Introduction
Developmental variations of the foot are common. Thus, they are a frequent source of concern to the family and a common reason for referral to an orthopedist.
Growth
The lower limb bud forms by about 4 weeks of gestation, and the foot develops over the next 4 weeks (Fig. 1).
Figure 1. Fetal foot development The limb bud appears by about 4 weeks of gestation and the foot is well formed by about 7 weeks.
The foot achieves its adult length earlier than the rest of the body (Fig. 2). Half of the adult length of the foot is achieved between 12 and 18 months of age. By comparison, half of adult height is achieved at 2 years, and half of the lower limb length by 3 to 4 years of age. Rapid foot growth requires frequent shoe changes in infancy and childhood.
Figure 2. Foot growth Dimeglio charts show the growth of the foot for girls (left) and boys (right). Note that growth of the foot slows earlier than growth in stature.
Arch Development
The longitudinal arch of the foot develops with advancing age (Fig. 3). The flatness of the infant’s foot is due to a combination of abundant subcutaneous fat and joint laxity common in infants. This joint laxity allows flattening of the arch when the infant stands, and the fatty foot further obscures the longitudinal arch.
Figure 3. Arch development The longitudinal arch develops with growth in childhood. Note the wide range of normal. Flatfeet fall within the normal range. From Staheli et al. (1987).
Normal Variability
Accessory centers of ossification are common about the foot (Fig. 4).
Figure 4. Common accessory ossification centers about the foot (A) Os trigonum (white arrow), (B) medial malleolar ossicle, (C) lateral malleolar ossicle, (D) accessory navicular (often painful), and (E) os vesalianum (yellow arrow).
Most fuse with the primary center and become part of the parent ossicle. Others remain as separate ossicles, usually attached to the parent bone by cartilage or fibrous tissue. These ossicles are clinically important because they may be confused with a fracture, and they may become painful when the syndesmosis or synchondrosis is disrupted. Such disruptions commonly involve the accessory navicular and an ossicle inferior to the lateral malleolus.
Foot in Systemic Disorders
Evaluation of the foot is a useful aid in diagnosing constitutional disorders. For example, polydactylism is seen in chondroectodermal dysplasia. Dysplastic nails are found in the nail–patella syndrome.
Nomenclature
To clarify this discussion, terms describing joint motion versus those describing deformities are defined separately (Fig. 5).
Figure 5. Nomenclature for normal joint motion and deformity Joint motion and deformity should be described independently.
The anatomical position is considered neutral. Often deformity is designated simply by describing the motion and adding the term deformity behind it. Thus, the subtalar joint fixed in inversion is referred to as an inversion deformity. Note that the description of great toe position is inconsistent with standard terminology. The reference point is the center of the foot rather than the center of the body. Thus, the position of the great toe toward the midline of the body is referred to as abduction.
Both bones and joints may be deformed. For example, medial deviation of the neck of the talus occurs in clubfeet. This contributes to the adduction deformity. Joint deformity is usually due to stiffness with fixation in a nonfunctional position. Limit the use of the terms varus and valgus to describe deformities.
Evaluation
Family History
Foot shape often runs in families (Fig. 6). If the deformity is present in an adult, inquiry about disability may help in managing the child’s problem.
Figure 6. Familial hallux varus Note the same deformity in the mother’s and daughter’s feet.
Screening Examination
Perform a screening examination. Look at the back for evidence of a spinal dysraphism that may account for a cavus foot. Assess joint laxity (Fig. 7), as this may be a cause of flexible flatfeet.
Figure 7. Generalized joint laxity This child’s thumb is easily opposed to the forearm. The child also has a flexible flatfoot.
Foot Examination
The diagnosis of most foot disorders can be made by physical examination. Bones and joints of the foot have little overlying obscuring soft tissue, thus deformity and swelling are easily observed. Furthermore, localization of the point of maximum tenderness (PMT) is readily established.
Observation
Observe the skin on the sole of the foot for signs of excessive loading (Fig. 8, 9). Excessive loading that causes calluses is not normal in children. Common sites of excessive loading include the metatarsal heads, the base of the fifth metatarsal, and under the head of the talus. The deformities that cause the calluses are likely to cause pain in adolescence.
Figure 8. Sole contact area Note the broad even weight distribution on the soles of these normal feet. Child is standing on a mirrored glass surface.
Figure 9. Examine the sole for signs of excessive loading Note the calluses under the metatarsal heads of both feet in this child with congenital toe malformations.
Observe the foot with the child standing. Note the alignment of the heel. Heel valgus is common. Note the height of the longitudinal arch. Next, ask the child to toe stand. A longitudinal arch is established in the child with a flexible flatfoot (Fig. 10). With the child seated and the foot unweighted, a longitudinal arch also appears in the child with a flexible flatfoot.
Figure 10. Flexible flatfeet The longitudinal arch absent on standing (white arrows) appears on toe standing (yellow arrows).
Range of Motion
Estimate the range of motion of the toes and the subtalar and ankle joints. Estimate subtalar joint mobility by the range of inversion and eversion motion. Assess ankle motion both with the knee flexed and extended and with the subtalar joint ieutral alignment (Fig. 11). Dorsiflexion to at least 20° with the knee flexed and to 10° with the knee extended should be possible.
Figure 11. Assessing ankle dorsiflexion Right angle (yellow) is neutral position. Assess dorsiflexion (red lines) with the knee extended and flexed to determine site and severity of triceps contractures.
Palpation
By palpation, determine if any tenderness is present. Determining the PMT is especially helpful in the foot because much of the foot is subcutaneous. The PMT is often diagnostic or at least helpful in making decisions regarding imaging.
Imaging
Whenever possible, radiographs of the feet should be taken with the child standing (Fig. 12). If radiographs are indicated, order AP and lateral projections. If subtalar motion is limited, an oblique view of the foot should be added to rule out a calcaneonavicular coalition. The ankle can be evaluated with AP and lateral radiographs. Order a “mortise” view if a problem such as an osteochondritis dissecans of the talus is suspected. Other special views such as flexion–extension studies may be helpful. Compare the radiographs to published standards for children.
Figure 12. Standing radiographs Standing radiographs allow the most consistent evaluation. In the adolescent with a skewfoot deformity, the talar inclination (yellow line), metatarsal axis (red line), and calcaneal pitch (orange line) are readily measured.
The normal range is broad and changes with age (Fig. 13). CT scans are useful in evaluating the subtalar joint for evidence of a talocalcaneal coalition. Bone scans are useful in confirming the diagnosis of an osteochondrosis, such as Freiberg disease. The scan will be abnormal before radiographic changes are present. MRI is useful for evaluating tumors.
Figure 13. Inclination of the talus by age The shaded area represents two standard deviations above and below the mean (heavy line). Note that the values change with age and that the normal range is very broad. From Vander Wilde et al. (1988).
Foot Pain
Foot pain in children is common and varied (Fig. 14, 15). During the first decade of life, foot pain is usually due to traumatic and inflammatory problems, such as injuries and infections, and is seldom due to deformity. During the second decade, foot pain is often secondary to deformity.
Figure 14. Classification of foot pain The causes of foot pain can be placed in categories for classification and diagnosis.
Figure 15. Foot pain localization Because the foot is largely subcutaneous, localization of the tenderness will often aid in establishing the diagnosis.
The cause of the foot pain can often be determined by the history and physical examination. Determining the PMT is especially useful about the foot because the structures are subcutaneous and easily examined (Fig. 16). This localization often allows a presumptive diagnosis.
Figure 16. Point of maximum tenderness The ankle is swollen and tenderness is present just anterior to the distal fibula, typical of a sprain.
Trauma
Stress–occult fractures Fractures without trauma history are not uncommon in infants and young children. They may be considered as part of the toddler fracture spectrum. Fractures of the cuboid, calcaneus, and metatarsal bones can be best identified by bone scans.
Tendonitis–fascitis Repetitive microtrauma is a common source of heel pain in children. This is most common about the os calcis either at the attachment of the heel-cord or the plantar fascia.
Infections
Infections of the foot are relatively common. Septic arthritis commonly affects the ankle and occasionally other joints of the foot. Osteomyelitis may occur in the calcaneus and other tarsal bones. Infection may be hematogenous or iatrogenic (heel sticks for blood sampling) or result from penetrating injuries.
Nail puncture wounds Nail puncture wounds are common injuries (Fig. 17, 18)
Figure 17. Nail puncture wound Erythema and a puncture wound (arrow) show the site of nail entry. Swelling is most prominent on the dorsum of the foot.
Figure 18. Needle penetration into heel Radiograph (left) shows brokeeedle. Photograph (right) shows site of entry of needle and surrounding inflammation
that may be complicated by osteomyelitis (Fig. 19). About 5% of nail penetrations become infected, but less than 1% develop osteomyelitis. Puncture wounds under the metatarsal are more likely to be caused by pseudomonas septic arthritis. Infections in the heel are commonly from staphylococcus or streptococcus.
Figure 19. Chronic osteomyelitis A nail puncture wound through a shoe was followed by this infection that involved the bone and joint (white arrow). The joint was destroyed. Chronic osteomyelitis of the first metatarsal (yellow arrow) is evident in the radiograph
Initial management Examine the foot and remove any protruding foreign material. Probing the wound will be unpleasant and unrewarding. Update tetanus immunization. Inform the family about the risk of infection and the need to return if signs of infection occur. Usually infections will show signs several days after the injury and include increasing discomfort, swelling on the dorsum of the foot, and fever.
Management of infection Culture the wound and obtain an AP radiograph of the foot to serve as a baseline. The time of onset of signs of an infection suggests the infecting agent. If the interval between penetration and infection is 1 day, the organism is likely to be streptococcus. If the interval is 3–4 days, staphylococcus is most likely, and if a week, pseudomonas. Children with pseudomonas infections were usually wearing shoes at the time of the penetration. Operative debridement and drainage are indicated in all pseudomonas infections. Drainage is also indicated in all infections that fail to improve promptly with antibiotic treatment.
Ingrown toenails Ingrown toenails (Fig. 20) are common infections resulting from a combination of anatomical predisposition, improper nail trimming, and trauma. Injury or constricting shoes or stockings may initiate the infection. In children prone to developing this problem, the nail is abnormal, often showing a greater lateral curvature of the nail into the nailbed.
Figure 20. Ingrown toenails Inflammed soft tissue around the ingrowail (red arrow). Photograph shows typical clinical appearance (white arrow).
Management of early infections Choose treatment based on the severity of the inflammation. Mild irritation requires only proper trimming of the nail and properly fitting shoes. Nails should be trimmed at right angles. Avoid trimming the nail to create a convex end. Instruct the family to trim the nail to create a concave end that leaves the nail edges extending beyond the skin to prevent recurrent ingrowth. Elevate the soft tissue from the nail plate with a wisp of cotton. Avoid forcefull packing. Repeat this several times if necessary to lift the inflamed soft tissue from the nail plate. If inflammation is more severe, rest, elevation, protection from injury, soaking to clean and promote drainage, and antibiotics may be necessary.
Management of late infections Persistent severe lesions require operative management. The hypertrophic chronic granulation tissue is excised, and removal of the lateral portion of the nail together with a portion of the nail matrix may be necessary to prevent recurrence.
Pauciarticular Arthritis
Pauciarticular arthritis may present with foot pain in the infant or young child. A limp, limited ankle or subtalar motion and swelling for more than 6 weeks duration suggests this diagnosis (Fig. 21). In contrast with septic arthritis, pauciarticular arthritis looks like it should hurt more than the child reports. The pain is often minimal.
Figure 21. Arthritis of the ankle This child has pauciarticular arthritis affecting the ankle.
Osteochondritis
Köhler disease Tarsal navicular osteochondritis, also known as Köhler disease, is an avascular necrosis most common in boys between 3 and 10 years of age (Fig. 22).
Figure 22. Köhler disease in a 5-year-old boy The tarsal navicular of the left foot is sclerotic (arrow) and the site of tenderness.
It also occurs uncommonly in girls 2 to 4 years of age. The disease produces inflammation, localized tenderness, pain, and a limp. Radiographic changes depend on the stage of the disease. The navicular first shows collapse and increased density. Patchy deossification follows. Finally, the navicular is reconstituted. Because healing occurs spontaneously, only symptomatic treatment is necessary. If pain is a significant problem, immobilize the foot in a short-leg walking cast for 6–8 weeks to reduce inflammation and provide relief of pain. Long-term follow-up studies show no residual disability.
Freiberg disease Metatarsal head osteochondritis, also known as Frieberg disease or infraction, is an idiopathic segmental avascular necrosis of the head of a metatarsal. It most commonly occurs in adolescent girls, 13–18 years, and involves the second metatarsal. Pain and localized tenderness (Fig. 23) are common.
Figure 23. Freiberg disease Tenderness over the head of the second metatarsal is usually present in Freiberg disease. Minimal changes are present in the radiograph (yellow arrow), and the bone scan shows increased uptake over the second metatarsal head (red arrow). The photograph shows the point of maximum tenderness (green arrow).
If the patient is seen early, a bone scan will show increased uptake and establish the diagnosis. Later, radiographs will show irregularity of the articular surface, sclerosis, fragmentation, and finally reconstitution. Residual overgrowth and articular irregularity may lead to degenerative changes and persistent pain. Treat with rest and immobilization to reduce inflammation. An orthosis to unweight the involved metatarsal head, sole stiffeners to reduce motion of the joint, and even a short-leg walking cast may be useful. For severe persisting pain, operative correction may be necessary. Options include joint debridement, excisional arthroplasty (proximal phalanx), interposition arthroplasty using the tendon of the extensor digitorum longus, and dorsiflexion osteotomy (Fig. 24) of the metatarsal (often the best choice).
Figure 24. Metatarsal osteotomy for pain due to Freiberg deformity This procedure moves the avascular segment of the metatarsal head away from the the joint
Sever disease, or calcaneal apophyseal osteochondrosis, is commonly diagnosed by heel pain and radiographic features of fragmentation and sclerosis of the calcaneal apophysis. These radiographic changes occur commonly in asymptomatic children (Fig. 25). Most heel pain in children is due to inflammation of the attachment of the plantar fascia or heel-cord.
Figure 25. Calcaneal apophysis In the normal child, this apophysis often shows sclerosis and fragmentation.
Impingement Pain
Os trigonum syndrome Compression of the ossicle in dancers often causes foot pain.
Mid tarsal impingement Mid foot pain is sometimes due to compression of articular margins often secondary to tarsal coalitions or heel-cord contracture (Fig. 26).
Figure 26. Impingement This is talar beaking associated with a tight heel-cord and impingement.
Syndesmosis Disruption
Disruption of the syndesmosis between the primary ossicle and a secondary center of ossification (accessory ossicle) is a common cause of pain in the feet of children and teenagers. This disruption is the equivalent of a stress injury of the cartilaginous or fibrous attachment. It becomes painful and tender (Fig. 27) unless healing is complete. The condition commonly recurs.
Figure 27. Accessory navicular The accessory navicular is located on the medial aspect of the foot (arrows). It often produces a prominence and is sometimes painful.
Accessory navicular is an accessory ossification center on the medial side of the tarsal navicular that occurs in about 10% of the population and remains as a separate ossification center in about 2%. They are classified into three types (Fig. 28).
Figure 28. Classification of accessory navicular Type 2 with disruption of the synchondrosis (red arc) and type 3 producing a prominence (arrow).
Type 1 is seldom symptomatic. Type 2 is most likely to have pain from disruption of the synchondrosis. Disruptions are common during late childhood and adolescence and are probably due to repetitive trauma. This disruption causes pain and localized tenderness. Type 3 causes a prominence that, if large, may cause irritation of the overlying skin.v
Manage pain with a short-leg cast or splint. If the pain persists, excision of the accessory navicular may be necessary. Simply excise the ossicle and a portion of the elongated primary navicular through a longitudinal split in the fibers of the posterior tibial tendon (Fig. 29).
Figure 29. Excision of accessory navicular The painful type 2 ossicle is removed, leaving the tendinous posterior tibial tendon attached to the navicular (arrow).
Avoid the more extensive Kidner procedure, which requires rerouting the tendon and does not improve the outcome.
Malleolar ossicles Ossification centers occur below the medial and lateral malleoli. Persisting ossicles under the lateral malleolus are most likely to be painful (Fig. 30). Manage first by cast immobilization. Rarely, excision or stabilization by internal fixation is necessary.
Figure 30. Lateral malleollar ossicle This ossicle was painful, not improved by casting, and evenutally required fusion with screw fixation.
Idiopathic Disorders
Tarsal tunnel syndrome Foot pain, Tinel’s sign over tarsal tunnel, dysesthesias, and delayed nerve condition suggest this diagnosis. This syndrome differs in children. Typically, the child is female, walks with the foot in varus, may elect to use crutches, and often requires operative release.
Reflex sympathetic dystrophy This syndrome usually affects the lower limb in girls (Fig. 31). Consider this diagnosis when the foot is swollen, stiff, cool, and generally painful. A history of injury is common. Pain assessment by the child is exaggerated and does not match the history or physical findings. See Chapter 3 for management.
Figure 31. Reflex sympathetic dystrophy The varus deformity of the left foot is due to reflex sympathetic dystrophy.
Foot Deformities
Foot deformities may cause pain due to pressure over bony prominences (Fig. 32) or to altered mechanics of the foot. Pain from deformity is usually not difficult to recognize.
Figure 32. Foot deform ities in a child with spina bifida Prominence of the head of the talus caused skin breakdown in the foot with diminished sensation.
Clubfoot
Clubfoot (CF) is a complex congenital deformity that includes components of equinus, cavus, adductus, varus, and internal rotation (Fig. 33). Clubfoot is also referred to as talipes equinovarus (TEV). It occurs in about 1 in 1000 births, is bilateral in half the cases, and affects males more frequently.
Figure 33. Typical appearance of bilateral clubfeet The deformity includes equinus, cavus, adductus, varus, and internal rotation.
Etiology
The cause of clubfeet is multifactorial. In affected families, clubfeet are about 30 times more frequent in offspring than for the general population. Fetal ultrasound screening shows the deformity in the first trimester (Fig. 34). Clubfoot can be associated with other congenital abnormalities such as neural tube defects, anomalies of the urinary or digestive system, and other musculoskeletal abnormalities. The clubfoot deformity can have different causes, as evidenced by the variability of expression and response to management.
Figure 34. Clubfoot on ultrasound at 16 weeks
Mild or positional clubfoot is a late intrauterine deformity (see Chapter 1) and corrects rapidly with cast treatment. At the other end of the severity spectrum, severe clubfoot behaves like a disruption, having an origin earlier in fetal life and requiring operative correction. Severe clubfoot is seen in conditions such as arthrogryposis (Fig. 35). Classic or idiopathic clubfoot is a multifactorial disorder, is relatively common, and occupies the middle range of the severity spectrum.
Figure 35. Severe clubfoot Note the prominent medial crease (arrow).
Pathology
The pathology of clubfoot is typical of a dysplasia. The tarsals are hypoplastic. The talus is most deformed; the size is reduced and the talar neck is shortened and deviated in a medial and plantar direction. The navicular articulates with the medial aspect of the neck of the talus due to the abnormal shape of the talus. The relationship of the tarsals are abnormal. The talus and calcaneus are parallel in all three planes. The midfoot becomes more medially displaced, and the metatarsals are adducted and plantarflexed. In addition to the deformities of cartilage and bone, the ligaments are thickened and the muscles hypoplastic. This results in a generalized hypoplasia of the limb with shortening of the foot and smallness of the calf (Fig. 36). Because the hypoplasia primarily involves the foot, limb length discrepancy is usually less than 1 cm. The foot is small, and split size shoes are often required. The amount of foot shortening is proportional to the severity of the clubfoot.
Figure 36. Reduction in leg size (Left) This girl with bilateral clubfeet has bilateral calf hypoplasia. (Below) The left clubfoot is more severe (red arrow) and is significantly shorter than the right foot with mild deformity. The degree of hypoplasia parallels the severity of the clubfoot deformity.
Natural History
Untreated, clubfoot produces considerable disability (Fig. 37). The dorsolateral skin becomes the weight-bearing area. Calluses form and walking becomes limited.
Operatively treated clubfeet are often stiff, weak, and may be in varus. These problems often cause considerable disability in adult life.
Figure 37. Untreated clubfeet These are the feet of a 13-year-old Cambodian boy with untreated clubfeet. A large callus and bursa have formed over the site of weight bearing on the dorsum of each foot.
Clinical Features
The diagnosis of clubfoot is not difficult and is seldom confused with other foot deformities. Sometimes severe metatarsus varus is confused with clubfoot, but the equinus component of clubfoot makes the differentiation clear. The presence of a clubfoot should prompt a careful search for other musculoskeletal problems.
Examine the back for evidence of dysraphism, the hips for dysplasia, and the knees for deformity. Perform a screening neurologic examination. Note the size, shape, and flexibility of the feet. Take radiographs of the spine or pelvis only if abnormalities are found on physical examination. Clubfoot is not associated with developmental hip dysplasia or spinal deformity.
Note the degree of stiffness of the foot (Fig. 38) and compare the size of the foot with the uninvolved foot. Marked differences in foot length suggest that the deformity is severe and foretell the need for operative correction. Document the components of the clubfoot deformity, the equinus, cavus, heel varus, forefoot adductus, and medial rotation.
Figure 38. Testing flexibility Assessing flexibility is a good way to determine the severity of the clubfoot.
Equinus is due to a combination of a plantar flexed talus, posterior ankle capsular contracture, and shortening of the triceps.
Cavus is due to a contracture of the plantar fascia with plantar flexion of the forefoot on the hindfoot.
Varus results from inversion of the subtalar joint.
Adductus and medial rotation are due to medial deviation of the neck of the talus, medial displacement of the talonavicular joint, and metatarsus adductus. Tibial rotation is normal.
Classification
A number of classifications for clubfoot have been proposed.
Etiologic classification This is based on the possible causes of clubfoot and include several types.
Positional clubfeet are flexible and thought to result from intrauterine position late in gestation. These resolve quickly with serial casting.
Idiopathic clubfeet include the classic forms with an intermediate degree of stiffness. They are multifactorial in etiology.
Teratologic clubfeet are associated with arthrogryposis, meningomyelocele, and other generalized disorders. These feet are very stiff and difficult to manage.
Pirani classification This classification is becoming widely used. It provides a numeric score based on three midfoot and three hindfoot features. Each is considered as normal, moderately abnormal, or severe abnormal. Make scores periodically during management to assess progress.
Midfoot scores are based on the lateral border, medial crease, and talar head coverage.
Hindfoot scores are based on the posterior crease, equinus rigidity, and the heel configuration.
Dimeglio classification This classification is based on stiffness. Range of motion in equinus, adduction, varus, and medial rotation are then given points. The sum of these points establishes the severity (Fig. 39).
Figure 39. Dimeglio classification Clubfoot stiffness in equinus (shown here), varus, rotation, and adduction are assessed. The sum of these scores is used to establish severity. The distribution of clubfeet into the four grades of severity are shown in the pie chart. Based on Dimeglio et al. (1995).
Imaging Studies
Radiographs, ultrasound, and MRI imaging are rarely used or necessary for assessment. Because active treatment usually occurs during early infancy, when ossification is incomplete, the value of radiographic studies is limited. Furthermore, because Ponseti management does not utilize radiographs, radiography is becoming less widely used than in the past. Ultrasound studies may become more widely used in the future. Radiographs become increasingly valuable with increasing age (Fig. 40). The common measures are as follows:
Figure 40. Radiographic evaluation of clubfoot On a maximum dorsiflexion radiograph, measure the tibial calcaneal angle (red lines). On resting or standing radiographs, note the parallelism between the axes of the talus and calcaneus (yellow lines).
Tibial calcaneal angle in maximal dorsiflexion is a measure of equinus. To fall into the normal range, the angle should be >10° above a right angle.
Lateral talocalcaneal angle is a measure of varus. Parallelism is a sign of residual heel varus.
AP calcaneocuboid alignment provides an assessment of the severity of the midfoot adduction and varus.
Navicular position Dorsal displacement of the navicular is a sign of malalignment of the midtarsal joints.
The value of radiographs is uncertain because long-term studies suggest that triceps strength, foot mobility, and plantar loading as measured clinically are more significant than static radiographic measures in assessing outcomes.
Routine screening radiographs of the pelvis are not necessary in children with clubfoot. Provide the same screening as for any normal child.
Management
The objective of management of clubfoot is to correct the deformity and retain mobility and strength. The foot should be plantigrade and have a normal load-bearing area. Secondary objectives include the ability to wear normal shoes, satisfactory appearance, and avoidance of unnecessarily complicated or prolonged treatment. The clubfoot is never fully corrected. When compared with a normal foot, all clubfeet show some residual stiffness, shortening, or deformity.
Management trends are influenced by data that suggest that maintaining mobility and triceps strength are more important than judging outcomes on radiographic criteria. Current trends favor early cast treatment (Fig. 41), Ponseti approach (Fig. 42), customized procedures (Fig. 43), and a greater focus on function and less on deformity.
Figure 41. Initial management with corrective casts Cast treatment is helpful in correcting or reducing clubfoot deformity. Padding is first applied. The shortleg portion is applied first as shown. This was extended to become a longleg cast to make it more effective.
Figure 42. Relating clubfoot severity to management Clubfoot management is often related to the severity of the clubfoot.
Figure 43. Approaches to management of clubfeet
Idiopathic clubfeet Start treatment as soon as possible after birth. Several approaches are used.
Ponseti management This approach has recently become the standard approach in most of the world. This management includes manipulation and casting to correct the deformities in an orderly sequence. Correct the cavus, rotate the foot from under the talus, and finally correct the equinus. Usually a percutaneous tenotomy is performed to facilitate equinus correction. Sometimes a transfer of the anterior tibialis (AT) is performed in early childhood. Rotational splinting is an essential part of management. Flexibility and strength are maintained with this approach.
French management emphasizes prolonged intense manipulations and splinting.
Traditional management usually includes initial casting and then one of several techniques for operative correction. Make the correction during the first year of life. Tailor the extent of the procedure to the severity of deformity [B]. Prevent recurrent deformity with night splinting.
Arthrogrypotic clubfeet Reduce the deformity by initial casting using the Ponseti technique. Individualize management depending upon the response. It may be necessary to perform percutaneous lengthenings of the flexor hallicus longus, the posterior tibialis and the heel-cord, then return to the casting sequence. In others, a posterior medial-lateral release may be necessary to correct deformity not resolved by castin.
Uncommon forms of clubfoot These occur in infants who have some underlying problem.
Non-idiopathic clubfeet These are clubfeet that occur in apparently normal infants but behave differently. These individuals have hypermobility and, with conventional treatment, may show overcorrection such as heel valgus. These overcorrections are less likely to occur with Ponseti management (Fig. 44) than with conventional management.
Figure 44. Ponseti management This child had serial casting, a percutaneous tenotomy (arrow), and an excellent outcome with a flexible, strong, plantigrade foot.
Syndrome associated clubfoot The classic clubfoot that occurs in arthrogryposis and mylomeningocele. Typically, these clubfeet are more difficult to correct and recurrence is more likely. Individualize management. Start with the Ponseti approach. If correction is not progressing at a satisfactory rate, consider a limited posteromedial release. Perform the releases subcutaneously; the casting may be resumed. Complete the correction by a posterior medial-lateral release later in the first year (Fig. 45). Be aware that recurrence is more likely and more difficult to control than seen with idiopathic clubfoot.
Figure 45. Operative correction This posterior release includes lengthening of the heel-cord (arrows) and opening of the joint capsule. Immobilization is provided by a long-leg cast.
Complications Are common in clubfoot management. They may be early or late. Recurrence is the most common early complication.
Recurrence Nearly half of clubfeet that are treated operatively recur and require additional treatment. Correct recurrent deformities with casts. Avoid repeated major operative procedures. Plan a final bony correction at the end of growth. Complications of this treatment are common.
Stiffness may result from excessive articular pressure during treatment, compartment syndromes complicating surgery, internal fixation, avascular necrosis of the talus, and operative scarring.
Weakness of the triceps jeopardizes function. Overlengthening and repeated lengthening procedures increase this risk.
Varus deformity commonly causes excessive plantar pressure over the base of the fifth metatarsal.
Overcorrection with a valgus hindfoot is common following operative correction. This is most likely in children with excessive joint laxity. Correction is challenging.
Salvage procedures These procedures may be necessary in special situations.
Talectomy Some surgeons perform an inital resection of the talus in teratologtic clubfeet as a primary procedure or more likely for salvage when other treatment fails.
External fixator Severe deformity in older children is sometimes best managed with the Ilizarov frame (Fig. 46). Use the frame to stretch soft tissues to achieve gradual correction. Be aware that recurrent deformity is a common and difficult problem. Provide postoperative splinting using an AFO. Position the foot in dorsiflexion to prevent recurrent deformity. This splint is important, but recurrence is still common.
Figure 46. Ilizarov frame This is an effective method of correcting severe deformity in the older child.
Bony corrections In severe clubfeet with recurrent deformity, delay recorrection until the end of growth. When possible, correct with osteotomies rather than arthrodeses to preserve what little joint motion remains. Bone procedures performed at the end of growth provide correction that is most likely to be permanent.
Ponseti Clubfoot Management
The Ponseti approach to management of clubfeet has been refined over a period of 50 years, has been shown to produce good long-term results, and is becoming the management standard throughout the world. This management shows 90+% success in idiopathic clubfeet (Fig. 47). It is also a good choice as the initial management of other forms of clubfoot as well.
Figure 47.
Correction is achieved by manipulation and cast correction in a definite sequence. Correction is usually achieved in 5 to 8 weekly sessions (casts). A percutaneous heel-cord tenotomy is commonly added to facilitate equinus correction. In many patients, a lateral transfer of the anterior tibialis is performed in early childhood. The mechanism of correction is best appreciated by using a skeletal model.
Principles
Pathology The calcaneus, navicular, and cuboid are adducted and inverted in relation to the talus and held in adduction and inversion by contracted ligaments and tendons (Fig. 48).
Figure 48.
Severity The severe clubfoot is characterized by a very short distance between the medial malleolus and tubercle of the navicular (Fig. 49).
Figure 49.
Early treatment Treatment should be started as soon after birth as possible to take advantage of the favorable fibroelastic properties at that age.
Manipulate the foot for a minute prior to cast application.
Casting Apply a long-leg cast to control all elements of the deformity, including rotation. Correct by weekly cast changes using well-molded long-leg plaster casts. Most clubfeet require 4 to 6 weeks with weekly cast changes.
Learning technique This technique is best learned under supervision of someone experienced with this technique. Faulty cast application may create deformities that are difficult to later correct.
Manipulation and Casting Sequence (Ponseti)
Correct cavus Supinate the pronated forefoot (Fig. 49 – E) by dorsiflexing the first metatarsal with the foot stabilized with a finger over the lateral aspect of the head of the talus (Fig. 50). This corrects the plantarflexion of the first ray. Immobilize the foot in marked supination in the cast (Fig. 51).
Figure 50. No caption available
Figure 51.
Correct adduction and varus With counterpressure by the thumb against the head of the talus (Fig. 52), abduct the supinated forefoot.
Figure 52.
Allow the calcaneus to evert under the talus in the subtalar joint. By full abduction of the midfoot and forefoot, the tight medial tarsal ligament contractures are overcome (Fig. 53).
Figure 53.
This correction allows the calcaneus to abduct, extend, and evert under the talus, correcting the heel varus. Be aware that this correction occurs at the subtalar level, not in the ankle joint. During the process of rotating and sliding the calcaneus under the talus, progressively increase the thigh-foot angle in the casts until about 70° is achieved (Fig. 54).
Figure 54. No caption available
Equinus correction Before dorsiflexing the foot, make certain the foot is fully abducted and the medial contracted ligaments and tendons are stretched out in the casts (Fig. 55). Correct equinus by dorsiflexing the fully abducted foot. Stop before creating a rocker bottom foot deformity. A percutaneous heel-cord tenotomy is necessary in about 90% of cases.
Figure 55.
Percutaneous tenotomy (Fig. 56) may be performed in the outpatient clinic or in the operating room one week after all of the other deformities are fully corrected.
Figure 56.
Provide general anesthesia or inject a small amount of local anesthesia (0.1 cc to avoid obscuring the tendon), or apply EMLA cream (lidocaine 2.5% + prilocaine 2.5%) one hour before the procedure. Insert a small blade just medial to the heel-cord about one centimeter above the calcaneus, feel the tendon with a blade, and divide from anterior to posterior, preserving the tendon sheath (Fig. 57).
Figure 57.
Immobilize in a long-leg cast (Fig. 58) for 3 weeks with the foot positioned in abduction and dorsiflexion. Mold the sole of the foot carefully to prevent rocker-bottom deformity. Extend the cast under the toes to stretch long toe flexors. Leave dorsum of the cast uncovered to allow dorsiflexion of the toes and to observe circulation of the foot.
Figure 58.
Post-Correction Management
Splinting is managed in a foot abduction orthosis (Fig. 59) full-time for 3 months.
Figure 59.
The width of the bar should equal the width of the infant’s shoulders. Use stiff, open-toed shoes on the bar. Place a plastizote pad above the heel to prevent the foot from slipping out of the shoes. Set the foot in about 70° foot abduction (lateral rotation) on the clubfoot side and about 45° on the normal side. The use of this splinting at nighttime for 3–5 years is an essential part of this management method (Fig. 60).
Figure 60.
Recurrence Recurrence can usually be corrected by a series of 2 or 3 long-leg casts, each worn for 2 weeks.
Tendon transfer If relapse occurs twice despite compliance with brace management, and the tibialis anterior tendon is strong and deforming, transfer the tendon to the third cuneiform during early childhood (Fig. 61).
Figure 61. No caption available.
Correct any fixed recurrence with a series of casts (needed for about 30% of feet). Avoid transfers before the cuneiform is ossified. Often a concurrent open heel-cord lengthening should be combined with the the AT tendon transfer. This balances the foot, prevents recurrence, and is a relatively simple procedure.
Common Errors in Management
Pronation Avoid pronation of the forefoot that accentuates the cavus component. Although the whole foot is supinated, the forefoot is in relative pronation, causing a cavus deformity.
Abduction of the foot Avoid abduction of the foot while the calcaneus is in varus to avoid posterior displacement of the lateral malleolus—an iatrogenic deformity.
Fixation on radiographs Good long-term results are related to mobility and strength, not radiographic appearance.
Relying on physical therapy alone without a period of cast immobilization allows relapse between therapy sessions, delaying correction.
Toe Deformities
Generalized Disorders
If a toe deformity is found, carefully examine the hands and feet of the child and of the parents. These deformities are sometimes manifestations of a generalized disorder (Fig. 62).
Figure 62. Syndromes associated with toe deformities
Cleft Foot Deformity
This rare deformity is transmitted as an autosomal dominant trait, is usually bilateral, and often involves the hands and feet (Fig. 63). A noninherited form is less common and is often unilateral. If it causes shoe-fitting problems, correct in late infancy or childhood by osteotomy and soft tissue approximation.
Figure 63. Cleft foot deformity These deformities are present in both the father and the son. The major problems are difficulties with shoe fitting and the unusual appearance.
Microdactyly
Small toes are often found in Streeter dysplasia and may be secondary to intrauterine hypotension, causing insufficient circulation to the toes (Fig. 64). No treatment is required.
Figure 64. Microdactyly
Syndactyly
Syndactyly is most common between the second and third toes, is usually bilateral and often familial. Fusion of the toes produces no functional disability and treatment is unnecessary. Look for some underlying problem if it involves more than two locations.
Polydactyly
Polydactyly or supernumerary digits are common (Fig. 65).
Figure 65. Excision of bifid great toe Half of the toe is removed. Excision of complex polydactyly is sometimes difficult.
They are most common in girls and in blacks and are sometimes inherited as an autosomal dominant trait. Most involve the little toe and duplication of the proximal phalanx with a block metatarsal or wide metatarsal head. Excise the extra digit late in the first year when the foot is large enough to make excision simple and before the infant is aware of the problem. Plan the procedure to minimize the scar, establish a normal foot contour, and avoid disturbing growth. Central duplications often cause permanent widening of the foot. Poor results are more likely for great toe duplications with persistent hallux varus and complex deformities (Fig. 66, 67).
Figure 66. Polydactyly Polydactyly causes a cosmetic and shoe fitting problem. Excision of the accessory toe is appropriate late in the first year.
Figure 67. Bracket epiphysis Toe deformities may be complex. In this case, the metatarsal epiphysis (yellow arc) is continuous for both toes. Excise the accessory digit and the adjacent portion of the growth plate.
Curly Toes
Curly toes (Fig. 68) are common in infancy and produce flexion and rotational deformities of the lesser toes. The deformity nearly always resolves spontaneously. Rarely, flexor tendinotomy is required for those that persist beyond age 4 years.
Figure 68. Curly toes This deformity may involve one or more toes and usually resolves spontaneously.
Claw Toes
Claw toes are usually associated with a cavus foot and are often secondary to a neurologic problem. Correction is usually part of the management of the cavus foot complex.
Hammer Toes
Hammer toes are secondary to a fixed flexion deformity of the proximal interphalangeal (PIP) joint (Fig. 69). The distal joint may be fixed or flexible. The condition is often bilateral, familial, and most commonly involves the second toes and less frequently the third and fourth. Operative correction is indicated in adolescence if the deformity produces pain or shoe-fitting problems. Correct by releasing the flexor tendons and fusing the PIP joint.
Figure 69. Hammer toe The fixed flexion deformity of the PIP joint of the second toe causes a callus (arrow) to form over the toe.
Mallet Toes
Mallet toes are due to a fixed flexion deformity of the distal interphalangeal (DIP) joint. These deformities are uncommon.
Overlapping Toes
Overlapping toes are common. Overlapping of the second, third, and fourth toes usually resolves with time. Overlapping of the fifth toe is more likely to be permanent (Fig. 70) and cause a problem with shoe fitting.
Figure 70. Overlapping toe This overlapping fifth toe persisted and required operative correction.
Overlapping of the fifth toe is often bilateral and familial. If overlapping becomes fixed, persists, and causes shoe-fitting problems, operative correction is appropriate. Correct with the Butler soft tissue alignment procedure (Fig. 71). This involves a double racket-handle incision, lengthening of the extensor tendon, releasing the joint contracture, and skin repair with the toe translated to a more plantar and lateral position.
Figure 71. Operative correction of overlapping toe Through a bucket handle incision (white line) lengthen the extensor tendon and capsule, correct the deformity, and close the skin, maintaining the correction (red line).
Hypertrophy
Hypertrophy (Fig. 72) is seen in children with Proteus syndrome, neurofibromatosis, or vascular malformation, or it can occur as an isolated deformity. Most show abnormal accumulation of adipose tissue, and some show endoneural and perineural fibrosis and focal neural and vascular proliferation. Management is difficult. Epiphysiodesis, debulking, ray resection, and through-joint amputations are ofteecessary. Recurrence is frequent, and several procedures are often required during childhood to facilitate shoe fitting.
Figure 72. Hypertrophy Overgrowth may cause severe shoe-fitting problems and require resection, epiphysiodesis, or amputation.
Cavus Deformity
A cavus foot is characterized by increased height of the longitudinal arch and is often associated with clawing of the toes and heel varus (Fig. 73). Cavus is most often physiological. It is simply the extreme end of the spectrum of normal variability of the shape of the longitudinal arch. This physiologic form is often familial. Pathologic forms of cavus deformity are usually neurogenic or myopathic.
Figure 73. Cavus–think spine The high arch should prompt an evaluation of the spine.
Physiologic Cavus
This deformity falls outside the normal range of ±2 SD in arch height (Fig. 74).
Figure 74. Normal values for foot contact area Contact area is described by the ratio of the arch width to the heel width. The mean value (green line), and two standard deviation levels for a low arch (blue line) and a high arch (red line) are shown. A foot is considered to have a cavus deformity if the arch contact area falls outside the ±2 SD level (light red area).
Often a parent’s feet have a high arch. The parent often volunteers that they have a “good” (high) arch. In fact, these parents are more likely to have pain than those with normal or low arches. The cavus is usually bilateral, with an onset in infancy. They may also have calluses under the metatarsal heads. The child’s musculoskeletal and neurologic screening examinations are normal, and clawing of the toes is absent. This is a diagnosis of exclusion. Occasionally, the teenager will complain of metatarsal pain. This is best managed by shock-absorbing shoeware and, if necessary, a soft shoe insert to unload the metatarsal heads.
Pathologic Cavus
Pathologic cavus is usually secondary to a neuromuscular disorder causing muscle imbalance. A major objective of management is to determine the underlying cause of the deformity.
Evaluation The neuromuscular disorders causing cavus deformities are often familial, so the family history is important. Look at the parents’ feet. Sometimes they may claim their feet are normal when they are clearly deformed. Perform a careful screening examination of the child. Examine the musculoskeletal system for other problems. Look for midline skin lesions over the spine (Fig. 75). A careful neurologic examination is essential. Check muscle strength. Examine the foot, noting the severity of the cavus, degree of rigidity, and presence of clawing of the toes and skin changes under the metatarsal heads.
Figure 75. Skin irritation with cavus deformity The cavus deformity increases the load on the metatarsal heads. If sensation is poor, as in the child with spina bifida, skin breakdown (arrow) is common.
Standing radiographs of the feet are useful in documenting the type and severity of the deformity. Special studies such as spine radiographs for spinal dysraphism, electromyography (EMG), DNA blood tests for Charcot–Marie–Tooth (CMT) disease, nerve conduction velocity measurements, and CPK determination for muscular dystrophy assessment may be necessary. Consultation with a neurologist may be appropriate. Establish the etiology of the cavus deformity (Fig. 76).
Natural history Because of the reduced area of plantar contact, deformity, and rigidity, cavus feet often cause considerable disability.
Figure 76. Classification of cavus deformity This classification includes the majority of causes of cavus feet. Pathologic cavus is often associated with neurologic disorders.
Types of Cavus Deformities
Congenital cavus is a rare deformity that may be due to intrauterine constraint or fixed deformity (Fig. 77). Assess the effect of growth.
Figure 77. A Congenital cavus This deformity gradually resolved during the first two years of growth. Note the calcaneal pitch (red line) and first metatarsal (yellow line) alignments.
Calcaneocavus results from weakness of the triceps. There is an increase in the calcaneal pitch, and a cavus deformity. Correct muscle imbalance, if possible. This deformity is seen in poliomyelitis (Fig. 78), in spina bifida, and following overlengthening of the triceps.
Figure 78. Hindfoot and forefoot cavus deformity Note the severe hindfoot cavus (orange arrow) secondary to weakness of the triceps from poliomyelitis. Note the forefoot cavus (yellow arrow). The white lines show the tibial axis, the red lines the calcaneal pitch, and the yellow lines the first metatarsal axis.
Cavovarus is the most common form. Muscle imbalance results in plantarflexion of the forefoot, inversion of the hindfoot, and a mild increase in the calcaneal pitch. This deformity is seen in CMT disease. Clawing of the toes is often seen.
Management
Follow a flowchart to manage (Fig. 79). The teenager will often complain of difficulty in fitting shoes, calluses over the claw toes and under the metatarsal heads, pain, and instability causing recurrent ankle sprains.
Figure 79. Cavus management flowchart From Mosca (2000).
Mild deformity Order shock-absorbing footwear and soft molded shoe inserts to broaden the load-bearing area of the foot.
Moderate or severe deformity This requires operative correction. Operations improve muscle balance, flatten the arch to broaden the weight-bearing surface, and correct toe deformity.
Flexible deformities or those in young children are best managed by a plantar medial release and appropriate tendon transfers. If performed during childhood, recurrence can occur.
Fixed deformities require correction in two stages. First, perform a soft tissue release, as described above. Follow this by osteotomies to correct bony deformity and tendon transfers to balance the foot. In most cases, perform a calcaneal osteotomy (Fig. 80) for calacaneocavus deformity and a dorsi flexion medial cuneiform osteotomy for cavovarus correction. Avoid arthrodesis whenever possible to maintain mobility and reduce the risk of degenerative arthritis of adjacent joints.
Figure 80. Calcaneocavus deformity This patient underwent a calcaneal dorsal displacement osteotomy to effectively reduce the cavus deformity.
Tarsal Coalitions
Coalitions are fusions between tarsal bones that cause a loss of inversion and eversion motion. They are often familial, may be unilateral or bilateral, and occur in both sexes equally. Coalitions may involve more than one joint. The fusion imposes increased stress on adjacent joints and sometimes causes degenerative arthritis, pain, and peroneal spasm. These symptoms usually develop during early adolescence. Often coalitions remain silent. Treatment is indicated only for intractible pain, not the mere existence of a coalition. Two common forms are present.
Calcaneonavicular (C-N) Coalitions
C-N coalitions are most common and sometimes identified on a lateral radiograph (Fig. 81) but are readily shown by an oblique radiograph of the foot (Fig. 82). The coalition may be composed of bone, cartilage, or fibrous tissue. Incomplete coalitions may show only narrowing or irregularity of the calcaneonavicular articulation.
Figure 81. “Ant-eater sign” The calcaneonavicular coalition is seen in lateral radiographs with this characteristic feature (arrows).
Figure 82. Calcaneonavicular coalition This C-N coalition is readily seen on oblique radiographs of the foot before resection (red arrows). Surgical resection (orange arrow) reduced discomfort and restored motion.
Manage symptomatic coalitions with a trial of immobilization (Fig. 83). Apply a short-leg walking cast for 4 weeks. The pain should disappear. If pain recurs soon after removal, operative correction is usually necessary. Resect the coalition and interpose extensor hallucis brevis muscle to prevent recurrence.
Figure 83. Flowchart for managing tarsal coalitions
Talocalcaneal (T-C) Coalitions
T-C coalitions usually involve the middle facet of the subtalar joint. Conventional radiographs are ofteormal, but sometimes the C-sign of Lateur may be present [C]. A special calcaneal or Harris view may show the fusion. The coalition is best demonstrated by CT scans of the foot [D].
Figure C C-sign of Lateur The C-sign of Lateur (arrow) is often present with subtalar coalitions
Figure D Subtalar coalition The middle facet subtalar coalition (arrow) is readily identified by CT imaging
Manage symptomatic coalitions with a trial using a short-leg cast. If pain recurs, consider operative resection. Assess the size of the coalition by CT imaging. Resection is likely to fail if coalitions exceed 50% of the joint. Technical problems are common [E]. Heel valgus may be increased by resection. Sometimes a calcaneal lengthening will be needed to correct this component. Outcomes for resection of subtalar coalitions are much less predictable than for the more common calcaneonavicular fusions. Advise the family of the potential for an unsatisfactory result and the possibility that additional procedures may be necessary.
Figure E Failed resection This resection failed because the coalition was not fully resected.
Other Coalitions
Other coalitions may occur at the talonavicular and naviculocuneiform joint. More extensive coalitions may be present in children with clubfeet, fibular hemimelia, and proximal focal femoral deficiencies. Pain and stiffness of the subtalar joint may occur with arthritis, tumors, and articular fractures. Consider these uncommon causes of pain if calcaneonavicular and talocalcaneal fusions are ruled out by radiography.
Tarsal Coalition Resection
Resection of tarsal coalitions is optimal management for refractory symptomatic coalitions. Resection of calcaneonavicular coalitions is much simpler and more consistently satisfactory than subtalar coalition resection. Subtalar coalitions often require secondary procedures due to continued pain, excessive valgus, or recurrence.
Calcaneonavicular Coalition Resection
This resection is based on the technique of Cowell (1970), as described by Gonzalez and Kumar (1990). Under tourniquet hemostasis [A], make a 4-cm incision over the sinus tarsi. Avoid the sural nerve and peroneal tendons in the inferior aspect of the wound. Deepen the incision to expose the extensor digitorum brevis muscle [B]. Detach the origin of the muscle from the calcaneus and elevate it from the underlying coalition and reflect the muscle distally [C]. Identify the coalition with a Freer elevator. If the location or extent of coalition is uncertain, identify it with the aid of imaging. Resect the coalition with an osteotome as a single block [D]. The resected block should be rectangular, not triangular in shape. Remove any cartilagenous remnants of the coalition from both the calcaneal and navicular sides of the resection. Confirm the resection with an oblique radiograph of the foot [G]. Apply bone wax to cut bony surfaces and place a heavy absorbable suture in the origin of the extensor muscle. Thread this suture on a straight needle and pass the needle through the skin in the midportion of the longitudinal arch. Apply traction to the suture to pull the origin of the extensor muscle into the space previously occupied by the coalition. Secure the suture through a pad and button [E]. Tie the suture with sufficient tension to maintain the position of the interposition but not so tight as to cause skin necrosis. The muscle interposed between the navicular and calcaneus prevents recurrence of the coalition [F]. Immobilize in a short-leg cast without weight bearing for 3 weeks. The patient should avoid weight bearing for another 3 weeks while regaining range of motion, and return to full activities as comfort permits.
Figure
Talocalcaneal Coalition Resection
Based on Olney and Asher (1987), this is a description of the resection of middle facet coalitions. Identify the coalition by CT scan [H].
Figure
Figure
Consider mapping the extent of the coalition, as success is related to size. Make a 5–6 cm incision over the sustentaculum tali [I]. Reflect the abductor hallucis plantar-ward and divide the flexor retinaculum. Retract the flexor digitorum and the neurovascular bundle [J].
Figure
Between these structures, identify the coalition by elevating the periosteum and marking the anterior and posterior margins of the subtalar joint with Keith needles [K]. If uncertain about the location of the coalition, use imaging. Resect the coalition with a power burr, osteotomes, or rongeurs. Make the resection 5–7 mm wide. Be certain that the entire coalition is resected by visualizing joint cartilage around the resected area and demonstrating increased subtalar motion [L]. Place bone wax on the cut surfaces and harvest autogenous fat from the buttock crease. Place this graft into the defect [M]. Secure the graft with sutures under the overlying periosteal margins. Repair the flexor retinaculum, reattach the abductor origin, and close the skin in layers. Apply a short-leg non-weight-bearing cast. Remove the cast in the clinic in 3 weeks. Maintaion-weight-bearing for an additional 4–6 weeks while initiating range-of-motion exercises.
Figure
Forefoot Adductus
Metatarsus Adductus and Varus
Adductus of the forefoot is the most common foot deformity. It is characterized by a convexity to the lateral aspect of the foot [A] or a dynamic abduction of the great toe [B]. The deformities fall into four categories [C].
Figure A Metatarsus adductus A convexity of the lateral border of the foot (red line) is the most consistent feature of this deformity.
Figure B Great toe abduction This is a dynamic deformity that resolves with time
Figure C Types of forefoot adductus and varus deformities The differential diagnosis of metatarsus adductus should include the rigid, nonresolving form, and the skewfoot.
Metatarsus adductus is a common intrauterine positional deformity. Because it is associated with hip dysplasia in 2% of cases, a careful hip evaluation is essential. Metatarsus adductus is common, flexible, benign, and resolves spontaneously.
Metatarsus varus is an uncommon rigid deformity that often persists and requires cast correction. Metatarsus varus does not produce disability and does not cause bunions, but it does produce cosmetic and occasionally shoe-fitting problems.
Skewfoot is discussed on the next page.
Great toe abduction is a dynamic deformity due to overactivity of the great toe abductor. It is sometimes called a “searching toe.” The condition improves spontaneously. No treatment is required.
Management
Evaluate by performing a screening examination, test for stiffness, and consider the child’s age [D]. Manage metatarsus adductus by documentation and observation [E].
Figure D Steps in managing forefoot adductus
Figure E Imaging the adducted foot The infant’s foot shape is recorded on a copy machine. The printout from the copy machine is compared to a photograph.
Manage metatarsus varus by serial casting [A and B] or bracing.
Figure A Long-leg cast for metatarsus varus This treatment of metatarsus varus is most effective, as the flexed knee provides control of tibial rotation. Using the thigh portion of the cast as a point of fixation (yellow arrow), the foot is laterally rotated (green arrow) and abducted (red arrow) to achieve the most effective correction.
Figure B Cast treatment of metatarsus varus This child with a persisting stiff deformity was corrected using these longleg casts. The knee is flexed to about 30° to control rotation. The foot is abducted in the casts. The casts are changed every 2–3 weeks until correction is completed.
Long-leg bracing is useful in the toddler. Serial casting is most effective. The deformity yields much more rapidly when the cast is extended above the flexed knee.
The following technique is useful to about age 5 years. Apply a short-leg cast first. As the cast sets, mold the forefoot into abduction and the hindfoot in slight varus-inversion. Finally, while holding the short-leg cast ieutral rotation and with the knee flexed about 30°, extend the cast to include the thigh. This long-leg cast allows both walking and effective correction.
In the older child, it may be best to accept the deformity, as it does not cause disability. If operative correction is selected, correct by opening wedge cuneiform and closing wedge cuboid osteotomies. Avoid attempting correction by capsulotomy or metatarsal osteotomies, as early and late complications are frequent.
Skewfoot
Skewfoot, Z-foot, and serpentine foot are all terms given to a spectrum of complex deformities. This deformity includes hindfoot plantarflexion, midfoot abduction, and forefoot adduction [D].
Figure D Skewfoot deformity Note the forefoot adduction in the photograph, the plantar flexed talus (red arrow), and the Z alignment (white lines).
A tight heel-cord is usually present in symptomatic cases. Skewfeet are seen in children with myelodysplasia; they are sometimes familial but are usually isolated deformities. There is a spectrum of severity. Some practitioners describe overcorrected clubfeet as skewfeet. Idiopathic skewfeet may persist and cause disability in adolescence and adult life.
Manage idiopathic skewfeet in young children by initial serial casting, correcting the forefoot adductus while carefully avoiding any eversion stress on the hindfoot. Document the effect of growth on the deformity. Most will persist. Plan correction in late childhood with heel-cord lengthening and osteotomies. Lengthen the calcaneus and medial cuneiform by opening wedge osteotomies [C].
Figure C Sequence of correction of skewfoot Calcaneal and cuneiform osteotomies and a heel-cord lengthening were performed. Note the changes in talar alignment between the preoperative (red arrows) and postoperative (yellow arrows) radiographs.
Bunions
A bunion is a prominence of the head of the first metatarsal [A].
Figure A Measurements for bunion assessment These values are usually present in bunion deformity.
It is most common in girls. In children, it is usually due to metatarsus primus varus, a developmental deformity characterized by an increased intermetatarsal angle [B] that exceeds about 9° between the first two rays.
Figure B Moderate bunion deformities The bunion is a prominence over the head of the first metatarsal. The left bunion (arrow) is most prominent here, and both are relatively moderate. Usually no active treatment is required for bunions of this severity.
Over time, the medial cuneiform becomes more trapezoid in shape and the metatarsal phalangeal joint subluxated. Hallux valgus is a secondary deformity aggravated by wearing shoes, as the great toe must be positioned in valgus to fit within a shoe. The normal hallux valgus angle is <15°. The combination of primary and secondary deformities causes the typical adolescent bunion [C].
Figure C Metatar sus primus varus An increased intermetatarsal angle (between red lines) is present in meta tar sus primus varus. The hallux valgus is a secondary deformity.
Bunions are often familial [D] and may occur in children with neuromuscular disorders [E]. Other factors may include pronation of the forefoot, joint laxity, and pointed shoes. Bunions are uncommon in barefoot populations.
Figure D Familial bunions Both mother and daughter have bunions.
Figure E Severe hallux valgus in cerebral palsy Note the absence of metatarsus primus varus and any prominence of the metatarsal head.
Evaluation Look for evidence of joint laxity, heel-cord contracture, pes planus, or other skeletal defects. Is the toe rotated? Is there a family history of bunions? If considering operative corection, order AP and lateral standing radiographs. Measure the intermetatarsal angle. Measure the distal metatarsal articular angle (DMAA). This is normally less than 8°. Is the metatarsal–phalangeal joint subluxated? Is the cuneiform–metatarsal articulation oblique? Note the relative lengths of the first and second rays.
Management Attempt to delay operative correction until the end of growth to reduce the risk of recurrence.
Shoes Encourage girls to avoid shoes with pointed toes and high heels, as they aggravate the deformity and increase discomfort.
Splints For nighttime use, splints may be effective but are difficult to use because of the required duration of management [F].
Operative Correction Correct bunions when symptoms are unacceptable and nonsurgical measures fail. Be aware that bunion correction in the child is complicated by the effects of growth and varied pathology.
Bunion Correction
Preoperative planning
Measure the metatarsal phalangeal angle [A]. This is normally 5°–15°. More severe deformities may indicate the need for a double-level osteotomy. Measure the DMAA. This is normally less than 8° [B]. Note the congruity for the first metatarsal-phalangeal joint. If the joint is congruous with significant angular deviation, a distal osteotomy is indicated to preserve this congruity. Note the relative lengths of the first and second metatarsals [C]. Note the obliquity of the cuneiform-metatarsal joint [D]. Assess the intermetatarsal angle [E]. This is normally below 10°. Higher values describe metatarsus primus varus, typical of juvenile onset bunions. If the first metatarsal is short, plan opening wedge osteotomies to maintain or improve length. Base choice of procedure on the pathological anatomy. Plan full correction, but not overcorrection; correct intermetatarsal and metatarsal phalangeal alignment while preserving normal metatarsal length relationships and congruity of the metatarsal phalangeal joint. Be careful to avoid sagittal plane deformity that causes uneven metatarsal loading.
Figure Technique (Peterson and Newman)
This procedure is indicated for moderate or severe deformity with congruity of the metatarsal-phalangeal joint [F]. Expose the distal metatarsal and excise the bony prominence of the bunion. Remove a wedge of bone from the distal metaphysis. This wedge is usually about 20°. Correct any malrotation. Make a second medial incision to expose the proximal metatarsal metaphysis. Perform an osteotomy, leaving the lateral cortex intact. Wedge open the osteotomy and insert the graft taken from the first osteotomy site. Fix with a longitudinal 3/16-inch smooth K wire. Close the wounds and apply a compressive dressing. Before discharge, apply a short-leg non-weight-bearing cast. At 6 weeks, remove the pin and apply a weight-bearing cast for 5–6 additional weeks.
Technique (Weiner et al.)
This is a modification of the Mitchell bunionectomy [G]. This procedure is indicated if the metatarsus primus varus is mild. The modification includes the use of smooth pin fixation and a trapezoidal step-off to preserve length.
Figure
Other Techniques
Other procedures include simple excision of the bunion prominence, opening wedge osteotomy of the cuneiform to correct excessive obliquity, and wedge osteotomies of the base of the proximal phalanx for complex bunions seen in children with neuromuscular disorders [H].
Figure Complications
Ray shortening causes uneven load bearing under the metatarsal heads.
Elevation or depression of the metatarsal heads creates increased loading under the depressed head or transferred loading to adjacent metatarsal heads if elevated.
Recurrence is common when bunions are corrected in late childhood. Bony remodeling reestablishes original deformity.
Overcorrection may follow excessive soft tissue releases [I].
Subluxation of the metatarsal-phalangeal joint may lead to arthritis.
AVN of first metatarsal head may occur if distal metatarsal osteotomy is combined with a lateral soft tissue release of the first metatarsal phalgeal joint.
Figure
Dorsal Bunion
The uncommon dorsal bunion [A] is due to an elevation of the first metatarsal. This elevation is caused by an imbalance between a stronger tibialis anterior and peroneus longus muscle. It is most common in operatively treated clubfeet. This can be corrected by a plantar flexion osteotomy of the medial cuneiform or metatarsal and muscle-balancing procedures.
Figure A Dorsal bunion This child’s bunion developed between the ages of 14 (yellow arrow) and 18 years (white arrows). The deformity was corrected by a plantar closing wedge osteotomy (red arrow) and lateral transfer of the anterior tibialis and transfer of the flexor hallucis longus to the first metatarsal.
Bunionette
Bunionette (tailor’s bunion) is a painful bony prominence on the lateral side of the fifth metatarsal head, often associated with an inflamed thickened bursa and callus formation. These deformities are developmental and involve an increased metatarsalphalangeal angle of the fifth toe and an increased intermetatarsal angle between the fourth and fifth toes. Management often requires a metatarsal osteotomy for correction.
Hallux Rigidus
This is a degenerative arthritis of the first metatarsal phalangeal joint due to repetitive trauma, which causes stiffness, limited dorsiflexion, and pain. Manage by protecting the joint with a shoe stiffener. If severe and persistent, correct by a dorsiflexion osteotomy [B] to move the arc of motion into more extension, improving functional motion and reducing discomfort.
.
Figure B Dorsal osteotomy for hallux rigidus A dorsal closing wedge osteotomy moved the arc of motion of the metatarsal phalangeal joint into a position for improved function.
Short Metatarsal
Shortening of one or more metatarsals may be due to a developmental abnormality as part of a generalized disorder or from trauma, infection, or tumors. It may the result of a premature growth plate closure that is bilateral and familial. Severe shortening may cause metatarsalgia and a cosmetic disability. Rarely, the deformity is severe enough to justify operative correction. This can be done by a single-stage lengthening technique [C] or by gradual distraction histiogenesis
Figure C Technique of metatarsal lengthening This one-stage lengthening is described by Baek and Chung (1998).
Vertical Talus
The vertical talus is the most severe and serious pathologic flatfoot. It is a congenital deformity that produces not only flattening but an actual convexity of the sole of the foot [A].
Figure A Vertical talus Note the convexity to the sole of the foot (red arrow) and the near vertical orientation of the talus on the radiograph (white line) and the plantarflexion of the calcaneus (yellow line).
Etiology
Vertical talus is usually associated with other conditions such as myelodysplasia and arthrogryposis [B].
Figure B Vertical talus associations This deformity usually occurs as part of a generalized problem.
Evaluation
Differentiate the stiff vertical talus from the benign plantar-flexed talus due to hypermobility.
Clinical The foot is stiff, with contractures of both the dorsiflexors and plantarflexors. The head of the talus projects into the plantar aspect of the foot, producing the convexity of the sole. Look at the parents’ feet for evidence of a genetic etiology [C].
Figure C Vertical talus in an adult Note the prominences on the sole of the foot causing calluses and pain with walking.
Imaging The diagnosis is suggested by a lateral radiograph of the foot showing the vertical orientation of the talus [A]. The calcaneus is also plantarflexed. The vertical talus may be confused with flexible oblique talus, a different condition. Make the differentiation by studying lateral plantarflexion and dorsiflexion radiographs of the foot [D]. The vertical talus will show stiffness and fixation in contrast to the flexible oblique talus, which shows a freely mobile mid- and hindfoot. Note especially the mobility of the calcaneus. If the calcaneus is fixed in plantarflexion in both views of the foot, the diagnosis is vertical talus.
Figure D Plantarflexed talus These radiographs were taken with the ankle in plantarflexion (upper) and then in dorsiflexion (lower). Note that on the extension view, the talus (yellow line) aligns with the first ray. On the plantarflexion view, the calcaneus becomes dorsiflexed. This study shows that the foot is flexible and consistnt with a deformity due to hypermobility of the talus and not a stiff foot as seen in the vertical talus
Management
Correct during the first year.
Serial casts Apply serial casts to stretch out the skin and the anterior soft tissues.
Anterior release Through a transverse incision [E] release the contracted ankle capsule and the talonavicular and calcaneocuboid joints. Place a K wire to secure the reduced navicular.
Posterior release Through a second transverse incision, lengthen the heel-cord and release the ankle capsule. Dorsiflex the foot to neutral. Immobilize in a long-leg cast.
Severe deformity In a more severe deformity in the untreated older child or for recurrent deformity, it may be necessary to resect the navicular and perform a subtalar fusion.
Figure E Operative correction The foot before the procedure with a plantarflexed navicular (1). An anterior release reduces the talus (2). A posterior release allows the foot to be dorsiflexed to a neutral position (3).
