Evaluation of the relationship between slow-waves of intracranial pressure, mean arterial pressure and brain tissue oxygen in TBI : a CENTER-TBI exploratory analysis

• Brain tissue oxygen (PbtO2) monitoring in traumatic brain injury (TBI) has demonstrated strong associations with globaloutcome. Additionally, PbtO2 signals have been used to derive indices thought to be associated with cerebrovascular reactivityin TBI. However, their true relationship to slow-wave vasogenic fuctuations associated with cerebral autoregulation remainsunclear. The goal of this study was to investigate the relationship between slow-wave fuctuations of intracranial pressure(ICP), mean arterial pressure (MAP) and PbtO2 over time. Using the Collaborative European NeuroTrauma EfectivenessResearch in Traumatic Brain Injury (CENTER-TBI) high resolution ICU sub-study cohort, we evaluated those patients withrecorded high-frequency digital intra-parenchymal ICP and PbtO2 monitoring data of a minimum of 6 h in duration. Digitalphysiologic signals were processed for ICP, MAP, and PbtO2 slow-waves using a moving average flter to decimate the highfrequency signal. The frst 5 days of recording were analyzed. The relationship between ICP, MAP and PbtO2 slow-wavesover time were assessed using autoregressive integrative moving average (ARIMA) and vector autoregressive integrativemoving average (VARIMA) modelling, as well as Granger causality testing. A total of 47 patients were included. The ARIMAstructure of ICP and MAP were similar in time, where PbtO2 displayed diferent optimal structure. VARIMA modellingand IRF plots confrmed the strong directional relationship between MAP and ICP, demonstrating an ICP response to MAPimpulse. PbtO2 slow-waves, however, failed to demonstrate a defnite response to ICP and MAP slow-wave impulses. Theseresults raise questions as to the utility of PbtO2 in the derivation of cerebrovascular reactivity measures in TBI. There isa reproducible relationship between slow-wave fuctuations of ICP and MAP, as demonstrated across various time-seriesanalytic techniques. PbtO2 does not appear to reliably respond in time to slow-wave fuctuations in MAP, as demonstratedon various VARIMA models across all patients. These fndings suggest that PbtO2 should not be utilized in the derivationof cerebrovascular reactivity metrics in TBI, as it does not appear to be responsive to changes in MAP in the slow-waves.These fndings corroborate previous results regarding PbtO2 based cerebrovascular reactivity indices. 

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Neurologi (hsv//swe)

MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Neurology (hsv//eng)

Nyckelord

Autoregulation

Brain tissue oxygen

Cerebrovascular reactivity

Traumatic brain injury

TBI

Publikations- och innehållstyp

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