Imaging in a Case of Cerebral Fat Embolism Syndrome

IF 0.3 Q4 SURGERY
Harsh Jain, J. Nair, K. Ganesh
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引用次数: 0

Abstract

A 62-year-old male presented to our emergency room intubated, with posttraumatic seizures and compound left femur fracture after suffering a road traffic accident. Glasgow Coma Scale (GCS) prior to seizure onset was 15. The computed tomography (CT) scan and magnetic resonance imaging (MRI) of the brain on admission were normal and the patient was taken up for emergency wound exploration and fixation of femur fracture. Postoperatively, sensorium did not improve on weaning sedation and GCS was E2VtM4. Initial noncontrast head CT showed no evidence of any infarcts or bleeds. Repeat MRI showed multiple punctate areas of diffusion restriction and corresponding punctate T2 hyperintensities in the subcortical white matter cerebellum and brainstem suggestive of cerebral fat embolism syndrome. These areas showed a diffusion restriction on diffusion-weighted imaging (DWI) sequences (►Fig. 1). Gradient recalled echo /susceptibility-weighted imaging (SWI) did not show microareas of blooming in the same distribution. Diffuse axonal injury was ruled out in our patient owing to normal MRI brain at admission. Early DWI in a typical case of Cerebral Fat embolism Syndrome (CFS) shows “starfield” appearance as multiple foci of high signal scatter predominantly in the border zones and deep gray nuclei bilaterally, similar to that seen in our case. In the subacute phase, DWI shows confluent bilateral symmetric periventricular and subcortical white matter cytotoxic edema and diffusion restriction. Microhemorrhages are seen as blooming foci in the white matte in T2 sequences but are better appreciated on SWI, theyare pathogenic of CFs. Up to one-third of all fat embolism casesmay showblooming on SWI, it was not seen in our case. MR spectroscopy shows the presence of lipid peaks within the lesions, a finding related to the nature of the emboli or associated necrosis.1–4 Fig. 1 (A) Magnetic resonance imaging brain axial image, T2weighted, showing multiple areas of hyperintensities in the cerebellum and the brainstem, corresponding to the diffusion restriction in the diffusion-weighted imaging (DWI). (B) Magnetic resonance imaging brain axial image, T2-weighted, showing multiple areas of hyperintensities in the subcortical white matter, corresponding to the diffusion restriction in the DWI. (C) Magnetic resonance imaging brain axial image, diffusion-weighted sequence, showing multiple punctuate areas of diffusion restriction in the cerebellum and brainstem. (D) Magnetic resonance imaging brain axial image, diffusion-weighted sequence, showing multiple punctuate areas of diffusion restriction in the subcortical white matter, in a “starfield” pattern. The diffusion restriction is seen predominantly in the border zones and deep gray nuclei bilaterally.
脑脂肪栓塞综合征1例影像学分析
一名62岁男性在道路交通事故后出现创伤后癫痫发作和左股骨复合骨折,经气管插管来到我们的急诊室。癫痫发作前格拉斯哥昏迷评分(GCS)为15。入院时脑部CT、MRI检查正常,急诊探查股骨骨折创面并固定。术后断奶镇静后感觉无改善,GCS为E2VtM4。最初的头部CT未见任何梗死或出血的迹象。重复MRI显示皮质下白质小脑和脑干多发点状扩散受限区及相应的点状T2高信号提示脑脂肪栓塞综合征。这些区域在扩散加权成像(DWI)序列上显示出扩散限制(►图2)。1)梯度回忆回声/敏感性加权成像(SWI)未显示相同分布的开花微区。本例患者入院时脑部MRI检查正常,排除弥漫性轴索损伤。典型脑脂肪栓塞综合征(CFS)的早期DWI表现为“星状区”,多灶高信号散在边界区,双侧深灰色核,与本病例相似。亚急性期,DWI显示双侧对称脑室周围和皮层下白质汇合性细胞毒性水肿和扩散受限。微出血在T2序列中被视为白色的开花灶,但在SWI上更容易被发现,它们是CFs的病原。高达三分之一的脂肪栓塞病例可能在SWI上出现,但在我们的病例中没有看到。磁共振光谱显示病灶内存在脂质峰,这一发现与栓子或相关坏死的性质有关。1 - 4图1 (A)磁共振成像脑轴向像,t2加权,显示小脑和脑干多处高信号区,对应于弥散加权成像(diffusion weighted imaging, DWI)中的弥散限制。(B)磁共振成像脑轴向像,t2加权,显示皮层下白质多处高信号区,与DWI上的扩散限制相对应。(C)磁共振成像脑轴向图像,弥散加权序列,显示小脑和脑干中多个间断的弥散限制区域。(D)磁共振成像脑轴向图像,扩散加权序列,显示皮层下白质中扩散受限的多个间断区域,呈“星场”模式。扩散限制主要出现在边界区和双侧深灰色核。
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来源期刊
CiteScore
0.40
自引率
0.00%
发文量
52
审稿时长
12 weeks
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