ORIGINAL ARTICLE
Perinatal outcome of placental massive perivillous fibrin deposition:
a case–control study
Louise Devisme1* , Claire Chauvière2, Hélène Franquet-Ansart1, Anastasia Chudzinski2, Morgane Stichelbout1,3,
Véronique Houfflin-Debarge2,4 and Damien Subtil2,4
1
Department of Pathology, Lille University Hospital CHRU, Lille Cedex, France
Jeanne de Flandre Hospital, Lille University Hospital CHRU, Lille Cedex, France
3
North of France University, Lille, France
4
EA 4489, Lille North of France University, Lille, France
*Correspondence to: Louise Devisme. E-mail: louise.devisme@chru-lille.fr
2
ABSTRACT
Objective The objectives of the study are to describe the obstetric outcomes associated with massive perivillous fibrin
deposition (MFD) compared with a control series and to determine if outcome differs according to the extent of fibrin
deposition.
Method Retrospective case–control study based on placentas analyzed over a consecutive 12-year period. MFD was
considered severe if it extended over more than 50% of the placenta and moderate between 25% and 50%.
Results During the study period, MFD was observed on 71 placentas, 39 severe and 32 moderate. Compared with the
142 control women, the 39 women with severe MFD more often had histories of autoimmune disease and intrauterine
fetal death. The case women with MFD were associated with elevated levels of maternal alpha-fetoprotein and with a
high risk of severe growth restriction and/or intrauterine death. Compared with the infants with moderate MFD, those
with severe MFD had also more abnormal umbilical artery Doppler velocimetry findings and more often intrauterine
deaths and lower birthweights.
Conclusion Regardless of their extent, MFD that covered at least 25% of the placenta was almost always accompanied
by severe growth restriction and by a high risk of intrauterine fetal death. Moreover, severe MFD tend to be associated
with autoimmune diseases of the mothers, and pregnancies show more often a pathologic Doppler of the umbilical
arteries and more often intrauterine fetal death that the moderate form. © 2017 John Wiley & Sons, Ltd.
Funding sources: None
Conflicts of interest: None declared
INTRODUCTION
Massive perivillous fibrin deposition (MFD) was first described
in the 1960s.1 It is defined by the existence of massive deposits
of fibrin extending over at least 25% of the placental volume,
whether they are observed to be central, transmural, or basal
(along the maternal floor).2
Even though its presence is associated with an increased risk of
growth restriction and intrauterine fetal death (IUFD),2–6 this
rare lesion remains relatively unstudied, and its cause unknown.
Thus, the frequency of growth restriction and the stillbirth rate,
associated with this placental lesion, are variable from one study
to another. The risk of recurrence is high in the first-trimester
abortion, but it seems to be lower when MFD is observed in
second-trimester or third-trimester placentas, at around 14%.2–7
The absence of studies comparing these cases with a control
population has prevented the formal establishment of a
relation between these lesions and the clinical manifestations
Prenatal Diagnosis 2017, 37, 323–328
observed. To improve knowledge of the clinical consequences
associated with MFD and to determine if outcome differs
according to the extent of fibrin deposition, we conducted a
retrospective comparative clinicopathologic study.
METHODS
This single-center continuous retrospective case–control study
covers the period from 1 January 2000 to 30 June 2013, in our
level 3 university hospital maternity unit. Cases and controls
come from a database of all the placental examinations
performed during this period in the department of pathology
at the request of the maternity department. Records of single
pregnancies at a gestational age of 22 weeks or more were
eligible for the study. The MFD diagnosis was based on the
following criteria: existence of massive fibrin deposits encasing
villi on microscopic examination of the placenta, regardless of
the potentially associated lesions (Figures 1 and 2). In the case
© 2017 John Wiley & Sons, Ltd.
10970223, 2017, 4, Downloaded from https://obgyn.onlinelibrary.wiley.com/doi/10.1002/pd.5013 by University Of Chicago - Librar, Wiley Online Library on [17/11/2022]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
DOI: 10.1002/pd.5013
Figure 1 Macroscopic sections of two placentas demonstrating massive grey-white diffuse deposition of fibrin occupying almost all the
parenchyma (a), compared with red and homogeneous sections of a normal placenta (b)
Figure 2 Low-power micrograph of two placentas showing massive perivillous fibrin eosinophilic fibrin surrounding strangled villi (a), while
villi are clearly visible in the free intervillous space of the normal placenta (b)
of recurrence in the same patient, only the index case was
retained.
Two controls were included for each case: the patients who
gave birth immediately before and after the case patient,
regardless of whether a placental examination was performed.
These controls were not matched with gestational or maternal
age, neither with race or ethnicity. All placentas were examined
after fixation in formalin. Systematic samples were taken from
healthy areas and embedded in three paraffin blocks (the cord
and membranes, central placenta and peripheral placenta).
Samples were also taken of any macroscopic lesions. The
blocks were cut to a 3-μm thickness and stained with
hematoxylin-eosin-safran. All slides were reread by a single
operator (L. D.). This pathologist was aware only of the Apgar
score and birth weight. We set up two groups according to
the magnitude of fibrin deposition. The first type, considered
severe, was defined by fibrin deposition occupying at least
50% of the villi and intervillous spaces.2 The second group
comprised the placentas where fibrin deposition occupied at
25% of the villi and intervillous space but did not reach 50%.
These deposits were called moderate.2
Prenatal Diagnosis 2017, 37, 323–328
Maternal and neonatal data were extracted and collected
from the medical files by a single investigator (C. C.). Data
collection was declared to the French Commission
Informatique et Liberté (DEC 16–67). Ethical approval was
not required for this retrospective study. We studied the
following patient characteristics: age, ethnicity, BMI,
smoking status during pregnancy, principal medical and
obstetric history. When available, these laboratory results
were also noted: alpha-fetoprotein and β-HCG in serum
screening for trisomy 21 (n < 2.5 MoM), alkaline
phosphatases (N < 2.5 N), transaminases (N < 3 N). The
clinical data collected during pregnancy concerned prenatal
hospitalization, any preeclampsia, defined according to the
ISSHP criteria8 and the uterine and umbilical artery Doppler
spectra. Data for pregnancy outcome included gestational
age, mode of labor onset, and mode of delivery. Data about
the newborn included: birthweight, umbilical artery pH, and
the occurrence of either neonatal intensive unit care
transfer or death before discharge. Fetal growth restriction
was defined according to the French curves derived from
2003 National Perinatal Survey.9,10 The birthweights
© 2017 John Wiley & Sons, Ltd.
10970223, 2017, 4, Downloaded from https://obgyn.onlinelibrary.wiley.com/doi/10.1002/pd.5013 by University Of Chicago - Librar, Wiley Online Library on [17/11/2022]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
L. Devisme et al.
324
325
observed were related to the median for gestational age, as
birthweight ratios.11
The analysis successively compared each of the MFD groups
(severe and moderate) with the control group and then
compared the two MFD groups with each other. Epidata 3.1
software (EpiData Association, Odense, Denmark) was used to
perform the analysis. Comparisons between the qualitative
data used the Chi-2 test or Fisher’s exact test, when the number
of individuals was low. Comparisons between the quantitative
variables used Wilcoxon’s nonparametric test. All the tests were
bilateral, and the significance level was set at P < 0.05. The
percentages are reported in parentheses, and means are
reported with the standard deviation of the distribution.
RESULTS
During the study period, 64 619 births took place in our
hospital, and 6971 placentas were analyzed (10.8%). Among
them, 79 placentas had lesions determined to be MFD (1.1%
of placental examinations, 0.1% of deliveries). As required by
the study protocol, eight placentas were excluded for the
following reasons: twin pregnancies (n = 2), gestational age
below 22 weeks (n = 1), recurrence of MFD (n = 5). Finally, the
study covered 71 placentas, 39 with severe MFD (>50%) and
32 moderate (25% to < 50%). In the group of 142 control
patients, three patients were excluded because of twin
pregnancies and were replaced.
Table 1 summarizes the characteristics of the case and
control patients. Compared with the control women, the case
patients with severe MFD were more often of African or West
Indian origin (15.4% vs 2.1%, P < 0.001)), or had a history of
IUFD (7.7% vs 0.0%, P = 0.009) or an autoimmune disease
(12.8% vs 2.1, P = 0.012). They were comparable to the control
patients for their other characteristics and history. The women
with moderate MFD were comparable to the control patients
except that more of the former smoked (41.9% vs 15.5%,
P = 0.002). Finally, compared with the women with moderate
MFD, the women with severe MFD were more often black
(African or West Indian, 15.4% vs 3.1%, P = 0.04) and smoked
less often (22.2% vs 41.9%, P = 0.05).
Pregnancy outcomes are described in Table 2. Severe MFD
was associated with an elevated level of alpha-fetoprotein
(>2.5 MoM) in one third of the cases (31.3% vs 0.0%,
P < 0.001), without any significant elevation of β-HCG, alkaline
phosphatases or transaminases. Clinically, more than half the
women with severe MFD were hospitalized before labor
(56.4% vs 14.1%, P < 0.001), and almost one in five had
preeclampsia (18.0% vs 0.7%, P < 0.001). More than half the
fetuses with severe MFD also had abnormal umbilical Doppler
spectra (60.0% vs 1.4%, P < 0.001), and nearly a quarter of them
died in utero (23.1 vs 0.0, P < 0.001), at a mean gestational age
of 31 weeks (range: 24–41 weeks). Preterm delivery was very
frequent in this severe MFD group, reaching 62.1% of
pregnancies (vs 6.4% in the control group, P < 0.001). Almost
one third of the women in this group gave birth very preterm
(≤32 weeks: 31.0 vs 0.7%, P < 0.001). Induced delivery was more
common in women with severe MFD, with a cesarean rate of
44.8% (vs 9.2% in controls, P < 0.001). Of the liveborn infants
in the severe MFD group, 93.1% were growth-restricted, with
birthweights below the third percentile (vs 3.5% of the controls,
P < 0.001). More than half the newborns with severe MFD were
transferred to the neonatal intensive care unit (55.2% vs 2.1%,
P < 0.001) (Table 2). There was one postnatal death: a child in
Table 1 Patient characteristics according to their group
1
Severe MFD
>50%
n = 39
Age (years)
29.6 ± 4.9
2
Moderate
MFD 25–50%
n = 32
31.4 ± 7.1
3
Controls
n = 142
30.1 ± 5.7
1
versus
3
2
versus
3
1
versus
2
0.62
0.27
0.21
<0.001
0.69
0.04
0.16
0.50
0.66
0.47
0.002
0.05
Ethnicity
White
23 (59.0)
23 (71.8)
111 (78.2)
North Africa
8 (20.5)
8 (25.0)
26 (18.3)
Sub-Saharan Africa, West Indies
6 (15.4)
1 (3.1)
3 (2.1)
0
2 (1.4)
Other
BMI (kg/m2)
Smokers
2 (5.1)
25.5 ± 6.1
24.8 ± 7.2
24.0 ± 5.8
8 (22.2)
13 (41.9)
22 (15.5)
Nulliparas
20 (51.3)
13 (40.6)
59 (41.5)
0.28
>0.99
0.37
History spont. abortion < 12 weeks
11 (28.2)
8 (25.0)
38 (26.8)
0.84
>0.99
0.76
History late miscarriage 12–21 weeks
2 (5.1)
0 (0.0)
1 (0.7)
0.12
>0.99
0.50
History IUFD
3 (7.7)
0 (0.0)
0 (0)
0.009
>0.99
0.24
History preeclampsia/HELLP
1 (2.6)
0 (0.0)
2 (1.4)
0.52
>0.99
>0.99
History deep vein thrombosis
1 (2.6)
0 (0.0)
3 (2.1)
>0.99
>0.99
>0.99
0 (0.0)
0 (0.0)
4 (2.8)
0.58
>0.99
5 (12.8)
0 (0.0)
3 (2.1)
0.012
>0.99
History known thrombophilia
Autoimmune diseasea
0.06
BMI, body mass index; IUFD, intrauterine fetal death.
a
Including one Antiphospholipid syndrome, one systemic scleroderma, one dermatopolymyositis, one mixed connective tissue disease and one Goujerot–Sjögren syndrome.
Prenatal Diagnosis 2017, 37, 323–328
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Perinatal outcome of placental massive perivillous fibrin deposition
Table 2 Pregnancy outcomes according to their group
1
Severe MFD
>50%
n = 39
2
Moderate MFD
25–50%
n = 32
3
Controls
n = 142
Alpha-fetoprotein > 2.5 MoM
5/16 (31.3)
β-HCG > 2.5 MoM
0/17 (0.0)
Alkaline phosphatases > 2.5 N
6/19 (31.6)
0/10 (0.0)
6/23 (26.1)
SGOT and /or TGP > 3 N
1/29 (3.5)
1/17 (5.9)
2/35 (5.7)
Prenatal hospitalization
Preeclampsia
22 (56.4)
7 (18.0)
2/78 (2.6)
>0.99
0.28
0.35
0.74
0.15
0.07
>0.99
13 (40.6)
3 (9.4)
18/30 (60.0)
6/24 (25.0)
9 (23.1)
35.1 ± 4.6
>0.99
1/9 (11.1)
Abnormal umbilical Doppler
Gestational age at birtha
<0.001
<0.001
11/20 (55.0)
In utero death
1
versus
2
0/67 (0.0)
15/32 (46.9)
1 (2.6)
2
versus
3
3/12 (25.0)
Abnormal uterine Doppler
Medically-indicated TOP
1
versus
3
1 (3.1)
2 (6.2)
36.8 ± 2.4
>0.99
>0.99
20 (14.1)
<0.001
<0.001
0.19
1 (0.7)
<0.001
0.02
0.49
0.15
0.06
0.57
5/21 (23.8)
<0.001
<0.001
1 (0.7)
0.39
0.34
>0.99
0 (0.0)
<0.001
0.03
0.10
<0.001
<0.001
0.06
1/70 (1.4)
39.1 ± 3.1
0.01
Preterm birth ≤ 32 weeks
9/29 (31.0)
3/29 (10.3)
1/141 (0.7)
<0.001
<0.001
0.05
Preterm birth ≤ 37 weeks
18/29 (62.1)
11/29 (37.9)
9/141 (6.4)
<0.001
<0.001
0.07
6/29 (20.7)
14/29 (48.3)
<0.001
<0.001
0.09
Mode of labor onseta
Spontaneous
112/141 (79.4)
Induction of labor
10/29 (34.5)
6/29 (20.7)
16/141 (11.3)
Cesarean before labor
13/29 (44.8)
9/29 (31.0)
13/141 (9.2)
18/29 (62.1)
18/29 (62.1)
1730 ± 770
2050 ± 690
27/29 (93.1)
Cesareana
Birthweight (g)a
<3d percentile
Umbilical artery pH < 7.15
Transferred to NICU
Inhospital neonatal death
4/28 (14.3)
16/29 (55.2)
1/29 (3.5)
<0.001
<0.001
>0.99
3390 ± 630
<0.001
<0.001
0.07
24/29 (82.8)
5/141 (3.5)
<0.001
<0.001
0.42
2/29 (6.9)
7/132 (5.3)
0.10
0.67
0.42
10/29(34.5)
3/141 (2.1)
<0.001
<0.001
0/29 (0)
20/141 (14.2)
0/141 (0)
>0.99
0.17
0.11
>0.99
MFD, massive perivillous fibrin deposition; NICU, neonatal intensive care unit; TOP, termination of pregnancy; SGOT, aspartate transaminase.
a
Excluding medical terminations of pregnancy and in utero deaths.
the severe MFD group, born at 32 weeks, weighing 810 g at
birth, below the first percentile. In the moderate case group,
findings were similar for pregnancies and neonates, with lower
proportions but always in the same direction and statistically
significant.
Finally, the comparison between the severe and moderate
MFD groups found no statistically significant differences for
laboratory, clinical or obstetric findings between the two
groups, except that abnormal umbilical Doppler spectra were
more frequent in the severe MPD group (60.0% vs 25.0%,
P = 0.01). Nonetheless, we also noted a trend toward more
IUFDs in the severe compared with the moderate MFD groups
(23.1 vs 6.2, P = 0.10) and toward a lower mean birthweight
(1730 ± 770 vs 2050 ± 690, P = 0.07).
DISCUSSION
Our work represents the first case–control study about MFD.
It shows that MFD is almost always associated with very
severe growth restriction, regardless of its extent once it
reaches the threshold of 25%. It is also associated with an
increased risk of IUFD, which reached 23% for the severe
Prenatal Diagnosis 2017, 37, 323–328
MFD cases. Moreover, we showed a significant association
between elevated alpha-fetoprotein in the second trimester
and MFD.
Massive perivillous fibrin deposition was found in 0.7% of
the placentas examined in our university pathology
department, which is consistent with the frequency of 0.5%
reported by others.2–4 Related to the number of deliveries, this
frequency was estimated at 0.07% in our study, double the
estimate of 0.03% by Bane et al.6 These variations may be
associated with the women’s ethnic origin and with the
indications for placental pathology examinations, which vary
between hospitals. In any article, these lesions are rare.
In our series, the increased risk of IUFD in the case group
was in accordance with the stillbirth rate estimated at 17% to
50% in the literature.3,4,12 The frequency of severe IUGR
reached 93%, which is much higher than for other placental
diseases. In comparison, the frequency of severe growth
restriction (below the third percentile) at our hospital is 30%
among the placentas of women with preeclampsia13 and 61%
among the placentas with chronic histiocytic intervillositis.14
Accordingly, severe growth restriction is the essential clinical
characteristic of MFD. This strong association has already been
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L. Devisme et al.
326
stressed, with growth restriction rates ranging from 31% to
100%, depending on the author.2–6,12 Some portion of these
variations may be explained by the different curves and cut
off points used.
The cases of growth restriction observed in our series were
mainly vascular placental, because 60% of them had abnormal
umbilical artery Doppler spectra, including more than 15%
with reverse flow or absent diastole. On the other hand, the
uterine Doppler spectra did not differ significantly from those
of the control group, a finding that does not support the
existence of maternal vascular damage. The preeclampsia rate
observed in our study was 18%: seven cases, only two severe.
This rate is moderate and close to the 20% found in women
with isolated growth restriction and abnormal umbilical
Doppler findings or among compromised fetuses between 24
and 36 weeks for whom the advantage of immediate delivery
was uncertain.15,16 This observation thus points in the same
direction as a impairment in the intraplacental blood flow in
the intervillous space and not a primary reduction in the
uteroplacental circulation.
Several authors have mentioned the association between
MFD and some autoimmune diseases, especially the
antiphospholipid syndrome.17,18 The association with these
diseases was significant in our series, although it concerned
only 13% (n = 5) of the women. Because each had a different
autoimmune disease, it is impossible to associate MFD onset
with any particular one.
Massive perivillous fibrin deposition can be definitively
diagnosed only by pathology examination, retrospectively.
Although some hyperechogenic placental features have been
described, potentially associated with oligohydramnios,12
there is no marker or antenatal sign specific for this disease.
Elevated maternal serum alpha-fetoprotein equal to or greater
than 2.5 MoM was found in almost one third of the cases in our
series. These high levels have long been known to be
associated with an excess of placental diseases, growth
restriction and IUFD,19 probably because of early and severe
thrombo-occlusive placental lesions. Although elevated
alpha-fetoprotein is not specific, it can be used as an early
marker of recurrence.20–22 Nonetheless, no data have been
published about the sensitivity of this examination. In our
study, a diagnosis of MFD was never mentioned during the
327
prenatal period. In practice, because of the risk of recurrence
in following pregnancies, the clinical management is
important but difficult and not well established so far. Dosage
of second trimester maternal serum alpha-fetoprotein,
ultrasound monitoring of fetal growth and ultrasounds
targeted to the placenta may be helpful to detecting a
recurrence and to provide an appropriated neonatal care.
Like all case–control studies, our analysis has several
limitations. In view of the absence of any obstetric pathology
in most of these control patients, some laboratory data,
velocimetric (Doppler) findings and most of the placental
examinations were unavailable for this group. Nonetheless,
the comparison with a control group is a strong point of our
study and makes it possible to demonstrate the highly
abnormal nature of these placental lesions once they reach
25% of the placental surface.
CONCLUSION
In our series, 88% of the neonates had severe growth
restriction, and half were born preterm. The rate of
intrauterine death was high at 15%, still higher than the 10%
risk of IUFD in cases of FGR with abnormal umbilical Doppler
or uncertain need for immediately delivery.15 To our
knowledge, no other placental pathology is associated with so
high a rate of growth restriction and of IUFD. Although rare –
less than 1% of the placental examinations in our series –
this pathology must be considered in cases of severe
apparently vascular growth restriction and normal maternal
uterine Doppler, especially if serum alpha-fetoprotein was
measured and found high during the second trimester of
pregnancy.
WHAT’S ALREADY KNOWN ABOUT THE TOPIC?
• Massive perivillous fibrin deposition is a rare idiopathic disorder
associated with a high risk of intrauterine growth restriction and
pregnancy loss.
WHAT DOES THIS STUDY ADD?
• Our study quantifies the risk of severe growth restriction and
intrauterine death regardless of the extent of the lesion.
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