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410 Non-neoplastic Lesions of the Placenta, Pathology of the Placenta
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of the uterus, and there is no or minimal
neovascularity.
• Histologic criteria :
• Microscopic examination of the placental
bed samples from hysterectomy specimen
shows extended areas of absent decidua
between villous tissue and myometrium
with placental villi attached directly to the
superficial myometrium.
• The diagnosis cannot be made on
just delivered placental tissue
nor on random biopsies of the placental bed.
Grade 2: Abnormally invasive placenta
(Increta)
• Clinical criteria:
• At laparotomy:
• Abnormal macroscopic findings over the
placental bed: bluish/purple coloring,
distension (placental “bulge”).
• Significant amounts of hypervascularity
(dense tangled bed of vessels or multiple
vessels running parallel craniocaudally
in the uterine serosa).
• No placental tissue seen to be invading
through the uterine serosa.
• Gentle cord traction results in the uterus
being pulled inwards without separation
of the placenta (so-called the dimple sign).
• Histologic criteria :
• Hysterectomy specimen or partial
myometrial resection of the increta area
shows placental villi within the muscular
fibers and sometimes in the lumen of the
deep uterine vasculature (radial or arcuat e
arteries).
Grade 3: Abnormally invasive placenta
(Percreta)
• Grade 3a: Limited to the uterine serosa
• Clinical criteria:
• At laparotomy:
• Abnormal macroscopic findings on uter-
ine serosal surface (as above) and placental tissue seen to be invading through
the surface of the uterus.
• No invasion into any other organ, includ-
ing the posterior wall of the bladder
(a clear surgical plane can be identified
between the bladder and uterus).
• Histologic criteria :
• Hysterectomy specimen showing villous
tissue within or breaching the uterine
serosa.
• Grade 3b: With urinary bladder invasion
• Clinical criteria:
• At laparotomy:
• Placental villi are seen to be invading
into the bladder but no other organs.
• Clear surgical plane cannot be identified between the bladder and uterus.
• Histologic criteria :
• Hysterectomy specimen showing villous
tissue breaching the uterine serosa and
invading the bladder wall tissue or
urothelium.
• Grade 3c: With invasion of other pelvic tissue/
organs
• Clinical criteria:
• At laparotomy:
• Placental villi are seen to be invading
into the broad ligament, vaginal wall,
pelvic sidewall, or any other pelvic
organ (with or without invasion of
the bladder).
• Histologic criteria :
• Hysterectomy specimen showing villous
tissue breaching the uterine serosa and
invading pelvic tissues/organs (with or
without invasion of the bladder)
(Jauniaux et al. 2019).
Placenta Accreta Spectrum (PAS) Pathologic
Classification (from the Perinatal
Subcommittee of the Society for Pediatric
Pathology):
• PAS Grade 1 – noninvasive: grossly adherent
placenta by manual palpation. Myometrial
cross sections show a smooth placental–
myometrial interface and uniform myometrial
thickness without thinning.
• PAS Grade 2 – superficial invasion: cross sections show an irregular placental–myometrial
interface without involvement of the outer
myometrium (i.e., with preservation of at
least 25% of the wall thickness relative to the
uninvolved myometrium).
Non-neoplastic Lesions of the Placenta, Pathology of the Placenta 411
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Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 72 Placenta percreta with disruption
of the uterine serosa
• PAS Grade 3A – deep invasion: cross sections
show an irregular placental–myometrial interface with involvement of the outer
myometrium (i.e., with preservation of less
than 25% of the wall thickness relative to the
uninvolved myometrium) and intact uterine
serosal surface.
• PA S Gra de 3D – deep invasion with disruption of the serosa: deeply invasive placenta
with disruption of the uterine serosal surface
(‘D’ for deep invasion with disruption)
(Fig. 72).
• PAS Grade 3E – deep invasion with adherent
extrauterine structures: placental invasion into
adjacent organs (most commonly bladder) or
extrauterine fibroadipose tissue, confirmed by
microscopy (“E” for extrauterine invasion).
• Basal plate myometrial fibers (BPMF) – microscopic findings of myometrial smooth muscle
fibers adherent to the basal plate (Fig. 73) with
or without intervening decidua inall specimens
other than hysterectomies or en-block
uteroplacental excisions (e.g., delivered placentas, curetting specimens). Should be
reported with the following information:
• Stage:
• Stage 1 – decidual present.
• Stage 2 – decidua absent.
• Size (mm) – linear dimension along the
basal plate in the largest focus.
• Number of separate foci.
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 73 Adherent basal plate myometrial
fibers
• An explanatory note: “Note: BPMF may be
an incidental finding, but may confirm noninvasive PAS in the appropriate clinical setting. Stage 1 BPMF is more likely to be an
incidental finding than Stage 2 BPMF
(without intervening decidua). Clinical correlation is recommended” (Hechtetal.2020).
A standardized protocol for pathologic
evaluation and reporting can be implemented
to assist in diagnosis and classification
(Dannheim et al. 2016
).
Macroscopy
In addition to the abnormalities described in the
classifications above, PAS disorders are very
often associated with placenta previa and may be
associated with marked thinning of the lower
uterine segment, particularly at the site of previous cesarean section scar (Fig. 74) (Dannheim
et al. 2016; Society of Gynecologic Oncology
et al. 2018; Hecht et al. 2020). Other common
findings include lower placental weight compared
to controls, likely related to lower gestational age
at delivery, and grossly incomplete maternal surface (Ernst et al. 2017).
Microscopy
PAS is defined histopathologically by a lack of
decidua between the chorionic villi and uterine
myometrium (Fig. 75) with chorionic villi
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Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 76 A cytokeratin 7 immunostain
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 74 Cross sections showing deep pla-
cental invasion (arrow) with marked thinning of the lower
uterine segment (arrowhead) at the site of a prior cesarean
section scar
highlighting extravillous trophoblast within myometrium
perivillous fibrin), and evidence of hemorrhage
(e.g., remote retromembranous hemorrhage, subchorionic/intervillous thrombi) are also seen in
association with PAS (Ernst et al. 2017).
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 75 Chorionic villi in abutting
myometrium in a case of placenta accreta
adhering to and/or invading into the myometrium.
Sometimes the villi are not seen in direct contact
with the myometrium and instead a layer of extravillous trophoblast (EVT) and fibrin is present in
the intervening space. EVT is often seen endovascularly and adjacent to damaged myometrium
(Dannheim et al. 2016; Hecht et al. 2020).
Chronic basal villitis, basal chronic plasma cell
deciduitis, villous changes of maternal vascular
underperfusion (e.g., infarction, increased syncytial knots, villous agglutination, increased
Immunophenotype
Immunohistochemical staining for CD10 can be
used to highlight decidual cells and compared to
cytokeratin (Fig. 76) or GATA-3 staining, which
highlight extravillous trophoblast (Dannheim
et al. 2016; Hech t et al. 2020). Recently, soluble
fms-like tyrosine kinase 1 (sFlt-1) has been shown
to be downregulated in invasive placentation
(Shainker et al. 2017).
Molecular Features
There are no well-defined molecular features of
PAS disorders to date.
Differential Diagnosis
Thinning of the lower uterine segment and the area
of scar from previous cesarean section can occur
physiologically and should not be overinterpreted
as placental invasion. This can be differentiated
from PAS disorders by the presence of decidua
overlying the area of thinning without adherence
of chorionic villi to the myometrium or scar tissue
(Dannheim et al. 2016; Hecht et al. 2020).
Finally, it is important to correlate with clinical
notes and radiologic findings in the setting of
disruption of the uterine wall, as true percreta
Non-neoplastic Lesions of the Placenta, Pathology of the Placenta 413
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and iatrogenic/intraoperative disruption are not
always distinguishable based on histopathology
exam alone (Dannheim et al. 2016; Hecht
et al. 2020).
Meconium-Associated Changes
Synonyms
Acute mecon ium exposure; Continuous meconium exposure; Meconium myonecrosis;
Meconium-laden macrophages; Meconiumstained amniotic fluid; Particulate meconium.
Definition
Meconium is the first passage of stool of the
newborn. When it appears prior to birth or during
labor, it results in meconium-stained amniotic
fluid (MSAF). This may indicate fetal distress.
Acute meconium exposure has been defined by
the presence of placental epithelial changes, while
continuous exposure is defined by the presence of
meconium-laden macrophages (Tamayev
et al. 2020).
Clinical Features
• Incidence
Intrauterine meconium passage is seen in
10–15% of term births, with MSAF identified
in 27.1% of post term births, 16.5% of term
births, and 5.1% of preterm births (Cimic and
Baergen 2016; Tamayev et al. 2020).
• Age
Meconium-stained amniotic fluid is seen more
frequently with increasing gestational age, particularly in post-term births (Tamayev et al.
2020). There is no known association with
maternal age.
• Sex
Meconium exposur e is not associated with a
particular fetal sex.
• Site
Placental membranes and chorionic plate; placental macrophages.
• Treatment
Urgent delivery may be necessary due to fetal
distress.
• Outcome
Acute meconium exposure is associated with a
higher rate of non-reassuring fetal heart rate
and adverse neonatal outcome. Continuous
exposure is associated with decreased placen-
tal weight (10th percentile for gestational age)
and higher frequency of cesarean delivery.
Neonatal MSAF inhalation can result in meco-
nium aspiration syndrome (MAS), resulting in
neonatal inflammatory pulmonary injury. This
is seen in approximately 5% of births with
MSAF. Longstanding meconium exposure
can result in myonecrosis of the umbilical and
chorionic vessels, which is associated with
umbilical vasoconstriction, fetal distress, intra-
uterine growth restriction, and intrauterine
fetal demise (Tamayev et al. 2020 ; Cimic and
Baergen 2016).
Macroscopy
Continuous or more longstanding meconium
exposure, when depositing on the membranes
and chorionic plate and/or taken up by placental
macrophages, results in green-brown discoloration of the fetal surface and some times the umbilical cord. Continuous meconium exposure is also
associated with decreased placental weight
(Tamayev et al. 2020).
Microscopy
Particulate meconium is orange-brown, extracellular, amorphous material that can be seen on the
surfaces of the placental membranes and chorionic plate. Meconium-la den macrophages typically appear light-brown and foamy, and most
often are seen within the stroma of the membranes
(Fig. 77) and chorionic plate, though they can be
identified in deeper layers down to the decidua.
These are felt to be a measure of longstanding
(continuous) meconium exposure. Meconium
present in the amniotic fluid will clear eventually,
through ingestion by placenta macrophages,
ingestion of amniotic fluid by the fetus, absorption
into the fetal blood, and transfer to the mother
(Tamayev et al. 2020).
The epithelial changes of acute meconium
exposure are characterized by columnar shape of
the amniocytes as well as vacuolar degeneration
N
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Molecular Features
There are no well-defined, specific molecular features of meconium-associated changes described
to date.
Differential Diagnosis
Meconium-laden macrophages should be differentiated from hemosiderin-laden macrophage.
Hemosiderin tends to be more refractile, while
meconium appears light brown and foamy.
However, this difference can sometimes be
challenging to discern, and stains can be of
assistance.
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 77 Meconium-laden macrophages
within the placental membranes
Acute funisitis and chorionic vasculitis secondary to meconium should be differentiated from the
effects seen in the setting of amniotic fluid infection/
acute chorioamnionitis (Grossman et al. 2019).
Increased Circulating Nucleated Red Blood
Cells
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 78 Amniocytes with columnar shape,
pigmentation, and vacuolization, consistent with acute
meconium exposure
(Fig. 78) (Tamayev et al. 2020). Vascular wall
myonecrosis is characterized by rounding up of
the muscle cells with cytoplasmic eosinophilia,
and nuclear pyknosis and/or loss of nuclear basophilia (Cimic and Baergen 2016). Features of both
fetal and maternal vascular malperfusion may also
be seen (Grossman et al. 2019).
Immunophenotype
Zinc coproporphyrin I (ZnCP-I) monoclonal antibody can be used to stain meconium-laden macrophages (Furuta et al. 2012). An iron stain can be used
to differentiate hemosiderin-laden macrophages.
Synonyms
Circulating erythroid precursors/erythroblasts/
normoblasts; Circulating nucleated erythrocytes;
Fetal erythroblastosis; Fetal normoblastemia.
Definition
Elevated nucleated red blood cells (nRBCs)
within the fetal vasculature, which is an indicator
of intrauterine stress (Redline 2008).
Clinical Features
• Incidence
Increased circulating fetal nRBCs are seen in
association with fetal/perinatal hypoxia, mater-
nal diabetes, maternal asthma, and other forms
of intrauterine stress (Boskabadi et al. 2017;
Daskalakis et al. 2008; Littner et al. 2003).
• Age
Increased circulating nRBCs have not been
shown to be associated with a particular mater-
nal or gestational age.
• Sex
Increased circulating nRBCs have not been
shown to be associated with a particular
fetal sex.
Non-neoplastic Lesions of the Placenta, Pathology of the Placenta 415
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• Site
Fetal circulation (within the chorionic vasculature, particularly the capillaries of the distal
villi).
• Treatment
Treatment may vary, depending on the cause of
fetal stress (e.g., intrauterine transfusion for
fetal anemia). Rapid delivery of the fetus/newborn may alleviate intrauterine stress and
reduce risk for morbidity and mortality. Therapeutic hypothermia is used in the setting of
perinatal asphyxia with signs of neonatal
encephalopathy (Frank et al. 2016).
• Outcome
Increased circulating nRBCs are seen in association with a diagnosis of cerebral palsy in
infants, perinatal intradural hemorrhage, fetal/
perinatal asphyxia, white matter and watershed
brain injury, infection, other causes of intrauterine stress, and fetal/neonatal death
(Redline 2008; Cohen et al. 2014; Frank et al.
2016; Boskabadi et al. 2017).
Macroscopy
There are no specific associated gross findings
associated with increased circulating fetal nRBCs.
Microscopy
Circulating nucleated red blood cells (Fig. 79)
have been quantified according to absolute number and as a relative measurement to circulating
white blood cells. The former calculates that
greater than 10 nRBCs per 10 high-power fields
correlates with an elevated absolute nRBC count
of 2.5 10
3
/mm3or greater (Redline 2008),
while the latter has been calculated as greater
than 11 nRBCs per 100 WBCs (Boskabadi
et al. 2017).
Elevated fetal nRBCs are associated with other
histopathologic lesions, including avascular villi
and chronic villitis (Redline 2008).
Immunophenotype
Erythroid-specific immunomarkers, such as
CD235, can be used to highlight nRBCs. Other
stains, such as myeloperoxidase, Giemsa, and
periodic acid Schiff (PAS), can be used in conjunction with morphology to help differentiate
between erythroid and myeloid precursors.
Molecular Features
Fetal nRBCs (both from the umbilical cord/placenta and those found in maternal circulation) can
be used for prenatal molecular diagnostics.
Differential Diagnosis
When increased circulating fetal nRBCs are seen,
specific causes should be considered, such as
erythroblastosis fetalis/hemolytic disease of the
fetus and newborn and fetal/fetomaternal hemorrhage. Nucleated red blood cells should also be
differentiated from circulating myeloid precursors, which may be increased in disease processes
such as the myeloid proliferations associated with
Down syndrome (i.e., transient abnormal
myelopoiesis, acute myeloid leukemia).
N
Non-neoplastic Lesions of the Placenta, Pathology of
the Placenta, Fig. 79 Increased nucleate red blood cells
within the fetal circulation
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