Single-level transforaminal interbody fusion for traumatic lumbosacral fracture-dislocation: a case report.

L5S1 fracture-dislocations are rare three-column injuries. The infrequency of this injury has led to a lack of a universally accepted treatment strategy. Transforaminal lumbar interbody fusion (TLIF) has been shown to be an effective approach for interbody fusion in degenerative indications, but has not been previously reported in the operative management of traumatic lumbosacral dislocation. The authors report a case of traumatic L5S1 fracture-dislocation in a 30-year-old male, presenting with a right-sided L5 neurologic deficit, following a street sweeper accident. Imaging revealed an L5S1 fracture-dislocation with fracture of the S1 body. Open reduction with TLIF and L5S1 posterolateral instrumented fusion was carried out within 24 hours of injury. Excellent reduction was obtained, and maintained at long-term follow-up, with complete resolution of pain and neurologic deficit. In this patient, L5S1 fracture-dislocation was treated successfully, with an excellent outcome, with a single level TLIF and instrumented posterolateral fusion at L5S1.

Cross-modulatory effects of clopidogrel and heparin on platelet and fibrin incorporation in thrombosis.

Pharmacologic inhibition of platelet activation and aggregation is a mainstay for reducing the incidence of arterial thrombosis, whereas anticoagulation is the primary approach for preventing the development of venous thrombosis. The effect of standard pharmacologic agents on their reciprocal vessel - anticoagulants on arterial thrombosis and platelet inhibitor on venous thrombosis - is relatively understudied. This study was designed to evaluate murine large-vessel arterial or venous thrombosis under conditions of either fibrin or platelet inhibition. In this study, heparin and clopidogrel were used as standard anticoagulant and platelet inhibitor, respectively, evaluating both large artery and vein thrombosis in mice, using in-vivo fluorescence imaging to simultaneously measure fibrin and platelet levels at the thrombus induction site. Heparin reduced both fibrin and platelet development in both arteries and veins, with stronger influences on fibrin accrual. Clopidogrel had a stronger effect in arteries, reducing both platelet and fibrin accumulation. Clopidogrel also reduced platelet accumulation with venous thrombosis, but the reductions in fibrin formation did not reach statistical significance. These findings illustrate the interactive role of platelet activity and coagulation in the development of large-vessel thrombosis, with inhibition of one thrombotic component showing profound effects on the other component in both arterial and venous thrombosis.