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Key Points

  • Positional abnormality of the fetal foot that results in it being fixed in adduction, supination, and varus, with concomitant soft-tissue abnormalities.

  • Incidence is 1 in 1000 livebirths.

  • Early amniocentesis (11-14 weeks of gestation) is associated with an increased incidence of clubfoot.

  • Fetuses with clubfoot should be referred to a facility capable of performing detailed fetal sonographic anatomic evaluation. Such a targeted scan should include measurement of amniotic fluid volume, observation for presence of amniotic bands, masses or abnormalities that could crowd the fetus, and assessment of fetal movement.

  • Associated abnormalities are seen in 23% to 61% of cases. More than 250 syndromes include clubfoot as one component.

  • If associated anomalies are seen, consider obtaining a karyotype. If clubfoot is isolated, a karyotype is not needed.

  • Treatment consists of stretching exercises, serial casting, and/or surgery. Surgery, if performed, is done at 2 to 12 months.

  • Recurrence risk depends on whether a syndrome is present. If clubfoot is isolated, complete family history information is needed to quote a risk.


The term clubfoot refers to a positional abnormality of the fetal foot, resulting in it being fixed in adduction, supination, and varus, with concomitant soft-tissue abnormalities (Drvaric et al., 1989). The Latin term talipes equinovarus (tali = ankle, pes = foot, equino = horse, varus = bent inward) (abbreviated as TEV) is used interchangeably with clubfoot.

Two general categories of clubfoot are recognized. Intrinsic clubfoot describes a foot that is rigid at birth with marked atrophy, fibrosis, and abnormal bony relationships. This form of clubfoot is generally treated by surgical intervention. Extrinsic clubfoot refers to a foot that is flexible at birth, although bony relationships may be abnormal. This type of clubfoot may be corrected conservatively, with manipulation and stretching (Kawashima and Uhthoff, 1990).

Even today, the cause of clubfoot is not precisely known. Most investigators agree that clubfoot is the result of an intrauterine developmental deformity, although controversy exists as to whether the cause is primarily muscular or neurologic in origin. The chief anatomic abnormality is the deformity of the talus, which is smaller than normal. Plantar and medial deviation of the head and neck of the talus also exists.

Bony malposition and subsequent development of contractures serve to keep the foot in a fixed position, resulting in forefoot adduction, midfoot supination, and hindfoot supination or equinus deformity (Drvaric et al., 1989). One hypothesis proposed for the cause of clubfoot involves a potential arrest in fetal development. The evidence for this relates to studies performed by Kawashima and Uhthoff (1990), who demonstrated that during normal embryologic development of the lower limb bud, the foot is first adducted in a position that resembles the clubfoot deformity at approximately 8 to 9 weeks of gestation (Figure 107-1) (Kawashima and Uhthoff, 1990). Movements ...

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