The Classic: Observations on Pathogenesis and Treatment of Congenital Clubfoot
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This Classic article is a reprint of the original work by Ignacio V. Ponseti and Jeronimo Campos, Observations on Pathogenesis and Treatment of Congenital Clubfoot. An accompanying biographical sketch on Ignacio V. Ponseti, MD, is available at DOI 10.1007/s11999-009-0719-8 and a second Classic article is available at 10.1007/s11999-009-0720-2. This article is ©1972 by Lippincott Williams and Wilkins and is reprinted with permission from Ponseti IV, Campos J. Observations on Pathogenesis and Treatment of Congenital Clubfoot. Clin Orthop Relat Res. 1972;84:50–60.
KeywordsAchilles Tendon Clubfoot Plaster Cast Tendon Insertion Deltoid Ligament
In the treatment of clubfoot, as in many other orthopedic disorders, the orthopedic surgeon is handicapped because of his ignorance of the primary causes of the deformity. Many scholarly studies blame congenital clubfoot on: abnormal leg muscle development , connective tissue genetic defect , defective cartilaginous anlage of the anterior part of the talus , intra-uterine compression , dislocation of the talonavicular joint , defect in peroneal muscle innervation , defective anterior horn cells , abnormal tendon insertions [14, 21], arrest of development , tight deltoid ligament , etc.
The clubfoot deformity has not been described in embryos, but it has been observed as early as the twelfth gestational week . We studied 6 congenital clubfeet, 2 in a 90-mm-long (crown to rump) male fetus, 2 in a 7-month premature fetus and 2 in a 3-day-old infant. The clubfeet were the only apparent abnormalities in our specimens.
We found in our dissections what Scarpa , Adams , and many other authors had found before us. Possibly no fundamental knowledge has been added to the anatomy of club-foot in the past 100 years, and it appears that the cause of this deformity cannot be determined from anatomic observations. Adams in 1866 emphasized the medial angulation of the neck of the talus which he observed in all dissected clubfeet. Recently Irani and Mary Sherman  believed this deviation to be the primary fault. Adams, however, regarded the “malformed condition of the astragalus as determined by the malposition of the navicular and the os calcis and that its altered form is evident adaptation to the altered position of these bones.” Scarpa, early in the nineteenth century, asserted that in infants who have not begun to walk “this obliquity of the body of the astragalus is very trifling when compared with that of the other bones of the tarsus.” Together with Adams most authors regard “the altered form of the astragalus as the result rather than the cause of the deformity.” In the same way, changes in muscles, tendons and ligaments observed at birth and believed to cause the deformity are most likely secondary. Not much can be added, to Scarpa’s assertion “that the essence of this congenital deformity of the feet consists in the twisting of the os naviculare, of the cuboids, and of the os calcis, around their smaller axis, into which morbid direction any drawn the cuneiform bones, those of the metatarsus, and of the phalanges of the toes, and that comparatively, the astragalus is the least displaced of all the other bones of the tarsus.” We do not know the cause of these displacements although it has been established that it is partly genetic .
The following hypothesis fits most known facts: Eversion of the foot is among the last movements acquired during a normal child’s development . An equinovarus position could possibly develop in a fetus with retarded or weak contractions of the peronei and foot dorsiflexors; since the plantar flexors and invertors are stronger muscles, once established the malposition will not correct spontaneously. It may become fixed if some abnormality in the connective tissue maturation occurs ; it will be unyielding at birth in disorders of muscle development (i.e., arthrogryposis) or of innervation (i.e., spina bifida).
In the treatment of clubfoot the orthopedist endeavors to align the tarsal and metatarsal bones in proper position with the leg. The aim is a supple, well-corrected foot; a normal foot is hardly ever obtained. Conservative treatment can only succeed when all foot and leg muscles are well developed and the infant can actively move the foot although tarsal joint motion range is very restricted. Rigid feet in infants with defective or absent muscles will need surgical correction.
Movements of the 3 tarsal joints occur simultaneously; therefore, adduction and inversion must be corrected together. Plaster cast wedgings delay correction .
There is no fixed axis of rotation for the tarsal joints; rather, these joints with their ligaments are suited for a complex movement around a moving axis . Attempts to tilt the os calcis under the talus on a hypothetical anteroposterior axis of motion  fail to correct heel inversion since the articular surfaces and ligaments of the talocalcaneal prevent this motion.
Inversion and adduction of the tarsus is corrected when the os calcis is shifted and turned laterally underneath the talus at the same time that the navicular and cuboid are shifted laterally. The deltoid, the calcaneotalar, and calcaneonavicular ligaments must he stretched. The spring ligament must be lengthened sufficiently to provide room between the sustentaculum tali and the navicular for the head of the talus.
- 4.Although the clubfoot is in severe supination, the front part of the foot is everted in relation to the heel (the first metatarsal is plantarflexed to a greater degree than the fifth metatarsal) and this relationship causes the cavus deformity . The cavus is corrected by inverting the forefoot (Fig. 3). The navicular, cuneiforms and metatarsals will thus be placed in straight alignment to form the lever arm needed for the correction of heel inversion (Fig. 4A).
Attempts to correct heel inversion by forcibly everting the forefoot fail, and the cavus deformity increases as the first metatarsal is further plantarflexed . This common maneuver causes false corrections .
The lateral shift of the os calcis, navicular, and cuboid in relation to the talus can only be accomplished if the talus is stabilized against rotation. Casts extending to below the knee will allow the leg, and therefore the talus, to rotate and heel inversion will not correct. Plaster casts will have to extend from toe to groin with the knee bent 90° (Fig. 4B).
The equinus is corrected last by dorsiflexing the foot in full valgus. To prevent recurrence of cavus and false correction of heel inversion the metatarsal heads must always be in a plane perpendicular to the leg (Fig. 4B) Correction of a severe equinus is radically shortened by subcutaneous heel-cord sectioning; a rockerbottom deformity and flattening of the superior articular surface of the talus are thus prevented .
The bones will remain well aligned when normal curvature profiles of joint surfaces have developed and when normal balance is reached in the pattern and strength of ligaments, tendons, and muscles in the leg and foot. This can be accomplished only gradually through many months of treatment. Denis Browne splints  or plaster casts are usually applied following weekly manipulative corrections. In our experience with severe cases false corrections and rockerbottom deformities are more common complications with splints than with casts, probably because the tarsometatarsal joints are much less rigid than the tarsal arid ankle joints. We prefer to control the correction obtained after gentle manipulation with well-molded, thinly padded toe-to-groin plaster casts which are changed every 4–7 days. If the heelcord is sectioned, the last cast is left on for 3 weeks. With proper manipulations and plaster cast technic the initial stage of treatment need not last much longer than 2 months. Joint molding and muscle development can then be accomplished by controlling the corrected position of the feet with a Denis Browne splint with well-fitted high-topped shoes attached in 75° outward rotation. In unilateral cases the shoe on the normal foot is attached in neutral rotation. The splints are left on full time for several months and then are discarded gradually, several hours a day, but remain applied at night for at least 5 or 6 years.
It is difficult to be certain when all components of clubfoot deformity are completely corrected. Although the position of the bones of the foot and their relationship to one another can be identified by palpation, false corrections can go undetected. Roentgenograms are useful to record the initial degree of deformity and to follow its correction. Only the central part of the tarsal elements, however, are ossified in infancy except for the navicular which does not ossify until the second or third year of age. Heel inversion can be estimated by measuring the talocalcaneal angle in anteroposterior roentgenograms  but the all-important relationship between the navicular and the head of the talus cannot be determined in the infant. One cannot be sure, therefore, that the correction is adequate. We consider the deformity corrected when the foot can be fully pronated and dorsiflexed. If this is no longer possible in a subsequent visit we believe that the deformity has relapsed.
Relapses, or incomplete correction, of the deformity are common in rigid feet with poor leg muscle development. The orthopedic surgeon cannot influence rigidity of connective tissue, but he can change muscle balance by transferring tendon insertions when necessary and thereby obtain correction in many cases.
The peroneal muscles are of necessity stretched by the deformed position of the foot and appear weaker than the supinators. Following the initial treatment, strength of the peronei and of foot dorsiflexors improve to normal in some children and maintain the foot well corrected. In some cases, however, the peronei remain weak and with a slight recurrence of heel inversion deformity the anterior tibial ceases to be a dorsiflexor and becomes purely a supinator . We treat the first recurrence with manipulation and toe-to-groin plaster casts changed each week for an average of 6 weeks. In most recurrences heel inversion is more resistant to conservative treatment than is equinus. We treat the second recurrence by another series of manipulations and plaster cast applications followed by anterior tibial transfer to the third cuneiform. The Achilles tendon is lengthened when necessary to correct equinus.
Until about 1948 a release of the soft tissues in the medial aspect of the foot  was the most commonly performed operation in this clinic for treatment of recurrences or incomplete corrections in severe clubfeet. In a review of the results of treatment in 1963  it was observed that medial release operations often leave extensive scarring and stiffness in the midtarsal joints and that early transfer of the anterior tibial tendon reduced greatly the need for this operation. During the past 20 years anterior tibial transfer has been the preferred operation for the treatment of relapsed foot supination. Bone and joint surgery has been rarely required for the correction of obstinate cases.
The results of anterior tibial transfers to the dorsum of the foot done in this clinic from 1950 to 1960 have been recently evaluated. Four hundred and ninety-one feet in 338 patients were treated during this period. Of these, 73 feet in 42 patients had an anterior tibial transfer. During the past year we have been able to see 34 of these patients with a total of 58 feet operated on. The operations were performed at ages ranging from 6 months to 10 years with an average of 5 years. The follow-up period ranged from 9 to 20 years with an average of 16 years.
The tendon was transferred to the third cuneiform in 43 cases and to the cuboid in 15. The tendon was transferred to its new attachment without changing its position underneath the ankle retinaculum except to provide a straight line of pull. In all cases the tendon was attached to the bone through a drill hole using a Bunnell pull-out suture. The foot was immobilized for 4 weeks in a toe-to-groin plaster cast. In addition to the anterior tibial transfer the Achilles tendon was lengthened in 11 feet; the extensor hallucis longus was recessed to the neck of the first metatarsal in 5 feet; and a medial release operation was done in 4 feet (one of these had already had a medial release operation 4 years earlier). The anterior tibial transferred in 2 feet with persistent supination following astragalectomy done 2 years before. Triple arthrodesis and anterior tibial transfer were done in 2 feet with relapse following medial release operations done 7 years previously.
Persistent or relapsed supination was treated with medial soft-tissue release in 4 feet 1–3 years following the tendon transfer, and one foot had a triple arthrodesis 10 years later. The last foot and one foot of the preceding group had medial release operations at the time of the transfer. The Achilles tendon was lengthened in 11 feet 1–10 years following the transfer. In 2 feet severe planovalgus following transfer of the anterior tibial tendon to the cuboid was treated by retransferring the tendon to the second cuneiform and Grice bone block.
The results were assessed by clinical and roentgenographic examination. We obtained AP and lateral roentgenograms of the feet with the patient standing and lateral roentgenograms with the feet in maximal dorsiflexion and in maximal plantarflexion. All patients are carrying on active lives and have no pain nor complaints referable to their feet. Most of them are or have participated in high school athletics. Clinically the heel was well aligned in 33 feet; it was in 10° of inversion or less in 15 feet and in slight eversion in 10 feet (4 feet of the last group had transfers to the cuboid; 2 of these 4 had retransfers to the second cuneiform and Grice bone block). In all cases the forefoot was well corrected except for 3 feet with 10–20° of adduction. A slight tendency of cock-up deformity in the metatarsophalangeal joint of the big toe was observed in 12 feet. The strength of the transferred anterior tibial was normal in 53, 4+ in 3 feet, and 3+ in the 2 feet with the retransferred tendon. Active ankle dorsiflexion was possible to more than 10° in 32 feet, from 10° to neutral in 21 feet, to 5° of equinus in 3 feet, and to 10° of equinus in 2 feet. Active ankle plantarflexion to more than 20° was seen in 48 patients. Plantarflexion was limited to 15° in 5 patients and to 10° in 5 patients. Subtalar motion was within normal limits in 30 feet, limited to about 50 per cent of normal in 18 feet, and absent in 10 feet.
This survey suggests that anterior tibial tendon transfer to the third cuneiform is a useful operation for the treatment of severe clubfeet which relapse following conservative treatment. Of the 58 feet surveyed, severe, foot supination recurred in only 5 and in 2 the deformity became grossly overcorrected. Heel inversion was completely corrected in three-fourths of the cases. Half of the cases had normal talar motions. Severe joint stiffness was seen in feet with medial soft-tissue releases. The 2 feet without tali gained good balance. As in all previous studies, for un-known reasons, difficult cases were encountered which yielded only to bone and joint surgery.
Morphological studies of 6 clubfeet (2 in a 90-mm crown to rump fetus, 2 in a 7-month-old fetus and 2 in a 3-day-old infant) gave no clues to the pathogenesis of this deformity. Anterior tibial tendon transfer to the third cuneiform is a useful operation for the treatment of cases of severe, relapsing clubfoot.
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