This document discusses various topics related to placental and gestational pathology including abortions, ectopic pregnancies, twin pregnancies, and placental malformations and pathology. It provides details on the definition, incidence, etiology, morphology and clinical features of abortions. It describes the predisposing factors, morphology and clinical features of ectopic pregnancies. It discusses the gross examination and types (monochorionic vs dichorionic) of twin placentas. Finally, it elaborates on the anatomy, development, functions and various malformations of the placenta like bilobed placenta, succenturiate lobes, membranacea, accreta, increta and percreta.

1. By:
Dr Prakriti Shukla
Department of Pathology

2.  Abortions
 Ectopic pregnancy
 Twin pregnancy
 Placental pathology and malformations of cord

3. Abortion
 Incidence : 40 – 80 %
 Etiology : infections,
mechanical disturbances,
endocrine diseases,
immunologic mechanisms and
inherited chromosomal abnormalities
 Definition : spontaneous abortions / miscarriage is defined as pregnancy
loss before 20 wks of gestation.

4.  Morphologic confirmation of the occurrence of pregnancy is one of the
challenging task for the pathologist.
 When fetal parts, gestational sac, viable chorionic villi are present , the task
is easy.
 If fetus is identified, determine whether macerated or normal, grossly
disorganized or focally abnormal.
 When gestational sac identified, check whether intact or ruptured and if
ruptured whether it contains cord stump or not.

5. PRODUCTS OF CONCEPTION REPRESENTED BY SMALL
EMBRYO AND CHORIONIC VILLI

6.  Necrotic villi (ghosts villi) are difficult to recognise since clumps of fibrin
simulate them
 Overall configuration and presence of shadows of stromal cells and
trophoblast are the main identifying criteria
 Chorionic villi absent - search for trophoblastic cells
 Intermediate trophoblastic cells resemble decidual cells
 Immunocytochemical stains for trophoblastic cells : hCG, hPL, SPI,
KERATIN

7. GHOST CHORIONIC VILLI EMBEDDED IN A CLOT

8. single syncitiotrophoblast cell strongly
immunoreactive to b-hCG despite the
presence of advanced necrotic changes
isolated intermediate trophoblast cells
strongly staining for keratin

9. FEATURES SUGGESTIVE OF INTRAUTERINE
IMPLANTATION
 Fetal parts
 Chorionic villi
 Trophoblastic cells
 Enlarged hyalinized spiral arterioles
 Fibrinoid matrix

10. ENDOMETRIAL PATTERN SUGGESTIVE OF
GESTATION BUT NOT PATHOGNOMIC
 Decidual Reaction
 Gestational Hyperplasia
 Arias Stella Reaction

11.  Decidual reaction :
 After implantation a generalised reaction occurs characterized by
change of endometrial glands which become hypersecretory whereas
the stroma becomes edematous.
 The stromal cells gradually become enlarged and filled with glycogen
and lipids( appear eosinophilic as their cytoplasm takes up pink stain
due to the presence of numerous mitochondria and intermediate
filaments)
 Gestational hyperplasia :
 Characterized by simultaneous presence in the endometrial mucosa
of glandular secretion, stromal edema, and deciduoid changes.
 The basal glandular cells acquire positivity for S- 100 protein

12.  Arias stella reaction :
 secretory or proliferative changes in the endometrial glands are
accompanied by prominent nuclear changes manifested by
hyperchromasia and marked enlargement.
 Normal or abnormal mitoses may also be present.
 Changes are focal can occur in cervix, endocervical polyps,
adenomyosis and endometriosis
 more often seen in postcurretage specimens
 May be seen in normal or ectopic pregnancy,H. mole, chorioca and
following exogenous hormones

13. DECIDUAL ARIAS STELLA GESTATIONAL
REACTION REACTION HYPERPLASIA

14.  In septic abortions , identification of the microorganism is a
must with large number of polymorphic neutrophils.

15. ECTOPIC PREGNANCY
 Definition :implantation of fetus in any site other than normal intrauterine
location.
 Most common site - fallopian tube
 Other sites – ovary, abdominal cavity, intrauterine portion of fallopian tube.
 Incidence- 1 in 150 pregnancy

16. Ectopic pregnancies occur when the fertilized ovum implants outside of the uterine
fundus. A tubal ectopic pregnancy, as diagrammed here, may proceed for several weeks,
but the enlargement can rupture the tube and lead to acute, life-threatening bleeding,
often about 6 weeks after a previous menstrual period.

17.  Predisposing factors: pelvic inflammatory diseases,
endometriosis,
appendicitis,
previous surgery and
intrauterine devices
 Morphology :
 Tubal hematoma
 Placental tissue composed of immature chorionic villi implants in the
lumen.
 Proper decidualization is lacking and growth of gestational sac leads
to tubal rupture and intraperitoneal haemorrhage

18. A positive pregnancy test (presence of human chorionic gonadotropin),
ultrasound, and culdocentesis with presence of blood are helpful in making the
diagnosis of ectopic pregnancy. Seen here is tubal epithelium at the right, with
rupture site and chorionic villi at the lower left.

19.  Clinical features
 Amenorrhea
 Severe abdominal pain
 Vaginal bleeding

20. PLACENTA

21. Placental Anatomy
 Shape : discoid.
 Diameter : 15-20 cm.
 Weight : 500 gm.
 Thickness : 2.5 cm at its center and gradually tapers towards
the periphery.
 Position : in the upper uterine segment (99.5%), either in the
posterior surface (2/3) or the anterior surface (1/3).
 Surfaces : fetal surface and maternal surface

23. FOETAL SURFACE
 Smooth, glistening and is covered by the amnion which is reflected on the
cord.
 The umbilical cord is inserted near or at the center of this surface and its
radiating branches can be seen beneath the amnion.

24. MATERNAL SURFACE
 Dull greyish red in colour and is divided into 15-20 cotyledons.
 Each cotyledon is formed of the branches of one main villus stem covered
by decidua basalis.

27. STRUCTURE:
Chorionic plate on fetal side
Basal plate on maternal side
Stem villi between the plates
Intervillous space between
stem villi filled with
maternal blood
27

28. Normal Chorionic Plate. The chorionic plate is covered by a layer of amnion and is
composed of mesoderm containing fetal vessels. • Beneath the chorionic plate is usually a
layer of subchorionic fibrin and villi. • The intervillus space (IVS) between the villi is filled
with maternal blood in vivo

29. DEVELOPMENT
Prelacunar stage:
Blastocyst Implantation:
24th day of menstrual cycle
on upper posterior uterine
wall
The embryonic pole of the
blastocyst is attached to the
endometrium
Syncytiotrophoblast (ST)
proliferates towards
decidua basalis & capsularis
Cytotrophoblast (CT)
differentiates to primary
mesoderm
29

30. PRELACUNAR STAGE

31. Early Lacunar stage:
Lacunar spaces form within ST around trabeculae
(cords of ST)
Lacunae enlarge and erode branches of uterine
arteries & veins – uteroplacental circulation
Primary villous stage:
Trabeculae convert to primary villi with invasion by
CT in central axis

32. 32
EARLY LACUNAR
STAGE
PRIMARY VILLOUS
STAGE

33. Secondary villous stage:
Primary mesodermal cells invade the primary villi
Tertiary villous stage:
Fetal vessels derived from umbilical vessels appear
within primary mesoderm
Numerous villi branch from tertiary villi in to
intervillous space (Labyrinthine structure)

34. 34
SECONDARY
VILLOUS STAGE
TERTIARY
VILLOUS STAGE

35. Chorionic villi at embryonic pole proliferate rapidly to from chorion
frondosum
Rest of the embryonic villi degenerate & disappear – chorion leave
(CL)
3rd
month of pregnancy – decidua capsularis & parietalis fuse with
regression of CL
Persistent chorionic frondosum + decidua basalis = human placenta

36. Primary villi- when trabeculae between lacunae of
syncytiotrophoblast and intermediate trophoblast are invaded by
cytotrophoblastic cells
Secondary villi – extraembryonic mesoderm invades primary villi
which thus develops mesenchymal core
Tertiary villi - when the mesenchymal cores of villi gets
vascularized

38. Layer Location Description
cytotrophoblast inner layer Single celled, inner layer of the
trophoblast
forms Syncytiotrophoblast
villous IT and Implantation site
IT
syncytiotrophoblast outer layer Thick layer of multinucleate
syncytium that lacks cell
boundaries and grows into the
endometrial stroma
Secretes hCG
Intermediate
trophoblast
implantation site, chorion,
villi (dependent on
subtype)
anchor placenta (implanation
site IT), unknown (chorionic &
villus IT)
TROPHOBLAST CELL TYPES

39. CT Villous IT Implant IT Chorionic
type IT
ST
Morph Round,
uniform,
granul cyt,
Polyhed.
Eosinoph
cyt,
Pleomorp&
large,
eosino cyt
Round to
polyhed,
eosin cyto
Linear,
multinuc,
Cytop
vacuoles
Growth cohesive cohesive infiltrating cohesive syncytial
CK + + + + + + + + + + + + + + + + + + + +
hCG - - -/ + - + + +
hPL - -/ + + + + + + + + +
Mel-CAM - + + + + + + + + -
PLAP - - + + + + + + + +
EMA - - - + + + -
Ki-67 25-50% >90% 0 3-10% 0

40. FUNCTIONS OF :
Villous Intermediate Trophoblast - maintains the
structural integrity of the villi that anchor placenta to
basal plate
Implantation Site Intermediate Trophoblast –
establishes the maternofetal circulation by invading the
spiral arteries
Chorionic-type Intermediate Trophoblast –
mechanical barrier to the maternal immune system

41. FUNCTIONS OF THE PLACENTA
1. Respiratory function
2. Nutritive function
3. Excretory function
4. Production of enzymes
5. Production of pregnancy associated plasma proteins (PAPP)
6. Barrier function
7. Endocrine function

42. PLACENTAL PATHOLOGY

43. EXAMINATION OF PLACENTA
Best examined in the fresh state immediately after delivery
A thorough evaluation can disclose abnormalities of clinical
significance ,contributing to the understanding of disabilities
among surviving children and be of great importance in the
resolution of medicolegal cases.

44. TWIN PREGNANCY
 Gross: type of twinning
 Monochorionic placenta – indicative of monozygotic
twins
 Dichorionic placenta – compatible with either
monozygotic or dizygotic twinning

45. MONOCHORIONIC PLACENTA
Stripping of amnion reveals a continuous chorionic plate
beneath the septum and major vascular anastomoses between
the twins

46. DICHORIONIC PLACENTA
Rough chorionic ridge at the base of the septum and lack
vascular anastomoses

48. CHORIONIC RIDGE AT THE BASE OF THE SEPTUM IN A
DICHORIONIC FUSED TWIN PLACENTA

49. These twin boys are at 9 weeks
gestational age in development.
Each twin has an amnionic cavity.
The amnions will eventually fuse
to form a diamnionic dividing
membrane.

50. The fetal surface of a normal term twin placenta is seen here. The dividing
membranes between the amniotic cavities occupied by the two fetuses are seen
between the cord insertions.

51. This is another twin placenta that has a normal discoid shape with dividing
membranes that separate the fetal amnionic cavities into equal halves. It is not
possible grossly to determine whether this is monochorionic or dichorionic.

52. Only a single amnionic cavity is present in this twin placenta. Note that the two
umbilical cords join and share circulation. Monoamnionic twins have more potential
problems. In this case, one twin was an "asymmetric" acardiac twin supported by the
heart of the remaining complete twin.

53. The placental blood vessels have been injected with a white fluid to reveal the
anastomosis across the dividing membranes of a monochorionic twin placenta in a
case of twin-twin transfusion syndrome. In general, this syndrome can be suspected
when one twin is at least 25% larger than the other.

54. PLACENTA BILOBATA
 the placenta is separated into lobes
 division is incomplete and the vessels
of fetal origin extend from one lobe to
the other before uniting to form the
umbilical cord.

55. BILOBED PLACENTA

56. SUCCENTURIATE LOBES
 small accessory lobe ≥1,develop in the membranes at a distant from the
periphery of the main placenta, to which they usually have vascular
connections of fetal origin
 incidence : 5%
 retained in the uterus after delivery and may cause serious hemorrhage
 accompanying vasa previa
- dangerous fetal hemorrhage at delivery

57. PLACENTA SUCCENTURIATE

58. PLACENTA MEMBRANACEA
 all of the fetal membranes are covered by functioning villi and the
placental develops as a thin membranous structure occupying the entire
periphery of the chorion
 serious hemorrhage d/t associated placenta previa or accreta

59. PLACENTA MEMBRANACEA

60. Abnormality Definition Clinical significance
Extrachorial
Placentation
 Circumvallate
Placenta
Circummarginate
placenta
 When the chorionic plate, which is on the
fetal side of the placenta, is smaller than
the basal plate, which is located on the
maternal side, the placental periphery is
uncovered
 Fetal surface of such a placenta presents
a central depression surrounded by a
thickened, grayish-white ring.
 Ring : composed of a double fold of
amnion and chorion with degenerated
decidua and fibrin in between
 Within the ring, the fetal surface presents
the usual appearance, except that the
large vessels terminate abruptly at the
margin of the ring
 Ring dose not have the central depression
with the fold of membranes
 Antepartum hemorrhage
- from placental abruption
and fetal hemorrhage
 Preterm delivery
 Perinatal mortaliy
 Fetal malformations
 less well defined

61. CIRCUMVALLATE PLACENTA

62. FENESTRATED PLACENTA
 Central portion of a discoidal placenta is missing
 In some instances, there is an actual hole in the placenta but more often
the defect involves only villous tissue with the chorionic plate mistakenly
considered to indicate that a missing portion of placenta

63. 1. Placenta accreta
 Placental villi adhere to
myometrium without
an intervening layer of
decidua
 Most often focal
2. Placenta increta
villi within the myometrium,
usually involving previous
cesarean section
3. Placenta percreta
villi penetrate through the
uterine wall to the serosa.
All forms associated with
increased postpartum bleeding,
which may necessitate
hysterectomy

64. PLACENTA
ACCRETA
 Gross and microscopic
appearance of placenta
accreta: penetration of
myometrium by chorionic
villi

65. AMNION NODOSUM : Small nodules < 1mm on the extraplacentar
membrane – pathognomonic of oligohydramnion
 tiny, light tan , creamy nodules in
the amnion made up of vernix
caseosa with hair, degenerated
squames and sebum
 Oligohydramnios
Found in :
 fetuses with renal agenesis
 prolonged preterm ruptured
membranes
 the placenta of the donor
fetus with twin-to-twin
transfusion syndrome

66. PLACENTAL INFLAMMATION
 Changes that are now recognized as various forms of degeneration and
necrosis were formerly described under the term placentitis
 Small placental cysts with grumous contents were formerly thought to be
abscesses.
 Nonetheless, especially in cases of preterm and prolonged membrane
rupture, bacteria invade the fetal surface of the placenta
→ chorioamnionitis

67. SUBCHORIONIC CYSTS

68. PLACENTAL
INFLAMMATION
1. Concentration of
inflammatory infiltrate on
the placental maternal side
2. Inflammatory changes
centered in umbilical vessels

69. NECROTIZING VILLITIS FROM LISTERIA
INFECTION

70. CHORIOAMNIONITIS
 Imflammation of the fetal membranes is usually manifestation of imtrauterine
infection
 Associated with prolonged membrane rupture and long labor
 Characteristic
clouding of the membranes
foul odor (depending on bacterial species and concentaraion )
 Definition
mono-and polymorphonuclear leukocytes infiltrate the chorion
 Leucocytes are found in amnionic fluid (amnionitis) or the umbilical cord(funisitis)
< 20 wks almost all polymorphonuclear leukocytes : maternal origin
> 20 wks: Inflammatory response : maternal & fetal
 Preterm deliveries : m/c

71.  Ascending portal of entry (vagina)
Cause of prematurity
 Microscopic study more valuable than “routine” cultures

72. ACUTE CHORIOAMNIONITIS

73. INTENSE INFLAMMATORY INFILTRATE OF
THE UMBILICAL CORD(FUNISITIS)

74.  According to some investigators these findings of inflammation may be
nonspecific and are not always associated with other evidence of fetal or
maternal infection
 Management
antimicrobial administration and expedient delivery

75. PLACENTAL INFARCTS
 m/c placental lesions
 Etiology : Preeclamptic toxemia ,
Essential hypertension,
Rh incompatibility and
Non toxic antepartum hemorrhage
 Incidence : 25% of placentas from uncomplicated term pregnancies
 Several types (by lesion sites )
- located at the placental margin (90%) , size <1cm(90%)
- underneath the chorionic plate - Subchorionic infarct downward with their apices
the intervillous space
- Intercotyledonary septa - meet and form a column of cartilage – like material
extending from the maternal surface to the fetal surface

76. OLD PLACENTAL INFARCT : LESION IS
WHITISH WITH HARD CONSISTENCY
1. fresh infarct: dark red
and firmer consistency
2. Old infarct: hard,white
mass of granular
appearance

77. GHOSTS OF CHORIONIC VILLI IN A LONG STANDING
PLACENTAL INFARCT
Microscopic:
1.crowding of villi
2.Virtual obliteration of
intervillous space
3.Marked congestion of villous
vessels
4.Old infarcts: mass of crowded
ghost villi seen

78. PLACENTAL SITE SUBINVOLUTION : SHOWING THICK-WALLED
VESSELS WHOSE LUMEN IS PARTIALLY OBLITERATED BY
ORGANIZING THROMBI
1. may result in vaginal bleeding
several weeks after delivery of
placenta
2. Curettage specimen : large
maternal vessels from placental
site partly filled with thrombi

79. --TUMORS OF THE PLACENTA-
Chorioangioma (Hemangioma)
 The resemblance components to the blood vessels and stroma of the
chorionic villus
 Benign tumor of placenta
 Incidence : 1%
 Hamartomas of primitive chorionic mesenchyme
 Diagnosis
larger chorioangiomas – sonographic findings
 Associated symptoms
small growths : asymptomatic
large tumors : hydramnios or antepartum hemorrhage
 Complication
associated with low birthweight
fetal death and malformations are uncommon

80. CHORIOANGIOMA (HEMANGIOMA)

81. TUMOURS OF PLACENTA gross:
 well circumscribed and
purplish mass,
 may protrude on fetal surface or
may remain localized in the
placental substance
 Microscopy:
 composed of network of
proliferating capillaries,
 mitoses may be present,
 degenerative changes are
common
 Associations:
 hydramnios,
 hemorrhage,
 premature delivery,
 premature placental seperation,
 placenta previa

82. Tumor Metastatic to the Placenta
 Malignant tumors rarely metastasize to the placenta
 Melanoma (1/3), leukemias and lymphomas 1/3
 Tumor cells usually are confined within the intervillous space
- the fetus : metastases (¼)
 Malignant cells seldom proliferate to cause clinical disease
Embolic Fetal Brain Tissue
 Fetal brain tissue occasionally is seen embolized to the placenta or fetal lungs
 Usually has been described with “traumatic” deliveries
 This phenomenon is not without precedent because brain tissue has been found in
pulmonary veins following head trauma in older children and adults

83. ABNORMALITIES OF CORD

84. Anatomy
 Origin : It develops from the connecting stalk.
 Length : At term, it measures about 50 cm.
 Diameter : 2 cm.

85. Structure: It consists of mesodermal connective tissue called Wharton's jelly,
covered by amnion.
It contains:
1. One umbilical vein carries oxygenated blood from the placenta to the
foetus
2. Two umbilical arteries carry deoxygenated blood from the foetus to the
placenta,
3. Remnants of the yolk sac and allantois
Insertion:
1. The cord is inserted in the foetal surface of the placenta near the center
"eccentric insertion" (70%) Or at the center "central insertion" (30%).

86. Here is a normal three vessel umbilical cord.
Note that there are two arteries towards the right and a single vein at
the left. Most of the cord consists of a loose mesenchyme with
intercellular ground substance (Wharton's jelly).

87. ABNORMALITIES OF CORD
1. Marginal insertion : in the placenta ( battledore insertion).
2. Velamentous insertion: in the membranes and vessels
connect the cord to the edge of the placenta.
 If these vessels pass at the region of the internal os , the
condition is called " Vasa praevia".

89. Velamentous insertion can cause rupture of one vessel,
but more often hypoxia.

90.  Seen above and below are
examples of "velamentous"
insertion of the umbilical cord in
which the major umbilical vessels
separate in the fetal membranes
before reaching the placental disk.
 Such a condition is of no major
consequence in utero, but could
lead to a greater chance for cord
trauma with bleeding during
delivery.
 Dividing membranes are seen at
the left in the twin placenta below.

91. ABNORMALITIES OF THE CORD
LENGTH
Long cord (>90cm) is result of fetal activity. The
more active fetus the longer the cord and opposite.
 Prolapse
 True knots
 Entanglement

92. Long cord can cause formation of true knots

93. This is another true umbilical cord knot

94. This is an umbilical cord pseudoknot. It is not a true knot, but just an
exaggerated loop of one of the umbilical arteries because it is longer
than the vein.

95. 1. True knot:
 when the foetus passes through a loop of the cord.
 If pulled tight, foetal asphyxia may result.
2. False knot:
localized collection of Wharton’s jelly containing a loop of umbilical
vessels

96. Excessive spiraling (normally clockwise from the fetal end) can cause
strictures, thrombosis and sometimes fetal demise. Spiraling is associated
with long cord and increased movement of fetus.

97. The fetus at the left is macerated from prolonged demise in utero. The cause of the
demise in this case is the marked twisting, or torsion, of the umbilical cord. A
macerated placenta is present at the right.

98. SHORT CORD
 Short cord (under 30 cm)
 Delay 2nd stage labor
 Abruptions
 Rupture
 CNS dysfunction
 Psychomotor impairments
 Congenital neuromuscular disease

99. SINGLE UMBILICAL ARTERY
 May be associated with other foetal congenital anomalies
 Must be confirmed by microscopic examination.

100. 101
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