Adult acquired flatfoot deformity (AAFD) is characterized by flattening of the longitudinal arch, increased forefoot abduction, and hindfoot valgus. Patients experience pain and a decline in foot function, with a painful, apropulsive gait. Appropriate nonoperative management can lead to decreased symptoms and functional improvement.
Initial treatment of stage 1 and 2 AAFD
Treatment of stage 3 and 4 AAFD in patients unwilling or unable to undergo surgical correction
Persistent pain and disability despite 3 to 6 months of treatment
Inability to tolerate conservative care (i.e., orthoses)
Progressive deformity despite appropriate care
Stage 1—Medial ankle pain, swelling. No deformity.
Stage 2—Arch flattening, hindfoot valgus, forefoot abduction. Correctable deformity.
Stage 3—Progressive, rigid deformity.
Stage 4—Valgus talar tilt, ankle arthrosis
HISTORY/INTRODUCTION/SCOPE OF THE PROBLEM
Adult acquired flatfoot deformity (AAFD) is a progressive disorder, causing pain and disability. In 1924, Dudley Morton stated that “no other disorder can compare with arch trouble in its baneful influence upon the working efficiency and welfare of the individual, mentally or physically.” Previously described as posterior tibial tendon insufficiency, AAFD is characterized by flattening of the medial longitudinal arch, hindfoot valgus, and forefoot abduction. This, in turn, produces a painful, apropulsive gait. There are many causes of AAFD, including posterior tibial tendon (PTT) insufficiency, arthritis, trauma, Charçot arthropathy, neuromuscular imbalance, seronegative inflammatory disorders, and corticosteroid injections.
Both static and dynamic structures play an important role in stability of the arch. Earlier studies have focused on the PTT as the main contributor to arch stability. Development of a painful flatfoot deformity is multifactorial, however, with degeneration of the PTT being only a part of the spectrum of the disease. Yeap et al. looked at 17 patients at a mean of 5.3 years after transfer of the posterior tibial tendon to the dorsum of the foot to regain active dorsiflexion. While 30% had mild flattening of the arch, none had a clinically significant flatfoot. Similarly, asymptomatic flatfoot may be a predisposition to the development of AAFD.
Functionally, the medial longitudinal arch consists of the calcaneal tuberosity, talus, sustentaculum tali, calcaneonavicular (spring) ligament, navicular, cuneiforms, and medial metatarsals. As weight is applied to the foot, the plantar ligaments become tight, which Van Borum et al. likens to function as an “upside-down leaf spring.” Both dynamic and static structures play a role in support of the arch.
The PTT has been shown to be the predominant dynamic supporter of the arch. With respect to the subtalar joint, the posterior tibial tendon has been shown to have a long moment arm, giving it greater mechanical advantage over the other hindfoot inverters in resisting flattening of the arch and pronation of the hindfoot. Thordarson and colleagues found the posterior tibial tendon to have the most significant arch-supporting function of the extrinsic tendons, with lesser contributions from the flexor hallucis longus, flexor digitorum longus, and peroneal longus. Loading of a cadaveric foot and its extrinsic tendons, without activation of the posterior tibial tendon, produces a tendency toward flattening. This tendency is reversed with loading of the posterior tibialis, suggesting an important role in arch maintenance. However, Hisateru et al., in a cadaveric study, looked at the effect of posterior tibial tendon release in an intact foot under cyclical loading to simulate gait. Initially, the osteoligamentous anatomy prevented flattening of the arch. After creation of a flatfoot through ligament attenuation and cyclical loading of the foot, restoration of posterior tibial tendon function was unable to restore normal hindfoot kinematics, demonstrating the importance of static restraints in arch stability.
The static support of the arch is supplied by the plantar aponeurosis, long plantar, short plantar, deltoid, and spring ligaments. The effect of the plantar fascia on arch stability is increased through the windlass mechanism. Division of the plantar fascia increases strain in the spring ligament and long planter ligament by 52% and 94%, respectively. The spring ligament complex is severely affected in AAFD and is often found torn or elongated on examination at surgery. Attenuation of the spring ligament allows the talus to plantar flex and adduct, and the remainder of the forefoot abducts around the head of the talus.
Hypermobility of the medial column, in conjunction with a contracture of the gastrocnemius muscle or triceps surae, has been implicated in development of AAFD. The triceps surae has the most significant arch-flattening effect of the posterior muscles. Isolated contracture of the triceps surae places increased stress on the forefoot and, thus, the arch itself. With a hypermobile medial column, this promotes further weakening and attenuation of the plantar ligaments, leading to progressive loss of the arch. As the arch continues to collapse, the talus subluxes anteriorly on the calcaneus. The midfoot subluxes dorsally and laterally around the head of the talus, a term coined dorsolateral peritalar subluxation. The heel goes into valgus, and the midfoot and forefoot assume an abducted position.
Patients with severe AAFD demonstrate decreased stride length, walking speed, and cadence, with a prolonged stance phase. The hindfoot remains maximally everted throughout stance phase, decreasing the shock absorption capability of the foot. If the hindfoot is unable to invert, the transverse tarsal joint remains unlocked and the foot is unable to form a rigid lever arm. Progression to heel rise is delayed and forward progression is decreased.
Patients with AAFD often present with complaints of vague, unilateral pain on the medial aspect of the ankle. The pain worsens throughout the day and with activity and is relieved with rest. In more advanced cases, lateral symptoms predominate, as the lateral process of the talus bottoms out in the sinus tarsi and the calcaneus impinges on the peroneal tendons and the fibula.
AAFD has been associated with hypertension, obesity, diabetes mellitus, seronegative spondyloarthropathies, and exposure to steroids. A history of foot or ankle trauma should be sought. Neurologic disorders such as cerebral palsy, stroke, closed head injury, or peripheral nerve injuries have been known to cause AAFD. Dysfunction relative to the L4-5 pathways is frequently noted.
The physical examination should begin with evaluation of the patient standing ( Figs. 28-1 and 28-2 ). The amount of valgus in the hindfoot and the “too-many-toes sign” is noted. When viewed from the front, the amount of collapse of the arch is evaluated. Observation of the patient’s gait demonstrates an antalgic, foot flat, apropulsive gait. Performing a single leg heel raise will be difficult, or impossible. Performing multiple heel rises may be a more sensitive indicator of PTT dysfunction.
Next, the foot is inspected for callosities. Callous under the second and third metatarsal head may be indicative of first ray dorsal hypermobility. Abnormal callous may be present along the medial midfoot at the navicular tuberosity. Swelling and tenderness along the posterior tibial tendon are noted. A thorough motor and neurovascular examination is then performed.
Range of motion of the foot and ankle is assessed. The mobility of the medial column is then evaluated. The first ray is then dorsiflexed and plantarflexed. More than 8 to 10 mm of sagittal plane motion is consistent with hypermobility. The subtalar joint is then held in neutral, and residual varus of the forefoot is noted. Ankle dorsiflexion is assessed through the Silverskiőld test. An equinus contracture with the leg extended, which is corrected with the knee bent, indicates an isolated gastrocnemeus contracture. If the equines does not correct with knee flexion, then a combined gastrocsoleus contracture is present.
While the diagnosis of AAFD is made by clinical examination, standard radiographs are performed to further delineate the magnitude and location of the deformity. Weight-bearing anteroposterior (AP) and lateral radiographs of the foot are performed, in addition to an AP ankle radiograph ( Figs. 28-3 and 28-4 ). The amount of deformity is determined by measuring the talo–first metatarsal angle on both the AP and lateral radiographs, noting also the location of the deformity. On the AP foot radiograph, the talonavicular coverage angle is determined.
On the AP ankle radiograph, impingement of the calcaneus on the fibula can be seen in advanced cases, as well as signs of arthrosis and tilt of the talus in the mortise. Hindfoot alignment views can be obtained to evaluate coronal displacement of the hindfoot in relation to the distal tibia. In cases of previous trauma, full-length tibia films and full-leg mechanical axis views can be beneficial.
PTT dysfunction was classified by Johnson and Strome in 1989. They described a continuum of three stages. Stage 1 is characterized by medial ankle pain and swelling without deformity. Patients are able to do a single-leg heel rise. The PTT is in continuity, with some degeneration. In stage 2, there is increased pain. Deformity is now present. The hindfoot is in valgus, collapse of the arch is noted, and a variable amount of forefoot abduction is present. The PTT is elongated or ruptured, and patients are unable to do a single-leg heel rise. Stage 3 demonstrates progressive deformity, which is now rigid. The pain may be medial or lateral secondary to impingement in the sinus tarsi or calcaneofibular abutment. Myerson added a stage IV to the classification, with valgus tilt of the talus in the mortise and early degeneration of the ankle.