Cerebral fat embolism after traumatic bone fractures: a structured literature review and analysis of published case reports

Abstract

Background: The incidence of cerebral fat embolism (CFE) ranges from 0.9-11%, with a mean mortality rate of around 10%. Although no univocal explanation has been identified for the resulting fat embolism syndrome (FES), two hypotheses are widely thought: the 'mechanical theory', and the 'chemical theory'. The present article provides a systematic review of published case reports of FES following a bone fracture.

Methods: We searched MEDLINE, Web of Science and Scopus to find any article related to FES. Inclusion criteria were: trauma patients; age ≥ 18 years; and the clinical diagnosis of CFE or FES. Studies were excluded if the bone fracture site was not specified.

Results: One hundred and seventy studies were included (268 cases). The male gender was most prominent (81.6% vs. 18.4%). The average age was 33 years (±18). The mean age for males (29 ± 14) was significantly lower than for females (51 ± 26) (p < 0.001). The femur was the most common fracture site (71% of cases). PFO was found in 12% of all cases. Univariate and multivariate regression analyses showed the male gender to be a risk factor for FES: RR 1.87 and 1.41, respectively (95%CI 1.27-2.48, p < 0.001; 95%CI 0.48-2.34, p < 0.001).

Conclusions: FES is most frequent in young men in the third decades of life following multiple leg fractures. FES may be more frequent after a burst fracture. The presence of PFO may be responsible for the acute presentation of cerebral embolisms, whereas FES is mostly delayed by 48-72 h.

Keywords: Cerebral fat embolism; Fat embolism syndrome; Patent foramen ovale.

Fig. 1

A simple model based on a fairground ‘test your strength’ hammer game might explain why higher energy impacts are more likely to result in fat emboli being ‘shot’ into the vascular compartment able to reach the upper body. Multiple organ involvement of fat embolization according to Peltier’s mechanical theory

Fig. 2

Oil Red O stained slides of the lung reveal extensive intravascular fat emboli within the peribronchiolar and alveolar vessels, as well as a perivascular fat globule and the presence of small lipid vesicles within alveolar macrophages

Fig. 3

Multiple intravascular fat emboli and focal areas of fat extravasation in the central nervous system of a young patient whose cause of death was a massive cerebral fat embolism

Fig. 4

An axial non enhanced computed tomography (NECT) scan performed on the first day (a) and 24 h later (b) show the appearance of diffuse cerebral edema with initial loss of normal gray-white matter differentiation (narrow white arrows), obliteration of CSF spaces (unfilled think arrow) and the “disappearing” of the basal ganglia (i.e., head of the right caudate nucleus) (filled thick arrow)

Fig. 5

Axial FLAIR (a) magnetic resonance imaging sequence shows the presence of numerous multifocal hyperintensities involving the deep white matter of both hemispheres (arrow), which correspond to innumerable tiny foci of diffusion restrictions on DWI (b) with low signal on ADC map (c) (arrow). These findings are the so-called “starfield” pattern characteristic of cerebral fat embolism syndrome. In the same patient, the SE-T1W (d) and T2* GRE (f) sequences, and the axial non enhanced computed tomography NECT scan (f) appear relatively normal