Slipped capital femoral epiphysis (SCFE) was first described by Ernst Muller, who called it Schenkelhalsverbiegungen im Jungesalter, meaning

"bending of the femoral neck in adolescence." The term slipped capital femoral epiphysis is a misnomer because the epiphysis is held in the acetabulum by the ligamentum teres; thus, the metaphysis actually moves proximally and anteriorly while the epiphysis remains in the acetabulum. Slipped capital femoral epiphysis (SCFE) is one of the most important pediatric and adolescent hip disorders encountered in medical practice. Although SCFE is a rare condition, an accurate diagnosis combined with immediate treatment is critical. Despite the fact that the underlying defect may be multifactorial (eg, mechanical and constitutional factors), SCFE represents a unique type of instability of the proximal femoral growth plate. Clinically, the patient may report hip pain, medial thigh pain, and/or knee pain; an acute or insidious onset of a limp; and decreased range of motion of the hip. SCFE is a common cause of hip and knee pain in children aged 1017. Slipped capital femoral epiphysis (SCFE) is not life threatening. However, untreated and complicated slipped capital femoral epiphysis can lead to deformity and early osteoarthrosis of the hip and, thus, can cause considerable morbidity. Factors that increase morbidity include avascular necrosis (AVN) of the hip and chondrolysis. Both of these may result in damage severe enough to warrant a salvage procedure, in the form of an arthrodesis or a total hip arthroplasty. Prompt diagnosis is critical to prevent further deformity and AVN. FUNCTIONAL ANATOMI SCFE results from a Salter-Harris type physeal fracture. In patients with SCFE, the epiphyseal growth plate is unusually widened, primarily due to expansion of the zone of hypertrophy. The hypertrophic zone, which constitutes 15-30% of the normal physis, can account for up to 80% of the width of the physeal plate in affected patients. Histologically, abnormal cartilage maturation, endochondral ossification, and perichondral ring instability occur. This leads to less organization of the normal cartilaginous columnar architecture. Slippage occurs through this weakened area. The position of the proximal physis normally changes from horizontal to oblique during preadolescence and adolescence, redirecting hip forces from compression forces to shear forces. There is an association between femoral neck retroversion and a reduced neckshaft angle with SCFE. These changes can increase the shear forces across the hip, leading to SCFE. [17] Other concomitant findings in the hip include inflammatory synovitis and disorganized collagen fibrils with accumulations of proteoglycans and glycoproteins within

the growth plate; however, whether these changes are a cause or a result of SCFE remains undetermined. ANATOMY