The Recurrence Prevention Committee, The Japan Obstetric Compensation System for Cerebral Palsy, Japan Council for Quality Health Care, Tokyo, Japan.
Department of Obstetrics and Gynecology, Mie University Graduate School of Medicine, Tsu, Mie, Japan.
Acta Obstet Gynecol Scand. 2023 Dec;102(12):1730-1740. doi: 10.1111/aogs.14675. Epub 2023 Sep 11.
With category II fetal heart rate tracings, the preferred timing of interventions to prevent fetal hypoxic brain damage while limiting operative interventions remains unclear. We aimed to estimate fetal extracellular base deficit (BD ) during labor with category II tracings to quantify the timing of potential interventions to prevent severe fetal metabolic acidemia.
A longitudinal study was conducted using the database of the Recurrence Prevention Committee, Japan Obstetric Compensation System for Cerebral Palsy, including infants with severe cerebral palsy born at ≥34 weeks' gestation between 2009 and 2014. Cases included those presumed to have an intrapartum onset of hypoxic-ischemic insult based on the fetal heart rate pattern evolution from reassuring to an abnormal pattern during delivery, in association with category II tracings marked by recurrent decelerations and an umbilical arterial BD ≥ 12 mEq/L. BD changes during labor were estimated based on stages of labor and the frequency/severity of fetal heart rate decelerations using the algorithm of Ross and Gala. The times from the onset of recurrent decelerations to BD 8 and 12 mEq/L (Decels-to-BD8, Decels-to-BD12) and to delivery were determined. Cases were divided into two groups (rapid and slow progression) based upon the rate of progression of acidosis from onset of decelerations to BD 12 mEq/L, determined by a finite-mixture model.
The median Decels-to-BD8 (28 vs. 144 min, p < 0.01) and Decels-to-BD12 (46 vs. 177 min, p < 0.01) times were significantly shorter in the rapid vs slow progression. In rapid progression cases, physicians' decisions to deliver the fetus occurred at ~BD 8 mEq/L, whereas the "decisions" did not occur until BD reached 12 mEq/L in slow progression cases.
Fetal BD reached 12 mEq/L within 1 h of recurrent fetal heart rate decelerations in the rapid progression group and within 3 h in the slow progression group. These findings suggest that cases with category II tracings marked by recurrent decelerations (i.e., slow progression) may benefit from operative intervention if persisting for longer than 2 h. In contrast, cases with sudden bradycardia (i.e., rapid progression) represent a challenge to prevent severe acidosis and hypoxic brain injury due to the limited time opportunity for emergent delivery.
对于 II 类胎心监护图，在限制手术干预的同时，预防胎儿缺氧性脑损伤的最佳干预时机仍不清楚。我们旨在通过测量有 II 类胎心监护图的产程中胎儿细胞外碱缺失（BD），来量化潜在干预措施以预防严重胎儿代谢性酸中毒的时机。
本研究为回顾性队列研究，使用日本脑性瘫痪产科补偿系统复发预防委员会的数据库，纳入了 2009 年至 2014 年期间胎龄≥34 周出生的严重脑瘫婴儿。这些病例被认为是由于胎儿心率模式从分娩时的正常模式转变为异常模式，与反复减速和脐动脉 BD≥12 mEq/L 相关，提示有产时缺氧-缺血性损伤。使用 Ross 和 Gala 的算法，根据产程阶段和胎儿心率减速的频率/严重程度来估计产程中的 BD 变化。从反复减速开始到 BD8 和 12 mEq/L（Decels-to-BD8、Decels-to-BD12）和分娩的时间被确定。根据从减速开始到 BD12 mEq/L时酸中毒进展的速度，将病例分为两组（快速进展组和缓慢进展组），通过有限混合模型确定。
快速进展组的 Decels-to-BD8（28 分钟比 144 分钟，p<0.01）和 Decels-to-BD12（46 分钟比 177 分钟，p<0.01）时间明显短于缓慢进展组。在快速进展组中，医生决定分娩胎儿的时间约为 BD8 mEq/L，而在缓慢进展组中，直到 BD 达到 12 mEq/L 才做出“决定”。
在快速进展组中，反复胎儿心率减速后 1 小时内，BD 达到 12 mEq/L，在缓慢进展组中 3 小时内达到 12 mEq/L。这些发现表明，有反复减速（即缓慢进展）的 II 类胎心监护图标记的病例，如果持续时间超过 2 小时，可能需要手术干预。相比之下，突然出现心动过缓（即快速进展）的病例，由于紧急分娩的时间机会有限，因此面临预防严重酸中毒和缺氧性脑损伤的挑战。
