Contact Dermatitis - treatment, symptoms and cause of Contact Dermatitis

Contact dermatitis is an inflammatory process in skin caused by an exogenous agent or agents that directly or indirectly injure the skin. This injury may be caused by an inherent characteristic of a compound irritant contact dermatitis (ICD). An example of ICD would be dermatitis induced by a concentrated acid or base. Agents that cause allergic contact dermatitis (ACD) induce an antigen-specific immune response. The clinical lesions of contact dermatitis may be acute (wet and edematous) or chronic (dry, thickened, and scaly), depending on the persistence of the insult. The most common presentation of contact dermatitis is hand eczema, and it is frequently related to occupational exposures. Occupation-related contact dermatitis represents a significant proportion of occupation-induced injury, affecting over 60,000 persons annually.

ICD is generally strictly demarcated and often localized to areas of thin skin (eyelids, intertriginous areas) or to areas where the irritant was occluded. Lesions may range from minimal skin erythema to areas of marked edema, vesicles, and ulcers. Chronic low-grade irritant dermatitis is the most common type of ICD and the most common area of involvement is the hands (see below). The most common irritants encountered are chronic wet work, soaps, and detergents. Treatment should be directed to avoidance of irritants and use of protective gloves or clothing.

ACD is a manifestation of delayed type hypersensitivity mediated by memory T lymphocytes in the skin. The most common cause of ACD is exposure to plants, specifically to members of the family Anacardiaceae; including the genera Toxicodendrun, Anacardium, Gluta, Mangifera, and Semecarpus. Poison ivy, poison oak, and poison sumac are members of the genus Toxicodendron and cause an allergic reaction marked by erythema, vesiculation, and severe pruritus. The eruption is often linear, corresponding to areas where plants have touched the skin. However, other allergens may be more difficult to identify, especially if the exposure is chronic and the skin becomes thickened and scaly. The sensitizing antigen common to these plants is urushiol, an oleoresin containing the active ingredient pentadecylcatechol. The oleoresin may adhere to skin, clothing, tools, and pets, and contaminated articles may cause dermatitis even after prolonged storage. Blister fluid does not contain urushiol and is not capable of inducing skin eruption in exposed subjects.

Treatment of Contact dermatitis

If ACD is suspected and an offending agent is identified and removed, the eruption will resolve. Usually, treatment with high-potency fluorinated topical glucocorticoids is enough to relieve symptoms while the ACD runs its course. For those patients who require systemic therapy, a tapering course over 2 to 3 weeks given as single morning doses is the preferred method.

Identification of a contact allergen can be a difficult and time-consuming task. Patients with dermatitis unresponsive to conventional therapy or with an unusual and patterned distribution should be suspected of having ACD. They should be questioned carefully regarding occupational exposures, topical medicaments, and oral medications. Common sensitizers include preservatives in topical preparations, nickel sulfate, potassium dichromate, thimerosal in ocular preparations, neomycin sulfate, fragrances, formaldehyde, and rubber-curing agents. Patch testing is helpful in identifying these agents, but should not be attempted on patients with widespread active dermatitis or on those taking systemic glucocorticoids.