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Classification
- Acute allergic angioedema (90% of cases)
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- IgE mediated mast cell degranulation and histamine release as in urticaria
- Non-allergic angioedema (bradykinin mediated)
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- Drug induced angioedema – ACE inhibitors
- Suspect a non-allergic drug reaction if the person is taking an angiotensin-converting enzyme (ACE) inhibitor.
- Drug induced angioedema – ACE inhibitors
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- Hereditary angioedema (HAE)
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- Autosomal dominant genetic abnormality
- C1-esterase-inhibitor deficiency or functional deficiency leading to the overproduction of bradykinin and a increase in vascular permeability
- Suspect hereditary angioedema (HAE) if there is a history of one of the parents being affected
- Acquired angioedema (AAE)
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- Acquired C1-esterase-inhibitor deficiency, usually secondary to lymphoma or connective tissue disorder e.g. SLE
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- Idiopathic angioedema
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- Usually a chronic and relapsing angioedema with an unknown cause
- More common in people with autoimmune disorders, such as systemic lupus erythematosus (SLE) and autoimmune thyroiditis
Allergic Angioedema | Non-Allergic Angioedema | Anaphylaxis |
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Differential Diagnosis
- Evolving anaphylaxis
- Cellulitis
- Erysipelas
- Lymphoedema
- SLE
- Contact dermatitis
Management in ED
- Rapidly developing angioedema Allergic angioedema without anaphylaxis: intravenous (IV) or intramuscular (IM) chlorphenamine and hydrocortisone
- For people with stable angioedema: Offer a non-sedating antihistamine (such as cetirizine, fexofenadine, or loratadine) for up to 6 weeks (use clinical judgement to determine the duration of treatment).If symptoms are severe, give a short course of an oral corticosteroid
- Hereditary Angioedema (suspect if there is a history of one of the parents being affected):
- does not respond to treatment with adrenaline, antihistamines and corticosteroids. Attacks of HAE should be treated with Icatibant (a bradykinin B2 receptor antagonist) or C1 esterase inhibitor concentrate (if available)-fresh frozen plasma .
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