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doi:10.1111/jpc.13075

REVIEW ARTICLE

Acute severe asthma

Colin VE Powell
Division of Population Medicine, School of Medicine, Cardiff University, Cardiff, Wales, United Kingdom

Abstact: Acute exacerbations of asthma are very common reasons for a presentation to emergency departments. This paper focuses on de-
ning the high-risk group, consideration of the concept of phenotypes of acute asthma, the assessment of severe and life-threatening exacer-
bations and an emphasis on the management of the more severe end of the exacerbation severity. A number of evidence-based guidelines exist
throughout the world and are all slightly different. This reects the poor evidence base for some of those recommendations. Thus, a large
variation of treatment drugs, doses and regimen are used and clearly not standardised. This paper aims to present a summary of the best

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evidence and discuss some of these controversies. The most important aspect of treating an exacerbation of acute asthma is to review
regularly and assess response to treatment. Severe and life-threatening episodes should be treated with early use of intravenous treatment
in a stepwise manner following the local guidelines. Non-invasive ventilation and high ow nasal cannulae delivery of oxygen in the emergency

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department are evolving modalities, but evidence for their use is currently limited.
Key words: acute severe exacerbation of asthma; bronchodilator; treatment.

Introduction
Ri History
Acute asthma is one of the commonest reasons for presentation to It is important to understand the patterns of asthma in children.3
an emergency department (ED),1 and in many cases, admissions to Over the last 30 years, there have been reports from a large num-
hospital may be preventable2 if managed effectively by the family ber of cohorts around the world describing different patterns of
co

and medical team involved with a childs care. The National
Asthma Campaign for Australia (NACA) 20143 and other best
practice guidelines4 and national guidelines5,6 are useful resources.
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wheeze, especially in the pre-school under ve age group.7 The
NACA classies the ages into two age groups of ages 0 to 5 years
and 6 years and over.3 The denitions used for asthma patterns in
children not taking a regular preventer are as follows:

Infrequent intermittent asthma

Key Points Symptom-free for at least 6 weeks at a time (symptoms up
A child should be considered as high risk when attending to once every 6 weeks on average but no symptoms
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the emergency department with an acute exacerbation of between are-ups)

their asthma when there is a combination of features of pre- Frequent intermittent asthma
vious severe asthma and one or more adverse psychological Symptoms more than once every 6 weeks on average but
factors no symptoms between are-ups
Dr

A stepwise approach to assessment and treatment should
include initial rapid assessment and commencing early treat-
ment, reassess severity within minutes of that treatment with
a more detailed assessment of clinical signs then review
response to treatment after that rst hour.
Evidence for the comparative choice of intravenous bronchodi-
lators is very limited. Until the evidence becomes available, the
choice of initial intravenous bronchodilators should be based
on local guidelines. Early non-invasive ventilation should be
considered when used by experienced clinicians.
Persistent asthma (mild) presents at least one of the following
daytime symptoms more than once per week but not every day
night-time symptoms more than twice per month but not
every week
Persistent asthma (moderate) shows any of the following
daytime symptoms daily
night-time symptoms more than once per week
symptoms sometimes restrict activity or sleep
Persistent asthma (severe) displays any of the following
daytime symptoms continual
night-time symptoms frequent
are-ups frequent
symptoms frequently restrict activity or sleep

Correspondence: Dr Colin VE Powell, Division of Population Medicine,

School of Medicine, Cardiff University, Cardiff, Wales, United Kingdom. The acute episode
Fax: 44 2920744822; email: Powellc7@cardiff.ac.uk
Mortality from acute asthma is fortunately rare. Condential
Conict of interest: None declared.
enquiry into deaths from asthma suggests that there are three
Accepted for publication 1 November 2015. major factors contributing to the increase risk of death.1

Journal of Paediatrics and Child Health 52 (2016) 187191 187

2016 The Author
Journal of Paediatrics and Child Health 2016 Paediatrics and Child Health Division (Royal Australasian College of Physicians)
Acute severe asthma CVE Powell

The severity of the disease: most children who have died
from asthma have persistent asthma; however, a minority
of children who have died have only mild-to-moderate dis-
ease.1,3,810 Previous near-fatal asthma, previous admission
in the last year, previous admission to paediatric intensive
care (PICU), heavy use of beta 2 agonists and repeat atten-
dances to the ED are all risk factors associated with risk of a
severe attack, near-fatal asthma or death.1,3
Medical management: inadequate treatment steroids, heavy
or increasing use of beta 2 agonists, inadequate monitoring
of the asthma and under use of written asthma plans and de-
lay in seeking help have all been associated with deaths from
asthma.1,3,810
Psychological factors: non-adherence, poorly perceived
symptoms, failure to attend clinics, conict between child
and parent or medical staff and family dysfunction are all
risk factors associated with risk of death from asthma.1,3,810
Impact
The pathophysiological changes and physiological responses to
those changes of increased airways obstruction, hypoxia,
hypercapnea and acidosis lead to the clinical signs that are used
to judge the severity of the episode and response to treatment.
The clinical signs are increased work of breathing, increased re-
spiratory rate, use of the respiratory accessory muscles, tachycar-
dia and pallor with sweating, anxiety and agitation and reduced
consciousness or exhaustion and cardiorespiratory and respira-
tory arrest or sudden death are well known. In older children,
lung function tests can be used as an objective assessment of
the severity of the obstruction, but in younger children, these
tests are not reliable or easy to complete during an exacerbation.
This causes a major problem for clinicians and researchers when
assessing the severity of an acute exacerbation and comparing
the responses to different treatments when relying on the clini-

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cal signs. There are many clinical asthma severity scores, which
have been developed for use in research particularly, but these
Pathophysiology do have problems of validity, reliability and predictive quality.16

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The pathophysiology of an acute exacerbation of asthma is well
described and is a combination of inammation, oedema and Examination
mucus production with bronchoconstriction and subsequent air-
way obstruction and airway plugging. Increased airways resis- The most important parameters in the assessment of the severity
Ri
tance with hyperination and air trapping causes a ventilation of acute childhood asthma are general appearance and mental
and perfusion mismatch within the lungs, and clinically, this state and work of breathing (accessory muscle use and reces-
leads to increased work of breathing and hypoxia and respiratory sion), as indicated in Table 1. Initial SaO2 in air, heart rate and
failure with eventual retention of carbon dioxide and develop- ability to talk are helpful but less reliable additional features.
co
ment of a respiratory acidosis. The increase in residual functional
capacity and lung volume increases the pulmonary vascular re-
sistance and strain on the right side of the heart. Acidosis and Table 1 Clinical features of severity of acute exacerbations
hypoxia will also cause pulmonary vasoconstriction, which adds
Symptoms Mild/ Severe Life-threatening
to the increased strain on the right side of the heart. During in-
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moderate
spiration, the high negative pressures generated by the effort of
inspiration will cause two processes: rstly, transcapillary uid Consciousness Alert 1
Drowsy or
movement into the airway causing airway oedema adding to unconscious
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the increased resistance to airow obstruction and secondly, an Respiratory Not severe Paradoxical Severe respiratory
increase left ventricular afterload and decrease cardiac output distress chest distress or poor
with an exaggerated decrease in systolic blood pressure made movement respiratory effort
worse during inspiration, manifesting as pulsus paradoxus.11 accessory
Dr

Based on studies of acute sudden asthma exacerbations and muscle use

the histopathology identied from asthma deaths, it is likely that and subcostal
there are four acute phenotypes of acute exacerbation of recession
asthma,915 although this still needs further clarity. Oximetry on >94% 9490% <90%
presentation
1 An acute anaphylaxis manifesting as sudden airways obstruction
(SaO2)
2 An acute episode of sudden respiratory collapse caused by
Speech Sentence Few words in Unable to speak
acute mucus plugging obstructing a major airway
in one one breath
3 A slow onset (type 1 exacerbation) where the episode takes
breath
hours to develop characterised by more airway inamma-
Respiratory <25 breaths >/= 25 breaths Bradypnoea
tion and oedema with less severity compared with type 2 rate per minute per minute (exhaustion)
exacerbation, less likely to be admitted to a PICU and longer Pulse rate Normal Tachycardia Cardiac dysrhythmia
length of stay in hospital, with more airway eosinophils at range or bradycardia
postmortem in those that have died. Skin colour Normal 1
Cyanosis
4 A fast onset (type 2 exacerbation) where the episode de- Wheeze Variable 1
Silent chest or
velops quickly over between 3 and 6 h characterised by intensity reduced air entry
mainly bronchospasm with more severity, more likely to
be admitted to PICU but shorter length of stay and recovery, *Not applicable may be the same as moderate and does not
with more airway neutrophils at postmortem in those that determine severity category.
have died.

188 Journal of Paediatrics and Child Health 52 (2016) 187191

2016 The Author
Journal of Paediatrics and Child Health 2016 Paediatrics and Child Health Division (Royal Australasian College of Physicians)
CVE Powell
Wheeze intensity, pulsus paradoxus and peak expiratory ow rate
are not reliable.36 Clinical signs of acute asthma correlate poorly
with the severity of the asthma attack, and none of the signs in iso-
lation are predictive of severity.16 The NACA guidelines3 classify an
acute attack into three levels of severity: mild and moderate
merged together and then severe and nally acute life-threatening
and suggest an initial rapid primary assessment focusing on ability
to speak, oxygen saturation in air at presentation, accessory muscle
use, conscious level, cyanosis and exhaustion. Complete a detailed
secondary assessment after initiating treatment.
Investigations
Chest x-ray is not generally required. Arterial blood gas and spi-
rometry are rarely required in the assessment of acute asthma in
children.
Differential diagnosis
It is worth considering other respiratory problems characterised by
cough, wheezing or breathlessness. During an acute episode of
wheezing, asymmetry on auscultation is often found due to mu-
cous plugging, but warrants consideration of foreign body. Consider
other causes of wheeze (e.g. bronchiolitis, mycoplasma infection,
aspiration, heart failure or foreign body). Chronically wheezy chil-
dren may have a diagnosis other than asthma such as cystic brosis,
cilial dyskinesia, immune dysfunction, developmental/congenital
abnormality (tracheomalacia), upper airway problems or bronchi-
ectasis. Protracted bacterial bronchitis and habit cough syndrome
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have also been recognised as a cause of chronic cough. There
may be clues in the family or perinatal history or the symptoms
and signs, which may suggest an alternative diagnosis to asthma.17
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Treatment
The most important aspect of treating an exacerbation of acute
asthma is to review regularly and assess response to treatment.
M
The NACA suggests the following approach.3 Initial assessment
and commencing treatment (rapid primary assessment), reassess
severity within minutes (secondary features), reassess after the
rst hour of treatment and then review after that rst hour.
Dr
The initial treatment for all exacerbations of asthma is well
established and is oxygen to keep the arterial oxygen saturation
above 92%, inhaled bronchodilators and steroids.3
Initial inhaled therapy
Using a pressurised metered dose inhaler (pMDI) and spacers for
inhaled beta 2 agonist administration is appropriate at the milder
level of severity and probably at the more severe end of the
spectrum too.3 There may be a question about the effectiveness
of using pressurised metered dose inhaler and spacer for admin-
istration of ipratropium bromide for mild-to-moderate exacerba-
tions and probably adds little to the effectiveness when in
combination with salbutamol and potentially associated with
more side effects.18 Giving three doses of nebulised ipratropium
bromide mixed with salbutamol in the rst hour is helpful in the
more severe end of the spectrum of exacerbations.19 There is some
evidence that more frequent doses can dry up secretions and lead
to worsening obstruction by plugging off smaller airways.20
Journal of Paediatrics and Child Health 52 (2016) 187191
2016 The Author
Journal of Paediatrics and Child Health 2016 Paediatrics and Child Health Division (Royal Australasian College of Physicians)
Acute severe asthma
Corticosteroids
Although there may be an issue about the use of systemic steroids
in children less than 5 years with wheezy illness,7 it seems
reasonable to treat those with systemic steroids when admitting
to hospital with a severe wheezy illness outside the bronchiolitis
age group and diagnosis.3,7 The NACA recommends a short
course of systemic corticosteroid therapy for children assessed
as having a moderate-to-severe acute asthma exacerbation or if
there is an incomplete response to beta-agonists.3 There is no
benet to intravenous steroids unless the child cannot take
medication orally or is unconscious,21 where methylpredniso-
lone (in an initial dose of 2 mg/kg, up to 60 mg, subsequent doses
1 mg/kg every 6 h on day 1, then every 12 h on day 2, then daily).
NACA recommends hydrocortisone at a dose of 810 mg/kg
(max 300 mg) initially, then 45 mg/kg/dose can be used,3,21,22
but most clinicians use 45 mg/kg as rst dose.2325
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An initial oral dose of 2 mg/kg prednisolone (maximum
60 mg) orally is recommended and subsequent daily doses of
1 mg/kg if required, although these doses need further evalua-
tion.21,22 A 3-day course is usually all that is required; in severe
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cases, a more prolonged course may be useful, and some may
need it tapering down over a longer period of time.3 There are
some recent papers suggesting that intermittent high-dose in-
Ri haled corticosteroids and leukotriene receptor antagonists have
a role in treating an acute exacerbation of asthma,22 but until
evidence becomes available, the NACA recommends using oral
corticosteroids only.3 A single dose of oral prednisolone has been
shown treat acute mild-to-moderate asthma in 70% of cases, but
these data have not been replicated recently,26 and so single dos-
ing for acute asthma treatment is not recommended. There are
current data to suggest that oral dexamethasone in shorter
course length compared with oral prednisolone may be equiva-
lent in outcome, but further studies are required to clarify this.27
Three national reviews of practice in the UK and Australia
show little variation of treatment for the milder end of the spec-
trum of severity of exacerbation, but the level of variation is
greatest for the more severe exacerbation and life-threatening
episodes.2325
Severe and life threatening exacerbations
These children account for about 510% of presentations to ED
with acute exacerbations1 and should be managed in a critical
care environment.
(i) Inhaled treatment
There is no agreed denition of what is maximal inhaled ther-
apy. NACA advises continuous nebulised bronchodilators of beta
2 agonists mixed with ipratropium bromide in this situation
(dose of 48 puffs (21 mcg/puff) every 20 min for the rst hour
if using pMDI or 250 mcg three times in the rst hour when
nebulised).3 Continuous nebulised treatment is considered to
be superior or at least equivalent to intermittent treatment.3
Nebulised magnesium sulfate (MgSO4) (150 mg nebulised every
20 min for the rst hour) may have a role in this more severe
group with shorter history (the type 2 exacerbation)28 and is
recommended for consideration in this scenario in the current
British Thoracic Society/Scottish Intercollegiate Guidelines
Network5 but not mentioned in NACA.3 Nebulised MgSO4 has
189
Acute severe asthma
not been shown to reduce the need for intravenous bronchodila-
tor treatment or intubation.28
Intravenous bronchodilators
The main problem with deciding which intravenous bron-
chodilator to use is that there are no good direct comparisons
with the three intravenous treatments commonly used. One
recent unblinded, three-way comparison by Singh et al. in
100 children aged between 1 and 12 years suggested that intra-
venous MgSO4 (50 mg/kg infusion over 20 min in 34 patients)
compared with intravenous terbutaline (10 g/kg as a bolus
followed by infusion of 0.1 g/kg/min increased to 1 g/kg/min
in 33 patients) and intravenous aminophylline (5 mg/kg bolus
followed by an infusion of 0.9 mg/kg in 33 patients) was
superior as the Clinical Asthma Severity score at 1 h was
reduced signicantly by four points in a scale of 012.29 There
is huge variation of treatment given in reality despite the
recommendations in the various guidelines.2325 Thus, the
guidelines vary with recommendations.36 The role of intrave-
nous bronchodilators, in addition to nebulised treatment,
remains unclear.3,6
Magnesium. The exact place for intravenous MgS04 in the
treatment of acute asthma in children has yet to be established.
It is clearly used widely; it is easy to give as a bolus and very
rarely given as an infusion.2325 Doses of between 40 and
100 mg/kg as a 20-min infusion have been used with varying
effects on lung function and asthma severity scores when com-
pared with placebo.30 The use of intravenous MgSO4 as second
line-treatment is endorsed by the NACA.3
co
Aminophylline. There is no evidence that there is a role for
aminophylline in children with mild-to-moderate exacerbations
of their asthma. However, if a child is unresponsive to maximal
inhaled therapy, then in the more severe and life-threatening
attacks, aminophylline at 10 mg/kg given over 1 h followed by
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an infusion of 1 mg/kg/h has been shown to have an effect on
outcome including intubation.31 However, recommended doses
and practice vary, with the commonest dose being 5 mg/kg
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loading dose over 20 min and an infusion of 1 mg/kg/h.2325
There is no doubt that vomiting and arrhythmias are serious
side effects from the higher doses of aminophylline, and they
may be the reason that it is not recommended or used in some
Dr
places.36,2325
Salbutamol. There are few clinical trial data on the effective-
ness of intravenous salbutamol. There are concerns that the
doses given are excessive and associated with side effects such
as lactic acidosis and hypokalemia. Further pharmacokinetic
and pharmacodynamic data are required along with head to
head comparisons with fully informed guidelines.32 Current
NACA guidelines suggest using salbutamol as third-line treat-
ment3 if the patient has not responded to continuous nebulised
treatment and add-on treatments such as MgSO4. They suggest
using a loading dose of 5 mcg/kg/min over 1 h and then an
infusion of 12 g/kg/min and monitoring electrolytes and acid
base balance and only on a critical care unit. The British
Thoracic Society/Scottish Intercollegiate Guidelines Network
guidelines suggest using a bolus of 15 g/kg (given over
10 min) in severe asthma and then a continuous intravenous
infusion at 15 g/kg/min thereafter.5 It is clear that there are
huge variations of practice, and clearly, some units do not use
salbutamol at all.2325
190
Journal of Paediatrics and Child Health 2016 Paediatrics and Child Health Division (Royal Australasian College of Physicians)
CVE Powell
Adrenaline
this bronchodilator is not mentioned in most paediatric guide-
lines.36 However, the Global Initiative on Asthma guidelines
suggest it may be of use.6 There is no doubt that some acute
asthma may be anaphylaxis,12 and intramuscular adrenalin
may well have a role.6 The dose suggested is 0.01 mg/kg up to
0.30.5 mg of 1:1000 epinephrine every 20 min for three doses
for acute asthma.6 This treatment is very rarely used in acute
asthma in a paediatric population.2325
Non-invasive ventilation
The NACA suggests considering bilevel positive airway
pressure if the patient shows signs of tiring or develops signs of
respiratory failure. This modality is being used.2325 It has been
shown in adults and children to improve gas exchange and
clinical improvement.11 There is debate as to whether this
should be used without3 or with11 sedation using ketamine or
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low-dose benzodiazepines. This modality clearly needs to be
used in a critical care environment where the skill and experi-
ence exist to manage successfully. Another evolving treatment
for use in the ED is high ow nasal cannula, but the current
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evidence for its use in acute asthma is poor.33 PICU management
is outside the remit of this paper.
Ri
Disposition
When a child is discharged from the ED or ward, consideration
of the childs preventative treatment is essential. It is important
to consider the childs overall control and denitions of good
control, partial control and poor control, and recommendations
for treatment are referenced in the NACA 2014 quick guide.3
Children should have a written action plan (which can be
preformatted and modiable4) and have their inhaler technique
reviewed before discharge. It is important that parents seek
further medical attention (preferably from their general practi-
tioner) should the patients condition deteriorates or if there is
no signicant improvement within 48 h of discharge. At dis-
charge, all patients should have an outpatient appointment or
appropriate follow-up arranged with a paediatrician and/or
family doctor. Parents should be informed of other sources of
information about asthma such as the Asthma Foundation. The
concept of an asthma discharge pack is useful to ensure all
aspects of discharge are considered. A child should be ready for
discharge when it is considered that they can be stable on 34 h
inhaled bronchodilators. This is often a subjective decision.36
References
1 Why asthma still kills. The National Review of Asthma Deaths (NRAD)
Condential Enquiry report, 2014. Available from: https://www.
rcplondon.ac.uk/sites/default/les/why-asthma-still-kills-full-report.pdf
[accessed 21 April 2015]
2 Ordonez GA, Phelan PD, Olinsky A, Robertson CF. Preventable factors
in hospital admissions for asthma. Arch. Dis. Child. 1998; 78: 1437.
3 National Asthma Council Australia. Australian Asthma Handbook,
Version 1.0. National Asthma Council Australia, Melbourne, 2014.
Website. Available from: http://www.asthmahandbook.org.au ISSN
22034722 National Asthma Council Australia Ltd, 2014. [accessed
21 April 2015]
Journal of Paediatrics and Child Health 52 (2016) 187191
2016 The Author
CVE Powell
4 http://www.asthmahandbook.org.au/. Royal Childrens Hospital,
Melbourne. Available from: http://www.rch.unimelb.edu.au/
clinicalguide/) [accessed 21 April 2015]
5 British Thoracic Society (BTS), Scottish Intercollegiate Guidelines
Network (SIGN). British Guideline on the management of Asthma. A
national clinical guideline. BTS/SIGN, Edinburgh, 2014. Available from:
http://www.sign.ac.uk/guidelines/fulltext/101/index.html [accessed 21
April 2015]
6 Global Strategy for Asthma Management and Prevention (Global
INitiative for Asthma GINA). Available from: http://www.ginasthma.org/
local/uploads/les/GINA_AtAGlance_2014.pdf. [accessed 21 April 2015]
7 Brand PL, Caudri D, Eber E et al. Classication and pharmacological
treatment of preschool wheezing: changes since 2008. Eur. Respir. J.
2014; 43: 11727.
8 Strunk RC, Mzrazek DA, Wolfson Fuhrmann GS, LaBrecque JF.
Physiologic and psychological characteristics associated with deaths
due to asthma in childhood. JAMA 1985; 254: 119398.
9 Robertson CF, Rubineld AR, Bowes G. Pediatric asthma deaths in
Victoria: the mild are at risk. Ped. Pulmonol. 1992; 12: 95100.
10 Martin AJ, Campbell DA, Gluyas PA et al. Characteristics of near fatal
asthma in children. Ped. Pulmonol. 1995; 20: 18.
11 Nievas IFF, Anand KJS. Severe acute asthma exacerbations in children:
a stepwise approach for escalating therapy in a pediatric intensive care
unit. JPPT 2013; 18: 88104.
12 Rainbow J, Browne GJ. Fatal asthma or anaphylaxis? Emerg. Med. J.
2002; 19: 4156.
13 Rodrigo G, Rodrigo C. Rapid-onset asthma attack. A prospective cohort
study about characteristics and response to emergency department
treatment. Chest 2000; 118: 154752.
Ri
14 Hyzy R, Travis W, Hanna E, Lyon-Callo S, Flaherty K, Rosenman K.
Slow-onset asthma deaths have more eosinophils and health care
co
utilization than rapid-onset deaths. Respir. Med. 2008; 103: 181926.
15 Ramnath V, Clark S, Camargo C. Multicenter study of clinical features of
sudden-onset versus slower-onset asthma exacerbations requiring
hospitalization. Respir. Care 2007; 52: 101320.
16 Bekhof J, Reimink R, Brand P. Systematic review: insufcient validation
ar
of clinical scores for the assessment of acute dyspnea in wheezing
children. Paediatr. Resp. Rev. 2014; 15: 98112.
17 Weinberger M, Abu-Hasan M. Pseudo-asthma: when cough, wheezing,
M
and dyspnea are not asthma. Pediatr. 2007; 120: 85564.
18 Powell CV, Cranswick NE. The current role of ipratropium bromide in an
acute exacerbation of asthma. J. Paediatr. Child Health 2015;
51: 7512.
19 Rodrigo GJ, Castro-Rodriguez JA. Anticholinergics in the treatment of
Dr
children and adults with acute asthma: a systematic review with meta-
analysis. Thorax 2005; 60: 7406.
Journal of Paediatrics and Child Health 52 (2016) 187191
2016 The Author
Journal of Paediatrics and Child Health 2016 Paediatrics and Child Health Division (Royal Australasian College of Physicians)
Acute severe asthma
20 Munro A, Maconochie I. Best evidence topic reports. Beta-agonists
with or without anti-cholinergics in the treatment of acute childhood
asthma? Emerg. Med. J. 2006; 23: 470.
21 Smith M, Iqubal S, Elliott TM, Rowe BH. Corticosteroids for hospitalized
children with acute asthma. (Review) Cochrane Database of Systematic
Reviews 2003; Issue 1. Art. No.: CD002886
22 Peter P van Asperen, Craig M Mellis, Peter D Sly, Colin Robertson The
Thoracic Society of Australia and New Zealand. The role of
corticosteroids in the management of childhood asthma. Available
from: http://www.thoracic.org.au/imagesDB/wysiwyg/
Steroidsinasthma_2010.pdf
23 Morris I, Lyttle MD, OSullivan R et al. Which intravenous
bronchodilators are being administered to children presenting with
acute severe wheeze in the UK and Ireland? Thorax 2015; 70: 8891.
24 Babl FE, Sheriff N, Borland M et al. Paediatric acute asthma management
in Australia and New Zealand: practice patterns in the context of clinical
practice guidelines. Arch. Dis. Child. 2008; 93: 30712.
25 Lyttle MD, OSullivan R, Doull I et al. Variation in treatment of acute
childhood wheeze in emergency departments of the United Kingdom
ra
and Ireland: an international survey of clinician practice. Arch. Dis.
Child. 2015; 100: 1215.
26 Storr J, Barry W, Barrell E, Lenney W, Hatcher G. Effect of a single oral
ve
dose of prednisolone in acute childhood asthma. Lancet 1987; 329:
87982.
27 Redman E, Powell CV. Prednisolone or dexamethasone for acute
exacerbations of asthma: do they have similar efcacy in the
management of exacerbations of childhood asthma? Arch. Dis. Child.
2013; 98: 9169.
28 Powell C, Kolamunnage-Dona R, Lowe J et al. Magnesium sulphate in
acute severe asthma in children (MAGNETIC): a randomised, placebo-
controlled trial. Lancet Respir Med. 2013; 1: 3018.
29 Singh S, Grover S, Bansal A, Chopra K. Randomised comparison of
intravenous magnesium sulphate, terbutaline and aminophylline for
children with acute severe asthma. Acta Paediatr. 2014; 103: 13016.
30 Rowe BH, Bretzlaff JA, Bourdon C et al. Magnesium sulphate for
treating exacerbations of acute asthma in the emergency department
(Cochrane Review). In: The Cochrane Library. Issue 3, Oxford: Update
Software 2001. [accessed 21 April 2015]
31 Yung M, South M. Randomised controlled trial of aminophylline for
severe asthma. Arch. Dis. Child. 1998; 79: 405410.
32 Starkey ES, Mulla H, Sammons HM, Padya H. Intravenous salbutamol
for childhood asthma: evidence based medicine? Arch. Dis. Child. 2014;
99: 8737.
33 Milsi C, Boubal M, Jacquot A et al. High-ow nasal cannula:
recommendations for daily practice in pediatrics. Ann. Intensive Care
2014; 30: 29.
191