Possible role of the C-reactive protein and white blood cell count in the pathogenesis of cerebral vasospasm following aneurysmal subarachnoid hemorrhage

The delayed ischemic neurologic deficit (DIND) is a common and potentially devastating complication in patients who have sustained subarachnoid hemorrhage (SAH). Recent evidence suggests that various constituents of the inflammatory response may be critical in the pathogenesis of this ischemic compl...

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Veröffentlicht in:Journal of neurosurgical anesthesiology 2006-01, Vol.18 (1), p.68-72
Hauptverfasser: Rothoerl, Ralf Dirk, Axmann, Cornelia, Pina, Ana-Luisa, Woertgen, Chris, Brawanski, Alexander
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Sprache:eng
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Zusammenfassung:The delayed ischemic neurologic deficit (DIND) is a common and potentially devastating complication in patients who have sustained subarachnoid hemorrhage (SAH). Recent evidence suggests that various constituents of the inflammatory response may be critical in the pathogenesis of this ischemic complication. The aim of this study was to evaluate the possible relationship between the C-reactive protein (CRP)/white blood cell (WBC) count and DIND. A total of 88 patients with acute SAH were included. CRP and WBC count were estimated on a daily basis. Outcome was evaluated 1 year after the initial ictus according to the Glasgow Outcome Scale. CRP levels on days 5, 6, 7, and 8 were statistically significantly higher in the group of patients developing a DIND (P < 0.025, P < 0.016, P < 0.011, P < 0.0002). WBC counts were higher in this patient group on days 1, 4, 5, 6, and 7 (P < 0.0253, P < 0.0087, P < 0.00167, P < 0.0026, P < 0.0045). Overall CRP values were higher with increasing severity of the initial ictus according to the Hunt and Hess Scale and to the outcome according to the Glasgow Outcome Scale from day 3 on. A statistically significant relationship between WBCs and outcome could not be observed. The presented data do not prove that WBCs and CRP values have a direct contribution to the pathogenesis of ischemic complications following SAH, but it supports the assertion that inflammation may present a common pathogenic pathway in the development of such complications.
ISSN:0898-4921
DOI:10.1097/01.ana.0000181693.30750.af