Abstract
BackgroundImpaired cerebrovascular reactivity in adult traumatic brain injury (TBI) is known to be associated with poor outcome. However, there has yet to be an analysis of the association between the comprehensively assessed intracranial hypertension therapeutic intensity level (TIL) and cerebrovascular reactivity.MethodsUsing the Collaborative European Neuro Trauma Effectiveness Research in TBI (CENTER-TBI) high-resolution intensive care unit (ICU) cohort, we derived pressure reactivity index (PRx) as the moving correlation coefficient between slow-wave in ICP and mean arterial pressure, updated every minute. Mean daily PRx, and daily % time above PRx of 0 were calculated for the first 7 days of injury and ICU stay. This data was linked with the daily TIL-Intermediate scores, including total and individual treatment sub-scores. Daily mean PRx variable values were compared for each TIL treatment score via mean, standard deviation, and the Mann U test (Bonferroni correction for multiple comparisons). General fixed effects and mixed effects models for total TIL versus PRx were created to display the relation between TIL and cerebrovascular reactivity.ResultsA total of 249 patients with 1230 ICU days of high frequency physiology matched with daily TIL, were assessed. Total TIL was unrelated to daily PRx. Most TIL sub-scores failed to display a significant relationship with the PRx variables. Mild hyperventilation (p < 0.0001), mild hypothermia (p = 0.0001), high levels of sedation for ICP control (p = 0.0001), and use vasopressors for CPP management (p < 0.0001) were found to be associated with only a modest decrease in mean daily PRx or % time with PRx above 0.ConclusionsCerebrovascular reactivity remains relatively independent of intracranial hypertension therapeutic intensity, suggesting inadequacy of current TBI therapies in modulating impaired autoregulation. These findings support the need for investigation into the molecular mechanisms involved, or individualized physiologic targets (ICP, CPP, or Co2) in order to treat dysautoregulation actively.
Highlights
MethodsImpaired cerebrovascular reactivity after traumatic brain injury (TBI) has emerged as a meaningful independent factor associated with mortality and poor functional outcome at 6 and 12 months post-injury [5, 20, 27, 28]
This limited change in monitored pressure reactivity index (PRx) occurred in parallel to a stable mortality level in the same cohort over the 25-year period. This corroborates similar findings from a smaller study of 48 TBI patients, evaluating factors impacting the ability to calculate cerebral perfusion pressure (CPP) optimum from PRx [24]. While these findings suggest that PRx is independent of current TBI therapies, they require robust corroboration in an analysis that accounts for the intensity of therapy
They suggest the need for further work on the molecular mechanisms or complex individual physiology involved in impaired cerebrovascular reactivity, so as to aid in the development of targeted therapies aimed at enhancing autoregulatory reserve, with the aim of increasing resilience to physiological insults and improving outcomes. The goal of this project was to assess the association between daily treatment intensity, as measured through the therapeutic intensity level (TIL) intermediate scoring system [12, 31], and daily measures of cerebrovascular reactivity, using the Collaborative European Neuro Trauma Effectiveness Research in TBI (CENTER-TBI) study high-resolution intensive care unit (ICU) sub-study cohort [13]
Summary
MethodsImpaired cerebrovascular reactivity after traumatic brain injury (TBI) has emerged as a meaningful independent factor associated with mortality and poor functional outcome at 6 and 12 months post-injury [5, 20, 27, 28]. A recent retrospective analysis assessed the last 25 years of experience with therapies guided by cerebral physiology monitoring in adult TBI This analysis suggested that, despite changes in Brain Trauma Foundation (BTF) ICP and cerebral perfusion pressure (CPP) targets, little to no impact on PRx was seen [7]. This limited change in monitored PRx occurred in parallel to a stable mortality level in the same cohort over the 25-year period. This corroborates similar findings from a smaller study of 48 TBI patients, evaluating factors impacting the ability to calculate CPP optimum from PRx [24]. There has yet to be an analysis of the association between the comprehensively assessed intracranial hypertension therapeutic intensity level (TIL) and cerebrovascular reactivity
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