Figure 160-1 Marked eyelid swelling may mimic the angioedema of anaphylaxis, but with ACD there is only localized pruritus and no associated systemic signs or symptoms. This case was caused by contact with the allergen in hair dye. (Adapted from Mark BJ, Slavin RG: Allergic contact dermatitis. Med Clin North Am 90:169-185, 2006.)
The one uniformly present feature of allergic contact dermatitis (ACD) is pruritus, without which the diagnosis of ACD is virtually excluded.
What To Do:
Attempt to determine the offending agent. Skin lesion distribution often provides a clue to the offending allergen. Question patients about potential exposure to topical medications (such as neomycin and benzocaine) or other potential allergens (such as sunscreens, moisturizing lotions, perfumes and other fragrances, nail polish, artificial nails, cosmetics, soaps, shampoos, hair dyes, household cleaners, laundry products, paints, rubbers, latex, adhesives, footwear, clothing, and plants such as poison ivy [Rhus toxicodendron]) (see Chapter 182). Metals in jewelry (e.g., nickel, chromium, cobalt) (Figure 160-2) and chemicals in clothing and footwear (e.g., resins, crease resistant finishes, leather dyes, rubber accelerators) (Figure 160-3, A and B) can be sources of cutaneous allergens. Vulvitis and balanitis may occur in patients who have an allergy to latex in condoms or ingredients in douches, contraceptive jellies, feminine hygiene products, or toilet paper.
Figure 160-2 The classic erythematous papulovesicular eruption of ACD on the back of this patient’s neck is caused by contact from nickel-plated jewelry. (Adapted from Mark BJ, Slavin RG: Allergic contact dermatitis. Med Clin North Am 90:169-185, 2006.)
Figure 160-3 A and B, Allergic contact dermatitis to leather shoes. Note the correspondence to sites of exposure. (Adapted from Bolognia J, Jorizzo J, Rapini R: Dermatology. St Louis, 2003, Mosby.)
Also evaluate for possible occupational exposure. Industries in which workers are at the highest risk for occupational skin diseases include food production, construction, printing, metal plating, machine tool operation, engine service, leatherwork, healthcare, cosmetology, and forestry. Specific chemical agents encountered on the job may reveal the underlying cause.
On physical examination, the appearance of the lesion in ACD often corresponds to the stage at which the patient presents. During the acute stage, there is marked erythema, edema, and vesicle formation. Edema predominates in areas of loose connective tissue, such as the eyelids or genitalia. Vesicles are usually multiple, may coalesce, and eventually will rupture during the subacute stage, leading to oozing and eroded skin with a characteristic eczematous appearance. Vesicles may be replaced by papules, crusting and scaling become more prominent than the erythema and edema, and, over time, lichenification and further scaling predominate during the chronic stage. These stages often overlap, and there is no sharp delineation between them.
Have the patient remove the offending allergen from the environment to avoid reexposure, and thoroughly wash the skin with a hypoallergenic soap such as Neutrogena.
For acute reactions with considerable edema and erythema—especially those with inflamed, oozing, or crusted lesions—frequent cool or cold compresses soaked with a 1:20 aluminum acetate (Burow) solution (Domeboro powder packets, two per pint of water) have cooling, soothing, and antiseptic effects. Cool baths can also help (Aveeno Colloidal Oatmeal, 1 cup, or 1 cup each of cornstarch and baking soda in half a bathtub of water).
For severe reactions, if there are no contraindications or relative contraindications (tuberculosis, peptic ulcer, diabetes, herpes, or severe hypertension), prescribe systemic corticosteroids, such as triamcinolone (Kenalog-40), 40 mg IM, or oral prednisone, 60 mg (or 1 mg/kg) for approximately 5 days, and then taper slowly over at least 2 weeks.
Systemic oral antihistamine therapy, such as hydroxyzine (Atarax, Vistaril), 25 to 50 mg q6h prn, helps control pruritus. The benefits may be nominal in the delayed-type reactions of ACD, but any reduction in pruritus, along with its soporific effects, will be appreciated by the patient.
For mild and localized reactions, corticosteroid ointments or gels, such as desoximetasone (Topicort) 0.25% ointment, 0.05% gel, or fluocinonide (Lidex) 0.05% cream, gel, or ointment, applied twice per day, have anti-inflammatory and antipruritic effects. They are usually effective within a few days and should be continued for 2 weeks. More severe local reactions can be treated with the very potent topical ointment or gel clobetasol (Temovate, Clobex), 0.05% bid. Topical steroids may be potentiated with occlusive dressings. Avoid long-term use (longer than 10 to 14 days) of these fluorinated corticosteroids on the face and genitalia, where they can cause atrophy. In general, higher potency steroids should be reserved for the extremities and torso.
Steroid creams may have greater cosmetic appeal than steroid ointments, but creams typically contain more potentially allergenic preservatives and fragrances. Ointments, on the other hand, penetrate more deeply into the skin, increasing their potency.
Impetigo resulting from superimposed bacterial infection (see Chapter 172) should be treated with systemic antibiotics, such as dicloxacillin (Dynapen), amoxicillin/clavulanate (Augmentin), 875 mg bid, cephalexin (Keflex), 500 mg qid, or erythromycin (Eryc), 250 mg qid × 10 days, or azithromycin (Zithromax), 500 mg, then 250 mg qd × 4 days. Consider antibiotics effective against community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) when these organisms are prevalent in your area. Avoid topical medications, because these are frequent allergic sensitizers.
When a precipitating agent cannot be determined, the patient should be referred for epicutaneous patch testing, which is considered the gold standard for diagnosing ACD. If patch testing fails to incriminate a likely allergen, and the diagnosis of ACD is still strongly considered, a detailed diary of the patient’s daily activities may help discover patterns of allergen exposure.
When the allergen cannot be avoided, wearing protective barriers is the next best preventive option. Gloves may be the most effective means of allergen protection. The ideal gloves are vinyl. They are waterproof and can be worn atop cotton gloves for greater comfort.
The contacted objects sometimes can be modified to become less allergenic themselves, such as nickel-plated fasteners and jewelry that is painted with a clear polyurethane varnish.
What Not To Do:
Do not allow patients to apply fluorinated corticosteroids for more than 10 to 14 days to the face or genital area, where they can produce premature aging of the skin with thinning and striae.
Do not prescribe a prepackaged steroid dose pack that is tapered over 6 days. It is usually inadequate for treatment of ACD and frequently results in rebound dermatitis.
Do not prescribe systemic steroids for secondary infections, such as cellulitis or erysipelas. Also, do not start steroids if there is a history of tuberculosis, diabetes, herpes, or severe hypertension, unless absolutely necessary and preferably in consultation with an appropriate specialist.
Do not recommend desensitization protocols (allergy shots). They have no role in treating delayed-type hypersensitivities to contact allergens.
Discussion
Allergic contact dermatitis is a delayed cutaneous hypersensitivity or cell-mediated immune reaction to small-molecular-weight chemicals, which act as haptens. To date, more than 3000 chemicals have been described to cause allergic dermatitis in human beings. Approximately 50 chemicals cause 80% of the reactions seen in clinical practice. ACD begins with a sensitization phase, in which these small molecules pass through the stratum corneum and are processed by Langerhans cells in the epidermis. Antigen-coupled Langerhans cells then leave the epidermis and migrate to the regional lymph nodes via the afferent lymphatics and present this antigen to naïve CD4+ T cells. These T cells proliferate into memory and effector T cells, which are capable of inducing ACD after repeat exposure to the allergen. This elicitation phase has a latency period that corresponds to the travel time for Langerhans cells to present the allergen to T cells plus the time for these T cells to proliferate, secrete cytokines, and home with other inflammatory cells to the site of contact. A contact allergic reaction normally appears 12 to 72 hours after exposure in a previously sensitized individual.
In addition to the history and appearance of the rash, its anatomic distribution may help distinguish ACD from other types of dermatitis. Because the more exposed areas of skin are more open to allergen encounter, the hands and face are the most common body parts presenting with ACD.
Head and Neck
The skin of the scalp tends to be thicker and have greater resistance to ACD than the face, ears, and neck. Hair dyes and shampoos often spare the scalp but involve the thin skin of the eyelids, ears, cheeks, and neck. Facial cosmetics may cause similar symptoms, and products applied to the hands, particularly nail polish, may be inadvertently transmitted to the face. Metals from jewelry piercings anywhere on the face and ears and topical antibiotics for the eyes and ears are common triggers of ACD.
Extremities
More than half of all cases of contact dermatitis involve the hands. The list of household and occupational materials that are frequently handled is extensive but should include supposed innocuous items, such as foods, moisturizers, musical instruments, and protective gloves. ACD frequently occurs on the dorsal side of the hands, where the skin is thinner and the density of Langerhans cells is greater than on the palmar side. Bracelets, watches, and rings may lead to ACD from metal exposure or exotic wood. Metals from keys and coins, and even the striking surfaces of matchboxes in pants pockets, may be the culprits in ACD of the upper legs.
Torso and Groin
Fragrances from deodorants may cause ACD involving the entire axillary vault, whereas formaldehyde, detergents, and dyes from clothes may preferentially involve the torso and axillary folds, with sparing of the vault. Rubber chemicals in the elastic of undergarments may affect the bra line and waistline. ACD of the periumbilical region is often caused by the metallic fasteners of belts and pants. Medicines, douches, and spermicides may cause contact dermatitis in the genital area, principally the vulva and adjacent thighs rather than the vaginal mucosa.
Knowledge of the common contact allergens will also be helpful in identifying a source of an ACD rash.
Poison Ivy
See Chapter 182.
Metals
Nickel is the most common metal allergen in the United States. Other frequent causes of metal allergy include chromium, cobalt, gold (gold sodium thiosulfate), and organic forms of mercury.
Medications
Topical antibiotics, such as neomycin and, to a much lesser extent, bacitracin, induce more ACD than any other class of medicines. Mupirocin may be a safe alternative. Topical anesthetics of the ester class (benzocaine and tetracaine) are frequently implicated in ACD. The amide class of anesthetics (lidocaine, dibucaine, and mepivacaine) is a rare sensitizer. Surprisingly, topical corticosteroids may be altered to induce allergenicity through both metabolism in the skin and degradative reactions within the pharmaceutical preparation. A preservative with the highest prevalence of positive skin patch tests is thimerosal, found principally in vaccines and numerous topical medicines for the eyes, ears, and nose.
Formaldehyde and Fragrances
Formaldehyde and formaldehyde releasers, such as quaternium-15, are the most common preservatives responsible for ACD other than thimerosal. These two preservatives are found in numerous cosmetics, moisturizers, and fabrics. Fragrances are widely used in cosmetics, fabrics, and topical medicines; in flavorings of foods, drinks, spices, and oral hygiene products; and in perfumes and colognes. Balsam of Peru is the fragrance most often implicated in ACD. In addition to the previously mentioned products, balsam of Peru is also found in sunscreens and shampoos.
Latex and Rubber Chemicals
Chemical accelerators and antioxidants are added to natural rubber latex during its vulcanization process. These chemicals are the primary sensitizers of ACD in rubber products. Of all the rubber products manufactured, latex gloves are the leading cause of ACD reactions.
Until patch testing can identify the specific offending agent, the patient should be instructed about avoidance of the most likely source of allergen that is inferred by the history and the distribution of the rash. A patient with facial dermatitis should be advised to avoid all cosmetics, hair products, facial creams, and lotions until the exact allergen has been identified.
Contact with blister fluid does not spread the allergen, but transfer of allergen remaining under the fingernails or reexposure to allergen persisting on fomites, such as clothing, can continue to spread the dermatitis.
Because corticosteroids halt lymphocyte proliferation and decrease cytokine production, they have become the mainstay of ACD therapy.
Local corticosteroid therapy is not necessary when systemic therapy is used. When using a topical steroid on the face, however, a less potent agent, such as hydrocortisone ointment 2.5% or desonide (Tridesilon) ointment 0.05%, is recommended.
It has been reported that 80% of cases of occupational contact dermatitis are attributable to irritant contact dermatitis (ICD) and 20% to allergic contact dermatitis (ACD). ICD results from skin-barrier disruption and subsequent release of inflammatory mediators without the requirement of previous sensitization. Mild irritants, such as water, soaps and detergents, typically cause chronic subclinical irritation, which is cumulative and eventually leads to clinically perceptible dermatitis. Work that requires frequent immersion in water causes maceration, and with frequent wetting and drying, proteins leach from the stratum corneum, which, in turn, causes breaks with chapping, scaling, and fissuring. Wetting and drying alone is a common cause of ICD, and soaps and detergents accentuate these reactions. Other industrial materials that may cause ICD include petroleum distillates, alkalis, acids, organic solvents, alcohols, chlorinated hydrocarbons, and glycols.
It is often impossible to use appearance to differentiate between allergic and irritant contact reactions. Acute ICD may present within minutes to hours after exposure, with sharply delineated areas of erythema, vesicles, and/or bullae. Chronic cumulative ICD presents with more scaling, fissuring, and lichenification (thickening of the epidermis with marked accentuation of the skin creases).
The mainstay of treating ICD is frequent moisturization and avoidance of irritants. The best agents for this purpose include plain petrolatum (Vaseline), Neutrogena Norwegian Formula Hand Cream, and Cetaphil Cream by Neutrogena. Data regarding the efficacy of topical steroids on ICD has been mixed in the past, but the results of a recent study support the traditional use of topical steroids to treat the inflammation associated with ICD.
Photocontact dermatitis is caused by the interaction between an exogenous chemical in the skin and the ultraviolet (UV) component of sunlight. The photosensitive agent may be a recently ingested drug, such as a sulfonamide, fluoroquinolone, tetracycline, oral contraceptive, or nonsteroidal anti-inflammatory drug, or may be a topically applied substance, such as cold tar extract. Clinically, only sun-exposed areas, such as the face, arms, and upper chest, are affected, whereas the skin under the chin, behind the ears, and on the upper eyelids is noticeably spared. A phototoxic reaction manifests as macular and tender erythema, which can resemble severe sunburn. With a photoallergic reaction, a delayed hypersensitivity reaction is induced by UV light, which chemically alters the sensitizing allergen in the skin. This reaction may produce a pruritic, papulovesicular, eczematous dermatitis similar to ACD.
Two types of contact urticaria have recently been recognized as subsets of contact dermatitis. In its nonallergic form, the urticaria remains localized to the site of contact and may be caused by direct mast-cell mediator release from fragrances, food preservatives, insect stings, caterpillar hairs, or topical medicines. Allergic contact urticaria requires previous exposure to sensitizing allergens, such as foods, metals, animal saliva, latex, industrial products, or topical medicines. Both forms of contact urticaria resemble noncontact urticaria, and their classic wheal and flare response usually appears within 30 minutes of exposure and may be relieved or reduced by simple washing. Although allergic contact urticaria may become generalized and even progress to angioedema or anaphylaxis, most cases of generalized urticaria, angioedema, and anaphylaxis result from ingested or internal causes rather than from contact or physical triggers (see Chapter 183).
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