Allergy and Immunology · 3 min read
Anaphylaxis, Urticaria and Angioedema
Anaphylaxis is an exam favorite because the correct first step, IM epinephrine, is so often delayed, and angioedema questions hinge on separating histamine from bradykinin.
Recognizing Anaphylaxis
Anaphylaxis is highly likely when there is acute onset of skin or mucosal involvement (hives, flushing, lip or tongue swelling) plus respiratory compromise, hypotension or end-organ dysfunction, or severe gastrointestinal symptoms; or acute hypotension, bronchospasm or laryngeal involvement after exposure to a known or highly probable allergen, even without skin findings. Up to 20% of episodes lack skin signs. Common triggers are foods, drugs (beta-lactams, NSAIDs, neuromuscular blockers, biologics), Hymenoptera venom and latex.
Management
There is no absolute contraindication to epinephrine in anaphylaxis, including older age and coronary disease. IM injection into the thigh gives faster, higher levels than subcutaneous injection. Patients taking beta-blockers may have refractory hypotension and bradycardia; glucagon (1–5 mg IV over 5 minutes, then an infusion of 5–15 µg/min) bypasses the beta receptor. Antihistamines treat only itching and hives, and corticosteroids neither treat acute symptoms nor reliably prevent biphasic reactions.
A biphasic reaction (return of symptoms without re-exposure, usually within 12 hours) occurs in about 5% of patients. Risk is higher with severe initial reactions and with more than one dose of epinephrine, so extend observation for those patients. Elevated tryptase supports mast cell activation, but a normal value does not exclude anaphylaxis, especially food-induced. Discharge every patient with 2 epinephrine auto-injectors (intranasal epinephrine is an approved alternative), an action plan and allergy referral.
Urticaria
Individual hives last under 24 hours and resolve without marks. Acute urticaria (under 6 weeks) is usually triggered by viral infection, drugs or foods. Chronic urticaria (6 weeks or more) is mostly chronic spontaneous urticaria, often autoimmune; extensive allergy testing is not indicated, and a complete blood count with erythrocyte sedimentation rate or C-reactive protein is enough unless history suggests otherwise. Inducible forms include dermatographism, cold, cholinergic and pressure urticaria.
Suspect urticarial vasculitis when lesions last more than 24 hours, burn rather than itch, leave purpura or hyperpigmentation, or occur with low complement; confirm by biopsy.
Histaminergic Versus Bradykinin Angioedema
| Feature | Histaminergic (mast cell) | ACE inhibitor | Hereditary (C1 inhibitor deficiency) |
|---|---|---|---|
| Urticaria or itching | Usually present | Absent | Absent |
| Typical sites | Lips, eyes, any skin | Tongue, lips, airway | Extremities, face, airway, bowel wall (abdominal pain) |
| Labs | Normal complement | Normal complement | Low C4; low C1 inhibitor level or function |
| Response to epinephrine | Good | Poor | Poor |
| Treatment | Epinephrine, antihistamines, steroids | Stop ACE inhibitor; airway; consider icatibant or fresh frozen plasma | C1 inhibitor concentrate, icatibant or ecallantide |
Angioedema from an angiotensin-converting enzyme (ACE) inhibitor can first occur after years of use, is more common in Black patients, and contraindicates all ACE inhibitors. An angiotensin receptor blocker carries a small risk and is usually acceptable; sacubitril-valsartan requires a 36-hour washout after the last ACE inhibitor dose. Hereditary angioedema begins in childhood or adolescence, is triggered by trauma, dental work, estrogen and stress, and is prevented long-term with lanadelumab, berotralstat or C1 inhibitor. Acquired C1 inhibitor deficiency presents after age 40 with low C1q and suggests lymphoproliferative disease or monoclonal gammopathy.
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