2. Case history
• A 14-year-old girl went for a birthday party. After having food in the party
she complained of uneasiness, crampy pain in abdomen, vomiting and
throat tightness. She was a known case of Asthma. When brought to the
emergency department she was having breathing difficulty, oxygen
saturation was 92% and had wheezing. She had rash as shown .
• What is the likely diagnosis?
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4. Learning objectives:
• At the end of this class the learner should be able to:
• Define Anaphylaxis and anaphylactoid reaction
• Enumerate common causes of anaphylaxis
• Pathophysiology of anaphylaxis
• Clinical features
• Management
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5. Definition:
• Anaphylaxis is an acute, severe, life-threatening allergic reaction in
presensitized individuals, leading to a systemic response caused by
the release of immune and inflammatory mediators from basophils
and mast cells.
• At least 2 organ systems are involved, such as the skin, the upper and
lower airways, and the cardiovascular, neurologic, and GI systems, in
this order of priority or in combination.
• Similar symptoms caused by nonimmunologic mechanisms are
termed anaphylactoid reactions/ pseudoanaphylaxis.
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7. Common causes
• Food:
• Pea nut, milk, egg, fish, tree nuts
and food additives.
• Medications:
• ß- lactam antibiotics, NSAIDS
• Venom:
• Hymenoptera
• Natural rubber latex
• Occupational allergens
• Diagnostic agents like
radiocontrast media.
• Immunomodulators and
recombinant biological agents
• Infliximab, rituximab, omalizumab
• Physical factors
• Exercise, cold, heat and sunlight
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8. Classification: World Allergy organization allergic disease
resource center: anaphylaxis
1. Anaphylaxis:
immunologic, particularly IgE-mediated reactions
2. Nonallergic anaphylaxis:
clinically identical to anaphylaxis; however, not immunologically
mediated
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9. Classification of immediate type life threatening allergic
reactions
1. IgE antibody mediated systemic anaphylaxis
2. IgE-mediated, local, life threatening laryngeal obstruction.
3. Immunologic but not IgE mediated anaphylaxis
4. Munchausen anaphylaxis: real or simulated factitious anaphylaxis
5. Anaphylactoid : non Ig E mediated
6. Idiopathic anaphylaxis: Cause cannot be identified.
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10. Epidemiology and pathogeneis
• Estimated prevalence between 1% and 17% of the total US
population, and 0.002% of the population may die from an
anaphylactic reaction.
• Other studies 0.05-2%
• Food allergies more common in children.
• Adults drug allergies more common.
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19. • Assessment : BLS
• Secure airways, maintain circulation.
• Give epinephrine: Dose and route
IM (1: 1000) IV / IO (1: 10,000) Endotracheal (1: 1000)
Children 0.01mg/kg (Max 0.3 mg) 0.01ml/kg (Max 1mg ) 0.1 mg/kg to max of
2.5mg diluted in 5-10
ml of sterile water
Adult 0.2 to 0.5 ml 1mg 2-2.5 mg diluted in 5-
10 ml of sterile water
Repeat dose 5-15 min 3-5 min 3-5 min
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20. • Oxygen for hypoxia.
• IV fluids for hypotension : 30ml/kg within 1st hour.
• Nebulization with salbutamol:
• children: 0.15 mg/kg nebulized every 20 minutes for 3 doses, then 0.15 to 0.3 mg/kg every 1-
4 hours when required;
• adults: 1.25 to 5 mg nebulized every 20 minutes for 3 doses, then every 1-4 hours when
required
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21. • H1 and H2 antagonists :
• Children: Diphenhydramine 1-2 mg/kg intravenously/intramuscularly;
• Adults: 25-50 mg intravenously/intramuscularly.
-and-
• Ranitidine: children: 1 mg/kg intravenously given over 5 minutes; adults: 50 mg
intravenously given over 5 minutes.
• Vasopressors: Iv epinephrine infusion.
• Glucagon: Adjunct along with epinephrine in patients on ß-blockers and CAD.
• Corticosteroids*:
• methylprednisolone: children and adults:1-2 mg/kg/day intravenously
• prednisone: children and adults: 0.5 to 1 mg/kg/day orally
• Atropine
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24. Summary
• Anaphylaxis is a life threatening event and a medical emergency.
• It could be IgE mediated or non – Ig E mediated (anaphylactoid).
• Food is the most common cause of anaphylaxis in children.
• Skin manifestation followed by respiratory symptoms are commonest.
• Treatment : Epinephrine.
• Prevention is possible.
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25. Bibliography
• BMJ Best Practice: Anaphylaxis
• Anaphylaxisda practice parameter update 2015. Ann Allergy Asthma
Immunol 115 (2015) 341e384
• Nelson Textbook of Pediatrics.
• Anaphylaxis. Textbook of Allergy for the clinician. P.K. Vedanthan et al.
CRC press.
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Classification of immediate-type, life-threatening allergic or
pseudoallergic reactions (CHEST)[4]
I. IgE antibody-mediated systemic anaphylaxis
• food
• medications
• venom
allergen immunotherapy
• blood products (including plasma and antibodies [intravenous immunoglobulin])
• monoclonal antibodies (e.g., omalizumab).
II. IgE-mediated, local, life-threatening laryngeal obstruction.
III. Immunologic but not IgE-mediated anaphylaxis
• mediated by anaphylatoxins C3a and C5a
• monoclonal antibodies against lymphocyte receptors
• other new biologic products.
IV. Munchausen anaphylaxis: real or simulated factitious anaphylaxis
• IgE-mediated, due to purposeful self-exposure to an allergen
• simulated: purposeful approximation of the vocal cords resulting in laryngeal stridor
• prevarication anaphylaxis: patient reports signs and symptoms of anaphylaxis on repeated occasions;
based on history, idiopathic anaphylaxis is suspected; however, never any documented signs and
symptoms by physicians.
V. Anaphylactoid: clinically indistinguishable from anaphylaxis, but not IgE-mediated; seen in response to
opiates, NSAIDs, and radiocontrast agents
• radiographic contrast medium (mechanism uncertain)
• pharmacologic.
VI. Idiopathic anaphylaxis: the cause cannot be identified
• generalized frequent: >6 episodes per year, or ≥2 episodes within a 2-month period
• generalized infrequent: less often than generalized frequent
• angioedema (potentially life-threatening) frequent: >6 episodes per year or ≥2 episodes within a 2-
month period
• angioedema (potentially life-threatening) infrequent: less often than angioedema frequent.
The clinical symptoms derive from proinflammatory and vasoactive mediators and cytokines released by
massive degranulation or release from basophils and mast cells
On subsequent exposure, binding of antigen to the IgE antibodies leads to bridging and triggers the
degranulation of mast cells. Histamine, prostaglandin D2, leukotrienes, platelet-activating factor, tryptase,
nitric oxide, and eosinophil and neutrophil chemotactic factors have diverse effects on target organs and lead
to the clinical manifestations of anaphylaxis.