Recently, Rached et al. published an article entitled ‘Slipped capital femoral epiphysis: reduction as a risk factor for avascular necrosis’ 1. The aim of the study was to identify high-risk factors associated with the complications of slipped capital femoral epiphysis (SCFE), especially avascular necrosis (AVN). The authors draw the conclusion that closed reduction and fixation between 24 h and 7 days and a greater slippage correction increased the risk of AVN. Although SCFE-associated AVN often progress to subchondral collapse and femoral head deformation, the concrete pathogenesis and etiology are still unclear; several risk factors have been postulated, including damage of the femoral head blood supply, increased intracapsular pressures, and repeated reduction. Peterson et al. 2 found that urgent reduction within 24 h may significantly reduce the occurrence of AVN. Maeda et al. 3 examined the effect of SCFE on femoral head blood supply; they found that before reduction, the vascular supply is damaged because of the slips. Herrera-Soto et al. 4 found that hip joint pressure increased in unstable SCFE, causing a tamponade effect that damages the blood supply. Although we could not interpret that AVN were caused by damaged blood supply and increased intracapsular pressures, at least they play a partial role in the pathophysiology of AVN.
Rached et al. 1 reported that an ‘unsafe window’ and degrees of correction are associated with the complication of AVN, conflicts with previous findings, and makes us more confused about the treatment of patients with SCFE. We found that slippage damages the blood supply and increases intracapsular pressures. It is not difficult to understand that the more severe the slips, the more obvious this effect. Rached et al. found that treatment during the ‘unsafe window’ and the correction angle are risk factors of AVN 1. We consider that severe SCFE may damage the vascular supply before the reduction, and earlier reduction does not contribute toward the risk of AVN; in contrast, an earlier stage of reduction may prove to be helpful 3. The ‘unsafe window’ and the correction angle are confounding factors in the study by Rached et al. We conclude that the degree of slips is a major risk factor of AVN, although we lack clinical evidence with large samples.
In brief, SCFE-associated AVN is a complex process that has still not been understood, but increasingly more studies have found that the levels of slippage are closely related to AVN. We believe that Rached et al.’s conclusion is assertive and requires verification in a future study. Further research is required to examine the pathogenesis of SCFE-associated AVN and how this devastating complication can be minimized.
Conflicts of interest
There are no conflicts of interest.
1. Rached E, Akkari M, Braga SR, Minutti MF, Santili C. Slipped capital femoral epiphysis: reduction as a risk factor for avascular necrosis. J Pediatr Orthop B. 2012;21:331–334
2. Peterson MD, Weiner DS, Green NE, Terry CL. Acute slipped capital femoral epiphysis: the value and safety of urgent manipulative reduction. J Pediatr Orthop. 1997;17:648–654
3. Maeda S, Kita A, Funayama K, Kokubun S. Vascular supply to slipped capital femoral epiphysis. J Pediatr Orthop. 2001;21:664–667
4. Herrera-Soto JA, Duffy MF, Birnbaum MA, Vander Have KL. Increased intracapsular pressures after unstable slipped capital femoral epiphysis. J Pediatr Orthop. 2008;28:723–728