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
Frederick A. Zeiler, Erta Beqiri, Manuel Cabeleira, Peter J. Hutchinson, Nino Stocchetti, David Menon, Marek Czosnyka, Peter Smielewski, Ari Ercole, Audny Anke, Ronny Beer, Bo‐Michael Bellander, Erta Beqiri, András Büki, Manuel Cabeleira, Marco Carbonara, Arturo Chieregato, Giuseppe Citerio, Hans Clusmann, Endre Czeiter, Marek Czosnyka, Bart Depreitere, Ari Ercole, Shirin Frisvold, Raimund Helbok, Stefan Jankowski, Danile Kondziella, Lars‐Owe Koskinen, Ana Kowark, David Menon, Geert Meyfroidt, Kirsten Moeller, David Nelson, Anna Piippo-Karjalainen, Andreea Rădoi, Arminas Ragauskas, Rahul Raj, Jonathan R. Rhodes, Saulius Ročka, Rolf Rossaint, Juan Sahuquillo, Oliver Sakowitz, Peter Smielewski, Nino Stocchetti, Nina Sundström, Riikka Takala, Tomas Tamošuitis, Olli Tenovuo, Peter Vajkoczy, Alessia Vargiolu, Rimantas Vilcinis, Stefan Wolf, Alexander Younsi, Frederick A. Zeiler
Abstract
Pressure reactivity index (PRx) and brain tissue oxygen (PbtO 2 ) are associated with outcome in traumatic brain injury (TBI). This study explores the relationship between PRx and PbtO 2 in adult moderate/severe TBI. Using the Collaborative European NeuroTrauma Effectiveness Research in Traumatic Brain Injury (CENTER-TBI) high resolution intensive care unit (ICU) sub-study cohort, we evaluated those patients with archived high-frequency digital intraparenchymal intracranial pressure (ICP) and PbtO 2 monitoring data of, a minimum of 6 h in duration, and the presence of a 6 month Glasgow Outcome Scale –Extended (GOSE) score. Digital physiological signals were processed for ICP, PbtO 2 , and PRx, with the % time above/below defined thresholds determined. The duration of ICP, PbtO 2 , and PRx derangements was characterized. Associations with dichotomized 6-month GOSE (alive/dead, and favorable/unfavorable outcome; ≤ 4 = unfavorable), were assessed. A total of 43 patients were included. Severely impaired cerebrovascular reactivity was seen during elevated ICP and low PbtO 2 episodes. However, most of the acute ICU physiological derangements were impaired cerebrovascular reactivity, not ICP elevations or low PbtO 2 episodes. Low PbtO 2 without PRx impairment was rarely seen. % time spent above PRx threshold was associated with mortality at 6 months for thresholds of 0 (area under the curve [AUC] 0.734, p = 0.003), > +0.25 (AUC 0.747, p = 0.002) and > +0.35 (AUC 0.745, p = 0.002). Similar relationships were not seen for % time with ICP >20 mm Hg, and PbtO 2 < 20 mm Hg in this cohort. Extreme impairment in cerebrovascular reactivity is seen during concurrent episodes of elevated ICP and low PbtO 2 . 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 PbtO 2 levels. Measures of cerebrovascular reactivity appear to display the most consistent associations with global outcome in TBI, compared with ICP and PbtO 2 .