Alterations in Cerebral Oxidative Metabolism following Traumatic Brain Injury

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Alterations in Cerebral Oxidative Metabolism following Traumatic Brain Injury Michael De Fazio • Richard Rammo • Kristine O’Phelan • M. Ross Bullock

Published online: 5 January 2011 Ó Springer Science+Business Media, LLC 2011

Abstract Background Traumatic brain injury (TBI) generates regional alterations in cerebral metabolism, leading to the potential evolution of persistent metabolic dysfunction. In the case of penetrating, firearm-related TBI, the pathophysiological mechanisms underlying these acute-phase metabolic derangements are not entirely understood— hindering the potential effectiveness of therapeutic intervention. The use of cerebral microdialysis to monitor biochemical alterations that occur, post-TBI, provides critical insight into the events that perpetuate neurological deterioration. Methods Cerebral microdialysis was used to monitor alterations in the brain tissue chemistry of a 22-year-old female patient who sustained a penetrating gunshot wound to the head. Extracellular glucose, lactate, pyruvate, and lactate pyruvate ratio (LPR) were monitored over the course of the first-week post-injury. Results Analysis of the microdialysate revealed sustained elevations in LPR with peaks in excess of those seen in patients who have sustained permanent ischemic injury. This interval of persistently elevated LPR was followed by M. De Fazio  R. Rammo University of Miami, Miller School of Medicine, Miami, Florida, USA K. O’Phelan (&) Department of Neurology and Jackson Memorial Hospital, University of Miami, Miller School of Medicine, Miami, Florida, USA e-mail: [email protected] M. Ross Bullock Department of Neurological Surgery, Jackson Memorial Hospital and Lois Pope LIFE Center, University of Miami, Miller School of Medicine, Miami, Florida, USA

a spontaneous reduction of values, to levels below the defined threshold for metabolic crisis, over a period of several days. Conclusions Microdialysis studies may significantly improve the understanding of the metabolic alterations that occur in patients who sustain a variety of forms of neurotrauma. Ultimately, monitoring these variations in brain tissue chemistry will improve the insight into the neuropathological mechanisms underlying penetrating traumatic brain injury, and enhance the therapeutic approach of these patients. Keywords Penetrating traumatic brain injury  Microdialysis  Cerebral oxidative metabolism  Lactate pyruvate ratio  Trauma

Introduction Traumatic brain injury (TBI) is one of the largest public health concerns in the United States. Data released from the Centers for Disease Control demonstrates, on average, approximately 1.7 million people sustain a TBI, annually, contributing to one-third (30.5%) of all injury related deaths in the US [1]. In particular, firearm-related trauma accounts for less than 10% of all traumatic brain injuries; however, reports indicate that 90.4% of gunshot wounds to the head (GSWH) result in death—making it the largest contributor of TBI-related mortality in the US [2]. Acute TBI results