Clubfoot Last Updates

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Clubfoot can be classified as (1) postural or positional or (2)

fixed or rigid. Postural or positional clubfeet are not true

clubfeet. Fixed or rigid clubfeet are either flexible (ie,

correctable without surgery) or resistant (ie, require surgical

release, though this is not entirely true according to the Ponseti

experience).

The Pirani, Goldner, Di Miglio, Hospital for Joint Diseases (HJD),

and classifications have been published, but none are

universally used.

History of the Procedure: In the past, clubfoot surgery was

performed in a way that did not differentiate severity. The same

procedure was performed for all patients. Recently, Bensahel has

proposed a more individualized approach (ie, addressing only the

structures that are required are released). The surgery is tailored

to the deformity. For example, if the forefoot is well corrected

externally rotated and there is no cavus but there is still

significant equinus, then a posterior approach alone should suffice

(see Intraoperative details).

Problem: See Relevant Anatomy.

Frequency: The incidence of clubfoot is approximately 1 case per

1000 live births in the United States. The incidence differs among

ethnicities. For example, it is close to 75 cases per 1000 live

births in the Polynesians, especially in places like Tonga.

The male-to-female ratio is 2:1. Bilateral involvement is found in

30-50% of cases. There is a 10% chance of a subsequent child being

affected if the parents already have a child with a clubfoot.

Etiology: The true etiology of congenital clubfoot is unknown. Most

infants who have clubfoot have no identifiable genetic, syndromal,

or extrinsic cause.

Extrinsic associations include teratogenic agents (eg, sodium

aminopterin), oligohydramnios, and congenital constriction rings.

Genetic associations include Mendelian inheritance (eg, diastrophic

dwarfism; autosomal recessive pattern of clubfoot inheritance).

Cytogenetic abnormalities (eg, congenital talipes equinovarus

[CTEV]) can be seen in syndromes involving chromosomal deletion. It

has been proposed that idiopathic CTEV in otherwise healthy infants

is the result of a multifactorial system of inheritance. Evidence

for this is as follows:

Incidence in the general population is 1 per 1000 live births.

Incidence in first-degree relations is approximately 2%.

Incidence in second-degree relations is approximately 0.6%.

If one monozygotic twin has a CTEV, the second twin has only a 32%

chance of having a CTEV.

Pathophysiology: Theories of the pathogenesis of clubfeet are as

follows:

Arrest of fetal development in the fibular stage

Defective cartilaginous anlage of the talus

Neurogenic factors: Histochemical abnormalities have been found in

posteromedial and peroneal muscle groups of patients with clubfeet.

This is postulated to be due to innervation changes in intrauterine

life secondary to a neurological event, such as a stroke leading to

mild hemiparesis or paraparesis. This is further supported by a 35%

incidence of varus and equinovarus deformity in spina bifida.

Retracting fibrosis (or myofibrosis) secondary to increased fibrous

tissue in muscles and ligaments: In fetal and cadaveric studies,

Ponseti also found the collagen in all of the ligamentous and

tendinous structures (except the Achilles tendon), and it was very

loosely crimped and could be stretched. The Achilles tendon, on the

other hand, was made up of tightly crimped collagen and was

resistant to stretching. Zimny et al found myoblasts in medial

fascia on electron microscopy and postulated them to cause medial

contracture.

Anomalous tendon insertions: Inclan proposed that anomalous tendon

insertions result in clubfeet. However, other studies have not

supported this. It is more likely that the distorted clubfoot

anatomy can make it appear that tendon insertions are anomalous.

Seasonal variations: on noted seasonal variations to be a

factor in his epidemiological studies in developing countries. This

coincided with a similar variation in the incidence of poliomyelitis

in the children in the community. Clubfoot was therefore proposed to

be a sequela of a prenatal poliolike condition. This theory is

further supported by motor neuron changes in the anterior horn in

the spinal cord of these babies.

Clinical: Seek a detailed family history of clubfoot or

neuromuscular disorders and perform a general examination to

identify any other abnormalities. Examine the feet with the child

prone, with the plantar aspect of the feet visualized, and supine to

evaluate internal rotation and varus. If the child can stand,

determine if the foot is plantigrade, if the heel is bearing weight,

and if it is in varus, valgus, or neutral.

Similar deformities are seen with myelomeningocele and

arthrogryposis. Therefore, always examine for these associated

conditions. The ankle is in equinus, and the foot is supinated

(varus) and adducted (a normal infant foot usually can be

dorsiflexed and everted so that the foot touches the anterior

tibia). Dorsiflexion beyond 90 degrees is not possible.

The navicular is displaced medially, as is the cuboid. Contractures

of the medial plantar soft tissues are present. The calcaneus is not

only in a position of equinus, but the anterior aspect is rotated

medially and the posterior aspect laterally.

The heel is small and empty. The heel feels soft to the touch (akin

to the feel of the cheeks). As the treatment progresses, it fills in

and develops a firmer feel (akin to the feel of the nose or of the

chin).

The talar neck is easily palpable in the sinus tarsi as it is

uncovered laterally. Normally, this is covered by the navicular, and

the talar body is in the mortise. The medial malleolus is difficult

to palpate and is often in contact with the navicular. The normal

navicular-malleolar interval is diminished.

The hindfoot is supinated, but the foot is often in a position of

pronation relative to the hindfoot. The first ray often drops to

create a position of cavus. The Ponseti method of closed management

of clubfeet through manipulations and casting describes the

elevation of the first metatarsal as a first step, even if it means

seemingly exacerbating the supination of the foot.

The tibia often has internal torsion. This assumes special

importance in the casting management of clubfeet, where care should

be taken to rotate the feet into abduction, avoiding spurious tibial

rotation through the knee.

Even following correction, the foot often remains short and the calf

thin.