gms | German Medical Science

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 impairment of pressure reactivity (PRx) after experimental subarachnoid hemorrhage correlates to outcome and recovery of cerebral blood flow

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  • Konstantin Hockel - Klinik für Neurochirurgie, Universitätsklinikum Tübingen, Tübingen, Deutschland
  • Nikolaus Plesnila - Institute for Stroke and Dementia Research, Klinikum der Unversität München, München, Deutschland
  • Martin Schuhmann - Klinik für Neurochirurgie, Universitätsklinikum Tübingen, Tübingen, 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. DocP 179

doi: 10.3205/17dgnc742, urn:nbn:de:0183-17dgnc7424

Published: June 9, 2017

© 2017 Hockel 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

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Objective: Disturbed cerebrovascular autoregulation (CA) has been identified as risk factor for secondary ischemic brain damage after SAH in patients. Monitoring of Pressure reactivity index (PRx), allowing for continuous and dynamic CA assessment, is more and more frequently used in the clinical but not in the experimental setting so far.

Methods: SAH was induced in Sprague-Dawley rats by endovascular puncture. In addition to monitoring regional cerebral blood flow (rCBF) in both hemispheres, intracranial pressure (ICP) and mean arterial blood pressure (MAP) were used to continuously calculate cerebral perfusion pressure (CPP) and PRx as measure for CA. Monitoring was continued for 60 minutes after SAH and subsequently mortality was assessed for 7 days (n=12). In a second group long-term monitoring was performed for 180 minutes after SAH and in sham operated animals (n=5 each).

Results: PRx is significantly higher (more disturbed CA) in the first hour after SAH compared to sham operated animals (0.20 vs. -0.04). This phenomenon exceeds the initial ictus and then slowly disappears over the next hours. Besides a more severe initial hemorrhage and a less pronounced recovery of rCBF non-surviving animals exhibited a tendency to more and longer impaired CA (46 vs. 40% of 1-hour monitoring after SAH). CPP in relation to rCBF and PRx allows for the assumption that CA plateau in severely altered and shifted to the right (higher CPP) after SAH.

Conclusion: Implementation of PRx monitoring in experimental SAH is feasible and adds valuable information about a frequently disturbed CA in the initial phase after SAH and may help evaluate the pathophysiology of early brain ischemia.