Ultrasound diagnosis of severe thrombotic placental damage in the second trimester: an observational study

Objectives To screen women with uteroplacental insufficiency between 18 and 26 weeks' gestation for sonographic evidence of destructive placental lesions, to observe the effect of low molecular‐weight heparin (LMWH) in these cases, and to compare the outcome with similar but untreated controls. Methods We screened 180 women at high risk for placental damage using 16‐week maternal serum screening (alpha‐fetoprotein and human chorionic gonadotropin), placental shape and texture, and uterine artery Doppler waveforms at the 18–20‐week level II examination. Serial gray‐scale examinations of placental texture were performed at 22, 24 and 26 weeks. LMWH was offered to women with ultrasound evidence of destructive placental lesions in the absence of intrauterine growth restriction and/or pre‐eclampsia. Results We prospectively identified six women (3.3%) with abnormal maternal serum screening and uterine artery Doppler in whom abnormal placental texture (echogenic cystic lesions) suggestive of destructive lesions in the placental parenchyma was found either at the 18–20‐week ultrasound examination (n = 4), or by 26 weeks of gestation (n = 2). All six received LMWH and had live births (gestational age at delivery, 33–37 weeks; birth weight, 1000–3200 g). A further 14 women were referred with similar multiparameter evidence of placental damage at or after 26 weeks, outside the screening study. All had significant fetal growth restriction and were therefore not offered heparin. In 9/14 cases there was a perinatal death. Ischemic and/or thrombotic placental pathology was confirmed in each case, but no maternal thrombophilia disorders were identified in the 20 women. Conclusions Integrated biochemical and ultrasound testing of placental function at 16–20 weeks of gestation, followed by serial placental gray‐scale ultrasound, may be an effective method of identifying a subset of pregnancies at high risk of adverse pregnancy outcome due to destructive lesions in the placental parenchyma. This strategy of identifying thrombo‐occlusive placental lesions before the development of pregnancy complications may prove useful in the design of trials to study the effectiveness of LMWH in the prevention of clinical complications resulting from thrombo‐occlusive placental disease. Copyright © 2004 ISUOG. Published by John Wiley & Sons, Ltd.