Transcript Anaphylaxis - Emory University Department of Pediatrics

This is a Test
It is ONLY a Test
A 16 y/o girl just passed out after receiving her
penicillin shot for strep throat (“doesn’t swallow
pills”). Which of the following will be most useful
to know in treating her:
A
B
C
D
Her Blood Pressure
Her Glucose level
Her Heart Rate
Your Heart Rate
Which of the following is the safest and most
efficient route to administer epinephrine in
an allergy emergency:
A
B
C
D
IV
Sub Q
IM
PR
Which of the following potential allergens do
not generally cross-react:
A. COX-2 inhibitors & Ibuprofen
B. Filberts & Pecans
C. Peanuts & Tofurky
D. Lobster & Shrimp
A first year PEM fellow attending conference
developed a sudden onset of urticaria, lip
swelling and DIB. The etiology is most
likely a reaction to:
A smelling someone else’s lunch
B a spider bite
C another “billing talk” by Dr Linzer
When advising parents/patients on how to
administer an “epi-pen” you should tell
them to:
A. hold it against the triceps and squeeze the
trigger
B. “stab” it into the anterior thigh
C. hold it against the lateral thigh and push
Which is NOT a clinical presentation of
anaphylaxis:
A.
B.
C.
D.
Vomiting and Diarrhea
Syncope
Altered Mental Status
Itchy Tongue
In counseling a 50kg 15 year old after a severe
episode of anaphylaxis to a bee sting your best
advice is that if they get stung again they first
should take
A.
B.
C.
D.
(2) 25mg diphenhydramine capsules PO
(5) tsp diphenhydramine elixer PO
.5mg epinephrine SQ
60mg prednisone PO
Which of the following treatments has been shown
to decrease the incidence of biphasic reactions:
A. Corticosteroids
B. Epinephrine
C. Diphenhydramine
D. Ranitidine
ANAPHYLAXIS
Michael Greenwald, MD
Pediatric Emergency Medicine
Emory University
Children’s Healthcare of Atlanta @ Egleston
Objectives
 Recognize
patients with, or at risk for,
anaphylactic reaction
 Understand the immunologic basis for
anaphylactic reactions
 Know the interventions appropriate for
anaphylactic reactions
 Know the appropriate medical follow-up
Historical Background



ana- backward
phylaxis- protection
Portier and Richet: reactions in dogs exposed to
sea anenome toxin
First documented case: Egyptian pharoah 2640
B.C. dies after wasp sting
Defining Anaphylaxis
 Acute
 Systemic
 Allergic (i.e. requires prior exposure)
Special Features of Anaphylaxis
 Spectrum
of severity
 Variety of manifestations
 Uniphasic, biphasic or protracted
Epidemiology
►
Top triggers: then
 penicillin
 insect venom
 food
►
► Top




triggers: now
Latex (27%)
Food (25%)
Drugs (16%)
Venoms (15%)
Anaphylaxis Epidemiology
►
84,000 cases/year in US
 1% fatal
 Kids > adults
► Food
Allergy
 under 4 y/o: 6-8%
 After 10 y/o: 2%
 29,000 cases food induced anaphylaxis/year
►
►
2000 hospitalizations
150 deaths; high association with asthma, peanut/tree nut allergy
 Peanuts are # 1 and increasing in Western nations
Hypersensitivity review: Gell and
Coombs Classification
Type I - Anaphylactic
Type II - Cytotoxic
Type III - Immune Complex
Type IV - Delayed Type
Type I - Anaphylactic
► Immediate:
Exposure to reaction < 30minutes
► Late Phase: Exposure to reaction: 2-12 hours





Exposure to reaction: <30minutes
Effector cell: IgE
Antigen: pollens, foods, drugs, venoms
Mediators: histamine, leukotrienes
Manifestations: anaphylaxis, allergic rhinitis, allergic asthma, urticaria
Type II - Cytotoxic
•
Exposure to reaction: variable (minutes to
hours)
•
•
•
•
Effector cell: IgG, IgM
Target: Red blood cells, Lung tissue
Mediators: Complement
Examples: Immune hemolytic anemia, Rh
hemolytic disease, Goodpasture syndrome
Type III - Immune Complexes
•
•
•
•
•
Exposure to reaction: 6 - 21 days
Effector cell: Antigen with Antibody
Target: Vascular endothelium
Mediators: Complement, Anaphylatoxin
Symptoms: fever, urticaria, arthralgia, arthritis,
lymphadenopathy
•
Examples: Serum sickness, PSGN
Type IV - Delayed Type
•
•
•
•
•
Exposure to reaction: 24-48 hours
Effector cell: Lymphocytes
Antigen: Chemicals, Mycobacterium tuberculosis
Mediators: Lymphokines
Examples: Contact dermatitis, Tuberculin skin reactions
Anaphylaxis and Her Cousin

Anaphylaxis
 IgE mediated
 IgG - immune complex mediated

Anaphylactoid
 direct stimulation of mast cells and basophils
 unknown mechanism
IgE - mediated Anaphylaxis
► Prior
exposure required
► Allergen-IgE binding induces release of mediators:




histamine
prostaglandins
platelet activating factor
tryptase
IgG -immune complex mediated
►
complement activated by immune complexes or
other agents
 Tissue antigens - RBC, WBC, Plts
 Serum proteins - Immunoglobulin, cryoprecipitin
►
anaphylatoxins: C3a, C5a
Anaphylactoid : Direct stimulation
direct stimulation of mast cells and basophils
► unknown mechanism - suspect high osmolarity
► examples: radiocontrast media (not assoc w/
iodine, shellfish allergy), mannitol, opiates, curare,
dextran, chemotherapeutic agents
►
Unexplained Anaphylaxis
►
Unknown mechanism:






ASA and other NSAIDS
preservatives
exercise
mastocytosis
cholinergic urticaria with anaphylaxis
progesterone: “catamenial anaphylaxis”
Unexplained Anaphylaxis
►
Idiopathic anaphylaxis: unknown trigger
 up to 37% of all reactions
 clinically indistinguishable from other forms
 particularly stressful to patients
Epidemiology
►
Patients at risk:
 Does atopic history matter?
 Who gets the worst reactions?
 Latex
Allergens
 Drugs
 Foods
 Venoms
 Latex
Defining Drug Reactions
►
Predictable Drug Reactions
 80% of all adverse effects
 dose dependent
 related to known pharmacological effect
►
Unpredictable Drug reactions
 not dose dependent
 occurs in susceptible individuals
 unrelated to known pharmacological effect
Drugs
►
Antimicrobials
 Penicillin: 2 potential groups of allergens
•
•
Major determinant: Benzyl penicilloyl
Minor determinants: penicillin, penicilloate, penilloate,
penicilloylamine
 Cephalosporins
 Sulfonamides
Drugs
►
NSAIDS
 bronchospasm in 2-10% of asthmatics
 unknown mechanism: IgE and mast cells not involved
Drugs
►
Macromolecules:
 protamine
 insulin
 IVIG
►2
recognized mechanisms
►IgA deficiency high risk
►slow infusion and pretreat
Drugs



Chemotherapeutic agents: L-Asparaginase
Vaccinations: MMR?
Immunotherapy
 17 fatalities reported 1985-1989 (10 million shots given
annually)
 precautions for medical facility:


observe 20 minute
medications and airway support available
Drugs

Radiocontrast media
 mast cell degranulation from anaphlatoxins of
complement cascade
►older
agents: Hypaque, Renigrafin
►mild reaction in 5%, severe - 1/1000,
40,000 exposures
 risk factors:
►atopic/asthma
►adult
history
death - 1/10-
Foods
 Tree
nuts: 1% Americans (3 million) allergic
 Legumes: 25-35% also allergic to tree nuts
 Shellfish
 Fish
 Milk
 Eggs
 Food additives: sulfites
Foods That May Contain Peanut Oil
Arachis oil (peanut oil)
► Baked Goods and mixes
► Biscuits, cookies, pastries
► Candy
► Cereals
► Chocolate
► Emulsifiers, flavorings
► Ethnic foods: African, Chinese,
Mexican, Thai, Vietnamese
►
Ice Cream
► Margarine
► Milk formula
► Satay Sauce (thai sauce)
► Soft drinks
► Soups
► Sunflower seeds
► Vegetable fats and oils
►
Venoms/Antivenins
5





major stinging insects in the US:
honeybees
wasps
yellow jackets
hornets
fire ants
 Rabies
and snake antivenin
Latex
► incidence
low, except for risk groups:
► >1000 episodes and 15 deaths attributed
► surgical and dental procedures highest risk
► RAST testing available
Exercise-induced

Variety of forms of exercise
 not heat alone
 not associated with atopy/asthma
 strong genetic predisposition

 histamine and parasympathetic tone, 
sympathetic tone
Exercise-induced
►
4 phases:
 Prodrome: fatigue, warmth, pruritis & erythema
 Early: urticaria, angioedema
 Fully established: (30’- 4 hours) stridor, choking,
N/V/D, syncope, hypotension
 Late: fatigue, warmth, headache, lasts up to 72 hours
Exercise-induced
►
Diagnosis: may resemble asthma or cholinergic
urticaria
 very unpredictable; some associated with foods
►
Management:
 recognize early signs and rest
 avoid hot, humid weather
 exercise with a partner
Symptoms
►
Manifestations in the “shock organs”
 skin, respiratory tract, gastrointestinal tract,
cardiovascular system
►
Why there?
 rich in mast cells
 sensitive to effects of mast cell mediators
 exposure to high concentrations of antigen
Skin
► Early
signs:
 Flushing, feeling warm
 Erythema
 Pruritis
► Urticaria
► Angioedema
► Pallor
Respiratory
►
Upper airway
 Nose & eyes: pruritis and watery discharge, sneezing
 Lips & tongue: swelling and pruritis
 Larynx & epiglottis: edema with hoarseness, dysphonia
to asphyxia
►
Bronchi: bronchospasm with wheezing,
decreased aeration, to apnea, asphyxia
Gastrointestinal
► not
only with food triggers
► crampy
abdominal pain, nausea, vomiting, watery
diarrhea, gastointestinal bleeding, fecal
incontinence
Cardiovascular
►
►
Intravascular volume depletion
Direct effects on the heart:
 arrythmias
 reduced contractility
 reduced coronary blood flow
Early: dizziness and confusion
► May progress to: syncope, seizures, loss of
consciousness shock, cardiac arrest
►
Other symptoms of anaphylaxis
►
►
►
►
Neurologic: HA, Mental Status changes
Uterine contraction
Urinary incontinence
Anxiety, Feeling of “impending doom”
Natural history of anaphylactic
reactions
►
Onset of reaction after exposure: seconds to
several hours. Depends on
 patient’s sensitivity
 dose of allergen
 route of entry
► Biphasic
reactions (1 – 28 hrs)
 5-23% in adults; 6% in kids
 Food, venom, medication induced anaphylaxis
 Second reaction may be worse
Making the correct diagnosis
►
May look just like:




Asthma exacerbation
Croup or foreign body aspiration
Cardiogenic syncope
food poisoning or gastroenteritis
Vasovagal vs. Anaphylaxis
►
Vasovagal
 pallor
 diaphoresis
 bradycardia or NSR
►
Anaphylaxis
 tachycardia
 flushing
 urticaria/pruritis/ bronchospasm
Differential Diagnosis
►
Related Diseases
 Serum Sickness
 Systemic Mastosytosis
 Urticaria Pigmentosa
►
Unique presentations
 MI, PE, CVA, Seizure, asphyxia, hypoglycemia
Making the correct diagnosis
►
Detailed history as close to the event as possible




All foods in prior 6-12 hours
Consider all ingredients
Look for likely suspects: e.g. legumes
Write it and keep it
► Prick
skin tests: Best Screening test
 high false positives; very low false negatives
 may require food challenge
Less common lab tests
► histamine
vs. tryptase level
 transient
 Tryptase NOT elevated in food-induced anaphylaxis
► RAST:
measures specific IgE,
 less sensitive than skin prick
 Useful in pt.s who can’t d/c antihistamines or w/skin condition
► Coombs
test - Type II
► complement levels - Type III
► patch testing - Type IV
Treatment




Prevention, education and observation
Early intervention
Medications
Managing a difficult airway
Early intervention: epinephrine
► Injection
Kits: Epipen, Ana-kit, Anaguard
► When to give?
► How to administer?
 location: SC vs IM, site of stinger
 dosing
 Inhaled epinephrine
► Precautions: Beta-blockers and Tricyclics
Medical adjuncts
►
Antihistamines
 Use in all cases
 H1 blockers: route and type
 H2 blockers
►
Steroids
 Use in all significant cases
 PO (liquid), IM or IV: 2mg/kg (max 60 mg?)
 Prevents delayed reactions
►
Bronchodilators & aminophylline
Supportive treatment and airway
issues
► Hypotension
may not respond to epinephrine
► Aggressive use of IVF + Trendelenberg, vasopressors if
necessary
► MAST trousers, glucagon and naloxone also reported
helpful
► Laryngeal edema and angioedema of the face pose
critical airway challenges
Prevention

Food allergies:
 Avoid entire food group if sensitive to one member (unless
proven safe)
 Canned fish (heated) may be tolerated if tested under
controlled setting
 Beware baked goods
 Learn ingredients, pseudonyms and synonyms

Drug allergies:
 desensitization: a temporary measure
 premedicate and observe closely
Prevention, education and
observation

Venom allergies:
 Don’t entice the insects: sights and smells
 Who gets venom immunotherapy?
 Educate
all caretakers
 4 hour observation/ hospital observation if not
resolving rapidly
Which of the following is the safest and most
efficient route to administer epinephrine in an
allergy emergency:
A IV
B Sub Q
C IM
D PR
Syncope after shot
A 16 y/o girl just passed out after receiving her penicillin
shot for strep throat (“doesn’t swallow pills”). Which of
the following will be most useful to know in treating her:
A
B
C
D
Her Blood Pressure
Her Glucose level
Her Heart Rate
Your Heart Rate
A first year PEM fellow attending conference
developed a sudden onset of urticaria, lip swelling
and DIB. The etiology is most likely a reaction to:
A smelling someone else’s lunch
B a spider bite
C another “billing talk” by Dr Linzer
Allergen Families
Which of the following potential allergens do not
generally cross-react:
A. COX-2 inhibitors & Ibuprofen
B. Filberts & Pecans
C. Peanuts & Tofurky
D. Lobster & Shrimp
Using the “Epi-Pen”
When advising parents/patients on how to
administer an “epipen” you should tell them to:
A. hold it against the triceps and squeeze the
trigger
B. “stab” it into the anterior thigh
C. hold it against the lateral thigh and push
Presentations of Anaphylaxis
Which is NOT a clinical presentation of anaphylaxis:
A.
B.
C.
D.
E.
Vomiting and Diarrhea
Syncope
Altered Mental Status
Itchy Tongue
None of the above
First line therapy
In counseling a 50kg 15 year old after a severe episode of
anaphylaxis to a bee sting your best advice is that if they
get stung again they first should take
A.
B.
C.
D.
(2) 25mg diphenhydramine capsules PO
(5) tsp diphenhydramine elixer PO
.5mg epinephrine SQ
60mg prednisone PO
Which of the following treatments has been shown
to decrease the incidence of biphasic reactions:
A. Corticosteroids
B. Epinephrine
C. Diphenhydramine
D. Ranitidine
Summary:
 Various
 May
mechanisms and presentations
resemble common illnesses
 Early
recognition and treatment
 Prevention
is critical