Appropriate Recognition and Management of Anaphylaxis · Appropriate Recognition and Management of...
Transcript of Appropriate Recognition and Management of Anaphylaxis · Appropriate Recognition and Management of...
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Appropriate Recognition and
Management of Anaphylaxis Session F4038
Mitchell R. Lester, MD FAAP Fairfield County Allergy, Asthma,
and Immunology Associates Norwalk, CT
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In the past 12 months, I have no relevant financial relationships with the manufacturer(s)
of any commercial product(s) and/or provider(s) of commercial services discussed in this CME activity. I do not intend to discuss
an unapproved/investigative use of a commercial product/device in my presentation. The minor differences between your handout and my talk do not affect the content of the
talk.
Disclosure $
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Learning Objectives At the conclusion of this CME activity,
the participant will be able to: 1. Describe and recognize anaphylaxis. 2. Identify the most common causes of
anaphylaxis. 3. Understand the importance of
identifying and treating anaphylaxis quickly.
4. Name the treatment of choice for anaphylaxis.
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Changes You Might Make in Your Practice
1. Reach for epinephrine first when treating anaphylaxis.
2. Have anaphylaxis mock-code drills.
3. Create an anaphylaxis management plan for your patients.
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•Richet and Portier, 1902 •During attempts to immunize dogs to the toxin of sea anemone, dogs that previously tolerated sub-lethal doses died after being given small doses. •Coined the term “anaphylaxis” (without protection).
•Opposite of prophylaxis. •Richet: 1913 Nobel Prize in Medicine.
From Whence “Anaphylaxis”?
Charles R. Richet, MD Paul J. Portier, MD
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What is Anaphylaxis?
J Allergy Clin Immunol. 2010,126(3):480e1-e42
One of three clinical scenarios: • Acute onset (minutes-hours) of a reaction
involving skin and/or mucosal tissue AND either respiratory compromise, hypotension OR symptoms of end organ dysfunction.
• Two or more of the following occurring rapidly after exposure to a likely allergen: skin/mucosal tissue, respiratory compromise, reduced blood pressure or associated symptoms, and/or persistent GI symptoms.
• Reduced blood pressure after exposure to a known allergen.
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•An acute multi-system reaction caused by the rapid release of mediators from tissue mast cells and peripheral blood basophils. • Immunologic mechanisms can be allergic (IgE-mediated) or non-IgE-mediated. •Non-immunologic anaphylactic reactions, formerly called anaphylactoid or pseudo-allergic reactions, also occur.
…But You Might Think of Anaphylaxis This Way…
Johansson SGO et al JACI 2004,113:832-6
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Prevalence of Anaphylaxis • Estimated risk in US: 1-3%.
• 3.3 to 4 million Americans at risk. • 1,433 to I,503 at risk for fatal reaction.
• Food: 150/yr., Antibiotics: 600/yr., Venom: 50/year.
• 5-year review of 1.15 million Canadians. • 0.95% of the population had epinephrine prescribed. • Dispensing rates 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.
• Conclusion: Anaphylaxis appears to peak in childhood, and then gradually decline.
J Allergy Clin Immunol 2001;108:622 J Allergy Clin Immunol 2002;110:341-8 J Allergy Clin Immunol 2002;110:647-51 Arch Int Med 2001;161,15-21
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• Estimates range from 10-100 per 100,000 person-yrs.
• 1983-87: 21 per 100,000 person-yrs. (95% confidence interval: 17 - 25). • Occurrence rate: 30 per 100,000 person-yrs.
• 2000: 49.8 per 100,000 person-yrs. • Increased over time. • Highest in children (70/100,000 person-yrs).
J Allergy Clin Immunol 1999;104:452-456. J Allergy Clin Immuno. 2009;122:1161–1165.
Incidence of Anaphylaxis
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Risk Factors for Anaphylaxis
Risk factors • Atopy Time since reaction • Age Economic status • Gender Season • Route and constancy of administration
Not risk factors • Race • Geography • Chronobiology Clin Exp Allergy. 2001;31.
J Allergy Clin Immunol. 2001;105
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Anaphylaxis Risks If You Are Atopic
Risk Factor • Idiopathic • Exercise • Latex • Radiocontrast media
Not Risk Factor • Penicillin • Insulin • Muscle relaxants • Hymenoptera venom
J Allergy Clin Immunol. 2004;113:536.
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• Females>males • Age 15 and older • Overall • Latex • Muscle relaxants • Aspirin/NSAIDs • Idiopathic
• Males>females • Younger than 15 yrs.
Gender and Risk of Anaphylaxis
J Allergy Clin Immunol. 2004;113:536.
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• Clinical diagnosis. • Careful history to identify cause. • Confirmed by elevated serum
tryptase. • Specific for mast cell degranulation.
• Refer to allergist for detailed history and specific testing.
Diagnosing Anaphylaxis
J Allergy Clin Immunol 2005;115:S483-523 J Allergy Clin Immunol 2010,126(3):480e1-e42
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Adapted from J Allergy Clin Immunol 2002;109:S181
Percent of children
Frequency of Symptoms in Anaphylaxis
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Signs and Symptoms of Anaphylaxis
Skin: Flushing, urticaria, angioedema, pruritus.
Respiratory: Nose: Symptoms of allergic rhinitis. Laryngeal*: Dysphonia, stridor,
dyspnea, asphyxiation, death. Lungs*: Wheezing, cough, chest
tightness, asphyxiation, death. * Potentially fatal
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Gastrointestinal: Nausea, vomiting, bloating, cramping, diarrhea.
Cardiovascular*: Tachycardia, hypotension, collapse, shock, bradycardia, death.
Other: Sense of impending doom, metallic taste, urinary urgency, uterine cramps.
Signs and Symptoms of Anaphylaxis
* Potentially fatal
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Differential Diagnosis Scombroid poisoning. Systemic mastocytosis. Hereditary angioedema. Samter’s triad. Vasovagal reaction. Cardiac arrhythmia. Hypoglycemia. Psychiatric conditions. Flushing syndromes. SIDS. J Investig Allergol Clin Immunol 2002;12:2-11
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Time to Demise in Anaphylaxis
Minutes from exposure to first arrest
0
5
10
15
20
25
30
35
<1 1-2 2.1-4.5 4.6-9.9 10-20 21-45 46-99 100-214 >215
Food Stings Drugs
Adapted from Clin Exp Allergy. 2000;30(8):1144-50.
# of
pat
ient
s
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Factors Affecting Prognosis
* Medications
Poor Prognosis Good Prognosis
Onset Early Late
Initiation of treatment Late Early
Route of exposure* Injection* Oral*
β-blocker use? Yes No
Underlying disease? Yes No
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Killers in Anaphylaxis
• Hypotension and shock. • Less frequent cutaneous/GI symptoms.
• Asphyxia (upper and/or lower). • Cardiac. • Hypotension. • Tachycardia. • Bradycardia. • Myocardial infarction. • Empty heart syndrome.
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Classification of Anaphylaxis
Adapted from Johansson, et al JACI 2004 and Simons JACI 2006
Anaphylaxis
Non-IgE Blood products, drugs, dextran,
immune complexes (Type II and III)
IgE (FcεRI) Food, venom, latex, drugs
(Type I)
Idiopathic
Non-Immunologic Immunologic
Physical Exercise, cold
Other Drugs, IV contrast, systemic mastocy-
tosis
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Not All Mast Cell Activation is IgE-Mediated
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Type I vs. Type II and III Hypersensitivity Reactions
Type 1 tend to be more severe. Higher rate of hypotension and arrest. Type 1 have higher tryptase level.
Clin Rev Allergy. 1991;9(3-4):249-258 Ann Fr Anesth Reanim. 1999;18(8):796-809 Anasthesiology 99:536,2003
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Adapted from Ann Allergy Asthma Immunol. 2004;92:464-468.
Causes of Anaphylaxis in Childhood
Number of Children
Food Drug Exercise Venom Other Idiopathic
25
15
0
5
10
20
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Food: Peanut, tree nuts, shellfish/fish, egg, milk. Medications: β-lactam and other antibiotics,
NSAIDs, muscle relaxants, biologicals, others. Latex. Venom: Bees, wasp, vespids, fire ants. Allergen immunotherapy, skin testing (rare). Exercise with food dependence. Seminal fluid.
Causes of IgE-Mediated Anaphylaxis
Neugut AI et al. Arch Intern Med 2001;161:15-21 Lazarou J et al. JAMA 1998;279:1200-5 J Allergy Clin Immunol 2010,126(3):480e1-e42
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Causes of Non-IgE-Mediated Anaphylaxis
Radiocontrast media. Medications: Opiates, IVIg, ACE inhibitors, vancomycin. Cellular elements. Physical: Exercise (without food), cold. Idiopathic. Mastocytosis. Scombroid poisoning. J Allergy Clin Immunol 2002;110:341-8 J Allergy Clin Immunol 2010,126(3):480e1-e42
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Iatrogenic Causes of Anaphylaxis
Radiocontrast media. Medications. Latex. Cellular elements (transfusions). Allergen immunotherapy.
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Temporal Patterns of Anaphylaxis •Uniphasic •Biphasic
• Return of symptoms (any severity) 1-8 hours after apparent resolution.
• Estimated: 2-3% of children and 5-20% of adults with severe episodes.
•Protracted • Up to 32 hours. • May not be prevented by steroids.
•Delayed Lieberman P. Ann Allergy Asthma Immunol 2005;95:21 Stark BJ, Sullivan TJ. J Allergy Clin Immunol. 1986;78:76 Lee JM, Greenes DS. Pediatrics. 2000;106(4):762-766. Popa VT, Lerner SA. Ann Allergy. 1984;53(2):151-155.
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Biphasic Reactions • 3-20% (or more). •Onset 4-8 hours later (or more). •Usually similar symptoms. •Risks:
• Ingested allergen. • Delay in onset of symptoms. • Severe reaction. • Delay in epi or > 1 epi dose.
•Comorbidities and medications. •GOMER or SIMER?
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Antigen Exposure
Treatment
Initial Symptoms
1-72 hours
Time
Uniphasic Anaphylaxis Treatment
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Biphasic Anaphylaxis
Antigen Exposure
Treatment
Initial Symptoms
Late-Phase
Symptoms
Treatment
1-8 hours
1-72 hours
Time
Treatment
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Antigen Exposure
Treatment
Initial Symptoms
1-72 hours
Time
Protracted Anaphylaxis Treatment Treatment
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Identifying the Trigger
History, history, history. • Timing of exposure. • Associated factors (exercise, meds). • Sequence of symptoms. • Treatment.
Testing for specific IgE. Other lab tests. Challenge tests?
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Testing in Anaphylaxis
Specific IgE can confirm or refute diagnostic suspicion. • Inhalants, foods, venom, some
medications. Lab tests for mast cell disease. • Mastocytosis. • Complement activation.
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Interpreting Allergy Tests • Positive test ≠ allergy. • Positive test = sensitization. • Presence of specific IgE
• Allergy = sensitization + mast cell activation with exposure. • Symptoms
• Therefore, do not test for random or irrelevant allergens.
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Types of IgE Allergy Testing In vivo: Skin tests • Choose appropriate allergens and controls. • No antihistamines or tricyclic antidepressants. • Positive test ≠ allergy: Correlate with history. • Skin prick test vs. Intradermal.
• Sensitivity/Specificity. • Venom, medications, aeroallergens.
In vitro: “RAST” • Less sensitive, more expensive, longer to get result. • Often harder to interpret. Positive test ≠ allergy. • Not influenced by medications or skin disease.
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Tests for Mast Cell Mediators in Anaphylaxis
0 30 60 90 120 150 180 210 240 270 300 330
Plasma histamine
Serum tryptase
24-hr N-methyl-histamine (urine)
Minutes Adapted from Anasthesiology. 2003;99:536. and JACI.2010,126(3):480e1-e42.
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• Random chart review (n=678) of patients with food allergy presenting to 21 North American emergency departments.
• Management: • Antihistamines: 72%. • Systemic corticosteroids: 48%. • Epinephrine: 16% (24% of severe reactions). • Respiratory meds (e.g., albuterol): 33%. • Self-injectable epinephrine at discharge: 16%. • Referred to an allergist: 12%.
Clark S et al. J Allergy Clin Immunol 2004;347-52
Anaphylaxis Rx in the ED
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The treatment of choice for anaphylaxis is: A. Adrenaline. B. Better give epinephrine or call your lawyer. C. Can’t justify anything better than epinephrine. D. Don’t give anything before epinephrine. E. Epinephrine F. F….well, just give the epi!
Allergy/Immunology Boards: Question #1
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If You Remember Nothing Else Today…
WHY?
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Treatment of Anaphylaxis
Onset of Action: • Epinephrine (IM):
•Antihistamines (IM, IV, or PO):
•Corticosteroids: (IM, IV, or PO):
Seconds.
Minutes.
Hours.
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When in Doubt…
Inject Epinephrine!
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Old Epinephrine is Better Than No Epinephrine
J Allergy Clin Immunol. 2004;113:837-844. J Allergy Clin Immunol. 2000;105:1025-30
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Rules from The House of God (#3)
“At a cardiac arrest, the first procedure is to take
your own pulse.” -Samuel Shem
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Management of Anaphylaxis Speed is critical: Circulation Airway
Breathing
Defibrillation
Epinephrine
Fluids Kemp and Lockey . 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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Management of Anaphylaxis
Kemp and Lockey . 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
Speed is critical: Circulation
Airway
Breathing
Epinephrine
Fluids
Defibrillation
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Management of Anaphylaxis
Kemp and Lockey . 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
Speed is critical: Circulation
Airway
Epinephrine
Breathing
Fluids
Defibrillation
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Management of Anaphylaxis
Kemp and Lockey . 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
Speed is critical: Circulation
Epinephrine Airway
Breathing
Fluids
Defibrillation
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Management of Anaphylaxis
Kemp and Lockey . 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
Speed is critical: Epinephrine Circulation
Airway
Breathing
Fluids
Defibrillation
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Secondary measures: • Patient in recumbent position; elevate legs. • Maintain airway (intubate or cricothyrotomy).
• Oxygen, 6-8 liters/minute.
• IV fluids for severe hypotension.
Management of Anaphylaxis
Kemp SF and Lockey RF. J Allergy Clin Immunol 2002;110:341-8
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Management of Anaphylaxis
Kemp SF and Lockey RF. J Allergy Clin Immunol 2002;110:341-8
• Secondary measures: • Epinephrine 1:1000, ½ dose into injection site. • Diphenhydramine or other H1-blocker. • Ranitidine or other H2-antagonist. • Albuterol nebulized solution. • Methylprednisolone 1-2 mg/kg per 24 hr.
• For refractory hypotension: • Dopamine 2-20 μg/kg/min. • Glucagon 20-30 μg/kg (max 1 mg in children)
over 5 min. then run at 5-15 μg/min.
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After the Anaphylaxis
Accidents are never planned. • Review the trigger and avoidance. • Recognize symptoms early. • React quickly.
Educate all caretakers. Create a management plan. • Emphasize & validate self-injectable
epinephrine.
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Anaphylaxis Action Plans
Home/school: • Triggers and symptoms to look for. • Medications to use with dose and order. • Where medications are kept and access. • What others should do.
Your office: • Allergy emergency practice drills. • What others should do.
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Anaphylaxis Action Plans
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Equipment and Medications for
Anaphylaxis Preparedness
Adapted from Allergy Asthma Proc. 2013;34(2):120-31.
Required: Epinephrine 1:1000 Oxygen IV fluids (0.9 NL saline) Tourniquets, syringes, Large bore needles
Optional: Diphenhydramine (IV/IM) Ranitidine (IV/IM) Corticostroids (IV)
Consider having: Epinephrine 1:10000 IV β-agonist/nebulizer IV pole/latex free gloves O2 Sat monitor Vasopressor ( e.g., dopamine)
Recommended: One-way valve facemask Oral airways (4-6 sizes) AED Glucagon
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Referral to the Allergist
Trigger identification. • History. • Testing.
Patient education. • Anaphylaxis in general. • Trigger avoidance. • Epinephrine auto-injector.
Detailed action plan.
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Changes You Might Make in Your Practice
1. Reach for epinephrine first when treating anaphylaxis.
2. Have anaphylaxis mock-code drills.
3. Create an anaphylaxis management plan for your patients.
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References Lieberman P (ed.), et al. The Diagnosis and Management of Anaphylaxis: An Updated Practice Parameter. J Allergy Clin Immunol. 2005;115(3):483-523. Lieberman P (ed.), et al. The Diagnosis and Management of Anaphylaxis Practice Parameter:2010 Update. J Allergy Clin Immunol. 2010,126(3):477-480e1-e42 (www.jacionline.org/article/S0091-6749(10)01004-3/fulltext) Samant SA, et al. Anaphylaxis: Diagnostic Criteria and epidemiology. Allergy Asthma Proc. 2013;34(2):115-9. Sampson HA et al., Second Symposium on the Definition and Management of Anaphylaxis: Summary Report. J Allergy Clin Immunol. 2006;117:391-7. Soar J, et al., Emergency Treatment of Anaphylactic Reactions-Guidelines for Health Care Providers. Resuscitation. 2008;77:157-69. Simons, FER. Anaphylaxis. J Allergy Clin Immunol. 2010,125(2):S161-181 Simons FE, et al. World Allergy Organization Anaphylaxis Guidelines: Summary. J Allergy Clin Immunol. 2011;127(3):587-593.e22. Wallace DV. Anaphylaxis in the allergist’s office: Preparing your office and staff for medical emergencies. Allergy Asthma Proc. 2013;34(2):120-31.