ANAPHYLAXIS

Slide 1.
Good Afternoon! I am presenting Anaphylaxis as a part CNE. Anaphylaxis is a
medical emergency which can be fatal in minutes, however, prompt early
recognition and treatment will improve patient outcome. Thus it is import for all of
us to know about Anaphylaxis.
SLIDE 2. Definition
Anaphylaxis is symptom complex accompanying acute reaction to a chemical
recognized as hostile by the immune system of a previously sensitized person.
This is the Classical Type I Hypersensitivity reaction.
Slide 3.
There is a associated entity called Anaphylactoid Reaction, which is a condition
which is clinically indistinguishable from anaphylaxis but pathophysiologic
mechanism is non-immunological or not determined.

Slide 4. Epidemiology

No evidence to suggest Age, Sex, Race, geography affect the incidence of

Anaphylaxis.

Atopy: does not increase in Anaphylaxis to Penicillin/Stings, but increases

the risk of anaphylaxis from Food & Latex exposure.

Outcome is Poor in patients with Asthma: due to Poor Adrenal

response to Antigen challenge.

Those who are on -Blockers, as on -Blockers Suppress Adrenal

response.

And those who are receiving Epidural Anesthesia/Analgesia with Local

anaesthetics due to chemical Sympathectomy.

Slide 5.
Anaphylaxis occurs only in Fit & Fine individuals. It is rare in ICU patients.
Adrenal response in sick patients pretreats anaphylaxis.
Notable exception is Asthma, where patients have depressed adrenal
response to stimulus.

Slide 6. Any antigen can trigger Anaphylaxis, but these are the common Causative
Substances triggering anaphylaxis in sensitized individuals.
1.
2.
3.
4.

Hormones: Insulin, Vasopressin, Parathormone

Enzymes: Trypsin, Chymotrypsin, Penicillinase, Streptokinase
Pollen: Ragweed, Grass, Flowering trees
Animal allergens: Dust mites, dander of animals,

5. Food: peanuts, milk, eggs, seafood, nuts, grains, gelatin

Slide 7.
6.
7.
8.
9.

Monoclonal antibodies
Hymenoptera Venom: Hornets, Wasps, Honeybee, Fire-ants
Polysaccharides: Dextran, Thiomersal
Occupational Exposure: Ethylene Oxide, Latex

Slide 8. These are the drugs which are common culprits in causing Anaphylaxis.
10.

Drugs:
a. Protamine
b. Antibiotics: Penicillins, Cephalosporins, Amphotericin B, Nitrofurantoin,
Quinalones
c. Chemotherapuetics: Carboplastin, Paclitaxel, Doxorubicin,
d. Local Anaesthetics: Procaine, Lidocaine
e. Muscle Relaxant: Suxamethonium, Gallamine, Pancuronium
f. Vitamins: Thiamine, Folic Acid,
g. Diagnostic Agent: Sodium dehydrocholate,

Slide 9 Now regarding pathophysiology .

Initially, a person is sensitized to a particular Ag when IgE is formed upon
initial contact with the Type B Lymphocytes. Then, IgE attaches itself to
Mast cells. During subsequent exposure, IgE triggers massive release of
Histamine and other immune mediators.
Histamine causes initial reaction, but cleared from blood rapidly. Other
inflammatory mediators like Leukotriene also play a role.
Slide 10. Pathophysiology
Over
o
o
o
o

all, mediators produce

Vasodilation: Hypotension, pulmonary edema
smooth muscle contraction: Bronchospasm
Increased glandular secretion: Chocking
Increased cell permeability: Laryngeal edema, Urticaria,
Hypovolemia, diarrhea.

Slide 11.Clinical Manifestation

Individuals differ how they manifest in terms of time and symptoms.
Hallmark of anaphylaxis is onset of some symptom within seconds to
minutes after exposure.
Most common routes: Injections > Ingestion
Upper airway: Lump in throat, hoarseness, Stridor
Lower Airway: Chest tightness, Bronchospasm, Audible wheeze,
Slide 12.
Skin:
o Piloerection, Flushing, feeling of warmth, generalized erythema

Characteristic lesion: well circumscribed, discrete wheels with raised

serpiginous, intensely pruritic, donot last >48 hrs
Angioedema of bowel mucosa may lead to diarrhea and circulatory
collapse.
o

Slide 13. These are pictures of typical lesions in anaphylaxis.

Slide 14. Diagnosis is mainly clinical.
Any History of exposure to some Antigen within last few minutes is of
highest importance.
Mast cell Serum Tryptase levels:
o Specific for Mast Cell Activation
o Appear within 1 hr of onset of reaction, but lasts only for 4 hrs.
o Anaphylaxis to food generally not associated with Tryptase elevation
[Prausnitz-Kustner reaction: clinically obsolete.]
Slide 15. Treatment of anaphylaxis should be initiated immediately.
Immediate recognition mandatory/ rule out NSAID triggered compliment
mediated reaction.
Inj. Adrenaline
o 0.3-0.5ml of 1:1000 (1mg/ml) SC/IM repeated @5-20 min intervals.
o IV 2.5mL of 1:10000 repeated as above
o If Adrenaline fails then Vasopressin/Methylene Blue can be tried.
Oxygen:
o Mask
o Intubation: if required
Slide 16.

Slide 16. If an extremity is injected with causative antigen then

o
o

Tourniquet should be applied to prevent spread of Ag.

Inj. Adrenaline 0.2 mlshould be infiltrated in to the site.

Fluid replacement is very important, several liters of IV fluid may be

required.
o Insert large bore IV lines (two No.)
o Volume expander (NS, Colloids)
Inotropic Support:
o Usually Cardiac function not affected
o Dopamine/Vasopressin/Noradrenaline/Adrenaline infusion
Slide 17. Ancillary treatment may not help in immediate treatment but help in later
consequences like edema, itching, and symptomatic relief.
o Antihistamines
o IV Steroids: Methyl prednisolone/Hydrocortisone.
o Bronchodilators: nebulized
Slide 18. Prevention /precaution:
Avoidance, Avoidance, Avoidance of the suspected Ag is most essential
part of prevention.

 Keep in mind following when a patient tells about sensitivity to a

substance.
o sensitivity of individual,
o Character of the drug
o Route of administration
Beta blockers are relatively contra-indicated in persons prone to
anaphylaxis [Eg. Hymenoptera venom sensitivity / Immunotherapy for
respiratory sensitivity]
Slide 19.
In person with h/o anaphylaxis/ sensitivity to a agent, choose an agent
structurally different from offending agent. Eg. Penicillin & cephalosporins.
Skin Test:
o No routine skin tests for antibiotics
o Skin test indicated only in persons with clinical history consistent
with IgE mediated reaction.
o Scratch test first, not intradermal test, as risk is higher in later.
Slide 20. Desensitization treatment is considered when an agents alternative is
not available. Desensitization can be done through Oral, IV, SC routes. Graded
doses of offending agent introduced to patient, starting with dose lower than
required to trigger a systemic response. Dose is doubled every subsequent session.
Desensitization taken up only in the set up equipped to handle possible
anaphylaxis and under specialists supervision.
Slide 21. Persons with Hymenoptera( Bee, Wasps) Venom sensitivity: Can be
prevented in following way..
o
o
o
o
o
o
o
o

Modification of lifestyle: Limitation of outdoor activity.

Exclude bare feet, perfumed toiletries, eating outdoors,
Clipping hedges, grass near living areas,
Regular clearing of trash and fallen fruits.
Avoiding bee attracting plants in gardens.
Wearing an information bracelet and carrying Adrenaline kit.
Desensitization treatment.
Lastly, IgG antibodies against hymenoptera Ag are being developed.