Brain Tissue Oxygen and Cerebrovascular Reactivity in Traumatic Brain Injury: A Collaborative European NeuroTrauma Effectiveness Research in Traumatic Brain Injury Exploratory Analysis of Insult Burden

Abstract

Pressure reactivity index (PRx) and brain tissue oxygen (PbtO2) are associated with outcome in TBI. This study explores the relationship between PRx and PbtO2 in adult moderate/severe TBI. Using the Collaborative European NeuroTrauma Effectiveness Research in Traumatic Brain Injury (CENTER-TBI) high resolution ICU sub-study cohort, we evaluated those patients with archived high-frequency digital intra-parenchymal ICP and PbtO2 monitoring data of a minimum of 6 hours in duration, and the presence of a 6 month Glasgow Outcome Scale -Extended (GOSE) score. Digital physiologic signals were processed for ICP, PbtO2 and pressure reactivity index (PRx), with the % time above/below defined thresholds determined. The duration of ICP, PbtO2 and PRx derangements was characterised.Associations with dichotomized 6-month GOSE (alive/dead, and favourable/unfavourable outcome; 4 or less = unfavourable), were assessed. A total of 43 patients were included. Severely impaired cerebrovascular reactivity was seen during elevated ICP and low PbtO2 episodes. However, most of the acute ICU physiologic derangements were impaired cerebrovascular reactivity, not ICP elevations or low PbtO2 episodes. Low PbtO2 without PRx impairment was rarely seen. % time spent above PRx threshold was associated with mortality at 6-months for thresholds of 0 (AUC 0.734, p=0.003), above +0.25 (AUC 0.747, p=0.002) and above +0.35 (AUC 0.745, p=0.002). Similar relationships were not seen for % time with ICP above 20 mmHg, and PbtO2 below 20 mmHg in this cohort. Extreme impairment in cerebrovascular reactivity is seen during concurrent episodes of elevated ICP and low PbtO2. However, the majority of the deranged cerebral physiology seen during the acute ICU phase is impairment in cerebrovascular reactivity, with most impairment occurring in the presence of normal PbtO2 levels.

The Impact of Vasopressor and Sedative Agents on Cerebrovascular Reactivity and Compensatory Reserve in Traumatic Brain Injury: An Exploratory Analysis

“…These methods are similar to those of prior works in the field. 10,14,28 Signal processing The following signal processing occurred using similar methodology, covered in other publications by our group and the senior author. 10,14,28 CPP was calculated as mean arterial pressure (MAP)-ICP.…”

“…10,14,28 Signal processing The following signal processing occurred using similar methodology, covered in other publications by our group and the senior author. 10,14,28 CPP was calculated as mean arterial pressure (MAP)-ICP. Pulse amplitude of ICP (AMP) was derived from the fundamental amplitude of the ICP waveform in the frequency domain, using Fourier analysis over a non-overlapping 10-sec moving window.…”

“…[7][8][9][10][11][12] Cerebrovascular reactivity is emerging as an important component to ongoing cerebral physiological dysfunction in the setting of current guideline-based therapies. 13,14 Further, impaired cerebrovascular reactivity has been demonstrated to be associated with computed tomography (CT) based pericontusion edema progression. 15,16 In addition, novel methods using cerebrovascular reactivity physiological targets, such as optimal cerebral perfusion pressure (CPPopt) [17][18][19][20] or individual ICP (iICP) thresholds, 21,22 have emerged in personalize treatment of patients with TBI.…”

The impact of hypertonic saline on cerebrovascular reactivity and compensatory reserve in traumatic brain injury: an exploratory analysis

“…Furthermore, it carries implications for prophylactic dosing of HTS in moderate/severe TBI. It is becoming more apparent that the time spent with abnormal cerebrovascular reactivity is associated with poorer 6-month outcome in moderate/severe TBI [20,24,45,48]. As such, if particular treatments lead to worse cerebrovascular reactivity, this may impact patient outcomes.…”

Traumatic brain injury neuroelectrochemical monitoring: behind-the-ear micro-instrument and cloud application

“…There is a growing consensus that continuous multimodal monitoring is critical for TBI patients [10,[38][39][40]. Brain neurochemical signals are subtle and complex and as such high-quality time-aligned clinical data are needed to identify changes, particularly in a highnoise clinical environment.…”