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370 Non-neoplastic Lesions of the Placenta, Pathology of the Placenta
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• Site
Stem and immature intermediate villi.
• Treatment
There is no specific treatment for
chorangiomatosis.
• Outcome
Multifocal chorangiomatosis is associated with
increased likelihood of fetal congenital anomaly, fetal growth restriction, and stillbirth
(Bagby and Redline 2011).
Macroscopy
There are no gross findings associated with
chorangiomatosis.
Microscopy
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 24 Peripherally hypercapillarized stem
and intermediate villi, consistent with chorangiomatosis
Chorangiomatosis has histologic characteristics
that overlap with chorangioma, but with somewhat normal villous architecture rather than
forming a nodular lesion (Fig. 23)(Oginoand
Redline 2000). The hypervasc ula ri ty of the
related to placental chorangioma and is character-
ized as a chorangioma-like lesion extending
directly into surrounding stem villi (Bagby and
Redline 2011).
lesion comes from peripheral hypercapillarization of mature stem and immature
intermediate villi (Fig. 24) (Amer and Heller
2010;Redline2015). Dysmorphic villi are seen
at increased frequency in placentas with multifocal chorangiomatosis (Bagby and Redline
2011).
Localize chorangiomatosis (“wandering
chorangioma”) is thought to be more closely
Immunophenotype
Muscle-specific actin can be used to differentiate
chorangiomas and chorangiomatosis from
chorangiosis by highlighting pericytes, which
form a contiguous perivascular layer in the former
two diagnoses but not in the latter. Reticulin stain
demonstrates a similar staining pattern in both
chorangiomas and chorangiomatosis – a loose
network of reticulin fibers – while it highlights
individual, thin, well-defined basement membranes around each capillary in chorangiosis
(Ogino and Redline 2000).
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 23 Enlarged, hypervascular stem and
intermediate villi with somewhat normal villous architecture, consistent with chorangiomatosis
Molecular Features
The association of multifocal chorangiomatosis with fetal congenital anomalies and dysmorphic villi suggests an underlying development
abnormality, though no specific molecular features have b een identified (Bagby and Redline
2011).
Differential Diagnosis
The differential diagnosis for chorangiomatosis
includes the other villous capillary lesions,
chorangiosis, and placental chorangioma (see
above).
Non-neoplastic Lesions of the Placenta, Pathology of the Placenta 371
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Villous Architectural Abnormalities
Delayed Villous Maturation (Maturation
Defect)
Synonyms
Distal villous immaturity; Variable villous maturation; Villous dysmaturity; Villous/placental maturation defect (Redline 2015; Khong et al. 2016).
Definition
Lack of maturation of distal villi in term or late
preterm placentas characterized by centralized
capillaries and reduced vasculosyncytial membrane formation (Redline 2015; Khong et al.
2016; Higgins et al. 2011).
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 25 Delayed villous maturation, char-
acterized by chorionic villi overall large for gestational age
with excessive stoma and centrally placed capillaries
Clinical Features
Macroscopy
• Incidence
Delayed villous maturation (DVM) is associated with multiparity, pregestational and gestational diabetes, and chronic umbilical cord
Placentas with DVM tend to have a decreased
fetoplacental weight ratio and placental weight
greater than 90th percentile for gestational age
(Redline 2012, 2015).
obstruction (Redline 2015; Higgins et al.
2011). Studies have identified it in around 6%
of placentas submitted for histopathologic
examination (Higgins et al. 2011).
• Age
Usually seen after 36 weeks and rarely before
34 weeks gestational age (Khong et al. 2016).
• Sex
DVM has not been shown to be associated with
a particular fetal sex.
• Site
Microscopy
DMV is characterized by a monotonous population of (at least 10) villi with excessive villous
stroma and centrally placed capillaries with
decreased vasculosyncytial membranes (Fig. 25).
At least 30% of one full-thickness slide should be
involved. It is graded as focal if present in only
one full-thickness section, and diffuse if present in
two or more full-thickness sections (Redline
2015; Khong et al. 2016).
Distal villi.
• Treatment
The following may be indicated in clinical
management if DVM is identified in placental
evaluation: maternal diabetes screen, suggest
weight loss if applicable, perform thirdtrimester fetal movement counts, and consider
delivery prior to 40 weeks gestational age in
subsequent pregnancies (Redline 2015).
Immunophenotype
Immunohistochemistry is not routinely used for
the diagnosis of DVM. Though, CD15 staining in
distal villous endothelial cells has been shown to
reflect physiologic immaturity or delayed maturation, while its expression is decreased in physiologically mature placentas and those with
accelerated maturation (Seidmann et al. 2014).
• Outcome
DVM is associated with fetal growth restriction and an increased risk of fetal and neonatal
death (Redline 2015; Higgins et al. 2011;
Jaiman et al. 2020).
Molecular Features
Genetic testing is not routinely used in the diagnosis of DVM. However, one study demonstrated
that 11 genes (ATXN7, C15orf41, CISD1, CRH,
N
372 Non-neoplastic Lesions of the Placenta, Pathology of the Placenta
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DAPK1, ECHS1, KMT2C, LPL, MTMR4,
PTPRB, RAB38) showed significant linear corre-
lation with pregnancy trimester/gestational age in
placentas with normal villous maturation, and that
samples from placentas with DVM had significant
shift in expression of four of these genes (ATXN7,
DAPK1, KMT2C, and MTMR4) below “normal”
in those with positive correlation to gestational
age, and above “norm al” in those with negative
correlation, suggesting that samples with DVM
appear molecularly younger than their true gestational age at delivery (Leavey et al. 2017).
Differential Diagnosis
The villi in DVM resemble those of a physiologically immature placenta, and thus the gestational
age should be kept in mind when making a histologic assessment. It has been recommended that
stages of maturation be used (typical histology for
less than 25 weeks ¼ very immature,
25–33 weeks ¼ immature, 34–38 weeks ¼ slightly
immature, and 39 weeks or more ¼ mature) to
assist with correlating gestational age with
expected villous morphology (Redline 2012).
Dysmorphic Villi
Synonyms
Atypical/abnormal villous morphology.
Definition
Villous archi tectural abnorm alities classically
seen in the setting of aneuploidy (Redline 2015).
placental mosaicism, placental mesenchymal
dysplasia (see below), fetal growth restriction,
and fetal developmental abnormalities (Dicke
et al. 2009; Carreon and Roberts 2020).
• Age
The majority of the literature regarding dysmorphic villous morphology revolves around
spontaneous abortions with aneuploidy, most
of which occur in the first trimester (Genest
et al. 1995; Redline et al. 1999). However,
villous dysmorphism is also seen to varying
degrees later in pregnancy, even at full-term
(Carreon and Roberts 2020).
• Sex
While dysmorphic villi on their own are not
associated with a particular fetal sex, placental
mesenchymal dysplasia, which by some is
thought to be a dramatic example of this pattern (Redline 2015), has a female predominance (Pawoo and Heller 2014).
• Site
Chorionic villi.
• Treatment
Not applicable.
• Outcome
As dysmorphic villous morphology is a predictor of aneuploidy and other genetic abnormalities, it is associated with spontaneous
abortion, fetal growth restriction, and other
placental and fetal developmental abnormalities (Genest et al. 1995; Redline et al. 1999;
Dicke et al. 2009; Carreon and Roberts
2020).
Clinical Features
• Incidence
Approximately 15% of clinically recognized
pregnancies end in early spontaneous abortions, and approximately half of them have
chromosomal abnormalities (Genest et al.
1995). Only a subset (17–25%) of these may
demonstrate abnormal villous morphology,
though when they do it is a sensitive predictor
of aneuploidy (Genest et al. 1995; Redline
et al. 1999). Dysmorphic villi are also seen in
placentas later in pregnancy in the setting of
aneuploidy and other genetic abnormalities,
Macroscopy
Placentas with aneuploidy and other genetic
abnormalities may demonstrate gross abnormalities, such as being small or large for gestational
age, or having a single umbilical artery.
The specific gross features of placental mesen-
chymal dysplasia are described below.
Microscopy
Villous architectural abnormalities, including
irregular contours, trophoblast inclusions, cystic
degeneration, edema, stromal overgrowth,
proximal-distal villous disproportion, abnormal
vascular patterning, and trophoblast hyperplasia
Non-neoplastic Lesions of the Placenta, Pathology of the Placenta 373
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(Figs. 26, 27, and 28) (Redline 2015; Genest et al.
1995; Redline et al. 1998).
The specific microscopic features of placental
mesenchymal dysplasia are described below.
Immunophenotype
Immunohistochemical stains are not routinely
used for diagnosis of dysmorphic villous morphology. However, it was recently discovered
that a subset of random clusters of dysmorphic
chorionic villi of third-trimester placentas demonstrate inverted discordant p57 expression (loss of
staining in the villous stromal cells, while
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 28 Dysmorphic villi with trophoblast
inclusions (arrows)
expression in the cytotrophoblast remains intact)
(Carreon and Roberts 2020).
Molecular Features
It has been p reviously reported that dysmorphic
villi are most commonly seen in spontaneous
abortus specimens with triploid karyotyp es, trisomies 7, 8, 13, 16, and 18, and monosomy
X (Redline et al. 1999), and that nonspecific trophoblast hyperplasia has been reported in the setting of trisomies 7, 15, and 22, monosomy X, and
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 26 Dysmorphic villi with irregular
contours and stomal hypercellularity
diandric triploidy (Redline et al. 1998).
The molecular features of placental mesenchymal
dysplasia are described below.
N
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 27 Dysmorphic villi with mild tro-
phoblast hyperplasia in a case of trisomy 21
Differential Diagnosis
Cases with dysmorphic villi should be differentiated from molar pregnancies (see the section on
gestational trophoblastic disease).
Placental Mesenchymal Dysplasia
Synonyms
Pseudopartial mole; Placentomegaly with massive hydrops of placental stem villi (Pawoo and
Heller 2014).
Definition
A rare placental stromal and vascular lesion characterized by placentomegaly, cystic dilation of the
374 Non-neoplastic Lesions of the Placenta, Pathology of the Placenta
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stem villi, and vascular abnormalities, sometimes
regarded as the most dramatic form of villous
dysmorphism (Faye-Petersen and Kapur 2013;
Pawoo and Heller 2014; Redline 2015).
Clinical Features
• Incidence
Placental mesenchymal dysplasia (PMD) is a
rare diagnosis (0.02% estimated incidence)
associated with Beckwith-Wiedemann syndrome (one-fourth to one-third of cases), transient neonatal diabetes mellitus, paternal
uniparental disomy 6, trisomy 13, and
Klinefelter syndrome (Faye-Petersen and
Kapur 2013; Pawoo and Heller 2014).
• Age
PMD has not been associated with a particular
maternal age.
• Sex
PMD has a female predominance (3.6–4.0:1);
the additional X chromosom e in Klinefelter
syndrome allows for male survival (see molecular features for additional information) (FayePetersen and Kapur 2013; Pawoo and Heller
2014).
• Site
Stem villi, chorionic plate vessels.
• Treatment
Not applicable.
• Outcome
Associated with intrauterine fetal growth restriction and fetal demise (Pawoo and Heller 2014).
Beckwith-Wiedemann syndrome includes
macrosomia, macroglossia, hemihyperplasia,
visceromegaly, abdominal wall defects, characteristic facies, renal anomalies, adrenal cytomegaly , and an increased risk of childhood
cancer (Faye-Petersen and Kapur 2013;GaillotDurand et al. 2018). Outside of BWS, PMD has
also been associated with fetal/infant hamartomas of the liver and lung, and hemangiomas
of the liver and skin (Faye-Petersen and Kapur
2013).
parenchyma will have scattered cystic structures,
resembling a partial mole. Stem villous vessels are
dilated and tortuous with occasional thrombosis.
The fetus is often structurally normal (FayePetersen and Kapur 2013; Pawoo and Heller 2014).
Microscopy
The typical histologic findings include enlarged,
fibromatous or edematous stem villi with cisterns
(Fig. 29) and/or abnormal, thick-walled vessels
(Fig. 30). Terminal villi are generally normal in
appearance; however, other villous capillary
lesions (e.g., chorangiosis, chorangioma,
chorangiomatosis) can be seen concurrently
(Faye-Petersen and Kapur 2013; Pawoo and
Heller 2014).
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 29 Enlarged villuswith central cistern
Macroscopy
Grossly, PMD presents with placentomegaly
(enlarged, thickened placental disc). The
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 30 Edematous villus with abnormal,
thick-walled vessels
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Immunophenotype
P57 is paternally imprinted and normally
expressed on the maternal allele of chromosome
11p15. In PMD, normal-appearing villi will demonstrate a normal staining pattern for p57 in which
both the villous stromal cells and cytotrophoblast
are positive. A subset of abnormal villi may show
loss of staining in the villous stromal cells, while
expression in the cytotrophoblast remains intact.
This is called a “discordant” staining pattern, as it
is the inverse of what is seen in a complete
hydatidiform mole (CHM), in which loss of
staining is seen in the cytotrophoblast (FayePetersen and Kapur 2013; Pawoo and Heller
2014).
Molecular Features
Cases of PMD demonstrate a diploid karyotype
(~80% 46,XX; ~20% 46,XY) with androgenic/biparental mosaicism identified in most cases. The pathogenesis of PMD is not completely understood,
though two possible pathways have been suggested.
In the first, fertilization is normal, but the initial
mitosis is abnormal, possibly due to failure of replication of the maternal genome prior to the first
cleavage with segregation of the paternal genome
and eventually leading to a diploid androgenetic
lineage. In the second pathway, the ovum is fertilized by two spermatozoa, with generation of one
daughter cell that is normal and one with paternal
disomy (Faye-Petersen and Kapur 2013; Pawoo and
Heller 2014; Kaiser-Rogers et al. 2006).
The genetic locus for Beckwith-Wiedemann
Syndrome (BWS) is on 11p15.5, and mosaic segmental loss of 11p15.5 gene imprinting has also
been associated with PMD. This region includes
the following genes: insulin growth factor 2 (IGF-
2; paternally expressed), H19, CDKN1C (encodes
KIP2
p57
; paternally silent), KCNQ1, and
KCNQ1OT1 (Faye-Petersen and Kapur 2013;
Gaillot-Durand et al. 2018).
trophoblastic proliferation/hyperplasia and
pseudoinclusions should be absent. These areusually conspicuous in molar pregnancies. Additionally, the fetus is often structurally normal besides
being growth-restricted in PMD, while the fetus in
a PHM is usually anomalous (an embryo/fetus a
rarely present in CHM). Finally, cases of PMD
will show a diploid karyotype usually with androgenetic/biparental mosaicism, while PHM will be
triploid. However, CHM will also be diploid.
Immunohistochemistry can be used to help differentiate between PMD and CHM. Because CHM is
diandric, less than 10% of villous cytotrophoblast
and stromal cells will express p57, as opposed to
the pattern described above for PMD. PHM will
demonstrate normal p57 staining (Faye-Petersen
and Kapur 2013; Pawoo and Heller 2014).
Malperfusion
Fetal Vascular Malperfusion
Synonyms
Fetal thrombotic vasculopathy; Fetal vascular
obstructive lesions (Redline and Ravishankar
2018).
Definition
Fetal vascular malperfusion (FVM) encompasses a
collection of lesions resulting from obstruction of
fetal blood flow.It can be divided into two patterns,
global/partial and segmental/complete, and can be
graded as low grade or high grade. Global/partial
FVM is usually associated with partial umbilical
cord obstruction, leading to lesions across much of
the placental parenchyma. Segmental/complete
FVM usually arises from thrombosis of large
fetoplacental vessels, resulting in complete
obstruction of the vessel, but affecting only those
villi downstream of the obstruction (Redline 2015;
Khong et al. 2016).
N
Differential Diagnosis
PMD should be differentiated from molar pregnancies (see the section on gestational trophoblastic disease), in particular partial hydatidiform
moles (PHMs). While there may be enlarged,
edematous villi with cisterns in PMD,
Clinical Features
• Incidence
Global/partial FVM is associated clinically
most often with chronic partial/recurrent
376 Non-neoplastic Lesions of the Placenta, Pathology of the Placenta
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intermittent umbilical cord obstruction. It can
also be seen in the setting of fetal polycythemia, cardiac insufficiency, and coagulopathy
(Redline 2015; Khong et al. 2016; Redlin e
and Ravishankar 2018).
Segmental/complete FVM results from
thrombosis of large fetoplacental vessels.
While stasis secondary to umbilical cord
obstruction is also the most common risk factor, risk for fetal vascular thrombosis may be
increased secondary to fetal coagulopathy
(e.g., protein C or S deficiencies, factor
V Leiden or MTHFR mutations), maternal
IgG antiphospholipid or antiplatelet antibodies
(which can cross over into fetal circulation),
and fetal inflammatory response and villitis of
various etiologies (Redline 2015; Redline and
Ravishankar 2018).
• Age
FVM is not associated with a particular maternal or gestational age.
• Sex
FVM is not associated with a particular
fetal sex.
• Site
FVM can involve any part of the fetal vascular
tree, from the fetus to the distal villi.
• Treatment
Complete/segmental FVM may prompt the following in clinical management: maternal/neonatal thrombophilia work-up, diabetes screen, and
maternal platelet evaluation (Redline 201 5).
• Outcome
Global/partial FVM is associated with fetal
death and central nervous system (CNS) injury.
When it is extensive, complete/segmental
FVM is associated with fetal death, fetal
growth restriction, and CNS injury (Redline
2015; Redline and Ravishankar 2018).
entanglements. The placenta is usually normal to
large for gestational age (possibly due to chronic
congestion secondary to decreased umbilical
venous return) and the fetoplacental weight ratio
is usually reduced. It is also associated with vascular ectasia, which is often most prominently
noted in the chorionic plate vessels. The segmental/complete pattern is associated with thrombosis
of large fetoplacental vessels (Redline 2015;
Khong et al. 2016; Redline et al. 2021).
Microscopy
There is potential for overlap in histopathologic
patterns of FVM depending on the etiology of
obstruction in fetal blood flow.
The global/partial pattern of FVM demonstrates histologic features of increased venous
pressure/outflow obstruction, such as vascular
ectasia, intramural
fibrin deposition in large
fetoplacental vessels, as well as poor perfusion
of the distal villi resulting in small foci (< 5 villi
per focus) of avascular or karyorrhectic villi
(Redline 2015; Khong et al. 2016).
The segmental/complete pattern includes
thrombosis of large fetoplacental vessels
(chorionic plate or stem villous vessels), and/or
stem vessel obliteration (obliteration of the vessel
lumen of a stem vill ous characterized by loss of
endothelial integrity followed by fibroblast
ingrowth; Figs. 31 and 32). These lead to larger
collections of degenerating downstream villi
Macroscopy
The global/partial pattern of FVM is associated
with obstructive umbilical cord lesions, including
hypercoiling (>3 coils/10 cm), excessive length
(>70 cm), true knots, strictures, thin cords
(<8 mm diameter), abnormal insertion sites
(marginal/membranous or furcate), tethering by
amnionic webs, or longstanding fetal
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 31 Stem vessel obliteration with loss
of endothelial integrity and fibroblast ingrowth
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Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 32 Stem vessel obliteration with near
complete fibroblast ingrowth
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 33 Villous stromal-vascular
karyorrhexis
characterized by stromal-vascular karyorrhexis
(Fig. 33) and eventual loss of vascularity
(avascular villi; Fig. 34), a pattern that was previously referred to as fetal thrombotic vasculopathy
(FTV). The definition of the former is
karyorrhexis of fetal cells, which can include
endothelial cells, stromal cells, nucleated erythrocytes, and leukocytes, with preservation of the
surrounding trophoblast. The quantitative criteria
for diagnosing stromal-vascular karyorrhexis and
avascular villi are the same, requiring identification of 3 or more foci of at least 2–4 terminal villi
with the respective pathologic abnormality
(Redline 2015; Khong et al. 2016).
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 34 A cluster of avascular villi
High-grade FVM is defined by finding more
than one focus of avascular villi with a cumulative
assessment of greater than or equal to 45 avascular
villi over 3 sections or an average of greater than
15 avascular villi per section full-thickness section (with or without thrombus), or two or more
thrombi in chorionic plate or major stem villi, or
multiple nonocclusive thrombi (Khong
et al. 2016).
Thrombosis, when identified, should be characterized by whether it is arterial or venous, occlusive or n onocclusive, and where in the fetal
vascular tree it is located (e.g., umbilical cord,
chorionic plate, stem vessel). The distribution
and extent of avascular villi should be described,
with small foci comprising 2–4 avascular terminal
villi, “intermediate foci” comprising 5–10 villi,
and large foci comprising more than 10 villi
(Khong et al. 2016).
Immunophenotype
Immunohistochemical stains are not routinely
used for the diagnosis of FVM.
Molecular Features
Genetic testing is not routinely used in the diagnosis of FVM.
Differential Diagnosis
Involutional and degenerative changes, including villous karyorrhexis and loss of vascularity,
can occur following fetal death and should be
N
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considered in the differential when assessing
placentas in this context. FVM can result in
fetal death, therefore this distinction can be
important. Umbilical cord abnormalities, large
vessel changes (e.g., ectasia, thrombosis, intramural fibrin), and sharply circumscribed foci of
avascular villi, in contrast to the more cellular
pattern seen in postmortem villous involution,
are indicative of FVM. Villitis of unknown etiology (described b elow) can also lead to stem
vessel obliteration and avascular villi, most
often when there is high-grade inflammation.
A diagnosis of FVM should not be made if any
adjacent villi show a lymphocytic infiltrate
(Khong et al. 2016;Heider2017;Redline
et al. 2021).
Loss of Integrity
Definition
Placental lesions of loss of fetal vascular integrity
resulting in hemorrhage and edema (Redline
2015).
Large Vessel Rupture (Fetal Hemorrhage)
Synonyms
Fetal exsanguination (large volume hemorrhage).
Definition
Rupture (spontaneous or iatrogenic) of large
fetoplacental vessels (chorionic and umbilical)
resulting in fetal hemorrhage.
Clinical Features
• Incidence
Large vessel rupture is associated with marginal or velamentous umbilical cord insertion
(particularly in the setting of vasa previa), placental previa, and other morphologic variations with membranous vessels and placental
shape abnormalities. These may result in spontaneous rupture during labor and delivery, or
increased risk of iatrogenic trauma during
procedures such as amniotomy or amniocentesis. Spontaneous large vessel rupture, no
matter the anatomy, may also occur in the
setting of severe inflammatory processes such
as meconium myonecrosis (see “Meconium-
Associated Changes” below). Of note, multi-
fetal gestations and pregnancies from in vitro
fertilization are at higher risk for vasa previa
(Redline 2015; Schmidt et al. 2005; Oyelese
et al. 1999).
• Age
Large vessel rupture is not associated with a
specific maternal or gestational age, though it
is seen more often in the context of labor and
delivery, later in gestation.
• Sex
Large vessel rupture has not been associated
with a particular fetal sex.
• Site
Umbilical cord and chorionic vessels.
• Treatment
Early diagno sis and management of vasa pre-
via is crucial for prevention of poor outcome.
Assessment of risk factors in concert with
risk factors identified at the 20-week anat-
omyscanmaypromptevaluationbytrans-
vaginal scan with color Doppler to rule out
vasa previa. If vasa previa, placenta prev ia,
or a low-lying placenta is identified, a repeat
transvaginal ultrasound is performed
~32 weeks gestational age to confirm the
diagnosis (a subset of cases may resolve
spontaneously). It is recommended that preg-
nancies with placenta previa are delivered by
cesarean section at 37 wee ks. It is
recommended th at pregnancies with vasa
previa are monitored closely, admitted when
cervical length is less than 2.5 cm, given
steroids, and delivered by cesarean sec tion
at 35–36 weeks. If vaginal bleeding, rupture
of membran es, or labor occurs prior to this,
cesarean delivery is performed as indicated
(Oyelese 2019).
In the setting of a known fetal hemorrhage
and depending on the clinical context and
severity (often based on gestational age and
fetal monitoring), management may range
from observation, to interventions such as
fetal intrauterine transfusion, to emergent
cesarean section delivery (Schmidt et al. 2005).
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• Outcome
Fetal hemorrhage can lead to fetal anemia and
hypovolemia, and their sequelae. Though rare,
fetal exsanguination and death can occur
(Schmidt et al. 2005). Of note, if vasa previa
goes undiagnosed, fetal/neonatal mortality is
approximately 56% (Oyelese 2019).
Macroscopy
Careful gross examination can reveal transected
membranous vessels, torn or ruptured chorionic
vessels, and tears of the umbilical cords. These are
usually accompanied by hematomas or overlying
blood clot (Fig. 35), which can help guide dissection. Sometimes, serial sections of suspicious
areas are needed for microscopic confirmation
(Schmidt et al. 2005).
Microscopy
Cross sections of involved vessels will confirm
vascular tear/rupture. Underlying inflammatory
processes, such as acute chorionic vasculitis or
meconium myonecrosis, may also be seen
(Schmidt et al. 2005).
Immunophenotype
Immunohistochemistry is not routinely used to
diagnose large vessel rupture, though special
stains such as trichome and elastic stains may be
used to evaluate vessels.
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 35 Umbilical cord with velamentous
insertion, disrupted velamentous vessels, and perivascular
hemorrhage/hematoma in a case of fetal exsanguination
Molecular Features
Genetic testing is not routinely used in the diagnosis of large vessel rupture.
Differential Diagnosis
Prenatal/perinatal large vessel rupture should be
differentiated from disruption and damage to the
placenta that might occur postnatally. For example, tearing of the membranes and avulsion of the
umbilical cord can occur during delivery of the
placenta after delivery of the neonate. Review of
the clinical history and procedural notes is usually
necessary.
Small Vessel Rupture (Fetomaternal
Hemorrhage)
Synonyms
Intervillous thrombus.
Definition
Disruption of the trophoblastic cells lining the
chorionic villi, resulting in fetal hemorrhage into
the intervillous space where fetal red blood cells
can subsequen tly enter maternal circulation
(Lewis et al. 2017).
Clinical Features
• Incidence
Fetomaternal hemorrhage (FMH) likely occurs
in every pregnancy, most without apparent
clinical significance. Less than 1% of cases
lose more than 15 mL, and the most widely
accepted cutoff considered to be significant is
30 mL, as this is covered by the standard
300 mg of Rh immune globulin administered
to prevent Rh sensitization. This volume of
FMH is estimated to occur in 3 per 1000 births.
However, this may not correlate with risk of
fetal morbidity/mortality, and thresholds of
80 mL and 150 mL have been proposed for
“large” or “massive” FMH, with incidences of
0.9 and 0.2 per 1000 births, respectively. FMH
has been reported to occur in 1.6–11% of stillbirths (Wylie and D’Alton 2010; Lewis
et al. 2017).
N
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