重度高胆红素血症新生儿苍白球磁共振成像特征及其临床意义

目的探讨苍白球MRI信号改变与高胆红素血症的严重程度及其相关因素关系,为胆红素脑病诊断与预后判定提供客观依据。方法36例高胆红素血症新生儿（TSB〉342μmoL／L）在生后10±6（2～34）]d接受头部MRI检查。场强1．5～3．0Tesla,扫描序列为T1WI,T2WI和DWI。2名不知被检者病史的放射科医师分析MRI结果。结果首次MRI有20例苍白球T1WI呈对称性高信号。有苍白球信号改变组的TSB、B／A及UCB均显著高于无改变组（605．28±89．19）μmoL／L vs．（438．19±67．89）μmoL／L,（1．08±0．18）vs．（0．77±0．16）,（555．49±92．3）μmoL／L vs．（412．01±54．8）μmoL／L,P=0．000],所有MRI-DWI均未见信号改变;TSB在342．0～427．5μmoL／L者9例,未见苍白球信号改变,427．5～513．0μmoL／L者7例,有改变者3例,超过525．0μmoL／L 20例,有改变者17例,黄疸程度与苍白球信号改变有密切关系（χ^2=15．000,P=0．000）;15例ABE苍白球T1WI均呈对称性的高信号（χ^2=17．601,P=0．000）,同时3例T2WI苍白球也呈对称性稍高信号（TSB分别为,745．3μmoL／L,735．7μmoL／L,707．6μmol/L）。7日内入院的25例中,16例苍白球有改变,平均入院时间显著晚于9例无改变者（121．5±39．9）h vs．（68．9±35）h,P〈0．03]。6例接受了第2次MRI,其中3例ABE有2例苍白球信号转为T2WI高信号,临床均表现脑瘫,另1例苍白球信号正常,但有听力异常;余3例非ABE患儿,2例苍白球信号转为正常,1例两次均无苍白球信号异常,目前发育正常。结论MRI T1WI苍白球对称性高信号,与高胆红素血症的严重程度及暴露时间密切关系,是新生儿ABE的重要表现特征。T1WI高信号转变为T2WI高信号可能提示预后不良。

Changes of globus pallidus in the newborn infants with severe hyperbilirubinemia

OBJECTIVE: The involvement of globus pallidus has been found in neonates with acute bilirubin encephalopathy (ABE), but so far the relationship between the severity of hyperbilirubinemia and changes of globus pallidus has not been studied further. The present study was conducted to understand possible relationship between the MRI signal changes of globus pallidus and severe hyperbilirubinemia in the neonates to provide evidences for diagnosis of bilirubin encephalopathy and prediction of outcome. METHODS: Thirty-six neonates with severe hyperbilirubinemia (total serum bilirubin, i.e., TSB > 342 micromol/L) received MRI examination in a magnetic field with the strength of 1.5 - 3.0 Tesla at ages of 10 +/- 6 (2 - 34) days of life, of whom 15 were assessed as acute bilirubin encephalopathy (ABE). Routine T1WI with three kinds of sequences (SE, IR and FFE), T2WI and DWI with two kinds of sequences (EPI-SE and DW SSh SENSE) were applied. Two neuroradiologists who knew nothing about the clinical history analyzed MRI findings. TSB, unconjugated bilirubin (UCB), conjugated bilirubin (CB) and albumin (ALB) in all these neonates were measured with the same methods and analyzer. RESULTS: Symmetric hyperintense globus pallidus was shown on T1WI in 20 neonates, of whom three had symmetric hyperintense globus pallidus on T2WI (TSB = 745.3 micromol/L, 735.7 micromol/L, 707.6 micromol/L, respectively) at the same time. Remarkably higher TSB, molar ratio of TSB and ALB (B/A) and UCB were found in 20 neonates with hyperintense globus pallidus as compared to 16 cases without changes of globus pallidus (P = 0.000). No abnormal signal changes were found on DWI for all neonates; 9 neonates with TSB ranged from 342.0 micromol/L to 427.5 micromol/L did not show any abnormalities of globus pallidus, 3 of 7 neonates with TSB ranged from 427.5 micromol/L to 513.0 micromol/L, but 17 of 20 neonates with TSB more than 513.0 micromol/L showed distinct hyperintense globus pallidus. Hyperintense globus pallidus on T1WI was related to the severity of hyperbilirubinemia (Fisher's Exact Test, P = 0.000). Hyperintense globus pallidus on T1WI was found in all the 15 neonates with ABE (Fisher's Exact Test, P = 0.000), at the same time, hyperintense globus pallidus on T2WI was found in 3 cases with severe ABE. Six infants received the second MRI at ages from 2 months to 12 months, two of three infants with ABE in neonatal period showed the signal changes of globes pallidus from T1WI hyperintensity to T2WI hyperintensity and they developed cerebral palsy. The other one with normal signal showed hearing dysfunction. Another three infants without history of ABE did not show abnormal signals of globus pallidus and developed normally. CONCLUSIONS: The symmetric involvement of globus pallidus with hyperintense signals on MRI T1WI indicates the severity of hyperbilirubinemia, which relates to time of exposure to hyperbilirubinemia and is a characteristic finding of ABE. The signal switch of hyperintense globus pallidus from T1WI to T2WI predicts poor outcome.