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

Brain tissue oxygen pressure-reactivity and delayed cerebral infarction after aneurysmal subarachnoid haemorrhage

Hirngewebssauerstoff-Reaktivität und "späte" zerebrale Infarkte nach aneurysmatischer Subarachnoidalblutung

Meeting Abstract

  • corresponding author Matthias Jaeger - Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Leipzig, Leipzig
  • M. Söhle - Klinik für Anästhesiologie und spezielle Intensivmedizin, Universitätsklinikum Bonn, Bonn
  • E. Kunze - Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Würzburg, Würzburg
  • J. Meixensberger - Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Leipzig, Leipzig

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.10.03

The electronic version of this article is the complete one and can be found online at: http://www.egms.de/en/meetings/dgnc2004/04dgnc0100.shtml

Published: April 23, 2004

© 2004 Jaeger et al.
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Outline

Text

Objective

To investigate the relation between an index of brain tissue oxygen pressure-reactivity (bPtiO2) and the occurrence of delayed cerebral infarction after severe aneurysmal subarachnoid haemorrhage (SAH).

Methods

In 51 patients after SAH H&H °III -°V monitoring of brain tissue oxygen (PtiO2) and cerebral perfusion pressure (CPP) was performed. The brain tissue oxygen pressure-reactivity index bPtiO2 was calculated every 30 seconds from bPtiO2=ΔPtiO2/ΔCPP, including data from the previous 12 hours of monitoring. Patients were divided into an infarction group (n=19) where delayed cerebral infarction occurred, and a non-infarction group (n=32).

Results

Median bPtiO2 over the whole monitoring period was significantly higher in the infarction group, as compared to the non-infarction group (0,25 vs. 0,12; p<0,001). Clinical data, transcranial Doppler values (TCD), and data of CPP and PtiO2 alone did not distinguish between groups. A step-down logistic regression analysis showed that bPtiO2 carries predictive information on the occurrence of delayed cerebral infarction, which is not contained in others factors.

Conclusions

These first data using bPtiO2 suggest that this parameter, which evaluates the long-term response of PtiO2 to CPP-changes, may differ between the infarction and non-infarction group. Furthermore, it may distinguish between those patients who ultimately develop delayed infarction after SAH, and those who do not. This is of interest, since standard criteria, such as clinical data, TCD, CPP, and PtiO2 alone did not differ between groups.