Urticaria 

  • Author: M Scott Linscott, MD, FACEP; Chief Editor: Pamela L Dyne, MD   more...
 
Updated: Apr 2, 2010
 

Background

Urticaria, commonly referred to as hives, is the most frequent dermatologic disorder seen in the ED. It appears as raised, well-circumscribed areas of erythema and edema involving the dermis and epidermis that are very pruritic. Urticaria may be acute (lasting less than 6 wk) or chronic (lasting more than 6 wk). A large variety of urticaria variants exist, including acute immunoglobulin E (IgE)–mediated urticaria, chemical-induced urticaria (non-IgE-mediated), urticarial vasculitis, autoimmune urticaria, cholinergic urticaria, cold urticaria, mastocytosis, Muckle-Wells syndrome, and many others.[1, 2]

Urticaria may be confused with a variety of other dermatologic diseases that are similar in appearance and are pruritic including atopic dermatitis (eczema), maculopapular drug eruptions, contact dermatitis, insect bites, erythema multiforme, pityriasis rosea, and others. Usually, however, the experienced clinician is able to distinguish these from urticaria because of its distinctive appearance (see the images below), the fact that it is intensely pruritic, and because it blanches completely with pressure.[3]

Urticaria developed after bites from an imported fUrticaria developed after bites from an imported fire ant. Urticaria associated with a drug reaction. Urticaria associated with a drug reaction.

Acute IgE-mediated urticaria is the most benign form of anaphylaxis. It usually occurs independently, but it may be accompanied by the more serious clinical manifestations of anaphylaxis: angioedema and anaphylactic shock. The etiologies of both acute and chronic urticaria are numerous (see Causes below). The etiologic agent is more likely to be identified in acute urticaria (40-60%) than in chronic urticaria (10-20%). The lesions of IgE-mediated urticaria usually last less than 24 hours and are often migratory, leaving no residual skin abnormalities. The lesions of urticarial vasculitis usually last longer than 24 hours, are both painful and pruritic, and often leave purpuric and hyperpigmented lesions.[4]

For more information, see Medscape's Allergy Resource Center.

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Pathophysiology

Urticaria results from the release of histamine, bradykinin, leukotriene C4, prostaglandin D2, and other vasoactive substances from mast cells and basophils in the dermis. These substances cause extravasation of fluid into the dermis, leading to the urticarial lesion. The intense pruritus of urticaria is a result of histamine released into the dermis. Histamine is the ligand for 2 membrane-bound receptors, the H1 and H2 receptors, which are present on many cell types. The activation of the H1 histamine receptors on endothelial and smooth muscle cells leads to increased capillary permeability. The activation of the H2 histamine receptors leads to arteriolar and venule vasodilation.[5, 6]

This process is caused by several mechanisms. The type I allergic IgE response is initiated by antigen-mediated IgE immune complexes that bind and cross-link Fc receptors on the surface of mast cells and basophils, thus causing degranulation with histamine release. The type II allergic response is mediated by cytotoxic T cells, causing deposits of immunoglobulins, complement, and fibrin around blood vessels. This leads to urticarial vasculitis. The type III immune-complex disease is associated with systemic lupus erythematosus and other autoimmune diseases that cause urticaria.[6]

Complement-mediated urticarias include viral and bacterial infections, serum sickness, and transfusion reactions. Urticarial transfusion reactions occur when allergenic substances in the plasma of the donated blood product react with preexisting IgE antibodies in the recipient. Certain drugs (opioids, vecuronium, succinylcholine, vancomycin, and others) as well as radiocontrast agents cause urticaria due to mast cell degranulation through a non — IgE-mediated mechanism. Urticaria from nonsteroidal anti-inflammatory drugs may be IgE-mediated or due to mast cell degranulation, and there may be significant cross-reactivity among the nonsteroidal anti-inflammatory drugs (NSAIDs) in causing urticaria and anaphylaxis.[7]

The physical urticarias in which some physical stimulus causes urticaria include immediate pressure urticaria, delayed pressure urticaria, cold urticaria, and cholinergic urticaria.[8] For some urticarias, especially chronic urticarias, no cause can be found, despite exhaustive efforts—the so-called idiopathic urticarias, although most of these are chronic autoimmune urticaria as defined by a positive autologous serum skin test (ASST).[9] This test is not specific for autoantibodies against a specific antigen or diagnostic of a specific disease state.[10] To date, no reliable test exists to identify with certainty if chronic urticaria is autoimmune or nonautoimmune in the specific patient.[11]

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Epidemiology

Frequency

United States

Acute urticaria affects 15-20% of the general population at some time during their lifetime.

International

The frequency of urticaria internationally is similar to that in the United States.

Mortality/Morbidity

Pruritus (itching) and rash are the primary manifestations of urticaria, and permanent hyperpigmentation or hypopigmentation are rare. Acute urticaria is usually self-limited and commonly resolves within 24 hours but may last up to 6 weeks. Chronic urticaria lasts more than 6 weeks. Neither acute nor chronic urticaria results in long-term consequences other than anxiety and depression. The depression can be severe enough to lead to suicide in rare cases. Also, many of the diseases associated with chronic urticaria may cause very significant morbidity and mortality.

Race

No variation in race is noted.

Sex

Incidence rates for acute urticaria are similar for men and women; chronic urticaria occurs more frequently in women (60%).

Age

Urticaria can occur in any age group, although chronic urticaria is more common in the fourth and fifth decades.

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Contributor Information and Disclosures
Author

M Scott Linscott, MD, FACEP  Professor, Division of Emergency Medicine, Professor of Surgery (Clinical), University of Utah School of Medicine

M Scott Linscott, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, and Utah Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Steven A Conrad, MD, PhD  Chief, Department of Emergency Medicine; Chief, Multidisciplinary Critical Care Service, Professor, Department of Emergency and Internal Medicine, Louisiana State University Health Sciences Center

Steven A Conrad, MD, PhD is a member of the following medical societies: American College of Chest Physicians, American College of Critical Care Medicine, American College of Emergency Physicians, American College of Physicians, International Society for Heart and Lung Transplantation, Louisiana State Medical Society, Shock Society, Society for Academic Emergency Medicine, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Mark W Fourre, MD  Program Director, Department of Emergency Medicine, Maine Medical Center; Associate Clinical Professor, Department of Surgery, University of Vermont School of Medicine

Disclosure: Nothing to disclose.

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Pamela L Dyne, MD  Professor of Clinical Medicine/Emergency Medicine, David Geffen School of Medicine at UCLA; Attending Physician, Department of Emergency Medicine, Olive View-UCLA Medical Center

Pamela L Dyne, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

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Urticaria developed after bites from an imported fire ant.
Urticaria associated with a drug reaction.
 
 
 
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