gms | German Medical Science

55. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e. V. (DGNC)
1. Joint Meeting mit der Ungarischen Gesellschaft für Neurochirurgie

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

25. bis 28.04.2004, Köln

Serum C-reactive protein correlates to the developement of a delayed ischemic lesion in the CT scan after aneurysmal SAH. Indicator for inflammatory pathogenesis of cerebral vasospasm or another epiphenomenon

Serum CRP korreliert zum Auftreten einer ischämischen Läsion im CT: Indikator für eine entzündliche Pathogenese des sogenannten zerebralen Vasospasmus oder Epihänomen

Meeting Abstract

  • corresponding author Ralf Rothoerl - Klinik und Poliklinik für Neurochirurgie, Klinikum der Universität Regensburg, Regensburg
  • C. Axmann - Klinik für Anästhesie, Klinikum der Universität Regensburg, Regensburg
  • J. Warnat - Klinik und Poliklinik für Neurochirurgie, Klinikum der Universität Regensburg, Regensburg
  • K. M. Schebesch - Klinik und Poliklinik für Neurochirurgie, Klinikum der Universität Regensburg, Regensburg
  • C. Woertgen - Klinik und Poliklinik für Neurochirurgie, Klinikum der Universität Regensburg, Regensburg
  • A. Brawanski - Klinik und Poliklinik für Neurochirurgie, Klinikum der Universität Regensburg, Regensburg

Deutsche Gesellschaft für Neurochirurgie. Ungarische Gesellschaft für Neurochirurgie. 55. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC), 1. Joint Meeting mit der Ungarischen Gesellschaft für Neurochirurgie. Köln, 25.-28.04.2004. Düsseldorf, Köln: German Medical Science; 2004. DocMO.10.05

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/dgnc2004/04dgnc0102.shtml

Veröffentlicht: 23. April 2004

© 2004 Rothoerl et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielf&aauml;ltigt, verbreitet und &oauml;ffentlich zug&aauml;nglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Objective

Cerebral vasospasm is a common and potentially devastating complication in patients who have sustained aneurysmal subarachnoid hemorrhage (SAH). Recently, convincing data have implicated a role of inflammation in the development and maintenance of cerebral vasospasm. Several studies suggest that various constituents of the inflammatory response, including adhesion molecules, cytokines, leukocytes, immunoglobulins, and complement, may be critical in the pathogenesis of cerebral vasospasm. Some of these inflammatory mediators are induced by acute phase proteins such as the C-reactive protein (CRP). The aim of this study was to evaluate the relationship of the C-reactive protein to the likelihood of a delayed neurological deficit after aneurysmal SAH.

Methods

Eighty-eight patients suffering from aneurysmal SAH were included in our study. The serum CRP, blood counts and TCD measurements were evaluated on a daily basis until day 8 after SAH. General clinical data, data concerning the treatment as well as the presence of a ischemic lesion on the discharge CT scan were recorded. Furthermore outcome data and data concerning infections such as pneumonia, ventriculitis etc. were collected.

Results

Thirty-seven patients (42%) developed delayed ischemic lesions. 59 patients showed a relevant infection (67%) but only 2 patients developed bacterial infections before day 7 after SAH. Serum CRP values increased from initially 16.6µg/l (range 0-68 µg/l) to 100.2µg/l (range 40.9µg/l-342µg/l) In the correlation analysis there was a statistically significant correlation of an increase of the serum CRP of day 3 to 4 after SAH to the development of a ischemic lesion on the discharge CT scan (p< 0.003). This increase did not correlate to the development of a bacterial infection. Serum leucocyte counts did not correlate to the serum CRP. However the increase correlated to the outcome data according to the Glasgow outcome Scale on discharge as well as the increase of flow velocities in the transcranial doppler measurements.

Conclusions

It is plausible that the inflammatory response may indeed represent a critical common pathway in the pathogenesis of cerebral vasospasm after SAH. Investigations into the nature of the inflammatory response accompanying SAH are needed to elucidate the precise role(s) of inflammatory events in SAH-induced pathologies.