Natural History of Slipped Capital Femoral Epiphysis : Journal of Pediatric Orthopaedics

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Natural History of Slipped Capital Femoral Epiphysis

Mathew, Smitha E. MD; Larson, A. Noelle MD

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Journal of Pediatric Orthopaedics 39():p S23-S27, July 2019. | DOI: 10.1097/BPO.0000000000001369
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Slipped capital femoral epiphysis (SCFE) occurs at a rate of 1 in 10,000 to 20,000 children.


A PubMed search was undertaken to evaluate recent SCFE literature. A convenience sample of articles were selected and summarized.


Most slips appear well tolerated long-term with ∼5% resulting in total hip arthroplasty (THA) at 20-year follow-up. Classic data reveals poor outcomes following closed reduction for treatment of SCFE. Improvements in intraoperative fluoroscopy and avoidance of pin penetration have reduced the rates of chondrolysis. Unfortunately, avascular necrosis remains a known risk in patients, occurring in 15% to 50% of patients following acute, unstable slips. This is the most common cause of THA in patients with SCFE. Rate of THA due to degenerative arthritis secondary to SCFE is more difficult to determine and occurs at a later age. Although realignment procedures to address anatomic abnormalities from SCFE have increased in popularity, it is unclear if this prevents degenerative arthritis and subsequently reduces the rate of THA. SCFE patients face an increased risk of disability and death due to their underlying medical comorbidities. Interventions for weight loss, blood pressure management, and lifestyle adjustments should be considered at the time of SCFE diagnosis.


SCFE remains a challenging and common condition for pediatric orthopedists. Although innovative techniques have been proposed, long-term outcome data still supports in situ pinning for stable slips, and in situ pinning with capsular decompression for unstable slips to minimize the risk of avascular necrosis.

Slipped capital femoral epiphysis (SCFE) is the most common hip disorder affecting adolescents between the ages of 9 and 16 years.1 SCFE occurs due to a weakened proximal femoral physis resulting in posterior and medial translation of the epiphysis relative to the metaphysis.2 The etiology is multifactorial; implicated factors include increased femoral retroversion, increased physeal obliquity, obesity, renal osteodystrophy, postradiation therapy to the pelvis, and endocrinopathies such as hypothyroidism, hypogonadism, and hypopituitarism.3–5

The annual incidence of SCFE is around 10 cases per 100,000 children.1 However, various epidemiological studies have shown the incidence to vary with ethnicity, gender and region, ranging from 4.4 to 10.8 cases per 100,000 children (Table 1).1,6–11 The mainstay of treatment for SCFE is in situ pinning, although osteotomies, open reduction, and capsular decompression have been described, particularly for severe, unstable slips.12,13

Reported Incidence of Slipped Capital Femoral Epiphysis

With the evolving treatment options for SCFE, it is important to consider the natural history of SCFE and reported results of in situ pinning to determine treatment efficacy. Thus, we aim to review long-term outcomes of SCFE patients treated with in situ pinning.


There is limited information regarding nonoperative management of SCFE. Carney and Weinstein14 reported on the natural history of 31 slips in 28 patients at a mean of 41-year follow-up and found that as long as the displacement was minimal, the outcome was acceptable. There were 17 mild, 11 moderate, and 3 severe slips. One mild slip developed chondrolysis, and 1 severe slip developed avascular necrosis (AVN) treated with cup arthroplasty. All moderate and severe slips had radiographic evidence of arthritis. At mean 41-year follow-up, mild slips had a mean Iowa Hip Rating of 92 points, moderate was at 87 points, and 75 points for the severe slips, with scores of 90 and above considered excellent. Ordeberg et al15 reported on 49 patients with untreated SCFE at 20 to 60 years follow-up. Most patients had few restrictions, with only 2 requiring surgery for degenerative arthritis. Thus, the natural history points to a low rate of disability, particularly in patients with mild slips who do not develop chondrolysis or AVN. Patient expectations, activity levels, and availability of arthroplasty may have changed since the mid to late-20th century, and it may be difficult to compare these classic reported results to current patient populations.


The most widely used technique for chronic stable SCFE is in situ pinning without attempts at reduction of the deformity. Complications such as AVN and chondrolysis are commonly seen with historic closed reduction attempts resulting in poor outcomes. At mean 31 years, Boyer et al16 reported on improved results for 83 hips treated without attempts at realignment (mean Iowa Hip Score 93 points) compared with 54 hips treated with realignment, with mean Iowa Hip Score around 70 points. Complications such as AVN or chondrolysis were also high in the realignment group (18 hips or 33%) compared with 6 in the in situ treatment group (7%). Three of the 6 cases of chondrolysis were secondary to spica cast placement, which is no longer performed. Carney et al17 also showed higher rates of chondrolysis and AVN with resulting poor outcomes in hips treated with forcible closed reduction. At a mean 41-year follow-up for 155 hips, in situ pinning was associated with the best outcomes and lowest risk of AVN or chondrolysis (Table 2).17–24 Wensaas et al22 showed satisfactory clinical and radiographic outcomes following in situ fixation irrespective of the method of treatment, which included screw fixation, bone-peg epiphysiodesis and bone-peg epiphysiodesis combined with corrective femoral osteotomy. The health-related quality of life measured by the EQ-5D index score of SCFE patients who underwent in situ pinning was comparable with Danish control patients.22 Thus, in situ pinning has become standard of care for treatment of stable SCFE, with low reported rates of arthroplasty (Table 2).

Outcomes of In Situ Pinning for Slipped Capital Femoral Epiphysis

Although SCFE treated with in situ pinning has demonstrated stable closure of the proximal femoral physis and favorable long-term clinical and radiologic outcomes, other studies have found that hip symptoms are common in adult SCFE patients. A study of SCFE patients treated between 1965 and 2005 demonstrated persistent hip pain in 33% SCFE patients who underwent in situ pinning, while at 10 years, 10% of patients had developed severe arthritis necessitating reconstructive surgery and at 20 years, 5% had undergone total hip arthroplasty (THA).18 Following in situ pinning of SCFE patients, need for additional/corrective surgeries ranged from 1% to 9% (Table 2). Although high grade slips have a higher rate of reconstructive procedures, even mild slips have been associated with labral degeneration and acetabular cartilage defects, leading to premature osteoarthritis.25

Although more severe deformity is associated with a higher rate of osteotomy, there is no correlation between severity of slip and need for THA. Some argue that a mild slip can be associated with greater acetabular damage because the rough metaphysis can slip into the acetabulum causing wear on the labrum and articular cartilage. Hip range of motion for severe slips may be restricted due to the deformity and thus due to decreased motion, the acetabulum and cartilage health can be preserved.25–28


The most serious early complications following SCFE are AVN and chondrolysis.29 The advent of intraoperative fluoroscopy has significantly reduced the frequency of intra-articular pins or screw penetration and thus the rates of chondrolysis. Thus, AVN is the primary early threat to hip joint function following SCFE and occurs almost exclusively in acute, unstable slips. Review of a total joints registry at a major tertiary referral center concluded that of the 33,731 primary hip arthroplasties performed from 1969 to 2007, only 0.1% (38 hips in 33 patients) was conducted for an indication of SCFE, the most common indication being AVN rather than degenerative arthritis secondary to femoroacetabular impingement (FAI).30 Further results showed that THA occurred earlier in patients with AVN (mean age: 20 y) as compared with patients with degenerative arthritis (38 y). Gent and Clark31 examined the Norwegian Arthroplasty Register and concluded that of the 72,301 hip replacements that were carried out, only 1.3% were for Perthes and SCFE combined. Thus, SCFE is a rare indication for THA, and THA performed for SCFE in the absence of AVN, an even less frequent occurrence.

Reported rates of THA following SCFE range from 2% to 28% at a mean of 18 to 38 years follow-up (Table 2). Because of the nature of long-term outcomes studies, only a subset of the entire cohort is found for follow-up, which may falsely inflate the rates of THA. Interestingly, up to 1.2% of the US population has undergone THA, showing only a marginally increased risk for SCFE patients, although certainly SCFE patients undergo THA at a younger age than patients with idiopathic osteoarthritis.30


Cam morphology is seen in idiopathic FAI patients as well as SCFE patients. Although literature reporting on FAI patients is frequently applied to the SCFE population, it is important to review the evidence to see if SCFE patients follow a similar course as that reported for idiopathic FAI. One may argue that SCFE patients represent a more sedentary population which may not be comparable to idiopathic FAI patients, who are primarily athletes.

Because of the subluxation of the femoral head, SCFE results in an altered neck-shaft angle and impingement due to residual capital deformity. The proximal femoral growth plate is normally tilted posteriorly and becomes more anteriorly tilted with growth. This posterior tilt is seen in the cam morphology secondary to SCFE, but not in subclinical SCFE signifying that subclinical SCFE has a unique morphology compared with the cam lesions typically seen in idiopathic FAI.32 Mild SCFE deformity has been shown to contribute to abnormal joint kinematics and the development of degenerative arthritis of the hip.18

FAI has also been shown to contribute to hip osteoarthritis in patients unaffected by SCFE. After unilateral THA, patients with FAI were at the high risk of undergoing THA on the opposite side, with 18% chance of contralateral THA within 20 years compared with 33% chance for patients with hip dysplasia or 15% chance for patients with normal hip morphology.33 In the CHECK study, 1002 patients with unilateral mild hip arthritis were followed prospectively for 5 years. The presence of a moderate cam-type deformity resulted in a 3.67 increased odds ratio for severe arthritis, and a severe cam lesion, indicated clinically by hip pain and a reduction in internal rotation of the hip (≤20 degrees), and radiographically by an increase in alpha angle (>60 degrees), with a 9.66 increased odds ratio for end-stage hip arthritis.34 Thus, FAI patients have a high risk of subsequent THA and degenerative changes. However, it is unclear whether idiopathic FAI patients are the same population as SCFE patients. At mean 20-year follow-up, 5% of SCFE patients have undergone THA due to degenerative arthritis not associated with AVN, which certainly represents increased risk compared with the average population.18 However, due to the rarity of the condition, it will be difficult to determine whether SCFE patients develop degenerative arthritis at the same rate as patients with idiopathic FAI.

In addition, SCFE patients differ from those with idiopathic FAI regarding their activity level. Risk factors for idiopathic cam lesions include a high level of involvement in athletics as an adolescent, particularly in sports that require internal rotation. Moats et al noted that early eighth and 11th century humans in North America did not have cam lesions, despite presumed strenuous physical activity, but that athletic programs in the context of a modern diet are now associated with an increased rate of cam lesions.35 SCFE seems to represent a different disease process altogether with increased body mass index, likely decreased activity level, and subsequent deformity of the physis. Thus, we feel that long-term outcomes reported for cam lesions without the formal diagnosis of SCFE should not be applied to the natural history of SCFE patients. The idiopathic cam lesion appears to be a different disease entity with likely a unique pathophysiology and prognosis compared with SCFE.


Interestingly, development of SCFE may portend severe underlying systemic disease. Escott and colleagues reported on a cohort of 64 patients with minimum 20-year follow-up from SCFE. First, they noted a 6 times higher mortality rate compared to age-adjusted US population. Mean body mass index over the study period increased from 27 to 37. In addition, 8% had diabetes, 9% had elevated blood sugar, 8% had chest pain, and 16% had hypertension in their 30s. There was no association between severity of slip, radiographic measures, and health-related quality of life. Thus, the authors stated that there should be increased focus on underlying metabolic health at the time of SCFE diagnosis.21


The risks of AVN for treatment of a stable slip with modern in situ pinning techniques approaches zero. Thus, the benefits from modern reconstructive procedures which may put the stable slipped hip at even slight risk for AVN must be carefully considered. For acute, unstable slips which have a high baseline risk of AVN, there may be an increased role for realignment procedures which themselves carry a risk of iatrogenic AVN. These procedures may be made safer with intraoperative monitoring of the blood supply to the femoral head.36 There is likely a role for capsular decompression for acute unstable SCFE, as elevated intracapsular pressures may contribute to poor perfusion of the femoral head. In addition, capsulotomy is a surgical procedure which can be performed either percutaneously or open and is readily performed by an on call surgeon without the need for specialized experience.37,38 The modified Dunn osteotomy is a technical procedure which involves capital realignment resulting in correction of the deformity and achievement of near anatomic restoration of the hip.39,40 However, it is associated with postoperative implant complications and AVN. Long-term follow-up studies are unavailable for the modified Dunn procedure to determine whether the risk for degenerative arthritis is in fact reduced by the resultant deformity correction. Two-year follow-up studies showed AVN rates ranging between 0% and as high as 26% (Table 3).13,39–41 These results should prompt careful reflection for each center as to whether in situ pinning is the better option for treatment of SCFE.

Rates of Avascular Necrosis With Modified Dunn Procedure

Thus, in order to determine if in situ pinning is the better option than realignment surgery, the natural history and the long-term outcomes of SCFE patients following in situ pinning has to be considered both in terms of residual symptoms and need for additional corrective surgeries.


Various treatment modalities have been described for the treatment of SCFE. AVN or chondrolysis are the greatest risk factors for early degenerative arthritis and hip replacement in SCFE. Thus, a primary concern should be avoidance of these 2 early complications. Over the years there have been significant changes in surgical techniques with some centers routinely performing realignment procedures for unstable or severe slips. Despite these advances, AVN has not been entirely eliminated. Recent work has outlined the poor prognosis of cam lesions; however, reconstructive procedures to date have not shown a decreased risk of arthritis following an offset procedure or trimming of the femoral head. Further, it is not altogether clear that the natural history of idiopathic cam lesions mirrors that for SCFE. Patients with moderate or severe slips have restricted motion, and in contrast to patients with idiopathic cam lesions, potentially a lower activity level which may reduce the wear on the native acetabulum. This may explain why the cam lesion is seemingly well tolerated in SCFE patients. Further, the morphology of a SCFE cam lesion may differ from that of an idiopathic cam lesion. Thus, natural history studies for SCFE should be restricted to patients with a known childhood diagnosis of SCFE.

Although acute unstable SCFE represents only 5% of the SCFE population, this group requires special consideration as they are at increased risk of complications. Future research should aim at attaining a better understanding of the articular cartilage and growth plate and development of newer modalities of treatment including growth friendly SCFE implants. Continued research must be focused on decreasing the rates of development of AVN and degenerative changes as well as early diagnosis and treatment of these complications, hence reducing the need for future arthroplasty and reconstructive surgeries in these patients.

Although, the greatest risk to the femoral head may be AVN, the greatest risk to the child is clearly the associated medical comorbidities and sequelae of obesity. Mortality rate following treatment of SCFE was 10% which was much higher than the crude accumulated US mortality rate between the ages of 12 and 32 years (1.4%).21 This was due to associated medical conditions leading to a decline in the health status, signifying that patients with SCFE are at risk of poor medical outcomes irrespective of treatment modality. A comprehensive program for intervention, weight loss, and nutrition should be considered as standard of care for SCFE patients with the hope of decreasing mortality and morbidity of chronic metabolic syndrome.

Verified and Valid Recommendation

In order to assess the outcomes of these new treatment approaches, it is important to have a solid understanding of the natural history and results of in situ pinning.

Use caution before undertaking procedures with a high risk of AVN, as the known detriment of AVN may outweigh the unproven benefit of restoring normal anatomy to the femoral head.

Consider a comprehensive endocrine/nutrition/weight loss program for SCFE patients. Long-term risks of mortality due to associated medical comorbidities are significant.

Reported rates of THA following childhood treatment of SCFE with in situ pinning ranges from 2% to 28% at mean 20-year follow-up.


1. Lehmann CL, Arons RR, Loder RT, et al. The epidemiology of slipped capital femoral epiphysis: an update. J Pediatr Orthop. 2006;26:286–290.
2. Aronsson DD, Loder RT, Breur GJ, et al. Slipped capital femoral epiphysis: current concepts. J Am Acad Orthop Surg. 2006;14:666–679.
3. DePuy J, Drennan JC. Correction of idiopathic: a comparison of result of early versus delayed posteromedial release. J Pediatr Orthop. 1989;9:44–48.
4. Ryan BR, Walters TR. Slipped capital femoral epiphysis following radiotherapy and chemotherapy. Med Pediatr Oncol. 1979;6:279–283.
5. Loder RT, Wittenberg B, DeSilva G. Slipped capital femoral epiphysis associated with endocrine disorders. J Pediatr Orthop. 1995;15:349–356.
6. Larson AN, Yu EM, Melton LJ III, et al. Incidence of slipped capital femoral epiphysis: a population-based study. J Pediatr Orthop B. 2010;19:9–12.
7. Herngren B, Stenmarker M, Vavruch L, et al. Slipped capital femoral epiphysis: a population-based study. BMC Musculoskelet Disord. 2017;18:304.
8. Witbreuk MM, van Royen BJ, Van Kemenade FJ, et al. Incidence and gender differences of slipped capital femoral epiphysis in the Netherlands from 1998-2010 combined with a review of the literature on the epidemiology of SCFE. J Child Orthop. 2013;7:99–105.
9. Murray AW, Wilson NI. Changing incidence of slipped capital femoral epiphysis: a relationship with obesity? J Bone Joint Surg Br. 2008;90:92–94.
10. Benson EC, Miller M, Bosch P, et al. A new look at the incidence of slipped capital femoral epiphysis in new Mexico. J Pediatr Orthop. 2008;28:529–533.
11. Kelsey JL. The incidence and distribution of slipped capital femoral epiphysis in Connecticut. J Chronic Dis. 1971;23:567–578.
12. Millis MB, Novais EN. In situ fixation for slipped capital femoral epiphysis: perspectives in 2011. J Bone Joint Surg Am. 2011;93(suppl 2):46–51.
13. Ziebarth K, Milosevic M, Lerch TD, et al. High survivorship and little osteoarthritis at 10-year followup in SCFE patients treated with a modified Dunn procedure. Clin Orthop Relat Res. 2017;475:1212–1228.
14. Carney BT, Weinstein SL. Natural history of untreated chronic slipped capital femoral epiphysis. Clin Orthop Relat Res. 1996;322:43–47.
15. Ordeberg G, Hansson LI, Sandström S. Slipped capital femoral epiphysis in southern Sweden. Long-term result with no treatment or symptomatic primary treatment. Clin Orthop Relat Res. 1984;191:95–104.
16. Boyer DW, Mickelson MR, Ponseti IV. Slipped capital femoral epiphysis. Long-term follow-up study of one hundred and twenty-one patients. J Bone Joint Surg Am. 1981;63:85–95.
17. Carney BT, Weinstein SL, Noble J. Long-term follow-up of slipped capital femoral epiphysis. J Bone Joint Surg Am. 1991;73:667–674.
18. Larson AN, Sierra RJ, Yu EM, et al. Outcomes of slipped capital femoral epiphysis treated with in situ pinning. J Pediatr Orthop. 2012;32:125–130.
19. de Poorter JJ, Beunder TJ, Gareb B, et al. Long-term outcomes of slipped capital femoral epiphysis treated with in situ pinning. J Child Orthop. 2016;10:371–379.
20. Boero S, Brunenghi GM, Carbone M, et al. Pinning in slipped capital femoral epiphysis: long-term follow-up study. J Pediatr Orthop B. 2003;12:372–379.
21. Escott BG, De La Rocha A, Jo CH, et al. Patient-reported health outcomes after in situ percutaneous fixation for slipped capital femoral epiphysis: an average twenty-year follow-up study. J Bone Joint Surg Am. 2015;97:1929–1934.
22. Wensaas A, Svenningsen S, Terjesen T. Long-term outcome of slipped capital femoral epiphysis: a 38-year follow-up of 66 patients. J Child Orthop. 2011;5:75–82.
23. Castaneda P, Ponce C, Villareal G, et al. The natural history of osteoarthritis after a slipped capital femoral epiphysis/the pistol grip deformity. J Pediatr Orthop. 2013;33(suppl 1):S76–S82.
24. Hagglund G, Hannson LI, Sandstrom S. Slipped capital femoral epiphysis in southern Sweden. Long-term results after nailing/pinning. Clin Orthop Relat Res. 1987;217:190–200.
25. Leunig M, Casillas MM, Hamlet M, et al. Slipped capital femoral epiphysis: early mechanical damage to the acetabular cartilage by a prominent femoral metaphysis. Acta Orthop Scand. 2000;71:370–375.
26. Klit J, Gosvig K, Magnussen E, et al. Cam deformity and hip degeneration are common after fixation of a slipped capital femoral epiphysis. Acta Orthop. 2014;85:585–591.
27. Futami T, Kasahara Y, Suzuki S, et al. Arthroscopy for slipped capital femoral epiphysis. J Pediatr Orthop. 1992;12:592–597.
28. Miese FR, Zilkens C, Holstein A, et al. Assessment of early cartilage degeneration after slipped capital femoral epiphysis using T2 and T2* mapping. Acta Radiol. 2011;52:106–110.
29. Lubicky JP. Chondrolysis and avascular necrosis: complications of slipped capital femoral epiphysis. J Pediatr Orthop B. 1996;5:162–167.
30. Larson AN, McIntosh AL, Trousdale RT, et al. Avascular necrosis most common indication for hip arthroplasty in patients with slipped capital femoral epiphysis. J Pediatr Orthop. 2010;30:767–773.
31. Gent E, Clarke NM. Joint replacement for sequelae of childhood hip disorders. J Pediatr Orthop. 2004;24:235–240.
32. Monazzam S, Bomar JD, Pennock AT. Idiopathic cam morphology is not caused by subclinical slipped capital femoral epiphysis an MRI and CT study. Orthop J Sports Med. 2013;1:2325967113512467.
33. Wyles CC, Heidenreich MJ, Jeng J, et al. The John Charnley Award: redefining the natural history of osteoarthritis in patients with hip dysplasia and impingement. Clin Orthop Relat Res. 2017;475:336–350.
34. Agricola R, Heijboer MP, Bierma-Zeinstra S, et al. Cam impingement causes osteoarthritis of the hip: a nationwide prospective cohort study (CHECK). Ann Rheum Dis. 2013;72:918–923.
35. Moats AR, Badrinath R, Spurlock LB, et al. The antiquity of the cam deformity: a comparison of proximal femoral morphology between early and modern humans. J Bone Joint Surg Am. 2015;97:1297–1304.
36. Schrader T, Jones CR, Kaufman AM, et al. Intraoperative monitoring of epiphyseal perfusion in slipped capital femoral epiphysis. J Bone Joint Surg Am. 2016;98:1030–1040.
37. Herrera-Soto JA, Duffy MF, Birnbaum MA, et al. Increased intracapsular pressures after unstable slipped capital femoral epiphysis. J Pediatr Orthop. 2008;28:723–728.
38. Ibrahim T, Mahmoud S, Riaz M, et al. Hip decompression of unstable slipped capital femoral epiphysis: a systematic review and meta-analysis. J Child Orthop. 2015;9:113–120.
39. Sankar WN, Vanderhave KL, Matheney T, et al. The modified Dunn procedure for unstable slipped capital femoral epiphysis: a multicenter perspective. J Bone Joint Surg Am. 2013;95:585–591.
40. Upasani VV, Matheney TH, Spencer SA, et al. Complications after modified Dunn osteotomy for the treatment of adolescent slipped capital femoral epiphysis. J Pediatr Orthop. 2014;34:661–667.
41. Slongo T, Kakaty D, Krause F, et al. Treatment of slipped capital femoral epiphysis with a modified Dunn procedure. J Bone Joint Surg Am. 2010;92:2898–2908.

femoroacetabular impingement; degenerative arthritis; osteonecrosis; avascular necrosis; slip

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