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Status asthmaticus
A severe form of asthma
Hypersecretion
Epitheal damage with
exposed nerve endings
Hypertrophy of goblet cells
and mucous glands
Status asthmaticus : Pathophysiology
Pathophysiology
Smooth
muscle
spasm
Airway
edema
Mucous
plugging
Asthma is primarily an inflammatory disease
Risk factors for fatal asthma
• Medical
– Previous attack with rapid/severe deterioration or
respiratory failure or seizure/loss of consciousness
• Psychosocial
– Denial ,non-compliance
• Family fear of inhalers
Lung Mechanics
• Hyperinflation
– Obstructed small airways cause premature airway
closure, leading to air trapping and hyperinflation.
• Hypoxemia
– Inhomogenous distribution of the affected areas
results in V/Q mismatch, mostly shunt.
Cardiopulmonary interactions
• Left ventricular load
– Spontaneously breathing children with severe asthma have
negative intrapleural pressure
as low as -35 cm H2O during almost the entire respiratory
cycle.
– Negative intrapleural pressure causes increased left
ventriculalr after load, resulting in risk for pulmonary edema
• Right ventricular load
– Hypoxic pulmonary vasoconstriction and lung hyperinflation
lead to increased right ventricular after load
Cardiopulmonary interactions
• Pulsus paradoxus
– It is the clinical correlate of cardiopulmonary
interaction during asthma. It is defined as exaggeration
of the normal respiratory drop in systolic BP:
• Normally <5 mm Hg, but >10mmHg in pulsus paradoxus
Pathophysiology
Severe air flow
obstruction
Incomplete exhalation Increased lung volume
Expanded small airwaysIncreased elastic recoil pressure
Increased expiratory flow Decreased expiratory resistance
Compenseted
Hyperinflation, normocapnia
Worsening airflow
obstruction
Decompenseted:
Severe hyperinflation, hypercapnia
Metabolism
VQ mismatch
Increased work
of breathing Dehydration
Hypoxia
Lactate
Ketones
Metabolic acidosis
Status asthmaticus by   Pushpa Raj Sharma
Types of exacerbation
• Mild asthma exacerbation
– Dyspnea on exertion or tachypnea in young
children.
– PEF< 70% predicted
– Prompt relief with inhaled with short acting beta
agonist.
– Home management
Moderate asthma exacerbation
• Dyspnea usually limits activity
– PEF 40-69%
– Relief with frequent inhaled short acting beta
agonists
– Hospistal/clinic management
– Anticipate 1-2 days of symptoms after treatment
onset
Severe exacerbation
• Dyspnea at rest, limiting conversation
– PEF less than 40% predicted
– Only partial relief with inhaled short acting beta 2
agonists
– Emergency department management
• Hospitalization likely
• Systemic corticosteroids and ipratropium
• Anticipate > 3 days symptoms
Life threatening exacerbation
• Unable to speak, severe dyspnea with
associated diaphoresis
– PEF <25% of predicted
– Minimal relief with inhaled short acting beta
agonist
– Emergency stabilazation
• PICU admission
• Frequent or continuous salbutamol nebs
• Systemic Corticosteroid and ipratroprium
• ABC management.
Assessment: impending respiratory failure
• Altered level of consciousness
• Inability to speak
• Absent breath sounds
• Central cyanosis
• Diaphoresis
• Inability to lie down
• Marked pulsus paradoxus
Status asthmaticus
Status asthmaticus
Management
• Oxygen 100% warm, humidified
– Delver by non breather mask or high flow nasal canula
• Nebulized salbutamol with ipratroium continuously
to hourly
• Systemic corticosteriod
• Adrenergic agonists:
– Epinephrine
– Terbutaline ( alterntive)
• Two intravenous line
Further management
(Hypercarbia is a failure of ventilation not oxygenation)
• Hypotension
– Fluid bolus of normal saline
– Chest xray ? Tension pneumothorax
(SIADH may be common in severe asthma)
• Magnesium 40-75 mg/kg
• Consider ketamine
• Consider non invasive ventilation: CPAP
• Heliox (helium to oxygen60:40)
• Avoid aminophylline or theophylline
Status asthmaticus
Status asthmaticus
Status asthmaticus
Status asthamaticus
Status asthmaticus
Why hesitate to intubate the asthmatic child?
Case scenario 1
• A 6 yr male with previous history of hospital
admission for difficulty in breathing without fever
and treatment with salbutamol MDI. Re 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 breath after every few seconds.
• Discuss your initial therapeutic approach.
Case Scenario 1
• Which of the following are mandatory in this
child with severe asthma?
(you may choose none, more than one or all)
– Arterial blood gas analysis (to detect onset of
respiratory acidosis)
– Continuous pulse oxymetry
– Chest radiograph (to rule out
penumomediastinum/ thorax
– Frequent determination of PFR
– Blood count to assess need for anesthetics
Scenario 2
• When nebulizing drugs during status asthmaticus, the
following statement about gas flow rate is correct:
A. The higher is the gas flow rate through the nebulizer, the
more particles will be deposited in the patient’s alveolar
space.
B. Most devices require a gas flow rate of 10-12 L/min to
generate optimal particle size.
C. Gas flow rates above 5L/min should be avoided to
maintain laminar flow in the nebulizer output.
D. The nebulizer device should not be driven by 100%
oxygen.

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Status asthmaticus by Pushpa Raj Sharma

  • 2. Hypersecretion Epitheal damage with exposed nerve endings Hypertrophy of goblet cells and mucous glands Status asthmaticus : Pathophysiology
  • 4. Risk factors for fatal asthma • Medical – Previous attack with rapid/severe deterioration or respiratory failure or seizure/loss of consciousness • Psychosocial – Denial ,non-compliance • Family fear of inhalers
  • 5. Lung Mechanics • Hyperinflation – Obstructed small airways cause premature airway closure, leading to air trapping and hyperinflation. • Hypoxemia – Inhomogenous distribution of the affected areas results in V/Q mismatch, mostly shunt.
  • 6. Cardiopulmonary interactions • Left ventricular load – Spontaneously breathing children with severe asthma have negative intrapleural pressure as low as -35 cm H2O during almost the entire respiratory cycle. – Negative intrapleural pressure causes increased left ventriculalr after load, resulting in risk for pulmonary edema • Right ventricular load – Hypoxic pulmonary vasoconstriction and lung hyperinflation lead to increased right ventricular after load
  • 7. Cardiopulmonary interactions • Pulsus paradoxus – It is the clinical correlate of cardiopulmonary interaction during asthma. It is defined as exaggeration of the normal respiratory drop in systolic BP: • Normally <5 mm Hg, but >10mmHg in pulsus paradoxus
  • 8. Pathophysiology Severe air flow obstruction Incomplete exhalation Increased lung volume Expanded small airwaysIncreased elastic recoil pressure Increased expiratory flow Decreased expiratory resistance Compenseted Hyperinflation, normocapnia Worsening airflow obstruction Decompenseted: Severe hyperinflation, hypercapnia
  • 9. Metabolism VQ mismatch Increased work of breathing Dehydration Hypoxia Lactate Ketones Metabolic acidosis
  • 11. Types of exacerbation • Mild asthma exacerbation – Dyspnea on exertion or tachypnea in young children. – PEF< 70% predicted – Prompt relief with inhaled with short acting beta agonist. – Home management
  • 12. Moderate asthma exacerbation • Dyspnea usually limits activity – PEF 40-69% – Relief with frequent inhaled short acting beta agonists – Hospistal/clinic management – Anticipate 1-2 days of symptoms after treatment onset
  • 13. Severe exacerbation • Dyspnea at rest, limiting conversation – PEF less than 40% predicted – Only partial relief with inhaled short acting beta 2 agonists – Emergency department management • Hospitalization likely • Systemic corticosteroids and ipratropium • Anticipate > 3 days symptoms
  • 14. Life threatening exacerbation • Unable to speak, severe dyspnea with associated diaphoresis – PEF <25% of predicted – Minimal relief with inhaled short acting beta agonist – Emergency stabilazation • PICU admission • Frequent or continuous salbutamol nebs • Systemic Corticosteroid and ipratroprium • ABC management.
  • 15. Assessment: impending respiratory failure • Altered level of consciousness • Inability to speak • Absent breath sounds • Central cyanosis • Diaphoresis • Inability to lie down • Marked pulsus paradoxus
  • 18. Management • Oxygen 100% warm, humidified – Delver by non breather mask or high flow nasal canula • Nebulized salbutamol with ipratroium continuously to hourly • Systemic corticosteriod • Adrenergic agonists: – Epinephrine – Terbutaline ( alterntive) • Two intravenous line
  • 19. Further management (Hypercarbia is a failure of ventilation not oxygenation) • Hypotension – Fluid bolus of normal saline – Chest xray ? Tension pneumothorax (SIADH may be common in severe asthma) • Magnesium 40-75 mg/kg • Consider ketamine • Consider non invasive ventilation: CPAP • Heliox (helium to oxygen60:40) • Avoid aminophylline or theophylline
  • 24. Status asthmaticus Why hesitate to intubate the asthmatic child?
  • 25. Case scenario 1 • A 6 yr male with previous history of hospital admission for difficulty in breathing without fever and treatment with salbutamol MDI. Re 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 breath after every few seconds. • Discuss your initial therapeutic approach.
  • 26. Case Scenario 1 • Which of the following are mandatory in this child with severe asthma? (you may choose none, more than one or all) – Arterial blood gas analysis (to detect onset of respiratory acidosis) – Continuous pulse oxymetry – Chest radiograph (to rule out penumomediastinum/ thorax – Frequent determination of PFR – Blood count to assess need for anesthetics
  • 27. Scenario 2 • When nebulizing drugs during status asthmaticus, the following statement about gas flow rate is correct: A. The higher is the gas flow rate through the nebulizer, the more particles will be deposited in the patient’s alveolar space. B. Most devices require a gas flow rate of 10-12 L/min to generate optimal particle size. C. Gas flow rates above 5L/min should be avoided to maintain laminar flow in the nebulizer output. D. The nebulizer device should not be driven by 100% oxygen.