BASICS OF ANAPHYLAXIS & ANAPHYLACTOID REACTION

1. ANAPHYLAXIS
&
ANAPHYLACTOID
REACTION DR VEENA MOHAN
JR1 ANESTHESIA

2. Hypersensitivity (also called hypersensitivity reaction or intolerance) refers to
undesirable reactions produced by the normal immune system, including allergies
and autoimmunity.
HYPERSENSITIVITY
Type I: reaction mediated by IgE antibodies.
Type II: cytotoxic reaction mediated by IgG or IgM antibodies
Type III: reaction mediated by immune complexes.
Type IV: delayed reaction mediated by cellular response.

3. immunoglobulin E (IgE) antibody against soluble antigen, triggering mast cell
degranulation.
TYPE I

4. TYPE II: IgG and IgM antibodies directed against
cellular antigens, leading to cell damage mediated by other
immune system effectors.

5. TYPE III
interactions of IgG, IgM, and, occasionally, IgA1 antibodies with antigen to form
immune complexes. Accumulation of immune complexes in tissue leads to tissue
damage mediated by other immune system effectors.

6. TYPES IV
T-cell–mediated reactions that can involve tissue damage mediated by activated
macrophages and cytotoxic T cells.

7. ANAPHYLAXIS
Sever immediate (type I) hypersensitivity reaction.
Acute multi-systemic allergic reaction involving the skin, airway, vascular
system, and GI on exposure to some allergens
Hormones
• Insulin
•Vasopressin
• Parathormone
Enzymes
• Trypsin
• Chymotrypsin
• Penicillinase
Pollens
• Ragweed
• Grass
• Seeds
Foods
• Egg
• Seafoods
• peaNuts
• Grains
• Beans
• Cottonseed oil
• Chocolate
Insect venom
• Paper wasp
• Honey bee
Occupational agents •
Rubber products
• Industrial chemicals
Drugs
• Penicillin
• NSAIDS
• Opioids
• ACEI

8. PATHOPHYSIOLOGY
a first exposure to an allergen activates a strong TH2 cell response.
It activate B cells specific to the same allergen,
differentiation into plasma cells,
antibody-class switch to production of IgE
(Fc) regions of the IgE antibodies bind to specific receptors on the surface of mast
cells throughout the body.
mast cells are primed for a subsequent exposure and the individual is sensitized to the
allergen.

10. On subsequent exposure, IgE activates the mast cells and triggers degranulation
Preformed components that are released from granules include
histamine,
serotonin
(Increases vascular permeability vasodilation &smooth-muscle
contraction)
Bradykinin
Leukotrienes
prostaglandins
cytokines ( tumor necrosis factor.)(Causes inflammation and stimulates cytokine
production by other cell types

11. CLINICAL PRESENTATIONS
TYPICAL PRESENTATION
Urticaria and Angioedema
Respiratory distress
Cardiovascular collapse with Hypotension
Vomiting
Headache or Dizziness

12. General
Pruritus
Metallic Taste in mouth
Naso-ocular
Itchy nose or eyes
Sneezing
Clear, watery Eye Discharge or Nasal discharge
Skin
Urticaria: Hives
Angioedema: Facial swelling and Lip swelling Sign
MILD CASES

13. MODERATE CASES
Neurologic
- Dizziness
- Weakness
Gastrointestinal
- Nausea, Vomiting
- Bloody Diarrhea
- Abdominal Pain
- Fecal urgency or Incontinence
Genitourinary
- Uterine cramps
- Urinary urgency or Incontinence Signs
SEVERE cases
Airway Compromise
 Hoarseness or Dysphonia
 Stridor
 Inability to manage own secretions
bronchospasm
 Dyspnea
 Tachypnea
 Hypoxia
Circulatory compromise
• Hypotension
• Tachycardia
• Hypoperfusion
• Syncope

15. Anaphylactoid reactions occur through a direct nonimmune- mediated release of
mediators from mast cells and/or basophils or result from direct complement
activation, but theypresent with clinical symptoms similar to those of anaphylaxis
ANAPHYLACTOID REACTION

16. • History
• Physical examination
• An increase in human α and β tryptase, the predominant mast
cell proteases,
• Allergy skin test
• • Radioallergosorbent test (RAST)
EVALUATION

17. PERIOPERATIVE ANAPHYLAXIS
Anaphylaxis is rare
Anaphylactoid reactions are more common
RISK FACTORS
• female gender,
• atopic history,
• preexisting allergies,
• previous anesthetic exposures

18. PERIOPERATIVE ANAPHYLAXIS
1.LOCAL ANESTHETICS:
IgE-mediated allergic reactions are usually due tothe paraaminobenzoic acid metabolite from
esters(PROCAINE, CHLORPROCAINE, BENZOCAINE) or methylparaben (a preservative).
2.MUSCLE RELAXANTS:
Succinylcholine contains a flexible molecule that can cross-link twomast cell IgE receptors induce
mast cell degranulation.
D-tubocurarine,doxacurium, atracurium, and mivacurium, are more likely to cause direct mast cell
degranulation
3.OPIOIDS
Rare
Morphine & MEPERIDINE cause non immunological histamine release
Rarely with INDUCTION AGENTS

19. TREATMENT
1. Immediate discontinuation of the anesthetic drugs and early administration of
epinephrine are the cornerstones of treatment.
2. Ensure large bore iv access
Airway support with 100% oxygen will increase oxygen delivery
IV crystalloid (2–4 l),,peds(20ml/kg)
Epinephrine is the drug of choice
α1 effects help to support the bloodpressure
β2 effects provide bronchial smooth-muscle relaxation.
5- to 10-μg IV bolus (0.2 μg/kg) doses for hypotension
0.1- to 0.5-mg IV doses in the presence of cardiovascular collapse.
In Pruritus and urticaria : 0.3 to 0.5 mL of 1:1000 (1.0mg/mL) epinephrine SC or IM

20. Histamine blockers
Diphenhydramine 0.5–1 mg/kg
Ranitidine 150 mg ,
Bronchodilators (e.g., ipratropium bromide nebulizers),
corticosteroids (e.g., hydrocortisone 1–5 mg/kg) decrease the airway swelling
Extubation should be delayed, because airway swelling and inflammation
may continue for 24 h.