• Jamin M Mulvey, Nicholas W C Dorsch, Yugan Mudaliar, and Erhard W Lang.
• Department of Intensive Care, University of Sydney, Westmead Hospital, Westmead Australia. jmulvey@ausdoctors.net
• Neurocrit Care. 2004 Jan 1;1(3):391-402.

AbstractTraumatic brain injury (TBI) is a major cause of morbidity and mortality with widespread social, personal, and financial implications for those who survive. TBI is caused by four main events: motor vehicle accidents, sporting injuries, falls, and assaults. Similarly to international statistics, annual incidence reports for TBI in Australia are between 100 and 288 per 100,000. Regardless of the cause of TBI, molecular and cellular derangements occur that can lead to neuronal cell death. Axonal transport disruption, ionic disruption, reduced energy formation, glutamate excitotoxicity, and free radical formation all contribute to the complex pathophysiological process of TBI-related neuronal death. Targeted pharmacological therapy has not proved beneficial in improving patient outcome, and monitoring and maintenance of various physiological parameters is the mainstay of current therapy. Parameters monitored include arterial blood pressure, blood gases, intracranial pressure, cerebral perfusion pressure, cerebral blood flow, and direct brain tissue oxygen measurement (ptiO2). Currently, indirect brain oximetry is used for cerebral oxygenation determination, which provides some information regarding global oxygenation levels. A newly developed oximetry technique, has shown promising results for the early detection of cerebral ischemia. ptiO2 monitoring provides a safe, easy, and sensitive method of regional brain oximetry, providing a greater understanding of neurophysiological derangements and the potential for correcting abnormal oxygenation earlier, thus improving patient outcome. This article reviews the current status of bedside monitoring for patients with TBI and considers whether ptiO2 has a role in the modern intensive care setting.

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