Dana V. Wallace, MD
ACAAI Immediate Past President
FACAAI, FAAAAI
Associate Clinical Professor
Nova Southeastern University
Fort Lauderdale, Florida
www.drdanawallace.com
drdanawallace@gmail.com
The Causes of Anaphylaxis:
Select Cases (1002)
Venom ?? 11-21%
(up to 65%)
Webb et al:J Allergy Clin Immunol 113:s241,2004
Anaphylaxis Incidence & Fatality

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


Incidence (lifetime) risk 1 to 3%1
Incidence rate of anaphylaxis 1-2%
Case-fatality rate is 0.65% to 1%1-2
Prevalence of food anaphylaxis unknown
Highest rate in children and adolescents
Best data for incidence is from outpatient
Rx for epinephrine auto-injectors
1Kemp SF. JACI 2002; 110:341-348.
2. Yocum, Michael et al: J Allergy Clin Immunol ,104:452-6. 1999
Variable Incidence of Foodinduced Anaphylaxis
Related Factors


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
Age
Regional diets
Food preparation
Amount of exposure
Timing of first exposure
Boyce, J. A., A. Assa'ad, et al. "Guidelines for the Diagnosis and Management of Food Allergy in
the United States: Summary of the NIAID-Sponsored Expert Panel Report.
" J Allergy Clin Immunol 126(6): 1105-18. [referred to as “NIAID Food Allergy Guidelines
2010” ]
Foods Allergy Prevalence
NIAID 2010 Guidelines
Children
Adults
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








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Cow’s milk (1-2 %)
Egg (1-2%)
Peanut (0.6%)
Shellfish (0.5%)
Fish (.2%)
Soybean
Wheat
Shellfish (2.8%)
Vegetables (0.01-13.7%
Fruits (0.02-8.5%)
Peanuts (0.6%)
Tree nuts (0.4-0.5%)
Fish (0.5%)
Gupta 2011 Pediatric Survey
Peanut
Gupta, R. S. Pediatrics 128(1): e9-17.
Major class 1 food allergens
 Cow's milk:
Caseins (, ,), -lactoalbumin, -lactoglobulin, serum
albumin
 Chicken egg:
Ovomucoid, ovalbumin, ovotransferrin
 Peanut:
Vicillin, conglutin, glycinin
 Soybean:
Glycinin, profilin, trypsin inhibitor
 Shrimp:
Tropomyosin **
 Lipid transfer proteins (LTPs): **
Apple, apricot, peach, plum, corn
POLLEN FOOD ALLERGY SYNDROME
Gastrointestinal food hypersensitivities:
Pollen food allergy syndrome or oral allergy
syndrome (OAS)
 Oral mucosal itching, swelling, tingling
 Elicited by a variety of plant proteins that cross-react with
airborne allergens
 Pollen allergic patients may develop symptoms following
the ingestion of vegetables foods:
- Ragweed allergic patients: Fresh melons and bananas
- Birch pollen allergic patients: Carrots, celery, apples,
pears, hazelnuts and kiwi
 Immunotherapy for treating the pollen-induced rhinitis
may or may not reduce oral allergy symptoms
J Allergy Clin Immunol. 2004; 113:808-809
Components of Pollen Food
Allergy Syndrome (PFAS)




A history of symptoms consistent with PFAS
Allergic sensitization to pollen
Allergic sensitization to a plant food
A known correlation between the plant food
and the pollen
Pollen Food Allergy Syndrome (PFAS)
Oral Allergy Syndrome + systemic reactions
 PFAS emphasizes that one may have not only
oropharyngeal symptoms but systemic symptoms 2-10%
of the time
 While usually associated only with raw foods, cooked
plant foods may provoke the PFAS
 Prick-by-prick testing to fresh food is preferred for most
fruits and vegetables
 Stable allergens, e.g. peanut, hazelnut, and pea may be
best detected with commercial extracts
 Consider duplicate testing when extracts are available
Food allergy:
Exercise-induced anaphylaxis
Exercise
Food
Temperature
Gastrin
Mediator release
- Histamine
- Others (LTD4,PAF, etc)
ANAPHYLAXIS
Exercise Anaphylaxis
Foods associated
Shellfish 16%
Alcohol 11%
Tomatoes 8%
Cheese 8%
Celery 7%
Strawberries, milk, wheat & or Omega- 5 gliadin,
other grains, peaches – each 5%
Advise early AM exercise before eating or >
4 hrs. after eating
Chong s-u, 35 al. Int Arch Allergy Immunol. 2002;120:19-26.
Exercise Anaphylaxis (EA)
Food-dependant
 Exercise leads to increased gut permeability
which thereby increases food allergen intake
 Patients with low levels of sIgE food antibodies
are tolerant until stressed by exercise
 In wheat-dependent AE, exercises activates
tissue transglutaminase, which results in high
molecular-weight omega-5 gliadin complexes
that bind IgE with increased intensity leading to
anaphylaxis
Lemon-Mule H. Current Allergy and Asthma Reports 2008. 8(3): 201-208.
New causes of Anaphylaxis
Cetuximab
Antibodies to oligosaccharide galactose-alpha-1,3
galactose present prior to Tx
Felt possibly to x-react with same oligosaccharides in
beef or pork; +/- parasites or histoplasmosis (not
established) 1
Cat allergic patients may have IgE to the cat IGA
galactose-α 1,3 galactose
Testing for IgE to cat has been suggested 2
Desensitization protocol has been used 3
1. Chung, NEJM 2008; 358-1109 2. Gronlund H et al. JACI 1009, 123:1189.
2. 3. Jerath MR at al. JACI 2009, 123: 260
Radiocontrast Anaphylactoid Rx
Not related to shellfish allergy
 Seafood Allergy is NOT a risk factor:
Possible origin of the myth:
– In 1975 Shehadi et. al noted the following
regarding patients reactions:
• 15% of patients gave an unconfirmed history
of shellfish allergy
• They surmised iodine in shellfish was
responsible for the allergy. [FALSE]
• They surmised iodine in shellfish cross-reacted
to iodine in RCM. [FALSE]
Shehadi WH. Am J Roentgenol. 1975; 124: 145-152.
Beaty AD. American Journal of Medicine. 2008; 121 (2): 158e.
Subsequent Reactions May Increase
in Severity with Time
1st Reaction
60
2nd Reaction
3rd Reaction
% of reactions
50
*
*
40
30
20
10
0
Peanut allergen
Tree nut allergen
Proportion of reactions rated severe
Simons et al, J Allergy Clin Immunol, 2004
Fatal Food-induced Anaphylaxis
Highest Risk Factors
 Peanuts and tree nuts account for up to 92% of
fatalities1,2
 Adolescents (14-17) and young adults highest risk
group1
 Asthma as a concurrent disease (>90% some studies),
esp. poorly controlled asthma2,3
 Cardiovascular disease in middle-aged & older
patients
 Delay between time of symptom onset and
administration of treatment (OR up to 7.3)2,4
 Improper epinephrine dosing, usually underdosing5
1. Bock, SA, et ak, JACI 2004; 107 (1) 191-3. 2. Sampson HA,et al., NEJM. 1992; 237:380384.3. Pumphrey R. Curr Opin Allergy Clin Immunol. 2004;4:285-290. 4. Amin HS, et al.
JACI 2006; 117:169-75.5. NIAID Food Allergy Guidelines 2010
ANAPHYLAXIS DX & TX
Clinical Criteria for Anaphylaxis
Anaphylaxis is likely if 1 or 3 set of criteria are fulfilled
Acute onset (min to hrs)
1–
Skin/mucosal symptoms
AND
– Airway compromise
OR
– ↓ BP or Associated
symptoms
3
Hypotension within min. to hrs. after
exposure to known allergen
2
Exposure to known
allergen + at least 2 items
below within min to hrs
–
–
–
–
Hx of severe reaction (2005)
Skin/mucosal symptoms
Airway compromise
↓ BP or Associated
symptoms
– GI symptoms with food
allergy
Symposium on the Definition and Management of Anaphylaxis: Summary report. Sampson HA, et al. JACI 2005;
115:584-59. Second symposium on the definition and management of anaphylaxis: summary report. Sampson HA,
et al. JACI 2006; 117(2): p. 391-7.
Symposium on the Definition & Management
of Anaphylaxis: Summary Report
“Caution: These criteria describe so called
classic cases of anaphylaxis. Other presentations may
also indicate anaphylaxis (e.g. early presentation,
generalized flushing; isolated presentation, sudden
hypotension only in a patient without evidence of
allergen exposure; classic presentation but with a nonallergenic cause, such as exercise)”
Sampson HA et al. J Allergy Clin Immunol 2005;115:584-91.
“ANAPHYLAXIS”
FUNCTIONAL DEFINITION
 An acute allergic reaction for which it is known
that there is potential for fatality
– Regardless of the severity of the presenting symptoms
– For which immediate treatment has been shown to
prevent progression of the disease process
Can Anaphylaxis occur on first
ingestion of a food?
 Usually, but not always, there is a history
of food allergy, with or without anaphylaxis
 First-time food ingestion can occur at any
age, more common in young children
 20% first time anaphylaxis events (to a
specific food exposure) occur in the
school setting
NIAID Food Allergy Guidelines 2010
Characteristics of Food-induced
Anaphylaxis
 Increasing in incidence in industrialized countries
 Food-induced anaphylaxis is not easily recognized,
delaying diagnosis
 Dx heavily dependent on
– Early recognition of specific signs and symptoms
– Timing of the reaction
– Concomitant factors and disease processes
 No tests, including prick, sIgE, challenge studies, can
predict the severity of IgE mediated reactions to
foods
NIAID Food Allergy Guidelines 2010
Most Frequent Signs and Symptoms of
Anaphylaxis: Regardless of cause
Manifestation
Percent
Urticaria/angioedema
87
Flush
50
Dyspnea/wheeze
46
Hypotension
30
Gastrointestinal
30
1. Lieberman P. Immunol Allergy Clin North Am. 2001;21:813-825.
25
Less Frequent Signs and
Symptoms of Anaphylaxis
Manifestation
Percent
Rhinitis
16
Headache
15
Substernal pain
6
Itch without rash
4.5
Seizure
1.5
1. Lieberman P. Immunol Allergy Clin North Am. 2001;21:813-825.
26
Signs and Symptoms of Foodinduced Anaphylaxis
Are they different?
 Up to 20% have no cutaneous symptoms
 Up to 70% of cases have respiratory
involvement (upper or lower airway)
 Up to 40% have GI Symptoms
 Up to 35% have cardiovascular
symptoms
 Other symptoms: anxiety, mental confusion,
lethargy, and seizures
NIAID Food Allergy Guidelines 2010
Cardiovascular co-morbidity
 Increased heart mast cells present with
ischemic heart dx & cardiomyopathy
 Mast cells accumulate at sites of
coronary atherosclerotic plaques
 IgE antibodies bound to heart mast
cells can trigger degranulation
 Anaphylaxis may trigger myocardial
ischemia due to plaque rupture
 15% of severe anaphylaxis present with
chest pain
 7% severe anaphylaxis present with an
arrhythmia
1. Kemp SF et al. Allergy 2008. 63(8): 1061-70.
2. Lieberman P et al. The diagnosis and management of anaphylaxis practice parameter: 2010 Update. J ACI 2010. 126 (3)
477-80, (AKA 2010 JTF Anaphylaxis PP)
LABORATORY TESTS IN THE DIAGNOSIS
OF ANAPHYLAXIS
Plasma histamine
Serum tryptase
A
M
O
U
N
T
24-hr Urinary histamine metabolite
0
30
60
90
120
150
180
MINUTES
210 240
270
300
330
Serum Tryptase
 Total Serum Tryptase in anaphylaxis may remain
within nl range, but if > 2 ng/ml above baseline it
has 0.73 sensitivity & 0.98 specificity for dx of
anaphylaxis1
 Usually not ↑ in food-induced
anaphylaxis
 ↑ more likely in hypotensive anaphylaxis
* Dr. Larry Schwartz lab, Virginia Commonwealth University
1. Brown SG et al. Emerg Med Austral 2004; 16:120
Time Course of Food-induced
Anaphylaxis
 Onset is usually minutes (e.g. 3-5) to a few
hours after exposure to food allergen
 Biphasic reactions occur in up to 20% of
cases (usually < 8 hours in food allergy)
NIAID Food Allergy Guidelines 2010
Biphasic Anaphylaxis
Treatment
Initial
Symptoms
Treatment
1-8 hours
0
Antigen
Exposure
SecondPhase
Symptoms
Classic Model
1-48 hours
New Evidence
Time
BIPHASIC ANAPHYLACTIC
REACTIONS
Characteristics
 Etiology not always clear
– Immunological, e.g. late-phase response
– Pharmacologic-medication effect has ended
 Usually involves same organ system
 Cannot be predicted based on severity of initial
reaction
Ellis AK, Day JH. Ann Allergy Asthma Immunol 2007;98:64-9.
Time Course of Food-induced
Anaphylaxis
 Onset is usually minutes (e.g. 3-5) to a few
hours after exposure to food allergen
 Biphasic reactions occur in up to 20% of
cases (usually < 8 hours in food allergy)
 Prolonged reactions occur in up to 20% of
cases
 Deaths reported 30 minutes to 2 hours
following exposure to food
NIAID Food Allergy Guidelines 2010
Onset of Anaphylaxis to
Cardiopulmonary Arrest
Pumphrey R. Curr Opin Allergy Clin Immunol. 2004;4:285Y290
Clinical Factors Affecting
Anaphylaxis Severity & Fatality




Psychiatric disease
Substance abuse
Beta-blockers
COPD
 PAF acetylhydrolase
factor deficiency
 Subclinical mastocytosis
 Previous anaphylaxis
1. Bock, SA, et ak, JACI 2004; . Sampson HA,et al., NEJM. 1992; 237:380-384.
3. Pumphrey R. Curr Opin 4. NIAID Food Allergy Guidelines 2010
Simons, E. et al. J Allergy Clin Immunol 2007;120:S2-24.)
Additional Risk Factors for
FA Anaphylaxis Fatality
 Multiple food allergens (3x increase)
 Shellfish (#1 allergen after age 14)
 Ingestant of allergen (No known report of fatality when
only skin contact)
 If there is no skin manifestations of anaphylaxis (delay in
diagnosis)
Many Mediators Cause
Anaphylactic Symptoms
 Leukotrienes
 Prostagandins
 Kinins
• Platelet activating
factor
• Interleukins
• Tumor necrosis
factor
• Histamine
Actions of Epinephrine:
Antagonize Effects of All Mediators
Epinephrine
 1-adrenergic
receptor
 Vasoconstriction
 Peripheral vascular
resistance
 Mucosal edema
 2-adrenergic
receptor
Insulin release
1-adrenergic
receptor
 Inotropy
 Chronotropy
2-adrenergic
receptor
 Bronchodilation
 Vasodilation
 Glycogenolysis
 Mediator release
Simons KJ, Simons FER. Curr Opin Allergy Clin Immunol. 2010;10:354-361.
Epinephrine Cardiovascular
Effects
 Enhances coronary blood flow
– Increased duration of diastole (vs. systole)
– Vasodilator effects caused by increased
myocardial contractility
 Vasoconstrictor effects on coronary arteries
would seem to be undesirable but it is
– Felt to be a minor effect compared to above
benefit
Kemp SF et al. Allergy 2008. 63(8): 1061-70.
False Sense of Security
 Food-induced anaphylaxis can have a mild
course and resolve spontaneously
– Most likely related to endogenous
production of vasoconstrictors
• Epinephrine
• Endothelin-I
• Angiotensin II
NIAID Food Allergy Guidelines 2010
Beta Blockers & ACE Inhibitors
 Exposure to β-adrenergic blocking agents is a risk factor
for more serious & Tx resistant anaphylaxis1,2,3
– May reduce the effect of exogenous epinephrine
– May reduce the effect of endogenous epinephrine
 ACE inhibitors (OR 2.7) are a risk for more severe
anaphylaxis (e.g. with venom immunotherapy)1,2
 ACE inhibitors “may” interfere with endogenous
compensatory mechanisms, resulting in more severe or
prolonged symptoms of food-induced anaphylaxis3
 No evidence of increased risk for ACE receptor
blockers
1. 2010 JTF Anaphylaxis PP) 2. Cox L. Allergy Immunotherapy- a practice parameter third update.
JACI 127(1 supp) S1-55. 3. NIAID Food Allergy Guidelines 2010
Steps in Treatment of
Anaphylaxis
 #1 Remove Allergen
#3 Call for help
 #2 Administer
Epinephrine
Supplies and Equipment for
Anaphylaxis Treatment in office





“NECESSARY”
Stethoscope and
sphygmomanometer
Epinephrine 1:1000
Oxygen
IV Fluids
Tourniquets, syringes,
hypodermic needles,
large-bore needles
2010 JTF Anaphylaxis PP
“CONSIDER HAVING”
 One-way valve facemask
 Diphenhydramine inj.
 Corticosteroids inj.
“MAYBE”
 Vasopressor (Dopamine)
 Glucagon
 Automatic defibrillator
 Oral airway
KEY POINTS ON GENERAL
ANAPHYLAXIS DX AND TX
 Anaphylaxis protocols are based on
consensus –not on evidence
 The more rapid the onset of signs and
symptoms following exposure to offending
stimulus, the more likely the reaction will
be severe and life-threatening.
 Delayed onset of anaphylaxis, with delayed
Tx, also introduces high risk
KEY POINT
# 1 DRUG F0R ANAPHYLAXIS
EPINEPHRINE
Adult- 1:1000 0.2-0.5 ml q 5 minutes (or less) PRN
Child-0.01 mg/kg , max 0.3 mg q 5 minutes (or less) PRN
IM in Lateral thigh (speaker preference)
1”
EPINEPHRINE
PREVENTS
Blocks further mediator release
TREATS
Reverses the end-organ effects of
Anaphylaxis
IM vs. SQ Epinephrine in Children
8+
- 2 minutes
(EpiPen®)
SHORTEST ONSET OF ACTION
Vastus Lateralis
34 +14 (5 – 120) minutes
p < 0.05
Deltoid
Time to Cmax after injection (minutes)
Simons: J Allergy Clin Immunol 113:838, 2004
Epinephrine IM: Time to Onset
Maximum
pharmacodynamic
effect occurs before 10
min
Adapted from Simons FER, et al.
J Allergy Clin Immunol. 1998;101:33-37.
Auto injectors
Needle Length found on auto
injectors
• 1.43 cm
• May not penetrate vastus
lateralis muscle
•42% women 1
•2% men1
•12% children2
Twinject
Epi-Pen
Adrenaclick
1. Song TT et al. Ann Allergy Asthma Immunol 2005;94:539-42.
2. Stecher D et al. Pediatrics 2009; 124 (1): 55-70.
Fatal Anaphylactic Reactions
 Most fatal reactions are unpredictable
– Appropriate management after recovery from a
severe reaction may be protective against a fatal
recurrence2
– Epinephrine used in 62% of fatal reactions
• 14% of time before cardiac arrest3
• 86% of time after cardiac arrest
1. Sampson HA, et al. N Engl J Med. 1992;327:380-384.
2. Pumphrey R. Curr Opin Allergy Clin Immunol. 2004;4:285-290.
3. Pumphrey RS. Clin Exp Allergy. 2000;30:1144-1150.
51
Epinephrine: Multiple doses
 Pt with food-induced anaphylaxis need
TWO doses of epinephrine required up to
20% of the time before recovery
 Repeat dosing may be required after 5-15
minutes (optimal dosing interval unknown)
NIAID Food Allergy Guidelines 2010
BIPHASIC ANAPHYLACTIC
REACTIONS
Treatment
 An insufficient dose of epinephrine given for the
primary response is considered a risk factor
 Steroids do not prevent, but there seems to be a
trend toward lower dose of corticosteroids
administered in patients with biphasic rx
[Administer adequate doses]
Ellis AK, Day JH. Ann Allergy Asthma Immunol 2007;98:64-9.
BIPHASIC ANAPHYLACTIC
REACTIONS
 Severity of 2nd event is variable but can be fatal
 No biphasic response occurred in patients who
had complete resolution of anaphylaxis
symptoms in < 30 minutes
 If occurs, consider overnight hospital observation
Ellis AK, Day JH. Ann Allergy Asthma Immunol 2007;98:64-9.
Lieberman P. Ann Allergy Asthma Immunol 2005;95:217-26
Epinephrine IM: Potential Side Effect
[These should not limit appropriate use]




Anxiety, fear, restlessness
Headache, dizziness, tremor, pallor
Palpitations, tachycardia
Increased risk with concurrent use of monamine
oxidase inhibitors, tricyclic antidepressants,
stimulant medications, cocaine abuse
 Increased risk with pre-existing cardiovascular
disease, aortic aneurysm, uncontrolled
hypertension, recent intracranial surgery
NIAID Food Allergy Guidelines 2010
Epinephrine IM: Potential Side Effect
[These should not limit appropriate use]
 Rare side effects:
–
–
–
–
–
–
Angina
Ventricular arrhythmias
Myocardial infarction
Pulmonary edema
Sudden sharp increase in BP
Intracranial hemorrhage
 More common with overdose any route
 More common with IV administration
NIAID Food Allergy Guidelines 2010
Severe Anaphylaxis Position
*
Position Patient Supine
Fatal cases associated with posture changes
(Pumphrey RSH. JACI 2003;112:451-2.)
 4 deaths occurred within seconds of a change to a more upright
position
 6 deaths occurred in individuals supported sitting up after
shock
 Postulated mechanisms
– • With sitting or standing venous return stops
– • Vena cava will empty within seconds
– • No blood flow to left heart results in pulseless electrical
activity
– • In this scenario epinephrine would likely not work
# 2 DRUG OXYGEN
 Optimally with all patients with anaphylaxis
 Any patient with Hypotension or respiratory
distress
 Any patient with 02 sat <95%
 Any patient requiring more than one Epi
injection
 Face mask recommended over nasal prongs.
 Start with 6-8 Liter/minute
#3 Drug IV FLUIDS
 For Hypotension (systolic <100) or any one who
has not responded to first IM Epinephrine
 When there is shock in spite of increased
vascular resistance
 10% severe anaphylaxis not reversible
with Epi*
 Select IV Fluids
– .9 NaCl (isotonic crystalloid)
– Hydroxyethyl starch (Hespan) (colloid) if saline not
effective
Bock SA, Munoz-Furlong A, Sampson HA. J Allergy Clin Immunol. 2001;107:191–193.
IV FLUIDS
 Administer rapidly 5-10 mg/kg
crystalloid over first 5-10 minutes,
and total of 20-30 ml/kg first hour
 Apply BP cuff to bag of fluid or
withdraw fluid and use a stopcock to
infuse with a large 50 cc syringe (see
picture)
 You may need to administer up to
50% of the intravascular volume
Second line drugs (office setting)
 Diphenhydramine 1-2 mg/kg parentally
 Ranitidine 50 mg (1 mg/kg children)
• IM same as IV for onset of action
• If IV administer over 5 minutes
 Leukotriene modifiers: no recommendation for
or against
 Atropine
 Bradycardia
 Βeta-Blocked anaphylaxis
 Dopamine
Antihistamines: Time to Suppression
Time to 50% suppression
101.2 min
79.2 min
51.7 min
Fexofenadine
Diphenhydramine IM
Diphenhydramine PO
Jones DH, et al. Ann Allergy Asthma Immunol. 2008;100(5):452-456.
Antihistamines
[A 2nd, 3rd, or 4th line drug]
 “The use of antihistamines is the most common
reason reported for NOT using epinephrine and
may place a patient at significantly increased
risk for progression toward a life-threatening
reaction.”
 H1 antihistamines are only useful for itching
and urticaria
 2nd generation H1 AH may be considered as
rapid onset and less sedation (e.g. cetirizine)
 H2 antihistamine use has minimal support
NIAID Food Allergy Guidelines 2010
H2-antihistamines
 In vitro studies suggest a benefit
 No adequate randomized and quasi-randomized
controlled trials comparing H2-antihistamines with
placebo or no intervention1
– No recommendations for clinical practice
 Avoid with food-induced anaphylaxis as may
interfere with food allergen digestion and
potentially augment a reaction2-3
1. Sheikh A, et al. Cochrane Database of Systematic Reviews 2007, Issue 1 .2.
Untersmavr E, et al. JACI 2003; 112:626-23. 3. Scholl I, et al. AM J Clin Nutr 2005;
81:154-60.
Additional Medications to consider
 Nebulized albuterol or levalbuterol for
bronchospasm1
Albuterol does not relieve airways edema!
1. 2010 JTF Anaphylaxis PP. JACI (in publication). 2. Brown SGA et al. Emerg Med J
2004;21:149-54. 3. Kill C et al. Int Arch Allergy Immunol 2004; 134:260-1. 4. Wenzel V et al.
N Engl J Med 2004; 350:105-13
CORTICOSTEROIDS






Limited data supporting usefulness in anaphylaxis
Never a substitute for Epi
Minimal benefit for initial treatment
4-6 hours before onset of action
Consider when a history of asthma
Questionable benefit for severe, prolonged and biphasic
reactions
 No difference in outcomes in severe IT anaphylaxis (37%
of non-fatal did not get steroids)
 Dosage is unknown (recommended dose is usually
methylprednisolone 1-2 mg/kg IV, 80-125 mg max or
prednisone 1 mg/kg PO, 60-80 mg max)
2010 Anaphylaxis PP. JACI)
NIAID Food Allergy Guidelines 2010
Additional Medications to consider
 Intravenous Epinephrine
– Bolus Dosage (1:10,000 dilution)10-20 mcg (0.1-0.2 ml of a
1:10,000 dilution) at initial dose of 0.75-1.5 mcg/kg2
– Repeat as necessary
 Vasopressors (Dopamine) for unresponsive hypotension
– Evidence suggest to use ≥ 10 mcg/kg/min IV2
 Vasopressin: esp. for cardiac arrest. It is a potent
vasoconstrictor, & inhibits NO and prostaglandin
generation 3-4
1. 2010 JTF Anaphylaxis PP. JACI (in publication). 2. Brown SGA et al. Emerg Med J
2004;21:149-54. 3. Kill C et al. Int Arch Allergy Immunol 2004; 134:260-1. 4. Wenzel V et al.
N Engl J Med 2004; 350:105-13
Glucagon
 For refractory hypotension in patients on βBlockers
 Initial dose of 1 to 5 mg IV followed by infusion of
5-15 mcg/min titrated against blood pressure
 Glucagon bypasses the β-adrenergic receptors
 Glucagon increases cAMP via stimulation of its own
receptor, producing bronchodilation and helping to
reverse hypotension
 Glucagon may induce nausea and vomiting
2010 JTF Anaphylaxis PP. JACI (in publication).
Epinephrine Auto-injections
Who needs one?
 Prescribe two doses of epinephrine for:
– Hx of prior systemic allergic reaction
– Patient with Food allergy (without hx of
anaphylaxis) and concomitant asthma
– Known food allergy to peanut, tree nut, fish,
and crustacean shellfish
(Even if no hx of
anaphylaxis)
– FPAS (oral allergy)
– All food allergic pts (??)
NIAID Food Allergy Guidelines 2010
Epinephrine for PFAS: Should one Rx?
 Up to 10% of patients with PFAS are at risk for a systemic
reaction
 Severe reactions can occur upon the first ingestion of a
food with cross-reactive allergens
 Systemic reactions to previously tolerated foods can occur
 The natural history of PFAS is unknown
 Peach, peanut, tree nuts, and mustard are high risk foods
for PFAS with systemic symptoms
 Rx for reactions of any severity to cooked plant foods
Discharge Plan for Patients with
Food-Induced Anaphylaxis
 Epinephrine (2 doses) must be available at
all times for patients at risk (e.g. school)
 Anaphylaxis emergency action plan
 Plan for monitoring auto-injector expiration
dates
 Plan for arranging further evaluation and/or
follow-up
 Printed info about anaphylaxis and its Tx
NIAID Food Allergy Guidelines 2010
ACAAI-ACEP
GO TO www.acaai.org and search for “SAFE”
Death
[We
Must
Prevent]
Patient Resources
 http://www.ncbi.nlm.nih.gov/pubmedhealth
 http://www.niaid.nih.gov/topics/foodallergy
/clinical/documents/faguidelinesexecsumma
ry.pdf
Physician Resources
 http://www.jacionline.org/article/S00916749(10)01566-6/fulltext
 http://allergyparameters.org/file_depot/010000000/3000040000/30326/folder/73825/2005%20Anaphyl
Thank You
DANA WALLACE, MD
drdanawallace@gmail.com
www.drdanawallace.com
username: medicalprofessional
password: allergy