BRUK PLACENTA development AND Amniotic fluid metabolism.ppt

PREPARED BY:- DR BRUKALEM G.(R-1)
MODERATOR:- DR HASAB
(CONSULTANT OBSTETRICIAN AND
GYNECOLOGIST)
Saturday, February 3, 2024
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ANATOMY AND ABNORMALITY
OF PLACENTA, MEMBRENE AND
AMINIOTIC FLUID
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Out lines
 Introduction
 Development of the placenta
 Placental function
 Placental anomalies
 Umbilical cord and anomalies
 Amniotic fluid and its disorders
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Placenta
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is a fetal organ consisting of
 umbilical cord
 membranes (chorion and amnion),
 and parenchyma
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Introduction
 Development of the placenta is a continuous process.
 Requires a receptive endometrium (decidua)
 The placenta is endocrine organ and an organ of transfer
between mother and fetus
 Normal site of implantation is posterior (2/3 of cases) or
anterior (1/3 of cases) wall of upper uterine segment
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Decidua
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This is a specialized, highly modified endometrium of pregnancy.
It is essential for hemochorial placentation
 The three regions of the decidua
 Decidua basalis - undersite of implantation
Decidua capsularis – overlies the enlarging blastocyst
Decidua parietalis – covering the rest of uterine cavity
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Trophoblast Development
 Human placental formation begins with the trophectoderm,
which gives rise to a trophoblast cell layer encircling the
blastocyst
By the 8th day after initial implantation
 The trophoblast differentiated to:-
 outer multinucleated syncytium of syncytiotrophoblast
 inner layer of primitive mononuclear cells of cytotrophoblast
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 Their invasiveness promotes implantation,
 their nutritional role and their endocrine function is essential to
maternal physiological adaptations and to pregnancy maintenance
exhibit the most variable structure, function, and developmental
pattern of all placental components
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Development of placenta
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 .
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 After implantation is complete it differentiate along pathways, giving rise to
Villous trophoblasts generate chorionic villi
Extravillous trophoblasts migrate into the decidua and
myometrium and also penetrate maternal vasculature further classified
classified as
 interstitial trophoblasts
 and endovascular trophoblasts
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 The interstitial trophoblasts invade the decidua and eventually
penetrate the myometrium to form placental bed giant cells.
 These trophoblasts also surround spiral arteries.
 The endovascular trophoblasts penetrate the spiral artery lumens and
remodel the lumen.
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 Some small cells appear between the embryonic disc and the
trophoblast and enclose a space that will become the amnionic cavity.
 Embryonic mesenchyme first appears as isolated cells within the
blastocyst cavity.
 When the cavity is completely lined with this mesoderm it is termed
the chorionic vesicle and its membrane now called the chorion is
composed of trophoblasts and mesenchyme
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 Some mesenchymal cells eventually will condense to form the
body stalk which joins to embryo to the nutrient chorion and
later develops in to the umbilical cord.
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FORMATION OF LACUNAE
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 Beginning approximately 12 days after conception the
syncytiotrophoblast deeply invade in the endometrium
 where vacuoles appear in the syncytium
 When these vacuoles fuse, they form large lacunae(future intervillous
spaces), and this phase of trophoblast development is thus known as the
lacunar stage
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FORMATION OF LACUNAE
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Development
of villi
Week 2 to week 3
 Primary villi:
cytotrophoblast+sync
ytiotrophoblast
 Secondary villi:
extraembryonic
mesoderm enter the
primary villi
 Tertiary villi:
extraembryonic
mesoderm =>CT+BV
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Cont..
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 Maternal arterial blood does not enter the intervillous space until
around day 15.
 By approximately the 17th day however fetal blood vessels are
functional and a placental circulation is established.
 The fetal placental circulation is completed when the blood vessels of
the embryo are connected with chorionic vessels.
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Placental growth and maturation
 In the first trimester placental growth is more than fetus
 at 17 weeks placental and fetal weights are approximately equal
 and at term placental weight is approximately one sixth of fetal weight .
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 Lobes vary from 15 to 20 are incompletely separated by grooves
of variable depth that overlie placental septa which arise from
folding of the basal plate.
 The total number of placental lobes remains the same and
continue to grow although less actively in the final weeks.
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Fetal- maternal circulation
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• Fetus:
umbilical A carries O2/nutrient depleted blood to cap. of chorion , exchange with
maternal blood of the intervillous space umbilical V
• Mother:
spiral A intervillous space uterine V
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 One truncal artery supplies one main stem villous and thus one
cotyledon.
 The amount of vessel wall smooth muscle decreases, and the vessel
caliber increases as it penetrates the chorionic plate.
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Anatomy
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At term
 Discoid organ
 weighs 450 g
 round to oval with a 22-cm diameter,
 central thickness of 2.5 cm
 composed of placental disc, extraplacental
membranes, and three-vessel umbilical cord
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,
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Two surfaces or plates
 Chorionic plate
umbilical cord is attached
 Basal plate
abuts the maternal endometrium
branching villi resemble a leafy tree
incompletely divided into between 10 and 40 lobes
 amnion is shiny but chorion is shaggy
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.
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Maternal and Fetal blood do not mix
Layers separating them
 Syncytiotrophoblast 1
 Cytotrophoblast 2
 Extraembryonic mesodrm 3
 Endothelial lining of fetal capillaries 4
By 4th month 2and 3 disappear and barrier
Becomes relatively leaky
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Bulk Flow/Solvent Drag
Differences in hydrostatic and osmotic pressures between
the
maternal and fetal circulations within the exchange barrier
drive water transfer by bulk flow, which drags along
dissolved
solutes
Mechanisms Transfer
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Conti..
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Endocytosis/Exocytosis
Endocytosis is the process by which molecules become
entrapped in invaginations of the microvillous plasma membrane
of the syncytiotrophoblast,active
transport- utilizes ATP to move solutes against a gradient, Na + K +
ATPase and Ca 2+ ATPase are two examples.
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Conti..
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Diffusion
Diffusion of any molecule occurs in both directions across
any barrier. When a concentration gradient exists—and/or
for charged species, an electrical gradient—one of these unidirectional
fluxes (rates of transfer) is greater in one direction
than it is in the other so that there is a net flux in one direction
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Function of the Placenta
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 Metabolic functions
 Respiratory function
 Excretory function
 Endocrine functions
 (PLACENTAL TRANSFER) Nutritional function
 Barrier function
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Metabolic functions
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 synthesizing appreciable amounts of glycogen
 Protein metabolism- At week 10, 1.5 g per day but at term rises to 7.5 g
 Lactate, a waste product of metabolism
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Respiratory function
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 Oxygen passes into the fetal blood by simple diffusion,
 Driven by an oxygen pressure gradient from the mother’s blood to the
fetus’s blood. Near the end of pregnancy,
 the mean PO2 of the mother’s blood in the placental sinuses is about 50
mm Hg, and the mean PO2 in the fetal blood after it becomes
oxygenated in the placenta is about 30 mm Hg.
 Therefore, the mean pressure gradient for diffusion of oxygen through
the placental membrane is about 20 mm Hg
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 The PCO2 of the fetal blood is 2 to 3 mm Hg higher than that of the
maternal blood.
 This small pressure gradient for carbon dioxide across the membrane is
more than sufficient to allow adequate diffusion of carbon dioxide,
 because the extreme solubility of carbon dioxide in the placental
membrane allows carbon dioxide to diffuse about 20 times as rapidly as
oxygen.
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Excretory function
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 same manner that carbon dioxide Waste products of the fetus are
passed to maternal blood by passive diffusion
 include especially the non protein nitrogen's such as urea, uric acid,
and creatinine.
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Endocrine functions
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 It Produce hormones
Two categories:
 peptide hormones (human chorionic gonadotropin [hCG],
human placental lactogen [hPL], cytokines, growth hormone
[GH], insulin-like growth factors [IGF's], corticotropin releasing
hormone [CRH], vascular endothelial growth factor [VEGF], placental
growth factor [PIGF]) and
 steroid hormones (estrogens, progesterone and glucocorticoids).
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1) Human chorionic gonadotrophin (hcG)
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 Produced by syncytiotrophoblasts (mostly),$ fetal kidney
 can be detected in the maternal blood and urine approximately 8 to
10 days after fertilization.
 glycoprotein molecular structure and function as LH,FSH,TSH
 Plasma levels doubling every 2 days in the first trimester, reaches
peak of 100,000mlu/ml about 60th day (at 8 to 10 wks of gestation)
 falls sharply after 16wks to 30,000mlu/ml and maintain at this level
until term
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 It is composed of two dissimilar α and β subunits which non
covalently held together.
 The α subunit is common to that TSH LH FSH and is encoded by a
single gene
 It is the β subunit that determines the biologic specificity of hCG
 Renal accounts for 30% of its metabolic clearance the remainder is
likely cleared by metabolism in the liver
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FUNCTIONS
- promotion of relaxin secretion by the corpus luteum
- regulates expansion of dNK cell numbers during early stages of
placentation
- hCG may promote uterine vascular vasodilatation and myometrial
smooth muscle relaxation
- maternal thyroid gland is also stimulated by large quantities of hCG
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2. Human placental lactogen (hPL)
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 also known as chorionic somatotropin,
 is a single-chain glycoprotein (22,300 Da)
 that has a high degree of amino acid sequence homology with both
human growth hormone (96%) and prolactin (67%).
 synthesized exclusively in the syncytiotrophoblast
 can be detected from the third week of gestation onward
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 plateau at around 36 weeks of gestation,
 at which time he daily production rate is approximately 1 g.
 production of hPL accounts for 5% to 10% of total protein
synthesis by placental ribosomes,
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Function
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 It promotes lipolysis, which increases circulating free fatty acid levels,
 promotes growth and differentiation of the mammary glandular tissue
in anticipation of lactation.
 potent angiogenic hormone and serve for fetal vasculature formation
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1 Estrogens
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 Produced by syncytiotrophoblasts
 hCG stimulates the synthesis of estrogen in the placenta
 At end of pregnancy, the daily production of placental estrogens
increases 30 times the mother’s normal level of production.
 the secretion placenta is quite different from secretion by the ovaries
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Placental Estrogen Production
 The placenta produces huge amounts of estrogens using blood-born
esteroidal precursors from the maternal and fetal adrenal glands.
 Near term, normal human pregnancy is hyper estrogenic state as
equivalent to 1000 ovulatory women.
 From 2-4 weeks secreted from c.luteum but later from placenta.
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 Dehydroepiandrosterone (DHEA) and its sulfate (DHEA-S) are C-19
steroids which are precursors and placenta had convert to estrone and
estradiol.
 This need four enzymes….
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 The fetal adrenal gland is important source of placental estrogen
precursors and it reflects the unique interactions of fetal adrenal
glands, fetal liver, placenta, and maternal adrenal glands.
 More than 90% of estradiol and estriol formed in
syncytiotrophoblast enters maternal plasma.
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Factors affecting estrogen production
 Fetal demise
 anencephaly
 adrenal hypoplasia
 placntal sulfatase deficiency
 placental aromatase deficiency
 Trisomy 21 Down Syndrome
 Deficiency in Fetal LDL Cholesterol Biosynthesis
 Fetal Erythroblastosis
 Gestational Trophoblastic Disease
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Function
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mainly a proliferative function on most reproductive and
associated organs of the mother.
 enlargement of the uterus,
enlargement of the breasts and growth of the breast ductal
structure, and
enlargement of the mother’s female external genitalia.
also relax the pelvic ligaments allow easier passage of the fetus
through the birth canal
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2 Progesterone
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In addition to being secreted in moderate quantities by the
corpus luteum at the beginning of pregnancy,
it is secreted later in tremendous quantities by the placenta,
averaging about a 10-fold increase during the course of
pregnancy,
utilize maternal cholesterol derived from low-density
lipoproteins (LDLs
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Function
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progesterone may be essential to maintain the secretory activity
of the endometrial glands.
decreases the contractility of the pregnant uterus,
contributes to the development of the conceptus even before
implantation,
although it may have immunomodulatory and appetite
stimulatory roles as well
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ABNORMALITIES OF THE PLACENTA
Bilobate
 Placentas may in frequently form as separate
nearly equally sized discs called bilobate placenta or bipartite
placenta or placenta duplex.
 In these the cord inserts between the two placental lobes either into a
connecting
chorionic bridge or into intervening membranes and may cross cervical
os result in vasa previa.
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 A placenta containing three or more equally sized lobes is rare
and termed multilobate.
 However more frequently one or more small accessory lobes
succenturiate lobes may develop in the membranes at a distance
from the main placenta.
 An accessory lobe may be retained in the uterus after delivery
and cause postpartum uterine atony and hemorrhage.
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Placentomegaly
 defines those thicker than 40mm and results from striking villous
enlargement .
 This may be secondary to maternal diabetes, severe maternal anemia,
fetal hydrops or infection caused by syphilis, toxoplasmosis,
cytomegalovirus.
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 Circummarginate placenta-failure of
chorionic plate to extend to this periphery and leads to a
chorionic plate that is smaller than the basal plate and fibrin and
old hemorrhage lie between the placenta and the overlying
amniochorion .
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 Circumvallate placenta- the peripheral chorion is thickened
opaque gray white circular ridge composed of double fold of
chorion and amnion.
 Clinically most pregnancies with extra chorial placenta have
normal outcome but circumvallate placenta was associated with
increased risk for ante partum bleeding and preterm birth.
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Placenta Accreta, Increta, and Percreta
 These placental abnormalities develop when trophoblast invades the
myometrium to varying depth to cause abnormal adherence.
 They are much more likely when there is placenta previa or when the
placenta implants over a prior uterine incision or perforation.
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Circulatory Disturbances
 Up to 30% of placental villi can be lost without untoward fetal effects
but extensive lesions can profoundly limit fetal growth.
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 Sub chorionic Fibrin Deposition
 Pre villous Fibrin Deposition- Maternal blood flow stasis
around villous results in fibrin deposition, diminished villous
oxygenation and syncytiotrophoblastic necrosis.
 Inter villous Thrombus- is a coagulated maternal blood
normally found in the intervillous space mixed with fetal blood
from a break in villous.
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 Maternal Floor Infarction- is fibrinoid deposition with in the
placental basal plate and impedes normal maternal blood flow in
to the intervillous space.
 These lesions are associated with miscarriage ,fetal growth
restriction, preterm delivery and
still births.
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Hematoma
 Retro placental hematoma-between the placenta and its adjacent
decidua.
 Marginal hematoma—between the chorion and decidua plate
known clinically as subchorionic hemorrhage.
 Subchorial thrombosis -along the roof of the intervillous space
and beneath the chorionic plate.
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 Sub amnionic hematoma- these are of fetal vessel origin
and found beneath the amnion but above the chorionic plate.
 Extensive retro placental, marginal, and subchorial collections
have been associated with higher rates of miscarriage,
placental abruption, fetal growth restriction, preterm delivery,
and adherent placenta.
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Placental Tumors
 Gestational Trophoblastic Disease
 Metastatic tumors
 Chorioangioma- these placental tumors have an incidence of
approximately 1%.
 Their characteristic sonographic appearance has a well circumscribed,
rounded, predominantly hypo echoic lesion near the chorionic surface.
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 Increased blood flow by color Doppler helps to distinguish these
lesions from other placental masses such as hematoma, partial
hydatidiform mole, teratoma, metastases, and leiomyoma.
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 Large tumors measuring >5cm may cause arterio-venous
shunting within the placenta that can cause fetal anemia and
hydrops.
 Hemorrhage, preterm delivery, amnionic fluid abnormalities,
and IUGR may also complicate large tumors.
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UMBILICAL CORD
 Most umbilical cords are 40 to 70cm long and vary from acordia to
300cm.
 Cord length is influenced positively by both amnionic fluid volume
and fetal mobility.
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 Short cords may be associated with IUGR, congenital
malformations, intrapartum distress, and a twofold risk of death.
 Excessively long cords are linked with cord entanglement or
prolapse and with fetal anomalies, acidemia, and demise.
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 Coiling- umbilical vessels spiral through the cord in left -
twisting direction.
coiling index = number of complete coils per centimeter.
sonographicaly -0.4
post delivery-0.2
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 Clinically, hypo-coiling has been linked with fetal demise where
as hyper-coiling has been associated with IUGR and
intrapartum fetal acidosis.
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 Vessel Number- The most common aberration is that of a
single umbilical artery with an incidence of 0.63% in live born
neonates, 1.92% with perinatal deaths, and 3% in twins.
 Major malformations frequently cardiovascular and
genitourinary have associated single umbilical artery.
 A single artery has also been associated with IUGR, prematurity,
aneuploidy and perinatal loss.
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 Insertion- The cord normally inserts centrally in to the
placental disc.
 Marginal insertion is a common variant sometimes referred to
as a battledore placenta in which the cord anchors at the
placental margin.
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 Velementous insertion-umbilical vessels spread within the
membranes at a distance from the placental margin surrounded
only by a fold of amnion and are vulnerable to compression,
which may lead to fetal hypo perfusion and acidemia.
 The incidence is approximately 1%, but more commonly seen
with placenta previa and multifetal gestations.
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 Furcate insertion- cord lose their protective Wharton jelly
shortly before they insert covered only by an amnion sheath and
prone to compression, twisting, and thrombosis.
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 Vasa Previa- This is particularly dangerous variation of
velamentous insertion in which the vessels within the
membranes overlie the cervical os.
 Common in bilobate or succenturiate placentas and second
trimester placenta previa, with or without later migration.
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Knots, Strictures, and Loops
 True knots are caused by fetal movement and are 1% of birth, common
and dangerous in monoamnionic twins.
 A cord stricture is a focal narrowing of its diameter that usually
develops near the fetal cord insertion.
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 Cord loops are coiling around various fetal parts during
movement is reported in 20 to 34 % of deliveries; two loops in
2.5 to 5% ; and three loops in 0.2 to 0.5%.
 Cord hematomas are uncommon and associated with abnormal
cord length, aneurysm, trauma, entanglement, umbilical vessel
venopuncture, and funisitis.
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Membranous structure
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 surrounds the developing fetus and forms the amniotic cavity
 composed of two layers:
- the amnion (inner layer) and
- the chorion (outer layer).
 fused approximately three months gestation
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CONTI…
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 Amniotic fluid (AF) is the liquid that surrounds the fetus after the
first few weeks of gestation
 Amniotic fluid
30 mL at 10 weeks
200 mL by 16 weeks
800 mL by the mid-third trimester
declines to about 500 mL at 42 weeks
 Early in pregnancy, is similar in composition to extracellular fluid
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first half of pregnancy, transfer of water and other small molecules
takes place
 across the amnion—transmembranous flow
 across the fetal vessels on placental surface —
intramembranous flow
 transcutaneous flow—across fetal skin.
SOURCES OF AMNIOTIC FLUID
Early gestation
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Late
gestation
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Major
 –Production: Fetal urine and fetal lung liquid
 –Clearance: Fetal swallowing and intramembranous pathway
Minor
 –Production —Secretions from the fetal oral-nasal cavities
 –Clearance —Transmembranous pathway.
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Four pathways play a major role in amnionic fluid
volume regulation
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Outflow = 1000 ml/day
1. Fetal swallowing
2. intramembranous
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Inflow = 1000 ml/day
1. Fetal Urine
2. Lung liquid
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AF regulation
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 –Secretion -Balanced -Absorption
 –AFV does not change significantly from day to day, but the AF itself is
completely replaced
 –Maximum at 38thwk of GA 800 –1000 ml then it will decrease till
term {b/c fetal renal system become functional}
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Physical characteristics
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Composition - (98-percent water)
- Carbohydrate, proteins, lipids, enzymes
Colorless
Meconium stained (green)
Golden color in Rh incompatibility
Greenish yellow (saffron) in post maturity
–Dark colored in concealed accidental hemorrhage
–Dark brown (tobacco juice) in IUD
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Measurement
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The actual volume of amnionic fluid is measured
 direct measurement and
 dye-dilution
These measurements have further been used to validate
sonographic fluid assessment techniques.
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Function
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 Shock absorber –protects from external trauma
 cushions the umbilical cord from compression
 Permits fetal movements –development of musculoskeletal
system, prevents adhesions
 Swallowing of AF enhances growth & development of GI
 AF volume maintains AF pressure –reduces loss of lung liquid
–pulmonary development
 Maintenance of fetal body temperature
 Some fetal nutrition, water supply
 Bacteriostatic properties: decreases potential for infection
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Sonographic Assessment
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 component of standard sonogram performed in the second
or third trimester
- only practical clinical method of assessing amniotic fluid volume
 two semi-quantitative techniques,
 the single deepest pocket of fluid or
 the amnionic fluid index (AFI)
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 The ultrasound transducer is held perpendicular to the floor and
parallel to the long axis of the woman.
 horizontal dimension -at least 1 cm
 largest vertical pocket of fluid is identified and measured
 No cord, fetal part
 Color Doppler is generally used to verify that umbilical cord
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1. Single Deepest Pocket
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 also called the largest or maximal vertical pocket of amnionic
fluid.
 normal if above 2 cm and less than 8 cm
 with values below and above this range indicating
oligohydramnios and hydramnios,
 multifetal gestations, a single deepest pocket of amnionic fluid is
assessed in each gestational sac, again using a normal range of
more than 2 cm to less than 8
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 not predictive of intrapartum or neonatal outcomes
 sensitivity 5%, specificity 98%
 SDP < 1 cm marked increase in perinatal morbidity and
mortality, which persisted even after correcting for birth defects
 Preferred over AFI -useful for the evaluation of pregnancies at
risk for an adverse pregnancy outcome
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2. Amnionic Fluid Index
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 The uterus is divided into four equal quadrants
 AFI is the sum of the single deepest pocket from each quadrant.
 The intraobserver variability of the AFI approximates 1 cm, and the
interobserver variability is about 2 cm
 normal is 5 cm to 25 cm
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 reliable in determining normal or increased amnionic fluid
 but was inaccurate in diagnosing oligohydramnios (leads to over
diagnosis of oligohydramnios
 So increase induction of labor & CD for fetal distress without
improving peripartum outcomes
 had a poor sensitivity for adverse pregnancy outcome
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 SDP and the AFI methods are equivalent in their prediction of adverse
outcomes and actual oligohydramnios and polyhydramnios in
singleton pregnancies,
 favors use of the SDP Than AFI
over diagnosis of oligohydramnios by AFI
Special Population
Gestational age 14 to 20 weeks
Multifetal pregnancy
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Problems
 low (oligohydramnios)
 high (polyhydramnios)
 Amniotic fluid embolism syndrome
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OLIGOHYDRAMNIOS
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 AFV < 95thcentile (AFI < 5 cm and SDP < 2 cm)
Anatomically < 200 mL at term
 complicates 1 to 2 percent of pregnancies
 always a cause for concern
 anhydramnios =no measurable pocket
 borderline Oligohydramnios: AFI between 5 and 8
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Etiology
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Early-Onset may reflect
. a fetal abnormality that precludes normal urination
. may represent a placental abnormality to impair perfusion
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By 18 weeks fetal kidneys are the main contributor AFV abnormalities
that lead to absent urine production include
Congenital Anomalies
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 bilateral renal agenesis,
 bilateral multicystic dysplastic
kidney,
 unilateral renal agenesis with
contralateral multicystic
dysplastic kidney,
 and the infantile form of
autosomal recessive polycystic
kidney disease
 bladder outlet obstruction. Examples
posterior urethral valves,
urethral atresia or stenosis,
the megacystis microcolon
intestinal hypoperistalsis syndrome.
 persistent cloaca and sirenomelia
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 2nd and Third trimester
• Usually
–PPROM: there will be full fetal bladder
–uteroplacental insufficiency: there will be empty fetal bladder
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FETAL
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 PROM (50%)
 IUGR
 IUFD
 –POSTTERM
PREGNANCY
Placental insufficiency
as with :
 Pre-eclampsia
 Essential hypertension
 –Chronic nephritis
MATERNAL
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Medication
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 ACE inhibitors
 angiotensin-receptor blockers
 NSAIDs
• fetal ductus arteriosus constriction which lower fetal urine
production
 •may result in acute & chronic renal insufficiency
111

Pregnancy Outcomes
DR BRUK
Fetal
•Abortion, prematurity, IUFD, deformity, malpresentation, fetal distress,
low APGAR
Maternal
• Increased morbidity, prolonged labor –due to Uxinertia
•Increased operative intervention {Malpresentation}
112

DR BRUK
 PROGNOSIS AND MANAGEMENT
• First trimester
– ominous usually - abortion
• Second trimester
underlying etiology and the severity of oligohydramnios
- borderline/low normal amniotic fluid volume generally have a good
prognosis
Preterm delivery, either spontaneous or indicated by maternal or fetal
complications, occurs in more than 50 percent of cases
113

DR BRUK
Third trimester
 - outcomes are related to umbilical cord compression, uteroplacental
insufficiency, meconium aspiration, and duration of oligohydramnios is
also a prognostic factor. Patients who present
 Timing of delivery
– If idiopathic oligohydramnios: 37 to 38 wks
– If etiology is known - manage accordingly
 Lung maturity is attained; lethal malformation; fetal jeopardy; severe
IUGR; severe oligohydramnios
114

DR BRUK
 Maternal hydration transiently increase amniotic fluid
volume and may have some .Does this improves clinical
outcome? Not unclear
115

HYDRAMNIOS
 This is an abnormally increased amniotic fluid volume, and it
complicates 1 to 2% of pregnancies.
 Hydramnios may be further categorized according to degree.
mild if the AFI is 25 to 29.9cm
moderate if 30 to 34.9cm ,
severe if 35cm or more
DR BRUK
116

 Moderate hydramnios accounts for about 20% , and severe
hydramnios approximately 15%.
 Severe hydramnios likely to have an underlying etiology and to
have consequences than mild hydramnios which is frequently
idiopathic and benign.
DR BRUK
117

 Etiology- include
- fetal congenital anomalies account 15%
-diabetes in 15 to 20%
-Congenital infection like CMV, toxoplasmosis, syphilis and
parvovirus
-red blood cell alloimmunization
DR BRUK
118

 The degree of hydramnios is associated with the likelihood of an
anomalous infant with 8% in mild hydramnios, 12% with
moderate, and more than 30% with severe hydramnios.
 If a fetal abnormality is encountered concurrent with
hydramnios, amniocentesis should be considered, because the
aneuploidy risk is increased.
DR BRUK
119

 Complications- include
- dyspnea
-orthopnea
-Edema
-placental abruption
-uterine dysfunction
-PPH
-PROM
-prematurity
-operative delivery
DR BRUK
120

TREATMENT
 Treat etiologies
 Treat complications- severe hydramnios with maternal respiratory
compromise amino-reduction may be needed.
 Approximately 1000 to 1500mL drawn over 30 minutes to restore
volume to upper normal range.
DR BRUK
121

DR BRUK
122

DR BRUK
 Incidence: Rare,between 1 and 12 cases per 100,000 deliveries
but catastrophic condition
 Maternal Mortality rate: 10 to 90 percent
 Neonatal Mortality rate: 20 and 60%
123

DR BRUK
 Cesarean or instrumental vaginal
delivery
 Precipitous or tumultuous labor
 Advanced maternal age (eg, ≥35
years)
 Placentaprevia,placentaaccrete/percr
eta/increta,or placental abruption
 Grand multiparity(≥5 live births or
stillbirths)
 Cervical lacerations
 Fetal distress
 Eclampsia
 Pharmacologic induction of
labor
 Uterine rupture
 Polyhydramnios
 Miscarriage, abortion,
amniocentesis
Risk factors
124

PATHOPHYSIOLOGY
DR BRUK
 amniotic fluid in maternal circulation acute pulmonary
hypertension and rapid RV failure ensue (usually lasting 15 to 30
minutes) followed by LV dysfunction LEADS
- hypoxemic respiratory failure
- Quick cardiovascular collapse
- systemic inflammation and noncardiogenic pulmonary edema
125

CLINICAL PRESENTATION
DR BRUK
 Timing
–90% occurs during labor & delivery, or immediately postpartum
–Rare: 48 hours after delivery, following 1st/ 2ndtrimester
abortion, amniocentesis, or abdominal/uterine trauma
126

DR BRUK
 Onset of symptoms
–90%: abrupt, catastrophic, and rapidly progressive
Hypotension due to cardiogenic shock
Hypoxemia and respiratory failure
DIC in the absence of other explanation
Coma or Tonic-clonicseizure
–The syndrome is best considered unpredictable and
unpreventable
127

MANAGMENT
DR BRUK
 There is no specific treatment for AFE.
 There are no data that any type of intervention improves
maternal prognosis with AFE.
 The goal of therapy is to correct hypoxemia and hypotension.
–Hemodynamic support (fluids/ vasopressors)
 A cautious approach is warranted since pulmonary edema is
common.
–Oxygenation
–Blood and blood products
128

References
Williams obstetrics 25th edition
DC Dutta’s text book of obstetrics, 7th ed
revised.
Gabbe obstetrics normal and problem
pregnancies,7th ed
Up to date 21.8
DR BRUK
129

DR BRUK 130

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