Management of Acute Urticaria

Dr. Paschal Madueke

Dermatology Unit,
Internal Medicine,
University of Benin Teaching Hospital
OUTLINE

• Background
• Epidemiology
• Classification
• Triggers
• Pathophysiology
• Presentation
• Investigations
• Prognosis
• Treatment
• References
BACKGROUND

• Urticaria is a common
disease with many different
clinical presentations.
• Dates back to the 18th
century, when the stinging
and burning was likened to
the sting of a nettle. Nettle plant (Urtica)
BACKGROUND

• Urticaria (hives, wheals, welts) is a hypersensitivity reaction

that may occur in isolation or associated with angio-edema
and/or anaphylaxis.
• Not contagious unless swollen hives contain a pathogen
• Mostly Benign but could progress to anaphylaxis and
angioedema
URTICARIA EXAMPLE
• Smooth
• Raised
• Well-cirmcumscribed
• Pruritic
• Erythematous
• Blanches with pressure
• 20 dermal oedema
• Erupts spontaneously,
persists for 2-24hrs, before
fading to leave normal
BACKGROUND

• Widespread Urticaria

Image Source: Dermatological society

EPIDERMIOLOGY

• Quite common
• Overall lifetime prevalence of 10-25%

• May occur at any age

• Chronic urticaria is more common in the 4th and 5th decades

of life
• No notable variation in race
EPIDEMIOLOGY

• A study on the Clinical Characteristics of Urticaria among

5360 Nigerians at LASUTH Dermatology clinic revealed:
• 1.76% of patients were diagnosed of Urticaria within a period
of 2 years
• 45.1% Males, 54.9% Females (ratio of 1.12)
• Majority had Chronic Urticaria (71.95%)

[Akinkugbe et al]
CLASSIFICATION

• A large variety of Urticaria variants exist

• May be persistent or episodic

• Spontaneous (“Ordinary”) Urticaria

– Acute (duration <6wks)

– Chronic (duration >6wks)

CLASSIFICATION

• Inducible Urticaria (Including physical urticaria)

– Mechanical: dermographism, delayed pressure urticaria
– Thermal: cold or heat induced

– Cholinergic: sweating or physical exertion (exercise-induced

anaphylaxis)
– Solar and Aquagenic urticaria

– Contact Urticaria (Immunologic or non-immunologic)

• Angioedema without wheals (Heriditary angioedema)

TRIGGERS

• The aetiologic agent is more likely to be identified in acute

urticaria (40-60%) than in chronic urticaria (10-20%).
• About 60% of Acute Generalized Urticaria is undertermined
TRIGGERS

• Known Triggers of Acute Urticaria:

– Infections (URTI, GIT infections, UTIs, fungal infections, malaria,
amebiasis, hepatitis, mononucleosis, HIV, parasitic infections, etc.)
– Caterpillars and moths
– Foods (shellfish, eggs, cheese, chocolate, nuts, berries, tomatoes)
– Drugs (penicillins. sulfonamides, salicylates, NAIDS, codeines,
antihistamines)
– Environmental agents (pollens, chemicals, plants, dust, mold)
– Latex exposure
– Others: undue skin pressure, cold, heat, exercise, emotional stress,
pregnancy, blood transfusion.
TRIGGERS

• Causes of chronic Urticaria includes triggers of acute urticaria

plus:
– Autoimmune disorders (SLE, RA, Polymyositis, thyroid
autoimmunity)
– Cholinergic (emotional stress, exercise, heat)
– Chronic medical illnesses (hypothyroidism,
hyperthyroidism, polycythemia vera, malignant neoplasms,
lymphoma)
– Mastocytosis
– Cold urticaria
PATHOPHYSIOLOGY
Pathophysiology

• May be Immunological or non-immunological but the end

result is the same
• Mast cell and basophil degranulation in the dermis results in
the release of:
– histamine
– bradykinin
– leukotriene C4
– Prostaglandin D2
– Pro-inflammatory cytokines
– Complement 5a
PATHOPHYSIOLOGY

• These substances cause extravasation of fluid into the

dermis, leading to the urticarial lesion.
• The pruritus in urticaria is as a result of the histamine
released into the dermis.
• The H1 and H2 histamine receptors play synergistic roles in
urticaria.
Pathophysiology

• H1 receptor - Increased capillary permeability of the

endothelial and smooth muscle cells
• H2 receptor - arteriolar and venule vasodilation
• This causes infiltration of

• Complex mechanisms bring about this process (Type 1

allergic IgE/IgG, Type 2 allergic response by cytotoxic T cells,
and Type 3 immune-complexes; SLE).
PATHOPHYSIOLOGY

• An autoimmune origin is one hypothesis for mast cell

activation.
• IgE- and IgG-dependent mechanisms form autoantibodies
– IgG autoantibodies to the alpha subunit of the Fc receptor
of the IgE molecule (35-40% of patients with chronic
urticaria).
– Less commonly, anti-IgE autoantibodies (5-10% of patients
with chronic urticaria)
– Both of which can activate mast cells and basophils to
release histamine (Auto-allergens)
Pathophysiology
Presentation

• Medical History
– Exclude precipitants (pressure, sun, heat, cold)
– How long does it take the urticaria to appear? (Dermographic
patients may notice wheals appear immediately wheals appear
immediately when the skin is rubbed/scratched, and lasts <1hr)
– Hx of itching, burning, pain
– How long does the marks last? (Delayed pressure urticaria may last
>72hrs as well as urticarial vasculitis)
– Hx of allergens; latex, foods like fish, eggs, nuts.
– Does the skin appear normal when the urticaria fades? (Urticarial
vasculitis will leave a bruising)
– Hx of wheezing and angioedema: lip and throat swelling
Presentation

• Hx of medications (salicylates, NSAIDS, ACEIs)

• Hx of symptoms suggesting underlying systemic disease
(fever, arthralgia, myalgia, diarrhea, weight loss)
• Family history of urticaria?
Physical Examination

• Smooth
• Erythematous
• Blanching
• Dermographism
• Does skin look normal after urticaria has faded?
• Swollen lips and tongues
• Assess patient using the urticarial activity score (A scoring
system used to follow-up and monitor urticaria; sum scores
over 4-7 days to monitor)
Physical Examination

Dermographism
Urticaria Activity Scoring

Score Wheals Itch

0 None None
1 Mild (<20 wheals/24hrs) Mild
2 Moderate (21-50 wheals/24hrs) Moderate
3 Intense or severe (>50 Intense or Severe
wheals/24hrs or large confluent
area of wheals)
Investigations

• Investigations are rarely necessary to diagnose Acute

urticaria if a careful history and detailed physical examination
is carried out to reveal the characteristic lesion.
• Specific Investigations
– Skin-prick testing or specific IgE quantification (if imediate reactions
are suspected eg. exposure to latex, food).
• Baseline (To exclude chronic urticaria and reassure patient):
– FBC (eosinophilia - helminthic infection)
– CRP/ESR (May be elevated esp. in Heriditary Fever Syndromes)
– TFT and Thyroid auto-antibodies
Investigations

• Others:
– Plasma or urinary histamine level
– Total Tryptase level (Marker of mast cell degranulation)
– Skin biopsy to rule out urticarial vasculitis (Confirmatory)
Differential Diagnoses

• Allergic contact dermatitis

• Atopic dermatitis
• Urticarial Vasculitis
• Drug eruptions
• Erythema multiforme
• Henoch Schonlein purpura (IgA Vasculitis)
• Scabies
• Pytiriasis Rosea
Prognosis

• Acute Urticaria can be controlled although it can persist for

some time (Good prognosis).
• Persists for 2-24hrs before fading to normal skin even without
treatment.
• May progress to anaphylactic shock and angioedema
• Scratching of the lesion may leave escoriation marks
• 50% of patients with chronic urticaria are clear within 6
months
• Urticaria with angio-oedema may persist for years.
TREATMENT
TREATMENT

• General Measures:
– Reasurrance
– Assess and monitor persistent disease using the UAS
– Counsel to minimize aggravating factors and triggers
– Advice dermographic patients not to scratch
– Minimize exposure to exacerbating drugs
– Prescribe a topical anti-pruritic agent eg. calamine lotion or
aqueous cream with 1% menthol
– Patient education
TREATMENT

• Specific Measures:
– Non-sedating H1 anti-histamine eg. Cetrizine, fexofenadine,
loratidine or rupatidine (40% of patients respond to this alone)
– Sedating H1 anti-histamine eg. chlorpheniramine 4-12mg,
hydroxyzine 10-50mg is useful at night, warn patient about feeling
drowsy in the morning, avoid if driving.
– H2 anti-histamine may be helpful eg. ranitidine
– Anti-leukotriene may also be helpful eg. montelukast 10mg.
– Systemic corticosteroids are usually effective when antihistamines
are not adequate (a low daily dose or alternate day)
• NB: long-term systemic corticosteroids are not recommended
TREATMENT

• Combined therapy: immunosuppressive agent (eg,

omalizumab, methotrexate,cysclosporin) may be required
• In Life-threatening Conditions (A/E):
– Anaphylactic shock, laryngeal oedema, hoarseness, stridor - IM
epinephrine 0.3-0.5mg
– Bronchospasm - Nebulized salbutamol, albuterol
TREATMENT
Conclusion

• Urticaria is a vascular reaction of the skin characterized by

wheals.
• It is Acute or chronic. Acute urticaria involves periodic
outbreaks of urticarial lesions that resolves in 6 wks
• Oral H1 anti-histamines are first line treatment for acute and
chronic urticaria
• 1st generation H1 anti-histamines can cause sedation
• Presence of systemic symptoms suggests the possibility of
chronic urticaria or urticarial vasculitis.
• Most acute urticaria will resolve on it’s own within 24hrs
References

• Habif clinical dermatology 7th edition

• Oxford Handbook of Dermatology: 2nd Edition, Chapter
11, Urticaria and Erythema pp 228-232
• Medscape: Urticaria Treatment & Management
• Thankiyouu!