Key Insights To Treating Talipes Equinovarus
- Volume 17 - Issue 4 - April 2004
- 11445 reads
- 0 comments
Since the first recognition of talipes equinovarus (TEV), the only treatment options have been closed reduction through manipulation with immobilizing techniques and surgical correction. The goal of treatment is ensuring a painless, plantigrade, supple foot with good range of motion and normal function. However, there has been a significant evolution in the treatment of TEV over the years. In fact, there are over 2,600 literature references on the subject.
TEV is an anatomically and etiologically complex condition. Understanding the morbid anatomy is crucial for successful conservative and surgical management.
The principal lesion is peritalar malposition with downward, medial and proximal navicular displacement. The greatest distortion is in the talus.1 Although the body and trochlea are almost normal, the neck is short, deviated medially and downward. The articular surface for the navicular is plantar and medial on the neck. Plantarflexion of the talus in the ankle mortise produces ankle equinus.
The navicular rotates so the forefoot becomes supinated and the navicular lies close to the tip of the medial malleolus. The calcaneus follows in the same direction while moving into varus around a rotational axis through its body with medial rotation in the transverse plane. The distal calcaneus is almost directly under the talar head. Its posterior portion elevates, goes into varus and moves laterally so that the superior and lateral surface come close to the fibular malleolus.
The cuboid and the rest of the distal foot follow this rotation. The calcaneocuboid facet faces more medially, adding to the adductus of the forefoot. Articular surface remodeling with ligament, joint capsule and muscle contractures make the deformity rigid.
It is a common misconception that the peritalar articulations are subluxed or dislocated.2 They are anatomically distorted in pathological positions, but are congruent and cohesive.2,3 Simple stretching will not relocate them. Correction requires shape change in the cartilage anlage.
Studies of the morbid anatomy of idiopathic TEV reveal several other findings.1,4 The calf muscles are almost always decreased in bulk.5-7 The initial thought was that decreased calf muscle diameter resulted from cast immobilization and other therapies, but one may also see this among untreated children. There are no regularly occurring abnormalities in muscle or nerve. There often are abnormalities in the anterior tibial artery. In some cases, it does not pass onto the dorsum of the foot. In other cases, there are anomalies as proximal as the trifurcation. The tendo-Achilles may insert more medially on the posterior calcaneus or the medial fibers may be contracted.1 There are no brain or spinal cord abnormalities.
A Review Of The Different Types Of TEV
There is a tendency to lump all forms of TEV together, but there are prognostic and therapeutic merits in classification.
Currently, there are four types of TEV. The idiopathic form is the most common. However, keep in mind that some studies suggest primary muscular and peripheral nerve etiologies in some cases of idiopathic TEV. There is also a polyallelic genetic component with severity influenced by the infant’s gender.8,9 Idiopathic TEV runs the spectrum from a mild flexible deformity to an extreme rigid deformity.
The postural (positional) form includes all TEV caused by in utero positioning and occult neurological disturbances with muscle imbalance. Therefore, this is not a pure category. The prognosis depends on the underlying pathophysiology.10,11
The teratological (teratogenic) form includes all TEV associated with multiple bone and joint pathologies. It includes diastematomyelia, myelomeningocele, tethered cord, arthrogryposis multiplex congenita and Streeter’s dysplasia.
The syndromic form includes all TEV associated with named syndromes in which TEV is a feature. Smith’s Recognizable Patterns of Human Malformation (although using the term generically) lists over 50 syndromes in which “clubfoot” is a regular or occasionally occurring feature.12