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OBSTETRICS SUPPLEMENT HANDOUT
TABLE OF CONTENTS
Maternal Anatomy
Menstrual Physiology
Fertilization
Placenta
Fetal Development
Maternal Physiology
Prenatal Care
Postpartum Changes
Postpartum hemorrhage
Dystocia

1
5
9
10
11
13
19
22
25
25

MATERNAL ANATOMY
EXTERNAL GENITALIA
SURFACE ANATOMY
Structure
Mons Pubis
Labia Majora

Labia Minora

Clitoris
Vestibule

Vestibular
Glands
Urethral
opening
Vestibular
bulbs
Vaginal
opening/hyme
n

escutheon
7-8x2-3x1-1.5cm
round ligaments terminate at their
upper borders
connective tissue with many
vessels, elastin fibers, and some
smooth muscle fibers
points downward and inward
toward the vaginal opening; rarely
exceeds 2 cm
functionally mature female
structure derived from the
embryonic urogenital membrane
perforated by six openings:
urethra, the vagina, two Bartholin
gland ducts, and two ducts of the
Skene glands
Bartholin glands, paraurethral
glands (Skene glands
diverticulum) minor vestibular
glands
lower two thirds of the urethra lie
immediately above the anterior
vaginal wall.
1 to 1.5 cm below the pubic arch
lie beneath the bulbocavernosus
muscle on either side of the
vestibule
vulvar hematoma.
Hymenal caruncles
Impreforate hymen

VESTIBULE

Functionally mature female structure of the


urogenital sinus of the embryo. Extends from
clitoris to forchette
STRUCTURES IN THE VESTIBULE
HYMEN

Non keratinized Stratified


squamous epithelium

During first coitus, first that


ruptures is usually at the 6 oclock
position

Caruncle Myrtiformes: Remnants of


hymen in adult female
GLANDUL
Periurethral Glands Skenes Glands
AR
Vulvovaginal Glands Bartholins
STRUCTU
Glands
RES
6

Vaginal introitus
OPENING

Urethral opening
S:

Paired Para urethral glands


opening

Paired Bartholin ducts opening


GLANDULAR STRUCTURES
PERIURETHRA
L GLANDS
Skenes
glands
Other
Lesser vestibular
name
glands
Male
Prostate
homolog
y
Type of
Tubulo alveolar
gland
Location
Adjacent to
the urethra
Patholog
Urethral
y
diverticulum

DIFFERENCE OF LABIA MAJORA AND LABIA


MINORA
LABIA MAJORA LABIA MINORA
HOMOLOGY
Scrotum
Ventral portion
of the penis
Skin of the
penis
LINING
Outer- KSSE
NKSSE
EPITHELIUM
Inner- NKSSE
NULLIPAROU
Lie in close
Not visible
S WOMEN
apposition
behind the non
Inner surface
separated labia
resembles the
majora
mucous
membrane
MULTIPAROU
Gape widely
Project beyond
S WOMEN
Inner surface
the labia majora
become skin like
GLANDS
(+) Hairfollicles
No hair follicles
(+) Sweat
No sweat glands
glands
(+) Sebaceous
(+) Sebaceous
glands
glands
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VULVOVAGINAL
GLANDS
Bartholins
glands
Greater vestibular
glands
Bulbourethral gland
Compound alveolar/
compound acinar
4 and 8 o clock of
the vagina
Bartholinss cyst/
abscess

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PERINEUM

closed
compartment

bounded deeply by the perineal


membrane and superficially by
Colles fascia
ischiocavernosus,
bulbocavernosus, and superficial
transverse perineal muscles;
Bartholin glands; vestibular
bulbs; clitoral body and crura;
and branches of the pudendal
vessels and nerve

ischiocavernos
us muscle

clitoral erection

bulbocavernos
us muscles

Bartholin gland secretion


Clitoral erection

superficial
transverse
perineal
muscles

may be attenuated or even


absent
Contributes to the perineal body

Urogenital (Anterior) Triangle: DEEP SPACE


Anterior Triangle (DEEP SPACE)

Clinical Significance

Boundary

Landmark

Anterior

pubic symphysis

Anterolatera
l

ischiopubic rami and ischial


tuberosities

Posterolater
al

sacrotuberous ligaments

posterior

coccyx

Continuou
s space
with the
pelvis

lies deep to the perineal membrane


and extends up into the pelvis
Contents: compressor urethrae and
urethrovaginal sphincter muscles,
external urethral sphincter, parts of
urethra and vagina, branches of the
internal pudendal artery, and the
dorsal nerve and vein of the clitoris

Ishorectal
fossae

wedge-shaped spaces found on


either side of the anal canal and
comprise the bulk of the posterior
triangle
Continuous space

PUDENDAL NERVE AND VESSELS


Roots

Anterior rami of the 2nd to 4th sacral


nerve

Course

between the piriformis and


coccygeus muscles and exits
through the greater sciatic foramen
in a location posteromedial to the
ischial spine
obturator internus muscle
pudendal canal (Alcock Canal)
enter the perineum and divides into
three terminal branches

Triangle
Anterior
Superficial
and deep

Posterior

Urogenital triangle
Boundaries:
Superrior- pubic rami
Lateral-ischial tuberosities
Posterior: superficial transverse
perineal muscle
Anal triangle
ischiorectal fossa, anal canal, anal
sphincter complex, and branches of the
internal pudendal vessels and pudendal
nerve

Urogenital (Anterior) Triangle: SUPERFICIAL


SPACE
Anterior Triangle (SUPERFICIAL SPACE)

Terminal Branches:
dorsal nerve
of the clitoris

skin of the clitoris

perineal
nerve

muscles of the anterior triangle and


labial skin

inferior
rectal

external anal sphincter, the mucous


membrane of the anal canal, and
the perianal skin

Landmark
for pudendal
nerve block

Ischial spine

Blood Supply

internal pudendal artery


VAGINA

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H-shaped
lower portion of the vagina is constricted
(urogenital hiatus in the levator ani)
Stratified squamous non keratinized epithelium
without glands
Upper part is more capacious
It extends from the vulva to the cervix.
Ruggae that has an accordion like distensability
Vaginal length:

Anterior wall: 6-8 cm

Posterior wall: 7-10 cm


Potential space: Lower third
CERVIX
ENDOCERVIX
EXOCERVIX
Supravaginal portion
Portio vaginalis
Extends from the isthmus
Extends from the
(Internal Os) to the ectocervix
squamo columnar
and contains the endocervical
junction to the
canal
external orifice
Single layer of mucous
Non keratinized
secreting highly ciliated
stratified
columnar epithelium which is
squamous
thrown into folds forming
epithelium
complex glands and crypts
Hormone Sensitive
Extensive amount of nerves
Few nerves only
Blood supply: Cervicovaginal branch of uterine artery
located at the lateral walls

Cervix: SQUAMO-COLUMNAR JUNCTION

Vesicovaginal septum

Separates the vagina from the bladder


and urethra
Rectovaginal septum

Separates the lower portion of the


vagina from the rectum
Rectouterine pouch of Douglas

Separates the upper fourth of the


vagina from the rectum

Upper vaginal vaults


Subdivided into anterior, posterior, and two
lateral fornices by the uterine cervix
Internal pelvic organs usually can be palpated
through their thin walls
Posterior fornix provides surgical access to the
peritoneal cavity

Prepubertal women
o Original SCJ at or near the exocervix
Reproductive Age women
o Eversion of endocervical epithelium and
exposure of columnar cells to the vaginal
environment
o Relocation of SJC down the Exocervix
Late adulthood / Post menopausal women
o SCJ at the endocervical canal
o Formation of transformation zone with
regrowth of the squamous epithelium

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UTERUS
SIZE

Nulliparous: 6 to 8 cm
(fundus=cervix) , 50-70 g
multiparous: 10 cm (cervix 1/3), 80 g
or more

Isthmus

Lower uterine portion

Fallopian
tubes

Attaches at the cornua

Posterior
wall

Completely covered by visceral


peritoneum

Anterior
wall

Only upper portion with peritonem


vesicouterine pouch

ENDOMETRI
UM

MYOMETRIU
M
SEROSA

STRATUM FUNCTIONALE

Shed during
menstruation

Supplied by the
Spiral Arteries

Superficial 2/3

Zona
Spongios
a
Zona
compact
a

STRATUM BASALE

Source of
Stratum Functionale
after menstruation

Supplied by the
Straight arteries

Basal 1/3

lympathics
Inner Longitudinal
Middle oblique
Outer longitudinal
lymphatics

SEGMENTS OF THE FALLOPIAN TUBE


Intramural Embodied
2% of ectopic
Interstitial within the
pregnancy
muscular wall Ectopic pregnancy at
of the uterus
this area result in
severe maternal
morbidity
Isthmus
The narrow
Most highly
portion of the
developed
tube that
musculature
adjoins the
Narrowest portion
uterus,
Preferred portion for
passes
applying clips for
gradually into
female sterilization
the wider,
Preferred portion for
lateral
tubal ligation
portion.
12% of ectopic
pregnancy
Ampulla
Widest and
Site of fertilization
most tortuous 80% of ectopic
area
pregnancy
Infundibul
Fimbriated
5% of ectopic
um
extremity
pregnancy
Tunnel
shaped
opening of
the distal end
of the
fallopian tube

LIGAMENTS OF THE UTERUS


Broad

Two wing-like structure that extend


ligament
from the lateral margins of the uterus
to the pelvic walls

Divide the pelvic cavity into anterior


and posterior compartments
Reproductive
Fallopian tubes
structures
ovaries
Vessels:
Ovarian arteries
Uterine arteries
Ligaments:
Ovarian ligament
Round ligament of
uterus
Cardinal

AKA Transverse Cervical Ligament or


ligament
Mackenrodt Ligament

Originated form the densest portion of


the broad ligament

Medially united to the supravaginal


wall of the cervix

Provide the major support of the


uterus and cervix

Maintain the anatomic position of the


cervix and upper part of the vagina
Uterosac

From posterolateral to the


ral
supravaginal portion of the cervix
ligament
encircling the rectum

Insert into the fascia over S2 and S3


Round

Extend from the lateral portion of the


Ligament
uterus, arising below and anterior to
origin of the oviducts, that is
continuous with the broad ligament,
outward and downward to the inguinal
canal
terminating at upper
portion of labium majus
FALLOPIAN TUBES

single layer of columnar cells, some of them


ciliated and others secretory.
No submucosa
supplied richly with elastic tissue, blood vessels,
and lymphatics
Sympathetic innervation
Diverticula

OVARIES
Lies on the posterior aspect of the broad ligament,
in the ovarian fossa
o lateral to the uterus in the pelvic sidewall
where the common iliac artery bifurcates
o ovarian fossa of Waldeyer
Are attached to the broad ligament by the
mesovarium.
They are not covered by peritoneum.

Ovaries: LAYERS
OUTER
Innermos
CORTEX t portion

INNER
MEDULL
A

Primordial and
Graafian follicles in
various stages of
development
Outermo

Tunica Albuginea- dull


st portion
and whitish fibrous
connective tissue
covering the surface of
the ovary

Germinal epithelium
of Waldeyer- a single
layer of cuboidal
epithelium over the
Tunica Albuginea

Composed of loose connective


tissue that is continuous with that of
the mesovarium.

Smooth muscle fibers that are


continuous with those in the
suspensory ligament.

Contains the stroma and blood


vessels of the ovary

PELVIS

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Pelvic Organs: BLOOD SUPPLY


MAJOR BLOOD SUPPLY TO THE FEMALE
REPRODUCTIVE SYSTEM
Pudenda
Internal Pudendal artery
Vagina
Vaginal Artery of the
Uterine Artery
Cervix
Cervicovaginal branch of
Uterine artery
Uterus
Uterine Artery
Fallopian tubes
Ovarian Artery
Ovaries
PARTICIPANTS IN THE COLLATERAL
CIRCULATION OF THE FEMALE PELVIS
Branches from

Ovarian artery
the Aorta

Inferior mesenteric

Lumbar and vertebral

Middle sacral arteries


Branches from

Deep iliac circumflex


the External

Inferior epigastric artery


Iliac Artery
Branches from

Medial femoral circumflex


the Femoral
artery
Artery

Lateral femoral
circumflex artery
Fals
e

ANT: lower abdomen


POST: lumbar vertebra
LATERAL: iliac fossa

L INEA TERMINALIS
Tru
e

Outlet increase by 1.5 -2.0 cm

PELVIC TENDENCY AND TYPE

Anterior dictates the tendency of the pelvis

Posterior dictates the type or character of the


pelvis
GYNECOID

ANDROI
D

ANTHROP
OID

PLATYPELLOID

FREQUENC
Y

50%

20%

25%

5% rarest

INLET
SHAPE

Round

Heart
Shaped

Vertically
oriented
oval

SIDEWALL
S

Straight

Converg
ent

Convergent

Horizontally
oriented
oval
Divergent,
then
convergent

ISCHIAL
SPINES

Non
promin
ent

Promine
nt

Prominent

Non
prominent

SACRUM

Inclined
neither
anterior
ly nor
posterio
rly

Straight =
pelvis
deeper
than other
3 types

Well curved
and rotated
backward

SIGNIFICA
NCE

Good
prognos
is for
vaginal
delivery

Increased
incidence
of Face
Delivery
Good
prognosis
for vaginal
delivery

Poor
prognosis
for vaginal
delivery

SUPERIOR BOUNDARY: Pelvic inlet


INFERIOR BOUNDARY: Pelvic outlet
ANTERIOR: Pubic Bones, Ascending Rami Of
Ischial Bones, Obturator Foramina
LATERAL: Ischial Bones and Sacrosciatic
Notch

Forward
and
straight
with
little
curvatur
e
Increase
d
incidenc
e of
Deep
Transver
se Arrest
Limited
posterior
space
for fetal
head,
poor
prognosi
s

EMBRYOLOGIC STRUCTURES AND DERIVATIVES


EMBRYOLOGIC
STRUCTURES
LABIOSCROTAL
SWELLING
UROGENITAL
FOLDS
PELVIC JOINTS

Anterior: symphysis pubis/arcuate ligament


of the pubis

Posterior: sacroiliac

Hormonal changes during pregnancy cause


laxity of these joints

By 3-5 months POST PARTUM, laxity has


regressed

Symphysis Pubis increase in width also


Increase mobility and displacement of the
sacroiliac joint
WHY THE DORSAL LITHOTOMY POSITION?

Upward gliding of sacroiliac joint is GREATEST


in the DORSAL LITHOTOMY POSITION

PHALLUS
(GENITAL
TUBERCLE)
UROGENITAL
SINUS

MALE

FEMALE

Scrotum

Labia Majora

Ventral
portion of the
penis
Penis

Labia Minora

Urinary
bladder
Prostate
gland

Urinary
bladder
Urethral and
Paraurethral
glands
Vagina

Prostatic
Utricle
Bulbourethral
glands
Seminal
colliculus

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Clitoris

Greater
vestibular
glands
Hymen
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PARAMESONEPHR
IC DUCT

Appendix of
testes

MESONEPHRIC
DUCT

Appendix of
Appendix of
epidydymis
vesiculosis
Ductus of
Duct of
epididymis
epoophoron
Ductus
Gartners
deferens
Duct
Ejaculatory
duct
Seminal
Vesicle
Ureter
Renal Pelvis
Calyces
Collecting system
Glomerulus
Renal Collecting Tubules
Testes
Ovary

METANEPHRIC
DUCT
URETERIC BUD
METANEPHRIC
MESENCHYME
UNDIFFERENTIAT
ED GONAD
CORTEX
MEDULLA
GUBERNACULUM

Seminiferous
tubules
Rete Testis
Gubernaculu
m testis

Hydatid of
Morgagni
Uterus and
Cervix
Fallopian
Tubes
Upper of
the vagina

Ovarian
Follicles
Rete Ovarii
Round
ligament of
uterus

MENSTRUAL PHYSIOLOGY
Overview of Menstrual Cycle

Spontaneous, cyclical ovulation occurs at 25- to


35-day intervals

Cyclical ovulation continues for almost 40 years


between menarche and menopause

Approximately 400 opportunities for


pregnancy, which may occur with intercourse on
any of 1,200 days (includes day of ovulation and
its two preceding days) during the reproductive
age of most women.

Menstrual cycle days 20 to 24 is the narrow


window of endometrial receptivity to blastocyst
implantation.

Mother and fetus coexist as two disctinct


immunological systems because of modifications
on both fetal and maternal tissues in a manner not
seen elsewhere.

Endometrium-decidua is the anatomical site of


blastocyst apposition, implantation, and placental
development.
Key Players:
1. Anterior pituitary
a. FSH
b. LH
2. Ovarian follicle
a. Theca cells
b. Granulosa cells
3. Estrogen
4. Progesterone
5. Endometrium
a. Basalis
b. Functionalis

OVARIAN CYCLE
Average cycle duration is approximately 28 days,
with a range of 25 to 32 days.
Follicular phase (days 1 to 14) is characterized by:
o Rising levels of estrogen
o Thickening of the endometrium

o Selection of dominant ovulatory follicle


Luteal phase (days 14 to 21), the corpus luteum
(CL) produces estrogen and progesterone, which
prepare the endometrium for implantation. If
implantation occurs, the developing blastocysts
will begin to produce hCG and rescue the CL, thus
maintaining progesterone production.

A. Follicular or preovulatory ovarian phase


FOLLICLE PROFILE
Event
Numbers
At Birth
2 Million oocytes
Puberty
400,000 follicles
Depletion rate
1,000 follicles/month
(puberty to 35y/o)
Total follicles released
400 follicles
during reproductive age
Atresia (apoptosis) of
99.9%
follicles
OOCYTE CYCLE

Primary Oocyte
o formed by 5th fetal month
o Started their first meiotic division
o Arrested in Prophase from 5th fetal month until
the onset of puberty
o Will complete the first meiotic division at the
onset of puberty

Secondary Oocyte
o Formed after completion of Meiotic I
o Release of the first Polar Body During ovulation
o Arrested in Metaphase II until fertilization
o Completion of 2ND Meiotic Division only occurs if
there is fertilization

Oocyte transforming growth factors:


1.
Growth differentiation factor 9 (GDF9)
2.
Bone morphogenetic protein 15 (BMP-15)
Functions:
1.
Regulate proliferation & differentiation of
granulosa cells (GC) as primary follicles grow
2.
Stabilize and expand the cumulus oocyte
complex in the oviduct
FOLLICLE DEVELOPMENT
1. Recruitment of primordial follicles.
2. Cohort will grow GC.
3. Selection of dominant follicle.
4. Dominant follicle increase GC.
5. Follicle produce estradiol & initiate expression of
LH receptors.
6. Appearance of LH receptors.

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7.

GC secrete progesterone which will cause LH


release.
8. GC produce inhibin B to inhibit FSH release.
9. Increase estradiol & inhibin production causes
drop of FSH
10. Drop of FSH causes failure of other follicles to
develop.
11. LH stimulates theca cells to produce
androstenediol.

HORMONE PRODUCTION

CORPUS LUTEUM
Key events:
1. Constant at 12 to 14 days.
2. Luteinization occurs after ovulation when the CL
develops.
3. Basement membrane separating the granulosalutein and theca-lutein cells breaks down
4. Day 2 postovulation, blood vessels and
capillaries invade the granulosa cell layer.
5. Increased capacity of granulosa-lutein cells to
produce progesterone is due to increased
access to steroidogenic precursors through
blood-borne LDL-derived cholesterol.
6. Just after ovulation, estrogen levels decrease.
7. Mid-luteal phase is a secondary rise that
reaches a peak production of 0.25 mg/day of
17B-estradiol.
8. Toward the end of the luteal phase, there is
secondary decrease in estradiol production.
9. Ovarian progesterone peaks at 25 to 50
mg/day during the midluteal phase. (With
pregnancy, CL continues progesterone
production in response to embryonic hCG)
10. CL is a transient endocrine organ that will
rapidly regress 9 to 11 days after ovulation.
LUTEOLYSIS
Luteolysis may be due to the following:
1.
Decreased levels of circulating LH in the late
luteal phase and
2.
Decrease LH sensitivity of luteal cells
3.
Apoptosis
Effects of luteolysis:
1.
Drop in circulating estradiol and progesterone
levels.
2.
Allows follicular development and ovulation
during the next ovarian cycle
3.
Signals the endometrium to initiate molecular
events that lead to menstruation.

Ovarian steroid production:


1.
Estrogen levels rise in parallel to growth of a
dominant follicle.
2.
Increase in its number of granulosa cells.
3.
GC are the exclusive site of FSH receptor
expression.
4.
Increase in FSH during the late luteal phase
stimulates increase in FSH receptors & ability of
cytochrome P450 to convert androstenedione
into estradiol.
B. Ovulation
OVULATION
Key events:
1.
Preovulatory follicles increase estrogen
secretion 34 to 36 hours before release of
ovum with LH surge.
2.
LH peaks 10 to 12 hours before ovulation.
3.
Resumption of meiosis 1 in the ovum and
release of first polar body.
4.
Cumulus cell produces more progesterone
and prostaglandin.
5.
Oocyte growth factors (GDF9 and BMP-15)
increases.
6.
Increase formation of hyaluronan-rich ECM
7.
Expansion occurs where cumulus cells lose
contact with one another and move outward from
the oocyte along the hyaluronan polymer.
8.
LH induces remodelling of the ovarian
extracellular matrix to allow release of the mature
oocyte.
9.
Activation of proteases on weakening of the
follicular basement membrane and ovulation.

D. Estrogen effects

17B- estradiol is the most biologically potent


naturally occuring estrogen secreted by granulosa
cells of the dominant follicles and luteinized
granulosa cells of the CL.

Estrogen is the essential hormonal signal on which


most events in the normal menstrual cycle
depend.

Estrogen receptor (ER-alpha & ER-beta) interaction


can promote synthesis of specfic m-RNAs and
proteins (e.g. estrogen and progesterone)

Acts at endothelial cell surface to stimulate nitric


oxide production, leading to its rapid vasoactive
properties.
E. Progesterone effects

Progesterone enters cells by diffusion and in


responsive tissues becomes associated with
progesterone receptors --- progesterone receptor
type A (PR-A) and B (PR-B)

PR-A can inhibit PR-B gene regulation.

Both PR-A and PR-B are expressed in endometrial


glands in the proliferative phase, such that both
receptors are involved with subnuclear vacuole
formation.

After ovulation, the glands continue to express


only PR-B through the midluteal phase. In contrast,
the stroma & predecidual cells express only PR-A
throughout the menstrual cycle.
ENDOMETRIAL CYCLE
LAYERS

C. Luteal or postovulatory ovarian phase


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Numerous mitotic figures

Late proliferative phase:

Days 11-14

Endometrium thickens from both glandular


hyperplasia and increased stromal ground
substance.

Functionalis layer glands are widely


separated, loose stroma is especially prominent.

Basalis layer glands are more crowded and


stroma is denser.

Endometrial histologic features:


o Proliferative phase straight to slightly coiled,
tubular glands are lined by pseudostratified
columnar epithelium with scattered mitoses.
o Early secretory phase coiled glands with a
slightly widened diameter are lined by simple
columnar epithelium that contains clear
subnuclear vacuoles. Luminal secretions are
seen.
o Late secretory phase serrated, dilated glands
with intraluminal secretion are lined by short
columnar cells.
o Menstrual phase fragmented endometrium
with condensed stroma and glands with
secretory vacuoles are seen in a background of
blood.
Layers of endometrium
o Basalis layer supplied by straight artery
o Functionalis layer supplied by spiral artery

A. Proliferative or preovulatory endometrial


phase
Features:

Straight to slightly coiled, tubular glands


are lined by pseudostratified columnar
epithelium with scattered mitoses.

Epithelial (glandular) cells, stromal


(mesenchymal) cells and blood vessels replicate
cyclically.

Functionalis layer is shed and regenerated from


the deepest basalis layer almost 400 times
during the reproductive lifetime of most women.

Day 5 of menses the epithelial surface of the


endometrium has been restored, and
revascularization is in progress.
Early proliferative phase:

Endometrium is thin, usually < 2 mm thick

Glands are narrow, tubular structures that are


almost a straight and parallel course from the
basalis layer toward the surface of the
endometrial cavity.

Mitotic figures are identified by day 5 of cycle,


and mitotic activity in both epithelium and stroma
persists until day 16 to 17, or 2 to 3 days after
ovulation.

Epithelial cell growth is regulated in part by


epidermal growth factor (EGF) and transforming
growth factor-alpha (TGF-a)

Stromal cell proliferation appears to increase


through paracrine and autocrine action of
estrogen and increased local production of VEGF,
which causes angiogenesis through vessel
elongation in the basalis.

Midcycle (near ovulation):

Glandular epithelium becomes taller and


pseudostratified.

Superficial epithelial cells acquire:


1.
microvilli (increase epithelial surface
area) and
2.
cilia (aid in the movement of
endometrial secretions during the secretory
phase)

Ovulation is evidenced by presence of


subnuclear vacuoles in 50% of glands
B. Secretory or postovulatory endometrial
phase
Early secretory phase:

coiled glands with a slightly widened diameter

lined by simple columnar epithelium that


contains clear subnuclear vacuoles.

Luminal secretions are seen.


Late secretory phase:

serrated, dilated glands with intraluminal


secretion are lined by short columnar cells.
Early secretory phase
Dating based on glandular epithelium.
Day 17:

glycogen accumulates in the basal portion


of glandular epithelium, creating subnuclear
vaculoes and pseudostratification (1st sign of
ovulation)
Day 18:

vacuoles move to the apical portion of the


secretory nonciliated cells
Day 19:

cells begin to secrete glycoprotein and


mucopolysaccharide contents into the lumen;

glandular cell mitosis ceases with secretory


activity.
Mid- to late-secretory phase
Dating is based on endometrial stroma
Days 21 to 24:

stroma becomes edematous

window of implantation

epithelial surface cells show decreased


microvilli and cilia

appearance of pinopodes, luminal protrusions


on the apical cell surface, in preparation for
blastocyst implantation.
Days 22 to 25:

stromal cells surrounding the spiral arterioles


begin to enlarge, and stromal mitosis
becomes apparent.

Predecidual transformation of upper 2/3 of


functionalis layer

Glands exhibit extensive coiling and luminal


secretions become visible
Days 23 to 28:

predecidual cells, which surround spiral


arterioles

Spiral artery activity


Midproliferative phase:

Arise from arcuate arteries, which are myometrial

Days 8-10
branches of the uterine vessels

Columnar surface epithelium

Lengthen at a rate greater than the rate of

Longer curving glands


increase in endometrial tissue height or thickness

Variable stromal edema


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Rapid angiogenesis is regulated through estrogenand progesterone-regulated synthesis of VEGF


Changes in blood flow through these vessels aid in
endometrial growth
Excessive coiling and stasis in blood flow coincide
with regression of CL function and lead to a
decline in endometrial tissue volume
Coiling leads to endometrial hypoxia and necrosis
Prior to endometrial bleeding, intense vasospasm
occurs to limit blood loss with menstruation

MENSTRUATION
Late premenstrual phase endometrium

Stromal infiltration by neutrophils, giving a


pseudoinflammatory appearance to the tissue

Endometrial stromal and epithelial cells


produce IL-8, which is a chemotactic activating
factor for neutrophils, and serves to recruit
neutrophils prior to menstruation

Invading leukocytes secrete enzymes that are


members of the matrix metalloproteinase
(MMP) family.

Rising level of MMPs tips the balance between


proteases and protease inhibitors, effectively
initiating matrix degradation.
Anatomical events

Marked changes in endometrial blood flow

Coiling of spiral arteries becomes sufficiently


severe that resistance to blood flow increases
strikingly, causing hypoxia or the endometrium

Resultant stasis is the primary cause of


endometrial ischemia and tissue degeneration.

Intense vasoconstriction & endometrial cytokine


changes, activation of proteases (MMP-1 & MMP-3)
Prostaglandins & menstruation

Role of prostaglandin:
o Vasoconstriction
o Myometrial contractions
o Upregulation of pro-inflammatory responses

Progesterone withdrawal increases expression of


inducible COX-2 enzyme to synthesize
prostaglandins and decrease expression of 15hydroxyprostaglandin dehydrogenase (PGDH),
which degrades prostaglandin

Increased prostaglandin production of stromal


cells along with increased prostaglandin receptor
density on blood vessels and surrounding cells.

PGF2-alpha
o Vasoconstriction of spiral arteries, causing the
uppermost endometrial zones to become
hypoxic
o Potent inducer of angiogenesis and vascular
permeability factors such as VEGF
Vasoactive peptides

Endothelin-1 is a potent vasoconstrictor as a


product of vascular endothelial cells.
o Degraded by enkephalinase, which is located in
endometrial stromal cells.
o Increase in its activity parallels with the
increase in progesterone levels after ovulation
o Enkephalinase activity is highest during the
midluteal phase and declines steadily
thereafter as progesterone plasma levels
decrease.
Activation of lytic mechanisms

Following vasoconstriction & endometrial cytokine


changes, activation of proteases (MMP-1 and MMP3) within stromal cells and leukocyte invasion
occurs to degrade the endometrial interstitial
matrix.

Origin of menstrual blood

Arterial bleeding is appreciably greater than


venous.

Endometrial bleeding appears to follow rupture of


an arteriole of a coiled artery, with consequent
hematoma formation.

With a hematoma, the superficial endometrium is


distended and ruptures.

Fissures develop in the adjacent functionalis layer,


and blood, as well as tissue fragments of various
sizes, are sloughed.

Hemorrhage stops with arteriolar constriction as


well as changes that accompany partial tissue
necrosis.

Endometrial surface is restored by growth of


flanges, or collars, that form the everted free ends
of the endometrial glands
Interval between menses

Modal interval of menstruation is 28 days.


Decidua

Specialized, highly modified endometrium of


pregnancy and is a function of hemochorial
placentation

Decidualization transformation of secretory


endometrium to decidua; dependent on estrogen
and progesterone and factors secreted by the
implanting blastocyst
Structure

3 parts
o Decidua basalis directly beneath blastocyst
implantation, modified by trophoblast invasion
o Decidua capsularis overlies the enlarging
blastocyst, and initially separates it from the
uterine cavity. Prominent during the 2nd month
of pregnancy.
o Decidua parietalis remainder of the uterine
lining
o Decidua vera when capsularis and parietalis
are joined later in pregnancy.

By 14 to 16 weeks AOG gestational sac


completely fills the uterine cavity and functionally
obliterated.

3 layers of decidua parietalis and basalis:


o zona compacta compact zone; part of zona
functionalis
o zona spongiosa spongy, middle portion, with
remnants of glands and numerous small blood
vessels; part of zona functionalis
o zona basalis basal zone which remains after
delivery and gives rise to new endometrium.
Reaction

Decidual reaction is completed only with


blastocyst implantation

Predecidual changes commence first during the


midluteal phase in endometrial stromal cells
adjacent to the spiral arteries and arterioles.

Endometrial stromal cells enlarge to form


polygonal or round decidual cells

Nuclei become round and vesicular, and the


cytoplasm becomes clear, slightly basophilic and
surrounded by a pericellular membrane

Pericellular matrix surrounding the decidual cells


may allow attachment of cytotrophoblasts through
cellular adhesion molecules.

Cell membrane also may provide decidual cell


protection against selected cytotrophoblastic
proteases.
Blood supply

Spiral arteries in the decidua parietalis retain a


smooth muscle wall and endothelium and thereby

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remain responsive to vasoactive agents that act


on their smooth muscle or endothelial cells.
Spiral arterioles and arteries are invaded by
cytotrophoblasts. As a consequence, the walls of
vessels in the basalis are destroyed. These
vascular conduits of maternal blood, devoid of
smooth muscle or endothelial cells, are not
responsive to vasoactive agents.
FERTILIZATION
EVENTS IN FERTILIZATION

Zygote cytoplasm is successively cleaved to form


a blastula, which consists of increasing smaller
blastomeres
At 32 -cell stage, the blastomeres form a morula,
which consists of an inner cell mass and outer cell
mass
The morula enters the uterine cavity at about 3
days post conception

BLASTOCYST FORMATION

Occurs when fluid secreted within the morula


forms the blastocyst cavity

Inner cell mass future embryo, is now called the


Embryoblast

The outer cell mass future placenta, is now


called the Trophoblast
IMPLANTATION

Blastocyst implants at around 7 days post


conception within the posterior superior wall of the
uterus

This is during the secretory phase of the


menstrual cycle, so implantation occurs within the
functional layer of endometrium.

1.
2.

3.

4.
5.

1.
2.
3.

The sperm binds to zona pellucida of the


secondary oocyte and triggers the acrosome
reaction, causing release of acrosomal enzymes
Sperm penetrates the zona pellucida and unite
with the oocytes plasma membrane, eliciting the
cortical reaction and rendering the secondary
oocyte impermeable to other sperm
Sperm and secondary oocyte cell membranes fuse
and contents of the sperm enter the cytoplasm
Male genetic material forms the male
pronucleus
Tail and mitochondria degenerate
Secondary oocyte completes meiosis II, forming a
mature ovum. The nucleus of the ovum is the
female pronucleus
The male and female pronuclei fuse to form a
zygote
POST CONCEPTION: WEEK 1
Cleavage
Blastocyst formation
Implantation

POST CONCEPTION: WEEK 2


EMBRYOBLAST

Differentiates into two distinct cell layers, the


Epiblast and Hypoblast, forming a Bilaminar
Embryonic Disk
o Epiblast -clefts develop within the Epiblast to
form the amniotic cavity
o Hypoblast -form the yolk sac
TROPHOBLAST

Cytotrophoblast divide mitotically

Syncytiotrophoblast
o Does not divide mitotically
o Produces the HCG
o Continues its growth into the endometrium to
make contact with the endometrial blood
vessels

EMBRYO PERIOD: WEEK 3-8


The beginning of the development of major organ
systems
Coincides with the first missed menstrual period
Period of high susceptibility to teratogen
Gastrulation is a process that establishes the 3
primary germ layers, forming a trilaminar
embryonic disk
o Ectoderm
o Endoderm
o Mesoderm

DERIVATIVES
LAYER
DERIVATIVES
Ectoderm
CNS and PNS
Sensory organs of seeing and hearing
Integument layer
Endoderm Lining of the GIR and Respiratory tract
Mesoderm Muscles
Cartilages
CVS
Urogenital System
RBC
EMBRYONIC PERIOD
Order of
Formation
CNS
First to develop and continues
post natal
Heart
Completed by 8 weeks
Upper limb
Completed by 8 weeks
Lower limb
Completed by 8 weeks
CLEAVAGE
External
Completed by 9 weeks
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genitalia

PERIOD OF TERATOGENICITY

DRUGS IN PREGNANCY
Category
Examples
Adequate and well-controlled human
studies have failed to demonstrate a
A risk to the fetus in the first trimester
Folic acid
of pregnancy (and there is no
evidence of risk in later trimesters).
Animal reproduction studies have
failed to demonstrate a risk to the
fetus and there are no adequate and
well-controlled studies in pregnant
Paracetamol,
women OR Animal studies have
B
amoxicillin,
shown an adverse effect, but
cephalexin,
adequate and well-controlled studies
in pregnant women have failed to
demonstrate a risk to the fetus in any
trimester.
Animal reproduction studies have
shown an adverse effect on the fetus
and there are no adequate and wellC
controlled studies in humans, but
paroxetine
potential benefits may warrant use of
the drug in pregnant women despite
potential risks.
There is positive evidence of human
fetal risk based on adverse reaction
data from investigational or marketing Phenytoin,
D experience or studies in humans, but tetracyclne,
potential benefits may warrant use of
aspirin,
the drug in pregnant women despite
potential risks.
Studies in animals or humans have
demonstrated fetal abnormalities
and/or there is positive evidence of
human fetal risk based on adverse
Thalidomide,
X reaction data from investigational or
isotretinoin
marketing experience, and the risks
involved in use of the drug in
pregnant women clearly outweigh
potential benefits.

AMNIOTIC FLUID

Normal amniotic fluid volume


o By 12 weeks = 60ml
o By 34-36 weeks = 1L
o By term = 840 ml
o By 42 weeks = 540 ml

Production of amniotic fluid


o Initially by amniotic epithelium
o Fetal kidneys and urine production
*Amniotic fluid volume is also dependent on the extent
of maternal plasma expansion

Removal and regulation of amniotic fluid


volume
o Fetal swallowing
o Fetal aspiration
o Exchange through skin and fetal membranes
THE PLACENTA AT TERM

Volume 497 Ml

Weight 508 grams (450-500 grams)

Surfaces
o Fetal

Covered with amniotic membrane giving


it white, glistening appearance

Where the umbilical cord arises


o Maternal

Attached to the decidua

Deep, bloody appearance arranged into


15-20 irregular lobes, cotyledons

Hofbauer cells
Circulation in the Mature Placenta

Fetal surface covered by amnion beneath which


the fetal chorionic vessels course chorionic villi
intervillous space decidual plate myometrium

FUNIS

Umbilcal cord

Two artery, one vein (left or right?)

Ave lenght: 55 cm

Wharton jelly- extracellular matrix of specialized


connective tissue

Anticlockwise spiral is present in 50 to 90 percent


of fetuses
PLACENTAL HORMONES

Trophoblast

Steroid hormones

hPL, hCG, parathyroid hormonerelated protein


(PTH-rP), calcitonin, relaxin, inhibins, activins, and
atrial natriuretic peptide

hypothalamic-like releasing and inhibiting


hormones: thyrotropin-releasing hormone (TRH),
gonadotropin-releasing hormone (GnRH),
corticotropin-releasing hormone (CRH),
somatostatin, and growth hormonereleasing
hormone (GHRH).

PLACENTA
FETAL TO MATERNAL MEMBRANES

Amnion
o Avascular; provides tensile strenght; first
identifiable at 7th to 8th day of life; from fetal
ectoderm

Chorion

Decidua parietalis (endometrium)


PLACENTAL STEROID HORMONES

Myometrium
Steroid
Nonpregnant

Serosa
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Pregnant
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Estradiol-17
Estriol
Progesterone
Aldosterone
Deoxycorticosterone
Cortisol

0.10.6
0.020.1
0.140
0.050.1
0.050.5
1030

1520
50150
250600
0.2500.600
112
1020

hCG

Almost exclusively produced by the placenta

Glycoprotein

Alpha and beta subunit

Functions: rescue and maintenance of function of


the corpus luteum, stimulates fetal testicular
testosterone secretion, materanl thyroid gland
stimulation (chorionic thyrotropins), promotion of
relaxin secretion

detectable in plasma of pregnant women 7 to 9


days after the midcycle surge of LH that precedes
ovulation.

Plasma levels increase rapidly, doubling every 2


days, with maximal levels being attained at 8 to
10 weeks

At 10 to 12 weeks, plasma levels begin to decline,


and a nadir is reached by about 16 weeks

Clearance: mainly hepatic, renal (30%)


hPL

Similar to hGH

detected in maternal serum as early as 3 weeks

Maternal plasma concentrations are linked to


placental mass, and they rise steadily until 34 to
36 weeks

production rate near term: approximately 1 g/day

Functions: Maternal lipolysis , anti-insulin or


"diabetogenic, potent angiogenic

Placental Estrogen Production

Conditions that Affect Hormone Levels in


Pregnancy
Condition

Findings

Fetal Demise

dec estrogen

PROGESTERONE

Source:
o First 6-7 weeks of pregnancy: Corpus luteum
(ovary)
o After 8 weeks: Placenta (Syncytiotrophoblast)

Function:
o Affects tubal motility, the endometrium,
uterine vasculature, and parturition
o Inhibits T lymphocytemediated tissue
rejection

Preferred precursor of progesterone biosynthesis


by the Trophoblast: Maternal plasma LDL
cholesterol

Fetal anencephaly

Dec estrogen (estriol)

Fetal adrenal
hypoplasia

absence of C19-precursors

Fetal-Placental
Sulfatase Deficiency

very low estrogen levels in


otherwise normal
pregnancies

Fetal-Placental
Aromatase Deficiency

virilization of the mother


and the female fetus

Trisomy 21Down
Syndrome

serum unconjugated
estriol levels were low

ESTROGEN

Pregnancy near term is hyperestrogenic

Produced exclusively by Syncytiotrophoblasts

Placenta produce all types of estrogen

Fetal Erythroblastosis

Elevated

Glucocorticoid
Treatment

Dec estrogen

Maternal Adrenal
Dysfunction

Dec estrogen

Gestational
Trophoblastic Disease

placental estrogen
formation is limited to the
use of C19-steroids in the
maternal plasma
estrogen produced is
principally estradiol

ESTROG
EN
Estradiol

Estrone

Estriol

SOURCE
Maternal ovaries for weeks 1 through 6
of gestation
After T1, the placenta is the major source
of circulating estradiol.
Maternal ovaries, adrenals, and
peripheral conversion in the first 4 to
6 weeks of pregnancy
The placenta subsequently secretes
increasing quantities
Produced almost exclusively by the
placental syncytiotrophoblast
Continued production depends on the
living fetus
Marker of fetal well being

FETAL DEVELOPMENT
Terms
Perinata
l
period

Period beginning 20 weeks AOG and


ending up to 28 completed days after
birth
It is recommended that this period be
defined as commencing at BW of 500
grams

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Neonata
l
period

Period after birth of an infant up to 28


completed days after birth

Fetal
period

Begins from 8 weeks after fertilization


or 10 weeks after onset of last menses

Embryo
nic
period

Commences beginning of the 3rd week


after ovulation and fertilization and lasts
up to 8 weeks AOG
8 weeks period from the time of
fertilization
10 weeks period from the time of the
last menstrual cycle/Ovulation

Abortus

Fetus or embryo removed or expelled


fro uterus during the first half of
gestation
20 weeks or less, or in the absence of
accurate dating criteria, born weighing
less than 500 grams

GESTATIONAL AGE vs. OVULATION AGE

Gestational age/menstrual age


o The time elapsed since the last menstruation
o Precedes fertilization/ovulation by 2 weeks

Ovulation age/post conceptional age


o Measures the actual age of the embryo from
the time of fertilization/ovulation
*A fetus that is 18 weeks AOG. What is the ovulation
age?
DETERMINING THE AGE OF THE FETUS

Naegeles Rule

Crown Rump Length (CRL)


o Measured from the superior to inferior pole of
the fetus preferably in extended position
o Used for First trimester

Biparietal Diameter (BPD)


o Measured at the outer to outer aspect of the
skull at the level of the occipitofrontal plane
o Used during the second and third trimester

breathe, but many will die because the


terminal sacs have not yet formed
28

crown-rump length is approximately 25 cm


skin is red and covered with vernix caseosa
pupillary membrane has just disappeared
from the eyes
born at this age has a 90-percent chance of
survival

36

CRL of 32
deposition of subcutaneous fat

40

average crown-rump length is about 36 cm


weight is approximately 3400 g

HEAD DIAMETERS

Bitemporal diameter (8.0cm)


o Greatest TRANSVERSE diameter of the head

Biparietal diameter (9.5 cm)

Occipitomental ( 12.5 cms)

Occipitofrontal (11.5 cms)


o The plane that corresponds to the greatest
CIRCUMFERENCE
o 34.5 cm

Suboccipitobregmatic ( 9.5 cms)


o
The plane that corresponds to the smallest
circumference of the head
o 32 cm
FETAL CIRCULATION

3 vessels (AVA)
o 2 arteries
o 1 vein

Three Shunts:
o Ductus venosus
o Foramen ovale
o Ductus arteriosus

FETAL PERIOD
AO
G
12

The uterus usually is just palpable above the


symphysis pubis,
crown-rump length is 6 to 7 cm.
Centers of ossification have appeared in
most of the fetal bones
fingers and toes have become differentiated
Skin and nails have developed and scattered
rudiments of hair appear.
external genitalia are beginning to show
definitive signs of male or female gender
spontaneous movements.

16

fetal crown-rump length is 12


Gender can be determined by experienced
observers by inspection of the external
genitalia by 14 weeks.
Quickening by multiparas

20

fetus now weighs somewhat more than 300


g, and weight begins to increase in a linear
manner.
fetus moves about every minute and is
active 10 to 30 percent of the time
downy lanugo covers its entire body

24

canalicular period of lung developmentis


nearly completed
fat deposition begins
fetus born at this time will attempt to

Fetal Blood

HEMATOPOIESIS
o yolk sac first site of hematopoiesis.
embryonic period
o Liver takes over up to near term
o Bone marrow starts at 4 mos AOG and
remains as the major site of blood formation
during adulthood

Erythrocytes nucleated and have a shorter life


span due to their large volume and are more
easily deformable

Fetal blood volume (125 ml/kg)


o Term infants = 80 ml/kg body weight
o Placenta = 45 ml/kg body weight

Fetal Hemoglobin

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o
o
o

Hemoglobin F
Hemoglobin A (adult hgb)
Hemoglobin A2

Fetal Circulation: CHANGES AFTER BIRTH

Foramen ovale functionally closed w/in


several minutes; anatomically fused 1 year after
birth

Ductus arteriosus functionally closed by


10-12 hours after birth; anatomically closed by
2-3 weeks

Ductus venosus constrict and becomes the


ligamentum venosum

testes or ovaries?
Dependent on the presence of SRY gene
present on the Y chromosome or the Testes
Determining region
Phenotypic Sex
o Is it a penis or a vagina?
o Dependent on the hormones produced
o
o

Kleihauer-Betke test

Rationale:
o Fetal RBCs are resistant to denaturating
effects of alkali.
o Motherr RBC are sensitive, thus may
hemolyze
FETAL PULMONARY SYSTEM

Presence of surfactant in the amnionic fluid is


evidence of fetal lung maturity (after 34 weeks)
Surfactant is formed in the type II pneumocytes
that line the alveoli
Starts to appear in the amniotic fluid at 28-32
weeks.
90% lipid and 10% proteins
o Phosphatidylcholines (lecithin) account for
80% of the glycerophospholipids
o Most active component
dipalmitoylphosphatidylcholine (DPPC)
o 2nd most active - phosphatidylglycerol
Alveolar development = just before birth 8 years
old

SEXUAL DIFFERENTIATION

MATERNAL PHYSIOLOGY

Genetic/Chromosomal Sex
o XX or XY?
o Dependent on the presence of Y chromosome
Gonadal Sex

CARDIOVASCULAR SYSTEM
Changes in cardiac function become apparent
during the first 8 weeks of pregnancy.
Cardiac output is increased as early as the fifth
week and reflects a reduced systemic vascular
resistance and an increased heart rate.
Resting pulse rate increases about 10 bpm.
Between 10 and 20 weeks, plasma volume
expansion begins and preload is increased.
Ventricular performance is influenced by both the
decrease in systemic vascular resistance and
changes in pulsatile arterial flow.

A. Heart

Heart is displaced to the left and upward and


rotated somewhat on its long axis. The apex is
moved somewhat laterally from its usual position,
causing a larger cardiac silhouette on chest
radiograph.

Pregnant women normally have some degree of


benign pericardial effusion, which may increase
the cardiac silhouette.

Normal pregnancy induces NO characteristic ECG


changes other than slight left-axis deviation as a
result of the altered heart position.

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B. Cardiac Sounds

Exaggerated splitting of the first heart sound with


increased loudness of both components

No definite changes in the aortic and pulmonary


elements of the second sound

Loud, easily heard third sound

Systolic murmur in 90% of pregnant patients


which was intensified during inspiration in some or
expiration in others, and disappeared shortly after
delivery.
C. Cardiac output

Mean arterial pressure and vascular resistance


decrease, while blood volume and basal metabolic
rate increase.

Cardiac output at rest, when measured in lateral


recumbent
position,
increases
significantly
beginning in early pregnancy. It continues to
increase and remain elevated during the
remainder of pregnancy.

During late pregnancy with a woman in SUPINE


position, the large pregnant uterus compresses
venous return from the lower body. It may
compress the aorta and cardiac filling may be
reduced with dimished cardiac output. Fetal
oxygen saturation is approximately 10% higher
when a labouring woman is in a lateral recumbent
position compared with supine. Upon standing,
cardiac output fall to the same degree as in the
non-pregnant woman.

During the 1st stage of labor, cardiac output


increases moderately. During the 2md stage, with
vigorous expulsive efforts, it is appreciably
greater. The pregnancy-induced increase is lost
after delivery.
D. Circulation and blood pressure

Brachial artery pressure when sitting is lower than


that when in the lateral recumbent supine
position.

Arterial pressure usually decreases to a nadir at 24


to 26 weeks and rises thereafter.

Diastolic pressure decreases more than systolic.

In about 10% of women, supine compression of


the great vessels by the uterus causes
significantly arterial hypotension, referred to as
the supine hypotensive syndrome. This may
directly affect fetal heart rate patterns. This also
occurs with hemorrhage or with spinal analgesia.

The components of the rennin-angiotensinaldosterone axis are increased in normal


pregnancy. These components are involved in
renal control of blood pressure via sodium and
water balance. Renin is produced by both the
maternal kidney and placenta, and increased renin
substrate (angiotensinogen) is produced by both
maternal and fetal liver. This increase in
angiotensinogen results, in part, from high levels
of estrogen production during normal pregnancy.
E. Cardiac natriuretic peptides

Atrial natriuretic peptide (ANP) and B-type


natriuretic peptide (BNP) are secreted by
cardiomyocytes in response to chamber-wall
stretching. These peptides regulate blood volume
by provoking natriuresis, dieresis, and vascular
smooth-muscle relaxation.

During pregnancy, plasma ANP are maintained in


the nonpregnant range despite increased plasma
volume. Median BNP levels are less than 20 pg/ml
and are stable across normal pregnancy. However,
these levels are increased in severe preeclampsia.
ANP-induced physiological adaptations participate
in the expansion of extracellular fluid volume and
the increase in plasma aldosterone concentrations
characteristic of normal pregnancy.

C-type natriuretic peptide (CNP), is secreted by


noncardiac tissues. This peptide appears to be a
major regulator of fetal bone growth.

F.

Prostaglandins
Renal medullary prostaglandin E2 synthesis is
increased markedly during late pregnancy and is
presumed to be natriuretic.
Prostacyclin (PGI2), the principal prostaglandin of
endothelium, is increased during late pregnancy
and regulates blood pressure and platelet
function. It also has been implicated in the
angiotensin resistance characteristic of normal
pregnancy.

G. Endothelin

Endothelin-1 is a potent vasoconstrictor in


endothelial and vascular smooth muscle cells and
regulates local vasomotor tone. It stimulates
secretion
of
ANP,
aldosterone,
and
catecholamines. There are endothelin receptors in
pregnant and nonpregnant myometrium. They are
also identified in the amnion, amniotic fluid,
decidua, and placental tissue. Vascular sensitivity
to endothelin-1 is not altered during normal
pregnancy. Vasodilating factors counterbalance
the endothelin-1 vasoconstrictor effects and
produce reduced peripheral vascular resistance.
H. Nitric Oxide

It is a potent vasodilator released by endothelial


cells and have important implication for modifying
vascular resistance during pregnancy.
PULMONARY SYSTEM
A. Anatomic Changes

Diaphragm rises about 4 cm during pregnancy.

Subcostal angle widens appreciably as the


transverse diameter of the thoracic cage increases
approximately 2 cm.

Thoracic circumference increases about 6 cm, but


not sufficiently to prevent a reduction in the
residual lung volume created by the elevated
diaphragm

Diaphragmatic excursion is actually greater in


pregnancy.
B. Pulmonary Function
Lung
Volumes
(ml)
Total lung
capacity

Tidal
volume

Residual
volume
Expirator
y reserve
volume
Inspirator
y
capacity
Inspirator

Nonpregna
nt

Term
Pregnan
cy

4,200

4,000

450

600

1,000

800

700

550

2,500

2,650

2,050

2,050

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Etiology

Resting minute
ventilation is also
increased. Can be
due to enhanced
respiratory drive
due to stimulatory
effects of
progesterone, low
expiratory reserve
volume and
compensated
respiratory
alkalosis.
Elevated
diaphragm

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y reserve
volume
Functiona
l residual
capacity
Vital
capacity

1,700

1,350

3,200

3,200

which shifts the curve back to the right. Reduced


PCO2 from maternal hyperventilation aids CO2
(waste) transfer from the fetus to the
mother while also facilitating O2 release to
the fetus.

Elevated
diaphragm

UNCHANGED

Respiratory rate is essentially unchanged.

Lung compliance is unaffected by pregnancy

Maximum breathing capacity and forced or timed


vital capacity are not altered appreciably
INCREASED

Airway conductance is increased possibly as a


result of progesterone

Amount of oxygen delivered into the lungs by the


increased tidal volume clearly exceeds O2
requirements imposed by pregnancy.

Total haemoglobin mass, and in turn total oxygencarrying capacity, increases appreciably.
DECREASED

Peak expiratory flow rates decline progressively as


gestation advances.

Total pulmonary resistance reduced possible as a


result of progesterone

Maternal arteriovenous oxygen difference is


decreased due to increased total oxygen carrying
capacity.
C. Acid-Base Equilibrium
Blood Gas
NonFirst
pregna
trimest
nt
er
HCO3
Not
(mEq/L
22-26
reported
)
PCO2
Not
(mmH
38-42
reported
g)
PO2
(mmH
90-100
93-100
g)
pH

7.38
7.42 (a)

7.36
7.52 (v)

Second
trimest
er

Third
trimest
er

Not
reported

16-22

Not
reported

25-33

90-98

92-107

7.40
7.52 (v)

7.41
7.53
7.39
7.45

(v)

(a)

(a) arterial; (v) venous

Increased awareness of a desire to breathe


early in pregnancy.
Physiologic dyspnea results from increased tidal
volume that lowers the blood PCO2 slightly,
which paradoxically causes dyspnea.
Increased respiratory effort, and in turn the
reduction in PCO2 is most likely induced in large
part by progesterone and to a lesser degree by
estrogen.
Progesterone appears to act centrally, where it
lowers the threshold and increases the
sensitivity of the chemoreflex response to
CO2.
To compensate for resulting respiratory
alkalosis, plasma bicarbonate levels decrease
from 26 to approximately 22 mmol/L
Although blood pH is increased only minimally, it
does shift the oxygen dissociation curve to the
left. This shift increases the affinity of maternal
hemoglobin for oxygen, thereby decreasing the
oxygen-releasing capacity of maternal blood.
Slight pH increase also stimulates an increase in
2,3-diphosphoglycerate in maternal blood

REPRODUCTIVE SYSTEM
A. Uterus

Non-pregnant weight of 70g to almost 1100 grams


by term.

Non-pregnant capacity of 10 ml to a total volume


of 5 to 20 liters by term

Uterine enlargement involves stretching and


marked hypertrophy of muscle cells, production
of new myocytes is limited.

Accumulation of fibrous tissue, particularly in the


external muscle layer, with an increase in elastic
tissue to strengthen the uterine wall

Uterine wall thins near term to only 1 to 2 cm.


It becomes soft and readily identable through
which the fetus can be palpated.

Uterine hypertrophy early in pregnancy probably


is stimulated by the action of estrogen and
perhaps that of progesterone. By 12 weeks,
increase in size is related predominantly to
pressure exerted by the expanding products of
conception.

Uterine enlargement most marked in the


fundus.

Early months of pregnancy fallopian tubes,


ovarian and round ligaments attach slightly below
the apex of the fundus

Later months of pregnancy fallopian tubes,


ovarian and round ligaments are located above
the middle of the uterus

Portion of the uterus surrounding placental site


enlarges more rapidly.

Arrangement of muscle cells:


o Outer hoodlike layer, which arches over the
fundus and extends into various ligaments
o Middle layer, dense network of muscle
fibers perforated in all directions by blood
vessels
o Internal layer, with sphincter-like fibers
around the fallopian tube orifices and internal
os of the cervix.
o Main portion of the uterine wall is formed by
the middle layer. Each cell in this layer has a
double curve so that the interlacing of any two
gives approximately the form of a figure 8.
When cells contract after delivery, they
constrict the penetrating blood vessels and act
as ligatures.

Pear shaped > globular form > spherical by 12


weeks > ovoid shape (length more than width)

Displaces intestines laterally and superiorly

Dextrorotation uterus undergoes rotation to the


right because of the rectosigmoid on the left side
of the pelvis.

There is tension exerted on the broad and round


ligaments.

Braxton Hicks contractions unpredictable,


sporadic and nonrhythmic contractons, every 10
to 20 minutes for some, intensity between 5 and
25 mmHg.

Total uterine blood flow from uterine and ovarian


arteries 450 to 650 mL/min
B. Cervix

Softening and cyanosis due to increased


vascularity and edema of the entire cervix,
together with hypertrophy and hyperplasia of
cervical glands.

Endocervical mucosal cells produce copious


amounts of a tenacious mucus that obstruct the
cervical canal soon after conception.

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Cervical Mucus is rich in Ig and cytokines and may


act as an immunological barrier to protect uterine
contents against infection.
Cervical mucus beading occurs as a result of
progesterone.
Arias-Stella
reaction

endocervical
gland
hyperplasia and hypersecretory appearance

C. Ovaries

Ovulation ceases and maturation of new follicles is


suspended.

Corpus luteum functions maximally during the first


6 7 weeks of pregnancy, produces progesterone.

Decidual reaction elevated patches of tissue


which bleed easily. Represents cellular detritus
from the endometrium that has passed through
the fallopian tubes.

Relaxin protein hormone secreted by the corpus


luteum, deciduas and placenta. Remodelling of
reproductive
tract
connective
tissue
to
accommodate pregnancy
D. Vagina & perineum

Chadwick sign increased vascularity affecting


vagina and results in violet discoloration
SKIN
a. Abdominal wall
1. Striae gravidarum or stretch marks
2. Diastasis recti rectus muscles separate in the
midline
b. Hyperpigmentation due elevated levels of
melanocyte-stimulating hormone; estrogen and
progesterone have melanocyte-stimulating effects

Linea nigra

Chloasma or melasma gravidarum

Pigmentation of areola and genital skin


c. Vascular changes

Vascular spiders or angiomas common on the


face, neck, upper chest and arms

Palmar erythema

Increased cutaneous blood flow serves to


dissipate excess heat generated by increased
metabolism

METABOLIC CHANGES
3rd trimester maternal basal metabolic rate is
INCREASED by 10 to 20%
WHO (2004) estimate of additional energy
demands:
o 1st tri 85 kcal/day
o 2nd tri 285 kcal/day
o 3rd tri 475 kcal/day

a. Weight gain

Attributable to uterus and its contents, breasts,


increase blood volume and extracellular fluid

Accumulation of cellular water, fat and protein

Average weight gain is approx. 12.5 kg or 27.5 lbs


b. Water metabolism
2. Increased water retention induced by resetting of
osmotic thresholds for thirst and vasopressin
secretion.
3. Mimimum amount of extra water during normal
pregnancy = 6.5 liters
o Amniotic fluid = 3.5 liters
o Maternal blood volume, uterus and breasts =
3.0 liters
4. Pitting edema of ankles and legs
o Increased venous pressure below the level of
the uterus due to partial vena cava occlusion
o Decrease in interstitial colloid osmotic pressure
c.

Protein metabolism

1.
2.
3.
4.

Fetus and placenta weigh about 4 kg and contain


approximately 500 g of protein
Remaining 500 g is added to uterus, breasts
primarily in the glands, and to hemoglobin and
plasma proteins
Nitrogen balance increased with gestational age
Maternal muscle breakdown is not required to
meet metabolic demands.

d. Carbohydrate metabolism

Pregnancy is characterized by mild fasting


hypoglycemia, postprandial hyperglycemia, and
hyperinsulinemia

Pregnancy-induced state of peripheral insulin


resistance occurs to ensure a sustained
postprandial supply of glucose to the fetus.
o Progesterone and estrogen, may act, directly or
indirectly to mediate this insensitivity
o Placental lactogen may increase lipolysis and
liberation of free fatty acids. Increased free
fatty acids may aid increased tissue resistance
to insulin

Pregnant women changes rapidly from a


postrprandial state characterized by elevated and
sustained glucose levels to a fasting state
characterized by decreased plasma glucose and
some amino acids
e. Fat metabolism

Lipids, lipoproteins and apolipoproteins increase


appreciably during pregnancy.

Increased insulin resistance and estrogen


stimulation are responsible for maternla
hyperlipidemia

Increased lipid synthesis and food intake


contribute to maternal fat accumulation during the
first two trimesters.

During 3rd trimester, fat storage declines or


ceases. This is a consequence of enhanced
lipolytic activity, and decreased lipoprotein lipase
activity reduces circulating triglyceride uptake into
adipose tissue. This transition to a catabolic state
favors maternal use of lipids as a source of energy
and spares glucose and amino acids for the fetus.

INCREASED levels during 3rd trimester:


o Triacylglycerol
o VLDL
o LDL
o
HDL

DECREASED levels after delivery: lipids,


lipoproteins and apolipoproteins
1. Leptin
o Primarily secreted by adipose tissue, some by
placenta
o Plays a role in body fat and energy expenditure
regulation
o May also help regulate fetal growth
o INCREASE and peak during the 2nd trimester
and plateau until term
o Abnormally elevated leptin have been
associated with preeclampsia and gestational
DM
2. Gherlin
o Secreted primarily by the stomach in response
to hunger.
o Cooperates with leptin in energy homeostasis
modulation
o Expressed also in placenta and likely has a role
in fetal growth and cell proliferation.
f.

Electrolyte and mineral metabolism

INCREASED
Iodine requirement

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DECREASED
Sodium
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Iron requirement

Potassium
Total serum calcium
(ionized & non-ionized)
Serum magnesium

HEMATOLOGIC CHANGES
a. Blood volume

Hypervolemia averages 40 to 45% above


nonpregnant blood volume after 32 to 34 weeks

Functions of hypervolemia:
o Meets the metabolic demands of the enlarged
uterus and its greatly hypertrophied vascular
system
o Provides abundant nutrients and elements to
support the rapidly growing placenta and fetus
o Protects the mother and fetus against the
deleterious effects of impaired venous return in
the supine and erect positions
o Safeguards the mother against the adverse
effects of parturition-associated blood loss

Maternal blood volume expands most rapidly


during the second trimester.

Blood volume expansion results from an increase


in both plasma and erythrocytes.

Moderate erythroid hyperplasia is present in the


bone marrow

Reticulocyte count is elevated slightly.

Elevated maternal plasma erythropoietin levels


peaks early during the 3rd trimester and
corresponds to maximal erythrocyte production.

Hemoglobin & hematocrit DECREASE slightly

Whole blood viscosity DECREASES.


b. Iron metabolism
1. Storage
o Total iron content of normal adult women: 2.0
to 2.5 grams. Most of this is incorporated in
hemoglobin or myoglobin.
o Iron stores of normal young women is
approximately 300 mg
2. Iron requirements
o Approximately 1,000 mg of iron is required for
normal pregnancy.
a. 300 mg - actively transferred to the fetus
and placenta.
b. 200 mg lost through normal excretion
routes, primarily in the GIT.
c. 500 mg required for the increase in total
circulating erythrocyte volume (approx
450 ml)
o The amount of dietary iron, together with that
mobilized from stores, will be insufficient to
meet the average demands imposed by
pregnancy.

Blastocyst must break through the


uterine cavity epithelial lining to invade
endometrial tissue

Trophoblast must replace endometrium


and vascular smooth muscle of maternal
blood vessels to secure adequate supply
for the placenta

Inflammatory environment is required to


secure cellular debris removal and
adequate repair of the uterine epithelium
o Midpregnancy (anti-inflammatory)

Period of rapid fetal growth and


development
o Parturition (recrudescence of inflammatory
process)

Influx of immune cells into the


myometrium
Suppressed activity:
o T-helper (Th) 1 cells

decreases secretion of IL-2, interferon-g,


and TNF-B

suppressed Th1 response is requisite for


pregnancy continuation

suppressed Th1 during pregnancy results


in remission of some autoimmune
disorders such as rheumatoid arthritis,
multiple sclerosis, and Hashimoto
thyroiditis

failure of Th1 suppression may be related


ot development of preeclampsia
o T-cytotoxic (Tc) 1 cells

Decreases secretion of IL-2, interferon-g,


and TNF-B
Upregulated activity:
o Th2 cells increase secretion of IL-4, IL-6 and
IL-13
o IgA and IgG in cervical mucus increase
o IL-1B in cervical and vaginal mucus is increased
during the 1st trimester
Vitamin K-dependent glycoprotein that inhibits
activation of factor X
Low levels may prove to be a risk factor for
otherwise unexplained recurrent early pregnancy
loss (Effraimidou and associates, 2009)

URINARY SYSTEM
a. Kidney

RENAL CHANGES IN NORMAL PREGNANCY


Paramete
Alteration
Clinical
r
relevance
Kidney size Approximately 1
Size returns to
cm longer of
normal
radiograph
postpartum
Dilatation
Resembles
Can be confused
hydronephrosis
with obstructive
3. Puerperium
on sonogram or
uropathy;
o During vaginal delivery & the first postpartum
IVP (more marked
Retained urine
days, only approximately half of the added
on right)
leads to collection
erythrocytes are lost from most women.
errors;
o Normal losses come from the following:
Renal infections
a. Placental implantation site
are more virulent;
b. Episiotomy or lacerations
May be
c. Lochia
responsible for
o Estimated blood loss:
distention
a. NSVD (singleton) 500 to 600 ml
syndrome;
b. CS or NSVD (Twin) 1,000 ml
Elective
pyelography
c. Immunologic functions
should be

Suppression of various humoral and cell-mediated


deferred to at
immunological functions occur to accommodate
least 12 weeks
the foreign semiallogenic fetal graft.
postpartum

Pregnancy is both a proinflammatory and


Renal
GFR & renal
Serum creatinine
antiinflammatory condition depending on the
function
plasma flow
decreases during
stage.
increase 50%
normal gestation

Three immunologic phases of pregnancy:


(>0.8 mg/dl
o Early pregnancy (pro-inflammatory)
creatinine already
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Maintenan
ce of acidbase

Decreased
bicarbonate
threshold;
Progesterone
stimulates
respiratory center

Plasma
osmolality

Osmoregulation
altered;
Osmotic
thresholds for
vasopressin (AVP)
release and thirst
decrease
Hormonal
disposal rates
increase

borderline);
Protein, amino
acid, and glucose
excretion all
increase
Serum
bicarbonate
decreased by 4-5
mEq/L;
PCO2 decreased
10 mmHg;
PCO2 or 40
mmHg already
represents CO2
retention
Serum osmolality
decreases 10
mOsm/L (serum
Na 5 mEq/L)
during normal
gestation
Increased
placental
metabolism of
AVP may cause
transient diabetes
insipidus during
pregnancy.

1. Loss of nutrients
o Amino acids and water-soluble vitamins
are lost in urine in greater amounts
2. Tests of renal function
o Serum creatinine DECREASED. Values above
0.9 mg/dl suggest underlying renal disease and
prompt investigation
o Creatinine clearance INCREASED about 30%
3. Urinalysis
o Glucosuria may NOT be abnormal. It can be
due to increase in GFR, together with impaired
tubular reabsorptive capacity for filtered
glucose. About 1/6 of pregnant women spill
glucose, but the possibility of DM should not be
ignored.
o Proteinuria NOT evident during pregnancy
except occasionally in slight amounts during or
soon after vigorous labor.
o Albumin excretion is minimal and ranges from
5 to 30 mg/day
o Hematuria is often a result of contamination
during collection. Common after difficult labor
and delivery because of trauma to the bladder
and urethra.

b. Ureters

Uterus rests upon ureters and laterally displaces it


and compresses them at the pelvic brim

Right ureter is dilated more than the left due to a


dextrorotated uterus and the right ovarian vein
complex lies obliquely over the right ureter.

Ureteral elongation and curvature formation


occurs due to distention
c.

Bladder
Bladder trigone is elevated by (>12 weeks):
o Increased uterine size
o Hyperemia
o Hyperplasia of bladders muscle and
connective tissue
Note: Elevation of trigone causes thickening of
posterior, or intraureteric origin

No mucosal changes

Increase in size and tortuosity of its blood vessels


Bladder pressure (primigravidas) increased from 8
cm H20 (early pregnancy) to 20 cm H20 (at term).
Absolute and functional urethral lengths
INCREASED
Maximal intraurethral pressure INCREASED from
70 to 93 cm H20, thus continence is maintained
End of pregnancy changes:
o Entire base of blader is pusched forward and
upward, converting normal convex surface to
concave due to presenting part
o Pressure of presenting part impairs drainage of
blood and lymph from the bladder base which
may lead to edema, and susceptibility to
trauma and infections
GASTROINTESTINAL TRACT
Appendix displaced upward and laterally as the
uterus enlarges, and it may reach the flank
Gastric emptying time is UNCHANGED. During
labor and administration of analgesic agents, it
becomes prolonged. General anesthesia may
cause regurgitation and aspiration during delivery.
Pyrosis (heartburn) reflux of acidic secretions
into the lower esophagus due to:
o Altered position of of the stomach
o Decreased LES tone
o Intraesophageal pressures are lower compared
to intragastric pressures
o Esophageal peristalsis has lower wave speed
and lower amplitude
Gums may become hyperemic and softened and
may bleed when mildly traumatized as with a
toothbrush
Epulis of pregnancy focal, highly vascular
swelling of the gums but regresses spontaneously
after delivery.
Pregnancy DOES NOT incite tooth decay.
Hemorrhoids are fairly common due to
constipation and elevated pressure in veins below
the level of the enlarged uterus.

a. Liver

NO INCREASE in liver size

Hepatic blood flow and diameter of the portal vein


is INCREASED

Increased levels:
o Total alkaline phosphatase almost doubles
o Total albumin
o Serum globin

Decreased levels:
o AST
o ALT
o GGT
o Bilirubin
o Serum albumin

Leucine aminopeptidase activity is markedly


INCREASED. This is increased with liver disease.
b. Gallbladder

Progesterone inhibits CCK-mediated smooth


muscle stimulation which impairs gallbladder
contraction

Impaired/reduced gallbladder contraction leads to


increased residual volume, and stasis with
associated increased bile cholesterol saturation of
pregnancy contributes to increased prevalence of
gallstone in multiparous women.

Intrahepatic cholestasis in pregnancy has been


linked to high circulating levels of estrogen, which
inhibit intraductal transport of bile acids.

Pruritus gravidarum is due to retained bile salts.


ENDOCRINE SYSTEM
a. Pituitary gland

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Enlarges by approximately 135% but rarely cause


visual disturbance from compression of optic
chiasma
Not essential for maintenance of pregnancy

1. Growth Hormone (GH)


o First trimester secreted predominantly from
maternal pituitary gland; serum and amniotic
fluid concentrations are within nonpregnant
values (0.5 to 7.5 ng.ml)
o At 8 weeks AOG growth hormone secreted by
placenta becomes detectable
o At 17 weeks AOG placenta is the principal
source of growth hormone secretion
o Maternal serum levels plateau after 28 weeks
at 14 ng/ml
o Amniotic fluid levels peak at 14 to 15 weeks
and slowly declines to reach baseline values
after 36 weeks.
o Maternal GH
Correlate positively with birthweight and
negatively with fetal growth restriction &
uterine artery resistance
o Placental GH
Differs from pituitary GH by 13 AA residues
Secreted by syncitiotrophoblasts in a
nonpulsatile fashion
Appears to have some influence on
fetal growth as well as the development
of preeclampsia
Major determinant of maternal insulin
resistance after midpregnancy
Fetal growth progresses in the
complete absence of placental GH
Not absolutely essential, but may act in
concert with human placental lactogen
and other somatolactogens to regulate
fetal growth.
2. Prolactin
o INCREASE markedly and usually 10-fold
greater at term (150 ng/ml)
o DECREASES after delivery even in women who
are breast feeding.
o There are pulsatile bursts of prolactin secretion
in response to suckling during early lactation.
o Increases prolactin level:
Estrogen stimulation increases the number
of anterior pituitary lactotrophs and may
stimulate release of prolactin
TRH
Serotonin
o Dopamine (prolactin-inhibiting factor) inhibits
prolactin secretion
o Functions of prolactin:
Ensure lactation
Initiate DNA synthesis and mitosis of
glandular epithelial cell and presecretory
alveolar cells of the breast (early
pregnancy).
Increases the number of estrogen and
prolactin galactopoiesis, and production of
casein, lactalbumin, lactose, and lipids.
o Present in amniotic fluid in high concentrations.
Up to 10,000 ng/ml at 20 to 26 weeks but
decrease and reach a nadir after 34 weeks.
Prolactin in amniotic fluid could be produced by
uterine decidua. Its function could be to
prevent water transfer from fetus into the
maternal compartment to prevent fetal
dehydration.
b. Thyroid gland

Thryroid hormone production INCREASED by 40


to 100% to meet maternal and fetal needs

c.

Thyroid gland undergoes moderate enlargement


as a result of glandular hyperplasia and increased
vascularity. Volume increase from 12 ml (first
trimester) to 15 ml (at term)
Normal pregnancy does not typically cause
significant thyromegaly. Goiter should be
investigated.
Thyroxin-binding globulin increases in the first
trimester and reaches its zenith at about 20
weeks, and stabilizes at approximately double
baseline values for the remainder of pregnancy
Total serum thyroxine INCREASE sharply between
6 and 9 weeks and reaches a plateau at 18 weeks
Free serum T4 rise slightly and peak along with
hCG levels, and return to normal
Total triiodothyronine (T3) INCREASE up to 18
weeks and plateaus.
Thyroid-releasing hormone (TRH) are NOT
INCREASED, but CROSSES the placenta and may
stimulate the fetal pituitary to secrete thyrotropin
TSH and hCG has identical a-subunits, thus hCG
has intrinsic thyrotropic activity and cause thyroid
stimulation.
Thyroid-stimulating hormone (TSH) or thyrotropin
DECREASES in more than 80% of pregnant
women, but remain normal for non-pregnant
women.
Normal suppression of TSH may lead to a
misdiagnosis of subclinical HYPERTHYROIDISM.
Parathyroid glands
Regulation of calcium concentration is closely
interrelated to magnesium, phosphate, PTH,
vitamin D, and calcitonin physiology
All markers of bone turnover INCREASED during
normal pregnancy and failed to reach baseline
level by 12 months postpartum
Calcium needed for fetal growth and lactation may
be drawn at least in part from the maternal
skeleton.
Acute or chronic decreases in plasma calcium or
acute decreases in magnesium stimulate the
release of PTH, and vice versa.
Action of PTH on bone resorption, intestinal
absorption, and kidney reabsorption is to increase
ECF calcium and decrease phosphate.

1. PTH and Calcium


o First trimester plasma PTH decrease initially
o Succeeding trimesters INCREASE
progressively
Due to lower calcium concentrations in
pregnancy as a result of increased plasma
volume, increased GFR, and maternal-fetal
transfer of calcium.
o Estrogen appears to BLOCK the action of PTH
on bone resorption, resulting in increase in PTH
o Physiologic hyperparathyroidism of
pregnancy occurs to supply the fetus with
adequate calcium.
2. Calcitonin and Calcium
o Calcium and magnesium increase the
biosynthesis and secretion of calcitonin
o Food ingestion & various gastric hormones (e.g.
gastrin, pentagastrin, glucagon, and
pancreozymin) also INCREASE calcitonin levels.
o Calcitonin acts to OPPOSE PTH and Vitamin D
to protect skeletal calcifications during times of
calcium stress, such as pregnancy and
lactation.
3. Vitamin D and Calcium
o 1, 25-diOH Vitamin D3 biologically active
compound, and stimulates resorption of

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calcium from bone and absorption from the
intestines
o Conversion to active Vitamin D3
Ingestion of Vit D or synthesis in the skin
LIVER Vitamin D converted to 25-OH Vit
D3
KIDNEY, DECIDUA & PLACENTA 25-OH Vit
D3 converted to 1, 25 diOH Vit D3
(biologically active form) which is
INCREASED in pregnancy.
o PTH, low calcium and phosphate levels
facilitates conversion of 25-OH Vit D3 to 1, 25
diOHVit D3
o Calcitonin OPPOSES conversion of Vit D to its
active form.
d. Adrenals undergo little morphological
change
1. Cortisol INCREASED
o Much of serum cortisol is bound by transcortin
(cortisol-binding globulin)
o Rate of adrneal cortisol secretion is not
increased, and probably it is decreased
compared with that of the nonpregnant state.
o Metabolic clearance rate is LOWER during
pregnancy because its half-life is nearly
doubled.
o During early pregnancy ACTH levels are
reduced strikingly
o As pregnancy progresses, ACTH and free
cortisol rises
o Elevation in cortisol may be a result of
resetting of the maternal feedback
mechanism to higher levels (Nolten and
Rueckert, 1981)
o In response to elevated progesterone levels
during pregnancy, an elevated free cortisol is
needed to maintain homeostasis (Keller-Wood
and Wood, 2001)
2. Aldosterone INCREASED
o As early as 15 weeks, maternal adrenal glands
secrete more aldosterone
o Sodium intake restriction increases aldosterone
secretion
o Increased aldosterone affords protection
against the natriuretic effect of progesterone
and ANP.
3. Deoxycorticosterone INCREASED
o Due to increased kidney production from
estrogen stimulation
o There is transfer of fetal deoxycorticosterone
into the maternal compartment due to high
levels in fetal blood.
4. DHEA-S DECREASED (serum and urine)
o Due to increased metabolic clearance through
externsive maternal hepatic 16a-hydroxylation
and placental conversion to estrogen
5. Androstenedione and testosterone INCREASED
o Maternal plasma androstenedione and
testosterone are converted to estradiol in the
placenta
o Increase in plasma SHBG retards testosterone
clearance
OTHER SYSTEMS
Musculoskeletal system

Progressive lordosis is observed. The lordosis


shifts the center of gravity back over the lower
extremities.

Sacroiliac, sacrococcygeal and pubic joints have


increased mobility during pregnancy.

Joint mobility may contribute to the alteration of


maternal posture and may cause discomfort in the
lower back.

Pelvic joints normally relax, particularly the


symphysis pubis. Most relaxation takes place in
the first half of pregnancy.
Symphyseal separation greater than 1 cm may
cause significant pain. Regression begins
immediately follwing delivery, and it is usually
complete within 3 to 5 months.

Eyes

Intraocular pressure decreases during pregnancy,


attributed to increased vitreous outflow.

Corneal sensitivity is decreased, particularly late


in gestation

Slight increase in corneal thickness due to edema.

Krukenberg spindles brownish-red opacities on


the posterior surface of the cornea have been
observed during pregnancy.

Visual function is unaffected by pregnancy, except


for transient loss of accommodation.
CNS

Women often report problems with attention,


concentration, and memory throughout pregnancy
and the early postpartum period.

Attention and memory were improved in women


with preeclampsia receiving magnesium sulfate
compared with normal pregnant women (Rana and
associates, 2006).

Mean blood flow in the middle and posterior


cerebral arteries decreased progressively from
non-pregnant state to late in the 3rd trimester.
Unknown clinical significance (Zeeman and coworkers, 2003)

Pregnancy does not appear to impact


cerebrovascular autoregulation.
o Sleep
Difficulty sleeping about 12 weeks to first
2 months postpartum with frequent
awakening, fewer hours of night sleep, and
reduced sleep efficiency.
Decreased frequency and duration of sleep
apnea episodes during pregnancy
compared postpartum
Supine position, average Pa)2 levels were
lower
Greatest disruption of sleep is seen
postpartum and may contribute to
postpartum blues or frank depression
PRENATAL CARE
Definition

A comprehensive antepartum care program that


involves a coordinated approach to medical care
and psychosocial support that optimally begins
before conception and extends throughout the
antepartum period. (AAP & ACOG, 2007)

A planned program of medical evaluation and


management, observation, and education of the
pregnant woman directed toward making
pregnancy, labor, delivery and the postpartum
recovery, a safe and satisfying experience.

It should provide opportunities for the following:


o Physician and patient to be better acquainted
o Physician to learn something about the
patients emotional attitude toward pregnancy
and labor
o Instruction for the patient and her husband in
optimal care for herself and the coming baby
o Optimal instruction of the patient and her
husband in a prepared childbirth program.
Components

Preconceptional care, Diagnosis of pregnancy,


Initial prenatal evaluation, follow-up prenatal visits
1. Diagnosis of pregnancy

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Established through signs and
symptoms, chorionic gonadotropin,
ultrasound recognition

Signs and symptoms of pregnancy


Sign or
Comments
symptom

Occurs 10 days after expected


menses

One to two episodes of bloody


Cessation
discharge, reminiscent of
of menses
menstruation, can be due to
blastocyst implantation or
implantation bleeding

Fern-like pattern Day 7 to 18 of


menses due to increased NaCl when
estrogen is produced.
Cervical

Beaded pattern Day 21 menses or


mucus
pregnancy due to decreased NaCl
influenced by progesterone that
prohibit ferning

Breast tenderness and tingling

>2 months: increased breast size,


delicate veins becomes visible,
nipples larger & more pigmented,
more erectile.
Breast

Colostrum can be expressed. Areola


changes
broader and deeply pigmented.

Glands of Montgomery which are


hypertrophic sebaceous glands
appear.

Breast striations may also appear


Chadwicks sign. Vaginal mucosa
Vaginal
becomes dark bluish or purplish red and
mucosa
congested.

Striae gravidarum or stretch marks

Diastasis recti. Rectus muscles


separate in the midline.

Linea nigra. Brownish-black


discoloration of linea alba

Chloasma or melasma gravidarum


Skin
(mask of pregnancy)
changes

Angiomas or vascular spiders.


Minute, red elevations on the skin of
the face, neck, upper chest and
arms. Often designated as nevus,
angioma or telangiectasia.

Palmar erythema

First few weeks. Anteroposterior


diameter is increased.
Changes

12 weeks AOG: body of uterus


in the
becomes globular, average diameter
uterus
is 8 cm.

6 to 8 weeks AOG: Hegars sign is


softening of the isthmus.

Goodells sign. Softening of the


cervix. The consistency of the
cervical tissue surrounding the
Changes
external os is more similar to that of
in the
the lips of the mouth.
cervix

Cervical softening is also noted in


women taking estrogenprogesterone pills.
Fetal

17 weeks: stethoscope
heart tone
10 weeks: doppler equipment

5 weeks: transvaginal sonography

Fetal heart rate: 110 to 160 bpm

Other sounds heard in the pregnant


abdomen:
1. Funic souffle rush of blood
through the umbilical
arteries. Sharp, whistling
sound, synchronous with
fetal pulse.
2. Uterine souffle soft,
blowing sound, synchronous
o

Fetal
movemen
ts

with maternal pulse. Heard


at lower portion of uterus
produced by dilated uterine
arteries.
18-20 weeks: Primigravid
16-18 weeks: Multigravid
20 weeks: examiner can begin to
detect fetal movements.

Presumptive

Probable

Positive

Symptoms
Nausea,
vomiting
Bladder
frequency/urgen
cy
Perception of
fetal movement
Breast
enlargement

Symptoms
Abdominal
distention
Braxton-Hicks

Signs
Secondary
amenorrhea
Chadwicks sign
Chloasma (face)
Linea nigra,
striae
Spider
telangiectasia
Breast changes
Thermal
changes

Signs
(+) Pregnancy
test
Abdominal
enlargement
Outlining of the
fetal parts
Hegars sign
Goodells sign
Ballotment

Signs
Fetal heart tone
Perception of
fetal movement
by examiner
Ultrasound
evidence

Pregnancy Test
1. Chorionic gonadotrophin
2. Ultrasound recognition (Transvaginal
ultrasound)

2. Initial prenatal evaluation

Major goals:
1. Define the health status of the mother and
fetus.
2. Estimate the gestational age.
3. Initiate a plan for continuing obstetrical
care.

Components of routine prenatal care


(Williams Obstetrics, 23rd edition)

COMPONENT

First
visit
+
+
+
+
+

History
Complete PE
Blood pressure
Maternal weight
Pelvic/cervical
exam
Fundal height
+
FHT & position
+
Hemoglobin
+
(Hgb) & Hct
Blood type & Rh
+
factor
Antibody screen
+
Pap smear
+
Urine protein
+
Urine culture
+
Rubella titer
+
Syphillis test
+
(VDRL)
Hepatits B
+
surface Ag
(HbsAg)
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15-20
weeks

24-28
weeks

29-41
weeks

+
+

+
+

+
+

+
+

+
+
+

+
+

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50 grams
OGCT/100g
OGTT
Gonococcal or
*
Chlamydial
culture
HIV
*
*High-risk women

+
*

Components of Initial Prenatal Evaluation:


A. Prenatal Record
Terminologies for prenatal record:
a. Nulligravida. Woman who is NOT now and
never has been pregnant.
b. Gravida. Woman who is or has been pregnant,
irrespective of the pregnancy outcome. With
the establishment of first pregnancy, she
becomes primigravida, and with successive
pregnancies, a multigravida.
c. Nullipara. Woman who has never completed a
pregnancy beyond 20 weeks gestation.
d. Primipara. Woman who has been delivered
only once a fetus or fetuses born alive or dead
with an estimated length of gestation 20 or
more weeks.
e. Multipara. Woman who has completed 2 or
more prenancies to 20 weeks or more. Parity is
determined by the number of pregnancies
reaching 20 weeks and not by the number of
fetuses delivered.
f. Gestational age or menstrual age is
calculated from the first day of last menstrual
period.
g. Ovulatory age or fertlization age, is 2 weeks
shorter than gestational age. Used by
embryologists and other reproductive
biologists.
h. First trimester is from conception to 14 weeks
gestation. Second trimester is up to 28 weeks
completed gestation. Third trimester from 29th
to 42nd week gestation.
Normal pregnancy duration
1. Non-viable pregnancy is less than or equal to 20
weeks gestation (140 days)
2. Viable pregnancy:

Preterm - >20 weeks to <37 weeks (141 to


<259 days)

Term 37 weeks to 42 weeks (259 294


days)

Post term - >42 weeks (294 days)


3. Term Pregnancy Categories (ACOG/SMFM: Replace
Phrase 'Term Pregnancy' With 4
Categories. Medscape. Oct 22, 2013.)

Early term: 37 weeks to 38 weeks, 6 days


has 7-fold higher risk for neonatal morbidity

Full term: 39 weeks to 40 weeks, 6 days

Late term: 41 weeks to 41 weeks, 6 days

Post term: 42 weeks and beyond


B. History

Menstrual history

Psychosocial screening
Nonbiomedical factors that affect mental and
physical well-being.
Screening for barriers to care:
1. lack of transportation
2. child care or family support
3. unstable housing
4. unintended pregnancy
5. communication barriers
6. nutritional problems
7. cigarette smoking, substance abuse
8. depression
9. domestic violence

Cigarette Smoking: spontaneous abortion, low


birthweight due to preterm delivery or fetal
growth restriction, infant and fetal deaths

(SIDS), placental abruption, placenta previa,


premature rupture of membranes
Ethanol: potent teratogen and causes fetal
alcohol syndrome, characterized by growth
restriction, facial abnormalities and CNS
dysfunction.
Illicit drugs include opium derivatives,
barbiturates and amphetamines which may
cause fetal distress, low birthweight.
Domestic violence refers to violence against
adolescent and adult females within the
context of family or intimate relationships.

C. Physical examination. Includes speculum and


pap smear, digital pelvic examination and rectal
exams.
D. Laboratory tests. Refer to table above.

Iron status for women during pregnancy and


the postpartum period. (CPG on Iron Deficiency
Anemia, November 2009)
Iron
Iron
Iron
deficiency
deficiency
sufficienc
Without
anemia
y
anemia
(IDA)
Hgb
11
Hgb
11
Hgb
<11
0
0
0
g/L
g/L
g/L
20 weeks
to
Ferriti 12
Ferriti <1 Ferriti <12
delivery
n
ug
n
2
n
ugL
L
ug
L
Hgb
12
Hgb
12
Hgb
<12
0
0
0
g/L
g/L
g/L
6 months
postpart Ferriti 15
Ferriti <1 Ferriti <15
um
n
ug
n
5
n
ugL
L
ug
L

Criteria for anemia in pregnancy by WHO and


US CDC (CPG on Iron Deficiency Anemia,
November 2009)
Trimester
Anemia if Hgb is less than
1st: 0-12 weeks
11.0 g/dl
2nd: 13-28 weeks
10.5 g/dl
3rd: 29 weeks to term
11.0 g/dl

Severity of anemia by WHO (CPG on Iron


Deficiency Anemia, November 2009)
Category
Severity
Hgb (g/dl)
1
Mild
9.5 10.5
2
Moderate
8.0 9.4
3
Severe
6.9 7.9
4
Very severe
<6.9

Recommendations on Detection and Diagnosis


of Diabetes Mellitus among Filipino Pregnant
Women (CPG on Diabetes Mellitus in
Pregnancy, November 2011)
o Diabetes mellitus recognized during
pregnancy should now be classified as
either gestational diabetes mellitus (GDM)
or over diabetes mellitus based on plasma
glucose levels.
o Universal screening for GDM is
recommended for Filipino gravidas.
o At the first prenatal visit, determine if the
gravid is high risk or not based on
historical and pregnancy risk factors.
o ALL FILIPINO gravidas are considered high
risk by race or ethnic group (Pacific
Islander) and should be screened for type
2 diabetes mellitus in the first prenatal
visit (fasting blood sugar [FBS] or
glycosylated hemoglobin [HbA1c] or
random blood sugar [RBS])

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o

E.

Diagnosis of OVERT DIABETES is given


among women with any of the following
results in their first visit.

FBS > 126 mg/dl (7 mmol/L)

RBS > 200 mg/dl (11.1 mmol/L)

HbA1c > 6.5%

2 hour 75 g OGTT > 200 mg/dl (11.1


mmol/L)
Diagnosis of GDM is made if any one (1) of
the following plasma values are exceeded:

FBS > 92 mg/dl (ADA/IADPSG/POGS

1 hour > 180 mg/dl

2 hour > 153 mg/dl (ADA/IADPSG) or >


140 mg/dl (WHO/POGS)
For Filipino gravidas with no other risk
factors aside from race or ethnicity and
the initial test (FBS, HbA1c or RBS) is
normal, screening for GDM should be done
at 24-28 weeks using a 2 hour 75 gram
OGTT. If there are other risk factors
identified, screening should proceed
immediately to 2 hour 75 gram OGTT at
first consult.
If the OGTT at 24-28 weeks is normal, the
woman should be re-tested at 32 weeks or
earlier if clinical signs and symptoms of
hyperglycemia are present both in the
mother and the fetus (e.g. polyphagia,
polyhdramnios, accelerated fetal growth,
etc)
OGTT should be performed in the morning
after an overnight fast of 8 hours following
the general instructions for the test.

Observe and overnight fast (at least 8


hours, but no more than 14 hours) prior
to testing.

Have an unrestricted diet (> 150 grams


of carbohydrates per day) for at least 3
days prior to the testing

Remain seated and should not smoke


during the test.
High Risk Pregnancies.

3. Subsequent prenatal visits


A. Prenatal Visits

Traditional: every 4 weeks until 28 weeks, every 2


weeks until 36 weeks, every week until term.
High-risk every week or as indicated.

WHO Model consists of a mean of 5 visits: once in


first trimester to screen for risk factors, then at 26,
32 and 38 weeks.
B. Prenatal Surveillance

Fetal surveillance: heart rate, size (current & rate


of change), amniotic fluid, presenting part and
station (late in pregnancy), activity

Maternal surveillance:
o Vital signs: BP, weight
o Symptoms: headache, altered vision,
abdominal pain, nausea and vomiting,
bleeding, vaginal fluid leakage, dysuria
o Abdominal Exam: fundal height
o Vaginal exam: confirms presenting part &
station, pelvic capacity, and cervical
consistency, effacement and dilatation
C. Assessment of Gestational Age

Fundal height between 20 and 34 weeks, the


height of the uterine fundus measured in
centimeters correlates closely with gestational age
in weeks.

Ancillary tests: Gestational diabetes, chlamydial


infection, gonococcal infection, fetal fibronectin
(vaginal fluid), GBS infection, genetic diseases.

Weight gain based on the BMI.

Category
Underwei
ght
Normal
Overweig
ht
Obese

BMI
(AsiaPacific)
<18.5

BMI
(ACOG)

Kilogra
ms

Pound
s

<19.8

28
40
25
35
15
25
11 20

18.5
24.9
25 29.9

19.8 26
26 - 29

12.5 18
11.5 16
7 11.5

>30

>29

5 9.1

III. Nutrition
Calories

Protein

Carbohydr
ates

Fats

Dietary
fiber

2000 calories/day + 300 kcal/day


(2nd & 3rd trimester)
9 grams/day
Protein deficiency may lead to
lowering of hemoglobin-producing
factors in the liver, which may result
in hypochromic anemia. Absorption of
calcium from intestinal tract may be
impaired.
Meats, mild and eggs are best
sources of protein.
150 grams/day in the first trimester.
225 grams/day at the end of
pregnancy.
50-100 grams/day according to FNRI
of the Philippines (1989) is sufficient
to prevent ketosis and other
symptoms of lack of dietary
carbohydrate.
Adequate carbohydrates seem to
lessen nausea and vomiting
15-25 grams/day
Most concentrated sources of energy,
providing more than twice the energy
value of an equivalent weight of
carbohydrates or protein.
No recommended level. Liberal intake
of fruits, vegetables and whole grain
cereals is highly recommended.
Promoting normal bowel functions
and bulk or satiety value to meals.
POSTPARTUM CHANGES

BREASTS & LACTATION


I. How breast milk protects babies against
infection. (DOH, 1991)
1. Breastfed babies have less diarrhea than
artificially-fed babies.
2. Fewer respiratory and middle ear infection.
3. Fewer infections because of the following:
a. Breast milk is clean and free of bacteria
b. Contains antibodies (immunoglobulin) to
many common infections, until he can make
his own antibodies.
c. Contains white blood cells to help fight
infection.
d. Contains bifidus factor which helps special
bacteria called Lactobacillus bifidus to grow
in the babys intestine. Lactobacillus bifidus
prevents other harmful bacteria from
growing and causing diarrhea.
e. Contains lactoferrin which binds iron.
Prevents the growth of some harmful
bacteria which need iron.
II. Other advantages of breastfeeding. (DOH,
1991)
1. Breast milk contains lipase which digests fat.
Breast milk is quickly and easily digested and a
breastfed baby may want to feed again more
quickly than an artificially-fed baby.
2. Breast milk is always ready to feed to the baby
and it needs no preparation.

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3.
4.
5.
6.
7.
8.

Breast milk never goes sour or bad in the breast


even if a woman does not feed her baby for
some days.
Breastfeeding helps to stop bleeding after
delivery.
Breastfeeding on demand helps to protect
against another pregnancy.
It helps them to bond, become attached to each
other and love each other.
It is free. You dont have to buy it.
It is exclusively for your baby and cannot be
served to other adults.

Protective Effects on Infants of Human Milk and


Breast Feeding (AAP, 1997)
Decreased
Possible protective
Incidence/Severity
effects
Diarrhea
Sudden infant death
Lower respiratory infection
syndrome
Otitis media
Type-1 Diabetes
Bacteremia
Inflammatory bowel
Bacterial meningitis
disease
Botulism
Lymphoma
Necrotizing enterocolitis
Allergies
Urinary infections
Chronic digestive
diseases
III. Composition of Human Breast
Component
Human milk
Water
Enough (87.2%
to 87.5%)
Bacterial
None
contamination
Anti-infection
Antibodies,
substances
leucocytes,
lactoferrin,
bifidus factor
Protein (Total)
1%
0.5%

Casein

lactalbumin 0.5%
Amino acids Enough for
Cysteine
growing brain
Enough

Taurine
Fats (Total)
4% average
Enough

Saturati
UNsaturated
on
Fatty acids
Enough for
linoleic acid
growing brain
(essential)
Enough

Cholesterol
Lipase to digest
Present
fat
Lactose (sugar)
7% (enough)
Salts (mEq/L)
Sodium

Chloride

Potassiu
m
Iron colostrum

Mature milk

6.5
12
14

Milk
Cow milk
More required
Likely
Antibodies not
active, absent
lactoferrin
4% too much
3% too much
0.5%
Not enough
Not present
4%
Too much
saturated
Not enough
Not enough

None
3% - 4% (not
enough)
25 (too much)
29 (too much)
35 (too much)

0.5 0.8 mg/L


0.2 0.3 mg/L

IV. Some Myths about Breastfeeding: (Thomson


Medical Center, Singapore. 2004)
1. It is painful & difficult to learn.
2. Breastfed babies cry more than bottle-fed
babies.
3. Breastfeeding tends to isolate mother and baby
from the rest of the family members.
4. It is embarrassing.
5. Spoils a baby and weaning is difficult.
6. Quality of breast milk depends on your mood.
7. Breastfeeding mother may have to give up food
she likes, become tied down and be unable to
work.
8. Breastfed babies need more water.
9. Breast milk lack iron.

V. How should breastfeeding begin. (DOH, 1991)


1. First feed

First feed should be on the delivery table.

Cover both mother and baby to keep them


warm.

Let the mother hold the baby close and let him
suck at the breast.

Sucking stimulates the production of oxytocin


which helps to deliver the placenta and stop
hemorrhage.

Baby gets valuable colostrums.

More likely to breastfeed for a long time. A


delay of even a few hours will result in failure
to breasfeed.
2. Rooming-in

There is no need for a mother and baby to rest


separately after a normal delivery.
3. Demand feeding

Let the mother pick up her baby and feed him


whenever he cries and she feels a need to feed
him.

Frequent sucking stimulates the production of


prolactin which helps the milk to come in
sooner.

It prevents engorgement of breasts.


4. Duration of feeds

More babies finish in 5-10 minutes, but some


like to take much longer, perhaps half an hour.
It does not matter.

Slow feeders take the same total amount of


milk as fast feeders.

Sucking in the wrong position causes sore


nipples.
5. Feeding from both breasts

Let the baby finish the first breast to make sure


that he gets the hindmilk. Let him take the
second breast if he wants to, but do not force
him.
6. Prelacteal feeds

Prelacteal feeds (e.g. formula, glucose water,


ampalaya juice, diluted honey) are NOT
necessary and they can be harmful.

Small amount of colostrum is ALL that a normal


baby needs at this time.
7. Extra water

Normal baby is born with a store of water which


keeps him well hydrated until the milk comes
in. He does not need drinks of water, they
interfere with breasfeeding.
8. Night breastfeeds

It is better if the mother breastfeeds the baby


at night as long as he wants to.

Night feeding helps to keep up the milk supply


because the baby sucks more.

Night feeds are especially useful for working


mothers.

Night feeds are important for child spacing.


9. Early weight changes

A baby may lose weight for the first few days


after delivery. He may lose up to 10% of his
birth weight.

When breastfeeding is started, the baby should


regain his birth weight in ten days.
10. Cleaning the breast

Frequent washing, especially with soap,


removes the natural oil from the nipple.

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The skin becomes dry and is more easily


damaged and fissured.

FAMILY PLANNING
Fertility Awareness-based (FAB) Methods

Family planning methods that attempt to identify


fertile time each cycle and then modify sexual
behavior.

Natural family planning (NFP) refers to sexual


abstinence during the fertile time.

Fertility awareness-combined methods (FACM)


refer to using barrier method during the fertile
time.

Various methods of periodic abstinence have


pregnancy rates estimated from 5 to 40 per 100
woman years. The unwanted pregnancy rate
during the first year of use is approximately 20%.
I.

II.

III.

Standard Days Method


Developed by the Institute for Reproductive Health
at Georgetown University
Avoid unprotected intercourse during cycle days 8
through 19.
Women must have regular monthly cycles of 26 to
32 days.
Cycle beads can be used to keep track of their
cycle.
Calendar Rhythm Method
Requires counting the number of days in the
shortest and longest menstrual cycle during a 6to 12-month span.
First fertile day 18 days are subtracted from the
shortest cycle.
Last fertile day 11 days are subtracted from the
longest cycle.
This is problematic because ovulation most often
occurs 14 days before the onset of the next
menses. This is not reliable.
Temperature Rhythm Method
The first scientific NFP method developed which
involves measuring changes in body temperature
after ovulation.
Immediately after ovulation, basal body
temperature, or the body temperature at complete
rest, dips slightly then rises by about 0.2 C to 0.5
C (0.4 F). It remains high until just before the next
period.
Follow a biphasic pattern, it remains low before
ovulation and higher after ovulation which is
caused by progesterone.
The woman has to take her temperature everyday,
upon waking up in the morning, before getting out
of bed, and after at least 3 hours of continuous
sleep.
She may take her temperature by mouth (under
the tongue) or by the axilla, but she has to use the
same route throughout the menstrual cycle. The
thermometer must be left in position for 5
minutes.
She must record it on a chart after taking it and
include other events like illness.
A coverline or baseline is drawn using the highest
temperature reading from day 6 to 10 of cycle and
watch out for 3 consecutive temperature readings
above the coverline which refers to the thermal or
temperature shift indicating that ovulation has
taken place.
The woman must abstain from intercourse from
the first day of menses through the 3rd day after
the increase in temperature.
With excellent compliance, the unwanted
pregnancy is approximately 2 percent the first
year.

IV.

V.

Cervical Mucus Rhythm Method


Also called Billings method, developed by John
Billings, depends on awareness of vaginal
dryness and wetness.
These are the consequences of changes in the
amount and quality of cervical mucus at different
times in the menstrual cycle.
The fertile mucus is brought about byt increasing
levels of estrogen and the infertile mucus by the
increase in progesterone.
Dry days after the menses are the indicators of
the preovulatory phase or the first infertile phase,
which are relatively infertile days.
Wet days signal the ovulatory phase and are
therefore fertile days. The fertile type mucus is
more copious, slippery/lubricative, stretchy and
wet. At times, it has the appearance of raw egg
white. This mucus makes it easy for the sperm to
travel through the cervix, uterus and the tubes to
meet the egg.
Last day of the wetness is called the peak day. Its
timing is around ovulation time. The 3 days after
the peak day or the post-peak days are still
considered fertile days, giving allowance for the
life span of the egg.
Ovulatory phase includes all days when the wet
sensation is first felt, including the Peak Day and
the 3 post-Peak days.
Abstinence is required from the beginning of
menses until 4 days after slippery mucus is
identified.
When used accurately, the first-year failure rate is
approximately 3 percent.
Symptothermal Method
Combines the use of changes in cervical mucus
onset of fertile period, changes in basal body
temperature end of fertile period, and
calculations to estimate the time of ovulation.
One also has to look out for other bodily changes
such as:
i. Feel and position of the cervix
1. Fertile: the cervix is far from the vaginal
opening and is open and softer
(consistency of the lips)
2. Not fertile: cervix is closed, firm (tip of the
nose) and close to the vulva
ii. Ovulation pain (Mittelschmerz)
iii. Mid-cycle bleeding or spotting
iv. Breast sensitivity
v. Skin changes
vi. Mood changes
To avoid pregnancy, the couple abstains from
vaginal intercourse on:
i. Alternate preovulatory days of no mucus or
dry mucus
ii. On all days of wet mucus
iii. The four days after the last day of wet mucus,
or the third day after temperature rise.

Contraceptive Failure Rates During the First


Year of Use
(Modified from Speroff and Darney, 2001, and
Trussell, 2004)
Method
Perfect Use
Typical Use
None
85
85
Calendar
9
20
Ovulation
3
Symptothermal
2
Post-ovulation
1
Withdrawal
4
27

Hormonal Contraceptives
I.
Combination hormonal contraceptives.
A. Mechanism of Action

Prevent ovulation by suppression of


hypothalamic gonodotropin releasing
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factors. Thus, prevents pituitary secretion
of FSH and LH.

Progestins action:
i. Prevent ovulation by suppressing
LH
ii. Thicken cervical mucus, thereby
retarding sperm passage.
iii. Render the endometrium
unfavourable for implantation.

Estrogen action:
1. Prevents ovulation by suppressing
FSH release.
2. Stabilizes the endometrium, which
prevents intermenstrual bleeding
also known as breakthrough
bleeding.
B. Composition

Monophasic pills progestin dose remains


constant throughout the cycle.

Multiphasic (bi-, tri- or quadriphasic) pills


dose frequently varied depending on the
number of dose changes within the cycle.
Some formulations, estrogen dose also
varies.

ESTROGEN
o Features:

Daily estrogen content varies from


10 to 50 ug of ethinyl estradiol,
and most contain 35 ug or less to
minimize adverse effects.
o Forms:
1. Ethinyl estradiol most common
2. Mestranol
3. Estradiol valerate
o

Side effects:
1. Breast tenderness
2. Fluid retention
3. Weight gain
4. Nausea
5. Headache

PROGESTIN
o Features:

Structurally related to
progesterone, testosterone, or
spironolactone

Binds variably to progesterone,


androgen, estrogen,
glucocorticoid, and
mineralocorticoid receptors which
explain pill-related side effects

Progestin related to testosterone


may impart androgenic side
effects such as acne and adverse
HDL and LDL levels.
o Forms:
1. Medroxyprogesterone acetate
mainly used in a progestin-only
injectable form
2. Nomegestrol acetate used in a
COC
3. Norethindrone acetate used in a
COC; non-acetate form used as
progestin-only
4. Norgestrel
5. Norgestimate
6. Ethynodiol diacetate
7. Levonorgestrel
8. Desogestrel
9. Dienogest
10. Drospirenone

Structurally similar to
spironolactone and have similar
effects to 25 mg of this diuretic
hormone.

Displays antiadrogenic
activities

Provides antialdosterone action


to minimize water retention

Antimineralocorticoid properties
that may cause potassium
retention and hyperkalemia.
Serum potassium level
monitoring for the first month is
recommended. Likeswise for
the following drugs:
NSAIDS, ACE inhibitors,
angiotensin II antagonists,
herparin, aldosterone
antagonists, and
potassium-sparing
diuretics.

Avoided in women with renal or


adrenal insufficiency or with
hepatic dysfunction.
o PROGESTIN-ONLY side effects:

Irregular uterine bleeding, such as


metrorhhagia or menorrhagia
(most frequently reported)

DO NOT significantly affect lipid


metabolism, glucose level,
hemostatic factors, liver function,
thyroid function, and blood
pressure.

NOT shown to increase risk for


thromboembolism, stroke, or CV
disease.

DMPA use shows increased LDL


and decreased HDL and may be
less favorable with cardiac or
vascular risks.

DO NOT impair mild production

NO increased risk of genital tract


or breast neoplasia

Weight gain and bone mineral


density loss are not prominent,
except for DMPA

Functional ovarian cysts develop


with greater frequency.
C. Administration

COCs are taken daily some for 21 days


with 7 pill-free interval or placebo.

Some provide 24 days of hormones


followed by 4 pill-free days (e.g. Yaz).

Ideally, women should begin on the first


day of a menstrual cycle.

There is a quick start method, wherein


the pills are started on ANY DAY,
regardless of cycle timing. A back-up
method is used during the first week. If the
woman is already pregnant during Quick
Start initiation, COCs ARE NOT
TERATOGENIC.

For maximum efficiency, pills should be


taken at the same time each day.

Spotting or bleeding is common with


initiation of COCs. It does not reflect
contraceptive failure and typically resolves
within one to three cycles.
D. Method-specific effects

Altered Drug Efficacy


o Three (3) groups of drugs that decrease
COC effectiveness:
1. Anti-TB drugs: rifampin and rifabutin
2. Anti-HIV drugs: efavirenz and
ritonavir-boosted protease inhibitors
3. Anticonvulsants: phytoin (Dilantin),
carbamazepine (Tegretol),
oxcarbazepine (Trileptal),

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barbiturates, primidone, and


topiramate (Topamax)
Metabolic changes
o COCs increase serum levels of
triglycerides and total cholesterol.
o Estrogen decreases LDL
o Estrogen increases HDL and VLDL
o OCP are NOT atherogenic
o Women with LDL >160 mg/dl or with
multiple additional risk factors for CV
disease, alternative methods are
recommended.
o Estrogen use related to increase in
fibrinogen and may of the clotting
factor levels and may lead to
thrombosis.
o COCs augment angiotensinogen
production and its conversion by renin
to angiotensin I which may be
associated with pill-induced
hypertension
o COCs increase SHBG which decrease
bioavailable testosterone
concentrations and improve androgenic
side effects.
o Risk of developing diabetes is NOT
increased.
o NO connection beteween COCs and
weight gain.
o OCP use related to elevated total
plasma thyroxine (T4) and thyroidbinding proteins
Cardiovascular effects
o Women using low-dose COCs
formulations rarely develop clinically
significant hypertension.
o Patients are advised to return 8 to 12
weeks after COC initiation for
evaluation of blood pressure and other
symptoms.
o COCs are permissible in women with
well-controlled uncomplicated
hypertension who are non-smokers,
otherwise healthy, and younger than
35.
o COCs use are NOT advisable for those
with severe forms of hypertension,
especially with end-organ involvement.
o Women with prior stroke or myocardial
infaction, COCs should NOT be
considered.
o Nonsmoking women younger than 35
years old has and extremely low risk of
ischemic and hemorrhagic strokes.
o COCs may be considered for women
with migraines that lack focal
neurological signs if they are otherwise
healthy, normotensive nonsmkers
younger than 35 years.
o VTE with COC use is only 3 to 4 per
10,000 woman-years and is lower than
the incidence of 5 to 6 per 10,000
woman-years estimated for pregnancy.
o Clinical factors that increase VTE with
COC use:

Thrombophilias

Hypertension

Obesity

Diabetes

Smoking

Sedentary lifestyle
o COCs are NOT recommended for
women within the first 4 weeks after
delivery.

E.

For all women, VTE risk with


drospirenone-containing COCs has been
shown.

Neoplasia
o Overall, COCs are not associated with
an increased risk for cancer.
o Protective effect against ovarian and
endometrial cancer
o Relative risk of cervical dysplasia and
cervical cancer is increased in current
COC users, but following 10 or more
years of disuse, risk returns to that of
never users.
o No evidence for increased risk of
hepatocellular cancer.
o Women with known tumores, COCs are
AVOIDED in those with benign hepatic
adenoma and hepatocellular
carcinoma.
o Women who are carriers of the BRCA1
and BRCA2 gene mutation, risks for
breast cancer are NOT INCREASED by
COC use.
o COCs appear to lower rates of benign
breast disease.

Non-contraceptive benefits of COCs


1. Increased bone density
2. Reduced menstrual blood loss and anemia
3. Decreased risk for ectopic pregnancy
4. Improved dysmenorrhea from endometriosis
5. Fewer premenstrual complaints
6. Decreased risk of endometrial and ovarian
cancer
7. Reduction in various benign breast diseases
8. Inhibition of hirsutism progression
9. Improvement of acne
10. Prevention of atherogenesis
11. Decreased incidence and severity of acute
salpingitis
12. Decreased activity of rheumatoid arthritis

II.

Injectable Progestin Contraceptives

Intramuscular depot medroxyprogesteron


acetate (Depo-Provera or Depo-Trust), 150 mg
every 3 months, injected into the deltoid or
gluteus muscle.

Mechanisms of action: ovulation inhibition,


increased cervical mucus viscosity, and
creation of an endometrium unfavourable for
ovum implantation.

Initial injection should begin within the first 5


days following menses onset. No back-up
contraceptive is required if initiated within 5
days of menses onset.

III.

Implants

Etonogestrel implant
o Thin, pliable progestin-containing cylinders
that are implanted subdermally and release
hormone over many years.
o Implanon

Single-rod implant with 68 mg of


etonogestrel covered by an ethylene
vinyl acetate copolymer cover.

Implant is placed subdermally on the


medial surface of the upper arm 8 to 10
cm from the elbow in the biceps groove
and aligned with the long axis of the
arm.

Provides contraception for 3 years and


then replaced at the same site or in the
opposite arm.

Method-specific adverse effects

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o

o
o

Branches of the medial antebrachial


cutaneous nerve can be injured if the
implant or insertion needle is placed too
deeply or if exploration for a lost implant is
aggressive.
Numbness and paresthesia over the
anteromedial aspect of the forearm
Nonpalpable devices may require
radiological imaging for localization

Insertion timing
o Etonogestrel implant: Ideally inserted within
5 days of menses. If inserted later in the
cycle, alternative contraception is
recommended for 7 days following
placement.
o Levonogestrel implant: Contraception is
established within 24 hours if inserted
within the first 7 days of the menstrual
cycle.
o Transitioning methods:

On the day of the first placebo COC pill

On the day of the next DMPA injection

Within 24 hours of taking the last POP


o Inserted before discharge following delivery,
miscarriage, or abortion

Intrauterine devices (IUD)

IUD are use and forget effective reversible


contraceptive methods that do not have to be
replaced for 5 or 10 years, depending on the
brand.

It is now better established that the major actions


of IUDs are contraceptive, NOT abortifacient.

Risk of pelvic infections is markedly reduced with


the currently used monofilament string and with
techniques to ensure safer insertion.

Risk of an associated ectopic pregnancy has been


clarified. Specifically, the contraceptive effect
decreases the absolute number of ectopic
pregnancies by approximately 50% compared with
that of women not using contraception. With
failure, pregnancy is more likely to be ectopic.

Within the uterus, an intense local endometrial


inflammatory response in induced, especially by
copper-containing devices. Cellular and humoral
components of this inflammation are expressed in
endometrial tissue and in fluid filling the uterine
cavity and fallopian tubes. These lead to
decreased sperm and egg viability.

With the LBG-IUS, in addition to an inflammatory


reaction, progestin release in long-term users
causes glandular atrophy and stromal
decidualization. Progestins create scant viscous
cervical mucus that hinders sperm motility.

4.

Need for transfusion.

Problems with the above definitions:


1. Clinical estimation of blood loss is frequently
inaccurate and the brisk nature of blood loss
during delivery or the presence of amniotic fluid
can make this more difficult.
2. Delay in obtaining laboratory results. Information
from laboratory tests would not reflect the
patients current hemodynamic status.
3. Any definition based on the need for transfusion is
difficult as there are differences in provider
practice patterns regarding transfusion.
Definition of obstetric hemorrhage combining
clinical and objective data (Bonnar, 2000)
Systoli
Blood
Hear
EBL
c BP
Signs &
volum
t
(ml)
(mmHg symptoms
e (%)
rate
)
500<10
10-15
Normal
None
1000
0
1000
Slight
Vasoconstrictio
100-150
15-25
decreas
n, weakness,
120
0
e
sweating
1500
120Restlessness,
25-35
80-100
140
pallor, oliguria
2000
2000
>14
Anuria, altered
35-45
60-80
0
consciousness
3000
Etiology and Risk Factors
Etiology
Pathophysiology
Overdistended
uterus

TONE
(Abnormal
uterine
contractilit
y)

TISSUE
(Retained
products
of
conception
)

Uterine
distortion/abnorma
lity

Accreta/Increta/Per
creta
Retained
placenta/membran
es

Laceration of the
cervix, vagina or
perineum

Surgical Methods

Tubal ligation

Vasectomy

Definition
The following are suggested definitions but there is a
lack of agreement on what constitutes excessive blood
loss:
1. Blood loss >500 ml for vaginal delivery and 1,000
ml for cesarean section (CS).
2. Blood loss >500 ml in the first 24 hours following
delivery.
3. Ten percent (10%) decrease in hemoglobin or
hematocrit level.

Chorioamnionitis

Uterine relaxing
drugs

Barrier Methods

Male Condoms

Diaphragm

POST-PARTUM HEMORRHAGE (PPH)

Uterine muscle
fatigue

TRAUMA
(Genital
tract
trauma)

Extension/lacerati
on at CS
Uterine rupture

Uterine inversion
THROMBIN
(Abnormali

Preexisting
clotting

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Risk Factors
Multiple gestation
Polyhydramnios
Macrosomia
Prolonged labor
Augmented labor
Prior PPH
Prolonged rupture
of membranes
(ROM)
Fibroids (myoma),
placenta previa
B-mimetics,
MgSO4,
anesthetic drugs
Prior uterine
surgery
Placenta previa
Multiparity
Manual placenta
removal
Succinturiate/acc
essory lobe
Precipitous
delivery
Macrosomia
Shoulder dystocia
Operative
delivery
Episiotomy (e.g.
mediolateral)
Deep
engagement
Malposition
Malpresentation
Prior uterine
surgery
Fundal placenta
Grand multiparity
Excessive
traction on
umbilical cord
History of
Coagulopathy or
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ties of
coagulatio
n)

abnormalities (e.g.
hemophilia,
vonWillebrands
disease,
hypofibrinogenemi
a)
DIC
HELLP
Anticoagulation

liver disease

Sepsis
Intrauterine
demise
Hemorrhage

General Management of PPH:


1. Initial management approach to obstetric
hemorrhage:
a. Assessment: constant awareness of the
hemodynamic status as well as evaluation to
determine the cause of bleeding.
b. Breathing: administration of oxygen
c. Circulation: obtaining intravenous (IV) access
and adequate circulating blood volume through
infusion of crystalloid and blood products.
Second large-bore IV catheter is needed
2. Notify the blood bank.
3. Simultaneous, coordinated, multi-disciplinary
management (OB-GYN, anesthesiologist,
hematologists, radiologists, nurses, laboratory and
blood bank technicians) to concur timely
management in the presence of obstetric
hemorrhage.
4. Preoperative preparedness is important especially
for patients identified as high risk.
Important Causes of PPH:
1. Uterine atony
2. Retained placenta
3. Uterine rupture
4. Genital tract trauma
5. Uterine inversion

DYSTOCIA
DYSTOCIA: PROBLEMS IN PASSENGER
Fetal Presentations and Conditions
1. Breech
2. External cephalic version
3. POP, OT
4. Brow and Face
5. Transverse/Oblique
6. Compound
7. Macrosomia
8. Shoulder dystocia
1. Breech

Planned CS has reduced risk for perinatal or


neonatal death/morbidity

Planned vaginal breech criteria:


o Skilled OB
o Facilities for possible CS available
o Woman is informed of risks
o EFW: 2500g to 4000g
o Continuous EFM
o Induction is NOT recommended. Oxytocin
augmentation if with hypotonic uterine
dysfunction.
o Passive 2nd stage without active pushing for
90 min allowing breech to descend into pelvis
o Once active pusching commences and
delivery not imminent after 60 min, CS is
recommended.

Delivery of the aftercoming head:


o assistant should apply suprapubic pressure to
favor flexion and engagement of fetal head
o Mauriceau-Smellie-Veit maneuver, or
o Use of Piper forceps

Spontaneous or assisted breech delivery is


acceptable. Fetal manipulation applied after
spontaneous delivery to the level of umbilicus.
Nuchal arms may be reduced by Lovset
maneuver.

Suspected breech
o Pre- or early labor ultrasound to assess type of
breech, fetal growth, EFW, attitude of fetal
head.
o If ultrasound is not available, CS is
recommended.
2. External cephalic version

ABSOLUTE Contraindications
o Where CS is required
o Anterpartum bleeding within the last 7 days
o Abnormal CTG
o Major uterine anomaly
o Ruptured membranes
o Multiple pregnancy (except delivery of the 2nd
twin)

RELATIVE Contraindications
o SGA fetus with abnormal Doppler
o Proteinuric preeclampsia
o Oligohydramnios
o Major fetal anomalies
o Scarred uterus
o Unstable lie

Manipulation of the fetus through the maternal


abdomen to a cephalic presentation.

Use of tocolysis with beta sympathomimetics may


increase success rate of ECV
3. POP, OT

Factors for incomplete rotation of fetal head:


o Poor contractions
o Faulty flexion of head
o Epidural anesthesia diminishes abdominal
muscular pushing & relaxes pelvic floor

Digital rotation of the fetus in the OP position.


4. Brow and Face
Brow
Expectant management, as long as FHR remains
reassuring and dilatation and descent are progressing
normally.
Face

Continuous EFM is mandatory because of increased


incidence of abnormal FHR patterns and/or fetal
compromise

Oxytocin can be used to augment labor using the


same precautions

Forceps, using Kielland forceps, may be used if the


mentum is anterior.
5. Transverse/Oblique
Both will benefit from a trial of version to cephalic
presentation following the criteria & recommendation
of ECV for breech.
6. Compound

If the hand has not prolapsed beyond the


presenting part, causing the hand to retract often
is accomplished. It can be ignored as long as labor
is progressing normally

If the hand or arm has prolapsed past the


presenting part, CS delivery is wise.
7. Macrosomia

Macrosomia: 4000 g (8 lb 13 oz) or 4500 g (9 lb 4


oz)

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Labor & vaginal delivery is NOT


CONTRAINDICATED for women with EFW up to 5 kg
in the absence of maternal DM
Indication for CS:
o >4,500 g, and
o prolonged 2nd stage or arrest of descent in 2nd
stage
Prophylactic CS:
o EFW > 5,000 g (w/o maternal DM)
o EFW > 4,500 g (w/ maternal DM)
Suspected macrosomia is NOT a contraindication
to attempted VBAC

8. Shoulder Dystocia
Shouder Dystocia Drill:
1. Call for HELP!
2. Generous EPISIOTOMY
3. SUPRAPUBIC pressure
4. McRoberts maneuver
If the Drill fails, attempt the following:
1. Delivery of posterior arm
2. Woods screw maneuver
3. Rubin maneuver
4. Zavanelli maneuver
5. Cleidotomy
6. Symphysiotomy
(supplementary)
Shoulder dystocia drill to better organize
emergency management:
1.

Call for helpmobilize assistants and anesthesia


and pediat- ric personnel. Initially, a gentle
attempt at traction is made. Drain the bladder if it
is distended.
2. A generous episiotomy may be desired to afford
room posteriorly.
3. Suprapubic pressure is used initially by most
practitioners because it has the advantage of
simplicity. Only one assis- tant is needed to provide
suprapubic pressure, while normal downward
traction is applied to the fetal head.
4. The McRoberts maneuver requires two
assistants. Each assistant grasps a leg and sharply
flexes the maternal thigh against the abdomen.
This is thesingle most effective intervention
and performed first.
These maneuvers will resolve most cases of shoulder
dystocia. If the above listed steps fail, the following
steps may be attempted, and any of the maneuvers
may be repeated:
5. Delivery of the posterior arm is attempted. With a
fully extended arm, however, this is usually
difficult to accomplish.
6. Woods screw maneuver is applied. Progressively
rotating the posterior shoulder 180 degrees in a
corkscrew fashion, the impacted anterior shoulder
could be released.
7. Rubin maneuver is attempted.

First, the fetal shoulders are rocked from side to


side by applying force to the maternal abdomen.

If this is not successful, the pelvic hand reaches


the most easily accessible fetal shoulder, which is
then pushed toward the anterior surface of the
chest. This maneuver most often abducts both
shoulders, which in turn produces a smaller
shoulder-to-shoulder diameter. This permits
displacement of the anterior shoulder from behind
the symphysis.

Other maneuvers:
o Zavanelli maneuver replaces or flexes the
fetal head back into the vagina, then CS is
performed.

o
o

Cleidotomy deliberate fracture of the


anterior clavicle to fee the shoulder
impaction.
Symphysiotomy intervening symphyseal
cartilage and much of its ligamentous support
is cut to widen the symphysis pubis

GUIDELINES FOR CESAREAN SECTION


Indications
1. Previous uterine scar
2. Abnormalities of the reproductive tract
3. Abnormalities of placenta, cord, membranes & AF
4. Infection in pregnancy
5. Maternal medical conditions
6. IUGR/FGR
7. Fetal congenital anomalies
8. CDMR (Maternal request)
1. Previous uterine scar

In the presence of scarred uterus, the following


are ABSOLUTE INDICATIONS for elective CS: (Level
III, Grade C)
o Previous classical or inverted T-uterine scar
o Uncertainty of type of previous CS scar
o Previous multiple low transverse segment
uterine scars
o Previous hysterotomy or myomectomy
entering the uterine cavity or extensive
transfundal uterine surgery
o Previous uterine rupture
o Presence of a contraindication to labor, such
as placenta previa/accreta, or
malpresentation
o No informed consent for VBAC

Failed trial of labor during VBAC.


2. Abnormalities of the reproductive tract

Presence of gynecologic tumors in pregnancy,


such as uterine myoma and/or adnexal masses,
are NOT ABSOLUTE indications for CS, unless they
cause dystocia

CS performed for those with a history of surgical


repair of obstetric and anal sphincters,
urinary incontinence and pelvic organ
prolapse because of risk of recurrences

Genital warts and genital cancers may be an


indication for CS if it obstructs the birth canal, or if
it is excessively bleeding, or in order to prevent
profuse bleeding

Presence of cervical stenosis is NOT A


CONTRAINDICATION to attempted vaginal delivery.
There is increased risk for CS.

Vaginal delivery for corrected imperforate hymen.

CS performed for those with history of complete


transverse vaginal septum and vaginal
agenesis due to risk of vaginal soft tissue
dystocia and lateral vault laceration
3. Abnormalities of the placenta, cord,
membranes and amniotic fluid

Vasa previa
o Elective CS between 35-37 weeks AOG
o Emergency CS for bleeding vasa previa

Placenta previa
o Any degree of placental overlap (>0 mm) at
the internal os after 35 weeks is an indication
for CS
o Previa within 1 cm of the internal os is an
indication for CS
o Elective CS for asymptomatic woman with
previa >37 weeks and for suspected accreta
>36 weeks

Abruptio placenta
o Emergency CS for abruptio placenta with fetal
compromise, severe uterine hyprtonus, life

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threatening bleeding or DIC, and remote from


vaginal delivery.
Cord prolapse
o Emergency CS for cord prolapse
o Cord prolapse with poor chances of viability,
vaginal delivery may be tried with informed
consent
o Ultrasound finding suggestive of forelying
cord or funic presentation is NOT an absolute
indication for CS
o Digital diagnosis of funic/cord presentation in
labor is an indication for CS
Chorioamnionitis or intra-amniotic infection
o Presence of clinical chorioamnionitis or intraamniotic infection is NOT an absolute
indication for CS.
Oligohydramnios
o Uncomplicated oligohydramnios is NOT an
absolute indication for CS

4. Infection in pregnancy

Herpes simplex virus


o CS for those who develop primary genital
herpes within 6 weeks of delivery
o CS for those with active genital lesions or
prodromal symptoms (e.g. vulvar pain or
burning) at the time of delivery

Hepatitis B virus
o Scheduled CS at 39 weeks with HBV profile as
follows:

HbeAg positive

HBV DNA copies >1,000,000

Not received oral antiretroviral therapy

Human papilloma virus


o Only for those with very large genital
warts causing pelvic outlet obstruction or
potential for excessive bleeding during
vaginal delivery

HIV
o Elective CS at 39 weeks to reduce risk of
MTCT provided:

Currently on highly active antiretroviral


therapy (HAART)

Viral load <400 copies/ml

On any ARV with viral load <50 copies/ml


5. Maternal medical conditions

Hypertensive complications
o Maternal indications

Deteriorating maternal condition

Uncontrolled hypertension despite drug


therapy

HELLP syndrome

Placental abruptio
o Fetal indications

Severe IUGR/FGR

Non-reassuring FHR pattern, repeated


Category II or III, refractory with
resuscitation, remote from delivery

BPP <4, done 6 hours apart

Doppler studies: ARED

Severe bronchial asthma


o CS is rarely needed.

Cardiac disease
o CS reserved for high-risk cardiac patients.

Gestational DM

Obesity
o Increased risk for CS

Macrosomia
6. IUGR/FGR

Deterioration in the fetal condition or when there


is an unripe cervix or when there are indications of
additional fetal compromise during labor

Viable fetus with IUGR when there is:

o
o
o
o

deterioration in the BPP


loss of variability on NST
severe oligohydramnios, and
failure to grow on serial biometry in the
presence of abnormal umbilical artery or
venous Doppler studies.

7. Fetal congenital anomalies

Fetuses with the following anomalies may benefit


from CS:
o Neural tube defects with fetus in breech
o Neural tube defects with sac >6 cm
o Cystic hygromas
o Sacrococcygeal teratomas >5 cm
o Hydrocephalus with BPD >10 cm or HC >36
cm

Elective CS
o Fetus with hypoplastic left heart syndrome
o Transposition of great arteries with intact
intraventricular septum that require urgent
neonatal atrial septostomy
8. Maternal request (CDMR)

If without clear indication or there is fear of


childbirth, the OB should provide counseling to
the patient.

Well-written informed consent with proper


approval by the hospitals ethics committee
should be secured before performing the CS.

Should be performed >39 weeks AOG, unless


there is documentation of fetal lung maturity.
9. Multiple pregnancy
10. Fetal malpresentation (Refer to Section III)
11. Abnormal labor patterns (Refer to Section II)
12. Abnormal FHR patterns (Refer to Section I)
Operative Recommendations
Timing of planned CS

Scheduled at 39 weeks
Pre-operative preparation for CS

Hemoglobin determination

Antimicrobial prophylaxis within 60 minutes preoperatively with either penicillins or


cephalosporins (1st or 2nd gen) Cefazolin 2g/IV (1st
gen), Cefuroxime 1.5 g/IV (2nd gen)

Alternative (if allergic): Clindamycin 600 mg/SIV

Morbid obese (BMI>35): double dose of antibiotic

Routine shaving not recommended. Clippers are


recommended than razors for excessive hair.
Techniques of CS

Transverse abdominal incision or Joel-Cohen


incision is preferred.

Placental delivery by controlled cord traction


rather than manual extraction

Blunt dissection of uterus was associated with


reduced mean blood loss compared to sharp
dissection.

Single layer closure was associated with


significant reduction in mean blood loss, duration
of operative time, post-operative pain but more
likely to result in uterine rupture.

Closure of both visceral and parietal


peritoneum after CS lead to LESS adhesions

Closure of subcutaneous tissue for >2 cm


subcutaneous fat.

Indwelling FC may be removed <24 hours after


CS
Anesthesia in CS

Uncomplicated elective CS may have modest


amounts of clear liquids up to 2 hours prior to
induction of anesthesia

Patient undergoing elective surgery should have a


fasting period for solids at least 6-8 hours prior to
induction.

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Aspiration prophylaxis: non-particulate antacids,


H2 receptor antagonists, metoclopramide
Post-CS care

No evidence to recommend a policy of delaying


oral fluids and food after CS

Remove the dressing 24 hours after the CS.

No evidence of adverse outcomes associated with


early postnatal discharge (3-4 days)

Sexual intercourse may be resumed as early as 2


weeks postpartum for as long as the patient feels
comfortable.

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Page 33 of 33