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Sonographic study of the decidua basalis in early pregnancy loss
Author(s) -
Wong H. S.,
Cheung Y. K.
Publication year - 2010
Publication title -
ultrasound in obstetrics and gynecology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.202
H-Index - 141
eISSN - 1469-0705
pISSN - 0960-7692
DOI - 10.1002/uog.7736
Subject(s) - decidua , medicine , pregnancy , gestation , echogenicity , obstetrics , placenta , andrology , gynecology , fetus , biology , ultrasound , radiology , genetics
Objectives To describe the sonographic findings in the decidua basalis layer in spontaneous early pregnancy loss and to compare them with those in normal pregnancy. Methods We reviewed 119 scans at 4–10 weeks' gestation from 110 patients who miscarried clinically at less than 13 weeks' gestation and 132 scans also at 4–10 weeks from 98 patients who had normal uncomplicated term pregnancies. The thickness and echogenicity of the decidua basalis layer were compared between pregnancies which suffered early loss and normal controls. Results Relative thinning of the decidua basalis was observed in cases of early pregnancy loss from 5–6 weeks onwards when compared with normal pregnancies. In embryonic pregnancies that subsequently miscarried, the decidua basalis did not show the rising trend in thickness that was observed in normal pregnancies. Shortly before and after embryonic demise, the decidua appeared relatively more echogenic compared with that in normal pregnancy and the placenta showed areas of hypoechogenicity. Embryonic demise was followed by disorganization of the decidual layer, which became difficult to recognize. Pregnancy with an empty sac showed a more gradual trend in the thinning of the decidua basalis, but the uniformity and echogenicity of the layer appeared to be relatively better preserved with time. Conclusion The decidua basalis layer in pregnancies that are destined to miscarry in the first trimester differs sonographically from that in normal pregnancies. The sonographic differences are suggestive of a defective decidual–placental complex resulting from deficient trophoblastic invasion. Copyright © 2010 ISUOG. Published by John Wiley & Sons, Ltd.