Adamson S J, Alessandri L M, Badawi N, Burton P R, Pemberton P J, Stanley F
Department of Neonatology, Princess Margaret Hospital for Children, Subiacco, Western Australia.
BMJ. 1995 Sep 2;311(7005):598-602. doi: 10.1136/bmj.311.7005.598.
Preliminary investigation of the contribution of adverse antepartum and intrapartum factors to neonatal encephalopathy in singleton neonates born full term.
Matched case-control study based on incidence density sampling of controls.
Two major teaching hospitals (one paediatric and one obstetric) and three peripheral maternity hospitals in Perth, Western Australia (population 1.2 million).
89 cases, all the full term singleton neonates born during an eight month period in 1992 who fulfilled one or more of six criteria during the first week of life (seizures, abnormal conscious state, persistent hypertonia or hypotonia, and feeding or respiratory difficulties of central origin). One full term control infant without neonatal encephalopathy was matched to each case by sex, hospital of delivery, time of day and day of the week of birth, and maternal health insurance status.
Odds ratio estimates of relative risk of neonatal encephalopathy associated with antepartum and intrapartum factors.
Estimated incidence of moderate or severe encephalopathy in first week of life was 3.75 per 1000 full term live births. Thirteen cases and no controls had evidence suggestive of important intrapartum hypoxia, and in only five of these cases was the neurological condition at birth attributed to events during the intrapartum period. Univariate conditional logistic regression analysis identified significant differences between cases and controls for maternal vaginal bleeding in pregnancy, maternal thyroxine treatment, congenital abnormalities, induction of labour, interval from membrane rupture to delivery, maternal pyrexia in labour, augmentation of labour, abnormal intrapartum cardiotocograms, and meconium in labour. Family history of convulsions also approached significance.
Our preliminary results suggest that intrapartum hypoxia, according to currently used criteria, was not the cause of neonatal encephalopathy in most cases in this population. Our findings suggest that many aetiologies of neonatal encephalopathy originate in the antepartum period.
初步调查足月单胎新生儿产前和产时不良因素对新生儿脑病的影响。
基于对照的发病率密度抽样的匹配病例对照研究。
西澳大利亚州珀斯的两家主要教学医院(一家儿科医院和一家产科医院)以及三家外围妇产医院(人口120万)。
89例病例,均为1992年8个月期间出生的足月单胎新生儿,这些新生儿在出生后第一周内符合六项标准中的一项或多项(惊厥、意识状态异常、持续性肌张力亢进或低下以及中枢性喂养或呼吸困难)。每例病例匹配一名无新生儿脑病的足月对照婴儿,匹配因素包括性别、分娩医院、出生时间和日期以及母亲的医疗保险状况。
与产前和产时因素相关的新生儿脑病相对风险的比值比估计值。
出生后第一周中度或重度脑病的估计发病率为每1000例足月活产儿中有3.75例。13例病例有提示重要产时缺氧的证据,而对照中无此情况,且其中仅5例病例出生时的神经状况归因于产时事件。单因素条件逻辑回归分析确定,病例与对照在以下方面存在显著差异:孕期母亲阴道出血、母亲甲状腺素治疗、先天性异常、引产、胎膜破裂至分娩的间隔时间、产时母亲发热、产程加速、产时异常胎心监护以及产时胎粪污染。惊厥家族史也接近显著水平。
我们的初步结果表明,根据目前使用的标准,产时缺氧并非该人群中大多数新生儿脑病的病因。我们的研究结果表明,新生儿脑病的许多病因起源于产前阶段。