Short Report
Monitoring extracellular concentrations of lactate, glutamate, and glycerol by in vivo microdialysis in the brain during liver transplantation in acute liver failure
Article first published online: 30 DEC 2003
DOI: 10.1053/jlts.2002.32283
Copyright © 2002 American Association for the Study of Liver Diseases
Additional Information
How to Cite
Tofteng, F. and Larsen, F. S. (2002), Monitoring extracellular concentrations of lactate, glutamate, and glycerol by in vivo microdialysis in the brain during liver transplantation in acute liver failure. Liver Transpl, 8: 302–305. doi: 10.1053/jlts.2002.32283
Publication History
- Issue published online: 30 DEC 2003
- Article first published online: 30 DEC 2003
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Abstract
Swelling of cerebral glial cells is a characteristic complication in patients with acute liver failure (ALF). This astrocyte edema may result in high intracranial pressure (ICP) and brain herniation before or during liver transplantation. Metabolic alterations responsible for the development of high ICP in patients with ALF are not fully understood. We describe changes in neurochemistry during liver transplantation using a cerebral microdialysis technique in a young man with severe ALF and cerebral edema. We found that the extracellular content of lactate ([lactate]ec) gradually increased during the operation. Becauce cerebral oxygen saturation and [lactate]ec to [pyruvate]ec ratio were within normal limits, hypoxia was not likely to be responsible for the increased [lactate]ec levels. Instead, we found that [lactate]ec levels correlated in this patient with arterial lactate concentrations during and after grafting (r2 = 0.96; P < .05), but did not correlate with arterial glucose concentrations (r2 = 0.20; P = not significant). Also, [glutamate]ec and [glycerol]ec levels were severely elevated before liver transplantation, but tended to decrease in the hours after grafting. These findings indicate disturbances in glutamate neurotransmission, arachidonic acid metabolism, and lactate flux across the blood-brain barrier in patients with ALF.

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