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 Type I immediate(IgE or IgG) – most common

 Type II Cytotoxic complement cascade (IgG or IgM) –Yes

 Type III Immune complex (IgG or IgM) – Yes

 Type IV Delayed T‐cell – No anaphylaxis

Allergic reactions that present as urticaria can progress to angioedema, resulting in histamine‐mediated facial or tongue swelling. Subsequently, airway obstruction might develop precipitously with obvious consequences. Angioedema also occurs without other manifestations of an allergic reaction and is due to non–histamine (bradykinin)‐mediated edema, such as the type that can develop from angiotensin‐converting enzyme inhibitors. This type of edema does not respond to conventional therapy of epinephrine, corticosteroids, and antihistamines. The patient may have been taking the medication for some time before such a reaction occurs. This can be confusing, as some assume that such a reaction would have occurred earlier in the course of taking the medication if the patient was going to exhibit one. It is vital to be able to distinguish between histamine and non–histamine‐mediated angioedema. Studies have shown that pruritus, uticaria, and angioedema associated with abdominal symptoms are more typical of non–histamine‐mediated angioedema, and airway maintenance and protection should be a priority focus [2].

Hereditary angioedema, on the other hand, does not represent a response to a specific allergen. However, it deserves mention because of its similar presentation to allergic reactions and other forms of angioedema. Hereditary angioedema is an autosomal dominant genetic disorder caused by a defect in the complement pathway that results in either a low C1 esterase level or a high level of dysfunctional C1 esterase. Symptoms can include pruritus, urticaria, wheezing, facial and tongue swelling, dizziness, hypotension, syncope, and gastrointestinal distress [3].