Anatomi plasenta normal

Khorioamnionitis akut
This is a view of the chorionic plate of
the placenta.
•Note the umbilical cord (white arrow)
•The chorionic plate is markedly
cloudy and opaque because the
chorion and amnion are infiltrated
with acute inflammotory cells

Note that the chorionic vessels are

barely visible (black arrow).
Epidemiology : •clinically evident in 0.5-10% of pregnancies

General Microscopic Description

• •Chorioamnionitis: membranes (amnion and chorion + parietal
decidua) show neutrophilic infiltrate. PMN's originate from maternal
vessels in parietal decidua and migrate into chorion and then
amnion.
• •Chorionitis: chorionic plate shows neutrophilic infiltrate. PMN's
orginate from maternal intervillous space and migrate into
subchorionic fibrin, chorion itself and then amnion
• •Funisitis: umbilical cord shows neutrophilic infiltrate. PMN's
orginate in the fetal vessels of the umbilical cord and migrate
sequentially through the muscular layers of the vessel and then into
the Wharton's jelly.
• •Chorionic vasculitis: chorionic vessels show neutrophils in wall.
PMN's originate in the fetal vessels of the chorionic plate and
migrate through the walls of the fetal vessels toward the amniotic
fluid
 Khorioamnionitis
General Gross Description
•membranes and chorionic plate appear
cloudy and occasionally have a yellow or
green tint
•in severe cases the umbilical cord may have
small yellow round lesions on its surface
which represent foci of PMN's (small
abscesses)
• Clinical Correlation
•associated with preterm birth
•only 8-25% of mothers have
symptoms such as fever, chills
•fetus may have decreased
biophysical profile score or
abnormal heart rate pattern
•can lead to congenital
pneumonia, gastroenteritis,
menigitis, sepsis although
most infants do not have
sepsis even with umbilical cord
inflammation
 Etiology :
• mostly bacteria
• low virulence organisms ,
normal flora of vagina or
• Acut chorionitis
• obvious pathogens such as
E.Coli, Mycoplasma,
Ureaplasma
Pathogenesis
bacteria ascending from vagina,
breaching cervical defenses
(mucus plug etc.)
bacterial colonization of
intrauterine space through
intact or ruptured membranes
• maternal and fetal acute
inflammatory response,
Epidemiology
• •clinically evident in 0.5-
10% of pregnancies
 Funisitis umbilical
• Funisitis • umbilical cord shows
neutrophilic infiltrate.
PMN's orginate in the
fetal vessels of the
umbilical cord and
migrate sequentially
through the muscular
layers of the vessel
and then into the
Wharton's jelly.
 Intervillositis kronis
• Clinical Correlation • Etiology Unknown
• May recur Pathogenesis Unknonwn,
• May be associated with decidual • Epidemiology
vascular thrombosis and • • May be associated with
euploid early spontaneous chronic non-specific villitis
losses. • • May be associated with
euploid spontaneous abortion

• he villi are separated by

maternal blood containing
numerous mononuclear
elements.
• The arrowheads point to two
mononuclear cells.
• The nucleated elements are a
combination of macrophages
and lymphocytes
 Infark plasenta hemorrhagik
General Gross Description
•Acute infarcts (2-3 days old) usually red
and firm
•Subacute infarct (3-5 days old) usually
pink-tan and firm
•Old infarcts usually white-tan and firm .
Wedge shaped with apex at maternal
surface
Etiology
• •Decidual vascular thrombosis or
• •Absence or abnormal conversion of
decidual vessels or
• •Fibrinoid necrosis and atherosis of
decidual vessels Can lead to a
cessation in blood supply to intervillous
space and subsequent collapse of
villous architecture and agglutination of
villi
Pathogenesis
•Cessation of blood supply to intervillous
space and subsequent collapse of
villous architecture and agglutination of
villi with death of villous trophoblast
followed by death of villous stroma and
fetal vessels,
Epidemiology
•Marginal infarcts (<1cm) present in 10%
of normal term deliveries
•More significant number and size of
infacts seen in preclampsia,
intrauterine growth retardation,anti-
phospholipid antibody syndrome
Infark Plasenta
Clinical Correlation

•Small infarcts are usually

asymptomatic

•Multiple infarcts associated

with preeclampsia or
severe hypertension may
involve enough of
placental parenchyma to
lead to fetal demise
 Fibrinoid nekrosis
Decidual Vasculopathy General Gross Description
Etiology • Unknown • Not grossly visible lesions in the
Pathogenesis blood vessels
• Unknown • Sequelae to decidual vasculopathy
• Blood vessels either fail to undergo may be grossly evident as a small
normal physiologic conversion or placenta (acceleration of villus
• develop pathologic changes maturation) or one displaying
following conversion, infarcts or abruption
Epidemiology General Microscopic Description
• Associated with pregnancy induced
hypertension • Unconverted vessels exhibit round
• Associated with anticardiolipin antibodies
cross section with a preserved
and lupus anticoagulant muscularis and intima
• Thrombosed vessels may exhibit
mural or occlusive thrombosis with
or without recanalization; thrombi
may organize with smooth muscle
proliferation
•
Lanjut General Microscopic Description

• Lymphocytes or plasma cells may involve the wall of the vessel

• Fibrinoid necrosis can be recognized as acellular, brilliantly
eosinophilic and glassy transformation of the vessel wall
• Atherosis, often accompanying fibrinoid necrosis, consists of an
intramural accumulation of foamy macrophages resembling cells seen
in atherosclerosis
• These changes may occur in converted or unconverted vessels

Clinical Correlation
• Severity of clinical disease does not correlate well with severity of
pathology
• Thrombosed vessels may result in villous infarct
• Necrotic vessels may rupture with abruption
• Unconverted vessels may respond to vasospasm and also lead to
abruption
 Desidua dengan trombosis
Decidual Vasculopathy General Gross Description
Etiology • Unknown • Not grossly visible lesions in the blood
vessels
Pathogenesis
• • Sequelae to decidual
• Unknown vasculopathy may be grossly evident
• Blood vessels either fail to undergo as a small
normal physiologic conversion • placenta (acceleration of villus
or develop pathologic changes following maturation) or one displaying infarcts
conversion, or
Epidemiology • abruption
• Associated with pregnancy induced • General Microscopic Description
hypertension • • Unconverted vessels exhibit
• Associated with anticardiolipin antibodies round cross section with a preserved
and lupus anticoagulant • muscularis and intima
• • Thrombosed vessels may exhibit
mural or occlusive thrombosis with or
• without recanalization; thrombi
may organize with smooth muscle
• proliferation
• • Lymphocytes or plasma cells
may involve the wall of the vessel
•
Lanjut desidua dg nekrosis
• Fibrinoid necrosis can be recognized as acellular, brilliantly
eosinophilic and glassy transformation of the vessel wall
• Atherosis, often accompanying fibrinoid necrosis, consists of an
intramural accumulation of foamy macrophages resembling cells seen
in atherosclerosis
• These changes may occur in converted or unconverted vessels

Clinical Correlation
• Severity of clinical disease does not correlate well with severity of
pathology
• Thrombosed vessels may result in villous infarct
• Necrotic vessels may rupture with abruption
• Unconverted vessels may respond to vasospasm and also lead to
abruption
 Quadriplet Plasenta
• Pathogenesis
Etiology • Most assisted reproduction cases result from
• May be secondary to assisted fertility with implantation of multiple zygotes resulting in
implantation of multiple zygotes "non-identical" twinning
• Unknown if sporadic • Sporadic cases may show a mixture of
monozygous and multizygous gestations
(also occasional monozygous twinning in
assisted reproduction),
 Quadriplet Plasenta
• Epidemiology
• Increasing maternal age
• Varies in racial groups
• Assisted reproductionGeneral
Gross Description
• Multiple placental disks with
and without fusion
• Membrane appearance will vary
depending on whether junctions
are dichorionic or onochorionic
General Microscopic Description
• Dichorionic diamniotic junctions
will show chorion intervening
between the two amnions
• Monochorionic diamniotic
junctions will show no chorion
intervening between the
amnions
Clinical Correlation
• Increased risk for morbidity and
mortality associated with
premature delivery
 Umbilical knot
There is a knot in the center of the cord.
•There is no swelling or hemorrhage in the cord
Etiology
indicating that the knot did not compress blood •excessively long umbilical cord
vessels.
General Gross Description (normal=54-61 cm)
•The umbilical cord is tied in a true knot
•Loose knots which do not affect circulation in cord show Pathogenesis
no color changes or swellings
•Tight knots which do affect the circulation lead to •probably fetal movement with a
hemorrhage on the fetal side of the knot and edema on the long cord allows knotting
placental side
Epidemiology: 0.4-0.5% of
deliveries

General Microscopic Description

•Tight knots can have compression
of Wharton's jelly and mural
thrombosis in umbilical vessels
Clinical Correlation
•associated fetal mortality = 10%
 Fetus abortus 16 minggu
Epidemiology
• Human pregnancy generates large
numbers of spontaneous losses.
• Estimates of the percentages of
conceptions that fail to reach term has
increased with the advent of early
detection methods.
• Greater than 25% of pregnancies end
spontaneously.
• Current estimates are that approximately
50% of first trimester losses (by far the
most common) are secondary to
chromosomal abnormalities.
• Increasing spontaneous abortion rate
with age.
• Some women are habitual aborters.
Spontaneous Abortion
Etiology
• Chromosomal abnormalities including triploidy,
trisomy (reported for every chromosome),
monosmy X (Turner's syndrome), among others.
• Problems with mainintaing implantation
including antiphospholipid antibody syndrome
• Unknown
Pathogenesis
• Chromosomal abnormalities may result in fetal
death with subsequent death of the placenta.
• Unknown what effect chromosomal
abnormalities have on the placenta's function.
• Antiphospholipid antibody syndrome is
associated with abnormal decidual
vascularization and thrombosis of decidual
vessels with abruption.
• Ascending infection leads to membrane rupture
and premature delivery.
• Anatomic cervical incompetence can also lead
to miscarriage.,
 Spontaneous Abortion
. Clinical Correlation
General Gross Description • Most women are not habitual
• An
empty sac or disorganized embryonic aborters.
tissues (identified by microscopy) may be
secondary to early fetal demise.
• Alternatively the fetus may be delivered within • An attempt to categorize the
the amnionic sac followed by the placenta. miscarriage as either secondary to
• chromosomal abnormalities or
General Microscopic Description euploidy is useful in the management
• Findings vary with etiology of the loss. of women with recurrent losses.
• Common to all is an implantation site with
acute hemorrhage and inflammation.
• Aneuploid losses may repeat with
• Decidualized endometrium is generally advanced maternal age. Also will
sloughed as well.
repeat if parent carries a balanced
• The villi may show infarct or intervillositis in translocation (very rare).
cases associated with euploidy.
• The villi may show a complex villus outline,
trophoblastic inclusions, and calcifications • Euploid losses may repeat but
in aneuploid gestations. intervention with aspirin and/or
• Histologic abnormalities can be demonstrated heparin may permit maintenance
in the fetus. of a subsequent pregnancy to
• viability.
•
 Placenta Accreta
Etiology • Unknown General Microscopic Description
Pathogenesis • Accreta may show adherent
• absent decidua at implantation site due myometrium along the basal plate
to scar or abnormal implantation site of the placenta
(cervix) • Increta/percreta show villi growing
• Permits deep invasion of trophoblast into or through myometrium
either into very superficial muscle
(accreta), deep muscle (increta) or Clinical Correlation
through the serosa (percreta), • Associated with uterine rupture,
Epidemiology hemorrhage, and failure to deliver
• Associated with placenta previa placenta
• Associated with previous C-sections
General Gross Description
• In simple accreta the maternal surface of
the placenta is shaggy and irregular with
variable amounts of fragmentation of the
cotyledons
• In increta or percreta the placenta cannot
be removed from the uterus at all and
rupture of the uterus is a common
complication
•