2022
DOI: 10.1016/j.placenta.2022.07.016
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Umbilical cord compromise versus other clinical conditions predisposing to placental fetal vascular malperfusion

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Cited by 12 publications
(8 citation statements)
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“…Our current material obtained in the Children's Hospital contained few hypertensive conditions of pregnancy, diabetes mellitus, infections, chronic FHR abnormalities, genetic thrombophilia, FGR, and oligohydramnios, i.e. the conditions known to be associated with FVM [28][29][30], but less frequently in our material than in UC compression [31]. Foetal growth restriction was reported to be associated with maternal background morbidities during pregnancy [32], representing a chronic repeated insult while "new" FGR cases (those following an appropriate for gestational age pregnancy) were characterized by a higher rate of FVM lesions and lower birth rate, probably representing "an accident" in placentation [33].…”
Section: Discussionmentioning
confidence: 98%
“…Our current material obtained in the Children's Hospital contained few hypertensive conditions of pregnancy, diabetes mellitus, infections, chronic FHR abnormalities, genetic thrombophilia, FGR, and oligohydramnios, i.e. the conditions known to be associated with FVM [28][29][30], but less frequently in our material than in UC compression [31]. Foetal growth restriction was reported to be associated with maternal background morbidities during pregnancy [32], representing a chronic repeated insult while "new" FGR cases (those following an appropriate for gestational age pregnancy) were characterized by a higher rate of FVM lesions and lower birth rate, probably representing "an accident" in placentation [33].…”
Section: Discussionmentioning
confidence: 98%
“…In our wide‐spectrum (gestational ages from 24th to 40th week) study population, numerous histopathologic alterations were identified in PE placentae, but the two entities of EO‐PE and LO‐PE were different in some respects: EO‐PE cases were characterized by diffuse DVH, AVM, certain decidual arteriopathies (i.e., signs of MVM), and large foci of AV, while LO‐PE cases had significantly increased infarcted areas and chorionic plate/stem vessel thrombosis compared to EO‐PE. DVH and avascular villi—accurately differentiated from infarcted areas—could be an evidence of pathological placentation in EO‐PE, while stem vessel thrombosis in the background of LO‐PE could be considered as consequence of different forms of umbilical cord pathology, and as a placental change associated with fetal cardiac failure, anemia, or fetal hypercoaguability 22 : in our study population, the presence of these entities could be found in the background of all of the LO‐PE cases (22 cases had thrombosis in the umbilical cord vessels, five cases had fetal cardiac failure, and two cases had fetal anemia, none of these backgrounds were found in the EO‐PE group).…”
Section: Discussionmentioning
confidence: 99%
“…However, UC abnormalities have been demonstrated to play a much larger role in the development of FVM than other clinical conditions (hypertensive conditions of pregnancy, diabetes mellitus, infections). 34 Additionally, placental vascular lesions (maternal vascular malperfusion and FVM) are inherently more difficult to reproducibly diagnose and grade than inflammatory lesions (villitis of unknown etiology and acute chorioamnionitis). 18 In summary, SUA is a specific cord anomaly predisposing to remote, advanced, and recent FVM, with a pathogenesis partially different from that of stasis induced FVM, likely because of the inherent conditions associated with SUA.…”
Section: Discussionmentioning
confidence: 99%