Bibliographic Details
| Title: |
Current Knowledge of Fetal Growth Restriction in Relation to Thrombosis at the Maternal‐Fetal Interface–Placenta and Umbilical Cord: A Literature Review |
| Authors: |
Yaxi Zhang, Yong Shao |
| Source: |
Reproductive, Female and Child Health, Vol 4, Iss 1, Pp n/a-n/a (2025) |
| Publisher Information: |
Wiley, 2025. |
| Publication Year: |
2025 |
| Collection: |
LCC:Reproduction
LCC:Women. Feminism |
| Subject Terms: |
fetal growth restriction, placenta, thrombosis, umbilical cord, Reproduction, QH471-489, Women. Feminism, HQ1101-2030.7 |
| More Details: |
ABSTRACT Background Fetal growth restriction (FGR), defined as estimated fetal weight or abdominal circumference below the 10th percentile for gestational age, is a common complication of pregnancy. Placental malperfusion is the most common cause of FGR. Thrombosis at the maternal‐fetal interface (placenta and umbilical cord) is closely related to FGR. Failure of spiral artery remodeling in early pregnancy can lead to obstruction of uteroplacental blood flow, contributing to the development of FGR. Umbilical cord thrombosis is rare, with umbilical artery thrombosis being associated with more severe adverse pregnancy outcomes. Virchow's triad of thrombosis–blood stasis, hypercoagulability, and endothelial damage ‐ are risk factors for thrombosis at the maternal‐fetal interface. Methods PubMed database was searched mainly using the terms ‘fetal growth restriction’ and “thrombosis”. Relevant articles retrieved were arranged to write this article. Results Umbilical cord abnormalities including intrinsic anatomical abnormalities, potential obstructive anatomical abnormalities, and transient anatomical abnormalities can cause placental thrombosis and fetal vascular malperfusion. Local hypercoagulability at the maternal‐fetal interface may be caused by physiological or pathological hypercoagulation in pregnant women, and abnormality in the placenta itself leading to a tendency for thrombosis is also getting recognized. Besides, vascular endothelial defects and immune reactions can cause damage to placental vascular endothelium, triggering local coagulation reactions. Conclusion Thrombosis at the maternal‐fetal interface is a complex process. Further understanding of this process can deepen our knowledge of the pathophysiological mechanisms underlying FGR and provide guiding opinions to medical practice in treating and preventing FGR. Clinical Trial Registration This study does not contain clinical trials. |
| Document Type: |
article |
| File Description: |
electronic resource |
| Language: |
English |
| ISSN: |
2768-7228 |
| Relation: |
https://doaj.org/toc/2768-7228 |
| DOI: |
10.1002/rfc2.70013 |
| Access URL: |
https://doaj.org/article/ef7394fdf452415cacb013498678fc8f |
| Accession Number: |
edsdoj.f7394fdf452415cacb013498678fc8f |
| Database: |
Directory of Open Access Journals |
