Key points

Introduction

Adult acquired flatfoot deformity is characterized by collapse of the medial longitudinal arch and loss of the mechanical advantage of the posterior-medial soft-tissue structures, including the posterior tibial tendon. Key¹ initially described a chronic partial rupture of the posterior tibial tendon in 1953.

Further literature confirmed an association with this abnormality and, in fact, “dysfunction” of this posterior tibial tendon with adult acquired flatfoot deformity. The clinical presentation of adult flatfoot can range from a flexible deformity with normal joint integrity to a rigid, arthritic flat foot. Conservative and surgical management of flatfoot deformity has been reviewed extensively in the literature, but debate still exists regarding the surgical management of stage II deformities, especially in the presence of medial column instability. Historically triple arthrodesis was a common surgical approach; however, the increased incidence and awareness of posterior tibial tendon dysfunction has stimulated a trend toward surgical interventions that involve joint preservation techniques.2,3

The purpose of this article is to review and discuss various surgical options for the correction of stage II flatfoot reconstructive procedures. The authors discuss their opinion that is not always necessary to transfer the flexor digitorum longus tendon to provide relief and stability in this patient population. The article focuses on the anatomy, diagnosis, and current treatments of flexible flatfoot deformity (Fig. 1).

Functional anatomy

The tibialis posterior arises from the posterior aspect of the tibia and is part of the deep posterior compartment. The tendon divides in the proximity to the navicular tuberosity into 3 slips: the anterior, middle, and posterior. The anterior slip is the largest of these, and also is the slip considered to be the continuation of the posterior tibial tendon proper. This slip inserts on to the navicular tuberosity, first cuneiform-navicular joint, and inferior first cuneiform. The middle tendon slip fans out like multiple tentacles that travel deep into the plantar vault of the foot inserting on the second and third cuneiform, lateral second metatarsal base, medial and lateral third metatarsal base, medial fourth metatarsal base, and cuboid. Occasionally there is a slip to the fifth metatarsal base. At the level of the midfoot this portion of tendon gives origin to the flexor hallucis brevis. The tendon also crosses deep to the peroneus longus and, in some instances, directly interacts with this tendon by tendinous attachment. The posterior component of the tibialis posterior travels lateral and posterior to insert on the sustentaculum tali.⁴ Ultrasonographic imaging of the tibialis posterior shows a mean width of 9.72 to 11.12 mm, thickness of 3.42 to 3.64 mm, and cross-sectional area of 2.66 to 3.07 mm² based on 3 observers. Magnetic resonance imaging (MRI) shows measurements of 10.65 to 11.11 mm width, thickness of 3.95 to 4.18 mm, and cross-sectional area of 3.17 to 4.06 mm².⁵

The flexor digitorum longus originates from the posterior tibia and interosseous membrane. The tendon courses under the sustentaculum tali as part of the deep posterior compartment. The tendon of the flexor digitorum longus traverses plantar to the flexor hallucis longus and travels anteriorly and laterally before it splits in to 4 slips, each inserting on their respective lesser digital distal phalanx. The tendon of the flexor digitorum longus also gives origin to the quadratus plantae.⁴ Ultrasonographic measurements of the flexor digitorum longus show a mean cross-sectional area of 1.59 to 176 mm².⁶

The course of the posterior tibial tendon runs slightly superior to the flexor digitorum longus. The flexor digitorum longus runs in a more axial fashion than the posterior tibial tendon. The higher angle of descent of the posterior tibial tendon places it in the ideal location for its strap-like, arch-supporting function.

When transferring the flexor digitorum longus to the posterior tibial tendon insertion, the flexor digitorum longus cannot recreate the trajectory of the posterior tibial tendon. Moreover, when transferring the flexor digitorum longus into the navicular or medial cuneiform, the tentacle-like insertions of the posterior tibial tendon are sacrificed.

In addition the spring ligament, the deltoid ligament complex, and the articular relationship of the talonavicular and subtalar joints can be affected in the presence of posterior tibial tendon dysfunction.

The vascularity of the posterior tibial tendon originates from branches of the posterior tibial artery. Superior to the medial malleolus, the posterior tibial tendon has vessels in the synovial sheath, which come from muscle tissue. Distally the insertion receives its blood supply from the periosteal tissue. In between is a zone of hypovascularity, which often corresponds to the site of the diseased tendon.⁷

Pathology

Biomechanical imbalance can lead to chronic microtrauma in the posterior tibial tendon. In addition, advanced age lessens tendon elasticity because of changes in collagen structure that create tendon weakness.⁸ Poor blood supply may stimulate this disease process and may preclude healing of the tendon, leading to a chronic inflammatory state that creates tenosynovitis and tendinosis. Deland and colleagues⁹ demonstrated that medial calcaneonavicular ligaments and the interosseous ligament are often implicated in posterior tibial tendon dysfunction. Other causes include medical conditions such as ligamentous laxity and trauma to the posterior tibial tendon. More common are biomechanical conditions associated with posterior tibial dysfunction. This patient population typically presents with an equinus contracture, a medial column instability that can lead to a forefoot varus and a hindfoot valgus.

Classification

Johnson and Strom¹⁰ described 3 stages of posterior tibial tendon dysfunction, with Myerson and Bluman¹¹ describing a fourth stage.

Stage I is described as painful tenosynovitis of the posterior tibial tendon. The patient is able to perform a single-limb heel rise. The hindfoot is supple. In this stage, a period of immobilization in a walking cast or walking boot followed by either ankle-foot orthosis or an orthotic can often manage this condition successfully.

Stage II is characterized by an elongated posterior tibial tendon, medial pain, and a mobile hindfoot valgus that corrects to neutral on heel rise. A single-limb heel-rise test shows marked weakness. There is a positive “too many toes” sign. Stage II can also be subdivided into IIA (<30% uncovering of talar head), IIB (>30% uncovering of talar head), and IIC, which is stage II posterior tibial tendon dysfunction with associated forefoot varus (Fig. 2).

Stage III is rigid hindfoot valgus that does not correct on double-limb heel rise. The patient may not be able to perform a double-limb heel rise, and is unable to perform a single-limb heel rise. There is a positive “too many toes” sign. There may be significant rearfoot arthritis. Pain is noted medially, and also can be lateral, owing to impingement of lateral talar process.¹⁰ Extra-articular osteotomies may be attempted to treat this stage; however, serious consideration should be given to fusion of the talonavicular and/or subtalar joint (Fig. 3).

Stage IV deformities are a progression of stage III, with associated tibiotalar valgus and possible arthrosis as a result of the prolonged hindfoot valgus.¹¹ The treatment of stage IV pes planovalgus is the same as for stage III; however, pain in the ankle joint must also be addressed by means of cautious monitoring, cartilage repair, fusion, or total ankle arthroplasty (Fig. 4).

It should be noted that this classification system is mentioned to provide an organized and categorized system to define the stages of the deformity. Clinicians must realize that there can be much overlap of findings from one stage to another, and there exists a spectrum of underlying abnormalities between these stages.

Other classification systems that describe the disorders associated with the dysfunction of the posterior tibial tendon also exist, but are beyond the scope of this article. The reader is encouraged to consult the corresponding references for more detail.12,13