Journal of Perinatology (2016) 00, 1–6

© 2016 Nature America, Inc., part of Springer Nature. All rights reserved 0743-8346/16
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ORIGINAL ARTICLE
The effect of placenta previa on fetal growth and pregnancy
outcome, in correlation with placental pathology
E Weiner1, H Miremberg1, E Grinstein1, Y Mizrachi1, L Schreiber2, J Bar1 and M Kovo1

OBJECTIVE: To compare the clinical characteristics and placental histopathology between pregnancies complicated by placenta
previa and controls.
STUDY DESIGN: Between 2009 and 2015, cesarean deliveries (CDs) of 119 pregnancies with placenta previa were identified from
which maternal outcomes, neonatal outcomes and placental pathology were reviewed. Results were compared with CDs matched
for maternal age and pregnancy complications (control group, n = 119). Placental lesions were classified into maternal and fetal
vascular supply lesions and inflammatory response. Composite neonatal outcome was defined as one or more of early neonatal
complications. Small-for-gestational age (SGA) was defined as birth weight ⩽ 10th percentile.
RESULTS: Placentas from the previa group had higher rates of weights o 10th percentile (P o 0.001) and of maternal and fetal
vascular supply lesions (P o0.001, for both). Higher rate of SGA (P = 0.003) and worse composite neonatal outcome (P o0.001) were
also observed in the previa group as compared with controls. After controlling for potential confounding bias using multivariable
logistic regression models, placenta previa remained statistically significantly associated with placental maternal (adjusted odds
ratio (aOR) 2.48, 95% confidence interval (CI) 1.2–4.9, P = 0.009) and fetal (aOR 7.05, 95% CI 2.4–20.2, P o0.001) vascular supply
lesions, SGA (aOR 10, 95% CI 2.3–44.2, P = 0.002) and adverse neonatal outcome (aOR 6.87, 95% CI 2.9–11.8, P o 0.001).
CONCLUSIONS: More placental vascular supply lesions, higher rate of SGA and worse neonatal outcome characterized pregnancies
with placenta previa in the current study. These findings may suggest that abnormal placentation is accompanied by suboptimal
implantation that interferes with fetal growth.
Journal of Perinatology advance online publication, 1 September 2016; doi:10.1038/jp.2016.140

INTRODUCTION growing fetus, is controversial.9,15–22 Notably, the effect of this

Placenta previa is described as suboptimal placental implantation abnormal placentation on placental histopathological lesions has
over or very near the internal cervical os. Most of the placenta not been addressed adequately.
previas that are observed by transvaginal ultrasound scans before The aim of the present study was to fill this gap and to compare
20 weeks of gestation will no longer be present near term.1,2 Only the clinical characteristics, neonatal and maternal outcomes and
1 in 200 pregnancies are complicated by persistent placenta previa the placental histopathology between pregnancies complicated
at delivery.3 The incidence of placenta previa appears to increase in by placenta previa and controls. Placental lesions were compared
a dose-dependent manner such that increasing number of prior using the classification to three major categories: placental
cesarean deliveries (CDs) is associated with increasing incidence maternal vascular supply lesions, placental fetal vascular supply
lesions, and lesions consistent with maternal and fetal inflamma-
rates of placenta previa in subsequent pregnancies.4 Other risk
tory response.23,24
factors for placenta previa include previous spontaneous and
elective pregnancy terminations, previous uterine surgeries,5
parity, advanced maternal age, smoking, cocaine use, multiple
MATERIALS AND METHODS
gestations, in vitro fertilization and prior placenta previa.6–8
The medical records of all women who underwent CDs for placenta previa
Pregnancies complicated by placenta previa have been asso-
between 24 and 42 weeks of gestation from January 2009 to April 2015
ciated with adverse maternal and neonatal outcomes. Preterm and were reviewed. The diagnosis of placenta previa was confirmed in all
early-term deliveries, prematurity, low Apgar scores, fetal and women by third trimester transvaginal ultrasound scans.25 In all cases,
neonatal death,9–11 maternal intrapartum and postpartum the placentas were sent to histopathology for evaluation, in accordance
hemorrhage, the need for blood transfusion, sepsis and hysterec- with the departmental policy that routinely performs placental analyses in
tomy3,9,12–14 were observed at increased rates in pregnancies all complicated pregnancies, and randomly also in women with an
complicated by placenta previa. uncomplicated pregnancy for research purposes.
The pathophysiology of placenta previa is still unclear. It appears Excluded from the study were multiple gestations, deliveries o24 weeks
of gestation, known fetal or neonatal malformation, cases with concurrent
to be associated with endometrial damage and uterine wall placenta accrete and cases with missing data.
scarring, which may interfere with the normal process of placental The control group included women who underwent an elective CD
implantation and development. Moreover, the possible effect of during the same time period, owing to malpresentation or previous CD, and
placenta previa, on placental function and consequently on the their placentas were sent for histopathological evaluation. The controls

1
Department of Obstetrics and Gynecology, The Edith Wolfson Medical Center, Affiliated with Sackler Faculty of Medicine, Tel Aviv University, Holon, Israel and 2Department of
Pathology, The Edith Wolfson Medical Center, Affiliated with Sackler Faculty of Medicine, Tel Aviv University, Holon, Israel. Correspondence: Dr E Weiner, Department of Obstetrics
and Gynecology, The Edith Wolfson Medical Center, Affiliated with Sackler Faculty of Medicine, Tel Aviv University, P.O. Box 5, Holon 58100, Israel.
E-mail: [email protected]
Received 16 April 2016; revised 28 June 2016; accepted 11 July 2016
 Placenta previa—histopathology, SGA, and pregnancy outcome
E Weiner et al
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were matched, on a 1:1 basis, to the study group (previa group) for maternal
age (±1 year) and pregnancy complications, including the presence of Table 1. Maternal characteristics
preeclampsia, diabetes mellitus and thrombophilias. For the purpose of the
Previa, n = 119 Control, n = 119 P-value
study, data were compared between the previa and control groups.
Approval was obtained from the Local Ethics Committee. Maternal age (years) 32.4 ± 4.3 31.9 ± 4.0 0.359
Gestational age (weeks) 35.8 ± 4.4 38.8 ± 2.9 o0.001
Data collection Nulliparity 30 (25.2) 56 (72.3) o0.001
The following data were collected from the admission file of each woman: BMI (kg m − 2) 24.6 ± 7.0 25.2 ± 6.1 0.486
age, gravidity, parity, previous CDs, gestational age (confirmed by first- Smoking 27 (22.7) 14 (11.8) 0.038
trimester ultrasonography), prepregnancy body mass index (BMI, kg m − 2), ART 19 (16.0) 9 (7.6) 0.069
cigarette smoking, pregnancies achieved by assisted reproductive Previous cesarean 0.9 ± 0.7 0.8 ± 0.6 0.238
techniques (ovulation induction or in vitro fertilization), and pregnancy deliveries
complications such as: preeclampsia, chronic hypertension, gestational Abbreviations: ART, assisted reproduction technology (ovulation induction
diabetes mellitus (A1 and A2), pregestational diabetes mellitus, and or in vitro fertilization); BMI, body mass index. Continuous variables are
thrombophilia (defined as any thrombophilia inherited or acquired that presented as mean ± s.d. and categorical variables as n (%). Bold values
necessitated thromboprophylaxis).26,27 indicate Po0.05.
The following data were collected from the surgical report and
postpartum file of each woman: hospitalization (days), preoperative
hemoglobin concentrations, 24 h postpartum hemoglobin concentration,
postpartum hemorrhage that necessitated the use of uterotonic medica- coils cm − 1, and hypocoiling was diagnosed in cases of umbilical coiling
tions, hysterectomy, uterine/hypogastric artery ligation, the need for re- index ⩽ 0.1 coils cm − 1.31 Abnormal cord insertion was defined as either
laparotomy, intensive care unit (ICU) admission, and the need for blood velamentous or marginal insertion.
product transfusion. Significant blood loss was defined as a difference in
hemoglobin concentration ⩾ 3 g dl − 1 between the preoperative and Statistical analysis
postpartum hemoglobin levels.
Data were analyzed with the SPSS software, version 21.0 (SPSS, Chicago, IL,
Immediately after birth, all neonates were examined by pediatricians.
USA). Continuous variables are presented as mean ± s.d. or median and
Birth weight percentile for gestational age was assigned using the updated
range, as appropriate. Categorical variables are presented as rate (%).
Israeli growth charts.28 Small-for-gestational age (SGA) was defined as
Continuous parameters were compared by Student’s t-test and categorical
actual birth weight ⩽ 10th percentile or ⩽ 5th percentile for gestational
variables by chi-square test or by Fisher’s exact test, as appropriate. P-value
age. The following information was collected from the neonatal records:
of o 0.05 was considered statistically significant.
Apgar scores, cord blood pH, neonatal hospitalization, neonatal ICU (NICU)
Composite placental maternal vascular supply lesions was defined as the
admissions, sepsis (positive blood or cerebrospinal fluid culture), need for
blood transfusion, need for phototherapy, respiratory distress syndrome, presence of one or more maternal vascular supply abnormalities, and
need for mechanical ventilation or support, necrotizing enterocolitis, composite placental fetal vascular supply lesions was defined as the
intraventricular hemorrhage (all grades), hypoxic ischemic encephalo- presence of one or more fetal vascular supply abnormalities.
pathy, seizures, and death. Composite adverse neonatal outcome was defined as one or more of
the following complications: neonatal sepsis, blood transfusion, photo-
therapy, respiratory morbidity (presence of respiratory distress syndrome,
Placental examination transient tachypnea of the newborn, mechanical ventilation or need for
Placental histopathology examinations were performed using our standard respiratory support), cerebral morbidity (presence of intraventricular
protocol by a single pathologist (LS). Placental lesions were classified by hemorrhage, seizures or hypoxic–ischemic encephalopathy), necrotizing
maternal or fetal origin, according to the criteria adopted by the Society for enterocolitis, or death.
Pediatric Pathology24 and as we previously reported.29 Briefly, placental Composite maternal hemorrhagic morbidity included one or more of
weight was determined 24 h after delivery, and the percentile was the following maternal surgical and postpartum complications: hyster-
determined according to placental weight charts.30 Each placenta was ectomy, uterine/hypogastric artery ligation, and the need for re-
fixed in formalin, and at least five samples were embedded in paraffin laparotomy, ICU admission, or the need for blood product transfusion.
blocks for microscopic assessment. To identify independent risk factors for the presence of placental weight
⩽ 10th percentile, placental maternal vascular supply lesions (composite)
and for placental fetal vascular supply lesions (composite), multivariate
Placental lesions logistic regression analyses were performed. Placental weight ⩽ 10th
Lesions of maternal vascular supply included: placental hemorrhages percentile, composite placental maternal vascular supply lesions and
(marginal and retro-placental), vascular changes associated with maternal composite placental fetal vascular lesions served as the dependent
malperfusion (acute atherosis and mural hypertrophy), and villous changes variables, whereas placenta previa, maternal age, gestational age, parity,
associated with maternal malperfusion (increased syncytial knots, villous smoking, thrombophilia and BMI served as independent variables.
agglutination, increased intervillous fibrin deposition, distal villous hypo- To identify independent risk factors for SGA (birth-weight ⩽ 10th
plasia and villous infarcts). percentile) and for adverse neonatal outcome, multivariate logistic
Lesions of fetal vascular supply were defined as findings consistent with regression analyses were performed. SGA and composite adverse neonatal
fetal thrombo-occlusive disease: vascular lesions (thrombosis of the outcome served as the dependent variables, whereas placenta previa,
chorionic plate and stem villous vessels) and villous changes (hypovas- maternal age, gestational age, parity, smoking, thrombophilia and BMI
cular, fibrotic and avascular villi). served as independent variables.
Findings consistent with chorioamnionitis were defined by the presence
of an inflammatory neutrophil infiltrate at two or more sites on the chorionic
plate and extraplacental membrane. Maternal inflammatory response was
divided into three stages: stage 1—characterized by the presence of a few
RESULTS
scattered neutrophils in the subchorionic space; stage 2—characterized by During the study period, 158 women with placenta previa, out of
many neutrophils (11–30 per high-power field) in the lower half of the 28 376 deliveries (0.56%), underwent CD. The study group included
chorionic plate; and stage 3—characterized by dense infiltrates of 119 women after excluding 39 cases, owing to multiple
neutrophils (430 per high-power field) throughout the chorionic plate. pregnancy,15 concurrent placenta accrete14 and incomplete data.10
Fetal inflammatory response was also divided into 3 stages: stage 1—early, Table 1 presents maternal and pregnancy characteristics of the
umbilical phlebitis; stage 2—intermediate, umbilical arteritis; and stage 3—
concentric umbilical perivasculitis (necrotizing funisitis).
study groups.
The umbilical cord was examined for the detection of hypercoiling and Women in the previa group were less likely to be nulliparous
abnormal cord insertion. Umbilical coiling index was calculated by dividing (P o 0.001), had a higher rate of cigarette smoking (P = 0.038) and
the total number of coils by the length of the cord in centimeters. gave birth at earlier gestational ages (35.8 ± 4.4 vs 38.8 ± 2.9 weeks,
Hypercoiling was diagnosed in cases of umbilical coiling index ⩾ 0.3 Po 0.001) as compared with controls. There were no differences

Journal of Perinatology (2016), 1 – 6 © 2016 Nature America, Inc., part of Springer Nature.
 Placenta previa—histopathology, SGA, and pregnancy outcome
E Weiner et al
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in maternal age, maternal BMI and the rate of pregnancies Table 2 presents the placental characteristics of the previa group
achieved by assisted reproductive techniques between the as compared with controls. Mean placental weight was signifi-
groups. As expected from the study design, both groups had cantly lower in the previa group as compared with the controls
similar rates of gestational or pregestational diabetes mellitus (432 ± 126 vs 498 ± 108 g, Po0.001, respectively). In addition, the
(10%), preeclampsia (0.8%) and thrombophilia (2.5%). previa group had a higher rate of placental weight below the 10th
percentile, (Po0.001). Higher rates of maternal placental vascular
lesions related to maternal malperfusion, placental hemorrhages
and composite placental maternal vascular supply lesions were
Table 2. Histopathological characteristics of the placentas
also detected in the previa group as compared with the control
Previa, Control, P-value group (P = 0.019, Po0.001, Po0.001, respectively). Additionally,
n = 119 n = 119 higher rates of placental lesions consistent with fetal thrombo-
occlusive disease, (vascular and villous), as well as higher rates of
Placental weight (g) 432 ± 126 498 ± 108 o0.001 composite fetal vascular lesions, were observed in the previa group
Placental weight o 10th 44 (37.0) 9 (7.5) o0.001 as compared with the controls (P = 0.024, P = 0.049, Po0.001,
percentile respectively). Moreover, placentas in the previa group had more
abnormal cord insertion as compared with the control group
Maternal vascular supply lesions
Placental hemorrhage 25 (21) 1 (0.8) o0.001 (16.5% vs 5.9%, P = 0.013). There were no significant between-
Vascular lesions related to 9 (7.6) 1 (0.8) 0.019 group differences in rates of placental inflammatory lesions and
maternal malperfusion abnormal coiling of the cord. Using multivariate logistic regression
Villous changes related to 33 (27.7) 30 (25.2) 0.769 analyses, composite placental maternal vascular supply lesions and
maternal malperfusion composite placental fetal vascular supply lesions were indepen-
Composite placental 61 (51.2) 32 (26.9) o0.001 dently associated with placenta previa (adjusted odds ratio
maternal vascular lesions (aOR) = 2.48, 95% confidence interval (CI) 1.2–4.9, P = 0.009 and
aOR 7.05, 95% CI 2.4–20.2, Po0.001, respectively). In addition,
Fetal vascular supply lesions
placental weight o10th percentile was also independently
Vascular lesions consistent 14 (11.8) 4 (3.4) 0.024
with FTOD associated with placenta previa (aOR = 6.58, 95% CI 2.6–16.7,
Villous lesions consistent 11 (9.2) 3 (2.5) 0.049 Po0.001) after controlling for background maternal confounders
with FTOD (maternal age, gestational age, parity, smoking, thrombophilia
Composite placental fetal 25 (21.0) 7 (5.9) o0.001 and BMI).
vascular lesions Neonatal outcome parameters are summarized in Table 3.
Increased rates of SGA neonates, below the 10th percentile and
Inflammatory lesions below the 5th percentile, were observed in the previa group as
MIR stages 1–3 4 (3.4) 11 (9.2) 0.106 compared with controls (15.1% vs 3.4%, P = 0.003 and 6.7% vs 0%,
FIR stages 1–3 2 (1.7) 4 (3.4) 0.683
P = 0.005, respectively). Neonates in the previa group had a longer
Umbilical cord findings hospitalization (12.7 ± 15.1 vs 4.8 ± 3.9 days, Po 0.001) and higher
Hypercoiling 22 (18.5) 13 (10.9) 0.142 rate of NICU admission (38.7% vs 14.3%, P o 0.001), as compared
Hypocoiling 21 (17.6) 11 (9.2) 0.086 with neonates in the control group. Composite neonatal outcome
Abnormal cord insertion 20 (16.8) 7 (5.9) 0.013 was worse in the previa group as compared with the control
group (45.3 vs 11.8%, P o 0.001). Using multivariate logistic
Abbreviations: FIR, fetal inflammatory response; FTOD, fetal thrombo-
regression analysis, SGA ⩽ 10th percentile (aOR 10.09, 95% CI
occlusive disease; MIR, maternal inflammatory response. Continuous
variables are presented as mean ± s.d. and categorical variables as n (%). 2.3–44.2, P = 0.002), NICU admission (aOR 3.87, 95% CI 2.5–12.3,
Bold values indicate P o0.05. P o0.001) and composite adverse neonatal outcome (aOR 6.87,
95% CI 2.9–11.8, P o0.001) remained independently associated

Table 3. Neonatal outcome

Previa, n = 119 Control, n = 119 P-value aORa 95% CIa

Birth weight (g) 3274 ± 332 2523 ± 462 o 0.001 — —

SGA ⩽ 10th percentile 18 (15.1) 4 (3.4) 0.003 10.09 2.3–44.2
SGA ⩽ 5th percentile 8 (6.7) 0 0.005 — —
Neonatal hospitalization (days) 12.7 ± 15.1 4.8 ± 3.9 o 0.001 1.68 1.1–6.5
NICU admission 46 (38.7) 17 (14.3) o 0.001 3.87 2.5–12.3
Umbilical cord pH ⩽ 7.1 1 (0.8) 1 (0.8) 1 — —
5-Min Apgar score ⩽ 7 5 (4.2) 1 (0.8) 0.212 — —
Respiratory morbidityb 29 (24.4) 4 (3.4) o 0.001 1.3 0.9–3.8
Cerebral morbidityc 3 (2.5) 0 0.247 — —
Neonatal sepsis 4 (3.4) 1 (0.8) 0.37 — —
Necrotizing enterocolitis 1 (0.8) 0 1 — —
Blood transfusions 10 (8.4) 1 (0.8) 0.01 — —
Phototherapy 31 (26.1) 8 (6.7) o 0.001 1.5 0.8–2.5
Neonatal death 1 (0.8) 0 1 — —
Composite adverse neonatal outcome 54 (45.3) 14 (11.8) o 0.001 6.87 2.9–11.8
Abbreviations: aOR, adjusted odds ratio; CI, confidence interval; NICU, neonatal intensive care unit; SGA, small for gestational age. Continuous variables are
presented as mean ± s.d. and categorical variables as n (%). aAfter controlling for background maternal confounders (maternal age, gestational age, parity,
smoking, thrombophilia and body mass index). bRespiratory morbidity includes the presence of respiratory distress syndrome or mechanical ventilation or the
need for respiratory support. cCerebral morbidity includes the presence of intraventricular hemorrhage (all grades) or seizures or hypoxic–ischemic
encephalopathy. Bold values indicate Po0.05.

© 2016 Nature America, Inc., part of Springer Nature. Journal of Perinatology (2016), 1 – 6
 Placenta previa—histopathology, SGA, and pregnancy outcome
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Table 4. Surgical and postpartum maternal complications

Previa, n = 119 Control, n = 119 P-value aORa 95 % CIa

Maternal hospitalization (days) 7.0 ± 2.1 4.3 ± 1.7 o0.001 2.3 1.5–4.9
Significant blood loss 39 (32.8) 6 (5) o0.001 4.36 2.6–17.3
PPH 13 (10.9) 4 (3.4) 0.041 — —
ICU admission 1 (0.8) 0 1 — —
Blood transfusion 31 (26.1) 7 (5.9) o0.001 1.9 0.9–1.6
Hysterectomy 1 0 1 — —
Uterine/hypogastric artery ligation 2 0 0.498 — —
Re-laparotomy 1 0 1 — —
Composite maternal hemorrhagic morbidity 32 (26.9) 7 (5.9) o0.001 5.32 2.4–15.3
Abbreviations: aOR, adjusted odds ratio; CI, confidence interval; ICU, intensive care unit; PPH, postpartum hemorrhage. Continuous variables are presented as
mean ± s.d. and categorical variables as n (%). PPH that necessitated the use of uterotonic medications. Significant blood loss—a difference in hemoglobin
concentration ⩾ 3 g dl − 1 between the preoperative and 24 postpartum hemoglobin levels. aAfter controlling for background maternal confounders (maternal
age, gestational age, parity, smoking, thrombophilia and body mass index). Bold values indicate Po0.05.

with placenta previa after controlling for background maternal biopsies in cases of placenta previa demonstrated a significantly
confounders (maternal age, gestational age, parity, smoking, higher trophoblastic giant cell infiltration in decidua and
thrombophilia and BMI). myometrial blood vessels,37 suggesting that placenta previa is
Table 4 presents the maternal postpartum outcome. As associated with normal physiological changes of the spiral arteries.
compared with the controls, women in the previa group had In the current study, we demonstrate that pregnancies
longer hospitalization (7.0 ± 2.1 vs 4.3 ± 1.7 days, Po0.001) and complicated by placenta previa were associated with SGA
higher rate of composite maternal hemorrhagic morbidity (26.9% neonates. SGA below the 10th percentile was independently
vs 5.9%, Po0.001). Using a multivariate logistic regression analysis, associated with placenta previa, aOR 10.09, 95% CI 2.3–44.2,
composite maternal hemorrhagic morbidity (aOR = 5.32, 95% CI P = 0.002. Indeed, the association between placenta previa and
2.4–15.3, Po0.001) and significant blood loss (aOR 4.36, 95% CI SGA has been studied with differing results, between no
2.6–17.3, Po0.001) remained independently associated with correlations,18–22 to increased risk.9,15–17 Our findings suggest an
placenta previa after controlling for background maternal con- etiopathogenesis for the development of SGA in pregnancies
founders (maternal age, gestational age, parity, smoking, throm- complicated with placenta previa, probably via the vascular
bophilia and BMI). compromise that is a result from abnormal placentation and is
expressed by placental maternal and fetal vascular supply lesions.
Several studies have reported an increased incidence of
DISCUSSION placental maternal vascular lesions in pregnancies complicated
In the present study, differences in the morphological appearance by SGA neonates, while others have demonstrated a combined
of placentas from pregnancies complicated by placenta previa as maternal and fetal compartment involvement in the development
compared with normal placental implantation were observed. of growth restriction and SGA neonates.38,39 Importantly, placental
Moreover, pregnancies with placenta previa were characterized by fetal vascular supply lesions are also known to be important
SGA neonates and worse maternal and neonatal outcomes. contributors to adverse pregnancy outcome.40,41 In the same line,
Placental pathology is a valuable link that may explain how worse neonatal outcome was observed in the current study in
underlying pathology results in adverse pregnancy outcomes. Yet, cases with placenta previa. Deliveries in pregnancies complicated
the effect of an abnormal implantation site, as in placenta previa, by placenta previa are more likely to occur preterm. It is well
on placental histopathology lesions is unknown. In the current established that late preterm birth is still associated with adverse
study, we observed that placentas from pregnancies complicated neonatal outcome, including respiratory morbidity, intraventricular
by placenta previa were smaller with higher rate of placental hemorrhage, sepsis work-ups, sepsis, phototherapy for hyperbilir-
weight below the 10th percentile. Additionally, these placentas ubinemia and neonatal death.42–44 However, in the current study
had significantly more of the characteristic vascular lesions adverse neonatal outcome was found to be independently
associated with placental hemorrhages, maternal malperfusion associated with placenta previa (aOR 6.87, 95% CI 2.9–11.8,
and fetal thrombo-occlusive disease, known to occur in pre- Po0.001), after adjustment for gestational age. These findings
eclampsia and fetal growth restriction.32 By multivariate regression also support our hypothesis that suboptimal implantation, as
analyses, placental weight o 10th percentile and placental occurs in placenta previa, results in abnormal placentation leading
vascular lesions (maternal and fetal) were independently asso- to placental malfunction with decreased placental perfusion.
ciated with placenta previa. In a recent review,33 it has been The increased composite maternal hemorrhagic morbidity
pointed out that developmental abnormalities of the maternal (26.9%), observed in pregnancies complicated by placenta previa,
stromal-vascular compartment of the placenta contribute to was expected, and it is in concordance with previous
placental dysfunction via malperfusion and loss of integrity. In studies.3,9,12–14 It probably reflects inadequate muscles contrac-
concordance with it, the current findings suggest that abnormal tions, at the lower uterine segment, hence bleeding ensues from
site of implantation may result in abnormal placental develop- the placental bed.
ment that may compromise fetal development. Notably, the Our study has several strengths. It is the first to our knowledge
higher rate of abnormal cord insertion observed in placenta previa that describes histopathological lesions in pregnancies compli-
as compared with controls is in concordance with others,34 and it cated by placenta previa and applies the placental histopathology
correlates with increased rate of placental vascular lesions.35 strict criteria that were validated and adopted by the Society of
Heidari et al.36 performed a stereological analysis of 10 placentas Pediatrics Pathology.24 In addition, a single pathologist who was
from pregnancies complicated by placenta previa and observed blinded to neonatal and maternal outcomes (but not to the
significant changes in the structure of the placenta as compared diagnosis of placenta previa) performed all histopathological
with controls. Yet, compared with our findings, placental bed evaluations. We could find a control group matched to the study

Journal of Perinatology (2016), 1 – 6 © 2016 Nature America, Inc., part of Springer Nature.
 Placenta previa—histopathology, SGA, and pregnancy outcome
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previa group by maternal age, pregnancy complications and 14 Spong CY, Mercer BM, D'Alton M, Kilpatrick S, Blackwell S, Saade G. Timing of
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Fetal Medicine, American Institute of Ultrasound in Medicine, American College of
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