pathophysiology
  20. 20. Pulsus paradoxus correlates with severity <ul><li>All patients who presented with FEV 1 of < 20% (of their best FEV 1 while well) had pulsus paradoxus </li></ul><ul><ul><li>Pierson RN. J Appl Physiol 1972;32(3):391-6 </li></ul></ul>: Pathophysiology
  21. 21. Cardiopulmonary interactions Negative intrapleural pressure Pulmonary edema Pulsus paradoxus Hyperinflation Hypotension Altered hemodynamics : Pathophysiology
  22. 22. Metabolism V/Q mismatch Hypoxia Dehydration Lactate Ketones Metabolic acidosis Increased work of breathing : Pathophysiology
  23. 23. Presentation <ul><li>Cough </li></ul><ul><li>Wheezing </li></ul><ul><li>Increased work of breathing </li></ul><ul><li>Anxiety </li></ul><ul><li>Restlessness </li></ul><ul><li>Oxygen desaturation </li></ul>Audible wheezes : reasonable airflow “ Silent chest” : ominous! : Presentation
  24. 24. Assessment <ul><li>Findings consistent with impending respiratory failure: </li></ul><ul><ul><li>Altered level of consciousness </li></ul></ul><ul><ul><li>Inability to speak </li></ul></ul><ul><ul><li>Absent breath sounds </li></ul></ul><ul><ul><li>Central cyanosis </li></ul></ul><ul><ul><li>Diaphoresis </li></ul></ul><ul><ul><li>Inability to lie down </li></ul></ul><ul><ul><li>Marked pulsus paradoxus </li></ul></ul>: Assessment
  25. 25. Clinical Asthma Score <ul><li> 0 1 2 </li></ul><ul><li>Cyanosis or None In air In 40% </li></ul><ul><li>PaO 2 >70 in air < 70 in air < 70 in 40% </li></ul><ul><li>Inspiratory B/S Nl Unequal or Absent decreased </li></ul><ul><li>Expir wheezing None Moderate Marked </li></ul><ul><li>Cerebral function Nl Depressed Coma </li></ul><ul><li>Agitated </li></ul><ul><ul><li>Wood DW. Am J Dis Child 1972;123(3):227-8 </li></ul></ul> 5 = impending resp failure : Assessment
  26. 26. Chest X-Ray <ul><ul><li>Not routinely indicated </li></ul></ul><ul><ul><li>Exceptions: </li></ul></ul><ul><ul><ul><li>Patient is intubated/ventilated </li></ul></ul></ul><ul><ul><ul><li>Suspected barotrauma </li></ul></ul></ul><ul><ul><ul><li>Suspected pneumonia </li></ul></ul></ul><ul><ul><ul><li>Other causes for wheezing are being suspected </li></ul></ul></ul>: Assessment
  27. 27. ABG <ul><ul><li>Early status asthmaticus: hypoxemia, hypocarbia </li></ul></ul><ul><ul><li>Late: hypercarbia </li></ul></ul><ul><ul><li>Decision to intubate should not depend on ABG, but on clinical assessment </li></ul></ul><ul><ul><li>Frequent ABGs are crucial in the ventilated asthmatic </li></ul></ul>: Assessment
  28. 28. Status Asthmaticus in Children <ul><li>Epidemiology </li></ul><ul><li>Pathophysiology </li></ul><ul><li>Presentation and assessment </li></ul><ul><li>Treatment </li></ul><ul><ul><li>Conventional </li></ul></ul><ul><ul><ul><li>General, ß-agonists, steroids, anticholinergics </li></ul></ul></ul><ul><ul><li>Advanced </li></ul></ul><ul><ul><ul><li>Mechanical ventilation, ketamine, inhalational anesthetics </li></ul></ul></ul><ul><ul><li>Unusual/Unproven </li></ul></ul><ul><ul><ul><li>Theophylline, magnesium, LTRAs, heliox, bronchoscopy </li></ul></ul></ul>
  29. 29. Oxygen <ul><li>Deliver high flow oxygen, as severe asthma causes V/Q mismatch (shunt) </li></ul>Oxygen will not suppress respiratory drive in children with asthma Schiff M. Clin Chest Med 1980;1(1):85-9 : Treatment
  30. 30. Fluid <ul><li>Judicious use of IV fluid necessary </li></ul><ul><ul><li>Most asthmatics are dehydrated on presentations - rehydrate to eu volemia </li></ul></ul><ul><ul><li>Over hydration may lead to pulmonary edema </li></ul></ul><ul><ul><li>SIADH may be common in severe asthma </li></ul></ul><ul><ul><ul><li>Baker JW. Mayo Clin Proc 1976;51(1):31-4 </li></ul></ul></ul>: Treatment
  31. 31. Antibiotics <ul><li>Most infections precipitating asthma </li></ul><ul><li>are viral </li></ul><ul><li>Antibiotics are not routinely </li></ul><ul><li>indicated </li></ul><ul><li>Johnston SL. Pediatr Pulmonol Suppl 1999;18:141-3 </li></ul>? : Treatment
  32. 32. ß-Agonists <ul><li>ß-receptor agonists stimulate ß 2 -receptors on bronchial smooth muscle and mediate muscle relaxation </li></ul><ul><li>Epinephrine </li></ul><ul><li>Isoproterenol </li></ul><ul><li>Terbutaline </li></ul><ul><li>Albuterol </li></ul>Relatively ß 2 selective Significant ß 1 cardiovascular effects : Treatment
  33. 33. ß-Agonists <ul><li>Less than 10% of nebulized drug reach the lung under ideal conditions </li></ul><ul><ul><li>Bisgaard H. J Asthma 1997;34(6):443-67 </li></ul></ul><ul><li>Drug delivery depends on </li></ul><ul><ul><li>Breathing pattern </li></ul></ul><ul><ul><li>Tidal volume </li></ul></ul><ul><ul><li>Nebulizer type and gas flow </li></ul></ul>: Treatment
  34. 34. ß -Agonists <ul><li>Delivery of nebulized drug </li></ul><ul><ul><li>Only particles between  m  are deposited in alveoli </li></ul></ul><ul><ul><li>Correct gas flow rate is crucial </li></ul></ul><ul><ul><li>Most devices require 10-12 L/min gas flow to generate correct particle size </li></ul></ul>: Treatment
  35. 35. <ul><li>ß -Agonists </li></ul><ul><li>Continuous nebulization is superior to intermittent nebulization </li></ul><ul><ul><li>More rapid improvement </li></ul></ul><ul><ul><li>More cost effective </li></ul></ul><ul><ul><li>More patient friendly </li></ul></ul><ul><ul><li>Papo MC. Crit Care Med 1993;21:1479-86 </li></ul></ul><ul><ul><li>Ackerman AD. Crit Care Med 1993;21:1422-4 </li></ul></ul>: Treatment
  36. 36. ß -Agonists <ul><li>Dosage </li></ul><ul><ul><li>Intermittent nebulization </li></ul></ul><ul><ul><ul><li>2.5 - 5 mg (0.5 - 1 ml of 0.5% solution), dilute with NS to 3 ml </li></ul></ul></ul><ul><ul><ul><li>Prediluted: 2.5 mg as 3ml of 0.083% solution </li></ul></ul></ul><ul><ul><ul><li>High dose: use up to undiluted 5% solution </li></ul></ul></ul><ul><ul><li>Continuous nebulization </li></ul></ul><ul><ul><ul><li>4-40 mg/hr </li></ul></ul></ul><ul><ul><ul><li>High dose: up to undiluted 5% solution (≈ 150 mg/hr) </li></ul></ul></ul>: Treatment
  37. 37. ß -Agonists <ul><li>Intravenous ß - Agonist </li></ul><ul><ul><li>Consider for patients with severe air flow limitation who remain unresponsive to nebulized albuterol </li></ul></ul><ul><ul><li>Terbutaline is i.v. ß-agonist of choice in US </li></ul></ul><ul><ul><li>Dosage: 0.1 - 10  g/kg/min </li></ul></ul><ul><ul><li>Stephanopoulos DE. Crit Care Med 1998;26(10):1744-8 </li></ul></ul>: Treatment
  38. 38. ß -Agonists <ul><li>Side effects </li></ul><ul><li>Tachycardia </li></ul><ul><li>Agitation, tremor </li></ul><ul><li>Hypokalemia </li></ul>: Treatment
  39. 39. ß -Agonists <ul><li>Cardiac side effects </li></ul><ul><ul><li>Myocardial ischemia known to occur with i.v. isoproterenol </li></ul></ul><ul><ul><li>No significant cardiovascular toxicity with i.v. terbutaline (prospective study in children with severe asthma) </li></ul></ul><ul><ul><li>Chiang VW. J Pediatr 2000;137(1):73-7 </li></ul></ul><ul><ul><li>Tachycardia (and tremor) show tachyphylaxis, bronchodilation does not </li></ul></ul><ul><ul><li>Lipworth BJ. Am Rev Respir Dis 1989;140(3):586-92 </li></ul></ul>: Treatment
  40. 40. Steroids <ul><li>Asthma is an inflammatory disease </li></ul><ul><li>Steroids are a mandatory element of first line therapy regimen (few exceptions only) </li></ul><ul><ul><li>Fanta CH: Am J Med 1983;74:845 </li></ul></ul>Effect of i.v. hydrocortisone vs. placebo : Treatment
  41. 41. Steroids <ul><li>Hydrocortisone 4-8 mg/kg x 1, then 2-4 mg/kg q 6° </li></ul><ul><li>Methylprednisolone 2 mg/kg x1, then 0.5-1 mg/kg q 4-6° </li></ul>: Treatment
  42. 42. Steroids <ul><li>Significant side effects </li></ul><ul><ul><li>Hyperglycemia </li></ul></ul><ul><ul><li>Hypertension </li></ul></ul><ul><ul><li>Acute psychosis </li></ul></ul><ul><ul><li>Unusual or unusually severe infections </li></ul></ul><ul><ul><ul><li>Steroids contraindicated with active or recent exposure to chickenpox </li></ul></ul></ul><ul><ul><li>Allergic reaction </li></ul></ul><ul><ul><ul><li>Reported with methylprednisolone, hydrocortisone and prednisone * </li></ul></ul></ul>* Vanpee D. Ann Emerg Med 1998;32(6):754. Kamm GL. Ann Pharmacother 1999;33(4):451-60. Schonwald S. Am J Emerg Med 1999;17(6):583-5. Judson MA. Chest 1995;107(2):563-5. : Treatment
  43. 43. Anticholinergics - Ipratropium <ul><li>Quaternary atropine derivative </li></ul><ul><li>Not absorbed systemically </li></ul><ul><li>Thus minimal cardiac effects </li></ul><ul><li>(But you will find a fixed/dilated pupil if the nebulizer mask slips over an eye!) </li></ul>: Treatment
  44. 44. Anticholinergics <ul><li>Change in FEV 1 is significantly greater when ipratropium was added to ß-agonists (199 adults) </li></ul><ul><li>Rebuck AS: Am J Med 1987;82:59 </li></ul><ul><li>Highly significant improvement in pulmonary function when ipratropium was added to albuterol (128 children). Sickest asthmatics experienced greatest improvement </li></ul><ul><li>Schuh S. J Pediatr 1995;126(4):639-45 </li></ul>: Treatment
  45. 45. Ipratropium Dose-Response Curve in Children (n=19, age 11-17 yrs) Dose (micrograms) Average increase in FEV 1 (over 4 hrs) <ul><ul><li>Davis A: J Pediatr 1984;105:1002 </li></ul></ul>: Treatment
  46. 46. Ipratropium <ul><li>Nebulize 250 - 500  g every 4-6 hours </li></ul>: Treatment Schuh S. J Pediatr 1995;126(4):639-45 Goodman and Gilman's. 9th ed. New York: McGraw-Hill; 1996
  47. 47. Intubation, Ventilation <ul><li>Absolute indications: </li></ul><ul><ul><li>Cardiac or respiratory arrest </li></ul></ul><ul><ul><li>Severe hypoxia </li></ul></ul><ul><ul><li>Rapid deterioration in mental state </li></ul></ul><ul><ul><li>Respiratory acidosis does not dictate intubation </li></ul></ul>: Treatment
  48. 48. Why hesitate to intubate the asthmatic child? <ul><li>Tracheal foreign body aggravates bronchospasm </li></ul><ul><li>Positive pressure ventilation increases risk of barotrauma and hypotension </li></ul><ul><li>Tuxen DV. Am Rev Respir Dis 1987;136(4):872-9 </li></ul><ul><li>> 50% of morbidity/mortality during severe asthma occurs during or immediately after intubation </li></ul><ul><li>Zimmerman JL. Crit Care Med 1993;21(11):1727-30 </li></ul>: Treatment
  49. 49. Intubation <ul><li>Preoxygenate, decompress stomach </li></ul><ul><li>Sedate (consider ketamine) </li></ul><ul><li>Neuromuscular blockade (may avoid large swings in airway/pleural pressure) </li></ul><ul><li>Rapid orotracheal intubation (consider cuffed tube) </li></ul>: Treatment
  50. 50. Immediately after intubation <ul><li>Expect hypotension, circulatory depression </li></ul><ul><li>Allow long expiratory time </li></ul><ul><li>Avoid overzealous manual breaths </li></ul><ul><li>Consider volume administration </li></ul><ul><li>Consider pneumothorax </li></ul><ul><li>Consider endotracheal tube obstruction (++ secretions) </li></ul>: Treatment
  51. 51. Mechanical ventilation <ul><li>Positive pressure ventilation worsens hyperinflation/risk of barotrauma </li></ul><ul><li>Thoughtful strategies include: </li></ul><ul><ul><li>Pressure-limited ventilation, TV 8-12 ml/kg, short T i , rate 8-12/min (permissive hypercapnia) </li></ul></ul><ul><ul><li>Cox RG. Pediatr Pulmonol 1991;11(2):120-6 </li></ul></ul><ul><ul><li>Pressure support ventilation using PS=20-30 cmH 2 O (may decrease hyperinflation by allowing active exhalation) </li></ul></ul><ul><ul><li>Wetzel RC. Crit Care Med 1996;24(9):1603-5 </li></ul></ul>: Treatment
  52. 52. Ketamine <ul><li>Dissociative anesthetic with strong analgesic effect </li></ul><ul><li>Direct bronchodilating action </li></ul><ul><li>Useful for induction (2 mg/kg i.v.) as well as continuous infusion (0.5 - 2 mg/kg/hr) </li></ul><ul><li>Induces bronchorrhea, emergence reaction </li></ul>: Treatment
  53. 53. Inhalational anesthetics <ul><li>Halothane, isoflurane have bronchodilating effect </li></ul><ul><li>Halothane may cause hypotension, dysrhythmia </li></ul><ul><li>Requires scavenging system, continuous gas analysis </li></ul>: Treatment
  54. 54. Theophylline <ul><li>Role in children with severe asthma remains controversial </li></ul><ul><li>Narrow therapeutic range </li></ul><ul><li>High risk of serious adverse effects </li></ul><ul><li>Mechanism of effect in asthma remains unclear </li></ul>: Treatment
  55. 55. Theophylline <ul><li>May have a role in selected, critically ill children with asthma unresponsive to conventional therapy: </li></ul><ul><ul><li>Randomized, placebo-controlled, blinded trial (n=163) in children with severe status asthmaticus </li></ul></ul><ul><ul><li>Theophylline group had greater improvement in PFTs and O 2 saturation </li></ul></ul><ul><ul><li>No difference in length </li></ul></ul><ul><ul><li>of PICU stay </li></ul></ul><ul><ul><li>Theophylline group had signifi- </li></ul></ul><ul><ul><li>cantly more N/V </li></ul></ul><ul><ul><li>Yung M. Arch Dis Child 1998;79(5):405-10. </li></ul></ul>: Treatment
  56. 56. Magnesium <ul><li>Smooth-muscle relaxation by inhibition of calcium uptake (=bronchodilator) </li></ul><ul><li>Dosage recommendation: 25 - 75 mg/kg i.v. over 20 minutes </li></ul>: Treatment
  57. 57. Magnesium <ul><li>Several anecdotal reports </li></ul><ul><li>Only one randomized pediatric trial </li></ul><ul><ul><li>Randomized, placebo-controlled, blinded trial (n=31) in children with acute asthma in ER (MgSO 4 25 mg/kg i.v. for 20 min) </li></ul></ul><ul><ul><li>Magnesium group had significantly greater improvement in FEV 1 /PEFR/FVC </li></ul></ul><ul><ul><li>Magnesium group more likely </li></ul></ul><ul><ul><li>to be discharged home </li></ul></ul><ul><ul><li>No adverse effects </li></ul></ul><ul><ul><li>Ciarallo L. J Pediatr 1996; 129 (6):809-14. </li></ul></ul>: Treatment
  58. 58. Leukotriene receptor antagonists (LTRAs) <ul><li>Asthmatic children have increased leukotriene levels (blood, urine) during an attack. Level falls as attack resolves </li></ul><ul><li>Sampson AP. Ann N Y Acad Sci 1991;629:437-9. </li></ul><ul><li>LTRA administration is associated with improvement in lung function in asthmatics </li></ul><ul><li>Gaddy JN. Am Rev Respir Dis 1992;146(2):358-63. </li></ul>
  59. 59. LTRAs <ul><li>Steroid administration to asthmatics has little effect on leukotriene levels </li></ul><ul><li>O'Shaughnessy KM. Am Rev Respir Dis 1993;147(6 Pt 1):1472-6. </li></ul><ul><li>Thus, LTRAs may offer additional benefits to asthmatics on steroids </li></ul><ul><li>Reiss TF. Arch Intern Med 1998;158(11):1213-20. </li></ul>
  60. 60. Intravenous LTRAs in moderate to severe asthma <ul><li>A single dose of i.v. montelukast (Singulair ®) was associated with significant improvement in lung function compared to standard therapy </li></ul>Camargo CA, Jr. Am J Respir Crit Care Med 2003;167(4):528-33.
  61. 61. LTRAs – Remaining questions <ul><li>Will they offer added benefit in the acute, severe asthmatic child already on ß-agonists, steroids, anticholinergics ? </li></ul><ul><ul><li>More rapid improvement in lung function/clinical score? </li></ul></ul><ul><ul><li>Reduced/shortened hospitalization? </li></ul></ul><ul><ul><li>Fewer PICU admissions? </li></ul></ul><ul><li>Cost ? </li></ul><ul><li>Adverse effects ? </li></ul>
  62. 62. Helium - Oxygen (Heliox) <ul><li>Helium lowers gas density (if at least 60% helium fraction) </li></ul><ul><li>Reduces resistance during turbulent flow </li></ul><ul><li>Renders turbulent flow less likely to occur </li></ul>: Treatment
  63. 63. Heliox <ul><li>Anecdotal reports of improved respiratory mechanics in non-intubated and intubated asthmatic children </li></ul><ul><li>Prospective, randomized, blinded cross-over study of heliox in non-intubated children with severe asthma (n=11) : no effect on respiratory mechanics or asthma score </li></ul><ul><li>Carter ER. Chest 1996;109(5):1256-61. </li></ul>: Treatment
  64. 64. Heliox <ul><li>Helium-oxygen (80:20) decreased pulsus paradoxus and increased PEFR in a controlled trial of adult patients </li></ul><ul><ul><li>Manthous CA. Am J Respir Crit Care Med 1995,151:310-314 </li></ul></ul><ul><li>Heliox may worsen dynamic hyperinflation </li></ul><ul><ul><li>Madison JM. Chest 1995,107:597-598 </li></ul></ul>: Treatment
  65. 65. Bronchoscopy, bronchial lavage <ul><li>Marked mucus plugging may render bronchodilating and anti-inflammatory therapy ineffective </li></ul><ul><li>“ Plastic bronchitis” has been described in asthmatic children </li></ul><ul><li>Combined bronchoscopy/lavage has been used in desperately ill asthmatic children </li></ul>: Treatment
  66. 66. Summary <ul><li>Severe asthma in children is increasing in prevalence and mortality </li></ul><ul><li>Aggressive treatment with ß-agonist, steroids and anticholinergic is warranted even in the sick-appearing child </li></ul><ul><li>Avoid intubation if possible </li></ul><ul><li>Mechanical ventilation will worsen bronchospasm and hyperinflation </li></ul><ul><li>Use low morbidity approach to mechanical ventilation </li></ul>
  67. 67. Prevention <ul><li>Steps toward prevention </li></ul><ul><li>1. Identify patients as at risk </li></ul><ul><li>2. Tell them about their risks </li></ul><ul><li>3. Organize treatment plan </li></ul><ul><li>4. Facilitate access to continued care </li></ul>
  68. 68. Case Scenario (1) <ul><li>A 6 y o black male with previous history of asthma is admitted with severe respiratory distress. He is wheezing, RR is 40/min, HR 145/min. He sits upright, leans forward, has retractions and looks very anxious. He correctly tells you his name and phone #, but has to take a breath after every few words. </li></ul><ul><li>Discuss your initial therapeutic approach. </li></ul>
  69. 69. Case Scenario (2) <ul><li>Which of the following are mandatory in this child with severe asthma? </li></ul><ul><li>(You may chose none, more than one or all) </li></ul><ul><li>Arterial blood gas analysis (to detect onset of respiratory acidosis) </li></ul><ul><li>Continuous pulse oximetry </li></ul><ul><li>Chest radiograph (to rule out pneumomediastinum/ –thorax) </li></ul><ul><li>Frequent determination of peak expiratory flow rate </li></ul><ul><li>White blood cell count with differential (to assess need for antibiotics) </li></ul>
  70. 70. Case Scenario (3) <ul><li>Given his current presentation: does this child need to be intubated and mechanically ventilated? </li></ul><ul><li>Discuss indications for intubation/mechanical ventilation in the child with severe status asthmaticus. </li></ul>
  71. 71. Case Scenario (4) <ul><li>When nebulizing drugs during status asthmaticus, the following statement about gas flow rates is CORRECT: </li></ul><ul><ul><ul><li>A. The higher the gas flow rate through the nebulizer, the more particles will be deposited in the patient’s alveolar space </li></ul></ul></ul><ul><ul><ul><li>B. Most devices require a gas flow rate of 10-12 L/min to generate optimal particle size </li></ul></ul></ul><ul><ul><ul><li>C. Gas flow rates above 5 L/min should be avoided to maintain laminar flow in the nebulizer output </li></ul></ul></ul><ul><ul><ul><li>D. The nebulizer device should not be driven by 100% oxygen </li></ul></ul></ul>
  72. 72. Case Scenario (5) <ul><li>In addition to administration of continuously nebulized beta-agonist and intermittent anticholinergic agonist, which of the following is almost mandatory? Discuss pros and cons for each. </li></ul><ul><ul><ul><li>A. Intravenous bolus of aminophylline, followed by infusion </li></ul></ul></ul><ul><ul><ul><li>B. Intravenous corticosteroid </li></ul></ul></ul><ul><ul><ul><li>C. Intravenous broad spectrum antibiotic </li></ul></ul></ul><ul><ul><ul><li>D. Intravenous beta-agonist infusion </li></ul></ul></ul><ul><ul><ul><li>E. Inhaled helium-oxygen mixture </li></ul></ul></ul>
  73. 73. Case Scenario (6) <ul><li>After 3 hours of therapy in the PICU, including high dose continuous albuterol, intermittent ipratropium, I.v. methylprednisolone as well as two infusions of magnesium sulfate, the child becomes obtunded. His O 2 saturations begin to drop below 85%. Is this an indication for intubation/mechanical ventilation? </li></ul><ul><li>If so, describe your approach to intubating this child. </li></ul><ul><li>How to prepare? Drugs? ETT size, route? Anticipated problems / complications? Initial pattern of ventilation? </li></ul>
  74. 74. Case Scenario (7) <ul><li>After you connect the child to the ventilator, he develops marked arterial hypotension. </li></ul><ul><li>What is your differential diagnosis? </li></ul><ul><li>What should you do? </li></ul>
  75. 75. Suggested Reading (part 1): <ul><li>1. Laitinen LA, Heino M, Laitinen A, et al. Damage of airway epithelium and bronchial reactivity in patients with asthma. Am Rev Respir Dis 1985;131(4):599-606. </li></ul><ul><li>2. Beakes DE. The use of anticholinergics in asthma. J Asthma 1997;34(5):357-68. </li></ul><ul><li>3. Barnes PJ. Beta-adrenergic receptors and their regulation. Am J Respir Crit Care Med 1995;152(3):838-60. </li></ul><ul><li>4. Miro A, Pinsky M. Cardiopulmonary Interactions. In: Fuhrman B, Zimmerman J, editors. Pediatric Critical Care. Second ed. St. Louis: Mosby; 1998. p. 250-60. </li></ul><ul><li>5. Stalcup SA, Mellins RB. Mechanical forces producing pulmonary edema and acute asthma. N Engl J Med 1977;297(11):592-6. </li></ul><ul><li>6. Rebuck AS, Pengelly LD. Development of pulsus paradoxus in the presence of airway obstruction. N Engl J Med 1973;288(2):66-9. </li></ul><ul><li>7. Papo MC, Frank J, Thompson AE. A prospective, randomized study of continuous versus intermittent nebulized albuterol for severe status asthmaticus in children. Crit Care Med 1993;21:1479-86. </li></ul><ul><li>8. Katz RW, Kelly HW, Crowley MR, et al. Safety of continuous nebulized albuterol for bronchospasm in infants and children [published erratum appears in Pediatrics 1994 Feb;93(2):A28]. Pediatrics 1993;92(5):666-9. </li></ul><ul><li>9. Schuh S, Johnson DW, Callahan S, et al. Efficacy of frequent nebulized ipratropium bromide added to frequent high-dose albuterol therapy in severe childhood asthma. J Pediatr 1995;126(4):639-45. </li></ul><ul><li>10. Fanta CH, Rossing TH, McFadden ER. Glucocorticoids in acute asthma: A critical controlled trial. Am J Med 1983;74:845-51. </li></ul>
  76. 76. <ul><li>Suggested Reading (part 2): </li></ul><ul><li>11 . Klein-Gitelman MS, Pachman LM. Intravenous corticosteroids: adverse reactions are more variable than expected in children. J Rheumatol 1998;25(10):1995-2002. </li></ul><ul><li>12. Stephanopoulos DE, Monge R, Schell KH, et al. Continuous intravenous terbutaline for pediatric status asthmaticus. Crit Care Med 1998;26(10):1744-8. </li></ul><ul><li>13. Chiang VW, Burns JP, Rifai N, et al. Cardiac toxicity of intravenous terbutaline for the treatment of severe asthma in children: a prospective assessment. J Pediatr 2000;137(1):73-7. </li></ul><ul><li>14. Ciarallo L, Sauer AH, Shannon MW. Intravenous magnesium therapy for moderate to severe pediatric asthma: results of a randomized, placebo-controlled trial. J Pediatr 1996;129(6):809-14. </li></ul><ul><li>15. Pabon H, Monem G, Kissoon N. Safety and efficacy of magnesium sulfate infusions in children with status asthmaticus. Pediatr Emerg Care 1994;10:200-3. </li></ul><ul><li>16. Yung M, South M. Randomised controlled trial of aminophylline for severe acute asthma. Arch Dis Child 1998;79(5):405-10. </li></ul><ul><li>17. Tuxen DV, Lane S. The effects of ventilatory pattern on hyperinflation, airway pressures, and circulation in mechanical ventilation of patients with severe airflow obstruction. Am Rev Respir Dis 1987;136(4):872-9. </li></ul><ul><li>18. Wetzel RC. Pressure-support ventilation in children with severe asthma. Crit Care Med 1996;24(9):1603-5. </li></ul><ul><li>19. Ibsen LM, Bratton SL. Current therapies for severe asthma exacerbations in children. New Horiz 1999;7(3):312-25. </li></ul><ul><li>20. Werner HA. Status asthmaticus in children: a review. Chest 2001;119(6):1913-29. </li></ul>

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