Stillbirths affects
1% of all pregnancies in US, amounting to nearly 24,000 deaths every year.
Recent advances in medicine has brought down the neonatal and infant mortality
considerably in last decade, but the decline is still birth rate is very slow.
A lack of understanding
of the mechanisms behind it coupled with inability to predict stillbirth has
prevented significant improvement in stillbirths’ rate.
Although altered
fetal growth and placental abnormalities are strongest predictors of stillbirths
but all patients with placental abnormalities do not end up in stillbirths, reflecting
our lack of understanding of this interrelationship.
This
population based case control study included 613 women who had stillbirths and 1747
women who had live births and who consented to placental pathological
examination from 59 hospitals in 5 geographic areas in the U.S.
Study was
published online August 18, 2017 in Journal PloS one.
About 15
placental pathologies were most prevalent in women with stillbirths and fetal
growth abnormalities.
Out of 15,
ten were also associated with fetal growth retardations. These are: single
umbilical artery; velamentous insertion; terminal villous immaturity;
retroplacental hematoma; parenchymal infarction; intraparenchymal thrombus;
avascular villi; placental edema; placental weight; ratio birth
weight/placental weight)
The other 5
(acute chorioamnionitis of placental membranes; acute chorioamionitis of
chorionic plate; chorionic plate vascular degenerative changes; perivillous,
intervillous fibrin, fibrinoid deposition; fetal vascular thrombi in the
chorionic plate) resulted in stillbirths without altered fetal growth.
Terminal
villous hypoplasia was equally common in live born and still born fetuses with
altered fetal growth.
Maternal factors
associated with still births were gestational hypertension/pre-eclampsia (20%
versus 11%, p<0.001), hypertension before pregnancy (11% versus 5%,
p<0.001), and pregestational diabetes (7% versus 2%, p<0.001)
Fetal
factors associated with still births were congenital malformations (13% versus
3%, p<0.001), lower birth weight (median 1,949 versus 3,321 grams,
p<0.001), and lower GA (median 33 versus 39 weeks, p<0.001).
The study
results suggest that different mechanisms exist for disruption in placental
function and the results vary according to timing of gestation. An acute insult
results in still births but no fetal growth alterations while a chronic, low
level insult results in fetal growth retardation which may end up in still
births.
Some of
these placental findings can be diagnosed with prenatal ultrasound and
pregnancies managed accordingly, Similarly, birth weight to placental weight
ratio could be estimated antenatally by ultrasound and those pregnancies with
abnormal ratio and at risk of stillbirths could benefit from early term delivery.
Access the
abstract, Full Text.
