Placenta

DR Nimco A Hassan
OBSTETRICS AND GYNAECOLOGY
1. Discuss anatomy, function and abnormalities
related to placenta.
2. Explain abnormalities related
to length of cord.

Placenta is a remarkable organ

Has a relative short life span, it undergoes rapid
growth ,differentiation and maturation.

A unique fetal –maternal communication
system which creates a hormonal environment
that helps initially to maintain pregnancy and
eventually initiates the events leading to
parturition
The human placenta is:
• Discoid
• Hemochorial
• Deciduate
Development of placenta-
Two sources
• Fetal – chorion Frondosum
• Maternal- decidua basalis
●
PLACENTA AT TERM:

Placenta is a discoid organ

15 – 20cm in diameter
3cm Thick at center
Weighs about 500gms
 Placental membrane

●
Total area-4 to 14 sq m
●
Similar to absorbtive area in adult git
●
In later part of pregnancy the membrane
thickness reduces from 0.025mm to0.002mm
●
Is classified as haemochorial
PLACENTAL BARRIER


Inspite of close proximity , there is no mixing of the maternal
and fetal blood.

They are separated by placental membranes or barrier.
 PLACENTAL
CIRCULATION

UTEROPLACENTAL FETOPLACENTAL
CIRCULATION CIRCULATION
UTEROPLACENTAL
CIRCULATION
• It is concerned with the circulation of maternal
blood through the intervillous space.
• Divided in 3 parts
1. Arterial circulation
2. Venous drainage
3. Circulation in intervillous space
• Blood in the intervillous space is temporarily outside maternal
circulatory system.

• These vessels discharge into the intervillous space through gaps in

the cytotrophoblastic shell.

• Blood flowing from spiral arteries is pulsatile and is propelled in

jet-like fountains by the maternal blood pressure.

• Welfare of the embryo and fetus chiefly depends on adequate

bathing of branch villi with maternal blood.

• Reduction in utero-placental circulation result in fetal hypoxia and

IUGR.
Arterial circulation
• About 120-200 spiral arteries open into
intervillous space.
Spiral artery remodelling
• There is cytotrophoblastic invasion into the spiral
arteries upto the intradecidual portion within
12weeks of pregnancy.

• Endothilial and muscoelastic media is destroyed

and replaced by fibrinoid material
• There is secondary invasion of trophoblast between
12-16 weeks.

• It extends upto the radial arteries within the

myometrium.

• SPIRAL ARTERIES are remodled into large bore

UTEROPLACENTAL ARTERIES.
INTERVILLOUS
HEMODYNAMICS

Volume of blood in mature placenta 500ml

Volume of blood in intervillous space 150ml

Blood flow in intervillous space 150ml

Pressure in intervillous space

1) During uterine contraction 30-50mm Hg
2)During uterine relaxation 10-15mm Hg

Pressure in supplying uterine artery 70-80mm Hg

Pressure in draning uterine vein 8mm Hg

FETOPLACENTAL
CIRCULATION
• Two umbilical arteries enter the chorionic plate
underneath the amnion, each supplying one half of
placenta.
• The arteries breakup into small branches which
enter the stems of chorionic villi.
• Each in turn divides the primary, secondary and
tertiary vessels of the corresponding villi.
• This system provides a very large area for exchange of
metabolic and gaseous products between maternal
and fetal blood streams.

• Well-oxygenated fetal blood in fetal capillaries passes

into thin walled veins.

• This follow chorionic arteries to site of attachment of

the umbilical cord, where they converge to form
umbilical vein.

• This large vessel carries oxygen-rich blood to the fetus.

 One (usual) or more small lobes of placenta, size of
cotyledon, may be placed at varying distances from
the placental margin.

 In cases of absenceof communicating

blood vessels, it is called placenta spuria.

 Incidence:
3%
 If the succenturiate lobe is retained, following
birth of the placenta, it may lead to:
1. Postpartum haemorrhage

2. Subinvolution

3. Uterine sepsis

4. Polyp formation
Whenever the diagnosis of missing lobe is made,
exploration of the uterus and removal of the lobe
under general anaesthesia is to be done.
The fetal surface is divided into a central depressed zone
surrounded

by a thickened white ring which is usually
complete.

Vessels radiate from the cord insertion as far as

the ring and then disappear from view.


The peripheral zone outside the ring is thicker

and the edge is elevated and rounded.

There is increased chance of:
 Abortion

Antepartum haemorrhage

FGR baby
 Preterm delivery

 Retained placenta or

membranes
 A thin fibrous ring is present at the margin of the
chorionic plate where the fetal vessels appear to
terminate.
• Encroachment of some part over the lower segment.

• Imperfect separation in the third stage.

• Chance of retained placenta is more and manual removal becomes difficult.

• These abnormalities are serious variations in which trophoblastic tissues invade the
myometrium to varying depths.

• They are much more likely with placenta previa or with implantation over a prior uterine
incision or perforation.
The condition is usually associated
• when the placenta is implanted in lower segment
(Placenta praevia)
or over the previously injured sites as in caesarean
section
dilatation and curettage operation
 manual removal
myomectomy
The diagnosis is only made
• during attempted manual removal when the plane of
cleavage between the placenta and uterine wall
cannot be made out.
• Ultrasound imaging, colour Doppler and MRI have all
been valuable in the diagnosis.
• Absence of decidua basalis
• Absence of Nitabuch’s fibrinoid layer
• Varying degree of penetration of the villi into the
muscle bundle (increta) or upto the
• serosal layer(percreta).
• The risk includes hemorrhage, shock,infection and
rarely inversion of the uterus.
Abnormal length of cord
Short cord
Less than 20cm
1. Prevent descent of the presenting part
specially during labour
2. Separation of normally situated placenta
3. Favour malpresentation
4. Acute inversion
5. Fetal growth restriction
6. Intrapartum distress
7. Failure of external version
8. Two fold risk of fetal death
Clinical Significance
• cord prolapse
• cord entanglement round the neck or the body
• True knot
• False knots
Battledore placenta
• The cord is attached to the margin of the placenta.
• If associated with low implantation of the placenta, there
is chance of cord compression in vaginal delivery leading
to fetal anoxia or even death; otherwise, it has got little
clinical significance.
Velamentous placenta

• The umbilical vessels spread within the membranes at

a distance from the placental margin, which they reach
surrounded only by a fold of amnion.
• Although their incidence is approximately 1 percent,
velamentous insertion develops in more commonly
with placenta previa and multifetal gestations.
If the leash of blood vessels happen to traverse through the
membranes overlying the internal os, infront of the presenting
part,the condition is called vasa praevia.
• In the presence of fetal bleeding, urgent delivery is
essential either vaginally or by caesarean section.
• The newborn's haemoglobin is estimated and if
necessary, blood transfusion be carried out.
• If the baby is dead, vaginal delivery is awaited.
Knots
False Knots
False knots appear as knobs protruding from the cord
surface and are focal redundancies of a vessel or Wharton
jelly, with no clinical significance.
FETAL CIRCULATION
 Fetal circulation

The hemodynamics of the fetal circulation undergoes profound changes soon

after birth (Fig. 4.2) due to— (1) cessation of the placental blood flow and
(2) initiation of respiration. The following changes occur in the vascular
system

 The umbilical vein carrying the oxygenated blood (80% saturated) from the
placenta, enters the fetus at the umbilicus and runs along the free margin of
the falciform ligament of the liver.
 In the liver, it gives off branches to the left lobe of the liver and receives the
deoxygenated blood from the portal vein. The greater portion of the
oxygenated blood, mixed with some portal venous blood, short circuits the
liver through the ductus venosus to enter the inferior vena cava (IVC) and
thence to right atrium of the heart.
 The O2 content of this mixed blood is thus reduced. Although both the ductus
venosus and hepatic portal/fetal trunk bloods enter the right atrium through
the IVC, there is little mixing.
The terminal part of the IVC receives blood from the right hepatic vein.In the
right atrium, most of the well oxygenated (75%) ductus venosus blood is
preferentially directed into the foramen ovale by the valve of the inferior vena
cava and crista dividens and passes into the left atrium.
Here it is mixed with small amount of venous blood returning from the lungs
through the pulmonary veins.
This left atrial blood is passed on through the mitral opening into the left
ventricle.Remaining lesser amount of blood (25%), after reaching the right
atrium via the superior and inferior vena cava (carrying the venous blood from
the cephalic and caudal parts of the fetus respectively) passes through the
tricuspid opening into the right ventricle
During ventricular systole, the left ventricular blood is pumped into the
ascending and arch of aorta and distributed by their branches to the
heart, head, neck, brain and arms.
The right ventricular blood with low oxygen content is discharged into the
pulmonary trunk. Since the resistance in the pulmonary arteries during
fetal life is very high, the main portion of the blood passes directly
through the ductus arteriosus into the descending aorta bypassing the lungs
where it mixes with the blood from the proximal aorta. 70% of the cardiac
output (60% from right and 10% from left ventricle) is carried by the
ductus arteriosus to the descending aorta. About 40% of the combined
output goes to the placenta through the umbilical arteries.
The deoxygenated blood leaves the body by way of two umbilical arteries
to reach the placenta where it is oxygenated and gets ready for
recirculation. The mean cardiac output is comparatively high in fetus and is
estimated to be 350 mL/kg/min.
CHANGES OF FETAL CIRCULATION AT BIRTH
1. Closure of the umbilical arteries: Functional closure is almost instantaneous preventing even slight
amount of the fetal blood to drain out. Actual obliteration takes about 2–3 months. The distal parts
form the lateral umbilical ligaments and the proximal parts remain open as superior vesical arteries.
2. Closure of the umbilical vein: The obliteration occurs a little later than the arteries, allowing
few extra volume of blood (80–100 mL) to be received by the fetus from the placenta. The
ductus venosus collapses and the venous pressure of the inferior vena cava falls and so also the
right atrial pressure. After obliteration, the umbilical vein forms the ligamentum teres and the ductus
venosus becomes ligamentum venosum (Fig. 4.2).
3. 3. Closure of the ductus arteriosus: Within few hours of respiration, the muscle wall of the
ductus arteriosus contracts probably in response to rising oxygen tension of the blood flowing
through the duct. The effects of variation of the O2 tension on ductus arteriosus are thought to be
mediated through the action of prostaglandins. Prostaglandin antagonists given to the mother
may lead to the premature closure of the ductus arteriosus. Whereas functional closure of
the ductus may occur soon after the establishment of pulmonary circulation, the anatomical
obliteration takes about 1–3 months and becomes ligamentum arteriosum.
4. 4. Closure of the foramen ovale: This is caused by an increased pressure of the left atrium combined
with a decreased pressure on the right atrium. Functional closure occurs soon after birth but
anatomical closure occurs in about 1 year time. During the first few days, the closure may be
reversible. This is evidenced clinically by the cyanotic look of the baby during crying when there
is shunting of the blood from right to left. Within 1 or 2 hours following birth, the cardiac output
is estimated to be about 500 mL/min and the heart rate varies from 120–140 per minute.
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