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Meconium-associated vascular necrosis (MAVN) is a histological abnormality of human placental chorionic vessels that is associated with poor neonatal outcome. We tested the hypothesis that MAVN shows apoptosis in the walls of chorionic vessels. Archival placental specimens with MAVN (n = 5) were compared with specimens from uncomplicated pregnancies at term (n = 5) and from placentas with intense chorionic vasculitis associated with acute chorioamnionitis with (n = 5) or without (n = 5) a clinical history of meconium in the amniotic fluid. Sections from all placentas were processed by the TUNEL method, and 2 observers who were blinded to specimen diagnosis quantified the immunofluorescent TUNEL staining in both the amnion-facing and villous-facing walls of the larger chorionic vessels in each specimen. Compared with the other 3 groups, only the amnion-facing wall of chorionic vessels in MAVN showed a significantly greater number of apoptotic cells. This was verified by morphological criteria and caspase 3 staining. There were limited or no detectable TUNEL-stained cells in either the villous-facing walls of vessels in the MAVN specimens or in any of the vessels of the placentas from uncomplicated pregnancies. There was a negligible level of apoptosis in chorionic vessels of placentas with intense chorionic vasculitis, with or without meconium, despite the inflammatory response or presence of meconium. We conclude that apoptosis contributes to the pathophysiology of MAVN.

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.

We compared the DNA content (DI) by cell image analysis with the karyotype and morphological phenotype of paraffin-embedded tissues from 51 spontaneous abortions. The study included 21 cases with triploid, 19 cases with diploid, and 11 cases with aneuploid (monosomic, trisomic, or mosaic) karyotype. Measurements were performed by image analysis on the trophoblastic and stromal cells of chorionic villi using 5-microm-thick, Feulgen-stained sections. At least 200 cells were analyzed. Results were interpreted using DI ranges of 1.3 to 1.7 for triploid and 0.9 to 1.1 for a diploid profile. All 21 cases with a cytogenetically confirmed triploid karyotype had DI values within the triploid range, and all 19 cases with a diploid karyotype had DI values within the diploid range. All of the trisomies and monosomies also had a DNA mass within the diploid range. However, eight cases with a triploid karyotype also had a peak in the diploid range: one case with a diploid karyotype and one case with a trisomic karyotype each had an additional peak in the triploid range. We did not find a morphological correlation either with image analysis or with karyotype. We conclude that cell image analysis is a reliable method for detection of triploidy in spontaneous abortions. This relatively rapid method allows visual discrimination of the areas to be analyzed, avoids the problem of maternal cell contamination, and may unmask mosaic karyotypes that would go unrecognized by cytogenetic studies alone.

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.