Posterior tibial tendon insufficiency is the most common cause of acquired adult flatfoot deformity. Although the exact etiology of the disorder is still unknown, the condition has been classified, on the basis of clinical and radiographic findings, into four stages. In stage I, there is no notable clinical deformity; patients usually present with pain along the course of the tendon and evidence of local inflammatory changes. Stage II is characterized by a dynamic deformity of the hindfoot. Stage III involves a fixed deformity of the hindfoot and typically also a fixed forefoot supination deformity but no obvious evidence of ankle abnormality. In stage IV, ankle involvement is secondary to long-standing fixed hindfoot deformities. The initial treatment of patients in any stage should be nonoperative, with immobilization, a nonsteroidal anti-inflammatory drug, and perhaps an orthotic device. Corticosteroid injections continue to be controversial. When nonoperative management fails, the treatment options consist of soft-tissue procedures alone or in combination with osteotomy or arthrodesis. Stage I insufficiency is generally treated with debridement and tenosynovectomy. Soft-tissue transfer does not appear to correct the underlying deformity in stage II disease; however, there is growing interest in joint-sparing operations that attempt to compensate for the underlying deformities with osteotomies or arthrodeses, supplemented with dynamic transfers to replace the insufficient posterior tibial tendon. Subtalar, double, or triple arthrodesis is the procedure of choice for stage III disease, frequently in conjunction with heel-cord lengthening. Tibiocalcaneal arthrodesis or pantalar arthrodesis is most commonly used to treat stage IV disease.
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Posterior tibial tendon insufficiency is the most common cause of acquired adult flatfoot deformity. Although the exact etiology of the disorder is still unknown, the condition has been classified, on the basis of clinical and radiographic findings, into four stages. In stage I, there is no notable clinical deformity; patients usually present with pain along the course of the tendon and evidence of local inflammatory changes. Stage II is characterized by a dynamic deformity of the hindfoot. Stage III involves a fixed deformity of the hindfoot and typically also a fixed forefoot supination deformity but no obvious evidence of ankle abnormality. In stage IV, ankle involvement is secondary to long-standing fixed hindfoot deformities. The initial treatment of patients in any stage should be nonoperative, with immobilization, a nonsteroidal anti-inflammatory drug, and perhaps an orthotic device. Corticosteroid injections continue to be controversial. When nonoperative management fails, the treatment options consist of soft-tissue procedures alone or in combination with osteotomy or arthrodesis. Stage I insufficiency is generally treated with debridement and tenosynovectomy. Soft-tissue transfer does not appear to correct the underlying deformity in stage II disease; however, there is growing interest in joint-sparing operations that attempt to compensate for the underlying deformities with osteotomies or arthrodeses, supplemented with dynamic transfers to replace the insufficient posterior tibial tendon. Subtalar, double, or triple arthrodesis is the procedure of choice for stage III disease, frequently in conjunction with heel-cord lengthening. Tibiocalcaneal arthrodesis or pantalar arthrodesis is most commonly used to treat stage IV disease.
Copyright remains with the authors and publisher.