Adult flatfoot refers to a deformity that develops after skeletal maturity is reached. Adult flatfoot should be differentiated from constitutional flatfoot, which is a common congenital non-pathologic foot morphology. There are numerous causes of acquired adult flatfoot, including fracture or dislocation, tendon laceration, tarsal coalition, arthritis, neuroarthropathy, neurologic weakness, and iatrogenic causes.
A person with flat feet has greater load placed on the posterior tibial tendon which is the main tendon unit supporting up the arch of the foot. Throughout life, aging leads to decreased strength of muscles, tendons and ligaments. The blood supply diminishes to tendons with aging as arteries narrow. Heavier, obese patients have more weight on the arch and have greater narrowing of arteries due to atherosclerosis. In some people, the posterior tibial tendon finally gives out or tears. This is not a sudden event in most cases. Rather, it is a slow, gradual stretching followed by inflammation and degeneration of the tendon. Once the posterior tibial tendon stretches, the ligaments of the arch stretch and tear. The bones of the arch then move out of position with body weight pressing down from above. The foot rotates inward at the ankle in a movement called pronation. The arch appears collapsed, and the heel bone is tilted to the inside. The deformity can progress until the foot literally dislocates outward from under the ankle joint.
The symptoms of PTTD may include pain, swelling, a flattening of the arch, and an inward rolling of the ankle. As the condition progresses, the symptoms will change. For example, when PTTD initially develops, there is pain on the inside of the foot and ankle (along the course of the tendon). In addition, the area may be red, warm, and swollen. Later, as the arch begins to flatten, there may still be pain on the inside of the foot and ankle. But at this point, the foot and toes begin to turn outward and the ankle rolls inward. As PTTD becomes more advanced, the arch flattens even more and the pain often shifts to the outside of the foot, below the ankle. The tendon has deteriorated considerably and arthritis often develops in the foot. In more severe cases, arthritis may also develop in the ankle.
First, both feet should be examined with the patient standing and the entire lower extremity visible. The foot should be inspected from above as well as from behind the patient, as valgus angulation of the hindfoot is best appreciated when the foot is viewed from behind. Johnson described the so-called more-toes sign: with more advanced deformity and abduction of the forefoot, more of the lateral toes become visible when the foot is viewed from behind. The single-limb heel-rise test is an excellent determinant of the function of the posterior tibial tendon. The patient is asked to attempt to rise onto the ball of one foot while the other foot is suspended off the floor. Under normal circumstances, the posterior tibial muscle, which inverts and stabilizes the hindfoot, is activated as the patient begins to rise onto the forefoot. The gastrocnemius-soleus muscle group then elevates the calcaneus, and the heel-rise is accomplished. With dysfunction of the posterior tibial tendon, however, inversion of the heel is weak, and either the heel remains in valgus or the patient is unable to rise onto the forefoot. If the patient can do a single-limb heel-rise, the limb may be stressed further by asking the patient to perform this maneuver repetitively.
Non surgical Treatment
Medical or nonoperative therapy for posterior tibial tendon dysfunction involves rest, immobilization, nonsteroidal anti-inflammatory medication, physical therapy, orthotics, and bracing. This treatment is especially attractive for patients who are elderly, who place low demands on the tendon, and who may have underlying medical problems that preclude operative intervention. During stage 1 posterior tibial tendon dysfunction, pain, rather than deformity, predominates. Cast immobilization is indicated for acute tenosynovitis of the posterior tibial tendon or for patients whose main presenting feature is chronic pain along the tendon sheath. A well-molded short leg walking cast or removable cast boot should be used for 6-8 weeks. Weight bearing is permitted if the patient is able to ambulate without pain. If improvement is noted, the patient then may be placed in custom full-length semirigid orthotics. The patient may then be referred to physical therapy for stretching of the Achilles tendon and strengthening of the posterior tibial tendon. Steroid injection into the posterior tibial tendon sheath is not recommended due to the possibility of causing a tendon rupture. In stage 2 dysfunction, a painful flexible deformity develops, and more control of hindfoot motion is required. In these cases, a rigid University of California at Berkley (UCBL) orthosis or short articulated ankle-foot orthosis (AFO) is indicated. Once a rigid flatfoot deformity develops, as in stage 3 or 4, bracing is extended above the ankle with a molded AFO, double upright brace, or patellar-tendon-bearing brace. The goals of this treatment are to accommodate the deformity, prevent or slow further collapse, and improve walking ability by transferring load to the proximal leg away from the collapsed medial midfoot and heel.
If conservative treatment fails surgical intervention is offered. For a Stage 1 deformity a posterior tibial tendon tenosynovectomy (debridement of the tendon) or primary repair may be indicated. For Stage 2 a combination of Achilles lengthening with bone cuts, calcaneal osteotomies, and tendon transfers is common. Stage 2 flexible PTTD is the most common stage patients present with for treatment. In Stage 3 or 4 PTTD isolated fusions, locking two or more joints together, maybe indicated. All treatment is dependent on the stage and severity at presentation with the goals and activity levels of the patient in mind. Treatment is customized to the individual patient needs.