Artikel
Cerebral microdialysis in severe head injury (SHI) and aneurysmal subarachnoid hemorrhage (SAH)
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Autoren
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Daniel Haux
- Department of Neurosurgery, University of Heidelberg, Heidelberg
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O. Sakowitz
- Department of Neurosurgery, University of Heidelberg, Heidelberg
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K. Kiening
- Department of Neurosurgery, University of Heidelberg, Heidelberg
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A. Sarrafzadeh
- Department of Neurosurgery, Charitè - Universitätsmedizin Berlin, Campus Virchow-Klinikum, Berlin
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A. Unterberg
- Department of Neurosurgery, University of Heidelberg, Heidelberg
| Veröffentlicht: | 23. April 2004 |
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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.
