1 - Gametogenesis & Early Development of The Fertilized Ovum v2

GAMETOGENESIS
IMPLANTATION
PLACENTATION
EARLY DEVELOPMENT
OF THE FERTILIZED OVUM
SPERMATOGENESIS
The testes are made up of a series of

convoluted seminiferous tubules
Spermatozoa are formed along the walls of
the tubules from the primitive germ cells
Controlled by (FSH)
Begins at puberty
During mans’ whole sexual life
SPERMATOGENESIS
The Interstial Cells of Leydig
- Nests of cells in between the tubules
- Secrete testosterone
- The process is controlled by (ICSH)

SPERMATOGENESIS
Prolipheration Maturation
• spermatogonia A → • spermatocyte I (diploid) →
• spermatogonia B → • spermatocyte II (haploid) →
• spermatocyte I • spermatid
(adolescence)
SPERMIOGENESIS
Acrozome, (Golgi)
Opposite: distal centriol→distal filament
CAPACITATION
Maturation
In the uterus / fallopian tubes
Capaciy of penetration
SPERMATOGENESIS
Spermatogonia
Primary Spermatocytes
meiotic division
Secondary Spermatocytes
Spermatids
Mature to form
Spermatozoa
They burry their heads in the Sertoli Cells (glycogen containing

cells in the tubules for nourishment).
OOGENESIS
The Ovary in the fetus & childhood
- During ovarian differentiation, germ cells undergo

mitotic divisions producing many thousands of stem
cells: oogonia
-- Part of the oogonia stop dividing mitotically and

enter the prophase of meiosis.
-- They are referred to as Primary oocyte
OOGENESIS
OOGENESIS
- The remaining oogonia continue dividing
- The total number reaches a peak at 4.5-5

months post conception (2 million
oogonia + 5 million oocytes in various
stages of meiotic prophase)
OOGENESIS
During the remaining of fetal life, the total No.
of cells decreases by oocyte degeneration
• At birth: the ovaries contain about 2 million
Oocytes.
• At 7 years of age: 300,000 cells.
• At 45-55 years: few hundreds of cells.
All Oocytes which reach the diplotene phase of

meiosis become enclosed by a layer of cells to
form the Primordial Follicles.
OOGENESIS
OOGENESIS
The ovary at puberty
• FSH stimulates the growth of primordial

follicles to form the Graafian Follicles.
• The enclosed germ cell is a primary
oocyte (diploid cell in the prophase of
meiosis).
OOGENESIS
OOGENESIS
OVULATION
The most significant changes which occur in the oocyte occur few hours before
ovulation.
Oocyte
(first maturation division)
Secondary oocyte (haploid cell)

+ First polar body
(second maturation division)
Not completed unless fertilization takes place
Female pronucleus + 2nd polar body

+ Male pronucleus
Zygote (Diploid No. of chromosomes).
FERTILIZATION
Site of fertilization:
Lateral third of fallopian tube.
Average time required for the sperm to

reach the ovum is about one hour (swim
rate 3mm/minute).
Fertilization
Fertilization
Fertilization
Following the entry

of the sperm into
the egg, a reaction
spreads over the
zona pellucida,
which prevents the
passage of further
sperms.
Fertilization
CLEAVAGE
• A first cleavage division occurs after 24

hours of fertilization.
• Subsequent divisions follow every about
22 hours.
• Divisions are normally into equal halves.
• The morula stage (16 cell stage).
• The balstocyst: free within the uterine
cavity on the fourth day.
Cleavage
Cleavage
58-cell blastocyst 107-cell blastocyst

Cleavage
IMPLANTATION
~ 5-6 days after fertilization

Protoplasmic processes grow out from the
cells of the blastocyst in closest proximity
to the Zona Pellucida. They traverse this
membrane and pass beyond their outer
surface.
IMPLANTATION
• 6-6.5 days after fertilization

The blastocyst becomes attached to the
Uterine mucosa (Implantation begins).
• After Implantation
The zona pellucida disappears.
• By the 9th – 10th day
The blastocyst becomes entrapped in the
mucosa of the dorsal wall of the Uterus.
EARLY DEVELOPMENT
1. The first period
- Starts at fertilization.
- Ends when the ovum is successfully implanted.
2. The second period
- Extends from the 3rd to the 8th week.
- All major organ Primordia appear
- The embryo assumes features which make it
recognizable as a human being.
3. The third period
- Is the fetal period from 3rd month until term.
EARLY DEVELOPMENT
In the blastocyst
- Fluid accumulates in the intercellular spaces
between the centrally placed cells.
- The inside of the cyst becomes lined by cells
which form the trophoblast.
- The inner aspect of the trophoblast is thickened
at one pole by the Inner Cell Mass.
- The Embryonic pole with the inner cell mass
penetrates first and most deeply into the decidua
in the uterine wall.
EARLY CHORIONIC DEVELOPMENT
After Implantation
- The trophoblast differentiates into:
• Syncytiotrophoblast.
• Cytotrophoblast.
- Later, Lacunar Spaces appear in the syncytium.
- The advancement of the trophoblastic
projections form the Early Villi.
- The Lacunar Spaces soon become filled
with maternal blood from eroded maternal
capillaries.
- Mesodermal cores become evident in the
villi on day 13.
- Fetal blood vessels appear subsequently.
- A fetal-placental circulation is established
when the heart starts to beat at 22 days
after fertilization.
- At day 16-17 the surface of the blastocyst is
covered by branching villi which are best
developed at the embryonic pole where the
placenta will become established. The chorion
here is called Chorion Frondosum.
- The smooth chorion covering the remainder of
the embryonic sphere is called Chorion Laeve.
EARLY CHORIONIC DEVELOPMENT
- The definitive number of stem villi is

established by 12 weeks of gestation.
- Placental growth there after continues
until term by a continuing increase in the
size of stem villi and more branching.
- At this stage the Lacunar spaces are
called the Intervillous Space.
CYTOTROPHOBLAST INVASION OF
DECIDUAL VESSELS
EARLY HUMAN DEVELOPMENT
Zygote
Blastomeres
Morula
Blastocyst
Embryo
Fetus
Conceptus
EMBRYONIC DEVELOPMENT AFTER
IMPLANTATION
Gametogenesis
&
Early Development Of The Fertilized Ovum
Spermatogenesis
The testes are made up of a series of convoluted -

seminiferous tubules
Spermatozoa are formed along the walls of the -

tubules from the primitive germ cells
This process is controlled by follicle stimulating

hormone (FSH)
The Interstial Cells of Leydig
Nests of cells in between the tubules -
Secrete testosterone -
The process is controlled by (ICSH) -

Spermatogonia
Primitive germ cells next to the
basement membranes of the seminiferous tubules
During adolescence mature into

Primary Spermatocytes
meiotic division
Secondary Spermatocytes
spermatids
Mature to form
spermatozoa
They burry their heads in the Sertoli
.Cells (glycogen containing cells in the tubules for nourishment)
Oogenesis
During ovarian differentiation, germ cells undergo -

mitotic divisions producing many thousands of stem
cells called oogonia
Part of the oogonia stop dividing mitotically and - -

.enter the prophase of meiosis
They are referred to as Primary oocyte - -
Oogenesis
The remaining oogonia continue dividing -
The total number reaches a peak at 4.5-5 months -

post conception (2 million oogonia + 5 million
oocytes in various stages of meiotic prophase)
OOgenesis
During the remaining of fetal life, the total No. of cells
decreases by oocyte degeneration
.At birth: the ovaries contain about 2 million Oocytes
.At 7 years of age: 300,000 cells
.At 45-55 years: few hundreds of cells
All Oocytes which reach the diplotene phase of meiosis -
become enclosed by a layer of cells to form the
.Primordial Follicles
FSH stimulates the growth of primordial follicles to -
.form the Graafian Follicles
The enclosed germ cell is a primary oocyte (diploid cell -
.in the prophase of meiosis)
Ovulation
The most significant changes which occur in the oocyte occur few
.hours before ovulation
Oocyte
)first maturation division(
Secondary oocyte (haploid cell)

First polar body +
)second maturation division(
Not completed unless fertilization takes place
Female pronucleus + 2nd polar body
Male pronucleus +
.Zygote (Diploid No. of chromosomes)
Fertilization
:Site of fertilization
.Lateral third of fallopian tube
Average time required for the sperm to reach the ovum -
.is about one hour (swim rate 3mm/minute)
Fertilization
Following the entry of the sperm into the egg, a reaction
spreads over the zona pellucida, which prevents the
.passage of further sperms
Cleavage
A first cleavage division occurs after 24 hours of -
.fertilization
- Subsequent divisions follow every about 22 hours.
- Divisions are normally into equal halves.
- The morula stage (16 cell stage).
- The balstocyst: free within the uterine cavity on the
fourth day.
Implantation
Approximately 5-6 days after fertilization

Protoplasmic processes grow out from the cells of the
blastocyst in closest proximity to the Zona Pellucida.
They traverse this membrane and pass beyond their
.outer surface
Implantation
days after fertilization 6-6.5

The blastocyst becomes attached to the Uterine mucosa
.(Implantation begins)
After Implantation
.The zona pellucida disappears
By the 9th – 10th day
The blastocyst becomes entrapped in the mucosa of the
.dorsal wall of the Uterus
Early development
:The first period
.Starts at fertilization -
.Ends when the ovum is successfully implanted -
:The second period
.Extends from the 3rd to the 8th week -
During this period, all major organ Primordia appear and -
the embryo assumes features which make it recognizable
.as a human being
:The third period
.Is the fetal period from 3rd month until term -
Early development
:In the blastocyst
Fluid accumulates in the intercellular spaces between the -
.centrally placed cells
The inside of the cyst becomes lined by cells which form -
.the trophoblast
The inner aspect of the trophoblast is thickened at one -
.pole by the Inner Cell Mass
The Embryonic pole with the inner cell mass penetrates -
.first and most deeply into the decidua in the uterine wall
Early Chorionic Development
:After Implantation
:The trophoblast differentiates into -
.Syncytiotrophoblast *
.Cytotrophoblast *
.Later, Lacunar Spaces appear in the syncytium -
The advancement of the trophoblastic projections form -
.the Early Villi
:After Implantation
The Lacunar Spaces soon become filled with maternal -
.blood from eroded maternal capillaries
.Mesodermal cores become evident in the villi on day 13 -
.Fetal blood vessels appear subsequently -
A fetal-placental circulation is established when the heart -
.starts to beat at 22 days after fertilization
:After Implantation
At day 16-17 the surface of the blastocyst is covered by -
branching villi which are best developed at the embryonic
pole where the placenta will become established. The
.chorion here is called Chorion Frondosum
The smooth chorion covering the remainder of the -
.embryonic sphere is called Chorion Lacve
:After Implantation
The definitive number of stem villi is established by 12 -
.weeks of gestation
Placental growth there after continues until term by a -
continuing increase in the size of stem villi and more
.branching
At this stage the Lacunar spaces are called the -
.Intervillous Space
DEVELOPMENT OF PLACENTA
PLACENTA’S MORPHOLOGY
AND FUNCTIONS
Prof. Vlad TICA, MD, PhD

FETAL TISSUES OF THE FETAL-
MATERNAL COMMUNICATION SYSTEM
 The extravillous and villous trophoblast
 Placental arm
 The fetal membranes (the amnion-chorion leave)

 Paracrine arm
 Human placenta : hemochorioendothelial type

BIOLOGY OF TROPHOBLAST
 Trophoblast is the most variable in structure, function and
development
 invasiveness provides for attatchment of blastocyst to
decidua of uterine cavity
 nutrition of the conceptus
 function as endocrine organ in human pregnancy
Essential to maternal physiological adaptations &

maintenance of pregnancy
 Differentiation
Cellular,
uninuclear
Syncytial
multinuclear
 Cytotrophoblast is the cellular progenitor of the
syncytiotrophoblast
Cytotrophoblast Syncytiotrophoblast
Morphologically uninuclear cells multinuclear giant cells
cell boders well demarcated lacking
nucleus single, distinct multiple & diverse
miotic figure present absent
Origin germinal cell cytotrophoblast
 After apposition & adherence, intrusion of cytotrophoblast
between endometrial epithelial cells
 facilitated by degradation of the extracellular matrix of
decidua catalyzed by
 urokinase-type plasminogen activator
 urokinase plasminogen activator receptor
 multiple metalloproteinase
 These functions of cytotrophoblasts invading the endometrium
are indistinguishable from those of metastasizing malignant
cells
 Implantation is dependent upon controlled trophoblast
invasion of maternal decidua and the spiral arteries -
mechanism for permitting and then for limiting trophoblast
invasion
INTEGRIN SWITCHING
 Coordinated & alternating process referred to as "integrin
switching“ - facilitates migration and then attachment of
trophoblasts in the decidua
 Integrin: one of four families of cell adhesion molecules

(CAMs = cell-surface receptors that mediate the adhesion of
cells to extracellular matrix proteins)
onfFN (oncofetal fibronectin)
 glycopeptide - trophouteronectin or trophoblast glue
 formed by extravillous trophoblast, including that of

chorion laeve
 critical role for migration and attachment of the

trophoblasts to maternal decidua
 facilitates separation of extraembryonic tissues from the
uterus at delivery
IMMUNOLOGICAL ACCEPTANCE OF THE CONCEPTUS
 Previous Theories:
 antigenic immaturity of the embryo-fetus
 diminished immunological responsiveness of the pregnant
woman
 decidua: immunologically privileged tissue site
 The acceptance and the survival of conceptus in the maternal

uterus must be attributed to immunological peculiarity of
the trophoblasts, not the decidua
 Uterine Large Granular Lymphocytes (LGL) - probably

lymphoid - natural killer cell lineage: speculated that involved
in the regulation of trophoblast invasion
 Expression of the major histocompatibility complex antigens
 HLA genes
 the products of multiple genetic loci of the MHC within
short arm of chromosome 6
 17 class I genes have been identified
 three classical genes

 A, B, C => major class I(a) transplantation antigens
 three other class I(b) genes

 E, F, G => class I HLA antigen
 HLA-G gene
 MHC class II antigens are absent from trophoblast at all
stages of gestation
 HLA-G antigen
 identified only in extravillous cytotrophoblast in decidua
basalis and chorion laeve
 not present in villous trophoblast, either in syncytium or in
cytotrophoblasts
 As gestation progresses, cells from inner cell mass of blastocyst

gradually develop both class I and II HLA antigen; these tissue
are not in direct contact with maternal tissue or blood
ORGANIZATION OF PLACENTA
 Trophoblast Ultrastructure
 Prominent microvilli of the syncytial surface (brush

border)
 pinocytotic vacuoles and vesicles
 absorptive and secretory placental function
 Chorionic Villi
 12th day
 Primary villi
 proliferation of cytotrophoblast extend into
syncytiotrophoblast
 Secondary villi
 mesenchymal cord, derived from cytotrophoblast, invade
solid trophoblast column
 Tertiary villi
 after angiogenesis occurs from the mesenchymal cores in
situ
 Characteristic of development of H-mole

 some villi, in which absence of angiogenesis results in a lack
of circulation, may distended with fluid and form vesicles
 Placental Cotyledons
 Certain villi of the chorion frondosum extend from

chorionic plate to the decidua and serve as anchoring villi
 Each of the main stem villi (truncal)

and their ramifications (rami)
constitute a placental cotyledon (lobe)
 For each cotyledon, a 2:1 ratio of artery

to vein to cotyledon
 Breaks in the Placental "Barrier "
 Passage of cells between mother and fetus in both directions
 A few fetal blood cells are found in the mother's blood
 Fetal leukocytes may replicate in the mother and leukocytes

bearing a Y chromosome have been identified in women for
up to 5 years after giving birth to a son
 Placetal Size and Weight
 Total number of cotyledons remains the same throughout
gestation
 Individual cotyledones continue to grow
 Placental weights vary considerably

PLACENTAL AGING
 Histologic changes that accompany placental growth and
aging are suggestive of increase in the efficiency of transport to
and exchange to meet increasing fetal metabolic requirements
 decrease in thickness of the syncytium
 partial reduction of cytotropholastic cell
 decrease in the stroma
 increase in the number of capillaries and approximation of these

vessels to the syncytial surface
 By 4 months:
 the apparent continuity of the cytotrophoblast is broken
PLACENTAL AGING
 At term:
 Covering of villi may be focally reduced to a thin layer of
syncytium with minimal connective tissue
 Fetal capillaries seem to abut the tropohoblast
 Villous stroma, cytotrophoblasts are markedly reduced
 villi appear filled with thin-walled capillaries
 Other changes suggestive of a decrease in the efficiency for

placental exchange:
 Thickening of the basement membrane of trophoblast capillaries
 Obliteration of certain fetal vessels

BLOOD CIRCULATION IN THE MATURE
PLACENTA
 A section through the placenta in
situ
 amnion → chorion → chorionic
villi → intervillous space →
decidual plate → myometrium
FETAL CIRCULATION
 2 umbilical arteries
 deoxygenated, or "venous-like" blood flows to the placenta
 separate at the chorionic plate to supply branches to the
cotyledons
 1 umbilical vein
 with a significantly higher oxygen content
MATERNAL CIRCULATION
 Intervillous space -> chorionic plate -> vein
 Spiral a., vein

 Ut. Contraction
 Intervillous space
 Ramsey's concept
THE PRINCIPLE FACTORS REGULATING
THE FLOW OF BLOOD IN THE
INTERVILLOUS SPACE
 arterial blood pressure
 intrauterine pressure
 pattern of uterine contraction
 factors that act specifically upon the arteriolar walls

THE AMNION
 Innermost fetal membrane and is contiguous with amnionic
fluid
 Avascular structure
 Provide almost all of the tensile strength of the fetal

membranes
 protect against rupture or tearing
 Reflected amnion
 Placental amnion
 Umbilical amnion
STRUCTURE
 single layer of cuboidal epithelial cells
 basement membrane
 acellular compact layer
 fibroblast-like mesenchymal cells
 zona spongiosa
 Missing element of human amnion

 smooth muscle cell, nerves, lymphatics, blood vessels
DEVELOPMENT
DEVELOPMENT
DEVELOPMENT
 Amnion epithelial cells
 derived from fetal ectoderm (embryonic disc)
 active metabolically; synthesis of tissue inhibitors of

metalloproteinase-1
 Amnion mesenchymal cells
 derived from the embryonic mesoderm
 synthesis of interstitial collagens that make up the compact

layer of the amnion
 highly capable of synthesizing cytokines - IL-6, IL-8, MCP-1

TENSILE STRENGTH
 Decidua and chorion laeve are quite elastic and can expand to
twice normal size during pregnancy
 Amnion provides the major strength of the membrane
 Tensile strength of amnion resides almost exclusively in the

compact layer
 composed of cross-linked interstial collagens I, III, and
lesser amounts of V and VI
UMBILICAL CORD (funis) Development
UMBILICAL CORD STRUCTURE AND FUNCTION
 diameter: 0.8 - 2.0 cm
 average length: 55 cm (usual length: 30 - 100 cm)
 Nodulation, false knot
 Extracellular matrix: Wharton's jelly

PLACENTAL FUNCTIONS
RESPIRATORY
IMMUNOLOGICA
NUTRIENT
L
PHISIOLOGY
OF PLACENTA
ENZYMATIC EXCRETORY
HAEMOPOETIC HORMONAL
MATERNO- PLACENTAL UNIT

PLACENTAL FUNCTIONS
 Transfer of nutrients and
waste products between the
mother & fetus
 TRANSFER  BARRIER
 RESPIRATORY  IMMUNOLOGICAL
 EXCRETORY
 ENZYMATIC
 NUTRITIVE
 HAEMATOPOETIC
 Produces or metabolizes the

hormones & enzymes
necessary to maintain the
pregnancy
TRANSFER
 Transport is facilitated by the close approximation of maternal
and fetal vascular systems within the placenta
 It is important to recognize that there normally is no mixing of

fetal and maternal blood within the placenta
TRANSFER
Oxygen, water, electrolytes •
First group Simple diffusion •
Second Glucose, acids, lipids, vitamins •

Active diffusion •
group
Thyroxin, hydrocortisone, HCG •
Third group Slow diffusion •
Immunological importance •
Fourth group Pinocytosis •
RESPIRATORY FUNCTION
 Intake of O2 & output of CO2 takes place by simple diffusion
 O2 supply to fetus rate of 5ml/kg/min

 achieved with cord flow of 165-330ml/min
EXCRETORY FUNCTION
 Waste products urea, uric acid, creatinine are excreted to

maternal blood by simple diffusion
NUTRITIVE FUNCTION
 Glucose is the major energy substrate provided to the placenta
and fetus
 It is transported across the placenta by facilitated diffusion

via hexoze transporters
 Although the fetus receives large amounts of intact glucose, a

large amount is oxidized within the placenta to lactate, which
is used for fetal energy production
TRANSPORT FUNCTION
 Amino acid concentrations in fetal blood are higher than in
maternal blood - active transport
 Lipids - TGs & FA directly transported from mother to fetus in

early pregnancy but synthesised in fetus later in pregnancy.
Thus, fetal fat has dual origin
 Water & electrolytes – Na+, K+, Cl- by simple diffusion. Ca,

Ph, iron by active transport
BARRIER FUNCTION
 Protective barrier to the fetus against noxious agents

circulating in maternal blood
IMMUNOLOGICAL FUNCTION
 Fetus & placenta contain paternally determined antigens,
foreign to the mother
 Inspite of this, no evidence of graft rejection
 Probably:
1. Fibrinoid & sialomucin coating of trophoblast may suppress
the troblastic antigen
2. Placental hormones, steriods, HCG have a weak
immunosuppressive effect, may be responsible for
producing sialomucin
Fetal, placental & maternal compartments
form an integrated hormonal unit
The feto-placental-maternal (FPM) unit

creates the
ENDOCRINE ENVIRONMENT
that maintains and drives the processes of

pregnancy and pre-natal development
PLACENTAL HORMONES
 Human Chorionic Gonadotropin (hCG)  Estrogen (E)
 Progesterone (P)
 Human Chorionic Somammotropin
(hCS) or Placental Lactogen (hPL)
 HYPOTHALAMIC-LIKE RELEASING
HORMONES
OTHER HORMONES
 GnRH
 Chorionic Adrenocorticotropin
 CRH
 Chorionic Thyrotropin
 cTRH
 Relaxin
 GH-RH
 PTH-rP
 hGH-V  PLACENTAL PEPTIDE HORMONES
 Neuropeptide-Y
 Inhibin & Activin
 ANP
To understand the FPM one should know:
1. The major hormones involved:
hCG
Progesterone
Estrogen
Human Chorionic Somatomammotropin (hCS)
(placental lactogen)
2. How the FPM compartments work together

to produce the steroid hormones
3. The transfer of hormones between

the FPM compartments
HUMAN CHORIONIC GONADOTROPIN
(hCG)
 Pregnancy hormone – glycoprotein
 Half life – 24 hrs
 Levels peak at 60-70 days, then remain at a low plateau for

the rest of pregnancy
 Placental GnRH have control of hCG

(hCG)
FUNCTIONS:
1. Rescue & maintenance of function of corpus luteum
 prevents degeneration of corpus luteum
 stimulates corpus luteum to secrete E + P which, in
turn, stimulate continual growth of endometrium
2. hCG stimulates Leydig cells of male fetus to produce

testosterone in conjunction with fetal pituitary
gonadotrophins. Thus indirectly involed in development
of external genitalia
3. Suppresses maternal immune function & reduces
possibility of fetus immunorejection
HUMAN CHORIONIC SOMAMMOTROPIN
(hCS) or PLACENTAL LACTOGEN
 Structure similar to growth hormone
 Produced by the placenta
 Levels throughout pregnancy
 Large amounts in maternal blood but DO NOT reach the

fetus
 Biological effects are reverse of those of insulin:
utilization of lipids; make glucose more readily available to
fetus, and for milk production.
 hCS levels proportionate to placental size
 hCS levels placental insufficiency

ESTROGEN (E)
 Forms:
 Estriol (most important )
 Estradiol
 Estrone
 Levels increase throughout pregnancy
 90% produced by placenta (syncytiotrophoblast)
 Placental production is transferred to both maternal and fetal

compartments
ESTROGEN (E)
 Two of the principle effects of placental estrogens are:
 Stimulate growth of the myometrium and antagonize

the myometrial-suppressing activity of progesterone
 In many species, the high levels of estrogen in late

gestation induces myometrial oxytocin receptors,
thereby preparing the uterus for parturition
 Stimulate mammary gland development
 Estrogens are one in a battery of hormones necessary for

both ductal and alveolar growth in the mammary gland
PROGESTERONE (P)
 80-90% is produced by placenta and secreted to both

fetus and mother
PROGESTERONE (P)
 Support of the endometrium to provide an
environment conducive to fetal survival
 If the endometrium is deprived of progestins, the
pregnancy will inevitably be terminated
 Suppression of contractility in uterine smooth

muscle, which, if unchecked, would clearly be a
disaster
 This is often called the "progesterone block" on the
myometrium
 ]
 Toward the end of gestation, this myometrial-

quieting effect is antagonized by rising levels of
PROGESTERONE (P)
 Progesterone and other progestins also potently inhibit
secretion of the pituitary gonadotropins luteinizing hormone
(LH) and follicle stimulating hormone (FSH)
 This effect almost always prevents ovulation from occuring

during pregnancy
Thank you !
PLACENTA
Immunological acceptance
Functions

 Fetus & placenta contain paternally determined antigens,
foreign to the mother
 Inspite of this, no evidence of graft rejection
 Probably:
Fibrinoid & sialomucin coating of trophoblast may suppress the
troblastic antigen
Placental hormones, steriods, HCG have a weak
immunosuppressive effect, may be responsible for producing
sialomucin
 The acceptance and the survival of conceptus in the maternal

uterus must be attributed to immunological peculiarity of
the trophoblasts, not the decidua
 Uterine Large Granular Lymphocytes (LGL) - probably

lymphoid - natural killer cell lineage: speculated that involved
in the regulation of trophoblast invasion
 Expression of the major histocompatibility complex antigens
 HLA genes
 the products of multiple genetic loci of the MHC within
short arm of chromosome 6
 17 class I genes have been identified
 three classical genes

 A, B, C => major class I(a) transplantation antigens
 three other class I(b) genes

 E, F, G => class I HLA antigen
 HLA-G gene
Expression of the major histocompatibility complex antigens
 MHC class II antigens are absent from trophoblast at all
stages of gestation
 HLA-G antigen
 identified only in extravillous cytotrophoblast in decidua
basalis and chorion laeve
 not present in villous trophoblast, either in syncytium or in
cytotrophoblasts
 As gestation progresses, cells from inner cell mass of blastocyst

gradually develop both class I and II HLA antigen; these tissue
are not in direct contact with maternal tissue or blood
PLACENTAL FUNCTIONS
RESPIRATORY
IMMUNOLOGICA
NUTRIENT
L
PHISIOLOGY
OF PLACENTA
ENZYMATIC EXCRETORY
HAEMOPOETIC HORMONAL
MATERNO- PLACENTAL UNIT

PLACENTAL FUNCTIONS
 Transfer of nutrients and
waste products between the
mother & fetus
 TRANSFER  BARRIER
 RESPIRATORY  IMMUNOLOGICAL
 EXCRETORY
 ENZYMATIC
 NUTRITIVE
 HAEMATOPOETIC
 Produces or metabolizes the

hormones & enzymes
necessary to maintain the
pregnancy
TRANSFER
 Transport is facilitated by the close approximation of maternal
and fetal vascular systems within the placenta
 It is important to recognize that there normally is no mixing of

fetal and maternal blood within the placenta
TRANSFER
Oxygen, water, electrolytes •
First group Simple diffusion •
Second Glucose, acids, lipids, vitamins •

Facilitated / Active diffusion •
group
Thyroxin, hydrocortisone, HCG •
Third group Slow diffusion •
Immunological importance •
Fourth group Pinocytosis •
RESPIRATORY FUNCTION
 Intake of O2 & output of CO2 takes place by simple diffusion
 O2 supply to fetus rate of 5ml/kg/min

 achieved with cord flow of 165-330ml/min
EXCRETORY FUNCTION
 Waste products urea, uric acid, creatinine are excreted to

maternal blood by simple diffusion
NUTRITIVE FUNCTION
 Glucose is the major energy substrate provided to the placenta
and fetus
 It is transported across the placenta by facilitated diffusion

via hexoze transporters
 Although the fetus receives large amounts of intact glucose, a

large amount is oxidized within the placenta to lactate, which
is used for fetal energy production
TRANSPORT FUNCTION
 Amino acid concentrations in fetal blood are higher than in
maternal blood - active transport
 Lipids - TGs & FA directly transported from mother to fetus in

early pregnancy but synthesised in fetus later in pregnancy.
Thus, fetal fat has dual origin
 Water & electrolytes – Na+, K+, Cl- by simple diffusion. Ca,

Ph, iron by active transport
BARRIER FUNCTION
 Protective barrier to the fetus against noxious agents

circulating in maternal blood
Fetal, placental & maternal compartments
form an integrated hormonal unit
The feto-placental-maternal (FPM) unit

creates the
ENDOCRINE ENVIRONMENT
that maintains and drives the processes of

pregnancy and pre-natal development
PLACENTAL HORMONES
 Human Chorionic Gonadotropin (hCG)  Estrogen (E)
 Progesterone (P)
 Human Chorionic Somammotropin
(hCS) or Placental Lactogen (hPL)
 HYPOTHALAMIC-LIKE RELEASING
HORMONES
OTHER HORMONES
 GnRH
 Chorionic Adrenocorticotropin
 CRH
 Chorionic Thyrotropin
 cTRH
 Relaxin
 GH-RH
 PTH-rP
 hGH-V  PLACENTAL PEPTIDE HORMONES
 Neuropeptide-Y
 Inhibin & Activin
 ANP
(hCG)
 Pregnancy hormone – glycoprotein
 Half life – 24 hrs
 Levels peak at 60-70 days, then remain at a low plateau for

the rest of pregnancy
 Placental GnRH have control of hCG

(hCG)
FUNCTIONS:
1. Rescue & maintenance of function of corpus luteum
 prevents degeneration of corpus luteum
 stimulates corpus luteum to secrete E + P which, in
turn, stimulate continual growth of endometrium
2. hCG stimulates Leydig cells of male fetus to produce

testosterone in conjunction with fetal pituitary
gonadotrophins. Thus indirectly involed in development
of external genitalia
3. Suppresses maternal immune function & reduces
possibility of fetus immunorejection
 Structure similar to growth hormone
 Produced by the placenta
 Levels throughout pregnancy
 Large amounts in maternal blood but DO NOT reach the

fetus
 Biological effects are reverse of those of insulin:
utilization of lipids; make glucose more readily available to
fetus, and for milk production.
 hCS levels proportionate to placental size
 hCS levels placental insufficiency

ESTROGEN (E)
 Forms:
 Estriol (most important )
 Estradiol
 Estrone
 90% produced by placenta (syncytiotrophoblast)
 Placental production is transferred to both maternal and fetal

compartments
ESTROGEN (E)
 Two of the principle effects of placental estrogens are:
 Stimulate growth of the myometrium and antagonize

the myometrial-suppressing activity of progesterone
 In many species, the high levels of estrogen in late

gestation induces myometrial oxytocin receptors,
thereby preparing the uterus for parturition
 Stimulate mammary gland development
 Estrogens are one in a battery of hormones necessary for

both ductal and alveolar growth in the mammary gland
PROGESTERONE (P)
 80-90% is produced by placenta and secreted to both

fetus and mother
PROGESTERONE (P)
 Support of the endometrium to provide an
environment conducive to fetal survival
 If the endometrium is deprived of progestins, the
pregnancy will inevitably be terminated
 Suppression of contractility in uterine smooth

muscle, which, if unchecked, would clearly be a
disaster
 This is often called the "progesterone block" on the
myometrium
 ]
 Toward the end of gestation, this myometrial-

quieting effect is antagonized by rising levels of
PROGESTERONE (P)
 Progesterone and other progestins also potently inhibit
secretion of the pituitary gonadotropins luteinizing hormone
(LH) and follicle stimulating hormone (FSH)
 This effect almost always prevents ovulation from occuring

during pregnancy
DIAGNOSIS OF PREGNANCY
DEFINITIONS
 Gravida = a pregnant woman. This refers to any pregnancy
regardless of duration
 Para = a woman who has delivered a viable young (not
necessarily living at birth). Para is used with numerals to
designate the number of pregnancies that have resulted in the
birth of a viable offspring
 Nulligravida = a woman who has never been pregnant

 Nullipara = a woman who has not delivered a child who
reached viability
 Primigravida = a woman pregnant for the first time

 Primipara = a woman who has delivered one child after the age
of viability
 is based on 3 groups of signs and symptoms:
 Presumtive
 Examination
 Investigations / lab tests

PRESUMPTIVE SIGNS AND SYMPTOMS
OF PREGNANCY
 Amenorrhea
 Nausea
 Vomiting
 Frequent urination
NAUSEA AND VOMITING
(MORNING SICKNESS)
NAUSEA AND VOMITING
(MORNING SICKNESS)
 Occurs in early morning during the first weeks of pregnancy
 Usually spontaneous and subsides in 6 to 8 weeks or by the 12th

to 16th weeks of pregnancy
 Hyperemesis gravidarum
 This is referred to as nausea and vomiting that is severe and lasts
beyond the 4th month of pregnancy
 It causes weight loss and upsets fluid and electrolyte balance of

the patient
FREQUENT URINATION
 Frequent urination is caused by pressure of the
expanding uterus on the bladder
 It subsides as pregnancy progresses and the

uterus rises out of the pelvic cavity
 The uterus returns during the last weeks of

pregnancy as the head of the fetus presses
against the bladder
 Frequent urination is not a definite sign since other factors can

be apparent (such as tension, diabetes, urinary tract infection,
or tumors)
BREAST CHANGES
 In early pregnancy- a slight, temporary enlargement of the
breasts → sensation of weight, fullness, and mild tingling
 Darkening of the areola - the brown part around the nipple
 Enlargement of Montgomery glands - the tiny nodules or
sebaceous glands within the areola
 Increased firmness or tenderness of the breasts
 More prominent and visible veins due to the increased blood
supply
 Presence of colostrum (thin yellowish fluid that is the
precursor of breast milk). This can be expressed during the 2nd
trimester and may even leak out in the latter part of the
pregnancy
BREAST CHANGES
VAGINAL CHANGES
 Chadwick's sign
 The vaginal walls have taken on a deeper color caused by the
increased vascularity because of increased hormones
 6th week
 It may also be noted with a rapidly growing uterine tumor or any

cause of pelvic congestion
 Leukorrhea
 An increase in the white / slightly gray
mucoid discharge that has a faint musty odor
 Due to hyperplasia of vaginal epithelial cells of the cervix
because of increased hormone level from the pregnancy

QUICKENING (FEELING OF LIFE)
 The 1st perception of fetal movement within the uterus
 It usually occurs toward the end of the 5th month because of spasmodic
flutter
 A multigravida can feel quickening as

early as 16 weeks
 A primigravida usually cannot feel

quickening until after 20 weeks
 Fetal movement early in pregnancy

is frequently thought to be gas
SKIN CHANGES
 Striae gravidarum (stretch marks)
 On the abdomen and/or buttocks caused
by ↑ production / sensitivity to adrenocortical
hormones during pregnancy
 These marks may be seen on a patient with

Cushing's disease / patient with sudden weight gain
 Chloasma
 The “mask of pregnancy“
 It is a bronze type of facial coloration seen more
on dark-haired women
 It is seen after the 16th week of pregnancy

SKIN CHANGES
 Linea nigra
 A black line in the midline of the abdomen that may run from the
sternum / umbilicus to the symphysis pubis
 Primigravida - 3rd month; keeps pace with the rising height of the
fundus
 Multigravida - before the 3rd month
NEURO-PSYCHOLOGICAL CHANGES
 Fatigue
 Common complaint by most patients
during the 1st trimester
 May be associated with sleepiness

 May also be a result of :
 anemia
 infection
 emotional stress
 malignant disease
 Irascibility
 Emotiveness
PROBABLE SIGNS OF PREGNANCY
 Those signs commonly noted by the physician upon examination of
the patient
 These signs include:

 uterine changes
 abdominal changes
 cervical changes
 basal body temperature
 positive pregnancy test by physician
 fetal palpation
UTERINE CHANGES
 Position
 12th week - the symphysis pubis
 36th week - the xiphoid process
 These guidelines are fairly accurate only as long as pregnancy is normal

and there are no twins, tumors, or excessive amniotic fluid
 Size
 Increases in width and length
approximately 5x its normal size
 Its weight increases from
50 grams to 1,000 grams
CERVICAL CHANGES
 Goodell's sign
 The cervix is normally firm like the cartilage at the end of the nose
 Softening of the cervix (firm like lips)
 Is present at 6 weeks of pregnancy
 Formation of a mucous plug

 This is due to hyperplasia of the cervical glands as a result of increased
hormones
 It serves to seal the cervix of the pregnant uterus and to protect it from
contamination by bacteria in the vagina
 The mucous is expelled at the end of pregnancy near or at the onset of

labor
BRAXTON-HICK'S CONTRACTIONS
 Painless uterine contractions occurring throughout pregnancy
 It usually begins about the 12th week of pregnancy and becomes

progressively stronger
 These contractions will, generally, cease with walking / other forms

of exercises
 Are distinct from contractions of true labor → do NOT cause the

cervix to dilate and can usually be stopped by walking
POSITIVE PREGNANCY TEST
BY THE CLINICIAN
 This may be misread by doing it too early / too late
 Even if the test is positive, it could be the result of ectopic pregnancy

/ hydatidiform mole (an abnormal growth of a fertilized ovum)
FETAL PALPATION
 This is a probable sign in early pregnancy
 The physician can palpate the abdomen and identify fetal parts
 It is not always accurate, a mass in the abdomen may be palpated

and mistakenly identified as an infant
POSITIVE SIGNS OF PREGNANCY
 Positive signs of pregnancy are those signs that are definitely
confirmed as a pregnancy
 They include:
 Fetal heart sounds
 Ultrasound scanning of the fetus
 Perception of fetal movements by the clinician
 X-ray
FETAL HEART SOUNDS
 The fetal heart begins beating by the 24th day following conception
 It is audible with a Doppler by 10 weeks of pregnancy and with a

fetoscope after the 16th week
 It is not to be confused with uterine souffle / swishlike tone from

pulsating uterine arteries
 The normal fetal heart rate is 120 - 160 beats

ULTRASOUND SCANNING OF THE FETUS
 The gestation sac can be seen and photographed
 An embryo as early as the 4th week after conception can be identified
 The fetal parts begin to appear by the 10th week of gestation

PERCEPTION OF FETAL MOVEMENT
 This is done by a trained examiner
 It is easily elicited after 24 weeks of pregnancy

X-RAY
 Identify the entire fetal skeleton by
the 12th week
 In utero, the fetus receives total body

radiation that may lead to
genetic / gonadal alterations
 An x-ray is NOT a recommended test

for identifying pregnancy
CHANGES OF THE CIRCULATORY SYSTEM
 Blood volume ↑ gradually by 30 to 50 %
 This results in ↓ concentration of red blood cells and hemoglobin
 This explains why the need for iron is so important during

pregnancy
 By the time pregnancy reaches term, the body has usually

compensated for the decrease resulting in an essentially normal
blood count
Lecture 3
DIAGNOSIS OF PREGNANCY.
MATERNAL ADAPTATION TO PREGNANCY.
LABORATORY TESTS IN PREGNANCY

DEFINITIONS

reached viability

of viability
DEFINITIONS
 Multigravida = a woman who has been pregnant more than
once
 Multipara = a woman who has delivered 2/more fetuses past

the age of viability.
 It doesn’t matter whether they are born dead or alive
 Grandmultipara = a woman who has had six or more births

past the age of viability
 Viability = refers to the capability of a fetus to survive outside

the uterus after the earliest gestational age (approximately 24
weeks gestation)
 In utero = refers to within the uterus

 Presumtive
 Examination
OF PREGNANCY
 Presumptive signs and symptoms of pregnancy are those signs
and symptoms that are usually noted by the patient
 These signs and symptoms are not proof of pregnancy, but will
suspicious of pregnancy
OF PREGNANCY
 Amenorrhea
 Nausea
 Vomiting
 Frequency Urination
 Breast Changes
 Vaginal Changes
 Skin Changes
 Quickening
 Fatigue
AMENORRHEA
 Amenorrhea is one of the earliest clues of pregnancy
 The majority of patients have no periodic bleeding after the

onset of pregnancy
 At least 20 % of women have some slight, painless spotting

during early gestation for no apparent reason and a large
majority of these continue to term and have normal infants
AMENORRHEA
 Other causes of amenorrhea:
 Menopause
 Stress (severe emotional shock, tension, fear, or a strong

desire for a pregnancy)
 Chronic illness (tuberculosis, endocrine disorders, or

central nervous system abnormality)
 Anemia
 Excessive exercise
NAUSEA AND VOMITING
(MORNING SICKNESS)
 Usually occurs in early morning during the first weeks of
pregnancy
 Usually spontaneous and subsides in 6 to 8 weeks or by the

twelfth to sixteenth week of pregnancy
beyond the 4 month of pregnancy

the patient
NAUSEA AND VOMITING
 Other causes of nausea and vomiting:
 Gastrointestinal disorders (hiatal hernias, ulcers, and

appendicitis)
 Infection (influenza, encephalitis)
 Emotional stress, upset (anxiety, anorexia nervosa)
 Indigestion
FREQUENCY URINATION
 Frequent urination is caused by pressure of the expanding
uterus on the bladder
 It subsides as pregnancy progresses and the uterus rises out of

the pelvic cavity
 The uterus returns during the last weeks of pregnancy as the

head of the fetus presses against the bladder

or tumors)
BREAST CHANGES
 In early pregnancy, changes start with a slight, temporary
enlargement of the breasts, causing a sensation of weight,
fullness, and mild tingling
supply
pregnancy
VAGINAL CHANGES
 Chadwick's sign: The vaginal walls have taken on a deeper
color caused by the increased vascularity because of
increased hormones
 It is noted at the 6th week when associated with
pregnancy
 It may also be noted with a rapidly growing uterine tumor
or any cause of pelvic congestion
 Leukorrhea: This is an increase in the white or slightly gray

 It is due to hyperplasia of vaginal epithelial cells of the
cervix because of increased hormone level from the
pregnancy
 This is the first perception of fetal movement within the uterus
 It usually occurs toward the end of the fifth month because of

spasmodic flutter
 A multigravida can feel quickening as early as 16 weeks
 A primigravida usually cannot feel quickening until after 18

weeks
 Once quickening has been established, the patient should be
instructed to report any instance in which fetal movement is
absent for a 24-hour period
 Fetal movement early in pregnancy is frequently thought to be
gas
SKIN CHANGES
 Striae gravidarum (stretch marks): Marks noted
on the abdomen and/or buttocks caused by increased
production or sensitivity to adrenocortical hormones during
pregnancy
 These marks may be seen on a patient with Cushing's
disease or a patient with sudden weight gain
 Chloasma (“mask of pregnancy“): It is a bronze type of facial

coloration seen more on dark-haired women
 Fingernails: Some patients note marked thinning and

softening by the 6th week
SKIN CHANGES
 Linea nigra: A black line in the midline of the abdomen that
may run from the sternum or umbilicus to the symphysis pubis
 This appears on the primigravida by the 3rd month and
keeps pace with the rising height of the fundus
 The entire line may appear on the multigravida before the

3rd month
FATIGUE
 This is a common complaint by most patients during the 1st
trimester
 Fatigue may also be a result of anemia, infection, emotional

stress, or malignant disease
 Probable signs of pregnancy are those signs commonly noted
by the physician upon examination of the patient

 uterine changes

UTERINE CHANGES
 Position: By the 12th week, the uterus rises above the
symphysis pubis and it should reach the xiphoid process by the
36th week of pregnancy
 These guidelines are fairly accurate only as long as
pregnancy is normal and there are no twins, tumors, or
excessive amniotic fluid
 Size: The uterine increases in width and length approximately

5x its normal size
 Its weight increases from 50 grams to 1,000 grams
UTERINE CHANGES
 Hegar’s Sign: This is softening of the lower uterine segment
just above the cervix
 When the uterine is compressed between examining fingers,

the wall feels tissue paper thin
 The physician will use bimanual maneuver simultaneously

(abdominal and vaginal) and will cause the uterus to tilt
forward
 The Hegar's sign is noted by the 6th to 8th week of pregnancy

UTERINE CHANGES
 Ballottement: This is demonstrated during the bimanual
exam at the 16th to 20th week
 Ballottement is when the lower uterine segment or the cervix is
tapped by the examiner's finger and left there, the fetus floats
upward, then sinks back and a gentle tap is felt on the finger
 This is not considered diagnostic because it can be elicited in
the presence of ascites or ovarian cysts
ABDOMINAL CHANGES
 This corresponds to changes that occur in the uterus, as the
uterus grows the abdomen gets larger
 Abdominal enlargement alone is not a sign of pregnancy
 Enlargement may be due to uterine or ovarian tumors, or

edema
 Striae gravidarum may also be classified as a probable sign of

pregnancy by the physician
CERVICAL CHANGES
 Goodell's sign: The cervix is normally firm like the cartilage at
the end of the nose
 The Goodell's sign is when there is marked softening of the
cervix
 This is present at 6 weeks of pregnancy
 Formation of a mucous plug: This is due to hyperplasia of

the cervical glands as a result of increased hormones
 It serves to seal the cervix of the pregnant uterus and to
protect it from contamination by bacteria in the vagina
 The mucous is expelled at the end of pregnancy near or at

 This involves painless uterine contractions occurring
throughout pregnancy

 These contractions will, generally, cease with walking or other

forms of exercise
 The Braxton-Hick's contractions are distinct from contractions

of true labor by the fact that they do not cause the cervix to
dilate and can usually be stopped by walking
BASAL BODY TEMPERATURE
 This is a good indication if the patient has been recording for
several cycles previously
 A persistent temperature elevation spanning over 3 weeks

since ovulation is noted
 Basal body temperature (BBT) is 97 % accurate

POSITIVE PREGNANCY TEST BY THE
CLINICIAN
 This may be misread by doing it too early or too late
 Even if the test is positive, it could be the result of ectopic

pregnancy or a hydatidiform mole (an abnormal growth of a
fertilized ovum)
FETAL PALPATION
 It is not always accurate, a mass in the abdomen may be

palpated and mistakenly identified as an infant
 They include:
 fetal heart sounds
 ultrasound scanning of the fetus
 palpation of the entire fetus
 palpation of fetal movements
 x-ray
FETAL HEART SOUNDS
 The fetal heart begins beating by the 24th day following
conception
 It is audible with a Doppler by 10 weeks of pregnancy and with

a fetoscope after the 16th week
 It is not to be confused with uterine souffle or swishlike tone

from pulsating uterine arteries
 The normal fetal heart rate is 120 to 160 beats
 Ultrasound Scanning of the Fetus: The gestation sac can be

seen and photographed
 An embryo as early as the 4th week after conception can be
identified
 Palpation of the Entire Fetus: Palpation must include the
fetus head, back, and upper and lower body parts
 This is a positive sign after the 24th week of pregnancy if the
woman is not obese
 Palpation of Fetal Movement: This is done by a trained

examiner.
 X-ray: An x-ray will identify the entire fetal skeleton by the 12th
week.
 In utero, the fetus receives total body radiation that may lead to
genetic or gonadal alterations
 An x-ray is not a recommended test for identifying pregnancy
 Actual Delivery of An Infant: Self-explanatory

TESTS UTILIZED TO DETERMINE
PREGNANCY
 Tests are based on the presence of human chorionic
gonadotropin (HCG) in the urine or blood
 Urine: can be performed accurately 42 days after the last
menstrual period or 2 weeks after the first missed period
 The first urine specimen of the morning is the best one to use
 Blood: Radioimmunoassays (RIA) can detect HCG in the

blood 2 days after implantation or 5 days before the first
menstrual period is missed
 NOTE: HCG levels peak between 50 to 90 days after the last
menstrual period
 Home pregnancy test kits are easily available and inexpensive.
CHANGES OF THE REPRODUCTIVE
SYSTEM DURING PREGNANCY
 Uterus
 By the time the pregnancy has reached term, the uterus will
have increased 5x its normal size:
 In length from 6.5 to 32 cm
 In depth from 2.5 to 22 cm
 In width from 4 to 24 cm
 In weight from 50 to 1000 grams

THE UTERUS
 The capacity of the uterus must expand to normally
accommodate a fetus and the placenta, the umbilical cord, 500
ml to 1000 ml of amniotic fluid, and the fetal membranes
 The abdominal contents are displaced to the sides as the uterus

grows in size, which allows for ample space for the uterus within
the abdominal cavity
 Growth of the uterus occurs at a steady, predictable pace
 Measurement of the fundal height during pregnancy is an

important factor that is noted and recorded
FUNDAL HEIGHT
 Growth that occurs too fast or too slow could be an indication
of problems
 The size of the uterus usually reaches its peak at 38 weeks

gestation
 The uterus may drop slightly as the fetal head settles into the
pelvis, preparing for delivery
 This dropping is referred to as "lightening."
 This is more noticeable in a primigravida than a multigravida

THE CERVIX
 The cervix undergoes a marked softening which is referred to as
the Goodell's sign
 Operculum: A mucus plug is formed in the cervical canal
 This is the result of enlarged and active mucus glands of the
cervix
 It serves to seal the uterus and to protect the fetus and fetal
membranes from infection
 The mucus plug is expelled at the end of the pregnancy
 This may occur at the onset of labor or precede labor by a few
days
 When the mucus is blood-tinged, it is referred to as a "bloody
show."
OTHER CHANGES
 Additional changes and softening of the cervix occur prior to
the beginning of labor
 Vagina
 Increased circulation to the vagina early in pregnancy
changes the color from normal light pink to a purple hue
which is known as the "Chadwick's sign."
THE OVARIES
 Follicle-stimulating hormone (FSH) ceases its activity due to
the increased levels of estrogen and progesterone secreted by
the ovaries and corpus luteum
 The FSH prevents ovulation and menstruation
 The corpus luteum enlarges during early pregnancy and may

even form a cyst on the ovary
THE CORPUS LUTEUM
 The corpus luteum produces progesterone to help maintain
the lining of the endometrium in early pregnancy
 It functions until about the 10th to 12th week of pregnancy when

the placenta is capable of producing adequate amounts of
progesterone and estrogen
 It slowly decreases in size and function after the 10th to 12th

week
CHANGES OF THE CIRCULATORY
 Blood volume increases gradually by 30-50 % (1500 ml to 3
units)
 This results in decrease concentration of red blood cells and

hemoglobin

pregnancy

compensated for the decrease resulting in an essentially
normal blood count
BLOOD CIRCULATION CHANGES
 Blood count is interpreted as anemia by the physician if the
hemoglobin falls below 10.5 grams per 100 ml and the
hematocrit drops below 30 %
 Increased blood volume compensates for hypertrophied

vascular system of enlarged uterus
 It improves the placental performance
 Blood lost during delivery, less than 500 cc is normal (300 to

400 cc is average)
CARDIAC OUTPUT
 Cardiac output increases about 30 % during the 1st and 2nd
trimester to accommodate for hypervolemia
 This is not a problem for patients with a normal heart
 A patient with a diseased heart is especially at risk for cardiac

decompensation 28 to 35 weeks of pregnancy when the blood
volume and cardiac load are at their peak; also, during labor
and immediately after delivery when rapid hemodynamic
changes occur
CHANGES OF THE CIRCULATORY
 Change in output is reflected in the heart rate
 It usually increases by 10 beats per minute
 Normally, the patient's blood pressure will not rise
 The lower extremities are often hampered in the last months

of pregnancy due to the expanding uterus restricting physical
movement and interfering with the return of blood flow
 This results in swelling of the feet and legs
CHANGES IN THE RESPIRATORY
 The respiratory rate rises to 18 to 20 to compensate for
increased maternal oxygen consumption, which is needed for
demands of the uterus, the placenta, and the fetus
 Women may feel out of breath and may need to sit a moment
to catch their breath
CHANGES OF BODY TEMPERATURE
DURING PREGNANCY
 A slight increase in body temperature in early pregnancy is
noted
 The temperature returns to normal at about the 16th week of

gestation
 The patient may feel warmer or experience "hot flashes"

caused by increased hormonal level and basal metabolic rate
CHANGES OF THE URINARY SYSTEM
DURING PREGNANCY
 The kidneys must work extra hard excreting the mother's own
waste products plus those of the fetus
 There is an increase in urinary output and a decrease in the

specific gravity
 The patient may develop urine stasis and pyelonephritis in the

right kidney
 This is due to pressure on the right ureter resulting from

displacement of the uterus slightly to the right by the sigmoid
colon
DURING PREGNANCY
 Frequent urination is a complaint during the 1st through 3rd
trimester
 As the uterus rises out of the pelvic cavity in early pregnancy,

pressure on the bladder decreases and frequency diminishes
 When lightening occurs during the final weeks of pregnancy,

pressure on the bladder returns to cause frequency
CHANGES OF THE SKELETAL SYSTEM
DURING PREGNANCY
 There is a realignment of the spinal curvatures during
pregnancy to maintain balance
 It is due to the increase in size of the uterus and pressure on
the abdominal wal
 The patient walks with head and shoulders thrust backward
and chest protruding outward to compensate
 This gives the patient a "waddling" gait
 There is a slight relaxation and increased mobility of the pelvic
joints, which allows stretching at the time of delivery of the
infant
CHANGES IN THE GASTROINTESTINAL
SYSTEM
 The uterus enlarges and rises up into the pelvic cavity
 This action displaces the stomach, intestines, and other

adjacent organs
 Peristalsis is slowed because of the production of the hormone

progesterone, which decreases tone and mobility of smooth
muscles
 This slowing enhances the absorption of nutrients and slows

the rate of secretion of hydrochloric acid and pepsin
GI CHANGES
 Flare-up of peptic ulcers is uncommon in pregnancy
 Slow emptying may increase nausea and heartburn (pyrosis)
 Relaxation of the cardiac sphincter may increase regurgitation

and chance for heartburn
 Movement through the large intestines is also slowed due to an

increase in water consumption from this area
 This increases the chance for constipation

CHANGES OF SELECTED GLANDS OF
THE ENDOCRINE SYSTEM DURING
PREGNANCY
 Parathyroid Gland: Increases in size slightly
 It meets the increased requirements for calcium needed for
fetal growth
 Posterior Pituitary: Near the end of term, the posterior

pituitary will begin to secrete oxytocin that was produced in
the hypothalamus and stored there
 It will serve to initiate labor
ENDOCRINE CHANGES
 Anterior Pituitary: At birth, It will begin to secrete prolactin
 This stimulates the production of breast milk
 Placenta: Acts as a temporary endocrine gland during

pregnancy
 It produces large amounts of estrogen and progesterone by
10 to 12 weeks of pregnancy
 It serves to maintain the growth of the uterus, helps to

control uterine activity, and is responsible for many of the
maternal changes in the body
CHANGES IN BODY WEIGHT DURING
PREGNANCY
Weight gain in pregnancy:
 There is a slight loss of pounds during early pregnancy if
the patient experiences much nausea and vomiting
 Weight gain of 2 to 4 lbs by the end of the 1st trimester
 A gain of a 1 lb. per wk is expected during the 2nd and 3rd

trimesters
 Monitoring of weight gain should be done in conjunction

with close monitoring of BP
BODY WEIGHT CHANGES DURING
PREGNANCY
 A lack of significant weight gain may be an indication of
intrauterine growth retardation (IUGR) of the infant
 Twin pregnancy: will require a higher caloric diet and expect a

higher weight gain than a single pregnancy
 Adequate protein intake emphasized to the patient for

development of the healthy fetus and proper diet reviewed at
each prenatal visit
 Normal weight gain is about 24 to 30 pounds (lbs) during

pregnancy
INVESTIGATIONS
 Urine tests:
 Test of hCG (human chorionic gonadotrophin)
 α and β (glycoprotein) subunit
 Cross reaction for alpha : LH, FSH, TSH (sharing of α
subunit)
 Morning specimen urine; repeat 1-2 weeks if necessary
 2 methods ; indirect and direct antibody test
 Serum hCG produced by synciotrophoblast; peaks at 10 weeks;

luteotropic & maintains corpus luteum until placental
steroidogenesis level is satisfactory
INVESTIGATIONS
 Urinary hCG
 False positive:
 Cross reaction to above hormones. Current test using
specific β-subunit
 Contamination by higher than normal urine protein
 Ovarian tumor
 False negative:
 Technical error
 Test done too early
 Abnormalities of pregnancy eg miscarriage
INVESTIGATIONS
 Sensitive serum assay: radioreceptor assay or
radioimmunoassay
 Advantage of sensitivity, allowing diagnosis of pregnancy
well before the first missed period
 More expensive, reserved for special indications eg ectopic

pregnancy, surveillance for molar pregnancy
FEATURES OF PREGNANCY TESTS
Feature Urine immunoassay Serum immunoassay
Slide test Tube test Radioimmuno Radioreceptor
assay (beta (alpha & beta
subunit) subunits)
Time for test 2 minutes 1-2 hours 1-2 hours 1 hour

result
Sensitivity 1,000-5,000 200 3-5 200
(Iu/l)
When 100% 42 28 20 28
accuracy can (few days after
be expected implantation)
(days after
LMP)
Cost + ++ ++++ +++

INVESTIGATIONS
Ultrasound
 Gestational sac by 5 weeks
 Fetal cardiac activity by 6-7 weeks, but 100% reliable at 8-
9 weeks
 What Should Be Seen In A First Trimester Pregnancy?
 The site of pregnancy
 The gestational sac, amniotic cavity including numbers
 The fetus and viability

WHAT SHOULD BE SEEN IN A 1 ST
TRIMESTER PREGNANCY?
 Earliest sign could be
thickened ET > 12mm
 4-5 weeks – gestational sac
(1-2 mm)
Double ring" (also known as

the "double decidual sign")
Gestational sac
Double ring
Correlation of serum ß-hCG
and gestional sac:
• TVS – small IUGS of 1-2mm
at ß-hCG 1500-2000 iu
BL
• TAS - at 6500 iu
IUGS
vag
INVESTIGATIONS
 Fetal ECG
 can be detected at 10 wks, but only reliable at 18-20 weeks
 Thermometry
 elevation of skin temperature (0.7%) over breast compared
with sternum
 Radiograph
 Fetal bones become visible on radiograph at 14-16 weeks
 Risk of radiation damage, NOT DONE !

INVESTIGATIONS
 Hormonal withdrawal test
 Large dose of estrogen/progesterone for 2-3 days
 Usually withdrawal bleed after 3-5 days, if not pregnant
 Possible harm; NOT DONE !

Lecture 4
Physiology of the uterine
muscle.
Labor's follow up.
Uterine contractile activ-
ity during labor
Prof. Vlad TICA, MD, P
Uterine contractile activity
during labor
1. The Myometrium
2. The Cervix
3. Labor Patterns
• Labor : thunderous uterine contractions
that effect
dilatation of the cervix and force the
fetus
through the birth canal
• False labor : myometrial contractions that

do not
cause cervical dilatation
unpredictability in occurrence
lack of intensity
brevity of duration
discomfort – confined to low ab-
domen & groin
The Myometrium
1. Anatomical and Physiological Considera-
tions
• Characteristics – advantage in the efficiency of
uterine
contractions & the delivery of
the fetus
① degree of shortening of smooth muscle cells
with
contraction
: magnitude greater than in striated mus-
cle cells
② forces can be exerted in smooth muscle
cells in
any direction
③ not organized in the same manner as skele-
tal muscle
- thick & thin filaments in long, random
Smooth Muscle (e.g.
myometrium)
Smooth muscle is found in the walls of blood vessels, tubular

organs such as the stomach and uterus. It has the ability to
stretch and maintain tension for long periods of time. It is not
under voluntary control and each cell exists as a discreet
independent unit that is innervated by a single nerve ending.
The myofilaments are loosely organized and attached to dense
Smooth Muscle (e.g. my-
ometrium)
•Does not contain
sarcomeres
• Contains > content

of actin than myosin
(ratio of 16:1)
• Myosin filaments at-

tached at ends of the
cell to dense
bodies
• Contains gap junc-

Smooth Muscle Contraction
• Depends on rise in free intracel-
lular Ca2+.
• Ca2+ binds with calmodulin.
– Ca2+ calmodulin complex joins with
and activates myosin light chain
kinase.
• Myosin heads are phosphory-

lated.
– Myosin heads binds with actin.
Mechanisms involved in
smooth muscle intracellular
calcium control
Functions of the SR in smooth muscle. A cartoon to demonstrate the
functions of the SR. 1: Contributing to Ca homeostasis and mainte-
nance of low resting level of intracellular [Ca] via sarco/endoplasmic
reticulum Ca-ATPase (SERCA) activity. 2: Contributing to relaxation
of the smooth muscle cell by taking up Ca via SERCA. 3: Contributing
to Ca signals and contraction by Ca release via IP3 receptor (IP3R)- or
ryanodine receptor (RyR)-gated Ca release channels and Ca puffs
and Ca sparks. 4: Contributing to excitability via Ca-activated K and
Cl channels. 5: Facilitation of Ca efflux on plasma membrane Ca-ATP-
ase (Ca pump) or Na/Ca exchanger, via vectorial release of Ca. 6:
Contributing to subcellular microdomains and organellar Ca home-
ostasis via Ca uptake and release between organelles. 7: Correct SR
The Myometrium
2. Biochemistry of Smooth Muscle Contractions
Contrac- Relax-
tion Myosin light chain ation
Myosin light chain
kinase 1) Decreased intracellular
Ca2+ activated Ca2+;
Phosphory- Ca2+ sequestration
lated
Myosin light 2) Dephosphorylation of
chain Acti
myosin light
n chain
Actin-Phosphorylated
Myowin 3) Inactivation of myosin
light chain
ATPase
kinase (e.g., by cyclic AMP-
ATP ADP dependent phosphory-
lation)
The Myometrium
3. The Three Stages of Labor
• First stage of labor
: begins when uterine contraction of suffi-

cient
frequency, intensity & duration are at-
tained
→ ends when cervix is fully dilatated
(10cm)
: stage of cervical effacement & dilatation

The Myometrium
• Second stage of labor

: begins when complete dilatation of cervix
→ ends with delivery of the fetus
: stage of expulsion of the fetus
• Third stage of labor

: begins after delivery of the fetus
→ ends with the delivery of the placenta
: stage of separation & expulsion of pla-
centa
The Myometrium
4. Clinical Onset of Labor
• Show (bloody show)
- sign of the impending onset of active la-

bor
- extrusion of mucus plug of the cervical
canal
→ discharge of small amount of blood-
tinged
mucus from vagina
The Myometrium
5. Uterine Contractions Characteristic of Labor
; muscular contractions, those of uterine
smooth
muscle of labor are painful
• cause of pain (not known definitely)

① hypoxia of contracted myometrium
② compression of nerve ganglia in cervix &
lower
uterus by the tightly interlocking muscle
bundles
③ stretching of cervix during dilatation
④ stretching of peritoneum overlying the
fundus
The Myometrium
• Ferguson reflex
: mechanical stretching of cervix enhances
uterine
activity
: manipulation of the cervix and stripping
the fetal
membranes is associated with an increase
in PGF2α
metabolite in blood
: exact mechanism : not clear
• Interval between contractions
: 10 minutes at the onset of the first stage
→ diminishes gradually
→ 1 minute or less in the second stage
The Myometrium
• Periods of relaxation between contractions

- essential to welfare of the fetus
- unremitting contraction of uterus com-
promises
uteroplacental blood flow, cause fetal
hypoxia
• Duration of contraction
: in active phase
Duration 30-90 seconds (average 60
sec)
Pressure 20-60 mmHg (average 40
mmHg)
The Myometrium
6. Differentiation of Uterine Activity
: During active labor, uterus is transformed
into
2 distinct parts
(1) Upper segment
① actively contracting
② becomes thicker as labor advances
③ quite firm or hard
(2) Lower segment
① relatively passive
② develops into a much thinly walled
passage
for the fetus
③ much less firm
The Myometrium
• Physiologic retraction ring
- As a result of the thinning of the lower
uterine
segment and the concomitant thickening
of the
upper, the boundary between the two is
marked
by a ridge on the inner uterine surface
• Pathologic retraction ring (the ring of Ban-

dle)
- When the thinning of the lower uterine
segment is
extreme, as in obstructed labor, the ring
The Myometrium
The Myometrium
7. Change in Uterine Shape
: each contraction produces elongation of
uterus with
decrease in horizontal diameter
→ important effect on labor process
① decrease in horizontal diameter

→ straightening of fetal vertebral column
② lengthening of uterus
→ longitudinal fibers are drawn taut
→ pulled upward the lower segment &
cervix
→ important factor in cervical dilatation
The Myometrium
8. Ancillary Forces in Labor
: After the cervix is dilated fully, the most
important
force in the expulsion of the fetus is that
produced
by increased maternal intrabdominal pres-
sure
“Pushing”
- increased intrabdominal pressure by con-
traction of
abdominal muscles, simultaneously with
forced
respiratory efforts with glottis closed
- important force in the expulsion of fetus
Thank You !
Lecture 5
PHASES OF PARTURITION
STAGES OF LABOR
MECHANISM OF NORMAL LABOR
IN OCCIPUT PRESENTATION
Prof. Vlad TICA, M.D., Ph. D.

• Labor : uterine contractions that effect dilatation of

cervix and force fetus through birth canal
• Parturition: bringing forth of young, encompass all

physiological processes involved in birthing
• Phase 0: Prelude to Parturition
• Phase 1: Preparation for Labor
• Phase 2: Process of Labor
• Phase 3: Parturition Recovery

PHASES OF PARTURITION & ONSET OF
LABOR
• Divide 4 uterine phases: correspond to major
physiological transient of myometrium and cervix
during pregnancy
PHASE 0: UT QUIESCENCE
• Uterine smooth m tranquility with maintenance of

cervical structural intergrity
• Unresponsive to natural stimuli, contractile paralysis
• Myometrium : quiescent state
• Cervix : firm unyielding
• Succesful anatomical structural integrity :essential
for successful parturition
• Some myometrial contraction occur not cause cervix
dilation  Braxton-Hicks contraction or false labor
PHASE 0: UT QUIESCENCE
• Braxton – Hicks contraction or false labor :

Myometrial contractions that do not cause cervical
dilatation
• unpredictability in occurrence
• lack of intensity
• brevity of duration
• discomfort – confined to low abdomen & groin
PHASE 1: PREPARATION FOR LABOR
• Uterine awakening or activation
• Progression of change in uterus during last 6-8

weeks of pregnancy
• Cervical change
• Myometrial change
CERVICAL CHANGE
• Initiation of parturition: Cx soften, yield, more
readily dilatable
• Fundus transformed to produce effective

contraction that drive fetus through Cx & birth canal
• Failure of coordinated interaction  unfavorable

preg outcome
CERVICAL CHANGE
• Change of state of bundles of collagen fiber
• Collagen breakdown ↑ & rearrangement of
collagen fiber bundles (No & size ↓)
• Chages in relative amount of glycosaminoglycans

(hyaluronic acid, ↑ capacity of Cx to retain water)
• Dermatan sulfate ↓ (need for collagen fiber
cross linking)
• Production of cytokine  degrade collgen
• Cx thinning, softening relaxation Cx initiate

diatation
CERVICAL CHANGE
• PG E2 & F2a : modification of collagen & alteration

in relative amount of glycosaminoglycans
 Cx softening or ripenning to facilitate induction of

labor
MYOMETRIAL CHANGE
• Increase Ut irritability & responsiveness to uterotonins
• Alterations in expression of key enzyme CAP

(contraction-associated proteins) - control
myometrum contractility
• Myometrial oxytocin R ↑
• Myometrial cell gap junction protein (ex connexin -43)
• Formation lower Ut segment

PHASE 2 OF PARTURITION: PROCESS OF
LABOR
• Active labor : Ut contrations bring about progressive
cervical dilatation & delivery
• 3 stage of labor
PHASE 2: PROCESS OF LABOR
1st STAGE OF LABOR

• begins when uterine contraction of sufficient fre-
quency, intensity & duration
• ends when Cx is fully dilatated (10cm)
• Stage of cervical effacement & dilatation
2nd STAGE OF LABOR

• begins when complete dilatation of Cx
• ends with delivery of fetus
• stage of expulsion of fetus
3rd STAGE OF LABOR

• begins after delivery of fetus
• ends with delivery of placenta and fetal membranes
• stage of separation & expulsion of placenta
4th STAGE OF LABOR

• begins after placenta and fetal membranes
• ends after 2 hours
• stage of immediate puerperium

1st STAGE OF LABOR: CLINICAL ONSET OF
LABOR
Formation of distinct lower & upper Ut segment:
• 2 distinct parts (anatomically & physiologically)
1. UPPER SEGMENT
• actively contracting
• becomes thicker as labor advances
• quite firm or hard
2. LOWER SEGMENT
• relatively passive
• develops into a much thinly walled passage for the fe-
tus
• much less firm
Sequence of development of segment & ring in uterus in
pregnant women at term & in labor
Cx near end of pregnacy Beginning effacement of Cx
before labor
Further effacement of Cx Cervical canal obliterated
CERVICAL CHANGE INDUCED DURING
1st STAGE OF LABOR
1st STAGE OF LABOR
2 phases of cervical dilatation:
1. LATENT PHASE
- more variable
- subject to sensitive changes by extraneous factors &
by sedation (prolongation) & myometrial stimulation
(shortening)
2. ACTIVE PHASE
- Acceleration phase - usually predictive of outcome
- Phase of maximum slope
- Deceleration phase
2nd STAGE OF LABOR: FETAL DESCENT
- In many nulliparas
① engagement accomplished before labor

begins
② further descent not occur until late in

labor
③ increased rates of descent are ordinarily

observed during the phase of maximum slope
Labor course divided fuctionally on basis of expected

evolution of dilatation & desecnt curves into 3
divisions
① PREPARATORY DIVISION
- latent & acceleration phases
② DILATATIONAL DIVISION
- phase of maximum slope of cervical dilatation
- most rapid rate of dilatation occur
③ PELVIC DIVISION
- deceleration phase & second stage while
concurrent with phase of maximum slope of fetal
descent
3rd STAGE OF LABOR: DELIVERY OF PLA-
CENTA & MEMBRANES
4th STAGE OF LABOR: IMMEDIATE
PUERPERIUM
PHASE 3 OF PARTURITION: PROCESS OF
LABOR
• Immediately after delivry & for 2 hours or so
thereafter, myometrium in state of rigid & persistent
contraction & retraction
 effect compression of large Ut vessels
 Severe PPH prevented
• Involution of Ut & reinstitution of ovulation
• Complete Ut involution : 4~6 wks
• Infertility persist as long as breast feeding is
continued ( lactation  anovulation & amenorrhea)
LIE, PRESENTATION, ATTITUDE & POSITION
FETAL LIE
• The relation of the long axis of the fetus to that of the
mother
• Longitudinal lie - found in 99% of labours at term
• Transverse lie - multiparity, placenta praevia, hydramnios,

uterine anomalies
• Oblique lie: unstable (become logitudinal or transversal)
• By abdominal palpation, vaginal examination, and

auscultation, or by technical means (USG, X-ray)
FETAL PRESENTATION
• The presenting part is the portion of the body of the

fetus that is foremost in the birth canal
• The presenting part can be felt through the cervix on

vaginal examination
• Longitudinal lie  cephalic presentation

 breech presentation
• Transverse lie  shoulder presentation

CEPHALIC PRESENTATION
• Head is flexed sharply  vertex / occiput presentation
• Head is extended sharply  face presentation
• Partially flexed  bregma presenting (sinciput

presentation)
• Partially extended  brow presentation

BREECH PRESENTATION
• Frank breech
• Complete breech
• Footling breech
ATTITUDE
• Posture of the fetus  folded on itself to accommodate

the shape of the uterus
• Flexed head, thighs, knees &feet
• The arms crossed over the chest
• Face presentation  extended concave contour of the

vertebral column
.
'
"
'
I
!
1\
1
1
A
B
i
i
c
D vertex )A( sinciput )B( brow )C( face )D(
Longitudinal lie. Cephalic presentation. Differences in attitude of

fetal body,
Note changes in fetal attitude in relation to fetal vertex as the fetal
head becomes less flexed.
I
I
Longitudinal lie. Frank breech Longitudinal lie. Complete breech

presentation. presentation.
Longitudinal lie. Incomplete, or footling,
breech presentation.
POSITION
The relation of an arbitrary chosen point of the fetal
presenting part to the Rt or Lt side of the maternal birth
canal
The chosen point
• Vertex presentation  occiput
• Face presentation  mentum
• Breech presentation  sacrum
Each presentation has two positions Rt or Lt
Each position has 3 varieties : anterior, transverse,
posterior OA
ROA LOA
ROT LOT
ROP LOP
OP
LONGITUDINAL LIE VERTEX PRESENTATION
LOA LOP
~
'
t
J
Right occiput posterior (ROP) Right occiput transverse (ROT)
Longitudinal lie. Vertex presentation

3
S
~
f
a
!
w
C
c
h
t
p
(
f
i
t
t
b
f
e
a
l Right occiput anterior (ROA)
FREQUENCY OF VARIOUS
PRESENTATIONS & POSITIONS AT TERM
• Vertex  96%
2/3 Lt
1/3 Rt
• Breech  3.5%
• Face 0.3%
• Shoulder 0.4%
Left mento-anterior Right mento-anterior Right mento-posterior
Longitudinal lie. Face presentation.

Left and right anterior and posterior positions.
~
Longitudinal lie. Breech presentation LSP

Transverse lie. Right acromio-dorso-posterior position (RADP).
The shoulder of the fetus is to the mother's right, and the back
is posterior.
MECHANISM OF LABOUR WITH OCCIPUT
PRESENTATIONS
THE CARDINAL MOVEMENTS OF LABOUR
1 - ENGAGEMENT
The greatest transverse diameter BPD passes through the
pelvic inlet
It may occur in the last few weeks of pregnancy or only in
labour especially in multipara
The fetus enters the pelvis in transverse or oblique
diameter
• LOT  40%
• ROT  20%
• OP  20% ROP > LOP
• ROA / LOA  20%
THE CARDINAL MOVEMENTS OF LABOUR
• Asynclitism
The sagittal sutures of the head deflects ant towards the

symphysis pubis or post towards the sacrum
2 - DESCENT
• In nullipara engagement takes place before the onset of
labour & further descent may not occur till the 2nd stage
• In multipara descent begins with engagement
• It is gradually progressive till the fetus is delivered
• It is affected by the uterine contractions & thinning of
the lower segment
Anterior asynclitism Normal synclitism Posterior asynclitism
Naegele's obliquity Litzmann's obliquity
Ear presentation
3-FLEXION
• The descending head meets resistance of pelvic floor,
Cx & walls of the pelvis  flexion
• The shorter suboccipito-begmatic is substituted for

the longer occipito-frontal
Lever action producing flexion of the head; conversion from
occipito-frontal to suboccipito-bregmatic diameter typically
reduces the anteroposterior diameter from nearly 12 to 9.5 cm
Four degrees of head flexion
Indicated by the solid line the
occipitomental diameter; the
broken line connects the
center of the anterior fontanel
with posterior fontanel:
A. Flexion poor
A B. Flexion moderate
c C. Flexion advanced
D. Flexion complete
Note that with flexion complete
the chin is on the chest, and
the suboccipitobregmatic
diameter, the shortest
anteroposterior diameter of the
fetal head, is passing through
the pelvic inlet.
A
c
D
4-INTERNAL ROTATION
• Turning of the head from the OT position  anteriorly
towards the symphysis pubis ie. Occiput moves from
transverse to anterior 45º
• Less commonly OT  posteriorly towards the sacrum
135º
• It is not accomplished till the head has reached the
spines
The levator ani muscles form a V shaped sling that
tend to rotate the vertex anteriorly
• It is completed by the time the head reaches the pelvic
floor 2/3 or shortly after ¼
EXTENSION
• When the flexed head reaches the vulva it undergoes
extension  the base of the occiput will be in direct
contact with the inferior margin of the symphysis
pubis
• Crowning  the largest diameter of the fetal head is

encircled by the vulvar ring
• The head is born by further extension as the occiput,

bregma, forehead, nose, mouth & chin pass
successively over the perineum
EXTERNAL ROTATION
RESTITUTION
• After delivery of the head it returns to the position it
occupied at engagement, the natural position relative
to the shoulders (oblique position)
• Then the fetal body will rotate to bring one shoulder
anterior behind the symphysis pubis (biacromial
diameter into the APD of the pelvic outlet)
• Restitution is followed by complete external rotation to
transverse position (occiput lies to next to left maternal
thigh)
• The anterior shoulder slips under the pubis
• By lateral flexion of the fetal body the post shoulder
will be delivered & the rest of the body will follow
3
0
2
Cardinal movements in
the mechanism of labor
2.Engagement;descent, flexion 6. Restitution (external rotation)
and delivery, left occiput
anterior position
3. Further descent, internal rotation
4. Complete rotation, beginning extension

3
0
4
t
l
v
a
b
f
Mechanism of labor for the left occiput transverse position, lateral

view. Posterior asynclitism (A) at the pelvic brim followed by lateral
flexion, resulting in anterior asynclitism (B) after engagement,
further descent (C), rotation, and extension (D)
OCCIPUT POSTERIOR POSITION
• Mechanism of labour is identical to OT & anterior

varieties
• The occiput rotate to the symphysis pubis through

135º instead of 90º or 45º
• If rotation does not occur  direct occiput posterior

or
partial rotation  transverse arrest
,
.
,
0
Mechanism of labor for right occiput posterior position,

anterior rotation
Lecture 6
BREACH PRESENTATION
TRANSVERSAL & OBLIQUE LIE
Prof. Vlad TICA, M.D., Ph. D.

TYPES OF BREECH
PRESENTATION
• Frank (65%): Hips are flexed,
knees are extended
• Complete (10%): The hips and
knees are flexed
• Incomplete (25%): The feet or
knees are the lowermost
presenting part:
• Single footling: one of the
lower extremities is
lowermost.
• Double footling: Both of the
lower extremities are
lowermost
Breech presentations:
A: Right sacrum posterior (RSP) position
B: Left sacrum anterior (LSA) position
TYPES OF BREECH
PRESENTATION
• Frank (65%): Hips are flexed,
knees are extended
• Complete (10%): The hips and
knees are flexed
• Incomplete (25%): The feet or
knees are the lowermost
presenting part:
• Single footling: one of the
lower extremities is
lowermost.
• Double footling: Both of the
lower extremities are
lowermost
BREECH PRESENTATION
PREDISPOSING FACTORS
• Prematurity
• Uterine abnormalities
• Malformation
• Fibroids
• Fetal abnormalities
• CNS Malformations
• Neck Masses
• Multiple gestations
• Previous breech delivery
BREECH PRESENTATION
Gestational age in weeks % Breech
21-24 33
25-28 28
29-32 14
33-36 9
37-40 7
BREECH PRESENTATION
DIAGNOSIS
• Palpation and ballottement
• Ultrasound
• Pelvic examination
• X-Ray studies
BREECH PRESENTATION
Leopold Maneuver
EXTERNAL CEPHALIC VERSION
MANAGEMENT
MANAGEMENT
TYPE OF DELIVERY
• Vaginal delivery:
• Spontaneous
• Partial breech extraction

• Total breech extraction
• Cesarean delivery
TYPES OF VAGINAL BREECH DELIVERY
• Spontaneous breech (rare): No manipulation of the

infant is necessary, other than supporting the infant
• Partial breech extraction: Fetus descend

spontaneously to where umbilicus is at the vaginal
introitus; then, the fetus is extracted completely
• Total breech extraction: The entire body is extracted.

This is indicated only if there is evidence of fetal
distress unresponsive to routine maneuvers and a
cesarean delivery is not possible.
CONDITIONS ARE UNFAVORABLE FOR
BREECH DELIVERY
• Fetus weight > 3500 g
• Unfavorable pelvis – Breech delivery does not allow

sufficient time for molding of the fetal head; thus, a
platypelloid or android pelvis decreases ability fetal
head to navigate maternal pelvis
• Hyperextension of the head – increases risk of cervical

spine injury
• Footlings- incidence of umbilical cord prolapse

increases with coiling of the umbilical cord around the
legs of the fetus
MORTALITY/MORBIDITY
• Increased birth trauma: As duration of umbilical cord

compression increases → deliver the infant more
rapidly → increasing birth trauma
• Decreased birth weight may result from preterm

delivery/growth restriction
• Incidence of prolapsed umbilical cord depends on type

of breech presentation : Footling 17%, Complete 5%,
Frank 0,5%
MECHANISM OF LABOR IN BREECH
DELIVERY
ASSISTED DELIVERY OF FRANK BREECH
Maneuver for delivery of the

head:
• The fingers of the left hand
are inserted into the infant’s
mouth of over mandible;
• The right hand exerts
pressure on the head from
above
MAURICEAU MANEUVER
MECHANISM OF LABOR IN BREECH
DELIVERY
• Piper forceps
• Modified Prague maneuver

DELIVERY OF THE AFTERCOMING HEAD
Application of Piper forceps, employing towel sling support.

The forceps are introduced from below, left blade first.
Aiming directly and intended positions on sides of the head
DELIVERY OF THE AFTERCOMING HEAD
MODIFIED PRAGUE MANEUVER
COMPLETE OR INCOMPLETE BREECH
EXTRACTION
COMPLETE OR INCOMPLETE BREECH
EXTRACTION
BREECH EXTRACTION
C-SECTION INDICATION
• A large fetus ( > 3.500 grams)
• A hyperextended fetus
• Uterine dysfunction
• Footling presentation
• Any degree of contraction or unfavorable shape

restriction
• Previous perinatal death or children suffering from

birth trauma
COMPLICATIONS
1. Perinatal morbidity and mortality from difficult delivery

2. Low birthweight from preterm delivery, growth
restriction, or bot
3. Prolapsed cord
4. Placenta praevia
5. Fetal, neonatal, and infant anomalies
6. Uterine anomalies and tumors

7. Multiple fetuses
8. Operative intervention, especially cesarean delivery
TRANSVERSE OR OBLIQUE PRESENTATION
1. DEFINITION
At the end of pregnancy or during of labor,
champ of pelvic inlet is not fetal head or fetal
breech
2. VARIETY
- shoulder right in dorso-anterior
- shoulder left in dorso-anterior
- shoulder right in dorso-posterior
- shoulder left in dorso-posterior
3. ETIOLOGY
• Mistake of accommodation: the grand cause of
transverse position is multipara (relax of uterine wall)
• Other cause can hydramnios, previa tumor, shortness

umbilical cord
• Uterine malformation
4. CLINICAL
• Inspection
• The uterus is developing transverse or oblique
• Palpation
• Hands explored base part of uterus on of pelvic
inlet can not contact fetal pole
• At middle of uterus fundus have no fetal pole

• At lateral face of uterus (right or left) can contact with

fetal pole or breech
• Multipara are rare on same plan of transverse
• Uterus malformation, the two poles can contact at

same higher at uterine body (back in anterior)
• In dorso-posterior, abdominal wall perception fetal

limps
• Auscultation:
• the fetal cardiac sound can receive a bite under
umbilical at cephalic side
• Digital exam:
• during pregnancy: the excavation is empty
(fingers are not contact the presentation)
• During labor: if membranes are not rupture, the sac

amniotic fluid is big volume (can not evaluation the
presentation)
• After rupture of membranes, the fingers are

perception:
. Shoulder and acromial protrusion
. Axillary furrow
• At profound permit contact:
. Costal
. Scapula
• In some cases, superior limp fall down in excavation,

vaginal, vulva with character cyanosis and edema
• The thumb turn to thigh of mother same name with of

shoulder that present
• Diagnostic of variety: must to know head, breech,

back, shoulder (right or left) situate at pelvic inlet
• When the hand is out side of vulva, sign of thumb
confirm the diagnosi
• X-ray: necessary in all cases, it confirme diagnostic
• Ultrasound: same of x-ray and position of placenta

5. DELIVERY
A. Ovular phenomenon:
The precocity of membranes rupture is favorable by
character of amniotic fluid sac (big volume in cervical
canal)
Uterus is empty of amniotic fluid and cord prolapses
B. Mechanic phenomenon:
• First time: weakness, head orient opposite trunk
(vertical). The shoulder is in center of basin.
Superficial exam, the presentation return
longitudinal
• Second time: engage of shoulder
• Third time: stop of progression (enclave).

C. Plastic phenomenon:
• is at region of shoulder, neck, back
D. Physiologic phenomenon:
• the dilatation of cervix is trouble: cause of dynamic
abnormal and ovular infection
• The cervix is edema, thick
• Lower segment still thick not contact with

presentation
• The uterine contraction is the trouble: the contraction

is normal until rupture of membrane but the
progression of presentation is stopped
• First irregular, then inertia or hypertonia with

hypercinesis
• The consequence of retraction is:
• Death of the fetus: the retraction provoke

diminution of blood fluid trans placenta and
infection
• Uterine rupture:
• the retraction of the myometrium of uterine body

provoke lower segment stretch (lower segment
rupture)
6. TREATMENT:
A. During of pregnancy:
- the surveillance of presentation is every days
- it can external version for cephalic presentation or
breech presentation at pelvic inlet (multipara)
- primipara: cesarean section at the end of
pregnancy
B. During of labor:
• Primipara:
• cesarean section
• Multipara:
• The membrane is intact:
• Complete dilatation of cervix: artificial rupture of
membrane and internal version
• Dilatation is incomplete: conservation of

membrane until complete dilatation
• The membranes are ruptured:
• Uterus is soft (not retracted) & fetus is alive:
• cesarean section if incomplete dilatation
• internal version if complete dilatation
• Uterus is retracted:
• Fetus is alive: cesarean section
• Fetus is dead: embryotomy

• Uterus is ruptured:
• after laparotomy and extraction of fetal mort and

placenta, the operation must suture of rupture or
hysterectomy
Lecture 6
DELIVERY OF PLACENTA
PUERPERIUM
LACTATION
Prof. Vlad TICA, M.D., Ph.D.

THIRD STAGE
• DELIVERY OF PLACENTA
 sign of placental separation (uterine sign, vulva sign,

cord sign)
 Modified Crede
 Brandt Andrew
 Controlled cord traction

DELIVERY OF THE PLACENTA
Controlled cord traction

• Prevent postpartum hemorrhage
 oxytocic drugs
• Syntocinon® : IV push, IV drip, IM
• Methergin® : IM, IV
REPAIRING EPISIOTOMY WOUND
Perineal tear during vaginal birth
• First-degree tear
• Second-degree tear
• Third-degree tear
• Fourth-degree tear
Repairing fourth-degree perineal tear

POSTPARTUM CARE: 10 BS
• Blood pressure
• Bladder
• Bloody discharge
• Basket
• Bowel
• Breast engorgement
• Breast feeding
• Baby
• Blue
• Brain
PUERPERIUM
• is defined as the time from the delivery of the
placenta through the first few weeks after the
delivery
• This period is usually considered to be 6 weeks in

duration
• By 6 weeks after delivery, most of the changes of

pregnancy, labor, and delivery have resolved and
the body has reverted to the nonpregnant state
• An overview of the relevant anatomy and

physiology in the postpartum period follows
PUERPERIUM
UTERUS
• The pregnant term uterus (not including baby,
placenta, fluids, etc) weighs approximately 1000 g
• In the 6 weeks following delivery, the uterus recedes
to a weight of 50-100 g
• Immediately postpartum, the uterine fundus is
palpable at or near the level of the maternal
umbilicus
• Thereafter, most of the reduction in size and weight
occurs in the first 2 weeks, at which time the uterus
has shrunk enough to return to the true pelvis
PUERPERIUM
UTERUS
PUERPERIUM
UTERUS
PUERPERIUM
UTERUS
• Over the next several weeks, the uterus slowly
returns to its nonpregnant state, although the
overall uterine size remains larger than prior to
gestation
• The endometrial lining rapidly regenerates, so
that by the 7th day endometrial glands are
already evident
• By the 16th day, the endometrium is restored
throughout the uterus, except at the placental
site
PUERPERIUM
UTERUS
• The placental site undergoes a series of changes
in the postpartum period
• Immediately after delivery, the contractions of
the arterial smooth muscle and compression of
the vessels by contraction of the myometrium
("physiologic ligatures") result in hemostasis
• The size of the placental bed decreases by half,
and the changes in the placental bed result in the
quantity and quality of the lochia that is
experienced
PUERPERIUM
UTERUS
• Immediately after delivery, a large amount of red
blood flows from the uterus until the contraction
phase occurs
• Thereafter, the volume of vaginal discharge
(lochia) rapidly decreases
• The duration of this discharge, known as lochia
rubra, is variable
• The red discharge progressively changes to
brownish red, with a more watery consistency
(lochia serosa)
• Over a period of weeks, the discharge continues
to decrease in amount and color and eventually
changes to yellow (lochia alba)
• The period of time the lochia can last varies,
although it averages approximately 5 weeks
PUERPERIUM
UTERUS
• The amount of flow and color of the lochia can
vary considerably
• 15% of women have continue to have lochia 6
weeks or more postpartum
• Often, women experience an increase in the
amount of bleeding at 7-14 days secondary to the
sloughing of the eschar on the placental site
• This is the classic time for delayed postpartum
hemorrhages to occur
PUERPERIUM
CERVIX
• The cervix also begins to rapidly revert to a
nonpregnant state, but it never returns to the
nulliparous state
• By the end of the first week, the external os
closes such that a finger cannot be easily
introduced
PUERPERIUM
VAGINA
• The vagina also regresses but it does not
completely return to its prepregnant size
• Resolution of the increased vascularity and
edema occurs by 3 weeks, and the rugae of the
vagina begin to reappear in women who are not
breastfeeding
• At this time, the vaginal epithelium appears
atrophic on smear
• This is restored by weeks 6-10; however, it is
further delayed in breastfeeding mothers because
of persistently decreased estrogen levels
PUERPERIUM
PERINEUM
• The perineum has been stretched and
traumatized, and sometimes torn or cut, during
the process of labor and delivery
• The swollen and engorged vulva rapidly resolves
within 1-2 weeks
• Most of the muscle tone is regained by 6 weeks,
with more improvement over the following few
months
• The muscle tone may or may not return to
normal, depending on the extent of injury to
muscle, nerve, and connecting tissues.
PUERPERIUM
ABDOMINAL WALL
• The abdominal wall remains soft and poorly toned

for many weeks
• The return to a prepregnant state depends greatly

on maternal exercise
PUERPERIUM
OVARIES
• The resumption of normal function by the ovaries
is highly variable and is greatly influenced by
breastfeeding the infant.
• The woman who breastfeeds her infant has a
longer period of amenorrhea and anovulation
than the mother who chooses to bottle-feed.
• The mother who does not breastfeed may ovulate
as early as 27 days after delivery.
• Most women have a menstrual period by 12
weeks; the mean time to first menses is 7-9
weeks
PUERPERIUM
OVARIES
• In the breastfeeding woman, the resumption of
menses is highly variable and depends on a
number of factors, including how much and how
often the baby is fed and whether the baby's food
is supplemented with formula.
• The delay in the return to normal ovarian function
in the lactating mother is caused by the
suppression of ovulation due to the elevation in
prolactin.
• ½ to ¾ of women who breastfeed return to
periods within 36 weeks of delivery
PUERPERIUM
BREASTS
• The changes to the breasts that prepare the body
for breastfeeding occur throughout pregnancy
• If delivery ensues, lactation can be established as

early as 16 weeks' gestation
• Lactogenesis is initially triggered by the delivery
of the placenta, which results in falling levels of
estrogen and progesterone, with the continued
presence of prolactin
• If the mother is not breastfeeding, the prolactin
levels decrease and return to normal within 2-3
weeks
PUERPERIUM
BREASTS
• The colostrum is the liquid that is initially
released by the breasts during the first 2-4 days
after delivery.
• High in protein content, this liquid is protective
for the newborn
• The colostrum, which the baby receives in the
first few days postpartum, is already present in
the breasts, and suckling by the newborn triggers
its release
PUERPERIUM
BREASTS
• The process, which begins as an endocrine
process, switches to an autocrine process; the
removal of milk from the breast stimulates more
milk production
• Over the first 7 days, the milk matures and
contains all necessary nutrients in the neonatal
period
• The milk continues to change throughout the
period of breastfeeding to meet the changing
demands of the baby
MANAGEMENT OF NORMAL PUERPERIUM
• The majority of mothers are perfectly well

during the puerperium and should be
encouraged to establish normal activities
• Immediately following the delivery of the

placenta observation of :
1. Vital signs (P, BP, Temp, R.R)
+ contraction of the uterus (uterin involution)
+ lochia (amount; colour and odder)
= every 5 min. for ½ hours, then every ½ hourly for

2 hours, then transfer the mother to the postnatal
ward and observation every 2 hours for 6 hourly;
then 6 hourly till discharge
2. Breast examination
+ lawer limb examination for the detection of signs

of DVT every day
3. The mother should be encouraged to pass urine

4. Early mobilization
5. Management of episiotomy; and perineum tears
6. In normal delivery the mother can go home 48

hours after delivery; and 72 hours in C-section
7. Diet regime
8. Postnatal visit
9. Advising for contraception and spacing of

pregnancy
BREAST FEEDING
LACTATION
• In those mothers who breast feed, lactation is the

most dominant physiological event of puerperium
• The primary function of breast feeding is to

continuing of nutrition for newborn
• The secondary functions:

 protection agonist infant infection
 inhibition of ovarian activity
 encouragement of uterine involution

PHYSIOLOGY OF LACTATION
• The major part of breast development occurs at

puberty before the first pregnancy
• So, only requires minimal hormonal stimulation for

production of milk
• The skin of the areola is relatively insensitive to

tactile stimuli during pregnancy but, much more
sensitive immediately after delivery
BREAST CHANGES
BREAST
MILK PRODUCTION
• Two similar independent mechanisms for

successful lactation :
1. Prolactin (PRL) release from A .p mammary

glandular tissue stimulation of milk
secretion
• PRL is long chain of polypeptide; it has only

physiological role that its action on lactating
breast
MILK PRODUCTION
2. Prolactin level during lactation depending on the

suckling ( strength , frequency and duration )
PRL release from A.p reaching
peak blood level at 30 -45 min. after suckling and
returns to the basal level 2 hours after suckling
 Adequate emptying of milk – secretary glands

MILK PRODUCTION
• Basal PRL is highest in the immediate puerperium

but:
 In breast feeding decline slowly as suckling
declines in later lactation revert to non pregnant
levels immediately after weaning (54 weeks)
 In bottle feeding reverted to non pregnant levels

immediately after delivery ( 10 weeks)
• So PRL appears essential for lactation due to

bromocriptin or dopamine agonist which is
selectively inhibits PRL secretion and decrease milk
secretion
MILK PRODUCTION
• Milk ejection reflex ( milk lead down ) mediated by

release of oxytocin from hypothalamus and (p.p):
 causing contraction of myoepithelial cells around
the milk –secretary
 dilatation of main ducts
So , Expelling milk from glands
• Oxytocin released in response to: suckling, and

sensory input like mother seeing or hearing their
baby crying
MILK PRODUCTION
• Highest levels of oxytocin occurring before suckling

in response to the baby cry
• Milk ejection reflex may be inhibited by emotional

stress and maternal anxiety and leads to failure of
lactation
• So, the key of both mechanisms activated by

suckling and mediated through neuro-
endocrianological pathways
BREAST FEEDING & FERTILITY
• The key event in lactating amenorrhea is suckling

induce changes in the hypothalamic sensitivity to
the feed back effects of ovarian hormones
• During lactation hypothalamus is more sensitive to

the negative feedback and less sensitive to the
positive feedback
In bottle feeding:
• PRL returns to level of non pregnant ovarian

follicular development ( E2 > 10 micro – gm ).
• And ovulation occur ( P4 >1 mg ) menstruation

by 14 weeks post-delivery
In breast feeding:
• During first week of suckling (60 min./day), the
ovarian activity is inhibited and menstruation is
suppressed
• At 32 weeks suckling has fallen to 25 min/day the
ovarian follicular activity returns to the normal
(anovulatory cycles)
• At 52 weeks normal ovulatory cycles occurs
• Breast feeding has important contraceptive effect
but not absolutely reliable especially after
menstruation returns, and (1-10%) of women will
conceive during lactation
Lecture 8
ECTOPIC PREGNANCY
ABORTION
ECTOPIC PREGNANCY
Definition
Implantation outside of the uterine cavity is
termed ectopic pregnancy
It is a condition that significantly jeopardizes the
mother because catastrophic bleeding may occur
when the implanting pregnancy erodes blood vessels
or ruptures of the tubal wall
IMPLANT LOCATIONS
Tubal 95% (80% ampullary portion)
Ovarian <1%
Abdominal 1-2%
Cervical 0.15%
Cornual 2%
ETIOLOGY
•Salpingitis have 6-fold increase the risk of ectopic
pregnancy
•Operation of tubal
•IUD(intrauterine device)
•Dysfunction of tubal
•Orther: endometriosis
OUTCOMES OF ECTOPIC PREGNANCY
Tubal abortion
8-12 weeks ampullary portion
Rupture of tubal pregnancy
5 weeks isthmic portion
Tubal abortion with subsequent implantation
on an intraperitoneal structure for example liver
pregnancy
CLINICAL MANIFESTATION OF ECTOPIC
PREGNANCY
Amenorrhea 70-80% 6-8 weeks
Abdominal and pelvic pain - the most common
symptom,which is present in nealy all patients. Pain is a result of
distented of tubal and irritation of peritoneum by blood
Irregular vaginal bleeding - results from the sloughing

of the decidua
Shock - result from amount of blood loss

Abdominal mass
PHYSICAL FINDINGS IN TUBAL
PREGNANCY
General findings:
Anemic or pale face
Pulse increased
BP decreased
T < 38 degree
ABDOMINAL EXAMINATION
Distention and tenderness with or without rebound
Decreased bowel sound
Shifting dullness positive
Mass
PELVIC EXAMINATION
Slightly open cervix with bleeding
Cervical motion tenderness
Adnexal tenderness
Adnexal mass
The uterus size may be normal or

enlarged
DIAGNOSTIC PROCEDURES
•Typical cases can be determined easy
•Early ectopic pregnancy or unrupture type

difficulty
•It is nessesary to need assistant examination

HCG test - 80-100% positive
•Urinary HCG level
•Blood HCG level
•If HCG negative,ectopic pregnancy does not be rule out
Type B Utrasound
Culdocentesis
•Aid in the identification of peritoneum bleeding
•Positive (noncloting blood)
•ectopic pregnancy may be confirmed
•Negative ectopic pregnancy does not be depletion
LAPAROSCOPY
It is a direct visualization and accurte method

to diagnosis ectopic pregnancy
Even laparoscopy, however, carries 2-5%

misdiagnosis rate, because an extremely early
tubal pregnancy gestation may not be identified
PATHOLOGY OF
ENDOMETRIUM
•Curettage of the uterine cavity can also help rule out

ectopic pregnancy
•Identification of chorionic villi in curetting may

identify an intrauterine pregnancy
DIFFERENTIAL DIAGNOSIS
Abortion
Acute salpingitis
Acute appendicitis
Rupture of corpus luteum
Torsion of ovarian cyst

TREATMENT OF ECTOPIC
PREGNANCY
Surgical treatment
Salpingectomy
Conservative operation
•Salpingostomy
•Segmental resection and tubal reanastomosis
NONSURGICAL THERAPY
Chemical therapy
Drug: MTX
Indications:
 The diameter of the mass < 3cm
 Unrupture
 Not significantly bleeding
 HCG level < 2000 U/L
ABORTION
DEFINITION
• Abortion is the termination of a pregnancy
before 28 weeks from the first day of the last
menstrual period and the fetus weight
<1000g
CLASSIFICATION
Early abortion <12W
Late abortion 12-28W
Spontaneous abortion
Artificial abortion
ETIOLOGY
Genetic factors
Maternal factors
•Infection
•Systemic factors heart disease sever anemia endocrine
•Reproductive tract abnormality
Immunologic factors
Enviromental factors – Toxin, Radiation,
smoking, alcohol
PATHOLOGY
1.Haemorrhage occurs
in the decidua basalis
leading to local necrosis
and inflammation
2. The ovum, partly or wholly detached, acts as a
foreign body and irritates uterine contractions. The
cervix begins to dilate.
3. Expulsion complete, The
decidua is shed during the next
few days in the lochial flow.
CLINICAL MANIFESTATION
 Haemorrhage is usually the first sign and may

be significantly if placental separation is
incomplete.
 Pain is usually intermittent, ‘like a small labrur’.

It ceases when the abortion is complete.
THREATENED ABORTION
•Low abdominal pain
•Vaginal bleeding
•Cervix is closed
•Unrupture of membrane
•Embryo survive
INEVITABLE ABORTION
•Bleeding increased
•Pain development
•Ruputure of membrane
•Cevix dilation
•Embryo tissue
incarcerated in the cervix
COMPLETE ABORTION
•Uterine contractions are
felt, the cervix dilates and
blood loss continues
•The fetus and placenta

are expelled complete, the
uterus contracts and
bleeding stops
•No further treatment is

needed
INCOMPLETE ABORTION
•In spite of uterine
contractions and cervical
dilatation, only the fetus and
some membranes are
expelled
•The placenta remains
partly attached and bleeding
continues
•This abortion must be
completed by surgical
methods
MISSED ABORTION
Is the retention of a failed intrauterine
pregnancy for a extended period, usually
defined as more than two menstrual cycles
RECURRENT ABORTION
It is a term used when a patient has had two or
more consecutive spontaneous abortions
SEPTIC ABORTION
TREATMENT OF ABORTION
 Incomplete abortion
Remove the embryo and placenta as soon as possible
 Negative pressure suction
 Embryulcia
 Missed abortion
Notice blood clot function prevent DIC
 Septic abortion
Broad-spectrum antibiotics
Removal of placental
tissue with ovum forceps.
Lecture 9
PRETERM AND POSTTERM

DELIVERY
PRETERM DELIVERY
DEFINITION OF TERMS
I. AS TO SIZE
Small-for-gestational age / fetal growth restriction / intrauterine
growth restriction (SGA/IUGR)
• newborns with birthweight below the 10th percentile for
gestational age
Large-for-gestational age (LGA)
• birthweight above the 90th percentile
Appropriate-for-gestational age (AGA)
• newborns with weight between the 10th and 90th percentiles
II. AS TO AOG
Preterm or premature birth
• neonates born too early
• delivery before 37 completed weeks
Term
• 37 – 42 weeks
Post term
• > 42 weeks
CAUSES OF PRETERM BIRTH
I. Medical and Obstetrical Complications
• Preeclampsia
• Fetal distress
• Fetal growth restriction
• Placental abruption
• Fetal death
• Spontaneous preterm labor with or without

prematurely ruptured membranes
II. Threatened Abortion
• Vaginal bleeding or spotting is associated with

increased incidence of subsequent pregnancy loss
prior to 24 weeks, preterm labor, and placental
abruption
III. Lifestyle Factors
1. Cigarette smoking
• Associated with 20 % of low-birthweight
neonates, 8 % of preterm births, and 5 % of
perinatal deaths
• 2- to 5-fold risk of preterm prematurely ruptured
membranes, a 1.2- to 2-fold risk of preterm
delivery, and a 1.5- to 3.5-fold risk of fetal growth
restriction
• increased incidence of ectopic pregnancy,
placental abruption, and placenta previa
2. inadequate maternal weight gain during

pregnancy
3. illicit drug
4. Other maternal factors:

• young or advanced maternal age
• poverty
• short stature
• vitamin C deficiency
• occupational factors: prolonged walking or
standing, strenuous working conditions, and long
weekly work hours
5. Psychological and physical stress - seldom been

formally studied but seem intuitively important
6. Both stress and higher levels of maternal serum

cortisol have been associated with spontaneous
preterm birth
7. significant link between low birthweight and

preterm birth in women injured by physical abuse
8. maternal depression was not associated with

birth prior to 35 weeks
IV. Genetic Factors
• gene for decidual relaxin is one candidate
• Fetal mitochondrial trifunctional protein defects

or polymorphism in the interleukin-1 gene
complex, 2-adrenergic receptor, or tumor necrosis
factor- α (TNF- α) may also be involved in preterm
membrane rupture
V. Chorioamnionitis
• Infection of the membranes and amnionic fluid

caused by a variety of microorganisms - possible
causes of ruptured membranes, preterm labor, or
both
• recovery of organisms from the chorioamnion was

significantly increased with spontaneous preterm
labor
IDENTIFICATION OF WOMEN AT RISK FOR
SPONTANEOUS PRETERM LABOR
1. Risk-Scoring Systems
• Not effective
2. Prior Preterm Birth

• strongly correlates with subsequent preterm labor
• risk of recurrent preterm delivery for women whose
first delivery was preterm was increased threefold
compared with that of women whose first neonate
was born at term
• More than a third of women whose first two
newborns were preterm subsequently delivered a
third preterm newborn
IDENTIFICATION OF WOMEN AT RISK FOR SPONTANEOUS
PRETERM LABOR
3. Incompetent Cervix
• recurrent, painless cervical dilatation and
spontaneous midtrimester birth in the absence of
spontaneous membrane rupture, bleeding, or
infection
4. Cervical Dilatation
• Asymptomatic cervical dilatation after midpregnancy
has gained attention as a risk factor for preterm
delivery, although some clinicians consider it to be a
normal anatomical variant, particularly in parous
women
• Recent studies suggested that parity alone is not
sufficient to explain cervical dilatation discovered
early in the third trimester
ULTRASONOGRAPHIC MEASUREMENT OF CERVICAL LENGTH
• mean cervical length at 24 weeks was about 35 mm, and

those women with progressively shorter cervices
experienced increased rates of preterm birth
• women with a previous preterm birth (< 32 weeks)
should undergo, on her next pregnancy, an ultrasound
examination of cervical length between 16 to 24 weeks
AOG; a shortened cervix ( < 25mm ) correlates with
another subsequent preterm birth before 35 weeks
ULTRASONOGRAPHIC MEASUREMENT OF CERVICAL LENGTH
• the value of cervical length to predict birth before

35 weeks is apparent only in women at high risk
for preterm birth
• routine cervical ultrasonography currently has no

role in the screening of normal-risk pregnant
women
• efficacy of cerclage for women with only a

shortened cervical length with no history of
recurrent midpregnancy loss is inconclusive
5. Signs and Symptoms
• painful or painless uterine contractions

• pelvic pressure
• menstrual-like cramps
• watery vaginal discharge
• pain in the low back

6. Ambulatory Uterine Monitoring
• an external tocodynamometer is belted around

the abdomen and connected to an electronic
waist recorder
• Uterine activity is transmitted via telephone daily
• Women are educated concerning signs and

symptoms of preterm labor, and clinicians are
kept apprised of their progress
• ACOG concluded that the use of this expensive,

bulky, and time-consuming system does not
reduce the rate of preterm birth
PRETERM LABOR
7. Fetal Fibronectin
• glycoprotein produced in 20 different molecular
forms by hepatocytes, fibroblasts, and endothelial
cells, and by fetal amnion
• Present in high concentrations in maternal blood
and in amnionic fluid which play a role in
intercellular adhesion during implantation and in
the maintenance of placental adhesion to the
decidua
• detected in cervicovaginal secretions in women
who have normal pregnancies with intact
membranes at term, and it appears to reflect
stromal remodeling of the cervix prior to labor
PRETERM LABOR
• fibronectin detection in cervicovaginal secretions

prior to membrane rupture was a possible marker
for impending preterm labor
• measured using an enzyme-linked
• immunosorbent assay
• values exceeding 50 ng/mL are considered
positive
• positive value for cervical or vaginal fetal
fibronectin assay, as early as 8 to 22 weeks -
powerful predictor of subsequent preterm birth
PRETERM LABOR
8. Bacterial Vaginosis
• not an infection, a condition in which the normal,
hydrogen peroxide–producing lactobacillus-
predominant vaginal flora is replaced with
anaerobes, Gardnerella vaginalis, Mobiluncus
species, and Mycoplasma hominis
• associated with spontaneous abortion, preterm
labor, preterm ruptured membranes,
chorioamnionitis, and amnionic fluid infection
• may precipitate preterm labor by a mechanism
similar to that proposed for amnionic fluid
infection
• screening and treatment have not been shown to
prevent preterm birth
PRETERM LABOR
9. Lower Genital Tract Infection

• Currently, screening and treatment to prevent
preterm birth in women with either Chlamydia
trachomatis or Trichomonas vaginalis is not
recommended
PRETERM LABOR
10. Salivary Estriol

• increased maternal salivary estriol concentration
and subsequent preterm birth
11. Periodontal Disease

• Oral bacteria - Fusobacterium nucleatum and
Capnocytophaga species, have been associated
with upper genital tract infection in pregnant
women
• sevenfold risk of preterm birth
INFECTIONS RELATED TO PRETERM
LABOR
INFECTION ETIOLOGY DIAGNOSTIC FEATURES MANAGEMENT
Bacterial Gardnerella vaginalis, -Vaginal pH > 4.5 Metronidazole 500
vaginosis Mobiluncus species, and -Homogenous vaginal mg BID for 7 days
Mycoplasma hominis discharge
- Amine odor when vaginal
secretions are mixed with
KOH
- Vaginal epithelial cells
heavily coated with bacilli
“clue cells”
- Gram staining of vaginal
secretions show few white
cells along with mixed flora
as compared with the
normal predominance of
lactobacilli
LABOR
Trichomoniasis and Trichomonas vaginalis - demonstration of - Routine screening

Candida Vaginitis Trichomonads by wet and treatmetn for this
mount of vaginal condition cannot be
secretions; Trichomondas recommended
are identified most - Metronidazole 250 mg
accurately by culture TID for 7 days
using Diamond medium, - Miconazole,
Direct immunoflorescent, Clotrimazole and
Monoclonal Ab staining is nystatin are effective
sensitive and specific for vaginal candidiasis
alternative
Lower genital tract Chlamydia - Genitourinary Erythromycin 500 mg
infection trachomatis Chlamydial infection at 24 PO QID for 7 days
weeks but not at 28 weeks
detected via ligase chain
reaction assay was
associated with a 2-fold
increase in subsequent
spontaneous preterm
birth
LABOR
Periodontitis Fusobacterium Teeth cleaning

nucleatum and and polishing;
Capnocytophaga deep root
species scaling and
planning plus
metronidazole
MANAGEMENT OF PRETERM LABOR
I. PRETERM RUPTURED MEMBRANES
• A history of vaginal leakage of fluid should

prompt a sterile speculum examination to
visualize gross vaginal pooling of amnionic fluid,
clear fluid from the cervical canal, or both
• Confirmation by ultrasonographic examination to

assess amnionic fluid volume; to identify the
presenting part; and if not previously determined,
to estimate gestational age
After confirmation of ruptured membranes, the

following steps are taken:
1. Cervical dilatation and effacement are estimated

visually during a sterile speculum examination
2. If < 34 weeks, if there are no maternal or fetal

indications for delivery, the woman and her fetus
are initially observed in the labor unit. Broad-
spectrum parenteral antimicrobials are begun to
prevent chorioamnionitis. Fetal heart rate and
uterine activity are monitored for cord
compression, fetal compromise, and early labor.
3. If < 34 weeks, betamethasone (two 12-mg doses

intramuscularly 24 hours apart) or
dexamethasone (6 mg intramuscularly every 12
hours for four doses) is given
4. If the fetal status is reassuring, and if labor does

not ensue, the woman is usually transferred to an
antepartum unit and observed for labor, infection,
or fetal jeopardy
• For pregnancies 34 weeks or beyond, if labor does

not begin spontaneously, then it is induced with
intravenous oxytocin unless contraindicated.
Cesarean delivery is performed for usual
indications, including failed induction of labor
• During labor or induction, a parenteral

antimicrobial is given for prevention of group B
streptococcal infection
PRETERM LABOR WITH INTACT FETAL MEMBRANES
Diagnosis
Criteria to document preterm labor:

• Contractions of four in 20 minutes or eight in 60
minutes plus progressive change in the cervix
• Cervical dilatation greater than 1 cm
• Cervical effacement of 80 percent or greater
PRETERM LABOR WITH INTACT FETAL MEMBRANES
• managed the same as for those with preterm
ruptured membranes
• The cornerstone of treatment is to avoid delivery
prior to 34 weeks, if possible
1. Amniocentesis to detect infection (not usually
indicated)
2. Steroid therapy to enhance fetal lung maturation
3. Thyrotropin-Releaasing hormone for fetal lung
maturation
4. Antenatal Phenobarbital and Vitamin K –
combination is not recommended for the
prevention of neonatal intraventricular
hemorrhage
INTERVENTIONS TO DELAY PRETERM
BIRTH
1. Antimicrobials – not recommended for the sole

purpose of preventing delivery
2. Emergency cerclage
3. Treatment for bacterial vaginosis

INHIBITION OF PRETERM LABOR
1. Bed rest
2. Hydration and sedation
3. Beta adrenergic receptor agonist

 Ritodrine
 Terbutaline, Isoxuprine
Beta adrenergic drugs
 Parenteral beta agonists prevent preterm
birth for at least 48 hours facilitating maternal
transport and giving of steroids
4. Magnesium sulfate
• Ionic magnesium in a sufficiently high concentration can
alter myometrial contractility
• role is presumably that of a calcium antagonist
• Clinical observations are that magnesium in
pharmacological doses may inhibit labor
• intravenously administered magnesium sulfate—a 4-g
loading dose followed by a continuous infusion of 2 g/hr—
usually arrests labor
5. Prostaglandin inhibitors (ex. Indomethacin)
6. Calcium channel blockers
• Nifedipine
7. Atosiban (oxytocin antagonist)
8. Nitric oxide donors (nitroglycerin) – not effective
RECOMMENDED MANAGEMENT OF
PRETERM LABOR
The following considerations should be given to

women in preterm labor:
1. Confirmation of preterm labor
2. For pregnancies less than 34 weeks in women
with no maternal or fetal indications for delivery,
close observation with monitoring of uterine
contractions and fetal heart rate is appropriate,
and serial examinations are done to assess
cervical changes
3. For pregnancies less than 34 weeks,
glucocorticoids are given for enhancement of
fetal lung maturation
RECOMMENDED MANAGEMENT OF
PRETERM LABOR
The following considerations should be given to women
in preterm labor:
4. For pregnancies less than 34 weeks in women who are
not in advanced labor, some practitioners believe it is
reasonable to attempt inhibition of contractions to
delay delivery while the women are given
glucocorticoid therapy and group B streptococcal
prophylaxis
5. For pregnancies at 34 weeks or beyond, women with
preterm labor are monitored for labor progression and
fetal well-being
6. For active labor, an antimicrobial is given for
prevention of neonatal group B streptococcal infection
INTRAPARTUM MANAGEMENT
1. Labor
• Continuous electronic monitoring is preferred
• Fetal tachycardia, especially with ruptured
membranes, is suggestive of sepsis
• Intrapartum acidemia may intensify some of the
neonatal complications usually attributed to
preterm delivery
2. Prevention of neonatal group B Streptococcal

infections
• The American College of Obstetricians and
Gynecologists, recommend either penicillin G or
ampicillin intravenously every 6 hours until
delivery for women in preterm labor
INTRAPARTUM MANAGEMENT
3. Delivery
• Staff proficient in resuscitative techniques commensurate
with the gestational age of the newborn and fully oriented
to any specific problems should be present
4. Prevention of neonatal intracranial hemorrhage

• Preterm newborns have germinal matrix bleeding that can
extend to more serious intraventricular hemorrhage
• It was hypothesized that cesarean delivery to obviate
trauma from labor and vaginal delivery might prevent these
complications
• This has not been validated by most subsequent studies
• hemorrhages related to whether or not the fetus had been
subjected to the active phase of labor, defined as the
interval before 5 cm cervical dilatation
• avoidance of active-phase labor is impossible in most
preterm births because the route of delivery cannot be
decided until the active phase labor is firmly established
POSTTERM DELIVERY
DEFINITION OF TERMS
• Postmature - infant with recognizable clinical

features indicating a pathologically prolonged
pregnancy
• Postdates - should be abandoned, because the

real issue in many postterm pregnancies is "post-
what dates?“
• Postterm or Prolonged Pregnancy - preferred

expression for an extended pregnancy
• “Postmature" is reserved for a specific clinical

fetal syndrome
• According to ACOG(1997) : 42 completed weeks

(294 days) or more from the first day of the last
menstrual period
Postmaturity Syndrome
Characteristic appearance / Features:

• wrinkled, patchy, peeling skin; a long, thin body
suggesting wasting; and advanced maturity
because the infant is open-eyed, unusually alert,
and appears old and worried-looking
• Skin wrinkling prominent on the palms and soles
• Nails are long
FETAL DISTRESS IN POSTTERM PREGNANCY
• antepartum fetal jeopardy and intrapartum fetal

distress were the consequence of cord
compression associated with oligohydramnios
• one or more prolonged decelerations preceded

three fourths of emergency cesarean deliveries
for fetal jeopardy
• findings are consistent with cord occlusion as the

proximate cause of fetal distress
• other correlates found were oligohydramnios and

viscous meconium
FETAL DISTRESS IN POSTTERM PREGNANCY
Prolonged fetal heart rate deceleration prior to
emergency cesarean delivery in a postterm pregnancy
with oligohydramnios
FETAL GROWTH RESTRICTION IN POSTTERM PREGNANCY
• stillbirths were more common among growth-

restricted infants who were delivered at 42 weeks
or beyond
• one third of the postterm stillbirths were growth

restricted
• morbidity and mortality were significantly

increased in the growth-restricted infants
MANAGEMENT OF POSTTERM PREGNANCY
• Antepartum interventions are indicated in cases

of postterm pregnancies
• When to induce? 41 or 42 weeks?
• 41 weeks with favorable cervix, induce lab or
• 41 weeks with unfavorable cervix, antepartum

fetal testing
• 42 weeks, whether the cervix is favorable or not,

labor is generally induced
UNFAVORABLE CERVIX
• A cervix that is closed, uneffaced with a bishop

score of less than 7
• women in whom there was no cervical dilatation

at 42 weeks had a twofold increased cesarean
delivery rate for "dystocia“
• cervical length of 3 cm or less determined by

transvaginal ultrasonography was predictive of
successful induction
UNFAVORABLE CERVIX
• The American College of Obstetricians and
Gynecologists (1997) has concluded that
prostaglandin gel can be used safely in postterm
pregnancies
Sweeping or stripping of the membranes:

• decreased the frequency of postterm pregnancy.
• stripping did not modify the risk for cesarean
delivery and maternal and neonatal infections were
not increased
Station of the vertex is important in predicting

successful postterm induction.
Table 37–3. Evaluation and Management of Postterm Pregnancy
1. Postterm pregnancy is defined as a pregnancy that has extended to or beyond 42 completed weeks.
2. Women with a postterm gestation who have an unfavorable cervix can either undergo labor induction or be managed
expectantly.
3. Prostaglandin can be used for cervical ripening and labor induction.
4. Delivery should be effected if there is evidence of fetal compromise or oligohydramnios.
5. It is reasonable to initiate antenatal surveillance between 41 and 42 weeks despite lack of evidence that monitoring improves
outcomes.
6. A nonstress test and amnionic fluid volume assessment should be adequate, although no single method has been shown to
be superior.
7. Many recommend prompt delivery in a woman with a postterm pregnancy, a favorable cervix, and no other complications.
From the American College of Obstetricians and Gynecologists (2004)

Lecture 10
FETAL DISTRESS
DEFINITION
•Fetal distress is the term commonly used to describe

fetal hypoxia
•It is a clinical diagnosis made by indirect methods and

should be defined as:
Hypoxia that may result in fetal damage / death if not
reversed or the fetus delivered immediately
•It includes acute distress and chronic distress

ETIOLOGY
Maternal:
 poor placental perfusion
 hypovolaemia
 hypotension
 myometrial hypertonus
• prolonged labor
• excess oxytocin
ETIOLOGY
Fetal:
 cord compression
• oligohydramnios
• entanglement
• prolapse
 pre-existing hypoxia or growth retardation
 infection
 cardiac
MECHANISM
• There are potentially limitless causes for fetal

distress, but several key mechanisms are usually
involved
• Contractions reduce temporarily placental blood

flow and can compress the umbilical cord
• If a women is in labor longer then this can cause

fetal distress via the above mechanism
MECHANISM
• Acute distress can be a result of:
 placental abruption
 prolapse of the umbilical cord (especially with
breech presentations)
 hypertonic uterine states
 use of oxytocin
• Hypotension can be caused by either epidural

anesthesia or the supine position, which reduces
inferior vena cava return of blood to the heart
• The decreased blood flow in hypotension can be a

cause of fetal distress
SIGNS AND SYMPTOMS
Acute fetal distress

SIGNS AND SYMPTOMS
• Cardiotocography signs:
 Increased / decreased fetal heart (tachycardia and
bradycardia), especially during and after a
contraction decreased varibility in the fetal heart rate
 Abnormal fetal heart rate (< 120 or > 160 bpm)

• A normal fetal heart rate may slow during a contraction
but usually recovers to normal as soon as the uterus
relaxes
• A very slow fetal heart rate in the absence of

contractions or persisting after contractions is
suggestive of fetal distress
SIGNS AND SYMPTOMS
• A rapid fetal heart rate may be a response to:
 maternal fever
 drugs
 hypertension
 amnionitis
• In the absence of a rapid maternal heart rate, a
rapid fetal heart rate = a sign of fetal distress
• For a diagnosis of fetal distress to be made, one or
more of the following must be present:
 persistent severe variable deceleration
 persistent and non-remediable late declarations
 persistent severe bradycardia
SIGNS AND SYMPTOMS
• Amniotic fluid is contaminated by meconium
• There are 3 degrees about contaminated
 I - slight contamination
• The color of the amniotic fluid = slight green
 II - mild contamination
• Color of the amniotic fluid = dark green
 III - severe contamination

• Color of the amniotic fluid is dark yellow.
• If the amniotic fluid is severely contamination, it
suggests the, fetal distress - it must be managed as
soon as possible
SIGNS AND SYMPTOMS
• Decreased fetal movement felt by the mother
• Biochemical signs - assessed by collecting a small

sample of baby‘s blood from a scalp prick through
the open cervix in labor:
 Fetal acidosis elevated fetal blood lactate levels
 A fetal scalp pH < 7.2 , Po2 >60mmHg suggests

fetal distress
Chronic Fetal Distress
SIGNS AND SYMPTOMS
• Decreased or disappear fetal movement:
 < 10 times per 12 hours is regarded as decreased
 With the first effect of hypoxia, the fetal movement

is increased
 If the hypoxia persists, the fetal movement is
decreased, and may disappear
 If the fetal movement lost, the fetal heart beat will
be disappearing within 24 hours
Cautions: Dangerous for the fetus if the fetal

movement disappear. Management immediately!!
SIGNS AND SYMPTOMS
• Abnormal cardiotocography signs:

 Slow fetal heart rate(<120bpm) or rapid
fetal heart rate (>180bpm) last more than
10 min in the absence of contractions is
suggestive of fetal distress
 The fetal heart rate > 160 bpm , especially

> 180 bpm, it suggests early hypoxia,
unless the maternal heart rate is faster
SIGNS AND SYMPTOMS
• FHR < 120bpm, typically less than 100bpm

 It is very danger for fetus
• The fetal heart rate normally show continuous

minor variations, with a range of about 5 bpm,
loss of base line variability implies that the
cardiac reflexes are impaired, either from the
effect of hypoxia or of drugs such as valium
 It may be serious
SIGNS AND SYMPTOMS
• Early deceleration: with each contraction the rate
often slows, but it returns to normal soon after
removal of the stress
• The early deceleration in the heart rate start within

30 seconds of the onset of the contraction and
return rapidly to the baseline rate
• It is not of serious significance as a rule and

indicate that while the fetus is undergoing some
stress the cardiac control mechanisms are
responding normally
EARLY DECELERATION
SIGNS AND SYMPTOMS
• Variable deceleration: no consistent relationship

with uterine contraction.
• It is sometimes caused by compression of the

umbilical cord between the uterus and the fetal
body, or because it is looped round some part of
the fetus
• Provided that it does not persist for more than a

few minutes it may have little significance, but
persistence for more than 15 minutes would call for
treatment
VARIABLE DECELERATION
SIGNS AND SYMPTOMS
• The most serious pattern of heart rate changes is

fetal bradycardia with loss of baseline variability
and late decelerations
• Decrease (defined as onset of deceleration to nadir

=30 seconds) and return to baseline FHR
associated with a uterine contraction.
• The deceleration is delayed in timing, with the

nadir of the deceleration occurring after the peak
on the contraction
LATE DECELERATION
BIOPHYSICAL PROFILE
• Biophysical Profile:
 Amniotic Fluid Volume Normal = 2 Points
 Non-Stress Test Result Positive = 2 Points
 Fetal Breathing Movements Active = 2 Points
 Fetal Extremity/Trunk Movements Active = 2 Points
 Fetal Movements Active= 2 Points
• If Biophysical Profile scores < 4 suggest fetal

distress
• Placental Insufficiency: Low estriol levels, E3 in

urine < 10mg/24h
TREATMENT
• Reposition patient: left-side-lying position
• Administer oxygen by mask
• Perform vaginal examination to check for

prolapsed cord
• Ensure that qualified personnel are in attendance

for resuscitation and care of the newborn
 Qualified personnel for resuscitation and care of

the newborn
TREATMENT
• Each of the following actions should be performed
and documented prior to starting a Cesarean
section for fetal distress:
 Perform vaginal exam to rule out imminent

vaginal delivery
 Initiate preoperative routines
 Monitor fetal heart tones (by continuous fetal

monitoring or by auscultation) immediately prior
to preparation of the abdomen
TREATMENT
• Ensure that qualified personnel are in
attendance for resuscitation and care of the
newborn
• STOP using oxytocin !

 Oxytocin can strengthen the contraction of
uterine which affects the baby's heart rate
INTRAUTERINE FETAL DEATH (IUFD)
DEFINITION:
• dead fetuses or newborns weighing > 500g or > 20
wks gestation
total births 1000 /4.5
DIAGNOSIS:
Absence of uterine growth
Serial ß-hcg
Loss of fetal movement
Absence of fetal heart
Disappearance of the signs & symptoms of pregnancy
X-ray Spalding sign
Robert’s sign
U/S 100% accurate Dx
CAUSES OF IUFD Maternal 5-10%
•Antiphospholipid antibody
•DM
Fetal causes 25-40% •HPT
•Chromosomal anomalies
•Trauma
•Birth defects
•Abnormal labor
•Non immune hydrops
•Sepsis
•Infections
•Acidosis/ Hypoxia
Placental 25-35% •Uterine rupture
•Abruption
•Postterm pregnancy
•Cord accidents
•Drugs
•Placental insufficiency
•Thrombophilia
•Intrapartum asphyxia
•Cyanotic heart disease
•P Previa
•Epilepsy
•Twin to twin transfusion S
•Severe anemia
•Chrioamnionitis
Unexplained 25-35%
A systematic approach to fetal death is valuable in
determining the etiology
B-Maternal History
HISTORY-1 I-Maternal medical conditions
•VTE/ PE
A-Family history •DM
•Recurrent abortions •HPT
•VTE/ PE •Thrombophilia
•Congenital anomalies •SLE
•Abnormal karyptype •Autoimmune disease
•Hereditary conditions •Severe Anemia
•Developmental delay Epilepsy
•
•Consanguinity
•Heart disease
II-Past OB Hx
•Baby with congenital anomaly / hereditary
condition
•IUGR
•Gestational HPT with adverse sequele
•Placental abruption
•IUFD
•Recurrent abortions
HISTORY-1
Specific fetal conditions
•Nonimmune hydrops
Current Pregnancy Hx •IUGR
•Maternal age •Infections
•Gestational age at fetal death •Congenital anomalies
•HPT •Chromosomal abnormalities
•DM/ Gestational D •Complications of multiple gestation
•Smooking , alcohol, or drug abuse
•Abdominal trauma
•Cholestasis
•Placental abruption Placental or cord complications
•Large or small placenta
•PROM or prelabor SROM •Hematoma
•Edema
•Large infarcts
•Abnormalities in structure , length
or insertion of the umbilical cord
•Cord prolapse
•Cord knots
•Placental tumors
2-EVALUATION OF STILL BORN INFANTS
Infant description Placenta

•Malformation •Weight
•Skin staining •Staining
•Degree of maceration •Adherent clots
•Color-pale ,plethoric •Structural abnormality
Umbilical cord •Velamentous insertion
•Prolapse •Edema/hydropic changes
•Entanglement-neck, arms, Membranes
legs •Stained
•Hematoma or stricture •Thickening
•Number of vessels
•Length
Amniotic fluid
•Color-meconium, blood
•Volume
INVESTIGATIONS-3 Fetal investigations
•Fetal autopsy
Maternal investigations
•Karyotype
•CBC
•Bl Gp & antibody screen specimen taken from cord(
•HB A1 C ,blood, intracardiac blood
•Kleihauer Batke test ,body fluid, skin, spleen
•Serological screening for Rubella placental wedge, or amniotic
•CMV, Toxo, Sphylis, Herpes & )fluid
•Fetography
Parovirus •Radiography
•Karyotyping of both parents (RFL,
Baby with malformation
Placental investigations
•Hb electrophorersis
•Chorionocity of placenta in
•Antiplatelet anbin tibodies
twins
•Throbophilia screening
•Cord thrombosis or knots
(antithrombin •Infarcts, thrombosis,
Protein C & S , factor IV leiden,
abruption
Factor II mutation, , lupus •Vascular malformations
anticoagulant, •Signs of infection
anticardolipin antibodies) •Bacterial culture for E.coli,
•DIC
.Listeria, gp B strpt
IUFD COMPLICATIONS
• Hypofibrinogenemia  4-5 wks after IUFD
• Coagulation studies must be started 2 wks after

IUFD
• Delivery by 4 wks or if fibrinogen  < 200mg/ml

PSYCHOLOGICAL ASPECT & COUNSELING
• A traumatic event
• Post-partum depression
• Anxiety
• Psychotherapy
• Recurrence 0-8% depending on the cause of IUFD

Lecture 11
COMPLICATIONS DURING PREGNANCY

PREGNANCY-RELATED COMPLICATIONS
• Hyperemesis Gravidarum
 Excessive Nausea and vomiting
• Electrolyte/acid base imbalance
• Significant weight loss
• Decreased turgor
• Decreased urine output
• High hematocrit
• Treatment
 Correct dehydration and inadequate nutrition
NURSING CARE FOR HYPEREMESIS
• Patient Education
 Reduce factors that trigger nausea and vomiting
 Keep accurate I&O
 Frequent, small meals
• Easley digested carbohydrates
• Eliminate foods with strong odors
• Drinking liquids between meals
• Reduce stress
SIGNS AND SYMPTOMS OF
HYPOVOLEMIC SHOCK
• Changes in fetal heart • Falling blood pressure
rate (increased, (hypotension)
decreased, less
• Decreased or absent
fluctuation)
urinary output (usually
• Rising, weak pulse less than 30 ml/hr)
(tachycardia) • Pale skin or pale
• Rising respiratory rate mucous membranes
(tachypnea)
• Cold, clammy skin
• Shallow, irregular
• Faintness
respirations; air hunger
• Thirst
DISSEMINATED INTRAVASCULAR
COAGULATION (DIC)
• A pathologic form of coagulation in which clotting
factors are consumed to such
extent that generalized
bleeding can occur, usually
associated with:
 abruptio placentae
 eclampsia
 intrauterine fetal demise
 amiotic fluid embolism

 hemorrhage
PREGNANCY COMPLICATED
BY MEDICAL CONDITIONS
• DIABETES MELLITUS
 Type 1 Diabetes mellitus
• Physiological disorder of the pancreas resulting in

insulin deficiency
 Type 2 Diabetes Mellitus
• Insulin resistance
• Familiar predisposition
 Gestational diabetes mellitus (GDM)

EFFECTS OF DIABETES IN PREGNANCY
• Maternal Effects
 Spontaneous abortion
 Gestational hypertension
 Preterm labor and premature rupture of the

membranes
 Hydramnios/ployhydramnios (excessive
amniotic fluid)
 Infections (vaginitis, UTI)
 Large for gestational age (LGA) fetus

EFFECTS OF DIABETES IN PREGNANCY
• Fetal/Neonatal effects
 Congenital abnormalities
 Macrosomia
 Intrauterine growth restriction

(IUGR)
 Birth injury
 Delayed lung maturity
 Neonatal: hypoglycemia, hypocalcemia,

hyperbilirubinemia/jaundice and polycythemia
GESTATIONAL DIABETES
• If woman cannot increase her insulin production,

then she will have periods of hyperglycemia
• Because fetus is continuously drawing glucose

from the mother, she will also experience
hypoglycemia between meals and during the
night
• During 2nd and 3rd trimester, fetus is at risk for

organ damage from hyperglycemia, because fetal
tissue has increased tissue resistance to maternal
insulin action
TREATMENT
• Diet
• Monitoring blood glucose levels
• Ketone monitoring
• Exercise
• Fetal assessment
CARE DURING LABOR OF THE WOMAN
WITH GDM
• Intravenous infusion of dextrose may be needed
• Regular insulin
• Assess blood glucose levels

hourly and adjust insulin
administration accordingly
CARE OF THE NEONATE OF A WOMAN WITH
GDM
• May have the following occur:
 Hypoglycemia
 Respiratory distress
• Injury related to macrosomia
• Blood glucose monitored closely for at least the

first 24 hours after birth
• Breastfeeding should be
encouraged
HEART DISEASE
• Manifestations
 Increased levels of clotting factors
 Increased risk of thrombosis
• If woman’s heart cannot handle increased

workload, then congestive heart failure (CHF)
results
• Fetus suffers from reduced placental blood flow

SIGNS OF CHF DURING PREGNANCY
• Persistent cough • Severe pitting edema of

the lower extremities /
• Moist lung sounds generalized edema
• Fatigue or fainting on • Palpitations

exertion
• Changes in fetal heart
• Difficulty breathing on rate
exertion  Indicating hypoxia /
growth restriction
• Orthopnea
TREATMENT
• Under care of both obstetrician and cardiologist
• Priority care is limiting physical activity

• Drug therapy
• May include:
• β-adrenergic blockers
• anticoagulants
• diuretics
• Vaginal birth is preferred because it carries less

risk for infection or respiratory complications
ANEMIA
• Anemia is the reduced ability of the blood to carry

oxygen to the cells
• Four types are significant during pregnancy

 Two are nutritional:
• Iron deficiency
• Folic acid deficiency
 Two are genetic disorders:
• Sickle cell disease

NUTRITIONAL ANEMIAS
• Symptoms:
 Easily fatigued
 Skin and mucous membranes

are pale
 Shortness of breath
 Pounding heart
 Rapid pulse (with severe anemia)

IRON DEFICIENCY ANEMIA
• RBCs are small (microcytic) and pale

(hypochromic)
• Prevention:
 Iron supplements
 Vitamin C may enhance

absorption
 Do not take iron with milk or antacids
• Calcium impairs absorption

IRON DEFICIENCY ANEMIA
• Treatment:
 Oral doses of elemental iron
 Continue therapy for about 3 months after

anemia has been corrected
FOLIC ACID DEFICIENCY ANEMIA
• Large, immature RBCs (megaloblastic anemia)
• Anticonvulsants, oral contraceptives, sulfa drugs,

and alcohol can decrease absorption of folate
from meals
• Folate is essential for normal

growth and development
• Prevention:
 Daily supplement of 400 mcg
(0.4 mg)
FOLIC ACID DEFICIENCY ANEMIA
• Treatment:
 Folate deficiency is treated with folic acid

supplementation
 1 mg/day (over twice the amount of the

preventive supplement)
• Dose may be higher for women

who have had a previous child
with a neural tube defect
GENETIC ANEMIAS
• Sickle cell anemia

 Autosomal recessive disorder
 Abnormal hemoglobin
 Causes erythrocytes to become distorted and sickle
(crescent) shaped during hypoxic or acidotic episodes
 Abnormally shaped blood cells do not flow smoothly
 Can clog small blood vessels
 Pregnancy can cause a crisis
 Massive erythrocyte destruction and vessel occlusion
 Risk to fetus if occlusion occurs in vessels that supply
the placenta
 Can lead to preterm birth, growth restriction, and fetal
demise
 Oxygen and fluids are given continuously throughout
labor
GENETIC ANEMIAS
• Thalassemia
 Pregnancy can cause a crisis
 Massive erythrocyte destruction and vessel occlusion
 Risk to fetus if occlusion occurs in vessels that supply

the placenta
 Can lead to preterm birth, growth restriction, and fetal

demise
 Oxygen and fluids are given continuously throughout

labor
 Genetic trait causes abnormality in one of two chains of

hemoglobin
GENETIC ANEMIAS
• Thalassemia
 β chain seen most often in United States
 Can inherit abnormal gene from each parent, causing β-

thalassemia major
 If only one abnormal gene is inherited, then infant will

have β-thalassemia minor
 Woman with β-thalassemia minor has few problems,

other than mild anemia
 Fetus does not appear affected
 Iron supplements may cause iron overload

GENETIC ANEMIAS
NURSING CARE FOR WOMEN WITH
ANEMIAS DURING PREGNANCY
• Teach woman which foods are high in iron and
folic acid
• Teach woman how to take supplements

 Do not take iron supplements at the same time when
drinking milk
 Do not take antacids with iron
 When taking iron, stools will be dark green to black
• The woman with sickle cell disease requires close

medical and nursing care
 Teach her to prevent dehydration and activities that
cause hypoxia
 Teach her to avoid situations where exposure to
infections are more likely
 Teach her to promptly report any signs of infections
INFECTIONS
• Acronym TORCH is used to describe infections

that can be devastating to the fetus or newborn:
 Toxoplasmosis
 Other infections (Coxsackievirus, Syphilis,

Varicella-Zoster Virus, HIV, and Parvovirus B19)
 Rubella
 Cytomegalovirus
 Herpes simplex
VIRAL INFECTIONS
• No effective therapy
• Immunizations can prevent some infections

CYTOMEGALOVIRUS (CMV)
• Infected infant may have: • Treatment:

 Mental retardation  No effective
treatment is known
 Seizures
 Therapeutic
 Blindness abortion may be
offered if CMV
 Deafness infection is
discovered early in
 Dental abnormalities pregnancy
 Petechiae
RUBELLA
• Mild viral disease

• Low fever and rash
• Destructive to developing fetus
 If it occurs early in pregnancy, it can disrupt formation
of major body systems
 If it occurs later in pregnancy, it can cause damage to

organs already formed
• If woman receives a rubella vaccine prior to

pregnancy, then she should not get pregnant for
at least 3 months
• Not given during pregnancy because vaccine is
from a live virus
RUBELLA
• Effects on embryo or fetus:
 Microcephaly (small head size)
 Mental retardation
 Congenital cataracts
 Deafness
 Cardiac effects
 Intrauterine growth restriction (IUGR)

HERPES VIRUS
• Two types:
 Type 1: Likely to cause fever blisters or cold
sores
 Type 2: Likely to cause genital herpes
• After primary infection, herpesvirus lies dormant

in the nerves and can reactivate at any time
• Initial infection during first half of pregnancy may

cause:
 spontaneous abortion
 IUGR
 preterm labor
HERPES VIRUS
• Infant can be infected in one of two ways:

 Virus ascends into the uterus after the
membranes rupture
 Infant has direct contact with infectious

lesions during vaginal delivery
• Neonatal herpes
 Can be either localized or disseminated
(widespread)
 High mortality rate

HERPES VIRUS
• Treatment and Nursing Care:
 Avoid contact with lesions
• If woman has active genital herpes when

membranes rupture or labor begins
 Cesarean delivery may be required if lesions

are present at time of delivery
 Mother and infant do not need to be isolated as

long as direct contact with lesions is avoided
HEPATITIS B
• Transmitted by blood, saliva, vaginal secretions,

semen, and breast milk; can also cross the
placenta
• Fetus may be infected transplacentally or by

contact with blood or vaginal secretions during
delivery
• Upon delivery, the neonate should receive a

single dose of hepatitis B immune globulin,
followed by the hepatitis B vaccine
RISK FACTORS FOR HEPATITIS B
• Intravenous drug users

• Persons with multiple sexual partners
• Persons with repeated infection with STI
• Health care workers with occupational exposure
to blood products and needle sticks
• Patients who are on hemodialysis
• Recipients of multiple blood transfusions or other
blood products
• Household contact with hepatitis carrier or
patient on hemodialysis
• Persons arriving from countries where there is a
higher incidence of hepatitis B
HUMAN IMMUNODEFICIENCY VIRUS (HIV)
• Virus that causes AIDS • Acquired in one of 3

• Cripples immune ways:
system  Sexual contact
• No known  Parenteral or mucous
membrane exposure to
immunization or infected body fluids
curative treatment  Perinatal exposure
• Infant may be
infected:
 Transplacentally
 Through contact with
infected maternal
secretions at birth
 Through breast milk
NURSING CARE IN HIV
• Educate the woman who is HIV positive on

methods to reduce the risk of transmission to her
developing fetus/infant
• Pregnant women with AIDS are more susceptible

to infection
• Breastfeeding is contraindicated for mothers who

are HIV positive
NONVIRAL INFECTIONS
• Toxoplasmosis
 A parasite acquired by contact with cat feces or
raw meat
 Transmitted through the placenta
 Congenital toxoplasmosis includes the

following possible signs:
• Low birth weight
• Enlarged liver and spleen
• Jaundice
• Anemia
NONVIRAL INFECTIONS
• Toxoplasmosis
 Treatment
• Therapeutic abortion
 Preventive measures
• Cook all meat thoroughly
• Wash hands and all kitchen surfaces after

handling raw meat
• Avoid uncooked eggs and unpasteurized
milk
• Wash fresh fruits and vegetables well
GROUP B STREPTOCOCCUS (GBS)
INFECTION
• Leading cause of • GBS significant cause
perinatal infection with of maternal
high mortality rate postpartum infection
 Symptoms include:
• Organism found in • Elevated
woman’s rectum, temperature within
vagina, cervix, throat, 12 h after delivery
or skin • rapid heart rate
• abdominal distention
• The risk of exposure to
the infant is greater if • Can be deadly to the
the labor is long or the infant
woman experiences
premature rupture of • Treatment
membranes  Penicillin
SEXUALLY TRANSMITTED INFECTIONS
(STI)
• Common mode of transmission is sexual
intercourse
• Infections that can be transmitted:

 syphilis
 gonorrhea
 chlamydia
 trichomoniasis
 condylomata acuminata
• Vaginal changes during pregnancy increase the

risk of transmission
URINARY TRACT INFECTIONS
• Pregnancy alters self- • May develop cystitis:

cleaning action due to  Burning with urination
pressure on urinary
structures  Increased frequency and
urgency of urination
• Prevents bladder from  Normal or slightly

emptying completely elevated temperature
• Retained urine • Pyelonephritis:

becomes more  High fever
alkaline
 Chills
 Flank pain or tenderness
 Nausea and vomiting

ENVIRONMENTAL HAZARDS DURING
PREGNANCY
• Substance abuse
 Questions should focus on how the information
will help nurses and physicians provide the
safest and most appropriate care to the
pregnant woman and her infant
• Alcohol
 A single episode of consuming two alcoholic
drinks can lead to the loss of some fetal brain
cells
RHESUS (Rh) ISOIMMUNIZATION
Rh ISOIMMUNIZATION
Blood groups (1900):
Antigens: Antibodies:
O (45%) AntiA+Anti B
A (40%) Anti B
B (10%) Anti A
AB (5%)
A and B : dominant
O : recessive
Other systems:
 kell-antikell,
 luther,
 Duffy, etc.
Rh ISOIMMUNIZATION
Rhesus factor (1940):
Agglutinogen (C,D,E) - mainly D

C,D,E - dominant antigen / d,e - recessive
Rh ISOIMMUNIZATION
- Rh positive (85%) - homozygous (DD) (35%),
or heterozygous (Dd) (50%)
Rh negative (15%)
- Incidence of Rh-ve in far east is about 1%
Rh ISOIMMUNIZATION
• So in response to introduction of foreign
protein (antigen)  production of antibody to
neutralize the antigen
• In ABO and other non Rh-incompatibility: It

usually causes mild anaemia, mainly as there
is no intrapartum boosting
• In Rhesus isoimmunization: mainly (D), but

C, E can produce antibodies
Rh ISOIMMUNIZATION
Feto-maternal haemorrhage: leakage of fetal
Rh+ cells in the Rh- maternal circulation
Examples:
- Spontaneous abortion
- Induced abortion
- APH
- E.C.V.
- Cordocentesis, CVS, amniocentesis
- Severe preeclampsia
- Ectopic pregnancy
- Caesarean section
- Manual removal of placenta
- Silent feto-maternal hage
Rh ISOIMMUNIZATION
Development of Rhesus antibodies: depends on
factors:
1- Inborn ability to respond
2- protection if ABO incompatible 1\10
3- Strength of Rh antigen stimumlus (CDe=R1)
4- Volume of leaking feta blood (0.25ml)
IgM (7 days) doesn’t cross placenta, then IgG

21 days - crosses placenta
1. Cleared by
Macrophage Mother
2. Plasma
stem cells Primary Response
• 6 wks to 6 M.
• IgM
IgM antibodies
Placental
The First Pregnancy is NOT Affected

Macroph. antigen
Presenting cell Mother
T- helper cell Secondary Response
• Small amount
B cell • Rapid
• IgG
IgG
Anti-D
Placental
Fetal Anemia
2 - If ABO is compatible:
Rh+ fetal cells  remain in circulation (life

span) until removed by (R.E.S)  destroyed
 liberating antigen (D)  isoimmunization
It takes time:
• 1st pregnancy is almost always not affected:
 1% - during labour or 3rd stage)
 10% - 6 months after delivery
 15% by the 2nd pregnancy
Rh ISOIMMUNIZATION
Kleihauer-Betke technique:
• (acid elution test) - measure amount of feto-

maternal haemorrhage
Rh ISOIMMUNIZATION
Mild Cases:
• fetal (RBC) destruction  from anti-D (IgG):
 anaemia  compensating haemopoiesis 
excess of unconjugated bilirubin
Severe Cases:
• excessive destruction of fetal (RBC)  severe
anaemia  hypoxia the tissues  cardiac or
circulatory failure  generalized edema  (H.
failure)  ascitis  IUFD
When excess of unconjugated bilirubin > (310-

350 mol/L)  It passes brain barrier 
(kernicterus)  permanent neurological and
mental disorders
Rh ISOIMMUNIZATION
Fetal and Neonatal Effects:
- Haemolytic anaemia of newborn Hb=14-18g/dl
- Icterus gravis neonatorum Hb=10-14g/dl
- Hydrops fetalis (Erythroblastosis fetalis)

MANAGEMENT OF Rh ISOIMMUNIZATION
I) PROPHYLAXIS
1 - Prevention of Rhesus isoimmunization: Anti D

(RhoD IgG)
• Standard dose for > 20 wks, and ½ standard

dose for < 20 wks - given within 72hours of
the incident
 500 iu = 100 ugm  neutralize 5ml
K-B test if large amount of leaking  another SD
if mother is Rh-, baby Rh+ with no
isoimmunization (checked by indirect or direct
Coombs test)
2 - A.P. administration of anti-D

• SD at 28 wks or at 28 and 36 wks will reduce
Rh isoimmunization
II) 1- Antibody Screening:
• for all pregnant women in ANC for irregular

antibodies (mainly for Rh- women), then start
at 20 wks , and every 4 weeks
2 - Management following detection of Rh
antibodies - in specialized centres
• Quantitative measures of antibodies +
husband genotype
 indirect Coombs
• Amniocentesis once necessary
• Obstetrical management based on timing of
I.U. transfusion (now cordocentesis +
fetoscopy) versus delivery
3 - Amniocentesis:
• Should be performed under ultrasound

guidance if titre > 1\16 = 0.5-1 ugm  2.5-5
I.U
• Timing: 1st amniocentesis - 10 weeks before

previous IUFD
• Start from 20-22 weeks, 2-4 weekly or more

frequent if needed
• Amniotic fluid analysis - spectrophotometry:

optical density at the height of optical density
deviation at wave length 450 nM
CORDOCENTESIS
• IU transfusion (cordocentesis) vs delivery :
 Using Liley’s chart
 Whitefield’s action line
LILEY’S CHART
WHITEFIELD’ ACTION LINE
• Alternatively follow up with Doppler study for
the fetal middle cerebral artery
• Prognosis depends on:
 obstetrical history
 paternal genotype
maternal history (blood transfusion, antibody
titre)
 amniocentesis results
• Delivery: Vaginal versus C-Section
• Intensive plasmaphoresis: when severe

cases anticipated, using continous flow
cell separator, as early as 12 wks
• Postnatal management: for the neonate:
 Direct Coombs test, blood group, Rh
type, Hb, bilirubin
 Mild cases: phototherapy - correction of
acidosis
 Severe cases: exchange transfusion
PREGNANCY INDUCED
HYPERTENSION
655
Index
 Diagnosis
 Etiology
 Pathogenesis
 Pathophysiology
 Prediction and Prevention
 Management
656
 Gestational Hypertension – 3.7% in 150,000
(National Center for Health Statics, 2001)
 Pregnancy-related hypertension :
 Pregnancy-related deaths (3201 in US, 1991-1997)
 Black women are 3.1x to die as white women
 Hypertensive disorders remain among the most

significant and intriguing unsolved problems in ob-
stetrics
657
Diagnosis
 Gestational hypertension
 Preeclampsia
 Eclampsia
 Superimposed preeclampsia (on chronic hy-
pertension)
 Chronic hypertension
658
Gestational hypertension
 BP≥ 140/90mmHg for first time during pregnancy
 No proteinuria
 BP returns to normal < 12 weeks’ postpartum
 Final diagnosis made only postpartum
 May have other signs or symptoms of preeclamp-

sia, for example, epigastric discomfort or thrombo-
cytopenia
659
Preeclampsia
￭ Minimum Criteria
- BP > 140/90 mmHg after 20 wks gestation
- Proteinuria ≥ 300mg/24hrs or ≥1+ dipstick
 Worsening proteinuria
 Epigastric or RUQ pain
 Thrombocytopenia
 severe vasospasm → microangiopathic hemolysis →
Platelet activation, aggregation
660
661
Eclampsia
 Preeclampsia + convulsion
 Seizures that cannot be attributed to other

causes in woman with preeclampsia
 Seizures are generalized and may appear be-

fore, during, of after labor
662
Chronic Hypertension
 BP > 140/90 mmHg before pregnancy or diag-

nosed before 20 wks gestation (not attributable
to gestational trophoblastic disease)
or
 Hypertension first diagnosed after 20 wks ges-
tation and persistent after 12 wks postpartum
663
Underlying Causes of Chronic Hypertensive Disorder
Essential familial hypertension (hypertensive vascular disease)
Obesity
Atrterial abnormalities
Renovascular hypertension
Coarctation of the aorta
Endocrine diorders
Diabetes mellitus
Cushing syndrome
Primary aldosteronism
Pheochromocytoma
Thyrotoxicosis
Glomerulonephritis (acute and chronic)
Renoprival hypertension
Chronic glomerulonephritis
Chronic renal insufficiency
Diabetic nephropathy
Connetive tissue disease
Lupus erythematosus
Systemic sclorosis
Periarteritis nodosa
Polycystic kidney disease
Acute renal failure 664
Preeclampsia superimposed on
Chronic Hypertension
 New-onset proteinuria ≥ 300mg/24hours in

hypertensive women but no proteinuria before
20 weeks’ gestation
 A sudden increase in proteinuria or blood

pressure or platelet count < 100,000/mm3 in
women with hypertension and proteinuria be-
fore 20weeks’ gestation
665
Etiology
 Vascular endothelial damage with vasospasm,
transudation of plasma, and ischemic and throm-
botic sequelae.
 Currently plausible potential cause (2003, Sibai)

 Abnormal trophoblastic invasion of Uterine vessels
 Immunological intolerance between maternal and feto-
placental tissues
 Maternal maladaptation to cardiovascular or inflamma-
tory changes of normal pregnancy
 Diatary deficiencies
 Genetic influences
666
667
 Lipid-laden cells → atherosis (Hertig, 1945)
 Obstruction of the spiral arteriolar lumen by athero-

sis may impair placental blood flow
 Placental perfusion → diminished

668
Increased Pressor Responses
Prostaglandins
Membrane phospholipid
 In preeclampsia
 Endothelial
Phospholipase prostacyclin (PGI2)
A2 Arachidonic acid production is de-
creased
 Thromboxane A2
COX1,2
(TXA2) secretion
by platelets is in-
creased
→ Increased sensitiv-
ity to infused an-
TXA2 PGI2, PGE2 giotensin II
→ vasoconstriction
Platelet 669
670
Cardiovascular System
Blood volume
 Blood volume in term

 Normal pregnancy : 5000ml
 Not pregnancy : 3500ml
 Eclampsia : 3500ml
 Hemoconcentration in preeclampsia
 Vasoconstriction and Endothelial dysfunction with
vascular permeability.
 Extravasion into the extracellular space (lung)
 Whereas, gestational hypertension have a normal
blood volume (Silver, 1998) 671
672
Blood and Coagulation
Platelet
 Thrombocytopenia → life threatening
 Severe disease: < 100.000/uL
 Platelet count → indication of delivery
 Platelet activation, aggregation, consumption → “exhau-

sion” → thrombocytopenia (Harlow, 2002)
 HELLP syndrome : hemolysis (H) , elevated liver enzymes

(EL), and low platelets (LP) (Weinstein, 982)
 20% of severe preeclampsia and eclampsia
 Adverse outcome : 40%
 Other complication - Liver
 Eclampsia (6%), Placental abruption (10%), ARF (5%),
pulmonary edema (10%), subcapsular liver hematoma
673
(1.6%)
Volume Homeostasis
Fluid and Electrolyte Changes
 Preclampsia
 Electrolyte unbalance
 Vigorous diuretic therapy
 Sodium restriction
 Administration of water with sufficient oxytocin to
produce antidiuretisis.
 Following eclamptic convertion -> lower HCO3
674
Liver
 Periportal hemorrhagic necrosis in the periphery of
the liver lobule
 Serum liver enzyme
 Nonfatal case
 Hepatic rupture(more rare), subcapsular hematoma
(more common).
 Spontaneous hepatic rupture mortality :30%
675
676
Brain
 Common Sx.
 Headache, visual disturbance / blindness – (rare, 4hr
to 8days) / Retinal detachement
 – associated convulsion (eclampsia) - Letharge,
confusion, blurred vision, coma
 Anatomical pathology
Gross hemorrhage – severe hypertension
 Postmortem cerebral lesion
 Edema, hyperemia, focal anemia, thrombosis,

hemorrhage
 CT - 50% hypodense cotical area – petechial hemor-
rhage and infarction site (at autopsy)
 MRI, EEG
677
678
Uteroplacental perfusion
 Vasospasm ->
 perinatal mortality and morbidity
 Measurement placental blood flow
 Inaccesibility, complexity, unsuitablity
 DHAS sulfate -> estradiol-17B (in placenta)
clearance rate
 Doppler
 Doppler measurement of blood velocity through uter-
ine artery.
-> estimate uteroplacental blood flow
679
Prediction
 Roll over test
 28-32 wks
 Lt. lat. Recumbent position -> supine position
 Hypertension abnormal
 Positive predictive value (true positive) : 33%
 Uric acid
 Decreased renal uric acid excretion -> elevated
serum uric acid level
 Uric acid level > 5.9mg/dL at 24wks ; PPV : 33%
 Uterine Artery Doppler Velocimetry

 Second trimester – uteroplacental vascular resis-
tance
 Sensitivity : 78%, PPV: 28% 680
Prevention
 Dietary Manipulation
 Salt restriction -> ineffective
 Low dose aspirin - controversial
 Prenatal Ca supplementation -> significant reduction in
BP and incidence of preeclampsia
 Antioxidants
 Chappel, 1999: 283 high risk women
 18-22wks , vit C & E versus placebo

 Significant reduction in preeclampsia (11% / 17%)
681
TREATMENT
GOAL
 To prevent the:
 Condition from becoming bad to worse
 Complications
OBSTETRIC MANAGEMENT
 Bedrest (either at home or in the hospital)
 Hospitalization (specialized personnel and equipment)
 Magnesium sulfate (or other antihypertensives for PIH)
 Fetal monitoring:
 fetal movement counting -
 nonstress testing
 biophysical profile
 Doppler flow studies
 Continued laboratory testing of urine and blood
 Corticosteroids
 Delivery of the baby
ANTIHYPERTENSIVES
 Goal: Blood Pressure < 150/100
 BP < 150/100 mmHg does not reduce risk to fetus or prevent
preeclampsia; Antihypertensives benefit mother only
 Do not reduce pregnancy complications
Diuretic Beta ACE inhibitors / Calcium Alpha

Blocker Angiotensin II receptor Channel Blockers
antagonist Blocker
Caution Not No No Caution
in Adversely effect fetal Myocardial
late and neonatal blood depressants
pregnancy pressure control, skull
defects,
oligohydramnios,
toxicity
Labetalol Arteriolar dilator
I/V Max 200 mg
2mg/min until satisfactory response
Oral 200 mg BID up to 1200mg
Hydralazine Vasodilator
(Apresoline) Causes tachycardia fluid retention
Oral 25 mg BD
IV 10mg in 10 ml saline in 20 minutes
Nitrates Isorbid dinitrate, Glyceryl trinitrate, isorbid mono nitrate
Methyldopa 250 – 500 mg 2-3 times/day

(Aldomet) Centrally acting Alph 2 receptor agonist
Sodium 0.5-1.5µgm/kgmin
Cyanide toxicity if treatment exceeds 3 days
Nitropruside
Nifedipine Vasodilator
(Adalet) no myocardial depression
10-20mg BD
EVALUATION
 Blood complete picture

 Platelet count
 Coagulation assay, PT, APTT, Fibrinogen, D - dimer
 Serum Urea/creatinine Electrolytes Uric Acid
 LFTs
 Urinolysis, Microscopy, 24 Hours specimen for protein and
creatinine clearence
 Type and screen Blood
TREATMENT OF ECLAMPSIA
 Stop convulsion (Thiopentone 50-100 mg)
 ABC
 Apply monitors (Pulse Oximeter, NIBP, ECG)
 I/V line
 Check BP repeatedly
 Administer MgSO4
 Treat hypertension
 Deliver baby
 Treatment of choice for Seizure = Magnesium Sulphate
4 - 6 grams in 20 minutes, followed by 1-2 gram / hr
 Monitor:
 Urine output
 Respiratory rate
 Patellar reflexes
 Serum levels - 4 hourly
5 mEq/L Therapeutic range

Loss of deep tendon reflexes
10 mEq/L Prolonged P-Q interval, Widening QRS
15 mEq/L Respiratory arrest
20 mEq/L Asystole
MgSO4
 CNS
 Depressant & Anticonvulsant
 CVS
 Mild Anti-hypertensive effect
 Neuromuscular Junction
 Inhibits Ach release
 Decrease membrane excitability
 Augment Non and depolarizing muscle relaxant
 Uterus
 Mild relaxant effect on vascular & uterine smooth muscle
 Improve uterine blood flow
 Neonatal depression
 Respiratory, hyporeflexia, decreased beat to beat variability
IMMEDIATE DELIVERY
 Severe Hypertension
 Progressive thrombocytopenia
 Liver dysfunction
 Progressive renal dysfunction
 Persistent headache
 Evidence of fetal jeopardy
 Premonitory signs of ECLAMPSIA

SPINAL ANESTHESIA
GENERAL ANESTHESIA
 Aspiration prophylaxis
 Thiopentone sodium induction
 Suxamethonium with cricoid pressure
 Attenute intubation response by deep anaesthesia & ligno-
cain
 Smaller ETT 6-6.5 mm (airway edema)
 Nondepolarizing agent after recovery from suxamethonium
Remember MgSO4
 2/3 rd MAC for adequate depth of anaesthesia
 MgSO4 intra and Post op period
 IBP line for continuous blood pressure monitoring
 Anti HTN drugs
Lecture 14
MULTIPLE PREGNANCY.
THE UTERINE RUPTURE

MULTIPLE PREGNANCY
MULTIPLE PREGNANCY
 Twin pregnancy represents 2 to 3% of all pregnancies
 The PNMR is 5 times that of singleton

DIZYGOTIC TWINS
 Most common represents 2/3 of cases
 Fertilization of more than one egg by more than one

sperm
 Non identical, may be of different sex
 Two chorion and two amnion
 Placenta may be separate or fused

FACTORS AFFECTING IT’S INCIDENCE
 Induction of ovulation, 10% with clomide and 30% with
gonadotrophins
 Increase maternal age ? Due to increase gonadotrophins

production
 Increases with parity
 Heredity usually on maternal side
 Race: Nigeria 1:22; North America 1:90

MONOZYGOTIC TWINS
 Constant incidence of 1:250 births
 Not affected by heredity
 Not related to induction of ovulation
 Constitutes 1/3 of twins

RESULTS FROM DIVISION OF
FERTILIZED EGG
0-72 hours Diamniotic dichorionic
4-8 days Diamniotic monochorionic
9-12 days Monoamnio monochorionic
>12 days Conjoined twins

FERTILIZED EGG
MONOZYGOTIC TWINS
 70% are diamniotic monochorionic
 30% are diamniotic dichorionic

DETERMINATION OF ZYGOSITY
 Very important as most of the complications

occur in monochorionic monozygotic twins
During pregnancy by USS
 Very accurate in the first trimester, two sacs, presence

of thick chorion between amniotic membranes
 Less accurate in the second trimester the chorion

become thin and fuse with the amniotic membranes
 Different sex indicates dizygotic twins
 Separate placentas indicates dizygotic twins

DETERMINATION OF ZYGOZITY
AFTER BIRTH
 By examination of the MEMBRANES, PLACENTA, SEX,
BLOOD group
 Examination of the newborn DNA and HLA may be

needed in few cases
COMPLICATIONS OF MULTIPLE GESTATION
Maternal Fetal
 Anemia  Malpresentation
 Hydramnios  Placenta previa
 Preeclampsia  Abruptio placentae
 Preterm labour  Premature rupture of the
 Postpartum hemorrhage membranes
  Prematurity
Cesarean delivery
 Umbilical cord prolapse
 Intrauterine growth
restriction
 Congenital anomalies
SPECIFIC COMPLICATIONS IN
MONOCHORIONIC TWINS
TWIN-TWIN transfusion
 Results from vascular

anastomosis between
twins vessels at the placenta
 Usually arterio (donor) venous (recipient)
 Occurs in 10% of monochorionic twins

MONOCHORIONIC TWINS
 Chronic shunt occurs, the donor

bleeds into the recipient so one is
pale with oligohydraminos while
the other is polycythemic with
hydraminos
 If not treated death occurs in 80-100% of cases

MONOCHORIONIC TWINS
Possible methods of treatment:
 Repeated amniocentesis from recipient
 Indomethacin
 Fetoscopy and laser ablation

of communicating vessels
OTHER COMPLICATIONS IN
MONOCHORIONIC TWINS
 Congenital malformation. Twice that of singleton.
 Umbilical cord anomalies. In 3 – 4 %.
 Conjoined twins. Rare 1:70000 deli varies. The

majority are thoracopagus
 PNMR of monochorionic is 5x that of dichorionic

twins (120 vs. 24 / 1000 births)
MONOCHORIONIC TWINS
- thoracopagus
- pigopagus
MONOCHORIONIC TWINS
- craniopagus
craniopagus parasiticus
- xyphopagus
MATERNAL PHYSIOLOGICAL ADAPTATION
 Increase blood volume and cardiac output
 Increase demand for iron and folic acid
 Maternal respiratory difficulty
 Excess fluid retention and edema
 Increase attacks of supine hypotension

DIAGNOSIS OF MULTIPLE PREGNANCY
 Positive family history mainly on maternal side
 Positive history of ovulation induction
 Exaggerated symptoms of pregnancy
 Marked edema of lower limb
 Discrepancy between date and uterine size
 Palpation of many fetal parts

 Auscultation of two fetal heart beats at two different
sites with a difference of 10 beats
 USS
 Two sacs by 5 weeks by TV USS
 Two embryos by 7 weeks by TV USS

ANTENATAL CARE
AIM
 Prolongation of gestation age, increase fetal weight
 Improve PNM and morbidity
 Decrease incidence of maternal complications

ANTENATAL CARE
Follow Up
 Every 2 weeks
 Iron and folic acid to avoid anemia
 Assess cervical length and competency

ANTENATAL CARE
Fetal Surveillance
 Monthly USS from 24 weeks to

assess fetal growth and weight
 A discordinate weight difference of >25% is abnormal

(IUGR)
 Weekly CTG from 36 weeks

3D USS – TWIN PREGNANCIES
METHOD OF DELIVERY
Vertex-Vertex (50%)
 Vaginal delivery, interval between

twins not to exceed 20 minutes
Vertex-Breech (20%)
 Vaginal delivery by senior obstetrician

METHOD OF DELIVERY
Breech-Vertex (20%)
 Safer to deliver by CS to avoid the

rare interlocking twins (1:1000 twins)
Breech-Breech (10%)
 Usually by CS
PERINATAL OUTCOME
 PNMR is 5 times that of singleton (30-50/1000 births)
 RDS accounts for 50% 0f PNMR. 2nd twin is more

affected
 Birth trauma – 2nd twin is 4 times affected than 1st
 Incidence of SB is twice that of singleton

PERINATAL OUTCOME
 Congenital anomalies is responsible for 15% of PNMR
 Cerebral hemorrage and birth asphyxia are responsible

for 10% of PNMR
 Cerebral palsy is 4 times that of singleton
 50% of twins babies are born with low birth (<2500

gms) from prematurity & IUGR
INTRAUTERINE DEATH OF ONE TWIN
 Early in pregnancy usually no risk
 In 2nd or 3rd trimester:
 Increase risk of DIC
 Increase risk of thrombosis in the a live one
 The risk is much higher in monochorionic than in

dichorionic twins
 The a life baby should be delivered by 32-34 weeks in
monochorionic twins
HIGH RANK MULTIPLE GESTATION
 Spontaneous triplets 1:8.000 births
 Spontaneous quadruplets 1:700.000 births
 The main risk is sever prematurity
 CS is the usual and safe mode of delivery
 High PNMR of 50-100 / 1000 births

COMPLICATIONS OF MULTIPLE PREGNANCY
A. MATERNAL:
1. Anemia due to increase demand
2. Increase incidence of PET(5 times)
3. Polyhydramnios in monochorionic monozygotic twins
4. Increase incidence of premature labor

COMPLICATIONS OF MULTIPLE
PREGNANCY
A. MATERNAL:
5. Increase incidence of CS. And operative delivery
6. Increase incidence of placenta praevia and abruptio

placentae
7. Increase incidence of hypotonic postpartum

hemorrhage
PREGNANCY
B. FETAL:
1. Increase perinatal morbidity and mortality
2. Prematurity with / without rupture of membrane
3. Increase incidence of malpresentation

PREGNANCY
B. FETAL:
4. Increase incidence of cord prolapse
5. Higher incidence of IUGR
6. Increase incidence of congenital anomalies

THE UTERINE RUPTURE
DEFINITION
 Separation of the muscular wall of the uterus
 Usually occurs during labor
 Occasionally happen during

the later weeks of pregnancy
CAUSES
During pregnancy
 Weak scar after previous
operations on the uterus
 History of cesarean section (VBAC - vaginal birth after

C-section)
 Myomectomy
 Excision of a uterine septum
 Previous perforation of uterus (D&C, hysteroscopy,

forceps delivery
CAUSES
During labor:
 uterine hyper-stimulation (oxytocin
with pitocin induction or
augmentation of labor)
 obstructed labor (macrosomia, fetopelvic
disproprotion)
 intrauterine manipulation (internal version, manual
removal of an adherent placenta)
 forcible dilatation (cervical tear)
 a weak scar (C-section or other
operations)
TYPES
 Incomplete rupture
 Complete rupture
 Depending on whether the

peritoneal coat is torn
through or not
SYMPTOMS AND SIGNS
1. Rupture of scar
 be gradual that symptom is very slight in incomplete
rupture
 abdominal pain wrongly attributed to the onset of labor
 severe pain and shock occurs in complete (suddenly

pain)
 fetal distress
 bleeding in vagina
SYMPTOMS AND SIGNS
2. Spontaneous rupture during obstructed labor
 prolonged labor
 violent uterine actions
 pathologic retraction ring
 disporpotion, malpresentation(transverse lie)
 fetal distress
 a sharp, tearing pain in lower abdomen
 pulse rapid
 blood pressure fall
 fetus may be felt in the abdominal cavity
PATHOLOGIC RETRACTION RING
SYMPTOMS AND SIGNS
3. Rupture by oxytocin drugs:
 be follow the administration of oxytocin
 the danger is less if the drug is given as a dilute

intravenous drip given in an increasing fashion
PROGNOSIS
 has a high mortality
 peri-natal morbidity is high

TREATMENT
 Women’s general condition must be improved
giving morphine, blood transfusion, glucose solution)
 immediate laparotomy
 hysterectomy
 wide-spectrum antibiotics
THANKS
FOR
YOUR
ATTENTION !
Lecture 15
GESTATIONAL
TROPHOBLASTIC
DISEASE

DEFINITION
 Gestational trophoblastic disease (GTD) is a group of
disease originated from placental villose trophoblastic
cells, including hydatidiform mole, invasive mole,
choriocarcinoma and a kind of less common
trophoblastic cell tumor in placenta
RELATIONS AMONG THE DISEASES
 Benign mole (hydatidiform mole) = abnormal
formation of placenta accompanied by the special
abnormal hereditary
 Invasive mole results from benign mole
 Choriocarcinoma and the trophoblastic cell tumor in

placenta may result from benign mole, term pregnancy,
abortion and ectopic pregnancy
CLASSIFICATIONS
Gestational Trophoblastic Disease (GTD)
Partial mole Invasive Chorio Placental site
I. Pathologic trophoblastic
Classification Complete mole mole carcinoma tumour
Pe
rsi
ste
nt
II. Clinical Benign GT
D
G.T. Neoplasia
Classification G.T.D. Malignant G.T.D.
βhCG based:
WHO, FIGO, ACOG 2004
Non metastatic Metastatic
& RCOG 2010
Low risk High risk

HYDATIDIFORM MOLE
DEFINITION
 Hydatidiform mole = an abnormal proliferation of the
trophoblast in which the terminal villi are transformed
into vesicles filled with clear viscid material (like grapes)
CLASSIFICATION
 Hydatidiform mole is
divided into:
 Complete
and
 Incomplete
ETIOLOGY
 is not clear
ETIOLOGY OF
COMPLETE HYDATIDIFORM MOLE
EPIDEMIOLOGY
 the morbidity of hydatidiform mole
is different in different area
INCIDENCE
 South East Asia is 1/500-600
 US and Europe: 1/500-2.000
 China: 1/1238
ETIOLOGY OF
HIGH RISK FACTORS
 nourishing status, social economy
 age: < 20 years old; > 35 and 40 years old
 hydatidiform mole history: if a patient has the history of

1 or 2 x hydatidiform mole, then the morbidity of the
hydatidiform mole when pregnant again is 1 % and 15-
20% respectively
ETIOLOGY OF
GENETIC FACTORS
 enucleate egg fertilization:

 chromosome karyotype of complete mole is diploid:
 90% is 46XX
 10% is 46XY
ETIOLOGY OF
INCOMPLETE HYDATIDIFORM MOLE
EPIDEMIOLOGY
 the morbidity of incomplete mole is much lower than

that of the complete type, and it is not associated with
age
ETIOLOGY OF
GENETIC FACTORS
 chromosome karyotype of 90% incomplete mole is

triploid
 The most common chromosome karyotype is 69XXY,

and then is 69XXX or 69XYY
PATHOLOGY
MACRO EXAMINATION
 mass of vesicles, vary in size,
grape-like and identifiable
embryonic or fetal tissues
MICRO EXAMINATION
 trophoblastic proliferation
 hydropic degeneration of the stroma
 absence of blood vessels or extreme scantiness of blood

vessels
PATHOLOGY
Complete mole Incomplete mole
Embryotic or fetal tissue - +
Villus stromal edema diffuseed localized
Trophoblastic hyperplasia diffuseed localized
Villus outline regular irregular
Villus stromal blood vessel - +
Karyotype diploid triploid / tetraploid

Normal trophoblastic Partial mole
Complete mole
Partial mole
Complete mole
COMPLETE MOLE
 Vaginal bleeding after amenorrhea
 Uterus is abnormally enlarged and become soft
 Theca lutein ovarian cyst
 Hyperthyroidism (plasma thyroxin
concentration elevates)
 Exaggerated early pregnancy
symptoms (nausea, vomitting, etc)
 Severe and early - onset PIH
THECA LUTEIN OVARIAN CYST
INCOMPLETE MOLE
 May have the major symptoms of complete mole, but it is

slightly manifested
 NO luteinizing cyst
 The histologic examination of

curettage sample may confirm
the diagnosis
PROGNOSIS
 Complete mole has the latent risk of local invasion or
telemetastasis
 The high-risk factors includes:
 β-HCG > 100.000 IU/L
 uterine size is obviously larger than that with the same gestational
time
 The luteinizing cyst is > 6 cm
 If >40 years old, the risk of invasion and metastasis = 37%
 If >50 years old, the risk of invasion and metastasis = 56%
 Repeated mole: the morbidity of invasion and metastasis increase

3-4 x
DIAGNOSIS
 β-HCG measurement
 US examination
 Detecting the fetal heart beat by ultrasound Doppler

COMPLETE HYDATIDIFORM MOLE WITH A COEXISTENT FETUS AT
13 WEEKS GESTATION
13 WEEKS GESTATION
 Abortion
 Multiple pregnancy
 Polyhydramnios
LONG STANDING MISSED ABORTION
WITH CYSTIC DEGENERATION OF THE PLACENTA

MANAGEMENT
 Emptying uterine cavity
 once the diagnosis is confirmed the
uterine cavity should be emptied as
soon as possible
 Hysterectomy
 over 40 years old with high-risk factors
 uterine size is over 14 gestational weeks
 Management of luteinizing cyst

EMPTYING UTERINE CAVITY
 Suction curettage has been performed
using 10 mm canula under US guidance
Canula
MANAGEMENT
 Preventive chemotherapy
 over 40 years old
 the β-HCG is over 100.000 IU/L before emptying mole
 the HCG regresion curve is not progressively declined
 uterus is obviously larger than the size of the amenorrhea
 luteinizing cyst is > 6 cm
 there is still over hyperplasia of trophoblastic cells in the

second curettage
FOLLOW UP
 β-HCG qw till normal
 QW x 3m
 Q2W x 3m
 QM x 6m
 Q6M x 2y
INVASIVE MOLE
DEFINITION
 Invasive mole = the hydatidiform mole invade the
uterine myometrium or metastasize to extrauterine tissue
BIOLOGIC BEHAVIOR
 Invasive mole villus may invade myometrium or blood
vessels or both, at beginning it spread locally, invade
myometrium, sometimes penetrate the uterine wall and
spread to the broad ligament or abdominal cavity
PATHOLOGY
MACRO EXAMINATION
 different size of vesicles in myometrium,
there may be or may not be primary
focus in uterine cavity
 when the invasion is near serosal layer
MICRO EXAMINATION
 villose structure and trophoblastic cells proliferation and
differentiation deficiency
 villose and trophoblastic cells can be found in most

PATHOLOGY
MACRO EXAMINATION
MICRO EXAMINATION
 irregular vaginal bleeding
 uterine subinvolution
 theca lutein cyst does not disappear after emptying uterus
 abdominal pain
 metastatic focus manifestation

DIAGNOSIS
 history and clinical manifestation
 successive measurement of β-HCG
 US examination
 X-ray and CT
 histological diagnosis
US DIAGNOSIS
DIAGNOSIS
CHORIOCARCINOMA
DEFINITION
 Choriocarcinoma is a highly malignant tumor, it can
metastasize to the whole body through blood circulation
damage tissues and organs, cause bleeding and necrosis
CHORIOCARCINOMA
 The most common metastatic site is lung, then vagina,
brain and liver
 50% gestational choriocarcinoma result from

hydatidiform mole (generally occurs over 1 year after
emptying the mole)
 The rate of occurrence after abortion or term delivery is

25% and 25% respectively, seldom occurs after ectopic
pregnancy
PATHOLOGY
MACRO EXAMINATION
 most choriocarcinoma occurs in uterus
 the tumor diameter = 2-10 cm
 cancer embolus is often found in parauterine veins
 ovarian luteinizing cyst may be formed
MICRO EXAMINATION
 the hyperplastic cytotrophoblastic cells and
syntrophoblastic cells invade the myometrium and blood
vessels accompanied by the bleeding and necrosis
MACRO EXAMINATION
MICRO EXAMINATION
 Vaginal bleeding
 Pain
 Uterine enlargement
 Mass
DIAGNOSIS
 Clinical features
 US
 β-HCG
 CT
 X-ray
 Pathology
 Hydatidiform mole
 Invasive mole
 Placental site trophoblastic tumors
 Rudimental placenta
LUNG METASTASES
VAGINA METASTASES
BRAIN METASTASES
LIVER METASTASES
ANATOMIC STAGING
 Stage I - disease confined to uterus
 Stage II - gestational trophoblastic tumor extending

outside uterus but limited to genital structures (adnexa,
vagina, broad ligament)
 Stage III - gestational trophoblastic disease extending to

lungs with or without known genital tract involvement
 Stage IV - all other metastatic sites

MANAGEMENT
 Chemotherapy
 Surgery
FOLLOW UP
 QM x 1y
 Q3M x 2y
 QY x 2y
 Q2Y
Lecture 16
ABNORMAL LABOR:
DYSTOCIA

ABNORMAL LABOR: DYSTOCIA
 When we last talked about childbirth, there are 4 major
influencing factors
 When one or more factors are abnormal or uncoordinated

= abnormal labor
 That may exist singly or in combination

ABNORMAL LABOR: DYSTOCIA
DEFINITION
 Generally, abnormal labor is very common whenever

there is disproportion between the presenting part of the
fetus and the birth canal
 Dystocia literally means difficult labor and is

characterized by abnormally slow progress of labor
CATEGORIES OF DYSTOCIA
According to the factors divided to 3 types:
1. Abnormalities of the powers (uterine contractility and

maternal expulsive effort)
2. Abnormalities of passenger (the fetus)
3. Abnormalities of the passage (the birth canal)

1. ABNORMALITIES OF THE POWERS
 Abnormalities of the uterine contractility and maternal
expulsive effort
 Either uterine forces insufficiently strong or

inappropriately coordinated to efface and dilate the
cervix - uterine dysfunction - or inadequate voluntary
muscle effort during the 2nd stage of labor
2. ABNORMALITIES OF PASSENGER
(THE FETUS)
 excessive fetal size
 malpositions
 congenital anomalies
 multiple gestation
3. ABNORMALITIES OF THE PASSAGE
(THE BIRTH CANAL)
 pelvic contraction
 soft tissue abnormalities of the birth canal
 masses or neoplasia
 aberrant placental location

UTERINE DYSFUNCTION
hypotonic primary
uterine inertia secondary
Uterine hypertonic
Dysfunction
uterine hypercontractility
1. ABNORMALITIES OF THE POWERS:
UTERINE INERTIA
1. ETIOLOGY
 Cephalopelvic disproportion / Fetal malposition

 Abnormal of uterine muscle
 Psychical factors
 Imbalance of endocrine system
 Administration of analgesia
 Others
i. Cephalopelvic disproportion / Fetal malposition
 The fetal head or presenting part could not close presses

to the cervix and lower uterine segment
 Fetopelvic disproportion arises from:
 diminished pelvic capacity
 excessive fetal size
 malpresentation
 Failure to progress in spontaneous / stimulated labor

 This term is used to include lack of progressive cervical
dilatation or lack of fetal descent
ii. ABNORMAL OF UTERINE MUSCLE
 Uterine muscle malfunction can result from uterine
overdistention or obstructed labor, or both (muscle
fiber excessive elongation and contractility decline)
 Polyhydramnios, macrosomia, multiple births (twins)
 Muscle fiber degeneration (past history of repeat uterus
infection, abortion, induction of labor or operation
 Myomas, pelvic tumors, myogenic dysplasia or malformed
uterus (didelphus, unicornous uterus)
iii. PSYCHICAL FACTORS
 fearing labor pain
 anxiety
 tension
 worried about: fetal safety, labor hemorrhage, injury
and dystocia
which eventually lead to uterine dysfunction and occur

uterine inertia
iv. OTHER FACTORS
 hormonal mechanism of uterine activity (deficiency of

oxytocin, estradiol, prostaglandin)
 excessive sedation, anesthesia, unripe cervix
 fatigue , early abdominal pressure
 overactive bladder filling (fetal presentation descent)

iv. OTHER FACTORS
 hormonal mechanism of uterine activity (deficiency of

oxytocin, estradiol, prostaglandin)
 excessive sedation, anesthesia, unripe cervix
 fatigue , early abdominal pressure
 overactive bladder filling (fetal presentation descent)

2.CLINICAL FINDINGS
 hypotonic uterine dysfunction (coordinated)

 Although there are still normal uterine contraction and
maintain the polarity, symmetry, and a certain rhythm, but
the contraction is weak and feeble, with short duration,
long interval and irregular
 when the contractions in the acme, no uterus uplift and

stiffen
2.CLINICAL FINDINGS
 When uterine contractions:

 the intrauterine pressure in the lower, and often <15 mmHg,
 as a finger pressing on the fundus of uterus a depression could

appear
 Maternal relative quiet, prolonged process (painless or

can endure )
 Fetal heart rate changes lately (no anoxia or lately)

2.CLINICAL FINDINGS
 hypertonic uterine inertia and uncoordinated

contractions
 often occur together, elevated resting tone of the uterus
 the exciting site of contraction is NOT from the horn of

uterus, and in a particular / multiple site, and with
uncoordinated rhythm, polarity inversion
2.CLINICAL FINDINGS
 When uterine contracts the fundus is no firm, and the mid

or lower uterine segment harder than that
 The uterus can NOT be completely relaxed, uterine cavity

pressure lasting with higher state, but the cervix no dilation
and fetal head NO descent progressively
 Maternal lasting abdominal pain and fidgety
 Fetal heart rate changes early (anoxia)

2.CLINICAL FINDINGS
 Failure to progress
 Lack of progressive cervical dilatation (primiparas):
 Prolonged latent phase > 16 hrs
 Prolonged active phase > 8 hrs, cervix dilation < 1.2

cm/hrs
 Protracted active phase > 2 hrs

2.CLINICAL FINDINGS
 Lack of fetal descent

 Prolonged descent > 1 cm/h
 Protracted descent > 1 h
 Prolonged labor > 24 hrs (the total stage of labor)

LABOR-PROCESS RANGE PLAN
LABOR-PROCESS RANGE PLAN
3. EFFECT ON MATERNAL AND FETUS
 Maternal - fatigue (prolonged progress)
- acidosis or dehydration
- infection (Prolonged progress , PROM)
- postpartum hemorrhage (insufficient contractility)
- cesarean section rate
- laceration
 Fetus - distress (uterine blood flow and fetal oxygenation )

- birth injury, intracranial trauma (obstructed labor,
rare)
- prolapse of umbilical cord
- stillbirth
4. MANAGEMENT
 Hypotonic: the rule of treatment = strengthen
contractions and prevent PPH
THE FIRST STAGE OF LABOR
 General management:  Physical methods:

 rest • massage uterus
 eat more liquid food • emptying the bladder
 sedation • stimulation nipple
 correct acidosis • artificial rupture of
 intravenous injection membranes (AROM)
4. MANAGEMENT
THE FIRST STAGE OF LABOR
 Drugs:
 Oxytocin: 2.5 U + 5% GS 500ml ( 5mU/ml, 8drop/min, at
the beginning)
 Diazepam: 10 mg iv (softening the cervix)
 Cesarean section:
 Following the above management still ineffective or
fetal distress
4. MANAGEMENT
THE SECOND STAGE OF LABOR

 Forceps or vacuum extractor:
 second stage of labor
 cervical fully dilated
 membranes ruptured
 fetal survival, presenting part below the level of ischial
spine
 Cesarean section:
 presenting part upward the level of ischial spine or fetal
distress
4. MANAGEMENT
 HYPERTONIC - the rule of treatment = Adjusted
contractions and resume a normal polarity and rhythm
 Sedative: Dolantin or Morphine - adjusted and resume

to a normal contractions
 Cesarean section: otherwise

UTERINE HYPERCONTRACTILITY
1. CLINICAL FINDINGS AND DIAGNOSIS
 Coordinated uterine hypercontractility:

 uterine contraction is normal and maintain the
normal polarity, symmetry and a certain rhythm
 the intensity strength and frequency enhanced
 Contraction with:
 long duration
 short interval
1. CLINICAL FINDINGS AND DIAGNOSIS
 Precipitate delivery (multiparas)
 the total stage of labor < 3 hrs
 the process of labor is too fast
 Birth injuries lacerations of the soft birth canal
 Fractures, intracranial hemorrhage of the newborn

 Postpartum hemorrhage
 Uterine inversion
 Infections
2. EFFECT ON MATERNAL AND FETUS
 Rupture of uterus
 PPH , infection
 Soft birth canal trauma
 Fetal distress
 Fetal death
 Stillbirth
3. MANAGEMENT
 Prophylaxis - reduced obstetric brutal operation
 Must be gentle, slightly and carefully
 Tocolytic sedatives inhibited contractions:

 Meperidin
 Magnesium sulfate
 Forceps / Vacuum extractor

CESAREAN SECTION
2. ABNORMALITIES OF PASSAGE
THE BIRTH CANAL
 pelvic contraction
 soft tissue abnormalities of the birth canal
 masses or neoplasia
 aberrant placental location

PELVIC CONTRACTION
 Bony pelvis - a main composing part of birth canal; its
size and shape have the direct relation to the course of
labor and delivery
 Any contraction of pelvic diameter that diminishes the
capacity can create dystocia
 There may be contractions of the:
 pelvic inlet,
 the midpelvis,
 the pelvic outlet or
 a generally contracted pelvis caused by combinations of
these
CONTRACTED PELVIC INLET
1. simple flat pelvis

 promontory of sacrum
(dotted line)
 forward dislocation
2. rachitic flat pelvis

 past history of rickets
CONTRACTED PELVIC INLET
1. CLINICAL FINDINGS
 Fetopelvic disproportion, malposition or

malpresentation (face and shoulder presentations are
encountered 3x more frequently)
 Uterine inertia and prolonged progress of labor

(prolonged latent phase, early active phase and
protracted active phase)
 Cord prolapse occurs 4-6 x more frequently

MIDPELVIC-OUTLET CONTRACTION
 Funnel shaped pelvic
 The spines are prominent, the pelvic sidewalls converge

MIDPELVIC-OUTLET CONTRACTION
CLINICAL FINDINGS
 Fetopelvic disproportion persistent occiput posterior

position or deep transverse arrest, molding of head and
caput succedaneum
 Protracted active phase / prolonged second stage

(secondary uterine inertia)
 Uterine rupture, perineal tears obstructed labor

GENERALLY CONTRACTION PELVIC
 Each pelvic plane is 2 cm less

than normal value or more
 Can be seen in shape more

short and small, well-balanced
women of type of figure
DIAGNOSIS
 A history of Rickets, bone tuberculosis, polio or pelvic

fracture (warrants careful review of previous radiographs
and possibly computed tomographic pelvimetry later in
pregnancy)
 Physical examination height, spine, lower limb disability

(height < 150cm , lateral curvature usually associated
with contracted pelvis)
DIAGNOSIS
 Pelvic measurement:
 external pelvimetry
 internal pelvimetry
(sterile vaginal examination)
DIAGNOSIS
 Pelvimetry
 diagonal conjugate = 12.5-13 cm
 bi-ischial diameter = 10 cm
 incisura ischiadica = 5-6 cm
 angle of subpubic arch = 90°

DIAGNOSIS
 The fetal position and dynamic monitoring of labor
 After onset of labor, in primipara, fetal head

unengagement, breech, shoulder presentation; birth
process has been slow (Prompt the contraction of pelvis)
MANAGEMENT
 Trial labor - under the effective uterine contractions

observed the progress of labor
 There is no reliable method for evaluating the adequacy
of the lower pelvic
 The vaginal examination should be performed early in
the course of labor
 With continuous fetal monitoring, fetal well-being may
be ensured
MANAGEMENT
 True inlet contracted: Cesarean section
 Midpelvic-outlet contraction: fetal head biparietal

diameter reached the level of the spines, and can be
depressed farther, the fetal presentation beyond station
plus 2, vaginal delivery usually is possible; otherwise
cesarean section
 Administration of oxytocin should avoided in true

midpelvic-outlet contraction
MANAGEMENT
 Generally contraction pelvic term fetus (birthweight >

3000 g) needed cesarean section
 The fetus is not big, fetopelvic is adaptation and without

complication can try to labor
 Deformed pelvic: cesarean section

SOFT-TISSUE DYSTOCIA
 Soft tissue canal:
 lower part of uterus, cervix, vagina previous scar of the
birth canal laceration
 cervical conization and cauterization

 cesarean section
 rape injury in a small child

 caustic abortifacient injury to vaginal vault and cervix
 Previous scaring of the birth canal may cause tissue

rigidity and dystocia
FETAL DYSTOCIA
 caused by:
 malposition and malpresentation
 excessive size of the fetus
 fetal malformation
 If no disproportion exists, the head readily enters the

pelvis, and vaginal delivery can be predicted
i. MALPOSITION AND MALPRESENTATION
a. vertex malposition
 persistent occiput posterior
 persistent occiput transverse 5%
 sincipital presentation 1.08%
 anterior asynclitism
 posterior asynclitism 0.5%-0.81%
b. brow presentation 0.03%-0.1%

c. face presentation 0.08% -0.27%
d. breech presentation 3%-4%
e. abnormal fetal lie - transverse/oblique lie 0.25%
PERSISTENT OCCIPUT POSTERIOR OR TRANSVERSE
POSITION (POP, POT)
DEFINITION:
 Up to later stage of delivery the occiput can’t rotate

anteriorly, persistent occiput posterior (POP) or
transverse position (POT)
 Most often , the result of malrotation of occiput anterior

position during labor (2/3)
ETIOLOGY:
 Abnormal pelvic - Anthropoid and android, transverse

narrowing of the midpelvis, the fetal head often engages in
OP or OT
 Bad flexion - fetal backbone near the maternal backbone,
which disadvantages fetus flexion
 Uterine inertia - influence fetal descent, flexion, internal
rotation
 Cephalopelvic disproportion - the pelvic cavity is narrow,
which limits fetal descent, flexion, internal rotation
 Others - placenta praevia, filling of bladder, myoma
CLINICAL FINDING AND SYMPTOMS
 Fetal head engages later at the onset of labor
 Concordant uterine inertia and slow dilatation of cervix,

induces prolonged active phase or 2nd stage
 Early use abdominal pressure before the cervix full dilate

TREATMENT
 The 1st stage:
 strengthen contractions, trial labor
 Latent phase:
 sufficient rest and nourishment (Pethidine or Diazepam)
 Active phase:
 AROM - cervix 3-4 cm, membranes intact. To induce fetal
head descending, strengthen contraction, and internal
rotation
 Oxytocin intravenous drip infusion (small dose, 2-2.5 u)
 Cesarean section - after treatment the labor is still not

TREATMENT
 The 2nd stage:
 Midwifery - BPD arrive the ischial spine plane or below,

s>+2 , to rotate the occiput to OA, vaginal delivery forceps
 Cesarean section - fetal head is much high or CPD

TREATMENT
 The 3rd stage:
 To prevent PPH - prolonged labor readily cause bleeding of

uterine inertia
 Oxytocin - large dose, intravenous drip infusion (20 u)
 Suture lacerations
 Antibiotic
DIAGNOSIS OF PREGNANCY.
MATERNAL ADAPTATION TO PREGNANCY.
LABORATORY TESTS IN PREGNANCY

DEFINITIONS

reached viability

of viability
 Presumtive
 Examination

OF PREGNANCY
 Amenorrhea
 Nausea
 Vomiting
 Frequent urination
AMENORRHEA
 Amenorrhea is one of the earliest clues of pregnancy
 The majority of patients have no periodic bleeding after the

onset of pregnancy
 20 % of women - slight, painless spotting during early

gestation for no apparent reason
 a large majority of these continue to term and have normal
infants
AMENORRHEA
 Other causes:
 Menopause
 Stress (severe emotional shock, tension, fear, or a strong

desire for a pregnancy)
 Chronic illness (tuberculosis, endocrine disorders, or

central nervous system abnormality)
 Anemia
 Excessive exercises
NAUSEA AND VOMITING
(MORNING SICKNESS)
 Occurs in early morning during the first weeks of pregnancy
 Usually spontaneous and subsides in 6 to 8 weeks or by the 12th

to 16th weeks of pregnancy
beyond the 4th month of pregnancy

the patient
NAUSEA AND VOMITING
(MORNING SICKNESS)
NAUSEA AND VOMITING
 Other causes:
 Gastrointestinal disorders (hiatal hernias, ulcers, and

appendicitis)
 Infection (influenza, encephalitis)
 Emotional stress, upset (anxiety, anorexia nervosa)
 Indigestion
FREQUENT URINATION
 Frequent urination is caused by pressure of the
expanding uterus on the bladder
 It subsides as pregnancy progresses and the

uterus rises out of the pelvic cavity
 The uterus returns during the last weeks of

pregnancy as the head of the fetus presses
against the bladder

or tumors)
BREAST CHANGES
 In early pregnancy- a slight, temporary enlargement of the
breasts → sensation of weight, fullness, and mild tingling
supply
pregnancy
BREAST CHANGES
VAGINAL CHANGES
 Chadwick's sign
 The vaginal walls have taken on a deeper color caused by the
increased vascularity because of increased hormones
 6th week
 It may also be noted with a rapidly growing uterine tumor or any

cause of pelvic congestion
 Leukorrhea
 An increase in the white / slightly gray
 Due to hyperplasia of vaginal epithelial cells of the cervix
because of increased hormone level from the pregnancy

 The 1st perception of fetal movement within the uterus
 It usually occurs toward the end of the 5th month because of spasmodic
flutter
 A multigravida can feel quickening as

early as 16 weeks
 A primigravida usually cannot feel

quickening until after 20 weeks
 Fetal movement early in pregnancy

is frequently thought to be gas
SKIN CHANGES
 Striae gravidarum (stretch marks)
 On the abdomen and/or buttocks caused
by ↑ production / sensitivity to adrenocortical
hormones during pregnancy
 These marks may be seen on a patient with

Cushing's disease / patient with sudden weight gain
 Chloasma
 The “mask of pregnancy“
 It is a bronze type of facial coloration seen more
on dark-haired women

SKIN CHANGES
 Linea nigra
 A black line in the midline of the abdomen that may run from the
sternum / umbilicus to the symphysis pubis
 Primigravida - 3rd month; keeps pace with the rising height of the
fundus
 Multigravida - before the 3rd month
NEURO-PSYCHOLOGICAL CHANGES
 Fatigue
 Common complaint by most patients
during the 1st trimester
 May be associated with sleepiness

 May also be a result of :
 anemia
 infection
 emotional stress
 malignant disease
 Irascibility
 Emotiveness
 Those signs commonly noted by the physician upon examination of
the patient

 uterine changes
 fetal palpation
UTERINE CHANGES
 Position
 12th week - the symphysis pubis
 36th week - the xiphoid process
 These guidelines are fairly accurate only as long as pregnancy is normal

and there are no twins, tumors, or excessive amniotic fluid
 Size
 Increases in width and length
approximately 5x its normal size
 Its weight increases from
50 grams to 1,000 grams
ABDOMINAL CHANGES
 Changes that occur in the uterus, as the uterus grows the abdomen
gets larger
 Abdominal enlargement alone is not a sign of pregnancy
 Enlargement may be due to uterine or ovarian tumors, or edema
 Striae gravidarum may also be classified as a probable sign of

pregnancy by the physician
CERVICAL CHANGES
 Goodell's sign
 The cervix is normally firm like the cartilage at the end of the nose
 Softening of the cervix (firm like lips)
 Is present at 6 weeks of pregnancy
 Formation of a mucous plug

 This is due to hyperplasia of the cervical glands as a result of increased
hormones
 It serves to seal the cervix of the pregnant uterus and to protect it from
contamination by bacteria in the vagina
 The mucous is expelled at the end of pregnancy near or at the onset of

labor
 Painless uterine contractions occurring throughout pregnancy

 These contractions will, generally, cease with walking / other forms

of exercises
 Are distinct from contractions of true labor → do NOT cause the

cervix to dilate and can usually be stopped by walking
BASAL BODY TEMPERATURE
 This is a good indication if the patient has been recording for several
cycles previously
 A persistent temperature elevation spanning over 3 weeks since

ovulation is noted
 Basal body temperature (BBT) is 97 % accurate

POSITIVE PREGNANCY TEST
BY THE CLINICIAN
 This may be misread by doing it too early / too late
 Even if the test is positive, it could be the result of ectopic pregnancy

/ hydatidiform mole (an abnormal growth of a fertilized ovum)
FETAL PALPATION
 It is not always accurate, a mass in the abdomen may be palpated

and mistakenly identified as an infant
 They include:
 Fetal heart sounds
 Ultrasound scanning of the fetus
 Perception of fetal movements by the clinician
 X-ray
FETAL HEART SOUNDS
 The fetal heart begins beating by the 24th day following conception
 It is audible with a Doppler by 10 weeks of pregnancy and with a

fetoscope after the 16th week
 It is not to be confused with uterine souffle / swishlike tone from

pulsating uterine arteries
 The normal fetal heart rate is 120 - 160 beats

ULTRASOUND SCANNING OF THE FETUS
 The gestation sac can be seen and photographed
 An embryo as early as the 4th week after conception can be identified

PERCEPTION OF FETAL MOVEMENT
 This is done by a trained examiner

X-RAY
 Identify the entire fetal skeleton by
the 12th week
 In utero, the fetus receives total body

radiation that may lead to
genetic / gonadal alterations
 An x-ray is NOT a recommended test

for identifying pregnancy
CHANGES OF THE CIRCULATORY SYSTEM
 Blood volume ↑ gradually by 30 to 50 %
 This results in ↓ concentration of red blood cells and hemoglobin

pregnancy

compensated for the decrease resulting in an essentially normal
blood count
BLOOD CIRCULATION CHANGES
 Blood count is interpreted as anemia by the physician if the
hemoglobin falls < 10.5 grams / 100 ml and the hematocrit drops <
30 %
 Increased blood volume compensates for hypertrophied vascular

system of enlarged uterus
 It improves the placental performance
 Blood lost during delivery < 500 ml is normal

CARDIAC OUTPUT
 Cardiac output ↑ about 30 % during the 1st and 2nd trimester to
accommodate for hypervolemia
 This is NOT a problem for patients with a normal heart
 Patients with a diseased heart → risk for cardiac decompensation 28

to 35 weeks of pregnancy (the blood volume and cardiac load are at
their peak)
 also, during labor and immediately after delivery when rapid
hemodynamic changes occur
 Change in output is reflected in the heart rate

 It usually ↑ by 10 beats / minute
BLOOD PRESSURE
 Normally, the patient's blood pressure will not rise

VENOUS RETURN
 The lower extremities are often hampered in the last months of
pregnancy due to the expanding uterus restricting physical
movement and interfering with the return of blood flow → swelling
of the feet and legs
CHANGES IN THE RESPIRATORY SYSTEM
 The respiratory rate ↑ to 18 to 20 to compensate for ↑ maternal

oxygen consumption (needed for demands of the uterus, the
placenta, and the fetus)
 Women may feel out of breath and may need to sit a moment to
catch their breath
CHANGES OF BODY TEMPERATURE
 A slight ↑ in body temperature in early pregnancy
 The temperature returns to normal at about the 16th week
 The patient may feel warmer or experience "hot flashes" caused by

increased hormonal level and basal metabolic rate
 The kidneys must work extra hard excreting the mother's own waste
products plus those of the fetus
 There is an ↑ in urinary output and a decrease in the specific gravity
 The patient may develop urine stasis and pyelonephritis in the right
kidney
 This is due to pressure on the right ureter resulting from

displacement of the uterus slightly to the right by the sigmoid colon
URINARY CHANGES
 Frequent urination is a complaint during the 1st through 3rd
trimester
 As the uterus rises out of the

pelvic cavity in early pregnancy,
pressure on the bladder decreases
and frequency diminishes
 When lightening occurs during

the final weeks of pregnancy,
pressure on the bladder returns
to cause frequency
CHANGES OF THE SKELETAL SYSTEM
 There is a realignment of the spinal curvatures during pregnancy to
maintain balance
 It is due to the ↑ in size of the uterus and
pressure on the abdominal wall
 The patient walks with head and shoulders

thrust backward and chest protruding
outward to compensate
 This gives the patient a "waddling" gait
 There is a slight relaxation and increased mobility of the pelvic

joints, which allows stretching at the time of delivery of the infant
SYSTEM
 The uterus enlarges and rises up into the
pelvic cavity
 This action displaces the stomach, intestines,

and other adjacent organs
 Peristalsis is slowed because of the production of the hormone

progesterone, which decreases tone and mobility of smooth muscles
 This slowing enhances the absorption of nutrients and slows the rate
of secretion of hydrochloric acid and pepsin
SYSTEM
 Flare-up of peptic ulcers is uncommon in pregnancy
 Slow emptying may ↑ nausea and heartburn (pyrosis)
 Relaxation of the cardiac sphincter may ↑ regurgitation and chance

for heartburn
 Movement through the large

intestines is also slowed due
to an ↑ in water consumption
from this area →
↑ the chance for constipation
CHANGES OF THE ENDOCRINE SYSTEM
 Parathyroid Gland
 ↑ in size slightly
 It meets the ↑ requirements for calcium needed for fetal growth
 Posterior Pituitary
 Near the end of term, the posterior pituitary will begin to secrete
oxytocin that was produced in the hypothalamus and stored there
 It will serve to initiate labor
CHANGES OF THE ENDOCRINE SYSTEM
 Anterior Pituitary
 At birth, It will begin to secrete prolactin
 This stimulates the production of breast milk
 Placenta
 Acts as a temporary endocrine gland
during pregnancy
 It produces large amounts of estrogen and

progesterone by 10 to 12 weeks of pregnancy
 It serves to maintain the growth of the uterus, helps to control uterine

activity, and is responsible for many of the maternal changes in the
CHANGES IN BODY WEIGHT
 Weight gain in pregnancy
 There is a slight loss of pounds during

early pregnancy if the patient
experiences much nausea and vomiting
 Weight gain of 1 to 2 kg by the end of

the 1st trimester
 A gain of a 400 mg per wk is expected during the 2nd and 3rd trimesters
 Monitoring of weight gain should be done in conjunction with close

monitoring of BP
CHANGES IN BODY WEIGHT
 A lack of significant weight gain may be an indication of intrauterine
growth retardation (IUGR) of the infant
 Twin pregnancy: will require a higher caloric diet and expect a higher
weight gain than a single pregnancy
 Adequate protein intake emphasized to the patient for development

of the healthy fetus and proper diet reviewed at each prenatal visit
 Normal weight gain is about 9 - 12 (10 – 15) kg during pregnancy

STAGES OF LABOR
MECHANISM OF NORMAL LABOR IN
OCCIPUT PRESENTATION
 Labor : uterine contractions that effect dilatation of
 Parturition: bringing forth of young, encompass all

 Phase 0: Prelude to Parturition
 Phase 1: Preparation for Labor
 Phase 2: Process of Labor
 Phase 3: Parturition Recovery

PHASES OF PARTURITION &
ONSET OF LABOR
 Divide 4 uterine phases: correspond to major
during pregnancy
PHASE 2 : PROCESS OF LABOR
 Active labor : Ut contrations bring about progressive
 4 stages of labor
1st STAGE OF LABOR
2 STAGE OF LABOR: FETAL DESCENT
nd
3rd STAGE OF LABOR:
DELIVERY OF PLACENTA & MEMBRANES
4th STAGE OF LABOR:
IMMEDIATE PUERPERIUM
PHASE 3 OF PARTURITION:
INVOLUTION
 Immediately after delivery & for 2 hours or so
 Involution of Ut & reinstitution of ovulation

 Complete Ut involution : 4~6 wks
 Infertility persist as long as breast feeding is continued
( lactation  anovulation & amenorrhea)
LIE, PRESENTATION, ATTITUDE &
POSITION
FETAL LIE
 The relation of the long axis of the fetus to that of the
mother
 Longitudinal lie - found in 99% of labours at term
 Transverse lie - multiparity, placenta praevia, hydramnios,

uterine anomalies
 Oblique lie: unstable (become logitudinal or transversal)
 By abdominal palpation, vaginal examination, and

POSITION
FETAL PRESENTATION
 The presenting part is the portion of the body of the fetus
that is foremost in the birth canal
 The presenting part can be felt through the cervix on

vaginal examination
 Longitudinal lie  cephalic presentation

 Transverse lie  shoulder presentation

POSITION
ATTITUDE
 Posture of the fetus  folded on itself to accommodate the
shape of the uterus
 Flexed head, thighs, knees &feet
 The arms crossed over the chest
 Face presentation  extended concave contour of the

vertebral column
vertex )A( sinciput )B( brow )C( face )D(
Longitudinal lie. Cephalic presentation. Differences in attitude of fetal

body,
Note changes in fetal attitude in relation to fetal vertex as the fetal head
becomes less flexed
POSITION
canal
The chosen point:
 Vertex presentation  occiput
 Face presentation  mentum
 Breech presentation  sacrum
Each presentation has 2 positions: Rt or Lt

posterior OA
ROA LOA
ROT LOT
ROP LOP
OP
LOA LOP
~
'
t
J

Right occiput anterior (ROA)
PRESENTATIONS & POSITIONS
AT TERM
 Vertex  96%
2/3 Lt
1/3 Rt
 Breech  3.5%
 Face 0.3%
 Shoulder 0.4%

~

Transverse lie. Right acromio-dorso-posterior position (RADP). The
shoulder of the fetus is to the mother's right, and the back is posterior
MECHANISM OF LABOUR WITH
OCCIPUT PRESENTATIONS
THE CARDINAL MOVEMENTS OF
1 - ENGAGEMENT
LABOUR
The greatest transverse diameter BPD passes through the pelvic
inlet
It may occur in the last few weeks of pregnancy or only in labour
especially in multipara
The fetus enters the pelvis in transverse or oblique diameter
 LOT  40%
 ROT  20%
 OP  20% ROP > LOP
 ROA / LOA  20%
 Asynclitism LABOUR
2 - DESCENT
 In nullipara engagement takes place before the onset of
 In multipara descent begins with engagement
 It is gradually progressive till the fetus is delivered
 It is affected by the uterine contractions & thinning of the
lower segment
Ear presentation
3-FLEXION
 The descending head meets resistance of pelvic floor, Cx

& walls of the pelvis  flexion
 The shorter suboccipito-begmatic is substituted for the

longer occipito-frontal
occipito-frontal to suboccipito-bregmatic diameter typically reduces
the anteroposterior diameter from nearly 12 to 9.5 cm
4-INTERNAL ROTATION
 Turning of the head from the OT position  anteriorly
 Less commonly OT  posteriorly towards the sacrum

135º
 It is not accomplished till the head has reached the

spines
The levator ani muscles form a V shaped sling that tend
to rotate the vertex anteriorly
 It is completed by the time the head reaches the pelvic

EXTENSION
 When the flexed head reaches the vulva it undergoes
contact with the inferior margin of the symphysis pubis
 Crowning  the largest diameter of the fetal head is

 The head is born by further extension as the occiput,

bregma, forehead, nose, mouth & chin pass successively
over the perineum
EXTERNAL ROTATION RESTITUTION
 After delivery of the head it returns to the position it
occupied at engagement, the natural position relative to
the shoulders (oblique position)
 Then the fetal body will rotate to bring one shoulder
 Restitution is followed by complete external rotation to
thigh)
 The anterior shoulder slips under the pubis
 By lateral flexion of the fetal body the post shoulder will
be delivered & the rest of the body will follow
Lecture 4
PHYSIOLOGY OF THE UTERINE
MUSCLE.
LABOR'S FOLLOW UP.
UTERINE CONTRACTILE ACTIVITY
DURING LABOR
UTERINE CONTRACTILE ACTIVITY
DURING LABOR
1. The Myometrium
2. The Cervix
3. Labor Patterns
LABOR
• thunderous uterine contractions that ef -
fect dilatation of the cervix and force the
fetus through the birth canal
FALSE LABOR
• myometrial contractions that do not

cause cervical dilatation
unpredictability in occurrence
lack of intensity
brevity of duration
discomfort – confined to low ab-
domen & groin
THE MYOMETRIUM
1. Anatomical and Physiological Considerations
• Characteristics – advantage in the efficiency of uterine
contractions & the delivery of the fetus
① degree of shortening of smooth muscle cells with
contraction
: magnitude greater than in striated muscle cells
② forces can be exerted in smooth muscle cells in
any direction
③ not organized in the same manner as skeletal mus-
cle
- thick & thin filaments in long, random bundles
→ greater shortening & force-generating capacity
④ multidirectional force generation
THE MYOMETRIUM
SMOOTH MUSCLE (e.g. Myometrium)
Smooth muscle - the walls of blood vessels, tubular organs (stomach

and uterus).
- ability to stretch and maintain tension for long periods of time.
- not under voluntary control, each cell exists as a discreet independent
unit that is innervated by a single nerve ending.
- myofilaments are loosely organized and attached to dense bodies
SMOOTH MUSCLE (e.g. Myometrium)
• Doesn’t contain sarcomeres
• Contains > content of actin

than myosin (ratio of 16:1)
• Myosin filaments attached

at ends of the cell to dense
bodies
• Contains gap junctions

SMOOTH MUSCLE CONTRACTION
• Depends on rise in free intracellular Ca2+
• Ca2+ binds with calmodulin
– Ca2+ calmodulin complex joins with and activates
myosin light chain kinase
• Myosin heads are phosphorylated

– Myosin heads binds with actin
• Relaxation occurs when Ca2+ concentration

decreases
MECHANISMS INVOLVED IN SMOOTH
MUSCLE INTRACELLULAR CALCIUM CONTROL
THE MYOMETRIUM
2. Biochemistry of Smooth Muscle Contractions
Contrac- Relax-
tion Myosin light chain ation
Myosin light chain
kinase 1) Decreased intracellular
Ca2+ activated Ca2+;
Phosphory- Ca2+ sequestration
lated
Myosin light 2) Dephosphorylation of
chain Acti
myosin light
n chain
Actin-Phosphorylated
Myowin 3) Inactivation of myosin
light chain
ATPase
kinase (e.g., by cyclic AMP-
ATP ADP dependent phosphory-
lation)
THE MYOMETRIUM
3. The Three Stages of Labor
a. First stage of labor
: begins when uterine contraction of sufficient

frequency, intensity & duration are attained
→ ends when cervix is fully dilatated (10cm)
: stage of cervical effacement & dilatation

a. FIRST STAGE OF LABOR
THE MYOMETRIUM
b. Second stage of labor
: begins when complete dilatation of cervix
→ ends with delivery of the fetus
: stage of expulsion of the fetus
c. Third stage of labor
: begins after delivery of the fetus
→ ends with the delivery of the placenta
: stage of separation & expulsion of placenta
2 & 3 STAGES OF LABOR
nd rd
THE MYOMETRIUM
4. Clinical Onset of Labor
• Show (bloody show)
- sign of the impending onset of active labor

- extrusion of mucus plug of the cervical canal
→ discharge of small amount of blood-
tinged mucus from vagina
THE MYOMETRIUM
5. Uterine Contractions Characteristic of Labor
• muscular contractions, those of uterine smooth
muscle of labor are painful
• cause of pain (not known definitely):
① hypoxia of contracted myometrium
② compression of nerve ganglia in cervix &
lower uterus by the tightly interlocking muscle
bundles
③ stretching of cervix during dilatation
④ stretching of peritoneum overlying the fun-
dus
THE MYOMETRIUM
• Ferguson reflex
: mechanical stretching of cervix enhances
uterine activity
: manipulation of the cervix and stripping the
fetal membranes is associated with an increase
in PGF2αmetabolite in blood
: exact mechanism : not clear
• Interval between contractions
: 10 minutes at the onset of the first stage
→ diminishes gradually
→ 1 minute or less in the second stage
THE MYOMETRIUM
• Periods of relaxation between contractions
- essential to welfare of the fetus
- unremitting contraction of uterus compro-
mises uteroplacental blood flow, cause fetal
hypoxia
• Duration of contraction
: in active phase
Duration 30-90 seconds (average 60 sec)
Pressure 20-60 mmHg (average 40 mmHg)
Duration of contraction in active
phase
THE MYOMETRIUM
6. Differentiation of Uterine Activity
: During active labor, uterus is transformed into 2 dis-
tinct parts:
(1) Upper segment
① actively contracting
② becomes thicker as labor advances
③ quite firm or hard
(2) Lower segment
① relatively passive
② develops into a much thinly walled passage
for the fetus
③ much less firm
THE MYOMETRIUM
THE MYOMETRIUM
• Physiologic retraction ring
- As a result of the thinning of the lower uterine
segment and the concomitant thickening of the
upper
- the boundary between the two is marked by a
ridge on the inner uterine surface
• Pathologic retraction ring (the ring of Bandle)
- When the thinning of the lower uterine seg-
ment is extreme, as in obstructed labor, the
ring is veryprominent
THE MYOMETRIUM
THE MYOMETRIUM
THE MYOMETRIUM
7. Change in Uterine Shape
: each contraction produces elongation of uterus
with decrease in horizontal diameter
→ important effect on labor process
① decrease in horizontal diameter
→ straightening of fetal vertebral column
② lengthening of uterus
→ longitudinal fibers are drawn taut
→ pulled upward the lower segment & cervix
→ important factor in cervical dilatation
THE MYOMETRIUM
8. Ancillary Forces in Labor
: After the cervix is dilated fully, the most impor-
tant force in the expulsion of the fetus is that
produced by increased maternal intraabdomi-
nal pressure
“Pushing”
- increased intraabdominal pressure by con-
traction of abdominal muscles, simultaneously
with forced respiratory efforts with glottis
closed
- important force in the expulsion of fetus
- similar to that involved in defecation
Thank You !
STAGES OF LABOR
MECHANISM OF NORMAL LABOR IN
OCCIPUT PRESENTATION

 Labor : uterine contractions that effect dilatation of
 Parturition: bringing forth of young, encompass all

 Phase 0: Prelude to Parturition
 Phase 1: Preparation for Labor
 Phase 2: Process of Labor
 Phase 3: Parturition Recovery

PHASES OF PARTURITION &
ONSET OF LABOR
 Divide 4 uterine phases: correspond to major
during pregnancy
PHASE 2 : PROCESS OF LABOR
 Active labor : Ut contrations bring about progressive
 4 stages of labor
1st STAGE OF LABOR
2 STAGE OF LABOR: FETAL DESCENT
nd
3rd STAGE OF LABOR:
DELIVERY OF PLACENTA & MEMBRANES
4th STAGE OF LABOR:
IMMEDIATE PUERPERIUM
PHASE 3 OF PARTURITION:
INVOLUTION
 Immediately after delivery & for 2 hours or so
 Involution of Ut & reinstitution of ovulation

 Complete Ut involution : 4~6 wks
 Infertility persist as long as breast feeding is continued
( lactation  anovulation & amenorrhea)
POSITION
FETAL LIE
 The relation of the long axis of the fetus to that of the
mother
 Longitudinal lie - found in 99% of labours at term
 Transverse lie - multiparity, placenta praevia, hydramnios,

uterine anomalies
 Oblique lie: unstable (become logitudinal or transversal)
 By abdominal palpation, vaginal examination, and

POSITION
FETAL PRESENTATION
 The presenting part is the portion of the body of the fetus
that is foremost in the birth canal
 The presenting part can be felt through the cervix on

vaginal examination
 Longitudinal lie  cephalic presentation

 Transverse lie  shoulder presentation

POSITION
ATTITUDE
 Posture of the fetus  folded on itself to accommodate the
shape of the uterus
 Flexed head, thighs, knees &feet
 The arms crossed over the chest
 Face presentation  extended concave contour of the

vertebral column
vertex )A( sinciput )B( brow )C( face )D(
Longitudinal lie. Cephalic presentation. Differences in attitude of fetal

body,
Note changes in fetal attitude in relation to fetal vertex as the fetal head
becomes less flexed
POSITION
canal
The chosen point:
 Vertex presentation  occiput
 Face presentation  mentum
 Breech presentation  sacrum
Each presentation has 2 positions: Rt or Lt

posterior OA
ROA LOA
ROT LOT
ROP LOP
OP
LOA LOP
~
'
t
J

Right occiput anterior (ROA)
PRESENTATIONS & POSITIONS
AT TERM
 Vertex  96%
2/3 Lt
1/3 Rt
 Breech  3.5%
 Face 0.3%
 Shoulder 0.4%

~

Transverse lie. Right acromio-dorso-posterior position (RADP). The
shoulder of the fetus is to the mother's right, and the back is posterior
MECHANISM OF LABOUR WITH
OCCIPUT PRESENTATIONS
1 - ENGAGEMENT
LABOUR
The greatest transverse diameter BPD passes through the pelvic
inlet
It may occur in the last few weeks of pregnancy or only in labour
especially in multipara
The fetus enters the pelvis in transverse or oblique diameter
 LOT  40%
 ROT  20%
 OP  20% ROP > LOP
 ROA / LOA  20%
 Asynclitism LABOUR
2 - DESCENT
 In nullipara engagement takes place before the onset of
 In multipara descent begins with engagement
 It is gradually progressive till the fetus is delivered
 It is affected by the uterine contractions & thinning of the
lower segment
Ear presentation
3-FLEXION
 The descending head meets resistance of pelvic floor, Cx

& walls of the pelvis  flexion
 The shorter suboccipito-begmatic is substituted for the

longer occipito-frontal
occipito-frontal to suboccipito-bregmatic diameter typically reduces
the anteroposterior diameter from nearly 12 to 9.5 cm
4-INTERNAL ROTATION
 Turning of the head from the OT position  anteriorly
 Less commonly OT  posteriorly towards the sacrum

135º
 It is not accomplished till the head has reached the

spines
The levator ani muscles form a V shaped sling that tend
to rotate the vertex anteriorly
 It is completed by the time the head reaches the pelvic

EXTENSION
 When the flexed head reaches the vulva it undergoes
contact with the inferior margin of the symphysis pubis
 Crowning  the largest diameter of the fetal head is

 The head is born by further extension as the occiput,

bregma, forehead, nose, mouth & chin pass successively
over the perineum
EXTERNAL ROTATION RESTITUTION
 After delivery of the head it returns to the position it
occupied at engagement, the natural position relative to
the shoulders (oblique position)
 Then the fetal body will rotate to bring one shoulder
 Restitution is followed by complete external rotation to
thigh)
 The anterior shoulder slips under the pubis
 By lateral flexion of the fetal body the post shoulder will
be delivered & the rest of the body will follow
DELIVERY OF PLACENTA
PUERPERIUM
LACTATION

THIRD STAGE
 DELIVERY OF PLACENTA
 Sign of placental separation (uterine sign, vulva sign, cord

sign)
 Modified Crede
 Brandt Andrew
 Controlled cord traction

Controlled cord traction

 Prevent postpartum hemorrhage
 Oxytocic drugs:
 Syntocinon® : IV push, IV drip, IM
 Methergin® : IM, IV
 Perineal tear during vaginal birth
 First-degree tear
 Second-degree tear
 Third-degree tear
 Fourth-degree tear
Repairing fourth-degree perineal tear

POSTPARTUM CARE: 10 BS
 Blood pressure
 Bladder
 Bloody discharge
 Basket
 Bowel
 Breast engorgement
 Breast feeding
 Baby
 Blue
 Brain
PUERPERIUM
 The time from the delivery of the placenta through the first
few weeks after the delivery
 This period is usually considered to be 6 weeks in duration
 By 6 weeks after delivery, most of the changes of pregnancy,

labor, and delivery have resolved and the body has reverted to
the nonpregnant state
PUERPERIUM
UTERUS
 The pregnant term uterus (not including baby, placenta, fluids,
etc) weighs approximately 1,000 g
 In the 6 weeks following delivery, the uterus recedes to a weight

of 50-100 g
 Immediately postpartum, the uterine fundus is palpable at or

near the level of the maternal umbilicus
 Thereafter, most of the reduction in size and weight occurs in

the first 2 weeks, at which time the uterus has shrunk enough
to return to the true pelvis
PUERPERIUM
UTERUS
PUERPERIUM
UTERUS
PUERPERIUM
UTERUS
 Over the next several weeks, the uterus slowly returns to its
nonpregnant state, although the overall uterine size remains
larger than prior to gestation
 The endometrial lining rapidly regenerates, so that by the 7th

day endometrial glands are already evident
 By the 16th day, the endometrium is restored throughout the

uterus, except at the placental site
PUERPERIUM
UTERUS
 Immediately after delivery, a large amount of red blood flows
from the uterus until the contraction phase occurs
 Thereafter, the volume of vaginal discharge (lochia) rapidly ↓
 The duration of this discharge - lochia rubra - is variable
 The red discharge progressively changes to brownish red, with a

more watery consistency (lochia serosa)
 Over a period of weeks, the discharge continues to ↓ in amount

and color and eventually changes to yellow (lochia alba)
 The period of time the lochia can last varies, although it averages
approximately 5 weeks
PUERPERIUM
UTERUS
 The amount of flow and color of the lochia can vary
considerably
 15% of women have continue to have lochia 6 weeks or more

postpartum
 Often, women experience an increase in the amount of

bleeding at 7-14 days secondary to the sloughing of the
eschar on the placental site
 This is the classic time for delayed postpartum hemorrhages to

occur
PUERPERIUM
CERVIX
 The cervix -rapidly reverts to a nonpregnant state, but it never
returns to the nulliparous state
 By the end of the first week, the external os closes such

that a finger cannot be easily introduced
PUERPERIUM
VAGINA
 The vagina also regresses, but it does not completely return to
its prepregnant size
 Resolution of the increased vascularity and edema occurs

by 3 weeks, and the rugae of the vagina begin to reappear in
women who are not breastfeeding
 At this time, the vaginal epithelium appears atrophic on smear
 This is restored by weeks 6-10; however, it is further delayed

in breastfeeding mothers because of persistently decreased
estrogen levels
PUERPERIUM
PERINEUM
 The perineum has been stretched and traumatized, and
sometimes torn or cut, during the process of labor and delivery
 The swollen and engorged vulva rapidly resolves within 1-2

weeks
 Most of the muscle tone is regained by 6 weeks, with more

improvement over the following few months
 The muscle tone may or may not return to normal, depending

on the extent of injury to muscle, nerve, and connecting
tissues
PUERPERIUM
ABDOMINAL WALL
 The abdominal wall remains soft and poorly toned for many
weeks
 The return to a pre-pregnant state depends greatly on

maternal exercise
PUERPERIUM
OVARIES
 The resumption of normal function by the ovaries is highly
variable and is greatly influenced by breastfeeding the infant
 The woman who breastfeeds her infant has a longer period of

amenorrhea and anovulation than the mother who chooses to
bottle-feed
 The mother who does not breastfeed may ovulate as early as

27 days after delivery
 Most women have a menstrual period by 12 weeks; the mean

time to first menses is 7-9 weeks
PUERPERIUM
BREASTS
 The changes to the breasts that prepare the body for
breastfeeding occur throughout pregnancy
 If delivery ensues, lactation can be established as early as 16

weeks' gestation
 Lactogenesis is initially triggered by the delivery of the

placenta → ↓ levels of estrogen and progesterone, with the
continued presence of prolactin
 If the mother is NOT breastfeeding, the prolactin levels ↓ and

return to normal within 2-3 weeks
PUERPERIUM
BREASTS
 The colostrum is the liquid that is initially released by the
breasts during the first 2-4 days after delivery
 High in protein content, this liquid is protective for the

newborn
 The colostrum, which the baby receives in the first few days
postpartum, is already present in the breasts, and suckling by
the newborn triggers its release
PUERPERIUM
BREASTS
 The process, which begins as an endocrine process, switches to
an autocrine process; the removal of milk from the breast
stimulates more milk production
 Over the first 7 days, the milk matures and contains all
necessary nutrients in the neonatal period
 The milk continues to change throughout the period of

breastfeeding to meet the changing demands of the baby
MANAGEMENT OF NORMAL
PUERPERIUM
 The majority of mothers are perfectly well during the
puerperium and should be encouraged to establish
normal activities
 Immediately following the delivery of the placenta

observation of :
PUERPERIUM
1. Vital signs (P, BP, Temp, R.R)
+ contraction of the uterus (uterin involution)
+ lochia (amount; colour and odder)
= every 5 min. for ½ hours,

then: every ½ hourly for 2 hours,
then: transfer the mother to the postnatal ward and
observation every 2 hours for 6 hours,
then: 6 hourly till discharge
PUERPERIUM
PUERPERIUM
2. Breast examination
3. The mother should be encouraged to pass urine

PUERPERIUM
PUERPERIUM
4. Early mobilization
+ lawer limb examination for the detection of signs of DVT
every day
5. Management of episiotomy; and perineum tears
6. In normal delivery the mother can go home 48 hours

after delivery; and 72 hours in C-section
7. Diet regime
8. Postnatal visit
9. Advising for contraception and spacing of pregnancy

BREAST FEEDING
LACTATION
 In those mothers who breast feed, lactation is the most
dominant physiological event of puerperium
 The primary function of breast feeding is to continuing of

nutrition for newborn
 The secondary functions:
protection agonist infant infection
inhibition of ovarian activity
encouragement of uterine involution

BREAST CHANGES
BREAST
MILK PRODUCTION
 2 similar independent mechanisms for successful
lactation :
1. Prolactin (PRL) release from anterior pituitary →

mammary glandular tissue → stimulation of milk
secretion
 PRL is long chain of polypeptide; it has only physiological

role that its action on lactating breast
MILK PRODUCTION
2. Prolactin level during lactation depending on the
suckling (strength , frequency and duration) → PRL
release from anterior pituitary → reaching peak blood
level at 30 -45 min. after suckling and returns to the basal
level 2 hours after suckling
 Adequate emptying of milk – secretary glands

MILK PRODUCTION
 Basal PRL is highest in the immediate puerperium, but:
 In breast feeding → ↓ slowly as suckling declines in later

lactation → revert to non-pregnant levels immediately
after weaning (54 weeks)
 In bottle feeding → reverted to non pregnant levels

immediately after delivery ( 10 weeks)
 So PRL appears essential for lactation due to

bromocriptin or dopamine agonist which is selectively
inhibits PRL secretion and ↓ milk secretion
MILK PRODUCTION
 Milk ejection reflex (milk lead down) mediated by release
of oxytocin from hypothalamus and posterior pituitary
 causing contraction of myoepithelial cells around the

milk –secretary
 dilatation of main ducts
So, expelling milk from glands
 Oxytocin released in response to: suckling, and sensory

input like mother seeing or hearing their baby crying
 The key event in lactating amenorrhea is suckling: induced

changes in the hypothalamic sensitivity to the feed back
effects of ovarian hormones
 During lactation hypothalamus is more sensitive to the

negative feedback and less sensitive to the positive
feedback
In breast feeding:
During first week of suckling (60 min/day), the ovarian

activity is inhibited and menstruation is suppressed
At 52 weeks normal ovulatory cycles occurs
Breast feeding has important contraceptive effect, but

not absolutely reliable especially after menstruation
returns, and 1-10% of women will conceive during lactation
ECTOPIC PREGNANCY.
ABORTION
ECTOPIC PREGNANCY
DEFINITION
?
ECTOPIC PREGNANCY
DEFINITION
 Implantation outside of the uterine cavity
 It is a condition that significantly jeopardizes the mother
 Catastrophic bleeding may occur when the implanting

pregnancy erodes blood vessels / ruptures of the tubal wall
IMPLANT LOCATIONS
 Tubal: 95% (80% ampullary portion)
 Ovarian: < 1%
 Abdominal: 1-2%
 Cervical: 0.15%
 Cornual: 2%
ETIOLOGY
 Salpingitis - 6x increase the risk of ectopic pregnancy
 Operation of fallopian tubes
 IUD (intrauterine device)
 Dysfunction of fallopian tubes
 Other: endometriosis
OUTCOMES OF ECTOPIC PREGNANCY
 Tubal abortion
 8-12 weeks - ampullary portion
 Rupture of tubal pregnancy

 5 weeks - isthmic portion
 Tubal abortion with subsequent implantation

 on an intraperitoneal structure, for example liver
pregnancy
CLINICAL MANIFESTATIONS
 Amenorrhea - 70-80% (6-8 weeks)
 Abdominal and pelvic pain - the most common symptom,

which is present in nealy all patients
 Pain is a result of distented of fallopian tube and irritation of
peritoneum by blood
 Irregular vaginal bleeding - results from the sloughing of

the decidua
 Shock - result from amount of blood loss
 Abdominal mass
PHYSICAL FINDINGS IN TUBAL
PREGNANCY
 Anemic / pale face
 Pulse ↑
 BP
 T < 38 ºC
ABDOMINAL EXAMINATION
 Distention and tenderness with or without rebound
 Decreased bowel sound
 Shifting dullness positive
 Mass
PELVIC EXAMINATION
 Slightly open cervix with bleeding
 Cervical motion tenderness
 Adnexal tenderness
 Adnexal mass
 The uterus size may be normal / enlarged

 Typical cases can be determined easy
 Early ectopic pregnancy / unruptured type - difficult
 It is necessary to need assistant examination

A. hCG TEST
 80-100% positive
 Urinary hCG level
 Blood hCG level
 If hCG negative, ectopic pregnancy does not be rule out
B. TYPE B ULTRASOUND
C. CULDOCENTESIS
 Aid in the identification of peritoneum bleeding
 Positive (noncloting blood)
 Ectopic pregnancy may be confirmed
 Negative ectopic pregnancy does not be depletion

D. LAPAROSCOPY
 It is a direct visualization and accurate method to diagnosis

ectopic pregnancy
 Even laparoscopy - 2-5% misdiagnosis rate
 an extremely early tubal

pregnancy gestation may
not be identified
PATHOLOGY OF ENDOMETRIUM
 Curettage of the uterine cavity can also help rule out ectopic
pregnancy
 Identification of chorionic villi in curetting may identify an

intrauterine pregnancy
 Abortion
 Acute salpingitis
 Acute appendicitis
 Rupture of corpus luteum
 Torsion of ovarian cyst

TREATMENT
SURGICAL TREATMENT
 Salpingectomy
 Conservative operation - Salpingostomy
 Segmental resection and tubal reanastomosis

TREATMENT
CHEMICAL THERAPY
 Drug: MTX
 Indications:
 The diameter of the mass < 3cm
 Unrupture
 Not significantly bleeding
 hCG level < 2000 UI/L

ABORTION
DEFINITION
 The termination of a pregnancy before 26 weeks from the

first day of the last menstrual period
CLASSIFICATION
 Early abortion: < 12 wks
 Late abortion: 12-28 wks
 Spontaneous abortion
 Artificial abortion
ETIOLOGY
 Genetic factors
 Maternal factors
 Infection
 Systemic factors, heart disease, sever anemia, endocrine
 Reproductive tract abnormality
 Immunologic factors
 Enviromental factors - Toxin, Radiation, smoking,

PATHOLOGY
1. Haemorrhage occurs in the

decidua basalis leading to local
necrosis and inflammation
PATHOLOGY
2. The ovum, partly or wholly

detached, acts as a foreign body
and irritates uterine contractions.
The cervix begins to dilate.
PATHOLOGY
3. Expulsion complete.
The decidua is shed during the
next few days in the lochial flow
 Haemorrhage
 usually the first sign
 may be significantly if placental separation is

incomplete
 Pain
 usually intermittent, ‘like a small labrur’
 it ceases when the abortion is complete

THREATENED ABORTION
 Low abdominal pain
 Cervix is closed
 Unruptured membranes
 Embryo survive
INEVITABLE ABORTION
 Bleeding increased
 Pain development
 Rupture of membranes
 Cervix dilation
 Embryo tissue incarcerated

in the cervix
COMPLETE ABORTION
 Uterine contractions are felt,
the cervix dilates and blood
loss continues
 The fetus and placenta are

expelled complete, the uterus
contracts and bleeding stops
 No further treatment is needed

INCOMPLETE ABORTION
 In spite of uterine contractions
and cervical dilatation, only the
fetus and some membranes are
expelled
 The placenta remains partly

attached and bleeding continues
 This abortion must be completed

by surgical methods
MISSED ABORTION
 Is the retention of a failed intrauterine pregnancy for a
extended period, usually defined as > 2 menstrual
cycles
RECURRENT ABORTION
 The patient has had two / more consecutive
spontaneous abortions
SEPTIC ABORTION
TREATMENT
INCOMPLETE ABORTION
 Remove the embryo and placenta as soon as possible
 Negative pressure suction
 Embryulcia
MISSED ABORTION
 Notice blood clot function prevent DIC
SEPTIC ABORTION
 Broad-spectrum antibiotics
REMOVAL OF PLACENTAL TISSUE WITH OVUM FORCEPS
REMOVAL OF PLACENTAL TISSUE WITH CURETTE
Lecture 9
PRETERM AND POSTTERM

DELIVERY

PRETERM DELIVERY
DEFINITION OF TERMS
I. AS TO SIZE
 Small-for-gestational age / fetal growth restriction /
intrauterine growth restriction (SGA/IUGR)
 newborns with birthweight below the 10th percentile for
gestational age
 Large-for-gestational age (LGA)

 birthweight above the 90th percentile
DEFINITION OF TERMS
II. AS TO AoG
 Preterm / premature birth
 neonates born too early
 delivery before 37 completed weeks
 Term
 37 – 42 weeks
 Post term
 > 42 weeks
I. Medical and Obstetrical Complications
 Preeclampsia
 Fetal distress
 Fetal growth restriction
 Placental abruption
 Fetal death
 Spontaneous preterm labor with / without prematurely

ruptured membranes
II. Threatened Abortion
 Vaginal bleeding or spotting is associated with ↑

incidence of subsequent pregnancy loss prior to 24 weeks,
preterm labor, and placental abruption
1. Cigarette smoking
 Associated with:
 20 % of low-birthweight neonates
 8 % of preterm births
 5 % of perinatal deaths
 2- to 5-fold risk of preterm PROM

 1.2- to 2-fold risk of preterm delivery
 1.5- to 3.5-fold risk of fetal growth restriction
 ↑ incidence of ectopic pregnancy, placental abruption,

and placenta previa
2. Inadequate maternal weight gain during pregnancy
3. Illicit drugs
4. Other maternal factors:

 young or advanced maternal age
 poverty
 short stature
 vitamin C deficiency
 occupational factors: prolonged walking or standing, strenuous
working conditions, and long weekly work hours
5. Psychological and physical stress
6. Physical abuse
IV. Genetic Factors
 Gene for decidual relaxin
 Fetal mitochondrial trifunctional protein defects or

polymorphism in the interleukin-1 gene complex, 2-adrenergic
receptor, or tumor necrosis factor- α (TNF- α) may also be
involved in preterm membrane rupture
V. Chorioamnionitis
IDENTIFICATION OF WOMEN AT RISK
FOR SPONTANEOUS PRETERM LABOR
1. Risk-Scoring Systems
 Not effective
2. Prior Preterm Birth

 Strongly correlates with subsequent preterm labor
 Risk of recurrent preterm = 3x
 > 1/3 of women whose first 2 newborns were preterm will

subsequently deliver a 3rd preterm newborn
3. Incompetent Cervix
 Recurrent, painless cervical dilatation and spontaneous
midtrimester birth in the absence of spontaneous
membrane rupture, bleeding or infection
4. Cervical Dilatation
 Asymptomatic cervical dilatation after midpregnancy,
although some clinicians consider it to be a normal
anatomical variant, particularly in parous women
ULTRASONOGRAPHIC MEASUREMENT
OF CERVICAL LENGTH
 Cervical length at 24 weeks = 35 mm, and those women with
progressively shorter cervices experienced ↑ rates of preterm
birth
 Women with a previous preterm birth (< 32 weeks) should
undergo, on her next pregnancy, an ultrasound examination of
cervical length between 16 to 24 weeks AOG; a shortened cervix
(< 25 mm) correlates with another subsequent preterm birth
before 35 weeks
ULTRASONOGRAPHIC MEASUREMENT
OF CERVICAL LENGTH
 The value of cervical length to predict birth < 35 weeks is
apparent only in women at high risk for preterm birth
 Routine cervical ultrasonography currently has NO role in the

screening of normal-risk pregnant women
5. Signs and Symptoms
 painful / painless uterine contractions
 pelvic pressure
 menstrual-like cramps
 watery vaginal discharge
 pain in the low back

 Glycoprotein - present in high concentrations in maternal
blood and in amnionic fluid which play a role in
intercellular adhesion during implantation and in the
maintenance of placental adhesion to the decidua
 Values > 50 ng/mL are considered positive
 Positive value for cervical / vaginal fetal fibronectin assay,

as early as 8 to 22 weeks - powerful predictor of
subsequent preterm birth
8. Bacterial Vaginosis
 NOT an infection, a condition in which the normal,
hydrogen peroxide–producing lactobacillus-predominant
vaginal flora is replaced with anaerobes (Gardnerella
vaginalis, Mobiluncus species and Mycoplasma hominis)
 Associated with spontaneous abortion, preterm labor,
preterm ruptured membranes, chorioamnionitis and
amniotic fluid infection
 May precipitate preterm labor by a mechanism similar to
that proposed for amniotic fluid infection
 Screening and treatment have not been shown to prevent
preterm birth
10. Salivary Estriol
 ↑ maternal salivary estriol concentration and
subsequent preterm birth
11. Periodontal Disease

 Oral bacteria - Fusobacterium nucleatum and
Capnocytophaga species, have been associated with
upper genital tract infection in pregnant women
 ↑ 7x risk of preterm birth
INFECTIONS RELATED TO
PRETERM LABOR
Bacterial Gardnerella vaginalis, - Vaginal pH > 4.5 Metronidazole
vaginosis Mobiluncus species, and - Homogenous vaginal 500 mg BID for 7
Mycoplasma hominis discharge days
- Amine odor when vaginal
secretions are mixed with
KOH
- Vaginal epithelial cells
heavily coated with bacilli
“clue cells”
- Gram staining of vaginal
secretions show few white
cells along with mixed flora
as compared with the normal
predominance of lactobacilli
PRETERM LABOR
Trichomoniasis and Trichomonas vaginalis - and specific alternative - Routine screening
Candida Vaginitis demonstration of and treatmetn for this
Trichomonads by wet mount condition cannot be
of vaginal secretions; recommended
Trichomondas are identified - Metronidazole 250
most accurately by culture mg TID for 7 days
using Diamond medium, - Miconazole,
Direct immunoflorescent, Clotrimazole and
Monoclonal Ab staining is nystatin are effective
sensitive for vaginal candidiasis
Lower genital tract Chlamydia trachomatis - Genitourinary Chlamydial Erythromycin 500 mg

infection infection at 24 weeks but not PO QID for 7 days
at 28 weeks detected via ligase
chain reaction assay was
associated with a 2-fold
increase in subsequent
spontaneous preterm birth
PRETERM LABOR
Periodontitis Fusobacterium Teeth cleaning
nucleatum and and polishing;
Capnocytophaga species deep root scaling
and planning
plus
metronidazole
I. PRETERM RUPTURED MEMBRANES
 A history of vaginal leakage of fluid should prompt a sterile

speculum examination to visualize gross vaginal pooling of
amnionic fluid, clear fluid from the cervical canal, or both
 Confirmation by ultrasonographic examination to assess

amnionic fluid volume; to identify the presenting part; and
if not previously determined, to estimate gestational age
 After confirmation of ruptured membranes, the following
steps are taken:
1. Cervical dilatation and effacement are estimated visually

during a sterile speculum examination
2. If < 34 weeks, if there are no maternal / fetal indications

for delivery, the woman and her fetus are initially
observed in the labor unit
 Broad-spectrum parenteral antimicrobials are begun to
prevent chorioamnionitis
 Fetal heart rate (FHR) and uterine activity are monitored
for cord compression, fetal compromise, and early labor
3. If < 34 weeks, betamethasone (two 12-mg doses intramuscularly
24 hours apart) or dexamethasone (6 mg intramuscularly every
12 hours for 4 doses) is given
4. If the fetal status is reassuring, and if labor does not ensue, the
woman is usually transferred to an antepartum unit and
observed for labor, infection, or fetal jeopardy
 For pregnancies 34 weeks or >, if labor does not begin

spontaneously, then it is induced with intravenous oxytocin
unless contraindicated. Cesarean delivery is performed for usual
indications, including failed induction of labor
 During labor / induction, a parenteral antimicrobial is given for

prevention of group B streptococcal infection
II. PRETERM LABOR WITH INTACT FETAL MEMBRANES
Diagnosis
Criteria to document preterm labor:
 Contractions of 4 in 20 minutes / 8 in 60 minutes + progressive

change in the cervix
 Cervical dilatation > 1 cm
 Cervical effacement of 80 % or greater

II. PRETERM LABOR WITH INTACT FETAL
MEMBRANES
 Managed the same as for those with preterm ruptured
membranes
 The cornerstone of treatment is to avoid delivery < 34
weeks, if possible
1. Amniocentesis to detect infection (not usually indicated)
2. Steroid therapy to enhance fetal lung maturation

3. Thyrotropin-Releasing Hormone for fetal lung maturation
INTERVENTIONS TO DELAY
PRETERM BIRTH
1. Antimicrobials - NOT recommended for the sole
purpose of preventing delivery
2. Emergency cerclage
3. Treatment for bacterial vaginosis

1. Bed rest
2. Hydration and sedation
3. β-adrenergic receptor agonists

 Ritodrine
 Terbutaline, Isoxuprine
 Parenteral β-agonists prevent preterm birth for at least 48 hours,

facilitating maternal transport and giving of steroids
4. Magnesium sulfate
 Ionic Mg in a sufficiently high concentration can alter myometrial
contractility
 Role is presumably that of a Ca antagonist
 Clinical observations are that Mg in pharmacological doses may inhibit labor
 Intravenously administered Mg sulfate - a 4 g loading dose followed by a
continuous infusion of 2 g/hr - usually arrests labor
5. Prostaglandin inhibitors (ex. Indomethacin)

6. Calcium channel blockers
 Nifedipine
7. Atosiban (oxytocin antagonist)

POSTTERM DELIVERY
DEFINITION OF TERMS
 Postmature - infant with recognizable clinical features
indicating a pathologically prolonged pregnancy
 Postdates - should be abandoned, because the real issue in

many postterm pregnancies is "post-what dates?“
 Postterm / Prolonged Pregnancy - preferred expression for

an extended pregnancy
 According to ACOG (1997): 42 completed weeks (294 days) or

more from the 1st day of the last menstrual period (LMP)
POSTMATURITY SYNDROME
 CHARACTERISTIC APPEARANCE / FEATURES
 Wrinkled, patchy, peeling skin
 A long, thin body suggesting wasting
 Advanced maturity because the infant is open-eyed, unusually alert,

and appears old and worried-looking
 Skin wrinkling prominent on the palms and soles
 Nails are long

FETAL DISTRESS IN
POSTTERM PREGNANCY
 Antepartum fetal jeopardy and intrapartum fetal distress
were the consequence of cord compression associated with
oligohydramnios
 One / more prolonged decelerations preced 3/4 of

emergency cesarean deliveries for fetal jeopardy
 Findings are consistent with cord occlusion as the proximate

cause of fetal distress
 Other correlates - oligohydramnios and viscous meconium

FETAL DISTRESS IN
POSTTERM PREGNANCY
Prolonged fetal heart rate (FHR) deceleration prior to
emergency cesarean delivery in a
postterm pregnancy with oligohydramnios
FETAL GROWTH RESTRICTION IN
POSTTERM PREGNANCY
 Stillbirths - more common among growth-restricted infants
delivered at 42 weeks or beyond
 1/3 of the postterm stillbirths - growth restricted
 Morbidity and mortality - significantly ↑ in the growth-

restricted infants
MANAGEMENT OF
POSTTERM PREGNANCY
 Antepartum interventions are indicated in cases of postterm
pregnancies
 When to induce? 41 or 42 weeks?
 41 weeks with favorable cervix, induce lab

or
 41 weeks with unfavorable cervix, antepartum fetal testing
 42 weeks, whether the cervix is favorable or not, labor is

generally induced
UNFAVORABLE CERVIX
 A cervix that is closed, uneffaced with a Bishop score of less
than 7
 Women in whom there was NO cervical dilatation at 42 weeks

had a 2x ↑ cesarean delivery rate for "dystocia“
 Cervical length of 3 cm or less determined by transvaginal

ultrasonography - predictive of successful induction
UNFAVORABLE CERVIX
 ACOG (1997) has concluded that prostaglandin gel can be
used safely in postterm pregnancies
 Sweeping / stripping of the membranes:

 ↓ the frequency of postterm pregnancy
 Stripping did NOT modify the risk for cesarean delivery and
maternal / neonatal infections were NOT ↑
 Station of the vertex is important in predicting successful

postterm induction
Lecture 10
FETAL DISTRESS.
INTRAUTERINE FETAL DEATH

DEFINITION
 Fetal distress is the term commonly used to describe fetal
hypoxia
 It is a clinical diagnosis made by indirect methods and should be

defined as:
 Hypoxia that may result in fetal damage / death if not reversed
or the fetus delivered immediately
 It includes acute distress and chronic distress

ETIOLOGY
 MATERNAL
 Poor placental perfusion
 Hypovolaemia
 Hypotension
 Myometrial hypertonus
 prolonged labor
 excess oxytocin
ETIOLOGY
 FETAL:
 Cord compression
 oligohydramnios
 entanglement
 prolapse
 Pre-existing hypoxia / growth retardation
 Infection
 Cardiac
MECHANISM
 There are potentially limitless causes for fetal distress, but
several key mechanisms are usually involved
 Contractions reduce temporarily placental blood flow and

can compress the umbilical cord
 If a women is in labor longer then this can cause fetal

distress via the above mechanism
MECHANISM
 Acute distress can be a result of:
 placental abruption
 prolapse of the umbilical cord (especially with breech presentations)
 hypertonic uterine states
 use of oxytocin
 Hypotension can be caused by either epidural anesthesia or the

supine position, which reduces inferior vena cava return of blood
to the heart
 The decreased blood flow in hypotension can be a cause of fetal

distress
ACUTE FETAL DISTRESS
SIGNS AND SYMPTOMS
 Cardiotocography signs:
 Increased / decreased fetal heart (tachycardia and

bradycardia), especially during and after a contraction
decreased varibility in the fetal heart rate
 Abnormal fetal heart rate (< 120 or > 160 bpm)
 A normal fetal heart rate may slow during a contraction but

usually recovers to normal as soon as the uterus relaxes
 A very slow fetal heart rate in the absence of contractions or

persisting after contractions is suggestive of fetal distress
SIGNS AND SYMPTOMS
 A rapid fetal heart rate may be a response to:
 maternal fever
 drugs
 hypertension
 amnionitis
 In the absence of a rapid maternal heart rate, a rapid fetal

heart rate = a sign of fetal distress
 For a diagnosis of fetal distress to be made, one / more of
the following must be present:
 persistent severe variable deceleration
 persistent and non-remediable late declarations
 persistent severe bradycardia
SIGNS AND SYMPTOMS
 Amniotic fluid is contaminated by meconium
 There are 3 degrees about contaminated:

 I - slight contamination
 The color of the amniotic fluid = slight green
 II - mild contamination
 Color of the amniotic fluid = dark green
 III - severe contamination

 Color of the amniotic fluid = dark yellow
 If the amniotic fluid is severely contaminated, it suggests

SIGNS AND SYMPTOMS
 Decreased fetal movement felt by the mother
 Biochemical signs - assessed by collecting a small sample of

baby‘s blood from a scalp prick through the open cervix in
labor:
 Fetal acidosis elevated fetal blood lactate levels
 A fetal scalp pH < 7.2 , Po > 60 mmHg suggests fetal distress

2
CHRONIC FETAL DISTRESS
SIGNS AND SYMPTOMS
 Decreased / disappear of fetal movement:
 < 10 times per 12 hours is regarded as decreased
 With the first effect of hypoxia, the fetal movement is

increased
 If the hypoxia persists, the fetal movement is decreased, and

may disappear
 If the fetal movement lost, the fetal heart beat will be

disappearing within 24 hours
CAUTIONS: Dangerous for the fetus if the fetal movement

SIGNS AND SYMPTOMS
 Abnormal cardiotocography signs:
 Slow fetal heart rate (< 120 bpm) or rapid fetal heart rate
(> 180 bpm) last more than 10 min in the absence of
contractions is suggestive of fetal distress
 The fetal heart rate > 160 bpm , especially > 180 bpm, it
suggests early hypoxia, unless the maternal heart rate is
faster
SIGNS AND SYMPTOMS
 FHR < 120 bpm, typically < 100 bpm

 It is very dangerous for fetus
 The fetal heart rate normally show continuous minor

variations, with a range of about 5 bpm, loss of base line
variability implies that the cardiac reflexes are impaired,
either from the effect of hypoxia or of drugs (valium)
 It may be serious
SIGNS AND SYMPTOMS
 Early deceleration: with each contraction the rate often
slows, but it returns to normal soon after removal of the
stress
 The early deceleration in the heart rate start within 30

seconds of the onset of the contraction and return rapidly to
the baseline rate
 It is NOT of serious significance as a rule and indicate that

while the fetus is undergoing some stress the cardiac
control mechanisms are responding normally
EARLY DECELERATION
SIGNS AND SYMPTOMS
 Variable deceleration: no consistent relationship with
uterine contraction
 It is sometimes caused by compression of the umbilical cord

between the uterus and the fetal body, or because it is
looped round some part of the fetus
 Provided that it does not persist for more than a few

minutes it may have little significance, but persistence for
more than 15 minutes would call for treatment
VARIABLE DECELERATION
SIGNS AND SYMPTOMS
 The most serious pattern of heart rate changes is fetal
bradycardia with loss of baseline variability and late
decelerations
 Decrease (defined as onset of deceleration to nadir =30

seconds) and return to baseline FHR associated with a
uterine contraction
 The deceleration is delayed in timing, with the nadir of the

deceleration occurring after the peak on the contraction
LATE DECELERATION
BIOPHYSICAL PROFILE
 Biophysical Profile:
 Amniotic Fluid Volume Normal = 2 Points
 Non-Stress Test Result Positive = 2 Points
 Fetal Breathing Movements Active = 2 Points
 Fetal Extremity/Trunk Movements Active = 2 Points
 Fetal Movements Active= 2 Points
 If Biophysical Profile scores < 4 suggest fetal distress

TREATMENT
 Reposition patient: left-side-lying position
 Administer oxygen by mask
 Perform vaginal examination to check for prolapsed cord
 Ensure that qualified personnel are in attendance for

resuscitation and care of the newborn
 NOTE: each institution shall define in writing the term

qualified personnel for resuscitation and care of the
newborn
TREATMENT
 Each of the following actions should be performed and
documented prior to starting a Cesarean section for fetal
distress:
 Perform vaginal exam to rule out imminent vaginal

delivery
 Initiate preoperative routines
 Monitor fetal heart tones (by continuous fetal

monitoring or by auscultation) immediately prior to
preparation of the abdomen
TREATMENT
 Ensure that qualified personnel are in attendance for

resuscitation and care of the newborn (each institution
shall define in writing the term qualified personnel for
resuscitation and care of the newborn)
 STOP using oxytocin !

 Oxytocin can strengthen the contraction of uterine
which affects the baby's heart rate
DEFINITIONS MUST BE GRASPED
 Baseline FHR:
 approximate mean FHR rounded to increments of 5 bpm

during a 10-minute segment, excluding periodic or
episodic changes, periods of marked FHR variability, and
segments of the baseline that differ by > 25 bpm
 In any 10-minute window, the minimum baseline

duration must be at least 2 minutes or the baseline for
that period is indeterminate
 Baseline FHR variability:
 Fluctuations in the baseline FHR =2 cycles / min
 These fluctuations are irregular in amplitude and

frequency, and are visually quantitated as the amplitude
of the peak to the trough in beats per minute as follows:
 amplitude range undetectable, absent FHR variability
 amplitude range greater than undetectable but = 5 bpm,

minimal FHR variability
 amplitude range 6 bpm - 25 bpm, moderate FHR variability
 amplitude range >25 bpm, marked FHR variability
 Bradycardia:
 a baseline FHR < 120 bpm
 Tachycardia:
 a baseline FHR > 160 bpm
 Early deceleration:
 A visually-apparent, gradual decrease (defined as onset
of deceleration to nadir = 30 seconds) and return to
baseline FHR associated with a uterine contraction
 The decrease is calculated from the most recently
determined portion of the baseline
 It is coincident in timing with the nadir of the
deceleration occurring at the same time as the peak of
the contraction
 In most cases the onset, nadir, and recovery of the
deceleration are coincident with the beginning, peak,
and ending of the contraction, respectively
 Variable deceleration:
 A visually-apparent, abrupt decrease in FHR below the

baseline

 The decrease in FHR below the baseline is = 15 bpm,

lasting = 15 seconds and = 2 minutes from onset to return
to baseline
 Late deceleration:
 A visually-apparent, gradual decrease (defined as onset

of deceleration to nadir = 30 seconds) and return to
baseline FHR associated with a uterine contraction

 The deceleration is delayed in timing, with the nadir of

the deceleration occurring after the peak on the
contraction
DEFINITION
 dead fetuses or newborns weighing > 500g or > 20 wks

gestation
INCIDENCE
 4.5 / 1000 total births

DIAGNOSIS
 Absence of uterine growth
 ↓ Serial ß-hCG
 Loss of fetal movement
 Absence of fetal heart
 Disappearance of the signs & symptoms of pregnancy
 X-ray →Spalding sign

→ Robert’s sign
 U/S → 100% accurate Dx
CAUSES OF IUFD
FETAL CAUSES (25-40%)
 Chromosomal anomalies
 Birth defects
 Non immune hydrops
 Infections
CAUSES OF IUFD
PLACENTAL CAUSES (25-35%)
 Abruption
 Cord accidents
 Placental insufficiency
 Intrapartum asphyxia
 Placenta praevia
 Twin to twin transfusion Syndrome
 Chrioamnionitis
CAUSES OF IUFD
MATERNAL CAUSES (5-10%)
 Antiphospholipid antibody  Uterine rupture
 DM  Postterm pregnancy
 HPT  Drugs
 Trauma  Thrombophilia
 Abnormal labor  Cyanotic heart disease
 Sepsis  Epilepsy
 Acidosis/ Hypoxia  Severe anemia

CAUSES OF IUFD
UNEXPLAINED (25-35%)
A systematic approach to fetal death is
valuable in determining the etiology
HISTORY
A. Family History
 Recurrent abortions
 VTE / PE
 Abnormal karyotype
 Hereditary conditions
 Developmental delay
HISTORY
B. Maternal History
1. Maternal medical conditions
 VTE/ PE
 DM
 HPT
 Thrombophilia
 SLE
 Autoimmune disease
 Severe Anemia
 Epilepsy
 Consanguinity
 Heart disease
HISTORY
B. Maternal History
2. Past OB Hx
 Baby with congenital anomaly / hereditary condition
 IUGR
 Gestational HPT with adverse sequele
 IUFD
 Recurrent abortions
HISTORY
B. Maternal History
3. Current Pregnancy Hx
 Maternal age
 Gestational age at fetal death
 HPT
 DM / Gestational D
 Smooking , alcohol or drug abuse
 Abdominal trauma
 Cholestasis
 PROM / prelabor SROM
SPECIFIC FETAL CONDITIONS
 Nonimmune hydrops
 IUGR
 Infections
 Chromosomal abnormalities
 Complications of multiple gestation

PLACENTAL / CORD COMPLICATIONS
 Large or small placenta
 Hematoma
 Edema
 Large infarcts
 Abnormalities in structure/length/insertion of the umbilical cord
 Cord prolapse
 Cord knots
 Placental tumors
EVALUATION OF STILL BORN INFANTS
INFANT DESCRIPTION
 Malformation
 Skin staining
 Degree of maceration
 Color-pale ,plethoric
UMBILICAL CORD
 Prolapse
 Entanglement-neck, arms, legs
 Hematoma / stricture
 Number of vessels
 Length
EVALUATION OF STILL BORN INFANTS
AMNIOTIC FLUID
 Color-meconium, blood
 Volume
PLACENTA
 Weight
 Staining
 Adherent clots
 Structural abnormality
 Velamentous insertion
 Edema/hydropic changes
MEMBRANES
 Stained
 Thickening
INVESTIGATIONS
MATERNAL INVESTIGATIONS
 CBC
 Bl Gp & antibody screen
 HB A1 C
 Kleihauer Batke test
 Serological screening for Rubella, CMV, Toxo, Sphylis, Herpes &
Parovirus
 Karyotyping of both parents (RFL, baby with malformation)
 Hb electrophorersis
 Antiplatelet anbin tibodies
 Throbophilia screening (antithrombin, Protein C & S , factor IV
leiden, Factor II mutation, , lupus anticoagulant, anticardolipin
antibodies)
 DIC
INVESTIGATIONS
FETAL INVESTIGATIONS
 Fetal autopsy
 Karyotype
(specimen taken from cord blood, intracardiac blood, body
fluid, skin, spleen, placental wedge or amniotic fluid)
 Fetography
 Radiography
INVESTIGATIONS
PLACENTAL INVESTIGATIONS
 Chorionocity of placenta in twins
 Cord thrombosis or knots
 Infarcts, thrombosis, abruption
 Vascular malformations
 Signs of infection
 Bacterial culture for E. coli, Listeria, group B streptococcus

IUFD COMPLICATIONS
 Hypofibrinogenemia → 4-5 wks after IUFD
 Coagulation studies must be started 2 wks after IUFD
 Delivery by 4 wks or if fibrinogen ↓ < 200mg/ml

PSYCHOLOGICAL
ASPECTS & COUNSELING
 A traumatic event
 Post-partum depression
 Anxiety
 Psychotherapy
 Recurrence 0-8% depending on the cause of IUFD

RHESUS (Rh) ISOIMMUNIZATION

Rh ISOIMMUNIZATION
Blood groups (1900):
Antigens: Antibodies:
O (45%) AntiA+Anti B
A (40%) Anti B
B (10%) Anti A
AB (5%)
A and B : dominant
O : recessive
Rh ISOIMMUNIZATION
Rhesus factor (1940):
Agglutinogen (C,D,E) - mainly D
C,D,E - dominant antigen
d,e - recessive antigen

Rh ISOIMMUNIZATION
- Rh positive (85%) - homozygous (DD) (35%),
or heterozygous (Dd) (50%)
- Rh negative (15%)
Examples of Rh factor: CDe , Cde cDE
Other systems:
 kell-antikell,
 luther,
 Duffy, etc.
Rh ISOIMMUNIZATION
• So in response to introduction of foreign
protein (antigen)  production of antibody to
neutralize the antigen
• In ABO and other non Rh-incompatibility: It

usually causes mild anaemia, mainly as there
is no intrapartum boosting
• In Rhesus isoimmunization: mainly (D), but

C, E can produce antibodies
Rh ISOIMMUNIZATION
Feto-maternal haemorrhage: during pregnancy
leakage of fetal cells in the maternal
circulation (Rh+ fetal cells in Rh- maternal
circulation
Examples:
- Spontaneous abortion
- Induced abortion
- Cordocentesis, CVS, amniocentesis
- Severe preeclampsia
- Ectopic pregnancy
- Caesarean section
- Manual removal of placenta
- Silent feto-maternal haemorrhage
Rh ISOIMMUNIZATION
Development of Rhesus antibodies: depends on
factors:
1- Inborn ability to respond
2- protection if ABO incompatible 1\10
3- Strength of Rh antigen stimulus (CDe)
4- Volume of leaking feta blood (0.25ml)
IgM (7 days) doesn’t cross placenta, then IgG

21 days - crosses placenta
1- If ABO is incompatible:
Red blood cells is easily destroyed, so not

reaching enough immunological component to
cause antibody response and reaction
2 - If ABO is compatible:
Rh+ fetal cells  remain in circulation (life

span) until removed  destroyed  liberating
antigen (D)  isoimmunization
It takes time:
• 1st pregnancy is almost always not affected:
 1% - during labour or 3rd stage)
 10% - 6 months after delivery
 15% by the 2nd pregnancy
1. Cleared by
Macrophage Mother
2. Plasma
stem cells Primary Response
• 6 wks to 6 M.
• IgM
IgM antibodies
Placenta
The First Pregnancy is NOT Affected

Macroph. antigen
Presenting cell Mother
T- helper cell Secondary Response
• Small amount
B cell • Rapid
• IgG
Anti-D IgG
Placenta
Fetal Anemia
Rh ISOIMMUNIZATION
Mild Cases:
• fetal (RBC) destruction  from anti-D (IgG):
 anaemia  compensating haemopoiesis 
excess of unconjugated bilirubin
Severe Cases:
• excessive destruction of fetal (RBC)  severe
anaemia  hypoxia the tissues  cardiac or
circulatory failure  generalized edema  (H.
failure)  ascitis  IUFD
When excess of unconjugated bilirubin > (310-

350 mol/L)  It passes brain barrier 
(kernicterus)  permanent neurological and
mental disorders
Rh ISOIMMUNIZATION
Fetal and Neonatal Effects:
- Haemolytic anaemia of newborn Hb=14-18g/dl
- Icterus gravis neonatorum Hb=10-14g/dl
- Hydrops fetalis (Erythroblastosis fetalis)

I) PROPHYLAXIS
1 - Prevention of Rhesus isoimmunization: Anti D

(RhoD IgG)
• Standard dose for > 20 wks, and ½ standard

dose for < 20 wks - given within 72hours of
the incident
• SD: i.m. injection: 500 iu = 100 ugm (UK),

1500iu = 300 ugm (USA)
 1500iu = 300 ugm  neutralize 15ml

 500 iu = 100 ugm  neutralize 5ml
(4ml+1ml)
 4ml = 4x20 f.cells = 80 fetal cells
Rh ISOIMMUNIZATION
Kleihauer-Betke technique:
• (acid elution test) - measure amount of feto-

maternal haemorrhage
• If 0,1-0,25 ml of fetal blood leakes (critical

volume)  isoimmunization represented by 5
fetal cells in 50 low power microscopic field of
peripheral maternal blood
• So 1 ml is represented by 20 fetal cells

K-B test if large amount of leaking  another SD

if mother is Rh-, baby Rh+ with no
isoimmunization (checked by indirect or direct
Coombs test)
2 - A.P. administration of anti-D

• SD at 28 wks or at 28 and 36 wks will reduce
Rh isoimmunization
II) 1- Antibody Screening:
• for all pregnant women in ANC for irregular

antibodies (mainly for Rh- women), then start
at 20 wks , and every 4 weeks
2 - Management following detection of Rh
antibodies
• Should be treated in specialized centres
• Quantitative measures of antibodies +

husband genotype
• Repeat titration (indirect Coombs, detecting

of antibodies)
• Amniocentesis once necessary
• Obstetrical management based on timing of

I.U. transfusion (now cordocentesis +
fetoscopy) versus delivery
3 - Amniocentesis:
• Should be performed under ultrasound

guidance if titre > 1\16 = 0.5-1 ugm  2.5-5
I.U
• Timing: 1st amniocentesis - 10 weeks before

previous IUFD
• Start from 20-22 weeks, 2-4 weekly or more

frequent if needed
• Amniotic fluid analysis - spectrophotometry:

optical density at the height of optical density
deviation at wave length 450 nM
CORDOCENTESIS
• IU transfusion (cordocentesis, in the past

intraperitoneal transfusion) versus delivery of
the baby:
 Using Liley’s chart
 Prediction chart (Queenan curve)

 Whitefield’s action line
LILEY’S CHART
WHITEFIELD’ ACTION LINE
• Alternatively follow up with Doppler study for
the fetal middle cerebral artery
• Prognosis depends on:

 obstetrical history
 paternal genotype
 maternal history (blood transfusion,
antibody titre)
 amniocentesis results
• Delivery: Vaginal versus C-Section

• Intensive plasmaphoresis: when severe

cases anticipated, using continous flow
cell separator, as early as 12 wks
• Postnatal management: for the neonate:

 Direct Coombs test, blood group, Rh
type, Hb, bilirubin
 Mild cases: phototherapy - correction of

acidosis
 Severe cases: exchange transfusion
Lecture 13
PREGNANCY
INDUCED
HYPERTENSION

INDEX
 Diagnosis
 Etiology
 Pathogenesis
 Pathophysiology
 Prediction and Prevention
 Management
 Long-term consequences
 Gestational Hypertension – 3.7% in 150,000
(National Center for Health Statics, 2001)
 Pregnancy-related hypertension:
 Pregnancy-related deaths (3201 in US, 1991-1997)
 Black women are 3.1 x to die as white women
 Hypertensive disorders remain among the most significant

and intriguing unsolved problems in obstetrics
DIAGNOSIS
 Gestational hypertension
 Preeclampsia
 Eclampsia
 Superimposed preeclampsia (on chronic hypertension)
 Chronic hypertension
GESTATIONAL HYPERTENSION
 BP ≥ 140/90mmHg for first time during pregnancy
 No proteinuria
 BP returns to normal < 12 weeks’ postpartum
 Final diagnosis made only postpartum
 May have other signs or symptoms of preeclampsia, for example,

epigastric discomfort or thrombocytopenia
PREECLAMPSIA
Minimum Criteria
 BP ≥ 140/90 mmHg after 20 wks gestation
 Proteinuria ≥ 300 mg/24 hrs or ≥1 + dipstick
Increased certainty of preeclampsia

 BP ≥ 160/110 mmHg
 Proteinuria 2.0 g/24 hrs or ≥2+dipstick
 Serum creatinine > 1.2mg/dl unless known to be previously elevated
 Platelets < 100.000/mm3
 Microangiopathic hemolysis (Increased LDH)
 Elevated ALT or AST
 Persistent headache or other cerebral or visual disturbance
 Persistent epigastric pain
PREECLAMPSIA
 Diastolic hypertension ≥ 95mmHg
 Worsening proteinuria
 Epigastric or RUQ pain
 Thrombocytopenia
SEVERITY OF PREECLAMPSIA
 Differentiation between mild & severe preeclampsia can be

misleading
 because apparently mild disease may progress rapidly to
severe disease
 Rapid ↑ in BP, followed by convulsions is usually preceded

by unrelenting severe headache or visual disturbances
1267
ECLAMPSIA
 Preeclampsia + convulsions
 Seizures that cannot be attributed to other causes in woman

with preeclampsia
 Seizures are generalized and may appear before, during

or after labor
CHRONIC HYPERTENSION
 BP ≥ 140/90 mmHg before pregnancy or diagnosed

before 20 wks gestation (not attributable to gestational
trophoblastic disease)
or
 HT first diagnosed after 20 wks gestation and persistent

after 12 wks postpartum
 Chronic HT
 BP ↓ during the 2nd and early 3rd trimesters in both
normotensive and chronically hypertensive women
 Underlying HT
 Essential familial HT (90%)
Underlying Causes of Chronic Hypertensive Disorder
 Essential familial hypertension (hypertensive vascular disease)
 Obesity
 Atrterial abnormalities
 Renovascular hypertension
 Coarctation of the aorta
 Endocrine diorders
 Diabetes mellitus
 Cushing syndrome
 Primary aldosteronism
 Pheochromocytoma
 Thyrotoxicosis
 Glomerulonephritis (acute and chronic)
 Renoprival hypertension
 Chronic glomerulonephritis
 Chronic renal insufficiency
 Diabetic nephropathy
 Connetive tissue disease
 Lupus erythematosus
 Systemic sclorosis
 Periarteritis nodosa
 Polycystic kidney disease
 Acute renal failure
 Chronic HT →
 ventricular hypertrophy
 cardiac decompensation
 cerebrovascular accidents
 renal damage
PREECLAMPSIA SUPERIMPOSED ON
 New-onset proteinuria ≥ 300 mg / 24hrs in hypertensive
women, but no proteinuria before 20 weeks’ gestation
 A sudden increase in proteinuria or blood pressure or

platelet count < 100,000/mm³ in women with HT and
proteinuria before 20 weeks’ gestation
INCIDENCE AND RISK FACTORS
 Nulliparous women
 Incidence: 5% (wide variation)
 Influence by:
 Parity, race, ethnicity, genetic predisposition
 Nulliparous
 Total: 7.6% / severe : 3.3% (Hauth, 2000)
 Risk factors:
 Chronic hypertension, multifetal gestation, maternal old age
(>35 yrs), obesity, African-American ethnicity
 Maternal weight and the risk of preeclampsia is
progressive
BMI (kg/m²) Morbidity (%)
<19.8 4.3
>35 13.3
Gestation:
- twin 13
- single 5 (Sibai, 2000)
 Smoking during pregnancy ↓ risk of HT during pregnancy

(Bainbridge,2005 ; Zhang, 1999)
 Placenta previa ↓ risk of HT

 Eclampsia
 Somewhat preventable
 Receive adquate prenatal care
 1976 (Williams Obstetrics 15th edition)

 1/700 deliveries (Parkland Hospital)
 1983-1986
 1/1150 deliveries
 1999
 1/1750 deliveries
 2000, National Vital Statistics Report, in US

 1/3250
ETIOLOGY
BASIC CONCEPTS
 Exposed to chorionic villi for the first time
 Exposed to a superabundance of chorionic villi, as with

twins / hydatidiform mole
 Have preexisting vascular disease
 Genetically predisposed to HT developing during

pregnancy
ETIOLOGY
BASIC CONCEPTS
 Vascular endothelial damage with vasospasm,

transudation of plasma and ischemic and thrombotic
sequelae
 Currently plausible potential cause (2003, Sibai)

 Abnormal trophoblastic invasion of uterine vessels
 Immunological intolerance between maternal and fetoplacental
tissues
 Maternal maladaptation to cardiovascular / inflammatory changes
of normal pregnancy
 Dietary deficiencies
 Genetic influences
ABNORMAL TROPHOBLASTIC INVASION
 In normal implantation, endovascular trophoblasts invade
the uterine spiral arteries
 In preeclampsia:
 Incomplete trophoblastic invasion
 The magnitude of defective trophoblastic invasion of the
spiral arteries correlated with the severity of the
hypertensive disorder (2000, Madazli)
 Using electron microscopy:

 Endothelial damage
 Insudation of plasma constituents into vessel walls
 Proliferation of myointimal cells
 Medial necrosis
 Lipid and macrophage accumulates in myointimal cells
 Lipid-laden cells → atherosis (Hertig, 1945)
 Obstruction of the spiral arteriolar lumen by atherosis may

impair placental blood flow
 Placental perfusion → diminished

IMMUNOLOGICAL FACTORS
THEORY
 Formation of blocking antibodies of placental antigenic
sites might be impaired
 Number of antigenic sites provided by the placenta is
unusually great compared with the amount of antibody, as
with multiple fetuses (Beer, 1978)
 Effective immunization by a previous pregnancy is lacking,
as in first pregnancies.
 The immunization concept was supported by their

observations that preeclampsia developed less often in
multiparas who had a prior term pregnancy (Mostello, 2002;
Trupin, 1996)
IMMUNOLOGICAL FACTORS
 Early 2nd trimester - Develop preeclampsia women
 Lower proportion of helper T cells (Th1)
 Th2 dominance, mediated by adenosine, which is found

in higher serum level in preeclamptic compared with
normotensive women (Yoneyama, 2002)
 These helper T lymphocytes secrete specific cytokines

that promote implantation, and their dysfunction may
favor preeclampsia (Hayashi, 2004; Whitecar, 2001)
THE VASCULOPATHY AND THE
INFLAMMATORY CHANGES
 The decidua contains an abundance of cells that, when
activated, can release noxious agents (Staff, 1999) →
mediators to provoke endothelial cell injury
 Preeclamsia due to an extreme state of activated

leukocytes in the maternal circulation (Faas, 2000)
 Cytokines: TNF-a, interleukin → oxidative stress
(highly toxic radicals)
 Potential benefit of antioxidants to prevent

preeclampsia (Chappell, 1999; Zhang, 2002)
NUTRITIONAL FACTORS
 Dietary deficiencies and excesses over the centuries have
been blamed as the cause of eclampsia
 Supplementation with various elements such as zinc,

calcium, and magnesium to prevent preeclampsia (John,
2002)
 Obesity - potent risk factor for preeclampsia
 C-reactive protein, an inflammatory marker, was shown to

be increase in obesity, which in turn was associated with
preeclampsia (Wolf, 2001)
GENETIC FACTORS
 Hereditary hypertension is linked to preeclampsia (Ness,
2003)
 Preeclampsia - eclampsia is highly heritable in sisters,

daughters, granddaughter and daughters-in-law (Chesley
and Cooper, 1986)
 60% concordance in monozygotic female twin pairs

(Nilsson, 2004)
 HLA-DR4 preeclampsia (Kilpatrick,1989)

PATHOGENESIS VASOSPASM
 Vascular constriction - resistance and subsequent HT
 Maldistribution, ischemia of the surrounding tissues -

blood flow - necrosis, hemorrhage, and other end-organ
disturbances
PATHOGENESIS
ENDOTHELIAL CELL ACTIVATION
 Unknown factors (from placenta) are secreted into the
maternal circulation
→ activation and dysfunction of the vascular endothelium.
 Damaged or activated endothelial cells secrete substances

→ promote coagulation and ↑ the sensitivity to vasopressors
→ changes in glomerular capillary endothelial morphology
→ ↑ capillary permeability
→ ↑ blood concentrations
1289
INCREASED PRESSOR RESPONSES
 Normally, pregnant women develop refractoriness to
infused vasopressors (Abdul-Karim an Assali, 1961)
 But, early preeclampsia women have increased vascular

reactivity to infused norepinephrine and angiotensin II (Raab,
1956)
PROSTAGLANDINS
Membrane phospholipid  In preeclampsia:
hospholipase A2  Endothelial prostacyclin
(PGI2) production is
Arachidonic acid decreased
 Thromboxane A (TXA2)
COX 1, COX 2 secretion by platelets is
increased
TXA2 PGI2, PGE2  sensitivity to infused

angiotensin II
1291
Platelet  vasoconstriction
NITRIC OXIDE
 Synthesized from L-arginine by endothelial cells (potent
vasodilator)
 Nitric oxide maintains the normal low-pressure vasodilated

state characteristic of fetoplacental perfusion (Myatt, 1992)
 Preeclampsia is associated with decreased endothelial nitric

oxide synthase expression, which increases cell
permeability (Wang, 2004)
ENDOTHELINS
 Endothelin-1 (ET-1):
 potent vasoconstrictors
 produced by human endothelium
 Plasma ET-1 is increased in normotensive pregnant women,

but women with preeclampsia have even higher levels (Ajne,
2003 ; Clark, 1992)
ANGIOGENIC FACTORS
 Vascular endothelial growth factor (VEGF), Placental
growth factor (PIGF),
 Which secretion increases in normal pregnancy
 Promote angiogenesis
 Induce nitric oxide
 Vasodilatory prostaglandins
 Paradoxically, VEGF is increased in serum from women with

preeclampsia, but its bioavailability is decreased (Baker, 1995 ;
Simmons, 2000)
PATHOPHYSIOLOGY
CARDIOVASCULAR SYSTEM
 Increased cardiac afterload caused by HT
 Cardiac preload in preeclampsia

 Pathologically diminished hypervolemia of pregnancy
 Iatrogenically increased by iv crystalloid or oncotic solution
 Extravasion into the extracellular space, especially the lung

HEMODYNAMIC CHANGES
 PREECLAMPSIA
 Cardiac output elevated before HT developed than

normal pregnancy
 With clinical onset of preeclampsia

 Marked reduction in cardiac output
 Increased peripheral resistance
 By contrast, Gestational HT
 Elevated cardiac outputs with development of HT
BLOOD VOLUME
 Blood volume in term
 Normal pregnancy : 5000ml
 Not pregnancy : 3500ml
 Eclampsia : 3500ml
 Hemoconcentration in preeclampsia
 Vasoconstriction and endothelial dysfunction with vascular
permeability
 Sevirity
 Whereas, gestational HT have a normal blood volume (Silver,
1998)
1299
BLOOD VOLUME
 With severe hemoconcentration, an acute fall in hematocrit
suggested resolution of preeclampsia
 Intravascular compartment in eclamptic women is usually
not underfilled
 vasospasm and endothelial leakage of plasma has contracted the
space to be filled
 It persist some time after delivery when the vascular endothelium
repairs
 Sensitive to vigorous fluid therapy to expand the contracted

blood volume to normal pregnancy levels.
 Sensitive to even normal blood loss at delivery
BLOOD AND COAGULATION
PLATELET
 Thrombocytopenia = life threatening
 Severe disease: < 100.000/uL
 Platelet count = indication of delivery
 Platelet activation, aggregation, consumption -“exhausion”

- thrombocytopenia (Harlow, 2002)
 HELLP syndrome : hemolysis (H) , elevated liver enzymes

(EL), and low platelets (LP) (Weinstein, 982)
 Neonatal thrombocytopenia
 Maternal thrombocytopenia (Prichard, 1987)
COAGULATION
 PT, aPTT, fibrinogen level (routine lab assessment of
coagulation) → preeclampsia management.
 FDP: unknown (but, hepatic derangements (Leduc, 1992))
 Thrombophilias :
 Clotting factor deficiencies → early onset preeclampsia
 Antithrombin
 Preeclampsia (Chang, 1992)
 Fibronectin
 Glycoprotein-vascular endothelial cell basement membrane
 Preeclampsia
FRAGMENTATION HEMOLYSIS
 Severe preeclampsia – hemolysis
 Peripheral blood change :

 Schizocytosis, spherocytosis, reticulocytosis
VOLUME HOMEOSTASIS
FLUID AND ELECTROLYTE CHANGES
PRECLAMPSIA
 ECF
 Pathologic retension : endothelial injury
 Electrolyte concentration do not differ.
 Electrolyte unbalance
 Vigorous diuretic therapy
 Sodium restriction
 Administration of water with sufficient oxytocin to produce
antidiuretisis
 Following eclamptic convertion -> lower HCO3

KIDNEY
 Proteinuria
 Preeclampsia-eclampsia
 Late
 24hr UA
 Anatomical changes
 Glomeruli : 20%
 Glomerular capillary endotheliosis
 Capillary endothelial swelling with subendothelial deposits of
protein materials
 Acute renal failure
 Tubular necrosis, cortical necrosis -> oligouria, anuria, rapidly
develped azotemia
 HELLP synd. , placental abruption, postpartum hemorrhage
LIVER
 Periportal hemorrhagic necrosis in the periphery of the
liver lobule
 Serum liver enzyme
 Nonfatal case
 Hepatic rupture(more rare), subcapsular hematoma (more
common).
 Treatment
 Surgical intervention, life saving
 Blood T/F
 Liver transplantation
 Spontaneous hepatic rupture - mortality : 30%
1307
LIVER
HELLP SYNDROME
 Hemolysis, Elevated Liver enzyme and Low Platelet
 20% of severe preeclampsia and eclampsia
 Adverse outcome : 40%
 Other complications
 Eclampsia (6%), Placental abruption (10%), ARF (5%),
pulmonary edema (10%), subcapsular liver hematoma (1.6%)
 Steroid Tx - controversial
BRAIN
 Common Sx
 Headache, visual disturbance – associated convulsion
(eclampsia)
 Anatomical pathology
 Gross hemorrhage – severe HT
 Chronic HT
 Postmortem cerebral lesions
 Edema, hyperemia, focal anemia, thrombosis, hemorrhage

BRAIN
 Neuroimaging study
 CT
 50% abnormal finding
 Hypodense cotical area – petechial hemorrhage and

infarction site (at autopsy)
 MRI
 Cerebral artery area - remarkable change
 Convulsion
BRAIN
 Cerebral Blood Flow
 Eclampsia: loss of autoregulation of cerebral blood

flow (Apollon, 2000)
 Hyperperfusion – similar in hypertensive encephalopathy.
 Increased cerebral perfusion –> headache
 Cerebral vasospasm
BRAIN
 Blindness
 Rare
 4hr to 8days
 Visual disturbance
 More common
 Retinal detachement
 Cerebral Edema
 Sx
 Letharge, confusion, blurred vision, coma
 Mental change, brain involvement. (CT, MRI)
 Sudden severe blood pressure elevatoin
 Electroencephalopgraphy
UTEROPLACENTAL PERFUSION
 Vasospasm →
 DHAS sulfate -> estradiol-17B Placental perfusion -> perinatal

mortality and morbidity
 Measurement
 Spiral a. : 500μm, 200 μm (preeclampsia)
 Placental blood flow

 Inaccesibility, complexity, unsuitablity
UTEROPLACENTAL PERFUSION
DOPPLER
 Doppler measurement of blood velocity through uterine

artery
-> estimate uteroplacental blood flow

PREDICTION AND PREVENTION
PREDICTION
 Lots of attemption to predict preeclampsia in early

pregnancy -> poor sensitivity, poor positive predictive value
 Roll over test

 28-32 wks
 Lt. lat. Recumbent position -> supine position
 Hypertension abnormal
 Positive predictive value (true positive) : 33% (Dekker, 1990 ; Friedman
and Lindhemier, 1999)
PREDICTION
 Uric acid
 Decreased renal uric acid excretion -> elevated serum
uric acid level
 Jacobson (1990)
 Uric acid level > 5.9mg/dL at 24wks ; positive predictive value :
33%
 Weerasekera and Peiris (2003)

 Serum uric acid levels did not vary significantly before the
detection of hypertension
PREDICTION
 Fibronectin
 Endothelial cell activation -> elevated serum cellular
fibronectin level (Brubaker, 1992)
 Clinical study, Paarlberg (1998)

 Low sensitivity: 69%
 Positive predictive value: 12%
 Clinical study, Chavarria (2003)

 16wks-20wks, 378 low-risk nulliparas
 Negative predictive value: 98%
PREDICTION
 Oxidative Stress
 Lipid peroxides level – antioxidants activity -> preeclampsia
prediction (Walsh, 1994)
 Markers
 Lipid peroxides: malondialdehyde
 Pro-oxidants : iron, transferrin, ferritin, blood lipids, TG, free
fatty acid, lipoproteins, Vit C & E
 Hyperhomocysteinemia
 Atherosclerosis risk factor (non pregnant)
PREDICTION
 Cytokines
 Released by vascular endothelium and leukocytes

 Interleukin, TNF – a
 CRP
 Not sufficiently predictive (Savvidou, 2002)

PREDICTION
 Placental peptides
 Corticotropin releasing hormone, chorionic gonadotropin,

activin A, inhibin A
 Angiogenic factor: VEGF, PlGF

PREDICTION
 Fetal DNA
 Identification of Fetal DNA in maternal serum -> prediction

of preeclampsia (Zhong, 2001)
 Endothelial activation and inflammation

PREDICTION
 Uterine Artery Doppler Velocimetry

 2nd trimester – uteroplacental vascular resistance (by Doppler
of uterine artery)
 Basic concepts
 Impaired trophoblastic invasion of the spiral arteries ->
uteroplacental blood flow
 Bower (1993)
 Sensitivity: 78%
PREVENTION
 Dietary Manipulation
 Salt restriction -> ineffective (Knuist, 1998)
 Prenatal Ca supplementation -> significant reduction in BP

and incidence of preeclampsia (Brucher, 1996)
PREVENTION
 Low dose aspirin
 60 mg aspirin - reduce the incidence of preeclampsia; selective

TXA2, dominance of endothelial prostacyclin (Hauth, 1998,
Wallenburg, 1986)
 Caritis, 1998; CLASP Collaborative Group, 1994; Hauth, 1993,

1998; Rotchell, 1998; Sibai, 1993a
 Low-dose aspirin was ineffective in preventing preeclampsia
PREVENTION
 Low dose aspirin
 60 mg aspirin - reduce the incidence of preeclampsia; selective

TXA2, dominance of endothelial prostacyclin (Hauth, 1998,
Wallenburg, 1986)
 Caritis, 1998; CLASP Collaborative Group, 1994; Hauth, 1993,

1998; Rotchell, 1998; Sibai, 1993a
 Low-dose aspirin was ineffective in preventing preeclampsia
PREVENTION
 Antioxidants
 Davidge, 1992
 Markedly reduced antioxidant activity in preeclampsia women
 Chappel, 1999
 283 high risk women
 18-22 wks , vit C & E versus placebo
PREVENTION
 Antioxidants
 Davidge, 1992
 Markedly reduced antioxidant activity in preeclampsia women
 Chappel, 1999
 283 high risk women
 18-22 wks , vit C & E versus placebo
TREATMENT
GOAL
 To prevent the:
 Condition from becoming bad to worse
 Complications
TREATMENT
 Specific treatment will be determined by the physician
based on:
 Pregnancy, overall health, and medical history
 Extent of the disease
 Tolerance for specific medications, procedures, or therapies
 Expectations for the course of the disease
 Patient’s opinion or preference

OBSTETRIC MANAGEMENT
 Bedrest (either at home or in the hospital)
 Hospitalization (specialized personnel and equipment)
 Magnesium sulfate (or other antihypertensives for PIH)
 Fetal monitoring may include:
 fetal movement counting - fetal kicks and movements
 change in the number/frequency: means fetus under stress.
 nonstress testing - measures the fetal heart rate in response to
the fetus' movements.
 biophysical profile - combines nonstress test with ultrasound
 Doppler flow studies
 Continued laboratory testing of urine and blood (for
changes that may signal worsening of PIH)
 Corticosteroids (help mature the lungs of the fetus)
 Delivery of the baby (if treatments do not control PIH or if the
fetus or mother is in danger)
ANTIHYPERTENSIVES
Diuretic Beta ACE inhibitors / Calcium Alpha
Blocker Angiotensin II receptor Channel Blockers
antagonist Blocker
Caution Not No No Caution
in Adversely effect fetal Myocardial
late and neonatal blood depressants
pregnancy pressure control, skull
defects,
oligohydramnios,
toxicity
Labetalol Arteriolar dilator
I/V Max 200 mg
2mg/min until satisfactory response
Oral 200 mg BID up to 1200mg
Hydralazine Vasodilator
(Apresoline) Causes tachycardia fluid retention
Oral 25 mg BD
IV 10mg in 10 ml saline in 20 minutes
Nitrates Isorbid dinitrate, Glyceryl trinitrate, isorbid mono nitrate
Methyldopa 250 – 500 mg 2-3 times/day

(Aldomet) Centrally acting Alph 2 receptor agonist
Sodium 0.5-1.5µgm/kgmin
Nitropruside Cyanide toxicity if treatment exceeds 3 days
Nifedipine Vasodilator
(Adalet) no myocardial depression
10-20mg BD
ANTIHYPERTENSIVES
 Alpha methyldopa 500 mg PO bid (up to 2 grams bid)
 Labetolol 200 mg PO bid (up to 1200 mg bid)
 Felodipine 5 mg PO daily (up to 20 mg daily)
 Hydrochlorothiazide
 Not usually initiated in pregnancy due to volume depletion
 May be continued if on pre-pregnancy - consult with local
expert opinion
 Nifedipine XL 30 mg PO bid (up to 120 mg daily)
 Hydralazine 10 mg PO tid (up to 25 mg tid

ANTIHYPERTENSIVES’ GOAL
 Blood Pressure < 150/100
(much higher than non-pregnant goal)
 Anti-hypertensives are not indicated for mild to moderate

chronic hypertension in pregnancy
 BP < 150/100 mmHg does not reduce risk to fetus or prevent

preeclampsia
 Antihypertensives benefit mother only
 Do not reduce pregnancy complications

PRE-OPERATIVE EVALUATION
INVESTIGATIONS
 Blood complete picture

 Platelet count
 Coagulation assay, PT, APTT, Fibrinogen, D - dimer
 Serum Urea/creatinine Electrolytes Uric Acid
 LFTs
 Urinolysis, Microscopy, 24 Hours specimen for protien and
creatinine clearence
 Type and screen Blood
IMMEDIATE DELIVERY
 Severe Hypertension
 Progressive thrombocytopenia
 Liver dysfunction
 Progressive Renal dysfunction
 Persistent headache
 Evidence of fetal jeopardy
 Premonitory signs of ECLAMPSIA

TREATMENT
 Treatment of choice for Seizure prophylaxis = Magnesium
Sulphate
 4 - 6 grams in 20 minutes, followed by 1-2 gram / hr
 Monitor:
 Urine output
 Respiratory rate
 Patellar reflexes
 Serum levels - 4 hourly
SERUM LEVELS OF
MAGNESIUM SULPHATE
5 mEq/L Therapeutic range
Loss of deep tendon reflexes
10 mEq/L Prolonged P-Q interval
Widening QRS complexes
15 mEq/L Respiratory arrest
20 mEq/L Asystole
ROLE OF MAGNESIUM SULPHATE
 CNS
 Depressant & Anticonvulsant
 CVS
 Mild Anti-hypertensive effect
 Neuromuscular Junction
 Inhibits Ach release
 Decrease membrane excitability
 Augment Non and depolarizing muscle relaxant
 Uterus
 Mild relaxant effect on vascular & uterine smooth muscle
FETAL EFFECTS OF MgSO4
 MgSO4 crosses the placenta
 Neonatal depression
 Respiratory
 Hyporeflexia
 Decreased beat to beat variability in heart rate

 Stop convulsion (Thiopentone 50-100 mg)
 ABC
 Apply monitors (Pulse Oximeter, NIBP, ECG)
 I/V line
 Check BP repeatedly
 Administer MgSO4
 Treat hypertension
 Deliver baby
ANAESTHESIA FOR C SECTION
 Spinal
 General
SPINAL ANAESTHESIA
 Best even in severe pre-eclampsia
 GA
Severe hypertensive response to intubation
Risk of difficult intubation due to airway edema
 Epidural
 Less reliable anaesthesia than spinal
 Risk of trauma to epidural vein
 Risk of hypotension 6 times less in pre eclamptic pregnant

woman
 .75% hyperbaric Bupivacain 11-12 mg with / without 15-20 µg
Fentanyl or Morphine 100-200 µg
GENERAL ANESTHESIA
 Aspiration prophylaxis
 Thiopentone sodium induction
 Suxamethonium with cricoid pressure
 Attenute intubation response by deep anaesthesia & lignocain
 Smaller ETT 6-6.5 mm (airway edema)
 Nondepolarizing agent after recovery from suxamethonium
Remember MgSO4
 2/3 rd MAC for adequate depth of anaesthesia
 MgSO4 intra and Post op period
 IBP line for continuous blood pressure monitoring
 Anti HTN drugs
Lecture 14
MULTIPLE PREGNANCY.
THE UTERINE RUPTURE

MULTIPLE PREGNANCY
MULTIPLE PREGNANCY
 Twin pregnancy represents 2 to 3% of all pregnancies
 The PNMR is 5 times that of singleton

DIZYGOTIC TWINS
 Most common represents 2/3 of cases
 Fertilization of more than one egg by more than one

sperm
 Non identical, may be of different sex
 Two chorion and two amnion
 Placenta may be separate or fused

DIZYGOTIC TWINS
FACTORS AFFECTING IT’S INCIDENCE
 Induction of ovulation, 10% with clomide and 30% with
gonadotrophins
 Increase maternal age ? Due to increase gonadotrophins

production
 Increases with parity
 Heredity usually on maternal side
 Race: Nigeria 1:22; North America 1:90

MONOZYGOTIC TWINS
 Constant incidence of 1:250 births
 Not affected by heredity
 Not related to induction of ovulation
 Constitutes 1/3 of twins

FERTILIZED EGG
0-72 hours Diamniotic dichorionic
4-8 days Diamniotic monochorionic
9-12 days Monoamnio monochorionic
>12 days Conjoined twins

FERTILIZED EGG
MONOZYGOTIC TWINS
 70% are diamniotic monochorionic
 30% are diamniotic dichorionic

During pregnancy by US
 Very accurate in the first trimester, two sacs, presence

of thick chorion between amniotic membranes
 Less accurate in the second trimester the chorion

become thin and fuse with the amniotic membranes
 Different sex indicates dizygotic twins
 Separate placentas indicates dizygotic twins

COMPLICATIONS OF MULTIPLE GESTATION
Maternal Fetal
 Anemia  Malpresentation
 Hydramnios  Placenta previa
 Preeclampsia  Abruptio placentae
 Preterm labour  Premature rupture of the
 Postpartum hemorrhage membranes
  Prematurity
Cesarean delivery
 Umbilical cord prolapse
 Intrauterine growth
restriction
MONOCHORIONIC TWINS
 Results from vascular

anastomosis between
twins vessels at the placenta
 Usually arterio (donor) venous (recipient)
 Occurs in 10% of monochorionic twins

MONOCHORIONIC TWINS
 Chronic shunt occurs, the donor

bleeds into the recipient so one is
pale with oligohydraminos while
the other is polycythemic with
hydraminos
 If not treated death occurs in 80-100% of cases

MONOCHORIONIC TWINS
Possible methods of treatment:
 Repeated amniocentesis from recipient
 Indomethacin
 Fetoscopy and laser ablation

of communicating vessels
MONOCHORIONIC TWINS
 Congenital malformation. Twice that of singleton.
 Umbilical cord anomalies. In 3 – 4 %.
 Conjoined twins. Rare 1:70000 deliveries. The majority

are thoracopagus
 PNMR of monochorionic is 5x that of dichorionic

twins (120 vs. 24 / 1000 births)
MONOCHORIONIC TWINS
- thoracopagus
- pigopagus
MONOCHORIONIC TWINS
- craniopagus
craniopagus parasiticus
- xyphopagus
MATERNAL PHYSIOLOGICAL ADAPTATION
 Increase blood volume and cardiac output
 Increase demand for iron and folic acid
 Maternal respiratory difficulty
 Excess fluid retention and edema
 Increase attacks of supine hypotension

 Positive family history mainly on maternal side
 Positive history of ovulation induction
 Exaggerated symptoms of pregnancy
 Marked edema of lower limb
 Discrepancy between date and uterine size
 Palpation of many fetal parts

 Auscultation of two fetal heart beats at two different
sites with a difference of 10 beats
 USS
 Two sacs by 5 weeks by TV USS
 Two embryos by 7 weeks by TV USS

ANTENATAL CARE
AIM
 Prolongation of gestation age, increase fetal weight
 Improve PNM and morbidity
 Decrease incidence of maternal complications

ANTENATAL CARE
Follow Up
 Every 2 weeks
 Iron and folic acid to avoid anemia
 Assess cervical length and competency

ANTENATAL CARE
Fetal Surveillance
 Monthly USS from 24 weeks to

assess fetal growth and weight
 A discordinate weight difference of >25% is abnormal

(IUGR)
 Weekly CTG from 36 weeks

3D USS – TWIN PREGNANCIES
METHOD OF DELIVERY
Vertex-Vertex (50%)
 Vaginal delivery, interval between

twins not to exceed 20 minutes
Vertex-Breech (20%)
 Vaginal delivery by senior obstetrician

METHOD OF DELIVERY
Breech-Vertex (20%)
 Safer to deliver by CS to avoid the

rare interlocking twins (1:1000 twins)
Breech-Breech (10%)
 Usually by CS
PERINATAL OUTCOME
 PNMR is 5 times that of singleton (30-50/1000 births)
 RDS accounts for 50% 0f PNMR. 2nd twin is more

affected
 Birth trauma – 2nd twin is 4 times affected than 1st

PERINATAL OUTCOME
 Congenital anomalies is responsible for 15% of PNMR
 Cerebral hemorrage and birth asphyxia are responsible

for 10% of PNMR
 Cerebral palsy is 4 times that of singleton
 50% of twins babies are born with low birth (<2500

gms) from prematurity & IUGR
INTRAUTERINE DEATH OF ONE TWIN
 Early in pregnancy usually no risk
 In 2nd or 3rd trimester:
 Increase risk of DIC
 Increase risk of thrombosis in the a live one
 The risk is much higher in monochorionic than in

dichorionic twins
 The life baby should be delivered by 32-34 weeks in
monochorionic twins
HIGH RANK MULTIPLE GESTATION
 Spontaneous triplets 1:8.000 births
 Spontaneous quadruplets 1:700.000 births
 The main risk is sever prematurity
 CS is the usual and safe mode of delivery
 High PNMR of 50-100 / 1000 births

COMPLICATIONS OF MULTIPLE PREGNANCY
A. MATERNAL:
1. Anemia due to increase demand
2. Increase incidence of PET(5 times)
3. Polyhydramnios in monochorionic monozygotic twins
4. Increase incidence of premature labor

PREGNANCY
A. MATERNAL:
5. Increase incidence of CS. And operative delivery
6. Increase incidence of placenta praevia and abruptio

placentae
7. Increase incidence of hypotonic postpartum

hemorrhage
PREGNANCY
B. FETAL:
1. Increase perinatal morbidity and mortality
2. Prematurity with / without rupture of membrane
3. Increase incidence of malpresentation

PREGNANCY
B. FETAL:
4. Increase incidence of cord prolapse
5. Higher incidence of IUGR
6. Increase incidence of congenital anomalies

THE UTERINE RUPTURE
DEFINITION
 Separation of the muscular wall of the uterus
 Usually occurs during labor
 Occasionally happen during

the later weeks of pregnancy
CAUSES
During pregnancy
 Weak scar after previous
operations on the uterus
 History of cesarean section (VBAC - vaginal birth after

C-section)
 Myomectomy
 Excision of a uterine septum
 Previous perforation of uterus (D&C, hysteroscopy,

forceps delivery
CAUSES
During labor:
 uterine hyper-stimulation (oxytocin
with pitocin induction or
augmentation of labor)
 obstructed labor (macrosomia, fetopelvic
disproprotion)
 intrauterine manipulation (internal version, manual
removal of an adherent placenta)
 forcible dilatation (cervical tear)
 a weak scar (C-section or other
operations)
TYPES
 Incomplete rupture
 Complete rupture
 Depending on whether the

peritoneal coat is torn
through or not
SYMPTOMS AND SIGNS
1. Rupture of scar
 be gradual that symptom is very slight in incomplete
rupture
 abdominal pain wrongly attributed to the onset of labor
 severe pain and shock occurs in complete (suddenly

pain)
 fetal distress
 bleeding in vagina
SYMPTOMS AND SIGNS
2. Spontaneous rupture during obstructed labor
 prolonged labor
 violent uterine actions
 pathologic retraction ring
 disporpotion, malpresentation (transverse lie)
 fetal distress
 a sharp, tearing pain in lower abdomen
 pulse rapid
 blood pressure fall
 fetus may be felt in the abdominal cavity
PATHOLOGIC RETRACTION RING
SYMPTOMS AND SIGNS
3. Rupture by oxytocin drugs:
 follows the administration of oxytocin
 the danger is less if the drug is given as a dilute

intravenous drip given in an increasing fashion
PROGNOSIS
 has a high mortality
 peri-natal morbidity is high

TREATMENT
 Women’s general condition must be improved
giving morphine, blood transfusion, glucose solution)
 immediate laparotomy
 Hysteroraphy / hysterectomy
 wide-spectrum antibiotics
Lecture 15
GESTATIONAL
TROPHOBLASTIC
DISEASE

DEFINITION
 Gestational trophoblastic disease (GTD) = a group of
disease originated from placental villose trophoblastic cells,
including hydatidiform mole, invasive mole, choriocarcinoma
and a kind of less common trophoblastic cell tumor in
placenta
RELATIONS AMONG THE DISEASES
 Benign mole (hydatidiform mole) = abnormal formation of
placenta accompanied by the special abnormal hereditary
 Invasive mole results from benign mole
 Choriocarcinoma and the trophoblastic cell tumor in

placenta may result from benign mole, term pregnancy,
abortion and ectopic pregnancy
CLASSIFICATIONS
Gestational Trophoblastic Disease (GTD)
Partial mole Invasive Chorio Placental site
I. Pathologic trophoblastic
Classification Complete mole mole carcinoma tumour
Pe
rsi
ste
nt
II. Clinical Benign GT
D
G.T. Neoplasia
Classification G.T.D. Malignant G.T.D.
βhCG based:
WHO, FIGO, ACOG 2004
Non metastatic Metastatic
& RCOG 2010
Low risk High risk

HYDATIDIFORM MOLE
DEFINITION
 Hydatidiform mole = an abnormal proliferation of the
trophoblast in which the terminal villi are transformed into
vesicles filled with clear viscid material (like grapes)
CLASSIFICATION
 Hydatidiform mole is
divided into:
 Complete
and
 Incomplete
ETIOLOGY
 is not clear
ETIOLOGY OF
EPIDEMIOLOGY
 the morbidity is different in different areas
INCIDENCE
 South East Asia is 1/500-600
 US and Europe: 1/500-2.000
 China: 1/1238
ETIOLOGY OF
HIGH RISK FACTORS
 nourishing status, social economy
 age: < 20 years old; > 35 and 40 years old
 history: if a patient has the history of 1 or 2 x hydatidiform

mole → the morbidity of the hydatidiform mole when
pregnant again is 1 % and 15-20% respectively
ETIOLOGY OF
GENETIC FACTORS
 enucleate egg fertilization:
 chromosome karyotype of complete mole is diploid:
 90% is 46XX
 10% is 46XY
ETIOLOGY OF
EPIDEMIOLOGY
 The morbidity of incomplete mole is much lower than that of

the complete type
 It is not associated with age

ETIOLOGY OF
GENETIC FACTORS
 Chromosome karyotype of 90% incomplete mole is triploid
 The most common chromosome karyotype is 69XXY, and

then is 69XXX or 69XYY
PATHOLOGY
MACRO EXAMINATION
 mass of vesicles, vary in size,
grape-like and identifiable
embryonic or fetal tissues
MICRO EXAMINATION
 trophoblastic proliferation
 hydropic degeneration of the stroma
 absence of blood vessels or extreme scantiness of blood

vessels
Normal
trophoblast
Partial mole Complete mole

Partial mole
Complete mole
COMPLETE MOLE
 Vaginal bleeding after amenorrhea
 Uterus is abnormally enlarged and become soft
 Theca lutein ovarian cyst
 Hyperthyroidism (plasma thyroxin

concentration elevates)
 Exaggerated early pregnancy

symptoms (nausea, vomitting, etc)
 Severe and early - onset PIH

THECA LUTEIN OVARIAN CYST
INCOMPLETE MOLE
 May have the major symptoms of complete mole, but it is

slightly manifested
 NO luteinizing cyst
 The histologic examination of

curettage sample may confirm
the diagnosis
PROGNOSIS
 Complete mole - latent risk of local invasion / telemetastasis
 High-risk factors:
 β-HCG > 100.000 IU/L
 Uterine size is obviously > than that with the same gestational
time
 The luteinizing cyst is > 6 cm
 If > 40 years old, the risk of invasion and metastasis = 37%
 If > 50 years old, the risk of invasion and metastasis = 56%
 Repeated mole: the morbidity of invasion and metastasis increase

3-4 x
DIAGNOSIS
 β-HCG measurement
 US examination
 Detecting the fetal heart beat by ultrasound Doppler

13 WEEKS GESTATION
13 WEEKS GESTATION
 Abortion
 Multiple pregnancy
 Polyhydramnios

MANAGEMENT
 Emptying uterine cavity
 once the diagnosis is confirmed the
uterine cavity should be emptied as
soon as possible
 Hysterectomy
 over 40 years old with high-risk factors
 uterine size is over 14 gestational weeks
 Management of luteinizing cyst

EMPTYING UTERINE CAVITY
 Suction curettage performed
using 10 mm cannula under US guidance
Canula
MANAGEMENT
 Preventive chemotherapy
 over 40 years old
 the β-HCG is over 100.000 IU/L before emptying mole
 the HCG regresion curve is not progressively declined
 uterus is obviously larger than the size of the amenorrhea
 luteinizing cyst is > 6 cm
 there is still over hyperplasia of trophoblastic cells in the

second curettage
FOLLOW UP
 β-HCG qw till normal
 QW x 3m
 Q2W x 3m
 QM x 6m
 Q6M x 2y
INVASIVE MOLE
DEFINITION
 Invasive mole = the hydatidiform mole invade the uterine
myometrium or metastasize to extrauterine tissue
BIOLOGIC BEHAVIOR
 Invasive mole villus may invade myometrium or blood vessels
or both, at beginning it spread locally, invade myometrium,
sometimes penetrate the uterine wall and spread to the broad
ligament or abdominal cavity
PATHOLOGY
MACRO EXAMINATION
 different size of vesicles in myometrium,
there may be or may not be primary
focus in uterine cavity
 when the invasion is near serosal layer
MICRO EXAMINATION
 villose structure and trophoblastic cells proliferation and
differentiation deficiency
 villose and trophoblastic cells can be found in most

PATHOLOGY
MACRO EXAMINATION
MICRO EXAMINATION
 irregular vaginal bleeding
 uterine subinvolution
 theca lutein cyst does not disappear after emptying uterus
 abdominal pain
 metastatic focus manifestation

DIAGNOSIS
 history and clinical manifestation
 successive measurement of β-HCG
 US examination
 X-ray and CT
 histological diagnosis
US DIAGNOSIS
DIAGNOSIS
CHORIOCARCINOMA
DEFINITION
 Choriocarcinoma is a highly malignant tumor, it can
metastasize to the whole body through blood circulation
damage tissues and organs, cause bleeding and necrosis
CHORIOCARCINOMA
 The most common metastatic site is lung, then vagina, brain
and liver
 50% gestational choriocarcinoma result from hydatidiform

mole (generally occurs over 1 year after emptying the mole)
 The rate of occurrence after abortion or term delivery is 25%

and 25% respectively, seldom occurs after ectopic pregnancy
PATHOLOGY
MACRO EXAMINATION
 most choriocarcinoma occurs in uterus
 the tumor diameter = 2-10 cm
 cancer embolus is often found in parauterine veins
 ovarian luteinizing cyst may be formed
MICRO EXAMINATION
 the hyperplastic cytotrophoblastic cells and
syntrophoblastic cells invade the myometrium and blood
vessels accompanied by the bleeding and necrosis
MACRO EXAMINATION
MICRO EXAMINATION
 Pain
 Uterine enlargement
 Mass
DIAGNOSIS
 Clinical features
 US
 β-HCG
 CT
 X-ray
 Pathology
 Hydatidiform mole
 Invasive mole
 Placental site trophoblastic tumors
 Rudimental placenta
LUNG METASTASES
VAGINA METASTASES
BRAIN METASTASES
LIVER METASTASES
ANATOMIC STAGING
 Stage I - disease confined to uterus
 Stage II - gestational trophoblastic tumor extending outside

uterus but limited to genital structures (adnexa, vagina, broad
ligament)
 Stage III - gestational trophoblastic disease extending to lungs

with or without known genital tract involvement
 Stage IV - all other metastatic sites

MANAGEMENT
 Chemotherapy
 Surgery
FOLLOW UP
 QM x 1y
 Q3M x 2y
 QY x 2y
 Q2Y
Lecture 17
ABNORMALITIES OF
PLACENTA
AND
UMBILICAL CORD
ABRUPTIO PLACENTAE
1. DEFINITION
 Separation of the normally situated placenta from its uterine
site of implantation after 20 weeks gestation, but before
delivery of the placenta
ABRUPTIO PLACENTAE
2. PLACENTAL GRADES
 Grade 0 - Patient asymptomatic. Small retroperitoneal clot

seen after delivery
 Grade 1 - Vaginal bleeding, may have abdominal

tenderness or slight uterine tetany, mom and baby not in
distress
 Grade 2 - Uterine tenderness, tetany with / without evidence

of bleeding, baby shows signs of distress
 Grade 3 - Uterine tetany, severe bleeding may not be visible.

Baby is dead. Mom often has coagulopathy
ABRUPTIO PLACENTAE
ABRUPTIO PLACENTAE
3. INCIDENCE
 Varies from 1/55 to 1/250 cases
 Incidence greater with increasing parity or history of
abruption
ABRUPTIO PLACENTAE
5. CONDITIONS ASSOCIATED WITH ABRUPTION:
 Hypertension - 5x higher
 Trauma
 Short umbilical cord
 Polyhydramnios
 IV cocaine use
 Uterine anomalies
ABRUPTIO PLACENTAE
5. CONDITIONS ASSOCIATED WITH ABRUPTION:
 OB history:
1. History of spontaneous abortions
2. Premature labor
3. Antepartum hemorrhage
4. Stillbirth / neonatal death
5. Parity > 7 - 6x greater
6. History of abruption - 30x greater
7. Cigarette smoking - decidual necrosis
ABRUPTIO PLACENTAE
6. SIGNS AND SYMPTOMS
 Depends on type of abruption:
 Mild c/o labor pains, may only have slight uterine
irritability
 May have no / only small amount of bleeding
 Severe knife-like pain with board-like abdomen

 May / may not see bleeding
 Uterus could be tender at point of separation or may be

generalized over entire abdomen
ABRUPTIO PLACENTAE
ABRUPTIO PLACENTAE
 Depends on type of abruption:
 Increased uterine distention - elevated fundal height
 Bleeding may be minimal or diffuse. Can be port-wine,

dark, or bright red
 Symptoms are determined by amount of blood lost
 Shock is severe
ABRUPTIO PLACENTAE
7. DIAGNOSIS
 Based on hystory, physical exam, lab values
 NO analgesia / anesthesia until diagnosis confirmed
 Vaginal bleeding with / without pain
 Increased uterine tone, tenderness
 Shock
 Fetal distress
 U/S for placental localization, position
 Palpation of abdomen, measure fundal height
 Confirm after delivery-inspect placenta
ABRUPTIO PLACENTAE
ABRUPTIO PLACENTAE
ABRUPTIO PLACENTAE
8. MATERNAL/ FETAL OUTCOME
 Mortality rate < 1%; if undetected until fetal death, mortality

rate is 10%
 DIC - 30%
 Renal failure from hypovolemia
 Amniotic fluid embolus
 Uterine rupture
 Postpartum endometritis
 Postpartum hemorrhage
ABRUPTIO PLACENTAE
ABRUPTIO PLACENTAE
9. MEDICAL MANAGEMENT
 US to R/O placenta praevia
 Bedrest (lateral position)
 IV with large bore catheter
 Type and crossmatch, CBC,
platelet count, fibrinogen, bleeding time
 Frequent vital signs
 Assess for signs of shock - cold, clammy skin, pale, anxious,
thirsty
 Assess FHR and uterine activity
ABRUPTIO PLACENTAE
 Mark top of fundus (check to see if rising)
 Observe for signs of vaginal bleeding
 C/S for fetal distress, maternal blood loss or compromise,
coagulopathy, poor labor progress
 Strict I & O
 Amniotomy to assess blood in fluid
 Oxygen per mask
 Avoid episiotomy
 Be aware of postpartum hemorrhage
COUVELAIRE UTERUS
 Occurs in severe abruptio placenta, when blood collects in

the uterine musculature beneath the uterine serosa, into
connective tissue of the broad ligaments and even into the
peritoneal cavity
 Suturing, followed by administration of IV oxytocin, usually

controls postpartum hemorrhage
COUVELAIRE UTERUS
COUVELAIRE UTERUS
PLACENTA PRAEVIA
1. DEFINITION
 Abnormally implanted placenta placed totally / partially in
the lower segment of the uterus, rather than in the fundus
 When the cervix begins to dilate and efface the placenta
separates, allowing bleeding form the open vessels
PLACENTA PRAEVIA
2. CLASSIFICATION
 Complete - internal os is completely covered by the placenta
 Partial - a portion of the cervical os is covered by the

placenta
 Marginal - The edge of the placenta extends to the edge of

the cervical os
PLACENTA PRAEVIA
PLACENTA PRAEVIA
3. INCIDENCE
 Depends on which trimester pregnancy is in:
 2nd trimester - 45 % in lower uterine segment
 3rd trimester - 0.5 to 1 % in lower uterine segment
 Occurs more often in multiparas - 80 %
 History of praevia - 12x more likely
 More common with history of abortions
 C/S, molar pregnancies, fibroids, uterine surgery

PLACENTA PRAEVIA
4. ETIOLOGY
 Unknown cause
 It is thought that when the embryo is ready to implant and

the decidua in the fundus is deficient, it will choose another
spot lower in the uterine segment
 Placentas are larger on the maternal side, cord often has

marginal or vellamentous insertion
 Suggests that the placenta was growing toward more
favorable decidua
PLACENTA PRAEVIA
4. ETIOLOGY
 Endometriosis after previous pregnancy
 Uterine scars - abortions, C/S, molar pregnancy
 Tumors altering contour of uterus
 Close pregnancy spacing
 Multiparity
 Large placenta - in multiple gestations or erythroblastosis
fetalis
 High altitudes
 Male fetus
PLACENTA PRAEVIA
5. DIAGNOSIS
 Painless bright red vaginal bleeding - usually 1st bleeding
episode not before 30 weeks
 Sometimes suspected with oblique / transverse lie
 Diagnosed by U/S
 80-90% - bleeding occurs without warning
 Uterus non-tender - no rise in fundal height
 Often occurs when sleeping
 1st episode usually scant, each episode more
 Shock
 May deliver by C/S, if placenta covers cervix
PLACENTA PRAEVIA
PLACENTA PRAEVIA
6. MATERNAL AND FETAL OUTCOME
 Mortality < 1%, morbidity = 20%
 Most will have at least one significant hemorrhage, 25% will

go into shock
 Vaginal and cervical lacerations occur more often with

vaginal delivery
 Poor endometrium may contribute to placenta accreta
 Fetal mortality 20% - prematurity, hypoxia, developmental

disorders
PLACENTA PRAEVIA
 Depends on gestational age and severity of bleed:
 Strict bedrest
 IV - large bore catheter (16 gauge)
 CBC, type & screen, platelet count, fibrinogen, bleeding

time
 If HCT < 30% → transfuse
 No pelvic exams
PLACENTA PRAEVIA
 Tocolysis for contractions
 No douching or intercourse
 Oxygen per mask
 Serial U/S to check for placental placement, fluid level,

fetal growth
 C/S for large blood loss

PLACENTA ACCRETA
1. DEFINITION
 a rare condition
 all or part of placenta adherent to the myometrium
 the normal spongy layer of decidua is absent / defective,

therefore placental villi grows down through the
endometrium into the myometrium
PLACENTA ACCRETA
2. TYPES
 Accreta - villi extends too

far into endometrium
 Increta - villi invade into

myometrium
 Percreta - villi invade through

myometrium to the serosa layer
PLACENTA ACCRETA
3. INCIDENCE
 1 / 7000
PLACENTA ACCRETA
4. PREDISPOSING FACTORS
 Implantation over a previous C/S scar / other surgical scar in

the uterine cavity
 Previous curretagge
 Prior history of endometritis / other endometrial trauma
 High parity
 Placenta previa sometimes precludes accreta

PLACENTA ACCRETA
 None until delivery
 Depends on depth, site of penetration, number of cotyledons
involved
 Partial accreta - some cotyledons may separate from the
uterine wall, leaving open, bleeding vessels
 The uterus is unable to contract because of the adherent
placenta still within the uterine cavity
 Profuse hemorrhage
 Total accreta - tearing occurs when doctor tries to deliver

placenta
 Uterine inversion may occur
PLACENTA ACCRETA
6. DIAGNOSIS
 Attempts to remove placenta reveals placental adherence
PLACENTA ACCRETA
7. OUTCOME
 Hemorrhage
 Shock
 Uterine inversion
 Hysterectomy
PLACENTA ACCRETA
8. TREATMENT
 Large bore IV catheter
 IV fluids, blood
 US
 Type and screen, CBC,
platelet count, fibrinogen, bleeding time
 Accurate I & O
 Assess vital signs
 D & C / hysterectomy
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
BILOBED PLACENTA
MULTILOBED PLACENTA
PATHOGENESIS
 Arise due to implantation in areas of

decrease uterine perfusion
 Example:
 Lateral implantation in between anterior and posterior
walls of the uterus with one lobe on the other and one on
the posterior wall
MULTILOBED PLACENTA
PATHOGENESIS
 Other local factors leading to multilobulation:
 Implantation over leiomyomas
 Area of previous surgeries
 In the cornu
 Over the cervical os

CIRCUMVALLATE PLACENTA
 The fetal surface of the placenta is exposed thorough a ring
of chorion and amnion opening around the umbilical cord
SUCCENTURIATE PLACENTA
 One or more accessory lobes of the villi have developed
 Vessels from the major to the minor lobes are only supported
by membrane
 This increases the likelihood that the minor lobe(s) are may
be retained during the third stage of labor
SUCCENTURIATE PLACENTA
ABNORMALITIES OF UMBILICAL CORD
LENGTH
 Mean length at term 55-60 cm
 Vascular occlusion by thrombi & true knots
 Excessively short umbilical cords may be instruments in

abruptio placenta & uterine inversion
SINGLE UMBILICAL ARTERY
 Absence of one umbilical artery
 0.85 % of all cords in singletons
 Infants with single-artery cord have

 18-30 % incidence of malformation
 34 % usually growth restricted
 17 % delivered preterm
SINGLE UMBILICAL ARTERY
 Incidence is increase in newborn of women with:
 DM
 Epilepsy
 Preeclampsia
 Anterpartum age
 Oligohydramnios
 Hydramnios
BATTLEDORE PLACENTA
 Cord inserted at / near the placental margin, rather than in
the center
VELAMENTOUS INSERTION OF
UMBILICAL CORD
 An abnormal condition in which umbilical vessel does not
insert into the placental mass but instead, traverse the fetal
membrane before it inserts into the umbilical cord
 Used to describe the condition in which the umbilical cord
inserts on the chorioamniotic membranes rather than on the
placental mass
 Incidence:
 1.1% in singleton pregnancies
 8.7% in twin gestations
 Spontaneous abortion
 33% between 9th & 12th wks AOG
 26 % between 13th & 16th
VASA PRAEVIA
 Rare circumstance that may occur with velamentous
insertion of the cord where umbilical vessels cross the
internal os presenting ahead of the fetus
 Requires a C/S
CORD ABNORMALITIES
KNOTS
 False knots
 Result from kinking of the vessels to accommodate length
of cord
 True knots
 Results from active fetal movement
CORD ABNORMALITIES
TORSION
 Result of fetal movement, cord normally becomes twisted
 Marked torsion  compromised fetal circulation
LOOPS
 Coiling of cord around the neck
 Incidence of nuchal cord coil once → 21 %
CORD ABNORMALITIES
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
 Associated with an extreme focal deficiency in Wharton’s jelly
THANKS !
Lecture 18
ABNORMALITIES OF
FETAL MEMBRANES &
AMNIOTIC FLUID

ABNORMALITIES OF FETAL
MEMBRANES & AMNIOTIC FLUID
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
CHORIOAMNIONITIS
 Inflammation of fetal membrane is a manifestation of an

intrauterine infection
 Frequently associated with prolonged membrane rupture and
long labor
 (+) mononuclears & polymorphonuclear leukocytes
infiltrating the chorion
CHORIOAMNIONITIS
DISORDERS OF THE AMNIOTIC FLUID
VOLUME
HYDRAMNIOS
 Defined as amniotic fluid index >24-25 cm
 Mild → moderate degrees = 2-3 L
 Incidence: 1 % of all pregnancies
 2/3 - idiopathic
 1/3 is associated with fetal anomalies, maternal DM or

multifetal gestation
HYDRAMNIOS
PATHOGENESIS
 Early in pregnancy
 Amnionic cavity is filled with fluid
similar in composition to ECF
 During 1st half of pregnancy

 Transfer of H2O & other small
molecules takes place not only
across the amnion but thru the
fetal skin
 2nd trimester

HYDRAMNIOS
SYMPTOMS
 Severe dyspnea
 Edema
DIAGNOSIS
 Clinical findings
 Uterine enlargements in association with difficulty in
palpating fetal small parts & in hearing FHT
 By US
 Large amounts of amniotic fluid can always be
demonstrated as an abnormally echo-free space between
fetus & uterine wall or placenta
HYDRAMNIOS
PROGNOSIS
 The more severe the hydramnios, the higher the perinatal

mortality rate
 Maternal complication associated with hydramnios

 Uterine dysfunction
 Postpartum hge
HYDRAMNIOS
MANAGEMENT
 Amniocentesis
 Principal purpose is to relieve maternal distress
 Amniotomy
 Disadvantage is cord prolapse
HYDRAMNIOS
MANAGEMENT
 Indomethacin therapy
 Impairs lung liquid production or enhances absorption
 Decrease fetal urine production
 Increase fluid movement across fetal membrane
 Dose: 1.5-3 mg/kg/day
 Disadvantage:
OLIGOHYDRAMNIOS
 Defined as amniotic fluid

index (AFI) < 5 cm
 Risk:
 Cord compression
OLIGOHYDRAMNIOS
CONDITIONS FREQUENTLY ASSOCIATED WITH
OLIGOHYDRAMNIOS
Fetal Maternal
 Chromosomal abnormalities  Uteroplacental insufficiency
 Congenital anomalies  Hypertension
 Growth restriction  Preeclampsia
 Demise  DM
 Postterm pregnancy
 Ruptured membranes
OLIGOHYDRAMNIOS
CONDITIONS FREQUENTLY ASSOCIATED WITH
OLIGOHYDRAMNIOS
Placenta Drugs
 Abruption  Prostaglandin synthetase
inhibitors
 Twin-twin transfusion
 ACE inhibitors
Idiopathic
OLIGOHYDRAMNIOS
EARLY-ONSET OLIGOHYDRAMNIOS
 Almost always evident when there is obstruction of fetal

urinary tract or renal agenesis
 Exposure to ACE inhibitors
 Fetal prognosis is poor

OLIGOHYDRAMNIOS
PULMONARY HYPOPLASIA
 Incidence @ birth: 1.1 – 1.4 in 1000 infants
 (+) when amnionic fluid is scant
 3 possibilities that account for pulmonary hypoplasia:

 Thoracic compression
 Lack of fetal breathing movement decreases lung inflow
 Failure to retain amnionic fluid or increase outflow with

impaired lung growth and development
OLIGOHYDRAMNIOS
OLIGOHYDRAMNIOS IN LATE PREGNANCY
 Amnionic fluid volume diminishes normally after 35 weeks
 Significant oligohydramnios
 Associated with increased risk of adverse perinatal
outcomes
 Fivefold increased cesarean delivery rate

AMNIOTIC FLUID EMBOLISM
 Amniotic fluid embolism (AFES) or anaphylactoid
syndrome of pregnancy
 Incidence: 1/8000 ~ 1/80000
 Maternal mortality: 60 ~ 90 %
 AFES & Pulmonary thromboembolism → 20% perinatal

maternal mortality
PATHOPHYSIOLOGY
 Entrance of amniotic fluid to

maternal circulation:
 Endocervical veins
 Placental insertion site
 Site of uterine trauma

PATHOPHYSIOLOGY
 Why Anaphylactoid Syndrome of Pregnancy?
1. Amniotic debris in non-AFES mother
2. Variability of clinical signs & symptoms and its severity

PATHOPHYSIOLOGY
 Proposed Mechanisms:
1. Host immune responses
2. Abnormal amniotic fluid, atypical substance

CLINICAL PRESENTATION
 Onset most commonly during labor & delivery
 Nonspecific symptoms: chills, nausea, vomiting, agitation
 Cardiorespiratory collapse occurred at presentation in the

majority
 Some have tonic-clonic seizure

 Major clinical findings:

 Hypoxia & respiratory failure
 Cardiogenic shock
 Disseminated intravascular coagulation (DIC)
 Each of the above can be the dominant presentation

 Signs & symptoms similar to anaphylactoid or septic shock
 Risk factors unknown?
 Etiology unkown?
HYPOXEMIA
 Due to ventilation / perfusion mismatching
 Some (15%) cases - bronchospasm
 50% - 1st hour death were due to hypoxia and cardiogenic

shock
 May result in neurologic impairment

HYPOXEMIA
 70% who initially survived developed pulmonary edema

 May be cardiogenic / noncardiogenic
 Evidence for endothelial-alveolar membrane damage →

capillary leak →
1. High protein concentration in lung edema fluid
2. Amniotic fluid debris in sputum & alveoli

DISSEMINATED INTRAVASCULAR COAGULATION (DIC)
 Major clinical findings:
 Hypoxia & respiratory failure
 Cardiogenic shock
 80% AFES develop DIC
 The temporal correlation is not constant among DIC,

cardiogenic shock, hypoxia
 When AFES occurs postpartum and DIC is the major early
finding, diagnosis may be delayed due to s/s mimics
DIAGNOSIS
 Via symptoms & signs  suspicion of AFES
 Other causes of sudden cardiorespiratory failure:
1. Hemorrhage
2. Air or pulmonary embolism
3. Anesthetic complications
4. Anaphylaxis
5. Sepsis
DIAGNOSIS
 Some authors require the amniotic fluid debris (eg. squamous

and trophoblastic cells, mucin, lanugo) from the distal port of
a pulmonary artery catheter to make the diagnosis
 But, amniotic fluid components commonly are present

in the maternal circulation in women with no signs &
symptoms of AFES
MANAGEMENT
 Aggressive monitor
 About maternal & fetal hypoxia
 Pharmacologic therapy
 Fluid support
 Correct coagulopathy as needed

MANAGEMENT
 Monitoring:
 SpO2
 EKG
 Arterial line
 Fetal monitor if onset prior to delivery
 Echocardiography
 CVP alone is not sufficient

MANAGEMENT
 Maternal Hypoxia
 Secure airway
 Intubation & Ventilation
 Small tidal volume (6~8 ml/kg)
 Normocapnia (~32 mmHg)
 PEEP
MANAGEMENT
 Fetal Hypoxia
 65% fatal AFES present before delivery
 Prevention of Fetal Hypoxia:
 Maternal PO2 keep > 47 mmHg; best above 65 mmHg
 Fetal umbilical vein PO2 >32 mmHg

 Fetal compensation by elevated Hb level & cardiac
output
MANAGEMENT
 Pharmacologic Therapy
 Inotropic & vasoactive agents:
 Norepinephrine
 Dopamine
 Dobutamine (often use norepinephrine in combination)

MANAGEMENT
 Fluid management
 Pulmonary artery catheter insertion first, if possible
 Avoid exacerbating pulmonary edema
 Initial management with vasopressor is preferred
 Correct coagulopathy with blood product as needed

PREMATURE RUPTURE OF THE
MEMBRANES
DEFINITIONS
 PROM is defined as amniorrhexis prior to the onset of labor

at any stage of gestation
 Amniorrhexis means spontaneous rupture of membranes as

opposed to amniotomy
 PPROM is used to defined that the patient who are preterm

with ruptured membranes, whether or not they have
contractions
MEMBRANES
ETIOLOGY AND RISK FACTORS
 Vaginal and cervical infections
 Abnormal membrane physiology
 Incompetent cervix
 Nutritional deficiencies
MEMBRANES
DIAGNOSIS
 It is based on the history of vaginal loss of fluid and

confirmation of amniotic fluid in the vaginal
 A sterile vaginal speculum examination should be performed
 Before labor, vaginal examination should not be performed
 Carry out a complete ultrasonic examination

MEMBRANES
OLIGOHYDRAMNIOS RESULTS IN:
 Fetal crowding with thoracic compression
 Restriction of fetal breathing
 Disturbances of pulmonary fluid production and flow
 Constaints placed on fetal movements in utero can also result

in positional skeletal abnormalities, such as talipes
equinovarus
DIAGNOSIS
MEMBRANES
 Confirmation of the diagnosis can be made by:
 Testing the fluid with nitrazine paper,

which will turn blue in the presence of
the alkaline amniotic fluid
 Placing a sample on a microscopic slide,

air drying, and examining for ferning
MEMBRANES
DIAGNOSIS OF OLIGOHYDRAMNIOS
 Ultrasonic definition has been standardized
 Criteria include:
1. Measure the amniotic fluid present in 4 quadrands by

vertical axis
2. AFI: total being called the amniotic fluid index
3. A value < 5 cm is considered abnormal

MEMBRANES
MANAGEMENT
 General considerations
 Conservative expectant management
 Management of chorioamnionitis
 Tests of pulmonary maturity

MEMBRANES
MANAGEMENT
 If PROM occurs at 36 weeks or later, condition of the cervix

is favorable, no spontaneous contractions, labor should be
induced after 6-12 hours
 If PROM occurs prior to 36 weeks’ gestation, we should

manage as followings:
MEMBRANES
LABORATORY TESTS
 Complete blood cells
 Gram stain and culture of amniotic fluid
 Pulmonary maturation studies of amniotic fluid

MEMBRANES
MANAGEMENT
Conservative expectant management
 The goal is to continue the pregnancy until the lung

profile is mature
 Take careful surveillance to diagnose subclinical infection and

chorioamnionitis
MEMBRANES
CLINICAL SIGNS & SYMPTOMS OF CHORIOAMNIONITIS
 Maternal temperature is > 38 0C
 Fetal tachycardia
 A tender uterus
 Uterine irritability on nonstress testing
 White blood cells elevates
 Measure the amniotic fluid by ultranography

MEMBRANES
MEMBRANES
MANAGEMENT OF CHORIOAMNIONITIS
 Use antibiotics depends on cultures and sensitivity
 Once antibiotics have been started, labor should be induced
 Vaginal delivery or cesarean section

MEMBRANES
MANAGEMENT
 Tocolytic therapy
 Corticosteriods
 Labor and delivery
They are just the same with preterm labor !

MEMBRANES
MANAGEMENT
Tests of pulmonary maturity:
 Lecithin/sphingomyelin (L/S) ratio maturity > 2
 Lamellar body number density (LBND)

 Maturity: > 46.000 LBND
MEMBRANES
MEMBRANES
MANAGEMENT
 Surfactant therapy
 It is effective
 Expensive
Lecture 19
ABNORMALITIES OF THE
PUERPERIUM

PUERPERIUM
PUERPERAL INFECTION
 is the commonest complication during puerperium, but largely

preventable
PUERPERIUM
PUERPERAL INFECTION
 Any bacterial infection of the genital tract after delivery
 Incidence: 6 %
 The most important cause of maternal death
 Temperature 38° C or higher recorded 2x in the first 10 days

postpartum, exclusive of the first 24 hours, and to be taken by
mouth by a standard technique at least 4x daily
PUERPERAL INFECTION
RISK FACTORS
 PROM
 Anemia
 Hemorrhage
 EP and CS
 Placenta retain
PUERPERAL INFECTION
MANIFESTATIONS
 Acute vulvitis vaginitis and cervicitis
 Uterine infection
 Adnexal infections
 Breast infection
 Urinary infection
 Septic pelvic thrombophlebitis
 Other incidental infections
PUERPERAL INFECTION
COMMON PATHOGENS
 Aerobes
 Group A, B, and D streptococci
 Gram-negative bacteria: Escherichia coli, Klebsiella
 Staphylococcus aureus
PUERPERAL INFECTION
COMMON PATHOGENS
 Anaerobes
 Petococcus species
 Petostreptococcus species
 Bacteroides fragilis group
 Clostridium species
PUERPERAL INFECTION
COMMON PATHOGENS
 Other
 Chlamydia trachomatis
 Mycoplasma species
PUERPERAL INFECTION
DIAGNOSIS
 History
 Physical examination and PV
 Lab finding
 Differential diagnosis
PUERPERAL INFECTION
TREATMENT
 Nutrition
 anemia prevention
 Antimicrobial treatment
 broad-spectrum, high dose, long time
 Drainage
 Treatment of thrombophlebitis
PUERPERIUM
PUERPERAL SEPSIS
 Definition
 Risk Factors for Puerperal Sepsis
 Diagnosis
 Management
 Complication
PUERPERAL SEPSIS
DEFINITION
 Infection of genital tract between delivery & 42 days after

delivery
 2 or > features to be present:

 Pelvic pain
 Fever: 38.5° C
 Vaginal D/S
 Smell of D/S
 Subinvolution
PUERPERAL SEPSIS
RISK FACTORS
 Anaemia
 Malnutrition
 DM
 Prolonged labor
 Obstructed labor
 Prolonged PPROM
 Frequent vaginal examinations
PUERPERAL SEPSIS
RISK FACTORS
 Operative delivery
 Un-repaired tears
 PPH
 Poor hygiene
 Poor aseptic technique for delivery
 Manipulations high in the birth canal
 Retained bits of placenta or membranes
 Pre-existing STDs
PUERPERAL SEPSIS
DIAGNOSIS
 Endometritis
 Subinvolution
 Pelvic cellulites
 Salpingitis & peritonitis
 Pelvic thrombophlebitis
 Septicaemia
PUERPERAL SEPSIS
MANAGEMENT
 Preventive
 Good antenatal care
 Proper intra-natal care
 Post natal care
 Curative
 General care
 Antibiotics for infection

PUERPERAL SEPSIS
COMPLICATIONS
 Septicaemia
 Septic shock
 DIC
 Pulmonary embolization
 Distant spread of infection
 Kidney failure
 Death
PUERPERAL SEPSIS
LATE COMPLICATIONS
 Menstrual problems
 Chronic pelvic pain
 Chronic PID
 Secondary infertility
INFECTIONS ASSOCIATED WITH
CHILDBIRTH PROCESS
(OTHER THAN PUERPERAL SEPSIS)
 Breast Problems
 Urinary Problems
 Venous Thrombosis
BREAST PROBLEMS
 Retracted / cracked nipples →
 Breast engorgement
 Mastitis
 Breast abscess →
 Failure of lactation
BREAST PROBLEMS
ENGORGEMENT
 2-4 days postpartum, if not breastfeeding
 Anytime whilst breastfeeding
 Conservative management:
 Tight bra, ice packs, analgesia
 Bromocriptine
BREAST PROBLEMS
MASTITIS
 Regional staph aureus infection
 Fever, focal erythema, oedema &
tenderness
 3rd - 4th week
 Uncommon
 >50% of cases are in primiparas
 Management:
 Feed or pump (overcome obstruction)
 Oral antibiotics
 Analgesia
 Aspiration/I&D for abscess (10%)
URINARY PROBLEMS
 Retention
 Incontinence
 Infection
VENOUS THROMBOSIS
 Due to hypercoagulable state of pregnancy
 Predisposing factors:
 Increasing maternal age
 Obesity
 Anaemia
 Dehydration
 Trauma
 Infection
PUERPERAL MORBIDITY
(OTHER THAN INFECTION)
 Secondary Hemorrhage
 Puerperal Psychic Problems
 Obstetric Palsy
SECONDARY HEMORRHAGE
DEFINITION
 Uterine bleeding by 24 hours after delivery
CAUSES
 Infection
 Retained bits of placenta & membranes
 Subinvolution
 Problems of incision (vulval haematoma, caesarean scar
dehiscence)
 Trophoblastic disease
PUERPERAL PSYCHIC PROBLEMS
 Postnatal blues
 Postnatal depression
 Puerperal psychosis
POSTNATAL BLUES
 50%
MANIFESTATIONS
 Tearful
 Sad
 Sleep disturbed
 Restless
 Headaches
 Poor concentration
MANAGEMENT
 Reassure, support
POSTNATAL DEPRESSION
 10-25% in 1st year
 Peak 3-4 weeks
 2/3 self limiting; 1/3 sustained/severe
 MANIFESTATIONS: Irritable, tired, decreased libido, guilt,

unable to cope, undue anxieties
 MANAGEMENT: psychotherapy, counselling, antidepressants

PUERPERAL PSYCHOSIS
 1/500-800
 5% commit suicide, 4% kill baby
 20% - again next pregnancy, 50% psychotic again later in life
MANIFESTATIONS
 Suspicious – denies pregnancy
and baby
 Delusions
 Hallucinations
 Confusion
 Cognitive impairment
RISK FACTORS
 Previous psychosis, unmarried, C/S, infection, perinatal death
OBSTETRIC PALSY
 Severe neuralgia due to pressure on lumbo-sacral nerve plexus
 Foot drop
 Rarely femoral, obturator or sciatic nerves may be involved
 Spontaneous recovery usually
 Physiotherapy is helpful
CONCLUSIONS
 Importance of history
 Systematic evaluation
 Proper advise & motivation regarding contraception
 Importance of immunization for new born
 Stress upon postnatal exercises

Lecture 20
PHYSIOPATHOLOGY OF THE FEMALE
REPRODUCTIVE SYSTEM.
HIPOTALAMO-PITUITARY-OVARIAN
AXIS.
ENDOMETRIAL CYCLE AND
MENSTRUATION
OVARIAN CYCLE
 As graafian follicle develops, primary
oocyte completes meiosis I
 One daughter cell (secondary oocyte)

receives cytoplasm
 Other daughter, now a small polar
body degenerates
 Secondary oocyte arrests at metaphase II

 Only fertilized ova complete
meiosis II
OVARIAN CYCLE
 Secondary oocyte is part of the graafian follicle
 Granulosa cells form a layer around outside of follicle
 Oocyte sits on a mound of this layer the cumulus oophorus
 Corona radiata – ring of granulosa cells enclosing the secondary

oocyte
 Zona pellucida – gelatinous layer between oocyte and radiata

forms barrier to sperm penetration
OVULATION
 10-14 days after start of
menstruation
 Only 1 follicle survives
 Others become atretic

follicles (degenerate)
 Surviving graafian follicle forms

bulge on surface of ovary
 Secretes increasing levels of estrogen
 Graffian follicle releases secondary oocyte
 Into uterine tube at ovulation

OVULATION FROM A HUMAN OVARY
FERTILIZATION
 If a sperm passes through the corona
radiata and zona pellucida and enters the
cytoplasm of the occyte
 now the oocyte completes meiosis II
 with formation of another polar body
 If not fertilized within 2 days, secondary

oocyte degenerates
OVARIAN CYCLE
 Following ovulation empty follicle under the influence of LH
becomes a corpus luteum
 which secretes progesterone and estradiol
 Non-fertile cycle, becomes corpus albicans (non-functional
remnant)
PITUITARY-OVARIAN AXIS
 Hormonal interactions between anterior pituitary and ovaries
 Anterior pituitary secretes luteinizing hormone (LH) and

follicle-stimulating hormone (FSH)
 Both promote cyclic changes in the ovaries
 Both are controlled by GnRH from hypothalamus

 FSH secretion slightly greater during early phase of
menstrual cycle
 LH secretion greatly exceeds FSH secretion prior to ovulation
 Not clearly understood but believed to result from negative
feedback effects
HYPOTHALAMIC- PITUITARY-OVARIAN
AXIS
MENSTRUAL (MONTHLY) CYCLE
 Approximately month-long cycle of ovarian activity
 humans, apes, old world monkeys
 Menstruation – characterized by shedding of endometrial

lining accompanied by bleeding
 And sexual receptivity anytime throughout the cycle
 Nonprimate female mammals have estrous cycles

 no shedding of endometrium and receptivity is limited
 estrous animals that bleed (dogs and cats) is due to high

estrogen that accompanies receptive period
MENSTRUAL CYCLE
 In humans is about 28 days
 Day 1 is taken to be the first day of menstruation
 Days 1 thru ovulation constitutes the follicular phase
 Time from ovulation to menstruation is luteal phase
 Endometrial changes are called: menstrual, proliferative and

secretory phases
FOLLICULAR PHASE
 Lasts from day 1 to ~13
 Dominated by growth and death

of a cohort of primary follicles
into secondary follicles
 with one survivor becoming a
graafian follicle
 which will undergo ovulation
 As follicles grow granulosa cells

secrete increasing amounts of
estradiol
 Reaching peak about day 12
FOLLICULAR PHASE
 Follicular growth and estradiol
secretion dependent on FSH
 FSH and estradiol induce

formation of FSH receptors in
granulosa cells
 Follicles increasingly sensitive
to the same level of FSH
 At same time – FSH and estradiol

recruit LH receptors in graafian
follicle
FOLLICULAR PHASE
 Rapidly rising estradiol secretion:
 Hypothalamus increases pulses
of GnRH
 Anterior pituitary sensitivity to
GnRH increases:
 results in greater LH secretion
 Positive feedback between

estrogen and anterior pituitary
 results in LH surge, peaks 16
hrs before ovulation and
causes ovulation
THE CYCLE OF OVULATION AND MENSTRUATION
THE LUTEAL PHASE
 After ovulation – LH causes empty follicle to become corpus
luteum
 which secretes Estrogen and Progesterone
 Progesterone levels rise and peak about a week after ovulation
 Development of new follicles and another ovulation inhibited

by:
 high progesterone and estrogen exert strong negative
feedback on LH and FSH
 inhibin from corpus luteum further suppresses FSH
THE LUTEAL PHASE
 No fertilization →
 corpus luteum regresses
 Estrogen and
Progesterone levels
decline
 with menstruation and

new cycle of follicle
development
CYCLIC CHANGES IN THE
ENDOMETRIUM
 Driven by cyclic changes in estrogen and progesterone levels
 Proliferative phase (menstration cycle) occurs during

follicular phase - ↑ levels of estrogen
 stimulates growth of endometrial lining and development of
spiral arteries
 causes cervical mucus to become thin and watery to allow
sperm penetration
ENDOMETRIUM
 Secretory phase occurs during
luteal phase – endometrium
becomes ready for implantation
 Progesterone stimulates
development of uterine glands
 Progesterone and Estrogen
cause endometrium to become
thick, vascular, and spongy
 Progesterone causes cervical
mucus to thicken and become
sticky
ENDOMETRIUM
 Menstrual phase results
from drop in Progesterone
and Estrogen following
corpus luteum degeneration
 Low progesterone:
constriction of spiral
arteries
 Blood flow stops followed
by necrosis and sloughing
of endometrium
ENDOCRINE
CONTROL OF
THE OVARIAN CYCLE
FACTORS AFFECTING MENSTRUAL
CYCLE
 Release of GnRH is regulated not only by hormonal feedback
but also by input from higher brain centers
 Olfactory system can send activity to hypothalamus in

response to pheromones
 Can cause the “dormitory effect” in which cycles of

roommates become synchronized
FACTORS AFFECTING MENSTRUAL
CYCLE
 Limbic system input to the hypothalamus:
 In times of stress can cause functional amenorrhea

(cessation of menstruation)
 Also occurs in very thin or athletic females with low body

weight
 may be related to reduced leptin secretion by small
adipocytes
CONTRACEPTIVE METHODS
 Oral contraceptive pills – synthetic estrogen and
progesterone
 Taken daily for 3 weeks after menstrual period
 Mimic corpus luteum, so that negative feedback inhibits

ovulation
 Placebo pills taken in 4th wk to permit menstruation

RHYTHM METHOD
 Involves daily measurement of oral basal body temperature (BT)
upon awakening because:
 ovarian steroids cause BT changes
 declining Estrogen on day of LH surge causes a slight drop in

BT
 rising Progesterone on day after LH peak causes elevated BT
MENOPAUSE
 Cessation of ovarian activity and menstruation roughly ~50
years
 Ovaries depleted of follicles produce no estrogen

 LH and FSH are high because of no negative feedback
 Lack of Estrogen from ovaries most responsible

for:
 Hot flashes, osteoporosis, and increased
risk of atherosclerosis
Lecture 21
DISORDERS OF THE
ENDOMETRIAL CYCLE.
PREMENSTRUAL SYNDROME.
PID
COMMON PROBLEMS
 Dysmenorrhea
 Amenorrhea
 Menopause
 Dysfunctional uterine bleeding
 Post menopsaual bleeding
 Premenstrual syndrome
 Leiomyoma
 Endometriosis
 Gynecological abdominal pain
FREQUENT TERMS
 HYPERMENORRHEA: Heavy or prolonged bleeding & regular
 MENORRHAGIA: Heavy bleeding
 METRORRHAGIA: Bleeding in between periods
 POLYMENORRHEA: Menses < 21 days, frequent period
 MENOMETRORRHAGIA: Prolonged flow with intermenstrual

bleeding
FREQUENT TERMS
 OLIGOMENORRHEA: Infrequent periods
 AMENORRHEA: Absent periods
 DYSPAREUNIA: Pain during intercourse
 DYSMENORRHEA: Painful menstruation
 MITTELSCHMERZ: Mid-cycle lower abdominal pains

associated with ovulation
DYSMENORRHEA
 Painful menses occurring within 24-48 hours of the onset of
menses
 Most common medical problem of young woman
 Variable disability for 50% of women during their reproductive

years
 10% of patient with incapacitating pain for 1-3 days month
 Either primary or secondary in nature
 Dysmenorrhea is a condition, not a disease; the underlying

cause must be diagnosed
PRIMARY DYSMENORRHEA
 Uncommon prior to menarche
 Most common in late teens
 Incidence increase until early adulthood then declines with
age
 Parity often decreases severity with each successive gestation
 No identifiable cause present
 Excessive PGF2α mediated uterine smooth muscle stimulation
 Cervical stenosis, uterine ischemia
 PGE2 vasodilator/platelet inhibitor increasing menstrual flow
H&P
 Initial onset usually within 2 years of menarche
 Sharp, diffuse colicky suprapubic abdominal pain radiates to
the back and last for 1-3 days
 Often described as labor pain
 Nausea, vomiting, diarrhea and headache secondary to
systemic effects of prostaglandins
 60% low back pain, 45% dizziness, nervousness
 Does not occur between cycle or with anovulatory conditions
 Dyspareunia uncommon and is suggestive of secondary
dysmenorrhea
 No anatomic or physiological causes present
TREATMENT
 PGE inhibitors – NSAID
 Combination OBCP (estrogen followed by progestin required

for PGE secretion from endometrium so combination reduces
natural cycle thus preventing ovulation and reducing PGE
production)
 Danazol (low dose testosterone) - helpful at times
 Progestin OBCP pills - reduce endometrial layer
 Severity lessen with parity secondary to previous cervical

dilation
SECONDARY DYSMENORRHEA
 Uncommon in early adulthood. Increases with age
 Occurrence & severity not effected by parity
 Pain is from inflammation, ischemia, stretch receptor,

hemorrhage or perforation which increase peritoneal irritation
 May occur between menstrual cycles, but increases with or

becomes more apparent during menses
 When occurs between cycles becomes chronic pelvic pain
CAUSES
 Extrauterine
 Endometriosis
 Inflammation
 Adhesions
 Tumors (benign & malignant)
 Non gynecologic systemic cause
 Intramural
 Adenomyosis
 Leiomyomata
 Intrauterine
 Leiomyomata
 Polyps
 IUD
 Infections cervical stenosis
 Endocervical adhesions,
 Congenital uterine abnormalities
H&P
 History often suggest etiology
 Usually initially mild and more general in nature
 Often associated with heavy flow suggesting
intramural/intrauterine etiologies
 Increase abdominal pain suggest extrauterine causes
 Abdominal symptoms, contour changes or pelvic fullness
suggest large leiomyomata or neoplasms
 Fever, chills, malaise, vaginal discharge, suggest inflammatory
 Coexisting infertility suggest endometriosis or chronic pelvic
inflammatory diseases
DYSMENORRHEA
DIAGNOSIS
 H & P with pelvic exam
 CBC
 Cultures
 Urine studies
 Pelvic & abdominal U/S
 CT scan
 Hysteroscopy
 Laparoscopy
 Possible open laparotomy
AMENORRHEA
 Defined as failure of menarche by age 16 regardless of
development or the absence of menstruation for 3-6 months
after menarche
 Typically menstruation start by age 12 with about 98% by age

16 & last from 24-38 days
 Mean development by age 14 getting earlier recently etiology
 Two different types: primary & secondary

AMENORRHEA
REMEMBER:
R/O
PREGNANCY
AMENORRHEA
PRIMARY
 Failure of development by 14 years of age
 Failure of menses by 16 years of age regardless of development
 Secondary to chromosomal (Turners 45XO) genital

agenesis/congenital abnormalities (absent vagina or
imperforated hymen), failure of pituitary-ovarian axis
AMENORRHEA
SECONDARY
 ****REMEMBER R/O PREGNANCY****
 Failure to menstruate for 3-6 months or 3 cycles after

menarche
 Ovarian failure most common i.e.: menopause, but can be

premature
 Outflow tract obstruction

AMENORRHEA
ETIOLOGY
 Reproductive Outflow Disorders:
 Mullerian agenesis - absence of either vagina or uterus
 Imperforated hymen
 Androgen insensitive
 Cervical stenosis

AMENORRHEA
ETIOLOGY
 Ovarian Disorders:
 Chronic anovulation
 Resistant ovary
 Gonadal dysgenesis
 Premature ovarian failure

AMENORRHEA
ETIOLOGY
 Pituitary Disorders:
 Hyperprolactinemia
 Various tumors
 Pituitary insufficiency
AMENORRHEA
ETIOLOGY
 Hypothalamic Disorders:
 Functional- Exercise, stress anorexia S/P
 OBC pill, obesity
 Drugs TCA, tranquilizers
 Neoplastic lesions
 Nonfunctional - space occupying lesions

AMENORRHEA
DIAGNOSTIC APPROACH
 History - extremely important in these cases, detailing the

physical sexual developmental, nutritional, medical, and
psychological history
 Details of possible endocrine symptoms i.e.: (virilization,

hypothyroid and diabetes)
 Exercise & weight loss (Body fat index)
 History anorexic or bulimia (menstruational anomalies are

often the presenting symptom in adolescent females)
 Emotional stress extremely important

AMENORRHEA
DIAGNOSTIC APPROACH
 Exam:
 Neuro for possible intracranial lesions
 Pelvic (limited external in adolescent)
 Secondary sex characteristics
 Any evidence of endocrine abnormalities

 Laboratory:
 hCG
 Prolactin
 TFT (T3/T4/TSH)
 LH/FSH
 Estrogen/progesterone
 Possible testosterone/DHEA-S
 CT/MRI
 Chromosome karyotyping
AMENORRHEA
DIAGNOSTIC APPROACH
 Progestin challenge test - MPA induced:
 If bleeding occurs, the cause is chronic anovulatory or oligo-

ovulatory
 If no withdrawal bleeding, the cause is either a low estrogen

state of anatomic
AMENORRHEA
TREATMENT
 Depends on the basic cause
 Goal to induce menstrual flow 3-4 /year
 Surgical - for any lesion/tumors/defects
 80-90% of CNS or pituitary tumors will need resection
 Absent genital: cosmetic surgery, but will never be functional

AMENORRHEA
TREATMENT
 Pharmacological - wide range usually long term
 Hypothalamic disorder - behavior or lifestyle changes
 Treat any hypothyroid and hyperprolactinimia with surgery

&/or Parlodel
 Ovulation can be induce by gonadotropins
 Cycles managed by either 10 day progestin withdrawal
 3-4/year or OBCP continuously
 If associated with DUB after R/O organic causes

STEIN-LEVENTHAL SYNDROME
 Is most common cause of chronic anovulation
 Can cause either amenorrhea / irregularity due to estrogen

breakthrough
 Triad: obesity-hirsutism-amenorrhea
 Also may include anovulation and infertility
 Thought to be X-linked
 HX of insulin resistance may be present

POLYCYSTIC OVARIAN SYNDROME
(PCOS)
 Etiology: Increased adrenal androgens with obesity related
increased extra-ovarian estrogens
 This leads to inappropriate follicular development with thecal

layer over-activity producing increased levels of androgens
 Both leading to elevated LH and decreased FSH
 Thus failure of conversion of progesterone to estrogen by

depressed granulosa cells
 This leads to premature, but slow regression of the follicle

leading to multiple cystic formation
(PCOS)
DIAGNOSIS
 ↑ LH and ↓ FSH
 ↑ near normal estrogens, progesterone ↓
 ↑ LH/FSH ratio
 U/S evidence ovarian enlargement with midsized cystic

follicles
TREATMENT
(PCOS)
 Intermittent progesterone interruption with OBCP
 Weight reduction ideal & often only issue needed
 If pregnancy is a non issue: periodic MPA withdrawal is

indicated 3-4x/year
 For pregnancy: Clomiphene / gonadotropins
 Hirsutism: spironolactone
ABNORMAL UTERINE BLEEDING
 Defined as alteration of normal flow
 Dysfunctional uterine bleeding (DUB) is most common cause

of abnormal uterine bleeding prior to menopause
 Heavy, prolonged or inter-menstrual
 Normal is for 3-7 day & 60-80 ml blood loss
 DUB increase to 7-18 day & 100-200 ml
 May have chronic Fe loss & anemia
 About 15% have regular ovulation but lack adequate corpus

function
REMEMBER:
R/O
PREGNANCY
ETIOLOGY
 Organic: coagulopathies, liver/renal disease, drugs (steroids,

chemo & Coumadin), obesity and endocrine abnormalities
(thyroid, diabetes & adrenal)
 Uterine: leiomyomas, polyps, endometrial hyperplasia, PID,

IUD, pregnancy, cancers & endocrine active tumors
 Non organic: persistent ovulatory failure, the most common

cause is the continuous acyclic estrogen production leading to
anovulation and endometrial proliferation
 DUB is the most common cause of bleeding in adolescent &

young adults
ANATOMIC CAUSES OF IRREGULAR BLEEDING
 Uterine lesions: myomas, polyps, endometrial carcinoma
 Cervical lesions: neoplasia, polyps, cervical inversion,

cervicitis, cervical condylomas
 Vaginal lesions: carcinoma, sarcoma, adenosis, laceration,

trauma, infections, foreign bodies
 Other: urethral carbuncle, urethral diverticulum, GI bleeding,

and various labial lesions
REMEMBER:
R/O
CANCER
DIAGNOSIS
 History: Previous customary cycles, episode of irregular

bleeding, heavy bleeding, sexual contact, STD, previous
surgery
 Exam: Pelvic for possible sites of internal bleeding

(vaginal/rectal), uterine or adnexal enlargement
 Lab: hCG, CBC, consider Prolactin Coag studies, TFT, LH,

FSH, estrogen and Progestin levels, U/S, CT/MRI
 May need biopsy, D&C, and hysteroscopy
 Treatment depends of etiology

Polypoid mucosa Hyper-stimulated mucosa
Fibroids Polyps
Adenocarcinoma
DYSFUNCTIONAL UTERINE BLEEDING
 Pathology is excluded
 Most patient anovulatory
 May be related to hypothalamic-pituitary axis resulting in

continued estrogenic stimulation of the endometrium
 The endometrium outgrows its blood supply partially
breaks down bleeding occurs in irregular manner
 Organic causes (thyroid, adrenal must be excluded)

 Epidemiology: Most common in extremes of reproductive
age (20% adolescents, 40% patients over 40)
 Hx: to exclude all other pathology
 Diagnosis - based on:

 history
 absence of ovulatory temperature changes
 low serum progesterone

TREATMENT
 DUB is most common cause of abnormal bleeding
 Unremarkable & negative workup
 Acute stable: MPA/OBCP 3 to 4 x usual dose
 Acute unstable: IV estrogen 25 mg q4 x6; if uncontrollable
need D&C with cytology
 Chronic: GnRH inhibitors, ergots, NSAID, various
progestin/estrogens/progest/OBCP combinations
 Surgical D&C, eletrocautery or laser endometrial ablation
 Hysterectomy is final option for significant refractory bleeding
without pathology
POST MENOPAUSAL BLEEDING

always abnormal
and is
CANCER
until proven otherwise

requires
a DEFINITIVE DIAGNOSIS
And if chronic, re-evaluate
EVERY YEAR
DIAGNOSIS
 History: Previous customary cycles, episode of irregular

bleeding, heavy bleeding
 Exam: Pelvic for possible sites of internal bleeding

(vaginal/rectal), uterine or adnexal enlargement
 Endometrial biopsy may be required
 Possible D&C and hysteroscopy may be helpful

TREATMENT
 HRT, if bleeding acyclic or last > 10 days
 If cyclic & before the 10 day & unresponsive to progesterone

increase requires biopsy
 HRT, if bleeding acyclic for > 6 months
 If heavy and persistent initially requires biopsy
 When in doubt, refer for biopsy

TREATMENT
 Depends on the final diagnosis refer for cancer / adenomatous

hyperplasia
 If cystic hyperplasia, proliferative endometrium increase

Progestin and repeat 4-6 months
 Secretory, non-proliferative or atrophic endometrium: normal

provide reassurance, but repeat 8-10 months if continues or for
any changes
 Never except insufficient sample or non definitive

PREMENSTRUAL SYNDROME
 Psychoneuroendocrine
 PMS is a clinical syndrome with physical & emotional

symptoms that increase just prior to the flow and rapidly
dissipates
 Nearly 100% with some degree of symptoms 50% present to

MD & 5% with severe symptoms
 Peak age is 30-45 with a + family history
 Often is associated with early perimenopause

 Increases with use OBCP
 40% + history of sexual abuse (double general)
 15% childhood sexual abuse (triple general)
 Increase with pregnancy complicated abortion, preeclampsia,

or postpartum depression
 Often linked with mid-life crises
 Symptoms rate mild, moderate, severe

ETIOLOGY
 Neurotransmitter dysfunction
 Steroid imbalance (estrogen/progesterone)
 Prostaglandin imbalance
 Fluid retention
 Vitamin deficiency (A, B6, B complex)
 Mineral deficiency (Mg, Zn & Ca)
 Psychosomatic illness
PRESENTATION
 Abdominal bloating
 Anxiety
 Breast tenderness
 Emotional liability
 Depression
 Fatigue
 Irritability
 Weight/water gain
DIAGNOSIS
 Clinical:
 Symptoms are cyclic & 2nd half of cycle
 Symptoms increase as cycle progress
 Symptoms are relief by menses onset
 Symptoms complete absence 2-3 days of menses onset
 Symptom free during rest of the cycle
 Symptoms present during 3 consecutive cycles

TREATMENT
 R/O organic disease & treat, if present
 Luteal-phase progesterone &/or estrogen
 Psychological support/reassurance/stress relief
 Nutritional supplementation vitamin B6/exercise
 Mild diuretic spironolactone
 Limit caffeine/smoking
 Trial of OBCP or Danazol/Leupron
 Trial of antidepressant/mild tranquilizer caution
 NSAID drug (flavor of the month - Naprosyn)
 Exercise
PELVIC INFLAMMATORY DISEASE
(PID)
 Spectrum disease involve cx, uterus, tubes
 Most often - ascending spread of microorganisms from vagina

& endocervix to endometrium, tubes, contiguous structures
 Incidence: acute PID 1-2% of young sexually active women

each year
PID
ETIOLOGY
 Neisseria gonorrhoeae common cause of PID
 85% of infection - sexually active female of reproductive age
 15% of infection occur after procedures that break cervical

mucous barrier
 Bacteria culture direct from tubal fluid common: N.

gonorrhoeae, C. trachomatis, endogenous aerobic, anaerobic,
genital mycoplasma spp.
PID
C. TRACHOMATIS
 produce mild form of salpingitis
 slow growth (48-72 hrs)
 intracellular organism
 insidious onset
 remain in tubes for months/years after initial colonization of

upper genital tract
 more severe tubes involvement

PID
N. GONORRHOEAE
 gram negative diplococcus
 rapid growth (20-40 min)
 rapid & intense inflammatory response
 2 major sequelae:
 infertility & ectopic pregnancy, strong asso. with prior
Chalamydia infection
PID
RISK FACTORS
 Strong correlation between exposure to STD
 Age of 1st intercourse
 Frequency of intercourse
 Number of sexual partners
 Marital status ; 33% - nulliparous

PID
RISK FACTORS
 Increased risk:
 IUD user (multifilament string
 surgical procedure
 previous acute PID
 Reinfection - untreated male partners 80%
 Decreased risk:
 barrier method
 OC
PID
DIAGNOSIS
 Common clinical manifestations:
 lower abdominal pain 90%
 cervical motion tenderness
 adnexal tenderness
 fever
 cervical discharge
PID
 acute appendicitis
 endometriosis
 torsion/rupture adx mass
 ectopic pregnancy
 lower genital tract infection

PID
 75% asso. endocervical infection & coexist purulent vaginal
discharge
 Fitz-Hugh-Curtis syndrome:
 1-10%
 perihepatic inflammation & adhesion
 s/s: RUQ pain, pleuritic pain, tenderness at RUQ on

palpation of the liver
 mistaken dx: acute cholecystitis, pneumonia

FITZ-HUGH-CURTIS SYNDROME
PID
DIAGNOSIS
 CBC
 ESR
 C-reactive protein
 Vaginal & cervical swab
 U/S, CT, MRI
 Culdocentesis
 Laparoscopic visualization
 most accurate method for confirm PID
 all pt. with uncertain dx, not response to Rx
 * -ve gram smear not R/O PID

PID
PID
SEQUELAE
 Infertility
 ¼ of pt have acute salpingitis
 occur 20%
 infertility rate increase direct with number of episodes of

acute pelvic infection
PID
SEQUELAE
 Ectopic pregnancy
 increase 6-10 fold
 50% occur in fallopian tubes (previous salpingitis)
 mechanism ; interfere ovum transport entrapment of ovum

PID
SEQUELAE
 Chronic pelvic pain
 4 x higher after acute salpingitis
 caused by hydrosalpinx, adhesion around ovaries
 should undergo laparoscope - R/O other disease
 TOA 10%
 Mortality:
 acute PID 1%
PID
TREATMENT
 Therapeutic goals:
 eliminate acute infection & symptoms
 prevent long-term sequelae

PID
TREATMENT
 Empirical ABx cover wide range of bacteria
 Treatment start as soon as culture & diagnosis is

confirmed/suspected
 failure rate, OPD oral ATB - 10-20%
 failure rate, IPD iv ATB - 5-10%
 reevaluate 48-72 hrs of initial OPD therapy

PID
TREATMENT
 Rx male partners & education for prevention reinfection
 Rx male partners - regimens for uncomplicated gonorrhoeae &

chlamydial infection
 Ceftriaxone 125 mg im, followed by:
 Doxycycline (100) 1x2ʘ pc x 7 days or
 Azithromycin 1gmʘ or
 Ofloxacin (300) 1x2ʘ pc x 7 days

PID
SURGICAL TREATMENT
 Laparotomy
 surgical emergencies
 definite Rx of failure medical treatment
 Laparoscopy
 consider in all pt with ddx of PID & without contraindication
 R/O surgical emergency
 Evidence of current / previous abscess
 Acute exacerbation of PID with bilateral TOA

PID
RUPTURED PELVIC ABSCESS
 Mortality rate 10%
 Can rupture spontaneous into:

 rectum
 sigmoid colon
 bladder
 peritoneal cavity
Lecture 22
PUBERTY & MENOPAUSE

OBJECTIVES
 Define puberty
 Mention period of onset of puberty
 Discuss the factors that affect the onset of puberty
 Describe how does puberty begin
 Describe the physical changes during puberty
 What is menopause
 Causes of menopause
 Stages of menopause
 Indications and signs
 Management
PUBERTY
DEFINITION
 The process of physical changes by which child's body
becomes an adult body capable of reproduction
PUBERTY
PERIOD OF ONSET
 The onset of puberty varies among individuals. Puberty usually
occurs in girls between the ages of 10 and 14
PUBERTY
FACTORS AFFECTING PUBERTY ONSET
 Leptin likely is one of multiple influences on
the hypothalamus which releases gonadotropin-releasing
hormone (GnRH)
 This in turn signals the pituitary gland to release luteinizing
hormone (LH) and follicle-stimulating hormone (FSH)
 A gene has been identified that appears to be critical for the

normal development of puberty
 The gene, known as GPR54, encodes a protein that appears to
have an effect on the secretion of GnRH by the hypothalamus
 Obesity
PUBERTY
HOW DOES PUBERTY BEGIN ?
 During childhood, the hypothalamus is extremely sensitive to

the negative feedback exerted by the small quantities of
estradiol & testosterone produced by the girls’ ovaries
PUBERTY
 As puberty approaches, the sensitivity of the hypothalamus
is decreased and subsequently, it increase the pulsatile
GnRH secretion initially at night
 The anterior pituitary responds by progressive secretion of

FSH and LH associated with increased secretion of growth
hormone
PUBERTY
 The ovaries respond to the
increase gonadotrophin
secretion by follicular
development & estrogen
secretion
 Estrogen causes development
of the genital organs and the
appearance of the secondary
sexual characters
 With increased estrogen
secretion, menarche and
cyclic estrogen secretion
occurs
PUBERTY
STAGES OF PHYSICAL CHANGES
PUBERTY
 Stage one
 The pre-puberty stage, girls haven’t marked

pubic hair and have only slightly elevated
breast tissue
PUBERTY
 Stage two
 Lasts from about 11.2 to 11.9 years
 Experience breast bud development and a

sparse growth of hair along the labia
 Growth is accelerated, and girls grow around

3 inches per year
PUBERTY
 Stage three
 Lasts from about age 12.4 to 12.7
 Breast tissue grows beyond the areola in the

absence of contour separation, and pubic
hair becomes pigmented, curled, and coarser
 Girls hit their growth peak velocity at this

PUBERTY
 Stage four
 Between the ages of 13.1 and 13.4 years
 Is marked by a projection of breast tissue and

adult-type pubic hair without spread to the
mid-thigh
 Growth decelerates at this stage, and slows to

PUBERTY
 Stage five
 Last from about 14 and one-half to 16 years
 Marked by adult-type hair and development

of adult breast contour
MENOPAUSE
DEFINITION
 The state of an absence of menstrual periods for 12
months
 Usually be expected in the

age range of 42–58
 Menopause occurs when a

woman's ovaries run out of
functioning eggs
CAUSES OF MENOPAUSE
1. NATURAL / PHYSIOLOGICAL MENOPAUSE
 part of a woman's normal aging process
 marks the end of a woman's potential childbearing years
 brought on by the ovaries gradually slowing down their
function
 FSH responsible for stimulating the growth of the woman's
eggs
 As menopause approaches, the remaining eggs become
less sensitive to FSH (hence FSH levels increase) and the
ovaries reduce their production of estrogen significantly
(hence, estrogen levels ↓)
CAUSES OF MENOPAUSE
2. INDUCED MENOPAUSE
 An early menopause can be related to:
 cigarette smoking
 higher body mass index
 racial/ethnic factors and financial strain
 illnesses
 chemotherapy and radiation

 surgical removal of the uterus and/or both ovaries
STAGES OF MENOPAUSE
1. PRE MENOPAUSE
 It is the phase before menopause covering a period of 5-10

years before the last menstrual cycle
STAGES OF MENOPAUSE
2. PERI MENOPAUSE
 It is the term describing the menopause transition years
 Production of most of the reproductive hormones, including
the estrogens, progesterone and testosterone, diminish and
become more irregular
 Fertility ↓, but is not considered to reach zero until the
official date of menopause (12 months after last menstrual
cycle)
 In the per menopause years, many women undergo
significant bodily changes resulting from hormonal
irregularity
 Most women will gain weight, especially in the lower abdomen,
buttocks, and thighs
MENOPAUSE
INDICATIONS AND SIGNS
 Vascular instability
 Hot flashes , including night sweats
 Increased risk of atherosclerosis
 Migraine
 Rapid heartbeat
MENOPAUSE
 Uro-genital atrophy
 Thinning of the membranes of the vulva, the vagina, the
cervix, and the outer urinary tract
 Itching
 Dryness
 Watery discharge
 Urinary frequency
 Urinary incontinence
 Urinary urgency
 Increased susceptibility to inflammation and infection
MENOPAUSE
 Skeletal
 Back pain
 Joint & muscle pain
 Osteopenia and the risk of osteoporosis

 Gradually developing over time
 Skin, soft tissue

 Breast atrophy
 Breast tenderness, swelling

MENOPAUSE
 Psychological
 Depression and/or anxiety
 Fatigue
 Irritability
 Memory loss, and problems with concentration
 Mood disturbance
 Sleep disturbances, poor quality sleep, light sleep, insomnia
 Sexual
 Decreased libido
 Problems reaching orgasm
 Vaginal dryness and vaginal atrophy
MENOPAUSE
PSYCHOLOGICAL
 The lack of estrogen and progesterone causes many changes

in women's physiology that affect their health and well-
being. These changes include:
 ↑ levels of total cholesterol and LDL-cholesterol, which ↑

the risk of coronary heart disease (CHD) in women
 During the reproductive years, estrogen prevents ↑ levels

of blood cholesterol and maintains the activity of estrogen
receptors in women, thus preventing the risk of CHD
MENOPAUSE
SKELETAL
 Calcium loss from the bones is ↑ in the first 5 years after the
onset of menopause, resulting in a loss of bone density
 This bone loss then tapers off until about the age of 75, when
calcium loss accelerates again
 This predisposes women to the risk of osteoporosis and bone

fractures
MENOPAUSE
 The body composition of menopausal women also changes,
with the percentage of body fat ↑ and muscle mass ↓
 The ↑ in body-fat percentage is believed to be partly due to
↓ physical activity
 ↓ muscle mass reduces the rate of basal metabolism, which

may be responsible for weight gain at this period of a
woman's life
 The abdominal-fat storage that occurs in women at this stage

↑ the risk for cardiovascular disease
MENOPAUSE
MANAGEMENT
(A) Hormone replacement therapy:
 The use of estrogen + progestin for a woman who has an intact
uterus, or estrogen alone for a woman who has had a hysterectomy
 Conjugated equine estrogens
 Selective Estrogen Receptor Modulators
(B) Symptoms management:

 Antidepressants
 GABA analogs
 Blood pressure medicines
 Alternative medicine
MENOPAUSE
MANAGEMENT
(C) Dietary and lifestyle changes:
 Cut down on red meat, organ meats such as liver and kidney, and
other foods high in iron, because they are not menstruating, so
their requirement for iron is ↓
 Water intake is emphasized in older women and men, since the
thirst sensation becomes dulled as people age
 ↓ their intake of total fat, saturated fat, and total calories to
balance their energy expenditure and prevent weight gain
 Intake of dietary fiber must be ↑ to prevent constipation
 Exercise is also very important for all older individuals
Lecture 23
PATHOLOGY OF VULVA,
VAGINA AND CERVIX

OBJECTIVES
 To understand some of the more common non-neoplastic
vulvar, vaginal and cervical lesions
 To understand the concept of vulvar dystrophy, vulval

intraepithelial neoplasia (VIN) and cervical squamous
intraepithelial lesion (SIL)
 To understand the common forms of vulvar, vaginal and

cervical carcinoma
NON-NEOPLASTIC EPITHELIAL
LESIONS
 These are non-neoplastic benign mucosal alterations of the
vulva
 Types:
 Lichen sclerosus
 Lichen simplex
 They are considered risk factors for vulvar neoplsia

LICHEN SCLEROSUS
 Grossly - yellowish, blue papules or
plaques that eventually coalesce into
thin, gray, parchment like areas
 Microscopically - atrophic epithelium,

dermal fibrosis and mononuclear
perivascular reaction
 It occurs in all age groups, but is most

common in postmenopausal women
 It is suggested to be an autoimmune
reaction
LICHEN SIMPLEX CHRONICUS
 "HYPERPLASTIC DYSTROPHY”
 It is the physiologic outcome to rubbing

the vulvar mucosa in response to
pruritus (caused by irritant exposure,
dermatitis and neoplsia)
 Grossly - an area of white plaques

termed leukoplakia
 Microscopically - a thickened
epithelium, hyperkeratosis and
leukocytic dermal inflammation
CONDYLOMA ACUMINATA
 A wart-like, verrucous lesion caused by
sexually transmitted HPV 6 and HPV 11
 Grossly - They occur anywhere on the ano-

genital surface, sometimes singly but more
often in multiple sites. They are red-pink
and range from a few mms to many cms in
diameter
 Microscopically - a sessile / branching

epithelial proliferation of stratified
squamous epithelium, some of which have
perinuclear cytoplasmic vacuolization
(koilocytosis)
VULVAR INTRAEPITHELIAL NEOPLASIA
(VIN)
 VIN is a premalignant intramucosal
epithelium changes that precedes invasive
carcinoma
 The VIN may be graded VIN II or VIN III

(carcinoma in situ)
 Caused by sexually transmitted HPV 16
 Cancer risk increases with age, and

spontaneous regression is more common
in younger patients
VULVAR NEOPLASM
 Represents 3% of all genital tract cancers in
women
 Approximately 90% of carcinomas are
squamous cell carcinomas
 90% of vulvar squamous cell carcinomas
are HPV related (type 16), usually
presenting as poorly differentiated
lesions, sometimes multifocal. They often
evolve from vulvar intraepithelial
neoplasia
 Non-HPV-related vulvar squamous
cell carcinoma occurs in older
individuals, is usually well differentiated
and unifocal, and is associated with
lichen sclerosis or other inflammatory
conditions
 The remainder are adenocarcinomas,

melanomas, or basal cell carcinomas,
EXTRAMAMMARY PAGET DISEASE
 Grossly - red, scaly sharply demarcated,
maplike area, mostly on the labia majora
 Microscopically - large, anaplastic,

vacuolated tumor cells lying singly or in
small clusters within the epidermis
 In a minority of cases there is an

underlying carcinoma of a vulvar or
perineal glands
VAGINAL MALIGNANT NEOPLASM
 Epithelial tumors:
 Squamous cell carcinoma
 Adenocarcinoma
 Non Epithelial tumors:

 Embryonal rhabdomyosarcoma
SQUAMOUS CELL CARCINOMA
 The most common type, accounting for

95% of cases
 The peak incidence is between 60-70 years

of age
 Grossly - either plaque like or occasionally

fungating
 They invade the cervix and perivaginal

structures as the urethra, urinary bladder
and rectum
ADENOCARCINOMA
 Rare, but important, because of the

increased frequency of clear cell
adenocarcinoma in young women whose
mothers were treated with diethylstilbestrol
(DES) during pregnancy (for threatened
abortion)
 These tumors are composed of glands lined

by vacuolated glycogen containing clear cells
SARCOMA BOTRYOIDES (EMBRYONAL
RHABDOMYOSARCOMA)
 Rare form of primary vaginal cancer
 Produce soft polypoid grape-like clusters that

may protrude from the vagina, formed of small
tumor cells with oval nuclei and embryonal
rhabdomyoblasts
 It is usually encountered in infants and children

younger than the age of 5 years
 It may occur in other sites, such as the urinary

bladder and bile ducts
CERVICITIS
 Cervicitis commonly comes to attention on
routine examination or because of marked
leukorrhea
Morphology
 Non specific cervicitis
 Acute nonspecific form - postpartum women
 usually caused by staphylococci or streptococci
with acute infiltration of neutrophils beneath the
lining mucosa
 The chronic nonspecific cervicitis - more common
 It consists of chronic inflammation, epithelial
regeneration, and squamous metaplasia of
columnar epithelium
 Specific cervicitis
 Specific form is caused by gonococcal infection,
herpes virus ulcerative lesions and changes caused by
Chlamydia
FEMALE GENITAL TRACT
 Embryology
 Anatomy
 Pathology
SEXUALLY TRANSMITTED DISEASES
A. Exclusively or regularly transmitted by sexual contact
Causal Agent Manifestations
VIRAL DISEASE
• HIV-I, HIV-II • Acquired Immunodeficiency
• Syndrome Herpes virus 1,2 (HSV-1,2)
• Herpes lesions
• Chlamydial, mycoplasmal
• Lymphogranuloma Venereum
• Chlamydia trachomatis (L. Type)
• C. Trachomatis, Ureaplasma • Non-gonorrheal Uretritis
Cervicitis
• Non-gonorrheal Uretritis, Cervicitis
• Urealyticum
CERVICAL HERPES
BACTERIAL DISEASE
• Neisseria Gonorrhoeae • Gonorrhea
• Treponema Pallidum • Syphilis (Lues Venerea)
• Haemophilus Ducreyi • Chancroid
• Calymmatobacterium Donovani • Granuloma Inguinale
PROTOZOAL
• Trichomonas Vaginalis • Trichomoniasis
BY ATHROPOD
• Phtirus Pubis • Pediculosis Pubis (Crabs)
TRICHOMONAS VAGINALIS
B. Transmissible sexually or by other means
 VIRAL
 Cytomegalovirus, Hepatitis B Virus, Epstein-Barr Virus,
Molluscum Contagiosum Virus
 BACTERIAL
 Group B Streptococci; Gram Negative Bacilli
 PROTOZOAL
 Enteromoeba Histolytica
CANDIDA ALBICANS
BARTHOLIN’S CYST
 Cystic dilation of the Bartholin gland due to obstruction of
Bartholin’s duct
 Usually preceded by acute infection and may result in a

Bartholin’s abscess
 Swelling in the posterior aspect of the labium majus (up to 5

cm), associated with pain and discomfort
 Occurs at all ages
 Cysts are either excised or opened permanently

BARTHOLIN’S CYST
VULVAR DYSTROPHY
 Lichen Sclerosis
 Occurs anywhere on the body
 All age groups, but most common after menopause
 Clinically: pale skin with atrophy
 Histologically: atrophy of epidermis and dense

sclerosis of dermis with a mononuclear cell infiltrate
about blood vessels
LICHEN SCLEROSIS
LICHEN SCLEROSIS
VULVAR DYSTROPHY - LICHEN SCLEROSIS
 Develops slowly, discomfort, predisposes to acute

infections
 Pathogenesis: unknown (genetic, hormones)
 It is not a pre-malignant lesion, but increases risk of

carcinoma slightly
VULVAR DYSTROPHY
 Squamous Hyperplasia
 Similar to Lichen Sclerosis
 Histologically: Hyperplasia of the vulvar squamous

epithelium with hyperkeratosis
 No significant increased risk of carcinoma
 Biopsy is indicated in all vulvar lesions

TUMORS OF THE VULVA
 Benign tumors
 Papillary hidradenoma
 Condyloma acuminatum
 Malignant tumors
 Carcinoma and vulvar intraepithelial neoplasia (VIN)
 Malignant melanoma
BENIGN TUMORS OF THE VULVA
 Papillary Hidradenoma
 Well circumscribed nodule, most commonly on labia

majora
 Benign proliferation of sweat glands, tubular ducts lined by

columnar cells and surrounded by myoepithelial cells
 Condyloma Acuminatum
 Benign papillary (wart-like) lesion on the mucosa of the

vulva, perianal region, urethra, cervix and vagina
 Caused by human papilloma virus (HPV types 6 and 11)
 Flat condyloma (HPV associated lesion) is usual pattern for

cervix
 Condyloma Acuminatum
 Histologically: papillary proliferation of squamous

epithelium with nuclear atypia and perinuclear
vacuolization (koilocytosis) in the surface cells
 Frequently regress spontaneously and are not precancerous

lesions
FLAT CONDYLOMA OF CERVIX
CONDYLOMA ACUMINATUM
HPV CHANGES
MALIGN TUMORS OF THE VULVA
 Carcinoma of the Vulva
 Uncommon malignancy (3% of all female genital cancers)
 Most occur in women over age 60 years
 The majority (85%) are squamous cell carcinoma
 Others include melanoma, adenocarcinoma, and basal cell

carcinoma
 Squamous Cell Carcinoma and Intraepithelial Neoplasia
(VIN)
 2 groups of squamous cell carcinoma differ in etiology:

pathogenesis and clinical presentation
 First group is associated with HPV, preceded by vulvar

intraepithelial lesion and multicentric
 Vulvar intraepithelial lesion (in situ carcinoma, Bowen’s

Disease) is frequently multicentric, 90% of cases associated
 2nd group of vulvar squamous cell carcinoma is associated
with vulvar dystrophy, unclear etiology
 Metastatic spread is linked to size and depth of tumor
 Most commonly involves regional lymph nodes, lung, and

liver
 Less than 2 cm in diameter have 60-80% 5-year survival rate

 Extrammamary Paget’s Disease
 Red sharply demarcated lesion on the labia majora
 Microscopic features are similar to Paget’s Disease of the

breast, clusters of anaplastic tumor cells within the
epidermis and its appendages
 These cells are surrounded by clear halo (micropoly-

saccharide)
 Very good prognosis (without invasion or associated

 Malignant Melanoma
 Rare tumors (5% of all vulvar cancers)
 Peak incidence is 6-7 decades
 Histologic and biologic characteristics are similar to

melanomas elsewhere
MALIGNANT MELANOMA
VAGINA
 Congenital Anomalies
 Premalignant and Malignant Neoplasms
 Vaginal intraepithelial neoplasia and squamous cell

carcinoma
 Adenocarcinoma
 Embryonal rhabdomyosarcoma
VAGINA
 Congenital Anomalies
 Garthner’s duct cysts: common, derived from Wolffian duct

rests, located on lateral wall of vagina submucosal cyst (up
to 2 cm)
 Mucous cyst: derived from Mullerian epithelium
 Atrasia
 Total absence of vagina

VAGINA
 Benign Tumors of the Vagina
 Skeletal muscle (rhabdomyoma)
 Stroma (stromal polyps)
 Leiomyoma
 Hemangioma
 Vaginal intraepithelial neoplasia and squamous cell

carcinoma
 Primary carcinoma of the vagina is extremely uncommon

 Associated with vaginal intraepithelial neoplasia
VAGINA
 Vaginal Adenocarcinoma
 Rare tumor
 Increased frequency (0.14%) of clear

cell adenocarcinomas in young women
(15-20 years), whose mothers had been
treated with diethylstilbestrol (DES) during pregnancy (for
threatened abortion)
 Composed of vacuolated, glycogen-containing cells (clear

cell)
VAGINA
 Vaginal Adenocarcinoma
 Vaginal adenosis is a possible precursor
 Careful follow-up of all DES-exposed women is mandatory
 Surgery and radiation (80% eradication rate)

VAGINA
 Embryonal Rhabdomyosarcoma (Sarcoma Botryoides)
 Very uncommon vaginal tumor
 Mostly seen in infants and children (under age of 5 years)
 Histologically: small, crowded, spindle cells with

cytoplasmic extensions from one end
 Locally invasive and may cause death by penetration into

peritoneum or obstruction of urinary tract
SARCOMA BOTRYOIDES
CERVIX
 Examination - Cuscoe or Sims’ speculum:
 Size, shape and consistency should be noted as well as any
discharge
 Ectocervix = stratified squamous epithelium
 Endocervical canal = columnar epithelium
 Junction = squamocolumnar
and adjacent is the
Transformation Zone
CERVICAL ECTOPY OR EROSION
 Endocervical epithelium advances on ectocervix- bright red
velvety appearance
 Occurs more in adolescence, pregnancy, use of OCP

 Can also result from labour
 Most cases asymptomatic
 Can cause leucorrhoea and post-coital bleeding
 Treatment - only if symptomatic

 Radial diathermy or cryosurgery
CERVICAL ECTOPY
 Complications
 secondary haemorrhage and infection
 cervical stenosis
CERVICITIS
 Non-specific condition difficult to define
 Common clinical diagnosis

CERVICAL POLYPS
 Develop from endocervix and protrude into vagina
 Usually asymptomatic
 Can cause intermenstrual and postcoital bleeding
 Rarely malignant
 Treat by avulsing and send for

histology
 Base should be cauterised-prevents regrowth

CERVICAL FIBROIDS
 Cervical leiomyomas similar to fibroids in other sites of uterus
 Pedunculated, sessile or grow to fill vagina and distort pelvic

organs
 Symptoms similar to other polyps
 Attempted extrusion can cause

colicky uterine pain
 Treatment by excision
NABOTHIAN FOLLICLES
 If process of squamous metaplasia results in obstruction of
cervical glands, retention cysts form- Nabothian follicles/cysts
 Linked to chronic cervicitis

CERVICAL CANCER
 Begins in the lining of the cervix
 Cells change from normal to pre-cancer (dysplasia)

and then to cancer
CERVICAL CANCER
3 Types:
 Squamous cell Carcinomas

 Cancer of flat epithelial cell
 80-90%
 Adenocarcinomas
 Cancer arising from glandular epithelium
 10-20%
 Mixed carcinoma
 Features both types
CERVICAL CANCER
STATISTICS
 10,520 new cases in the U.S. this year
 3,900 will die

 50% are diagnosed between ages 35 and 55
 20% at the age of 65 or over
 Rarely occurs in women younger than 20
 Noninvasive is four times more common
 74% decrease in deaths between 1955 and 1992 in the U.S.
 Death rate continuous to decline by 2% a year
LIFETIME PROBABILITY OF DEVELOPING CANCER,
BY SITE, WOMEN, US, 1998-2000
Site: Risk
All sites 1 in 3
Breast 1 in 7
Lung & bronchus 1 in 17
Colon & rectum 1 in 18
Uterine corpus 1 in 38
Non-Hodgkin lymphoma 1 in 57
Ovary 1 in 59
Pancreas 1 in 83
Melanoma 1 in 82
Urinary bladder 1 in 91
Uterine cervix 1 in 128
Source: DevCan: Probability of Developing or Dying of Cancer Software, Version 5.1 Statistical Research and Applications
Branch, NCI, 2003. http://srab.cancer.gov/devcan
CERVICAL CANCER
SIGNS AND SYMPTOMS
 Menstrual bleeding is longer and heavier than usual
 Bleeding after menopause or increased vaginal discharge
 Bleeding following intercourse or pelvic exam
 Pain during intercourse
Source: American Cancer Society

CERVICAL CANCER
RISK FACTORS
 Human papillomavirus infection (HPV) – Primary factor
 HPV 16, HPV 18, HPV 31, HPV 33, HPV 45
 50% are caused by HPV 16 AND 18
 Sexual behavior
 Smoking
 HIV infection
 Chlamydia infection
 Diet
 Oral contraceptives
 Multiple pregnancies
 Low socioeconomic status
 Diethylstilbestrol (DES)
 Family history
CERVICAL CANCER
PREVENTION
 Avoiding the risk factors

 Especially HPV
 Help for low-income women (NBCCEDP)
 Having the Pap Test

 3 years after first vaginal intercourse or by age 21
 Have test annually

CERVICAL CANCER
DIAGNOSIS
 Cervical Cytology (Pap Test)

 Cells are removed from the cervix and examined under the
microscope
 Can detect epithelial cell abnormalities:
 Atypical squamous cells
 Squamous intraepithelial lesions
 Squamous cell carcinoma (likely to be invasive)

CERVICAL CANCER
DIAGNOSIS
 Additional testing:
 Colposcopy
 Cervix is viewed through a colposcope and the surface of the
cervix can be seen close and clear
 Cervical Biopsies
 Colposcopic biopsy – removal of small section of the abnormal area
of the surface
 Endocervical curettage – removing some tissue lining from the
endocervical canal
 Cone biopsy – cone-shaped piece of tissue is removed from the cervix

CERVICAL CANCER
STAGING
 FIGO System (International Federation Of Gynecology and Obstetrics)
 5 stages (0 to 4):
 Stage 0 - Carcinoma in situ
 Stage 1 - Invaded cervix, but has not spread
 Stage 2 - Has spread to nearby areas, not leaving pelvic area
 Stage 3 - Cancer has spread to the lower part of the vagina
 Stage 4 - Cancer has spread to nearby organs; metastasis

CERVICAL CANCER
SURVIVAL RATE
 5-year survival rate is 92% for earliest stage
 71% for all stages combined

CERVICAL CANCER
TREATMENT
 Surgery
 Preinvasive cervical cancer
 Cryosurgery
 Laser surgery
 Conization
 Invasive cervical cancer
 Simple hysterectomy
 Removal of the body of the uterus and cervix
 Radical hysterectomy and pelvic lymph node dissection
 Removal of entire uterus, surrounding tissue, upper part of the vagina, and
lymph nodes from the cervix
 Radiation
 Chemotherapy
WHAT’S NEW IN CERVICAL CANCER
RESEARCH AND TREATMENT?
 HPV test
 HPV vaccine
 Radical trachelectomy procedure
 Other clinical trials

Lecture 25
PATHOLOGY OF THE UTERUS

CONGENITAL MALFORMATIONS OF
THE FEMALE GENITAL TRACT
1. MÜLLERIAN AGENISIS
MAYER –ROKITANSKY-KUSTER-HUSER SYNDROME
 Etiology ?
 Failure of müllerian duct development → absence of the upper
vagina, cx & uterus (uterine reminants may be found)
 The ovaries & fallopian tubes are present
 Normal 46XX ♀ with normal external genitalia
 Pt present with primary amenorrhea
 47% have associated urinary tract anomalies
 12% skeletal anomalies
 Treatment:
 Psychological counseling
 Surgical:
 vaginoplasty
 excision of uterine reminant (if it has functioning endometrium)
 vaginal dilators
2. DISORDERS OF LATERAL FUSION OF

THE MÜLLERIAN DUCTS
Incidence
 ? 0.1-2%
 4% of infertile pt
 6-10% recurrent abortion pt
 Most pt can conceive without difficulty
 ↑ incidence of :
 recurrent abortions
 premature birth
 fetal loss
 fetal malpresentation
 C/S
 cx incompetence
 Shortly after menarche → if there is obstruction to uterine
blood flow
 Difficulty in intercourse → longitudinal vaginal septum
 Dysmenorrhea / menorrhagia
 Abnormality detected on D&C
 U/S, laparoscopy or laparotomy
 Palpable mass
 Complications of pregnancy
 HSG → during infertility or RFL investigations
NON OBSTRUCTIVE MALFORMATIONS OF THE
MÜLLERIAN DUCTS
3. DISORDERS OF VERTICALE FUSION
OF THE MÜLLERIAN DUCTS
A. VAGINAL SEPTUM
 Faults in the junction between the müllerian tubercle & the
urogenital sinus → could be very thick or thin
 85% in upper two third of the vagina
 Pt present primary amenorrhea, hematocolpos, mass or

cyclic abdominal pain
 ↑ incidence of endometriosis
 Rx → surgical excision
4. UNUSUAL CONFIGURATION OF
VERTICAL/LATERAL FUSION DEFECTS
 Combined lateral & verticale defects
 Do not fit in other categories
Complete vaginal obstruction Incomplete vaginal obstruction Complete vaginal obstruction with
common double uterus
5. DEFECTS OF THE EXTERNAL
GENITALIA
 Ambigious genitalia → congenital adrenal hyperplasia
(hermaphrodites)
 Defects of the clitoris → uncommon → bifid clitoris
hypertrophied → androgen effect
IMPERFORATE HYMEN
 Hymen is formed at the junction of the urogenital sinus &
sinovaginal bulbs
 Pt presents with primary amenorrhea with cyclic abdominal
pain or hematocolpos /hematometria
 Rx → cruciate incision
UTERINE LEIOMYOMA
UTERINE LEIOMYOMA
DEFINITION
 It is a benign disease of the muscular wall of the uterus
composed primarily of smooth muscle
INCIDENCE
 They are the most common pelvic
tumors
 It is found in:
 25% of white women
 50% of black women

UTERINE LEIOMYOMA
ETIOLOGY
 Unknown
 Each individual myoma is unicellular in origin
 Estogens - no evidence that it is a causative factor , it has been
implicated in growth of myomas
 Myomas contain estrogen receptors in ↑ concentration than
surrounding myometrium
 Myomas may ↑ in size with estrogen therapy & in pregnancy
and ↓ after menopause
 They are not detectable before puberty
 Progestrone ↑ mitotic activity & reduce apoptosis in size
 There may be genetic predisposition
UTERINE LEIOMYOMA
PATHOLOGY
 Frequently multiple
 May reach 15 cm in size / larger
 Firm
 Spherical / irregularly lobulated
 Have a false capsule
 Can be easily enucleated from surrounding myometrium

UTERINE LEIOMYOMA
CLASSIFICATION
 Submucous leiomyoma
 Pedunculated submucous
 Intramural / interstitial
 Subserous / subperitoneal
 Pedunculated abdominal
 Parasitic
 Intraligmentary
 Cervical
SECONDARY CHANGES
1. BENIGN DEGENERATION
 Atrophic
 Hyaline → yellow, soft gelatinous areas
 Cystic → liquefaction follows extreme hyalinization
 Calcific → circulatory deprivation → precipitation of Ca
carbonate & phosphate
 Septic → circulatory deprivation → necrosis → infection
 Myxomatous (fatty) → uncommon, follows hyaline or cystic
degeneration
 Red degeneration - during pregnancy: aseptic degeneration
& infarction with venous thrombosis & hemorrhage; painful
but self-limiting; may result in preterm labor & rarely DIC
2. MALIGNANT TRANSFORMATIONc
 Transformation to leiomyosarcomas occurs in 0.1 - 0.5 %
UTERINE LEIOMYOMA
SYMPTOMS
 Symptomatic in only 35-50%
 Symptoms depend on location, size, changes & pregnancy

status
Abnormal uterine bleeding
 The most common 30%
 Heavy / prolonged bleeding (menorrhagia) → iron deficiency

anemia
UTERINE LEIOMYOMA
SYMPTOMS
Abnormal uterine bleeding
 Submucous myoma produce the most pronounced symptoms

of menorrhagia, pre & post-menstrual spotting
 Bleeding is due to interruption of blood supply to the

endometrium, distortion & congestion of surrounding vessels
or ulceration of the overlying endometrium
 Pedunculated submucous  areas of venouse thrombosis &

necrosis on the surface  intermenstrtual bleeding
UTERINE LEIOMYOMA
SYMPTOMS
Pain
 Vascular occlusion → necrosis, infection
 Torsion of a pedunculated fibroid → acute pain
 Myometrial contractions to expel the myoma
 Red degeneration → acute pain
 Heaviness fullness in the pelvic area
 Feeling a mass
 If the tumor gets impacted in the pelvis → pressure on nerves
→ back pain radiating to the lower extremities
 Dyspareunia if it is protruding to vagina
UTERINE LEIOMYOMA
SYMPTOMS
Pressure effects
 If large may distort or obstruct other organs like ureters,
bladder or rectum → urinary symptoms, hydroureter,
constipation, pelvic venous congestion & LL edema
 Rarely a posterior fundal tumor → extreme retroflexion of the

uterus distorting the bladder base → urinary retention
 Parasitic tumor may cause bowel obstruction
 Cervical tumors → serosanguineous vaginal discharge,

bleeding, dyspareunia or infertility
UTERINE LEIOMYOMA
SYMPTOMS
Infertility
 The relationship is uncertain
 27-40% of women with multiple fibroids are infertile → but
other causes of infertility are present
 Endocavitary tumors affect fertility more
Spontaneous abortion
 ~2X N → incidence before myomectomy 40%
after myomectomy 20%
 More with intracavitary tumors
UTERINE LEIOMYOMA
DIAGNOSIS
Examination
 Most myoma are discovered on routine bimanual pelvic exam
or abdominal examination
 Retroflexed retroverted uterus → obscure the palpation of
myomas
Laboratory findings
 Anemia
 Depletion of iron reserve
 Rarely erythrocytosis → pressure on the ureters → back
pressure on the kidneys → ↑ erythropoietin
 Acute degeneration & infection → ↑ESR, leucocytosis, & fever
UTERINE LEIOMYOMA
DIAGNOSIS
Imaging
 Pelvic U/S - very helpful in confirming the Dx & excluding
pregnancy / particularly in obese Pt
 Saline hysterosonography → identify submucous myoma that
may be missed on U/S
 HSG → intrauterine leiomyoma
 MRI → highly accurate in delineating the size, location & no.
of myomas, but not always necessary
 IVP → ureteral dilatation or deviation & urinary anomalies
 Hysteroscopy → identification & removal of submucous
myomas
UTERINE LEIOMYOMA
 Usually easily diagnosed
 Exclude pregnancy
 Exclude other pelvic masses
 Ovarian Ca
 Tubo-ovarian abscess
 Endometriosis
 Adenexa, omentum or bowel adherent to the uterus
 Exclude other causes of uterine enlargement:
 Adenomyosis
 Myometrial hypertrophy
 Endometrial Ca
UTERINE LEIOMYOMA
 Exclude other causes of abnormal bleeding:
 Endometrial hyperplasia
 Endometrial or tubal Ca
 Uterine sarcoma
 Ovarian Ca
 Polyps
 Adenomyosis
 DUB
 Endometriosis
 Exogenouse estrogens
 Endometrial biopsy / D&C is essential in the evaluation of
abnormal bleeding to exclude endometrial Ca
UTERINE LEIOMYOMA
COMPLICATIONS IN PREGNANCY
During labor
 Uterine inertia
 Malpresentation
 Obstruction of the birth canal
 Cervical or isthmic myoma → necessitate CS
 PPH
UTERINE LEIOMYOMA
TREATMENT
Depends on:
 Age
 Parity
 Pregnancy status
 Desire for future pregnancy
 General health
 Symptoms
 Size
 Location
UTERINE LEIOMYOMA
TREATMENT
A. Emergency measures
 Blood transfusion/ PRBC to correct anemia
 Emergency surgery indicated for:

 infected myoma
 acute torsion
 intestinal obstruction
 Myomectomy is contraindicated during pregnancy

UTERINE LEIOMYOMA
TREATMENT
B. Specific measures
 Most cases asymptomatic → no treatment
 Postmenopausal → no treatment
 Other causes of pelvic mass must be excluded
 The Dx must be certain
 Initial follow up every 6 M → to determine the rate of growth

of the myoma
UTERINE LEIOMYOMA
TREATMENT
B. Specific measures
 Surgery is contraindicated in pregnancy
 The only indication for myomectomy in pregnancy is torsion

of a pedunculated fibroid
 Myomectomy is not recommended during CS
 Pregnant women with previous multiple myomectomy /

especially if the cavity was entered → should be delivered by
CS to ↓ risk of scar rupture in labor
UTERINE LEIOMYOMA
TREATMENT
C. GnRH agonists
 ↓ size of the myomas 50% maximum
 This shrinkage is achieved in 3M of RX
 Amenorrhea & hypoestrogenic side-effects occur
 Osteopososis may occur if Rx last > 6M
 It is indicated for:
 ↓ bleeding from myoma except for the polypoid submucous type
 Preoperative to ↓ size → allow for vaginal hysterectomy,

myomectomy, laparoscopic myomectomy
UTERINE LEIOMYOMA
TREATMENT
D. Supportive measures
 PAP smear & endometrial sampling for all Pt with irregular
bleeding
 Before surgery:
 Correct Hb
 Prophylactic antibiotics
 Mechanical & antibiotic bowel preparation → if difficult surgery

is anticipated
UTERINE LEIOMYOMA
TREATMENT
E. Surgical measures
 Evaluation for other neoplasia
 Myomectomy
 For symptomatic pt who wish to preserve fertility
 Open myomectomy
 Laparoscopic myomectomy
 Hysteroscopic myomectomy
 Hysterectomy
 Vaginal hysterectomy
 Abdominal hysterectomy
 Uterine artery embolisation
ENDOMETRIAL CANCER
ENDOMETRIAL CANCER
CAUSE
 The exact cause is unknown
 Estrogen
ENDOMETRIAL CANCER
RISK FACTORS
 Sex, age, class, race, family history
 Irregular menstrual periods
 Early first menstruation / late menopause
 Low parity / nulliparity
 Infertility
 Obesity
 Diabetes
 Hypertension
 Estrogen replacement therapy and/or Tamoxifen
ENDOMETRIAL CANCER
SYMPTOMS
 Unusual vaginal spotting
 Bleeding
 Discharge
 Pain in the pelvic region
 Presence of a lump
ENDOMETRIAL CANCER
DIAGNOSIS
ENDOMETRIAL CANCER
DIAGNOSIS
ENDOMETRIAL CANCER
DIAGNOSIS
ENDOMETRIAL CANCER
DIAGNOSIS
ENDOMETRIAL CANCER
DIAGNOSIS
ENDOMETRIAL CANCER
DIAGNOSIS
ENDOMETRIAL CANCER
TREATMENT
 The stage of cancer is determined
 International Federation of Gynecology and Obstetrics (FIGO)

adopted a staging and grading (G1-G3) system
 FIGO stages are:
 Stage I - Cancer is limited to the uterus - 70%
 Stage II - Cancer involves the uterus and cervix - 10-15%
 Stage III - Cancer has spread out of the uterus but restricted to
pelvic region
 Stage IV - Cancer has spread to the bladder, bowel, or other
distant locations
ENDOMETRIAL CANCER
TREATMENT
ENDOMETRIAL CANCER
TREATMENT
 Radiation therapy
 Chemotherapy
 Hormonal therapy
 Alternatives
ENDOMETRIAL CANCER
PROGNOSIS
 Since it is possible to detect endometrial cancer early, the
chances of curing it are excellent !
ENDOMETRIAL CANCER
PREVENTION
 Women report any abnormal vaginal bleeding / discharge to

the doctor
 Controlling obesity, blood pressure, and diabetes help reduce
risk
 Using birth control helps prevent endometrium cancer
 Taking medication that produces estrogen ask about receiving

progesterone
 If you are at risk, get screened regularly
ENDOMETRIOSIS
ENDOMETRIOSIS
DEFINITION
 Endometriosis is a disease in
which endometrial glands and
stroma implant and grow in
areas outside the uterus
 Most commonly implants are

found in the pelvis
 Lesions may occur at distant sites:

pleural cavity, liver, kidney, gluteal
muscles, bladder, etc.
ENDOMETRIOSIS
PREVALENCE
 Prevalence 2-50% of women;

21-47% of infertility cases
 Exposure to ovarian hormones

appears to be essential
 No known racial or
socioeconomic predilection
 Severe disease may occur in

families
ENDOMETRIOSIS
ETYOLOGY
 Sampson's theory: Retrograde menses and peritoneal
implantation
 Most women retrograde menstruate
 Meyer's theory: Coelomic metaplasia
 Low incidence of pleural disease
 Halban's theory: Hematogenous or lymphatic spread to
distant tissues
 Does not explain gravity dependent disease sites
 Immunogenic defect
 Relative Risk to siblings 2.3 overall

 Relative Risk to sibs if severe endo 15
ENDOMETRIOSIS
RISK FACTORS
 Single/nulliparous
 Early menarche
 Non oral contraception
 Non smoker shorter cycle/longer duration of flow
 Dysplastic naevus syndrome, melanoma

CLASSIFICATION
Stage II (Mild)
Stage I (Minimal)
Stage IV (Severe)
Stage III (Moderate)
ENDOMETRIOSIS
SYMPTOMS
 90% severe dysmenorrhea
 70% chronic pelvic pain
 75% dyspareunia
 55% infertility
ENDOMETRIOSIS
PHYSICAL FINDINGS
 Tender nodules along the uterosacral ligaments or in

the cul-de-sac, especially just before menses
 Pain or induration without nodules commonly in the

cul-de-sac or rectovaginal septum
 Uterine or adnexal fixation, or an adnexal mass

ENDOMETRIOSIS
DIAGNOSIS
 Direct visualization of implants
 Laparoscopically
 Conscious pain mapping
 Imaging of endometriomas
 MR appears to be best (3 mm
implants)
 Ultrasound helpful in office setting
 Biochemical markers
ENDOMETRIOSIS
TREATMENT OF PAIN
 NSAIDS: all significantly better than placebo, studies vary

which one is best
 Naproxen > mefanemic acid > aspirin
 Naproxen = ibuprofen
 Naproxen only drug with significant SEs

TREATMENT OF PAIN
MEDICAL MANAGEMENT (OVARIAN SUPPRESSION,
REMOVAL OF ESTROGEN)
 Oral contraceptives, progestin, danazol
 GnRH agonist with add-back
 Alternating GnRH agonist and OCs
 Aromatase inhibitors
ENDOMETRIOSIS
LIMITATIONS OF DRUG THERAPY
 Only shrinks some types of endometriosis which are oestrogen

sensitive ie red and blister appearance not brown, black and
white
 Shrinkage not complete - ussualy leaves micro disease
 Results for infertility treatment no better than no treatment
 Does not deal with adhesions

TREATMENT OF INFERTILITY
 Removal of disease
 Laparoscopy - surgery improve conception rates at all stages
Conservative; Presacral neurectomy, LUNA
Semiconservative, Radical
 Endometriosis may recur in 15%
 Ovulation induction
 Gonadotropins with ovarian suppression
 Insemination with either clomiphene or FSH
 Medical suppression of ovarian function

 No benefit
Thank you !

1 - Gametogenesis & Early Development of The Fertilized Ovum v2

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1 - Gametogenesis & Early Development of The Fertilized Ovum v2

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GAMETOGENESIS

The testes are made up of a series of

- Nests of cells in between the tubules

- The process is controlled by (ICSH)

They burry their heads in the Sertoli Cells (glycogen containing

The Ovary in the fetus & childhood

- During ovarian differentiation, germ cells undergo

-- Part of the oogonia stop dividing mitotically and

The Ovary in the fetus & childhood

- The remaining oogonia continue dividing

- The total number reaches a peak at 4.5-5

All Oocytes which reach the diplotene phase of

The ovary at puberty

• FSH stimulates the growth of primordial

Secondary oocyte (haploid cell)

Not completed unless fertilization takes place

Female pronucleus + 2nd polar body

Average time required for the sperm to

Following the entry

• A first cleavage division occurs after 24

58-cell blastocyst 107-cell blastocyst

~ 5-6 days after fertilization

• 6-6.5 days after fertilization

- The definitive number of stem villi is

The testes are made up of a series of convoluted -

Spermatozoa are formed along the walls of the -

This process is controlled by follicle stimulating

Nests of cells in between the tubules -

The process is controlled by (ICSH) -

During adolescence mature into

The Ovary in the fetus & childhood

During ovarian differentiation, germ cells undergo -

Part of the oogonia stop dividing mitotically and - -

The Ovary in the fetus & childhood

The remaining oogonia continue dividing -

The total number reaches a peak at 4.5-5 months -

Secondary oocyte (haploid cell)

Approximately 5-6 days after fertilization

days after fertilization 6-6.5

Prof. Vlad TICA, MD, PhD

 The fetal membranes (the amnion-chorion leave)

 Human placenta : hemochorioendothelial type

 function as endocrine organ in human pregnancy

Essential to maternal physiological adaptations &

 Integrin: one of four families of cell adhesion molecules

 glycopeptide - trophouteronectin or trophoblast glue

 formed by extravillous trophoblast, including that of

 critical role for migration and attachment of the

 The acceptance and the survival of conceptus in the maternal

 Uterine Large Granular Lymphocytes (LGL) - probably

 17 class I genes have been identified

 three classical genes

 three other class I(b) genes

 As gestation progresses, cells from inner cell mass of blastocyst

 Prominent microvilli of the syncytial surface (brush

 Characteristic of development of H-mole

 Certain villi of the chorion frondosum extend from

 Each of the main stem villi (truncal)

 For each cotyledon, a 2:1 ratio of artery

 Passage of cells between mother and fetus in both directions

 A few fetal blood cells are found in the mother's blood

 Fetal leukocytes may replicate in the mother and leukocytes