Urticaria

Urticaria (hives)

Dr Sami Aldaham

Goals and Objectives

• You have to be able to
  • Describe the morphology of urticaria
  • Distinguish between acute and chronic urticaria

Urticaria

• Urticaria (hives) is a vascular reaction of the skin characterized by wheals surrounded by a red halo or flare (area of erythema)
  • Cardinal symptom is PRURITUS (itch)
  • Urticaria = pruritus
  • Urticaria is caused by swelling of the upper dermis
  • Up to 20% of the population experience urticaria at some point in their lives

Angioedema

• Angioedema can be caused by the same pathogenic mechanisms as urticaria

• The pathology is in the deep dermis and subcutaneous tissue and swelling is the major manifestation

• Angioedema commonly affects the face or a portion of an extremity

• Involvement of the lips, cheeks, and periorbital areas is common, but angioedema also may affect the tongue, pharynx, larynx and bowels.

• May be painful or burning, but not pruritic

• May last several days

Examples of Urticaria

Example of Angioedema

Urticaria & Angioedema

• Urticaria and angioedema may occur in any location together or individually.
• Angioedema and/or urticaria may be the cutaneous presentation of anaphylaxis, so assessment of the respiratory and cardiovascular systems is vital.

Clinical Findings

• Lesions typically appear over the course of minutes, enlarge, and then disappear within hours
• Individual wheals rarely last >12hrs
• Surrounding erythema will blanch with pressure

Clinical Classification

• Acute urticaria = new onset urticaria < 6 weeks
• Chronic urticaria = recurrent urticaria (most days) > 6 weeks

Common Causes of Acute Urticaria

1. Idiopathic
2. Food reactions: Shellfish, nuts, fruit
3. Infections: Upper respiratory, streptococcal infections, helminthes
4. Drug reactions
5. IV administration
6. Blood products, contrast agents

Etiology of Chronic Urticaria

1. Idiopathic: over 50% of chronic urticaria RR
2. Physical urticarias: many patients with chronic urticaria have physical factors that contribute to their urticaria
   • These factors include pressure, cold, heat, water (aquagenic), sunlight (solar), vibration, and exercise
   • Cholinergic urticaria is triggered by heat and emotion
   • The diagnosis of pure physical urticaria is made when the sole cause of a patient’s urticaria is a physical factor
3. Chronic autoimmune: possibly a third or more of patients with chronic urticaria
4. Other: infections, ingestions, medications

Dermatographism

• Most common form of physical urticaria
• Sharply localized
• edema or wheal
• within seconds to minutes after the skin has been rubbed

#ospe

Pathophysiology

• Immunologic mediated urticaria
• The mast cell is the major effector cell in urticaria
• Non – immunologic mediated urticaria

1- Immunologic Urticaria

• Antigen binds to IgE on the mast cell ⇒
• Mast cell degranulation ⇒
• histamine releasing ⇒
• Histamine binds to H1 and H2 receptors to cause arteriolar dilatation ⇒
• venous constriction ⇒
• increased capillary permeability.

2- Non-Immunologic Urticaria: Not dependent on the binding of IgE receptors

• Some drugs (aspirin) ⇒
• Unknown: pharmacologic mechanism ⇒
• Affect the arachidonic acid metabolism ⇒
• release of histamine from mast cells.

3- Physical stimuli

• Physical stimuli
• direct mast cell degranulation
• Induced histamine release

DIAGNOSIS

1. Urticaria is a clinical diagnosis

2. A detailed history and physical exam should be performed

3. Many times patients will not present with urticaria during their clinic visit

4. show patients photographs of urticaria and ask if their lesions appear similar

5. Ask patients to take photos of their lesions / bring them to their office visit

Allergy Testing

• Allergy testing is not routinely performed in patients with chronic urticaria.

• Skin prick testing may reveal sensitivities to a variety of allergens that may not be .relevant to the patient’s urticaria

Natural History and Prognosis

• In most patients, chronic urticaria is an episodic and self-limited disorder

• Average duration of disease is two to five years

• Symptoms of chronic urticaria can be severe and impair the patient’s quality of life (QOL)

Treatment

Antihistamines

Oral H1 antihistamines are the first-line treatment for acute and chronic urticaria

1. First-generation H1 antihistamines are less well-tolerated due to sedation used also in atopic dermatitis

2. Second-generation H1 long acting antihistamines are well tolerated with fewer sedative and anticholinergic effects

The following are examples of H₁ antihistamines: 1st Generation

• Diphenhydramine (OTC)
• Hydroxyzine (Rx,generic)
• Chlorpheniramine (OTC)

2nd Generation

• Cetirizine (OTC)
• Loratadine (OTC)
• Fexofenadine (OTC)

Referral to Dermatologist and indication of skin biopsy

Biopsy should be performed in patients with one or more of the following features:

• Individual lesions that persist beyond 48 hours, are painful rather than pruritic, or have accompanying petechial characteristics
• Systemic symptoms
• Lack of response to antihistamines
• Lesions that leave pigmentation changes upon resolution

Take Home Points

1. Urticaria (hives) is a vascular reaction of the skin characterized by wheals surrounded by a red halo or flare.
2. Urticaria is classified as acute or chronic. Acute urticaria is defined as periodic outbreaks of urticarial lesions that resolve within six weeks.
3. Over 50% of chronic urticaria is idiopathic.
4. Oral H1 antihistamines are first-line treatment for acute and chronic urticaria.
5. 1st generation H1 antihistamines can cause sedation.
6. The presence of systemic symptoms should signal the possibility that an urticarial rash is not ordinary urticaria.

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Urticaria

Characteristics and Causes

• Time to onset: immediate, accelerated (hours), or delayed (days).
• Type I hypersensitivity reactions: antibiotics (cephalosporins, and sulfonamides), local anesthetics, radiocontrast media, blood products, and gamma globulin.
• Non-immune urticaria: radiocontrast media and long-acting ACE-inhibitors (due to changes in vascular response to bradykinin).
• Mast cell degranulation by non-IgE mechanisms: opiate analgesics, anesthetic muscle relaxants, and Vancomycin (Red Man Syndrome, which can be worsened by concommitant opiate use).