The Flexible Flatfoot in the Adults
The adult acquired flatfoot deformity is characterized by flattening of the medial longitudinal arch with insufficiency of the supporting posteromedial soft tissue structures of the ankle and hindfoot.
Although the etiology of this deformity can be arthritic or traumatic in nature, it is most commonly associated with posterior tibial tendon dysfunction (PTTD). Developmental etiologies also may be responsible for a flexible flatfoot deformity. These include conditions associated with soft tissue laxity (Ehlers-Danlos and Marfan syndromes), accessory navicular, and neuro-muscular diseases. Extrinsic factors are less common but can result from trauma involving the medial structures in an eversion type injury.
Two potential mechanical causes of an acquired flatfoot deformity include medial column instability and a contracture of the Achilles tendon or gastrocnemius fascia. With the former, medial column instability results in forefoot varus and a compensatory hindfoot valgus. With the latter, a tight Achilles tendon or gastrocnemius fascia results in transmission of dorsiflexion forces from the ankle to the transverse tarsal joint and midfoot. This leads to midfoot collapse and hindfoot valgus with lateral peritalar subluxation of the navicular and subfibular impingement.
An acquired flexible flatfoot deformity is most often associated with Posterior Tibial tendon (PTT) dysfunction. Biomechanic overloading as described above can lead to chronic microtrauma in the tendon. With advancing age, the tendon’s elastic compliance decreases because of changes in collagen structure, thus creating a pathologic sequence where tendon weakening results in failure of the static stabilizers of the arch. Poor blood supply may initiate this process or may prevent an adequate healing response, resulting in chronic inflammation, tenosynovitis, and tendinosis.
Patients usually complain of medial ankle and hindfoot pain that radiates to the arch of the foot or proximally to the leg. As the deformity progresses, there may be a complaint of lateral or sinus tarsi pain caused by subfibular impingement. Although some patients will attribute a nonspecific traumatic event to the pain, most patients will relate a gradual onset of the pain with loss of the medial plantar arch over recent months or years.
On physical examination, it is helpful to evaluate the patient in short pants with both shoes off. This allows the clinician to note the alignment of not only the foot and ankle, but also the knee. With genu valgus, an individual’s center of gravity may be altered and more load may be placed on the medial ankle and PTT. Comparison of tread wear on the shoes may reveal more posteromedial wear than the opposite side. On examination of the standing patient from behind, the presence of hindfoot valgus can be noted and measured, and the “too many toes” sign can be identified. The patient should be asked to perform a double leg heel rise so that the presence or absence of hindfoot inversion can be identified. Next, the patient is asked to perform a single leg heel rise on the affected side noting that inability to do so is consistent with PTTD.
Examination sitting should include assessment of ankle and subtalar range of motion. Ankle motion should be measured with the knee extended and flexed with the transverse tarsal joint locked and unlocked. This will allow the examiner to assess for Achilles tendon and gastrocnemius contractures. Palpation of the posteromedial ankle and hindfoot may reveal tenderness, swelling, or fullness. The sinus tarsi, talar dome, and navicular tuberosity should be palpated. Callus formation over the subluxated talar head may be noted. For patients who have a flexible flatfoot, reduction of the talonavicular joint and correction of the hindfoot valgus/forefoot abduction is possible. Lastly, the PTT strength is tested with resistance against the inverted and plantarflexed foot.
Clinical examination and radiographs (in weight bearing Position) are usually sufficient to establish the diagnosis of PTTD. In certain instances, however, the use of MRI can be helpful to confirm the diagnosis, evaluate the amount of pathology in the PTT and spring ligament complex, and detect bone edema.
STAGES of PTTD
Stage I consists of painful synovitis of the tendon. Nevertheless, tendon length and function are maintained so there is no deformity.
Stage II disease, there is progressive tendon dysfunction and a flexible flatfoot deformity develops.
Stage III involves a rigid deformity with stiffness and often arthritis of the midfoot and hindfoot.
Stage IV consists of tibiotalar valgus, usually with associated arthritic changes.
The stage and progression of the flatfoot deformity will generally determine the degree and duration of the conservative treatment. The initial treatment of the adult flexible flatfoot deformity (stage II PTTD) focuses on improving symptoms by decreasing the forces transmitted through the posteromedial hindfoot. The patient should be encouraged to lose weight, modify repetitive loading activities, and use supportive shoes.
(Eric Giza, MDa,*, Gerard Cush, MDb, Lew C. Schon, MD)