Cerebral microdialysis monitoring: determination of normal and ischemic cerebral metabolisms in patients with aneurysmal subarachnoid hemorrhage.
OBJECTIVE
The success of treatment for delayed cerebral ischemia is time dependent, and neuronal monitoring methods that can detect early subclinical levels of cerebral ischemia may improve overall treatment results. Cerebral microdialysis may represent such a method. The authors' goal was to characterize patterns of markers of energy metabolism (glucose, pyruvate, and lactate) and neuronal injury (glutamate and glycerol) in patients with subarachnoid hemorrhage (SAH), in whom ischemia was or was not suspected.


METHODS
By using low-flow intracerebral microdialysis monitoring, central nervous system extracellular fluid concentrations of glucose, pyruvate, lactate, glutamate, and glycerol were determined in 46 patients suffering from poor-grade SAH. The results in two subgroups were analyzed: those patients with no clinical or radiological signs of cerebral ischemia (14 patients) and those who succumbed to brain death (five patients). Significantly lower levels of energy substrates and significantly higher levels of lactate and neuronal injury markers were observed in patients with severe and complete ischemia when compared with patients without symptoms of ischemia (glucose 0 compared with 2.12+/-0.15 mmol/L; pyruvate 0 compared with 151+/-11.5 micromol; lactate 6.57+/-1.07 compared with 3.06+/-0.32 mmol/L; glycerol 639+/-91 compared with 81.6+/-12.4 micromol; and glutamate 339+/-53.4 compared with 14+/-3.33 micromol). Immediately after catheter placement, glutamate concentrations declined over the first 4 to 6 hours to reach stable values. The remaining parameters exhibited stable values after 1 to 2 hours.


CONCLUSIONS
The results confirm that intracerebral microdialysis monitoring of patients with SAH can be used to detect patterns of cerebral ischemia. The wide range from normal to severe ischemic values calls for additional studies to characterize further incomplete and possible subclinical levels of ischemia.
Schulz
M K
MK
Department of Neurosurgery, Odense University Hospital, Denmark. m.schultz@imbmed.ou.dk
Wang
L P
LP
Tange
M
M
Bjerre
P
P
D000328:Adult; D000368:Aged; D001921:Brain / Q000098:blood supply / Q000378:metabolism*; D001926:Brain Death / Q000175:diagnosis / Q000378:metabolism; D002545:Brain Ischemia / Q000175:diagnosis / Q000378:metabolism*; D002533:Cerebral Angiography; D005110:Extracellular Space / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D018698:Glutamic Acid / Q000378:metabolism; D005990:Glycerol / Q000378:metabolism; D006801:Humans; D019344:Lactic Acid / Q000378:metabolism; D017551:Microdialysis / Q000379:methods*; D008875:Middle Aged; D008991:Monitoring, Physiologic / Q000379:methods*; D019289:Pyruvic Acid / Q000378:metabolism; D020521:Stroke / Q000175:diagnosis / Q000378:metabolism; D013345:Subarachnoid Hemorrhage / Q000175:diagnosis / Q000378:metabolism*
D019344:Lactic Acid; D018698:Glutamic Acid; D019289:Pyruvic Acid; D005947:Glucose; D005990:Glycerol