INTRODUCTION Angioedema and urticaria are common transient phenomena that result from mast cell degranulation with the release of mediators that promote vascular permeability, causing proteins and fluids to extravasate into the extracellular space. In urticaria fluid collects within the dermal tissue, whereas in angioedema fluid collects in the deeper subcutaneous space. The causes of mast cell degranulation are varied and include both immunologic and nonimmunologic mechanisms. Systemic involvement may include rhinitis, bronchospasm, or anaphylaxis. Severe reactions may lead to syncope, bronchial asthma, and hypotension. In rare cases both urticaria and angioedema may be triggered by exercise. Acute cases reach a peak in one to three days and usually fade in 7-21 days. In chronic cases the condition waxes and wanes for months or may even persist for years. There may be recurrent attacks separated by months to years. Inciting allergens are numerous and include foods, cosmetics, ophthalmic preparations, and environmental contactants. A hereditary form of angioedema is caused by a deficiency of the C1 esterase inhibitor, a component of complement.
CLINICAL PRESENTATION Urticaria is characterized by edema and erythematous wheals which appear as pink edematous papules and plaques with normal overlying epidermis. They are accompanied by burning, stinging, and itching. Lesions may have blanched halos or may be so edematous as to be blanched themselves. They are rarely limited to the eyelids and may occur randomly scattered over the body. Associated edema of the lips, hands, and feet is common. The clinical finding of angioedema is an erythematous evanescent, eyelid swelling accompanied by severe pruritius. In both conditions the reaction usually occurs within 30 to 60 minutes after exposure to an allergen, though a delayed reaction of four to six hours can also occur. No one lesion lasts over 24 hours, but new ones may occur. Reactive conjunctival vascular dilation can also lead to boggy and sometimes massive conjunctival chemosis.
Angioedema and Urticaria (Contd.)
HISTOPATHOLOGY Angioedema is characterized by edema of the deep dermis and/or subcutis, which is recognized in histological sections as separation of the collagen bundles. Venules may appear dilated. There may be a sparse perivascular and interstitial infiltrate of lymphocytes, neutrophils, and eosinophils, though inflammatory cells are absent in hereditary angioedema.
TREATMENT The key to treatment is to determine the underlying cause since urticaria is always present secondary to an underling immunologic process. Elimination of the inciting factor is curative. Allergy testing may be useful for recurrent cases. In acute urticaria, an etiology is found 20% to 30% of the time and most commonly includes drugs, food or food additives, intravenous radio-opaque contrast medium, hymenoptera stings, infections, or systemic inflammatory diseases. Marked emotional tension may precipitate or exacerbate the condition. Cold, pressure, and sunlight may trigger urticaria in rare familial or sporadic cases. Often, however, the cause cannot be determined. Cold compresses often give relief. Use of subcutaneous epinephrine injection may be necessary for hypotension or airway involvement. In chronic cases the etiology is found in less than 5% of cases.
Angioedema and Urticaria (Contd.)
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