Scientific Basis of Management
Clubfoot is not an embryonic malformation. A normally developing foot turns into aclubfoot during the second trimester of pregnancy. Clubfoot is rarely detected with
ultrasonography before the 16th week of gestation. Therefore, like developmental
hip dysplasia and idiopathic scoliosis, clubfoot is a developmental deformation.
A 17-week-old male fetus with bilateral clubfoot, more severe on the left, is
shown [1]. A section in the frontal plane through the malleoli of the right clubfoot
[2] shows the deltoid, tibionavicular ligament, and the tibialis posterior tendon to
be very thick and to merge with the short plantar calcaneonavicular ligament. The
interosseous talocalcaneal ligament is normal.
A photomicrograph of the tibionavicular ligament [3] shows the collagen fibers to
be wavy and densely packed. The cells are very abundant, and many have spherical
nuclei (original magnification, x475).
The shape of the tarsal joints is altered relative to the altered positions of the
tarsal bones. The forefoot is in some pronation, causing the plantar arch to be more
concave (cavus). Increasing flexion of the metatarsal bones is present in a lateromedial
direction.
In the clubfoot, there appears to be excessive pull of the tibialis posterior abetted
by the gastrosoleus and the long toe flexors. These muscles are smaller in size
and shorter than in the normal foot. In the distal end of the gastrosoleus, there is an
increase of connective tissue rich in collagen, which tends to spread into the tendo
Achillis and the deep fasciae.
In the clubfoot, the ligaments of the posterior and medial aspect of the ankle and
tarsal joints are very thick and taut, thereby severely restraining the foot in equinus
and the navicular and calcaneus in adduction and inversion. The size of the leg
muscles correlates inversely with the severity of the deformity. In the most severe
clubfoot, the gastrosoleus is seen as a muscle of small size in the upper third of the
calf. Excessive collagen synthesis in the ligaments, tendons, and muscles may persist
until the child is 3 or 4 years of age and might be a cause of relapses.
Under the microscope, the bundles of collagen fibers display a wavy appearance
known as crimp. This crimp allows the ligaments to be stretched. Gentle stretching
of the ligaments in the infant causes no harm. The crimp reappears a few days later,
allowing for further stretching. That is why manual correction of the deformity is
feasible.
Kinematics
The clubfoot deformity occurs mostly in the tarsus. The tarsal bones, which are
mostly made of cartilage, are in the most extreme positions of flexion, adduction,
and inversion at birth. The talus is in severe plantar flexion, its neck is medially and
plantarly deflected, and its head is wedge-shaped. The navicular is severely medially
displaced, close to the medial malleolus, and articulates with the medial surface of
the head of the talus. The calcaneus is adducted and inverted under the talus.
As shown in a 3-day-old infant [4 opposite page], the navicular is medially
displaced and articulates only with the medial aspect of the head of the talus. The
cuneiforms are seen to the right of the navicular, and the cuboid is underneath it.
The calcaneocuboid joint is directed posteromedially. The anterior two-thirds of the
calcaneus is seen underneath the talus. The tendons of the tibialis anterior, extensor
hallucis longus, and extensor digitorum longus are medially displaced.
No single axis of motion (like a mitered hinge) exists on which to rotate the tarsus,
whether in a normal or a clubfoot. The tarsal joints are functionally interdependent.
The movement of each tarsal bone involves simultaneous shifts in the adjacent
bones. Joint motions are determined by the curvature of the joint surfaces and by the
orientation and structure of the binding ligaments. Each joint has its own specific
motion pattern. Therefore, correction of the extreme medial displacement and inversion
of the tarsal bones in the clubfoot necessitates a simultaneous gradual lateral
shift of the navicular, cuboid, and calcaneus before they can be everted into a neutral
position. These displacements are feasible because the taut tarsal ligaments can be
gradually stretched.
The correction of the severe displacements of the tarsal bones in clubfoot requires
a clear understanding of the functional anatomy of the tarsus. Unfortunately, most
orthopaedists treating clubfoot act on the wrong assumption that the subtalar and
Chopart joints have a fixed axis of rotation that runs obliquely from anteromedial
superior to posterolateral inferior, passing through the sinus tarsi. They believe that
by pronating the foot on this axis, the heel varus and foot supination can be corrected.
This is not so.
Pronating the clubfoot on this imaginary fixed axis tilts the forefoot into further
pronation, thereby increasing the cavus and pressing the adducted calcaneus against
the talus. The result is a breach in the hindfoot, leaving the heel varus uncorrected.
In the clubfoot [1], the anterior portion of the calcaneus lies beneath the head of
the talus. This position causes varus and equinus deformity of the heel. Attempts to
push the calcaneus into eversion without abducting it [2] will press the calcaneus
against the talus and will not correct the heel varus. Lateral displacement (abduction)
of the calcaneus to its normal relationship with the talus [3] will correct the
heel varus deformity of the clubfoot.
Correction of clubfoot is accomplished by abducting the foot in supination while
counterpressure is applied over the lateral aspect of the head of the talus to prevent
rotation of the talus in the ankle. A well-molded plaster cast maintains the foot in
an improved position. The ligaments should never be stretched beyond their natural
amount of give. After 5 days, the ligaments can be stretched again to further
improve the degree of correction of the deformity.
The bones and joints remodel with each cast change because of the inherent properties
of young connective tissue, cartilage, and bone, which respond to the changes
in the direction of mechanical stimuli. This has been beautifully demonstrated by
Pirani [5], comparing the clinical and magnetic resonance imaging appearance
before, during, and at the end of cast treatment. Note the changes in the talonavicular
joint and calcaneocuboid joint. Before treatment, the navicular (red outline) is
displaced to the medial side of the head of the talus (blue). Note how this relationship
normalizes during cast treatment. Similarly, the cuboid (green) becomes aligned
with the calcaneus (yellow) during the same cast treatment.
Before applying the last plaster cast, the tendo Achillis may have to be percutaneously
sectioned to achieve complete correction of the equinus. The tendo Achillis,
unlike the tarsal ligaments that are stretchable, is made of non-stretchable, thick,
tight collagen bundles with few cells. The last cast is left in place for 3 weeks while
the severed heel-cord tendon regenerates in the proper length with minimal scarring.
At that point, the tarsal joints have remodeled in the corrected positions.
In summary, most cases of clubfoot are corrected after five to six cast changes
and, in many cases, a tendo Achillis tenotomy. This technique results in feet that
are strong, flexible, and plantigrade. Maintenance of function without pain has been
demonstrated in a 35-year follow-up study.
