placenta%20MD.pptx

Developement of placenta ,umbilical cord and
membranes
Directed by
Esraa Hamdy Abo Zaid
Under supervision
Nashwa El shenawy
Prof of Obstetrics and Gynecology

Placenta
Chorio – decidual membrane
Embryology:
 The development of placenta involves the following
1. Development of decidua basalis from endometrium.
2. Development of chorion.
3. Combination of decidua basalis ( from mother ) and
chorion frondosum ( from fetus ) to form placenta.

Decidua:
 Specialized , Highly modified endometrium of pregnancy.
Decidualization:
 Transformation of secretory endometrium to decidua It is dependent
on estrogen , Progesterone and factors secreted by the implanting
blastocyst.
 The special relationship that exists between the decidua and the
envading trophoblast appears defies the law of transplantation
immunology.

Decidual structure:
 It is classified into three parts based on anatomical location
1. Decidua basalis: decidua directly beneath blastocyst implantation is
modified by trophoblast envision.
2. Decidua capsularis: overlies the enlarging blastocyst and initially
separates the conceptus from the rest of the uterine cavity , It is
prominent during the second month of pregnancy.
3. Decidua parietalis the remainder lining of uterus .

During early pregnancy:
• Three is space between capsularis & Parietalis because
gestational sac does not fill the entire uterine cavity.
By 14 to 16 Weeks gestation :
• The expanding sac has enlarged to completely fill the uterine
cavity, The resulting apposition of the decidua capsularis and
parietalis creates decidua vera & The uterine cavity is
functionally obliterated.

 The decidua parietalis and basalis are composed of three layers:
1. Zona compacta : surface or compact zone.
2. Zona spongiosa : Middle portion or spongy zone.
3. Zona basalis : basal zone remains after delivery and gives rise to new
endometrium.
Zona compacta & spongiosa together form zone functionalis.

Decidual blood supply
1. Decidua capsularis : As a consequence of implantation the
blood supply to capsularis is lost as embryo grows.
2. Decidua parietalis : Supplied by spiral arteries which retain
smooth muscle wall & endothelia and thereby remain
responsive to vasoactive agents.
3. Decidua basalis : Spiral arterial system supplying decidua
basalis is altered remarkably. these spiral arterioles and arteries
are invaded by cytotrophoblasts , during this process.

The vessel walls in basalis are destroyed only a shell with
out smooth muscle or endothelial cells
So these blood vessels ( uteroplacental vessels ) are not
responsive to vasoactive agents conversely the fetal
chorionic vessels which transport blood between
placenta & fetus contain smooth muscle & thus do
respond to vasoactive agents.

Decidua basalis
contributes to formation of placental basal plate and differs Histologically
from decidua parietalis in two important respects.
1. Spongy zone of basalis consists mainly of Arteries and widely dilated veins
and by term glands disappeared.
2. The decidua basalis is invaded by many interstitial trophoblast cells &
trophoblastic giant cells which commonly penetrate the upper
myometrium.
The NitaBuch layer is a zone of fibrinoid degeneration in which invading
trophoblasts meet the decidua basalis if decidua is defective as in placenta
accreta the NitaBuch layer is usually absent.

Development of chorion and formation of chorionic villi
Human placental formation begins with trophectoderm which appears
at morula stage, It gives rise to trophoblast cell layer encircling the
blastocyst.

Differentiation of trophoblast:
By 8th day post fertilization, after initial
implantation the trophoblast has differentiated
into outer multi nucleated syncytium = primitive
syncytiotrophoblast and an inner layer of
primitive mononuclear cells = cytotrophoblast.

Syncytio trophoblast
Cytotrophoblast
 Amorphous cytoplasm
without cell borders
 Nuclei are multiple and
varies in size and shape
 Well demarcated cell border
 Single nucleus
 Ability to undergo DNA
synthesis and mitosis.

After implantation is complete:
 Trophoblast further differentiate along two
Extra villous trophoblasts Villous trophoblasts gives rise to
= Not villi chorionic villi . transport O2,
Migrate into decidua & Myometrium and nutrient and other compounds
ALSO penetrate maternal vasculature. Between fetus & Mother
Thus coming into contact ē various maternal stages primary
Cell types classified into secondary
Tertiary
classified into
Interstitial trophoblasts Endovascular
Invade decidua & Myometrium trophoblasts
to form placental bed giant cells which penetrate floating Anchoring
they surround spiral arteries. Spiral Artery lumen villi villi

All around chorionic vesicle finger like processes develop from
syncytiotrophoblast and called syncytial trabeculae they are separated
by spaces called lacunae.

This occurs 12 days after conception.
After invasion of superficial decidual capillary walls
lacunae become filled ē maternal blood.
Placental organization
1. Development of primary villi
with deeper blastocyts invasion into the decidua cyto
trophoblastic cells grow in the center of each syncytial
trabeculum to form primary villous composed of core
of cytotrophoblast surrounded by
syncytiotrophoblast.

 The cytotrophoblast cells pierce the distal ends of the syncytial
trabeculae = primary villi and spared deep to decidua basalis and
capsularis to meet & fuse with cytotrophoblast cells from adjacent
trabeculae. As a result continuous layer called cytotrophoblast shell
develops deep to decidua basalis & capsularis this shell separates the
syncytiotrophablast of chorionic vesicle from decidua preventing more
erosion of uterus by syncytiotrophoblast.

 This cytotrophoblast proliferation at villous tips produce the
trophoblastic cell columns that form anchoring villi which has no
mesoderm or fetal vessels it is trophoblastic cell columns that are
anchored to the decidua at basal plate.

Development of secondary villi:
These are formed when extraembryonic mesoderm
grows in the center of cytotrophoblast cells of
primary villi this occurs 12th day after fertilization.
3. Development of tertiary villi :This formed when villous
mesoderm gives rise to Arterioles capillaries &
venules which join the blood vessels of the umbilical
cord & feotus.

Decidual septa:
 Number of decidual septa project into the
intervillous spaces from the decidua basalis.
These septa do not reach the chorionic plate. They
have a core of decidua basalis in the center covered
by cytotrophoblast & syncytiotrophoblast the septa
incompletely divide placenta into 25
-
15 spaces called
cotyledons.

Trophoblast formation are divided to
 Villous trophoblast : Trophoblast that arranged in villous
pattern it is further divided to
A. Anchoring villi formed of cyto & syncytiotrophoblast.
B. Floating = free = branching villi formed of fetal
vessels + Extraembryonic mesoderm + cyto +
cyncytiotrophoblast.

2. Extra villous trophoblast this trophoblast does not
form villi – it invades the decidua reaching the
myometrium & invades decidual spiral arterioles and
it is subdivided into
A. Interstitial trophoblast
B. Endovascular trophoblast

Fate of chorionic villi
All the chorionic vesicle is surrounded by villi in
which
1. The villi related to decidua capsularis degenerate
compression by the expanding chorionic vesicle.
2. The villi related to decidua basalis enlarge to form
( chorion frondosum ).

Which chorion frondosum combine which decidua
basalis to form placenta.
Although maternal venous sinuses are tapped early
in implantation maternal arterial blood does not
enter the inter villous space until around day 15.
Approximately at Day 17 fetal blood vessels are
functional and placental circulation is established.

Invasion of spiral Arteries
These events occur in 1st half of pregnancy
completed by 18 to 20 WKS.
Spiral artery modification are carried out by two
population of extra villous trophoblast.
Interstitial trophoblast surround Arteries
endovascular trophoblast penetrate spiral Artery
lurnen.
This remodeling converts narrow lumen, muscular
Arteries into dilated, low resistance uteroplacental
vessels.

Placental Growth:
• 1st trimester placental growth is more rapid than that of the fetus.
• 17 postmenstrual weeks placental & fetal weights are
approximately equal.
• At term placental weight one sixth of fetal weight.

Morphology of placenta
Placental disc :
1. site of implantation:
 Upper uterine segment posterior in 60%of cases and anterior in 40% ,
If inserted in lower uterine segment partial or total it is placenta
previa.
2. Weight At term typical placental weighs 1/6 fetal weight = 500gm.
3. Shape discoid round to oval.
4. Diameter 18-22 cm in diameter.

5. Thickness at center 25mm.
6. Surfaces has 2 surfaces
Maternal surface : that lies against uterine wall. It is
basal plate which is divided by clefts into 15-20
portions = cotyledons.
Fetal surface : chorionic plate into which umbilical
cord insert typically near center visible large fetal
vessels that originate from cord vessels then spread
& branch a cross chorionic plate.

In tracing these two features are clinically important
•Fetal Arteries invariably cross over veins which is
important when taking a fetal arterial blood sample.
•Fetal vessels do not reach periphery of placenta
important to determine that no other lobes are
missed.
Chorionic plate and it’s vessels are covered by thin
amnion which can be easily peeled away from post-
delivery specimen.

Extra placental membranes
Amnion amniotic epithelium covering the fetal
surface of the placenta.
Amnion & chorion that extend from placental edge.
Abnormality in size = weight = thickness
1. Small placenta no universal definition but if <15cm
diameter & it is associated é LBW.

2. Placentomegaly placenta thicker than 40mm by
ultrasound.
Causes :
(a) large retro placental hematoma.
(b) Collection of blood or fibrin é massive peri villous
or inter villous fibrin deposition.
(c) Villous enlargement due to maternal causes DM,
Anemia or fetal causes Hydrops, anemia or infection
by syphilis, toxoplasmosis, CMV, parvovirus.

Variation in placental Morphology
1. Bilobate placenta = bipartite placenta = placenta
duplex

 The cord insert between two placental lobes either into a connecting
chorionic bridge ( bilobate ) or into intervening membranes (
bipartite ) multilobate = more equivalently sized lobes is rare.
2. Placenta succenturiate placenta é small succenturiate
lobe ( s ) that develop in membranes at a distance from main placenta.

Clinical complication:
1. These lobes have vessels that pass through the
membranes and if these vessels overlie the cervix
and create vasa previa dangerous fetal He can
follow vessel laceration.
2. An accessary lobe can also be retained in the
uterus after delivery post partum Hge & atony.
3. Placenta membranacea :
 This placenta é large diameter like amembrane and villi cover all or
nearly all the uterine cavity.

4. Ring shaped placenta:
May be a variant of placenta membrancea. This
placenta is annular and a partial or complete ring of
placental tissue is present.
5. Placenta fenestrate the central portion of
placental disc is missing.

6. Placental mesenchymal dysplasia:
 Cystic vesicles are seen é this rare condition correspond to enlarged
stem villi but unlike molar pregnancy trophoblast proliferation is not
excessive.

7. Circumvallate placenta the periphery of chorion is
thickened , opaque , gray – white circular ridge composed of double fold
of chorion & amnion.

8. Circummarginate placenta
The chorionic membranes insert inward from
the margin of placental edge unlike
circumvallate placenta , the placental edge is
not central depression & rolled up.

Variation of placental site:
Placenta previa partial or total encroachment of
placenta on lower uterine segement a low lying ,
marginal previa , partial previa , complete previa.
Placental calcification & grading
 It occurs é advancing gestation , smoking , maternal serum ca levels.

• These Hyperechoic deposit can easily be seen by U/S and aggrading
scale from 0 to 3 reflects calcification é numerical grade.
• Grade 0 placenta is Homogenous , lacks calcification and displays a
smooth , Flat chorionic plate.
• Grade 1 placenta scattered echogenicities , subtle chorionic plate.
• Grade 2 placenta shows echogenic stippling at basal plate , large.

Placental Abnormal attachment
Abnormal placental adherence placenta accreta .
Abnormal detachment placental abruption.
Vascular pathologies of placenta
Placental Fibrin deposition :
(a) Subchorionic (b) Perivillous
 Slow of maternal blood
flow in the intervillous
space. It appears as white,
Firm, round elevated
plaques with in placental
fetal surface.
 Slow of maternal blood flow
around on individual villus result
in fibrin deposition & can lead to
diminished villous O2 .
 They are small, yellow - white
placental nodules are only visible
with in parenchyma of a cut
placenta.

Infraction : chorionic Villi receive O2 solely from maternal
Circulation supplied to the intervillous space any obstruction
to this supply by uteroplacental disease can cause infarction.
They are common lesions in mature placenta.
Hematoma: several types of hematoma
A. Retroplacental hematoma, between placenta & decidua e.g
placental abruption is large & clinically significant.
B. Marginal hematoma between chorion & decidua at
placental periphery known clinically as subchorionic Hge.
C. Sub amniotic hematoma from fetal blood vessels, beneath
the amnion but above chorionic plate.

D. Subchorial thrombus along roof of intervillous space & beneath
chorionic plate.
By U/S Hyperechoic to isoechoic in 1st wk after Hg.
Hypoechoic at 1 to 2 WKS.
Anechoic after 2WKs.
Placental thrombosis :
a) Intervillous collection of coagulated maternal blood normally found in
the intervillous space + fetal blood from a break in a villus .
 If recent rcd, around or oval vary in size up to > 1 cm.
 old white-yellow round or oval.
a) Fetal arteries thrombosis:
 Fetal arteries that divide & send branches out across placental
surface. this will obstruct fetal blood flow distal to obstruction
affected portions of the villus become non functional.
 there are thrombi limited numbers are normally found in mature
placentas.

C. Vascular lesions affecting villous capillaries
1) Chorangiosis number of capillaries with in terminal villi
≥ 10 capillaries to be present in ≥ 10 villi in ≥ 10 field through
a 10x microscope lens.
2) Chorangiomatosis number of capillaries in stem villi
But not terminal villi.
Clinical significance remains unclear.

Placental tumors :
1) Chorioangioma : Benign placental tumors have components
similar to blood vessels & stroma of chorionic villus
incidence 1%.
In some cases fetal to maternal Hge across tumor capillaries
leads to elevated level of maternal serum alpha – fetoprotein
( MSAFp).
U/S well-circumscribed-rounded hypoechoic lesion lying near
the chorionic plate & protruding into amniotic cavity.
Cavity. By color doppler increase blood flow distinguish these
lesions from other placental masses e.g hematoma.

2. Gestational trophoblastic neoplasia
3. Metastatic tumors
 Maternal malignant tumor rarely metastasize to placenta
Fetal malignant tumors rarely metastasize to placenta.
Development of fetal membranes
Fetal membranes are extra embryonic mesoderm
Chorion
Amnion

Early during development a space develops from the dorsal cell of
inner cell mass (ectoderm).
Epithelial cells of Amnion derived from Fetal ectoderm and called
amnioblastic cells.
Amnion 1st identifiable at 7th or 8th day of embryo development
initially a minute vesicle small sac that covers the dorsal
embryo surface.
As amnion enlarges it engulfs the growing embryo which
prolapses into cavity.
Human amnion lacks smooth muscle calls, nerves, blood vessels
and lymphatics.

Amnion Epithelium is metabolically active & involved in
solute & Water transport for amniotic fluid Hemostasis &
produce Bioactive compounds é both autocrine & paracrine
responses that include production of IL8, PGE2 , fetal
fibronectin and collagenase.
Proteoglycans are responsible for tensile strength of amnion.
Such factors modulate change in membrane properties during
labor.

Amniotic fluid :
Early pregnancy it is an ultrafiltrate of maternal plasma.
 2nd trimester consists largely from extracellular fluid that
diffuses through the fetal skin thus reflects composition of fetal
plasma.
After 20 Wks cornification of fetal skin prevents this diffusion
and amniotic fluid is produced by .
1) Largely From Fetal urine ,kidneys produce urine 12 weeks
by 18 weeks 7 to 14 ml per day.
2) Pulmonary fluid Small proportion of Amniotic volume.
3) Fluid filtering through placenta accounts for rest.
4) Desquamated fetal cells, vernix, lanugo bec these are
hypotonic, the net effect is that amniotic fluid osmolality
decreases é advancing gestation.

Volume :
Volume at each Wk is variable.
Volume by 10 ml per week at 8weeks.
Volume by 60 ml per week at 21 weeks.
Then peaks at 34 weeks .
At term average volume 1000 ml.
 Functions :
 Cushion to fetus, Musculoskeletal development
protection from trauma, maintain temperature
minimal nutritive function.

•Chorioamnion abnormalities :
1.Chorioamnionitis .
2.Amnion nodosum numerous, small, light tan
nodules on the amnion overlying the chorionic plate
these may be scraped off the fetal surface & contain
deposits of fetal squamous & fibrin reflects
prolonged & severe oligohydramnious.

3. Amniotic band sequence : Amnion bands Constrict or
amputate fetal parts.
U/S : often identifies the sequelae of this sequence rather
than the bands them salves.
Management : Fetoscopic laser interruption of band in highly
selected antepartum cases .

4. Amnionic sheet normal amniochorion
draped over a preexisting uterine synechia .
It poses little fetal risk.

 Development of umbilical card :

•At first Embryo is 3 layer flattened disc (trilaminar
embryo) interposed between Amnion (fetal
ectoderm side) & yolk sac (fetal endoderm side).
Fetal dorsal surface=ectoderm grows faster than
the ventral surface = endoderm resulting in folding
of the embryo in all direction such that the
ectoderm is now on the outer surface of the whole
embryo then the mesoderm in the middle and the
endoderm in the center of the embryo.

 The amniotic sac enlarges as well, squeezing &
forming the umbilical card.
 As pregnancy advances yolk sac become smaller &
it’s pedicle relative longer.
 By the 3rd month (middle of it) the expanding
amnion fuses with chorion leave & covers the pulging
placental disc & lateral surface of body stalk = called
umbilical card.

Primitive umbilical card :
1. Connecting stalk containing allantois and 4 umbilical vessels
(2 Arteries , 2 veins).
2. Yolk stalk is covered by vitelline vessels and surrounded by
extraembryonic coelom which contains loops of intestine if
persist umbilical hernia.

 Definitive umbilical cord:
Some structures disappear
Loops of intestine return into the abdomen.
The extraembryonic coelom is closed.
The allantois, yolk stak and vitelline vessels are
obliterated.
Rt umbilical vein disappears.
 At term Umbilical card contain ,
1 vein + 2 Arteries.

Umbilical card abnormalities :
 Length:
A. excessive long card cord entanglement,
prolapse and fetal anomalies.
B. shorts cord < 30 cm failure of engagement descant,
malpresentation.

Vessel number:
four vessel cord- rare, e congenital anomalies.
The most common aberration is that single umbilical artery
(SUA) which is associated e fatal anomalies.
 Cysts:
A. True cysts: are epithelium-lined remnants of allantoic or
vitelline duct - located closer to fetal insertion
B. Pseudocysts: more common, from local degeneration of
Wharton jelly, and where along cord.

 Insertion of cord:
1. Eccentric insertion: no identifiable fetal risk.
C. Marginal insertion: common, called battledore placenta
cord anchors at placenta margin.
D. Velamentous insertion: vessels (umbilical) travel with the
membrane before reaching the placental margin
incidence 1% - twin 6% - more common é placenta previa.
4. Furcate insertion: umbilical vessels lose their protective
Wharton jelly shortly before insertion, they are covered by
amnion sheath, prone to compression, twisting, thrombosis.

Vasa previa: fetal vessels travel within the membranes and
overlie cervical os. They can be torn é cervical dilatation or membrane
rupture antepartum Hge from rapid fetal bleeding.

 Vascular abnormalities:
Cord hematoma: rare, follow rapture of umbilical vessel
Still birth, intrapartum abnormal fetal Heart rate.
Umbilical cord vessel thrombosis: rare, 70% venous 20%
venous & arterial, 10% arterial still birth, fetal growth
restriction, intrapartum fetal distress.
Umbilical vein varices by color Doppler
Umbilical Artery Aneurysm d.t congenital thinning vessel wall
é decrease support from Wharton jelly fetal compromise &
death.

Knots, strictures & loops
True knots 1% of births, formed from fetal movement
if found in singleton fetuses – still birth 4 to 10 fold
False knots: focal redundancy & folding of vessels
Cord strictures: focal narrowing of diameter usually near
fetal cord insertion site.

cord loops: common coiling & round various fetal parts
during movement
Nuchal cord: common vaginal delivery is suitable since despite
their frequency nuchal cord & cords wrapped around body are
not associated é greater rates of adverse perinatal outcome.
Funic presentation :umbilical cord is presenting part in lab
uncommon, associated with malpresentation identified by
U/S color flow Doppler overt or occult cord prolapse at term
cesarean delivery is recommended.

placenta%20MD.pptx

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