Association of Age and Sex With Multi-Modal Cerebral Physiology in Adult Moderate/Severe Traumatic Brain Injury: A Narrative Overview and Future Avenues for Personalized Approaches.

The impact of age and biological sex on outcome in moderate/severe traumatic brain injury (TBI) has been documented in large cohort studies, with advanced age and male sex linked to worse long-term outcomes. However, the association between age/biological sex and high-frequency continuous multi-modal monitoring (MMM) cerebral physiology is unclear, with only sparing reference made in guidelines and major literature in moderate/severe TBI. In this narrative review, we summarize some of the largest studies associating various high-frequency MMM parameters with age and biological sex in moderate/severe TBI. To start, we present this by highlighting the representative available literature on high-frequency data from Intracranial Pressure (ICP), Cerebral Perfusion Pressure (CPP), Extracellular Brain Tissue Oxygenation (PbtO2), Regional Cerebral Oxygen Saturations (rSO2), Cerebral Blood Flow (CBF), Cerebral Blood Flow Velocity (CBFV), Cerebrovascular Reactivity (CVR), Cerebral Compensatory Reserve, common Cerebral Microdialysis (CMD) Analytes and their correlation to age and sex in moderate/severe TBI cohorts. Then we present current knowledge gaps in the literature, discuss biological implications of age and sex on cerebrovascular monitoring in TBI and some future avenues for bedside research into the cerebrovascular physiome after TBI.

Sedation and cerebrovascular reactivity in traumatic brain injury: another potential avenue for personalized approaches in neurocritical care?

BACKGROUND: Impaired cerebrovascular reactivity appears to be linked to worse global outcome in adult traumatic brain injury (TBI). Literature suggests that current treatments administered in TBI care, in the intensive care unit (ICU), fail to greatly impact recorded cerebrovascular reactivity measures. In particular, the impact of sedation on cerebrovascular reactivity in traumatic brain injury (TBI) remains unclear in vivo. The goal of this study was to preliminarily assess the relationship between objectively measured depth of sedation and cerebrovascular reactivity in TBI. METHODS: Within, we describe a case series of 5 adult TBI patients with TBI, during which objective high-frequency physiology for sedation depth, using bispectral index (BIS), and both intracranial pressure (ICP) and arterial blood pressure (ABP) were recorded. Pressure reactivity index (PRx) and RAP (a metric of cerebral compensatory reserve) were derived. Relationships between cerebrovascular reactivity and compensatory reserve monitoring with BIS metrics were explored using descriptive plots. RESULTS: A total of 5 cases in our prospectively maintained database with high-frequency physiology for ICP, ABP, and BIS. Through error bar plotting, it can be seen that each patient displays a parabolic relationship between BIS and PRx. This suggests a potential "optimal" depth of sedation where cerebrovascular reactivity is the most intact. CONCLUSIONS: This small series highlights the potential impact of depth of sedation on cerebrovascular reactivity in TBI. It suggests that there may be an individual optimal depth of sedation, so as to optimize cerebrovascular reactivity. Further study of objective depth of sedation and its impact on cerebrovascular physiology in TBI is required.