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68. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)
7. Joint Meeting mit der Britischen Gesellschaft für Neurochirurgie (SBNS)

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

14. - 17. Mai 2017, Magdeburg

Variation of blood injection velocity in a new experimental model of non-aneurysmal SAH: any influence on intracranial pressure and cerebral perfusion in the acute phase?

Meeting Abstract

  • Catharina Conzen - Universitätsklinikum der RWTH Aachen, Neurochirurgische Klinik, Aachen, Deutschland
  • Katrin Becker - Universitätsklinikum der RWTH Aachen, Neurochirurgische Klinik, Aachen, Deutschland
  • Walid Albanna - Universitätsklinikum der RWTH Aachen, Neurochirurgische Klinik, Aachen, Deutschland
  • Anke Höllig - Universitätsklinikum der RWTH Aachen, Neurochirurgische Klinik, Aachen, Deutschland
  • Hans Rainer Clusmann - Universitätsklinikum der RWTH Aachen, Neurochirurgische Klinik, Aachen, Deutschland
  • Ute Lindauer - Universitätsklinikum der RWTH Aachen, Neurochirurgische Klinik, Aachen, Deutschland
  • Gerrit Schubert - Universitätsklinikum der RWTH Aachen, Neurochirurgische Klinik, Aachen, Deutschland

Deutsche Gesellschaft für Neurochirurgie. Society of British Neurological Surgeons. 68. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), 7. Joint Meeting mit der Society of British Neurological Surgeons (SBNS). Magdeburg, 14.-17.05.2017. Düsseldorf: German Medical Science GMS Publishing House; 2017. DocDI.26.05

doi: 10.3205/17dgnc335, urn:nbn:de:0183-17dgnc3350

Veröffentlicht: 9. Juni 2017

© 2017 Conzen et al.
Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). Lizenz-Angaben siehe http://creativecommons.org/licenses/by/4.0/.


Gliederung

Text

Introduction: Aneurysmal subarachnoid hemorrhage (aSAH) is hallmarked by rapid increase of intracranial pressure (ICP) and acute hypoperfusion contributing to early brain injury. Non-aneurysmal SAH (naSAH) is assumed to result in less dramatic ICP changes and possibly preserved cerebral perfusion, thereby resulting in a better neurological outcome. The purpose of our study was to develop an experimental model of naSAH by variation of injection velocity in order to determine the role of intracranial pressure variability on acute changes of cerebral perfusion after SAH.

Method: SAH in rats was induced by cisternal injection of 0.5ml arterial blood (AB) or 0.5ml normal saline (NS) in predefined time frames: group AB1 0.5ml/1min (n=8), group AB10 0.5ml/10min (n=11), group AB30 0.5ml/30min (n=7), group NS1 0.5ml/1 min (n=9); group NS10 0.5ml/10min (n=10). 11 sham-operated animals served as controls without any injection. Regional cortical blood flow (CBF), intracranial pressure (ICP) and mean arterial blood pressure (mABP) were recorded for 6 h after SAH.

Results: Maximum increase of ICP was highest in the rapid injection group (AB1, p<0.001), but significance was lost after 60 minutes. ICP was significantly higher in the AB groups when compared to the NS groups throughout the observation period (plateau phase >1h post SAH, p<0.001). Maximum increase of mABP was significantly higher in the rapid injection group (AB1) compared to AB10 and AB30 (p<0.001). With NS injection (NS1, NS10), no significant difference in mABP was detected pre- and post SAH. CBF decreased significantly in AB1, AB10 and AB30 compared to baseline pre-SAH (p<0.001, p<0.001, p<0.01 resp.). Maximum decrease was reached at different time points (AB1 at 1min, AB10 at 12min, AB30 at 70min post SAH). Significant hypoperfusion was observed for 112mins in group AB1, 165mins in group AB10 and 90mins in group AB30. NS injection led to a transient increase of CBF (p<0.01).

Discussion: Higher velocity of blood injection is associated with a higher increase of ICP, but changes do not extend beyond the hyperacute phase. Acute hypoperfusion is observed at all blood injection velocities, but not with saline injection. Variation of injection velocity may facilitate investigation of different SAH entities (aSAH vs naSAH) and their respective acute and chronic stages.