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Online ISSN 1827-1596
Vuille-Dit-Bille R. N. 1, Ha-Huy R. 2, Tanner M. 1, Stover J. F. 1
1 Division of Surgical Intensive Care Medicine, Department of Surgery, University Hospital Zürich, Zürich, Switzerland;
2 Cardiovascular Therapy Research, Department of Internal Medicine, University Hospital Zürich, Zürich, Switzerland
BACKGROUND: Cerebral 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 SjvO2 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 (SjvO2).
METHODS:Arterial 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. SjvO2, lactate and paCO2 were determined in routine blood gas analysis. Calculated AJVD indirectly reflects cerebral uptake (positive values) or cerebral release (negative values).
RESULTS:During pharmacologic coma an increase in ICP approaching 20 mmHg was associated with significantly reduced paCO2 (4.7±0.5 kPa; mean±standard deviation), markedly decreased SjvO2 (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.
CONCLUSION: During pharmacologic coma increased ICP was associated with significantly decreased SjvO2 which coincided only with a trend to increased cerebral glutamate release. Calculated AJVDglu appears to be inferior in unmasking altered brain metabolism compared to SjvO2 whenever ICP is increased.