Pruritis, or generalized itching, is the most common presenting skin complaint. It can be a particularly annoying and sometimes debilitating problem for athletes, who place great demands on their skin. Since pruritis may be caused by a particular skin disease or may occur without evidence of any specific skin disorder, diagnosis can be challenging for the clinician.
Making the diagnosis even more difficult is the fact that athletes often attempt various treatment regimens, including the use of over-the-counter remedies, which can alter the appearance of the skin, before seeking professional advice. When an athlete presents with a complaint of itching, one should consider eczematous dermatitis, infections, parasite infestations, insect bites and systemic diseases. For the purposes of this column, let us take a closer look at eczematous dermatitis.
Eczematous dermatitis represents an inflammatory response of the skin to many different external and internal stimulants or agents. It is the most common cause of pruritis in the athlete. The most frequently encountered conditions that fall into this category include xerosis, atopic dermatitis, lichen simplex chronicus and contact dermatitis.
Also known as chronic winter itch or winter dry skin, xerotic eczema represents the most frequent cause of itching in the athlete. This condition is characterized by dehydration with redness, dry scaling and fine superficial cracking of the skin. Although these changes can occur in patches over several parts of the body, one commonly sees these changes on the lower legs.
This xerotic and pruritic condition frequently occurs during the winter and in areas where the humidity is very low. The skin becomes extremely dry and scaly, and starts to show accentuated skin lines (xerosis). If the process continues, there is redness with thin, long, horizontal superficial cracks appearing in the skin. The most severe form of this condition can result in deep fissuring that becomes secondarily infected. At this point, pain becomes the primary symptom as opposed to pruritis.
Xerotic eczema develops as a result of decreased skin surface lipids. Cleansers and deodorant soaps predispose the patient to water loss and a decrease in the water reservoir within the stratum corneum. This dryness causes generalized pruritis, which, in turn, leads to rubbing and scratching, causing disorganization of the surface lipid balance. Frequent bathing in hot water increases water loss from the skin while it dries. 
Treatment of xerotic eczema involves educating the athlete about skin care. Talk to athletes about decreasing their number of baths or, better yet, taking only one short, lukewarm shower a day. Emphasize the use of mild, unscented, moisturizing soaps. Encourage them to use topical emollients containing lanolin, glycerin, urea, lactic acid or other alpha-hydroxy acids. In severe cases of pruritis, patients should apply group V or VI topical corticosteroids two to three times daily.
Using a room humidifier can also be very helpful for patients. Also encourage them to lower the heat in their home since it will help reduce skin water loss due to evaporation. Remind them that less moisture is needed to maintain a high relative humidity at the lower temperatures.
Also known as atopic or allergic eczema, atopic dermatitis is another common skin condition that causes pruritis in athletes. Atopic dermatitis represents a chronically relapsing skin eczema that may begin in infancy, childhood, adolescence or adulthood. Therefore, taking a good history is important in making a proper diagnosis. There is frequently a family history of atopic dermatitis, associated allergic rhinitis and asthma. In many adolescent and adult cases, patients may have previously had eczema that went into remission.
Atopic dermatitis usually occurs as an erythematous papulovesicular eruption that evolves into a dry, scaly dermatitis with accentuated skin lines. The skin distribution of the rash varies somewhat with age, with the flexural surfaces, face, wrists, knees, hands and feet showing xerosis, lichenification and papular eruptions in adolescents and adults.
One may diagnose atopic dermatitis by combining the clinical symptoms, especially the extremely pruritic rash, with the typical appearance and distribution, and the tendency toward a chronic and recurrent course. The personal or family history of asthma, seasonal allergies and eczema also plays a significant role in reaching a diagnosis. The emotional stress and increased temperatures that often occur in sports activities may also worsen the pruritis and subsequent dermatitis.
When treating atopic dermatitis, one strives to eliminate inflammation, provide hydration and control the factors, such as stress, that cause exacerbation.
Topical therapy includes:
• moisturizers with urea or lactic acid;
• bathing in tepid water with bath oils;
• low-potency group V or VI corticosteroids for mild to moderate rashes; and
• group II to IV corticosteroids applied two to three times a day for severe lichenified dermatoses
Oral medications may include antihistamines to control pruritus. In rare severely resistant cases, one may employ a short course of corticosteroids. Use the lowest potency of topical corticosteroid that controls a patient’s symptoms and avoid systemic corticosteroids if possible to prevent rebound flares after treatment.
Lichen simplex chronicus, or circumscribed neurodermatitis, is a pruritic condition that occurs as variably sized patches of thick, lichenified skin that one most commonly sees on the outer lower portion of the lower leg and the ankle. This condition arises on skin that previously looked normal and represents the response of the predisposed skin to repeated scratching and rubbing. External factors such as an insect bite or friction from a shoe may play a role in initiating the lesion.
Emotions appear to play a role in perpetuation of the condition. Once the area becomes lichenified from rubbing or scratching, there may be pleasure derived from additional scratching of the pruritic area. This effect probably explains the high rate of recurrence of this chronic condition.
Patients often complain of pruritis that is much greater than one might expect from the appearance of the lesion. The fully developed lesion presents as a sharply demarcated patch of thickened skin. It is red and edematous during its early stage and subsequently becomes dry, scaly, excoriated and hyperpigmented. This condition may also appear on the soles. Keep in mind that this condition may appear on the soles and it is often misdiagnosed as callus or psoriasis.
Patient education is key as one has to break the “itch-scratch” cycle. However, since scratching may take place subconsciously or at night, occlusive dressings are preferable for chronic lesions. They provide a barrier to prevent scratching and permit the medication to work for longer periods of time.
One can reapply topical corticosteroids and antipruretics under modified Unna boots weekly or reapply them under an occlusive plastic dressing that is changed once or twice a day. Cortisone-impregnated adhesive, such as Cordran Tape, is convenient for this purpose. While intralesional cortisone injections are often used to treat lichen simplex chronicus, one should avoid using these for lesions on the ankle and foot. In chronic recurrent eruptions, psychological consultations may be necessary to help resolve the condition.
When an athlete presents with a pruritic skin condition, one should always consider contact dermatitis. There are two main types of contact dermatitis: irritant contact dermatitis and allergic contact dermatitis.
Contact dermatitis arises from mechanically or chemically irritating substances. Since this condition is not immunologically mediated, the concentration of the irritant must exceed a threshold before the reaction can take place. 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 or sunscreens.
Allergic contact dermatitis, in contrast, is secondary to acquired hypersensitivity to a specific allergen. 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 contact with the same antigen, resulting in erythematous pruritic vesicles and papules. Common allergens include the resins from the Rhus plants (poison ivy, oak and sumac), paraphenylenediamines (blue/black dyes), nickel compounds, rubber compounds and chromates (tanned leather and metal parts). Topical medications such as antibiotics, antihistamines, menthol and salicylate products can also act as allergens.
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 and vesiculation. Irritant contact dermatitis is generally localized and looks more like a severe burn with large blisters or marked erythema and edema.
The first step for either of these conditions is avoiding exposure to the suspected causative agent throughout the treatment program and afterward. Use wet dressings and cold compresses to dry oozing secretions, soften scales and crusts, cleanse purulent wounds and relieve itching and burning. Use topical corticosteroids in the strength necessary to relieve the pruritis and reduce the erythema. This can usually be accomplished within seven to 14 days. Oral antihistamines are often helpful in reducing the itching and, in severe cases, a brief regimen of oral corticosteroids may be indicated.
Although pruritic conditions can be potentially debilitating for athletes, treatment can sometimes be simple. However, it is important to understand how dermatitis and other conditions can contribute to pruritis in order to make appropriate treatment recommendations.
Dr. Caselli (pictured) is a staff podiatrist at the VA Hudson Valley Health Care System in Montrose, N.Y. He is also an Adjunct Professor at the New York College of Podiatric Medicine and a Fellow of the American College of Sports Medicine.
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