Urticaria And Angio-Edema: Health Significance To The Skin And Its Clinical Presentations
Acute Pressure Urticaria
A General Clinical Overview
The urticarias are transient, localized, itchy swelling of the skin. They start suddenly as erythematous patches which become raised and the center fades as the edema develops in the dermis. Generally, they subside in a few hours but rarely, they persist longer than 48 hours. Angio-edema is the term used to denote the same process occurring in the subcutaneous tissues. This leads to deep swellings which often affect the eyelids, lips, and tongue. They cause a burning sensation or pain. Angio edema and urticaria often coexist, although each may occur separately.
Common precipitating agents:
- Drugs: Aspirin, other antirheumatic drugs, penicillin, other antibiotics, plasma or blood products and prophylactic sera.
- Foods: Eggs, fish, meat, chocolate, vegetables, cheese, nuts etc
- Inhaled allegens: Pollens, fungal, particles, animal hairs, house dust etc, which show seasonal variation.
- Physical stimuli: Friction of clothes, exercise, sweating, cold, sunlight, pressure, heat, water. The term cholinergic unrticaria is given to those urticarias provoked by exercise or sweating.
- Infections: Helminthic parasites, fungal infections (superficial mycosis and candidiasis), bacterial infections, infectious mononucleosis, and other viral infections.
- Insect bites: Bees, wasps, mosquitoes and other blood sucking insects, bed bugs, fleas etc.
- Psychogenic factors: Frustration and emotional stress.
- Physical urticarias: These are urticarias in which physical factors such as friction, cold or sunlight trigger the rash.
In many cases, the patient may not be aware of the causative agent. A physical urticaria is more probable, if individual lesions disappear within 30 minutes of withdrawal of the causative agent. Provocative tests are available to determine the causative factors. Lesions in areas exposed to light are diagnostic of solar urticaria.
In some cases, a positive family history of urticaria, angio-edema, or suddent death may be forthcoming. In familial cases, the disease manifests from childhood with urticaria, edema glottis or abdominal pain. Some of these cases show deficiency of C1 esterase inhibitor.
The lesions start as rapidly developing raised erythematous, well demarcated wheals. Which are severely pruritic. The lesion may start discretely in several areas and become confluent, or may remain localized. At times, the lesions may be linear. The center becomes pale as the margins extend. Later, the whole part may become uniformly swollen, warm, indurated and erythematous- the sharp margins fading away. The erythema fades on pressure. Purpura and arthralgia develop in some cases.
Angio-edema occurring in locations such as the tongue, pharynx or larynx leads to rapid respiratory obstruction and unless this is relieved, asphyxia and death may follow. In some cases, the patient may go into shock.
© 2014 Funom Theophilus Makama