Major C A, Lewis D F, Harding J A, Porto M A, Garite T J
Department of Obstetrics and Gynecology, University of California, Irvine 92668.
Am J Obstet Gynecol. 1994 Jan;170(1 Pt 1):102-6. doi: 10.1016/s0002-9378(94)70392-2.
The null hypothesis states that prolonged antenatal indomethacin exposure within 24 hours of delivery does not increase the incidence of necrotizing enterocolitis in the low-birth-weight neonate.
The neonates of patients receiving indomethacin tocolysis admitted in preterm labor (N = 56) were compared with the neonates of preterm labor patients who received no indomethacin tocolysis (N = 703). These neonatal groups were then compared with regard to gestational age at delivery, birth weight, mode of delivery, antenatal magnesium and steroid exposure, incidence of respiratory distress syndrome, perinatal depression, sepsis, umbilical catheterization, and feeding rates and volumes. The overall incidence of necrotizing enterocolitis, mortality secondary to necrotizing enterocolitis, and the intervals from delivery and feeding to necrotizing enterocolitis diagnosis were also compared. The association between necrotizing enterocolitis and the duration of indomethacin exposure and the interval from exposure to delivery for both the indomethacin and control groups was determined.
The incidence of necrotizing enterocolitis in neonates who were delivered within 24 hours of maternal indomethacin therapy was 20% compared with 9% in the control group (p = 0.005). The incidence of necrotizing enterocolitis in neonates with > 48 hours of antenatal indomethacin exposure was 26.4% compared with 4.1% in those with < 48 hours exposure (p = 0.042). The interval from first feeding to necrotizing enterocolitis development was significantly shorter in the indomethacin group versus the control group (2.1 +/- 3.0 vs 6.8 +/- 6.3 days) (p = 0.001), as was the mean interval from delivery to development of necrotizing enterocolitis (10.2 +/- 3.7 vs 15.2 +/- 3.8 days) (p = 0.019).
Antenatal indomethacin exposure occurring within < or = 24 hours of delivery and of at least 48 hours' duration is associated with a significant increase in the incidence of necrotizing enterocolitis in the low-birth-weight neonate.
无效假设表明，在分娩24小时内长时间产前使用吲哚美辛不会增加低体重新生儿坏死性小肠结肠炎的发病率。
将接受吲哚美辛保胎治疗的早产患者的新生儿（N = 56）与未接受吲哚美辛保胎治疗的早产患者的新生儿（N = 703）进行比较。然后比较这些新生儿组的分娩时孕周、出生体重、分娩方式、产前镁和类固醇暴露情况、呼吸窘迫综合征的发病率、围产期抑郁、败血症、脐导管插入术以及喂养率和喂养量。还比较了坏死性小肠结肠炎的总体发病率、坏死性小肠结肠炎继发的死亡率以及从分娩和喂养到坏死性小肠结肠炎诊断的间隔时间。确定了吲哚美辛组和对照组中坏死性小肠结肠炎与吲哚美辛暴露持续时间以及从暴露到分娩的间隔时间之间的关联。
母亲接受吲哚美辛治疗后24小时内分娩的新生儿中，坏死性小肠结肠炎的发病率为20%，而对照组为9%（p = 0.005）。产前吲哚美辛暴露超过48小时的新生儿中，坏死性小肠结肠炎的发病率为26.4%，而暴露时间少于48小时的新生儿中这一发病率为4.1%（p = 0.042）。与对照组相比，吲哚美辛组从首次喂养到发生坏死性小肠结肠炎的间隔时间明显更短（2.1±3.0天对6.8±6.3天）（p = 0.001），从分娩到发生坏死性小肠结肠炎的平均间隔时间也是如此（1组为10.2±3.7天，对照组为15.2±3.8天）（p = 0.019）。
在分娩≤24小时内且持续至少48小时的产前吲哚美辛暴露与低体重新生儿坏死性小肠结肠炎的发病率显著增加有关。
