A club foot is one in which the navicular bone and the forefoot are medially situated relative to the talus (metatarsus adductus) and the calcaneus is directly locked under the talus, so that the heel is in varus, and in equinus.

There are generally considered to be four types of club feet. One is a positional deformity, related to the foot being held in a bad position in utero. This deformity is corrected after application of only one or two corrective casts. The second type, which most of this section is concerned with, is the anatomic club foot. Club feet may also be associated with muscle absence, such as arthrogryposis or clear muscle imbalance, such as myelodysplasia.

While the overall incidence is about 1 in 1000 births, a first-degree relative of an affected individual has a relative risk of 20 to 30. Some populations, such as the Hawaiians, have a much higher incidence at about 6 in 1000. The inheritance pattern is multifactorial with a threshold effect, and is subject to environmental influences.

Muscle imbalance has been suggested to play a role in the aetiology. Alterations in muscle fibre types suggest that it might be a dystrophy or a neuropathy. Numbers of muscles do not appear to be reduced. The primary deformity has been seen to reside in the talus, which shows foreshortening of the head. The condition can be produced by intrauterine insults, including administration of insulin to animal embryos.

Treatment of the condition never produces a perfectly normal foot. The calf is always smaller than normal and the foot is usually one or two shoe sizes smaller. Most patients, however do not have muscle deficiencies, and if the condition is well treated, it will not recur, nor does it need long-term bracing. It remains to be seen how much of a factor the treatment effect contributes to the smaller foot and calf: 50 per cent of foot growth is presumably complete by the age of 2. If a child spends a good part of that time in casts, growth is likely to be suppressed.

It is obviously important to determine the type of club foot being treated. The initial treatment is the same, with application of a cast. An arthrogrypotic foot is then treated differently from an ananatomical club foot, however. Tendon releases are ultimately necessary; thus, in an arthrogrypotic foot, lengthening of tendons is not sufficient.

The diagnosis is suggested on manipulation of the foot; it is more supple, and it is easier to achieve more correction when the deformity is positional. The arthrogrypotic foot is suggested by the presence of dimpling, suggesting loss of subcutaneous fat, and contractures (Fig. 4) 2599. Attempts to stimulate muscle activity by tickling the bottom of the foot, or stroking over various muscle groups fail. Radiographs of the leg show absent or diminished musculature. Dislocation of the hip occurs at a higher frequency in club foot patients; rigid dislocations, or abnormalities at other joints may suggest arthrogryposis multiplex congenita, a generalized condition.

The defect in the anterior tibial muscle does not necessarily indicate an underlying neurological problem. The anatomical club foot cannot be adequately dorsiflexed, and the muscle is functioning at a mechanical disadvantage. If the toe extensors and the peroneal muscles are functional the patient probably has no neurological problem.

The first method of treating club foot is casting. The foot is always manipulated first, and then plastered. In the early days of club foot casting, the foot was dorsiflexed before correction of the varus component. This causes the forefoot to come up, but not the hind-foot, creating a rocker bottom deformity. Surgeons then tried to swing the foot into valgus, while at the same time keeping it in equinus. The key to modern management, whether by casting or by surgery, is to recognize that the key feature of club foot is the locking of the calcaneus under the talus. The subtalar joint is an oblique axis joint, so that the foot goes into dorsiflexion and valgus at the same time, or and into varus and inversion. For the heel to be dorsiflexed, the calcaneus cannot be locked under the talus, but must be able to be swung out laterally. Some of the dorsiflexion of the foot also occurs at the subtalar joint. It follows then, that in casting, one tries to evert the heel, and at the same time bring it up and out.

The success of casting and manipulation can be assessed on radiographs taken after about 3 months. Lateral views are usually taken on a dorsiflexion frame, while the anteroposterior radiographs are taken with the patient weight-bearing. If the foot is corrected, the calcaneus and talus cross on the lateral view. Lines drawn through the long axis of the bones form an angle of about 30 to 50° (Fig. 6) 2601. The anteroposterior view also shows the bones to be disengaged, with the talus pointing to the first metatarsal, and the calcaneus pointing to the fifth metatarsal, forming an angle of about 20 to 40°. An acceptable foot can usually be produced by prolonged casting: casting for 9 months to 1 year is not uncommon. However, ligaments are usually stronger than the bones in children, and casting can cause crushing or deformation of the foot. The round bones in the foot have circular growth plates, a fact not often appreciated because there is no secondary ossification centre around them. Casting can cause significant deformities, such as flat topped tali, and the foot then becomes rigid. Club feet treated with prolonged casting invariably recur. The impression that corrected club feet need bracing for many years is derived from experience with incompletely corrected feet. Only those with an arthrogrypotic or neurological cause need prolonged bracing.

Casting is usually continued for about 3 months, with changes weekly for the first month or 6 weeks, and then biweekly. Particular care is required in children with insensate feet, such as those with myelodysplasia, since they will not be fretful even if the cast is exerting too much pressure. Some surgeons have suggested that operations delayed until about 1 year of age have better results. These surgeons temporize by performing subcutaneous Achilles tenotomies. However, joints tend to develop in the wrong places, and a substantial part of foot growth is finished by that time. We usually operate after the age of 3 months if casting has failed, preferably at around 5 or 6 months, when the child is a little bigger and stronger.

All surgical procedures are essentially similar. An incision is made from the first metatarsal to the dorsum of the talonavicular joint, down around the medial malleolus, dipping over the abductor hallucis, and then up along the interval between the tendon Achilles and the posterior compartment. Some surgeons prefer the Cincinnati incision, which is a horizontal incision that runs medially and laterally around the foot. This incision permits exposure to the lateral ankle structures, but a wide medial exposure also allows access to the lateral ligaments.

In an anatomical club foot, the Achilles tendon, the posterior tibial tendon, and the tendons of the flexor hallucis longus and the flexor digitorium longus are Z-lengthened. The neurovascular bundle is identified and followed into the plantar surface of the foot, where the overlying deep muscles and fascial band are incised. The talonavicular joint is freed, and the subtalar joint, including the posterior capsule, is released. One great area of controversy is whether the interosseous ligaments should be released, and if so, to what degree. The objections to releasing them completely are based on the potential of obtaining a severe flat foot. However, complete release of all of the interosseous ligaments is advisable. The calcaneus is then positioned under the talus, facing laterally, and with just a trace of valgus. This position is held with a pin through the calcaneus and talus, and up into the tibia. The talonavicular joint is held in position with a second pin to avoid subluxation of the navicular bone on to the neck of the talus. This approach gives a mild flat foot, with a trace of medial overhang, but there are no problems with recurrence, and the foot does not require bracing. A programme to strengthen all the foot muscles is then initiated. Sometimes they need a mild University of California at Berkeley type arch support.

One of the major breakthroughs of the last several years has been the understanding of residual internal rotation deformity in patients with club feet. It had been thought that the internal rotation was largely secondary to internal tibial torsion. Whether there is internal torsion initially is questionable as patients who have been in a cast for several months show marked external tibial torsion, because the interosseous ligaments give fairly easily in response to the casting. Persistent internal rotation is due to the fact that the lateral border of the calcaneus is still bound by the calcaneal-fibula ligaments posteriorly. This prevents rotation of the calcaneus, so that the back becomes medial and the front faces laterally. This deformity is corrected by releasing these ligaments and rotating the calcaneus at the time of pin placement.

Patients presenting late with uncorrected club feet have generally undergone salvage procedures. In children of 8 years old or more, extensive releases give poor results, because the joints are already formed. In these cases, an attempt is made to accept the basic deformity, but to make the feet more plantigrade. The operations usually consist of metatarsal osteotomies and removal of a lateral wedge from the heel. More extensive releases can be performed on older patients, perhaps up to the age of 8 years. There is generally relative overgrowth of the lateral border of the foot, and some of the bone has to be removed from that side.

Uncorrected club feet in a mature individual require a triple arthrodesis.

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