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7/24/2019 Allergic Emergencies and Anaphylaxis How To Avoid Getting Stung.pdf
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reactions are usually responses to inhaled antigens,
particularly house dust mites. However, allergies are
also responsible for at least 400-800 deaths in the
United States each year.4,5Recent studies suggest that
there may be 30 cases of anaphylaxis per year per
100,000 individuals.6 In northern climates, anaphylaxis
is most common in the summer months, reflecting the
impact of insect stings.
Pathophysiology: A Simple Primer
Allergic reactions are developed hypersensitivities to
antigens.Antigens are proteins recognized by the
human host as foreign. Alternatively, haptensare
incomplete antigens incapable of causing allergic
reactions, but which become antigenic when bound to
certain proteins. Allergies develop by recurrent
exposure to antigens over time. There is a strong
familial tendency toward atopic disorders linked
to a histocompatibility locus on chromosome 11. 7,8
However, the precise mechanisms that prompt the
immune system to identify antigens as foreign are
not well understood.
The Immune ResponseClassical allergy, also termed immediate hypersensitivity,
is an immune-mediated reaction. The classification
system proposed by Gell and Coombs distills this
complex response into four categories. (SeeTable 1.)
With hypersensitivity, antigen-processing cells (i.e.,
macrophages and other cell types) recognize some
allergens as foreign. They release cytokines and other
mediators to transform B-lymphocytes into plasma
cells, which in turn produce antigen-specific immuno-
globulin.9Antibodies of the IgE class and IgG 4subclass
are most important in the pathogenesis of allergy.10,11T
helper and suppressor cells modulate the production of
these antibodies. (See Figure 1.)
IgE antibodies bind to the cell membranes of
receptor cells, mainly mast cells and basophils. There,they lie in wait for antigens. When subsequent antigen
contact occurs, these receptors are activated via adenyl
cyclase inhibition, calcium channel stimulation, and
other mechanisms. In response, the cells release
preformed mediators as well as producing secondary
agents.12These include such substances as histamine,
leukotriene C4, prostaglandin D2, and tryptase.
Stimulation of the production and release of
inflammatory mediators may bypass the IgE-mediated
pathways. For example, anaphylactoid reactionsrelease
Table 1. Classification Of Immunologic Reactions(Gell And Coombs).
Type Mediator Reaction
I IgE (Rarely IgG4) Immediate
II IgG, IgM (Cell-Ag) Cytotoxic
III Ag-Ab complexes Immune complex
IV T cells Cell-mediated
Note: This classification is an oversimplication.
Adapted from: Middleton E Jr., et al. Allergy: Principles and Practice.St. Louis: Mosby; 1998.
Figure 1. Sensitization Phase Of Allergy (Antigen-Induced Immune Stimulation).
(Genetic predisposition)
T suppressor cells
Cytokinesproduced
Antigen-specific IgE Plasma cells
B cells activatedT helper cells activated
Antigen Processing Cell(macrophage and others)
Allergen
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Urticaria is both the mildest and most common
type of systemic allergic reaction. Also termed hives,
urticaria presents as well-circumscribed, pruritic
wheals involving the superficial dermis. Urticaria
occurs in up to 20% of people during their lifetimes,
and is termed acute if it lasts less than six weeks.15
Angioedema involves the deeper layers of the
skin, including subcutaneous tissue, and presents as
well-demarcated localized edema. The skin, gas-
trointestinal tract, and upper airway are most com-monly involved. Respiratory tract angioedema is
potentially fatal. Hereditary angioedema (HAE) is an
autosomal dominant condition caused by lack of a
functional C1 esterase inhibitor.16The facial, airway, or
extremity edema is often associated with abdominal
pain, nausea, vomiting, and diarrhea.
Anaphylaxis is a clinical syndrome characterized
by a severe reaction of multiple organ systems to an
antigen-induced, IgE-driven mediator release in
previously sensitized individuals. Hypotension,
bronchoconstriction, and severe upper airway obstruc-
tion are presenting components of anaphylaxis.
Individuals with anaphylaxis may have one, two, or all
of these conditions. (SeeTable 3.)
Causes Of Hypersensitivity Reactions
Table 4 presents a list of some causes of hypersensitiv-
Mast Celland
Basophil
Classic Allergic Reaction Late-Phase Reaction
Flushing Eosinophil infiltration
Hypotension Neutrophil infiltration
Increased mucus production Fibrin deposition
Pruritis Mononuclear infiltration
Smooth muscle contraction Tissue destruction
Vascular leakage
Minutes Hours
Figure 3. Time Course Of Allergic Reaction. Table 2. HypersensitivityReactions.
Hypersensitivity reactions canbe of varied severity, depend-
ing upon:
Degrees of hypersensitivity Specific IgE concentration
Allergen affinity
Number of mast cellsand basophils
Quantity, route, and rate ofantigen exposure
Pattern and quantity ofmediator release
Target organ sensitivityand responsiveness
Table 4. Causes Of Hypersensitivity Reactions.*
IgE Mediated
Drugs (e.g., antimicrobials, nonsteroidals)
Food (e.g., peanuts, tree nuts, fish, shellfish, eggs, certain
fresh fruits)
Environmental (e.g., house dust mites, pollens, molds, otherinhaled proteins)
Soaps, lotions, detergents
Envenomations (e.g., Hymenoptera)
Snake antivenin
Latex
Miscellaneous: cold, light, vibration, pressure, exercise
Non-immunologic Causes
Drugs (e.g., narcotics, neomycin, d-tubocurare, salicylates,nonsteroidals)
Radiocontrast agents
*This list is not intended to be all-inclusive.
Table 3. Frequency Of Occurrence Of SignsAnd Symptoms Of Anaphylaxis.
Signs/Symptoms Percent
Urticaria and angioedema 88%
Dyspnea, wheeze 47%
Dizziness, syncope, hypotension 33%
Nausea, vomiting, diarrhea, cramping abdominal pain 30%
Flush 46%
Upper airway edema 56%
Headache 15%
Rhinitis 16%
Substernal pain 6%
Itch without rash 4.5%
Seizure 1.5%
Adapted from: Middleton E Jr., et al. Allergy: Principles and Practice.St. Louis: Mosby; 1998.
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ity reactions. A wide variety of allergens is responsible
for anaphylaxis; some are widespread, such as peanuts
or shellfish, while others are sporadic, including
reactions to vaccines or even semen. The most common
precipitants in children include foods (57%), drugs
(11%), Hymenoptera venom (12%), exercise (9%),
idiopathic (6%), vaccines (2%), additives (1%), specific
immunotherapy (1%), and latex (1%).17
EnvenomationsThere are slightly fewer than 100 cases of sting-related
deaths in the United States each year. Hymenoptera
(e.g., wasps, bees, and fire ants) venom precipitates
serious systemic reactions in 1-3% of patients.18 Once a
patient has a severe systemic reaction from a Hy-
menoptera sting, up to 35-60% will experience anaphy-
laxis to a subsequent sting.19,20Other arthropods
besides Hymenoptera can cause anaphylaxis, including
the kissing bug and a variety of ticks.
Drugs And MedicationsWhile numerous medications can cause allergic
reactions, the most important drug allergy involves
penicillin. Penicillin is responsible for three-quarters of
all deaths from drug-related anaphylaxis. Fatal
anaphylaxis occurs approximately once per 7,500,000
exposures, leading to approximately 100 deaths each
year in the United States.21Parenteral (IM or IV)
penicillin is much more likely to produce anaphylaxis
than orally administered drugs. In fact, only six
fatalities have ever been reported with oral penicillin.22
While penicillin allergy may be more frequent in
people with atopy, a family history of penicillin allergy
does not predict individual sensitivity.
Not all adverse reactions patients experience in
regards to the beta-lactam drugs are allergic in nature.
In particular, most children who develop erythematous
rashes associated with amoxicillin are able to tolerate
beta-lactams and even amoxicillin without problems in
10 Allergy Pearls
1. Hypoxia k ills. Hoarseness or stridor should prompt
immediate concern about a severe hypersensitivity
reaction. Use epinephrine and supplemental oxygen
in this setting and determine the need for intubation.
2. Treat shock. Give small, repeated aliquots of IV
epinephrine to patients in shock. Subcutaneousepinephrine is inadequate.
3. Recognize limits. Antihistamines and steroids may
not be effective in managing acute angioedema.
4. Whos in tr ouble? Voice change, hoarseness, stridor,
and dyspnea suggest the need for airway control in
patients with angioedema. Palatal edema is an
ominous sign in all allergic reactions.
5. Its a famil y affair. Hereditary angioedema presents
with recurrent extremity, gastrointestinal, and upper-airway edema without urticaria. A family history of
similar problems is an important hint. Treat hereditary
angioedema with fresh frozen plasma.
6. Around the blo ck. Patients with allergic reactions
who are on beta-blockers may not respond to
standard therapy. Remember glucagon for serious
hypersensitivity, as well as inhalational ipratroprium if
bronchospasm predominates.
7. Prevention. Prevention of further allergic reactions is
key. Referral for immunotherapy is important for
systemic hypersensitivity reactions to Hymenoptera
stings, including bees, wasps, and fire ants.
Recognition of the precipitating agent or event
requires a careful historythen educate the patient
on future avoidance.
8. Self-stimulation. Epinephrine self-injectable
syringes save lives if patients have serious allergic
reactions outside the hospital. Give a prescription for
several, so the patient can store them in different
placeshome, car, work, and so on. Teach the patient
how and when to use it.
9. Allergy is an acquir ed disorder. Patients who
state or think they cannot be allergic to something
because they have taken it before without problems
often are making a critical mistake. Patientsmay develop angioedema after discontinuing an
ACE inhibitor.
10. Be suspicious . Remember to include anaphylaxis
in the differential diagnosis of shock. Hypotension
with isolated difficulty breathing, chest pain,
back pain, and subtle angioedema often are not
recognized as early anaphylaxis. Delays in
diagnosis can be fatal.
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the future.23In one study of 86 consecutive children
with antibiotic use for upper respiratory infection who
developed a rash, 80% were younger than 3 years of
age. Most (85%) had nonspecific erythematous rash,
but 15% had an urticarial rash. When these patients
were re-challenged with the suspected antibiotics
while healthy, none developed rash.24
A particularly interesting reaction to procaine
penicillin is Hoignes syndrome. This dramatic but
non-allergic phenomenon is an idiosyncratic responseto procaine (Bicillin C-R, Wycillin) characterized
by psychosis, anxiety, hallucinations, hypertension,
and tachycardia.25Patients who suffer this effect
do not need to avoid beta-lactams in the future
(only procaine).
Penicillin Allergy And Cephalosporin Use
Penicillin allergy is an absolute contraindication to
cephalosporin use only if severe angioedema or
anaphylaxis occurs with penicillin. Estimates of cross-
sensitivity of cephalosporins and penicillins vary
widely, ranging from 2% to 16%.26However, even in
patients with a stated penicillin allergy, true anaphy-
laxis to cephalosporins is extremely rare (< 0.02%).27
In fact, cross-reactions appear limited to patients given
first-generation cephalosporins; studies of second-
and third-generation cephalosporins show no increase
in allergic reactions in patients who have a history
of penicillin allergy.27In addition, penicillin skin
tests do not predict the likelihood of allergic reactions
to cephalosporins in patients with histories of penicil-
lin allergy.
Aspirin And Nonsteroidal Anti-inflammatory Drugs
Certain agents precipitate hypersensitivity reactions byaltering arachidonic acid metabolism (e.g., salicylates
and nonsteroidals). These drugs inhibit the degrada-
tion of arachidonic acid by cyclooxygenase, allowing
production of more inflammatory allergic mediators
through an alternate lipoxygenase pathway. The new
cyclooxygenase II inhibitors appear to avoid this
biochemical problem.
Aspirin and older NSAIDs remain an important
cause of serious allergic reactions. These drugs may
precipitate bronchospasm in as many as 20% of
asthmatic patients.28A history of nasal polyps may
increase the likelihood of an allergic reaction.
Illicit DrugsA substantial number of hypersensitivity reactions are
non-immunologic and precipitated through direct
mediator release from effector cells.29 For example,
injecting opiates into an upper-extremity vein may
cause swelling and erythema in that arm. Smoking
crack cocaine can produce a pulmonary syndrome of
crack lung,characterized by fever, eosinophilia, and
pulmonary infiltrates.30
LatexTwo-thirds of latex reactions are mild and local (e.g.,
hand erythema and itching), but some patients develop
fatal anaphylaxis.31Latex sensitization has been
reported in about 2.6% of nurses, 9% of surgeons, and
29% of spina bifida patients. In one study of dental
students, 10% developed some form of latex sensitivity
by the end of their four years of training.32 Children
with spina bifida can have such frequent and striking
hypersensitivity reactions to latex that a joint councilsuggests that they have all medical, surgical, and
dental procedures performed in a latex-controlled
environment regardless of a history of latex allergy.33
Radiocontrast MediaAs with latex and medication allergies, anaphylaxis
due to radiocontrast media is an important iatrogenic
affliction. While the vast majority of these reactions
are not immunologic in nature, a few patients may
have an IgE-mediated component to radiocontrast
allergy.34 One to two percent of patients exposed to
these agents suffer an anaphylactoid reaction, with
fatal results in 1 per 50,000-100,000.35This adds up to
an estimated 2667 reactions with 500 deaths annually
in the United States.36
Risk factors for radiocontrast reactions include
previous allergic reactions to these agents (35%
recurrence rate), history of atopy, shellfish allergy,
increased age, dehydration, renal or hepatic dysfunc-
tion, and cardiac disease. Other considerations
involve dye factors such as dose, osmolality, or ionic
content.37A history of asthma or use of beta-blockers
may be among the strongest predictors of a contrast-
associated reaction.38
Methods of risk reduction for radiocontrastreactions include using another imaging technique that
does not involve these agents, using nonionic low-
osmolality agents, and pre-treating 12-24 hours prior to
dye load.39Administering diphenhydramine 1 mg/kg
every six hours and prednisone 1 mg/kg over that
period reduces the reaction rate to radiocontrast media
to under 5% for patients with previous reactions.40One
study demonstrated a very low reaction rate if low-
osmolality, non-ionic agents were used.41However, the
costs associated with these more expensive imaging
dyes are substantial.41
Food AllergiesFood allergies are the predominant cause of anaphy-
laxis seen in the ED.42While food allergy occurs in
about 1.4% of young children and 0.3% of adults, most
reactions are minor.43
Anaphylactic reactions to foods usually occur
immediately after the food is ingested.44Of interest, as
many as one-third of patients with food allergy
demonstrate a biphasic reaction. Many can experience
prolonged symptoms, lasting as long as several
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weeks.45Some food allergies occur only when particu-
lar food is followed by exercise.46In addition to
causing urticaria or respiratory symptoms, food
allergens frequently precipitate a gastrointestinal
insurrection. Patients typically complain of nausea,
vomiting, abdominal cramping, and/or diarrhea.
Some food hypersensitivity reactions are due to
agents added during food production (e.g., penicillins
and sulfites). A limited number of foods are respon-
sible for the vast majority of food-induced allergicreactions. In children, the culprits include milk, eggs,
peanuts, fish, and tree nuts; in adults, prime offenders
consist of peanuts, tree nuts, fish, and shellfish.47As
the American palate expands toward the gourmet,
emergency physicians are seeing reactions to new
foods, such as kiwi-chamomile tea. Peanut allergies are
both common and severe, leading some airlines to stop
serving this staple as the in-flight snack. Of all aller-
gies, however, some consider beer anaphylaxis to be
the most tragic.48
There are several interesting non-allergic food
reactions known collectively as the restaurant syn-
dromes.The Chinese restaurant syndrome is a
reaction to MSG that consists of chest pain, facial
burning, flushing, paresthesias, sweating, dizziness,
headaches, palpitations, nausea, and vomiting. Symp-
toms usually begin during or shortly after the meal but
can be delayed for up to 14 hours.49
Scombroid poisoning occurs after eating spoiled
fish, usually tuna, mackerel, or mahi-mahi (dolphin).
Symptoms include flushing (usually a sunburn-type
rash), urticaria, headache, nausea, vomiting, and
abdominal cramping.50This reaction due to
histamine-like toxins can be treated with diphenhy-
dramine or cimetidine.
Exercise
Other poorly understood mechanisms cause directmediator release from allergy effector cells. Exercise-
induced allergy is usually limited to urticaria and nasal
congestion, but some reactions are fatal.39More than
50% of patients with exercise-induced reactions have
atopy, and more than half of those with exercise-
induced anaphylaxis develop the syndrome only if
they ate just prior to marked exertion.51Prevention
includes modifying the exercise activity, avoiding
high-risk foods within four hours of exercise, and
prophylaxis with antihistamines and leukotriene-
receptor antagonists.
Diagnosis Of Hypersensitivity Reactions
The diagnosis of an allergic reaction often depends
upon the patient drawing a connection between an
exposure and subsequent hives or wheezing. However,
making the correct diagnosis is complicated when
Table 5. Diagnosis Of Hypersensitivity Reactions.
History
Precipitating event:Medications, including OTCs (especially NSAIDs)
Foods (peanuts, nuts, fresh fruits, fish, shellfish,eggs, milk)
Environmental exposures
Physical agents/events
Previous episodes:
Frequency
Duration
Effects of treatment
Physical Exam
Vital signs
Skin
Urticaria
Angioedema
Upper respiratory tract
Rhinitis
Oral and laryngeal edema
Lower respiratory tract
Bronchospasm
Increased secretions
Cardiovascular
Hypotension
Tachycardia (rarely bradycardia)
Dysrhythmias
Cardiac arrest
Gastrointestinal tract
Abdominal colic
Vomiting (nausea)
Diarrhea
Central nervous system
Confusion
Agitation
Coma
Eyes
Conjunctivitis
Chemosis
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chest discomfort, back pain, or vascular collapse occurs
in isolation, especially if the patient is confused or
moribund. Serious allergic reactions may occasionally
be confused with vasovagal episodes after an injection,
sting, or other exposures.
Although identifying the etiology often depends
on an appropriate history, a physical exam demonstrat-
ing urticaria, angioedema, bronchospasm, or vascular
collapse provides a compelling diagnostic picture.
(SeeTable 5.) Occasionally, therapeutic intervention
must be based on the physical findings alone; clinical
improvement with therapy may be the best and only
diagnostic confirmation.
HistoryThe single most important question to ask of a
patient with an allergic reaction is How is your
breathing?The inability to answer this question
speaks volumes. Syncope and dyspnea are the most
acutely worrisome complaints during an allergic
reaction. Other symptoms with dangerous overtones
include hoarseness, a lumpin the throat, chest pain,or trouble swallowing.
The next priority is to determine the time course of
the reaction. Most people likely to die of anaphylaxis
have dramatic progression of symptoms. Severe
reactions are characterized by shortness of breath,
syncope, or lightheadedness within 30 minutes of
exposure. The more rapid the progression of symp-
toms, the greater the need for emergency intervention.
Many patients with allergic reactions complain of
generalized pruritus in addition to real or imagined
swelling of various body parts. Gastrointestinal
symptoms are frequent, and may include crampy
abdominal pain, nausea, vomiting, and diarrhea. Yet,while skin and respiratory complaints are common,
some patients with severe allergic reactions may have
no pruritus or dyspnea. Anaphylaxis can produce
isolated cardiovascular collapse.52
Identifying The Agent
Clearly, the physician would like to identify the
inciting agent. Recognizing the precipitant (seeTable 4)
of a hypersensitivity reaction can prevent or ameliorate
subsequent episodes by avoidance or possibly immu-
notherapy. Patients who believe they have had an
allergic reaction are eager to provide a variety of
theories as to the possible allergen. Unfortunately,because the tempo of allergic reactions is so var iable,
the assumed connection between an exposure and a
reaction may be misleading. Certainly, a list of medica-
tions and new environmental exposures (soaps,
perfumes, foods, and so on) is helpful. A careful
inventory must include over-the-counter (OTC)
medications, which many patients fail to recall unless
prompted. It is important to realize that anyone may
become sensi tized to almost anything, even after
decades of tolerance. The fact that they never had a
reaction to shellfish in the past does not eliminate
shellfish from the list of current suspects.
Past Medical And Family History
Past medical history is important, particularly the
history of prior allergic reactions. If the patient re-
counts a distant history of sulfa allergy, this may
incriminate a current drug such as Silvadene cream.
Family history of drug allergies is less significant. The
fact that the patient has a family history of penicillin
allergy may increase the possibility of multiple drug
allergies, but not necessarily penicillin.53
Physical Exam inat ion
The physical exam in hypersensitivity reactions should
initially focus on the immediate life threatslaryn-
gospasm and hypotension.
Airway
Evaluate the patient for stridor, drooling, and signs of
respiratory distress. The patient in extremis may be
bolt upright, strap muscles bulging, and ribs retracting.An inability to speak, muffled voice, or hoarseness
may reflect the need for urgent intubation. Ask the
patient to open his or her mouth, if he or she is able.
Palatal edema is an important sign that may presage
laryngeal edema. Upper airway edema is present on
autopsy in about 60% of fatal cases.54Visualization of
the cords with a fiberoptic scope or ENT mirror may be
helpful in some cases if suspicion for laryngeal edema
is high despite a normal palate. Upper respiratory
findings in allergic reactions include rhinitis and
laryngeal edema.
Some patients with psychological problems
present with factitious stridor, known asMunchausensstridor. These patients intentionally adduct their vocal
cords and can appear to be in profound respiratory
distress. Indirect laryngoscopy can reveal the non-
anatomic nature of the stridor. Or more simply, ask the
patient to cough during the acute episode, which may
cause the stridor to disappear for a brief period.55
Breathing
The patient with laryngospasm may demonstrate a
paradoxical torso movement, with sternal collapse
accompanied by abdominal distention on inspiration.
Tachypnea may represent bronchospasm or can be due
to increased metabolic demand. Bronchospasm withincreased airway secretions reflects lower airway
involvement. Wheezing is frequent in severe reactions,
and should be distinguished from stridor, which is a
more ominous sign. Stridor tends to be loudest over
the larynx or sternal notch, while wheezing is more
prominent in the lateral fields.
Circulation
Severe hypersensitivity reactions may present with
circulatory collapse, hypoperfusion, and tachycardia.
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However, the moribund patient may be bradycardic,
and dysrhythmias are seen in some cases. Quickly
determine the presence of shock by evaluating pulses,
skin perfusion, and mental status.
Skin And M ucous Membra nes
The most typical manifestations in allergy are found by
carefully evaluating the skin and upper respiratory
tract. Isolated urticaria or angioedema may be early
signs of a serious allergic reaction, especially if it
involves the lips, tongue, or palate. Detection of
urticaria may require palpation in dark-skinned
patients. Some patients with urticaria demonstrate an
unusual skin reaction called dermatographism.
Drawing on their back with a finger will cause the skin
to develop wheals in the stimulated area. Acute
conjunctival hyperemia and swelling of the sclera
(chemosis) also suggests an allergic reaction. (SeeTable
5.) Angioedema may be difficult to recognize in its
early stages, and the patient or family may be most
helpful with confirming early changes.
Laboratory EvaluationThe laboratory evaluation of allergic reactions in the
ED has limited utility. Define the level of oxygenation,
realizing that hypoperfusion may limit the ability of
pulse oximetry to accurately report oxygen saturation.
Consequently, arterial blood gas (ABG) analysis may
be more useful than pulse oximetry in anaphylactic
shock. Metabolic acidosis is common in severe anaphy-
laxis.56Other laboratory tests available to the emer-
gency physician are not useful in the initial evaluation
of hypersensitivity reactions but may be used to
eliminate alternate diagnoses.
While the emergency physician is concerned with
stabilizing the patient, a future consulting physician
will likely be concerned with the etiology of the
patients reaction. Allergists believe that tests which
confirm an event as allergic can have future utility.
Serum histamine peaks early and transiently, and for
this reason is unlikely to be helpful. Serum tryptase
levels, however, peak 1 to 1.5 hours after the onset of
anaphylaxis and remain elevated far longer than
Table 6. Differential Diagnosis Of Anaphylaxis And Anaphylactoid Reactions.
Physical factors
Exercise
Cold, heat, sunlight
Airway disease
Reactive airway disease
Epiglottitis
Foreign body
Pulmonary embolism
Cardiovascular disease
Dysrhythmias
Myocardial ischemia
Capillary leak syndrome
Flush syndromes
Carcinoid
Postmenopausal
Chlorpropamidealcohol
Medullary carcinoma thyroid
Restaurant syndromes
Monosodium glutamate (MSG)
Scombroid poisoning
Sulfites
Shock
Hemorrhagic
Cardiogenic
Endotoxic
Excess endogenous production of histamine
Systemic mastocytosis
Urticaria pigmentosa
Leukemias
Psychiatric disease
Panic attacks
Munchausens stridor
Neurologic
Vasovagal syncope
Seizure
Stroke
Drug reaction
Red man syndrome (vancomycin)
Reaction to anti-seizure medication
Miscellaneous
Hereditary angioedemaProgesteroneanaphylaxis
Urticarial vasculitis
Pheochromocytoma
Hyperimmunoglobulin E, urticaria syndrome
Adapted from: Middleton E Jr., et al. Allergy: Principles and Practice.St. Louis: Mosby; 1998.
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plasma histamine. Elevated tryptase levels persist
for five hours after the onset of symptoms.57However,
the utility of this test for emergency management
remains unknown.58
Differential Diagnosis
A number of disorders mimic allergic reactions. (See
Table 6.) Necrotizing vasculitis, erythema multiforme,
and serum sickness may cause urticaria. Cutaneousmastocytosis is a rare disorder that causes reddish-
brown macules and papules that develop urticar ia and
itching if traumatized. Systemic mastocytosis is
another rare disorder that causes episodic flushing
with or without urticaria.
Angioedema is most commonly allergy-mediated,
but it also may occur in its acquired and hereditary
forms. Hereditary angioedema is due to a deficiency of
C1esterase inhibitors. Hereditary angioedema is
suggested by a family history (i.e., autosomal domi-
nant inheritance), absence of urticaria and itching,
prominence of recurrent self-limited attacks of circum-
cised subepithelial edema of the skin, and involvement
of the gastrointestinal tract (e.g., abdominal colic) and
upper respiratory tract (e.g., airway angioedema).59
It is usually a clinical diagnosis, because the definitive
test, a functional assay of C1esterase inhibitor, is
not rapidly available. Recognizing hereditary an-
gioedema is very important because it is not respon-
sive to epinephrine, antihistamines, or corticosteroids.
Fresh frozen plasma infusion will abolish acute
episodes, and danazol reduces attack frequency.
Acquired angioedema may occur with some
lymphoproliferative disorders.
Angiotensin-converting enzyme (ACE) inhibitors
may produce angioedema, predominantly of the upper
airway. This idiosyncratic reaction may begin soon
after starting the medication or suddenly arise after
years of symptomless use. This disorder responds
poorly to standard allergic therapy and is mainly due
to unmetabolized kinins.60 Aggressive airway manage-
ment is particularly important because serious upper
airway angioedema may threaten the ability to breathe.
Occasionally, urticaria and angioedema must be
differentiated from contact sensitivity, which is a
localized, vesicular eruption progressing to chronic
skin thickening with continued allergen exposure.
Atopic dermatitis occasionally mimics hypersensitivity
reactions.61 The lack of abrupt-onset or migratory
patterns common with typical urticaria may signify a
non-allergic disorder.
Treatment Of Allergic Reactions
The major causes of death from hypersensitivity
reactions are respiratory failure and circulatory
collapse. Consequently, identify and treat shock and
respiratory insufficiency. Patients with severe reactions
need emergent resuscitation and require a team
approach. Monitoring should include ECG leads, pulse
oximetry, and serial automated blood pressure mea-
surements. Invasive hemodynamic and urine output
monitoring are important in severe hypersensitivity
reactions, particularly in the elderly and those with
significant concomitant medical problems.
AirwayThe most immediate threat to life in an allergic
reaction is upper airway obstruction. If the patient
is not profoundly hypotensive, allow him or her to
Cost-Effective Strategies In DealingWith Acute Allergic Reactions And Angioedema
1. Do not order radiographs or laboratory tests in most
patients with acute allergic reactions.
Laboratory tests (e.g., CBC and electrolytes) are
not usually indicated in patients with acute
allergic reactions.
Risk M anag ement Caveat : Laboratory tests may be useful
in diagnosing maladies that mimic allergic reactions.
For example, shortness of breath may be due to cardiac
ischemia or acute anemia, in which case an ECG or stat
hemoglobin may be helpful.
2. Do not order chest x-rays in patients with acute
allergic reactions and mild respiratory distress.
In many cases, respiratory distress in mild allergic
reactions is due to bronchospasm. This can be treated
effectively with nebulized beta-adrenergic agonists.
Risk M anag ement Caveat : A chest radiograph may be
used to exclude pneumonia and pneumothorax in
patients with atypical presentations for allergy.
3. Use less expensive, generic medications.
Many patients can be treated effectively with generic
diphenhydramine and cimetidine, rather than more
expensive H1and H
2antihistamines. In fact, most of the
studies regarding H1and H
2blockers in allergy were
done using diphenhydramine and cimetidine.
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sit upright and make best use of his or her respiratory
mechanics. All dyspneic patients require 100%
oxygen by face mask. Heliox may improve
ventilation in severe airway compromise
by reducing airway turbulence.
Some patients may require urgent or emergent
intubation; however, massive swelling of the tongue
or upper airway may pose a nightmarish scenario
for the emergency physician. Orotracheal intubation
is usually preferred to the nasotracheal route because
mucosal edema may limit success and cause bleeding
during the latter approach. If time permits, look at
the back of the patients throat. If you are unable to
see the entirety of the soft palate, the intubation will
be challenging.62
Rapid-sequence intubation (RSI) is the most
commonly employed approach to emergency intuba-
tion. However, it may create special problems in the
patient with pronounced airway edema. If a breathing
patient is given paralytics but is unable to be intubated
secondary to distorted anatomy associated with
anaphylaxis, upper airway obstruction may render thebag valve mask useless. There are several alternatives
to RSI in the patient with airway edema. Awake
intubation is often suggested. If time permits, such
patients may be pretreated with nebulized lidocaine to
anesthetize the airway and with a sedative agent as
indicated. Fiberoptic nasotracheal intubation is another
alternative. The emergency physician may decide to
involve the anesthesiologist in this procedure depend-
ing upon his or her degree of experience with this
technique. If RSI is ultimately chosen for the patient
with airway edema, be prepared to perform an imme-
diate cricothyroidotomy if intubation fails. Being
prepared in this instance involves applying Betadine tothe patients neck and having an opened
cricothyroidotomy tray at the bedside. (Dont let the
patient see the tray, especially if the Betadine on their
neck alarms them.)
Epinephrine is an important adjunct in
patients with upper airway edema, as described
in subsequent sections.
BreathingWhile patients with anaphylaxis certainly demonstrate
wheezing, most profound respiratory distress is due
to upper airway problems rather than bronchospasm.
As with all aspects of anaphylaxis, epinephrine byany route can decrease the bronchospastic component
of this disease. Inhaled epinephrine may be useful
in mitigating both bronchospasm and laryngeal
edema (i.e., 0.5 mL of epinephrine nebulized in 2.5
mL of saline).63
Other inhaled sympathomimetics such as albuterol
and metaproterenol are useful for allergy-induced
bronchospasm. Nebulized ipratropium bromide
(Atrovent) will also ameliorate bronchospasm, particu-
larly in allergy patients on beta-blockers. While often
recommended by older textbooks for allergic broncho-
spasm, there is no empiric evidence for the use of
aminophylline in anaphylaxis.
CirculationAfter airway obstruction, shock is the most likely cause
of death from anaphylaxis. Hypotensive patients
require large-bore IVs and aggressive resuscitation.
Epinephrine is the drug of choice in severe allergic
emergencies. Epinephrine has alpha-agonist activity
that improves vascular tone, and beta activity that
bronchodilates and stimulates the heart. In addition,
epinephrine blocks the release of allergic mediators
through cyclic-AMP stimulation.
There are no absolute contraindications to the use o f
epinephrine in a true anaphylactic emergency. Epinephrine
is safe even for older adults. In one study on asthma,
patients as old as 96 years of age were safely given
three doses of epinephrine. In this study there was no
significant difference in ventricular arrhythmias
between patients younger than 40 vs. those older than
40 years old, and the mean arterial pressure, heart rate,and respiratory rate decreased with treatment in the
older population.64
In mild-to-moderate reactions where peripheral
perfusion is maintained, give epinephrine subcutane-
ously or intramuscularly at 0.01 mg/kg (i.e., 0.1 mL/
kg) up to 0.3 to 0.5 mg (1:1000 solution=1 mg/mL).
Some authorities believe that the IM route is so
safe and effective that the subcutaneous route
should be abandoned.65
The appropriate dose, concentration, and route of
epinephrine delivery in anaphylactic shock have not
been studied. The following recommendations are
based on non-peer-reviewed, published recommenda-tions and the experience of the authors. In more severe
reactions, give 1-5 mL of a 1:10,000 solution (0.1 mg/
mL) intravenously over two to three minutes. Alterna-
tively, one can titrate an epinephrine infusion (1 mg in
250 cc D5W=4 mcg/cc) to symptoms and signs.66 The
low-dose titration method may be most appropriate for
patients at risk for cardiac complications from epi-
nephrine therapy.67Cardiac monitoring is appropriate
for all patients receiving intravenous epinephrine.68
If vascular access cannot be obtained in the
intubated patient, intratracheal dosing using 1-5 mL of
1:10,000 epinephrine can be used. Sublingual injection
of epinephrine is another consideration.
Complications Of Epineph rine
Complications of epinephrine used for allergic reac-
tions are rare. In one case, a patient was given epineph-
rine for a presumed allergic reaction and suffered a
fatal intracranial bleed. The crucial issue here involved
the fact that the patient was not having an allergic
reaction but was in the midst of a hypertensive crisis.
He had a blood pressure of 220/160 mmHg prior to
receiving the drug.69In another case, a 30-year-old man
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developed a myocardial infarction after self-adminis-
tering an Epi-Pen for an episode of idiopathic anaphy-
laxis. The patient had numerous risk factors for
coronary artery disease.70All told, there are only a
handful of cases in the English-language literature that
document adverse outcomes when epinephrine is used
to treat allergic reactions.66,68,71
Non-pharmacologic TherapyFluids are an important adjunct in the treatment of
anaphylaxis. Some patients with anaphylactic shock
are unresponsive to epinephrine, possibly due to
secretion of endogenous epinephrine, norepinephrine,
and production of angiotensin II.72,73
Use large volumes of IV crystalloid to resuscitate
severely allergic patients with hypoperfusion. Resusci-
tation may require several liters of isotonic saline or
lactated Ringer s solution to replete the intravascular
space. Avoid hypo-osmolar and dextrose-containing
solutions, which quickly ooze into the extravascular
space from the associated capillary leak syndrome.
The Pneumatic Antishock Garment (PASG)(formerly known as MAST) has been used to treat
shock associated with allergic reactions.74,75However,
this device has not been subject to rigorous study in
patients with anaphylaxis.
Additional InterventionsDecrease Antigen Loa d
If possible, eliminate the antigen or delay its absorp-
tion. (See Clinical Pathway: Treatment Of Allergic
Reactionson page 13.) If the antigenic material was
injected into an extremity, as in the case of an enveno-
mation, some authorities suggest applying a loose
tourniquet to impede lymphatic but not arterial flow.Bees, but not wasps, may leave a stinger in the wound,
attached to a glob of bee parts (the venom sac). If a
stinger is present, remove it by scraping rather than
compression; squeezing the venom sac can inject more
antigen. Local application of ice may delay central
antigen delivery, but it may also cause cold injury to
local tissue.
The utility of decreasing the gastric absorption of
an ingested antigen remains unknown. While the use
of charcoal seems reasonable in this situation, there is
essentially no clinical or laboratory data supporting
its use.
Antihistamines
The use of H1-blocking antihistamines (e.g., diphenhy-
dramine) is standard therapy in patients with allergic
reactions. The dose for mild reactions is usually
diphenhydramine or hydroxyzine 25 to 50 mg given
PO or IM. Oral alternatives with limited sedation are
cetirizine 10 mg or loratadine 10 mg.76,77
Patients with more severe reactions should be
treated with intravenous H1antihistamines. In these
cases, most authorities recommend diphenhydramine
50 to 75 mg IV.
H2blockers (e.g., cimetidine), either alone or in
combination with an H1agent, are also useful in the
treatment of allergic reactions. The best-studied H2antagonist is cimetidine. It is usually given in a 300 mg
dose (PO, IM, or IV). The H2blockers offer a non-
sedating alternative (or addition) to the H1blockers
and seem equally effective.78,79 One study of 93 patients
compared diphenhydramine and cimetidine and found
them both useful in treating acute allergic reactions.78
Runge et al found cimetidine and diphenhydramine
togethermore effective than either alone in treating
acute urticaria in 39 patients.80There are also some
data indicating that cimetidine may be effective when
H1antihistamines are not.81
CorticosteroidsAlthough antihistamines may be sufficient in mild
allergic reactions, they are inadequate if used alone for
severe anaphylaxis. Corticosteroids are useful in most
allergic reactions that require an ED visit. They block
arachidonic acid production through cell membranestabilization; however, this effect may take several
hours. Steroids also attenuate the late-onset component
of hypersensitivity reactions, although the significance
of this component of allergy is unclear. Prednisone is
effective in the outpatient management of acute
urticaria, resolving rash and itching significantly faster
than placebo.82 Although optimal dosing has not been
studied, prednisone 1 mg/kg/d used for three to five
days appears reasonable. This short course does not
require a tapering dose. Consider risks and benefits in
patients with diabetes mellitus or peptic ulcer disease.
Inhaled corticosteroids mitigate allergic effects isolated
to the respiratory tract and may be particularly usefulin allergic rhinitis.83
GlucagonThe patient with a significant hypersensitivity reaction
who is taking beta-blocker drugs poses a special
challenge. These patients often respond poorly to
epinephrine. In case of epinephrine failure, consider
the use of glucagon in these patients. This drug may
also be effective in anyone with anaphylaxis who is
unresponsive to other therapies. Glucagon bypasses
the receptors obstructed by the beta-blockers.84 Its
positive chronotropic and inotropic effects are inde-
pendent of catecholamine receptors, possibly throughstimulation of cAMP synthesis.
The use of glucagon for allergic reactions in
patients taking beta-blockers is based on case reports.85
Since glucagon is short-acting, it may be dosed at 1-2
mg IV every five minutes titrated to symptomatic
improvement. Some patients may require a glucagon
drip at 1-5 mg/h. Common side effects include
hyperglycemia, nausea, and vomiting.
Cont inued on page 14
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Clinical Pathway: Treatment Of Allergic Reactions
Allergenexposure PO charcoal
Loose tourniquet if peripheral Stinger removal by scraping
Local SC epinephrine 0.01 mg/kg? Ice?
Urticaria and/or mildangioedema
Bronchospasm
Oral
Sting, bite
Poorresponse
Goodresponse
H1and/or H
2antagonist
PrednisoneRarely epinephrine SC
Inhaled sympathomimetic Inhaled ipratropium (Atrovent)
Ensure adequate oxygenation (Intubate if necessary)
Epinephrine 1:10,000 solution in 1 cc aliquots IV q 2-3 min until
improvedAND/OR 1 mg in 250 cc D
5W, titrate to response
Aggressive IV normal saline or Ringers lactate (2-3 L/h
if hypoperfusion)
Hemodynamic and O2saturation monitoring
H1and/or H
2antagonist
Corticosteroid
Consider glucagonIV, especially if onbeta-blockers
Taper epinephrineand IV fluid
Consider disposition
This cl inical pa thw ay is intended to supplement, rather tha n
subst i tute, professional jud gm ent an d m ay be chang ed
depending upon a pat ient s individu al n eeds. Failure to com ply
wi th this pathw ay does not represent a breach of the standard
of care.
Copyright2000 Pinnacle Publishing, Inc. Pinnacle Publishing (1-800-788-1900) grants permission to reproduce this
Emergency Medicine Practicetool for institutional use.
Hypersensitivityreaction
Airwayangioedema,
anaphylaxis
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Controversies In Practice
Approach To ACE AngioedemaAngioedema is an immunologically mediated, non-IgE
edema that is generally restricted to the soft tissues of
the head and neck. Antihistamines and steroids may
not be effective in managing acute angioedema,86
leaving some patients at risk for upper airway obstruc-
tion. Many emergency physicians wonder, Whenshould these patients be admitted, and how should
their airways be managed?Unfortunately, there are
few data available to answer this question.
Ishoo et al retrospectively studied 93 episodes of
angioedema.87Intubation or tracheostomy was necessary
in nine (9.7%) of the cases. Voice change, hoarseness,
stridor, and dyspnea were significantly associated with
the need for airway control. These authors suggest that
patients with facial rash, facial edema, lip edema, or soft
palate edema may be managed with supportive care and
observation. Alternatively, they suggest that patients with
laryngeal edema or progressing symptoms be admitted
to an ICU setting. In addition to being a retrospective
study based on a relatively small number of patients, the
admission algorithm developed by these authors was not
prospectively validated.
ACE-inhibitor angioedema is not known to be
biphasic; thus, patients who stabilize and improve tend
to do well. It seems reasonable that patients who
present to the ED with lip or tongue swelling and no
respiratory signs or symptoms can be monitored in the
ED to determine whether the condition improves or
worsens over the course of several hours. In one
retrospective chart review over an eight-year period,
no case of ACE-inhibitor mediated angioedema
required intubation or surgical airway.88Obviously,
such patients must be instructed not to take their ACE
inhibitor and to return immediately for any worsening.
On the other hand, all cases of ACE-inhibitor-induced
angioedema are not benign, and the literature is full of
case reports of respiratory compromise.89,90Patients
with respiratory complaints, palatal edema, or progres-
sive course require admission and are candidates for
intubation; patients whose symptoms have plateaued
may be watched . . . with a cricothyroidotomy tray atthe bedside!
Cont inued f rom page 12
Ten Excuses That Dont Work In Court
1. I thought he had cardiogenic shock. He complained of
chest pain.
Anaphylaxis can present initially with chest discomfort,
hypotension, and tachycardia. Urticarial wheals may beabsent. Unfortunately, this patient did not get the
epinephrine he needed until he developed ventricular
fibrillation. Now this physician is consulting with the
hospital lawyer.
2. I thought it was just hives involving the lips
and tongue.
This patient actually had angioedema related to ACE
inhibitor use. The diphenhydramine and steroids he
received for an allergic reaction were ineffective for his
angioedema, and the patient collapsed on the way home
with airway obstruction. Angioedema is non-IgE-mediated and usually involves the head and neck.
Angioedema due to ACE inhibitor use may not respond
to antihistamines or steroids, but may progress rapidly to
upper airway obstruction.
3. I didnt think the patient was at risk for a
contrast reaction.
This patient got IV contrast for a head CT to exclude HIV-
related toxoplasmosis. Unfortunately, he developed
acute renal failure and is now a candidate for
hemodialysis. Risk factors for radiocontrast media
reactions are a prior history of similar reactions, a history
of asthma, increased age, dehydration, renal or hepaticdysfunction, beta-blocker use, and cardiac disease.
4. Since he collapsed during exercise, I thought he had a
heart attack.
Exercise-induced allergic reactions are usually associated
with urticaria and nasal congestion, but sometimes they
are fatal. If the treating physician had spoken with the
patients wife, he would have learned that the patient
develops allergic symptoms during exercise and forgot
his Singulair today.
5. I thought this was just simple urticaria.The patient was treated with diphenhydramine and
released with the diagnosis of allergic reaction.
Unfortunately, the treating physician ignored the
patients fever, myalgias, arthralgias, and use of penicillin
10 days ago. This physician thought about possible
serum sickness later that night and called the patient to
return for re-evaluation. The patient returned the next
morning with a creatinine of 5.0 mg/dL.
Cont inued on page 15
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Management Of Recurrent UrticariaSome patients treated in the ED for mild-to-moderate
allergic reactions are discharged and return later with
recurrent symptoms. The first step in managing these
patients is to carefully repeat the history and physical,
looking for keys to the diagnosis that were possibly
missed on the first visit, such as new body products,
clothing, pets, or medications. Occult infections and
malignancy may present with urticaria, and the
physical examination should look for these etiologies.
Blood work is usually not part of the initial visit for
urticaria; however, for recurrent cases a CBC may be
helpful in identifying an occult processes such as a
myeloproliferative diseases including thrombocytosis,
which will cause histamine release.91Some clinicians
obtain a sedimentation rate on patients with recurrent
urticaria in an attempt to identify underlying inflam-
matory processes; unfortunately, the lack of sensitivity
and specificity of this test limits its usefulness.92
Pharmacologic management of recurrent urticaria
should involve either switching the patient to another
category of antihistamine (remember, there are eightcategories of antihistamine, each with its own thera-
6. I didnt think about prescribing an Ana-Kit.
Having a patient die following ED discharge from
anaphylaxis after ano t he r bee sting is a definite
malpractice risk. These kits contain epinephrine anddiphenhydramine. Self-administered medications should
be prescribed at ED discharge following an allergic
reaction due to an envenomation. The one caveat is that
older patients with cardiac disease should not use
epinephrine unless i n ext remis.
7. I didnt think that patient with angioedema
needed intubation.
One retrospective study associated voice change,
hoarseness, stridor, and dyspnea with the need for
airway control. Consider airway control in patients
with these findings (although not all patients withthese signs and symptoms require emergent
intubation). Unfortunately, this emergency physician
did not control the airway despite stridor, and now
the patient has a large cricothyroidotomy hole in
his neck.
8. I didnt use epinephrine because he was so old. I
thought he would do okay with Benadryl and steroids.
He didnt. Epinephrine is the drug of choice for life-
threatening anaphylaxis. When the chips are down,
nothing else will do. It is indicated even in elderly
patients and those with a history of hypertension and
cardiac disease whenever they have a dangerousallergic reaction.
9. I just didnt understand why that patient did not
respond to standard therapy.
Patients on beta-blockers may not respond to standard
anti-allergy therapy, including epinephrine. One
alternative in this setting is glucagon. This physician now
wishes he had thought of using glucagon in this patient
who developed anaphylactic shock.
10. I didnt think it could be hereditary angioedema
because it is so rare.Although hereditary angioedema is an unusual
diagnosis in the ED, the treatment of this disorder is
different enough from standard angioedema or
allergic reactions to merit note. These patients can
be treated with fresh frozen plasma in addition to
airway management. Being aware of the possible
need for FFP in hereditary angioedema may save a
patients life, as well as preclude a large retainer for
your defense lawyer.
Ten Excuses That Dont Work In Court(continued)
peutic profile). Another approach is to add an H2-
blocker or steroids. In one double-blind, randomized,
prospective trial, adding prednisone to an antihista-
mine regimen shortened the clinical duration of
urticaria without apparent adverse effects.82
A crucial component to managing patients with
recurrent urticaria is education about the natural
history of allergic reactions. Tell these patients they
should expect a waxing and waning course. While the
medication may mitigate the severity of symptoms
(i.e., itching and rash), it will not completely extirpate
those symptoms. When patients have realistic expec-
tations about their allergic reaction, they are less
likely to return to the ED.
Disposition: Admission, Discharge,Or Observation?
The disposition of allergy patients requires significant
clinical judgment. Most patients with allergic reac-
tions can be discharged. Hospitalize or observe
patients with severe reactions such as airway an-
gioedema, persistent bronchospasm, hypoperfusion,
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or cardiac problems, especially if the condition is not
promptly resolved by therapy. Other high-risk groups
include those on beta-blocker therapy who have
significant reactions and those with severe late-phase
or prolonged reaction. Some patients who have
problematic social situations (such as no phone) or live
far from medical care may also require admission or
prolonged observation. (SeeTable 7.)
The amount of time a patient needs to be observed
after an allergic reaction is also unknown. Most
authorities suggest that patients with significant
allergic reactions should be observed for four to six
hours if discharge is being considered. When they are
discharged, instructions must include immediate
return to the ED for shortness of breath or syncope.
Discharge MedicationsBecause some reactions are biphasic, drugs prescribed
at discharge may blunt a late allergic relapse. Prescribe
H1and/or H2antagonists for at least 24 to 48 hours,
and corticosteroids for several days, to modify any
delayed inflammatory response. Montelukast andother leukotriene-receptor antagonists may inhibit
exercise-induced anaphylaxis.93
If a patient had a severe reaction to a food or insect
sting, prescribe self-administered injectable epineph-
rine (Epi-Pen or Ana-Kit, both available in adult and
pediatric strengths). Make sure the patient knows
when and how to use the device.
Education And ReferralRemember to educate the patient about antigen
avoidance. Aspirin is present in many over-the-counter
combination medications, and cross-sensitivity with
other non-steroidal agents may exist. With predictable
exposure to agents that might initiate the allergy
mechanism (e.g., iodinated radiocontrast agents),
pretreatment with antihistamines and corticosteroids
may be appropriate. Recommend Medic Alert bracelets
for those with severe allergies.
Finally, make an allergist referral on a case-by-case
basis. This is most appropriate for patients with
anaphylaxis due to Hymenoptera stings. Immuno-
therapy has become the standard of care for severe
(i.e., not simple, localized) stinging insect reactions and
may reduce the risk of anaphylaxis with re-sting from
60% to about 5%.94,95 Immunotherapy may not be
necessary for children who have isolated hives after
bee stings. In one study, children who had only
cutaneous reactions were not at risk for future anaphy-
laxis to stings.96
Summary
Allergy is a complex illness that involves inflammatory
mechanisms. Most patients with allergic reactions have
mild symptoms. However, life-threatening airway
angioedema as well as anaphylaxis require prompt
recognition and aggressive therapy. Patients in distress
require appropriate oxygenation and occasionally
intubation. Epinephrine and IV fluids remain the
mainstays of therapy for severe reactions. Give antihis-
tamines and corticosteroids for most reactions.
Above all, treat allergic reactions with respect.
The average emergency physician will encounter
many severe hypersensitivity reactions during his
or her career.
References
Evidence-based medicine requires a critical appraisal
of the literature based upon study methodology and
number of subjects. Not all references are equally
robust. The findings of a large, prospective, random-
ized, and blinded trial should carry more weight than a
case report.
To help the reader judge the strength of each
reference, pertinent information about the study, such
as the type of study and the number of patients in the
study, will be included in bold type following the
reference, where available. In addition, the mostinformative references cited in the paper, as deter-
mined by the authors, will be noted by an asterisk (*)
next to the number of the reference.
1. Cohen SG. The pharaoh and the wasp.Allergy Proc
1989;10:149-151. (Historical article)
2. Portier P, Richet C. De laction anaphylactique des certain
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3. Lichtenstein LM. Allergy and the immune system. Sci Am
1993 Sep;269(3):116-124. (Review)
4. Yunginger JW, Nelson DR, Squillace DL, et al. Laboratory
Table 7. Disposition Of Hypersensitivity Reactions.
When in doubt, hospitalize:
All severe reactions not promptly resolved by therapy:
Airway angioedema, bronchospasm
Hypoperfusion or cardiac problem
All patients on beta-blocker therapy
Anticipated severe late-phase reaction (for example, if there is history of the same in the past)
Patients with inadequate support system
Discharge plan:
Observe patients significant reactions for at least four to six hours prior to discharge
Prescribe H1and/or H
2antagonists for at least 24-48 hours
Consider steroids (for most allergic reactions)
Beta-agonists
Education about antigen avoidance
Self-injectable epinephrine
Appropriate referral
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1981;36:857-865.
5. Schwartz HJ, Yunginger JW, Schwartz LB. Is unrecognized
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10. Cohen JJ. The immune system: An overview. In: Middleton
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3rded. St Louis: Mosby; 1988. (Textbook)
11. Ishizaka K, Ishizaka T. Identification of gamma-E-
antibodies as a carrier of reaginic activity.J Immunol
1967;99(6):1187-1198. (Review)
12. McNeil HP, Austen KF. Biology of the mast cell. In: Frank
M, et al, eds. Immunological Diseases.5th
ed. Boston: Little,Brown; 1995. (Review)
*13. Brady WJ Jr, Luber S, Carter CT, et al. Multiphasic
anaphylaxis: An uncommon event in the emergency
department.Acad Emerg Med 1997;4(3):193-197. (Retrospec-
tive; 1,261 patients)
14. Reisman RE, Livingston A. Late-onset allergic reactions,
including serum sickness, after insect stings.J Allergy Clin
Immunol 1989 Sep;84(3):331-337. (10 patients)
15. Soter NA. Urticaria and angioedema. In: Fitzpatrick TB, et
al, eds. Dermatology In General Medicine. 4thed. New York:
McGraw-Hill; 1993. (Textbook)
16. Frank MM, Gelfand JA, Atkinson JP. Hereditary an-
gioedema: The clinical syndrome and its management.Ann
Intern Med 1976;84(5):580-593. (Review)
17. Novembre E, Cianferoni A, Bernardini R, et al. Anaphylaxisin children: Clinical and allergologic features. Pediatrics
1998;101(4):E8. (Retrospective; 95 episodes)
18. Settipane GA, Boyd GK. Anaphylaxis from insect stings:
Myths, controversy and reality. Postgrad Med
1989;86(2):273-281. (Review)
19. Van der Linden PWG, Struyvenberg A, Kraaijenhagen RJ, et
al. Anaphylactic shock after insect-sting challenge in 138
persons with a previous insect-sting reaction.Ann Intern
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Physician CME Questions
31. The most common cause of death in patients with
a severe allergic reaction is:
a. cerebrovascular accident.
b. circulatory collapse.
c. complications of medical therapy.
d. multiple organ failure.
e. respiratory failure.
32. IV epinephrine is not indicated in which of the
following allergic reaction situations?
a. An 8-year-old female with hypotension and
severe tachycardia
b. A 32-year-old male with hoarseness and
stridor
c. A 38-year-old male with airway angioedema
d. A 48-year-old female with urticaria alone
e. A 64-year-old male with hypotension and
abdominal pain
33. All of the following are potential causes of
anaphylactic shock except:
a. C1esterase inhibitor deficiency.
b. exercise.
c. Hymenoptera stings.
d. latex.
e. peanut oil ingestion.
34. A patient on beta-blocker therapy presentshypotensive and bradycardic shortly after
multiple bee stings. Epinephrine does not help.
Which medication should be given next?
a. cimetidine.
b. diphenhydramine.
c. glucagon.
d. high-dose epinephrine.
e. methylprednisolone.
35. A young female presents with vomiting and
diarrhea along with facial and hand swelling, as
well as airway stridor. She has experienced thisbefore but never has had urticaria. Other family
members have a similar problem. The medication
of choice is:
a. cimetidine.
b. epinephrine.
c. fresh frozen plasma.
d. hydroxyzine.
e. methylprednisolone.
36. A patient with known severe penicillin allergy is
accidentally given an oral dose of penicillin. He
is asymptomatic so far. Treatment should include
which of the following?
a. Benadryl
b. Intravenous epinephrine
c. Or al charcoal
d. Prednisone
e. Subcutaneous epinephrine
37. Which of these clinical scenarios is not sugges-
tive of an allergic reaction?
a. Acute back pain with hypotension
b. Acute bronchospasm with hypotension
c. Confusion with fever of 103F
d. Isolated facial angioedemae. Urticaria with vomiting and diarrhea
38. The most frequent cause of allergic
symptoms is:
a. food sensitivity.
b. inhaled antigens.
c. insect s tings.
d. medicat ions.
e. non-immunogenic.
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Physician CME Information
This CME enduring material is sponsored by Carolinas HealthCare System
and has been planned and implemented in accordance with the Essentials
and Standards of the Accreditation Council for Continuing Medical
Education. Credit may be obtained by reading each issue and completing
the post-tests administered in December and June.
Target Audience:This enduring material is designed for emergency
medicine physicians.
Needs Assessment:The need for this educational activity was determined
by a survey of medical staff, including the editorial board of this publica-
tion; review of morbidity and mortality data from the CDC, AHA, NCHS,
and ACEP; and evaluation of prior activities for emergency physicians.
Date of Original Release:This issue ofEm ergency Medicine Practice
was published April 1, 2000. This activity is eligible for CME credit through
April 1, 2001. The latest review of this material was March 28, 2000.
Discussion of I nvestigational Information:As part of the newsletter,
faculty may be presenting investigational information about
pharmaceutical products that is outside Food and Drug Administration
approved labeling. Information presented as part of this activity is
intended solely as continuing medical education and is not intended
to promote off-label use of any pharmaceutical product.Disclosure of
Off-Label Usage:This issue ofEm ergency Medicine Practice discusses no off-
label use of any phamaceutical product.
Faculty Disclosure: In compliance with all ACCME Essentials, Standards,
and Guidelines, all faculty for this CME activity were asked to complete afull disclosure statement. The information received is as follows: Dr.
OBrien. Dr. Howell, Dr. Zull, and Dr. Salomone report no significant
financial interest or other relationship with the manufacturer(s) of any
commercial product(s) discussed in this educational presentation.
Accreditation:Carolinas HealthCare System is accredited by the
Accreditation Council for Continuing Medical Education to sponsor
continuing medical education for physicians.
Credit Designation: Carolinas HealthCare System designates this
educational activity for up to 2 hours of Category 1 credit toward the
AMA Physicians Recognition Award. Each physician should claim only
those hours of credit actually spent in the educational activity.Emergency
Medicine Practice is approved by the American College of Emergency Phy-
sicians for 24 hours of ACEP Category 1 credit (per annual subscription).
Earning Credit:Physicians with current and valid licenses in the United
States, who read all CME articles during each Em ergency Medicine Practice
six-month testing period, complete the CME Evaluation Form distributed
with the December and June issues, and return it according to the
published instructions are eligible for up to 2 hours of Category 1 credit
toward the AMA Physicians Recognition Award (PRA) for each issue. You
must complete both the post-test and CME Evaluation Form to receive
credit. Results will be kept confidential. CME certificates will be mailed to
each participant scoring higher than 70% at the end of the calendar year.
Class I
Always acceptable, safe
Definitely useful
Proven in both efficacy
and effectiveness
Must be used in the
intended manner for
proper clinical indications
Level o f Evidence:
One or more largeprospective studies
are present (with
rare exceptions)
Study results consistently
positive a
Recommended