Presentation
Pedestrian versus car low speed accident with multiple long bone fractures. Slow to wake up.
Patient Data
Innumerable punctate foci of susceptibility artifact are present throughout the cerebellar hemispheres, pons and midbrain, corpus callosum (particularly within the splenium), periventricular and subcortical white matter and the posterior frontal and parietal cortex, best seen on the susceptibility-weighted sequence. Numerous foci of diffusion restriction are present within the same regions, notably the left cerebellar hemisphere, bilateral periventricular white matter and frontal and parietal cortices. No filling defects, beading or aneurysm identified within the circle of Willis. No hydrocephalus or extra-axial fluid collection identified. The visualized orbits and paranasal sinuses are unremarkable.
Case Discussion
Fat embolism syndrome is a rare complication of long bone fractures, with an incidence of 1-11%, and mortality rate of 10%. Following long bone fractures, fat globule from marrow pass into the venous sinuses and may from there enter the arterial circulation via one of two mechanisms - right to left shunt (eg PFO) or direct filtration of microglobules through the pulmonary capillaries.
Clinical presentation is highly variable and multiple organ systems can be affected. The classic clinical triad of fat embolism syndrome is that of respiratory distress, petechial rash and neurological changes.
Cerebral fat embolism can be difficult to diagnose clinically, as symptoms are often non-specific, ranging from mild confusion to, seizures, focal neurology and coma. CT is typically normal, but may show evidence of edema or sometimes hemorrhage. MRI shows bilateral and symmetric microhemorrhages (SWI - walnut kernel pattern) and tiny foci of cytotoxic edema (DWI/ADC - starfield pattern) with a subcortical and deep white matter, including subcortical U-fibers, corpus callosum, and internal capsule distribution.
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