Subtalar dislocations are a rare entity accounting for only 1% to 2% of all dislocations. This injury, also termed a peritalar dislocation, describes dislocation of the talus from both the calcaneus and navicular bones (Fig. 23–42). Subtalar dislocations may be classified as medial or lateral depending on the position of the foot relative to the distal tibia. The more common medial type represents 80% to 85% of all subtalar dislocations.54,55 Medial subtalar dislocations are known as Basketball Foot or Acquired Clubfoot.55 Lateral subtalar dislocations are less common. Lateral subtalar dislocations have been called Acquired Flatfoot.55 Anterior and posterior subtalar dislocation may also occur but are unusual.
Subtalar dislocation (medial).
Dislocation of the talus above the ankle mortise and below the calcaneus and navicular bones is termed a total talar dislocation and is extremely rare.56) With total talar dislocations, the talus is completely dislocated out of the ankle mortise and rotated such that the inferior articular surface points posteriorly and the talar head points medially.
Subtalar dislocations can occur after both low-energy (e.g., stepping off a curb) and high-energy (e.g., fall from a height) trauma.54–57 A medial subtalar dislocation typically follows an inversion and plantar flexion injury. The talocalcaneal and talonavicular ligaments rupture as the bones of the foot are displaced medially.
In lateral dislocations, there is a forcible eversion of the foot. The talar head is forced through the capsule of the talonavicular joint and the calcaneus. The remainder of the forefoot displaces laterally from the talus.
The patient will present with a relatively obvious deformity of the foot (Fig. 23–43). There is generally marked pain, swelling, and tenderness. With medial dislocations, the foot will be displaced medially and the talus palpable laterally. The skin is taut over the lateral surface of the foot and the vascular supply is often compromised. Open dislocations may also occur and should be suspected whenever there is disruption of the skin laterally.
Subtalar dislocation (medial).
Routine views including AP, lateral, and oblique are usually adequate in demonstrating a subtalar dislocation (Fig. 23–44). Fractures are associated in approximately two-thirds of cases.57,58 Malleolar, talar neck, and osteochondral fractures are the most common. Postreduction films are required for documentation as well as to exclude the presence of occult fractures. Postreduction CT identifies additional fractures and changes the management in nearly half of the cases.58
Radiographs of a subtalar dislocation (medial). A. AP and B. lateral.
Subtalar dislocations are associated with fractures (tarsal, malleolar, talar neck, and osteochondral) and ligamentous injury.
The emergency management of closed injuries includes analgesics and prompt reduction to avoid the complication of skin necrosis (Video 23–1). If prompt consultation is not available, an attempt at closed reduction should be made.59,60
Video 23-1: Subtalar joint dislocation reduction.
The knee is held in flexion to relax the gastrocnemius and allow for an easier reduction. To reduce a medial dislocation, traction is applied to the foot and heel in line with the deformity. Countertraction is applied to the leg. This is followed by pressure over the talar head with an abduction force concomitantly applied to the forefoot. Lateral dislocations are reduced by firm traction followed by adduction over the forefoot. Subtalar dislocations are irreducible in almost a third of the cases.61 Medial subtalar dislocations have a higher rate of successful reduction than lateral dislocations which require open reduction in half of the cases.61,62
Subtalar dislocations may be complicated by the development of several significant disorders.
AVN of the talus
Loss of ankle motion and traumatic arthritis
Ischemic skin loss secondary to underlying talar pressure
MTP dislocations are a rare injury and usually occur in a dorsal direction. Dislocations of the great toe MTP are more common than the lesser toes.25 MTP dislocations are classified as simple or complex based on the presence of interposed soft tissues or sesamoid bones (Fig. 23–45). The interphalangeal (IP) joint can be dislocated in a dorsal or volar direction. IP dislocations, like MTP dislocations, are rare.42
Dislocations of the MTP joint are secondary to axial load with extreme dorsiflexion of the proximal phalanx. Classically, this injury occurs in football players competing on artificial turf.63 If the force generated does not result in a dislocation, a sprain is diagnosed, commonly referred to as “turf toe.” With greater forces (e.g., motor vehicle collisions), the plantar capsule avulses and a dorsal dislocation of the proximal phalanx on the metatarsal occurs. Medial or lateral MTP dislocations are the result of injury forces that abduct or adduct the toe.
Patients with dislocation of the MTP joint present with pain, swelling, inability to walk, and visible deformity. Typically, the toe is hyperextended, resting on the dorsum of the metatarsal. The sesamoid may be palpable on the dorsal aspect if the dislocation is complex. Patients with IP dislocations will present with similar findings. If swelling is significant, the deformity might not be as obvious (Fig. 23–46A).
Dorsal dislocation of the right great toe interphalangeal joint. (A). Patient photograph (arrow). (B). AP radiograph. (C). Oblique radiograph.
MTP dislocations may be diagnosed on the AP view, as there is generally an overlap between the distal metatarsal and proximal phalanx. IP dislocations are best seen on the AP and oblique views (Figs. 23–46B and C). With a complex MTP dislocation, the volar plate of the great toe, along with the sesamoid, entraps the phalanx on the dorsal surface of the metatarsal.
IP dislocations are frequently associated with fractures.
IP dislocations may be treated with closed reduction followed by dynamic splinting. Unstable reductions require early referral for internal fixation. Dorsal MTP dislocations are reduced using hyperextension with distal traction (Fig. 23–47 and Video 23–2) Stable reductions require a hard-soled shoe and dynamic splinting. Dislocations resistant to reduction have interposed soft tissues and usually require open reduction though successful percutaneous reduction has been reported.64 Unstable reductions or crepitus after reduction, suggesting an intra-articular loose body, are also indications for operative repair.
Reduction of the metatarsophalangeal joint. A. Traction is applied in the line of deformity. B. Hyperextension is used to reproduce the injuring force. C. With traction maintained, reduction is accomplished.
Foot Compartment Syndrome
For a full discussion of compartment syndrome, refer to Chapter 4. This section will address unique aspects of compartment syndrome of the foot. The foot is the most challenging location in the body to diagnose compartment syndrome because the presentation is subtle. The emergency physician should have a high index of suspicion for this diagnosis to avoid the chronic sequelae of a missed diagnosis.
The foot contains a total of nine separate compartments. Three compartments—the medial, lateral, and central (superficial)—run along the entire plantar surface of the foot (Fig. 23–48). The medial compartment is located inferior and medial to the first metatarsal and contains the abductor hallucis and flexor hallucis brevis muscles. The lateral compartment is found inferior and lateral to the fifth metatarsal. This compartment contains the abductor digiti minimi and flexor digiti minimi brevis. The central (superficial) compartment contains the flexor digitorum longus and brevis muscles.
The compartments of the sole of the foot. (Image used with permission from Eric Brader, MD)
The remaining six compartments do not run along the entire length of the foot (Fig. 23–49). These compartments include the four interosseous compartments and the calcaneus and adductor compartments. The four interosseous compartments exist dorsally between the metatarsals. These compartments contain the interosseous muscles. The calcaneus compartment is deep to the central compartment within the heel of the foot. This compartment contains the quadratus plantae muscle and communicates with the deep posterior compartment of the leg through the flexor retinaculum. The adductor compartment is within the deep plantar aspect of the forefoot and contains the adductor hallucis muscle.
Cross-section schematic of the compartments of the foot at the level of the proximal metatarsal head.
Like compartment syndromes in other parts of the body, fractures are a major cause of foot compartment syndrome along with significant crush injuries, infection, and iatrogenic causes.65 The fractures most likely to produce a compartment syndrome in the foot include multiple metatarsal fractures, Lisfranc fracture–dislocations, and intra-articular calcaneal fractures.65 Foot compartment syndrome occurs after 10% of intra-articular calcaneal fractures.11,65 Of these, one-half develop a claw toe deformity due to contracture of the quadratus plantae muscle within the calcaneal compartment. In one study, foot compartment syndrome was due to calcaneal fractures in 42%, multiple metatarsal fractures in 25%, and Lisfranc fracture–dislocation in 17%. The remaining 17% of patients did not have injury to the foot, but suffered from foot swelling due to more proximal orthopedic injuries (tibia plafond, open femur, tibial plateau).66 Delayed presentations of up to 36 hours have been reported in patients who sustained less severe mechanisms of trauma (kicked in the foot during a soccer game).67
As with all compartment syndromes, the degree of pain is out of proportion to the injury, but it is generally more vague and ill-defined. The pain is not relieved by immobilization or with pain medication. The pain caused by compartment syndrome in the foot may be exacerbated by elevation.
The affected compartment will be tense on examination. Pain with passive dorsiflexion of the toes is an important sign. After several hours, signs of neurologic compromise may appear, including numbness, burning, and paresthesias. Again, these findings are less dramatic in the foot when compared with other locations of the body.
The emergency physician must have a high index of suspicion for this condition in patients with significant bony or soft-tissue injuries or in patients who present after minor trauma with pain that appears out of proportion to what is expected. Orthopedic consultation should be obtained and compartmental pressure readings are measured. Treatment involves decompression with an emergent fasciotomy.
Puncture wounds to the plantar aspect of the foot are associated with a higher rate of infection than similar wounds elsewhere on the body. The penetrating agents include needles, nails, glass, wood splinters, thorns, and toothpicks. Retained foreign bodies are present in 3% of cases and include pieces of clothing, rust, gravel, or dirt. The presence of a foreign body is associated with soft-tissue infection and osteomyelitis.
Ten percent of patients experience late infection. In a study by Fitzgerald and Cowan,68 132 of 774 children examined with puncture wounds experienced cellulitis and 16 had osteomyelitis. The most common bacterial pathogens causing soft-tissue infections are staphylococci including MRSA and streptococci, whereas pseudomonas causes 90% of the cases of osteomyelitis. Other organisms that cause osteomyelitis include Escherichia coli, Staphylococcus aureus, and mixed flora.69,70
Puncture wounds of the foot can be separated into five types depending on the degree of penetration, infection, and the presence of the foreign body. Type I involves superficial cutaneous penetration into the epidermis or the dermis with no signs or symptoms of infection.71 Type II puncture wounds are subcutaneous or involve a joint without signs or symptoms of infection. This is the most common type of puncture wound. Type III puncture wounds are divided into those that involve soft-tissue infection including septic arthritis and a retained foreign body (type IIIA) and those with penetration of the foreign body into the bone (type IIIB). Type IV puncture wounds are associated with osteomyelitis.
Findings on physical examination are usually minimal immediately following injury and include a small laceration or puncture wound (Fig. 23–50A). If the injury is several days old, the original wound may be partially healing. In these cases, the patient is usually presenting because of erythema, discharge, warmth, and pain associated with an infection. If the presence of a foreign body is unclear, use a cotton-tip applicator to palpate around the puncture site and ask the patient if there is any area of significant tenderness. If the wound is tender, there is a greater likelihood of a retained foreign body and the location of tenderness is where the foreign body will likely be.
Plantar foreign body removal. A. Plantar puncture wound. B. Radiograph demonstrates a triangular glass foreign body. C. Fluoroscopy is used to locate the glass. D. The glass is grasped and removed.
Plain radiographs should be taken when a patient presents with a puncture wound and the examiner is uncertain if a retained foreign body is present. Glass and metal are usually easily seen on radiographs (Fig. 23–50B). To localize a metal foreign body, ultrasonography or fluoroscopy is useful. These modalities are especially useful because real-time images can be obtained that will also aid in the removal of larger foreign bodies. For radiopaque foreign materials, removal is aided because the clinician can visualize both the instrument and the foreign body (Fig. 23–50C and D). Ultrasonography and CT better demonstrate plastic or wood foreign bodies.
Because of the high rate of infection, these wounds require special attention. The treatment of superficial, noninfected puncture wounds (type I) includes tetanus and local wound care. The patient is instructed to clean the area twice daily and wear a protective covering. If there is discomfort when walking, non–weight-bearing activities are recommended. When the depth of the wound cannot be determined, the penetration should be assumed to be deep and the wound treated as such.
Deeper wounds (type II) usually require exploration. A local anesthetic or a regional nerve block (ankle block of sural and posterior tibial nerves) should be administered. Multiple options for exploration exist, and the best method is unknown. Blunt probing with splinter forceps may simply force objects deeper. Excision of a block of tissue around the puncture will aid in foreign body removal and assist in irrigation (Fig. 23–51). Extending the uninfected wound is recommended to remove wood or other contaminated objects or when a nail puncture occurs through a shoe. These injuries are especially likely to become infected. To prevent the inoculation of healthy tissues, the wound should not be closed. It must be noted, however, that it is not necessary to remove a foreign body if it is inert, asymptomatic, not a threat to function, and not within a joint. Unfortunately, prophylactic antibiotics have not been shown to reduce the infection rate.70
Technique for detecting and removing a foreign body within a plantar puncture wound. A. Palpate around the wound with a cotton-tipped applicator. The site of greatest tenderness is the location of the foreign body. B. A small 2- to 3-mm elliptical incision is made toward the presumed location of the foreign body. C. The tissue is removed with forceps. The foreign body may be located within the tissue.
Puncture wounds that are infected and have a foreign body (type IIIA) require antibiotics and surgical intervention. When penetration of foreign material is into bone (type IIIB), the foreign body must be surgically removed with curettage of the osseous defect, debridement of soft tissue, copious lavage, and open packing. Empiric intravenous antimicrobial agents are administered, pending intraoperative cultures results.
Puncture wounds of the foot that result in osteomyelitis (type IV) are unusual. The condition does occur and wider recognition of the entity will help in prevention and early diagnosis. Once infection develops in a puncture wound, one must be aggressive, including surgical exploration of the wound, debridement, and removal of all foreign material.69,71
Rupture of the Achilles tendon is relatively common, occurring in 18 per 100,000 persons.72 This condition is misdiagnosed in 20% to 30% of cases because of insignificant pain or an incomplete examination. The diagnosis is delayed more commonly in those patients injured while not participating in sports and patients with a high BMI. This delay is due to a lower index of suspicion and a technically difficult examination.73 This injury is more common in men between the ages of 30 and 50 years who participate in recreational sports (weekend warrior). This condition also occurs in serious athletes.74 Chronic oral corticosteroid administration and fluoroquinolone usage predisposes to rupture.72,73 Rupture of the Achilles tendon occurs most commonly at the narrowest portion of the tendon, approximately 2 to 6 inches above its point of attachment to the calcaneus.75
The mechanisms of injury include an extra stretch applied to a taut tendon, forceful dorsiflexion with the ankle in a relaxed state, or direct trauma to a taut tendon. Only one-third of patients will have symptoms prior to rupture. Patients report a sudden onset of pain and the sensation that they were struck or kicked in the back of the leg. An audible snap may be heard.
The patient complains of acute pain in the lower calf that makes walking almost impossible. A partial tear may be difficult to diagnose and is often misdiagnosed as a strained muscle; however, most Achilles tears are complete.
On examination, diffuse swelling and bruising is present and there may be loss of plantar flexion (Fig. 23–52). A palpable defect may be present, unless swelling is severe. The patient will have some ability to plantar flex the ankle because of the action of the posterior tibial muscle, but weakness will be noted.
Achilles tendon rupture of the right foot. Note the edema in the heel and loss of plantar flexion when compared with the uninjured side.
Several clinical tests are described to aid in the diagnosis. The calf-squeeze test is performed while the patient lies prone on the examination table with the feet hanging off the edge. The calves are squeezed bilaterally and the foot is observed for plantar flexion. If a complete rupture is present, little or no foot movement will occur (Fig. 23–53 and Video 23–3). The description of this test is commonly credited to Thompson; however, it was described 5 years earlier by Simmonds.76–78
Video 23-3: Thompson test in a patient with Achilles tendon rupture on the left leg.
Thompson test. A. When the Achilles mechanism is intact, squeezing the calf will cause plantar flexion of the foot. B. In patients with a ruptured Achilles tendon, there is no plantar flexion. (Image used with permission from Melissa Leber, MD)
Other tests include the knee flexion test and sphygmomanometer test. To perform the knee flexion test, the supine patient is asked to flex the knee to 90 degrees. The foot is observed during this movement and will fall into neutral or dorsiflexion when a tendon tear is present. The sphygmomanometer test is performed by inflating the cuff to 100 mm Hg while wrapped around the midcalf. The foot is dorsiflexed and the manometer pressure is noted. When the tendon is intact, the pressure should rise to approximately 140 mm Hg.72
Radiographs are usually not necessary to make the diagnosis. A lateral radiograph of the ankle may reveal loss of the regular configuration between the superior aspect of the calcaneus and the posterior aspect of the tibia (Kager triangle). When rupture is present, this space becomes smaller.75 Bedside ultrasound can confirm the diagnosis, but it is an operator dependent test (Fig. 23–54). MRI can confirm the diagnosis, but it is not required in the emergency department.
Ultrasound of an Achilles tendon rupture. Courtesy of Eric Brader, MD.
Achilles tendon rupture should be treated with ice, analgesics, and immobilization in the “gravity equinus position” with the ankle plantar flexed to a comfortable position. Crutches should be given and the patient instructed not to bear weight. Referral to an orthopedic surgeon should be made within 2 days.
There continues to be controversy regarding the most appropriate treatment for Achilles tendon rupture.79–82 Nonsurgical treatment consists of splint immobilization in 20 degrees of plantar flexion for 2 weeks to allow hematoma consolidation. Following this period, the lower extremity is immobilized in a short-leg cast or removable boot with an elevated heel for 6 to 8 weeks.79 After immobilization is complete, gradual range of motion is initiated and a 2-cm heel lift is weaned over the next 2 months. Disadvantages of this method include decreased muscle strength due to lengthening of the healed tendon and a higher rate of recurrent rupture (8%–39%).75
Surgical treatment is frequently preferred in younger or more athletic patients. Range of motion exercises can be initiated 3 to 7 days after surgery, but a walking boot must be worn for 6 weeks. Outcomes after surgery reveal improved strength when compared with nonoperative management. Risk of recurrent rupture is significantly decreased (approximately 5%).80–82 Disadvantages of this treatment method include higher costs and postsurgical complications (infection, skin sloughing, nerve injury). In patients whom the diagnosis is delayed for less than 1 week, surgical treatment is generally preferred. If managed nonoperatively, these patients exhibit tendon lengthening upon healing that inhibits muscle strength.
The Achilles tendon constitutes the distal insertion of the gastrocnemius and soleus muscles into the calcaneus. Achilles tendinopathy is a painful condition due to inflammation of the Achilles tendon. This condition is also referred to as Achilles tendonitis, tenosynovitis, peritendinitis, paratenonitis (acute disease), tendinosis (chronic disease), and achillodynia.83,84
The acute phase of Achilles tendinopathy is secondary to acute overexertion, blunt trauma, or chronic overuse and muscle fatigue.83,84 Achilles tendinopathy is the third most common problem in distance runners and is the most frequent injury in ballet dancers.85 The annual incidence in elite runners is 7% to 9%.86 Improper muscle flexibility, increased foot pronation, and leg-length discrepancy are other predisposing factors for this condition.
Patients present with swelling and tenderness around the tendon. Fine crepitus is perceived on motion of the foot due to the presence of fibrin exudate within the paratenon. In most cases, the tender region is well localized, and the patient holds the foot plantar flexed to relieve the discomfort. Passive dorsiflexion will aggravate the pain. There often is a palpable nodular thickening over the tendon or peritendinous tissues as previously described.87 Morning stiffness is common, but typically pain is increased with activity and relieved by rest.88
The diagnosis is made on clinical grounds. Ultrasonography and MRI are confirmatory but are not necessary.
Conservative management includes decreasing activity and elevating the heel inside the shoe with a small felt pad. The runner should be encouraged to perform sustained stretching exercises of the Achilles complex. Oral anti-inflammatory agents may be used, whereas steroid injections should be avoided as they may lead to rupture. Eccentric loading exercises are recommended. Ice is used after activity. If the pain is acute and other measures have not helped, then a short-leg walking cast can be used for 10 days. Injectible therapies such as platelet-rich plasma have had variable results.87 Operative treatment to release the thickened tenosynovium is recommended in patients who do not respond to a 6-month trial of conservative treatment.79
This condition is the most common cause of heel pain and represents up to 15% of foot problems.89,90 The typical patient is 40 to 60 years old, but it occurs at an earlier age in runners, where the incidence is as high as 10%.91 The patient presents with pain on the undersurface of the heel on standing or walking, and relief with rest. Frequently, patients note pain after a period of bed rest that lessens after some activity, but then becomes severe again after an increased duration of weight bearing.
Plantar fasciitis develops as an inflammatory and degenerative condition at the site of origin of the plantar fascia (medial tuberosity of the calcaneus). Irritation of the periosteum results in secondary subperiosteal ossification and the development of a bone spur.
The condition is most commonly secondary to overuse. Several risk factors have been identified including occupations that involve excessive walking or standing, poorly cushioned footwear, obesity, and running. Patients who are excessive pronators (pes planus) or have reduced ankle dorsiflexion are also at a higher risk of developing plantar fasciitis.89
Local tenderness is noted to palpation at the anteromedial surface of the calcaneus where the plantar fascia attaches (Fig. 23–55). Passive dorsiflexion of the toes accentuates the pain. The pain and tenderness are always anterior to the heel with radiation to the sole being a frequent accompaniment.
Palpation in this area is painful in patients with plantar fasciitis. A calcaneal spur is shown which is commonly associated with this condition. (Image used with permission from Melissa Leber, MD)
The condition is bilateral in up to one-third of cases. When plantar fasciitis is bilateral, it is associated with rheumatologic conditions such as rheumatoid arthritis, systemic lupus erythematosus, and gout.
The diagnosis of plantar fasciitis is a clinical one in most cases. Radiographs or bone scan may be useful to rule out other diagnoses, such as a calcaneal stress fracture.
Radiographs demonstrate a calcaneal bone spur in 50% of cases. Heel spurs occur on the plantar aspect of the calcaneus at the attachment of the plantar aponeurosis where a bony prominence develops and extends across the plantar surface of the bone. Many patients with a calcaneus spur are asymptomatic, however, and 15% to 25% of the general population have these spurs.92
Several therapies exist to treat plantar fasciitis including rest, physical therapy, stretching, change in footwear, arch supports, orthotics, night splints, anti-inflammatory agents, and surgery. With proper treatment, 80% of patients will see a resolution of their symptoms within 12 months. Early treatment within 6 weeks of the development of symptoms is thought to hasten recovery.89,93
The ED treatment should include rest, ice, and nonsteroidal anti-inflammatory drugs (NSAIDs). The patient should be instructed to use a heel pad (one-half inch), arch support to reduce the stretch of the plantar fascia, or taping (Fig. 23–56A to C).92,94 In addition, the patient should be advised not to walk barefoot and replace worn out footwear.
A. Planter fascia taping technique. B. Heel pad for treating plantar fasciitis. C. Plantar fascia arch support padding. D. Stretches for plantar fasciitis.
Stretching exercises of the Achilles tendon should also be prescribed (Fig. 23–56D). The best method for performing these stretches is to lean against a wall with the forefoot while keeping the heel on the ground and knees straight. The patient should be instructed to stand approximately 1 ft away from the wall with the opposite foot and gradually lean the hips forward until the Achilles is felt to stretch. This position is held for 10 seconds and then repeated three times. The stretch should be performed frequently during the day (up to five times) initially and then a couple of times a day to prevent recurrence.
Another method that can be employed in the ED is strapping the plantar aspect of the foot. Using a roll of 2-inch tape, several pieces are measured out that extend along the plantar aspect of the foot from the head of the fifth metatarsal to the head of the first metatarsal. The strips are applied so that they overlap by one-fourth to one-half inch. The tape should be bow strung in the arch area.
Local steroid–anesthetic injection along the medial aspect of the heel often provides relief but may be associated with fat pad atrophy and is recommended in resistant cases. Steroid injections can be done using ultrasound to guide needle placement.96,97 Steroid injections may predispose to rupture.94 In a recent study, the injection of Botulinum toxin A in the calf muscles produced faster and more sustained results than intralesional steroids.90 Plantar fascial release, including the first layer of intrinsic muscles, has been shown to be effective in recalcitrant cases.95 Endoscopic plantar fasciotomy is a reasonable option where conservative therapy has failed.96
The calcaneal fat pad is composed of multiple fibroelastic tissue compartments composed of adipose cells. A painful heel pad is due to atrophy of the subcalcaneal fat pad and repetitive heel loading during walking. This condition is common, especially in the elderly. Obesity and prolonged ambulatory activity, particularly on hard floors, aggravates the condition. Furthermore, acute stress on the pad may rupture or strain the compartments, causing temporary loss of compressibility.
On examination, pain is generalized over the whole heel. Pain is especially prominent on standing and rest gains relief. Radiographs may demonstrate a smooth undersurface of the calcaneus in some patients; otherwise, they are normal. Conservative treatment includes rest, NSAIDs, and a dispersion pad (U pad). A flexible heel protector is a tight-fitting plastic that cups the heel and squeezes all of the fat under the calcaneus, providing more cushioning. Over-the-counter silicone-based heel cushions are also available. To prevent recurrence, shoe modification with heel dispersion padding or a foot orthotic is used and the patient is referred to an appropriate clinician.
Two bursae are involved in inflammatory processes around the heel. The retrocalcaneal bursa is located between the calcaneus and the Achilles tendon. The posterior calcaneal bursa is located more superficially between the Achilles tendon and the skin (Fig. 23–57).97
The posterior calcaneal bursa and the retrocalcaneal bursa.
Posterior calcaneal bursitis is usually secondary to friction from ill-fitting shoes and is especially common in women who wear high heels.98 The bursa is usually distended with fluid and visibly inflamed. In chronic cases, the bursa and overlying skin is thickened with tenderness and swelling noted in the back of the heel. In retrocalcaneal bursitis, the patient complains of pain on motion and localized tenderness is noted to palpation just anterior to the Achilles tendon.
The treatment of calcaneal bursitis is rest, heat, NSAIDs, and elevation. In patients with posterior calcaneal bursitis, proper fitting shoes with low heels are essential. The back of the shoe may have to be cut out in acute cases. Local anesthetic–steroid injection provides prompt relief of symptoms.
A simple bone cyst is a relatively common bone tumor and accounts for about 3% of all bone tumors. Males are more commonly affected in their first and second decades of life. A simple bone cyst can be asymptomatic or it may produce localized pain and swelling. The radiograph demonstrates a cystic structure in the bone. Steroid injection therapy has been shown to be successful and is preferable to surgical curettage.99
Bones and ligaments maintain the normal resting position of the foot. The muscles act to protect the bones and ligaments from excessive stress. Foot pain on standing, therefore, is not muscular in etiology but mechanical, osseous, or ligamentous. Pain on walking, however, may be muscular or from other soft tissues.
The foot has two arches, a longitudinal and transverse arch. The longitudinal arch extends from the calcaneus to the metatarsal heads. The transverse arch runs across the metatarsals. The arches are maintained by skeletal components held in place by ligaments. The longitudinal arch is maintained by the relationship of the talus and the calcaneus, the interosseous ligaments, the long and short plantars, and the spring ligament. The function of this arch is to provide a springboard for weight bearing and forward motion. When the ligaments are stretched by excessive weight, pressure, or poor muscle tone, the foot is strained. Foot strain can be acute, subacute, or chronic. Acute foot strain is seen most commonly after recent overuse, such as occurs with prolonged standing. Chronic foot strain is secondary to excessive stresses on normal structures or normal stresses on abnormal structures.
As mentioned, most patients with these injuries have recently increased activity levels. In other cases, excessive weight and exercise or incorrectly fitting shoes may be the causative factors. The patient complains of pain over the inner border of the foot with standing or walking and relief with rest. The patient has tenderness over the strained ligament that is often well localized under the navicular and anterior and posterior arches. Passive dorsiflexion of the foot intensifies the pain and plantar flexion is usually painless. The patient may have such significant strain that he or she may be unable to bear weight and complains of pain radiating to the calf.
The treatment of the acute form of foot strain that is most commonly seen in the ED is rest and hot soaks. Support for the longitudinal arch can be provided with a sponge rubber pad fitted into the shoe. Acute foot strain subsides with simple rest and gradual return to activity. All these patients should be referred for podiatric consultation to avoid complications such as ligamentous elongation, joint inflammation, degeneration, and arthrosis.
Metatarsalgia is characterized by pain and tenderness of the plantar heads of the metatarsals. It occurs when the transverse arch becomes depressed and the middle metatarsal heads bear a disproportionate amount of the weight. It is seen in patients with cavus deformity of the foot and in patients who wear high-heeled shoes.
In normal weight bearing, the first metatarsal head and the two sesamoids bear one-third of the body’s weight. In the flattened foot, the second, third, and fourth metatarsal heads bear greater weight. There are many common factors that cause the syndrome of metatarsalgia. These include ligamentous stretching that permits the transverse arch to become more relaxed and subject to strain, muscle weakness of the intrinsics, and traumatic factors. Metatarsalgia is a symptom, not a disease, and refers only to pain around the metatarsal heads.
The patient presents with pain and decreased willingness to bear weight in the forefoot. The dorsum of the foot may be edematous. Tenderness is noted at the middle of the shafts with flexion or extension of the toes. Pain subsides with rest and non–weight-bearing but recurs with any exertion. The site of initial tenderness is over the metatarsal heads.
The treatment must be directed at the causative factor and is symptomatic initially, which may include anti-inflammatory agents. The patient must be instructed to use low-heeled shoes only. Ultrasound has been used to treat this condition and metatarsal pads fitted to the patient’s foot have yielded good results.100 Referral to a podiatrist is indicated on a nonurgent basis.
Morton neuroma is an entrapment neuropathy of the interdigital nerve (Fig. 23–58). This condition most commonly affects middle-aged women and is usually unilateral. Morton neuroma is a type of metatarsalgia characterized by sudden attacks of sharp pain that radiates to the toes.101 The cutaneous branches of the digital nerves divide on the plantar aspect of the transverse metatarsal ligament and supply the nerves to the sides of the toes.
Pathologically, the neuroma is a fusiform swelling occurring proximal to the bifurcation of the nerve that consists primarily of proliferative connective tissue and an amorphous eosinophilic material which may be the result of a nonspecific inflammatory neuritis or some type of localized arteritis. The deposition of these materials is followed by slow degeneration of the nerve fiber.101
The patient usually complains of a burning pain localized to the plantar aspect of the metatarsal heads, which radiates to the toes and may be accompanied by paresthesias and numbness. The most common site is between the second and third metatarsals. The pain is usually described as a lancinating, sharp pain that feels “like walking on a stone.” Initially, the pain occurs only with walking or standing but later persists even at rest. The patient obtains relief by removing the shoe and massaging the foot. This relieves the pressure between the metatarsal heads.
After these sudden attacks, the tenderness may persist for days. The foot appears normal; however, on firm palpation, one finds a small area of exquisite tenderness located in the web space. In late stages, one may elicit crepitation and palpate a small tumor in the web space. This condition can be differentiated from other causes of metatarsalgia because pressure between the metatarsal heads reproduces the pain.
If the toes are hyperextended at the MTP joint, a throbbing type of pain occurs in the involved toes. The most useful clinical test for the diagnosis of Morton neuroma is to perform a web space compression test. Severe pain is produced by squeezing the metatarsal heads together with one hand and simultaneously compressing the involved web space with the thumb and the index finger of the opposite hand. This compression test can also produce a painful and palpable click called a Mulder’s sign.102
The differential diagnosis includes a foreign body, an epithelial cyst, and a traumatic bursitis.
There are several important components of the treatment of Morton neuroma. First, the patient’s footwear must be examined to make sure that the forefoot and the toe box are large enough. Steroid injection within the affected area followed by ultrasound, forefoot mobilization, and a temporary metatarsal pad also will decrease symptoms. If these conservative measures fail, the patient is referred for surgical treatment, which consists of division of the transverse ligament with or without the excision of the neuroma.101 Alcohol injections under ultrasound guidance has also been used which may obviate the need for surgery.103
Navicular Stress Fracture
Navicular stress fracture is a relatively uncommon injury most often seen in elite level athletes with repetitive push-off activities such as sprinters and gymnasts.104 The navicular most commonly succumbs to stress in the central third. Because this bone is relatively avascular, similar to its counterpart in the wrist, it is prone to developing delayed union or nonunion if not diagnosed and treated properly. The patient will complain of pain that is insidious in onset. Palpation of the proximal dorsal portion of the navicular will elicit tenderness and is the key to making the diagnosis. Like stress fractures in the rest of the body, plain radiography is not sensitive and the clinician will need to rely on bone scan, CT, or MRI. Treatment includes non–weight-bearing immobilization for 6 weeks followed by a gradual return to activity.105 Screw fixation is required for those patients that develop nonunion or do not respond to conservative treatment.104 Some authors have advocated operative fixation to promote an earlier return to sports participation but this has not been clearly demonstrated.104
Metatarsal Stress Fracture
No discussion of painful disorders of the forefoot would be complete without including stress fractures of the metatarsals, called March fractures. The patient usually gives a history of an increase in physical activity with no clear history of preceding trauma.
On examination, there is tenderness at the middle of the shaft of the third metatarsal, which is the one most commonly involved. The pain is worse with ambulation and flexion or extension of the toes and subsides with rest. Initial radiographs are negative but within 2 weeks, a callus is seen in the midshaft of the metatarsal (Fig. 23–59). MRI has replaced bone scan as the test of choice in patients with negative x-rays but suspected stress fracture.106
March fracture of the third metatarsal.
When the fracture involves the first, third, fourth, and distal aspect of the second metatarsals, the treatment is symptomatic with relative rest. Patients may benefit from a walking boot or crutches if the pain is severe. Once tenderness to palpation and pain with ambulation has resolved, the patient may gradually commence activity. Cardiovascular fitness can be maintained with pool running, or cycling.
Stress fractures at the base of the second metatarsal should be treated with weight-bearing rest for a period of 6 weeks. CT or MRI may be needed to rule out a subtle Lisfranc fracture in this location.107 Diaphyseal fractures of the fifth metatarsal are prone to nonunion and these patients should be non–weight-bearing for 6 to 10 weeks.107
Most of the bursae in this area are “adventitial bursa”. They are found in the joints of the foot that are exposed to pressure, often from a shoe. The most common sites include:
Dorsal IP joints of the toes
Medial first MTP joint
Lateral fifth MTP joint
In acute bursitis, the patient presents with tenderness to palpation of the involved site along with erythema and edema. The treatment includes elimination of the inciting cause. One must protect the area from further irritation using ice therapy, NSAIDs, and steroid injection therapy to relieve swelling and acute pain.
The first metatarsal sesamoids can become inflamed following trauma or an increased amount of ambulation. Examination demonstrates point tenderness beneath the metatarsal head that increases with dorsiflexion of the MTP joint. Low-heeled shoes and a metatarsal bar proximal to the metatarsal heads are usually satisfactory to alleviate the symptoms. Taping of the great toe, slight plantar flexion, and anti-inflammatory drugs are also useful. If persistent, sesamoid stress fracture needs to be ruled out.
The navicular is the last tarsal bone to ossify and is subject to AVN, which usually occurs between the ages of 4 and 6 years and is often bilateral.108 The etiology of this disorder is unclear, but the condition is usually self-limited and tends to spontaneous recovery.
On examination, the patient is most often a boy between the ages of 4 and 10 years who complains of pain over the region of the navicular, usually accompanied by a limp. Palpation elicits tenderness over the navicular and there is usually no history of trauma.
Radiographs of the foot should be obtained with comparison views that demonstrate an increased density and loss of the trabecular pattern of the navicular, which is irregular in outline and often has a crushed appearance (Fig. 23–60).
Radiograph of a 5 year old demonstrates increased density and irregular appearance of the tarsal navicular consistent with AVN (arrow). Courtesy of Melissa Leber, MD.
The treatment consists of protecting the bone in the acute stage with restricted activity and casting for 6 to 8 weeks in more severe cases. Complete ossification occurs in 2 to 3 years and no permanent disability is expected.
Initially described by Dr. Alfred Freiberg, this entity is an AVN of a metatarsal head, most commonly the second metatarsal.109 Freiberg disease is five times more common in females than males.109,110 There is no consensus on the cause, whether the etiology is repetitive trauma, vascular, or multifactorial.
Most commonly, an adolescent or a female in her early twenties presents with forefoot pain that increases with activity.109,110 Stiffness, limp, and vague pain are the primary complaints. Tenderness and decreased range of motion will be noted.
Radiographs will demonstrate sclerosis and flattening of the metatarsal head, which may show collapse in more advanced cases (Figs. 23–61 and 23–62).111
Frieberg disease is noted in the distal second metatarsal.
MRI demonstrating Frieberg disease in a 17-year-old female. Courtesy of Melissa Leber, MD.
Initial therapy includes anti-inflammatory medications, immobilization, limited weight bearing, and orthopedic follow-up. Further treatments may include physical therapy, orthotics, and steroid injections. Surgery is reserved for refractory cases.109,111
Synovial herniation occurs after a chronic sprain that is accompanied by weakness of the capsules of one of the many joints of the foot. A frequent site is near the peroneal tendon insertion distal to the lateral malleolus where it may be quite large. Another site is at the dorsum of the foot. In this case, the ganglion arises along the long extensor tendon sheath or the tarsal joints. The treatment is surgical removal; however, in some cases, aspiration followed by a pressure dressing may yield good results.
The tarsal tunnel is located on the medial aspect of the foot posterior to the medial malleolus. It is formed by the flexor retinaculum, which makes up the roof of the tunnel. Tarsal tunnel syndrome results from compression of the posterior tibial nerve within the fibro-osseous tunnel (Fig. 23–63).112 Pes planus is a common cause of this condition because increased abduction of the forefoot and valgus deviation of the hindfoot increase tension on the nerve.98 Tarsal tunnel syndrome is commonly seen in athletes involved in strenuous sporting activities which places a great deal of stress on the tibiotalar joint.113
Medial view of the ankle demonstrating the course of the posterior tibial nerve within the tarsal tunnel.
Patients complain of an insidious onset of pain described as burning in nature. It originates at the medial malleolus and radiates to the sole and heel. The pain is increased with activity and decreased with rest. Paresthesia, dysesthesia, and hypesthesia may be present within the same distribution. However, the presentation varies, with some patients complaining of pain only in the metatarsal area, whereas others note pain along the lateral aspect of the foot. About one-half of patients state that the pain radiates superiorly along the medial side of the calf. Rubbing of the foot seems to offer temporary relief.
The feature that clinches the diagnosis is a positive Tinel sign, with pain radiating down the medial or lateral plantar nerve distribution on percussion of the nerve within the canal.114 Pain is also reproduced by dorsiflexion and eversion of the foot. The diagnosis can be confirmed by nerve conduction studies.
Orthotics, stretching, rest, and NSAIDs are prescribed. Steroid and local anesthetic injection of the tunnel at the point where percussion tenderness is maximal will also be effective in relieving symptoms.115 Surgical release of the flexor retinaculum is the treatment of choice for this condition, and patients should be appropriately referred when the diagnosis is suspected.112
Lateral Plantar and Calcaneal Nerve Entrapment
The posterior tibial nerve gives rise to the medial and lateral plantar nerves and the calcaneal nerve. The lateral plantar and calcaneal nerves can become entrapped between the deep fascia of the abductor hallucis muscle and the medial caudal margin of the quadratus plantar muscle. The result is pain within the nerves’ distribution—the heel.
Approximately 10% to 15% of athletes with chronic unresolved heel pain have entrapment of these nerves. The patient presents with chronic heel pain that is dull, aching, or sharp in character. The pain may radiate into the ankle and is intensified by walking or running. Point tenderness over the first branch of the lateral plantar nerve deep to the abductor hallucis muscle is present. Variable success rates have been shown with orthotics. Frequently, these patients require surgical neurolysis.
Medial Plantar Nerve Entrapment
This condition is most commonly known as jogger’s foot. Entrapment of the medial calcaneal branch of the posterior tibial nerve causes acute irritation and inflammation and chronic fibrosis and neuroma formation. The patient complains of aching pain along the medial border of the heel that is more severe on weight bearing but does not radiate further into the foot. If the foot is in hyperpronation, this tends to aggravate the condition further. Anti-inflammatory agents and a custom molded orthotic are useful. If the patient does not respond after several months, referral for operative neurolysis is indicated.
Sural nerve entrapment occurs secondary to recurrent ankle sprains and running. The patient presents with a shooting pain and paresthesias, typically extending to the lateral foot border, which is confirmed by local tenderness, a positive Tinel sign, and occasionally an area of hyperesthesia. A trial of NSAIDs is useful; however, injection therapy should be tried and orthotics may be necessary. If conservative therapy fails, surgical release usually is definitive.
Ski Boot Compression Syndrome
In this condition, pain is felt on the dorsum of the foot when the deep peroneal nerve is injured (Fig. 23–64). The nerve is superficial and a contusion to the dorsum of the foot or compression by the “tongue” of a ski boot will cause nerve injury and pain. The deep peroneal nerve can also be entrapped, most commonly under the inferior extensor retinaculum. The superficial peroneal nerve can be entrapped at its exit from the deep fascia. Recurrent ankle sprains or repetitive trauma from running causes both of these entrapment neuropathies.
Anterior view of the foot demonstrating the deep peroneal nerve.
This nerve supplies sensation to the area between the first and second toes and the patient has pain radiating to this region. When entrapment is the cause, the pain is reproduced with either dorsiflexion or plantar flexion. Superficial neuropathy is suggested by pain, paresthesias, or numbness over the outer border of the distal calf, dorsum of the foot, and ankle, but sparing the first web space.
On examination, light palpation evokes severe pain over the dorsum of the foot. When entrapment is the cause, there may be point tenderness where the nerve emerges from the deep fascia. Sensation in the web space between the first and second toes is almost absent and the sensation over the remainder of the dorsum of the foot is decreased.
For ski boot compression syndrome, the treatment includes elevation of the extremity, ice packs, and mild analgesics, with resolution usually occurring in 36 hours; however, sensation may not return to normal for up to 4 weeks. In refractory cases, injection of steroids is recommended. Entrapment neuropathies are also treated with conservative modalities such as NSAIDs, orthotics, or injection therapy. Neurolysis is reserved for cases of intractable pain or atrophy.
Diabetic Foot Ulcers and Infection
Diabetic foot ulcers are common conditions seen in the ED. They develop in 15% of diabetics. In diabetics that require foot amputation, 85% had ulceration initially.116 Foot ulcers occur in diabetics with and without neuropathy. The annual incidence of foot ulcers is 2% in diabetics, but increases to 7.5% in diabetics with peripheral neuropathy. Peripheral neuropathy results in a loss of protective mechanisms because the patient can no longer sense when an injury has occurred. Other predisposing factors in the development of a diabetic foot ulcer include calluses, peripheral vascular disease, and deformity.117 Trauma is a common precipitant, which may be as minor as improperly fitted shoes.
The evaluation of a patient with foot ulceration should include a thorough sensory examination and palpation of the peripheral pulses. If foot pulses are present, neuropathy is the major cause of the ulcer.118 Ischemic ulcers should be recognized by clinical examination and evaluated for the possible need of revascularization. Neuropathic ulcers are subdivided into mild, moderate, or severe, depending on the depth of the ulcer and the presence or absence of bone involvement.
Infection is a common complication (Fig. 23–65A). The ulcer provides an easy entry for bacteria in a patient with a diminished resistance to infection. Infection is defined as the presence of local signs and symptoms (erythema, warmth, induration, and pain) combined with either systemic symptoms or purulent discharge. Infections are typically polymicrobial with aerobic gram-positive, gram-negative, and anaerobic organisms present. Osteomyelitis is present in up to two-thirds of diabetic foot ulcers.119 The ability to touch bone with a blunt sterile instrument had a positive predictive value for osteomyelitis of 89% in one study.120 A radiograph should be obtained to look for evidence of osteomyelitis (bone destruction or periosteal reaction) or gas in the surrounding soft tissues (Fig. 23–65B). When infection is present, a deep-tissue culture should be obtained and is superior to superficial swab specimens for identifying the causative organism.121
A. A necrotic diabetic foot infection. B. Radiograph of the same patient demonstrating gas in the tissues.
The treatment of neuropathic ulcers includes the avoidance of pressure to the ulcer (i.e., non–weight-bearing with crutches or a walking cast/shoe). Debridement of necrotic tissue, callus, and infected foreign material is crucial and is best performed with a scalpel.118 Soaking of the wound macerates the tissue but does not debride the necrotic tissue and should be avoided. Enzymatic chemical debridement and whirlpool soaks are not useful. Surgical treatment is indicated for severe claudication, intractable rest pain, necrosis, or nonresponding ulcers.122
The choice of dressing is important. A sterile nonadherent gauze dressing is preferred to either plain gauze or occlusive/semiocclusive dressing. Newer dressings contain cellulose or collagen–protease modulating materials or hyaluronan and are designed to promote healing.118
Clinical signs of infection are treated with antibiotics. Empiric choices for mild foot infections include clindamycin, levofloxacin, trimethoprim–sulfamethoxazole, or amoxicillin–clavulanic acid for outpatient therapy. Intravenous antibiotics for inpatient care include imipenem, piperacillin–tazobactam, or broad-spectrum cephalosporins. Vancomycin should also be considered to cover resistant gram-positive organisms. Soft-tissue infections usually require 1 to 2 weeks of therapy, whereas patients with osteomyelitis require 6 weeks or more of treatment. Surgical debridement of infected bone is also important in eradicating osteomyelitis.
One of the most important aspects in treating patients with diabetic foot ulcers is to make certain that they are referred to an appropriate clinic where preventive care at 2- to 3-month intervals can be performed. Blood sugar control, pressure reduction, debridement, and antibiotics when necessary are critical measures. Preventive care includes nail care and removal of any calluses as well as fitting the patient with appropriate shoes.
Verruca vulgaris are common and occur on the plantar surface of the feet. Plantar warts cause signiﬁcant pain with standing and walking. These lesions appear as a firm white growth, which is flat or raised. Warts can be differentiated from calluses and corns by superﬁcial sharp debridement of the lesions which reveals punctate black dots that are thrombosed capillary vessels in patients with warts.123 Spontaneous regression is quite common in children, almost 50% of warts disappear within 6 months. Unfortunately, warts are more persistent in adults. Mosaic warts can occur when small warts coalesce.124
Treatments can be categorized as topical, intralesional, oral, and destructive.123 Large plantar warts are treated conservatively with weekly paring and the application of a keratolytic agent such as salicylic acid. Painful lesions are treated with more invasive techniques including cryotherapy with liquid nitrogen, local curettage, laser therapy, and electrosurgery. These patients should be referred for therapy.
Although surgical removal has been shown to be effective, complications include pain and wound healing. Topical treatments use salicyclic acid preparations, podophyllotoxin, retinoids, silver nitrate, and topical immunotherapeutic agents.
The ingrown toenail, or onychocryptosis, is a commonly occurring problem that is easily treated in the ED (Fig. 23–66). This condition must be distinguished from subungual exostosis, which is a benign condition that can look like an ingrown nail.125,126 An ingrown toenail occurs when the lateral margins of the nail dig into the surrounding nail fold and cause discomfort that may lead to a paronychial infection. The causes of this condition include excessive external pressure (i.e., poorly fitted shoes), improperly trimmed nails, or hyperhidrosis.127 The condition is most common in 20- to 30-year-old individuals, and most often involves the great toe.127
The treatment depends on the stage at which the condition is seen. In the early stages, the examiner will notice only erythema and some swelling of the nail fold where the nail is penetrating the skin. At this stage, treatment should consist of warm soaks and elevation of the leading corner of the nail with a cotton pledget soaked in an antiseptic solution. The patient should be advised on how to trim the nails properly and cautioned against wearing shoes that are narrow or have a high heel.
In the later stages, when the nail fold is acutely inflamed or there is a paronychial infection, excision of the lateral nail plate is accompanied by lateral matricectomy.128 To perform this procedure, the great toe is prepped with povidone–iodine solution and blocked with a local anesthetic (Video 23–4). A fine scissors or hemostat is used to carefully lift the lateral nail plate. A scissors is then used to cut the nail plate and the nail is removed. The nail matrix is now exposed and the tissue can be ablated with a cotton-tipped applicator soaked with phenol or electrocautery (Fig. 23–67 and Video 23–5). It is important that the nail matrix is ablated beneath the nail fold or a portion of the nail will grow back.
Video 23-4: Blocking the large toe.
Local anesthetic is injected around the entire circumference of the toe.
Ingrown toenail removal. A. After a hemostat is used to elevate the ingrown toenail, cut the nail plate with scissors. B. The lateral portion of the nail plate is removed. C. The nail matrix is now exposed. D. A cotton tip applicator soaked in phenol is used to destroy the nail bed matrix of the toe so that this portion of the toenail does not grow back.
This is an uncommon benign bony tumor that manifests as a painful, firm hyperkeratotic nodule at the free edge of the nail plate.126 Subungual exostosis forms over the distal portion of the distal phalanx and is most common in the great toe. The patient presents with complaints of pain and swelling along with increased sensitivity of the toe over the exostosis. The toe deviates laterally, causing difficulty with walking. Subungual exostosis more commonly affects women than men by a ratio of 2:1.126 Most lesions occur in children and young adults. The treatment for the condition is surgical removal.
Hallux valgus (bunion) is a deformity in which the large toe deviates laterally and a bony prominence develops over the medial aspect of the first metatarsal head and neck. The medial portion of the first metatarsal head enlarges and a bursa forms over the medial MTP joint that may become inflamed and thickened. It is this bursitis that may bring the patient to the ED. Treatment is the application of warm moist soaks to the region. A pad is placed over the medial aspect of the toe for comfort. A large number of different surgical procedures have been described for this common condition. These patients should be referred to a podiatrist for definitive care.