Temporal course of autonomic dysfunction in severe traumatic brain injury

Document Type

Conference Proceeding

Publication Date

10-25-2025

Publication Title

Intensive Care Med Exp

Keywords

biological marker, adult, arterial pressure, autonomic dysfunction, autonomic nervous system function, benchmarking, clinical article, comparative effectiveness, conference abstract, controlled study, drug therapy, electrocardiogram, electrocardiography, entropy, female, human, intensive care unit, male, physiologic monitoring, pressoreceptor reflex, randomized controlled trial, sympathetic tone, traumatic brain injury, waveform

Abstract

Introduction. Early autonomic dysfunction (eAD) is a recognized critical but understudied component of secondary injury in severe traumatic brain injury (TBI). Using high-resolution physiologic waveform data obtained from multi-modal monitoring in the BOOST-3 trial, we analyzed measures of autonomic nervous system function over the first five days post-injury. Methods. We performed a retrospective analysis of cardiac waveform data collected via Moberg analytics from 42 patients enrolled in BOOST-3 with available data. BOOST-3 is a randomized clinical trial to determine the comparative effectiveness of two strategies for monitoring and treating patients with TBI in the intensive care unit setting. eAD metrics were derived from continuous arterial blood pressure (ABP) and electrocardiogram (ECG) waveforms. The primary analysis focused on changes in key AD indices, including time-domain (root mean square of successive differences [RMSSD], standard deviation of NN intervals [SDNN], percentage of successive normal-to-normal intervals differing by more than 50 ms [pNN50] and baroreflex sensitivity), frequency-domain metrics (low to high-frequency ratio [LF/HF]), and signal entropy over the first 5 days following injury. We analyzed beat-to-beat measurements averaged over one hour epochs. Results. Preliminary analysis of the first 42 patients revealed significant variation in eAD parameters within the first 24 h (Fig. 1). Specifically, RMSSD decreased from a median of 26 ms on day 1 to 21 ms by day 5. Similarly, SDNN decreased from 31 ms on day 1 to 27 ms by day 5. The LF/HF ratio decreased from 1.3 on day 1 to 1.1 by day 5. Baroreflex sensitivity (BRS) showed a rise and fall, with median values peaking to 8.7 ms/mmHg and decreasing to 5.2 ms/mmHg by day 5. Conclusions. eAD is prevalent in severe TBI and evolves over time, with significant changes in key metrics such as RMSSD, SDNN, pNN50, LF/HF, and BRS, indicating reduced parasympathetic and increased sympathetic activity. This study leverages high-resolution physiologic monitoring to characterize these changes, providing insights into potential prognostic and therapeutic implications. Further analysis of the full dataset will refine our understanding of eAD in severe TBI.

Volume

13

Issue

1

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