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Structure of the Human Placenta and Pathomorphological Changes in Placental Insufficiency
Fig. 24.3a Embryo and chorion frondosum. EB = embryo; AC = amni-
otic cavity; YS =yolk sac; CH = chorion frondosum.
24
Amnion
Decidua capsularis
Chorionic cavity
Decidua parietalis
Fig. 24.4 Diagram showing the relationship between the embryonic
membranes and uterine wall.
a Week 8 postconception.
Amniotic cavity
Chorion
frondosum
Decidua basalis
Fig. 24.3b Histological appearance of an embryo, with the amniotic
cavity and chorion frondosum (H & E, ⫻10). EB = embryo AC = amni-
otic cavity; CP = chorionic plate; VL = villus; YS = yolk sac.
Amnion
Chorion laeve
Decidua capsularis
Decidua parietalis
Amniotic cavity
Decidua basalis
Placenta
b Week 15 postconception.
232
Capillary
Cytotrophoblast
Stroma
Syncytiotrophoblast
Fig. 24.5 Mesenchymal villus with a “sprout.” (Modified from Kaufmann and Scheffen.).
Structure of the Villous Tree
As the growth of the placenta progresses,different types of villi
become increasingly distinct
Mesenchymal villi. “Mesenchymal villi” are trophoblastic
sprouts, initially fungiform, that are the precursors of all the
other villi (Fig. 24.
5). They are comparable in structure to the
primary and secondary villi that form during early development and consist of a centrally located, proliferating cytotrophoblast and an outer syncytiotrophoblast. They are invaded
by mesenchymal cells and subsequently vascularized with the
formation of new villi
11
Immature intermediate villi. Large-caliber, immature interme-
diate villi predominantly develop from the mesenchymal villi
25, 26
.
.
Structure of the Human Placenta
during the first and second trimesters. They are distinguished
by a coarse-meshed reticular stroma with blood vessels and
small, intercommunicating stromal channels (Fig. 24.
6a).
These channels provide transit routes for the Hofbauer cells—
fetal tissue macrophages that play an integral role in host
defenses and influence the morphogenesis and angiogenesis of
the villi
6, 10, 50
.
Mainstem villi. The immature intermediate villi are transformed into mainstem villi that connect the chorionic plate
with the villous tree. Each villous stem branches into firstorder through fourthth-order rami and first-order through
tenth-order ramuli. The mainstem villi are characterized by a
condensed fibrous stroma, large afferent and efferent blood
vessels with a distinct tunica media, and a paravascular fibrous
cuff (Fig. 24.
6b). Their function is to stabilize the villous tree
and thus the circulation of blood. The dominant process that
occurs during the first and second trimesters is the expansion
of the villous tree
11
.
Mature intermediate villi and terminal villi. During the third
trimester, by contrast, predominantly mature intermediate
villi are formed from the mesenchymal villi. They contain
many arterioles, capillaries, and venules and are direct precursors of the terminal villi (Fig. 24.
6c). The terminal villi are
equipped with numerous capillaries that have undergone sinusoidal transformation and cause the villous surface to protrude, forming “metabolic membranes” (Fig. 24.
6d). Thus, the
dominant process in the third trimester is maturation of the
villi rather than growth of the villous tree
Figure 24.
7 shows a high-power view of a fetal villous tree
11
.
that includes mainstem, intermediate, and terminal villi.
The development of the terminal villi is dependent on
capillary growth in the mature intermediate villi. Once capil-
Specific Obstetric Problems
a
c
Fig. 24.6 The different types of villi in the human placenta.
a Immature intermediate villus with a reticular stroma, stromal chan-
nels, and Hofbauer cells (H & E, ⫻200). SC = stromal channel HB =Hofbauer cell; FBV = fetal blood vessel; TB =trophoblast; IVLS = inter-
villous space.
b Mainstem villus with a fibrous stroma and paravascular fibrous cuff
(H & E, ⫻100).
FS = fibrous stroma PF = paravascular fibrous cuff; FBV =fetal blood
vessel.
c Mature intermediate villus with many arterioles, capillaries, and
venules (H & E, ⫻200). FBV = fetal blood vessel TB = trophoblast.
d Terminal villi with sinusoids and metabolic membranes (H& E,
⫻1000). S = sinusoid MM = metabolic membrane; TB = trophoblast;
IVLS = intervillous space.
b
d
233
Structure of the Human Placenta and Pathomorphological Changes in Placental Insufficiency
lary growth exceeds the length of the villus, the capillary becomes coiled and causes a passive outpouching of the villous
surface. This process creates a cluster-of-grapes pattern of terminal branches that represent new terminal villi. Imbalances
between capillary and villous growth can lead to various disturbances of villous
maturation
Microstructure of the Terminal Villus
Cytotrophoblast. The terminal villus is approximately
30–80
µm in size (Fig. 24.8). With advancing gestation, the
inner cytotrophoblast becomes more and more fragmentary. It
provides a stem cell pool for the outer syncytiotrophoblast,
with oxygen apparently serving as an important regulator.
Hypoxic damage to the syncytiotrophoblast stimulates proliferation of the cytotrophoblast, followed by fusion of the
6
cells
.
Syncytiotrophoblast. The outer syncytiotrophoblast is no
longer capable of cell division. It shows increasing differentiation and its functions include hormone production.
24
Fig. 24.7 High-power view of a villous tree (semithin section, H & E,
⫻200). MVL = mainstem villus IMVL = intermediate villus ; TMVL =terminal villus.
Villous capillaries. With sinusoidal expansion of the fetal
villous capillaries, the syncytial nuclei and organelles are
pushed aside. The trophoblastic and capillary basement membranes partially fuse together, forming the metabolic membrane that is so essential for metabolic and gaseous exchange.
In the mature placenta, approximately 25–40% of the surface
area of the terminal villi consists of these vasculosyncytial
membranes, which are 0.5–1
6, 27
.
µm in thickness
46
.
234
Sinusoid
Macrophage
Metabolic
membrane
Fig. 24.8a Schematic diagram of the microstructure ofa terminal villus.
Syncytiotrophoblast
Cytotrophoblast
Capillary
Fig. 24.8b Transmission electron micrograph of the metabolic membrane of a terminal villus. S = sinusoid; ST = syncytiotrophoblast;
MM = metabolic membrane; ER = erythrocyte; ECN = endothelial cell
nucleus; IVLS = intervillous space; basement membrane of trophoblast (arrowheads); basement membrane of capillary (arrows).
Maturation of the Placenta
Structure of the Human Placenta
The maturation of the placenta serves to shorten the distance
between the maternal and fetal blood. Becker
5
defined four
signs of placental maturity that can be useful in the qualitative
assessment of placental maturation.
First sign of maturity: a steady decrease in villous diameters
accompanied by an increase in the total villus surface area.
Second sign of maturity: increasing vascularization of the villi
and sinusoidal transformation of the villous capillaries. This
process starts at about the end of the 5th month of gestation,
increases markedly during the final six weeks, and reaches its
high point at term. The villus stroma is drastically reduced,
causing a substantial decrease in the fetomaternal diffusion
pathway.
Third sign of maturity: decreasing thickness of the villus trophoblast with advancing gestation, accompanied by displacement of the trophoblastic nuclei and the formation of metabolic membranes. The trophoblastic nuclei move to the sides
and form nuclear bridges between adjacent villi. This creates a
supportive “external cytoskeleton”
5
that interlinks the villi and
prevents collapse of the villous network in response to significant changes in maternal blood pressure. The formation of
metabolic membranes and trophoblastic bridges is the criterion for the third sign of placental maturity. As vascularization
of the villi increases, the “diffusion placenta” is progressively
transformed into a “vascularization placenta”
5
.
Fourth sign of maturity: luminal narrowing of the large arterial
vessels of the mainstem villi and the formation of paravascular
fibrous cuffs. This leads to stiffening of the vessels, and the resulting pressure constriction with a slowing of flow in the
downstream vascular system serves to decompress the pressure-sensitive peripheral villi and protect the delicate sinusoids in the terminal villi
5
.
Vascular Architecture of the Villous Tree
By about the 6th week after fertilization, an embryoplacental
circulation is established by the fusion of allantoic vessels from
the umbilical cord with the capillaries that develop locally in
the villi
pressure gradients that exist in the afferent and efferent vessels.
Umbilical cord. The umbilical cord transmits a vein carrying
arterialized blood along with two arteries, which anastomose
near the placenta in 96 % of cases in order to equalize pressures
and distribute the blood more uniformly (Hyrtl’s anastomosis).
6, 13
. Different wall structures result from the different
Fig. 24.9 Arrangement of the fetal blood vessels in a cluster of terminal villi.
dothelial and muscle cells, creating a “musculoendothelial system” that is important in local autonomic vasoregulation, since
the placenta is devoid of nerves
36
.
Terminal villi. The capillaries of the terminal villi, which lack a
tunica media, show local dilatative, sinusoidal transformations
that serve to decelerate the blood flow (Fig. 24.
9). To ensure an
optimum transfer of substances and gaseous exchange, the
fetal blood passes successively through the capillary loops of
2–5 adjacent terminal villi before it returns to the postcapillary
venule
6, 27
.
Regulation of Villous Blood Flow
From 40 % to 57% of the fetal cardiac output flows through the
two umbilical arteries into the placenta. The rate of umbilical
blood flow at term is approximately 110(ml/min)/kg body
weight. The arterial fetal blood pressure is approximately
53 mmHg, the intravillous capillary pressure is approximately
35 mmHg, and the umbilical venous pressure is about
20 mmHg
driving force, it appears that there is a peripheral regulation of
villus blood flow. Immunohistochemical studies have demonstrated the presence of contractile actin- and desmin-positive
myofibroblasts in the vessels and stroma of the villi (Fig.24.
It may be that substances such as catecholamines, angiotensin,
and prostaglandin exert a hormonal control of villous blood
flow.There can be no neural regulation of villous blood flow, as
the placenta is devoid of nerves
46
. While the fetal heart beat represents an important
46
.
10).
Specific Obstetric Problems
Villous tree. Each villous tree is supplied by a centrally located
artery and an accompanying vein, which progressively branch
into arterioles, capillaries, and venules. The vessel walls are
characterized histologically by an almost complete absence of
elastic fibers. Numerous processes pass between the en-
235
Structure of the Human Placenta and Pathomorphological Changes in Placental Insufficiency
flows radially into the intervillous space, which is now of capillary size. These areas are characterized histologically by the
presence of numerous terminal villi. With their closely packed
arrangement, these villi significantly slow the movement of
maternal blood, permitting an optimum fetomaternal exchange of gas and nutrients. The oxygen-depleted venous maternal blood then flows back through the subchorionic space
and regions between the villous trees into the veins of the basal
plate and into the marginal sinus. As a result, the distribution
and direction of maternal blood flow are regulated essentially
by the varying density of the villi within the placentones
Morphology and Physiological Transformation of the Maternal Basal-Plate Vessels
Fig. 24.10 Immunohistochemical detection of actin-positive myofibroblasts in the fetal vessel walls and villous stroma (⫻200). TB = trophoblast; FBV = fetal blood vessel; VLS = villous stroma.
Concept of the Placentone
24
The “placentone” is a fetomaternal functional unit comprised
of a fetal villous tree (cotyledon) and the maternal spiral artery
that supplies it
chiefly as a growth and regeneration area, while the peripheral
portions are for the fetomaternal exchange of gas and
nutrients
Gas and nutrient transfer. By injecting contrast material into
cannulated spiral arteries, Beck
maternal blood first collects in a centrally located, loosely
structured cavity in the placentone (Fig. 24.
42
. The central portions of the placentone serve
42
.
4
showed that the oxygen-rich
11). From there it
The maternal blood vessels of the basal plate increasingly undergo regressive changes during the course of pregnancy. Extravillous trophoblastic cells play an essential role in this pro-
6, 9, 38, 39
cess
. Figure 24.12 shows a cross section of the basal
plate with a maternal spiral artery and a villus anchored in the
basal plate, with adjacent cytotrophoblastic and syncytiotrophoblastic cells.
Extravillous trophoblastic cells. Some of the proliferating cy-
totrophoblasts fuse, as described above, to form the outer syncytiotrophoblasts. Others invade the placental bed and the maternal preplacental vessels. Similarly to tumor cells, these cytotrophoblastic cells show an altered expression of adhesion
molecules and matrix molecules and leave the villous basement membrane
6, 7,9, 43
deeply infiltrate the decidua, losing their cellular cohesion.
After reaching a depth of more than five cell layers from the
villous basement membrane, they stop dividing and start to
4, 33
.
. These extravillous trophoblastic cells
236
Subchorionic space
Spiral artery
Fig. 24.11 Schematic diagram of maternal blood flow in a fetomaternal functional unit (placentone; red = arterial blood, blue = venous
blood).
Capillary regionCentral cavityVenous ostium
AVL
FBV
ST
BM
eVT
Fig. 24.12 Schematic diagram showing the histological structure of
the basal plate with an adjacent anchoring villus and the arrangement
of the villous and extravillous trophoblasts. (Modified from Benirschke
and Kaufmann
ST = syncytiotrophoblast; BM = basement membrane; SA = spiral
artery; F = fibrinoid; D = decidua; VLT = villous trophoblast; eVT = extravillous trophoblast.
FSA
6
.) AVL= anchoring villus; FBV= fetal blood vessel;
eVT
VLT
D
differentiate. In the process, these cells form a “matrix-type fibrinoid”—a modified basement membrane material in nonpolarized form whose functions include creating a barrier to
further trophoblast invasion
6
. This “intermediate” trophoblast
located outside the villi fulfills at least some of the criteria of a
malignant tumor invading the maternal tissue. This infiltration
is controlled and self-limiting, however
43
.
Intravascular trophoblast invasion. The preplacental maternal
arteries are also invaded and remodeled by trophoblastic cells.
This process is marked by a decrease of muscular and elastic
fibers in the arteries and an increase in intramural f ibrinoid
deposits (Fig. 24.
13)
6, 14, 38
.
Two stages can be distinguished in this process. An initial
stage of intravascular trophoblast invasion occurs in just the
8th to 10th weeks of gestation and mainly affects arteries located in the central area of the placental bed
32
. A second wave
of trophoblast invasion occurs in the 14th to 16th weeks of gestation. In this stagethe cells migrate into myometrial segments
of the maternal arteries and transform them into broad, relatively stiff channels that are exempt from local vasoregulation.
The luminal diameters of the vessels are increased from ap-
proximately 200
µm to 1000–2000 µm where they open into
the intervillous space, with a corresponding decline of flow re-
Placental Insufficiency
Fig. 24.13 Physiological fetal trophoblast invasion of a maternal preplacental blood vessel (H & E, ⫻200). SA =spiral artery D = decidua; ex-
travillous trophoblastic cells (arrows).
sistance
wall changes fail to occur in maternal hypertensive disorders of
pregnancy
6
. It has been theorized that these physiological vessel
8, 39
.
Specific Obstetric Problems
Placental Insufficiency
Definition and Etiology of Placental Insufficiency
From a pathoanatomical standpoint, placental insufficiency refers to a decline in the performance of the organ as a result of
demonstrable structural abnormalities.
Intraplacental causes. A disturbance of metabolic and exchange processes in the placenta can result from a reduction of
perfusion capacity, diffusion capacity, or both
various causes:
➤
Deficient placental growth (in weight and/or area of attachment)
➤
Abnormalities of villous maturation
➤
Decreased blood flow (maternal and/or fetal)
➤
Parenchymal inflammation
➤
Tumors
Extraplacental causes. Placental insufficiency may also have
extraplacental causes. Preplacental or postplacental abnormalities of the maternal or fetal circulatory system are generally not accessible to pathoanatomical diagnosis.
The placenta normally undergoes a continuous increase in
size and weight during the course of pregnancy, accompanied
by maturation of the villous trees with a reduction in villous diameters and increasing vascularization. The resulting decrease
of impedance can be quantified by Doppler sonography of the
umbilical arteries. In several studies in which the histomorphological findings in placentas were correlated with Doppler
flow measurements, abnormal Doppler velocity waveforms
46
. It can have
were found to be associated with significantly smaller placen-
tas (reduced area of attachment and volume) and lower fetal
weights
19,20, 47
. Moreover, it was common to find markedly reduced numbers of vessels and metabolic membranes per villus
in groups with zero or negative flow
21, 47, 48
.
The results in these cases point to the presence of an overriding disorder that is responsible both for the smaller fetoplacental dimensions and for the underdifferentiation of the
villous trees, leading to frank placental insufficiency
47
.Itmay
be that an implantation abnormality with reduced fetal trophoblastic invasion of the maternal basal plate and spiral arteries may be the cause of placental dysfunction in these cases
22
The further clinical course in cases with Doppler abnormalities
is critically influenced by the extent of the placental reserve
capacity.
Placental Compensatory Mechanisms
The human placenta has a number of compensatory mechanisms at its disposal:
➤
Initially, placental dysfunction evokes an increase in fetal
and/or maternal blood flow.
➤
More serious disturbances of villous maturation can evoke a
compensatory increase in placental growth.
➤
With a primary small placenta or a placenta whose
functional parenchyma has been reduced by extensive obliterative lesions, an acceleration of placental maturation may
be observed
5, 46
.
.
237
Structure of the Human Placenta and Pathomorphological Changes in Placental Insufficiency
with decreased vascularization, thin vascular tunica media,
Classification of Placental Insufficiency by its Progression
Acute and chronic forms. A distinction is drawn between acute
and chronic forms of placental insufficiency. The acute form
develops in minutes or hours and causes a global impairment
of oxygenand other gaseous exchange followed by intrauterine
asphyxia (acute respiratory insufficiency). Chronic placental
insufficiency develops over a period of weeks or months and
leads to intrauterine growth retardation (nutritional insufficiency)
5
.
Morphological Counterparts of Latent or Overt Placental Insufficiency
Disorders of Villous Maturation
and the absence of a paravascular fibrous cuff (persistence of
immature intermediate villi). This maturation defect may
occur in the setting of chromosome abnormalities, diabetes
mellitus, or blood group isoimmunization.
Chromosome abnormalities. Chromosome abnormalities such
as trisomies, triploidies, and XO monosomies usually lead to
pregnancy loss during the first 12 weeks. Other possible effects
are abnormal fetal development or intrauterine death in later
stages of pregnancy, particularly with numerical chromosome
anomalies
46
. A cytogenetic analysis should be done whenever
possible, since morphological examination of the placenta
rarely identifies criteria that can prove a genetic anomaly. It is
common, however, to find underweight placentas with large,
immature “cat’s paw” villi resulting from abnormal villous
branching. These changes are considered part of the phenotype
of the underlying chromosome disorder
46
.
Timing and consequences. Villous maturation disorders may
occur in early pregnancy, when the dominant processes are
placental growth and the expansion of the villous trees, or in
later pregnancy when the dominant process is placental matu-
24
ration. A severe villous maturation disorder occurring in early
gestation leads to fetal loss. Maturation defects that occur in
advanced stages of pregnancy can cause fetal growth retardation but may also lead to intrauterine death. In evaluating
villous maturation disorders, it is important to take into account fetal weight and dimensions and compare them with
those of the placenta, e.g., by determining the placental-fetal
index.
Arrested Villous Maturation
Figure 24.14 shows an example of arrested villous matura-
46
tion
, known also as maturity arrest5or persistent immaturi-
6
ty
. The histological features are compared with a normally
branched villous network in the 28th week of gestation. Villous
maturation may become arrested in early or late pregnancy,
appearing histologically as large-caliber, poorly branched villi
Diabetes mellitus. Arrest of villous maturation is a common
finding in pregnant women with poorly controlled diabetes
mellitus. It is characterized by poor villous branching with hypoplastic blood vessels, microcystic edema, and poor differentiation of the chorionic epithelium as a possible response to
maternal hyperglycemia
46
. The children of these mothers show
hyperinsulinism combined with accelerated longitudinal
growth, visceromegaly, obesity, and corresponding weight
12
gain
. Appropriate correction of the diabetic metabolism can
prevent the development of these changes
6, 46
.
Rhesus incompatibility. Another disease that may be as-
sociated with arrested villous maturation is rhesus incompatibility (Fig. 24.
14a). In this condition it is common to find large-
caliber, immature villi with coarse villous edema and numerous erythroblasts in the fetal capillaries. Rhesus incompatibility is an immunohemolytic anemia that develops when
anti-erythrocyte maternal antibodies cross the placental barrier. The fetal anemia and hypoxia evoke a dramatic increase in
the fetal cardiac output. The resulting cardiomegaly with heart
failure and hypoxic capillary-wall damage are considered the
238
Fig. 24.14a Arrest of villous maturation in rhesus incompatibility
(28th week of gestation, H & E, ⫻200).
Fig. 24.14b Normally branched villous network (28th week of gesta-
tion, H & E, ⫻200).
Placental Insufficiency
major causes of fetal and placental edema, which may progress
to hydrops
ing into the intervillous space are occasionally observed
6, 46
. Even villous capillary-wall ruptures with bleed-
6
.Fetal
erythropoiesis is increased, and there are increased numbers
of immature nucleated precursor cells.
Electron microscopy of affected placental villi demonstrates necrotic syncytiotrophoblasts, hyperplasia of the cytotrophoblasts, and thickening of the villous basement mem-
24
brane
tions
. These changes may be caused by direct immune reac-
49
.
In some cases, villous immaturity evokes a compensatory
increase in placental growth and ineffectual capillary proliferation in the immature intermediate villi
5
. For villous maturation to become arrested, maternal antibodies must cross the
placental barrier in early pregnancy, when the villous trees are
still immature. The placental changes take some time to
develop, and therefore a histological diagnosis cannot be made
before the 26th week of gestation
placenta in Fig. 24.
14b shows a normal degree of development
46
. For comparison, the
for the 28th week of gestation.
Retarded Villous Maturation
An example of retarded villous maturation46is shown in
Fig. 24.
villous deficiency
15a . Also known as retarded maturity
6
, this maturation disorder can be diagnosed
by the second trimester of pregnancy. Histological sections
show insufficient branching of the fetal villous trees with a
deficiency of terminal villi and decreased vascularization of
the villi. Since the metabolic membranes are reduced in number, the diffusion path is lengthened. The intrauterine fetal
supply can be maintained only through compensatory placental hyperplasia. These placentas often show a poor compensatory capacity at birth, however, and this can lead to acute
fetal/neonatal hypoxia
5
. Retarded villous maturation can occur
in conditions such as postdate pregnancy, poorly controlled
diabetes mellitus, and blood group isoimmunization, but often
there is no discernible cause. For comparison, Fig. 24.
shows the appearance of a largely mature placenta in the 40th
week of gestation.
5
or terminal
15b
Dissociated Villous Maturation Disorder with
Prevalence of Immaturity
Figure 24.16a shows an example of a dissociated villous maturation disorder “with prevalence of immaturity”
week of gestation. The fetal cotyledons have an approximately
normal branching pattern, but they show a focal or extended
failure of organization into different types of villi in terms of
stromal and vascular development
46
. This villous maturation
disorder does not appear before the late second trimester. It is
on a continuum with retarded villous maturation.
Histological examination shows a markedly decreased
capillary content in the villi, which are still bordered predominantly by two trophoblastic layers. Diffusion capacity is again
compromised by a decreased number of metabolic membranes. Figure 24.
16b illustrates normal placental develop-
ment for the 38th week of gestation.
46
in the 38th
Chorangiosis
Chorangiosis46is a villous maturation disorder characterized
by hyperplasia of the villous capillaries, which often show insufficient sinusoidal transformation (Vogel type I chorangiosis,
Fig. 24.
This disorder may be manifested as early as the first trimester
and is often viewed as an attempt by the placenta to compensate for primary placental hypotrophy or a secondary decrease
in placental size due to extensive infarctions. Chorangiosis may
also occur in association with maternal anemia, poorly controlled diabetes mellitus, blood group isoimmunization, pregnancies at high altitudes, or a maternal cyanotic heart defect
chronic hypoxemia leads to endothelial proliferation with increased fetal capillarization of the villi and increased tortuosity
of those vessels
duction of growth factors by fetal macrophages that have been
damaged by hypoxia
normally developed for the 34th week of gestation.
17a). The diffusion path is correspondingly lengthened.
6, 46
. Studies in experimental animals have shown that
3
. The pathogenesis has been related to the pro-
37
. Figure 24.17b shows a placenta that is
Specific Obstetric Problems
Fig. 24.15a Retardation of villous maturation (40th week of gesta-
tion, H & E, ⫻100).
239
Fig. 24.15b Mature placenta (40th week of gestation, H & E, ⫻100).
Structure of the Human Placenta and Pathomorphological Changes in Placental Insufficiency
Fig. 24.16a Dissociated maturation defect with prevalence of imma-
turity (38th week of gestation, H & E, ⫻200).
24
Fig. 24.17 a Vogel type I chorangiosis (34th week of gestation, H & E,
⫻200).
Fig. 24.16b Mature placenta (38th week of gestation, H & E, ⫻200).
Fig. 24.17 b Normally branched villous network (34th week of gesta-
tion, H & E, ⫻200).
240
Accelerated Villous Maturation
Accelerated villous maturation6is commonly seen, for example, in underweight placentas that have a small basal area
and extensive adjacent obliterative placental lesions. It is
characterized by asynchronous maturation of the fetus and
placenta, and many authors interpret it as an attempted compensatory response by the placenta. Known also as premature
villous maturation
ance of an almost fully mature placenta while the fetus is still
immature and appropriate for dates.
5
, this disorder has the histological appear-
Deficiency of Intermediate Villi
Figure 24.18 a shows the histological appearance of this defi-
46
ciency
which the intermediate villi are decreased in number. Normally fibrosed mainstem villi and myriad terminal villi dominate the picture. As a result, the perfusion capacity of the
—a focal or generalized villous maturation disorder in
placenta is diminished. Since the placenta has no additional
growth reserves, it is pushed to the limit in terms of fetal
supply and, according to Becker
comparison, Fig. 24.
normal-for-date placenta in the 29th week of gestation.
18b shows the appearance of an essentially
5
, requires“rescue by birth.” For
Fetal Obliterative Vascular Diseases
Obliterative fetal vascular diseases most commonly occur in
the large endplate vessels and mainstem villous vessel, causing
fibrous narrowing or even occlusion of the vessel lumina.
Endarteropathy obliterans. A typical representative of these
diseases is endarteropathy obliterans, which is defined as reactive fibrous tissue proliferation in the vessel walls in response
to intrauterine insults
large mainstem villous vessel that has been narrowed by
fibrous plaque. In most cases the precipitating cause of this
process cannot be determined either clinically or morphologi-
5, 46
. Figure 24.19 shows an originally
Placental Insufficiency
Fig. 24.18a Deficiency of intermediate villi (29th week of gestation,
H&E, ⫻40).
Fig. 24.19 Endarteropathy obliterans in a mainstem villous vessel
(MG, ⫻100).
Fig. 24.18b Normally branched villous network (29th week of gesta-
tion, H & E, ⫻40).
Specific Obstetric Problems
Fig. 24.20 Endarteritis obliterans in a mainstem villous vessel (H & E,
⫻200).
cally. Endarteropathy obliterans may be found in the setting of
intrauterine infections, diabetes mellitus, blood group isoimmunization, autoimmune disorders, maternal nicotine abuse,
and other conditions
5, 46
.
Endarteritis obliterans. This is an obliterative process in which
inflammatory infiltrates or pathogenic organisms can be iden-
46
tified
genital syphilis or rubella (Fig. 24.
HIV-associated vasculopathy. Jimenez et al.
. Endarteritis obliterans most commonly occurs in con-
20).
23
were able to detect allantoic vasculopathyin 18 of 34 placentas from HIV-positive mothers. Histological sections revealed foci of endothelial
cell necrosis, media proliferation, altered collagen synthesis, fibrinoid vessel wall insudation, mononuclear infiltration, and
complicating thrombus formation. These vascular changes
may be the result of abnormal immune responses. The presence of these changes showed a positive correlation with clinical manifestations of maternal immune suppression, i.e., less
than a 1 : 1 ratio of maternal T
cells and a fall in the T
lymphocyte count to less than 500/µL.
4
helper cells to T8suppressor
4
The same authors observed villous maturation defects with
prevalence of immaturity in more than one-third of the
placentas examined. The villous immaturity may have resulted
from the vasculopathy. Inflammatory changes in the placental
parenchymaand/or the fetal membranes are no more common
in HIV-infected mothers than in the general population.
The detection of vasculopathy in the allantoic vessels is not
specific for HIV infection, nor does it provide evidence of any
fetal infection that may be present
23
.
Fetal thrombi. Fetal thrombi with luminal narrowing or occlusion are most commonly found in large mainstem villous vessels and endplate vessels. Many of these thrombi are conglutination thrombi that have formed in a setting of endarteritis or
endarteropathy. Figure 24.
21 shows endplate vessels occupied
by older fetal thrombi that are already becoming organized.
Thrombi may be found in small or large villous vessels as a re-
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