Posterior tibial tendon insufficiency (PTTI) is the most common cause of acquired pes planus in adults. The posterior tibialis muscle originates along the proximal one-third of the tibia and intraosseous membrane. Distally, its tendon travels posteriorly and inferiorly through the medial malleolar groove and inserts on the navicular, cuneiforms, cuboid, and bases of the second, third, and fourth metatarsals.

Causes / typical injury mechanism: While the exact mechanism of PTTI is not known, it is thought to be a progressive disease due to a combination of degenerating factors including inflammation, trauma, and ischemia. However, it can also occur more abruptly in the case of trauma as the result of partial or complete tendon rupture.

Classic history and presentation: Due to the progressive nature of the disease, symptoms tend to develop and evolve over time.

• Early in the course, symptoms include pain and swelling in the medial aspect of the foot and ankle, with weakness and difficulty standing on tiptoes.
• As the disease progresses, later symptoms include collapse of the longitudinal medial arch, leading to the classic flatfoot deformity.
• Additionally, patients can experience more lateral ankle pain due to fibular compression against the calcaneus.

Prevalence:

• Age – PTTI is more prevalent in women older than 40 years, most often in the sixth decade of life.
• Sex / gender – PTTI predominately affects women.

Risk factors: Risk factors include increased age, obesity, diabetes mellitus, chronic steroid use, congenital flatfoot deformity, and inflammatory arthropathies.

Pathophysiology: While the pathophysiology of PTTI has classically been described as a progressive degeneration of the tendon due to repeated loading and microtrauma, other etiologies have also been explored. One such includes a hypovascular region in the mid-portion of the tendon behind the medial malleolus that receives a relatively poor blood supply. This region is in a watershed zone of the tendon between the proximal portion, which receives its arterial supply via the posterior tibial artery, and the distal tendon and insertion, which are supplied by both the posterior tibial and dorsalis pedis arteries.

The posterior tibial tendon works with the gastrocnemius / soleus complex to stabilize the hindfoot and support the longitudinal arch. As the posterior tibial tendon degenerates and becomes less efficient, more stress is placed on the medial ligamentous structures, such as the spring ligament, talocalcaneal interosseous ligament, and superficial deltoid, in order to support the longitudinal arch. As more stressed is placed on these structures, they attenuate, leading to progressive loss of the arch and abduction of the mid-foot. Additionally, the calcaneus can drift into valgus malalignment, resulting in contracture of the Achilles tendon.

Grade / classification system: Classification and staging was originally proposed by Johnson and Strom, consisting of 3 stages. However, a fourth stage was subsequently added by Myerson.

Stage I – Tenosynovitis, normal tendon function and no deformity. Patients will be able to perform a single heel rise.

Stage II – The tendon is incompetent or ruptured. Patients exhibit a flexible flatfoot deformity and will not be able to perform single heel rise.

• IIA: normal forefoot (anteroposterior [AP] foot radiograph: < 30% talar head uncoverage)
• IIB: forefoot abduction (AP foot radiograph: > 30%-40% talonavicular uncoverage, "too many toes" sign)

Stage III – Fixed flatfoot deformity with rigid forefoot abduction and hindfoot valgus, evidence of subtalar arthritis, and inability to perform a single heel rise.

Stage IV – Valgus deformity of the tibiotalar joint secondary to deltoid ligament insufficiency.