gms | German Medical Science

65. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

11. - 14. Mai 2014, Dresden

Controlled temporary hypercapnia for treatment of delayed cerebral ischemia after SAH – Results of a phase 1 study

Meeting Abstract

  • Thomas Westermaier - Department of Neurosurgery, University Hospital Wuerzburg, Wuerzburg, Germany
  • Christian Stetter - Department of Neurosurgery, University Hospital Wuerzburg, Wuerzburg, Germany
  • Ekkehard Kunze - Department of Neurosurgery, University Hospital Wuerzburg, Wuerzburg, Germany
  • Nadine Willner - Department of Neurosurgery, University Hospital Wuerzburg, Wuerzburg, Germany
  • Judith Holzmeier - Department of Neurosurgery, University Hospital Wuerzburg, Wuerzburg, Germany
  • Christian Kilgenstein - Department of Anaesthesia and Critical Care, University Hospital Wuerzburg, Wuerzburg, Germany
  • Jin-Yul Lee - Department of Neurosurgery, University Hospital Wuerzburg, Wuerzburg, Germany
  • Ralf-Ingo Ernestus - Department of Neurosurgery, University Hospital Wuerzburg, Wuerzburg, Germany
  • Norbert Roewer - Department of Anaesthesia and Critical Care, University Hospital Wuerzburg, Wuerzburg, Germany
  • Ralf Michael Muellenbach - Department of Anaesthesia and Critical Care, University Hospital Wuerzburg, Wuerzburg, Germany

Deutsche Gesellschaft für Neurochirurgie. 65. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC). Dresden, 11.-14.05.2014. Düsseldorf: German Medical Science GMS Publishing House; 2014. DocDI.11.08

doi: 10.3205/14dgnc183, urn:nbn:de:0183-14dgnc1837

Veröffentlicht: 13. Mai 2014

© 2014 Westermaier et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Objective: Today, there is no specific treatment for the prevention or treatment of delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (SAH). This study was designed to assess if the basic physiological mechanism of CO2-regulation of cerebral blood flow (CBF) can be used to enhance cerebral perfusion in patients with poor-grade SAH and high risk to develop DCI and secondary infarction.

Method: Patients met the inclusion criteria if they had suffered poor grade aneurysmal SAH (Hunt/Hess grade 3-5, Fisher grade 3), were supplied with an external ventricular drainage, received early clipping or coiling of the aneurysm, and were mechanically ventilated. Once a day between day 4 and 14, the arterial partial pressure of carbon dioxide (PaCO2) was lowered from baseline values of 40 mmHg to 30 mmHg, then increased to 40, 50 and 60 mmHg, respectively, by a modification of the respiratory volume. Intracerebral CBF measurement and transcutaneous brain tissue oxygen saturation (StiO2) were the primary end points.

Results: 10 patients were included in the study. No trial-related complications were noted. CBF increased significantly to 128 ± 15% and 146 ± 21% of baseline when PaCO2 was elevated to 50 and 60 mmHg, respectively. Simultaneously, StiO2 increased to 107 ± 3% and 113 ± 3% of baseline, when PaCO2 was elevated to 50 and 60 mmHg, respectively. ICP remained constant. However, a surplus drainage of CSF was registered during hypercapnia. After returning to baseline ventilation parameters, CBF and StiO2 slowly returned to normal without a rebound effect. No patient developed DCI.

Conclusions: During the whole observation period – between day 4 and 14 after SAH – hypercapnia resulted in an increase of CBF and StiO2 without a rebound effect after returning to baseline ventilation parameters and without negative side effects. Hypercapnia may yield a therapeutic potential in patients who suffered from aneurysmal SAH and are prone to develop delayed ischemia.