Rajiv Limaye and others describe the clinical condition, treatment options and treatment planning for PTTD in the foot and ankle unit at University Hospital of North Tees and Hartlepool
Introduction
Posterior tibial tendon dysfunction (PTTD) is a commonly seen problem of the foot and ankle, and the most common cause of Adult Acquired Flatfoot Deformity (AAFD) [1]. It can be secondary to trauma (like ankle fracture [6], ankle sprain [7], or a direct blow to the tendon [8]), chronic tenosynovitis (due to traumatic, degenerative or inflammatory arthritis), posterior tibial tendon (PTT) tear (partial or complete) or due to accessory navicular/tarsal coalition.
The posterior tibial muscle originates from the posterior aspects of the tibia, fibula and interosseous membrane and runs through the deep posterior compartment of the leg. Its tendon runs posterior to the medial malleolus and inserts into the navicular tuberosity with multiple insertions across the plantar aspect of the midfoot [2]. The malleolus rather sharply changes the direction of the pull of the muscle. A relative hypovascular zone exists in the retromalleolar region [3]. Functionally, the tibialis posterior is the main inverter of the midfoot and the primary dynamic stabilizer of the medial longitudinal arch [4,5]. It elevates the medial longitudinal arch causing the midfoot and hindfoot to form a rigid lever that allows the gastrocnemius to act with greater efficiency during the toe off phase of the gait cycle [4].
Histological examination suggests that tendon degeneration, rather than tendinitis, leads to the tibialis posterior tendon becoming fibrotic due to repeated microtrauma [9]. However, some controversy does remain about the underlying cause of this tendinosis [10–16]. The relative hypovascularity of the tendon in the retromalleolar area [3,10], a sharp turning of the tendon behind the medial malleolus and the over pull of the opposing peroneus brevis muscle [16] have also been suggested as contributory factors. A compromised reparative response to tissue injury due to the limited vascularity characterized by mucinous degeneration, fibroblast hypercellularity, chondroid metaplasia and neovascularization result in marked disruption of collagen bundle, which in turn may predispose the tendon to rupture under physiologic loads [11].
Patient presentation, clinical findings and treatment options depend on the stage of the disease. Most controversy exists around managing stage II disease [18]. This is further compounded by the failure of an adequate classification system by which similar pathologic deformities may be compared [18]. In this article we will describe the clinical condition, treatment options and treatment planning in our foot and ankle unit.
Clinical presentation and evaluation
PTTD is more common in females and the prevalence increases with age. Risk factors include obesity, hypertension, diabetes mellitus, corticosteroid use, inflammatory arthropathies and previous injuries. Athletes involved in activities that put excessive force on the foot, such as basketball, football, tennis, hockey and running on banked tracks, are also at higher risk [17].
Patients present with insidious onset of medial hindfoot pain with or without an associated swelling. Advanced disease presents with pain on the lateral side. Symptoms are aggravated by standing and walking. Patients may also complain of changes in their walking pattern, difficulty in taking long strides, running, stair climbing or walking on uneven ground.
Examination reveals a unilateral flatfoot comprised of a flattened medial longitudinal arch, hindfoot valgus and midfoot abduction, depending on the stage of the disease. There is inability to do the single heel raise test and the “too many toes” sign is characteristic of this condition. The patient walks with an antalgic gait, with decreased stride length and poor heel raise. Tenderness along the PTT is present early in the disease, however subfibular and sinus tarsi tender