Notes

The patient is intubated.

Numerous tiny ( <1.5 mm) foci of SWI susceptibility are noted supra and
infratentorially , with diffuse white matter involvement, as well as
bilateral internal capsules, basal ganglia, thalami, splenium of corpus
callosum, brainstem and bilateral cerebellar hemispheres.

There is no evidence of gross intracranial hemorrhage. No evidence of acute infarction, edema or mass effect.
Patchy periventricular and deep white matter T2 FLAIR hyperintensities are
noted, in keeping with mild chronic microangiopathic changes.

Ventricles, sulci and cisterns are age-appropriate. No hydrocephalus. No
midline shift. Normal flow-void signal from the major intracranial vessels
is maintained.

Mucosal thickening noted in bilateral ethmoidal air cells and sphenoid
sinuses. There is trace fluid in the mastoid air cells bilaterally.

IMPRESSION:
Striking numerous tiny foci of SWI susceptibility are demonstrated
diffusely in the brain parenchyma supra and infratentorially, also
involving the splenium of corpus callosum, internal capsules, brainstem and bilateral cerebellar hemispheres. These are nonspecific. Allowing for provided history of recent trauma and multiple fractures, we favor it to represent changes related to fat emboli.

Similar imaging findings have also been described in blood dyscrasias and DIC. Diffuse axonal injury and cerebral amyloid angiopathy are included in the differential diagnosis, however considered less likely.

There is no evidence of gross intracranial cranial hemorrhage. No edema or mass effect.