Abstract
In situ fixation of slipped capital femoral epiphysis (SCFE) results in residual deformity that can cause femoroacetabular impingement (FAI). It is unknown what factors could help differentiate patients who are more likely to become symptomatic. We performed a retrospective review of 55 hips treated with in situ pinning for SCFE and subsequent secondary deformity correction procedure for symptomatic FAI and compared them to 39 asymptomatic hips with SCFE deformity using multivariable analysis. Case patients were slightly older than controls (12.6 vs 11.3 years, p = 0.0002) but had similar BMI. The mean epiphyseal-diaphyseal angle was 56° in cases versus 44° in controls (p = 0.0019). Cases were significantly more likely to have obligate external rotation with hip flexion, external foot progression, flexion <90°, antalgic limp, and Trendelenburg lurch. On radiographs, most cases had a head-neck offset ≤0 mm, a distinct metaphyseal corner prominence, acetabular retroversion, and an alpha angle ≥60°. Most controls also had head-neck offset ≤0 mm. Pre-pinning, older age (OR = 1.98 per year, p = 0.0016) and initial epiphyseal-diaphyseal angle (OR = 1.04 per degree, p = 0.018) significantly increased the odds of having symptomatic FAI. Post-pinning, external foot progression increased the odds of symptomatic FAI by 10.48 (p = 0.017), and an alpha angle ≥60° resulted in 11.4 times higher odds of symptomatic FAI (p = 0.011). The linear correlation between epiphyseal-diaphyseal and alpha angle was poor (r = 0.28). Older age and initial epiphyseal-diaphyseal pre-pinning mildly increased the odds of eventual symptomatic FAI. This information can help the surgeon to predict which patients may develop symptomatic FAI.
Keywords: Slipped capital femoral epiphysis, Femoroacetabular impingement
1. Introduction
Three-dimensional deformity in slipped capital femoral epiphysis (SCFE) results from anterior translation and external rotation of the metaphysis along with relative epiphyseal retroversion. Gold standard treatment with in situ fixation is effective at stabilizing the physis and minimizes the risk of avascular necrosis.1 However, residual deformity of the proximal femur alters hip mechanics and leaves patients susceptible to intra-articular damage through femoroacetabular impingement (FAI).2 In the short term, FAI may result in pain, decreased range of motion, and abnormal gait, and in the long term, contributes to osteoarthritis progression.3 Damage to the labrum and acetabular cartilage has been reported to occur within months after a slip.4 However, previous studies have not consistently shown a predictable correlation between intra-articular pathology and slip severity using standard measures.5 A study of 121 SCFE patients 22 years after in situ pinning found worse clinical outcomes and higher grades of osteoarthritis for patients with radiographic FAI, which was seen in almost 80% of patients.6 Another study 30–40 years post-pinning showed inferior outcomes with radiographic FAI morphology, even when the slip was mild.7 Therefore, factors other than the slip angle are likely to play a role, but the specific morphologic components that predispose to poor outcomes have yet to be identified.
Interest in dedicated treatment of post-SCFE deformity to improve both immediate function and facilitate hip preservation has risen as evidence on the adverse effects of FAI accumulates.8 The most commonly used techniques for treating post-SCFE deformity include open or arthroscopic osteochondroplasty and intertrochanteric osteotomy (ITO). Each has demonstrated effectiveness for reducing FAI symptoms and normalizing radiographic and clinical signs associated with progressive degenerative changes.9 However, osteochondroplasty for SCFE is an evolving procedure with only short-term results available. Data for ITO spans up to 27 years10 but still only captures patients in young adulthood. For symptomatic patients, the decision to intervene is fairly straightforward with a goal of improving current symptoms. Difficulty arises when considering whether asymptomatic patients with evidence of FAI pathology should be treated prophylactically. Several authors argue that intervention is likely to be more successful long term if performed before irreversible intra-articular damage occurs.11 The theoretical arguments are compelling, but evidence to show that treating post-SCFE deformity will change the natural progression towards early arthritis is lacking.12 Given the potential for complications, the judgement of whom to operate on and when is an imperative avenue of research. Since many patients function well for decades after a slip,13 it is difficult to justify the risks of deformity correction without knowledge about which patients are most likely to benefit.
To our knowledge, no previous studies have compared SCFE patients who develop symptomatic FAI to those who remain asymptomatic. Therefore, the purposes of this study are to: (1) Describe the clinical and radiographic parameters of patients who developed early symptomatic impingement and (2) compare those patients with a group of asymptomatic SCFE controls to identify early clinical indicators of future symptomatic FAI. The significance is to provide appropriate counseling and potentially identify patients most likely to benefit from early deformity correction.
2. Materials and methods
2.1. Study design
This study was IRB approved and conducted in accordance with the STROBE (Strengthening the Reporting of Observational studies in Epidemiology) statement. We retrospectively reviewed all patients who had been treated for SCFE with in situ pinning at a tertiary children's hospital from January 1, 2011 to December 31, 2018. Patients who underwent a second surgical procedure for symptomatic FAI were identified as cases (Fig. 1). The FAI diagnosis included primarily pain with activities requiring hip flexion or prolonged walking or sitting, a positive anterior impingement test that recreated the patient's normal pain, and decreased flexion and/or internal rotation. Controls were patients who had undergone in situ pinning of SCFE during the study period but reported to be pain free during follow-up. Exclusion criteria were pre-slips, incomplete clinical and radiographic data, and the development of AVN or chondrolysis following in situ pinning. Patients who reported pain or restricted motion that was not functionally limiting enough to undergo a secondary surgery were also excluded. Acceptable follow-up for controls was determined based on the median time between in situ pinning and presentation with symptomatic FAI in cases.
Fig. 1.
Frog leg lateral x-ray of a case patient with bilateral moderate slips (A) who underwent bilateral open osteochondroplasty for symptomatic FAI (B).
2.2. Variables
The electronic medical records were reviewed for potential risk factors. Patient related variables included age, BMI, and sex. Additional pre-pinning data included the initial epiphyseal-diaphyseal angle, slip chronicity, and stability. Potential risk factors post-pinning were grouped into 3 categories: (1) physical exam, (2) gait, and (3) radiographic parameters. Radiographic measurements were performed by a pediatric orthopedic surgery fellow. Physical exam-associated factors included range of motion and a positive impingement sign. Gait variables were external foot progression, antalgic limp, and Trendelenburg lurch. AP and frog leg lateral radiographs from the clinic visit when a patient first complained of pain in cases or the most recent follow-up in controls were assessed for the epiphyseal-diaphyseal angle, alpha angle (normal <55°), head-neck offset (normal = 8–9 mm),14 presence of a discretely visible metaphyseal corner prominence, acetabular retroversion, lateral center edge angle (LCEA), and Tönnis angle. Slip severity was determined by the Southwick method.15 The epiphyseal-diaphyseal angle was used in comparative analysis rather than the slip angle to permit focused assessment of the involved extremity and to avoid introducing error for hips in which the contralateral side could not be accurately measured. For quality control, we determined if the SCFE screw head was medial to the intertrochanteric line, which can be an independent source of impingement.16
2.3. Statistical analysis
The Fischer exact and Mann-Whitney U tests were used to assess for statistical differences between the cases and controls. Significant variables were then stepwise selected into separate pre- and post-pinning multivariable models from which odds ratios with 95% confidence intervals were calculated. Variables of clinical importance were force entered into the final model. Linear correlation was assessed by the Pearson correlation coefficient. A p-value of <0.05 was considered significant.
3. Results
3.1. Participants
We identified 55 case and 39 control hips. Four case patients and 2 control patients had bilateral slips. The median interval between in situ pinning and presentation with symptomatic FAI was 8 months (range 1–49 mo). The median follow-up for controls was 17 months (range 8–55 mo).
3.2. Descriptive data
The mean age of cases and controls at the time of their SCFE pinning was significantly different at 12.5 (range: 11–15) and 11.4 (range: 9–15) years old respectively (p = 0.002). Mean BMI in both groups was 28.3. The majority of patients were males, and the majority of slips were stable and chronic. A greater percentage of case patients had unstable slips at the time of presentation (25 vs 3%, p = 0.017). The mean pre-pinning epiphyseal-diaphyseal angle was 56° in cases versus 44° in controls (p = 0.0019). Forty cases and 34 controls had a mild or moderate slip according to Southwick classification. The triradiate cartilage was open in 29% of cases versus 64% of controls (p = 0.012). There was no significant difference in the proportion of hips with a screwhead medial to the intertrochanteric line (p = 0.83). Pre-pinning patient demographics and slip characteristics are displayed in Table 1.
Table 1.
Demographics and Slip characteristics.
| Cases N = 55 Count (%) |
Controls N = 39 Count (%) |
p-value | |
|---|---|---|---|
| Age | 12.6 ± 1.3 | 11.4 ± 1.29 | 0.0002a |
| BMI | 28.3 ± 5.8 | 28.3 ± 5.57 | 0.84 |
| Male | 34 (62) | 28 (72) | 0.38 |
| Unstable | 14 (25) | 1 (3) | 0.017a |
| Chronic | 32 (58) | 19 (49) | 0.12 |
| Open triradiate cartilage | 20 (36) | 25 (64) | 0.012a |
| Initial epiphyseal-diaphyseal angle | 55.5 ± 19.4 | 43.6 ± 17.2 | 0.0019a |
| Initial Southwick slip angle | 45.3 ± 18.5 | 34 ± 17.3 | 0.0029a |
Denotes significant difference on univariate analysis.
On post-pinning clinical exam, significantly more cases had obligate external rotation (61.8% vs 28.2%, p = 0.0003), flexion less than 90° (40% vs 7.7%, p = 0.0004), external foot progression (38.2% vs 12.8%, p < 0.0001), antalgic limp (53% vs 2.9%, p < 0.0001), and Trendelenburg lurch (56% vs 8.6%, p < 0.0001). On radiographs, significantly more cases had head-neck offset ≤0 mm (87% vs 59%, p = 0.003), distinct metaphyseal corner prominence (62% vs 21%, p < 0.0001), acetabular retroversion (67% vs 21%, p < 0.0001), and alpha angle ≥60° (75% vs 23%, p < 0.0001) (Fig. 2). The post-pinning epiphyseal-diaphyseal angle was 52° in cases versus 40° in controls (p = 0.0003). Mean alpha angle was significantly higher in cases (67.1 vs 51.3, p < 0.0001), and mean head-neck offset was significantly lower (0 mm vs 1.5 mm, p = 0.003). The LCEA and Tönnis angle were similar in both groups. Table 2 presents the post-pinning data. The alpha angle had a weak linear correlation to the epiphyseal-diaphyseal angle (r = 0.28, p = 0.006) (Fig. 3).
Fig. 2.
Bar graph showing the post-operative characteristics of case patients versus controls. All variables were significantly different on univariate analysis.
Table 2.
Post-operative clinical examination and radiographic findings.
| Variable | Cases N = 55 Count (%) |
Controls N = 39 Count (%) |
p-value |
|---|---|---|---|
| Screwhead medial to intertroch line | 16 (29) | 19 (49) | 0.083a |
| Epiphyseal-diaphyseal angle | 52.2 ± 16.9 | 39.5 ± 14.4 | 0.0003a |
| Southwick slip angle | 41.8 ± 16.9 | 30 ± 14.6 | 0.0008a |
| Alpha angle | 67.1 ± 10.8 | 51.3 ± 11 | <0.0001a |
| Alpha angle ≥60° | 42 (76) | 9 (23) | <0.0001a |
| Head-Neck Offset ≤0 mm | 48 (87) | 23 (59) | 0.003a |
| LCEA | 27 ± 5.0 | 27 ± 5.0 | n/a |
| Tönnis angle | 11 ± 4.3 | 11 ± 2.5 | n/a |
| Acetabular retroversion | 37 (67) | 8 (21) | <0.001a |
| Metaphyseal corner | 34 (62) | 8 (21) | <0.0001a |
| Flexion <90° | 22 (42) | 2 (6.1) | 0.0004a |
| Positive Drehmann sign | 34 (62) | 9 (23) | 0.0003a |
| Positive Impingement test | 35 (76) | 9 (25) | <0.0001a |
| Trendelenburg lurch | 20 (56) | 3 (8.6) | <0.0001a |
| External Foot Progression | 21 (68) | 5 (16) | <0.0001a |
| Antalgic Limp | 16 (53) | 1 (2.9) | <0.0001a |
LCEA = lateral center edge angle.
Denotes significant difference on univariate analysis.
Fig. 3.
Scatter plot showing the relationship between the epiphyseal-diaphyseal angle on the y-axis and alpha angle on the x-axis. Cases (squares) have alpha angles clustered at 60 and higher while controls (diamonds) have values mostly below 60 for the same slip angle (r = 0.28).
3.3. Predictors of symptomatic FAI
Pre-pinning, multivariable analysis identified modest predictive effects of chronological age, which increased the odds of symptomatic FAI by 1.98 times per year (CI: 1.30–3.03, p = 00016) and initial epiphyseal diaphyseal angle, which increased the odds by only 1.04 times per degree (CI: 1.01–1.07, p = 0.018). Our data suggested age 12 as an inflection point where risk increases since only 18% of controls versus 47% of cases were older than 12, but this only trended towards statistical significance (p = 0.071). In a separate analysis for post-pinning data, stepwise selection identified external foot progression and alpha angle as significant factors. Epiphyseal-diaphyseal angle was force entered into the model to account for the significant difference between case sand controls. Acetabular retroversion was also force entered into the final model given its known association with FAI.17 In the final model, greater predictive effect was found with external foot progression, which increased the odds of symptomatic FAI by 10.48 (CI: 1.5–71.6, p = 0.017), and an alpha angle ≥60° (Fig. 4), which resulted in 11.4 times higher odds (CI: 1.75–74.5, p = 0.011). The epiphyseal-diaphyseal angle was not significant (p = 0.371).
Fig. 4.
Radiographic measurement of the alpha angle. Lines are drawn connecting the center of the femoral head to the mid-point of the narrowest part on the femoral neck and from the center of the femoral head to the point where the sphericity of the femoral head ends. A metaphyseal prominence is also visible.
4. Discussion
The first purpose of this study was to report the clinical and radiographic profile of patients who develop symptomatic FAI in the setting of post-SCFE deformity. The median time from in situ pinning to presentation with symptoms was only 8 months, and 80% (44/55) developed symptoms within two years. We found that cases were likely to be older and have a closed triradiate cartilage at the time of their in-situ pinning. The majority of cases had obligate external rotation, positive impingement sign, metaphyseal prominence, head neck offset ≤0 mm, acetabular retroversion, and alpha angle ≥60°. Approximately a third had flexion <90°, external foot progression, and Trendelenburg lurch. In contrast, the only abnormality found in a majority of asymptomatic controls was a head neck offset ≤0 mm (Table 2, Fig. 5). Therefore, a decreased head-neck offset is not a particularly useful parameter to distinguish post-SCFE patients who are most prone to symptomatic FAI, despite the measurement's relevance in the standard radiographic assessment of FAI. Cases did not have pathologically increased LCEA or decreased Tönnis angle.
Fig. 5.
Radiographic illustration of a patient with no offset between the anterior neck and head.
The second purpose of this study was to compare post-SCFE deformity symptomatic cases to asymptomatic controls to determine if certain variables might be useful in predicting progression to symptomatic FAI. Our pre-pinning multivariable analysis showed initial epiphyseal-diaphyseal angle only had a mild effect at 1.04. Older age had a modest effect with a 2-fold increase in risk. Our data suggests that age >12 shifts risk higher, but this finding was only a trend. In the final post-pinning model, external foot progression had a more impressive effect of a 10 times increased odds of developing symptoms. An alpha angle ≥60° increased odds the most by a factor of 11.4. In contrast to the pre-pinning model, epiphyseal-diaphyseal angle was not significant. Only 2 controls had an alpha angle ≥60° and external foot progression. Although they denied symptoms, their most recent x-rays showed radiographic evidence of impingement (Fig. 6).
Fig. 6.
Frog leg lateral radiographs of a control patient with an alpha angle greater than 60 and external foot progression. The patient initially had a prominence (A) that was eroded over time through contact with the acetabular rim (B).
Our finding of an alpha angle ≥60° increasing the odds of FAI is consistent with the radiographic definition of a cam lesion and several other published studies. In a study of 58 hips,7 SCFE patients with abnormal alpha angles had worse outcomes. While that study found a significant association between the slip and alpha angle, our cohort had a weak linear correlation between these two measurements. We observed that patients with the same slip angle had different alpha angles, as could be expected from a three-dimensional deformity. Our work also supports a radiographic study18 that reported alpha angles could range from 40 to 94 in slips <30°. The relevance of an elevated alpha angle has also been demonstrated through delayed gadolinium-enhanced magnetic resonance imaging of cartilage (dGEMRIC) correlations between angles >60° and degenerative changes—even in the absence of symptoms.19
External foot progression can represent retroversion of the capital femoral epiphysis, a compensatory strategy for avoiding FAI,20 or both. Femoral retroversion is also a risk factor in for SCFE and therefore may be a pre-existing condition.21 Retroversion through the femoral shaft has been shown to increase hip contract stresses with flexion and can be an independent source of FAI through a pincer-type mechanism.22 Alternatively, femoral neck retroversion can be a consequence of SCFE. With post-SCFE cam-type lesions, retroversion of the femur is a second hit that could account for why some patients with similar proximal head-neck geometry experience more pain and joint deterioration.23 A study of 265 hips with FAI found femoral retroversion increased the odds of developing osteoarthritis by 1.6.24 Since symptomatic FAI can be a precursor to osteoarthritis, these results are consistent with our finding that external foot progression, a surrogate for femoral retroversion, increased risk independent of the alpha angle. External foot progression may also be an adaptive behavior to avoid FAI by rotating the cam away from the socket.23 Support for this explanation comes from the fact that 52% (11/21) of our cases with external foot progression also had a Drehmann sign.
The major strength of our study is the design in which we utilized other patients with post-SCFE deformity as controls and were able to perform multivariable analysis. Other studies have compared SCFE patients to normal populations, but this is less helpful when trying to determine the risk for a patient who does have altered anatomy. Since the slip angle does not always directly correlate with the degree of intra-articular damage from FAI, we evaluated risk factors from multiple spheres including demographics, radiographs, physical examination, and gait observation. Although our numbers were small, this is still one of the largest reports of symptomatic FAI in SCFE patients.
Our study has several limitations. The key weaknesses are the retrospective design and small numbers. Proportional matching was not possible due to high loss to follow-up of controls. We included controls who had at least 8 months of follow-up since this was the median time to presentation with symptoms in our cases, but it is possible they will become symptomatic in the future. Also, our study only examined patients who became symptomatic during adolescence, and our results cannot be used to assess lifetime FAI risk. Additionally, we were underpowered to accurately assess how some variables contributed to the overall risk of developing symptoms. Each additional pathologic finding may incrementally increase risk, but larger and longer-term studies are necessary to develop a comprehensive predictive model. Finally, 3D imaging may provide greater detail in identifying which aspects of the deformity contribute most to the development of symptoms than the plain radiographs utilized.
In conclusion, we have shown that the slip angle is not the most important variable for differentiating the risk of symptomatic FAI in post-SCFE deformity in the short term. Slips of similar severity as defined by slip angle were found to have variable amounts of translation and rotation as indicated by the alpha angle. Differences in three-dimensional geometry are clearly important. External foot progression could be a consequence of pre-existing or acquired femoral retroversion, which exacerbates impingement from the residual deformity. Each year increase in age doubles risk, likely due to less remodeling potential, and age >12 trended towards a stratification point. Our recommendation is to assess for an alpha angle ≥60° and external foot progression in all post-SCFE patients. Patients with these findings should be counseled about the increased likelihood of developing symptoms, which helps families set expectations. By the time our cases underwent a second surgery, the vast majority had a labral tear and nearly a quarter had acetabular cartilage damage. Thus, knowing earlier that these patients are at risk for becoming symptomatic could allow the surgeon to offer surgery sooner and possibly prevent some of the intra-articular damage from occurring. Future studies are still needed to determine whether intervention alters the natural history of osteoarthritis progression and how delaying treatment until symptoms develop impacts that progression.
Source of funding
This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.
Footnotes
Investigation performed at Texas Children's Hospital, Houston, TX.
Contributor Information
Melissa M. Allen, Email: MAllen5@augusta.edu.
Ramesh B. Ghanta, Email: Ramesh.Ghanta@bcm.edu.
Matthew Lahey, Email: Mattlahey94@gmail.com.
Scott B. Rosenfeld, Email: sbrosenf@texaschildrens.org.
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