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

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Comparison of early pathophysiology of subarachnoid hemorrhage with/without intraventricular hemorrhage and intracerebral hemorrhage in a porcine hemorrhage model

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  • B. Orakcioglu - Neurochirurgische Klinik und Poliklinik, Universitätsklinikum Heidelberg, Heidelberg, Deutschland
  • presenting/speaker M. M. Kentar - Neurochirurgische Klinik und Poliklinik, Universitätsklinikum Heidelberg, Heidelberg, Deutschland
  • E. Santos - Neurochirurgische Klinik und Poliklinik, Universitätsklinikum Heidelberg, Heidelberg, Deutschland
  • Y. Uozumi - Neurochirurgische Klinik und Poliklinik, Universitätsklinikum Heidelberg, Heidelberg, Deutschland; Department of Neurosurgery, National Defense Medical College, Tokorozawa, Japan
  • O. W. Sakowitz - Neurochirurgische Klinik und Poliklinik, Universitätsklinikum Heidelberg, Heidelberg, Deutschland
  • A. Unterberg - Neurochirurgische Klinik und Poliklinik, Universitätsklinikum Heidelberg, Heidelberg, Deutschland

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. DocDO.01.07

doi: 10.3205/12dgnc024, urn:nbn:de:0183-12dgnc0248

Published: June 4, 2012

© 2012 Orakcioglu 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.

Outline

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Objective: Unexpected subarachnoid hemorrhage (SAH) with intraventricular extension (IVH) may result in attempts to create intracerebral hemorrhage (ICH) in swine. We investigated early pathophysiological changes in experimental SAH/IVH and ICH using multiparametric neuromonitoring.

Methods: 12 male swine (30–35 kg) were divided in two groups, a SAB/IVH group (gr1, n = 5) and an ICH group (gr 2, n = 7). All animals were sedated, mechanically ventilated and 4 right parietal cerebral monitoring probes were inserted (ICP; CBF; PbrO2; microdialysis) into the supposed perihemorrhagic zone (PHZ) of a planned subcortical ICH. A volume of 3 ml was applied. Online monitoring of all relevant physiological parameters was permanently obtained up to 12 hours post hemorrhage. The clot formation was confirmed post mortem as subarachnoid with/ without intraventricular haemorrhage or ICH alone.

Results: In 19% of ICH inductions solid clot formation could not be reached, but SAH/IVH was present. In the gr1 hematoma induction resulted in an immediate increase of ICP. The ICP progressively increased and peaked at 10.7 ± -4.4 mmHg mean ICP, but remained under pathologic values. CBF was subsequently increased from 36.9 ± -13.1 to 39.2 ± -7.4 ml / 100 mg/min attempting to compensate CPP related decrease of PbrO2 from 28 ± 6.9 mmHg to 14.7 ± 2.5 mmHg. LP-ratio non-significantly increased from 28.9 ± 4.6 to 35.2 ± 12.2. In ICH animals CBF decreases from 36.5 ± 12.7 to 27.9 ± 10.9 ml / 100 mg/ml resulted in mild significant LP-ratio increase from 26.7 ± 13.4 to 46.1 ± 18.1 arguing for an ischemic perihemorrhagic zone.

Conclusions: In porcine SAH/IVH ICP increase leads to significant PbrO2 decreases and compensatory relative CBF increase in the early phase after SAH. Neurometabolic effects in this acute phase could not be detected in SAH. However, in ICH rCBF was clearly reduced which may be explained by local for toxic effects of the solid clot in the early phase. This model can serve as a basis for further research in experimental SAH and neuromonitoring.