GLORIA Module 8: Anaphylaxis

Report
GLORIA Module 8:
Anaphylaxis
Updated: June 2011
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(GLORIA™)
Global Resources In Allergy (GLORIA™) is the
flagship program of the World Allergy
Organization (WAO). Its curriculum educates
medical professionals worldwide through
regional and national presentations. GLORIA
modules are created from established guidelines
and recommendations to address different
aspects of allergy-related patient care.
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The World Allergy Organization is an international
coalition of 89 regional and national allergy and
clinical immunology societies.
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advocate in the field of allergy, advancing
excellence in clinical care, education, research
and training through a world-wide alliance of
allergy and clinical immunology societies
GLORIA Module 8:
Anaphylaxis
WAO Expert Panel
Richard F. Lockey, USA
Michael A. Kaliner, USA
F. Estelle R. Simons, Canada
Cassim Motala, South Africa
Bob Lanier, USA
Additional contributor: Aziz Sheikh, UK
Definition of anaphylaxis
Anaphylaxis is a severe life-threatening generalized or
systemic hypersensitivity reaction.
It is commonly, but not always, mediated by an allergic
mechanism, usually by IgE.
Allergic (immunologic) non-IgE-mediated anaphylaxis also
occurs.
Non-allergic anaphylactic reactions, formerly called
anaphylactoid or pseudo-allergic reactions, may also occur.
Johansson SGO et al JACI 2004,113:832-6
Revised nomenclature for anaphylaxis
Anaphylaxis
Allergic anaphylaxis
IgE- mediated
anaphylaxis
Johansson SGO et al JACI 2004,113:832-6
Non-allergic anaphylaxis
Immunologic, nonIgE-mediated
anaphylaxis
Gell and Coombs classification of
hypersensitivity
Type I
Type II
Type III
Type IV
Immediate hypersensitivity
Cytotoxic reactions
Immune complex reactions
Delayed hypersensitivity
Anaphylaxis can occur through Types I, II and III
immunopathologic mechanisms
Kemp SF and Lockey RF. J Allergy Clin Immunol 2002;110:341-8
Mechanisms of allergic anaphylaxis
…a severe, acute, systemic
allergic reaction caused by the
rapid, IgE-mediated release of
potent mediators such as
histamine from tissue mast cells
and peripheral blood basophils
Acutely released mediators of
anaphylaxis
• degranulation of mast cells and basophils causes the release of:
- preformed granule-associated substances, eg histamine,
tryptase, chymase, carboxypeptidase, and cytokines
- newly-generated lipid-derived mediators, eg prostaglandin D2,
leukotriene (LT) B4, LTC4, LTD4, LTE4, and platelet activating
factor.
Kemp SF and Lockey RF. J Allergy Clin Immunol 2002; 110:341-8
Primary symptoms of anaphylaxis
• Skin:
flushing, itching, urticaria,
angioedema
• Gastrointestinal:
nausea, vomiting, bloating,
cramping, diarrhea
• Other:
feeling of impending doom,
metallic taste
• Respiratory:
dysphonia, cough, stridor,
wheezing, dyspnea, chest
tightness, asphyxiation, death
• Cardiovascular: tachycardia,
hypotension, dizziness,
collapse, death
Comments about anaphylaxis signs
and symptoms
• skin symptoms occur most commonly ( > 90% of patients)
• skin, oral, and throat symptoms are often the first ones noted
• respiratory symptoms occur in 40% to 70% of patients
• gastrointestinal symptoms occur in about 30% of patients
• shock occurs in about 10% of patients
• signs and symptoms are usually seen within 5 to 30 minutes
• the more rapid the onset, the more serious the reaction
Lieberman P. In: Middleton’s Allergy: Principles and Practice, 6th edition, Mosby Inc., St. Louis,
MO, 2003
Biphasic and protracted anaphylaxis
•
biphasic anaphylaxis is defined as return of symptoms after
resolution of initial symptoms, without subsequent allergen
exposure
•
usually, symptoms return within 1 to 8 hours (sometimes longer)
•
up to 20% of anaphylactic reactions are biphasic
•
patients with biphasic anaphylaxis may require more epinephrine to
control initial symptoms
•
in protracted anaphylaxis, symptoms may be continuous for 5-32 hrs
Lieberman P. Ann Allergy Asthma Immunol 2005;95:217-26
Biphasic/late-phase reaction
Cellular infiltrates: 3 to 6 hours (LPR)
Eosinophil
Histamine
CysLTs, GM-CSF,
TNF-, IL-1, IL-3, PAF,
ECP, MBP
IL-4, IL-6
Allergen
3 to 6 hours
Basophil
Histamine,
CysLTs,
TNF-, IL-4, IL-5, IL-6
(CysLTs, PAF,
IL-5)
Monocyte
PGs
CysLTs
Proteases
Mast cell
EPR 15 min
(Early-Phase Reaction)
CysLTs, TNF-, PAF,
IL-1
Lymphocyte
IL-4, IL-13, IL-5,
IL-3, GM-CSF
Return
of
Symptoms
Differential diagnosis of anaphylaxis
• vasovagal reactions
• flushing
• mastocytosis
• carcinoid syndrome
• hyperventilation syndrome
• globus hystericus
• hereditary angioedema
• other types of shock, eg. cardiogenic, septic
• scombroid poisoning
Montanaro A and Bardana EJ Jr. J Investig Allergol Clin Immunol 2002;12:2-11
Incidence and prevalence of anaphylaxis
• “anaphylaxis in the US: an investigation into its epidemiology"
- on the basis of a literature review, more than 1.21% of the
population may be affected
• independent US Omnibus Studies (2002 and 2003)
- 32 million have had 2 or more symptoms
- 18 million diagnosed
- 11 million have suffered a life-threatening reaction
Neugut AI et al. Arch Intern Med 2001;161:15-21
Dey, L.P. Independent omnibus studies. Data on file. 2002-2003
Incidence and prevalence of
anaphylaxis (cont.)
•
•
•
•
5-year review of 1.15 million persons in Manitoba, Canada
dispensing patterns of epinephrine for out-of-hospital treatment
0.95% of the general population had epinephrine dispensed
dispensing rates in the general population varied with age
- 1.44% for individuals <17 years of age
- 0.9% for those 17-64 years of age
- 0.32% for those >65 years of age
• interpretation: anaphylaxis from all triggers, occurring out of
hospital, appears to peak in childhood, and then gradually decline
Simons FER et al. J Allergy Clin Immunol 2002;110:647-51
International collaborative study of
severe anaphylaxis
•
Objective
•
•
To quantify the risk of anaphylaxis due to drugs and other
exposures in hospital patients
Methods
•
•
•
•Epidemiology
Hospitals in Sweden, Hungary, India and Spain
Incident cases 1992-1995
Clinical diagnosis using a priori agreed criteria, independent
of presumed trigger
1998;9:141-46
International collaborative study of
severe anaphylaxis (cont.)
•
Main findings
•
•
•
•
•
•Epidemiology
123/481,752 i.e. risk of 15-20/100,000 admissions
33% males
Median age ~53
79% respiratory symptoms; 70% cardiovascular symptoms;
49% both
Death in 2% of cases
1998;9:141-46
UK anaphylaxis death register
•
Objective
•
•
To understand the circumstances leading to fatal
anaphylaxis
Methods
•
•
•
Running since 1992; ONS mortality data coded for
anaphylaxis since 1993
Detailed information obtained from medical records,
medical staff, coroners officers and mast cell serum tryptase
Adrenaline rarely used before cardiac arrest
Pumphrey RSH, Clin Exp Aller 2000; J Clin Pathol 2000; Novartis Found Symp 2004
UK anaphylaxis death register (cont.)
•
Main findings
•
•
•
•
•
~20 recorded deaths/year i.e. ~1:2.8 million
50% iatrogenic; 25% food and 25% venom
~50% died from asphyxia (food) and 50% from shock
(iatrogenic and venom)
Median time to death:
5 mins if iatrogenic; 15 mins venom; and 30 mins food
Adrenaline rarely used before cardiac arrest
Pumphrey RSH, Clin Exp Aller 2000; J Clin Pathol 2000; Novartis Found Symp 2004
Hong Kong ED
Objective
To describe the epidemiology, clinical features and
management of anaphylaxis
Methods
Retrospective review of all age patients in one ED, 19992003
Clinical diagnosis of anaphylaxis
Main findings
~1/2800 attendances for anaphylaxis
Smit DV et al. J Emer Med 2005;28:381-88
Agents that cause anaphylaxis:
IgE-dependent triggers
•
•
•
•
•
foods (eg peanut, tree nuts, seafood)
medications (eg, β-lactam antibiotics)
venoms
latex
allergen immunotherapy
• diagnostic allergens
• exercise (with food or medication cotrigger)
Kemp SF and Lockey RF, J Allergy Clin Immunol 2002;110:341-8
• hormones
• animal or human proteins
• colorants (insect-derived, eg. carmine)
• enzymes
• polysaccharides
• aspirin and NSAIDs (possibly through
IgE)
Risk of anaphylaxis
• estimated risk in US: 1-3%
• fatalities per year in the US:
- food-induced: 150
- antibiotic-induced: 600
- venom-induced: 50
Kemp SF and Lockey RF, J Allergy Clin Immunol 2002;110:341-8
Food-induced anaphylaxis
• many anaphylactic reactions are caused by food
- accidental food exposures are common and unpredictable
- anaphylaxis from food can occur at any age, but children, teens
and young adults are at highest risk
• prevalence of peanut allergy has doubled in children <5 years of age
in the last 5 years
• seafood allergy is reported by 2.3% of the US population, and is
more common in adults than in children
Sampson HA. J Allergy Clin Immunol 2004;113:805-19 Sicherer
SH et al. J Allergy Clin Immunol 2004;114:159-65
Most common food allergies
•
•
•
•
•
•
•
•
peanut
tree nut
seafood
fin fish
milk
egg
soy
wheat
Fatal food-induced anaphylaxis
• in a retrospective analysis of 32 deaths in patients age 2-33 years
- peanut and tree nuts caused >90% of reactions
- most patients had a history of asthma
- most did not have injectable epinephrine available
at the time of their reaction and death
Bock SA et al. J Allergy Clin Immunol 2001;107:191-3
Hymenoptera stings
• 0.5% to 5% of the US population is allergic to Hymenoptera
venom(s)
- bees
- wasps
- yellow jackets
- hornets
- fire ants
• at least 50 deaths per year
• incidence rising due to
- increased numbers of fire ants and Africanized bees
- increased numbers of people engaged in outdoor activities
Neugut AI et al. Arch Intern Med 2001;161:15-21
Iatrogenic anaphylaxis
• estimated 550,000 serious allergic reactions to drugs/year in US hospitals
• most common drug triggers
- penicillin (highest number of documented deaths from anaphylaxis)
- sulfa drugs
- non-steroidal anti-inflammatory drugs
- muscle relaxants
• most common biologic triggers
- anti-sera for snakebite
- anti-lymphocyte globulin
- vaccines
- allergens
Neugut AI et al. Arch Intern Med 2001;161:15-21
Lazarou J et al. JAMA 1998;279:1200-5
Latex-induced anaphylaxis
• <1% of the US general population
• prevalence is highest among healthcare workers
• latex gloves, especially if powdered, are a common trigger
• repeated exposure leads to higher risk
• incidence increased dramatically in the mid-1980s, but has
decreased progressively with more use of non-powdered latex
gloves and use of non-latex gloves
Neugut AI et al. Arch Intern Med 2001;161:15-21
Peri-operative anaphylaxis
• neuromuscular blocking drugs (muscle relaxants), eg
suxamethonium, rocuronium, alcuronium, atracurium
• induction agents, eg thiopentone, propofol, alfathesin
• other: including local anesthetics, antibiotics, protamine,
and latex
• predisposing factors: atopy, asthma; previous exposure
Fisher M. In: Anaphylaxis, John Wiley & Sons Ltd., Chichester, UK, 2004:193-206
Allergen immunotherapy-induced
anaphylaxis
• fatal reactions are uncommon: 1 per 2,000,000 injections
• risk factors for fatality include:
- dosing errors
- poorly controlled asthma (FEV1 < 70%)
- concomitant β-blocker use
- lack of proper equipment and trained personnel
- inadequate epinephrine treatment
Stewart GE and Lockey RF. J Allergy Clin Immunol 1992;90:567-78
Bernstein DI et al, J Allergy Clin Immumol 2004;113:1129-36
Food-dependent exercise-induced
anaphylaxis
• reported in USA, Thailand and Japan
• most commonly occurs in females, and from late teens to mid30’s
• triggered by exercise 2-4 hours after ingesting offending food
• foods implicated: wheat, seafood, fruit, milk,celery and fish.
• associations: asthma, positive skin prick tests to foods
• mechanism: two signals required
Aunhachoke K et al. J Med Assoc Thai 2002;85:1014-8
Aihara Y et al. J Allergy Clin Immunol 2001;108:1035-9
Anaphylaxis from immune causes
other than IgE
• cytotoxic (Type II)
- transfusion reactions to cellular elements (IgG, IgM)
• immune aggregates (Type III)
- intravenous immunoglobulin
- Dextran (possibly)
Kemp SF and Lockey RF, J Allergy Clin Immunol 2002;110:341-8
Anaphylaxis: non-immunologic causes
MULTIMEDIATOR COMPLEMENT ACTIVATION/ACTIVATION
OF CONTACT SYSTEM
• radiocontrast media
• ethylene oxide gas on dialysis tubing (possibly through IgE)
• protamine (possibly)
• ACE-inhibitor administered during renal dialysis with sulfonated
polyacrylonitrile, cuprophane, or polymethylmethacrylate dialysis
membranes
Kemp SF and Lockey RF, J Allergy Clin Immunol 2002;110:341-8
Anaphylaxis: non-immunologic causes
NONSPECIFIC DEGRANULATION OF MAST
CELLS
AND BASOPHILS
• opiates
• physical factors:
- exercise (no food or medication co-trigger)
- temperature (cold, heat)
Kemp SF and Lockey RF, J Allergy Clin Immunol 2002;110:341-8
Idiopathic anaphylaxis
• common in adults who are referred to allergists for evaluation
of anaphylaxis
• uncommon in children
• negative skin tests, negative dietary history, no associated
diseases eg. mastocytosis
• preventive medication: oral corticosteroids, H1 & H2
antihistamines, anti-leukotrienes
• deaths rare
• may gradually improve over time
Lieberman PL et al. J Allergy Clin Immunol 2005;115:S483-S523
Most common precipitating causes
Country
Precipitating agents
USA
Insect venom and drugs,
immunotherapy, foods, radio
contrast media, NSAID
China, Korea
Drugs - antibiotics and anesthetic
agents
India
Australia
China
Japan
Antibiotics, radio contrast agents
and anesthetic agents plus blood
products, insulin and growth
hormones
Peanuts
Foods in children, insect stings,
latex and drugs in adults
De Bruyne JA and Lee BW. Allergy Clin Immunol Int: J World Allergy Org 2004;16:137-41
-Adrenergic blockade
• by mouth or topically
• paradoxical bradycardia, severe hypotension and
bronchospasm
• can exacerbate disease and impede treatment
• selective β-blockers can produce clinically significant adverse
respiratory effects even in mild-moderate asthma and COPD;
not studied in anaphylaxis
Lieberman PL et al. J Allergy Clin Immunol 2005;115:S483-523
Diagnosing anaphylaxis
• clinical diagnosis based on clinical presentation and exposure history
• flushing and tachycardia are invariably present, other cutaneous
symptoms (hives, itch) may be absent
• anaphylaxis may be difficult to diagnose, especially when patients
present with bradycardia (instead of tachycardia, which is usual)
• very rarely, patients present only with profound hypotension. The
exposure to some inciting event is one key to the diagnosis in this rare
circumstance
Lieberman PL et al. J Allergy Clin Immunol 2005;115:S483-523
Diagnosing anaphylaxis (cont.)
• careful history to identify possible causes
• can be confirmed by an elevated serum tryptase level
- specific for mast cell degranulation
- remains elevated for up to 6 hours
- may not be elevated, especially in food allergy
• refer to allergist for specific testing
Lieberman PL et al, J Allergy Clin Immunol 2005;115:S483-523
Laboratory tests in the diagnosis of
anaphylaxis
Plasma histamine
Serum tryptase
24-hr Urinary histamine metabolite
0
30
60
90
120
150
180
210
240
270
300
330
Problems with laboratory tests
• histamine and tryptase levels may not correlate with each other
• histamine level was elevated in 42 of 97 patients in the
Emergency Department, but only 20 of 97 had an elevated
tryptase level
• histamine levels also correlated better with symptoms and signs
• plasma histamine levels only remain elevated for one hour after
symptom onset; therefore, this test is usually not practical
Lin RY et al. J Allergy Clin Immunol 2000;106:65-71
Diagnosing anaphylaxis
Allergists can identify specific causes by:
• complete and accurate medical/allergy history
• skin tests/specific IgE levels
- foods
- insect venoms
- drugs (some)
• challenge tests:
(selected patients, physician-monitored, preferably in hospital)
- foods
- NSAIDs
- exercise
Simons FER. J Allergy Clin Immunol 2006;117:367-77
Office management of anaphylaxis:
checklist of equipment and drugs required
• stethoscope and sphygmomanometer
• tourniquets, syringes, needles (including large bore 14gauge)
• injectable epinephrine (adrenaline) 1:1000
• oral airway and endotracheal tubes
• oxygen, and equipment to administer it
• diphenhydramine (or similar) injectable antihistamine
• corticosteroids for IV injection
• vasopressor (eg dopamine, noradrenaline)
• glucagon
• automatic defibrillator
Physician-supervised management
of anaphylaxis
I. Speed is critical:
a) assess airway, breathing, circulation, and mentation
b) epinephrine, IM into the muscle of the anterolateral thigh;
1:1000 dilution, 0.3 - 0.5 mL (0.01 mg/kg in children);
repeat, every 5-15 minutes as necessary.
Kemp S and Lockey R. J Allergy Clin Immunol 2002;110:341-8
Simons FER et al. J Allergy Clin Immunol 1998;101:33-7
Simons FER et al. J Allergy Clin Immunol 2001;108:871-3
Physician-supervised management
of anaphylaxis
II. Secondary measures:
a) place patient in recumbent position and elevate his/her
legs
b) maintain airway (endotracheal tube or cricothyrotomy)
c) oxygen, 6 - 8 liters/minute
d) normal saline IV; volume expanders (colloid solution) for
severe hypotension
Kemp SF and Lockey RF. J Allergy Clin Immunol 2002;110:341-8
Physician-supervised management of
anaphylaxis
III. Other measures:
a)
epinephrine 1:1000, ½ dose (0.1- 0.2 mg) into reaction site
diphenhydramine, 50 mg IV or orally (1.25 mg/kg, up to 50 mg
dose for children); maximum daily dose: adults 400 mg;
children 200 mg
b)
ranitidine, 50 mg in adults and 12.5 - 50 mg (1 mg/kg) in
children,
dilute in 5% D/W, total 20 ml, inject slowly IV, over 5 minutes
(cimetidine 4 mg/kg OK for adults, dose not established for
children)
Kemp SF and Lockey RF. J Allergy Clin Immunol 2002;110:341-8
Physician-supervised management
of anaphylaxis
•
for bronchospasm
- nebulized albuterol (salbutamol) 2.5 - 5 mg in 3 ml normal saline
•
for refractory hypotension
- dopamine, 400 mg in 500 ml normal saline IV 2 - 20 μg/kg/min
- glucagon, 1- 5 mg (20 - 30 μg/kg, max 1 mg in children), IV over 5
minutes followed with continuous IV infusion 5-15 μg/min
- methylprednisolone, 1- 2 mg/kg per 24 hr
Kemp SF and Lockey RF. J Allergy Clin Immunol 2002;110:341-8
Measures to reduce the incidence of
drug-induced anaphylaxis
General measures
• obtain detailed history of previous adverse reactions to drugs
• avoid drugs that cross-react with any agents to which patient is
sensitive
• administer drugs orally rather than parenterally when possible
• check all drugs for proper labeling
• monitor patients closely for 20 to 30 minutes after injections
Lieberman P. In: Middleton’s Allergy: Principles and Practice, 6th edition,
Mosby Inc., St. Louis, MO, 2003
Measures to reduce the incidence of
anaphylaxis
• identify causative factors; provide specific instructions about
avoidance
• have patient wear Medic Alert® or carry other medical identification
• teach self-injection of epinephrine and caution patients to keep it with
them at all times
• repeat instructions each year
• re-evaluate use of -adrenergic blocking agents, ACE inhibitors,
monoamine oxidase inhibitors, and tricyclic antidepressants
Simons FER, J Allergy Clin Immunol 2006;117:367-77
Measures to reduce the incidence of
anaphylaxis
Use preventive techniques when patients need to undergo a procedure
or take an agent which places them at risk, such as:
- pretreatment
- provocative challenge (selected patients, physician-monitored,
preferably in hospital)
- desensitization (selected patients, physician-monitored,
preferably in hospital)
Lieberman P. In: Middleton’s Allergy: Principles and Practice,
6th edition, Mosby Inc., St. Louis, MO,2003Q
Prevention of anaphylactic reactions to
radiocontrast media (RCM) in adults
•
•
•
•
prednisone 20-50 mg orally 12,7, and 1 hours before administration of RCM
diphenhydramine 50 mg orally/intramuscularly 1 hour prior to RCM
ephedrine 25 mg orally 1 hour before RCM administered
another approach:
- give oral non-sedating H1antihistamine and H2 antihistamine at 12 and 1
hours before exposure
Lieberman P et al. J Allergy Clin Immunol 2005, 115:5483-5523
Specific advice for food-induced
anaphylaxis: patient education
• teach patients about risk management
• complete avoidance of a food is difficult
• patients must always be prepared with:
- a written Anaphylaxis Emergency Action Plan
- self-injectable epinephrine (adrenaline)
- Medic Alert®-type identification
Sampson HA, J Allergy Clin Immunol 2004;113:805-19
Simons FER, J Allergy Clin Immunol 2006;117:367-77
Specific advice for food-induced
anaphylaxis: patient education
• teach patients to avoid allergens
- read product labels
- identify alternative names for ingredients
- identify “hidden” ingredients
• avoid high-risk foods (eg baked goods) and high-risk situations
(eg buffets)
• avoid sharing food, utensils, or dishes
- minute amounts of allergen can be life-threatening
• provide educational materials, available from Food Allergy and
Anaphylaxis Network - FAAN (www.foodallergy.org)
Sampson HA, J Allergy Clin Immunol 2004;113:805-19
Simons FER, J Allergy Clin Immunol 2006;117:367-77
Venom-induced anaphylaxis
• normal reactions: local pain, erythema, mild swelling
- large local reaction: extended swelling, erythema
• anaphylaxis: usual onset within 5-30 minutes
- cutaneous: pruritus, urticaria, flushing, angioedema
- respiratory: dyspnea, wheezing, stridor, dysphonia
- cardiovascular: tachycardia, hypotension, dizziness,
faintness
• in a patient who has already experienced anaphylaxis from a
sting, the risk of anaphylaxis to a subsequent sting is 30%-60%
Freeman TM, N Eng J Med 2004;351:1978-84
Specific advice for venom-induced
reactions: Patient education
• teach patients methods of risk reduction (avoidance strategies)
• keep injectable epinephrine on hand at all times, in key
locations
• develop a written emergency action plan, and update it yearly
• always wear a Medic Alert®-type identification
• consult an allergist to determine need for venom
immunotherapy
Freeman TM, N Eng J Med 2004;351:1978-84
Simons FER. J Allergy Clin Immunol 2006;117:367-77
Specific advice for venom-induced
reactions: immunotherapy
• medical criteria
- history of any systemic reaction in adults
- history of life-threatening reaction in children
- positive venom skin test or increased specific IgE level
• therapy is >97% effective
- less than 3% risk for systemic reaction to subsequent stings vs
30% to 60% risk without immunotherapy
Golden DBK, N Eng J Med 2004:351:668-74
Moffit JE et al. J Allergy Clin Immunol 2004;114:869-86
Factors affecting prognosis
Factor
Poor
Prognosis
Good
Prognosis
Onset of symptoms
Early
Late
Initiation of treatment
Late
Early
Route of exposure
Injection
Oral*
β-adrenergic blocker use
Yes
No
Presence of underlying disease
Yes
No
* true for drugs, not foods
Anaphylaxis in the emergency
department
• chart review study in 21 North American Emergency Departments
• random sample of 678 charts of patients presenting with food
allergy
• management:
- 72% received antihistamines
- 48% received systemic corticosteroids
- 16% received epinephrine (24% of those with severe reactions)
- 33% received respiratory medication (eg. inhaled albuterol)
- only 16% received Rx for self-injectable epinephrine at discharge
- only 12% referred to an allergist
Clark S et al. J Allergy Clin Immunol 2004;347-52
Referral to allergy/immunology
specialist
• risk assessment: detailed history; coordinate allergy tests and
other investigations
• risk management:
- patient education (about allergen avoidance measures)
- medication review
- self-administered epinephrine
- immunotherapy (for hymenoptera allergy)
- premedication (for idiopathic anaphylaxis)
- new therapies
Simons FER, J Allergy Clin Immunol 2006;117:367-77
Important resources
•
•
•
•
•
•
•
www.foodallergy.org
www.latexallergyresources.org
www.aaaai.org
www.acaai.org
www.worldallergy.org
resources for: patients, families, health-care professionals
practical advice, up-to-date scientific information, promotion of
research, legislation, etc.
Summary
• anaphylaxis: release of inflammatory mediators from mast cells
and basophils (IgE-mediated or non-IgE mediated)
• symptoms: within minutes of exposure to triggering agent (less
commonly can be delayed, biphasic or protracted)
• common triggers: foods, drugs, latex, hymenoptera stings;
idiopathic
• first-line of treatment: injected epinephrine (adrenaline)
• hallmarks of management: education and prevention
World Allergy Organization (WAO)
For more information on the World Allergy
Organization (WAO), please visit
www.worldallery.org or contact the:
WAO Secretariat
555 East Wells Street, Suite 1100
Milwaukee, WI 53202
United States
Tel: +1 414 276 1791
Fax: +1 414 276 3349
Email: [email protected]

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