Dermatology · PANCE / PANRE

Urticaria (Acute and Chronic)

Written & clinically reviewed by Ryan Busch, PA-C · Updated August 2026 · Report an error

Transient pruritic edematous wheals from mast cell degranulation; acute (<6 wks) or chronic (≥6 wks).

Also known as: urticaria, hives, wheals, chronic spontaneous urticaria, CSU, angioedema

Overview

An inflammatory disorder of the dermis characterized by transient, pruritic, edematous wheals (hives), each lasting <24 hours, with normal-appearing skin between flares. Often accompanied by angioedema (deeper dermal/subcutaneous edema). Classified by duration: acute (<6 weeks) and chronic (≥6 weeks).

Epidemiology

Lifetime prevalence ~20% for acute urticaria. Chronic spontaneous urticaria (CSU) affects ~0.5-1% of adults; female predominance 2:1; peak ages 20-40.

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Question 1DermatologyMedium
A 28-year-old woman presents with a 3-day history of an intensely itchy, recurrent rash. She reports raised, pink, well-circumscribed plaques on her trunk and arms that last a few hours, fade completely, then recur in new locations, with each individual lesion resolving within 24 hours and leaving no bruising or skin discoloration. She has no fever, joint pain, mucosal lesions, or breathing difficulty. On examination, stroking her forearm with a tongue depressor produces a linear wheal, and the intervening skin appears entirely normal. Which of the following is the most likely diagnosis?
  • AErythema multiforme
  • BAcute urticaria
  • CContact dermatitis
  • DUrticarial vasculitis
Reveal answer & full explanation
Correct answer: B — Acute urticaria
  • AErythema multiforme
  • BAcute urticaria✓
  • CContact dermatitis
  • DUrticarial vasculitis

Why Acute urticaria is correct

  • Transient, migratory, intensely pruritic wheals in which each individual lesion lasts under 24 hours and resolves with completely normal skin in between is the classic, defining presentation of urticaria; a course under 6 weeks makes it acute.
  • The lesions fade without residual purpura, scarring, or pigment change, and the patient lacks systemic involvement (no fever, arthralgia, mucosal lesions, or airway symptoms).
  • A linear wheal produced by stroking the skin is dermographism, the most common physical (inducible) urticaria, further supporting mast cell-mediated hives.

Why the others are wrong

  • Urticarial vasculitis produces wheal-like lesions that persist beyond 24 hours, burn or hurt rather than itch, and leave residual purpura or hyperpigmentation, with leukocytoclastic vasculitis on biopsy; her fleeting, cleanly resolving lesions argue against it.
  • Erythema multiforme produces fixed target lesions with a dusky center, often with mucosal involvement and an HSV or drug trigger; the lesions last days rather than hours and do not migrate.
  • Contact dermatitis is an eczematous, often vesicular eruption confined to the site of allergen contact with a delayed, persistent course, not transient migratory wheals appearing across the trunk and arms.
Question 2DermatologyMedium
A 34-year-old woman has had daily itchy hives for the past 4 months. Individual wheals are raised, pink, and migratory, each fading within several hours and leaving completely normal skin behind. She has no fever, joint pain, or residual bruising, and no identifiable food or drug trigger. Past history includes Hashimoto thyroiditis, and TPO antibodies are elevated. A diagnosis of chronic spontaneous urticaria is made. Which of the following best explains the findings?
  • AImmune complex deposition driving leukocytoclastic vasculitis of dermal vessels
  • BIgE-mediated sensitization to a recently ingested dietary food allergen
  • CBradykinin accumulation from deficient C1 esterase inhibitor activity
  • DIgG autoantibodies cross-link the high-affinity IgE receptor on mast cells
Reveal answer & full explanation
Correct answer: D — IgG autoantibodies cross-link the high-affinity IgE receptor on mast cells
  • AImmune complex deposition driving leukocytoclastic vasculitis of dermal vessels
  • BIgE-mediated sensitization to a recently ingested dietary food allergen
  • CBradykinin accumulation from deficient C1 esterase inhibitor activity
  • DIgG autoantibodies cross-link the high-affinity IgE receptor on mast cells✓

Why IgG autoantibodies cross-link the high-affinity IgE receptor on mast cells is correct

  • Chronic spontaneous urticaria (CSU) is largely a non-IgE immunologic process: in roughly a third of patients, IgG autoantibodies target the alpha subunit of the high-affinity IgE receptor (FcεRI) or target IgE itself, cross-linking the receptor and driving mast cell and basophil degranulation.
  • Released histamine, leukotrienes, and prostaglandins cause vasodilation, increased capillary permeability, and plasma extravasation into the dermis, producing transient pruritic wheals with normal skin between flares.
  • The association with autoimmune thyroid disease (Hashimoto, elevated TPO antibodies) and the absence of an external IgE trigger fit this autoimmune CSU mechanism. Per EAACI/AAAAI guidance, management starts with second-generation H1 antihistamines, up-titrated to as much as 4x dose, with omalizumab (anti-IgE) as the preferred add-on.

Why the others are wrong

  • Bradykinin accumulation from deficient C1 esterase inhibitor activity — this is the mechanism of hereditary angioedema, which causes angioedema WITHOUT urticaria/wheals and is unresponsive to antihistamines; this patient has classic itchy wheals.
  • IgE-mediated sensitization to a recently ingested dietary food allergen — true IgE food allergy causes acute urticaria minutes to hours after a specific exposure, not daily wheals for months with no identifiable trigger.
  • Immune complex deposition driving leukocytoclastic vasculitis of dermal vessels — urticarial vasculitis produces lesions that last more than 24 hours, burn rather than itch, and leave residual purpura/pigmentation; here each wheal fades within hours and leaves normal skin.
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Risk factors

  • Acute: viral infections (most common in children), foods (peanuts, tree nuts, shellfish, eggs, dairy, soy), medications (NSAIDs, antibiotics, opioids, contrast media), insect stings, latex
  • Chronic spontaneous: autoimmune disease (thyroid disease in 25%, ANA positive in ~30%, autoimmune antibodies against FcεRI or IgE), atopic disease, stress
  • Chronic inducible: physical triggers (cold, heat, pressure, vibration, sun, water, exercise, cholinergic)
  • Drugs: NSAIDs, ACE inhibitors (angioedema without urticaria — bradykinin-mediated), opioids (direct mast cell activation)

Pathophysiology

Mast cell and basophil degranulation releases histamine, leukotrienes, prostaglandins, cytokines → vasodilation, increased capillary permeability, plasma extravasation into dermis (wheal) or deeper tissue (angioedema). Triggers: IgE-mediated (food/drug allergy), non-IgE immunologic (autoantibodies in CSU), direct mast cell activators (opioids, contrast), complement-mediated (urticarial vasculitis, hereditary angioedema), pseudoallergic (NSAIDs via COX-1 inhibition).

Clinical presentation

Symptoms

  • Intense pruritus (rarely burning or stinging)
  • Sudden onset of wheals lasting minutes to <24 hours each, fluctuating in location
  • Angioedema: face (lips, eyelids), hands, feet, genitalia, larynx — may compromise airway
  • Systemic symptoms (anaphylaxis): dyspnea, wheezing, syncope, GI distress — IM EPINEPHRINE

Signs / physical exam

  • Wheals: well-circumscribed raised pink or pale-centered plaques with surrounding flare; size mm to >10 cm; round, oval, polycyclic, annular; resolve without scarring or pigment change
  • Dermographism: linear wheal where skin is stroked — most common physical urticaria
  • Cholinergic urticaria: small (1-3 mm) wheals with surrounding flare after exercise, hot showers, emotional stress
  • Cold urticaria: wheal/angioedema in areas of cold contact; positive ice cube test
  • Angioedema: deeper, often asymmetric, non-pitting swelling of face, lips, tongue, extremities; LESS pruritic, more burning/painful

Classic findings

Transient migratory pruritic wheals lasting <24 hours each, with completely normal skin between.

Differential diagnosis

  • Urticarial vasculitis — Individual lesions >24 hours, painful/burning rather than itchy, residual purpura/pigmentation; biopsy = leukocytoclastic vasculitis; check complement, ANA, SSA, hep C
  • Erythema multiforme — Target lesions, dusky center, fixed >24 hours, mucosal involvement; HSV or drug trigger
  • Mastocytosis / mastocytoma — Persistent reddish-brown macules/papules with Darier sign (urticate on stroking); elevated tryptase
  • Hereditary angioedema (HAE) — Angioedema WITHOUT urticaria, family history, recurrent abdominal pain attacks, low C4 and C1-INH levels
  • ACE-inhibitor angioedema — Angioedema without urticaria, often facial/tongue, days to years after starting ACEi
  • Anaphylaxis — Urticaria + 1 more system: respiratory, hypotension, GI; rapid onset; epinephrine
  • Atopic dermatitis — Chronic eczematous lesions, lichenification, flexural; not transient
  • Contact urticaria — Wheals at site of contact with latex, food, plants; immediate or delayed

Diagnostic workup

Diagnostic criteria

Clinical: characteristic wheals lasting <24 hours each, total episode duration determines acute vs chronic; angioedema without urticaria requires HAE/ACEi workup.

Labs

  • Acute urticaria: usually no workup needed unless trigger unclear — careful history identifies most triggers (foods, drugs, infections)
  • Chronic spontaneous urticaria: limited testing per international guidelines — CBC with differential, CRP/ESR, TSH/free T4 and TPO antibodies (screen autoimmune thyroid)
  • If suspicion of urticarial vasculitis: skin biopsy, C3/C4, ANA, RF, hepatitis B/C, complement profile
  • If suspicion of hereditary angioedema: C4 (low during AND between attacks), C1-INH level and function, C1q
  • Autologous serum skin test or basophil activation test for autoimmune CSU (research/specialty)
  • Specific IgE / skin prick testing only for clinically suspected food/drug allergy with consistent history

Imaging

  • Not indicated

Diagnostic algorithm

flowchart TD
  A[Itchy wheal,<br/>each lasting <24 h] --> B{Duration of episode}
  B -->|<6 weeks| C[Acute urticaria]
  B -->|≥6 weeks| D[Chronic urticaria]
  C --> E[Identify trigger:<br/>infection, food, drug]
  D --> F[Limited workup: CBC, CRP, TSH, TPO Ab]
  E --> G[2nd-gen H1 antihistamine<br/>± short prednisone course]
  F --> G
  G --> H{Controlled in 2-4 wks?}
  H -->|No| I[Up-titrate H1 antihistamine<br/>to 4x dose]
  I --> J{Controlled?}
  J -->|No| K[Add omalizumab<br/>or cyclosporine]
  A --> L{Wheal lasts<br/>>24 h, painful,<br/>leaves purpura?}
  L -->|Yes| M[Urticarial vasculitis<br/>Biopsy + autoimmune workup]
  A --> N{Angioedema<br/>without wheals?}
  N -->|Yes| O[Check C4, C1-INH<br/>ACEi history → Hereditary AE or ACEi reaction]
Urticaria evaluation and step-care management algorithm.

Treatment

First-line

  • Identify and avoid trigger (when identified)
  • Step 1: second-generation non-sedating H1 antihistamine at standard dose — cetirizine 10 mg, levocetirizine 5 mg, fexofenadine 180 mg, loratadine 10 mg, desloratadine 5 mg, bilastine 20 mg daily
  • Step 2 (inadequate response after 2-4 weeks): up-titrate H1 antihistamine to 2-4x standard daily dose (EAACI/AAAAI guidelines)
  • Step 3: add omalizumab 300 mg SC every 4 weeks (anti-IgE biologic) — highly effective for CSU; alternatively trial cyclosporine 2-5 mg/kg/day
  • Step 4: cyclosporine or other immunomodulator (mycophenolate, dapsone)
  • Acute severe urticaria with angioedema: short course oral prednisone 0.5-1 mg/kg/day × 5-7 days (avoid long-term use)
  • Anaphylaxis or laryngeal angioedema: IM epinephrine 0.3-0.5 mg adult / 0.01 mg/kg pediatric in anterolateral thigh — first-line; airway, IV fluids, H1+H2 blockers, steroids as adjuncts

Chronic inducible (physical) urticaria

  • Identify trigger and avoid (cold, pressure, heat, sun, vibration)
  • Cold urticaria — cetirizine 4x daily, omalizumab, rupatadine; carry EpiPen
  • Cholinergic urticaria — antihistamines, avoid extreme exertion/heat
  • Solar urticaria — sun avoidance, broad-spectrum SPF 50+, antihistamines, phototherapy desensitization

Hereditary angioedema

  • Acute: IV C1 esterase inhibitor concentrate, ecallantide, icatibant
  • Prophylaxis: lanadelumab, berotralstat, attenuated androgens (danazol; rarely used now)
  • NOT responsive to antihistamines, epinephrine, or steroids

ACEi-induced angioedema

  • Discontinue ACE inhibitor permanently (cross-reactivity with ARBs ~10% — avoid if possible)
  • Supportive care; refractory cases may respond to icatibant

Second-line / adjunct

  • Avoid first-generation sedating antihistamines (diphenhydramine, hydroxyzine) as routine therapy — sedation, anticholinergic effects, and short half-life make them inferior to second-generation agents
  • H2 antagonist (famotidine) addition has modest benefit
  • Leukotriene receptor antagonist (montelukast) sometimes added, especially for NSAID-sensitive patients
  • Counsel: most chronic urticaria resolves within 1-5 years

Complications

  • Anaphylaxis with airway compromise — life-threatening
  • Sleep disturbance, decreased quality of life, depression, work/school impairment
  • Adverse effects from chronic systemic corticosteroids (avoid if possible)
  • Misdiagnosis as drug allergy → unnecessary medication restriction

PANCE pearls

  • Individual wheals lasting >24 hours, painful rather than itchy, with residual purpura = urticarial vasculitis — biopsy.
  • Angioedema WITHOUT urticaria → think hereditary angioedema or ACE inhibitor reaction; antihistamines and steroids do NOT work.
  • Up-titration of second-generation H1 antihistamines to 4x dose is safe, evidence-based, and recommended BEFORE adding other agents.
  • Omalizumab is the most effective add-on for chronic spontaneous urticaria refractory to high-dose antihistamines.
  • Acute urticaria + respiratory or hemodynamic symptoms = anaphylaxis = IM epinephrine FIRST, not antihistamines.

References

  • EAACI/GA²LEN/EDF/WAO 2022 — International EAACI/GA²LEN/EuroGuiDerm/APAAACI Guideline for the Definition, Classification, Diagnosis and Management of Urticaria (Zuberbier et al., Allergy 2022)
  • AAAAI/ACAAI 2014 — Practice Parameter Update: Chronic Urticaria (Bernstein et al., J Allergy Clin Immunol 2014)
  • WAO 2020 — World Allergy Organization Anaphylaxis Guidance 2020 (Cardona et al., World Allergy Organ J 2020)

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Acne VulgarisRosaceaAtopic Dermatitis (Eczema)Allergic and Irritant Contact DermatitisSeborrheic DermatitisPsoriasisLichen PlanusPityriasis RoseaTinea Infections (corporis, capitis, pedis, cruris, versicolor)Cutaneous CandidiasisScabiesPediculosisImpetigoHerpes Zoster (Shingles)

Differentials & related conditions

Erythema Multiforme

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