Relationship Between Measures of Cerebrovascular Reactivity and Intracranial Lesion Progression in Acute TBI Patients: an Exploratory Analysis

Abstract

Background: Failure of cerebral autoregulation and progression of intracranial lesion have both been shown to contribute to poor outcome in patients with acute traumatic brain injury (TBI), but the interplay between the two phenomena has not been investigated. Preliminary evidence leads us to hypothesize that brain tissue adjacent to primary injury foci may be more vulnerable to large fluctuations in blood flow in the absence of intact autoregulatory mechanisms. The goal of this study was therefore to assess the influence of cerebrovascular reactivity measures on radiological lesion expansion in a cohort of patients with acute TBI.

Methods: We conducted a retrospective cohort analysis on 50 TBI patients who had undergone high-frequency multimodal intracranial monitoring and for which at least two brain computed tomography (CT) scans had been performed in the acute phase of injury. We first performed univariate analyses on the full cohort to identify non-neurophysiological factors (i.e., initial lesion volume, timing of scan, coagulopathy) associated with traumatic lesion growth in this population. In a subset analysis of 23 patients who had intracranial recording data covering the period between the initial and repeat CT scan, we then correlated changes in serial volumetric lesion measurements with cerebrovascular reactivity metrics derived from the pressure reactivity index (PRx), pulse amplitude index (PAx), and RAC (correlation coefficient between the pulse amplitude of intracranial pressure and cerebral perfusion pressure). Using multivariate methods, these results were subsequently adjusted for the non-neurophysiological confounders identified in the univariate analyses.

Results: We observed significant positive linear associations between the degree of cerebrovascular reactivity impairment and progression of pericontusional edema. The strongest correlations were observed between edema progression and the following indices of cerebrovascular reactivity between sequential scans: % time PRx > 0.25 (r = 0.69, p = 0.002) and % time PAx > 0.25 (r = 0.64, p = 0.006). These associations remained significant after adjusting for initial lesion volume and mean cerebral perfusion pressure. In contrast, progression of the hemorrhagic core and extra-axial hemorrhage volume did not appear to be strongly influenced by autoregulatory status.

Conclusions: Our preliminary findings suggest a possible link between autoregulatory failure and traumatic edema progression, which warrants re-evaluation in larger-scale prospective studies.

Keywords: Neurophysiological monitoring; Traumatic brain injury; Traumatic intracranial hemorrhage.

Fig. 1

Representative set of segmented traumatic lesions on CT. Left: initial image; Right: segmented lesion(s). a Contusion core (blue) and peri-contusional edema (magenta), b epidural hematoma (green), c subdural hematoma (dark blue), d subarachnoid hemorrhage (red) and trace parafalcine extra-axial blood (dark blue). Right frontal hyperdensity in a and d represents the tip of the intracranial probe

Fig. 2

Scatter plot matrix of correlations between cerebrovascular reactivity status and radiological lesion progression. Recording interval between initial and repeat scan (n = 23). Correlation coefficients are shown in the top middle portion of each scatter plot. Δ Core, absolute difference in volume (mL) for contusion core between initial and repeat scan; Δ Edema, absolute difference in volume (mL) for peri-contusional edema between initial and repeat scan; Δ Extra-axial, absolute difference in total volume (mL) of extra-axial hemorrhage between initial and repeat scan, PAx pulse amplitude index (correlation between pulse amplitude of intracranial pressure and mean arterial pressure), PRx pressure reactivity index (correlation between intracranial pressure and mean arterial pressure, RAC correlation between pulse amplitude of intracranial pressure and cerebral perfusion pressure