Porter & Schon: Baxter's The Foot and Ankle in Sport, 2nd ed.

Section 2 - Sport Syndromes

Chapter 11 - Dermatologic, infectious, and nail disorders

Kevin Gebke






Dermatologic disorders: environmental/anatomic



Dermatologic disorders: traumatic



Infectious disorders



Nail disorders





Athletes present with a wide range of dermatologic afflictions, including traumatic conditions, anatomic abnormalities, and various infections. Identifying patterns of wear and anatomic variation may give key insight into the cause of the presenting complaint. The purpose of this chapter is to discuss the more common disorders seen in sports medicine and to give insight into the treatment options. The ultimate goal is to assist in early recognition of common problems and to prevent performance impairment in our athletic patients. Initial examination of the foot and ankle always should include a thorough inspection of the skin and nails.


Dermatologic Disorders: Environmental/ Anatomic

Contact Dermatitis

Contact dermatitis ( Fig. 11-1 ) is fairly common in an athletic population. Athletes encounter multiple exposures, including adhesive tape, compound of benzoin, topical medications (antibiotics, antifungals, and antiseptics), and rubber-containing sports equipment. Some athletes even have reactions to the leather products of which most sports shoes are composed. Contact dermatitis presents as an inflammatory response of the skin to an offending irritant. The main pathologic feature of contact dermatitis is intracellular edema of the epidermis, resulting in intraepidermal vesicle and bullae formation in acute cases. In chronic cases, a presentation with papules, scarring, and lichenification can be seen.[1] Allergic contact dermatitis will be seen in individuals who previously have been sensitized to the allergen. A delayed hypersensitivity reaction will be seen over the course of several hours. In athletes, contact dermatitis is seen most commonly on the dorsum of the foot and toes. Fisher[2] stressed that the moist environment within the athletic shoe is a major component in the development of contact dermatitis. It was stated that feet that were kept dry would not develop this form of dermatitis.


Figure 11-1  Contact dermatitis.  (From Habif, Clinical dermatology, St Louis, 2004, Mosby: p. 92, Figure 4-16.)


The initial approach to treatment of contact dermatitis is to remove exposure to the offending agent. A wet compress with an astringent such as aluminum acetate is effective in soothing the affected areas. Topical and systemic steroids are used for their anti-inflammatory and mineralocorticoid effects. Antihistamines are used when significant pruritus is associated with the dermatitis. As the dermatitis starts to resolve, it is advocated to apply emollients to moisturize the healing skin.


Clinical pearls in treatment and prevention of contact dermatitis include regular changing of damp footwear, avoidance of potentially irritating or allergenic substances applied to the foot and ankle, and early identification of signs and symptoms of dermatitis. It is recommended to maintain a high index of suspicion for secondary bacterial infections and to treat with systemic antibiotics as needed.


Injury induced by cold exposure has been recognized for thousands of years.[3] Frostbite involves the skin and potentially the soft tissues of the foot and ankle in athletes that are exposed to prolonged cold environments. Injury can occur, however, even with brief exposure of an unprotected foot to a cold, conductive surface (metal, concrete). Several terms are used to describe this phenomenon, including frostnip, chilblains, and frostbite. Frostnip is described as nonfreezing injury to the skin tissues that can commonly be seen in the toes. Associated symptoms include numbness and tingling. Cellular injury is absent in frostnip. Chilblains is associated with a more significant nonfreezing cold injury seen at temperatures below 59°F in which mild tissue damage is seen in the form of minor vascular injury and tissue swelling. Frostbite is the destruction of body tissues because of freezing (below 32°F) and ice crystal formation in the tissues, which causes cell lysis and tissue destruction. The tissue damage seen in association with frostbite is caused by two distinct mechanisms. First, ice crystal formation in the intracellular space leads to cellular dehydration and destruction. Second, damage to the vascular endothelium leads to inefficient delivery of blood to the injured tissues, further complicated by edema and swelling. Ultimately, further cell deterioration is seen secondary to hypoxia.[4]

Several classification schemes have been used to categorize frostbite injury. Historically, frostbite has been categorized into four degrees of injury, with first degree being described as a numb central white plaque with surrounding erythema. Second-degree injury is described as blister formation of clear or milky fluid with surrounding erythema and edema, all seen within the first 24 hours. Third-degree injury is characterized by blisters filled with a dark fluid, possibly appearing hemorrhagic, that eventually results in a black eschar within a couple of weeks. Fourth-degree injury generally refers to complete tissue necrosis. Considering that it is nearly impossible to classify frostbite into one of these categories on initial presentation, many clinicians simply describe frostbite as either superficial or deep. Superficial frostbite includes the first- and second-degree types described and deep describes the third- and fourth-degree categories. Physical examination findings on initial presentation can allow the clinician to arrive at a general prognosis. Findings such as sensation to pinprick, normal skin color, and enlarged blisters with clear fluid are favorable indicators that predict more of a superficial injury. On the other hand, if dark fluid-filled blisters; hard, nondeforming skin; and nonblanching cyanosis are seen, this is more diagnostic of a deeper injury. Patients with frostbite of the foot are likely to have involvement of the toes. They typically will complain of symptoms of numbness and tingling with possible associated electric–shock-type sensations. Symptoms of cold sensitivity, sensory loss, and hyperhidrosis may be described for months to years following the injury.

The diagnosis of frostbite is made on the basis of history and physical examination. It is difficult to predict the degree of tissue injury for weeks following the exposure. With severe injury, it may take months before a clear delineation of viable versus nonviable tissue can be made. There is no current radiologic technique that can reliably distinguish the line of demarcation of injured tissues in the immediate postinjury period. Continued research using technetium scintigraphy and magnetic resonance techniques is needed to identify whether any available radiographic procedure may allow for early distinction of viable tissues.[4]

The treatment of frostbite injuries can be divided into three phases, including initial evaluation, acute care, and long-term follow-up. McCauley et al.[5] described a treatment protocol for frostbite. This protocol can be applied to active individuals who suffer injuries to the lower extremity. Initially, the athlete should be admitted for rapid rewarming of the affected area in warm water (104° to 108°F for 15 to 30 minutes or until thawing has completed). After the completion of rewarming, the affected parts should be treated as follows: white blisters should be debrided and topical treatment with aloe vera should be applied every 6 hours. Hemorrhagic blisters should be left intact, with topical aloe vera administration every 6 hours. The patient's lower extremities should be elevated and splinted as needed. The athlete should be given antitetanus prophylaxis. Regular administration of anti-inflammatory medications is recommended. Analgesia should be accomplished using narcotic medications. Antibiotic coverage should be started and continued for the first 2 to 3 days or until signs of superinfection have cleared. Daily hydrotherapy should be implemented for 30 to 45 minutes at a temperature of 104°F. Lastly, the patient should avoid smoking during this time to prevent peripheral vasoconstriction. When evaluating and treating patients with frostbite, the clinician should avoid rubbing the involved region because this can cause additional damage to the injured tissue. It also is important to ensure that there is not a possibility of refreezing after the rewarming process has taken place. If the potential for refreezing exists, rewarming should be delayed until further cold injury can be avoided. If refreezing does occur, significantly more tissue injury can manifest. Most athletes with frostbite injuries of the foot and ankle will present with findings consistent with a superficial injury. After rewarming, the athlete can be treated in an outpatient setting using appropriate topical formulations and analgesics. Close follow-up is necessary.


Clinical pearls in the treatment and prevention of frostbite include many commonsense principles. First of all, athletes should be educated on the use of appropriate clothing not only to protect the lower extremities but also to help maintain core body temperature. As the core body temperature begins to decrease, blood is shunted away from the lower extremity, further predisposing to frostbite injury. Adequate hydration should be stressed. Regular changing of damp socks and footwear should be recommended. Lastly, during times of anticipated cold exposure, it should be recommended that the athlete wear two pairs of socks, with the inner layer made of synthetic fiber such as polypropylene to wick away water from the skin and an outer layer made of wool or cotton for increased insulation.


Hyperhidrosis is defined as excessive sweating outside the range required for normal thermal regulation. It typically presents in early childhood or adolescence and can affect the soles of the feet. The condition can be idiopathic or secondary to systemic disease, metabolic disorder, febrile illness, or medication use. Three forms of hyperhidrosis are described, including emotionally induced, localized, and generalized. The sole of the foot can be affected by the emotionally induced and localized types. It occurs equally in both sexes and there seems to be a predisposition in those of Japanese descent.

Athletes will seek medical attention most commonly after they have suffered secondary effects from the plantar hyperhidrosis. They will describe excessive sweating in this area and a history of recurrent skin maceration, blistering, dermatitis, and/or infections. Depending on the pattern of hyperhidrosis described, a workup for an underlying systemic disorder may be justified. People who develop hyperhidrosis later in life warrant a workup for systemic disease on presentation.

The treatment for hyperhidrosis can be challenging. Topical agents such as glutaraldehyde solution can be administered in an attempt to reduce perspiration through the denaturation of keratin with resultant occlusion of the pores of the sweat glands. Aluminum compounds such as aluminum chloride function as antiperspirants and can be used topically, as well. Darrigrand et al.[6] studied the application of antiperspirants to the feet of cadets in an attempt to decrease foot sweat accumulation and injuries. They demonstrated a 50% decrease in foot sweat accumulation and a reduced occurrence of trench foot and friction blisters. There was, however, an increased incidence of contact dermatitis. Oral administration of anticholinergic agents such as propantheline, glycopyrrolate, benztropine, and oxybutynin also has been advocated. In addition, neuromuscular blocking agents such as botulinum toxin can be used to inhibit transmission of nerve impulses at the neuromuscular junction of skeletal muscle and/or the autonomic ganglia. It is recommended to perform a nerve block of the posterior tibial nerve and the sural nerve before to botulinum toxin treatment for plantar hyperhidrosis.[7]


Clinical pearls in the treatment of hyperhidrosis include early multimodality intervention in an attempt to control sweating. It is important to remember that hyperhidrosis is not associated with mortality, but multiple morbidities can be seen that will impair athletic participation and performance. Many times, a dermatologist will need to be consulted, especially if botulinum toxin therapy is considered.


Hyperkeratosis ( Fig. 11-2 ) in the form of corns and calluses is a standard feature for many athletes. These lesions are produced as pressure and friction are applied repeatedly to the skin overlying the osseous structures. In an attempt to protect from skin breakdown, the body produces these regions of hyperkeratotic tissue. Many athletes who have symptoms related to their hyperkeratosis complain of localized pain and discomfort. Interestingly, the hyperkeratotic tissue itself is not what causes the pain, but rather underlying bursitis and nerve irritation. The most common types of hyperkeratosis include helomas, tylomas, and intractable plantar keratoma. Helomas are synonymous with corns and usually are found on the toes. Tylomas also are known as calluses and they usually are found over bony prominences, especially in the region of the metatarsal heads. Intractable plantar keratoma is defined as a cone-shaped keratotic plug within a tyloma.


Figure 11-2  Hyperkeratosis (corn).  (From Habif, Clinical dermatology, St Louis, 2004, Mosby: p. 928, Figure 27-5.)


Corns usually are broken down into two types. Hard corns are located over the lateral aspect of the proximal interphalangeal (PIP) joint of the fifth toe or over the proximal or distal interphalangeal joints of the second, third, and fourth toes dorsally. Athletes with hammertoe deformities and mallet-toe deformities are particularly predisposed to developing hard corns.

Soft corns appear between the toes and can be attributed to the moist environment and high pressure seen with improper footwear. Large, hyperkeratotic, boggy masses can appear over time and develop central ulceration. The most common location is the interdigital space of the third, fourth, and fifth toes.

Treatment of hard corns can be achieved using scalpel debridement techniques and/or regular buffing with a pumice stone. The athlete should be educated on proper footwear, with close attention to an appropriate size toe box to ensure adequate toe spacing and decreased potential for rubbing. Soft corns can be treated with debridement of the loose skin and adjustments in footwear. The athlete should be encouraged to attempt to keep the feet as dry as possible and can be instructed on the placement of padding between the toes. Surgical treatment usually is aimed toward correction of an underlying bony deformity but is rarely necessary.

Calluses are seen almost universally on the feet of athletes. As described earlier, this is the body's response to wear and tear. Many times, athletes are protected from skin breakdown and potential infection by this hyperkeratotic process. Callus formation becomes problematic when there is an overproliferation of the keratin tissue leading to underlying bursitis, neuroma, or neuritis.[8] Intractable plantar keratoma is a highly painful lesion in the region of the plantar aspect of the metatarsal heads. Intractable plantar keratoma can be extensive and symptomatic enough to affect an athlete's performance.[9]Deformities of the metatarsophalangeal joint that produce increased plantarflexion in this area lead to the development of intractable plantar keratoma in the metatarsal head regions receiving the most plantar pressure.

Calluses should be treated systematically. Early scalpel debridement and intervention by means of footwear changes are essential. Daily work on these lesions with a pumice stone or callus file should be advocated. Metatarsal pad fabrication and placement of custom foot orthotics will aid in prevention of recurrence.


Clinical pearls for treatment of hyperkeratotic conditions primarily focus on prevention. Try to personalize footwear for your athletes through identification of predisposing factors such as bony deformities, lesions currently present, and history of previous complications. Also, avoid aggressive treatment to prevent exacerbation of symptoms and always assess for other potential causes (viral warts).


Xerosis simply is severely dried skin. Skin drying is more pronounced in cold environments and especially during the winter months in temperate regions. Low humidity in the air leads to increased drying of the skin that manifests as roughening and fine scaling. In more severe forms of xerosis, the scaling becomes coarser and fissures may occur. Athletes that are exposed to chemicals (swimmers) and adhesives are particularly at risk. For the most part, xerosis is a benign condition and athletes will complain of pruritus in the lower leg and dorsal foot. This drying can predispose to fissure formation, allowing fungal or bacterial organisms to colonize the area.

The treatment of xerosis should include regular emollient therapy. More severe cases respond well to 12% lactate lotion. Temporary relief of pruritus symptoms can be achieved using antihistamines such as diphenhydramine and cetirizine.


Clinical pearls for the treatment and prevention of xerosis include decreasing shower frequency and duration, minimizing hot water use, using regular emollient therapy, and protecting from epidermal excoriation.


Sun exposure for prolonged periods of time in barefoot sports such as sand volleyball, swimming, and surfing lead to light-induced skin changes manifest as either suntan or sunburn. A suntan is the body's protection mechanism from photoinjury after exposure to ultraviolet light. Suntan occurs in two stages; the first stage involves a photochemical change of existing melanin to produce a darkening of the skin color, whereas the second stage involves the synthesis of new melanin in the dermal layer that typically becomes visible within 72 hours.[10] Sunburn occurs as a response to excess ultraviolet exposure with the degree of damage being dependent on duration of exposure and sensitivity of the skin. Individuals with a light complexion are much more predisposed to this type of injury. The dorsum of the foot is a region that is not often sun exposed and is prone to severe burn. Sunburn reaction occurs in several stages, including immediate erythema, delayed erythema, vascular permeability with the development of edema and blisters, and finally desquamation. Immediate erythema is seen within a few minutes before fading. This gives way to a delayed erythema after a period of time. With more severe injury, vascular permeability with intradermal edema and epidermal blister formation will be seen within the span of a few hours. The desquamation process takes place within a week, giving way to new skin, albeit sun-damaged skin. Sun damage has an additive effect. Long-term changes increase the risk of skin cancers such as melanoma, squamous cell carcinoma, and basal cell carcinoma.

Treatment after sun exposure depends on the degree of injury. Less severe burns can be treated with cool, wet compresses, emollient therapy, and protection from further exposure. Severe burns may need to be treated with a 4- to 6-day course of oral steroids in an attempt to prevent intense immune reaction. Again, it should also be stressed that these injuries should be protected from further ultraviolet exposure.


The key clinical pearl for sunburn treatment and prevention is preparation. Any anticipated sun exposure should be preceded by application of a sunscreen compound. Sun protection factor (SPF) is an indicator of sunscreen efficacy, with a higher SPF being more protective. When treating sunburn acutely, topical anesthetic preparations containing benzocaine should be avoided secondary to a photosensitization effect.


Dermatologic Disorders: Traumatic

Black heel (calcaneal petechiae, talon noir)

Darkening of the posterior and posterolateral aspect of the heel was first described by Crissey and Peachey[11] in basketball players. This discoloration is caused by repeated lateral shearing force of the epidermis sliding over the rete pegs of the papillary dermis, resulting in intraepidermal hemorrhage.[12] The dark appearance gave rise to the terms black heel and calcaneal petechiae. In addition to basketball players, black heel ( Fig. 11-3 ) has been described in other sports that require frequent starting and stopping such as lacrosse and football. The pathophysiologic changes previously described are caused by heel trauma from rubbing against the back of the shoe. It is seen most commonly in adolescents and young adults and usually is asymptomatic. Sports activities should not be limited by this condition.



Figure 11-3  Black heel.  (From Habif, Clinical dermatology, St Louis, 2004, Mosby: p. 375, Figures 12-18a and b.)


The diagnosis of black heel usually will be readily apparent by history and physical examination. The lesions usually appear as multiple petechiae with central aggregation and scattered satellite patches. Often the dyschromia is horizontally arranged across the posterior and lateral aspect of the heel but can be seen in circular and oval patches, as well. If the diagnosis is in doubt, other diagnoses such as viral warts and malignant melanoma must be considered. Rarely, skin biopsy with histochemical staining is required to confirm the diagnosis of black heel and to rule out malignant melanoma.[13]

The treatment of black heel is quite simple. The clinician should educate and reassure the athlete that this condition is benign and will resolve with cessation of the causal mechanism.


The most important clinical pearl in black heel evaluation is distinguishing this lesion from malignant melanoma. If there is any doubt, an excisional biopsy should be performed with dermatopathology evaluation. Black heel can be prevented by placing a felt pad in the heel of the shoe. If a cosmetic effect is desired, the lesion can be pared down with a scalpel with nearly complete clearance of the dyschromia.

Piezogenic pedal papules

The term piezogenic refers to “pressure giving rise to.” Piezogenic papules occurring in the heel are more common than previously thought. Zaidi et al.[14] described 80 subjects out of a random sample of 100 people to have these pedal papules. They arise from herniation of the subcutaneous fat into the dermis. Their presence is identified easily while pressure is being applied, but they usually disappear with the removal of that force. The distribution of piezogenic papules in an athletic population is primarily along the medial and lateral plantar heel pad. The potential exists for these lesions to become painful, especially in long-distance runners, who place a great deal of repetitive stress on their feet. When painful, piezogenic papules can be detrimental to athletic performance. It is thought that the pain associated with the papular lesions is secondary to inflammatory changes in the deep dermal layers.[15]

Treatment options for piezogenic papules are limited. Some degree of symptomatic relief may be achieved with heel cups or shoe orthotics. There are no medical or surgical therapies described for this malady.


Regarding treatment pearls, with piezogenic pedal papules it is more of a case of what not to do than what to do. Corticosteroid injections into painful lesions are contraindicated. If steroid injections are administered, the athlete will be predisposed to fat atrophy and weakening of the supportive collagen matrix in this region that can be complicated by an even more painful heel.

Friction blisters

Repetitive rubbing of the skin has been shown to produce blisters in multiple controlled trials. These frictional forces cause a mechanical separation of the epidermal cells at the level of the stratum spinosum. With continued mechanical trauma and separation of the epidermal cells, midepidermal necrosis will occur and a clear transudate will accumulate in this space.[16] These blisters are more likely to occur in skin areas that have a thick, horny layer held tightly to underlying structures, such as the soles of the feet.[17] Moisture of the foot can either exacerbate or relieve the degree of frictional force present. A damp skin surface will see an increase in the frictional force, whereas very moist/wet feet actually will benefit from a lubrication effect. Friction blisters can be seen in many parts of the body in many types of athletes but are most common on the feet of distance runners. In addition to a damp environment, friction blisters also can be caused by poorly fitted shoes, bulky socks that bunch up and cause an area of increased pressure, and training on hard surfaces such as concrete or pavement.

The diagnosis of friction blisters usually can be made by history alone. A physical examination will identify a bullous-appearing lesion corresponding to the region of discomfort. Friction blisters tend to be tender to palpation and are fluctuant when pressure is applied. The clinician should examine the region surrounding a friction blister carefully to evaluate for the possibility of a superficial infection (cellulitis).

The consensus is that blisters should be drained, multiple times if needed, within the first 24 hours. Cortese et al.[18] described a shorter healing time with this early intervention. They also stressed that the blister region healed more rapidly if the overlying roof was kept intact. Again, close attention should be paid for signs of infection, with appropriate use of systemic antibiotics to treat early cellulitis or impetigo. Placement of padding (moleskin) over the blister region is advocated until healing has occurred.


Clinical pearls for the treatment and prevention of friction blisters focus primarily on decreasing the amount of frictional force across a given dermatologic region. Some studies including Knapik et al.[19] have shown foot antiperspirants to be efficacious in the reduction of foot blisters during recreational sports activities. It should be noted, however, that the use of antiperspirants on the feet as a prevention for friction blisters is controversial. Also, the use of antiperspirant agents is confounded by a high incidence of irritant contact dermatitis, which can be more debilitating than the original friction blisters. Knapik et al.[20] identified a reduction in frictional blister formation with the use of polyester-lined socks. With this information, now it is recommended that endurance athletes use acrylic-based socks or thin polyester socks combined with a thick polypropylene sock. Neoprene insoles combined with appropriately fitted shoes are a great starting point for those initiating training activities. Early exposure to low-intensity frictional coefficients allows for cellular adaptation and epidermal thickening which may reduce the likelihood of blisters, as well.[17]


Infectious Disorders

Viral warts

It is estimated that approximately 10% of the adolescent population in the United States is affected by plantar warts ( Fig. 11-4 ). With this in mind, it becomes evident that many athletes will fall into this category. Human papillomavirus (HPV) types 1, 2, and 4 are responsible for this form of hyperkeratotic lesion. After exposure to the virus, HPV attacks the epidermal layers of damaged, cracked skin. Unlike viral wart lesions elsewhere on the body, plantar warts grow deep into the tissue secondary to the constant pressure application to the sole of the foot. Plantar warts seem to thrive in the warm, moist environment of the shoe. The virus typically is encountered by direct contact of the bare foot to a surface harboring the virus. Johnson[21] identified that the use of public locker rooms increased the risk of contracting plantar warts, especially when the subjects used communal showers.


Figure 11-4  Plantar warts.  (From DeLee J, Drez D, Miller, M: DeLee and Drez's orthopedic sports medicine, ed 2, Philadelphia, 2002, Elsevier, Figure 30-J-73.)


The diagnosis of plantar warts can be challenging because these lesions sometimes are difficult to distinguish from callus formation. Athletes will present with symptoms of pain in the region corresponding to the lesion. Direct observation may identify centralized cratering of a warty lesion. If the diagnosis remains in doubt, the hyperkeratotic tissue should be pared away using a no. 15 blade scalpel until the hypertrophic epithelium gives way to a dermal layer revealing multiple “seeds.” These seeds represent the thrombosed vessels that supply the warty lesion.[22] Localized spread along the plantar surface results in a cluster of warty lesions that may resemble a mosaic. Plantar warts can be seen anywhere along the plantar surface but tend to spare the region corresponding to the metatarsal heads.

Plantar warts are benign, and most will resolve spontaneously. Many forms of therapy have been described to eradicate plantar warts. Close attention should be paid to the potential adverse reactions associated with a given therapy. If lesions are causing symptoms of pain or impairment in function, a noninvasive therapeutic approach should be considered. Paring of the hyperkeratotic superficial layer should be followed by regular application of keratolytic agents such as salicylic acid (15% to 60%), cantharidin, or dichloroacetic acid. Daily application of these topical therapies with regular use of a pumice stone will aid in the gradual resolution of plantar warty lesions without significant impairment in function. Multiple other therapeutic modalities are described, including cryotherapy, injection therapy, immunotherapy, electrical therapy, chemical destruction, and surgical therapy.[23] More aggressive/invasive treatments should be reserved for recalcitrant cases of plantar warts that have not responded to conservative management.


The first clinical pearl to remember is that plantar warts cause localized pain symptoms but can be overlooked on physical examination. Many athletes present with painful plantar lesions that are mistaken as overuse injuries such as metatarsal stress fractures because a plantar dermatologic examination was not performed. Encouraging the use of shower thongs or sandals in communal showers can reduce the risk of HPV exposure. Surgical treatment should be strongly discouraged because the resultant scar tissue can lead to symptoms of continued pain.

Tinea pedis

The term athlete's foot refers to the most common infection in sports participants. Fungal infection of the feet usually affects the interdigital spaces, especially between the fourth and fifth toes. The warm, moist environment within an athletic shoe provides an ideal environment for fungus to prosper. The dermatophyte linked to tinea pedis ( Fig. 11-5 ) in most cases is Trichophyton rubrum. Less commonly, Trichophyton mentagrophytes and Epidermophyton floccosum are isolated. Men are affected more commonly than women or children. A 70% rate of lifetime incidence is estimated.[24] Much like the viruses associated with plantar warts, dermatophytes can survive on the warm, moist floors of locker rooms and communal showers.


Figure 11-5  Tinea pedis.  (From Rakel: Textbook of family practice, ed 6, Philadelphia, 2002, WB Saunders, Figure 41-28.)


The interdigital spaces are most commonly affected in tinea pedis; however, a moccasin distribution also can be identified on physical examination. The “moccasin” distribution refers to scaling along the medial and lateral sides of the foot and potentially also the plantar surface. Physical examination findings will vary depending on the stage of infection. Early infection presents as fine scaling with associated pruritus. As the infection progresses, maceration of the superficial skin occurs, with gradual epidermal breakdown. At this point, superinfection by resident bacteria progresses skin breakdown and increases symptomatology. Leyden and Kligman[25] demonstrated progressively decreased rates of fungal recovery as the severity of symptoms worsened. Conversely, more severe symptomatology correlated with increasing numbers of resident aerobic bacteria, especially large colony diphtheroids. In rare cases, highly inflamed sterile vesicles and pustules can be seen distant from the tinea infection. This is referred to as a “dermatophytid” or “id” reaction, representing an immunologic response to the fungus.[26]

Dermatophyte infections of the interdigital space usually respond well to topical therapy with antifungal agents of the imidazole and allylamine groups. Examples from these groups include clotrimazole 1% and terbinafine, respectively. Other potential choices include econazole, ketoconazole, miconazole, oxiconazole, ciclopirox, naftifine, and butenafine. Topical therapy must be continued for 4 weeks with clotrimazole and 1 to 4 weeks with terbinafine. Patients with moccasin-type tinea pedis can be difficult to treat and occasionally will require oral antifungal therapy. Oral antifungals include itraconazole, terbinafine, fluconazole, ketoconazole, and griseofulvin. Fluconazole should be administered 150mg daily for a total of 2 to 4 weeks for recalcitrant cases. If the diagnosis of tinea pedis is in doubt after several weeks of topical and/or oral therapy, a potassium hydroxide preparation with microscopic examination for hyphae should be performed to confirm the diagnosis. Oral antibiotic therapy should be prescribed for severe cases with associated cellulitis. Immunocompromised individuals are especially prone to this complication. Coverage for typical skin flora including Staphylococcus and Streptococcusis appropriate. First-line therapy is dicloxacillin 500mg every 6 hours for 7 days (Gilbert et al.[27]). Erythromycin can be substituted if penicillin is contraindicated. Other interventions in treating tinea pedis include the use of drying agents such as aluminum acetate solution and keratolytic agents such as ammonium lactate lotion.

The prevention of tinea pedis is challenging.


Clinical pearls include education of athletes to avoid direct contact of the feet with flooring in showers and locker rooms. Also, maintaining a dry environment for the feet can limit the potential for fungal growth. Lastly, sharing footwear and towels should be discouraged.


Nail Disorders

Subungual hematoma

Many sports predispose participants to direct foot trauma, especially to the toes. This trauma may be in the form of repetitive pounding against the anterior shoebox or it may be suffered as a result of another player's stepping on the foot. Subungual hematoma ( Fig. 11-6 ) formation can occur as a result of this trauma. Blood collects in the space between the nail bed and the toenail, with pain generated from increasing pressure within this space. Symptoms range from mild discomfort to extreme pain. Acute traumatic injuries tend to be more painful. Associated injuries include phalanx fractures and soft-tissue contusion.


Figure 11-6  Subungual hematoma.  (From Habif, Clinical dermatology, St Louis, 2004, Mosby: p. 882, Figure 25-36.)


The evaluation process for a subungual hematoma should include a thorough history, including the timing of the injury and musculoskeletal, neurologic, and vascular assessment. With repetitive pounding injuries as seen in runners and tennis players, the physical examination may reveal early subungual discoloration, but this may be delayed. Acute traumatic injuries usually will have a more obvious subungual bloody accumulation that is identified easily on examination.

The treatment for subungual hematoma depends on symptomatology and the degree of involvement. Athletes presenting with extreme pain, especially with a brief period of symptoms, will benefit from a decompression procedure. Decompression can be achieved in one of three ways: a battery-operated cautery device can be used to burn a small hole through the nail, a large-diameter needle can be used to bore into the nail to create a hole, or a paper clip tip can be heated to burn through the nail plate as well. All of these interventions will allow the blood to drain, effectively relieving the pressure and pain. On occasion, a nail bed laceration will be identified. This requires nail removal and laceration repair.[28] Early intervention will allow for prevention of nail dystrophy and further impairment.


Clinical pearls for the prevention of subungual hematoma include working with athletes to choose appropriate footwear. Excessive forefoot anterior motion and tight dorsal toe boxes can exacerbate this problem. During the recovery phase from subungual hematoma, it is beneficial to provide pressure relief over the involved toes by cutting the leather overlying the involved digits.[29]


Ingrown toenails can lead to severe functional impairment, especially in those who depend on their feet in competition. Onychocryptosis ( Fig. 11-7 ) is the most common of all toenail problems in athletes, and the lateral margins of the great toe are most often affected. The condition also can be complicated by paronychia formation, which can lead to osteomyelitis or sepsis. Ingrown toenails can be seen secondary to abnormal nail plate anatomy or secondary to external factors. Abnormal nail plate anatomy can be hereditary or secondary to previous trauma. When there is an improper fit of the nail plate in the nail groove, sharp spicules of the lateral nail margin are driven gradually into the dermis of that region. A foreign body reaction is seen, leading to localized erythema, edema, purulence, and granulation tissue. Compromise of the tegument can lead to the introduction of typical skin flora into the break in the skin. Typically, ingrown toenails are divided into three stages: the first stage involves erythema, edema, and focal tenderness. The second stage is marked by crusting and expressible purulence at the nail fold and nail plate junction. The third stage shows signs of chronic infection, with protuberant granulation tissue extending over and under the nail plate. The prevalence of ingrown toenails is 3:1, male to female.[30] The factors that put athletes at risk for onychocryptosis include improper nail care (aggressive nail trimming), excessive foot moisture, and repetitive trauma.


Figure 11-7  Onychocryptosis (ingrown toenail).  (From Habif, Clinical dermatology, St Louis, 2004, Mosby: p. 881, Figure 25-35.)


Initial evaluation for onychocryptosis should involve a thorough history and focused physical examination. Symptoms described will vary from minimal discomfort to incapacitating pain. A family history of ingrown nails or a previous history of similar problems may aid in determining the underlying cause. Physical examination of type 1 lesions will reveal erythema, edema, and tenderness to palpation in the involved nail border. The nail can be lifted easily to identify an intact layer of skin within the nail groove. Type 2 lesions will be characterized by crusting at the nail fold and nail plate junction, with or without an expressible purulence. Lifting the lateral nail border will reveal early dermal breakdown. Stage 3 lesions appear very uncomfortable and have signs of chronic infection and extensive granulation tissue (proud flesh). Evaluation of nail morphology may point toward a specific causal factor (incurvated nail plate, subungual exostosis, or nail dystrophy).

Treatment approach to ingrown nails varies depending on the stage of involvement. Ilfeld[31] described a successful therapy for onychocryptosis with stage 1 findings. The treatment consisted of placement of a collodion-coated cotton wisp between the edge of the ingrown nail and the adjacent soft tissue. This waterproof barrier allows for immediate pain relief and provides a firm runway for further growth of the nail. This procedure may need to be repeated after 3 to 6 weeks or sooner if displacement occurs. A similar intervention can be applied initially for stage 2 involvement. The collodion-coated cotton wisp can be inserted between the lateral nail edge and the soft tissues if there is not significant spicule formation. If there is a component of the nail that has broken through the dermal layer that prevents placement in a reasonable fashion, the lateral nail border should be removed. This therapeutic approach is contiguous with that recommended for stage 3 onychocryptosis. Wedge-shaped nail resection is recommended on the involved side in the following manner: first, a digital block should be performed using 1% or 2% lidocaine injection at the base of the digit. Next, a tourniquet should be placed proximal to the toenail. After thorough cleansing with Betadine solution, a nail splitting scissors should be inserted under the ingrown nail plate parallel to the lateral nail fold. On meeting resistance proximally in the region of the matrix, the wedge should be cut and removed. Any granulation tissue present should be treated with silver nitrate application or removed via curettage. Wound care following this procedure entails regular application of wet compresses until inflammation has subsided. Gentle cleansing is recommended but should be delayed for the first 24 to 48 hours. For cases of recurrent ingrown nails, athletes may require the use of liquid phenol for permanent destruction of the lateral nail matrix. This should be applied immediately after wedge resection, with care taken to avoid the soft tissues other than the nail matrix.

Ingrown toenails will be encountered on a fairly regular basis.


Clinical pearls for the treatment of this malady include early intervention in an attempt to avoid advanced-stage lesions. Treatment interventions can lead to symptom exacerbation and further loss of performance capacity. There is not absolute contraindication to participation after nail resection unless the athlete has signs/symptoms of systemic infection. Participation should be based on pain tolerance. Nail resection should be reserved for those athletes who are unable to perform or whose schedule allows for a period of recovery. Lastly, complete nail extraction should be avoided if possible because this can predispose to further nail dystrophies.

Onychomycosis (tinea unguium)

Onychomycosis ( Fig. 11-8 ) is the most common cause of toenail thickening. Up to 20% of the population in various age groups is afflicted with this problem.[10] The most common pathogens include the dermatophytes Trichophyton rubrum and Trichophyton mentagrophytes. Less commonly, Candida albicans and nonpathogenic fungi are implicated. The most common distribution is the distal subungual region. Other patterns include white superficial onychomycosis, proximal subungual onychomycosis, and Candida onychomycosis. In distal subungual onychomycosis, the dermatophytes invade the distal area of the nail bed leading to the development of an accumulation of hyperkeratotic debris. This subsequent nail thickening causes separation from the underlying nail bed and allows the fungus to grow further into the substance of the plate. With time, this invasion slowly moves more proximally with the potential to involve the entire nail. Proximal subungual onychomycosis is caused by the same organisms, but is more associated with immunosuppressed states. Psoriasis should be kept high on the differential diagnosis because this disorder can cause similar nail features. Factors that predispose individuals to the development of onychomycosis are humidity, heat, trauma, diabetes mellitus, and underlying tinea pedis.[32]


Figure 11-8  Onychomycosis.  (From Rakel: Textbook of family practice, ed 6, Philadelphia, 2002, WB Saunders, Figure 41-30.)


Historically, affected individuals will present with a chronic history of gradual nail thickening and discoloration. Runners seem to be predisposed to this condition secondary to repetitive trauma to the nail from contact with the toe box, whereas basketball players are more predisposed secondary to the direct trauma of having their toes stepped on by other competitors. Physical examination will reveal hyperkeratosis of the nail bed, with a yellowish to brown discoloration and onycholysis. The diagnosis should be confirmed with both a potassium hydroxide (KOH) examination and a fungal culture.

On confirmation of a fungal offending agent, therapeutic modalities can be discussed. Within recent years, effective systemic antifungal therapy has become available for the treatment of onychomycosis. Included in the treatment options are fluconazole, itraconazole, and terbinafine. These drugs have replaced griseofulvin as the systemic treatment options. Terbinafine should be administered at a dosing schedule of 250mg/day for a total of 12 weeks. Itraconazole can be administered at 200mg/day for a total of 12 weeks or through pulse dosing at 400mg/day for the first week of 4 consecutive months. Lastly, fluconazole is an option at 150mg once weekly for a total of 6 to 12 months (Gilbert et al27). Extreme care should be taken to avoid the use of these medications in individuals with hepatic insufficiency. A review of potential drug interactions also is advocated.

Onychomycosis is a fairly benign entity but can be complicated by symptoms of localized pain or secondary bacterial infection. Many athletes will opt to defer systemic treatment, but those who wish to proceed with therapy should be monitored closely for adverse reactions or drug interactions. Educating the individual that it may take 6 to 12 months for the nail to grow out will minimize the number of callbacks within the first few months.



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