| Autor: |
Mathieu F; Division of Neurosurgery, University of Toronto, Toronto, Ontario, Canada.; Division of Anaesthesia, University of Cambridge, Cambridge, United Kingdom.; Department of Clinical Neurosciences, University of Cambridge, Cambridge, United Kingdom., Zeiler FA; Division of Anaesthesia, University of Cambridge, Cambridge, United Kingdom.; Section of Neurosurgery, Department of Surgery, Rady Faculty of Health Sciences, University of Manitoba, Winnibeg, Manitoba, Canada.; Department of Human Anatomy and Cell Science, Rady Faculty of Health Sciences, University of Manitoba, Winnibeg, Manitoba, Canada.; Biomedical Engineering, Faculty of Engineering, University of Manitoba, Winnibeg, Manitoba, Canada., Ercole A; Division of Anaesthesia, University of Cambridge, Cambridge, United Kingdom., Monteiro M; Biomedical Image Analysis Group, Imperial College London, London, United Kingdom., Kamnitsas K; Biomedical Image Analysis Group, Imperial College London, London, United Kingdom., Glocker B; Biomedical Image Analysis Group, Imperial College London, London, United Kingdom., Whitehouse DP; Division of Anaesthesia, University of Cambridge, Cambridge, United Kingdom., Das T; Department of Radiology, Addenbrooke's Hospital, University of Cambridge, Cambridge, Cambridge, United Kingdom., Smielewski P; Brain Physics Laboratory, Division of Neurosurgery, Addenbrooke's Hospital, University of Cambridge, Cambridge, Cambridge, United Kingdom.; Division of Neurosurgery, Addenbrooke's Hospital, University of Cambridge, Cambridge, Cambridge, United Kingdom., Czosnyka M; Brain Physics Laboratory, Division of Neurosurgery, Addenbrooke's Hospital, University of Cambridge, Cambridge, Cambridge, United Kingdom.; Institute of Electronic Systems, Warsaw University of Technology, Warsaw, Poland., Hutchinson PJ; Division of Neurosurgery, Addenbrooke's Hospital, University of Cambridge, Cambridge, Cambridge, United Kingdom., Newcombe VFJ; Division of Anaesthesia, University of Cambridge, Cambridge, United Kingdom., Menon DK; Division of Anaesthesia, University of Cambridge, Cambridge, United Kingdom. |
| Abstrakt: |
Failure of cerebral autoregulation has been linked to unfavorable outcome after traumatic brain injury (TBI). Preliminary evidence from a small, retrospective, single-center analysis suggests that autoregulatory dysfunction may be associated with traumatic lesion expansion, particularly for pericontusional edema. The goal of this study was to further explore these associations using prospective, multi-center data from the Collaborative European Neurotrauma Effectiveness Research in TBI (CENTER-TBI) and to further explore the relationship between autoregulatory failure, lesion progression, and patient outcome. A total of 88 subjects from the CENTER-TBI High Resolution ICU Sub-Study cohort were included. All patients had an admission computed tomography (CT) scan and early repeat scan available, as well as high-frequency neurophysiological recordings covering the between-scan interval. Using a novel, semiautomated approach at lesion segmentation, we calculated absolute changes in volume of contusion core, pericontusional edema, and extra-axial hemorrhage between the imaging studies. We then evaluated associations between cerebrovascular reactivity metrics and radiological lesion progression using mixed-model regression. Analyses were adjusted for baseline covariates and non-neurophysiological factors associated with lesion growth using multi-variate methods. Impairment in cerebrovascular reactivity was significantly associated with progression of pericontusional edema and, to a lesser degree, intraparenchymal hemorrhage. In contrast, there were no significant associations with extra-axial hemorrhage. The strongest relationships were observed between RAC-based metrics and edema formation. Pulse amplitude index showed weaker, but consistent, associations with contusion growth. Cerebrovascular reactivity metrics remained strongly associated with lesion progression after taking into account contributions from non-neurophysiological factors and mean cerebral perfusion pressure. Total hemorrhagic core and edema volumes on repeat CT were significantly larger in patients who were deceased at 6 months, and the amount of edema was greater in patients with an unfavourable outcome (Glasgow Outcome Scale-Extended 1-4). Our study suggests associations between autoregulatory failure, traumatic edema progression, and poor outcome. This is in keeping with findings from a single-center retrospective analysis, providing multi-center prospective data to support those results. |
