Anaphylaxis is a potentially life-threatening hypersensitivity reaction that requires immediate treatment to prevent shock or death. It is most often triggered by allergens that cause mast cell degranulation and the release of histamine and other mediators. Local anesthetics can occasionally cause anaphylactic reactions. Management involves epinephrine injection, antihistamines, corticosteroids, oxygen, IV fluids and monitoring for biphasic reactions. Sensitivity testing can help identify causative agents to prevent future episodes. Proper anaphylaxis management training is crucial for dental professionals.

1. MANAGEMENT OF ANAPHYLAXIS
FOLLOWING LOCAL ANAESTHESIA
AASTHA MOZA
1st YR PG

2. OVERVIEW
• Hypersensitivity
• Definition of Anaphylaxis
• History of anaphylaxis
• Criteria of anaphylaxis
• Mechanism
• Anaphylaxis following local anaesthesia
• Clinical manifestations
• Management
• Anaphylactic shock
• Prevention (Sensitivity tests)
• Anaphylactic reaction VS anaphylactoid reaction
• Differential Diagnosis

3. WHAT IS HYPERSENSITIVITY ?
• Immune responses that normally are protective, also are capable of causing tissue injury.
• Originated from the idea that persons who mount immune responses against an antigen
are sensitized to that antigen, so pathologic or excessive reactions represent
manifestations of a hypersensitive state.
• Hypersensitivity reactions can be subdivided into four types based on the principal
immune mechanism responsible for injury.

4. Anaphylactic
(immediate,
homocytotropic ,
antigen induced ,
antibody mediated)

5. Anaphylaxis is an exaggerated potentially life-threatening hypersensitivity
reaction to a previously encountered antigen. Response is mediated by antibodies
of the IgE class of Immunoglobulins, cause release of histamine and other
chemical mediators.
Characterised by a number of signs and symptoms, alone or in combination,
which occur within minutes to a few hours, after exposure to a provoking agent.

6. HISTORY OF ANAPHYLAXIS
The term anaphylaxis was coined by Charles Richet and Paul
Portier when they tried to immunize dogs with actinia extracts, but
after a repeated injection of a small amount of the toxin the dog died
within 25 min.
Richet described toxic effects of these extracts very precisely in
several dog experiments and concluded that there were two different
toxins, ‘thalassine', which induced violent pruritus and urticaria but
was not fatal, ‘congestine', which led to an intestinal and
cardiovascular congestion with finally lethal outcome.
In trying to find a name he wanted to express ‘lack of protection' and
should have used the word ‘aphylaxis’.
.

7. Causes of Anaphylaxis
IgE-Mediated
Reactions
Cytotoxic and Immune
Complex –
Whole Blood, Serum,
Plasma, Fractionated
Serum Products
Non-immunologic Mast
Cell Activators
Idiopathic Anaphylaxis
• Local anaesthetics
• Latex
Anaphylatoxins C3a,
C4a and C5a cause
mast cell and basophil
degranulation
Cold temperature,
Increased physical
activity
Signs and symptoms of
anaphylaxis can occur
without a recognizable
cause.

8. CRITERIA OF ANAPHYLAXIS

9. Shaker MS, Wallace DV, Golden DB, Oppenheimer J, Bernstein JA, Campbell RC, Dinakar C, Ellis A, Greenhawt M, Khan DA, Lang DM. Anaphylaxis–a 2020 Practice Parameter Update,
Systematic Review and GRADE Analysis. Journal of Allergy and Clinical Immunology. 2020 Jan 28.

10. MECHANISM
Type 1 reaction is mediated by
humoral antibodies of IgE type in
response to antigen.
Genetic basis: 50% chance that a
child born to both parents allergic to
an antigen predispose to it.
Environmental pollutants: Proposed
hypotheses states that increased
mucosal permeability allows greater
entry of allergen which in turn leads
to raised IgE levels.

11. First contact of host with antigen, sensitization takes place.
B lymphocytes get activated and differentiate to form IgE secreting plasma cells.
IgE antibodies bind to Fc receptors present in plenty on surface of mast cells of type 1
reaction. ( cells are fully sensitized for next event)
Second contact with same antigen IgE antibodies on surface of mast cells / basophils are so
firmly bound to Fc receptors that it causes membrane lysis , influx of sodium and water ,
degranulation of mast cell – basophil (complex).
Proinflammatory chemical mediators
• Histamine
• Platelet activating factor
• Chemotactic factors of anaphylaxis for neutrophils and eosinophils are released.
• Increased vascular permeability
• smooth muscle contraction
• increased gastric secretion
• immediate vasoconstriction followed by prolonged vasodilatation

12. ANAPHYLAXIS FOLLOWING LOCAL
ANAESTHESIA

13. Immediate response- 5 to 30 mins after exposure to an allergen and subsiding in 60 mins.
(stimulated by mast cells and lipid mediators)
• Vasodilatation
• Smooth muscle spasm
Late response-
(Stimulated by cytokines 2-8 hours later)
Histamine release is chiefly responsible for redness, urticaria, angioedema.
Itching on the episode of anaphylaxis is due to the interaction with H1 and H2 receptors
near C fibres.
Biphasic and fatal anaphylaxis
ANAPHYLAXIS FOLLOWING LOCAL
ANAESTHESIA

14. • Ester and Amide(Incidence of <1%) local anaesthetics both are responsible for causing
a anaphylactic reaction though rare.
• Historically most allergic reactions were ascribed to procaine.
• Antigenicity of procaine and other ester compounds is associated with PABA.
• Methylparaben used as a preservative(antioxidant) having a bacteriostatic , fungistatic
action helps to prevent contamination but its phenol like action acts by denaturation of
proteins and antimetabolite property of p- hydroxy benzoic acid.
Anaphylaxis following local anaesthesia

15. MANAGEMENT
J ALLERGY CLIN IMMUNOL VOLUME 110,
NUMBER 3
Immediate intervention
• Assessment of CAB
• Administer aqueous epinephrine 1:1000 dilution, 0.3-0.5 mL (0.01 mg/kg in children;
maximum dose, 0.3 mg), intramuscularly/SC into the arm (deltoid) every 5 minutes, as
necessary, to control symptoms and blood pressure. The arm permits easy access for the
earliest administration of epinephrine. However, intramuscular injection into the
anterolateral thigh (vastus medialis) produces higher and more rapid peak plasma levels.
• Alternatively, an epinephrine autoinjector ( EpiPen [0.3 mg] or EpiPen Jr [0.15 mg]) may
be administered through clothing into the anterolateral thigh. Repeat every 5 minutes as
necessary (avoid toxicity).

16. General measures
• Place subject in recumbent position and elevate lower extremities.
• Establish and maintain airway.
• Administer oxygen at 10-15 L/min.
• Administer normal saline intravenously for fluid replacement and venous access.
• A venous tourniquet above the reaction site might decrease absorption of an injected allergen
( local anaesthetic)
MANAGEMENT

17. Specific measures
• Aqueous epinephrine 1:1,000, one half dose (0.1-0.2 mg), at the reaction site after
injection might delay allergen absorption.
• Diphenhydramine, 50 mg or more in divided doses orally or intravenously, with
maximum daily dose of 300 mg (5 mg/kg) for children and 400 mg for adults.
• For bronchospasm resistant to epinephrine, administer nebulized albuterol, 2.5-5 mg in 3
mL. Levalbuterol is a consideration for albuterol-intolerant subjects.
• Systemic glucocorticosteroids, such as methylprednisolone 1-2 mg/kg per 24 hours, are
usually not helpful acutely but might prevent prolonged reactions or relapses

18. SKIN MANIFESTATIONS
ORAL Antihistamines Benadryl 25-
50mg / IM Diphenhydramine 25-
50mg
RESPIRATORY MANIFESTATIONS
Epinephrine IM/SC 0.3mg , Oxygen
therapy, Maintain Airway, IM
Diphenhydramine 25-50mg ,
Aminophylline 250-500mg IV
SHOCK
Epinephrine IM/SC 0.3mg ,
BLS/CPR as indicated, EMS
activation
Speca SJ, Boynes
SG, Cuddy MA.
Allergic reactions
to local anesthetic
formulations.
Dental Clinics.
2010 Oct
1;54(4):655-64.

19. RATIONALE TO USE EPINEPHRINE:
• Vasoconstrictor to antagonize the vasodilatation produced by chemical mediators of
anaphylaxis.
• Stimulation of alpha and beta receptors (CVS)
• Bronchodilatation by beta-2 receptors

20. ANTI HISTAMINICS : competitive antagonists are H1 receptors , penetrate BBB ,
highly sedating(Diphenhydramine).
LEUKOTRIENES: Synthesized from AA using 5 Lipoxygenase(FLAP)
LTC4 , LTD4 are slow reacting substance of anaphylaxis (SRS-A) due to powerful
Bronchoconstriction action.
RATIONALE TO USE ANTI HISTAMINICS:

21. RATIONALE TO USE CORTICOSTEROIDS:
Hematopoietic system Inflammatory system Immune system
Glucocorticoids
Sequestration of
lymphocytes, basophils
in circulation.
Glucocorticoids(Anti-
inflammatory agent )
Inhibition of chemotaxis
Increased production of
annexins (lipocortins )
Inhibition of
phospholipase A2
(involved in production
of leukotrienes and
prostaglandins )
• Inhibition of
chemotaxis
• Catabolism of
immunoglobulin G

22. ANAPHYLACTIC SHOCK
A severe mostly fatal systemic hypersensitivity reaction to an allergen. The condition may
occur within seconds from time of exposure to sensitizing factor and is marked by
respiratory distress and vascular collapse.
Ranging from mild bronchospasm to full blown anaphylactic shock with generalized
oedema including bronchospasm and hypotension ultimately causing cardiac arrest.
Treatment:
Primary management:
• Adrenaline 0.5-1 mg or 50-100 microgram intravenously to maintain blood pressure.
• Crystalloid solutions (normal saline, Ringer’s lactate)
• Leg end elevation
Secondary:
• Chlorpheniramine maleate
• Hydrocortisone 100mg intravenously

23. Nanavati RS, Kumar M, Modi TG,
Kale H. Anaphylactic shock
management in dental clinics: an
overview. Journal of the
International Clinical Dental
Research Organization. 2013 Jan
1;5(1):36

24. LOCAL ANAESTHETIC SENSITIVITY TESTS
AND HYPERSENSITIVITY
• SKIN PRICK TEST
• DERMAL TEST
• PATCH TEST
Thyssen JP, Menné T, Elberling J, Plaschke P, Johansen JD. Hypersensitivity to local anaesthetics–
update and proposal of evaluation algorithm. Contact Dermatitis. 2008 Aug;59(2):69-78

25. ANAPHYLACTIC REACTION VS
ANAPHYLACTOID REACTION
IMMUNE MEDIATED REACTION NON IMMUNE MEDIATED
REACTION
IgE ANTIBODY PLAYS A MAJOR
ROLE
NO ROLE OF IgE ANTIBODY
ALLERGEN ( ANTIGEN) REACTS
WITH IgE ANTIBODY AND FORMS
A COMPLEX RESPONSIBLE FOR
MAST CELL DEGRANULATION AND
SUBSEQUENT RELEASE OF
HISTAMINE.
ALLERGEN CAUSES DIRECT RELEASE
OF HISTAMINE WITHOUT
DEGRANULATION.

26. DIFFERENTIAL DIAGNOSIS
• Systemic Mastocytosis
• Angiodema
• Medullary thyroid Carcinoma
• Malignant carcinoid syndrome

27. REFERENCES
• Stanley Malamed 11th edition
• Scully’s medical problems in dentistry 7th edition
• Kubo M. Mast cells and basophils in allergic inflammation. Current opinion in immunology.
• Ring J, Beyer K, Biedermann T, Bircher A, Duda D, Fischer J, Friedrichs F, Fuchs T, Gieler U, Jakob T, Klimek
L. Guideline for acute therapy and management of anaphylaxis. Allergo journal international. 2014 May
1;23(3):96-112.
• Simons FE, Ardusso LR, Bilò MB, El-Gamal YM, Ledford DK, Ring J, Sanchez-Borges M, Senna GE, Sheikh A,
Thong BY. World Allergy Organization anaphylaxis guidelines: summary. Journal of Allergy and Clinical
Immunology. 2011 Mar 1;127(3):587-93.