Anaphylaxis 

Anaphylaxis 
 Introduction
o Anaphylaxis is an acute, potentially fatal, multiorgan system reaction
caused by the release of chemical mediators from mast cells and
basophils.The classic form involves prior sensitization to an allergen with
later reexposure, producing symptoms via an immunologic mechanism.
Anaphylaxis 
 Causes
o A)IgE mediated mast cell degranulation
o Food- peanuts,fish,milk,egg,etc.
o Insect stings- bee venom.
o Drugs and chemicals- penicillin and other antibiotics, i.v anaesthetic agents,
latex particles.

o B)Non IgE mediated degranulation

o Aspirin
o Radiocontrast media
o Exercise
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 Pathophysiology
 The traditional nomenclature for anaphylaxis reserves the term anaphylactic
for reactions mediated by immunoglobulin E (IgE) and the term
anaphylactoid for IgE-independent events, which are clinically
indistinguishable. The World Allergy Organization has recommended
replacing this terminology with immunologic (IgE-mediated and non–IgE-
mediated [eg, IgG and immune complex complement–mediated]) and
nonimmunologic anaphylaxis (events resulting in sudden mast cell and
basophil degranulation in the absence of immunoglobulins)
Anaphylaxis 
 The physiologic responses to the release of anaphylaxis mediators include
smooth muscle spasm in the respiratory and gastrointestinal (GI) tracts,
vasodilation, increased vascular permeability, and stimulation of sensory
nerve endings. Increased mucous secretion and increased bronchial smooth
muscle tone, as well as airway edema, contribute to the respiratory
symptoms observed in anaphylaxis.
Anaphylaxis 
 Cardiovascular effects result from decreased vascular tone and capillary
leakage. Hypotension, cardiac arrhythmias, syncope, and shock can result
from intravascular volume loss, vasodilation, and myocardial dysfunction.
Increased vascular permeability can produce a shift of 35% of vascular
volume to the extravascular space within 10 minutes.
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 These physiologic events lead to some or all of the classic symptoms of
anaphylaxis: flushing; urticaria/angioedema; pruritus; bronchospasm;
laryngeal edema; abdominal cramping with nausea, vomiting, and diarrhea;
and feeling of impending doom. Concomitant signs and symptoms can
include rhinorrhea, dysphonia, metallic taste, uterine cramps, light-
headedness, and headache.
 Interleukin (IL)–4 and IL-13 are cytokines important in the initial
generation of antibody and inflammatory cell responses to anaphylaxis
Anaphylaxis 
 Vasodilation, hypotension, and flushing are mediated by both H 1 receptors
and H2 receptors. H1 receptors alone mediate coronary artery
vasoconstriction, tachycardia, vascular permeability, pruritus,
bronchospasm, and rhinorrhea. H2 receptors increase atrial and ventricular
contractility, atrial chronotropy, and coronary artery vasodilation. H3
receptors in experimental models of canine anaphylaxis appear to influence
cardiovascular responses to norepinephrine. The importance of H 3 receptors
in humans is unknown.
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 Clinical presentation
 Cutaneous/ocular - Flushing, urticaria, angioedema, cutaneous and/or
conjunctival pruritus, warmth, and swelling
 Respiratory - Nasal congestion, rhinorrhea, throat tightness, wheezing,
shortness of breath, cough, hoarseness
 Cardiovascular - Dizziness, weakness, syncope, chest pain, palpitations
 Gastrointestinal - Dysphagia, nausea, vomiting, diarrhea, bloating, cramps
 Neurologic - Headache, dizziness, blurred vision, and seizure (very rare and
often associated with hypotension)
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 Symptoms usually begin within 5-30 minutes from the time the culprit
antigen is injected but can occur within seconds. If the antigen is ingested,
symptoms usually occur within minutes to 2 hours. In rare cases, symptoms
can be delayed in onset for several hours.
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 D/D
o Vasodepressor (vasovagal) reaction
o Hereditary angioedema
o Pulmonary embolism
o Myocardial dysfunction
o Foreign body aspiration
o Pheochromocytoma
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 Investigations
 CBC
 CT/MRI
 IgE
 CXR
 ECHO
 LFT
 RFT
 Sr.Electrolytes
 ABG
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 Management
 Anaphylaxis is an acute medical emergency. So immediate management
includes
 Prevent further contact
 Ensuring airway patency
 O2 administration
 BP control
 Prompt administration of adrenaline