Anaphylaxis

Lisa J. Kobrynski, MD, MPH

Anaphylaxis is a clinical syndrome characterized by an abrupt, severe, life-threatening

event with cutaneous, respiratory, cardiovascular, and gastrointestinal symptoms mediated
by IgE and non-IgE immunologic reactions to a particular antigen. Several other syndromes
have symptoms that may mimic those of anaphylaxis, and a rapid diagnostic laboratory test
is not readily available in most emergency departments. Thus, it is important that
physicians in the emergency department are familiar with the signs and symptoms of
anaphylaxis and are able to distinguish this condition from disorders presenting with
similar symptoms. Prompt recognition of anaphylaxis and initiation of treatment with
epinephrine in a timely fashion is critical to prevent fatalities. This article will review the
pathophysiology of anaphylaxis, the common triggers, the clinical findings, the treatment
and prevention of this disorder.
Clin Ped Emerg Med 8:110-116 ª 2007 Published by Elsevier Inc.

KEYWORDS anaphylaxis, anaphylactoid, angioedema, epinephrine

T he term anaphylaxis was originally used to refer to

severe allergic reactions, mediated by immunoglo-
bulin (Ig) E, necessitating exposure, sensitization, and
reexposure to a particular agent. Later on, the term
anaphylactoid reaction was used to refer to a similar
clinical syndrome occurring due to other immunologic
responses to a foreign antigen. In many ways, these 2
entities are clinically indistinguishable. In this article,
anaphylaxis will be used as a descriptive term to
denote a clinical syndrome characterized by an abrupt,
severe, life-threatening event with cutaneous, respira-
tory, cardiovascular, and gastrointestinal symptoms
mediated by IgE and non-IgE immunologic reactions
to a particular antigen.
Pathophysiology
Anaphylaxis occurs when a foreign antigen elicits an
immunologic response in an individual leading to the
release of histamine and other chemokines causing
systemic symptoms. This response can occur secondary
to preformed IgE molecules because of the formation of
antigen-antibody complexes or due to direct mast cell
degranulation. The commonly associated symptoms of
anaphylaxis are caused by the release of inflammatory me-
diators such as histamine, leukotrienes, anaphylatoxins
C3a and C5a (slow releasing substance of anaphylaxis),
neuropeptides, platelet-activating factor, tryptase, chy-
mase, and prostaglandins. These mediators are responsible
for peripheral vasodilation, bronchoconstriction, urtica-
ria, and angioedema because of increased vascular perme-
ability, chemotaxis of eosinophils, activation of
complement, and coronary vasoconstriction.
Anaphylaxis can occur after reexposure to an antigen,
frequently a foreign protein, which binds preformed
antigen specific IgE bound to the high affinity IgE receptor
on the surface of mast cells. Once antigen is bound, cross-
linking of the IgE molecules on the cell surface occurs and
the mast cell degranulates, releasing histamine, tryptase,
and other enzymes. Histamine is a potent vasodilator and
bronchoconstrictor and causes urticaria, angioedema,
flushing, hypotension, vomiting, and diarrhea.
Anaphylaxis can also occur when an antigen binds
IgG and complement in the serum to form immune
complexes. Activation of complement results in the
release of C3a, C5a, and the slow releasing substances
of anaphylaxis. These substances also cause contraction
Division of Allergy and Immunology, Emory University School of
Medicine, Atlanta, GA.
Reprint requests and correspondence: Lisa J. Kobrynski, MD, MPH,
Division of Allergy and Immunology, Emory University School of
Medicine, 2015 Uppergate Dr., Atlanta, GA 30322.

110 1522-8401/$ - see front matter ª 2007 Published by Elsevier Inc.

doi:10.1016/j.cpem.2007.04.006
Anaphylaxis
of bronchial smooth muscle, vasodilation, and induce
the release of other mediators from mast cells and
basophils.
Still, other substances will cause abnormalities in the
arachadonic acid pathway, leading to the release of
metabolites such as leukotrienes. These substances
mainly cause bronchoconstriction. Other agents have
been shown to cause the release of histamine from mast
cells without the presence of specific IgG or IgE antibody.
These reactions have been called banaphylactoidQ reac-
tions, but the symptoms are identical to anaphylactic
reactions, differing only in the mechanism of the reaction
such that sensitization and the formation of specific
antibody is not required.
Epidemiology
The exact incidence of anaphylactic reactions is not
known. Estimates derived from retrospective reviews and
analyses of published literature put the annual incidence
rates for anaphylaxis between 3 and 21 per 100 000
person years [1-5]. This is likely an underestimation and
the occurrence rates could be as high as 590 per 100,000
[6]. The rate of fatality from anaphylaxis is also
unknown, and estimates vary widely. Is has been
estimated that between 1443 and 1503 deaths occur each
year due to anaphylaxis for a fatality rate of 0.002% [2].
Overall, there may be a slight increase in the frequency of
anaphylactic reactions in females, especially in cases due
to aspirin or latex [7,8]. Anaphylaxis occurs in all age
groups, but children are more likely to experience
anaphylaxis due to foods and antibiotics. In children
with spina bifida and ventriculoperitoneal shunts, and in
health care workers, the risk of anaphylaxis is linked to
repetitive exposures to agents such as latex. A similar
situation occurs in diabetic patients exposed to prot-
amine. The most common identifiable causes are foods
and drugs, particularly penicillin.
Etiology
A large variety of agents can trigger anaphylactic
reactions (Table 1). The risk of developing anaphylaxis
after exposure to any of these agents is increased by
decreasing the time interval between the first exposure
and subsequent reexposures, by intravenous (IV) admin-
istration, and by a history of atopic disease. Food-induced
anaphylaxis accounts for one third to one half of pediatric
cases [5,6,9]. The cause of anaphylaxis may remain
unidentified in up to two thirds of patients [8].
Clinical Findings
The symptoms and signs of anaphylaxis may vary in
timing of onset, symptom progression, and severity.
Table 2 shows the commonly seen symptoms of anaphy-
111
Table 1 Causes of anaphylaxis.
IgE-mediated
Antibiotics (eg, penicillins, cephalosporins, vancomycin,
neomycin, amphotericin B)
Foreign proteins (eg, serum, insulins, asparaginase,
chymopapain, venoms, penicillinase, blood,
blood products, protamine, antithymocyte globulins, latex)
Other medications (eg, allergen extracts,
methylprednisolone, local anesthetics, vaccines,
thiopental)
Foods (eg, milk, eggs, wheat, soy, peanuts, tree nuts,
shellfish, fish, corn, seeds, bananas)
Immune complex–mediated
Biologics (eg, blood, blood products, immunoglobulin)
Medications (methotrexate)
Radiocontrast media
Arachadonic acid pathway
Acetylsalicylic acid and nonsteroidal anti-inflammatory
agents
Tartrazine
Direct histamine release
Medications (eg, opiates, iron-dextran, thiamine, mannitol,
pentamidine)
Radiocontrast media
Dextran
laxis. These symptoms may occur in any order, although
cutaneous symptoms are generally one of the first
manifestations of an anaphylactic reaction, followed by
respiratory and cardiovascular symptoms. However, if
there is rapid progression, cutaneous symptoms may be
delayed or not apparent at the time of presentation.
Cardiovascular collapse can be the presenting sign of
anaphylaxis. Although signs and symptoms of anaphy-
laxis usually appear within 5 to 30 minutes after
exposure, occasionally, symptoms will not develop for
several hours. Rapid onset of symptoms after exposure is
associated with a more severe and life-threatening course
of anaphylaxis. Between 5% and 20% of patients may
experience a recurrence of anaphylaxis 8 to 12 hours after
the initial presentation [10-12]. Biphasic episodes are
more likely to occur if administration of epinephrine was
delayed or if multiple doses were required to treat the
initial event. About 1% of patients will experience
protracted anaphylaxis with symptoms lasting up to
32 hours. Fatal reactions are more common in the setting
of protracted anaphylaxis [11].
Cutaneous symptoms include urticaria, flushing, and
angioedema. These symptoms occur in over 90% of cases
[8]. Less commonly (2%-5%), pruritus without rash will
occur. Respiratory symptoms occur secondary to airway
edema and bronchoconstriction and include dyspnea,
wheezing (45%-59%), stridor, or dysphonia (20%-50%),
and rhinorrhea (8%-20%). Signs of cardiovascular
involvement include chest pain (6%), hypotension
(15%-30%), and syncope/dizziness (30%-35%). Cardiac
dysrhythmias can occur due to vagal effects or myocardial
112
Table 2 Signs and symptoms of anaphylaxis.
Cutaneous: flushing, pruritus, urticaria, angioedema
Oral: pruritus, edema of lips and tongue, metallic taste
Nasal: pruritus, rhinorrhea, sneezing, congestion
Respiratory: laryngeal edema, dysphagia, dysphonia, chest
tightness, shortness of breath, wheezing, cough
Cardiovascular: faintness, syncope, chest pain,
hypotension, dysrhythmia
Gastrointestinal: nausea, abdominal pain/cramping,
vomiting, diarrhea
Other: feeling of impending doom, sweating, uterine
contractions, incontinence
ischemia. The most frequent gastrointestinal symptoms
are diarrhea and abdominal cramps (25%-30%), most
likely secondary to contraction of smooth muscle in the
gastrointestinal tract and increased mucus secretion.
Nausea and vomiting occur in 20% of cases. Less
common manifestations of anaphylaxis include headache
(3%-5%), blurry vision (1%), and seizures (1%) [8,13].
Many patients report experiencing a feeling of impending
doom at the onset of anaphylaxis.
Differential Diagnosis
Numerous clinical conditions may mimic anaphylaxis,
and it can be difficult to distinguish these entities from
anaphylaxis, especially when a patient is seen after the
episode (Table 3). The diagnosis of anaphylaxis requires
a careful medical history with particular attention to the
circumstances preceding the onset of symptoms, the
order and time course of symptoms, and the response to
treatment. The following cases illustrate some of the
clinical situations commonly mistaken for anaphylaxis.
Case 1
A 16-year-old male adolescent presents to his pediatrician
for his yearly sports physical. While in the office, he
receives his tetanus booster immunization. Five minutes
later, he appears diaphoretic, pale, and complains of
feeling dizzy. He has a syncopal episode in the office. His
vital signs are the following: heart rate, 50; blood
pressure, 85/40 mm Hg; and respiratory rate, 22. He
regains consciousness after being placed in the Trende-
lenburg position but complains of nausea and vomits a
short time later.
The occurrence of a syncopal episode, associated with
a traumatic or painful event accompanied by bradycardia
and hypotension, is characteristic of a vasovagal reaction.
Although diaphoresis, dizziness, hypotension, and syn-
cope can be symptoms of anaphylaxis, the absence of
cutaneous symptoms such as urticaria, flushing or
angioedema, and the presence of bradycardia can dis-
tinguish a vasovagal reaction from anaphylaxis. Typically,
vasovagal reactions result from venous pooling causing a
paradoxical stimulation of the vagal nerve, leading to
L.J. Kobrynski
vasodilation and bradycardia. Generally, the only treat-
ment required is to place the patient in the supine or
Trendelenburg position.
Case 2
A 15-year-old cheerleader complains of the sudden onset
of difficulty breathing during the homecoming football
game. She tells a teammate that her throat feels tight, and
she can’t take a breath. She uses her albuterol inhaler
without relief then collapses on the field. Emergency
medical services are called, and on arrival, they find a
pale, thin girl in moderate respiratory distress. Her heart
rate is 120, respirations are 30 and shallow, and she has
audible inspiratory and expiratory wheezing. Her blood
pressure is normal. She receives oxygen and albuterol and
begins to improve slightly after her second nebulizer
treatment. According to her parents, who arrived in the
emergency department (ED) a short while later, she has
experienced several of these sudden battacksQ since their
divorce 6 months ago.
Acute episodes of dyspnea with wheezing and dizziness
not responsive to albuterol can be seen in patients with
vocal cord dysfunction (VCD). Typically, this entity is seen
in adolescent girls, who are high achievers, with multiple
stressors at home and at school. The symptoms are brought
on by involuntary adduction of the vocal cords, causing
upper airway obstruction with wheezing heard during
both inspiration and expiration. Approximately half of the
patients with VCD will have asthma as well; however,
wheezing episodes due to VCD do not respond to
bronchodilators or corticosteroids. The lack of cutaneous
symptoms and hypotension can help distinguish VCD
from anaphylaxis. The diagnosis of VCD can be confirmed
by direct visualization of the vocal cords during an
episode. During inspiration and phonation of certain
vowel sounds, there is inappropriate adduction of the
Table 3 Differential diagnosis.
Sign/symptom Differential
Hypotension Vasovagal reaction
Hypovolemic/septic shock
Flushing Carcinoid syndrome
Red man syndrome
Scromboid fish poisoning
Monosodium glutamate ingestion
Urticaria Urticaria pigmentosa/mastocytosis
Scromboid fish poisoning
Respiratory distress Asthma exacerbation
(wheezing) Vocal cord dysfunction
Airway foreign body
Angioedema Hereditary angioedema
Serum sickness
Syncope Vasovagal reaction
Pseudoanaphylaxis
(procaine penicillin)
Adapted with permission from Ref. [13].
Anaphylaxis
vocal cords anteriorly with a characteristic diamond-
shaped posterior glottic chink [14]. Spirometry performed
during a symptomatic episode frequently shows flattening
of the inspiratory loop of the flow-volume curve. Therapy
for this disorder must include evaluation and counseling
regarding stressors, as well as the recognition of the cause
of the wheezing and dyspnea. Speech therapy may be
helpful in teaching patients breathing techniques for
relaxing the vocal cords during an episode.
Case 3
A 7-year-old boy presents to the ED with the sudden
onset of flushing of the face and chest and hives over the
torso, headache, and diarrhea. His family had just
returned home after eating dinner at their favorite sushi
restaurant when his symptoms began. According to the
parents, they have eaten at this restaurant before, and he
has eaten fish and shellfish previously without any
problems. During the meal tonight, he ate several pieces
of tuna sashimi and some rice. On exam, he is irritable
and complains of headache and some abdominal pain.
His face and chest are flushed and warm to the touch. He
has some large confluent hives over his trunk and neck.
Respiratory rate is mildly elevated, heart rate is elevated,
and blood pressure is decreased. He has normal breath
sounds. He receives diphenhydramine and a fluid bolus
and begins to feel better within 15 to 20 minutes.
Scromboid poisoning occurs after ingestion of hista-
mine in spoiled fish. The histamine is produced by the
conversion of histidine to histamine by bacteria in the
fish. This occurs after the fish have been caught, primarily
if they are not kept at a cold-enough temperature before
consumption. The fish have a normal smell and taste, and
the histamine is not destroyed by cooking. Scromboid
poisoning is seen mainly after consumption of fish such
as tuna, mackerel, mahi-mahi, or herring [13]. The
severity of symptoms is related to the amount of
histamine ingested, thus, smaller persons are more likely
to experience symptoms. The onset of symptoms occurs
minutes to several hours after the meal, and symptoms
last for several hours. The presence of elevated plasma
histamine without elevated tryptase is consistent with
scromboid poisoning. Treatment with antihistamines and
fluid boluses (if hypotension is present) are helpful in
alleviating the symptoms, although the course is generally
self-limited.
Other flushing syndromes that can mimic anaphylaxis
include bred-man syndrome,Q cutaneous flushing after
administration of vancomycin; carcinoid syndrome, with
release of histamine and other mediators from the
carcinoid tumor; and monosodium glutamate ingestion.
One other condition that can mimic anaphylaxis, with
potentially fatal complications is hereditary angioedema
(HAE). Hereditary angioedema is an autosomal dominant
condition where there is an absence of a functional C1
esterase inhibitor protein (C1INH), leading to the uncon-
113
trolled activation of the complement cascade. This may be
triggered by physical stressors such as an injury, dental
and abdominal surgery, or infection and may also be
triggered by certain medications. Angioedema occurs
without the presence of pruritus or urticaria and can
involve the face, larynx, gastrointestinal tract, and
extremities [15]. Epinephrine has little effect on the
angioedema during an acute attack, and antihistamines
and corticosteroids are also ineffective. Hereditary angioe-
dema is diagnosed by demonstrating a qualitative or
quantitative deficiency of C1INH. Frequently, C4 is
decreased during an acute episode [16]. Androgenic
steroids such as danazol and stanazolol are of limited
usefulness during acute attacks but are effective in
preventing a recurrence. The most promising therapy
for HAE is C1INH concentrates [17], and clinical trials are
underway in this country. Fresh frozen plasma and
antifibrinolytics may also have a role in the acute
management of HAE [16,18]. Airway management is
critical in patients with laryngeal edema, and intubation
should be considered early in the course of the attack.
Diagnosis
The diagnosis of anaphylaxis rests on the pattern of the
clinical signs and symptoms, along with a history of
exposure to a known trigger. Careful attention must be
paid to possible exposures (foods, medications, latex, insect
stings, radiographic contrast media, and blood products)
during the 2 to 4 hours before the onset of symptoms.
Laboratory testing may be helpful in diagnosing some of
the other disorders listed in the differential. An abnormal
C1INH or functional assay, along with a decrease in C4, is
seen in patients with symptoms due to HAE. Patients with
scromboid poisoning may have elevated plasma histamine
levels with normal serum tryptase levels. Blood serotonin
and urinary vanillylmandelic acid will be elevated in
patients with carcinoid syndrome.
A rise in total serum tryptase levels has been reported to
occur in anaphylaxis [19]. Plasma histamine levels rise
within minutes of the onset of symptoms and only remain
elevated for 30 to 60 minutes [20]. Thus, its usefulness as
a diagnostic test is limited. The rise in serum tryptase
occurs within 60 minutes, and levels can remain elevated
for up to 6 hours after the onset of symptoms [20].
However, serum tryptase may not be elevated in food
induced anaphylaxis [21]. Serum tryptase may also be
useful in distinguishing anaphylaxis from systemic mas-
tocyctosis. There are two forms of tryptase in the serum.
Alpha-tryptase is produced and secreted constitutively by
mast cells, whereas beta-tryptase is released during mast
cell degranulation. Therefore, levels of beta-tryptase are
elevated during anaphylaxis and levels of alpha-tryptase
remain elevated in systemic mastocytosis [22].
Following an episode of anaphylaxis, identification of
specific IgE against a suspected trigger, such as a food, an
114 L.J. Kobrynski

insect venom, or a medication, either by skin prick Table 4 Dosing of medications for treatment of anaphylaxis
testing or radioallergosorbent testing (RAST) can help to Drug Dose/route
confirm allergic sensitivity to this agent. The absence of a Epinephrine 1:1000 0.1 mg/kg IM
positive test does not rule out the possibility of an IgG or (max, 0.5 mL)
immune complex mediated reaction and is not helpful for 1:10 000 0.01mg/kg IV over
agents known to cause direct degranulation of mast cells, 1-2 minutes
such as radiocontrast media. Continuous infusion:
0.1Mg/kg/minute
Diphenhydramine 1-1.25 mg/kg (max, 50 mg)
Treatment (H1 blocker) PO/IM/IV
Ranitidine (H2 blockers) 1 mg/kg IV (max, 50 mg)
Rapid initiation of treatment, particularly administration
Cimetidine 4 mg/kg IV (max, 300 mg)
of epinephrine, is essential in the treatment of anaphy- given slowly
laxis. Fatalities may be prevented by the early use of Hydrocortisone 1-2 mg/kg IV
epinephrine. The treatment of anaphylaxis and the (corticosteroids)
drugs and doses employed are presented in Figure 1 Prednisone 1-2 mg/kg PO (max 80 mg)
and Table 4. The immediate interventions should occur mild episodes
nearly simultaneously. Methylprednisolone 1-2 mg/kg IV
Epinephrine should be administered intramuscularly (max 125 mg)
(IM), preferably in the lateral aspect of the thigh. B -Agonists (bronchodilators- 0.25-0.5 ml in 2 ml saline
Absorption occurs more rapidly with IM injection, albuterol)
compared to the subcutaneous route. In addition, Volume expanders (normal 20 mL/kg rapid bolus
saline, Ringer’s lactate)
injection into the lateral thigh results in more rapid and
Dopamine (vasopressor) 5-20 M g/kg/min
higher plasma concentrations than injection into the Glucagon (B -blockade) 1-5 mg IV
deltoid muscle [23]. The initial IM dose can be repeated
at 10- to 15-minute intervals. Intravenous epinephrine is
recommended if there is persistent hypotension and no response to IM administration. Careful monitoring for
arrhythmias is important with use of the IV route.
Epinephrine can also be administered intraosseously or
via the endotracheal tube, or injected sublingually, if IV
access cannot be obtained. In the case of an anaphylactic
reaction after an insect sting or injection of allergen
extract or vaccine, a venous tourniquet should be placed
above the injection site, and epinephrine should be
injected locally to slow the absorption (the tourniquet
should be released every 5 minutes for 2 to 3 minutes and
not used for more than 30 minutes total).
Antihistamines, both H1 and H2 blockers, are useful
adjunctive treatment to epinephrine. They are especially
effective in relieving pruritus and urticaria. The combi-
nation of H1 and H2 agents is superior to the use of an H1
antagonist alone [24]. These agents have a slower onset of
action than epinephrine and should be considered as an
adjunct to epinephrine administration. The main role of
corticosteroids in the management of anaphylaxis is to
prevent recurrence of symptoms or protracted anaphy-
laxis. Administration of corticosteroids is advisable in
moderate to severe cases of anaphylaxis.
Hypotension due to anaphylaxis should be treated by
placing the patient in the Trendelenburg position, unless
respiratory symptoms are prohibitive, and by giving fluid
replacement with a crystalloid solution. Some sources
prefer normal saline over lactated Ringers because it may
potentially contribute towards metabolic acidosis [25].
Up to 30 mL/kg during the first hour may be required for
children. If volume replacement does not correct hypo-
Figure 1 Treatment algorithm for anaphylaxis. tension, IV epinephrine should be administered either as
Anaphylaxis 115

a bolus of 0.1 to 0.3 mL of 1:10 000 dilution given over reactions involving cutaneous symptoms without respira-
several minutes or as a continuous infusion of 0.1 lg/kg tory difficulty. If symptoms progress, or if there is a history
per minute with a maximum dose of 10 lg/min. of rapidly progressing symptoms, epinephrine should be
Alternately, a dopamine infusion of 5 to 20 lg/kg/min administered as well.
can be used for refractory hypotension. Other important preventative measures include the
Patients taking a b-adrenergic blocking medication can following:
have protracted anaphylaxis, often refractory to epinephr-
ine treatment. In this case, glucagon has been shown to be – Wearing a medical alert bracelet
– Providing the family, daycare, and school with an
effective in the treatment of hypotension through its
emergency plan (Fig. 2) [29]
inotropic effects. An IV bolus of 1 to 5 mg can be followed
– Administering drugs by the oral route, rather than
by an infusion of 5 to 15 lg/min [26].
IV
Any patient presenting to the ED for treatment of
– Providing schools and daycare centers with
anaphylaxis should be observed for a period of time
detailed instructions regarding food avoidance
depending on the severity of the reaction. For mild cases,
– Avoid the use of b-blockers and angiotensin-
2 hours may be sufficient. Patients with severe anaphy-
laxis, with respiratory compromise and hypotension, converting enzyme inhibitors
– Desensitization for specific medications if no
should be observed in the hospital overnight. This is
alternatives are available
essential because of the risk of a biphasic reaction, which
– Immunotherapy for insect venom
occurs in 6% of cases [11]. Medications needed for the
– Pretreatment with antihistamines and corticoste-
resolution of the symptoms (antihistamines, H2 blockers,
roids before the use of radiocontrast media.
corticosteroids) should be continued for 24 to 48 hours
after discharge. Referral to an allergist is recommended to (1) assist in
counseling the patient regarding avoidance measures,
particularly for foods and insects; (2) assist in the
Discharge
It is very important that patients are instructed in
measures to prevent a recurrence and to provide the
patient and family with the tools (education and a
preloaded epinephrine autoinjector syringe) necessary
to treat future episodes, should they occur. In cases where
the trigger is fairly certain, such as a food, medication, or
insect sting, complete avoidance is an absolute necessity.
Confirmation of IgE-mediated hypersensitivity can be
made through skin prick testing or RAST testing. In cases
where the trigger is unknown, allergy testing may be
useful in identifying possible allergic triggers. Although a
blood sample for RAST testing can be obtained in the ED
during the acute event, skin prick testing should not be
done for at least 2 weeks after the anaphylactic reaction
due to a refractory period that can occur resulting in
anergy to the triggering agent.
Because 30% to 35% of patients will have a recurrence
[27,28], all patients should be instructed in the proper use
of a preloaded epinephrine syringe and provided with a
prescription for this medication before discharge from the
ED or hospital. Epinephrine autoinjectors should be kept
readily available at home, school, daycare, camp, and
sporting events. The family should be instructed to use
epinephrine in cases of anaphylaxis involving any respi-
ratory difficulty or angioedema of the airway, which is
demonstrated by hoarseness, stridor, drooling, or swelling
of the tongue. Once epinephrine is administered, the
patient should be immediately transported to the nearest
ED. The family should also have diphenhydramine
(liquid) available in case of a milder reaction and should Figure 2 Emergency action plan. Adapted with permission from
be instructed to give this as the first line medication for Ref. [29].
116
identification of possible triggers; (3) provide further
education regarding management of anaphylaxis; and (4)
determine if desensitization (eg, penicillin) or immuno-
therapy (eg, insect venom) is indicated and to begin
therapy [13].
Summary
Anaphylaxis remains a serious, frequently underrecog-
nized problem, which is eminently treatable given prompt
recognition. Fortunately, fatalities due to anaphylaxis are
uncommon. The risk of fatality is increased in patients
with asthma, in cases where the triggering agent was
injected intravenously and when the administration of
epinephrine is delayed. Physicians should be familiar with
the signs and symptoms of anaphylaxis and the conditions
which mimic anaphylaxis in order to initiate prompt life-
saving treatment. However, the role of the ED physician
does not stop after the symptoms have subsided. It is
imperative that patients receive education before discharge
to help prevent and treat recurrence of anaphylaxis. Early
treatment of symptoms with epinephrine is life-saving, and
all patients who have experienced an episode of anaphy-
laxis should carry an epinephrine autoinjector syringe.
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