Talipes equinovarus
Overview
A clubfoot, or talipes equinovarus[1] (TEV), is a birth defect. TEV is classified into 2 groups Postural TEV or Structural TEV. Without treatment, persons afflicted often appear to walk on their ankles, or on the sides of their feet. It is a common birth defect, occurring in about one in every 1,000 live births. Approximately 50% of cases of clubfoot are bilateral. In most cases it is an isolated dysmelia. This occurs in males more often than in females by a ratio of 2:1. There are different causes for clubfoot depending on what classification it is given. Structural TEV is caused by: genetic factors, such as Edwards syndrome, a genetic defect with three copies of chromosome 18. Growth arrests at roughly 9 weeks and compartment syndrome of the affect limb are also causes of Structural TEV. Genetic influences increase dramatically with family history. It was previously assumed that postural TEV could be caused by external influences in the final trimester such as intrauterine compression from oligohydramnios or from amniotic band syndrome. However, this is countered by findings that TEV does not occur more frequently than usual when the intrauterine space is restricted. [2] Breach Birth presentation is also another known cause. TEV may be associated with other birth defects such as spina bifida cystica. Use of MDMA (Ecstasy) and smoking [3] while pregnant has been linked with this congenital abnormality
Symptoms
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 neurologic 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 that they cause medial contracture.1, 2, 9 * Anomalous tendon insertions: Inclan proposed that anomalous tendon insertions result in clubfeet.10 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: Robertson noted seasonal variations to be a factor in his epidemiologic studies in developing countries.11 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.
Treatment
Clubfoot is treated with manipulation by podiatrists, physiotherapists, orthopedic surgeons, specialist nurses, or orthotists by providing braces to hold the feet in orthodox positions, serial casting, or splints called knee ankle foot orthoses (KAFO). Other orthotic options include Dennis-Brown bars with straight last boots, ankle foot orthoses and/or custom foot orthoses (CFO). In North America, manipulation is followed by serial casting, most often by the Ponseti Method. Foot manipulations usually begin within two weeks of birth. Even with successful treatment, when only one side is affected, that foot may be smaller than the other, and often that calf, as well. Extensive surgery of the soft tissue or bone is not usually necessary to treat clubfoot; however, there are two minimal surgeries that may be required: 1. Tenotomy (needed in 80% of cases) is a release (clipping) of the Achilles tendon - minor surgery- local anesthesia 2. Anterior Tibial Tendon Transfer (needed in 20% of cases) - where the tendon is moved from the first ray (toe) to the third ray in order to release the inward traction on the foot. Of course, each case is different but the main idea is that extensive surgery is not needed to treat clubfoot. Extensive surgery may lead to scar tissue developing inside the child's foot. The scarring may result in functional, growth and aesthetic problems in the child's foot because the scarred tissue will interfere with the normal development of the foot. A child who has extensive surgery may require on average 2 additional surgeries to correct the issues presented above. In stretching and casting therapy the doctor changes the cast multiple times over a few weeks, gradually stretching tendons until the foot is in the correct position of external rotation. The heel cord is released (percutaneous tenotomy) and another cast is put on, which is removed after three weeks. To avoid relapse a corrective brace is worn for a gradually reducing time until it is only at night up to four years of age