Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.597845
Title: Regional ischaemia following acute head injury
Author: Coles, J. P.
Awarding Body: University of Cambridge
Current Institution: University of Cambridge
Date of Award: 2004
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Abstract:
15Oxygen positron emission tomography (15O PET) has been used to demonstrate ischaemia and define physiological thresholds predictive of tissue viability in stroke. Unfortunately, it is difficult to translate such data to clinical head injury due to concurrent use of sedative agents, the metabolic effects of trauma, and the lack of  a priori knowledge regarding the location of ischaemia. While ischaemia may be prominent in perilesional areas, it may also be observed in structurally normal brain. The methodological basis of 15O PET is discussed with consideration of the steady-state 15O model. These studies utilised phantom and control data to address the processing of imaging datasets, the precision of repeated measurements in interventional studies and the reliability of voxel-based measures of ischaemia. The methodology developed in these studies was used as a basis for the experimental work in patients. Head injured patients within 24 hours of ictus, showed evidence of regional ischaemia that was not detected by common bedside monitoring techniques, such as jugular bulb oximetry. Although the absolute volume of brain at risk was variable, it had important implications in terms of outcome. Evidence of an increased gradient for oxygen diffusion and impaired oxygen unloading were associated with structural evidence of microvascular collapse and perivascular oedema. This suggests that mechanisms other than simple perfusion-limited ischaemia may be responsible for tissue hypoxia in head injury. Moderate hyperventilation increased the volume of brain at risk of ischaemia injury, both by reducing perfusion, and by increasing oxygen demand. Brain regions that were unable to increase oxygen extraction to meet increased oxygen demand showed a fall in cerebral metabolism. Elevation of cerebral perfusion pressure above 70 mmHg does not benefit the injured brain in the absence of significant cerebral ischaemia.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.597845  DOI: Not available
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