Orthopaedic Surgery - Clubfoot

Basics

Clubfoot, also known as talipes equinovarus, is a complex congenital deformity of the foot that is present at birth.

The deformity consists of three major components: equinus of the heel, varus with internal rotation of the hindfoot, and adduction of the forefoot.

Components of the Deformity

Equinus describes a plantarflexed position of the ankle and heel.

Varus refers to inward turning of the hindfoot, while forefoot adduction causes the front of the foot to deviate medially.

Together, these abnormalities cause the foot to point downward and inward.

Weight-Bearing Pattern

If the deformity remains untreated, the child may bear weight along the lateral border or even the dorsolateral aspect of the foot rather than on the plantar surface.

This abnormal loading can eventually lead to callus formation, pain, and gait difficulty.

Classification

Clubfoot can be divided broadly into two categories.

The first is isolated or idiopathic clubfoot, in which no other congenital abnormality is identified.

The second is syndromic or secondary clubfoot, occurring in association with other congenital or neuromuscular disorders.

Syndromic Clubfoot

Associated conditions include amniotic band syndrome, arthrogryposis, myelodysplasia, diastrophic dysplasia, Larsen syndrome, Freeman–Sheldon syndrome, Möbius syndrome, and Loeys–Dietz syndrome.

Clubfeet associated with these conditions are usually more rigid, more severe, and more resistant to nonoperative treatment than idiopathic clubfeet.

They therefore have a greater likelihood of requiring surgical correction.

Bony Anatomy

The talar neck is characteristically directed medially and plantarward.

The talonavicular relationship is also abnormal, contributing substantially to the medial and plantar displacement of the foot.

Foot Size

The involved foot is usually smaller than normal.

In unilateral cases, the affected foot may be slightly shorter than the contralateral side, generally by less than approximately 1 cm.

The calf may also remain smaller because of associated muscle hypoplasia.

Epidemiology

Clubfoot occurs in approximately 1 in every 1,000 live births.

Males are affected about twice as often as females, producing a male-to-female ratio of roughly 2:1.

Risk Factors

A positive family history substantially increases the likelihood of clubfoot.

Important risk factors include having an affected parent or sibling and the presence of congenital disorders known to be associated with clubfoot.

Associated Congenital Disorders

Conditions linked with clubfoot include amniotic band syndrome, arthrogryposis, myelodysplasia, Möbius syndrome, Freeman–Sheldon syndrome, Larsen syndrome, diastrophic dysplasia, and Loeys–Dietz syndrome.

Certain teratogenic drug exposures during pregnancy, historically including aminopterin, have also been associated with congenital foot deformities.

Genetics

Idiopathic clubfoot is believed to have a multifactorial or polygenic inheritance pattern with variable penetrance.

No single genetic abnormality explains most idiopathic cases.

Familial Risk

When one child has clubfoot, the risk to a subsequent sibling has historically been estimated at approximately 2–6%.

If a parent has clubfoot, the risk to each child has been estimated at approximately 10%.

Etiology

The exact cause of idiopathic clubfoot remains uncertain.

A genetic contribution is strongly suspected, although environmental and developmental factors may also participate.

Associated Conditions

Clubfoot may occur together with other congenital musculoskeletal or neurologic abnormalities.

The presence of other deformities should prompt evaluation for an underlying syndrome or neurologic disorder.

Diagnosis

Signs and Symptoms

The diagnosis is usually evident from the appearance of the newborn foot.

The foot is excessively turned downward and inward, often with a deep medial crease.

Older Children

Untreated clubfoot in an older child can cause difficulty walking, poor shoe fit, painful callosities, and abnormal weight-bearing.

Severe untreated cases may result in walking on the lateral or dorsal aspect of the foot.

Pain

Pain is uncommon in infancy but may develop in older children or adults if the deformity remains uncorrected or becomes rigid.

Physical Examination

The typical examination demonstrates heel equinus, hindfoot varus or supination, and adduction of the midfoot and forefoot.

Together, these findings produce the characteristic appearance of a curved or “kidney-shaped” foot.

Medial Crease

A prominent medial or plantar crease is commonly present.

The foot projects medially from the leg and may resemble the shape of a club.

Flexibility

The examiner should determine how much of the deformity can be passively corrected.

Flexibility is important for assessing severity and planning treatment.

Muscle Function

Ankle and toe muscle activity should be evaluated.

The absence of active toe dorsiflexion may indicate more severe neuromuscular involvement and is associated with a less favorable prognosis.

Calf Hypoplasia

A smaller calf is a characteristic feature.

Even after successful correction of the foot position, some degree of calf hypoplasia usually persists.

Imaging

General Role of Radiographs

Radiographs are not routinely necessary for the diagnosis or early treatment of typical idiopathic clubfoot.

They may be useful when there is concern for underlying bony fusion, atypical anatomy, or when operative treatment is being planned.

Simulated Weight-Bearing Views

When imaging is obtained in a young child who cannot stand, simulated standing AP and lateral radiographs may be used.

Obtaining adequate images can be difficult because of the rigid deformity.

Positioning

The foot should be corrected as close to neutral as possible during imaging.

A Plexiglas plate or similar device may be used to hold the foot in position.

AP Radiograph

On the AP view, the forefoot is typically markedly adducted.

In a normal foot, the talus roughly aligns with the first metatarsal and the calcaneus with the fifth metatarsal.

Kite Angle

The angle between the longitudinal axes of the talus and calcaneus is known as the talocalcaneal or Kite angle.

On an AP radiograph, the normal angle is approximately 20–40°.

Kite Angle in Clubfoot

In clubfoot, the talus and calcaneus are nearly parallel.

As a result, the AP talocalcaneal angle is substantially reduced.

Lateral Radiograph

The lateral view demonstrates the equinus position of the foot.

In a normal foot, the lateral talocalcaneal angle is approximately 35–50°.

Lateral Talocalcaneal Angle in Clubfoot

In clubfoot, the talus and calcaneus remain relatively parallel in the sagittal plane, producing a markedly decreased talocalcaneal angle.

These angular relationships can help assess the adequacy of correction.

Pathological Findings

The principal bony abnormality is medial deviation of the talar neck with subluxation of the talonavicular joint.

Soft-tissue abnormalities are also prominent.

Muscle Abnormalities

Histologic studies have demonstrated that muscle fibers on the affected side may be smaller than normal.

This contributes to the characteristic calf hypoplasia.

Soft-Tissue Contracture

The fascia, tendons, and joint capsules on the medial and posterior aspects of the foot are thickened and contracted.

These soft-tissue abnormalities contribute to the rigidity of the deformity.

Differential Diagnosis

Metatarsus Adductus

Severe metatarsus adductus can resemble clubfoot because the forefoot is turned inward.

The key difference is that metatarsus adductus does not have the fixed hindfoot equinus component characteristic of true clubfoot.

Treatment

General Principles

Treatment should begin as soon as practical after birth.

The current standard for most idiopathic clubfeet is serial manipulation and casting using the Ponseti method.

Ponseti Method

The Ponseti technique gradually corrects the deformity through a specific sequence of gentle manipulations followed by long-leg casting.

Correction proceeds progressively rather than attempting to force the foot immediately into a normal position.

Correction Sequence

The forefoot is gradually abducted while the heel and talus are stabilized.

This corrects the cavus, adduction, and hindfoot varus components.

Equinus is corrected last, after the foot has been brought into appropriate alignment.

Long-Leg Casting

A cast is applied from the toes to above the knee to maintain each stage of correction.

The cast is typically changed at approximately weekly intervals until adequate correction is achieved.

Duration of Casting

Correction often requires approximately 6–8 weeks, although the number of casts varies with the severity and rigidity of the deformity.

Achilles Tenotomy

Persistent equinus is very common after correction of the other components.

A percutaneous Achilles tenotomy is therefore frequently performed to obtain adequate ankle dorsiflexion.

Post-Correction Bracing

After successful correction, maintenance bracing is essential to reduce recurrence.

A foot-abduction brace, commonly consisting of shoes attached to a Denis Browne-type bar, is used.

Brace Schedule

The brace is generally worn essentially full-time during the initial post-correction period and subsequently during sleep and naps for several years.

Adherence to bracing is one of the most important factors in preventing recurrence.

Physical Therapy

Stretching

Stretching of the heel cord and medial soft tissues may be helpful.

However, stretching alone is usually insufficient to correct a true clubfoot.

Maintenance of Correction

Exercises are most useful after casting as an adjunct to preserve ankle and foot flexibility.

They should not substitute for appropriate casting and bracing.

Medication

Medication has little role in the routine correction of clubfoot.

Botulinum toxin has been investigated as an adjunct to casting and splinting in selected cases, but it is not a standard substitute for established Ponseti treatment.

Surgery

Indications

Surgery is reserved primarily for persistent or recurrent deformity that cannot be adequately corrected with repeat casting and less invasive measures.

Modern Ponseti treatment has substantially reduced the need for extensive surgical release.

Treatment of Relapse

Recurrent deformity can frequently be managed with repeat casting, repeat Achilles tenotomy, or anterior tibialis tendon transfer.

The specific treatment depends on the pattern and flexibility of the recurrence.

Anterior Tibialis Tendon Transfer

An anterior tibialis tendon transfer may be useful in a child with recurrent dynamic supination after initial successful correction.

The tendon is repositioned to rebalance the foot during gait.

Extensive Surgical Release

If casting fails completely, more extensive surgery may be necessary.

The goal is to release contracted structures while avoiding excessive dissection that could lead to stiffness and scarring.

Medial Release

Medial procedures may include lengthening or release of the posterior tibial tendon and flexor tendons, together with release of contracted medial structures.

Posterior Release

Posterior correction may require Achilles tendon lengthening and release of contracted posterior joint capsules.

Minimize Capsular Dissection

Extensive capsular release should be minimized whenever possible because over-dissection increases the risk of postoperative stiffness, scarring, weakness, and later pain.

Temporary Fixation

Pins may occasionally be used to maintain correction after surgical release.

When used, they may remain in place for several weeks while the soft tissues heal.

Repeat Surgery

A minority of children treated surgically may require additional procedures later because of recurrent deformity or residual imbalance.

Historically, repeat surgery has been required in approximately 10–20% of surgically treated patients.

Follow-Up

Referral

Children with suspected clubfoot should be referred to an orthopaedic surgeon experienced in pediatric foot deformity and Ponseti treatment.

Early specialist management improves the likelihood of successful nonoperative correction.

Prognosis

With appropriate treatment, most children achieve a plantigrade, functional foot that allows normal or near-normal walking and activity.

Residual Differences

Certain features cannot be fully corrected.

The affected foot often remains somewhat smaller, the calf may remain thinner, and slight limb or foot shortening may persist.

These differences usually have little effect on overall function.

Complications

Residual Deformity

Incomplete correction may leave persistent equinus, varus, adduction, or cavus.

Residual deformity may interfere with shoe wear or gait.

Rocker-Bottom Foot

Overly forceful correction, particularly dorsiflexion before adequate correction of hindfoot and forefoot alignment, can produce a rocker-bottom deformity.

This should be avoided through proper sequential correction.

Overcorrection

Excessive correction can result in hindfoot valgus or other alignment abnormalities.

Stiffness

Extensive surgical treatment may result in a stiff foot.

This is one reason modern management emphasizes serial casting and limited procedures whenever possible.

Pain

Pain can develop later in childhood or adulthood, particularly if residual deformity, overcorrection, stiffness, or degenerative changes are present.

Patient Monitoring

Long-Term Follow-Up

Children require regular follow-up for several years because recurrence may occur even after an initially successful correction.

Timing of Recurrence

Idiopathic clubfoot may recur through approximately 6–7 years of age, although most relapses occur during the first several years of life.

Monitoring for Relapse

Follow-up should assess ankle dorsiflexion, hindfoot alignment, forefoot adduction, dynamic supination, brace adherence, gait, and shoe fit.

Management of Recurrence

Early recurrence can often be successfully treated with repeat Ponseti casting, Achilles tenotomy, or anterior tibialis tendon transfer, avoiding the need for extensive surgery.