Status asthmaticus


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Diagnosis and management of Asthma and status asthmaticus in children

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Status asthmaticus

  1. 1. STATUSSTATUS ASTHMATICUSASTHMATICUS DR FARHAN SHAIKH MD;DNB (Peds), Fellow Pediatric Critical Care, Consultant Pediatric Intensivistcademic Coordinator NABH Assessor for Quality Rainbow Children’s Hospital
  2. 2. DefinitionDefinition “Condition of progressively worsening bronchospasm, unresponsive to standard therapy” “Status Asthmaticus”.Derek S,Wheeler et al The respiratory Tract in Pediatric Critical illness and Injury.Springer-Verlag London Limited 2009
  3. 3. EpidemiologyEpidemiology • In contrast to cancer, heart diseases etc, asthma lacks a standardized , consensus definition. • Inspite of that, there is strong evidence that worldwide, its incidence is rising. • Since 1980 its frequency has aproximately doubled. Committeee TIS.International Survey of Asthma and Allergy in Childhood;Lancet 1998;351:1225-1232 KellerMB et al.Epidemiology of Asthma.Semin Respir Crit Care Med 2002;23:317-329
  4. 4. Mortality andMortality and MorbidityMorbidity Mortality and morbidity is steadily rising world wide. Probable causes of it.. •Under-medication •Inadequate use of steroids •Lack of recognition of the severity of asthma Berney P et al.Variation in the prevalance of respiratory symptoms,self reported asthma attacks,and use of asthma medications in the European Community Respiratory Health Survey (ECRH).Eur Respir J 1996;9:687-695
  5. 5. Two clinical subsets..Two clinical subsets.. Type1 Or Slow onset & late arrival: Those children who had long history of poorly controlled severe asthma , often with past h/o respiratory failure •It is the most common variety. •Most of the times preventable. •Pathologic examination shows extensive mucous plugging, edema, eosinophilic infilterates. Papiris S et al.Clinical review:Severe Asthma.Critical Care 2002;6:30-44
  6. 6. Type 2 OR Fast-onset: Mild history of asthma, often without any past history of hospitalization being brought with sudden onset bronchospasm and rapid progression to cardiac arrest and death. •If recognized and managed early, they respond faster to Beta agonists and mechanical ventilation as compared to Type 1. •Pathologic examination shows empty airway, void of mucous plugging and more neutrophils than eosinophils. Papiris S et al.Clinical review:Severe Asthma.Critical Care 2002;6:30-44
  7. 7. Risk factors for fatalRisk factors for fatal AsthmaAsthma •Severe rapid progression of symptoms •Respiratory failure requiring intubation •Seizures or loss of consciousness •Associated psychiatric disorder “Status Asthmaticus”.Derek S,Wheeler et al The respiratory Tract in Pediatric Critical illness and Injury.Springer-Verlag London Limited 2009
  8. 8. PATHOGENESISPATHOGENESIS • It is a disease of inflammation. Two principal hallmarks.. A) Airway (or bronchial) hyperresponsiveness B)Inflammation “Status Asthmaticus”.Derek S,Wheeler et al The respiratory Tract in Pediatric Critical illness and Injury.Springer-Verlag London Limited 2009
  9. 9. • Asthma begins in childhood is often associated with atopy, • Atopy: genetic susceptibility to produce IgE, specific to common airborne allergens (e.g. dust, animal dander etc) • Asthmatic children respond to these allergens, by increased activation of CD4 T helper (Th) cells.
  10. 10. •Atopic children mainly respond with a T helper type 2 (Th2) immune response, •Non-atopic children respond through T helper type 1 (Th1) immuse response “Status Asthmaticus”.Derek S,Wheeler et al The respiratory Tract in Pediatric Critical illness and Injury.Springer-Verlag London Limited 2009
  11. 11. • Atopic children, through Th2 immunological response, activate allergic airway inflammation via IL-4,5,6,9 and IL-13 and via B-cells release of IgE. • IgE binds with Fc receptors of mast cells and causes release of histamine,mast cell tryptase and prostaglandins. • Non atopic children, through Th1, produce interferon (IFN)-Gamma, IL-2, and lymphotoxins “Status Asthmaticus”.Derek S,Wheeler et al The respiratory Tract in Pediatric Critical illness and Injury.Springer-Verlag London Limited 2009
  12. 12. Role of Airway SmoothRole of Airway Smooth Muscles (ASM)Muscles (ASM) • Recently shown to synthesize and release many cytokines, chemokines and mediators. • ASMs of asthmatic children are shown to possess Fc receptor just like mast cells, which bind with IgE and produce these responses. “Status Asthmaticus”.Derek S,Wheeler et al The respiratory Tract in Pediatric Critical illness and Injury.Springer-Verlag London Limited 2009
  13. 13. Role of Exhaled NitricRole of Exhaled Nitric Oxide measurementsOxide measurements • In asthmatic patients, due the inflammation, there is increased gene expression and production of inducible Nitric Oxide synthase (iNOS) leading to production of Nitric Oxide. • Exhaled Nitric Oxide levels appear to correlate with the severity of asthma and can be used for monitoring of these children DeNicolaLK et al.Exhaled nitric oxide as an indicator of severity of asthmatic inflammation.Pedaitr Emerg Care 2000;16:290-295 Nelson BV e al Expired NO as a marker for childhood asthma.J Pediatr 1997;130:423-427
  14. 14. Airflow ObstructionAirflow Obstruction A) Acute Bronchoconstriction A) Airway edema A) Chronic mucous plugging A) Airway remodeling
  15. 15. A) Acute bronchoconstriction is mainly mediated through release of IgE B) Airway edema develops 6-24 hours following the allergen challenge also known as late asthmatic response. C) Mucous production is more prominent in Th2 cell response in children with atopy D) Airway remodeling is associated with structural changes due to long standing inflammation and significantly affect the extent of reversibility of airway obstruction.
  16. 16. Airway edemaAirway edema Acute Bronchoconstriction Acute Bronchoconstriction Chronic mucous plugging Chronic mucous plugging Increased airway resistance Airway remodeling Airway remodeling
  17. 17. Increased airwayIncreased airway resistance leads to..resistance leads to.. • Increased work of breathing • Marked reduction in FEV1 and FVC. • In severe cases, during expiration, as it is a passive process it will promote air trapping
  18. 18. Leatherman, Crit Care Med 1996; 24:541 Air trapping and Auto PEEP generation
  19. 19. set PEEP auto PEEP pressure time PIP PIP No active exhalation or inspiratory effort Treats lungs as single compartment
  20. 20. Inhalation Exhalation AutoPEEP Time Flow Air trapping & Auto PEEPAir trapping & Auto PEEP on Flow-Time scalaron Flow-Time scalar
  21. 21. No return to base line Air trapping and autoAir trapping and auto PEEEP on F-V LoopPEEEP on F-V Loop
  22. 22. Effects of auto PEEP & lungEffects of auto PEEP & lung hyperinflationhyperinflation • Flattening of the diaphragm, thus reducing its efficiency • Reduction in the venous return to the right atrium thus reduces Right Ventricular preload. • Worsening of the lung compliance
  23. 23. • Hyperinflation will cause premature closure of airways during expiration thus aggravating air trapping further and worsening gas exchange by causing V-Q mismatch • Excessive work of breathing (to create negative intrathoracic pressure) will be required during inspiration to overcome the auto PEEP thus increasing the left ventricular afterload.
  24. 24. Clinical manifestationClinical manifestation A child in status asthmaticus brought in the ER should be assessed systematicaly.. •Neurological assessment to look for hypoxic irritability, confusion, inability to recognize parents or even unconsciousness •Child preferring to sit in tripod position to improve diaphragmatic excursions
  25. 25. • Tachypnoea in most cases. • Bradypnea in impending respiratory failure • Grunting, flaring of alae nasi, use of accessory muscles or in late cases, see-saw breathing (chest moving inwards during inspiration) • Older children speaking in short phrases or only in words.
  26. 26. Tachycardia due •to anxiety , •acidosis, •fever, •and hypoxia Pulsus paradoxus (more than 10mmHg change in systolic pressure between inspiration & expiration) in severe airway obstruction.
  27. 27. Role of Oxygen saturation monitoringRole of Oxygen saturation monitoring (the 5(the 5thth Vital sign)Vital sign) •Improvement in SpO2 after Beta agonist inhalor therapy predicts better outcome. •Respiratory failure rarely occurs in patients presenting to hospitals with SpO2 above 92% •Low SpO2 (below 92% at room air) at the time of admission independently predicts risk factor of more severity and longer stay in hospital. Cook T et al., Pediatric asthma: A correlation of clinical treatment and oxygen saturation. Hawaii Med J 1995;54: 665-668 Carruthers DM et al., Arterial blood gas analysis or oxygen saturation in the assessment of acute asthma ? Thorax 1995;50:186-188
  28. 28. Mild Moderate Severe H/O intermittent wheezing Few or no hospitalizayions Frequent hospitalizations (No PICU admissions) Chronic medications < treatments Previous PICU admission, chronic medications > 2 treatments Normal neurologically Anxious, Restless Inability to recogognize parents, Coma, seizures No cyanosis at room air, good air enrty bilaterally, normal speech Cyanosis on < 1.0 FiO2 Decreased air entry with wheezing Speaks in phrases or partial sentences Cyanosis on 1.0 FiO2 Silent Chest, Speaks single words or short phrases Tachycardia, no pulsus paradoxus (PP) Tachycardia, Pulsus paradoxus(PP) (10-20mmHg) Tachycardia, or in late cases bradycardia,PP >20 mmHg PEFR 70-90% predicted or baseline PEFR 50-70% predicted or baseline PEFR <50% of predicted or baseline FEV1/FVC 85% FEV1/FVC 75% FEV1/FVC 45% SpO2 > 95% SpO2 90-95% <90% PaO2 > 80 PaCO2 < 35 PaO2 60-80 PaCO2 <50 PaO2 > 60 PaCO2 > 50
  29. 29. Modified Becker’sModified Becker’s ScoreScore SCORE Resp. Rate Wheezing Insp : Exp. ratio Accessory muscle use 0 < 30 None 1 : 1.5 None 1 30 - 40 Terminal expiration 1 : 2.0 One site 2 41-50 Entire expiration 1 : 3.0 Two sites 3 > 50 Inspiration and entire expiration > 1 : 3 Three sites or Neck strap use Scores from 0 to 12 , 0 being minimal disease severity
  30. 30. Role of ABGRole of ABG • ABG is not predictive of outcome. • In mild to moderate cases, ABG may show normal Oxygenation with respiratory alkalosis. • In Moderate to severe cases, the PaO2 falls and may even show respiratory and metabolic acidosis • Serial ABGs are more useful in assessing response to treatment. “Status Asthmaticus”.Derek S,Wheeler et al The respiratory Tract in Pediatric Critical illness and Injury.Springer-Verlag London Limited 2009
  31. 31. Metabolic AcidosisMetabolic Acidosis • Accumulation of lactate due to increased work of breathing • Oxygen demand/supply mismatch • Dehydration due to poor oral intake and insensible losses • Reduced cardiac output • and V/Q mismatch in lungs
  32. 32. HypokalemiaHypokalemia Most common form of dys-electrolytemia •Mostly due to Beta-agonist administration •Use of glucocorticoids can cause unwanted mineralocorticoid effects leading to hypokalemia “Status Asthmaticus”.Derek S,Wheeler et al The respiratory Tract in Pediatric Critical illness and Injury.Springer-Verlag London Limited 2009
  33. 33. • Associated SIADH can lead to hyponatremia and fluid overload, particularly if large amount of hypotonic fluids administered. • This can cause pulmonary edema too. “Status Asthmaticus”.Derek S,Wheeler et al The respiratory Tract in Pediatric Critical illness and Injury.Springer-Verlag London Limited 2009
  34. 34. MANAGEMENTMANAGEMENT • PROTOCOLIZED , SYSTEMATIC APPROACH TO THE TREATMENT OF CHILDREN WITH STATUS ASTHMATICUS SIGNIFICANTLY IMPROVES THE OUTCOME. “Status Asthmaticus”.Derek S,Wheeler et al The respiratory Tract in Pediatric Critical illness and Injury.Springer-Verlag London Limited 2009
  35. 35. Case ScenarioCase Scenario
  36. 36. A 7 yr girl with a history of.. • recurrent exacerbations of asthma was brought to hospital with a sudden onset of severe respiratory distress 2 hours earlier.
  37. 37. In Emergency departmentIn Emergency department  Conscious, mildly agitated  Talking in sentences of 3-4 words  Intercostal & subcostal retractions  RR- 45/min,  HR- 140/min, pulsus paradoxus of 10-20mmHg  SpO2 92% in 6 L /min oxygen flow  Breath sounds were decreased with moderate wheezing over all lung fields. Assessment?  Moderate Status Asthmaticus  What next?
  38. 38. OxygenOxygen •Oxygen should be given in such a way to keep the SpO2 above 92% •Some adult studies have shown that in severe status asthmaticus Oxygen administration can worsen PaCO2 elimination, mechanism unknown. •However in children no evidence to support this and Oxygen administration is recommended. “Status Asthmaticus”.Derek S,Wheeler et al The respiratory Tract in Pediatric Critical illness and Injury.Springer-Verlag London Limited 2009
  39. 39. SystemicSystemic CorticosteroidsCorticosteroids • Meta analysis by Rowe et al reviewed 30 RCTs that evaluated administration of corticosteroids in children and adults with status asthmaticus concluded that “early corticosteroids in severe asthma improves survival and reduces morbidity “ • A Cochrane Collaboration review of seven RCTs involving 426 children, concluded that “use of corticosteroids produces improvement in outcomes in children with severe asthma”. Rowe BH, et al., Effectiveness of steroid therapy in acute exacerbation of asthma: a metaanalysis. Am J Emerg Med 1992; 10:301-310. Smith M et al., Corticosteroids for the hospitalised children with acute asthma. Cochrane Database Sys Rev 2003;CD 002886.
  40. 40. • Recommendation is to start corticosteroids in first 48 hours of management of status asthmaticus • Methyl prednisolone 2-4 mg/ kg / day divided every 6 hourly IV will maintain plasma steroid concentration of 100-150mcg cortisol/100ml • No special role of “High dose” corticosteroids • Oral route is equally efficatious as IV or IM but not recommended in severe cases. Collins JV et al., Intravenous corticosteroids in the treatment of acute bronchial asthma. Lancet 1970; 21: 1047-1049
  41. 41. • Peak anti-inflammatory effects of corticosteroids become evident from 6 hours and 12 hours after first dose. • A Cochrane collaboration review of 12 RCTs involving 863 patients (children and adults) concluded that “Administration of corticosteroids within 1 hour of presentation to ER significantly reduces admission rate”. Rowe BH et al.Era;y emergency department treatment of acute asthma with systemic corticosteroids.Cochrane database Syst Rev 2001;1:CD002178
  42. 42. Mechanism of action of steroids in Status asthmaticus still under study, proposed mechanisms are.. Genomic effects (takes 6-24 hours) •Inhibition of pro-inflammatory gene expression •Up-regulation of Beta adrenergic receptors expression Non genomic effects (start almost immediately): Membrane stabilization and effects on ion channels.
  43. 43. InhaledInhaled CorticosteroidsCorticosteroids • Not recommended in Management of severe status asthmaticus. • Severe airway obstruction and mucous plugging may limit delivery of steroids to the site of action • Several studies have compared various inhaled steroids with intravenous corticosteroids and came to similar conclusion that IV corticosteroid was superior in reducing mortality and morbidity. “Status Asthmaticus”.Derek S,Wheeler et al The respiratory Tract in Pediatric Critical illness and Injury.Springer-Verlag London Limited 2009
  44. 44. Beta- AdrenergicBeta- Adrenergic AgonistsAgonists Epinephrine : •Subcutaneous 1 : 1000. 1mg/ml.0.01ml/kg/dose every 15-20 minutes may be repeated 3 times •Nebulized form not studied in Status asthmaticus. •Once considered treatment of choice, nowadays not used frequently because IV corticosteroids with newer Beta agonist (Salbutamol) are very effective. “Status Asthmaticus”.Derek S,Wheeler et al The respiratory Tract in Pediatric Critical illness and Injury.Springer-Verlag London Limited 2009
  45. 45. • Subcutaneous Epinephrine OR subcutaneous Terbutaline (0.01ml/kg of 1 : 1,000 terbutaline OR 1 mg/ml, max 0.3 – 0.5 ml) is recommended in severe Status asthmaticus, where child is decompensating on Inhaled Beta agonists. • Subcut Terbutaline is safe in children and adults but not recommended below 2 years age “Status Asthmaticus”.Derek S,Wheeler et al The respiratory Tract in Pediatric Critical illness and Injury.Springer-Verlag London Limited 2009
  46. 46. SalbutamolSalbutamol • Several studies have demonstrated superior efficacy of inhaled Beta2 agonist as compared to sub cut. Epinephrine • Fixed dose (2.5 mg Salbutamol in 2.5 ml saline) is as efficacious as calculated dose (0.1mg/kg) in moderate Status Asthmaticus. • In severe Status Asthmaticus, “high dose” (0.30mg/kg) salbutamol is more effective than “Low dose” (0.1mg/kg) Tinkelman DG et al., Comparison of nebulized terbutaline and subcutaneous epinephrine in the treatment of acute asthma. Ann Allergy 1983; 50:398-401 Uden DL et al., Comparison of nebulized terbutaline and subcutaneous epinephrine in the treatment of acute asthma. Ann Emer Med 1985; 14:229-232.
  47. 47. Nebulisor Vs InhalorsNebulisor Vs Inhalors • Available evidence suggests that there is no difference between MDIs with spacers compared with nebulizers, regardless of the severity of acute Asthma and both options are reasonable in the routine care in ER in mild to moderate cases. • However in acute severe Asthma continuous salbutamol Nebulization is the most appropriate choice in critically ill child. Amirav I et al., Metered dose inhaler accessory devices in acute asthma.Arch Pediatr Adolesc Med 1997;151:876-882 Scarfone RJ et al., Beta 2 agonist in acute asthma: the evolving state of the art. Pediatr Emer Care 2002;18:442-447.
  48. 48. • Continuous nebulization provides sustained stimulation of the Beta-adrenergic receptors in the airways. Side effects: Hypokalemia, muscle cramps, Tremors, tachycardia. • Beta2 agonists at higher doses have shown to reduce anti inflammatory actions of steroids by reducing its binding to its action receptors. • Adcock IM, et al., High concentration of beta adrenergic agonistinhibite DNA binding of glucocorticoids in human lung in vitro. Biochem Soc Trans 1995; 23:217S • Peters MJ, et al., Beta agonist inhibition of steroid receptor DNA binding activity in human lung. Am Rev Respir Dis 1993;147: A 772 • Peters MJ, et al., Beta adrenoreceptors agonists interfere with glucocorticoid receptor DNA binding in rat lung. Eur J Pharmacol 1995;289: 275-281
  49. 49. TerbutalineTerbutaline • It is selective Beta2 receptor agonist • No RCTs on its use in Status asthmaticus in children or adults. • It can be tried in children unresponsive to continuous salbutamol nebulizations > 2year age • It can be given subcut, IV or Nebulzed form. • More studies needed to support its more active role in status Asthmaticus. “Status Asthmaticus”.Derek S,Wheeler et al The respiratory Tract in Pediatric Critical illness and Injury.Springer-Verlag London Limited 2009
  50. 50. Levo salbutamolLevo salbutamol • Salbutamol exists as a 50 : 50 mixture of two mirror image enantiomers-the active R-Salbutamol and S –Salbutamol. • Studies have shown that S-Salbutamol can promote bronchoconstriction. • Levo salbutamol is pure R-salbutamol. • Studies in children have not shown any clear benefit of Levo over regular salbutamol. Scarfone RJ,et al., Beta 2 agonists in acute asthma:the evolving state of the art. Pediatr Emer Care 2002 ; 18:442-447
  51. 51. IV SalbutamolIV Salbutamol • Can be used as bolus (5-15mcg / kg) or continuous infusion (1 mcg /kg / min to clinical improvement or greater than 20% increase in heart rate) • One study suggested no clinical differences between IV sulbutamol and IV Aminophylline in status asthmaticus. • IV Sulbutamol can casue tachycardia, tremors and cardiac arrhythmias. Roberts G,et al., Intravenous salbutamol bolus compared with an aminophylline infusion in children with severe asthma. A randomized control trial. Thorax 2003;30:306-310.
  52. 52. Ipratropium BromideIpratropium Bromide • Parasympathetic nerve fibres are mainly supplied to larger central airways and stimulate bronchoconstriction and mucous secretion. • Sympathetic nerves are supplied to peripheral smaller airways and cause bronchodilation. Studies have shown synergistic effect when Ipratropium bromide is used along with salbutamol.(Salbotamol acting on peripheral airways and Ipratropium bromide on proximal) “Status Asthmaticus”.Derek S,Wheeler et al The respiratory Tract in Pediatric Critical illness and Injury.Springer-Verlag London Limited 2009
  53. 53. MagnesiumMagnesium • Exact mechanism of action in Status asthmaticus not known • It may treat underlying hypo magnesemia (Hypo Mg can occur due to continuous Beta agonist therapy,) • Mg acts as Calcium antagonist reducing Ca uptake by muscles and causing relaxation.
  54. 54. doses: •IV 0.1ml/kg of 50% MgSO4 (50-75 mg / kg (Max 2 gram) over 20- 30 minutes, every 4 – 6 hourly •Aim to keep Sr Mg above 4 mg% to have optimum broncodilatation • Side effects: Nausea, facial flushing. When Sr Mg is > 12 mg% loss of deep tendon reflexes, muscle weakness and respiratory depression.
  55. 55. TheophyllineTheophylline • Although effective bronchodilator, its use has reduced as Beta2 agonists are sufficient in most cases. • It produces bronchodilatation without causing V/Q mismatch • while Terbutaline infusion causes bronchodialatation along with hypoxic vasoconstriction leading to some V/Q mismatch “Status Asthmaticus”.Derek S,Wheeler et al The respiratory Tract in Pediatric Critical illness and Injury.Springer-Verlag London Limited 2009
  56. 56. • Theophylline’s diuretic effects may also reduce excess alveolar fluid and microvascular permeability Theophylline also .. • increases respiratory drive, • improves mucociliary clearance, • improves contractility of diaphragm • and reduces pulmonary vascular resistance Monserrat JM, et al., Gas exchange response to intravenous aminophylline in patient with severe exacerbation of asthma. Eur Respir J 1995;8:28-33. Bell M et al., Low dose theophylline increases urine output in diuretic dependent critically ill children. Intensive Care Med 1998; 24: 1099-1105
  57. 57. • Three recent trials in critically ill children (including ventilated children) used theophylline along with steroids, Beta2 agonist inhalor therapy, Oxygen and mechanical ventilation and found positive role of theophylline in Status Asthmaticus. • They have recommend to use other safer options first, before starting theophylline • Serum theophylline concentration should be followed closely. (keep below 10-12 mg/ml) Yung M et al., Randomized controlled trial of aminophylline for severe acute asthma. Arch Dis Child 1998; 79: 405-410. Ream RS, et al., Efficacy of IV theophylline in children with severe status asthmatics.Chest 2001;119(5):1480-1488.
  58. 58. Back to our Scenario..Back to our Scenario..
  59. 59. Medical ManagementMedical Management Oxygen by NRM at 10L/min Steroids •Hydrocortisone: 4mg/kg stat f.b 2mg/kg every 6hr o Methyl Prednisolon IV: 2-4 mg/kg every 6hr on D1 1mg/kg every 12 hr D2 1mg/kg every day Bronchodilator Nebulisation: Continuous o Salbutamol: 0.1-0.3 mg/kg o Ipratropium bromide: 250microgram/dose as TID or QID IV Fluids full maintenance in dehydrated child, 2/3rd maintenance in well hydrated child (risk of SIADH)
  60. 60. As the distress persisted, Magnesium Sulphate (50%) – o 0.1ml/kg (50mg/kg) I.V over 20min f.b 0.06ml/kg/hr(30mg/kg/hr) o Target Mg level – 1.5-2.5 mmol/lt Respiratory distress persisted and still the air entry was absent over both lung fields… Aminophylline infusion – o Loading dose 5mg/kg f.b o Maintainance – 1mg/kg/hr
  61. 61. After 1hrAfter 1hr Conscious but • More agitated • Increasing respiratory effort, RR – 55/min • Spo2 88% in 10 lt/min • Skin warm and well perfused • ABG: pH 7.2, pCo2 65, paO2 75, BE 8
  62. 62. How will you proceed?How will you proceed? • Non-invasive assisted ventilation using full-face mask continous positive airway pressure (CPAP) at 5- 6 cmH 2 0. • Medical management continued
  63. 63. Over the next hourOver the next hour • No significant improvement in ventilation and oxygenation • Increasingly fluctuating conscious state and • Markedly decreased peripheral perfusion • Decreased respiratory effort • Bradycardia
  64. 64. MechanicalMechanical ventilationventilation Risks associated with use of mechanical ventilation in Status Asthmaticus include.. •Risk of barotrauma •Cardiovascular instability Many experts feel mechanical ventilation should be avoided in status asthmaticus in children at all costs. Werner HA,et al., Status asthmaticus in children. A review. Chest 2001;119: 1913-1929. Mansmann HC,et al., Treatment of severe respiratory failure during status asthmaticus in children and adolescents using high flow oxygen and sodium bicarbonate. Ann Allergy Asthma Immunol 1997;78(1):69-73.
  65. 65. • Decision to intubate should be based on clinical situation and NOT on blood gas. • Worsening acidosis,worsening hypoxia,deteriorating sensorium, bradycardia etc are some indications. • RSI should be by most experienced person • More than 50% of complication in ventilated patients in Status Asthmaticus occur at the time of intubation. Werner HA,et al., Status asthmaticus in children. A review. Chest 2001;119: 1913-1929.
  66. 66. How will you Intubate ?How will you Intubate ? Rapid sequence Intubation • Preparation: of personnel, equipment & establish monitoring. • Preoxygenation: for 2-3 min with 100% O2. • Pretreatment: Ketamine 1- 2mg/kg • Paralysis: Rocuronium, Vecuronium • Positioning and pressure • Period of apnoea • Placement and proof :Tracheal intubation • Post intubation monitoring
  67. 67. KetamineKetamine • Dissociative anaesthetic. Produces bronchodilatation by.. • Drug induced release of catecholamines • Inhibition of vagal tone • Direct bronchial muscle relaxation
  68. 68. • Its controversial in non-intubated patients, as it can cause laryngospasm, increased bronchial secretions and hallucinations • Current recommendation is to use under strict monitoring in status asthmaticus with impdending respiratory failure or in intubated patiens. Howton JC et al., Randomized double blind placebo controlled trial of intravenous ketamine in acute asthma. Ann Emerg Med 1996;27(2): 170-175.
  69. 69. • High PIP is usually required to overcome airway resistance • Clinical goal is to buy time so that effects of steroids and bronchodilators start and break the cycle of inflammation and bronchospasm.
  70. 70. Strategy: •Use PRVC mode: Constant Vt in face of changing lung compliance and advantage of decelerating flow pattern. •Low Vt : 4 – 6ml/kg •Short Ti •Accept higher paCO2 (upper limit still unknown, but keep the Ph above 7.2 •Use PEEP just below the auto PEEP
  71. 71. auto-PEEP 10 cm H2O trigger effort = 10 cm H2O auto-PEEP 3 cm H2O trigger effort = 3 cm H2O PEEP 7 cm H2O PEEP 10 cm H2O PEEP 10 cm H2O Auto-PEEP should be measured with set PEEP = 0
  72. 72. • HFO has been described to be useful in status asthmaticus • ECMO in refractory Status Asthmaticus has been been used Duval EL, et al., Status asthmaticus treated by high frequency oscillator ventilation. Pediatr Pulmono 2000;30(4): 350-353. Tobias JD, et al., Therapeutic options for severe, refractory status asthmaticus:inhalational anaesthatic agents, extracorporeal membrane oxygenation and helium/ oxygen ventilation. Pediatr Anaesth 1997;7(1): 47-57.
  73. 73. Back to Scenario..Back to Scenario..
  74. 74. What will be the initial ventilatorWhat will be the initial ventilator settings ?settings ? • Tidal volume – 6-8 lt/min • I:E ratio 1:3, • PIP–To achieve the target TV (avoid peak pressure > 30 ) • PEEP – 80% of the intrinsic PEEP • Fio2 – 100%
  75. 75. What sedation will youWhat sedation will you use ?use ? • Ketamine Infusion @ 10-40 microgm/kg/min or • Morphine infusion 40mcg/kg/min (some concern about histamine release, but safe) • Midazolam infusion @ 1-4 microgm/kg/min • Intermittent neuromuscular paralysis with Pancuronium 0.1mg/kg ( avoid as much as Possible to prvent critical care Myopathy)
  76. 76. After 12 hoursAfter 12 hours • ABG- PH-7.2, PcO2-70, PaO2-80 , HCO3-30 • Patient is hemodyanamically stable, SpO2 95% • Tidal Volume – Improved What will you do now ?
  77. 77. •Permissive hypercapnia •Tolerating PH till 7.2 if pt hemodyanmically stable Landmark article by Darioli and Perett in 1984 demonstrated approach of “permissive hypercarbia” by using low Vt and low rates dramatically reducing barotrauma and mortality Darioli R, et al., Mechanical controlled hypoventilation in status asthmaticus. Am Rev Respir Dis 1984;129:385-387.
  78. 78. After 24 hrsAfter 24 hrs • ABG: PH- 7.15, PCo2- 80, paO2- 60, HC03- 35 sPO2: 85% • Blood pressure: 80/50 mmHg requiring Dopamine
  79. 79. What will you do now?What will you do now? • Optimize bronchodilatation, sedation • Urgent X ray chest to rule out pneumothorax • Intermittently disconnecting the pt from ventilator, manual bagging and squeezing the chest
  80. 80. After 36 hrAfter 36 hr • Child better o PH – 7.25, Pco2 50, paO2 90 HC03 28 • Blood pressure: 100/60mmHg • Minimal wheezing
  81. 81. Course-Course- • Aminophylline infusion discontinued • Bronchodilatation freq reduced • Sedation decreased to promote spontaneous breathing • Neuromuscular paralysis stopped • FiO2 decreased to 40% • Decrease PIP by 2 as TV delivery improved
  82. 82. After 48 hrsAfter 48 hrs  Child spontaneously breathing  Minimal wheeze  ABG pH 7.3. PCO2 45 PaO2 100 HCO3 25
  83. 83. • Put on SIMV/PS mode f.b CPAP/PS • Stopped sedation and paralysis • Minimal wheeze • Nebulisation continued • Child extubated to high flow oxygen and nebulization continued
  84. 84. Some otherSome other modalities..modalities..
  85. 85. Helium OxygenHelium Oxygen 86 Poiseuille’s lawPoiseuille’s law R = Airflow resistanceR = Airflow resistance n = gas viscosityn = gas viscosity l = length of the tubel = length of the tube r = radiusr = radius R =R = 8 n l8 n l ΠΠ rr44 Helium is used to reduce viscosity and thus the resistance.
  86. 86. • A recently published trial suggests continuous use of Salbutamol nebulization along with Helium-Oxygen mixture results in a greater clinical improvement compared to when use with only 100% Oxygen. Kim IK et al,Helium/oxygen- driven albutrol nebulization in the treatment of children with moderate to severe asthma exacerbations.A randomized control trial.Pediatrics 2005;116:1127-1133
  87. 87. Leukotriene ModifyingLeukotriene Modifying AgentsAgents • Antagonise Leukotrienes thus reversing bronchoconstriction and improves mucociliary function. • Found useful in chronic asthma. • Growing interest in their use in status asthmaticus but no pediatric studies till date and only few adult studies available. Reiss TF et al.Effect of Monteleukast, a potent cysteinyl leukotrien receptor antagonist,on bronchodilatation in asthmatics patients treated with and without inhaled steroids.Thorax 1997;52:45-48
  88. 88. Volatile anestheticVolatile anesthetic • Mainly Isoflurane is found to be safe and useful in status asthmaticus. • Causes direct bronchodilatation and inhibits vagal tone. • Inline gas analyzer is needed along with system to scavenge exhaled gas is necessary. • Useful in refractory status asthmaticus. Wheeler DS et al, Isoflurane therapy for status asthmaticus in children:a case series and protocol.Pediatr Critic Care Med 2000;1(1):55-59
  89. 89. SUMMING UP!!SUMMING UP!! Knowing the “red flag signs”, to predict who will like to be very sick •Past h/o recurrent wheezing, PICU admission •Presenting with SpO2 <92% at room air. •Presence of hypoxic irritability, altered sensorium •Tachycardia, in late stages bradycardia •Use of accessory muscles of respiration •Elder child speaking in short phrases
  90. 90. • Start high flow Oxygen (10 L/min by Non rebreathing mask • Start continuous Nebulaization with salbutamol with Oxygen • Start steroids in FIRST hour of arrival. • In moderate case, can try Oral Prednisolone, other wise give IV steroids • Can give Ipratropium bromide nebulization along with Salbutamol • Can even start MgSO4 in the first one or two hours in cases of severe Asthma
  91. 91. • Think about using Aminophylline in more severe cases. • Can give subcutaneous Epinephrine at this stage. • Try CPAP if still no response. • Ventilation is considered when there is impending respiratory failure, bradycardia,altered sensorium • ABG not used to decide about intubation.
  92. 92. • Ketamine with a paralytic for the RSI by experienced person • Ventilation with Low rates, shorter Ti,low Tidal Volume (4- 6ml/kg) and PEEP 70-80% of the auto PEEP. • Permissive hypercarbia (allowing higher PaCO2 as long as child’s ph is 7.2 or above)
  93. 93. Once you see theOnce you see the improvement..improvement.. 1. Stop infusion Gradually MgSo4, Aminophylline 2. Decrease the frequency of Nebulization 1- 4 hrly 3. Continue Steroids for total for 3 to 5 days 4. Shift to oral once started on oral feeds 5. Discharge on Preventer Regimen