Posterior hip dislocations: a cadaveric angiographic study

Avascular necrosis (AVN) of the femoral head after a traumatic posterior hip dislocation (Thompson and Epstein type I) has been hypothesized to occur due to changes in blood flow. However, to the best of our knowledge of the English literature, a human cadaveric angiographic study has never been performed to delineate these vascular changes. Six fresh frozen human cadavers were used to examine the effects of posterior hip dislocation on the extraosseous and intraosseous blood supply to the femoral head and neck. After a forceful posterior hip dislocation was performed on the cadavers, the proximal vessels were injected with a radioopaque colored latex liquid polymer (Microfil) and examined under cinefluoroscopy. The contra lateral hips were used as controls and were examined in a similar manner. Both hips of the cadavers were harvested, and a macroscopic and microscopic examination was performed. The cine-fluoroscopic examination delineated the dynamic effects of posterior dislocation on the surrounding vasculature. Filling defects were most notable at the junction of the external iliac and common femoral arteries. Filling defects were also present in the circumflex vessels. Compared to controls, the common femoral and circumflex vessel filling defects were statistically significant (p < 0.004). These defects were secondary to an apparent stretching and twisting of the artery caused by the pull and rotation of the dislocated hip. A number of collateral vessels from the gluteal arteries were also demonstrated on fluoroscopic examination. The macro and microscopic examination did not show a qualitative or a quantitative difference in the amount of latex present in the dislocated and control groups. Based on the results of this study, changes in the extraosseous blood flow to the dislocated hip do occur. The vessels that appear to be most affected by the dislocation are the common femoral and circumflex vessels. However, these extraosseous changes do not consistently result in changes in the intraosseous blood flow possibly due to collateral circulation. Relocating the femoral head in a traumatic posterior hip dislocation may provide earlier blood flow to the femoral head by relieving tension across the femoral and circumflex vessels. Delayed relocation could contribute to the development of AVN in the femoral head by not only inducing immediate ischemia at the time of injury but by also producing a progressive and delayed form of arterial damage in the femoral and circumflex vessels. AVN may not be an absolute outcome of posterior hip dislocations due to preexisting collateral circulation and/or the preservation of the femoral circumflex vessels.