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© 1999 The Journal of Bone and Joint Surgery, Inc.
Current Concepts Review - Acquired Flatfoot in Adults Due to Dysfunction of the Posterior Tibial Tendon* , SOUTH PORTLAND, MAINE , ATLANTA, GEORGIA , SALT LAKE CITY, UTAH
Dysfunction of the posterior tibial tendon is increasingly recognized as an etiology leading to acquired flatfoot in adults. Increased awareness of this condition during the past fifteen years has resulted in intensive study of the basic science and pathophysiology behind this clinical syndrome. New regimens for clinical assessment and treatment have been developed. Although much progress has been made in the recognition and treatment of this condition, many controversies and unanswered questions remain. This article will review the current thinking with regard to the pathophysiology, clinical evaluation, and decision-making process for the treatment of this common, debilitating condition.
Kulowski, in 1936, was the first, to our knowledge, to describe tenosynovitis of the posterior tibial tendon39. Almost twenty years later, Fowler discussed tibialis posterior syndrome and described a series of patients who had had operative treatment of that condition19. In 1963, Williams described the operative treatment of tenovaginitis of the posterior tibial tendon73. In 1969, Kettelkamp and Alexander reported on repair of spontaneous rupture of the posterior tibial tendon35. Little else was written regarding the problems emanating from dysfunction of the posterior tibial tendon until others rekindled interest in this subject during the 1980s28,32,33,44-46. Many authors have described the progressive nature of acquired flatfoot that occurs following the onset of dysfunction of the posterior tibial tendon in an adult4,9,12,20,22,26,27, and a multitude of treatment regimens have been reported2,5,7,8,13,15,19,21,23,25,28,30,32,35,38,40,46,48,52,57,58,61,66,67,71,72.
The posterior tibial muscle originates in the proximal one-third of the leg, from the posterior aspect of the fibula, the intermuscular septum, and the posterior tibial cortex. The posterior tibial tendon runs in a separate fibro-osseous groove behind the medial malleolus. From this point, the tendon runs distally in a tenosynovial sheath and terminates in multiple insertions, including the plantar aspect of the navicular and medial cuneiform bones64. The tendon courses posterior to the axis of rotation of the ankle joint and medial to that of the subtalar joint. This path results in the posterior tibial muscle functioning as a plantar flexor of the ankle and an invertor of the foot43,47. The posterior tibial tendon is the initiator of inversion of the hindfoot at the subtalar joint after the foot-flat portion of the stance phase of the gait cycle42,70. As the hindfoot inverts through the subtalar joint, the axes of the talonavicular and calcaneocuboid joints become nonparallel and the foot goes from being flexible at heel-strike to rigid during the heel-rise and toe-off phases of gait. With inversion of the hindfoot during heel-rise, the insertion of the Achilles tendon shifts medial to the axis of rotation of the subtalar joint. This firmly secures the inversion of the hindfoot and the position of the transverse tarsal joints, making the entire length of the foot a rigid lever that lifts and propels the body during the last phases of single-limb stance20,46,65. The primary antagonist of the posterior tibial tendon is the peroneus brevis muscle, which everts the hindfoot and abducts the midfoot. The posterior tibial muscle is more than two times stronger than the peroneus brevis muscle, and their relative strengths are implied by their respective cross-sectional areas (average, 16.9 compared with 6.7 square centimeters)70. The functional importance of this difference is appreciated when it is considered that the posterior tibial tendon is required to act during the full-weight-bearing phases of the gait cycle, whereas the peroneus brevis acts to evert the foot and unlock the transverse tarsal joints in the non-weight-bearing swing phase of gait70.
Many etiologies have been proposed as the underlying cause of dysfunction of the posterior tibial tendon. Jahss hypothesized that there is an impingement mechanism at the level of the fibro-osseous groove, posterior to the medial malleolus29. It has been noted that interruption of the normal pattern of insertion of the posterior tibial tendon through an accessory navicular is associated with an increased prevalence of dysfunction of the posterior tibial tendon36. Frey et al. pointed out a distinct area of hypovascularity within the posterior tibial tendon, behind the medial malleolus, and suggested that this area is predisposed to degeneration and subsequent tendinopathy18. However, a large percentage of abnormalities of the posterior tibial tendon occur distal to this region. The inflammatory arthropathies have been implicated in degeneration and dysfunction of the posterior tibial tendon, with chronic tenosynovitis leading to degeneration and dysfunction10,12,35,50,51,56. Injection of corticosteroids in the vicinity of the tendon sheath has been implicated in rupture of the posterior tibial tendon27. Many authors have suggested that some patients who have congenital pes planus later may have dysfunction of the posterior tibial tendon as a result of chronic mechanical overload and degenerative tendinosis1,14,20,28,32,33,35,44. Acute trauma with partial or complete disruption of the tendon also can cause dysfunction of the posterior tibial tendon53,74. Mosier et al. described the histopathological characteristics of posterior tibial tendon specimens that were obtained during operative reconstruction in adults who had acquired flatfoot55. Those authors clearly showed that the underlying pathological mechanism in chronic dysfunction of the posterior tibial tendon is degenerative tendinosis with no evidence of inflammation. Dysfunction of the posterior tibial tendon also has been associated with ipsilateral valgus gonarthrosis69. The posterior tibial tendon unit has a great deal of power but acts through a relatively short excursion. This may predispose the musculotendinous unit to become weak and dysfunctional with changes as small as one centimeter in resting length, regardless of the underlying etiology70. Once the posterior tibial tendon has been weakened, a common mechanical pathway leads to a progressive flatfoot deformity. At heel-strike, with the hindfoot in valgus and the transverse tarsal joints unlocked, the gait cycle progresses to the foot-flat phase. At this point, without the normal inversion power of the posterior tibial tendon, the peroneus brevis keeps the foot everted and the insertion of the Achilles tendon remains lateral to the axis of rotation of the subtalar joint. During subsequent heel-rise, the midfoot remains unlocked and flexible. The plantar ligaments of the midfoot then are subjected to the forces generated by the gastrocnemius-soleus complex and body weight. Over time, these medial soft-tissue longitudinal arch restraints become attenuated21,32. The unchecked eversion force of the peroneus brevis and the permanent shift of the insertion of the Achilles tendon lateral to the subtalar axis of rotation convert these two musculotendinous units into constant deforming forces. Loss of the longitudinal arch results in a fixed equinus deformity of the hindfoot and contracture of the Achilles tendon15,31,58. This process continues and, if unchecked, results in deformity, including valgus and equinus deformity of the hindfoot, pes planus, and abduction of the forefoot20,32,33,44,46. Over time, this can lead to degenerative arthritis of the hindfoot and midfoot. If this deformity persists, valgus deformity and degenerative arthritis of the ankle can occur33.
During the evaluation of acquired flatfoot in an adult, it should be kept in mind that there are many potential causes, only one of which is dysfunction of the posterior tibial tendon. Other known etiologies include traumatic disruption of the ligaments of the midfoot, a previously unrecognized tarsal coalition, inflammatory arthritis, tarsometatarsal osteoarthritis, Charcot arthropathy, and neuromuscular disease26,47. Because of the increased awareness of dysfunction of the posterior tibial tendon, and possibly because of changes in societal demographics and activity levels, acquired flatfoot in adults due to dysfunction of the posterior tibial tendon is now likely to be encountered often in the musculoskeletal specialist's practice.
History Patients who are seen early in the disease process usually describe an insidious onset of vague, activity-aggravated pain on the medial side of the foot and ankle. Fatigue or weakness of the foot and ankle is a common symptom46. On careful questioning, approximately one-half of patients recall a remote traumatic event, such as stepping awkwardly off of a curb and forcibly everting the foot47. There may be problems with balance or increased difficulty with walking on uneven ground. Later in the disease process, activity-related pain in the areas of the sinus tarsi and the lateral malleolus may become more prevalent, presumably because the deformity causes impingement of the lateral structures of the foot and ankle during weight-bearing33,58. There may be pain on the lateral side of the foot and ankle after the symptoms on the medial side have abated. This suggests that the tenosynovitis on the medial side dissipates after elongation of the posterior tibial tendon and the subsequent onset of deformity. Patients may note a new onset of unilateral flatfoot deformity or progression of a preexisting flatfoot deformity. In the subsequent stages of the disease, there may be generalized pain, stiffness, and soft-tissue swelling in the hindfoot; these symptoms are consistent with the development of osteoarthritis of the subtalar and transverse tarsal joints. It is important to recognize the broad spectrum of symptoms caused by dysfunction of the posterior tibial tendon and to expect to encounter them in a variety of age-groups.
Physical Examination The examination begins with the patient standing with the legs, ankles, and feet unclothed to allow observation of alignment. The surgeon should look for asymmetrical swelling, abduction of the forefoot, or pes planus. When observed from behind with the patient's knees pointing directly forward, asymmetrical pes planovalgus will be indicated by the so-called too-many-toes sign. This sign is positive when more of the lesser toes are visible lateral to the ankle joint on the involved side than on the uninvolved side32. The patient should perform a bilateral heel-rise. Dysfunction of the posterior tibial tendon will be apparent if there is asymmetrical or incomplete inversion of the hindfoot during this maneuver46. A more sensitive and specific finding is difficulty in performing (or an inability to perform) a single-limb heel-rise32,33,68. This test is performed with the uninvolved foot in the air and the hands resting lightly on a vertical surface. Incomplete inversion of the heel, difficulty in performing (or an inability to perform) a heel-rise, and a sensation of weakness all are highly suggestive of dysfunction of the posterior tibial tendon. Patients also may feel pain medially along the course of the posterior tibial tendon while performing this maneuver. When a patient has early or subtle symptoms, repetitive single-limb heel-rise with comparison with the contralateral, asymptomatic side is helpful58. In the absence of dysfunction of the posterior tibial tendon, an individual should easily be able to perform five to ten consecutive single-limb heel-rises47. With the patient seated on the examination table, the posterior tibial tendon is palpated. In patients who have chronic dysfunction, the tendon is approximately one and one-half times the normal size55. This can be noted, by an experienced examiner, in a patient who is not morbidly obese if there is an absence of generalized pedal edema. Soft-tissue swelling and tenderness can be noted as well. Tenderness can be elicited anywhere along the course of the tendon as far distal as its primary insertion on the navicular. The motor strength of the posterior tibial tendon can be assessed by asking the patient to invert the foot against resistance. The foot should be placed in a fully plantar flexed position to ensure that the anterior tibial tendon is not substituting for the posterior tibial tendon. Alternatively, motor strength can be assessed by placing the foot in maximum passive eversion and plantar flexion and then asking the patient to invert the foot actively against resistance. This position also prevents substitution by the anterior tibial tendon. It is important to note that the demonstration of active motor power and the absence of a palpable defect do not rule out dysfunction of the posterior tibial tendon. It is common for the patient to have some intact function of the posterior tibial tendon. Only in advanced stages will total dysfunction be grossly evident on manual examination; hence, the importance of the too-many-toes sign and the single-limb heel-rise test47,68. Next, the passive range of motion of the hindfoot and midfoot is assessed. If valgus angulation of the hindfoot was noted on standing alignment, it is important to assess whether or not this deformity can be corrected fully by the examiner. The hindfoot should be examined with the ankle plantar flexed because contracture of the Achilles tendon often occurs as part of the flatfoot process15,31,54,58. Such a contracture usually is not passively correctable. For the assessment of the forefoot, valgus angulation of the hindfoot is corrected to neutral with one hand and the contralateral hand is used to determine the flexibility and correctability of abduction and supination of the forefoot. During the evaluation of dysfunction of the posterior tibial tendon, two critical questions must be answered. First, it must be determined if the patient has an asymmetrical flatfoot deformity or a preexisting flatfoot deformity that has worsened over time. Second, it must be determined if the deformity can be passively corrected by the examiner and thus whether it is flexible.
Clinical Staging (Table I)
Stage-1 disease is characterized by pain and tenderness in the posterior tibial tendon without asymmetrical clinical and radiographic deformity. The tendon has a normal resting length, and the hindfoot may invert normally during heel-rise. In stage 2, asymmetry between the flatfoot and the normal foot is noted on clinical evaluation or radiographs. Elongation or disruption of the posterior tibial tendon must have occurred in order for deformity to be present. The deformity remains flexible and can be reduced by the examiner while the hindfoot is held in equinus. The hallmark of stage-3 disease is loss of flexibility of the hindfoot deformity on physical examination. This stage may be accompanied by degenerative arthritis of the hindfoot or midfoot as seen on radiographs. Stage-4 disease is characterized by the same findings as in stage 3, in addition to valgus deformity and arthritis of the ankle.
Radiographic Evaluation Once a general impression has been obtained, the surgeon should quantify the extent of the flatfoot deformity. This is particularly helpful when the surgeon is following a patient with serial examinations and documenting progression from stage 1 to stage 2. In patients who have bilateral pes planovalgus, a subtle asymmetry in the measurements may suggest progression on the involved side. There are many different approaches to the measurement of flatfoot deformity on plain radiographs. Sangeorzan et al. described a method utilizing angular measurements63. On the anteroposterior radiograph of the foot, the angle between the longitudinal axis of the talus and the first metatarsal may be used to identify abduction of the forefoot. The anteroposterior relationship of the talus to the navicular is defined by the talonavicular coverage angle. This angle consists of three points: the center of the articular surface of the talar head, the center of the articular surface of the navicular, and the midpoint of the line connecting the edges of the articular surface of the talus. On the lateral radiograph, the talometatarsal angle is determined by drawing the longitudinal axes of the first metatarsal and the talus49. We prefer a technique that utilizes linear measurements6. On the anteroposterior radiograph of the foot, the degree of abduction of the forefoot is quantified by measuring the degree to which the talar head is not covered by the navicular. A linear measurement is made from a fixed point on the medial aspect of the talar head to a fixed point on the medial edge of the navicular. This same measurement is made on the contralateral foot with use of the same osseous landmarks, and the results are compared. It has been our clinical experience that this is a sensitive method for documenting asymmetrical abduction of the forefoot (Fig. 1). Next, measurements are made on the bilateral lateral radiographs made with the patient standing. This is done by drawing a horizontal line parallel to the inferior border of the base of the fifth metatarsal and measuring perpendicularly to the anterior-inferior corner of the medial cuneiform (Figs. 2-A and 2-B). The radiographs of the two feet are then compared. This technique originally was described for the assessment of deformity at the tarsometatarsal joint16, but we have found it to be helpful in the evaluation of pes planovalgus deformity. In a normal arch, the base of the medial cuneiform is higher than the base of the fifth metatarsal. In a foot with a pes planovalgus deformity, the height of the medial cuneiform above the level of the fifth metatarsal decreases and may even become a negative value. The bilateral anteroposterior radiograph of the ankle is used to measure the total height of the ankle, from the superior margin of the talar body to the base of the radiograph. This value is compared with the height of the contralateral ankle. Asymmetrical flatfoot can be documented on the basis of a shorter height on one side (Fig. 3).
Use of Other Imaging Modalities
Nonoperative Treatment In patients who have acute stage-1 disease, a below-the-knee cast worn for four to six weeks can be helpful for initially controlling the symptoms of tendinitis or tenosynovitis66. Weight-bearing while the cast is worn should be allowed only if it does not cause pain. After the cast has been removed, use of a full-length custom orthotic device helps to support the longitudinal arch and to reduce strain on the posterior tibial tendon. The orthosis should provide support to the medial longitudinal arch and correction of the valgus angulation of the hindfoot and the abduction of the forefoot with use of a medial heel-wedge and a medial column post30,66. It is helpful to perform the evaluation and fitting for the orthotic device before the cast is applied. The device can be made while the patient is wearing the cast and will therefore be ready for use as soon as the cast is removed. If the findings of the initial evaluation suggest that the tendinitis is chronic or less severe, the patient can proceed to use the orthotic device without first wearing the cast. We do not believe that corticosteroid injections should be used in the treatment of dysfunction of the posterior tibial tendon, as the underlying etiology often is not of an inflammatory nature17,18,22,26,27,53,55. Some authors have noted a relationship between previous corticosteroid injections and rupture of the posterior tibial tendon27. A trial of three to six months is adequate to determine if nonoperative care has been successful. If clinical improvement is noted, the patient may need the orthotic device indefinitely. Routine follow-up at six-to-twelve-month intervals is recommended as the symptoms may recur or the condition may progress to stage 2 despite initial improvement. Recurrence of symptoms in a patient who has a well fitted orthotic device may indicate the need for operative treatment. In stage-2 disease, the posterior tibial tendon has become permanently elongated and the medial plantar ligaments have become attenuated21,32,55; however, the flatfoot deformity remains flexible except for the tight gastrocnemius-soleus complex. The treatment is much the same as that for patients who have stage-1 disease, although more intensive orthotic management may be necessary. The goal is to alleviate pain and to correct and control the flexible deformity. If semirigid orthotic devices are ineffective, consideration should be given to a University of California at Berkeley Laboratory-type orthotic device, which is more rigid and provides lateral buttressing of the forefoot to help to control more severe flexible abduction deformities of the forefoot. If the deformity is particularly severe, an ankle-foot orthosis may be needed66. Again, a three-to-six-month period should be adequate to determine if nonoperative care will be sufficient. In stage-3 disease, there is a rigid deformity of the hindfoot; there also may be stiffness of the midfoot as well as arthritis of the hindfoot and midfoot. Orthotic devices for these patients must be more accommodative; corrective-type devices may be poorly tolerated because of the rigidity of the deformity. The goals of treatment are relief of pain and correction of any remaining flexibility of the deformity. An ankle-foot orthosis may be necessary to prevent further progression of the valgus angulation of the hindfoot and the abduction of the forefoot66. Some patients may tolerate an articulated ankle-foot orthosis better. In this late stage of the disease, the ankle and the knee are at risk for arthritic changes secondary to malalignment of the limb. (A more thorough discussion of the use of orthoses, including modifications in shoewear, for the treatment of dysfunction of the posterior tibial tendon can be found in three excellent reviews, by Chao et al.7, Lin et al.40, and Sferra and Rosenberg66.) The nonoperative treatment of stage-4 disease typically involves the use of a solid ankle-foot orthosis. The orthosis should be used to try to correct only the part of the deformity that is flexible. The rigid components cannot be corrected with a brace; pain and problems with the skin may increase if the brace provides too much correction in a patient with a rigid deformity. Although nonoperative care can be very effective for alleviating symptoms and preventing progression of a flatfoot deformity, the surgeon should be aware of the potential for progression to more advanced stages of dysfunction of the posterior tibial tendon. Operative treatment should be considered after a three-to-six-month trial of nonoperative care has failed. Postponement of operative treatment may lead to progression of the deformity and the stage of the disease.
Operative Treatment In stage-2 disease, progressive flatfoot deformity has begun and may be longstanding. Many gross changes in the posterior tibial tendon may be visible at this stage. These changes include yellow discoloration; loss of the smooth, glistening surface; longitudinal tears; and enlargement of the tendon, often to one and one-half times its normal width. Critical assessment of the musculotendinous unit is required at the time of the operation, as the muscle belly may have irreversibly lost its elasticity44,47. This may be noted on direct observation when tension is applied to the posterior tibial tendon. If the musculotendinous unit is found to be inelastic, transfer of the flexor digitorum longus to the posterior tibial tendon is not recommended44,47. In patients who have early stage-2 disease with minimum degenerative changes in the posterior tibial tendon and normal muscle elasticity, retention of the posterior tibial tendon and side-to-side transfer to the flexor digitorum longus tendon may be considered28,44,67. Tendon transfer alone has been described in patients who have stage-2 disease20,32,46; however, this procedure often fails to correct the deformity. Without correction of the flatfoot deformity, postoperative function may deteriorate over time8,29,59. Supplementation of transfer of the flexor digitorum longus tendon with one procedure or a combination of procedures is currently under investigation48,57,58,61. The early results of these combined procedures are promising. Soft-tissue reconstruction of the spring ligament complex has been advocated by some authors11,21. Reconstruction of the medial column with advancement of the osteoperiosteal flap, with or without an arthrodesis of the medial column, has been described5,13,52. Lengthening of the lateral column with use of a tricortical iliac-crest bone graft, either at the level of the anterior process of the calcaneus or by distraction arthrodesis of the calcaneocuboid joint, has been shown to reproducibly restore the height of the medial longitudinal arch and to reduce the abduction deformity of the forefoot1,3,60,61,63. Medial displacement calcaneal osteotomy has been advocated by some authors for the correction of pes planus and has been used alone or in combination with procedures for lengthening of the lateral column38,41,48,57,61. A potential criticism of the use of a medial displacement calcaneal osteotomy alone is that it inconsistently restores the height of the medial longitudinal arch57. It is important to recognize that contracture of the Achilles tendon may occur concurrently with the pes planovalgus deformity32,54,58, and this may necessitate lengthening of the Achilles tendon at the time of the osteotomy of the hindfoot15,48,54,61. Limited arthrodesis of either the subtalar or the talonavicular joint, alone or as a supplement to tendon transfer, has been described for the treatment of dysfunction of the posterior tibial tendon23,25,37. Correction of flatfoot deformity with arthrodesis of the talonavicular joint successfully restores the height of the medial longitudinal arch and appears to provide lasting correction25. However, this procedure may result in a nearly complete loss of motion of the subtalar and transverse tarsal joints3. We believe that, in the absence of arthritis of the subtalar or talonavicular joint, other joint-preserving procedures should be considered. A double or triple arthrodesis will alleviate pain in patients who have stage-2 disease, but such relief is traded for loss of motion and related function2,3,24. Currently, there is much controversy with regard to which technique or combination of techniques is preferable. Short-term follow-up studies have shown that the early results of tendon transfer in conjunction with a supplemental procedure are promising57,61. However, the long-term results must be evaluated in order to determine if they are indeed better than those obtained with a triple arthrodesis. For stage-3 disease, characterized by a rigid valgus deformity of the hindfoot and often accompanied by degenerative arthritis of the hindfoot and midfoot, arthrodesis is the procedure of choice. If there is isolated involvement of the subtalar joint, an isolated arthrodesis of that joint may be warranted in addition to débridement of the posterior tibial tendon and transfer of the flexor digitorum longus23. If the arthritis is limited to the talonavicular joint, consideration can be given to correction of the deformity and arthrodesis of that joint alone25. In our experience, these clinical scenarios have been rare and a triple arthrodesis usually has been needed to correct all of the components of the rigid deformity and to alleviate pain in the involved joints. In patients who have stage-3 disease, the goal of treatment is to reduce pain that occurs during walking. Avoidance of progressive arthritis of the proximal and distal joints is also a theoretical goal. Therefore, it is important not to perform the triple arthrodesis with the hindfoot in situ but, rather, to correct the deformity of the foot23. In patients who have stage-4 disease, operative treatment should be considered after nonoperative treatment has failed. As the disease affects the ankle as well as the subtalar, talonavicular, and calcaneocuboid joints, care must be taken to determine which site is causing most of the symptoms. If the pain is isolated to the ankle joint, an arthrodesis should be considered. If the pain is primarily in the tarsal joints, a triple arthrodesis is the procedure of choice. Many patients have pain in both the ankle and the tarsal joints, necessitating a pantalar arthrodesis. In all instances, the remaining deformity should be corrected with an arthrodesis in order to maximize the function of the surrounding joints that are not included in the arthrodesis.
Acquired flatfoot in adults is a common clinical entity. It may present as progression of congenital pes planovalgus or as new-onset unilateral flatfoot. Although there are many causes of acquired flatfoot in adults, dysfunction of the posterior tibial tendon is now a commonly recognized etiology. Dysfunction of the posterior tibial tendon itself has many potential etiologies. Flatfoot deformity secondary to dysfunction of the posterior tibial tendon is due primarily to the loss of balance between the muscles that invert and evert the hindfoot. With the onset of dysfunction of the posterior tibial tendon, the hindfoot fails to invert during the heel-rise and toe-off phases of gait. This begins to occur when the antagonist peroneus brevis becomes stronger than the tibialis posterior and the posterior tibial tendon becomes too weak to invert the weight-bearing foot. Without inversion of the hindfoot, the transverse tarsal joints fail to lock and abnormal stress is transmitted to the medial plantar ligaments. Over time, a progressive flatfoot deformity develops. Early recognition of dysfunction of the posterior tibial tendon is important because of the progressive natural history of the disease. Effective treatment is now available for patients with all stages of the disease and can be determined after the stage has been identified. The diagnosis and staging of dysfunction of the posterior tibial tendon remains primarily a clinical process. Imaging studies other than plain radiographs should be used only for selected patients. Although, in the last two decades, great strides have been made in the understanding, recognition, and treatment of dysfunction of the posterior tibial tendon, there remain many unanswered questions, clinical debate, and controversy. The fact that effective treatment is available magnifies the importance of recognizing the disease at the time of presentation, identifying its stage, and remaining knowledgeable regarding current techniques of operative and nonoperative care.
*No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article. No funds were received in support of this study.
#Department of Orthopaedics, University of South Alabama, 2451 Fillingim Street, Mobile, Alabama 36617.
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