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GLORIA Module 8:

Anaphylaxis

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GLORIA™ is supported by unrestricted educational grants from

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Global Resources in Allergy (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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World Allergy Organization (WAO)

The World Allergy Organization is an


international coalition of 77 regional and
national allergy and clinical immunology
societies.

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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

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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

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REVISED NOMENCLATURE FOR ANAPHYLAXIS

Anaphylaxis

Allergic anaphylaxis Non-allergic anaphylaxis

IgE- mediated Immunologic, non-


anaphylaxis IgE-mediated
anaphylaxis
Johansson SGO et al JACI 2004,113:832-6

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GELL AND COOMBS CLASSIFICATION
OF HYPERSENSITIVITY REACTIONS

Type I Immediate hypersensitivity


Type II Cytotoxic reactions
Type III Immune complex reactions
Type IV 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

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Manifestasi dan mekanisme reaksihipersensitivitas

Tipe Manifestasi Mekanisme

I Reaksi hipesensitivitas = Biasanya IgE


Reaksi cepat
II Antibodi terhadap sel = IgG atau IgM
Reaksi Sitotoksik
III Kompleks antibodi-antigen = Biasanya IgG
Reaksi kompleks imun
IV Reaksi hipersenitivitas lambat Sel T yang disensitisasi

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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

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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

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PRIMARY SYMPTOMS OF ANAPHYLAXIS

• Skin: • Respiratory:
flushing, itching, urticaria, dysphonia, cough, stridor,
angioedema wheezing, dyspnea, chest
tightness, asphyxiation, death
• Gastrointestinal:
• Cardiovascular: tachycardia,
nausea, vomiting, bloating,
hypotension, dizziness,
cramping, diarrhea
collapse, death
• Other:
feeling of impending doom,
metallic taste

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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

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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

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BIPHASIC/LATE-PHASE REACTION
Cellular infiltrates: 3 to 6 hours (LPR)
Eosinophil
CysLTs, GM-CSF,
Histamine IL-4, IL-6 TNF-, IL-1, IL-3, PAF,
ECP, MBP

Allergen
3 to 6 hours Basophil
Histamine,
(CysLTs, PAF, CysLTs, Return
IL-5) TNF-, IL-4, IL-5, IL-6
of
Monocyte Symptoms
PGs CysLTs CysLTs, TNF-,
PAF, IL-1
Proteases

Mast cell Lymphocyte


IL-4, IL-13, IL-5,
IL-3, GM-CSF
EPR 15 min
(Early-Phase Reaction)

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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

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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

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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

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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

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AGENTS THAT CAUSE ANAPHYLAXIS:
IgE-DEPENDENT TRIGGERS
• foods (eg peanut, tree nuts, seafood) • hormones
• medications (eg, β-lactam antibiotics) • animal or human proteins
• venoms • colorants (insect-derived, eg.
• latex carmine)
• allergen immunotherapy • enzymes
• diagnostic allergens • polysaccharides
• exercise (with food or medication co- • aspirin and NSAIDs (possibly through
trigger) IgE)

Kemp SF and Lockey RF, J Allergy Clin Immunol 2002;110:341-8

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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

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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

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MOST COMMON FOOD ALLERGIES

• peanut
• tree nut
• seafood
• fin fish
• milk
• egg
• soy
• wheat

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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

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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

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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

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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

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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

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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

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FOOD-DEPENDENT EXERCISE-INDUCED
ANAPHYLAXIS
• reported in USA, Thailand and Japan
• most commonly occurs in females, and from late teens to mid-30’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

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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

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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

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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

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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

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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
Antibiotics, radio contrast
India agents and anesthetic agents
plus blood products, insulin and
growth hormones
Australia
China Peanuts
Japan 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

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-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

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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

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DIAGNOSING ANAPHYLAXIS (cont’d)

• 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

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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

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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

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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

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OFFICE MANAGEMENT OF ANAPHYLAXIS
CHECKLIST OF EQUIPMENT AND DRUGS REQUIRED
• stethoscope and sphygmomanometer
• tourniquets, syringes, needles (including large bore 14-gauge)
• 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

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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

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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

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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

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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

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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, 6 th edition, Mosby Inc., St. Louis, MO, 2003

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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

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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, 6 th edition, Mosby Inc., St. Louis, MO,2003

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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

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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

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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

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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

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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

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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

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FACTORS AFFECTING PROGNOSIS

Factor Poor Good


Prognosis 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

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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

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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

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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.

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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

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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: info@worldallergy.org

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Manifestasi dan mekanisme reaksihipersensitivitas

Tipe Manifestasi Mekanisme

I Reaksi hipesensitivitas = Biasanya IgE


Reaksi cepat
II Antibodi terhadap sel = IgG atau IgM
Reaksi Sitotoksik
III Kompleks antibodi-antigen = Biasanya IgG
Reaksi kompleks imun
IV Reaksi hipersenitivitas lambat Sel T yang disensitisasi

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