Fetal and maternal vascular lesions
Section snippets
Development of the circulation
The fetal–placental circulation is established at approximately 5 weeks of development when the developing vessels of the placenta connect with the allantoic (umbilical) vessels derived from the embryo. The villous vessels develop in situ in what are then known as “tertiary” villi. The vessels from the fetus grow and elongate over the course of development. Outside of the umbilical cord, it is not possible to distinguish arteries from veins except by position on the fetal surface.1, 2
The
Maternal vascular lesions and effects
Pathologic changes associated with abnormalities in utero-placental blood flow are the most common diagnoses made in gross and microscopic pathology.5 Because of their frequency, assessment of their impact on a fetus is often difficult based on the pathology alone. Appropriate sampling of the placenta is critical to diagnosis.6 In the normal term placenta, maternal blood flow to villi varies with location. The best arterial perfusion occurs in the central placental areas of both linear extent
Fetal vascular lesions
Fetal vascular lesions are clearly recognized to be important findings in infants who later are found to have cerebral palsy or other neurologic defects.13 In most cases, this type of outcome appears to be a combination of antepartum factors, coupled with some perinatal insult. These antenatal processes may particularly lower the threshold for injury. A recent study found that more than half of placentas from medicolegal consultations have severe fetal vascular lesions, a more than five-fold
Interactions of fetal and maternal vascular lesions
Fetal and maternal vascular processes are often seen as separate entities in their effects on a pregnancy, usually in mild and/or early disease. As there is progression, however, the close relationship of the two circulations engenders interactions of one on the other. Lesions in both circuits are commonly seen together in diseased placentas.
The most common etiology for poor fetal growth is maternal vascular underperfusion in the context of preeclampsia. The fetus becomes hypovolemic and the
Conclusion
Maternal uteroplacental perfusion abnormalities are important causes of perinatal morbidity, as they are common precursors to growth restriction, oligohydramnios, preterm delivery, and intrauterine death. Consequently, these same abnormalities are also the most common findings in examined placentas and generally need fetal and clinical correlation for meaningful evaluation. In contrast, fetal vascular lesions are considerably less common, but their recognition is particularly important as they
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Cited by (29)
Placental pathology
2017, Reproductive and Developmental ToxicologyType 1, type 2 and gestational diabetes mellitus differentially impact placental pathologic characteristics of uteroplacental malperfusion
2015, PlacentaCitation Excerpt :We found that women with T2DM or GDM shared placental pathologic features related to uteroplacental malperfusion. Uteroplacental malperfusion is thought to be due to decreased or abnormal uterine artery blood flow and has been associated with intrauterine fetal growth restriction and fetal death [5]. Pathologic features consistent with uteroplacental malperfusion include placental infarcts, accelerated villous maturation, and an increase in maternal vascular lesions such as decidual vasculopathy [7,20,21].
Placental hypoxia: The lesions of maternal malperfusion
2015, Seminars in PerinatologyCitation Excerpt :Infarctions due to occlusion of maternal spiral arteries are common at term,35,36 particularly in the placental periphery, and are generally of little clinical significance. Such infarctions in a preterm placenta or occupying more than 5% of the placental volume are both abnormal and clinically significant.35,36 The second type of placental infarction includes those central lesions not centered on the placental basal plate (and not due to occlusion of a specific spiral artery).
Placental infarction identified by macroscopic examination and risk of cerebral palsy in infants at 35 weeks of gestational age and over
2011, American Journal of Obstetrics and GynecologyPlacental fetal thrombotic vasculopathy in severe congenital anomalies prompting EXIT procedure
2011, PlacentaCitation Excerpt :Therefore, an umbilical cord compromise or/and fetal heart failure might have been operative in that series, unlike in our cases with polyhydramnios and a likely mechanical interference with blood return from the placenta by intrathoracic mass. The most serious risk associated with placental FTV is thromboembolic disease of the fetus, cerebral palsy, and perinatal liver disease [25–27,39–41], Placental FTV was found in 23 placentas of 125 neurologically impaired term infants who were the focus of clinical negligence litigation [42], which could explain the complicated short-term and long-term postnatal outcome related to fetal thromboembolic complications. The possibility of neonatal coagulopathy should be considered in management of the neonates after EXIT procedures as routine laboratory evaluation of the patient’s coagulation status may not be predictive either of severe placental FTV in EXIT [43] or ECMO nonsurvivors with thrombohemorrhagic complications [44].