Predicting vasospasm after aneurismal subarachnoid hemorrhage with C reactive protein levels

Abstract

<p> <span style="font-size:10.0pt;font-family:;" "=""><span style="font-family:Verdana;">Aim: The interest of inflammatory marker increased in the last years, even in preventing clinical outcome after subarachnoid hemorrhage (SAH). Our objective was to study the relationships between C-reactive protein levels and clinical outcome and the development of cerebral vasospasm after aneurismal SAH. Methods: One hundred adult patients with aneurismal SAH were prospectively evaluated. Glasgow Coma Scale (GCS) score, Hunt and Hess grade, Fisher grade, CT scans, digital subtraction angiography studies, transcranial doppler (TCD) and daily neurological examinations were recorded. Serial serum CRP measurements were obtained on d</span><span style="font-family:Verdana;">aily between admission and 10th day</span><span style="font-family:Verdana;">s. Glasgow Outcome Scale (GOS) and the modified Rankin Scale (mRS) were used to predict outcome. Results: A progressive increase in the CR</span><span style="font-family:Verdana;">P levels from the admission to the 3rd p</span><span style="font-family:Verdana;">ostictal day was observed, followed by a slow decrease until the 9th day. Hemodynamic changes in TCD were associated with higher serum CRP levels. Patients with lower GCS scores presented with increased CRP levels. Patients with higher Hunt and Hess grades on admission developed significantly higher CRP serum levels. Patients with higher admission Fisher grades showed increased levels of CRP. A statistically significant inverse correlation was established in our series between CRP serum levels and GOS and mRS scores on discharge and CRP levels. Conclusion: Increased CRP levels were strongly associated with poor clinical outcome. CRP levels can predict cerebral vasospasm and delayed ischemic deficits with higher statistic significance. There are relationships between hemodynamic chances in TCD and higher CRP levels.</span></span> </p

C-reactive protein and vasospasm after aneurysmal subarachnoid hemorrhage1

“…Pathogenesis of vasospasm is due to smooth muscle contraction (entry and release of calcium and activation of calcium / calmodulin-dependent myosin light-chain kinase), endothelial injury (nitric oxide and endothelin-1 derangement), inflammation (inflammatory cytokines, intercellular adhesion molecules and genetic upregulation of inflammatory, proliferative and extracellular matrix-regulating genes) and vessel remodeling 1,3,[10][11][12][13] .…”