Scheuermann ’ s Kyphosis : Diagnosis , Management , and Selecting Fusion Levels

Scheuermann’s kyphosis (SK) is a rigid structural deformity of the thoracic spine defined radiographically as three or more contiguous vertebrae with at least 5 of wedging anteriorly. Prevalence of the disease is thought to be between 0.4% and 10%. The true cause of SK remains unclear; however, various theories include growth irregularities, mechanical factors, genetic factors, and/or poor bone quality as the causes. Patients with mild disease (less than 70 ) generally have a favorable prognosis with good clinical outcomes. Most patients with SK are successfully treated nonsurgically with observation, anti-inflammatory medications, and physical therapy. Surgical intervention is indicated in patients with greater than 70 to 75 thoracic curves, greater than 25 to 30 thoracolumbar curves, intractable pain, neurologic deficit, cardiopulmonary compromise, or poor cosmesis. Because of advances in posterior spinal instrumentation, surgery can typically be performed through a posterior-only approach. When surgical treatment is planned, appropriate selection of the upperand lower-instrumented vertebrae is important to achieve a wellbalanced spine, preserve motion segments, and reduce the risk of junctional kyphosis. Scheuermann’s kyphosis (SK) is a rigid spinal kyphosis affecting the mid-thoracic or thoracolumbar spine, which was first described by Holger Werfel Scheuermann in 1920.1,2 The condition is associated with anterior wedging of the vertebrae, end plate irregularities, and Schmorl’s nodes.3 In 1964, Sorensen4 was the first to define SK radiographically by the presence of at least three adjacent vertebrae wedged a minimum of 5 . Prevalence of the disease is thought to be between 0.4% and 10%,4,5 affecting men and women equally.6 The etiology of SK remains unclear; however, multiple theories have been proposed. Scheuermann1 believed that osteonecrosis of the vertebral ring apophysis resulted in longitudinal growth arrest of the anterior vertebral body, thus causing a wedging of the vertebrae. Schmorl postulated that disk material herniated through the vertebral end plates lead to loss of disk height, vertebral body wedging, and node formation.3 Both these early theories have since been called into question. Some authors noted a familial predilection for the disease, including a high rate of heritability and an autosomal dominant pattern, suggesting possible genetic causes.4 Growth hormone abnormalities have also been implicated as a causative factor; however, the true cause of the disease remains unknown. Zeeshan M. Sardar, MD, MSc

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