Imaging in a Case of Cerebral Fat Embolism Syndrome
A 62-year-old male presented to our emergency room intubated, with posttraumatic seizures
and compound left femur fracture after suffering a road traffic accident. Glasgow
Coma Scale (GCS) prior to seizure onset was 15. The computed tomography (CT) scan
and magnetic resonance imaging (MRI) of the brain on admission were normal and the
patient was taken up for emergency wound exploration and fixation of femur fracture.
Postoperatively, sensorium did not improve on weaning sedation and GCS was E2VtM4.
Initial noncontrast head CT showed no evidence of any infarcts or bleeds. Repeat MRI
showed multiple punctate areas of diffusion restriction and corresponding punctate
T2 hyperintensities in the subcortical white matter cerebellum and brainstem suggestive
of cerebral fat embolism syndrome. These areas showed a diffusion restriction on diffusion-weighted
imaging (DWI) sequences ([Fig. 1]). Gradient recalled echo /susceptibility-weighted imaging (SWI) did not show microareas
of blooming in the same distribution. Diffuse axonal injury was ruled out in our patient
owing to normal MRI brain at admission.
Fig. 1 (A) Magnetic resonance imaging brain axial image, T2-weighted, showing multiple areas
of hyperintensities in the cerebellum and the brainstem, corresponding to the diffusion
restriction in the diffusion-weighted imaging (DWI). (B) Magnetic resonance imaging brain axial image, T2-weighted, showing multiple areas
of hyperintensities in the subcortical white matter, corresponding to the diffusion
restriction in the DWI. (C) Magnetic resonance imaging brain axial image, diffusion-weighted sequence, showing
multiple punctuate areas of diffusion restriction in the cerebellum and brainstem.
(D) Magnetic resonance imaging brain axial image, diffusion-weighted sequence, showing
multiple punctuate areas of diffusion restriction in the subcortical white matter,
in a “starfield” pattern. The diffusion restriction is seen predominantly in the border
zones and deep gray nuclei bilaterally.
Early DWI in a typical case of Cerebral Fat embolism Syndrome (CFS) shows “starfield”
appearance as multiple foci of high signal scatter predominantly in the border zones
and deep gray nuclei bilaterally, similar to that seen in our case. In the subacute
phase, DWI shows confluent bilateral symmetric periventricular and subcortical white
matter cytotoxic edema and diffusion restriction.
Microhemorrhages are seen as blooming foci in the white matte in T2 sequences but
are better appreciated on SWI, they are pathogenic of CFs. Up to one-third of all
fat embolism cases may show blooming on SWI, it was not seen in our case. MR spectroscopy
shows the presence of lipid peaks within the lesions, a finding related to the nature
of the emboli or associated necrosis.[1]
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