gms | German Medical Science

55. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e. V. (DGNC)
1. Joint Meeting mit der Ungarischen Gesellschaft für Neurochirurgie

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

25. bis 28.04.2004, Köln

Cerebral microdialysis in severe head injury (SHI) and aneurysmal subarachnoid hemorrhage (SAH)

Meeting Abstract

  • corresponding author Daniel Haux - Department of Neurosurgery, University of Heidelberg, Heidelberg
  • O. Sakowitz - Department of Neurosurgery, University of Heidelberg, Heidelberg
  • K. Kiening - Department of Neurosurgery, University of Heidelberg, Heidelberg
  • A. Sarrafzadeh - Department of Neurosurgery, Charitè - Universitätsmedizin Berlin, Campus Virchow-Klinikum, Berlin
  • A. Unterberg - Department of Neurosurgery, University of Heidelberg, Heidelberg

Deutsche Gesellschaft für Neurochirurgie. Ungarische Gesellschaft für Neurochirurgie. 55. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC), 1. Joint Meeting mit der Ungarischen Gesellschaft für Neurochirurgie. Köln, 25.-28.04.2004. Düsseldorf, Köln: German Medical Science; 2004. DocJM III.02

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/dgnc2004/04dgnc0010.shtml

Veröffentlicht: 23. April 2004

© 2004 Haux 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 vervielf&aauml;ltigt, verbreitet und &oauml;ffentlich zug&aauml;nglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Objective

Cerebral ischemia is a serious complication in both patients with severe traumatic head injury (SHI) and aneurysmal subarachnoid hemorrhage (SAH). Metabolic deterioration can be detected by cerebral microdialysis (MD). Does MD provide additional information in both SHI and SAH patients?

Methods

Overall 42 SHI-patients (38±22 ys, GCS<9) and 164 SAH-patients (51±13 ys, WFNS 1-5) were monitored by MD analyzed hourly for glucose, lactate, lactate/pyruvate (L/P) ratio, glutamate and glycerol using a bedside device (CMA 600, Sweden). (A) In SHI-patients, ptiO2 (Licox, Germany) was additionally monitored for hypoxic episodes (ptiO2 < 10mmHg for ≥5 min) and compared to changes in MD. (B) In SAH-patients who developed cerebral vasospasm during monitoring (N=25), MD parameters were analyzed in relation to clinical deterioration. In 13 SAH-patients, MD was correlated to regional cerebral blood flow (rCBF, by 15O-H2O-PET) and glucose metabolism (18F-FDG-PET, N=21) within MD region.

Results

(A) In 68% of SHI-patients, hypoxic episodes were present, mainly caused by hyperventilation (decrease in endtidal CO2 < 30 mmHg, 78%), an ICP elevation > 20 mmHg (62%) and a decreased cerebral perfusion pressure < 60 mmHg (41%). During hypoxic episodes glutamate concentrations were four times higher (35.6 ±29.5 µmol) compared to baseline values but did not precede changes in ptiO2 or ICP. (B) In SAH-patients with acute neurological deficits (N=44), glutamate and lactate or L/P ratio levels were initially high or increased secondarily (p<0.005). Patients with delayed ischemic neurological deficits had significantly higher glutamate and lactate concentrations on days 1-8 after surgery (p<0.01) and a higher L/P ratio on days 1, 3-5 and 7 after surgery compared to asymptomatic patients (n=59; p<0.05). In 84% of these patients, clinical deterioration was most frequently anticipated by an increase in glutamate (-9 hours), lactate (-5.5 hours) and the L/P ratio (-4 hours).

Conclusions

In SHI, MD reflects metabolic changes during secondary insults but supplies no additional information to well established monitoring techniques. In contrast, especially in high-grade SAH patients, MD provides valuable information about impending ischemia.