Contact urticaria may be immunologic (allergic) or non-immunologic (non-allergic). The immunologic form is an immediate hypersensitivity reaction (IgE-mediated) that occurs when the skin is directly exposed to an allergen. It may rarely be complicated by anaphylaxis and is more common in atopic individuals. Substances that have been found to cause this reaction include latex, foods (meat, raw potato, and fish), preservatives, disinfectants, fragrances, formaldehyde, epoxy resin hardeners, several woods, and therapeutic drugs. Non-immunologic contact urticaria often occurs without previous sensitization and usually remains localized. Substances that cause non-immunologic contact urticaria include benzoic acid, sorbic acid, cinnamic acid, cinnamic aldehyde, nicotinic acid esters, insects, nettles and other plants, foodstuffs (fish, mustard, cayenne pepper, thyme), as well as materials related to the medical industry (alcohol, benzocaine, tincture of benzoin, witch hazel, balsam of Peru, DMSO).

In both of these forms, contact with the inciting agent triggers an inflammatory reaction in which capillary permeability changes. Fluid leaks into the area of contact, causing a wheal and flare reaction. These wheals (hives) are raised areas of the skin that are pink or red in color and often intensely pruritic. Individual wheals, once formed, are self-limiting and will subside when exposure to the causative substance has ceased. Prevention of this condition by avoiding known causative agents is the best treatment.

Contact urticaria can be differentiated from cellulitis based on time course and exposure history. Contact urticaria develops and resolves quite quickly, whereas cellulitis, by comparison, is a more indolent and progressive process.