Talipes equinovarus, commonly known as “clubfoot,” is a congenital deformity of the foot (Figure 1). The condition is characterized by an exaggerated arch (cavus), a convex curved outer border of the foot (adductus), inversion of the heel (varus) and plantar flexion (equinus) that may involve one or both feet. Taken together, these deformities cause the foot to resemble a club, hence the name. Clubfoot is often idiopathic and seen as an isolated birth defect, but it can also be caused by an underlying congenital disorder in approximately 20% of cases.
Structure and Function
The foot can be divided into three regions: the hindfoot, the midfoot, and the forefoot.
The hindfoot consists of the talus and the calcaneus. These bones are joined at the subtalar joint to allow for inversion and eversion. The talus also articulates with the tibia and fibula at the ankle, to allow for dorsiflexion and plantarflexion.
The bones of the midfoot are the navicular, the cuboid, and the three cuneiform bones. The midfoot forms the arch of the foot and serves as a shock absorber.
The forefoot consists of the metatarsals and phalanges.
Clubfoot deformity primarily affects the hindfoot and midfoot. Pathological features include an abnormally small calcaneus, talus, and navicular - though all of the bones in a clubfoot are slightly smaller than normal – and contracted ligaments between the hindfoot and midfoot. There is, accordingly, a plantarflexion deformity of the ankle (talocrural) joint, medial subluxation of the talonavicular and calcaneocuboid joints and inversion and adduction of the calcaneus, navicular, and cuboid.
The deformity can extend distally to the forefoot where there can be plantar flexion of the 1st metatarsal (cavus) and adduction of all metatarsals. The deformity can also extend proximally to the calf, with atrophy, fibrosis and shortening of the muscle-tendon units of the posteromedial leg muscles seen.
There are many theories about the etiology of clubfoot, but the definitive cause is still unknown. In the past, experts believed the positioning of the foot in the womb caused the deformity; today it is known that clubfoot is associated with multiple genetic abnormalities that influence the muscle contractile complex and bone development. For example, Gurnett et al (PMID: 18950742) found that abnormalities of the PITX gene, responsible for early limb development, has been associated with familial clubfoot.
Clubfoot is a congenital deformity that is immediately apparent at birth. Fetal ultrasound can diagnose clubfoot as early as the second trimester.
The affected foot is characteristically adducted (“varus”), plantarflexed (“equinus”), and possesses an exaggerated arch (“cavus”). Depending on the severity, the foot may be more or less rigid. Half of all cases will involve both feet. In unilateral clubfoot, the involved foot, calf, and leg will be smaller and shorter than the unaffected side. Even after correction of the deformity, the foot, calf, and leg may have some residual differences including atrophied calf muscles, a shorter leg, and a smaller foot. These residuals are not necessarily clinically significant.
Despite its dramatic deformities, clubfoot is not necessarily painful. However, if children begin to walk prior to successful correction of the deformity, they will bear weight on the dorsolateral aspect of the foot. This abnormal gait can cause focal loading on a small area and can be painful.
Clubfoot is detectable via prenatal ultrasound in the second trimester. Early detection is important because it can prompt discussion with parents about treatment options and early screening for underlying neuromuscular diseases.
X-rays are not particularly useful in clubfoot evaluation because the neonatal bones are immature and poorly ossified. Radiographs are more useful for measuring progress in clubfoot treatment and long-term follow-up.
Clubfoot occurs in 1 in 1000 births and affects males twice as frequently as females. Approximately 50% of all cases are bilateral and 25% have a positive family history of clubfoot. In the US, incidence ranges across ethnic groups from 0.4 in 1000 in the Chinese population to 7 in 1000 in the Polynesian population.
Most cases are idiopathic but about 20% are due to a genetic or chromosomal abnormality. The most common of these are disorders of the nervous system including myelomeningocele and arthrogryposis. These cases tend to be stiffer and more resistant to standard treatment than idiopathic cases.
Metatarsus adductus is a congenital foot deformity that is superficially similar to clubfoot. Metatarsus adductus is characterized by the forefoot (metatarsus) pointing inward (adductus) with normal positioning and mobility of the hindfoot, forming a “C” shape. The incidence of metatarsus adductus is approximately the same as clubfoot. Examination of the hindfoot can distinguish metatarsus from clubfoot, since the hindfoot has normal mobilitiy in metatarsus adductus but cannot dorsiflex or evert normally in clubfoot.
Other congenital foot deformities include talipes calcaneovalgus (dorsiflexed and abducted foot) and vertical talus (rigid foot deformity similar to talipes calcaneovalgus). These deformities are structurally and visually distinct from clubfoot.
Clubfoot may be seen in association with spina bifida, arthrogryposis, and amniotic band syndrome. The evaluator should therefore pay close attention to the spine and motor function of the extremities.
Positional clubfoot is similar to clubfoot in that the foot is in equinus and varus. It is caused by a restrictive uterine environment that forces the baby’s feet into an abnormal position. However, the foot and bony anatomy are completely normal in positional clubfoot, and the deformities usually correct without treatment.
Although clubfoot is most often an idiopathic birth defect, some cases are secondary to underlying neuromuscular conditions such as spina bifida. Thus, the presence of clubfoot should prompt a close diagnostic evaluation to exclude these conditions.
Treatment Options and Outcomes
Treatment options for clubfoot include serial casting, bracing, physical therapy, and surgery.
The standard of care for uncomplicated clubfoot deformities is the Ponseti Method, which involves repeated manipulation and casting (Figure 2) to guide the growth of the foot toward normal alignment. The child’s foot is manually stretched toward the correct position, and a cast is then applied to maintain the correction. This process is repeated weekly over the course of 4-6 weeks.
At the end of the serial casting phase of treatment, most children will require a minor operation (percutaneous Achilles tendon tenotomy) to lengthen the Achilles tendon and release the foot from residual plantar flexion. Rarely, patients may also require a transfer of the tibialis anterior from its normal insertion on the first metatarsal to a new insertion on the third. This transfer will reduce supination of the foot with dorsiflexion. The operation is usually performed after age 3 years. If the Ponseti Method of casting, bracing, and tenotomy is applied correctly, it will be successful in more than 95% of cases.
After casting, the child must wear a foot abduction brace (Figure 3) at night for four or five years to maintain the correction. Without bracing, the deformity will likely recur because the muscles of the foot will pull it back into an abnormal position.
Recurrence (despite bracing) occurs in approximately 10% of patients, and most will respond to a repeated course of manipulation and casting; a few will require additional surgery to prevent further relapse.
Although the Ponseti Method is highly effective in idiopathic clubfeet, some patients (especially those who present late or whose deformities are secondary to neuromuscular disease) will not respond to non-operative treatment and will require surgical intervention.
Surgery is normally performed at 9-12 months of age. The goal of surgery is to correct all the deformities in one operation. The surgical procedure varies from patient to patient but generally involves releasing all joint capsule contractures, lengthening any shortened muscle-tendon units, and realigning the bones of the foot.
Compared to the results of non-surgical methods, the long-term outcomes from surgery are associated with more pain, stiffness, deformity, and muscle weakness. However, it is important to note that surgery is reserved for patients with more severe disease. Accordingly, this is a not a true head-to-head comparison.
Even with optimal treatment, the corrected clubfoot will be functionally normal but structurally different than the unaffected foot. The affected foot is often smaller (requiring a different shoe size) and less mobile than the other foot. Additionally, the calf muscles in the affected leg may also be smaller. In some cases of clubfoot, the affected leg will stop developing prematurely. Even if this were to occur, the affected leg will usually be no more than ½ inch shorter than the other leg – a clinically insignificant discrepancy. Rarely, there will be a difference in limb length sufficiently large that a surgery will be needed to lengthen the affected leg.
Risk Factors and Prevention
Honien et al (PMID: 11032161) found that family history of clubfoot is a major risk factor for developing clubfoot (OR = 6.52). Smoking exposure in utero is also associated with increased risk of clubfoot (OR = 1.34). This risk is dramatically increased in babies that already have a past family history of clubfoot (OR = 20.30). As a result, mothers with a positive family history of clubfoot should be strongly urged not to smoke while pregnant to minimize the risk of their child having clubfoot.
Clubfoot can be identified in the second trimester using fetal ultrasound. This can provide an opportunity for counseling about genetic testing for associated conditions as well as education about the treatment and prognosis of the condition.
Figure-skater Kristi Yamaguchi, soccer star Mia Hamm, and NFL quarterback Troy Aikman were all born with clubfeet but still attained great success as professional athletes.
Clubfoot is uniformly treated at a very early age in the US, but in low-income countries it is not uncommon to see older children with neglected clubfoot (a deformity that was never treated), residual clubfoot (a deformity that was incompletely treated and retains aspects of the deformity years later), and recurrent clubfoot (a deformity that was completely treated but reverted back due to insufficient bracing). These forms of clubfoot can severely decrease quality of life by subjecting patients to physical disability and alienation.
Horses walk on their toes; hence, a deformity of plantar flexion that places the toes in lone contact with the ground is called "equinus.”
Clubfoot, Talipes equinovarus, Ponseti Method
Recognize the gross manifestations of clubfoot and differentiate these from other congenital foot deformities. Explain treatment options for clubfoot, including the Ponseti Method of serial casting, bracing, and tenotomy. Describe the possible outcomes of clubfoot treatment, including restoration of normal form and function, residual deformity, and recurrent deformity.
*Additional Peer Review completed after Foot and Ankle Textbook print.
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