{'fraction_non_alphanumeric': 0.018301610541727673, 'fraction_numerical': 0.005124450951683748, 'mean_word_length': 5.358139534883721, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
[Brain CT and MRI findings in fat embolism syndrome].

To elucidate brain CT and MRI findings in fat embolism syndrome (FES), we retrospectively analyzed images from 5 patients with FES during the acute and subacute stages. Brain CT examinations demonstrated brain edema in 2 patients and transient spotty low density lesions in 2 patients. Three patients showed no abnormalities. Brain MRI, however, showed brain abnormalities in all patients during the acute stages. These were revealed as spotty high signal intensity lesions on T2WI, and some showed low intensity on T1WI. These spotty lesions were considered to reflect edematous fluid occurring as a result of the unique pathophysiological condition of FES. While the spotty high signal intensity lesions on T2WI were distributed in the cerebrum, cerebellum, brain stem, thalamus, basal ganglia, internal capsule and corpus callosum, cerebral and cerebellar spotty lesions were characteristically located along the boundary zones of the major vascular territories. This characteristic location might be induced by a hypoxic brain condition in FES because the numerous fat globules present in this condition can block entire brain capillaries. This characteristic signal location on T2WI is a useful indicator for differentiating FES from the primary intra-axial brain injury in patients with multifocal trauma.