THE MERCK VETERINARY MANUAL
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Overview of Urticaria

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Urticaria is characterized by multiple plaque-like eruptions that are formed by localized edema in the dermis and that often develop and disappear suddenly. It occurs in all domestic animals but most often in horses. Allergic urticaria may be exogenous or endogenous. Exogenous hives may be produced by toxic irritating products of the stinging nettle, the stings or bites of insects, topical medications, or exposure to chemicals (eg, carbolic acid, turpentine, carbon disulfide, or crude oil). Nonimmunologic factors such as pressure, sunlight, heat, exercise, psychologic stress, and genetic abnormalities may precipitate or intensify urticaria. Pruritus is not always present, particularly in horses.

Sensitive animals, particularly short-haired dogs and purebred horses, also rarely may exhibit dermographism, a phenomenon wherein pressure applied to the skin produces linear urticarial lesions. The clinical significance is unknown.

Endogenous urticaria may develop after exposure to topical, inhaled, or a ingested allergens or administration of medications; it has been seen mostly in horses and dogs. In horses, it has been noted in the course of GI conditions, particularly severe constipation or inflammation of the intestinal mucosa. A unique form of urticaria in cattle has been described chiefly in the Channel Island breeds (Jersey, Guernsey), which become sensitized to the casein in their own milk (“milk allergy”); it occurs in cases of milk retention or unusual engorgement of the udder with milk. Urticaria has been seen in bitches during estrus. In young horses, dogs, and pigs, urticaria may be associated with intestinal parasites. Angioneurotic edema is a life-threatening variant of urticaria in which there is diffuse subcutaneous edema, often localized to the head, limbs, or perineum. In horses, dermatophytosis (ringworm) and pemphigus foliaceus may present as urticaria early in the diseases. In horses, vasculitis may also present with urticaria.

The wheals or plaques appear within a few minutes or hours of exposure to the causative agent. In severe cases, the cutaneous eruptions are preceded by fever, anorexia, or dullness. Horses often become excited and restless. The skin lesions are elevated, round, flat-topped, and 0.5–8 in. (1–20 cm) in diameter; they may be slightly depressed in the center. They can develop on any part of the body but are seen mainly on the back, flanks, neck, eyelids, and legs. In advanced cases, they may be found on the mucous membranes of the mouth, nose, conjunctiva, rectum, and vagina. In general, the lesions disappear as rapidly as they arise, usually within a few hours.

In sheep, lesions usually are seen only on the udder and hairless parts of the abdomen. In pigs, eruptions have been seen around the eyes, between the hindlegs, and on the snout, abdomen, and back.

In general, the prognosis is favorable. Fatalities are rare and are probably due to anaphylaxis or associated angioedema involving the respiratory passages.

Chronic urticaria is a diagnostic challenge. All allergens in an environment should be considered potential causes, and elimination of exposure instituted, if possible. Persistent urticarial lesions, particularly those that progress to thickened crusts, should be biopsied.

Acute urticaria usually disappears spontaneously. The rapid-acting glucocorticosteroids, eg, hydrocortisone sodium succinate or prednisolone sodium succinate or hemisuccinate are reported to be useful. Dexamethasone (0.1 mg/kg) has been useful in dogs, cats, and horses. Antihistamines are of questionable value and may induce urticaria if given IV. Epinephrine may be given in life-threatening situations. The lesions promptly disappear but return rapidly if the allergen is not eliminated. Usually, local treatment of the lesions is not necessary. In chronic urticaria in horses, the antihistamine hydroxyzine at 0.4–0.8mg/kg, bid, or the tricyclic antidepressant doxepin (which has antihistaminic properties) at 0.6 mg/kg, bid, may be useful.

Last full review/revision May 2013 by Stephen D. White, DVM, DACVD

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