Resuscitation · 2026
3-Dimensional quantification of ischemic brain injury in post-cardiac arrest patients with hypoxic-ischemic brain injury.
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Ambwani Gaurav, Larkey Connor A, Limaye Warda, Griesdale Donald E, Sekhon Mypinder S, Guest Will, Hoiland Ryan L
Аннотация
INTRODUCTION: Brain tissue hypoxia and ischemia are central to the pathophysiology of hypoxic-ischemic brain injury (HIBI). Magnetic resonance imaging (MRI) techniques including diffusion-weighted imaging (DWI) and associated apparent diffusion coefficient (ADC) maps offer a non-invasive method for identifying ischemic tissue, but their use is often limited to the provision of summary data. We developed a reproducible, semi-automated analysis pipeline to three-dimensionally quantify and anatomically localize ischemic brain injury using DWI-ADC data in HIBI patients.
METHODS: A retrospective cohort of post-cardiac arrest patients with HIBI (n = 10) was included. MRI preprocessing included skull stripping, spatial normalization to MNI152 space, and anatomical parcellation using FreeSurfer atlases. Ischemic regions were defined by an ADC threshold (<650e-6 mm2/s), and lesion burden was computed voxel-wise by segment, hemisphere, and tissue type. Susceptibility-weighted imaging (SWI) hypointensities were also quantified.
RESULTS: Ischemic injury was spatially heterogeneous but consistently affected the putamen, thalamus, and posterior cortical regions (e.g., pericalcarine and perirolandic cortices). The overall mean relative lesion volume was 28.4 ± 14.1% of total brain volume, with greater involvement in white matter (33.3 ± 17.8%) than gray matter (24.1 ± 11.4%; P = 0.005). Overlap of SWI and ADC hypointensities was minimal (<1% of all voxels), indicating negligible confounding by intraparenchymal blood.
DISCUSSION: We present a robust, observer-independent workflow for anatomically resolved quantification of ischemic injury in HIBI. Atlas-based segmentation integrated with voxel-intensity ADC analysis, enabled generation of granular data on the pattern and extent of ischemic brain injury following cardiac arrest.
METHODS: A retrospective cohort of post-cardiac arrest patients with HIBI (n = 10) was included. MRI preprocessing included skull stripping, spatial normalization to MNI152 space, and anatomical parcellation using FreeSurfer atlases. Ischemic regions were defined by an ADC threshold (<650e-6 mm2/s), and lesion burden was computed voxel-wise by segment, hemisphere, and tissue type. Susceptibility-weighted imaging (SWI) hypointensities were also quantified.
RESULTS: Ischemic injury was spatially heterogeneous but consistently affected the putamen, thalamus, and posterior cortical regions (e.g., pericalcarine and perirolandic cortices). The overall mean relative lesion volume was 28.4 ± 14.1% of total brain volume, with greater involvement in white matter (33.3 ± 17.8%) than gray matter (24.1 ± 11.4%; P = 0.005). Overlap of SWI and ADC hypointensities was minimal (<1% of all voxels), indicating negligible confounding by intraparenchymal blood.
DISCUSSION: We present a robust, observer-independent workflow for anatomically resolved quantification of ischemic injury in HIBI. Atlas-based segmentation integrated with voxel-intensity ADC analysis, enabled generation of granular data on the pattern and extent of ischemic brain injury following cardiac arrest.