Excerpt from Acquired Flatfoot

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History of the Procedure

Kulowski first described tenosynovitis of the posterior tibial tendon in 1936. Key described surgical findings of partial posterior tibial tendon rupture in 1953. In 1974, Goldner et al described the surgical treatment of 9 patients with posterior tibial tendon dysfunction. In the early 1980s, Jahss (1982), Mann (1982), and Johnson (1983) recognized posterior tibial tendon dysfunction as a common cause of acquired adult flatfoot.

Problem

Adult flatfoot refers to a deformity that develops after skeletal maturity is reached. It should be differentiated from constitutional flatfoot, which is a common congenital nonpathologic foot morphology.

Etiology

There are numerous causes of acquired adult flatfoot, including fracture or dislocation, tendon laceration, tarsal coalition, arthritis, neuroarthropathy, neurologic weakness, and iatrogenic causes. The most common cause of acquired adult flatfoot is posterior tibial tendon dysfunction. This article focuses primarily on the diagnosis and treatment of this condition.

The etiology of posterior tibial tendon dysfunction is varied; it is attributed to degenerative, inflammatory, and traumatic causes. In 1 study, 60% of patients were obese or had diabetes mellitus, hypertension, previous surgery or trauma to the medial foot, or treatment with steroids. Myerson has described 2 subsets of patients with posterior tibial tendon dysfunction. One patient group was younger with associated enthesopathies at multiple sites, a higher incidence of HLA-B27 positivity, and a significant family history for inflammatory disease and psoriasis, thus suggesting a seronegative spondyloarthropathy. The other patient group was older and had isolated dysfunction, suggesting a purely mechanical degenerative cause.

Arthropathies can result in posterior tibial tendon dysfunction as well. In 1 study, 11% of 99 rheumatoid patients were found to have posterior tibial tendon pathology. A zone of tendon hypovascularity exists 1-1.5 cm distal to the medial malleolus, continuing 14 mm distally. Poor blood supply in this area of the tendon, where it takes a sharply curving course around the medial malleolus, could result in tendon degeneration and may explain a mechanical cause for tendon rupture.

A study by Dyal et al compared weight-bearing radiographs of symptomatic feet with posterior tibial tendon dysfunction to those of the contralateral asymptomatic feet. Interestingly, there was strong correlation between the measurements of both feet, leading the authors to suggest that a predisposing constitutional flatfoot may be a possible etiologic factor in the development of dysfunction. The authors cautioned against using radiographic measurements alone for diagnosis.

Pathophysiology

The medial longitudinal arch has both passive and active support. The 3 most important static contributors to arch stability in order of importance are the plantar fascia, the long and short plantar ligaments, and the spring ligament (calcaneonavicular ligament). The spring ligament forms a sling for the talar head, which prevents medial and plantar migration of the talar head and provides static arch support. The major dynamic stabilizer for the arch is the posterior tibial tendon.

Contraction of the posterior tibial tendon causes inversion of the midfoot and elevation of the medial longitudinal arch through its broad insertion on the navicular, cuneiforms, medial 3 metatarsal bases, and cuboid.

The posterior tibial tendon also indirectly affects hindfoot inversion due to its course running behind the medial malleolus and its close association with the deep deltoid and spring ligaments. With hindfoot inversion, the axes of the talonavicular and calcaneocuboid joints diverge, and the transverse tarsal joint (Chopart joint) becomes locked, which transforms the foot into a rigid lever.

Loss of posterior tibial function due to stretching or rupture of the tendon removes the primary inverter of the foot and leaves the primary and secondary everters of the foot, the peroneus brevis and longus, relatively unopposed. Therefore, posterior tibial dysfunction leads to flattening of the medial longitudinal arch, forefoot abduction, and hindfoot valgus. During the late stance phase of gait, the patient loses push-off strength due to inability to invert the hindfoot and achieve forefoot rigidity. With loss of the posterior tibial tendon function, the powerful gastrocsoleus complex acts at the talonavicular joint instead of at the level of the metatarsal heads.

The talar head is then pushed downward and medially, stretching the calcaneonavicular (spring) ligament. Continued weight bearing on the medial side of the heel eventually leads to deltoid ligament insufficiency and valgus instability of the ankle. Three-dimensional CT analysis of patients with acquired flatfoot has documented subluxation of the subtalar joint with less contact between all 3 facets of the calcaneus and talus compared to controls.

Clinical

The patient with posterior tibial tendon dysfunction initially complains of pain and swelling in the medial ankle and midfoot during weight bearing. Over time, the patient may notice loss of the arch and the tendency to walk on the inner border of the foot. Loss of push-off strength during gait occurs, and the patient may develop a limp. As the patient's heel displaces into valgus and the forefoot abducts, pressure between the calcaneus and fibula may develop, causing painful impingement between the lateral ankle and calcaneus. Abnormal wear of the medial heel and inner border of shoe wear may also be noted.

The patient is first examined while standing, allowing comparison of the symptomatic to the asymptomatic foot. Arch height is assessed and compared to the asymptomatic foot. In later stages of posterior tibial tendon dysfunction, the arch is lowered and the forefoot abducted. Viewing the patient's foot from behind allows the examiner to evaluate forefoot abduction and heel valgus. The toes visible lateral to the heel are counted. The finding of 1 or 2 toes visible lateral to the heel is normal. In cases of significant forefoot abduction, 3 or more toes are visible. This too-many-toes sign is a test to confirm forefoot abduction (see Image 1).

The angle that the heel forms with the longitudinal axis of the lower leg also should be measured. This posterior tibiocalcaneal angle is increased in cases of significant heel valgus. The patient should then be asked to stand on 1 foot and rise up on the toes. The patient usually needs to hold on to the examining table or wall for balance during this maneuver. Normally, the heel inverts as the posterior tibial muscle contracts and as the gastrocsoleus fires. In cases of posterior tibial tendon dysfunction, the heel does not invert, and the patient finds this single-limb heel rise maneuver painful, difficult, or impossible (see Image 2).

The patient then is examined seated on the examining table, and the course of the posterior tibial tendon is palpated for tenderness. Swelling along the posterior tibial tendon heath may be noted, and fluid may be palpated within the sheath. Posterior tibial strength is tested by holding the forefoot in a position of plantar flexion and eversion and asking the patient to invert the foot. During this maneuver, the posterior tibial tendon should be palpated to assess its continuity. The sinus tarsi and distal fibular area also should be palpated for tenderness because in later stages of posterior tibial tendon dysfunction, these areas of impingement may also be painful. The knee is extended, the foot is held in a subtalar neutral position, and passive ankle dorsiflexion is measured.

Usually, 10-20° of dorsiflexion is possible, but in cases of long-standing pes planus, dorsiflexion past neutral is often limited because of the development of a plantar flexion contracture. During the final stages of posterior tibial tendon dysfunction, the subtalar joint may be fixed in eversion, and inversion to neutral may be impossible. Finally, forefoot flexibility is assessed by pronating and supinating the forefoot while holding the heel in neutral position. Although the subtalar joint may be flexible, the transverse tarsal joint may have become fixed in varus, preventing plantigrade positioning of the forefoot (see Image 3). This finding has important implications for surgical treatment.

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