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400 Non-neoplastic Lesions of the Placenta, Pathology of the Placenta
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preterm deliveries (20.8%) and is seen in 34%
of pregnancies with spontaneous preterm labor
and delivery, 29% of pregnancies with preterm
prelabor rupture of mem branes, and 70% of
late preterm births. Additionally, it was found
in 60% of cases with fetal death. This associated with fetal death has led to theories that CC
may represent a form of maternal anti-fetal
rejection (Kim et al. 2015a).
• Age
CC is not associated with a specific maternal or
gestational age.
• Sex
CC is not associated with a particular fetal sex.
• Site
Fetal chorionic layer.
• Treatment
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 62 Placental membranes with lym-
phocytic inflammatory infiltrate (Photomicrograph courtesy of Fusun Gundogan, MD [Women and Infants
Hospital of Rhode Island])
There is no specific treatment for CC to date.
• Outcome
CC is associated with spontaneous abortion,
villitis of unknown etiology (Katzman 2015;
Kim et al. 2010).
intrauterine growth restriction, preterm labor,
preterm prelabor rupture of membranes, and
preterm birth (Kim et al. 2010).
Immunophenotype
The lymphocytic infiltr ate is composed predomi-
Macroscopy
CC does not usually give rise to gross abnormalities (Katzman 2015).
nantly of T cells, which can be highlighted by
immunohistochemical stains for T-cell markers,
such as CD3 (Katzman 2015).
Microscopy
CC is characterized by a lymphocytic inflammatory infiltrate of the fetal chorionic surface or
within the chorionic layer of the free membranes
(Fig. 62). The infiltrate is often patchy, but usually
more prominent in the fetal surface than the free
membranes. It canbe graded and staged as follows:
• Grade 1: Greater than two foci of patchy
inflammation.
• Grade 2: Diffuse inflammation.
• Stage 1: Amniotropic lymphocytic infiltration
was limited to the chorionic trophoblast layer,
sparing the chorioamniotic connective tissue.
• Stage 2: Lymphocytic infiltration into the
chorioamniotic connective tissue present.
CC is can be seen concurrently with other
chronic inflammatory lesions, such as chronic
Molecular Features
Genetic testing is not routinely used in the diagnosis of CC. However, mRNA expression of
CXCl9, CXCL10, and CXCL11 (antiangiogenic T-cell chemokines) has been shown
to be significantly higher in chorioamniotic
membranes with CC compares to those without
(Kim et al. 2010
).
Differential Diagnosis
CC should be differentiated from acute chorioamnionitis. Notably, these can sometimes overlap,
suggesting an infectious etiology for a subset of
cases of CC.
Lymphoplasmacytic Deciduitis
Synonyms
Chronic deciduitis.
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Definition
Chronic inflammation of the decidua (of the basal
plate or free membranes) composed of lymphocytes and plasma cells, the etiology of which is
uncertain, though both chronic infection and
immune mechanisms have been implicated (Kim
et al. 2015a).
Clinical Features
• Incidence
Thought to affect 1–2% of all pregnancies
(Kim et al. 2015a).
• Age
Lymphoplasmacytic deciduitis is not associated
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 63 Decidua with lymphoplasmacytic
inflammation
with a specific maternal or gestational age.
• Sex
Lymphoplasmacytic deciduitis is not associated with a particular fetal sex.
• Site
Decidua.
• Treatment
There is no treatment for lymphoplasmacytic
Differential Diagnosis
Chronic inflammatory cells, predominantly lymphocytes, are normally present in small numbers
in the decidua and should not be mistaken for
lymphoplasmacytic deciduitis, which is a much
heavier infiltration most often with a component
of plasma cells (Khong et al. 2000).
deciduitis to date.
• Outcome
Eosinophilic/T-cell Fetal Vasculitis
Associated with preterm labor, fetal growth
restriction, and fetal death (Kim et al. 2015a;
Edmondson et al. 2009).
Synonyms
Eosinophilic T-cell Fetal Vasculitis; Eosinophilic/
Macroscopy
T-cell Chorionic Vasculitis.
Lymphoplasmacytic deciduitis does not give rise
to gross abnormalities.
Definition
A form of chorionic vasculitis characterized by an
Microscopy
A diagnosis of lymphoplasmacytic deciduitis can
be made if plasma cells are present within the
inflammatory infiltrate composed of eosinophils
and T-cells, the etiology and significance of which
is unclear (Fraser and Wright 2002).
decidua (Fig. 63) or, in the absence of plasma
cells, if lymphocytic inflammation is diffuse
Clinical Features
(Khong et al. 2000).
• Incidence
Immunophenotype
Immunohistochemical staining for CD138 can be
used to highlight plasma cells.
Studies have reported Eosinophilic/T-cell Vasculitis (E/TV) in 0.197–0.572% of placentas
examined (Fraser and Wright 2002; Jacques
et al. 2011).
Molecular Features
There are no well-characterized molecular features of lymphoplasmacytic deciduitis described
to date.
• Age
The majority of cases are identified in placentas delivered at term (>37 weeks gestational age) (Jacques et al. 2011).
N
402 Non-neoplastic Lesions of the Placenta, Pathology of the Placenta
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• Sex
One study showed a predominance of female
fetuses; however, this may be a reflection of the
small study group size (Jacques et al. 2011).
• Site
Fetal/chorionic vessels.
• Treatment
Not applicable.
• Outcome
E/TV has not been shown to be associated with
any clinical maternal conditions or fetal outcomes (Fraser and Wright 2002; Jacques
et al. 2011).
Non-neoplastic Lesions of the Placenta, Pathology of
Macroscopy
There are no gross abnormalities seen in E/TV.
Microscopy
E/TV is often focal, involving a single chorionic
the Placenta, Fig. 65 Chorionic vessel with eosinophilic
and lymphocytic infiltrate radiating away from the fetal
surface (above the pictured field), toward the intervillous
space (below the pictured field) (Photomicrograph courtesy of Fusun Gundogan, MD [Women and Infants Hospital of Rhode Island])
vessel infiltrated by eosinophils, sometimes
accompanied by T cells (Fig. 64). Curiously, the
infiltrate usually radiates away from the fetal surface/amniotic fluid and toward the intervillous
space (Fig. 65). Mural thrombi can be seen in
association with this lesion. It may be seen in
Immunophenotype
Immunohistochemical staining for CD3 can be
used to highlight the T cells. Both CD4- and
CD8-positive T cells have been shown to be pre-
sent (Jacques et al. 2011).
association with other chronic inflammatory
lesions, such as villitis of unknown etiology
(Fraser and Wright 2002; Jacques et al. 2011).
Molecular Features
There are no well-characterized molecular fea-
tures of E/TV described to date.
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 64 Chorionic vessel infiltrated by
eosinophils and lymphocytes (Photomicrograph courtesy
of Fusun Gundogan, MD [Women and Infants Hospital of
Rhode Island])
Differential Diagnosis
E/TV should be differentiated from the chorionic
vasculitis seen in acute chorioamnionitis.
Chronic Histiocytic Intervillositis
Synonyms
Chronic intervillositis of unknown etiology;
Chronic intervillositis; Intervillitis (Bos et al.
2018); Massive perivillous histiocytosis.
Definition
A rare idiopathic inflammatory lesion character-
ized by a maternal intervillous histiocytic inflam-
matory infiltrate and associated with early fetal
death and a high rate of recurrence in subsequent
pregnancies (Redline 2015).
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Clinical Features
• Incidence
Chronic histiocytic intervillositis (CHI) has
been associated with maternal autoimmune
disease (e.g., Sjogren’s syndrome, systemic
lupus erythematosus, autoimmune thyroiditis,
celiac disease) (Mekinian et al. 2015;Chen
and Roberts 2018). It is rare, affecting less
than 1% of all pregnancies, and its prevalence
is not completely understood but is thought to
vary depending on gestational age (Chen and
Roberts 2018). It has been shown to affect 9.6
per 1000 spontaneous abortions, 0.6 per
1000 second and third-trimester placentas,
and 80 per 1000 patients with a history of
prior spontaneous abortion (Boyd and
Redline 2000).
• Age
Mothers affected by CHI do not appear to be of
advanced maternal age. Additionally, CHI
appears to be more prevalent in spontaneous
abortions in the first trimester (Boyd and
Redline 2015; Chen and Roberts 2018).
• Sex
CHI is not associated with a particular
fetal sex.
• Site
Intervillous space.
• Treatment
There is some evidence suggesting that aspirin,
heparin, and immunosuppressive therapies
may have some effect in decreasing adverse
pregnancy outcomes and increasing the likelihood of live birth (Mekinian et al. 2015;
Redline 2015).
• Outcome
CHI is strongly associ ated with miscarriage,
fetal growth restriction, preterm birth, and
early intrauterine fetal demise, and has the
highest rate of recurrence of any placental
lesion (Redline 2015; Mekinian et al. 2015;
Bos et al. 2018).
Microscopy
CHI is characterized by a maternal hist iocytic
infiltrate in the intervillous space without accom-
panying villitis of unknown etiology (described
above) and occasionally is seen in association
with maternal floor infarction (described below)
(Redline 2015). The following diagnostic criteria
have been proposed for CHI (of unknown
etiology):
Criterion I: An infiltrate is present in the
intervillous space.
Criterion II: Approximately 80% of the mononu-
clear cells in the intervillous space are CD68positive cells.
Criterion III: 5% or more of the intervillous space
should be occupied by an infiltrate.
Exclusion criterion:
Criterion IV: Cases with clinical or histopatholog-
ical signs of infection should be excluded (Bos
et al. 2018).
Immunophenotype
Immunohistochemistry for CD68 can be used to
highlight histiocytes (Fig. 66) (Boyd and Redline
2000; Bos et al. 2018).
N
Macroscopy
No specific gross abnormalities have been
described in CHI (Chen and Roberts 2018).
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 66 CD68 immunostain highlighting
clusters of histiocytes in the intervillous space
404 Non-neoplastic Lesions of the Placenta, Pathology of the Placenta
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Molecular Features
No definitive molecular features have been
described in CHI to date.
Differential Diagnosis
CHI should be differentiated from intervillositis
of infectious etiology.
Other Placental Processes
This section discusses placental lesions that do not
classically fall into the categories of vascular or
inflammatory processes as described above
(Redline 2015).
Massive Perivillous Fibrin(oid) Deposition
(Maternal Floor Infarction)
Synonyms
Diffuse perivillous fibrin(oid) deposition; Massive perivillous fibrin(oid) deposition; Maternal
floor infarction.
Definition
Maternal floor infarction (MFI) and massive
perivillous fibrin deposition (MPVFD) are a
spectrum of rare idiopathic lesions associated
with recurrent perinatal morbidity and mortality,
characterized (as the name implies) by widespread perivillous fibrin deposition w ith villous
entrapment and atrophy, rather than ischemic
injury (maternal floor “infarction” is a misnomer) (Redline 2015, 2021; Faye-Petersen and
Ernst 2013).
Clinical Features
• Incidence
MFI/MPVFD affect 0.028–0.5% of deliveries
(Faye-Petersen and Ernst 2013). It is associated with maternal autoimmune disease, thrombophilia, and gestational hypertension
(Redline 2015).
• Age
MFI/MPVFD have not been shown to be associated with a particular maternal age. Recurrent
MFI/MPVFD may be more common in first-
trimester spontaneous abortions compared to
second- and third-trimester placentas
(Katzman and Genest 2002).
• Sex
MFI/MPVFD are not associated with a particular fetal sex.
• Site
Maternal surface with variable, sometimes
transmural, extension into the middle and subchorial zones.
• Treatment
Not known.
• Outcome
Strongly associated with recurrent miscarri age,
severe fetal growth restriction, early fetal
death, preterm birth, and fetal CNS injury
(Redline 2015).
Macroscopy
Placentas are usually small-for-gestational age
with a firm, yellow-white, thickened-appearing
maternal surface. O ccasionally, MFI/MPVFD
result in a normal or increased weight due to
the heaviness of abundant fibrinoid and/or
extravillous cytotrophoblast proliferation.
Cross sections show a friable and granular
appearance with fibrinoid material deposited in
a lattice-like network or “ rind” from the basal to
subchorial zone (Faye-Petersen and Ernst
2013).
Microscopy
MFI/MPVFD are characterized by increa sed
perivillous/intervillous space fibrinoid deposi-
tion along the basal plate with varying degrees
of upward extension into the midzonal and sub-
chorionic regions (Fig. 67). The chorionic villi
can demonstrate variable histologic appearance
with atrophy and loss of histologic detail, as
well as loss of syncytiotrophoblasts and villous
vascularity (Fig. 68). MFI/MPVFD may be
accompanied by foci of villitis and
intervillositis, lymphoplasmacytic deciduitis,
and foci of true infarctio n. MFI and MPVFD
are terms often used interchangeably, as they
are thought to represent a spectrum of the same
pathologic process. Historically, classic MFI
was defined as involving the basal villi of the
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Molecular Features
There are no well-defined molecular features of
MFI/MPVFD to date.
Differential Diagnosis
MFI/MPVFD must be differentiated from normal
perivillous fibrinoid deposition and villous ische-
mia/infarction. Villous infarction is characterized
by collapse of villi and obliteration of the
intervillous space with necrosis of the villi,
whereas MFI/MPVFD demonstrates preserved
spacing between villi with much more prominent
perivillous fibrin and more atrophic/fibrotic villi
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 67 Perivillous fibrin with extension
into the midzonal region
rather than necrotic. The gross appearance of vil-
lous infarcts is also quite different, usually being
distinct triangular or rounded lesions.
The avascular villiof fetalvascular malperfusion
(a.k.a. fetal thrombotic vasculopathy) can resemble
those of MFI/MPVFD, but will have scant perivillous fibrinoid.
Finally, due to the variable presence of villitis
and intervillositis, MFI/MPVFD should also be
differentiated from chronic villitis and
intervillositis, including infectious etiologies,
villitis of unknown etiology (VUE), and chronic
histiocytic intervillositis (CHI) (discussed above).
The classic gross appearance and finding of perivillous fibrinoid deposition as the predominant
pattern helps in the diagnosis of MFI/MPVFD.
Additionally, MFI/MPVFD will not show stem
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 68 Chorionic villi surrounded by
perivillous fibrin with loss of histologic detail
villous vasculitis or thrombosis (as in VUE) and
will only have focal or patchy intervillous inflammation (Faye-Petersen and Ernst 2013).
N
entire materna l floor with a thickness of 3 mm or
greater in at least o ne slide, whereas MPVFD
was used to describe expansion of the lesioninto
the overlying parenchyma toward the fetal surface. Transmural MPVFD is defined as encasing
at least 50% of the villi on at least one slide , and
borderline MPVFD is defined as encasing
25–50% of the villi on at least one slide
(Redline 2015, 2021; Faye-Petersen and Ernst
2013).
Immunophenotype
Immunohistochemical studies are not typically
used in the diagnosis of MFI/MPVFD.
Abnormal Placental Weight or Shape
Synonyms
Abnormal fetoplacental ratio; Abnormal placental
surface shape; Accessory/succenturiate lobe;
Bilobed/bilobate/bipartite placenta; Circummarginate placenta; Circumvallate placenta; Multilobed/multilobate/multipartite placenta; Placenta
fenestrata; Placenta membranacea.
Definition
Normal placental shape is described as a round to
oval disc, measuring approximately 22 cm in
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diameter and 2 – 2.5 cm in thickness, with a centrally placed umbilical cord, inserting an average
of 9 cm from the disc edge (Rathbun and
Hildebrand 2021; Salafia et al. 2010). The
fetoplacental weight ratio (FPR) is the ratio of
fetal/neonatal birthweight to the placental weight,
which varie s depending on gestational age. Low
FPR is thought to be indicative of impaired placental function or impaired environment (Salafia
et al. 2007).
Clinical Features
• Incidence
Bilobed placentas occur in 2–8% and
succenturiate placentas occur in 5% of cases
(Rathbun and Hildebrand 2021). Accessory
lobes are associated with placental implantation
overlying leiomyomas, the cervical os, and areas
of prior surgery , as well as implantation within
the cornu (Rathbun and Hildebran 2021). Recent
studies have shownthat accessorylobes are more
common with in vitro fertilization (IVF) after
frozen embryo transfer (10.4%) compared to
fresh embryo transfer (5.2%) (Sacha et al.
2020), and bilobate placentas a re more common
after IVF in general (Salafiaetal.2012).
• Age
Accessory lobes are associated with advanced
maternal age (Rathbun and Hildebrand 2021).
It has been also shown that placentas that are
larger or thicker in the first trimester remain
that way at delivery (Salafia et al. 2012).
• Sex
Abnormal placental shape is not associated
with a particular fetal sex.
• Site
Placental disc.
• Treatment
No treatment for abnormal placental shape is
known to date. However, while modification of
placental development is unlikely , some theorize
that therapeutic interventions may be possible in
the future to counteract the effects of placental
dysfunction (Longtine and Ne lson 2011).
• Outcome
Abnormalities in placental proportions have
been shown to modify placental function and
efficiency. Irregular placental weight and shape
have been associated with lower fetal/neonatal
birthweight. Bilobed, multilobed, and
succenturiate placentas are associated with
increased risk of vasa previa and retained placen-
tal tissue. Circumvallate placentas are associated
with premature rupture of membranes, preterm
delivery , and placental abruption (Longtine and
Nelson 2011; Rathbun and Hildeb rand 2021).
Macroscopy
Abnormal placental shape with non-central umbilical insertion point. Accessory (or succenturiate)
lobes are lobes that develop in the membranes apart
from the main placental disc, connected by fetal
vessels running within the placental membranes
(Fig. 69
). Bilobed placentas are those with two
lobes of roughly equal size. Circumvallate and
circummarginate placentas are both extrachorial,
meaning a rim of placental tissue extends beyond
the vascular plate. The rim in circumvallate placentas is raised, while that of circummarginate
placentas is flat. Placenta membranacea is a rare
abnormality in which the placental disc is very
large and thin, due to aberrant covering of the
fetal membranes by chorionic villi (partially or
diffusely). Placenta fenestrate is also a rare abnormality, which is characterized by areas of atrophy,
lacking villous tissue. Usually the chorionic plate
remains intact, but rarely there is a true hole
(Rathbun and Hildebrand 2021).
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 69 Placental disc with accessory
(succenturiate) lobe (bottom left)
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Microscopy
Features of both maternal uteroplacental and
fetoplacental insufficiency have been described
in association with abnormal placental shape
(Salafia et al. 2010).
Immunophenotype
Abnormalities of placenta shape are not associated with a particular immunophenotype.
Molecular Features
It is thought that epigenetics contributes to fetal
programming, which likely involves its effect on
placental gene expression and/or placental function (Longtine and Nelson 2011).
Differential Diagnosis
Gross abnormalities of placental shape should be
differentiated from each other and from placental
disruption secondary to iatrogenic etiologies (e.g.,
disruptions of the disc during manual extraction).
Correlation with clinical , radiologic, and procedural notes is very important in this setting.
Abnormal Umbilical Cord Length, Shape, or
Insertion Site
Synonyms
Cord stricture; False knots; Furcate insertion;
Hypercoiled or hypocoiled umbilical cord; Marginal/Battledore insertion; Membranous/
velamentous insertion; Single umbilical artery;
True knots; Umbilical cord masses.
Definition
The umbilical cord should be centrally inserted on
the placental disc and located approximately 9 cm
from the disc edge on average (Sala fia et al. 2010).
Most measure 55–60 cm in length (Pinar and
Carpenter 2010).
Clinical Features
• Incidence
Velamentous insertion is seen in 0.5–1.5% of
placentas with a higher frequency in twin placentas (up to 9%). Marginal insertion is seen in
7% of placentas. True knots are seen in 0.5% of
placentas, but are more common in pregnancies with male fetuses and monoamnionic
twins, and those from multiparous mothers
(Pinar and Carpenter 2010).
• Age
Umbilical cord abnormalities are not associated with particular maternal or
gestational ages.
• Sex
True knots are more common in male fetuses
(Pinar and Carpenter 2010).
• Site
Umbilical cord.
• Treatment
Umbilical cord abnormalities may result in
fetal distress, necessitating urgent delivery.
While modification of placental development
is unlikely, some theorize that therapeutic
interventions may be possible in the future to
counteract the effects of placental dysfunction
(Longtine and Nelson 2011).
• Outcome
Eccentric umbilical cord insertion is thought
to negatively influence placental efficiency –
the more eccentric a cord, the less efficient
the placenta. Placentas with non-centrally
placed co rds tend to be thicker a nd heavier,
though the placental shape itself does not
appear to be otherwise altered. Marginal
and velamentous insertion, on the other
hand, are associated with s mall p lacentas.
All eccentric insertions appear to be associated with decreased birthweight.
Ve lamentous i nsertion and true knots are
seen in 1% of stillbirths, and true knots are
associated with a perinatal mortality rate of
8–11%. A recent study demonstrated that
19% of stillbirths were associated with
umbilical cord abnormality. Long umbilical
cords are associated with fetal entanglements, whereas short cords are associated
with decreased fetal movement, amniotic
bands, limb defects, and multiple malformation syndromes. Both hypercoiling and
hypocoiling are associated with stillbirth,
fetal intolerance to labor, and intrauterine
growth restriction (Longtine and Nelson
N
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Non-neoplastic Lesions of the Placenta, Pathology of
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 70 Placenta with velamentous umbil-
ical cord insertion
the Placenta, Fig. 71 Cross section of a two-vessel
umbilical cord (single umbilical artery)
vasculopathy (avascular villi and/or villous stromal
2011; Yampolsky e t al. 2009; Pinar and
karyorrhexis) (Tantbirojn et al. 2009).
Carpenter 2010;Hammadetal.2020).
Immunophenotype
Macroscopy
Velamentous cords are characterized by insertion
Immunophenotyping is not routinely used in the
diagnosis of umbilical cord abnormalities.
into the fetal membranes (Fig. 70), connected to
the placental disc by membranous fetal vessels.
Marginal (or Battledore) insertion is defined as
insertion at or within 2 cm of the disc edge.
Furcate umbilical cords demonstrate loss of
Wharton’s jelly before insertion into the disc,
resulting in exposure of the umbilical vessels.
Umbilical cord strictures are due to deficiency of
Molecular Features
Some umbilical cord abnormalities (e.g., short
cord, single umbilical artery) (Fig. 71) are associated with other congenital malformations, which
raises the possibility of an underlying genetic
aberration. Single umbilical artery specifically is
associated with aneuploidy.
Wharton’s jelly along the umbilical cord. False
knots are not actual knots, as opposed to true
knots, but instead are foci of umbilical vascular
ectasia. Abnormally long cords are defined as
>70 cm, and short cords are defined as <40 cm
at term. Hypercoiling and hypocoiling are defined
as 0.3 coils per centimeter and 0.1 coil per
centimeter, respectively. Masses of the umbilical
cord are rare. Those most commonl y seen are
Differential Diagnosis
Gross abnormalities of the umbilical cord and its
insertion should be differentiated from each other
and from disr uption and injury secondary to iatrogenic etiologies (e.g., avulsion of the cord during manual extraction). Correlation with clinical,
radiologic, and procedural notes is very important
in this setting.
benign, including hemangiomas, and cysts of
allantoic and vitelline duct remnants. Teratomas
can very rarely present as umbilical cord masses
(Pinar and Carpenter 2010).
Morbidly Adherent Placentas (Placenta
Accreta Spectrum)
Microscopy
Umbilical cord abnormalities can result in changes
secondary to restricted fetal blood flow, including
vascular ectasia, thrombosis, and fetal thrombotic
Synonyms
Invasive placentation; Placenta accreta spectrum
(PAS); Placenta accreta; Placenta increta; Placenta
percreta.
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Definition
Disorders of abnormal placentation due to failure
of decidualization and invasion of chorionic villi
and trophoblast into the uterine myometrium,
resulting in morbid adherence and retention of
placental tissue with maternal morbidity and mortality secondary to obstetrical hemorrhage (Hecht
et al. 2020).
Clinical Features
• Incidence
One in 272 reported in 2016, increasing from
1 in 2510–4017 in the 1970s and 1980s; incidence increased with each cesarean delivery
(Hecht et al. 2020).
• Age
There is an increased risk of PAS disorders
with advanced maternal age, though this may
be due to increased numbers of cesarean sections in the setting of higher gravity and parity
and increased frequency of uterine instrumentation compared to controls (Ernst et al. 2017).
• Sex
PAS disorders are not associated with a particular fetal sex.
• Site
Placental-myometrial interface.
• Treatment
Most commonly requires cesarean delivery
followed by total hysterectomy when there is
lack of uterine-placentalseparation. Antenatal
diagnosis is critical in order to allow for
proper management at the time of delivery,
which usually requires a multidisciplinary
care team (e.g., maternal-fetal medicine, pelvic surgery, urology, i nterventional radiology,
anesthesiology, critical care, neonatology,and
transfusion medicine). Conservative managementwithuterinepreservationispossibleina
small number of cases that have only focal placental adherence, with removal of placental or
uteroplacental tissues without hysterectomy.
Expectant management, where the placenta is
left partially or entirely in situ, is associated
with a high risk of morbidity and high risk of
recurrence (Society of Gynecologic Oncology
et al. 2018).
• Outcome
Associated with a high risk of maternal morbidity and mortality, particularly when it is not
diagnosed antenatally and managed by an
experienced clinical team (Society of Gynecologic Oncology et al. 2018).
Classifications
Abnormally Invasive Placenta (AIP)
Classification:
• Placenta accreta: a lack for decidua between
the placental villi and uterine myometrium
with abnormal adherence of the placental chorionic villi to the myometrium.
• Placenta increta: a lack for decidua between the
placental villi and uterine myometrium with
invasion of chorionic villi into the myometrial
wall.
• Placental percreta: a lack for decidua between
the placental villi and uterine myometrium
with invasion of chorionic villi into and
through the myometrial wall, breaching the
serosa and invading into surrounding structures (e.g., adipose tissue, bladder, colon)
(Collins et al. 2016, 2018).
International Federation of Gynecology and
Obstetrics (Fédération Internationale de
Gynécologie et d’Obstétrique/FIGO)
Classification:
Grade 1: Abnormally adherent placenta (placenta
adherenta or accreta)
• Clinical criteria:
• At vaginal delivery:
•
No separation with synthetic oxytocin
and gentle controlled cord traction.
• Attempts at manual removal of the placenta results in heavy bleeding from the
placenta implantation site requiring
mechanical or surgical procedures.
• If laparotomy is required (including for
cesarean delivery):
• Same as above.
• Macroscopically, the uterus shows no
obvious distension over the placental
bed (placental “bulge”), no placental tissue is seen invading through the surface
N
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