Dr. Farah, Asst. prof. pathology

1. PLACENTAL DISORDERS

2. Introduction
 Diseases of pregnancy and pathologic
conditions of the placenta are important
causes of fetal intrauterine or perinatal death,
congenital malformations, intrauterine growth
retardation, maternal death, and morbidity for
both mother and child.

3. Normal placenta anatomy
 Placenta is derived from both maternal
and fetal tissues.
a) The m ate rnalpo rtio n o f the place nta has
irregular grooves dividing it into
cotyledons which are composed of sheets
of decidua basalis and remnants of blood
vessels.
b) The fe talpo rtio n o f the place nta is
co m po se d of numerous functional units
called chorionic villi and comprise the

5. Chorionic villi
 In the chorionic villi they
form an extensive
capillary system, bringing
fetal blood in close
proximity to maternal
blood.
 Chorionic villi composed
of delicate mesh of
central stroma
surrounded by two
discrete layers of

6. Disorders of Early Pregnancy
 Spontaneous Abortion
 Ectopic Pregnancy
Disorders of Late Pregnancy
 Twin Placentas
 Abnormalities of Placental Implantation
 Placental Infections
 Preeclampsia and Eclampsia

7. Disorders of Early Pregnancy
Spontaneous Abortion
Spontaneous abortion, or “miscarriage,” is
defined as pregnancy loss before 20 weeks of
gestation.
 Most of these occur before 12 weeks.
 10 to 15% of clinically recognized pregnancies
terminate in spontaneous abortion
 However, using sensitive HCG assays, it has
been determined that an additional 20% of
early pregnancies in otherwise healthy women

8. ETIOLOGY
 The mechanisms leading to early loss of
pregnancy are unknown. However, multiple
fetal and maternal causes of spontaneous
abortion have been identified.
 Among the most important are the following
 Fetal chromosomal anomalies, such as
aneuploidy, polyploidy, and translocations, are
present in approximately 50% of early
abortuses.
 Maternal endocrine factors, including luteal-
phase defect, poorly controlled diabetes, and

9.  Physical defects of the uterus, such as
submucosal leiomyomas, uterine polyps, or
uterine malformations, may prevent or disrupt
implantation
 Systemic disorders affecting the maternal
vasculature, such as antiphospholipid
antibody syndrome, coagulopathies, and
hypertension
 Infections with protozoa (Toxoplasma),
bacteria (Mycoplasma, Listeria), or a number
of viruses. Ascending infection is particularly

10. Ectopic Pregnancy
 Ectopic pregnancy refers to implantation of the
fetus in a site other than the normal
intrauterine location
 The most common site is the extrauterine
fallopian tube (approximately 90% of cases).
 Other sites include the ovary, the abdominal
cavity, and the intrauterine portion of the
fallopian tube (cornual pregnancy)
 Ectopic pregnancies account for 2% of

11. RISKFACTORS OF ECTOPIC PREGNANCY
 Pelvic inflammatory disease resulting in
intralumenal fallopian tube scarring (chronic
salpingitis)
 Peritubal scarring and adhesions, which may
be caused by appendicitis, endometriosis, and
previous surgery
 Intrauterine contraceptive device(associated
with twofold increase of ectopic pregnancy)

12. MORPHOLOGY
 In each abnormal location, the fertilized ovum
develops as usual, forming placental tissue,
amniotic sac, and fetus. The host implantation
site may also develop decidual changes.
 Tubal pregnancy is the most common cause
of hematosalpinx (blood-filled fallopian tube)
and should always be suspected when a tubal
hematoma is present.

13. Consequences of Ectopic Pregnancy
 With time the growth of the gestational sac
distends the fallopian tube, causing thinning of
the wall and rupture. The rupture frequently
results in massive intraperitoneal hemorrhage,
which sometimes is fatal.
 Less commonly the tubal pregnancy may
undergo spontaneous regression and
resorption, or be extruded through the
fimbriated end of the tube into the abdominal
cavity (tubal abortion).

14. Clinical Features
 Rupture of a tubal pregnancy is a medical
emergency.
 The clinical course of ectopic tubal pregnancy
is characterized by
 the onset of moderate to severe abdominal
pain and
 vaginal bleeding 6 to 8 weeks after last
menstrual period, correlating with distention
and then rupture of the fallopian tube, causing
hemorrhagic shock with signs of an acute
abdomen, and therefore early diagnosis is

15. Diagnosis of ectopic pregnancy
Diagnosis is based on
 Determination of chorionic gonadotropin titers,
 Pelvic sonography,
 Endometrial biopsy (which shows decidua
without chorionic villi or implantation site) and/or
 Laparoscopy

16. Disorders of Late Pregnancy
Twin Placentas
 Twin pregnancies arise from fertilization of two
ova (dizygotic) or from division of one fertilized
ovum (monozygotic).
 There are three basic types of twin placentas
a) diamnionic dichorionic (which may be fused),
b) diamnionic monochorionic, and
c) monoamnionic monochorionic.

17. Monochorionic placentas imply monozygotic (identical) twins
Dichorionic placentation may occur with either monozygotic
or dizygotic twins

18. Complication
 Complication of monochorionic twin pregnancy is
twin-twintransfusionsyndrome.
Monochorionic twin placentas have vascular
anastomoses that connect the circulations of the
twins, and in some cases these connections
include one or more arteriovenous shunts
If these shunts preferentially increase blood flow
to one twin at the expense of the second, one
twin will be underperfused, while the second will
be fluid overloaded.

19. Abnormalities of Placental
Implantation
Placentaprevia
 Conditioninwhichtheplacentaimplants inthe
loweruterinesegment orcervix
 Often leading to serious third trimester
bleeding.
 A complete placenta previa covers the internal
cervical os and thus requires delivery via
cesarean section to avert placental rupture
and fatal maternal hemorrhage during vaginal
delivery

20. Placenta completely covers
the top of cervix
Placenta partially covers
the top of the cervix

21.  Placenta accreta occurs when all or part of
the placenta attaches abnormally to
the myometrium (the muscular layer of the uterine
wall).
 Caused by partial or complete absence of the
decidua, such that the placental villous tissue
adheres directly to the myometrium, which leads to
a failure of placental separation at birth.
 It is an important cause of severe, potentially life
threatening postpartum bleeding.
 Common predisposing factors are
Placenta accreta

22.  Three grades of abnormal placental attachment
are defined according to the depth of invasion:
a) Accreta – chorionic villi attach strongly to the
myometrium (but does not penetrate it), rather
than being restricted within the decidua basalis
b) Increta – chorionic villi invade into the
myometrium
c) Percreta – chorionic villi invade through the
myometrium (penetrates the entire myometrium
to the uterine serosa)

24. Placental Infections
 Infections in the placenta develop by two
pathways:
(1) Ascending infection through the birth canal and
(2) Hematogenous (transplacental) infection
 Ascending infections are by far the most common
and are virtually always bacterial
 Localized infection of the membranes produces
premature rupture of membranes and preterm
delivery.
 The amniotic fluid may be cloudy with purulent
exudate, and histologically the chorionamnion

25.  The infection frequently elicits a fetal response
consisting of a “vasculitis” of the umbilical and
fetal chorionic plate vessels.
 Uncommonly, bacterial infections may result
from hematogenous spread to the placenta,
leading to acute villitis
 Several hematogenous infections, classically
components of the TORCHgroup
(toxoplasmosis and others [syphilis,
tuberculosis, listeriosis], rubella,
cytomegalovirus, herpes simplex), can affect

26. Preeclampsia and Eclampsia
Preeclampsia is a systemic syndrome
characterized by widespread maternal
endothelial dysfunction that presents during
pregnancy with hypertension, edema, and
proteinuria
 Preeclampsia should be distinguished from
gestational hypertension that can develop in
pregnancy without proteinuria.
 It occurs in about 3% to 5% of pregnant women,
usually in the last trimester and more commonly
in primiparas (women pregnant for the first time).

28. Pathogenesis
 Although the exact mechanisms leading to
development of preeclampsia are still being
investigated, it is clear that the placenta plays
a central role in the pathogenesis of the
syndrome, since the symptoms disappear
rapidly after delivery of the placenta.
 The critical abnormalities in preeclampsia are
1) Diffuse endothelial dysfunction,
2) Vasoconstriction (leading to hypertension),
and
3) Increased vascular permeability (resulting in

29. Pathogenesis (Cont.)
The principal pathophysiologic aberrations appear to
be the following:
 Abnormal placental vasculature
 Endothelial dysfunction and imbalance of
angiogenic and antiangiogenic factors
 Coagulation abnormalities

30. Abnormal placental vasculature
In normal pregnancy, the
musculoelastic walls of the
spiral arteries are invaded by
trophoblasts, permitting them to
dilate into wide vascular
sinusoids.
In preeclampsia and eclampsia,
this vascular remodeling is
impaired, the musculoelastic
walls are retained and the
channels remain narrow.
Decreased uteroplacental blood

31. Endothelial dysfunction and imbalance of
angiogenic and antiangiogenic factors
 Balance between pro-angiogenic (VEGF and TGFβ)
and anti-angiogenic factors (soluble so luble fm s-like
tyro sine kinase sFlt and soluble endoglin) is
essential for the normal function of placenta.
 There imbalance are hypothesized to result in
endothelial cell dysfunction, vascular hyperreactivity,
and end-organ microangiopathy
 When placenta-derived anti-angiogenic factors i.e,
sFlt and endoglin are overexpressed together, rats
develop nephrotic-range proteinuria, severe
hypertension, and fetal growth restriction, the

32.  Thus, it seems that sFlt1 and soluble endoglin
are key mediators that link the placenta to the
characteristic maternal endothelial dysfunction
of preeclampsia.

33. Coagulation abnormalities
 Preeclampsia is associated with
hypercoagulability which is likely related to the
reduced endothelial production of PGI2, a potent
antithrombotic factor, and increased release of
procoagulant factors
 This hypercoagulable state may lead to the
formation of thrombi in arterioles and capillaries
throughout the body, but particularly in the liver,
kidneys, brain, and pituitary.

35. MORPHOLOGY
 Placental abnormalities include:
a) Infarcts, which can be a feature of normal
pregnancy, but are much more numerous with
severe preeclampsia or eclampsia
b) Retroplacental hemorrhages
c) Premature maturation of placental villi associated
with villous edema, hypovascularity, and increased
production of syncytial epithelial knots
d) Fibrinoid necrosis and focal accumulation of lipid
containing macrophages (acute atherosis) of
decidual vessels

36.  liverlesions when present, take the form of irregular,
focal, subcapsular, and intraparenchymal
hemorrhages
 fibrin thrombi in the portal capillaries
 foci of hemorrhagic necrosis
 kidney lesions are variable.
 Glomeruli show marked swelling of endothelial cells,
amorphous dense deposits on the endothelial side
of the basement membrane, and mesangial cell
hyperplasia.
• bilateral renal cortical necrosis (widespread and

37. Clinical Features
 Preeclampsia most commonly starts after 34
weeks of gestation but begins earlier in women
with hydatidiform mole or preexisting kidney
disease, hypertension, or coagulopathies.
 The onset is typically insidious, characterized by
hypertension and edema, with proteinuria following
within several days. Headaches and visual
disturbances are serious events and are indicative
of severe preeclampsia, often requiring delivery.
 Eclampsia is heralded by central nervous system
involvement, including convulsions and eventual

39. MANAGEMENT
 For term pregnancies: delivery is the
treatment of choice regardless of disease
severity.
 In preterm pregnancies, where delivery may
not be in the best interest of the fetus, patients
with mild disease can be managed expectantly
by closely monitoring the mother and fetus.
 Eclam psia, se ve re pre e clam psia with m ate rnal
e nd-o rg an dysfunctio n, fe talco m pro m ise , o r
the HELLP syndro m e are indicatio ns fo r
de live ry re g ardle ss o f g e statio nalag e .

40. COMPLICATIONS AND CONSEQUENCES
 Hypercoagulability,
 Acute renal failure, and
 Pulmonary edema
 HELLP syndrome
 Although in most instances preeclampsia has no
lasting sequelae, recent studies indicate that
about 20% of affected women develop
hypertension and microalbuminuria within 7 years
of a pregnancy complicated by preeclampsia.
 There is also a twofold increase in the long term

41. THANKYOU