The Foot

The Foot

Vincent S. Mosca


The assessment and management of foot deformities and malformations in children and adolescents are based on principles, not techniques, due to the complexity and variety of the pathologic conditions and the complexity of the foot itself. An orthopaedist managing these conditions must have

  • An appreciation of the age-related physiologic variations in the shape of the foot

  • An understanding of the natural history of each variation and deformity

  • An appreciation of the effect of a chosen intervention on growth and development of the foot as well as the effect of growth and development on a chosen intervention

  • A thorough and working knowledge of the most unique “joint” in the human body, the subtalar joint complex, which is a combination of the talocalcaneal (subtalar) joint, plus the talonavicular and calcaneocuboid joints (transtarsal or Chopart joints)

  • The ability to obtain, and the commitment to evaluate, only weight-bearing or simulated weight-bearing radiographs

  • A dedication to preserving joint motion by utilizing softtissue releases and osteotomies instead of arthrodeses

  • A complete understanding of the phrase: “The foot is not a joint” (1)

The first principle to embrace is that “the foot is not a joint” (1), although it is often discussed as if it were another joint in the body, such as the hip, knee, shoulder, or elbow. It is a unique part of the musculoskeletal system comprised of 26 bones with countless articulations. It is extremely unusual for only one portion of the foot or only one joint of the foot or ankle to be congenitally or developmentally deformed. Its many joints are usually deformed or malaligned in rotationally opposite directions, “as if the foot was wrung out like a towel” (1). As examples, note that there is inversion of the subtalar joint and pronation of the forefoot on the hindfoot in a cavus foot and eversion of the subtalar joint and supination of the forefoot on the hindfoot in a flatfoot. And one cannot ignore the adjacent ankle joint as a potential site of additional deformity. The orthopaedist must identify all deformities preoperatively, if possible, and have a treatment plan that addresses each one individually and, usually, concurrently. There is no justification for creating a compensating deformity or incompletely correcting a deformity in order to avoid an additional procedure, particularly one that can usually be carried out during the same operative session.

The child’s foot often looks different than that of an adult. In fact, there is so much variation in shape that the foot of one child can look quite different than that of another child. Agerelated physiologic variations of the child’s foot, such as flexible metatarsus adductus, positional calcaneovalgus, and flexible flatfoot, must be identified as normal, but not average, shapes in order to avoid inappropriate and potentially harmful interventions. This feature of physiologic variation is also seen in the long bones of the child’s lower extremities in conditions such as genu varum, genu valgum, femoral anteversion, and tibial torsion (2, 3). There are age-related average shapes and normal ranges of shapes. The natural history is for spontaneous change
from the normal shapes of the child to those of the adult through normal growth and development. Externally applied forces cannot modify these physiologic shape variations of the long bones. And the long-term health consequences of persistent physiologic variations of the long bones have yet to be proven.

An understanding of the natural history of each foot shape variation and deformity is of paramount importance. Eightyfive to ninety-five percent of feet with metatarsus adductus correct spontaneously with little if any long-term disability even with mild to moderate residual deformity (4, 5 and 6). Essentially all calcaneovalgus “deformities” correct spontaneously (7). Flexible flatfoot is almost ubiquitous at birth and is present in approximately 23% of adults, most of whom are asymptomatic (8). The height of the longitudinal arch increases spontaneously during the first decade of life in most children (9, 10). There is a wide range of normal arch heights at all ages (particularly in young children) (9, 10). Most feet with accessory naviculars (11, 12) and approximately 75% of feet with tarsal coalitions (13) are asymptomatic and do not need treatment, whereas one can expect the onset of symptoms from the rest to develop in late childhood or early adolescence. Conversely, all congenital clubfoot and congenital vertical talus deformities persist and cause disability unless treated.

The natural history of an intervention must also be fully appreciated and considered in relation to the natural history of the deformity or condition. Unfortunately, although there are few good natural history studies on deformities and variations of the child’s foot, there are fewer good long-term follow-up studies on operative intervention for these conditions. It seems most reasonable that the default should logically go to the natural history of the condition.

Unique challenges facing those who manage foot deformities in children are the consideration of the effect of a chosen intervention on growth and development of the foot as well as the effect of growth and development on a chosen intervention. Early reconstruction of foot deformities in children normalizes the stresses on the bones and joints to allow more normal development. Delay results in the development or persistence of abnormalities in the shapes of the bones and joints that makes reconstruction more difficult. Furthermore, procedures that affect or potentially affect growth in a positive or in an adverse way must be used judiciously. Conversely, one must consider how the early positive result of an intervention may change as the child grows. Cavus foot deformity is most commonly a manifestation of muscle imbalance from an underlying neuromuscular disorder. In some cases, the disorder is static (cerebral palsy) or can be stabilized but may recur (tethered cord in myelomeningocele). In others, the disorder is progressive and the rate and extent of neuromuscular deterioration may not be predictable (Charcot-Marie-Tooth [CMT]). It is difficult to establish precise muscle balance in any cavus foot, and it is well known that growth as well as progressive neurologic deterioration can undo an excellent early result of intervention. The child and family must be made aware that there are no panaceas and more surgery may be needed in the future. The surgeon must also remember this admonition, avoid burning bridges, and keep reasonable options available for future surgeries.

Although most congenital clubfeet and many congenital vertical talus deformities respond to nonsurgical or minimally invasive management, some undergo operative releases in the first year of life when the foot is 8 to 9 cm in length. The hope is that the correction of these deformities, located at the foundation of the human body, will be maintained through 14 to 16 years of growth and a doubling to tripling in the length of the foot. Problems, including recurrence, overcorrection, pain, and stiffness, as well as plans for their management, should be anticipated.

There is no other “joint” in the human body with the unique anatomy and three-dimensional motion of the subtalar joint complex. This complex consists of two components, the talocalcaneal or subtalar joint, plus the talonavicular and calcaneocuboid or transtarsal joints. These four bones, several important ligaments, and multiple joint capsules function together as a unit. Terms that apply to sagittal and coronal plane alignment and motions, such as varus, valgus, abduction, adduction, flexion, extension, supination, and pronation, do not necessarily apply to the subtalar complex because its axis of motion is in neither the sagittal nor coronal plane. Inversion and eversion are terms that, in my opinion, define the motions of this complex, but they need to be better defined and understood by all that use them.

Almost 200 years ago, Scarpa (14) saw similarities between the subtalar joint complex and the hip joint. He compared the femoral head to the talar head and the pelvic acetabulum to his so-called acetabulum pedis (AP). The latter is a cup-like structure made up of the navicular, the spring ligament, and the anterior end of the calcaneus and its facets. Although it is not a perfect comparison, I believe that the two anatomic areas share certain features that make the comparison both valid and worthwhile. The hip, a pure ball-and-socket joint with a central rotation point, is comprised of two bones, one intra-articular ligament, and a joint capsule. The subtalar joint is not an independent ball-and-socket joint, though the combined motions of the subtalar joint and the immediately adjacent ankle joint give the impression of a ball-and-socket joint. In fact, the subtalar joint has an axis of motion that is in an oblique plane that is not frontal, sagittal, or coronal, thus creating motions that are best described with the unique terms inversion and eversion. The stable structure in the hip joint is the acetabulum (the socket), while the stable structure in the subtalar joint complex is the talus (the ball). Inversion is comprised of plantar flexion, supination, and internal rotation of the AP around the head of the talus (15). Eversion is a combination of dorsiflexion, pronation, and external rotation of the AP around the talar head. The static position of inversion of the subtalar joint is called hindfoot varus and is found in cavovarus feet and clubfeet. Hindfoot valgus is the static position of the everted subtalar joint and is seen in flatfeet and skewfeet. It is essential that all who manage foot deformities have a thorough and working knowledge of this most unique joint complex.

It is important to evaluate deformity both clinically and radiographically with the foot in the weight-bearing position. That is the baseline against which the corrected foot will be judged. A flexible flatfoot appears to have an arch, and a normal foot may appear to have a cavus or clubfoot deformity when dangling in the air.

Deformities of the child’s foot should be corrected by means of soft-tissue releases to align the joints and osteotomies to correct residual deformities. Arthrodesis should be reserved for the older child, adolescent, or adult with established degenerative arthrosis of a joint or with such severe deformity that correction cannot be achieved with soft-tissue releases and osteotomies. Long-term follow-up studies have demonstrated that arthrodesis of even the small joints of the child’s foot should be avoided because of the risk of developing degenerative arthrosis at the adjacent unfused joints (16, 17 and 18). Arthrodesis of the subtalar joint, particularly triple arthrodesis, leads to stress transfer to the ankle (19, 20, 21, 22, 23, 24, 25, 26 and 27). The development of degenerative arthrosis at that important joint is a potentially disastrous outcome.

Correction of foot deformities must be combined with balancing of muscle forces in order to help prevent recurrence. Balancing muscle forces in a mobile foot is much more challenging than in one that has undergone arthrodesis. This challenge must be accepted.

There is a great need for more natural history studies on deformities and variations in the shape of the child’s foot, as well as long-term follow-up studies on the interventions used to treat these conditions. The message must be to exhibit caution with interventions until it is clear that the treatment is not potentially worse than the condition.

All of these principles apply to the congenital and developmental deformities and other conditions that will now be presented individually and alphabetically, not in order of importance, incidence, or complexity.

FIGURE 29-1. Accessory navicular. A: Type I. B: Type II. C: Type III. (From the private collection of Vincent S. Mosca, MD.)


Accessory Navicular


The accessory tarsal navicular is the most common accessory bone in the foot, occurring in between 4% and 14% of the population (8, 11, 28). It is frequently bilateral and occurs more commonly in females. Geist (28) recognized a higher incidence of accessory naviculars in young patients evaluated radiologically than in cadaver studies.


McKusick (29) believed that the accessory navicular was inherited as an autosomal dominant trait. Geist (28) reported that there are three types: (a) a sesamoid bone within the substance of the posterior tibial tendon, (b) a separate bone with a true articulation (synovial joint) with the navicular, and (c) an ossicle with a synchondrosis to the main navicular.

Clinical Features.

Pain, tenderness, and callus formation may develop over the firm prominence distal to the talar head on the plantar-medial aspect of the midfoot starting in adolescence. There may be a coexistent flexible flatfoot (30, 31, 32 and 33), but there is not conclusive evidence that there is a cause-and-effect relationship between the two conditions as was historically believed (12). The prominence of an accessory navicular is in close proximity to the head of the talus, which is prominent in a flexible flatfoot. Inverting and everting the subtalar joint with one’s thumb on the prominence is helpful for differentiating the two. If the prominence moves, it is an accessory navicular. If it remains stationary, it is the head of the talus.

Individuals with an accessory navicular may present for evaluation because of the prominence, but more commonly they present because of pain at the site. The typical patient is an active adolescent girl with a history of minor trauma who presents with pain, callus formation, tenderness, redness, and, occasionally, swelling over the bony prominence. Maximum tenderness is elicited by upward pressure under the prominence. Because of the frequency of this anatomic variation in the general population, one must be careful not to assume that a radiographic finding of an accessory navicular is the cause of the foot pain without thorough evaluation (34).

Radiographic Features.

An accessory navicular can usually be seen on standing AP and lateral radiographs, but a lateral oblique view (opposite to the standard medial oblique view that is generally obtained) may be necessary for identification. There are three types of accessory naviculars (35) (Fig. 29-1). Type I is a rarely symptomatic, small pea-sized sesamoid bone located in the center of the most distal portion of the tibialis posterior tendon. Type II, the most frequently symptomatic type, is a bullet-shaped ossicle joined to the tuberosity of the navicular by a syndesmosis or synchondrosis. Type III is a large, horn-shaped navicular that probably results from fusion of a type II with the body of the navicular over time.


There is proliferating vascular mesenchymal tissue, cartilage proliferation, and osteoblastic and osteoclastic activity in the tissue between the ossicle and the main body of the navicular in painful type II accessory naviculars (35). These histologic findings are consistent with healing microfractures, substantiating the opinion that pain at this site is related to chronic, repetitive stress. There are at least two other possible sources of pain. One is pain from pressure on the skin overlying the bony prominence. The other is tendinitis in the tibialis posterior, the tendon in which the ossicle resides. Any or all of these sources may exist in the same painful foot.

Natural History.

Accessory naviculars are for the most part asymptomatic. If symptoms do occur, a period of protection from stress and injury generally returns the patient to the asymptomatic state (32).

Cavus Foot Deformity


Cavus is a manifestation of a neuromuscular disorder with muscle imbalance, until proven otherwise. At least two-thirds of patients who seek treatment for a painful high arch will have an underlying neurologic problem, and over half of these will have Charcot-Marie-Tooth (CMT) disease (43, 44). There are many other causes of cavus foot deformity. It is helpful to consider those that cause unilateral versus bilateral deformity when developing a differential diagnosis for your patient (Table 29-1). The number of cases termed “idiopathic” cavus foot continues to decrease as diagnostic methods improve.

Calcaneocavus deformity is seen almost exclusively in children with myelomeningocele and poliomyelitis due to a specific pattern of muscle imbalance seen in many of these children.


The incidence of cavus is variable and is related to the prevalence of neuromuscular disorders at any point in time.

TABLE 29-1 Causes of Cavus Foot Deformity


Charcot-Marie-Tooth disease

Friedreich ataxia

Dejerine-Sottas interstitial hypertrophic neuritis


Roussy-Lévy syndrome

Spinal muscular atrophy



Spinal cord tumor


Spinal dysraphism (tethered cord)

Muscular dystrophy

Cerebral palsy—paraparesis or quadriparesis (although usually planus deformities)

Familial (consider Charcot-Marie-Tooth disease)

Clubfoot/recurrent clubfoot

Idiopathic cause (diagnosis of exclusion)


Traumatic injury of a peripheral nerve or spinal root nerve




Spinal cord tumor


Spinal dysraphism (tethered cord)

Tendon laceration

Overlengthened Achilles tendon

Cerebral palsy—hemiparesis

Clubfoot/recurrent clubfoot

Compartment syndrome of the leg

Severe burn of the leg

Crush injury of the leg

Clinical Features.

The clinical features depend on the underlying etiology. Some of the underlying neurologic abnormalities are known at the time of presentation and some are not, some are treatable and some are not, and some are static and some are progressive. The resultant muscle imbalance, however, always leads to progressive foot deformity. The clinical manifestations are instability of gait with frequent falling, a feeling that the ankle is “giving out,” and a history of repeated ankle sprains. Instability may be secondary to muscle weakness, sensory loss, or deformity (45). Painful callosities develop under the metatarsal heads, lateral to the base of the fifth metatarsal, and over the dorsum of the proximal interphalangeal (PIP) joints of the progressively clawing toes. In the calcaneocavus foot, callus formation occurs primarily under the calcaneus; however, exaggerated callus formation under all metatarsal heads can occasionally be seen.

A history of progressive change in foot shape and function must be ascertained, even in situations of a known underlying neurologic abnormality. A sudden increase in cavus deformity in a child with myelomeningocele or lipomeningocele could represent evidence of a tethered spinal cord.

Medical, birth, and developmental histories, as well as a review of systems, are mandatory in searching for underlying causes of cavus foot. A family history of cavus foot deformity should be investigated as an aid to diagnosis. Charcot-Marie-Tooth disease, an autosomal dominant disorder with variable phenotypic expression, is one of the most common causes of cavus foot deformity (43). Examination of other family members can often be revealing, because a subtle cavus foot may be present.

A detailed neurologic examination, including motor, sensory, and reflex testing, of the upper and lower extremities is mandatory. The spine must be examined for deformity, midline defects, hairy patches, dimples, or other evidence of spinal dysraphism. The Trendelenburg test should be performed.

The foot is examined with the child seated, standing, and walking. Cavovarus is the most common specific form of cavus foot deformity and can be caused by many different underlying neurologic disorders. The longitudinal arch is excessively elevated along the medial border of a weight-bearing foot (Fig. 29-2). The lateral border of the foot is convex and plantigrade, and the base of the fifth metatarsal is prominent and often callused. The hindfoot is in varus alignment. Atrophy of the intrinsic muscles is apparent. There may or may not be contracture of the gastrocnemius or the triceps surae. In many cases, as in most cavovarus deformities secondary to CMT, the forefoot equinus gives the false impression of a hindfoot equinus (46). The thigh-foot angle is usually neutral, despite the internal rotation deformity in the subtalar joint. The reason is that external tibial torsion is always associated with a developmental cavovarus deformity. The two rotational deformities are in opposite directions and cancel each other out. It is important to discuss this with the patient and family, because the external tibial torsion will become obvious after correction of the foot deformity.

Despite differences in the patterns of muscle imbalance that create cavovarus, the pattern of deformity development is fairly constant (47, 48 and 49). The first metatarsal becomes plantar-flexed, giving the appearance of pronation of the forefoot on the hindfoot. The deformity is flexible at first but becomes rigid with time. The plantar fascia and the other
plantar soft tissues become contracted. The incompletely ossified bones change shape due to excessive compression on their plantar aspects (Hueter-Volkmann law). The normal tripod structure of the foot becomes unbalanced. Bearing weight on the plantar-flexed first metatarsal causes the forefoot to supinate in relation to the tibia, thereby allowing the fifth metatarsal head to touch the ground. Because the forefoot is rigidly pronated in relation to the hindfoot, the subtalar joint is thereby driven into inversion, or varus (48) (Fig. 29-3). This flexible hindfoot varus deformity eventually becomes rigid as the plantar-medial soft tissues of the subtalar joint contract. The cavovarus foot, therefore, has two major rotational deformities in opposite directions from each other: pronation of the forefoot and supination (varus and inversion are other descriptive terms) of the hindfoot. It appears as if the foot is wrung out (1). Determination of the flexibility or rigidity of each deformity is important when planning an operation. Flexible deformities are treated with tendon transfers, and inflexible deformities are treated with soft-tissue releases, osteotomies, and, occasionally, arthrodeses. Coleman and Chestnut (50) devised the block test to help evaluate the flexibility of the hindfoot (Fig. 29-4). The patient stands with a block of wood under the lateral border of the foot to recreate the tripod while allowing the first metatarsal to plantar-flex. A flexible varus deformity of the hindfoot will correct to valgus alignment. One that is already contracted and rigid will not. In the first situation, surgery for deformity correction is confined to the forefoot. In the latter case, forefoot and hindfoot procedures are needed.

FIGURE 29-2. Cavovarus deformity in this individual with Charcot-Marie-Tooth disease. A: The arch is elevated only along the medial border of the foot. B: Varus and adduction can be appreciated. (From the private collection of Vincent S. Mosca, MD.)

FIGURE 29-3. The tripod effect. The hindfoot must assume a varus position when weight bearing if the first metatarsal is fixed in plantar flexion (9). Initial contact of plantar-flexed first metatarsal (4). Fifth metatarsal makes contact through supination of the forefoot (arrow), which also drives the hindfoot into varus. (From Paulos L, Coleman SS, Samuelson KM. Pes cavovarus. Review of a surgical approach using selective soft-tissue procedures. J Bone Joint Surg Am 1980;62: 942-953, with permission.)

FIGURE 29-4. The Coleman block test for determination of hindfoot flexibility. The flexible varus deformity of the hindfoot (A) corrects to valgus (B) when the plantar-flexed first metatarsal is allowed to drop down off the edge of the block of wood as in this example. Failure to correct to valgus indicates the need for surgical correction of the hindfoot deformity, in addition to the procedures on the forefoot. (From Coleman SS, Chesnut WJ. A simple test for hindfoot flexibility in the cavovarus foot. Clin Orthop 1977;123:60-62, with permission.)

The arch is elevated across the entire midfoot in the calcaneocavus deformity (Fig. 29-5). The calcaneus is dorsiflexed and vertically aligned, giving it the appearance of posterior truncation. The plantar heel pad is thickly callused from excessive pressure over a small surface area.

Radiologic Features.

Standing AP and lateral radiographs of the foot are indicated on initial evaluation. According to Meary (51), there is normally a straight-line relationship between the axis of the talus and that of the first metatarsal on the lateral view. In essentially all cavovarus foot deformities, those two lines intersect within the body of the medial cuneiform, indicating that site as the center of rotation of angulation (CORA) (52), with the apex of the angulation directed dorsally (Fig. 29-6A). A calcaneal pitch (CP) >30 degrees is also indicative of a cavus deformity. The hyperdorsiflexion of the calcaneus seen on the radiographs confirms that the apparent clinical equinus deformity is, in fact, forefoot equinus, that is, cavus (Fig. 29-6). Inversion or varus deformity of the hindfoot is indicated on the AP radiograph by parallelism between the talus and calcaneus and by adduction at the talonavicular joint. It is also manifest as the intersection of the axis of the talus and that of the first metatarsal (the CORA) (52) at the talonavicular joint or within the head of the talus (Fig. 29-7A).

FIGURE 29-5. Calcaneocavus deformity in a child with myelomeningocele. A: Transtarsal cavus with thick callosities under the calcaneus and the metatarsal heads. B: Radiograph of the calcaneocavus “pistol-grip” deformity. (From the private collection of Vincent S. Mosca, MD.)

I obtain a standing AP Coleman-type block test radiograph to document the flexibility of the hindfoot. I find that the clinical and radiographic block tests are more reliable if a Plexiglas block is placed under the lateral metatarsal heads alone with the heel on the X-ray plate/platform (Fig. 29-7).

An AP pelvis radiograph is indicated because of the known association of Charcot-Marie-Tooth disease with progressive hip subluxation and dysplasia. Standing AP and lateral radiographs of the spine are indicated if any physical examination findings suggest spinal dysraphism, spine tumor, or diastematomyelia.

FIGURE 29-6. Lateral radiograph of a cavovarus foot deformity before (A) and after (B) a medial cuneiform plantar-based opening-wedge osteotomy. The axis lines of the first metatarsal and the talus cross each other in the body of the medial cuneiform, indicating that as the site of deformity, that is, the CORA. (From VS. Ankle and foot: pediatric aspects. In: Beaty J, ed. Orthopaedic Knowledge Update 6. Rosemont, IL: American Academy of Orthopaedic Surgeons, 1999:583, with permission.)

Other Diagnostic Studies.

Consultation by a pediatric neurologist is in the best interest of the child. Although most cavus foot deformities are caused by CMT, a progressive genetically determined neuromuscular disorder for which there is no known treatment, it is vital to identify and correct a treatable neurologic disorder before treating the foot. An MRI of the spine along
with DNA blood tests for CMT, electromyogram with nerve conduction studies, and muscle biopsy may be indicated.

FIGURE 29-7. Standing block test radiograph with Plexiglas under the lateral metatarsal heads. The flexibility or rigidity of the subtalar joint can be documented by assessing alignment at the talonavicular joint using the talus-first metatarsal angle. A: Without block. B: With block, the hindfoot varus is corrected as indicated by abduction of the 1st metatarsal axis in relation to the axis of the talus. (From the private collection of Vincent S. Mosca, MD.)


Several patterns of muscle imbalance can create the cavovarus deformity. A common pattern is that seen in CMT (47, 49). Denervation begins in the intrinsic muscles of the foot (49). The weakened lumbricals allow the long toe extensors to extend the metatarsophalangeal joints and the long toe flexors to flex the interphalangeal joints, thereby creating claw toe deformities. These same forces create elevation of the longitudinal arch during gait by the windlass effect of the plantar fascia (53) (Fig. 29-8). The intrinsic muscles undergo atrophy, fibrosis, and shortening that lead to secondary contracture of the plantar fascia. This creates a bowstring between the anterior and posterior pillars of the arch that draws them closer and produces equinus of the forefoot on the hindfoot. The tibialis anterior, a dorsiflexor of the first metatarsal, becomes weak, while the peroneus longus, a plantar flexor of the first metatarsal, remains relatively strong (42). The extensor hallucis longus is involuntarily recruited in an attempt to provide additional dorsiflexion strength along the medial column of the foot, but it creates a paradoxical effect of plantar flexion due to the windlass effect of the plantar fascia. The first metatarsal starts to plantar-flex, and, with time, this creates more contracture and shortening along the plantar-medial than the plantar-lateral border
of the foot. The forefoot becomes rigidly pronated in relation to the hindfoot. The tripod effect (48) accounts for the varus position that the hindfoot must assume during weight bearing due to the fixed pronation of the forefoot. Also contributing to the varus deformity of the hindfoot is the muscle imbalance between the tibialis posterior, an invertor of the subtalar joint, that remains strong and the peroneus brevis, an evertor of the subtalar joint, that becomes weak (47). The subtalar joint eventually becomes rigidly deformed in varus because of contracture of the plantar-medial soft tissues, including those of the subtalar joint complex. Although the triceps surae does not become contracted in CMT, it does in some of the other diseases that cause cavus.

FIGURE 29-8. The windlass effect of the plantar fascia. The drum, or pulley, of the windlass is the head of the metatarsal. The handle is the proximal phalanx. The cable that is wound under the drum, through its attachment to the plantar pad of the metatarsophalangeal joint, is the plantar fascia. Dorsiflexion of the toes creates elevation of the longitudinal arch. (From Hicks JH. The mechanics of the foot. II. The plantar aponeurosis and the arch. J Anat 1954;88:25-30, with permission.)

The calcaneocavus deformity develops when there is little or no strength in the triceps surae, but strength exists in the muscles that plantar-flex the forefoot and toes. The tibialis posterior, peroneus brevis and longus, flexor hallucis longus, and flexor digitorum longus (FDL) bypass the calcaneus and plantar-flex the entire forefoot on the hindfoot without creating varus. Contracture of the plantar fascia, elongation of the paralyzed triceps surae, and preservation of functional strength in the tibialis anterior contribute to the dorsiflexion posture of the calcaneus.

Natural History.

Muscle imbalance from both static and progressive neuromuscular disorders leads to progressive increase in the severity and stiffness of cavus foot deformities, though the rate of progression varies considerably.

Cleft Foot (Ectrodactyly)


The cleft foot is a rare condition with an overall occurrence rate of 1 per 90,000 live births (84). In the most common form of this condition, the malformation is bilateral, usually associated with cleft hands, and has an autosomal dominant pattern of inheritance with incomplete penetrance (84, 85 and 86) (Fig. 29-24). In the less common form, the cleft foot is unilateral without associated hand malformation, and there is no evidence of familial inheritance. The incidence of this form is 1 in 150,000 (84). Approximately 10% of cleft feet have no family history (87). Boys are affected more frequently than girls.


The apical ectodermal ridge (AER) induces normal development of limb buds by interaction with the underlying mesenchyme (88). A defect of the AER, by genetic or toxic influences, could induce osseous syndactyly by deficient differentiation, polydactyly by excessive differentiation, or a central defect by another mechanism. Watson and Bonde (89) proposed that cleft formation was the result of selective damage to a specific region in the AER localized to the second or third ray, which is the typical area for deficiency in a cleft foot. They further proposed that the extent and duration of damage to the AER would relate to both the width and depth of the defect.

FIGURE 29-25. Cleft foot classification according to Blauth and Borisch. (From Blauth W, Borisch NC. Cleft feet. Proposals for a new classification based on roentgenographic morphology. Clin Orthop 1990; 258:41-48, with permission.)

Clinical Features.

Variations of the malformation known as cleft foot range from a mere deepening of the interdigital commissure to the typical central ray deficiency to the monodactylous foot (90). The width of the foot at the metatarsal heads is excessive in comparison with the hindfoot, particularly in those feet with a greater deficiency of rays. And in these feet with greater ray deficiencies, there are often exaggerated hallux valgus and fifth toe varus orientations (Fig. 29-24). Anomalies associated with cleft foot include cleft hand, cleft lip and palate, deafness, urinary tract abnormalities, triphalangeal thumb, and tibial hemimelia.

Radiographic Features.

Blauth and Borisch (90) have classified cleft foot into six groups based on the number of metatarsal bones (Fig. 29-25). They identified two additional forms: a polydactylous type and a diastatic type. The latter is characterized by monodactyly with lower leg diastasis or tibial aplasia or both. Other variations of morphology in this condition, such as crossbones and synostoses, are also described by the authors (Fig. 29-26). In addition to radiographs of the foot, renal ultrasonography is indicated to rule out renal abnormalities, as they are frequently associated with cleft foot.


The pathoanatomy is one of variable degrees of failure of formation with occasional duplication and malorientation of bones. Synostoses may be seen at the margins of the cleft and in the tarsals (90). Often a hallux valgus deformity results from the pull of conjoined flexor and extensor tendons, resulting in an abduction force.

Natural History.

Many patients with cleft foot function well and can wear regular shoes without pain or compromise of function, while others do well with accommodative shoe wear. For such individuals, no surgical treatment is required.
However, in many cases of cleft foot, there is a marked increase in the width of the forefoot (Fig. 29-24), making it difficult or impossible to find shoes that fit comfortably. Painful callosities develop over the medial and lateral metatarsal heads.

FIGURE 29-26. A: This patient had a mild cleft foot with a transverse metatarsal bridging the cleft and widening the foot. B: With repair of the cleft and removal of the transverse metatarsal, a healthy foot resulted. (From the private collection of Vincent S. Mosca, MD.)

Clubfoot (Congenital Talipes Equinovarus)


The incidence of clubfoot is 0.93 to 1.5 per 1000 live births in Caucasians (93, 94 and 95), 0.6 per 1000 in Asians, 0.9 per 1000 births in Western Australia (96), and 6.8 per 1000 in Hawaiians, Polynesians, and Maorians (97). Boys are affected twice as often as girls are, and bilateral involvement is seen in approximately 50% of cases (93, 94, 98).

FIGURE 29-27. Preoperative (A) and postoperative (B) radiographs of symptomatic cleft foot treated with osteotomies. (From the private collection of Vincent S. Mosca, MD.)

Wynne-Davies (94, 95) determined that the occurrence rate is 17 times higher than the normal population for first-degree relatives, is 6 times higher for second-degree relatives, and approximates the normal population risk for third-degree relatives. Unaffected parents with an affected son have a 1 in 40 (2.5%) chance of having another son with the disorder, while the risk to a subsequent daughter is very low. Unaffected parents with an affected daughter have a 1 in 16 (6.5%) chance of having a son with clubfoot and a 1 in 40 (2.5%) chance of seeing the deformity in another daughter. The chances are about one in four that a subsequent child will have a clubfoot if a parent and child have the disorder. There is a 32.5% rate of concordance in monozygotic twins and a 2.9% rate in heterozygotic twins.

FIGURE 29-28. Clubfoot deformity is associated with forefoot supination, deep medial creases, and equinovarus of the hindfoot. (From the private collection of Vincent S. Mosca, MD.)


Clubfoot is probably etiologically heterogeneous. Genetics clearly plays a part. The observations of Wynne-Davies (94, 95) on occurrence rates led her to propose that clubfoot is inherited as a dominant gene with reduced penetrance or multifactorial inheritance. Cowell and Wein (98) concluded that the data could be accounted for using a multifactorial inheritance model. Complex segregation analysis using a regressive
logistic model was used by Rebbeck et al. (99) to conclude that the probability of having clubfoot was explained by the mendelian segregation of a single gene with two alleles plus the effects of some other factors that are yet to be elucidated.

TABLE 29-2 Syndromes with Which Clubfoot Is Commonly Associated


Constriction bands (Streeter dysplasia)

Prune belly

Tibial hemimelia

Möbius syndrome

Freeman-Sheldon syndrome (whistling face) (autosomal dominant)

Diastrophic dwarfism (autosomal recessive)

Larsen syndrome (autosomal recessive)

Opitz syndrome (autosomal recessive)

Pierre Robin syndrome (X-linked recessive)

The proximate cause of the genetic message is debated with fervor, based on a small number of personal observations by a large number of investigators. There may be validity in many of the discordant studies if, in fact, clubfoot is a clinical manifestation that can result from multiple causes and mechanisms. Among the proposed theories are in utero molding (100), primary muscle lesion (101), primary bone deformity (germ plasm defect) (102), primary vascular lesion (103), intrauterine enteroviral infection (104), developmental arrest (105), primary nerve lesion (106), abnormal tendon insertion, retracting fibrosis (107), and abnormal histology (108).

Environmental factors may modulate the genetic expression of the disorder. Skelly et al. (109) demonstrated an increased risk of clubfoot for mothers who smoked during pregnancy. The data were particularly convincing because the risk increased with increased numbers of cigarettes smoked per day. Honein et al. (110) also identified maternal smoking as a significant etiologic factor. The joint effect of family history of clubfoot and maternal smoking during pregnancy was more than additive, suggesting a genetic-environmental interaction.

Other associations with clubfoot have been identified, such as increased ligament laxity in families of children with clubfoot (111) and increased internal hip rotation in a limb with a clubfoot (112). The implications of these findings are yet unknown.

Clinical Features.

The deformities of the clubfoot fit the acronym CAVE. They are cavus (plantar flexion of the forefoot on the hindfoot), adductus of the forefoot on the midfoot, varus (or inversion) of the subtalar joint complex, and equinus of the ankle. These deformities are not passively correctable. The severity of the deformities and associated findings vary from foot to foot, even in bilateral cases. There is a single (occasionally double) posterior ankle skin crease (Fig. 29-29). The calcaneus is difficult to palpate within the fatty heel pad, resulting on the so-called empty heel pad sign. A deep transverse skin crease crosses the midfoot and extends under the longitudinal arch. Assessment of tibial torsion in a newborn with a clubfoot is unreliable. The head of the talus can be seen and palpated on the dorsolateral aspect of the midfoot/hindfoot just anterior to the ankle joint. This is due to excessive inversion of the subtalar joint complex around the talus. An examiner’s thumb can be placed on the dorsolateral aspect of the head of the talus as a solid fulcrum around which one can attempt to evert the subtalar joint. In an idiopathic clubfoot, the navicular will not fully align with the head of the talus and displace the examiner’s thumb.

FIGURE 29-29. Clubfoot (left) with single heel crease and healthy foot (right) with multiple heel creases. (From the private collection of Vincent S. Mosca, MD.)

The foot and calf are smaller than the contralateral side. Little and Aiona (113) noted a leg length discrepancy of >0.5 cm in 18% of children with unilateral clubfoot and 4% with bilateral deformities. In those with unilateral deformity and discrepancy, the tibia is short in 89% and the femur is short in 43%. Spiegel and Loder (114) found a leg length discrepancy of >0.5 cm in 32 of 47 patients with a unilateral clubfoot, a frequency that is perhaps more accurate.

In 2009, Howlett and Mosca (112) reported increased internal hip rotation in limbs with clubfoot deformity. Because this was a clinical study, it was not possible to determine if this finding was due to femoral anteversion, acetabular anteversion, or both. There was at least 10 degrees greater internal hip rotation, and 10 degrees less external rotation, ipsilateral to a unilateral clubfoot compared to the nonaffected limb in >80% of cases. Children with bilateral clubfoot deformities had at least 10 degrees greater internal hip rotation than that reported for age-matched normal controls (115). There might be genetic implications for this finding that are yet to be elucidated, but the clinical implications are significant. An in-toeing gait in a child with a clubfoot could represent persistence or recurrence of the clubfoot deformity, but, if the in-toeing is due to increased internal hip rotation, it must be identified and differentiated before considering inappropriate treatment of a well-corrected clubfoot.

A complete physical examination of the child is indicated to rule out a neurogenic or syndromic etiology for the deformity (Table 29-2). Muscle testing and sensory examination should be part of the initial examination in all patients, as clubfoot has been found to be associated with absent anterior compartment muscles and lesions involving the innervation to the anterior and lateral compartment muscles. A finding as subtle as adducted and contracted thumbs across the palms will identify a child with clubfeet as having arthrogryposis. Examination of the hips in a newborn is an important part of the musculoskeletal screening exam, but there is no reported increased risk for developmental dysplasia of the hip in children with clubfoot (116, 117).

Classification of the severity and rigidity of the clubfoot is important for the comparison of treatment modalities. Several classification systems have been proposed (120, 121 and 122, 125, 163, 173, 528), but none has been universally accepted. They all suffer from excessive subjectivity and only fair reproducibility.

Clinical Classification of Clubfoot.

With respect to classification of clubfeet, important clinical features must be documented. Included in these features are

  • The severity and rigidity of the deformities

  • Depth of the skin creases (Fig. 29-29)

  • Tightness and contractility of the muscles

Although there are a number of classification systems in use, two of them seem to be of particular value in attempting to classify clubfeet at the initiation of treatment. One of these classification systems was defined by Dimeglio et al. (121) and the second by Pirani (122, 123). The classification systems apply a point score to a number of physical findings, which, when totaled, leads to a “grade of involvement.” Flynn et al. (124) showed a good correspondence between the classification systems of Dimeglio and Pirani. They found a correlation coefficient of 0.83 with the Dimeglio system and 0.9 with the Pirani system when applied by three individuals. The correlation improved in both systems after the initial 15 feet were scored. Wainwright et al. (125) compared four classification systems: Dimeglio, Catteral, Harold and Walker, and Ponseti and Smoley, and determined that the Dimeglio system was the most reproducible. Both the Dimeglio and the Pirani point systems attempt to differentiate between mildly affected feet requiring little treatment and those that are extremely severe. If the outcomes of treatment are to be compared, a valid classification system must be employed before the initiation of treatment.

FIGURE 29-30. Dimeglio’s classification system for clubfoot deformity rates the position of the foot relative to equinus, varus, foot rotation, and forefoot medial deviation. These are scored from 0 to 4 on the basis of severity. Finally, the depths of posterior crease, medial crease, cavus, and muscle condition are each assigned a 0 or 1 point score. Total score ranges from 0 to 20 points, correlating with the severity of the clubfoot deformity. (From Dimeglio A, Bensahel H, Souchet P, et al. Classification of clubfoot. J Pediatr Orthop B 1995;4:129-136, with permission.)

One should create a checklist with either or both of the systems and attempt to score clubfeet at the initiation of treatment. Each of the scoring systems can be applied in <2 minutes. In the Pirani system, isolated physical findings, including the severity of deformity, the depth of skin creases, and the degree of certain pathoanatomic variations of the midfoot and the hindfoot, are each given severity scores of 0, 0.5, or 1 with a maximum possible score of 6. In the Dimeglio system (Fig. 29-30), the deviations of the foot—equinus, varus, adductus, and foot rotation—are scored based on the degree of deformity. Scores for the depth of skin creases, presence of cavus, and the condition of the muscles are combined to give a maximum possible score of 20. Choose one and attempt to grade clubfeet on the basis of these clinical criteria.

Radiographic Features.

There is no consensus on the role of radiographs in the diagnosis and management of the clubfoot (121, 122). However, it should be stated that the diagnosis of clubfoot in the newborn can and should be based solely on clinical findings. The intended role of radiographs in the assessment of foot deformities is to demonstrate the relationships between bones. This is accomplished by first drawing the axis of each bone, and herein lies the limitation of this imaging modality. There is little ossification of the bones in the normal newborn foot, and there is a delay in ossification in the clubfoot (126). The ossific nucleus of the talus is not centrally located in the cartilaginous anlage (127, 128). The ossific nucleus of the talus is between the head and neck and may be spherical in shape for the first several weeks of life. Ossification of the navicular does not begin until age 3 to 4 years in children with clubfoot and even then is eccentric. Brennan et al. (129) identified an even more fundamental problem when they showed very poor reproducibility in positioning the clubfoot for the radiograph. These factors make it unrealistic to consider radiographs of the newborn and infant clubfoot as objective data. The age or point at which radiographs become reliable is unclear.

Despite these limitations, there might be a role for radiographs to confirm correction of the clubfoot deformities or to help identify the site(s) of residual deformity in the child who is several months old and has been undergoing serial manipulation and casting. In the latter situation, the information can be helpful for surgical planning, particularly if one ascribes to à la carte surgery (118, 119, 130). The AP view is obtained with the foot pressed against the radiographic plate with a dorsiflexion and external rotation force (120, 131) (Fig. 29-31A). This will place the subtalar joint in its most everted and corrected position. The lateral radiograph is obtained with the foot dorsiflexed and maximally everted, but also with the leg internally rotated to assure a true lateral view of the ankle (manifest by the projection of the fibula within the posterior half of the tibia) (Fig. 29-31B). The talocalcaneal and talus-first metatarsal angles are measured on both views (10). The axis of the talus and calcaneus normally diverge from each other and the axis of the talus and the first metatarsal normally form a nearly straight line on both views. The tibiotalar and tibiocalcaneal angles are measured on the lateral view (10). The axis of the talus normally aligns almost perpendicular to the tibia and the calcaneus dorsiflexes above a right angle with the tibia. The alignment of the calcaneus and cuboid are assessed on the AP view (132).

FIGURE 29-31. A: Simulated weight-bearing anteroposterior radiograph of clubfoot. The talus (small straight arrow) and calcaneus (large straight arrow) are parallel, rather than divergent. The metatarsals are markedly adducted in relation to the talus. The cuboid ossification center (curved arrow) is medially aligned on the end of the calcaneus, rather than in the normal straight alignment. B: Maximum dorsiflexion lateral radiograph of clubfoot. The talus and calcaneus are somewhat parallel to each other and plantar-flexed in relation to the tibia. (From the private collection of Vincent S. Mosca, MD).

A second point at which radiographs may be helpful is intraoperatively to confirm the adequacy of correction of the deformities. The low dose radiation and convenience of minifluoroscopy make that technology desirable. The third indication for radiographs could be at some substantial time after surgery to confirm maintenance of deformity correction. Alternatively, the third point at which radiographs are obtained is when recurrence or other secondary deformities are identified.

Other Imaging Studies.

In response to the limitations of radiographs, ultrasound techniques are evolving for the assessment of the infant clubfoot during nonoperative and operative treatment (133, 134, 135, 136 and 137). Early results seem promising; however, availability of the technology in orthopaedic outpatient clinics
is currently limited. Arthrography, computerized tomography (138), and magnetic resonance imaging (127, 139, 140) may have a role in research or in the evaluation of postsurgical deformities, but do not have a role in the routine assessment of the idiopathic clubfoot.

Intrauterine Diagnosis.

The intrauterine diagnosis of clubfoot has become increasingly frequent with the routine use of fetal ultrasonography during pregnancy. This has implications for the orthopaedist, who is being consulted by prospective parents regarding the diagnosis, possible relationship to syndromes, treatment options, and prognosis. It appears that the earliest that a clubfoot can be diagnosed by ultrasound with accuracy is 12 weeks of gestational age. With sequential studies, there is an increased ability to visualize the deformity, relating either to the progressive development of a clubfoot deformity or perhaps the accuracy with which it can be seen. According to Keret et al. (141), the clubfoot deformity has been detected in routine studies in approximately 60% of cases, which is indicative of some degree of false-negative assessment. In 86% of cases, the deformity is identified by 23 weeks of gestational age, but still others are recognized up to 33 weeks. The diagnosis is made on ultrasound by the fixed position of the foot in an equinovarus position, not deviating from this on sequential observations (Fig. 29-32). Three-dimensional ultrasound may provide a more accurate diagnosis than standard ultrasound studies (142).

In studies of large populations using routine in utero ultrasound (143), the recognition of clubfoot deformity varies from 0.1% to 0.4% (144). Because postnatal studies suggest an occurrence rate at birth between 0.1% and 0.6%, one can assume a rather low false-negative rate. The false-positive rate for in utero diagnosis of clubfoot using ultrasound varies from 30% to 40%, depending on the series and the criteria (144, 145, 146 and 147). A term functional false-positive rate has been used in cases in which a foot may have the appearance of remaining in a plantar-flexed, varus, and medially deviated position but can passively be corrected to neutral during exam just following birth. The foot is characterized with a score of 0, 1, or 2 using the Dimeglio classification system and has been classified by some authors as a positional clubfoot. Such a foot requires only parent-administered exercise, and no long-term deformity results. With the advancement of ultrasound and increase in experience, the accuracy of diagnosis will steadily increase.

FIGURE 29-32. The clubfoot is diagnosed by ultrasound in utero when there is persistent medial deviation and equinus of the foot relative to the tibia. (From the private collection of James R. Kasser, MD.)

The ability to recognize syndromes associated with skeletal malformations is also increasing with time (142, 148). The combination of technologic advances and improved expertise in obtaining and interpreting images will certainly lead to further progress in recognizing fetal structural abnormalities. This brings one to the question of the need for amniocentesis and karyotyping if an isolated clubfoot deformity is found. In 1998, Shipp and Benacerraf (149) and Rijhsinghani et al. (144) suggested that amniocentesis and karyotyping were necessary to identify associated syndromes when clubfoot was identified. Malone et al. (150), in the year 2000, showed that in 57 cases of isolated clubfoot deformity out of 27,000 prenatal exams, there were no unrecognized associated abnormalities. Therefore, the recommendation is that karyotyping not be done in cases where a diagnosis of isolated clubfoot deformity was made. This still appears controversial, and a geneticist should be consulted about the need for amniocentesis if the question arises.

There is no attempt to provide any therapeutic intervention once an intrauterine diagnosis of clubfoot is made. The orthopaedist is only involved in counseling the family about the etiology, treatment, and prognosis, which generally alleviates fears and guilt, dispels myths, allows the parents to make personal decisions concerning the pregnancy, and allows for an improved emotional state for the family during the remainder of the pregnancy and the delivery of their child.


The deformities of the clubfoot are created, in part, by malalignment of the bones at the joints and, in part, by deformation in the shapes of the bones (102, 127, 138, 139 and 140, 151, 152, 153, 154, 155, 156, 157, 158, 159 and 160). The neck of the talus is short and deviated plantar-medially on the body of the talus (102, 153, 157, 158, 159 and 160). This directs the articular cartilage of the head of the talus in the same plantar-medial direction. Anatomic dissections (158) and MRI scan images (139, 140, 153) confirm that there is a varus deformity of the distal end of the calcaneus creating a medial tilt of its articular surface at the calcaneocuboid joint. Howard and Benson (157) and Epeldegui and Delgado (156) found that the anterior facet of the calcaneus is tilted medially in relation to the middle facet in the clubfoot, indicating that the location of the varus deformity is between the two facets (Fig. 29-33). Epeldegui and Delgado (156) performed elegant microdissections of the feet of 75 stillborns, some of which had clubfoot deformities. He specifically studied the bony and softtissue anatomy of the talocalcaneonavicular joint, which he, like Sarrafian, called the AP and Scarpa (14) termed the pes acetabulum. The AP is an ellipsoid articular cavity that holds and rotates around the head of the talus, comparable to the relationship between the pelvic acetabulum and the femoral head at the
hip joint. Its bony elements are the posterior articular surface of the navicular and the anterior and posterior articular facets of the calcaneus. Epeldegui found that the soft tissues of the AP were likewise markedly different in shape and orientation in the clubfoot from the normal foot. The shape of the medial cuneiform has not been studied in the newborn, but it is trapezoid shaped in the older child with residual forefoot adductus deformity. The subtalar joint complex is severely inverted, a combination of internal rotation and plantar flexion. The axis of rotation is in the interosseus talocalcaneal ligament. The AP is inverted around the plantar-medially-deviated head and neck of the talus, thereby aligning the navicular at or near the medial malleolus. The calcaneus is rotated downward and inward resulting in parallel alignment with the talus in the frontal and sagittal planes. The posterior part of the calcaneus is tethered to the fibula by the calcaneofibular ligament. There is a varus deformity of the distal end of the calcaneus with medial deviation of a congruous calcaneocuboid joint in many clubfeet (78, 139, 140, 153, 155, 156, 157, 158 and 159, 161). There may be medial subluxation of the cuboid on the distal calcaneus in some feet (152, 162). The plantar fascia, short plantar muscles, and spring ligament are contracted. The Achilles, tibialis posterior, flexor hallucis longus, and flexor digitorum communis tendons are contracted. The posterior capsules of the ankle and talocalcaneal joints are contracted.

FIGURE 29-33. Navicular (1). The axis of the anterior facet of the calcaneus (2) is tilted medially in relation to the axis of the middle facet (3) in the clubfoot (image on left) compared with the normal foot (image on right). (From Epeldegui T, Delgado E. Acetabulum pedis. Part I: talocalcaneonavicular joint socket in normal foot. J Pediatr Orthop B 1995;4:9, with permission.)

Tibial torsion and the position of the talus in the ankle are debated. McKay (154) believes the talus is in neutral alignment, Goldner (163) believes that it is internally rotated, and Carroll (151, 152, 155) believes that it is externally rotated. A recent three-dimensional MRI study of clubfeet revealed an externally rotated position of the talus in clubfoot compared with normal feet (127).

The muscles are abnormal in both anatomical insertion and intrinsic structure (101, 106). Muscles in clubfoot are smaller than normal and there is an increase in intracellular connective tissue within the gastrocsoleus and posterior tibial muscles. A predominance of type I muscle fiber has been seen in posterior and medial muscle groups. Electron microscopic studies have shown loss of myofibrils and atrophic fibers, suggesting a regional neuronal abnormality as well (108).

The ligaments are thick, with increased collagen fibers and increased cellularity (107). This is particularly true of the calcaneonavicular ligament or spring ligament and the posterior tibial tendon sheath (164). An electron microscopic study of medial ligaments in clubfoot identified myofibroblasts, which could be responsible for fibroblastic contracture in the postoperative clubfoot. Fukuhara et al. (165) showed myofibroblast-like cells in the deltoid and spring ligaments. Together, the thickened and shortened ligaments with contractile fibroblasts may
produce a significant component of the clubfoot pathology. Sano et al. (166) confirmed these findings, showing that cells of the medial ligamentous structures contained vimentin uniformly and myofibroblasts in some cases. More recently, Khan et al. (167) were unable to show myofibroblast-like cells in clubfeet, and van der Sluijs and Pruys (168) demonstrated normal collagen cross-linking in clubfeet.

Finally, abnormal vasculature in the foot is frequently present (169). The dorsalis pedis artery in many cases is absent or altered. Katz et al. (170) showed deficient dorsalis pedis flow in 45% of clubfeet compared to 8% of normal controls. In the more severely affected feet requiring surgery, the incidence of dorsalis pedis abnormality was 54%, whereas those successfully treated with cast therapy had an abnormality in dorsalis pedis flow in only 20% of cases. These data suggest that the severity of clubfoot may in some way relate to the vascular abnormality frequently seen in this condition.

Natural History.

The untreated clubfoot persists as a rigid, unsightly deformity. A large, callused bursa develops over the dorsolateral aspect of the hyperflexed midfoot which functions as the weight-bearing surface of the foot (Fig. 29-34). In the most extreme cases, the toes point backward during ambulation. Specially made footwear is required to accommodate the deformity. Surprisingly, untreated adults in certain cultures and environments will have little pain for many years and can function adequately. Their function is similar to that of individuals with Syme amputations when not wearing their prostheses. City-dwelling adolescents and adults with untreated clubfoot experience pain and disability with ambulation on paved sidewalks and hard floors.

Surgical Correction of Clubfoot (Figs. 29-44, 29-45, 29-46, 29-47, 29-48, 29-49, 29-50, 29-51, 29-52, 29-53 and 29-54)

General anesthesia with supplemental caudal epidural anesthesia has been shown to decrease the postoperative narcotic requirement, provide good pain control for several hours after surgery, and shorten the hospital stay (218).

The most useful type of skin incision(s) is debated, but this is certainly less important than the procedures performed under the skin, as long as all components of the deformity can be exposed and treated safely and effectively (Fig. 29-44).

Most surgeons use the Cincinnati incision (219) because it is extensile, cosmetic, and safe, as long as it is placed at least 1 cm proximal to the deep posterior ankle skin crease. Lower placement may risk slough of the heel pad. The Cincinnati incision can be used for revision surgery, even crossing longitudinal scars from previous surgery. Another approach is Carroll’s two-incision technique (152, 180). It is safe and extensile, but less cosmetic.

The operation typically begins with heel cord lengthening and posterior release of the ankle and subtalar joints, with release of the calcaneofibular ligament (Figs. 29-45, 29-46, 29-47, 29-48, 29-49 and 29-50).

Residual cavus, adductus, and varus require a plantarmedial release that starts with release of the plantar fascia and the three origins of the abductor hallucis muscle from the calcaneus (Figs. 29-11, 29-51).

If the talonavicular joint is not normally aligned at this point, the posterior tibial tendon is lengthened (Figs. 29-12, 29-51, 27-52 and 29-53).

If still not aligned, the talonavicular joint capsule is released judiciously, starting medially and carefully progressing plantar and dorsal. Once there is a straight talus-first metatarsal angle visualized on minifluoroscopy, no further release is necessary. Excessive release of the talonavicular joint can lead to unrecoverable subluxation/dislocation and must be avoided (Figs. 29-12, 29-51, 27-52 and 29-53).

The interosseous talocalcaneal ligament is always left intact. Percutaneous releases of the flexor hallucis longus and flexor digitorum longus (FDL) tendons at the base of the toes or supramalleolar lengthenings of these tendons are preferable to lengthening these tendons in the midfoot. Finally, the posterior tibial and Achilles tendons are repaired under slight tension with the joints in anatomic alignment to avoid postoperative weakness (Fig. 29-54).

Debate surrounds the need for internal fixation with wires. Procedures that involve more extensive capsular releases tend to require fixation. One of the many challenges of wire fixation is the inability to accurately determine the proper alignment of the bones and joints. There is minimal ossification of the tarsal bones in infants, so the accuracy of radiographic analysis is marginal at best. Pinning in a poor alignment is perhaps as likely as pinning in the anatomic position. I personally do not use wire fixation, but instead depend on sufficient, but not excessive, softtissue releases and fluoroscopic guidance to produce proper joint alignment. Others prefer internal fixation.

Before closure of the wound, some steps should be taken to minimize the bleeding in the foot because this can cause considerable swelling, which may necessitate splitting or removal of the cast. Release the tourniquet and achieve wound hemostasis before closure. Approximate the subcutaneous tissues with interrupted absorbable sutures, and approximate the skin edges with a running subcuticular absorbable suture, such as 4-0 Monocryl.

Apply a solid long-leg cast with the foot in the fully corrected position and with the knee bent 90 degrees and the thigh-foot angle set at 45 degrees outward. Attempts at early motion with a hinged cast, as advocated by McKay (154, 178), have not been widely utilized. At 6 weeks, the cast and the pins, if utilized, are removed in the office. Another long-leg cast is applied and maintained for 4 to 6 weeks, depending on the age of the child. After the final cast is removed, there are options for maintaining deformity correction. One is to utilize a FAB, as is used in the Ponseti method after cast correction. Another option is to use an ankle-foot orthosis in an overcorrected position, either day and night or at nighttime only. Generally speaking, special shoes are not required, but the use of arch supports or simple shoe modifications may be of benefit in selected cases.

In a severe clubfoot that has not responded well to casting, it may not be possible to immediately approximate the edges of the Cincinnati incision with the foot in the fully corrected position without compromising the circulation of the skin. It has been suggested to leave the skin edges separated with the foot in the fully corrected position and allow for wound closure by secondary intent (220). Alternatively, the skin edges can be approximated (with or without a pin inserted across the talonavicular joint), the cast can be applied with the foot in plantar flexion, and the foot can be manipulated safely into further dorsiflexion during a cast change under anesthesia 1 to 2 weeks later (175, 176 and 177, 219).

Surgical Complications and Their Management.

The laundry list of operative complications was mentioned earlier. The approach to management of some of the postoperative deformities will now be discussed.

Surgical Correction of Clubfoot (Figs. 29-44, 29-45, 29-46, 29-47, 29-48, 29-49, 29-50, 29-51, 29-52, 29-53 and 29-54)

FIGURE 29-44. Surgical Correction of Clubfoot. The incisions used for clubfoot surgery vary widely and are more numerous than can be described here. All have been used successfully, but what is done beneath the incision is far more important to the result than the incision itself. Turco (175) described a straight incision that ran from the base of the first metatarsal, under the medial malleolus, until it reached the Achilles tendon (A). He pointed out that a proximal extension of the incision along the Achilles tendon was contraindicated and that no undermining of the wound should be done. Ignoring these two admonitions has led to many wound problems. Crawford et al. (219) described an incision popularized by Giannestras in Cincinnati (B). This transverse incision begins on the medial side of the foot, over the naviculocuneiform joint. From there, the incision passes posteriorly to cross just beneath the tip of the medial malleolus. It continues across the back of the ankle at least 1cm proximal to the posterior heel crease and continues laterally to pass under the lateral malleolus, ending at the sinus tarsi. Although some surgeons have abandoned this incision because of wound complications, many more report using it routinely without problems. It is my incision of choice. Some surgeons prefer to use two incisions: one posterior and one medial, with a third incision laterally over the calcaneocuboid joint, if this is necessary. Carroll (152) has described a medial incision with three limbs (C). The center of the calcaneus, the front of the medial malleolus, and the base of the first metatarsal form a triangle. The center part of this incision is parallel to the base of the triangle, whereas the proximal part angles toward the center of the heel and the distal part crosses over the dorsum of the foot. The posterior incision (not shown) runs from a point in the midline about 4 cm above the tibiotalar joint obliquely to a point midway between the Achilles tendon and the lateral malleolus.

FIGURE 29-45. The patient is positioned prone for the clubfoot operation. The foam head cradle used by anesthesiologists to support the head serves as an excellent support for the prone infant. The foot can be raised with a folded sheet underneath it to allow better access to it. The skin is divided sharply down to the Achilles tendon. It is important to preserve the sheath of the tendon. This is best accomplished by leaving the sheath attached to the subcutaneous tissue. Therefore, the incision in the skin and subcutaneous tissue is carried directly down onto the tendon, passing through its filmy sheath. Then the tendon is exposed circumferentially by gently teasing its sheath away with a small elevator. A large amount of proximal exposure can be achieved by placing the blade of a Senn or Langenbeck retractor proximally and pulling upward while “toeing in” on the retractor. Divide the tendon in a Z fashion. This starts proximally with a cut in the middle of the tendon. It should be sufficiently long because it is often surprising how much length is needed in a severe clubfoot. When the knife reaches the calcaneus, it is turned medially to detach the medial half of the tendon from the calcaneus. The medial half is detached to lessen the varus force. With the Senn retractor elevating the skin proximally, the lateral half of the tendon is detached proximally. Both halves are dissected free. Sutures can be passed through the free end of both halves to act as handles to aid with later repair.

FIGURE 29-46. The next step is to open the deep posterior compartment, a distinct anatomic compartment that can be opened by incising it with a knife. Starting proximally, the fat under the Achilles tendon is sharply incised in a longitudinal straight line. As this incision is deepened, the fascial boundary of the compartment is encountered and, beneath it, more fat in the posterior compartment. Often, after this incision is completed, the anatomic structures in the posterior compartment come instantly into view (A). In the severe clubfoot, the normal anatomic relationships may not be appreciated. In such cases the incision may come down directly over the posterior tibial nerve, as illustrated here. Note the flexor hallucis longus just lateral to the nerve. This structure is the first landmark to identify in the posterior compartment and is easily recognized as the only tendon passing behind the medial malleolus in which the muscle belly extends this low. This is easily remembered as the only muscle with “beef at the heel.” A small periosteal elevator is used to dissect beneath this muscle, staying in close contact with the posterior capsule. This dissection is continued around the medial side of the ankle as far as the posterior aspect of the medial malleolus. The dissection is facilitated by opening the sheath of the flexor hallucis longus tendon longitudinally until the sustentaculum tali is encountered. This is the point at which the tendon can no longer be seen and is the landmark that identifies the subtalar joint, as that joint is immediately adjacent to the sustentaculum tali. This early and definitive identification of the subtalar joint helps ensure subsequent proper identification of the ankle joint which is often difficult, especially in severe deformities. The neurovascular bundle is elevated with the fatty tissue around it. A vessel loop can be used to gently retract the bundle. If a plantar release will be performed later in the procedure, it is easiest to dissect the neurovascular bundle out at this point to facilitate its exposure from the medial incision. A Senn or Langenbeck retractor can be used to retract all these structures, giving a clear view of the posterior capsules from the midline to the medial malleolus (B). Allowing the foot to go into plantar flexion makes this exposure even easier.

FIGURE 29-47. The lateral side of the capsules must now be exposed in the same manner. This is most easily accomplished by incising the fascia over the peroneal muscle bellies. These muscles are enveloped in fat and fascia lateral to the flexor hallucis longus, whose muscle belly is shown exposed along the neurovascular bundle. After the muscle tissue is identified, a scissors is used to open this fascial envelope around the peroneal muscles and tendons (A). This incision should be carried to the point where the peroneal tendons curve under the lateral malleolus so that these tendons can be retracted sufficiently to permit a complete division of the calcaneofibular ligament, which lies beneath the peroneal tendon sheath (B). This completes the exposure of the posterior aspect of the tibiotalar and subtalar joints.

FIGURE 29-48. The next step is to open the posterior joints. In a severe clubfoot, the posterior edge of the calcaneus may be in direct contact with the posterior border of the tibia, obscuring the talus. To facilitate this exposure, the fibrofatty tissue over the posterior aspect of the joints is sharply excised with a knife. The subtalar joint, which has already been identified following release of the flexor hallucis longus tendon sheath down to the sustentaculum tali, can be released from medial to lateral with a scalpel or scissors. The peroneal tendons are retracted and the incision in the capsule is continued around the lateral side, including release of the calcaneofibular ligament.

FIGURE 29-49. The tibiotalar joint can be identified proximal to the subtalar joint by palpation and inspection while the foot is plantar and dorsiflexed. The fibrofatty tissue is first excised with a knife, and then the scissors is inserted with one blade in the joint and the other outside the joint. The capsule is opened around the medial side until the FDL tendon is identified. Two notes of caution: ensure that the neurovascular structures are retracted and go slowly behind the medial malleolus to avoid dividing the FDL and posterior tibial tendons and the deep deltoid ligament. As the foot is dorsiflexed, the dome of the talus comes into view. Cutting the talofibular ligament usually makes the largest difference in the amount of dorsiflexion that is obtained.

FIGURE 29-50. Although many illustrations of clubfoot surgery show the ligaments of the posterior capsule as distinct structures, the surgeon rarely sees them this way because they are merely condensations of the continuous posterior capsule. Occasionally, the posterior talofibular ligament and the calcaneofibular ligament stand out, the latter appearing like a tendon. The geographic cuts in the posterior capsule of the tibiotalar and subtalar joints divide the ligaments as shown: the posterior tibiotalar ligament (A), the posterior talofibular ligament (B), the tibiofibular ligament (C), the calcaneofibular ligament (D), and the deltoid ligament (E). The deltoid ligament consists of several parts. One part of the deltoid ligament, referred to as the deep deltoid ligament (anterior tibiotalar part of the deltoid ligament), is attached to the talus and, in the opinion of many surgeons, should not be divided in order to avoid the complication of lateral subluxation of the talus. Division of this part of the deltoid ligament is avoided by limiting the capsulotomy of the tibiotalar joint up to the posterior aspect of the medial malleolus. If it is desired to divide this portion of the deltoid ligament as a part of the operation, as is done in the procedure described by Goldner (191), it should be repaired.

FIGURE 29-51. A: The plantar-medial release is performed through the antero-medial extension of a Cincinnati incision. A vessel loop surrounds the posterior tibial neurovascular bundle (blue arrow) posterior to the medial malleolus. The proximal edge (black arrow) of the laciniate ligament (a.k.a. flexor retinaculum) is exposed. B: The laciniate ligament is released with scissors. C: The lowest (1) of the 3 origins of the abductor hallucis muscle is released from the calcaneus superficial to the lateral plantar neurovascular bundle. D: The plantar fascia and short toe flexors are next released superficial (plantar) to the lateral plantar neurovascular bundle. Release of those soft tissues using the tunnel of the NV bundle for guidance obviates injury to those important structures. E: The thin septum (2) of the abductor hallucis that separates the medial and lateral plantar NV bundles is divided under direct vision. F: The most dorsal origin (3) of the abductor hallucis, which is dorsal to the medial plantar NV bundle, is released. This completes the superficial plantar-medial release.

FIGURE 29-51. (continued) G: The tibialis posterior and flexor digitorum longus are released from their respective tendon sheaths. H: The deep plantar-medial release begins with z-lengthening of the tibialis posterior. The talonavicular joint capsule is release medially, extending to varying degrees dorsal and plantar, as required, to enable eversion of the subtalar joint. (From the private collection of Vincent S. Mosca, MD.)

FIGURE 29-52. With the posterior tibial tendon detached, it is easy to identify the talonavicular joint in a normal foot. However, in a clubfoot it must be remembered that the navicular is displaced medially, causing it to lie on the medial side of the neck of the talus and closer than normal to the medial malleolus.

FIGURE 29-53. In addition, the space between the tuberosity of the navicular and the medial malleolus is filled with dense, fibrous tissue. If the surgeon knows the anatomy, this tissue can be excised with a knife. A scissors is used to open the talonavicular joint. This joint is found by directing the scissors distally toward the first metatarsal between the neck of the talus and the navicular (A). The error is to cut transversely across the foot as if the anatomic relationship between the navicular and the talus were normal. This is especially dangerous if done with a knife because it is not difficult to inadvertently divide the cartilaginous neck of the talus. At the same time, the surgeon should be careful to avoid opening the naviculocuneiform joint. This will further devascularize the navicular and tend to destabilize it permitting it to rotate out of position. The talonavicular joint capsule should be released primarily on the medial and plantar aspects, as those are the most contracted portions. The dorsomedial capsule should be released only to the extent that it limits eversion of the subtalar joint. Excessive release of the talonavicular joint capsule might result in hypermobility and dorsal subluxation of the navicular, a difficult situation from which to recover. (Much of the capsule in this drawing has been removed for clarity, but this should not be done during the surgery.) The plantar aspect of the joint may remain tight even after the capsule is cut. To free it, the plantar calcaneonavicular (spring) ligament and the anterior portion of the deltoid ligament inserting into the navicular (tibionavicular ligament) must be divided. Because these ligaments are condensations of the capsules, they will be divided when the capsules between the talus and the navicular dorsomedially and the calcaneus and the cuboid on the plantar aspect are opened. This can be done with a scissors or a knife when the surgeon is certain that he or she has identified the joint. Plantar and lateral to the talonavicular joint, and almost in line with it, is the medial side of the calcaneocuboid joint (B). This medial capsule can be opened, but additional release is sometimes necessary. Because the peroneus longus tendon crosses the most plantar and lateral aspect of this joint, it should be retracted. The medial capsule of the calcaneocuboid joint, like all the other capsules, can be opened safely with a scissors, although some experienced surgeons prefer to use a knife.

FIGURE 29-54. Repair of the Achilles tendon is all that remains to be done posteriorly. This should be done after the completion of the entire release and after the foot is reduced. The tendon may be repaired end to end with a Kessler type of stitch or side to side. The repair should be under modest tension to avoid unnecessary weakening of the gastrocnemius muscle.

Recurrent and Residual Deformity.

Recurrent and residual deformities of the surgically, and nonsurgically, treated clubfoot in the young child are first treated with a series of manipulations and long-leg cast applications using Ponseti’s method. Repeat soft-tissue release, using an à la carte approach, is indicated if the deformities cannot be corrected nonoperatively. In the older child, one or more osteotomies may be necessary to correct residual deformities that are identified after the joints are aligned by soft-tissue releases.

Residual midfoot adduction and supination are often a problem after clubfoot correction. The deformity is commonly referred to as the “bean-shaped foot.” The symptoms are difficulty with rigid shoe wear and walking on the lateral border.

In the past, painful midfoot adduction was often treated by metatarsal osteotomies (459, 460) or tarsometatarsal capsulotomies (Hyman-Herndon procedure) (456). More recently, however, these operations have been used less frequently because they either fail to provide the desired correction or they result in painful stiff joints (457, 458, 461, 462).

Painful residual adductus of the midfoot in the older child can be treated with an opening-wedge osteotomy of the medial cuneiform (77, 221), a closing-wedge osteotomy of the cuboid (222), or both (223, 224 and 225) (Figs. 29-55, 29-56, 29-57, 29-58, 29-59, 29-60 and 29-61).

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Jul 21, 2016 | Posted by in ORTHOPEDIC | Comments Off on The Foot

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