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单绒毛膜性双胎一胎胎死:如何预测存活的共同胎儿的脑损伤?

Single fetal demise in monochorionic twins: How to predict cerebral injury in the survivor co-twin?

机构信息

Universidad Autónoma de Madrid, Madrid, Spain.

Department of Obstetrics and Gynecology, La Paz University Hospital, Madrid, Spain.

出版信息

Acta Obstet Gynecol Scand. 2023 Aug;102(8):1125-1134. doi: 10.1111/aogs.14604. Epub 2023 Jun 3.

DOI:10.1111/aogs.14604
PMID:37270671
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10378013/
Abstract

INTRODUCTION

The aims of the study were to evaluate perinatal outcome in monochorionic (MC) twins complicated with single intrauterine fetal death, spontaneously vs after fetal therapy, and to assess antenatal events that increase the risk of cerebral injury.

MATERIAL AND METHODS

Historical cohort study of MC pregnancies with single intrauterine fetal death diagnosed or referred to a tertiary referral hospital (2012-2020). Adverse perinatal outcome included termination of pregnancy, perinatal death, abnormal fetal or neonatal neuroimaging and abnormal neurological development.

RESULTS

A total of 68 MC pregnancies with single intrauterine fetal death after 14 weeks of gestation were included. Sixty-five (95.6%) occurred in complicated MC pregnancies (twin to twin transfusion syndrome: 35/68 [51.5%]; discordant malformation: 13/68 [19.1%], selective intrauterine growth restriction: 10/68 [14.7%], twin reversed arterial perfusion sequence: 5/68 [7.3%] and cord entanglement in monoamniotic twins: 2/68 [2.94%]). In 52 cases (76.5%) single intrauterine fetal demise occurred after fetal therapy and in 16 (23.5%) occurred spontaneously. Cerebral damage included 14/68 cases (20.6%): 6/68 cases (8.82%) were prenatal lesions and 8/68 cases (11.8%) were postnatal. Risk of cerebral damage tended to be higher in the spontaneous death group (6/16, 37.5%) compared to the therapy-group (8/52, 15.38%) (p = 0.07). The risk increased with gestational age at intrauterine death (OR 1.21, 95% CI: 1.04-1.41, p = 0.014) and was higher in those surviving co-twins who developed anemia (OR 9.27, 95% CI: 1.50-57.12, p = 0.016). Pregnancies complicated with selective intrauterine growth restriction tended to be at higher risk for neurological damage (OR 2.85, 95% CI: 0.68-11.85, p = 0.15). Preterm birth rate (<37 weeks of pregnancy) was 61.7% (37/60). Seven of eight postnatal cerebral lesions (87.5%) were related to extreme prematurity. Overall perinatal survival rate was 88.3% (57/68) and 7% (4/57) of children had an abnormal neurological outcome.

CONCLUSIONS

Risk of cerebral damage in single intrauterine fetal death is especially high when it occurs spontaneously. Gestational age at single intrauterine fetal death, selective intrauterine growth restriction and anemia of the surviving co-twin are the main predictors for prenatal lesions and might be useful in parent counseling. Abnormal postnatal neurological outcome is closely related to extreme prematurity.

摘要

介绍

本研究旨在评估因胎儿治疗或自发性因素而导致的单绒毛膜(MC)双胎一胎宫内死亡的围产儿结局,并评估增加脑损伤风险的产前事件。

材料和方法

对在三级转诊医院诊断或转诊的 14 周后发生单胎宫内胎儿死亡的 MC 妊娠进行回顾性队列研究(2012-2020 年)。不良围产儿结局包括终止妊娠、围产儿死亡、胎儿或新生儿神经影像学异常和神经发育异常。

结果

共纳入 68 例 14 周后发生单胎宫内胎儿死亡的 MC 妊娠。65 例(95.6%)发生在复杂的 MC 妊娠中(双胎输血综合征:35/68 [51.5%];不一致的畸形:13/68 [19.1%],选择性宫内生长受限:10/68 [14.7%],双胎反向动脉灌注序列:5/68 [7.3%],单羊膜囊双胎的脐带缠绕:2/68 [2.94%])。在 52 例(76.5%)中,单胎宫内胎儿死亡发生在胎儿治疗后,在 16 例(23.5%)中发生自发性死亡。脑损伤包括 14/68 例(20.6%):6/68 例(8.82%)为产前病变,8/68 例(11.8%)为产后病变。与治疗组(8/52,15.38%)相比,自发性死亡组(6/16,37.5%)脑损伤的风险更高(p=0.07)。风险随宫内死亡时的胎龄而增加(OR 1.21,95%CI:1.04-1.41,p=0.014),存活的同胎中出现贫血的风险更高(OR 9.27,95%CI:1.50-57.12,p=0.016)。选择性宫内生长受限的妊娠更倾向于发生神经损伤(OR 2.85,95%CI:0.68-11.85,p=0.15)。早产率(<37 周妊娠)为 61.7%(37/60)。8 例产后脑损伤中有 7 例(87.5%)与极早产有关。总的围产儿存活率为 88.3%(57/68),7%(4/57)的儿童有神经发育异常。

结论

当单胎宫内胎儿死亡为自发性时,脑损伤的风险特别高。单胎宫内胎儿死亡时的胎龄、选择性宫内生长受限和存活的同胎贫血是产前病变的主要预测因素,可能有助于对父母进行咨询。异常的产后神经发育结局与极早产密切相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6d5/10378013/33b7c12eed28/AOGS-102-1125-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6d5/10378013/853adfcad8e6/AOGS-102-1125-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6d5/10378013/cc9a3ef87d5f/AOGS-102-1125-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6d5/10378013/33b7c12eed28/AOGS-102-1125-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6d5/10378013/853adfcad8e6/AOGS-102-1125-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6d5/10378013/cc9a3ef87d5f/AOGS-102-1125-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6d5/10378013/33b7c12eed28/AOGS-102-1125-g004.jpg

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