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

Clinical experience after 5 years of metabolic monitoring in severe SAH

Klinische Erfahrungen im metabolischen Monitoring bei schwerer SAB nach 5-jähriger Anwendung

Meeting Abstract

  • corresponding author Bernd M. Hölper - Städtisches Klinikum Fulda, Klinik für Neurochirurgie
  • B. M. Hoelper - Klinik für Neurochirurgie, Klinikum Fulda, Fulda
  • F. Soldner - Klinik für Neurochirurgie, Klinikum Fulda, Fulda
  • M. Janka - Klinik für Neurochirurgie, Klinikum Fulda, Fulda
  • R. Behr - Klinik für Neurochirurgie, Klinikum Fulda, Fulda

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. DocMO.10.06

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Veröffentlicht: 23. April 2004

© 2004 Hölper et al.
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Cerebral metabolic monitoring after subarachnoid haemorrhage (SAH) is mainly intended to detect impending ischemia which is mostly due to vasospasm. After diagnosis of severe cerebral vasospasm as one of the most common causes of ischemia, several therapeutic possibilities such as triple-H therapy or transluminal balloon angioplasty (TBA) can be initiated. In this report, we describe our five year experience of metabolic monitoring in severe SAH concerning the possibilities of detecting cerebral ischemia as well as surveillance of vasospasm treatment.


32 intubated and controlled ventilated patients with severe SAH were monitored by bilateral microdialysis (=MD, CMA 600), unilateral ptiO2 (Licox) as well as ICP and brain temperature (Rehau), daily transcranial Doppler measurement, time-locked recording of MAP, blood gas analysis, laboratory data, respirator settings and pharmacological triple-H therapy. Serial CCT was performed to identify regional cerebral ischemia. In cases of intractable severe cerebral vasospasm, TBA was performed.


In 19% cerebral ischemia occurred without pathological MD measurements due to placement of MD catheters outside the ischemic region. ptiO2 < 10mmHg was highly sensitive to impending ischemia visible in CCT if located in or closed to the relevant area. Interstitial lactate was significantly higher (4-6mmol/l) in ischemic patients over the complete monitoring time compared to the non-ischemic group (2-3mmol/l), while lactate/pyruvate ratio (>35) and glutamate (>20mmol/l) was only significantly different over the first days after monitoring was initiated. Temporary or long-lasting metabolic parameters improved in 4 of 6 patients following TBA, while no changes were found in two patients.


The local measurement of current applicable metabolic monitoring limits the value of these techniques to detect impending cerebral ischemia in SAH. Even using bilateral MD monitoring ischemia still occurred in vascular territories not under surveillance. However, if both MD and ptiO2 catheters are placed in tissue of risk, in our experience both techniques are very sensitive and reliable. In therapy refractory vasospasm, TBA can be performed, but metabolic improvement was only seen in limited local but not in widespread diffuse vasospasm of several vessels in this small series.