• A J Johnston, L A Steiner, D A Chatfield, M R Coleman, J P Coles, P G Al-Rawi, D K Menon, and A K Gupta.
• University of Cambridge Department of Anaesthesia, Box 93, Cambridge CB2 2QQ, UK. ajj29@cam.ac.uk
• Br J Anaesth. 2003 Dec 1; 91 (6): 781-6.

BackgroundFlow-metabolism coupling is thought to be deranged after traumatic brain injury, while the effects of propofol on flow-metabolism coupling are controversial. We have used a step increase in target plasma propofol concentration in head injured patients to explore flow-metabolism coupling in these patients.MethodsTen patients with a moderate to severe head injury received a step increase in propofol target controlled infusion of 2 microg x ml(-1). Cerebral tissue gas measurements were recorded using a multimodal sensor, and regional chemistry was assessed using microdialysis. Arterial-jugular venous oxygen differences (AVDO(2)) were measured and all patients had cortical function monitoring (EEG).ResultsThe step increase in propofol led to a large increase in EEG burst-suppression ratio (0% (range 0-1.1) to 46.1% (range 0-61.7), P<0.05); however, this did not significantly change tissue gas levels, tissue chemistry, or AVDO(2).ConclusionsFlow-metabolism coupling remains intact during a step increase in propofol after traumatic brain injury. The EEG burst-suppression induced by propofol after traumatic brain injury does not appear to be a useful therapeutic tool in reducing the level of regional ischaemic burden.

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