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A few cases of food-induced angioedema may present in the ED, and angioedema is extremely rare in the pediatric population. Most cases occur at sites where the coagulation pathway is activated, for example, the cornea, skin, upper respiratory tract, and lower airway (such as the larynx and trachea). Airway management is rapidly becoming a more viable option in the treatment of life-threatening laryngeal angioedema. The point-of-care evidence base for the role of corticosteroids and C1-INH is growing.
A number of complex, heterogeneous technologies are used to diagnose and treat angioedema. These include histamine- and bradykinin-sensitive imaging methods, laboratory assays, specialized imaging modalities, recombinant DNA technology, and pharmacy compounding.
Angioedema is defined as a swelling (at least in part) secondary to a sudden and transient increase in vascular permeability. Histamine-mediation accounts for approximately 75% of non-HAE angioedemas, and bradykinin-mediated angioedema accounts for approximately 15% of non-HAE angioedemas. The mechanism of these vasoactive substances in swelling appears to be precipitation of protein C1 inhibitor, which occurs in the initiation phase of angioedema. Histamine leads to the release of bradykinin, which in turn activates infiltrating granulocytes and other immune system cells, which initiates the inflammatory process with edema. Patients with HAE are prone to excessive and life-threatening edema secondary to serum kallikrein deficiency. The clinical manifestation of HAE includes recurrent, unexplained upper respiratory tract and gastrointestinal tract disease. Type I involves reduced functional C1 inhibitor, whereas Types II and III are caused by a reduction in functional C1 inhibitor and C1q, respectively. Both serum and tissue kallikrein are detectable at the time that the acute flare occurs. Most patients with HAE Type I are treated early with daily plasma-derived C1-INH. C1-INH is a highly effective treatment, but factors that bear on outcomes for HAE patients include access to C1-INH replacement therapy and the timing of diagnosis and initiation of treatment. d2c66b5586