Surgical Treatment of Cavus Foot

 

 

 

DEFINITION

A cavus foot deformity in children develops from muscle imbalance that leads to forefoot pronation in relation to the hindfoot. When well established, it is readily recognizable by an abnormally high medial arch that persists with weight bearing (FIG 1).

Commonly a result of hereditary sensory motor neuropathy (HSMN), it is frequently difficult to determine the underlying cause.

 

 

ANATOMY

 

The plantar fascia is an extensive fibrous structure that spans the foot between the medial aspect of the calcaneal tuberosity and the transverse metatarsal ligaments at the metatarsal heads (FIG 2). It stabilizes the arch of the foot and protects the underlying neurovascular structures from injury.

 

During the gait cycle, the plantar fascia assists in the dynamic changes of the arch.

 

 

At heel strike, there is forefoot supination and heel inversion, whereas eccentric contraction of the quadriceps muscles absorbs much of the energy.

 

During midstance, there is unlocking of the midtarsal joints with hindfoot pronation and internal tibia rotation.

 

At toe off, the plantar fascia helps lock the midtarsal joints to assist the foot to be a rigid lever for forward propulsion.

 

This is termed the windlass effect, when passive dorsiflexion at the metatarsophalangeal joints tightens the plantar fascia, leading to elevation of the medial arch and tarsal joint stability (FIG 3).

 

PATHOGENESIS

 

In progressive conditions such as HSMN, there is muscle imbalance with weakness of the intrinsic, tibialis anterior, and peroneus brevis muscles. This can lead to a relative overpull of the peroneus longus and posterior tibialis muscles.

 

 

 

FIG 1 • A 17-year-old girl with HSMN type 1A. Cavus right foot deformity with high arch, plantar crease, apex of deformity at the midfoot, and claw toes.

 

 

Clinical muscle testing shows that although both peroneal muscles are weak, the larger peroneus longus muscle retains relatively more strength. Differential peroneal nerve compression at the proximal fibula is

postulated to cause relative sparing of the peroneus longus innervation.5

 

Computed tomography (CT) imaging studies in Charcot-Marie-Tooth disease, a major category of HSMN, showed early foot intrinsic muscle atrophy with sparing of the abductor hallucis and involvement of the peroneus

brevis, peroneus longus, and flexor hallucis longus muscles.13

 

Magnetic resonance imaging (MRI) studies have shown dominance in the size of the peroneus longus muscle versus the tibialis anterior.16

 

The muscle imbalance and intrinsic muscle weakness lead to an unopposed extensor digitorum longus, hyperextension of the lesser toe metatarsophalangeal joints, and phalangeal joint flexion by the long and short toe flexors.

 

 

There is an exaggeration of the windlass effect with claw toe deformities.

 

 

 

FIG 2 • Plantar view of plantar fascia.

 

 

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FIG 3 • A,B. Windlass effect. The foot is an arch. If the plantar tissues tighten and become shorter, the fixed length of the arch forces it to become taller.

 

 

The first metatarsal becomes even more plantarflexed by the action of the peroneus longus and with time becomes fixed in this position.

 

The plantar aspect of the foot assumes a tripod position, resulting in hindfoot varus (FIG 4).

 

The cavus foot remains a rigid lever throughout stance phase, leading to increased stress and lack of shock absorption, pain, and callosities.

 

 

 

FIG 4 • A,B. Tripod effect. Weight bearing is shared between the heel and medial and lateral columns of the forefoot. If the medial column is in plantarflexion, the heel is forced into varus with weight bearing.

 

NATURAL HISTORY

 

Cavus foot is rarely present at birth but develops with time.

 

The natural history depends on the underlying diagnosis. The underlying cause affects the outcome, so determination of cause is essential. An underlying diagnosis can be found in the brain, spinal cord, peripheral nerves, or the foot itself.

 

Cavus foot deformity can be either progressive or nonprogressive.

 

Cavus foot deformity involves either a dorsiflexion deformity of the calcaneus or a forefoot plantarflexion deformity.

 

The most common cause of progressive bilateral cavus foot deformity is HSMN. HSMN is a group of progressive peripheral nerve diseases and has a heterogeneous genetic classification.

 

 

Charcot-Marie-Tooth disease involves types I and II HSMN, with HSMN IA the most common type seen in 60% of patients with HSMN.

 

 

HSMN type I has myelin degeneration, type II is the axonal degeneration form, and type III (Dejerine-Sottas disease) is more severe and presents in infancy.

 

There are more than 17 different genetic loci determined for Charcot-Marie-Tooth disease.

 

The prognosis for these progressive conditions is less favorable than for the nonprogressive disorders.

 

The natural history of HSMN is related to the underlying type.

 

 

Progression of muscle involvement begins initially in the intrinsic muscles, followed by the anterior compartment, the peroneal muscles, and then the posterior muscles.14

 

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The foot can assume a cavovarus, calcaneocavus deformity, or even a valgus deformity and may have more unilateral severity (HSMN type III).4

 

Associated hip dysplasia may be asymptomatic or may present with symptoms. Acetabular dysplasia may be the first indicator of HSMN.3

 

In progressive conditions that are left untreated, a flexible and correctable foot may become rigid with structural bony changes. This can lead to inability to participate in athletics and pain and difficulty with shoe wear and normal walking. Treatment is recommended when the foot is still flexible.

 

Unilateral cavus foot can have a number of causes. The idiopathic variety may be progressive, with an unpredictable natural history.

 

Patients with nonprogressive conditions, as seen in cerebral palsy or spinal cord disorders, may fare better but still can have long-term problems with athletics, metatarsalgia, plantar fasciitis, and iliotibial band

syndrome.9

 

Calcaneocavus deformity is often seen with nonprogressive conditions such as spina bifida or clubfoot deformity with an overlengthened heel cord. Problems include heel pain or heel pad ulceration if sensation is deficient and weak or no push-off or crouch gait if not braced.

 

PATIENT HISTORY AND PHYSICAL FINDINGS

 

The physical examination is used to determine the underlying diagnosis and to determine characteristics of the cavus foot deformity that would indicate surgical correction is needed.

 

Physical examination should include observation of the spine and its range of motion. Skin changes, scoliosis, or kyphosis may represent an underlying spinal cord abnormality.

 

The upper extremities are evaluated for intrinsic muscle wasting and weakness. Atrophy or weakness in the hand suggests HSMN.

 

The clinician evaluates hip range of motion and looks for Trendelenburg gait. Bilateral hip dysplasia newly diagnosed in a teenager is highly suggestive of HSMN.

 

Lower extremities are evaluated for size, muscle strength, and firmness and tenderness along the course of major nerves. Bilateral calf atrophy is seen with spina bifida and may be present in severe HSMN. Unilateral atrophy may be seen with diastematomyelia, tethered spinal cord, or split cord malformation.

 

 

 

FIG 5 • A,B. In the Coleman block test, the patient bears weight with the lateral border of the foot on a 2-cm block while the first metatarsal is allowed to drop down off the edge of the block. If hindfoot varus corrects to neutral position, the hindfoot is flexible and the medial forefoot is the source of hindfoot varus.

 

 

A neurologic examination is performed. Patients with HSMN may have decreased sensation to light touch,

position sense, or vibration. There may be obvious weakness of the anterior tibialis muscle, preventing ability to heel walk. Deep tendon reflexes may be decreased or absent in HSMN and Friedreich ataxia.

 

The foot is examined for deformity (cavus, cavovarus, or calcaneocavus). Bilateral deformity is typical for HSMN. Unilateral deformity may be present with a structural abnormality. The clinician locates the apex of the midfoot deformity and determines whether the foot is rigid or flexible. The hindfoot is rarely in equinus.

 

The Coleman block test is performed (FIG 5).

 

The toes are examined for any deformities. Cavus foot may not have associated toe abnormality. Rigid claw toe abnormality requires surgical treatment.

 

IMAGING AND OTHER DIAGNOSTIC STUDIES

 

Bilateral standing anteroposterior (AP) and lateral radiographs are standard.

 

 

On the lateral weight-bearing radiograph, the clinician should determine the calcaneal pitch; greater than 30 degrees indicates chronic gastrocnemius-soleus weakness (FIG 6A).

 

The Meary angle, the angle between the shaft of the first metatarsal and the axis of the talus, is normally 0 degree.

 

Ankle equinus, forefoot equinus, the amount of cavus, and the apex of the midfoot deformity are determined.

 

With the foot positioned for the Coleman block test, a lateral radiograph of the foot can document the degree of hindfoot correction.1

 

In the patient with known or possible HSMN, a standing AP pelvis view is obtained to screen for the presence of hip dysplasia.17

 

Standing full-length posteroanterior and lateral spine radiographs are obtained when a spinal abnormality is suspected or if the underlying diagnosis is in question.

 

MRI of the entire brainstem and cervical, thoracic, and lumbar spine is performed when a spinal cord tumor, syrinx, tethered cord, or Chiari I malformation is of concern (FIG 6B,C).

 

Nerve conduction and electromyelographic (EMG) studies may be done to evaluate for HMSN. In HMSN type I, motor nerve conduction is markedly slowed. In HMSN type II, there is near-normal motor nerve conduction but EMG

 

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evidence of denervation. Molecular DNA testing of peripheral blood may be used for diagnosing HSMN; therefore, sural nerve biopsy is generally not necessary.

 

 

 

FIG 6 • A. A 15-year-old boy with HSMN type 1A with severe bilateral cavus foot deformity. Lateral standing radiograph of right foot. The Meary angle, measured between the axis of the talus and the first metatarsal, is 25 degrees, but it should be 0 degrees. The calcaneal pitch angle, measured between the horizontal and the plantar aspect of the calcaneus, is 26 degrees but should be less than 20 degrees. B. A 5-year-old girl with 28-degree right thoracic scoliosis. MRI T1-weighted sagittal view of large cervical thoracic syrinx with Chiari I malformation at foramen magnum. C. MRI T1-weighted axial view showing large central cord syrinx (asterisk).

 

DIFFERENTIAL DIAGNOSIS

Hemiplegic cerebral palsy

Spastic diplegic cerebral palsy with calcaneocavus foot deformity if the Achilles tendon has been overlengthened

Friedreich ataxia Myelodysplasia

Chiari I malformation with syringomyelia and scoliosis Diastematomyelia and split cord malformation Poliomyelitis

Spinal cord tumors

 

Guillain-Barré syndrome

Peripheral nerves: HSMN types I and II Sciatic nerve injury

Peripheral nerve tumor

Silent compartment syndrome after tibia or foot fracture Residual deformity of clubfoot

Idiopathic

Subtalar tarsal coalition (rare)

Severe limb length discrepancy leading to a fixed equinus gait

 

 

NONOPERATIVE MANAGEMENT

 

Nonoperative management is appropriate for mild or nonprogressive deformity.

 

 

 

Inserts that support the lateral forefoot and eliminate hindfoot inversion may be helpful. Gel heel cups and replacing worn athletic shoes assist the stiff foot in energy absorption.

 

Extra-depth shoes and orthotics that unload pressure points may help in more advanced cases.

 

SURGICAL MANAGEMENT

 

Surgical treatment is necessary for more severe nonprogressive cases or for progressive cases. The functional goal is to correct the cavus deformity and to obtain a mobile, plantigrade, and well-balanced foot while avoiding common pitfalls. Treatment is best performed when the foot is still

 

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flexible. Staged procedures, correcting deformity first and balancing muscles at a later stage, may be safer for the foot.12

 

Specific principles for surgical decision making include the following:

 

 

Surgical management is usually needed when there is an identified functional problem or progression of the deformity. For progressive cavus deformity, it is better to use simple procedures early.

 

Plantar fascia release is the initial procedure of choice in young children with nonprogressive deformity. We prefer to do this through a medial plantar incision with postoperative serial corrective casting used to gain further correction. Plantar fascia release is generally done with other procedures.

 

The surgeon can correct any underlying muscle imbalance with tendon transfers or lengthening or by bony correction of the lever arm that the muscles work through.

 

In a more rigid deformity, a forefoot osteotomy is used to correct the pronated medial forefoot.

 

 

The goal is to correct the fixed deformity while preserving joint mobility. The site of the osteotomy is determined by the location of the deformity apex. The most common are first metatarsal dorsal closing, medial cuneiform plantar opening, and midfoot wedge osteotomies. If the fixed cavus deformity on the medial side of the foot is severe enough, the first metatarsal dorsal osteotomy can be combined with the

medial cuneiform plantar opening osteotomy.11

 

For marked and rigid forefoot equinus (FIG 7), a more extensive midfoot osteotomy is used; this is typically needed during the patient's second decade of life.20

 

Calcaneal osteotomy is used if the Coleman block test indicates a fixed heel varus. We recommend a slide osteotomy through a lateral approach, although a lateral closing wedge alone or combined with the slide may also be used for more correction. Tendon transfers are frequently required to achieve a balanced foot. These

may involve a transfer of the relatively strong posterior tibialis tendon to the dorsum of the foot,1 a Jones procedure in which the extensor hallucis tendon is transferred to the neck of the first metatarsal with fusion of the great toe interphalangeal (IP) joint, a split or complete anterior tibialis tendon transfer if the muscle has

preserved strength, or a transfer of the peroneus longus to the peroneus brevis.21

 

 

 

FIG 7 • An 18-year-old girl with HSMN type 1A with marked cavus and fixed midfoot deformity and shortening. Owing to her age and the degree of rigid deformity, a midfoot osteotomy is required.

 

 

Calcaneal cavus deformity may need a posterior sliding calcaneal osteotomy to increase the calcaneal lever arm. We prefer this to be a crescent-shaped cut. A plantar fascia release facilitates posterior sliding of the distal fragment.

 

Triple arthrodesis is used as a salvage procedure for rigid hindfoot deformity. We are reluctant to recommend

this for a foot with sensory deficit because the long-term outcome when this procedure is used is poor.19 With a triple arthrodesis, tendon transfers may still be necessary to maintain a balanced foot.

 

Preoperative Planning

 

 

Intraoperative epidural anesthesia may be continued in the postoperative period. Preoperative antibiotics are given.

 

A tourniquet allows optimal visualization of the operative site.

 

In patients with HSMN, the surgeon must be very careful about tourniquet use because the sciatic and femoral nerves in the thigh are very sensitive to the pressure and time effects of the tourniquet. We recommend the minimal pressure needed and less than 1 hour of inflation time.

 

Positioning

 

The patient is positioned supine on a radiolucent imaging table.

 

Approach

 

A combination of surgical procedures may be needed to fully correct the foot deformity.

 

For most deformities, an extensive plantar release is used.

 

As the extensor hallucis longus muscle function may be spared in HSMN, the Jones procedure is useful for the child with a plantarflexed medial column and dynamic great toe hyperextension during swing phase. It is generally combined with a medial or midfoot osteotomy.

 

For more extensive and rigid deformity, an osteotomy may be needed. A younger patient may require only an osteotomy of the proximal first metatarsal or first cuneiform. A midfoot wedge osteotomy is useful for the rigid midfoot deformity in an adolescent or young adult when the midfoot does not sufficiently correct after the plantar fascia release. If the lateral and medial aspects of the midfoot are in equinus, an osteotomy across the entire midfoot will more reliably correct the deformity than a medial column osteotomy.

 

An alternative to the dorsal closing midfoot osteotomy is a technique where the deformity is corrected by excising the navicular and doing a dorsal closing osteotomy of the cuboid. The excision of the navicular is done through a medial incision and the dorsal closing osteotomy of the cuboid is done through a lateral incision. The advantage of this technique is that it does not fuse any joints in the midfoot. It does correct the deformity and the

articular surface of the cuneiforms now articulates with the head of the talus.10

 

 

The lateral calcaneal slide osteotomy is used to correct fixed hindfoot varus that does not correct with the Coleman block test.

 

 

Advantages include use of a simple single cut with control of the amount of correction needed.

 

The posterior slide calcaneal osteotomy is useful in the calcaneocavus foot with a high calcaneal pitch angle.

 

 

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Incisions should be longitudinal and placed over the areas of relevant pathology (FIG 8).

 

 

A cavus foot is short and will be lengthened in the course of treatment. It may be safer to obtain some of the correction with postoperative corrective casts rather than doing all of the correction at the initial surgery.

 

 

 

FIG 8 • Cavus deformities typically require a combination of procedures. For this right foot, incisions for an extensive plantar medial release, modified Jones procedure, midfoot osteotomy, and posterior tibialis tendon lengthening are drawn. The midfoot osteotomy is at the apex of the deformity.

 

TECHNIQUES

• Plantar Release

A longitudinal incision is made medially over the plantar fascia. Sharp knife dissection is used through the skin and subcutaneous fat (TECH FIG 1A).

The abductor hallucis is the first structure identified and is released off its deep fascia (TECH FIG 1B).

The fascia deep to the abductor hallucis is next exposed. The posterior tibial nerve and artery are identified proximally and followed distally by releasing the overlying fascia. Note the division of the posterior tibial nerve into its plantar medial and lateral branches.

Posterior to the neurovascular bundle, the plantar fascia is exposed as it attaches to the medial tubercle of the calcaneus.

 

 

 

 

TECH FIG 1 • A. Plantar medial incision. Because the foot will be lengthened, the incision should be placed longitudinally and gentle sharp dissection used. B. The abductor hallucis muscle has been dissected off its deeper fascia, and the plantar aponeurosis and muscles have been isolated posterior to the neurovascular bundle.

 

 

The flexor digitorum brevis, quadratus plantae, and abductor digiti quinti muscles are released at their proximal origins with Mayo scissors.

 

Capsulotomies of the medial talonavicular and subtalar joints may be needed if superficial release is not adequate to achieve correction.2

 

Severe cases may need posterior tibialis tendon lengthening or transfer.

 

The incision is loosely closed with interrupted sutures. By widely spacing the sutures, blood can drain and not cause excessive postoperative pressure.

 

In severe cases, serial casting may be necessary after the release.

 

 

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• Medial Column Osteotomy

   

  A plantar medial release should also be performed if an osteotomy is required.

   

  A stiff forefoot, an older patient, or painful forefoot calluses indicate the need for an osteotomy.

   

  Depending on the apex of the deformity, the osteotomy can be performed on the medial cuneiform or the first metatarsal. In a younger child, it may be safer to avoid the proximal metatarsal physis and perform a medial cuneiform osteotomy.

   

  The osteotomy can be performed either as a first metatarsal dorsal-based closing wedge osteotomy or as a medial cuneiform plantar-based open wedge.

   

  The first metatarsal dorsal closing wedge osteotomy does not require a bone graft, has one bony surface to heal, and can be held closed with a single screw. However, it may shorten the metatarsal slightly.

   

   

   

  TECH FIG 2 • A. Proximal incomplete dorsal-based closing wedge osteotomy of proximal metatarsal. The plantar aspect of the metatarsal and soft tissues are left intact to act as a hinge to allow closure of the osteotomy. Steinmann pins are placed to accurately guide the bony cuts. B. The plantar hinge remains intact for proper closure. A screw or percutaneous pin holds the osteotomy closed. C. Plantar opening wedge osteotomy of the medial cuneiform. D. The dorsal hinge must remain intact. A triangular bone graft is inserted in the plantar aspect. Fixation is with a single screw, percutaneous wire, or suture on the plantar surface.

   

   

  The first cuneiform plantar open wedge osteotomy requires only a single cut, the amount of correction can be fine-tuned after the bone has been cut, and it does not shorten the foot, but a bone graft is required to hold it open, typically a freeze-dried allograft.

   

  For a proximal, dorsal-based oblique closing wedge first metatarsal osteotomy, a longitudinal incision is made directly over the proximal metatarsal; be careful to protect the dorsal digital nerve (TECH FIG 2A,B).

   

  Subperiosteal dissection of the proximal metatarsal is performed; be careful to leave the plantar periosteum and soft tissue intact.

   

  Two small-diameter Steinmann pins are drilled at the site of the bone cuts, converging at the plantar apex. The apex of the correction is quite proximal and plantar. A bony and soft tissue posterior hinge is left intact so that the osteotomy is an incomplete closing wedge.

   

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  A small oscillating saw is used to make the bone cuts. The wires are used to guide the cuts toward the plantar apex. A small osteotome and pituitary rongeur may be used to remove some of the bone at the apex.

   

  When sufficient bone has been removed from the apex, the cut ends can be slowly closed together while maintaining integrity of the bony hinge. A wire, screw, or dorsal plate can be used to secure the corrected osteotomy.

   

  In a younger child with an open metatarsal physis or when the deformity apex is at the medial cuneiform, the opening wedge osteotomy can be performed at this level (TECH FIG 2C,D).

   

  • Modified Jones Procedure

     

    Two incisions are used, a dorsal transverse incision over the great toe IP joint and a longitudinal incision over the distal first metatarsal (TECH FIG 3).

    Interphalangeal Joint Fusion

     

    Through the transverse incision over the IP joint, the incision is carried down to the extensor hallucis tendon.

     

     

    The tendon is transected at the level of the IP joint, and the IP joint capsule is incised transversely. Continue with the no. 15 blade to expose the articular distal aspect of the proximal phalanx.

     

    A rongeur is used to remove the articular cartilage and some of the subchondral cortical bone on both sides of the IP joint. Only a minimal amount of bone is removed.

     

    A cannulated 4.0-mm screw is used for fixation. This is placed by retrograde insertion of a guidewire through the center of the distal phalanx, exiting distally just plantar to the nail.

     

     

     

    TECH FIG 3 • Two incisions are used: one transverse over the IP joint and the other longitudinal along the distal first metatarsal.

     

     

    The IP joint is then reduced in a neutral position, and the screw is inserted; be careful to provide compression at the IP joint.

     

    Proper length places the tip of the screw into the proximal aspect of the proximal phalanx.

    Transfer of the Extensor Hallucis Tendon to the Metatarsal Neck

     

    A longitudinal skin incision is made over the distal first metatarsal.

     

    The extensor hallucis tendon is identified and isolated distally until its cut end can be pulled into the incision.

     

    A 0 suture whipstitch is placed into the distal tendon.

     

    Subperiosteal exposure of the distal metatarsal allows a transverse drill hole to be made in the metatarsal neck.

     

    The drill diameter is roughly the diameter of the extensor hallucis longus tendon.

     

    A wire or suture passer aids passage of the extensor hallucis longus tendon through the hole.

     

    After the medial column or midfoot osteotomy is secured, the end of the extensor hallucis longus tendon is secured to itself (TECH FIG 4).

     

     

     

    TECH FIG 4 • After denuding the IP joint articular cartilage, a 4.0-mm screw transfixes this joint. A whipstitch is placed into the cut end of the extensor hallucis longus tendon (inset) and the tendon is passed through a transverse drill hole and sutured to itself.

     

     

     

     

• Midfoot Osteotomy

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  The osteotomy is placed at the apex of the deformity, which should be proximal to any plantar calluses (TECH FIG 5A,B).

   

  Too distal placement results in a rocker bottom residual deformity.

   

  If the deformity is severe, a triple arthrodesis may be needed to bring the forefoot into a plantigrade position.

   

  Muscle balancing procedures will still be required because the foot will further deform with time if imbalance remains.

   

  Several types of osteotomies have been described.6, 7, 20

   

  We recommend a simple procedure that uses a truncated wedge placed at the apex of the deformity.

   

  Once cut, the distal fragment may be laterally rotated to compensate for excessive medial column flexion.

   

  A long, single dorsomedial skin incision is used at the apex of the deformity.

   

  It is more effective to place the osteotomy proximally so that correction is achieved at the level of the deformity; it is generally at the navicular cuneiform joint.

   

   

   

  TECH FIG 5 • A,B. Midfoot osteotomy is centered at the apex of the deformity, typically through the naviculocuneiform joint. Rotation can be added to decrease the excessive amount of medial column plantarflexion. C. Neurovascular structures are protected with two Hohmann retractors.

   

   

  The Hohmann retractors are placed dorsal and plantar, with the entire midfoot exposed (TECH FIG 5C).

   

  Smooth Steinmann pins are inserted to define the proximal and distal aspects of the osteotomies. The osteotomy is cut with the oscillating saw and completed with osteotomes and rongeurs. A dorsal-based wedge of bone is removed; it can be a triangle for moderate deformities or a truncated trapezoid for more significant deformities.

   

   

  Fixation is with two threaded Steinmann pins, which are removed in 4 to 6 weeks. The incision is loosely closed with interrupted sutures.

   

  The foot is casted for 6 weeks with toe-touch weight bearing. Because of the potential for nonunion, an additional 6 weeks of weight-bearing casting should be considered.

   

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• Calcaneal Osteotomies

  Lateral Calcaneal Slide Osteotomy

   

  The incision is placed lateral to the calcaneus, parallel to the peroneal tendons.

   

  The peroneal tendons are reflected proximally to gain access to the lateral aspect of the calcaneus tubercle.

   

  A sharp Hohmann retractor is placed just anterior to the Achilles insertion and another is placed plantar

  and distal.

   

  Fluoroscopy can be used to check the orientation of the osteotomy by the position of the retractors (TECH FIG 6A).

   

  A 1-inch osteotome or saw is used to make the osteotomy across the calcaneus to the opposite cortex. A smooth lamina spreader is used to distract the fragments, and the medial cortex can be freed up with a pituitary rongeur and a Cobb elevator.

   

  The calcaneal tubercle with the heel is then slid medially about 50% of its width. The correct position is for the heel to be underneath and in line with the tibial shaft (TECH FIG 6B). A laterally based wedge can also be removed if more correction is needed.

   

   

   

  TECH FIG 6 • A. Lateral exposure of the calcaneus for calcaneal slide osteotomy. The peroneal tendon sheath is divided and the tendons are reflected proximally. One Hohmann retractor is placed anterior to the Achilles tendon insertion and a second is placed distally on the plantar aspect of the calcaneus. B. Posterior view of the foot showing the lateral slide calcaneal osteotomy. C. The distal tubercle with the heel pad is positioned underneath the tibia. Fixation is with a threaded Steinmann pin for 3 weeks.

   

   

   

  TECH FIG 7 • Crescent-shaped calcaneal osteotomy allows posterior positioning of the calcaneus to improve the lever arm function of the gastrocnemius-soleus muscles and to decrease the point pressure on the heel.

   

   

  A large threaded Steinmann pin is placed in the sinus tarsi and directed toward the most posteroinferior aspect of the tubercle (TECH FIG 6C).

   

  The pin is removed in the clinic in 3 weeks. A cast is used for a total of 6 weeks.

  Posterior Slide Calcaneal Osteotomy

   

   

  A lateral approach to the calcaneus is used, similar to the lateral slide osteotomy. Hohmann retractors are placed for protection and orientation.

  An oblique straight cut may be used, but we prefer a curved cut using a Chiari chisel (TECH FIG 7). Once cut, the distal calcaneal fragment is slid posterior and transfixed with a threaded Steinmann pin. Because the bone may continue to bleed, loose interrupted suture closure and a bulky dressing are used. The pin is removed in 3 weeks, and the foot is casted for a total of 6 weeks.

   

   

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  PEARLS AND PITFALLS

   

  Failure to diagnose underlying spine condition

  • A child presenting with a foot problem must always have the spine examined.

  • A markedly small foot or calf may be a sign of a split cord malformation or diastematomyelia.

     

    Failure to diagnose a structural lesion of a major nerve

  • The clinician must examine the entire lower limbs along the course of major nerves to detect a localized peripheral nerve tumor or site of nerve compression.

     

    Failure to diagnose HSMN ▪ Bilateral cavus may be subtle.

    • The clinician should always ask about a family history of cavus feet or peripheral neuropathy.

    • Sometimes, there is not an established diagnosis of HSMN in the family. In these cases, the family members may need to be examined.

    • The hand and foot intrinsics are examined.

    • HSMN may initially present as bilateral adolescent hip dysplasia.

       

      Missing a diagnosis with a very treatable lesion

  • Several conditions may cause a cavus foot deformity. Subtalar coalition generally causes a rigid valgus hindfoot deformity but may cause a spastic hindfoot varus (FIG 9).

 

Insufficient surgical procedure ▪ With adolescence, severe cavus deformities often require a more

extensive midfoot osteotomy to correct the deformity.

 

Severe idiopathic cavus foot deformity often requires repeat surgical procedures

• The family should be warned that further surgical procedures may be necessary with time as the child grows and the deformity changes.

 

 

FIG 9 • Spastic hindfoot varus.

 

 

 

POSTOPERATIVE CARE

 

After a plantar release, the foot should be wrapped with soft, bulky cotton and casted with minimal external correction.

 

At 2 weeks, the sutures are removed and gentle correction is obtained. This may require serial casting for up to 6 weeks.

 

After a midfoot or forefoot osteotomy, weight bearing is restricted until the osteotomy has healed, generally about 6 weeks.

 

 

OUTCOMES

Long-term outcome studies are limited for progressive conditions such as HSMN.15

One study demonstrated that patients with Charcot-Marie-Tooth disease that had a first metatarsal osteotomy and soft tissue procedures had lower rates of degenerative changes and lower rates of

reoperations when compared with patients treated with a triple arthrodesis.18 This study seemed to confirm that patients treated with procedures that attempt to rebalance the foot and keep a mobile foot have a better outcome than those treated with an arthrodesis.

Triple arthrodesis for progressive cavus deformity has a poor long-term outcome. Results are further compromised by technical problems at the time of surgery as well as from undercorrection and overcorrection.

Most patients with a progressive cavus deformity and a triple arthrodesis performed as a teenager had significant foot problems by their 30s.19

Nonprogressive deformities such as spastic cavovarus with equinus can be surgically balanced with acceptable results.

Progressive deformities may require several surgeries during childhood followed by a triple arthrodesis at maturity. The patient and family should be warned about this possibility.

 

COMPLICATIONS

 

Femoral or sciatic nerve injury from tourniquet. This can occur with excessive pressure or time on the tourniquet or even with minimal time and pressure. The tourniquet time should be under 1 hour, using minimal pressure needed for visualization.

Plantar medial incision dehiscence if excessive correction is attempted at the time of surgery Pressure sores in patients with HSMN

Surgical correction of midfoot deformity distal to the apex may result in a rocker bottom foot deformity. Nonunion of the midfoot osteotomy8

Persistent midfoot cavus if the deformity is too severe for a medial column or midfoot osteotomy

Persistent hindfoot varus if deformity is fixed and a calcaneal osteotomy is not performed

 

 

 

REFERENCES

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1. Azmaipairashvili Z, Riddle EC, Scavina M, et al. Correction of cavovarus foot deformity in Charcot-Marie-Tooth disease. J Pediatr Orthop 2005;25:360-365.

    

2. Bradley GW, Coleman SS. Treatment of the calcaneocavus foot deformity. J Bone Joint Surg Am 1981;63(7):1159-1166.

    

3. Fuller JE, DeLuca PA. Acetabular dysplasia and Charcot-Marie-Tooth disease in a family. A report of four cases. J Bone Joint Surg Am 1995;77(7):1087-1091.

    

4. Ghanem I, Zeller R, Seringe R. The foot in hereditary motor and sensory neuropathies in children [in French]. Rev Chir Orthop Reparatrice Appar Mot 1996;82:152-160.

    

5. Guyton GP. Peroneal nerve branching suggests compression palsy in the deformities of Charcot-Marie Tooth disease. Clin Orthop Relat Res 2006;451:167-170.

    

6. Jahss MH. Evaluation of the cavus foot for orthopedic treatment. Clin Orthop Relat Res 1983;(181):52-63.

    

7. Japas LM. Surgical treatment of pes cavus by tarsal V-osteotomy. Preliminary report. J Bone Joint Surg Am 1968;50(5):927-944.

    

8. Levitt RL, Canale ST, Cooke AJ, et al. The role of foot surgery in progressive neuromuscular disorders in children. J Bone Joint Surg Am 1973;55(7):1396-1410.

    

9. Lutter LD. Cavus foot in runners. Foot Ankle 1981;1:225-228.

    

10. Mubarak SJ, Dimeglio A. Navicular excision and cuboid closing wedge for severe cavovarus foot deformities: a salvage procedures. J Pediatr Orthop 2011;31(5):551-556.

     

11. Mubarak SJ, Van Valin SE. Osteotomies of the foot for cavus deformities in children. J Pediatr Orthop 2009;29(3):294-299.

     

12. Paulos L, Coleman SS, Samuelson KM. Pes cavovarus. Review of a surgical approach using selective soft-tissue procedures. J Bone Joint Surg Am 1980;62(6):942-953.

     

     

13. Price AE, Maisel R, Drennan JC. Computed tomographic analysis of pes cavus. J Pediatr Orthop 1993;13:646-653.

     

     

14. Sabir M, Lyttle D. Pathogenesis of pes cavus in Charcot-Marie-Tooth disease. Clin Orthop Relat Res 1983;(175):173-178.

     

     

15. Schwend RM, Drennan JC. Cavus foot deformity in children. J Am Acad Orthop Surg 2003;11:201-211.

     

     

16. Tynan MC, Klenerman L, Helliwell TR, et al. Investigation of muscle imbalance in the leg in symptomatic forefoot pes cavus: a multidisciplinary study. Foot Ankle 1992;13:489-501.

     

     

17. Walker JL, Nelson KR, Heavilon JA, et al. Hip abnormalities in children with Charcot-Marie-Tooth disease. J Pediatr Orthop 1994;14:54-59.

     

     

18. Ward CM, Dolan LA, Bennett DL, et al. Long-term results of reconstruction for treatment of a flexible cavovarus foot in Charcot-Marie-Tooth disease. J Bone Join Surg Am 2008;90(12):2631-2642.

     

     

19. Wetmore RS, Drennan JC. Long-term results of triple arthrodesis in Charcot-Marie-Tooth disease. J Bone Joint Surg Am 1989;71(3):417-422.

     

     

20. Wilcox PG, Weiner DS. The Akron midtarsal dome osteotomy in the treatment of rigid pes cavus: a preliminary review. J Pediatr Orthop 1985;5:333-338.

     

     

21. Younger ASE, Hansen ST Jr. Adult cavovarus foot. J Am Acad Orthop Surg 2005;13:302-315.