This article appeared in a journal published by Elsevier.

The attached
copy is furnished to the author for internal non-commercial research
and education use, including for instruction at the authors institution
and sharing with colleagues.
Other uses, including reproduction and distribution, or selling or
licensing copies, or posting to personal, institutional or third party
websites are prohibited.
In most cases authors are permitted to post their version of the
article (e.g. in Word or Tex form) to their personal website or
institutional repository. Authors requiring further information
regarding Elseviers archiving and manuscript policies are
encouraged to visit:
http://www.elsevier.com/copyright

Author's personal copy

Symposium: Allergy

Prevention and treatment of

anaphylaxis

ngoing. A recent consensus document has defined anaphylaxis

o
as a serious allergic reaction that is rapid in onset and may cause
death; the document also proposed diagnostic criteria for use in
research and clinical care (see Table 1).2 Generally speaking, a
diagnosis of anaphylaxis can be made if there is involvement of
the respiratory or cardiovascular systems during an allergic reaction. Less severe reactions may be defined as anaphylaxis if there
is a high index of suspicion for allergic reaction in the setting of
a previously diagnosed allergy. In considering the approach to
treatment and prevention of anaphylaxis, it is important to consider the risk factors for anaphylaxis and fatal anaphylaxis.

Mimi LK Tang
Liew Woei Kang

Abstract

Epidemiology

Anaphylaxis is a systemic allergic reaction that involves the respiratory

and/or cardiovascular systems. Less severe reactions may be defined as
anaphylaxis if there is a high index of suspicion for allergic reaction in the
setting of previously diagnosed allergy. The prevalence of anaphylaxis is
rising at an alarming rate in Westernised societies. The true prevalence
of anaphylaxis in childhood is not well documented, but studies from
Australia suggest it may be as high as one in 170 among pre-school aged
children. Intramuscular adrenaline remains the cornerstone of treatment
for the acute episode. Maintaining a supine posture, oxygen and fluid
support are important adjunct measures. Whether corticosteroids and
antihistamines are beneficial remains inconclusive. Long-term management centres on risk minimisation through prevention of repeat episodes,
education of patients/parents in the recognition and emergency treatment of allergic reactions, and optimal management of co-morbidities
especially asthma. Identification and avoidance of the allergen trigger are
fundamental to prevention. However, avoidance of food triggers is difficult and accidental exposures are common. Education of patients/parents
on recognition and treatment of allergic reactions is, therefore, essential
and should be supported by provision of an anaphylaxis action plan.
An adrenaline auto-injector allows early treatment of anaphylaxis occurring in the community and represents an important aspect of long-term
management. However, controversy remains as to who might benefit from
carrying this device. Some authoritative bodies recommend selective provision to children identified as being at high risk of anaphylaxis or fatality
from anaphylaxis. Whether or not an adrenaline auto-injector is provided,
risk minimisation strategies should be implemented for all children with
known allergy where ongoing exposure is likely (e.g. food, insect sting).

Rates of allergic disease have increased dramatically in the

past three decades. The different allergic conditions have not
increased simultaneously. Worldwide, time trends reveal that
the earlier rise in childhood asthma prevalence has reached a
plateau, and that the rising prevalence of allergic rhinoconjunctivitis and eczema appear to be slowing.3 In contrast, there is a

Clinical criteria for diagnosing anaphylaxis

Anaphylaxis is highly likely when any one of the following three
criteria are fulfilled:
1. Acute onset of an illness (minutes to several hours)
with involvement of the skin, mucosal tissue, or both
(e.g. generalised hives, pruritus or flushing, swollen
lips-tongue-uvula)
AND AT LEAST ONE OF THE FOLLOWING:
a. Respiratory compromise (e.g. dyspnea, wheezebronchospasm, stridor, reduced PEF, hypoxemia)
b. Reduced BP or associated symptoms of end-organ
dysfunction (e.g. hypotonia [collapse], syncope,
incontinence)
2. Two or more of the following that occur rapidly after exposure
to a likely allergen for that patient (minutes to several hours):
a. Involvement of the skin-mucosal tissue (e.g.
generalised hives, itch-flush, swollen lips-tongue-uvula)
b. Respiratory compromise (e.g. dyspnea, wheezebronchospasm, stridor, reduced PEF, hypoxemia)
c. Reduced BP or associated symptoms (e.g. hypotonia
[collapse], syncope, incontinence)
d. Persistent gastrointestinal symptoms (e.g. crampy
abdominal pain, vomiting)
3. Reduced BP after exposure to known allergen for that patient
(minutes to several hours):
a. Infants and children: low systolic BP (age-specific) or
greater than 30% decrease in systolic BP*
b. Adults: systolic BP of less than 90 mmHg or greater
than 30% decrease from that persons baseline

Keywords anaphylaxis; childhood; prevention; treatment

Introduction
Portier and Richet first described anaphylactic reactions in the
1900s.1 Despite numerous advances in the understanding and management of anaphylaxis, there has been confusion surrounding
the definition of anaphylaxis and efforts to address this are

Mimi LK Tang MBBS PhD FRACP FRCPA is an Associate Professor and Director
of the Department of Allergy and Immunology, Royal Childrens
Hospital, Melbourne, Australia.

Adapted from Sampson et al.1 PEF, peak expiratory flow; BP, blood
ressure.
p
*Low systolic blood pressure for children is defined as: less than 70
mmHg from 1 month to 1 year; less than [70 mmHg + (Age x 2)] from 1
to 10 years, and less than 90 mmHg from 11 to 17 years.

Liew Woei Kang MBBS MRCPCH FAMS (Paediatrics) is a Clinical Fellow at the
Department of Allergy and Immunology, Royal Childrens Hospital,
Melbourne, Australia.

PAEDIATRICS AND CHILD HEALTH 18:7

Table 1

309

2008 Elsevier Ltd. All rights reserved.

Author's personal copy

Symposium: Allergy

c ontinuing exponential rise in the prevalence of food allergy and

anaphylaxis.4,5 Admissions to hospital for anaphylaxis, which
are likely to reflect more severe cases, demonstrate these recent
increases. In the UK, hospital admissions for anaphylaxis rose
seven-fold from 50 to 360 per 100,000 population in a period of
13 years from 1990/1 to 2003/4.4 Similarly, in Australia, admissions for anaphylaxis rose from 362 to 803 per 100,000 population in 11 years from 1993/4 to 2004/5.5 Anaphylaxis to foods in
children aged 04 years accounted for most of this rise.6
The population prevalence of anaphylaxis has been difficult to
quantify, largely due to a lack of universal consensus on the definition of anaphylaxis, and the use of varying methodologies and
sample populations. Published figures are likely to have underestimated the true prevalence. Recently proposed consensus definitions
for anaphylaxis will assist the acquisition of accurate prevalence
data.1 Previously published population studies7 have estimated
the prevalence of anaphylaxis to be 1030 per 100,000 population,
while the lifetime prevalence is estimated to be 0.052.0%.8 Anaphylaxis appears to be more common in young children with an
Australian survey of parent-reported allergy identifying that one in
170 children had experienced at least one episode of anaphylaxis.9
Food allergy is the most common cause of anaphylaxis in children. Two recent retrospective Australian paediatric emergency
department chart review revealed that food (5685%) was the principle allergen implicated.10,11 Of note, no cause was identified in
32% of cases and only 21% of cases had a reaction to a previously
known allergen.10 Less common causes included: medications,
insect stings, latex, immunotherapy-related reactions, exercise, cold
and idiopathic causes. This is in contrast to adults, in whom drugs
and insect venom are more common triggers.12 Consistent with this,
hospital admissions for food-induced anaphylaxis occurred predominantly in children aged 04 years, while admissions for non-food
causes of anaphylaxis occurred predominantly in adults 35 years
and the elderly, and to a lesser extent in 1534 year olds.6

Consistent risk factors for death from food-induced anaphylaxis identified from the reported UK and US15,18 series include:
active asthma (43/48 fatalities in the UK series required daily
treatment for asthma and a further three were known to avoid
steroids; in addition, 10/32 had varying degrees of asthma exacerbation leading up to the fatal reaction; all in the US series had
asthma although further details of severity or activity were not
available); age 1130 years (65% and 54% in the US and UK
series, respectively); peanut or tree nut allergy (81% and 38%
in the US and UK series, respectively); unavailability or delayed
use of adrenaline (87% and 81% in the US and UK series, respectively); and previous severe reactions (noted in 27% of cases in
UK series).15 Pumphrey determined that the incidence rate for
fatal anaphylaxis among 1524 year olds with nut allergy was
2.3 per 100,000, which is 10 times higher than the overall rate
of fatal anaphylaxis. In contrast, death in children less than 10
years of age is uncommon (13% and 15% in the US and UK
series, respectively).15,18 These findings emphasise the importance of optimal management of asthma, and particular caution
in adolescents/young adults with nut allergy.
Almost all patients in the US series had a previous history of
reaction to the food allergen, yet most were not aware that the
allergen was present within the food ingested.18 A total of 12 of
31 (39%) and 18 of 48 (38%) in the US and UK series, respectively, involved foods catered or prepared away from home,15,18
highlighting the difficulties in achieving strict avoidance particularly with commercially prepared foods.14 Carrying an adrenaline
auto-injector may not always prevent death. Seven of 48 cases in
the UK series and 4/31 cases in the US series died despite early
and repeated administration of adrenaline that was not expired,
suggesting that in some instances adrenaline may not be sufficient to prevent death. Furthermore, for deaths due to insect
stings or drugs, the fatal episode was the first reaction in most
cases,13 and in a recent UK series, over half the deaths occurred
in patients whose previous reaction had been mild, so that it was
unlikely that a doctor would have recommended that they carry
an adrenaline auto-injector pen and they would have been less
likely to be compliant with carrying one.15 Inadequate education and failure to use an adrenaline auto-injector even when
prescribed remains a feature, with 10 of 19 fatalities due to failing to carry or use the device correctly.15 In the UK series, most
subjects had not been referred to an allergist. Together, these
findings highlight that inadequate education and/or understanding of the principles of strict allergen avoidance, early recognition of allergic reactions and their appropriate management are
common features for anaphylaxis fatalities.

Fatal anaphylaxis
Fatalities are rare and estimated to occur in less than 2% of cases
of anaphylaxis, which equates to 13 per million population.7
National statistics for fatal anaphylaxis are available from the
UK where a prevalence of one death per year for each 3 million
population was reported.13 In Australia, between 1997 and 2004,
there were 106 deaths in which anaphylaxis or angioedema was
certified as the underlying or associated cause of death.6
Foods are the second most common cause of fatality from
anaphylaxis in the UK, with peanuts and tree nuts causing
almost half of these.12 A careful search for fatal cases of foodinduced anaphylaxis in the UK identified 48 deaths over a 7-year
period between 1999 and 2006.15 The frequency of deaths caused
by food-induced anaphylaxis in the United States is estimated
at 150 deaths per year.16 A voluntary US registry of fatal foodinduced anaphylaxis maintained by the American Academy of
Allergy Asthma and Immunology (AAAAI) and the Food Allergy
and Anaphylaxis Network (FAAN) recorded 32 cases of fatal
food-induced anaphylaxis between 1994 and 199917 and a further 31 cases between 2001 and 2006.18 Interestingly, the rate of
fatal food-induced anaphylaxis has remained stable over the past
decade in both the UK and the US, and does not appear to have
risen in line with the rising rates of food allergy or anaphylaxis.

PAEDIATRICS AND CHILD HEALTH 18:7

Management of anaphylaxis
The management of anaphylaxis may be considered to include:
treatment of the acute episode
long-term management comprising risk minimisation strategies to prevent future episodes and facilitate optimal treatment of a future episode.
Acute management
There are many published international guidelines for the emergency management of anaphylaxis.19 The evidence base for anaphylaxis management is limited to expert opinion or case series.
310

2008 Elsevier Ltd. All rights reserved.

Author's personal copy

Symposium: Allergy

All guidelines agree that adrenaline (0.01 mg/kg, maximum dose

0.5 mg, 1:1000 concentration, administered intramuscularly every
515 minutes as necessary) is the first-line treatment for anaphylaxis. Its effects include: increasing the peripheral vascular resistance; blood pressure and coronary artery perfusion; reducing
angioedema and urticaria (-adrenergic effects); increasing heart
rate and contraction (1-adrenergic effects); inducing bronchodilation and inhibiting release of inflammatory mediators (2adrenergic effects). Intramuscular administration into the lateral
thigh achieves higher and faster peak plasma concentration than
injection in the deltoid or subcutaneous administration.20 There
are no absolute contraindications to the use of adrenaline, but
patients with underlying cardiac disease may be at risk of tachyarrhythmia. There continues to be reluctance by patients with anaphylaxis to seek medical attention and for physicians to administer
adrenaline for severe symptoms. In a survey of FAAN conference
participants, only 35% of subjects with severe symptoms sought
medical attention and only 6% received pre-hospital adrenaline.
Even for repeat severe episodes, only 33% received pre-hospital
adrenaline, although 73% sought medical attention.21
In patients with severe hypotension refractory to intramuscular adrenaline and fluid support, intravenous adrenaline 0.1 g/
kg/min may be initiated (under the direction by intensive care
or emergency physicians as deaths have been associated with
this approach1). Administration of intravenous glucagon may be
of benefit if the patient is on -blockers. Glucagon is thought
to reverse refractory hypotension and bronchospasm by activating adenylate cyclase independent of the -receptors (children:
2030 g/kg, maximum 1 mg intravascularly over 5 minutes, followed by infusion 515 g/min, titrated to clinical response).

12 mg/kg/dose of methylprednisolone every 6 hours. Oral prednisolone 1 mg/kg, up to 50 mg may be used in milder episodes.
Observation: continued observation is essential after treatment
of an anaphylactic reaction, as the reaction might recur when the
effect of intramuscular adrenaline wears off, and because of the
risk of biphasic reactions. A biphasic reaction is reported to occur
in 120% of cases.24 There are no consistently reported risk
factors for biphasic reactions but delay in administration or inadequate dose of adrenaline given for the primary response, and
the omission of corticosteroids have been implicated. Review of
anaphylaxis admissions to the Royal Childrens Hospital in Melbourne over a 5-year period found a median time to biphasic
reaction of 6.5 hours (IQR 1.516 hours), and the requirement
of more than one dose of adrenaline or a fluid bolus for management of the presenting episode as risk factors for a biphasic
reaction.25 The observation period should be individualised on
the basis of severity of initial reaction, reliability of the patient
and access to care.1,24 As most second responses occur within 8
hours (range 178 hours) of the first event, an observation period
of 68 hours has been suggested for most patients, with more
prolonged observation (24-hour) in those with severe or refractory symptoms.
Discharge planning: all patients that have experienced an anaphylactic reaction should receive advice about trigger avoidance
(where identified) and a follow-up appointment with an allergist.
An adrenaline auto-injector should be prescribed as severe reactions are followed by a subsequent severe reaction in up to 71%
of subjects.26 Education in the early recognition and treatment
of allergic reactions and anaphylaxis, and training in the use of
the adrenaline auto-injector must also be provided, supported
by a personalised anaphylaxis action plan (See below: Risk
minimisation and prevention of anaphylaxis). Allergen-specific
immunotherapy is indicated in insect sting anaphylaxis as it can
prevent future reactions and improve quality of life.

Posture, airway and fluid support: there is consensus that

patients should be placed in a supine position (unless contraindicated by respiratory distress or vomiting)19 as a change to
an upright posture may have contributed to fatality in some
cases of anaphylaxis.22 Intravenous fluid resuscitation (20 ml/
kg) for cardiovascular involvement is important. Airway support
and oxygen should be administered for respiratory distress. An
inhaled 2-agonist (e.g. salbutamol or adrenaline) may be a useful adjunct to relieve airway bronchospasm but intramuscular
adrenaline must still be considered as the first-line therapy.

Risk minimisation and prevention of anaphylaxis: long-term

management
The fundamental basis of long-term management is risk minimisation. This is achieved through:
prevention of future episodes
education of patients and their carers in the early recognition
and treatment of allergic reactions
management of co-morbidities that increase the risks associated with anaphylaxis.
The risk of a child with specific allergy (food, insect sting, latex)
having an anaphylactic reaction is difficult to quantify. Risk minimisation strategies should be implemented for all children with
specific allergy. These strategies may, but do not necessarily,
include the provision of an adrenaline-auto-injector.

Antihistamine and corticosteroid: there is lack of agreement in

international guidelines on the use of antihistamines and corticosteroids for the treatment of acute anaphylaxis.19 Antihistamines
are effective in relieving cutaneous symptoms of pruritus and
urticaria. However, there is no evidence of their efficacy in relieving respiratory and gastrointestinal symptoms or shock. A recent
Cochrane meta-analysis found insufficient evidence to support
their use for the treatment of anaphylaxis.23 Furthermore, the
use of first generation sedating antihistamines may cause drowsiness, thus complicating the early identification of anaphylaxis,
and should be avoided. The use of corticosteroids in anaphylaxis
is largely empirical and extrapolated from their use in other allergic conditions (e.g. asthma) for prevention of the delayed phase
of reaction. It has been suggested that their use might prevent a
protracted or biphasic reaction. As the onset of action is slow,
steroids are not useful in the acute management stage. If given,
the dose of intravenous corticosteroid should be equivalent to

PAEDIATRICS AND CHILD HEALTH 18:7

Prevention of future episodes: Trigger avoidance when there

has been a previous allergic reaction and the trigger has been
identified, strict avoidance offers one approach to prevention of
anaphylaxis. Avoidance of medications and latex can generally
be successfully achieved; however, avoidance of food allergens
is more difficult. Accidental exposures to hidden food allergens, especially in commercially prepared food, are common
311

2008 Elsevier Ltd. All rights reserved.

Author's personal copy

Symposium: Allergy

and account for most anaphylaxis fatalities due to peanut and

tree nut allergy.14 Furthermore, almost 80% of patients who
presented to the Emergency Department for anaphylaxis did not
have a previous reaction to the suspected allergen.10 Allergen
avoidance is, therefore, only partially effective as a prevention
strategy for anaphylaxis.
In educating patients and/or parents regarding avoidance of
food allergens, information should be provided on the different
terms that can be used to describe the relevant allergen, and on
how to read food labels to detect hidden allergens. Food labelling laws in many countries have implemented the use of simplified terminology to assist in the identification of hidden food
allergens, although imported goods may still be problematic. For
example, in Australia, the EU and US, it is now legislated that
common food allergens must be listed on the ingredients list if
any of the ingredients are derived from common allergens. May
contain traces of warnings have caused confusion. Currently,
there is no legal requirement for food manufacturers to provide
this declaration. Therefore, a food that does not bear this warning label is just as likely to contain the allergen as a food that
does. Improved labelling laws that require declaration of the true
risk of contamination with allergen may help to resolve these
difficulties. For example, statements such as this food has been
produced on the same line as foods containing peanut, or no
peanut products are manufactured on this line would allow a
person to make an informed decision regarding the likely risk for
contamination with peanut. Interestingly, however, patients and
families appear less likely to heed these more specific declarations than a may contain traces of declaration so educational
support would be required.27 Special attention should be paid
to avoidance strategies at school, day-care, friends homes and
restaurants. It should be emphasised that the patient should not
take a food if its ingredients cannot be verified.
Immunotherapy allergen-specific immunotherapy can
reduce the risk of anaphylaxis but is currently limited to insect
sting anaphylaxis. Other immune-modulatory therapies being
explored include anti-IgE therapy, recombinant food proteins,
peptide immunotherapy, oral immunotherapy, sublingual immunotherapy and Chinese herb FAHF-2.

prior to the arrival of an ambulance and is anticipated to prevent

death as delayed administration of adrenaline is reported to be a
risk factor for fatality. It may, therefore, be suggested that among
children with food allergy, those who would benefit from carrying an adrenaline auto-injector are those who will later experience an anaphylaxis reaction. However, most children with food
allergy will not experience an anaphylaxis reaction; 810% of
children have a food allergy, while 0.5% of children are reported
to have experienced an anaphylaxis reaction.9 How then might
we identify those who are at increased risk of anaphylaxis?
Subsequent reactions following a previous severe reaction
(anaphylaxis) are reported to be similarly severe in up to 70% of
subjects.26 A history of an anaphylaxis reaction, therefore, represents a logical indication for the provision of an adrenaline autoinjector. Nevertheless, 2045% of mild allergic reactions may be
followed by a severe reaction,26,29 so additional indicators are
required to identify those at increased risk for anaphylaxis where
there is no previous history of anaphylaxis. The presence of coexisting asthma is associated with more severe allergic reactions
to foods, providing another predictor for anaphylaxis, although
the specificity is poor since food allergy and asthma frequently coexist.30 Risk factors for fatal anaphylaxis have been used to guide
indications for adrenaline auto-injectors in cases where there is
no history of anaphylaxis. These include the presence of active
asthma, being an adolescent or young adult, having peanut or
tree nut allergy, and distance from medical assistance. Caveats to
basing the provision of adrenaline auto-injectors on the presence
of risk factors for fatal anaphylaxis are that risk factors for death
may be different to those for the development of anaphylaxis per
se, and they have poor specificity since most food allergic children have one or more of these risk factors whereas a minority of
children with food allergy will have anaphylaxis. Nevertheless,
in the absence of more accurate clinical and/or laboratory markers for the identification of those individuals who are at risk of
severe or fatal allergic reactions, these risk factors offer a practical approach to assist in the decision of whether to prescribe an
adrenaline auto-injector for children with food allergy.
Such an approach has been adopted in Australia with the
development of national prescribing guidelines for the EpiPen,
and a similar approach has been recommended in the EU and
discussed in the UK (Table 2).31,32 Absolute indications for a selfinjectable adrenaline device include: previous cardiovascular or
respiratory reaction (anaphylaxis) to a food, insect sting, latex or
exercise, and idiopathic anaphylaxis. Relative indications include
a history of a previous systemic reaction (non-anaphylactic)
and one or more of the following risk factors: poorly controlled
asthma; adolescent or young adult; peanut or tree nut allergy;
and remoteness of home from medical facilities.32 The Australian
prescribing guidelines also suggest that an adrenaline auto-injector would not normally be recommended for a positive skin test
or RAST test in the absence of clinical reaction, or for localised
allergic reactions and mild systemic reactions in the absence of
the preceding risk factors (Table 2).
It remains controversial whether two devices or a device with
two doses should be provided to cater for the potential requirement of a second dose of adrenaline. A study of food-induced
anaphylaxis occurring in the community found that 10% of
children and 25% of adults (overall 18%) received a second
dose of adrenaline.33 Similarly, 21% of adults presenting to an

Risk minimisation: Adrenaline auto-injectors several selfinjectable adrenaline devices containing a fixed dose of either
0.3 mg or 0.15 mg adrenaline are available in many countries.
A device containing two doses has recently become available in
the US (Twinject). While there is no self-injectable adrenaline
device for infants under 15 kg body weight, mild overdosing in
otherwise healthy children appears safe.28
An adrenaline auto-injector should be considered where
there is ongoing risk for anaphylaxis and also exposure to a trigger. Most experts agree that an adrenaline auto-injector is not
required for anaphylaxis due to medications since avoidance
should be possible. In the case of food allergy, the issue of who
should carry an adrenaline auto-injector is more controversial.
Some experts would suggest that all children with proven food
allergy should carry such a device, while others would recommend more limited provision. In considering the merits of either
approach, it is helpful to consider what benefit may be conferred
by having this device. The availability of an adrenaline autoinjector allows early treatment of anaphylaxis in the community

PAEDIATRICS AND CHILD HEALTH 18:7

312

2008 Elsevier Ltd. All rights reserved.

Author's personal copy

Symposium: Allergy

EpiPen prescribing guidelines

Indications for prescribing
self-injectable adrenaline

Australia

European Union

Recommended:

Previous anaphylaxis to food, latex, insect sting or

exercise and idiopathic anaphylaxis (if the patient is
considered to be at continuing risk)

Previous cardiovascular or respiratory reaction

to a food, insect sting or latex
Exercise-induced anaphylaxis

Idiopathic anaphylaxis

Child with food allergy and co-existent

persistent asthma

May be recommended:

History of a previous systemic (non-anaphylactic)

reaction and one or more of the following risk factors:

Any reaction to small amounts of a food (e.g.

airborne food allergen or contact only via skin)
History of only a previous mild reaction to

peanut or a tree nut

Food allergic reaction in a teenager

Home remote from medical facilities

poorly-controlled asthma

adolescent or young adult

peanut or tree nut allergy

remoteness of home from medical facilities

Not normally recommended:

Asthma patients without anaphylaxis or generalised

allergic reactions
Positive skin test or RAST test in the absence of

clinical reaction
Family (rather than personal) history of anaphylaxis

Local reactions or generalised skin rash (only) to

insect stings in children

Resolved food allergy

Table 2

EpiPen.38 Paediatricians in a major teaching hospital also had

poor ability to demonstrate the use of an EpiPen and only 37%
would have successfully administered adrenaline to a subject.39
It is considered that education and training will improve physician knowledge and patient/carer willingness to carry and use
an adrenaline auto-injector device.35 A recent study reported
that empowerment is the most significant factor associated with
increased parent comfort in using the EpiPen.40
Adolescents represent a particularly important cohort for education. A total of 2.3% of teenagers have food allergy,41 yet they
account for more than half of deaths from food anaphylaxis.15,18
Adolescents tend to have minimal parental supervision, and are
known to engage in risk-taking behaviours as part of their journey towards independence. Adolescents list social isolation as
the most difficult aspect of living with food allergy and 62% had
been teased about their condition, which may promote risk taking.41 In a study exploring risk taking and coping strategies in
adolescents and young adults with food allergy, 71% were found
to have had anaphylaxis; of these 37% had not received epineph
rine, and 38% did not have their adrenaline auto-injectors
with them although 89% stated they carried their device with
them most or all of the time.41 There was limited awareness of
at risk situations (e.g. parties, eating out, sport). Risk taking
was common with 54% eating foods known to contain allergen
and 17% doing this several times a month or more and 44%
a few times a year. Specific attention to education of teenagers
and their peers is required to support this at risk population in
implementing prevention and risk minimisation strategies. For
younger children, specific training of staff in schools and day-care

mergency Department with food-induced anaphylaxis required

E
a second dose of adrenaline.34
Anaphylaxis education whether or not an adrenaline autoinjector is prescribed, appropriate training of at-risk individuals
and their families in the early recognition and first aid treatment
of anaphylaxis is an essential aspect of prevention and risk minimisation. Education is an ongoing process and needs regular
reinforcement. Important concepts include the definition of anaphylaxis, the rationale for and approach to strict allergen avoidance, early recognition of a mild or moderate allergic reaction
and of anaphylaxis, and what to do in the event of an allergic
reaction or anaphylaxis. Education is supported by the provision
of the anaphylaxis action plan. If an adrenaline auto-injector
has been prescribed, this must be accompanied by additional
hands-on training in the use of the device. There is continued
reluctance for patients/carers and physicians to use and prescribe adrenaline auto-injectors. Knowledge in the management
of anaphylaxis also remains inadequate for both groups.35 Only
38% of subjects with anaphylaxis sought medical attention and
of these only 31% were provided with EpiPen prescriptions (75%
of subjects with repeat anaphylaxis sought medical attention, but
only 33% received an EpiPen).21 Even with education strategies
in place from a specialist allergy clinic, 30% of parents do not
always carry the EpiPen and 40% have concerns regarding its
use in an emergency situation.36 Parents of children who have
been provided with an adrenaline auto-injector are deficient in
their knowledge of the symptoms of anaphylaxis, as well as the
use of the device, using it in only 29% of recurrent anaphylactic
reactions.37 A total of 69% of parents report problems using the

PAEDIATRICS AND CHILD HEALTH 18:7

313

2008 Elsevier Ltd. All rights reserved.

Author's personal copy

Symposium: Allergy

centres/kindergartens should be provided since children spend a

significant amount of time in these settings. Public health policy
may be developed to support this, and training of staff in schools
and day-cares is now legislated and funded by the Government
in some states of Australia. Educational efforts directed to restaurants and food manufacturers are essential but currently lacking.
Personalised anaphylaxis emergency action plan anaphylaxis education should be supported by the provision of a personalised anaphylaxis action plan. Although the evidence for their
benefit is limited to case studies, they are thought to promote
patient empowerment and improve health outcomes.42 Various
anaphylaxis action plans are available (e.g. www.allergy.org.
au, www.allergyuk.org, www.aaaai.org). The use of a personalised anaphylaxis action plan is essential for anyone carrying
an adrenaline auto-injector. These plans assist the parent/patient
in management of anaphylaxis episodes in the community setting by clearly describing symptoms of an allergic reaction/anaphylaxis and the appropriate actions to take in the event of an
allergic or anaphylactic reaction. They often contain illustrated
instructions on the use of adrenaline auto-injectors. A similar

action plan should also be provided to any child with confirmed

diagnosis of food allergy or insect sting allergy who does not
carry an adrenaline auto-injector (a sample plan is shown in
Figure 1). These plans would not include instructions for use of
an adrenaline auto-injector but would nevertheless outline the
symptoms and signs of an allergic reaction or anaphylaxis and
the appropriate action to be taken in the event of a reaction.
Management of co-morbidities: most anaphylaxis fatalities
have been associated with active asthma that is suboptimally
controlled. Therefore, regular assessment of asthma should be
performed and disease control optimised. Patients requiring
beta-blockers should be considered for alternative medications,
as adrenergic blockade may interfere with the action of adrenaline when administered.

Conclusions
Anaphylaxis is emerging as a significant public health concern
in Western societies. Long-term management centres on risk

Action plan for Allergic Reactions

Name
Date of Birth

Mild to moderate allergic reaction

Photo

Tingling in the mouth

Swelling in the lips, face, eyes
Hives or welts
Abdominal pain, vomiting or diarrhoea
Action

Known allergies

Stay with the child and monitor closely

Give antihistamine
Call parents/emergency contact
Watch for signs of severe reaction

Patient emergency contact:

1. Name
Ph: No 1
Ph: No 2
2. Name
Ph: No 1
Ph: No 2
Plan prepared by:
Dr
Signed
Date

Severe allergic reaction

Difficulty/noisy breathing
Swelling of tongue
Swelling/tightness in throat
Difficulty talking and/or hoarse voice
Wheeze or persistent cough
Loss of consciousness and/or collapse
Pale and floppy (young children)
Action
Phone ambulance
Contact parent/carer

Figure 1 Sample personalised allergic reaction action plan.

PAEDIATRICS AND CHILD HEALTH 18:7

314

2008 Elsevier Ltd. All rights reserved.

Author's personal copy

Symposium: Allergy

inimisation and prevention of future episodes. All children with

m
a defined allergy (e.g. food, insect sting, medication, latex) and
their parents should be provided with advice on allergen avoidance. An individualised action plan, and education on the early
recognition of allergic reactions and their management should
also be provided. The decision as to who should be provided
with an adrenaline auto-injector remains controversial. As most
allergic reactions to foods are not anaphylactic, it is suggested
that not all children with food allergy require a personal adrenaline auto-injector. Instead, adrenaline auto-injectors could be
selectively provided to children identified as being at increased
risk of anaphylaxis using identified risk factors for anaphylactic
reactions and fatal anaphylaxis. A previous anaphylactic reaction is a clear risk factor for future anaphylaxis episodes and
represents a definite indication for provision of an adrenaline
auto-injector where it is not possible to avoid the allergen trigger
(e.g. food allergy, insect sting). Where there is a history of systemic allergic reaction without anaphylaxis, risk factors for fatal
anaphylaxis may be used to determine the need for an adrenaline auto-injector poorly controlled asthma, adolescents and
young adults, peanut or tree nut allergy, or remote location. This
tailored approach to the provision of adrenaline auto-injectors
has been recommended in the EU and Australia. Importantly,
children with food, insect venom or other specific allergy who
remain at risk for anaphylaxis and have not been provided with
an adrenaline auto-injector should nevertheless receive education and advice on allergen avoidance, a detailed action plan
that outlines the symptoms and signs of allergic reactions and
their appropriate management, as well as education on the early
recognition of allergic reactions and their management.

10 Braganza SC, Acworth JP, McKinnon DR, et al. Paediatric emergency

department anaphylaxis: different patterns from adults. Arch Dis
Child 2006; 91: 15963.
11 De Silva I, Mehr S, Tey D, Tang MLK. Paediatric anaphylaxis: a 5 year
retrospective review. Allergy, in press.
12 Brown SG, Mullins RJ, Gold MS. Anaphylaxis: diagnosis and
management. Med J Aust 2006; 185: 2839.
13 Pumphrey RS. Fatal anaphylaxis in the UK, 19922001. Novartis
Found Symp 2004; 257: 11628 [discussion: 12832, 15760,
27685].
14 Pumphrey RS. Anaphylaxis: can we tell who is at risk of a fatal
reaction? Curr Opin Allergy Clin Immunol 2004; 4: 28590.
15 Pumphrey RS, Gowland MH. Further fatal allergic reactions to food
in the United Kingdom, 19992006. J Allergy Clin Immunol 2007;
119: 10189.
16 Sampson HA. Anaphylaxis and emergency treatment. Pediatrics
2003; 111: 16018.
17 Bock SA, Munoz-Furlong A, Sampson HA. Fatalities due to
anaphylactic reactions to foods. J Allergy Clin Immunol 2001; 107:
1913.
18 Bock SA, Munoz-Furlong A, Sampson HA. Further fatalities caused by
anaphylactic reactions to food, 20012006. J Allergy Clin Immunol
2007; 119: 10168.
19 Alrasbi M, Sheikh A. Comparison of international guidelines for the
emergency medical management of anaphylaxis. Allergy 2007; 62:
83841.
20 Simons FE. First-aid treatment of anaphylaxis to food: focus on
epinephrine. J Allergy Clin Immunol 2004; 113: 83744.
21 Simons ECW, Muoz-Furlong A, Furlong TJ, Sicherer SH.
Management of food-induced anaphylaxis by caregivers and medical
professionals: a survey. J Allergy Clin Immunol 2006; 117(suppl 1):
S1345.
22 Pumphrey RS. Fatal posture in anaphylactic shock. J Allergy Clin
Immunol 2003; 112: 4512.
23 Sheikh A, Ten Broek V, Brown SG, et al. H1-antihistamines for the
treatment of anaphylaxis: cochrane systematic review. Allergy 2007;
62: 8307.
24 Tole JW, Lieberman P. Biphasic anaphylaxis: review of incidence,
clinical predictors, and observation recommendations. Immunol
Allergy Clin North Am 2007; 27: 30926 viii.
25 Tang M. Anaphylaxis in childhoodrisk factors for biphasic reactions.
J Allergy Clin Immunol 2005; 115: S137.
26 Vander Leek TK, Liu AH, Stefanski K, et al. The natural history of
peanut allergy in young children and its association with serum
peanut-specific IgE. J Pediatr 2000; 137: 74955.
27 Hefle SL, Furlong TJ, Niemann L, et al. Consumer attitudes and risks
associated with packaged foods having advisory labeling regarding
the presence of peanuts. J Allergy Clin Immunol 2007; 120: 1716.
28 Simons FE, Gu X, Silver NA, et al. EpiPen Jr versus EpiPen in young
children weighing 15 to 30 kg at risk for anaphylaxis. J Allergy Clin
Immunol 2002; 109: 1715.
29 Ewan PW, Clark AT. Long-term prospective observational study
of patients with peanut and nut allergy after participation in a
management plan. Lancet 2001; 357: 1115.
30 Roberts G, Lack G. Food allergy and asthma what is the link?
Paediatr Respir Rev 2003; 4: 20512.
31 McLean-Tooke AP, Bethune CA, Fay AC, et al. Adrenaline in the
treatment of anaphylaxis: what is the evidence? BMJ 2003; 327:
13325.

References
1 Portier P, Richet C. De laction anaphylactique de certains venins.
C R Sances Mem Soc Biol Paris 1902; 54: 170.
2 Sampson HA, Munoz-Furlong A, Campbell RL, et al. Second
symposium on the definition and management of anaphylaxis:
summary reportsecond National Institute of Allergy and Infectious
Disease/Food Allergy and Anaphylaxis Network symposium. J Allergy
Clin Immunol 2006; 117: 3917.
3 Asher MI, Montefort S, Bjorksten B, et al. Worldwide time trends in
the prevalence of symptoms of asthma, allergic rhinoconjunctivitis,
and eczema in childhood: ISAAC Phases One and Three repeat
multicountry cross-sectional surveys. Lancet 2006; 368: 73343.
4 Gupta R, Sheikh A, Strachan DP, et al. Time trends in allergic
disorders in the UK. Thorax 2007; 62: 916.
5 Mullins RJ. Paediatric food allergy trends in a community-based
specialist allergy practice, 19952006. Med J Aust 2007; 186: 61821.
6 Poulos LM, Waters AM, Correll PK, et al. Trends in hospitalizations
for anaphylaxis, angioedema, and urticaria in Australia, 19931994
to 20042005. J Allergy Clin Immunol 2007; 120: 87884.
7 Moneret-Vautrin DA, Morisset M, Flabbee J, et al. Epidemiology of
life-threatening and lethal anaphylaxis: a review. Allergy 2005; 60:
44351.
8 Clark S, Camargo Jr. CA. Epidemiology of anaphylaxis. Immunol
Allergy Clin North Am 2007; 27: 14563.
9 Boros CA, Kay D, Gold MS. Parent reported allergy and anaphylaxis
in 4173 South Australian children. J Paediatr Child Health 2000; 36:
3640.

PAEDIATRICS AND CHILD HEALTH 18:7

315

2008 Elsevier Ltd. All rights reserved.

Author's personal copy

Symposium: Allergy

32 Muraro A, Roberts G, Clark A, et al. The management of anaphylaxis

in childhood: position paper of the European academy of
allergology and clinical immunology. Allergy 2007; 62: 85771.
33 Uguz A, Lack G, Pumphrey R, et al. Allergic reactions in the
community: a questionnaire survey of members of the anaphylaxis
campaign. Clin Exp Allergy 2005; 35: 74650.
34 Oren E, Banerji A, Clark S, et al. Food-induced anaphylaxis and
repeated epinephrine treatments. Ann Allergy Asthma Immunol
2007; 99: 42932.
35 Simons FE. Anaphylaxis, killer allergy: long-term management in the
community. J Allergy Clin Immunol 2006; 117: 36777.
36 Hu W, Grbich C, Kemp A. Parental food allergy information needs: a
qualitative study. Arch Dis Child 2007; 92: 7715.
37 Gold MS, Sainsbury R. First aid anaphylaxis management in children
who were prescribed an epinephrine auto-injector device (EpiPen).
J Allergy Clin Immunol 2000; 106: 1716.
38 Arkwright PD, Farragher AJ. Factors determining the ability of parents
to effectively administer intramuscular adrenaline to food allergic
children. Pediatr Allergy Immunol 2006; 17: 2279.
39 Mehr S, Robinson M, Tang M. Doctor how do I use my EpiPen?
Pediatr Allergy Immunol 2007; 18: 44852.
40 Kim JS, Sinacore JM, Pongracic JA. Parental use of EpiPen for children
with food allergies. J Allergy Clin Immunol 2005; 116: 1648.
41 Sampson MA, Munoz-Furlong A, Sicherer SH. Risk-taking and coping
strategies of adolescents and young adults with food allergy.
J Allergy Clin Immunol 2006; 117: 14405.
42 Choo K, Sheikh A. Action plans for the long-term management of
anaphylaxis: systematic review of effectiveness. Clin Exp Allergy
2007; 37: 10904.

Adolescents and young adults represent a high-risk group and

account for more than half of deaths from food anaphylaxis
Risk factors for fatal anaphylaxis include: active asthma;
being an adolescent/young adult; nut allergy; delayed
administration of adrenaline
Intramuscular adrenaline remains the cornerstone of
treatment for the acute episode. Maintaining a supine
posture, oxygen and fluid support are important adjunct
measures
Long-term management centres on risk minimisation through:
prevention of repeat episodes by avoidance of
identified triggers
education of patients/parents in the early recognition
and emergency treatment of allergic reactions, supported
by provision of a personalised anaphylaxis action plan
optimal management of co-morbidities especially asthma
Avoidance of food triggers may be difficult accidental
exposures commonly occur, particularly if food is prepared
outside the home
An adrenaline auto-injector should be provided where
there is ongoing risk of anaphylaxis and also exposure to a
trigger. Current practice is varied. One suggested approach
is to assess the risk for future anaphylaxis based upon the
severity of previous reactions and presence of risk factors for
fatal anaphylaxis
An adrenaline auto-injector is indicated if there is a history of
previous anaphylaxis to a food, insect sting, latex or exercise,
and for idiopathic anaphylaxis
An adrenaline auto-injector may be considered if there is a
history of systemic allergic reaction without anaphylaxis AND if
one or more of the following risk factors for fatal anaphylaxis
are identified: poorly controlled asthma; adolescent/young
adult; peanut or tree nut allergy; remote location
The need for adrenaline auto-injectors should be re-assessed
at regular intervals since food allergy may resolve or risk
factors for fatal anaphylaxis may develop

Practice points
Anaphylaxis is a severe systemic allergic reaction that
involves the respiratory and/or cardiovascular system
Food allergy is the most common cause of anaphylaxis in
children

PAEDIATRICS AND CHILD HEALTH 18:7

316

2008 Elsevier Ltd. All rights reserved.