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66th Annual Meeting of the German Society of Neurosurgery (DGNC)
Friendship Meeting with the Italian Society of Neurosurgery (SINch)

German Society of Neurosurgery (DGNC)

7 - 10 June 2015, Karlsruhe

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Cerebral alterations after multiple trauma and hemorrhagic shock

Meeting Abstract

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  • Nina Vogt - Klinik für Neurochirurgie, Universitätsklinikum Gießen
  • Daphne Eschbach - Klinik für Unfall,- Hand,- und Wiederherstellungschirurgie, Universitätsklinikum Marburg
  • Christiane Herden - Institut für Veterinär-Pathologie, Universität Gießen
  • Eberhard Uhl - Klinik für Neurochirurgie, Universitätsklinikum Gießen
  • Elke Roeb - Medizinische Klinik II, Gastroenterologie, Universitätsklinikum Gießen
  • Karsten Schöller - Klinik für Neurochirurgie, Universitätsklinikum Gießen

Deutsche Gesellschaft für Neurochirurgie. 66. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC). Karlsruhe, 07.-10.06.2015. Düsseldorf: German Medical Science GMS Publishing House; 2015. DocDI.19.04

doi: 10.3205/15dgnc207, urn:nbn:de:0183-15dgnc2078

Published: June 2, 2015

© 2015 Vogt 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: Multiple trauma (MT) including hemorrhagic shock (HS) might lead to cerebral hypoperfusion and brain damage. Therefore, we studied the cerebral sequelae of polytrauma with tibia fracture, pulmonary contusion, liver laceration and controlled HS with subsequent reperfusion in a newly developed porcine model. Furthermore, the neuroprotective effects of a mild hypothermia were examined.

Method: Domestic pigs (weight 30-42kg) were randomly assigned to two groups with induction of a standardized MT incl. controlled hemorrhage (45-50% blood volume) and subsequent reperfusion after 90 (T90) or 120min (T120), as well as to a sham-group. In two additional groups (TH90, TH120) mild hypothermia (33°C, 12h) was induced following trauma/ reperfusion. Pressure controlled ventilation was carried out after tracheotomy in all groups. Intracranial pressure (ICP), cerebral oxygenation (ptiO2) and brain temperature were monitored for 48h with a NEUROVENT®-PTO probe. Serum Protein S100B (S100B) and neuron specific enolase (NSE) levels were measured by ELISA. The extent of cerebral inflammation was quantified on HE-stained brain slices using a 3-point score.

Results: ICP was not affected by trauma or reperfusion. Directly after MT/HS, however, cerebral perfusion pressure (CPP) (p<0.001) and ptiO2 (p=0.007) decreased compared to sham animals. After reperfusion both parameters showed a delayed recovery. S100B (p=0.02 vs. sham) and NSE (p=0.006 vs. sham) increased only temporarily as a result of MT/HS in the T120 min group. Cerebral inflammation was detectable in all normothermic groups, presumably due to long-term ventilation. Mild hypothermia reduced inflammation in the TH90 group (p=0.017 vs. T90) without any effect on serum markers or monitoring parameters.

Conclusions: There is no permanent cerebral impairment after MT/HS when reperfusion is initiated within 120min. The temporary increase of S100B and NSE seems to be associated with trauma severity. Hypothermia appears to have some neuroprotective effects on inflammation when initiated early. However, further differentiated investigations of the morphological brain damage considering the protective potential of hypothermia are ongoing.