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58. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e. V. (DGNC)

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

26. bis 29.04.2007, Leipzig

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Bedside assessment of CPP-independent changes of cerebral circulation in neurosurgical patients using a thermodiffusion probe – Comparison with experimental data in non-injured brain

Kontinuierliche patientennahe Einschätzung CPP-unabhängiger Veränderungen der zerebralen Zirkulation mittels Thermodiffusionssonde in Patienten mit neuronaler Schädigung – Ein Vergleich mit tierexperimentellen Daten

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  • corresponding author J. Soukup - Klinik für Anästhesiologie und Operative Intensivmedizin der MLU Halle
  • M. Menzel - Klinik für Anästhesiologie und Operative Intensivmedizin der MLU Halle
  • T. Marx - Klinik für Neurochirurgie der MLU Halle
  • C. Holz - Klinik für Neurochirurgie der MLU Halle
  • I. Bramsiepe - Klinik für Anästhesiologie und Operative Intensivmedizin der MLU Halle
  • L. Sanchin - Klinik für Neurochirurgie der MLU Halle

Deutsche Gesellschaft für Neurochirurgie. 58. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC). Leipzig, 26.-29.04.2007. Düsseldorf: German Medical Science GMS Publishing House; 2007. DocP 007

The electronic version of this article is the complete one and can be found online at: http://www.egms.de/en/meetings/dgnc2007/07dgnc262.shtml

Published: April 11, 2007

© 2007 Soukup et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.

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Objective: Monitoring of cerebral perfusion pressure (CPP) and thus CPP-directed therapy offers a means of maintaining sufficient cerebral blood flow (CBF) to ensure that the oxygen supply to the brain. The concept is limited by the inability to calculate the influence of CPP-independent parameter on cerebral perfusion (i.e. controlled mild hyperventilation). The purpose of the present study was to determine the impact of variations of arterial pCO2 during controlled hyperventilation on regional cerebral blood flow (rCBF) and brain tissue oxygenation (ptiO2) in non – injured brain (animal experiment) and in patients with neuronal injury.

Methods: 10 patients with a GCS<8 after severe head trauma (n=4) and intracerebral bleeding (n=6) and 9 anaesthetized pigs were analyzed. Extended neuromonitoring, including an intraparenchymal intracranial pressure sensor (NEUROVENT-PT), a miniaturized thermodiffusion probe to measure the regional cerebral blood flow (rCBF, QFlow™-System) and a miniaturized Clark-type sensor in the animal experiment (Licox®) or a multiparameter probe (Neurotrend®) in the clinical setup to measure ptiO2, were placed carefully in the frontal cortex. After a 2-hour stabilization period (etCO2 ~ 37-40 mmHg) a controlled mild hyperventilation (etCO2 ~ 28-30 mmHg) was performed.

Results: In patients controlled hyperventilation (arterial pCO2 37,5±3,8mmHg vs. 29,3±4,5mmHg) lead to a significant reduction of the mean rCBF (34±4 ml/100g/min vs. 21,8±4,8ml/100g/min; p<0,0001). According to the known physiology, hyperventilation reduces the mean ptiO2 significant from 33±13mmHg to 11±7mmHg (p<0,001). There was no significant correlation between CPP and rCBF (R2= 0,302). In most of the patients the correct placement of the rCBF-probe was difficult, thatswhy re-placements were necessary. In the animal experiment controlled hyperventilation from paCO2 45,0±2,3 mmHg to 24,0±2,3mmHg lead to a significant reduction of the rCBF, (33±2,6ml/100g/min to 21±3,2ml/100g/min (p<0,0001) and the brain tissue oxygenation. (ptiO2 von 20,3±7,5mmHg to 10,5±4,5mmHg; p<0,0001) as well.

Conclusions: The availability of continuous bed-side rCBF-measurement offers the possibility to assess individual regional cerebral perfusion, requirering a standardized placement procedure of the rCBF-probe. Our results are comparable with those of the current literature. Comparing our clinical data (injured brain) to our results of the animal experiment (non-inured brain) the CO2-regulation is more sensitive in patients after neuronal injury.