Dermatology Made Easy is based on the most popular topics from DermNet NZ's vast array of material. The book combines the essential focus of the ‘Made Easy’ book series with the authority and knowledge base of DermNet NZ's unparalleled resources.
Author and Chief Editor: Dr Amanda Oakley, Dermatologist, Hamilton, New Zealand, January 2015.
Urticaria is characterised by weals (hives) or angioedema (swellings, in 10%) or both (in 40%). There are several types of urticaria. The name urticaria is derived from the common European stinging nettle 'Urtica dioica'.
A weal (or wheal) is a superficial skin-coloured or pale skin swelling, usually surrounded by erythema (redness) that lasts anything from a few minutes to 24 hours. Usually very itchy, it may have a burning sensation.
Angioedema is deeper swelling within the skin or mucous membranes, and can be skin-coloured or red. It resolves within 72 hours. Angioedema may be itchy or painful but is often asymptomatic.
Acute urticaria is urticaria, with or without angioedema, that is present for less than 6 weeks. It is often gone within hours to days.
One in five children or adults have an episode of acute urticaria during their lifetime. It is more common in atopics. It affects all races and both sexes.
Urticarial weals can be a few millimetres or several centimetres in diameter, coloured white or red, with or without a red flare. Each weal may last a few minutes or several hours, and may change shape. Weals may be round, or form rings, a map-like pattern or giant patches.
Acute urticaria can affect any site of the body and tends to be distributed widely.
Weals are due to release of chemical mediators from tissue mast cells and circulating basophils. These chemical mediators include histamine, platelet-activating factor and cytokines. The mediators activate sensory nerves and cause dilation of blood vessels and leakage of fluid into surrounding tissues. Bradykinin release causes angioedema.
Several hypotheses have been proposed to explain urticaria. The immune, arachidonic acid and coagulation systems are involved, and genetic mutations are under investigation.
Acute urticaria can be induced by the following factors but the cause is not always identified.
Severe allergic urticaria may lead to anaphylactic shock (bronchospasm, collapse).
A single episode or recurrent episodes of angioedema without urticaria can be due to an angiotensin-converting enzyme (ACE) inhibitor drug.
Acute urticaria is diagnosed in people with a short history of weals that last less than 24 hours, with or without angioedema. A thorough physical examination should be undertaken to look for underlying causes.
Biopsy of urticaria can be non-specific and difficult to interpret. The pathology shows oedema in the dermis and dilated blood vessels, with variable mixed inflammatory infiltrate. Vessel-wall damage indicates urticarial vasculitis.
The main treatment for acute urticaria in adults and in children is with an oral second-generation antihistamine chosen from the list below. If the standard dose (eg 10 mg for cetirizine) is not effective, the dose can be increased fourfold (eg 40 mg cetirizine daily). They are best taken continuously rather than on demand. They are stopped when the acute urticaria has settled down. There is not thought to be any benefit from adding a second antihistamine.
Although systemic treatment is best avoided during pregnancy and breast feeding, there have been no reports that second-generation antihistamines cause birth defects. If treatment is required, loratidine and cetirizine are currently preferred.
Conventional first-generation antihistamines such as promethazine or chlorpheniramine are no longer recommended for urticaria.
In addition to antihistamines, the triggers for urticaria should be avoided where possible. For example:
If non-sedating antihistamines are not effective, a 4 to 5-day course of oral prednisone (prednisolone) may be warranted in severe acute urticaria, particularly if there is angioedema. Systemic steroids do not speed up resolution of symptoms.
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