Burns Charlotte M, Rutherford Mary A, Boardman James P, Cowan Frances M
Department of Paediatrics, Hammersmith Hospital, Imperial College Healthcare NHS Trust, London, England.
Pediatrics. 2008 Jul;122(1):65-74. doi: 10.1542/peds.2007-2822.
Symptomatic neonatal hypoglycemia may be associated with later neurodevelopmental impairment. Brain injury patterns identified on early MRI scans and their relationships to the nature of the hypoglycemic insult and neurodevelopmental outcomes are poorly defined.
We studied 35 term infants with early brain MRI scans after symptomatic neonatal hypoglycemia (median glucose level: 1 mmol/L) without evidence of hypoxic-ischemic encephalopathy. Perinatal data were compared with equivalent data from 229 term, neurologically normal infants (control subjects), to identify risk factors for hypoglycemia. Neurodevelopmental outcomes were assessed at a minimum of 18 months.
White matter abnormalities occurred in 94% of infants with hypoglycemia, being severe in 43%, with a predominantly posterior pattern in 29% of cases. Cortical abnormalities occurred in 51% of infants; 30% had white matter hemorrhage, 40% basal ganglia/thalamic lesions, and 11% an abnormal posterior limb of the internal capsule. Three infants had middle cerebral artery territory infarctions. Twenty-three infants (65%) demonstrated impairments at 18 months, which were related to the severity of white matter injury and involvement of the posterior limb of the internal capsule. Fourteen infants demonstrated growth restriction, 1 had macrosomia, and 2 had mothers with diabetes mellitus. Pregnancy-induced hypertension, a family history of seizures, emergency cesarean section, and the need for resuscitation were more common among case subjects than control subjects.
Patterns of injury associated with symptomatic neonatal hypoglycemia were more varied than described previously. White matter injury was not confined to the posterior regions; hemorrhage, middle cerebral artery infarction, and basal ganglia/thalamic abnormalities were seen, and cortical involvement was common. Early MRI findings were more instructive than the severity or duration of hypoglycemia for predicting neurodevelopmental outcomes.
有症状的新生儿低血糖可能与后期神经发育障碍有关。早期MRI扫描所识别的脑损伤模式及其与低血糖损伤性质和神经发育结局的关系尚不明确。
我们研究了35名足月婴儿,这些婴儿在出现有症状的新生儿低血糖(中位血糖水平:1 mmol/L)后进行了早期脑部MRI扫描,且无缺氧缺血性脑病的证据。将围产期数据与229名足月、神经功能正常的婴儿(对照对象)的等效数据进行比较,以确定低血糖的危险因素。至少在18个月时评估神经发育结局。
94%的低血糖婴儿出现白质异常,其中43%为重度异常,29%的病例主要表现为后部模式。51%的婴儿出现皮质异常;30%有白质出血,40%有基底节/丘脑病变,11%有内囊后肢异常。3名婴儿出现大脑中动脉供血区梗死。23名婴儿(65%)在18个月时表现出损伤,这与白质损伤的严重程度和内囊后肢受累有关。14名婴儿表现为生长受限,1名婴儿巨大儿,2名婴儿的母亲患有糖尿病。与对照对象相比,病例组中妊娠高血压、癫痫家族史、急诊剖宫产和复苏需求更为常见。
与有症状的新生儿低血糖相关的损伤模式比先前描述的更多样化。白质损伤并不局限于后部区域;可见出血、大脑中动脉梗死和基底节/丘脑异常,且皮质受累很常见。早期MRI检查结果在预测神经发育结局方面比低血糖的严重程度或持续时间更具指导意义。