The Pediatric Foot

Pes planus is a term
describing any condition of the foot in which the longitudinal arch is
lowered. It is important to distinguish between physiologic pes planus
and pes planus secondary to pathologic conditions.

Physiologic pes planus (hypermobile flatfoot, flexible
flatfoot) is characterized by varying degrees of loss of the
longitudinal arch of the foot on weight bearing. The foot assumes an
apparent pronated posture with abduction of the forefoot and varying
degrees of heel valgus (Figure 20-5). The
important distinguishing characteristic between physiologic and
pathologic pes planus is flexibility. In the physiologic type, the foot
remains flexible.

Ninety percent of normal children younger than 2 years
have varying degrees of pes planus. This is due to the normal joint
hypermobility in this age group and the normal infant fat pad along the
medial aspect of the foot (Figure 20-6). In
addition, the normal wide-based stance assumed by newly standing or
walking children causes the weight-bearing line to fall medial to first
or second ray, resulting in the hypermobile foot assuming a pes planus
posture.

Between 3 and 5 years of age, the normal longitudinal
arch develops in most patients. It is estimated that by age 10 years,
only 4% of the population have persistent pes planus.

The normal longitudinal arch of the foot is determined
by maintenance of the normal relations between the bones of the foot.
These relations are maintained by the supporting ligamentous and
capsular structures and can be affected by functional stresses applied
to the foot in weight bearing and by muscle contraction. The foot
musculature does not maintain the longitudinal arch. Its purpose is to
maintain balance, adjust the foot to uneven ground, and propel the
body. Biomechanically, when the foot is supinated, the articulations of
the midfoot are “locked,” and the foot is a rigid structure. When the
foot is pronated, however, greater mobility is allowed at the midfoot
joints, and maximal motion can occur at the talonavicular and
calcaneocuboid joints. The position of heel valgus and forefoot
abduction with lowering of the longitudinal arch is often referred to
as a pronated foot, while in actuality,
the forefoot is supinated to varying degrees in relation to the hind
foot. Thus, in true physiologic pes planus, as the calcaneus assumes a
valgus position, the lateral aspect of the forefoot is in contact only
with the ground if the forefoot supinates to some degree in relation to
the hindfoot.

The normal weight-bearing pattern includes ground
contact with the lateral border of the foot and with the first and
fifth metatarsals. In pes planus, as the calcaneus assumes a more
valgus position, the talar head loses some of its support and assumes a
more vertically oriented position, with

subsequent loss of the normal arch (Figure 20-7).
Body weight shifts medially, altering the normal weight-bearing pattern
and causing increasing ground contact with the medial aspect of the
foot. With time, the Achilles tendon may shorten and act as an everter
of the foot, accentuating the deformity.

Many theories have been advanced over the years about
the cause of physiologic pes planus, most centering around abnormal
bone configuration, muscle imbalance, or ligamentous laxity. The origin
of persistent physiologic pes planus, however, remains unknown. Many
patients have a positive family history of a similar condition or
evidence of generalized ligamentous laxity. Physiologic pes planus may
also be associated with obesity. A positive family history should be
sought for conditions associated with joint laxity, such as Marfan and
Ehlers-Danlos syndromes. Physiologic pes planus is occasionally seen as
a residual of the calcaneal valgus foot deformity (discussed later). It
is important to obtain a family history of treatment of similar
conditions because this may have significant bearing on the patient
education necessary in prescribing treatment modalities to the family.

Most children with physiologic pes planus are
asymptomatic. They are brought in by their parents because of the
assumption that flatfeet are abnormal and harmful to their child if not
treated. Occasionally, some children may complain of symptoms that are
referable to foot strain after prolonged activity and generally
relieved by rest. Associated leg aches are not uncommon in patients who
present with symptomatic pes planus, but because these are present in a
large portion of normal people, a cause-and-effect relation is
difficult to establish.

Each patient should be thoroughly examined for excessive
joint laxity manifested by the ability to hyperextend the metacarpal
phalangeal joints,

appose
the thumb to the forearm, and hyperextend the elbows and knees. The
foot has normal to slightly increased subtalar motion. In weight
bearing, varying degrees of loss of the longitudinal medial arch are
noted. The heel is in valgus and the forefoot in abduction (see Figure 20-5).
With loss of the longitudinal arch on weight bearing, the center of
gravity is shifted medially to the second metatarsal or medially to the
first metatarsal. The patient may have a toe-in gait in an attempt to
shift the weight-bearing axis laterally.

Foot flexibility may be demonstrated in two ways: by
examining the feet in the resting position and by the tiptoe test. The
patient should be examined with legs dangling over the examination
table (see Figure 20-5). In this position, the
physiologic pes planus foot assumes a normal contour to the
longitudinal arch. In the tiptoe test, the patient’s feet are observed
when the patient walks on tiptoes (see Figure 20-5).
In this position, the normal arch is restored, with the heel going to a
neutral or slightly varus position. Muscle strength of the foot should
be normal.

It is important to rule out hypermobile flatfoot associated with a short Achilles tendon by history and physical examination (Figure 20-8).
This condition, which is often familial, is evidenced by contracture of
the gastrocnemius in association with the same clinical features as
described previously. This condition is usually symptomatic and
associated with long-term disability. These patients can usually
correct the deformity by involuntary muscular effort, as demonstrated
by the patient restoring the arch by standing on tiptoes.

In
addition, in the nonweight-bearing position, the normal arch is
generally present. Contracture of the Achilles tendon is best assessed
with the knee in extension and the talonavicular joint locked in
inversion so that dorsiflexion is measured only at the ankle. The
radiographic features of this condition are characteristic (Figure 20-9).
These patients may also show evidence of hypermobility at the midtarsal
joints, which allows the heel to touch the floor despite a contracted
Achilles tendon. Without treatment, this condition may cause severe
disabling pain.

In the child presenting with a complaint of flatfeet,
pathologic causes of pes planus must be ruled out. These causes include
congenital vertical talus, oblique talus, tarsal coalition, tumor,
foreign body reaction, and Köhler disease of the navicular and
accessory navicular. Accessory navicular bones are seen in about 12% of
the population and are a normal variant. Two patterns are evident. In
one pattern, the accessory navicular is a sesamoid bone within the
posterior tibial tendon (Figure 20-10). It is
anatomically separate from the navicular and usually does not cause
symptoms. In the second form, the accessory navicular is in close
association with the navicular as an ossification center, causing a
change in shape of the navicular. This type may be associated with
pain, particularly during adolescence (Figure 20-11).
Accessory navicular is not a cause of hypermobile flatfoot, but because
both conditions are common, they may present together. Accessory
naviculars may be treated symptomatically, but excision may be required
if conservative measures fail.

The foot with a vertical talus assumes a convex plantar surface that is rigid and has characteristic radiographic findings (Figures 20-12, 20-13 and 20-14).
Neuromuscular causes of pes planus, such as cerebral palsy and muscular
dystrophy, can be diagnosed by their typical diagnostic
characteristics. The most severe form of physiologic pes planus is
referred to as an oblique talus because of
its radiologic appearance. It has features similar to vertical talus on
the standing lateral view, but normal alignment is restored on plantar
flexion lateral radiographs. Tarsal coalitions have rigidity of
subtalar motion, may be associated with peroneal spastic flatfoot, and
are diagnosed radiographically (Figures 20-15, 20-16, 20-17 and 20-18).
Other causes of pes planus include the so-called skewfoot or Z-foot
(see metatarsus adductus) and surgically overcorrected clubfeet.

Radiographs are generally not indicated in the
asymptomatic child with a physiologic pes planus. In severe cases,
standing anteroposterior (AP) and lateral radiographs should be
obtained. On the normal standing AP radiograph, the talocalcaneal angle
should be between 15 and 35° (Figure 20-19).
Diversion of the AP talocalcaneal angle to greater than 35° is evidence
of heel valgus. The midtalar line passing medial to the first
metatarsal with the navicular displaced laterally is evidence of
forefoot abduction. On the standing lateral radiograph, the normal
lateral talocalcaneal angle is between 25 and 50°. The talus first
metatarsal angle should be about 0°. On the lateral view, the exact
location of loss of longitudinal arch can be determined. This sag may
occur at the talonavicular joint, first naviculocuneiform joint, and
first metatarsocuneiform joint, or combinations thereof. On the
standing lateral radiograph, the talus is more vertically oriented,
with the metatarsals and the calcaneus in a more horizontal position
than normal because of flattening of the arch (see Figure 20-7).

If the patient presents with a painful flatfoot, oblique
views and Harris views (radiograph taken from behind the foot with the
x-ray beam at a 45° angle) may be helpful in defining a tarsal
coalition or a pathologic process. If tumor, infection, or a stress
fracture is suspected, bone scanning may be helpful. Computed
tomography (CT) is indicated if talocalcaneal tarsal coalition is
suspected (see Figure 20-18). The diagnosis of physiologic pes planus is one of exclusion.

The natural history of physiologic pes planus is
unfortunately clouded by medical and nonmedical mythology. To most
parents and many physicians and paramedical personnel, flatfeet are
considered

a significant health problem. Unfortunately, good natural history data on this condition are lacking.

Treatments offered in the past have been based on the
assumption that patients will have problems in the future if the
condition is not treated. In normal children, aged 1 to 3 years, whose
parents bring them in for concerns over flatfeet, reassurance and
explanation of the cause of pes planus are essential. The parents
should be informed about the presence of the normal fat pad, the normal
hyperlaxity of

infancy,
the often familial nature of the condition. They should also be
reassured that, in most children, an arch will develop by 5 years of
age. The parents should be informed of the benign natural history of
the condition. Appropriate literature should be supplied to the family
so they can reassure themselves and other family members who may expect
some treatment because of what they have heard from others, what they
have read, or treatment they underwent as children. Many parents are
under the false assumption that so-called corrective shoes are
responsible for the natural development of the longitudinal arch.

The same conservative recommendations apply to all other
children with the diagnosis of physiologic pes planus. The educational
aspects of the natural history of the condition cannot be
overemphasized. The parents should be instructed that treatment
modalities offered in the past were offered without any scientific
basis. A recent prospective randomized study of patients with flexible
flatfeet treated by corrective shoes and inserts revealed that all
patients improved moderately after 3 years of treatment, and no greater
improvement was seen in patients who were treated vigorously, even
those treated with custom-made inserts. All treatments in the past,

including exercises, varying shoe modifications, and inserts, have been proved to be ineffective.

In a child with a painful flexible flatfoot, the
diagnosis must be reassessed and sources of painful flatfeet
eliminated. Prophylactic treatment of any type is unwarranted.
Treatment for flexible flatfeet is only indicated if the patient
presents with pain, usually in the foot or calf, or if the patient has
severe excessive shoe wear. The discomfort in the foot and the
associated leg aches, which occur in about 15 to 30% of normal people,
should be treated symptomatically with acetaminophen, local heat, and
massage. If fatigue symptoms or discomfort with increasing activity
persists, shoe modifications can be considered. It is important to
emphasize that these modifications are not corrective. High-top tennis
shoes with a good longitudinal arch can usually be recommended. If
symptoms persist, other noncorrective adaptive measures may be tried,
such as a medial heel wedge, a long shoe counter, or a navicular pad.

For the more severe symptomatic physiologic pes planus
that fails to respond to conservative measures, a more formal shoe
orthotic, such as a University of California Biomechanics Lab insert or
custom-made insert, may distribute body weight more evenly across the
sole of the foot and take the pressure off the prominent talar head.
These modalities, however, are expensive, must be changed frequently
with foot growth, and have no scientific basis for their use. The use
of shoe modification inserts tends to label the child as having a
problem. The use of these devices to appease parents or grandparents
should be discouraged.

In young patients with hypermobile flatfoot and a short
tendo Achilles, heel cord stretching exercises should be instituted. If
symptoms develop or the contracture persists, tendo Achilles
lengthening can be considered. The only operative indications in true
physiologic pes planus flatfoot are severe malalignment problems
causing excessive abnormal shoe wear or pain. Achilles tendon
stretching or casting may be of some benefit. Surgical options for
these indications are rarely indicated. In the past, these options
included soft tissue procedures alone; arthrodeses of the various
tarsal joints; osteotomies; and combined osteotomies, arthrodeses, and
soft tissue procedures, all with the goal of restoring the normal
longitudinal arch, relieving pain, and preserving as much motion as
possible. Results of these procedures have been poor.

The term tarsal coalition refers to the union of two or more tarsal bones by fibrous, cartilaginous, or bony tissue. This entity is often called peroneal spastic flatfoot
because of the high association with contracture of the peroneal
tendons. The most common sites of coalition are between the calcaneus
and the navicular and between the talus and calcaneus. The most common
talocalcaneal coalition is

between
the sustentaculum and the talus, with rare coalitions involving the
anterior or posterior facet. Other tarsal coalitions are much less
common. The coalitions may be complete or partial. When the coalition
is fibrous, it is called a syndesmosis. When the coalition is cartilaginous, it is referred to as synchondroses. A bony union is referred to as a synostosis. Tarsal coalition represents the most common nonneuromuscular cause of pathologic pes planus.

The true incidence of tarsal coalition is unknown. It is
estimated, however, that less than 1 to 2% of the population is
affected. Although tarsal coalitions may be multiple, rarely is there
more than one coalition per foot. Bilateralness, however, is common.

Demonstration of coalitions in fetal specimens lends
support to the theory of failure of segmentation as the origins of
tarsal coalitions (Figure 20-20). This
incomplete segmentation of the mesenchymal anlage of the tarsal bones
gives rise to the fibrous or cartilaginous coalition, which may ossify
later in life. Bilateralness has been reported in up to 70% of
calcaneonavicular coalitions and in 20 to 50% of talocalcaneal
coalitions. Tarsal coalitions are thought to be an inherited condition,
with the most widely accepted pattern being autosomal dominant
inheritance with variable penetrance.

Because the true incidence of tarsal coalitions in the
population is unknown, the natural history is uncertain. It is apparent
that many patients with tarsal coalitions have no symptoms, and many
patients with coalitions treated symptomatically can go well into adult
life without persistent pain or disability. Symptoms most commonly
develop when the coalition begins to ossify. Ossification of the
coalition restricts subtalar motion. This alteration in subtalar
mechanics leads to increased stress at adjacent joints, particularly
the ankle and talonavicular joints. If a coalition remains fibrous
(syndesmosis), symptoms may never develop because of the mobility
allowed through the syndesmosis. With increasing ossification of a
cartilaginous (synchondrosis) coalition, decreased mobility ensues,
increasing the likelihood of the patient developing clinical symptoms.
The altered subtalar joint mechanics over time may lead to degenerative
joint disease in adjacent joints, causing persistent pain and
disability. The limited subtalar motion also causes increased laxity in
adjacent joints, particularly the ankle joint, leading to increased
incidence of sprains and secondary joint alterations.

The typical patient with tarsal coalition presents
during the second decade of life with pain or decreased subtalar
motion. Occasionally, the patient complains of a limp, discomfort in
the calf region, or nonspecific foot pain. The pain is often localized
to the anterior, medial, or lateral aspect of the subtalar joint or to
the talonavicular region. The onset of pain is usually insidious or
associated with a traumatic event such as a nonresolving ankle sprain.
Pain is usually made worse by activities like running and jumping or
prolonged standing; it is usually relieved by rest. The symptom onset
depends on the nature of the coalition (fibrous, cartilaginous, or
bony) and the specific joint involved. Children with the rare
talonavicular coalition may present between 2 and 4 years of age.
Typically, patients with calcaneonavicular coalitions present between 8
and 12 years of age, and those with talocalcaneal coalitions between 12
and 14 years of age. In any child presenting with a painful rigid foot,
tarsal coalition must be ruled out.

Physical examination in patients with tarsal coalition
generally reveals decreased hindfoot or midfoot motion, or both. Most
commonly, the heel is in valgus and the forefoot in abduction (Figure 20-21).
The patient may walk with an antalgic gait, and if symptoms are
long-standing and the pain is significant, disuse atrophy may be noted
on calf measurements. In about half of cases, contractures of the
peroneal muscles is present. This is evidenced by prominence of the
peroneal tendons in the lateral aspect of the ankle and foot (Figure 20-22). Attempt at inversion of the deformity causes pain and discomfort along the peroneal region (Figure 20-23).
The peroneal tendons are contracted secondary to prolonged positioning
of the foot in valgus. True muscle spasms of the peroneal tendons are
rare. Increased ankle ligamentous laxity is most commonly seen in
patients with long-standing symptoms, particularly those with
talocalcaneal coalitions. There may also be varying degrees of loss of
the longitudinal arch. Pathologic conditions affecting the subtalar
joint, including tumors, rheumatoid arthritis, and traumatic injuries,
may mimic the physical findings of tarsal coalition.

When tarsal coalitions are suspected, standing AP, lateral, and 45° medial oblique radiographs should be obtained (see Figure 20-15).
The diagnosis of a calcaneonavicular coalition can usually be made on
these standard radiographs. The 45° medial oblique radiograph usually
demonstrates this coalition. If the coalition is fibrous or
cartilaginous, however, it may not be obvious on plain radiographs.
Other findings that indicate a possible calcaneonavicular coalition
include elongation at the anterior portion of the calcaneus to a point
of close proximity to the navicular and irregular, sclerotic

margins of the two bones in close approximation (see Figure 20-16).

Before the development of CT scanning, talocalcaneal
coalitions were often difficult to diagnose. In suspected talocalcaneal
coalitions, Harris views taken from behind the foot at an angle 45°
from the horizontal demonstrate the posterior and medial facets of the
subtalar joint. Normally, these are parallel, but coalitions may be
diagnosed by the loss of the parallel orientation between the two
facets, presence of fusion, or irregular or sclerotic surfaces (see Figure 20-17).
Other types of tomography also have been used to demonstrate
talocalcaneal coalitions; however, CT is the diagnostic method of
choice for demonstrating these coalitions. Coronal sections should be
obtained to document the coalition (see Figure 20-18).
These sections not only document the presence of the coalition but also
clearly define its extent. CT scans are most helpful in planning
surgical management of this condition.

In patients with talocalcaneal coalitions, abnormal
subtalar mechanics may be evident radiographically by secondary
adaptive changes. These changes include dorsal beaking or lipping at
the head or neck of the talus (see Figure 20-16).
This is secondary to stretching of the talonavicular ligaments because
of the navicular impinging on the head of the talus. The lateral aspect
of the talus may appear broadened, with the undersurface of the talar
neck having a concave appearance. There may be apparent narrowing of
the posterior talocalcaneal joint space and inability to determine the
definition of the middle talocalcaneal articulation.

Radiographs of the ankle joint may demonstrate an
apparent ball-and-socket ankle—manifest by convexity of the dome of the
talus on both the AP and lateral views. In patients presenting with
repeated ankle sprains and radiographic evidence of a ball-and-socket
ankle, tarsal coalition should be sought. In these cases, the
radiographic changes at the ankle joint are secondary to long-standing
ankle instability and adaptive changes of the tibial talar articulation.

Initial management of calcaneonavicular coalitions
should be nonoperative because the natural history indicates that many
patients have no symptoms, and the literature review of various
treatment programs indicates some success with nonoperative treatment.
Nonoperative treatment measures are based on immobilizing the subtalar
joint. Shoe orthotics, ankle-foot orthoses, nonsteroidal
anti-inflammatory agents, and activity restriction may be tried as a
first line of treatment. If these fail, a period of cast immobilization
with a short-leg walking cast for 3 to 6 weeks should be tried. If
symptoms recur or are not alleviated by conservative measures, surgical
excision is indicated. The most commonly used surgical technique is
wide excision of the bar and interposition of either extensor digitorum
brevis tendons or fat. Patients are immobilized in a cast for about 7
to 10 days, followed by range of motion exercise and protected weight
bearing. Full weight bearing is allowed in 4 to 6 weeks. The main
indication for surgery is pain relief, not restoration of joint motion,
although with calcaneonavicular bar excisions, restoration and
maintenance of joint motion can be expected if the patient does not
have secondary degenerative joint disease changes. If symptoms persist
and secondary degenerative joint disease is present in the adjacent
joints, triple arthrodesis remains the only option for relief of the
patient’s symptoms. Success rates of surgery in calcaneonavicular
coalitions are best in young patients

with
cartilaginous bars and no evidence of degenerative joint disease at the
talonavicular joint. Talar beaking is not a contraindication for
surgery because it does not necessarily represent degenerative changes.

The treatment of talocalcaneal coalitions is somewhat
more difficult. Usual treatment should center around nonoperative
measures as indicated previously for calcaneonavicular coalitions. If
these nonoperative measures fail to provide lasting relief of the
patient’s symptoms, resection of the coalition with interposition of
fat or bone wax should be considered. Specific criteria for
resectability of these coalitions are lacking. Long-term series with
large numbers of patients are unavailable. Contraindications to
resection, however, are an extensive coalition and degenerative joint
disease at the adjacent joints. In these circumstances, subtalar fusion
or triple arthrodesis should be considered. The most common cause of
failure in surgical management of tarsal coalitions is incomplete
resection.

Congenital vertical talus is a rare deformity of the
foot. It is characterized by a rigid flatfoot deformity, with the
plantar aspect of the foot having a convex contour. The heel is in
valgus, and the forefoot is abducted (see Figure 20-12). This entity has also been called congenital convex pes planus, congenital convex pes valgus, and congenital flatfoot with talonavicular dislocation. All these terms are descriptive either of the clinical or radiographic appearance of the foot.

Congenital vertical talus rarely exists alone. It is
usually associated with other congenital abnormalities, musculoskeletal
defects, or disorders of the central nervous system. There is a high
incidence of congenital vertical talus in children with
myelomeningocele (10% having congenital vertical talus), congenital hip
dysplasia, and several trisomies (13 to 15%, 18%). This entity is more
common in boys than girls, and there appears to be a familial tendency.
It may be bilateral, but if unilateral, it may be associated with a
pathologic condition of the opposite foot, including clubfoot,
metatarsus adductus, or calcaneal valgus deformity.

Clinically, the condition can be diagnosed at birth. The
involved foot is usually smaller than the opposite side with decreased
circumference of the calf. In the newborn, the dorsal aspect of the
foot may be in close approximation to the distal aspect of the tibia,
similar to the foot position in the calcaneal valgus deformity. Unlike
calcaneal valgus, however, this position is rigid, and the foot cannot
be flexed in a plantar direction. The sole of the foot has a convex
appearance, the rocker-bottom deformity. The hindfoot is in the
equinovalgus position with the Achilles tendon contracted. The forefoot
is in the abducted dorsiflexed position. The head of the talus is
easily palpable on the plantar medial aspect of the foot at the apex of
the foot convexity. The deformity is rigid; it cannot be manipulated
into the normal position. The head of the talus is covered
dorsolaterally by the displaced navicular. Attempts at manipulation
fail to reduce the talonavicular joint. The clinical appearance may
mimic a hypermobile flatfoot or calcaneal valgus deformity. In both
these conditions, however, normal relations, particularly the
talonavicular relation, can be restored by plantar flexion.

AP and simulated standing or standing lateral
radiographs should be obtained. Standing or simulated standing lateral
radiographs reveal the calcaneus to be in equinus and talus to be
vertically oriented parallel to the long axis of the tibia (see Figure 20-13).
Because of the extreme plantar flexion of the talus, only the posterior
aspect of dome articulates with the distal aspect of the tibia. In
children younger than 3 to 5 years of age, the navicular is not
ossified, and hence the talonavicular dislocation can only be inferred
by noting that the forefoot is displaced dorsally in relation to the
talus. Occasionally, a concave depression may be noted on the talar
neck induced by the dorsolateral subluxation of the navicular. Once the
navicular is ossified, the talonavicular dislocation is easily
demonstrated. Radiographs may also demonstrate disruption of the
calcaneocuboid joint with dorsolateral displacement of the cuboid. The
diagnosis can be confirmed radiographically by a forced plantar flexion
lateral view.

In congenital vertical talus, the normal bony relations
are not restored on the plantar flexion lateral view. The long axis of
the talus is plantar to the cuboid, as opposed to dorsal, and the long
axis of the metatarsals cannot be brought into collinear alignment with
the long axis of the talus (see Figure 20-13).

Pathoanatomic studies of a few specimens of congenital
vertical talus confirm the anatomic distortions evident by the clinical
and radiographic presentation. The specimens reported are similar in
their clinical features, all demonstrating hindfoot valgus, equinus
deformity, and the dorsolateral subluxation of the navicular on the
talus. The talus itself may be hypoplastic with a facet joint on the
dorsal neck at the point of articulation with the

navicular.
The sustentaculum talus is hypoplastic and the anterior facet joint
absent. The peroneal and posterior tibialis tendons are displaced
dorsally, resulting in muscle imbalance. The cause of this condition is
unknown.

The natural history of congenital vertical talus depends
not only on the foot deformity but also on any associated
musculoskeletal or central nervous system disorder. In general, without
treatment the ambulatory patient develops significant callosities over
the head of the talus. This results in pain and skin breakdown over the
talar head. The gait of these children is awkward, and shoeing may be a
significant problem.

The treatment of congenital vertical talus depends on
whether associated conditions are present. In the isolated deformity,
surgical correction is almost always necessary. The foot should be
manipulated to try to stretch the dorsolateral soft tissues. The
manipulations are followed by casting with a long-leg cast changed at
weekly intervals. The purpose of the manipulation and casting is to
stretch the dorsolateral constricted soft tissues to minimize surgical
complications, particularly skin necrosis. Manipulation and casting
should be begun immediately at birth and continued for 6 to 10 weeks.
Surgical correction is then performed either as a single or multistage
procedure. The surgical correction involves lengthening the contracted
dorsolateral structures, reducing the talonavicular or calcaneocuboid
(or both) joint subluxations, and correcting of the equinus deformity
through a posterior capsulotomy of the ankle and subtalar joint and
Achilles tendon lengthening. Reinforcement of the soft tissue
structures on the plantar aspect of the navicular by use of the
posterior tibial tendon is generally indicated (see Figure 20-14).
In older children (over 2.5 years of age), surgical correction is often
accompanied by an extra-articular subtalar arthrodesis at the time of
surgical correction or as an adjunctive procedure at a later time.
Surgical corrections are aimed at restoring normal bony alignment and
muscle balance. Complication rates of surgery are high and include
aseptic necrosis of the talus, loss of reduction, and stiffness,
particularly of the subtalar joint. Success rates are better in
children treated surgically when younger than 1 year of age. Tendon
transfers may be needed at a later date to restore muscle balance. In
the adolescent or adult with untreated or recurrent congenital vertical
talus, triple arthrodesis may be the only way to restore normal bony
alignment.

Calcaneal valgus (pes calcaneal valgus, talipes
calcaneal valgus, congenital talipes calcaneal valgus) is one of the
most common foot deformities seen at birth. The entire foot is held in
the dorsiflexed everted position, and in its most severe form, the foot
lies adjacent to the anterior border of the tibia (Figure 20-24).
Calcaneal valgus is thought to be secondary to intrauterine molding. It
is most common in firstborn children and in children of young mothers.
It has a female predominance of 1:0.6 and is estimated to occur in 1 of
every 1,000 live births.

Clinically, the foot is held in dorsiflexion near the
tibia with the forefoot in varying degrees of abduction and the heel in
varying degrees of valgus. The peroneal tendons may be subluxated
anterior to the lateral malleolus. The soft tissues on the dorsal and
lateral aspect of the foot are contracted and restrict plantar flexion
and inversion. There may be

a
transverse crease just distal to the ankle joint on the dorsal aspect
of the foot. The foot can generally be manipulated to neutral or just
short of the neutral position and, occasionally in mild cases, just
beyond this position (Figure 20-25).
The deformity may be accompanied by a mild abduction of the forefoot in
varying degrees of heel valgus. There is an occasional association of
this deformity with external rotation contractures in the hip and with
other conditions thought to be secondary to intrauterine molding
deformities (e.g., congenital hip dysplasia and torticollis).

It is important to rule out neuromuscular causes of
calcaneal valgus deformity, such as myelomeningocele and
arthrogryposis, as well as congenital vertical talus. In congenital
vertical talus, the Achilles tendon is contracted, the hindfoot is in
equinus, and there is a rocker-bottom deformity. Half the cases of
vertical talus are associated with a neuromuscular deformity. All cases
of posteromedial bowing of the tibia are associated with a calcaneal
valgus deformity of the foot.

Radiographs are not necessary to make the diagnosis of
pes calcaneal valgus. The foot can be palpated to show normal alignment
with no subluxation at the talonavicular joint. Radiographs are only
necessary when the diagnosis is in question. It is important to
stimulate the foot to make certain that the plantar flexors are present.

The natural history of pes calcaneal valgus is one of
spontaneous correction. Persistence of some of the deformity may lead
to a flexible flatfoot. Casting is rarely necessary. Treatment should
be directed at instructing the parents in stretching exercises. The
foot should be gently manipulated into plantar flexion and inversion.
In general, the deformity is corrected by 2 to 4 months of age. If it
is persistent, however, manipulation and casting can be considered.

Köhler disease is an osteochondrosis that affects the
tarsal navicular. It is a self-limited condition characterized by pain
or swelling in the area of the tarsal navicular in association with
certain radiographic features. It occurs in the age range of 4 to 7
years, with 80% of cases occurring in boys. One-fourth to one-third of
cases are bilateral.

The cause of Köhler disease is unknown, but it is
thought to be related to repetitive trauma and interruption of blood
supply to the tarsal navicular. The tarsal navicular is the last bone
of the foot to ossify. The appearance of the ossification center varies
and is gender related. In girls, the tarsal navicular ossifies between
18 months and 2 years of age. In boys, the ossification occurs between
2.5 and 3 years of age. The normal ossification center has a smooth
contour and uniform density. In otherwise normal children who have
delay in appearance of the ossification center of the navicular,
however, it may appear flat or fragmented with multiple ossification
centers of increased density and irregular contour. Several
ossification centers may eventually coalesce to form the navicular.
Postmortem studies of the navicular in children reveal that the blood
supply is tenuous, being supplied by only a single vessel until age 6
years.

Köhler disease is more common in patients (male or
female) in whom ossification is delayed. The pathogenesis may be
secondary to traumatic interruption of the vasculature to the tarsal
navicular at a crucial stage in ossification.

Clinically, children present to the physician with
complaints of pain and tenderness to palpation over the tarsal
navicular. Localized swelling is occasionally evident. There may be
palpable thickening of the soft tissues around the tarsal navicular.
Many affected children walk with an antalgic gait and bear

weight
on the lateral aspect of the foot to avoid pressure over the medial
aspect and the tarsal navicular. Active and passive range of motion are
normal.

Radiographically, the navicular shows evidence of flattening, sclerosis, and irregular ossification (Figure 20-26).
On the standing lateral view, the navicular has a decreased AP diameter
with evidence of varying amounts of flattening. Multiple centers of
ossification may be present. As mentioned previously, these
radiographic features may be a normal variation in as many as one-third
of children, particularly those who have late-onset ossification.
Therefore, the diagnosis of Köhler disease is made only with the
combination of the clinical signs, symptoms, and the radiographic
features.

Children with clinical Köhler disease may have similar
radiographic changes in the opposite navicular and be totally
asymptomatic. In the normal child, the radiographic appearance is
assumed to be secondary to coalescence of multiple ossification
centers, while in the child with Köhler disease, the radiographic
features represent the changes of avascular necrosis, with invasion by
granulation tissue, resorption of necrotic trabeculae, and deposition
of new bone.

The natural history of Köhler disease is relatively
benign. No long-term disabilities have been reported in patients who
have Köhler disease despite lack of treatment. In most cases, the
navicular assumes a relatively normal appearance within 1 to 3 years
after symptom onset.

Treatment of the condition is designed to relieve
symptoms and not to hasten the reparative process. Treatment for Köhler
disease is nonsurgical and depends on the magnitude of symptoms. In
patients with mild symptoms, restriction of activities may be all that
is necessary. In children with more severe symptoms, a longitudinal
arch support can be considered to more evenly distribute the patient’s
body weight in weight bearing. These measures, in conjunction with
avoidance of strenuous activities such as jumping and running, usually
relieve symptoms. In patients with more severe symptoms, immobilization
in a short-leg cast for 3 to 4 weeks usually provides good relief of
symptoms. The patient may need to use crutches with touch weight
bearing for a short time but then may bear full weight on the cast as
long as symptoms do not recur. Cast treatment should be continued until
the patient is asymptomatic. In severe cases, the use of a short-leg
walking cast improves the natural history of symptoms dramatically but
has no effect on the radiographic course of the disease. Without
treatment, most patients have intermittent symptoms for 1 to 3 years
that is activity related and relieved by rest.

Freiberg infarction is another type of osteochondrosis.
Specifically, it is an aseptic necrosis of the metatarsal head.
Three-fourths of cases occur in girls, and the second metatarsal head
is the most commonly involved, although the disease may affect the
third or fourth metatarsal head. Freiberg disease rarely occurs before
the age of 13 or 14 years.

The origin of Freiberg infarction is unknown, but it is
thought to be similar to that of osteochondritis dissecans of the knee.
The second metatarsal is the longest and the most rigid metatarsal. It
is subjected to the greatest amount of stress in walking. Freiberg
infarction is sometimes seen with an accompanying stress fracture of
the metatarsal.

Clinically, patients present with pain and tenderness
around the second metatarsophalangeal joint. They may complain of
stiffness and have a limp secondary to the pain. On physical
examination, the discomfort is well localized. There may be palpable
swelling at the second metatarsophalangeal joint. Pain may be elicited
on passive range of motion.

Motion
may be limited and painful. The history may be one of exacerbations and
remissions, with pain aggravated by activity and relieved by rest.

Radiographically, the second metatarsal head may have a
flattened, enlarged appearance with areas of increased sclerosis and
fragmentation. The affected metatarsophalangeal joint may be narrowed,
and in long-standing disease, secondary degenerative changes may be
evident (Figure 20-27).

The natural history of Freiberg infarction is variable.
In many cases, the condition is self-limited, with revascularization of
the affected metatarsal head. The disease process may leave the
metatarsal head deformed. Many patients have no pain or discomfort and
good range of motion. In some cases, however, the disease course
involves exacerbations and remissions. Significant deformity may ensue,
and secondary degenerative changes may occur at the metatarsophalangeal
joint.

The goal of treatment is to obtain healing of the
aseptic necrosis. Initial treatment should be symptomatic. Symptomatic
treatment includes decreasing activities and using metatarsal pads
inserted in the shoe or metatarsal bars on the sole of the shoe. These
two measures are designed to allow for weight bearing on the metatarsal
neck as opposed to the metatarsal head to decrease the stresses applied
to the metatarsal head. In patients who have more acute symptoms, a
short-leg walking cast with or without crutches may provide relief. If
the joint is free of degenerative changes and symptoms persist, removal
of the necrotic fragment alone may provide symptomatic relief. A foot
orthosis designed to provide pressure relief over the second metatarsal
head may be used on a long-term basis once the acute symptoms have
subsided or after surgical removal of the necrotic segment. Mild
symptoms may be treated by an orthosis alone.

In patients with long-standing symptoms who fail
nonoperative treatment, surgical treatment may be offered. This may
include removal of the loose fragment and resection of the base of the
proximal phalanx. Alternatively, resection of the metatarsophalangeal
joint may be required, with syndactylization of the second and third
toe to avoid significant shortening that may follow resection of the
metatarsophalangeal joint. This usually provides good relief of
symptoms.

Sever disease, or calcaneal apophysitis, is one of the
most common overuse syndromes seen in growing children. It most
commonly occurs in the age range of 6 to 12 years and is thought to be
due to repeated microtrauma. Most affected children are extremely
active. This condition may thus represent chronic strain at the
insertion of the tendo Achilles.

Affected children present with activity-related pain
over the posterior aspect of the calcaneus. Physical examination
reveals tenderness to compression over the calcaneal apophysis.
Symptoms may cause discomfort with passive ankle dorsiflexion. The
condition must be differentiated from other sources of heel pain in
young children (Table 20-1).

In normal children, the calcaneal apophysis appears at an average of 5.6 years of age in girls (range,

3 to 8.5 years) and 7.9 years of age in boys (range, 6 to 10 years). In
many normal children, the calcaneal apophysis may appear fragmented and
then coalesce from two to three separate ossification centers. This
normal ossification variant, in combination with symptomatology, is
considered diagnostic of Sever disease (Figure 20-28).
If patients have bilateral symptoms, radiographs are often not
necessary. In unilateral cases, however, radiographs of both feet
should be obtained to rule out other causes of heel pain, such as
retrocalcaneal bursitis, stress fractures, infection, rheumatologic
conditions, and neoplastic lesions.

Sever disease is a self-limiting condition. In cases of
severe symptoms, activity restriction may be necessary. If this alone
does not relieve symptoms or if symptoms are acute, a short-leg walking
cast may be applied for 3 to 4 weeks. This usually is adequate to
curtail symptoms. Longer periods of casting or activity restriction of
up to 1 to 3 months may be necessary in some cases. No long-term
disability or deformity has been reported from Sever disease.

A wide variety of terms are used to describe this clinical entity, including metatarsus
adductus, metatarsus varus, skew foot, serpentine foot, pes adductus,
metatarsus adductovarus, hooked forefoot, metatarsus internus, and congenital metatarsus varus.
These terms unfortunately are used inconsistently throughout the
medical literature. The two most widely used terms are metatarsus
adductus and metatarsus varus, which describe slightly different
forefoot variations but are synonymous. In this condition, the forefoot
is generally adducted and occasionally inverted (varus) at the
tarsometatarsal joint, and the hindfoot is generally neutral to valgus (Figure 20-29; see Figure 20-19).
Metatarsus adductus is present at birth but often is overlooked by the
family until the child is between 3 months and 1 year of age.

Metatarsus adductus is the most common congenital foot
deformity. Its incidence is 1 in 1,000 live births. It has a female
predominance of 4:3 and a 5% incidence of the condition in first-degree
relatives. There is no known pattern of inheritance, but the risk of a
second sibling being affected is 1 in 20. Two-thirds of patients have
involvement of both feet. There is a strong association between
metatarsus adductus and congenital hip dysplasia and dislocation.

The cause of metatarsus adductus is unknown. It is
thought to be secondary to intrauterine molding because 59% of patients
are firstborn children. Other etiologic theories include peroneal
muscle weakness with overactive anterior tibialis and posterior
tibialis; abnormal insertion of the tibialis posterior tendons on the
first cuneiform rather than their usual site on the navicular; and
posture habits caused by prone, sleeping with the buttocks elevated,

hips
and knees in complete flexion, feet adducted and tucked beneath the
buttocks, and sitting on the adducted feet. Persistent soft tissue
contractures may lead to secondary tarsal changes, making the deformity
rigid with time.

Clinically, the deformity is present at birth but
usually not noticed by the parents until the child begins to crawl or
walk. Occasionally, patients present to a physician in the toddler
years when the parents complain of the child in-toeing or having
difficulty wearing shoes. On physical examination, all the metatarsals
are adducted and the forefoot is occasionally in varus (see Figure 20-29).
The heel is in neutral to slight valgus. The great toe is often widely
separated from the second toe, and the base of the fifth metatarsal and
the cuboid are prominent on the lateral aspect of the foot. The medial
border of the foot is concave, and the lateral border is convex. Medial
tibial torsion often accompanies metatarsus adductus. The Achilles
tendon is not tight, and the foot can be fully dorsiflexed at the ankle
joint. The deformity is often accentuated by overactivity in the
abductor hallucis and the short toe flexors.

The deformity is often classified subjectively as mild,
moderate, or severe, depending on whether the forefoot can be passively
corrected to neutral or to an overcorrected position. Severe
deformities are rigid and not passively correctable. The ratio of
supple to rigid deformity is about 10:1. The term serpentine foot is often used for a rigid adducted forefoot with an accompanying heel valgus.

The heel bisector should pass through the second toe. In
a mild deformity, the bisector passes through the third toe; in a
moderate deformity, it passes between the third and fourth toes or just
the fourth toe; and in a severe deformity, the heel bisector passes
between the fourth and fifth toes. The deformity is said to be flexible
or passively correctable if the forefoot (second toe) can be passively
abducted beyond the heel bisector (see Figure 20-29).
Many patients exhibit dynamic hallux varus, whereby the great toe
deviates medially during stance phase but the metatarsals are normally
aligned.

Radiographs are not required to make the diagnosis of
metatarsus adductus. Radiographs can, however, document deformity and
are used by some to classify the deformity. Radiographs, if taken,
should be in the standing position or with the foot resting in a
simulated standing position on the radiograph cassette. Radiographs
demonstrate sharp medial angulation of the tarsometatarsal joints, with
the first metatarsal being more severely adducted than the fifth (see Figure 20-19).
Normally, a line drawn through the longitudinal axis of the first
metatarsal is parallel or diverges laterally from a line drawn through
the longitudinal axis of the talus. In metatarsus adductus, the first
metatarsal line falls medial to the talar line. In the weight-bearing
or simulated weight-bearing film, the calcaneal line should bisect the
cuboid and the base of the fourth metatarsal. In metatarsus adductus,
the calcaneal line passes through the lateral portion of the cuboid and
through the base of the fifth metatarsal. Heel valgus is evidenced by a
greater than 35° AP talocalcaneal angle and by medial and forward
displacement of the head of the talus in relation to the anterior
portion of the calcaneus. The navicular

(generally not seen on radiographs in this age group) is neutral or displaced laterally on the talar head (see Figure 20-19).

The natural history of metatarsus adductus is generally
benign. It is estimated that 85 to 90% of cases resolve spontaneously
without treatment. In childhood, persistent metatarsus adductus leads
to an in-toeing gait and occasional complaints of stumbling or
tripping. Adults with uncorrected metatarsus adductus rarely complain
of pain but may have hallux valgus and bunions. Shoe wear may be a
problem in patients with uncorrected metatarsus adductus. Patients may
complain of pain in the lateral foot and in the tarsometatarsal joints.
Shoes may irritate this area. It is thus important in infancy to select
patients who require treatment.

Treatment decisions for metatarsus adductus are based on
the passive correctability of the deformity. In patients in whom the
deformity corrects by stimulation of the lateral border of the foot or
in those in whom the heel is stabilized, the deformity can be passively
corrected or overcorrected, and only observation is necessary. Most
cases correct spontaneously. In most large series, if the foot remained
passively correctable, the deformity had corrected spontaneously by the
age of 3 years. Parents should not be encouraged to do manipulations.
Manipulations by parents are generally poorly done and may accentuate
heel valgus and only minimally correct forefoot adduction. There is no
scientific validity for the use of straight-last or reverse-last shoes
in the treatment of metatarsus adductus. Denis Browne splints should
not be used because they may accentuate heel valgus.

In patients with rigid, severe, nonpassively correctable
metatarsus adductus, manipulation and casting are indicated. Two main
components of the deformity, adduction of the metatarsals and varying
degrees of valgus of the heel, must be corrected simultaneously.
Improper manipulation and casting treatment of metatarsus adductus lead
to a pronation deformity of the foot. A flatfoot with residuals of
metatarsus adductus and severe heel valgus is a significantly worse
problem than the original deformity.

The hindfoot deformity is corrected by supinating the
calcaneus underneath the talus. With the calcaneus supinated, the
cuneiform, navicular, and cuboid bones are inverted, bringing the bases
of the metatarsals in proper alignment with the talus and calcaneus
(see Figure 20-19). The metatarsals are then
abducted, with counterpressure applied over the cuboid bone. It is
important not to pronate the forefoot because a cavus deformity will
result. The manipulations of the foot are sustained for several
minutes, and this is followed by the application of a thinly padded,
well-molded, toe-to-groin plaster cast changed at biweekly intervals
until the foot is in the slightly overcorrected position. Complete
correction usually requires 3 to 4 long-leg plaster applications. The
casting treatment is complete when the lateral aspect of the foot is no
longer convex, the heel is in a neutral to slight valgus position, and
the forefoot has been completely corrected past neutral. Successful
treatment of metatarsus adductus by manipulations and casting in
patients older than 8 months of age is not likely, and surgical
correction may be necessary.

Surgical correction for metatarsus adductus is indicated
only in patients with significant cosmetic or shoe-wearing problems. In
patients younger than 2 years of age with rigid metatarsus adductus,
first metatarsal cuneiform capsulotomy and release of the abductor
hallucis, followed by casting, is usually successful. In older
children, corrective bone surgery may be necessary.

Talipes equinovarus is the term most commonly used for clubfeet. Talipes is a generic term for any foot deformity that centers around the talus. Equinus implies that the foot is flexed in the plantar direction. The term talipes equinocavovarus
is sometimes used to denote the varying amounts of cavus of the
forefoot evident in patients with clubfeet. In the clubfoot, the heel
is in varus, and the first metatarsal is in severe plantar flexion,
while the fifth metatarsal is normally aligned with the cuboid and
calcaneus (Figures 20-30 and 20-31; see Figure 20-19). Cavus is caused by eversion of the forefoot in relation to the hindfoot.

Clubfoot is a complex foot deformity that is readily
apparent at birth. All clubfeet are not of the same severity, although
all have the basic components of adduction and inversion of the
forefoot and midfoot, heel varus, and fixed equinus. The soft tissue
changes vary from mild to severe. Clubfoot should best be thought of as
a spectrum of deformities. Clubfoot may occur as an isolated disorder
or in combination with various syndromes and other associated
anomalies, such as arthrogryposis, sacral agenesis, amniotic bands,
Larsen syndrome, diastrophic dwarfism, Freeman-Sheldon syndrome, and
myelodysplasia.

The incidence of idiopathic clubfoot is estimated to be
1 to 2 per 1,000 live births. It has a male predominance of 2:1 and an
incidence of bilateralness estimated to be about 50%. There is an
increased incidence in certain racial and ethnic groups, such as
Polynesians, Maoris, and South African blacks, with a much higher
incidence if the patient has a positive family history for clubfoot.

The origin of congenital clubfoot in otherwise normal
patients remains unknown. Many theories have been advanced, including
intrauterine molding defect, blastemic defect of the tarsal cartilage,
primary nerve lesion with secondary muscle dysfunction, vascular
abnormalities, arrested embryonic development, abnormal tendon
insertions, and primary fibrotic contracture. The most widely accepted
theory is that of polygenic inheritance modified by environmental
factors.

Clinically, the deformity is readily apparent at birth.
The child presents with the foot in severe supination with a fixed
equinus deformity, heel varus, forefoot and midfoot adduction, and
varying amounts of cavus. The involved foot is generally smaller than
the opposite side with varying amounts of calf atrophy.

The head of the talus is prominent and easily palpable
on the dorsolateral aspect of the foot. Depending on the severity of
the cavus deformity, there may be a deep skin crease across the plantar
medial aspect of the midfoot. The foot cannot be passively manipulated
into the neutral position.

Radiographs are often useful in documenting the
deformity. The calcaneus, talus, and cuboid are usually ossified at
birth. The navicular does not ossify until about 3 years of age. The
normal values of

bony relations on standing AP and lateral views of the foot are somewhat variable and age dependent (Figure 20-32).

Radiographs are useful in documenting the deformity
(photographs are also useful for this purpose), for follow-up, in
assessing the results of nonoperative treatment, and in planning for
operative correction of the deformity if necessary. It is best to
obtain the initial radiographs in the maximally corrected position.
This position varies depending on the flexibility of the individual
clubfoot.

In the clubfoot deformity, the talus and calcaneus
exhibit parallelism on both the AP and lateral radiographs, indicating
hindfoot varus and equinus (see Figure 20-31).
The talus first metatarsal angle is negative, indicating adduction of
the forefoot. Because of the inversion of the forefoot, the metatarsals
appear overlapped. The cuboid is medially displaced on the AP view,
indicating the adduction at the midfoot; and on the lateral view, the
first metatarsal is in plantar flexion to a greater degree than the
fifth metatarsal, indicating cavus deformity.

Pathoanatomically, many specimens of clubfeet have been described, all showing varying degrees of similar abnormalities (see Figure 20-31).
In the clubfoot, the talar body is in plantar flexion with the neck
angulated medially. The navicular articulates with the medial aspect of
the talar neck, and the navicular tuberosity is in close approximation
with the medial malleolus. The calcaneus is directly underneath the
talus, and the cuboid is medially displaced beneath the navicular. The
midfoot is thus adducted and inverted in relation to the talus. The
dorsal tendons are medially displaced, and the head of the talus is
prominent laterally.

Anatomically, the involved talus is generally smaller
than the noninvolved side, with the neck in varying degrees of medial
deviation. The navicular is wedged-shaped laterally, with a prominent
tuberosity. The calcaneus is small, often with an absent anterior
facet. The posterior facet shows varying degrees of hypoplasia and may
be linked directly to the middle facet. In unilateral deformities, the
foot is always smaller than the noninvolved side, and the calf has
varying degrees of atrophy. The tuberosity of the navicular is held in
close approximation to the talar neck, the sustentaculum and the medial
malleolus by the shortened, thickened tibionavicular ligament,
calcaneonavicular ligament, and sheath of the posterior tibial tendon.

Clubfoot deformity, regardless of origin or associated
clinical problems, results in a severe handicap unless corrected. The
surface area for weight bearing is the lateral aspect of the foot;
without treatment, even an otherwise normal patient develops pressure
sores and sinuses by the fourth or fifth decade of life (Figure 20-33).

The criteria for successful treatment of a clubfoot
deformity vary in the orthopaedic literature. Some judge success only
by radiographic criteria, others by function, and others by certain
clinical criteria. Thus, the literature on treatment is difficult to
compare.

The goal of treatment in clubfoot deformity is to obtain
and maintain the foot in plantargrade position. Treatment should be
initiated immediately on diagnosis, preferably within the first week of
life. Treatment for the newborn with clubfoot is by manipulation and
then casting to maintain the correction obtained through manipulation.
Corrections begun at a later age may be more difficult owing to
ligamentous contracture and joint deformity. Toe-to-groin plaster casts
are used to maintain the corrections obtained through manipulation. The
equinus deformity is the last deformity corrected to prevent
development of a rocker-bottom foot. Casts are changed at weekly
intervals, and most deformities are corrected in 5 to 7 casts.
Successful treatment rates by casting regimens alone vary in the
literature from 85 to 95%. Night splinting is often used for prolonged
periods (several years) to maintain correction.

Depending on the initial severity, clubfeet have a
natural tendency to recur. The more severe and rigid the initial
deformity, the greater the risk of recurrence. Recurrences may be
treated by serial manipulations and casting followed by occasional
tendon transfers to correct for any muscle imbalance.

The small percentage of deformities that fail to respond
to manipulation and casting or that recur may require extensive
posterior, medial, and lateral soft tissue releases. The releases are
best done at a young age but can be done satisfactorily in children
until 5 years of age.

In children older than 3 years of age, lateral column
shortening procedures (decancellation of the cuboid or wedge resection
of the cuboid in excision of the anterior end of the calcaneus) are
often performed in conjunction with posteromedial releases. This is
because the greater length of the lateral foot column compared with the
medial foot column is thought to be secondary to the medial soft tissue
contractures.

The major complications of the extensive posterior,
medial, subtalar, and lateral releases performed for residual,
resistant, or recurrent clubfoot include skin sloughing on
posteromedial aspect of the foot, overcorrection of the deformity,
residual forefoot adductus, stiffness, and incomplete correction of the
deformity.

Triple arthrodesis may be necessary for recurrent or
persistent clubfoot deformity in older children. These procedures are
best offered to the patient at 10 to 12 years of age, when foot growth
is complete.

This entity is also called habitual toe-walking, hereditary tendo Achilles contracture, or congenital short tendo calcaneus.
Parents notice that the child is walking on the toes either all or most
of the time. Idiopathic toe-walking is thought to be an inherited
condition because up to 70% of patients have a positive family history.
The condition is bilateral and predominantly affects boys (3:1). About
20% of these children have evidence of a learning disability, and an
occasional child carries the diagnosis of hyperkinesia with minimal
brain dysfunction.

When a child begins to stand and walk, toe-walking is a
normal gait variation. Generally, within the first 6 months after
walking, the gait may progress from the toe-toe gait or an occasional
toe-toe gait to a toe-heel gait and eventually to a heel-toe gait. The
mature heel-toe gait pattern is generally established by the time a
child is 3 years of age. Careful history of gait development should be
obtained in each patient who presents with a chief complaint of
toe-walking. Patients with the diagnosis of idiopathic toe-walking have
nearly always walked on their toes.

Physical examination includes range of motion of the
upper and lower extremities as well as a careful neurologic examination
and observation of the patient’s gait. Variable amounts of contracture
and restriction of ankle dorsiflexion are noted. The amount of
contracture or restriction of motion may not be symmetric. These
patients have normal sensory examinations and no evidence of muscle
weakness. Deep tendon reflexes should be intact

without
evidence of hyperactivity. The spine should be evaluated for evidence
of hair patches, dimpling, hyperpigmentation, or nevi, which are
suggestive of spinal dysraphism. There should be minimal or no
contracture of the hamstrings, and the patient should have good control
of the upper extremities.

The child’s gait should be carefully evaluated. Many
patients with idiopathic toe-walking can walk on their heels and have a
heel-toe gait periodically, but the observed gait pattern usually is
toe-toe. Idiopathic toe-walkers with heel cord contractures can
generally get their heels down in standing only through knee
hyperextension (Figure 20-34).

Idiopathic toe-walking is the diagnosis of exclusion.
All conditions that may be associated with an equinus deformity and
contracture of the tendo Achilles must be ruled out. Cerebral palsy can
be ruled out by the absence of increased deep tendon reflexes,
hypertonicity, hamstring contractures, and the lack of posturing
abnormalities of the upper extremity during gait. Gait analysis may be
of help in differentiating the idiopathic toe-walker from the cerebral
palsy patient. Other conditions, such as spinal dysraphism, muscular
dystrophy, tethered spinal cord, or other central nervous system
dysfunctions, must be ruled out. Electromyographs, motor nerve
conduction studies, spine films, CT scan of the brain, or MRI may be
necessary. Muscle biopsy to rule out muscular dystrophy is also
warranted on occasion. Any child with a unilateral deformity,
particularly of recent onset, should have an etiologic source sought. A
neurologic consultation is often in order.

The typical patient with idiopathic toe-walking has no
abnormal findings other than those referable to the equinus deformity
with varying degrees of contracture of the Achilles tendon. They have
normal sensation, no pain, and no muscle dysfunction.

Treatment of the condition varies according to the age
of the patient and the degree of contracture of the Achilles tendon. In
patients who are younger than 3 to 4 years of age and have no or
minimal contracture of the Achilles tendon, passive range of motion and
stretching exercises are indicated. The child’s progress should be
monitored carefully. If ankle dorsiflexion to at least 10° cannot be
restored by this method in 3 to 4 months, serial casts should be
applied. If, however, the ankle can be passively dorsiflexed to neutral
or beyond, but the child habitually toe-walks, use of a hinged or
nonhinged ankle foot orthosis is an option to prevent plantar flexion.
These orthoses can be used for a period of weeks to months, depending
on the clinical situation. The patient should be continually
reevaluated and progress reassessed. In most cases, serial casting in
dorsiflexion for 4 to 6 weeks is usually sufficient to resolve the
problem. Many patients require postcasting ankle-foot orthoses, passive
range of motion, and careful follow-up to ensure that the condition
does not recur. In most cases, these noninvasive procedures provide
resolution of the problem. For the child who fails to respond to serial
casting or is otherwise not a candidate for this procedure, Achilles
tendon lengthening provides uniformly good results. Surgical Achilles
tendon lengthening is followed by 3 weeks in a nonweight-bearing
short-leg cast, then 3 weeks in a weight-bearing short-leg cast.
Recurrences after this procedure are rare.

The parents’ or grandparents’ perception of an abnormal
position of the legs of an infant or the way a child walks frequently
results in medical consultation.

Unfortunately, these concerns often result in unnecessary, costly treatment.

In the newborn, the proximal femur (femoral head, neck,
and trochanter) is usually anteverted about 40° in relation to the
transcondylar axis of the distal femur. The intermalleolar axis of the
distal tibia in relation to the interplateau axis of the proximal tibia
is in about 3° of lateral rotation. During the first year of life,
femoral anteversion decreases by about 8° and thereafter decreases by
about 1° per year until the adult configuration of about 10 to 15° of
anteversion is reached at maturity. Tibial version also increases
throughout life until the adult lateral version of 15 to 20° is reached
at maturity. Version of more than two standard deviations beyond the
mean is referred to as torsion.

Any child who is brought in for evaluation because the
parents perceive an abnormality should be carefully checked to see
whether the child is merely in the normal stages of development or has
a torsional problem. The most common torsional problems are femoral
antetorsion and medial tibial torsion. The normal values for version
vary according to the age of the patient (Figure 20-35).
The cause of the torsional problems is unknown but may be due to
persistent version or genetic factors. Postnatal sitting and sleeping
postures have been implicated as mechanisms that either cause torsional
abnormalities or contribute to their lack of resolution, but no
conclusive proof exists. Excessive ligament laxity on a genetic basis
has been thought by some investigators to contribute to persistent
femoral antetorsion in that many children with femoral antetorsion have
accompanying physiologic pes planus, genu recurvatum, and excessive
lumbar lordosis. The latter two may actually be compensatory measures
for femoral antetorsion.

Any child brought in by parents for complaints of
in-toeing should have a careful history and physical examination. The
history should include the age at which the parents first noted the
deformity, how they think it affects the child’s function, and any
perceived disability because of the deformity. Sleeping and sitting
postures should be assessed and a complete history of normal growth and
development obtained. The age at onset of walking should be evaluated.
Any delay in development of walking beyond 18 months of age may be
suggestive of a neuromuscular abnormality such as cerebral palsy. A
family history of similar problems should be sought.

Careful physical examination must include a complete
neurologic examination and a torsional profile of the patient. The most
common abnormalities seen are those of femoral antetorsion, medial
tibial torsion, and metatarsus adductus. Other conditions, such as an
overactive abductor hallucis, clubfoot deformity, or dynamic in-toeing
because of muscle imbalance, must be ruled out.

The parents may complain that the child’s problem is
worse at the end of the day or when tired, which may indicate failure
of compensatory mechanisms. The problem may be of great concern to
parents, who often scold the child for walking in a way that is more
comfortable because of the child’s rotational profile.

The child should be observed walking and running in an
unobstructed area. The position of the patella and the feet should be
noted. The physician should assess the foot progression angle. The foot
progression angle is the axis of the foot as the child walks along an
imaginary line of progression. This can be estimated or special paper
(footprint paper) can be used to assess the foot progression angle.
Negative foot progression angles designate in-toeing; positive foot
progression angles designating outtoeing. The normal foot progression
angle is usually positive.

Hip rotation should be assessed with the hip in
extension in the prone position. The knee is flexed to 90°, and
rotation is assessed medially and laterally in relation to the gluteal
cleft. The pelvis should be stabilized, and no force should be exerted
on the limb. Internal and external rotation are assessed and compared
with normal, age-matched values (Figures 20-36 and 20-37).

Tibial rotation is next assessed by use of either the thigh-foot or transmalleolar axis (Figure 20-38).
In most cases, the thigh-foot axis is sufficient. Tibial rotation can
be assessed in several ways. With the patient in the prone position and
the knees flexed to 90°, the thigh-foot axis can easily be assessed and
compared with normal, age-matched values. If the patient has a foot
deformity, the transmalleolar axis should be used. The transmalleolar
axis is assessed by placing the thumb and index finger on the medial
and lateral malleoli, respectively, to define the intermalleolar axis;
a perpendicular axis is then defined, and the angles between the
perpendicular and intermalleolar axis and the long axis of the thigh
are assessed. A simpler assessment of the intermalleolar axis is done
with the patient sitting with the legs hanging free over the table and
the knees at 90°. The thumb and index finger can be placed on the
medial and lateral malleoli, respectively, and the intermalleolar axis
can be assessed in relation to the tibial tubercle, determining the
degree of tibial rotation.

The patient’s feet should be examined for evidence of
metatarsus adductus and residual deformity secondary to previous
clubfoot treatment. The cause of the patient’s in-toeing gait may be
one or more abnormalities in the lower extremity. Occasionally, a
rotational profile of the parent may reveal a torsional problem that
explains the torsional problem in the child or lack of resolution of
the problem in the older child.

Radiographs or special studies are rarely necessary in
children with torsional problems. In the infant, congenital hip
dysplasia must be ruled out, and if clinical examination warrants,
radiographs may be necessary. Determination of version is best done by
CT or MRI with cuts through the axis of the femoral neck and the
femoral condyles. Torsion of the tibia is easily measured clinically,
and hence radiographs or special studies are rarely necessary.

The natural history of torsional problems is one of
gradual resolution, and hence treatment of these conditions is rarely
necessary. Treatment by devices such as corrective shoes, twister
cables, and alteration of sleeping or sitting habits have never been
shown to affect the natural history of these conditions and should
therefore be avoided. Education of the family regarding the natural
history of these conditions is important. The family should be
reassured that most torsional problems resolve spontaneously in the
course of normal growth. The parents should also be reassured that if
there is a positive family history of torsional problems, complete
resolution may not occur, but in most cases, no functional disability
ensues.

Infants and children before walking age may be brought
in by parents for complaints of the feet pointing out. Careful
examination of the hips should be done to rule out congenital hip
dysplasia. External rotation contractures are normal in the infant and
gradually resolve with time. Treatment is never indicated.

In a child who has not reached walking age comes in with
the parents complaining of one foot turning out, a careful hip
examination should be performed to rule out any associated congenital
hip dysplasia. In general, the out-turned foot is the more normal foot
because this condition usually coexists with metatarsus adductus or
medial tibial torsion on the opposite side. The natural history should
be explained to the parents and observation recommended.

In the prewalking years, the most common cause of
in-turning of the lower extremities is metatarsus adductus. Congenital
hip dysplasia must, however, be ruled out.

In the walking child between 1 and 3 years of age, the
most common cause of in-toeing is medial tibial torsion, which may or
may not be accompanied by metatarsus adductus. Reassurance and
observation is the treatment of choice.

In the older child, particularly after 3 years of age,
medial femoral torsion is a common cause of an in-toeing gait. Natural
history studies indicate that medial femoral torsion is not associated
with degenerative joint disease over the long term, and hence
observation is the only treatment warranted. Radiographs or special
studies are not indicated unless there is asymmetry.

Surgical treatment for medial tibial torsion or medial
femoral torsion is rarely indicated. Surgical correction can be
considered in cases of medial tibial torsion if the child is older than
8 years of age (when spontaneous correction is no longer possible),

if
the discrepancy is more than three to four standard deviations from the
mean, and if the deformity is causing the child significant functional
or cosmetic problems. Supramalleolar osteotomy is usually the treatment
of choice when surgical correction is contemplated.

Lateral tibial torsion is not an uncommon problem and
usually does not resolve with age. Lateral tibial torsion can be
considered for correction if it is greater than 30° and causes
significant functional or cosmetic deformity to the child (see Figure 20-37).

Medial femoral torsion can be considered for correction
if the child is older than 8 years of age and has more than three
standard deviations from the mean of torsional deformity (medial
rotation greater than 85°, lateral rotation less than 10°, or
anteversion greater than 50°). Consideration can be given for
correction either at the intertrochanteric level or the supracondylar
region; most surgeons prefer the intertrochanteric region. In
teenagers, closed intramedullary rotational osteotomy can be considered.

In a certain number of children with severe femoral
antetorsion, lateral tibial torsion compensates for the deformity.
Surgical treatment should be avoided because the rotational osteotomies
would need to be performed in the femur and the tibia, and subsequent
patellofemoral malalignment problems could ensue.