Adult acquired flatfoot deformity, primarily posterior tibial tendon dysfunction, in many cases can be successfully managed with conservative treatment modalities including early immobilization, long-term bracing, physi?cal therapy, and anti-inflam?matory medications. Adult acquired flatfoot deformity (AAFD), the painful flatfoot deformity in adults, is a major cause of disability for a patient and can be a challenge for foot and ankle specialists.
Causes of an adult acquired flatfoot may include Neuropathic foot (Charcot foot) secondary to Diabetes mellitus, Leprosy, Profound peripheral neuritis of any cause. Degenerative changes in the ankle, talonavicular or tarsometatarsal joints, or both, secondary to Inflammatory arthropathy, Osteoarthropathy, Fractures, Acquired flatfoot resulting from loss of the supporting structures of the medial longitudinal arch. Dysfunction of the tibialis posterior tendon Tear of the spring (calcaneoanvicular) ligament (rare). Tibialis anterior rupture (rare). Painful flatfoot can have other causes, such as tarsal coalition, but as such a patient will not present with a change in the shape of the foot these are not included here.
Your feet tire easily or become painful with prolonged standing. It’s difficult to move your heel or midfoot around, or to stand on your toes. Your foot aches, particularly in the heel or arch area, with swelling along the inner side. Pain in your feet reduces your ability to participate in sports. You’ve been diagnosed with rheumatoid arthritis; about half of all people with rheumatoid arthritis will develop a progressive flatfoot deformity.
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.
Until recently, operative treatment was indicated for most patients with stage 2 deformities. However, with the use of potentially effective nonoperative management , operative treatment is now indicated for those patients that have failed nonoperative management. The principles of operative treatment of stage 2 deformities include transferring another tendon to help serve the role of the dysfunctional posterior tibial tendon (usually the flexor hallucis longus is transferred). Restoring the shape and alignment of the foot. This moves the weight bearing axis back to the center of the ankle. Changing the shape of the foot can be achieved by one or more of the following procedures. Cutting the heel bone and shifting it to the inside (Medializing calcaneal osteotomy). Lateral column lengthening restores the arch and overall alignment of the foot. Medial column stabilization. This stiffens the ray of the big toe to better support the arch. Lengthening of the Achilles tendon or Gastrocnemius. This will allow the ankle to move adequately once the alignment of the foot is corrected. Stage 3 acquired adult flatfoot deformity is treated operatively with a hindfoot fusion (arthrodesis). This is done with either a double or triple arthrodesis – fusion of two or three of the joints in hindfoot through which the deformity occurs. It is important when a hindfoot arthrodesis is performed that it be done in such a way that the underlying foot deformity is corrected first. Simply fusing the hindfoot joints in place is no longer acceptable.