Tibialis posterior muscle arises from the posterior aspect of the tibia and fibula and from the interosseous membrane. PTT passes immediately behind the medial malleolus, through a fibrous tunnel which is covered by the flexor retinaculum. After contouring the malleolus, the tendon begins to fan out. It has a wide insertion including the navicular, the sustentaculum tali, first cuneiform bones, and the bases of the second, third, and fourth metatarsals. The PTT is an important dynamic stabilizer of the medial arch and the most powerful inverter of the foot (Gluck et al. 2010). The spring ligament complex is the static soft tissue support of the talonavicular joint and also plays a key role in its biomechanics (Boss and Hintermann 2002). The PTT does not have a mesotenon.

A retromalleolar hypovascular region (Fig. 34.1) has been observed and can be implicated in degenerative changes of the tendon (Frey et al. 1990; Manske et al. 2015). The posterior tibial tendon is usually supplied by two vessels entering the tendon approximately 4.5 cm proximal and 2.0 cm distal to the medial malleolus (Manske et al. 2015).

Inflammatory, degenerative, functional, and traumatic processes might lead to PTT dysfunction at different levels (Yao et al. 2015). Inflammatory diseases (e.g., lupus or rheumatoid arthritis) are more common in younger patients (Myerson 1997; Otis and Gage 2001). Chronic overuse and consequent tendon deterioration have been noticed to occur more often and more frequently in late to middle age, women, and obese (Myerson 1997; Otis and Gage 2001). However, degeneration due to overtraining with repetitive microtrauma has also been described among young athletes, particularly in running and sports requiring repeated and rapid changes in direction (Ribbans and Garde 2013; Supple et al. 1992). Inflammatory changes, tendon tears, and tenosynovitis have been connected to activity levels around 1500 to 2000 cycles per hour (Bare and Haddad 2001).

Other risk factors include hyperpronation or anomalous anatomy, ligamentous laxity, diabetes mellitus, hypertension, and corticosteroid therapy (Yao et al. 2015). Moreover, Probasco et al. recently stated that an increased valgus orientation of the subtalar joint is more frequent among patients with adult acquired flatfoot when compared to controls (Probasco et al. 2015). Acute trauma is rarely the cause of tendon dysfunction or rupture (Trnka 2004).

The precise mechanisms leading to PTT degeneration remain unclear. The combination of the hypovascular zone and abnormal mechanical forces experienced behind the medial malleolus where the tendon acutely changes direction in several activities might play a role (Trnka 2004).

A patient suffering from PTT tendinopathy might refer isolated posteromedial ankle pain. The natural history is usually slow, with insidious onset of complaints which can cause delay in searching for assistance. However, on clinical examination one can find local tenderness, medial pain (sometimes irradiating to the calf), positive PTT provocation test, or inability to walk on tiptoes. Over time, patients may notice progressive collapse of the medial longitudinal arch (acquired flatfoot) and increased hindfoot valgus. The shoe soles may show signs of increased wear on the medial side, and they may report difficulty standing on their toes due to pain and weakness.

Pain usually worsens with walking and progressively affects sports and activities of daily living (Trnka 2004). On later stages of the disease, patients often report that pain shifts laterally as the fibula begins to impinge against the calcaneus while the medial pain often disappears (Yao et al. 2015). At these stages sports activities are severely compromised if possible at all.

Examination (Fig. 34.2) should begin with inspection through all sides while standing (including podoscope for plantar view). The examiner should search for increased valgus angulation of the hindfoot and abduction of the forefoot. Both these features are reflected in a positive “too many toes” sign, in which more toes are visible on the lateral side of the affected foot when viewed from behind given the increased hindfoot valgus and forefoot abduction (Johnson 1983).

Next, the “heel-rise test” (Fig. 34.2) is performed to assess severity of the condition (Johnson 1983). The patient is asked to attempt to rise onto the ball of the affected foot while keeping the contralateral foot lifted off the ground. The normal foot is also tested for comparison. A positive test is considered if the affected hindfoot will either remain in valgus abduction during the heel raise (once the PTT fails to invert it) or the patient will refer important pain limiting this movement. It might be required to repeat the test a few times for proper assessment. Hintermann and Gächter have described another useful test: the first metatarsal rise sign (Hintermann and Gachter 1996). The patient is asked to stand in full weight bearing on both feet. The examiner will then externally rotate the shin of the affected foot with one hand. In the presence of marked PTT insufficiency, the head of the first metatarsal will be lifted off the floor (fixed supination of the first ray).

Subsequent clinical examination can be managed with the patient seated. The PTT should be palpated throughout its course to assess for a palpable gap, crepitation, tenderness, or swelling. The lateral side of the foot should also be palpated once subfibular tenderness may be an indication of calcaneofibular impingement. Palpation and strength assessment should be repeated with resisted inversion and compared to the opposite side. The foot is held in slight plantarflexion and eversion to isolate the posterior tibialis from the synergistic action of tibialis anterior (Myerson and Corrigan 1996). The patient is then asked to invert and further plantarflex the foot against resistance, while the examiner palpates for the posterior tibialis tendon to determine its integrity and the painful site. The mobility of the ankle and the subtalar joint should be carefully assessed given the implication in the method of treatment. Range of motion at the subtalar joint will progressively decrease with the progression of the condition, and eventually the hindfoot will assume a fixed valgus deformity. The forefoot and midfoot will try to compensate for this by progressively adopting a supinated position, which is best appreciated with the heel in a neutral position. This is another critical part of the examination because a fixed supination deformity of the forefoot is an important consideration in the subsequent selection of treatment (Yao et al. 2015).

It is also mandatory to assess the Achilles tendon for contracture. This is often associated with chronic hindfoot valgus once the Achilles tendon adopts an abnormal position lateral to the axis of the subtalar joint, leading to tendon shortening over time (Yao et al. 2015).

Radiographies assess global foot and ankle morphology and alignment and are helpful in later stages of these disorders. In early stages, they are often normal.

Standing anteroposterior and lateral view (Fig. 34.2) radiographs of both feet and ankles as well as mortise views of the ankle joint should be ordered. The collapse of the longitudinal arch on a lateral weight-bearing radiograph might be noticed in any of the following measurements, especially if asymmetric: calcaneal inclination angle (angle between the calcaneal inclination axis and the supporting surface, considered low if less than 20°), talometatarsal angle (angle between the axis of the talus and the axis of the first metatarsal, normally between 0° and 10°), or the distance of the medial cuneiform from the floor (normally between 15 and 25 mm) (Slovenkai 1997).

Uncovering of the talar head might be recognizable on an anteroposterior view. With increased forefoot abduction deformity, the navicular slides laterally, leading to subluxation of the talonavicular joint which is abnormal if more than 15% of the talar head is uncovered (Slovenkai 1997). Plain radiographs might also show talar tilt; calcaneofibular impingement; arthritic changes of the tibiotalar, subtalar, and talonavicular joints; and signs of enthesopathy in the form of bony irregularities and hypertrophic changes at the navicular insertion site of the posterior tibialis tendon (Kong and Van Der Vliet 2008).

MRI (Fig. 34.3) and ultrasound, despite known limitations in low-grade PTT disease, are useful in identifying different pathologies, such as tenosynovitis (longitudinal) ruptures, degenerative changes, or adhesions (Cooper et al. 2007; Lhoste-Trouilloud 2012). Moreover, MRI can be useful in identifying spring and deltoid ligament injuries (Kong and Van Der Vliet 2008; Nallamshetty et al. 2005).

CT scan is useful in identifying bone ossicles (Fig. 34.3) and deformities, namely, secondary to fractures which might cause persistent damage to the tendon (Kong and Van Der Vliet 2008).

When dealing with diagnosis of PTT disorders, one must also consider and rule out subtalar arthritis, Müller-Weiss disease, Lisfranc joint pathology, consequences of fractures or bone ossicles, PTT subluxation, coalition, Charcot arthropathy, spring ligament injury, and deltoid ligament injury.

Johnson and Strom proposed a classification system correlating the severity of PTT dysfunction and subsequent adaptations of the foot to treatment recommendations (Johnson and Strom 1989). This classification was further refined by Myerson (Myerson 1997) and Bluman (Bluman et al. 2007) (Table 34.1 summarizes one of the most popular classification systems). Further classifications have been proposed, and all try to correlate major clinical findings and treatment options (Haddad et al. 2011). Treatments of PTT disorders include conservative and surgical options depending on the severity of the condition.

In the early stages of the disease, conservative treatment is recommended. This comprises modification of activity, cryotherapy, physiotherapy, medication, insoles, corrective shoes (medial heel and sole wedge), and orthosis (Kulig et al. 2009).

In common patients, when a trial of 3–6 months of conservative treatment has failed with progression of symptoms (Ribbans and Garde 2013; Bare and Haddad 2001), tendoscopy represents an option with increased popularity (Khazen and Khazen 2012; van Dijk et al. 1997). Tendoscopy (Fig. 34.4) is considered in grade I (Khazen and Khazen 2012; Chow et al. 2005; van Dijk et al. 1997) and selected cases of early grade II cases (Lui 2007). However, one must consider that particularly in patients with inflammatory diseases, the process of tendon degradation secondary to synovitis might be more aggressive, and surgical treatment is considered earlier (6-week trial of conservative treatment) (Myerson et al. 1989).

More complex approaches include the combined treatment of spring and deltoid ligaments as recently described by Lui et al. (Lui 2015, 2016a). Posterior arthroscopic approach (Fig. 34.3) has also been described and might also be used for the removal of bone ossicles in post-traumatic cases (Hua et al. 2015). However, these approaches should be further validated by clinical evidence before widespread recommendation.

Currently, indications for posterior tibial tendon tendoscopy (van Dijk et al. 1997; Pereira et al. 2014) include:

PTT tendoscopy enables diagnostic confirmation of symptomatic partial tendon tear (false positives and false negatives have been described on MRI and ultrasound) (van Sterkenburg et al. 2010b). Partial tendon tears can be definitively treated endoscopically. However, if that is not the case, it will help to diminish open surgical approach thus contributing in the worst-case scenario to lower the incision, diminish postoperative pain, and contribute to earlier rehabilitation. The tendoscopic procedure can be converted to a “guided” mini-open approach, which is still less invasive than the standard open procedure (Pereira et al. 2014).

The tibialis anterior muscle (Fig. 34.7) originates from the lateral tibial condyle and interosseous membrane. The musculotendinous junction occurs at the transition of the middle and distal thirds of the tibia. The ATT has its main insertions at the medial cuneiform and the inferomedial base of the first metatarsal; however, different types of distal insertions have been described in the literature (Varghese and Bianchi 2014). The ATT courses within a synovial sheath during most of its course, deep to the extensor retinaculum of the ankle and foot. It is the strongest dorsiflexor of the foot (accounts for more than 80% of the strength required for this movement) while also contributing to inversion (Ouzounian and Anderson 1995). It also controls deceleration of the foot after heel strike. It is innervated by the deep peroneal nerve. Peterson et al. described a zone of hypovascularity (Petersen et al. 2000); however, Geppert et al. had opposed to this theory stating that ATT has no sustainable hypovascular zones (Geppert et al. 1993). It receives vascular supply from the anterior tibial artery proximally and the medial tarsal arteries distally. The ATT’s bursa is found close to its insertion, between the tibialis anterior tendon and the medial cuneiform bone.