The Ankle And Foot

Chapter 12 The Ankle and Foot


The ankle and foot perform two major roles: they support the body and propel it forward. In the process of performing these functions, several painful conditions may develop. Many of these develop in the forefoot and are often the result of poorly fitted shoes.



Anatomy


The ankle is a hinge joint composed of the articular surfaces of the lower portion of the tibia, talus, and medial and lateral malleoli (Fig. 12-1). The stability of this joint or “mortise” is maintained by the malleoli and their ligaments, which grasp the talus and prevent medial and lateral displacement. The talus and socket are both broader in front, an arrangement that provides maximum stability when the ankle is in dorsiflexion or neutral, and this prevents posterior displacement. Only movements of dorsiflexion and plantar flexion occur at the ankle.


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Fig. 12-1 Bones of the ankle and heel. A, The talus is held in position in the mortise by the malleoli and ankle ligaments. B, The articular surface of the talus is wider anteriorly than posteriorly. The ankle is therefore more stable in neutral or slight dorsiflexion when the wider anterior portion of the talus fits in the mortise. It is unstable in plantar flexion. Wearing high-heeled shoes may therefore lead to chronic ankle and calf pain. Eversion and inversion movements take place in the subtalar (talocalcaneal) joint.


The foot is composed of 26 bones, 12 of which are components of the medial and lateral longitudinal arches (Fig. 12-2). Strong fascial supports maintain these arches and prevent collapse (Fig. 12-3). Eversion and inversion movements of the foot take place in the hindfoot at the subtalar joint. Injury or disease that affects this joint will cause pain in the region of the heel when walking on uneven or irregular surfaces. Abduction and adduction movements occur in the midfoot or midtarsal joints.


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Fig. 12-2 Roentgenogram of the foot. N, Navicular; T, talus; CA, calcaneus; CU, cuboid; CN, cuneiforms, medial, intermediate, and lateral. The foot is divided into the forefoot (phalanges and metatarsals), midfoot (tarsals), and hindfoot (talus and calcaneus).


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Fig. 12-3 The plantar fascia. It may be affected by Dupuytren’s contracture in a similar manner to the hand. It may also become inflamed, especially at the medial attachment to the calcaneus (plantar fasciitis).


During normal walking, when the heel strikes, the calcaneus everts to cushion impact. At the toe-off position, the heel then rolls into varus to provide power.



Flatfoot


Flatfoot is a common disorder that is defined as a depression or loss of the medial longitudinal arch of the foot. It is usually combined with valgus or eversion of the heel and abduction of the forefoot. An apparent flatfoot (“fat foot”) is present in many children up to the age of 2 years because of the presence of a fat pad in the area of the longitudinal arch. As the fat pad atrophies with weight bearing, the normal arch usually becomes visible. Flatfoot is usually one of two types: flexible or rigid. It occurs in conjunction with an accessory navicular bone in the foot, and it also results when a rupture of the posterior tibial tendon has occurred. It is also seen in the late stages of Charcot arthropathy, when collapse and reversal of the longitudinal arch can develop.



FLEXIBLE FLATFOOT


Flexible or hypermobile flatfoot is a benign disorder frequently seen in both adults and children. It is usually bilateral. The condition is often hereditary and varies in severity. It is occasionally associated with a tight Achilles tendon (heel cord). The tight heel cord tends to hold the heel in eversion. With growth, stretching of the deltoid ligament on the medial side of the ankle may occur.




ClINICAL FEATURES


Symptoms are rare but may consist of pain, burning, and easy fatigability. With weight bearing, the heels are everted, and the forefoot appears pronated and abducted (Fig. 12-4). The child often “breaks down” the medial counter of the shoe. When it is not bearing weight, the foot often looks normal. Absence of the medial arch is apparent, and the foot is mobile without any fixed deformity. The child with flatfoot can usually form a good arch when asked to stand on tiptoe. The heel rolls into its usual varus position, and normal strength is apparent. A mild genu valgum (knock-knee) or internal tibial torsion may be present. With the heel inverted, passive dorsiflexion of the ankle will be limited if the heel cord is tight.


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Fig. 12-4 Flatfoot deformity with eversion (valgus) of the heels and loss of the normal longitudinal arch.


A lateral roentgenogram taken with the foot bearing weight may reveal a loss of the normal arch and plantar flexion of the talus (Fig. 12-5). Some secondary bony changes may be present in the adult.


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Fig. 12-5 Lateral weight-bearing roentgenogram revealing plantar flexion of the talus.




TREATMENT


The treatment of flexible flatfoot in the child is controversial. The disorder is considered a normal variant in most cases, and only reassurance is needed. The natural history is spontaneous correction in the majority of cases with maturity. Symptoms are rare during childhood and uncommon even in the adult with moderately severe deformity. Actually, most foot pain in young adults is caused by an abnormally high rather than an abnormally low arch. Shoe corrections and orthotics used for this condition are of uncertain benefit. An arch cannot be “created” by supporting it. Exercises are of doubtful value, except for those that stretch the tight heel cords (Fig. 12-6). These exercises cure many cases associated with heel cord contractures. A soft arch support may be tried if symptoms are present. Surgery is reserved for symptomatic cases but is rarely necessary. No treatment is needed in most cases.


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Fig. 12-6 Heel cord stretching exercises. The legs are internally rotated; the forefeet are placed on a 2.5-cm board, and the patient leans forward.




RIGID FLATFOOT


Rigid or peroneal spastic flatfoot differs from flexible flatfoot in that the deformity is not passively correctable and is present whether weight bearing or not. This condition is usually secondary to a tarsal coalition or arthritis in the hindfoot. Tarsal coalitions are congenital cartilaginous or bony bridges that may be found between the two bones of the hindfoot or between either of these bones (usually the calcaneus) and the navicular. The resultant loss of motion in the hindfoot leads to local irritation and protective “spasm” in the peroneal muscles, producing the flatfoot appearance. This may be caused by attempts at compensation by the muscles to correct the alignment by pulling against the deformity. The condition is bilateral in half of the cases. Most cases of coalition are not symptomatic.



CLINICAL FEATURES


The onset of the disorder is usually gradual and begins in early adolescence if it is caused by a coalition. This may be because of the more solid ossification of the bar that occurs at this age. Stiffness and a painful limp are the most common initial symptoms. Tenderness and pain may be present over the peroneal tendons or in the hindfoot. The heel is frequently everted, and subtalar motion is limited and painful. The forefoot may be abducted. Passive stretching of the peroneal tendons by forefoot adduction and inversion frequently reproduces the pain. Swelling will be present if the disorder is secondary to a rheumatoid process. Roentgenograms may reveal arthritic changes in the hindfoot or the presence of a coalition (Fig. 12-7). Computed tomography (CT) and magnetic resonance imaging (MRI) are valuable in determining the extent of the condition.


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Fig. 12-7 Tarsal coalition. An incomplete calcaneonavicular bar is present (arrow). The anterior process of the calcaneus is abnormally prolonged.



TREATMENT


Symptomatic treatment is indicated in early cases. Rest, heat, and nonsteroidal antiinflammatory drugs (NSAIDs) are usually helpful. A short leg walking cast may be worn intermittently to relieve symptoms followed by a light brace or orthotic. Surgery is necessary in some cases.




POSTERIOR TIBIAL TENDINOPATHY/RUPTURE


The posterior tibial tendon is commonly involved in a spectrum of overuse disorders. These can range from simple acute pain as a result of tendinitis to complete rupture. The underlying pathology is now considered to be more degenerative than inflammatory, perhaps the result of some distant traumatic event with ischemia. Although the name tendinitis is still used, these disorders are often discussed under the general term tendinopathy or tendinosis because inflammatory pathology is usually absent, hence the changing terminology.


Simple degeneration causes painful medial swelling and tenderness along the tendon sheath. There is usually no history of trauma, and the onset of symptoms is insidious. Stretching the tendon increases symptoms, and active inversion reproduces pain. Weight bearing is difficult. Treatment includes NSAIDs, gentle stretching, rest, orthotics, and the use of a cast boot. Steroid injections are probably not indicated because they could lead to further weakening of the tendon.


Further deterioration of the tendon could lead to rupture and the development of an acquired flatfoot deformity. Overuse, attrition, and failure are the cause. (Acute rupture of healthy tendon is unusual.) The condition is common, but the diagnosis can be difficult and is often missed until the patient discovers the loss of the arch. Usually, there is a history of previous pain, and the patient may have even had treatment for “tendinitis” in the same area. There is often only minimal pain after rupture, probably because the tendon is no longer attached and is no longer subject to stretch. Normally, the posterior tibial tendon locks the heel in varus, but without it, the heel does not move into inversion with push-off, and the gait is thus weakened. Clinically, the tendon sheath may be empty, and the heel everts with weight bearing. The medial arch is lower, and swelling and mild tenderness may be present. Inversion of the heel and forefoot against resistance is weak. There is also difficulty in performing the single heel rise test, in which the patient tries to rise on the ball of the foot on the affected side (Fig. 12-8). Heel valgus and forefoot abduction also increase gradually, and, as a result, when looking from behind, “too many toes” are visible with the patient standing (Fig. 12-9).


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Fig. 12-8 Single heel rise for posterior tibial tendon function. In an abnormal test, the patient cannot rise onto the ball of the foot. Some older patients may have difficuly with this test because of problems with balance.


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Fig. 12-9 The “too many toes” sign, right foot, indicative of posterior tibial tendon rupture. When viewed from behind, there is increased forefoot abduction, increased heel valgus and flattening of the arch causing more toes to appear lateral to the ankle.


Patients with complete ruptures and partial ruptures that do not respond to medical treatment should be referred. Many patients with complete rupture do well with nonsurgical care and do not require reconstruction.



Clubfoot


Congenital clubfoot, or talipes equinovarus, is a fixed deformity that is present at birth. It is frequently bilateral, and a hereditary factor is often present. The cause is unknown.




CLINICAL FEATURES


The deformity consists of three major components, none of which is passively correctable. This lack of correctability distinguishes clubfoot from other common foot deformities (which may be caused by intrauterine molding and usually resolve without treatment). The three components are equinus of the ankle and forefoot, varus of the heel, and adduction of the forefoot (Fig. 12-10). The medial border of the foot is concave, and the lateral border is convex.


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Fig. 12-10 Bilateral clubfeet (talipes equinovarus).



TREATMENT


Early referral to an orthopedic specialist is needed, because treatment needs to begin within the first few days of life. The initial management consists of manipulation of the foot to stretch the contracted soft tissues, followed by the application of a corrective cast. The cast is changed at weekly intervals, and the foot is further manipulated until complete correction is obtained. This method of treatment frequently succeeds if it is begun immediately. Surgery is required when casting fails. The procedures range from simple heel cord lengthening to wide soft tissue releases.



Calcaneovalgus


Talipes calcaneovalgus is the most common neonatal foot disorder. It is characterized by excessive eversion and dorsiflexion of the foot. The cause is unknown, but positional compression in utero is likely. In contrast to clubfoot, the deformity is not fixed and may be easily overcorrected.



CLINICAL FEATURES


The deformity is easily diagnosed shortly after birth. Marked laxity of the ligaments of the foot and ankle is obvious, and the foot can often be dorsiflexed so that the toes touch the anterior aspect of the tibia (Fig. 12-11). The heel cord may appear to be severely stretched.


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Fig. 12-11 Talipes calcaneovalgus.



TREATMENT


Mild cases require no treatment. More severe cases respond well to passive stretching exercises. Corrective casts may be necessary for a short period of time. A mild flatfoot deformity may persist, but there is no evidence that a calcaneovalgus deformity will become a flexible flat foot. Most cases seem to resolve spontaneously.



Kohler’s Disease (Osteonecrosis of the Tarsal Navicular)


The tarsal navicular may undergo avascular necrosis similar to what occurs in other bones. The cause of all of these disorders is not completely understood, but interference with the circulation to the bone is thought to be the usual cause of the ischemia. The onset of this disorder is about the age of 5 years. A painful limp is the usual initial complaint. Local pain, tenderness, and swelling over the navicular bone are frequently present.


The roentgenographic appearance is usually characteristic. Flattening, sclerosis, and irregularity of the navicular are usually present (Fig. 12-12).


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Fig. 12-12 Kohler’s disease (arrow).


Protection from excessive trauma, sometimes by the use of a short walking cast for 7 to 8 weeks, is sufficient treatment in most cases. Spontaneous recovery is the rule, and complete reossification of the navicular usually occurs within 2 to 3 years.



Ankle Sprains


The sprain is the most common of all ankle injuries and may be the most common injury in sports. Most of these (85%) involve the lateral ligament complex as a result of excessive inversion. Medial sprains involving the deltoid ligament are rare. The anterior talofibular (ATF) ligament is usually injured first in the typical lateral sprain (Fig. 12-13). More severe injuries involve the calcaneofibular (CF) ligament. Only rarely is the posterior talofibular ligament involved. The injuries are often graded I, II, and III, with I being mild and II being moderate. Grade III injuries are more severe, with instability resulting from rupture of the ATF and CF ligaments. Inversion (varus) sprains may also cause marked hemorrhage of the peroneal muscles and even peroneal nerve damage. The subtalar joint may also be injured.


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Fig. 12-13 The lateral ankle ligaments, anterior and posterior talofibular (PTF) and calcaneofibular (CF). Also shown are the anterior inferior tibiofibular (AITF) ligament and the beginning of the interosseous membrane (IM).


Other ligamentous ankle injuries are much less common, but the anterior inferior tibiofibular (AITF) ligament, deltoid ligament, and interosseous membrane may be involved in eversion and rotational injuries. Damage to the tibiofibular syndesmosis is sometimes called a “high sprain” because of pain above the ankle from injury to the interosseous membrane. On rare occasions, the fibula may even be separated from the tibia.




CLINICAL FEATURES


The symptoms will depend on the severity of the injury. There is often a history of a “pop” at the time of injury. Mild sprains may cause only slight loss of function, but with more severe injuries, swelling and pain are significant and prohibit further use of the limb. Syndesmotic sprains often appear more benign because of minimal swelling. However, the pain and disability are greater than the clinical appearance would suggest, and the patient may be unable to bear weight.


Physical examination is important. Hemorrhage and local tenderness are present at the site of injury. Careful palpation can localize the site of damage. Tendon function should be assessed, and any bony tenderness should be noted. The clinical evaluation of stability is sometimes helpful since it may determine the course of treatment, although this part of the examination may need to be deferred because of pain. Stability of lateral injuries can be assessed by the anterior drawer and talar tilt tests (Fig. 12-14). The anterior drawer is the most reliable test and least painful in the acute stage. Positive test results indicate complete rupture of the ATF and CF ligaments and a grade III injury. Motor function should always be evaluated.


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Fig. 12-14 Tests for ankle instability. A, Inversion stress test. B, Anterior drawer test with the foot slightly plantar flexed.


In syndesmotic injuries, the area of tenderness is more anterior and proximal. Dorsiflexion of the foot and compressing the ankle mortise (the “squeeze” test) may provoke pain, and the ankle may feel spongy.


Roentgenographic evaluation is always performed, and because the mechanism of injury that causes a lateral sprain is the same as that which causes an avulsion fracture of the base of the fifth toe, the film should include the fifth metatarsal base to rule out fracture of the small toe. If the injury is in a child or adolescent with open growth plates, tenderness over the fibular malleolus (even with normal roentgenographic findings) implies the more likely growth plate fracture rather than a lateral sprain, and a cast is usually necessary. Opinions vary on the usefulness of arthrograms, tenograms, and stress films (Fig. 12-15). A good clinical examination is usually sufficient to determine stability.


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Fig. 12-15 A, Stress roentgenography of the ankle revealing severe lateral instability, with tilting of the talus. B, The anterior drawer test.



TREATMENT


Regardless of the severity, almost all sprains are treated nonoperatively. At first, all injuries are elevated, and a soft compression dressing is applied for comfort and to help control swelling. Ice (1 hour on, 1 hour off) is applied, and crutches are used for ambulation. Rest, ice, compression, and elevation (RICE) are continued for 1 to 2 days. Anti-inflammatory medication has been recommended in the past for these injuries because it was thought that suppressing the local inflammation could allow faster recovery from sprains and other similar soft tissue injuries. The use of these drugs under these circumstances has been the source of considerable debate, mainly because prostaglandins play important roles in the healing process and these medications block their production. The effects of NSAIDs on soft tissue healing are not clear, and any apparent benefits may only be because of their analgesic effects. Whether these drugs are helpful or harmful in these cases has not been determined. Crutches are frequently needed for 2 to 3 days. Heat is never used.


The next phase of treatment is rehabilitation, which includes early active range-of-motion exercises (circumduction) and weight bearing as tolerated (Fig. 12-16). “Alphabet” exercises (writing the alphabet in capital letters with the great toe) are begun, and in 4 to 5 days, exercise against resistance is added. Wrapping or bracing with a stabilizing orthosis may also be helpful. Static bicycling may be added after 1 week, along with fast walking.


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Fig. 12-16 Ankle exercises. A-C, Range of motion (dorsiflexion, plantar flexion, circumduction, and writing the alphabet with the great toe). D-G, Strengthening exercises using a rubber strap (invertors, evertors, plantar flexors, and dorsiflexors). H, Static one-leg standing with eyes closed. I, Toe raises. J, Heel cord stretches. Each exercise is performed 10 to 15 times. Ice is applied for a few minutes before and after each exercise period, and the exercises are performed 3 times each day.


If the pain is particularly severe or the patient requires independence, a short leg walking cast may be applied for 2 to 4 weeks. A removable fracture cast boot is also a good option to control excessive pain.


Casting is used less frequently now because of concern over the temporary loss of motion and atrophy that occur, which require some time for restoration of function following cast removal. However, cast treatment has many advocates and should still be considered, especially in those patients who might require independent walking. Other options for painful sprains include various short leg orthoses that immobilize the ankle and foot, such as the ankle–foot orthosis (AFO). These are usually weight-bearing appliances that can be removed for exercise. They are worn for about 4 weeks. A compression stocking can help control swelling.


The treatment of severe sprains with instability remains somewhat controversial, but they are usually treated in the same manner as other sprains with a functional rehabilitation program. Although the results of surgical repair of unstable acute sprains are excellent, surgery is usually reserved for chronic instability in the high-level professional athlete or those with significant syndesmotic separations.


NOTE: Lateral sprains of any severity may also cause lingering symptoms for weeks and months. Some syndesmotic sprains take even longer to heal (55 days vs 35 days for lateral sprains), and heterotopic ossification may even develop in the interosseous membrane. (Unless symptoms occur, long-term results are not usually affected by such ossification.) If healing seems delayed, the following conditions should be considered: (1) talar dome fracture, (2) reflex sympathetic dystrophy, (3) chronic tendinitis, (4) peroneal tendon subluxation, (5) another occult fracture—such as that involving the anterior superior process of the calcaneus or the lateral process of the talus, (6) poor rehabilitation, and (7) the high sprain. Evaluation at this point should start by another clinical examination and simply repeating the plain roentgenograms (Fig. 12-17). CT, bone scan, or MRI may be indicated at a later time.


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Fig. 12-17 Fracture of the anterior superior process of the calcaneus (arrow). This injury may not unite and cause chronic pain.


Ankles that are chronically unstable because of lateral ligamentous laxity may benefit from the application of a 0.3-cm lateral heel and sole wedge to prevent inversion. Taping or bracing during vigorous activities is also helpful, as are strengthening exercises. Continuing symptoms may require surgical reconstruction of the lateral ligaments to relieve symptoms of instability, although late traumatic arthritis or chronic instability is rare regardless of treatment.


NOTE: Evidence-based studies suggest the following: (1) there are no significant differences in outcomes between surgical and nonsurgical treatment of acute lateral ligament injuries of the ankle; and (2) ultrasound therapy appears to be of no benefit in the treatment of acute ankle sprains.



Tarsal Tunnel Syndrome


Nerve entrapment rarely may occur in the foot by compression of the posterior tibial nerve beneath the flexor retinaculum at the ankle. This retinaculum arises from the medial malleolus and inserts into the medial aspect of the calcaneus (Fig. 12-18). Space-occupying lesions, local tendinitis, traction injuries, fibrosis secondary to fractures, or deformities of the heel and foot can all compromise the tunnel and cause pressure on the posterior tibial nerve. The disorder is controversial, and there are many unanswered questions regarding its diagnosis and incidence.


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Fig. 12-18 The tarsal tunnel. The posterior tibial nerve runs beneath the flexor retinaculum.




CLINICAL FEATURES


The symptoms are often vague in contrast to other compression neuropathies such as carpal tunnel syndrome. As a result, the diagnosis is often delayed. Burning pain, numbness, and tingling may be present in the sole of the foot. The Valleix phenomenon (proximal radiation of the pain) may occur. The exact location of these symptoms is variable. They are frequently worse with activity. The pain may even radiate into the calf. It may be difficult to differentiate tarsal tunnel syndrome from plantar fasciitis, and the two may even occur together. (With tarsal tunnel syndrome, pain lingers after walking ceases in contrast to fasciitis, where pain stops with rest.) Sensory loss and intrinsic muscle weakness are rarely present. Tinel’s sign may be positive over the tarsal tunnel, and sustained eversion or compression of the tunnel may reproduce symptoms. Nerve conduction studies may be abnormal in some cases but are often inconclusive, and despite improvements in electrical testing, tarsal tunnel syndrome can be difficult to diagnose.



TREATMENT


Hindfoot deformity may be treated with an orthosis. A medial heel wedge or heel seat may be used in an attempt to remove traction from the nerve. Surgical release of the entrapment may be indicated in selected patients with a clear diagnosis if symptoms persist, but the results are often mixed.



Subluxation of Peroneal Tendons


Sudden, forceful dorsiflexion of the foot accompanied by contraction of the peroneal muscles may cause a tear in the retinaculum that holds these tendons in their groove behind the lateral malleolus. This may allow the tendons to acutely or chronically sublux over the lateral malleolus (Fig. 12-19). The condition can also follow a severe lateral ankle sprain.


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Fig. 12-19 Subluxing peroneal tendons.




CLINICAL FEATURES


The diagnosis usually is easily made. The tendons are seen or felt to lie over the lateral malleolus. The subluxation can often be reproduced by the patient in chronic cases.



TREATMENT


Acute cases are treated by reduction and immobilization in a short leg walking cast for 4 weeks or open repair of the retinaculum. Chronic cases are usually treated surgically by reconstruction of the retinaculum.



Osteochondritis Dissecans of the Talus (Talar Dome Fracture)


This condition is characterized by the formation of a small area of necrotic bone on the articular surface of the talus. The cause is usually traumatic, and the medial aspect of the talus is the area most commonly involved. It is often the lesion causing persistent symptoms after a “sprain” that does not heal. The necrotic fragment may even become detached from its base, becoming a loose body.




CLINICAL FEATURES


The onset is gradual, and a history of injury may be absent. The disorder usually occurs during adolescence or early adulthood. A painful limp and chronic swelling in the ankle with activity are common complaints. Examination of the ankle with the foot in plantar flexion may reveal an area of point tenderess over the articular surface of the talus. Ankle motion is frequently restricted. Occasionally, if the fragment is detached, intermittent locking may occur, but this is rare because the loose body usually settles into a joint recess and attaches to the soft tissue.


Roentgenographic examination usually reveals the characteristic lesion. MRI and CT are helpful in questionable cases (Fig. 12-20). They are also useful in determining the status of the lesion.


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Fig. 12-20 A, Radiographic image and (B and C) CT scans showing osteochondritis dissecans of the talus. The arrow indicates the talar dome fracture.



TREATMENT


The undisplaced fragment is treated by prolonged abstinence from weight bearing until the lesion heals. Cast immobilization is frequently indicated. Persistent symptoms or detachment of the fragment may require surgical intervention.



Disorders of the Hindfoot



PLANTAR FASCIITIS (“PAINFUL HEEL SYNDROME”)


The plantar fascia extends from the calcaneus to the proximal phalanges of each toe and plays an important role in gait. It is a common site of pain that frequently develops near its attachment at the medial tubercle of the calcaneus and along the medial longitudinal arch. The etiology is probably overuse with the development of degeneration and microtears. The role of inflammation is unclear. Both heels are frequently affected. This bilateral involvement may be an early symptom of other inflammatory disorders, such as rheumatoid arthritis, gouty arthritis, or ankylosing spondylitis (when it is often referred to as enthesitis or enthesopathy). Risk factors include tight heel cords (reduced ankle dorsiflexion) and obesity. Men and women are affected equally, and runners are more often affected.



CLINICAL FEATURES


The pain is usually felt directly beneath the calcaneus but may be present in the area of the medial arch. The discomfort is characteristically worse with the first steps in the morning or after periods of prolonged sitting and later in the day after weight-bearing activities. Morning pain usually lessens as the foot “warms up.” Examination reveals local point tenderness in the area of involvement, usually the medial tubercle of the calcaneous. The pain may be aggravated by direct pressure or by maneuvers that place the fascia under a strain, such as dorsiflexing the toes and ankle. Some patients have a tight heel cord.


Roentgenographic findings are usually normal but may reveal a traction spur on the os calcis that is directed distally (Fig. 12-21). The significance of this osteophyte in the etiology of symptoms is unknown. It may be a response to muscle tension and is frequently found in the asymptomatic foot. It is not considered the cause of pain. A stress fracture or other bony disorder may need to be ruled out in some cases (Fig. 12-22).


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Fig. 12-21 Roentgenography of the os calcis shows the distally directed traction osteophyte on its inferior aspect (arrow). The patient should be reassured that even though a “spur” may be present, it is not sharp as the name might suggest, but rather it is round and smooth, and the relationship between heel pain and heel spurs has never been established.


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Fig. 12-22 Stress fracture of the calcaneus.



TREATMENT


Taping, relief pads, heel cups, cushions, and various orthoses have all been used with only modest success. Over-the-counter pads and cups are as effective as more expensive orthoses. No treatment designed to cushion the heel seems to help, probably because heel strike may not be the cause of the problem. Exercises that stretch the heel cord and plantar fascia may help, but they should not be performed in the acutely painful foot. Only a gentle pulling sensation should be felt. Cold or ice as counterirritants may promote temporary relief. A heel lift or high-heeled shoe may relieve pain in some cases. Oral anti-inflammatory medication is used as necessary. Many patients will benefit from local infiltration of the tender area with a steroid/lidocaine mixture (Fig. 12-23). The injection may be repeated three to four times. (Avoid injecting the superficial tissue, which could cause fat pad necrosis.) Application of a short leg walking cast or removable cast-boot for 6 weeks is often very beneficial. Custom-fitted tension night splints that hold the foot in slight dorsiflexion are used in some resistant cases. Physical therapy is not usually recommended. Extracorporeal shock wave therapy has even been tried, but the results are inconclusive.


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Fig. 12-23 Injection site for plantar fasciitis. Injection should be through the sole into the area of maximum tenderness. A 25- or 27-gauge needle should be used and the medication injected slowly as some pain may occur. The total volume should be no greater than 1.5 mL.

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Jun 12, 2016 | Posted by in ORTHOPEDIC | Comments Off on The Ankle And Foot

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