Contact dermatitis is a type of eczema that is caused by an external agent that produces an inflammatory reaction of the skin. The appearance of the eruption and a careful history often provide clues as to the offending agent.
Contact dermatitis is divided into two major types based on etiology: irritant and allergic contact dermatitis.
Also known as nonallergic contact dermatitis, irritant contact dermatitis (ICD) is an inflammatory cutaneous eruption that is not caused by an allergen, but rather results from a direct toxic effect of a single or repeated application of a chemical or physical insult to the skin. Irritants are often found in the home and workplace and include water, soaps, detergents, solvents, acids, alkalis, and friction. For example, underarm shaving, deodorants, and antiperspirants can produce an irritant contact dermatitis after repeated contact.
ICD may affect anyone, providing they have had enough exposure to the irritant. Patients who have atopic dermatitis are more likely to develop ICD as a result of their inherent skin sensitivity and defective barrier function.
The eruption of ICD is confined to the area(s) of exposure or insult, as exemplified by diaper rash (see Chapter 4: Eczema in Infants and Children, Fig. 4.28), scaly dry hands from overwashing, habitual lip licking, or areas where a topical medication or an adhesive was applied (Figs. 13.5-13.8).
The diagnosis and cause of ICD is based on a careful history and ruling out of allergic contact dermatitis (ACD).
Management consists of avoidance or minimizing contact with the offending agent and treatment, if necessary.
Allergic contact dermatitis (ACD) is a true allergic or hypersensitivity reaction that precipitates an eczematous dermatitis. ACD is a delayed-type (type IV) hypersensitivity reaction that occurs when the skin comes in contact with an allergen (antigen) to which an individual has previously been sensitized.
Poison ivy and oak (discussed below) and nickel are the most common contact allergens. Other common allergens found in home and work environments include components of jewelry, metals, cosmetics, topical medications, and rubber compounds; namely, thimerosal (a mercurial preservative), neomycin (a topical antibiotic), formaldehyde (found in shampoo and cosmetics), paraphenylenediamine (found in certain hair dyes) (Fig. 13.8), and quaternium-15 (a preservative often found in cosmetics) are also potential allergens.
ACD occurs only in sensitized persons. ACD is not dose dependent, and it may spread extensively beyond the site of original contact. ACD is seen less commonly in infants, the elderly, and African-Americans.
In the United States, poison ivy and poison oak are the principal causes of ACD. Poison ivy is found throughout the country, whereas poison oak is found more commonly in the western United States and poison sumac (a small related tree), is found only in woody, swampy areas. Poison ivy, oak, and sumac were formerly members of the genus Rhus (hence the term Rhus dermatitis) but now are classified into the genus Toxicodendron, a member of the Anacardiaceae family (Figs. 13.9 and 13.10).
Pentadecylcatechol and heptadecylcatechol are the sensitizing allergens in the plants' resinous oils (urushiol). These invisible oils may reach the skin not only from direct contact, but also through garden tools, pet fur, golf clubs, or the smoke of a burning plant. Identical or related antigens are found in the resin of the Japanese lacquer tree, ginkgo trees, cashew nut shells, the dye of the India marking nut (used as a clothing dye in India), and the skin of mangoes. All cause similar skin rashes in sensitized people.
In the eastern United States, poison ivy dermatitis occurs mainly in the spring and summer. In the western and southeastern United States, where outdoor activity is common all year, it may occur in any season.
The characteristic eruption consists of intensely pruritic linear streaks of erythematous papules, juicy vesicles, and bullae (blisters), which give the appearance of having been caused by an outside agent (Fig. 13.11). The rash typically occurs 2 days after contact with the plant, but initial reactions have been noted within 12 hours of contact and as long as 1 week later.
The distribution of lesions is characteristic. Generally, exposed areas of the body are affected first. The rash may later involve covered areas that have come into contact with the plant oil. The external vulva or perianal areas may be affected in women (Fig. 13.12). In men, involvement of the penis is sometimes a diagnostic sign.
Further dissemination, or autoeczematization (see later in this chapter), is believed to occur through hematogenous spread and subsequent immune-complex deposition in the skin. This spread may occur within 5 to 7 days after the initial exposure, and the resulting rash may last for 3 weeks or more.
Plant Dermatitis other than Toxicodendron (e.g., Reactions to Meadow Grass and other Plants) Scabies (see Chapter 29: Bites, Stings, and Infestations) Herpes Zoster (see Chapter 17: Mucocutaneous Manifestations of Viral Infections) |
A limited eruption and mild itching may be relieved by the following:
In severe cases with widespread eruption and marked pruritus, topical therapy may require supplementation with systemic agents, as follows:
SEE PATIENT HANDOUT Burow Solution IN THE COMPANION eBOOK EDITION. |
Other Common Examples of Allergic Contact Dermatitis
Eyelid contact dermatitis: The thin skin of the eyelids contributes to its sensitivity and susceptibility to allergic and irritant reactions (e.g., poison ivy, cosmetics, nickel). Not uncommonly, ACD of the eyelids, as well as on the face and fingers, may occur from the application of artificial acrylic nails. Patients generally touch their face and eyelids often without being aware of it (Fig. 13.13).
Airborne contact dermatitis: Chemicals in the air may produce airborne CD which usually manifests on the eyelids, but may affect other exposed areas, particularly the head and the neck.
Diagnosis of ACD
Patients should be questioned regarding their daily habits and occupational exposures.
The distribution and shape of the eruption may point to a specific allergen. For example, dermatitis from rubber in underpants (Fig. 13.14), neomycin in eardrops (Fig. 13.15), hair dyes, nickel in earrings (Fig. 13.16), or to an adhesive (Fig. 13.17).
Patch testing is used to identify specific allergens in patients with histories suggestive of ACD (Fig. 13.18A,B). The standardized, commercially available allergens are fixed in dehydrated gel layers, taped against the skin of the patient's back for 48 hours and are then removed. A final reading is performed after 96 hours. The presence of erythema, papules, or vesicles (i.e., an acute eczematous reaction) at the site where the chemical is applied is a strongly positive reaction. A bullous reaction is extremely positive.
Interpretation of patch test results and correlation with clinical findings require experience and are generally performed by dermatologists.
Systemic Drug Reactions (see Chapter 26: Adverse Cutaneous Drug Eruptions) |