University of Sydney, Cerebral Palsy Alliance, University of Notre Dame Australia, Darlinghurst, New South Wales, the Centre for Child Health Research, University of Western Australia at the Telethon Institute for Child Health Research, Perth, and the Cerebral Palsy Alliance, University of Notre Dame Australia, Grace Centre for Newborn Care, the Children's Hospital at Westmead, the University of Sydney, and the University of Sydney, Sydney Adventist Hospital, Sydney, Australia; the Department of Neurology, Children's National Medical Centre, Washington, DC; and the National Institute of Neurological Disorder and Stroke, National Institutes of Health, Bethesda, Maryland.
Obstet Gynecol. 2013 Oct;122(4):869-877. doi: 10.1097/AOG.0b013e3182a265ab.
To examine the antecedents of cerebral palsy and of perinatal death in singletons born at or after 35 weeks of gestation.
From a total population of singletons born at or after 35 weeks of gestation, we identified 494 with cerebral palsy and 508 neonates in a matched control group, 100 neonatal deaths, and 73 intrapartum stillbirths (all deaths in selected birth years). Neonatal death and cerebral palsy were categorized as without encephalopathy, after neonatal encephalopathy, or after neonatal encephalopathy considered hypoxic-ischemic. We examined the contribution of potentially asphyxial birth events, inflammation, fetal growth restriction, and birth defects recognized by age 6 years to each of these outcomes and to intrapartum stillbirths.
The odds of total cerebral palsy after potentially asphyxial birth events or inflammation were modestly increased (odds ratio [OR] 1.9, 95% confidence interval [CI] 1.1-3.2 and OR 2.2, 95% CI 1.0-4.2, respectively). However, potentially asphyxial birth events occurred in 34% of intrapartum stillbirths and 21.6% of cerebral palsy after hypoxic-ischemic encephalopathy. Inflammatory markers occurred in 13.9% and 11.9% of these outcomes, respectively. Growth restriction contributed significantly to all poor outcome groups. Birth defects were recognized in 5.5% of neonates in the control group compared with 60% of neonatal deaths and more than half of cases of cerebral palsy without hypoxic-ischemic encephalopathy. In children with cerebral palsy, a potentially asphyxial birth event, inflammation, or both were experienced by 12.6%, whereas growth restriction, a birth defect, or both were experienced by 48.6% (P<.001).
Fetal growth restriction and birth defects recognized by age 6 years were more substantial contributors to cerebral palsy and neonatal death than potentially asphyxial birth events and inflammation.
: II.
探讨胎龄 35 周及以上单胎儿脑瘫和围产儿死亡的发病因素。
在胎龄 35 周及以上的所有单胎儿中，我们共识别出 494 例脑瘫患儿和与之匹配的 508 例对照组新生儿、100 例新生儿死亡和 73 例产时胎儿死亡（所有死亡均发生在特定年份）。我们将新生儿死亡和脑瘫分为无脑损伤、伴有新生儿脑病、伴有新生儿脑病且考虑为缺氧缺血性脑病。我们检测了可能导致窒息的分娩事件、炎症、胎儿生长受限和 6 岁前发现的出生缺陷对以上结局和产时胎儿死亡的影响。
伴有可能窒息的分娩事件或炎症的患儿发生总脑瘫的风险适度增加（比值比 [OR] 1.9，95%置信区间 [CI] 1.1-3.2 和 OR 2.2，95% CI 1.0-4.2）。然而，可能窒息的分娩事件发生于 34%的产时胎儿死亡和 21.6%的缺氧缺血性脑病后脑瘫患儿中。在这些患儿中，分别有 13.9%和 11.9%的患儿出现炎症标志物。生长受限对所有预后不良的患儿均有重要影响。在对照组中，5.5%的新生儿存在出生缺陷，而在新生儿死亡患儿中，60%存在出生缺陷，超过一半的无脑损伤性脑瘫患儿存在出生缺陷。在脑瘫患儿中，有 12.6%的患儿经历过可能窒息的分娩事件、炎症或两者皆有，而 48.6%的患儿经历过生长受限、出生缺陷或两者皆有（P<.001）。
与可能窒息的分娩事件和炎症相比，6 岁前发现的胎儿生长受限和出生缺陷是脑瘫和新生儿死亡的更重要的发病因素。
Ⅱ。
