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## Complete Summary

#### GUIDELINE TITLE

The diagnosis and management of anaphylaxis: an updated practice
parameter.

#### BIBLIOGRAPHIC SOURCE(S)

The diagnosis and management of anaphylaxis: an updated practice
parameter. J Allergy Clin Immunol 2005 Mar;115(3 Suppl):S483-523. \[232
references\]
[PubMed](http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15753926)

#### GUIDELINE STATUS

This is the current release of the guideline.

This guideline updates a previous version: Joint Council of Allergy,
Asthma and Immunology. The diagnosis and management of anaphylaxis. J
Allergy Clin Immunol 1998 Jun;101(6 Pt 2):S465-S528.

### COMPLETE SUMMARY CONTENT

 SCOPE\
 METHODOLOGY - including Rating Scheme and Cost Analysis\
 RECOMMENDATIONS\
 EVIDENCE SUPPORTING THE RECOMMENDATIONS\
 BENEFITS/HARMS OF IMPLEMENTING THE GUIDELINE RECOMMENDATIONS\
 CONTRAINDICATIONS\
 QUALIFYING STATEMENTS\
 IMPLEMENTATION OF THE GUIDELINE\
 INSTITUTE OF MEDICINE (IOM) NATIONAL HEALTHCARE QUALITY REPORT
CATEGORIES\
 IDENTIFYING INFORMATION AND AVAILABILITY\
 DISCLAIMER

### SCOPE

#### DISEASE/CONDITION(S)

Anaphylaxis and anaphylactoid reactions, including:

-   Anaphylaxis to foods

-   Latex-induced anaphylaxis

-   Anaphylaxis during general anesthesia, the intraoperative period,
    and the postoperative period

-   Seminal fluid-induced anaphylaxis

-   Exercise-induced anaphylaxis

-   Idiopathic anaphylaxis

-   Anaphylaxis and allergen immunotherapy vaccine

-   Anaphylaxis to drugs

#### GUIDELINE CATEGORY

Diagnosis\
Evaluation\
Management\
Prevention\
Risk Assessment\
Treatment

#### CLINICAL SPECIALTY

Allergy and Immunology\
Emergency Medicine\
Family Practice\
Internal Medicine\
Pediatrics

#### INTENDED USERS

Physicians

#### GUIDELINE OBJECTIVE(S)

To improve the care of patients by providing the practicing physician
with an evidence-based approach to the diagnosis and management of
anaphylactic reactions

#### TARGET POPULATION

Patients at risk for anaphylactic or anaphylactoid reactions

#### INTERVENTIONS AND PRACTICES CONSIDERED

**Evaluation/Diagnosis/Risk Assessment**

1.  Patient history

2.  Signs and symptoms

3.  Diagnostic tests (e.g., skin prick tests, food challenges, in vitro
    testing)

4.  Laboratory tests (e.g., serum tryptase)

5.  Intensive evaluation, including a meticulous history (idiopathic
    anaphylaxis)

**Prevention/Management**

1.  Patient education (early treatment, self-administration of
    epinephrine, and use of medical condition identification bracelet)

2.  Avoidance measures

3.  Prophylaxis with glucocorticosteroids and antihistamines

4.  Allergen immunotherapy

5.  Desensitization to medications

**Treatment**

1.  Epinephrine and oxygen

2.  Volume replacement with colloid or crystalloids

3.  Immunotherapy

4.  Cardiopulmonary resuscitation and advanced cardiac life support for
    cardiopulmonary arrest during anaphylaxis

5.  Transport to emergency or intensive care facility

6.  Individualized follow-up

7.  Consultation with allergist-immunologist

#### MAJOR OUTCOMES CONSIDERED

-   Mortality due to anaphylaxis

-   Recurrence of anaphylaxis or anaphylactoid reactions

-   Utility of diagnostic interventions

### METHODOLOGY

#### METHODS USED TO COLLECT/SELECT EVIDENCE

Searches of Electronic Databases

#### DESCRIPTION OF METHODS USED TO COLLECT/SELECT THE EVIDENCE

A comprehensive search of the medical literature was conducted with
various search engines, including PubMed, using appropriate search
terms.

#### NUMBER OF SOURCE DOCUMENTS

Not stated

#### METHODS USED TO ASSESS THE QUALITY AND STRENGTH OF THE EVIDENCE

Weighting According to a Rating Scheme (Scheme Given)

#### RATING SCHEME FOR THE STRENGTH OF THE EVIDENCE

Ia Evidence from meta-analysis of randomized controlled trials

Ib Evidence from at least one randomized controlled trial

IIa Evidence from at least one controlled study without randomization

IIb Evidence from at least one other type of quasiexperimental study

III Evidence from nonexperimental descriptive studies, such as
comparative studies

IV Evidence from expert committee reports or opinions or clinical
experience of respected authorities or both

#### METHODS USED TO ANALYZE THE EVIDENCE

Systematic Review

#### DESCRIPTION OF THE METHODS USED TO ANALYZE THE EVIDENCE

Published clinical studies were rated by category of evidence and used
to establish the strength of the clinical recommendations.

#### METHODS USED TO FORMULATE THE RECOMMENDATIONS

Expert Consensus

#### DESCRIPTION OF METHODS USED TO FORMULATE THE RECOMMENDATIONS

Not stated

#### RATING SCHEME FOR THE STRENGTH OF THE RECOMMENDATIONS

A.  Directly based on category I evidence

B.  Directly based on category II evidence or extrapolated
    recommendation from category I evidence

C.  Directly based on category III evidence or extrapolated
    recommendation from category I or II evidence

D.  Directly based on category IV evidence or extrapolated
    recommendation from category I, II, or III evidence

NR Not rated

#### COST ANALYSIS

A formal cost analysis was not performed and published cost analyses
were not reviewed.

#### METHOD OF GUIDELINE VALIDATION

Peer Review

#### DESCRIPTION OF METHOD OF GUIDELINE VALIDATION

A workgroup chaired by Phillip Lieberman, MD, prepared the initial
draft. The Joint Task Force then reworked the initial draft into a
working draft of the document. The working draft of this updated
parameter was reviewed by a large number of experts on anaphylaxis
selected by the sponsoring organizations. This document represents an
evidence-based and broadly accepted consensus viewpoint on the diagnosis
and management of anaphylaxis.

### RECOMMENDATIONS

#### MAJOR RECOMMENDATIONS

This practice parameter includes algorithms for the initial evaluation
and management of a patient with a history of an episode of anaphylaxis
and for the treatment of acute anaphylaxis accompanied by annotations
(numbered to correspond to the algorithms). Guideline recommendations
are presented in the form of summary statements. After each statement is
a letter that indicates the strength of the recommendation. Grades of
recommendations are defined at the end of the Major Recommendations
field.

**[Algorithm for Initial Evaluation and Management of a Patient with a
History of Anaphylaxis]{.underline}**

**Annotation 1: Is the history consistent with a previous episode of
anaphylaxis?**

All individuals who have had a known or suspected anaphylactic episode
require a careful and complete review of their clinical history. This
history might elicit manifestations, such as urticaria, angioedema,
flushing, pruritus, upper airway obstruction, gastrointestinal symptoms,
syncope, hypotension, lower airway obstruction, and/or dizziness.

Of primary importance is the nature of the symptoms characterizing the
event. Essential questions to be asked are as follows:

1.  Were there cutaneous manifestations, specifically pruritus, flush,
    urticaria, and angioedema?

2.  Was there any sign of airway obstruction involving either the upper
    airway or the lower airway?

3.  Were there gastrointestinal symptoms (i.e., nausea, vomiting, or
    diarrhea)?

4.  Were syncope or presyncopal symptoms present?

At this point, it should be noted that the absence of cutaneous symptoms
puts the diagnosis in question because the majority of anaphylaxis
includes cutaneous symptoms, but their absence would not necessarily
rule out an anaphylactic or anaphylactoid event.

The history should concentrate on agents encountered before the
reaction. Whenever appropriate, the information should be obtained from
not only the patient but also family members or other witnesses. The
complete sequence of events must be reviewed, with special attention
paid to the cardiorespiratory symptoms. Medical records, including
medication records, can often be useful in evaluating the history,
physical findings, and treatment of the clinical event. In addition, the
results of any previous laboratory studies (e.g., serum tryptase levels)
might be helpful in making the diagnosis of anaphylaxis or
distinguishing it from other entities.

**Annotation 1A: Consider consultation with an allergist-immunologist**

Patients with anaphylaxis might be first seen with serious and
life-threatening symptoms. Evaluation and diagnosis, as well as
long-term management, can be complex. The allergist-immunologist has the
training and expertise to obtain a detailed allergy history, coordinate
laboratory and allergy testing, evaluate the benefits and risks of
therapeutic options, and counsel the patient on avoidance measures. For
these reasons, patients with a history of anaphylaxis should be
considered for referral to an allergy-immunology specialist.

**Annotation 2: Pursue other diagnoses or make appropriate referral**

Other conditions that should be considered in the differential diagnosis
include the following: (1) vasodepressor (vasovagal-neurocardiogenic)
syncope; (2) syndromes that can be associated with flushing (e.g.,
metastatic carcinoid); (3) postprandial syndromes (e.g., scombroid
poisoning); (4) systemic mastocytosis; (5) psychiatric disorders that
can mimic anaphylaxis, such as panic attacks or vocal cord dysfunction
syndrome; (6) angioedema (e.g., hereditary angioedema); (7) other causes
of shock (e.g., cardiogenic); and (8) other cardiovascular or
respiratory events.

**Annotation 3: Is cause readily identified by history?**

The history is the most important tool to establish the cause of
anaphylaxis and takes precedence over diagnostic tests. A detailed
history of all ingestants (both foods and drugs) several hours before
the episode should be obtained. In addition, the labels for all packaged
foods ingested by the patient in this period of time should be reviewed
because a substance added to the food (e.g., carmine) could be
responsible. A history of any preceding bite or sting should be
obtained. The patient\'s activities (e.g., exercise, sexual activity, or
both) preceding the event should be reviewed. Patient diaries might be a
useful adjunct in confirming and identifying the cause of anaphylaxis.

**Annotation 4: Consider idiopathic anaphylaxis**

Idiopathic anaphylaxis is a diagnosis of exclusion that should be made
only after other causes of anaphylaxis and other differential diagnoses
have been considered.

**Annotation 5: Are further diagnostic tests indicated: immediate
hypersensitivity or in vitro tests, challenge tests?**

Immediate hypersensitivity tests or in vitro specific immunoglobulin E
(IgE) tests and/or challenge tests might be appropriate to help define
the cause of the anaphylactic episode. However, the history might be so
specific that none of the above tests are necessary.

**Annotation 6: Diagnosis established on basis of history, risk of
testing, limitation of tests, patient refuses test, other management
options available, management**

There might be circumstances in which allergy skin tests, in vitro
specific IgE tests, and/or challenge tests might not be warranted. In
general, this might apply when the clinician (with the consent of the
patient) decides to proceed with management on the basis of the history
and physical examination.

For example, the clinical history of anaphylaxis to a specific agent
might be so strong that testing is unnecessary (or dangerous).
Conversely, the medical history of anaphylaxis might be sufficiently
mild or weak that management can proceed in the absence of testing. If
avoidance can be easily and safely accomplished, testing might not be
necessary.

Furthermore, testing or challenge with reagents to a suspected allergen
might not be available, or the accuracy of the test might be in
question. In addition, for patients with a history of anaphylaxis,
challenge tests (and, to a lesser extent, skin tests) might be
hazardous.

**Annotation 7: Testing identifies specific cause of anaphylaxis**

Skin tests or in vitro tests that determine the presence of specific IgE
antibodies can identify specific causes of anaphylaxis. Causes of
anaphylaxis that can be defined in this way include foods, medications
(e.g., penicillin and insulin), and stinging insects. For the majority
of medications, standardized testing either by in vivo or in vitro means
is not available. Such tests are only valid when the reaction is due to
a true anaphylactic event (IgE-mediated reaction) and not as a result of
an anaphylactoid (non-IgE-mediated) reaction.

In general, skin testing is more sensitive than in vitro testing and is
the diagnostic procedure of choice for evaluation of most potential
causes of anaphylaxis (e.g., penicillin, insect stings, and foods). It
is essential that the correct technique for skin testing be used to
obtain meaningful data regarding causative agents of anaphylaxis. When
possible, standardized extracts should be used (occasionally fresh food
extracts will be superior to available standardized extracts). If the
skin testing extract has not been standardized (e.g., latex, protamine,
or antibiotics other than penicillin), the predictive value is
uncertain. If skin testing is performed, it should be done under the
supervision of a physician who is experienced in the procedure in a
setting with appropriate rescue equipment and medication.

The accuracy of in vitro testing depends on the reliability of the in
vitro method, the ability to interpret the results, and the availability
of reliable testing material. The clinical significance of skin test or
in vitro test results depends on the ability to correlate such results
with the patient\'s history.

If tests for specific IgE antibodies (i.e., skin tests, in vitro tests,
or both) do not provide conclusive evidence of the cause of anaphylaxis,
challenge with the suspected agent can be considered. Challenge
procedures might also be appropriate in patients with anaphylactoid
reactions (e.g., reactions to aspirin or other nonsteroidal
anti-inflammatory drugs). Challenges with suspected agents must be done
carefully by individuals knowledgeable in the challenge procedure and
with expertise in managing reactions to the challenge agent if they
should occur.

**Annotation 8: Reconsider clinical diagnosis, reconsider idiopathic
anaphylaxis, consider other triggers, consider further testing,
management**

At this stage in the patient\'s evaluation, it is particularly important
to consider other trigger factors and diagnoses. The medical history and
laboratory test results should be reviewed. Further testing for specific
IgE antibodies should be considered. Laboratory studies that might be
helpful include serum tryptase measurement, as well as urinary
5-hydroxyindoleacetic acid, methylhistamine, and catecholamine
measurement. Idiopathic anaphylaxis is a diagnosis of exclusion (see
\"Idiopathic anaphylaxis\").

Management of anaphylaxis episodes should follow annotation 10 (see
algorithm).

**Annotation 9: Diagnosis made of specific cause of anaphylaxis**

The diagnosis of a specific cause of anaphylaxis might be supported by
the results of skin tests, in vitro IgE tests, and/or challenge tests
(particularly double-blind, placebo-controlled challenge tests).

**Annotation 10: Management of anaphylaxis**

When anaphylaxis has occurred because of exposure to a specific agent
(e.g., food, medication, or insect sting), patients should be educated
about agents or exposures that would place them at risk for future
reactions and be counseled on avoidance measures that might be used to
reduce risk for such exposures. Patients who have had anaphylactic
reactions to food should be instructed on how to read food ingredient
labels to identify foods that they should avoid. Patients with
anaphylaxis to medications should be informed about all cross-reacting
medications that should be avoided. Should there be a future essential
indication for use of incriminated medications, it might be helpful to
educate patients about applicable management options (e.g., medication
pretreatment and use of low-osmolarity agents in patients with a history
of reactions to radiographic contrast media or desensitization for
drugs, such as antibiotics). Patients who have had anaphylactic
reactions to insect stings should be advised about avoidance measures to
reduce the risk of insect stings and are candidates for insect venom
immunotherapy (see \'\'Stinging insect hypersensitivity: a practice
parameter update\'\'). Patients who have had anaphylaxis should carry
self-injectable epinephrine for use if anaphylaxis develops. There might
be exceptions to this (e.g., anaphylaxis to penicillin). Patients should
also carry identification indicating that they are prone to anaphylaxis
and indicating the responsible agent. Patients taking beta-blockers are
at increased risk during anaphylaxis.

**[Algorithm for the Treatment of Acute Anaphylaxis]{.underline}**

**Annotation 1. Anaphylaxis preparedness**

It is important to stress that management recommendations are subject to
physician discretion and that variations in sequence and performance
rely on physician judgment. Additionally, a determination of when a
patient should be transferred to an emergency facility depends on the
skill, experience, and clinical decision making of the individual
physician. Preparedness, prompt recognition, and appropriate and
aggressive treatment are integral to parts of successful management of
anaphylaxis. A treatment log will assist in accurately recording
progress.

Recommendations depend on practice resources and the proximity to other
emergency assistance. Stocking and maintaining anaphylaxis supplies with
regular written documentation of contents and expiration dates and ready
availability of injectable epinephrine, intravenous fluids and needles,
oxygen and mask cannula, airway adjuncts, and stethoscope and
sphygmomanometer are bare essentials. (An example of a supply checklist
is included in Figure 4 in the original guideline document. Not all
items need to be present in each office.)

Regular anaphylaxis practice drills, the contents of which are left to
the discretion and qualifications of the individual physician, are
strongly recommended. Essential ingredients are identification of a
person who will be responsible for calling emergency medical services
and the person who will document treatment and time each is rendered.
The emergency kit should be up to date and complete. Everyone who will
be directly involved in patient care should, for example, be able to
easily locate necessary supplies and rapidly assemble fluids for
intravenous administration.

**Annotation 2. Patient presents with possible-probable acute
anaphylaxis**

Anaphylaxis is an acute life-threatening reaction, usually but not
always mediated by an immunologic mechanism (anaphylactoid reactions are
IgE independent), that results from the sudden systemic release of mast
cells and basophil mediators. It has varied clinical presentations, but
respiratory compromise and cardiovascular collapse cause the most
concern because they are the most frequent causes of fatalities.
Urticaria and angioedema are the most common manifestations of
anaphylaxis but might be delayed or absent in rapidly progressive
anaphylaxis. The more rapidly anaphylaxis occurs after exposure to an
offending stimulus, the more likely the reaction is to be severe and
potentially life-threatening.

Anaphylaxis often produces signs and symptoms within minutes of exposure
to an offending stimulus (see comments in text in the original guideline
document), but some reactions might develop later (e.g., \>30 minutes
after exposure). Late-phase or biphasic reactions, which occur 8 to 12
hours after the initial attack, have also been reported. Protracted and
severe anaphylaxis might last up to 32 hours, despite aggressive
treatment.

Increased vascular permeability, a characteristic feature of
anaphylaxis, allows transfer of as much as 50% of the intravascular
fluid into the extravascular space within 10 minutes. As a result,
hemodynamic collapse might occur rapidly with little or no cutaneous or
respiratory manifestations.

**Annotation 3. Initial assessment supports potential anaphylaxis**

Initial assessment should determine whether history and physical
findings are compatible with anaphylaxis. The setting of the episode and
the history might suggest or reveal the source of the reaction.
Evaluation should include level of consciousness (impairment might
reflect hypoxia), upper and lower airways (dysphonia, stridor, cough,
wheezing, or shortness of breath), cardiovascular system (hypotension
with or without syncope and/or cardiac arrhythmias), the skin (diffuse
or localized erythema, pruritus, urticaria, and/or angioedema), and the
gastrointestinal system (nausea, vomiting, or diarrhea). In addition,
some patients might have symptoms of lightheadedness, headache, uterine
cramps, feeling of impending doom, and unconsciousness.

The vasodepressor (vasovagal) reaction probably is the condition most
commonly confused with anaphylactic and anaphylactoid reactions. In
vasodepressor reactions, however, urticaria is absent, the heart rate is
typically bradycardic, bronchospasm or other breathing difficulty is
generally absent, the blood pressure is usually normal or increased, and
the skin is typically cool and pale. Tachycardia is the rule in
anaphylaxis, but it might be absent in patients with conduction defects,
with increased vagal tone caused by a cardioinhibitory (Bezold-Jarisch)
reflex, or who take sympatholytic medications.

**Annotation 4. Consider other diagnosis**

Other diagnoses that might present with signs and/or symptoms
characteristic of anaphylaxis should be excluded. Like anaphylaxis,
several conditions might cause abrupt and dramatic patient collapse.
Among conditions to consider are vasodepressor (vasovagal) reactions,
acute anxiety (e.g., panic attack or hyperventilation syndrome),
myocardial dysfunction, pulmonary embolism, systemic mast cell
disorders, foreign-body aspiration, acute poisoning, hypoglycemia, and
seizure disorder. Specific signs and symptoms of anaphylaxis might
present singly in other disorders. Examples are urticaria-angioedema,
hereditary angioedema, and asthma.

**Annotation 5. Immediate intervention**

The clinician should remember that anaphylaxis occurs as part of a
continuum. Symptoms not immediately life-threatening might progress
rapidly unless treated promptly. Treatment recommendations are subject
to physician discretion, and variations in sequence and performance rely
on physician judgment. Additionally, a determination of when a patient
should be transferred to an emergency or intensive care facility depends
on available resources and the skill, experience, and clinical decision
making of the individual physician.

1.  Assess airway, breathing, circulation, and level of consciousness
    (altered mentation might suggest the presence of hypoxia).

2.  Administer epinephrine. Aqueous epinephrine 1:1000 dilution (1
    mg/mL), 0.2 to 0.5 mL (0.01 mg/kg in children, maximum 0.3-mg
    dosage) intramuscularly or subcutaneously every 5 minutes, as
    necessary, should be used to control symptoms and increase blood
    pressure. Consider dose-response effects. Note: If the clinician
    deems it appropriate, the 5-minute interval between injections can
    be liberalized to permit more frequent injections. Intramuscular
    epinephrine injections into the thigh have been reported to provide
    more rapid absorption and higher plasma epinephrine levels in both
    children and adults than intramuscular or subcutaneous injections
    administered in the arm. However, similar studies comparing
    intramuscular injections with subcutaneous injections in the thigh
    have not yet been done. Moreover, these studies were not performed
    in patients experiencing anaphylaxis. For this reason, the
    generalizability of these findings to the clinical setting of
    anaphylaxis has not been established. Although intuitively more
    rapid absorption and higher epinephrine levels would seem desirable,
    the clinical significance of this finding is not known. No data
    support the use of epinephrine in anaphylaxis through a
    nonparenteral route. However, alternative routes of administration
    have been anecdotally successful. These include, for example,
    inhaled epinephrine in the presence of laryngeal edema or sublingual
    administration if an intravenous route cannot be obtained.
    Endotracheally administered dosages have also been proposed for use
    when intravenous access is not available in intubated patients
    experiencing cardiac arrest.

**Annotation 6. Subsequent emergency care that might be necessary
depending on response to epinephrine**

1.  Place patient in the recumbent position and elevate the lower
    extremities, as tolerated symptomatically. This slows progression of
    hemodynamic compromise, if present, by preventing orthostatic
    hypotension and helping to shunt effective circulation from the
    periphery to the head and to the heart and kidneys.

2.  Establish and maintain airway. Ventilatory assistance through a
    1-way valve facemask with an oxygen inlet port (e.g., Pocket-Mask
    \[Laerdalâ, Preparedness Industries, Ukiah, Calif\] or similar
    device) might be necessary. Ambubags of less than 700 mL are
    discouraged in adults in the absence of an endotracheal tube because
    ventilated volume will not overcome 150 to 200 mL of anatomic dead
    space to provide effective tidal volume. (Ambubags can be used in
    children, provided the reservoir volume of the device is
    sufficient.) Endotracheal intubation or cricothyroidotomy might be
    considered where appropriate and provided that clinicians are
    adequately trained and proficient in this procedure.

3.  Administer oxygen. Oxygen should be administered to patients with
    anaphylaxis who have prolonged reactions, have pre-existing
    hypoxemia or myocardial dysfunction, receive inhaled beta-agonists
    as part of therapy for anaphylaxis, or require multiple doses of
    epinephrine. Continuous pulse oximetry and/or arterial blood gas
    determination (where available) should guide oxygen therapy where
    hypoxemia is a concern.

4.  Consider a normal saline intravenous line for fluid replacement and
    venous access. Lactated Ringer\'s solution might potentially
    contribute to metabolic acidosis, and dextrose is rapidly
    extravasated from the intravascular circulation to the interstitial
    tissues. Increased vascular permeability in anaphylaxis might permit
    transfer of 50% of the intravascular fluid into the extravascular
    space within 10 minutes. Crystalloid volumes (e.g., saline) of up to
    7 L might be necessary. One to 2 L of normal saline should be
    administered to adults at a rate of 5 to 10 mL/kg in the first 5
    minutes. Patients with congestive heart failure or chronic renal
    disease should be observed cautiously to prevent volume overload.
    Children should receive up to 30 mL/kg in the first hour. Adults
    receiving colloid solution should receive 500 mL rapidly, followed
    by slow infusion. Aqueous epinephrine 1:1000, 0.1 to 0.3 mL in 10 mL
    of normal saline, can be administered intravenously over several
    minutes and repeated as necessary in cases of anaphylaxis not
    responding to epinephrine injections and volume resuscitation.
    Alternatively, an epinephrine infusion can be prepared by adding 1
    mg (1 mL) of a 1:1000 dilution of epinephrine to 250 mL of D5W to
    yield a concentration of 4.0 micrograms/mL. This solution is infused
    at a rate of 1 to 4 micrograms/min (15 to 60 drops per minute with a
    microdrop apparatus \[60 drops per minute = 1 mL = 60 mL/h\]),
    increasing to a maximum of 10.0 micrograms/min. If an infusion pump
    is available, an alternative 1:100,000 solution of epinephrine (1 mg
    \[1 mL\] in 100 mL of saline) can be prepared and administered
    intravenously at an initial rate of 30 to 100 mL/h (5 to 15
    micrograms/min), titrated up or down depending on clinical response
    or epinephrine side effects (toxicity). A dosage of 0.01 mg/kg (0.1
    mL/kg of a 1:10,000 solution; maximum dose, 0.3 mg) is recommended
    for children. Alternative pediatric dosage by the \"rule of 6\" is
    as follows: 0.6 times body weight (in kilograms) = the number of
    milligrams diluted to a total of 100 mL of saline; then 1 mL/h
    delivers 0.1 microgram/kg/min. Note: Because of the risk for
    potentially lethal arrhythmias, epinephrine should be administered
    intravenously only during cardiac arrest or to profoundly
    hypotensive patients who have failed to respond to intravenous
    volume replacement and several injected doses of epinephrine. In
    situations in which hemodynamic monitoring is available (e.g.,
    emergency department or intensive care facility), continuous
    hemodynamic monitoring is essential. However, use of intravenous
    epinephrine should not be precluded in a scenario in which such
    monitoring is unavailable if the clinician deems administration is
    essential after failure of several epinephrine injections. If
    intravenous epinephrine is considered essential under these special
    circumstances, monitoring by available means (e.g., every-minute
    blood pressure and pulse measurements and electrocardiographic
    monitoring, if available) should be conducted.

5.  Consider diphenhydramine, 1 to 2 mg/kg or 25 to 50 mg per dose
    (parenterally). Note: H~1~ antihistamines are considered second-line
    therapy to epinephrine and should never be administered alone in the
    treatment of anaphylaxis.

6.  Consider ranitidine, 50 mg in adults and 12.5 to 50 mg (1 mg/kg) in
    children, which might be diluted in 5% dextrose to a total volume of
    20 mL and injected intravenously over 5 minutes. Cimetidine (4
    mg/kg) can be administered intravenously to adults, but no pediatric
    dosage in anaphylaxis has been established. Note: In the management
    of anaphylaxis, a combination of diphenhydramine and ranitidine is
    superior to diphenhydramine alone. However, these agents have a much
    slower onset of action than epinephrine and should never be used
    alone in the treatment of anaphylaxis. Both alone and in
    combination, these agents are second-line therapy to epinephrine.

7.  Bronchospasm resistant to adequate doses of epinephrine: consider
    inhaled beta-agonist (e.g., nebulized albuterol, 2.5 to 5 mg in 3 mL
    of saline and repeat as necessary).

8.  Hypotension refractory to volume replacement and epinephrine
    injections: consider vasopressor infusion. Continuous hemodynamic
    monitoring is essential. For example, dopamine (400 mg in 500 mL of
    5% dextrose) can be infused at 2 to 20 micrograms/kg/min and
    titrated to maintain systolic blood pressure of greater than 90 mm
    Hg.

9.  Consider glucagon infusion when concomitant beta-adrenergic blocking
    agent complicates treatment. Glucagon dosage is 1 to 5 mg (20 to 30
    micrograms/kg \[maximum dose, 1 mg\] in children) administered
    intravenously over 5 minutes and followed by an infusion (5 to 15
    micrograms/min) titrated to clinical response.

10. Consider systemic glucocorticosteroids for patients with a history
    of idiopathic anaphylaxis or asthma and patients who experience
    severe or prolonged anaphylaxis. Glucocorticosteroids usually are
    not helpful acutely but potentially might prevent recurrent or
    protracted anaphylaxis. If given, intravenous glucocorticosteroids
    should be administered every 6 hours at a dosage equivalent to 1.0
    to 2.0 mg/kg/d. Oral administration of glucocorticosteroids (e.g.,
    prednisone, 0.5 mg/kg) might be sufficient for less critical
    anaphylactic episodes.

11. Consider transportation to emergency department or intensive care
    facility.

**Annotation 7. Cardiopulmonary arrest during anaphylaxis**

1.  Cardiopulmonary resuscitation and advanced cardiac life support
    measures.

2.  High-dose epinephrine administered intravenously (i.e., rapid
    progression to high dose). A common sequence is 1 to 3 mg (1:10,000
    dilution) slowly administered intravenously over 3 minutes, 3 to 5
    mg administered intravenously over 3 minutes, and then a 4 to 10
    microgram/min infusion. For children, the recommended initial
    resuscitation dosage is 0.01 mg/kg (0.1 mL/kg of a 1:10,000 solution
    up to 10 mg/min rate of infusion) repeated every 3 to 5 minutes for
    ongoing arrest. Higher subsequent dosages (0.1 to 0.2 mg/kg; 0.1
    mL/kg of a 1:1,000 solution) might be considered for unresponsive
    asystole or pulseless electrical activity.

3.  Rapid volume expansion.

4.  Atropine and transcutaneous pacing if asystole and/or pulseless
    electrical activity are present.

5.  Prolonged resuscitation is encouraged, if necessary, because efforts
    are more likely to be successful in anaphylaxis.

6.  Transport to emergency department or intensive care facility, as
    setting dictates.

**Annotation 8. Observation and subsequent follow-up**

Observation periods must be individualized because there are no reliable
predictors of biphasic or protracted anaphylaxis on the basis of initial
clinical presentation. Follow-up accordingly must be individualized and
based on such factors as clinical scenario and distance from the
patient\'s home to the closest emergency facility. After resolution of
the acute episode, patients should be provided with an epinephrine
syringe and receive proper instruction for self-administration in case
of a subsequent episode. In circumstances in which an
allergist-immunologist is not already involved, it is strongly
recommended that individuals who have experienced acute anaphylaxis
should receive consultation from an allergist-immunologist regarding
diagnosis, prevention, and treatment.

**Annotation 9. Consider consultation with an allergist-immunologist**

After acute anaphylaxis, patients should be assessed for future risk for
anaphylaxis. The allergist-immunologist can obtain a detailed history,
coordinate allergy diagnostic testing, evaluate the risks and benefits
of therapeutic options, train and retrain in self-administration of
epinephrine, and provide counseling on avoidance measures (the most
effective treatment for most causes of anaphylaxis). Consultation with
an allergist-immunologist is recommended when:

1.  The diagnosis is doubtful or incomplete.

2.  The symptoms are recurrent or difficult to control.

3.  Help is needed in evaluation and management of medication use or
    side effects.

4.  Help is needed in medical management or adherence to treatment.

5.  Help is needed in the diagnosis or management of IgE-mediated
    reactions or identification of allergic triggers.

6.  The patient is a candidate for desensitization (e.g., penicillin) or
    immunotherapy (e.g., venom-specific immunotherapy).

7.  The patient requires daily medications for prevention.

8.  The patient requires intensive education regarding avoidance or
    management.

9.  Help is needed with new or investigative therapy.

10. Treatment goals have not been met.

11. Anaphylaxis is complicated by one or more comorbid conditions or
    concomitant medications.

12. The patient has requested a subspecialty consultation.

**[Summary Statements]{.underline}**

**Evaluation and Management of the Patient with a History of Episodes of
Anaphylaxis**

1.  The history is the most important tool to determine whether a
    patient has had anaphylaxis and the cause of the episode. (C)

2.  A thorough differential diagnosis should be considered, and other
    conditions should be ruled out. (C)

3.  Laboratory tests can be helpful to confirm a diagnosis of
    anaphylaxis or rule out other causes. Proper timing of studies
    (e.g., serum tryptase) is essential. (B)

4.  In the management of a patient with a previous episode, education is
    necessary. Emphasis on early treatment, specifically the
    self-administration of epinephrine, is essential. (C)

5.  The patient should be instructed to wear and/or carry identification
    denoting his or her condition (e.g., Medic Alert jewelry). (C)

**Management of Anaphylaxis**

6.  Medical facilities should have an established protocol to deal with
    anaphylaxis and the appropriate equipment to treat the episode. In
    addition, telephone numbers for paramedical rescue squads and
    ambulance services might be helpful to have on hand. (B)

7.  Anaphylaxis is an acute, life-threatening systemic reaction with
    varied mechanisms, clinical presentations, and severity that results
    from the sudden systemic release of mediators from mast cells and
    basophils. (B)

8.  Anaphylactic (IgE-dependent) and anaphylactoid (IgE-independent)
    reactions differ mechanistically, but the clinical presentations are
    identical. (C)

9.  The more rapidly anaphylaxis develops, the more likely the reaction
    is to be severe and potentially life threatening. (C)

10. Prompt recognition of signs and symptoms of anaphylaxis is crucial.
    If there is any doubt, it is generally better to administer
    epinephrine. (C)

11. Any health care facility should have a plan of action for
    anaphylaxis should it occur. Physicians and office staff should
    maintain clinical proficiency in anaphylaxis management. (D)

12. Epinephrine and oxygen are the most important therapeutic agents
    administered in anaphylaxis. Epinephrine is the drug of choice, and
    the appropriate dose should be administered promptly at the onset of
    apparent anaphylaxis. (A/D)

13. Appropriate volume replacement either with colloid or crystalloids
    and rapid transport to the hospital is essential for patients who
    are unstable or refractory to initial therapy for anaphylaxis in the
    office setting. (B)

**Anaphylaxis to Foods**

14. Severe food reactions have been reported to involve the
    gastrointestinal, cutaneous, respiratory, and cardiovascular
    systems. (D)

15. The greatest number of anaphylactic episodes in children has
    involved peanuts, tree nuts (i.e., walnuts, pecans, and others),
    fish, shellfish, milk, and eggs (C). The greatest number of
    anaphylactic episodes in adults is due to shellfish (C). Clinical
    cross-reactivity with other foods in the same group is unpredictable
    (B). Additives can also cause anaphylaxis (C).

16. Anaphylactic reactions to foods almost always occur immediately.
    Symptoms might then subside, only to recur several hours later. (A)

17. The most useful diagnostic tests include skin tests and food
    challenges. In vitro testing with foods might be appropriate as an
    alternative screening procedure. (C)

18. Double- or single-blind placebo-controlled food challenges can be
    done in patients with suspected food allergy in a medical facility
    by personnel experienced in performing the procedure and prepared to
    treat anaphylaxis. (B)

19. Patient education should include discussion about avoidance and
    management of accidental ingestion. (C)

20. Schools might present a special hazard for the student with food
    allergy. Epinephrine should be available for use by the individuals
    in the school trained to respond to such a medical emergency. (C)

**Latex-Induced Anaphylaxis**

21. Latex (rubber) hypersensitivity is a significant medical problem,
    and 3 groups are at higher risk of reaction: health care workers,
    children with spina bifida and genitourinary abnormalities, and
    workers with occupational exposure to latex. (C)

22. Skin prick tests with latex extracts should be considered for
    patients who are members of high-risk groups or who have a clinical
    history of possible latex allergy to identify IgE-mediated
    sensitivity. Although a standardized, commercial skin test reagent
    for latex is not available in the United States, many allergy
    centers have prepared latex extracts from gloves to be used for
    clinical testing. It should be noted, however, that such extracts
    prepared from gloves demonstrate tremendous variability in content
    of latex antigen. In vitro assays for IgE to latex might also be
    useful, although these tests are generally less sensitive than skin
    tests. (C)

23. Patients with spina bifida (regardless of a history of latex
    allergy) and other patients with a positive history of latex allergy
    ideally should have all medical-surgical-dental procedures performed
    in a latex-safe environment and as the first case of the day. (D)

24. A latex-safe environment is an environment in which no latex gloves
    are used in the room or surgical suite and no latex accessories
    (catheters, adhesives, tourniquets, and anesthesia equipment) come
    into contact with the patient. (D)

25. In health care settings general use of latex gloves with negligible
    allergen content, powder-free latex gloves, and nonlatex gloves and
    medical articles should be considered in an effort to minimize
    exposure to latex allergen. Such a combined approach might minimize
    latex sensitization of health care workers and patients and should
    reduce the risk of inadvertent reactions to latex in previously
    sensitized individuals. (C)

**Anaphylaxis during General Anesthesia, the Intraoperative Period, and
the Postoperative Period**

26. The incidence of anaphylaxis during anesthesia has been reported to
    range from 1 in 4,000 to 1 in 25,000. Anaphylaxis during anesthesia
    can present as cardiovascular collapse, airway obstruction,
    flushing, and/or edema of the skin. (C)

27. It might be difficult to differentiate between immune and nonimmune
    mast cell-mediated reactions and pharmacologic effects from the
    variety of medications administered during general anesthesia. (B)

28. Thiopental allergy has been documented by using skin tests. (B)

29. Neuromuscular blocking agents, such as succinylcholine, can cause
    nonimmunologic histamine release, but there have been reports of
    IgE-mediated mechanisms in some cases. (B)

30. Reactions to opioid analgesics are usually caused by direct mast
    cell-mediator release rather than IgE-dependent mechanisms. (B)

31. Antibiotics that are administered perioperatively can cause
    immunologic or nonimmunologic generalized reactions. (B)

32. Protamine can also cause severe systemic reactions through
    IgE-mediated or nonimmunologic mechanisms. (B)

33. Latex is a potent allergen, and IgE-mediated reactions to latex
    during anesthesia have been clearly documented. Patients with
    multiple surgical procedures (e.g., patients with spina bifida) and
    health care workers are at greater risk of latex sensitization.
    Precautions for latex-sensitive patients include avoiding the use of
    latex gloves and latex blood pressure cuffs, as well as latex
    intravenous tubing ports and rubber stoppers from medication vials.
    (B)

34. Blood transfusions can elicit a variety of systemic reactions, some
    of which might be IgE mediated or mediated through other immunologic
    mechanisms. (B)

35. Methylmethacrylate (bone cement) has been associated with
    hypotension and various systemic reactions, although no IgE
    mechanism has yet been documented. (C)

36. The evaluation of IgE-mediated reactions to medications used during
    anesthesia can include skin testing to a variety of anesthetic
    agents. (B)

37. The management of anaphylactic or anaphylactoid reactions that occur
    during general anesthesia is similar to the management of
    anaphylaxis in other situations. (B)

**Seminal Fluid-Induced Anaphylaxis**

38. Anaphylaxis caused by human seminal fluid has been shown to be due
    to IgE-mediated sensitization by proteins of varying molecular
    weights. (B)

39. Localized seminal plasma hypersensitivity has been well described
    and is likely IgE mediated on the basis of successful response to
    rapid seminal plasma desensitization. (C)

40. History of atopic disease is the most consistent risk factor.
    However, anecdotal case reports have been associated with
    gynecologic surgery, injection of anti-RH immunoglobulin, and the
    postpartum state. (C)

41. The diagnosis is confirmed by means of skin and/or in vitro tests
    for serum-specific IgE by using proper reagents obtained from
    fractionation of seminal fluid components. (C)

42. Prevention of reactions to seminal fluid can be accomplished by
    barrier use of condoms. (C)

43. Immunotherapy to properly fractionated seminal fluid proteins has
    been universally successful in preventing anaphylaxis to seminal
    fluid, provided the sensitizing seminal fluid fractions are used as
    immunogens. Successful intravaginal graded challenge with
    unfractionated seminal fluid has been reported in a few cases, but
    the duration of protection is unknown. (C)

44. Localized and/or systemic seminal plasma hypersensitivity is not
    associated with infertility. (D)

**Exercise-Induced Anaphylaxis**

45. Exercise-induced anaphylaxis is a form of physical allergy.
    Premonitory symptoms can include diffuse warmth, itching, and
    erythema. Urticaria generally ensues, with progression to confluence
    and often angioedema. Episodes can progress to include
    gastrointestinal symptoms, laryngeal edema, and/or vascular
    collapse. (B)

46. Factors that have been associated with exercise-induced anaphylaxis
    include medications (e.g., aspirin and other nonsteroidal
    anti-inflammatory drugs) or food ingestion before and after
    exercise. (C)

47. Patients with exercise-induced anaphylaxis might have a higher
    incidence of personal and/or family history of atopy. (C)

48. Medications used prophylactically are not useful in preventing
    exercise-induced anaphylaxis. (C)

49. If exercise-induced anaphylactic episodes have been associated with
    the ingestion of food, exercise should be avoided in the immediate
    postprandial period. (C)

50. Patients with exercise-induced anaphylaxis should carry epinephrine
    and should wear and/or carry Medic Alert identification denoting
    their condition. They should have a companion with them when
    exercising. This companion should be versed in the use of an EpiPen.
    (D)

**Idiopathic Anaphylaxis**

51. The symptoms of idiopathic anaphylaxis are identical to those of
    episodes related to known causes. (C)

52. Patients with idiopathic anaphylaxis should receive an intensive
    evaluation, including a meticulous history to rule out a definite
    cause of the events. (C)

53. There might be a need for specific laboratory studies to exclude
    systemic disorders, such as systemic mastocytosis. This might
    include a serum tryptase level when the patient is asymptomatic, a
    ratio of beta-tryptase to total tryptase during an event, and
    selective allergy skin testing. (C)

**Anaphylaxis and Allergen Immunotherapy Vaccines**

54. There is a small risk of near-fatal and fatal anaphylactic reactions
    to allergen immunotherapy injections. (C)

55. Patients with asthma, particularly poorly controlled asthma, are at
    higher risk for serious systemic reactions to allergen immunotherapy
    injections (C). Patients taking beta- adrenergic blocking agents are
    at higher risk for serious systemic reactions to allergen
    immunotherapy injections. (B)

56. Allergen immunotherapy vaccines should be administered only by
    health care professionals trained in the recognition and treatment
    of anaphylaxis, only in health care facilities with the proper
    equipment for the treatment of anaphylaxis, and in clinics with
    policies and procedures that minimize the risk of anaphylaxis. (D)

**Anaphylaxis to Drugs**

57. Low-molecular-weight medications induce an IgE-mediated reaction
    only after combining with a carrier protein to produce a complete
    multivalent antigen. (B)

58. Penicillin is the most common cause of drug-induced anaphylaxis. (C)

59. Penicillin spontaneously degrades to major and minor antigenic
    determinants, and skin testing with reagents on the basis of these
    determinants yields negative results in about 90% of patients with a
    history of penicillin allergy. (B)

60. The negative predictive value of penicillin skin testing (for
    immediate-type reactions) is between 97% and 99% (depending on the
    reagents used), and the positive predictive value is at least 50%.
    (B)

61. The extent of allergic cross-reactivity between penicillin and
    cephalosporins is unknown but appears to be low. Four percent of
    patients proved to have penicillin allergy by means of penicillin
    skin testing react to cephalosporin challenges. (C)

62. Patients with a history of penicillin allergy who have negative
    penicillin skin test responses might safely receive cephalosporins.
    (B)

63. Patients with a history of penicillin allergy who have positive
    penicillin skin test responses might (1) receive an alternate
    (non-beta-lactam) antibiotic, (2) receive a cephalosporin through
    graded challenge, or (3) receive a cephalosporin through rapid
    desensitization. (F)

64. Aztreonam does not cross-react with other beta lactams, except
    ceftazidime, with which it shares a common R-group side chain. (B)

65. Carbapenems should be considered cross-reactive with penicillin. (C)

66. Diagnosis of IgE-mediated reactions to non-beta-lactam antibiotics
    is limited by a lack of knowledge of the relevant allergenic
    determinants and/or metabolites. (C)

67. Aspirin and nonsteroidal anti-inflammatory drugs are the second most
    common cause of drug-induced anaphylaxis. (C)

68. Anaphylactic reactions to aspirin and nonsteroidal anti-inflammatory
    drugs appear to be medication specific and do not cross-react with
    structurally unrelated aspirin or other nonsteroidal
    anti-inflammatory drugs. (D)

**Prevention of Anaphylaxis**

69. Major risk factors related to anaphylaxis include, but are not
    limited to, prior history of such reactions, concomitant
    beta-adrenergic blocker therapy, exposure, or atopic background.
    Atopic background might be a risk factor for venom- and
    latex-induced anaphylaxis and possibly anaphylactoid reactions to
    radiographic contrast material but not for anaphylactic reactions to
    medications.

70. Avoidance measures are successful if future exposure to drugs,
    foods, additives, or occupational allergens can be prevented.
    Avoidance of stinging and biting insects is also possible in many
    cases. Prevention of systemic reactions during allergen
    immunotherapy is dependent on the specific circumstances involved.

71. Avoidance management should be individualized, taking into
    consideration factors such as age, activity, occupation, hobbies,
    residential conditions, access to medical care, and the patients\'
    level of personal anxiety.

72. Pharmacologic prophylaxis should be used to prevent recurrent
    anaphylactoid reactions to radiographic contrast material,
    fluorescein, as well as to prevent idiopathic anaphylaxis.
    Prophylaxis with glucocorticosteroids and antihistamines markedly
    reduces the occurrence of subsequent reactions.

73. Allergen immunotherapy with the appropriate stinging insect venom
    should be recommended for patients with systemic sensitivity to
    stinging insects because this treatment is highly (90 to 98%)
    effective.

74. Desensitization to medications that are known to have caused
    anaphylaxis can be effective. In most cases the effect of
    desensitization is temporary, and if the medication is required some
    time in the future, the desensitization process must be repeated.

75. Patient education might be the most important preventive strategy.
    Patients should be carefully instructed about hidden allergens,
    cross-reactions to various allergens, unforeseen risks during
    medical procedures, and when and how to use self-administered
    epinephrine. Physicians should educate patients about the risks of
    future anaphylaxis, as well as the benefits of avoidance measures.

**[Definitions]{.underline}**:

**Strength of Recommendation**

A.  Directly based on category I evidence

B.  Directly based on category II evidence or extrapolated
    recommendation from category I evidence

C.  Directly based on category III evidence or extrapolated
    recommendation from category I or II evidence

D.  Directly based on category IV evidence or extrapolated
    recommendation from category I, II, or III evidence

**Category of Evidence**

Ia Evidence from meta-analysis of randomized controlled trials

Ib Evidence from at least one randomized controlled trial

IIa Evidence from at least one controlled study without randomization

IIb Evidence from at least one other type of quasiexperimental study

III Evidence from nonexperimental descriptive studies, such as
comparative studies

IV Evidence from expert committee reports or opinions or clinical
experience of respected authorities or both

#### CLINICAL ALGORITHM(S)

Algorithms are provided in the original guideline document for:

-   The initial evaluation and management of a patient with a history of
    an episode of anaphylaxis

-   The treatment of acute anaphylaxis

### EVIDENCE SUPPORTING THE RECOMMENDATIONS

#### TYPE OF EVIDENCE SUPPORTING THE RECOMMENDATIONS

The type of supporting evidence is identified for each recommendation
(see \"Major Recommendations\").

### BENEFITS/HARMS OF IMPLEMENTING THE GUIDELINE RECOMMENDATIONS

#### POTENTIAL BENEFITS

Identification, prevention, and management of anaphylaxis and
anaphylactoid reactions

#### POTENTIAL HARMS

-   Because of the risk for potentially lethal arrhythmias, epinephrine
    should be administered intravenously only during cardiac arrest or
    to profoundly hypotensive subjects who have failed to respond to
    intravenous volume replacement and several injected doses of
    epinephrine.

-   Cimetidine, 4 mg/kg in adults, should be administered slowly because
    rapid intravenous administration might produce hypotension.
    Cimetidine should not be administered to children with anaphylaxis
    because no dosages have been established.

-   Often, but not always, pruritis of the oral tissues or nausea is the
    initial complaint after food challenge.

-   There is a small risk of near-fatal and fatal anaphylactic reactions
    to allergen immunotherapy injections. Patients with asthma,
    particularly poorly controlled asthma, and patients taking
    beta-adrenergic blocking agents are at higher risk for serious
    systemic reactions to allergen immunotherapy injections.

### CONTRAINDICATIONS

#### CONTRAINDICATIONS

Beta-adrenergic blockade is a relative contraindication for allergen
immunotherapy.

### QUALIFYING STATEMENTS

#### QUALIFYING STATEMENTS

-   This is a complete and comprehensive document at the current time.
    The medical environment is a changing environment, and not all
    recommendations will be appropriate for all patients.

-   Because this document incorporated the efforts of many participants,
    no single individual, including those who served on the Joint Task
    Force, is authorized to provide an official American Academy of
    Allergy, Asthma, and Immunology (AAAAI) or American College of
    Allergy, Asthma, and Immunology (ACAAI) interpretation of these
    practice parameters. Any request for information about or an
    interpretation of these practice parameters by the AAAAI or ACAAI
    should be directed to the Executive Offices of the AAAAI, the ACAAI,
    and the Joint Council of Allergy, Asthma, and Immunology.

-   These parameters are not designed for use by pharmaceutical
    companies in drug promotion.

-   This parameter was edited by Dr Nicklas in his private capacity and
    not in his capacity as a medical officer with the Food and Drug
    Administration. No official support or endorsement by the Food and
    Drug Administration is intended or should be inferred.

-   The Joint Task Force on Practice Parameters recognizes that there
    are different, although appropriate, approaches to the diagnosis and
    management of anaphylactic reactions that often require flexible
    recommendations. Therefore the diagnosis and management of
    anaphylactic reactions must be individualized on the basis of unique
    features in particular patients.

### IMPLEMENTATION OF THE GUIDELINE

#### DESCRIPTION OF IMPLEMENTATION STRATEGY

An implementation strategy was not provided.

#### IMPLEMENTATION TOOLS

Clinical Algorithm

For information about
[availability](#identifying-information-and-availability), see the
\"Availability of Companion Documents\" and \"Patient Resources\" fields
below.

### INSTITUTE OF MEDICINE (IOM) NATIONAL HEALTHCARE QUALITY REPORT CATEGORIES

#### IOM CARE NEED

Getting Better\
Living with Illness\
Staying Healthy

#### IOM DOMAIN

Effectiveness\
Patient-centeredness\
Safety\
Timeliness

### IDENTIFYING INFORMATION AND AVAILABILITY

#### BIBLIOGRAPHIC SOURCE(S)

The diagnosis and management of anaphylaxis: an updated practice
parameter. J Allergy Clin Immunol 2005 Mar;115(3 Suppl):S483-523. \[232
references\]
[PubMed](http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15753926)

#### ADAPTATION

Not applicable: The guideline was not adapted from another source.

#### DATE RELEASED

1998 Jun (revised 2005 Mar)

#### GUIDELINE DEVELOPER(S)

American Academy of Allergy, Asthma and Immunology - Medical Specialty
Society\
American College of Allergy, Asthma and Immunology - Medical Specialty
Society\
Joint Council of Allergy, Asthma and Immunology - Medical Specialty
Society

#### GUIDELINE DEVELOPER COMMENT

These guidelines were developed by the Joint Task Force on Practice
Parameters for Allergy and Immunology, which is sponsored by the
American Academy of Allergy, Asthma, and Immunology, the American
College of Allergy, Asthma, and Immunology and the Joint Council of
Allergy, Asthma and Immunology.

#### SOURCE(S) OF FUNDING

Funded by the American Academy of Allergy, Asthma, and Immunology
(AAAAI), the American College of Allergy, Asthma, and Immunology (ACAAI)
and the Joint Council of Allergy, Asthma and Immunology (JCAAI).

#### GUIDELINE COMMITTEE

Joint Task Force on Practice Parameters\
Work Group on Diagnosis and Management of Anaphylaxis

#### COMPOSITION OF GROUP THAT AUTHORED THE GUIDELINE

*Chief Editors*: Phillip Lieberman, MD, Departments of Medicine and
Pediatrics, University of Tennessee, College of Medicine, Memphis,
Tennessee; Stephen F. Kemp, MD, Departments of Medicine and Pediatrics,
University of Mississippi Medical Center, Jackson, Mississippi; John
Oppenheimer, MD, Department of Internal Medicine, New Jersey Medical
School, Pulmonary and Allergy Associates, Morristown, New Jersey; David
M. Lang, MD, Allergy/Immunology Section, Division of Medicine, Director,
Allergy and Immunology Fellowship, Training Program, Cleveland Clinic
Foundation, Cleveland, Ohio; I. Leonard Bernstein, MD, Departments of
Medicine and Environmental Health, University of Cincinnati College of
Medicine, Cincinnati, Ohio; Richard A. Nicklas, MD, Department of
Medicine, George Washington Medical Center, Washington, DC

**Work Group on Diagnosis and Management of Anaphylaxis**

*Contributors*: John Anderson, MD, Aspen Medical Center, Fort Collins,
Colorado; David I. Bernstein, MD, Department of Clinical Medicine,
Division of Immunology, University of Cincinnati College of Medicine,
Cincinnati, Ohio; Jonathan A. Bernstein, MD, University of Cincinnati
College of Medicine, Department of Internal Medicine, Division of
Immunology/Allergy Section, Cincinnati, Ohio; Jordan N. Fink, MD,
Allergy-Immunology, Departments of Pediatrics and Medicine, Medical
College of Wisconsin, Milwaukee, Wisconsin; Paul A. Greenberger, MD,
Division of Allergy and Immunology, Northwestern University Feinberg
School of Medicine, Chicago, Illinois; Dennis K. Ledford, MD, Department
of Medicine, University of South Florida College of Medicine and the
James A. Haley V.A. Hospital, Tampa, Florida; James T. Li, MD, PhD, Mayo
Clinic, Rochester, Minnesota; Albert L. Sheffer, MD, Brigham and
Women\'s Hospital, Boston, Massachusetts; Roland Solensky, MD, The
Corvallis Clinic, Corvallis, Oregon; Bruce L. Wolf, MD, Vanderbilt
University, Nashville, Tennessee

#### FINANCIAL DISCLOSURES/CONFLICTS OF INTEREST

Disclosure of potential conflict of interest: P. Lieberman-none
disclosed. S. F. Kemp has consultant arrangements with MedPointe
Pharmaceuticals. J. Oppenheimer-none disclosed. D. M. Lang-none
disclosed. I. L. Bernstein-none disclosed. R. A. Nicklas-none disclosed.
J. A. Anderson-none disclosed. D. I. Bernstein-none disclosed. J.
Bernstein is on the Speakers\' Bureau for Merck, GlaxoSmithKline,
AstraZeneca, Aventis, Medpointe, Pfizer, Schering-Plough, and IVAX. J.
N. Fink-none disclosed. P. A. Greenberger-none disclosed. D. K.
Ledford-none disclosed. J. Li-none disclosed. A. L. Sheffer-none
disclosed. R. Solensky-none disclosed. B. L. Wolf-none disclosed. J.
Blessing-Moore-none disclosed. D. A. Khan has consultant arrangements
with Pfizer; receives grants/research support from AstraZeneca; and is
on the Speakers\' Bureau for Pfizer, Merck, Aventis, and
GlaxoSmithKline. R. E. Lee-none disclosed. J. M. Portnoy-none disclosed.
D. E. Schuller is on the Speakers\' Bureau for Boehringer-Ingelheim.
S.L. Spector has had consultant arrangements with, has received
grants/research support from, and has been on the Speakers\' Bureau for
Abbott, Allen & Hanburys, AstraZeneca, Boehringer-Ingelheim,
GlaxoSmithKline, Fisons, Forest, ICN, Key, Eli-Lilly, 3M, Miles, Muro,
Pfizer, Purdue Frederick, Schering-Plough, Wallace, and Witby. S. A.
Tilles-none disclosed.

#### GUIDELINE STATUS

This is the current release of the guideline.

This guideline updates a previous version: Joint Council of Allergy,
Asthma and Immunology. The diagnosis and management of anaphylaxis. J
Allergy Clin Immunol 1998 Jun;101(6 Pt 2):S465-S528.

#### GUIDELINE AVAILABILITY

Electronic copies: Available in Portable Document Format (PDF) from the
[Joint Council of Allergy, Asthma, and Immunology (JCAAI) Web
site](http://www.jcaai.readyportal.net/file_depot/0-10000000/20000-30000/27387/folder/63948/AllerRhin_PT12003.pdf).

Print copies: Available from JCAAI, 50 N. Brockway, Ste 3-3 Palatine, IL
60067.

#### AVAILABILITY OF COMPANION DOCUMENTS

None available

#### PATIENT RESOURCES

None available

#### NGC STATUS

This summary was completed by ECRI on October 1, 1998. The information
was verified by the guideline developer on December 15, 1998. This NGC
summary was updated by ECRI on May 10, 2005. The updated information was
verified by the guideline developer on May 23, 2005.

#### COPYRIGHT STATEMENT

This NGC summary is based on the original guideline, which is subject to
the guideline developer\'s copyright restrictions. Reproduced with the
permission from the American College of Allergy, Asthma, and Immunology.

### DISCLAIMER

#### NGC DISCLAIMER

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