Division of Maternal-Fetal Medicine, Columbia University Irving Medical Center, New York, NY; Department of Obstetrics and Gynecology, Columbia University Irving Medical Center, New York, NY.
Division of Maternal-Fetal Medicine, Columbia University Irving Medical Center, New York, NY; Department of Obstetrics and Gynecology, Columbia University Irving Medical Center, New York, NY.
Am J Obstet Gynecol MFM. 2020 May;2(2):100082. doi: 10.1016/j.ajogmf.2019.100082. Epub 2020 Jan 7.
Preterm birth is the leading cause of neonatal morbidity and mortality. Individuals who survive preterm birth are at a higher risk for many long-term adverse effects, including neurodevelopmental deficits. There are many well-established risk factors for worse neurologic outcomes spanning the prenatal and postnatal periods; however, investigators have yet to assess whether the cause of preterm birth has an impact on neurodevelopment.
Our objective was to assess whether neurologic outcomes differ by children born via indicated versus spontaneous preterm birth.
We performed secondary analysis of a multicenter trial assessing magnesium for neuroprotection in women at risk for preterm delivery from 24 to 31 weeks. We included women with live, nonanomalous, singleton gestations who delivered preterm; we excluded women whose children were missing 2-year follow-up information for reasons other than perinatal demise. The primary exposure was type of preterm birth: (1) spontaneous if the child's mother presented with preterm labor or ruptured membranes, or (2) indicated if the child was delivered preterm iatrogenically. The primary outcome was death (including stillbirths, neonatal intensive care unit deaths, and deaths after discharge) or an abnormal Bayley II score by 2 years of age, defined as a Mental Developmental Index score or Psychomotor Developmental Index score 2 standard deviations below the mean. Secondary outcomes included death or Mental Developmental Index and Psychomotor Developmental Index scores 1 standard deviation or less, and neonatal morbidities associated with prematurity. Bivariate analyses of baseline characteristics by exposure were conducted. A logistic regression model was fitted to adjust for confounders.
Of 1678 subjects, 1631 (97.2%) underwent spontaneous preterm birth and 47 (2.8%) underwent indicated preterm birth. Baseline maternal demographics and gestational age at delivery were similar between groups (29.6 weeks ± 7.8 versus 28.8 weeks ± 2.5, P = .07). A Psychomotor Developmental Index score 2 standard deviations or less below the mean or death occurred in 340 (20.9%) spontaneous preterm birth subjects and 17 (36.2%) indicated preterm birth subjects (P = .01). When adjusting for confounders, there remained an increased probability of a Psychomotor Developmental Index scores 2 standard deviations or less or death in indicated preterm birth subjects (P = .02). Although not statistically significant, indicated preterm birth was also associated with higher odds of Mental Developmental Index scores 2 standard deviations or less or death, Psychomotor Developmental scores 1 standard deviation or less or death, and Mental Developmental Index scores 1 standard deviation or less or death (1.76, 1.59, and 1.45, respectively). Limiting the analysis to small for gestational age infants, there was no difference in neurologic outcomes. The same was true for when we excluded small for gestational age infants from our analysis. However, after adjusting for small for gestational age, the odds of a Psychomotor Developmental Index score 2 standard deviations or less or death remained significant higher in the indicated preterm birth group (adjusted odds ratio, 1.98; 95% confidence interval, 1.01-3.88).
In this cohort of pregnant women who delivered preterm, indicated deliveries were associated with worse psychomotor development than were spontaneous deliveries. Other outcomes appeared to be poor, but our numbers were limited. This finding should be confirmed in a larger cohort of women undergoing medically indicated preterm deliveries.
早产是新生儿发病率和死亡率的主要原因。存活下来的早产儿面临许多长期不良影响的风险更高，包括神经发育缺陷。有许多已确立的风险因素可导致产前和产后神经发育不良；然而，研究人员尚未评估早产的原因是否会对神经发育产生影响。
我们的目的是评估因有医学指征的早产与自发性早产的新生儿神经发育结果是否不同。
我们对一项多中心试验进行了二次分析，该试验评估了镁对有早产风险的孕妇（妊娠 24 周至 31 周）的神经保护作用。我们纳入了有活产、非畸形、单胎妊娠且早产分娩的孕妇；排除了因围产期死亡以外的其他原因导致 2 年随访信息缺失的儿童。主要暴露因素为早产类型：（1）自发性，如果孩子的母亲出现早产宫缩或胎膜破裂；（2）有医学指征的，如果孩子因医疗原因早产。主要结局是死亡（包括死胎、新生儿重症监护病房死亡和出院后死亡）或 2 岁时出现贝利二世评分异常，定义为精神发育指数或运动发育指数评分低于平均值 2 个标准差。次要结局包括死亡或精神发育指数和运动发育指数评分 1 个标准差或更低，以及与早产相关的新生儿并发症。根据暴露情况对基线特征进行了双变量分析。使用逻辑回归模型进行调整，以控制混杂因素。
在 1678 名受试者中，1631 名（97.2%）发生自发性早产，47 名（2.8%）发生有医学指征的早产。两组间的基线产妇人口统计学特征和分娩时的孕龄相似（29.6 周±7.8 与 28.8 周±2.5，P=0.07）。340 名（20.9%）自发性早产的受试者和 17 名（36.2%）有医学指征的早产受试者出现精神运动发育指数评分低于平均值 2 个标准差或死亡（P=0.01）。在调整混杂因素后，有医学指征的早产受试者的精神运动发育指数评分低于平均值 2 个标准差或死亡的可能性仍然增加（P=0.02）。虽然没有统计学意义，但有医学指征的早产也与更高的精神发育指数评分低于平均值 2 个标准差或死亡、运动发育评分低于平均值 1 个标准差或死亡、精神发育指数评分低于平均值 1 个标准差或死亡的几率相关（分别为 1.76、1.59 和 1.45）。将分析限制在小于胎龄儿，神经发育结局没有差异。当我们将小于胎龄儿从分析中排除时，情况也是如此。然而，在调整了小于胎龄儿后，有医学指征的早产组的精神运动发育指数评分低于平均值 2 个标准差或死亡的几率仍然显著更高（调整后的优势比，1.98；95%置信区间，1.01-3.88）。
在这组接受早产分娩的孕妇中，有医学指征的分娩与自发性分娩相比，与较差的精神运动发育相关。其他结果似乎较差，但我们的数量有限。这一发现应在接受有医学指征的早产分娩的更大孕妇队列中得到证实。
