Posterior Tibial Tendon Dysfunction in the Adult: Current Concepts

Transcription

1 38 Posterior Tibial Tendon Dysfunction in the Adult: Current Concepts Benjamin E. Stein, MD Lew C. Schon, MD Abstract The management of posterior tibial tendon dysfunction in adults has evolved substantially, and controversy persists regarding a specifi c recommended algorithm for treatment. The current focus is on early diagnosis and treatment of this disorder with joint-sparing surgeries, such as corrective osteotomies and tendon transfers, when nonsurgical modalities have been exhausted. It is helpful to be familiar with the pertinent pathophysiolog y and diagnostic pearls associated with posterior tibial tendon dysfunction, its treatment options, pertinent literature, and technique tips for the procedures currently being used. Instr Course Lect 2015;64: The management of posterior tibial tendon dysfunction (PTTD), also referred to as adult-acquired flatfoot deformity, has evolved substantially since it was first recognized as a distinct entity in the 1950s. 1,2 The management of this complex disorder is controversial, and different philosophic approaches to treatment are advocated by leaders in the field. Historically, surgical management was reserved for the later stages of the disease and focused on definitive deformity correction with triple arthrodesis to establish a stable and plantigrade foot. Adjacent joint arthrosis Dr. Schon or an immediate family member has received royalties from DJ Orthopaedics, Arthrex, Darco, Tornier, and Zimmer; is a member of a speakers bureau or has made paid presentations on behalf of Tornier, Biomet, Zimmer, and Biomimetics; serves as a paid consultant to or is an employee of Biomet, Biomimetics, Guidepoint Global, Gerson Lehrman Group, Tornier, Wright Medical Technolog y, and Zimmer; serves as an unpaid consultant to Royer Biomedical and Carestream Health; has stock or stock options held in Tornier, Royer Biomedical, Bioactive Surgical, and Healthpoint Capital; has received research or institutional support from Royer Biomedical, Zimmer, Tornier, Arthrex, Spinesmith Holdings, Biomimetics, and Biomet; has received nonincome support (such as equipment or services), commercially derived honoraria, or other non research-related funding (such as paid travel) from Bioactive Surgical, Concepts in Medicine, Smith & Nephew, Endoscopy, Orthohelix, Chesapeake Surgical Biocomposites, Olympus, and OMeGA; and serves as a board member, owner, offi cer, or committee member of the American Foot and Ankle Society. Neither Dr. Stein nor any immediate family member has received anything of value from or has stock or stock options held in a commercial company or institution related directly or indirectly to the subject of this chapter. of the midfoot and the ankle tended to develop in such rigidly corrected feet. 3-5 Surgeons now focus on recognizing and diagnosing this disease at an early stage and use both nonsurgical and surgical techniques to maximize foot function and preserve range of motion. This can be accomplished by using joint- sparing surgical procedures, such as tendon transfers, calcaneal and midfoot osteotomies, and ligament reconstructions. This chapter focuses on the current concepts and treatments used in the management of PTTD in its earlier stages. Function and Dysfunction The posterior tibial tendon is the crucial dynamic stabilizer of the foot during gait. The tendon functions as a plantar flexor of the ankle and an invertor of the subtalar joint complex as well as an adductor and a supinator of the forefoot. 6 It drives inversion of the hindfoot during the stance phase of gait, which maximizes the mechanical advantage of the Achilles tendon during toe rise and also adducts and plantarflexes the 2015 AAOS Instructional Course Lectures, Volume

2 Foot and Ankle navicular on the talar head, thereby buttressing the medial longitudinal arch against collapse. 7 The dynamic stability conferred by the posterior tibial tendon is complemented by static stability from the bony architecture and soft-tissue structures, including the calcaneonavicular (spring) ligament, the talonavicular capsule, the plantar fascia, and the deltoid ligament. 8,9 Eventual attenuation of these static tissue structures also contributes to the progressive deformity seen in PTTD. 10 The dysfunction of the posterior tibial tendon that precipitates the deformity is likely multifactorial. Believed to be an overuse and age-related phenomenon, posterior tibial tendon degeneration typically occurs in the areas of maximal anatomic stress. 6,11,12 Vascular studies of the posterior tibial tendon also have demonstrated that the retromalleolar region is a relatively hypovascular zone. 13,14 In this region, the tendon experiences the most mechanical stress between the motion segments of the ankle and hindfoot complex. After a tendon injury has occurred, an inflammatory cascade is initiated that increases the local metalloproteinase activity and leads to further tendon injury. 15,16 Congenital flatfoot is often asymptomatic; however, greater stress, which is likely the result of medial column deficiency and increased subtalar motion, may result in increased stress on the posterior tibial tendon as patients age. 17 This structural predisposition may lead to a propensity for long-term tendon degeneration and dysfunction. 18 Medical comorbidities, including obesity, systemic steroid use, diabetes mellitus, fluoroquinolone use, and inflammatory conditions such as rheumatoid arthritis and seronegative spondyloarthropathies also can contribute to tendon rupture or dysfunction. 19,20 In some cases, progressive adult planovalgus deformity can be caused primarily by a failure of the talonavicular capsuloligamentous complex rather than the posterior tibial tendon. Diagnosis and Physical Examination The physical examination begins by observing a patient with suspected PTTD. With the patient standing, the position of the affected extremity is evaluated from multiple angles to assess overall limb alignment, the height of the midfoot arch, the degree of midfoot abduction, and heel alignment. Medial talar head prominence and the presence of any skin changes on the plantar aspect of the foot also should be noted. While viewing both extremities from the front, the examiner should determine whether there is concurrent genu valgum. By observing the standing patient from behind, the examiner should look for pathologic midfoot abduction, which is seen with the too many toes sign, and also for the degree of heel valgus (Figure 1). To assess the maintenance of the medial arch during clinical examination, this chapter s authors have developed and use a simple manual method ( fingometer method) that is shown in Figure 2. If there is a loss of medial arch height but the hindfoot alignment remains neutral or physiologic, then the cause may be advanced midfoot arthritis and collapse, not PTTD. The patient should then be observed during dynamic gait to allow the examiner to assess the cadence of his or her gait, the condition of the arch of the foot during stance, and the presence or the absence of heel inversion during toe-off. Figure 1 Clinical photograph of a patient with stage II posterior tibial tendon dysfunction with severe heel valgus, collapse of the medial arch, and severe midfoot abduction. With the patient still standing, the traditional single- and double-stance heel rise tests are performed to assess posterior tibial tendon function. The examiner should observe the ability to invert the hindfoot with a single-heel rise and compare this with the contralateral hindfoot during a double-heel rise. Difficulty or pain with multiple repetitions may be a sign of early tendon pathology. Other foot and ankle pathology, such as Achilles tendon dysfunction and painful midfoot arthritis, can lead to false-positive results with this test. With the patient seated, the examiner begins palpating the pertinent anatomic areas. The length of the posterior tibial tendon is palpated, noting areas of tenderness, swelling, warmth, and any palpable defects in continuity. The lateral hindfoot, the sinus tarsi, and the distal fibula are palpated because tenderness in these areas can develop in more severe and chronic cases as a result of subfibular impingement. Next, passive range of motion of the affected ankle and hindfoot should be assessed and compared with the contralateral side. Hindfoot motion can be AAOS Instructional Course Lectures, Volume 64

3 Posterior Tibial Tendon Dysfunction in the Adult: Current Concepts Chapter 38 measured as the angle defined by the position of the second metatarsal shaft in relation to the long axis of the tibial shaft. The foot should be brought from a fully abducted and everted position to the fully inverted and adducted position. A decreased arc of hindfoot motion can indicate advanced osteoarthritis, which may preclude treatment with joint- sparing procedures. Passive ankle motion is assessed with the knee extended and flexed to 90, and the Silfverskiöld test is used to determine the degree of gastrocnemius muscle contracture. This test specifically measures gastrocnemius contracture by alternately relaxing and incorporating the muscle because of its origin proximal to the knee joint; maximal ankle dorsiflexion is assessed in each state. Assuming that the hindfoot valgus is flexible, it is important to hold the heel in a corrected neutral position to accurately gauge the degree of equinus contracture. It also is important to check for fixed forefoot varus deformity during this portion of the examination. The final component of the examination should focus on posterior tibial tendon power and motor function. The foot is positioned passively in a maximally plantarflexed and inverted position to isolate the tendon. The patient should be asked to hold this position when the foot is released while keeping the toes relaxed. If there is an inversion lag or the patient cannot maintain this position against resistance, then there may be attenuation or stretching of the tendon. Tendon power should then be further assessed along its entire range of excursion by testing against resistance at the neutral position and the fully everted position. For clinical grading, 5/5 is defined by full power against the entire range of passive tendon Figure 2 Photographs demonstrating the fi ngometer method for clinical assessment of the medial longitudinal arch. A, The long fi nger is seated as deeply as possible under the medial arch. B, The thumb is used to mark the length that the long fi nger is seated. C, The fi nal depth measurement is noted and compared with the contralateral side. excursion, and 5 /5 is for less than full power compared with the unaffected side. With the presence of an inversion lag, the power is defined as 4/5, which is further subclassified as 4, 4, or 4+ depending on tendon power. The ability to maintain inversion 20 beyond the midline against resistance is graded as 4+, and the inability to maintain inversion beyond the midline is graded as 4. By carefully assessing and documenting these examination findings on serial office visits, interval improvement or deterioration can be followed. Imaging A standard series of standing AP, lateral, and oblique radiographs of the foot as well as AP and mortise views of the ankle are useful in evaluating a patient with symptomatic flatfoot deformity. For comparison, additional radiographs of the contralateral side should be obtained in patients with congenital flatfoot. If there is any proximal deformity of the hip or the knee, full-length standing radiographs should be obtained. Measurements of the foot are taken in both the AP and lateral planes to quantify the findings associated with this deformity. On the lateral radiograph, the important parameters are the calcaneal pitch, the lateral talocalcaneal angle, the lateral talometatarsal angle, and the medial cuneiform height (Figure 3). On the AP radiograph, the important parameters are the talometatarsal angle and the percentage of talar head uncoverage (Figure 4). The techniques for performing these measurements can vary greatly, and no standard has yet been established. It is common for patients to bring previous imaging studies, such as MRIs and ultrasound studies, when presenting for examination. Although these studies can provide additional information regarding pathology in the soft tissues and joints, the findings do not usually dictate the treatment approach. Consequently, the routine use of MRI for PTTD is not necessary unless there 2015 AAOS Instructional Course Lectures, Volume

4 Foot and Ankle Figure 3 A, Lateral radiograph of a normal foot. The circled area is enlarged in the insert. B, Lateral radiograph of a pes planus foot showing a decrease in the talocalcaneal angle, extension of the talometatarsal angle, loss of medial cuneiform height, and obliteration of the sinus tarsi in a patient with posterior tibial tendon dysfunction. Inserts show sinus tarsi: shoulder of the talus/gissane angle. is concern for additional pathology that may potentially alter the surgical plan, such as possible attenuation of the deltoid ligament or peroneal tendon involvement. Standing clinical photographs are routinely obtained, and the patient may be videotaped while walking to document the degree of clinical severity. Classification PTTD is best understood as a syndrome with a spectrum of clinical presentations ranging from recent onset tendinitis with minimal deformity to long-standing tendon dysfunction with advanced deformity. In 1989, Johnson and Strom 21 proposed a general classification system for PTTD that is based on clinical and radiographic findings. Patients with stage I PTTD have swelling and pain along the posterior tibial tendon and do not have progressive planovalgus deformity. The tendon pathology is usually restricted to tenosynovitis, without attenuation or elongation of the tendon. With regard to the function of the posterior tibial tendon, these patients have no inversion lag and are able to perform an isolated single-stance heel rise. However, repetitive stresses may reveal slight weakness compared with the contralateral side. Posterior tibial tendon degeneration with elongation has begun to develop in patients with stage II PTTD. These patients also exhibit varying degrees of flexible planovalgus deformity. Early in this stage, the patient may be able to perform a single-stance heel rise (although painful), but may soon lose the ability to do so. Several authors have subclassified this stage with the severity of the deformity and the presence of lateral subfibular pain, which are used as the parameters for these addi tional stages. 22,23 For use in their practice, this chapter s authors have informally subclassified stage II PTTD into three types based on the degree of talonavicular uncoverage and resultant abduction deformity. Types IIa and IIb are defined by less than 40% uncoverage and between 40% to 50% uncoverage, respectively. In the treatment algorithm (Table 1), these subgroups usually can be managed with a joint-sparing procedure, such as a lateral column lengthening. Type IIc PTTD is defined as uncoverage of greater than 50%. In these patients, fusion procedures may be indicated. In stage III PTTD, a rigid planovalgus deformity has developed. On clinical examination, these patients demonstrate severe hindfoot valgus and midfoot valgus with the too many toes sign and frequently a fixed forefoot varus deformity. There is substantial lateral pain associated with subfibular impingement. Because of the rigidity of the deformity at this stage, fusion is frequently required. Patients with stage IV PTTD have chronic valgus loading of the ankle joint, with subsequent arthritic changes and joint erosion. 24 These patients have lateral pain partially from subfibular impingement and lateral ankle joint arthritis. As the severity of the ankle deformity worsens, the deltoid ligament becomes attenuated and can rupture. Treatment of this stage will include reconstructive surgery for the foot deformity as well as the ankle deformity. Treatment Stage I PTTD The mainstay of treatment of patients with stage I PTTD is nonsurgical management. This includes bracing and/ AAOS Instructional Course Lectures, Volume 64

5 Posterior Tibial Tendon Dysfunction in the Adult: Current Concepts Chapter 38 Figure 4 A, AP radiograph of a normal foot. B, AP radiograph demonstrating the increased talometatarsal angle and increased talonavicular uncoverage in the foot of a patient with posterior tibial tendon dysfunction. or orthotics, activity modification, and physical therapy after symptoms have largely resolved. This chapter s authors typically begin with a period of bracing for 6 weeks to allow for diminished inflammation and improved symptomatology. The specific bracing used depends on the severity of symptoms, with a tall, controlled ankle motion (CAM) walking boot used for the most severely symptomatic patients and an off-the-shelf PTTD brace for patients with more moderate symptoms. This brace was designed to limit eversion while also incorporating a support strap that lifts the medial arch and an adjustable pneumatic bladder for additional arch support. Frequently, patients are started with the CAM boot initially and then graduated to the brace as their symptoms allow. Other braces also can be used and have been described in the literature, including standard lace-up braces, custom ankle foot orthoses, and Arizona-type braces. 25,26 Shoe modification and orthotics provide adequate support and relief only in mildly symptomatic cases with minimal tendinopathy. 27 Routine oral anti-inflammatory medications can be used; injectable corticosteroids are not commonly used because these have been shown to lead to further attenuation and potential posterior tibial tendon rupture. 20,21 After a patient s symptoms have resolved, formal physical therapy can be started to focus on strengthening the posterior tibial tendon and the remaining musculature of the posterior compartments. In a patient with a tight heel cord, it also is important to focus on stretching the gastrocnemius-soleus complex. Several studies have shown that these therapeutic strengthening and stretching regimens in conjunction with orthotic treatment achieve clinical benefit Despite prolonged nonsurgical treatment with bracing and therapy, some patients remain symptomatic. In these refractory cases, alternative modalities of treatment can be considered, including shock-wave therapy or bone marrow aspirate concentrate injections. In vitro studies have shown that these modalities have beneficial effects on tenocytes. 16,32,33 It is important to note that after a bone marrow aspirate concentrate injection, there is a period of increased pain, so this chapter s authors routinely recommend 4 to 6 weeks of postinjection bracing for these patients. For stage I PTTD, some authors have described isolated tenosynovectomy for refractory cases, but only moderate success has been reported. 34,35 Although there can be success with an isolated tendon procedure, an adjunctive alignment procedure, such as arthroereisis and/or osteotomies, is more likely to optimize the chances of a positive outcome. Stage II PTTD The management of stage II begins with nonsurgical treatment that 2015 AAOS Instructional Course Lectures, Volume

6 Foot and Ankle Table 1 Surgical Algorithm for Stage II Posterior Tibial Tendon Dysfunction Lateral AP Radiograph Radiograph Procedures TN Uncoverage (%) AP T1MTA Lateral T1MTA Clinical Examination and Heel Valgus FDL transfer <20% <15 <10 <5 valgus; <5 side-to-side difference; inverts 20 beyond midline FDL transfer and subtalar arthroereisis 20-30% <20 <10 <5 valgus; inverts 20 beyond midline; obesity or systemic factor FDL transfer and MDCO 20-40% <35 <20 <20 valgus; <10 side-to-side difference; unable to invert beyond midline FDL transfer, MDCO, and subtalar arthroereisis <40% <40 <25 <20 valgus; <10 side-to-side difference; obesity or other systemic factor FDL transfer and LCL 40-50% <50 <25 >20 valgus; unable to invert beyond midline FDL transfer, MDCO, and lateral column lengthening >50% >50 >25 >20 valgus; unable to invert beyond midline TN = talonavicular, T1MTA = talus-fi rst metatarsal angle, FDL = fl exor digitorum longus, MDCO = medial displacement calcaneal osteotomy. fo cuses on bracing and the therapy modalities as previously outlined for stage I. After these nonsurgical modalities have been exhausted without clinical improvement, the focus of treatment shifts to surgical management. The determination of the appropriate surgical treatment is predicated on the clinical and radiographic examination as well as patient-specific medical and functional factors. The treatment algorithm used in the institution of this chapter s authors reflects the various procedures available to correct the broad spectrum of deformity encountered. This algorithm does not determine the final treatment plan. Patient-specific issues, such as medical comorbidities (for example, obesity, diabetes, and steroid use) and intraoperative findings will further guide surgical treatment. For example, a residual intraoperative equinus contracture may necessitate an adjunctive Strayer procedure for contractures of less than 15 or Achilles tendon lengthening for more severe contractures. Surgical Procedures Medial Displacement Calcaneal Osteotomy The medial displacement calcaneal osteotomy (MDCO) is the cornerstone procedure for reconstructing a flexible flatfoot. It shifts the mechanical pull of the Achilles tendon medially and the weight-bearing axis of the heel closer to the long axis of the tibia. These biomechanical advantages lead to improved inversion power and restoration of the medial longitudinal arch. This chapter s authors obtain approximately 1 cm of medial translation, and fixation is achieved with one or two 6.5- or 7.3-mm cannulated, partially threaded cancellous screws. A crushplasty of the prominent lateral cortex is performed to optimize the lateral contour and also improve bone apposition (Figure 5). Flexor Digitorum Longus Tendon Transfer After posterior tibial tendon incompetence is demonstrated, the flexor digitorum longus (FDL) remains the optimal choice for augmentation or replacement. The FDL and the posterior tibial tendon are in-phase muscles with similar lines of pull, and the FDL can match the strength of the peroneus brevis. The transfer is rarely performed as an isolated procedure and is usu ally accompanied by an MDCO as well as additional corrective osteotomies. This chapter s authors prefer to use an interference screw for FDL fixation within the navicular bone tunnel, which allows for harvesting the tendon more proximally and minimizes the need for additional dissection. The free suture ends of the whipstitch also are secured over the bone as a bridge to the posterior tibial tendon insertion to provide an additional point of fixation. The transfer is tensioned before fixation to obtain approximately 15 of plantar flexion and 15 of inversion. The posterior tibial tendon is not routinely excised if it appears salvageable, but it is instead débrided of any degenerative-appearing tendon, and the FDL transfer is used for augmentation rather than replacement (Figure 6). Outcome studies of FDL transfer with a medial displacement AAOS Instructional Course Lectures, Volume 64

7 Posterior Tibial Tendon Dysfunction in the Adult: Current Concepts Chapter 38 Figure 5 Intraoperative photograph (A) of a medial displacement calcaneal osteotomy after lateral ridge crushplasty, with additional fl uoroscopic images demonstrating axial (B) and lateral (C) views after medial translation and fi xation. The calcaneal osteotomy is slid approximately 1 cm for severe valgus and fi xed with 6.5- or 7.3-mm screws. Figure 6 Intraoperative photograph of the fl exor digitorum longus transferred into the navicular tunnel after interference screw fi xation. Note the preservation of the pos te r ior tibial tendon. calcaneal osteotomy have demonstrated good results, with mean maximal improvement achieved between 10 and 14 months. 36,37 Lateral Column Lengthening Initially described by Evans 38 in 1975 and later modified by Mosca 39 in 1995, lateral column lengthening has remained a popular tool in the treatment of flexible flatfoot deformity It is used either as the primary corrective osteotomy or combined with other osteotomies. Several adverse effects have been described with this procedure, including lateral column overload and restriction of subtalar range of motion. 41,42 In addition to the traditional Evans osteotomy, other osteotomies, including stepcut and Hintermann osteotomies, have been described to achieve lateral column lengthening. 43,44 Lateral column lengthening procedures are typically reserved for severe forefoot abduction with talonavicular uncoverage of 40% to 50%. This osteotomy is performed only if the MDCO alone does not provide adequate correction. If lateral column lengthening is performed, Hintermann s modification is used, with the osteotomy performed along the sinus tarsi, between the posterior and middle facets (Figure 7). In the experience of this chapter s authors, the modified lateral column lengthening osteotomy achieves better graft incorporation, less restriction of subtalar motion, and no calcaneocuboid subluxation compared with Evans more distal osteotomy. A biplanar femoral neck allograft soaked in bone marrow aspirate concentrate is used. This osteotomy is typically performed in conjunction with an MDCO, and, because of its more proximal position, fixation can be achieved across both osteotomies with a cannulated, partially threaded screw. Cotton Osteotomy If residual fixed forefoot varus remains after the other corrective procedures, a dorsal opening wedge osteotomy of the medial cuneiform, also known as a Cotton osteotomy, can be performed. 45 The medial cuneiform is exposed with a dorsomedial approach. The extensor hallucis longus and the dorsal neurovascular bundle are retracted and protected, and a transverse osteotomy is performed without violating the plantar cortex. An approximately 7-mm wedge-shaped graft is prepared from a femoral head allograft that is soaked in bone marrow aspirate concentrate. Internal fixation is not generally used (Figure 8). Clinical and radiographic studies (CJ Humbyrd, MD, et al, San Diego, CA, unpublished data presented at the American Orthopaedic Foot and Ankle Society annual meeting, 2012) have reported good results with this procedure. 46 Arthroereisis The role of arthroereisis in the management of the adult flexible flatfoot is controversial. This chapter s authors use this procedure in conjunction with an MDCO and FDL transfer for patients with more severe deformity; obesity; or 2015 AAOS Instructional Course Lectures, Volume

8 Foot and Ankle Figure 7 Intraoperative AP and lateral (insert) fl uoroscopic views after a Hintermann-type lateral column lengthening osteotomy. The Hintermann-type osteotomy is performed through the sinus tarsi between the posterior and middle facets and exits the tarsal canal medially. The biplanar wedge femoral neck allograft is then inserted. Figure 8 A, Clinical photograph of a patient with fi xed forefoot varus deformity. Postoperative AP (B), oblique (C), and lateral (D) radiographs show a healed Cotton osteotomy of the medial cuneiform with restored lateral talometatarsal alignment and medial cuneiform height. certain medical comorbidities, such as diabetes or chronic steroid use. The addition of an arthroereisis to an MDCO and FDL transfer has been shown to provide improved correction in a cadaver flatfoot model. 47 Arthroereisis (Figure 9) is performed under fluoroscopic guidance with a small incision centered over the sinus tarsi. A guidewire is placed across the interval between the posterior and middle facets of the talus, and the appropriately sized implant is inserted across the lateral half of the talar neck. The implant is designed to limit pathologic eversion and block the talus from rotating plantarly and medially. Preoperatively, contralateral heel valgus is assessed and an attempt is made to replicate this degree of valgus after final implant insertion on the affected extremity. Clinical studies have thus far demonstrated promising results at midterm follow-up, but persistent lateral pain has been described; as a result, the implant sometimes must be removed. 48,49 If the implant needs to be removed, the correction is often maintained because of the concomitant procedures. Stages III and IV PTTD In the later stages of PTTD, a rigid deformity of the hindfoot complex exists; thus, joint salvage procedures are no longer indicated. Surgical treatment of stages III and IV usually involves a triple arthrodesis. When planning and performing these fusion procedures, it is critical to ensure that the appropriate final alignment is achieved. This should be tailored to the patient, taking into consideration the patient s contralateral hindfoot position as well as the spe cific characteristics of his or her gait. If no arthrosis is present, a AAOS Instructional Course Lectures, Volume 64

9 Posterior Tibial Tendon Dysfunction in the Adult: Current Concepts Chapter 38 Figure 9 A, Photograph of an arthroereisis implant. Intraoperative fl uoroscopic images showing implantation of the arthroereisis implant (B) and the implant in place (C). When in place, the implant should not cross beyond the midline of the talar neck on an AP radiograph. D, Lateral radiograph showing an arthroereisis implant in place. double-hindfoot arthrodesis with sparing of the calcaneocuboid joint may be at tempted. This spared motion segment may prevent progressive degeneration of the four to five metatarsocuboid articulations. Thus far, this has led to good results without substantial compromise to union rates. 50 The presence of valgus ankle arthritis in patients with stage IV PTTD also must be addressed with a corrective supramalleolar osteotomy, an ankle arthroplasty, or arthrodesis. Summary The treatment of PTTD is complex and controversial. As the focus in surgical management has shifted to earlier intervention and joint-sparing reconstructions, ongoing debate has ensued regarding the optimal approach and the specific procedures used. A comprehensive trial of nonsurgical treatment should always be used initially. When the patient s level of dysfunction and/ or pain does not improve satisfactorily with nonsurgical treatment, then the discussion should shift to selecting an appropriate surgical plan. Despite differing opinions, there is growing consensus in the need to achieve the goals of preserving motion, reestablishing alignment, and ultimately restoring patient function. References 1. Key JA: Partial rupture of the tendon of the posterior tibial muscle. J Bone Joint Surg Am 1953;35(4): Lapidus PW, Seidenstein H: Chronic non-specific tenosynovitis with effusion about the ankle: Report of three cases. J Bone Joint Surg Am 1950;32(1): Pell RF IV, Myerson MS, Schon LC: Clinical outcome after primary triple arthrodesis. J Bone Joint Surg Am 2000;82(1): Coetzee JC, Hansen ST: Surgical management of severe deformity resulting from posterior tibial tendon dysfunction. Foot Ankle Int 2001;22(12): Saltzman CL, Fehrle MJ, Cooper RR, Spencer EC, Ponseti IV: Triple arthrodesis: Twenty-five and fortyfour-year average follow-up of the same patients. J Bone Joint Surg Am 1999;81(10): Supple KM, Hanft JR, Murphy BJ, Janecki CJ, Kogler GF: Posterior tibial tendon dysfunction. Semin Arthritis Rheum 1992;22(2): Kapandji I: The Physiolog y of the Joints. New York, NY, Churchill Livingston, 1970, pp Niki H, Ching RP, Kiser P, Sangeorzan BJ: The effect of posterior tibial tendon dysfunction on hindfoot kinematics. Foot Ankle Int 2001;22(4): Van Boerum DH, Sangeorzan BJ: Biomechanics and pathophysiology of flat foot. Foot Ankle Clin 2003;8(3): Deland JT, de Asla RJ, Sung I-H, Ernberg LA, Potter HG: Posterior tibial tendon insufficiency: Which ligaments are involved? Foot Ankle Int 2005;26(6): Jahss MH: Spontaneous rupture of the tibialis posterior tendon: Clinical findings, tenographic studies, and a new technique of repair. Foot Ankle 1982;3(3): Petersen W, Hohmann G, Pufe T, et al: Structure of the human tibialis posterior tendon. Arch Orthop Trauma Surg 2004;124(4): Frey C, Shereff M, Greenidge N: Vascularity of the posterior tibial tendon. J Bone Joint Surg Am 1990;72(6): Petersen W, Hohmann G, Stein V, Tillmann B: The blood supply of the posterior tibial tendon. J Bone Joint Surg Br 2002;84(1): Bridgeman JT, Zhang Y, Donahue H, Wade AM, Juliano PJ: Estrogen receptor expression in posterior tibial tendon dysfunction: A pilot study. Foot Ankle Int 2010;31(12): Han SH, Lee JW, Guyton GP, Parks BG, Courneya J-P, Schon LC: Effect of extracorporeal shock wave therapy on cultured tenocytes. Foot Ankle Int 2009;30(2): Cozen L: Posterior tibial tenosynovitis secondary to foot strain. Clin Orthop Relat Res 1965;42: Dyal CM, Feder J, Deland JT, Thompson FM: Pes planus in patients with posterior tibial tendon insufficiency: Asymptomatic versus symptomatic foot. Foot Ankle Int 1997;18(2): AAOS Instructional Course Lectures, Volume

10 Foot and Ankle 19. Myerson M, Solomon G, Shereff M: Posterior tibial tendon dysfunction: Its association with seronegative inflammatory disease. Foot Ankle 1989;9(5): Holmes GB Jr, Mann RA: Possible epidemiological factors associated with rupture of the posterior tibial tendon. Foot Ankle 1992;13(2): Johnson KA, Strom DE: Tibialis posterior tendon dysfunction. Clin Orthop Relat Res 1989;239: Deland JT: Adult-acquired flatfoot deformity. J Am Acad Orthop Surg 2008;16(7): Bluman EM, Title CI, Myerson MS: Posterior tibial tendon rupture: A refined classification system. Foot Ankle Clin 2007;12(2): , v. 24. Myerson MS: Adult acquired flatfoot deformity: Treatment of dysfunction of the posterior tibial tendon. Instr Course Lect 1997;46: Chao W, Wapner KL, Lee TH, Adams J, Hecht PJ: Nonoperative management of posterior tibial tendon dysfunction. Foot Ankle Int 1996;17(12): Augustin JF, Lin SS, Berberian WS, Johnson JE: Nonoperative treatment of adult acquired flat foot with the Arizona brace. Foot Ankle Clin 2003;8(3): Janisse DJ, Wertsch JD, Del Toro DR: Foot orthoses and prescription shoes, in Redford JB, Basmajian JV, Trautman P, eds: Orthotics, Clinical Practice and Rehabilitation Technolog y, New York, NY Churchill Livingstone, 1995, pp Kulig K, Burnfield JM, Requejo SM, Sperry M, Terk M: Selective activation of tibialis posterior: Evaluation by magnetic resonance imaging. Med Sci Sports Exerc 2004;36(5): Kulig K, Lederhaus ES, Reischl S, Arya S, Bashford G: Effect of eccentric exercise program for early tibialis posterior tendinopathy. Foot Ankle Int 2009;30(9): Alvarez RG, Marini A, Schmitt C, Saltzman CL: Stage I and II posterior tibial tendon dysfunction treated by a structured nonoperative management protocol: An orthosis and exercise program. Foot Ankle Int 2006;27(1): Lin JL, Balbas J, Richardson EG: Results of non-surgical treatment of stage II posterior tibial tendon dysfunction: A 7- to 10-year followup. Foot Ankle Int 2008;29(8): Baksh N, Hannon CP, Murawski CD, Smyth NA, Kennedy JG: Platelet-rich plasma in tendon models: A systematic review of basic science literature. Arthroscopy 2013;29(3): Mazzocca AD, McCarthy MB, Chowaniec DM, et al: The positive effects of different platelet-rich plasma methods on human muscle, bone, and tendon cells. Am J Sports Med 2012;40(8): Teasdall RD, Johnson KA: Surgical treatment of stage I posterior tibial tendon dysfunction. Foot Ankle Int 1994;15(12): Crates JM, Richardson EG: Treatment of stage I posterior tibial tendon dysfunction with medial soft tissue procedures. Clin Orthop Relat Res 1999;365: Guyton GP, Jeng C, Krieger LE, Mann RA: Flexor digitorum longus transfer and medial displacement calcaneal osteotomy for posterior tibial tendon dysfunction: A middle-term clinical follow-up. Foot Ankle Int 2001;22(8): Myerson MS, Badekas A, Schon LC: Treatment of stage II posterior tibial tendon deficiency with flexor digitorum longus tendon transfer and calcaneal osteotomy. Foot Ankle Int 2004;25(7): Evans D: Calcaneo-valgus deformity. J Bone Joint Surg Br 1975;57(3): Mosca VS: Calcaneal lengthening for valgus deformity of the hindfoot: Results in children who had severe, symptomatic flatfoot and skewfoot. J Bone Joint Surg Am 1995;77(4): Phillips GE: A review of elongation of os calcis for flat feet. J Bone Joint Surg Br 1983;65(1): Tien TR, Parks BG, Guyton GP: Plantar pressures in the forefoot after lateral column lengthening: A cadaver study comparing the Evans osteotomy and calcaneocuboid fusion. Foot Ankle Int 2005;26(7): Ellis SJ, Williams BR, Garg R, Campbell G, Pavlov H, Deland JT: Incidence of plantar lateral foot pain before and after the use of trial metal wedges in lateral column lengthening. Foot Ankle Int 2011;32(7): Vander Griend RA: Z osteotomy of the calcaneus. Tech Foot Ankle Surg 2008;7: Hintermann B, Valderrabano V, Kundert HP: Lengthening of the lateral column and reconstruction of the medial soft tissue for treatment of acquired flatfoot deformity associated with insufficiency of the posterior tibial tendon. Foot Ankle Int 1999;20(10): Cotton FJ: Foot statics and surgery. N Engl J Med 1936;214: Hirose CB, Johnson JE: Plantarflexion opening wedge medial cuneiform osteotomy for correction of fixed forefoot varus associated with flatfoot deformity. Foot Ankle Int 2004;25(8): Vora AM, Tien TR, Parks BG, Schon LC: Correction of moderate and severe acquired flexible flatfoot with medializing calcaneal osteotomy and flexor digitorum longus transfer. J Bone Joint Surg Am 2006;88(8): Needleman RL: A surgical approach for flexible flatfeet in adults including a subtalar arthroereisis with the MBA sinus tarsi implant. Foot Ankle Int 2006;27(1): Fernández de Retana P, Alvarez F, Bacca G: Is there a role for subtalar arthroereisis in the management of adult acquired flatfoot? Foot Ankle Clin 2012;17(2): Sammarco VJ, Magur EG, Sammarco GJ, Bagwe MR: Arthrodesis of the subtalar and talonavicular joints for correction of symptomatic hindfoot malalignment. Foot Ankle Int 2006;27(9): AAOS Instructional Course Lectures, Volume 64