Pulmonary embolism after adult spinal deformity surgery.

STUDY DESIGN: Retrospective review. OBJECTIVE: To determine the incidence and identify the associated risk factors of pulmonary embolism (PE) in patients who receive pharmacologic thromboprophylaxis after adult spinal deformity surgery. SUMMARY OF BACKGROUND DATA: The risk of PE after adult spinal deformity surgery is reported to be as high as 2.2%. However, the incidence and associated risks of PE in the same patient population who receive postoperative pharmacologic thromboprophylaxis is unknown. METHODS: The study included 361 adult patients with spinal deformity who underwent 407 corrective spinal procedures for scoliosis, kyphosis, or kyphoscoliosis. The incidence of PE was determined and compared with a study (historical control) of similar patients undergoing similar surgery but without postoperative pharmacologic thromboprophylaxis. Their demographic information, American Society of Anesthesiologists score, operative time, surgical approach, surgical complexity, and intraoperative blood loss were also analyzed to determine the presence of associated risk factors. RESULTS: Despite universal pharmacologic thromboprophylaxis, 10 pulmonary emboli (2.4%) were diagnosed. Patients undergoing anterior spinal surgery were at a significantly higher risk than those undergoing posterior spinal surgery (P = 0.024). The right-side anterior approach was also associated with a significantly higher incidence of PE compared with the left-sided anterior approach (P = 0.018). Although the rate of PE after posterior spinal surgery did not differ from the historical control, the rate of PE after anterior surgery was reduced by 50% compared with the historical control. Age, gender, estimated blood loss, operative time, revision status, and the number of fusion levels were not significant variables for PE. There were 2 epidural hematomas requiring decompression (0.48%) and 1 wound hematoma (0.24%). CONCLUSION: Although pharmacologic thromboprophylaxis probably does not have a role after posterior spinal surgery, the data in this study suggest that it does lower the incidence of PE after anterior spinal surgery.

High-dose ibuprofen for reduction of striatal infarcts during middle cerebral artery occlusion in rats.

OBJECT: Ibuprofen is an antiinflammatory drug that disrupts leukocyte-endothelial cell interactions by limiting expression of endothelial adhesion molecules such as intercellular adhesion molecule-1 (ICAM-1), also known as CD54. The authors hypothesized that ibuprofen could reduce the size of the infarct associated with transient focal ischemia by inhibition of ICAM-1 expression, and they evaluated its effects in rats treated with middle cerebral artery (MCA) occlusion. Ibuprofen treatment was compared with mild systemic hypothermia, which is known to be neuroprotective and is commonly used during neurosurgical procedures. METHODS: The maximum ibuprofen dose (240 mg/kg/day) that could be tolerated with no systemic toxicity was established in the initial experiments. In the efficacy experiment, rats were pretreated with vehicle, ibuprofen, or hypothermia (33 degrees C) prior to 2 hours of MCA occlusion; then their brains were harvested at 24 hours of reperfusion for histological studies. End-ischemic cerebral blood flow (CBF) was evaluated using [14C]iodoantipyrine autoradiography in additional cohorts. Expression of ICAM-1 within ischemic compared with nonischemic caudate nucleus and putamen (striatum) or cortex was evaluated using immunohistochemical studies. Compared with vehicle treatment, ibuprofen produced a 46.2% reduction (p = 0.01) in striatal infarcts, which was comparable to hypothermia (48.7% reduction, p = 0.02). Ibuprofen did not alter end-ischemic CBF in any region studied, and the ibuprofen treatment group had the lowest proportion of animals with marked ICAM-1 staining. CONCLUSIONS: Ibuprofen given in maximum tolerated doses reduces the striatal infarct size after focal cerebral ischemia. The neuroprotective mechanism does not work through preservation of intraischemic CBF and is consistent with inhibition of ICAM-1 expression; however, at the doses used in this study, other effects of ibuprofen on platelet and endothelial function are possible.