Abstract

We aimed to explore the stratification of physiological factors affecting cerebral perfusion pressure, including arterial oxygen tension, arterial carbon dioxide tension, mean arterial pressure, intracranial pressure (ICP), and blood-brain barrier (BBB) status, with respect to primary or secondary brain injury (PBI or SBI) after out-of-hospital cardiac arrest (OHCA). Among the retrospectively enrolled 97 comatose OHCA survivors undergoing post-cardiac arrest (PCA) care, 46 (47.4%) with already established PBI (high signal intensity (HSI) on diffusion-weighted imaging (DWI) had higher ICP (p = 0.02) and poorer BBB status (p < 0.01) than the non-HSI group. On subgroup analysis within the non-HSI group to exclude the confounding effect of already established PBI, 40 (78.4%) patients with good neurological outcomes had lower ICP at 24 h (11.0 vs. 16.0 mmHg, p < 0.01) and more stable BBB status (p = 0.17 in pairwise comparison) compared to those with poor neurological outcomes, despite the non-significant differences in other physiological factors. OHCA survivors with HSI on DWI showed significantly higher ICP and poorer BBB status at baseline before PCA care than those without HSI. Despite the negative DWI findings before PCA care, OHCA survivors have a cerebral penumbra at risk for potentially leading the poor neurological outcome from unsuppressed SBI, which may be associated with increased ICP and BBB permeability.

Highlights

  • Based on the “two-hit model,” hypoxic-ischemic brain injury (HIBI) can be divided into two phases, namely, primary and secondary injury, which occur during cardiac arrest (CA) and immediately after return of spontaneous circulation (ROSC), respectively [3]

  • Characteristics and physiological factors (PFs) Associated with high-signal intensity (HSI) on diffusion-weighted image (DWI)

  • HSI on DWI obtained before post-cardiac arrest (PCA) care

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Summary

Introduction

Out-of-hospital cardiac arrest (OHCA) survivors suffer from hypoxic-ischemic brain injury (HIBI), with a high risk of mortality or incidence of poor neurological outcomes without regaining consciousness [1,2]. Based on the “two-hit model,” HIBI can be divided into two phases, namely, primary and secondary injury, which occur during cardiac arrest (CA) and immediately after return of spontaneous circulation (ROSC), respectively [3]. The neuroprotective strategies for managing secondary brain injury, including physiological, pharmacological, or surgical interventions, induce limited improvement of patient outcomes, as the primary brain injury is crucially involved in the possible occurrence of advanced brain injury before applying neuroprotective strategies [4,5]. Studies have reported irreversible brain damage in OHCA survivors through an analysis of the ratio of gray–white matter ratio attenuation (GWR) in brain computed tomography (CT) performed within 24 h of ROSC [6,7,8]

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