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Adult Cavovarus Foot Abstract Cavovarus foot deformity, which often results from an imbalance of muscle forces, is commonly caused by hereditary motor sensory neuropathies. Other causes are cerebral palsy, cerebral injury (stroke), anterior horn cell disease (spinal root injury), talar neck injury, and residual clubfoot. In cavovarus foot deformity, the relatively strong peroneus longus and tibialis posterior muscles cause a hindfoot varus and forefoot valgus (pronated) position. Hindfoot varus causes overload of the lateral border of the foot, resulting in ankle instability, peroneal tendinitis, and stress fracture. Degenerative arthritic changes can develop in overloaded joints. Gait examination allows appropriate planning of tendon transfers to correct stance and swing-phase deficits. Inspection of the forefoot and hindfoot positions determines the need for soft- tissue release and osteotomy. The Coleman block test is invaluable for assessing the cause of hindfoot varus. Prolonged use of orthoses or supportive footwear can result in muscle imbalance, causing increasing deformity and irreversible damage to tendons and joints. Rebalancing tendons is an early priority to prevent unsalvageable deterioration of the foot. Muscle imbalance can be corrected by tendon transfer, corrective osteotomy, and fusion. Fixed bony deformity can be addressed by fusion and osteotomy. C avovarus foot can present in childhood or adulthood as either progressive or fixed, depending on the underlying cause and its severity. Cavovarus foot deformities are categorized by etiology. The four main causes of the adult cavovarus foot are neurologic, traumatic, the result of residual clubfoot, and idiopathic (Table 1). Etiology Neurologic The hereditary motor and sensory neuropathies (HMSNs) that cause cavus foot deformity are mostly motor, rather than congenital or progressive. 1 Muscle imbalance usually predominates in agonist-antagonist pairs, such as a weak anterior tibial muscle with a strong peroneus longus, or a weak peroneus brevis with a strong tibialis posterior muscle. Subgroups of the HMSNs have in- cluded Charcot-Marie-Tooth (CMT) disease and Dejerine-Sottas disease; however, gene analysis is rapidly changing the classification and un- derstanding of HMSNs. For example, 17 variants of CMT disease have been determined with gene map- ping. Subgroups now include demyelinating and axonal patholo- gies subdivided into autosomal- dominant, autosomal-recessive, and X-linked transmission groups. Be- cause there is no definitive diagnos- tic technique for patients with an HMSN, the diagnosis is made based Alastair S. E. Younger, MB, ChB, MSc, ChM, FRCSC, and Sigvard T. Hansen, Jr, MD Dr. Younger is Director, Foot and Ankle Program, Providence Health Care, and Clinical Associate Professor, The Division of Lower Limb Reconstruction and Oncology, Department of Orthopaedics, University of British Columbia, Vancouver, BC, Canada. Dr. Hansen is Chief, Foot and Ankle Service, and Professor and Chairman Emeritus, Department of Orthopaedics, University of Washington, Harborview Medical Center, Seattle, WA. None of the following authors or the departments with which they are affiliated has received anything of value from or owns stock in a commercial company or institution related directly or indirectly to the subject of this article: Dr. Younger and Dr. Hansen. Reprint requests: Dr. Younger, Univer- sity of British Columbia, 401-1160 Burrard Street, Vancouver, BC V6Z 2E8 Canada. J Am Acad Orthop Surg 2005;13:302- 315 Copyright 2005 by the American Academy of Orthopaedic Surgeons. 302 Journal of the American Academy of Orthopaedic Surgeons on the appearance of the foot and a positive family history. Peripheral neuropathy usually causes weakness of the intrinsic muscles, followed by more proximal involvement. The long flexor and extensor tendons overpower the lum- brical and interosseus muscles, causing flexion at the interphalangeal joints and hyperextension at the metatarsophalangeal joints. Sublux- ation followed by dislocation at the metatarsophalangeal joint causes the plantar pad to migrate distal to the metatarsal head, bringing the thinner, more proximal skin under the weight-bearing metatarsal head. Proximal weakness may affect peroneal and tibial nerve distribution. 2 Relative weakness of the anterior tibialis and the peroneus longus muscles causes plantar flexion of the first ray relative to the lesser metatarsal heads. In time, these deformities become fixed. The combination of the relatively strong tibialis posterior and peroneus longus muscles with the weak peroneus brevis and tibialis anterior muscles results in a hindfoot varus and forefoot valgus (pronated) position. In patients with CMT disease, the peroneus longus is hypertro- phied with normal muscle architec- ture, creating imbalance in relation to the tibialis anterior muscle. 3 Re- cruitment of the extensor hallucis in the absence of a functional tibialis anterior further drives down the first metatarsal head via the windlass mechanism on the medial plantar fascia. Patients also often present with forefoot adduction and plantar flexion of the first ray. When a secondary equinus deformity develops at the ankle, the patient with ad- vanced involvement walks with a high-stepping drop-foot gait with hyperextension of the knee. Other neurologic and congenital causes of cavovarus foot include conditions with more profound proximal involvement (eg, amyotrophic lateral sclerosis [Lou Gehrig’s disease], Huntington’s chorea, Friedreich’s ataxia) that often make addressing foot deformity a lower priority. Depending on the area of the motor cortex involved and the resultant weakness and spasticity, patients with cerebral palsy may have a planovalgus (66%) or cavovarus deformity (34%) (23 of 35 and 12 of 35 patients, respectively). 4 Mulier et al 5 reported on 17 patients with tendon transfer for equinovarus. Foot involvement in cerebral palsy varies in nature and presentation. Equinus is rarely seen alone, and a varus or valgus component is almost always associated with a tight heel cord. The deformity varies between the swing and stance phases of gait, particularly in patients with a flexible deformity . Adult patients with intracerebral bleeding or closed head injury may develop subsequent equinus and equinovarus deformities. The suc- cess of treatment depends on the degree and severity of central involvement. Patients with poor cognition or with extensive stroke-related motor, proprioceptive, or sensory deficits are poor candidates for reconstructive surgery. In some wheelchair-bound patients, tendon releases may be indicated to assist in shoe wear or transferring or to re- solve pressure sores. A delay of 18 to 24 months between cerebral injury and reconstructive surgery is advis- able because of the possibility of var- ious degrees of functional recovery. Poliomyelitis affects the anterior horn cells in the spinal cord and causes a lower motor neuron paraly- sis that affects specific spinal roots. The level of root involvement determines whether patients develop a cavovarus, planovalgus, or calcaneus gait pattern. Depending on the extent and pattern of deformity, patients with poliomyelitis may benefit from limited foot fusions or osteotomies as well as in-phase and out-of-phase muscle transfers. Congenital multiple arthrogrypo- sis is usually obvious by its other manifestations, resulting in a stiff fixed equinovarus foot deformity. Amyotrophic lateral sclerosis and spinal muscular atrophy also can result in progressive cavovarus foot position. A unilateral progressive cavovarus foot may be caused by an instrinsic spinal cord lesion. In a re- view of 43 patients with diastema- tomyelia, 11 had a cavus foot and 4 had a clubfoot. 6 Progression of cavus foot is an indication for tethered cord release. 7 Pes cavus associated with scoliosis suggests a neurologic origin for both conditions. 7 Traumatic The muscle contractures created by deep posterior compartment syndrome cause the tibialis posterior and the flexor digitorum longus muscles to pull the foot into an equinus and cavovarus position. Severe scarring after burns, crush injuries, or venous stasis may pull the foot into the cavovarus position. A talar neck fracture malunion can leave the distal portion of the talar neck in a shortened, dorsally and medially translated position, resulting in a fixed varus position of the subtalar, talonavicular, and calcaneocuboid joints. 8 Four Primary Causes of Adult Cavovarus Foot Neurologic Hereditary motor and sensory neuropathies Cerebral palsy Aftereffects of cerebral injury (stroke) Anterior horn cell disease (spinal root injury) Spinal cord lesions Traumatic Compartment syndrome Talar neck malunion Peroneal nerve injury Knee dislocation (neurovascular injury) Residual clubfoot Idiopathic Table 1 Alastair S. E. Younger, MB, ChB, MSc, ChM, FRCSC, and Sigvard T. Hansen, Jr, MD Volume 13, Number 5, September 2005 303 Injury to the deep branch of the peroneal nerve or to the L5 nerve root resulting in peroneal muscle weakness leaves the action of the tibialis posterior and long toe flexor muscles unopposed, causing hindfoot and forefoot varus. For example, knee dislocation with permanent injury to the peroneal nerve may lead to an equinocavovarus position of the ankle or foot, requiring multiple tendon transfers early in treatment. Heel varus may subject the peroneus brevis tendon to repetitive injury, resulting in a degenerative tear and possible rupture. Loss of the peroneus brevis tendon can progress to a significant cavovarus foot. Residual Clubfoot The untreated or partially treated clubfoot can result in a persisting cavovarus and equinus position in adults, with the foot fixed in a char- acteristic hindfoot and forefoot varus position. Other residual prob- lems may include an overlengthened heel cord, causing a calcaneus gait or restricted ankle motion secondary to a flat-topped talus. 9 Idiopathic In some patients, an underlying cause is not found. The genetic pat- terns of some HMSNs are still un- known, offering promise that many of the presently idiopathic causes will be better understood in the fu- ture. Idiopathic peripheral neuropathy is the most distressing cause of a cavus foot, often presenting early with neuropathic ulcers and sensory imbalance as well as motor involvement. In all cases, early muscle rebalancing by transfers and osteotomies is required, as are ongoing physiotherapy and shoe modifica- tions. Clinical Presentation Patients often present with pain caused by increased stress on one part of the foot. Overload of the cuboid region occurs with the hindfoot and forefoot varus position seen in patients with clubfoot. Patients with CMT disease may overload the lateral border of the foot, the first metatarsal head, 10 or the lateral metatarsal heads. This increased load can cause stress fractures, most commonly in the fifth metatarsal. In runners, the cavus foot position causes increased load on the metatarsal heads and on the calcaneus. 11 The varus position of the hindfoot also may result in lateral ankle instability, with the lateral collater- al ligaments being continuously overloaded by the medially displaced moment arm of the Achilles tendon. Symptomatic metatarsalgia is caused by distal migration of the fat pad underneath the metatarsal heads in association with claw toe deformity. Prolonged weight bearing in the cavus position may cause overload of the ankle and of the joints of the so-called triple-joint complex (ie, the subtalar, talonavicular, and calcaneocuboid joints). Secondary degenerative change occurs in the overloaded medial aspect of the ankle joint, often associated with varus tilt of the talus and concomitant lateral ligament laxity. A family history of similar deformity indicates a hereditary cause. Spontaneous occurrence of a unilateral clubfoot, especially when ac- companied by other neurologic symptoms, suggests a spinal cord lesion, necessitating additional work- up. Physical Examination Patients should be examined while walking and standing, and limb alignment and the weight-bearing posture of the foot should be assessed. The presence of foot drop, hyperextension of the great or lesser toes, and varus or valgus positioning of the forefoot and hindfoot may be appreciated during the swing phase of gait. Stance phase is analyzed from heel strike to toe-off. The position of calluses should reinforce the observations of gait. The range of motion of all surrounding joints should be measured. The heel cord is tested for tightness with the knee both flexed and extended. Lack of change in equinus deformity between the two positions may indicate a mechanical block to ankle dorsiflexion from a tight posterior capsule or anterior osteophytes. Oc- casionally, an isolated contracture of the soleus causes restriction of ankle dorsiflexion with the knee in both flexion and extension. Equinus with the knee straight, and increased dorsiflexion with the knee flexed, indicate a tight gastrocnemius muscle. Function and strength of all muscles and nerve roots in the region should be mapped at least twice. The power or strength of each muscle is tested against active resistance ap- plied by the examiner, and the results are graded using the Medical Research Council scale. The grading of muscular response in this scale ranges from 0 to 5: grade 0, no contraction; grade 1, flicker or trace of contraction; grade 2, active movement with gravity eliminated; grade 3, active movement against gravity; grade 4, active movement against gravity and resistance; and grade 5, normal power. Tendons are palpated to determine whether they are a source of pain. Tendon imbalance may cause dynamic deformity (eg, the peroneus longus may be recruit- ed to compensate for a weak peroneus brevis). The dynamic deformity causes a plantarflexed position of the first ray and an increased cavus deformity. Complete neurologic examination also should include reflexes, sensation, and vibratory response. A Coleman block test should be performed to separate forefoot- driven hindfoot varus from an intrinsic or tibialis posterior muscle– driven hindfoot varus. A flexible hindfoot with a fixed plantarflexed first ray will correct with the Cole- man block test, indicating that cor- Adult Cavovarus Foot 304 Journal of the American Academy of Orthopaedic Surgeons rection of the forefoot position should correct the hindfoot varus (Fig. 1). Failure of the hindfoot varus to cor rect indicates a fixed hindfoot deformity that may require both a hindfoot procedure to correct the varus (eg, calcaneal osteotomy or subtalar fusion) and a dorsiflexion osteotomy of the first ray. 10 The results of the Coleman block test must be interpreted in the context of the remainder of the physical examination because a patient with fixed hindfoot varus and a valgus position of the forefoot still requires correction of the forefoot position. When in doubt, a lateralizing calcaneal osteotomy should be performed because the varus deformity of the hindfoot remains undercorrected in all but the mildest cases. Radiographic Evaluation Weight-bearing anteroposterior and lateral views of the foot and ankle are required, along with a calcaneal axial view. Oblique views of the foot are occasionally helpful to visualize changes at the tarsometatarsal joint level. Patients with a cavus foot position often have a degenerative spur in the posterior aspect of the subtalar joint. A lateral radiograph of the patient performing a Coleman block test will indicate the degree of correction obtainable with a first ray osteotomy. A modified Cobey view may be a better guide for hindfoot alignment than a calcaneal axial view. 12 A Canale view of the talar neck is best for finding talar neck fracture and malalignment. 13 Com- puted tomography (CT) scans also may be of value in assessing hindfoot position, but they provide only a simulated weight-bearing view. 14 A CT scan of the foot allows more ac- curate assessment of degenerative changes within the foot. Techne- tium 99m bone scanning can assist in identifying involved joints. Anes- thetic blocks of symptomatic joints can be identified fluoroscopically and can assist in determining the source of pain. Nonsurgical Treatment Orthoses An orthotic device may be fashioned to broaden the weight-bearing area in the foot. Because custom orthoses are expensive and the high- arched foot is hard to fit, patients initially may wish to modify an off-the-shelf insert. Commercially available metatarsal pads may be added to a foam rubber insert. Pa- tients with first metatarsal head overload may need a cutout for the first metatarsal head. Carpet felt also can be added to the shoe, with a cutout for the first metatarsal head. If the modified shoe insert works, a custom-made tridensity or semirigid orthosis can be fashioned using the prefabricated insert as a tem- plate. A metatarsal pad can be added to the semirigid or tridensity orthosis, with a metatarsal head cutout. Hard orthoses are often poorly toler- ated by patients with rigid cavus feet. A high-arched orthosis actually may increase ankle instability and may need to be modified. A high boot or an off-the-shelf ankle brace may be used. Braces that lace up are easier to fit inside a shoe or boot and offer stabilization similar to that of plastic upright ankle braces. Patients with muscle weakness often benefit from a full-length custom ankle-foot orthosis (AFO) to prevent foot drop. Orthotic modifi- cations can be integrated into the AFO, providing more control over ankle instability than would a brace Figure 1 The Coleman block test. A, On initial examination, the hindfoot is in varus. B, The patient stands with a book or block under the lateral side of the forefoot, and the hindfoot is reexamined. Heel varus correction indicates that the hindfoot deformity is flexible and that the varus position is secondary to the plantarflexed first ray, or valgus position of the forefoot. Alastair S. E. Younger, MB, ChB, MSc, ChM, FRCSC, and Sigvard T. Hansen, Jr, MD Volume 13, Number 5, September 2005 305 alone. Patients with an equinus deformity may require a brace to prevent its progression. A splint should be worn every night when the equinus contracture is progressing. Brac- ing also is important for maintaining correction after heel cord lengthening. Often a full clamshell brace or bivalved cast is required because the deformity will overcome the correction obtainable with a posterior brace and anterior straps. Shoe Wear The high-arched foot may be difficult to fit inside a shoe, particularly a slip-on style of shoe. Initially, an off-the-shelf lace-up shoe with an extra-deep toe box will accommo- date the foot. A lace-up boot has the added benefit of allowing more room for the arch and providing some degree of ankle stability. Extra depth and custom shoes may be required to fit insertable orthoses, AFOs, and very-high-arched-foot or claw toe deformities. Surgical Treatment Surgical goals, expectations, and recovery times should be clearly out- lined to the patient. All normal joints should be preserved when possible. In patients with muscle imbalance, well-planned osteotomies and tendon transfers provide more reli- able outcomes than does triple ar- throdesis. Symptomatic degenerative joints should be fused and contracted soft tissues released. Contracted tendons also should be released or transferred, or the muscle-tendon junction fractionally lengthened. Osteotomies, tendon transfers, or releases can correct muscle imbalance in most patients with a neurogenic cavovarus foot. Although some surgeons recom- mend initial treatment with orthoses and bracing, others believe that, in some cases, surgical inter- vention is indicated as soon as the diagnosis is made. A cavovarus clawfoot is a progressive deformity in the presence of muscle imbalance. Therefore, the muscle imbalance must be corrected to stop the progression before fixed deformity and unsalvageable secondary joint de- generation occur. Correction of muscle imbalance requires transfer of the two most deforming muscles— the long peroneal and tibialis posterior tendons. Consideration should be given to a lateralizing calcaneal osteotomy and dorsiflexion osteotomy of the first ray. Soft-Tissue Release and Tendon Lengthening In the equinovarus foot, contractures affect the structures of the plantar and medial aspects. Depend- ing on the position and extent of the contracture, a posteromedial release will be required. A tight heel cord can be addressed with either a gastrocnemius recession (slide) or heel cord lengthening (Table 2). These procedures are performed for hindfoot equinus deformities, which only are diagnosed by reviewing lateral weight-bearing radiographs. Forefoot equinus is measured using the talo-first metatarsal angle (normal, 0° to 3°). Hindfoot equinus is measured by a decreasing calcaneal pitch angle as the ankle plantarflexes. For the patient with a unilateral cavus foot, comparison with a weight-bearing lateral radiograph of the normal side is helpful. When the gastrocnemius component alone is tight, a gastrocnemius recession can be performed. The range of passive ankle dorsiflexion is examined with the knee in both flexion and extension. If the range does not change and if the palpated Achilles tendon does not feel tight, then a mechanical block to dorsiflexion is likely present, caused by a tight posterior capsule, anterior osteophytes, or a tight soleus component. A weight-bearing lateral radiograph of the ankle may illustrate impinging anterior osteophytes. For open heel cord lengthening, the incision is made just posterior and medial to the ankle joint. The Achil- les tendon is identified through this incision by deep dissection. The neurovascular bundle is identified when an extensive release is planned. 15 A percutaneous heel cord lengthening also can be performed, although over- lengthening may result in a calcaneus gait and weakness in plantar flexion. A split tibialis posterior tendon transfer should be performed at the same time if the hindfoot is in varus during the stance phase of gait. 16 The flexor digitorum longus is lengthened Soft-Tissue Release and Tendon-Lengthening Procedures Range of Forced Ankle Dorsiflexion (degrees) With the Knee in Flexion Range of Forced Ankle Dorsiflexion (degrees) With the Knee Extended Procedure >10 <5 Gastrocnemius recession 0 to 10 5 (dorsiflexion) to 20 (plantar flexion) Gastrocnemius recession and/or open heel cord lengthening <0 20 (plantar flexion) Open heel cord lengthening or percutaneous Achilles tendon lengthening <0 Does not change with knee flexion; heel cord not tight Ankle joint débridement and posterior release <0 Does not change with knee flexion; heel cord tight Percutaneous Achilles tendon lengthening and posterior release if the foot does not correct Table 2 Adult Cavovarus Foot 306 Journal of the American Academy of Orthopaedic Surgeons or transferred if the toes are flexed with the foot in a neutral position. The flexor hallucis longus tendon may be released at the knot of Henry, transferred, or fractionally lengthened at any level at which it can be safely exposed. 17 Transfer into a very weak or paralyzed peroneus brevis can be very effective. An isolated gastrocnemius recession is performed using a midcalf medial incision over the palpable junction of the gastrocnemius with the heel cord. The tissue plane between the sural nerve, the fascia, and the tendon is developed. The isolated gastrocnemius tendon is sec- tioned, and adequate ankle dorsiflexion with the knee extended is confirmed after the release. Soft-tissue contractures may prevent the ankle joint from correcting after tendon release (Fig. 2). In this situation, the deltoid ligament can be released at the posterior aspect of the medial malleolus. The ankle and subtalar joint capsule also may need to be released. After isolating the neurovascular bundle, the capsule is identified anterior and posterior to the tibialis posterior tendon. As with a clubfoot, it may help to divide the posterior aspect of the syndesmosis between the tibia and fibula to allow the talus to rotate posteriorly in the ankle mor tise. The fat and fascia surrounding the superficial and deep compartments also can be scarred or contracted and may need to be released (Fig. 2). The midfoot may be held in the equinovarus position. Release of the plantar fascia will allow correction and can be performed by multiple small incisions, excision, or exten- Figure 2 A, Weight-bearing lateral radiograph of a 44-year-old man with a cavovarus foot deformity associated with severe equinus secondary to multiple sclerosis. B, Weight-bearing lateral radiograph of the normal contralateral foot confirmed that most of the deformity was at the level of the ankle joint, with only a small portion secondary to midfoot cavus. C, Weight-bearing lateral radiograph of the foot in panel A taken 6 months postoperatively. A posteromedial release was performed. Single-stage correction was achieved with a cast change under anesthetic at 2 weeks. Claw toe deformities were treated by interphalangeal fusions, and residual forefoot valgus deformity was corrected by a dorsiflexion osteotomy of the first ray. Calcaneal osteotomy was not required because the foot corrected beyond neutral. Eight months postoperatively, the patient ambulated for 1 hour with a single cane, which was used more for balance than to relieve pain. Alastair S. E. Younger, MB, ChB, MSc, ChM, FRCSC, and Sigvard T. Hansen, Jr, MD Volume 13, Number 5, September 2005 307 sile release from the calcaneus. 18 Midfoot cavus deformities should be addressed by a plantar fascia release, with releases of the deep muscles and their tendon sheaths as necessary. 19 An extensive release of the talonavicular joint capsule also may be required. If the soft-tissue releases fail to correct the foot position, then osteotomies or fusions will be required to correct the foot to neutral. After trauma and a compartment syndrome, correction may require tendon releases, resection of infarct- ed tissue within the muscle, and ad- vancement of muscle tendon units as well as tendon transfers or corrective osteotomies and fusions. 20,21 In Volkmann’s ischemic contracture, a significant length of the necrotic and scarred tendon and muscle may need to be removed to ensure a permanent release. This extensive surgical procedure requires exacting preoper- ative knowledge of the neurovascular anatomy of the extremity. Tendon Transfer Out-of-phase transfers (eg, tibialis posterior to tibialis anterior tendon transfer) are recommended for younger patients with lower motor neuron pathology. The anterior transfer of the flexor digitorum longus and flexor hallucis longus tendons has been used as an out-of- phase transfer for stroke patients. 22 Specific requirements must be met. (1) The transferred muscle should both be strong enough and have an appropriate excursion to perform the function of the substituted muscle. 18 A grade of power will be lost after the transfer. (2) The transferred tendon should be inserted close to the substituted tendon and routed in a comparatively direct line. (3) The transferred tendon should be routed in a tendon sheath, either its own or the sheath of the substituted tendon, or within tissues that will allow it to glide. (4) The nerve and blood supply of the transferred tendon should not be damaged. (5) The joints on which the tendon is to act must be functional (ie, have a reasonable range of motion, be stable, and have minimal deformity). (6) The tendon should be attached directly to bone, or indirectly by another tendon using a tendon weave, and it should be in slight to moderate tension. For example, the tibialis posterior tendon can be transferred through the interosseous membrane and inserted into the medial cuneiform via a weave into the tibialis anterior. Agonists are preferable to antagonists. 18 Tendon transfers can be categorized according to whether they affect gait in either the swing phase or stance phase 5,23,24 (Ta- bles 3 and 4). Debate exists as to the donor morbidity of the transferred tibialis posterior tendon. In the cavus foot position, the released tendon does not cause a subsequent planovalgus deformity because the bones and ligaments of the foot apparently are able to maintain the medial arch. In contrast, the tibialis posterior ten- In-Phase Tendon Transfers for Swing Phase and Stance Phase Phase Donor Recipient Indication Concomitant Procedure Swing Extensor hallucis longus Tibialis anterior Clawed first ray; weak dorsiflexion First ray IP fusion; MTP joint release Extensor hallucis longus Peroneus tertius (complete or split) Weak dorsiflexion with inversion on swing phase First ray IP fusion; MTP joint release Extensor digitorum brevis Extensor digitorum longus stump Clawtoes IP fusions or excisions; MTP joint releases Extensor digitorum longus Peroneus tertius Clawed lesser toes; weak dorsiflexion IP fusions or excisions; MTP joint releases Tibialis anterior (complete or split) Peroneus tertius Excessive forefoot inversion during swing phase — Stance Flexor hallucis longus Peroneus brevis Weak ankle eversion Calcaneal osteotomy Flexor hallucis longus Peroneus longus Flexible forefoot varus Midfoot fusion Peroneus longus Peroneus brevis Weak ankle eversion Calcaneal osteotomy Peroneus brevis Peroneus longus Weak ankle eversion and flexible forefoot varus Calcaneal osteotomy Tibialis posterior (complete or split) Peroneus brevis Weak ankle eversion Calcaneal osteotomy Tibialis posterior (complete or split) Peroneus longus Forefoot varus and weak ankle eversion Calcaneal osteotomy IP = interphalangeal, MTP = metatarsophalangeal Table 3 Adult Cavovarus Foot 308 Journal of the American Academy of Orthopaedic Surgeons don is an essential part of the medial column in a flexible planovalgus foot. For stroke patients, a heel cord lengthening on its own is rarely suf- ficient because the tight tibialis posterior tendon will cause a varus heel position once the foot is corrected. 16 Therefore, a tibialis posterior tendon lengthening or transfer will be required at the same time. Exces- sive lengthening of the heel cord should be avoided because increased cavus deformity or a calcaneus gait may develop. 25 An overlengthened heel cord also will result in weakness in plantar flexion, poor gait progression at toe-off, and, in some cases, anterior impingement in the ankle joint. Additionally, increased energy may be required for gait because the quadriceps muscle is re- cruited to prevent the patient from falling forward. Failure to release tight long toe flexors may result in a poorer outcome and require a second release. 26 Appropriate releases or tendon transfers allow the foot to be brought into the neutral position and improve or prevent bracing. Walking ability is related to the age at surger y and the degree of paraly- sis. 22 In patients with hemiplegia, anterior transfer of the flexor digitorum longus and flexor hallucis longus may assist dorsiflexion power. 27 Osteotomy The lateralizing calcaneal osteotomy can effectively reduce the varus moment arm of the Achilles tendon at the ankle during stance phase; this osteotomy also can reduce the additive contribution of the Achilles tendon toward the tibialis posterior in favor of the peroneus brevis during toe-off. The patient with an in- ternally rotated distal tibia also tends to have a varus moment of the Achilles tendon at the ankle. The degree of tibial rotation can be assessed by CT. 28 An osteotomy is indicated for a mild to moderate fixed deformity that persists after appropriate tendon releases in a patient without arthritic change in the surrounding joints. Osteotomy also may be indicated in combination with fusion when the foot position cannot be corrected by fusion alone. For example, after an ankle fusion, the hindfoot may correct completely, but the forefoot may be left with plantar flexion of the first ray. Thus, a dorsiflexion osteotomy through the first tarsometatarsal joint or in the proximal me- taphysis would be indicated. Distal tibial osteotomy may be of value in a patient with forefoot varus, hindfoot varus, and varus alignment at the ankle joint. A supramalleolar osteotomy with a lateral closing wedge will bring the foot flat to the ground and redistribute the force within the ankle joint. Supramalleolar derotational osteotomy also may be beneficial. Ro- tating the distal tibia changes the direction of the moment arm of the Achilles tendon. External rotation osteotomy of the distal tibia in- creases the valgus moment at the subtalar joint and unlocks the subtalar joint. McNicol et al 29 reported successful outcomes in patients with polio and other neurologic etiologies who were treated with rotational osteotomy to externally rotate the foot. In most cases of cavovarus foot, the foot is correctly aligned on the tibia after the talonavicular joint has been released. Calcaneal Osteotomy When the hindfoot does not pas- sively correct to neutral, a lateralizing calcaneal osteotomy must be performed, with or without a subtalar fusion. Because hindfoot varus is difficult to assess, calcaneal osteotomy should be done when there is any residual hindfoot varus. The calcaneal osteotomy will correct the foot during heel strike and at rest and, more important, will lateralize the moment arm o f the Achilles tendon during toe-off. In a patient with a mobile midfoot and hindfoot, a lateralizing calcaneal osteotomy in- creases the load on the medial border Out-of-Phase Tendon Transfers for Swing-Phase Deficit Donor Recipient Indication Concomitant Procedure Tibialis posterior Tibialis anterior and/or peroneus tertius Weak dorsiflexion caused by lower motor neuron pathology, or nerve or muscle injury Heel cord lengthening Peroneus longus Peroneus tertius Weak dorsiflexion Tibialis posterior transfer; heel cord lengthening Flexor hallucis longus and digitorum longus Fourth metatarsal through interosseous membrane Weak dorsiflexion caused by stroke Short flexor release; lengthening of heel cord or tibialis posterior Flexor digitorum longus Extensor hood Intrinsic deformity of toes Interphalangeal joint fusion or excision Table 4 Alastair S. E. Younger, MB, ChB, MSc, ChM, FRCSC, and Sigvard T. Hansen, Jr, MD Volume 13, Number 5, September 2005 309 of the foot during toe-off. A dorsiflexion osteotomy of the first ray or a dorsiflexion fusion of the first tarsometatarsal joint should be performed at the same time if the first ray is plantarflexed, as is common in CMT disease. In many patients with a cavovarus foot requiring a lateralizing calcaneal osteotomy, a posterior and medial osteophyte is present in the subtalar joint. If this is the only ev- idence of degenerative change and is mildly symptomatic, the osteophyte can be excised medially by dissect- ing just anterior to the flexor digitorum longus. The Dwyer closing wedge osteotomy weakens the moment arm of the Achilles tendon and often cannot achieve full correction. 30 A sliding calcaneal osteotomy without excision is usually preferable 17 (Fig. 3). In this procedure, a posterior lateral incision is made. The calcaneal cut is made transverse to the long axis of the foot to prevent shortening or lengthening of the osteotomy. The medial cut should not penetrate close to the sustentaculum tali because of the proximity of the neurovascular bundle to this groove. A skin mark can be made medially halfway between the neurovascular bundle and the tuberosity of the calcaneus. A finger of the surgeon’s nondominant hand is placed on the mark, and the saw is directed to this point. After mobilizing both the tuberosity fragment and the deep investing fascia surrounding the Achilles tendon, lateral translation is performed. The osteotomy is held with two screws. Anteroposterior, lateral, and calcaneal axial views of the ankle should be taken intraoper- atively. The lateral aspect of the tuberosity fragment is trimmed and can be used for bone graft elsewhere. Posterior calcaneal osteotomy with plantar release has been used to correct hindfoot cavus associated with a weak gastrocnemius-soleus complex. By sliding the tuberosity of the calcaneus posteriorly and superi- orly using an oblique osteotomy, the position of the calcaneus is corrected and the lever arm of the weak triceps surae muscle is augmented 31 (Fig. 4). Posterior calcaneal osteotomy should not be performed in the presence of anterior ankle joint impingement. In this procedure, a lateral incision is made using a portion of the L- Figure 3 Lateralizing sliding calcaneal osteotomy. A, A posterior lateral incision is made. B, Once the soft tissues have been retracted, the calcaneus is cut with a saw. C, The medial cut should not penetrate close to the sustentaculum tali. D and E, The osteotomy is held with two proximal-distal transcalcaneal screws. F and G, Alternative screw positions. (Adapted with permission from Hansen ST Jr [ed]: Functional Reconstruction of the Foot and Ankle. Philadelphia, PA: Lippincott Williams and Wilkins, 2000, p 369.) Adult Cavovarus Foot 310 Journal of the American Academy of Orthopaedic Surgeons or J-shaped calcaneal fracture incision. This incision can be combined with a sinus tarsi incision if correction of varus is incomplete after a subtalar fusion. The osteotomy be- gins anterior to the Achilles tendon insertion and the insertion of the plantar fascia. An osteotomy posterior to the plantar fascia will destabi- lize the osteotomy. The osteotomy should be transverse. An oblique osteotomy lengthens or shortens the tuberosity of the calcaneus, and lengthening the calcaneus may re- strict the correction of var us because the soft-tissue envelope may become too tight. An oblique osteotomy ex- iting anteriorly on the medial wall may damage the neurovascular bundle. The osteotomy site is released from the medial soft tissues using a periosteal elevator or curved curet. The Achilles tendon sheath is released to improve displacement of the tuberosity fragment; the investing fascia will prevent translation of the Achilles tendon. The tuberosity fragment is held by two screws. Af- ter placing the distal screw, the supe- rior aspect of the posterior fragment of the osteotomy is then rotated medially and transfixed with a second screw. Radiographic views (eg, lateral ankle and Broden views) are ob- tained to ensure that the screws do not penetrate the subtalar joint. Lateral Column Shortening Because lateral column shortening corrects hindfoot varus, forefoot varus, and forefoot abduction, it is ideally suited to correct the position of a residual clubfoot. Lateral column shortening can be performed through the cuboid, the lateral aspect of the calcaneus, or the calcaneocuboid joint. 18 This procedure is indicated when the foot fails to correct after medial talonavicular release. Talar Neck Osteotomy A malreduced talar neck fracture can result in dorsal and medial translation of the distal portion of the talar neck as well as shortening of it. This results in a cavovarus position of the foot. The malunion locks the triple-joint complex, causing a pain- ful rigid foot with overload of the lateral border. Components of rotation and translation also coexist within the subtalar and midtarsal joints as well as at the malunion, causing overload of the triple-joint complex (subtalar, talonavicular, and calcaneocuboid joints). 8 A talar neck osteotomy may be performed when the surrounding joints are well preserved. A preoper- ative CT scan is needed to assess the amount of correction required. If necessary, intact blood supply to the body is confirmed with magnetic resonance imaging. The risks of this procedure include failure to correct all components of the deformity, nonunion of the distraction graft, and osteonecrosis of the talar body. 32 Dorsiflexion Osteotomy of the First Ray Dorsiflexion osteotomy of the first ray is indicated for a symptomatic plantarflexed first ray with pain in the forefoot secondary t o overload of the first metatarsal head. It is also indicated for a symptomatic plantarflexed first ray with pain over the lateral border of the foot resulting from supination caused by forefoot- driven hindfoot varus. Clawing of the first ray with a dorsal contracture of the metatarsophalangeal joint and a tight extensor tendon are often seen in conjunction. Dorsiflex- ion osteotomy or fusion of the first tarsometatarsal joint also is indicated if the hindfoot corrects to neutral when a Coleman block test indicates a forefoot-driven hindfoot varus. Dorsiflexion fusion of the first tarsometatarsal joint should be con- sidered when the tarsometatarsal joint is hypermobile and a strong peroneus longus plantarflexes the first ray. Care should be taken not to over-shorten or over-elevate the first ray. Excessive correction can result in hallux rigidus and transfer metatarsalgia. 23 A plantar fascia release may be required at the same time to allow elevation of the first ray. The proximal cut of the tarsometatarsal fusion is almost parallel to the joint and is perpendicular to an imaginary line running through the talus and the navicular Figure 4 Posterior calcaneal osteotomy for hindfoot cavus. A, Normal relationship of the hindfoot bones. B, Position of the hindfoot secondary to a weak triceps surae. The osteotomy is made from the lateral aspect. C, The posterior tuberosity fragment is displaced in a dorsal and posterior direction to restore length, reduce the arch, and improve the moment arm of the weak triceps surae muscle. The screws are placed in parallel across the osteotomy site. (Adapted with permission from Hansen ST Jr [ed]: Functional Reconstruction of the Foot and Ankle. Philadelphia, PA: Lippincott Williams and Wilkins, 2000, p 373.) Alastair S. E. Younger, MB, ChB, MSc, ChM, FRCSC, and Sigvard T. Hansen, Jr, MD Volume 13, Number 5, September 2005 311 [...]... multiple proximal metatarsal osteotomies (Jahss osteotomy) because metatarsalgia will develop under a residual plantarflexed ray Journal of the American Academy of Orthopaedic Surgeons Alastair S E Younger, MB, ChB, MSc, ChM, FRCSC, and Sigvard T Hansen, Jr, MD Figure 6 Midfoot osteotomy to correct midfoot cavus A, Transverse cross-sectional view of the midtarsus showing the relative anatomy of the... alignment view Foot Ankle Int 1995;16:572-576 Canale ST, Kelly FB Jr: Fractures of the neck of the talus: Long-term evaluation of seventy-one cases J Bone Joint Surg Am 1978;60:143-156 Van Bergeyk AB, Younger A, Carson B: CT analysis of hindfoot alignment in chronic lateral ankle instability Foot Ankle Int 2002;23:37-42 Saraph V, Zwick EB, Uitz C, Linhart W, Steinwender G: The Baumann procedure for fixed... Crenshaw AH (ed): Campbell’s Orthopaedics, ed 7 St Louis, MO: Mosby, 1987, vol 4, pp 2925-3061 Sherman FC, Westin GW: Plantar re- Journal of the American Academy of Orthopaedic Surgeons Alastair S E Younger, MB, ChB, MSc, ChM, FRCSC, and Sigvard T Hansen, Jr, MD 20 21 22 23 24 lease in the correction of deformities of the foot in childhood J Bone Joint Surg Am 1981;63:1382-1389 Santi MD, Botte MJ: Volkmann’s . patients with an HMSN, the diagnosis is made based Alastair S. E. Younger, MB, ChB, MSc, ChM, FRCSC, and Sigvard T. Hansen, Jr, MD Dr. Younger is Director, Foot and Ankle Program, Providence Health. institution related directly or indirectly to the subject of this article: Dr. Younger and Dr. Hansen. Reprint requests: Dr. Younger, Univer- sity of British Columbia, 401-1160 Burrard Street, Vancouver,. injury Knee dislocation (neurovascular injury) Residual clubfoot Idiopathic Table 1 Alastair S. E. Younger, MB, ChB, MSc, ChM, FRCSC, and Sigvard T. Hansen, Jr, MD Volume 13, Number 5, September 2005

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