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低血糖症与缺氧缺血性脑病。

Hypoglycaemia and hypoxic-ischaemic encephalopathy.

作者信息

Boardman James P, Hawdon Jane M

机构信息

MRC Centre for Reproductive Health, University of Edinburgh, Edinburgh, UK.

出版信息

Dev Med Child Neurol. 2015 Apr;57 Suppl 3:29-33. doi: 10.1111/dmcn.12729.

DOI:10.1111/dmcn.12729
PMID:25800489
Abstract

The transition from fetal to neonatal life requires metabolic adaptation to ensure that energy supply to vital organs and systems is maintained after separation from the placental circulation. Under normal conditions, this is achieved through the mobilization and use of alternative cerebral fuels (fatty acids, ketone bodies, and lactate) when blood glucose concentration falls. Severe hypoxia-ischaemia is associated with impaired metabolic adaptation, and animal and human data suggest that levels of hypoglycaemia that are tolerated under normal conditions can be harmful in association with hypoxia-ischaemia. The optimal target blood glucose level for ensuring adequate energy provision in hypoxic-ischaemic encephalopathy (HIE) remains unknown. However, recent data support guidance to maintain a blood glucose concentration of 2.5 mmol/L or more in neonates with signs of acute neurological dysfunction, which includes those with HIE, and this is higher than the accepted threshold of 2 mmol/L in infants without signs of neurological dysfunction or hyperinsulinism.

摘要

从胎儿期到新生儿期的转变需要代谢适应,以确保在与胎盘循环分离后,重要器官和系统的能量供应得以维持。在正常情况下,当血糖浓度下降时,可通过动员和使用替代脑燃料(脂肪酸、酮体和乳酸)来实现这一点。严重缺氧缺血与代谢适应受损有关,动物和人类数据表明,正常情况下可耐受的低血糖水平在与缺氧缺血相关时可能有害。在缺氧缺血性脑病(HIE)中,确保充足能量供应的最佳目标血糖水平仍不清楚。然而,最近的数据支持在有急性神经功能障碍迹象的新生儿(包括患有HIE的新生儿)中维持血糖浓度在2.5 mmol/L或更高的指导建议,这高于无神经功能障碍或高胰岛素血症迹象的婴儿所接受的2 mmol/L阈值。

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Abnormalities in evoked potentials associated with abnormal glycemia and brain injury in neonatal hypoxic-ischemic encephalopathy.与新生儿缺氧缺血性脑病时异常血糖和脑损伤相关的诱发电位异常。
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