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Urticaria

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urticaria hives skin wheals

A series of three clinical photographs demonstrating the dermatological resolution of urticaria (hives) across three anatomical regions: the knee joint (A), the lateral waist (B), and the elbow (C). The images show characteristic wheals—edematous, circumscribed, and slightly elevated skin lesions. Panel A displays the knee area with subtle, flesh-colored to slightly erythematous elevations and an uneven skin texture consistent with resolving wheals. Panel B shows the lateral waist with faint, linear, and confluent dermal edema. Panel C depicts the elbow where the lesions have largely flattened, leaving only minimal, faint markings on the skin surface. The progression illustrates the transient nature of urticarial lesions as they gradually diminish in size and elevation. This visual serves as an educational reference for identifying skin morphology in the recovery phase of an acute urticarial reaction, emphasizing the characteristic lack of secondary skin changes (such as scaling or scarring) during the resolution of wheals.

A series of three clinical photographs demonstrating the dermatological resolution of urticaria (hives) across three anatomical regions: the knee joint (A), the lateral waist (B), and the elbow (C). The images show characteristic wheals—edematous, circumscribed, and slightly elevated skin lesions. Panel A displays the knee area with subtle, flesh-colored to slightly erythematous elevations and an uneven skin texture consistent with resolving wheals. Panel B shows the lateral waist with faint, linear, and confluent dermal edema. Panel C depicts the elbow where the lesions have largely flattened, leaving only minimal, faint markings on the skin surface. The progression illustrates the transient nature of urticarial lesions as they gradually diminish in size and elevation. This visual serves as an educational reference for identifying skin morphology in the recovery phase of an acute urticarial reaction, emphasizing the characteristic lack of secondary skin changes (such as scaling or scarring) during the resolution of wheals.

A clinical photograph showing a close-up of a child's lower extremity demonstrating urticaria. The image displays multiple raised, edematous skin lesions known as wheals or hives. These lesions are characterized by pale-to-skin-colored central swellings of varying sizes and irregular shapes, surrounded by a distinct zone of erythema (redness). The distribution is scattered across the leg, illustrating the typical appearance of a hypersensitivity reaction or allergic response. This image serves as an educational reference for identifying cutaneous manifestations of urticaria, focusing on the morphology of superficial dermal edema and associated inflammatory flare.

A clinical photograph showing a close-up of a child's lower extremity demonstrating urticaria. The image displays multiple raised, edematous skin lesions known as wheals or hives. These lesions are characterized by pale-to-skin-colored central swellings of varying sizes and irregular shapes, surrounded by a distinct zone of erythema (redness). The distribution is scattered across the leg, illustrating the typical appearance of a hypersensitivity reaction or allergic response. This image serves as an educational reference for identifying cutaneous manifestations of urticaria, focusing on the morphology of superficial dermal edema and associated inflammatory flare.

Clinical photograph of a pediatric patient's bilateral lower limbs demonstrating classic urticaria (hives). The image shows multiple discrete and confluent wheals distributed across the thighs. Morphologically, the lesions are characterized by raised, edematous, superficial swellings of varying sizes. The central portions of the wheals appear pale or skin-colored, while the peripheries exhibit varying degrees of erythema. These findings represent a type I hypersensitivity reaction or mast cell degranulation, leading to dermal edema. This visual evidence is a key diagnostic clinical sign for acute urticaria, commonly used in dermatology and pediatric curricula to differentiate transient wheals from other types of papular eruptions or inflammatory skin conditions.

Clinical photograph of a pediatric patient's bilateral lower limbs demonstrating classic urticaria (hives). The image shows multiple discrete and confluent wheals distributed across the thighs. Morphologically, the lesions are characterized by raised, edematous, superficial swellings of varying sizes. The central portions of the wheals appear pale or skin-colored, while the peripheries exhibit varying degrees of erythema. These findings represent a type I hypersensitivity reaction or mast cell degranulation, leading to dermal edema. This visual evidence is a key diagnostic clinical sign for acute urticaria, commonly used in dermatology and pediatric curricula to differentiate transient wheals from other types of papular eruptions or inflammatory skin conditions.

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Urticaria (Hives)

Urticaria - raised erythematous wheals on the arm
Fig. Urticaria: erythematous, raised wheals on the arm (Rosen's Emergency Medicine)
Urticaria wheals on a child's lower limb
Fig. Classic urticaria with pale wheals and surrounding erythema in a pediatric patient

Definition & Epidemiology

Urticaria (hives) is one of the most common cutaneous reaction patterns, characterised by transient, pruritic, edematous wheals involving the superficial dermis. It may occur in isolation or as part of a systemic anaphylactic reaction. Approximately 15-20% of the population experiences urticaria at some point in their lifetime. Acute urticaria is equally common in both sexes; chronic urticaria is more prevalent in women in their 40s and 50s, with a peak of chronic spontaneous urticaria (CSU) between the third and fourth decade. Women are nearly twice as likely as men to develop urticaria. Half of all patients with chronic urticaria have disease for 5 years or more.
Chronic urticaria is defined by recurrence over a period of ≥6 weeks and is often of unknown cause. Statistical analysis shows 66-93% of chronic urticaria is CSU, 4-33% is physical urticaria, and 1-7% is cholinergic urticaria.
  • Goldman-Cecil Medicine, p. 4300
  • Rosen's Emergency Medicine, p. 2413

Pathophysiology

Urticaria results from local degranulation of mast cells with the release of histamine and other mediators. This can be triggered by immunologic or nonimmunologic mechanisms:
MechanismExamples
IgE-mediated (Type I)Foods, drugs, insect stings, latex
Immune complex/complementInfections, serum sickness
AutoimmuneFunctional IgE or IgG autoantibodies against FcεRI or IgE
Direct mast cell degranulationNSAIDs, opioids, radiocontrast media, vancomycin
Bradykinin-mediatedACE inhibitors, hereditary angioedema
Vasoactive stimuliPhysical stimuli (cold, pressure, heat, light)
Key mediators include histamine, bradykinin, kallikrein, acetylcholine, and slow-reacting substance of anaphylaxis (SRS-A). IL-31 levels correlate with itch intensity. Functional IgG autoantibodies against the high-affinity IgE receptor (FcεRI) are found in ~30-50% of CSU patients, representing an autoimmune subtype.
  • Goldman-Cecil Medicine, p. 4301
  • Dermatology 2-Volume Set 5e, p. 125
  • Harrison's Principles, p. 2851

Classification

1. Acute Urticaria (< 6 weeks)

  • Drug reactions (antimicrobials, NSAIDs, opioids, ACE inhibitors, radiocontrast)
  • Food reactions (seafood, tree nuts, eggs, peanuts, strawberries)
  • Infections: viral (rhinovirus, EBV, hepatitis, coxsackievirus), bacterial, parasitic
  • Insect stings/bites
  • Transfusion reactions

2. Chronic Urticaria (≥ 6 weeks)

A. Chronic Spontaneous Urticaria (CSU)
  • No identifiable external trigger
  • May have autoimmune component (anti-FcεRI or anti-IgE antibodies)
  • Angioedema accompanies wheals in ~33-67% of CSU patients
B. Inducible (Physical) Urticaria
SubtypeTriggerKey Feature
Symptomatic dermographismFirm stroking of skinMost common physical urticaria; wheal within 30 min
Cold urticariaCold exposureRisk of anaphylaxis with cold water immersion
Cholinergic urticariaHeat, exercise, emotionSmall wheals (1-3 mm) with large surrounding erythema
Pressure urticariaSustained pressureDelayed onset 4-8 hours
Solar urticariaUV/visible lightConfined to sun-exposed areas
Aquagenic urticariaWater (any temperature)May be associated with polycythemia vera
Vibratory urticariaVibrationOccupational; some familial (ADGRE2 mutations)
Exercise-induced anaphylaxisExertion ± foodMay progress to vascular collapse
C. Rare/Syndromic
  • Urticarial vasculitis
  • Mastocytosis (cutaneous or systemic)
  • Hereditary angioedema (HAE) - bradykinin-mediated, NO pruritus, NO urticaria
  • CIAS1/NLRP3-associated: familial cold autoinflammatory syndrome (FCAS), Muckle-Wells syndrome
  • Schnitzler's syndrome, Gleich's syndrome
  • Harrison's Principles, p. 2851 (Table 363-1)
  • Rosen's Emergency Medicine, p. 2413
  • Fitzpatrick's Dermatology, p. 718

Clinical Features

Morphology:
  • Circumscribed, raised, pruritic, evanescent areas of edema in the superficial dermis
  • Individual wheals last < 24 hours (new lesions continuously develop)
  • Pale/white centers with red borders ("wheal and flare")
  • May be erythematous or whitish when edema is marked
  • Sizes range from a few mm to several cm; may be annular, polycyclic, or map-like
Angioedema = edema extending into deep dermis/subcutaneous tissue; lasts longer (1-3 days); common at lips, eyelids, tongue, larynx, GI tract.
Warning features suggesting urticarial vasculitis: lesions lasting > 36 h, painful (not pruritic), scarring - warrants biopsy.
Key distinguishing feature of HAE: NO pruritus, NO urticaria; GI colic attacks; laryngeal edema; FAILS H1 antihistamines; low C4 and C1INH.
  • Fitzpatrick's Dermatology, p. 717
  • Harrison's Principles, p. 2851

Differential Diagnosis

  • Drug eruption / morbilliform exanthem
  • Erythema multiforme (targetoid; fixed > 24 h)
  • Urticarial vasculitis
  • Angioedema (non-urticarial types)
  • Bullous pemphigoid (urticarial phase)
  • Polymorphous eruption of pregnancy
  • Erythema marginatum
  • Systemic mastocytosis
  • Sweet's syndrome

Diagnosis

Acute urticaria

  • History alone is usually sufficient
  • Allergen-specific IgE testing or skin prick testing when a specific trigger is suspected

Chronic urticaria

LevelTests
Routine (all CSU)Differential blood count, ESR and/or CRP
Extended (guided by history)Avoidance of suspected triggers; H. pylori testing; thyroid hormones + autoantibodies; autologous serum skin test (ASST) for autoantibodies; allergy skin tests; serum tryptase (if mastocytosis suspected); skin biopsy (if vasculitis suspected)
Inducible urticaria: Provocation and threshold testing (ice cube test for cold urticaria, dermographometer for dermographism, UV lamp for solar urticaria, etc.) - usually establishes the diagnosis directly.
Isolated angioedema without urticaria: Check C4, C1INH antigen and function, C1q protein to rule out HAE and acquired C1INH deficiency.
  • Fitzpatrick's Dermatology (Table 41-1)
  • Harrison's Principles, p. 2852

Treatment

Step-Up Approach (EAACI/GALEN Guidelines)

Step 1 - First-line: Second-generation H1 antihistamines (non-sedating)
  • Cetirizine, fexofenadine, loratadine, desloratadine, levocetirizine
  • Preferred over first-generation agents (diphenhydramine, hydroxyzine) due to lack of sedation and anticholinergic side effects
  • Can be up-dosed to 4× the standard daily dose if standard dosing is insufficient
Step 2 - Add-on agents (if H1 blockade inadequate)
  • H2 antagonist (famotidine, ranitidine) - modest additional benefit
  • Leukotriene receptor antagonist (montelukast 10 mg/day) - particularly useful in aspirin/NSAID-sensitive urticaria
  • First-generation antihistamine at night (e.g. hydroxyzine for sedation-aided sleep)
Step 3 - Refractory chronic urticaria: Omalizumab
  • Omalizumab (anti-IgE monoclonal antibody): approved for CSU in patients ≥12 years
  • 300 mg SC every 4 weeks is the standard dose for CSU
  • Effective and rapidly acting; approved for chronic inducible urticaria as well
  • A 2025 meta-analysis confirms efficacy and safety in pediatric CSU (PMID: 40545961)
Step 4 - Cyclosporin / immunosuppressants
  • For CSU refractory to omalizumab
  • Cyclosporin A (calcineurin inhibitor) - targets T-cells and mast cells
  • Hydroxychloroquine, dapsone, or colchicine for urticarial vasculitis
Systemic corticosteroids:
  • Not recommended chronically (long-term toxicity)
  • Short courses (14-21 days with taper) acceptable for moderate-severe acute urticaria
  • Useful in pressure urticaria, vasculitic urticaria, or refractory angioedema
For specific subtypes:
  • Cold urticaria: antihistamines 30-60 min before cold exposure; avoid cold water immersion
  • Cholinergic urticaria: non-sedating antihistamines
  • Solar urticaria: phototherapy for tolerance induction
  • HAE: NOT treated with antihistamines - use C1INH concentrate, icatibant (bradykinin B2 receptor antagonist), ecallantide, or lanadelumab for prophylaxis
  • Harrison's Principles, p. 2852
  • Rosen's Emergency Medicine, p. 2414
  • Dermatology 2-Volume Set 5e, p. 125
  • Goldman-Cecil Medicine, abstract
  • Katzung Pharmacology 16e

Common Causes Summary

CategoryExamples
DrugsPenicillin (most common antibiotic), aspirin/NSAIDs, opioids, ACE inhibitors
FoodsSeafood, tree nuts, peanuts, eggs, strawberries, lobster
InfectionsRhinovirus, EBV, hepatitis, coxsackievirus, H. pylori, Candida, parasites
PhysicalDermatographism, cold, pressure, heat, exercise
Systemic diseasesSLE, lymphoma, carcinoma, hyperthyroidism, juvenile RA
InhalantsPollens, mold, animal dander, dust mites
ContactLatex, topical medications, cosmetics, animal saliva
Idiopathic~50% of chronic urticaria - no cause found

Recent Evidence (2024-2026)

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