Food and drug reactions and anaphylaxis
Emergency department anaphylaxis:
A review of 142 patients in a single year
Anthony F. T. Brown, MB ChB, FRCP, FRCS(Ed), FACEM, FFAEM,
David McKinnon, MB BS, and Kevin Chu, MB BS, MS, FACEM Brisbane, Australia
Background: There are few data on the incidence, clinical fea-
tures, and management of patients with acute anaphylaxis pre-
senting to the emergency department. We investigated all pre-
sentations to one department during the course of a year to
improve current awareness of this medical emergency.
Objective: The purpose of the study was to describe the clini-
cal features, management, and outcome of anaphylaxis presen-
tations to a single Australian adult emergency department in a
single year, 1998-1999.
Methods: This was a retrospective, case-based study of adult
patients (≥13 years of age) attending a single emergency
department in Brisbane, Australia, during the year 1998-1999.
The medical records of 304 patients satisfying the relevant dis-
charge diagnostic codes were studied. We determined inci-
dence, sex ratio, age, clinical features, management, disposal,
asthma prevalence, and causes in patients presenting with
acute allergic reactions and anaphylaxis.
Results: In all, 162 emergency department patients with acute
allergic reactions and 142 emergency department patients with
anaphylaxis, including 60 whose anaphylaxis was severe, were
seen during the year, for an anaphylaxis presentation incidence
of 1 in 439. One patient died; this gave a case fatality rate of
0.70%. Cutaneous features were present in 94% of the patients
with anaphylaxis. Of those with severe anaphylaxis, 35% had
dizziness/syncope before hospital presentation, 25% laryngeal
edema, and 21.7% systolic hypotension on hospital presenta-
tion. A cause was recognized in 73% of the anaphylaxis cases;
most commonly, the causative agent was a drug, insect venom,
or food. Adrenaline was used in 57% of the severe cases before
hospital presentation or in the hospital. The emergency depart-
ment alone definitively cared for 94% of all patients, though
only 43% severe anaphylaxis cases were referred for follow-up.
Conclusion: The emergency department anaphylaxis presentation
incidence of 1 in 439 cases is greater than previously recognized,
though death remains rare. In three fourths of cases, a precipitant
was identified, a fact that emphasizes the need for a detailed ini-
tial history. Definitive management in the emergency department
alone is possible in most cases, provided that the appropriate use
of adrenaline and the need for allergy clinic follow-up are appre-
ciated. (J Allergy Clin Immunol 2001;108:861-6.)
From the Department of Emergency Medicine, Royal Brisbane Hospital.
Received for publication February 1, 2001; revised July 20, 2001; accepted
for publication July 24, 2001.
Reprint requests: Assoc. Prof. Anthony F. T. Brown, Department of Emer-
gency Medicine, Royal Brisbane Hospital, Brisbane, QLD, 4029, Aus-
tralia.
Copyright © 2001 by Mosby, Inc.
0091-6749/2001 $35.00 + 0 1/87/119028
doi:10.1067/mai.2001.119028
Key words: Angioedema, anaphylaxis, epinephrine (adrenaline),
histamine H1 antagonists (antihistamines), histamine h2 antago-
nists, immediate hypersensitivity, urticaria
The term anaphylaxis was introduced in 1902 by
Portier and Richet.1 Although the etiologic distinction
between immune-mediated anaphylactic reactions and
nonimmune anaphylactoid ones is important,2 the label is
now commonly used to describe both of these clinical
syndromes.3 There are remarkably few data on the inci-
dence of this potentially fatal condition, which appears to
be increasing,4,5 despite likely under-reporting by both
physicians and patients alike.6
Existing data on anaphylaxis come from a wide vari-
ety of patient categories, including the general popula-
tion,6 emergency department (ED) visits,5,7,8 hospital
admissions,4,9 and specialist allergy/immunology clin-
ics,10 as well as from selected groups, such as anaphy-
laxis during anesthesia,11,12 drug-related anaphylax-
is,13,14 food-related anaphylaxis,15,16 and anaphylaxis
associated with hymenopteran stings.17,18 These het-
erogenous data are difficult to interpret inasmuch as there
is no universally accepted clinical definition of anaphy-
laxis. An author might use a grading system from I to
IV,19 might require 1 feature of generalized mediator
release with at least 1 additional feature from multisys-
tem involvement,6 or might reserve the term anaphylaxis
for severe systemic allergic reactions with either
hypotension or marked respiratory difficulty.5 Alterna-
tively, a temporal basis is used7 or a constellation of
symptoms and signs is given with no precise specifica-
tions of which symptoms and signs should be present, to
what degree these should be present, or in which combi-
nation they should be present.4,10,20-22
Accordingly, the purpose of our study was to add to
the literature a clearly defined description of the epi-
demiologic character, clinical features, and management
of a large group of acute, undifferentiated patients pre-
senting with clinical anaphylaxis to a single adult ED.
METHODS
A retrospective, case-based, adult study was performed on all
patients presenting to a single emergency department (ED) during 1
year, from July 1, 1998, to June 30, 1999, with final ED Interna-
tional Classification of Diseases–9th revision–Clinical Modification
(ICD-9-CM) discharge diagnostic codes under the following 4
major headings: allergy/allergic reaction; anaphylactic shock or
reaction; angioedema; and urticaria.23 The facility, designed for the
861
862 Brown, McKinnon, and Chu
Abbreviations used
ACE: Angiotensin-converting enzyme
ED: Emergency department
ICD-9-CM: International Classification of Diseases–9th
revision–Clinical Modification
IM: Intramuscular(ly)
IV: Intravenous(ly)
LMO: Local medical officer
treatment of adults, was a tertiary referral university-affiliated
teaching hospital in the northern suburbs of Brisbane, a semitropi-
cal state capital city with a population of 1.3 million on the east
coast of Australia. This hospital, which directly serves a local pop-
ulation of 485,000, recorded a total of 62,361 ED attendances from
all causes in patients aged 13 years and older during the study peri-
od. Children were not included, inasmuch as they are seen at a near-
by pediatric hospital.
The department is staffed 24 hours per day (1) by 8 training ED
registrars (postgraduate years 4 to 9) who are supervised 16 hours per
day by 7 attending ED specialists (available for immediate callback)
and (2) by 4 teams of 5 residents (postgraduate years 1 to 3). It is rep-
resentative of most major urban Australasian EDs but has considerably
higher senior staff levels than equivalent departments in the United
Kingdom. Each of the patients was presenting for the first time and
was either self-referred or referred by a local medical officer (LMO).
None of the cases was an interhospital transfer for tertiary care. The
study was approved by the Royal Brisbane Hospital Executive. Formal
institutional review board assessment was waived by the Executive in
view of the study’s retrospective and observational nature.
ICD-9-CM codes
The 4 major ICD-9-CM diagnostic categories included 23 rele-
vant subheading codings. Because several codings appeared in more
than 1 subheading list, a total of 16 ICD-9-CM discharge codes
were included in our study (Table I).
Exclusions
All patient notes with relevant ICD-9-CM discharge codes were
reviewed in detail by a single, trained data abstractor (D.M.). Thir-
teen patient charts had insufficient documentation for an allergic or
anaphylactic reaction to be clearly defined, and 37 patient charts
were missing or unavailable on multiple callings. This left a total of
304 patient presentations that formed the study population seen in
the single year.
Definitions
The 304 patient presentations were divided into 2 groups:
patients with acute allergic reactions confined to cutaneous symp-
toms alone were separated from those considered to have anaphy-
laxis, according to the following definitions:
1. Acute allergic reaction. Patients with evidence of generalized
mediator release restricted to cutaneous findings alone, such
as generalized rash, pruritus, rhinitis/conjunctivitis, urticaria,
local edema, and angioedema without any other systemic
symptoms or signs.
2a. Mild to moderate anaphylaxis. Patients with any of the findings
listed for acute allergic reaction with additional respiratory,
cardiovascular, gastrointestinal, or neurologic features or pre-
senting with any of these additional features alone in the set-
ting of an allergic reaction. The additional features included a
history of shortness of breath or dyspnea, wheeze, hoarseness,
and nausea or vomiting. Physical findings recorded on arrival
J ALLERGY CLIN IMMUNOL
NOVEMBER 2001
in the ED or within 30 minutes of arrival included the presence
of bronchospasm, systolic blood pressure >90 mmHg, respira-
tory rate <25/min, and a normal Glasgow Coma Scale score.
2b. Severe anaphylaxis. Patients with any of the findings listed for
mild to moderate anaphylaxis but with potentially life-threat-
ening symptoms or signs. These included any one or more of
the following: history of loss of consciousness, syncope, or
dizziness or light-headedness at any time; systolic blood pres-
sure on arrival in the ED or within 30 minutes of arrival of <90
mmHg; a Glasgow Coma Scale score on arrival or within 30
minutes of arrival of <15, related to cardiovascular system col-
lapse and/or neurologic dysfunction from hypoperfusion,
hypoxia, and the direct effect of mediators. Also included
were patients with any 1 or more of the following: history of
shortness of breath, wheeze, hoarseness or bronchospasm plus
any 1 or more of stridor, cyanosis, laryngeal edema or a respi-
ratory rate ≥25/min on ED arrival or within 30 minutes from
respiratory system dysfunction.
Further data abstracted for each group included the causative
agent (if known), previous history of asthma or allergy to the
causative agent, treatment before hospital presentation, treatment in
the hospital, discharge treatment, and information on whether dis-
charge advice was given. Descriptive statistics were calculated;
results are expressed either as means ± SDs and ranges or as per-
centages. ANOVA was used to compare continuous variables
between multiple groups. SAS 6.12 statistical software (SAS Insti-
tute, Inc, Cary, NC) was used to perform the analysis.
RESULTS
There were 162 patients with acute allergic reactions
and 142 patients with anaphylaxis. The mean age was 35.3
years (SD, 15.6; range, 14-88 years) for the patients with
acute allergic reactions and 37.3 years (SD, 15.8; range,
14-86 years) for the patients with anaphylaxis. Females
outnumbered males by a ratio of 3:2 in both groups.
Sixty patients had severe, potentially life-threatening
anaphylaxis. Their mean age was 39.7 years (SD, 16.7;
range 14-86 years), but this was not statistically different
from the mean age of 35.6 years (SD, 14.9; range 14-85
years) for the 82 patients with mild to moderate anaphy-
laxis or from the mean age in the acute allergic reaction
group (P = .16).
Clinical features
The clinical features of the 162 patients with acute
allergic reactions and the 142 patients with anaphylaxis
are presented in Table II. Seven patients had mild to mod-
erate anaphylaxis without cutaneous features, and all but
2 of the patients with severe anaphylaxis (96.6%) had
cutaneous features. Overall, 133 (94%) of the 142
patients with anaphylaxis had cutaneous features.
The additional respiratory, cardiovascular, gastroin-
testinal, and neurologic features in the patients with ana-
phylaxis are shown in Table III. One 60-year-old man
who collapsed after a bee sting arrived in electromechan-
ical dissociation and died.
Causative agents
The causative agent was known in 57% of the patients
with acute allergic reactions and 73.0% of the patients
with anaphylaxis. The most common category of causes
J ALLERGY CLIN IMMUNOL Brown, McKinnon, and Chu 863
VOLUME 108, NUMBER 5

TABLE I. ICD-9-CM discharge codes included in study group

Major category and subheadings (indented)

Allergy, allergic reaction (995.3)

Specified allergen (477.8) Food ingested (693.1)
Anaphylactic shock (999.4) Inhalant (477.9)
Angioneurotic edema (995.1) Serum (999.5)
Bee sting (989.5) Urticaria (708.0)
Drug, medicinal substance and biological (995.2)
Anaphylactic shock or reaction, (correct substance properly administered) (995.0)
Immunization (999.4) Following sting (989.5)
Wrong substance given (977.9) Following serum (999.4)
Angioedema, allergic, any site, with urticaria (995.1)
Hereditary (277.6)
Urticaria (708.9)
Angioneurotic edema (995.1) Due to plants (708.8)
Allergic (708.0) Due to serum (999.5)
Due to drugs (708.0) Idiopathic (708.1)
Due to food (708.0) Larynx (995.1)
Due to inhalants (708.0)

TABLE II. Cutaneous features of patients with acute allergic reactions, mild/moderate anaphylaxis and life threatening
anaphylaxis
No. of patients (%)

Acute allergic reaction Mild/moderate anaphylaxis Life-threatening anaphylaxis All Anaphylaxis

Pruritus 128 (79) 43 (52.4) 37 (61.7) 80 (56.3)

Erythema
Local 30 (18.5) 5 (6.1) 5 (8.3) 10 (7.0)
Generalized 106 (65.4) 50 (61.0) 43 (71.7) 93 (65.5)
Urticaria 77 (47.5) 39 (47.6) 31 (51.7) 70 (49.3)
Angioedema 43 (26.5) 34 (41.5) 23 (38.5) 57 (40)
Local edema 11 (6.8) 3 (3.7) 2 (3.3) 5 (3.5)
Rhinitis/conjunctivitis 4 (2.5) 7 (8.5) 1 (1.7) 8 (5.6)
Totals 162 82 60 142

TABLE III. Additional respiratory, cardiovascular, gastrointestinal, and neurologic features in patients with anaphylaxis
No. of patients (%)

Feature Mild/moderate anaphylaxis Life-threatening anaphylaxis Total

Dyspnoea 28 (34.1) 33 (55.0) 61 (43)

Wheeze 28 (34.1) 22 (36.7) 50 (35.2)
Hoarseness 1 (1.2) 13 (21.7) 14 (9.9)
Loss of consciousness 0 3 (5.0) 3 (2.1)
Syncope/dizziness 0 21 (35.0) 21 (14.8)
Vomiting 13 (15.9) 14 (23.3) 27 (19.0)
Stridor 0 2 (3.3) 2 (1.4)
Bronchospasm 12 (14.6) 14 (23.3) 26 (18.3)
Cyanosis 0 2 (3.3) 2 (1.4)
Laryngeal edema 0 15 (25.0) 15 (10.6)
SBP <90 mmHg 0 13 (21.7) 13 (9.2)
GCS <15 0 4 (6.7) 4 (2.8)
Respiratory rate ≥25 3 (3.7) 16 (26.7) 19 (13.4)
Totals 82 60 142

SBP, Systolic blood pressure; GCS, Glasgow Coma Scale score.

in the anaphylaxis group was drugs (28% of all cases);
this was followed by insects (17.5%) and food (17%).
Drug-related causes included antibiotics in 17 cases
(cephalosporins, 6; penicillins, 5; trimethoprim, 3; others,
3), nonsteroidal anti-inflammatory agents in 10 cases,
angiotensin-converting enzyme (ACE) inhibitors in 6
cases, and intravenous (IV) contrast in 4 cases; other
drugs were involved in the remaining 3 cases. Insect caus-
es included wasp in 8 cases, tick in 2 cases, ant in 1 case,
bee in 1 case, and caterpillar in 1 case; in 12 cases, the
864 Brown, McKinnon, and Chu
TABLE IV. Treatment data for 142 patients with anaphylaxis
Prehospital
Histamine H1 antagonists 35 (24.7)
Histamine H2 antagonists 3 (2.1)
Steroids 22 (15.5)
Adrenaline 26 (18.3)
*Denominator for discharge data is 133 because 8 patients who were admitted to intensive care (or as medical patients) and 1 patient who died were excluded.
insect type was unknown. Food causes included fish and
seafood in 13 cases, nut in 4 cases, mango or lemon drink
in 2 cases, and other foods in 3 cases. There were 15 mis-
cellaneous causes. No causes were apparent or temporal-
ly related in 27% of the patients with anaphylaxis.
Comorbidity
The prevalence of asthma in patients with anaphylaxis
was 23.2%, though we did not specifically record other
atopic conditions. More than one fourth of patients (28.2%)
had a known preexisting allergy to the causative agent.
Treatment before presentation at the
hospital
Thirty-five patients with anaphylaxis (24.7%) received
histamine H1 antagonists, 22 (15.5%) steroids, and 26
(18.3%) adrenaline before presentation at the hospital
(Table IV). Six patients were self-medicated with adren-
aline (total dose range, 300-600 µg), 9 received adrena-
line from their LMO (dose range, 300-1000 µg), and 11
received adrenaline from an ambulance officer. Adrena-
line was administered IV in 3 patients (doses: 2000 µg
for the patient who received cardiopulmonary resuscita-
tion, 200 µg, and 300 µg). Otherwise, all prehospital
adrenaline doses were administered subcutaneously or
intramuscularly (IM).
Treatment in the hospital
One hundred two patients (72%) were given histamine
H1 antagonists, 86 (60.5%) histamine H2 antagonists, and
106 (74.5%) steroids in the hospital. An additional 39
patients (27.4%) received adrenaline (Table IV), 12 IM
and 27 IV, usually diluted to 1:100,000 and titrated at 1
mL (10 µg) per minute to an initial dose between 0.75
and 1.5 µg/kg, with mandatory vital signs and electro-
cardiographic monitoring.
Disposition of patients with anaphylaxis
Forty-seven patients with anaphylaxis (33%) were dis-
charged directly from our ED after a period of monitor-
ing (median duration [hours:minutes], 6:32; range, 4:01
to 9:15). Eighty-seven patients (61%) were admitted to
the ED observation ward, 4 (3%) to the intensive care
unit, and 4 (3%) to a general medical ward. On discharge
from the ED service, 64% patients were given histamine
H1 antagonists, 38% were given histamine H2 antago-
nists, and 71% were given oral steroids. Seven patients
J ALLERGY CLIN IMMUNOL
NOVEMBER 2001
No. of patients (%)
In hospital Total prehospital and/or in hospital Discharge*
102 (72) 121 (85) 85 (64)
86 (60.5) 88 (62) 51 (38)
106 (74.5) 113 (78) 94 (71)
39 (27.4) 57 (40) 7 (5.3)
received replacement self-injectable adrenaline. Follow-
up care was arranged at the allergy clinic for 31 patients
(23%) and at medical outpatient facilities for 3 patients
(2%); 13 patients (10%) were to receive follow-up care
from their LMO. An additional 21 patients (16%)
received discharge advice. Of the 60 patients with severe
anaphylaxis, 43% received follow-up, including 27%
who were referred to the allergy clinic, 10% who were
referred to their LMO, and 6% who were referred to
medical outpatient facilities.
DISCUSSION
This is the largest reported series of patients present-
ing to a single adult ED in 1 year with anaphylaxis or an
acute allergic reaction. It is the first comprehensive
review from Australasia and was aimed at expanding the
currently limited data on the true incidence of anaphy-
laxis.6,24,25 In light of the recognized lack of agreement
on definitions,26 we required evidence of cutaneous fea-
tures as well as additional multisystem involvement; this
was similar to the approach used by Yocum et al6 in a
population-based epidemiologic study in the United
States. Individual chart audit excluded patients with iso-
lated asthma, rash or rhinitis, and so forth if there was no
clear acute precipitating factor or no cutaneous and sys-
temic allergic features. Severe anaphylaxis was defined
by the presence of potentially life-threatening features, as
suggested by Stewart and Ewan5 in their ED study in the
United Kingdom. It was impossible to exclude a signifi-
cant underlying comorbid condition in apparently severe
reactions, though all patients were discharged within 24
hours or had improved rapidly in that time in the inten-
sive care unit or medical ward.
Our data confirm that anaphylaxis is more common
than previously recognized. Our annual incidence was 1
in 439 ED cases, of which just under half (ie, approxi-
mately 1 in 1000 cases) were severe. The population inci-
dence of ED cases, given a static catchment area, was 1
adult presentation per 3400 people per year. These are
greater than existing ED attendance figures, which typi-
cally indicate an incidence of anaphylaxis presentations
of 1:1100 ED cases8 and an incidence of severe anaphy-
laxis presentations of 1:1500 ED cases.5 Our data are
nevertheless likely to reflect underestimation, inasmuch
as some cases might have gone unrecognized and others
been treated or resolved spontaneously before presenta-
J ALLERGY CLIN IMMUNOL
VOLUME 108, NUMBER 5
tion at the hospital. Still other patients might have died
before hospital presentation; we did not study the local
coroner’s cases. The fact that only 1 of our patients died
means that the annual case fatality rate was 1:142 ana-
phylaxis cases, or 0.70%; this compares with a rate of
0.65% reported by Yocum et al6 from data collected from
1983 to 1987. These fatality rates are higher than other
figures (ranging from 0.05%27 to 0.002%28), though the
numbers of deaths recorded are still too small to allow
the drawing of any conclusions.
Overall, 94% of all our patients with anaphylaxis had
cutaneous features; in contrast, some authors have
reported that all of their patients had cutaneous manifes-
tations.6,29,30 Patients with acute anaphylaxis might
indeed present without cutaneous markers because of
treatment before hospital presentation, the spontaneous
resolution of cutaneous signs, or the complete absence of
such signs, particularly in patients presenting with the
rapid onset of laryngeal edema or circulatory shock,6,31
as in our 9 cases without cutaneous features.
ACE inhibitors were the most common cause of
angioedema, and the most common single cause of ana-
phylaxis was fish (including seafood), though because of
inconsistent data recording, individual cases could not be
separated further. Our findings were similar to those in 2
other ED evaluations,5,7 though other authors have recog-
nized an increasing role of food-induced anaphylaxis.4,10,15
No cause was apparent in 27% of our cases; this is similar
to rates reported by Yocum et al6 (32%) and Kemp et al10
(37%). The absence of a recorded cause in our series might
simply reflect the retrospective nature of data collection.
A history of known asthma was recorded in 23.2% of
our patients with anaphylaxis; this compared with a
prevalence of diagnosed asthma in eastern Australia in
1993 of 7.2% in adults and 17.5% in primary school chil-
dren.32 The higher prevalence of asthma in our study is in
line with findings in 2 other studies,6,10 but it is not as
dramatic as the 96% atopy rate seen in Ewan’s15 series of
62 patients with nut allergy.
A preexisting allergy to the causative agent was known
in 28.2% of patients, which is similar to the rate of 24% of
patients reported in Ewan’s5 ED series. However, of major
concern is the fact that among our patients with anaphy-
laxis, 2 of 6 reacting to cephalosporins, 2 of 5 reacting to
penicillins, 1 given trimethoprim, 4 of 10 reacting to non-
steroidal anti-inflammatory drugs, and 3 of 6 reacting to
ACE inhibitors were already known to be allergic. One of
these 12 instances resulted in a severe reaction (to peni-
cillin). We were unable to determine whether there had
been a failure of patient record documentation, an inade-
quate or absent physician inquiry, or simply insufficient
notice taken. All of these iatrogenic cases were avoidable,
and they serve to emphasize the need for the taking of a
careful drug and allergy history in every ED patient.
The use of H1 antihistamines and steroids was much as
expected, though the additional use of H2 with H1 anti-
histamines reflected local ED policy,31,33,34 supported
recently in a randomized, controlled trial.35 Adrenaline,
oxygen, and fluids, however, continue to be the first-line
Brown, McKinnon, and Chu 865
therapy in anaphylaxis.21,26,33,34,36,37 Adrenaline was
usually given subcutaneously or IM before hospital pre-
sentation; however, 27 of 39 patients received adrenaline
IV in the hospital (the remaining 12 patients received
adrenaline IM in the hospital). The majority (57%) of
patients with severe anaphylaxis received adrenaline
either before hospital presentation or in the hospital,
including all those with laryngeal edema and hypoten-
sion. Some patients with syncope, dizziness, and altered
conscious levels before hospital presentation recovered
spontaneously, and others with wheeze responded to β-2
agonists. Spontaneous recovery5,33,37 and recovery after
treatment with oxygen, fluids, and specific bronchodila-
tors is well recognized,38,39 though the subjective nature
of the symptoms and the likelihood of panic or hyper-
ventilation in some patients might have distorted the
data. Adrenaline must continue to be used appropriately
in acute anaphylaxis,3,5,21,26,33,34 despite a reluctance in
some to give it to adults5,40,41 or children.42,43 Arguments
about recommended doses, route, dilution, and timing
should not obscure adrenaline’s vital role.33,44-47
Finally, though virtually all cases of anaphylaxis can be
managed in the ED and observation ward, it is clear that
greater use of referrals to allergy specialists is necessary.
There is a wide variation in reported allergy clinic referral
rates, from 0%5,7 to as much as 79%,48 but in our series it
was inadequate. An educational program to increase
awareness is now in place in our ED, particularly for
patients in whom the reaction is significant, the stimulus is
unknown or unavoidable, and attacks are recurrent.26,33,49
In addition, all data presented were collected retrospec-
tively and were thus prone to reporting bias. We are cur-
rently planning to participate in a prospective, multicenter
Australian ED study of anaphylaxis presentations.
CONCLUSION
Our data suggest that patients with anaphylaxis present
to the ED more commonly than is realized; 1 severe case
can be expected every week in a moderate-sized depart-
ment. A precipitant will be recognized in approximately
three fourths of cases, emphasizing the need for taking a
detailed history on presentation and the importance of
giving advice on future avoidance. More than 90% of
patients with anaphylaxis will have cutaneous features,
but their absence in 6% does not preclude the diagnosis.
Finally, though the large majority of patients can be defin-
itively managed in the ED alone, a clear management
guideline stressing the importance of the appropriate use
of adrenaline and the need for allergy referral is essential.
We thank Dr Roger Prentice for his advice and Ms Monique
Cichocki for her expert manuscript preparation.
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