• R N Vuille-Dit-Bille, R Ha-Huy, M Tanner, and J F Stover.
• Division of Surgical Intensive Care Medicine, Department of Surgery, University Hospital Zürich, Switzerland.
• Minerva Anestesiol. 2011 Sep 1;77(9):870-6.

BackgroundCerebral metabolic impairment is feared to induce secondary brain damage following traumatic brain injury (TBI). The present study was designed to assess the temporal profile of calculated arterio- jugular venous differences in glutamate (AJVDglu) and SjvO(2) in patients subjected to continuous pharmacologic coma. Metabolic impairment was assumed to be reflected by increased jugular venous glutamate levels and decreased jugular venous oxygen saturation (SjvO(2)).MethodsArterial and jugular venous blood was drawn once daily for up to 14 days from 14 patients to assess the temporal profile. Plasma glutamate was measured by high performance liquid chromatography. SjvO(2), lactate and paCO(2) were determined in routine blood gas analysis. Calculated AJVD indirectly reflects cerebral uptake (positive values) or cerebral release (negative values).ResultsDuring pharmacologic coma an increase in ICP approaching 20 mmHg was associated with significantly reduced paCO(2) (4.7 ± 0.5 kPa; mean ± standard deviation), markedly decreased SjvO(2) (66.0 ± 4.2%) without reaching ischemic values, and a trend to more negative AJVDglu values (-6.0 ± 14.3 μmol/L), suggesting cerebral glutamate release. Arterio- jugular venous lactate difference (AJVDlac) remained unchanged.ConclusionDuring pharmacologic coma increased ICP was associated with significantly decreased SjvO(2) which coincided only with a trend to increased cerebral glutamate release. Calculated AJVDglu appears to be inferior in unmasking altered brain metabolism compared to SjvO(2) whenever ICP is increased.

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