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Chen et al. Neuroimmunol Neuroinflammation 2018;5:31 I http://dx.doi.org/10.20517/2347-8659.2018.23 Page 5 of 7

One major and four minor criteria must be present to formally diagnose FES. Neither of these diagnostic
tools includes brain imaging, which seems to be the most specific. CFES is a clinical diagnosis, but specific
findings on neuroimaging studies can be strongly supportive. The purpose of a CT scan is to rule out certain
stroke mimics and detect hemorrhage, not necessarily to rule in the diagnosis of ischemic stroke. CT scans
may not be sensitive enough to detect an ischemic stroke, especially if it is small, acute (especially within
24 h of the stroke onset), or in the posterior fossa (i.e., brainstem and cerebellum areas). In other words, a
normal CT scan does not rule out the diagnosis of ischemic stroke. Noticeably, it is important to underline
that a careful examination of brain-CT findings, such as the topography and density measurements of round
lesions (such as round hypodense lesions, -40 HU) , were enough to confirm the clinical suspicion of CFE .
[3]
[3]
This is important because in some cases the MRI cannot be available or would be impossible to perform.
MRI is more sensitive and demonstrates multiple small hyperintense, intracerebral lesions. There were great
amounts of hyperintense lesions on MRI T2-weighted scans. The most characteristic MRI finding is the
starfield pattern, demonstrating scattered foci of high-intensity restricted diffusion on diffusion-weighted
imaging [7,10] . This is most apparent in the acute phase, from 4 h to the first few days from the time of injury.
Such widespread petechial hemorrhage and bland microinfarction have been demonstrated on autopsy . In
[11]
our case, the initial brain-CT scan was normal, while MRI showed extensive cortical and subcortical regions
fat embolism which led to disturbance of consciousness. There are few differential diagnoses of disseminated
hyperintense lesions on T2-weighted scans which include diffuse axonal injury, areas of vasogenic edema
associated with microinfarcts, and demyelinating diseases which were ruled out by history and clinical
[12]
scenario, in our case. Of note, in some patients who sustained severe trauma, both CFE and diffuse axonal
injury (DAI) could be the cause of altered consciousness in the absence of marked intracranial lesions in
cranial CT . However, distinguishing CFE and DAI can be difficult clinically. Generally, DAI develops
[13]
immediately after the insult, whereas CFE occurs 24 to 72 h after the trauma and even after internal fixation
for the fractures . It was reported that there was no significant difference between diagnostic performance
[13]
of diffusion tensor imaging (DTI) and conventional MRI in CFES, but a difference in directional diffusivities
was clearly identified between CFES and DAI.

There are currently no disease-specific treatment guidelines for FES or CFES other than supportive care to
address both intrinsic lung pathology and airway protection in the setting of neurological impairment .
[2]
Pharmacological intervention, including administration of heparin, dextran, aspirin, statin, albumin, and
steroids and glucose loading, proved to be ineffective [14,15] . Corticosteroids have been extensively studied with
variable results, and their use is controversial. In cases of fulminant FES, corticosteroids may be considered.
Gupta et al. propose a regimen of methylprednisolone 1.5 mg/kg IV every 8 h for 6 doses in a select
[16]
group of patients with long bone or pelvic fractures at high risk of developing FES and without significant
contraindications. In our case, the patient was treated with methylprednisolone injection (80 mg twice a day).
The side effects of corticosteroids such as promoting coagulation and ulcer, disorder of electrolyte metabolism
should be emphasized. Anticoagulation has been shown to prevent stroke in patients with cardioembolic
and other noncardioembolic sources. However, the early use of anticoagulants has been associated with
hemorrhagic transformation. Hitherto, there is insufficient evidence to support that routine administration
of anticoagulation agent is effective and safe for FES. One possible benefit from anticoagulation for fat
embolism may potentially decrease the risk of deep vein thrombosis. Early surgical stabilization should
be considered. Early fixation of fractures within 24 h has been recommended to prevent further trauma at
the injury site, thus decreasing the incidence of FES. The prognosis of CFES is variable, depending on the
severity of the manifestations and on the quality and timing of treatment. Most of patients recovered fully
from this disease, and other survivors remained in cognitive disorder, and some even die [3,7,15] .

In summary, we highlight that CFES could develop within hours after long bone fractures. Neurologic
manifestations of CFES vary greatly. Neuroimaging is critical in the diagnosis of CFES. The brain-CT scan
indicating the presence of round, hypodense lesions within the range of fat (-40 HU) suggests fat embolism.