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. Fisher² 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.

Frostbite

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.

Hyperhidrosis

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

Hyperkeratosis

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.

Xerosis

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.