Stable thoracolumbar fracture is a common injury. The factors that determine its outcome are unclear. Aspects of injury severity were analysed for their ability to predict outcome by controlling other outcome-affecting factors (patient's pre-injury health status, legal aspects, associated injuries, etc.). No reliable disc injury severity grading system was available and therefore a new system was developed. A prospective observational study of 44 conservatively treated patients with stable fractures between T11 and L5 was conducted. Bony injury severity was scored based on comminution, apposition and kyphosis parameters. Disc injury severity was scored by the new scale based on variables – Herniation, Indentation, Height decrease and Signal change – seen in MRI. Ten outcome domains (five domains of pain and function each) were assessed at 1 to 2 years from injury. The data was analysed by non-parametric correlation and stepwise-linear regression analysis to assess the predictive value of different variables (patient factors, injury factors and social factor) to outcome. The correlation coefficients between injury severity and outcome were consistently higher with disc injury severity than bony. Disc injury severity showed highest predictive value for both pain (29%) and functional (16%) outcomes, whereas the bony injury severity parameters (kyphosis, etc.) and the posterior ligament injury severity provided no prediction of outcome. According to AO classification, the fractures were A1, A2, A3 and B1; in this spectrum of injuries, the AO classification had no prediction of outcome. The disc injury score also had a good predictive value for final disc degeneration. Disc injury severity should be gauged in advising prognosis and treatment. The new disc injury severity grading system showed good construct validity.
Ten percent of fractures end in delayed or non-union. NSAIDs have been linked to an inhibitory action on fracture repair for three decades yet the mechanism of action remains to be elucidated. Cancer research has identified that NSAIDs impede cell proliferation by inhibiting angiogenesis. It is proposed that a similar mechanism occurs in the induction of NSAID induced non-union. We have investigated this hypothesis in a randomised placebo control trial of the NSAID rofecoxib using a murine femoral fracture. All animals had an open femoral fracture treated using an external fixator. Outcomes measures included x-ray, histology and biomechanical testing, with laser Doppler used to assess blood flow across the fracture gap. Radiology showed similar healing patterns in both groups; however, at the later stages (day 32) the NSAID group had significantly poorer healing. Histological analysis showed that controls healed quicker (days 24 and 32), with more callus (day 8) and less fibrous tissue (Day 32). Biomechanical testing showed controls were stronger at day 32. Both groups exhibited a similar pattern of blood flow; however NSAIDs exhibited a lower median flow from day 4 onwards (significant at days 4, 16 and 24). Positive correlations were demonstrated between both histological and radiographic assessments of healing, with increasing blood flow. NSAID animals exhibited lower flows and poorer healing by all outcomes. Regression analysis demonstrates, however, that the negative effect of NSAIDs on fracture repair is independent of its inhibitory action on blood flow. COX-2 inhibitors are marketed as having cleaner side effect profiles and are widely used in trauma patients. Following development of a novel method of analysing functional vascularity across a fracture gap, we have demonstrated that the COX-2 inhibitor rofecoxib has a significant negative effect on blood flow at the fracture gap alongside inhibiting fracture repair.
