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360 Non-neoplastic Lesions of the Placenta, Pathology of the Placenta
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Molecular Features
Genetic testing is not used routi nely in the diagnosis of DVH.
Differential Diagnosis
Distal villous distribution varies somewhat, and
is normally decreased in the subchorionic areas
and the periphery of the placental disc. For this
reason, be sure to follow the recommended definitions of DVH for diagnosis and sampling as
outlined in the Amsterdam consensus (fullthickness sections taken from the central twothirds of the disc) (Khong et al. 2016).
Late: Accelerated Villous Maturation
Synonyms
Placental villous hypermaturation; Villous
hypermaturity.
Definition
Maturation of the terminal villi beyond what is
expected for the gestational age.
Clinical Features
• Incidence
Accelerated villous maturation (AVM) is asso-
ciated with preeclampsia and preterm labor
(Khong et al. 2016).
• Age
The number of villi with syncytial knots is one
of the elements used to judge placental matu-
ration. The average percentages of villi with
syncytial knots have been shown to be 28% at
term (37–40 weeks), 21–22% at 35–36 weeks,
~18% at 34 weeks, 13–15% at 27–33 weeks,
and ~5–11% at 20–26 weeks; however, overlap
is seen in the ranges of villi with syncytial
knots between gestational ages (Loukeris
et al. 2010).
• Sex
AVM has not been shown to be associated with
a particular fetal sex.
• Site
Terminal villi of the lower (basal) two-thirds of
the placental parenchyma.
• Treatment
Treatment varies depending on the underlying
clinical syndrome, symptoms, and severity. If
evidence of severe global/partial maternal vascular malperfusion is seen, the following may
be indicated in clinical management: evaluate
maternal cardiovascular status, glucose tolerance, thrombophilia, and renal function; suggest
weight loss if applicable; consider aspirin therapy, uterine artery Doppler, early third-trimester
placental ultrasounds, and early delivery in subsequent pregnancies (Redline 2015).
• Outcome
AVM is associated with fetal growth restriction, preterm birth, and fetal death (Khong
et al. 2016; Morgan et al. 2013; Jaiman et al.
2020). Severe global/partial maternal
malperfusion recurs in 10–25% of subsequent
pregnancies (Redline 2015).
Macroscopy
Lesions associated with maternal vascular
malperfusion are associated with placental hypoplasia and are often seen concurrently with placental infarction and retroplacental hemorrhage
(discussed in further detail below) (Khong
et al. 2016).
Microscopy
AVM is characterized by terminal villi that are
small or short and with increased syncytial knots
for gestational age (Khong et al. 2016) (Fig. 10
Syncytial knots are defined as multilayered aggregates with at least 5 syncytiotrophoblastic nuclei,
which are protruding from the villous surface and
are not in contact with any of the adjacent villi
(Loukeris et al. 2010). At term, knots on more
than 33% of villi is considered increased (Khong
et al. 2016).
AVM is usually seen in a pattern of crowded,
hypermature villi with intervillous fibrin deposition, alternating with areas of villous paucity, the
latter of which would qualify for a diagnosis of
distal villous hypoplasia if comprising at least
30% of one full-thickness slide (see above)
(Khong et al. 2016; Redline 2015). Foci of villous
agglutination (“microinfarcts”), clusters of
).
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Segmental/Complete
Villous Infarct(s)
Synonyms
Placental infarct(s); Villous infarction.
Definition
Lesions are characterized by villous collapse and
necrosis secondary to spiral artery thrombosis
(Becroft et al. 2002).
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 10 High power view of accelerated
villous maturation in a premature placenta with small terminal villi and increased syncytial knots
adherent distal villi and fibrin with fibrosis and
karyorrhexis of the villous stro ma, may also be
seen (Redline 2015; Ernst 2018).
Immunophenotype
Immunohistochemical stains are not routinely
used for the diagnosis of AVM.
Molecular Features
Genetic testing is not used routi nely in the diagnosis of AVM. However, one study demonstrated
that 11 genes (ATXN7, C15orf41, CISD1, CRH,
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 AVM had significant
shift in expression above “normal” in genes with
positive correlation to gestational age, and below
“normal” in genes with negative correlation,
suggesting that samples with AVM appear molecularly olderthan their true gestational age at delivery (Leavey et al. 2017).
Differential Diagnosis
Areas adjacent to placental infarction can show
villous crowding with increased intervillous fibrin
and other histologic changes, and thus should not
be used for the diagnosis of AVM (Khong
et al. 2016).
Clinical Features
• Incidence
Villous infarcts are seen in association with
thrombophilia (e.g., Factor V Leiden mutation,
prothrombin gene variant), autoimmune dis-
ease (e.g., systemic lupus erythematosus/anti-
phospholipid antibody syndrome), maternal
hypertension, and pre-eclampsia (Becroft
et al. 2002; Franco et al. 2011).
• Age
In term placentas, single infarcts, particularly
at the placental margin, are not unusual; how-
ever, any infarct in a preterm placenta is con-
sidered abnormal (Redline 2015; Khong
et al. 2016).
• Sex
Placental infarction has not been shown to be
associated with a particular fetal sex.
• Site
Placenta disc, particularly the basal
parenchyma.
• Treatment
Treatment varies depending on the underlying
clinical syndrome, symptoms, and severity.
• Outcome
Villous infarcts are associated with fetal
growth restriction, perinatal brain lesions, still-
birth, and intrauterine fetal demise (Becroft
et al. 2002
; Franco et al. 2011).
Macroscopy
Infarcts are classically firm, wedge-shaped
lesionsinvolving the basal parenchyma,sometimes
with central hemorrhage (Khong et al. 2016).
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They are initially red in color as acute infarcts and
become progressively more tan-yellow as they age
(Ernst 2018). Suspected infarcts should be quanti-
fied (number of lesions and estimated percentage of
total parenchymal volume) (Khong et al. 2016).
Aspecific subset of infarctions, infarction
hematomas, appears differently. They are rounded,
pale, tan-pink lesions with central hemorrhage/
hematoma and form due to disruption of
vasculopathic decidual arterioles, resulting in a
high-pressure bleed with necrosis of the surrounding villi due to rapid expansion of the intervillous
space and the subsequent compression. Because of
this gross appearance, they are also known as
rounded intraplacental hematomas (Fitzgerald
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 12 High power view of a placental
infarction with villous necrosis, crowding, and degenera tion
et al. 2011).
Lesions associated with maternal vascular
malperfusion, such as villous infarcts, are associated with placental hypoplasia (Khong et al. 2016).
Microscopy
Placental infarcts are characterized by villous
crowding and collapse into the intervillous space
(Fig. 11). Early lesions demonstrate loss of
nuclear basophilia and patchy infiltration by neutrophils. As infarcts age, coagulative necrosis
becomes more obvious, with progressive
pyknosis, karyorrhexis, loss of nuclear detail,
and degeneration of villi (Fig. 12) (Ernst 2018;
Khong et al. 2016).
When central hemorrhage is identified within
an infarct and histology confirms that it is encased
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 13 Low power view of an infarction
hematoma (a.k.a. hypertensive infarct) characterized by its
rounded shape with central hemorrhage/hematoma
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 11 Low power view of a placental
infarction (right) with villous necrosis and crowding
by infarcted villi, the term infarction hematoma
should be used (Fig. 13) (Khong et al. 2016).
Immunophenotype
Immunohistochemical stains are not routinely
used for the diagnosis of placental infarction.
Molecular Features
Genetic testing is not used routi nely in the diagnosis of placental infarction, though particular
maternal thrombophilic mutations may
increase risk.
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Differential Diagnosis
Intervillous thrombi and chorangiomas (discussed
below) may appear grossly similar to villous
infarcts, but appear histologically very different.
Villous infarction should also be differentiated
from massive perivillous fibrin deposition
(maternal floor infarction; see below), which
appears grossly as a tan-yellow band involving at
least 25% of the basal parenchyma and histologically will have less villous collapse with more pronounced fibrin filling the intervillous space.
Loss of Integrity
Synonyms
Placental abruption; Retroplacental hemorrhage/
hematoma.
Definition
Retroplacental hemorrhage arising from maternal vasculature, which can be arterial or venous
in nature, central or marginal in location, temporally acute or chronic, and falls into several
subtypes that are discussed below. Placental
abruption is a clinical diagnosis, while
retroplacental hemorrhage/hematoma is the
descriptor for the pathologic finding (Redline
2015; Khong et al. 2016).
Abruptio Placenta (Arterial)
Synonyms
Retroplacental hemorrhage/hematoma.
Definition
Spiral artery rupture leading to retroplacental
hemorrhage (Redline 2015; Khong et al. 2016).
Clinical Features
• Incidence
Abruptio placenta may be seen in association
with preeclampsia secondary to incompletely
remodeled spiral arteries due to ischemia-
reperfusion or atherosis, as well as vasoactive
drugs (e.g., cocaine, nicotine), shear stress
(e.g., trauma, uterine rupture), multiple
gestation, and acute chorioamnionitis
(Redline 2015; Oyelese and Ananth 2006).
Clinical placental abruption complicates
approximately 1% of deliveries with pathologic evidence of abruption in about 4% of
examined placentas (Oyelese and Ananth
2006).
• Age
Advanced maternal age is associated with
increased risk of clinical placental abruption
(Oyelese and Ananth 2006).
• Sex
Some literature has suggested that male fetal
sex is associated with an incre ased risk of
clinical placental abruption (Oyelese and
Ananth 2006).
• Site
Retroplacental, classically central/nonmarginal.
• Treatment
Variable, depending on the clinical presentation,
gestational age, and degree of maternal and fetal
compromise, ranging from increased clinical
monitoring to supportive treatment and blood
transfusion to emergent delivery. Most cases
lead to immediate delivery (Redline 2015).
• Outcome
Clinical placental abruption is associated
with increased risk of preterm premature rupture of membranes and preterm delivery, fetal
death, and maternal complications including
disseminated intravascular coagulopathy,
renal failure, obstetric hemorrhage sometimes necessitating blood transfusions, hysterectomy, and death (Oyelese and Ananth
2006).
Macroscopy
Usually non-marginal retroplacental hemorrhage
and/or hematoma with evidence of high-pressure
flow , including large volume, indentation of the
basal plate, and extension into the intervillous
space (Redline 2015; Khong et al. 2016). Acute
hemorrhage will appear as loosely adherent, fresh
blood clot on the maternal surface, while chronic
lesions will form firmer, more adherent hematomas
sometimes with adjacent villous infarction (Ernst
2018).
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Microscopy
Abruptio placenta is characterized microscopically by accumulation of blood beneath the basal
plate and dissection through the decidua,
compressing the intervillous space (Figs. 14 and
15). There is resultant villous crowding, conges-
tion, and intravillous hemorrhage (Figs. 14 and
16). Sometimes there are associated changes of
villous infarct. As hemorrhage becomes chronic,
it becomes organized into hematoma occasionally
with associated hemosiderin-laden macrophages.
When seen in association with acute
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 16 High power view of a placental
abruption with intravillous hemorrhage
chorioamnionitis, the term “inflammatory abruption” may be used (Redline 2015; Khong et al.
2016; Ernst 2018).
Immunophenotype
Immunohistochemical stains are not routinely
used for the diagnosis of abruptio placenta.
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 14 Low power view of a placental
abruption with hemorrhage dissecting the decidua (bottom
left) and overlying chorionic villi with intravillous
hemorrhage
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 15 High power view of a placental
abruption with hemorrhage dissecting the decidua
Molecular Features
Genetic testing is not used routinely in the
diagnosis of abruption. Though, there is significant recurrence risk with abruption and several
studies have suggested that there may be genetic
risk factors. One meta-analysis identified seven
polymorphisms with statistically significant
association with abruption: F5 Arg506Gln, F5
Met385Thr, F2 G2021 0A, MTHFR A1298C,
MTHFD1 Arg653Gln, NOS3 Glu298Asp, AGT
Met235Thr. The majority of the implicated
genes are involved in thrombophilia or hemodynamics (Zdoukopoulos and Zintzaras 2008).
Differential Diagnosis
Retroplacental hemorrhage should be differentiated grossly from blood clot naturally associated with the basal plate after delivery. In the
latter, it should easily dissociate from the placental disc a nd should not be associated with
indentation o f the maternal surface. See below
for descriptions of the other subtypes of
retroplacental hemorrhage.
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Marginal Abruption (Venous)
Acute
Synonyms
Retroplacental hemorrhage/hematoma.
Definition
Rupture of maternal veins at the edge of the placental disc (Redline 2015).
Clinical Features
• Incidence
Marginal abruption is associated with sudden
changes in uterine shape (e.g., rupture of mem-
branes, cervical insufficiency), poor anatomic
support (e.g., lower uterine segment implanta-
tion), increased maternal venous pressure, and
chorioamnionitis (Redline 2015).
• Age
Advanced maternal age is associated with
increased risk of clinical placental abruption
(Oyelese and Ananth 2006).
• Sex
Some literaturehas suggestedthat male fetal sex
is associated with an increased risk of clinical
placental abruption (Oyelese and Ananth 2006).
• Site
Retroplacental, marginal.
• Treatment
As opposed to the arterial bleed of abruptio
placenta (see above), the venous bleed from
marginal abruption generally leads to less
severe vaginal bleeding and may not necessi-
tate delivery (Redline 2015).
• Outcome
Acute marginal abruption is associated with
preterm birth, but only rarely fetal hypoxia
(Redline 2015).
Macroscopy
Marginal retroplacen tal and retromembranous hemorrhage with organizing blood clots/ hematoma and
green-brown discoloration of the placental membranes, consistent with chorioamnionic hemosiderosis when chronic. There may or may not be
compression of adjacent pare nchyma.
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 17 Subchorionic hemorrhage in a
case of marginal abruption
Microscopy
Marginal retroplacental and retromembranous
hemorrhage/hematoma with intravillous and
sometimes subchorionic hemorrhage (Fig. 17).
Immunophenotype
Immunohistochemical stains are not routinely used
for the diagnosis of acute marginal abruption.
Molecular Features
Marginal (venous) abruption is not generally associated with genetic factors, though, clinical placental abruption is not always differentiated into
subtypes and some literature has suggested potential genetic risk factors (see “Abruptio placenta”
above).
Differential Diagnosis
Retroplacental hemorrhage should be differentiated
grossly from blood clot naturally associated with
the basal plate after delivery. In the latter, it should
easily dissociate from the placental disc and should
not be associated with indentation of the maternal
surface. See above and below for descriptionsof the
other subtypes of retroplacental hemorrhage.
Chronic
Synonyms
Retroplacental hemorrhage/hematoma.
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Definition
Rupture of maternal veins that does not progress
immediately to delivery, resulting in weeks to
months of bleeding (Redline 2015).
Clinical Features
• Incidence
Marginal abruption is associated with sudden
changes in uterine shape (e.g., rupture of mem-
branes, cervical insufficiency), poor anatomic
support (e.g., lower uterine segment implanta-
tion), increased maternal venous pressure, and
chorioamnionitis (Redline 2015).
• Age
Advanced maternal age is associated with
increased risk of clinical placental abruption
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 18 Multiple hemosiderin-laden mac-
rophages within the chorionic plate in a case of chronic
marginal abruption
(Oyelese and Ananth 2006).
• Sex
Some literaturehas suggestedthat male fetal sex
is associated with an increased risk of clinical
placental abruption (Oyelese and Ananth 2006).
• Site
Retroplacental, marginal.
sometimes subchorionic hemorrhage. Hemosiderinladen macrophages can usually be ide ntified within
the placental membranes or along the chorionic
plate, and are often prominent (chorioamnionic
hemosiderosis; Fig. 18)(Redline2015; Khong
et al. 2016).
• Treatment
As opposed to the arterial bleed of abruptio
placenta (see above), the venous bleed from
marginal abruption generally leads to less
Immunophenotype
Immunohistochemical stains are not routinely used
for the diagnosis of chronic marginal abruption.
severe vaginal bleeding and may not necessitate delivery (Redline 2015).
• Outcome
Acute marginal abruption is associated with
preterm birth, but only rarely fetal hypoxia.
Chronic marginal abruption develops when
acute marginal abruption does not lead to delivery within weeks to months (Redline 2015).
Molecular Features
Marginal (venous) abruption is not generally
associated with genetic factors, though, clinical
placental abruption is not always differentiated
into subtypes and some literature has suggested
potential genetic risk factors (see “Abruptio pla-
centa” above).
Macroscopy
Marginal retroplacental and retromembranous
hemorrhagewith organizing blood clots/hematoma
and green-brown discoloration of the placental
membranes, consistent with chorioamnionic
hemosiderosis. Circumvallate membrane insertion
is also typical (Redline 2015).
Microscopy
Marginal retroplacen tal and retromembranous hemorrhage/organizing hematoma with intravillous and
Differential Diagnosis
Retroplacental hemorrhage should be differenti-
ated grossly from blood clot naturally associated
with the basal plate after delivery. In the latter, it
should easily dissociate from the placental disc
and should not be associated with indentation of
the maternal surface. See above for descriptions
of the other subtypes of retroplacental
hemorrhage.
Hemosiderin pigment is typically more granu-
lar (Fig. 19) and refractile than meconium;
Non-neoplastic Lesions of the Placenta, Pathology of the Placenta 367
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at high altitude, smoking and air pollution,
gestational hy pertension and preeclampsia,
diabetes mellitus, place ntal abruption, umbilical cord abnormalities, and fetal thrombotic vasculopath y (see be low) (Sung and
Baergen 2019). It has been estimated to affect
up to 7% of placentas (Sung and Baergen
2019).
• Age
Chorangiosis is found predominantly in term
placentas (Ogino and Redline 2000).
• Sex
Chorangiosis has not been shown to be associ-
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 19 The typical granular appearance of
hemosiderin pigment in macrophages within the placental
membranes
ated with a particular fetal sex.
• Site
Terminal and intermediate villi.
• Treatment
however, it can sometimes be difficult to make
this differentiation. Iron staining can be used to
discern hemosiderin-laden macrophages from
meconium-laden macrophages.
Treatment varies depending on the underlying
clinical syndrome, symptoms, and severity.
• Outcome
Chorangiosis is associated with lower Apgar
scores (Sung and Baergen 2019).
Fetal Stromal-Vascular Lesions
Macroscopy
Developmental
Chorangiosis is associated with increased placen-
tal weight (Sung and Baergen 2019), though it is
Definition
Placental lesions associated with abnormalities in
chorionic villous stromal and vascular develop-
worth considering that this might be confounded
by the fact that it is associated with maternal
diabetes.
ment and architecture (Redline 2015).
Microscopy
Villous Capillary Lesions
Defined by Altshuler in 1984 as at least 10 vas-
cular profiles in 10 or more terminal/intermedi-
Chorangiosis
ate villi in at least ten 10x microscopic fields of
3 or more random, noninfarcted areas of the
Synonyms
Villous hypervascularity.
placenta (“rule of 10s”)(Stanek2016;Sung
and Ba ergen 2019), though most ac cept the
criteria of more than 10 vascular profiles in
Definition
Hypercapillarization of terminal villi is thought to
result from placental hypoxia (Redline 2015;
10 or more terminal/intermediate villi in several
regions of the placenta (Ogino and Redline
2000)(Fig.20).
Stanek 2016).
Immunophenotype
Clinical Features
Muscle-specific actin can be used to differentiate
chorangiomas and chorangiomatosis from
• Incidence
Chorangiosis has been seen in association
with various conditions, including pregnancy
chorangiosis by highlighting pericytes, which
form a contiguous perivascular layer in the former
two diagnoses but not in the latter. Reticulin stain
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Clinical Features
• Incidence
Chorangiomas occur in 1 in 100 placentas
(Amer and Heller 2010).
• Age
Chorangiomas are identified most frequently at
32–37 weeks gestational age (Ogino and
Redline 2000).
• Sex
Chorangiomas have not been shown to be
associated with a particular fetal sex.
• Site
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 20 A focus of chorangiosis (at least
10 terminal/intermediate villi with at least 10 vascular
profiles)
Most often found at the margin of the placenta
disc just beneath the chorionic plate (Amer and
Heller 2010).
• Treatment
Several techniques have been used to
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).
Additionally, it should be noted that if CD31 or
CD34 are used to highlight vascular endothelium,
vascular profiles may be visualized at higher numbers compared to what is visualized on hematoxylin and eosin-stained slides (Ogino and Redline
2000; Stanek 2016).
devascularize chorangiomas, including suture
ligation, alcohol ablation, microcoil embolization, and laser thermocoagulation. Polyhydramnios can specifically be treated with
amniodrainage, and intrauterine transfusion
can be used to treat fetal hydrops. Occasionally, there can be spontaneous degeneration of
the tumor resulting in regression of symptoms
(Amer and Heller 2010).
• Outcome
In most cases, chorang iomas are small and of
no clinical significance. However, if more than
4 cm in size, they are associated with negative
Molecular Features
Genetic testing is not routinely used in the diagnosis of chorangiosis.
clinical impact, including polyhydramnios,
fetal cardiomegaly, hydrops fetalis, intrauterine growth restriction, preterm delivery, and
neonatal mortality. The latter is generally sec-
Differential Diagnosis
The differential for chorangiosis includes the
ondary to high output heart failure (Amer and
Heller 2010).
other villous capillary lesions, chorangioma, and
chorangiomatosis (see below).
Macroscopy
When large enough to be seen grossly,
Chorangioma
chorangiomas appear as nodular lesions most
often arising at the margin of the placental disc
Synonyms
Placental hemangioma.
or beneath the chorionic plate. Their cut surfaces
are varia ble in appearance, ranging from red-
brown and congested, to tan and fleshy, to
Definition
A benign placental vascular tumor arising in stem
villi (Redline 2015).
fibroma-like or even myxoma-like. Calcification
and infarction are common degenerative changes
(Amer and Heller 2010).
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Microscopy
Chorangiomas appear as well-defined masses
composed of capillary vascular channels in variable amounts of fibrous to collagenized stroma
surrounded by trophoblast which is occasionally
hyperplastic (Amer and Heller 2010) (Figs. 21
and 22).
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 mem-
branes around each capillary in chorangiosis
(Ogino and Redline 2000).
Molecular Features
Though no specific molecular features have been
elucidated, recurrence of chorangiomas in subse-
quent pregnancies and cooccurrence of fetal hem-
angiomas suggest genetic predisposition (Ogino
and Redline 2000).
Differential Diagnosis
The differential diagnosis includes the other vil-
lous capillary lesions, chorangiosis (see above),
and chorangiomatosis (see below).
Multifocal Chorangiomatosis
Synonyms
Diffuse chorangiomatosis.
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 21 Low power view of a cross section
of chorangioma abutting the basal plate (bottom)
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 22 Medium power view of a cross
section of chorangioma
Definition
A more pervasive developmental abnormality
characterized by hypervascularization of stem
and immature intermediate villi, sharing some
features with chorangiosis and placental
chorangioma (Redline 2015; Bagby and Redline
2011).
Clinical Features
• Incidence
Studies have demonstrated that chorangiomatosis affects 0.5–1% of placentas and is asso-
ciated with advanced maternal age and
multigravidity (Ogino and Redline 2000;
Bagby and Redline 2011).
• Age
Chorangiomatosis is most commonly seen in
preterm placentas (<32 weeks) and is associated with advanced maternal age (Bagby and
Redline 2011).
• Sex
Chorangiomatosis has not been shown to be
associated with a particular fetal sex.
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