@article{ref1,
title="Intra- and extra-cranial injury burden as drivers of impaired cerebrovascular reactivity in traumatic brain injury",
journal="Journal of neurotrauma",
year="2018",
author="Zeiler, Frederick Adam and Donnelly, Joseph and Nourallah, Basil and Thelin, Eric Peter and Calviello, Leanne and Smieleweski, Peter and Czosnyka, Marek and Ercole, Ari and Menon, David",
volume="35",
number="14",
pages="1569-1577",
abstract="Impaired cerebrovascular reactivity has been associated with outcome following traumatic brain injury (TBI), but it is unknown how it is affected by trauma severity. Thus, we aimed to explore the relationship between intra-cranial (IC) and extra-cranial (EC) injury burden and cerebrovascular reactivity in TBI patients. We retrospectively included critically ill TBI patients. IC injury burden included detailed lesion and computerized tomography (CT) scoring (ie. Marshall, Rotterdam, Helsinki and Stockholm Scores) on admission. EC injury burden were characterized using the injury severity score (ISS) and APACHE II score. Pressure reactivity index (PRx), pulse amplitude index (PAx) and RAC were used to assess autoregulation/cerebrovascular reactivity. We used univariate and multi-variate logistic regression techniques to explore relationships between IC and EC injury burden and autoregulation indices. A total of 358 patients were assessed. ISS and all IC CT scoring systems were poor predictors of impaired cerebrovascular reactivity. Only subdural hematomas and thickness of SAH (p<0.05, respectively) were consistently associated with dysfunctional cerebrovascular reactivity. High age (p<0.01 for all) and admission APACHE II scores (p<0.05 for all) were the two variables strongest associated with abnormal cerebrovascular reactivity. In summary, diffuse IC injury markers (thickness of SAH and the presence of a SDH) and APACHE II were most associated with dysfunction in cerebrovascular reactivity after TBI. Standard CT scoring systems and evidence of macroscopic parenchymal damage are poor predictors, implicating potentially both microscopic injury patterns and host response as drivers of dysfunctional cerebrovascular reactivity. Age remains a major variable associated with cerebrovascular reactivity.<p /> <p>Language: en</p>",
language="en",
issn="0897-7151",
doi="10.1089/neu.2017.5595",
url="http://dx.doi.org/10.1089/neu.2017.5595"
}