• Most cases are idiopathic (multifactorial inheritance pattern with significant environmental influence).
• Infrequently, neuromuscular imbalance may underlie the deformity (cerebral palsy, myelomeningocele, lipomas of the cord, caudal or sacral agenesis, polio, arthrogryposis, fetal alcohol syndrome).

• Many anatomic abnormalities have been postulated as causing clubfoot: anomalous or deficient muscles, myoblasts, mast cells, abnormal primary bone formation, joint and muscle contractures, vascular anomalies (absent dorsalis pedis artery), nerve anomalies, and abnormalities of the fibrous connective tissue.
• Interruption of the development of the embryonic foot has also been suggested.

• Prevalence is 1 to 1.4 per 1,000 live births.
• The risk of deformity increases by 20 to 30 times where there is an affected first-degree relative. Male:female ratio is 2:1.

• Distinguish other deformities of the foot:
  • Metatarsus adductus or varus (heel is in neutral position)
  • Calcaneovalgus (foot is in valgus)
  • Vertical talus (foot is in valgus, heel in equinovalgus)
• Many children with clubfoot will also have tibial tortion.

• Family history of clubfoot (3%)
• Onset of deformity (congenital or developmental)

• The neuromuscular system for neuromuscular etiologies such as lumbosacral sinuses, dimples, and lipomas
• The hips for hip dysplasia
• The neck for torticollis

• X-ray studies (after 3 months of age)
• Tarsal bones are poorly ossified in the newborn. Diagnosis is clinical.
• At 3 to 6 months of age, anteroposterior (AP) and lateral x-ray films in dorsiflexion (maximal correction) may help in defining residual deformity. The beam should be focused on the hindfoot for both the AP and lateral x-rays, as the measured angles will be hindfoot angles.
• Decreased talocalcaneal angle on the AP and lateral views (25 degrees or less) confirm persistent deformity.
• Medial displacement of the cuboid on the calcaneus and persistent plantar flexion of the forefoot on the hindfoot (talar to first metatarsal angle) indicate more complex deformities.

• Initial treatment is serial (weekly) manipulation and casting.
• Taping may be useful for treatment of the infant requiring ICU care; access to the feet should be maintained for blood tests.
• Failure to correct the deformity completely by manipulation within 3 to 9 months should lead to surgical treatment.

• Realignment of the deformity is the goal and should be achieved at surgery or by casting.
• Most surgeons cast the feet for 3 months postoperatively.
• Some brace the feet for 6 months.
• Remember, the cause of the deformity is not corrected. Only the alignment of the bones and lengthening of the soft tissues are corrected.
• Depending on the severity of the deformity, calf narrowing and weakness, and ankle and subtalar stiffness, a difference between the feet of one to two shoe sizes and even a leg-length discrepancy will be present in all corrected clubfeet.
• There will also be decreased ankle and subtalar motion as compared to the normal.
• Adolescent children with clubfeet often will get leg cramps and will tire easily while doing normally strenuous activities in sports.
• All true recurrences should lead to further evaluation for neuromuscular or syndrome causes that might have been missed in the infant.

Q: How can a rigid clubfoot be distinguished from a positional clubfoot?
A: During initial evaluation of the child, it is important to assess the amount of flexibility in a clubfoot. This can be most easily done by flexing the hip to 90 degrees, flexing the knee to 90 degrees, and then gently trying to turn the forefoot into a straight position lined up with the thigh. If the foot easily spins around into a normal position, it can be assumed that this is a flexible or positional clubfoot. If deformity persists, this is a rigid deformity. If possible, the examining physician should palpate the heel to see if the os calsis comes out of its equinus position filling the heel pad. In some children, particularly with a rocker bottom sole, the heel pad looks as if it is in the correct position, but the os calsis remains in equinus with the posterior aspect of the os calsis proximal to the heel pad.

Q: What percentage of clubfeet are successfully treated by casting?
A: To some extent, the amount of success depends on how much correction is desired. Occasionally, cast correction will provide a partial correction. Some feet, after casting, can be held in the corrected position, only to spin back to the clubfoot deformity when released. Positional clubfeet are likely to improve with casting in perhaps 80% of cases. Rigid clubfeet are much less likely to be corrected by casting. The success rate in the rigid feet is likely to be about 10% to 20%.

Q: What will be the permanent disability of a congenital clubfoot deformity?
A: While casting and surgical correction of a congenital clubfoot can realign the bones, the surgery does little to correct the underlying neuromuscular problems. As a result, all children with rigid clubfeet are likely to have a leg-length inequality (usually less than 1.5 in.), a smaller foot (usually one to two sizes), calf narrowing that cannot be significantly improved with exercise, and joint stiffness (ankle, subtalar, and midfoot). Even children with optimal realignment of the deformity will notice their inability to perform gymnastic activities or running activities requiring normal range of motion of the ankle and foot. Many will complain of the inability to keep up with their peer group during adolescent and young-adult sports activities.

Q: How soon should an infant with congenital clubfoot be referred to an orthopedic surgeon?
A: If casting is to be even partially successful, cast treatment should begin within the first week or two of life. Clearly, medical and life-threatening conditions will take precedence over the treatment of the clubfoot. Access to the feet for IV or blood studies will interfere with a casting regimen. Casting should begin as soon as is practical. It may even be possible to begin taping of the foot as an alternative to casting, which will still allow IV access to the feet. Referral to an orthopedic surgeon should therefore follow as soon as is practical.

Hamel J, Becker W. Sonographic assessment of clubfoot deformity in young children. J Pediatr Orthop B 1996;5(4):279–286.

Johnston CE II, Hobatho MC, Baker KJ, Baunin C. Three-dimensional analysis of clubfoot deformity by computed tomography. J Pediatr Orthop B 1995;4(1):39–48.

Napiontek M. Clinical and radiographic appearance of congenital talipes equinovarus after successful nonoperative treatment. J Pediatr Orthop 1996;16(1):67–72.

Yamamoto H, Muneta T, Morita S. Nonsurgical treatment of congenital clubfoot with manipulation, cast, and modified Denis Browne splint. J Pediatr Orthop 1998;18(4):538–542.