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for signs of overuse, including atrophy and striae, is important while
managing this chronic condition.

FIGURE 65.4 Dyshidrotic eczema. (Reprinted with permission from Craft N, Taylor E,
Tumeh PC, et al. VisualDx: Essential Adult Dermatology . Philadelphia, PA: Lippincott
Williams & Wilkins; 2010.)


FIGURE 65.5 Contact dermatitis from a softball glove. Note the striking distribution of
the dermatitis with a sharp cut-off on the third and fourth fingers corresponding to
where the fingers contacted the inside of the glove.

Contact Dermatitis
Contact dermatitis is an inflammatory reaction of the skin caused by an
allergen (allergic contact dermatitis) or a primary irritant (irritant contact
dermatitis). Acute eruptions have intense pruritus, severe erythema, edema,
vesicles, and erosions with serous discharge and crusting ( Fig. 65.5 ). A
specific distribution with a sharp demarcation between involved and
unaffected skin may be a clue to this diagnosis. Subacute reactions have
mild erythema, dry scale, less vesiculation, and mild thickening of the skin.
Chronic exposures may result in lichenification, fissures, scales,
excoriations, and hyperpigmentation. Itching, distribution, and the surface
changes described above are key components that can help differentiate
acute contact dermatitis from acute skin infections such as cellulitis.
Treatment of contact dermatitis includes avoidance of allergens or
irritants and use of thick emollients and topical corticosteroids when
needed. When oral corticosteroids are needed for severe or widespread


contact dermatitis, a longer treatment course with a slow taper over 14 days
will decrease the risk for rebound dermatitis.

Allergic Contact Dermatitis
Allergic contact dermatitis is caused by a classic delayed T-cell–mediated
hypersensitivity reaction (type IV). Repeated exposure causes an allergic
sensitization. The eruption is delayed after the initial exposure for up to 7 to
10 days. Repeated exposures can cause the rapid appearance of an acute
dermatitis (within 12 to 24 hours). Rhus dermatitis, caused by an oleoresin
in the sap of poison ivy, poison oak, or poison sumac plants, is the most
common cause of allergic contact dermatitis in the United States. Delayed
exposure may occur because of contact with objects that have had contact
with the plants (e.g., shoe laces, dogs). Typical presentation includes
pruritus and erythema followed by development of papules, vesicles, and
bullae, sometimes in a linear arrangement ( Fig. 65.6 ). Burning of plants
leads to aerosolization of the allergen, and may cause a widespread and
severe outbreak on exposed skin surfaces, including severe edema of the
eyelids and lips in some cases. “Black dot poison ivy” can occur when a
concentrated amount of the oleoresin gets deposited on the surface of the
skin and oxidizes, creating a central black eschar surrounded by an acute
dermatitis. This entity has been confused with a pigmented lesion or an
insect bite. If possible, the black eschar should be removed by soaking or
debridement to minimize spread of the resin. Other plants, flowers, pollens
(especially ragweed), clothing, shoes, metals (e.g., nickel in jewelry),
cosmetics, adhesive tape, and latex-containing products can also cause an
allergic contact dermatitis. Nickel dermatitis occurs on earlobes as a result
of nickel-containing earrings and on the abdomen due to pant buttons or
belt buckles. Shoe dermatitis usually occurs on the dorsal surfaces of the
feet, sparing interdigital spaces, in a symmetric manner.


FIGURE 65.6 Allergic contact dermatitis caused by poison ivy. (Reprinted with

permission from Stedman’s Medical Dictionary . 28th ed. Philadelphia, PA: Lippincott
Williams & Wilkins; 2005.)

Allergic contact dermatitis is rare in neonates because of their impaired
ability to react to allergens. By 3 to 8 years of age, children react to