Kim and Fischer Allergy, Asthma & Clinical Immunology 2011, 7(Suppl 1):S6

http://www.aacijournal.com/content/7/S1/S6 ALLERGY, ASTHMA & CLINICAL

IMMUNOLOGY

REVIEW Open Access

Anaphylaxis
Harold Kim1,2*, David Fischer3

Abstract
Anaphylaxis is an acute, potentially fatal systemic reaction with varied mechanisms and clinical presentations.
Although prompt recognition and treatment of anaphylaxis are imperative, both patients and healthcare
professionals often fail to recognize and diagnose early signs and symptoms of the condition. Clinical
manifestations vary widely, however, the most common signs are cutaneous symptoms, including angioedema,
urticaria, erythema and pruritus. Immediate intramuscular administration of epinephrine into the lateral thigh is
first-line therapy, even if the diagnosis is uncertain. The mainstays of long-term management include specialist
assessment, avoidance measures, and the provision of an epinephrine auto-injector and an individualized
anaphylaxis action plan. This article provides an overview of the causes, clinical features, diagnosis and acute and
long-term management of this serious allergic reaction.

Introduction anaphylaxis are: foods, particularly, peanuts, tree nuts,

Anaphylaxis is defined as a serious allergic reaction that shellfish and fish, cow’s milk, eggs and wheat; medica-
is rapid in onset and may cause death [1,2]. The preva- tions (most commonly penicillin), and natural rubber
lence of anaphylaxis is estimated to be as high as 2%, latex. Exercise, aspirin, non-steroidal anti-inflammatory
and appears to be rising, particularly in the younger age drugs (NSAIDs), opiates, and radiocontrast agents can
group [3-5]. also cause anaphylaxis, but anaphylactic reactions to
The more rapidly anaphylaxis develops, the more these agents often result from non-IgE-mediated
likely the reaction is to be severe and life-threatening mechanisms. In other cases, the cause of anaphylactic
[4]. Therefore, prompt recognition and management of reactions is unknown (idiopathic anaphylaxis). In chil-
the condition are imperative. However, anaphylaxis is dren, anaphylaxis is most often caused by foods, while
often under-recognized and treated inadequately. Diag- venom- and drug-induced anaphylaxis is more common
nosis and management are challenging since reactions in adults [4,7-9]. Table 1 provides a more comprehen-
are often immediate and unexpected. Furthermore, sive list of the potential causes of anaphylaxis.
there is no single test to diagnose anaphylaxis in routine Co-morbidities and concurrent medications may also
clinical practice [3,6]. This article will provide an over- affect the severity of anaphylactic reactions and patient
view of the causes and clinical features of anaphylaxis as response to treatment. For example, patients with
well as strategies for the accurate diagnosis and manage- asthma and cardiovascular disease are more likely to
ment of the condition. experience a poor outcome from anaphylaxis. Concur-
rent administration of beta-blockers can interfere with
Causes the patient’s ability to respond to epinephrine, the first-
Most episodes of anaphylaxis are triggered through an line of treatment for anaphylaxis (discussed later).
immunologic mechanism involving immunoglobulin E Furthermore, the use of angiotensin-converting enzyme
(IgE) which leads to mast cell and basophil activation (ACE) inhibitors and angiotensin receptor blockers
and the subsequent release of inflammatory mediators (ARBs) can impact a patient’s compensatory physiologic
such as histamine, leukotrienes, tryptase and prostaglan- response to anaphylaxis, leading to more severe reac-
dins. Although any substance has the potential to cause tions [10].
anaphylaxis, the most common causes of IgE-mediated
Signs and symptoms
* Correspondence: hlkimkw@gmail.com Since anaphylaxis is a generalized reaction, a wide vari-
1
University of Western Ontario, London, Ontario, Canada ety of clinical signs and symptoms involving the skin,
Full list of author information is available at the end of the article

© 2011 Kim and Fischer; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative
Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and
reproduction in any medium, provided the original work is properly cited.
Kim and Fischer Allergy, Asthma & Clinical Immunology 2011, 7(Suppl 1):S6 Page 2 of 7
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Table 1 Causes of anaphylaxis antigen, but may occasionally occur as late as 1 hour
Common: post exposure. Symptoms usually follow a uniphasic
• Foods: most commonly peanuts, tree nuts, egg, seafood and fish, course, with resolution of symptoms within hours of
cow’s milk, wheat
• Medications: most commonly antibiotics
treatment. However, up to 20% of reactions follow a
• Insect stings (bees and wasps) biphasic course characterized by an asymptomatic per-
• Natural rubber latex iod of 1-8 hours followed by recurrent symptoms [13].
• Unidentified (no cause found; idiopathic anaphylaxis)
Less common:
• Exercise Diagnosis
• Semen The diagnosis of anaphylaxis is based primarily on
• Food additives: monosodium glutamate, metabisulfite
• Hormonal changes: menstrual factors clinical signs and symptoms, as well as a detailed
• Topical medications description of the acute episode, including antecedent
• Transfusions activities and events. Diagnostic criteria for anaphylaxis
were published by a multidisciplinary group of experts
in 2005 and 2006, and are shown in Table 3[1,2]. A
gastrointestinal and respiratory tracts, and cardiovascular diagnosis of anaphylaxis is highly likely when any one
system can be observed (see Table 2). The most common of the criteria listed in Table 3 is fulfilled. Since the
clinical manifestations are cutaneous symptoms, including evaluation and diagnosis of anaphylaxis is often com-
urticaria and angioedema, erythema (flushing), and pruri- plex, referral to an allergist with training and expertise
tus (itching) [11]. Patients also often describe an impend- in the identification and management of anaphylaxis
ing sense of death (angor animi). Death due to should be considered.
anaphylaxis usually occurs as a result of respiratory
obstruction or cardiovascular collapse, or both. Evidence History
suggests that there is a direct correlation between the The history is the most important tool to establish the
immediacy of symptom onset and the severity of the epi- cause of anaphylaxis and should take precedence over
sode, with the more rapid the onset, the more severe the diagnostic tests. It should elicit information about clini-
event [12]. It is important to note that the signs and symp- cal manifestations (e.g., urticaria, angioedema, flushing,
toms of anaphylaxis are unpredictable and may vary from pruritus, airway obstruction, gastrointestinal symptoms,
patient to patient and from one reaction to another. syncope, and hypotension); agents encountered before
Therefore, the absence of one or more of the common the reaction, such as foods, medications or insect bites/
symptoms listed in Table 2 does not rule out anaphylaxis, stings, as well as the patient’s activities preceding the
and should not delay immediate treatment. event (e.g., exercise, sexual activity). The absence of
The signs and symptoms of anaphylaxis typically cutaneous symptoms puts the diagnosis in question
develop within minutes after exposure to the offending since the majority of anaphylactic episodes include

Table 2 Signs and symptoms of anaphylaxis [6,11]

Skin Gastrointestinal:
• Urticaria (hives) • Nausea
• Angioedema (swelling) • Vomiting
• Erythema (flushing) • Abdominal pain
• Pruritus (itching) • Diarrhea

Respiratory: Neurologic:
• Upper airway: • Light-headedness
– Nasal congestion • Dizziness
– Sneezing • Confusion
– Hoarseness
– Cough
– Oropharyngeal or laryngeal edema
• Lower airway: dyspnea Oral:
– Bronchospasms • Itching
– Wheezing • Tingling or swelling of the lips, tongue or palate
– Chest tightness
Cardiovascular: Other:
• Hypotension • Sense of impending doom
• Dizziness • Anxiety
• Syncope
• Tachycardia
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Table 3 Clinical criteria for diagnosing anaphylaxis [1,2]

Anaphylaxis is highly likely when any 1 of the following 3 criteria is fulfilled following exposure to an allergen:
1 Acute onset of an illness (minutes to several hours) with involvement of the skin, mucosal tissue, or both (e.g., generalized hives,
pruritus or flushing, swollen lips-tongue-uvula) and at least 1 of the following:
a. Respiratory compromise (e.g. dyspnea, wheeze, bronchospasm, stridor, reduced PEF, hypoxemia)
b. Reduced BP or associated symptoms of end-organ dysfunction (e.g. hypotonia [collapse], syncope, incontinence)
2 2 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., generalized hives, itch-flush, swollen lips-tongue-uvula)
b. Respiratory compromise (e.g., dyspnea, wheeze, bronchospasm, stridor, reduced PEF, hypoxemia)
c. Reduced BP or associated symptoms (e.g., hypotonia [collapse], syncope, incontinence)
d. Persistent GI symptoms (e.g., painful abdominal cramps, vomiting)
3 Reduced BP after exposure to a known allergen for that patient (minutes to several hours):
a. Infants and children: low systolic BP (age specific) or > 30% decrease in systolic BP*
b. Adults: systolic BP < 90 mmHg or > 30% decrease from that person’s baseline
PEF = Peak expiratory flow; BP: blood pressure; GI: gastrointestinal
* Low systolic blood pressure for children is age specific and defined as: < 70 mmHg for age 1 month to 1 year; < 70mmHg + [2 x age] for age 1 to 10 years; <
90mmHg for age 11 to 17 years.

cutaneous symptoms; however, their absence does not dysfunction, acute poisoning; hypoglycemia; and seizure
rule out anaphylaxis [4]. disorders [4,14].

Additional diagnostic tests Treatment

The diagnosis of a specific cause of anaphylaxis may be Acute management
supported by the results of skin tests and/or in vitro The acute treatment of anaphylaxis begins with rapid
IgE tests [4]. These tests can determine the presence assessment of the airway, breathing and circulation. Epi-
of specific IgE antibodies to foods, medications (e.g., nephrine is the drug of choice for anaphylaxis and
penicillin), and stinging insects. However, for the should be given immediately to any patient with a sus-
majority of medications, standardized skin tests and/or pected anaphylactic episode. Treatment should be pro-
in vitro tests are not available. In general, skin testing vided even if the diagnosis is uncertain since there here
is more sensitive than in vitro testing and is the diag- are no contraindications to the use of epinephrine [6].
nostic procedure of choice for the evaluation of most The recommended dosing of epinephrine for the acute
IgE-mediated causes of anaphylaxis (if available for the treatment of anaphylaxis is 0.01 mg/kg up to a maxi-
relevant trigger or allergen). If skin testing is per- mum of 0.5 mg administered intramuscularly every 5–
formed, it should be done under the supervision of a 20 min as necessary [6]. Intramuscular administration
physician who is experienced in the procedure in a set- into the lateral thigh is recommended as it allows for
ting with appropriate rescue equipment and medica- more rapid absorption and higher plasma epinephrine
tion available [4]. levels compared to subcutaneous administration [10].
The clinical diagnosis of anaphylaxis can sometimes Glucagon should also be considered in patients using
be supported by the documentation of elevated concen- beta-blockers.
trations of mast cell and basophil mediators such as All patients receiving emergency epinephrine must be
plasma histamine or serum or plasma total tryptase. transported to hospital immediately (ideally by ambu-
However, it is critical to obtain blood samples for these lance) for evaluation and observation. Patients should
measurements as soon as possible after the onset of also be placed in a recumbent (supine) position with the
symptoms since elevations are transient. lower extremities elevated, unless this is precluded by
shortness of breath or vomiting [6,15,16].
Differential diagnosis As mentioned earlier, patients with asthma, particu-
Other diagnoses that might present with signs and/or larly those with poorly controlled asthma, are at
symptoms characteristic of anaphylaxis should be increased risk of a fatal reaction. In these patients, ana-
excluded. The most common conditions that mimic phylaxis may be mistaken for an asthma exacerbation
anaphylaxis include: vasodepressor (vasovagal/neurocar- and inappropriately treated solely with asthma inhalers.
diogenic) reactions (which are characterized by hypoten- Therefore, if there are ongoing asthma symptoms in an
sion, pallor, bradycardia, weakness, nausea and individual with known anaphylaxis, epinephrine should
vomiting); acute respiratory decompensation from severe be given [6].
asthma attacks, foreign body aspiration and pulmonary Oxygen therapy should also be considered in any
embolism; vocal cord dysfunction; acute anxiety (e.g., patient with symptoms of anaphylaxis, particularly for
panic attack or hyperventilation syndrome); myocardial those with prolonged reactions. Intravenous fluids
Kim and Fischer Allergy, Asthma & Clinical Immunology 2011, 7(Suppl 1):S6 Page 4 of 7
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(crystalloid solutions or colloid volume expanders) Prescription for an epinephrine auto-injector

should also be provided since massive fluid shifts can A prescription for an epinephrine auto-injector should
occur rapidly in anaphylaxis due to increased vascular be provided to all patients who have experienced ana-
permeability. Volume replacement is particularly impor- phylaxis previously, including those who have had any
tant for patients whose hypotension persists despite epi- rapid-onset systemic allergic reaction (gastrointestinal,
nephrine injections. Supportive therapy such as inhaled respiratory, cardiac); diffuse hives to any food or insect
beta2-agonists (for patients experiencing bronchospasm) stings; or any rapid-onset (i.e., minutes to hours) reac-
and antihistamines (for control of cutaneous symptoms) tion of any severity to the highest risk foods such as
can also be helpful, but should never replace epinephr- peanut, tree nuts, fish, and shellfish [6].
ine as first-line therapy. Vasopressors, such as dopa- There are currently two epinephrine auto-injectors
mine, can also be considered if epinephrine injections available in North America: EpiPen ® and Twinject ® .
and volume expansion with intravenous fluids fail to Both products come in two dosages (0.15 mg and 0.30
alleviate hypotension. Glucocorticosteroids have a slow mg), which are prescribed according to weight. The
onset of action and, therefore, these agents have not 0.30 mg dosage should be used for those weighing 30
been shown to be effective for the acute treatment of kg or more, and the 0.15 mg dosage for children
anaphylaxis. Theoretically, however, they may prevent weighing between 15–30 kg. Certain sources recom-
biphasic or protracted reactions and, hence, are often mend switching to the 0.30 mg dose at 25 kg rather
given on an empirical basis. To date, there is no conclu- than 30 kg [16]. These devices should be stored prop-
sive evidence that the administration of glucocorticos- erly (avoiding temperature extremes) and replaced
teroids prevents a biphasic response [4]. before the expiration date. More information on these
If intramuscular epinephrine and intravenous fluids auto-injectors is available at http://www.epipen.ca and
fail to improve anaphylactic symptoms, intravenous http://www.twinject.ca.
infusions of epinephrine may be required; however, Upon prescription of an epinephrine auto-injector,
these infusions should be given by a physician who is healthcare providers must instruct the patient on how
trained and experienced in its use and has the capacity and when to use the device. Instructions on proper use
for continuous blood pressure and cardiac monitoring. should be reviewed verbally and accompanied by a DVD
Figure 1 provides a simplified algorithm for the acute and/or written material, and should be reinforced
management of anaphylaxis. annually.
Following acute treatment, patients should be
observed for a period of time due to the risk of a bipha- Education on avoidance measures
sic response or possible recurrence of the reaction as Patients and their caregivers should be educated about
epinephrine wears off. The observation period should be agents or exposures that may place them at risk for
individualized based on the severity of the initial reac- future reactions, and should be counselled on avoidance
tion and access to care. Experts have recommended measures that may be used to reduce the risk for such
observing patients for 4 to 6 hours following an anaphy- exposures. Avoidance strategies should be individua-
lactic reaction, with prolonged observation times for lized, taking into consideration factors such as relevant
patients with severe or refractory symptoms [6]. triggers, age, activity, occupation, hobbies, residential
conditions, access to medical care, and the patient’s
Long-term management level of personal anxiety. Individuals who have had ana-
The mainstays of long-term management for patients phylactic reactions to foods should be instructed to read
who have experienced an anaphylactic episode include: food labels carefully, watching for hidden ingredients
specialist assessment, a prescription for an epinephrine such as “natural flavour” or “spices” that may indicate
auto-injector, patient and caregiver education on avoid- the presence of allergens (e.g., peanut, tree nuts, milk,
ance measures, and the provision of an individualized egg, shellfish, fish, sesame, soy and wheat), as well as
anaphylaxis action plan. “may contain” warnings [4]. Recent evidence suggests
that peanut allergic children can be desensitized to pea-
Specialist assessment nut by feeding them increasing amounts of peanut
After acute anaphylaxis, patients should be assessed for under close supervision [17]. Similar results have been
their future risk of anaphylaxis, ideally by an allergist. noted for egg and milk allergy. Although these results
These specialists are experienced in identifying and con- are promising, further confirmatory studies in this area
firming the cause of anaphylaxis, educating patients on are needed before routinely recommending desensitiza-
appropriate avoidance strategies, drafting an anaphylaxis tion procedures to patients with these food allergies (for
action plan, and advising whether immunotherapy is more information, see article on Food Allergy in this
appropriate [4,6]. supplement).
Kim and Fischer Allergy, Asthma & Clinical Immunology 2011, 7(Suppl 1):S6 Page 5 of 7
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Anaphylaxis?

Assess ABC: Airway, Breathing, Circulation

Intramuscular epinephrine
x 0.01 mg/kg up to a maximum of 0.5 mg
x Repeat every 5–20 min if needed

x Call 911 for immediate transfer to

hospital
x Lie patient flat and raise patient’s
legs (if breathing not impaired)

Oxygen and IV fluids Supportive therapy:

x Inhaled beta2-agonists (for
bronchospasms)
x Antihistamines (for
cutaneous symptoms)
No improvement
x Vasopressors
x Glucocorticosteroids

IV epinephrine*

Figure 1 Simplified algorithm for the acute management of anaphylaxis. IV: intravenous *Should be given by a physician trained in the use
of IV epinephrine with capacity for continuous blood pressure and cardiac monitoring

Patients with anaphylaxis to medications should be Induction of drug tolerance procedures temporarily
informed about all cross-reacting medications that modify a patient’s immunologic or non-immunologic
should be avoided. Should there be a future essential response to a drug through the administration of
indication for use of the medication causing anaphy- incremental doses of the drug. However, drug toler-
lactic reactions, it may be helpful to educate patients ance is usually maintained only as long as the drug is
about possible management options, such as medica- administered; therefore, the procedure needs to be
tion pretreatment and use of low osmolarity agents in repeated in the future if the patient requires the drug
patients with a history of reactions to radiographic again after finishing a prior therapeutic course (for
contrast media, or induction of drug tolerance proce- more information, see article on Drug Allergy in this
dures (also known as drug desensitization) [4]. supplement).
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Patients who have had an anaphylactic reaction to an and emergency protocols [6]. Important information that
insect sting should be advised about avoidance measures should be included in this plan is shown in Table 4[6,18].
to reduce the risk of future stings. Such measures Examples of such a plan, along with other relevant infor-
include: being alert when eating outdoors (as wasps are mation and materials, can be downloaded at Anaphylaxis
attracted to food), wearing shoes and long pants when Canada (http://www.anaphylaxis.ca) or the Food Allergy
in fields, and having nests or hives near the patient’s and Anaphylaxis Network (http://www.foodallergy.org; a
home removed [14]. Patients who have previously US-based association). Action plans should be reviewed
experienced venom-induced anaphylaxis are often candi- annually and updated if necessary. A copy of the plan
dates for venom immunotherapy, which is successful in should be made available to all relevant persons, such as
preventing anaphylaxis in up to 98% of patients (see day-care providers, teachers, and employers. Recommen-
article on Allergen Immunotherapy in this supplement). dations for the management of anaphylaxis in schools and
Subjects at high risk of a reaction to latex include: other community settings [15] are available through the
healthcare workers, children with spina bifida and geni- Allergy Safe Communities website at http://www.allergysa-
tourinary abnormalities; and workers with occupational fecommunities.ca.
exposure to latex. Patients with spina bifida (regardless
of a history of latex allergy) and patients with a positive Conclusions
history of latex allergy should have all medical-surgical- Anaphylaxis is an acute, potentially fatal systemic reac-
dental procedures performed in a latex-safe environ- tion with varied mechanisms and clinical presentations.
ment. This is an environment in which no natural rub- Prompt recognition and treatment of anaphylaxis are
ber latex gloves are used in the room or surgical suite imperative; however, both patients and healthcare pro-
and in which there are limited latex-based accessories fessionals often fail to recognize and diagnose anaphy-
(catheters, adhesives, tourniquets, anesthesia equipment laxis in its early stages. Diagnostic criteria which take
or devices) which come in contact with the patient [4]. into account the variable clinical manifestations of ana-
Patients should also obtain and wear medical identifica- phylaxis are now available and can assist healthcare pro-
tion (such as a MedicAlert bracelet/necklace) that indi- viders in the early recognition of the condition.
cates that they have experienced anaphylaxis as well as the Immediate intramuscular administration of epinephrine
responsible agent. Patients should also be instructed to into the lateral thigh is first-line therapy for anaphylaxis.
avoid drugs that might increase their susceptibility and/or Acute management may also involve oxygen therapy,
complicate the management of an anaphylactic event, intravenous fluids, and adjunctive therapies such as anti-
such as beta-blockers, ACE inhibitors, or ARBs [4]. histamines or inhaled beta2-agonists. The mainstays of
long-term management include specialist assessment, a
Anaphylaxis action plan prescription for an epinephrine auto-injector, patient
A comprehensive, individualized anaphylaxis action plan and caregiver education on avoidance measures, and the
should be prepared which defines roles and responsibilities provision of an individualized anaphylaxis action plan.

Table 4 Components of an anaphylaxis action plan [6,18]

Contact details
• Names and contact details for emergencies, including family members, allergist/immunologist and family doctor
• Contact details for local emergency or ambulance services
Allergens/Triggers
• Clear identification of allergens/triggers to be avoided
– Include generic and proprietary names of drugs and possible cross-sensitivities, if relevant
How to recognize the signs and symptoms of anaphylaxis
• Mouth: itching, swelling of lips/tongue
• Throat: itching, tightness, closure, hoarseness
• Skin: itching, hives, eczema, swelling, flushing
• Gut: vomiting, diarrhea, abdominal pain
• Lung: shortness of breath, cough, wheeze
• Heart: hypotension, dizziness, syncope, tachycardia
• Neuro (or head): light-headedness
• Other: feeling of impending doom, anxiety
Medications prescribed and when they should be used
• Epinephrine auto-injectors (first-line); should include detailed instructions (with photographs, if possible) on how to correctly administer
the auto-injector device (for daycare, school and/or office staff)
• Antihistamines (for cutaneous symptoms)
• Inhaled beta2-agonists (for bronchospasm)
Where medication is stored at home, work or school
Kim and Fischer Allergy, Asthma & Clinical Immunology 2011, 7(Suppl 1):S6 Page 7 of 7
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Key take-home messages definition and management of anaphylaxis: summary report – Second
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Acknowledgements 13. Stark BJ, Sullivan TJ: Biphasic and protracted anaphylaxis. J Allergy Clin
This article has been published as part of Allergy, Asthma & Clinical Immunol 1986, 78:76-83.
Immunology Volume 7 Supplement 1, 2011: Practical guide for allergy and 14. Ellis AK, Day JH: Diagnosis and management of anaphylaxis. CMAJ 2003,
immunology in Canada. The full contents of the supplement are available 169:307-11.
online at http://www.aacijournal.com/supplements/7/S1 15. Canadian Society of Allergy and Clinical Immunology: Anaphylaxis in
schools & other settings. CSACI;, 2 2009.
Author details 16. Sicherer SH, Simons FE, Section on Allergy and Immunology American
1
University of Western Ontario, London, Ontario, Canada. 2McMaster Academy of Pediatrics: Self-injectable epinephrine for first-aid
University, Hamilton, Ontario, Canada. 3University of Western Ontario, management of anaphylaxis. Pediatrics 2007, 119:638-46.
London, Ontario, Canada. 17. Burks A: Peanut allergy. Lancet 2008, 371:1538-46.
18. Muraro A, Roberts G, Clark A, Eigenmann PA, Halken S, Lack G, Moneret-
Competing interests Vautrin A, Niggemann B, Rancé F, EAACI Task Force on Anaphylaxis in
Dr. Harold Kim is the past president of the Canadian Network for Respiratory Children: The management of anaphylaxis in childhood: position paper
Care and co-chief editor of Allergy, Asthma &Clinical Immunology. He has of the European academy of allergology and clinical immunology. Allergy
received consulting fees and honoraria for continuing education from 2007, 62:857-71.
AstraZeneca, GlaxoSmithKline, Graceway Pharmaceuticals, King Pharma,
Merck Frosst, Novartis, and Nycomed. doi:10.1186/1710-1492-7-S1-S6
Dr. David Fischer is a member of the Board of Directors of the Canadian Cite this article as: Kim and Fischer: Anaphylaxis. Allergy, Asthma &
Society of Allergy & Clinical Immunology. He has received consulting fees Clinical Immunology 2011 7(Suppl 1):S6.
and honoraria for continuing education from AstraZeneca, GlaxoSmithKline,
Graceway Pharmaceuticals, King Pharma, Merck Frosst, Novartis, Paladin Labs
and Nycomed.

Published: 10 November 2011

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