Introduction
Slipped capital femoral epiphysis (SCFE) is one of the most common adolescent hip conditions that have potential long-term sequelae and are dependent on the severity of the SCFE [
1]. SCFE can be classified into two groups: stable and unstable according to Loder et al. [
2]. A stable SCFE is defined as one where the patient is able to ambulate, with or without crutches, regardless of the duration of symptoms, whereas an unstable SCFE is defined as one where the patient cannot ambulate, with or without crutches, regardless of the duration of symptoms. This classification system is the most useful because of its correlation with prognosis by estimating the risk of osteonecrosis of the femoral head that was reported as 47 % for unstable SCFE in this classic paper [
2].
The management of unstable SCFE remains controversial, with little consensus on the best treatment and with most recommendations made with level IV evidence [
3]. However, in situ pinning remains the gold standard for the management of unstable SCFE [
4]. The literature suggests that urgent reduction with internal fixation and decompressive arthrotomy results in the lowest rate of osteonecrosis of the femoral head for unstable SCFE [
3]. The current controversies regarding the treatment of unstable SCFE include the role of hip decompression, the timing of intervention, the role of reduction, the type of surgical fixation, and the post-operative management. The goals of treatment of unstable SCFE include the avoidance of osteonecrosis and chondrolysis of the femoral head, prevention of further slippage, and correction of proximal femoral deformity. More recently, the role of surgical dislocation in the management of moderate and severe unstable SCFE has become popularized because of the advantage of anatomically correcting the acute proximal femoral deformity and, thus, preventing osteoarthritis secondary to femoroacetabular impingement, with reported rates of osteonecrosis ranging from 0 to 6.7 % [
5,
6].
Osteonecrosis of the femoral head is the most significant complication in patients with unstable SCFE. The rate of osteonecrosis varies between studies and has been reported to range from 3 to 58 % [
7]. A recent review of unstable SCFE reported an overall rate of osteonecrosis of 23.9 % with multiple treatment modalities used and limited data concerning complications after treatment of unstable SCFE [
8]. The etiology of osteonecrosis of the femoral head remains unknown and is most likely multifactorial due to disruption or kinking of the retinacular vessels to the epiphysis or vascular tamponade due to increased intracapsular hip pressure. Kinking of the retinacular vessels has been demonstrated in an angiographic study of unstable SCFE with restoration of blood supply after reduction [
9]. Increased intracapsular hip pressure has also been studied in unstable SCFE. Herrera-Soto et al. [
10] measured the intracapsular joint pressure in 13 unstable SCFE. The mean intracapsular joint pressure of the unstable SCFE measured 48 mm Hg, which increased to 75 mm Hg after manipulative reduction and dropped to 17 mm Hg after capsulotomy and decompression.
The aim of our study was to systematically review the literature that compares hip decompression to no hip decompression of unstable SCFE. The primary outcome analysis involved the rate of osteonecrosis of the femoral head.
Discussion
Hip decompression was associated with a 16.2 % pooled rate of osteonecrosis of the femoral head compared to 22.2 % for no hip decompression in patients with unstable SCFE. The current study revealed no statistically significant difference in the observed rate of osteonecrosis in unstable SCFE when comparing hip decompression and no hip decompression. The results were consistent across different assumptions. The extent to which this statement reflects the true outcome of comparison requires an understanding of the limitations in the current literature and included studies and consideration of the conduct and interpretation of the results of the analyses. The ability to detect a difference is further confounded by the relatively small sample size. Although our study assessed the effect of hip decompression, there was varied reporting regarding the key determinants of unstable SCFE known to influence the rate of osteonecrosis, and none of the included studies reported effect estimates adjusted for these potential confounders.
Intracapsular hip pressure is increased after traumatic femoral neck fractures and, thus, increased intracapsular hip pressure is a known cause of osteonecrosis in femoral neck fractures in children [
24,
25]. Decompression of the hip joint can decrease the intracapsular hip pressure and the incidence of osteonecrosis in femoral neck fractures in children [
26]. Soto-Hall et al. [
27] was the first to measure intracapsular hip pressure in a traumatic SCFE and found a significant increase in the intracapsular hip pressure after reduction (58 mm Hg) compared to the pre-reduction pressure of 12 mm Hg. More recently, Herrera-Soto et al. [
10] suggested that unstable SCFE behave like intracapsular hip fractures. Patients with unstable SCFE have intracapsular hip pressures increased to levels higher than those of a compartment syndrome causing a tamponade effect by occluding the venous and arteriole vasculature caused by hematoma formation and effusion. Herrera-Soto et al. [
10] observed a 67 % elevation in the intracapsular hip pressure of unstable SCFE after gentle manipulation from 45 to 75 mm Hg. The increase in intracapsular pressure returned to normal values after capsulotomy with a mean pressure of 17 mm Hg. The difference between pre-capsulotomy and post-capsulotomy intracapsular hip pressures was statistically significant. Hence, the authors recommended a capsulotomy to decompress unstable SCFE, especially if gentle manipulation is attempted.
Parsch et al. [
28] observed pure blood in 82.8 % of arthrotomies and 17.2 % had a blood-stained rose or clear effusion in a series of 64 consecutive cases of unstable SCFE. In two of the three cases that developed osteonecrosis, blood was drained following hip decompression. Another important variable for the treatment of unstable SCFE is the timing of reduction. Peterson et al. [
21] suggested that acute displacement of the femoral epiphysis compromises the blood flow which may be restored by a timely reduction for the unstable SCFE. Both Petersen et al. [
21] and Gordon et al. [
18] reported lower rates of osteonecrosis in patients treated within 24 h compared to those treated after 24 h. Thus, emergent treatment and hip decompression either with capsulotomy or aspiration is currently recommended in all unstable SCFE to optimize blood flow to the femoral head [
4].
There is currently no comparative study demonstrating the superiority of decompression over no decompression in terms of lowering the intracapsular hip pressure of unstable SCFE and preventing osteonecrosis of the femoral head. Surveys of both the European and North American pediatric orthopedic societies showed that hip decompression was recommended by 29 % of European and 35 % of North American pediatric orthopedic surgeons [
29,
30]. Our systematic review identified nine studies [
2,
15‐
22] (level III/IV) that compared the rate of osteonecrosis in patients who underwent hip decompression compared to no hip decompression. The one retrospective cohort study included in the analysis was of good methodological quality using the Newcastle–Ottawa Scale with limitations in the comparability domain. Because of the small number and type of included studies, we did not incorporate quality in our sensitivity analysis. The simplest approach is to judge studies on specific domains of quality that are most relevant to the control of bias for that particular study.
Our findings are consistent with the literature, with an overall rate of osteonecrosis of 19.5 %. We found that hip decompression was not associated with a lower rate of osteonecrosis in patients with unstable SCFE. Sensitivity analyses revealed no significant change in the OR of osteonecrosis when no bony and bony procedures were performed with hip decompression in unstable SCFE. However, orthopedic surgeons may consider hip decompression of unstable SCFE as an option that can potentially decompress the intracapsular hip pressure and optimize the blood flow to the femoral head.
Our analysis has a limitation due to the paucity of studies addressing this pivotal issue. There were only nine eligible published studies, but we chose to perform the meta-analysis to provide more generalizable results on the effect estimate. The only outcome measure examined in this meta-analysis was the rate of osteonecrosis. This is a clinically relevant and important outcome and the definition of osteonecrosis was the same amongst the nine studies. Other important factors, such as the time of intervention, the role of reduction, the type of fixation, and post-operative management, could not be controlled for in this analysis and require further study. The limited number of studies addressing these factors permits limited conclusions from the current study. These factors will particularly vary from center to center and variations in clinical skill, implant use, and patient assessment will further confound the results because of these inconsistencies. In addition, others have expressed a concern regarding the different and variable definitions for stable and unstable SCFE [
31]. However, the definition of unstable SCFE was uniform amongst the studies included in our analysis. Publication bias was not significant in our meta-analysis.
There has recently been a change of approach to unstable SCFE with urgent reduction, decompression and fixation or open reduction, and fixation using surgical dislocation. The rate of osteonecrosis has been reported to be as low as 8 %, but larger series are required in order to determine the safe approach to unstable SCFE using these surgical techniques [
7]. Despite these surgical advancements, Carney et al. [
1] concluded that in situ pinning without reduction is the most common treatment worldwide, with the fewest complications.
Our study has only assessed the effect of hip decompression on the rate of osteonecrosis for unstable SCFE, which is one of many factors that may influence osteonecrosis. Hence, the cumulative evidence at present does not indicate an association between hip decompression and a lower rate of osteonecrosis for unstable SCFE. However, orthopedic surgeons may opt to decompress unstable SCFE to decrease intracapsular hip pressure and optimize the blood flow to the femoral head. The results of our meta-analysis are based on observational studies and, thus, further attention should be directed to studies of good methodological quality. Therefore, multicenter prospective cohort studies are required and will be able to answer this question with more certainty and a higher level of evidence.