4.2 Article

Placenta in intrauterine fetal demise (IUFD): a comprehensive study from a tertiary care hospital

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JOURNAL OF MATERNAL-FETAL & NEONATAL MEDICINE
卷 32, 期 23, 页码 3939-3947

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TAYLOR & FRANCIS LTD
DOI: 10.1080/14767058.2018.1479390

关键词

Delayed villous maturation; fetal inflammatory response; fetal vascular malperfusion; maternal inflammatory response; maternal vascular malperfusion parenchymal loss; villitis

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Background: Intrauterine fetal demise (IUFD) is an unpredictable and challenging obstetric complication. Its etiology is multifactorial with more than 60% attributed to the placental cause. The present study was done with a primary objective of understanding the placental lesions underlying IUFD. Methods: In this retrospective observational study, IUFD cases (>22 weeks) between January 2012 and September 2015 were collected from pathology database. The clinical details with ultrasound findings were collected from mother's charts. The lesions were classified into (A) maternal vascular malperfusion (MVM) including retroplacental hematomas, (B) fetal vascular malperfusion (FVM), (C) inflammatory lesions, and (D) idiopathic. The contributor to fetal death was classified as direct, major, minor, unlikely, or unknown. Placental findings of fetal hypoxia were recorded. Results: The study included 100 cases of IUFD. The mean maternal age was 26 years (18-36 years). Primipara were 46. There were 65 early preterm (PT) (<34 weeks), 20 late PT (34 weeks to <37 weeks) and 15 term (>37 weeks) IUFD. The mean gestation age was 30 weeks. The ratio of male:female fetuses was 1:1.7. Relevant obstetric complications included preeclampsia (n = 39), intrauterine growth restriction (IUGR) (n = 7), pre-gestational diabetes (n = 7), bad obstetric history (n = 6), oligohydramnios (n = 5). The mean placental weight was 256 g. Maternal vascular malperfusion had the highest incidence (30%), followed by combined maternal and FVM (10%). Exclusive inflammatory lesions and FVM were seen in 12 and 6%, respectively. No cause was identified in 18%. Direct contributor to IUFD was identified in 51 cases and major, minor, unlikely contribution in 21, 11 and nine cases, respectively. In nine cases, it was unknown. Lesions indicating fetal hypoxia were noted in 35 cases. In both early and late PT, MVM featured more commonly (23 and 5%). In term placentas, the most common cause was idiopathic. Conclusions: Lesions of MVM were the most common cause of IUFD and served as a direct contributor to fetal demise.

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