Last Updated on April 4, 2021 by frcemuser

Classification

• Acute allergic angioedema (90% of cases)

• • IgE mediated mast cell degranulation and histamine release as in urticaria
• Non-allergic angioedema (bradykinin mediated)

• • Drug induced angioedema – ACE inhibitors
    • Suspect a non-allergic drug reaction if the person is taking an angiotensin-converting enzyme (ACE) inhibitor.

• • Hereditary angioedema (HAE)

• • • 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)

• • • Acquired C1-esterase-inhibitor deficiency, usually secondary to lymphoma or connective tissue disorder e.g. SLE
• Idiopathic angioedema

• • 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

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 .