Suppr超能文献

胎儿窒息与儿童神经病理学及缺陷的关系。

Relationship of fetal asphyxia to neuropathology and deficits in children.

作者信息

Low J A

机构信息

Department of Obstetrics and Gynecology, Queen's University, Kingston, Ontario.

出版信息

Clin Invest Med. 1993 Apr;16(2):133-40.

PMID:8513613
Abstract

Neuropathological studies suggest that the majority of the fetal asphyxial complications resulting in brain damage in either preterm or term fetus occur before the onset of labor. Anoxia because of the rapid sequence of events will usually result in death of the fetus. Hypoxia of 1-3 h duration may account for brain damage and deficits in children who survive. The threshold for brain damage is a severe acidosis with a pH < 7.0 in conjunction with systemic hypotension. The prevalence of antepartum fetal asphyxia and the frequency of deficits in such children have not been established. The prevalence of intrapartum fetal asphyxia determined biochemically is 2%. The majority of these children develop normally because of fetal cardiovascular compensatory mechanisms which protect the brain. However, beyond the threshold of asphyxia in either the preterm or term fetus, neuropathology may develop leading to deficits in some children.

摘要

神经病理学研究表明,导致早产或足月胎儿脑损伤的大多数胎儿窒息并发症发生在分娩开始之前。由于一系列快速事件导致的缺氧通常会导致胎儿死亡。持续1 - 3小时的缺氧可能是存活儿童脑损伤和缺陷的原因。脑损伤的阈值是pH < 7.0的严重酸中毒并伴有全身性低血压。产前胎儿窒息的患病率以及此类儿童缺陷的发生率尚未确定。通过生化方法确定的产时胎儿窒息患病率为2%。这些儿童中的大多数由于保护大脑的胎儿心血管代偿机制而正常发育。然而,无论是早产还是足月胎儿,一旦超过窒息阈值,可能会发展为神经病理学改变,导致一些儿童出现缺陷。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验