Most placentae are either round or oval.

Variations are comman –

Multiple placentae with a single fetus
Cord insertion between 2 placentae : either
into the chorionic bridge / into the
membranes
Bilobed or placenta bilobata
Placenta succenturata
Placenta memranacea
Ring shaped placenta
Placenta fenestrata
Extrachorial placenta
-circumvallate placenta
-Placenta marginata
Multilobed placenta
Bilobed or placenta bilobata
› Incidence 2-8% of placentas
› Roughly equal size lobes are separated by a
segment membranes
› Umbilical cord may insert in either of the lobes or
in velamentous fashion or in between the lobes
Also known as bipartrite placenta or placenta
duplex
Placenta containing 2 or more lobes is rare &
is called Multilobate placenta.
Incidence :5%
Small accessory lobes develop at a small
distance from the main placenta.
2 fold increase in twin placentae
Accessory lobe may be retained after
delivery causing PPH
Accompanying vasa praevia may cause fetal
hemorrhage (APH)
If the communicating membranes do not
have vessels it is called placenta supuria.
Pathogenesis: Abnormal placentation
- Arise due to implantation in areas of
decreased uterine perfusion
- Lateral implantation in between anterior and
posterior walls of the uterus with one lobe on the
anteriors and one on the posterior wall
Other local factors leading to multilobulation:

› Implantation over leiomyomas

› Area of previous surgeries
› In the cornu
› Over the cervical os

› Succenturate lobe : Results when one or more small

accessory lobes are developed in the membranes at
the a distance from the periphery of the main
placenta
Whole/large part of placenta is covered by
functioning villi , large & thin placenta ; may
be associated with praevia or accereta.
Incidence 1:6000 deliveries
Annular in shape
May be horse-shoe shaped
because of atrophy of a part
of placental ring.
Complete ring of placental
tissue may be present .
May be associated with
- APH
- PPH
- IUGR
Rare anomaly
Central portion of discoid placenta is
missing. Rarely there may be an actual hole
in placenta.
More often the defect involves the villous
tissue & the chorionic plate remains intact.
Clinically it may prompt a search for a
retained placental
Chorionic plate (fetal side ) is smaller than
basal plate .
So membranes are not inserted at the
periphery of placenta.
These may be fibrin deposition in b/w the
membranes.
There may be plication or folding of
membranes ( circumvallate placenta)
In placenta circummarginata there is no
folding of membranes
Fetal surface has a central
depression surrounded by
thickened grey white ring
composed of a double fold
of chorion, amnion,
degenerated decidua &
fibrin deposits .

Large vessels terminate at

the margins of the placenta
when seen from the fetal
surface.
Risks of circumvallate placenta
APH
Fetal Hemorrhage
PT delivery
Placental insufficiency
Perinatal mortality
PLACENTA ACCERATA , INCRETA &
PERCRETA
Abnormalities are serious variations.
Trophoblastic cells invade the myometrium
to varying depths.
Placenta accreta
› Accounts for 75-78%
› Placenta attached directly to the muscles of the
uterine wall
Placenta increta
› Accounts for 17% of cases
› Placenta extends into the uterine muscles
Placenta percreta
› 5-7% placenta extends through the entire wall of the
uterus
Incidence of 1 in 7,000 deliveries
Incidence maybe increase because of the
increase no. of women with prev CS
Risk factors:
› Placenta previa
› Placental located underlying the previous uterine
scar
› Multiple pregnancies
› Prev. D & C
Torrential hemorrhage is a frequent
complication.
¼ of term pregnancies
2/3 pregnancies complicated by severe
HPNsive disease
Result from occlusion of maternal vascular
supply
Principal histopath features:
› Fibrinoid degeneration of trophoblast
› Calcification
› Ischemic infarction from adhesion of spiral arteries
 Placental perfusion disorders many disrupt
blood flow.
a) To the placenta
b) With in placenta
c) To the fetus through the villi. Many of these
lesions are found in normal mature placenta
Functional reserve of placenta is great. It
may loose 30% of it’s villi without any fetal
effects.
Maternal floor infarcts:
Deposition of dense fibrinoid layer on
placental basal plate
thick white & fibrin corrugated surface acts as
a blockade to blood flow.
Associated with:
IUGR
PT Labor
Still births May recur in
subsequent pregnancies.
Etiology is not well defined.
May be associated with maternal
thrombophillias.
Degenerative lesions of placenta have 2
etiological factors:
› Changes assoc with aging of trophoblast
› Impairment of uteroplacental circulation causing
infarction
Small calcareous nodules or plaques
frequently observed on the maternal surface
of the placenta
Visualized in USG
>33 weeks POG
› More than half of the placenta have some degree
of calcification w/c increase until term
Thrombosis of a stem artery produces
sharply demarcated area of avascularity
Single artery thrombosis
› (+) 4.5% of placenta from normal pregnancy
› (+)10% involving diabetic women
Thrombosis of single fetal stem artery will
deprive only 5% of the villi of their blood
supply
Length
› Mean length at term 50-60 cm
› Vascular occlusion by thrombi & true knots
› Excessively short umbilical cords may be
instrumental in abruptio placenta & uterine inversion
› Short cords are associated with
› - IUGR & OLIGOHYDRAMNIOS
› - CMF & CHROMOSOMAL ABERRATIONS
› - Intrapartum fetal death
› - 2 folds risk of death
Long cords are associated with-
Cord entanglement
Cord prolapse
CMF
FETAL DISTRESS& DEMISE
Lean cords are associated with IUGR
Large diameter cords are associated with
macrosomia
Clinical utility of parameter – unclear
Cord vessels spiral through the cord
UCI - is the no. of complete coils divided by
the cord length in cm
Antenatal UCI has the lower sensitivity than
the measurement postpartum
Hyper coiling is linked with fetal demise,
IUGR & intrapartum hypoxia
Abnormal UCI has been related to trisomies
& single umbilical artery
Single umbilical artery :
Results due to atrophy of the previously
existing umbilical artery

4 vessel cord :
- Quiet uncomman
- May be a venous remnannt
- Association with CMF is not clear
Absence of one umbilical artery

INCIDENCE : - 0.63 % in live births

- 1.92 % in perinatal deaths
- 3 % in twins
Incidence is increased in women with :
Diabetes
Epilepsy
PET
APH
Oligohydramnios
Hydramnios
Chromosomal abnormalities
About 30% of all infants with only one umbilical artery
have congenital anomalies
› Associated CMF :
› Aneuploidies
 Tracheo-oesophagial fistula
 Renal agenesis
 Imperforate anus
› Vertebral defects
› 34% are growth restricted
› 17% deliver preterm
Rarely umbilical artery may fail to split
Shared ,fused lumen
May involve the entire length or may be
partial (towards the placental insertion site)
Hyrtl Anastomosis :
Anastomosis b/w the two umb. Arteries with in 3
cm of placental incertion site
Acts as a pressure equalising system b/w the two
umbilical Aa.
Improves placental perfusion during uterine
contractions /during compression of one of the
umbilicalarteries.
Usually the cord is inserted at or near the
center of the fetal surface of placenta.
Various cord insertion variations are:
› Battledore placenta
› Furcate insertion
› Velamentous insertion
› Vasa praevia
Insertion site is normal

Umbilical vessels lose their protective

wharton’s jelly shortly before insertion.

Vessels are covered only by the

amnion(vulnerable to compression)
An abnormal condition in which umbilical vessel does not
insert into the placental mass but instead, traverse the fetal
membrane at a short distance from the placental margin.

They are surrounded only by a fold of amnion(vulnerable to

compression).

More common with placenta praevia and multiple pregency

Incidence :
› 1.1% in singleton pregnancies
› 8.7% in twin gestations
› Spontaneous abortion
33% between 9th & 12th wks AOG
26 % between 13th & 16th
Incidence : 1 in 5200 pregnancies

Assoc with Velamentous insertion when some

of the fetal vessels in the membrane cross the
region of the internal os & occupy a position of
the presenting part

These vessels are not only vulnerable to

compression but also to laceration.
 Bilobate placenta
Succenturiate placenta
2nd trimester placenta praevia
Pregnancies conceived by IVF

Haemorrhage from vasa praevia may lead

to instant fetal death and should always be kept as a
D/D in all cases with APH / IPH

Elective CS is planned in case diagnosis is

confirmed .
Identified as echogenic parrallel / circular line
near the cervix

USG has low sensitivity

Doppler is recommended in suspected cases

Knots : False knots
Result from kinking of the vessels to accommodate
length of cord and are due to redundancies of
Umbilical vessels / Wharton’s jelly.
True knots
Results from active fetal movement
Incidence 1%
More common in monoamniotic twins
Active fetal movements create true knots
Risk of still births is increased 5 to 10 folds in
those with true knots.
FHR abnormalities are common during labor
but cord blood PH values are normal
The cord is frequently coiled around the fetus

More likely with longer cords

Loops around fetal neck are termed a nuchal cord

(uncommon cause of adverse PN outcome)

Contractions may compress the nuchal cord and cause

FHR decelerations and low umbilical artery

Incidence :
› 1 loop of Nuchal cord 20-34%
› 2 loops of nuchal cord 2.5-5%
› 3 loops of nuchal cord 0.2-0.5%
Associated with-
› Short cord
› Trauma
› Entanglement
May result from rupture of varyx(venous)
May be iatrogenic
May be found along the course of the cord
True cysts:
› Epithelium lined
› Remnants of the allantois
› Coexist with patent urachus

False Cysts:
Due to degeneration of wharton’s jelly.
Single cyst may resolve completely
Multiple cysts may be associated with miscarriage
/aneuploidy.
Focal narrowing of cord diameter near fetal
insertion
Pathological findings- absent of wharton’s
jelly and stenosis of cord vessels.
Most cases are still borns.
Hematoma
› Usually results from rupture of varix, usually of
umbilical vein with effusion of blood into cord

Stricture
› Most but not all infants with cord stricture are
stillborn
› Assoc with an extreme focal deficiency in
wharton’s jelly
Meconium staining
› Staining of amniotic membrane within 1-3 hrs
after meconium passage
› Neonatal mortality rate
3.3% in the group with meconium-stained
membrane compared with 1.7% in those without
staining