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68th Annual Meeting of the German Society of Neurosurgery (DGNC)
7th Joint Meeting with the British Neurosurgical Society (SBNS)

German Society of Neurosurgery (DGNC)

14 - 17 May 2017, Magdeburg

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Early Hypothermia attenuates neurological deficits and brain damage after experimental SAH

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  • Nadine Lilla - Würzburg, Deutschland
  • Christoph Rinne - Klinik für Anästhesiologie, Universitätsklinikum Würzburg, Würzburg, Deutschland
  • Judith Weiland - Universitätsklinikum Würzburg, Neurochirurgische Klinik und Poliklinik, Würzburg, Deutschland
  • Stefan Köhler - Deutschland, Deutschland
  • Ralf-Ingo Ernestus - Universitätsklinikum Würzburg, Neurochirurgische Klinik und Poliklinik, Würzburg, Deutschland
  • Thomas Westermaier - Universitätsklinikum Würzburg, Neurochirurgische Klinik, Würzburg, 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. DocMO.01.05

doi: 10.3205/17dgnc005, urn:nbn:de:0183-17dgnc0050

Published: June 9, 2017

© 2017 Lilla et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. See license information at http://creativecommons.org/licenses/by/4.0/.

Outline

Text

Objective: Metabolic exhaustion in ischemic tissue is the basis for a detrimental cascade of cell damage eventually ischemic cell death. In the acute stage of subarachnoid hemorrhage (SAH), a sequence of global and focal ischemia occurs threatening brain tissue to undergo ischemic damage. This study was conducted to investigate whether early therapy with moderate hypothermia can offer neuroprotection after experimental SAH in rats.

Methods: 20 male Sprague-Dawley rats were subjected to SAH by the endovascular filament model and treated by active cooling (34° C) from 15 to 180 minutes after vessel perforation or served as controls by continuous maintainance of normothermia (37.5° C). Mean arterial blood pressure (MABP), intracranial pressure (ICP), and local CBF over both hemispheres were continuously measured. Neurological assessment was performed 24 hours later. Hippocampal damage was assessed by H.E.- and Caspase-3 staining.

Results: By a slight increase of MABP in the cooling phase and a significant reduction of ICP, hypothermia improved cerebral perfusion pressure (CPP) in the first 60 minutes after SAH. Accordingly, a trend to increased CBF was observed during this period. Thereafter, CBF was lower in hypothermic animals. The rate of injured neurons was significantly reduced in hypothermia-treated animals (4.5 ± 3 %) compared to normothermic controls (20.8 ± 4 %). The number of Caspase 3 positive neurons in the hippocampal CA1-field was reduced but did not reach the level of significance.

Conclusion: In this study, the effects of very early temporary hypothermia was investigated. The results of this series cannot finally answer whether this form of treatment permanently attenuates or only delays ischemic damage. In the latter case, slowing down metabolic exhaustion by hypothermia may still be a valuable treatment during this state of ischemic brain damage and prolong the therapeutical window for possible causal treatments of the acute perfusion deficit. Therefore, it may be useful as a first-tier therapy in suspected SAH.