Anaphylaxis
D E FI N I T ION
Acute life-threatening multisystem syndrome caused by sudden release of
mast cell- and basophil-derived mediators into the circulation.
AE T IOLOGY
Can be classified as:
Immunologic: IgE-mediated or immune complex/complement-mediated. Non-immunologic:
mast cell or basophil degranulation without the involvement of antibodies (e.g. reactions
caused by vancomycin, codeine, ACE inhibitors).
Inflammatory mediators such as histamine, tryptase, chymase, histamine-releasing factor,
PAF, prostaglandins and leucotrienes cause bronchospasm, " capillary permeability and
# vascular tone, resulting in tissue oedema.
Common allergens include drugs (e.g. penicillin), radiological contrast agents, latex, insect
stings, egg, peanuts, shellfish and fish. Anaphylaxis may occur following repeated
administration of blood products in patients with selective IgA deficiency (as a result
of formation of anti-IgA antibodies). Anaphylaxis can also be induced by exercise.
E P IDEMIOLOGY
Relatively common. Anaphylaxis occurs in 1 in 5,000 exposures to
parenteral penicillin or cephalosporins.
1–2 % of patients receiving IV radiocontrast experience a hypersensitivity reaction (often
minor). 0.5–1 % of children suffer from peanut allergy. 1 in 700 patients have selective
IgA deficiency.
H ISTORY
Acute onset of symptoms on exposure to allergen:
. Wheeze, shortness of breath or sensation of choking.
. Swelling of lips and face.
. Pruritus, rash.
The severity of previous reactions does not predict the severity of future reactions. Patients
may have a history of other allergic hypersensitivity disorders e.g. asthma, allergic rhinitis.
Biphasic reactions occur 1–72 h after the first reaction in up to 20% of patients.
EXAMINA T I ON
Tachypnoea, wheeze, cyanosis.
Swollen upper airways and eyes, rhinitis, conjunctival injection.
Urticarial rash (erythematous wheals).
Hypotension, tachycardia.
INVE S T I G A T IONS
The diagnosis of anaphylaxis is made clinically.
Serum tryptase (measured within 15 min–3 h after onset of symptoms), or histamine levels
(measured preferably within 30 min after symptom onset) and urinary metabolites of
histamine (which may remain elevated for several hours after symptom onset) can support
the clinical diagnosis. Normal levels of these mediators do not exclude the possibility of
anaphylaxis.
After the attack:
Allergen skin testing: Identifies allergen. It should be performed by an allergy specialist,
because of the risk of anaphylaxis and the skill required for proper interpretation.
IgE immunoassays: E.g. radioallergosorbent tests (RASTs) to identify food-specific IgE in the
serum.
MANAGEMENT
Stop any suspected drugs.
Resuscitation according to principles of airway, breathing and circulation.
Secure airway and give 100 % O2. Intubation and transfer to ITU may be necessary so
anaesthetist must be informed early.
Adrenaline IM (0.5 mL of 1:1,000). This can be repeated every 10 min according to response
of pulse and BP.
Antihistamine IV (10mg chlorpheniramine).
Steroids IV (100mg hydrocortisone).
Anaphylaxis (continued)
IV crystalloid or colloid to maintain blood pressure. If hypotensive, lie patient flat with head
tilted down.
Treat bronchospasm with salbutamolipratropium inhaler. Aminophylline IV infusion may
be required.
Advice: Educate on use of adrenaline pen for IM administration. Provide Medicalert bracelet.
Make note in patient’s notes and drug charts. Referral to an allergy specialist for
identification of the culprit allergen and education in allergen avoidance.
COMPL I C A T IONS
Respiratory failure, shock, death.
P ROGNOS I S
Good if prompt treatment given.
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