Comatose Patients with Cardiac Arrest: Predicting Clinical Outcome with Diffusion-weighted MR Imaging

Purpose: To examine whether the severity and spatial distribution of reductions in apparent diffusion coefficient (ADC) are associated with clinical outcomes in patients who become comatose after cardiac arrest.

Materials and Methods: This was an institutional review board–approved, HIPAA-compliant retrospective study of 80 comatose patients with cardiac arrest who underwent diffusion-weighted magnetic resonance imaging. The need to obtain informed consent was waived except when follow-up phone calls were required; in those cases, informed consent was obtained from the families. Mean patient age was 57 years ± 16 (standard deviation); 31 (39%) patients were women. ADC maps were semiautomatically segmented into the following regions: subcortical white matter; cerebellum; insula; frontal, occipital, parietal, and temporal lobes; caudate nucleus; putamen; and thalamus. Median ADCs were measured in these regions and in the whole brain and were compared (with a two-tailed Wilcoxon test) as a function of clinical outcome. Outcome was defined by both early eye opening in the 1st week after arrest (either spontaneously or in response to external stimuli) and 6-month modified Rankin scale score.

Results: Whole-brain median ADC was a significant predictor of poor outcome as measured by no eye opening (specificity, 100% [95% confidence interval {CI}: 86%, 100%]; sensitivity, 30% [95% CI: 18%, 45%]) or 6-month modified Rankin scale score greater than 3 (specificity, 100% [95% CI: 73%, 100%]; sensitivity, 41% [95% CI: 29%, 54%]), with patients with poor outcomes having significantly lower ADCs for both outcome measures (P ≤ .001). Differences in ADC between patients with good and those with poor outcomes varied according to brain region, involving predominantly the occipital and parietal lobes and the putamen, and were dependent on the timing of imaging.

Conclusion: Spatial and temporal differences in ADCs may provide insight into mechanisms of hypoxic-ischemic brain injury and, hence, recovery.

© RSNA, 2009

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Article History

Published in print: 2009