Key Insights On Treating Early Adult-Acquired Flatfoot Deformity
- Volume 20 - Issue 9 - September 2007
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When a patient presents to the office complaining of medial ankle pain, one should consider several differential diagnoses. These include an ankle sprain, posterior tibialis or flexor digitorum longus tenosynovitis, a rupture or tarsal tunnel syndrome.
However, if the patient is middle-aged, female, mildly obese and has had medial ankle pain for several months, there should be a high index of suspicion of insufficient posterior tibialis (PT) tendon leading to adult-acquired flatfoot (AAF) syndrome. When the loss of PT tendon function due to partial or complete rupture occurs, the development of a progressive flatfoot deformity in adults is often missed.
The rupture of the PT tendon was first described in 1953. In 1969, Kettelkamp and Alexander published results of their surgical exploration of the PT tendon and reported that one cannot obtain satisfactory results in patients with delayed repair and a loss of tendon substance.1 Mann and Thompson reported a series of 17 patients with PT tendon rupture. The duration of treatment for these patients was 43 months and in all but two of the patients, there was an incorrect initial diagnosis.2
In the adult population, researchers have reported progressive flatfoot deformity with degenerative disease of the PT tendon leading to partial rupture. The failure of the tendon is due to degeneration of the PT tendon in the middle-aged population secondary to acute angulation of the tendon as it passes posterior to the medial malleolus and the zone of hypovascularity distal to the medial malleolus.3
Currently, clinicians use the terms posterior tibial tendon dysfunction (PTTD) or AAF deformity interchangeably with a diagnosis based on the Johnson and Strom classification.4 The treatment dilemma occurs with treatment options of late Stage I or early Stage II PTTD with suspected partial rupture of the PT tendon.
An Anatomical Overview Of The PT Tendon
The PT tendon runs posterior and medial to the axis of the ankle joint, and medial to the axis of the subtalar joint. The PT tendon functions as a plantar-flexor of the ankle and an invertor of the subtalar joint complex. The PT muscle starts the process of inversion of the hindfoot during gait by bringing it into a neutral position and maximizing the mechanical advantage of the laterally positioned Achilles tendon as one rises onto the forefoot. The PT muscle drives the position of the hindfoot and determines the flexibility of the foot by its control over the transverse tarsal joints.
The loss of the force of inversion of the muscle explains why patients with PT tendon insufficiency have only a limited ability or are completely unable to rise onto their toes from a position of single leg stance. The PT muscle normally is antagonistic to the peroneus brevis muscle when there is a lack of opposition of the peroneus brevis muscle. This leads to the clinical deformities one sees in patients with rupture or dysfunction of the PT tendon.
The medial capsular and ligamentous structure of the hindfoot and midfoot plays a role in the development of flatfoot deformities. The talonavicular joint capsule, the spring ligament and deltoid ligament complexes become attenuated and they have been implicated in the progressive loss of the medial longitudinal arch of the foot and the ankle dysfunction one sees in longstanding cases of PTTD.
Recognizing the progressive nature of PTTD is very important.
What You Should Know About The Johnson And Strom Classification Of PTTD
The classification by Johnson and Strom is useful in developing algorithms for treatment of AAF deformity.4 However, this classification does not predict the outcome of treatment and does not consider the contracted gastrocnemius.
The Johnson and Strom classification identifies different stages of PTTD. Stage I is characterized as PT tendon dysfunction with tenosynovitis, with or without intratendinous degeneration. The tendon is not elongated and the hindfoot is not in a valgus position. The muscle strength is diminished but no noticeable foot deformity is present. The foot is in normal alignment when the patient is standing.