STRUCTURE AND

FUNCTION
OF PLACENTA INCLUDING
PLACENTAL
INSUFFICIENCY

DEFINITION:
Placenta is a fleshy structure that develops
mostly from fetal chorionic tissue and
maternal decidua during pregnancy. It lies
implanted on the uterine wall. It is
connected with fetus through umbilical
cord in the amniotic cavity .It maintains
pregnancy and carries vital fetal functions.
The human placenta is discoid because of
its shape; hemochorial, because of direct
contact of chorion with the maternal blood

DEVELOPMENT OF THE
HUMAN PLACENTA
Decidua : It is the name given to
endometrium during pregnancy.
Decidua basalis
Decidua capsularis
Decidua parietalis

 Early Trophoblast
Syncitio trophoblast / Plasmodia
trophoblast
Cytotrophoblast / Langhans
layer
Extra embryonic mesoderm

Formation of chorionic villi

The essential element of
placenta are small finger like
projection called villi.
The villi are formed as offshoots from
the surface of the trophoblast. As it
along with the underlying extraembryonic mesoderm, constitutes
the chorion, the villi arising from it
are called chorionic villi

 The villi related to the decidua

capsularis are transitory and after
some time they degenerate. This
part of the chorion becomes smooth
and is called the chorion laevae.
The part of the chorion that helps
form the placenta is called the
chorion frondosum.

Stages in formation of
chorionic villi
Primary villi: consist of a central
core of cytotrophoblast covered by a
layer of syncitio trophoblast.
Adjoining villi are separated by an
intervillous space.

 Secondary villi: It shows 3 layers.

Ouuter syncitiotrophoblast, an
intermediate layer of cytotrophoblast
and an inner layer of extra
embryonic mesoderm.
Tertiary villi: It is like secondary
villi except that there are blood
capillaries in the mesoderm.

 Details of the process of villus

formation

 Placental ageing
Villi changes:
Decreasing thickness of the syncitium and
appearance of syncitial knots.
Partial disappearance of Langhans cells.
Decrease in the stromal tissue including
Hofbauer cells.
Obliteration of some vessels and marked
dilatation of the capillaries.
Thickening of the basement layer of the fetal
endothelium and the cytotrophoblast.
Deposition of fibrin on the surface of the villi.

 Decidual changes: Degeneration of

Nitabuchs
layer
(area
where
trophoblast cells meet the decidua)
Intervillous space :
-White infarcts
-Rohrs stria

STRUCTURE OF PLACENTA
AT FULLTIME PREGNANCY
Naked Eye Anatomy:

It is disc like spongy fleshy

structure , thick at centre but thin at
edge.

It weighs 500gm.It measures

from 15-20cm in diameter and
2.5cm at the centre.Its volume is
500 ml; surface area 243 sq.cm.

 Fetal surface: covered with whitish

smooth and glistening amniotic
membrane
and
umbilical
cord
attached at or near the centre.
Branches of umbilical vessels are
visible on this surface radiating from
umbilical cord. Amniotic membrane
can be peeled of from underlying
chorionic plate except at umbilical
cord.

 Maternal surface: looks dull red

and shows 15-20 lobes or maternal
cotyledons which are separated by
sulci. Each sulcus corresponds to
decidual septum. It is covered with a
thin greyish layer of deciduacompact layer and spongy layer that
comes away with basal plate at the
time of separation .Numerous small
greyish calcified white infarcts are
visible on this surface.

 Margin : It is formed by fusion of

basal and chorionic plates and is
continuous with two membraneschorion leave and amnion.
Attachments: Placenta is attached
to upper part of posterior or anterior
wall of uterine cavity near fundus.
Placental separation:It normally
separates after birth of baby through
spongy layer of decidua.

Micro anatomy
At term 4/5th of placenta is of
fetal origin. Decidual plate and
maternal sinus blood belong to
mother. Structure of placenta
from fetal to maternal are:

 Amniotic membrane: A thin layered

cubical epithelium on a thin layer of
avascular connective tissue.
Chorionic plate: A sheet of
connective tissue with branching
umbilical vessels. Maternal surface is
coated with anchoring and nutritive
placental villi . Fetal surface is coated
with amniotic membrane

 Basal plate: It consist of the

following from outside inwards.
Part of the compact and spongy layer of
the deciduas basalis.
Nitabuch layer (area of fibrinoid
degeneration, wher trophoblast cells
meet the deciduas.)
Cytotrophoblastic shell.
Syncitiotrophoblast.

Intervillous space: It is lined on

the inner side by the chorionic plate
and outer side by the basal plate,
limited on the periphery by the
fusion of the two plates.It is lined
internally on all sides by the
syncitiotrophoblast and is filled with
slow flowing maternal blood.

 Stem villi:
These arise from the chorionic plate and extends
to the basal plate. Functional unit of the placenta
is called a fetal cotyledon or placentome,
which is derived from a major primary stem
villus. Functional subunit is called a lobule which
is derived from a tertiary stem villi. About 60
stem villi persist in human placenta. Thus each
cotyledon (totalling 15-29) contains 3-4
major stem villi. The fetal capillary system
within the villi is almost 50 km long. Thus, while
some of the villi are anchoring the placenta to
the deciduas, the majority are free within the
intervillous space and are called nutritive villi

 Structure of a terminal villus: It

has got following structure from
outside inwards:
Outer syncitiotrophoblast
Cytotrophoblast
Basement membrane
Central stroma containing fetal capillaries,
primitive mesenchymal cells, connective
tissue and a few phagocytic (hofbauer
cells that can trap maternal antibodies
crossing through the placenta) cells.

PLACENTAL CIRCULATION
The fetal circulation system

Fetal blood comes via the two umbilical arteries, arteria

umbilicales in the villi and leaves the placenta through a
single navel vein, the vena umbilicalis .

The pressure in the fetal vessels and their villus

branches always lies over that of the intervillous space.
This protects the fetal vessels from collapse.
arterial pressure: 50mm of Hg
venous pressure: 20mm of Hg

1 Umbilical arteries

2 Umbilical vein

3 Fetal capillaries

The maternal circulation system

Via the spiral arteries (80 -100 mm Hg) that

come from the uterine arteries (Aa. uterinae),
maternal blood gets into the intervillous spaces.
Subsequently the blood leaves the intervillous
spaces via the uterine veins that are arranged in
the periphery of the intervillous space.
The flow of the placental blood amounts to 600
cm3/min and the pressure in the spiral arteries to
70 mm Hg. In the intervillous spaces the pressure
falls to only 10 mm Hg .The blood in the intervillous
space is exchanged 2-3 times per minute.

1 Spiral arteries
2 Uterine veins
3 Intervillous spaces
A Basal plate

The placental
membrane(barrier)
In the first trimester it consists of the syncytiotrophoblast, the
cytotrophoblast (Langhans' cells), the villus mesenchyma (in which
numerous ovoid Hofbauer cells that exhibit macrophage properties are
found) and the fetal capillary walls.

1
2
3
4
5
6

Intervillous space
syncitiotrophoblast
cytotrophoblast
villus mesenchyma
fetal capillaries
Hofbauer macrophage

 During the 4th month the

cytotrophoblast disappears from the
villus wall and the thickness of the
barrier decreases while the surface
area increases (roughly 12 m2
towards the end of the pregnancy).
In the 5th month the fetal vessels
have multiplied their branches and
gotten closer to the villus surface.

1
2
3
4
5
6

Intervillous space
Syncytiotrophoblast
Cytotrophoblast
Villus mesenchyma
Fetal capillaries
Hofbauer macrophages

 During the 6th month the nuclei of

the syncytiotrophoblast group
together in the so-called proliferation
knots. The other zones of the
syncytiotrophoblast lack nuclei and
are adjacent to the capillaries
(exchange zones).

1 Intervillous space (with maternal blood)

2 Placental barrier of a terminal villus
3 Fetal capillaries
4 Merged basal membranes of the fetal capillary and of the
syncythiothrophoblast
5 Endothelial cells
6 Rare cytotrophoblast cells
7 Basal membrane of the capillaries
8 Basal membrane of the trophoblast portion
9 Syncytiotrophoblast with proliferation knots (nuclei rich region)

PLACENTAL FUNCTIONS

TRANSPORT FUNCTION: The placental

membranes actively control the transfer of a wide
range of substances by 5 major mechanisms
Simple diffusion
Facilitated transport
Active transport
Pinocytosis
Bulk flow of water and some solutes result
from hydrostatic and osmotic pressures

 Respiratory function
Excretory function
Nutritive function
Glucose
Lipids
Amino Acids
Water and electrolytes
Hormones

ENZYMATIC FUNCTION
STORAGE FUNCTION
BARRIER FUNCTION
IMMUNOLOGICAL FUNCTION
ENDOCRINE FUNCTIONS: The placenta
produces hormones that are vital to the survival
of fetus. It includes following.
Protein hormones: hCG, hPL PS -1G
Steroid hormones: Estrogen
(estriol,estradiol,estrone) , Progesterone.

Human chorionic gonadotrophin (hCG)

Functions:
It stimulates the secretion of estrogen and progesterone by
the corpus luteum and prevents involution of the corpus
luteum at end of menstrual cycle thereby preventing
spontaneous abortion.
It stimulates Leydig cells of the male fetus to produce
testosterones that causes male sex organs to grow.
It has got immuno-suppressive activity which may inhibit
the maternal process of immunorejection of the fetus as a
homograft.
It is also used as basis for pregnancy test.

Human placental lactogen (hPL) / Human

chorionic somatomammotrophin (hCS):

Functions:
Proteolysis and lipolysis in mother and
promotes transfer of glucose and amino
acids to the fetus.
It antagonizes insulin action, high level of
maternal insulin promotes protein synthesis.
Stimulates breast development to prepare
for lactation.

Pregnancy specific -1 glycoprotein (PS -1G

Function: It is a potent immuno-suppressor of
lymphocyte proliferation and prevents rejection of
the conceptus.
Human chorionic thyrotrophin (hCT) and
Human chorionic corticotrophin (hCC
Function: Accelerating the activity of thyroid,
adrenal cortex and pancreas to meet the
additional needs during pregnancy.

 Functions of steroid hormones :(estrogen and

progesterone)
Estrogen causes hypertrophy and hyperplasia of the uterine
myometrium, thereby increasing the accommodation
capacity and blood flow of the uterus.
Progesterone in conjunction with estrogen stimulates
growth of the uterus, causes decidual changes of the
endometrium required for implantation and it inhibits
myometrial contraction.
Proliferation and hypertophy of the ducts in breast are due
to estrogen while those of lobulo- alveolar system are due
to combined action of estrogen and progesterone
Both the steroids are required for the adaptation of the
maternal organs to the constantly increasing demands of
the growing fetus

 Progesterone maintains uterine quiescence, by

stabilizing lysosomal membranes and inhibiting
prostaglandins synthesis. Estrogen and
progesterone are antagonistic in the process of
labour.
Estrogen sensitizes the myometrium to oxytocin
and prostaglandins. It ripens the cervix.
Progesterone along with hCG and decidual
cortisol inhibits T- lymphocyte mediated tissue
rejection and protects the conceptus.
Together they cause inhibition of cyclic fluctuating
activity of gonadotrphin-gonadal axis thereby
preserving gonadal function.

PLACENTAL GRADING
Grade
Grade
Grade
Grade

0:
1:
2:
3:

placental
placental
placental
placental

age
age
age
age

12-24 weeks
30-32 weeks
36 weeks
38 weeks

ABNORMALITIES OF
PLACENTA AND CORD
PLACENTA SUCCENTURIATA

PLACENTA EXTRACHORIALIS:
Circumvallate Placenta

 Placenta marginata

 PLACENTA MEMBRANECAE
BIPARTITE PLACENTA
TRIPARTITE PLACENTA
Placenta in multiple pregnancy

Abnormal placental attachment or

separation
Placenta accreta/percreta/increta
Placental abruption
Placenta praevia

CORD ABNORMALITIES
BATTLEDORE PLACENTA

VELAMENTOUS PLACENTA

 Abnormal length of cord

long cord (>100 cm)
short cord (<40 cm)
Cord Knots
Cord Vessels
Thromboses

PLACENTAL INSUFFICIENCY
Definition: Placental insufficiency is
a complication of pregnancy in which
the placenta cannot bring enough
oxygen and nutrients to a baby
growing in the womb.
Etiology
Effects

Risks to the fetus

8-fold higher risk of death during delivery
5-fold higher risk of poor oxygenation at birth that may
lead to cerebral palsy and other complications
Hypothermia, or low body temperature
Hypoglycemia, or low blood sugar
30 to 40% chance of learning disabilities
Premature delivery
Poor tolerance of labor
Increased chance of cesarean birth
Increased chance of having birth defects
Increased chance of meconium aspiration, in which the
baby inhales some of the amniotic fluid during labor
Polycythemia, which is an excess of red blood cells
Hypocalcemia, which is too little calcium in the blood

 Treatment
Side effects of the treatment
Monitoring the condition
Preventing the condition

INTRA UTERINE GROWTH

RETARDATION
Definition: Intrauterine growth restriction refers
to a fetus whose weight is below the 10th
percentile of the average for its gestational age.
Etiology:
Maternal:
Constitutional : Small women, maternal genetic
and racial background are associated with small
babies.
Poor maternal nutrition before and during the
pregnancy

 Maternal diseases: Heart disease, preeclampsia or

eclampsia, anemia, chronic renal disease etc.
Toxins: Alcohol abuse, drug addiction, smoking
Fetal:
Structural anomalies: cardiovascular, renal or others
Chromosomal abnormality: Turners syndrome ,trisomies
(13.18,21)
Infection: TORCH agents
Multiple pregnancy: there is mechanical hindrance to
growth and excessive fetal demand.
Placental:
Poor uterine blood flow to the placenta for along time.
Placental pathology: Placenta praevia , abruption,
infarction etc

BIBLIOGRAPHY
Pritchard JA, Grant NF. Williams obstetrics. 17th edition.
Connecticut: Appleton century crafts;1985
Dawn CS. Textbook of obstetrics and neonatolgy. 16th
edition. Kolkata: Dawn book publishers; 2004
Dutta DC. Textbook of obstetrics. 6th edition. Kolkata: New
Central Book Agency; 2004
Orshan SA. Maternity, Newborn and Womens health
nursing. Philadelphia: Lippincott Williams and Wilkins ;
2008
Ladewig PW, London ML, Olds SB. Maternal newborn
nursing. California: Addison Wesley nursing; 1994
Lowdermilk DL, Perry SC. Maternity and womens health
care. 8th edition Missouri: Mosby; 2004

 Pilliteri A. Maternal and child health nursing. Philadelphia:

Lippincott Williams and Wilkins; 1999
Fraser DM, Cooper MA. Myles textbook for midwives. 14th
edition. London: Churchill Livingstone; 2003
Reeder J.S , Martin L.L , Griffin KD .Maternity Nursing
Family , Newborn and Womens Health Care .18th edition .
Philadelphia : Lippincott; 1997.
Jacob Annamma . A Comprehensive Textbook of Midwifery .
2nd edition . New Delhi : Jaypee Brothers Medical Publishers
Pvt Ltd ;2008
Novak C.J ,Broom B.L . Maternal and Child Health Nursing.
9th edition . Missouri : Mosby Inc ; 1999.
Varney H, Kriebs JM , Gregor CL. Varneys textbook of
midwifery . 4th edition . New Delhi: Elsevier; 2005

 Daftary SN, Chakravarti S. Manual of obstetrics .2 nd edition.

New Delhi: Elsevier;2005
Mudaliar AL, Menon MK. Clinical obstetrics.10 th edition. Chennai:
Orient Longman; 2005.
Baergen R. Macroscopic examination of the placenta
immediately following birth. Journal of Nurse midwifery. 1997
.September; 42(5)
McFarlain B. IUGR . Journal of Nurse midwifery. 1994. April;
39(2)
http: //www. ScienceDirect .com- Placenta Placental Findings
Contributing to Fetal Death.
http:// www.aafp.org/patient info
http://www. News medical.net placenta tag
http:// www.health on.com
http://www.womens healthnews.com
http://www.pubmed.com