Clubfoot deformity primarily affects the hindfoot and midfoot. The pathological changes seen include an abnormally small calcaneus, talus, and navicular 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 calcaneocubid joints and i-nversion and adduction of the calcaneus, navicular, and cuboid. Last, there is also
The deformity can extent distally to the forefoot where there can be plantar flexion (“equinus”) and inversion (“varus”) of the metatarsals .Clubfoot deformity also causes and proximally to the calf, with atrophy, fibrosis and shortening of the muscle-tendon units of the posteromedial leg (calf) muscles seen.
There are many theories about the etiology of clubfoot but the definitive cause is still unknown. In the past, experts believed that the deformity was caused by the foot being stuck in the wrong position in the womb; today it is known that clubfoot is associated wioth 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 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. Some parents will might know as early as the second trimester if the clubfoot is diagnosed via fetal ultrasound.
X-rays are not particularly useful in clubfoot evaluation because (1) clubfoot is grossly visible at birth, and (2) the neonatal bones are immature and poorly ossified. Radiographs are more useful for measuring progress in clubfoot treatment and long-term follow-up. Understanding the orientation of the bones may be important if considering surgical intervention or determining the extent of correction achieved by casting or surgery. Typical radiographic findings include: plantarflexion, loss of the normal antero-posterior talo-calcaneal angle (Kite’s angle), a misshapen talus, and medial subluxation of the navicular and cuboid.
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 24-50% 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.
Clubfoot is one of several congenital foot deformities. Metatarsus adductus is a congenital foot deformity that is superficially similar to clubfoot. It is Metatarsus adductusis characterized by the forefoot (metatarsus) pointing inward (adductus) with normal positing and mobility of the hindfoot, forming a “C” shape. The incidence of metatarsus adductus is approximately the same as clubfoot. Metatarsus adductus is distinguished from clubfoot by an examination of the hindfoot, which has normal mobility in metatarsus adductus but cannot be appropriately dorsiflexed or everted in the case of clubfoot.
Certain conditions, including spina bifida, arthrogryposis, and amniotic band syndrome can cause clubfoot and should also be on the differential. Further diagnostic evaluation . 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 cause caused by a restrictive uterine environment that forces the baby’s feet into an abnormal position. However, it is different from CTEV classic clubfoot in that the foot and bony anatomy are completely normal while congenital/syndromic clubfoot has abnormal bony anatomy. It is easily corrected by stretching and casting.
Although clubfoot is most often an idiopathic birth defect, it is important to note that some cases are secondary to underlying neuromuscular conditions such as spina bifida. Thus, children diagnosed with clubfoot should receive further the presence of clubfoot should be deemed a red flag, prompting a close diagnostic evaluation to catch exclude these conditions.
Treatment options and outcomes
The standard of care in the U.S. is the Ponseti Method, which involves repeated manipulation and casting 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 or biweekly over the course of 4-6 weeks.
Toward the end of the serial casting phase of treatment, 80% of these most children will undergo require a minor operation (percutaneous Achilles tendon tenotomy) to lengthen the Achilles tendon and release the foot from plantarflexion. Some Rarely, patients may also require lateral a transfer of the tibialis anterior – moving it from its normal insertion of on the first metatarsal to a new position insertion on the third – to . This transfer will reduce supination of the foot with dorsiflexion. If the Ponseti Method of casting, bracing, and tenotomy is applied correctly, it will be successful in >95% more than 95% of cases.
After casting, the child must wear a foot abduction brace at night for up to 4 a few years to maintain the correction. In the case of inadequate bracing or noncompliance in bracing, Without bracing, the deformity will likely recur because the muscles of the foot will pull it back into an abnormal position. This
Recurrence (despite bracing) occurs in approximately 10% of patients. Approximately one quarter of these patients who relapse , and most will respond to a repeated course of manipulation; a few will require additional surgery to prevent further relapse. Since it is largely the responsibility of the parents to ensure daily compliance with the brace, it is vital to stress the importance of bracing to parents.
Figure: Denis-Brown brace, a type of foot-abduction brace used to maintain the correction. http://en.wikipedia.org/wiki/Club_foot#mediaviewer/File:Botas.JPG
Although the Ponseti Method is highly effective in idiopathic clubfeet, some clubfeet – patients (especially those in older children or those that present late or whose deformities are secondary to neuromuscular disease – ) will be resistant not respond to this non-operative treatment regimen and will require more dramatic 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. Metal pins are used to maintain the proper alignment post-operatively.
Compared to the results of non-surgical methods, surgical intervention for clubfoot the long-term outcomes from surgery is associated with foot arthritis in adulthood, increased more pain, stiffness, deformity, and muscle weakness. Failure rates are high – as much as 25% – in part because surgery is often performed on complex clubfoot cases that have been recalcitrant to other methods of correction. (Of course, it must be noted that surgery is reserved for tougher cases so this is not a true head-to-head comparison.)
Even with optimal treatment, the corrected clubfoot will be functionally normal but structurally dissimilar from the unaffected foot. The affected foot may be 1 to 1 ½ sizes smaller 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 before the other leg, leading to a significant difference in limb length differences . In these cases, it will be necessary to surgically lengthen the affected leg, most often with the Iliazarov method.
Risk factors and prevention