Tendon Disorders of Foot and Ankle Part 3- Tibialis Posterior

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Tendon Disorders of the Foot and Ankle, Part 3 : The Posterior Tibial Tendon George S. Gluck, Daniel S. Heckman and Selene G. Parekh Am J Sports Med 2010 38: 2133 originally published online March 29, 2010 DOI: 10.1177/0363546509359492 The online version of this article can be found at: http://ajs.sagepub.com/content/38/10/2133

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Clinical Sports Medicine Update

Tendon Disorders of the Foot and Ankle, Part 3

M

The Posterior Tibial Tendon George S. Gluck,* MD, Daniel S. Heckman,* MD, and Selene G. Parekh,yz§ MD, MBA From the *Department of Orthopaedic Surgery, University of North Carolina School of Medicine, Chapel Hill, North Carolina, and the zDivision of Orthopaedic Surgery and §Fuqua Business School, Duke University, Durham, North Carolina

This article provides a review of posterior tibial tendon pathology and the authors’ preferred management. The tibialis posterior musculotendinous unit is the most powerful inverter of the foot and an important dynamic stabilizer of the arch. In the stance phase of the gait cycle, it serves as an initiator of both ankle plantar flexion and subtalar inversion. This creates a rigid midfoot by stabilizing the transverse tarsal joint, and allows for increased power generation by the gastrocsoleus complex through toe-off.

Injuries to the posterior tibialis tendon include traumatic laceration and dislocation, as well as tenosynovitis and tendinopathy, which can lead to attenuation and rupture. If these injuries are not addressed, significant clinical deformity and disability can result.

Keywords: posterior tibial tendon deficiency; tenosynovitis; accessory navicular; subtalar arthrodesis

contribute to degenerative changes of the tendon.20 The PTT divides anterior to the tuberosity of the navicular.

An anterior slip, which is in direct continuity with the main tendon, inserts onto the tuberosity of the navicular, the inferior aspect of the capsule of the medial naviculocuneiform joint, and the inferior surface of the medial cuneiform. A second slip attaches to the plantar surfaces of the middle and lateral cuneiforms and the cuboid, as well as to the bases of the corresponding metatarsals.50 The tibialis posterior tendon is an important dynamic stabilizer of the arch and the most powerful inverter of the foot.35,36 It is roughly twice the size of the flexor hallucis longus (FHL) and flexor digitorum longus (FDL) tendons, and slightly smaller than the tibialis anterior tendon.50 The clinical deformity associated with PTT dysfunction (PTTD) reflects the loss of support from the spring, deltoid, and talocalcaneal interosseous ligaments as well as from the talonavicular capsule and the plantar fascia. Normally, the deltoid ligament provides stability to the tibiotalocalcaneal joint complex.16,58 With clinical progression of PTTD, the deltoid ligament becomes attenuated and the talus begins to tilt in the ankle joint, leading to a valgus deformity of the hindfoot.13 Deland et al13 demonstrated that no abnormality can be seen radiographically in a cadaveric model when there is dysfunction of the PTT alone, and that a static deformity occurs only when there is also associated ligamentous damage.

ANATOMY The tibialis posterior muscle is the most central muscle in the leg. Located in the deep posterior compartment, it originates at the upper third of the leg on the posterior borders of the tibia, fibula, and interosseous membrane.

The tendon forms in the distal third of the leg and passes immediately posterior to the medial malleolus where it changes direction acutely.32 A groove in the posteromedial aspect of the distal part of the tibia holds the posterior tibial tendon (PTT) but is not deep enough to keep the tendon from bow-stringing or dislocating after an injury.56 The flexor retinaculum, which is adjacent to the medial malleolus, tethers the tendon and keeps it in the groove, preventing dislocation. Distally, this retinaculum blends with the sheath of the tibialis posterior tendon and the superficial deltoid ligament. The PTT does not have a mesotenon, and there is an area of relative hypovascularity immediately distal to the medial malleolus that may y Address correspondence to Selene G. Parekh, MD, MBA, 3609 SW Durham Dr., Durham, NC 27707 (e-mail: selene.parekh@gmail.com).

The authors declared that they had no conflicts of interests in their authorship and publication of this contribution.

The American Journal of Sports Medicine, Vol. 38, No. 10 DOI: 10.1177/0363546509359492 Ó 2010 The Author(s)

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ACUTE INJURY Traumatic Lacerations of the PTT Traumatic lacerations of the PTT can occur directly or indirectly in association with an ankle fracture or dislocation,46 a calcaneal fracture, or a traumatic fall. If left untreated, the traumatic PTT tear can result in the same pes planus deformity seen in attritional ruptures.23 Imaging of the soft tissue structures is not usually required with a laceration, as local wound exploration should lead to an accurate diagnosis. In the setting of delayed treatment where the wound was closed primarily without exploration, or in the setting of a closed injury, MRI can be helpful. An ‘‘empty’’ tendon sheath can be diagnosed with high accuracy with MRI, with a sensitivity of 95%, a specificity of 100%, and an overall accuracy of 96%.59 Ultrasonography, although highly userdependent, can allow for real-time dynamic examination of the tendon.30 If possible, primary repair should be attempted at the time of wound exploration, followed by cast immobilization to allow for adequate healing to occur.2,17 In the event that primary repair is not possible, an FDL tendon transfer may be performed.66 If a hindfoot valgus deformity has occurred, a medial calcaneal slide osteotomy may also be necessary.

Authors’ Preferred Treatment of Primary Tears of the PTT. In the setting of an acute rupture of the PTT, our preference is to proceed with a primary repair as acutely as possible to minimize contracture of the proximal PTT stump and scarring of the tendon ends due to a delay in treatment. The patient is placed supine on the operating room table and a thigh tourniquet is applied. A rolled bump may be placed under the contralateral hip if the normal external rotation of the ipsilateral limb will not allow for adequate visualization of the posteromedial aspect of the ankle. An incision is centered along the course of the PTT, from the navicular to approximately 3 cm proximal to the tip of the medial malleolus. The tendon sheath is carefully opened with a knife, taking care to protect the remaining portion of the PTT. If possible, the ruptured ends are reapproximated with a running Krackow stitch placed in each of the free ends with a nonabsorbable suture. The ends of the tendon are brought together and the sutures are tied while holding the foot in maximal plantar flexion and inversion. A 0 Vicryl suture (Ethicon, Johnson & Johnson, Somerville, New Jersey) is then placed in a running fashion around the rupture site to enhance the repair.

If the tendon ends cannot be opposed, or if the tear is chronic in nature with fraying and discoloration (Figure 1), then an FDL tendon transfer is performed. If the rupture is chronic in nature and a hindfoot valgus deformity has occurred, then a medial calcaneal slide osteotomy is also performed. See the discussion below of our preferred treatment for stage 2 PTTD for details of this procedure.

In the operating room, the patient is placed in a bulky Jones splint in slight plantar flexion and inversion. Two weeks following surgery, sutures are removed and a short-leg nonweightbearing cast is applied. Four weeks later, the patient is allowed to bear weight, protected in

Figure 1. Intraoperative photograph of a chronic rupture with fibrous healing of the posterior tibial tendon. a controlled ankle motion (CAM) boot. Physical therapy is started for range of motion (ROM), strengthening, and modalities as needed. Ten weeks following surgery, the CAM boot is discontinued and physical therapy is maintained until the tendon repair or transfer has achieved maximal strength.

Dislocation of the PTT Dislocation of the PTT is an uncommon injury, with less than 40 cases reported in the English literature. The most common mechanism is forced dorsiflexion and eversion of the ankle with the foot inverted while the PTT is contracted. It has been reported in association with medial malleolar fractures, and both minor and major ankle trauma.54 Magnetic resonance imaging is useful for demonstrating a dislocation of the PTT medial to the medial malleolus. Moderate edema surrounding the tendon can also be seen.51 A few case reports exist in the literature, with the largest series by Ouzounian and Myerson.54 Their series included 6 acute traumatic dislocations and 1 chronic dislocation that was attributed to multiple local steroid injections. The average length of time to diagnosis was 9 months, with all patients requiring surgery after failed nonoperative treatment. The retinaculum was found to be absent, torn, redundant, or avulsed with a fibrocartilaginous rim. Reconstruction was performed with either reattachment through drill holes, imbrication, or primary repair where appropriate. If the retromalleolar groove was found to be shallow, a deepening procedure was also performed. All patients had postoperative immobilization in a short-leg cast followed by

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physical therapy. Five patients were asymptomatic on follow-up, with 1 patient having continued difficulty.

Various other methods of stabilization have been used.

These include suture anchor repair of the retinaculum and reconstruction using a periosteal sleeve or Achilles tendon flap. Overall, most authors report good to excellent results with the majority of patients returning to preinjury activity levels.24,51,54 Authors’ Preferred Treatment of PTT Dislocation. The patient is placed supine on the operating room table and a thigh tourniquet is applied. A bump may be placed under the contralateral hip if the normal external rotation of the ipsilateral limb will not allow for adequate visualization of the posteromedial aspect of the ankle. An incision is centered along the course of the PTT, from the navicular to approximately 4 cm proximal to the tip of the medial malleolus. The retinaculum is examined; if it is torn off of the medial malleolus, the tear is extended to expose the PTT. If the sheath is attenuated, it is carefully opened with a knife, taking care to protect the PTT. The PTT is then examined for any longitudinal tears. If present, the PTT tear is repaired with a nonabsorbable running suture.

The malleolar groove is examined. If shallow, it must be deepened. Under fluoroscopic guidance, a guide pin from a 4-0 cannulated screw system is placed, starting from the tip of the medial malleolus, and inserted proximally and posteriorly, parallel to the cortex of the groove. The guide pin is advanced proximally until the tip of the pin touches the posterior cortex on the lateral view. The guide pin is then overdrilled with a 4.0-mm drill bit and checked radiographically. The guide pin is removed and the malleolar groove is deepened with a bone tamp and mallet.

Next, the retinaculum is repaired; if it is torn from the medial malleolus, the sheath is reattached to the bone through drill holes, using a nonabsorbable suture. If the sheath is attenuated, it is imbricated with a nonabsorbable suture. Care is taken to ensure that the retinaculum is not overtightened, to prevent constriction of the PTT. In the operating room, the patient is placed in a bulky Jones splint with the foot in slight plantar flexion and inversion. Two weeks following surgery, sutures are removed and a short-leg nonweightbearing cast is applied. Four weeks later, the patient is allowed to bear weight, protected in a CAM boot. Physical therapy is started for ROM, strengthening, and modalities as needed. Ten weeks following surgery, the CAM boot is discontinued and physical therapy is continued until maximal strength is achieved.

SYMPTOMATIC ACCESSORY NAVICULAR The accessory navicular is one of 38 accessory bones that have been identified in the foot.53 It can be unilateral or bilateral and is significantly more prevalent in females.

Symptoms usually develop after 5 years of age and are most common in early adolescence.41 Patients often complain of pain over the medial aspect of the midfoot with weightbearing, walking, and strenuous activity or from wearing narrow shoes. Pain can be reproduced by palpation

over the accessory navicular and PTT insertion, or by resisting active foot inversion.14 Symptoms are more likely to be acute in adults, especially after trauma with a foot eversion injury. In children, the presenting complaint is often more chronic and related to pressure on the medial prominence from the shoe.10 The classification system includes 3 types, which are based on radiographic appearance. Geist22 was the first to perform a radiographic study on the accessory navicular, and he expanded on previous work to include the 3 types that are recognized today. When the accessory navicular exists as an ossicle within the substance of the PTT, it is considered type 1. Type 2 is defined by a synchondrosis that joins it to the navicular.62 In cases where it has fused to the navicular, it is considered a type 3.22 In addition to plain radiographs and CT scans of the foot (Figure 2), bone scintigraphy and MRI can help to identify a symptomatic accessory navicular by localizing increased technetium uptake or fluid and marrow edema, respectively.

Nonoperative treatment, regardless of classification, consists of shoe wear modification to relieve pressure over the tender area, nonsteroidal anti-inflammatory medication, braces, and orthotics such as a University of California at Berkeley Laboratory–type orthotic device (UCBL) or medial heel wedge to minimize tension of the PTT at the insertion. Some advocate corticosteroid injections targeted at the synchondrosis.10 In the acute setting, in patients who are exquisitely tender, a short-leg walking cast or removable fracture boot may be tried. Results of nonoperative treatment range in success from 13% to 33%.22,25 Operative treatment generally incorporates removal of the accessory navicular with either primary PTT repair in stage 1 or reconstruction in stages 2 and 3. Kidner34 is well known for his classic description of the procedure for symptomatic accessory navicular. It involved accessory navicular excision and PTT reconstruction by reattaching a wafer of bone and the PTT to the navicular with chromic suture. Leonard et al39 proposed the modification of passing the PTT through a drill hole. Successful outcomes have been achieved with both primary repair and reconstruction of the PTT, regardless of stage.22,37,39,42 Some authors advocate other modifications, such as the use of suture anchors in the navicular or resection of the synchondrosis and fusion with screw fixation.42,61,67 Authors’ Preferred Treatment of the Accessory Navicular. The patient is placed supine on the operating room table and a thigh tourniquet is applied. A bump may be placed under the contralateral hip if the normal external rotation of the ipsilateral limb will not allow for adequate visualization of the posteromedial aspect of the ankle. An incision is centered along the course of the PTT, from the navicular to 1 cm proximal to the tip of the medial malleolus. The PTT sheath is identified and carefully opened sharply. The PTT is identified and followed distally to the accessory navicular. The accessory navicular is palpated. The PTT is sharply dissected off the accessory navicular and the navicular bone as distally as possible. The accessory navicular is then excised. The distal attachments of the PTT are preserved if the accessory navicular can be removed from the tendon without complete tenotomy. A

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Figure 2. Imaging of an accessory navicular: A, AP view of a synchondrosis type; B, axial CT image. nonabsorbable suture is placed in a modified Kessler-type fashion over the distal aspect of the PTT. A drill hole is then placed in a dorsal to plantar direction with a drill bit to create a hole large enough to allow passage of the tendon. With use of a suture passer, the PTT is brought through the hole plantar to dorsal. The foot is held in maximal inversion and plantar flexion. A series of No. 2 nonabsorbable horizontal mattress sutures are placed through the tendon and into the surrounding periosteum and capsule at the dorsal aspect of the drill hole. The 2 free ends of the No. 2 nonabsorbable suture from the tip of the PTT are then tied back onto the PTT proximally. The sheath is closed with 2-0 Vicryl sutures. The subcutaneous tissue is closed with 2-0 Vicryl sutures. Staples are used to close the skin.

The patient is placed in a bulky Jones splint with the foot in slight plantar flexion and inversion. Two weeks following surgery, staples are removed and a short-leg nonweightbearing cast is applied. Four weeks later, the patient is allowed to bear weight, protected in a CAM boot. Physical therapy is started for ROM, strengthening, and modalities as needed. Ten weeks following surgery, the CAM boot is discontinued and physical therapy is maintained until maximal strength is achieved.

POSTERIOR TIBIAL TENDON DEFICIENCY AND ACQUIRED FLATFOOT DEFORMITY The first published description of tendinitis and insufficiency of the PTT is credited to Kulowski in a 1936 article.38 Subsequently, articles by Fowler19 and Williams70 discussed the syndromic nature of the disease and the role of

surgical intervention to alter its natural history. The use of an FDL transfer to treat progressive flatfoot deformity was originally described by Goldner et al23 in 1974 and popularized in the early 1980s by Jahss31and Mann and Thompson.45 Although PTTD is a common clinical entity, an exact incidence is difficult to determine. Causative risk factors have not been definitively identified, but certain associations have been made. Several authors have noted the incidence of PTT pathology or rupture as higher in middleaged women who have coexisting obesity.21,28,32,45 Other clinical entities that have been found to contribute to the development of PTTD include diabetes mellitus, hypertension, steroid exposure, or previous trauma or surgery in the medial foot region. Holmes and Mann28 studied 67 patients with PTT rupture. The authors noted that almost 60% of their patients had a history of at least 1 of these aforementioned conditions.

Insufficiency of the PTT is mainly a clinical diagnosis.

Symptoms early in the disease process are predominantly pain around the posteromedial aspect of the ankle. It is often worsened with activity and can radiate along to the arch of the foot. Fatigue or weakness of the foot and ankle is also associated with this condition, and patients may complain of decreased endurance with walking or difficulty walking on uneven surfaces. Swelling and pain along the course of the PTT, particularly several centimeters proximal to the insertion on the navicular, are also common.

Patients may also begin to complain of pain on the lateral aspect of the ankle and progressive ‘‘turning out’’ of the foot as the disease progresses and deformity with impingement of lateral structures occurs. Although PTTD can lead to flatfoot deformity, there are other potential causes of this deformity that must be considered. Other causes

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include tarsal coalition, inflammatory arthritis, traumatic disruption of the ligaments of the midfoot, tarsometatarsal osteoarthritis, Charcot arthropathy, and neuromuscular disease.

On physical examination, after both legs, ankles, and feet are exposed, inspection should be made for any areas of swelling or malalignment. Gait analysis should be performed to identify any asymmetries or antalgic components. Forefoot abduction and pes planus deformities should be noted. Observation of the alignment of the extremity from behind with the patient facing away from the examiner will reveal pes planovalgus deformity by the ‘‘too-many-toes’’ sign. Heel valgus should also be noted.

Once heel valgus exceeds the normal range of about 5° to 10°,63 the Achilles tendon moves lateral to the axis of the subtalar joint and contractures of the Achilles tendon can develop. Single-limb heel raise should always be tested or, more easily, a patient can be asked to walk on his or her toes for a short distance. Individuals with normal foot and ankle strength and mechanics should be able to complete 5 to 10 single-limb heel raises without difficulty.

Incomplete inversion of the heel, difficulty or inability to raise the heel, or sensations of weakness or pain while performing this test are highly suggestive of PTTD. Tenderness is first noted over the course of the PTT, but can develop over the tip of the lateral malleolus as lateral impingement occurs in the latter stages of disease.56 Strength should be assessed by having the examiner hold the patient’s foot in plantar flexion, eversion, and abduction. The patient is then asked to plantar flex and invert the foot against resistance. Strength deficits of 20% to 30% or more can be detected in stage 2 disease.29 Subtalar mobility should also be checked. If mobile, dorsiflexion of the ankle should be tested with the knee both flexed and extended while passively correcting any valgus angulation of the heel. This allows for the evaluation of an Achilles tendon contracture.

A widely accepted classification system, proposed by Johnson and Strom32 and later modified by Myerson,48 clarifies treatment recommendations based on the severity of PTTD and adaptation of the foot to collapse of the medial longitudinal arch (Table 1).

Stage 1 Stage 1 disease is characterized by tenderness over the PTT with a variable amount of edema and warmth, consistent with tendinosis or tenosynovitis. Mild weakness may be present with single-limb heel raise or manual testing, which should reproduce posteromedial pain at a minimum.

Tenderness along the course of the PTT is present. Hindfoot inversion and overall clinical alignment and mobility should be normal. Radiographs should not show any degenerative changes or deformity, while MRI may show enhancement surrounding the PTT on T2-weighted imaging (Figure 3), consistent with inflammation and edema.

Ultrasound may show fluid around the PTT. Nonoperative treatment depends on the level of symptoms reported by the patient. With acute or severe disease,

immobilization is recommended with a cast or removable fracture boot. Weightbearing is allowed, and nonsteroidal anti-inflammatory drugs are used for pain relief. After a 4- to 6-week period of immobilization, patients are encouraged to use an arch support with a medial heel wedge and a medial column post.63 In those with more chronic or mild symptoms, orthotic support may be the initial recommendation. Physical therapy for ankle strength and flexibility, with focus on the tibialis posterior, is introduced as the patient improves and symptoms allow. Treatment is continued for 3 to 6 months before surgical intervention is considered. Prolonged orthotic use and periodic evaluations to monitor for progression may be necessary in patients who respond to nonoperative treatment.

Operative treatment of stage 1 disease includes tenosynovectomy, in addition to debridement or repair of degenerative areas or tears.64 Both open and tendoscopic techniques have been described. An open procedure allows clear identification and inspection of the local anatomy.

One, small, retrospective study reported complete relief in 6 of 7 patients 11 months after synovectomy with or without tendon debridement. These patients all failed at least 6 weeks of immobilization. The 1 operative failure had extensive intrasubstance degeneration and required tendon transfer after further disease progression.11 Posterior tibial tendoscopy allows for improved cosmesis and potentially less surgical pain and scarring. Two publications on tendoscopic techniques had similar results in small patient groups without reported complication other than entering the wrong tendon sheath initially.4,7,68 Authors’ Preferred Treatment of PTTD Stage 1. We do not routinely use corticosteroid injections, as the disease is considered more degenerative than inflammatory.28,32,48 The patient is placed supine on the operating room table and a thigh tourniquet is applied. A bump may be placed under the contralateral hip if the normal external rotation of the ipsilateral limb will not allow for adequate visualization of the posteromedial aspect of the ankle. An incision is centered along the course of the PTT, from the navicular to 4 cm proximal to the tip of the medial malleolus. The PTT sheath is identified and carefully opened sharply. Oftentimes, there are dense adhesions between the tendon and the sheath, such that dissection of the tendon must be performed extremely carefully. Synovitic tissue will appear brownish red. This is meticulously removed with a rongeur.

The tendon is examined for any fusiform edema or tears. If present, tears of the tendon should be repaired with a tubularization procedure using a nonabsorbable suture.

The sheath is then reapproximated and closed with an absorbable suture. The subcutaneous tissues are also closed with absorbable suture. The skin is closed with staples. The patient is placed in a bulky Jones splint with slight plantar flexion and inversion.

Two weeks following surgery, sutures are removed and the patient is allowed to bear weight as tolerated in a CAM boot. Aggressive physical therapy is started for ROM, strengthening, and modalities as needed. Six weeks following surgery, the CAM boot is discontinued and physical therapy is maintained until maximal strength is achieved.

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TABLE 1 Stages of Posterior Tibial Tendon Dysfunctiona Stage 1 Tendon pathology Deformity

Tenosynovitis 6 degeneration Absent

Clinical findings

Medial pain Mild pain with heel raise Mild weakness with hindfoot inversion

Nonoperative treatment

Medial heel 1 sole wedge Period of immobilization Therapy Tenosynovectomy Repair

Operative treatment

Stage 2

Stage 3

Stage 4

Degeneration 1 elongation Flexible pes planovalgus Medial 6 lateral pain Too-many-toes sign Marked pain with heel raise 6 unable to perform Marked weakness with hindfoot inversion

Degeneration 1 elongation Fixed pes planovalgus Medial 6 lateral pain Too-many-toes sign Unable to perform heel raise Marked weakness with hindfoot inversion

Degeneration 1 elongation

Orthotic support (molded, articulated AFO)

Rigid AFO

FDL tendon transfer Calcaneal osteotomy Lateral column lengthening Heel cord lengthening

Triple arthrodesis

Fixed pes planovalgus Medial 6 lateral pain Too-many-toes sign Unable to perform heel raise Marked weakness with hindfoot inversion Pain/crepitus with tibiotalar motion Rigid AFO

Tibiotalocalcaneal arthrodesis Triple arthrodesis with total ankle arthroplasty (experimental)

a

AFO, ankle-foot orthosis; FDL, flexor digitorum longus

Figure 3. A T2-weighted MRI axial cut showing increased fluid within the posterior tibial tendon sheath.

Stage 2 Stage 2 disease is characterized by the presence of clinical pes planus deformity that is flexible with a varying degree of heel valgus and a positive too-many-toes sign. This sign

is characterized by the visibility of the lateral toes extending into the field of view when the foot is viewed from behind the heel (Figure 4). Tenderness and swelling persist, but weakness and difficulty with single-limb heel raises increases.

Common radiographic findings are decreased lateral talocalcaneal pitch angle and uncovering of the talar head. On MRI, enlargement and abnormal signal of the PTT can be appreciated when compared with the peroneal, FDL, and FHL tendons (Figure 5).

Radiographic analysis of the foot and ankle is important, not only to evaluate for arthrosis but also to document preoperative deformity. Evaluation should include bilateral weightbearing AP and lateral views of the foot and ankle. A variety of angular and linear methods of measurement have been described.5 The AP view of the ankle is obtained to evaluate valgus tilt of the talus and subfibular impingement. On the AP view of the foot, the talo–first metatarsal angle can be measured, and should be close to parallel. On the lateral weightbearing view of the foot, the lateral talocalcaneal and calcaneal pitch angles are noted. Loss of calcaneal pitch and an increased lateral talocalcaneal angle can be seen in flatfoot deformity. Divergence of the talo–first metatarsal angle can also be seen (Figure 6). Magnetic resonance imaging can be a helpful adjunct when planning the treatment for PTTD, and can help identify ligamentous and PTT pathology. Relevant findings include intrasubstance tears or degeneration of the PTT, enlargement of the PTT to more than twice the diameter of the FHL or FDL tendons, edema surrounding

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Figure 4. Too-many-toes sign.

Figure 6. Clinical diagrams showing normal and pathologic alignment of the flatfoot in AP and lateral views.

Figure 5. A T1-weighted MRI axial cut showing enlargement and abnormal signal within the posterior tibial tendon (PTT).

FDL, flexor digitorum longus; FHL, flexor hallucis longus. the PTT, and gross tears or attenuation of the spring ligament complex. In one report, MRI was found to have increased sensivitiy for the extent of PTT degeneration when compared with intraoperative evaluation.9 The presence of a deformity suggests that elongation or disruption of the PTT has occurred, along with attenuation of stabilizing ligamentous structures. These include the deltoid ligament, the talocalcaneal interosseous ligament, and the spring ligament complex consisting of the superomedial calcaneonavicular ligament (incorporated with the medial talonavicular capsule) and the inferior/plantar calcaneonavicular ligament.12 The deformity remains flexible with relatively normal subtalar motion, but a gastrocnemius-soleus contracture may be present. This stage can be further

separated into patients without lateral ankle pain (stage 2A) and those with lateral ankle pain (stage 2B). Lateral pain indicates further progression with symptomatic collapse of the medial arch.

Nonoperative treatment is similar to that for stage 1 disease, except that the prescribed orthosis must be more rigid, with increased lateral buttressing of the forefoot. A supramalleolar orthotic or molded articulated ankle-foot orthosis (AFO) may serve to control deformity and reduce symptoms.6 A rigid orthosis can provide a permanent solution for patients who find it helpful. One study by Lin et al40 demonstrated a 70% success rate at a 7- to 10-year follow-up for nonoperative treatment of stage 2 PTTD using a double upright AFO for an average bracing period of 14 months.

Operative treatment remains an area of some controversy. Treatment usually incorporates dynamic support with tendon transfer to replace or augment the PTT, along with bony procedures to improve static alignment. Mainstays include a flexor tendon transfer, usually with the FDL, and a medializing calcaneal osteotomy.21,33,47,50 Use of the FHL for reconstruction has been recommended as well,23 but requires a more complicated dissection and has increased donor morbidity secondary to functional deficit. Furthermore, while the FHL is significantly stronger than the FDL, the FDL is located in a more optimal anatomic position for transfer.50 Heel cord or a gastrocnemius recession and lateral column lengthening through the neck of the calcaneus or the calcaneocuboid joint have also been incorporated into reconstructive procedures to correct equinus contracture and forefoot adduction, respectively.15,49,52 A repair of the spring ligament is an additional soft tissue procedure that can be used to augment the reconstruction.28 Some authors also advocate

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a lateral column lengthening through the calcaneocuboid joint with arthrodesis, as opposed to an Evans-type osteotomy at the calcaneal neck to prevent increased pressure across the calcaneocuboid joint.50A clinical study addressing this issue found no significant differences in objective outcome measures or patient satisfaction at 1 year.65 Authors’ Preferred Treatment of PTTD Stage 2. The patient is placed supine on the operating room table and a thigh tourniquet is applied. A bump may be placed under the contralateral hip if the normal external rotation of the ipsilateral limb will not allow for adequate visualization of the posteromedial aspect of the ankle. If the patient has a hindfoot valgus deformity and a gastrocsoleus complex contraction, an Achilles tendon lengthening is performed first. The foot is held by an assistant approximately 1 foot off of the table. Three hemisections are performed percutaneously in the Achilles tendon. Two exit the tendon laterally and one exits medially in an alternating fashion.

A No. 15 blade is brought through the tendon parallel to the long axis of the tibia. It is then turned 90° and a hemisection is performed. This is done 1 to 2 cm proximal to the insertion site, then at approximately 4 cm, and finally at approximately 6 cm proximal to the insertion site. After the 3 hemisections are completed, the foot is held in neutral and the Achilles tendon is slowly lengthened such that 10° to 15° of dorsiflexion is obtained. All 3 wounds are closed with staples.

Next, attention is directed to the posteromedial ankle.

An incision is centered along the course of the PTT, from the navicular to approximately 4 cm proximal to the tip of the medial malleolus. The PTT sheath is identified and opened sharply. The PTT is examined to ensure that a tendon transfer is required. If a transfer is needed, the PTT is transected at the proximal extent of the incision. The residual distal portion is then mobilized and resected off of the navicular. Dissection is continued medially along the foot.

The abductor hallucis is reflected inferiorly. The origin of the flexor hallucis brevis is identified and released to gain access in the midfoot. The FDL and FHL tendons are then identified (Figure 7A). Any connection between the 2 tendons is released. With all of the toes held in maximal plantar flexion at the same level, a tacking suture is placed at the level of the knot of Henry, tenodesing the FDL and FHL tendons together. The FDL tendon is then transected at the level of the first metatarsal, proximal to the tenodesis. A Kessler suture is placed in the tip of the FDL tendon with a No. 2 nonabsorbable suture (Figure 7B). The spring ligament is carefully examined. If attenuated, it must be repaired, in a pants-over-vest manner.

To perform a spring ligament repair, the talonavicular joint is held reduced and the amount of attenuated tissue is marked. Nonabsorbable suture is placed from the distal segment to the proximal marks and from the proximal segment to the distal mark. A small incision is made in the floor of the PTT sheath to communicate with the FDL tendon sheath. The FDL is transferred into the PTT sheath proximally. The medial pole of the navicular is identified.

A drill hole is made dorsal to plantar through the medial pole of the navicular. The FDL is then pulled from plantar to dorsal through the drill hole (Figure 7C). The foot is

placed into maximum plantar flexion and inversion and the FDL is sewn back on itself with No. 2 nonabsorbable suture (Figure 7D). An additional nonabsorbable suture is placed into the periosteum to secure fixation. The spring ligament sutures are then tied. The tendon sheath is closed with running absorbable sutures. The subcutaneous tissue is closed with absorbable sutures. The skin is closed with staples.

If there is a hindfoot valgus deformity, a medial calcaneal slide osteotomy is performed prior to fixation of the tendon. An incision is made over the lateral aspect of the calcaneus just posterior to the peroneal tendons. It is carried down through subcutaneous tissues with care to avoid injury to the sural nerve. Dissection is carried down to the level of the lateral wall calcaneus. Subperiosteal dissection is carried out around the lateral wall. The guidewire from a 7.0-mm cannulated screw system is introduced into the posteroinferior aspect of the calcaneus, perpendicular to the plane of the planned osteotomy. It is introduced up to the depths of the threads. The osteotomy is then performed with a sagittal saw through the posterior aspect calcaneus.

The posterior fragment is displaced approximately 5 to 10 mm medially. The guidewire is driven across for provisional fixation. The prominent lateral shelf of the calcaneus osteotomy is tamped down to avoid impingement on the peroneal tendons. The position of the pin is checked radiographically. It is then overdrilled and fixed with a 7-mm partially threaded screw (Figure 8). Rigid fixation must be obtained. The guidewire is then removed from the wound. The wound is irrigated and closed with absorbable sutures followed by staples for the skin.

The patient is placed in a bulky Jones splint with slight plantar flexion and inversion. Two weeks following surgery, sutures are removed and a short-leg nonweightbearing cast is applied. Four weeks later, the patient is allowed to bear weight, protected in a CAM boot. Physical therapy is started for ROM, strengthening, and modalities as needed. Ten weeks following surgery, the CAM boot is discontinued and physical therapy is maintained until maximal strength is achieved.

Stages 3 and 4 Stage 3 is characterized by loss of hindfoot deformity flexibility and an increase in lateral-sided ankle pain. Forefoot supination may be present to compensate for fixed hindfoot valgus in order to maintain a plantigrade foot. This is a fixed deformity that cannot be passively corrected. In addition to clinical and radiographic malalignment, degenerative changes of the subtalar, talonavicular, and calcaneocuboid joints may be present. Routine plain radiographs of the foot and ankle may be further supplemented

by CT imaging to help identify arthrosis in these joints.

Over time, without surgical correction or treatment to prevent progression, patients with stage 3 PTTD progress to stage 4. This is characterized by arthrosis involving the ankle joint as well.48 Nonoperative treatment of stage 3 and stage 4 disease incorporates a progressively more rigid AFO, such as an

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Figure 7. Intraoperative photographs of flexor digitorum longus (FDL) transfer for posterior tibial tendon (PTT) reconstruction. A, the flexor hallucis longus (FHL) as it passes superior to the FDL at the knot of Henry. B, the FDL after tenotomy and tagging with a suture. C, the FDL after it has been pulled through a drill hole in the navicular. D, the FDL tied to itself after the PTT reconstruction.

Arizona-type brace or an articulated AFO. At this point, the goal is to prevent progression by accommodating any rigid deformity, correcting any correctable deformity, and controlling pain.34,64 Bracing will prevent progressive deformity, but progressive arthrosis can still occur because of abnormal mechanics during weightbearing.6 Surgical intervention should be considered if patients do not obtain relief within 3 to 6 months, or if they cannot tolerate bracing.

The goals of operative treatment in stage 3 disease are to re-create a plantigrade weightbearing surface and maintain the integrity of the ankle through arthrodesis by realigning the hindfoot.50 Single, double, and triple fusions have been used to treat stage 3 PTTD. Fusions can be selective with an isolated talonavicular arthrodesis, talonavicular and calcaneocuboid arthrodesis, or an isolated subtalar arthrodesis. Double fusions of the talonavicular and calcaneocuboid joints may be indicated in cases where clinical deformity consists of forefoot abduction and varus, but the subtalar joint remains painless and passively

correctable.8,43 Similarly, isolated subtalar arthrodesis may be indicated where forefoot abduction and varus are reducible, and the transverse tarsal joints are pain-free and without evidence of arthrosis.44,60 Isolated talonavicular arthrodesis can be performed to facilitate limited correction in the setting of a painless, flexible subtalar joint, but it will still significantly limit forefoot motion.1 It can be complicated by the development of pain at the intact calcaneocuboid joint. It is not commonly performed, but can be successful in older, lower demand patients.27,45,55 Lengthening the Achilles tendon to increase ankle dorsiflexion and decrease midfoot loading is also an important aspect of surgical treatment, and it may serve to limit progressive arthrosis.18 Triple arthrodesis is commonly performed for this condition, and a 2-incision technique is recommended as it provides superior visualization for preparation of all fusion sites.50 Triple arthrodesis can provide reliable pain relief, but patients often continue to have some residual pain.69 It is important to ensure proper

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Figure 8. Radiographs of the calcaneal osteotomy after fixation with a 7-mm cannulated compression screw: A, lateral view; B, Harris axial heel view. alignment of the hindfoot, as not doing so can alter tibiotalar joint mechanics and loading.57 There is a high rate of postoperative complications, and some patients will still develop ankle arthrosis.3,48 Despite these problems, patient satisfaction remained high in multiple studies.3,8,18,55 Stage 4 PTTD represents the end of the natural progression of the disease. It can also develop after triple arthrodesis with residual malalignment. Treatment options are based on whether the valgus ankle deformity can be reduced. It is also important to rule out fibular stress fractures and lateral talar dome osteonecrosis. If the ankle joint is reducible, fusion can be revised if previously performed.26 Medial displacement calcaneal osteotomy,58 deltoid ligament reconstruction,37 or a combination of the two can also be considered, but there are no reports of the longterm results available. If the ankle joint is irreducible, options include arthrodesis or arthroplasty. Arthrodesis can be performed using external fixation, internal fixation, or retrograde intramedullary nailing. A variety of implants are available for ankle arthroplasty, but the procedure is still not widely accepted and long-term results are not available in this subset of patients.

Authors’ Preferred Treatment of PTTD Stage 3. The patient is placed supine on the operating room table and a thigh tourniquet is applied. A bump may be placed under the contralateral hip if the normal external rotation of the ipsilateral limb will not allow for adequate visualization of the posteromedial aspect of the ankle. If the patient has a hindfoot valgus deformity and a gastrocsoleus complex contraction, an Achilles tendon lengthening is performed first. This is performed as described in our preferred treatment for stage 2 PTTD. An incision is made from the tip of the fibula toward the base of the fourth metatarsal. It is carried down through the subcutaneous tissues. Care is taken to avoid injury to the sural nerve and lateral branches of superficial peroneal nerve. Dissection is carried down to the interval between the peroneal tendon, sinus tarsi, and extensor digitorum brevis muscle. The extensor digitorum brevis is elevated and reflected medially. This gives access to both the subtalar and calcaneocuboid joints. The interosseous ligament is

then divided off the origin of the superior aspect of the calcaneus. Using a series of rongeurs and curets, the remaining subchondral bone from the posterior, middle, and anterior facets of the subtalar joint is removed to the level of cancellous bone. The joint surfaces are then feathered with a 0.25-in osteotome. A 2-mm drill bit is used to create puncture holes in the subchondral bone of both bony surfaces. The surfaces are prepared so that when they are reduced, the heel remains in 5° of residual valgus.

Attention is then turned to the calcaneocuboid joint. A distractor is placed. Again, using a series of rongeurs and curets, all remaining subchondral bone is removed down to the level of cancellous surfaces, taking care to preserve the saddle shape of the calcaneocuboid joint. The joint surfaces are then feathered with a 0.25-in osteotome. A 2-mm drill bit is used to create puncture holes in the subchondral bone of both bony surfaces.

Attention is then directed dorsomedially. An incision is made over the dorsal aspect of the talonavicular joint. This is carried out through the subcutaneous tissue with care to avoid injury to the saphenous nerve and vein. Dissection is carried down to the level of the joint capsule. A dorsal capsulotomy is created and the talonavicular joint is exposed by dissecting the capsule off the dorsal surface of the navicular. Using a distractor, all remaining subchondral bone is removed from the head of the talus and proximal undersurface of the navicular. This is removed down to the level of cancellous bony surfaces. Once this is completed, the cancellous surfaces are feathered with a 0.25-in osteotome.

A 2-mm drill bit is used to create puncture holes in the subchondral bone of both bony surfaces.

The subtalar joint is first reduced, giving the heel 5° of residual valgus. A guidewire from a 7.0-mm screw system is introduced into the neck of the talus, through the body of the talus, and into the calcaneus. Fluoroscopic views are obtained to confirm good position of the guidewire. The talus is overdrilled and a 7.0-mm screw is placed. The talonavicular joint is then reduced to restore normal alignment of the arch and bring the forefoot into neutral alignment.

With the talonavicular joint held reduced, the guide from a staples system is placed and overdrilled. Two staples

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are placed to span the talonavicular joint. Attention is then turned to the calcaneocuboid joint. Reduction is confirmed, and a locking staple system guide is placed and overdrilled.

A locking staple and respective screws are placed and the staple is compressed. Final fluoroscopic views are obtained.

The patient is placed in a bulky Jones splint in neutral dorsiflexion and plantar flexion, with 5° of valgus. Two weeks following surgery, sutures are removed and a short-leg nonweightbearing cast is applied. Four weeks later, the patient is placed in a CAM boot, but remains nonweightbearing. Eight to 10 weeks following surgery, after radiographic evidence of healing is seen, patients are allowed to bear weight in a CAM boot. The CAM boot is discontinued at week 12.

SUMMARY Both acute and chronic PTT injury can result in significant disability for the patient. As such, it is important that clinicians be able to recognize PTT pathology and be familiar with treatment options. This article serves to provide a brief review of PTT disorders and presents surgical methods for treatment. We would like to emphasize that the techniques presented in this article represent our preferred methods for surgical treatment. Although we have been pleased with our clinical outcomes, we do recognize that controversy remains regarding the appropriate treatment for some of these conditions.

An online CME course associated with this article is available for 1 AMA PRA Category 1 CreditTM at http://ajsm-cme.sagepub.com. In accordance with the standards of the Accreditation Council for Continuing Medical Education (ACCME), it is the policy of The American Orthopaedic Society for Sports Medicine that authors, editors, and planners disclose to the learners all financial relationships during the past 12 months with any commercial interest (A ‘commercial interest’ is any entity producing, marketing, re-selling, or distributing health care goods or services consumed by, or used on, patients). Any and all disclosures are provided in the online journal CME area which is provided to all participants before they actually take the CME activity.

In accordance with AOSSM policy, authors, editors, and planners’ participation in this educational activity will be predicated upon timely submission and review of AOSSM disclosure. Noncompliance will result in an author/editor or planner to be stricken from participating in this CME activity.

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