Histopathological analysis of the placental lesions in pregnancies complicated with IUGR and stillbirths in comparison with noncomplicated pregnancies

Günyeli, İlker; Erdemoğlu, Evrim; Ceylaner, Serdar; Zergeroğlu, Sema; Mungan, Tamer

doi:10.5152/jtgga.2011.19

Cited by 19 publications

(9 citation statements)

References 22 publications

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“…The most relevant change was the ischemia, also with an increase in the fibrin and calcification deposition, reflecting the effect of uteroplacental vessel ligation on the placenta. This finding is also in accordance with previous clinical [60, 61] and experimental data [45, 46, 62] where placental histology assessment evidenced higher levels of fibrin deposition, placenta infarction, and calcifications in IUGR.…”

Section: Discussionsupporting

confidence: 93%

Structural Brain Changes during the Neonatal Period in a Rabbit Model of Intrauterine Growth Restriction

et al. 2020

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Background: Intrauterine growth restriction (IUGR) is associated with abnormal neurodevelopment, but the associated structural brain changes are poorly documented. The aim of this study was to describe in an animal model the brain changes at the cellular level in the gray and white matter induced by IUGR during the neonatal period. Methods: The IUGR model was surgically induced in pregnant rabbits by ligating 40–50% of the uteroplacental vessels in 1 horn, whereas the uteroplacental vessels of the contralateral horn were not ligated. After 5 days, IUGR animals from the ligated horn and controls from the nonligated were delivered. On the day of delivery, perinatal data and placentas were collected. On postnatal day 1, functional changes were first evaluated, and thereafter, neuronal arborization in the frontal cortex and density of pre-oligodendrocytes, astrocytes, and microglia in the corpus callosum were evaluated. Results: Higher stillbirth in IUGR fetuses together with a reduced birth weight as compared to controls was evidenced. IUGR animals showed poorer functional results, an altered neuronal arborization pattern, and a decrease in the pre-oligodendrocytes, with no differences in microglia and astrocyte densities. Conclusions: Overall, in the rabbit model used, IUGR is related to functional and brain changes evidenced already at birth, including changes in the neuronal arborization and abnormal oligodendrocyte maturation.

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Section: Discussionsupporting

confidence: 93%

Structural Brain Changes during the Neonatal Period in a Rabbit Model of Intrauterine Growth Restriction

et al. 2020

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“…Although placental infarction can be found in both normal and abnormal pregnancies, this lesion presents clinico-morphological significance when it affects at least an average of 10-20% of the placental volume. The relationship between fetal hypoxia, subsequent IUGR and the presence of multiple placental infarction lesion has already been reported in literature [28]. In the present study, different degrees of placental infarction were detected in 28 (87.5%) cases of the study group, results similar with those previously published [29].…”

Section:  Discussionsupporting

confidence: 92%

Morphological and histopathological changes in placentas of pregnancies with intrauterine growth restriction

Vişan

Bălan

Costea

et al. 2020

Rom J Morphol Embryol

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“…Placental dysfunction, and abnormalities also have a well-known association with poor pregnancy outcome [ 28 - 30 ]. It has also been suggested that the fetus at risk may stop movement to conserve energy in the presence of placental dysfunction [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

A triple risk model for unexplained late stillbirth

Warland

Mitchell

2014

BMC Pregnancy Childbirth

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BackgroundThe triple risk model for sudden infant death syndrome (SIDS) has been useful in understanding its pathogenesis. Risk factors for late stillbirth are well established, especially relating to maternal and fetal wellbeing.DiscussionWe propose a similar triple risk model for unexplained late stillbirth. The model proposed by us results from the interplay of three groups of factors: (1) maternal factors (such as maternal age, obesity, smoking), (2) fetal and placental factors (such as intrauterine growth retardation, placental insufficiency), and (3) a stressor (such as venocaval compression from maternal supine sleep position, sleep disordered breathing). We argue that the risk factors within each group in themselves may be insufficient to cause the death, but when they interrelate may produce a lethal combination.SummaryUnexplained late stillbirth occurs when a fetus who is somehow vulnerable dies as a result of encountering a stressor and/or maternal condition in a combination which is lethal for them.

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Histopathological analysis of the placental lesions in pregnancies complicated with IUGR and stillbirths in comparison with noncomplicated pregnancies

Cited by 19 publications

References 22 publications

Structural Brain Changes during the Neonatal Period in a Rabbit Model of Intrauterine Growth Restriction

Structural Brain Changes during the Neonatal Period in a Rabbit Model of Intrauterine Growth Restriction

Morphological and histopathological changes in placentas of pregnancies with intrauterine growth restriction

A triple risk model for unexplained late stillbirth

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