1 Clubfoot has an incidence of approximately 1 in 1000 live births. In the majority the condition is labelled as ‘idiopathic’, although the deformity is associated with myelomeningocele, amniotic band syndrome (Streeter’s dysplasia) and arthrogryposis. Population and twin studies suggest a genetic component but the mode of inheritance does not follow a distinctive pattern. In the presence of a gene mutation, such as polymorphism in the methylenetetrahydrofolate reductase gene (MTHFR), other factors will predispose the child to contraction of the soft tissues of the foot and abnormal talar development. Deformity is exacerbated by a reduction in maternal amniotic fluid (oligohydramnios), hence the prevalence of the condition in children born during the summer months, and by disturbances in neuromuscular function producing ipsilateral calf muscle hypoplasia.

2 The primary deformities are those of hindfoot equinus and varus with forefoot adductus and supination. This positioning is secondary to medial and plantar deviation of the talar neck, medial rotation of the calcaneus and medial displacement of the navicular and cuboid. This leads to a parallel and superimposed positioning of the talus upon the calcaneus (angle <20°) and a negative talus/first metatarsal angle as shown in Figure 1.2a and b On a dorsiflexion lateral film the talocalcaneal angle is reduced (< normal 35°; Fig. 1.2c and d).

3 A gradual improvement in anatomical alignment is achieved by sequential stretching. The key, according to Ponseti, is a reversal of the cavus by dorsiflexion of the first metatarsal during the initial stage of treatment. Supination and equinus are accepted until the metatarsal is adequately dorsiflexed. Reduction in the cavus unlocks the midfoot. Subsequent correction occurs by using the uncovered talar head as a lateral fulcrum. As the forefoot is then abducted, the heel externally rotates and dorsiflexes, reversing the equinus. The position is held by applying a dynamic splint, as shown in Figure 1.3, or plaster casts applied with the knee in at least 70° of flexion. It is necessary for the physician or a trained therapist to see the child weekly to ensure that the splintage is holding the foot in the corrected position. After 2 or 3 months, if an adequate correction has been achieved, the feet may be splinted out with an abduction bar attached to the shoes. This will be used full time for 3 months and then required as a night splint to age 3 or 4 (Fig. 1.4).

4 The optimal timing of surgery and the exact procedures required remain a matter of some debate. The majority of surgeons would probably agree that at least a lengthening of the Achilles tendon should be considered after 3 months if conservative measures fail. In Edinburgh, an extended posteromedial release through a transverse Cincinnati incision is favoured for the recalcitrant foot (Fig. 1.5), creating a mobile and plantigrade foot. The foot is immobilized in plaster following surgery to maintain the corrected position. The success of surgery relates to the compliance with bracing. Studies from the Ponseti Clubfoot Center in New York suggest that two-thirds of those non-compliant with bracing had recurrence of deformity, with one-third of these requiring more extensive surgery than Achilles tenotomy and anterior tibial tendon transfer. In contrast, only 14% of those compliant with bracing had recurrences and none required extensive surgery.

• Clubfoot is the most common orthopaedic deformity at birth and requires careful early management.