Posterior tibial tendon dysfunction and treatment of stage II disease

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 tenderness occurs in advanced stages.

PTTD was initially classified by Johnson and Strom (1989) into three stages and modified by Myerson (1996), who added a fourth stage. Stage I comprised of painful tenosynovitis without any deformity. Stage II consisted of reducible hindfoot valgus. Stage III included rigid hindfoot valgus. Presence of ankle deformity formed stage IV. As the classification described by Johnson and Strom does not help directly in treatment planning, further classifications have been suggested. One of the recent ones has been from Haddad et al. (2011) who further sub-divided stage II into five subtypes [18].

Weight-bearing foot and ankle anteroposterior (AP) and lateral radiographs help in the initial evaluation of the disease. Radiographs may appear normal in stage I, show signs of arch collapse in stage II, subtalar arthritis in stage III and talar tilt in stage IV disease. On the weight-bearing lateral view, lateral talometatarsal angle or Meary’s angle is the angle formed by the intersection of the long axis of the talus and the first metatarsal. Normally these two lines are parallel. With loss of the medial longitudinal arch and abduction of the midfoot the lateral talometatarsal angle increases [19]. On the weight-bearing AP radiographs, the talonavicular coverage angle can be used to assess the extent of midfoot abduction [20]. This angle is formed by drawing a line from the edges of the articular surface of the talar head and another line from the edges of the articular surface of the navicular. An angle of greater than 10 degrees represents increased midfoot abduction [21].

CT scans provide information on the status of the bones and joints helping detect tarsal coalitions and assess hindfoot arthritis [21].

MRI provides an accurate assessment of the soft tissues, including PTT, spring ligament, deltoid ligament and even the functional status of a muscle (i.e. fatty replacement versus normal muscle signal) [22]. However, the detailed abnormal findings are often not clinically relevant [21].

Ultrasonography is a quick, low-cost modality that can provide an accurate assessment of the PTT [23], but its results are very user dependant [24].

 

Literature review

All stages of the disease are initially managed conservatively with casts, braces or specific orthotics and NSAIDs. Stage I rarely requires operative management [21]. Persistent symptoms may require a PTT debridement/decompression.

There are a variety of options available to manage stage II PTTD, which can be divided into soft tissue procedures and bony procedures. Bony procedures can further be subdivided into displacement osteotomy, lateral column, medial column and joint sacrificing procedures. The procedures and their rationale are listed in the Table 1. Joint sacrificing procedures are reserved as salvage options in stage II PTTD.

 

Stage III disease requires hindfoot arthrodesis/joint sacrificing procedures [25], whereas stage IV, due to the tibiotalar involvement, requires tibiotalocalcaneal or pantalar arthrodesis. However, bony alignment correction with deltoid ligament reconstruction has also been described [26], but currently lacks sufficient evidence.

Medial displacement calcaneal osteotomy (MDCO) and posterior tibial tendon transfer is the most common combination used to treat stage II PTTD [27]. Brodsky et al. performed a prospective gait analysis on 12 patients who underwent this combination and found statistically significant improvement in cadence, stride length and ankle push-off [28]. Myerson et al. [29], Fayazi et al. [30], Wacker et al. [31], Guyton et al. [32], and Sammarco and Hockenbury each published retrospective reviews demonstrating a high rate of successful results with short to intermediate follow-up [21].

 

Our experience

Between January 2012 and January 2015, a total of 23 patients with symptomatic stage IIB PTTD underwent MDCO with FDL transfer to the navicular tuberosity. Inclusion criteria were asymmetrical flat foot with supination deformity of forefoot, pain and swelling on medial ankle, inability to perform single heel raise, markedly reduced or absent strength of inversion (MRC<2), with a mobile hindfoot. Patients with infection, diabetes, hindfoot arthritis and neuroarthropathy were excluded from the study.

Each patient was selected after failing a trial of conservative management for six months, which included casts, braces, specific orthoses and NSAID use.

Before the surgical procedure, all the patients had a preoperative MRI for detailed analysis of the PTT and supporting structures. All patients were evaluated using the pre-op and post-op Manchester Oxford Foot Questionnaire (MOXFQ) and VAS score to obtain a standardised outcome.

 

 

Surgery on all the patients was carried out by the same surgeon, using the same techniques.

Post-operatively, patients were given a below knee back slab for two weeks, by the end of which suture removal was done and a below knee cast for a further four weeks was applied. Patients were kept non-weight bearing for the duration of these six weeks followed by cast removal and partial to full weight bearing walking as tolerated by the individual. All the patients received DVT prophylaxis for the entirety of the six-week duration.

Out of the 23 total patients, 15 (65.21 per cent) were females while eight (34.78 per cent) were males. The average follow-up duration was 25 months. Quantified MOXFQ scores indicated good to excellent results in 18 patients (78.2 per cent), satisfactory results in four (17.4 per cent) and unsatisfactory in one patient (4.3 per cent) who had ongoing pain.

One case progressed to stage IIC, for which Evan’s procedure was done. Two patients required calcaneal screw removal due to undue implant prominence.

In our centre, we believe combined calcaneal osteotomy with FDL transfer provides good pain relief and satisfactory function in stage IIB PTTD.

 

Discussion

As the PTT weakens there is progressive collapse of the medial arch, placing additional stress on the supporting structures [33] like the spring ligament (especially the superomedial component) and deltoid ligament [21,35]. This leads to reduced height of the medial arch, increased load on the first metatarsal, plantar medial rotation of the talus, hindfoot valgus and forefoot abduction [34,35]. The Achilles tendon migrates laterally with the heel, causing it to act as an everter of the hindfoot. This leads to the axes of the talonavicular and calcaneocuboid joints becoming parallel to each other, thus uncoupling the mechanism of locking the transverse tarsal joints and preventing the formation of a rigid lever arm. Additionally, contracture in the Achilles tendon can lead to an equinus deformity.

Direct repair of the PTT was attempted earlier, but proved unsatisfactory [36,37]. Isolated tendon transfer augmentation, which initially showed good results, failed within a few years as it did not address the original deforming forces [38].

Gleich described a medial closing wedge calcaneal osteotomy in 1893 to restore the calcaneal pitch angle [39]. Koutsogiannis recommended a posterior calcaneal displacement osteotomy in 1971 [40]. Myerson described the MCDO with adjunctive FDL transfer in 1995. Since then numerous clinical and biomechanical studies have reported the success of this procedure [18]. FDL transfer restores medial arch stability and MDCO repositions the axis of the pull of the Achilles tendon medial to the subtalar joint. MDCO also helps to protect the transferred FDL tendon, off-loads the plantar surface of the first and second metatarsal heads and reduces the contact stresses in tibiotalar joint [18]. Brodsky et al. performed a prospective gait analysis on 12 patients who underwent this combination and found statistically significant improvement in cadence, stride length and ankle push-off [28]. Myerson et al. [29], Fayazi et al. [30], Wacker et al. [31], Guyton et al. [32], and Sammarco and Hockenbury each published retrospective reviews demonstrating a high rate of successful results with short to intermediate follow-up [21]. Alan et al., in their retrospective review of 24 patients, noted that patients who had PCDO with FDL transfer did significantly better than those without FDL transfer [41].

Lateral column lengthening was originally described for paediatric flatfoot [41] and this can be achieved by either a calcaneocuboid distraction arthrodesis or anterior calcaneal osteotomy. It causes adduction and plantar flexion of the midfoot, therefore correcting the deformity [43]. Some case series have shown the use of this procedure to treat stage II PTTD with satisfactory results [44,45]. However, complications like gait abnormality, lateral overload, graft failure/non-union and painful metal work were relatively high [45-48].

Double calcaneal osteotomy consists of MDCO and anterior calcaneal osteotomy using a tricortical graft [49,50]. It gives more anatomic correction and can treat all aspects of the stage II PTTD deformity [21]. One retrospective review showed a high rate of patient satisfaction with intermediate follow-up and considerable radiographic improvement with respect to the midfoot and forefoot [49]. Complications included removal of implants due to pain, calcaneocuboid arthritis and lateral foot overload [48]. Presently there is insufficient clinical evidence to make a specific recommendation for this procedure.

Subtalar arthroereises is the use of an implant to restrict eversion of the subtalar joint [51,52]. Originally described for paediatric flatfoot, it does not treat the aetiology of the deformity. Complications included foreign body reaction, implant failure, persistent sinus tarsi pain and osteonecrosis of the talus [53,54].

Joint sacrificing procedures such as subtalar arthrodesis, double arthrodesis and triple arthrodesis limit motion and increase the stresses on other joints. They are reserved as salvage procedures in stage II PTTD. One thing to bear in mind is the relative non-union rate of different joints in a triple arthrodesis. Making use of bone graft and meticulous technique is of paramount importance [55].

In our experience, the treatment of stage II PTTD with MDCO and FDL transfer at our centre gives consistent good to excellent results with low rates of complication, which matches the results in published literature.

 

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Authors:

M Salim – Foot/Ankle Fellow,

Harry Clark – Research Assistant,

Devangna Bhatia – Research Assistant,

Rajiv Limaye – Consultant Orthopaedic Surgeon, University Hospital of North Tees and Hartlepool, UK