PLACENTA AND ITS

ABNORMALITIES
अपरा

(सु. श. 4/24)
तदैव च आर्तवम् अधोगमने गर्भेण
प्रतिहतं आहरपरिनामतः च प्रतिदिनं
उपचियमानं I (INDHU)
PLACENTA

•Discoid
•Hemochorial
•Decidua
•Fetomaternal organ
•2 surfaces – maternal and fetal
 FORMATION OF PLACENTA
Implantation
ZONA HATCHING

IMPLANTATION
INTERSTISIAL
IMPLANTATION

Trophoblast of the
blastocyst invades the
endometrium of uterus.
Blastocyst burrows deeper
and deeper into the uterine
mucosa till the whole of it
DECIDUA –SHEDS OFF
DECIDUA - uterine endometrium
after implantation

•When morula reaches the uterus, the

endometrium is in secretory phase.
•After implantation, the features of
endometrium, which are seen during
secretory phase of menstural cycle are
maintained and intensified.
DECIDUAL REACTION: the stromal cells
enlarge becomes vacuolated and store
glycogen and lipids.
DECIDUA BASALIS:
• Also inferred as decidual plate.
• The portion of decidua where the placenta is
to be formed (deep to the developing
blastocyst)
• Firmly united to the chorion.
• Store large amounts of lipids and glycogen.

DECIDUA CAPSULARIS:
• Part of the decidua which separates the
embryo from uterine lumen.

DECIDUA PARIETALIS:
• Part lining the rest of the uterine cavity.
FORMATION OF CHORIONIC VILLI

•Functional element of placenta – very

small finger like process/ villi
•Villi – capillaries through which fetal
blood circulates
surrounded my maternal blood
exchange b/w maternal and fetal
circulation takes place
through the tissues forming the
walls of the villi
•Villi are formed as offshots from the
surface of the trophoblast
• Chorionic villi are first
formed all over the
trophoblast and grow into
the surrounding decidua.
• Villi related to decidua
capsularis are transitory
and degenerated after
sometime – this part of
chorion become smooth
and is called the chorion
laevae.
• Villi that grow into the
decidua basalis undergo
considerable
development.
 Decidual plate

Chorionic plate
 Syncytiotrophoblast grows into the endometrium
As the endometrium is eroded some of its blood vessels are opened up and
blood from them fills the lacunar space

Each trabeculus - initially made of syncytiotrophoblast

- later cells of cytotrophoblast begin to multiply and grow into
each trabeculus

i.e., - central core – cytotrophoblast

10 villus - outer layer – syncytiotrophoblast
- surrounded by maternal blood filling the lacunar space –
Intervillous space

Extra embryonic mesoderm invades 10 villus

 Core – mesoderm
20 villus Covered by – cytotrophoblast
syncytiotrophoblast

Blood vessels are seen in mesoderm

Core – mesoderm with blood vessels

30 villus Covered by – cytotrophoblast
syncytiotrophoblast

Blood vessels of villus establish connection with circulating system of

embryo
• Fetal blood – circulates through villi
• Maternal blood – circulates through intervillous space
Stages of chorionic villi formation
10 villi
• Central core of cytotrophoblast
• Covered by layer of syncytiotrophoblast
• Adjoining villi – separated by intervillous space

20 villi – 3 layers
• Outer – syncytiotrophoblast
• Intermediate - cytotrophoblast
• Inner extra embryonic mesoderm

30 villi
• Similar to 20 villi
• Blood capillaries in the mesoderm
1st formed villi are attached on Anchoring villi which consists of

Truncus • stem
chorii

• divides into
Rami number of
chorii branches

• Finer branches
Ramuli which is attached
to the
chorii cytotrophoblastic
shell
• Anchoring villi give off numerous
branches that grow into the intervillous
space as free villi.
•New villi also sprout from the chorionic
side of the intervillous space.
• Ultimately, almost the whole
intervillous space becomes filled with
villi. As a result the surface area
available for exchange b/w maternal
and fetal circulation becomes
enormous.
 FURTHER DEVELOPMENT OF PLACENTA
 Placenta gets subdivided into a number of lobes by septa that
grow into intervillous space from the maternal side.
 Each lobe – maternal cotyledon
 Appearance when viewed from maternal side:
Base of the septa – grooves
Cotyledons – convex areas bounded by grooves
Number of lobes – 15-20
Each lobe contains – a number of anchoring villi and their branches
one such villi constitutes fetal cotyledon
At full term – 6-8ll diameter
Maternal surface –* formed by decidual plate
*rough
*subdivided into cotyledons
Fetal surface – *formed by chorionic plate lined by amnion
*smooth
*umbilical cord is attached
 Cotyledon (15-20)

Chorionic villi

Lacunar/intervillous spaces
A. fetal surface of the placenta. Note the site of cord
insertion (arrow head). A1: placental border with the
insertion of the amniotic membranes.
B. Distribution of the chorionic vessels in the fetal placental surface
from the site of cord insertion (arrow head). B1: chorionic vessels
with the cross between an artery (upper) and a vein (under)
(arrow).
C. Maternal surface of the placenta. Note the subdivision of the
surface in numerous maternal cotyledons. C1: maternal
cotyledons
PLACENTAL MEMBRANES/ BARRIER
Ma
ter
nal
blo Fe m b ra n e
me
od tal
S e pa rate d by a

bl
oo
d
placental barrier
In placenta,
Maternal blood circulates through intervillous space
Fetal blood circulates through blood vessels in villi
They do not mix with each other

Membrane composition:
• Endothelium of fetal blood vessel and its basement membrane
• Surrounding mesoderm (connective tissue)
• Cytotrophoblast and its basement membrane
• Syncytiotrophoblast From fetal side

Importance : interchange of oxygen, nutrition and waste products

 Placental
barrier

1
2
 PLACENTAL CIRCULATION
Placental circulation consists of independent circulation of blood in
two systems:
• UTEROPLACENTAL CIRCULATION
• FETOPLACENTAL CIRCULATION
UTEROPLACENTAL CIRCULATION (maternal circulation):

• A mature placenta volume -500 ml

• 350 ml being occupied in the villi system
• 150 ml lying in the intervillous space.
• intervillous blood flow at term -500–600 ml /minute,
• the blood in the intervillous space is completely replaced about
3–4 times per minute.
• intervillous space pressure
• 10–15 mmHg during uterine relaxation
• 30–50 mmHg during uterine contraction.
• the fetal capillary pressure in the villi -20–40 mm hg.
 ARTERIAL CIRCULATION:
About 120–200 spiral arteries open into the intervillous space
by piercing the basal plate randomly at numerous sites. Normally,
there is cytotrophoblastic invasion into the spiral arteries initially up
to the intradecidual portion within 12 weeks of pregnancy. Not only
the endothelial lining is replaced but also the musculoelastic media
is destroyed and replaced by fibrinoid material. There is a secondary
invasion of trophoblast between 12 weeks and 16 weeks extending
up to radial arteries within the myometrium. Thus, spiral arteries
are converted to large bore uteroplacental arteries. The net effect is
funneling of the arteries which reduces the pressure of the blood to
70–80 mmHg before it reaches the intervillous space. It thus
increases the blood flow.
Trophoblast cells that do not take part in villous structure are
known as extravillous trophoblast (EVT).
FETOPLACENTAL CIRCULATION:
• umbilical arteries chorionic plate underneath the
amnion, each supplying one half of the placenta.
• The arteries small branchesenter the stems of the
chorionic villi.
• Each dividesprimary, secondary and tertiary vessels of
the corresponding villi.
• Maternal and fetal bloodstreams flow side by side, but
in opposite direction. =This counter current flow .
facilitates material exchange between the mother and
fetus.
• villous capillary pressure -20–40 mm Hg.
• The fetal blood flow through the placenta -400 mL/min.
FUNCTIONS OF PLACENTA
 FUNCTIONS OF PLACENTA
• Transport -O2,H2O,electrolytes and nutrition [in the
form of carbohydrates, lipids, polypetitides, amino
acids, vitamins]from maternal to fetal blood
• A full term fetus --25ml of O2 /min from maternal
blood.
• Excretion of CO2, urea and other waste products
produced by the fetus into the maternal blood
• Maternal anitibodies [IgG] reaching the fetus
through placenta give the fetus immunity against
some infections (Eg, diphtheria,measles)
•Acts as a barrier and prevents many bacteria and other harmful
substance from reaching the fetus. However most viruses [including
poliomyelitis, rubella] and drugs taken by the mother enter the
fetal circulation and can produce congenital malformation.
As a rule, maternal hormones do not reach the fetus, however
synthetic progestins and synthetic estrogens easily cross the
placenta and can have adverse effects on the fetus (including CA in
later life)
•Preventing antigenic reactions b/w fetal and maternal blood.
•Placenta synthesis several hormones (probably produced in
syncytiotrophoblast)
 PLACENTAL HORMONES
The placenta secretes large number of hormones , the most
important are
STEROID HORMONES
Estrogen : Progressively increases during pregnancy (peak
before onset of labor). Stimulate growth of the myometrium and
antagonize the myometrial suppressing activity of progesterone
stimulate mammary gland development.
Progesterone : Until the end of the 8th week the corpus
luteum continues to secrete progesterone , with gradual cessation
of corpus luteum function, the placenta become responsible for its
secretion which reaches the peak just before labor.
Progestins, including progesterone, have two major roles during
pregnancy:
Support of the endometrium
Suppression of contractility in uterine smooth muscle
 PROTIEN HORMONES

• Human chorionic gonadotrophin : detected in maternal

plasma by radioimmunoassay at 6days after fertilization and
in urine soon after that and this forms the basis of the
pregnancy test. It reaches the peak at 10-11weeks of
gestation
• Human placental lactogen : its main action is to reset the
CHO and fat metabolism of the mother and ensure adequate
supply of energy and glucose to the fetus.
• Relaxin : detected in maternal plasma 8-10 days after
ovulation , its important to inhibit uterine contraction in early
pregnancy
hCS (somatomammotropin) – anti insulin effect of mother
Increase plasma levels of glucose and amino acids in
maternal circulation
In this way it increases availability of these materials
for the fetus
It also enhances glucose utilization by the fetus
 Progesterone
hCG
Maintains the corpus luteum during the initial
period of pregnancy hCS
Maintains the pregnancy

Relaxin
Oestriol
Lactogenic function
Growth stimulation

Inhibits myometrial contractions

10 20 30 40 Weeks
6 12
 Progesterone
hCG

hCS

Relaxin
Oestriol

10 20 30 40 Weeks
6 12
 PLACENTAL GRADING (GRANNM
CLASSIFICATION)

Its an ultrasound grading system of placenta based on its

maturity.
This primarily affects the extent of calcification.
 • < 18 weeks
• Uniform echogenicity
Grade 0 • Smooth chorionic plate

• 18-29 weeks
• Occasionally paranchymal
Grade 1 calcification/ hyperechoic
area
• Subtle indentations of
chorionic plate
 • 30-38 weeks
• Occasional basal calcification/
Grade 3 hyperechoic area
• Deeper indentations of the
chorionic plate

• >39weeks
• Significant basal plate
Grade 4 calcification
• Chorionic plate interrupted by
indentations (frequently
calcified) that reach up to the
basal plate
 PLACENTAL PATHOLOGY

a) PLACENTAL ANATOMY
• PLACENTAL THICKNESS – Small placenta
Placentomegaly
• PLACENTAL GRADING – Placental calcification
Placental venous lake
• VARITION IN PLACENTAL MORPHOLOGY
 INCREASED THICKNESS
An abnormally increased placental thickness falls under the
spectrum of placetomegaly. This can happen with a number of
conditions and is associated with increased risk of placental
insufficiency.
Causes include:upper limit of normal variation
fetal macrosomia
fetal hydrops
TORCH infections
maternal medical conditions
maternal anemia
maternal diabetes
If the placenta is thickened and contains cysts, then other entities
should be considered:
partial molar pregnancy
triploidy
placental mesenchymal dysplasia
MIMICS
An important mimic for a thickened placenta is an
isoechoic abruption. A transient myometrial contraction can also
mimic a thickened placenta.

DECREASED THICKNESS
An abnormally decreased placental thickness can be seen
with:
• pre-eclampsia
• intrauterine growth restriction (IUGR)
• placenta membranacea (extremely rare)
 SMALL PLACENTA

A small placenta if observed on antenatal ultrasound can arise from a

number of situations. They include:
• variation in placental morphology: where only part of the placenta is
seen
• bilobed placenta: with only one lobe seen
• succenturiate lobe: with either main lobe or succenturiate lobe not
seen
• hypertensive states in pregnancy: with presence of placental infarcts
• chromosomal anomalies
• trisomy
• dygynic triploidy: with extra chromosomal set from maternal origin
• ​IUGR
• intrauterine infection
 PLACENTAL CALCIFICATION

Placental calcification has been considered a manifestation of “aging” of the

placenta. It commonly increases with gestational age.
Delayed placental calcification
• maternal diabetes
• Rh sensitization
Accelerated placental calcification
• normal placental maturity
• maternal thrombotic disorders
• hypertension
• IUGR
• maternal cigarette smoking
• maternal SLE
 VARIATION IN PLACENTAL MORPHOLOGY

There can be several variations in placental morphology. These include:

• Bilobed placenta: two near equal size lobes

• Succenturiate lobe(s): one of more smaller accessory lobes
• Circumvallate placenta: rolled placental edges with smaller chorionic plate
• Circummarginate placenta
• Placenta membranacea
• Placenta fenestrata
• Zonary placenta
 CIRCUMMARGINATE PLACENTA

Circummarginate placenta is an uncommon variation in placental morphology.

The chorionic membranes insert inward from the margin of placental edge,
similar to circumvallate placenta, but unlike circumvallate placenta, the
placental edge is not thickened and rolled up, and there is no central
depression.
 PLACENTA MEMBRANACEA

Placenta membranacea, also known as a placenta diffusa, is an extremely

uncommon variation in placental morphology in which the placenta develops as a
thin membranous structure occupying the entire periphery of the chorion.

EPIDEMIOLOGY
The estimated incidence is ~1:20,000-40,000 pregnancies .

ASSOCIATIONS
abnormal placental adherence: reported in up to 30% of cases .

PATHOLOGY
In this situation all of the fetal membranes are covered by functioning villi and the
placenta develops as a thin membranous structure occupying the entire periphery of
the chorion. The placental mass can often be thin (1-2 cm ) and even disrupted.
 PLACENTA FENESTRATA

Placenta fenestrata is one of the variations in placental morphology, which is

characterized by one or more areas of focal placental atrophy lacking villi
and covered only by the chorion membrane
b) PLACENTAL DEVELOPMENTAL ABNORMALITIES
• PLACENTA PREVIA

• SPECTRUM OF ABNORMAL PLACENTAL VILLOUS ADHERENCE

Placental accreta
Placental increta
Placental percreta

• ANORMALITIES OF CORD INSETION

• ABRUPTIO PLACENTA

• PLACENTAL MASSES
 PLACENTA PRAEVIA

Placenta praevia refers to an abnormally low lying placenta such that it lies
close to, or covers the internal cervical os. It is a common cause
of antepartum hemorrhage.
Placenta praevia is potentially life-threatening condition for both mother and
infant. As such, antenatal diagnosis is essential to adequately prepare for
childbirth.

EPIDEMIOLOGY
Placenta praevia has an incidence of 1/200 pregnancies.
 CLASSIFICATION
Praevia is divided into four grades depending on the relationship and distance
to the internal cervical os:

Sometimes grades I and II are termed a "minor" or "partial" placenta praevia,

and grades III and IV are termed a "major" placenta praevia
Clinical presentation
 PLACENTAL INFARCTION

Placental infarction refers to a localized area of ischemic villous necrosis. It is a

significant cause of placental insufficiency.

EPIDEMIOLOGY
A localized infarction can occurs in up to ~12.5% (range 5-20%) of all gestations.

PATHOLOGY
It usually results from an interrupted maternal blood supply

LOCATION
Placental infarcts are more common at the periphery of the placenta.
 PLACENTAL INSUFFICIENCY
Placental insufficiency is a term given to a situation where the placenta cannot
bring enough oxygen and nutrients to the growing fetus.

CLINICAL PRESENTATION
Fetuses may present with intra-uterine growth restriction
(IUGR) (especially asymmetrical IUGR).

PATHOLOGY
It can be primarily caused by three main mechanisms :
• Impairment in maternal circulation
Maternal hypertension
Maternal thrombophilic disorders
• Impairment in fetal circulation
Placental implantation over a fibroid
• Vascular thrombosis (e.G placental infarction)
 BATTLEDORE PLACENTA
Placenta battledore (batyldoure = a beating instrument) is a term
describing a placenta where the umbilical cord is attached at the margin.
Occurs 7- 9% in singleton pregnancies and 24-33% in twin pregnancies and
may effect placental function/fetal growth. The description probably comes
from the similarity to a bat or paddle
 VASA PRAEVIA
Vasa praevia refers to a situation where there are aberrant fetal vessels crossing
over or in close proximity to the internal cervical os, ahead of the fetal presenting
part. These vessels are within the amniotic membranes, without the support of
the placenta. Vasa praevia is a rare but potentially catastrophic cause
of antepartum hemorrhage.

PATHOLOGY
Vasa previa can be of two types:
TYPE I (present in ~ 90% of cases with vasa praevia 3): abnormal fetal vessels
connect a velamentous cord insertion with the main body of the placenta
TYPE II
• Abnormal vessels connect portions of a bilobed placenta
• Placenta with a succenturiate lobe: due to this association, vasa praevia
needs to be excluded in patients with variant placental morphology
These vessels are unsupported by Wharton jelly or placental tissue and are at risk
of rupture during labor.
VASA PRAEVIA
PLACENTAL CYST
PLACENTAL TUMORS
HYDATIDIFORM MOLE
TWIN PREGNANCY
 PLACENTAL FUSION

Placental fusion is a phenomenon that can occur in a twin pregnancy. This can
occur to varying degrees. Determination of chorionicity on ultrasound can
sometimes be difficult if there has been a placental fusion.
PLACENTA – THE LEAST UNDERSTOOD
ORGAN
THANK YOU