Avascular necrosis (AVN) of the femoral head after a traumatic posteri
or hip dislocation (Thompson and Epstein type I) has been hypothesized
to occur due to changes in blood flow. However, to the best of our kn
owledge of the English literature, a human cadaveric angiographic stud
y has never been performed to delineate these vascular changes. Six fr
esh frozen human cadavers were used to examine the effects of posterio
r 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 wit
h a radioopaque colored latex liquid polymer (Microfil) and examined u
nder cinefluoroscopy. The contra lateral hips were used as controls an
d were examined in a similar manner. Both hips of the cadavers were ha
rvested, and a macroscopic and microscopic examination was performed.
The cine-fluoroscopic examination delineated the dynamic effects of po
sterior dislocation on the surrounding vasculature. Filling defects we
re most notable at the junction of the external iliac and common femor
al arteries. Filling defects were also present in the circumflex vesse
ls. Compared to controls, the common femoral and circumflex vessel fil
ling defects were statistically significant (p < 0.004). These defects
were secondary to an apparent stretching and twisting of the artery c
aused by the pull and rotation of the dislocated hip. A number of coll
ateral vessels from the gluteal arteries were also demonstrated on flu
oroscopic examination. The macro and microscopic examination did not s
how 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 h
ip do occur. The vessels that appear to be most affected by the disloc
ation are the common femoral and circumflex vessels. However, these ex
traosseous changes do not consistently result in changes in the intrao
sseous blood flow possibly due to collateral circulation. Relocating t
he femoral head in a traumatic posterior hip dislocation may provide e
arlier 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 immed
iate ischemia at the time of injury but by also producing a progressiv
e and delayed form of arterial damage in the femoral and circumflex ve
ssels. AVN may not be an absolute outcome of posterior hip dislocation
s due to preexisting collateral circulation and/or the preservation of
the femoral circumflex vessels.