Ruess Lynne, Dent Carly M, Tiarks Hailey J, Yoshida Michelle A, Rusin Jerome A
Department of Radiology, Nationwide Children's Hospital, 700 Children's Drive, Columbus, OH, 43205, USA,
Pediatr Radiol. 2014 Nov;44(11):1393-402. doi: 10.1007/s00247-014-3006-0. Epub 2014 Oct 11.
Deep white matter hemorrhagic venous infarction with subsequent cavitation due to necrosis and liquefaction has been described in neonates and may be associated with infection and meningitis. In our experience, the MRI pattern of these lesions is confused with the pattern seen with cerebral abscesses.
The purpose of our study was to characterize the MRI findings of post infarction necrosis and liquefaction after hemorrhagic deep white matter venous infarction in infants and to distinguish these lesions from cerebral abscesses.
An institutional review board approved a retrospective review of imaging records to identify all patients with cerebral venous infarction at a children's hospital during a 10-year period. Nine infants had deep white matter hemorrhagic venous infarction with white matter fluid signal cavitary lesions. A diagnosis of cerebral abscess was considered in all. The imaging and laboratory findings in these patients are reviewed and compared to descriptions of abscesses found in the literature.
There were six female and three male infants. The mean age at presentation was 20 days (range: 0-90 days), while the corrected age at presentation was less than 30 days for all patients. Seven patients presented with seizures and signs of infection; one infant presented with lethargy and later proved to have protein C deficiency. MRI was performed 0-12 days from presentation in these eight patients. Another patient with known protein C deficiency underwent MRI at 30 days for follow-up of screening US abnormalities. There were a total of 38 deep cerebral white matter fluid signal cavitary lesions: 25 frontal, 9 parietal, 2 temporal, 2 occipital. Larger lesions had dependent debris. All lesions had associated hemorrhage and many lesions had evidence of adjacent small vessel venous thrombosis. Lesions imaged after gadolinium showed peripheral enhancement. Three lesions increased in size on follow-up imaging. Three patients, two with meningitis confirmed via microbiology and one with presumed meningitis by CSF counts, underwent surgical aspiration of a total of six lesions. All specimens were sent for pathology and culture and were negative for microorganisms.
Recognizing the MR appearance of cavitary necrosis and liquefaction after deep white matter cerebral venous infarction in neonates can distinguish this entity from cerebral abscess and potentially avoid an unnecessary neurosurgical aspiration procedure.
新生儿中曾有深部白质出血性静脉梗死伴随后续因坏死和液化形成空洞的描述,且可能与感染及脑膜炎相关。根据我们的经验,这些病变的MRI表现与脑脓肿的表现相混淆。
我们研究的目的是描述婴儿深部白质出血性静脉梗死后梗死灶坏死和液化的MRI表现,并将这些病变与脑脓肿相鉴别。
机构审查委员会批准了一项对影像记录的回顾性研究,以识别一家儿童医院10年间所有患有脑静脉梗死的患者。9名婴儿患有深部白质出血性静脉梗死伴白质液性信号空洞性病变。所有病例均考虑脑脓肿的诊断。对这些患者的影像和实验室检查结果进行回顾,并与文献中报道的脓肿描述进行比较。
有6名女婴和3名男婴。就诊时的平均年龄为20天(范围:0 - 90天),所有患者的校正年龄均小于30天。7名患者出现惊厥和感染体征;1名婴儿表现为嗜睡,后来证实患有蛋白C缺乏症。这8名患者在就诊后0 - 12天进行了MRI检查。另一名已知蛋白C缺乏症的患者在30天时进行了MRI检查,以随访筛查超声发现的异常情况。共有38个深部脑白质液性信号空洞性病变:25个位于额叶,9个位于顶叶,2个位于颞叶,2个位于枕叶。较大的病变有下沉的碎屑。所有病变均伴有出血,许多病变有相邻小静脉血栓形成的证据。钆增强后成像显示病变周边强化。3个病变在随访成像时增大。3名患者,2名经微生物学确诊为脑膜炎,1名经脑脊液计数推测为脑膜炎,共对6个病变进行了手术抽吸。所有标本均送去做病理和培养,微生物检查均为阴性。
认识新生儿深部脑白质静脉梗死后空洞性坏死和液化的MR表现,可将此病变与脑脓肿相鉴别,并可能避免不必要的神经外科抽吸手术。