Histologic Examination of the Placenta in the Growth-Retarded Fetus

Abstract

This investigation was undertaken to determine whether histologic examination of the placenta contributed to a better understanding of the cause of intrauterine fetal growth retardation. Placentas were examined of 151 liveborn infants whose birthweights were in the lower 10th percentile for gestational age. One or more histologic aberrations were found in 139 (92%) cases, in contrast to one or more antenatal risk factors (primarily hypertension) in 77 (51%) cases or a gross placental abnormality (primarily abruption) in 46 (30%) cases. Compared with placentas belonging to appropriately sized fetuses, histologic signs of uteroplacental vascular insufficiency, chronic inflammation, and hemorrhagic endovasculitis were significantly more common in the study group. The primary histologic condition was supportive of prior clinical impressions in 61 (40%) cases, contradictory in 23 (15%) cases, or solely contributory to explaining the growth retardation in 55 (36%) cases. Placental histologic examination may clarify a cause for delayed fetal growth, especially after a normotensive pregnancy.

Placental Pathology in Early-Onset and Late-Onset Fetal Growth Restriction

“…Similarly, several microscopic abnormalities have been reported more frequently in FGR placentas, none of which are present in the majority of affected cases in any study, and almost all of which may be encountered in other non-FGR pregnancies, including [2,3,4,5,6,7,9,10,11,12,13,14,15,16,17,18,19,20,21,22,23,24,25]: villous infarcts (an example from a placenta in a case of FGR is shown in figure 1a, b), placental abruption/retroplacental haemorrhage, villous morphological abnormalities suggestive of reduced uteroplacental and/or fetoplacental flow (‘hypoxic' lesion) such as syncytiotrophoblast ‘knots', excess cytotrophoblast cells, thickened trophoblastic basement membrane, villous fibrosis, hypovascular terminal villi, reduced villous volume, reduced intervillous space, and non-specific inflammatory lesions [villitis of unknown aetiology (VUE)]. In addition, histological features indicating defective remodelling of spiral arteries into uteroplacental vessels may be identified, such as inadequate ‘physiological change', fibrinoid necrosis and acute atherosis (a dense perivascular lymphocytic infiltrate with intimal arterial foamy macrophages; see fig.…”

“…First, it should be noted that, overall, approximately one quarter of placentas associated with FGR/SGA (however defined) lack any morphological abnormality on routine macroscopic and histological examination [1]. In those cases with lesions present, the most frequent macroscopic abnormality that occurs with increased frequency in FGR placentas is patchy placental infarction, being present in around 25% of term FGR versus 10% of controls [2,3,4,5,6,7,8,9,10,11,12,13,14]. This finding illustrates a common theme when interpreting placental findings in FGR, that the frequency of several ‘lesions' is increased, but since such lesions are only present in a minority of affected cases and are also found in some normal controls, and since non-FGR is far more frequent than FGR in the population, the positive predictive value of such findings for pathological FGR in any given unselected case will be very low.…”

Placental pathology and neurodevelopment of the infant with intrauterine growth restriction

“…Evidence for impaired uteroplacental blood flow was specifically examined, namely placental infarction and accelerated villous maturation, as previously recommended (Naeye 1987, Naeye 1989, Burke et al 1995. Similar to other studies, these placental pathologies were found to be associated with growth restriction (Boyd 1985, Rayburn 1989, Salafia 1992. It is not suggested, however, that the placental infarcts caused the growth restriction, but rather they were a marker for more widespread changes in the uteroplacental circulation which result in IUGR.…”

“…The present study investigated infants born with growth restriction, with birthweight >2SDs below the mean for gestational age, which contrasted with many other studies that included infants with less severe growth retardation (Rayburn 1989, Salafia 1992. Evidence for impaired uteroplacental blood flow was specifically examined, namely placental infarction and accelerated villous maturation, as previously recommended (Naeye 1987, Naeye 1989, Burke et al 1995.…”

Histopathological study of placentae in intrauterine growth retardation pregnancies in a tertiary care hospital and correlation with fetal birth weight

“…So, the patterns of lesions are more important in elucidating the casual pathways by which placental histopathology is translated into IUGR 5 and histology examination of placenta may clarify a cause for delayed fetal growth. 6 The severity of placental abnormalities expressed as cumulative number of placental lesions is a significant risk factor for IUGR. 7 Redline et al 8 demonstrated that five chronic patterns of placental injury are significantly increased in placentas from pregnancies complicated by IUGR.…”