ADULT ACQUIRED FLATFOOT DEFORMITY: TREATMENT OF POSTERIOR TIBIAL TENDON INSUFFICIENCY
October 27th, 1995
Mark S. Myerson, MD
Acquired flatfoot deformity caused by posterior tibial tendon (PTT) insufficiency is a common clinical problem. Management, which depends on the severity of symptoms and stage of the disease, include nonoperative and surgical options such as rest, antiinflammatory medication, or immobilization and tendon transfer, calcaneal osteotomy, and alternative methods of arthrodesis, respectively.
Anatomy and Pathophysiology
The posterior tibial muscle forms part of the deep posterior compartment of the calf. It originates from the proximal third of the tibia and the interosseous membrane, and passes immediately posterior to the medial malleolus, where it changes direction acutely.1 A groove in the posteromedial aspect of the distal tibia secures the PTT but is not sufficient to keep the tendon from bowstringing or dislocating after injury.2 The flexor retinaculum adjacent to the medial malleolus tethers the PTT in position. Distally, this retinaculum blends with the PTT sheath 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, which may be a cause of tendon degeneration.3 The PTT divides in front of the tuberosity of the naviculum into an anterior slip, which is in direct continuity with the main tendon, and inserts onto the tuberosity of the naviculum, the inferior capsule of the medial naviculocuneiform joint, and the inferior surface of the medial cuneiform. A second slip attaches to the plantar surface of the middle and lateral cuneiforms and the cuboid and the bases of the corresponding metatarsals.4
The PTT passes posterior to the axis of movement of the ankle and medial to the axis of the subtalar joint. Because of its insertion on the naviculum and the plantar aspect of the midtarsus, the PTT acts to plantarflex as well as invert the mid part of the foot, with an action that occurs primarily across the transverse tarsal joints (talonavicular and calcaneocuboid). The PTT therefore functions predominantly to invert the midfoot and to elevate the medial longitudinal arch rather than having a specific effect on the hindfoot. However, the tendon does have a supportive action indirectly on the calcaneus and hindfoot due to its action within the pulley behind the medial malleolus.1
With PTT insufficiency, the medial longitudinal arch collapses, the subtalar joint everts, the heel assumes a valgus position, and the foot abducts at the talonavicular joint. This excessive movement around the talus suggests that the loss of function occurs as a result of PTT insufficiency via its insertion on the naviculum, or through secondary stretching of the calcaneonavicular (spring) ligament.5 Loss of function of the PTT results in heel valgus, probably due to the ligamentous expansions into the sustentaculum and the fibrocartilaginous support on the medial aspect of the talus. Once the heel assumes a more valgus position, the Achilles tendon begins to act as an everter of the calcaneus, since it is now lateral to the axis of rotation of the calcaneus.
PTT insufficiency therefore results in the reversal of its primary actions with internal rotation of the tibia and talus and flattening of the medial longitudinal arch. Secondary changes result in ankle equinus, and a more horizontal subtalar joint and valgus heel. The associated contracture of the Achilles tendon results in increased sagittal plane motion through the subtalar rather than the tibiotalar joint. As the deformity progresses, this eventually causes impingement of the calcaneus against the fibula and associated lateral foot and ankle pain.
The clinical deformity associated with PTT insufficiency also involves loss of its ligamentous support including the spring, deltoid, and talocalcaneal interosseous ligaments as well as the talonavicular capsule and plantar fascia. The deltoid ligament has a substantial stabilizing function on the tibiotalocalcaneal joint complex.6-10 Deltoid ligament insufficiency occurs with increasing deformity, particularly if the hindfoot becomes rigid, leading to valgus tilting of the tibiotalar joint.6,10,11 Deland et al.11 demonstrated in a cadaver model that no radiographic abnormality occurs with PTT insufficiency alone, and static deformity occurs only when associated ligamentous damage is also present.11 One cannot extrapolate these data to the clinical situation directly, since the ligamentous changes that occur are highly variable. However, it is important to recognize that rupture of the PTT is associated with changes in the ligamentous support of the hindfoot.
Etiology and Tendon Rupture
The etiology of PTT is varied, ranging from inflammatory synovitis to degenerative ruptures and, occasionally, acute trauma. Most studies have identified an increased incidence of PTT rupture in middle-aged obese women.12-15 Holmes and Mann16 reported that in 67 patients diagnosed with rupture of the PTT, 60% had positive medical histories including hypertension, obesity, diabetes, prior surgery or trauma about the medial aspect of the foot, or treatment with steroids. Although it is unlikely that acute trauma plays a substantial role in rupture of the PTT and only a few patients can recall a mild sprain or minor injury about the foot and ankle, the PTT is at risk for injury because of its close proximity to the medial malleolar sulcus. For example, acute rupture of the PTT has been demonstrated in association with a closed ankle injury.17 It should be noted, however, that the incidence of this injury is rare.
There appears to be an association between PTT insufficiency and steroid injection. Jahss1 reported that 3 of 10 patients who had received corticosteroid injections developed PTT dysfunction. In this study, patients who received multiple steroid injections around the medial aspect of the foot were diagnosed with PTT rupture months to years later.1 Holmes and Mann demonstrated that corticosteroid injection about the PTT or oral intake of corticosteroids increased the likelihood of PTT rupture.16
It is likely that under normal circumstances an intrinsic abnormality or failure, rather than extrinsic trauma, causes PTT rupture, perhaps because of the direction of the PTT as it passes behind the medial malleolus, the relative hypovascularity of the tendon, or intrinsic degeneration associated with an inflammatory disorder. Frey et al3 showed that there is a zone of hypovascularity in the PTT that begins 1 to 1.5 cm distal to the medial malleolus and extends 1 cm further distally. This area is the most often reported site of clinical degeneration. Neither the flexor digitorum longus (FDL) nor the flexor hallucis longus (FHL) pass as acutely behind the malleolus as does the PTT, which may explain the rarity of injury to the former two tendons.1
PTT dysfunction has also been linked to seronegative inflammatory disorders, a group of acute and chronic rheumatic diseases that are clinically, genetically, and pathologically related to conditions such as ankylosing spondylitis, Reiter's syndrome, and psoriasis rather than to rheumatoid arthritis. Myerson et al,18 for example, reported on a group of young patients with inflammation and/or rupture of the PTT who had seronegative inflammatory disorder and manifestations of enthesopathy. Anzel et al19 suggested that PTT rupture was associated in patients with rheumatoid arthritis, but other authors have found no strong relationship between rheumatoid arthritis and PTT rupture.12,16,18 Flatfoot deformity associated with rheumatoid arthritis is more likely to be caused by synovitis of the talonavicular and subtalar joints.20
The position, function, and neurovascular status of both feet is determined. Both feet should be examined with the patient standing, with the lower extremity visible. The foot should be inspected from above as well as from behind the patient since hindfoot valgus is best appreciated when the foot is viewed posteriorly. Johnson13 described the "more toes sign": with more advanced deformity and abduction of the forefoot, more of the lateral toes become visible when viewed from behind the patient.13 The patient is asked to attempt to rise up on the ball of one foot while the other is suspended off the floor. This single heel rise test is an excellent determinant of PTT function. Under normal circumstances, as the patient begins to rise off of the forefoot, the tibialis posterior, which inverts and stabilizes the hindfoot, is activated. The gastrocnemius-soleus muscle group then pulls up the calcaneus and the heel rise is accomplished. However, with PTT dysfunction, the heel inversion is weak, and the heel either remains in valgus or the patient is unable to rise up on the forefoot. If a single heel rise is possible, the foot may be stressed by asking the patient to perform this manoeuver repetitively.
The strength of the PTT is evaluated against resistance by requesting the patient to plantarflex and invert the foot. When testing for PTT strength, the examiner should hold the hindfoot in plantarflexion and eversion and the forefoot in abduction. This eliminates the synergistic action of the anterior tibial muscle and more accurately quantifies the strength of the PTT. The tendon should be palpated while resisting inversion. Occasionally, an acquired flatfoot deformity is due not to rupture of the PTT but to a tear of the spring or deltoid ligament.15
By palpation, the location of maximum pain and tenderness is established. In the early stages of PTT dysfunction, most of the discomfort is located medially along the course of the tendon, and the patient reports fatigue and aching on the plantar-medial aspect of the foot and ankle. As PTT dysfunction progresses, maximum pain occurs laterally in the sinus tarsi due to impingement of the fibula against the calcaneus.
After locating the sites of pain and tenderness, the subtalar and ankle joints are assessed for mobility and the presence of an Achilles tendon contracture. With increasing heel valgus, the axis of the Achilles tendon is lateral to the ankle joint and shortening of the gastrocnemius-soleus muscle group occurs. If the subtalar joint is mobile, the clinician should check ankle dorsiflexion while passively correcting the heel valgus, since dorsiflexion may be occurring through the transverse tarsal and not the ankle joint. When reducing the heel valgus into neutral, the position of the forefoot is assessed. With minimal deformity, the forefoot remains plantigrade with the subtalar joint reduced. However, as the flatfoot deformity worsens, a fixed supination deformity of the forefoot occurs with the subtalar joint reduced, which has an impact on treatment (see later under "Management"). With more advanced PTT dysfunction, rigidity of the subtalar joint may be present and it may not be possible to reduce the valgus deformity.
It is apparent that a clinical continuum of PTT dysfunction exists, ranging from tenosynovitis through fixed deformity. Any grading or staging system of PTT dysfunction is therefore somewhat arbitrary. It is however useful to describe it in stages in order to better present treatment alternatives in a logical manner. In 1989, Johnson and Strom21 described the clinical stages of PTT dysfunction.21 Stage I is characterized by pain associated with swelling on the medial aspect of the foot and ankle. The tendon is normal in length, and tendinitis is present associated with mild degeneration. Mild weakness and minimal deformity are present. In Stage II, the tendon is torn, the limb is weak, and the patient is unable to stand on tiptoe on the affected foot. Secondary deformity is present as the midfoot pronates and the forefoot abducts across the transverse tarsal joint. The subtalar joint, however, remains flexible. In Stage III, degeneration of the tendon is present, the deformity is more severe, and the hindfoot is rigid. A further stage, not presented by Johnson and Strom21 includes valgus tilting of the talus with early degeneration of the ankle joint.
Anteroposterior and lateral radiographs of both feet and a mortise view of both ankles while bearing weight is recommended for evaluating flatfoot deformity.20 With flatfoot deformity, the anteroposterior radiograph shows abduction of the forefoot across the transverse tarsal joint, with the navicular sliding laterally on the talar head. The lateral radiograph shows a decrease in the talometatarsal angle and the height of the medial cuneiform to the floor. In advanced cases, talonavicular subluxation and dislocation associated with degenerative osteoarthrosis in the posterior facet of the subtalar joint may occur.1
It should be emphasized that the diagnosis of PTT insufficiency is made based on thorough examination of the foot and radiographs, which confirm the extent of deformity and the presence of arthritis. Magnetic resonance imaging (MRI) is not required to make the diagnosis nor does it assist in planning treatment. Although some authors believe that MRI is a useful diagnostic tool in evaluating PTT insufficiency,22-24 other clinicians consider that MRI is used far too commonly in clinical practice and that its clinical usefulness is questionable.15,16
Nonoperative treatment should be attempted for most symptomatic patients with any stage of PTT dysfunction. Most patients with stage-I disease or tenosynovitis respond to nonoperative treatment. Patients with more advanced stage-II or stage-III deformity also benefit from nonoperative treatment, but the risk of progressive deformity has to be considered when planning these treatments.
A patient presenting with acute tenosynovitis has pain along the medial aspect of the ankle associated with swelling and is able to perform a single heel rise test, but with pain. Resisted inversion is painful but still strong. These patients should be treated with rest, appropriate antiinflammatory medication, and immobilization. Corticosteroid injections are not recommended. Immobilization may be obtained with either a rigid short leg cast or a removable cast boot device. Removable stirrup braces are not sufficient, since they do not always limit motion in the sagittal plane, which is part of the pathologic process. Patients are allowed to walk in the cast or boot during an immobilization period of 6 to 8 weeks to prevent overuse and subsequent rupture. At this time, a decision must be made regarding the need for further treatment. If the patient has markedly improved, ambulation may begin in a stiff-soled shoe with a medial heel and sole wedge to invert the hindfoot. With mild to moderate improvement, a more prolonged trial of casting or placing the patient in a stirrup ankle brace may be tried.
Chao et al25 have demonstrated that when the flatfoot deformity is caused by a nonfunctioning PTT, the deformity is usually progressive. However, they showed that a molded ankle foot orthosis or a rigid orthotic support controlled the deformity and alleviated symptoms in many elderly patients with a relatively sedentary lifestyle. They concluded that surgical treatment, therefore, should be considered only for patients who fail an adequate trial of orthotic support or bracing.
Many surgical options are available for treating PTT dysfunction that has failed to improve with a thorough nonoperative treatment program. The type of surgical correction is determined by the patient's age and activity level, the presence of obesity, and the extent of deformity. Defining the clinical stages (as outlined above) is a useful guide to surgical correction and is summarized in the treatment algorithm presented in Table 1. In general, the clinician should perform the least invasive procedure that will provide decreased pain and improved function. One should consider the implications of each procedure with respect to the function of the rest of the foot and ankle, particularly as it pertains to arthrodesis.
Surgical Pathology. The surgical pathology varies according to the underlying etiology of PTT dysfunction. Myerson et al.18 demonstrated that patients with seronegative inflammatory disorders had a proliferative synovium that adhered to the tendon 18. In these patients, the tendon was often attenuated and contained longitudinal fissures, and a chronic nonspecific inflammatory infiltrate was noted histologically.18 In patients with degenerative tendinosis, the tendon sheath is edematous and thickened. Fibrous adhesions are usually present and extend from the inner aspect of the tendon, often posteriorly. If a tear is present, it is commonly located 1 to 2 cm distal to the medial malleolus. Partial or complete rupture of the tendon occurs approximately 2 cm proximal to the tubercle of the naviculum. In most cases, the scarred tendon associated with longitudinal fissuring is adherent to the tendon sheath. It is common to find longitudinal fissures in the posterior aspect of the tendon lying in proximity to the deeper soft tissues and tendon sheath.1,18
I have noted that the extent of clinical and radiographic deformity does not always correlate with PTT degeneration, and I have identified severe unilateral flatfoot deformity associated with an intact PTT.15 In such patients, a rupture of the spring ligament, talonavicular capsule, or deltoid ligament was present, but the PTT was grossly normal and intact.
Tenosynovectomy. Patients with tenosynovitis present with an acute onset of pain and swelling along the medial aspect of the foot immediately inferior the medial malleolus. This is associated with aching of the foot and inability to stand or walk for long distances. Tenderness is present to direct palpation over the tendon. PTT strength is present to resisted inversion, and the patient is able to perform a single or repetitive heel rise, albeit with pain. If the patient shows no improvement after 6 weeks of nonoperative care, then tenosynovectomy should be considered. This is particularly important in younger patients who may have developed tenosynovitis associated with a seronegative inflammatory disorder. This tenosynovitis appears to be particularly aggressive and is associated with inflammatory infiltrate into the tendon and tendon rupture unless treated expeditiously.18
A tenosynovectomy may be performed under ankle block anesthesia.26 A posteromedial incision is made from the musculotendinous junction to the insertion of the PTT. It is useful to preserve a 1-cm strip of the tendon sheath adjacent to the medial malleolus to prevent later dislocation of the PTT, which may occur if the sheath and flexor retinaculum are not repaired.2,27 The tendon sheath is opened and the tendon is inspected.
If an inflammatory tenosynovitis is associated with a seronegative disorder, the tenosynovitis adheres to and infiltrates the sheath and the tendon; this tissue should be thoroughly debrided. Tenosynovitis associated with stage-I degenerative tendinosis is less florid, and bulbous swelling of the tendon with longitudinal fissuring (particularly on the posterior surface) is typically present. These fissures are debrided and the tendon splits repaired with a 4-0 nonabsorbable suture material. Any bulbous tendon degeneration should be excised and the tendon should be thinned out to pass behind the malleolus satisfactorily. After the debridement, the retinaculum immediately posterior to the medial malleolus is repaired, but the tendon sheath is otherwise left open to prevent subsequent tendon adhesions.
It is unlikely that young patients with tenosynovitis associated with a seronegative inflammatory disorder require other surgical treatments.18 Tenosynovectomy is usually sufficient unless attritional tearing of the tendon has already occurred. This was substantiated by Teasdall and Johnson,27 who recommended treatment of stage-I PTT dysfunction with synovectomy and debridement. In their report, 84% of the patients reported subjective improvement with return of function of the PTT.
In older patients with stage-I disease, but with more advanced tendon degeneration than the patient's symptoms would have suggested, it is important to consider additional surgery to the tenosynovectomy to support the diseased tendon. If one assumes that the tenosynovitis is a manifestation of early degeneration of the tendon, then the underlying pathologic process may continue to worsen after a simple tenosynovectomy. In these patients, some authors have advocated performing a side-to-side tenodesis of the FDL tendon to the PTT1,24,28 or calcaneal osteotomy in addition to tenosynovectomy.29
Calcaneal Osteotomy. The concept of treating the valgus heel with a calcaneal osteotomy is well described and understood. The medial shift of the calcaneus alters the biomechanical axis of the lower limb, reducing the valgus thrust on the hindfoot. By displacing the calcaneus medially, it re-directs the pull of the gastrocnemius-soleus muscle group slightly medial to the axis of the subtalar joint. This effectively places the Achilles tendon slightly medially, increasing its varus pull on the hindfoot. This operation was first performed by Gleich30 in 1893 in an attempt to displace the posterior calcaneal tuberosity both medially and inferiorly in order to restore the calcaneal pitch angle. Subsequently, other authors have reported on treatment of flatfoot with osteotomy.29,31-34 The osteotomy as performed by Rose31 is performed by resecting a triangular portion of bone from the posterior-inferior fragment, thereby creating a medial ridge that passes medial to the inner side of the cephalad fragment and locks the osteotomy. This creates both varus angulation and medial displacement of the calcaneus, which is reported to be stable.31,33
The osteotomy as recommended by Myerson et al,29 Saxby and Myerson,34 Fairbank et al,6 and Koutsogiannis35 is a simpler medial translational osteotomy of the posterior calcaneus. The indications for this procedure are in conjunction with a flexor tendon transfer for stage-II PTT dysfunction or combined with tenosynovectomy for more advanced stage-I deficiency. The patient is placed in the lateral decubitus position and an incision is made inferior and parallel to the peroneal tendons and posterior to the sural nerve. The incision extends from the upper border of the calcaneus anterior to the retrocalcaneal space, to the inferior border of the calcaneus deep to the plantar fascia. The incision is deepened to the periosteum and the soft tissues are retracted with a self-retaining retractor. The periosteum is reflected and the transverse osteotomy is made in the calcaneus with an oscillating saw in line with the skin incision. The cut is made at right angles to the lateral border of the calcaneus and is inclined posteriorly at an angle of approximately 45o to the plane of the foot. No wedge is removed from the calcaneus and no attempt is made to tilt the tuberosity into varus.15 A laminar spreader is inserted into the osteotomy site, and the medial soft-tissue attachments at the calcaneus are relaxed by spreading the laminar spreader. The laminar spreader is withdrawn, and the posterior calcaneal tuberosity is translated medially by 10 mm and secured with cannulated cancellous lag screw (Fig. 1).
Lengthening of the lateral column of the foot with osteotomy of the neck of the calcaneus and interposition of a tricortical bone graft in adults has recently gained popularity.36 Evans37 described an osteotomy of the calcaneus 1.5 cm proximal to the calcaneocuboid joint, lengthening the calcaneus and interposing the osteotomy with bone graft. Other authors38,39 have since corroborated these findings clinically and radiographically. Sangeorzan et al40 subsequently described the effect of calcaneal lengthening on relationships among the hindfoot, midfoot, and forefoot. They found improvement in the lateral talocalcaneal angle, lateral talometatarsal angle, anteroposterior talometatarsal angle, calcaneal pitch angle, and talonavicular coverage angle. However, anecdotal experience has also documented increasing incidence of calcaneocuboid joint symptoms as a result of stress on this joint. When lateral column lengthening is performed in the adult for acquired flatfoot, lengthening should probably be done through the calcaneocuboid joint itself with a tricortical bone graft. The indication for lateral column lengthening through a bone block interposition in the calcaneocuboid joint is a patient who has stage-II deformity with lateral foot pain, a mobile subtalar joint, and no fixed supination deformity of the forefoot when the heel is reduced into neutral from the valgus position. Lengthening of the lateral aspect of the hindfoot, whether through a calcaneal osteotomy or through the calcaneocuboid joint by arthrodesis, is an excellent option since in vitro studies have documented that motion of the talonavicular joint, and to some extent that of the subtalar joint, is still maintained.41,42 This may therefore have a positive effect on stress of adjacent joints, thereby indirectly reducing the incidence of adjacent arthrosis, including the ankle.
Flexor Tendon Transfer. Flexor tendon transfer is performed for stage-I or stage-II PTT insufficiency associated with weakness, hindfoot valgus, medial foot pain, and a mobile subtalar joint. Funk et al,12 Johnson,13 Mann,43 and Mann and Thompson14 recommended using the FDL tendon to substitute for the ruptured PTT. Goldner et al5 recommended the use of the FHL for reconstruction for PTT insufficiency. However, the dissection is more complicated, the neurovascular bundle is in closer proximity to the FHL, and the donor deficit is more substantial. Although the FHL muscle is markedly stronger than the FDL, the proximity of the PTT to the FDL makes the latter a more suitable tendon for transfer. The FDL tendon is detached distally and re-routed through the under-surface of the naviculum through a drill hole. The incision is made along the entire length of the PTT from the musculotendinous junction distally beyond the naviculum in line with the first metatarsal (Fig. 2). The PTT sheath is opened, the tendon is inspected, and the PTT is cut transversely adjacent to the medial malleolus, leaving a 1-cm stump attached to the naviculum distally.
Chronic rupture of the PTT may be associated with atrophy and fibrosis of the posterior tibial muscle. If the posterior tibial muscle remains healthy, ie not scarred, a tenodesis of the FDL tendon to the cut distal end of the PTT adjacent to the medial malleolus may be performed. The normal excursion of the PTT is approximately 1 cm. If there is no excursion of the PTT when pulling on it in a distal direction, the muscle is either scarred or fibrotic, and a tenodesis to the FDL should not be performed.
The sheath posterior to the PTT is opened and the FDL tendon is identified. The FDL sheath is split open longitudinally and distally. The plane of dissection is performed dorsal to the abductor hallucis and flexor digitorum brevis muscles. Once the FHL and FDL tendons are identified, the FDL tendon is cut, transected, and pulled proximally (Fig. 3). The FDL tendon should be cut as far distally as possible but under direct vision. It is not necessary to perform a tenodesis of the FHL to the stump of the FDL. Multiple interconnections between the FDL and FHL are present, making the FDL quite suitable for use with PTT reconstruction.44
The periosteum over the naviculum is dissected and a 4.5-mm drill hole is made from dorsal to plantar in the medial tuberosity of the naviculum (Fig. 4). The tendon is then passed from plantar to dorsal and secured under moderate tension. Before suturing the FDL tendon, a vertical ellipse approximately 8-mm in width is removed from the talonavicular capsule extending from the dorsal aspect of the joint toward the spring ligament inferiorly (Fig. 5). It is sutured once the FDL tendon has been transferred and attached. To avoid overstretching the FDL muscle, the tension on the FDL tendon is set half way between maximum tension and maximum relaxation (Fig. 6).15
At the completion of the reconstruction, the foot should rest in a slight equinovarus position. If a tourniquet is used, a suction drain should be inserted and removed 24 hours later. No weight-bearing is permitted for 4 weeks, after which partial weight-bearing is permitted in either a short leg cast or a hinged range of motion walker boot for 4 additional weeks. By 8 weeks, full ambulation in a shoe is begun with an ankle stirrup brace and physical therapy strengthening modalities are initiated (Fig. 7).
Arthrodesis. An arthrodesis is indicated in a patient with PTT insufficiency who presents with lateral foot pain, a rigid valgus hindfoot, or a deformity of the hindfoot that, when corrected into neutral, is associated with a fixed supination deformity of the forefoot. Numerous arthrodesis procedures have been described, including isolated talonavicular,45-47 talonavicular and calcaneocuboid,48 subtalar,49 or a triple arthrodesis.50-53 According to Johnson and Lester,49 it does not make much difference which of the arthrodesis procedures is performed, since fusion of any one of the hindfoot joints effectively blocks hindfoot motion, and it is more important to avoid further stress on any adjacent joints. They noted that it was important not to disturb the position of the calcaneocuboid and talonavicular joints; however, this is not always possible, particularly if the deformity is rigid and a fixed supination deformity of the midfoot and forefoot occurs when reducing the subtalar joint into a neutral position. The technique reported by Johnson and Lester49 includes a morcellized bone graft obtained from the anterior iliac crest, which is inserted into the anterior subtalar joint with temporary fixation provided by a Steinmann pin introduced percutaneously from the neck of the talus dorsally into the calcaneus inferiorly.
Although triple arthrodesis has a long and successful history for the treatment of neuromuscular deformities in children, fewer reports are available on its outcome in adults, particularly with respect to planovalgus deformity in the hindfoot. A triple arthrodesis is indicated for fixed hindfoot deformity associated with lateral foot pain. The goals of the triple arthrodesis procedure should be to realign the hindfoot; to establish a plantigrade weight-bearing surface of the hindfoot, midfoot, and forefoot; to maintain the integrity of the adjacent joints, particularly the ankle; and to avoid incisional neuromas.
The technique of triple arthrodesis should be meticulous. The single incision approach on the lateral aspect of the foot places both the sural nerve and the lateral cutaneous branch of the superficial peroneal nerve at risk for incisional neuroma, and it does not allow visualization of most of the talonavicular joint.54 Therefore, the triple arthrodesis procedure should be performed with two incisions. The first incision parallels the inferior surface of the peroneal tendons from the tip of the fibula over the sinus tarsi; the second incision lies medial to the anterior tibial tendon, extending from the tibiotalar joint to the naviculocuneiform joint. Laterally, the contents of the sinus tarsi are excised and, using a sharp osteotome or chisel, the joints are denuded of articular cartilage. The correction is performed by adequate subtalar and talonavicular rotation, not by resection of bone wedges.
It is particularly important to pay attention to the recess between the naviculum and the cuboid. At this joint surface, the four bones, ie the talus, navicular, calcaneus, and cuboid, may come into contact with each other. If an arthrodesis can be obtained in this location, the foot is invariably stable despite what may appear to be a radiographic nonunion of one of the other joints. This concept has been supported by Jahss et al.55 and referred to as a quadruple arthrodesis.
The two-incision method utilizes internal fixation and compression fixation. I prefer using lag screw fixation to staples or other methods of internal fixation and have found it unnecessary to use bone graft. Provided that rigid compression fixation is used across the three joints and broad bleeding bone joint surfaces are present, the incidence of nonunion is negligible with this technique (Fig. 8).
Some clinicians advocate fixing the talonavicular joints first15; others believe that the subtalar joint should be corrected first. It is my belief that by realigning the medial column, the talonavicular joint is the key to the rest of the foot. The forefoot is adducted and plantarflexed across the talonavicular joint and held secure with a temporary cannulated guide pin(s). Laterally, the subtalar joint follows, and the heel at this stage invariably is corrected to slight valgus. When stabilizing the calcaneocuboid joint, it is very important to forcefully elevate the cuboid to prevent any inferior sag that may later result in malunion and pain along the lateral weight-bearing surface of the foot.
It is far preferable to leave the foot in valgus than in neutral or varus, despite the possibility of impingement between the fibula and the calcaneus that may still occur in some of these patients with more advanced deformity. Nonetheless, if internal fixation is used, one must be careful not to over-correct the foot by internally rotating the subtalar joint and adducting the forefoot across the transverse tarsal joint. An in situ arthrodesis that leaves the calcaneus in marked valgus will place undue stress on the tibiotalar joint. Based on these findings, Jahss (M. H. Jahss, personal communication) recommended adding a medial displacement osteotomy of the calcaneus to a triple arthrodesis in the presence of fixed hindfoot deformity. The advantages of this medial displacement osteotomy may be to normalize the weight-bearing surface of the hindfoot and increase the distribution of weight-bearing force across the medial ankle, thereby reducing the stress on the tibiotalar joint and the deltoid ligament.6,10,29,56,57 This is certainly an option for fixed valgus deformity associated with valgus tilting of the ankle, but every effort should be made to reduce the deformity intraoperatively.
Unfortunately, the results of triple arthrodesis in older adults with flatfoot deformity are disappointing, since many of these patients experience later problems with the ankle. Graves et al50 concluded that triple arthrodesis in older patients relieved or lessened the pain, but they cautioned that this procedure should be used only in a salvage attempt for fixed deformity because of the high rate of postoperative complications. With severe deformity, the hindfoot may become rigid in valgus and, in this fixed position, the talus may begin to tilt into valgus in the tibiotalar joint, perhaps as a result of attritional changes in the deltoid ligament. In many of these patients, the triple arthrodesis will fail (Fig. 9). Johnson and Lester49 were perhaps the first to recognize this fact; they recommended a tibiotalocalcaneal arthrodesis primarily to reverse this problem.
Lateral column lengthening arthrodesis for the treatment of severe planovalgus deformity of the foot has been performed successfully, with excellent results and maintained correction.37,58 The indications for performing the lateral column lengthening are a patient who would benefit from an arthrodesis, ie who has a valgus deformity, but one that is not fixed. In a patient who has a flexible foot with medial symptoms and stage-I49 deformity, a tendon transfer should be sufficient. It is the patient with a flexible hindfoot and stage-II deformity for whom the lateral column lengthening procedure may be performed.59 Options for bone graft include autograft from the iliac crest or allograft, which is far easier and involves less morbidity. However, it is important to advise patients of the latter's potential complications, particularly nonunion.60 I prefer to use femoral head allograft, contouring a trapezoidal block of bone in two planes. The trapezoid is fashioned so that it is wider dorsally and laterally and narrower medially and inferiorly. The widest portion dorsal and lateral measures 12 mm in width; medially and dorsally it tapers to 9 mm. Similarly, on the plantar surface, the trapezoid tapers to 8 mm on both sides to adduct the midfoot and plantarflex the hindfoot (Fig. 10). The lengthening arthrodesis is performed by means of distraction by inserting into the joint a laminar spreader that is removed once the bone graft is tamped and secured into place. The use of a smooth laminar spreader (without attached teeth) facilitates the insertion of the bone graft and the extraction of the spreader as the bone graft is tamped into place. Although securing the bone graft with fixation may not be necessary since it is inserted under compression, I nevertheless prefer to use either a cannulated screw or a percutaneous Kirschner wire to hold the graft.
The options for nonoperative and operative treatments of the acquired flatfoot deformity in the adult are numerous. Although each classification or treatment regimen has its flaws, the algorithm provided should help the clinician with treatment with decision-making according to a biomechanical basis.
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Fig. 1. The calcaneus is shifted 1 cm medially and secured with a cannulated screw. [Reprinted by permission from: Myerson MS, Corrigan J, Thompson F, Schon LC: Tendon transfer combined with calcaneal osteotomy for the treatment of posterior tibial tendon insufficiency: a radiological investigation. Foot Ankle Int 16:713, 1995. © Williams & Wilkins]
Fig. 2. The posteromedial incision for the tendon transfer. [Reprinted by permission from: Myerson MS, Corrigan J, Thompson F, Schon LC: Tendon transfer combined with calcaneal osteotomy for the treatment of posterior tibial tendon insufficiency: a radiological investigation. Foot Ankle Int 16:714, 1995. © Williams & Wilkins]
Fig. 3. The FDL tendon is cut as distally as possible under direct vision. [Reprinted by permission from: Myerson M: Posterior tibial tendon insufficiency. In Myerson M (ed): Current Therapy in Foot and Ankle Surgery, pp 128. St. Louis, Mosby-Year Book Inc, 1993.]
Fig. 4. A 4.5-mm drill hole is made in the naviculum from dorsal to plantar. [Reprinted by permission from: Myerson M: Posterior tibial tendon insufficiency. In Myerson M (ed): Current Therapy in Foot and Ankle Surgery, pp 129. St. Louis, Mosby-Year Book Inc, 1993.]
Fig. 5. A vertical ellipse over the talonavicular capsule is excised before suturing the FDL tendon transfer.
Fig. 6. The FDL tendon is sutured under tension to the stump of the PTT or periosteum overlying the naviculum. A tenodesis of the proximal stump of the FDL tendon to the cut PTT is performed. [Reprinted by permission from: Myerson MS, Corrigan J, Thompson F, Schon LC: Tendon transfer combined with calcaneal osteotomy for the treatment of posterior tibial tendon insufficiency: a radiological investigation. Foot Ankle Int 16:714, 1995. © Williams & Wilkins]
Fig. 7. Preoperative (A, B) and postoperative (C, D) anteroposterior and lateral radiographs in a patient with PTT insufficiency treated with calcaneal osteotomy and FDL tendon transfer.
Fig. 8. Preoperative (A, B) and postoperative (C, D) anteroposterior and lateral radiographs in a patient with substantial flatfoot deformity treated with a triple arthrodesis.
Fig. 9. Valgus tilt of the tibiotalar joint occurred 28 months after triple arthrodesis in this 63-year-old patient.
Fig. 10. Preoperative (A, B) and postoperative (C, D) anteroposterior and lateral radiographs in a patient with lateral foot pain and a flexible hindfoot deformity associated with PTT insufficiency treated with a calcaneocuboid joint bone block distraction arthrodesis and FDL tendon transfer.