gms | German Medical Science

63rd Annual Meeting of the German Society of Neurosurgery (DGNC)
Joint Meeting with the Japanese Neurosurgical Society (JNS)

German Society of Neurosurgery (DGNC)

13 - 16 June 2012, Leipzig

Correlation of brain edema and perfusion deficit in the acute phase after experimental subarachnoid hemorrhage

Meeting Abstract

  • T. Westermaier - Neurochirurgische Klinik, Universitätsklinikum Würzburg
  • J. Eriskat - Neurochirurgische Klinik, Universitätsklinikum Würzburg
  • E. Kunze - Neurochirurgische Klinik, Universitätsklinikum Würzburg
  • G.H. Vince - Neurochirurgische Klinik, Universitätsklinikum Würzburg
  • R.I. Ernestus - Neurochirurgische Klinik, Universitätsklinikum Würzburg

Deutsche Gesellschaft für Neurochirurgie. Japanische Gesellschaft für Neurochirurgie. 63. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit der Japanischen Gesellschaft für Neurochirurgie (JNS). Leipzig, 13.-16.06.2012. Düsseldorf: German Medical Science GMS Publishing House; 2012. DocP 016

DOI: 10.3205/12dgnc403, URN: urn:nbn:de:0183-12dgnc4032

Published: June 4, 2012

© 2012 Westermaier et al.
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Outline

Text

Objective: In a number of patients suffering from subarachnoid hemorrhage (SAH) the development of severe brain edema can be observed. Little is known about the time-course of brain-swelling, its course and pathogenesis. This study was performed to investigate the development of brain edema and its correlation with perfusion parameters after experimental SAH.

Methods: Male Sprague-Dawley rats were randomly assigned to one of six experimental groups. They were subjected to SAH using the endovascular filament model or served as controls. Intracranial pressure (ICP) and Local cerebral blood flow (LCBF) were measured continuously. Animals were sacrificed under anesthesia without induction of SAH (control group) or 15, 30, 60, 180 or 360 minutes after SAH. Brain water content was determined using the wet/dry-weight method.

Results: After induction of SAH, LCBF rapidly decreased and ICP sharply increased. ICP gradually recovered and had almost returned to baseline values 6 hours after SAH. In contrast, brain water content continuously increased until 6 hours after SAH. Significant correlations were observed between brain water content and the extent of the perfusion deficit in animals sacrificed after 180 and 360 minutes.

Conclusions: Brain water content progressively increases for at least 6 hours after experimental SAH. A significant correlation with the perfusion deficit after SAH suggest that the development of brain edema is directly related to the extent of ischemia and acute vasoconstriction in the first hours after SAH.