Dynamic MR imaging patterns of cerebral fat embolism: a systematic review with illustrative cases

Abstract

Different MR imaging patterns of cerebral fat embolism have been reported in the literature without a systematic review. Our goal was to describe the patterns, explore the relationship between disease course and the imaging patterns, and discuss the underlying mechanism. We reveal 5 distinctive MR imaging patterns: 1) scattered embolic ischemia occurring dominantly at the acute stage; 2) confluent symmetric cytotoxic edema located at the cerebral white matter, which mainly occurs at the subacute stage; 3) vasogenic edematous lesions also occurring at the subacute stage; 4) petechial hemorrhage, which persists from the acute to the chronic stage; and 5) chronic sequelae, occurring at late stage, including cerebral atrophy, demyelinating change, and sequelae of infarction or necrosis. Underlying mechanisms of these imaging patterns are further discussed. Recognition of the 5 evolving MR imaging patterns of cerebral fat embolism may result in adjustment of the appropriate management and improve the outcome.

Fig 1.

Quality of Reporting of Meta-analysis standards (QUOROM) flow diagram of articles included in this systematic review.

Fig 2.

Bar graph of case numbers and positive proportion of each pattern against time.

Fig 3.

A 25-year-old man with a traumatic tibial bone fracture. Rapid consciousness decline was noted at postfracture day 1, and the brain MR imaging was performed at postfracture day 2. Axial DWI (A) and corresponding axial ADC image (B) demonstrate scattered spot diffusion-restricted lesions in the bilateral striatum, left posterior internal capsule, insula, operculum, and periventricular white matter (type 1 pattern).

Fig 4.

Another 19-year-old man with a traumatic tibial bone fracture. Stupor was noted at postfracture day 1, and the brain MR imaging was delayed to postfracture day 7 due to unstable vital signs. Serial axial DWI (A–D) and axial ADC images (E and F) demonstrate confluent cytotoxic edematous lesions in periventricular and subcortical white matter of the frontal, parietal, and temporal lobes; corpus callosum; and cerebellar peduncle bilaterally, which are type 2A patterns (asterisks). Axial ADC (E), corresponding FLAIR (G), and contrast-enhanced T1WI (H) demonstrate dot-shaped vasogenic edema with faint enhancement, which is a type 2B pattern (arrows).

Fig 5.

Serial axial SWI images of the second case at postfracture week 3 (A–D) demonstrate numerous petechial hemorrhages in the subcortical and periventricular white matter, cerebellar hemisphere and peduncle, and posterior corpus callosum bilaterally. Corresponding images of the same level at postfracture week 5 (E) and 3 months (F) demonstrate no significant interval change (type 2C pattern).

Fig 6.

Axial FLAIR images of the second case at postfracture day 7 (A) and 3 months (B) demonstrate brain volume loss and demyelination change at the late stage of CFE (type 3 pattern).