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Table of Contents    
Year : 2012  |  Volume : 60  |  Issue : 1  |  Page : 100-102

Fat embolism syndrome mimicker of diffuse axonal injury on magnetic resonance imaging

1 Department of Radio-diagnosis and Imaging, PGIMER, Chandigarh, India
2 Department of Orthopedics, PGIMER, Chandigarh, India

Date of Submission30-Sep-2011
Date of Decision01-Oct-2011
Date of Acceptance05-Dec-2011
Date of Web Publication7-Mar-2012

Correspondence Address:
Vivek Gupta
Department of Radio-diagnosis and Imaging, PGIMER, Chandigarh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.93597

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How to cite this article:
Kumar S, Gupta V, Aggarwal S, Singh P, Khandelwal N. Fat embolism syndrome mimicker of diffuse axonal injury on magnetic resonance imaging. Neurol India 2012;60:100-2

How to cite this URL:
Kumar S, Gupta V, Aggarwal S, Singh P, Khandelwal N. Fat embolism syndrome mimicker of diffuse axonal injury on magnetic resonance imaging. Neurol India [serial online] 2012 [cited 2021 Aug 2];60:100-2. Available from:


Fat embolism syndrome is most commonly associated with long bone and pelvic fractures. [1] The syndrome occurs mostly in adults and rarely in children, as in children, the bone marrow contains more of hematopoietic tissue and less of fat. The patients usually develop features within 24 to 72 h after trauma. Neurological features present in the early stages and often occur after the onset of respiratory distress. Brain magnetic resonance imaging (MRI) is a valuable tool in evaluating fat embolism syndrome. We report a case of fat embolism syndrome with unique MRI findings.

A 27-year-old man sustained fractures of shaft right femur, right tibia and fibula in a roadside accident and was conscious at the time of admission with Glasgow Coma Score (GCS) of 15. Patient underwent open reduction and internal fixation of femoral fracture one day after the accident. Postoperatively after 24 h, patient developed dyspnea and altered mental status. Multiple punctate skin rashes were observed on anterior chest wall and in axillary regions on Day 2 after surgery. Blood gas analysis showed mild hypoxemia, with a PaO 2 of 74 mm Hg and a PaCO 2 of 27.1 mm Hg and HCO 3 -16.7 m mol/l. MRI of the brain T2-WI [Figure 1]a-c and Fluid attenuated inversion recovery [FLAIR] images [Figure 2]a-c revealed multiple foci of high signal intensity within the brain parenchyma involving the white matter (subcortical white matter and centrum semiovale), corpus callosum as well as in basal ganglia and thalami. On diffusion-weighted sequence [Figure 3]a-c with a b value of 1000 mm/s2, these lesions showed high signal intensity, with low signal on apparent diffusion coefficient [ADC] images [Figure 3]d-f suggesting restricted diffusion. He was conservatively managed and recovered from the event in three weeks without any neurological deficit.
Figure 1: Axial T2WI demonstrating multiple foci of high signal intensity involving the basal ganglia and thalami (a), the corpus callosum splenium (b) as well as subcortical white matter and centrum semiovale (c)

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Figure 2: FLAIR coronal images showing hyperintense signal of centrum semiovale (a) and corpus callosum splenium (b, c)

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Figure 3: DW images with b value of 1000 mm/s2, shows lesions as high signal intensity (a-c). The corresponding ADC images (d-f), demonstrate low signal intensity more marked in corpus callosum splenium (white arrow in e)

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Fat embolism syndrome includes a triad: Hypoxemia, neurologic abnormalities, and petechial skin rashes. [2] Neurological features include confusion and drowsiness or seizure, acute confusional state is the most common. All neurological deficits are transient and fully reversible.

The incidence of fat embolism syndrome after bone fractures is about 0.9-2.2%. [3] Fat embolism syndrome has been found to be rarely associated with non-traumatic conditions such as diabetes, pancreatitis, sickle cell disease, liposuction, and decompression sickness. [4] The fat droplets of small size may pass through the lung and reach the systemic circulation causing embolisation to the brain, skin and kidney. [5] The generalized and transient neurotoxic event occurring at the time of fat embolism, is due to the toxic effect of local free fatty acids release. The mechanisms of brain lesions are occlusion of cerebral blood vessels by fat emboli, breach in blood-brain barrier by chemical effects of free fatty acids or by change in solubility of fat in blood after injury. Butteriss et al., [6] also stated that primary blood-brain barrier breakdown as a result of arteriolar occlusion causes combination of both infarction and diffuse cerebral toxicity in the pathophysiology of brain injury.

MRI confirms the diagnosis by better depiction of lesions. Though MRI findings are definite in a given clinical setting they alone are not specific and can be observed in diffuse axonal injury (DAI), and demyelination. [7] In a case of DAI the abnormal neurological features appear immediate after to injury and associated with loss of consciousness, whereas in fat embolism syndrome cerebral features appear generally after orthopedic intervention. In demyelination there will be no history of trauma and no restriction is seen on diffusion weighted images. FLAIR and conventional T2W sequences show multiple diffuse foci of hyperintensity in white matter, subcortical, periventricular, and centrum semiovale regions. In the majority of cases restricted diffusion foci giving characteristic "star field pattern" are seen in the centrum semiovale. However, patchy and confluent-restricted diffusion as seen in our patients may also be seen rarely. [8] In some cases infarcts involving gray and white matter may be seen. [9] Our patient was atypical showing more confluent white matter lesions, and involvement of the corpus callosum. Susceptibility-weighted imaging (SWI) may reveal several punctate foci of low signal intensity in the bilateral cerebral and cerebellar white matter, predominantly in the corticomedullary junction and splenium of the corpus callosum. These punctate foci of low signal intensity are petechial hemorrhages that cannot be detected by other MR sequences. [10]

 » References Top

1.Ereth MH, Weber JG, Abel MD, Lennon RL, Lewallen DG, Ilstrup DM, et al. Cemented versus noncemented total hip arthroplasty-embolism, hemodynamics, and intrapulmonary shunting. Mayo Clin Proc 1992; 67:1066-74.  Back to cited text no. 1
2.Johnson MJ, Lucas GL. Fat embolism syndrome. Orthopedics 1996; 19:41-9.  Back to cited text no. 2
3.Müller C, Rahn BA, Pfister U, Meinig RP. The incidence, pathogenesis, diagnosis, and treatment of fat embolism. Orthop Rev 1994;23:107-17.  Back to cited text no. 3
4.Ten Duis HJ. The fat embolism syndrome. Injury 1997;28:77-85.  Back to cited text no. 4
5.Saigal R, Mittal M, Kansal A, Singh Y, Kolar PR, Jain S. Fat Embolism Syndrome. J Assoc Physicians India 2008;56:245-9.  Back to cited text no. 5
6.Butteriss DJ, Mahad D, Soh C, Walls T, Weir D, Birchall D. Reversible cytotoxic cerebral edema in cerebral fat embolism. AJNR Am J Neuroradiol 2006; 27:620-3.  Back to cited text no. 6
7.Ryu CW, Lee DH, Kim TK, Kim SJ, Kim HS, Lee JH, et al. Cerebral fat embolism: Diffusion-weighted magnetic resonance imaging findings. Acta Radiol 2005;46:528-33.  Back to cited text no. 7
8.Chen JJ, Ha JC, Mirvis SE. MR imaging of the brain in fat embolism syndrome. Emerg Radiol 2008;15:187-92.  Back to cited text no. 8
9.Simon AD, Ulmer JL, Strottmann JM. Contrast-enhanced MR imaging of cerebral fat embolism: Case report and review of the literature. AJNR Am J Neuroradiol 2003;24:97-101.  Back to cited text no. 9
10.Zaitsu Y, Terae S, Kudo K, Tha KK, Hayakawa M, Fujima N, et al. Susceptibility-Weighted Imaging of Cerebral Fat Embolism. J Comput Assist Tomogr 2010;34:107-12.  Back to cited text no. 10


  [Figure 1], [Figure 2], [Figure 3]

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