Congenital clubfoot (CCF) is a deformity that seriously affects the function of the foot, with an incidence of about 1 per 1,000, accounting for 85% of the incidence of foot deformities, and a male:female ratio of about 2:1. The cause of the disease is still unclear, and there are various theories, such as: neuromuscular lesions, abnormal skeletal development, abnormal vascular development, genetic theory, soft tissue anomalies, and intrauterine developmental block theory. There are also theories of intrauterine growth retardation.
The Ponseti method has been recognized as the best method for the treatment of CCF in the neonatal period, and currently, our department adopts the method of plaster fixation with small needle closure and release for CCF in some cases. The following is an excerpt of the treatment evolution for the parents’ reference.
1, the etiology of congenital clubfoot.
1.1 Muscle and neuropathy theory
Some scholars believe that CCF is the result of muscle imbalance in early fetal life. Skeletal, joint and soft tissue contractures are secondary to adaptive changes in muscle strength imbalance, and the changes in muscle strength are based on neurological abnormalities. It is believed that the disease is a neuromuscular disease.
1.2 Vascular developmental abnormalities
Angiography of the CCF foot revealed vascular abnormalities in the foot, and the tarsal sinus area was depleted of blood flow and disorganized in vascular arrangement. The vascular changes are obvious in early fetal life, and this defect originates from vascular rupture or developmental defect, which leads to ischemia or thrombosis resulting in hypoxia, affecting the formation of limb buds, and finally leading to clubfoot deformity.
1.3 Soft tissue developmental abnormalities
The fibrous tissues in the muscles, tendons, tendon sheaths and fascia of the posterior calf of the sick foot of the child were significantly increased, and it is presumed that soft tissue contracture may be the primary lesion.
1.4 Skeletal developmental abnormalities
Most scholars believe that the primary pathologic changes in CCF are in the tarsus of the foot, mainly in the talus, where the ossification grooves are disorganized and the cartilage channels are more numerous compared to the ossification centers, resulting in a relatively small and deviated ossification center in the talus. The talus is deformed and smaller than normal, the neck is rotated inward and in the metatarsal plane, and the cervical body angle is reduced. The navicular surface of the talus is shifted to the medial and metatarsal surfaces. The talocalcaneal joint is subluxated and the anterior part of the talar talus is detached from the ankle point, resulting in contracture and fibrosis of the posterior aspect of the subtalar joint and the Achilles tendon and then a horseshoe deformity.
1.5 Intrauterine fetal growth retardation
It is also believed that CCF is the result of embryonic developmental block in utero. When certain factors affect the development of the foot, the position of the foot stops at a certain stage and remains until the fetus is formed, which may be the cause of CCF.
1.6 Regional growth disorder
CCF may be a regional growth disorder with the following clinical features: (1) the foot and lower leg on the affected side are smaller than on the healthy side, and the heavier the deformity, the more pronounced it is; (2) during the growth phase of the foot, even if the deformity is satisfactorily corrected, it can still develop and recur later. This suggests that the internal tissue behind the diseased foot and leg is more delayed than the anterolateral development.
1.7 Genetic theory
Epidemiological studies suggest that genetics plays an important role in the development of CCF. It is now recognized that the occurrence of CCF is the result of the combined effect of genetic and environmental factors.
2.Clinical manifestations and pathological features
Deformity: including forefoot inversion, ankle horseshoe, heel inversion, tibial internal rotation. All groups of muscles in the lower leg are poorly developed and in a state of atrophy, especially internal, posterior and metatarsal contractures, posterior contracture is serious with Achilles tendon contracture, and the pathology increases with age. When the child walks, the stride is difficult for one side to walk with a limp, and the walking is unstable for both sides.
3.Treatment method: modified Ponseti therapy
The treatment principle of congenital clubfoot is the earlier the better, because with the growth of age, the shaping force of the foot cartilage is gradually weakened, should be started immediately after birth, and good results can be expected within 3 months, most of the children through early correct manipulation and appropriate external fixation can obtain satisfactory treatment results, severe deformity through manipulation to make the contracture tissue loose, laying the foundation for surgical treatment. The Ponseti method for the treatment of CCF was first reported in 1963, i.e. early correction of congenital clubfoot by continuous plaster orthosis with subcutaneous Achilles tendon severance and foot abduction orthotic brace. This method is easy to operate, less invasive, less expensive, and has good efficacy in long-term follow-up, with a reported success rate of 92%. This non-surgical treatment has fewer complications than surgical treatment, painless walking, and better functional recovery.
3.1 Manipulation plus continuous tubular plaster fixation: The child is placed in supine position, and under nursing or sleep state, the first manipulation is performed to fully stretch the contracted ligaments and muscles on the medial and metatarsal sides of the foot, so that the displacement of the bone and joint can be reset; the child flexes the hip and knee, the doctor holds the upper part of the ankle with the index and middle fingers, and the thumb is placed on the head of the talus, and pushes the head of the talus to reset the talonavicular joint; the first metatarsal is pulled to make the foot rotate backward and then abduct The forefoot is pulled so that the foot is first rotated and then abducted to correct the forefoot inversion and high arch. Repeat the operation for 5-10 minutes each time, and be gentle with the magnitude of the technique and force, depending on whether the child is crying or not. In the selected corrected position, the knee is flexed at 90° and fixed in a long-legged tubular cast with the upper end reaching the middle or lower 1/3 of the thigh to avoid cast dislodgement, while maintaining moderate external rotation of the lower leg. The cast was changed every 7-10 days. Through 3-8 consecutive plaster orthoses, the talofibular joint can be reset, the heel bone is abducted and externally rotated under the talus, and the heel bone is internally rotated subsequently corrected.
3.2 Percutaneous small needle Achilles tendonotomy: after the foot inversion and heel inversion are fully corrected, if 10°~15° plantar flexion remains uncorrected, Achilles tendonotomy is performed. Under local anesthesia in an outpatient setting, the Achilles tendon is cut percutaneously with a small needle. After surgery, the plaster tube was fixed at 60°-70° of foot abduction and 10°-15° of dorsiflexion for 3 weeks.
3.3 Wearing orthopedic brace: 3 weeks after percutaneous Achilles tendon lengthening, remove the cast and immediately wear a foot abduction brace, keeping the affected side abducted at 70°, the healthy side abducted at 45°, and dorsiflexed at 10°~20°. The brace was worn all day for 3 months, and then at night and during daytime naps until 4 years of age. However, the compliance of the child and the family often directly affects the recurrence of horseshoe foot deformity, so it is necessary to improve the compliance by various means to strive for better long-term results.
4. Discussion:
Dr. Ponseti believes that the high arch of the horseshoe foot is related to the inversion or rotation of the hindfoot, which is the result of hyperflexion of the first metatarsal, as opposed to the forefoot rotation of the hindfoot. Therefore, to correct the horseshoe foot, the forefoot must first be rotated back to correct the high arch deformity, and then the forefoot must be abducted, and the inversion and inversion of the hindfoot must be corrected at the same time; to correct the inversion and inversion of the tarsus of the horseshoe foot, the navicular bone, dice bone, and heel bone must be gradually moved outward at the same time before only after they are externally turned to a neutral position; when the foot is sufficiently abducted, the horseshoe foot is corrected by percutaneous Achilles tendon lengthening so as not to crush the talus.
Histological studies of the fetus have revealed that the neonatal ligaments are rich in collagen eggs, which are wavy, wrinkled, and cell-rich, and are easily stretched; slow strains on the ligaments do not cause any damage, and the wrinkles reappear after a few days, allowing further strains, so the clubfoot can be corrected by rotating the posterior abduction maneuver while applying an opposing force to the lateral aspect of the talar head to avoid rotation of the talus. A well-formed cast fixes the foot in the corrected position, and the cast is replaced in 5-7 days with gradual distraction to achieve correction.
According to the footprint length curve, the foot grows fastest in the first month after birth and linearly, and the growth rate decreases significantly after one month, so the neonatal period is the best period for shaping, the cast is easy to tie, and the deformity is easy to correct. Correction at this time does not affect the development of the child’s movements such as sitting, crawling, standing and walking, and the deformity is corrected before the toddler.