Complete Recovery of Perfusion Abnormalities in a Cardiac Arrest Patient Treated with Hypothermia: Results of Cerebral Perfusion MR Imaging
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Therapeutic hypothermia in cardiac arrest patients is associated with favorable outcomes mediated via neuroprotective mechanisms. We report a rare case of a 32-year-old male who demonstrated complete recovery of signal changes on perfusion-weighted imaging after therapeutic hypothermia due to cardiac arrest. Brain MRI with perfusion-weighted imaging, performed three days after ending the hypothermia therapy, showed a marked decrease in relative cerebral blood flow (rCBF) and delay in mean transit time (MTT) in the bilateral basal ganglia, thalami, brain stem, cerebellum, occipitoparietal cortex, and frontotemporal cortex. However, no cerebral ischemia was not noted on diffusion-weighted imaging (DWI) or fluidattenuated inversion recovery (FLAIR) sequences. A follow-up brain MRI after one week showed complete resolution of the perfusion deficit and the patient was discharged without any neurologic sequelae. The mechanism and interpretation of the perfusion changes in cardiac arrest patients treated with therapeutic hypothermia are discussed.
Abstract
Therapeutic hypothermia in cardiac arrest patients is associated with favorable outcomes mediated via neuroprotective mechanisms. We report a rare case of a 32-year-old male who demonstrated complete recovery of signal changes on perfusion-weighted imaging after therapeutic hypothermia due to cardiac arrest. Brain MRI with perfusion-weighted imaging, performed three days after ending the hypothermia therapy, showed a marked decrease in relative cerebral blood flow (rCBF) and delay in mean transit time (MTT) in the bilateral basal ganglia, thalami, brain stem, cerebellum, occipitoparietal cortex, and frontotemporal cortex. However, no cerebral ischemia was not noted on diffusion-weighted imaging (DWI) or fluidattenuated inversion recovery (FLAIR) sequences. A follow-up brain MRI after one week showed complete resolution of the perfusion deficit and the patient was discharged without any neurologic sequelae. The mechanism and interpretation of the perfusion changes in cardiac arrest patients treated with therapeutic hypothermia are discussed.
참고문헌 (7)
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