Placenta

SAMPLING AND
DEFINITIONS OF
PLACENTAL LESIONS
Presenter- Dr. Pannaga P Kumar
Moderator- Dr. Anisha T S
AMSTERDAM PLACENTAL WORKSHOP GROUP CONSENSUS STATEMEN
Khong et al
Arch Pathol Lab Med- Vol 140, July 2016

INTRODUCTION
 The placenta is crucial for fetal growth and survival,
performing the most important functions of many
somatic organs before birth.
 Thus, pathologic processes interfering with placental
function may result in abnormalities of fetal growth or
development, malformation, or stillbirth, and
 There is increasing recognition that some long-term
(especially neurologic) disabilities can be traced to injury
occurring before birth.

PLACENTA
 This is a fetomaternal organ.
 It has two components:
o Fetal part – develops from the chorionic frondosum
o Maternal part – derived from the decidua
 The placenta and the umbilical cord are a transport
system for substances between the mother and the
fetus.

PLACENTA AT TERM
 Fleshy
 Weight-500gm
 Diameter- 15-20 cm
 Thickness-2.5 cm
 Spongy to feel
 Occupies 30% of the uterine wall
 Two surfaces- Maternal and fetal
 4/5th of the placenta is of fetal origin and 1/5 is of
maternal origin

MATERNAL SURFACE
Irregular, divided into
convex areas
(cotyledons)
FETAL SURFACE
Smooth, transparent,
covered by amnion with
umbilical cord attached
near its center &
umbilical vessels
radiating from it

MATERNAL SURFACE
 Cotyledons –about 15
to 20 slightly bulging
villous areas. Their
surface is covered by
shreds of decidua
basalis from the uterine
wall.
 After birth, the placenta
is always carefully
inspected for missing
cotyledons.
 Cotyledons remaining
attached to the uterine
wall after birth may
cause severe bleeding.

FETAL SURFACE
 This side is smooth and
shiny. It is covered by
amnion.
 The umbilical cord is
attached close to the
center of the placenta.
 The umbilical vessels
radiate from the
umbilical cord.
 They branch on the
fetal surface to form
chorionic vessels.
 They enter the
chorionic villi to form
arteriocapillary-
venous system.

PLACENTA
 Margins of the placenta are formed by fused chorionic
and the basal plate
 Placenta is attached to the upper part of the uterine
body either at the posterior or anterior wall
 After delivery ,placenta separates with the line of
separation being through decidua spongiosum
(intermediate spongy layer of the decidua basalis

PLACENTA- GROSS
ABNORMALITIES
BATTLEDORE PLACENTA VELAMENTOUS INSERTION OF CORD

STRUCTURE OF PLACENTA
 Placenta is
limited by the
amniotic
membrane on
the fetal side
and by the
basal plate on
the maternal
 Between these
two lies the
intervillous
space filled with
maternal blood
and stem villi
with their

 Amniotic membrane- single
layer of cuboidal epithelium
loosely attached to adjacent
chorionic plate and does not
take part in placental
formation.
 Chorionic plate- forms the
roof of the placenta
From outside inwards consists
of
 Syncitotrophoblast
 Cytotrophoblast
 Extraembryonic mesoderm
with branches of umbilical
vessels

 Basal Plate- forms the
floor From outside
inwards it consist of
 Compact and spongy
layer of decidua
basalis
 Layer of Nitabuch
 Cytotrophoblastic
shell
 Syncytiotrophoblast
Basal plate is perforated
by the spiral arteries
allowing entry of
maternal blood into
intervillous space

DECIDUA
DEFINITION:
1. It is the functional layer of endometrium of the gravid
(pregnant) uterus.
2. It includes the endometrium of fundus & body of
uterus
3. The endometrium of the cervix does not form a part of
decidua.
STEPS OF FORMATION (DECIDUAL REACTION):
1. The endometrium becomes thicker & more vascular
2. The endometrial glands become full of secretion
3. The connective tissue cells enlarge due to
accumulation of lipid & glycogen.
4. They are called “decidual cells”

DECIDUA
 Decidua basalis: It
lies at the site of
implantation ,it forms
the maternal part of
the placenta
 Decidua capsularis:
it covers the
conceptus
 Decidua parietalis:
the rest of the
endometrium that
lines the body & the
fundus.

DECIDUA- HISTOLOGY
 The hypersecretory glandular epithelium of the
endometrium, which is progestationally induced, affords
the proper environment for implantation
 Decidual cells of the endometrium are characterized as
epithelioid and polygonal.
 Their small rounded nuclei are generally situated
centrally in abundant pale eosinophilic, often
vacuolated, cytoplasm.
 The cytoplasm is rich in glycogen and glycoproteins. In
regions of decidual tissue, where trophoblastic
derivatives are not present, nuclear content is diploid.

 Layer of Nitabuch - is a fibrinous layer formed at the
junction of cytotrohoblastic shell with decidua due to
fibrinoid degeneration of syncitotrohoblast
 It prevents excessive penetration of the decidua by the
trophoblast
 Nitabuch membrane is absent in placenta accreta and
other morbidly adherent placentas

Stem (Anchoring villi )
 Arise from the chorionic plate and extend to the basal plate
 Fetal cotyledon (60-100 ) – derived from one major primary stem
villus and is the structural unit of placenta
 Maternal cotyledon (15-20 ) contains 3-5 fetal cotyledons
 Villus is the functional unit of placenta
 Total surface of the villi for exchange varies between 4-14 sq meters
Intervillous space:
 Numerous branch villi arising from the stem villi project into this
space
 It is lined internally on all sides by the syncytiotrophoblast and is
filled with maternal blood

VILLI- GROSS
 The villous parenchyma is discoid and occupies the
space beneath the chorionic plate.
 The substance of the parenchyma is red and “beefy.” On
sectioning, it appears relatively homogeneous in contour
and texture, such that significant irregularities denote
abnormalities within the villous parenchyma.
 Many abnormalities, however, are common and when
focal or minimal in quantity, can be considered as
normal variants. Examples include small infarcts and
perivillous fibrin deposition.

VILLI- GROSS
 On occasion, the placental parenchyma has spherical
defects (usually 1 to 2 cm in greatest dimension), which
represent the so-called jet lesions.
 These cleared areas within the villous parenchyma
represent pressure heads from maternal decidual
vascular flow.
 It is not uncommon to histologically identify a small zone
of acute infarction peripheral to these lesions.
 Calcification is a common phenomenon in the mature
placenta. Calcification has been used to diagnose
placental maturity by ultrasonographic evaluation during
pregnancy.

VILLI- HISTOLOGY
 The histologic variations in placental architecture are largely
dependent on the developmental state at which observations
are made.
 The syncytiotrophoblast, the outer cell layer surrounding villi,
possesses a brush border.
 Microvilli that constitute this border are felt to be involved in
pinocytotic activity Vacuoles within the cytoplasm of these
cells are indicative of the absorptive and secretory activities
of the syncytiotrophoblast.
 Syncytiotrophoblasts are composed of pyknotic (often
multiple) nuclei that are hyperchromatic.

VILLI- HISTOLOGY
 The cytotrophoblastic nuclei are more round and open.
 On occasion, cytotrophoblasts may possess mitotic
figures. Ultrastructurally, the cytotrophoblast has fewer
organelles than does the syncytiotrophoblast. Most
prominent are large mitochondria, which may be
numerous.
 Extravillus trophoblasts are major constituents of the cell
columns that form the deepest structural components of
the implantation site.

CORD- EMBRYOLOGY
 The open region on the ventral surface of the developing
embryo diminishes in size and then forms the early
umbilicus. Through this structure extend both the yolk
stalk and the body stalk, as well as the allantois.
 This cylindrical structure elongates, and its surface
becomes covered by the expanding amnion. This is a
single-layered epithelium on a layer of connective tissue.
 Therefore, the developing umbilical cord contains the
yolk stalk, a pair of vitelline blood vessels, the allantois,
and the allantoic blood vessels (two arteries and one
vein) and is covered by amnionic epithelium.

CORD- GROSS
 The gross anatomic features of the umbilical cord
that are of importance are the location of its
insertion in the placental disk, its length, and the
number of vessels.
 The presence of true knots may be considered
normal when there is no adverse outcome, yet
this occurrence may lead to fetal demise when the
knot is tight.
 The presence of vascular tortuosities (false knots)
is common and rarely of clinical significance.
 The finding of meconium staining and the
presence of surface plaques are definitely

CORD- GROSS
 The normal umbilical cord is pearly white and
somewhat translucent.
 The length of the umbilical cord has great
significance, principally when it is excessively long
or excessively short.
 Cord length has been shown to vary with
gestational age, and measurements indicate that
the cord elongates as gestation proceeds.
 At approximately 20 weeks’ gestational age, the
average cord length is 32 cm.
 The normal length of the umbilical cord at term
has been determined to be, on average, between
55 and 65 cm

CORD- HISTOLOGY
 Histologic examination of the umbilical cord shows
several distinct layers. On the surface is a well-
defined single layer of amnionic epithelium. The
epithelium is squamoid and, in the region of fetal cord
insertion, often becomes multilayered and closely
resembles its epidermal contiguity.
 Deep to the amnionic epithelium that comprises the
surface of the cord is the substance of Wharton’s jelly.
This material largely is composed of
mucopolysaccharides (hyaluronic acid and chondroitin
sulfate).
 Embedded within the substance of Wharton’s jelly are
the umbilical vessels.

CORD- HISTOLOGY
 The vasculature of the umbilical cord is composed of
two arteries and one vein.
 The arteries possess no internal elastic lamina and have
a double-layered muscular wall. Each of these muscular
layers is composed of a network of interlacing smooth
muscle bundles.
 The vein does have an inner elastic lamina. The
umbilical vein, which generally has a larger diameter,
possesses a thinner muscular coat consisting of a single
layer of circular smooth muscle.

PLACENTAL BARRIER
 This is a composite structure that separating the fetal
blood from the maternal blood.
 It has four layers:
 Syncytiotrophoblast
 Cytotrophoblast
 Connective tissue of villus
 Endothelium of fetal capillaries
 After the 20th week, the cytotrophoblastic cells disappear
and the placental membrane consists only of three
layers.

PLACENTAL BARRIER
 It separates fetal from maternal blood.
 It prevents mixing of them.
 It is an incomplete barrier as it only prevents large molecules
to pass ( heparin & bacteria)
 But cannot prevents passage of viruses(e.g. rubella), micro-
organisms(toxoplasma, treponema pallidum) drugs and
hormones.

MEMBRANES
 The placental membranes consist of the amnion and the
chorion.
AMNION
 The amnion, which constitutes the innermost aspect of the
embryonic cavity, develops from the margin of the embryonic
disk.
 As the embryonic disk begins to take the form of a tube, the
amnionic periphery also folds inward and its attachment to
the ventral body is defined.
 The amnionic cavity subsequently develops by the process of
cavitation The amnionic cavity remains filled with amniotic
fluid, which by the end of gestation amounts to approximately
1 L.

CHORION
 The chorion forms the base for the peripherally radiating
villi and serves to encapsulate the embryo and the
developing amnion.
 As the early implantation embryo develops, the
embryonic tissues (the trophoblast and its mesodermal
investments) continue to expand in a spherical fashion.
 The inner aspect of the condensation of mesoderm,
which forms the inner capsular structure deep to the
peripheral trophoblast, is also termed chorion.
 In the region that becomes the placental disk proper,
chorionic villi continue to develop beneath these
structures, and the placenta proper or the chorion
frondosum is defined.

CHORION
 The region of the chorion that covers the expanded
amnionic cavity forms what has been termed chorionic
laeve.
 This constitutes the reflected membranes and is
discerned from the membranous covering of the
chorionic plate.
 Chorionic villi in the region of the laeve (which delimits
the sac containing amnionic fluid) atrophy by pressure,
although remnants of villous tissue may be found in
association with this structure.
 In the region of the chorion frondosum, the fetal blood
vessels invest the chorionic plate. Such vessels only
occur in the chorion; the amnion is an avascular

GROSS ANATOMY-
MEMBRANES
 The fetal membranes have a particular and
characteristic appearance in normal deliveries. The
sac, when viewed from the fetal surface, is clear and
often has a bluish hue, and the amnion is devoid of
vasculature.
 Remnants of atrophied vasculature may be seen in
the overlying chorion and appear as filamentous
streaks.
 The chorionic plate also has a characteristic blue
sheen and, as described previously, the distribution of
chorionic vessels has a characteristic appearance.
 It is not infrequent to find a peripheral nodule on the
surface of the disk membranes. This normal nodule is
the remnant of the fetal yolk sac

INTRODUCTION
 A systematic review concluded that pathology of the
placenta, cord, or membranes is attributed as a cause or
contributory to stillbirth in 11% to 65% of cases in
various classifications, depending on the classification
used.
 Following protocols and definitions can be applied by
general practice pathologists and improve the value of
placental pathology and perinatal autopsy reports.

PLACENTAL WEIGHT
 Description of the placenta should include the placental
weight trimmed of extraplacental membranes and
umbilical cord, and notation of whether the placenta was
fresh or ﬁxed when measured.
 Any prior sampling of the placental parenchyma should
also be documented. Any disruption of the basal plate
should be noted.
 The placental weight is a surrogate for placental
function, and fetoplacental weight ratio has been
suggested as a possible indicator of adequacy of
placental reserve capacity in fetal growth restriction
(FGR)

PLACENTAL DISK
DIMENSIONS
 Description of the placenta should include the
measurement of the placenta in three dimensions:
 maximal linear dimension (length),
 greatest dimension of the axis perpendicular to this
linear measurement (width),
 mural minimal and maximal thickness.

DESCRIPTION OF UMBILICAL
CORD
 Description of the umbilical cord should include
 average diameter of the cord;
 length;
 site of insertion in relation to the center/margin of the
placenta, determined by measuring the distance
between the insertion site and the nearest placental
margin;
 presence of strictures;
 and whether the cord appears to be hypocoiled or
hyper coiled.
 segmental or localized areas of hyper coiling should
be recorded.
 direction of coiling (handedness) should be noted if
possible.

 Thin umbilical cords are associated with FGR, whereas
thick cords are associated with maternal diabetes and
with fetal hydrops.
 Excessively long and short cords can be associated with
adverse outcomes.
 Marginal (<1 cm from the nearest margin) and
velamentous insertions, but not peripheral (<3 cm from
the nearest margin) insertions, are associated with an
increased risk of adverse pregnancy outcomes,
including preterm delivery.

 Hypocoiling (<1 coil per 10 cm) and hypercoiling (>3
coils per 10 cm) may be associated with adverse
outcomes in some cases.
 Opinion was divided about the best way to assess
coiling, especially because cords are often incompletely
submitted
 Fixation of the cord will affect the length and therefore
the coiling index, underscoring the importance of stating
whether the placenta was fresh or ﬁxed when pathologic
examination was performed.

DESCRIPTION OF
MEMBRANES
 Description of the membranes should include the
color/opacity and completeness.
 Recording the shortest distance between the site of
rupture to the placental edge may be useful in some
cases of placenta previa if the rupture was at the edge,
but the group was divided on this recommendation.
 If circumvallate or circummarginate, the percentage of
the circumference involved should be noted.

Sampling of Cord, Membranes,
and Placental Disk
 Submit 4 blocks as a minimum:
 1 block to include a roll of the extraplacental membranes
from the rupture edge to the placental margin, including
part of the marginal parenchyma;
 2 cross sections of the umbilical cord, one from the fetal
end and another approximately 5 cm from the placental
insertion end.
 Three other blocks each containing a full thickness
section of normal-appearing placenta parenchyma
should be submitted.

 Full-thickness samples should be taken from within the
central two-thirds of the disc and include one adjacent to
the insertion site itself.
 If the transmural thickness is greater than the length of
the cassette, two options are available: the upper third
(chorionic plate and subjacent tissue) and lower third
(basal aspect) of the parenchyma can be submitted in
one cassette, or the gross slice can be divided into two
and submitted in two cassettes
 A full-thickness sample should be taken from close to
the umbilical cord insertion site to document fetal
vascular ectasia and fetal and/or maternal inﬂammatory
response.

DESCRIPTION OF LESIONS
 Grossly identiﬁed lesions should be described with
either an estimate of the percentage of the total
parenchymal volume they affect or a measurement of
the two maximal dimensions of each lesion.
 The number of lesions of the same gross appearance
should be counted and stated as being single or
multiple.
 The location(s) of the lesions should be stated: central/
paracentral or peripheral. Lesions that are
microscopically different may appear similar grossly.
 A block of the lesion (one of each type of lesion) should
be sampled, with adjacent normal parenchyma if
possible, in up to 3 additional blocks

Figure 5. Chronologic dating of infarcts is easier in the fixed placenta because
the lesions are better demarcated: the older infarcts appear tan colored,
whereas the fresher ones appear red and congested.
Figure 6. Fresh placental abruption resulting in marked congestion of the
overlying placental parenchyma.

MATERNAL VASCULAR
MALPERFUSION OF THE
PLACENTAL BED
 Effects of inadequate spiral artery remodeling or spiral
artery pathology manifest as a spectrum that includes
FGR and preeclampsia, high-velocity malperfusion may
be detrimental to placentation in early pregnancy and
placental function in later pregnancy.
 Gross ﬁndings include placental hypoplasia, infarction,
and retroplacental hemorrhage
 Microscopic ﬁndings include abnormalities of villous
development, which can be separated into distal villous
hypoplasia, and accelerated villous maturation

INFARCTION
 Whether they are recent or remote.
 When histology confirms that the hemorrhage is
encased by infarction, the proposed term infarction
hematoma should be used.
 Infarcts can be suspected by their generally pyramidal
shape and usual involvement of the basal parenchyma
or maternal floor of the placenta.
 Gross chronologic dating of infarcts is easier in the fixed
placenta because the lesions are better demarcated

CHRONICITY OF INFARCTION
 Early infarcts are seen as crowding and congestion of
villi, which may be hemorrhagic, accompanied by early
loss of nuclear staining of the stroma. There may also
be migration of neutrophils into the intervillous space,
which may be compressed or obliterated.
 Later changes include necrotic changes (pyknosis and
karyorrhexis of trophoblast), loss of trophoblast nuclear
staining, and eventually ghost villi.

RETROPLACENTAL
HEMORRHAGE
 When a retroplacental hemorrhage is associated with
indentation of the placental parenchyma, the indentation
should be described, and two dimensions (length and
width) or the percentage of maternal surface area
involved should be recorded.
 Any clot that is separate from the placenta but submitted
in the specimen container should be weighed and, if
possible, measured in three dimensions.
 At least one sample of the area of retroplacental
hemorrhage should be submitted for histology, which
should include part of the basal plate.

RETROPLACENTAL
HEMORRHAGE
 Grossly, there is blood accumulation on the maternal
surface, with congestion and/or hemorrhage within or
compression of the overlying parenchyma.
 Microscopically, there is blood accumulation beneath
and dissecting the decidua and compression of the
overlying intervillous space, with villous crowding,
congestion, and/or intravillous hemorrhage with touching
villi; there is also a smudged appearance, as evidence
of early coagulation necrosis of the syncytiotrophoblast
nuclei, and pale appearance of syncytiotrophoblast
nuclei

DISTAL VILLOUS HYPOPLASIA
(DVH)
 Deﬁned as the paucity of villi in relation to the
surrounding stem villi.
 The villi are thin and relatively elongated-appearing, and
syncytial knots are increased.
 The diagnosis should be made when the features are
seen in the lower two-thirds and involve at least 30% of
1 full-thickness parenchymal slide.
 It may be further graded as focal— ﬁnding of lesion in 1
full-thickness slide only—or diffuse— present in 2 or
more full-thickness slides sampled. Diffuse distal villous
hypoplasia is associated with early-onset FGR.

Distal villous hypoplasia: there is a paucity of villi, many of which are thin
and elongated (hematoxylin-eosin, original magnification)

ACCELERATED VILLOUS
MATURATION
 Presence of small or short hypermature villi for
gestational period, usually accompanied by an increase
in syncytial knots.
 It is diagnosed by identifying a diffuse pattern of term-
appearing villi with increased syncytial knots and
intervillous ﬁbrin, usually alternating with areas of villous
paucity.
 Accelerated villous maturation is a common pattern that
may be found in mild, moderate, or severe forms of
placental insufﬁciency, which includes FGR,
preeclampsia, and preterm labor.

DECIDUAL ARTERIOPATHY
 The elements include acute atherosis, ﬁbrinoid
necrosis with or without foam cells, mural
hypertrophy, chronic perivasculitis , absence of
spiral artery remodeling, arterial thrombosis,
and persistence of intramural endovascular
trophoblast in the third trimester.

FETAL VASCULAR
MALPERFUSION
 The lesions described under this umbrella of FVM are
likely to be due to obstruction in fetal blood flow that
could result from a number of conditions (eg, umbilical
cord lesions, hypercoagulability, complications of fetal
cardiac dysfunction, such as hypoxia, etc.)
 Findings consistent with FVM are thrombosis, segmental
avascular villi, and villous stromalvascular karyorrhexis.
Other possible markers, such as vascular intramural
fibrin deposition, stem vessel obliteration/fibromuscular
sclerosis, and vascular ectasia, should also be sought.

 Two patterns of FVM are recognized, and either may be
low grade or high grade.
 The first is segmental FVM, indicating thrombotic
occlusion of chorionic or stem villous vessels, or stem
vessel obliteration—although the distribution of the
lesions is segmental, the thrombus or obstruction would
be expected to result in complete obstruction to the villi
downstream.
 The second is global FVM, indicating partially obstructed
umbilical blood flow with venous ectasia, intramural
fibrin deposition in large vessels, and/ or small foci (,5
villi per focus) of avascular or karyorrhectic villi—the
obstruction is partial or intermittent, but the lesions can

 High-grade FVM is manifest by the ﬁnding of
 more than one focus of avascular villi (a cumulative
assessment of >45 avascular villi over 3 sections
examined or an average of >15 villi per section) with or
without thrombus, or
 2 or more occlusive or nonocclusive thrombi in chorionic
plate or major stem villi, or multiple nonocclusive
thrombi.

THROMBOSIS
 Arterial or venous.
 The location(s) of the thrombosis should be speciﬁed as
to whether it is at the umbilical, chorionic plate, or stem
vessel vascular level, or any combination thereof.

Avascular villi
 Distribution and extent.
 The criteria for avascular
villi that have been
published previously are
amended slightly.
 Small foci are the ﬁnding of
3 or more foci of 2 to 4
terminal villi showing total
loss of villous capillaries
and bland hyaline ﬁbrosis
of the villous stroma.
Intermediate foci are 5 to
10 villi, and large foci are
more than 10 villi.

Intramural fibrin deposition
 Isolated -if there is no more than one such lesion per
slide.
 Whether the lesion is recent or remote should be noted.
 The location of the fibrin deposition is subendothelial or
intramuscular, and thus intramural.
 It is also noted that the depositions are, by definition,
nonocclusive.
 The criteria for intramural fibrin deposition have been
published previously: fibrin or fibrinoid deposition
(subendothelial or intramuscular) within the wall of large
fetal vessels (indicates recent), with calcification
(indicates remote)

VILLOUS STROMAL-VASCULAR
KARYORRHEXIS
 3 or more foci of 2 to 4
terminal villi showing
karyorrhexis of fetal cells
(nucleated erythrocytes,
leukocytes, endothelial
cells, and/or stromal
cells) with preservation
of surrounding
trophoblast

STEM VESSEL OBLITERATION
In stem vessel obliteration there is marked thickening of
the vessel wall and resultant obliteration of the vascular
lumen.
VASCULAR ECTASIA
The cause of vascular ectasia is not clear at this stage and
may be nonspeciﬁc or related to umbilical cord
compromise in combination with FVM. Vascular ectasia is
characterized by the ﬁnding of vessels that are four times
the luminal diameter of the surrounding corresponding
vessel.

DELAYED VILLOUS
MATURATION
 The lesion is defined by a monotonous villous
population (defined as at least 10 such villi) with
centrally placed capillaries and decreased
vasculosyncytial membranes, recapitulating the
histology in early pregnancy.
 The diagnosis should be made when it is present in at
least 30% of 1 full-thickness parenchymal slide.
 Grading:
 focal, which is a finding of the lesion in 1 full-thickness
parenchymal slide only, and
 diffuse, which is a presence in 2 or more full-thickness
slides sampled.

Ascending Intrauterine Infection
 Describing the topography of the inflammation will allow
separation of the maternal from the fetal inflammatory
response.
 This is thought to be important because there is
evidence that poor fetal outcomes are more often
associated with a fetal inflammatory response.
 Chronicity of inflammation may have clinical implications
different from those of a purely acute response, and
should therefore be documented

SUBCHORIAL INFLAMMATION
 The presence of neutrophils in the subchorial
intervillous space or beneath the chorion laeve
layer in the absence of inflammation
elsewhere, should be reported as
subchorionitis.
 Involvement of artery or vein or both should be
speciﬁed.

REPORTING FORMAT
 Histologic acute inﬂammation in the placenta,
extraplacental membranes, and umbilical cord be
reported as: acute chorioamnionitis (or acute chorionitis)
with/without fetal inflammatory response in (specify)
chorionic vessels, umbilical vein, and/or umbilical artery
(or arteries).

VILLITIS OF UNKNOWN
ETIOLOGY
 Histologic diagnosis and, although it may have a
variable distribution, evidence indicates that 3
parenchymal blocks will identify 62% of villitis.
 It is usually lymphohistiocytic: although the presence of
rare plasma cells does not exclude the diagnosis.

VILLITIS OF UNKNOWN
ETIOLOGY
Grading Schema
 Low grade is defined as the presence of inflammation
affecting fewer than 10 contiguous villi in any one focus,
with more than one focus required for the diagnosis.
 High grade is defined as the presence of multiple foci,
on more than one section, at least one of which shows
inflammation affecting more than 10 contiguous villi

 Low-grade lesions should be further classiﬁed as
a) focal when they are seen in one slide, all foci affecting
fewer than 10 villi, with more than one focus required
for diagnosis;
b) or as multifocal when they are present in more than
one slide, all foci affecting fewer than 10 contiguous
villi.
 High-grade lesions should be further classiﬁed as
a) patchy when there are multiple foci, with at least one
focus with 10 or more contiguous villi, and seen in one
or more slides;
b) or as diffuse when more than 30% of all distal villi are
involved

Vascular Damage
 When inflammatory cells damage vessels that
have a muscular wall, the term villitis with stem
vessel obliteration should be used.
 When avascular villi are seen in a placenta
with villitis, the report should designate the
finding as chronic villitis with associated
avascular villi.
 Villitis may cause impairment of the
fetoplacental circulation. Such damage is
associated with adverse effects, such as
neurologic impairment

 When possible, the distribution of the foci of
villitis should be reported as being located
parabasal/ paraseptal, randomly in the
midparenchyma or subchorionic zone, or
combinations thereof.

 Entities reported to be associated with villitis,
such as eosinophilic/T-cell vasculitis, chronic
intervillositis, and chronic deciduitis, should be
noted.

Placenta

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