S lipped C ap i t al F emo ra l Epiphysis How to Evaluate with a Review and Update of Treatment Andrew G. Georgiadis,
MD
a
, Ira Zaltz,
MD
b
KEYWORDS Slipped capital femoral epiphysis SCFE Hip disorders, pediatric Chondrolysis Dunn osteotomy Osteonecrosis Avascular necrosis Medial circumflex femoral artery KEY POINTS Slipped capital femoral epiphysis (SCFE) is a common adolescent hip disorder. 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. 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 Pare´, a barber surgeon for the King of France.1 Later, Mu¨ller described a deformity he termed “bending of the neck of the femur in adolescence.”2 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,3 rickettsial disorders,2 infection,4 endocrine disturbances, and “periosteal atrophy [. . .] tending to produce a point of weakness at the epiphyseal line.”5 Sprengel6 cadaverically proved epiphyseal separation and proposed that SCFE stemmed from fracture. The first etiologic categorization, performed by Key,5 comprehensively classified proximal femoral varus due to Perthes, infection, Charcot
Disclosure: None. a Department of Orthopaedic Surgery, Henry Ford Hospital, Detroit, MI 48202, USA; b Orthopaedic Surgery, William Beaumont Hospital, 30575 Woodward Avenue, Royal Oak, MI 48073, USA E-mail address: [email protected] Pediatr Clin N Am 61 (2014) 1119–1135 http://dx.doi.org/10.1016/j.pcl.2014.08.001 pediatric.theclinics.com 0031-3955/14/$ – see front matter Ó 2014 Elsevier Inc. All rights reserved.
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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.3,7 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.8 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
Fig. 1. Specimen from 18-month-old human cadaver. Evident is the complete independence of the lateral epiphyseal arteries investing the epiphysis and the ascending metaphyseal vessels ending at the physeal plate. This independence persists until physeal closure in adolescence. (From Trueta J. The normal vascular anatomy of the human femoral head during growth. J Bone Joint Surg Br 1957;39-B(2):358–94; with permission.)
Slipped Capital Femoral Epiphysis
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 Harrison9 described the intraosseous and extraosseous proximal femoral vascular anatomy in adult hips through a series of detailed histologic dye studies.9,10 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.11 Ganz and colleagues12 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 colleagues13 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 colleagues14 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. Speer15 described a growth spurt around age 7 resulting in asymmetric neck lengthening and increased verticality of the physis. Mirkopulos and colleagues16 found that subjects with
Fig. 2. During adolescence, terminal branches of the ascending metaphyseal circulation do not cross the closing physis, instead they end in the hypertrophic zone of the growth plate. (From Trueta J. The normal vascular anatomy of the human femoral head during growth. J Bone Joint Surg Br 1957;39-B(2):358–94; with permission.)
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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.15,17 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.15,18 Physiologic shear forces have been shown capable of displacing an adolescent proximal femoral epiphysis ex vivo18,19 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).15,17,20 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.21 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
Fig. 3. Normal proximal femoral physis with extracellular matrix primarily in the resting zone and excellent columnar organization of developing chondrocytes (A). Proximal femoral physis of an SCFE patient showing extracellular matrix in the proliferating and hypertrophic zones (B) and a frank cleft in the hypertrophic zone with disorganized ECM and erythrocytes invasion (C). Those arrows are demonstrating alcian-blue positivity (proteoglycan content) in the proliferative zone. (From Ippolito E, Mickelson MR, Ponseti IV. A histochemical study of slipped capital femoral epiphysis. J Bone Joint Surg Am 1981;63(7):1109–13; with permission.)
Slipped Capital Femoral Epiphysis
stability but decreases in size and surface area during childhood and adolescence as peripheral physeal cupping increases. Liu and colleagues22 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.23,24 A stature test can be used to identify patients with SCFE and a concomitant endocrine abnormality.25 Patients with SCFE who were below the tenth percentile for height comprised 90.9% of all endocrinopathies. Loder and colleagues26 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 (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. Loder and colleagues27 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
Fig. 4. Three dimensional CT reconstructions of the epiphyseal tubercle in the posterosuperior epiphysis, decreasing in normative size as a child ages. Also appreciable is the increase in physeal cupping over time. (From Liu RW, Armstrong DG, Levine AD, et al. An anatomic study of the epiphyseal tubercle and its importance in the pathogenesis of slipped capital femoral epiphysis. J Bone Joint Surg Am 2013;95:e341–8; with permission.)
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Table 1 Odds ratios of atypical SCFE based on deviations from norms of age, weight, and height Group
Odds Ratio
Age 16 y
7.4
Height
MD
a
, Ira Zaltz,
MD
b
KEYWORDS Slipped capital femoral epiphysis SCFE Hip disorders, pediatric Chondrolysis Dunn osteotomy Osteonecrosis Avascular necrosis Medial circumflex femoral artery KEY POINTS Slipped capital femoral epiphysis (SCFE) is a common adolescent hip disorder. 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. 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 Pare´, a barber surgeon for the King of France.1 Later, Mu¨ller described a deformity he termed “bending of the neck of the femur in adolescence.”2 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,3 rickettsial disorders,2 infection,4 endocrine disturbances, and “periosteal atrophy [. . .] tending to produce a point of weakness at the epiphyseal line.”5 Sprengel6 cadaverically proved epiphyseal separation and proposed that SCFE stemmed from fracture. The first etiologic categorization, performed by Key,5 comprehensively classified proximal femoral varus due to Perthes, infection, Charcot
Disclosure: None. a Department of Orthopaedic Surgery, Henry Ford Hospital, Detroit, MI 48202, USA; b Orthopaedic Surgery, William Beaumont Hospital, 30575 Woodward Avenue, Royal Oak, MI 48073, USA E-mail address: [email protected] Pediatr Clin N Am 61 (2014) 1119–1135 http://dx.doi.org/10.1016/j.pcl.2014.08.001 pediatric.theclinics.com 0031-3955/14/$ – see front matter Ó 2014 Elsevier Inc. All rights reserved.
1120
Georgiadis & Zaltz
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.3,7 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.8 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
Fig. 1. Specimen from 18-month-old human cadaver. Evident is the complete independence of the lateral epiphyseal arteries investing the epiphysis and the ascending metaphyseal vessels ending at the physeal plate. This independence persists until physeal closure in adolescence. (From Trueta J. The normal vascular anatomy of the human femoral head during growth. J Bone Joint Surg Br 1957;39-B(2):358–94; with permission.)
Slipped Capital Femoral Epiphysis
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 Harrison9 described the intraosseous and extraosseous proximal femoral vascular anatomy in adult hips through a series of detailed histologic dye studies.9,10 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.11 Ganz and colleagues12 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 colleagues13 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 colleagues14 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. Speer15 described a growth spurt around age 7 resulting in asymmetric neck lengthening and increased verticality of the physis. Mirkopulos and colleagues16 found that subjects with
Fig. 2. During adolescence, terminal branches of the ascending metaphyseal circulation do not cross the closing physis, instead they end in the hypertrophic zone of the growth plate. (From Trueta J. The normal vascular anatomy of the human femoral head during growth. J Bone Joint Surg Br 1957;39-B(2):358–94; with permission.)
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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.15,17 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.15,18 Physiologic shear forces have been shown capable of displacing an adolescent proximal femoral epiphysis ex vivo18,19 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).15,17,20 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.21 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
Fig. 3. Normal proximal femoral physis with extracellular matrix primarily in the resting zone and excellent columnar organization of developing chondrocytes (A). Proximal femoral physis of an SCFE patient showing extracellular matrix in the proliferating and hypertrophic zones (B) and a frank cleft in the hypertrophic zone with disorganized ECM and erythrocytes invasion (C). Those arrows are demonstrating alcian-blue positivity (proteoglycan content) in the proliferative zone. (From Ippolito E, Mickelson MR, Ponseti IV. A histochemical study of slipped capital femoral epiphysis. J Bone Joint Surg Am 1981;63(7):1109–13; with permission.)
Slipped Capital Femoral Epiphysis
stability but decreases in size and surface area during childhood and adolescence as peripheral physeal cupping increases. Liu and colleagues22 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.23,24 A stature test can be used to identify patients with SCFE and a concomitant endocrine abnormality.25 Patients with SCFE who were below the tenth percentile for height comprised 90.9% of all endocrinopathies. Loder and colleagues26 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 (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. Loder and colleagues27 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
Fig. 4. Three dimensional CT reconstructions of the epiphyseal tubercle in the posterosuperior epiphysis, decreasing in normative size as a child ages. Also appreciable is the increase in physeal cupping over time. (From Liu RW, Armstrong DG, Levine AD, et al. An anatomic study of the epiphyseal tubercle and its importance in the pathogenesis of slipped capital femoral epiphysis. J Bone Joint Surg Am 2013;95:e341–8; with permission.)
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Table 1 Odds ratios of atypical SCFE based on deviations from norms of age, weight, and height Group
Odds Ratio
Age 16 y
7.4
Height
