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Year : 2021  |  Volume : 69  |  Issue : 2  |  Page : 538--539

The Devastating Starfield Pattern of Cerebral Fat Embolism

Enambir S Josan1, Gabriel A Zaietta2, Girendra V Hoskere2,  
1 Department of Pulmonary and Critical Care – MetroHealth Medical Center, Cleveland, OH USA 44109, USA
2 Department of Pulmonary and Critical Care - East Tennessee State University, Johnson City, TN, USA 37614, USA

Correspondence Address:
Dr. Enambir S Josan
2500 Metrohealth Drive, Dept. of Pulmonary and Critical Care, Cleveland, OH
USA




How to cite this article:
Josan ES, Zaietta GA, Hoskere GV. The Devastating Starfield Pattern of Cerebral Fat Embolism.Neurol India 2021;69:538-539


How to cite this URL:
Josan ES, Zaietta GA, Hoskere GV. The Devastating Starfield Pattern of Cerebral Fat Embolism. Neurol India [serial online] 2021 [cited 2021 Jun 21 ];69:538-539
Available from: https://www.neurologyindia.com/text.asp?2021/69/2/538/314561


Full Text



A 22-year-old male presented with bilateral femur fractures after a 20-feet fall and underwent rapid external fixation of long bones. He was Glasgow coma scale of 15 on presentation but deteriorated shortly after procedure, developed respiratory failure, and was intubated. Diffusion-weighted imaging (DWI) on Magnetic Resonance Imaging (MRI) brain showed multiple, tiny, slightly hyperintense areas of punctate signal abnormality involving bilateral cerebral hemispheres [Figure 1], corpus callosum, cerebellar hemispheres, and brainstem that were also seen in T2 and FLAIR (Fluid attenuated inversion recovery). The pattern was consistent with starfield like presentation of diffuse fat emboli. The T2 star/gradient echo sequences did not show any areas of dark signal intensity to indicate associated hemorrhagic component. Overt parenchymal edema wasn't noted and craniocervical junction was grossly unremarkable.{Figure 1}

Cerebral fat embolism syndrome (CFES) is a devastating complication of fat embolization syndrome which is almost exclusively due to long bone fracture.[1] It clinically presents as sudden onset of hypoxia, altered mental status, and petechial rash in setting of long bone fracture.[1] Neurological deficits are often transient and reversible although permanent morbidity has been noted as well.[2],[3] MRI brain is diagnostic in the appropriate clinical setting with a starfield like pattern on T2 and DWI.[4] The multiple, non-confluent, small foci of punctate white matter hyperintensity (starfield pattern of white spots on dark background) is representative of micro-embolic infarcts and toxic effects of free fatty acids.[3],[4] It usually involves subcortical cerebral white matter, basal ganglia, thalami, and centrum semiovale.[2] The degree of involvement can be graded and correlates with severity of neurological decompensation, while the resolution of lesions is noted to match clinical recovery.[3] Other etiologies of disseminated T2-hyperintense lesions include demyelinating diseases, diffuse axonal injury, vasogenic edema due to microinfarcts, and glotic foci. Diffusion restriction can differentiate the chronic pathologies.[5] Vascular parkinsonian syndromes and Wilson disease may also show subcortical involvement, but with more confluent T2 hyperintensities.[6]

Early clinical suspicion with rapid fixation of fracture is targeted for prevention.[1] In patients who develop CFES, management is mainly supportive with early resuscitation, ventilator support for hypoxia, stroke prophylaxis with aspirin, and seizure prophylaxis with antiepileptics.[7]

Our patient was young and would have been a candidate for long-term ventilator support with tracheostomy and nutritional support with percutaneous gastrostomy. However, given the poor prognosis secondary to traumatic injuries, the family chose to withdraw care leading to demise.

Acknowledgement

Dr. Mudher Al Shathir and Dr. Amanda Vanlandingham for care provided for this patient.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

References

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