Inflammatory Diseases
Angioedema
Angioedema
Etiology • Usually triggered by ingested antigens (eg, shellfish, nuts,
fruits, medications) • Mechanism associated with immunoglobulin E (IgE)-mediated
mast cell degranulation with subsequent histamine release • Drug reactions resulting in release of inflammatory mediators
(bradykinin) • Some cases have a genetic basis: C1 esterase inhibitor deficien-
cy or inhibitor dysfunction (autosomal recessive) • May be correlated with disease states characterized by the
presence of circulating immune complexesfruits, medications) • Mechanism associated with immunoglobulin E (IgE)-mediated
mast cell degranulation with subsequent histamine release • Drug reactions resulting in release of inflammatory mediators
(bradykinin) • Some cases have a genetic basis: C1 esterase inhibitor deficien-
cy or inhibitor dysfunction (autosomal recessive) • May be correlated with disease states characterized by the
Clinical Presentation • Soft, diffuse, painless swelling of face, lips, and neck • Overlying skin and oral mucosa appear noninflamed • Mucosa may become secondarily erythematous, ulcerative, or,
rarely, vesicular • Usually short-lived (24–48 hours)
Diagnosis • Nonspecific histology • Correlation of history and clinical findings
Differential Diagnosis • Trauma (physical, cold) • Cellulitis • Vascular malformation • Acute contact stomatitis • Melkersson-Rosenthal syndrome (early stages) • Orofacial granulomatosis (early stages)
Treatment • Elimination of possible etiologic/precipitating factor(s) • Antihistamines, corticosteroids, adrenaline
Prognosis • Good to excellent