Allergic Emergencies and Anaphylaxis How To Avoid Getting Stung PDF

EMERGENCY MEDICINE PRACTICE
A N E V I D E N C E - B A S E D A P P ROAC H T O E M E RG E N C Y M E D I C I N E
April 2000
Allergic Emergencies
and Anaphylaxis:
How To Avoid Getting Stung
Volume 2, Number 4
Authors
LLERGIC reactions span a wide spectrum of clinical presentationsfrom the minor irritant of hay fever to the dramatic systemic
disruption known as anaphylaxis. Recognizing allergic phenomena can
be a challenge. While urticaria represents an obvious hypersensitivity
reaction, distinguishing an allergic etiology of syncope or chest pain is
more difficult. Many serious allergic reactions present with atypical
symptoms, making immediate diagnosis difficult.
Emergency physicians are often faced with difficult management
decisions surrounding allergic reactions. When should patients with ACE
inhibitor angioedema be admitted, or even prophylactically intubated?
How does one manage recurrent urticaria?
This issue of Emergency Medicine Practice suggests a plan for prompt,
effective management. Central principles include recognizing the highrisk patient, an organized approach to the seriously ill, and protecting
the patient from future allergic problems.
History And Epidemiology

Anaphylaxis was recognized even in ancient times. In 2640 B.C., the
Pharaoh Menes died of a wasp sting, and an early medical archivist
chiseled this event on the kings tomb.1 (Ironically, he forgot to sign the
inscription, making it the worlds most tardy medical record.) At the
beginning of the 20 th century, Portier and Richet reported a fatal systemic
reaction in a dog from a second injection of a previously tolerated foreign
protein. 2 In their 1902 paper, they coined the term anaphylaxis, derived
from the Greek words ana (against) and phylax (protect) to mean without
protection.
Approximately 20% of the U.S. population is allergic.3 Minor allergic
Editor-in-Chief
Stephen A. Colucciello, MD, FACEP,
Director of Clinical Services, Department of Emergency
Medicine, Carolinas Medical
Center, Charlotte, NC; Assistant
Clinical Professor, Department of
Emergency Medicine, University
of North Carolina at Chapel Hill,
Chapel Hill, NC.
Associate Editor
Andy Jagoda, MD, FACEP, Associate
Professor of Emergency
Medicine, Mount Sinai School of
Medicine, New York, NY.
Editorial Board
Judith C. Brillman, MD, Residency
Director, Associate Professor,
Department of Emergency
Medicine, The University of

New Mexico Health Sciences
Center School of Medicine,
Albuquerque, NM.
W. Richard Bukata, MD, Assistant
Clinical Professor, Emergency
Medicine, Los Angeles County/USC
Medical Center, Los Angeles, CA;
Medical Director, Emergency
Department, San Gabriel Valley
Medical Center, San Gabriel, CA.
Francis M. Fesmire, MD, FACEP,
Director, Chest PainStroke
Center, Erlanger Medical Center;
Assistant Professor of Medicine,
UT College of Medicine,
Chattanooga, TN.
Michael J. Gerardi, MD, FACEP,
Clinical Assistant Professor,
Medicine, University of Medicine
and Dentistry of New Jersey;
Director, Pediatric Emergency
Medicine, Childrens Medical
Center, Atlantic Health System;
Chair, Pediatric Emergency

Medicine Committee, ACEP.
Michael A. Gibbs, MD, FACEP,
Residency Program Director;
Medical Director, MedCenter Air,
Center; Associate Professor of
Charlotte, NC.
Gregory L. Henry, MD, FACEP, CEO,
Medical Practice Risk Assessment,
Inc., Ann Arbor, MI; Clinical
Professor, Department of
of Michigan Medical School, Ann
Arbor, MI; President, American
Physicians Assurance Society,
Ltd., Bridgetown, Barbados, West
Indies; Past President, ACEP.
Jerome R. Hoffman, MA, MD, FACEP,
Professor of Medicine/
Emergency Medicine, UCLA
John OBrien, MD
Assistant Residency Director, Department of
Emergency Medicine, Orlando Regional Medical
Center; Clinical Assistant Professor of Medicine,
University of Florida College of Medicine, Orlando, FL.
John M. Howell, MD
Chairman, Department of Emergency
Medicine, Georgetown University Medical
Center, Washington, DC.
Peer Reviewers
David N. Zull, MD, FACEP, FACP
Associate Professor of Medicine/Associate Chief
Medicine, Northwestern University, Chicago, IL.
Joseph A. Salomone III, MD, FAAEM
Residency Director, Department of Emergency
Medicine; Associate Professor, Truman Medical Center/
UMKC School of Medicine, Kansas City, MO.
CME Objectives
Upon completing this article, you should be able to:
1. list common precipitants of allergy, both immunemediated and anaphylactoid etiologies;
2. identify appropriate therapeutic interventions for
allergic reactions;
3. discuss approaches to high-risk patients with severe
allergy and those who respond poorly to therapy;
4. describe techniques to prevent future allergic
reactions; and
5. describe indications for hospitalization of allergic
reactions, as well as appropriate outpatient
disposition techniques.
Date of original release: April 1, 2000.

Date of most recent review: March 28, 2000.
See Physician CME Information on back page.
School of Medicine; Attending

Physician, UCLA Emergency
Medicine Center;
Co-Director, The Doctoring
Program, UCLA School of
Medicine, Los Angeles, CA.
John A. Marx, MD, Chair and Chief,
Center, Charlotte, NC; Clinical
Professor, Department of
Chapel Hill, NC.
Michael S. Radeos, MD, FACEP,
Attending Physician in
Emergency Medicine, Lincoln
Hospital, Bronx, NY; Research
Fellow in Emergency Medicine,
Massachusetts General Hospital,
Boston, MA; Research Fellow in
Respiratory Epidemiology,
Channing Lab, Boston, MA.
Steven G. Rothrock, MD, FACEP,
FAAP, Assistant Professor of

of Florida; Orlando Regional
Medical Center, Orlando, FL.
Alfred Sacchetti, MD, FACEP,
Research Director, Our Lady of
Lourdes Medical Center, Camden,
NJ; Assistant Clinical Professor
of Emergency Medicine,
Thomas Jefferson University,
Philadelphia, PA.
Corey M. Slovis, MD, FACP, FACEP,
Medicine, Vanderbilt University
Hospital, Nashville, TN.
Mark Smith, MD, Chairman,
Medicine, Washington Hospital
Center, Washington, DC.
Thomas E. Terndrup, MD, Professor
and Chair, Department of
of Alabama at Birmingham,
Birmingham, AL.
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.
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.4,5 Recent 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.
The Immune Response

Classical 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. (See Table 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 immunoglobulin.9 Antibodies of the IgE class and IgG4 subclass
are most important in the pathogenesis of allergy.10,11 T
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.12 These 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 reactions release
Pathophysiology: A Simple Primer

Allergic reactions are developed hypersensitivities to
antigens. Antigens are proteins recognized by the
human host as foreign. Alternatively, haptens are
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
Table 1. Classification Of Immunologic Reactions

(Gell And Coombs).
Type
Mediator
Reaction
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).

Allergen
T suppressor cells
Antigen Processing Cell

(macrophage and others)
Cytokines
produced

T helper cells activated
(Genetic predisposition)
B cells activated
Emergency Medicine Practice
Antigen-specific IgE
Plasma cells
April 2000
in the biochemistry of allergy.
mediators without involving antibodies. Many stimuli

can precipitate mast cells and basophils to produce and
release mediators without antibody involvement.
Occasionally, it is unclear whether a reaction is truly
immune-mediated or anaphylactoid, with the classic
example being hypersensitivity reactions to nonsteroidal anti-inflammatory agents. These drugs cause
allergic symptoms through either or both pathways.
(See Figure 2.) From an emergency perspective, the
clinical aspects of anaphylaxis are more important than
the immunochemical details. For this reason, we do not
need to distinguish an anaphylactic from an anaphylactoid reaction.
Types Of Reactions
The classic allergic reaction frequently becomes evident
seconds to minutes after exposure to a triggering antigen.
In rare situations, a delay of several hours may occur,
especially with some oral ingestions. (See Figure 3 on
page 4.) However, the sooner a reaction occurs after antigen
exposure, the more likely it is to be severe.
Although a biphasic phase of severe allergy has
been reported, there are conflicting data regarding the
importance of the delayed component. In one study of
1,261 patients with allergic reactions, only two had
late-phase recurrences, and these involved only mild
facial edema.13 In another report, 10 patients, aged 6 to
78 years, had allergic reactions one to two weeks after
an insect sting; two of them had severe anaphylactic
symptoms, including throat edema.14
Allergic reactions vary widely in severity and
depend on many factors. (See Table 2 on page 4.) These
include the degree of hypersensitivity of the individual
as well as the quantity, rate, and route of antigen
exposure. Other issues include the pattern and quantity of mediator release as well as target organ sensitivity and responsiveness.
The Allergic Stew

Histamine operates on at least three receptors to cause
smooth muscle contraction, enhanced vascular permeability, increased airway mucous production, and
chemotaxis of eosinophils and neutrophils.
Leukotrienes are much more potent mediators of
allergy and were previously characterized as the
slow-reacting substance of anaphylaxis. Eosinophil
and neutrophil chemotactic factors recruit white cells
that regulate the inflammatory mechanism. Kallikreins,
prostaglandins, and other mediators are also important
Figure 2. Allergy Mechanism.
IgE-Mediated
Antigen
Non-IgE-Mediated or Anaphylactoid
Mast Cell
or
Basophil
Medications: Radio-iodinated contrast agents, salicylates,

opiates, etc.
Physical Factors: Temperature, pressure, exercise, etc.
Psychogenic: Anxiety, stress, etc.
Release of Mediators of Inflammation
April 2000
Preformed
Histamine
Eosinophil Chemotactic
Factor
Neutrophil Chemotactic
Factor
Kallikreins
Others
Newly Synthesized
Leukotrienes
Prostaglandins
Platelet Activating Factor
Various Lipoxygenase
Products
Others
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, gastrointestinal tract, and upper airway are most commonly involved. Respiratory tract angioedema is
potentially fatal. Hereditary angioedema (HAE) is an
autosomal dominant condition caused by lack of a
functional C1 esterase inhibitor.16 The 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 obstruction are presenting components of anaphylaxis.
Individuals with anaphylaxis may have one, two, or all
of these conditions. (See Table 3.)
Causes Of Hypersensitivity Reactions

Table 4 presents a list of some causes of hypersensitiv-
Table 2. Hypersensitivity
Reactions.
Figure 3. Time Course Of Allergic Reaction.
Mast Cell
and
Basophil
Degrees of hypersensitivity
Hours
Specific IgE concentration
Allergen affinity
Minutes
Hypersensitivity reactions can

be of varied severity, depending upon:
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
Number of mast cells

and basophils
Quantity, route, and rate of
antigen exposure
Pattern and quantity of
mediator release
Target organ sensitivity
and responsiveness
Vascular leakage
Table 3. Frequency Of Occurrence Of Signs

And Symptoms Of Anaphylaxis.
Table 4. Causes Of Hypersensitivity Reactions.*

IgE Mediated
Signs/Symptoms
Percent
Drugs (e.g., antimicrobials, nonsteroidals)
Urticaria and angioedema
88%
Dyspnea, wheeze
47%
Dizziness, syncope, hypotension
33%
Nausea, vomiting, diarrhea,

cramping abdominal pain
Environmental (e.g., house dust mites, pollens, molds, other

inhaled proteins)
30%
Soaps, lotions, detergents
Flush
46%
Envenomations (e.g., Hymenoptera)
Upper airway edema
56%
Snake antivenin
Headache
15%
Latex
Rhinitis
16%
Miscellaneous: cold, light, vibration, pressure, exercise
Substernal pain
Food (e.g., peanuts, tree nuts, fish, shellfish, eggs, certain

fresh fruits)
6%
Itch without rash
4.5%
Seizure
1.5%
Non-immunologic Causes
Drugs (e.g., narcotics, neomycin, d-tubocurare, salicylates,
nonsteroidals)

Radiocontrast agents
* This list is not intended to be all-inclusive.
April 2000
Drugs And Medications
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
While 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.21 Parenteral (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
Envenomations
There 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 Hymenoptera sting, up to 35-60% will experience anaphylaxis to a subsequent sting.19,20 Other arthropods
besides Hymenoptera can cause anaphylaxis, including
the kissing bug and a variety of ticks.
10 Allergy Pearls
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.
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 sho ck. Give small, repeated aliquots of IV
epinephrine to patients in shock. Subcutaneous
epinephrine is inadequate.
8. Self-stimula tion. 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.
3. Recogniz e 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.
9. Aller gy is an acquir ed disor der. 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. Patients
may develop angioedema after discontinuing an
ACE inhibitor.
5. Its a famil y affair . Hereditary angioedema presents

with recurrent extremity, gastrointestinal, and upperairway edema without urticaria. A family history of
similar problems is an important hint. Treat hereditary
angioedema with fresh frozen plasma.
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.
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.
April 2000
Latex
the future.23 In 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 response
to procaine (Bicillin C-R, Wycillin) characterized
by psychosis, anxiety, hallucinations, hypertension,
and tachycardia.25 Patients who suffer this effect
do not need to avoid beta-lactams in the future
(only procaine).
Two-thirds of latex reactions are mild and local (e.g.,

hand erythema and itching), but some patients develop
fatal anaphylaxis. 31 Latex 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 council
suggests that they have all medical, surgical, and
dental procedures performed in a latex-controlled
environment regardless of a history of latex allergy.33
Radiocontrast Media
As 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 50,000-100,000.35 This 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 dysfunction, and cardiac disease. Other considerations
involve dye factors such as dose, osmolality, or ionic
content.37 A history of asthma or use of beta-blockers
may be among the strongest predictors of a contrastassociated reaction.38
Methods of risk reduction for radiocontrast
reactions include using another imaging technique that
does not involve these agents, using nonionic lowosmolality agents, and pre-treating 12-24 hours prior to
dye load.39 Administering 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.40 One
study demonstrated a very low reaction rate if lowosmolality, non-ionic agents were used.41 However, the
costs associated with these more expensive imaging
dyes are substantial.41
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 crosssensitivity of cephalosporins and penicillins vary
widely, ranging from 2% to 16%. 26 However, even in
patients with a stated penicillin allergy, true anaphylaxis to cephalosporins is extremely rare (< 0.02%).27
In fact, cross-reactions appear limited to patients given
first-generation cephalosporins; studies of secondand third-generation cephalosporins show no increase
in allergic reactions in patients who have a history
of penicillin allergy.27 In addition, penicillin skin
tests do not predict the likelihood of allergic reactions
to cephalosporins in patients with histories of penicillin allergy.
Aspirin And Nonsteroidal Anti-inflammatory Drugs

Certain agents precipitate hypersensitivity reactions by
altering arachidonic acid metabolism (e.g., salicylates
and nonsteroidals). These drugs inhibit the degradation 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. 28 A history of nasal polyps may
increase the likelihood of an allergic reaction.
Food Allergies
Illicit Drugs
Food allergies are the predominant cause of anaphylaxis seen in the ED.42 While 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. 44 Of 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
A 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
April 2000
weeks.45 Some food allergies occur only when particular food is followed by exercise.46 In 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 responsible for the vast majority of food-induced allergic
reactions. In children, the culprits include milk, eggs,
peanuts, fish, and tree nuts; in adults, prime offenders
consist of peanuts, tree nuts, fish, and shellfish. 47 As
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 allergies, however, some consider beer anaphylaxis to be
the most tragic.48
There are several interesting non-allergic food
reactions known collectively as the restaurant syndromes. 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. Symptoms 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.50 This reaction due to
histamine-like toxins can be treated with diphenhydramine or cimetidine.
Exercise
Other poorly understood mechanisms cause direct
mediator release from allergy effector cells. Exerciseinduced allergy is usually limited to urticaria and nasal
congestion, but some reactions are fatal.39 More than
50% of patients with exercise-induced reactions have
atopy, and more than half of those with exerciseinduced anaphylaxis develop the syndrome only if
they ate just prior to marked exertion.51 Prevention
includes modifying the exercise activity, avoiding
high-risk foods within four hours of exercise, and
prophylaxis with antihistamines and leukotrienereceptor 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.

Lower respiratory tract
Bronchospasm
Increased secretions
History
Precipitating event:
Medications, including OTCs (especially NSAIDs)
Foods (peanuts, nuts, fresh fruits, fish, shellfish,
eggs, milk)
Environmental exposures
Physical agents/events
Cardiovascular
Hypotension
Tachycardia (rarely bradycardia)
Dysrhythmias
Cardiac arrest
Previous episodes:
Frequency
Duration
Effects of treatment
Gastrointestinal tract
Abdominal colic
Vomiting (nausea)
Diarrhea
Physical Exam
Vital signs
Central nervous system

Confusion
Agitation
Coma
Skin
Urticaria
Angioedema
Eyes
Conjunctivitis
Chemosis
Upper respiratory tract

Rhinitis
Oral and laryngeal edema
April 2000
reaction to shellfish in the past does not eliminate

shellfish from the list of current suspects.
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 demonstrating urticaria, angioedema, bronchospasm, or vascular
collapse provides a compelling diagnostic picture.
(See Table 5.) Occasionally, therapeutic intervention
must be based on the physical findings alone; clinical
improvement with therapy may be the best and only
diagnostic confirmation.
Past Medical And Family History

Past medical history is important, particularly the
history of prior allergic reactions. If the patient recounts 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 Examination
History
The physical exam in hypersensitivity reactions should

initially focus on the immediate life threatslaryngospasm and hypotension.
The 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 lump in 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 symptoms, 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
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.54 Visualization 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 as Munchausens
stridor. These patients intentionally adduct their vocal
cords and can appear to be in profound respiratory
distress. Indirect laryngoscopy can reveal the nonanatomic 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
Identifying The Agent

Clearly, the physician would like to identify the
inciting agent. Recognizing the precipitant (see Table 4)
of a hypersensitivity reaction can prevent or ameliorate
subsequent episodes by avoidance or possibly immunotherapy. 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 variable,
the assumed connection between an exposure and a
reaction may be misleading. Certainly, a list of medications 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 sensitized to almost anything, even after
decades of tolerance. The fact that they never had a
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 with
increased 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.
April 2000
Laboratory Evaluation
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.
The 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 anaphylaxis.56 Other laboratory tests available to the emergency 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
Skin And Mucous Membranes

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. (See Table
5.) Angioedema may be difficult to recognize in its
early stages, and the patient or family may be most
helpful with confirming early changes.
Table 6. Differential Diagnosis Of Anaphylaxis And Anaphylactoid Reactions.

Excess endogenous production of histamine
Systemic mastocytosis
Urticaria pigmentosa
Leukemias
Physical factors
Exercise
Cold, heat, sunlight
Airway disease
Reactive airway disease
Epiglottitis
Foreign body
Pulmonary embolism
Psychiatric disease
Panic attacks
Munchausens stridor
Neurologic
Vasovagal syncope
Seizure
Stroke
Cardiovascular disease
Dysrhythmias
Myocardial ischemia
Capillary leak syndrome
Drug reaction
Red man syndrome (vancomycin)
Reaction to anti-seizure medication
Flush syndromes
Carcinoid
Postmenopausal
Chlorpropamidealcohol
Medullary carcinoma thyroid
Miscellaneous
Hereditary angioedema
Progesterone anaphylaxis
Urticarial vasculitis
Pheochromocytoma
Hyperimmunoglobulin E, urticaria syndrome
Restaurant syndromes
Monosodium glutamate (MSG)
Scombroid poisoning
Sulfites

Shock
Hemorrhagic
Cardiogenic
Endotoxic
April 2000
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 management 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.
plasma histamine. Elevated tryptase levels persist

for five hours after the onset of symptoms. 57 However,
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. Cutaneous
mastocytosis is a rare disorder that causes reddishbrown macules and papules that develop urticaria 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
C 1 esterase inhibitors. Hereditary angioedema is
suggested by a family history (i.e., autosomal dominant inheritance), absence of urticaria and itching,
prominence of recurrent self-limited attacks of circumcised 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 C1 esterase inhibitor, is
not rapidly available. Recognizing hereditary angioedema is very important because it is not responsive 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
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 measurements. Invasive hemodynamic and urine output
monitoring are important in severe hypersensitivity
reactions, particularly in the elderly and those with
significant concomitant medical problems.
Airway
The 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 Dealing

With Acute Allergic Reactions And Angioedema
In many cases, respiratory distress in mild allergic
reactions is due to bronchospasm. This can be treated
effectively with nebulized beta-adrenergic agonists.
Risk Management Caveat: A chest radiograph may be
used to exclude pneumonia and pneumothorax in
patients with atypical presentations for allergy.
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 Management 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.
3. Use less expensive, generic medications.

Many patients can be treated effectively with generic
diphenhydramine and cimetidine, rather than more
expensive H 1 and H2 antihistamines. In fact, most of the
studies regarding H1 and H 2 blockers in allergy were
done using diphenhydramine and cimetidine.
2. Do not order chest x-rays in patients with acute

allergic reactions and mild respiratory distress.
10
April 2000
recommended by older textbooks for allergic bronchospasm, there is no empiric evidence for the use of
aminophylline in anaphylaxis.
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 intubation. 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 the
bag 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 depending 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 immediate cricothyroidotomy if intubation fails. Being
prepared in this instance involves applying Betadine to
the 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.
Circulation
After 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 of
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 subcutaneously 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 recommendations 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. Alternatively, 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 epinephrine therapy.67 Cardiac 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.
Breathing
While 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 by
any 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, particularly in allergy patients on beta-blockers. While often
April 2000
Complications Of Epinephrine
Complications of epinephrine used for allergic reactions are rare. In one case, a patient was given epinephrine 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.69 In another case, a 30-year-old man
11
50 to 75 mg IV.
H 2 blockers (e.g., cimetidine), either alone or in
combination with an H1 agent, are also useful in the
treatment of allergic reactions. The best-studied H 2
antagonist is cimetidine. It is usually given in a 300 mg
dose (PO, IM, or IV). The H2 blockers offer a nonsedating alternative (or addition) to the H 1 blockers
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
together more effective than either alone in treating
acute urticaria in 39 patients.80 There are also some
data indicating that cimetidine may be effective when
H 1 antihistamines are not.81
developed a myocardial infarction after self-administering an Epi-Pen for an episode of idiopathic anaphylaxis. The patient had numerous risk factors for
coronary artery disease.70 All 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 Therapy
Fluids 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. Resuscitation 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.74,75 However,
this device has not been subject to rigorous study in
patients with anaphylaxis.
Corticosteroids
Although 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 membrane
stabilization; 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 useful
in allergic rhinitis.83
Additional Interventions
Decrease Antigen Load
If possible, eliminate the antigen or delay its absorption. (See Clinical Pathway: Treatment Of Allergic
Reactions on page 13.) If the antigenic material was
injected into an extremity, as in the case of an envenomation, 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.
Glucagon
The 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 independent of catecholamine receptors, possibly through
stimulation 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.
Antihistamines
The use of H1-blocking antihistamines (e.g., diphenhydramine) 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 H1 antihistamines. In these
cases, most authorities recommend diphenhydramine
Continued on page 14
12
April 2000
Clinical Pathway: Treatment Of Allergic Reactions

Oral
PO charcoal
Sting, bite
Hypersensitivity
reaction
Airway
angioedema,
anaphylaxis
Allergen
exposure
Urticaria and/or mild

angioedema
H1 and/or H2 antagonist
Prednisone
Rarely epinephrine SC
Bronchospasm
Inhaled sympathomimetic
Inhaled ipratropium (Atrovent)
Loose tourniquet if peripheral

Stinger removal by scraping
Local SC epinephrine 0.01 mg/kg?
Ice?
Ensure adequate oxygenation (Intubate if necessary)

Epinephrine
1:10,000 solution in 1 cc aliquots IV q 2-3 min until
improved AND/OR
1 mg in 250 cc D5W, titrate to response
Aggressive IV normal saline or Ringers lactate (2-3 L/h
if hypoperfusion)
Hemodynamic and O2 saturation monitoring
H1 and/or H2 antagonist
Corticosteroid
Consider glucagon
IV, especially if on
beta-blockers
This clinical pathway is intended to supplement, rather than

substitute, professional judgment and may be changed
depending upon a patients individual needs. Failure to comply
with this pathway does not represent a breach of the standard
of care.
Poor
response
Good
response
Taper epinephrine
and IV fluid
Consider disposition
Copyright 2000 Pinnacle Publishing, Inc. Pinnacle Publishing (1-800-788-1900) grants permission to reproduce this
Emergency Medicine Practice tool for institutional use.
April 2000
13
Continued from page 12
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.88 Obviously,
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.89,90 Patients
with respiratory complaints, palatal edema, or progressive course require admission and are candidates for
intubation; patients whose symptoms have plateaued
may be watched . . . with a cricothyroidotomy tray at
the bedside!
Controversies In Practice
Approach To ACE Angioedema
Angioedema 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 obstruction. Many emergency physicians wonder, When
should 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.87 Intubation 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
Ten Excuses That Dont Work In Court

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 hepatic
dysfunction, beta-blocker use, and cardiac disease.
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 be
absent. Unfortunately, this patient did not get the
epinephrine he needed until he developed ventricular
fibrillation. Now this physician is consulting with the
hospital lawyer.
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.
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-IgEmediated 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.
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.
3. I didnt think the patient was at risk for a

contrast reaction.
This patient got IV contrast for a head CT to exclude HIVrelated toxoplasmosis. Unfortunately, he developed
Continued on page 15
14
April 2000
Management Of Recurrent Urticaria
peutic profile). Another approach is to add an H2blocker or steroids. In one double-blind, randomized,
prospective trial, adding prednisone to an antihistamine 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 expectations about their allergic reaction, they are less
likely to return to the ED.
Some 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.91 Some clinicians
obtain a sedimentation rate on patients with recurrent
urticaria in an attempt to identify underlying inflammatory 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 eight
categories of antihistamine, each with its own thera-
Disposition: Admission, Discharge,

Or Observation?
The disposition of allergy patients requires significant
clinical judgment. Most patients with allergic reactions can be discharged. Hospitalize or observe
patients with severe reactions such as airway angioedema, persistent bronchospasm, hypoperfusion,
Ten Excuses That Dont Work In Court
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 dangerous
allergic reaction.
6. I didnt think about prescribing an Ana-Kit.

Having a patient die following ED discharge from
anaphylaxis after another bee sting is a definite
malpractice risk. These kits contain epinephrine and
diphenhydramine. 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 in extremis.
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.
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 with
these 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.
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.
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-
April 2000
(continued)
15
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. Immunotherapy 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 anaphylaxis to stings.96
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. (See Table 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 Medications
Because some reactions are biphasic, drugs prescribed
at discharge may blunt a late allergic relapse. Prescribe
H 1 and/or H2 antagonists for at least 24 to 48 hours,
and corticosteroids for several days, to modify any
delayed inflammatory response. Montelukast and
other 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 epinephrine (Epi-Pen or Ana-Kit, both available in adult and
pediatric strengths). Make sure the patient knows
when and how to use the device.
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 antihistamines 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.
Education And Referral

Remember to educate the patient about antigen
avoidance. Aspirin is present in many over-the-counter
References
Table 7. Disposition Of Hypersensitivity Reactions.
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, randomized, 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 most
informative references cited in the paper, as determined by the authors, will be noted by an asterisk (*)
next to the number of the reference.
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 H1 and/or H2 antagonists for at least 24-48 hours
1.
Consider steroids (for most allergic reactions)

Beta-agonists
2.
Education about antigen avoidance

3.
Self-injectable epinephrine
Appropriate referral
4.
16
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April 2000
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April 2000
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17
67. Brown AF. Therapeutic controversies in the management of

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73. Silverman HJ, Van Hook C, Haponik EF. Hemodynamic
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74. Bickell WH, Dice WH. Military antishock trousers in a
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75. Oertel T, Loehr MM. Bee-sting anaphylaxis: The use of
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77. Kaliner MA. Nonsedating antihistamines: Pharmacology,
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78. Moscati RM, Moore GP. Comparison of cimetidine and
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*80. Runge JW, Martinez JC, Caravati EM, et al. Histamine
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81. Yarbrough JA, Moffitt JE, Brown DA. Cimetidine in the
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82. Pollack CV, Romano TJ. Outpatient management of acute
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84. Pollack CV. Utility of glucagon in the emergency department. J Emerg Med 1993;11:195. (Review)
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46. Horan RF, Sheffer AL. Food-dependent exercise-induced
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56. Fawcett WJ, Shepard JN, Soni NC, et al. Oxygen transport
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59. Borum ML, Howard DE. Hereditary angioedema: Complex
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60. Anderson MW, deShazo RD. Studies of the mechanism of
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18
April 2000
86. Thompson T, Frable MA. Drug-induced, life-threatening

angioedema revisited. Laryngoscope 1993;103(1 Pt 1):10-12.
(Case report; 36 patients)
*87. Ishoo E, Shah UK, Grillone GA, et al. Predicting airway risk
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33. All of the following are potential causes of

anaphylactic shock except:
a. C1 esterase inhibitor deficiency.
b. exercise.
c. Hymenoptera stings.
d. latex.
e. peanut oil ingestion.
34. A patient on beta-blocker therapy presents
hypotensive 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 this
before 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. Oral charcoal
d. Prednisone
e. Subcutaneous epinephrine
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.
37. Which of these clinical scenarios is not suggestive of an allergic reaction?

a. Acute back pain with hypotension
b. Acute bronchospasm with hypotension
c. Confusion with fever of 103F
d. Isolated facial angioedema
e. Urticaria with vomiting and diarrhea
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
April 2000
38. The most frequent cause of allergic

symptoms is:
a. food sensitivity.
b. inhaled antigens.
c. insect stings.
d. medications.
e. non-immunogenic.
19
Physician CME Information
39. Which of the following is not a risk

factor for significant radio-contrast
media reactions?
a. History of previous reaction
b. Increased age
c. Beta-blocker use
d. History of asthma
e. Male sex
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 A udienc e: This enduring material is designed for emergency
medicine physicians.
Needs A ssessmen t: The need for this educational activity was determined
by a survey of medical staff, including the editorial board of this publication; review of morbidity and mortality data from the CDC, AHA, NCHS,
and ACEP; and evaluation of prior activities for emergency physicians.
40. The following are all examples of mainly

non-immunogenic activators of the allergic
mechanisms except:
a. anxiety.
b. exercise.
c. narcotics.
d. radio-iodinated contrast agents.
e. snake antivenin.
Date of O riginal R elease: This issue of Emergency 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 nvestiga tional I nformation: 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 of Emergency Medicine Practice discusses no offlabel use of any phamaceutical product.
Facult y Disclosur e: In compliance with all ACCME Essentials, Standards,
and Guidelines, all faculty for this CME activity were asked to complete a
full 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.
Class Of Evidence Definitions

Each action in the clinical pathways section of Emergency
Medicine Practice receives an alpha-numerical score based on
the following definitions.
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 of Evidence:
One or more large
prospective studies
are present (with
rare exceptions)
Study results consistently
positive and compelling
Class IIa
Safe, acceptable
Clinically useful
Considered treatments
of choice
Level of Evidence:
Generally higher levels
of evidence
Results are consistently
positive
Class IIb
Safe, acceptable
Clinically useful
Considered optional or
alternative treatments
Level of Evidence:
Generally lower or
intermediate levels
of evidence
Generally, but not
consistently, positive results
Accreditation: Carolinas HealthCare System is accredited by the

Accreditation Council for Continuing Medical Education to sponsor
continuing medical education for physicians.
Class III:
Unacceptable
Not useful clinically
May be harmful
Level of Evidence:
No positive high-level data
Some studies suggest or
confirm harm
Credit D esigna tion: 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 Physicians for 24 hours of ACEP Category 1 credit (per annual subscription).
Earning C redit: Physicians with current and valid licenses in the United
States, who read all CME articles during each Emergency 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.
Indeterminate
Continuing area of research
No recommendations until
further research
Level of Evidence:
Evidence not available
Higher studies in progress
Results inconsistent,
contradictory
Results not compelling
Publisher : Robert Williford. Vice Presiden t/General Manager : Connie Austin.

Executiv e Editor: Heidi Frost.
Direct all editorial or subscription-related questions to Pinnacle

Publishing, Inc.: 1-800-788-1900 or 770-992-9401
Fax: 770-993-4323
Pinnacle Publishing, Inc.
P.O. Box 769389
Roswell, GA 30076-8220
E-mail: emer gmed@pinpub .com
Adapted from: The Emergency

Cardiovascular Care Committees
of the American Heart Association
and representatives from the
resuscitation councils of ILCOR:
How to Develop Evidence-Based
Guidelines for Emergency Cardiac
Care: Quality of Evidence and
Classes of Recommendations; also:
Anonymous. Guidelines for
cardiopulmonary resuscitation and
emergency cardiac care. Emergency Cardiac Care Committee and
Subcommittees, American Heart
Association. Part IX. Ensuring
effectiveness of community-wide
emergency cardiac care. JAMA
1992;268(16):2289-2295.
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Allergic Emergencies and Anaphylaxis How To Avoid Getting Stung PDF

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EMERGENCY MEDICINE PRACTICE

History And Epidemiology

Medicine, The University of

Chair, Pediatric Emergency

Date of original release: April 1, 2000.

School of Medicine; Attending

FAAP, Assistant Professor of

familial tendency toward atopic disorders linked

reactions are usually responses to inhaled antigens,

The Immune Response

Pathophysiology: A Simple Primer

Table 1. Classification Of Immunologic Reactions

IgE (Rarely IgG4)

IgG, IgM (Cell-Ag)

Note: This classification is an oversimplication.

Figure 1. Sensitization Phase Of Allergy (Antigen-Induced Immune Stimulation).

Antigen Processing Cell

Emergency Medicine Practice

in the biochemistry of allergy.

mediators without involving antibodies. Many stimuli

The Allergic Stew

Figure 2. Allergy Mechanism.

Medications: Radio-iodinated contrast agents, salicylates,

Release of Mediators of Inflammation

Emergency Medicine Practice

Urticaria is both the mildest and most common

extremity edema is often associated with abdominal

Causes Of Hypersensitivity Reactions

Figure 3. Time Course Of Allergic Reaction.

Specific IgE concentration

Hypersensitivity reactions can

Classic Allergic Reaction

Increased mucus production

Smooth muscle contraction

Number of mast cells

Table 3. Frequency Of Occurrence Of Signs

Table 4. Causes Of Hypersensitivity Reactions.*

Drugs (e.g., antimicrobials, nonsteroidals)

Urticaria and angioedema

Dizziness, syncope, hypotension

Nausea, vomiting, diarrhea,

Environmental (e.g., house dust mites, pollens, molds, other

Soaps, lotions, detergents

Envenomations (e.g., Hymenoptera)

Upper airway edema

Miscellaneous: cold, light, vibration, pressure, exercise

Food (e.g., peanuts, tree nuts, fish, shellfish, eggs, certain

Itch without rash

Adapted from: Middleton E Jr., et al. Allergy: Principles and Practice.

Emergency Medicine Practice

Drugs And Medications

ity reactions. A wide variety of allergens is responsible

While numerous medications can cause allergic

1. Hypoxia k ills. Hoarseness or stridor should prompt

8. Self-stimula tion. Epinephrine self-injectable

3. Recogniz e limits . Antihistamines and steroids may

9. Aller gy is an acquir ed disor der. Patients who

5. Its a famil y affair . Hereditary angioedema presents

10. Be suspicious . Remember to include anaphylaxis

6. Around the blo ck. Patients with allergic reactions

Emergency Medicine Practice

the future.23 In one study of 86 consecutive children