Introduction The purpose of the study was to evaluate the differences in individual histopathologic placental lesions in pregnancies complicated by early‐onset (<32 weeks at diagnosis) and late‐onset (≥32 weeks at diagnosis) fetal growth restriction (FGR). Material and methods A cohort study of 440 singleton pregnancies complicated by FGR, diagnosed according to standard ultrasonographic criteria, followed up and delivered at the same institution between 2010 and 2016. Placental lesions were classified according to the Amsterdam Placental Workshop Consensus Criteria. Pathologic examination of placentas from 113 healthy singleton term pregnancies served as controls. Binary and multinomial logistic regression models were used to evaluate the independent association of placental lesions with the type of FGR. Results In our cohort the prevalences of early and late FGR were 37.3% (164/440) and 62.7% (276/440), respectively. The overall rates of preeclampsia (69/164 vs 59/276, P < 0.01) and absent/reversed umbilical artery pulsatility indices (61/164 vs 14/276, P < 0.001) were higher among early FGR than late FGR. Placental characteristics from early and late FGR pregnancies differed mainly in regard to maternal vascular malperfusion scores rather than fetal scores, with preeclampsia found to be a cofactor modulating the rates and severity of associated lesions. In the binary logistic analysis, recent infarcts (OR 2.44, 95% CI 1.2‐5), distal villous hypoplasia (OR 1.8, 95% CI 1.0‐3.2), atherosis (OR 2.71, 95% CI 1.35‐5.47), persistent endovascular trophoblasts (OR 1.67, 95% CI 1.03‐2.7), and a reduced fetal/placental weight score (OR 0.27, 95% CI 0.2‐0.38) were independently associated with an increased likelihood of early FGR compared with late FGR. The sensitivity, specificity, and area under the curve of the model were 60% (95% CI 51.2‐66.2), 89.1% (95% CI 84.9‐92.3), and 0.81 (95% CI 0.77‐0.85), respectively, suggesting a fair to good predictive value. Conclusions Individual placental lesions suggestive of increased rates of ischemia, defective remodeling of spiral arteries, peripheral hypoxia interfering with villus development, and reduced placental efficiency were significantly more common in early FGR than late FGR.

Objectives To construct a nomogram of fetal stomach, and to prospectively determine the clinical value of stomach measurement in pathological cases. Methods A cross‐sectional prospective study was conducted between 14 and 40 weeks in well‐dated, low‐risk, singleton pregnancies. Stomach dimensions were acquired in longitudinal plane in which maximal stomach length was measured, and in axial plane in which were measured: antero‐posterior and latero‐lateral. Stomach maximal and axial 1st to 99th centiles were calculated for each gestational‐week. Results Five hundred fifty‐four measurements were performed. A cubic polynomial regression model best described the correlation between stomach size and gestational age. The correlation coefficient (r2) was 0.627 and 0.754 (p < 0.001) for the stomach axial and maximal diameters, respectively. Intra‐ and interobserver variability had high interclass correlation coefficients (>0.9). Nomograms were created for predicted stomach axial and maximal 1st, 3rd, 10th, 25th, 50th,75th, 90th, 95th, 97th, and 99th centiles. The nomogram correctly detected 92.3% (12/13) of pathological cases including three bowel obstruction, eight esophageal atresia, and two hypotonic syndromes. Conclusions The present study provides updated nomograms of the fetal stomach. Clinical application of these nomograms may assist in preventing unnecessary investigation in falsely perceived small or large stomachs and may improve the in utero detection of true pathologies.