Review Article
Sports Medicine 9 (2): 100-119, 1990 0112-1642/90/0002-0 I 00/$1 0.00/0 © ADiS Press Limited
All rights reserved. SPORT2 247A
Common Cutaneous Disorders in Athletes Robert 1. Conklin Department of Dermatology, University of British Columbia, Vancouver, British Columbia, Canada
Contents
Summary ............................... ............. ..... ........... .............................................. .. ..... .................. 101 I. Sun-Related Disorders ......................................................................................................... 102 1. 1 Acute Sun-Related Disorders ............................ .................................. .......... .. .............. 102 1.2 Chronic Sun-Related Disorders ........................ ...... ... ................................................... 1.3 Treatment of Sun-Related Disorders ........................................ .................................... 1.4 Prevention of Sun-Related Disorders ................................................... ......... ..... ......... 2. Infections ....................................................................................................... .. ....... ............... 2.1 Viral Infections .............................................................................................................. 2.2 Bacterial Infections .................. .......................................... .. .......... ..... ..................... ...... 2.3 Fungal Infections ............................................................................................ ..... .......... 2.4 Mixed Fungal and Bacterial Infections ................ ............. .............. .............. ............... 2.4.1 Interdigital Tinea Pedis ........ ................................................................................
102 103 103 104 105 106 107 107 107
2.4.2 Otitis Externa ........................................................................................................ 108 2.5 Nail Infections ..... ................ ............................. ............... ..... ......... ... .............................. 109 2.6 Tinea Versicolor (Pityriasis Versicolor, Pityrosporum Versicolor) ..... .. ....... ... ....... ... 109 3. Acute Trauma ....................................................................................................................... 110 3.1 Contusions .............................. .................................................................. ...................... 110 3.2 Black Heel ............. ...................................................................................... .. .............. ... 110 3.3 Black Toe ............................................................................... .................. ... ....... .. ....... .. .. 110 3.4 Jogger's N ipple .... ..... ........... .... ......... ...................... ...... ........ ... .. ........ ......... .. .. ..... ......... .,. III 3.5 Foot Blisters .......... .................. ............................ ........................................................... III 4. Chronic Trauma ....... ...... ................................. ............................. ........................................ III 4.1 4.2 4.3 4.4
Callus ......... ............. .................. ......... ................... ........................................ .................. Corns ...... .... ....... ........................ ........................... ........................ ............... .................... Paronychia ....................................................................................... ....... .............. .......... Other Chronic Injuries ............. ........................................................................ .. ...........
III 112 113 113
Cutaneous Disorders in Athletes
5. Aggravation of Previous Skin Disorders ............................................................................ 6. Allergic Contact Dermatitis ................................................................................................. 7. Hyperhidrosis ........................................................................................................................ 7.1 Miliaria ............................................................................................................................ 7.2 Palmar and Plantar Hyperhidrosis ...............................................................................
Summary
101
114 114 115 115 115
Athletic activity may cause or aggravate skin disorders, which in turn may diminish athletic performance. Since many sporting activities necessitate prolonged exposure to the sun, athletes must avoid painful sunburn which will adversely affect their performance. Drugs and chemicals also may cause photoallergic and/or phototoxic reactions, including polymorphous light eruption and athletes should thus avoid photosensitising drugs and chemicals. The effects of chronic ultraviolet exposure include ageing, pigmentation and skin cancers. The most effective protection against excessive exposure to sunlight is the use of sunscreens, although inadequate application and poor protection in the UV A spectrum may diminish their effectiveness and contact allergies may create other problems. Viral, bacterial and fungal infections are common in athletes due to heat, friction and contact with others. Herpes simplex may be treated with any drying agents (e.g. alcohol) as they are as effective as more expensive topical agents such as acyclovir. Molluscum contagiosum may be spread by close contact or water contact and is treated by superficial incision, cryotherapy or standard wart varnishes. Plantar wart infection is transmitted by swimming pool decks, changing rooms and hand-to-hand from weights in gymnasiums. Plantar warts presenting with pain may be aggressively treated, by blunt dissection, but painless ones are best treated conservatively. Impetigo and folliculitis often develop after trauma. Antibiotics are effective against mild infections while abrasions and lacerations should be cleansed and dressed with occlusive dressings. Diphtheroid bacteria in moist footwear may produce pitted keratolysis and erythrasma. Tinea pedis is common in athletes and probably originates in swimming pools, gymnasium floors and locker rooms. Interdigital, dry-moccasin and pustular-midsole forms can be distinguished. The latter two forms respond to topical antifungal agents, while the interdigital form, a mixed fungal/bacterial infection, is treated with debridement, antibiotics and drying routine similar to the therapy of otitis externa. Nail infections by a variety of organisms may appear as onycholysis with or without paronychia and should be treated with the appropriate antibiotics. Tinea versicolor occurs in heat and humidity. Since Pityrosporum orbiculare is part of the normal flora it often recurs, necessitating regular treatment. Acute trauma injuries include contusions, black heel or petichiae of the heel, black toe (bleeding under the nail), 'jogger's nipple' caused by chafing, and foot blisters. Chronic trauma may result in calluses, corns and paronychia. Plantar corns can be disabling and may be caused by overly tight shoes or abnormalities in biomechanics; treatment includes restoring normal foot function and minimal surgical procedures. Paronychia is treated best by wedge resection. Sweat and friction may aggravate pre-existing psoriasis, acne, atopic dermatitis and allergic contact dermatitis. Allergic contact dermatitis may be caused by dyes, rubber chemicals or glues associated with sports equipment, by detergents or fabric softeners, by plants such as poison ivy/oak or allergies to antibiotics or anaesthetic salves. Hyperhidrosis may cause miliaria [treated with hydrocortisone (cortisol») or palmer and plantar hyperhidrosis. Drying routines, tackifiers and special grips may aid the athlete and tap water iontophoresis likewise may be effective.
102
1. Sun-Related Disorders For many athletes, exposure to the sun is a necessary part of training and competition. For some it is sought for cosmetic benefit. 1.1 Acute Sun-Related Disorders
Athletes need to avoid painful sunburn which will adversely affect performance in the following 6 to 72 hours. Sunburn is induced mainly by ultraviolet light B (UVB) [290 to 320nm]. Severe sunburn is associated with fever, chills, nausea and vomiting. The skin types most likely to develop sunburn and long term consequences of ultraviolet skin damage are skin types I and 2 (skin types: 1 always bums, never tans; 2 always bums, tans minimally; 3 bums moderately, tans gradually; 4 bums minimally, tans well; 5 never bums, tans deeply. There is a definite correlation between ease of burning and red hair and freckles (Azizi et al. 1988). Drug-induced photosensitivity may be phototoxic or photoallergic. Photo toxic drug reactions may appear simply as severe sunburn with variable pruritus. Photoallergic eruptions may be urticarial or maculopapular, manifesting like any drug reaction. Drugs associated with photosensitivity include antibiotics, sulphonylureas, thiazides, phenothiazines, non-steroidal anti-inflammatory drugs and topical chemicals, such as, tars, perfumes antiseptics, anaesthetics, plants and sunscreens (Demis 1988). Some of these photosensitisers may be both phototoxic and photoallergic. Most photosensitivity reactions are induced by ultraviolet light in the range of 320 to 400nm, the so-called UVA spectrum. Present sunscreens do not screen UVA reactions very well. A common acute reaction to the sun is polymorphous light eruption. By definition, it is not due to any known drug nor chemical. Polymorphous light eruption (Gschnait et al. 1983; Holzle et al. 1982, 1987; Morison & Stem 1982; Ortel et al. 1986), as the name implies, can present as maculopapular, papulovesicular, or erythema multi-
Sports Medicine 9 (2) 1990
forme-like, usually very pruritic, lesions. It tends to appear mostly after a long winter when tan has faded, particularly when the later winter and early spring have been cloudy and the athlete finds himself exposed to strong late spring sun. As the summer progresses, tan develops and the reaction diminishes (Holzle 1982). It may diminish in later years and, contrary to some belief, does not significantly progress to lupus erythematosis (Jansen & Karvonen 1984). For further reading on less common disorders, the reader is referred to reviews of lupus erythematosis (Callen et al. 1985; Tuffanelli et al. 1985) and solar urticaria (Kojima et al. 1986). 1.2 Chronic Sun-Related Disorders Many athletes are unable to avoid regular sun exposure. In addition, in the last 40 years, it has been 'tres chic' to be tanned. This attitude contrasts with rapidly increasing skin cancer statistics. In the USA this year there will be 22 000 melanomas diagnosed and over 5000 people will die (Johnson & Lookingbill 1984) and about 500000 new nonmelanoma skin cancers will be diagnosed. Athletes are not immune. Examination of a group of female golfers (Hanke et al. 1985) showed a high rate of precancers and cancers. Four of 51 female professional golfers had skin cancers before age 43 and most of them were skin type I or 2. These burning skin types not only have little melanocyte protection, but a high proportion of phaeomelanin. UV -Exposed phaeomelanin induces free radicals, creating chromosomal aberrations (Azizi et al. 1988). Despite public education, only two-thirds of people under 30 use sunscreen when exposed to the sun and many use sunscreens only to 'get a tan'. Clearly, the tanning craze can be considered a public health risk on a par wth alcohol, tobacco and overeating. Both UVB (290 to 320nm) and UV A (320 to 400nm) can produce chronic damage to the skin. UVA once was considered fairly innocuous because it is a 1000-fold less burning to the skin than UVB. However, we now know that sun produces
103
Cutaneous Disorders in Athletes
Fig. 1. Some of the many cutaneous effects of chronic sun exposure: lentigenes. guttate hypomelanosis and basal cell carcinoma.
500 to 1000 times as much UV A as UVB over the whole year (Kligman 1987), so the exposure to UV A is significant. UV A is far more penetrating than UVB, more damaging to collagen and elastic fibres, and may have immunosuppressive effects, contributing to local or distant cancers (Bruyneel-Rapp et al. 1988; Deleo 1988; Kligman 1987; O'Dell et al. 1980; Urbach 1986). Therefore, 'getting a tan' without burning can be dangerous. The effects of chronic ultraviolet exposure include ageing (wrinkles, elastosis, comedones), pigmentation (melasma, lentigenes, freckles), pigment fatigue (guttate hypermelanosis) and skin cancers (melanoma, basal cell and squamous cell carcinoma) [fig. Il. Other possible chronic effects of light are actinic reticuloid (Vandermaesen et al. 1986) and damage to larger blood vessels (O'Brien 1987).
1.3 Treatment of Sun-Related Disorders
Acute sunburn is treated with cooling compresses, such as tap water, Burows compresses (aluminium acetate/benzothonium chloride) and analgesics. Topical and oral nonsteroidal anti-inflammatories have been tried (Lichenstein et al. 1987; Snyder & Eaglestein 1974), but must be used immediately after sun exposure (therefore it is too
late when the burn first appears) and have limited duration of effect (Eaglestein et al. 1979). Chemical- and drug-induced photosensitivities are treated by topical or oral steroids in the acute phase and the offending drug or chemical, such as perfume or antiseptic in soap, must be eliminated. Polymorphous light eruption is managed by oral or topical steroids in the short term. Severe cases of polymorphous light eruption require treatment with UVB or psoralen and UV A (PUV A) [Addo et al. 1987; Holzle et al. 1982; Murphy et al. 1987] if sunscreens are not helpful (Gschnait et al. 1983; Holzle et al. 1987; Ortel et al. 1986). Chronic skin damage is mostly irreversible (Kligman et al. 1987). However, there is hope for some improvement of aging effects, such as wrinkles, elastosis, comedones, pigmentation, solar keratoses with the application of tretinoin (vitamin A acid) 0.05% to 0.1 % cream applied daily for at least 4 to 6 months and then indefinitely (Kligman 1986; Weiss et al. 1988). However, this cream helps only if further sun is avoided. There is some interest in simple measures to reduce the incidence of cancer, based on animal studies. These measures include diet, simple antioxidants, such as ascorbic acid (vitamin C), carotenoids and oral retinoids (Deleo 1988). Again, none of these measures is comparable to protection from the sun. 1.4 Prevention of Sun-Related Disorders Avoidance of the sun prevents most sun-related disorders. Everyone should limit sun exposure to the hours when the sun is not too strong, preferably 2 hours before or after high noon. Athletes unable to avoid the high sun hours should be aware that light loosely woven cotton, light foundation cosmetic, shade and light clouds may protect only partially (Editorial 1979). Photosensitising drugs and chemicals should be avoided. Attempts to protect from sun exposure by prior use of j1-carotene pills, so-called cosmetic tan accelerators containing tyrosine (Jaworsky et al. 1987) and canthaxanthine are not effective. Canthaxanthine produces worrisome retinal deposits (Lober 1985) and is banned in many countries.
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Suntan beds provide special hazards. Many patrons of suntan beds are young and have skin types 1 and 2 (Diffey 1986). Although there are studies that show pure UV A protects partially from the adverse effects ofUVB (Bech-Thomsen et al. 1988; Roser-Maass et al. 1982), UVB and UVA are cocarcinogens when used at the same time (BruyneelRapp et al. 1988; Urbach 1986). Since UVA lamps in sun parlors emit some UVB with the UVA (BechThomsen et al 1988; Morison 1988), such exposure is dangerous. There are many other problems with sunlamp parlors; doses are poorly monitored and many patrons fail to use eye protection which help prevent UV A-induced cataract formation (Bruyneel-Rapp et al. 1988). The most effective protection from excessive sun exposure is the use of sunscreens. Sunscreens are rated by the solar protection factor (SPF). An SPF of 15 means that with the sunscreen applied the skin will take about 15 times longer to bum. Waterproof sunscreens protect for 80 minutes in water and water resistant for 40 minutes (Warrick 1987). In the USA, sun oils, sunscreens and lip protectors accounted for over $350 million in sales in 1981 (Johnson et al. 1984). Sunscreens are clinically proven to help protect against the chronic, long term, damaging effects of ultraviolet radiation (Kligman et al. 1980; Lowe 1988). However, there are a number of problems associated with sunscreen use. Proper total body coverage requires 20 to 30g, costing US$35 for a 2week holiday (Lynfield 1984; Stenberg & Lanko 1985), so the sunscreen may be applied too thinly in order to save money. Inadequate application reduces SPF drastically. Skiers, climbers and boaters often fail to protect the undersurfaces, for example under the chin, where reflected light from snow can bum (Editorial 1979). Although patients may be aware of their skin type (Stem & Montaz 1984), they often underestimate it (Rampen et al. 1988) and choose too weak a sunscreen. SPF refers to UVB but not to UVA protection, so an SPF-15 sunscreen may only protect about SPF-4 for UV A (Diffey & Farr 1985). Since patients often use sunscreens to 'get a tan', they are increasing their overaU UV A exposure. Sunscreens protect poorly in the
UVA spectrum, so they are not effective against nearly all chemical and drug reactions, most cases of polymorphous light eruptions, and probably do not prevent cancer and ageing changes as much as hoped. Touted as UVA screens, oxybenzone and the newer ingredients Parasol 1789 and eusolax 8024 provide only several SPFs for UVA, e.g. they would reduce UVA exposure by only 35% in northern latitudes in the summer (Diffey & Farr 1985; Kaidbey & Gange 1987; Lowe et al. 1987). Sunscreens have no effect on skin damage from heat (Dover et al. 1989) and wind (Owens et al. 1974), both contributors to the damaging effects of ultraviolet on the skin. Due to failure to protect from UV A, modem sunscreens still are not as protective as the complete sunblocks containing zinc oxide and titanium dioxide, which have the disadvantage of opaque color. Further research into new chemicals will likely improve UV A protection in sunscreens (Gschnait et al. 1984). There is some evidence sunscreens may slightly increase hyperthermia risk, particularly for long distance runners (Lee 1982; WeUs et al. 1984). Further work is needed to determine if this is a vehicle or active ingredient effect. Finally, contact aUergy can develop to the additives in the base, the active ingredients, para-aminobenzoic acid (PABA), oxybenzone and homosalicylate (Rietschel & Lewis 1978; Thompson et al. 1977). Sunscreens may be shunned in some sports because of greasiness and irritation to the eyes (Hanke et al. 1985). Use of high SPF, such as the 30 to 40 range religiously coupled by avoidance of fatty foods containing vitamin D, may render the athlete vitamin D-deficient (Prystowski 1988) or require vitamin D supplements. Overall, the benefits of sunscreen outweigh these disadvantages by a substantial margin.
2. Infections Bacteria (Duncan 1969), fungi (Allen & King 1978) and viruses thrive in a moist, warm environment, the conditions which exist under athletic
105
Cutaneous Disorders in Athletes
clothing and footwear. Frictional trauma then damages the skin, increasing bacterial adherence and then penetration of the organisms (Cole & Silverberg 1986). 2.1 Viral Infections Herpes simplex may occur in athletes due to body contact (James et a1. 1984; White & GrantKels 1984). The term herpes gladiatorus derives from the high incidence in wrestlers, almost 20% in one study (Becker et a1. 1988). It is the responsibility of coaches and their informed athletes to restrict contact with others during the acute vesicular stage and preferably till the crusts have healed. Herpes can produce morbidity with primary infection, recur frequently and is difficult to treat. Herpetic keratitis leading to blindness is always a risk. Topical acyclovir is not helpful in recurring herpes infections (Corey 1982). Any drying agent, for example alcohol, is as good as more expensive topicals, such as acyclovir and idoxyuridine. It is seldom warranted to consider long term oral acyclovir for prophylaxis, because its remarkable effectiveness is balanced by high cost of continuous treatment and concern about the development of resistant strains (Raab 1983) and more severe flares when medication is finally discontinued. Similarly, molluscum contagiosum may develop with close contact and trauma (Mobacken & Nordin 1987) and is generally felt to spread with water contact in pools. Molluscum is treated by superficial incision, cryotherapy, cantherone or even standard wart varnishes, all with reasonable success. Curettage may result in mild scarring. Wart virus infection is a problem for athletes. It is likely that plantar warts are transmitted from swimming pool decks and shower rooms and hand warts from weight apparatus in gyms. They spread more in moist environments, as in running shoes and under gloves. Wart-prone athletes might try to reduce further exposure by drying powders for feet (Gentles et a1. 1974) and wear sandals in gyms and shower rooms. Warts may be more common in calluses which occur in athletes (Kantor & Bergfeld 1988).
Fig. 2. Plantar wart undergoing salicylic acid therapy.
Treatment of warts in athletes must take into account short term disability. There are many techniques for removal of warts of the hands. Cryotherapy is the most popular. The blister produced provides an ideal environment for rapid healing under the wart. However, after cryotherapy athletes must avoid heavy pressure to the palms for a week after to prevent large blood blisters. Blood blisters may be more common in those on nonsteroidal anti-inflammatories, which reduce platelet function. Plantar warts (fig. 2) have been treated many ways, some of which are listed in table I. Disabling plantar warts may be best treated by blunt dissection (Pringle & Holms 1982). I prefer a simple modified approach: superficial incision around the boundary of the wart, curettage of the wart, pinching it to render temporary haemostasis, application of monsel or aluminum chloride 30% for more permanent haemostasis, then application of liquid nitrogen or 70% trichloroacetic acid (fOllowed quickly by alcohol wash) to the cavity to remove any remnants of wart. This is followed by strict antiseptic care as the defect heals by secondary retention. Painless plantar warts are best treated by long term 50% salicylic acid surrounded by a corn cushion and occluded by tape. This is applied continuously, changing it every 2 days with regular scissor-blade paring of the wart, for a duration of about a month . In this way the athlete may get rid of the wart painlessly, without loss of training.
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Table I. Some plantar wart treatments (Conklin 1987)
Treatment
Frequency
Result
Pain
Ulceration
Scarring
50% salicylic acid paste Cantharidine Electrosurgerya Cryotherapy Laser Blunt dissection Excision a Blenoxane IL
Daily for 3-6 weeks Frequent Several Every other week Several Once Once Several
Good Poor
Little Few days Week 3 days Few days Few days Week Few days
None None Weeks Little Weeks Weeks None None
None
a b
Good Fair Good Good Good Good
None Often b Rare Minimal Minimal Frequent b Rare
Not recommended. Scarring can result in permanent pain.
2.2 Bacterial Infections Bacterial infections, such as impetigo and folliculitis, often develop after trauma. Although streptococcal impetigo and folliculitis are common in association with footballers (Dorman 1981) and North American football (Bartlett et al. 1982), Staphylococcus aureus has emerged as the predominant organism in impetigo (Coskey & Coskey 1987). Antibiotics such as oral erythromycin and cloxacillin, or topical antibiotics such as mupericin (Gratton 1987) and fucidic acid (Pakrooh 1977/78), may be equally effective against mild infections. Abrasions and lacerations should be cleansed briefly with hydrogen peroxide, then dressed. Sports-related abrasions, turf burns and blisters and other wounds heal more rapidly with occlusive dressings (Alper 1986; Eaglestein et al. 1987; Levy et al. 1987; Millikan 1987; Reed & Clark 1985). Sensitisation and irritation to these dressings are rare, but occasionally infections can occur in dirty wounds. Due to pus build-up, vapour-impermeable dressings should be changed several times in the first few days, but care should be taken in the removal of adhesive dressings to prevent removal of the new epithelium. Vapour-permeable transparent dressings and hydrocolloid-absorbent dressings may reduce exudate build-up and reduce need for dressing changes. All these dressings are generally very expensive. For clean wounds, plastic film (Katz
1986), and for exudative wounds, zinc oxideimpregnated gauze (Erickson 1986) attached with elastic tape, may be as effective and are considerably less expensive. Opinions differ whether an antibacterial effect from neomycin, bacitracin, polymyxin, bactroban, silver sulfadiazine or benzoyl peroxides is needed under such dressings, but theymay improve re-epithelialisation (Eaglestein et al. 1988; Hirschman 1988; Millikan 1987; Reed & Clark 1985). In contrast, most topical antiseptics may delay healing if used repeatedly (Reed 1985). A wide variety of diphtheroid bacteria thrive in the moist environment of athletic footwear. Some of these bacteria may produce pitted keratolysis and erythrasma. Pitted keratolysis is a benign disorder, is usually asymptomatic and appears as 'moth-eaten' pits studding the overhydrated plantar skin.
Table II. Drying routine for feet
Hydrous aluminum chloride 20-30% in alcohol Permanganate 1 tab/L Tea soaks 1 bag/L Tannic acid powder (Zeasorb) Cotton socks Removal of footwear more often Gentian violet compress Castellani's paint Glutaraldehyde application Iontophoresis
Cutaneous Disorders in Athletes
107
Erythrasma is another diphtheroid infection, involving the web spaces. It can also appear in the axillary and groin areas and occasionally on the trunk, where it appears as patchy dryness (Sindhupak et al. 1985), occasionally resembling tinea versicolor. It can be quite itchy. Between the toes it resembles the dry form of tinea pedis and fluoresces a coral colour with Wood's lamp. Both these diphtheroid infections respond well to drying routine (table II) and, if necessary, to topical erythromycin and modern antifungals, such as imidazoles. 2.3 Fungal Infections Athlete's foot (tinea pedis) seems relatively common in sportsmen (Gentles 1975) and probably originates commonly from swimming pools, gymnasium floors and locker rooms (Gentles et al. 1974). Athletes foot can be classified (Leyden & Kligman 1978) into 3 types: interdigital, dry-moccasin and pustular-midsole types. They are diagnosed clinically and by a simple lab technique, the KOH exam. KOH (potassium hydroxide 10 to 20% aqueous) is applied by dropper to a slide of scrapings, then allowed to sit under a cover-slip for 10
minutes or gently heated. Then the scrapings are examined microscopically for hyphae. The moccasin form is usually asymptomatic and appears as a fine, powdery dryness of the skin of the foot in the distribution a moccasin would cover. The moccasin type is chronic, frequently relapses after treatment, and requires constant application of antifungal topical prepar&tions (see table III). A substitute Whitfield's ointment can be formulated; benzoic acid 6%, salicylic acid 3% in vanishing cream base (Logan et al. 1987). This formulation is also less greasy than standard Whitfield's ointment. The pustular form is often itchy. It can appear identical to pustular psoriasis of the sole, so KOH examination is valuable. It readily responds to topical antifungals applied for at least 2 weeks. The interdigital form, the commonest form of athlete's foot, is really a mixed fungal and bacterial infection (see next section). 2.4 Mixed Fungal and Bacterial Infections
2.4.1 I nterdigital Tinea Pedis The most common mixed infection in athletes is the common interdigital tinea pedis. It involves the web spaces usually between the third and fifth
Table III. Topical antifungal agents (Conklin 1987)
Agent
Gram-positive bacteria
Nystatin Natamycin Amphotericin Whitfield's Undecylenics Tolnaftate Imidazolesc
+/-
Ciclopirox Haloprogin Tioconazole Itraconazole Naftifine HC1
+
+ +
? ?
Candida
+ +/+ +/-
+ + +/+ + +
Tinea
+ + + + + + + + ++
a
Nail mold.
b c
Cost (Editorial 1988): L = low; M = medium; H = high; M-H = medium to high. Miconazole, clotrimazole, econazole, bifonazole.
Mold a
Irritation
? ?
? ?
+
+/+/+/+/? ?
? ?
Costb
L M H L L L M M-H M-H M-H M-H M-H
108
Sports Medicine 9 (2) 1990
Normal toewebs Staphylococci (non-pathogenic, antibiotic producing strains) Diphtheroids Micrococci
DermatophytosiS simplex Occlusion Moisture
Normal flora ......
C02 pH
Dermatophytes (penicillin-producing) Staphylococcus
(penicillin-resistant) Heat
Increasing moisture C02, pH and dilution "
of natural antibiotics
Dermatophytosis complex Non-lipophilic diphtheroids (e.g. Brevibacterium) Keratinolysis
Gram-negative infection Non-lipophilic Fewer dermatophytes Increasing Gram-negatives (antifungal factors)
Fig. 3. The emergence of penicillin-producing dermatophytes encourages staphylococci that produce penicillinase, diphthe-
roids that are penicillin resistant, and diphtheroids that produce substances toxic to fungi and are keratolytic. Removal of protective keratin may allow Gram-negatives to penetrate, which then may produce antifungal factors, establishing their foothold.
toes. It can be subdivided into a simplex (dry form), complex (wet form) and Gram-negative bacterial form. A scheme is presented in figure 3, which explains how more complex forms of tinea develop from microenvironment and bacterial interactions (Leyden 1982; Leyden & Kligman 1978; Terlecky & Axler 1983). It is perhaps understandable that bacteria playa role when in the web space there is 100 to 1000 times the bacteria of other skin surfaces (Noble & Somerville 1974). The simplex form infects the crease of the web space. It is also called the dry form because it is scaly and is not very wet. The simplex form mayor may not be itchy. The predominant organisms are species of dermatophyte fungi. Differential diagnosis of the simplex form includes erythrasma and psoriasis. This form can be treated well by the older narrow spectrum topical antifungals (table II). The common complex form is constantly wet with shoes off for long periods, because of tight web spaces. It is often itchy or somewhat sore. The complex form harbours more diphtheroids than the simplex form and, occasionally, pathogenic Staphylococcus organisms. When Staphylococcus predominates, adjacent skin may be involved. Differ-
ential diagnosis includes soft corns, and web space psoriasis. Broad spectrum antifungals (table III) are effective against most of these organisms. The least common but most bothersome form (Abramson 1983) is the Gram-negative form, manifesting as erosion, crusting, and pain of any web space and adjacent skin. The predominant organisms are Gram-negative bacteria, although lesser numbers offungi and diphtheroids may also be found. Severe cases require debridement (King & King 1986) and systemic (Eaglestein et al. 1983) or topical antibacterials based on culture and sensitivity or antiseptics such as 0.5% silver nitrate or castellani paint (King & King 1986). Long term use of drying routine or inexpensive topical antifungals such as tolnaftate powder (Leyden & Kligman 1975) may reduce the recurrence rate significantly. Patients with recurrent, severe disease might be checked for diabetes (Eaglestein et aI. 1983). 2.4.2 Otitis Externa This mixed infection is common in swimmers. It shares many characteristics with Gram-negative tinea pedis (chronic moisture, Gram-negative staphylococci, chronic duration, management by de-
Cutaneous Disorders in Athletes
109
bridement, antibiotics and drying). Debris, wax must be gently debrided, wicks of aluminium chloride or Burow's solution (aluminium acetate/ benzethonium chloride), 20% silver nitrate applied 3 times a day for 3 days (Smathers 1977). For resistant cases, cultures are of value followed by oral antibiotics. Ear plugs are contraindicated if the activity includes diving (Levine 1980). Regular cleaning of the ear canal with dry cue tip is contraindicated as it may remove the protective wax layer and injure the ear canal. Regular use of Burow's solution may prevent recurrence. 2.5 Nail Infections Infections of the nails by a variety of organisms may appear as onycholysis (lifting of the free end of the nail) with or without paronychia. Often the nail pigment produced by the organism hints at the type of organism involved (table IV). However, mixed infections can occur, so that determination of the organism depends on KOH and culture. Treatment of the Candida and bacterial form require appropriate antibiotics applied to the paronychial area or, in the case of distal subungual yeast infections, applied under the free end of the nail. Candida paronychia is best treated by topical antifungal applied under the proximal nail fold (table III). Broad spectrum antifungals are best because staphylococci are often present. Gram-negative paronychia are treated by gentamycin or po-
Table IV. Characteristics of nail infections (Conklin 1987). The most common type, termed onychomycosis, usually refers to the fungal type Organism
Onycholysis
Paronychia
Pigmentation
Candida
+/+ +/+/+/-
+
W/Y W/Y/O
+/+/-
8/G
Dermatophyte Pseudomonas Proteus
Molds Staphylococcus Colour: W
=
o = orange.
white; Y
8
W/Y/O
+ yellow; 8
black; G
green;
Iymyxin and onycholysis by any of the appropriate anti yeast antibiotics (table III). The commonest form of nail infection is onychomycosis, caused by dermatophytes, which tend to invade damaged nails (Baran & Badillet 1982) of athletes. There are 3 main forms of onychomycosis. The commonest form is the distal subungual form, characterised by onycholysis and coloured subungual debris. It is very difficult to treat successfully as recurrence rates are high. The usual treatment is oral griseofulvin, administered until the nail is apparently regrown. The length of treatment depends on the length of time for the diseased portion of the nail to grow out. A totally diseased nail, measured 15mm from the free end, may require at least 8 months' treatment. Treatment with griseofulvin, griseofulvin with nail removal, topical antifungals with nail removal and 28% tioconazole with griseofulvin (Hay 1987) all show poor long term remission rates. Remission rates may be improved by indefinite topical antifungal application to the nails and feet following regrowth (Zaias & Drachman 1983). Use of oral ketoconazole for tinea unguum is not indicated, considering the risk of liver toxicity after long term use of this drug (Lewis et al. 1984). 2.6 Tinea Versicolor (Pityriasis Versicolor, Pityrosporum Versicolor) Tinea versicolor is caused by the dimorphic fungus, Pityrosporum orbiculare, found normally in the human skin appendages. There may be some infectivity from person to person, for example, Shelley and Shelley (1987) noted transmission to several persons who had worn the same diving suit. However, it probably emanates from the patient's own pores, growing as colonies on the surface of the skin in persons with poor general or local immunity to the organism. Severe cases are reported in diabetics. Tinea versicolor seems to occur more often in conditions of humidity and heat. It may be itchy, but is mainly of cosmetic concern to the athlete who has to bare the torso. In the infected stage, it consists of faint tan coloured, fine powdery sealey
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Table V. Topical treatment of tinea versicolor. The lotions and shampoos are generally applied 15 to 30 minutes daily for a week and the creams once or twice a day for about 4 days to eradicate the organism 1. 2. 3. 4. 5. 6. 7. 8. 9.
2.5% Selenium sulfide shampoo or lotion 30% Sodium thiosulfate - 6 weeks (EI-Gothamy 1975) 2% Sulfur lotion (Bamford 1983) 2% Salicylic acid shampoo (Bamford 1983) 1% Zinc pyrethione shampoo - 5 mintues (Faergemann & Djarv 1982) 50% Propylene glycol in water (Faergemann & Frederickson 1980) 5% Benzoyl peroxide gel - nightly (Prestia 1983) Econazole nitrate (Vicik et al. 1984) Ciclopirox (Cullen et al. 1985)
macules which occur most commonly on the trunk. Scratching the macules reveals the talcum powderlike scale which indicates that treatment is necessary. KOH-stained mount of the fine scale reveals many short hyphae and some small round yeast forms, i.e. spaghetti and meatballs. Wood's lamp will reveal yellowish fluorescence. Tinea versicolor is easy to treat with a variety of chemicals, which usually have to be applied frequently for fairly long periods (table V). Since Pityrosporum orbiculare is part of the normal flora, it often recurs, requiring regular topical prophylactic treatment, e.g. once or twice per week. Even oral ketoconazole treatment carries a significant recurrent rate (Alteras et al. (1987), requiring regular treatments, such as ketoconazole 400mg once per month (Rausch & Jacobs 1984). Although serious liver toxicity from this drug is uncommon and seems to develop after continuous use (Lewis et al. 1984), it is not known what the risks would be for long term intermittent administration for this benign disease. Treatment or even sun exposure will eradicate the organism, but leave non powdery white patches that contrast with the normal tanned skin. This will remain for several months. Differential diagnosis includes pityriasis rosea and seborrhoeic dermatitis. It is interesting that seborrhoeic dermatitis may be in part due to this organism (Green et al. 1987). The depigmented, inactive stage may be confused with vitiligo and idiopathic guttate hypomelanosis.
Pityrosporum folliculitis (Back et al. 1985) is relatively common in athletes and often appears as an itchy, fine papulopustular eruption of the trunk. It resembles acne, which usually is not itchy and miliaria. KOH will often reveal significant pityrosporum organisms. Treatment is identical to regular tinea versicolor.
3. Acute Trauma The athlete is susceptible to acute injuries, such as contusions in contact sports and friction problems, such as blisters and petechiae, both aggragated by moisture. 3.1 Contusions Acute injuries such as contusions are treated by several 15-minute ice packs followed by heat 24 hours later (Kantor & Bergfeld 1988). 3.2 Black Heel Black heel or petechiae of the heel usually occurs in sports where there are sudden stops, such as basketball. It is painless, of sudden onset, and usually occurs at the beginning of the season when callus has not yet formed. Padding prevents recurrence as it holds the heel firmly and cushions it (Ayers & Milban 1972; Kantor & Bergfeld 1988; Levine 1980; Verbov 1973). Similar lesions have been reported on the pressure points of the fingers of weightlifters (Izumi 1974). 3.3. Black Toe Black toe (fig. 4a) is due to mild bleeding under the nail and is caused by pressure of the toe against the toe box of a shoe or continual deformation of the nail plate with running. It is particularly common with marathon-distance running (fig. 4b). Because it develops suddenly, it should not be confused with nevi nor melanoma of the nail matrix or nail bed. It is surprisingly painless when evolving, but can be uncomfortable for a few days af-
[[I
Cutaneous Disorders in Athletes
panel over the breast prevents this problem (Levit 1977). 3.5 Foot Blisters Blisters are due to friction, warmth, and moisture. Saturation of shoes from running through puddles drastically increases blistering. Drying of the skin with powder, lubrication with vaseline, and proper fitting shoes prevent blisters. Draining the blisters several times in the first 24 hours and application of firm occlusive dressings aids healing time (Levine 1980).
4. Chronic Trauma Chronic trauma to the skin can result in hyperkeratosis, in the form of calluses. A callus is the skin's way of protecting against blistering. However, when corns develop in the callus, there can be pain and disability. 4.1 Callus Fig. 4. (a) Black toe, after 1st marathon. (b) Same toes after 8 marathons. Note the black toe. with evidence of fungus , the tenting of the second toe and the evidence of fungus infection of the third toe. The fungus infection is secondary to trauma and there is no evidence of tinea of the skin of the foot.
terwards. It is difficult to prevent even with proper fitting shoes. If continual, chronic onycholysis, thickening and fungal infection (fig. 4b) of the nail may supervene (Baran & Badillet 1982). 3.4 Jogger's Nipple This is a painful chafing of the nipples due to friction of cotton type T-shirts. It usually occurs after long runs in cool conditions when the nipple is erect and when the shirt is moist, increasing friction. It is more common in males now (Nequin 1977) because female runners generally wear firm, well-padded brassieres. Taping, ointment and wearing running shirts with a smooth silk-type
Callus is accentuated by moisture, pressure and friction. It can occur anywhere there is regular moisture and friction. Short application of friction might increase proliferation of the epidermis for days (MacKenzie 1974). Therefore regular use of pumice stone may actually feed calluses. Calluses are best reduced professionally with a blade or treated chemically (see below). Certain sports may be associated with chafing and callusing in unusual places, for example, pulling boat hands (Toback et al. 1985) and rower's rump (Tomecki & Mikesell 1987). Padding usually helps prevent these conditions. The majority ofhyperkeratoses develop on the feet where friction and moisture are the greatest. Foot calluses without corns are usually painful only if deep fissures develop in the brittle skin. These calluses are reduced by compounds such as 20% salicylic acid, 12% lactic acid and urea 20% in cream bases applied for a few hours under plastic film occlusion or salicylic acid or lactic acid in flexible collodion (Kantor & Bengfeld 1988). Reducing
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Fig. S. Vascular corn with hallux rigidis and possible lack of fat pad under the Ist metatarsal.
moisture and fixing the heel with heel inserts to prevent motion also help. 4.2 Corns Corns commonly develop in pressure places due to deformity of the foot. There is always a bony protuberance below the skin which the point of the corn is directed towards. The bone may be normal but out of position and pressing the skin from the inside. An example is hammer toes where the corns occur on the dorsal aspect or tips of the toes. Corns may be particularly disabling when they occur on plantar skin. Terminology is confusing for such plantar lesions, which include a number of poorly defined entities, such as porokeratosis plantaris (Mandojana et al. 1984), neurovascular corns and keratoses in calluses (McCarthy & Montgomery 1986). I believe that the plantar corns found in the middle of calluses are the most common type of plantar corn and are caused by direct pressure, shearing forces and for some corns under the metatarsal heads, opposing movement of the metatarsal heads, pinching the skin internally. These plantar corns-in-calluses (fig. 5) are usually solitary, but can be multiple, making differentiation from multiple warts difficult (table VI). Because 3 times the bodyweight is distributed to the pressure places of the feet while running, these corns can be very painful and should be reduced if pain interferes with
training. Haemorrhage in plantar corns is painful and can be a sign of diabetes (Rosen et al. 1985). Plantar corns and calluses may be caused by use of overly tight shoes, but in athletes, who generally wear footwear with good padding (Cook et al. 1985), abnormalities in biomechanics may contribute more to corns and calluses (Gibbs & Boxer 1982). A knowledge of abnormal mechanics of the foot is necessary for assessment and management of plantar corns. For example, rearfoot varus, a common biomechanical problem (McPoil et al. 1988), can lead to many types of hyperkeratosis, such as Haglund's deformity (a hyperkeratotic nodule of the back of the heel) and calluses and corns under the middle 3 metatarsals. Expanding the example, rearfoot varus with rigid first ray can contribute to hyperkeratosis under the first and fifth metatarsals, and, if severe, on the lateral aspect of the fifth metatarsal. However, sometimes pressure from tight fitting shoes can contribute to corns of the lateral aspect of the fifth toe (fig. 6) and soft corns between the fourth and fifth toes. Paring of the corns provides only temporary benefits. However, treatment plans usually require restoring the normal function of the foot (orthotics) recommending roomier, padded shoes and sometimes minimal surgical procedures (Gibbs & Boxer 1982) rather than simply paring and recommending roomier shoes. Firm orthotics are helpful, but expensive and sometimes soft orthotics or simple padding will suffice (Schneider 1988) for lesser corns.
Table VI. Differences between plantar warts and corns Parameter
Plantar wart
Plantar corn
Site Surrounding skin Onset
Any Usually normal Fairly rapid Often young Unrelated
Pressure places Usually callus Slow Usually older Heel varus. Pes cavus None usually 'Glassy' By direct pressure
Age Deformity Vessels Translucency Tenderness
Punctuate None By pinching
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Cutaneous Disorders in Athletes
ity is packed with iodoform gauze which acts as both haemostatic agent and antiseptic. This is changed in a few days. The patient is instructed in trimming the nails straight across, reduction of hyperhidrosis and tight shoes and consideration of mechanical problems to help prevent recurrence. If the problem recurs the nail is removed in the same manner, but a narrow cue tip with 70% phenol is rotated into the cavity under the proximal nail fold for 20 seconds, rinsed copiously with alcohol, then dressed (Cameron 1981; Haneke 1986; PagIiano 1987). The phenol destroys the matrix permanently (Morkane et aL 1984; Young & Rutherford 1987). 4.4 Other Chronic Injuries
Fig. 6. (a) Lateral corn of the 5th toe due to tight shoes. In thi s case due to hard suede material. (b) Same toe I month later. after suede material slit to relieve the pressure.
4.3 Paronychia Chronic trauma may also contribute to paronychia. Paronychia of the lateral nail fold is aggravated by biomechanic abnormalities (Gibbs & Boxer 1982), tight shoes, hyperhidrosis, improper trimming (Haneke 1986; Scher 1983) and poor resistance to infection, such as in diabetes. The simplest treatment is surgical wedge resection. This is done by use of an anaesthetic nerve block, tourniquet, nail splitter and forceps to remove a narrow wedge of nail from the affected side. The cav-
Chronic damage to the toe nails may result in other nail dystrophies (Gibbs 1985), such as thickening and tenting (fig. 4b) which may be somewhat painful. Such nails may be removed without destruction of the matrix and may not recur if the mechanical problem is rectified (Stone 1984). It is valuable to send the specimen for fungus culture which might also have to be treated. Such nails may also be removed by 40% urea in paste, applied for a week or two. The surrounding skin is protected by tape or moleskin (Averill & Scher 1986). The nail can be lifted off the nail bed, often relatively easily without anaesthetic. Very thick nails have to be pretreated by paring them first for this chemical method to be effective. Chronic injury to the skin, such as chafing of the thighs, can be reduced by modern occlusion dressings, then application of ointment to the site to reduce friction before activity. Intertrigo of the groin in heavy muscled individuals is due to friction , maceration, humidity, bacteria. It differs from tinea cruris (dermatophyte infection of the upper thigh) because tinea cruris involves mostly the upper thigh and intertrigo, mostly the skin of the inguinal crease. Intertrigo responds to Burow's compresses, vioform HC (iodochlorhydroxyquine/hydrocortisone cream), or topical antibiotic ointment and mild soap. Wear-
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Sports Medicine 9 (2) 1990
ing of smooth stretch apparel and lubrication prevents recurrence.
5. Aggravation of Previous Skin Disorders Common pre-existing skin disorders can be aggravated by athletic activity. Sweat and friction aggravate psoriasis (Rosenberg & Noak 1988) and acne (Mills & Kligman 1975). Atopic dermatitis is often aggravated by infection, sweat and friction (Hanifen 1984; Scholtz 1965). Juvenile plantar dermatosis, a common plantar disorder in young atopic athletes, can be cleared by strict avoidance of excessive moisture (Ashton et at. 1985). Allergic contact dermatitis is worse under conditions of sweat and friction, both of which allow the chemicals to penetrate the skin easily. All of these disorders can trouble the athlete. Acne aggravated by athletic pads and helmets may be reduced somewhat by soft absorbent materials. The treatment of acne in the athlete is discussed elsewhere (Conklin 1988). Reduction of sweating is one of the principles of the management of atopic dermatitis (Hanifen 1984; Scholtz 1965). Psoriasis may actually be koebnerised by friction (Rosenberg & Noak 1988). The Koebner phenomenon describes the actual induction ofpsoriasis in previously normal skin by trauma.
6. Allergic Contact Dermatitis Sweating and perspiration may aggravate allergic contact dermatitis. Moisture tends to leach out the chemicals in running shoes, such as chromates, dyes, rubber chemicals and glues (Cronin 1980). The dermatitis usually occurs on the dorsal aspect of the foot (fig. 7). Allergy to shoe chemicals may be reduced markedly by drying routines (table II), particularly tannic acid powder applied heavily to the socks (Fisher 1973). Allergy to glue and rubber dye in swimming goggles has been described (Fisher 1986). Allergy to tape used to be more common with rubber based tapes (Cooper & Fair 1978; Cronin
Fig. 7. Allergic contact dermatitis to running shoes. Note it usually involves the dorsal foot.
1978; Editorial 1977). Both the rubber and benzoin tackifiers cause allergy. Tape reactions are relatively uncommon now because cloth tapes use acrylic adhesives (Heskel et at. 1982; Jordan 1975; Marks & Rainey 1984). Sweating tends to leach out detergents and fabric softeners in fabrics, creating dermatitis in the sweating areas, such as the antecubital fossae and periaxillary areas and groin. Friction contributes dermatitis around the shoulders, neck, waist, and upper inner thighs. Allergy to plants, such as poison ivy/oak (Baer 1986), properly termed Rhus dermatitis, is well known in hikers. Allergy may be preventable by application of linoleic dimers which may protect for 12 hours (Orchard et at. 1986). Occasionally allergy can occur to other plants as well, producing
Cutaneous Disorders in Athletes
the typical linear, pigmented or vesicular dermatitis. Among the most common causes of contact allergy in athletes are antibiotic and anaesthetic salves applied to abrasions or chafed areas. Allergies can occur to antiseptics (Marks & Rainey 1984) and to fucidin and bacitracin, and commonly to neomycin and benzocaine. Also relatively common is allergic contact dermatitis to benzoin used to toughen skin and prevent blistering (Cooper & Fair 1978). An incidence of allergy to tincture of benzoin of 0.3% has been reported in military recruits and a better substitute suggested, namely, Mastisol (gum mastic-styrase liquid compound which does not contain gumbenzoin) [James et al. 1984]. Irritant skin reaction can occur from fibreglass from hockey sticks or under tape when it is repeatedly removed and reapplied to one area. Photosensitivity can occur from many topical medications.
7. Hyperhidrosis Hyperhidrosis without trauma causes 2 distressing problems: miliaria and palmar hyperhidrosis. 7.1 Miliaria Miliaria (Dobson & Lobitz 1957) is an itchy vesicular, usually papular (miliaria rubra) and occasionally pustular eruption, most common on the trunk, under conditions of high humidity and occlusion of clothing. The pustular form is due to staphylococcal infection of the sweat gland pore, analagous to folliculitis which is infection of the hair follicle (for those unsure of its appearance, the papular and pustular forms occur almost universally to various degrees under diapers of babies). It most commonly affects athletes not acclimatised to humid climate on the trunk. It resolves well after a few hours of air conditioning and application of hydrocortisone (cortisol) lotion. The vesicular form, miliaria crystallina, occurs commonly on sweating after sunburn. The pustular form is rare, and an
liS
extension of the papular form, both forms partly due to bacterial overgrowth in the occluded pore. 7.2 Palmar and Plantar Hyperhidrosis Hyperhidrosis of the hands or feet can be a problem for the athlete. It is often hereditary and triggers with emotional stress. As previously discussed, moist feet contribute to tinea, bacterial infections, warts, contact allergy, and frictional problems. It is also associated with unpleasant odour due to bacterial products. Drying routine, outlined in table II, helps to reduce odour. Persons with moderate palmar hyperhidrosis engaged in racket sports will benefit from wraparound grip material, which usually sold in small rolls in sports shops. Rackets should be purchased with handles a bit narrower to accommodate these materials, which are often composed of a thin polyester base fabric laminated with a thin coating of polyurethane. The polyurethane is buffed to create a mild frictional surface. These materials provide for cushioning, friction, mild tackiness, and moisture absorption and come in many different brands, some of which offer various types of wraps, differing in degrees of these qualities. Severe sweating of the palms interferes with gripping in gymnastics, weightlifting, baseball, golf, bowling and racket sports. It is also socially embarrassing. In some of these gripping sports, tackifiers and special grips and grip wraps help. However, tackifiers, formaldehyde, methanamine (formaldehyde releaser) and even glutaraldehyde may sensitise (fig. 8). Soaks or compresses consisting of solutions of saline, Epsom salts and Burow's have little effect. Glutaraldehyde application and tea soaks have to be used regularly and discolour the hands. Formaldehyde, glutaraldehyde and aluminium chloride may irritate the skin causing it to peel. In addition formaldehyde is a potential carcinogen. Generally, the efficacy of these treatments is minimal, particularly where hyperhidrosis is marked (White 1986). Cervical sympathectomy results in permanent hot, dry palms and there are risks with the operation. For many years there has been interest in tap
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weeks. The Fischer unit seems more rapid in action, although this has not been quantitated by direct comparison (Sto!man 1987; White 1986).
References
Fig. 8. Contact allergy to fonnaldehyde used to dry the palms.
water iontophoresis as a treatment for palmar and plantar hyperhidrosis (Bouman & Leutzer 1952). Tap water iontophoresis is the introduction of water into the sweat ducts, by means of weak electrical current which results in poral closure. Research has led to the use of apparatus, such as the Fischer unit (Stolman 1987), Drionic unit (Akins et al. 1987; Elgart 1987) and other units (Holzle 1987). The Drionic unit costs about US$150.00 to purchase and requires fairly expensive batteries. The Drionic unit works only on the part of the hand or foot in contact with the pads, so is not as effective as the Fischer unit, where the hand is immersed. However, it is inexpensive compared to the Fischer unit which requires many physiotherapy visits. The Drionic unit requires a 30-minute treatment for 8 to 20 days for palms (and twice as many treatments for feet) to obtain dryness for up to 4
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Cutaneous Disorders in Athletes
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