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目的探讨严重高胆红素血症新生儿急性胆红素脑病(ABE)发生的危险因素。方法选择本院2010年1月至2012年12月诊治的胎龄≥35周、血清胆红素(TSB)峰值>425μmol/L且资料完整、进行了头颅核磁共振及脑干听觉诱发电位检查的患儿,根据是否符合ABE的诊断标准分为病例组和对照组,对一般资料、母孕期情况、合并症、围生期缺氧、黄疸的发生发展过程及实验室指标共22项临床因素进行单因素分析,对其中13项进行多因素Logistic回归分析。结果病例组43例,对照组30例,单因素分析显示,病例组出生后体重下降程度、TSB峰值、平均每日胆红素上升值及B/A值均高于对照组,差异有统计学意义(P<0.05);多因素分析提示,严重黄疸诊断日龄、围生期缺氧史及酸中毒与ABE的发生相关,OR(95%可信区间)分别为0.545(0.413~0.962)、36.589(1.114~1202.032)、7.963(1.294~49.010),P均<0.05。结论在严重高胆红素血症新生儿中,严重黄疸诊断日龄越小,曾有围生期缺氧史和(或)伴有酸中毒者,ABE发生风险越高;而母乳喂养、出生后体重下降多、存在母子血型不合溶血、葡萄糖-6-磷酸脱氢酶缺陷则可能是严重高胆红素血症的原因。加强黄疸的监测、对严重高胆红素血症患儿积极纠正酸中毒,可能有助于预防胆红素脑病。
Objective To explore the risk factors of acute bilirubin encephalopathy (ABE) in neonates with severe hyperbilirubinemia. Methods The data of our hospital from January 2010 to December 2012 with gestational age ≥35 weeks, peak TSB value> 425μmol / L and complete data were examined by MRI and brainstem auditory evoked potentials Children were divided into case group and control group according to the diagnostic criteria of ABE. Twenty-two clinical factors including general information, pregnancy status, complications, perinatal hypoxia, development of jaundice and laboratory parameters Univariate analysis, of which 13 were multivariate Logistic regression analysis. Results In the case group, there were 43 cases in the control group and 30 cases in the control group. Univariate analysis showed that the body weight loss, TSB peak, mean daily bilirubin and B / A values in the case group were significantly higher than those in the control group (P <0.05). Multivariate analysis suggested that the diagnosis of severe jaundice on day-old, perinatal hypoxia and acidosis were associated with the occurrence of ABE. The OR (95% confidence interval) were 0.545 (0.413-0.962) 36.589 (1.114 ~ 1202.032), 7.963 (1.294 ~ 49.010), all P <0.05. Conclusions In neonates with severe hyperbilirubinemia, the smaller the diagnosis of severe jaundice, the perinatal history of hypoxia and / or acidosis, the higher the risk of ABE. However, breastfeeding and birth After weight loss, there is maternal and child blood group incompatible hemolysis, glucose-6-phosphate dehydrogenase deficiency may be the cause of severe hyperbilirubinemia. To strengthen the monitoring of jaundice, positive correction of acidosis in children with severe hyperbilirubinemia, may help prevent bilirubin encephalopathy.