Anaphylaxis — Emergency Symptoms, Causes & First Aid Guide — Symptoms, Causes & Treatment | MyMedicPlus

Anaphylaxis is a severe, potentially life-threatening systemic hypersensitivity reaction characterised by the rapid onset of airway, breathing, and/or circulatory compromise, usually with skin and mucosal involvement. It occurs when a previously sensitised immune system is re-exposed to a trigger allergen (or, in non-IgE-mediated forms, through direct mast cell activation), causing sudden massive mast cell and basophil degranulation — releasing histamine, leukotrienes, prostaglandins, platelet-activating factor, and cytokines. These mediators cause systemic vasodilatation (profound fall in blood pressure), bronchospasm, increased vascular permeability (oedema of soft tissues including the larynx and tongue), and increased mucus secretion. Without immediate treatment with intramuscular adrenaline (epinephrine), anaphylaxis can progress to fatal airway obstruction, circulatory collapse, or both within minutes. The incidence of anaphylaxis is 50-112 episodes per 100,000 person-years, with a lifetime prevalence of 0.5-2% globally and rising trends in food-triggered anaphylaxis, particularly in children. Despite the severity, anaphylaxis death is uncommon — approximately 1-3 per million population annually — but entirely preventable with timely adrenaline administration. Misidentification, delayed diagnosis, and delayed adrenaline are the key modifiable causes of preventable anaphylaxis deaths.

The most common triggers are foods (peanuts, tree nuts, shellfish, fish, cow's milk, hen's eggs, wheat, and sesame — accounting for 33-56% of anaphylaxis cases; peanut and tree nut are most likely to be severe and fatal), insect venom (bee, wasp, and hornet stings — the commonest cause of anaphylaxis in adults in the UK), medications (beta-lactam antibiotics including penicillin — the leading drug cause; NSAIDs, radiocontrast agents, chemotherapy agents, biological therapies including monoclonal antibodies, and neuromuscular blocking agents used during anaesthesia — a common cause of peri-operative anaphylaxis), and latex (particularly occupational risk in healthcare workers and rubber industry workers). Exercise-induced anaphylaxis can occur alone or as a cofactor with food (food-dependent exercise-induced anaphylaxis — FDEIA). Non-IgE-mediated mechanisms (direct mast cell activation or complement activation) cause anaphylactoid reactions: radiocontrast media, opioids, vancomycin (red man syndrome), and some chemotherapy agents. Risk factors for severe or fatal anaphylaxis: previous severe anaphylaxis; asthma (the strongest risk factor for fatal anaphylaxis — increases risk 8-fold); cardiovascular disease; mastocytosis (elevated mast cell burden amplifies severity); beta-blocker and ACE inhibitor use (impairs cardiovascular compensation and adrenaline response); delayed adrenaline administration; and delayed hospital attendance.

Anaphylaxis typically develops within minutes (usually 5-30 minutes) of allergen exposure, though reactions to food may be delayed by 30-60 minutes or more. The clinical presentation involves at least two body systems (skin/mucosa, respiratory, cardiovascular, or gastrointestinal). Skin and mucosal symptoms (present in 80-90% but absent in some cardiovascular presentations): urticaria (generalised hives — raised, erythematous, itchy welts), angioedema (swelling of lips, tongue, throat, eyelids, and extremities — particularly dangerous when involving the larynx causing stridor and airway obstruction), flushing, and generalised pruritus. Respiratory symptoms: bronchospasm (wheeze, cough, chest tightness — particularly prominent in asthmatic patients), upper airway stridor from laryngeal oedema, hoarseness, and progressive respiratory failure. Cardiovascular symptoms: hypotension (systolic below 90 mmHg), tachycardia, pallor, loss of consciousness — anaphylactic shock; cardiovascular collapse may dominate in drug-induced anaphylaxis with absent skin signs (up to 20% of peri-operative anaphylaxis). Gastrointestinal symptoms: nausea, vomiting, crampy abdominal pain, and diarrhoea — common in food-triggered anaphylaxis. Neurological: dizziness, confusion, severe anxiety, and a 'sense of impending doom' — a distinctive symptom reported by many anaphylaxis patients. Recognition of anaphylaxis without skin involvement (in cardiovascular or respiratory collapse alone) requires high clinical suspicion in any patient who has received an allergen-containing substance.

Anaphylaxis is a clinical diagnosis made at the bedside based on the rapid onset of characteristic multi-system symptoms following allergen exposure — diagnostic criteria are met when any of three validated clinical criteria sets are fulfilled (WAO, NIAID/FAAN, or NICE). During the acute event: no specific test is required before giving adrenaline — treatment must not be delayed for investigations. Serum mast cell tryptase: drawn at 1-3 hours after reaction onset (peak tryptase is most useful 60-90 minutes after symptom onset) — elevated above the individual's baseline (normal reference is below 11.4 mcg/L in most labs) supports the diagnosis of anaphylaxis, particularly in cases without prominent skin symptoms; baseline (non-acute) tryptase measured more than 24 hours after the reaction is used for comparison; persistently elevated baseline tryptase (above 11.4 mcg/L) raises suspicion of mastocytosis. Post-event allergy investigation — performed at least 4-6 weeks after the acute reaction: skin prick testing (SPT) and intradermal testing with the suspected allergen, and specific serum IgE (ImmunoCAP) — to confirm the triggering allergen and guide avoidance and immunotherapy. These investigations must never be performed during the acute reaction. 24-hour urine or serum histamine may be used in research but is rarely useful clinically due to rapid metabolism. Bone marrow biopsy and serum tryptase are indicated when systemic mastocytosis is suspected.

Intramuscular adrenaline (epinephrine) is the life-saving first-line treatment and must be administered immediately — delay is the primary cause of preventable anaphylaxis death. Dose: 500 mcg (0.5 mg) IM in adults (0.3 mg for children 6-12 years; 0.15 mg for children under 6) into the anterolateral outer thigh — which has the fastest and most reliable absorption; IV adrenaline is reserved for cardiac arrest under monitoring. Adrenaline reverses vasodilatation (restoring blood pressure), bronchodilates airways, stabilises mast cell membranes (stopping further mediator release), and reduces angioedema. Call emergency services (999/112/911) immediately. The patient should be positioned flat with legs elevated (Trendelenburg position) — unless airway compromise requires sitting up; do not allow sudden standing. Second IM adrenaline dose: administer after 5-15 minutes if no improvement or if symptoms recur. Supportive measures — given after adrenaline and never instead of it: IV fluid resuscitation (crystalloid bolus 500-1000 mL for hypotension); supplemental oxygen; inhaled salbutamol for bronchospasm; H1 antihistamines (chlorphenamine) and H2 antihistamines (ranitidine) reduce urticaria but do not treat anaphylaxis and must not delay adrenaline; IV or oral corticosteroids (hydrocortisone 200 mg IV or prednisolone 50 mg orally) may reduce late-phase reactions but evidence for preventing biphasic anaphylaxis is limited. All anaphylaxis patients require hospital observation for 4-12 hours post-adrenaline (minimum 4 hours from last adrenaline dose) to monitor for biphasic anaphylaxis. Upon discharge: prescription of two adrenaline auto-injectors (EpiPen 300 mcg — adult; EpiPen Jr 150 mcg — paediatric), written emergency action plan, patient and carer training on recognition and device use, and urgent specialist allergy referral within 4 weeks.

Untreated anaphylaxis rapidly progresses to fatal respiratory and cardiovascular failure. Fatal laryngeal oedema — progressive swelling of the tongue, oropharynx, and larynx causing complete airway obstruction and asphyxiation — is the cause of most anaphylaxis deaths from food allergens (particularly peanut and tree nut). Cardiovascular collapse (anaphylactic shock) from systemic vasodilation and capillary leak causes refractory hypotension, cardiac arrhythmias, and cardiac arrest — the predominant mechanism in fatal drug-induced anaphylaxis and insect venom anaphylaxis. Hypoxic brain injury from prolonged circulatory compromise — even after successful resuscitation from cardiac arrest — can cause permanent neurological disability. Biphasic anaphylaxis — recurrence of severe symptoms 1-72 hours after apparent full recovery, without re-allergen exposure — occurs in 5-20% of cases and can be as severe or more severe than the initial reaction, requiring the mandatory hospital observation period even after apparent full symptom resolution. Severe asthma patients who experience anaphylaxis are at particular risk of death from bronchospasm refractory to initial adrenaline. Psychological sequelae — anxiety disorders, PTSD, and eating restrictions from fear of allergic reactions — affect approximately 30% of patients after severe anaphylaxis and significantly impair quality of life.

Strict avoidance of identified triggers is the cornerstone of prevention. Always carry two adrenaline auto-injectors (EpiPens) and know how to use them. Wear a medical alert bracelet. For food allergy: read all food labels carefully, inform restaurants, and be aware of cross-contamination risks. For insect venom allergy: venom immunotherapy (VIT) for bee or wasp allergy is highly effective, reducing risk of future anaphylaxis by over 95%. Develop and rehearse an emergency action plan with family and caregivers. Schools, workplaces, and carers should be informed and trained.

Call emergency services (999/112/911) immediately for any suspected anaphylaxis — do not wait to see if symptoms improve. Administer an adrenaline auto-injector (EpiPen) as soon as anaphylaxis is suspected and call for emergency help. Even if symptoms appear to resolve after adrenaline, all patients must be taken to hospital — biphasic reactions can occur 1–72 hours later. After any anaphylactic episode, seek urgent referral to an allergy specialist for allergen identification, allergen immunotherapy discussion, and comprehensive anaphylaxis action planning. See your GP promptly if you experience any significant allergic reaction (generalised urticaria, lip swelling, breathlessness after a food or sting exposure) even if it did not reach full anaphylaxis — this may predict future severe reactions and warrants specialist assessment.