URTICARIA (HIVES)

Dr. Gazi Asma Sultana

Associate Professor & Head of the Dept.
Department of Deramtology & Venereology
Tairunnessa Memorial Medical College and Hospital
 INTRODUCTION

• Urticaria is extremely common.

• It is estimated that approximately 15%-25% of the population experiences on

urticarial illness at some time in their life.

Of these up to

- 40% experience urticarial alone

- 10% angioedema alone

- 50% have both urticarial and angioedema

 DEFINITION

• Urticaria is vascular reaction of the skin characterized by the appearance of the

wheals, white or red evanescent plaques, generally surrounded by a red halo or

flare and associated with severe itching, stinging or pricking sensation.

• The eruption may also consists of macular erythema or papules and may be

localized or generalized, the latters being the more common. The eruption

usually favors the covered areas, such as trunks, buttocks or chest.

 DEFINITION (Cont.)

• Subcutaneous swelling (angioedema) especially of eyelids or lips may

accompany the wheals or occurs alone. Angioedema any target the GIT or

respiratory tract, resulting in abdominal pain, coryza, asthma and respiratory

problems. Respiratory tract involvement can produce airway obstructioin.

CLASSIFICATIONS
 According to duration

• Acute Urticaria – Producing evanescent wheals that individually rarely lasts

more than 12 Hrs, with complete resolution of the urticaria with in 6 weeks of

onset. More likely to have an identifiable trigger.

• Chronic Urticaria – Daily episodes of urticaria and or angioedema lasting

more than 6 weeks is designated as chronic urticaria which predominantly

affects adults and is twice as common in women as in men. Less likely to have

an identifiable trigger
 According to Pathogenesis
• Immunologic urticaria
- IgE depended (Type I hypersensitivity) e.g specific antigen sensitivities
of physical urticaria.
- Complement mediated (Serum sickness urticarial vasculitis)
• Nonimmunologic urticaria
- Direct (Produce by mast cell degranulation) e.g opiates, radiocontrast
dye
- Indirect (Aspirin and other NSAIDS)
 According to cause

• Idiopathic urticaria – More than 75% of chronic urticaria is idiopathic.

• Physical urticaria – Includes dermatographic, cold , heat, cholinergic,

aquagenic, solar, vibratory and exercise induced.

EM like
 Etiologic Factors
Drugs, Food, Infections are the most common.

• Drugs – Are probably the most common causes of urticaria and angioedema.
Penicillin and related antibiotics are the most frequent offenders.

• Aspirin – Aspirin exacerbates chronic urticaria in at least 30% of patients.

Aspirin, Salicylates, NSAIDS, Opiates, X-ray contrast media and ACE-inhibitors
commonly cause urticaria by non immunogenic mechanisms.
Patients may have the triad of allergic rhinitis or asthma,
episodes of food induced anaphylaxis and increased frequency of sensitivity to
aspirin and other NSAIDS.
 Etiologic Factors (Cont.)

• Food – Foods are a frequent cause of acute urticaria, whereas in chronic

urticaria food is a less frequent factor. The most allergic foods are chocolate,

shellfish, nuts, peanuts, tomatoes, strawberries, melons, pork, cheese, garlic,

onions and spices. Eggs and milk cause urticaria in children.

[Non allergic foods – Lamb, beef, rice, potato, carrots, string beans, peas,

squash, apple sauce, tapioca, preserved pears, peaches or cherries, Ry-krisp

crackers, butter, sugar, tea with out milk or lemon and coffee with out cream]
 Etiologic Factors (Cont.)

• Food additives – Natural food additives include yeast, salicylates,

citric acid, egg and fish albumin. Synthetic additives the most
important of which are azo dye, benzoic acid derivatives and penicillin.

[Yeast containing foods are- bread and bread stuffs, sausages, wine,
beer, grapes, cheese, vinegar, pickled foods, katchup.

Food containing azo dyes and benzoic acid include candy, soft drinks,
jelly, marmalade, custards, puddings, various cakes and pancake mixes,
mayonnaise, ready made salad dressings]
 Etiologic Factors (Cont.)

• Infections - The possibility of localized infection in the tonsils, a tooth,

sinuses, gallbladder, prostate, bladder or kidney should be considered as a
possible cause in case of acute or chronic urticaria

• Emotional stress

• Menthol – Mentholated cigarettes, candy & mint, cough drops, aerosol sprays
and topical medications are among these.

• Neoplasms – Urticaria has been associated with carcinomas and Hodgkin’s

diseases.
 Etiologic Factors (Cont.)

• Inhalants – Grass pollens, house dust mites, feathers, formaldehyde, acrolein

(produced when frying with lard or by smoking cigarettes containing glycerin as

a hygroscopic agent), castor bean or soyabean dust, cooked lentils, cotton

seed, animal dander, cosmetics, aerosols, pyrethrum, orris and molds have

been known to cause urticaria.

 Etiologic Factors (Cont.)

• Viruses – Hepatitis B and Hepatitis C may cause urticaria.

• Parasites – Many of the helminthic infestations may cause urticaria.

• Alcohol
 Pathophysiology of Urticaria
Non-immunologic factors Immunologic factors

Chemical histamine liberators Types II and III

Alternative
eg. Opiates, polymyxin antibiotics, complement
complement
thiamine activation
pathway action

Anaphylatoxins (C3a, C5a) Type I IgE

Physical agents, e.g.
mediated
cold, heat, sunlight

genetic factors

modulating factors
released mediators
endogenous (particularly histamine)
Cholinergic hormone

vasodilating Small blood

factors vessel
vasodilation

URTICARIA
 PATHOGENESIS
1st exposure to an antigen

IgE antibody production with in 1-3 weeks

IgE antibody binds firmly by the Fc region to basophil and mast cells

Individuals are sensitized or primed to that particular antigen

 PATHOGENESIS (Cont.)
Re exposure of sensitized individual with same allergen

Allergens bind with IgE

Cross linkage of adjacent IgE antibody

Activation of mast cells with release of mediators

 PATHOGENESIS (Cont.)
o Mediators released from must cells after activations-
• Primary or preformed mediators
- Histamin
- Adenosin
- Eosinophil Chemotactic Factor
- Neutrophil Chemotactic Factor
- Enzymes
- Heparin
• Secondary or newly synthesized mediators
- Leukotrians
- PGD2
- Platelet Activating Factors.
 Diagnosis

• Detailed history
• including has pt ever had urticaria before
• were there any unusual exposures immediately prior to the
episode
• Does the patient have pictures?
• Physical Exam
• If the patient does not have lesions at time of
exam, consider showing them photos of urticaria as
an example
 Diagnosis (cont)
• Laboratory testing – Acute Urticaria
• Allergy testing if specific trigger can be implicated (would possibly include
skin prick testing or immunocap testing for IgE to specific food or drug)

• Laboratory testing – Chronic Urticaria*

• CBCD
• UA
• ESR
• LFTs

*These results are often normal so there is no clear consensus that these must
be done
 TREATMENT
• Acute urticaria
- Antihistamines
• Chronic urticaria
- Antihistamines (Long acting)
*1/3rd cases of Chronic idiopathic urticaria –
- Plasmapheresis
- I/V immunoglobin
- Cyclosporin
Angioedema
 Characteristics

• Similar process to urticaria

• Occurs deeper in subcutaneous tissue

• “Swelling” due to extravastation of fluid into tissues from vasodilators

• Typically seen in areas with little connective tissue such as lips, face, mouth,
uvula and genitalia

• Can occur in bowel wall which manifests as colicky abdominal pain

 Characteristics (cont)

• Rapid onset (typically minutes to hours)

• Often asymmetric in distribution

• Often in non-gravitationally dependent areas such as lips, mouth, face, tongue

• Can be associated with urticaria, sometimes with allergic reaction or part of

anaphylaxis, or may occur in isolation

*Can be life-threatening if associated with airway compromise

 Hereditary Angioedema

• Usually presents in second decade of life

• May be seen in younger children or even into 30’s

• Edema can be present in different organs and can alter presentation:

• Tongue – most serious as can cause obstruction

• Face
• Trunk
• Genitals
• GI track – can resemble SBO and have pt go for emergent surgery
• Extremities

• Attacks usually last 2-5 days

 Hereditary Angioedema

• aka Quincke’s Edema

• NO PRURITIS OR URTICARIA, + PAIN

• Low C4, C1, C1q, C2 levels

• Low or dysfunctional plasma C1 esterase inhibitor protein.

• 25% of deaths from laryngeal edema

• Tx of choice: fresh frozen plasma, stanazol, tranexamic acid

 Acquired Angioedema

• Symptoms same as HA, but NO family history.

• Usually occurs at night, pt wakes up with it.

• Acute evanescent circumscribed edema

• Affects most distensible tissues: eyelids, lips, earlobes, genitalia, mouth, tongue,
larynx.

• Swelling is subcutaneous, not dermal.

• Overlying skin is not affected.

 Hospital Treatments – Acute Episode
What treatments should be given?
• C-1-esterase inhibitor if available
• FFP – should be second line treatment today
• Carries same risk as blood transfusion
• Intubation precautions
• Volume support
• On discharge
• Start prophylaxis ideally with C-1-esterase inhibitor
• Refer to allergy/immunology for care
• Confirm with repeat C-4, C-1-esterase inhibitor level and functional
assay.
 Thank you
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