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British Journal of Anaesthesia, 2003, Vol. 91, No. 6 781-786
© 2003 The Board of Management and Trustees of the British Journal of Anaesthesia

Clinical Investigations

Effects of propofol on cerebral oxygenation and metabolism after head injury

A. J. Johnston1,3, L. A. Steiner1,3, D. A. Chatfield1,3, M. R. Coleman3, J. P. Coles1,3, P. G. Al-Rawi2, D. K. Menon1,3 and A. K. Gupta1

1 University of Cambridge Department of Anaesthesia, Box 93, 2 Academic Neurosurgery, Box 167, and 3 University of Cambridge Wolfson Brain Imaging Centre, Addenbrooke’s Hospital, Cambridge CB2 2QQ, UK

*Corresponding author. E-mail: ajj29@cam.ac.uk

Background. Flow-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.

Methods. Ten patients with a moderate to severe head injury received a step increase in propofol target controlled infusion of 2 µg ml–1. Cerebral tissue gas measurements were recorded using a multimodal sensor, and regional chemistry was assessed using microdialysis. Arterial-jugular venous oxygen differences (AVDO2) were measured and all patients had cortical function monitoring (EEG).

Results. The 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 AVDO2.

Conclusions. Flow-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.

Br J Anaesth 2003; 91: 781–6


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