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Status Asthmaticus in
Children
Soumya Ranjan Parida
Basic B.Sc. Nursing 4th
year
Sum Nursing College
Chronic inflammatory disorder of the medium and small
airways.
These airways are hypersensitive to certain “triggers” in
t...
Status Asthmaticus in
Children
Definition: Status Asthmaticus is a
life threatening form of asthma
defined as “a condition...
Epidemiology
Pathophysiology
Presentation and Assessment
Treatment
Topics Covered
Risk factors for fatal asthma
Medical
– Previous attack with rapid/severe
deterioration or respiratory failure or
seizure/...
Status Asthmaticus in
Children
Epidemiology
Pathophysiology
– Cytokines
– Airway pathology
– Autonomic nervous system
– Pu...
Pathophysiology
Asthma is primarily an
inflammatory disease
Mucous pluggingMucous plugging
Smooth muscleSmooth muscle
spas...
Inflammatory cytokines
Activated mast cells and
lymphocytes produce pro-
inflammatory cytokines
(histamine, leukotrienes,
...
Airway
The irritable and inflamed airway is
susceptible to obstruction
triggered by
– Allergens
– Infections
– Irritants i...
Irritable and damaged
airway
HypersecretionHypersecretion
Epithelial damage with
exposed nerve endings
Epithelial damage w...
Autonomic nervous system
Bronchodilation Bronchoconstriction
SympatheticSympathetic Circulating catecholaminesCirculating ...
Lung mechanics
Hyperinflation
– Obstructed small airways cause
premature airway closure, leading to air
trapping and hyper...
Severe airflowSevere airflow
obstructionobstruction
IncompleteIncomplete
exhalationexhalation
Increased lungIncreased lung...
Cardiopulmonary
interactions
Left ventricular load
– Spontaneously breathing children
with severe asthma have negative
int...
Cardiopulmonary
interactions
Right ventricular load
– Hypoxic pulmonary vasoconstriction and
lung hyperinflation lead to i...
Cardiopulmonary
interactions
Pulsus paradoxus
– P. paradoxus is the clinical correlate of
cardiopulmonary interaction duri...
Pulsus paradoxus correlates
with severity
All patients who presented with
FEV1 of < 20% (of their best FEV1
while well) ha...
Cardiopulmonary
interactions
Negative intrapleuralNegative intrapleural
pressurepressure
Pulmonary edemaPulmonary edema Pu...
Metabolism
V/Q mismatchV/Q mismatch
HypoxiaHypoxia
DehydrationDehydration
LactateLactate KetonesKetones
Metabolic acidosis...
Presentation
Cough
Wheezing
Increased work of breathing
Anxiety
Restlessness
Oxygen desaturation
Chest tightness
Shortness...
Assessment
Findings consistent with impending
respiratory failure:
– Altered level of consciousness
– Inability to speak
–...
Clinical Asthma Score
0 1 2
Cyanosis or None In air In 40%
PaO2 >70 in air < 70 in air <70 in 40%
Inspiratory B/S Nl Unequ...
Chest X-Ray
– Not routinely indicated
– Exceptions:
Patient is intubated/ventilated
Suspected barotrauma
Suspected pneumon...
ABG
– Early status asthmaticus: hypoxemia,
hypocarbia
– Late: hypercarbia
– Decision to intubate should not depend
on ABG,...
Differential Diagnosis of
wheezing
Bronchiolitis
Pneumonia-viral, bacterial, atypical
Congenital abnormalities: larnygotra...
Oxygen
Deliver high flow
oxygen, as severe
asthma causes V/Q
mismatch (shunt)
Oxygen will not suppress respiratory drive
i...
Fluid
Judicious use of IV fluid necessary
– Most asthmatics are dehydrated on
presentations - rehydrate to euvolemia
– Ove...
Antibiotics
Most infections precipitating asthma
are viral
Antibiotics are not routinely
indicated
??
Treatment
ß-Agonists
ß-receptor agonists stimulate ß2-
receptors on bronchial smooth
muscle and mediate muscle
relaxation
Epinephrin...
ß-Agonists
Less than 10% of nebulized drug
reach the lung under ideal conditions
Drug delivery depends on
– Breathing patt...
ß -Agonists
Delivery of nebulized
drug
– Only particles between
0.8 - 3 mm are
deposited in alveoli
– Correct gas flow rat...
•ß -Agonists
Continuous nebulization superior to
intermittent nebulization
–More rapid improvement
–More cost effective
–M...
ß -Agonists
Dosage
– Intermittent nebulization
O.1-2.5mg (0.5% solution), dilute with NS to
3 ml
High dose: use up to undi...
ß -Agonists
Intravenous ß - Agonist
– Consider for patients with severe air
flow limitation who remain unresponsive
to neb...
ß -Agonists
Side effects
Tachycardia
Agitation, tremor
Hypokalemia
Treatment
ß -Agonists
Cardiac side effects
– Myocardial ischemia known to occur with
i.v. isoproterenol
– No significant cardiovascu...
Steroids
Asthma is an inflammatory
disease
Steroids are a mandatory
element of first line therapy
regimen (few exceptions ...
Steroids
Hydrocortisone 4-8 mg/kg x 1,
then 2-4 mg/kg q 6°
Methylprednisolone 2 mg/kg x1,
then 0.5-1 mg/kg q 4-6°
Treatment
Steroids
Significant side effects
– Hyperglycemia
– Hypertension
– Acute psychosis
– Unusual or unusually severe
infection...
Anticholinergics - Ipratropium
Quaternary atropine derivative
Not absorbed systemically
Thus minimal cardiac effects
(may ...
Anticholinergics
Change in FEV1 is significantly greater
when ipratropium was added to ß-
agonists (199 adults)
Highly sig...
Ipratropium
Dose-Response Curve in Children (n=19,
age 11-17 yrs)
0
0.1
0.2
0.3
0.4
7.5 25 75 250
Dose (micrograms)Dose (m...
Ipratropium
Nebulize 250 - 500 mg every 6 hours
Treatment
Intubation, Ventilation
Absolute indications:
– Cardiac or respiratory arrest
– Severe hypoxia
– Rapid deterioration in me...
Why hesitate to intubate
the asthmatic child?
Tracheal foreign body
aggravates
bronchospasm
Positive pressure
ventilation ...
Intubation
Preoxygenate, decompress stomach
Sedate (consider ketamine)
Neuromuscular blockade (may avoid
large swings in a...
Immediately after
intubation
Expect hypotension, circulatory
depression
Allow long expiratory time
Avoid overzealous manua...
Mechanical ventilation
Positive pressure ventilation
worsens hyperinflation/risk of
barotrauma
Thoughtful strategies inclu...
Ketamine
Dissociative anesthetic with strong
analgesic effect
Direct bronchodilating action
Useful for induction (2 mg/kg ...
Inhalational anesthetics
Halothane, isoflurane have
bronchodilating effect
Halothane may cause hypotension,
dysrhythmia
Re...
Theophylline
Role in children with severe asthma
remains controversial
Narrow therapeutic range
High risk of serious adver...
– Loading Dosage :6-7mg/kg
– Maintenance Dosage; as per age
– 6wk-6mth :0.5mg/kg/hr
– 6mth-1yr : 0.7mg/kg/hr
– 1yr-9yr : 1...
Theophylline
May have a role in selected,
critically ill children with asthma
unresponsive to conventional
therapy:
– Rand...
Magnesium
Smooth-muscle relaxation by
inhibition of calcium uptake
(=bronchodilator)
Dosage recommendation: 25 - 75
mg/kg ...
Magnesium
Several anecdotal reports
Only one randomized pediatric
trial
– Randomized, placebo-controlled, blinded trial (n...
Helium - Oxygen (Heliox)
Helium lowers gas density (if at least
60% helium fraction)
Reduces resistance during turbulent
f...
Heliox
Helium-oxygen (80:20) decreased
pulsus paradoxus and increased PEFR in
a controlled trial of adult patients
Heliox ...
Bronchoscopy, bronchial
lavage
Marked mucus plugging may render
bronchodilating and anti-inflammatory
therapy ineffective
...
Summary
Severe asthma in children is increasing in
prevalence and mortality
Aggressive treatment with ß-agonist, steroids ...
Management of Asthma Exacerbations in Acute Care Setting
Initial Assessment
• History, physical examination (auscultation,...
Reassess after 1 Hour
Physical Examination, PEF, O2 saturation and other tests as needed
Criteria for Moderate Episode:
• ...
Good Response within 1-2
Hours:
• Response sustained 60 min after
last
treatment
• Physical exam normal: No
distress
• PEF...
Admit to Acute Care Setting
• Oxygen
• Inhaled 2-agonist ― anticholinergic
• Systemic glucocorticosteroid
• Intravenous ma...
Status asthmaticus
Status asthmaticus
Status asthmaticus
Status asthmaticus
Status asthmaticus
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Status asthmaticus

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Status asthmaticus

  1. 1. Status Asthmaticus in Children Soumya Ranjan Parida Basic B.Sc. Nursing 4th year Sum Nursing College
  2. 2. Chronic inflammatory disorder of the medium and small airways. These airways are hypersensitive to certain “triggers” in the environment. Intermittent and recurrent episodes of... – Wheezing – Shortness of breath – Chest tightness – Cough - night, early morning Usually reversible Asthma cannot be cured but its symptoms can be controlled with proper environmental changes and medication. What is Asthma ?
  3. 3. Status Asthmaticus in Children Definition: Status Asthmaticus is a life threatening form of asthma defined as “a condition in which a progressively worsening attack is unresponsive to the usual appropriate therapy with adrenergic drugs and that leads to pulmonary insufficiency.”
  4. 4. Epidemiology Pathophysiology Presentation and Assessment Treatment Topics Covered
  5. 5. Risk factors for fatal asthma Medical – Previous attack with rapid/severe deterioration or respiratory failure or seizure/loss of consciousness Psychosocial – Denial, non-compliance – Depression or other psychiatric disorder – Dysfunctional family : Epidemiology: Epidemiology
  6. 6. Status Asthmaticus in Children Epidemiology Pathophysiology – Cytokines – Airway pathology – Autonomic nervous system – Pulmonary mechanics – Cardiopulmonary interactions – Metabolism Presentation and assessment Treatment
  7. 7. Pathophysiology Asthma is primarily an inflammatory disease Mucous pluggingMucous plugging Smooth muscleSmooth muscle spasmspasm Airway edemaAirway edema
  8. 8. Inflammatory cytokines Activated mast cells and lymphocytes produce pro- inflammatory cytokines (histamine, leukotrienes, PAF,PGD2), which are increased in asthmatics’ airways and bloodstream :: PathophysiologyPathophysiology
  9. 9. Airway The irritable and inflamed airway is susceptible to obstruction triggered by – Allergens – Infections – Irritants including smoke – Exercise – Emotional stress – GE reflux – Drugs – Other factors Pathophysiology
  10. 10. Irritable and damaged airway HypersecretionHypersecretion Epithelial damage with exposed nerve endings Epithelial damage with exposed nerve endings Hypertrophy of goblet cells and mucus glands Hypertrophy of goblet cells and mucus glands Pathophysiology
  11. 11. Autonomic nervous system Bronchodilation Bronchoconstriction SympatheticSympathetic Circulating catecholaminesCirculating catecholamines stimulate ß-receptorsstimulate ß-receptors -- ParasympatheticParasympathetic Vagal signals stimulateVagal signals stimulate bronchodilating Mbronchodilating M22 -- receptorsreceptors Vagal signals stimulateVagal signals stimulate bronchoconstricting Mbronchoconstricting M33-- receptorsreceptors Nonadrenergic-Nonadrenergic- noncholinergicnoncholinergic (NANC)(NANC) Release of bronchodilatingRelease of bronchodilating neurotransmitters (VIP, NO)neurotransmitters (VIP, NO) Release of tachykininsRelease of tachykinins (substance P, neurokinin A)(substance P, neurokinin A) Pathophysiology
  12. 12. Lung mechanics Hyperinflation – Obstructed small airways cause premature airway closure, leading to air trapping and hyperinflation Hypoxemia – Inhomogeneous distribution of affected areas results in V/Q mismatch, mostly shunt Pathophysiology
  13. 13. Severe airflowSevere airflow obstructionobstruction IncompleteIncomplete exhalationexhalation Increased lungIncreased lung volumevolume Increased elasticIncreased elastic recoil pressurerecoil pressure IncreasedIncreased expiratory flowexpiratory flow Expanded smallExpanded small airwaysairways Decreased expiratoryDecreased expiratory resistanceresistance Compensated:Compensated: Hyperinflation,Hyperinflation, normocapnianormocapnia Decreased expiratoryDecreased expiratory resistanceresistance Decompensated:Decompensated: Severe hyperinflation, hypercapniaSevere hyperinflation, hypercapnia WorseningWorsening airflowairflow obstructionobstruction Pathophysiology
  14. 14. Cardiopulmonary interactions Left ventricular load – Spontaneously breathing children with severe asthma have negative intrapleural pressure (as low as -35 cmH2O) during almost the entire respiratory cycle – Negative intrapleural pressure causes increased left ventricular afterload, resulting in risk for pulmonary edema Pathophysiology
  15. 15. Cardiopulmonary interactions Right ventricular load – Hypoxic pulmonary vasoconstriction and lung hyperinflation lead to increased right ventricular afterload Pathophysiology
  16. 16. Cardiopulmonary interactions Pulsus paradoxus – 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. ExpirExpir Inspir NlNl P.P. paradoxusparadoxus InspirExpirExpir Pathophysiology
  17. 17. Pulsus paradoxus correlates with severity All patients who presented with FEV1 of < 20% (of their best FEV1 while well) had pulsus paradoxus Pathophysiology
  18. 18. Cardiopulmonary interactions Negative intrapleuralNegative intrapleural pressurepressure Pulmonary edemaPulmonary edema Pulsus paradoxusPulsus paradoxus HyperinflationHyperinflation HypotensionHypotension Altered hemodynamicsAltered hemodynamics Pathophysiology
  19. 19. Metabolism V/Q mismatchV/Q mismatch HypoxiaHypoxia DehydrationDehydration LactateLactate KetonesKetones Metabolic acidosisMetabolic acidosis Increased workIncreased work of breathingof breathing Pathophysiology
  20. 20. Presentation Cough Wheezing Increased work of breathing Anxiety Restlessness Oxygen desaturation Chest tightness Shortness of breath Audible wheezes : reasonable airflowAudible wheezes : reasonable airflowAudible wheezes : reasonable airflowAudible wheezes : reasonable airflow ““Silent chest” : ominous!Silent chest” : ominous!““Silent chest” : ominous!Silent chest” : ominous! Pathophysiology
  21. 21. Assessment Findings consistent with impending respiratory failure: – Altered level of consciousness – Inability to speak – Absent breath sounds – Central cyanosis – Diaphoresis – Inability to lie down – Marked pulsus paradoxus
  22. 22. Clinical Asthma Score 0 1 2 Cyanosis or None In air In 40% PaO2 >70 in air < 70 in air <70 in 40% Inspiratory B/S Nl Unequal or Absent decreased Expir wheezing None Moderate Marked Cerebral Nl Depressed Coma function Agitated ≥≥ 5 = impending resp failure5 = impending resp failure
  23. 23. Chest X-Ray – Not routinely indicated – Exceptions: Patient is intubated/ventilated Suspected barotrauma Suspected pneumonia Other causes for wheezing are being suspected Assessment
  24. 24. ABG – Early status asthmaticus: hypoxemia, hypocarbia – Late: hypercarbia – Decision to intubate should not depend on ABG, but on clinical assessment – Frequent ABGs are crucial in the ventilated asthmatic Assessment
  25. 25. Differential Diagnosis of wheezing Bronchiolitis Pneumonia-viral, bacterial, atypical Congenital abnormalities: larnygotrachelmalacia, vocal cord paralysis, tracheal or bronchial stenosis, gastro-esophageal reflux, vascular ring. Enlarged lymph nodes from infection or tumor Foreign bodies in trachea, bronchus, or esophagus Cystic Fibrosis Aspergillus Anaphylaxis Toxic fume exposure
  26. 26. Oxygen Deliver high flow oxygen, as severe asthma causes V/Q mismatch (shunt) Oxygen will not suppress respiratory drive in children with asthma Treatment
  27. 27. Fluid Judicious use of IV fluid necessary – Most asthmatics are dehydrated on presentations - rehydrate to euvolemia – Overhydration may lead to pulmonary edema – SIADH may be common in severe asthma Treatment
  28. 28. Antibiotics Most infections precipitating asthma are viral Antibiotics are not routinely indicated ?? Treatment
  29. 29. ß-Agonists ß-receptor agonists stimulate ß2- receptors on bronchial smooth muscle and mediate muscle relaxation Epinephrine Isoproterenol Terbutaline Albuterol Relatively ßRelatively ß22 selectiveselective Significant ßSignificant ß11 cardiovascularcardiovascular effectseffects Treatment
  30. 30. ß-Agonists Less than 10% of nebulized drug reach the lung under ideal conditions Drug delivery depends on – Breathing pattern – Tidal volume – Nebulizer type and gas flow Treatment
  31. 31. ß -Agonists Delivery of nebulized drug – Only particles between 0.8 - 3 mm are deposited in alveoli – Correct gas flow rate is crucial – Most devices require 10-12 L/min gas flow to generate correct particle size Treatment
  32. 32. •ß -Agonists Continuous nebulization superior to intermittent nebulization –More rapid improvement –More cost effective –More patient friendly Treatment
  33. 33. ß -Agonists Dosage – Intermittent nebulization O.1-2.5mg (0.5% solution), dilute with NS to 3 ml High dose: use up to undiluted 0.5% solution – Continuous nebulization 0.5mg/kg/hr High dose: up to undiluted 5% solution (≈ 150 mg/hr) Treatment
  34. 34. ß -Agonists Intravenous ß - Agonist – Consider for patients with severe air flow limitation who remain unresponsive to nebulized albuterol – Terbutaline is i.v. ß-agonist of choice – Loading dosage :10mcg/kg in 10 min – Maintenance Dosage: 0.5 – 5.0 mcg/kg/min Treatment
  35. 35. ß -Agonists Side effects Tachycardia Agitation, tremor Hypokalemia Treatment
  36. 36. ß -Agonists Cardiac side effects – Myocardial ischemia known to occur with i.v. isoproterenol – No significant cardiovascular toxicity with i.v. terbutaline (prospective study in children with severe asthma) – Tachycardia (and tremor) show tachyphylaxis, bronchodilation does not Treatment
  37. 37. Steroids Asthma is an inflammatory disease Steroids are a mandatory element of first line therapy regimen (few exceptions only) Treatment
  38. 38. Steroids Hydrocortisone 4-8 mg/kg x 1, then 2-4 mg/kg q 6° Methylprednisolone 2 mg/kg x1, then 0.5-1 mg/kg q 4-6° Treatment
  39. 39. Steroids Significant side effects – Hyperglycemia – Hypertension – Acute psychosis – Unusual or unusually severe infections Steroids contraindicated with active or recent exposure to chickenpox – Allergic reaction Reported with methylprednisolone, hydrocortisone and prednisone* Treatment
  40. 40. Anticholinergics - Ipratropium Quaternary atropine derivative Not absorbed systemically Thus minimal cardiac effects (may find a fixed/dilated pupil if the nebulizer mask slips over an eye!) Treatment
  41. 41. Anticholinergics Change in FEV1 is significantly greater when ipratropium was added to ß- agonists (199 adults) Highly significant improvement in pulmonary function when ipratropium was added to albuterol (128 children). Sickest asthmatics experienced greatest improvement Treatment
  42. 42. Ipratropium Dose-Response Curve in Children (n=19, age 11-17 yrs) 0 0.1 0.2 0.3 0.4 7.5 25 75 250 Dose (micrograms)Dose (micrograms) Average increase in FEVAverage increase in FEV11 (over 4 hrs)(over 4 hrs) Treatment
  43. 43. Ipratropium Nebulize 250 - 500 mg every 6 hours Treatment
  44. 44. Intubation, Ventilation Absolute indications: – Cardiac or respiratory arrest – Severe hypoxia – Rapid deterioration in mental state – Respiratory acidosis does not dictate intubation Treatment
  45. 45. Why hesitate to intubate the asthmatic child? Tracheal foreign body aggravates bronchospasm Positive pressure ventilation increases risk of barotrauma and hypotension > 50% of morbidity/mortality during severe asthma occurs during or immediately after intubation Treatment
  46. 46. Intubation Preoxygenate, decompress stomach Sedate (consider ketamine) Neuromuscular blockade (may avoid large swings in airway/pleural pressure) Rapid orotracheal intubation (consider cuffed tube) Treatment
  47. 47. Immediately after intubation Expect hypotension, circulatory depression Allow long expiratory time Avoid overzealous manual breaths Consider volume administration Consider pneumothorax Consider endotracheal tube obstruction (++ secretions) Treatment
  48. 48. Mechanical ventilation Positive pressure ventilation worsens hyperinflation/risk of barotrauma Thoughtful strategies include: – Pressure-limited ventilation, TV 8-12 ml/kg, short Ti, rate 8-12/min (permissive hypercapnia) – Pressure support ventilation using PS=20-30 cmH2O (may decrease hyperinflation by allowing active exhalation) Treatment
  49. 49. Ketamine Dissociative anesthetic with strong analgesic effect Direct bronchodilating action Useful for induction (2 mg/kg i.v.) as well as continuous infusion (0.5 - 2 mg/kg/hr) Induces bronchorrhea, emergence reaction Treatment
  50. 50. Inhalational anesthetics Halothane, isoflurane have bronchodilating effect Halothane may cause hypotension, dysrhythmia Requires scavenging system, continuous gas analysis Treatment
  51. 51. Theophylline Role in children with severe asthma remains controversial Narrow therapeutic range High risk of serious adverse effects Mechanism of effect in asthma remains unclear Treatment
  52. 52. – Loading Dosage :6-7mg/kg – Maintenance Dosage; as per age – 6wk-6mth :0.5mg/kg/hr – 6mth-1yr : 0.7mg/kg/hr – 1yr-9yr : 1mg/kg/hr – 9yr-12yr : 0.9mg/kg/hr – 12yr-ad : 0.7mg/kg/hr Theophylline Treatment
  53. 53. Theophylline May have a role in selected, critically ill children with asthma unresponsive to conventional therapy: – Randomized, placebo-controlled, blinded trial (n=163) in children with severe status asthmaticus – Theophylline group had greater improvement in PFTs and O2 saturation – No difference in length – of PICU stay – Theophylline group had signifi- 0 10 20 30 40 50 60 Prior 6 hr 12 hr 24 hr FEV 1 (%) Placebo Theophylline Treatment
  54. 54. Magnesium Smooth-muscle relaxation by inhibition of calcium uptake (=bronchodilator) Dosage recommendation: 25 - 75 mg/kg i.v. over 20 minutes Treatment
  55. 55. Magnesium Several anecdotal reports Only one randomized pediatric trial – Randomized, placebo-controlled, blinded trial (n=31) in children with acute asthma in ER (MgSO4 25 mg/kg i.v. for 20 min) – Magnesium group had significantly greater improvement in FEV1/PEFR/FVC – Magnesium group more likely – to be discharged home – No adverse effects 0 10 20 30 40 50 60 50 min 80 min 110 min Placebo Magnesium Treatment
  56. 56. Helium - Oxygen (Heliox) Helium lowers gas density (if at least 60% helium fraction) Reduces resistance during turbulent flow Renders turbulent flow less likely to occur Treatment
  57. 57. Heliox Helium-oxygen (80:20) decreased pulsus paradoxus and increased PEFR in a controlled trial of adult patients Heliox may worsen dynamic hyperinflation Treatment
  58. 58. Bronchoscopy, bronchial lavage Marked mucus plugging may render bronchodilating and anti-inflammatory therapy ineffective “Plastic bronchitis” has been described in asthmatic children Combined bronchoscopy/lavage has been used in desperately ill asthmatic children Treatment
  59. 59. Summary Severe asthma in children is increasing in prevalence and mortality Aggressive treatment with ß-agonist, steroids and anticholinergic is warranted even in the sick- appearing child Avoid intubation if possible Mechanical ventilation will worsen bronchospasm and hyperinflation Use low morbidity approach to mechanical ventilation
  60. 60. Management of Asthma Exacerbations in Acute Care Setting Initial Assessment • History, physical examination (auscultation, use of accessory muscles, heart rate, respiratory rate, PEF or FEV1, oxygen saturation, arterial blood gas if patient in extremis) Initial Treatment • Oxygen to achieve O2 saturation ≥ 90% (95% in children) • Inhaled rapid-acting 2-agonist continuously for one hour. • Systemic glucocorticosteroids if no immediate response, or if patient recently took oral glucocorticosteroid, or if episode is severe. • Sedation is contraindicated in the treatment of an exacerbation.
  61. 61. Reassess after 1 Hour Physical Examination, PEF, O2 saturation and other tests as needed Criteria for Moderate Episode: • PEF 60-80% predicted/personal best • Physical exam: moderate symptoms, accessory muscle use Treatment: • Oxygen • Inhaled 2-agonist and inhaled anticholinergic every 60 min • Oral glucocorticosteroids • Continue treatment for 1-3 hours, provided there is improvement Criteria for Severe Episode: • History of risk factors for near fatal asthma • PEF < 60% predicted/personal best • Physical exam: severe symptoms at rest, chest retraction • No improvement after initial treatment Treatment: • Oxygen • Inhaled 2-agonist and inhaled anticholinergic • Systemic glucocorticosteroids • Intravenous magnesiu Reassess after 1 Hour Physical Examination, PEF, O2 saturation and other tests as needed
  62. 62. Good Response within 1-2 Hours: • Response sustained 60 min after last treatment • Physical exam normal: No distress • PEF > 70% • O2 saturation > 90% (95% children Incomplete Response within 1-2 Hours: • Risk factors for near fatal asthma • Physical exam: mild to moderate signs • PEF < 60% • O2 saturation not improving Improved: Criteria for Discharge Home • PEF > 60% predicted/personal best • Sustained on oral/inhaled medication Home Treatment: • Continue inhaled 2-agonist • Consider, in most cases, oral glucocorticosteroids • Consider adding a combination inhaler • Patient education: Take medicine correctly Review action plan Close medical follow-up Poor Response within 1-2 Hours: • Risk factors for near fatal asthma • Physical exam: symptoms severe, drowsiness, confusion • PEF < 30% • PCO2 > 45 mm Hg • P O2 < 60mm Hg
  63. 63. Admit to Acute Care Setting • Oxygen • Inhaled 2-agonist ― anticholinergic • Systemic glucocorticosteroid • Intravenous magnesium • Monitor PEF, O Admit to Intensive Care • Oxygen • Inhaled 2-agonist + anticholinergic • Intravenous glucocorticosteroids • Consider intravenous 2-agonist • Consider intravenous theophylline • Possible intubation and mechanical ventilation Reassess at intervals Poor Response (see above): • Admit to Intensive Care Incomplete response in 6-12 hours (see above) • Consider admission to Intensive Care if no improvement within 6-12 hours Improved: Criteria for Discharge Home • PEF > 60% predicted/personal best • Sustained on oral/inhaled medication Home Treatment: • Continue inhaled 2-agonist • Consider, in most cases, oral glucocorticosteroids • Consider adding a combination inhaler • Patient education: Take medicine correctly Review action plan Close medical follow-up Improved

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