• Robert Vink, Kartik D Bahtia, and Peter L Reilly.
• Discipline of Pathology, School of Medical Sciences, University of Adelaide, Adelaide, SA 5005, Australia. Robert.Vink@adelaide.edu.au
• Acta Neurochir. Suppl. 2008 Jan 1;102:189-92.

BackgroundWhile it is understood that raised intracranial pressure (ICP) after traumatic brain injury (TBI) may negatively impact on brain tissue oxygenation (PbtO2), few studies have characterized the inter-relationship between these two variables, particularly in a large animal model that replicates the human gyrencephalic brain. The current study uses an ovine model to examine the dynamics of ICP and PbtO2 after TBI.Materials And MethodsFive 2-year-old male Merino sheep were anesthetized with isoflurane and impacted in the left temporal region using a humane stunner. ICP and PbtO2 were then monitored over the following 4 h using a Codman ICP Express monitoring system and a LICOX brain tissue oxygen monitoring system, respectively. Two additional sheep were anesthetized and monitored as sham (uninjured) controls.FindingsMean ICP 60 min following TBI was over 25 mmHg (p < 0.05 versus controls) and by 4 h, values were consistently greater than 30 mmHg (p < 0.001). With respect to PbtO2, values fell from mean control values of 52 +/- 11 to 20 +/- 4 mmHg by 60 min (p < 0.001) and by 4 h to 14 +/- 3 mmHg (p < 0.01). The sigmoidal relationship between the two variables included a negative linear correlation when ICP was between 13 to 27 mmHg.ConclusionsOur results suggest that TBI results in early changes in ICP that are associated with profound declines in PbtO2, and may indicate the need for earlier management of ICP after TBI.

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