Abstract
Introduction The precise contribution of the posterior longitudinal ligament (PLL) and disc annulus in the burst fracture setting and their potential relative roles during intra operative reduction manoeuvres remains unclear. The anatomical attachments of the posterosuperior fragment most often associated with canal occlusion and potential neurological compromise are not well described in a reproducible model.
Methods Burst fractures were induced using a pendulum impact tester. The jig allowed for accurate positioning in all planes and for precise delivery of both the magnitude and vector of the impact force. This allowed for creation of fracture all three major groups of the AO classification. The A3 (burst fracture) was produced in 10 cadaveric sheep spines by delivering a neutral force vector on a physiologically flexed spine. The morphology of the fracture was confirmed by CT. Subsequent laminectomy was performed and the anatomical attachments of the large fragments were identified.
Results The PLL was identified following laminectomy in each case. In six of the ten spines there had been significant disruption of the longitudinal structure of the PLL .In a further two cases there had been stripping of the PLL from the posterior aspect of the vertebral body in association with the retropulsed canal fragment. Subsequent excision of the PLL from the posterior aspects of vertebral body and discs did not compromise the attachment of the retropulsed fragment to the disc annulus in any case.
Discussion This study confirms the anatomical relationship between disc fragment and disc annulus in the burst fracture setting. The strong attachment between fragment and disc facilitate rotation of the fragment about this hinge and into the canal. Subsequent intraoperative reduction of this fragment by restoration of disc height may require contribution both from this annular attachment and from tension set up in an intact PLL. The relative contributions of each of these structures in the reduction manoeuvre remains unclear.
The abstracts were prepared by Assoc Prof Bruce McPhee. Correspondence should be addressed to him at the Division of Orthopaedics, The University of Queensland, Clinical Sciences Building, Royal Brisbane Hospital, Herston, Brisbane, 4029, Australia.
