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Objective: The purpose of this study was to compare the screening efficiency of the umbilical artery systolic to diastolic ratio (S/D), pulsatility index (PI), and absent end-diastolic flow (AEDF) for adverse pregnancy outcomes and placental abnormalities in small for gestational age (SGA) fetuses., Methods: We conducted a retrospective cohort study of Doppler examinations of 161 nonanomalous SGA fetuses. The reliability of the S/D and PI were quantified by intraclass correlation coefficients. The association of the S/D, PI, and AEDF with adverse outcomes and placental abnormalities was compared by the chi(2) test., Results: There was a simple association of Doppler results with adverse outcomes, which was mitigated when controlled for gestational age. For all measures of adverse outcomes, the specificity of abnormal Doppler results exceeded the sensitivity, and the negative predictive value was greater than the positive predictive value. Comparing the S/D with the PI, there was no significant difference in the sensitivity; however, the specificity of the PI was at least 90% and exceeded that of the S/D for all outcomes. The intraclass correlation coefficients of the S/D and PI were similar, indicating no difference in reliability. Placental abnormalities were significantly more common in cases with abnormal Doppler values (positive predictive value, 94%) with no overlap in the types of placental lesions in most cases., Conclusions: As an initial screen for adverse outcomes in SGA fetuses, the umbilical artery Doppler S/D, PI, and AEDF were imprecise. However, these measures were all strongly and similarly predictive of placental abnormalities, especially lesions of maternal underperfusion and fetal vascular obstruction.

Frequently, placentas sent for pathologic examination include a clinical diagnosis that does not suggest a specific placental lesion. Pathologists who do not have great experience in this field may need some assistance with selecting the pertinent placental lesions to look for. This brief outline is included to define these conditions and present a list of the specific placental lesions that deserve consideration. The placental examination should be directed with the goal of identifying or noting and recording specifically the presence or absence of the relevant pathologic lesions. The syndromes or conditions considered in this context include neonatal encephalopathy, preterm birth, fetal growth restriction, maternal diabetes mellitus, thrombophilias, HELLP syndrome, and fetal hydrops.

The purpose of this study was to assemble and test the reliability of a complete set of the placental reaction patterns seen with chronic fetal vascular obstruction in the hope that this might provide a standardized diagnostic framework useful for practicing pathologists. Study cases (14 with fetal vascular obstructive lesions, 6 controls) were reviewed blindly by seven pathologists after agreement on a standard set of diagnostic criteria. Majority vote served as the gold standard and 80% of the 180 diagnoses rendered (9 diagnoses each for 20 cases) were agreed upon by at least six of the seven scores. The sensitivity of individual diagnosis relative to the group consensus averaged 83% (range, 69-100%) and specificity averaged 91% (range, 86-100%). Reproducibility was measured by unweighted kappa-values and interpreted as follows: < 0.2, poor; 0.2-0.6, fair/moderate; > 0.6, substantial. Kappa values for lesions of distal villi were generally superior to those for lesions involving large fetal vessels: avascular villi (0.49), villous stromal-vascular karyorrhexis (0.58), and villitis of unknown etiology (VUE) with stem villitis and avascular villi (0.65) versus large vessel thrombi (any vessel, 0.34; chorionic plate vessel, 0.40) and intimal fibrin cushions (recent, 0.47; remote, 0.78). Reproducibility for a global impression of any villous change consistent with chronic fetal vascular obstruction was substantial (0.63), while that for a more severe subgroup was moderate (0.44). Three points are worthy of emphasis. Our system separately recognizes, but later combines, uniformly avascular villi and villous stromal-vascular karyorrhexis as manifestations of the same underlying process. We propose that this combined group of villous lesions be dichotomized with the terms fetal thrombotic vasculopathy or extensive avascular villi (and/or villous stromal-vascular karyorrhexis) being reserved for the group with 15 or more affected terminal villi per section. Scattered foci of avascular villi (and/or villous stromal-vascular karyorrhexis) could be used to describe less severe cases. Finally, we distinguish VUE with stem villitis and avascular villi (obliterative fetal vasculopathy) as a distinct process with substantial perinatal morbidity.

Thrombi in the fetal circulation of the placenta cause a pattern of clustered fibrotic villi called fetal thrombotic vasculopathy (FTV), which has been associated with serious injuries to neonates, especially brain injuries. Correlation of FTV with visceral thrombi in autopsy specimens might lead to a more accurate estimate of the prevalence of somatic thrombi as a significant and underrecognized cause of prenatal injury or perinatal death, and show the potential validity of placental FTV as an indicator of thrombotic lesions in the fetus and newborns who survive. Clinicopathologic correlation was used to perform a 3-year retrospective autopsy review. We identified 16 cases (19%) among 84 perinatal autopsy specimens in which placental FTV was associated with stillbirth, intrapartum, or neonatal death. Two liveborn neonates survived 2.5 hours, and one for 24 hours; there was one intrapartum death, and the rest were stillborn. Clinical evidence of severe central nervous system (CNS) injury to two of the liveborn infants was evident at birth. Twelve stillborns died from 12 to 48 hours before delivery. Placental FTV had features of organization that clearly antedated the fetal death. Autopsy findings confirmed somatic thrombi in six cases (37.5%) of the 16 with FTV, including cerebral thrombi or infarcts (three cases), renal thromboemboli (three cases), and pulmonary thromboemboli (two cases). One mother had history of deep vein thrombosis, and four of eight tested had abnormal coagulation test results. Placental FTV indicates a significant probability of thrombi in the fetus and represents an important, possibly underrecognized cause of perinatal mortality and neonatal injury. Parental coagulopathy as a significant factor in prenatal injury and death deserves more comprehensive study. The placenta remains an undervalued and underutilized surgical specimen in the evaluation of perinatal injury, especially cerebral palsy.

Fetal vessels in the placentas of 11 of 15 infants with cerebral palsy contained thrombi. An alternate basis for the injury was identified in the four placentas without thrombi. Autopsy findings in one infant who died at age 1 month confirmed the presence of cerebral thrombi and infarcts. It is concluded that thrombotic events in utero may explain the pathogenesis of many instances of cerebral palsy and that identification of a coagulopathy in parents could potentially identify those at risk and provide a basis for preventive treatment during pregnancy.

The complex double circulation of the placenta adds diversity to the kinds of changes caused by thrombi and bleeding. Different lesions may have different clinical implications for the mother and fetus. The clinical history may be extremely important in directing the pathologic examination and in evaluating the significance of vascular lesions.

Objective: Our aim was to find out whether patients delivered preterm because of preterm labor or preterm premature rupture of membranes can be categorized according to clinical characteristics and placental pathologic findings., Study Design: We performed a case-control study of 105 patients who were delivered preterm, 42 because of preterm labor and 63 because of premature rupture of membranes, and 105 patients who were delivered at term after uncomplicated pregnancies., Results: Maternal placental vascular lesions were present in 14 (34.1%) patients with preterm labor, 19 (35.1%) patients with premature rupture of membranes, and 9 (11.8%) control patients (odds ratios 3.8 and 4.0, 95% confidence intervals 1.3 to 11.1 and 1.5 to 10.8, p = 0.0065 and 0.0022, respectively). Infection of the products of conception was found in 16 patients (38%) with preterm labor, 23 patients (36.5%) with premature rupture of membranes, and 19 control patients (18%) (odds ratios 2.7 and 2.6, 95% confidence intervals 1.1 to 6.6 and 1.2 to 5.6, p = 0.017 and 0.01, respectively). Patients with maternal placental vasculopathy had significantly different characteristics compared with those of infected patients., Conclusions: It is possible to identify two subgroups of patients among those who are delivered preterm because of preterm labor or premature rupture of membranes, one with infection of the products of conception and another with maternal placental vasculopathy.

Vascular lesions, most often mediated by thrombi, are second only to infections as a cause of fetal injury in the later weeks of pregnancy. In our experience many pathologists who examine placentas fail to conduct a proper search for vascular lesions and some even fail to recognize those exposed by their examination. This review is intended to define the typical clinical background or circumstances that suggest the presence of significant vascular problems, to define techniques calculated to display them well, and to identify criteria for diagnosis. Further research is needed to evaluate the prevalence of maternal and fetal hypercoagulable states and thrombi as a cause of fetal injury.

Very large chorioangiomas are a rare but well recognized cause of neonatal morbidity, while small ones are clinically insignificant. This study emphasizes that some chorioangiomas of intermediate size may be causally related to intrauterine growth retardation, and that they may be surprisingly difficult to detect in the unfixed placenta.