Contact Dermatitis

ICD is a nonspecific inflammatory reaction to toxic substances contacting the skin. Numerous substances can irritate the skin, including

Properties of the irritant (eg, extreme pH, solubility in the lipid film on skin), environment (eg, low humidity, high temperature, high friction), and patient (eg, very young or old) influence the likelihood of developing ICD. ICD often can be divided into categories:

Occupational ICD is ICD caused by one or more of the many possible work-related skin irritants. It can be acute, chronic, or cumulative.

Atopic disorders increase risk of ICD because of impaired skin barrier function and lower threshold for skin irritation.

Phototoxic dermatitis ( see Chemical photosensitivity Chemical photosensitivity ) is a variant in which a topical (eg, perfumes, coal tar) or ingested (eg, psoralens) agent becomes a skin toxin only after exposure to ultraviolet light, most typically long-wave ultraviolet light (UVA). Phototoxic dermatitis, therefore, occurs only in UV-exposed skin, typically with a sharp demarcation.

ACD is a type IV, T-cell–mediated, delayed-type hypersensitivity reaction to an environmental allergen that has 2 phases:

In the sensitization phase, allergens are captured by Langerhans cells (dendritic epidermal cells). When activated by innate immunity cascades, these cells migrate to regional lymph nodes, where they process and present the antigen to naive, antigen-specific T cells. When a naive T cell recognizes its antigen via binding to its T-cell receptor, it expands clonally and differentiates into memory/effector T cells. The sensitization phase, which is asymptomatic, may be brief (6 to 10 days for strong sensitizers such as poison ivy) or prolonged (years for weak sensitizers such as sunscreens, fragrances, and glucocorticoids). During differentiation, sensitized T cells become able to express cutaneous homing antigens (eg, cutaneous lymphocyte antigens) that enable them to migrate from cutaneous capillaries to the epidermis. When antigen-presenting cells present the antigen to the sensitized T cells, the T cells can expand and trigger an inflammatory reaction at that location (elicitation phase of ACD), resulting in the characteristic symptoms and signs of ACD.

Multiple allergens can cause ACD (see table Causes of Allergic Contact Dermatitis Causes of Allergic Contact Dermatitis ). Nickel sulfate is the most common contact allergen in most populations. The Toxicodendron species of plant (eg, poison ivy, poison oak, poison sumac) accounts for a large percentage of ACD, including moderate and severe cases. The offending allergen is urushiol.

Photoallergic contact dermatitis is a variant of ACD, in which a substance becomes sensitizing only after it undergoes structural change triggered by ultraviolet light. Reactions may extend to non–sun-exposed skin. Typical causes include fragrances (eg, musk ambrette, sandalwood), nonsteroidal anti-inflammatory drugs, and sunscreen filters.

Acute ICD is more painful than pruritic. Signs range from erythema, scaling, and edema to erosions, crusting, and blistering. Chronic and cumulative ICD is more often pruritic.

ACD is more pruritic than painful. Skin changes range from erythema, scaling, and edema, through vesiculation to severe swelling with bullae. Changes often occur in a pattern, distribution, or combination that suggests a specific exposure, such as linear streaking on an arm or leg (eg, due to brushing against poison ivy) or circumferential erythema (under a wristwatch or waistband). Linear streaks are almost always indicative of an external allergen or irritant.

The site of contact is where the allergen contacted the skin, very often the hands, because they touch so many substances. Although the palms and the palmar sides of the fingers are most exposed, ACD often starts in the web spaces between fingers because the thick stratum corneum prevents or delays allergen penetration on the palms and palmar sides of the fingers (also on the soles). With airborne exposure (eg, perfume aerosols), areas not covered by clothing are predominantly affected. Although ACD is typically limited to the site of contact, it may later spread because of scratching and autoeczematization (id reaction, a dermatitis at sites remote from the site of the initial inflammatory problem or infection). Because of the time needed to recruit and expand T cells in the epidermis, ACD typically takes ≥ 1 day after exposure to become noticeable and takes 2 to 3 days to become further aggravated (crescendo reaction). (In contrast, ICD typically decreases in intensity [decrescendo reaction] after 1 or 2 days.)