UrticariaMANAGEMENT

SYSTEMIC AND MISCELLANEOUS PRESENTATIONS · 12 SECTIONS

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734 items

☷ Legend

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Cardiovascular Presentations71▾

Respiratory Presentations52▾

Neurological Presentations83▾

Gastrointestinal Presentations74▾

Genitourinary and Reproductive Presentations48▾

Infectious Disease Presentations148▾

Trauma Presentations89▾

Toxicologic Presentations80▾

Psychiatric Presentations26▾

Musculoskeletal and Rheumatologic Presentations96▾

Dermatology Presentations23▾

Environmental and Exposure Presentations27▾

Hematologic and Oncologic Presentations36▾

Pediatric-Specific Presentations19▾

Endocrine and Metabolic Presentations45▾

ENT and Maxillofacial Presentations27▾

Ophthalmologic Presentations19▾

Obstetric Presentations23▾

Systemic and Miscellaneous Presentations17▾

Allergic Transfusion Reaction Anaphylaxis Angioedema Benedikt's Syndrome Cannabis-induced hyperemesis Eczema (acute flare)Gradenigo's Syndrome Horner's Syndrome (Acute)Huntington's Disease (Acute Presentation)Kanavel's Signs Lemierre's Syndrome Procedural sedation Radiation exposure Retained products of conception Sever's Disease Urticaria Venous air embolism

01Approach to the Critical Patient/attcp44

Anaphylaxis recognition and exclusion

›Immediate anaphylaxis screen

›Urticaria plus systemic involvement

›Hypotension (SBP < 90 mmHg)

›Bronchospasm or stridor

›Laryngeal or oropharyngeal edema

›GI symptoms with urticaria

›Abdominal pain

›Vomiting or diarrhea

›Neurological involvement

›Lightheadedness or syncope

›Loss of consciousness

›If anaphylaxis not excluded, treat as anaphylaxis

›Epinephrine 0.3–0.5 mg IM anterolateral thigh (1:1000 solution)

›Repeat every 5–15 minutes if inadequate response

›No absolute contraindications in anaphylaxis

›Supine position with legs elevated

›Unless respiratory distress or vomiting

›IV access and fluid resuscitation

›0.9% NaCl 1–2 L bolus for hypotension

Airway threat assessment

›Airway compromise triggers

›Lingual or laryngeal angioedema

›Hoarseness or voice change

›Stridor on inspiration

›Oropharyngeal swelling progression

›Progressive dysphagia

›Drooling

02History/hx88

Symptom characterization

›Urticarial lesion features

›Onset timing and acuity

›Acute urticaria less than 6 weeks

›Chronic urticaria 6 weeks or more

›Individual wheal duration

›Less than 24 hours is typical of urticaria

›Greater than 24 hours with residual skin change suggests vasculitis

›Lesion quality

›Pruritic (typical of histamine-mediated)

›Burning pain rather than itch (suggests vasculitis)

›Distribution

›Localized vs generalized

›Pressure-exposed areas (physical urticaria)

›Angioedema features

›Location

›Lip, tongue, eyelid, genital

›Laryngeal or glottic involvement

›Onset speed

›Rapid onset suggests IgE-mediated

›Slower onset over hours suggests bradykinin-mediated

›Absence of wheals with isolated angioedema

›Suggests hereditary angioedema or ACE inhibitor-induced

Trigger identification

›Food triggers

›Common IgE-mediated foods

›Tree nuts and peanuts

›Shellfish and fish

›Eggs and dairy

›Temporal relationship

›Ingestion within 2 hours of reaction onset

›Histamine-rich foods

›Aged cheese, cured meats, fermented foods, alcohol

›Medication triggers

›NSAIDs and aspirin

›Present in up to 30% of chronic urticaria exacerbations

›Mechanism via prostaglandin E2 suppression (non-IgE)

›ACE inhibitors

›Bradykinin-mediated angioedema (not histamine-mediated)

›Discontinue and observe for 6 weeks

›Beta-lactam antibiotics

›Most common drug-induced trigger in children

›Opioids and vancomycin

›Direct mast cell degranulation (non-IgE mediated)

›Physical triggers

›Dermographism (pressure)

›Cold exposure (cold urticaria)

›Heat or exercise (cholinergic urticaria)

›Solar exposure (solar urticaria)

›Infectious triggers

›Viral URIs

›Most common trigger in children (up to 23%)

›H. pylori

›Hepatitis B or C

›UTI or GI infection

Alarm features in history

›Anaphylaxis symptom screen

›Dyspnea, wheezing, stridor

›Abdominal pain, vomiting, diarrhea

›Lightheadedness, syncope, palpitations

›Throat tightness or voice change

›Vasculitis clues

›Wheals lasting more than 24 hours

›Burning pain rather than pruritus

›Residual ecchymosis or hyperpigmentation

›Fever and arthralgias

›Systemic disease clues

›Fever, night sweats, weight loss (lymphoma)

›Joint pain, uveitis (autoimmune disease)

›Cold intolerance, fatigue (hypothyroidism)

Risk factors and background history

›Atopic history

›Asthma

›Allergic rhinitis

›Eczema

›Prior episodes

›Previous urticaria or angioedema

›Known triggers identified

›Prior epinephrine auto-injector use

›Autoimmune comorbidities

›Autoimmune thyroiditis (most common autoimmune comorbidity)

›SLE, Sjögren syndrome, rheumatoid arthritis

›Celiac disease

›Family history

›Hereditary angioedema (autosomal dominant, types 1–3)

›Cryopyrin-associated periodic syndrome (CAPS)

›Atopic disease in family

›Occupational and social exposures

›Latex exposure

›Chemical occupational exposure

›Travel history (parasitic infections)

›Hepatitis or HIV risk factors

03Physical Exam/exam59

Skin and lesion assessment

›Urticarial lesion characteristics

›Raised, erythematous wheals

›Blanching on diascopy (distinguishes from purpura)

›Sizes ranging from mm to cm

›Distribution mapping

›Localized vs generalized

›Dermatome or pressure pattern

›Residual skin changes

›Ecchymosis or hyperpigmentation (vasculitis marker)

›No residual change expected with typical urticaria

›Angioedema assessment

›Non-pitting swelling in dermis and subcutaneous tissue

›Lip, periorbital, tongue, genital sites

›Asymmetric distribution common

›Darier sign

›Stroking lesion produces urtication (mastocytosis marker)

›Dermographism test

›Firm stroking of skin produces linear wheal

›Simple dermographism (mechanical stimulus only)

Airway and upper respiratory exam

›Oropharyngeal inspection

›Tongue and uvular swelling

›Uvular angioedema as early laryngeal predictor

›Floor of mouth induration

›Drooling (inability to swallow secretions)

›Muffled voice or hot-potato voice

›Neck assessment

04Differential Diagnosis/ddx50

Life-threatening diagnoses

›Anaphylaxis

›ICD-10 T78.2 (anaphylactic shock, unspecified)

›Urticaria plus hypotension, bronchospasm, or GI symptoms

›Must be excluded in every ED presentation

›Angioedema with airway compromise

›ICD-10 T78.3 (angioneurotic edema)

›Laryngeal or glottic involvement

›ACE inhibitor-induced or hereditary angioedema variants

›Stevens-Johnson syndrome / TEN

›ICD-10 L51.1 / L51.2

›Painful non-pruritic rash with mucosal involvement

›Cannot-miss drug reaction differential

Urticaria mimics

›Urticarial vasculitis

›ICD-10 L95.1

›Wheals lasting greater than 24 hours

›Burning pain, residual ecchymosis

›Biopsy shows leukocytoclastic vasculitis

›Erythema multiforme

›ICD-10 L51.0

›Fixed target lesions (non-migratory)

›Post-infectious (HSV) or drug-related

›Bullous pemphigoid

›ICD-10 L12.0

›Urticarial prodrome before blistering

›Predominantly older adults

›Contact dermatitis

05Laboratory Tests/lt53

Emergency and acute workup

›Allergy and mast cell markers

›Serum tryptase

›Elevated within 1–3 hours of anaphylaxis (peak 30–60 min)

›Sensitivity 36–68% for anaphylaxis

›Useful to confirm retrospective anaphylaxis diagnosis

›Draw within 1–3 hours of onset for best yield

›Baseline tryptase for suspected mastocytosis

›Greater than 20 mcg/L suggests systemic mastocytosis

›Acute urticaria labs (selective use)

›Complete blood count

›Eosinophilia suggesting parasitic or drug reaction

›Leukocytosis suggesting infectious trigger

›Comprehensive metabolic panel

›Renal and hepatic function if systemic symptoms

›Glucose for metabolic context

Chronic urticaria workup (outpatient, not acute ED)

›Thyroid screening

›TSH

›Autoimmune thyroiditis is the most common autoimmune comorbidity

›Anti-TPO antibodies if TSH abnormal

›Anti-thyroid peroxidase (anti-TPO)

›Positive in subset of chronic spontaneous urticaria

›Does not change acute management

›Inflammatory and autoimmune markers

›ESR and CRP

›Elevated in vasculitis and systemic inflammation

›Markedly elevated ESR supports urticarial vasculitis

06Diagnostic Tests/dt56

Scoring Systems

›Urticaria Activity Score (UAS7)

›Weekly urticaria severity assessment

›Number of wheals per day (0–3)

›Pruritus intensity per day (0–3)

›Maximum score 42 over 7 days

›Score greater than 16 indicates moderate-severe disease

›Used for chronic spontaneous urticaria monitoring

›Guides step-up therapy decisions

›Not designed for acute ED use

›Urticaria Control Test (UCT)

›4-question validated patient-reported outcome

›Score range 0–16

›Score less than 12 indicates poor disease control

›Used to titrate chronic urticaria therapy

›Angioedema Activity Score (AAS)

›Angioedema severity and frequency tracking

›7-day recall period

›Useful for hereditary angioedema monitoring

›Anaphylaxis severity grading (Ring and Messmer classification)

›Grade I: Cutaneous symptoms only

›Grade II: Mild multi-organ involvement

›Grade III: Life-threatening anaphylaxis

›Grade IV: Cardiac/respiratory arrest

MRI

›MRI role in urticaria

›Not indicated for routine urticaria evaluation

›No established role in acute or chronic urticaria workup

07Disposition/dispo41

Admission criteria

›Indications for hospital admission

›Anaphylaxis requiring epinephrine or hemodynamic support

›Incomplete resolution after two doses of epinephrine

›Persistent hypotension or bronchospasm

›Airway-compromising angioedema

›Laryngeal, glottic, or lingual edema

›Threatened or established airway compromise

›Refractory urticaria with ongoing systemic symptoms

›Symptoms not responding to ED antihistamine therapy

›Concern for serious underlying etiology

›Suspected urticarial vasculitis with systemic involvement

›Serum sickness with hemodynamic instability

Observation criteria

›Indications for observation (4–8 hours)

›Post-anaphylaxis monitoring

›Minimum 4–6 hours after epinephrine administration

›Biphasic anaphylaxis risk within 8 hours

›Longer observation for severe initial reactions

›Angioedema involving face, neck, or oropharynx

›Good response to treatment but progression risk

›Reassess airway at 1–2 hour intervals

Discharge criteria

›Safe discharge requirements

›Isolated urticaria without systemic symptoms

›No angioedema involving airway

›No hemodynamic instability

›Symptoms improving or resolved with antihistamines

08Treatment/t107

Anaphylaxis management

›First-line anaphylaxis treatment

›Epinephrine IM anterolateral thigh

›Adults: 0.3–0.5 mg (1:1000 solution)

›Repeat every 5–15 minutes as needed

›Auto-injector equivalent: 0.3 mg adult, 0.15 mg pediatric

›IV fluid resuscitation

›0.9% NaCl 1–2 L IV bolus for hypotension

›Repeat 500 mL boluses as needed for hemodynamic response

›Supplemental oxygen

›High-flow oxygen for bronchospasm or hypoxemia

›Target SpO2 greater than 94%

›Second-line adjuncts (anaphylaxis)

›Diphenhydramine IV 25–50 mg

›Adjunct only; does not treat core anaphylaxis

›Not a substitute for epinephrine

›Ranitidine IV 50 mg or famotidine IV 20 mg (H2 blocker)

›Additive to H1 blocker in anaphylaxis

›Limited evidence but low risk

›Methylprednisolone IV 125 mg

›Reduces biphasic reaction risk (evidence conflicting)

›May blunt late-phase inflammation

›Bronchodilator therapy

›Salbutamol (albuterol) 2.5 mg nebulized for bronchospasm

›Repeat every 20 minutes as needed

Acute urticaria pharmacotherapy

›First-line: Second-generation H1 antihistamines

›Cetirizine 10 mg oral once daily

›Minimal sedation at standard doses

›Onset 1 hour

›Loratadine 10 mg oral once daily

›Non-sedating

›Preferred for driving and occupational safety

›Fexofenadine 180 mg oral once daily

›Non-sedating

›No cardiac effects

›Levocetirizine 5 mg oral once daily

›Active enantiomer of cetirizine

›AFP first-line recommendation

›Adjunct in acute setting

›Diphenhydramine 25–50 mg oral or IV (first-generation H1)

›Significant sedation limits outpatient use

›Suitable for acute ED symptom relief

›Avoid as sole long-term agent

›H2 blocker addition (ranitidine or famotidine)

›Additive effect when combined with H1 blockers

›Limited evidence but low-risk adjunct

›Short-course corticosteroids for acute refractory urticaria

›Prednisone 40–50 mg oral daily for 3–5 days

›Evidence of benefit is conflicting (RCT data mixed)

›Reduces symptom burden and recurrence at 1 week

›Not recommended for chronic urticaria long-term

›Methylprednisolone IV for severe refractory cases

›125 mg IV single dose in ED setting

›Transition to oral prednisone on discharge

Chronic spontaneous urticaria stepwise management

›Step 1: Standard-dose second-generation H1 antihistamine

›Cetirizine, loratadine, fexofenadine, or levocetirizine once daily

›Daily dosing preferred over PRN for best control

›Reassess at 2–4 weeks

›Step 2: Up-titrate H1 antihistamine (up to 4x standard dose)

›Cetirizine up to 40 mg daily

›Off-label but supported by EAACI/GA2LEN/EDF/WAO guideline

›Monitor for sedation at higher doses

›Reassess symptom control with UCT score

›Step 3: Adjunct agents

›Leukotriene receptor antagonist

›Montelukast 10 mg oral once daily

›Evidence conflicting; may benefit NSAID-exacerbated urticaria

›H2 blocker addition

›Ranitidine 150 mg twice daily or famotidine 20 mg twice daily

›Additive with H1 blockers; evidence limited

›Hydroxyzine or doxepin at bedtime for nocturnal symptoms

›Hydroxyzine 25–50 mg at bedtime

›Doxepin 10–25 mg at bedtime (tricyclic with potent H1 activity)

›Step 4: Omalizumab for antihistamine-refractory CSU

›Omalizumab 300 mg SC every 4 weeks

›FDA-approved for chronic spontaneous urticaria 12 years and older

›Response typically within 4–8 weeks

›JAMA 2024 review: most effective add-on therapy

›Class I recommendation for refractory CSU

›Observe 30–60 minutes post-injection for anaphylaxis

›Rare but reported

›Step 5: Immunosuppressive therapy (specialist-initiated)

›Cyclosporine 3 mg/kg/day oral for omalizumab-refractory cases

›Off-label use

›Monitor blood pressure and renal function

›Maximum 5 mg/kg/day

›Other immunosuppressants (mycophenolate, dapsone) second-line

Hereditary angioedema acute attack treatment

›HAE-specific therapy (antihistamines ineffective)

›C1 esterase inhibitor concentrate IV

›Berinert 20 units/kg IV for acute attacks

›Onset within 30–60 minutes

›Icatibant 30 mg SC

›Bradykinin B2 receptor antagonist

›Single dose; repeat in 6 hours if inadequate response

›Tranexamic acid oral (if specific HAE therapy unavailable)

›Antifibrinolytic; limited acute efficacy

›Do NOT administer epinephrine, antihistamines, or corticosteroids as primary therapy

›May provide temporary relief but do not treat mechanism

Non-pharmacologic management

›Trigger avoidance counseling

›NSAIDs and aspirin avoidance

›Substitute acetaminophen for analgesia

›Alcohol avoidance (histamine-releasing effect)

›Tight-fitting clothing avoidance (physical urticaria)

›Excessive heat and stress minimization

›Contraindicated treatments

›Topical antihistamines (not effective for urticaria)

›Topical corticosteroids (not effective for urticaria)

›Long-term systemic corticosteroids for chronic urticaria (AFP guideline)

09Special Populations/sp89

Pregnancy

›Urticaria in pregnancy overview

›Prevalence and mechanisms

›Hormonal shifts alter immune regulation in pregnancy

›Increased susceptibility to IgE-mediated reactions

›Pruritic urticarial papules and plaques of pregnancy (PUPPP) is a specific pregnancy dermatosis

›Differential diagnosis in pregnancy

›PUPPP vs. allergic urticaria (PUPPP appears late third trimester, periumbilical)

›Pemphigoid gestationis (rare, autoimmune)

›Intrahepatic cholestasis of pregnancy (pruritus without wheals)

›Antihistamine safety in pregnancy

›First-line: Loratadine or cetirizine

›Preferred based on reassuring safety data

›Category B equivalent (no established teratogenicity)

›Chlorpheniramine as alternative (older safety data available)

›Avoid fexofenadine in first trimester (limited data)

›Diphenhydramine acceptable in second trimester

›Avoid near term (neonatal withdrawal risk)

›Corticosteroid use in pregnancy

›Short course prednisone acceptable for severe acute urticaria

›Use lowest effective dose and shortest duration

›Cleft palate risk is theoretical; benefit-risk favors use for severe disease

›Anaphylaxis in pregnancy

›Epinephrine is NOT contraindicated in pregnancy

›Maternal hemodynamic stability is fetal priority

›IM epinephrine 0.3 mg as in non-pregnant adults

›Fetal monitoring recommended after severe anaphylaxis

›Obstetrics consultation

Geriatric

›Urticaria in older adults overview

›Differential diagnosis considerations

›Bullous pemphigoid urticarial prodrome more common in elderly

›Drug reactions more frequent (polypharmacy)

›ACE inhibitor-induced angioedema risk increased with age

›Antihistamine safety in older adults

›Avoid first-generation antihistamines (diphenhydramine, hydroxyzine)

›Anticholinergic burden increases fall risk

›Cognitive impairment and delirium risk (Beers Criteria)

›Urinary retention risk in men with prostatic hypertrophy

›Preferred agents: Loratadine, cetirizine, fexofenadine

›Low anticholinergic burden

›Cetirizine: mild sedation at higher doses, use 5 mg starting dose

›Reduce dosing for renal impairment

›Cetirizine 5 mg daily if eGFR less than 30 mL/min

›Levocetirizine 2.5 mg every other day if eGFR 10–30 mL/min

›Omalizumab in older adults

›Effective and generally well-tolerated

›No dose adjustment required for age alone

›Monitor for injection-site reactions

›Anaphylaxis considerations in older adults

›Attenuated tachycardia response due to beta-blockade or autonomic dysfunction

›Glucagon 1–5 mg IV if beta-blocker blunts epinephrine response

›Higher risk of cardiovascular complications during anaphylaxis

›Kounis syndrome (coronary vasospasm)

›ECG monitoring indicated

Pediatrics

›Urticaria in children overview

›Epidemiology

›Most common urticaria trigger in children is viral URI (up to 23%)

›Beta-lactam antibiotics are the most common drug trigger

›Food-induced urticaria more common in younger children

›Acute urticaria dominates in pediatric population

›Chronic urticaria less common than adults

›Most pediatric cases are acute and self-limited

›Antihistamine dosing in children

›Cetirizine

›6 months to 2 years: 2.5 mg once daily

›2–5 years: 2.5 mg once or twice daily (max 5 mg/day)

›6 years and older: 5–10 mg once daily

›Loratadine

›2–5 years: 5 mg once daily

›6 years and older: 10 mg once daily

›Fexofenadine

›6–11 years: 30 mg twice daily

›12 years and older: 180 mg once daily

›Diphenhydramine

›1–12 years: 1.25 mg/kg per dose every 4–6 hours (max 25 mg/dose)

›12 years and older: 25–50 mg every 4–6 hours

›Anaphylaxis in children

›Epinephrine auto-injector dosing

›15–30 kg: 0.15 mg (EpiPen Jr)

›Greater than 30 kg: 0.3 mg (EpiPen)

›IM epinephrine 0.01 mg/kg (1:1000 solution), max 0.5 mg

›Omalizumab in children

›Approved for chronic spontaneous urticaria 12 years and older

›300 mg SC every 4 weeks

›Ages 6–11 years: off-label use; specialist decision

›Pediatric-specific considerations

›Avoid first-generation antihistamines in young children when possible

›Paradoxical excitation in children under 2 years

›Stool ova and parasites if eosinophilia present

›Parasitic infections are a trigger in endemic areas

10Background/b86

Epidemiology

›Prevalence and incidence

›Lifetime prevalence of urticaria: approximately 20% of the general population

›Acute urticaria affects up to 15–20% of the population at least once

›Chronic spontaneous urticaria prevalence 0.5–1% globally

›Global burden

›BMC Public Health 2025: urticaria burden increased 1990–2021

›Younger age groups carry the highest disease burden

›Environmental risk factors include air pollution (ozone, particulates)

›Sex distribution

›Female predominance, especially for chronic spontaneous urticaria

›Estimated female-to-male ratio 2:1 for CSU

›Classification

›Acute urticaria: less than 6 weeks duration

›Chronic urticaria: 6 weeks or more

›Chronic spontaneous urticaria (CSU): no identifiable external trigger

›Chronic inducible urticaria: reproducible physical trigger

›80–90% of chronic urticaria cases are idiopathic (chronic spontaneous)

›AFP 2026 guideline data

›Etiology breakdown (acute)

›Infections most common in children (viral URIs up to 23%)

›Drug reactions major cause in adults

›Food allergy cause in 10–15% of acute urticaria cases

›No cause identified in up to 50% of acute cases

Pathophysiology

›Core mechanism: mast cell activation

›Histamine release from dermal mast cells

›Causes vasodilation and increased vascular permeability

›Produces erythema, edema (wheal), and pruritus (flare)

›IgE-mediated type I hypersensitivity

›Antigen crosslinks IgE on mast cell surface

›Immediate degranulation within minutes

›Late-phase reaction (eosinophil/basophil) at 2–8 hours

›Non-IgE-mediated mast cell degranulation

›Direct mast cell activation (opioids, vancomycin, radiocontrast)

›Complement activation (transfusion reactions)

›NSAIDs: prostaglandin E2 suppression shifts toward leukotriene production

›Angioedema pathophysiology

›Histamine-mediated angioedema

›Deeper dermal and subcutaneous mast cell activation

›Co-occurs with urticaria in ~50% of cases

›Responds to antihistamines

›Bradykinin-mediated angioedema

›ACE inhibitor-induced: bradykinin accumulation from ACE inhibition

›Hereditary angioedema (HAE): C1 esterase inhibitor deficiency

›Does NOT respond to antihistamines, epinephrine, or corticosteroids

›Autoimmune mechanisms in chronic spontaneous urticaria

›Type IIb autoimmune: IgG autoantibodies against IgE or FcεRI receptor

›Activates mast cells and basophils independently of IgE

›Elevated IgE levels in subset of CSU patients

›JAMA 2024 review: IgE pathobiology supports omalizumab mechanism

›Thyroid autoantibodies (anti-TPO) associated with subset of CSU

›Mechanism unclear; euthyroid patients can still have reactive urticaria

Therapeutic Considerations

›Antihistamine pharmacology

›Second-generation H1 antihistamines are first-line

›Minimal CNS penetration and sedation at standard doses

›Inverse agonists at H1 receptor (not simply competitive antagonists)

›Continuous dosing more effective than PRN use (NEJM 2022)

›Dose escalation rationale

›Up to 4x standard dose used in CSU (EAACI/GA2LEN/EDF/WAO guideline)

›Higher H1 receptor occupancy achieved at supranormal doses

›H2 receptor role

›H2 receptors present on skin vasculature

›Additive vasodilation blockade when H2 combined with H1 blockers

›Omalizumab mechanism and evidence

›Anti-IgE monoclonal antibody

›Binds free IgE preventing mast cell and basophil activation

›Reduces FcεRI receptor density on mast cells

›JAMA 2024 (Kolkhir et al.): CSU comprehensive review

›Omalizumab 300 mg q4 weeks most effective for refractory CSU

›Class I recommendation for antihistamine-refractory CSU

›Response assessment

›Complete response in 40–60% of patients

›Partial response in additional 20%

›Non-responders may have HAE overlap or alternative diagnosis

›Corticosteroid limitations

›Short courses acceptable for acute refractory urticaria

›Prednisone 40–50 mg for 3–5 days (evidence conflicting per ACEP)

›RCT (American Journal of Emergency Medicine 2021) did not show benefit of adding IV corticosteroids to antihistamines in acute urticaria

›Long-term use contraindicated in chronic urticaria

›Adrenal suppression, metabolic consequences

›AFP guideline recommendation

›Natural history and prognosis

›Acute urticaria: most cases resolve within days to weeks

›Spontaneous resolution without specific trigger identified in majority

›Chronic urticaria remission rates

›Approximately 50% achieve remission within 1–5 years (NEJM 2022)

›Disease may wax and wane over years

11Patient Discharge Instructions/pdi31

copy discharge instructions

›Discharge instructions for Urticaria (Hives)

›What you have been diagnosed with

›Urticaria (hives) is a skin condition causing raised, itchy, red welts

›Individual welts usually disappear within 24 hours but new ones may appear

›Most cases of acute hives are temporary and resolve on their own within days to weeks

›Your medications

›Take your antihistamine tablet every day as prescribed, not just when hives appear

›Taking it daily gives better control than waiting until symptoms start

›If you were given a steroid tablet (prednisone), take it with food and complete the full course

›What to avoid

›Avoid ibuprofen, naproxen, aspirin, and other NSAID pain relievers — use acetaminophen (Tylenol) instead

›Avoid alcohol (may worsen hives)

›Avoid tight-fitting clothing and excessive heat

›Avoid any food or substance you suspect triggered this episode

›Follow-up instructions

›See your family doctor within 1–2 weeks if hives persist

›If you have had hives for more than 6 weeks, a more detailed allergy workup is needed

›If you received an epinephrine auto-injector prescription, fill it today and carry it at all times

›Photograph your skin lesions on your phone when they appear — they may be gone by the time you see a doctor

›Return to the emergency department immediately if you experience

›Difficulty breathing, wheezing, or throat tightness

›Swelling of the tongue, lips, or throat

›Feeling faint, dizzy, or losing consciousness

›Chest pain or rapid heartbeat with hives

›Abdominal pain, vomiting, or diarrhea with hives

›Hives that rapidly spread despite antihistamines

›Worsening hives after epinephrine auto-injector use (call 911)

12References/r30

Guidelines and key sources

›Primary clinical guidelines

›Semenya AM, Pienkowski S, Bhatnagar P. Acute and Chronic Urticaria: Evaluation and Treatment. American Family Physician. 2026.

›Primary clinical management reference for this document

›PMID 41839072

›Zuberbier T, et al. EAACI/GA2LEN/EDF/WAO Guideline for the Definition, Classification, Diagnosis and Management of Urticaria. Allergy. 2018.

›International consensus guideline

›Dose escalation of H1 antihistamines and omalizumab recommendation

›Bernstein JA, Lang DM, Khan DA, et al. The Diagnosis and Management of Acute and Chronic Urticaria: 2014 Update. Journal of Allergy and Clinical Immunology. 2014.

›US-focused management guideline

›Key review articles

›Kolkhir P, Bonnekoh H, Metz M, Maurer M. Chronic Spontaneous Urticaria: A Review. JAMA. 2024.

›Comprehensive CSU review including omalizumab evidence

›Lang DM. Chronic Urticaria. New England Journal of Medicine. 2022.

›Natural history, prognosis, and stepwise therapy

›Yosipovitch G, Maderal AD, Elman SA. Chronic Spontaneous Urticaria. JAMA Dermatology. 2025.

›Updated clinical review

›Marzano AV, et al. Urticarial Vasculitis. Journal of Allergy and Clinical Immunology. 2022.

›Differential diagnosis and biopsy criteria

›Pediatric and special population references

›Bezirganoglu H, et al. The common triggers of urticaria in children admitted to the pediatric emergency room. Pediatric Dermatology. 2022.

›Pediatric trigger data and beta-lactam association

›Foley G. Urticaria. Clinical Guide to Paediatrics. 2022.

›Pediatric clinical framework

›Trial and epidemiology data

›Palungwachira P, et al. A Randomized Controlled Trial of Adding Intravenous Corticosteroids to H1 Antihistamines in Patients With Acute Urticaria. American Journal of Emergency Medicine. 2021.

›IV corticosteroid adjunct RCT; no significant benefit demonstrated

›Tan S, Chen Z, Lin T. Global, Regional, and National Burden of Urticaria (1990-2021). BMC Public Health. 2025.

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Evidence & Review

Reviewed by SymptomDx Medical Team · Last reviewed August 18, 2026

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