Prevalence of venous thromboembolic events after elective major thoracolumbar degenerative spine surgery.

STUDY DESIGN: A case-control study. OBJECTIVE: The purposes of this study were to establish the prevalence of venous thromboembolic disease in patients undergoing elective major thoracolumbar degenerative spine surgery and identify risk factors. SUMMARY OF BACKGROUND DATA: Venous thromboembolic events (VTE) are a serious complication of orthopedic surgery, but the prevalence of VTE after elective thoracolumbar degenerative spine surgery is not well known. METHODS: This was a case-control study of 5766 consecutive elective thoracolumbar degenerative spine surgeries. Symptomatic pulmonary emboli (PE) were diagnosed by spiral chest CT scans, nuclear scintigraphic ventilation-perfusion, and angiography. Deep vein thromboses (DVT) were diagnosed by venous duplex scans. The prevalence of VTE was analyzed according to patient demographic variables and type of surgery performed. RESULTS: The prevalence of developing a VTE was 1.5% (89/5766), with a prevalence of symptomatic PE of 0.88% (51/5766) and DVT of 0.66% (38/5766). There were 47% males and 53% females with a mean age of 60.3 years. In patients undergoing 5-segment fusions the prevalence of PE was 3.1% (P=0.022). Patients who had ≥4 segments fused had a prevalence of PE of 1.7% (P=0.014). The odds of having a PE in those above 65 years at the time of surgery were 2.196 times as large as for those below 65 years. Noncontributory factors included sex, instrumentation, and revision surgery. CONCLUSIONS: This case-control study of 5766 patients who underwent elective thoracolumbar degenerative spine surgery revealed a prevalence of VTE of 1.5%, with a prevalence of PE of 0.88% and DVT of 0.66%. Patients with increasingly extensive surgery had a higher risk of PE, specifically those undergoing fusion of ≥5 segments.

Role of raf-1 kinase in diabetes-induced accelerated apoptosis of retinal capillary cells.

Small molecular weight G-proteins serve as fundamental signaling switches that regulate cell fates by coupling receptor activation to downstream effector pathways. H-Ras, a small molecular weight G-protein, in its active form, recruits Raf. Activated Raf via a signaling transduction pathway regulates apoptosis. Our previous studies have shown that H-Ras has an important role in the loss of retinal capillary cells in diabetes. The purpose of this study is to investigate the role of Raf-1 in the development of diabetic retinopathy. Bovine retinal endothelial cells were incubated in 5 mM or 20 mM glucose in the presence of Raf-1 kinase inhibitor (10µM of GW5074), activator (200µM of ZM336374) or mitogen activated protein kinase inhibitor (30µM of PD098059) for five days. Apoptosis of endothelial cells was analyzed by ELISA and activation of Raf-1 and its downstream signaling proteins by determining genes and protein expressions. Inhibition of Raf-1 kinase repressed glucose-induced apoptosis of the cells by 75%, and this was accompanied by attenuation of activation of MAP kinase, ERK-1, nuclear transcriptional factor and caspase-3. In contrast, ZM336374 further increased glucose-induced apoptosis by 50%, and activated the signaling molecules and caspase 3 by over 30%. Further, PD098059 alone also attenuated glucose-induced apoptosis of retinal endothelial cells. These findings demonstrate that accelerated loss of retinal capillary cells in diabetes is mediated via Raf-1 kinase activation. Modulation of Raf-1 kinase activity could, in part, regulate apoptosis of retinal endothelial cells, which may ultimately contribute to the development of diabetic retinopathy.