of Oncology and Onco-haematology, University of Milan, Milan, Italy.
2 Dino Ferrari Centre, Neuroscience Section, Department of Pathophysiology and Transplantation (DEPT), University of Milan, Milan, Italy.
3 Department of Internal Medicine, Rare Diseases Centre, General Medicine Unit, Fondazione IRCCS Ca' Granda, Ospedale Maggiore Policlinico, Milan, Italy.
4 Neurology Unit, Fondazione IRCCS Ca' Granda, Ospedale Maggiore Policlinico, Milan, Italy.
| This is an Open Access article distributed
under the terms of the Creative Commons Attribution License
(https://creativecommons.org/licenses/by-nc/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
To the editor
1. Pre- and
post-cerebral fat embolism (CFE) brain magnetic resonance imaging (MRI)
with susceptibility-weighted sequences. Normal brain
fluid-attenuated inversion recovery (FLAIR) MRI sequences performed 6
months before the index event (left side, A and B).
Susceptibility-weighted imaging (SWI) sequences performed 24 hours
after intubation. Multiple, punctuate, widespread, hypointense lesions
are distributed in the cerebellum (C), basal ganglia, splenium of
corpus callosum (D), and subcortical white matter bilaterally (E),
(walnut kernel pattern). These alterations are consistent with the
accumulation of haemosiderin in the context of diffuse
microhaemorrhages from small-vessel occlusion by fat emboli. FLAIR
images at 24 hours after intubation show scattered, monomorphic,
hyperintense lesions in the deep grey structures (short arrow) and
splenium of the corpus callosum (long arrow) not present in the pre-CFE
brain imaging (A and B).