Status asthmaticus

STATUSSTATUS
ASTHMATICUSASTHMATICUS
DR FARHAN SHAIKH
MD;DNB (Peds), Fellow Pediatric Critical Care,
Consultant Pediatric Intensivistcademic Coordinator
NABH Assessor for Quality
Rainbow Children’s Hospital

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

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

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

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

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

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

PATHOGENESISPATHOGENESIS
• It is a disease of inflammation.
Two principal hallmarks..
A) Airway (or bronchial) hyperresponsiveness
B)Inflammation

• 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.

•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

• 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

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.

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

Airflow ObstructionAirflow Obstruction
A) Acute Bronchoconstriction
A) Airway edema
A) Chronic mucous plugging
A) Airway remodeling

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.

Airway edemaAirway edema
Acute
Bronchoconstriction
Acute
Bronchoconstriction
Chronic
mucous
plugging
Chronic
mucous
plugging
Increased
airway
resistance
Airway
remodeling
Airway
remodeling

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

Leatherman, Crit Care Med 1996; 24:541
Air trapping and
Auto PEEP
generation

set PEEP
auto PEEP
pressure
time
PIP
PIP
No active exhalation or inspiratory effort
Treats lungs as single compartment

Inhalation
Exhalation
AutoPEEP
Time
Flow
Air trapping & Auto PEEPAir trapping & Auto PEEP
on Flow-Time scalaron Flow-Time scalar

No return to
base line
Air trapping and autoAir trapping and auto
PEEEP on F-V LoopPEEEP on F-V Loop

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

• 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.

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

• 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.

Tachycardia due
•to anxiety ,
•acidosis,
•fever,
•and hypoxia
Pulsus paradoxus (more than 10mmHg change in systolic
pressure between inspiration & expiration) in severe airway
obstruction.

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

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

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

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

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

HypokalemiaHypokalemia
Most common form of dys-electrolytemia
•Mostly due to Beta-agonist administration
•Use of glucocorticoids can cause unwanted mineralocorticoid
effects leading to hypokalemia
Pediatric Critical illness and Injury.Springer-Verlag London Limited 2009

• Associated SIADH can lead to hyponatremia and
fluid overload, particularly if large amount of
hypotonic fluids administered.
• This can cause pulmonary edema too.
2009

MANAGEMENTMANAGEMENT
• PROTOCOLIZED , SYSTEMATIC APPROACH TO THE
TREATMENT OF CHILDREN WITH STATUS ASTHMATICUS
SIGNIFICANTLY IMPROVES THE OUTCOME.

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.

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?

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.

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.

• 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

• 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

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.

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.
2009

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.

• 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

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.

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.

• 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

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.
2009

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

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.

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)

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.

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.

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

• 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

• 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.

Back to our Scenario..Back to our Scenario..

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)

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

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

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

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

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.

• 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.

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

KetamineKetamine
• Dissociative anaesthetic.
Produces bronchodilatation by..
• Drug induced release of catecholamines
• Inhibition of vagal tone
• Direct bronchial muscle relaxation

• 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.

• 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.

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

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

• 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.

Back to Scenario..Back to Scenario..

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%

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)

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 ?

•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.

After 24 hrsAfter 24 hrs
• ABG: PH- 7.15, PCo2- 80, paO2- 60, HC03- 35 sPO2: 85%
• Blood pressure: 80/50 mmHg requiring Dopamine

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

After 36 hrAfter 36 hr
• Child better
o PH – 7.25, Pco2 50, paO2 90 HC03 28
• Blood pressure: 100/60mmHg
• Minimal wheezing

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

After 48 hrsAfter 48 hrs
 Child spontaneously breathing
 Minimal wheeze
 ABG pH 7.3. PCO2 45 PaO2 100 HCO3 25

• 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

Some otherSome other
modalities..modalities..

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.

• 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

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

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

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

• 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

• 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.

• 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)

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

THANKTHANK
YOU!!
STAY HUNGRY… STAY FOOLISH… STEVE JOBS

Status asthmaticus

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