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Slipped capital femoral epiphysis (SCFE) is a disorder in which the capital femoral epiphysis is displaced from the metaphysis through the physeal plate.

"Slipped Capital Femoral Epiphysis ." Children . Children, n.d. Web. 08/03/2010. <

Pathology (organ, cell, system)

SCFE is a Salter-Harris type 1 fracture through the hypertrophic zone of the physeal cartilage. There is an intrinsic weakness in the physeal cartilage and stress around the hip causes a shear force to be applied at the growth plate, causing the epiphysis to move posteriorly and inferiorly. SCFE is typically seen in overweight males with obesity or other endocrinopathies. Obesity results in increased shear stress across the physeal plate, which is already oriented more vertically and posteriorly. The almost exclusive incidence of SCFE during the adolescent growth spurt indicates a hormonal role.

Unlike a Salter Harris injury which occurs between the proliferating and the hypertrophic zones; in SCFE, the slip occurs in the layer of cartilage adjacent to the zone of provisional calcification.

In SCFE, the zone of hypertrophy is thickened, and the normal columnar arrangement of chondrocytes is lost. Chondrocyte clustering and disarray are evident.

Ultrastructural studies show defective collagen fibrils and defects in collagen banding in the zone of hypertrophy and changes in the proteoglycan and glycoprotein concentrations in the zone of proliferation, with increased glycoprotein staining in the territorial matrix and increased proteoglycan staining in the extraterritorial matrix.

Agamanolis DP, Weiner DS, Lloyd JK.   Slipped capital femoral epiphysis: a pathological study. II. An ultrastructural study of 23 cases.   J Pediatr Orthop .   Jan-Feb   1985;5(1):47-58.

Ponseti IV, McClintock R.   The pathology of slipping of the upper femoral

epiphysis.   J Bone Joint Surg Am .   Jan   1956;38-A(1):71-83.  



The capital femoral epiphysis is the ball of the hip joint while the acetabulum is the socket. The epiphysis should sit squarely on the femoral neck. The epiphyseal plate, also known as the growth plate or physis, is made of pliable cartilaginous material and it allows for the elongation of the femur through chondrocyte proliferation on the epiphyseal side. 

In SCFE, the acetabulum, by embracing the femur head, helps shear off the femoral neck through the cartilage growth zone, especially if the cartilage is thick, soft, if the forces are high, and/or if there’s scarred tissue outside the bone (making for an abnormal “fulcrum”).

“Slipped Capital Femoral Epiphysis” 08/07/2010.

Differential Diagnosis

Stress fracture
Toddler's fracture (minimally displaced spiral fracture of the tibia)
Soft tissue contusion
Ankle sprain

Septic arthritis
Lyme disease
Tuberculosis of bone
Postinfectious reactive arthritis

Spinal cord tumors
Tumors of bone
Benign: osteoid osteoma, osteoblastoma
Malignant: osteosarcoma, Ewing's sarcoma

Juvenile rheumatoid arthritis
Transient synovitis
Systemic lupus erythematosus

Developmental dysplasia of the hip
Sickle cell
Congenitally short femur

Legg-Calvé-Perthes disease
Slipped capital femoral epiphysis
Tarsal coalitions
Osteochondritis dissecans (knee, talus)

Cerebral palsy, especial mild hemiparesis
Hereditary sensory motor neuropathies

Leet, Arabella, and David Skaggs. "Evaluation of the Acutely Limping Child." American Family Physician 61. (2000): 1011-8. Web. 3 Aug 2010. <>.



The overall incidence of idiopathic SCFE in the United States between 1997 and 2000 was 10.80 cases/100,000 children. The relative incidence of SCFE was 3.94 times higher in black children and 2.53 times higher in Hispanic children than in white children. The incidence rate was significantly higher in boys (13.35 cases/100,000 children) than in girls (8.07 cases/100,000 children). Higher incidence rates of SCFE were found in the Northeast and West when compared with rates in the Midwest and the South, suggesting that climate plays a role in the onset of SCFE.


Lehmann CL et al. J Pediatr Orthop. 2006 May-Jun;26(3):286-90.              



The etiology of SCFE is unknown although it is thought to be multifactorial. A genetic predisposition with an autosomal dominant pattern of transmission is suggested, in addition to environmental factors

Indeed, most cases of SCFE are idiopathic. However, several characteristics suggest involvement of endocrine abnormalities in the onset of idiopathic SCFE. The onset of SCFE occurs at the growth spurt when longitudinal growth is at its peak and endocrine changes are significant (ex. Increase in GH). GH stimulates liver cells to produce and secrete IGFs. IGF receptors are located in the proliferating and upper hypertrophic chondrocytes in the growth plate, where cell proliferation is dominant. Therefore, GH indirectly stimulates cell proliferation of the growth plate chondrocytes to induce longitudinal growth and stimulate local synthesis of IGFs by chondrocytes. Due to GH function, growth plate cartilage is probably the most fragile physiologically during the growth spurt.


Many patients with SCFE tend to be obese. Obesity causes an increase in shear stress on the growth plate. In addition to the mechanical bearing; often, obese children suffer from type 2 diabetes mellitus. Insulin reacts through the same receptor as for IGFs and is known to be one of the systemic factors that

stimulates chondrocytes in the growth plate. An increase in cell proliferation in the growth plate would result in its widening and the growth plate would then be prone to slippage.  (

In females, SCFE rarely occurs after menarche. Estrogen is known to suppress growth hormone (GH) secretion and to stimulate endochondral

ossification of the growth plate. That said, marked obesity is associated with increased androgen production and increased peripheral conversion of androgen to estrogen.This suggests that obesity is not the only etiological factor from an endocrine perspective.

J Orthop Sci (2004) 9:214–219

Clinical manifestations

The most common findings of presentation of SCFE include pain, limping and decreased ROM at the hip. Hip or groin pain in an obese, peripubertal child is highly suggestive of SCFE. However, hip pain is absent in as many as 50% of the children with SCFE, including upto 8% with a painless limp. Pain is localized to the knee and/or distal thigh in 23% to 46% of cases. Previous studies have noted that distal thigh and/or knee pain often results in significant misdiagnosis of SCFE, delay in diagnosis, incresead slip severity, etc.

Symptoms of SCFE are generally present for weeks to several months prior to presentation to the orthopedist. Although patients report a specific inciting event as the cause of pain in approzimately 50% of cases, severe trauma is rarely reported.

The limp in children with SCFE is due to several gait deviations. Hip abductor weakness manifests as a Tredelenburg gait. If there’s marked pain, an antalgic gait will be present as well. Hip rotation is abnormal because of both the abnormal anatomy and the synovitis that accompany SCFE. Loss of hip internal rotation is combined with preservation of external rotation.  Children with unilateral involvement have significant asymmetry of foot and knee progression angles with a unilateral Tredelenburg gait, whereas children with bilateral SCFE present with a more “waddling” gait bilaterally, and bilateral external foot and knee progression.

Lovell W, Winter R. Lovell and Winter’s pediatric orthopedics, Volume 2. Accessed via Google books on 08/06/10.


Late presentation, complications

Delay in diagnosis of slipped capital femoral epiphysis ( SCFE ) in the pediatric and adolescent hip has important implications in terms of long-term hip outcome. Delayed diagnosis is associated with increased slip severity. Increased slip severity is associated with a higher risk of short-term complications from treatment such as avascular necrosis and chondrolysis. Increased slip severity is also associated with poorer long-term outcome including pain, limitation of motion, and degenerative joint disease . The burden of disease from SCFE may be substantial, because it is estimated that a relatively large percentage of adult hip osteoarthritis stems from sequelae of pediatric hip disease .


Kocher MS. et al. Pediatrics Vol. 113 No. 4 April 2004, pp. e322-e325


Nutritional factors

Low-calorie foods and exercise may prevent the development of obesity, one of the risk factors of SCFE.


Radiographic evidence

Often, early in the course of a slipped capital femoral epiphysis, the anteroposterior radiograph is normal since the initial early slippage is posterior. Consequently, a lateral radiograph must always be obtained. Lateral views are more sensitive for detecting mild degrees of slip. Cross-table lateral views are also often cited as more reliable than frog-lateral views which may be due to difficulties with the positioning of these children. The early sign seen on the lateral radiograph is a minimal posterior step-off at the anterior epiphyseal-metaphyseal junction, or physeal plate.  On anteroposterior radiographs, subtle early signs include Klein's line and the blanch sign of Steel.

Klein's line is a line drawn along the superior surface of the femoral neck. The epiphysis should normally project superiorly to it whereas in early slipped capital femoral epiphysis, the epiphysis is flush with it.

The blanch sign of Steel on the anteroposterior radiograph represents superimposition of the posteriorly displaced epiphysis on the femoral neck.

The degree of slip is commonly quantified as the amount of femoral head displacement as a percentage of the femoral neck diameter. Slips have been categorized as mild, moderate and severe. This measurements, however, should be used only in the evaluation of SCFE prior to remodeling of the proximal femoral head.

Loder, RT. Slipped Femoral Capital Epiphysis: Radiologic Decision Making. AAFP. Printed May 1 st 1998.


Laboratory evidence

Because the rate of endocrinopathy in children with SCFE is relatively low, recommendations are made against the routine screening of patients with SCFE without clinical evidence of an endocrinopathy. Burrow et al. reported that a person’s height below the 10 th percentile was the only useful screening characteristic for endocrine abnormalities. The sensitivity and the negative predictive value of using height below the 10 th percentile as a cutoff was reported to be at least 90%. Hence routine screening of all patients with SCFE for any potential endocrine disease is not warranted. For children with suspected endocrine disease, thyroid function tests should be carried out. GH levels should be checked in children with short stature.

Lovell W, Winter R. Lovell and Winter’s pediatric orthopedics, Volume 2. pg 1096-1099. Accessed via Google books on 08/06/10.


Psychosocial impact of disease

In the likelihood of disability, some psychosocial implications include disability, unemployment, depression, lack of independence etc.


Risk factors

Risk factors may include: obesity, medications (such as steroids), thyroid dysfunction, radiation treatment in the region of the proximal femur, chemotherapy and bone problems related to kidney disease (renal osteodystrophy).




Of course, there’s no prevention for SCFE. However, once the diagnosis is made, weight bearing should be forbidden to minimize amount of slip which can compromise blood supply to femoral head and cause avascular necrosis.


Treatment options

Once the diagnosis of SCFE is made, the child is admitted to the hospital and should not be allowed to bear weight as it may result in osteonecrosis.

The goals of early treatment of SCFE are early detection, prevention of further slipping, and avoidance of complications. In addition, care of the unaffected hip through careful observation or prophylactic treatment cannot be forsaken.

The goal of early manipulation is to decrease the proximal femoral deformity. Spica casting and internal fixation are two methods of manipulation. With the advent of improved imaging techniques, cannulated screw systems and decreased operative morbidity, there is little role for nonsurgical treatment in children with SCFE.

The goal of in-situ fixation is to prevent slip progression. In-situ fixation is currently the preferred initial treatment for cases of SCFE of all degrees in most centers because of the relative simplicity of this extensively and well-documented technique.


Lovell W, Winter R. Lovell and Winter’s pediatric orthopedics, Volume 2. pg 1096-1099. Accessed via Google books on 08/06/10.


Outcomes  of treatment

Several long-term historical results of treatment showed that symptomatic treatment or fixation in situ gave excellent results, with only 2% needing a reconstructive procedure. Closed reduction or spica cast treatment had a combined rate of AVN and chondrolysis of 13%, with 35% needing a reconstructive procedure; femoral neck osteotomy resulted in a combined rate of AVN and chondrolysis of 30%, with 15% needing a reconstructive procedure.


Wright, JG. Evidence-based orthopedics:the best answers to clinical questions. Pg 224-227.

Complications of treatment

Complications of in-situ fixation may be either iatrogenic or may be due to the natural history of SCFE. The two most severe complications are osteonecrosis and chondrolysis. Osteonecrosis may be the natural seqeula of an unstable SCFE or may result from pin placement problems, whereas chondrolysis may occur because of unrecognized pin penetration. Other complications include further slipping, growing off the screw, loosening or failure of SCFE fixation, proximal femoral fracture, limb-length discrepancy, early osteoarthritis and sciatic nerve neuropraxia.

Other potential complications include bleeding and infection.


Lim, YJ et al. Journal of Orthopedic Surgery 2007;15(3):334-8


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