Predicting vasospasm after aneurismal subarachnoid hemorrhage with C reactive protein levels

Flávio R Romero,Roberto C Gabarra,Antônio J M Cataneo,Marco A Zanini,Daniele C Cataneo,Luis G Ducati

doi:10.4236/health.2013.57a5001

Abstract

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 daily between admission and 10th days. Glasgow Outcome Scale (GOS) and the modified Rankin Scale (mRS) were used to predict outcome. Results: A progressive increase in the CRP levels from the admission to the 3rd postictal 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.

Highlights

Cerebral vasospasm is the major cause of delayed morbidity following aneurysmal subarachnoid hemorrhage (SAH)
A multiple inflammatory mechanisms are directly involved in the pathogenesis of cerebral vasospasm, with increased levels of various soluble adhesion molecules and cytokines have been detected in the plasma and cerebrospinal fluid (CSF) of patients with SAH [2,3,6,7,8,9]
The inclusion criteria were as follows: 1) diagnosis of aSAH and cerebral aneurysms established by a CT scan and four-vessel DS angiography study; 2) patient age > 18 years; 3) patient admission to our institutions within the first 24 hours postictus

Summary

Introduction

Cerebral vasospasm is the major cause of delayed morbidity following aneurysmal subarachnoid hemorrhage (SAH). A multiple inflammatory mechanisms are directly involved in the pathogenesis of cerebral vasospasm, with increased levels of various soluble adhesion molecules (such as E-selectin, intercellular adhesion molecule-1, and vascular adhesion molecule-1) and cytokines (such as IL-6 and IL-1) have been detected in the plasma and cerebrospinal fluid (CSF) of patients with SAH [2,3,6,7,8,9]. The measurement of sensitive inflammatory markers such as CRP significantly increases our ability to predict with accuracy and prevent or appropriately treat coronary thrombotic events [10,11,12,13]. Previous clinical studies have shown that elevated levels of high-sensitivity CRP could predict the development of coronary vasospasm [8,9]

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