Acute Severe Asthma in

Children
Ajay Goenka
 Specific Learning
Objectives
• Definition and mechanisms
• Initial assessment
• Manage a case of acute severe
asthma
• Outline the recent advances, newer
concepts.
• Principles of management of a child
with life threatening asthma.
 Definition
It is a life threatening form of asthma
defined as : a condition in which a
progressively worsening attack is
unresponsive to the usual
appropriate therapy that leads to
pulmonary insufficiency.
 Mechanisms of Status Asthmaticus

Bronchospasm
Mucous
Hypersecretion Mucosal edema

Increased resistance to air flow

Atelectasis Uneven Hyperinflation

ventilation
deadspace compliance
Abnormal
pCO2 V/Q
pO2 alveolar
hypoventilation WOB
 Initial assessment of acute asthma in
children aged >2 years in A&E
Moderate Severe Life threatening
exacerbation exacerbation asthma

• SpO2 92% • SpO2 <92% • SpO2 <92%

• PEF 50% best/ predicted
(>5 years)
• No clinical features of severe
asthma
• Heart rate:
- 130/min (2-5 years)
- 120/min (>5 years)
• Respiratory rate:
- 50/min (2-5 years)
- 30/min (>5 years)
• PEF <50% best/ predicted • PEF <33% best/ predicted
(>5 years) (>5 years)
• Too breathless to talk • Silent chest
or eat • Poor respiratory effort
• Heart rate: • Agitation
- >130/min (2-5 years) • Altered consciousness
- >120/min (>5 years) • Cyanosis
• Respiratory rate:
- >50/min (2-5 years)
- >30/min (>5 years)
• Use of accessory neck
muscles
_____________________________________________________________________________

Asthma score:
0 1 2

1. PaO2 70-100 in air < 70 in air < 70 in 40%

2. Cyanosis none in air in 40%

3. Inspir. BS none unequal Dec. to absent

4. Access. Mus. none moderate maximal

5. Exp. Wheeze none moderate marked

6. Cerebral normal depressed Coma

or agitated
Dec 8, 2021
_____________________________________________________________________________
6
Asthma score:
Clinical asthma score > 5 signifies
impending respiratory failure

Clinical asthma score > 7 plus PCO2 >

65 signifies existing respiratory
failure.
 Status Asthmaticus
Oxygen
• Relative hypoxemia:
– V/Q mismatch
– hypoventilation
• Hypoxemia bronchoconstriction
 agonists impair hypoxic pulmonary
vasoconstriction shunt
• Oxygen to keep pulse ox > 92%
 Status Asthmaticus
Beta2 Agonist Therapy

• Mainstay of • Mode of delivery:

therapy – Inhaled vs
• Rapid onset Systemic
– Intermittent vs
• Selective  2: Continuous
– Metaproterenol – Nonintubated vs
– Terbutaline Intubated
– Albuterol
 Intravenous 
Agonists
• Most studies:
– inhaled therapy > to IV  agonist
• Greater side effects with IV
• Potential benefit severe bronchospasm
• Experience anecdotal with severe SA
• IV Terbutaline:
– bolus 10 mcq/kg
– infusion 0.1-4.0 mcq/kg/min
 Status Asthmaticus
Subcutaneous  Agonists

• Epinephrine/Terbutaline
• No advantage over inhaled  agonists
• Increased side effects
• Indications:
– inability to cooperate with inhalation
therapy
– rapidly decompensating patient
– failure to respond to inhaled beta-agonists
 Status Asthmaticus
Anticholinergics

Airway
 agonist
Sympathetic
Parasympatheti
Xc

Vagolytics
 Status Asthmaticus
IV or oral Corticosteroids
• Recommended dose
– Prednisone or methylprednisolone
• suggested initial dose 2 mg/kg
• 1 mg/kg IV q 6 hours (max 60 mg) x 48
hours,
• then 1mg/kg q 12 hours for 3-5 days
 Status Asthmaticus
IV Theophylline

• Phosphodiesterase inhibitor
• Randomized trials (x2) - no benefit
over standard 2agonists and/or
corticosteroids
• Uncertain benefit in episodes
unresponsive to all other therapy
 Management of acute asthma
in children aged >2 years in A&E
Moderate Severe Life threatening
exacerbation exacerbation exacerbation
• ß2 agonist 2-10 puffs via • Give nebulised ß2 agonist:
spacer ± facemask salbutamol (2-5 years: 2.5mg; >5 years: 5mg) or terbutaline
• Reassess after 15 minutes (2-5 years: 5mg; >5 years: 10mg) with oxygen as driving gas
• Continue oxygen via facemask/nasal prongs
• Give prednisolone (2-5 years: 20mg; >5 years 30-40mg) or
IV hydrocortisone (2-5 years: 50mg; >5 years: 100mg)

RESPONDING NOT RESPONDING IF LIFE THREATENING FEATURES PRESENT

• Continue inhaled • Repeat inhaled Discuss with senior clinician, PICU team or
ß2 agonists ß2 agonist every paediatrician. Consider:
1-4 hourly 20-30 minutes • Chest x-ray and blood gases
• Add soluble oral • Add soluble oral • Repeat nebulised ß2 agonists plus ipratropium
prednisolone prednisolone bromide 0.25mg nebulised every 20-30 minutes
- 20mg (2-5 years) - 20mg (2-5 years) • Bolus IV salbutamol 15g/kg of 200g/ml
- 30-40mg - 30-40mg (>5 years) solution over 10 minutes
(>5 years) • IV aminophylline
 Response to treatment of acute asthma
in children aged >2 years in A&E
Moderate Severe Life threatening
exacerbation exacerbation exacerbation

NOT RESPONDING TO IF POOR RESPONSE TO

RESPONDING TO TREATMENT
TREATMENT TREATMENT

DISCHARGE PLAN ARRANGE ADMISSION ARRANGE IMMEDIATE

•Continue ß2 agonists 1-4 hourly prn (lower threshold if concern over TRANSFER TO PICU
•Consider prednisolone social circumstances)
20mg (2-5 years) 30-40mg
(>5 years) daily for up to 3 days
•Advise to contact if not controlled
on above treatment
•Provide a written asthma action
plan
•Review regular treatment
•Check inhaler technique
•Arrange follow up
 CASE 1
• A 4 year old child was admitted to the
paediatric wards at 10 am with a 24 h history of
cough and wheeze. He had been seen previously
as an outpatient by a colleague and diagnosed as
having asthma. He usually inhaled 200 µg of
budesonide twice a day using a large volume
spacer and had excellent inhaler technique. Until
the day before admission his symptoms had
been well controlled. Despite bronchodilator
treatment for most of the day, he continued to
deteriorate and needed oxygen via a face mask
at 5 l/min to maintain oxygen saturations above
92%.
 Drug delivery: large-volume
spacer versus nebuliser
• There is good evidence to support the view that
pressurised metered dose inhalers (pMDI) in
combination with large volume spacers are at least as
effective as nebulisers

• In mild attacks two to four puffs of salbutamol (200–

400 µg) may be sufficient,

• But in moderate or severe attacks 10 puffs of

salbutamol may be required.
• During this time it is difficult to administer
supplemental oxygen
• For children who do not initially require
supplemental oxygen, ß2 agonists given via a
pMDI+spacer are less likely to provoke hypoxia or
tachycardia than when the same drug is given by a
nebuliser.

• Recent experience from Australia in the use of

large volume spacers found that only 3% of children
admitted to hospital with an exacerbation of
asthma were unable to use a pMDI+spacer, although
7.5% of 200 admissions eventually received
nebulisation.
 Intermittent versus
continuous nebulisation
• Salbutamol reaches its maximal bronchodilating
effects at relatively low doses.

• Increasing the dosage does not increase the

absolute bronchodilatation but does prolong the
bronchodilator effect.

• Continuous nebulisation in low dosages (0.15 mg/kg

in 5 ml) is the most effective
• sustained stimulation of the pulmonary ß2
receptors
• prevents the rebound bronchoconstriction that may
occur with intermittent therapy.
 Combined inhaled
anticholinergics and ß2
agonists
• The evidence also supports the use of nebulised
ipratropium bromide (125–250 µg per dose) in
addition to ß2 agonists for the first 2 h of a
severe attack in children.
• A systematic review and meta-analysis
demonstrated a reduction in hospital admissions
and a significant increase in spirometric
parameters compared with those who did not
receive anticholinergics.
• Children who received more than two
doses did even better.
• If symptoms are refractory to initial ß2
agonist treatment, then ipratropium
bromide mixed with the nebulised ß2
agonist solution should be given.
• It is recommended that this is
repeated every 20 min for the first
hour and every 4 h thereafter.
 Steroids in acute asthma:
route and dose
• Children with an acute exacerbation of asthma should
receive steroid treatment as early as possible.

• This has been shown to reduce the risk of admission

to hospital and prevent a relapse .

• The available data suggest that intravenous steroids

are no more effective than oral steroids and both
begin to work within 3–4 h.

• Intravenous hydrocortisone (4 mg/kg) should

therefore be reserved for children who are unable to
tolerate oral fluids.

•
• . Doses of 1–2 mg/kg are currently
recommended for children with acute severe
asthma.
• The widely held practice of doubling the
inhaled corticosteroid dosage in an acute
exacerbation has been tested in children and
has been found to be wanting.
 CASE 2
• A 10 year old child is admitted at 8 pm following
an acute asthma attack triggered by a cold. He
had been well controlled until 2 weeks
previously, but his parents had noticed a gradual
increase in symptoms over the last fortnight and
suspect that he had stopped taking his inhalers.
• He has not had any salbutamol prior to admission
as he is unable to generate a high enough
inspiratory flow to activate his dry powder
inhaler. His oxygen saturations are 90% in high
flow oxygen and he is halfway through his
second 5 mg salbutamol nebuliser and received
oral steroids. He is pale with marked
respiratory distress and a respiratory rate of
40/min.
Intravenous salbutamol: bolus
versus infusion

• The exact role of intravenous treatment for the

management of acute severe asthma in childhood remains
controversial.

• In selected children it appears to be effective and offers

benefits above and beyond those seen with inhaled
treatment alone.

• Initial loading dose of salbutamol (15 µg/kg over 5 min) as

without this it takes 10–20 h for a plateau concentration
to be reached followed by a continuous infusion (1–5
µg/kg/min).
• If a child is ill enough for treatment with
intravenous salbutamol, or intravenous
aminophylline as below, to be considered,
this should be in a high-dependency unit or
in a paediatric intensive care setting
wherever possible.
• Hypokalaemia is a common consequence of
salbutamol administration
 Intravenous aminophylline
versus salbutamol versus
nothing

• limited data to suggest an improvement in lung function indices

at 6 h following intravenous aminophylline,
• There is no apparent reduction in symptoms, in the number of
nebuliser treatments required or in the length of hospital stay.
.
• Aminophylline infusions are associated with unpleasant side-
effects with a three-fold increase in the risk of vomiting.
 Magnesium
• Bronchodilator:
– inhibits cellular Ca++ uptake/release
– stabilizes most cell membranes

• Intravenous magnesium sulphate is a safe and

established treatment for acute asthma in adults.
• However, there is only limited experience of its use
in childhood.
• However, its place in the treatment of acute
severe asthma remains unclear .
• Doses of up to 50 mg/kg/day have been used for
asthma in the emergency department.
 Leukotriene receptor
antagonists in acute asthma
• Cysteinyl leukotrienes have been shown to be mediators of inflammation
in asthma and marked elevations occur during acute asthma episodes.
• In adults who were admitted to hospital with acute asthma. Intravenous
montelukast in addition to standard treatment, gave a more rapid
recovery in FEV1 over a 2 h period .They also needed less ß 2 agonist and
fewer treatment failures occurred compared to placebo.
• Oral montelukast (4 mg) has been shown to be more effective than
placebo in children between 2 and 5 years of age with mild to moderate
acute asthma, significantly reducing respiratory distress during the
first 4 h
• However, its role in more severe asthma or in addition to oral steroids
remains unknown.
 Levalbuterol versus
salbutamol

• Acute asthma is usually treated with

salbutamol. This is a racemic mixture
of (R)-salbutamol and (S)-salbutamol,
but the bronchodilator effects of
salbutamol are mediated
predominantly by the (R)-salbutamol
isomer, levalbuterol.
• A randomised controlled trial in
children, however, comparing
levalbuterol to combined treatment
with racemic mixture salbutamol and
ipratropium bromide showed no
benefit in terms of hospital
admissions or respiratory distress
 Status Asthmaticus
Ketamine

• Dissociative anesthetic
• Direct bronchodilator
• Potentiates catecholamines
• Bronchorrhea
• Other side effects:
– tachycardia
– BP
 Status Asthmaticus
Inhaled Anesthetics

• Halothane, enflurane, isoflurane

• Mechanisms:
 2 agonist effect
– vagolytic
– direct airway relaxation
• No randomized (level I) trials
 Status Asthmaticus
Helium - Oxygen (HELIOX)

• Blend of 80:20 helium:oxygen

• Biologically inert
• Insoluble in human tissue
• No deleterious effects
• Low density gas
– Air: 1.29 g/l
– O2: 1.43 g/l
– Helium: 0.17 g/l
 Status Asthmaticus
Helium - Oxygen (HELIOX)
• Most recent case reports and clinical studies
have found mixed results in the role of heliox
for use in asthma
 Status Asthmaticus
“Mechanical” Support

• BiPAP
• Intubation/Mechanical Ventilation
• Extracorporeal Life Support
 Status Asthmaticus
Non invasive Ventilation

• Positive-pressure by nasal mask (BiPAP)

• Potential benefits:
– airway stenting
– improve V/Q match
• CPAP improved hypoxemia in asthmatic
children
 Status Asthmaticus
Intubation

• Best done semi-electively

– earlier rather than later
• Drugs of choice:
– Atropine
– Ketamine/Midazolam
– Succinylcholine
 Status Asthmaticus
Intubation
• Usually last resort
• Potential M&M
• Mortality rate
– in adults 0 - 40%
– in children 0 – 5%
 Status Asthmaticus
Mechanical Ventilation

• GOALS:
– Rest inspiratory muscles
– Protect airway
– Provide adequate gas exchange
NOT normal exchange
– Avoid barotrauma, catastrophe
 Status Asthmaticus
Mechanical Ventilation Indications

Coma
Absolute:
Respiratory or cardiac arrest

Cyanosis and hypoxemia on O2

PaCO2 greater than 50 and rising >
Relative: 5mmHg/hr
Deteriorating mental status
Minimal chest movement/air exchange
Pneumothorax
 Status Asthmaticus
Mechanical Ventilation

• Key approach: permissive hypercapnia

(“controlled hypoventilation”)
• tolerate pCO2 to keep pH > 7.20 - 7.25
• prolonged expiratory time
• rate, inspiratory time
• tidal volume
• PEEP: auto-PEEP
 Therapies NOT Recommended

• Antibiotics
• Empiric, aggressive hydration
• Chest PT
• Mucolytics
• Sedation??
SUMMARY
 Treatment of acute asthma
in children aged >2 years

Children with life threatening asthma or SpO2 <92% should receive high
flow oxygen via a tight fitting face mask or nasal cannula at sufficient flow
rates to achieve normal saturations
Inhaled ß2 agonists are first line treatment for acute asthma *
pMDI and spacer are preferred delivery system in mild to moderate
asthma
Individualise drug dosing according to severity and adjust according to
response
IV salbutamol (15mg/kg) is effective adjunct in severe cases

* Dose can be repeated every 20-30 minutes

 Steroid therapy for acute
asthma in children aged >2 years
Give prednisolone early in the treatment of acute asthma attacks
• Use prednisolone 20mg (2-5 years), 30-40mg (>5 years)
• Those already receiving maintenance steroid tablets should
receive 2 mg/kg oral prednisolone up to a maximum dose of 60
mg
• Repeat the dose of prednisolone in children who vomit and
consider IV steroids
• Treatment up to 3 days is usually sufficient, but tailor to the
number of days for recovery
Do not initiate inhaled steroids in preference to steroid tablets
to treat acute childhood asthma
 Other therapies for acute
asthma in children aged >2 years

If poor response to 2 agonist treatment, add nebulised ipratropium

bromide (250mcg/dose mixed with 2 agonist) *
Aminophylline is not recommended in children with mild to moderate
acute asthma
Consider aminophylline for children in high dependency/intensive care
with severe or life threatening bronchospasm unresponsive to maximal
doses of bronchodilators and steroid tablets
Do not give antibiotics routinely in the management of acute childhood
asthma
ECG monitoring is mandatory for all intravenous treatments
* Dose can be repeated every 20-30 minutes
 Hospital admission for acute
asthma in children aged >2 years
Children with acute asthma failing to improve after 10 puffs of 2 agonist
should be referred to hospital. Further doses of bronchodilator should be given
as necessary whilst awaiting transfer
Treat with oxygen and nebulised 2 agonists during the journey to hospital

Transfer children with severe or life threatening asthma urgently to hospital to

receive frequent doses of nebulised 2 agonists (2.5-5mg salbutamol or 5-10
mg terbutaline)
Decisions about admission should be made by trained physicians after repeated
assessment of the response to further bronchodilator treatment
Consider intensive inpatient treatment for children with SpO 2 <92% on air after
initial bronchodilator treatment
 Treatment of acute asthma
in children aged <2 years

Oral 2 agonists are not recommended for acute asthma in infants

For mild to moderate acute asthma, a pMDI with spacer is the optimal
drug delivery device
Consider steroid tablets in infants early in the management of moderate
to severe episodes of acute asthma in the hospital setting
Steroid tablet therapy (10 mg of soluble prednisolone for up to
3 days) is the preferred steroid preparation
Consider inhaled ipratropium bromide in combination with an inhaled 2
agonist for more severe symptoms
 Report Card: Status
Asthmaticus Therapy
Oxygen A
 Agonists
Inhaled A+
IV B
Ipratropium A
Corticosteroids A
Magnesium B+
Report Card: Status Asthmaticus Therapy

Ketamine C
HELIOX B-
Inhaled Anesthesia C+
BiPAP C+
Methylxanthines D
QUESTIONS??