Definition

The tibialis posterior muscle, originating from the proximal tibia and fibula, passes distally with a broad insertion on the plantar aspect of the navicular, cuneiform, cuboid, and metatarsal bases and normally functions to invert the subtalar joint and to adduct the forefoot. Its principal antagonist is the peroneus brevis, which normally everts the subtalar joint and abducts the forefoot. Posterior tibial tendon dysfunction is a condition, as its name suggests, that is characterized by the loss of function of the posterior tibial tendon. This disabling problem may be caused by trauma, degeneration, or inflammatory arthritides and is most commonly seen in late middle-aged, obese women. These pathologic processes can lead to reduction of effective excursion of the tendon or even rupture, resulting in progressive loss of the medial arch, midfoot abduction, and forefoot pronation. Additional risk factors include obesity, diabetes, hypertension, ligamentous laxity, steroid use, and previous involvement in high-impact sports. Posterior tibial tendon dysfunction is the most common cause of acquired flatfoot in the adult. Usually, posterior tibial tendon dysfunction is a chronic, progressive process, but spontaneous rupture can occur in patients receiving long-term steroid therapy or after trauma.

In regard to pathophysiology, the posterior tibial tendon functions in concert with the gastrocnemius-soleus complex to stabilize the hindfoot. The longitudinal arch is stabilized primarily by bone articulations and ligamentous structures (spring ligament, talocalcaneal interosseous ligament, superficial deltoid) and only secondarily supported by the posterior tibial tendon. The initial pathologic change is typically tendinosis of the posterior tibial tendon with maintenance of the longitudinal arch. As the tendon becomes less efficient, more stress is placed on the medial ligamentous structures, which attenuate, leading to progressive loss of the arch and abduction of the midfoot. The posterior tibial tendon begins to atrophy while the flexor digitorum longus hypertrophies in an attempt to compensate. Next, the calcaneus will drift into a valgus malalignment, changing the lever arm of the Achilles and causing a heel cord contracture. Finally, the peroneus brevis becomes an unopposed antagonist and exacerbates the deformity.

Symptoms

Patients, most commonly middle-aged women, primarily complain of pain on the inner or medial aspect of the ankle and the hindfoot. As the insufficiency progresses, pronation increases, leading to pain over the dorsolateral aspect of the midfoot. Typically, this results in a gradual loss of the arch associated with a corresponding increase in pain.

Rarely, there is a history of a rapid collapse from rupture after an acute injury. There have been only six reported cases in the literature of athletes (basketball players and runners) younger than 30 years with acute posterior tibial tendon ruptures.

Physical Examination

The physical examination reveals swelling confined to the area around the medial malleolus. In general, there is tenderness along the course of the tendon, and there may be exquisite tenderness just distal to the medial malleolus where the tendon most commonly tears.

Assessment of the lower extremity in the weight-bearing position best demonstrates the essential elements of the deformity: valgus hindfoot (calcaneovalgus), midfoot abduction, and forefoot pronation. This complex deformity clinically demonstrates a “too many toes” sign, that is, when the feet are viewed from behind, there appear to be more toes on the affected side than on the unaffected side. The severity of the patient’s presentation depends on the chronicity of the insufficiency and the magnitude of the tendon dysfunction. The medial longitudinal arch of the foot may be entirely lost.

The anterior tibial tendon may become more visible than on the normal side as the patient, subconsciously, tries to regain the arch. Patients may have difficulty walking on their tiptoes or have difficulty performing a one-sided toe-stand while holding on to the clinician’s hands. The heel fails to invert into a varus position. Asking the patient to invert the plantar-flexed foot against resistance can be overcome by the clinician’s hand. Assessment of the patient on the couch reveals altered posture of the foot due to the unopposed action of the peroneus brevis. A callosity can be seen in the region of the medial plantar aspect of the midfoot.

Posterior tibial tendon dysfunction can be classified in three stages that are correlated to the treatment. Stage I is a tenosynovitis, normal tendon function, and no deformity. Stage II is a spectrum of disease that includes tendinosis but also posterior tibial tendon dysfunction and weakness. Loss of the medial arch and progressive valgus of the heel with mild lateral impingement can be seen. Early in stage II, the patient may be able to perform a single heel raise, but as this stage progresses, this function is lost. Most important, the flexibility of the foot is maintained with nearly normal subtalar, midtarsal, and forefoot motion. This continuum of disease may progress to stage III as the deformity becomes more rigid and subtalar degeneration occurs with subsequent decreased motion. Lateral tenderness is present because of impingement of the distal fibula on the calcaneus. A heel cord contracture is also apparent in most cases.