What Is the Cause of Avascular Necrosis in Unstable Slipped Capital Femoral Epiphysis and What Can Be Done to Lower the Rate?

Abstract

An unstable slipped capital femoral epiphysis (SCFE) is associated with a high rate of avascular necrosis (AVN). Etiology of the AVN is not completely known and likely multifactorial. Potential causes are a tear/anatomic disruption of the retinacular vessels to the epiphysis, kinking of the retinacular vessels, or vascular tamponade due to increased intracapsular pressure. A review of the recent literature of unstable SCFE was performed to abstract various potential causes of AVN. The overall rate of AVN was 21% (88 of 417). Kinking of the retinacular vessels was demonstrated angiographically in 5 unstable SCFEs where the vessels did not fill in 3; in 1 the vascularity returned after reduction. Intracapsular joint pressure was measured in 13 unstable SCFEs with an average of 48 mm Hg on the unstable side compared with 23 mm Hg in the opposite normal hip. After manipulative reduction the pressures increased to 75 mm Hg, and dropped markedly to 17 mm Hg after capsulotomy and decompression. Although a complete tear of the vessels is another possibility, there are no described cases in the literature. Means to lower AVN depends upon its etiology. In 28 unstable SCFEs urgent reduction, internal fixation and decompressive arthrotomy resulted in a rate of 14% (4 of 28). Urgent open reduction through an anterior approach with smooth Kirschner wire fixation resulted in a rate of 5% (3 of 64). The modified Dunn procedure using a surgical dislocation resulted in a rate of 8% (2 of 26). Larger and combined series will be needed to determine the best treatment to minimize the rate of AVN in the unstable SCFE. With today's present techniques, AVN in the unstable SCFE will never be a "never" event.