Summary
Urticaria, also known as welts, hives, or wheals, is characterized by the appearance of intensely pruritic erythematous plaques.[1] It appears clinically as pruritic, pale, blanching swellings of the superficial dermis that last for up to 24 hours. Lesions may be small, large, giant, oval, or annular.[Figure caption and citation for the preceding image starts]: Acute urticaria: typical whealsFrom the collection of Adam Reich, MD, PhD [Citation ends].
[Figure caption and citation for the preceding image starts]: Typical lesions seen in acute or chronic urticariaFrom the collection of Stephen Dreskin, MD, PhD [Citation ends].
[Figure caption and citation for the preceding image starts]: Urticaria: whealsFrom the collection of Adam Reich, MD, PhD [Citation ends].
Urticaria affects 10% to 25% of the population and can occur in any age group.[2] It is a mast-cell-driven disease. The triggering mechanisms for mast-cell activation in urticaria are not well defined but seem to be multiple and diverse.[3]
Urticaria is classified according to duration of symptoms:
Acute urticaria: the occurrence of spontaneous wheals, angioedema, or both for <6 weeks[1][2][3]
Chronic urticaria: urticaria that has been continuously or intermittently present for ≥6 weeks.[1][3][4]
Chronic urticaria is classified into 2 subtypes:[3]
Chronic spontaneous urticaria: spontaneous appearance of wheals, angioedema, or both ≥6 weeks due to known or unknown causes.
Inducible urticaria, for example delayed pressure urticaria, heat urticaria, solar urticaria, symptomatic dermatographism, vibratory angioedema, aquagenic urticaria, cholinergic urticaria, and contact urticaria.
Urticaria complicated by angioedema
Some people have urticaria that is complicated by angioedema, a swelling of the deeper dermis and tissues (e.g., mucosal surfaces), with laryngeal edema potentially causing respiratory distress and death.[3] Angioedema is commonly associated with urticaria and may occur at any age.[5] It may not necessarily be seen at the first urticarial episode, but risk of angioedema increases with greater exposure to the allergenic substance.[6]
Clinical presentation of angioedema may include nonpitting edema of the subcutaneous tissues involving lips, face, neck and extremities and/or submucosal tissues affecting the oral cavity, larynx and gastrointestinal system.[7] Associated symptoms may also be present. These are dependent on the underlying etiology. Examples include flushing, bronchospasm, abdominal pain, diarrhea and vomiting.[7] Angioedema without urticaria should prompt further evaluation.[1][Figure caption and citation for the preceding image starts]: Angio-oedema of the lips in a patient who also has urticariaFrom the collection of Stephen Dreskin, MD, PhD [Citation ends].
Differentials
Common
- Acute spontaneous urticaria
- Chronic spontaneous urticaria
- Chronic inducible (physical) urticaria
- Drug eruptions
- Insect bite
- Viral exanthem
- Atopic dermatitis
- Allergic contact dermatitis
- Irritant contact dermatitis
Uncommon
- Erythema multiforme
- Stevens-Johnson syndrome
- Auriculotemporal syndrome
- Bullous pemphigoid
- Cutaneous mastocytosis
- Systemic mastocytosis
- Mast cell activation syndrome
- Urticarial vasculitis
- Transfusion reactions
- Serum sickness
- Cold-induced urticaria, Muckle-Wells syndrome, neonatal multisystem inflammatory disease
- Anaphylaxis
Contributors
Authors
Marilyn Li, MD
Associate Professor of Clinical Pediatrics, Clinician Educator
Director, Quality Improvement and Educational Activities For The Breathmobile Program
Keck School of Medicine, USC
Los Angeles
CA
Disclosures
ML is an unpaid board member of the California Society of Allergy Asthma and Immunology (CSAAI). ML has created CME content on asthma, anaphylaxis, and immunotherapy.
Kenny Y.C. Kwong, MD
Clinical Associate Professor of Pediatrics
Division of Allergy-Immunology
Los Angeles General Medical Center
Los Angeles
CA
Disclosures
KYCK is a consultant and independent contractor for Thermo-Fisher Scientific Immunodiagnostics Division (Phadia).
Acknowledgements
Dr Marilyn Li and Dr Kenny Y.C. Kwong would like to gratefully acknowledge Dr Nanette Silverberg, and Dr Mary Lee-Wong, previous contributors to this topic.
Disclosures
NS and MLW declare that they have no competing interests.
Peer reviewers
Christopher Parrish, MD
Assistant Professor
Pediatrics and Internal Medicine
Division of Allergy and Immunology
UT Southwestern
TX
Disclosures
CP declares that he has no competing interests.
Amor Kachamoune, MD
Assistant Professor
New York University School of Medicine
New York
NY
Disclosures
AK declares that he has no competing interests.
Bettina Wedi, MD
Professor
Head of Allergy Division
Department of Dermatology and Allergy
Hannover Medical School
Hannover
Germany
Disclosures
BW declares that she has no competing interests.
Patient information
Dermatitis (seborrheic) of the body
More Patient information
Log in or subscribe to access all of BMJ Best Practice
Use of this content is subject to our disclaimer