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ANAPHYLAXIS
• Anaphylaxis is a serious type-
1 hypersensitivity allergic
reaction that is rapid in onset
and may cause death.
• On the first exposure to
antigen, memory B-cells are
produced which, on the
second exposure produce
immune response.
• The term comes from the
Ancient Greek: ‘Ana’ means
against, and the ‘Phylaxis’
means protection.
SIGNS AND SYMPTOMS:
CAUSES:
FOOD : Common triggering foods vary around the world.
-Western cultures: ingestion of or exposure to peanuts, wheat,
nuts, seafood like shellfish, milk, and eggs.
-Middle East: Sesame
-Asia: rice and chickpeas.
MEDICATION :
-most common are β-lactam antibiotics (such as penicillin) followed
by aspirin and NSAIDs. [Anaphylaxis to penicillin or cephalosporins
occurs only after it binds to proteins inside the body with some
agents binding more easily than others.]
-chemotherapy, vaccines, protamine and herbal preparations.
- Some medications (vancomycin, morphine, x-ray contrast among
VENOM :
-from stinging or biting insects such as
Hymenoptera (ants, bees, and wasps) or
Triatominae (kissing bugs) cause anaphylaxis in
susceptible people.
-Previous reactions, that are anything more
than a local reaction around the site of the
sting, are a risk factor for future anaphylaxis.
OTHER FACTORS : People with atopic diseases
such as asthma, eczema, or allergic rhinitis are
at high risk of anaphylaxis from food, latex.
-physical factors, biological agents such as
semen, latex, hormonal changes, food additives
such as monosodium glutamate and food
colors, and topical medications.
-exercise-induced anaphylaxis.
-idiopathic anaphylaxis.
PATHOPHYSIOLOGY:
• IMMUNOLOGIC MECHANISM:
-IgE binds to the antigen.
-Antigen-bound IgE then activates
FcεRI receptors on mast cells and
basophils.
-Release of inflammatory mediators
such as histamine.
-Increase the contraction of bronchial
smooth muscles, trigger vasodilation,
increase the leakage of fluid from
blood vessels, and cause heart muscle
depression.
- There is also an immunologic
mechanism that does not rely on IgE,
• NON-IMMUNOLOGIC
MECHANISM:
-Involve substances that
directly cause the
degranulation of mast cells and
basophils.
-Agents such as contrast
medium, opioids, temperature
(hot or cold), and vibration.
-Sulfites may cause reactions
by both immunologic and non-
immunologic mechanisms.
DIAGNOSIS:
• Anaphylaxis is diagnosed on the basis of a person's signs and
symptoms.
• any two of the following occurs within minutes or hours of
exposure to an allergen there is a high likelihood of
anaphylaxis:
a. Involvement of the skin or mucosa
b. Respiratory difficulties
c. Low blood pressure
d. Gastrointestinal symptoms
• Allergy testing:
• Help in determining the trigger.
Skin allergy testing is available for
certain foods and venoms.
• Blood testing for specific IgE can
be useful to confirm milk, egg,
peanut, tree nut and fish allergies.
• Skin testing is available to confirm
penicillin allergies, but is not for
other medications.
• Non-immune forms of anaphylaxis
can only be determined by history
or exposure to the allergen in
question.
• Post-mortem findings:
• In a person who died from anaphylaxis, autopsy may show an
"empty heart" attributed to reduced venous return from
vasodilation and redistribution of intravascular volume from the
central to the peripheral compartment.
• Other signs are laryngeal edema, eosinophilia in lungs, heart
and tissues, and evidence of myocardial hypoperfusion.
• Laboratory findings could detect increased levels of serum
tryptase, increase in total and specific IgE serum levels.
MANAGEMENT:
• EPINEPHRINE:
• Drug of choice with almost no
contraindications.
• Given intramuscularly into the mid
anterolateral thigh as soon as the diagnosis is
suspected. The injection may be repeated
every 5 to 15 minutes and second dose given
if required.
• Subcutaneous administration has delayed
absorption.
• Intravenously given using a dilute
epinephrine solution.
• ADJUNCTS:
• Antihistamines-have poor effect, given along with epinephrine.
• Corticosteroids-poor effect but given to decrease risk of
biphasic anaphylaxis.
• Nebulized salbutamol effective for bronchospasm that does
not resolve with epinephrine.
• Methylene blue used in those not responsive to other measures
due to its presumed effect of relaxing smooth muscle.
RESEARCH:
• There are ongoing efforts to develop sublingual epinephrine to
treat anaphylaxis.
• Subcutaneous injection of the anti-IgE antibody omalizumab is
being studied as a method of preventing recurrence, but it is
not yet recommended.
THANK YOU
• -AKSHMALA SHARMA
•

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Anaphylaxis

  • 2. • Anaphylaxis is a serious type- 1 hypersensitivity allergic reaction that is rapid in onset and may cause death. • On the first exposure to antigen, memory B-cells are produced which, on the second exposure produce immune response. • The term comes from the Ancient Greek: ‘Ana’ means against, and the ‘Phylaxis’ means protection.
  • 4.
  • 5. CAUSES: FOOD : Common triggering foods vary around the world. -Western cultures: ingestion of or exposure to peanuts, wheat, nuts, seafood like shellfish, milk, and eggs. -Middle East: Sesame -Asia: rice and chickpeas. MEDICATION : -most common are β-lactam antibiotics (such as penicillin) followed by aspirin and NSAIDs. [Anaphylaxis to penicillin or cephalosporins occurs only after it binds to proteins inside the body with some agents binding more easily than others.] -chemotherapy, vaccines, protamine and herbal preparations. - Some medications (vancomycin, morphine, x-ray contrast among
  • 6. VENOM : -from stinging or biting insects such as Hymenoptera (ants, bees, and wasps) or Triatominae (kissing bugs) cause anaphylaxis in susceptible people. -Previous reactions, that are anything more than a local reaction around the site of the sting, are a risk factor for future anaphylaxis. OTHER FACTORS : People with atopic diseases such as asthma, eczema, or allergic rhinitis are at high risk of anaphylaxis from food, latex. -physical factors, biological agents such as semen, latex, hormonal changes, food additives such as monosodium glutamate and food colors, and topical medications. -exercise-induced anaphylaxis. -idiopathic anaphylaxis.
  • 7. PATHOPHYSIOLOGY: • IMMUNOLOGIC MECHANISM: -IgE binds to the antigen. -Antigen-bound IgE then activates FcεRI receptors on mast cells and basophils. -Release of inflammatory mediators such as histamine. -Increase the contraction of bronchial smooth muscles, trigger vasodilation, increase the leakage of fluid from blood vessels, and cause heart muscle depression. - There is also an immunologic mechanism that does not rely on IgE,
  • 8.
  • 9. • NON-IMMUNOLOGIC MECHANISM: -Involve substances that directly cause the degranulation of mast cells and basophils. -Agents such as contrast medium, opioids, temperature (hot or cold), and vibration. -Sulfites may cause reactions by both immunologic and non- immunologic mechanisms.
  • 10. DIAGNOSIS: • Anaphylaxis is diagnosed on the basis of a person's signs and symptoms. • any two of the following occurs within minutes or hours of exposure to an allergen there is a high likelihood of anaphylaxis: a. Involvement of the skin or mucosa b. Respiratory difficulties c. Low blood pressure d. Gastrointestinal symptoms
  • 11. • Allergy testing: • Help in determining the trigger. Skin allergy testing is available for certain foods and venoms. • Blood testing for specific IgE can be useful to confirm milk, egg, peanut, tree nut and fish allergies. • Skin testing is available to confirm penicillin allergies, but is not for other medications. • Non-immune forms of anaphylaxis can only be determined by history or exposure to the allergen in question.
  • 12. • Post-mortem findings: • In a person who died from anaphylaxis, autopsy may show an "empty heart" attributed to reduced venous return from vasodilation and redistribution of intravascular volume from the central to the peripheral compartment. • Other signs are laryngeal edema, eosinophilia in lungs, heart and tissues, and evidence of myocardial hypoperfusion. • Laboratory findings could detect increased levels of serum tryptase, increase in total and specific IgE serum levels.
  • 13. MANAGEMENT: • EPINEPHRINE: • Drug of choice with almost no contraindications. • Given intramuscularly into the mid anterolateral thigh as soon as the diagnosis is suspected. The injection may be repeated every 5 to 15 minutes and second dose given if required. • Subcutaneous administration has delayed absorption. • Intravenously given using a dilute epinephrine solution.
  • 14. • ADJUNCTS: • Antihistamines-have poor effect, given along with epinephrine. • Corticosteroids-poor effect but given to decrease risk of biphasic anaphylaxis. • Nebulized salbutamol effective for bronchospasm that does not resolve with epinephrine. • Methylene blue used in those not responsive to other measures due to its presumed effect of relaxing smooth muscle.
  • 15. RESEARCH: • There are ongoing efforts to develop sublingual epinephrine to treat anaphylaxis. • Subcutaneous injection of the anti-IgE antibody omalizumab is being studied as a method of preventing recurrence, but it is not yet recommended.