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Describe anaphylaxis with its causes, mechanism and management.

Pathology · 2nd Professional — Para-Clinical

Definition

Anaphylaxis is a severe, rapidly developing, generalised type I hypersensitivity reaction that is potentially fatal.

Anaphylactoid reactions are clinically identical but not IgE-mediated — caused by direct mast cell degranulation (radiocontrast, opioids, vancomycin) and may occur on first exposure

Common Causes

Group	Examples
Drugs	Penicillin and other beta-lactams, aspirin and NSAIDs, radiocontrast media, anaesthetic agents
Foods	Peanut, tree nuts, shellfish, egg, milk
Venoms	Bee and wasp stings
Biological products	Antivenom, antisera, vaccines, blood products (in IgA deficiency)
Latex	Gloves; important in health workers and in spina bifida

Mechanism and Clinical Features

Antigen cross-links IgE on sensitised mast cells and basophils → Explosive degranulation throughout the body → histamine, tryptase, leukotrienes, prostaglandins, PAF → Widespread vasodilatation → profound hypotension → Increased permeability → angio-oedema, laryngeal oedema, loss of circulating volume → bronchospasm → wheeze and respiratory failure → Death from airway obstruction or circulatory collapse, sometimes within minutes

System	Features
Skin (80–90%)	Urticaria, flushing, itch, angio-oedema of lips and eyelids
Respiratory	Stridor from laryngeal oedema; wheeze; hoarseness — the commonest cause of death
Cardiovascular	Hypotension, tachycardia, collapse
Gastrointestinal	Cramping pain, vomiting, diarrhoea
Other	A sense of impending doom; incontinence

CLINICAL PEARL

Skin signs are absent in up to 20%, and their absence has cost lives. Anaphylaxis presenting as sudden hypotension or bronchospasm without a rash is easily mistaken for shock or asthma of another cause. If the onset is sudden and follows an exposure, treat as anaphylaxis: adrenaline given unnecessarily is far safer than adrenaline withheld.

Management

Adrenaline 0.5 mg (0.5 mL of 1:1000) intramuscularly into the anterolateral thigh, repeated every 5 minutes as needed — the only treatment that saves life
It reverses every mechanism: alpha-1 causes vasoconstriction, beta-1 supports the heart, beta-2 relieves bronchospasm and stabilises mast cells
Remove the trigger; lie the patient flat with legs raised (never sit them up, which can cause fatal empty-ventricle syndrome)
High-flow oxygen and rapid intravenous fluids
Antihistamines and corticosteroids are second-line, and do nothing for the acute crisis; steroids may reduce the late phase
Observe for 6–12 hours — a biphasic reaction occurs in up to 20%

Applied Aspects

Serum tryptase taken within a few hours confirms mast cell degranulation retrospectively
Every patient must be referred for allergy testing and given an adrenaline auto-injector with training in its use
Beta-blockers make anaphylaxis resistant to adrenaline; glucagon is used in that situation
Always ask about drug allergy before prescribing, and record it prominently — penicillin anaphylaxis remains a preventable cause of death
Anaphylaxis after antivenom or antisera is a real risk in Indian practice, and adrenaline must be drawn up before the infusion is started

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