Slipped capital femoral epiphysis (SCFE) involves displacement of the proximal femoral metaphysis relative to a fixed epiphysis, usually during a period of rapid growth and unique physeal susceptibility. Patients have characteristic clinical, histologic, and radiologic features. Several clinical signs and medical diagnoses should prompt radiologic and laboratory workup. Limp or hip or knee pain in a patient 10 to 16 years old should include SCFE in the differential. If confirmed, appropriate treatment involves proximal femoral physeal stabilization and/or realignment. The optimal surgical treatment of severe SCFE and its late sequela remain an evolving and controversial subject.
Key points
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Slipped capital femoral epiphysis (SCFE) is a common adolescent hip disorder.
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The physis is uniquely susceptible to lysis during specific periods of growth, and the risk of epiphyseal displacement is compounded by normal proximal femoral development, physeal orientation, acetabular morphology, and endocrinologic factors.
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Rapid diagnosis can be made by careful clinical history, examination, and performance of anteroposterior and frog-lateral radiographs.
Introduction
The earliest report of slipped capital femoral epiphysis (SCFE) is widely attributed to a 1572 French text, Cinq Livres de Chirurgie , by Ambroise Paré, a barber surgeon for the King of France. Later, Müller described a deformity he termed “bending of the neck of the femur in adolescence.” By 1898 there were 22 publications on coxa vara in the German literature alone. The suspected source of deformity in these early studies included fracture, rickettsial disorders, infection, endocrine disturbances, and “periosteal atrophy [. . .] tending to produce a point of weakness at the epiphyseal line.”
Sprengel cadaverically proved epiphyseal separation and proposed that SCFE stemmed from fracture. The first etiologic categorization, performed by Key, comprehensively classified proximal femoral varus due to Perthes, infection, Charcot arthropathy, rickets, congenital deformities, and arthritic causes, with an emphasis on slipped epiphyses. Late nineteenth and early twentieth century investigators differentiated traumatic and insidious proximal femoral epiphyseal separation and suggested early treatment include three or more months of hip spica casting. Subtrochanteric cuneiform osteotomies were performed as early as 1900 for a variety of fixed proximal femoral deformities in adolescents, including healed or remodeled SCFE.
Introduction
The earliest report of slipped capital femoral epiphysis (SCFE) is widely attributed to a 1572 French text, Cinq Livres de Chirurgie , by Ambroise Paré, a barber surgeon for the King of France. Later, Müller described a deformity he termed “bending of the neck of the femur in adolescence.” By 1898 there were 22 publications on coxa vara in the German literature alone. The suspected source of deformity in these early studies included fracture, rickettsial disorders, infection, endocrine disturbances, and “periosteal atrophy [. . .] tending to produce a point of weakness at the epiphyseal line.”
Sprengel cadaverically proved epiphyseal separation and proposed that SCFE stemmed from fracture. The first etiologic categorization, performed by Key, comprehensively classified proximal femoral varus due to Perthes, infection, Charcot arthropathy, rickets, congenital deformities, and arthritic causes, with an emphasis on slipped epiphyses. Late nineteenth and early twentieth century investigators differentiated traumatic and insidious proximal femoral epiphyseal separation and suggested early treatment include three or more months of hip spica casting. Subtrochanteric cuneiform osteotomies were performed as early as 1900 for a variety of fixed proximal femoral deformities in adolescents, including healed or remodeled SCFE.
Pathophysiology
The underlying pathologic condition in SCFE involves a mechanical overload to the proximal femoral physis causing anterior translation and external rotation of the metaphysis with respect to the upper femoral epiphysis. At-risk patients are of a characteristic age, with certain epidemiologic, anatomic, histologic, and endocrinologic factors.
Vascular Anatomy
The vascular supply to the proximal femoral epiphysis undergoes series of developmental stages described by Trueta. Before 3 months of age, the developing chondropeiphysis has a significant contribution from the artery of the ligamentum teres, a robust and nearly vertical ascending metaphyseal circulation, and a horizontal precursor to the lateral epiphyseal arteries emanating from the greater trochanter. By 18 months of age, the lateral epiphyseal arteries are the dominant contributors to the femoral head because the ascending metaphyseal arteries no longer cross the physeal plate ( Fig. 1 ) and the artery of the ligamentum teres disappears between 6 months and 3 years of age. Complete independence of the metaphyseal and epiphyseal circulations persists to adulthood. During adolescence and immediately preceding physeal closure, an increasingly rich metaphyseal circulation begins to invest the subphyseal region, ascending to terminate in the hypertrophic zone of the physeal plate ( Fig. 2 ) that is the cellular layer through which most SCFE occurs. This metaphyseal supply to the neck arises from the extracapsular arterial ring, distinct from the epiphyseal circulation.
Preceding these experiments, Trueta and Harrison described the intraosseous and extraosseous proximal femoral vascular anatomy in adult hips through a series of detailed histologic dye studies. The medial circumflex femoral artery (MFCA) supplies lateral epiphyseal branches that become the dominant vascular contribution to the femoral head by age 18 months and persists into adulthood. The MFCA ascends the posterolateral femoral neck and, once intracapsular, is invested by a fibrous sheath and adjacent venular system. Ganz and colleagues performed detailed dye investigations of the MFCA and lateral epiphyseal vessels, the protection of which can allow for complex surgical exposure of the hip by preservation of the epiphyseal circulation.
Osseous and Physeal Anatomy
Multiple factors differentiate SCFE from a physeal fracture, including antecedent physeolysis, slower displacement, and intact periosteum. Variations in proximal femoral and acetabular anatomy contribute to the pathogenesis of SCFE and physeal instability.
Gelberman and colleagues described relative femoral retroversion in SCFE hips (averaging 1.0° vs 6.3° of anteversion) and postulated that abnormal torsional stresses, stemming from decreased anteversion, could contribute to rotational instability across the developing growth plate. Later, Sankar and colleagues investigated acetabular anatomy after treatment of unilateral SCFE, demonstrating acetabular retroversion and overcoverage in the unaffected hip, a finding with implications for SCFE development and the development of posttreatment impingement.
The femoral neck-shaft angle decreases from 160° at birth to an average of 125° degrees by adolescence, along with changes in physeal orientation. Speer described a growth spurt around age 7 resulting in asymmetric neck lengthening and increased verticality of the physis. Mirkopulos and colleagues found that subjects with unilateral SCFE had steeper physes than both their unaffected contralateral hips and age-matched controls. A 14° increase in radiographic slope occurred between 1 and 18 years, with the most rapid increase occurring between ages 9 and 12. This higher physeal inclination angle and resultant increase in shear vector parallel to the growth plate may contribute to epiphyseal translation and development of a SCFE. Because physiologic loads can create shear forces in excess of six times body weight, obesity further contributes to epiphyseal instability.
The perichondrial ring contributes to the load-carrying capacity of the physeal plate. Because the perichondrial ring thins and attenuates during adolescence, less shear force is necessary to cause epiphyseal displacement. Physiologic shear forces have been shown capable of displacing an adolescent proximal femoral epiphysis ex vivo furthering the mechanical contribution to SCFE development.
Although the precise pathogenesis is unclear, physeal cellular columnar height and organization are significantly altered in SCFE. Because the perichondrial ring is thinned, the large surface area of the undulating, interlocking mammillary processes provide the greatest internal support of the normal physis. In contrast, SCFE is characterized by physeal widening up to 12 mm (normal range: 2–6 mm), a widened hypertrophic zone comprising 60% to80% of the physeal height, enlargement of chondrocytes, cellular columnar disorganization, higher proteoglycan and extracellular matrix concentrations throughout the physis, and a general disruption in orderly chondrocyte differentiation and endochondral ossification ( Fig. 3 ). Radiographic physeal widening implies a mechanically weakened physis susceptible to unlocking of the mammillary processes and further destabilization.
The epiphyseal tubercle is an anatomic feature receiving increased attention. It is a prominence consistently located among the mammillary processes of the posterosuperior quadrant of the epiphysis. The tubercle averages 4 mm in height, is always below the foramina for the lateral epiphyseal vessels, and is postulated to confer mechanical strength to the physeal plate. It is considered a possible keystone for physeal stability but decreases in size and surface area during childhood and adolescence as peripheral physeal cupping increases. Liu and colleagues postulate that the epiphysis internally rotates on the epiphyseal tubercle and that a widened physis could contribute to epiphyseal dislodgement. Because the lateral epiphyseal arteries are immediately adjacent to and above the epiphyseal tubercle, this could explain the low rate of osteonecrosis in chronic, stable slips (ie, minimal displacement of the lateral epiphyseal vessels) ( Fig. 4 ).
Related Conditions
Suspicion of an endocrinologic disturbance in the pathogenesis of SCFE arose due to the known stippling effect of congenital hypothyroidism because thyroid hormone (T3) is necessary for normal skeletal development and chondrocyte differentiation. Although a common presentation of SCFE is that of an obese, hypogonadal male during the adolescent growth spurt, most SCFEs occur in the absence of endocrine disorder.
A stature test can be used to identify patients with SCFE and a concomitant endocrine abnormality. Patients with SCFE who were below the tenth percentile for height comprised 90.9% of all endocrinopathies. Loder and colleagues described the prognostic implications of an age-weight and age-height test to distinguish a typical (idiopathic) from an atypical (usually endocrine-related) SCFE. Subjects were grouped into six categories based on age (<10 years, 10–16 years, >16 years) and weight or height (greater or less than the fiftieth percentile). In combined variable models, extremes of age and weight; height and weight; and age, height, and weight were associated with increased odds-ratios of an atypical slipped epiphysis ( Table 1 ). Because these tests all have high negative predictive value, an orthopedic surgeon can be reasonably confident that an SCFE is idiopathic when the age-weight, age-height, and stature tests are negative.
| Group | Odds Ratio |
|---|---|
| Age <10 or >16 y | 7.4 |
| Height <50th percentile | 6.0 |
| Age and height | |
| Age <10 or >16 y | 5.8 |
| Height <50th percentile | 15.0 |
| Weight and height | |
| Weight <50th percentile | 7.4 |
| Height <50th percentile | 12.8 |
| Age, weight, and height | |
| Age <10 or >16 y | 4.9 |
| Weight <50th percentile | 4.5 |
| Height <50th percentile | 14.1 |
Loder and colleagues published a review of all previously reported slipped capital epiphyses in patients with endocrine disturbances, separating subjects into three groups: hypothyroidism, growth hormone deficiency, and all others. Hypothyroidism was the most common diagnosis (40% of 85 subjects) and the development of SCFE usually antedated the diagnosis of thyroid disturbance. All subjects with growth hormone deficiency (25%) had been diagnosed before developing an SCFE, experienced the shortest symptom duration before a slip diagnosis, and 92% developed a slip during their hormone replacement therapy. All subjects with other endocrine disturbances, such as panhypopituitarism, craniopharyngioma, and multiple endocrine neoplasia (35%), were diagnosed later in adolescence (average age 17.4 years) and an average of 3 years from first SCFE symptoms. Bilaterality is more commonly reported in endocrine-related SCFE, with many unilateral presentations progressing to contralateral involvement within the first 18 months. Increased rates of SCFE have also been demonstrated in subjects with renal osteodystrophy and secondary hyperparathyroidism, postradiation, hypogonadism, and Down syndrome.
A unique combination of histologic, vascular, anatomic, and endocrinologic factors affect physeal stability and the pathogenesis of SCFE. The proximal femoral physis represents an area of rapid cellular proliferation vulnerable to instability, is characterized by a unique temporal susceptibility that can be heightened by the body’s endocrinologic milieu, and is nourished by a fragile blood supply.
Clinical evaluation
Patients with slipped capital epiphyses can present to a physician in a delayed or acute fashion with implications for epiphyseal stability. Patients commonly present with longstanding symptoms lasting months. The most common presentations include limp and pain in the affected groin, lateral or posterior hip, thigh, or ipsilateral knee. Knee pain in SCFE is referred by a reflex arc involving somatic sensory nerves ending at the same spinal level ( Fig. 5 ). This differs from radiating pain caused by irritation of obturator nerve branches that course to the medial knee. Knee pain, present in 15% to 50% of SCFE, leads to high rates of misdiagnosis, extra radiographs, higher grade SCFE at treatment, and errant surgical procedures directed at nonexistent knee disease. A stable slip, Medicaid insurance, and distal thigh or knee pain are the strongest independent predictors of a delay in diagnosis of SCFE.
Altered gait patterns in SCFE include components of antalgic, waddling, or Trendelenburg gait, with an externally rotated foot progression angle. Only a small percentage of limp in SCFE is painless. Motion can be severely restricted in multiple planes and rotational profiles should be compared bilaterally. Patients may have weak hip abduction, decreased hip flexion, decreased internal rotation, obligate external rotation with hip flexion (Drehmann sign), and the development of synovitis precipitating a flexed posture or even hip flexion contracture. A positive Drehmann sign is elicited when the examiner passive flexes the supine patient’s hip, which then falls into obligate external rotation and abduction.
Reviews of large national databases report an SCFE incidence rate of 10 per 100,000, with a 1.4:2.0 female/male ratio. The average age of diagnosis is 12 years, and most patients presenting outside of ages 10 and 16 represent atypical SCFE possibly associated with endocrinologic diagnoses. Blacks, Hispanics, and Pacific Islanders have significantly greater incidence rates than whites. There has been a consistent finding of higher SCFE incidence north of 40° latitude, with the greatest incidences in the United States found in the Northeast and West. A seasonal incidence pattern has also been noted, with most northern latitudes presenting in the summer months, and most southern latitudes in the winter. Recent data have indicated a trend to decreased age and increased frequency of bilaterality at first presentation, suspected to correlate with increasing rates of childhood obesity.
Bilateral SCFE at first presentation has traditionally been reported in approximately 20%, with higher rates in patients with endocrinopathy. The incidence of metachronous slip, affecting 15% to 36% of SCFE, may provide justification for prophylactic pinning of the unaffected hip in at-risk patients. Almost 90% of metachronous SCFE presents within the first 18 months after treatment of the index slip.
Radiographic evaluation
The primary radiographic test used in suspected SCFE remains an anteroposterior (AP) and frog pelvis radiograph. Klein and colleagues described a line drawn along the superior neck on the AP image that should intersect the epiphysis. Failure to do so comprises a positive Trethowan sign and may indicate a slipped femoral epiphysis. The sensitivity of this line has been questioned, reportedly missing 61% of SCFE and underdiagnosing patients in a preslip phase. Green and colleagues found similarly low sensitivity of this line, proposing a modification wherein the amount of the epiphysis that is lateral to the Klein line was compared between the two hips on the AP image, with a 2 mm side-to-side difference highly suspicious of SCFE. There are numerous subtle radiographic findings indicating early slippage, including widening and irregularity of the affected physis, sharpening of the metaphyseal border of the head, loss of anterior concavity to the head-neck junction on the lateral view, and subtle periosteal elevation ; however, lateral radiographs are generally more sensitive than the AP images, particularly in the earliest phases of slipping ( Fig. 6 ). Most SCFE is characterized by anterior translation and external rotation of the metaphysis relative to the epiphysis, which, on an AP projection, is located posterior and inferior to the metaphysis. As a result, the total epiphyseal height may appear decreased and a double-density or metaphyseal blanch sign described by Steel can be present. Chronic SCFE can result in uncovering and resorption of the superior metaphysis, with periosteal reaction, osseous formation, and breaking along the inferomedial neck ( Fig. 7 ).
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