How To Handle Contact Dermatitis In Athletes

Whenever an athlete presents with an acute vesicular or chronic scaling inflammatory condition of the skin, one must consider contact dermatitis. Often, the activities of these athletes may lead the practitioner to an initial diagnosis of conditions such as friction trauma, infection and pedal hyperhidrosis while treatment of the actual condition, contact dermatitis, is significantly delayed. Contact dermatitis can manifest itself in several ways, including primary irritant contact dermatitis, allergic contact dermatitis and photoallergic contact dermatitis. Irritant contact dermatitis is the non-allergic type that arises from mechanically or chemically irritating substances. Since this condition is not immunologically mediated, the concentration of an irritant must exceed a threshold before the reaction can take place. This threshold may be very high, according to the irritancy of the compound. Since sensitization is not necessary, an irritant reaction may occur immediately after the athlete comes in contact with the material. Irritant contact dermatitis may be caused by adhesive tape, topical medications, antiseptics, insect repellents, cosmetics, oily sunscreens or a leakage of “cold-pack” chemicals. Allergic contact dermatitis, in contrast, is a delayed T cell-mediated immune response to the antigen, usually a low-molecular weight hapten (see “Sources Of Allergenic Contact Dermatitis In Athletes” below). Unlike irritant contact dermatitis, this condition has an induction period of five to seven days before the first appearance of hypersensitivity. The peak reaction of the skin occurs 24 to 48 hours after being challenged with the same antigen. This manifests in inflammation and formation of small pruritic vesicles and papules. If the reaction is severe, the vesicular phase may proceed to bullae formation. If one removes the sensitizing agent, the skin soon heals within a short period of time. When there is repeated exposure to the causative agent, the skin reaction becomes rapid and severe. One factor that exacerbates allergic contact dermatitis is repeated exposure to heat or constant warmth which may occur within a shoe. This causes increased perspiration, which allows the well-recognized sensitizers within shoe materials to become problematic, and promotes the spread of the vesicular or pruritic papules. Be aware that the general appearance of these papules may lead to the misdiagnosis of tinea pedis. Appropriate treatment of contact dermatitis is frequently delayed because of this misdiagnosis and long-term treatment with topical antifungal agents. It is often difficult to tell the difference between irritant contact dermatitis and allergic contact dermatitis. In general, allergic contact dermatitis appears more polymorphic, with erythema, vesiculation and edema. Irritant contact dermatitis is generally localized and looks more like a severe burn with large blisters or marked erythema and edema. Photodermatitis (photoallergic contact dermatitis) is less common than the other two forms of contact dermatitis. It can occur when one applies certain topical agents to the skin of the lower extremities before sun exposure. This type of eruption can be mediated by the T-cell system. If the problem is not immunologically mediated yet sunlight is still required to activate the condition, it is known as a phototoxic reaction. Identifying Possible Sources Of Contact Dermatitis Athletic tape, especially that which is rubber-based, has been identified as the most common contact allergen among athletes. Rubber-based tape is now frequently replaced with tape made of cloth and other adhesives, such as p-Tert-butylphenol formaldehyde resin (PTBP-FR) and acrylics, because of their durable, flexible and rapidly adherent qualities. Nickel is the most frequently identified allergen of patients undergoing patch testing. Athletes are probably predisposed to nickel allergy. The significant factor in its development is not so much the nickel concentration in the object or coating but the amount released into the skin during exposure to human sweat. The dermatitis appears at contact sites of metal chains, buckles, clasps and other gold-plated items first covered with nickel. Running shoes and athletic gear contain rubber accelerators, antioxidants and other rubber additives that are common causes of contact allergy. Among the potential allergens are thioureas, thiurams, carbamates, N-isopropyl-N-phenyl-p-phenylenediamine (IPPD) and mercaptobenzothiazole (MBT). It has also been reported that the dye found in the insoles of certain running shoes has caused contact dermatitis in runners. Allergen alternatives include shoes made mostly of polyurethane and those with components that are patch-test negative. Swimmers and divers are exposed to numerous rubber-containing articles such as masks, goggles, diving suits, fins and fin straps. Scuba-diver dermatitis may be caused by IPPD, thiuram and p-phenylenediamine black rubber antioxidants. In wetsuits, rubber accelerators are the most important allergens. Of these, diphenylthiourea was identified as having the highest overall sensitization potential. For thiourea-sensitive individuals, Rubatex Corporation manufactures a grade of closed-cell neoprene without thiourea. Be Aware Of Possible Plant Allergens Outdoor exercise exposes athletes to plants, which are among the most common causes of contact dermatitis. When patients present with suspected contact allergies, you should ask them about their contact with plants. The Rhus plants, which include poison ivy, oak, and sumac and contain the allergen urushiol, are the most common cause of allergic contact dermatitis in North America. Their resins remain allergenic and, since they do not evaporate, may cling to clothing, sporting equipment and pets for months. Even in the winter, the stem and dead leaves may carry the resins. Contact with these resins results in a rash that most commonly appears on exposed skin as linear streaks with vesicles. The blister fluid does not contain the resin and does not spread the condition. Plant extracts are now popular in topical medications and cosmetics. Athletes using these “natural remedies” are particularly susceptible to the development of contact allergy. There are reports of allergic contact dermatitis with witch hazel, which is used as an antipruritic; tea tree oil, a eucalyptol-containing anti-acne/fungal treatment; and chamomile, an essential oil with presumed sedative and antiinflammatory effects. When Topical And Oral Medications Can Cause Allergic Dermatitis Medications, particularly topical agents, are often responsible for localized or generalized allergic dermatitis. Almost any topical antibiotic can produce contact allergy with neomycin and bacitracin being among the most common perpetrators. Topical acyclovir and imidazole antifungal agents are also potential antigens. Topical anesthetics (eg., benzocaine) and topical antihistamines (eg., diphenhydramine, doxepin) may cause allergic contact dermatitis. Diphenhydramine can also act as an occasional photosensitizer. Methylsalicylate, a topical analgesic, can cause both an irritant and allergic dermatitis in athletes. Athletes who are allergic to sunscreens containing p-aminobenzoic acid (PABA) may have a cross-reaction with benzocaine, p-aminosalicylic acid, sulfonylurea antidiabetic agents, procainamide or thiazide diuretics. Oral medications taken by athletes may also be allergenic. This is particularly the case with nonsteroidal agents, especially piroxicam, and antibiotics such as ciprofloxacin, nalidixic acid, sulfonamides and tetracyclines, which are photosensitizers. Contact dermatitis is also frequently caused by over treatment with topical medications for tinea pedis and hyperhidrosis, and overuse of lotions and creams for softening callosities. Arriving At A Solid Diagnosis The treatment of contact dermatitis begins with determining the cause. It is helpful to ask whether the eruptions are aggravated by weather changes, employment, sports activity changes or vacations away from work or home environments. The history should also include a detailed account of topical cosmetics, creams and ointments, as well as any recent changes in clothing, including shoes, hosiery and socks. It’s also helpful to ask if the patient or his or her family has a history of similar conditions. You may employ a patch test for known or suspected agents. One can employ patch tests by either applying a series of the most common sensitizers in the hope that one will show a positive response or doing a patch test with specific suspect agents to demonstrate whether a particular allergy exists. Once you have established the differential diagnosis (including tinea pedis, lichen simplex chronicus, atopic dermatitis, urticaria and others) and strongly suspect contact dermatitis, you may proceed with treatment. Exploring The Various Treatment Options Obviously, the first key is for the patient to avoid exposure to the suspected causative agent throughout the treatment program and afterward. Wet dressings and cold compresses help to dry oozing secretions, soften scales and crusts, and cleanse purulent wounds. Cold compresses are also beneficial in relieving burning, itching and paresthesia caused by irritant contact dermatitis through the cooling and drying effect of the solution. In cases in which the contact dermatitis primarily involves the foot, one may immerse the area in a foot bath of cold to warm water mixed with aluminum acetate (Burrow’s solution), diluted 1:10, for 15 to 20 minutes. Topical steroids are the mainstay of treatment for contact dermatitis. There are five types of topical corticosteroid formulations: ointments, gels, creams, lotions and solutions. Ointments are the most efficacious but creams have greater cosmetic appeal. Lotions, gels and solutions are preferred for hair-bearing areas of the body. Topical corticosteroid preparations vary greatly in potency and are categorized into seven groups with group I being superpotent and group VII having the lowest potency. Examples of commonly used steroids include clobetasol propionate (Temovate cream 0.05%) from group I, triamcinolone acetonide (Kenalog cream 0.01%) from group IV (medium potency) and hydrocortisone (Hytone cream 1%) from group VII. Be sure to remind patients that they should not apply medium-potency and superpotent topical corticosteroids to the face or body folds for longer than two weeks. One may use systemic corticosteroids to treat more severe forms of contact dermatitis as long as there are no obvious contraindications. In most cases of contact dermatitis involving the lower extremities, a relatively short course of oral therapy of not more than two weeks is recommended. You may recommend systemic antihistamines to reduce itching but let patients know they have an undesirable sedative effect. One should also consider nonsedating antihistamines such as fexofenadine (Allegra) and loratidine (Claritin) as they minimize drug interactions. The chronic form of contact dermatitis can also be managed by avoiding the contact allergen or establishing a barrier. For example, when it comes to contact dermatitis secondary to rubber materials in footgear, you may apply a topical corticosteroid cream to the foot, proceed to apply talcum powder and have the patient wear a heavy white sock. Have the patient change the sock frequently during the day to prevent dampness which brings out the rubber material within the shoe. Secondary control of perspiration via activated charcoal insoles will also help reduce hyperhidrosis and bromhidrosis, and reduce the amount of inflammatory response to a contact irritant on the feet. Dr. Caselli is an Adjunct Professor in the Department of Orthopedic Sciences at the New York College of Podiatric Medicine. He is also a Staff Podiatrist at the VA Hudson Valley Health Care System.
 

References:

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