Placenta and Placental Hormones: PDV
The Ovarian & Endometrial Cycle
Menstruation
- Process of endometrial tissue shedding with
hemorrhage that is dependent on sex
steroid hormone-directed changes in blood
flow in the spiral arteries
- Monthly shedding of the lining of the
endometrium
- Desquamation of the endometrium
purpose of which is to form a new growth of
the endometrial layer in preparation for
pregnancy
Spiral arteries
- Found in the functionalis layer
- Terminal branches of uterine artery
- Main arteries which are involved in the
changes that happen during pregnancy
- are insterspersed in the myometrium
After delivery, myometrium has to
compress or contract to tighten the
interspersed spiral artery to prevent
postpartum bleeding
Uterine artery
- Comes from the internal iliac artery/
hypogastric artery
- Supply the lateral portions of the uterus
Hypogastric artery
- Branch of common iliac artery
Common iliac artery
- Branch of abdominal artery
Ovarian artery
- Supply the fundal portion of the uterus
The uterus must be properly nourished and
supplied with a lot of vasculature because it
needs a lot of these blood vessels to supply
with the necessary blood at the time of
pregnancy.
This is also associated with changes with
regards to malignancy wherein its spread
has something to do with the vasculature
supplying the uterus
Upper third of the posterior wall of the uterus/
decidua
- blastocyst implant after it has undergone
changes from fertilization
Decidua
- Endometrium of the pregnancy
Normal menstrual cycle: 28 days
It is important to identify which part of this cycle
would belong to the first or second part because
this would give us the idea when to suggest to
the patient when they are likely ovulating or
when is their best chance of getting pregnant
The Ovarian & Endometrial Cycle
- Complex interaction:
Hypothalamus-pituitary axis
Ovaries
Genital Tract
The hypothalamus would have to secrete GnRH
to stimulate the pituitary gland to produce FSH
and LH
FSH and LH would have its effect over the
ovaries for it to secrete estrogen and
progesterone
Estrogen and progesterone would then have its
consequent effect over the endometrium
There is no direct effect on the endometrium
since it does not have the receptors for estrogen
& progesterone the stimulation would have to
come from the ovaries
- Average cycle: 28 days
- Range: 21 to 25 days (<21 and >35
considered abnormal)
- Duration: 2-6 days (1 day bleeding and 10
days bleeding considered abnormal
uterine bleeding
- Amount: 20-60 ml (<20ml and >60ml
abnormal)
Quantify the amount by number of
pads used
Qualify the type of pad used
Follicle Stimulating Hormone (FSH)
- Responsible for feeding the growing follicle
for more estrogenized effect happening to
the follicle during the first part of the cycle
After the follicles grows too much, there will
be a negative feedback to the hypothalamus
to stop production of GnRH
LH will now increase to facilitate ovulation
Ovulation primary purpose is to expel the
ovum inside the mature follicle
Problems affecting the hypothalamus and
pituitary gland would have its effect on the
end organ causing irregular bleeding (ex.
Amenorrhea)
Strenuous activities GnRH FSH
e rogen leads to unovulatory cycles
Overweight patients e rogen d e o
increased peripheral conversion of
androstenedione in the adipose cells to
estrone contributing to the thickening of the
lining of the uterus unovulatory menses
Stress causes abnormal/ Irregular
menstruations
Ovarian Cycle
- 2 phases:
Follicular (preovulatory) formation/
growth of follicle
Luteal (postovulatory) ovum is
being readies to be expelled from
the mature follicle in preparation for
the meeting with the sperm
From the time we have been conceived in
utero, at 20 weeks 6-7 million oocytes
formed
These oocytes undergo degeneration,
atresia/ follicular atresia
At birth 1-2million oocytes left
Puberty 300,000available for ovulation
Only 400-500 will be released for ovulation
Follicular phase
- Recruitment of the follicles from the resting
pool after which a cohort if formed
- Growth to the antral stage cohort
- From the cohort, the meanest of the follicles
would have to survive the effects of FSH
selected graafian follicle/mature follicle
Graafian follicle contains the egg
to be extruded
1

- These changes undergo two cell-two
gonadotropin theory
Formation of progesterone happens
when this is inside the thecal cells
In the presence of LH in the thecal
cells, C19 steroids are converted
into cholesterol
Cholesterol converted into
androstenedione which crosses the
basement membrane
With the action of FSH attaching to
a receptor in the granulosa cell part
in the presence of cAMP,
androstenedione is converted to
estrone
Estrone converted to the potent
17 - estradiol
17 - estradiol goes out of the
granulosa cell and have its effect on
the endometrium
TAKE NOTE: Theca cells LH
(True Love)
Granulosa cells
FSH (Girl Friend)
- Follicle must be ready for ovulation to
happen
Ovulation
- Onset of gonadotropin surge 34-46 hours
before ovulation
- Peak of LH 10-12 hours before ovulation
Ovulatory kit recognizes the high
level of LH which indicates ovulation
- In the presence of progesterone and
prostaglandins, a stigma happens over the
wall of the graafian follicle weak portion
ruptures release of oocyte-cumulus
complex
Graafian follicle contains fluid
noted on ultrasound as fluid in the
cul de sac indicates ovulation
- Symptomatic indications:
breast tenderness due to
hormone stimulation
pain in hypogastric area due to
fluid coming out from the follicle
that irritates the peritoneal cavity
Luteal Phase
- primarily responsible for the formation of the
corpus luteum
corpus luteum produces
progesterone
- proge erone, e rogen
- If no pregnanct happens, corpus luteum
regresses and menstruation happens
- Responsible for luteinization and
neovascularization edematous
endometrial lining to have the necessary
stroma for the implantation of the blastocyst
Vascular endothelial growth factor
responsible for neovascularization
- Lifespan is dependent on the presence of
LH and HCG
During pregnancy corpus luteum
is maintained continuous
production of progesterone
pregnancy goes on until term
Placenta takes over production of
progesterone after 8-12 weeks
No pregnancy corpus luteum
regresses 9-11 days after ovulation
Placenta and Placental Hormones: PDV
due to decrease LH and decreased
LH sensitivity of luteal cells
Estrogen
- 17 - estradiol Most biologically potent
- Secreted by the granulosa cells coming from
the dominant follicle and the luteinized
granulosa cells of the corpus luteum
- Has 2 receptors:
E rogen recep or (ER )
responsible for most of the changes
in the endometrium
E rogen recep or (ER ) glands
and stroma
- Roles:
Synthesis of proteins from receptor-
specific gene transcription
At the cell surface: stimulate nitric
acid production in endothelial cells
Replication of the endometrium
Progesterone
- Predominant hormone in the luteal phase
- Mediated through nuclear hormonal
receptors
- 2 receptors:
Proge erone recep or
Proge erone recep or
responsible for most of the glandular
secretion during the luteal phase of
the cycle
- Subnuclear vacuolation indication of high
levels of progesterone and that ovulation
has started
Endometrial Cycle
- Has 2 phase:
Proliferative phase (preovulatory)
Secretory phase (postovulatory)
- Synonymous with the menstrual cycle
First day of the endometrial
cycle is the first day of the
menses
- Can be dated based on the:
Epithelial (glandular)
Stromal (mesenchymal)
Presence of blood vessels
More tortuous vessels on
the latter part of the cycle
and more compact stroma
needed for the implantation
of the blastocyst
Proliferative Phase
- Corresponds to the follicular phase of the
ovarian cycle
- Production of estradiol
- Largely stimulated by estrogen
- Day 5 restoration and revascularization of
the endometrium to help rebuild/
proliferation of the endometrium for the next
cycle
Evident by the presence of
thin, tubular and narrow
glands
- Reepithelialization and angiogenesis stops
bleeding
Estrogen is responsible
because it increases
vascular endothelial growth
factor needed for
angiogenesis
2

- Hyperplasia and increase in stromal ground
substance
Estrogen induces growth
factor gene expression in
stromal cells
- Makes the cycle variable (5-7 days; 21-30
days)
Luteal phase of the ovarian
cycle and secretory phase
in endometrial cycle os
constant in duration 12-
14 days
Best time for patient to get pregnant:
- Ask the patient her cycles for the last 4-5
months
- Compute the intervals from which this
patient has her normal cycles
- Subtract 14
- E . If pa ien normal c cle i 29 da 29-
14= 15 day 15 is the time the patient is
fertile ovulates
Inform couple to have
sexual contact for 3
consecutive days for
successful conception to
happen
Secretory Phase
- Part of the cycle that tells us that ovulation
has happened
- Dating based on the histology of glandular
epithelium
- Day 17: glycogen accumulation,
pseudostratification, subnuclear vacuoles
are noted over the apical portion of the
endometrium over the peripheral portion
first sign of ovulation
GnRH & LH
Proge erone
Ovum has been extruded
from graafian follicle
- Phase where there are a lot of tortuous
glands and a lot of mitosis is happening
- Day 18: vacuoles moved to the apical
portion
- Day 19: glycoprotein and
mucopolysaccharide contents released;
mitotic activity ceases
- Day 21-24: stroma becomes edematous
- Day 22-25: stromal mitosis apparent
Day 20-24: window of implantation
(endometrium must be ready for
successful implantation)
Pinopods protrusions of the apical
surface in to the lumen; helpful
during the time of implantation
Continuous growth of spiral arteries
at this time for continuous
nourishment of the endometrium in
preparation for the decidua
Day 22 I m read for o da in
the endometrium
Decidualizarion
- Happens because of preogesterone
If corpus luteum is rescued and
there is continued secretion of
progesterone, the endometrium will
be decidualized
LH and HCG maintains the corpus
luteum; basis for the pregnancy test
Placenta and Placental Hormones: PDV
Mentruation
- Corpus luteum production of progesterone
drops
- Psuedoinflammatory appearance
- Infiltration of leukocytes important key
factors in the initiation of the extracellular
matrix breakdown of the functionalis layer of
the decidua
- Severe coiling of the arteries causing
hypoxia of the endometrium and
consequently endometrial ischemia tissue
degeneration
Same mechanism happens in
patients with abruption placenta
Abruption placenta placenta
becomes detached from the decidua
because a hematoma happens
between the decidua and plancenta
The same manner that a ruptured,
coiled artery may produce
hematoma, thus causes the
shedding of the functionalis layer
with the basalis layer still intact
(basalis layer is left for endometrial
growth to happen
- Infiltration of neutrophils one to two days
before menstruation: (IL-8)
- MCP-1= monocytes
Pain during menses:
- Because of the effect of the prostaglandins
par ic larl PGF2 causes
vasiconstriction
- Vasoactive peptides-- endothelin-
enkephalinase system vasoconstrictors
Vasoconstriction endometrial
ischemia manifested as
dysmenorrhea/ pain
After endometrial ischemia, tissue
desquamation will no ensue
Changes in the ovarian and endometrial
cycle are the bases whether a patient will be
highly successful in achieving pregnancy or
not
Effects of progesterone and estrogen does
not only focus on the ovaries and the
endometrium
It also has its effect on the body causing a
rise in the basal body temperature one
basis in predicting ovulation
Progesterone has a thermogenic effect
causes the increase in basal body
temperature and the feverish feeling during
pregnancy
The moment the temperature rises and that
temperature is sustained after 14 days
chances of pregnancy has likely happened
3
 Placenta and Placental Hormones: PDV
FERTILIZATION
N ri ion of he de eloping embryo
- Birth 2,000,000 oocytes
- Adolescence 400,000 Endocrine f nc ion secretes hormones

- Reproductive period 400 undergo EMBRYOBLAST make up the inner cell

maturation -> ovulation mass which becomes the embryo, umbilical
cord, and
Primary follicles amnion
st
1 meiotic division: arrested in prophase of
(completed just before ovulation) Remember: TOE (Trophoblast:Outer,
nd
2 meiotic division halted in metaphase Embryoblast:Enner)
(completed upon fertilization of ovum)

- Oocytes must be fertilized within 12 hours IMPLANTATION

(cannot survive for more than 24 hours) - 6-7 days after fertilization
- happens in the Ampulla (*Fallopian tube is
7-8 cm) Stages:

A. Apposition blastocyst adherence to the upper

Upon fertilization, the oocyte undergoes many part of the posterior uterine wall (superficial
changes: adherence)

o Embryonic pole (contains the embryoblast)

attaches first
o Implantation window adhesion of
trophoblast and endometrium is maximal
and is only present at
this time

vitro fertilizations
***Dra. said that there is a step called
Adherence hich i j a deeper implan a ion
1. Zygote - formed by fusion of 2 haploid
gametes (46 chromosomes) B. Invasion penetration of the blastocyst to the
- union of the egg and the sperm inner 1/3 layer. Cells of the trophoblast of the
2. Blastomere further divisions (myosis and implanting embryonic pole proliferate to form 2
mitosis) make the zygote go through different layers:
stages as it
travels in the fallopian tube (2 cell stage, 4 cell, 8 1. Syncitiotrophoblast outer layer facing
cell, 16 cell) It will happen three days in the maternal tissue; fused
fallopian tube. 2. Cytotrophoblast remaining unfused
O Transported by peristaltic and cellular components
ciliary movement
3. Morula solid ball of cells formed; Remember: SOCI (syncitio:outer; cyto:inner)
enters uterine cavity 3 days after fertilization or
once it reaches the 16 cell stage ** Trophoblast invasion does not penetrate beyond the
- the one that enters the uterine cavity and inner third of myometrium
rd
implants in the upper 3
(Ectopic/Tubal pregnancy implants in the Germinal cell

fallopian tube) Camp

On FM

* later on it will accumulate more fluid between - Trophoutronectin

the cells/blastomeres or when there is fluid Cytotrophoblast
- Trophoblastic glue
accumulation it becomes the blastocyst
Facilitates separation of tissue
at delivery
4. Blastocyst: implants on endometrial lining
(6-7 days after fertilization)
Syncitiotrophoblast
- the fluid accumulation will cause Secretory cell
preferential flow (the cells to be pushed on one
side). One side is called inner cell mass which
C. Other developments after implantation
will become the embryon and the outer cell
Prelacunar & lacunar stages
mass is the placenta and trophoblast.
Trophoblast invasion
- Most of the blastocyst cells make up
Villous development
the TROPHOBLAST (outer wall that becomes
Development of chorion and decidua
the fetal membranes and the placenta)
1. Prelacunar stage
TROPHOBLAST (functions)
- Characteristic feature: solid
syncitiotrophoblast mass with finger-like extensions
invading the endometrium
A achmen of bla oc o he er
1

2. Lacunar stage
-DAY 8: Formation of lacunae (confluence of
vacuoles in the syncitiotrophoblast)
-Trabeculae: separating syncitiotrophoblast
- DAY 12: Uterine epithelium closes over
implantation site
*Completed syncitiotrophoblast covered by
layer of incomplete cytotrophoblast
3. Trophoblast invasion of the
endometrium
- Signal of invasion: proliferation and
migration of cytotrophoblast at the bottom of the shell
- Significance of this event:
o Further invasion of the blastocyst
o Helps the maternal vessels adapt to
pregnancy conditions
o Anchorage of the developing
placenta
- Trophoblast is seen as an irritant and
causes release of hormones that promote
endometrial stroma
proliferation and enlargement = formation of
decidual cells
- Syncitiotrophoblast invasion causes the
maternal endometrial vessels to disintegrate
causing maternal blood to enter through the
lacunae (remember that these were formed
during the lacunar stage )
o The syncitio now becomes the
capillary walls and forms new lacunae -> complete
perfusion of
the entire lacunar system
o Spiral arteries erode due to deeper
invasion = increase intralacunar
pressure = FIRST REAL maternal
circulation of the placenta
4. Villous development
- Lacunar system is transformed into the intervillous
space
- Primary villi: longitudinal cell columns that protrude
into the lacunae
- Secondary villi: transformed when mesenchymal
cells from extraembryonic chorionic plate invade the
villi
- Tertiary villi: marked by the appearance of capillaries
in villous stroma
o Complete fetoplacental circulation: established at
th
5 week
Fun Fact:
Embryo 8 eek and belo ; adpole looking
Fetus - 8 weeks and above
Placenta and Placental Hormones: PDV
- fe al a me he hape of a h man
5. Development of Chorion and Decidua
a. Decidua basalis
- Decidua at implantation site/the placenta
- Chorionic villi at this site will proliferate and form
the chorion frondosum / leafy chorion (fore runner of
the placenta)
- Very vascular
b. Decidua capsularis
- Envelops the blastocyst after completion of
implantation
- Covers/encapsulates the embryo
- Covers the side facing the endometrial cavity
- Chorionic villi here degenerates & becomes
avascular because of pressure due to growth
blood is compromised = chorion laeve / smooth
chorion (to avoid misspelling, remember that chorion
laeve is spelled like leave, but the vowels are
alphabetically arranged LAEVE)
c. Decidua parietalis
- Rest of the decidua that is not in contact with
blastocyst
** There is this vestigial cavity between the decidua
capsularis and parietalis.
- After 14 16 (15) weeks the smooth Chorion and
Decidua Capsularis fuse together with the Decidua
Parietalis due to the growth of the fetus and
becomes Decidua Vera
- Clinical Significance: Before 15 weeks,
intrauterine infection can set in due to the
communication between the two (ascending
infection). After 15 weeks, the fetus is protected from
the ascending infection.
Con ac be een he moo h Chorion and
Decidual surface of uterine wall allows
paraplacental exchange.
(Sabi ni Williams 24/E)
The decidua parietalis and basalis are composed of
three layers.
1. Zona Compacta surface
2. Zona Spongiosa middle; with remnants of
glands and numerous small blood vessels
3. Zona Basalis Contains the endometrial gands
and stroma
The ona compac a and pongio a oge her form
the zona functionalis. The basal zone MUST remain
after delivery and give rise to new endometrium
because without it the woman becomes infertile.
The Ni ab ch la er i a one of fibrinoid
degeneration in which invading trophoblasts meet
the decidua basalis. If the decidua is defective, as in
placenta accreta, the Nitabuch layer is usually
ab en Thi la er hich epara e he ba ali from
the placenta and the myometrium.
(Sorry, may tin ro i a di o pero hi lang inabi
ni a oooo, e an ko ano ng hi b i abo
the Fibrion/ Nitabuch layer. So I got that statement
from Williams)
DECIDUALIZATION
- Change that occurs in the endometrium in
response to blastocyst implantation
2
 Placenta and Placental Hormones: PDV
- The endome ri m ran form in o he decid a rd
(3 trimester) exchange due to high degree of
because of hormones. with fetal vascularisation & large
- Decidualized endometrial cells are called branching exchange surface
decidual cells angiogenesis - prominent sites for hormone
Remember: Decidua is the endometrium of the production
pregnant woman - high degree of fetal
Con ain a fe T cell b no B cell (rea on h capillaries & dilated
trophoblast is not recognized by the endometrium) sinusoids (responsible for
D. Ba ali : con ain ma ernal macrophage /c slowing down blood flow to
are able to phagocytose cell debris and immune Terminal villi provide ample time for
complexes w/ fetomaternal exchange; area
- Walls of spiral arteries have no nonbranching of greatest diffusional
macrophages and are thus invaded by the Angiogenesis exchange)
trophoblastic cells (decrease in - MAIN site of fetomaternal
- Macrophage function inhibited by VEGF and exchange
progesterone increase in
placental GF) (O2, CO2, H2O
PLACENTA transfer)
- Major source of nutrients of the fetus in - reduction in terminal villi =
utero may lead to fetal hypoxia
- Produce hormones that maintain the
pregnancy
- Main function: oxygenate blood from fetus
- Insight into prenatal life
- Helpful in caring for neonate
- Plan the future care for mother/child
- Fetal side of the placenta: glistening, covered
by amnion
- Maternal side: rough ; attached in the D.
Basalis
- Main cell comprises of the Trophoblast
** Basically, villi are present in the placenta to
Characteristics of Placenta: facilitate exchange of nutrients, oxygen, etc between
the mother and the fetus. Thus, blood flow and BP
- HEMOCHORIAL control is very important in the intervillous space.
o HEMO: Maternal blood (from spiral arteries) is
localized only to the outsides of the endothelium of - Major mechanism in the pathogenesis of
the maternal vascular system intrauterine growth restriction (IUGR) with
- Directly bathes the syncitiotrophoblast absence of reverse end-diastolic umbilical flow
(where exchange of gases & nutrients occur) (ARED)

o CHORIO: chorion-placenta separated from - Myofibroblasts are present in stem and anchoring
fetal blood by endothelial wall of fetal capillaries villi to help relax the capillaries when there is an
o Fetal capillary blood confined in the villous increase in pressure in IV space
core
o There is no mixing of maternal and fetal blood NONVILLOUS PARTS OF PLACENTA
(may come in close contact but never mixing)
- Separated by the placental barrier 1. Extravillous trophoblasts
composed of the ff layers: - Responsible for invasion of maternal tissues and
Syncitiotrophoblast lining the vessels
intervillous space
C o rophobla (Langhan cell )
Trophoblastic basal lamina
Connective tissue
Fetal endothelium

VILLOUS
Villi Type Function
- Mechanically support the
structures of the villous trees
Stem Villi - Negligible part in
fetomaternal exchange and
endocrine activity
- Growth centers of villous
Immature trees
intermediate (placentones) 2. Fibrinoid
villi - principal sites of exchange - Nonfibrous, noncellular, homogenous
during first 2 trimesters
Mature - contain capillaries, arterioles, 3. Decidualized endometrial stroma (see decidua
intermediate venules on page 1)
villi - important for fetomaternal
3

PLACENTONE THEORY OF SCHUHMANN &
WEHLER Placentone:
fetomaternal circulatory unit is composed of 1
villous tree + related centrifugally perfused
intervillous space
The arrows represent the maternal blood at it enters
the center of the villious tree and leaves through the
clefts between neighboring villious trees.
- One or a few villous trees = 1 placental lobule/
maternal cotyledon
- 15-20 lobes divided by Fibro septae
- to check: put on a table and look for
missing segments (incomplete can cause maternal
hemorrhage/infection/suninvolution)
Placenta and Placental Hormones: PDV
FACTORS REGULATING BLOOD FLOW TO
PLACENTA
1. Blood pressure of mother increased BP of
mother will decrease blood flow to the placenta; Low
BP poor circulation Hypoxic baby
2. Intrauterine pressure will also decrease blood
flow to placenta
3. Type of uterine contraction
Ex. Hypertonic contractions (one after
another)/Tetanic No relaxation = no pooling of
blood
4. Factors affecting arteriolar wall PTH and
Endothelin I (chorionic vessels)
ABNORMAL:
H-mole (Hyatidiform mole)

VASCULOGENESIS & ANGIOGENESIS IN

PLACENTA
- Normal vessel formation is regulated by the ff:
VEGF (Vascular Endothelial Growth Factor), partial
pressure of Oxygen in the fetoplacental vessels
Imbalance in an of he e ma lead o
preeclampsia/ IUGR

- Vessel formation involves 2 processes:

- Placenta develops; with fertilization; with
implantation
1. Vasculogenesis de novo formation from
- No fetus
mesodermally derived precursor cells
- Pregnancy is a lot bigger than expected because of
2. Angiogenesis creation of new vessel
the rapid growth of the placenta
branches from pre-existing ones
- Grows every 2 days (twice the amount)
Branching angiogene i : Principal
- Swollen and avascular
type; occurs during development of the villi =
- Vesicles that are grape like
primitive
- Proliferation of the trophoblastic cells
capillary network; mainly
stimulated by VEGF
Nonbranching angiogene i :
Coincide with development of
mature intermediate villi
rd
(3 trimester) and terminal villi;
lasts until term

REGULATORS OF A & V
1. VEGF
- potent stimulator of growth and survival of
blood vessels
o High levels in early pregnancy promotes
formation of widely branched low resistance
capillaries (branching angiogenesis)
o Decreased levels in second half of
pregnancy
o Affected by O2 levels; low O2 levels
stimulate upregulation of VEGF ->
compensatory formation of blood vessels
2. PlGF
- High levels in second half of pregnancy, during the
period of the most dramatic nonbranching
angiogenesis
- Small caliber compared to the rest of the umbilical
cord (normal length: 55 100 cm). If more than that
it can twist and wrap around the fetus/cord coil
sudden fetal death
***Always monitor the fetal movement thus report
changes in fetal movement to see the location of the
umbilical cord
- Umbilical cord i co ered i h Whar on jell and
contains 2 arteries and 1 vein. The absence of 1
artery is the most common vascular anomaly in the
human being but it is compatible with life.

** Balance between VEGF & PlGF = balance

between branching & nonbranching angiogenesis
** if VEGF > PlGF: predominance of branching
angiogenesis = highly branched, convoluted, short,
terminal villi (seen in preplacental & uteroplacental
hypoxia)
** if PlGF > VEGF: predominance of
nonbranching angiogenesis = long filiform terminal
villi
(seen in postplacental hypoxia) - Umbilical cord is capable of having blood vessel
anomalies. Some are tortious and we call these
varix/varices or some call it as a pseudoknot.
4
 Placenta and Placental Hormones: PDV
Underneath it is just an accumulation of blood increased fetoplacental
vessels which are swollen similar to the concept of flow impedance
varicose veins in pregnant women.

- This is because of the redundancy of the umbilical
cord, some twists/ screw like along the length of the
umbilical cord. The tighter this twist becomes
untoward events can happen to the fetus.
- Long cord and had undergone twisting or torsion.
Mother will verbalize that no fetal movement is felt.
Upon examination,no more cardiac activity.
Evacuation/Induced labor is important because
leaving the fetus in utero will lead to DIC. Cesarean
section is not needed unless there are some other
maternal indications.
FETAL CIRCULATION
- Uteroplacental arteries are branches
of myometrial arteries. As they enter the decidua,
they are also
called spiral arteries (due to spiral course)
- Deoxygenated blood is carried to the
placenta via 2 umbilical arteries in the umbilical cord
- Single umbilical vein carries oxygenated
blood back to fetus
- Umbilical vessels enter placenta and branch
into capillary networks
- Exchange of substances passively diffuse
from capillary networks to intervillous space
- Maternal blood bathes
syncitiotrophoblast -> oxygenated blood returns
from placenta to the fetus
through the single umbilical vein
- Maternal oxygen supply has a strong impact
on villous growth and differentiation
o Low maternal O2 may lead to
underdevelopment of the villous and cause fetal
hypoxia
- No actual mixing of fetal and maternal blood
just diffusion and osmosis
PLACENTAL AGING
- Premature placenta may affect fetal growth
- As it ages, there is also an increasing impairment
of function
Characteristics/Features of aging:

o Decrease syncytial thickness

o Lo of Langhan cell
o Decrease stroma
o Increased capillaries
o Thickened basement membrane
o Obliteration of blood vessel villi
o Fibrin deposits
- Pathologic placenta
o Hydropic degeneration of placenta (occurs
in molar pregnancies)
- Nuchal Cord coil sudden fetal death (most
common) ***

PLACENTAL MEMBRANES
Different Origins of Fetal Hypoxia 3 distinct layers:
1. Amnion
Hypoxia Causes 2. Chorion laeve/smooth chorion
maternal anemia, 3. Decidua capsularis
Preplacental
cyanotic maternal
hypoxia
cardiac diseases, Trophoblast is subdivided into:
mother, placenta, &
pregnancy in high a. Basal chorion cells surrounding the
fetus are hypoxic
altitude implantation pole
Uteroplacental o Becomes the chorion frondosum (tree
Impairment in
Mother (normal) like) with appearance of the 1st villi
uteroplacental circulation
Placenta and fetus b. Capsular chorion cells surrounding the
(preeclampsia)
(hypoxic) anti-implantation pole
IUGR w/o umbilical end- o Degenerates by 3rd week, intervillous
Postplacental
diastolic flow space obliterates, trophoblastic cells fuse to
Fetus (hypoxic) Mother
form chorion laeve (smooth chorion)
(normoxic) Placenta
Poorly developed
( h pero ia
terminal villous AMNION
- higher O2 levels
capillaries, absent - Composed of inner layer of epithelial cells
than normal)
capillary branching = - Easily separated from underlying chorion
5
 Placenta and Placental Hormones: PDV
- Contains Amniotic Fluid - Contains 2 arteries & 1 vein (left umbilical vein;
- Avascular - no blood vessels; obtains nutrition right vein disappears early in life)
and O2 from surrounding chorionic fluid, amniotic - Artery deoxygenated blood; Vein
fluid, and fetal oxygenated
surface vessels **Chorionic vessels branches of these
- Intramniotic lipid synthesis umbilical vessels seen on the surface of the
- Greater tensile strength than chorion placenta
- to maintain pregnancy until 9 months - central wider vessels and periphery
- if weak (ex. infection) there might be a smaller
rupture Amnionitis
- Amnionic epithelium flat, cuboidal
to columnar cells - Intraabdominal portion of the duct atrophies and
o Exclusive source of PGE2 di appear . If i remain : Meckel di erticulum
o Source of interleukins - Average length: 55cm (range: 30-100cm)
(regulateprostaglandin synthesis) Diameter: 0.8 2cm
Prostaglandins: significant role in
initiation and maintenance of uterine Possible pathologies:
contractions
Intraamnionic infections induce False knots: folding and tortuosity of vessels
production of IL -> increase PG longer than umbilical cord
production Pro r ion of Whar on jell
o Produce leukotrienes Constriction of some portions of the cord
o Produces Endothelin I potent Torsion of umbilical cord
vasoconstrictor (if increased, it will * Usually in very long cords
compromise circulation with fetus IUGR Ma ca e fe al dea h
(Intraunterine Growth restriction), amniotic Mi concep ion: if he mbilical cord i rro nding
fluid homeostasis; promotes H2O transfer the neck, it will cause death of the baby and is an
across epithelia of other organs immediate indication to do a caesarean section.
o Contains carbonic anhydrase isoenzymes NOT TRUE! For it to actually cause death, it has to
(responsible for regulating pH of amniotic fluid to be tightly wrapped around the neck.
7.0) Cord coil
- E racell lar ma ri i called Whar on jell
- Contain oxytocin receptors
- Membrane that contains amniotic fluid PLACENTAL HORMONES:
- Solute and water transport to maintain
A.F> Hemostasis 1. Estrogen
- Produces hormones: Pregnancy is hyperestrogenic state
o Parathyroid hormone related protein Syncitiotrophoblast
Vasodilator (must in balance with Endothelin Ovaries 2-4 weeks post-ovulation
I) 7th Week > 50% placenta
o Enkaphalinase
- Modulates chorionic vessel tone and blood flow
Precursors
Source of Amniotic Fluid: DHEAs (main)
1. Possible secretory process of amnionic epithelium Androstenodione
2. Filtration of fluid from maternal vessels via Testosterone
deciduas parietalis and chorion laeve
3. Filtration from fetal vessels or in the chorionic Decreased Estrogen
plate and via umbilical cord Fetal Anencephaly
4. Urination of fetus Maternal Adrenal Dysfunction
5. Filtration from intracorporeal fetal vessels via Maternal ovarian androgen producing
fetal skin tumors
**Functioning GI, GU, Pulmonary, Integumentary to Placental sulfatase deficiency
have normal amount 1000cc / 1L towards term Placental aromatase deficiency
Hydramnios more than 1L may be cause by Glucocorticoid Treatment
problems in circulation/GI/Atresia/obstruction and Deficiency in fetal LDL synthesis
less is oligohydramnios may have problems in
Decreased fetal adrenal utilization of
GU/renal agenisis/obstruction
LDL
UMBILICAL CORD
2. Progesterone
- 18 days: embryo is a flattened disc between
Source: Syncitiotrophoblast
amnion and yolk sac
Utilization of Maternal LDL
- Middle of 3rd month: amnion obliterates the
exocoelom, fuses with chorion laeve and covers the
* when there is ovulation there is Trophoblast
bulging placental disc and the lateral surface of the
formation and implantation there is Corpus Luteum
body stalk
production source of progesterone fro the next 6 -
- Body stalk called funis or umbilical cord
7 weeks. After that, the placenta takes over.
- Must be in the central or para central area to get
better blood flow
3. Human Chrorionic Gonadotrophins (HCG)
- Fetal umbilicus to the fetal surface of the
Syncitiotrophoblast
placenta
Alpha & Beta Subunits

6
 Placenta and Placental Hormones: PDV
Structural related to LH, FSH and TSH
Alpha sub-units identical
Beta sub-units are distinct
Beta subunit: basis for pregnancy kit (5
drop of rine in he indo of he ki
= 1 line means negative and 2 lines
means positive) The kit contains
antibodies coagulation happens with
HCG
Hormone of pregnancy
Increases between 9-10 weeks AOG
down at term
Amount is directly related to no of
Trophoblast
Doubles every 2 days if negative, try
again after 2 days

Significance: Increased HCG means increased

TSH thus the thyroid gland enlarges
symptoms of hyperthyroidism. Same correlation
goes to an enlarged ovaries because of FSH
thus we need monitoring.

• Functions
Rescue & maintenance of corpus
Luteum
Stimulate Leydig cells of the fetal
testes
Induces ovulation (Infertile women)
• Increased HCG
Multiple pregnancies
Fetal hydrops
H-mole
Choriocarcinoma

4. Human Placental Lactogen (HPL)

Chorionic Somatotropin
Chorionic Growth Hormone
Syncitiotrophoblast
Detected on 2nd or 3rd week of
fertilization
Structurally related to Human growth
hormone and human prolactin
• HPL Synthesis
Stimulated by insulin
Inhibited by PGE2 & PGF2
alpha
Greatest hormone in humans
Present within 5-10 days after
conception
Concentration rises till 34-36
th th
weeks AOG *peak 6 7
month
Proportional to placental mass
• Metabolic actions of HPL
Lipolysis and increased
circulating free fatty acid
reason why it is a Diabetogenic
Anti-insulin
Increased maternal insulin
CHON synthesis thus no fetal
starvation
A.A. for transport of fetus thus
no fetal starvation

********There are others but you can just read on

i . I i and I q o e Nice o Kno . If o are
not nice, then you know what to do. :P

7

MATERNAL ADAPTATIONS TO PREGNANCY
REPRODUCTIVE TRACT
A. Uterus
1. Increase in size (attributed to the ff
changes:)
To accommodate the growing fetus,
placenta, amniotic fluid
- At term, uterine contents = 5L 20L,
weight: 1100g
70 g and is almost solid,
except for a cavity of 10 mL or less
By the end of pregnancy 500 to 1000 times greater
Thinning of the wall (1-2cm at thickness at term)
Hypertrophy of smooth muscle (myometrial) cells
(hypertrophy > hyperplasia)
- Production of new myocytes is limited
- because of the stretch it becomes more
of hypertrophy
Increase in fibrous & elastic tissues
- Adds strength to uterine wall
o Increase in size and
number of lymphatics & blood vessels
Hypertrophy of nerves
o Asymmetrical enlargement
= more pronounced at the FUNDUS
- More rapid growth at the part of the
uterus surrounding the placental site
- Early pregnancy the fallopian tubes
and ovarian and round ligament attach
only slightly below the apex of the
fundus.
- Later months, located above the middle
In ectopic pregnancies: growth still takes
place because of the
hormones
Stimuli for change:
- Before 12 weeks: Hormonal -
(estrogen & progesterone)
- Polyamines (spermidine, spermine,
putrescine)
- After 12 weeks:
mechanical distension by uterine
contents is responsible thus it still
stretches outside labor
occur entirely in response to mechanical distention
by the products of conception, because similar
uterine changes are observed with ectopic
pregnancy
Myocyte Arrangement
- uterine musculature: 3 strata
Hoodlike layer arches over the fundus and extends
to the various ligaments
Middle layer dense network perforated in all
directions by the BV. Forms most of the
uterine wall. Each cell has a double
c r e like an 8 crucial because
the cells contract after delivery, they
constrict penetrating blood vessels
and thus act as ligatures.
Internal Layer w/ spincter like fibers around the FT
orifices and internal cervical os.
2. The uterus becomes an
abdominal organ (from being a pelvic
organ)
Few weeks piriform/ pear
Becomes ovoid/globular (end of 12th week)
MATERNAL PHYSIOLOGY: PDV
Due to a more rapid increase in length than
width
Shape pushes uterus out of pelvic cavity
displace the intestines laterally and
superiorly, almost the tip of liver
o Dextrorotation (right) caused by the
rectosigmoid colon on the left side of the pelvis
o Standing causes extension of the pelvic inlet axis.
The abdominal wall supports the uterus maintains
the relation between the long axis uterus and axis
of the pelvic inlet.
o Supine uterus falls back t the vertebral column
and adjacent great vessels.
o Stretching of myometrium
o Fundal
o Round & broad ligament are located already
midway the uterus due to its ascent to the
abdomen because of the tilting of the
dextrorotation
o Consistency soft uterus if because of pregnancy
and solid if tumor of the musculature
Vascularity causes softness
Bimanual examination - One hand at the
vagina/cervix one hand at the abdomen top (one
interal + one external)
Proce ed o ge he ol me
Upper limit fundus to note the number of weeks
Size is important in knowing if the baby is growing
well SGA or too big; rapid growth; GDM
Tape measure put one end at the symphysis pubis
another is on the top part (fundus)
- correspondence in height in cm and weeks
ex.. 18 weeks = 18 cm but after 36 it will become
smaller
20 weeks at level of umbilicus
16 weeks 2 finger breadths below the umbilicus
24 weeks 2 -3 finger breadths above the umbilicus
Appendix pushed up but this does not mean that we
do not check on the possibility of Appendicitis if
with right lower quadrant pain
Myoma can cause the uterus to enlarge
3. + Hegar sign
Softening of the isthmus +
disappearance -> replaced by the lower uterine
segment
Reappears after delivery
4. Contractions
Early pregnancy: painless, irregular
contractions because of the stretch in muscles
o 2nd trimester: contractions detected by
bimanual palpation
Braxton - Hicks contractions: appear
unpredictably, sporadically, nonrhythmic
- Strong palpable irregular contractions (5
25mm Hg)
- Encountered usually during last two weeks
of pregnancy
- May occur every 10 to 20 minutes
- May cause false labor pains
Factors affecting contractility:
- Estrogen increased function of the
biochemical contractile system of uterine
smooth muscle
- Progesterone maintains high membrane
potential to block myometrial activity
- Biochemical control: increase contraction
of actomyosin, increase muscle excitability
through Ca, PGE2 and PGF2
- ANS innervations
1

* Know the difference between the contractions:
before labor and towards labor
5. Uteroplacental Blood Flow
Placental perfusion is dependent on total uterine
blood flow
Increase progressively during pregnancy
Estimates range from 500 to 750 mL/min
Nonpregnant woman is 5000 mL/min
Uterine veins reduced elastin content and
adrenergic nerve density increased venous
caliber and distensibility..
Uterine artery diameter doubled by 20 weeks
17 -estradiol has been shown to promote
uterine artery vasodilation and reduce uterine
vascular resistance
B. Cervix
* speculum bivalve instrument used for IE
1. + G de (as early as 1
mo after conception)
Softening of the cervix due to: (parang lips)
- Increased vascularity & edema
- Hyperplasia & hypertrophy of the
cervical glands = leukorrhea
(excessive secretions)
- can also be caused by hormonal
2. Cyanosis of the cervix
Not all bluish cervix are pregnant; cervical
cyanosis may also be caused by oral
contraceptives
Violicious in color
3. Rearrangement of collagen-rich
connective tissue
For maintenance of pregnancy, dilatation during
labor, repair following parturition
Decreases collagen and proteoglycan
concentrations and increases water content
- regulated in part by localized estrogen
and progesterone metabolism
4. Cervical Glands
Marked proliferation: by the end of pregnancy -
occupy up to one half of the entire cervical mass
Cervical extension, or eversion, of the
proliferating columnar endocervical glands
(tissue tends to be red and velvety and bleeds
even with minor trauma)
5. Mucoid plug
Produced by endocervical mucosal cells due to
hypertrophy and hyperplasia of the glands
Rich in immunoglobulins and cytokines
Acts as a barrier w/in cervix, prevents bacteria
from entering uterine cavity through the vagina
o During contraction, mucoid plug is
extruded = bloody show
Stimuli for these changes: estrogen &
progesterone
* anti-bacterial and immunologic
6. Changes in cervical mucus (as
seen on a glass slide)
Beading/crystallization (progesterone induced)
Ferning (arborisation of crystals)
Result of amniotic fluid leakage
MATERNAL PHYSIOLOGY: PDV
Estrogen * sa lecture both E
and P daw but more of P
meaning ferning i n normal in
pregnancy
7. Others
o Basal cells near the squamocolumnar junction
- prominent in size, shape, and staining
qualities (Estrogen
induced)
Arias-Stella reaction
o - both endocervical gland hyperplasia and
hypersecretory appearance, which makes
the differentiation of these and atypical
glandular cells on Pap smear particularly
difficult
C. Ovaries
1. Amenorrhea (due to arrested
follicular maturation and ovulation)
2. + Corpus Luteum (until 6-7wks
AOG)
Produce progesterone
Releases relaxin remodels CT of repro tract +
allow successful pregnancy & labor
upon decrease in hormone it will be rescued by
HCG
Estrogen and Progesterone -
no release of FSH and LH;
source is placenta kaya raw
parating mataas ang level
3. Extrauterine decidual reaction
(On and beneath the surface of the ovaries is
common)
- Elevated patches of tissue bleed easily and
may (resemble freshly torn adhesions)
Similar decidual reactions are seen on the uterine
serosa and other pelvic, or even
extrapelvic, abdominal organs
o These areas arise from subcoelomic mesenchyme
(progesterone stimulation and histologically
appear similar to progestin-
stimulated intrauterine endometrial stroma)
4. Increased caliber of ovarian veins
from 0.9 to 2.6 cm at term
5. Pregnancy Luteoma
Overexaggeration of the luteinization reaction of
normal ovary
Not true malignancies but are large masses
o Difficult to differentiate from other ovarian
neoplasms
o May cause maternal virilization, female fetus
USUALLY not affected (due to protective
role of trophoblast
converting androstenedione to estrogen)
Self-limited; resolves after delivery
6. Hyperreactio Luteinalis (Theca-
Lutein Cyst)
- benign ovarian lesion; usually bilateral cystic
ovaries are moderately to massively
enlarged
Due to exaggerated physiologic follicle stimulation
Tumor related to an increase in hCG
- May also be seen in hyperthyroid patients due to
structurally similarity between TSH
and hCG
2

Usually found in large placenta, multiple fetuses and
anti-D alloimmunization
May also cause virilization during pregnancy (due to
high testosterone and androstenedione)
- Sx: temporal balding, hirsutism,
clitoromegaly
Self-limited; resolution follows delivery
D. Fallopian Tubes
1. Little hypertrophy of muscle layer
2. Flattened epithelium
3. FT torsion (may result from
increasing size of the uterus in the presence of
ovarian cyts)
MATERNAL PHYSIOLOGY: PDV
Exchange happens in terminal villi composed of
layers of syncy., basal lamina, and endothelial cells
Late pregnancy, diffusion barrier thins 5 mm surface
12m2
Large amounts of Progesterone, Estrogen, hCG,
hPL and other secretory products are released by
syncytiotrophoblast directly into intervillous space
Maternal circulation
Placental hormones largely responsible maternal
physiology
BREASTS
In preparation for lactation
1. Breast tenderness & paresthesias
(early pregnancy) ***

E. Vagina and Perineum After 2nd month

1. Increased vascularity and 2. Enlargement of mammary glands

hyperemia
In skin & muscles of perineum and vulva
2. + C ad c
Violet color of the vagina
Due to increased vascularity
3. Vaginal changes that prepare for
delivery:
Increase in mucosal thickness
Loosening of connective tissue
Hypertrophy of smooth muscle cells
Hypertrophy of the papillae of vaginal epithelium
fine, hobnailed appearance
4. Increased volume of cervical
secretions within vagina
Thick white discharge
pH 3.5-6 due to increased production of lactic acid
from glycogen in epithelium (by
Lactobacillus acidophilus
Bartholin gland cyst 1-cm common
PLACENTA (APMC only not discussed)
o At first missed menstrual period
o Due to hypertrophy and hyperplasia of glands in
preparation for lactation
o Increase in fatty tissue
3. Delicate veins become visible
4. Nipples: deeply pigmented, enlarge,
more erectile
After first few months
5. Expression of colostrums (end of
first trimester)
Thick yellowish fluid expressed from nipples after
gentle massage
1st evidence of secretory activity
6. Broader and more deeply pigmented
areola
happens after # 5
forms a mottled secondary areola
7. Hypertrophic glands of Montgomery
Sebaceous glands found scattered through the
areola

Anchor developing fetus to the uterine wall **Extensive increase in breast size may also cause
exchange of nutrients and fetal wastes striations on the skin of the breast similar to the
Direct homeostatic adj. to meet changing fetal needs striations in the abdomen
by secreting hormones and others into mat. **No relation between prepregnant breast size and
Circulation volume of milk production
Disc shaped measures 22cm in diameter and
2.5cm thick at the end of pregnancy SKIN
Chorionic plate: facing fetus
Penetrated at center AVA -> tree-like vili which is A. Blood Flow
rooted at chorionic plate and extended to basal plate 1. Increased metabolism in pregnancy =
(maternal decidual + extravillious excess heat production = increased cutaneous
syncytiotrophoblast) blood f low to release heat
60 -70 villuos trees 100,000 intermediate and
terminal villi B. Abdominal Wall
1. Striae gravidarum
Length 90 km with finer branches of arterioles and
venules terminate grape-like (sinusoidal dilated Stretch marks
capillaries) Begins at midpregnancy
Entire villous tree ensheathed in a continuous layer Reddish, glistening, silvery lines that represent the
of syncytiotrophoblast overlay a discon. layer of cicatrices from previous striae, slightly
cytotrophoblastic cells. depressed streaks commonly found
Chorionic plate fused at edges with basal plate to in abdominal skin and some in the breasts & thighs
form hollow cavity Risk factors: weight gain during pregnancy, younger
Intervillous spaceperfused with Maternal blood maternal age, family history
enter spiral erteries branch off the radial arteries * change in the Biometrical components of the skin
in the myometrium and exits by way of * disruption of the skin weight
uteroplacental veins 2. Diastasis recti
o Separation of rectus muscles at
the midline
3
 MATERNAL PHYSIOLOGY: PDV
o Due to inability of the abdominal
wall to withstand the tension

C. Hyperpigmentation (may also be caused by

oral contraceptives)
1. Linea nigra
Midline of the abdominal skin (linea alba) is
hyperpigmented to a brownish- black color
2. Cholasma or melasma gravidarum
Mask of pregnancy
Irregular brownish patches of varying size on the
face and neck A. Weight Gain
caused by melanocyte-stimulating hormone 2nd o Most of the weight is contributed by
month until term the uterus and its contents plus
hypervolemia and extravascular
3. Pigmentation of areola & genital skin fluid increase.
Disappear/regress after delivery o Increase in cellular water and
deposition of new fat and protein
Stimuli: (maternal reserves)
Increased melanocyte-stimulating hormone
(elevated at 2nd month of pregnancy until o increase BMR
term) o Weight gain: (average: 12.5kg or
Estrogen & progesterone (melanocyte stimulating 27.5lb) more than normal DM
effect) o Causes:
Uterus + contents
D. Vascular Changes Breasts
1. Angiomas (vascular spiders) Increase in blood volume
Minute, red elevations on the skin (face, neck Increase in extravascular
upper chest, arms) with radicles branching ECF
out from a central lesion Increase in cellular water
Aka nevus, angioma or telangiectasis and fat/protein deposition =
* can be seen in liver diseases maternal reserves
o 1st trimester: 2 lbs gain (5lbs wt loss
2. Palmar Erythema = normal)
Due to hyperestrogenemia o 2nd trimester: 11 lbs (1-2lbs/wk)
rd
Disappear after pregnancy o 3 Trimester 11 lbs
3. Increased cutaneous blood flow
serves to dissipate excess heat generated by B. Metabolism Changes
increased metabolism
1. Water
* important to do differential diagnosis because
these changes can still happen in other serious o There is increased water retention,
diseases mostly attributed to a fall in plasma
ex. Cervix discoloration OC pills osmolality induced by resetting
threshold for thirst and vasopressin
action.
o Water content (of the fetus)
at term: 3.5 L. + 3.0 L more as a
result of increased maternal blood
METABOLIC CHANGES volume.
o The minimum amount of extra water
the woman can hold: 6.5 L.
o Increase of venous pressure below
the level of the uterus as a
consequence of partial occlusion of
the vena cava produces
accumulation of fluid in the ankles
and legs.

2. Proteins

o The fetus and placenta = 4 kg with a

protein content of 500 g.
o Another 500 g. is added to the
uterus as contractile proteins, to the
breasts as found in the glands, and
to the maternal blood as hemoglobin
and plasma proteins.
o Daily supplement of protein is
needed growth or fetus and
mother
o Higher concentrations in fetal
4

o Largely regulated by the placenta
not only concentrates AA into the
fetal circulation +protein synthesis,
oxidation, and transamination of
some nonessential AA
3. Carbohydrates
o Normal pregnancy is characterized
by mild fasting hypoglycemia,
postprandial hyperglycemia and
hyperinsulinemia.
Increased insulin response to
glucose.
Increased peripheral uptake of
glucose.
Suppressed glucagons
o Increased concentration of free fatty
acids from lipolysis (enhanced by
hPL) facilitate increased tissue
resistance to insulin.
o Insulin sensitivity in late normal
pregnancy 45 to 70% lower than
non pregnant
o Nitrogen Balance
Increased with gestational age
Urinary excretion of 3-
methylhistidine did not change
no maternal muscle
breakdown
Turnover rate of nonessential
serine decreases across
gestation
o Accelerated Starvation
Post-prandial: elevated and
sustained glucose to a fasting
state: decreased plasma
glucose and some AA
Plasma concentrations of FFA,
Triglycerides and cholesterol
are higher
Pregnancy-induced switch in
fuels from glucose to lipids
Prolonged fasting ketonemia
4. Fats
o Concentrations of all lipids are
usually increased in pregnancy
(includes lipoproteins and
apolipoproteins)
o Increased insulin-resistance and
estrogen stimulation during
pregnancy Maternal
Hyperlipidemia
st nd
o 1 and 2 trimester maternal fat
accumulation increase in lipid
synthesis and food intake
rd
o 3 trimester Fat storage decrease:
enhanced lipolytic activity
(increased hPL effect) and
decreased lipoprotein lipase activity
reduces Triglyceride uptake into
adipose tissue
favors maternal use of lipids
o Hyperlipidemia
Triacylglycerol and cholesterol
levels in VLDL, LDL and HDL
rd
increased during 3 trimester
Associated with endothelial
dysfunction
Endothelium-dependent
vasodilation responses
MATERNAL PHYSIOLOGY: PDV
improve across pregnancy
because of the increased
HDL-cholesterol
concentration likely inhibit
LDL oxidation thus
protecting the endothelium
Increased CV disease may
be related to other factors
other than
hypercholesterolemia
o LDL-C peaks at about 36 weeks
(consequence of hepatic effects of
estradiol)
o HDL-C peaks at 25 weeks but
nd
decreases by the 32 week.
o Lactation speeds decrease change
in levels
nd
5. Increased leptin levels (peak in 2
trimester; plateau in term 2 to 4 times
higher in nonpregnant)
o Secreted by adipose tissue

o Regulate body fat and energy
expenditure
o Increase is partially
due to increased weight gain
o Deficiency:
1. Anovulation and infertility
2. Increase causes
preecplampsia and GDM
o Leptin is also produced by placenta
o May play a role in regulation of
growth
o Placental weight is correlated with
leptin levels (UC blood
measurement)
o Leptin and adiponectin cytokine
involved in fetal growth
6. Increase ghrelin levels (Increase in
mid-pregnancy and decrease until term)
o Produced by the placenta
o Role in fetal growth and cell
proliferation
o Regulates GH secretion
7. Electrolyte and mineral Metabolism
NORMAL: 1000 mEq of Na and 300 mEq of K
o Large accumulations of sodium and
potassium that decreases in the
plasma.
o Increase in their glomerular filtration,
but the excretion of these
electrolytes are unchanged as a
result of increased tubular
resorption
o Serum concentrations are
decreased slightly because of
expanded plasma volume
o Progesterone counters
aldo erone effec on na ri e i
and kaliuresis.
o CALCIUM - plasma levels decline,
follows lowered plasma Albumin
concentrations decrease in the
amt. of circulating protein-bound
nonionized calcium
Serum ionized Ca levels
remain unchanged
Fetus demands on maternal
5

Ca: doubing of maternal
intestinal Ca absorption by
1,25-dihydroxyvitamin D3
o MAGNESIUM: plasma levels
decline. Lowered plasma proteins
cause little of the minerals that are
bound.
o PHOSPHATE: within non pregnant
range. The renal threshold for
inorganic phosphates excretion is
elevated in pregnancy due to
increased calcitonin.
o IODINE: Increase during normal
pregnancy
Maternal Thyroxine (T4)
production increases to
maintain maternal
euthyroidism and to transfer
thyroid hormones to the
fetus early in the gestation
before the fetal thyroid
functioning
Fetal Thyroid hormone
increases during the 2nd
half of pregnancy -- this
contributes to increased
maternal iodine
requirements because
iodide crosses the placenta
Primary route of Iodine
extractions is through the
kidney in the early part of
pregnancy the iodide
glomerular filtration rate
increases by 30 to 50
percent
Placenta has the ability to
store Iodine
o IRON: pregnancy induces minimal
change in iron metabolism.
HEMATOLOGIC CHANGES
A. Blood Volume
- Maternal blood volume increases during pregnancy
(to about 40-45% more than the usual). Increase in
both.
- A fetus is not essential in the production of
hypervolemia, a hyadatidiform cyst also produces
increased ECV.
Functions:
Meet the demands of the enlarged uterus
Oxygen delivery
Protect both mother and fetus from the
deleterious effects of impaired venous return
supine/erect
Safegaurd the mother against adverse
effects of parturition increase blood loss
Usual blood loss in vaginal
delivery = 500-600ml
Usual blood loss in caesarean
delivery or twins = 1000ml
st
- Begins to increase during the 1 tri. By 12
menstrual weeks, plasma volume expands by
approximately 15%
nd
- Most rapid during the 2 trimester; slower during
rd
3 trimester to plateau during the weeks
MATERNAL PHYSIOLOGY: PDV
- Expansion is both plasma > erythrocytes (average
450mL)
- Moderate erythroid hyperplasia in bone marrow
- Reticulocyte count is slightly elevated
- Slightly elevated reticulocyte count during
pregnancy. Followed by increased levels of
rd
erythropoietin peaking at 3 trimester and
corresponds to maximal erythrocyte production.
- delicate/may cause heart failure: Heart may not be
able to handle BV at times of greater increase in
BV/CO
(immediately after delivery) maximal Work Load
Contraction increase pump
Postpartum extra fluid in the circulatory system
comes back into circulatory system; increase in
venous return and decrease in intraabdominal
pressure
First week puerperium: mobilization of fluid from
interstitium to vascular compartment; increases
blood flow back to heart
B. Hemoglobin and Hematocrit
o Decreases slightly during pregnancy.
o Due to increase in plasma voume (dilution
effect) physiologic anemia
o Whole blood viscosity also goes down with it
o Hgb average: 12.5 mg/dL; can go as low as
11.0 mg/dL (if low: iron deficiency rather than
pregnancy hypervolemia)
C. Iron
1. Storage Iron
o Total iron content in women: 2-2.5 g.
o Hemoglobin and Myoglobin
o Iron stores 300mg
2. Iron Requirements
o The iron requirement for normal
pregnancy is 1000 mg.
o 300 mg.: actively transferred to the fetus
and placenta
o 200 mg.: lost through various routes (GI)
o As blood erythrocyte volume expand,
more iron is needed, Thus another 500
mg is required, because 1 mL. RBC
contains 1.1 mg at an expanded volume
of 450 mL.
o The requirement becomes increased,
especially during the second half. It now
become about 6-7 g a day from
exogenous sources.
3. Pueperium
o 500 to 600mL of predelivery whole blood
are lost with vaginal delivery of a single
fetus
o CS or with twins: 1000mL
o Bleeding after birth: Originating from the
placental implantation site, the placenta
itself, the laceration/episiostomy, and in
the lochia.
IMMUNOLOGICAL FUNCTIONS
- Pregnancy reduces the effects of a variety of
cellular and humoral mediated immune
re pon e in order o accommoda e he foreign
semiallogenic fetal graft
6

- proinflammatory and antiinflamatory depending
on the stage
Stages:
1. Proinflammatory early pregnancy
- during the implantation and
placentation, the blastocyst must break
through the uterine cavity. Trophoblast
must replace endothelium and vascular
S. muscle of the BV to have good B.
flow these processes causes
invading, dying and repairing needing an
inflammatory envi.
2. Antiinflammatory - Midpregnancy
- fetal Gand D anti-inflammatory state
is needed
3. Influx of Immune Cells - Partuition
- in the myometrium to promote
recrudescence of an inflammatory
process
- Important inflammatory component
S pre ion of Th and Tc 1 cell hich
decreases secretion of IL-2 interferon-y and TNF-B
S pre ed Th1 prerequisite for
pregnancy continuation
- Explains pregnancy related remission of
autoimmune disorders (R. arthritis, Multiple
Sclerosis and Hashimoto thyroiditis - Th1
mediated) Th1 suppression failure causes
preeclampsia
preg la ion of Th2 increase IL-4, IL-6
and IL-13
Cer ical m c peak Ig A and G
st
IL-B in cervical and vaginal mucus 1
trimester : 10 fold greater
* WBC increase indicator in infection (5-10k/mm)
- sometimes goes over 10k
A. Leukocytes
nd
o 2 tri and after - depressed
polymorphonuclear leukocyte
chemotaxis and adherence functions
Relaxin impairs the
Neutrophil activation
o Depressed Leukocyte functions =
improvement of some autoimmune
MATERNAL PHYSIOLOGY: PDV
o During labor and the early puerperium,
values may become markedly elevated,
attaining levels of 25,000/ L
NORMAL: 5,000-12,000/µL.
o 3rd trimester, the percentages of
granulocytes and CD8 T lymphocytes
are significantly increased, along with a
concomitant reduction in the
percentages of CD4 T lymphocytes and
monocytes
B. Inflammatory Markers
o Leukocyte Alkaline Phosphatase (LAP)
is increased beginning quite early in
pregnancy
o 1000-fold increased response of C-
reactive protein (acute-phase serum
reactant) increasing during labor
o Elevated ESR (Erythrocyte
Sedimentation Rate) due to increased
globulins and fibrinogen
rd
o 2nd and 3 tri: C3 and C4 are also
increased
o Procalcitonin - a normal precursor of
calcitonin, increase at the end of the 3rd
trimester and through the first few
postpartum days. Elevated in severe
bacterial infections but remain low in
viral infections and nonspecific
inflammatory disease
C. Coagulation and Fibrinolysis
o The coagulation cascade is activated
during normal pregnancy.
o Increased concentrations of all clotting
factors except XI and XIII
o Clotting time no significant change
considering the substantive
physiological increase in plasma volume
in normal pregnancy, such increased
concentrations represent a markedly
augmented production of these
procoagulants
o Progressive increases in the level and
rate of thrombin generation throughout
gestation. These returned to
preconceptional levels by 1 year after
pregnancy
o The percentage in high-molecular
weight fibrinogen is unchanged
contributing to the increased ESR
o Levels of coagulation factors can be
duplicated by the administration of
estrogen plus progestin contraceptive
tablets
o Tissue plasminogen activator (tPA)
converts plasminogen into plasmin,
which causes fibrinolysis and produces
fibrin-degradation products such as D-
dimers decreased fibrinolytic activity
o Platelets:
Decreased slightly during pregnancy
o 213,000/ L compared i h
250,000/ L in nonpregnan con rol
women partially due to
hemodilutional effects.
Increased platelet consumption,
leading to a greater proportion of
younger and therefore larger
platelets
7

Midpregnancy: Increase production
of thromboxane A2, which induces
platelet aggregation (Because of
splenic enlargement)
o Regulatory Proteins:
- natural inhibitors of coagulation:
Proteins C and S and antithrombin
Resistance to Activated C,
along with a decrease in free
protein S and factor V
(neutralizing factor Va and VIIIa)
Increase in factor VIII
Constant antithrombin
o Spleen:
Enlarges by 50% - by the end of
pregnancy
Cause of this splenomegaly is
unknown, but it might follow the
increased blood volume and/or
the hemodynamic changes of
pregnancy
CARDIOVASCULAR SYSTEM
o The most important changes in the CVS
is apparent during the first 8 weeks of
pregnancy.
o Brachial systolic blood pressure,
diastolic blood pressure, and central
systolic blood pressure are all
significantly lower 6 to 7 weeks from the
last menstrual period
th
o CO is increased at 5 week and reflects
a reduced systemic vascular resistance
and an increased HR
o Increase Resting Pulse (10 bpm)
- P. Volume expansion and
Preload (bet. 10 20 weeks)
o Ventricular performance during
pregnancy is influenced by the decrease
in the systemic vascular resistance and
changes in pulsatile arterial flow
o Vascular Resistance:
Human Vascular endothelial cells
express estrogen receptors and in
response to Estradiol rapidly
increase vasodilating NO and PGI2
A. Heart
o The heart is displaced to the left and
upward as a result of diaphragmatic
enlargement
o It is also somewhat rotated on its long
axis Apex moved laterally Larger
cardiac silhouette in radiograph
o Some degree of pericardial effusion
o Slight deviation of electrical axis to the
left (ECG) because of altered position
but no characteristic changes in ECG
o Alterations in cardiac sounds:
Exaggerated splitting of the first
nd
heart sound; no change in 2 ;
and a loud easily heard 3
rd
sound.
Systolic murmur (90%)
intensified at inspiration;
disappears shortly after delivery;
more volume handled by the
heart. Diastolic murmur
cardiac disease
Soft Diastolic murmur (10%)
from the breast vasculature
MATERNAL PHYSIOLOGY: PDV
o Ventricular function during pregnancy is
normal (as estimated by the Braunwald
ventricular function graph)
1. Remodelling (please compare to
Williams because it says differently
compared to this)
o Due to high levels of estrogen and
progesterone
o Increase in preload + increased blood
volume = increase in left atrial diameter
o Increased aortic distensibility +
decreased VR = decreased afterload
o Response to circulating levels of
Estrogen and Progesterone
o Increase in preload develops in concert
with the increment in BV increase in
left atrial diameter
o 5 months after hypertrophy = mild
residual persists
B. Cardiac Output
o Arterial blood pressure and vascular
resistance are decreased, while ECV,
maternal weight and metabolic rates
increase.
o Increased in 6 weeks
o 4.8 L/min before fertilization and 7 after
st
1 tri
o Increase in CO accompanied by a
modest decrease in mean blood
pressure - from a decline in diastolic
pressure
o CO is HIGHER in the RECUMBENT
position; because in the supine position,
the uterus impedes cardiac venous
return from the IVC Cardiac filling
may be reduced
o CO becomes appreciably greater at the
nd
2 stage of labor with forceful expulsion.
o In multifetal pregnancies, there is also
increase in CO predominantly because
of greater SV and HR.
Left atrial diameter and left
ventricular end-diastolic diameter
are also increased due to
augmented preload
The increased heart rate and
inotropic contractility imply that
cardiovascular reserve is reduced
C. Hemodynamic Function in Late Pregnancy
o Increases in HR, SV, and CO.(although
increase in CO LV func as measured by
Stroke work remains similar to
nonpregnant)
o Decrease in Systemic vascular and
Pulmonary vascular resistance.
o Decrease Colloid Osmotic pressure
o No change in pulmonary capillary wedge
pressure, and central venous pressure
D. Circulation and Blood Pressure
o Brachial Artery pressure: Sitting <
Lateral recumbent supine
o BP returns to baseline at term
o Labor: increase in CO and BP
o After labor: CO initially increases then
decreases within the first hour to reach
baseline 2 weeks postP
o Atrial pressure decreases to a nadir at
24 -26 weeks and rises after
o Decrease: Diastolic > Systolic
8

o Antecubital venous pressure =
unchanged
o Supine: femoral V. pressureincrease
o Venous BF in the legs is retarded except
when in lateral recumbent
o Blood stagnation in the lower extremities
during latter pregnancy - occlusion of
the pelvic veins and inferior vena cava
by the enlarged uterus
o Elevated venous pressure returns to
normal when the pregnant woman lies
on her side and immediately after
delivery dependent edema frequently
experienced and to the development of
varicose veins in the legs and vulva, as
well as hemorrhoids + predispose to
deep-vein thrombosis.
1. Supine Hypotension
o Supine Hypotensive Syndrome
- compression of great vessels by
uterus
o Uterine arterial pressure < Brachial
artery affects fetal HR pattern
Increase Venous return compressed IVC (supine)
below the level of the uterus edema and
varicose veins
Othrostatic hypotension
Increase volume and increased blood vessel and
blood con ainer = pre re no increa ed generall
low in 2dn trimester
Ex. 80-85 MAP
Preecplamsia increase in BP
E. Renin, Angiotensin II and Plasma Volume
o RAA axis controls salt and water volume.
All components of the system are
increased during pregnancy.
o Renin is produced by maternal kidney
and placenta
o Increased Renin substrate (angiotensin)
produced in fetal and maternal liver
o Actual hormones are secreted by the
maternal kidney and the uteroplacental
unit; increase attributed to increased
st
estrogen secretion (most important 1
trimester)
o Sensitivity to angiotensin II = increased
because of vessel wall refractoriness
(lost after delivery of placenta 15 to 30
mins)
o Prostaglandin vascular response to
Angiotensin II
o Exogenous progesterone does not
restore angiotensin II refractoriness to
women with gestational hypertension,
this can be done with infusion of its
major metabolite, 5 -
dihydroprogesterone
F. Cardiac Natriuretic Peptides
o ANP and BNP (B-type NP) secrete by
cardiomyoctes in response to stretch
o Unchanged despite increase in plasma
volume
o Provokes Natriuresis, Diuresis and
Vasculer SM relaxation
o BNP and NT pro-BNP (amino-terminal
pro-brain NP)
screening for depressed LV
systolic function (for preggy and non-preggy)
MATERNAL PHYSIOLOGY: PDV
- increase (severe preeclamsia)
due to increased cardiac strain from induced
afterload
o ANP
- participate in extracellular fluid
expansion and in increased plasma aldosterone
o CNP (C-type NP)
- predominantly noncardiac tissues
- fetal bone growth regulator
G. Prostaglandin
o Increase production of prostaglandin
play a central role in regulating vascular
tone, BP and Na balance
o Renal Medullary Prostaglandin E2
synthesis increases during late
pregnancy and presumed to be
natriuretic
o PGI2 (prostacyclin)
- prostaglandin of endothelium
increased during late
pregnancy and regulates BP
and platelet function
- Implicated in angiotensin
resistance
- Ratio with thromboxane in urine
and blood related to preeclampsia pathogenesis
H. Endothelins
o Endothelin-1 is produced in the endothelial
cells and vascular smooth muscle to
regulate vasomotor tone by inducing
vasoconstriction.
o It has been identified in the amnion, amniotic
fluid, deciduas and placental tissue.
o It is stimulated by angiotensin II, Arg-
vassopressin, and thrombin
o It can stimulate secretion of ANP,
aldosterone and catecholamines.
I. Nitric Oxide
o Potent vasodilator endothelial cells
o Imp. Mediators of placental vascular tone
and dev.
o Abnormal associated with preeclampsia
RESPIRATORY TRACT
Facts:
The diaphragm rises about 4 cm. during
pregnancy
Subcostal angle widens as transverse
diameter of the thoracic cage widens by +
2 cm.
+ 6 cm. to the thoracic circumference. But
this adaptation not sufficient to prevent
residual volume created by think elevated
diaphragm
Greater diaphragmatic excursion
9
 MATERNAL PHYSIOLOGY: PDV
o Increased respiratory effort in turn
reduction in PCO2
- induced by Progesterone in a
lesser degree by Estrogen

Proge erone appear o ac cen rall , here i

lowers the threshold and increases the sensitivity of
the chemoreflex response to CO2 increases
Ventilatory drive
* Progesterone is also sensitive to PO2 hypoxic
A. Pulmonary Function state (high altitude/exercise)
1. Functional residual capacity (FRC) decreases * Hyperventilation high circulating concentrations
by approximately 20 to 30 percent or 400 to 700 mL of progesterone
during pregnancy o Respiratory Alkalosis
Composition: - Minute ventilation increases during
a. Expiratory reserve volume which pregnancy
decreases 15 to 20 - To compensate moderate
percent or 200 to 300 mL decrease in plasma bicarbonate from 26 mmol to 22
b. Residual volume which decreases 20 to mmol minimal increase in the pH shifts the
125 percent or 200 to 400 mL. oxygen dissociation curve to the left increases the
FRC and re id al ol me decline d e o diaphragm affinity of maternal hemoglobin for oxygen (Bohr
elevation, and significant reductions are observed by effect)
the sixth month with a progressive decline across - BUT offset because the slight pH
pregnancy increase also stimulates an increase in 2,3-
2. Inspiratory capacity (the maximum volume that diphosphoglycerate in maternal erythrocytes
can be inhaled from FRC) shifts the curve back to the right reduced Pco2
- increases by 5 to 10 percent or 200 to 250 mL from maternal hyperventilation aids carbon dioxide
during pregnancy (waste) transfer from the fetus to the mother while
3. Total lung capacity (the combination of FRC and also aiding oxygen release to the fetus
inspiratory capacity)
- unchanged or decreases by less than 5 percent at * Gas exchange across the placenta similar to gas
term exchange in lungs th arterial supply to the placenta
is low O2 high CO2 after equilibration with maternal
4. Tidal Volume and Resting Minute Ventilation blood umbilical venous blood has taken on O2 and
Increase (but RR unchanged) delivered CO2
o Increase in RMV * Difference bet. Uterine and umbilical venous blood
a. Stimulated by progesterone is due to the high rate of O2 extraction and CO2
b. Low expiratory reserve volume production by the syncytiotrophoblast and by the
c. Compensated respiratory alkalosis relatively large areas of the placenta that are
5. Peak expiratory flow rates unavailable for exchange.
- increase progressively * Despite low PO2and the metabolic activity of
6. Lung compliance syncytio., the O2 content in umbilical venous blood
- unaffected is the similar to maternal arterial blood because of
7. Airway conductance higher affinity of hemoglobin in fetal blood
- increased and total pulmonary resistance reduced * PCO2, Bicarb and pH are all the same in umbilical
- possibly as a result of progesterone venous blood
8. Maximum breathing capacity and forced or Although the CO is increased, the lowered Hgb
timed vital capacity content of blood accounts for poor oxygen delivery =
- not altered appreciably PHYSIOLOGIC ANEMIA OF PREGNANCY (lowered
9. Critical closing volume atrial oxygen tension)
- (the lung volume at which airways in the dependent
parts of the lung begin to close during expiration) URINARY SYSTEM
unclear if it is higher in pregnancy
10. Total pulmonary resistance A. Kidneys
- reduced o The size of the kidney increases slightly
- Due to progesterone during pregnancy. (About 1.5 cm.
- Hormones of pregnancy will relax airway longer than normal)
smooth muscle = increase functional dead space = o Afferent and efferent and glomerular
decrease airway resistance arterioles are major sites of resistance in
blood flow.
B. Oxygen Delivery
1. Maternal hemoglobin 1. GFR and RBF is INCREASED.
nd
- (in increased pH) has greater affinity for oxygen - Where GFR can rise up to 25% 2
thus increasing total oxygen-carrying capacity. week after conception and 50% by the
nd
2. Maternal atriovenous oxygen difference beginning of the 2 trimester
- decreased. Effects for hyperfiltration:
1. Hypervolemia-induced
C. Acid Base Balance hemodilution
o Physiologic Dyspnea - lowers the protein
- Increased TV that lowers the blood concentration and oncotic pressure of
PCO2 slightly plasma entering the glomerular
microcirculation
2. Increase in Renal Plasma Flow
10

- 80% increase before the
st
end of the 1 trimester
Ele a ed GFR per i n il erm
increase urination
- Nonselective and selective inhibition of
NO synthase isoforms attenuate the
renal hemodynamic changes
2. Marked GFR during puerperium
st
1 post partum day from the reduced
glomerular capillary oncotic pressure
3. Reversal of the gestational hypervolemia
and hemodilution
- still evident on the first postpartum day,
eventuates by the second week postpartum
4. Relaxin
- mediating both increased GFR
and renal blood flow
- increases endothelin and nitric
oxide production in the renal circulation renal
vasodilation and decreased renal afferent and
efferent arteriolar resistance increase in renal
blood flow and GFR.
- increase vascular gelatinase
activity renal vasodilation, glomerular
hyperfiltration, and reduced myogenic reactivity
of small renal arteries
- enchances NO production by an
C. Ureter (HYDRONEPHROSIS / HYDROURETER)
endothelin B receptor-mediated mechanism
5. Urinary flow and sodium excretion
- Late in pregnancy average less than half
the excretion rate in the supine position than in
the recumbent position.
- Increased excretion of nutrients via the
urine. Such nutrients include amino acids and
water-soluble
vitamins.
B. Renal Function Test
1. The plasma concentration of both urea
and creatinine (0.7 to 0.5 mg/dL)
- often decrease in pregnancy
attributed to the increased GFR. Much is lost
in the urine.
2. Creatinine Clearance
- Increased 30% (Nonpregnant: 100 115
mL/min)
D. Bladder
- Decreased serum level
- very useful test to estimate renal function.
o During the day, women tend to
accumulate the water in the
form of dependent edema.
o During the night at recumbent
mobilize fluid with diuresis
URINE IS DILUTE
MATERNAL PHYSIOLOGY: PDV
Failure of a pregnant woman to excrete
concentrated urine after 18 hours of
fluid restriction DOES NOT
NECESSARILY signify renal damage
3. Urinalysis
o Glucosuria in pregnancy is not
immediately abnormal; increased
GFR + low reabsorptive capacity of
the tubules account for glucose in
the urine.
o Hematuria difficult labor and
delivery trauma to the bladder
and urethra
o Proteinuria is not always evident
- Excretion rate of more than 150
mg/day aforementioned hyperfiltration
and possible reduction of tubular
reabsorption, significant proteinuria
during pregnancy is usually defined as a
protein excretion rate of at least 300
mg/day
- Measuring Urine Protein:
1. Dipstick BUT renal
concentration and dilution of urine is not
accounted for
2. 24- hour affected by urinary
tract dilatation errors related to both
retention and timing (remaining urine may
have formed hours before collection). Advice
pt. hydration and lateral recumbent for 45
to 60 minutes. Discard first
collection. Final hour place in recumbent
again at the end of this hour final
collected urine is incorporated into
the total collected volume.
3. CHO/ Crea ration promising
approach data can be obtained quickly
and collection errors avoided. BUT CHO per
unit of Crea excreted ir not constant
o With the uterus rising out the pelvis, the
ureters may be compressed laterally
displaces and compresses at the pelvic brim
o There is unequal degree of dilatation
because of the compression on the:
LEFT: Sigmoid colon
RIGHT: Greater compression by
dextrorotation of the uterus + R. ovarian
Vein complex is dilated and lies
obliquely over the R. ureter
o Can also be caused by elevated
Progesterone levels
o Ureteral elongation accompanies distention
frequently thrown into curves especially
the smaller one which become angulated
o Estrogen: growth promoting
o Progesterone: generalized atony of the UT
musculature slowing musculature
o Hypertrophy in ureter
o Return dapat within 6 weeks postpartum
o Few before 12 weeks
o Increased uterine size, the hyperemia that
affects all pelvic organs,
o Hyperplasia of bladder muscle and
connective tissues elevate the trigone
thickening of its posterior, or intraureteric,
margin marked deepening and widening
of the trigone.
11

o There are no mucosal changes other than
an increase in the size and tortuosity of its
blood vessels
o Bladder pressure from 8 to 20 cm H2O and
to compensate for reduced bladder capacity
absolute and functional urethral length
increase (6.7 and 4.8 mm respectively)
o Increase pressure (70 93 cmH2O)
Pressure effect pushed by the uterus
polyuria
Happens because:
st
1. 1 trimester enlarged uterus
rd
2. 3 tri pushing of the presenting
part/fetus
o Toward the end of pregnancy
-(particularly in nulliparas in whom the
presenting part often engages before labor)
the entire base of the bladder is pushed
forward and upward the normal convex
surface into a concavity
As a result, difficulties in diagnostic and
therapeutic procedures are greatly
increased.
- pressure from the presenting part impairs
blood and lymph drainage from the bladder
base, often rendering the area edematous,
easily traumatized, and possibly more
susceptible to infection + marked
hypervascularity
o Stasis UTI/pyelonephritis
Gastrointestinal Tract
A. Pregnancy Gingivitis
o Gums are hyperemic and softened and may
bleed when brushing
o Subsides postpartum
o Due to increased Estrogen
o ep li gra idar m pyogenic granuloma;
focal and highly vascular swelling of the
gums; spongy with raised nodule, ptyalism
and excessive salivation
B. Stomach and intestines
o Displaced by the enlarging uterus
o Vomiting
o Appendix, for instance, is usually displaced
upward and somewhat laterally as the
uterus enlarges. At times, it may reach the
right flank
o Progesterone decreased motility
o Estrogen decreased Hydrochloric acid
o Slow emptying increase SI absorption
(ferrous and calcium) and LI absorption of
water increased constipation
C. Pyrosis (heartburn)
o Common during pregnancy and is most
likely caused by reflux of acidic secretions
into the lower esophagus
o Although the altered stomach position
probably contributes to its frequency,
o Lower esophageal sphincter tone also is
decreased (due to progesterone)
o Intraesophageal pressures are lower and
intragastric pressures higher in pregnant
women. At the same time, esophageal
peristalsis has lower wave speed and lower
amplitude
D. Gastric emptying time
o Unchanged during each trimester
MATERNAL PHYSIOLOGY: PDV
o During labor, however, and especially after
administration of analgesic agents, gastric
emptying time may be appreciably
prolonged = Do not feed
o Danger of Gen. Anesthesia regurgitation
and aspiration of food-laden or highly acidic
gastric contents
o Decreased motility = prolonged transit time
= better ferrous & Ca & H2O absorption
o Can cause increased
flatulence/constipation/ bloated
o Mechanical displacement on rectosigmoid
area = constipation and hemorrhoid
formation
F. Liver
o Does not enlarge
o Increase in hepatic arterial and portal
venous blood flow
o Total ALP activity can double - the increase
is contributed by the heat-stable placental
ALP isoenzyme, Serum Aspartate
transaminase (AST), alanine transaminase
(ALT) and y-glutamyl transpeptidase (GGT)
and bilirubin levels are usually lower in
pregnancy
o Serum albumin concentration decreases. By
late pregnancy, albumin concentrations may
be near 3.0 g/dL (approximately 4.3 g/dL in
nonpregnant women)
o Total body albumin levels are increased,
o However, because of pregnancy-associated
increased plasma volume. Serum globulin
levels are also slightly higher
o Leucine aminopeptidase (proteolytic liver
enzyme) whose serum levels may be
increased with liver disease. Its activity is
markedly elevated in pregnant women. The
increase, however, results from a
pregnancy-specific enzyme(s) with distinct
substrate specificities
o Pregnancy-induced aminopeptidase has
oxytocinase and vasopressinase activity that
occasionally causes transient diabetes
insipidus
G. Gallbladder
o Reduce Gallbladder contractility
increased residual volume
o Progesterone potentially impairs gallbladder
contraction by inhibiting cholecystokinin-
mediated smooth muscle stimulation, which
is the primary regulator of gallbladder
contraction.
o Impaired emptying, subsequent stasis, and
an increased bile cholesterol saturation
increased prevalence of cholesterol
gallstones in multiparas
o cause intrahepatic cholestasis and pruritus
gravidarum from retained bile salts
o Intrahepatic cholestasis has been linked to
high circulating levels of estrogen, which
inhibit intraductal bile acid transport
Increased progesterone levels and genetic
factors have been implicated in the
pathogenesis
ENDOCRINE SYSTEM
A. Pituitary glands
o Enlarges during pregnancy (138%)
o Size can compress the optic chiasma to
reduce visual fields but impaired vision is
rare
12

o Due to Estrogen-stimulated hypertrophy and
hyperplasia of the lactotrophs
o Maternal serum prolactin levels parallel the
increasing size
o Gonadotrophs decline in number, and
corticotrophs and thyrotrophs remain
constant.
o Somatotrophs are generally suppressed due
to negative feedback by the placental
production of growth hormone.
o Involutes rapidly thereafter and reaches
normal size by 6 months postpartum
o Pituitary gland not necessarily essential
because women without it can still take
supplements and have a normal pregnancy
o Posterior lobe increase in oxytocin
production especially nearing term
o Increase vascularity is not much
enlargement Ischemia bec. of
hemorrhage hypopituiotarism/ knock out
blood supply panpi i ari m (Sheehan )
B. Growth Hormone
st
o At the 1 trimester, from the maternal
pituitary gland
o GH in the serum and AF are at non-
pregnant values (0.5 to 7.5 ng/mL).
o 8 weeks secreted by the placenta is
detectable
o 17 weeks placenta is the source of GH
th
o Serum values of GH increase by the 10
week and plateau after 28 weeks. (from 10
to 14 ng/mL)
th th
o GH in the AF peaks by the 14 15 week,
th
and reach baseline by the 36 week.
C. Placental growth hormone
o (differs from pituitary growth hormone by 13
amino acid residues)
o secreted by syncytiotrophoblast in a
nonpulsatile fashion
o to have some influence on fetal growth as
well as preeclampsia development
o major determinant of maternal insulin
resistance after midpregnancy.
o Maternal serum levels correlate positively
with birthweight but negatively with fetal-
growth restriction and uterine artery
resistance fetal growth still progresses in
the complete absence of this hormone.
o Although not absolutely essential, the
hormone may act in concert with placental
lactogen and somatolactogens to regulate
fetal growth
D. Prolactin
o Prolactin has a 10-fold increase in the
maternal blood (150 ng/mL)
o After delivery, there is a paradoxical
decrease even in breastfeeding women
o Pulsatile burst of prolactin in response to
sucking.
o Estrogen can increase the activation of the
lactotrophs in the pituitary
o TRH increases prolactin
o Serotonin also increases prolactin secretion.
o Its principal function is Lactation
o Early in pregnancy initiate DNA synthesis
and mitosis of glandular epithelial cells and
presecretory alveolar cells of the breast
o Increases prolactin and estrogen receptors
in the cell
MATERNAL PHYSIOLOGY: PDV
o Promotes mammary alveolar cell RNA
sysnthesis, galactopoiesis and production of
casein, lactalbumin, lactose and lipids The
amniotic fluid also contains appreciable
amounts of prolactin, probably secreted by
the decidua
o Impairs water transfer from the fetus into the
maternal compartment, thus preventing fetal
dehydration
E. Oxytocin and ADH
o Secreted from the posterior pituitary.
o Levels of antidiuretic hormone, also called
vasopressin, do not change
Please note: Further discussion daw nasa
Chapters 21 (p. 426) and 36 (p. 672) Nakakalula
na kasi idagdag isang chapter nanaman yun.
F. Thyroid
st
o 1 tri - increase of thyroxine- binding globin
(TBG) in response to Estrogen
o Thyroidal activating substances are also
made in the placenta.
o The thyroid is controlled by both thyrotrophin
and hCG during normal and abnormal
pregnancies
o Increase clearance of iodide and losses to
the fetus during gestation, may result to a
iodine deficiency state.
o Hyperplasia of the glandular tissue +
st
vascuarity. (volume increase 12 mL 1 tri to
15 mL at del) inversely proportional to serum
thyrotropin
o Increased hCG production indeed causes
activation of the thyroid.
o Minimal transfer of thyroxine from mother to
child somewhere in advanced age.
o Thyrotropin-releasing hormone (TRH) is
secreted by the hypothalamus stimulates
thyrotrope cells of the anterior pituitary
release thyroid-stimulating hormone (TSH)
or thyrotropin.
o TRH levels are not increased during normal
pregnancy. However, this neurotransmitter
does cross the placenta and may serve to
stimulate the fetal pituitary to secrete
thyrotropin
o Pregnancy causes TG to increase
THproduction = mild hyperthyroid state
o Full blown lang sa DM
13

Explanation to the figure above:
1. Maternal changes include a marked and early
increase in hepatic production of thyroxine-binding
globulin (TBG) and placental production of human
chorionic gonadotropin (hCG).
2. Increased thyroxine-binding globulin increases
serum thyroxine (T4) concentrations.
3. hCG has thyrotropin-like activity and stimulates
maternal free T4 secretion inhibits maternal
secretion of thyrotropin. Except for minimally
increased free T4 levels when hCG peaks, these
levels are essentially unchanged.
4. Fetal levels of all serum thyroid analytes increase
incrementally across pregnancy.
5. Fetal triiodothyronine (T3) does not increase until
late pregnancy
G. Iodine
o Increase
o If low intake low thyroxine and increased
TSH
o For the fetus, early exposure to thyroid
hormone is essential for the nervous
system, and
o Iodine deficiency is the most common
preventable cause of impaired neurological
development
H. Parathyroid gland and Calcitonin
o Acute or chronic decreases in plasma
calcium or acute decreases in magnesium
stimulate parathyroid hormone (PTH)
release.
o increased calcium and magnesium levels
suppress PTH levels.
o Action on: Bone resorption, intestinal
absorption, and kidney reabsorption is to
increase extracellular fluid calcium
concentrations and decrease phosphate
levels
o Fetal skeleton miniralization requires 30g of
rd
Ca: 3 tri
o Ca absorbed gradually increases
rd
400mg/day at 3 tri
o Ca absorption is mediated by elevated
maternal 1,25 dihydroxyvitamin D -- this
occurs despite decreased levels during early
pregnancy of PTH, which is the normal
stimulus for active Vit D prod.
st
o PTH at 1 tri is low and increases after
MATERNAL PHYSIOLOGY: PDV
o Increased production of active vitamin D is
likely due to placental production of either
PTH or a PTH-related protein (PTH-rP)
o Outside pregnancy and lactation, PTH-rP is
usually only detectable in serum of women
with hypercalcemia due to malignancy
o During pregnancy, PTH-rP concentrations
increase significantly - synthesized in both
fetal tissues and maternal breasts
o Intensified levels are attributed to the fact
that maternal calcium stores are low.
o PTH is blocked by estrogen.
o Physiological hyperparathyroidism of
pregnancy.
- Calcium and magnesium increase the
biosynthesis of calcitonin.
- Opposes the action of PTH by lowering
plasma calcium.
- Since pregnancy causes calcium stress,
levels of calcitonin are generally higher.
o Calcitonin
- C cells that secrete calcitonin are derived
embryologically from the neural crest and are
located predominantly in the perifollicular areas of
the thyroid gland
- Increased by gastric hormones (Gastrin,
Pengastrin, Glucagon and pancreozymin + food
ingestion)
I. Adrenal Glands
1. Cortisol
o Considerable increase in cortisol serum
concentration but much is bound to
transcortin - cortisol-binding globulin
o Adrenal secretion rate of this
glucocorticoid is probably decreases
o Metabolic clearance rate is lower
because its half-life is doubled
o Estrogen and OC change in level
o During early pregnancy, the levels of
circulating adrenocorticotropic hormone
(ACTH), also known as corticotropin, are
reduced strikingly As pregnancy
progresses, ACTH and free cortisol
levels rise equally and strikingly This
apparent paradox is not understood
completely
Probable reasons:
a. some suggest that the
higher free cortisol levels observed in pregnancy
result from a
re e ing of he ma ernal feedback
mechanism to higher levels
b. might result from tissue
refractoriness to cortisol
c. antagonistic action of
progesterone on mineralocorticoids Elevated
progesterone
elevated free cortisol homeostasis
o Elevated maternal cortisol and
aldosterone secretion are necessary to
maintain the normal increase in plasma
volume during late pregnancy
2. Aldosterone
o 15 weeks maternal adrenals secrete
increased aldosterone
rd
o 3 tri 1mg/day
o IF Na intake is restricted Aldosterone is
elevated
14

o Considerable increase in secretion in
order to protect the mother from the
natriuretic effect of preogesterone and
ANP.
o Levels of renin and angiotensin II
substrate normally are increased,
especially during the latter half of
pregnancy rise to increased plasma
levels of angiotensin II, which acts on
the zona glomerulosa of the maternal
adrenal glands and accounts for the
markedly elevated aldosterone secretion
o Increased aldosterone - protection
against the natriuretic effect of
progesterone and atrial natriuretic
peptide
o Modulating trophoblast growth and
placental size
3. Deoxycorticosterone
o Increased rise near 1500 pg/mL at term
(>15 fold)
o Represents increased kidney
production caused by estrogen
stimulation
o Increased in fetal > maternal blood
4. Androgen
o Maternal plasma levels of both
androstenedione and testosterone are
increased during pregnancy
o Both androgens are converted to
estradiol in the placenta, which
increases their clearance rates
o Conversely, increased plasma sex
hormone-binding globulin in pregnant
women retards testosterone clearance
production rates of maternal
testosterone and androstenedione
during human pregnancy are increased.
o The source of this increased C19-
steroid production is unknown, but it
likely originates in the ovary.
o Little or no testosterone in maternal
plasma enters the fetal circulation as
testosterone. Even when massive
testosterone levels are found in the
circulation of pregnant women, as with
androgen-secreting tumors,
testosterone concentrations in umbilical
cord blood are likely to be undetectable
This results from the near complete
trophoblastic conversion of testosterone
to 17 -estradiol
o Maternal serum and urine levels of
dehydroepiandrosterone sulfate are
decreased during normal pregnancy
because of increased metabolic
clearance through extensive maternal
hepa ic 16 -hydroxylation and placental
conversion to estrogen
MUSCULO-SKELETAL
o Progressive lordosis is a characteristic
feature of pregnancy.
o The body is compensating for the
anterior position of the enlarging uterus.
The lordosis shifts the weight back over
the lower extremes.
o Increased mobility in the following
joints:
Sacroiliac
Sacrococcygeal
MATERNAL PHYSIOLOGY: PDV
Pubic joints
o Some symphyseal separation likely
accompanies many deliveries, those
greater than 1 cm may cause significant
pain
o Marked lordosis is already characterized
by anterior neck flexion and slumping of
the shoulder girdle which may produce
traction to the median and ulnar nerves -
--- causes pain and discomfort +
numbness
o Normal relaxation of pelvic joints
a. Due to hormones of pregnancy
b. Allow for expansion during childbirth
c. Joint laxity and mobility may
cause lower back pain in later
pregnancy
o Postpartum tailbone pain
- Due to the tailbone being flattened
and p hed o ard a bab head
passes through the pelvic outlet
during labor and delivery
o Expansion of rib cage
o Shoulders become imbalanced
Muscles that elevate shoulders/
internal rotators = tighten
Muscles that depress
shoulders/external rotators =
weaken
o Carpal tunnel syndrome compression
of the medial nerve as it passes thorugh
the wrist
o Upper extremities
Swelling, fluid retension and
increased BV can compress
tissues in extremities especially
rd
at 3 tri hand pain,
numbness upon waking up
EYES
o Even with pituitary hypertrophy, the optic
tracts are compressed, but no significant
change in vision is observed.
o Decrease in intraocular pressure due to
increased vitreous outflow.
o Decreased corneal sensitivity.
Thickness may also change as a
consequence of edema.
o Krukenberg spindles are brownish red
opacities on the posterior surface of the
cornea. Hormonal effects are causing
this phenomenon.
o Transient but reversible loss of
accommodation reflex.
CNS
o Problems with attention, concentration
rd
and memory significantly at 3 trimester
o Difficulty in sleeping, frequent
awakenings, reduce sleep efficiency and
fewer hours of sleep
o Mean blood flow in the middle and
posterior cerebral arteries decreased
(progressively from 147 and 56 mL/min
when nonpregnant to 118 and 44
mL/min late in pregnancy, respectively)
SLEEP
o 12 eek ge a ion and e ending
through the first 2 months postpartum,
15
 MATERNAL PHYSIOLOGY: PDV
women have difficulty with going to
sleep, frequent awakenings, fewer hours
of night sleep, and reduced sleep
efficiency
o The frequency and duration of sleep
apnea episodes were reported to be
decreased significantly in pregnant
women compared with those postpartum
o In the supine position, however, average
Pao2 levels were lower
o The greatest disruption of sleep is encountered
postpartum and may contribute to postpartum
blues or to frank depression

16
 OB: Fetal Growth and Development
FETAL GROWTH & DEVELOPMENT
I. Determination of Gestational Age/ Menstrual
Age
It is the time elapsed since the first day of the last
menstrual period.
Time that precedes conception.
Starting time:
- 2 weeks before ovulation and fertilization
- Nearly 3 weeks before implantation.
AVERAGE: 280 days, or 40 weeks from the first
day of the last menstruation.
corresponds to 9 1/3 months or 10 units
containing 28 days each. The unit of 28 days has
been referred to as a LUNAR MONTH of pregnancy.
Computing for the Age of Gestation (AOG):
menstrual age
in weeks, not months
based on LMP
LMP: April 20-23,2014
Today: Aug.6, 2014
Month No. of days for the month
April 10
(April has 30 days, since April 20
was the LMP, subtract 20 from 30)
May 31
June 30
July 31
August 6 (since today is Aug 6)
Total: 108 days/ 7= 15-16 weeks AOG 2
nd
trimester
Computing for Expected Date of Delivery (EDD)
Naegele R le
1. Subtract 3 months or add 9 months from the
given date
2. Add 7 days to the first day of LMP.
LMP: April 20,2014
4 20
-3 +7
1 27 Jan 27, 2015 is the EDD
This is not the exact date, it is only an
approximation
Delivery must be more or less +/- 2 weeks from
the EDD
If baby is delivers > 2 weeks the EDD post
term baby
More conveniently, pregnancy is divided into
three trimesters (each 13-14 weeks long),
because obstetrical milestones are easier to
plot.
Trimester dividing pregnancy into 3 groups;
used as reference periods
Sonographic estimate of gestational age is
usually a few days later than that determined by
the last period
Term pregnancy: 37 weeks and above
Fetus starts from union of sperm and egg
which forms zygote
<20 weeks gestation abortion
>20 weeks gestation preterm birth
Death inside uterus with AOG of <20weeks
miscarriage/ missed abortion
Red mentioned by Dra. Coloma
Yellow highlight lumabas sa samplex
Death inside uterus with AOG of >20 weeks
Intrauterine Fetal Death (IUFD)
nd
Still birth 2 half/ later part of pregnancy
Placenta previa low lying placenta; causes
bleeding
Embryo term used up to 10 weeks AOG
Fetus AOG >10weeks
II. Morphologic Growth
A. Zygote and Blastocyst Development
first 2 weeks after ovulation and then fertilization
undergoes implantation 6-7 days after fertilization
58-cell blastocyst form the 5 embryo producing
cells (the inner cell mass)
Remaining 53 cells form the placenta
trophoblast
aka Blastocyst form in which it will implant in
the uterine cavity; part of the product will
become the fetus; part will become the
placenta
B. Embryonic Period
rd
It begins at the start of the 3 weeks after
ovulation/fertilization which coincides with the time
the next menstruation would start.
From cell mass endoderm, ectoderm &
mesoderm different organ system derived from
these layers
primitive chorionic villi form
lasts 8 weeks
organogenesis takes place
hCG levels may now be measured (+ pregnancy
test)
The embryonic disc, body stalk are defined. The
chorionic sac is about 1 cm. in diameter.
Week Development
3 fetal blood vessels in the chorionic
villi appear
embryonic disc, body stalk are
defined
chorionic sac: 1cm in diameter
4 cardiovascular system has formed
& true circulation established within
the embryo and between embryo
and chorionic villi
the chorionic sac assumes a 2-3
cm diameter, and the embryo is 4-5
mm. in length
Middle Primitive heart
of 4 Arm and leg buds, and the amnion
begins to unsheathe the body stalk
to be the future umbilical cord
6 the embryo is now about 22-24
mm. in length
Fingers and toes
heart completely formed
head is larger than trunk
Arms bend at the elbow
Upper lip and external ears are
visible
C. Fetal Period
Occur at about 8 weeks after fertilization, or 10
weeks after onset of LMP.
Fetus is about 4 cm. long
1
 OB: Fetal Growth and Development
Red mentioned by Dra. Coloma

Yellow highlight lumabas sa samplex

period of growth and maturation of the structures many neonate born at this age die because
formed in the embryonic period terminal sac required for gas exchange have not yet
there is increase in size and functionality of the formed; some may survive with intensive neonatal
different systems care
Crown-to-rump length (CRL)/ sitting height CRL= 21cm
more accurate in determining AOG than standing
th
height due to the variability to maintain arms and 26 week
legs extended nociceptors present all over the body
Length is a more accurate criterion of gestational Neural pain system is developed
age than weight
th
28 week
th
11 week CRL= 25 cm
round head= ½ CRL weight= 1100 g.
Eyes closed Thin reddish skin covered in vernix caseosa
external genitalia not distinguishabke (mixture of fatty secretions of fetal sebaceous glands
physiological herniation of the gut: and desquamated epidermal cells)
intestines are located outside abdominal cavity Disappearance of papillary membrane; eyes
within abdominal end partially open
of the umbilical cord peak of isolated eye blinking
neonate born at this age has 90% survival without
th
12 week physical or neurological impairment
Uterus can be palpable above the pubic
nd
symphisis. 32 week
CRL approximately 6-7 cm. CRL= 28 cm
Centers of ossification have appeared in fatal weight= 1800 g
bones skin surface still red and wrinkled
Fingers and toes are well differentiated toenails present
Skin and nails + scattered rudiments of hair testes start to descend
External genitalia are beginning to show evidence birth of this age has good survival rate as long as
of gender given proper care
th
Spontaneous fetal movements; respond to stimuli 36 week
intestines normally located within abdomen CRL= 32cm
Weight= 2500g
th
14 week Because of deposition of subcutaneous fat, the
gender can be determined by inspection body has become more rotund, and wrinkles
of genitalia disappear
birth at this age has excellent chance of survival
th
16 week
th
CRL approximately 12 cm 40 week
Weight of about 110 g Average CRL is 36 cm. and weighs about 3600 g.
Eye movements at 16-18 weeks (coincides with Fetus is fully develop and fully functional
midbrain maturation) testes in scrotum
forearm and lower legs are crossed, fingers chest is prominent, breast protrude
flexed fingernails extend beyond fingertips
bone ossifications allow identification of bones pinae of ear contain cartilage
thru x-ray
III. Fetal-Maternal Communication System
th
20 week PLACENTA
midpoint of pregnancy has 2 parts: Decidua maternal part; chorion
fetus weighs more than 300g frondosum fetal part
Skin becomes less transparent and downy lanugo The vessels that go into the placenta go into
hairs covers the entire body the chorion frondosum it affixes itself into
Scalp hair the endometrium and then it will attach itself
fetal breathing movements become regular to the decidua basalis (invasion)
moves about every minute; active 10-20% of the Gross interface between baby and mother
time At the final structural level, they interface
CRL= 16cm at the intervillous space
Intervillous space-- space between the
th
24 week villi which is a fetal structure but what
fetus now weighs approximately 630 g. goes into this space is maternal blood
Wrinkled skin, with fat deposition. therefore it is where the interface is
Head is still quite large, with eyebrows and The transfer oxygen: MOTHER to FETUS
eyelashes fairly recognizable. The release of CO2 and metabolic wastes:
CANALICULAR PERIOD of the lungs, where the FETUS to MOTHER
bronchi and bronchioles including the alveoli Achieved by way of the nutritive component the
develop placental arm of the FMCS
Fetal lung pneumocytes begin production
of surfactant
2
 OB: Fetal Growth and Development
There is no direct communication between the
fetal and maternal blood because of the lining of the
chorion frondosum
Fetal capillaries contain the fetal blood in
the chorionic villi
Maternal blood remains in the intervillous
spaces
No gross intermingling of the macromolecular
constituents of the two circulations
Eliminates wastes to mother
Receives nutrients for the baby
O2 & CO2 exchange very vital; essential
function of respiration; assumes function of the lungs
Assumes function of the GI (absorption of
nutrients) & GU (elimination of waste)
Blood that passes through the GI and GU
of the fetus are still deoxygenated blood
so less nutrients are extracted and less
wastes eliminated
The placenta also ages efficient only up to a
certain point; eventually degenerates decreased
efficiency
>40 weeks AOG adverse effects on
baby due to less efficient placenta
THE INTERVILLOUS SPACE
Contains maternal blood (primary unit of
maternal-fetal transfer)
blood from maternal spiral arteries directly bathes
the trophoblasts.
To transfer nutrients to the fetus, blood enters the
intervillous space and the nutritive substance is
delivered to the syncitiotrophoblasts.
The same route is used to eliminate the fetal
metabolic wastes.
Thus the chorionic villi and intervillous space
function as the fetal lung, GIT and kidney.
Although renal function is not yet maximum, fetal
urine comprises a major portion of the amniotic fluid
after 16 weeks AOG
Fetal urination:
2.2 mL/h at 22 weeks
10 mL/h at 30 weeks
50 mL/h at term
The residual volume of the placenta at term is
about 140 mL. This increases by twice before
dlivery.
Uteroplacental blood flow is estimated 700-900
mL/min near term.
The blood pressure of the intervillous space is
less than uterine artery pressure, but greater than
uterine venous pressure.
Uterine venous pressure is greatly dependent on
the relative position of the mother.
FETAL CAPILLARIES
Contains the fetal blood.
The hydrostatic pressure of the fetal capillaries
traversing the chorionic villi is NOT different from
that of the intervillous space.
During normal delivery, the blood pressure of the
fetal capillaries should parallel the pressure of the
amniotic fluid and intervillous space. Otherwise, the
capillaries would collapse and fetal blood flow would
cease.
Red mentioned by Dra. Coloma
Yellow highlight lumabas sa samplex
PHYSIOLOGY OF PLACENTAL TRANSFER
A. Chorionic Villus
Substances that transfer from mother to fetus
should traverse the following:
1. Syncitiotrophoblast
2. Villous stroma
3. Fetal capillary wall
Throughout pregnancy, the syncitiotrphoblast
actively or passively permit, facilitate and adjust the
total amount of nutrients that enter the fetus.
After midpregnancy, the Langhans cells
(cytotrophoblasts), lining the innermost layer of the
chroionic villi, will decrease and will consist primarily
of syncitiotrophoblasts.
B. Regulation of Placental Transfer
The syncitiotrophoblast is the fetal tissue interface
of the whole system.
Maternal-facing surface: Complex microvillus
structure.
Fetal-facing surface: Site of transfer to the
intravillous space through which the fetal capillaries
traverse.
Variables of Maternal-Fetal Substance Transfer:
1. Concentration of the substance in the
maternal plasma; extent to which is it is
protein bound.
2. Rate of maternal blood flow
3. Area available for exchange
4. Physical properties of the tissue barrier
between the blood in the intervillous space
and capillary.
5. Biochemical machinery of the palcenta
6. Amount of substance metabolized by the
placenta
7. Area of exchange across fetal capillaries
8. Concentration of substance in the fetal
blood.
9. Specific binding or carrier proteins in the
fetal or maternal circulation.
10. Rate of fetal blood flow through the villus
capillaries.
C. Mechanism of Transfer
* study what substances are transferred via simple
diffusion and facilitated diffusion
Simple Diffusion occurs among substances with
molecular mass <500Da (These include oxygen,
CO2, water, most electrolytes and anesthetic gases)
Insulin, steroid hormones and thyroid hormones
cross the placenta but at very slow rates.
Large molevular weight substances do not pass
the placenta unless it is mediated by a specific
trophoblast receptor mediated mechanism (IgG)
D. Transfer of Oxygen and Carbon Dioxide
The transfer of oxygen is blood flow limited
The average oxygen saturation of the intervillous
space is about 65-75% with partial pressures of 30-
35 mmHg.
the placenta is highly permeable to carbon
dioxide, which traverses the chorionic villus by
diffusion more rapidly than oxygen
Despite the low PO2 the fetus still survives
because of the following mechanisms:
3
 OB: Fetal Growth and Development
1. High cardiac output
2. Increased oxygen carrying capacity of fetal
hemoglobin.
3. Higher concentration of hemoglobin
compared to the adult.
Near term, the PCO2 in the umbilical arteries
averages about 50 mmHg, about 5 mmHg more
than maternal blood.
Fetal blood has less affinity for CO2 thus favoring
release to the maternal blood.
IV. Fetal Nutrition
During the first 2 months, the embryo consists
mainly of water. As gestation progress, more solids
are being added.
Because of the small amount of yolk, the embryo-
fetus is dependent on the mother for nutrition during
the first 2 months.
During the first few days after implantation,
blastocyst nutrition is derived from the interstitial fluid
of the endometrium and surrounding maternal
tissue.
Three major storage depots from the mother:
1. Liver
2. Adipose tissue
3. Muscles
Together with the storage-hormone
insulin, they are intimately involved in the
metabolism of the nutrients absorbed from
the maternal gut
A. Glucose in Fetal Growth
Minimize use of the glucose by the mother so that
is can be given to the fetus.
Glucose is the major nutrient for fetal growth and
energy.
hPL block glucose uptake and use of glucose,
and promotes the mobilization of fatty acids by
maternal tissues.
B. Glucose Transport
GLUT-1 and GLUT-3 primarily facilitate glucose
uptake by the placenta and are located in the
plasma membrane of the synctiotrophoblast
microvilli
GLUT-1 expression is essential for
decidualization; it increases as pregnancy advances
and is induced by almost all growth factors
Fetal size is not only dependent on age, but also
on efficiency of nutrient transport, availability, and a
number of cofactors.
Fetal Macrosomia: Hyperinsulinemia, increased
levels of selected growth factors, increased GLUT
expression in the syncitiotrophoblast.
C. Leptin
contributes to angiogenesis, hemopoiesis,
osteogenesis, pulmonary maturation, and
neruroendocrine, immune and reproductive
functions.
expressed in synctiotrophoblast and fetal vascular
endothelial cells
rises approximately 34 weeks and are correlated
with fetal weight
abnormal levels: preeclampsia and growth
disorders
Red mentioned by Dra. Coloma
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D. Free Fatty Acids and Triacylglycerols.
newborn fat= 50% of body weight
Neutral fats (triacylglycerols) does not cross the
placenta. Lipoprotein lipase, present ONLY on the
maternal side, will hydrolyze neutral fats to allow
glycerol to enter.
Glycerol will be acetylated in the fetal liver into
triglycerides.
LDL can be taken in as an alternate mechanism
to acquire fatty acids and amino acids.
LDL particle taken up by receptor mediated
endocytosis.
LDL is hydrolyzed by the lysosomal enzymes in
the syncitium to give rise to:
1. Cholesterol for progesterone synthesis
2. Free amino acids including essential ones.
3. Essential fatty acids, such as linoleic acid.
E. Amino Acids
The placenta can concentrate large amounts of
amino acids
They are then transferred to the fetal circulation
by simple diffusion
AA concentration in umbilical cord plasma >
maternal villous or arterial plasma
transport influenced by gestational age and
environmental transport such as heat stress,
hypoxia and under- and over-nutrition, as well as
hormones such as glucocorticoid, GH and leptin
F. Proteins
Proteins transfer is limited. Except for IgG.
IgG crosses the placenta via endocytosis and
trophoblast Fc receptors
IgM can be found in the fetal blood only if there is
an infection.
G. Ions and Trace Metals
Iodide transport is a carrier-mediated process and
is energy requiring as well.
Zinc is greater in fetal plasma; Copper is greater
in maternal plasma
Important copper-requiring enzymes are
neccesarry for fetal development
Deficiency in copper results in inadequate
collagen cross-linking thus diminishing
tensile strength in tissues
H. Heavy Metals
Achieved using a heavy metal binding protein
metallothionein-1 which can sequester zinc, copper,
lead and cadmium.
Cadmium from cigarette smoke is sequestered by
metallothionein that is why it cannot be found in fetal
circulation.
Copper is also sequestered by metallothionein-1.
That is why it is less in fetal blood.
I. Calcium and Phosphorus
actively transported from mother to fetus
calcium: for fetal skeletal mineralization
parathyroid hormone related protein: acts as
surrogate PTH; expressed in cytotrophoblast
4
 OB: Fetal Growth and Development
J. Vitamins
Concentration of Vitamin A (retinol) is greater in
the fetal blood.
Vitamic C is transferred through a carrier
mediated process.
Vitamin D metabolites are greater in maternal
plasma, hydroxylation takes place in the placenta.
V. FETAL ORGAN SYSTEM DEVELOPMENT
FETAL HEAD
Very important in obstetrics, since it is an
essential feature in labor
Adaptation between the fetal head and the
mo her pel ic o le
composed primarily of skull with face occupying a
small part
SKULL
Composed of 2 frontal, 2 parietal, 2 temporal,
upper portion of occipital bone and wings of the
sphenoid
These bones are separated by sutures.
1. Frontal suture between 2 frontal bones
2. Sagittal between 2 parietal bones
3. 2 coronal between the frontal and
parietal bones
4. 2 lambdoid between posterior margins
of the parietal bones and upper margin
of the occipital bone
In vertex position, all except the temporal
suture can be palpated (useful in monitoring
position and presentation of fetal head)
When several sutures meet, they form an
irregular space covered in a membrane
the FONTANEL.
1. Greater/anterior fontanel (Bregma)
lozenge- shaped space between the
coronal and sagittal structures.
Red mentioned by Dra. Coloma
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2. Lesser/posterior fontanel
triangular shaped; intersection of the
sagittal and lambdoid sutures.
3. Temporal/ Caesarian fontanel
junction of the lambdoid and
temporal sutures
Palpation and localization of these fontanels can
determine the position and presentation of the baby.
DIAMETERS OF THE NEWBORN HEAD:
1. Occipitofrontal (11.5 cm) From a point just
above the root of the nose to the most
prominent part of the occipital bone; seen if
bab head i no fle ed
2. Biparietal (9.5 cm) Greatest transverse
diameter of the head; from one parietal bone
to the other.
3. Bitemporal (8 cm) Greatest distance
between two temporal bones.
4. Occipitomental (12.5 cm) Chin to most
prominent portion of the occiput.
5. Suboccipitobregmatic (9.5 m) line drawn
from the middle of large fontanel to the
undersurface of the occipital bone where it
joins the neck; shortest diameter that can
pass through during normal cephalix
delivery; seen when fetal head is completely
flexed
6. Trachelobregmatic (9.5) line drawn from
the bregma to the undersurface of the fetal
mentum/ mandible
Plane of occipitofrontal diameter greatest
circumference of the head; averages 34.5cm
Plane of suboccipitobregmatic diameter
smallest circumference; 32cm
MOLDING: Intrapartum process; Consider the
thin layer of fibrous tissue which allows a degree of
considerable shifting and sliding as the head adapts
to the shape and size of the pelvis.
Fetopelvic disproportion leading indication
for caesarean delivery
FETAL BRAIN
From midpregnancy onwards, it is possible to
identify fetal age from characteristic external
appearance
Myelination of the ventral roots of the
cerebrospinal nerves and brainstem begin at about
th
6 month.
It is completed at birth.
The lack of myelin and ossification of the fetal
skull allows the physician to see the fetal brain
throughout gestation.
CNS & SPINAL CORD;
Neuronal proliferation and migration proceed
along with gyral growth and maturation
Myelination of the ventral roots of the
cerebrospinal nerves and brainstem begins at
approximately 6 months but most myelination occurs
after birth
20-24 weeks complete neuronal
proliferation and migration
nd
2 half of gestation organizational events
proceed with gyral formation and
5
 OB: Fetal Growth and Development
proliferation, differentiation, and migration of
cellular elements
The spinal cord extends along the entire length of
the vertebral column in the embryo, but after it grows
more slowly
By 24 weeks, the spinal cord
extends up to S1
At birth to L3
Adult to L1
Spinal cordmyelination begins at the midgestation
and continues through the first year of life.
th
8 week: synaptic responses that promote trunk
and neck flexion.
AMNIOTIC FLUID
In early pregnancy, it is an ulatrafiltrate of
maternal plasma; usually comes from amniotic
membrane= 50ml
Consists of ECF that diffuses from the fetal skin
nd
reflecting the composition of fetal plasma by the 2
triemster
As cornification of the skin begins at about 20
weeks AOG, the fetal urine becomes a major
component of amniotic fluid (fetal kidneys start
producing urine at 12 weeks)
Fetal urine consists of increased quantities of
urea, creatinine and uric acid. It also contains
desquamated epithelials, lanugo, vernix and various
secretions.
Amniotic fluid contains glycerophospholipids,
pulmonary cells, desquamated fetal cells, vernix,
lanugo and various secretions.
The volume of amniotic fluid increases with age:
10 mL. per week after 8 weeks
60 mL per week after 21 weeks
Peaks at 34 weeks
Midpregnancy: 400ml
peak volume: 1000ml (36-38weeks)
>42 weeks AOG= decrease in AFV
Functions:
1. Cushions the fetus for musculocutaneous
growth and trauma protection.
2. Maintains temperature
3. Minimal nutritive function
4. Contains EGF and EGF like growth factors
5. Promote growth and differentiation of lungs
and GIT by swallowing and inspiring
amniotic fluid.
Ultrasound is usually used to measure AF
index
- How to measure: uterus is divided
into 4 equal quadrants AF is
measured vertically in single
deepest pocket of each quadrant
add the 4 values to ger AFI
- Interpretation:
< 5cm oligohydramnios (may indicate fetal lung
hypoplasia)
> 24cm polyhydramnios
AF can also determine maturity of the lung
- Movement of AF in and out of fetal
lungs= increase in
glycerophospholipids & pulmonary
cells
- Movement is regulated by fetal
breathing movements
Red mentioned by Dra. Coloma
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CARDIOVASCULAR SYSTEM
* study fetal blood circulation favorite questions in
quizzes
blood from mother goes through the placenta and
goes to the fetus via umbilical cord
fetal blood does not need to enter the pulmonary
vasculature to be oxygenated; most RV output
bypasses the lungs
fetal heart chambers work in parallel, not in series
effectively supplies brain and heart more highly
oxygenated blood
umbilical cord has 3 vessels: 2 arteries and 1 vein
oxygen and nutrients are delivered from the
placenta by the single umbilical vein
O gena ed blood en er he bab
umbilicus, then goes up to the liver and
umbilical vein is then divided into 2
umbilical vein is divided into:
1. Ductus venosus
- Major branch of the umbilical vein
- Transverses the liver to enter/join the
IVC directly
- Carries highly oxygenated blood directly
to the heart
2. Portal sinus/ portal vein
- Carries blood to the hepatic veins
primarily on the left side of the liver, and
oxygen is extracted
Deoxygenated blood from liver flows to
IVC, which also receives less oxygenated
blood from the lower body
ventricles work in parallel
well oxygenated blood enters LV, which supplies
brain and heart
less oxygenated blood enters RV, supplies the
rest of the body
well oxygenated blood tends to course along the
medial aspect of the IVC
less oxygenated blood flows along the lateral
vessel wall
Once blood enters the RA, upper interaterial
septum (crista dividens) shunts well
oxygenated blood from the medial side of
the IVC through the foramen ovale into the
left heart then to the heart and brain
After extraction of oxygen, the less
oxygenated blood then returns to the RA
through the SVC
Less oxygenated blood SVC RA & RV
The SVC courses inferiorly and anteriorly as
it enters the RA, ensuring that less well-
oxygenated blood returning from the brain
and upper body will be shunted into the RV
The ostium of the coronary sinus lies just
superior to the tricuspid valve so that less
oxygenated blood from the heart returns to
the RV
90% of less oxygenated blood exiting the
RV is shunted through the ductus arteriosus
to the descending aorta
The remaining RV output returns to the
placenta through the 2 hypogastric arteries
The blood picks up oxygen and nutrients in
the placenta and is recirculated through the
umbilical vein
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 OB: Fetal Growth and Development
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blood in the RV is 15-20% less saturated than
blood in the LV due to the shunting of less O2 blood
to the RV
STREAMING OF FLOW
Streaming effect high oxygenated blood
passes though the medial side and less
oxygenated blood passes though the lateral
side and they are all brought together by
the IVC to the RA. By the presence of the
crista dividens, the streaming is maintained
such that highly oxygenated blood goes
through the foramen ovale into the LA and
then to the LV then goes into the
circulation.
The less oxygenated blood goes to the RA
then to the RV then goes to the pulmonary.
The lower part of the pulmonary has a
structure that connects to the descending
aorta, which is the ductus arteriosus.
Through it, the less oxygenated blood goes
to the descending aorta.
On the other hand, less oxygenated blood
from the upper part of the body goes into
the SVC, then goes into the RA then to the
RV.
The referred blood from the ductus
venosus goes to through the foramen ovale
to the LA. It then goes to the LV and from
this it goes to the ascending aorta which
supply the coronaries of the heart and then
it goes up to the neck to supply the brain
Heart and brain priority; need more highly
oxygenated blood
Upper part of the descending aorta
supplies the lungs and the viscera (since
lungs are not functional, they receive the
less oxygenated blood)
inadequate closure there will be a
problem and must close within 1 year to
completely close
- Ductus arteriosus functionally closes
10-96 hours after birth; anatomically
closes 2-3 weeks after birth; eventually
becomes ligamentum arteriosum
- Ductus venosus functionally closes
10-96 hours afterbirth; anatomically
closes 2-3 weeks after birth
(walang sinabi sa Williams tungkol sa closure ng
ductus arteriosus pero sabi sa group discussion
pareho lang sila ng ductus venosus)
3. Fetal cardiac output is higher
- To compensate for the high affinity of
oxygen to HgbF
HgbF tightly binds O2 more so
lesser O2 is available to the
circulation fetal heart
compensates by increasing
cardiac output to meet the
demand
FETAL CIRCULATION

Circulatory Changes at Birth

umbilical vessels, ductus arteriosus, foramen
ovale and ductus venosus normally constrict or
collapse due to shift in pressure
expansion of lungs and closure of ductus
arteriosus blood from RV enters the pulmonary
vasculature to become oxygenated before it returns
to the left heart
ventricles now work in series, not in parallel
more distal portions of the hypogastric arteries
undergo atrophy and obliteration within 3-4 days
after birth and become umbilical ligaments
intraabdominal remnants of umbilical vein form
ligamentum teres
ductus venosus constricts 10-96 hours after birth
and closes by 2-3 weeks formation of ligamentum
venosum
umbilical arteries become umbilical ligaments

Difference from Adult:

1. Functions in parallel (adult heart works in
series)
- There is a pathway for the oxygenated
blood and pathway for deoxygenated
blood
2. Interconnection of fetal circulation is
possible because of the 3 shunts:
- Foramen ovale closes immediately at
birth; in some instances if there is
7
 OB: Fetal Growth and Development
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fetoplacental blood volume at term= 125ml/ kg of

fetal weight
Hepmoglobin has a timing of production,
depending on the chains that it contains.

Fetal Hemoglobin
YOLK SAC: Gower 1, Gower 2 and Portland
LIVER: HbF (fetal hemoglobin)
hemoglobin produced by fetus
binds more O2 (12-15G/DL)
Lesser binding with 2,3-DPG= higher
affinity of Hgb for O2
Persistence of HgF in newborns of
diabetic women is usually due to hypomethylation of
the q
gene (genes are not turned off continued
production of HgbF)
BONE MARROW: adult-type hemoglobin A
SHUNT 1 Foramen Ovale hemoglobin produced when baby is born
SHUNT 2 Ductus Arteriosus binds 2,3-DPG more avidly than HgbF= lowered
affinity of Hgb for O2
In pregnancy, maternal 2,3-DPG levels
are increased
As term approaches, less HgbF and more
HgbA are produced (at term, 3/4 are Hgb A)

Functional difference between HbA and

HbF. Fetal RBC that contain HbF bind
more oxygen. Because HbA binds more
rapidly with 2-3DPG reducing its capacity
for oxygen binding.
The switch from HbF to HbA is driven by
glucocotricoids.

FETAL BLOOD
st
1 site: Yolk sac/ Mesoblastic Period (can be seen in
ultrasound up to 10 weeks)
function: early source of blood cells up to
8 weeks
nd
2 site: Liver/ Hepatic Period
8-32weeks
Final site: Bone Marrow/ Myeloid Period
32 weeks and above
The fir RBC relea ed in o fe al circ la ion are
usually macrocytic and nucleated. Occupying a
volume of 180 fL, but decreases to 105-115 fL at
term.
Hemoglobin concentration at midpregnancy is
about 12 g/dL, which rises to about 18 g/dL by term.
Fetal erythrocytes have shorter life span due to
large size but lengthens to approximately 90 days at
term.
RBC production is chiefly controlled by fetal
erythropoietin
It is produced in response to bleeding, labor and
isoimmunization (hypoxic stress)
Liver is the production site before the renal cells
mature
After birth, erythropoietin may not be detectable
for up to 3 months
Coagulation Factors
With the exception of fibrinogen, the fetus
produces adult-type procoagulant, fibrinolytic and
anticoagulant proteins by 12 weeks.
Fetal leves of factor II, VII, IX, X, XI as well as
prokallikerin, protein S & C, antithrombin and
plasminogen are low (low vitamin K dependent
dependent factors)
Requirement of Vit K to reduce risk of
hemorrhage at birth to prevent hemorrhagic
disease of the newborn because coagulation factors
decrease further first few days after birth
Fetal fibrinogen appears 5 weeks. It forms a less
compressible clot and the fibrin monomer has lower
degree of aggregation.
Fibrin stabilizing factor or factor XIII is decreased
significantly compared to the adults.
Bleeding is not significant during cordocentesis,
because amniotic fluid thromboplastins and factors
in he Whar on jelly facilitate clotting at the
puncture site.
Fetal Plasma Proteins
1. Albumin
2. LD
3. AST
4. GGT
5. Alanin transferase
These proteins increase with gestational age.
At birth, the concentration of plasma proteins of
the fetus parallel that of the mother.

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 OB: Fetal Growth and Development
IMMUNOGLOBULINS
A. IgG
Transport to the fetus begins by 16 weeks.
A large bulk is acquired by the last 4 weeks of
pregnancy.
Adult values are not attained until 3 years of age
Pass freely from the mother to the fetus (all IgG
will be coming from the mother)
transfer of IgG from mother to fetus may also be
harmful hemolytic disease of the fetus and
newborn results from D-antigen alloimmunization
(Rh incompatibility)
Rh (-) mother, Rh (+) baby no effect on first
nd
pregnancy; 2 pregnancy is affected because
mother has already developed antibodies
st
Exception: 1 pregnancy may be affected/
immunoglobulins of the mother will act on the
fetus if there will be a break in the barrier of the
fetal and maternal circulation (ex. Tearing of
the placenta in placenta previa, invasive
procedures done to the mother that may break
the barrier)
Prophylactic anti-Rh prophylaxis is given to the
mother; any bleeding to an Rh (-) mother will
warrant administration of anti-Rh (Rhogam)
B. IgM
Not transported from mother to fetus.
Very little IgM is produced by the fetus, and that
which is produced may include an antibody to the
maternal T lymphocytes.
produced in response to antigenic stimulus
Increased levels may be found in newborns with
congenital infections/ TORCH viruses like rubella,
CMV, or toxoplasmosis
C. IgA
Acquired in the colostrums of breast fed infants
Provides adequate mucosal protection from
enteric organisms
helpful in preventing diarrhea in newborn
LYMPHOCYTES
B lymphocytes appear in the liver by 9 weeks,
and become apparent in the blood and spleen by 12
weeks AOG.
T lymphocytes in the fetal thymus are released by
14 weeks AOG.
Lack of responsive B lymphocytes to polyclonal
activators and lack of proliferating T cells result to
poor response to immunization and bacterial
capsular polysaccharides
MONOCYTES
are able to process and present antigen when
tested with maternal antigen-specific T CELLS
GASTROINTESTINAL TRACT
10-12weeks: Swallowing begins; coincident with
active peristalsis of the small intestines and ability to
transport glucose actively
stimuli for swallowing: thirst, gastric emptying,
change in AF composition; fetal taste buds may also
play a role
Volume of swallowed amniotic fluid is smaller
than the total volume, so it doe n r n o .
AF regulation is substantially affected by fetal
swallowing.
Red mentioned by Dra. Coloma
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Hydramnios due to accumulation
of AF; common if swallowing is
inhibited
Esophageal atresia most common
anomaly associated with increase
AF
Average of 200-760 mL/day swallowed AF.
Swallowing also serves to remove insoluble
debris that is shed into the amniotic sac and
sometimes abnormally excreted into it.
Intrinsic factor is detectable by 11 weeks
stomach emptying stimulated primarily by volume
Pepsinogen by 16 weeks
Movement of AF in the GIT stimulates growth and
development of the alimentary canal
Impaired swallowing= impaired growth and
development of GIT
MECONIUM
passed after birth and sometimes during labor
Consists not only of AF debris, but of products of
secretion such as:
1. Glycerophospholipids in the lungs
2. Desquamated fetal cells
3. Lanugo scalp hair
4. Vernix
The dark greenish black appearance is due to
biliverdin pigments.
can be passed due to normal bowel peristalsis in
mature fetus or from vagal stimulation
Arginine Vasopressin hypoxia stimulated;
stimulated colonic smooth muscle to contract,
resulting to intraamnionic defecation
Why is there meconium passage?
- Normal bowel peristalsis (can signify
maturation of the GI tract)
At around 32 weeks, some
fetuses can already produce
meconium
- Hypoxia/fetal distress (stimulates
pituitary gland to produce Arginine
Vasopressin stimulates contraction of
the smooth muscles of the colon
meconium passage/ intraamniotic
defecation)
LIVER
serum liver enzyme levels increase with
gestational age
System of conjugation of bilirubin is immature
when the fetus is younger.
The small amount conjugated is excreted through
the biliary tract into the intestines and is ultimately
oxidized to biliverdin.
th
12 week: unconjugated bilirubin is excreted into
the amniotic fluid and transferred across the
placenta.
bidirectional placental transfer excess
unconjugated bilirubin from mother readily passes to
the fetus and the AF; conjugated bilirubin is not
exchanged to any significant degree between
mother and fetus
fetal cholesterol most from hepatic synthesis;
large demand for LDL by fetal adrenal glands
Glycogen is present ay low levels in the liver. But
as the fetus nears term, the values rise at least two
to three times than normal adult liver glycogen.
Values fall precipitously after birth.
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 OB: Fetal Growth and Development
PANCREAS
Insulin can be identified by 9-10 weeks and
detectably in fetal plasma at 12 weeks.
The fetal pancreas has the ability to respond to
hyperglycemia by secreting insulin
Glucagon is apparent by 8 weeks
Most pancreatic enzymes are produced by 16
weeks, and lipases are present as early as 14
weeks.
URINARY SYSTEM
2 primitive urinary system: pronephros and
mesonephros
metanephros forms the final kidney
The pronephros involutes by 2 weeks.
The mesonephros produced urine at 5 weeks will
degenerate by 11-12 weeks.
Between 9-12 weeks, the ureteric buds and
nephrogenic blastema unite to form the
metanephros.
th
By the 14 week, the Loop of Henle becomes
functional and reabsorption occurs
More nephrons are added until 36 weeks, and
formation will continue until after birth.
fetal kidneys produce urine but have limited ability
to concentrate and modify pH
The urine is HYPOTONIC to plasma, and has low
electrolyte concentration
Less Na, K, Cl
More urea, creatinine, uric acid
Causes AF to also be hypotonic
High renal vascular resistance and low filtration
fraction
Receive only 2-4% of CO as compared to the 15-
18% of the newborn.
KIDNEYS
Not essential for survival in utero
important in the control of AF volume and
composition
nephrons are formed until 36 weeks AOG (In
preterm, it continues after birth)
After 20 weeks, if there is problem with the
kidney oligohydramnios because majority of AF
comes from fetal urine complication:
inadequate AF will result to poorly developed
fetal lungs pulmonary hypoplasia
RBF and urine formation is controlled by:
1. RAA System
2. Sympathetic nervous system
3. Prostaglandins
4. Kallikrein
5. ANP
GFR increases with gestational age
< 0.1 mL/min 12 weeks
0.3 mL/min 20 weeks
Formation of urine that appear in the bladder
begins by 12 weeks.
7-14 mL/day by 18 weeks
27ml/hr or 650 mL/day at term
- Decreased urine formation may
result to fetal hypoxic state
PULMONARY SYSTEM
The presence of surface-active materials
(surfactant) in the AF is indicative of fetal lung
maturity.
Red mentioned by Dra. Coloma
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ANATOMICAL MATURATION
Three stages:
1. Pseudoglandular stage
- growth of intrasegmental bronchial tree
- between 6-16 weeks
- the lungs appear like glands.
2. Canalicular stage
- 16-26 weeks
- bronchial cartilage plates extend
peripherally
- each terminal bronchiole give rise to
respiratory bronchioles subsequently
dividing into multiple saccular ducts
3. Terminal Sac stage
- begins at 26 weeks
- respiratory bronchioles give rise to
primitive alveoli or terminal sac
- extracellular matrix develop from
proximal to distal lung segments
- type II cells produce surfactant
- most importance stage because alveoli
is fully developed and produces
surfactant
4. Alveolar stage:
- begins at 32 weeks
- alveolar epithelial lining thins to improve
gas exchange
- an extracellular matrix develops from
proximal to distal lung segments until
term
At birth only 15% of the alveoli are formed, this
continues until about 8 years of childhood.
If there is an insult before stage 3 occurs,
there will be a decreased growth and
development of the pulmonary tree. Baby
may survive but will present with pulmonary
hypoplasia.
LUNGS
Air sacs expand no sooner than 28 weeks (before
28 weeks, surfactant expand the lungs)
full maturation starts at 32 weeks
Morphological or functional immaturity at birth
Respiratory Distress Syndrome (RDS)
factors that accelerate fetal lung maturity:
Corticosteroids (Betamethasone,
Dexamethasone)
- Usually given when preterm baby is
expected to hasten the process of
the maturation of the lungs to
greatly improve respiratory
compliance of baby to decrease
incidence of RDS
- Cortisol natural stimulus for lung
maturation and augmentation of
surfactant synthesis
- Used in neonatal surfactant therapy
(prenatal& postnatal) reduced
incidence of RDS
- Recommended to give steroids at
24-34 weeks
- Maximum period of effectivity is 26-
32 weeks
- Duration of effect is only 1 weeks (If
baby is delivered 1 week after
administration of surfactant, there is
no effect)
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 OB: Fetal Growth and Development
- Multiple courses of steroid will have
detrimental effect
Indicators of lung maturation:
Examine amniotic fluid
Lecithin/ sphingomyelin ration (L/S ratio)
- 1:1 (34weeks AOG)
- 2 ( 36 weeks AOG)
- >2 (mature lungs)
Phosphatidylglycerol
Foam shake test
- Indirectly measures
phosphatidylglycerol
Lamellar body count
- Reliable test to asses fetal pulmonary
maturity
SURFACTANT
rd
become highly available in the 3 trimester
Keeps the terminal sacs from collapsing because
they must be kept expanded despite the pressure
imparted by tissue-to air interface
In utero, there is water to alveoli interface
alveoli constantly being bathed in AF
During delivery, when baby takes first breath
air goes into alveoli and if there is no
surfactant, the lungs will collapse
Low surfactant RDS
surface active material present in mature lungs
formed by Type II pneumocytes
Multivesicular bodies that produce lamellar
bodies spread in alveolus and prevent
collapse
Lamellar bodies where surfactant is
formed
Capacity of fetal lungs to produce
surfactant establish lung maturity
lack of surfactant RDS
Composition:
Lipid (glycerophospholipid) 90%
- Phosphatidylcholines (lecithins)
80%: Major component of surfactant
- Dipalmitoylphosphatidylcholine
principle active component of surfactant
- Phosphatidylglycerol 8-15%; second
most surface active
glycerophospholipid; has stabilizing
feature which prevent lung collapse
- Phosphatidylinositol 4%
Proteins 10%
- surfactant A (SP-A) major apoprotein;
its synthesis is increased by treatment
of fetal lung tissue with CAMP
analogues, epidermal GF and
triiodothyronine
RESPIRATION
th
Movements can be detected by the 11 week
AOG. Wherein the lungs must be able to move
enough to provide itself with oxygen and eliminate
CO2
respiratory muscles develop early
th
4 month: respiratory movements detected
(content of AF moves in and out of respiratory tract)
meconium passage poses danger in babies
because it may be aspirated to the lungs
Red mentioned by Dra. Coloma
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ENDOCRINE GLANDS
A. Pituitary Gland
The two components of the hypophysis develop
separately:
1. Anterior pituitary gland/
ADENOHYPOPHYSIS
de elop from oral ec oderm or Ra hke po ch
Differentiates into 5 cell types which secrete 6
protein hormones:
a. Lactotrophs produce prolactin (PRL)
b. Somatotrophs produce growth
hormones (GH)
c. Corticotrophs produce corticotropin
(ACTH) (detected as early as 7 weeks)
d. Thyrotrophs produce thyrotropin or
thyroid stimulating hormone (TSH)
e. Gonadotrophs produce FSH and LH
GH, LH and ACTH have been
indentified by 13 weeks.
2. Posterior pituitary gland/
NEUROHYPOPHYSIS neuroectoderm
Well developed by 10-12 weeks
Oxytocin and arginine vasopressin (AVP)
INTERMEDIATE LOBE
cells of this structure begin to disappear before
term and are absent from the adult pituitary
Prod c ion of -MSH and -Endorphins
B. Thyroid
It is able to synthesize hormones by 10-12 weeks
AOG, and TSH, thyroxine and TBG are
demonstrable by 11 weeks.
Normal fetal levels of free T3 and T4 and TBG
increase steadily throughout pregnancy.
By 36 weeks:
TSH is higher than adult levels
T3 is lower than adult levels
T4 is similar to adult levels
Fetal thyroid hormone is essential to normal
development of all tissues, especially the brain.
Placenta prevents passage of maternal thyroid
hormones to the fetus by rapidly deiodinating
maternal T4 to T3 to form reverse T3, a relatively
inactive thyroid hormone.
Maternal T4 prevent antenatal
cretinism in fetuses with thyroid
agenesis
Changes immediately after birth:
Atmospheric cooling activates secretion of
TSH to increase T4 levels maximal 24-36
hours after birth
Simultaneous elevations in T3
C. Adrenal Glands
They are larger than the standard adult size.
The bulk is made up of the inner or fetal zone of
adrenal cortex and involutes rapidly after birth
Sources: Dra. Coloma, Williams 24thEd, Notes from
higher years, LALALA-LALA, samplex
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OB: Fetal Growth and Development
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1
DIAGNOSIS OF PREGNANCY Usually most noticeable at 1st few
1. Presumptive signs and symptoms that weeks of pregnancy
involve other organ systems but most Easy fatigability is normal in pregnancy
prominent in reproductive tract due to increased BMR
2. Probable o However, always check with cardio and
3. Positive 100% chance that the woman is pulmo first to be sure that it is not caused by an
pregnant underlying cardio or pulmo condition
PRESUMPTIVE EVIDENCE Differential Diagnosis:
Symptoms Medicine daw (Kapagod e. Alam daw yan ng
A. NAUSEA w/ or w/o VOMITING Nanay niya. Ikaw? Alam ba ng nanay mo yun?)
Begins at 6 weeks Higher metabolic rate
Peak: 60 70 days (9-10 weeks) = peak of Big tummy
hCG (hCG ne er ero )
First 2-3 months: 50% of pregnant D. PERCEPTION OF FETAL MOVEMENT
women have peculiar distaste for food, food (Quickening)
idiosyncrasies, and other GI disturbances Quickening: first perception by the mother of
o Morning sickness (may also occur other fetal movement
times of the day) o Slight flutter or some brisk movement w/in
Correlates with the amount of circulating serum abdomen
hCG Primigravidas: usually felt at 18-20 weeks
Hyperemesis gravidarum: persistent o May mistake this as peristalsis or
vomiting aggravated by inability to take in food spasms of the GI system
o Can lead to severe dehydration Multigravidas: usually felt at 16-18 weeks
and ketonuria Increases in intensity & frequency as
pregnancy progresses
Management: At about 20 weeks, depending on maternal
Frequent, small feedings habitus, an examiner can begin to detect fetal
Avoidance of fatty food; light, dry, low fat diet movements.
Ice chips Differential Diagnosis:
Anti-emetics occasionally Peristalsis
For severe vomiting (dehydration) who are Taong magaling magkontrol ng muscle
unable to take in food and anti-emetics, hospitalize Hoks lang yun spelled as (Etch-O-A-X)
and correct fluid and electrolyte imbalance ***tapos biglang segue ng:
o Get serum electrolyte levels 1. Pseudosyosis false pregnancy very
Do an ultrasound to check for the desperate of pregnancy that they feel all these
presence of conditions that may increase hCG changes
levels 2. Ectosyesis ectopic pregnancy
1. Hyperplacentosis (multiple gestations or
molar pregnancies) E. BREAST SYMPTOMS
2. Fetal hydrops Estrogen: stimulate mammary duct system
3. Mother carrying a fetus with DS Progesterone: stimulate alveolar components
4. H-mole: gestational trophoblastic disease Breast tenderness & engorgement (esp in
Increases hCG to hundred thousands early pregnancy)
No baby is involved o Mastodynia tenderness; tingling to
5. Polycystic ovary frank pain (first weeks of pregnancy)
A subunit of hCG can interact with LH and cause Described by some px as tightness of heaviness of
hCG to increase the breasts
6. Choriocarcinoma **Less obvious changes in multiparas breasts may
contain a small amount of milky material/colostrums
Differential Diagnosis: for months or years after the birth or their last child,
Nakakasuka raw katabi mo especially if child was breastfed.
Hormone problems
GI problems Signs
F. CESSATION OF MENSTRUATION
B. DISTURBANCES IN URINATION - the endometrium will not shed
2nd and 3rd months: most prominent during - prolonged release of Progesterone
this time because the Corpus Luteum does not die
o Uterus is still pelvic organ and is quite rescued by hCG
adjacent to the bladder Earliest sign of pregnancy
Enlarging uterus puts pressure on urinary Not a reliable indicator of pregnancy (esp
bladder causing the ff: if px does not have a regular menstrual cycle)
o Irritability o Dribbling o Nocturia o Highly suspect pregnancy: 10 or more
o Frequent UTI Differentail Diagnosis days after expected onset of menses
Disappears as uterus rises (end of the 1st o 2nd missed period enhances suspicion
trimester) and becomes an abdominal organ o note the amount, interval and duration of normal
Symptoms may reappear again near menses for comparison
term when presenting part emerges Many non-pregnant factors may cause a
delay in menstruation:
C. FATIGUE Irregular cycles
Emotional Stress
1
Chronic disease Perceptible elevation of body temperature
Drugs for longer than 3 weeks
Endocrine disorders o Due to thermogenic effect of progesterone
Lactation
Genitourinary tumors Differential Diagnosis:
Luteal phase body temperature increase by 0.3
Uterine bleeding after conceptions may occur 0.5oC of the basal body temperature in the
occasionally and may be mistaken for follicular phase
menstruation (25%) - Luteal > follicular phase temperature
o Usually 1 or 2 episodes of bloody Hyperthyroid
discharge in the 1st month of pregnancy
o Usually lesser in amount and paler in J. SKIN PIGMENTATION CHANGES
color Due to an increase in estrogen and progesterone ->
o Physiological; due to blastocyst stimulates Melanocyte Stimulating Hormone ->
implantation hyperpigmentation
o Resolves spontaneously 1. Cholasma (melasma gravidarum)
o Mask of pregnancy
Differential Diagnosis: o Irregular brownish patches of varying size on
Stress Hypothalamic face & neck
Hormonal changes o Usually over forehead, bridge of nose,
Increase in hCG H-mole cheekbones, neck
Anovulatory (irregular cycles/gap) remember ha o More prominent in those with dark complexion
the cycle depends on ovulation and this causes the o Intensified by exposure to sunlight
production of progesterone and then stays for 2 o Disappear or regress after delivery
weeks on without ovulation the woman only gets
Estrogen stimulation then the shedding of the 2. Linea Nigra
Endometrium depends on how much that supply o Midline of the abdominal skin (linea alba
can ppor he prolifera ing pha e ( a ahead of line from symphysis pubis to xiphoid process) is
our Gyne) hyperpigmented to a brownish-black color
- ex. PCOS hormonal imbalance there is o Due to the stimulation of melanophores by
no dominant follicle and then the cohort stays as is increased MSH secondary to increased Estrogen
small non progressive that is why the
appearance of ha im la e (pin ol ni a bigla 3. Striae gravidarum or stretch marks
kasi may tumunog na phone) o Begins at midpregnancy or late
pregnancy when there is increased tension to skin
G. ANATOMICAL BREAST CHANGES o Reddish, slightly depressed streaks
Enlargement of the mammary glands commonly found in abdominal skin (some may
Delicate veins become visible (6-8wks be found in breasts and thighs)
after conception) Indicates recent rupture of muscle fibers
Nipples: deeply pigmented, enlarged, May turn silvery white after delivery
more erectile/everted o Due to the separation of the underlying
Areola: enlarged and more deeply pigmented collagen tissue & appear as irregular scars
Striations may be present if breast o Risk factors: weight gain during pregnancy,
size is extensive younger maternal age, family history
Hypertrophic glands of Montgomery
o Seen as small elevations scattered in the 4. Spider telangiectesia
areola o Vascular and stellate marks
o Minute, red elevations on the skin (face, neck,
Expression of colostrum (16th week) upper chest, arms) with radicles branching out from
o Thick, yellowish fluid expressed from breasts a central lesion
by gentle massage o Due to high levels of estrogen
REMEMBER! There is no relation between pre- o Blanch when compressed
pregnant breast size & volume of milk production o Palmar erythema associated sign
during lactation
Differential Diagnosis: **These changes may be absent in pregnant women.
Tumor - Enlargement They may also be present in non-pregnant
Oral Contraceptive - Tenderness women who are taking estrogen-progestin
contraceptives
H. CHANGES IN VAGINAL MUCOSA
Occurs on the 6th week **There are other states where in the Estrogen is
+ Chadwick s sign increased such as:
o Dark-bluish or purplish-red color of the Liver diseases not able to breakdown the
vagina Estrogen manifestations of Estrogen increase
- includes increase in cervical softening but can
also be due to Estrogen-Progestin contraceptives Differential Diagnosis:
o Due to increased vascularity Use of cosmetics
- Photon damage in the skin
Differential Diagnosis: Reaction to skin whitening products
Oral Contraceptives

I. THERMAL CHANGES PROBABLE EVIDENCE

2
 Therefore, fern pattern in seen from day 7 to 18 of
Signs the cycle due to estrogen production
o Progesterone: lowers NaCl concentration =
A. ABDOMINAL ENLARGEMENT inhibit fernin
- After the day 21, there is beading or cellular
At 12 weeks: uterus fundus felt at appearance
symphysis pubis - During pregnancy, progesterone effect
At 16-22 weeks: growth is more rapid as predominates despite enormous estrogen produced
uterus rises out of pelvis into the abdomen - Therefore, if thin, fern-patterned mucus is seen =
At a certain period in pregnancy, tape pregnancy is UNLIKELY
measure height is equal to the age of gestation
(16-32 weeks) E. BRAXTON HICKS CONTRACTION
o The measurement from symphysis False labor pain
pubis to the uterine fundus (w/ empty bladder) = Strong, PALPABLE, VISIBLE, irregular
AOG contractions
o Makes fundic height very useful in (5-25mmHg)
gauging AOG especially if px cannot recall LMP or Usually felt most in the last two weeks of
no ultrasound is available pregnancy
o Ex. at 20 weeks = 20cm (28 weeks)
Abdominal enlargement more o May occur early in pregnancy but not as
pronounced in multigravida then primigravida strong
o Multigravida: Distended, more lax, o Increase in number when abdomen is
flaccid, pendulous abdomen due to previous massaged/stimulated
pregnancies Of short duration (true labor: long duration,
- Especially if (+) hx of multifetal more pain, regular)
pregnancies, polyhydramnios, fetal macrosomia
F. BALLOTEMENT
B. CHANGES IN UTERINE SHAPE, 20th week: Amniotic fluid volume is greater
SIZE, CONSISTENCY than fetus
Internal and external
fetus Procedure (internal ballottement):
o Growth is limited to anteroposterior 1. Insert fingers in vagina
diameter 2. Place upward pressure on fundus
o 12 weeks: uterus is somewhat globular (average 3. Use other hand to palpate
diameter: 8 cm) Findings: You will feel a rounded structure that
On bimanual examination: uterus is will hit/bounce back on your finger
elastic or exceedingly soft compared to firm, External ballottement: When examiner moves
doughy non pregnant uterus uterus side to side (with both palms on each side of
uterus), feels like something is floating/bouncing
+ He a against the palms
o 6-8 weeks Not a positive sign because if there is a
o Softening of the isthmus and fundus mass in the uterus, you will also elicit the same
(compared to the firm cervix) reaction.
- Softening is very significant that
uterus and cervix seem to be separate organs G. OUTLINING OF THE FETUS
- Makes it compressible on bimanual Myomas or ovarian overgrowths may be
examination mistaken for the fetal head
+ G de
o As early as 4 weeks H. POSITIVE ENDOCRINE TESTS
o Softening of the cervix due to increased hCG (detected as early as 8-9 days after
vascularity of tissue ovulation)
o produced by fetal trophoblasts: maintains
C. CHANGES IN THE CERVIX the corpus luteum, the main site of progesterone
6-8 weeks: softening production before the placenta kicks in
o May also be caused by estrogen- progestin o hCG in serum/urine basis for pregnancy
contraceptives tests
- hCG is a heterodimer composed of two
o Firm cervix: nose/nasal cartilage dissimilar subunits ( and )
External cervical os & cervical canal o increase from day of implantation (doubling
become patulous (open/distended) to allow time: 1.4-2 days)
insertion of fingertip o peak: 60-70 days
o Internal os should remain close o concentration declines slowly until lowest
level is reached at about 16 weeks
D. CHANGES IN CERVICAL MUCUS pregnancy tests are targeted to detecting
Mucus crystallization the subunit of hCG
o Necessary for production of fern pattern o subunit: similar to LH, FSH, TSH not
nonspecific though reliable indicator of pregnancy that s why the
o Depends on an increased NaCl concentration subunit is used
* Cervical mucus is relatively rich in NaCl when * Although each immunoassay detects a slightly
estrogen is produced (not progesterone). different mixture of hCG variants, its free subunits,

3
or its metabolites, all are appropriate for pregnancy - Visualization of cardiac activity and fetal pole
testing - Also used to measure CRL

Sandwich-type immunoassay. o Fetal echocardiography

a monoclonal an ibod again he -subunit is - Demonstrated as early as 6-8 wks AOG
bound to a solid phase support o Doppler ultrasound
The attached antibody is then exposed to and - Heard at 10 th week
binds hCG in the serum or urine specimen. A o Stethoscope
second antibody is then added, binds to another - Easiest & simplest way
i e on he hCG molec le, and and iche he th
bound hCG between the two antibodies. - Disadvantage: hear FHT at 18 week
In some assays, the second antibody is linked to Other sounds heard:
an enzyme, such as alkaline phosphatase. 1. Uterine soufflé
When substrate for the enzyme is added, a color Soft, blowing sound synchronous with maternal
develops. The color intensity is proportional to the pulse
amount of enzyme and thus to the amount of the Heard in the later months of pregnancy
second antibody bound. Produced by the passage of blood through the
This is a function of the hCG concentration in the dilated uterine vessels
test sample. Heard most distinctly near the lower portion of
The sensitivity for the laboratory detection of hCG the uterus (hypogastric area of abdomen)
in serum is as low as 1.0 mIU/mL using this 2. Funic soufflé or umbilical cord soufflé
technique Sharp, whistling sound that is synchronous with fetal
extremely sensitive immunoradiometric assays, the pulse
detection limit is even lower Caused by the rush of blood through the umbilical
arteries
**False positive hCG results are rare with the May not be heard consistently
sandwich type immunoassay 3. Sound from movements of fetus
o Possible causes of false +: 4. Maternal pulse
Presence of circulating serum factors Pulsation of aorta is unusually loud
(heterophilic antibodies usually seen in women who 5. Gurgling gas in mother s GIT
work with animals) that may interact with hCG Sounds from maternal internal peristalsis
antibody
Elevated hCG levels may also reflect molar B. PERCEPTION OF FETAL MOVEMENT BY
pregnancy and its associated cancers EXAMINER
Other rare causes of positive assays without Active fetal movement may be seen and felt
pregnancy are: by the
(1) exogenous hCG injection used for weight loss examiner
(2) renal failure with impaired hCG clearance In advanced pregnancies, fetal movements
(3) physiological pituitary hCG can be visualized by inspection
(4) hCG-producing tumors that most commonly o Visible bowel movements are rarely seen
originate from gastrointestinal sites, ovary, bladder, Usually occurs late in pregnancy (after 20th
or lung week)
o Detected earlier with real times sonography
Home pregnancy tests: 75 percent
sensitivity, high C. RECOGNITION OF THE EMBRYO OR FETUS
false negative rate BY ULTRASOND TECHNIQUES
o Detection limit: 12.5mIU/mL Detects fetal heart activity
Commercially available tests involve At 5 weeks, gestational sac may be seen
the ff: agglutination-inhibition, radio-immunoassay, o 2mm sac = 16 days from ovulation or 10 days
enzyme- linked absorbent assay (ELISA), from implantation
immunochromatography At 6 weeks, fetus w/in sac & fetal heart beat
detected
6-12 weeks: CRL measurement is
POSITIVE EVIDENCE predictive of gestational
A. IDENTIFICATION OF FETAL HEART TONES Preferred is transvaginal sees signs of
Auscultation of fetal heart tones apart from pregnancy by 4-5 weeks
mother s own pulse is a positive sign that there is a - gestational sac is seen in the decidua change in
viable pregnancy the endometrium for the pregnancy state form a
o How to do it: Get maternal pulse and FHT sac like thing 5-6 weeks a white rim forms which
simultaneously Maternal pulse and fetal heart tone is the gestational sac
must not be synchronous - yolk sac and embryo, as time goes by
- Maternal thyrotoxicosis or fever can mimic the fetal separates
heart tone due to increased maternal HR - in the UTZ there will be a flicker which is
o Usually FHT is faster than the mother s (110-150 he hi e hing (Y p, hindi ni a ina abi ano yun)
beats per minute) - look for the sac in other areas because it
might be ectpic
Different ways to listen to FHT (arranged
from the earliest to the latest): ** J read he book for hi proce r o read
o Ultrasound (real time sonography) back (I g e placen a )
- Heard at the 5th weeks ** X-ray the pelvic bone covers the fetal bones
- Most accurate o mahirap rin i o.

4

Other information that could be verified by ultrasound
presence of blighted ovum
number of foetuses
ectopic gestation
presenting part
fetal anomalies
hydramnios
detection of IUGR
Differential Diagnosis
Other conditions may result in enlargement of the
abdomen and may be mistaken for a pregnancy
o myomas (esp fundal solitary subserous variety)
o adenomyosis
o solid ovarian masses
o hematometra
PSEUDOCYESIS
Imaginary or spurious pregnancy
o Have nausea, vomiting,
quickening, sensation of fluid coming out (amniotic
fluid)
o Feel majority of signs and symptoms but
they are not pregnant
Usually seen in women who are nearing
menopause or those with a strong desire to become
pregnant
Other risk factors:
o Obese, emotional problems (strong desire to
become pregnant), > 35 y/o
Women with pseudocyesis are usually
hard to convince that they are not pregnant
o Do an ultrasound! (most convincing method)
o Bimanual exam may also be done
- Uterus will be seen as small & (-) positive
signs of pregnancy
IDENTIFICATION OF FETAL LIFE & DEATH
In 50% of cases, cause of death is
unexplainable
Pregnancy tests are not reliable because
trophoblasts continue to produce hCG for several
days or weeks after fetal demise
Ultrasound to confirm nonviability
o If not available do bimanual pelvic exam &
auscultation of FHT with stethoscope
Decrease in uterine size
o Due to collapse/shrinkage of fetal skeleton
o Collapse of skull w/ liquefaction of fetal brain
Clinical Findings that indicate non-viability of the fetus
1. Cessation of fetal movements or an
appreciable decrease in activity
2. Cessation of vomiting for hyperemetic px
3. Weight decreases/returns to normal
4. Cessation of fetal movement usually
the most noticeable sign in fetal demise that
occurs in the period after quickening
o Position changes due to amniotic fluid may
be mistaken for fetal movements
5. Loss of breast turgor & engorgement
6. If previously hypertensive, BP decreases.
7. Decrease in fundic height
8. Internal exam: soft collapsible fetal skull
may be felt through soft cervix that has already
started to dilate
9. No fetal heart tone
10. Tobacco stained amniotic fluid highly
suggestive of fetal demise
11. Ultrasound may show
oligohydramnios/anhydramnios and particulate
matters floating in scanty AF
Radiographic Evidence nice to know - not used
anymore
1. Spalding s sign: overlapping of the fetal
skull bones due to liquefaction of the brain
2. Robert s sign: gas bubbles in the fetus
3. Exaggeration of fetal spine curvature
Extra from the book:
Sonographic Recognition of Pregnancy
Transvaginal sonography
early pregnancy imaging and is commonly used to
accurately establish gestational age and confirm
pregnancy location
First sonographic evidence of pregnancy: A
gestational sac a small anechoic fluid collection
within the endometrial cavity
Seen with transvaginal sonography by 4 to 5
eek ge a ion
Fluid collection, however, can also be seen within
the endometrial cavity with an ectopic pregnancy
and is termed a pseudogestational sac or
pseudosac
Further evaluation may be warranted if this is the
only sonographic finding, particularly in a patient
with pain or bleeding.
Normal gestational sac implants eccentrically in the
endometrium (whereas a pseudosac is seen in the
midline of the endometrial cavity)
Other potential indicators of early intrauterine
pregnancy:
Anechoic center surrounded by:
1. single echogenic rim the intradecidual sign
2. two concentric echogenic rings surrounding the
gestational sac the double decidual sign
sonography yields equivocal findings the so-
called pregnancy of unknown location, then serial
serum hCG levels can also help differentiate a
normal intrauterine pregnancy from an extrauterine
pregnancy or an early miscarriage
Visualization of the yolk sac
- a brightly echogenic ring with an
anechoic center
confirms with certainty an intrauterine location for
the pregnancy and can normally be seen by the
middle of the fifth week.
after 6 weeks, an embryo is seen as a linear
structure immediately adjacent to the yolk sac, and
cardiac motion is typically noted at this point
Up o 12 eek ge a ion, he cro n-rump length
is predictive of gestational age within 4 days
5
TETRALOGY, TERATOGENS AND FETOTOXIC CRITERIA FOR DETERMINING TERATOGENICITY
AGENTS

Birth defects

- Nearly 70% of birth defects do not have an

obvious etiology, and those with identified
cause are more likely to be genetic than
teratogenic

Tetralogy
- Study of birth defects and their etiology
Teratogen
- came from Greek work teratos, meaning
monster
- Any agent that acts during embryonic or fetal
development to produce a permanent
alteration of form or function Although all criteria may not be required to establish
- May be a drug or any chemical substance, a teratogenicity, the following tenets must be
physical or environmental factor (heat or considered:
radiation), a maternal metabolite (such as in
PKU or diabetes), a genetic abnormality of an
infection
- Causes structural abnormalities
Hadegen The defect has been completely characterized
- Is an agent that interferes with normal – done because various genetic and
maturation and function of an organ environmental factors may produce
- Named after the god Hades similar anomalies
Trophogen – it is easiest to prove causation if a
- An agents that alters growth rare exposure produces a rare defect,
when at least 3 cases with the same
exposure have been identified and
Both Hadegen and trophogen affect
when defect is severe
development in the fetal period or after birth ,
The agent must cross the placenta
when exposures are often difficult to
– Transport must be sufficient quantity
document
to directly influence embryonic or fetal
Teratogen is used to refer to these types of
development or to alter maternal or
agents
placental metabolism to exert an
Hydroxyprogesterone caproate
indirect effect
- Only medication approved between 1996 and o Placental transfer depends
2011 specifically for pregnancy for recurrent on:
preterm birth prevention 1. Maternal metabolism
Pregnant women are excluded protein binding and
from drug trials to protect the storage, molecular size,
embryo and fetus from potentially electrical charge and lipid
harmful effects of a medication solubility
and because pregnancy 2. Placental metabolism
physiology affects the medication. CYP 450 enzyme
Trofurantoin and Sulfonamides systems
- Appropriate for first trimester use if no suitable Exposure must occur during a critical period
alternative is available of development:
- First-line agents for treatment and prevention 1. Preimplantation period
st
of UTI beyond 1 trimester – 2 weeks from fertilization to
implantation
– Kno n a he all or none
period
– As zygote undergoes
cleavage, an insult
damaging large number of
cells causes embryonic
death
– Compensation is possible if
only few cells are damaged
2. Embryonic period
nd th
– 2 -8 week
– Organogenesis
– most crucial period with
regard to structural
malformations
1
 3. Fetal Period
– >8weeks
– Continued maturation and
functional development
– Certain organs remain
vulnerable (ex. Brain
development susceptible
to environmental influences
such as alcohol exposure)
A biologically plausible association is
supportive
– Because birth defects and
medication exposures are
both common, they may
be temporarily but not
causally related
Epidemiological findings must be consistent
– Important criterion for
teratogenicity: 2 or more
high-quality
epidemiological studies
report similar findings
The suspected teratogen causes defect in
animal studies
– Human teratogenicity is Teratogens
more likely is an agent
produces adverse effects - Act by disturbing specific physiological
in animals process, which may in turn lead to abnormal
Exception: thalidomide potent cellular differentiation, altered tissue growth,
human teratogen but produces no or cell death
defects in several animal species - Exposure may result in multiple effects
Failure to employ these tenets and criteria has because pathophysiological processes may
contributed to erroneous conclusions be induced by various cell types and tissues
regarding the safety of some widely used - May produce similar phenotypic abnormalities
drugs. because different teratogens may disturb
similar processes
Low-risk teratogens

- Medications that produce defects in fewer Fetal genome

than 10 per 1000 maternal exposures
- Ex. Corticosteroids, lithium, trimethropin and
methimazole
- Genetic composition has been linked to
susceptibility to teratogenic effects of specific
medications
- Ex. Fetuses exposed to hydantoin are more
likely to develop anomalies if homozygous for
a gene mutation that results in abnormally low
levels of epoxide hydrolase

Disruption of Folic Acid Metabolism

- Fetal neural tube defects, cardiac defects and

oral clefts can be a result of folic acid
metabolic pathway disturbances

Folate

- Essential for methionine production, which is

required for gene methylation and thus
production of proteins, lipids and myelin
Anticonvulsants such as
phenytoin, carbamazepine,
valproic acid and phenobarbital
– May either impair folic acid
absorption or act as folic
acid antagonist

Paternal exposures

- Exposures to drugs and environmental

influences may increase risk of adverse fetal
outcome
- Proposed mechanisms:
2
 induction of a gene mutation or
chromosomal abnormality in
sperm
– 64 days germ cells
mature into sperm
– Exposure during the 2
months before conception
could cause gene
mutations
Epigenetic pathways suppress
germ-cell apoptosis or interfere
with imprinting
During intercourse, the
developing embryo is exposed to
a teratogenic agent in seminal
fluid
- Exposure to mercury, lead, solvents,
pesticides, anesthetic gases or
hydrocarbons associates with early
pregnancy loss

General rule: Since no adequate and well-

controlled studies in pregnant women for most
medications, and because animal
reproduction studies are not always predictive
of human response, any medication in
pregnancy must be carefully considered and
only used if clearly needed.

Known and Suspected Teratogens:

1. Alcohol
- Most potent and prevalent teratogen
- One of the most frequent nongenetic cause of
mental retardation
- Leading cause of preventable defects in the
US
Fetal alcohol syndrome
– alcohol-related fetal defects
– include dysmorphic facial
features, pre- or postnatal
growth impairment, and CNS
abnormalities that may be
structural, neurological or
functional
Fetal alcohol spectrum disorder
– an umbrella term that
includes the full range of
prenatal alcohol damage that
may not meet the criteria for
fetal alcohol syndrome
Other alcohol-related major and minor
birth defects include cardiac and renal
anomalies, orthopedic problems and
abnormalities of the eyes and ears
- There is unknown minimum amount of alcohol
required to produce adverse fetal
consequences
Binge drinking believed to pose
particular high risk for alcohol-related
birth defects and increases risk for
stillbirth
2. Anticonvulsant medications
- No anticonvulsant drugs are considered truly
afe in pregnanc
- Most medications used to treat epilepsy has
been proven or suspected to confer an
increased risk for fetal malformations
Several older anticonvulsants
produce a constellation of
malformations similar to fetal
hydantoin syndrome
Valproic aicd
– confers the greatest risk;
significantly increases risk for
malformations
– children with in utero
exposure are reported to
have significantly lower IQ
scores at age 3 compared
with those exposed to
phenytoin, carbamazepine or
lamotrigine
Topimarate
– Among the newer agents, it is
reported to confer a risk for
orofacial clefts at least
fivefold higher than in
unexposed pregnancies
- Most frequently reported anomalies:
– Orofacial clefts
– Cardiac malformations
– Neural tube defects
3

3. ACE inhibitors & ARBs
- ACE inhibitors
– considered fetotoxic and result in
ACE-inhibitor fetopathy
– causes fetal hypotension and renal
hypoperfusion, with subsequent
ischemia and anuria
Normal renal development depends
on the renal-angiotensin system
Reduced perfusion may cause fetal-
growth restriction and calvarium
maldevelopment, whereas
oligohydramnios may result in
pulmonary hypoplasia and limb
contractures
- ARBs
– Since it has same mechanism of
action as ACEI, concerns regarding
fetotoxicity has been generalized to
include this entire mediation class
4. Antifungal Medications
- Fluconazole
– Has been associated with a pattern of
congenital malformations resembling
the autosomal recessive Antley-Bixler
Syndrome
– Abnormalities include: oral clefts,
abnormal facies and cardiac, skull,
long bone and joint abnormalities
reported only with chronic high-dose
treatment in the first trimester (400-
800mg daily)
5. Anti-inflammatory Agents
- NSAIDs
– Includes both aspirin and traditional
NSAIDs such as ibuprofen and
indomethacin
– Low dose aspirin, 100mg daily or
lower, does not confer increased risk
for constriction of the ductus
arteriosus or for adverse infant
outcomes
– High dose aspirin and NSAIDs should
be avoided particularly during the
third trimester
– NSAIDs may cause adverse fetal
effects when taken in late pregnancy
Indomethacin may cause
constriction of the fetal ductus
arteriosus resulting in
pulmonary hypertension; may
also decrease fetal urine
production and thereby
reduce amniotic fluid
volume presumed due to
an increase in vasopressin
levels and vasopressin
responsiveness
Fetal ductal constriction is
more likely when drug is
rd
taken in the 3 trimester for
longer han 72 ho r d ra ion
- Leflunomide
– Pyrimidine-synthesis inhibitor used to
treat rheumatoid arthritis
– Contraindicated in pregnancy
because when given at or below
human-equivalent doses in several
animal species, it is associated with
multiple abnormalities
Abnormalities include
hydrocephalus, eye
anomalies, skeletal
abnormalities and embryo
death
– its active metabolite is detectable in
plasma for up to 2 years following its
discontinuation
Women of childbearing
potential who discontinue this
medication should consider
cholestyramine treatment/
washout, followed by
verification that serum levels
are undetectable on 2 tests
performed 14 days apart
6. Antimicrobial Drugs
- Aminoglycosides
– Preterm infants treated with
gentamicin or streptomycin have
developed nephrotoxicity and
ototoxicity
- Chloramphenicol
– Gray baby syndrome was described
in neonates who received this
medication
Preterm infants were unable
to conjugate and excrete the
drug manifested abdominal
distention, respiratory
abnormalities, an ashen-gray
color and vascular collapse
- Nitrofurantoin
– First trimester exposure include a
fourfold increased risk for hypoplastic
left heart syndrome and
micropthalmia/ anopthalmia and a
twofold increased risk for clefts and
atrial septal defects
- Sulfonamides
– Often combined with trimethroprim
and used to treat various infections
during pregnancy such as MRSA
– First trimester exposure increases risk
for anencephaly and left ventricular
outflow tract obstruction, choanal
atresia, and diaphragmatic hernia
– Displaces bilirubin from protein
binding sites which may worsen
hyperbilirubinemia if given near time
of preterm delivery
- Tetracyclin
– Associated with yellowish-brown
discoloration of deciduous teeth when
used after 25 weeks
7. Antineoplastic Agents
- Cyclophosphamide
– Alkylating agent that inflicts a
chemical insult on developing fetal
tissues and leads to cell death and
heritable DNA alterations in surviving
cells
– Increases pregnancy loss and
reported malformations include
skeletal abnormalities, limb defects,
cleft palate and eye abnormalities
4
 – Surviving infants may have growth
abnormalities and developmental
delays
– Environmental exposures increase
risk for spontaneous abortion
- Methotrexate
– folic acid antagonist
– a potent teratogen
– used for cancer chemotherapy,
immunosuppression, nonsurgical
treatment of ectopic pregnancy and
as an abortifacient
– can cause defects known collectively
known as fetal methotrexate-
aminopterin syndrome includes
cranio n o i i h clo er-leaf skull,
wide nasal bridge, low set ears,
micrognathia and limb deformities
2
– 50mg/m dose given to treat ectopic
pregnancy
Dose is increased to induce
elective abortion
- Tamoxifen
– Nonsteroidal selective estrogen-
receptor modulator (SERM)
– Used as an adjuvant to treat breast
cancer
– Women who become pregnant while
on therapy or within 2 months of its
discontinuation should be appraised
for long-term risk of diethylstrilbestrol
(DES)- like symptoms
– Exposed infants should be monitored
for carcinogenic effects for up to 20
years
- Trastuzumab
– Recombinant monoclonal antibody
directed to the human epidermal
growth factor 2 (HER 2) protein
– Used to treat breast cancers that over
express HER2 protein
– Associated with oligohydramnios,
anhydramnios and fetal urine faiure
– May result in fetal pulmonary
hypoplasia, skeletal abnormalities and
neonatal death
8. Antiviral Agents
- Ribavirin
– Nucleoside analogue
– Component therapy for hepatitis C
infection
– Causes multiple defects in multiple
animal species
– Women are recommended to use two
forms of contraception while on this
therapy and delay childbrearing for 6
months following drug administration
- Efavirenz
– Nucleoside reverse transcriptase
inhibitor used to treat HIV infection
– CNS abnormalities following human
exposure
9. Endothelin-Receptor Antagonists
- Teratogenic for mice; no human data
available
10. Sex Hormones
- Testosterone and Anabolic Steroids
– Exposure of a female fetus may
cause virilization and may result in
ambiguous genitalia similar to that
encountered in cases of congenital
adrenal hyperplasia
– Labioscrotal fusion first trimester
exposure
– Phallic enlargement later fetal
exposure
- Danazol
– Used to treat endometriosis,
premenstrual syndrome and
fibrocystic breast disease
– 40% of exposed female fetuses were
virilized
– May cause dose-related pattern of
clitoromegaly, fused labia and
urogenital sinus malformation
- Diethylstilbestrol
– In utero exposure increases risk for
vaginal and cervical intraepithelial
neoplasia
– Has been associated with genital tract
abnormalities in exposed fetuses of
both genders
Women may have
hypoplastic, T-shaped uterine
cavity, cervical collars, hoods
septa and coxcombs and
withered fallopian tube;
slightly higher rates of earlier
menopause and breast
cancer
Men may develop
epididymal cyst, microphallus,
hypospadias, cryptorchidism
and testicular hypoplasia
11. Immunosuppressant Medications
- Corticosteroids
– Associated with clefts in animal
studies
– Prednisolone active metabolite of
prednisone; inactivated by placental
enzyme 11-beta-hydroxysteroid
dehydrogenase 2 and does not
effectively reach the fetus
- Mycophenolate Mofetil
– Potent immunosuppressant used to
prevent rejection in organ-transplant
recipients
– Also used for autoimmune disease
such as lupus nephritis
– May cause abortion
– Surviving infants may have
malformations (usually ear
deformities)
12. Radioiodine
- Radioactive iodine -131 is used to treat
thyroid cancer and thyrotoxicosis and for
diagnostic thyroid scanning
- Contraindicated in pregnancy because it
readily crosses the placenta and is then
concentrated in the fetal thyroid gland by 12
weeks
- Causes irreversible fetal hypothyroidism and
may increase risk for childhood bearing
thyroid cancer
5
13. Lead
- Associated with fetal-growth abnormalities
and with childhood development delay and
behavioral abnormalities
- There is no lead exposure that is considered
safe in pregnancy
14. Mercury
- Prenatal exposure causes disturbances in
neuronal cell division and migration and lead
to a range of defects from developmental
delay microcephaly and severe brain damage
Principal concern for prenatal mercury
exposure is the consumption of
certain species of large fish
Advice not to eat shark, swordfish,
king mackerel, or tilefish, and
consumption of albacore tuna should
be limited to 6ounces per week
15. Psychiatric Medications
- Lithium
– Associated with Ebstein anomaly
– Exposure near delivery findings
typically persist 1-2 weeks and may
include hypothyroidism, diabetes
insipidus, cardiomegaly, bradycardia,
ECG abnormalities, cyanosis and
hypotonia
Ebstein anomaly
– a cardiac abnormality
characterized by apical
displacement of the
tricuspid valve
– often results in severe
tricuspid regurgitation
and marked right atrial
enlargement, which
confer significant
morbidity
Fetal Echocardiography
should be considered for
pregnancies exposed to
lithium in the first trimester
- Selective Serotonin- and Norepinephrine-
Reuptake Inhibitors
– As a class, not considered major
teratogens
– Exception: paroxetine associated
with increased risk for cardiac
anomalies particularly atrial and
septal defects
Paroxetine should be avoided
in women planning pregnancy
and fetal ECG should be
considered for those with 1
st
trimester exposure
– May cause neonatal behavioral
syndrome jittering, irritability, hyper-
or hypotonia, feeding abnormalities,
vomiting, hypoglycemia,
thermoregulatory instability and
respiratory abnormalities; neonatal
effects are typically mild and self-
limited, lasts for only about 2 days
– Late-pregnancy exposure to SSRI
may manifest severe adaptation
abnormalities, including seizures,
hyperpyrexia, excessive weight loss
and respiratory failure; also
associated with pulmonary
hypertension of the newborn
- Antipsychotic Medications
– Exposed neonates have manifested
extrapyramidal muscle movements
and withdrawal symptoms, including
agitation, abnormally increased or
decreased muscle tone, tremor,
sleepiness, feeding difficulty and
respiratory abnormalities
16. Retinoids
- Vitamin A derivatives
- Among the most potent human teratogens
- Isotretinoin, acitretin and bexarotene highly
teratogenic when orally administered
- Inhibits neural-crest migration during
embryogenesis resulting in neural crest
defects termed retinoic acid embryopathy
retinoic acid embryopathy
involve the CNS, face, heart
and thymus
- specific anomalies: ventriculomegaly,
maldevelopment of facial bones and cranium,
microtia or anotia, micrognathia, cleft palate,
conotruncal heart defects and thymic aplasia
or hypoplasia
- Isotretinoin
– First trimester exposure is associated
with high rate of pregnancy loss and
fetal malformations
- Acitretin
– Was introduced to replace etretinate
which is a lipophilic retinoid with such
a long half-life that birth defects
resulted more than 2 years after
therapy was discontinued
- Bexarotene
– Causes abnormalities in rats such as
eye and ear abnormalities, cleft palate
and incomplete ossification
– Males with partners who could
become pregnant are advised to use
condoms during sexual intercourse
while taking this drug and for one
month after discontinuing therapy
- Topical retinoids
– Initially used to treat acne; popular
treatment for sun damage that they
are called cosmeceuticals
– Include tretinoin and tazarotene
– Tretinoin was reported to cause
malformations following topical
administration
- Vitamin A
– Has 2 natural forms: Beta- carotene &
Retinol
Retinol is a preformed vitamin
A which has been associated
with cranial neural-crest
6
 defects when >10,000IU per 19. Herbal Medicines
st
day is consumed in the 1
trimester
Avoid doses >3,000IU daily

17. Thalidomide & Lenalidomide

- Thalidomide
– most notorious human teratogen
– causes malformations in 20% of
fetuses exposed between 34-50 days
menstrual age
– characteristic malformation:
phocomelia absence of one or
more long bones which result in the
hands or feet being attached to the
trunk by a small rudimentary bone
– cardiac malformations, GI
abnormalities and other limb
reduction defects are also common
Important Teratological
Principles:
1. The placenta is not a perfect
barrier to the transfer of toxic
substance from mother to
fetus
2. There is extreme variability in
species susceptible to drugs
and chemicals. Because
thalidomide produced no
defects in experimental mice
and rats, it had been
assumed to be safe for
humans
3. There is a close relationship
between exposure timing and
defect type.
Upper-limb phocomelia
thalidomide exposure
during days 27-30
Lower-limb phocomelia
days 30-33
Gallbladder aplasia days
42-43
Duodenal atresia days
40-47
18. Warfarin
- Vitamin K antagonist and a potent
anticoagulant
- Has low molecular weight and readily crosses
the placenta causing embrotoxic and fetotoxic
effects
-
th th
Exposure between 6 -9 week warfarin
embryopathy (characterized by stippling of the
vertebrae and femoral epiphyses and by nasal
hypoplasia with depression of the nasal bridge
- Affected infants may also have choanal
atresia resulting to respiratory distress
- Increased risk of embryopathy in women who
require >5mg daily
- May result in hemorrhage into fetal structures
st
when used beyond 1 trimester causing
abnormal growth and deformation from
scarring
- Abnormalities may include agenesis of the
corpus callosum, cerebellar vermian agenesis
(Dandy-Walker Malformation), micropthalmia
and optic atrophy
- Affected infants at risk for blindness, deafness
and developmental delays
20. Recreational Drugs
- Amphetamines
– In utero exposure associated with
fetal-growth restriction and with
behavioral abnormalities in both
infancy and early childhood
- Cocaine
– Most adverse outcomes result from its
vasoconstrictive and hypertensive
effects
– Can cause serious maternal
complications such as
cerebrovascular hemorrhage,
myocardial damage and placental
abruption
– May be associated with cleft palate,
CV abnormalities and urinary tract
abnormalities
– Also associated with fetal growth
restriction and preterm delivery
– Children exposed as fetuses
increased risk for behavioral
abnormalities and cognitive
impairments
- Opiods- Narcotics
– Periconceptional exposure
Increased risk for spina bifida,
gastroschisis and cardiac anomalies
– Strongly associated with fetal and
neonatal effects
– Heroin-addicted mothers increased
risk of preterm birth, placental
abruption, fetal growth restriction and
fetal death (due to effects of repeated
narcotic withdrawal on the fetus and
placenta)
Neonatal Narcotic Withdrawal
- called the neonatal
abstinence syndrome;
manifest in 90% of exposed
infants

7
 - characterized by CNS gastroschisis, cleft lip and palate and hand
irritability leading to abnormalities
seizures if untreated, along - Dose response reduction in fetal growth
best-documented adverse reproductive
with tachypnea,
outcome from smoking
episodes of apnea, poor - Newborns of mother who smoke weigh an
feeding and failure average of >200g than newborns of
to thrive nonsmokers
- at risk neonates - Doubles the risk of low birth rate and
monitored using scoring increases risk of fetal growth restriction
system - Growth disparity detected sonographically
between 10-20weeks
- severely affected
- Women who stop smoking early in
neonates treated with pregnancy generally have neonates with
opioids normal BW
Methadone - Has also been linked to subfertility and
- synthetic opioid routinely spontaneous abortions, increase risk for
offered to pregnant women to placenta previa and placental abruption and to
obviate uncontrolled narcotic preterm delivery
withdrawal
- increases risk of preterm
birth and fetal-growth
restriction
- Miscellaneous drugs
– Marijuana not associated with
human fetal anomalies; teratogenic
to animals if given in high doses
– Phencyclidine (PCP) or angel dust
not associated with congenital
anomalies; most exposed newborns
experience withdrawal symptoms
characterized by tremors, jitterness,
and irritability
– Toluene common solvent used in
paints and glue; exposure reported to
have significant fetal risks
Toluene embryopathy
- toluene abuse in early
pregnancy
- phenotypically similar to
fetal alcohol syndrome
- Abnormalities: pre- and
postnatal growth deficiency,
microcephaly and
characteristic face and hand
findings (includes midface
hypoplasia, short palpebral
fissures, wide nasal bridge
and abnormal palmar creases

21. Tobacco
- Cigarette smoke contains a complex of
mixture of nicotine, cotinine, cyanide,
thiocyanate, carbon monoxide, cadmium, lead
and various hydrocarbons
- Fetotoxic
- Have vasoactive effects and reduce oxygen
levels
- Not considered a major teratogen, although
associated with selected birth defects
- Vasoactive properties could produce
congenital defects related to vascular
disturbances
- Increased risk for cardiac anomalies has been
reported and may be dose-related
- Maternal smoking is associated with
hydrocephaly, microcephaly, omphalocele,

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 Prenatal, tetralogy, immunizations, drugs, high risk pregnancy: EMR, JV-C & PDV

Prenatal Care
INITIAL PRENATAL EVALUATION
Prenatal Care ini ia ed a oon a here a rea onable likelihood of pregnanc .
Major goals are to:
define the health status of the mother and fetus
estimate the gestational age
initiate a plan for continuing OB care

The initial plan for subsequent care may range from relatively infrequent routine visits to prompt hospitalization
because of serious maternal or fetal disease.

Prenatal Record
Use of a standardized record within a perinatal health care system greatly aids antepartum and
intrapartum management
Standardized Documentation
o allow communication and care continuity between providers
o enable objective measures of care quality to be evaluated over time and across different clinical
settings

Definitions
1. Nulligravida - not currently nor has ever been pregnant
2. Gravida - is currently pregnant or has been in the past, irrespective of the pregnancy outcome.
Primiravida first pregnancy
Multigravida with successive pregnancies
3. Nullipara - ne er comple ed a pregnanc be ond 20 eek ge a ion.
ha en been pregnan
had a spontaneous or elective abortion(s)
an ectopic pregnancy
4. Primipara delivered only once, born alive or dead with >20wks AOG.
NB: 500g BW threshold definition for parity
- controversial: this is used to differentiate stillborn from an abortus
- <500g of BW = common
5. Multipara - completed two or more pregnancies to >20 wks AOG.

PARITY
number of pregnancies reaching 20 weeks
not increased if multiples are delivered in a given pregnancy (twins, tripltes, quadruplets = P 1)
stillbirth does not lower this number

OB SCORE: GP (T-P-A-A)
Term: >37wks (37 - 42)
Preterm: >20wks but <37wks
Post term: >42 weeks
Abortus: <20wks
o Ectopic (tubal pregnancy) | H-mole
Ali e: c rren l UNTIL NOW!

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 Prenatal, tetralogy, immunizations, drugs, high risk pregnancy: EMR, JV-C & PDV

OB Scoring Sample Cases

E.R. S b ec JV-C a d PDV S b ec

1. 25yo CC: missed menses Case 1:

LMP: July 3-7, 2014 Patient: A.P.
(+) pregnancy test AOG= 19weeks
OB Hx: OB History:
- 2009: pu 37-38wks NSD male 2.7Kg - 2013: 38 weeks delivered by NSD
- 2010: pu 8-9wks abortion
- 2012: pu 36-37wks NSD female 2.6Kg Answer: G2 P1
G4P2 (1-1-1-2) Case 2:
2. 25yo CC: missed menses Patient: L.T., 40y/o,
LMP: July 3-7, 2014 AOG= 28 weeks
(+) pregnancy test OB History:
OB Hx: - 2004: 37 weeks delivered to a live
- 2009: pu 37-38wks NSD male 2.7Kg baby
- 2010: pu 8-9wks abortion - 2006: abortion 15 weeks
- 2012: twin preg 26-27wks, del. By 1° LT - 2007: delivered 32 weeks via NSD
o A 600g; B 700g which died
o Died after 2 days
G4P2 (1-2-1-1) Answer: G4 P2 (T1 P1 A1 L1)
3. 25yo CC: missed menses Case 3:
LMP: July 3-7, 2014 Patient: L.C., 35y/o
(+) pregnancy test AOG= 9weeks
OB Hx: OB History:
- 2009: pu 37-38wks NSD male 2.7Kg - 2009: twin pregnancy 32weeks, 1 died
- 2010: pu 8-9wks abortion - 2010: right salphingectomy with
- 2012: twin preg 39-40wks, del by 1° LT ectopic pregnancy
o A 2600g; B 2700g - 2012: 32 weeks delivered by NSD
G4P2 (3-0-1-3)
4. 25yo CC: missed menses Answer: G4 P2 (T0 P3 A1 L2)
LMP: July 3-7, 2014 Case 4:
(+) pregnancy test Patient: A.T., 30y/o
OB Hx: AOG= 28 weeks
- 2009: pu 37-38wks NSD male 2.7Kg OB History:
- 2010: pu 8-9wks abortion - 2005: H Mole, suction curettage done
- 2012: pu 39-40wks IUFD 3.5kg - 2006: twin pregnancy via cesarean at
o IntraUterine Fetal Death 34 weeks
G4P2 (2-0-1-1) - 2007: ectopic pregnancy, right
5. 25 yo G1P0 10-11wks AOG PRIMI salphingectomy
- (+) Fetal Heart Tone Doppler - 2008: completion curettage
As clinicians, we must know the ffing: - 2009: IUFD at 23 weeks
LMP with AOG & EDD
Examine total health of Pt. Answer: G6 P2 (T0 P3 A3 L2)
Head to toe Case 5:
Look for an o her problem Patient: 39y/o
that may affect pregnancy AOG= 36weeks
Diagnosis of Pregnancy OB History:
Lab test are usually last to - 2009: Twin pregnancy, 8 weeks,
perform completion curettage done
To verify/confirm reliability of - 2010: NSD at 36 weeks
OB history. - 2011: Twin pregnancy, 37 weeks, 1
died
- 2013: ectopic pregnancy

Answer: G5 P2 (T2 P1 A3 L2)

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 Prenatal, tetralogy, immunizations, drugs, high risk pregnancy: EMR, JV-C & PDV

According to Dra.: Fundic height in cm is equal to gestational

Good prenatal care= good delivery age at 16 32 weeks

3 major objectives: Ultrasound

1. Determine AOG
2. Assess fetal well-being
3. Initiate a plan of continuing care
Minimum of 4 prenatal care is recommended
Twin Pregnancy count as G1; P1 if >20
weeks; but is counted separately for TPAL
H mole count as G1
Curretage, ectopic pregnancy count as
abortus (<20weeks)
Normal Pregnancy Duration
st
280days / 40weeks mean duration from 1 day of
normal LMP
Mean Pregnancy Duration: 281 days with SD of
13days
Divided into 3 equal epochs (approx. 3mos /
14wks)
First Trimester
o Period of Organogenesis
o Spontaneous abortion takes place
Second Trimester
o Period of organ maturation
Third Trimester
o Dx of HPN disorders for mothers
EDD (Expected Delivery Date): Naegele Rule
st
1 day of LMP + 7days 3mos + 1year =
EDD
Gestational Age / Menstrual Age
Assumes pregnancy begun 2 weeks before
ovulation
Used by clinicians to mark temporal events
during pregnancy
Ovulatory Age / Fertilization Age
Used by embryologists and other
reproductive biologists
Typically two weeks earlier
Precise knowledge of fetal age is imperative for ideal
OB managemen , eek of ge a ion comple ed i
a clinically appropriate unit for use.
For 33 completed weeks and for days
4/7
o Either 33 weeks or 33+4
Timing from ovulation add 267 days to last
ovulation date to determine EDC
Timing from quickening movement perceived
from 16th to 18th week (multipara); 18th 20th
week (primipara)
- this method is more useful as a confirmation of
other parameters
Height of the Fundus
Fundus above pubic symphysis: 12 wks
- Fundus halfway between
symphysis and umbilicus: 16 wks
Fundus at level of umbilicus: 20 wks
Fundus just below the ensiform cartilage: 36
wks
o The fundus will remain here until
onset of labor (esp in multipara)
o Fundal height drops at time of
lightening (in primipara)
Useful in detecting common obstetrical
problems that cluster in each trimester
1st term: spontaneous abortions
3rd term: pregnancy-induced hypertension
Previous and Current Health Status
Menstrual History
Clinically important
Gestational or Menstrual age number of
weeks since the onset of LMP
Ovulatory cycles without a Hx of regular,
predictable, cyclic, spontaneous menses
o Difficulty in accurate dating of
pregnancy
o by Hx and PE
Normal Cycle: 28days, ovulation takes place on the
th
14 day
Irregular Cycle: >28-30days, ovulation is beyond day
14
Chronic anovulation menstrual period with
a very much longer and irregular intervals
NOTES:
I important to ascertain whether or not
steroidal contraceptives were used before
the pregnancy
o ovulation may not have resumed 2
weeks after the onset of the last
withdrawal bleeding. Instead, may
have occurred at an appreciably
later and highly variable date
o Use of sonography in early
pregnancy
Clarify gestational age
Obstetrical History Gravidity, Parity, and OB
score
Medical and Surgical History DM, Thyroid,
HPN, Asthma, Seizure disorder
If patient is positive for any of the medical and
surgical history, patient is considered as a high- risk
px.
Other pertinent history:
- Includes complete past and family history & a
good obstetric resume
- Obstetric resume should emphasize the ff:
Menstrual history
Evidence of infertility
Careful inquiry into previous pregnancy
Time in gestation when labor occurred
Duration, type of delivery and complications
W eight and sex of baby
Woman reac ion o c rren pregnanc
Symptoms during pregnancy
Dietary History nutritional adequacy
Post-partum course
Infan wellbeing
PHYSICAL EXAM
A. MATERNAL EVALUATION
- Do a complete PE from head to foot
- Obtain the ff:
o BP actual and extent of change

3
 Prenatal, tetralogy, immunizations, drugs, high risk pregnancy: EMR, JV-C & PDV

o Maternal weight actual and extent of Considered negative if

change fetal head is engaged
o Fundic height distance over 2. Cephalic prominence
abdominal wall from the top of the symphysis If on the same side as fetal
pubis to the top of the fundus small parts = head is
- At 20-34 wks AOG is equal flexed and vertex is
the presenting part
to the fundic height in cm) If on same side as fetal
- Therefore if baby is 28 back = head is extended
wks AOG and is only 25cm fundic height, consider and presenting part is the
SGA or consider wrong LMP date given face
B. VAGINAL EXAMINATION
- Vaginal exam during 1st visit
o Fetal heart tones (subsequent only if indicated)
- 110-160bpm o However at term: done weekly to
- First heard in most women bet 16- 19 weeks determine consistency, effacement,
with a standard nonamplified stethoscope and dilatation of the cervix;
- Doppler ultrasound: 10 weeks presenting part, station of PP,
- Ultrasound: 5 weeks clinical mensuration of pelvis
o C/I if with hx of vaginal bleeding
o Leopold s maneuver - Diagnosis of presentation may be obtained
accurately during labor when cervix is dilated
- Presentations identified as follows:
Leopold s Maneuver o Vertex sutures and fontanels
- Provides information on o Face portions of fetal face
o Position o Breech sacrum & ischial
tuberosities
o Presenting part o Shoulder acromion
o Extent to w/c presenting part has descended into
pelvis C. PELVIC EXAMINATION
- Performed during latter m o n t hs o f - Insert speculum into vagina and is able
to visualize abnormalities in the vagina and the
pregnanc y (3rd trimester) and during intervals cervix
between uterine contractions of labor - Usually done during initial prenatal care
- First 3 maneuvers are done with the doctor - Do systematically: Inspection -> Palpation
on the right side of the bed and facing the upper part o Inspect vulva for lesions
of the patient o Observe whether perineum is
anatomically
- 4th maneuver done facing the lower part of the intact or lacerated
mother o Vaginal discharge/bleeding
1st maneuver: Fundal Grip o Polyps
- Screening for cervico-vaginal infections
o Determines what fetal part and
occupies fundus cervical cancer is now considered routine
o Sensation of large nodular body = in prenatal care
buttocks or lower extremities at o Obtain cervical scrape
fundus in cephalic presentation o Inspect cervix for Chadwick s
sign and local esions (ex.
o Hard, freely movable, ballotable part Nabothian cysts occlusion cyst
fetal head at fundus in breech position of endocervical glands bulging
o Use fingertips of both hands beneath exocervical mucosa)
nd
2 maneuver: Umbilical Grip
o Determine location of fetal back Subsequent Assessments
o Palms are placed on each side of 1. Cervical culture for N gonorrhoeae
mother s abdomen and gentle but deep 2. Hgb electrophoresis
pressure is exerted 3. HIV titer by ELISA Western blot if HIV + by
o Hard resistant convex structure fetal ELISA
back 4. Glucose screening for DM; all pregnant
o Numerous nodulations - fetal small women should be tested
parts a. OGTT Oral Glucose Tolerance Test
3rd maneuver: Pawlic/Pawlik s Grip
st
- performed during the 1 trimester if the patient is at
o Determine what is occupying the high risk for DM
pelvic inlet Family history
o Use of thumb and fingers of one hand Age > or = to 35 y/o
o Movable, round and hard body fetal Previous birth of large baby
head not engaged
o Considered negative if lower pole of (+) sugar in urine
the fetus is fixed in the pelvis or
engaged b. GCT Glucose Challenge Test
- performed if patient is not a high risk patient
4th maneuver: Pelvic Grip - done at 24 28 weeks AOG
o Determine whether head is - Threshold value: 130 mg/dL if Glucose is greater
extended or flexed that this, do OGTT
1. Engagement occurs if both 5. MSAF at 15 -18 weeks (Usually with
hands converge from each other since presenting HCG, estriol)
part has entered the pelvis
If head is not engaged,
the cephalic prominence is
palpated

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 Prenatal, tetralogy, immunizations, drugs, high risk pregnancy: EMR, JV-C & PDV
Psychosocial Screening
Psychosocial Issues
These are nonbiomedical factors that affect
one men al and ph ical ell-being.
Women should be screened regardless of
social status, education level, race, or
ethnicity.
o seek barriers to care,
communication obstacles, nutritional
status, unstable housing, desire for
pregnancy
o safety concerns that include intimate
partner violence, depression, stress
o use of substances such as tobacco,
alcohol, and illicit drugs
performed on a regular basis (at least
once/trimester)
o to identify important issues and
reduce adverse pregnancy
outcomes
o Results to a less likely preterm or
low- birthweight newborns delivery,
and decreased rate of gestational
DM, premature rupture of
membranes, and vaginal bleeding
Cigarette Smoking
Potential teratogen
twofold risk of placenta previa, placental
abruption, and premature membrane rupture
likely to be preterm, have lower BW, and die
of SIDS (sudden infant death syndrome)
ri k for pon aneo abor ion, fe al dea h,
and fetal digital anomalies
e po re in ero: ri k of a hma, infan ile
colic, childhood obesity
Pathophysiological Mechanisms
fetal hypoxia
o increased carboxyhemoglobin
o reduced uteroplacental blood flow
direct toxic effects of nicotine and other
compounds in smoke
o Nicotine transfer is so efficient that
fetal nicotine exposure is greater
than that of the mother
o E po ed fe e : HR ariabili
due to impaired autonomic
regulation
Smoking Cessation
First and subsequent prenatal visits
counseling and effective intervention options
are recommended
Cessation at preconception = GREATEST
BENEFIT
Quitting at any stage of Pregnancy =
improved perinatal outcomes
Fi e A of Smoking Ce a ion
- 15min. counseling approach
1. ASK about smoking at the first and
subsequent prenatal visits.
- To improve assessment accuracy,
patients should choose the ffing statement
that best describes her smoking status:
o I smoke regularly now; the same as
before pregnancy
o I smoke regularly now, b I e c
down with pregnancy. I smoke every
once in a while
o I have quit smoking before
pregnancy, and I do not currently
smoke
o If smoking abstinence has already begun,
then reinforce her decision to quit,
congratulate on her success, and
encourage her continued abstinence.
For persistent smokers, proceed to the ffing steps:
2. ADVISE with clear, strong statements that
explain the risks of continued smoking to the
woman, fetus, and newborn
3. ASSESS he pa ien illingne o a emp
cessation
4. ASSIST with pregnancy-specific, self-help
smoking cessation materials
5. ARRANGE to track smoking abstinence
progress at subsequent visits
Alcohol - Ethyl alcohol or ethanol
potent teratogen causes fetal syndrome
o characterized by growth restriction,
facial abnormalities, and CNS
dysfunction
Pregnant women, aged 35-44 y/o, white,
college graduates or employed, should
abstain from using any alcoholic beverages.
Illicit Drugs
Agents may include heroin and other
opiates, cocaine, amphetamines,
barbiturates, and marijuana
Chronic use of large quantities is harmful to
the fetus
o fetal-growth restriction, low
birthweight, and drug withdrawal
soon after birth.
Methadone maintenance for heroin abuse
o 10-30mg OD with titration PRN
Buprenorphine
o Monotherapy or in combination with
Naloxone
o Less commonly used
Intimate Partner Violence
Major public health problem
pattern of assaultive and coercive behaviors
o include physical injury,
psychological abuse, sexual assault,
progressive isolation, stalking,
deprivation, intimidation, and
reproductive coercion
Domestic Violence prevalent during
routine prenatal screening aside from
preeclampsia
Could lead to adverse perinatal outcomes
such as preterm delivery, fetal-growth
restriction, and perinatal death.
Domestic Violence Screening
Use at the first prenatal visit, again at least
1/trimester, and at the postpartum visit
Done privately and away from family
members
Clinical Evaluation
- thorough, general PE should be completed at the
initial prenatal encounter
Pelvic examination is performed as part of
the evaluation
5
 Prenatal, tetralogy, immunizations, drugs, high risk pregnancy: EMR, JV-C & PDV

Cervix is visualized employing a speculum Risk factors include unmarried status, recent
lubricated with warm water or water-based change in sexual partner or multiple
lubricant gel concurrent partners, < 25 years of age,
- Bluish-red passive hyperemia: inner-city residence, history or presence of
characteristic but not of itself diagnostic other STD , and little or no prenatal care
nd
- Nabothian cysts prominent dilated- Test of Cure 2 test ffing treatment.
occluded cervical glands (beneath o Recommended during 3-4wks after
ectocervical mucosa) Tx completion
- The cervix is not normally dilated
except at the external os Pregnancy Risk Assessment
- Pap smear - identification cytological SUBSEQUENT PRENATAL VISITS
abnormalities 4-week intervals until 28 weeks
- Bimanual examination is completed by every 2 weeks until 36 weeks
palpation weekly until delivery
- consistency, length, and dilatation
of the cervix - complicated preganancies = 1-2weeks
- to uterine and adnexal size | bony interval visits
pelvic architecture | any vaginal or o twin pregnancies
perineal anomalies - re rn i i e er 2 k = o come
Fetal presentation determined at the latter o emphasis on prenatal nutrition and
part of pregnancy education
Lesions of the cervix, vagina, or vulva
evaluated by colposcopy, biopsy, culture, or Prenatal Surveillance
dark-field examination A e men of he mo her and he fe ell-
Perianal region - visualized with DRE as being at each return visit
required for complaints of rectal pain, - Fetus: Evaluation of the heart rate, growth,
bleeding, or mass amniotic fluid volume, and activity
- Mother: BP, weight, extent of change
Gestational Age Assessment - Symptomatic headache, nausea, vomiting,
one of the most important aspects of altered vision, abdominal pain, bleeding,
prenatal care vaginal fluid leakage, and dysuria are
Treatment for the development of pregnancy sought
complica ion dependen on fe al age - Measurement of uterine size (symphysis
Based on Uterine Size: to fundus).
o 6wks gestation small orange - In late pregnancy, vaginal examination
o 8wks pregnancy large orange provides valuable information
o 12wks - grapefruit o Confirmation of the presenting part
Crown-Rump Length (CRL) and its station
st
o Most accurate during 1 trimester o Clinical estimation of pelvic capacity
Sonographic interrogation General configuration, amniotic
o Provision of an estimated fluid volume adequacy, cervical
gestational age during the latter consistency, effacement, and
pregnancy dilatation
o With declining accuracy Fundal Height
Between 20 and 34 weeks
Laboratory Tests uterine fundus height (cm) = gestational age
Initial Blood Tests in weeks
complete blood count o used to monitor fetal growth and
blood type with Rh status determination amnionic fluid volume.
an antibody screen o distance along the abdominal wall
top of the symphysis pubis
Universal HIV testing recommended part for op of he f nd
prenatal care o bladder must be emptied before
with patient notification and right of refusal fundal measurement
refused or declined RECORDED in o if used alone, fetal growth restriction
prenatal record (FGR) can be undiagnosed
Obese patient or presence of uterine mass
All pregnant women should also be (Leiomomata) limits accuracy
screened for hepatitis B virus and syphilis o Ultrasound can be used
and with immunity to rubella at the initial visit
Fetal Heart Sounds
Routine Urine Analysis - FH Rate: 110 160bpm
Urine culture: performed for the treatment of - Doppler ultrasound 10weeks
asymptomatic bacter ria = mp oma ic - Standard nonamplified Stethoscope
UTI development 16weeks; 20weeks in majority (80%); 22wks
for all women
Cervical Infections - Because the fetus moves freely in amnionic
st
Chlamydia trachomatis screened at 1 prenatal fluid
rd
visit, with additional 3 trimester testing (high risk) site on the maternal abdomen where
Neisseria gonorrhoeae G(-) diplococci fetal heart sounds can be heard best will
vary
6
 Prenatal, tetralogy, immunizations, drugs, high risk pregnancy: EMR, JV-C & PDV
Sonography
provides invaluable information regarding
fetal anatomy, growth, and well-being
used at least once during the entire
pregnancy
only be performed when there is a valid
medical indication
o used with lowest possible US exposure
setting
Subsequent Laboratory Tests
- Fetal aneuploidy screening 11-14wks
and/or 15-20wks
- Serum screening for neural tube defects
15-20wks
- Hct & Hgb determination + syphilis serology
(if prevalent) repeated at 28-23wks
- ri k for HIV acquisition repeated testing
rd
at 3 trimester
- ri k for Hep B infec ion retested at the
time of hospitalization for delivery
- D (Rh) negative and unsensitized women
Ab screening test repeated at 28-29wks +
anti-D Ig administration (if remained
unsensitized)
Group B Streptococcal (GBS) Infection
- Between 35-37 AOG attain vaginal and
rectal GBS cultures
- Intrapartum antimicrobial prophylaxis (+)
cultures
Gestational Diabetes
- All should be screened for gestational DM
o by history, clinical factors
- routine laboratory testing (bet. 24-28wks)
most sensitive approach
Selected Genetic Screening
- offered to those at increased risk based on family
history, ethnic or racial background, or age
- Tay-Sachs disease Eastern European
Jewish / French Canadian ancestry
- -thalassemia - Mediterranean, Southeast
Asian, Indian, Pakistani, or African
ancestry
- -thalassemia - Southeast Asian or
African ancestry
- sickle-cell anemia - African,
Mediterranean, Middle Eastern,
Caribbean, Latin American, or Indian
descent
- Trisomy 21 - with advanced maternal age.
NUTRITIONAL COUNSELING
Weight Gain Recommendations
st th
1 half of 20 century
- Recommended wt gain = limited to <20lb or
9kg
- prevent gestational hypertension and fetal
macrosomia.
1970s at least 25lb or 11-12kg gain
- prevent preterm birth and fetal-growth
restriction
prepregancy BMI basis for weight gain
foc of d : lo bir h eigh ne born obe i
- increased risks for gestational HPN
(preeclampsia) & DM, macrosomia,
cesarean delivery
- do e rela ed o prenatal weight gain.
- Maternal weight gain during pregnancy
influences birthweight
Severe Undernutrition
severe nutritional deficiencies - consequence of
social, economic, or political disaster
Dutch Hunger Winter
- Intense nutritional deprivation in Netherlands
- Rations reached 450kcal/day
o With generalized malnutrition
- Smith (1947), correlates the influence of
starvation to birth wt. during late pregnancy
- Intense dietary deprivation = impaired brain
development
Barker hypothesis
- Earl ar a ion = CNS anomalies,
schizophrenia, and schizophrenia-spectrum
personality disorders
- Mid to Late pregnancy deprivation = light,
short, thin at birth
o incidence of dimini hed gl co e
tolerance, HPN, reactive airway
disease, dyslipidemia & CAD
- Concept of Fetal Programming
o Adult morbidity and mortality ~ fetal
death
Weight Retention after Pregnancy
- Maternal Weight Loss:
at delivery (12lb or 5.5kg)
ensuing 2wks (9lb or 4kg)
between 2wks and 6mos postpartum
(5.5lb or 2.5kg)
- Gain > Loss; thus, 3lb or 1.4kg of weight is
retained.
- gain d ring pregnanc = po par m
loss
- No relationship bet. Pre-pregnancy BMI or
weight gain and weight retention
Recommended Dietary Allowances
- Iron, Zinc, Selenium, Vit A, B6, C, and D =
with potential toxic effects in intake >2x the
RDA
- Excessive Vit A (>10,000 IU/day) -
teratogenic
Calories
- Pregnancy requires 80,000kcal on the last
20wks.
- Recommended increase from 100 to
300kcal/day is advised during pregnancy
o should not be divided equally during
the course of pregnancy
- Used as a means of energy source and for
the sparing of protein metabolism, used
for fetal growth and development
Protein
- Used for the growth and remodeling of fetus,
placen a, er , and brea , a ell a
maternal blood volume
7
 Prenatal, tetralogy, immunizations, drugs, high risk pregnancy: EMR, JV-C & PDV
nd
- 2 half of pregnancy = 1000g of CHON are larger infants with bigger head
deposited, amounting to 5-6g/day circumference
o orni hine, gl cine, a rine, and - 30mg zinc from 12-16wks AOG
proline maternal plasma level until delivery = no improvement
o gl amic acid and alanine conc. in birthweight
During pregnancy - Low-birthweight infants of mothers with zinc
- Supplied from: animal source (meat, milk, pplemen a ion = ri k of ac e diarrhea,
eggs, cheese, poultry, fish) dysentery, impetigo
- Milk and dairy products source of CHON
and calcium for pregnant or lactating women Magnesium
- Mineral deficiency during pregnancy still has
Minerals no recognized consequence.
Iron
- Iron and iodine minerals not found in diets
the supply adequate calories for weight gain. Trace Metals
- 300mg of Fe transferred to the fetus and - Copper, Selenium, Chromium and
placenta Manganese (Cu, Se, Cr, Mn) (+) roles in
- 500mg of Fe added into the maternal Hgb certain enzyme functions
mass - Selenium deficiency fatal cardiomyopathy
Nearly all is used after mid-pregnancy in young children and reproductive-aged
- At least 27mg of elemental iron (FDA: women
30mg) supplement per day given to - Oversupplementation Selenium Toxicity
pregnant women
Amount contained in most prenatal Potassium - decreased by 0.5mEq/L during
vitamins (as Fe fumarate, sulfate, midpregnancy on the maternal plasma
gluconate)
If taken daily throughout the latter half Fluoride
of pregnancy = adequate requirement - no beneficial evidence on fluoride
+ protection of preexisting Fe stores supplementation during pregnancy
Also provide for Fe requirements of - no alteration on fluoride metabolism
lactation - ingestion does not increase concentration in
- 60-100mg of elemental Fe/day for large breast milk for lactating women
women, has twin fetus, late pregnancy
supplementation, irregular Fe intake, or with Vitamins
depressed Hgb levels Folic Acid
- IDA woman responds well to oral iron salts - 400mcg = ne ral be defec a
- Iron supplementation during the first four preconceptional period
months of pregnancy is not required - Level A recommendation
Avoids risk of aggravating nausea and o 0.4 to 0.8 mg of folic acid per day
st
vomiting - 4mg/day 1 mon h before concep ion 1
- Iron intake at bedtime or empty stomach = trimester
ab opr ion & ad er e GI reac ion o recurrence risk of NTD
o Consumed as a separate
Iodine supplement, not as multivitamins.
- RDA: 220mcg
- Iodized salt and bread products Vitamin A
recommended to offset the increased fetal -
req. and maternal renal loss of iodine malformations
- Maternal hypothyroidism = cretinism with - Accutane Vit A derivative isotretinoin
neurodevelopmental defect in children o Most potent teratogen
- -carotene found in fruits and vegetables
Calcium o incidence of toxicity
- pregnant woman retains approximately 30g - Deficiency
of calcium o <
rd
- Most is deposited in the fetus late in o night blindness 3 trimester
pregnancy o ri k of ma ernal anemia and
- Represents only 2.5% of total maternal spontaneous preterm birth
calcium Vitamin B12
most of which is in bone and can - pla ma transcobalamins (carrier) =
readily be mobilized for fetal growth maternal plasma B12
- in e inal ab orp ion and progre i e - naturally only in foods of animal origin
retention throughout pregnancy o strict vege arian = B12 infan
o Profound in breast-fed infant
Zinc - Vi C inge ion = f nc ional deficienc of
- Severe zinc deficiency - poor appetite, B12
suboptimal growth, and impaired wound - Deficienc : ri k of ne ral be defec
healing o Still controversial
- RDA = 12mg during pregnancy
- 25mg zinc supplementation at Vitamin B6 Pyridoxine
midpregnancy = higher zinc plasma level =
- 2mg supplement for high risk inadequate
nutrition
8
 Prenatal, tetralogy, immunizations, drugs, high risk pregnancy: EMR, JV-C & PDV

o substance abusers, adolescents, - Avoidance of high risk of falling / abdominal

and those with multifetal gestations ra ma & c ba di ing ( ri k of
- Vi B6 + do lamine = na ea and decompression sickness)
vomiting - e erci e or ph ical ac i i = re = (+)
Vitamin C outcome
- RDA = 80 to 85 mg/day o For pregnant women who are
- Most water soluble vitamins decline during having:
pregnancy but higher in the cord=blood level pregnancy-associated
Vitamin D hypertensive disorder
- Fat soluble vitamin with active metabolic preterm labor, placenta
form previa
- in e inal calci m ab orp ion & promo e severe cardiac or
bone mineralization and growth pulmonary disease
- Source: endogenous synthesis from sunlight multiple or suspected
& dietary intake growth-restricted fetuses
- Deficiency: disordered skeletal homeostasis,
congenital rickets, and fractures in the Seafood Consumption
newborn - Fi h = pro ein, a . fa , (+) omega-3 fatty
- Recommended intake = 15mcg/day (600 IU acids
per day) - Fish and shellfish = (+) trace amount of Hg
- 25-hydroxyvitamin D serum level lab test (methylmercury)
for suggestive deficiency o Shark, swordfish, king mackerel,
Pragmatic Nutritional Surveillance and tile fish
Advise the pregnant woman to eat what she o Not given to pregnant and lactating
wants in amounts she desires and salted to women
taste - Recommendation: nmt 12oz or 2 servings of
Ensure that food is amply available for canned tuna / week & nmt 6oz of albacore
socioeconomically deprived women or white tuna
Monitor weight gain - goal of approx. 25-35 - Limitation: if Hg content is unknown = nmt
lbs in women with a normal BMI 6oz / week overall fish consumption
Explore food intake by dietary recall
periodically to discover the occasional Lead Screening
nutritionally errant diet - Maternal exposure = several adverse
Give tablets of simple iron salts that provide maternal and fetal outcomes
at least 27 mg of elemental iron daily o Mother: (+) gestational HPN,
o Give folate supplementation before spontaneous abortion
and in the early weeks of pregnancy o Fetus: low birthweight, and
o Provide iodine supplementation in neurodevelopmental impairments
areas of known dietary insufficiency -
Recheck Hct or Hgb concentration at 28- - =
32wks AOG to detect significant decreases undergo chelation therapy

COMMON CONCERNS Automobile and Air Travel

Employment - Encouraged to wear properly positioned
- (+) pregnancy = 12 workweeks of unpaid three-point restraints
leave o Throughout pregnancy while on
o For birth and care of newborn child automobiles
- pregnanc complica ion ri k : o Lap portion placed under
o Ph icall demanding = ra e of abdomen and across upper thighs
preterm birth, fetal-growth o Belt snug comfortably
restriction, or gestational HPN o Shoulder belt between the breasts
o 5x risk of preeclampsia - (+) availability of airbags
o Occ pa ional fa ig e = ri k of - Air travel = properly pressurized aircraft = no
premature membrane rupture harmful effect
# of hours standing - Can safely fly up to 36wks of AOG
Intensity of physical and - Significant risk: infectious disease
mental demands acquisition, lower venous thromboembolism
Environmental stressors
- Management: adequate period of rest, Coitus
limitation of work or play, minimization of - A oidance if ri k of abor ion, placen a
physical work previa, or preterm labor
- ge a ion = coi freq enc
Exercise - Intercourse late in pregnancy = not harmful
- Not limited to pregnant women provided that - Oral-vaginal intercourse is occasionally
they do not become excessively fatigued or hazardous
risk injury - (+) fetal air embolism result of air blown
- encouraged to engage in regular, moderate- during cunnilingis at late pregnancy
intensity physical activity for >30mins daily.
- Activity = reviewed for potential risks Dental Care
- Par of prena al e amina ion enco rage
good dental hygiene

9
 Prenatal, tetralogy, immunizations, drugs, high risk pregnancy: EMR, JV-C & PDV

o Periodontal disease = preterm labor - Morning sickness due to be worse in the

- Dental carries not aggravate by pregnancy morning though can continue throughout the
- Pregnancy not contraindicated to dental day.
treatment and dental radiographs - Treatment: minimization of symptoms but
seldom provides complete relief
Immunization o Frequent small meals
- Exposure to thimerosal vaccine preservative o Herbal remedy ginger
= neuropsychological disorders o Vit B6 + doxylamine
o Still under controversy o Phenothiazine or H1-receptor
- three-agent Tdap vaccine - tetanus toxoid, blocking antiemetics
reduced diphtheria toxoid, and acellular - Hyperemesis gravidarum severe
pertussis vomiting = dehydration, electrolyte and acid-
o d e o per i infec ion base disturbance, starvation ketosis
o dea h ri k for infants still
dependent on passive immunization Backache
from maternal Ab - Lower back pain excessive strain or
Vaccine is initiated at significant bending, lifting, or walking
2months of age o Reduced by squatting rather than
o 27-36 wks AOG - optimal passive bending over; using a pillow for
antibody transfer of Ab to the fetus support while sitting; high-heeled
- Influenza vaccine given at any gestation shoes
age during flu season - Progre ing ge a ion = complain
o prenatal maternal accina ion = o Prevalent on obese women or (+)
infant influenza incidence/ febrile history of low back pain\
respiratory illness (first 6 months of - Severe pain = require thorough orthopedic
life) examination
- postpartum MMR vaccine - susceptible to o pregnancy-associated osteoporosis,
rubella disc disease, vertebral
o will not cause congenital rubella osteoarthritis, or septic arthritis
syndrome even if used during - muscular spasm = acute strain or fibrositis
pregnancy - usually responds to analgesics, heat, and
o no contraindication while breast rest
feeding o Tylenol for chronic pain
o NSAID ed in hor co r e =
Biological Warfare and Vaccines fetal effects
- smallpox vaccine - live attenuated vaccinia o Muscle relaxants (cyclobenzaprine
virus (Flexeril) or baclofen) added as
o may result to abortion, stillbirth, or needed
neonatal death - ac e pain (+) ph ical herap o
o contraindicated during pregnancy or stability and strength of spine and hip
to pre-pregnant women within o (+) sacroiliac joint stabilizing support
28days of vaccination belt
o if administered inadvertently at early o Essential for the increase load of
pregnancy = not an indication for pregnancy
termination - Multimodal therapy - combination of manual
o (+) infection direct contact or chiropractic therapy, exercises, and patient
victim of bioterrorist = benefit > risk education
of vaccination o Re l o pain and disability
- Anthrax vaccine - no live bacteria
o Only for occupationally exposed Varicosities and Hemorrhoids
citizens (Veterinarians, Lab workers, - Venous leg varicosities = congenital
military personnel) predi po i ion & i h ad ancing age
o No potential fetal risk - Fac or: lo er e remi ie eno pre re,
prolonged standing
Caffeine - Symptoms: cosmetic blemishes, mild to
- heavy intake (5cups or 500mg of caffeine e ere di comfor req ire rest + feet
per da ) = abor ion ri k elevation
- moderate intake (<200mg daily) no - Vulvar varicosities co-exist with leg
reported risk varicosities
- no a ocia ion i h pre erm bir h b ih o Become massive and almost
risk for fetal growth impairment incapacitating
- limited intake = <300mg or three 5-oz cups o (+) rupture = severe blood loss
of percolated coffee o Treatment: fitted pantyhose -
lower extremity varicosities
Nausea and Vomiting foam rubber pad suspended
st
- Common complaints during 1 half of across the vulva by a belt
pregnancy (+) pressure on dilated
st nd
- Usually commence between 1 and 2 veins
mi ed men r al period 14-16wks AOG for bothersome
vulvar varicosities

10
 Prenatal, tetralogy, immunizations, drugs, high risk pregnancy: EMR, JV-C & PDV

- Hemorrhoids - rectal vein varicosities due to

pel ic eno pre re Cord Blood Banking

o Pain and swelling relieved by umbilical cord blood transplantations = Tx
topical anesthetics, warm soaks and for hemopoietic cancers and various genetic
stool softening agents conditions
o External hemorrhoid thrombosis 2 types of cord blood banks
relieved by incision and clot removal o Public banks promotion of
under local analgesia allogenic donation, for use by
related or unrelated recepients
Heartburn Similar to blood product
- One of the most common complaints donation
- Gastric reflux into the lower esophagus o Private banks for storage of stem
- Result from upward displacement and cell f re a ologo e ih
compression of stomach by uterus + LES fees for initial processing and
relaxation annual storage
- Relie ed b hort meal frequency,
bending over / lying flat, antacids (Al(OH)3, Identification of High Risk Preganncy
Mg(OH)2, Mg trisilicate) A. Medical History
Asthma, cardiac disease, DM, drug and alcohol use,
Pica and Ptyalism epilepsy (on medication), family hx of genetic
- Pica craving for strange food problems (Down Syndrome, PKU),
o Pagophagia - ice hemoglobinopathy, hypertension, prior DVT or
o Amylophagia - starch pulmonary embolism, psychiatric illness, COPD,
o Geophagia - clay chronic renal disease
- Can be riggered by severe iron deficiency
- Ptyalism distressed by profuse salivation
o Stimulation after starch ingestion
B. Obstetrical History
Sleeping and Fatigue Age >35 y/o, caesarean delivery, incompetent
- earl pregnanc = (+) fa ig e, leep req iremen cervix, prior fetal structural/chromosomal
- soporific effect of progesterone abnormality, prior
st
- 1 trimester: nausea and vomiting neonatal death, prior fetal death, prior
rd
- lesser extent than 3 trimestral pregnancy preterm delivery or preterm ruptured membranes,
rd
- 3 trimester: general discomfort, urinary frequency, prior LBW (<2500g), uterine leiomyomas or
dyspnea malformation
- poor leep efficienc , a akening, age
4 (deep) and rapid-eye movement sleep C. Initial Lab Tests
- short sleep duration, (+) snore, HIV
restless leg syndrome, (+) sleep disturbance Rh positive
- Diphenhydramine (Benadryl) can be helpful Initial examination condylomata

Leukorrhea
- aginal di charge d ring pregnanc
- Most instances are not pathologic
- e rogen = m c ecre ion b cer ical gland
- Contributing factor
Speculu
Dischar
m Dx Tx
ge
Finding
Foamy/f
Hanging Metroni
Tricho rothy,
Strawbe drop dazole
monas yellow/g st
rry NSS (after 1
vaginal reen,
cervix Trichom trimeste
is leucorrh
onas r)
ea
Reddish Flagellat
Candid
vaginal e
a Cheesy Nystatin
- Thayer
albican white, /
pruritus/ Martin
s/ curd- Micona
burning Agar
Chlamy like zole
sensatio Pseudo
dia
n hyphae
Clue
Grayish, cells
Gardin rotten Hanging
ella fishy drop Metroni
vaginal odor w/ 10% dazole
is pH < KOH (+
4.5 amine
test)

11
 Drugs, Immunizations and High Risk

Drugs & Immunizations

Pharmacokinetics in Pregnancy
o Ideal drug for treatment
Efficacious for maternal indication
Minimally transported through the placenta & in event of passage, exerts minimal effect
on the fetus
Drug characteristics that influence tolerability & adherence to dosage & dosing schedule
Must not exacerbate conditions common in pregnancy: emesis, GIT changes, glucose
intolerance, hypertension
o Therapeutic consideration: Effects on fetus > Maternal factors
o Physiologic changes in pregnancy significantly affect pharmacokinetics in pregnant patient

Physiologic Change Effect on PK Examples

GIT Variable bioavailability of oral Most oral preparations

GIT motility, gastric pH, nausea preparations
& vomiting
Respiratory Increased alveolar uptake of inhaled Inhaled anesthetics
Hyperventilation, TV Pulmonary drugs
blood volume
Cardiovascular Increased volume of distribution
: Cardiac output (40%), plasma
volume (50%) & total blood volume
(40%)
Body space Further increase in volume of
: Maternal aqueous, fatty tissue distribution
space (peak at 10-30wks), body
water (ECF: 40% maternal, 60%
feto-placental)
Metabolic Increased free-drug fractions of Diazepam, phenytoin, valproic acid
rd
: Albumin (25%) protein-bound drugs specially in 3
: Steroid hormones competing for trimester
protein binding sites
Serum Progesterone Increased cytochrome metabolism Phenytoin, carbamazepine, valproic
of drugs acid
Serum Estrogen Decreased cytochrome oxidase Theophylline & caffeine
metabolism of some drugs
Renal Increased renal excretion & Lithium, digoxin, ampicillin
Renal blood flow (50%) leading to creatinine clearance (doubled)
GFR (50%)
Net effect expected decrease in steady state concentration if a normal dose is
administered, higher dose will be needed
Important in theory, but often not clinically significant, exceptions
Drugs exclusively eliminated via renal route
o Lithium & Digoxin
o Increase in renal clearance decreased serum concentration
o Narrow therapeutic range serum concentration monitoring
Anti-epileptics
o Carbamazepine, valproic acid & phenytoin
o Increase in: hepatic metabolism, renal clearance & plasma volume +
Decreased protein binding decrease in effective serum concentration
Feto-placental Pharmacokinetics
o Drugs reaching the fetus are almost always administered to the mother
o Maternal administration Placenta Fetal serum Placenta Maternal excretion
o Cotyledons (Maternal lobes)
Raised areas on the basal surface of the placenta intimately related to several fetal
cotyledons
Allows maternal circulation to be superimposed onto the fetus
Passage of solutes (require passing through the syncytiotrophoblast either
Directly through its cytoplasm more common
Via a network of specific transporters less common
o 3 Compartments to cross: Maternal blood trophoblastic cytoplasm fetal circulation
Simple diffusion major transport mechanism
Ra e of ran por i dic a ed b ol e
Molecular weight
Degree of ionization

1
 Drugs, Immunizations and High Risk

Protein-binding
Relative concentration across the compartments
Factors involved in drug transfer across the placenta
Physiochemical properties of drug: highly lipid soluble, non-ionized, low
molecular weight (<200daltons) & low protein-binding easily cross the placental
barrier
Transfer of flow-limited drugs is affected by maternal serum drug concentration &
placental blood flow: Higher maternal drug concentration create a greater
concentration gradient causing rapid placental transport
Compounds that alter blood flow also alter maternal drug disposition &
consequently placental transfer
Placental metabolism (dealkylation, hydroxylation, demethylation) influence drug
ran por o a le er degree han ma ernal me aboli m infl ence
Fetal metabolism plays a part but may change during pregnancy

Fetal Pharmacokinetics also play a role in determining the net effect of drugs on the fetus
o Maternal blood flow to the placenta
Increases gradually during gestation
10 weeks 50mL/min
38 weeks 600mL/min (peak)
Increases the fetal drug exposure as pregnancy progresses
o Protein-binding capacity
Fetal plasma (vs maternal)
Albumin where acidic drugs bind to, higher by 15%
a1-Acid Glycoprotein where basic drugs bind to, lower by 37%
Protein-binding capacity lower
Leads to a greater free drug fraction that enter fetal circulation
Propanolol & lidocane basic drugs
Ampicillin & benzylpenicillin drugs with low affinity for fetal proteins
Less protein-binding, less a1GP More free drug in circulation Greater risk for
toxicity
o Ionization
pH: Fetal plasma & amniotic fluid (more acidic) vs maternal blood
Ionization is favored ion-trapping of basic drugs in fetal compartment greater risk for
toxicity
o Hepatic metabolism
st
Fetal liver has cytochrome oxidase responsible for 1 pass effect in the fetus, less
metabolizing capacity vs maternal
Modulated by ductus venosus shunt & may vary by 30-70%
Maternal estrogen Decrease activity of cytochrome oxidase Decrease hepatic
metabolism of drugs Increase circulating drug concentration greater risk for toxicity
o Renal clearance
Fetal kidney is immature low GFR
GFR increases with AOG but peaks only at 2-4mL/min at term because it receives only
3% of CO (vs 25% in adults)
Cation secretion high, efficient clearance of cimetidine
Anionic drug secretion very low, inefficient clearance of penicillin
o Reabsorption
Fetal urine Amniotic fluid May be swallowed by the fetus
Renally excreted drugs & metabolites may be reabsorbed

Generalities on Pharmacokinetics (Maternal, placental, fetal)

o Drugs that are large, highly protein-bound, ionized in maternal plasma & poorly absorbed into the
maternal bloodstream
Rarely cross the placenta
Usually confined in the maternal compartment
Exhibit minimal effect on the fetus
o Drugs that cross the placenta exhibit greater toxicity for the fetus than for the mother due to
Decreased protein binding
Ion-trapping
Poor metabolism
Poor excretion

2
 Drugs, Immunizations and High Risk

Guidelines for Prescribing & Counseling in Pregnancy

o Generalities
Rule of thumb:
st
Drug intake in the pregnant patient is generally avoided especially in the 1
trimester when fetus exhibits highest risk for congenital malformations
Consider non-pharmacologic treatments
If absolutely necessary,
Preference must be given to drugs with proven safety: Classes A & B
Monotherapy is preferred
Drug combinations agents must be introduced one at a time
Exposure of fetus to agent must be kept to a minimum: Lowest possible dose &
shortest possible effective treatment duration
Systemic administration should be avoided (inhalation & topical vs oral & IV)
Benefits >>> Risk to fetus & mother
o Bacterial infections
Penicillins (B) preferred agents & probably the safest antimicrobial in pregnancy
Erythromycin (B) for penicillin-allergic patients
Use with caution: Cephalosporins (B), Chloramphenicol (B) & Metronidazole (C)
o Tuberculosis
Rifampicin, Isoniazid, Ethambutol no increased risk for congenital malformation
Use drugs with caution
o Colds, cough
Always aim for symptomatic relief with fluids & rest
Antihistamines use with relative safety
Chlorpheniramine (B)
Tripolidine (D)
Diphenhydramine (C) more rapid-onset of rebound congestion in pregnancy;
use for no longer than 2-4days
Pseudoephedrine (C) generally safe
Cough suppressants
Guaifenesin (C)
Dextromethorphan (C)
Avoid preparations with alcohol & iodine
o Nausea & vomiting
Treated conservatively when effective: Rest, small frequent meals & acupressure
st
Emetrol 1 line
Vitamin B6 (A) + Doxylamine (B)
Use with caution: Promethazine (C) & Metaclopramide (C)
o Pain Relief
Paracetamol (B) pain reliever & antipyretic of choice
Ibuprofen (B)
Local anesthetics (Xylocaine) useful but do not combine with Epinephrine
Narcotics for sever pain Codeine, Demerol & Morphine
Mother addictive potential
Fetus respiratory depression
o Diarrhea
Kaolin & Pectin (B) anti-diarrheal of choice, not absorbed systematically
Loperamide (B) most probably safe
o Asthma
Treatment is same with non-pregnant patient
Theophylline (B)
Salbutamol (B) via aerosol
Steroids (B) & Leukotrienes (B) safe for pregnancy
o Epilepsy
Emphasize risk for malformations (5% with epipleptics, 3% in others)
Avoid drug combinations & use therapeutic drug monitoring
Therapy is maximized before pregnancy & may consider slowly withdrawing if patient has
been seizure-free for 2-3years
No justification for shifting from a teratogen to one with no available data
Phenobarbital (B) no increased frequency in minor/major defects
Carbamazepine (D) teratogenic potential is influenced by genetics (epoxide
hydroxylase levels)
Valproic Acid (D) 1-2% risk of spina bifida, associated with minor craniofacial
deformities
o HPN
Methyldopa (C) most widely used, unparalleled safety record in pregnancy
b-Blockers, except Atenolol (D) non-teratogenic but may cause growth restriction
nd rd
Hydralazine no adverse fetal effects; used for the 2 & 3 trimester

3
 Drugs, Immunizations and High Risk

NaNitroprusside readily crosses the placenta & may cause accumulation of cyanide, no
adequate data
o Hyperthyroidism
Propylthiouracil used more often than carbamazepine, less lipid-soluble & more protein-
bound, this transported less well to fetus & breast milk

Immunization During Pregnancy

o Generalities
Vaccines that generate maternal immune response may also become protective to the
fetus when maternal antibodies pass through the placenta
Detrimental when sufficient amount of maternal antibodies are transmitted as to interfere
with the development of natural antibodies in the fetus
Maternal reactions to vaccination may adversely affect fetal support & development
Fever
Hypersensitivity
Risks are theoretical no available clinical evidence; Benefits >>>> Risk
Live vaccines carry greater theoretical risk of vertical transmission & are
contraindicated
Measles
Mumps
Rubella
o Tetanus-Diphtheria Vaccine (Td)
Safe in pregnancy - toxoid
Booster shots for previously immunized: okay
Unimmunized must be given the complete 3-dose series
nd
Preferred schedule: after 2 trimester with each dose given 4 weeks apart
ONLY VACCINE routinely indicated for all susceptible pregnant patients
o Hepatitis A Vaccine
Not established if safe/not
Killed vaccine - theoretical risk is low but safety is not determined
May be indicated for high-risk patients
o Hepatitis B Vaccine
Safe in pregnancy, no known detrimental effects on the fetus
Indicated in patients: >1 sexual partners in the last 6months, concurrent STD, IV drug
use, HBsAg-positive partner
o Human Papillomavirus Vaccine
Not recommended in pregnancy
Has been related to some adverse outcomes in pregnancy but data is limited
o Influenza Vaccine (Inactivated)
Safe in pregnancy, no adverse fetal outcomes reported
Recommended during influenza season, pregnant who become infected are at increased
risk for severe complications
o Measles, Mumps & Rubella Vaccine
Live vaccines - should not be administered in pregnant patients
Vaccinated women should not be advised to get pregnant for 28 days after administration
Congenital Rubella Syndrome in fetus (no documented case yet)
o Pneumococcal Vaccine
Not established if safe/not
No adverse effects reported
o Polio Vaccine
Safe but avoided
No adverse effects reported but avoided due to theoretical risks
High-risk patients may be considered for vaccination
o Tetanus-Diphtheria-Pertussis Vaccine
Safe in pregnancy
Maternal pertussis Abs may be protective to the infant in early life (preferred over tetanus
toxoid alone)
o Varicella Vaccine
Not safe in pregnancy - unknown effects in fetus
Avoided entirely in pregnancy
Lower virulence than the wild type
o BCG - Not recommended; No Harmful effects reported
o Typhoid Vaccine - Not established; No available data
o Rabies Vaccine
Safe as post-exposure prophylaxis
Consequences of rabies >>> Risk of vaccination

4
Drugs, Immunizations and High Risk

5
 Drugs, Immunizations and High Risk

Identification of High-Risk Pregnancy

Maternal Age
Less than 18
More than 30 (Nullipara) or 35 (Multipara)
Advanced age is inimical to the fetus
Nearly 2-fold greater risk of fetal death
Maternal Height
Small women
o Birth trauma
o Cesarean section
o Congenital anomalies
Less than 5ft contracted pelvis
Weight: Obesity increased fetal growth, hypertensive disorders, gestational diabetes, increased need for
cesarean section

Social Factors
Smoking IUGR, mean weight non-smokers is 3148g vs 2982g for smokers (165g deficit)
Potential teratogen
2-fold risk of placenta previa, placental abruption, and premature membrane rupture
Likely to be preterm, have lower BW, and die of SIDS (sudden infant death syndrome)
Ri k for pon aneo abor ion, fe al dea h, and fe al digi al anomalie
E po re in ero: ri k of a hma, infan ile colic, childhood obe i
o Low birthweight infants, premature labor, abruptio placenta, bleeding, premature rupture of
membranes
o Effects of smoking
CO inactivates fetal and maternal Hgb
Vasoconstrictor effect of nicotine = induce placental abrution
Reduced appetite = reduced caloric intake
Decreased maternal plasma volume
Unexplained predisposition to ill effects of nicotine that persists even after quitting smoking
o Fetal hypoxia
increased carboxyhemoglobin
reduced uteroplacental blood flow
o Direct toxic effects of nicotine and other compounds in smoke
Nicotine transfer is so efficient that fetal nicotine exposure is greater than that of the mother
o E po ed fe e : HR ariabili d e o impaired a onomic reg la ion
Cessation
o First and subsequent prenatal visits
counseling and effective intervention options are recommended
Cessation at preconception = GREATEST BENEFIT
Quitting at any stage of Pregnancy = improved perinatal outcomes
o Fi e A of Smoking Ce a ion: 15min. co n eling approach
ASK about smoking at the first and subsequent prenatal visits.
To improve assessment accuracy, patients should choose the ffing statement that
best describes her smoking status:
o I smoke regularly now; the same as before pregnancy
o I moke reg larl no , b I e c do n i h pregnanc . I moke e er once
in a while
o I have quit smoking before pregnancy, and I do not currently smoke
If smoking abstinence has already begun, then reinforce her decision to quit,
congratulate on her success, and encourage her continued abstinence.
o (For persistent smokers, proceed to the ffing steps)
ADVISE with clear, strong statements that explain the risks of continued smoking to the
woman, fetus, and newborn
ASSESS he pa ien illingne o a emp ce a ion
ASSIST with pregnancy-specific, self-help smoking cessation materials
ARRANGE to track smoking abstinence progress at subsequent visits
Drugs
Illicit drug use - intrauterine & fetal distress (opium, barbiturates, amphetamines, methadone, heroin and other
opiates, cocaine, amphetamines, barbiturates, and marijuana)
Chronic use of large quantities is harmful to the fetus: fetal-growth restriction, low birthweight,
and drug withdrawal soon after birth.
Methadone maintenance for heroin abuse; 10-30mg OD with titration PRN
Buprenorphine - monotherapy or in combination with Naloxone; Less commonly used
Antibiotics little harmful effect
o Tetracycline brownish discoloration of deciduous teeth & premature cessation of long bone growth
6
 Drugs, Immunizations and High Risk

o Chloramphenicol cardiac fail re in neona e (Gra ndrome) if gi en la e in pregnanc

o Streptomycin congenital deafness, effects auditory nerve

Alcohol (Ethanol)
Potent teratogen - causes fetal syndrome
o characterized by growth restriction, facial abnormalities, and CNS dysfunction
Pregnant women, aged 35-44 y/o, white, college graduates or employed, should abstain from using any
alcoholic beverages.
Readily crosses the placenta
Moderate use no proven pathologic changes
Delirium tremens
o Seen in affected newborns
o Newborn is depressed at birth soon becomes extremely hyperactive with sweating tremors &
episodes of twitching of the face & extremities
Chronic use fetal craniofacial, limb & CV defects, prenatal & postnatal growth restriction
Heavy drinking (5 or 6 drinks of wine, beer or distilled spirits a day) during pregnancy can cause fetal alcohol
syndrome
o Undersized infants
o Mentally deficient
o Multiple deformities affecting head, face, limbs, heart, CNS
Even moderate consumption is related to a variety of problems

Intimate Partner Violence

Major public health problem
Pattern of assaultive and coercive behaviors - include physical injury, psychological abuse, sexual assault,
progressive isolation, stalking, deprivation, intimidation, and reproductive coercion
Domestic Violence prevalent during routine prenatal screening aside from preeclampsia. SCREENING;
o Use at the first prenatal visit, again at least 1/trimester, and at the postpartum visit
o Done privately and away from family members
Could lead to adverse perinatal outcomes such as preterm delivery, fetal-growth restriction, and perinatal
death.

Obstetrical History (Multiparity)

Incidence of Abruptio placenta, placenta previa, postpartum hemorrhage, uterine rupture, twinning,
dysfunctional labor & congenital anomalies increase with parity
Caesarean delivery, incompetent cervix, prior fetal structural/chromosomal abnormality, prior neonatal death,
prior fetal death, prior preterm delivery or preterm ruptured membranes, prior LBW (<2500g), uterine
leiomyomas or malformation
Premature Rupture of Membranes (PROM)
Rupture of fetal membranes prior to onset of labor
3 clinical significance
o Presenting part is not fixed in the pelvis possibility of cord prolapse & subsequent compression is
increased
o Labor is quite likely to occur
o Intrauterine infection
Management:
o Immediate delivery if there is evidence of
Chorioamnionitis
Vaginal bleeding
Fetal distress
o Induce labor with IV oxytocin/prostaglandin
Intrauterine Fetal Growth Restriction (IUGR)
th
Fetus is less than the 10 percentile if weight for AOG curve
Maternal Risk Factors - Diagnosis begins with identification of risk factors
Social: Poor weight in pregnancy, smoking, poor socio-economic status
Obstetrical: Previous IUGR infant, repeated abortions, stillbirths & neonatal death
Medical: Hypertension, renal disease, multiple UTIs, liver disease, cardiac disease,
hemoglobinopathies, thrombophilias
Screening methods: Abdominal palpation, fundic height, amniotic fluid volume estimate
Diagnosis
Confirmed by Ultrasound (BPD, femur length, HC, abdominal diameter & circumference)
Reduced abdominal circumference most sensitive biometric measure
Doppler velocity wave form analysis of fetal vessels best method in evaluating IUGR

Reduction of IUGR Incidence

st nd
1. Prophylaxis with acetylsalicylic acid started on 1 /2 trimester
2. Heparin before conception
Post-term pregnancy
7
 Drugs, Immunizations and High Risk

Dysmaturity
Completed >42 weeks AOG
Impairment of nutritional supply
Parchment-like skin
Reduced weight - subcutaneous tissue scaling
Complications
Sharp rise in both fetal & neonatal mortality after 42 weeks AOG
Fetal injury from fetopelvic disproportion
Asphyxial damage from fetal distress with increased risk of mental subnormality &
neurologic deficit
Pre-term birth
Delivery before 37weeks AOG
Accounts for 2/3 of infant death
Administration of corticosteroid
To mothers in preterm labor
Between 24-34 weeks
Reduces neonatal mortality by reducing RDS, Intraventricular Hemorrhage (IVH) & Necrotizing
Enterocolitis (NEC)
Fetal Macrosomnia
Excessive-sized infants are born to multiparas (Gestational/overt diabetes, obesity)
Complications with vaginal delivery
o Asphyxia
o Fetal stress & trauma
Mental subnormality
Clavicular fracture
Brachial plexus injury
o Vaginal lacerations/hematoma & pelvic relaxation
Multiple pregnancies
Twinning occurs nearly 2% of gestations
o Contributes to 15% of infants weighing less than 2.5kg (half of which is preterm)
o Account for undergrowth neonates
Maternal complications
o Pre-eclampsia, eclampsia 3x more frequent
o Premature labor PROM
st
o Premature separation of placenta after delivery of 1 of the twins
o Hemorrhage & trauma
Fetal complications
o Fetal death due to abnormal fetal/placental development
o Circulatory competition
o Umbilical cord accidents
o Abruptio placenta/cord prolapse asphyxia CNS injury: Cerebral palsy, mental retardation
o Twin-twin transfusion anemia in one, plethora in the other
o Double ovum twins FARE BETTER than single ovum twins
Hydramnios & Oligohydramnios
o AFI by ultrasound is critical in antenatal surveillance
o Hydramnios AFI > 25cm LGA, Congenital abnormalities
o Oligohydramnios AFI < 5cm poor perinatal outcome

UTI
Major cause of premature delivery, fetal death & maternal mortality
Multiparas > Primigravidas
Bacteriuria Acute pyelonephritis
Outlook is good if treated

DM - prematurity is a problem because of

Spontaneous premature labor
Tendency to deliver early delivery prior to term is induced in poorly controlled diabetic gravidas to avoid fetal
death in utero
Thyroid Disorders
Hypothyroidism: Stillbirths
Hyperthyroidism: LBW infants
Medical History
Asthma, cardiac disease, DM, drug and alcohol use, epilepsy (on medication), family hx of genetic problems
(Down Syndrome, PKU), hemoglobinopathy, hypertension, prior DVT or pulmonary embolism, psychiatric
illness, COPD, chronic renal disease
Initial Lab Tests
HIV, Rh positive, Initial examination condylomata

8
 Drugs, Immunizations and High Risk

Indications for Antepartum Fetal Monitoring Postnatal motor & intellectual impairment
Premature delivery
Tests Notes

CBC depends on the AOG/trimester - to determine hemtologic status

st
1 trimester 11g as normal - to r/o anemia
nd
2 trimester 10.5g as normal
rd
3 trimester 11g
* anything below is Abnormal

Urinalysis, Urine culture & sensitivity - to evaluate for UTI and renal function
- to check for asymptomatic bacteremia

Blood group, Rh - to determine blood type, Rh status and risk of isoimmunization

Serologic test for syphilis (RPR, - to detect previous or currents infections

VDRL) - if positive, do specific treponemal tests (FTA-ABS and MHA-TP)

Hep B surface Ag Do at 3rd trimester for cost- effectiveness

If positive:
- Use double glove delivery
- Give baby immunoglobulin
and Hep B vaccine immediately after delivery

Rubella Titer Approx 85% of mothers have evidence of prior infection

If px is seronegative, special precautions needed Vaccination is then
required postpartum

Cervical cytology (Pap Smear) To screen for cervical dysplasia/cancer

Indication: hx of sexual contact of at least 3 years (because you want to
detect the pre-cancer stage)
- Repeat every year
Patients at risk for uteroplacental insufficiency: Congenital abnormalities
Prolonged Pregnancy Need for specific therapy
DM
HPN
Previous stillbirth
Suspected IUGR
Advanced maternal age
Multiple gestations with discordant growth
Anti-phospholipid syndrome
Tests suggest fetal compromise
Suspected IUGR
Decreased fetal movement
Oligohydramnios
Routine antepartum surveillance

Obstetric conditions & management that may be

influenced by antepartum testing

Preterm delivery
Route of delivery
Bed rest
Observation
Drug therapy
Operative intervention in labor
Neonatal intensive care
Termination of pregnancy for a congenital
anomaly
Aspects of fetal condition that might be reduced
by antepartum testing

Perinatal death
IUGR
Non-reassuring fetal status (Intrapartum)
Neonatal asphyxia

9
Ultrasound

Technology

- Real-time image on the ultrasound screen is produced by sound waves reflected back from fluid and
tissue interfaces of the fetus, amnionic fluid, and placenta.
- Sector array transducers (w/ groups of piezoelectric crystals) working simultaneously in arrays
electrical energy into sound waves (synchronized pulses)
- Dense tissue such as bone produces high-velocity reflected waves = as bright echoes - hyperechoic
- Fluid generates few reflected waves and appears dark or anechoic.
- Sound waves traveling at a frequency above 20,000 hertz (cycles per second).
- Higher-frequency transducers = better image resolution
- Lower frequencies = penetrate tissue more effectively
nd
- 2 trimester, a 4- to 6-megahertz abdominal transducer is often in close enough proximity to the fetus
rd
- 3 trimester - lower frequency 2- to 5-megahertz transducer may be needed for penetration, but can lead
to compromised resolution. This explains when imaging obese patients and why low-frequency
transducers are needed to reach the fetus through maternal tissues.
- Early pregnancy, a 5- to 10-megahertz vaginal transducer may provide excellent resolution, because the
early fetus is close to the transducer

Fetal Safety

Sonography

valid medical indication, using the lowest possible exposure setting to gain necessary information the
ALARA principle as low as reasonably achievable.
no causal relationship has been demonstrated between diagnostic ultrasound and recognized adverse
effects in human pregnancy
required to display two indices: the thermal index and the mechanical index.
o Thermal index
measure of the relative probability that the examination may raise the temperature,
potentially enough to induce injury.
The potential for temperature elevation is higher with longer examination time and is
greater near bone than in soft tissue.
higher with pulsed Doppler applications than with routine B-mode scanning.
First trimester, if pulsed Doppler is needed for a clinical indication, the thermal index
ho ld be 1.0, and e po re ime ho ld be kep a hor a po ible, all no
longer than 5 to 10 minutes
To document the embryonic or fetal heart rate, M-mode imaging should be used instead
of pulsed Doppler imaging

*Also, theoretical risks are greater during organogenesis than later in gestation.

o Mechanical index
measure of likelihood of adverse effects related to rarefractional pressure, such as
cavitation which is relevant only in tissues that contain air.
Microbubble ultrasound contrast agents are not used in pregnancy for this reason.
No adverse effects have been reported because fetuses cannot contain gas bodies
U e of onograph for an nonmedical p rpo e, ch a keep ake fe al imaging, i
considered contrary to responsible medical practice and is not condoned by the Food and
Drug Administration

Operator Safety

Musculoskeletal discomfort
Main risk factors for injury during transabdominal ultrasound are
o awkward posture,
o sustained static forces
o various pinch grips while maneuvering the transducer
o maternal habitus
Guidelines to avert injury
1. Position the patient on the table close to you elbow is close to your body (less than 30 degrees
shoulder abduction, keeping your thumb facing up)
2. Adjust the table or chair height so that your forearm is parallel to the floor
3. If seated, use a chair with back support, support your feet, and keep ankles in neutral position. Do not
lean toward the patient or monitor.
4. Face the monitor squarely and position it so that it is viewed at a neutral angle, such as 15 degrees
downward.
5. Avoid reaching, bending, or twisting while scanning.
6. Frequent breaks may avoid muscle strain. Stretching and strengthening exercises can be helpful.

10
First Trimester Sonography

Early pregnancy can be evaluated using transabdominal or transvaginal sonography, or both

The components listed in Table 10-2 should be assessed
The crown-rump length (CRL) is the most accurate biometric predictor of gestational age
o The CRL should be obtained in a sagittal plane and include neither the yolk sac nor a limb bud
o If carefully performed, it has a variance of only 3 to 5 days
o Correlation with real age at 1st trimester: 
+/- 3 5 days
At 2nd trimester: +/- 7 days
At 3rd trimester: +/- 21 days
First-trimester sonography can reliably diagnose
o anembryonic gestation
o embryonic demise
o ectopic pregnancy
o gestational trophoblastic disease
Multifetal gestation can be identified early, and this is the optimal time to determine chorionicity
Ideal time to evaluate the uterus, adnexa, and cul-de-sac (pouch of peritoneum behind the uterus which
becomes filled with blood when an ectopic pregnancy ruptures)
Cervical length and the relationship of the placenta to the cervical os are best evaluated in the second
trimester
An intrauterine gestational sac is reliably visualized with transvaginal sonography by 5 weeks, and an
embryo with cardiac activity by 6 weeks
The embryo should be visible transvaginally once the mean sac diameter has reached 20 mm otherwise
the gestation is anembryonic
Cardiac motion is usually visible with transvaginal imaging when the embryo length has reached 5 mm
If an embryo less than 7 mm is not identified to have cardiac activity, a subsequent examination is
recommended in 1 week
Demise is diagnosed if the embryo has reached 10 mm without cardiac motion, taking into consideration
the standard error of the ultrasound measurements

Nuchal Translucency (NT)

o a component of first-trimester
aneuploidy screening, has had a major
impact on the number of pregnancies
receiving late first-trimester ultrasound
examination
o represents the maximum thickness of
the subcutaneous translucent area
between the skin and soft tissue
overlying the fetal spine at the back of
the neck
o measured in the sagittal plane
between 11 and 14 weeks using
precise criteria > or = to 3mm is
abnormal
o Screening for trisomy 18&21
o Check for fetal breathing, movement,
and tone -Tone is measured as closing
of fetal hands
o When the nuchal translucency is
increased, the risk for fetal aneuploidy
and various structural anomalies
including heart defects is significantly
elevated
o Aneuploidy screening - nuchal
11
 translucency measurement in
conjunction with assessment of
maternal serum human chorionic
gonadotropin and pregnancy-
associated plasma protein A levels

First-Trimester Fetal Anomaly Detection

Assessment for selected fetal abnormalities in an at-risk pregnancy is another indication for first-trimester
sonography
Anatomy visible at 11 to 14 weeks, to coincide with sonography performed as part of aneuploidy
screening
Wi h c rren echnolog , i i no reali ic o e pec ha all major abnormali ie de ec able in he econd
trimester may be visualized in the first trimester
Identification varies considerably according to the specific abnormality. For example, reported detection
rates are extremely high for anencephaly, alobar holoprosencephaly, and ventral wall defects. However,
only one-third of major cardiac anomalies have been identified, with no detected cases of microcephaly,
agenesis of the corpus callosum, cerebellar abnormalities, congenital pulmonary airway malformations, or
bowel obstruction
Thus, as first-trimester sonography is unreliable for detection of many major abnormalities, it should not
replace second-trimester anatomical evaluation

Second- and Third-Trimester Sonography

There are three types of examinations: standard, specialized, and limited

1. Standard sonographic
The fetal anatomical structures that should be evaluated during the examination may be adequately
assessed after approximately 18 weeks
When examining twins or other multiples, documentation also includes the number of chorions and
amnions, comparison of fetal sizes, estimation of amnionic fluid volume within each sac, and fetal sex
determination
2. There are several types of specialized examinations.
The targeted examination is a detailed anatomical survey performed when an abnormality is suspected
on the basis of history, screening test result, or abnormal findings from a standard examination
A targeted examination is performed and interpreted by an experienced operator. It includes the
anatomical structures listed in Table 10-5 (OPA! Kalma! Nandito yan. See chart below), along with
additional views of the brain and cranium, neck, profile, lungs and diaphragm, cardiac anatomy, liver,
shape and curvature of the spine, hands and feet, and any placental abnormalities
The physician performing the examination further determines whether other examination components will
be needed on a case-by-case basis
Other specialized examinations include fetal echocardiography and Doppler evaluation, biophysical
profile and additional biometric measurements.

12
3. A limited examination
performed to address a specific clinical
question (Examples include amnionic fluid
volume assessment, placental location, or
evaluation of fetal presentation or viability)
In most cases, a limited examination is appropriate only
when a prior standard or targeted examination has
previously been performed

Fetal Biometry
Equipment software derives the estimated gestational age from the crown-rump length.
Formulas are similarly used to calculate estimated gestational age and fetal weight from
measurements of the biparietal diameter, head and abdominal circumference, and femur length
The estimates are most accurate when multiple parameters are used and when nomograms derived
from fetuses of similar ethnic or racial background living at similar altitude are selected
Even the best models may over- or underestimate fetal weight by as much as 15 percent
Various nomograms for other fetal structures, including the cerebellum diameter, ear length,
interocular and binocular distances, thoracic circumference, and kidney, long bones, and feet lengths,
may be used to address specific questions regarding organ system abnormalities or syndromes

In the second trimester

Use of ultrasound: Check for anatomic disorders
Enough amniotic fluid can be found to serve as contrast which will allow easier visualization
Best time to see congenital anomalies
Biparietal diameter (BPD) most accurately reflects the gestational age, with a variation of 7 to 10
days.
measured in the transthalamic view, at the level of the thalami and cavum septum pellucidum (CSP),
from the outer edge of the skull in the near field to the inner edge of the skull in the far field
The head circumference (HC) is also measured in the transthalamic view, either by placing an ellipse
around the outer edge of the skull, or by measuring the occipital-frontal diameter (OFD) and
calculating the circumference from the BPD and OFD.
The cephalic index, which is the BPD divided by the OFD, is normally approximately 70 to 86 percent.
If the head shape is flattened dolichocephaly, or rounded brachycephaly, the HC is more reliable
than the BPD. Dolichocephaly and brachycephaly may be normal variants or may be secondary to
positional changes or oligohydramnios. However, dolichocephaly can occur with neural-tube defects,
and brachycephaly may be seen in fetuses with Down syndrome
Whenever the skull shape is abnormal, craniosynostosis and other craniofacial abnormalities are a
consideration
The femur length (FL) correlates well with both BPD and gestational age. It is measured with the
beam perpendicular to the long axis of the shaft, excluding the epiphysis. For gestational age
estimation, it has a variation of 7 to 11 days in the second trimester
A mildly foreshortened femur one that is 90 percent or less than that expected for gestational age
has been used as a minor marker for Down syndrome.
A femur length that is dramatically foreshortened prompts an evaluation for a skeletal dysplasia
In general, the normal range for the FL to abdominal circumference (AC) ratio is 20 to 24 percent. A
FL/AC < 16 percent suggests a lethal skeletal dysplasia, particularly if other skeletal abnormalities are
present
The abdominal circumference has the greatest variation, up to 2 to 3 weeks, for gestational age
estimation.
The AC is measured around the outer border of the skin. This is a transverse image at the level of the
stomach and the confluence of the umbilical vein with the portal sinus
Of the biometric parameters, AC is most affected by fetal growth.
a small abdominal circumference has been used as an early indicator of fetal-growth restriction
Variability of the estimated gestational age and of fetal weight increases with advancing gestation.
Individual measurements are least accurate in the third trimester. Although estimates are improved by
averaging multiple parameters, if one parameter differs significantly from the others, consideration is
given to excluding it from the calculation. The outlier could result from poor visibility, but it could also
indicate a fetal abnormality or growth problem.
Menstrual dates are generally considered confirmed if an estimated gestational age (EGA) based on
a sonographic first-trimester crown-rump length is within 1 week or if the EGA from biometry at 14 to
20 weeks is within 10 days

13
In the third trimester
the accuracy of sonography is only within 3 to 4 weeks. Sonographic evaluation performed to monitor
fetal growth should typically be performed at least 2 to 4 weeks after a prior examination

Use of ultrasound: For establishing the functions of the fetus
Growth result of function (SGA, LGA, etc)
Surveillance high-risk pregnancies Have to make a decision whether to keep baby in utero or
deliver him/her 

Can also do biometery, biophysical scoring, Doppler velocimetry
Reflects oxygenation of fetus

Manifest if well oxygenated

Brain sparing in the fetus: Blood is well distributed during critical times to the heart, brain, etc. if baby
manifests with a score of ZERO tone, breathing or movement = baby is very hypoxic!
Remember that you only do surveillance at a time when the baby can survive ex-utero. Do not perform
antenatal surveillance during the first trimester because baby is not yet able to survive ex utero

Amnionic Fluid
volume evaluation is a component of every second- or third-trimester sonogram.
Oligohydramnios
- volume is below normal range, and
- subjective crowding of the fetus is often noted
Hydramnios also called polyhydramnios is defined as
- volume above normal
Measurements include either the single deepest vertical fluid pocket or the sum of the deepest
vertical pockets from each of four equal uterine quadrants the amnionic fluid index
Reference range ha e been e abli hed for bo h mea remen from 16 eek ge a ion on ard
The single deepest vertical pocket is normally between 2 and 8 cm, and the amnionic fluid index
normally ranges between 8 and 24 cm

Fetal Anatomical Evaluation

Important goal of second- and third-trimester sonography is to systematically evaluate fetal anatomy
and determine whether specific anatomical components appear normal or abnormal
If a single ultrasound examination is planned for the purpose of evaluating fetal anatomy, the
American College of Obstetricians and Gynecologists (2011) recommends that it be performed at 18
to 20 weeks.
o At this gestational age range, complex organs such as the fetal brain and heart can be
imaged clearly enough to visualize many major malformations.
Technical factors such as maternal habitus, abdominal wall scarring, fetal size, and fetal position may
limit adequate visualization, and these limitations should be noted in the report.
If imaging is suboptimal, a follow-up examination may be helpful. If an abnormality is identified or
suspected during a standard examination of fetal anatomy, specialized sonography is indicated.

Second-Trimester Fetal Anomaly Detection.

The sensitivity of sonography for detecting fetal anomalies varies according to factors such as
gestational age, maternal habitus, fetal position, equipment features, examination type, operator skill,
and the specific abnormality in question
This reflects inclusion of anomalies with minimal or no sonographic detection, such as microcephaly,
anotia, choanal atresia, cleft palate, bile duct atresia, Hirschsprung disease, anal atresia, and
congenital skin disorders. These are mentioned because clinicians tend to focus on abnormalities
amenable to sonographic detection, whereas families may find those not readily detectable no less
devastating.
Most anomalous infants approximately 75 percent occur in pregnancies that are otherwise low-
risk, that is, without an indication for specialized sonography.

DOPPLER
When sound waves strike a moving target, the frequency of the waves reflected back is shifted proportionate
to the velocity and direction of that moving target a phenomenon known as the Doppler shift
- Because the magnitude and direction of the frequency shift depend on the relative motion of the moving
target, Doppler can be used to evaluate flow within blood vessels

* I did not include the Doppler equation. If you are soooo into this Doppler topic, feel free to use your book
and see how t is being computed. Turo mo sa akin tapos magpre-pretend akong nakikinig. Promise! You
on e en no ice he difference.

Continuous wave Doppler equipment

has two separate types of crystals one transmits high-frequency sound waves, and another
continuously captures signals

14
 In M-mode imaging, continuous wave Doppler is used to evaluate motion through time, however, it
cannot image individual vessels

Pulsed-wave Doppler
uses only one crystal, which transmits the signal and then waits until the returning signal is received
before transmitting another one
It allows precise targeting and visualization of the vessel of interest
Configured to allow color-flow mapping such that blood flowing toward the transducer is displayed in
red and that flowing away from the transducer appears in blue.

Umbilical Artery
subjected to more rigorous assessment than has any previous test of fetal health
differs from other vessels in that it normally has forward flow throughout the cardiac cycle
the amount of flow during diastole increases as gestation advances a function of decreasing
placental impedance.
(the computation I was encouraging you to explain to me)
The S/D ratio normally decreases from approximately 4.0 at 20 weeks to 2.0 at term, and it is
generally less than 3.0 after 30 weeks - Because of downstream impedance to flow, more end-
diastolic flow is observed at the placental cord insertion than at the fetal ventral wall abnormalities
such as absent or reversed end-diastolic flow will appear first at the fetal cord insertion site. The
International Society of Ultrasound in Obstetrics and Gynecology recommends that umbilical artery
Doppler measurements be made in a free loop of cord
Recommended that assessment be performed close to the ventral wall insertion to optimize
reproducibility
The waveform is considered abnormal if the S/D ratio is above the 95th percentile for gestational age.
In extreme cases of growth restriction, end-diastolic flow may become absent or even reversed Such
reversal of end-diastolic flow has been associated with greater than 70-percent obliteration of the
small muscular arteries in placental tertiary stem villi (oh e inaral mo na ba equation?)
useful adjunct in the management of pregnancies complicated by fetal-growth restriction, and it has
been associated with improved outcome in such cases
not recommended for complications other than growth restriction and as a screening tool for
identifying pregnancies that will subsequently be complicated by growth restriction
Abnormal umbilical artery Doppler findings should prompt a complete fetal evaluation if not already
done, as such findings are associated with major fetal anomalies and aneuploidy
The Society for Maternal Fetal Medicine has recommended that so long as fetal surveillance remains
reassuring, pregnancies with fetal-growth restriction and absent end-diastolic flow in the umbilical
artery may be managed expectantly until delivery at 34 weeks, and those with reversed end-diastolic
flow managed expectantly until delivery at 32 weeks

Ductus Arteriosus
used primarily to monitor fetuses exposed to indomethacin and other nonsteroidal antiinflammatory
agents (NSAIDs)
Indomethacin, which is used by some for tocolysis, may cause ductal constriction or closure,
particularly when used in the third trimester
The resulting increased pulmonary flow may cause reactive hypertrophy of the pulmonary arterioles
and eventual development of pulmonary hypertension
ductal constriction is often reversible after NSAID discontinuation. Because ductal constriction is a
potentially serious complication that should be avoided, the duration of NSAID administration is
typically limited to less than 72 hours, and women taking NSAIDs are closely monitored so that these
can be discontinued if ductal constriction is identified

Uterine Artery
estimated to increase from 50 mL/min early in gestation to 500 to 750 mL/min by term
Doppler waveform is characterized by high diastolic flow velocities and by highly turbulent flow
Increased resistance to flow and development of a diastolic notch are associated with later
development of gestational hypertension, preeclampsia, and fetal-growth restriction
women with chronic hypertension who had increased uterine artery impedance at 16 to 20 weeks
were at increased risk to develop superimposed preeclampsia.
the predictive value of uterine artery Doppler testing is low, and screening is not recommended in
either high-risk or low-risk pregnancies
technique has not been standardized, frequency of assessment has not been established, and criteria
for an abnormal test have not been determined

perinatal benefits of uterine artery Doppler screening have not yet been demonstrated. (BOOM
Lakas! Yung akala mo yun na pero paasa lang pala. Minsan sayang [tulad ng oras na ginugol mo sa
pagbasa nitong anti sleepiness opinion ko] pero malay natin sa katagalan malalaman nilang,
importante rin pala)

15
 Middle Cerebral Artery

fetal anemia detection and fetal-growth restriction evaluation.

Ana omicall , he pa h of he MCA i ch ha flo of en approache he ran d cer head-on,
allowing for accurate determination of flow velocity
imaged in an axial view of the head at the base of the skull, ideally within 2 mm of the internal carotid
artery origin
Velocity measurement is optimal when the insonating angle is close to zero, and no more than 30
degrees of angle correction should be used. In general, velocity assessment is not performed in other
fetal vessels, because a larger insonating angle is needed and confers significant measurement error
When fetal anemia is present, the peak systolic velocity is increased due to increased cardiac output
and decreased blood viscosity
This has permitted the reliable, noninvasive detection of fetal anemia in cases of blood-group
alloimmunization.
In most referral centers, MCA peak systolic velocity has replaced invasive testing with amniocentesis
for fetal anemia detection
MCA Doppler has also been studied as an adjunct in the evaluation of fetal-growth restriction
Fetal hypoxemia is believed to result in increased blood flow to the brain, heart, and adrenal glands,
leading to increased end-dia olic flo in he MCA. Thi phenomenon, brain- paring, i ac ally a
misnomer, as it is not protective for the fetus but rather is associated with perinatal morbidity and
mortality

Ductus Venosus
imaged as it branches from the umbilical vein at approximately the level of the diaphragm
Fetal position poses more of a challenge in imaging the ductus venosus than it does with either the
umbilical artery or the middle cerebral artery.
The waveform is biphasic and normally has forward flow throughout the cardiac cycle
The first peak reflects ventricular systole, and the second is diastolic filling. These are followed by a
nadir during atrial contraction termed the a-wave.
progression of Doppler findings in preterm fetuses with growth restriction, such that umbilical artery
Doppler abnormalities occur first, followed by those in the middle cerebral artery and then the ductus
venosus
wide variability in manifestation of these abnormalities.
When severe fetal-growth restriction is present, cardiac dysfunction may lead to flow in the a-wave
that is decreased, absent, and eventually reversed, along with pulsatile flow in the umbilical vein
abnormalities have potential to identify preterm growth-restricted fetuses that are at greatest risk for
adverse outcomes
recently concluded that Doppler assessment of vessels other than the umbilical artery has not been
shown to improve perinatal outcome and that its role in clinical practice remains uncertain

Additional/summary from Lalala-lala:

NORMAL AND ABNORMAL FETAL ANATOMY

1. Brain and Spine

Standard sonographic evaluation of the fetal brain includes 3 transverse (axial) views:
a. Transthalamic view
- Used to measure the biparietal diameter (BPD) and head circumference (HC) and includes
the midline falx , cavum septum pellucidum (CSP), and thalami.
CSP space between the 2 laminae that separate the frontal horns
Inability to visualize a normal CSP may indicate midline brain abnormality such as
corpus callosum, labor holoprosencephaly, or septo-optic dysplasia (de Morsier
syndrome)
b. Transventricular view
16
 - Includes the lateral ventricles, which contain echogenic choroid plexus
- The ventricles are measured in their atrium, which is the confluence of their temporal and
occipital horns
c. Transcerebellar view
- Obtained by angling the transducer back through the posterior fossa
- The cerebellum and cisterna magna are measured
- Between 15 to 20 weeks, the nuchal skinfold thickness may be measured
- From between 15 until 22 weeks, cerebellar diameter in millimeters is roughly equivalent to
the AOG
Cisterna magna normally measures 2-10mm; its effacement is present in the Chiari
II malformation
Imaging of the spine includes evaluation of the cervical, thoracic, lumbar and sacral regions
Representative spinal images for record keeping
- often obtained in sagittal and coronal plane
Real-time imaging
- should include evaluation of each spinal segment in the transverse plane more sensitive for
abnormality detection
Transverse images
— demonstrate 3 ossification centers
Anterior ossification center
— represent the vertebral body
Posterior ossification center
— junction of vertebral laminae and pedicles
Ossification of the spine proceeds in a cranial-caudal fashion
Ossification of upper sacrum (S1-S2) not visible sonographically <16 weeks
Ossification of entire sacrum not visible until 21 weeks
nd
Difficult to detect some spinal anomalies during the early 2 trimester
Examples of spinal abnormalities: spina bifida, caudal regression sequence and
sacrococcygeal teratoma
- More subtle spinal abnormalities may be visible which include:
Diastematomyelia
— longitudinal cleft or splitting of the spinal cord itself
Hemivertebrae
— a component of the vertebral, anal, cardiac, trachea-esophageal fistula, renal,
limb (VACTERL) association
If brain or spinal abnormality is identified, specialized sonography is indicated
Fetal magnetic resonance (MR) imaging
— useful in further characterizing CNS abnormalities

17
Neural Tube Defects

- result from incomplete closure of the neural tube by the embryonic age of 26-28 days
nd
- 2 most common class of malformations after cardiac anomalies
- Can be prevented with folic acid supplementation

a. Anencephaly
- Characterized by absence of the cranium and telencephalic structures, with the skullbase and
orbits covered only by angiomatous stroma

b. Acrania
- Absence of the cranium, with protrusion of disorganized brain tissue
Both anencephaly and acrania are generally grouped together and ancencephaly is
considered to be the final stage of acrania
Lethal anomalies diagnosed in late first trimester
Second trimester all cases may be diagnosed
Third trimester hydramnios from impaired swallowing is common

c. Cephalocele
- Herniation of the meninges through a cranial defect, typically located in the midline occipital
region
Encephalocele brain tissue herniates through the skull defect
- Associated hydrocephalus and microcephaly are common
- Surviving infants have high incidence of neurological deficits and developmental impairment
- Important feature of the autosomal recessive Meckel-Gruber syndrome
Meckel-Gruber syndrome includes cystic renal dysplasia and polydactyly

18
 Amnionic band sequence cephalocele not located in the occipital midline

d. Spina Bifida
- Defect in the vertebrae, typically the dorsal arch, with exposure of the meninges and spinal
cord
- Most cases are open spina bifida defect includes skin and soft tissues
Myelomeningocele herniated of the meningeal sac containing neural elements
Meningocele only a meningeal sac is present
nd
- May be reliably diagnosed in 2 trimester sonography due to two characteristic findings:
Lemon sign scalloping of the frontal bones
Banana sign anterior curvature of the cerebellum with effacement of the cisterna
magna
These findings are manifestations of the Chiari II malformation
Chiari II malformation (Arnold-Chiari malformation)
— Occurs when downward displacement of the spinal cord pulls a portion of the
cerebellum through the foramen magnum and into the upper cervical canal
- Children with this defect require multidisciplinary care to address problems related to the
defect, shunt, swallowing, bladder and bowel function and ambulation; they are also at
increased risk for latex allergy
Ventriculocytomegaly
— Frequent sonographic finding particularly after midgestation
— More than 80% of infants with spina bifida require ventriculoperitoneal shunt
placement
— Distention of the cerebral ventricles with CSF as a nonspecific marker of
abnormal brain development
— Atrial width of 10-15mm mild ventriculomegy
— Atrial width of >15mm overt or severe ventriculomegaly
(normal atrium: 5-10mm from 15 weeks to term)
o CSF Produced by the choroid plexus, which is an epithelium-lined
capillary core and loose connective tissue found in the ventricles
o Dangling choroid plexus found with severe ventriculomegaly
— The larger the atrium, the greater the likelihood of abnormal outcome
o Enlarged ventricle may be due to another CNS abnormality such as
Dandy-Walker malformation or holopreoscencephaly
o Dandy-Walker malformation or holopreoscencephaly may be due to an
obstructive process such as aqueductal stenosis or secondary to a
destructive process such as porencephaly or an intracranial teratoma

19
 — Initial evaluation: specialized exam of fetal anatomy, fetal karyotyping, and
testing for congenital infections

Agenesis of the Corpus Callosum

— Corpus callosum major fiber bundle connecting reciprocal regions of the
cerebral hemispheres
— Normal cavum septum cannot be visualized sonographically and frontal horns
are displaced laterally
— There is mild enlargement of the atria posteriorly ventricles has a
charac eri ic eardrop appearance
— Associated with other CNS and non-CNS anomalies, aneuploidy and many
genetic sundromes
Holoproscencephaly
— Prosencephalon fails to divide completely into 2 separate cerebral
hemispheres and into underlying diencephalic structures
— Main forms:
a. Alobar
- most severe form
- a single monoventricle, with or without a covering mantle of cortex,
surrounds the fused central thalami
b. Semilobar
- partial separation of the hemisphere occurs
c. Lobar
- characterized by a variable degree of fusion of frontal structures

20
 - should be considered when a normal cavum septum pellucidum cannot
be visualized
— May be associated with anomalies of the orbits and eyes (hypotelorism,
cyclopia, or micropthalmia), lips (median cleft), or nose (ethmocephaly,
cebocephaly and arhinia with probiscus)
o This is because the differentiation into two hemispheres is induced by
prechordal mesenchyme, which is also responsible for the
differentiation of the midline face

Dandy-Walker Malformation Vermian Agenesis

— posterior fossa abnormality characterized by agenesis of the cerebellar
vermis, posterior fossa enlargement and elevation of thee tentorium
— Sonographically, fluid in the enlarged cisterna magna visibly communicates
with the fourth ventricle through the cerebellar vermis defect, with visible
separation of the cerebellar hemisphere
— Associated with numerous genetic and sporadic syndromes, congenital viral
infections and teratogen exposure
o inferior vermian agenesis also called Dandy-Walker variant; term used
when only the inferior portion of the vermis is absent
Sacrococcygeal Teratoma
— Germ cell tumor; one of the most common tumors in neonates
— Believed to arise from totipotent cells along Hensen node, anterior to the
coccyx
— 4 types:
a. Type 1 predominantly external with a minimal presacral component
b. Type 2 predominantly external but with a significant intrapelvic
component
c. Type 3 predominantly internal but with abdominal extension
d. Type 4 is entirely internal with no external component
— Sonographically, appears as a solid and/or cystic mass that arises from the
anterior sacrum and usually extends inferiorly and externally as it grows
— Solid components often have varying echogenicity, appear disorganized
and may grow rapidly with advancing gestation
— Internal pelvic components more challenging to visualize, consider fetal
MR imaging
— Hydramnios is frequent
— Hydrops may develop from high-output cardiac failure (either due to tumor
vascularity or secondary to bleeding within the tumor and resultant anemia)
— >5cm tumor cesarean delivery and classical hysterectomy may be needed

Caudal Regression Sequence Sacral Agenesis

— Rare; characterized by absence of sacral spine and often portions of lumbar
spine
— Sonographically, spine appears abnormally short, lacks normal lumbosacral
curvature and terminates abruptly above the level of the iliac wings
o Because sacrum does not lie between iliac wings, they are abnormally
clo e oge her and ma appear hield-like
— There may be abnormal positioning of lower extremities and lack of normal
tissue development
— Should be differentiated from sirenomelia
o Sirenomelia single fused lower extremity in the midline
2. Face and Neck
- Micrognathia
— abnormally small jaw; should be considered in the evaluation of hydramnios
— identified by fetal profile

21
- Facial clefts
— 3 main types:
a. Cleft lip and palate
- involves the lip, may also involve hard palate
- may be unilateral or bilateral
o If cleft in upper lip is visible, a transverse image at the level of the
alveolar ridge may demonstrate that the defect also involves primary
palate
b. Isolated cleft palate
- begins at the uvula; may involve soft palate and occasionally involves the hard
palate
- does not involve the lip
- described using specialized 2- and 3-D sonography
- not visualized during standard ultrasound exam
c. Median cleft lip
- found in association with several conditions which include agenesis of the
primary palate, hypotelorism, and holoprosencephaly
- may be associated with hypertelorism and frontonasal hyperplasia, formerly
called median cleft face syndrome

- Cystic Hygroma
— Venolymphatic malformation in which fluid filled sacs extend from the posterior neck
st
— May be diagnosed in the 1 trimester
— Believed to develop when lymph from head fails to drain into the jugular veins and
accumulates instead in the jugular lymphatic sacs
— 70% are associated with aneuploidy
nd
— If diagnosed on 2 trimester, 75% of aneuploidy cases are 45,X Turner syndrome
st
— If diagnosed on 1 trimester, trisomy 21 and 45,X are common, followed by trisomy
18
— In the absence of aneuploidy, there is increased risk for cardiac anomalies that are
flow-related (hypoplastic left heart and coarctation of the aorta)
— May be part of a genetic syndrome
o Noonan syndrome an autosomal dominant disorder that shares
several features with Turner syndrome, including short stature,
lymphedema, high-arched palate and often pulmonary valve stenosis
— Large cystic hygromas found in hydrops fetalis, rarely resolve and carry poor
prognosis
— Small hygromas may undergo spontaneous resolution and if fetal karyotype and
ECG results are normal, the prognosis may be good

22
3. Thorax
- Lungs appear as homogeneous structures surrounding the heart and best visualized 20-25
weeks AOG
- In a four-chamber view of the chest: (lungs: 2/3, heart 1/3)
- Thoracic circumference measured at the skin line in a transverse plane at the level of the
four-chamber view
- Congenital Diaphragmatic Hernia
— Defect in the diaphragm through which abdominal organs herniate into the thorax
o 75% of cases left sided
o 20%-- right sided
o 5%-- bilateral
— Targeted sonography and fetal ECG should be performed
— Reduction in survival rate if with associated abnormalities
— If without associated abnormalities, major cause of death are pulmonary hypoplasia
and pulmonary hypertension
— Sonographically, most frequent finding with left sided defect is repositioning of the
heart tp the mid or right thorax
— Associated findings: stomach bubble or bowel peristalsis in the chest and wedge
shaped mass which is the liver located anteriorly in left hemithorax
— Large lesions impaired swallowing and mediastinal shift resulting in hydramnios
and hydrops

- Congenital Cystic Adenomatoid Malformation (CCAM)

— Abnormality presents with hamartomatous overgrowth of terminal bronchioles that
communicated with the tracheobronchial tree
— A.k.a CPAM (congenital pulmonary airway malformations)
— Sonographically, there is a well-circumscribed mass that may appear solid and
echogenic or may have one or multiple variably sized cysts
— Usually involves one lobe and has blood supply from the pulmonary artery and drains
into pulmonary veins
— Large mass hydrops fetalis and hypoplasia may result
— Macrocystic lesions with cyst >5mm
— Microcystic <5mm
- Extralobular Pulmonary Sequestration
— A.k.a. bronchopulmonary sequestration
— An acce or l ng b d eq e ered from he racheobronchial ree a mass of
nonfunctioning lung tissue
— Extralobar most cases diagnosed prenatally; developed in their own pleura
23
 — Interlobar most sequestrations present in adulthood; within the pleura of another
lobe
— Sonographically, Extralobar Pulmonary Sequestration (ELS) presents as
homogeneous, echogenic thoracic mass; it may resemble microcystic CCAM,
however,blood supple in from systemic circulation
- Congenital High Airway Obstruction Sequence (CHAOS)
— Rare; results from laryngeal or tracheal atresia
— Normal egress of lung fluid is obstructed and the tracheobronchial tree and lungs
become massively distended
— Sonographically, lungs appear brightly echogenic and the bronchi are dilated with
fluid
— Flattening and eversion of diaphragm and compression of the heart is common
— Venous return impaired and ascites develops
— A feature of the autosomal recessive Fraser syndrome
4. Heart
- Cardiac malformations most common class of congenital anomalies
- 90% of cardiac defects multifactorial or polygenic in origin
nd
- Routine 2 trimester sonography identified approximately 40% of major cardiac anomalies
before 22 weeks
- Specialized sonography identified 80%
- Basic Cardiac Exam
— Standard cardiac assessment includes 4 chamber view
— Evaluation of rate and rhythm and evaluation of left and right ventricular outflow tracts
— Evaluation of outflow tracts aid in detection of anomalies such as tetralogy of fallot,
transposition of great bessels and truncus arteriosus, which are not initially
appreciated in 4 chamber view
- Four-Chamber view
— A transverse image of the fetal thorax at the level immediately above the diaphragm
— Allows evaluation of cardiac size, position in the thorax, cardiac axis, atria and
ventricles, foramen ovale, atrial septum primum, interventricular septum and
atrioventricular valves
o Atria and ventricles should be same size
o Apex of the heart should form 45-degree angle with the left anterior chest
wall

- Fetal Echocardiography
— Specialized examination of fetal cardiac structure and function designed to identify
and characterize abnormalities
— Indications: suspected fetal cardiac anomaly, extracardiac anomaly, chromosomal
abnormality, fetal arrhythmia, hydrops, increased nuchal translucency, monochorionic
twin gestation, first-degree relative to a fetus with congenital cardiac defect, in vitro
fertilization, maternal anti-Ro or anti-La antibodies, exposure to medications
associated with increased cardiac malformation risks, and maternal metabolic
disease associated with cardiac defects

24
- Ventricular Septal Defect
— Single most common cardiac congenital anomaly
— A defect may be appreciated in the membranous or muscular portion of the
interventricular septum in the four-chamber view
— Color Doppler demonstrates flow through the defect
— Imaging of the left ventricular outflow tract may demonstrate discontinuity of the
interventricular septum as it becomes the wall of the aorta

- Echocardial Cushion Defect

— A.k.a. atrioventricular (AV) septal defect or AV canal defect
— Echocardial cushions are the crux of the heart and defects jointly involve the atrial
septum primum, interventricular septum, and medial leaflets of the mitral and
tricuspid valve
— May develop with heterotaxy syndrome more likely to have conduction system
abnormalities resulting in third-degree AV block
o Atrial isomerism heat and/ or abdominal organs are on the incorrect side
- Hypoplastic Left Heart Syndrome
— Postnatal treatment consists of a three stage palliative repair or a cardiac
transplantation
— Morbidity remains high and developmental delays are common
— Sonographycally, the left side of the heart may appear so small that it is difficult to
appreciate a ventricular chamber
— There may be no visible inflow or outflow and may be reversal pf flow in the ductus
arteriosus
- Tetralogy of Fallot
— Characterized by four components:
o Ventricular septal defect (VSD)
o Overriding aorta
o Pulmonary valve abnormality
o Right ventricular hypertrophy
— Due to the location of the VSD, it is often not visible in the four-chamber view, which
may appear normal
- Cardiac Rhabdomyoma
25
 — Most common cardiac tumor
— Appear as well circumscribed echogenic masses, usually within ventricles and
outflow tracts
— May be one or multiple; may increase in size during gestation; inflow or outflow
obstruction may result
— No obstruction good prognosis
— Largest in the neonatal period and tends to regress as children grow
o If fetal rhabdomyoma is identified, in the absence of a family history,
evaluation of parents for clinical manifestations of neurofibromatosis should
be considered
- M-Mode (Motion-mode imaging)
— A linear display of cardiac cycle events, with time on x-axis and motion on y-axis
— Used frequently to measure fetal heart rate
— If with abnormal heart rate and rhythm, it permits separate evaluation of atrial and
septal waveforms
— Useful in characterizing arrhythmias and their response to treatment

-Premature Atrial Contractions

— A.k.a. atrial extrasystoles
— Most common fetal arrhythmia and frequent finding
— Represent cardiac conduction system immaturity
— Typically resolve later in gestation or in the neonatal period
— May be conducted and sound like an extra beat
— With handheld doppler or fetoscope, they sound like a dropped beat
o The dropped beat may be demonstration with M-mode evaluation to be the
compensatory pause that follows the premature contraction
5. Abdominal Wall
- Standard examination: assess integrity of the abdominal wall at the level of the cord insertion
- Gastroschisis and omphalocele collectively termed ventral wall defects; relatively common
fetal anomalies; both associated with elevated maternal serum alpha-fetoprotein
- Gastroschisis
— Full-thickness abdominal wall defect typically located right of the umbilical cord
insertion
— Bowel herniates through defect into the amniotic cavity
— One major common anomaly in fetuses of younger mothers and average maternal
age of 20 years

26
 - Omphalocele
— Forms when the lateral ectomesodermal folds fail to meet in the midline, leaving the
abdominal contents covered onlu by a two-layered sac of amnion and peritoneum
into which the umbilical cord inserts
— Is a component of syndromes such as Beckwith-Wiedemann, cloacal extrophy, and
pentalogy of Cantrell
- Body Stalk Anomaly
— A.k.a. limb-body-wall complex or cyllosoma
— Rare, lethal anomaly characterized by abnormal formation of the body wall
— No abdominal wall is visible and there is extrusion of the abdominal organs into the
extraamniotic coelom
— There is close approximation or fusion of the body to the placenta and an extremely
short umbilical cord
— Acute-angle scoliosis is another feature
— Amniotic bands are often identified

6. Gastrointestinal Tract
- 14 weeks Stomach is visible
nd rd
- 2 and 3 trimester liver, spleen, gallbladder and bowel can be identified
- Nonvisualization of stomach may be due to impaired swallowing (underlying causes
include: esophageal atresia, craniofacial abnormality or CNS or musculoskeletal abnormality)
- Bowel may appear bright or echogenic, which may indicated small amounts of swallowed
intraamnionic blood (particularly in elevated maternal serum alpha-fetoprotein)
o Bowel that appears as bright as fetal bone confers a slightly increased risk
for underlying GI malformations, cystic fibrosis, trisomy 21 and congenital
infection
- Gastrointestinal Atresia
— Obstruction and proximal bowel dilatation
— The more proximal the obstruction, the more likely there is hydramnios
o Hydramnios associated with proximal small bowel obstruction may be severe
enough to results in maternal respiratory compromise or preterm labor
o This may necessitate amniocentesis, a.k.a. amnioreduction
— Esophageal atresia
- may be suspected if stomach is not visualized and hydramnios is present
- 90% of cases present with tracheoesophageal fistula which allows fluid to enter the
stomach; this results to a problem in prenatal detection
— Duodenal atresia
- characterized by sonographic double-bubble sign, which represents distention of the stomach
and the first part of the duodenum; this finding is usually not present before 22-24 weeks

7. Kidneys and Urinary Tract

- Fetal kidneys
st
— visible adjacent to spine by 1 trimester and routinely by 18 weeks AOG
— become les echogenic and a rim of perinephric fat aids visualization of their margin
— produce most of amniotic fluid after 18weeks AOG
— urine production increases from 5mL/ hr at 20weeks to 50mL/hr at term
- 20mm length of kidney at 20 weeks; increasing by 1.1mm each week
- Unexplained oligohydramnions suggests a placental or urinary tract abnormality

27
 nd
- Normal amniotic fluid volume in 2 half of pregnancy urinary tract patency with at least 1
functioning kidney

- Renal Pelvis dilatation

— May be transient or physiological
— May represent urinary tract abnormality which is confirmed in the neonatal
period
— Either uteropelvic function junction (UPJ) obstruction or vesicoureteral reflex
(VUR)
o Renal pelvis is measured anterior-posterior in the transverse plane
nd rd
o Pelis dilated > 4mm in 2 trimester or 7mm in 3 trimester
- Uteropelvic Junction Obstruction
— Most common anomaly associated with renal pelvis dilatation
— Affects males more than females
— Obstruction is functional rather than anatomical
- Duplicated Renal Collecting System
— Occurs when the upper and lower poles of the kidney (known as moieties) are each
drained by separate ureter
— More common among females
— Sonographically, an intervening tissue band separates 2 distinct renal pelves
o Hydronephrosis and/or ureteral dilatation develops due to abnormal dilatation
of one or both ureters within the bladder a relationship descried by Weigert-
Meyer rule
o Upper pole of ureter develops obstruction from a uterocele within the
bladder
o Lower pole has a shortened intravesical segment that predisposes to
vesicoureteral reflux

- Renal Agenesis
— When kidney is absent, the ipisilateral adrenal gland typically enlarges to fill the renal
fossa termed as lying down adrenal sign

28
 — Absence of renal artery Demonstrated by color Doppler imaging of the descending
aorta
— If bilateral no urine if formed resulting to hydramnios which leads to pulmonary
hypoplasia, limb contractures and a distinctively compressed face Potter Syndrome
o If these abnormalities resulting from decreased AF is not caused by renal
agenesis Potter Sequence
- Multicystic Dysplastic Kidney
— Severe form of renal dysplasia which results in a nonfunctioning kidney
— Nephrons and collecting duct do nor form normally
— Primitive ducts are surrounded by fibromuscular tissue
— Ureter is atretic
— Sonographically, kidneys contain numerous smooth walled cysts of varying sizes that
do not communicated with the renal pelvis and are surrounded by echogenic cortex
— If isolated and unilateral prognosis is good
— If bilateral associated with decreased AF volume leading to Potter sequence poor
prognosis

- Bladder Outlet Obstruction

— Distal obstruction of urinary tract
— More common in males
— Common etiology: posterior urethral valves
— There is dilatation of the bladder and proximal urethra ke hole ign
— Bladder wall is thick
— If with oligohydramnios poor prognosis due to pulmonary hypoplasia
— Outcome may be poor even with normal AF volume
- Polycystic Kidney Disease
— Only the infantile form of autosomal recessive polycystic kidney disease (ARPKD) is
diagnosed prenatally
o ARPKD
chronic, progressive disease that involves kidney and liver
results in cystic dilatation of the renal collecting ducts and congenital
hepatic fibrosis
has wide phenotypic variability from lethal pulmonary hypoplasia at birth
to hepatic manifestations in the late childhood and adulthood
— Infantile characterized by abnormally large kidneys that fill and distend fetal
abdomen and have a solid glass texture
— Severe oligohydramnios poor prognosis
o Autosomal Dominant Polycystic Kidney Disease (ADPKD)
more common; does not manifest until adulthood
may have mild renal enlargement, increased renal echogenicity, and
normal AF volume
differential diagnosis: several genetic syndromes, aneuploidy or normal
variant
8. Skeletal Abnormalities
- 2 types of skeletal dysplasias:
Osteochondrodysplasias generalized abnormal development of the bone and/or
cartilage
Dystoses abnormalities of individual bones (ex. Polydactyly)

29
 o In addition to these malformations, skeletal abnormalities include
deformations (ex. clubfoot) and disruptions (ex. Limb-reduction defects)
- Skeletal Dysplasias
— 2 groups account for most cases:
o Fibroblast growth factor 3 (FGFR 3) chondrodysplasia group
Include achondroplasia and thanatophoric dysplasia
Achondroplasia
- a.k.a. heterozygous achondroplasia
- most common nonlethal skeletal dysplasia
- inherited in an autosomal dominant fashion
- characterized by long bone shortening that is predominantly
rhizomelic, an enlarged head with frontal bossing, depressed nasal
bridge, exaggerated lumbar lordosis and a trident configuration of the
hands
- sonographically, femur and humerus measurements <5% until early
rd
3 trimester
Thanatophoric dysplasia
- most common lethal skeletal disorder
- characterized by severe micromelia and affected fetuses may
develop a characteristic cloverleaf skull deformity due to
craniosyntosis
o Osteogenesis imperfect and decreased bone density group
— Evaluation include survey of every long bone, hands and feet, skull size and shape,
clavicles, scapulae, thorax and spine
o Micromelia involvement of all long bones
o Rhizomelia Involvement of proximal long bones
o Mesomelia involvement of intermediate long bones
o Acromelia involvement of distal long bones
— Note for degree of ossification and presence of bowing and fractures narrows
differential diagnosis and suggests specific skeletal dysplasia
o Lethal dysplasias frequently characterized by profound long bone
shortening (<5%) and by femur length-to-abdominal circumference ratios
(<16%)
o Indicative of pulmonary hypoplasia:
- thoracic circumference is 80% of the abdominal circumference
- thoracic circumference <25%
- cardiothoracic circumference ratio >50%

— Osteogenesis imperfecta represents a group of skeletal dysplasias characterized

by hypomineralization
o There are multiple types but type IIa (a.k.a. perinatal form) is lethal and
characterized by profound lack of skull ossification such that gentle pressure
on maternal abdomen from the ultrasound transducer results in visible skull
deformation
o Other features: multiple in- ero frac re and rib ha appear beaded
— Hypophosphatasia skeletal dysplasia that results in severe hypomineralization;
inherited in autosomal recessive fashion
- Clubfoot Talipes Equinovarus
— Deformed talus and shortened Achilles tendon

30
 — Affected food abnormally fixed and positioned with equinus (downward pointing),
varus (inward rotation) and forefoot adduction
— Sonographically, footprint is visible in the same plane as the tibia and fibula

- Limb-Reduction Defects
— Absence of all or part of one or more extremity
o Amelia absence of an entire extremity
o Phocomelia absence of one or more leg bones with hands or feet attached
to the trunk; associated with thalidomide exposure
— Associated with the following:
o Roberts syndrome an autosomal recessive condition characterized by
tetraphocomelia
o Clubhand deformity associated with trisomy 18 and also a component of
the thrombocytopenia-absent radius syndrome
o Chorionic villi sampling performed <10 weeks AOG

THREE- AND FOUR- DIMENSIONAL SONOGRAPHY

3-D sonography

- Not routinely used during standard exam

- Not a required modality but may be a component of various specialized evaluations
- Uses a special transducer
o After a region of interest is identified, a 3-D volume is acquired that renders to diplay
images of any plane (axial, sagittal, coronal or even oblique) within that volume
o Sequential slices can be generated (similar to CT scan and MRI)
- Can evaluate intracranial anatomy in the sagittal plane (ex. corpus callosum) and imaging of
the palate and skeletal system
- Static and obtained by processing of a volume of stored images

4-D Sonography

- A.k.a. real time 3-D sonography

- Allows rapid reconstruction of the rendered images to convey the impression that the
scanning is in real time
- Can improve visualization of cardiac anatomy
- Useful in postprocessing algorithms and techniques (ex. spatiotemporal image correlation/
STIC which us used to evaluate complex heart anatomy and function)
o addition of an inversion-mode algorithm may aid in imaging of blood flow within the
heart and great vessels and may permit measurement of ventricular blood volume

31
PRENATAL DIAGNOSIS - Exposed to excessive medication or to
Dr. Gonzalez environmental hazards
- History of down syndrome or some other
Prenatal Diagnosis chromosomal abnormality is present
- Science of identifying structural or functional - The fetus is detected to be at increased risk
abnormalities birth defects in the fetus for NTD
- Appropriate counseling and optimize
outcome
- Fetal therapy
o Blood product transfusion Neural Tube Defects
nd
o Administration of medication - 2 most common congenital malformation
o Amioreduction/amnioinfusion - Family history
o Fetal thoracentesis - Aneuploidy-trisomy 13 and 18, triploidy
o Fetal surgery - Hyperglycemia
o Laser or radiofrequency ablation of - Hyperthermia
vascular anastomoses - Coumadin
- Aminopterin
Benefits of Prenatal Diagnosis - Thalidomide
- Determines the outcome of pregnancy and - Anticonvulsants: valproic and
identifies possible complications that can carbamazepine
arise during birth
- It can be helpful in improving the outcome of Folic Acid
pregnancy using fetal treatment - Reduce risk of NTD by 70%
- Screening can help couples prepare for the - Low risk: 0.4 mg/day
birth of a child with an abnormality - High risk: 4 mg/day prior to pregnancy up to
st
the 1 trimester
Etiology of Birth Defects
- Malformation PRENATAL DIAGNOSIS OF NTD
o Most common type of structural fetal Alpha Fetoprotein
abnormality - Glycoprotein synthesized by the fetal yolk
o An intrinsic abnormality sac and later by the GIT and liver
programmed in development - Major serum protein of the embryo and early
regardless of whether precise fetus
genetic etiology is known - Concentration increases steadily in both
- Deformation fetal serum and AF until 13 weeks gestation
o A genetically normal fetus develops - Major source of AFP in AF is fetal urine
abnormally because of mechanical - Some proteins cross the fetal membrane to
forces imposed by the uterine enter maternal circulation
environment - After 13 weeks gestation, both the fetal
- Disruption serum and AF levels normally decreases
o More severe change in form or while those in maternal serum continue to
function that occurs when rise until late in pregnancy
genetically normal tissue is modified
as a result of specific insult Maternal Serum AFP
- Performed at 15-20 weeks AOG
Techniques - Upper limit of normal 2.0 or 2.5 MoM
- Non-invasive o Detection rate of 90% for
o Ultrasound anencephaly
o X ray o Detection rate of 80% for spina
o Magnetic resonance bifida
- Invasive - Abnormal test
o Fetoscopy o Counseling
o Amniocentesis o Targeted sonography
o Chorionic villus sampling o Amniocentesis
o Percutaneous umbilical cord
sampling Amniocentesis
- Amniotic fluid AFP
Prenatal Diagnosis - Acetylcholinesterase
- The pregnant woman >/35 at the time of o Most sensitive and specific in
delivery determining NTD
- She or her parents have had a previous o Leaks directly from the exposed
child with a chromosomal abnormality neural tissue
- History of recurrent abortions, or her - Sensitivity: 90%
h band pre io ife e perienced
several miscarriages Elevated MSAFP
- The couple is known to be carriers of a - NTD
chromosomal translocation - Intestinal obstruction
- The pregnant woman is affected with type I - Cyctic hygroma
DM, epilepsy, etc. - Sacrococcygeal teratoma
- Exposed to viral infections (rubella or - Omphalocoele, gastroschisis
cytomegalovirus) - Urinary obstruction

1
 - Renal anomalies polycystic, absent PRENATAL DIAGNOSIS OF DOWN SYNDROME
kidneys - 11-14 weeks
- Sonographic evaluation
*Ultrasound 99% accuracy with NTD o Nuchal translucency
- Maternal serum anylate screening
NTDs o Increase serum hCG levels
- Anencephaly o Pregnancy associated plasma
- Spina bifida protein A (PAPP-A): lower
- Cephalocoele - Detection rate: 79-87%
- Encephalocoele
Second Trimester Screening
Anencephaly - Triple creen
- Failure of closure at the cranial end of the o Low MSAFP
neural tube (26-28 weeks) o Increased hCG
- Absence of the cranium and telencephalon o Low levels of unconjugated estriol
- Hydramnios o Detection rate: 61-70%
- Lethal during neonatal period - Q ad creen
o Low MSAFP
*Acrania: only cranium is absent; with brain o Low unconjugated estriol
o Increased hCG
Spina Bifida o Increased inhibin A
- Failure of distal closure during early o Detection rate: 80%
embryogenesis
- Defect in the vertebrae, typically the dorsal Integrated Screen
arch with exposure of the meninges and - First trimester screen and Quad test
spinal cord - Detection rate: 94-96%
- Associate with various degree of motor
impairment, lower limb paralysis or INVASIVE TECHNIQUES
dysfunction and incontinence - Embryoscopy
- Associated with hydrocephalus >> poor - Fetoscopy
prognostic factor for intellectual - Amniocentesis
development - Chorionic villus sampling
- Spina bifida occulta - Cordocentesis
o Vertebral shisis covered by normal
soft tissues Embryoscopy
st
- Spina bifida aperta - Performed in the 1 trimester (up to 12
o Full thickness defect of the skin, weeks AOG)
underlying soft tissues and vertebral - A rigid endoscope is inserted via the cervix
arches and exposing the neural in the space between the amnion and the
canal chorion, under sterile conditions and U/S
o Meningocoele guidance, to visualize the embryo for the
Defect is covered by thin diagnosis of structural malformations
meningeal membrane
o Myelomeningocoele Fetoscopy
nd
Presence of neural tissue - Performed during the 2 trimester (after 16
inside the sac weeks AOG)
- A fine-caliber endoscope is inserted into the
*Spina bifida: compatible with life amniotic cavity and U/S guidance, for the
- Common problem: urinary/fecal retention visualization of the embryo to detect the
o Management: catheterization every presence of structural abnormalities
6 hours - Also used for fetal blood and tissue
sampling
Cephalocoele - Associated with a 3-5% risk of miscarriage;
- Herniation of meninges through a cranial therefore, it is suprseded by detailed U/S
defect scanning
- Most common: midline occipital region
nd
- Meckel-Gruber syndrome 2 Trimester Amniocentesis
o Cephalocoele - 15-20 weeks
o Cystic renal dysplasia - Fetal karyotyping
o Polydactyly - Cytogenetic studies
- Enzyme and DNA
Encephalocoele - Alpha fetoprotein
- Incomplete skull formation with extrusion of - Acetylcholinesterase
varying amount of brain tissue
- Most common: occipital area Early Amniocentesis
- Associate with hydrocephalus and - 11-14 weeks
microcephaly - Less fluid can be withdrawn
- Neonatal mortality rate: 40% - Increased culture failure rate
- Intellectual impairment and neurologic - Higher rates of abortion (2.5% vs 0.7%)
sequelae: 80% - Higher rates of talipes equinovarus
*Compatible with life

2
 o Oligohydramnios, damage to the - Fetal anemia (alloimmunization)
vascular supply of the developing o Blood transfusion into the umbilical
leg vein
- Higher rates of fluid leakage - Fetal pleural effusion
- Not recommended by ACOG o Fetal thoracentesis
- Gastroschisis
Amniocentesis o Amnioexchange
- Lung maturity Replace AF with NSS
o L/S ratio o Intestines exposed to AF >> harmful
o Phosphatidylglycerol - Fetal thyrotoxicosis
o Lamellar body count o Propylthiouracil
**Use 10 cc of AF; Coulter - Fetal arrhythmia
counter (machine used?) o Antiarrhythmic agents digoxin,
- Chorioamnionitis verapamil, propranolol
o C l re and en i i i , Gram ain o May be given to the mother
- Meconium staining o Through the umbilical cord or
- Complications intramuscular
o Fetal and maternal trauma
o AF leakage **Karyotyping result
o Vaginal spotting - Cordocentesis: 2 weeks
o Chorioamnionitis - CVS: 4 weeks
o Abortion
o Preterm labor

Chorionic Villus Sampling

- Performed at 10-13 weeks
- Transcervically or transabdominally
- Cytogenetic studies
- Fetal karyotype
- Enzyme and DNA analysis
- Results are available earlier
- Early CVS (7 weeks) increased incidence
of limb reduction and oromandibular defects
- Complications
o Vaginal bleeding
o Abortion
o Infection
o Limb abnormalities

Corodocentesis
- Prenatal diagnosis of blood disorder
- Isoimmunization
- Fetal viral and bacterial infections
- Rapid fetal karyotyping
- Metabolic and biochemical analysis
- DNA analysis
- Acid-base analysis
- Immunologic studies
- Complications
o Fetal loss
o Chorioamnionitis
o Ruptured membranes
o Bleeding
o Severe bradycardia

Fetal Tissue Biopsy

- Muscle biopsy
o Muscular dystrophy
o Mitochondrial myopathy
- Skin biopsy

Fetal Therapy
- Twin-to-twin transfusion syndrome
o Unbalance vascular anastomoses
that connect the 2 fetal circulations
Twins: 1 LGA
(polyhydramnios), 1 SGA
(oligohydramnios)
o Amnioreduction
o Septostomy
o Laser occlusion of placental
vascular anastomoses
3
OB1: Passages
Lectures per Facilitator
YELLOW - Dr. Lee

BLUE Dr. Gonzalez

RED Dr. Mariano

Pelvic Bones
composed of four bones:
o sacrum
o coccyx
o two innominate bones
o Each is formed by the fusion of
three bones
the ilium, ischium, and
TRUE PELVIS important portion especially
pubis (Fig. 2-16)
during childbearing
o Both are joined to the sacrum @
o Described as: in er ed J haped
sacroiliac synchondroses and to
an obliquely truncated
one another @ symphysis pubis
bent cylinder
with greatest height posteriorly
o Linea Terminalis superior border
o Iliopectineal line
o Imaginary line w/c separates
true from false pelvis
o Pelvic Outlet inferior margin
o sidewalls of the true pelvis of an adult
woman somewhat converge
o Ischial Spines extends from the
middle of the posterior margin of each
ischium
These are of great obstetrical
importance
distance between them - represents
the shortest diameter of the true
pelvis
also serve as valuable landmarks
o assessment of level to
which the presenting part
of the fetus has descended
into the true pelvis
conceptually divided into false and true
these aid pudendal nerve block
components
placement
True Pelvis False Pelvis o sacrum - posterior wall of the true pelvis
Below the Above the upper anterior margin
LOCATION linea linea corresponds to the
terminalis terminalis
promontory that may
P: anterior P: Lumbar be felt during
surface of Vertebra bimanual pelvic
sacrum L: Iliac examination in women
L: inner Fossa with a small pelvis
surface of A: Lower provide a landmark for clinical
ischial bones portion of pelvimetry
& sacrosciatic anterior Normally, it has a marked
notches & abdominal vertical & a less pronounced
BOUNDARIES ligaments wall horizontal concavity
A: pubic
ABNORMAL: undergo
bones,
important variations
ascending
straight lines
superior rami
from the promontory
of the ischial
to the tip of the
bones, &
sacrum = 10cm
obturator
foramina distance along the
concavity = 12 cm

Pelvic Joints
ANTERIORLY: pelvic bones - joined together by the
symphysis pubis
consists of fibrocartilage and the superior &
inferior pubic ligaments
o latter ligament - frequently designated
the arcuate ligament of the pubis
POSTERIORLY: pelvic bones - joined by articulations
between the sacrum and the iliac portion of the innominate
bones to form the sacroiliac joints

1
 These joints in general have a limited degree (Diagonal conjugate - 1.5 to 2cm)
of mobility = <11.5 cm means inadequate
during pregnancy
o there is remarkable relaxation of
these joints at term
o caused by upward gliding of the
sacroiliac joint
The displacement may increase the diameter
of the outlet by 1.5 to 2.0 cm.
o greatest in the dorsal lithotomy
position
o main justification for a vaginal
delivery
increase in pelvic outlet diameter occurs only
if the sacrum is allowed to rotate posteriorly 2. Transverse diameter
o will not occur if the sacrum is forced o constructed at right angles to the
anteriorly by the weight of the obstetrical conjugate
maternal pelvis against the delivery o represents the greatest distance
table or bed between the linea terminalis on either
side
Sacroiliac joint mobility = successful McRoberts o can be mea red
maneuver o usually intersects the obstetrical
o Release of an obstructed shoulder conjugate at a point approx. 5 cm in
cases of shoulder dystocia front of the promontory and measures
(+) labor difficulty approx. 13 cm
These changes have also been attributed to the
success of the modified squatting position to 3. Two oblique diameters
hasten second-stage labor o extends from 1 sacroiliac synchondrosis
o squatting position -
diameter & pelvic outlet diameter o Each eminence - minor
NOTE: These latter observations are unconfirmed, but this elevation
position is assumed for birth in many societies. marks the union site
of the ilium & pubis
Planes and Diameters of the Pelvis o These oblique diameters average < 13
The pelvis is described as having 4 imaginary planes: cm
1. The plane of the pelvic inlet the superior strait
2. The plane of the pelvic outlet the inferior strait
3. The plane of the midpelvis the least pelvic Midpelvis and Pelvic Outlet
dimensions Midpelvis
4. The plane of greatest pelvic dimension no o measured at the level of the ischial
obstetrical spines
significance. o lower margin of the anterior symphysis
Pelvic Inlet o also called the midplane or plane of
called he perior rai & i al o he perior least pelvic dimensions (Fig. 2-19)
plane of the true pelvis
bounded by the promontory & alae of the sacrum
(P), by the linea terminalis (L), and by the
horizontal pubic rami & the symphysis pubis (A)
During labor, fetal head engagement is defined
b he fe al head biparie al diame er pa ing
through this plane
o To aid this passage, the inlet of the
female pelvis more nearly round
(gynecoid) than ovoid
compared with the male pelvis

Four diameters of the pelvic inlet are usually described:

1. AnteroPosterior described using specific
landmarks
o Most cephalad
o AP diameter true /anatomic conjugate
Not measurable o During labor, the degree of fetal head
o Extends from the upper most margin of descent into the true pelvis may be
the symphysi described by station
promontory midpelvis and ischial spines
serve to mark zero station.
Obstetrical Conjugate o The interspinous diameter = 10 cm or
o Clinically important (not measurable) slightly greater
o Shortest distance between sacral usually the smallest pelvic
promontory and symphysis pubis = diameter
smallest diameter important in cases of
o Normally measure > 10cm obstructed labor
o Can be mea red direc l i h o AP diameter thru the level of the ischial
examining fingers spines normally measures at least 11.5
Diagonal conjugate distance from cm.
lowest margin (inferior border) of the o Can only be estimated thru an Internal
Exam
Clinical purpose measured with Feel for the sacrum
estimation
2
 ✓curvature =
adequate midpelvis
(12cm)
Feel the ischial spines
+ prominent = small
interspinous/bispinous
diameter
Converge of sidewalls
✗ convergent walls
Pelvic Outlet
o consists of two approximately triangular
areas
boundaries mirror the perineal
triangle
o have a common base
a line drawn between the two
ischial tuberosities
o apex of the posterior triangle - tip of the
sacrum
o lateral boundaries - sacrotuberous
ligaments and the ischial tuberosities
o anterior triangle - formed by the
descending inferior rami of the pubic
bones
These rami unite at an angle of
90-100 degrees to form a
rounded arch under which the
fetal head must pass
o Clinically, three diameters of the pelvic
outlet usually are described:
AnteroPosterior diameter
Transverse diameter
Posterior Sagittal diameter
NOTE: Unless there is significant pelvic bony disease, the
pelvic outlet seldom obstructs vaginal delivery.
o Thing to assess are:
o Subpubic Arch
✗ measure the angle
determine either wide
(>90) or not
o Bituberous diameter
At least 8cm (nlt 8cm)
Try to see if clenched
fist can fit
Can be mea red
during IE
Pelvic Shapes
The Caldwell-Moloy ( 33, 34) ana omical cla ifica ion of
the pelvis
based on shape, and its concepts aid an
understanding of labor mechanisms
greatest transverse diameter of the inlet
its division into anterior and posterior segments
o used to classify the pelvis as gynecoid,
anthropoid, android, or platypelloid.
posterior segment determines the
type of pelvis
anterior segment determines the
tendency
These are both determined
because many pelves are not
pure but are mixed types
E.g. a gynecoid pelvis w/ an
android tendency
o P pelvis = gynecoid
o A pelvis = android
shaped
From viewing the four basic types in Figure 2-20, the
configuration of the gynecoid pelvis would intuitively seem
suited for delivery of most fetuses. Indeed, Caldwell (1939)
reported that the gynecoid pelvis was found in almost half
of women.
o Gynecoid Pelvis most suited for fetal delivery
o Extreme android pelvis poor Dx for VSD
o Anthropoid type 33% of women
Tests for assessment of pelvic adequacy:
Diagonal conjugate determination (11.5-12cm)
Assess engagement
Müller-Hillis Manuever
o Pushes fundus downward then if the
head of the fetus reaches the ischial
spine = (+) adequate
o Head is at ischial spine = station 0 =
head is engaged
o Engagement when the bipareital
diameter of the flexed head is at the
level of the pelvic inlet
Indications for Xray Pelvimetry
Fetal delivery by breech or vaginally
o If head is flexed or if the head will fit
(+) previous injury to pelvis (fracture/trauma/hip
replacement) / (+) polio infection
o changes in pelvic configuration
previous CS
All PRIMIs w/ breech presentation are delivered
adbominally
Generally, clinical pelvimetry is done for PRIMIs &
mothers who did not deliver vaginally during
previous pregnancies
Patient must be in dorsal lithotomy position
o When legs are elevated, AP diameter
increases
Clinical Obstetrics
(+) pelvic contractions = difficulty in vaginal
delivery
o indication for CS
o Types of contraction
Inlet contraction
Inlet & Midpelvis contraction
Midpelvis contraction
Midpelvis & outlet contraction
Outlet contraction lowest
incidence
Trial of Labor
o Except for those with:
Placenta previa
Breech in a PRIMI
Malpresentation
All are indicated for
CS
G2P
st
o 1 Pregnancy: CS
nd
o 2 Pregnancy: vaginally
request for pelvic scan before
proceeding.
3
PASSENGER 1. Cephalic Presentation
— Full flexion is ordinarily achieved
because occipital condyles are
located near the posterior aspect of
3P the skull
As head enters the inlet, the
1. Passages longer segment of the lever
2. Passenger yields to the pressure and
3. Power flexion results
— Classified according to the
relationship between the head and
Fetal orientation relative to the maternal pelvis is body of the fetus:
described in terms: a. Vertex or occiput
presentation
1. Fetal lie head is fully flexed sharply
2. Fetal presentation so that the chin is in contact
3. Fetal attitude with the thorax
4. Fetal position presenting anteroposterior
diameter is the
suboccipitobregmatic
FETAL LIE (9.5cm at term)
occipital/ posterior
- Relation of the fetal long axis to that of the (triangular) fontanel is the
mother presenting part
- It can be: longitudinal, transverse, or oblique
b. Face presentation
fetal neck is hyperextended
1. Longitudinal Lie so that the occiput and back
— present in >99% of labors at term come in contact, and the face
— Long axis of the fetus parallel to the is foremost in the birth canal
long axis of uterus presenting AP diameter is
As term approaches, the uterine cavity submentobregmatic or
most often accommodates the fetus in tracheobregmatic (9.5cm at
longitudinal lie with either fetal head term)
(cephalic) or breech presenting allows advancement through
pelvis but vaginal delivery
2. Transverse Lie may result to cervical spinal
— Perpendicular to the long axis of the cord injury
mother chin/ mentum presenting
— Predisposing factors: multiparity, part
placenta previa, hydramnios, uterine
anomalies c. Sinciput presentation
— The shoulder is usually over the pelvic Partially flexed fetal head
inlet with the fetal head lying in one iliac Anterior (large diamond
fossa and the breech in the other shaped) fontanel or bregma
— Less common is the presenting part
— Potentially serious; when membranes Military attitude
rupture, cord prolapse commonly follows AP diameter is
— Indication for cesarean section because occipitofrontal (12.5cm at
labor will cause a ruptured uterus term)

3. Oblique Lie d. Brow presentation

— Fetal and maternal axes may cross at a Partially extended fetal
45-degree angle head
— Unstable and becomes longitudinal and AP diameter is
transverse during labor occipitomental plane
(13.5cm at term; longest AP
diameter)
FETAL PRESENTATION Frontum/ Frontal bone
and orbits presenting part
- Presenting part portion of the fetal body
that is either foremost within the birth canal The sinciput and brow
or in close proximity to it presentations are usually
- Typically can be felt thought the cervix on transient. As labor progresses,
vaginal examination both presentations almost
In longitudinal lie: presenting part is always convert into vertex and
either fetal head (cephalic) or breech face presentations by neck
presentation flexion and extension,
In transverse lie: shoulder is the respectively.
presenting part o Vertex neck flexion
o Face neck extension

1
 o Failure to do so can
lead to dystocia
Peculiarity in fetal attitude,
particularly extension of the
vertebral column as seen in
frank breeches may also
prevent fetus from turning
Implantation of placental in
lower uterine segment which
may distort normal
intrauterine anatomy

a. Frank breech presentation

Lower extremities are flexed
at the hips and extended at
the knees
Fetal feet lie in close
proximity to the head

Term fetus usually presents

with vertex because uterus is
piriform or pear shaped

Cephalic pole
composed of fetal head only
slightly larger than the
breech
Podalic Pole
Breech and flexed
extremities
bulkier and more mobile
than the cephalic pole
b. Complete breech
presentation
One or both knees are
flexed
Thighs are flexed over the
abdomen, legs are flexed
upon the thighs and the feet
present at the level of the
buttocks

At 32 weeks, amniotic cavity is

large compared with the fetal
mass and the fetus is not
crowded by the uterine walls.

As fetal mass increases, the

ratio of amniotic fluid volume
decreases results to the
uterine walls more apposed
closely to the fetal parts
c. Incomplete breech
presentation
If presenting part is breech, One or both hips are not
fetus most often changes flexed, and one or both feet
polarity to make use of the or knees lie below the
roomier fundus for its bulkier breech, such that a foot or
and more mobile podalic knee is lowermost in the
pole Incidence of breech birth canal
presentation decreases with Possible complication:
gestational age compression of a prolapsed
cord or a cord entangled
2. Breech Presentation around the extremities as
— Considered when fetus presents the breech fills the pelvis
with buttocks towards the pelvis and
the bitrochanteric diameter
(9.5cm) presents
— Presented by the sacral prominence
— 3 general presentations: frank,
complete and footling presentations
— May result from circumstances that
prevent normal version from taking
place such as:
Septum that protrudes into
the uterine cavity

2
 Footling breech an
incomplete breech with one or
both feet below the breech
Single footling one leg is
completely extended and the
other is flexed
Double footling both legs
are extended below the level of
the buttocks
3. Shoulder Presentation
— Shoulder or acromion is presenting
into the pelvic inlet in transverse lie
— Bisacromial diameter (11.0cm)
presents
4. Compound Presentation
— Fetal hand or foot prolapses
alongside the presenting vertex or
breech
— Causes: conditions that prevent
complete occlusion of the pelvic
inlet by the presenting part
Combination of hand with
vertex or breech tends to
resolve spontaneously as
labor advances
Combination of foot and
fetal head tends to be
complicated with cord
prolapse
FETAL ATTITUDE or POSTURE
- Relation of fetal parts to one another
- The fetus forms an ovoid mass that
corresponds roughly to the shape of the
uterine cavity
- The fetus becomes folded or bent; the back
becomes markedly convex; the head is
flexed with the chin in contact with the chest;
the thighs are flexed over the abdomen; legs
are bent at the knees; arches of feet rest
upon the anterior surface of the legs this
characteristic feature results partly from the
mode of growth of the fetus and partly from
a process of accommodation to the uterine
cavity
- In cephalic presentations, arms are usually
crossed over the thorax or become parallel
to the sides.
- The umbilical cord lies in the space between
the arms and lower extremities.
Abnormal exceptions to this
attitude: fetal head becomes
more extended from vertex to
face presentation resulting
from change in fetal attitude
from convex (flexed) to
concave (extended) contour of
the vertebral column.
FETAL POSITION
- Relationship of an arbitrarily chosen portion
of the fetal presenting part to the right or left
side of the birth canal (According to
Williams)
According to APMC, fetal
position is the relationship of
the chosen portion of the fetal
presenting part in reference to
one of the four quadrants or to
the transverse diameter of the
maternal birth canal
- For each presentation there may be 2
positions right or left
- Determining points:
Vertex presentation occiput
Face presentation chin (mentum)
Breech presentation sacrum
Presenting part may either be
right or left position
Left occipital (LO) and right
occipital (RO)
Left mental (LM) and right
mental (RM)
Left Sacral (LS) and right
sacral (RS)
VARIETIES OF PRESENTATIONS AND
POSITIONS
- Relationship of a given position of the
presenting part to the anterior, transverse, or
posterior portion of the maternal pelvis for
more accurate orientation
- Presenting part in right or left positions may
be directed anteriorly (A), transversely (T),
or posteriorly (P)
- There are 6 varieties for each of the 3
presentations
In an occiput presentation, the
presentation, position and variety
may be abbreviated in clockwise
fashion as:
Acromion (scapula)
portion of the fetus arbitrarily
chosen for orientation with the
maternal pelvis in shoulder
presentations
may be directed wither posteriorly
or anteriorly and superiorly and
inferiorly
All transverse lies are referred to as
shoulder presentations
Transverse lie, with back up or back
down, is clinically important when
deciding incision type for cesarean
delivery
3
 1. Abdominal Palpation Le d
Maneuver
— Conducted systematically employing
4 maneuvers
— Mother lies supine and comfortable
positioned with her abdomen bared
— May be difficult to perform in obese
patient, excessive amniotic fluid or if
placenta is implanted anteriorly
— Can be performed throughout the
latter months of pregnancy and
during and between contractions of
labor
— Can be used to estimate size of
fetus

a. LM 1 (Fundic Grip)
Identification of which fetal
pole (either cephalic or
podalic) occupies uterine
fundus
Breech felt as large,
nodular mass
Head felt as hard and
round and is more mobile
and ballotable

b. LM 2 (Umbilical Grip)
Palms are placed on either
side of the maternal
abdomen, and gentle but
deep pressure is exerted
Fetal back felt as hard
and resistant structure
Fetal extremities felt as
numerous small, irregular
mobile parts
Identify if fetal back is on the
right or left side and where
the fetal heart sound is best
appreciated
Fetal orientation
can be determined
by noting whether
the back is directed
anteriorly,
transversely or
posteriorly

c. LM 3 (Pa c/ Pa G )
Performed by grasping with
the thumb and fingers on
one hand the lower portion
of the maternal abdomen
just above the symphysis
pubis
To determine what is
occupying the pelvic inlet
If presenting part is not
engaged movable mass is
felt (usually the head
DIAGNOSIS OF FETAL PRESENTATION AND
POSITION d. LM 4 (Pelvic Grip)
Examiner faces the
- Several methods may be used: abdominal mo her fee
palpation, vaginal examination, auscultation Tips of the first 3 fingers of
and sonography each hand are used in
- Rarely used: radiographs, computed exerting deep pressure in
tomography or MRI the direction of the axis in
the pelvic inlet

4
 Determine whether head is — Determines vertex presentations
extended or flexed and positions through palpation of
If cephalic various fetal sutures and fontanels
prominence is on — Face and breech presentations
the same side as identified by palpation of facial
the fetal small features and fetal sacrum
parts head is — Comprises 4 movements:
st
flexed and is in 1 : Examiner inserts 2
vertex presentation fingers into the vagina and
If cephalic presenting part is found
prominence is on Differentiation of
the same side as vertex, face and
the fetal back breech is readily
head is extended accomplished
nd
and face is the 2 : If vertex presentation,
presenting part fingers are directed
Tells us if there is posteriorly and then swept
engagement forward over the fetal head
Difficult to assess toward the maternal
engagement if symphysis
breech presentation During this
If presenting part is movement, the
not engaged can fingers necessarily
be determined if cross the sagittal
both hands meet, suture and its linear
hands should have course is delineated
rd
a meeting point or 3 : The positions of the 2
they should fontanels are ascertained;
intersect at one Fingers are passed to the
point; cephalic most anterior extension of
prominence is on the sagittal suture and the
the same side as fontanel encountered there
that of the fetal back is examined and identified.
Deeply engaged Then with a sweeping
indicative that the motion, the fingers pass
lower fetal pole is in along the suture to the other
the pelvis; cephalic end of the head until the
prominence is no other fontanel is felt and
longer palpable on differentiated
th
the ipsilateral side 4 : Established the station
as that of the fetal or extent to which the
back presenting part has
descended into the pelvis
Various sutures and
fontanels are
located readily
using these
maneuvers.

2. Vaginal Examination
— Inconclusive in diagnosing fetal
presentation and position when
done before labor because
palpation is done through closed
cervix and lower uterine segment
— Usually done during onset of labor
and after cervical dilatation

5
 Examples:

1. Right Occiput Transverse (ROT)

LM 1: Breech
3. Auscultation LM 2: fetal back right (FBR)
- does not provide very reliable information LM 3: Cephalic
concerning fetal presentation and position LM 4: Cephalic prominence (CP) is
- fetal heart sounds best heard through fetal on the contralateral side
back
- The point of maximal intensity of fetal heart
sounds in cephalic presentation is usually Unless the examiner tells you that her
midway between the maternal umbilicus and fingers did not meet, there is (-) engagement
the anterior superior spine of the ilium
- Breech presentation above the level of the
umbilicus

4. Sonography and Radiography

- Can aid fetal position identification,
especially in obese women or in women with
rigid abdominal walls

DETERMINING FETAL POSITION:

2. Left Mentum Posterior (LMP)

LM 1: Breech
LM 2: FBR
LM 3: Cephalic
LM 4: CP is ipsilateral to fetal back;
(-) engagement

*T e a e e e a
facing the examiner

A Anterior

P Posterior

R Right (per ain o he mo her right, not

he e aminer )

L Left (per ain o he mo her lef , no

3. Left Sacral Anterior (LSA)
he e aminer ) LM 1: Cephalic
LM 2: Fetal back left
T Transverse
LM 3: Breech
LM 4:

6
 If heart tones is heard above the umbilicus
breech presentation

If heart tones is heard below the umbilicus

cephalic presentation

Asynclitism

- Lateral deflection of the sagittal suture to a

more anterior or posterior position in the
4. Left Acromio-dorso posterior pelvis
LM 1: (-) - Anterior asynclitism if sagittal suture
LM 2: Head left; buttocks right approaches the sacral promontory, more of
LM 3: (-) the anterior parietal bone presents itself to
LM 4: (-) the examining fingers
- Posterior asynclitism sagittal suture lies
close to the symphysis, more of the
posterior parietal bone will present

5. Right Acromio-dorso anterior (RADA)

LM 1: (-)
LM 2: Head right; buttocks left
LM 3: (-)
LM 4: (-) Passenger factors that affect vaginal delivery:

1. Presentation: cephalic vaginal; breech

On Internal Exam: abdominal delivery
2. Varieties of cephalic presentation: face
Breech presentation usually abdominal delivery
- If there is difficult in reaching for the part 3. Multiple gestation
- Soft area 4. Size of the baby
- If soles of the feet is felt 5. Maturity of the baby
- If straight line is felt between the ischial Preterm disproportion of the size
tuberosity and anal opening of the head and chest; better to
- If finger is put is put inside anal opening, deliver abdominally
there is meconium

Face or Cephalic Presentation

- If one side of the triangle is formed when
palpating for the malar eminence and the Sources: Williams, APMC, Group discussion
mouth
- When finger is put inside the mouth, the
baby sucks the fingers

For compound presentations wherein the

hand goes over the head
- Longer fingers are felt
- There is grasp reflex

Compound presentation is differentiated

from breech by:
- Shape of the soles are different clumpier
compared to palm of the hands
- There i fanning (babin ki ign) hen ole
of the feet is stroked

7
Fetal Contributions to Initiation of Parturition
mature human fetus provides the signal to initiate
parturition
o signals transmitted in several ways to
suspend uterine quiescence.
fetus may provide a signal thru a blood-borne
agent that acts on the placenta
o Although signals may arise from the
fetus
the uterus and cervix likely first
must be prepared for labor
before production & release of
uterotonin
Uterine Stretch and Parturition
Fetal Growth important component in uterine
activation (Phase 1 of Parturition)
o Significant myometrial tensile stress
& AF pressure flow
o (+) uterine activation
stretch is required for induction
of specific contraction-
associated proteins (CAPs)
stretch - increases expression
of the gap junction protein
connexin 43 and of
oxytocin receptors
Gastrin-releasing peptide
a stimulatory agonist
for smooth muscle
increased by stretch in
the myometrium
Other Hypothesis: stretch plays an integrated
role with fetal- maternal endocrine cascades
of uterine activation
Clinical support for a role of stretch
o multifetal pregnancies - greater risk for
preterm labor than singletons
preterm labor - common in
pregnancies complicated by
hydramnios
o (+) role for uterine stretch is considered
Mechano-Transduction cell signaling systems
used by stretch to regulate the myometrial cell
that includes:
activation of cell-surface receptors or ion
channels
transmission of signals through
extracellular matrix
release of autocrine molecules that act
directly on myometrium
For example, Fibronectin (EC matrix protein) + -
5 integrin receptor (its cell-surface receptor)
o induced in the rodent by stretch
o aid force transduction during labor
contraction by anchoring hypertrophied
myocytes to the uterine EC matrix.
Fetal Endocrine Cascades Leading to Parturition
(+) ability of the fetus to provide endocrine
signals initiate parturition
Liggins and associates (1967, 1973) used
sheep
o signal comes from the fetal
hypothalamic pituitary adrenal
(HPO) axis
o exact mechanisms regulating human
parturition - more difficult to prove
o all evidence humans are not regulated
in the exact manner seen in the sheep
Even so, activation of the human fetal
hypothalamic pituitary adrenal placental
axis
o considered a critical component of
normal parturition.
o
preterm labor
As in the sheep, steroid products of the human
fetal adrenal gland
o (+) effects on the placenta and
membranes
o transform myometrium from a quiescent
to contractile state.
A key component in the human - unique ability of
Placental Corticotropin-Releasing Hormone (CRH)
Production.
A CRH hormone identical to maternal and fetal
hypothalamic CRH
o synthesized by the placenta in relatively
large amounts
One important difference is that, unlike
hypothalamic CRH, which is under GC (-
)feedback
o cortisol - stimulate placental CRH
production
o thru activation of the transcription factor,
nuclear factor kappa B (NF- B)
o This ability create a feed-forward
endocrine cascade that does not end
until delivery
st
(from midgestation to term)
o In the last 12 weeks, CRH plasma levels
rise exponentially
o peaking during labor and then falling
precipitously after delivery
CRH the only trophic hormone-releasing factor
to have a specific serum binding protein.
o During most of pregnancy, CRH-binding
protein (CRH-BP) binds most maternal
o -BP
levels in both maternal plasma and
levels of bioavailable CRH
In pregnancie in hich he fe (+) re ed
from various complications
o
maternal plasma
o as compared with those seen in normal
gestation
o placenta -
concentration
For example, women with
preeclampsia = 4x placental
CRH content
than in those from normal
pregnancies
ge a ion & ecre ion of placen al CRH in
complicated pregnancies
o may play a role in fetal adrenal cortisol
synthesis
o may result in the supranormal levels of
umbilical cord blood cortisol
as noted in stressed neonates
Corticotropin-Releasing Hormones and Parturition Timing
Placental CRH (+) play several roles in
parturition regulation
o
Late in pregnancy (phase 2 or 3 of parturition)
o
myometrial cell Ca levels via PKC
(protein kinase C) activation
1
 Oxytocin - acts to attenuate CRH-stimulated
accumulation of cAMP in myometrial tissue
CRH augments the contraction-inducing potency
of a given dose of oxytocin in human myometrial
strips
o CRH -
response to PGF2
o 19-
steroid synthesis
production
(+) shifting of the
estrogen-to-
progesterone ratio
promote the
expression of a series
of myometrial
contractile proteins.
o rising level of CRH at the end of gestation reflects
a fetal-placental clock
o CRH levels vary greatly among women
o -
more accurate predictor of pregnancy
outcome than is a single measurement
o In this regard, the placenta and fetus, through
endocrinological events, influence the timing of
parturition at the end of normal gestation.
Fetal Lung Surfactant and Parturition
Surfactant protein A (SP-A) - produced by the
fetal lung
o required for lung maturation
o im
- production
A concentrations in AF = (+)
migration into the myometrium
and induce NF- B
NF- B - activates inflammatory
response genes in the
myometrium
promote uterine
contractility
This model supports the
supposition that fetal signals
play a role in parturition
initiation
SP-A is expressed by the human amnion and
decidua
o Present in AF (amniotic fluid)
o prompts signaling pathways in human
myometrial cells
The exact mechanisms by which SP-A
activates myometrial contractility in
women, however, remains to be clarified
SP-A selectively inhibits PGF2 in the term
decidua & AF concentration of SP-
Fetal Anomalies and Delayed Parturition
= prolonged gestation
o The e na ral e perimen incl de
fetal anencephaly with adrenal
hypoplasia and those with inherited
placental sulfatase deficiency.
o The broad range of gestational length
seen with these disorders calls into
question the exact role of estrogen in
human parturition initiation.
Other fetal abnormalities do not prolong human
pregnancy
o
entry of fetal urine into AF
o
secretions
Thus, a fetal signal through the paracrine arm of
the fetal-maternal communication system does
not appear to be mandated for parturition
initiation
Some brain anomalies of the fetal calf, fetal
lamb, and sometimes the human fetus
o delay the normal timing of parturition.
o (+) fetal anencephaly = prolonged
human gestation (374 days or 53
weeks)
attributable to anomalous fetal
brain-pituitary-adrenal function.
Very small adrenal
glands and only 5-
10% as large of those
of a normal fetus at
term
caused by developmental
failure of the fetal zone
accounts for most of
fetal adrenal mass
and production of
C19-steroid hormones
Such pregnancies are associated with delayed
labor and suggest that the fetal adrenal glands
are important for the timely onset of parturition
Phase 3: Uterine Stimulation
synonymous with uterine contractions
o that bring about progressive cervical
dilatation and delivery.
uterotonin theory of labor initiation
o Phase 1 suspension & Phase 2
o # of uterotonins (important) = success of
phase 3 (Active labor)
Uterotonins - candidates for labor induction
includes:
o oxytocin, prostaglandins, serotonin,
histamine, PAF, angiotensin II, and
many others.
o (+) stimulate smooth muscle contraction
through G-protein coupling
Oxytocin and Phase 3 of Parturition
Late in pregnancy, during phase 2 of parturition
o 50-
oxytocin receptors
o
responsiveness to oxytocin.
o Moreover, prolonged gestation = delay
in the increase of these receptors
Oxytocin q ick bir h
st
o 1 uterotonin to be implicated in
parturition initiation
o nanopeptide, synthesized as a
prohormone in the magnocellular
neurons of the SON (supraoptic) & PVN
(paraventricular).
o transported with its carrier protein,
neurophysin
along the axons to the neural
lobe of the posterior pituitary
gland in membrane-bound
vesicles for storage and later
release.
o converted enzymatically to oxytocin
during transport
Role of Oxytocin in Phase 3 and 4 of Parturition
2
 logically suspected in parturition initiation.
First, in addition to its effectiveness in inducing
labor at term
o oxytocin is a potent uterotonin and
occurs naturally in humans.
Subsequent observations provide additional
support for this theory:
and decidual tissues near the end of gestation
(2) oxytocin acts on decidual tissue to
promote prostaglandin release
(3) synthesized directly in decidual and
extraembryonic fetal tissues and in the placenta
Although little evidence suggests a role for
oxytocin in phase 2 of parturition
o abundant data support its important role
during second-stage labor & in the
puerperium - phase 4 of parturition
Specifically, there are
levels:
(1) during second-stage labor - end of
phase 3 of parturition
(2) in the early puerperium
(3) during breast feeding
Immediately after delivery of the fetus, placenta,
and membranes
o Completion of parturition phase 3
o (+) firm and persistent uterine
contractions and myometrial retraction
hemorrhage
o Oxytocin - causes persistent
contractions
o Oxytocin infusion in women promotes
encode proteins essential for
uterine involution
These include interstitial
collagenase, monocyte
chemoattractant protein-1, IL-8,
and urokinase plasminogen
activator receptor.
Therefore, oxytocin action at
the end of labor may be
involved in uterine involution
Prostaglandins and Phase 3 of Parturition
(+) critical role in phase 3 of parturition
o mediators
noncomplicated pregnancies
First, levels of prostaglandins, or their metabolites
o In amnionic fluid, maternal plasma, and
maternal urine
Second, Tx of pregnant women with PG =
abortion or labor at all gestational stages
o At any route of administration
(+) giving of prostaglandin H synthase type 2
(PGHS-2) inhibitors to pregnant women
o Delay onset of spontaneous labor & may
arrest preterm labor
Last, PG Tx of myometrial tissue in vitro
o causes contraction
o dependent on the prostanoid tested &
physiological status of the tissue treated.
Uterine Events Regulating Prostaglandin Production.
During labor, PG production within the
myometrium and decidua
o efficient mechanism of activating
contractions.
o For example, PG synthesis is high and
unchanging in the decidua
during phase 2 and 3 of
parturition
o 2 in the
decidua at term
regulatory step in PG action in
the uterus.
myometrium synthesizes PGHS-2 with labor
onset
o most PG likely comes from the decidua
The fetal membranes and placenta also produce
PGs
o Primarily PGE2, but also PGF2
o detected in AF at all gestational stages
o
demonstrable after labor begins
o results to the dilatation of the cervix &
decidual tissue exposure
o
those in the upper compartment
follow an inflammatory
labor.
o Together, the increases in cytokines and
prostaglandins
degrade the EC matrix =
weakening of fetal membranes.
o inflammatory mediators
aid cervical dilatation
alterations to the lower uterine
segment
It can be envisioned that they, along
with the increased prostaglandin levels
measured in vaginal fluid during labor,
add to the relatively rapid cervical
changes that are characteristic of
parturition.
Endothelin-1
family of 21-amino acid peptides
o powerfully induce myometrial
contraction
endothelin A receptor - preferentially expressed
Endothelin-1
o produced in myometrium of term
gestations
o able to induce synthesis of other
contractile mediators
such as PG and inflammatory
(+) requirement of endothelin-1 in normal
parturition physiology
However, there is evidence of pathologies
associated with aberrant endothelin-1 expression
o such as premature birth and uterine
leiomyomas
Angiotensin II
2 G-protein-linked angiotensin II receptors
expressed in the uterus: AT1 and AT2
o nonpregnant women - AT2 receptor is
predominant
o
expression
Angiotensin II binding to the plasma-membrane
receptor = contraction
During pregnancy, vascular smooth muscle (+)
expression of AT2 receptor
o refractory to the pressor effects of
infused angiotensin II
In myometrium near term, angiotensin II may be
another component of the uterotonin system of
parturition phase 3
3
 Contribution of Intrauterine
Tissues to Parturition
the amnion, chorion laeve, and decidua parietalis
o have a potential role in parturition
initiation
o plays an alternative role
The membranes and decidua
o make up an important tissue shell
around the fetus
o serves as a physical, immunological,
and metabolic shield
to protect against untimely
initiation of parturition.
Late in gestation, however, the fetal membranes
may indeed act to prepare for labor.
Amnion
Provides virtually all of the tensile strength of the
fetal membrane
o (+) resistance to tearing and rupture
avascular tissue
highly resistant to penetration by leukocytes,
microorganisms, and neoplastic cells
constitutes a selective filter
o to prevent fetal particulate-bound lung
and skin secretions from reaching the
maternal compartment
o maternal tissues are protected from
amnionic fluid constituents
myometrial function
amnionic-fluid embolism
Several bioactive peptides and prostaglandins
that cause myometrial relaxation or contraction
are synthesized in amnion
landin
2 and PGHS-2
Accordingly, many hypothesize that PG regulate
events leading to parturition.
Amnion - major source for AF prostaglandins
o (+) role in activation of cascades =
promote membrane rupture
o n-derived PG on
uterine quiescence & activation
due to PG transport from the
amnion thru the chorion to
access maternal tissues
limited by expression of the
inactivating enzyme,
prostaglandin dehydrogenase.
Chorion Laeve
primarily protective tissue layer
(+) immunological acceptance
enriched with enzymes that inactivate
uterotonins:
o prostaglandin dehydrogenase (PGDH) -
inactivates amnion-derived PG
o oxytocinase
o enkephalinase
(+) chorionic rupture =
adjacent decidua and myometrium
labor.
o - stimulated matrix
metalloproteinase activity
associated with membrane
rupture
o It would further allow prostaglandin entry
into the maternal compartment
to promote myometrial
contractility
progesterone - maintains chorion PGDH
expression
cortisol - decreases PGDH expression.
o
levels
part of progesterone withdrawal
Decidua
A metabolic contribution of decidual activation to
parturi- tion initiation is an appealing possibility
for both anatomical and functional reasons.
(+) generation of decidual uterotonins
o paracrine action on contiguous
myometrium is intuitive.
(+) steroid metabolizing enzymes expression
o 20 -HSD and eroid 5 R1
may regulate local
progesterone withdrawal
Decidual activation is characterized by:
o increased proinflammatory cells
o increased expression of proinflammatory
cytokines, PG and uterotonins
Uterotonins such as oxytocin
receptors and connexin 43
Cytokines produced in the decidua
o increase uterotonin production
(principally prostaglandins)
o act directly on myometrium to cause
contraction.
o Examples: tumor necrosis factor-
(TNF- ) and in erle kin 1, 6, 8, and 12.
also can act as chemokines
recruit to the
myometrium
neutrophils and
eosinophils
further increase
contractions and labor
There is uncertainty whether prostaglandin
concentration or output from the decidua
increases with term labor onset.
Olson and Ammann (2007) suggest that the
major regulation of decidual prostaglandin action
is not their synthesis but rather increased PGF2
receptor expression.
Summary: Regulation of Phase 3 and 4 of Parturition
It is likely that multiple and possibly redundant
processes contribute to the success of the three
active labor phases once phase 1 of parturition is
suspended and phase 2 is initiated.
Phase 3
o -protein-
coupled receptors
(+)interaction of actin and
myosin = force generation.
Simultaneously, (+) alteration of cervical
proteoglycan composition and collagen structure
o promotes tissue distensibility and
increased compliance.
NET RESULT:
o initiation of coordinated myometrial
contractions
with sufficient amplitude and
frequency
= cervical dilatation & pushing
of fetus thru birth canal
Multiple regulatory ligands orchestrate these
processes and vary from endocrine hormones
4
such as oxytocin to locally produced
prostaglandins.
In phase 4 of parturition
o Initiation of a complicated series of
repair processes
to resolve inflammatory
responses
to remove glycosaminoglycans,
proteoglycans, and structurally
compromised collagen.
Simultaneously, (+) synthesis of matrix and
cellular components = complete uterine
involution. (+) reformation of dense connective
tissue and structural integrity of the cervix

5
OB1 Biochemical Aspects of Parturition (Part II)
th
- from 24 Ed. OB. Williams
Fetal Contributions to Initiation of Parturition
mature human fetus provides the signal to
initiate parturition
o signals transmitted in several ways
to suspend uterine quiescence.
fetus may provide a signal thru a blood-
borne agent that acts on the placenta
o Although signals may arise from the
fetus
the uterus and cervix likely
first must be prepared for
labor before production &
release of uterotonin
Uterine Stretch and Parturition
Fetal Growth important component in
uterine activation (Phase 1 of Parturition)
o Significant myometrial tensile
stress & AF pressure flow
o (+) uterine activation
stretch is required for
induction of specific
contraction-associated
proteins (CAPs)
stretch - increases
expression of the gap
junction protein
connexin 43 and of
oxytocin receptors
Gastrin-releasing peptide
a stimulatory
agonist for smooth
muscle
increased by stretch
in the myometrium
Other Hypothesis: stretch plays an
integrated role with fetal- maternal
endocrine cascades of uterine activation
Clinical support for a role of stretch
o multifetal pregnancies - greater risk
for preterm labor than singletons
preterm labor - common in
pregnancies complicated by
hydramnios
o (+) role for uterine stretch is
considered
Mechano-Transduction cell signaling
systems used by stretch to regulate the
myometrial cell that includes:
activation of cell-surface receptors
or ion channels
transmission of signals through
extracellular matrix
release of autocrine molecules that
act directly on myometrium
For example, Fibronectin (EC matrix protein)
+ -5 integrin receptor (its cell-surface
receptor)
o induced in the rodent by stretch
o aid force transduction during labor
contraction by anchoring
hypertrophied myocytes to the
uterine EC matrix.
Fetal Endocrine Cascades Leading to Parturition
(+) ability of the fetus to provide endocrine
signals initiate parturition
Liggins and associates (1967, 1973) used
sheep
o signal comes from the fetal
hypothalamic pituitary adrenal
(HPO) axis
o exact mechanisms regulating
human parturition - more difficult to
prove
o all evidence humans are not
regulated in the exact manner seen
in the sheep
Even so, activation of the human fetal
hypothalamic pituitary adrenal
placental axis
o considered a critical component of
normal parturition.
o
preterm labor
As in the sheep, steroid products of the
human fetal adrenal gland
o (+) effects on the placenta and
membranes
o transform myometrium from a
quiescent to contractile state.
A key component in the human - unique
Placental Corticotropin-Releasing Hormone
(CRH) Production.
A CRH hormone identical to maternal and
fetal hypothalamic CRH
o synthesized by the placenta in
relatively large amounts
One important difference is that, unlike
hypothalamic CRH, which is under GC (-
)feedback
o cortisol - stimulate placental CRH
production
o thru activation of the transcription
factor, nuclear factor kappa B (NF-
B)
o This ability create a feed-forward
endocrine cascade that does not
end until delivery
st
Tri)
o In the last 12 weeks, CRH plasma
levels rise exponentially
o peaking during labor and then falling
precipitously after delivery
CRH the only trophic hormone-releasing
factor to have a specific serum binding
protein.
o During most of pregnancy, CRH-
binding protein (CRH-BP) binds
inactivation
o -BP
levels in both maternal plasma and
levels of bioavailable CRH
In pregnancies in which the fetus (+)
re ed from ario complica ion
o
1
 and maternal plasma
o as compared with those seen in
normal gestation
o placenta -
concentration
For example, women with
preeclampsia = 4x placental
CRH content
than in those from normal
pregnancies
ge a ion & ecre ion of placen al CRH
in complicated pregnancies
o may play a role in fetal adrenal
cortisol synthesis
o may result in the supranormal levels
of umbilical cord blood cortisol
as noted in stressed
neonates
Corticotropin-Releasing Hormones and Parturition
Timing
Placental CRH (+) play several roles in
parturition regulation
o may enhance fetal cortisol
placental CRH
Late in pregnancy (phase 2 or 3 of
parturition)
o (+) modification in the CRH receptor
myometrial cell Ca levels via PKC
(protein kinase C) activation
Oxytocin - acts to attenuate CRH-stimulated
accumulation of cAMP in myometrial tissue
CRH augments the contraction-inducing
potency of a given dose of oxytocin in
human myometrial strips
o CRH -
in response to PGF2
o 19-
steroid synthesis
ns
production
(+) shifting of the
estrogen-to-
progesterone ratio
promote the
expression of a
series of myometrial
contractile proteins.
o rising level of CRH at the end of gestation
reflects a fetal-placental clock
o CRH levels vary greatly among women
o the rat
more accurate predictor of
pregnancy outcome than is a single
measurement
o In this regard, the placenta and fetus,
through endocrinological events, influence
the timing of parturition at the end of normal
gestation.
Fetal Lung Surfactant and Parturition
Surfactant protein A (SP-A) - produced by
the fetal lung
o required for lung maturation
o
SP-A concentrations in AF =
(+) fluid macrophages
the myometrium and induce
NF- B
NF- B - activates
inflammatory response
genes in the myometrium
promote uterine
contractility
This model supports the
supposition that fetal signals
play a role in parturition
initiation
SP-A is expressed by the human amnion
and decidua
o Present in AF (amniotic fluid)
o prompts signaling pathways in
human myometrial cells
The exact mechanisms by which
SP-A activates myometrial
contractility in women, however,
remains to be clarified
SP-A selectively inhibits PGF2 in the term
decidua & AF concentration of SP-
term
Fetal Anomalies and Delayed Parturition
production = prolonged gestation
o The e na ral e perimen incl de
fetal anencephaly with adrenal
hypoplasia and those with inherited
placental sulfatase deficiency.
o The broad range of gestational
length seen with these disorders
calls into question the exact role of
estrogen in human parturition
initiation.
Other fetal abnormalities do not prolong
human pregnancy
o
AF
o
secretions
Thus, a fetal signal through the paracrine
arm of the fetal-maternal communication
system does not appear to be mandated for
parturition initiation
Some brain anomalies of the fetal calf, fetal
lamb, and sometimes the human fetus
- o delay the normal timing of
parturition.
o (+) fetal anencephaly = prolonged
human gestation (374 days or 53
weeks)
attributable to anomalous
fetal brain-pituitary-adrenal
function.
Very small adrenal
glands and only 5-
10% as large of
those of a normal
fetus at term
caused by developmental
2
 failure of the fetal zone
accounts for most
of fetal adrenal
mass and
production of C19-
steroid hormones
Such pregnancies are associated with
delayed labor and suggest that the fetal
adrenal glands are important for the timely
onset of parturition
Phase 3: Uterine Stimulation
synonymous with uterine contractions
o that bring about progressive cervical
dilatation and delivery.
uterotonin theory of labor initiation
o Phase 1 suspension & Phase 2
production
o # of uterotonins (important) =
success of phase 3 (Active labor)
Uterotonins - candidates for labor induction
includes:
o oxytocin, prostaglandins, serotonin,
histamine, PAF, angiotensin II, and
many others.
o (+) stimulate smooth muscle
contraction through G-protein
coupling
Oxytocin and Phase 3 of Parturition
Late in pregnancy, during phase 2 of
parturition
o 50-
myometrial oxytocin receptors
o ne
contractile responsiveness to
oxytocin.
o Moreover, prolonged gestation =
delay in the increase of these
receptors
Oxytocin q ick bir h
st
o 1 uterotonin to be implicated in
parturition initiation
o nanopeptide, synthesized as a
prohormone in the magnocellular
neurons of the SON (supraoptic) &
PVN (paraventricular).
o transported with its carrier protein,
neurophysin
along the axons to the
neural lobe of the posterior
pituitary gland in
membrane-bound vesicles
for storage and later
release.
o converted enzymatically to oxytocin
during transport
Role of Oxytocin in Phase 3 and 4 of Parturition
logically suspected in parturition initiation.
First, in addition to its effectiveness in
inducing labor at term
o oxytocin is a potent uterotonin and
occurs naturally in humans.
Subsequent observations provide additional
support for this theory:
myometrial and decidual tissues near the
end of gestation
(2) oxytocin acts on decidual tissue to
promote prostaglandin release
(3) synthesized directly in decidual and
extraembryonic fetal tissues and in the
placenta
Although little evidence suggests a role for
oxytocin in phase 2 of parturition
o abundant data support its important
role during second-stage labor & in
the puerperium - phase 4 of
parturition
oxytocin levels:
(1) during second-stage labor - end
of phase 3 of parturition
(2) in the early puerperium
(3) during breast feeding
Immediately after delivery of the fetus,
placenta, and membranes
o Completion of parturition phase 3
o (+) firm and persistent uterine
contractions and myometrial
retraction
hemorrhage
o Oxytocin - causes persistent
contractions
o Oxytocin infusion in women
myometrial genes
encode proteins essential
for uterine involution
These include interstitial
collagenase, monocyte
chemoattractant protein-1,
IL-8, and urokinase
plasminogen activator
receptor.
Therefore, oxytocin action at
the end of labor may be
involved in uterine involution
Prostaglandins and Phase 3 of Parturition
(+) critical role in phase 3 of parturition
o
noncomplicated pregnancies
First, levels of prostaglandins, or their
o In amnionic fluid, maternal plasma,
and maternal urine
Second, Tx of pregnant women with PG =
abortion or labor at all gestational stages
o At any route of administration
(+) giving of prostaglandin H synthase type 2
(PGHS-2) inhibitors to pregnant women
o Delay onset of spontaneous labor &
may arrest preterm labor
Last, PG Tx of myometrial tissue in vitro
o causes contraction
o dependent on the prostanoid tested
& physiological status of the tissue
treated.
3
Uterine Events Regulating Prostaglandin
Production.
During labor, PG production within the
myometrium and decidua
o efficient mechanism of activating
contractions.
o For example, PG synthesis is high
and unchanging in the decidua
during phase 2 and 3 of
parturition
o 2 in the
decidua at term
regulatory step in PG action
in the uterus.
myometrium synthesizes PGHS-2 with labor
onset
o most PG likely comes from the
decidua
The fetal membranes and placenta also
produce PGs
o Primarily PGE2, but also PGF2
o detected in AF at all gestational
stages
o
demonstrable after labor begins
o results to the dilatation of the cervix
& decidual tissue exposure
o
with those in the upper compartment
follow an inflammatory
labor.
o Together, the increases in cytokines
and prostaglandins
degrade the EC matrix =
weakening of fetal
membranes.
o inflammatory mediators
aid cervical dilatation
alterations to the lower
uterine segment
It can be envisioned that they, along
with the increased prostaglandin
levels measured in vaginal fluid
during labor, add to the relatively
rapid cervical changes that are
characteristic of parturition.
Endothelin-1
family of 21-amino acid peptides
o powerfully induce myometrial
contraction
endothelin A receptor - preferentially
Endothelin-1
o produced in myometrium of term
gestations
o able to induce synthesis of other
contractile mediators
such as PG and
inflammatory mediators
(+) requirement of endothelin-1 in normal
parturition physiology
However, there is evidence of pathologies
associated with aberrant endothelin-1
expression
o such as premature birth and uterine
leiomyomas
Angiotensin II
2 G-protein-linked angiotensin II receptors
expressed in the uterus: AT1 and AT2
o nonpregnant women - AT2 receptor
is predominant
o
expression
Angiotensin II binding to the plasma-
membrane receptor = contraction
During pregnancy, vascular smooth muscle
(+) expression of AT2 receptor
o refractory to the pressor effects of
infused angiotensin II
In myometrium near term, angiotensin II
may be another component of the uterotonin
system of parturition phase 3
Contribution of Intrauterine
Tissues to Parturition
the amnion, chorion laeve, and decidua
parietalis
o have a potential role in parturition
initiation
o plays an alternative role
The membranes and decidua
o make up an important tissue shell
around the fetus
o serves as a physical, immunological,
and metabolic shield
to protect against untimely
initiation of parturition.
Late in gestation, however, the fetal
membranes may indeed act to prepare for
labor.
Amnion
Provides virtually all of the tensile strength of
the fetal membrane
o (+) resistance to tearing and
rupture
avascular tissue
highly resistant to penetration by leukocytes,
microorganisms, and neoplastic cells
constitutes a selective filter
o to prevent fetal particulate-bound
lung and skin secretions from
reaching the maternal compartment
o maternal tissues are protected from
amnionic fluid constituents
myometrial function
amnionic-fluid embolism
Several bioactive peptides and
prostaglandins that cause myometrial
relaxation or contraction are synthesized in
amnion
prostag
PLA2 and PGHS-2
Accordingly, many hypothesize that PG
regulate events leading to parturition.
Amnion - major source for AF
prostaglandins
o (+) role in activation of cascades =
4
 promote membrane rupture
o n-derived PG
on uterine quiescence & activation
due to PG transport from
the amnion thru the chorion
to access maternal tissues
limited by expression of the
inactivating enzyme,
prostaglandin
dehydrogenase.
Chorion Laeve
primarily protective tissue layer
(+) immunological acceptance
enriched with enzymes that inactivate
uterotonins:
o prostaglandin dehydrogenase
Parturition
(PGDH) - inactivates amnion-
derived PG
o oxytocinase
o enkephalinase
influence adjacent decidua and myometrium
during labor.
o - stimulated matrix
metalloproteinase activity
associated with membrane
rupture
o It would further allow prostaglandin
entry into the maternal compartment
to promote myometrial
contractility
progesterone - maintains chorion PGDH
expression
cortisol - decreases PGDH expression.
o
PGDH levels
part of progesterone
withdrawal
Decidua
A metabolic contribution of decidual
activation to parturi- tion initiation is an
appealing possibility for both anatomical and
functional reasons.
(+) generation of decidual uterotonins
o paracrine action on contiguous
myometrium is intuitive.
(+) steroid metabolizing enzymes expression
o 20 -HSD and eroid 5 R1
may regulate local
progesterone withdrawal
Decidual activation is characterized by:
o increased proinflammatory cells
o increased expression of
proinflammatory cytokines, PG and
uterotonins
Uterotonins such as
oxytocin receptors and
connexin 43
Cytokines produced in the decidua
o increase uterotonin production
(principally prostaglandins)
o act directly on myometrium to cause
contraction.
o Examples: tumor necrosis factor-
(TNF- ) and in erle kin 1, 6, 8, and
12.
also can act as chemokines
recruit to the
myometrium
neutrophils and
eosinophils
further increase
contractions and
labor
There is uncertainty whether prostaglandin
concentration or output from the decidua
increases with term labor onset.
Olson and Ammann (2007) suggest that the
major regulation of decidual prostaglandin
action is not their synthesis but rather
increased PGF2 receptor expression.
Summary: Regulation of Phase 3 and 4 of
It is likely that multiple and possibly
redundant processes contribute to the
success of the three active labor phases
once phase 1 of parturition is suspended
and phase 2 is initiated.
Phase 3
o -
protein-coupled receptors
stores
(+)interaction of actin and
myosin = force generation.
Simultaneously, (+) alteration of cervical
proteoglycan composition and collagen
structure
o promotes tissue distensibility and
increased compliance.
NET RESULT:
o initiation of coordinated myometrial
contractions
with sufficient amplitude and
frequency
= cervical dilatation &
pushing of fetus thru birth
canal
Multiple regulatory ligands orchestrate these
processes and vary from endocrine
hormones such as oxytocin to locally
produced prostaglandins.
In phase 4 of parturition
o Initiation of a complicated series of
repair processes
to resolve inflammatory
responses
to remove
glycosaminoglycans,
proteoglycans, and
structurally compromised
collagen.
Simultaneously, (+) synthesis of matrix and
cellular components = complete uterine
involution. (+) reformation of dense
connective tissue and structural integrity of
the cervix
5
 STAGES OF LABOR
Stages of labor
- Belong to phase 3 of parturition (processes/ stimulation)

Early phase of labor/ Phase 1 Parturition

Characterized by quiescent phase
Uterus should not contract excepts during episodes of Braxton-hicks contractions
We need the uterus to be relaxed because it still has a growing fetus inside that needs all the
space and all the time to develop until it reaches term

Phase 2 Parturition (preparedness/ preparation)

major changes happen both in uterus and cervix
Cervix needed for dilatation end effacement at the time of delivery
Uterus needed for contraction
— Formation of lower uterine segment happens
Isthmus/ isthmic portion forms lower uterine segment
Lower uterine segment passive segment
Upper portion more active segment; where contraction happen and receives all the action
from the uterus
Uterotubal portion Site/ pacemaker of contractions of the uterus; where all the actions
would have to come from
Uterine smooth muscles generate multidirectional courses that would generate
contractions, but these contractions must come from the upper segment/ fundus of the
uterus

What happens to the cervix during phase 2?

— Uterus and cervix is being prepared
Uterus
prepared for more contractions to happen
more gap junctions are being stimulated, more connexin 43 are there and more
contractile proteins are available for the release of oxytocin for more stimulation of
oxytocin receptors and therefore more uterine contractions
Cervix
must always be closed during phase 1 to prevent any form of miscarriage
At the time patient enters labor and delivery, there will be breakdown of collagen
fibers, particularly
Dermatan sulfate holds the fibers of the cervix together in such a way that it
does not give in to any Braxton-hicks contraction during the phase 1 parturition
A competent cervix is very important because we want to keep the pregnancy
intact, only to open by the time the pregnancy is to be delivered/ terminated
because the fetus is already term
Cervix becomes dilated due to more absorption of water due to the presence of
hyaluronic acid
Hyaluronic acid GAG that helps retain water making the cervix softer, flexible
and more pliable to whatever changes that would come from the uterus from the
upper segment
At the time the cervix is ready, the formation of the lower uterine segment makes
he pa ien e perience a cer ain form of dropping do n of he bab kno n a
lightening
Lightening decrease in fundic height may be felt; head may already occupy
the lower uterine segment, ready to be engaged/ enter the pelvic inlet in
preparation for labor

Phase 3 of Parturition
— Time of activation/ stimulation
— Define the different stages of labor

1
 st
1 Stage of Labor: Clinical Onset of Labor
- Encompasses the onset of cervical dilatation and effacement and ends with full (10cm) cervical dilatation and
effacement
- In some women, beginning of forceful uterine contractions that effect delivery
- In others, labor initiation is marked by spontaneous release of a small amount of blood-tinged mucus from the
vagina or b d
Show/ bloody show
— extrusion of mucus plug that had previously filled the cervical canal during
pregnancy
— it indicates that labor is already in progress and will likely ensure in hours to
days

o Cervical Changes
two fundamental changes due to contraction forces: Effacement and dilatation
1. Cervical Effacement
— thinning
— obli era ion or aking p of he cer i o ard he lo er erine egmen
shortening of the cervical length
— normal cervical length: 3cm
If there is 50% cervical effacement noted cervical length of 1.5cm from
the lower uterine segment until the edge of the cervix
2
 If cervix is 4cm dilated and 80% effaced means there is more
shortened cervical length, cervical length of 0.6cm
Fully dilated cervix or 100% effacement cervix is completely in
complement with that of the lower uterine segment, therefore lip of the
cervix is not felt anymore
— Length of the cervix at the time of labor
— manifest clinically by shortening of the cervical canal from a length of
approximately 2cm to a mere circular orifice with almost paper-thin edges
Internal cervical os --muscular fibers at this the level are pulled upward, or
aken p , in o he lo er erine egmen
External cervical os remains temporarily unchanged
— may be compared to a funneling process in which the whole length of a narrow
cylinder is converted into a very obtuse, flaring funnel with a small cervical
opening
effacement is sometimes accomplished before active labor begins due
to increased myometrial activity
— causes expulsion of the mucous plug as the cervical canal is shortened
2. Cervical Dilatation
— The force exerted by the presenting part makes the cervix open, increasing the
cervical diameter
Internal os diameter measured to measure the cervical dilatation
Patulous cervix external os is open, internal os is still closed; seen in
multiparus patients
During internal exam, insert fingers inside, separate the labia using the
thumb and pinky, insert one finger at a time, rotate 280 degrees and
search/ palpate for the cervix
Evaluate if arching is already in the cervix early onset of labor
Regular pains, regular contractions, ruptured membranes verify using
speculum exam if bag of water is indeed ruptured by observing for pooling
of fluid in the posterior lip of the speculum, check for cervical dilatation,
check for the bloody show
During the entire time of pregnancy, uterus is protected from the vaginal
environment by the mucus plug and once labor starts, the mucus plug is
expelled because of the contractions exposes what is inside the uterine
cavity with that of the vaginal environment
How to look for the cervix? Insert finger downward, posteriorly, reach for
the posterior fornix and then turn upwards and midline and feel for a
depression that your fingers may feel into, feel for the crater cervical os
If patient is still preterm/ not yet into labor, cervix is still pointing
downwards and you will have to go through the posterior fornix to reach
for the cervical os
If patient is in true labor, by the time that fingers are put inside, the cervix
will be meeting you right in the middle
— 10cm dilation for an average-size fetal head to pass through the cervix
— Presenting part descends somewhat as the cervix dilates
nd
During 2 stage of labor: nulliparas presenting part descends slowly
and steadily; multiparas rapid descent
— created by the centrifugal pull exerted on the cervix this is because the lower
segment and cervix have lesser resistance during a contraction
As uterine contractions cause pressure on the membranes, hydrostatic
action of the amniotic sac dilates cervical canal
Absence of intact membranes still with effective pressure of the
presenting part against the cervix and lower uterine part
Early rupture of membranes does no retard cervical dilation as long as
presenting fetal part is positioned to exert pressure against cervix and
lower uterine segment
— Divided into:
a. Latent phase
Its duration is more variable and sensitive to changes by extraneous
factors
Sedation may prolong latent phase; Myometrial stimulation may
shorten it
Has little bearing on course of labor
b. Active phase
Subdivided further into:
Acceleration phase
Phase of maximum slope
Deceleration phase
Usually predicted of labor outcome
During this phase, completion of cervical dilatation is accomplished
by cervical retraction about the presenting part

3
 Cervical effacement + dilation formation of the forebag of amniotic fluid (leading portion of fluid and
amniotic sac located in front of presenting part

o Uterine Labor Contractions

— Painful uterine smooth muscle contractions
— Cause is unknown, but several possibilities have been suggested:
1. Hypoxia of the contracted myometrium (similar to angina pectoris)
2. Compression of nerve ganglia in the cervix and lower uterus by contracted interlocking
muscle bundles
3. Cervical stretching during dilatation
4. Stretching of the peritoneum overlying the fundus
Paracervical infiltration with local anesthetic usually produces pain relief with contractions
— Involuntary and independent of extrauterine control
— Its intensity and frequency cannot be diminished by neural blockade from epidural anesthesia
Ferguson reflex mechanical stretching of cervix enhances uterine activity
Manip la ion of he cer i and ripping he fe al membrane associated with increase blood
levels of prostaglandin F2a metabolite (PGFM)

Interval between contractions diminishes gradually (from 10 minutes to as little as 1 minute or

nd
less) in the 2 stage of labor
Periods of relaxation between contractions essential for fetal welfare
Unremitting contractions compromise uteroplacental blood flow causing fetal hypoxemia
Active-phase labor 30-90 seconds (average 1 min) duration of contraction
Normal labor has variable contraction intensity
40mmHg (range: 20-60mmHg) amniotic fluid pressures generated by contractions during
spontaneous labor

o Distinct Lower and Upper Uterine Segments

— anatomical uterine divisions become increasingly evident
— can be differentiated by abdominal palpation even before membranes rupture
Upper segment
— firm during contractions
— contracts, retracts and expels fetus
— its myometrium does not relax to its original length after contractions
— becomes relatively fixed at a shorter length
— contracts down on its diminishing contents, but myometrial tension remains constant
Uterine musculature is kept in firm contact with uterine contents
As a consequence of retraction, each successive contraction commences
where it predecessor left off resulting to a slightly smaller upper part of the
uterine cavity with each successive contraction shortening of the muscular
st
fibers leads to thickening of the upper active segment throughout the 1 and
nd
2 stage of labor
This process continues resulting to a thickened upper uterine segment
immediately after deliver
Upper segment retraction decrease in volume of its contents
Lower segment
— softer, distended and more passive
— dilate together with cervix and form a greatly expanded, thinned-out tube through
which fetus can pass
— Its musculature must stretch, particularly in early labor when cervical dilatations is
minimal, to facilitate the decrease in the volume of contents in the upper segment
— Its relaxation mirrors the same gradual progression of retraction
With labor, successive lengthening of the fibers of the lower segment is
accompanied by thinning

4
 Lower segment thinning + upper segment thickening= physiological retraction
ring
Physiologic retraction ring boundary between the upper and lower
segments
Pathological retraction ring (ak.a. Bandl ring) abnormal condition
described as a prominent ring during extreme thinning of lower uterine
segment; seen in obstructed labor
— this mechanism is imperative because if entire myometrium (including lower segment and cervix)
were to contract simultaneously and with equal intensity decreased net expulsive force
Upper Segment Lower Segment

- active - passive

- firm during - softer

contraction
- contracts - dilates
- retracts - distends/ stretches

- expels fetus - forms a tube for

fetus to pass
- shortens - lengthens

- thickens - thinnig

o Changes is Uterine Shape during labor

— elongation of ovoid uterine shape with a decrease in horizontal diameter during each contraction
— importance in labor process:
1. Increase in fetal axis pressure
— Decreased horizontal diameter serves to straighten the fetal vertebral column
resulting in the upper pole of the fetus pressed firmly against the fundus and
lower pole is further thrusted downward
— Lengthening of ovoid shape 5-10cm
2. With the lengthening of the uterus, the longitudinal muscle fibers are drawn taut
— Lower segment and cervix are the only parts of the uterus that are flexible
pulled upward and around the lower pole of the fetus

o Ancillary Forces in Labor

produced by maternal intraabdominal pressure
Pushing contraction of the abdominal muscles simultaneously with forced respiratory efforts
with the glottis closed
Force is similar to that of defecation but with greater intensity
Importance of intraabdominal pressure shown in prolonged descent in labor in paraplegic
women and those with dense epidural block
nd
Increased in intraabdominal pressure is necessary to complete the 2 stage of labor (only
nd
instruct the patient to push during the 2 stage of labor/ if 10cm or fully dilated)
5
 st
Pushing in the 1 stage of labor is unnecessary may exhaust the mother and harm the fetus
by increasing intrauterine pressures
nd
2 Stage of Labor: Fetal Descent
- from full cervical dilatation until the expulsion of the fetus
Patient may have full cervical effacement but still not fully dilated
- part of the labor where mother plays the most active role
- time when the patient is asked to push (success of the vaginal delivery largely comes from the effort of the
mother in pushing)
only ask mother to push by the time that she is fully dilated avoid exhausting the mother
exhaustion of mother during pushing may be indicative of cesarean/ abdominal delivery
- Nulliparas engagement of fetal head is accomplished before labor begins
- Head may not further descend until late in labor
- Descent pattern of labor a typical hyperbolic curve is formed when station of fetal head is plotted as a
function of labor duration
Station descent of fetal biparietal diameter in relation to a line drawn between maternal ischial
spines
- Active descent takes place after filatation has progressed
Nulliparas increased rate of descent are observed ordinarily during cervical dilatation phase of
maximum slope
At this time, speed of descent is maximal and is maintained until the presenting part reaches the
perineal floor

o Pelvic Floor Changes During Labor

— Birth Canal supported and is functionally closed by several layers of tissues that together form
the pelvic floor
— Marked changes in the biomechanical properties of levator ani muscle and fibromuscular
connective tissue covering its upper and lower surfaces and of the vaginal wall during
parturition results from altered extracellular matrix structure or composition
Levator ani
— Consists of pubovisceral, puborectalis and iliococcygeus muscles
— Close the lower end of the pelvic cavity as a diaphragm
Concave upper and a convex lower surface
— Varies in thickness from 3-5mm; thicker in margins encircling the rectum and
vagina
— Undergoes hypertrophy during pregnancy forms a thick band that extends
backwards from the pubis and encircles the vagina about 2cm above the plane
of the hymen
— Draws both the rectum and vagina forward and upward in the direction of the
symphysis pubis upon contraction and thereby acts to close the vagina
— Posterior and lateral portions of the pelvic floor occupied bilaterally by the piriformis and
coccygeus muscles

6
 st
In the 1 stage of labor intact membranes and fetal presenting part serve to dilate the
upper vagina
Stretching of the levator ani muscle fiber most marked change
Accompanied by thinning of the central portion of the perineum from a wedge- shaped,
5cm thick tissue mass to a thin, almost transparent membranous structure less than 1cm
thick.
When perineum is distended maximally, anus becomes dilated and presents an opening
that varies from 2-3cm in diameter and though which the anterior wall of the rectum bulges

rd
3 Stage of Labor: Delivery of Placenta and Membranes
- Fetal deliver until the expulsion of the placenta
- Begins immediately after fetal delivery and involves separation and expulsion of the placenta and membranes
- As neonate is born, uterus spontaneously contracts
- By the time the newborn is completely delivered:
uterine cavity is nearly obliterated
Uterus consists of an almost solid mass of muscle, several centimeters thick, above the thinner
lower segment
Uterine fundus below the level of the umbilicus
- Sudden decrease in uterine size accompanied by a decrease in the area of the placental implantation site
Placenta increases in thickness, but because of limited placental elasticity, it is forced to buckle
Resulting tension pulls weakest layer (decidua spongiosa) from that placental implantation site
Placental separation due to disproportion created between relatively unchanged placental size
and the reduced size of the implantation site
- Cleavage of placenta aided greatly by the loose structure of the spongy decidua
- Hematoma formed between the separating placenta/ decidua and the decidua that remains
attached to the myometrium; usually a result rather than the cause of placental separation

o Fetal Membrane Separation and Placental Extrusion

— Great decrease in uterine cavity surface area simultaneously throws fetal membranes
(amniochorion and the parietal decidua) into innumerable folds
— Membranes remain in situ until placental separation is nearly completed
— Causes of peeling off of membranes from the uterine walls:
further contraction of myometrium
traction exerted by the separated placenta

7
 Increase abdominal pressure facilitated expulsion after the placenta has separated
rd
Completion of 3 stage accomplished by alternately compressing and elevating the fundus
while exerting minimal traction on the umbilical cord
Retroplacental hematoma either follows the placenta or is found within the inverted sac formed
by the membranes

2 Mechanisms of Placental Expulsion:

1. Schultze mechanism
— Blood from the placental site pours into the membrane sac and does not escape
externally until after extrusion of the placenta
— Central mechanism of placental deliver
— Shiny side comes out (Shiny Shultze)
— Not much blood is coming out at this point because the placental will form like
an umbrella which will be filled up by blood that will come out later on (placenta
comes out first)
— Retroplacental type of hematoma will be formed
2. Duncan mechanism
— the placenta separates first at the periphery and blood collects between the
membranes and the uterine wall escapes from the vagina
— placenta descends sideways and its maternal surface appears first
— peripheral type of placental circulation
— reddish part comes out/ maternal side comes out first (DirtyDuncan)
— cotylidons will be seen
— blood will come out first before the placenta that will come out later on
CS(Central Schultze)
MD (Maternal Duncan)
th
4 Stage of Labor
- first hour after the placental delivery
- gives overview of how much bleeding the patient has had during labor and delivery
500 ml expected blood loss for vaginal deliver
1L for CS
>500ml blood loss in vaginal delivery or >1L for CS manifested in the changes in the vital signs
st
of the patient during the 1 hour of delivery
- more frequent monitoring is needed for early detection of excess bleeding and early treatment/ management

Signs that patient has excess bleeding during the first hour after delivery:
- Checheck HR increased
>90bpm indica e ha ome hing i rong i h he pa ien ; peak in ide he pa ien agina and
see if the patient is bleeding too much (is she soaking the bed linen because of too much blood
loss)
- Check for BP Hypotension
- Check urine output decreased

Initial IE tells you:

- dilatation
- effacement
- station of the presenting part
- presentation
- whether bag of water in intact or not

8

TOPICS:
2nd-4th Stage of Labor
Episiotomy & Episiorraphy
Uterine Atony
Second(24
BLACK Stage
TH EDofWilliams)
Labor ORANGE (LaLaLaLa Notes)
begins with complete cervical dilatation
(10cm) and ends with fetal delivery
o median duration is approx 50min
(nulliparas) and about 20min
(multiparas)
In a woman of higher parity with a previously
dilated vagina and perineum
o two or three expulsive efforts after full
cervical dilatation may suffice to
complete delivery.
Conversely, second stage may become
abnormally long in women:
o with a contracted pelvis
o with a large fetus
o with impaired expulsive efforts from
conduction analgesia or sedation
Robinson and colleagues (2011) found that
increasing maternal body mass index did not
interfere with the second stage of labor
Duration of Labor
Our understanding of the normal duration of
labor may be clouded by the many clinical
variables that affect conduct of labor in
modern obstetrical units.
the mean length of first- and second-stage
labor
o was approx 9 hours in nulliparous
women w/o regional analgesia
(Upper Limit of 18.5hr)
o Corresponding times for multiparous
women were a mean of 6 hours (UL:
13.5 hrs)
labor onset is defined as the time when a
woman recalled:
o regular, painful contractions q3-5 min
-> cervical change
Parity nulliparous versus multiparous and
cervical dilatation at admission were
significant determinants of the length of
spontaneous labor.
o The median time from admission to
spontaneous delivery for all
parturients
Equates to 3.5 hours (UL:
10.1 hours)
These results suggest that normal human
labor is relatively short.
Risk Factors for prolonged 2nd Stage:
o Maternal weight / weight gain
o Nulliparity
o Use of conduction/regional
anesthesia
o Fetal OP (occiput posterior) position
o Increased BW
Management of the Second Stage of Labor
With full cervical dilatation (onset of the
second stage) -> begins to bear down
With descent of the presenting part -> (+)
develops the urge to defecate.
Uterine contractions and the accompanying
expulsive forces
o may now last 1min and recur at an
interval no longer than 5.5mins
the median duration of the second stage:
o 50 minutes in nulliparas
abnormal if >2hr w/o
anesthesia; >3hrs w/
anesthesia
o 20 minutes in multiparas
abnormal if >1hr w/o
anesthesia; >2hrs w/
anesthesia
Monitoring of the fetal heart rate and
interpretation of second-stage electronic fetal
heart rate patterns should be assessed
Expulsive Efforts
In most cases, bearing down is reflexive and
spontaneous during second-stage labor.
o Occasionally, a woman may not
employ her expulsive forces to good
advantage and coaching is desirable.
o legs should be half-flexed -> push with
them against the mattress
When the next uterine contraction begins
o (+) instructed to exert downward
pressure (straining to defecate)
A woman is not encouraged to push beyond
the completion of each contraction.
o Instead, she and her fetus should be
allowed to rest and recover.
During this period of actively bearing down
o the fetal HR appears to be slow (STAT
auscultation after contraction) but
should recover to normal before the
next expulsive effort
Several positions during the second stage have
been recommended to augment pushing
efforts.
o supported upright position than
recumbent one
Upright positions include
sitting, kneeling, squatting, or
resting with the back at a 30-
degree elevation.
Fetal and obstetrical outcomes appear to be
unaffected whether pushing is coached or
uncoached during second-stage labor
o Women coached to push during
second-stage labor had decreased
bladder capacity and decreased first
urge to void compared with women
encouraged to push or rest as desired.
(+) head descends through the pelvis ->
perineum begins to bulge and the overlying
skin becomes stretched.
o (+) fetal scalp visible through the
vulvar opening
o At this time, the woman and her fetus
are prepared for delivery
Management of 2nd Stage of Labor
1. Monitoring of Fetus and Mother
a. Low Risk Pregnancies
i. FHR q15min after each
contraction
ii. Fetal heart tones best heard
after contraction or 1-2mins
before peak of contractions
b. High Risk Pregnancies
i. FHR q5min
c. Slowing of FHR during this stage
maybe due to compression of head
during descent (but not all)
i. Other reasons: cord
compression or tightening of
1
 nuchal cord, premature
placental separation
d. Monitor FHR after contractions
i. Determines the response of
FHR to temporary loss of
oxygenation
2. When do we ask mothers to push?
a. 2nd stage of labor
b. during contractions with full cervical
dilatation
3. Preparation for Delivery
a. Assume a dorsal lithotomy position
leg flexed
i. Asked to breathe normally
until start of contraction when
they are asked to strain down
ii. Push sustained as long as
possible
iii. Ideal position because it inc.
pelvic outlet diameter
b. Strict asepsis and antisepsis (sterile
gown, cap, mask)
i. Perineal area scrubbed w/
antiseptic solution
ii. Apply antiseptic first before
sterile drapes are applied
4. Delivery of the Head and Episiotomy
a. Perineal opening becomes ovoid to
circular with the descent of the fetal
presenting part
b. Perineum is stretched to almost paper
thin
c. Crowning event wherein fetal head is

encircled by the vulvar ring
i. sign that episiotomy can be
done
Active Management of Labor
(+) concept that a disciplined, standardized labor

management protocol reduced the number of
cesarean 
deliveries for dystocia. 
 firmness
Two of its components amniotomy and
oxytocin 
have been widely used 
 boggy uterus suggests uterine
With this protocol, labor is diagnosed when
painful 
contractions are accompanied by: 
 If uterus is firm but with
o complete cervical effacement
o blood ho 
 vaginal lacerations
o ruptured membranes
Women with such findings are committed to
delivery within 12 hours.
o Pelvic examination -> performed q1hr
(for the next 3hr) -> 2-hour intervals
thereafter
o amniotomy is performed - dilatation has
not increased by at least 1 cm/hr
o Progress is again assessed at 2 hours
high-dose oxytocin infusion is
started unless dilatation of at
least 1 cm/hr is documented
Women are constantly attended by midwives.
If membranes rupture before admission,
oxytocin is begun for no progress at the 1-hour
mark.
This type of management somewhat shortened
labor but did not affect the cesarean delivery
rate
THIRD STAGE OF LABOR Stage of Placental
Separation and Expulsion
Begins after delivery of fetus until delivery of
the placenta
o Usually begins 5-10mins after fetal
delivery
o May require <10min but may last as
long as 30mins
If beyond this, consider active
intervention
Interference in the absence of
hemorrhage may cause:
hemorrhage, uterine inversion,
and placental entrapment
Signs of Placental Separation
o Calkin s Sign (earliest)
Change in uterine shape from
discoid -> globular (contraction)
o Blood how from the vagina
Cord lengthening
o Uterus rises in abdomen as placenta
descends to lower uterine segment or
vagina
(+) upward uterine displacement
rd
Active Management of 3 Stage of Labor
o Before, they used to just wait for the
placenta to go out. Now, there is
active management
Get anesthesia for uterine
relaxation
(+) gloving & sterile
gowning -> insert fingers
inside (remove remnants
similar to tearing of pages
in a book)
o Do gentle and downward cord traction
o One hand is placed on the abdomen
and uterus is pushed cephalad until
placenta reached intoitus
When majority of placenta is
out, gently grasp with both
hands and pull while twisting
the placenta allowing
separation of the fetal
membranes
o Massage fundus until contraction is felt
Palpate abdomen to confirm
reduction in size of uterus and
Ongoing blood loss and soft
atony
ongoing blood loss
(+)Consider cervical or
o Start oxytocin drip or give ergot
derivatives (contraindicated to Px with
HPN)
FOURTH STAGE OF LABOR
1hr immediately ffing placental delivery
critical period and where lacerations are repaired
(+) admini ra ion of ero onic ake place
o for tx of postpartum hemorrhage as the
result of uterine atony
Uterine tone and perineum should be evaluated
frequently
Maternal BP and pulse should be recorded STAT
after delivery & q15min for the first 2hrs.
o Recommended by the American
Academy of Pediatrics and the
American College of Obstetricians and
Gynecologists (2012)
Examination for completeness of the ffing
structures:
o Placenta, membranes, and umbilical
cord
2
 Birth Canal Lacerations

Lower genital tract lacerations

o involves the cervix, vagina, or perineum
Perineal tears - follows any vaginal delivery &
classified as BCL
3rd and 4th-degree lacerations - higher-order
lacerations
o Short-term assoc. with éblood loss,
puerperal pain, and wound disruption or
infection risk
o Long-term (0.25-6%) linked with inc.
rates of anal incontinence and
dyspareunia.
Risk factors for these more complex lacerations
o midline episiotomy, nulliparity, longer
second- stage labor, precipitous
delivery, persistent OP position,
operative vaginal delivery, Asian race,
and inc. fetal BW
Epidural analgesia was found to be protective
Mediolateral episiotomy - most powerful predictor of
wound disruption.

Episiotomy

Greek episton pubic region plus tomy to cut.

o incision of the pudendum the external
genital organs.
Perineotomy incision of the perineum
the term episiotomy often is used synonymously
with perineotomy
o common to practice
midline incision è creating a median or midline
episiotomy
begin at midline and directed laterally and
downward away from the rectum -> mediolateral
episiotomy Episiotomy Type and Timing

Before episiotomy, analgesia may be provided thru:

Episiotomy Indications and Consequences
episiotomy - common obstetrical procedure
o use has inc. over the past 30 years
(age-adjusted rate)
Primipara common practice to cut an episiotomy
(1970s)
o Easier to repair due to a straight surgical
incision
Less operative pain, improved healing, prevention
of pelvic floor disorders with episiotomy
o Still has no evidence
Routine Episiotomy - assoc with dec. incidence of
anal sphincter & rectal tears but with inc.
incidence of anterior perineal trauma
o (+) anal sphincter incontinence inc.
risk of higher-order lacerations
fecal and flatal incontinence
increased rates of posterior perineal trauma,
surgical repair, and healing complications
o women managed with a restrictive use
of episiotomy
o routine used by the American College of
Obstetricians and Gynecologists
(2013a)
episiotomy should be considered for indications
such as:
o shoulder dystocia, breech delivery,
macrosomic fetuses, operative vaginal
deliveries, persistent OP positions
o other instances in which failure to
perform an episiotomy will result in
significant perineal rupture
FINAL RULE: no substitute for surgical judgment
and common sense
o Labor epidural analgesia
o bilateral pudendal nerve blockade
o infiltration of 1% lidocaine
Bleeding from the episiotomy
o During the interval b/w incision and
delivery due to unnecessarily early
administration
(+) Lacerations - If performed too late
Typically, episiotomy is completed when the
head is visible during a contraction to a diameter
of approximately 4 cm, that is, crowning.
When used in conjunction with forceps delivery,
most perform an episiotomy after application of
the blades.
Technique
For midline episiotomy
o fingers - insinuated between the
crowning head and the perineum
o scissors - positioned a 6 o clock on he
vaginal opening and directed posteriorly
o incision length - varies from 2 to 3 cm
depending on perineal length
and degree of tissue thinning
incision is customized for
specific delivery needs
should stop before reaching
external anal sphincter.

3
 For mediolateral episiotomy
scissors - po i ioned a 7 o clock or a 5
o clock
incision - extended 3 to 4 cm toward the
ipsilateral ischial tuberosity
inc. in severe perineal lacerations
(+) protective effect against higher-order
lacerations when used during operative vaginal
delivery
midline episiotomy is superior - third and fourth-degree
extensions

perineal suturing
oincrease dose for those with epidural
analgesia
Hemo a i and ana omical re ora ion /o
suture
o Essential for episiorrhaphy (repair)

Repair of Episiotomy or Perineal Laceration

episiotomy repair - deferred until the placenta has
been delivered.
o permits undivided attention to the signs
of placental separation and delivery
o Advantage
repair is not interrupted or
disrupted by the obvious
necessity of delivering the
placenta
specially if manual
removal must be
performed that may
disrupt a newly
repaired episiotomy.
o major disadvantage:
continuing blood loss until the
repair is completed
(+) Direct pressure from an
applied gauze sponge
will help to limit blood loss.
Adequate analgesia is imperative
o Local lidocaine
Used solely or as a supplement
to bilateral pudendal nerve
blockade.
o women w/o regional analgesia
(+)high levels of pain during
continuous or interrupted closure (+)similar
postoperative pain scores
o less suture material and faster
procedure = less pain
Blunt needles suitable & dec. incidence of
needlestick injuries
o The suture material commonly used is
2 0 chromic catgut
o Sutures made of polyglycolic acid
derivatives are also used
o Synthetic materials advantage is dec.
postsurgical pain
though occasionally require
suture removal from the repair
site because of pain or
dyspareunia
maybe reduced using a
rapidly absorbed
polyglactin 910 (Vicryl
Rapide).
Repair of a mediolateral episiotomy is similar to a midline
repair.

4

Fourth-Degree Laceration Repair
Two methods are used to repair a laceration
involving the anal sphincter and rectal mucosa.
o first is the end-to-end technique -
which we prefer
o second is the overlapping technique.
essential to approximate the torn edges of the
rectal mucosa with sutures placed in the rectal
muscularis approximately 0.5 cm apart
o choice is to use 2 0 or 3 0 chromic gut
o next is to cover this muscular layer by
o reapproximation of the internal anal
sphincter
o Finally, there are isolation,
approximation and suturing of the cut
ends of the external anal sphincter
together end-to-end with three or four
interrupted stitches
o remainder of the repair is the same as
for a midline episiotomy.
The overlapping technique - alternative method to
approximate the external anal sphincter
(+) recommends perioperative antimicrobial
prophylaxis
o for the reduction of infectious morbidity
assoc with higher-order perineal injury
repair
o single dose of a cephalosporin (2nd-
generation) is suitable
clindamycin for penicillin-
allergic women
Postoperatively, stool softeners should be given
o prescribed for a week
o enemas and suppositories should be
avoided.
Unfortunately, normal function is not always ensured even
with correct and complete surgical repair. Some women
may experience continuing fecal incontinence caused by
injury to the innervation of the pelvic floor musculature
Postepisiotomy Pain
Pudendal nerve blockade - aid relief of perineal
pain postoperatively
Locally applied ice packs - help reduce swelling
and allay discomfort
Topical application of 5% lidocaine ointment
o was not effective in relieving episiotomy
or perineal laceration discomfort
Analgesics such as codeine give considerable
relief
o pain may be a signal of a large vulvar,
paravaginal, or ischiorectal fossa
hematoma or perineal cellulitis
these sites should be examined
carefully if pain is severe or
persistent
o In addition to pain, urinary retention may
complicate episiotomy recovery
For those with second-degree or greater
lacerations
o intercourse is usually proscribed until
after the first puerperal visit
usually at 4 to 6 weeks.
CAUSES OF OBSTETRICAL HEMORRHAGE
The most important causes because of their
incidence or consequence of severe obstetrical
hemorrhage and their contribution to maternal
mortality rates
Fatal hemorrhage is most likely in circumstances in
which blood or components are not immediately
available.
the ability to provide prompt resuscitation of
hypovolemia and blood administration is an
absolute requirement for acceptable obstetrical
care.
Uterine Atony
most frequent cause of obstetrical hemorrhage
o failure of the uterus to contract
sufficiently after delivery and to arrest
bleeding from vessels at the placental
implantation site
some bleeding is inevitable during third stage labor
as the placenta begins to separate
o the Duncan mechanism of placental
separation immediate escape of the
blood from the implantation site to the
5
 vagina
o the Schultze mechanism remained
concealed behind the placenta and
membranes until the placenta is
delivered
With bleeding during the third stage
o uterus should be massaged if it is not
contracted firmly
o After the signs of separation, placental
descent is indicated by the cord
becoming slack.
Placental expression should be attempted by
manual fundal pressure
If bleeding continues, then manual removal of the
placenta may be necessary

Separation and delivery of the placenta by cord traction,

especially when the uterus is atonic, may cause uterine
inversion

Third-Stage Bleeding

Manual Placental Removal

o Indicated if significant bleeding persists
after delivery of the infant and while the
placenta remains partially or totally
attached
adequate analgesia is
mandatory
aseptic surgical technique
should be used.
o the placenta is peeled off its uterine
attachment Risk Factors
similar motion to that used in
separating the pages of a book In many women, uterine atony can at least be
o After its removal, trailing membranes are anticipated well in advance of delivery
removed the ability to identify which individual woman will
by carefully teasing them from experience atony is limited
the decidua Risk factors for retained placenta are similar
(+) use of ring forceps The magnitude of risk imposed by each of these
Another method is to wipe out the uterine cavity factors shown in Table 41-2 varies considerably
with a gauze-wrapped hand between reports

Uterine Atony after Placental Delivery

fundus should always be palpated following
placental delivery
o to confirm that the uterus is well
contracted
o If it is not firm, then do vigorous fundal
massage
prevents postpartum
hemorrhage from atony
o Simultaneously, 20 units of oxytocin in
1000mL of crystalloid solution
IV admin of 10 mL/min (dose of
200mU/min)
Proven to be effective
Higher concentrations are
minimally more effective
Never give Oxytocin (undiluted bolus)
Can develop serious
hypotension or cardiac
arrhythmias
o Primiparity has been cited as a risk factor
o High parity is a long-known risk factor for uterine
atony.
o The overdistended uterus - prone to hypotonia after
delivery
o Inc. risk for women with a large fetus,
multiple fetuses, or hydramnios
o Labor abnormalities predispose to atony
o Includes hyper- or hypotonic labor
o Labor induction or augmentation
o with either prostaglandins or oxytocin
o more likely to be followed by atony
o woman who has had a prior postpartum
hemorrhage
o risk for recurrence with a subsequent
delivery
Evaluation and Management

With immediate postpartum hemorrhage

o careful inspection is done to exclude
birth canal laceration
o bleeding can be caused by retained
placental fragments
do routine inspection of the
placenta after delivery
If a defect is seen, uterus
should be manually explored ->

6
 fragment removal
o Occasionally, retention of a
succenturiate lobe may cause post-
partum hemorrhage
During examination for lacerations and causes of
atony
o uterus is massaged and uterotonic
agents are administered
Uterotonic Agents
several compounds that prompt the postpartum
uterus to contract
One of these is routinely selected and given to
prevent postpartum bleeding
o by ensuring uterine contractions.
also used to treat uterine atony with bleeding
(+) given prophylactically will prevent most cases of
uterine atony
When atony persists despite preventive measures
o Ergot derivatives have been used for
Bleeding Unresponsive to Uterotonic Agents
second- line treatment
includes methylergonovine
(Methergine) and ergonovine
Only methylergonovine is
currently manufactured in USA
Given IM, (+) rapidly stimulate
tetanic uterine contractions (for
45mins)
0.2mg of either drug is
a common regimen
Disadvantage:
if given IV = dangerous
HPN with women w/
preeclampsia
severe HPN
concomitant use of
protease inhibitors
(HIV infection)
o E- and F-series prostaglandins
2nd line agents for atony in the
more recent years
Carboprost tromethamine
(Hemabate)
15-methyl derivative of
prostaglandin F2á
dose of 250 ìg (0.25
mg) IM Tx for
uterine atony (>25yrs)
can be repeated if
necessary o 15- to 90-
minute intervals (max
of 8doses)
Another pharmacological effect
pulmonary airway and
vascular constriction.
should not be used for
asthmatics and those
with suspected
amnionic-fluid
embolism
Side Effects (in descending
order of frequency):
Diarrhea
Hypertension
Vomiting
Fever
Flushing
Tachycardia
severe hypertension given to
women with preeclampsia
can cause arterial oxygen
desaturation
E-series prostaglandins have been used to prevent
or treat atony
o Dinoprostone (prostaglandin E2)
20-mg suppository per rectum
or per vaginam q2h
It typically causes diarrhea
which is problematic for the
rectal route whereas vigorous
vaginal bleeding may preclude
its use per vaginam
o Sulprostone (PGE2 IV) - used in
Europe, but not available in US
o Misoprostol (Cytotec) - synthetic
prostaglandin E1 analogue
evaluated for both prevention
and treatment of atony and
postpartum hemorrhage
From a systematic review, oxytocin and ergot
preparations administered after delivery were
more effective than misoprostol for prevention of
postpartum hemorrhage
Hemorrhage that persists despite uterine massage
and continued uterotonin administration may be
from a yet unrecognized genital tract laceration
(uterine rupture)
Thus, if bleeding persists after initial measures for
atony have been implemented, then the following
management steps are performed immediately
and simultaneously:
1. Begin bimanual uterine compression
which is easily done and controls
most cases of continuing
hemorrhage
This technique is not simply fundal
massage.
o The posterior uterine wall is
massaged by one hand on the
abdomen
o while the other hand is made into
a fist and placed into the vagina
This kneads the anterior
uterine wall through the
anterior vaginal wall
Concurrently, the uterus is
also compressed between
the two hands
2. Immediately mobilize the emergent-care
obstetrical team to the delivery room
and call for whole blood or packed red
cells
3. Request urgent help from the
anesthesia team.
4. Secure at least two large-bore IV
catheters
crystalloid with oxytocin is
continued simultaneously with
blood products
Insert an indwelling Foley
catheter
o for continuous urine
output monitoring.
5. Begin volume resuscitation with rapid
intravenous infusion of crystalloid
6. With sedation, analgesia, or anesthesia
established and now with optimal
exposure
once again manually explore the
uterine cavity
o for retained placental
fragments
o for uterine
abnormalities, including
lacerations or rupture.
7. Thoroughly inspect the cervix and
vagina again for lacerations that may
have escaped attention.
8. If the woman is still unstable or if there is
7
 persistent hemorrhage hemorrhage from atony and these includes:
(+)blood transfusions are given o uterine compression sutures
o pelvic vessel ligation
o angiographic embolization
At this juncture, after causes other than atony have o hysterectomy
been excluded and after hypovolemia is
reversed, several other measures are considered
if bleeding continues. Their use depends on
several factors such as parity, desire for
sterilization, and experience with each method.

Uterine Packing or Balloon Tamponade

Uterine packing was popular to treat refractory

uterine atony (1st half of the 20th century)
o (+) concealed bleeding and infection
subsequently fell from favor
Newer techniques have been described that
alleviate some of these concerns
o In one technique, the tip of a 24F Foley
catheter with a 30-mL balloon
guided into the uterine cavity
and filled with 60 to 80 mL of
saline
(+) open tip permits continuous
drainage of blood from the
uterus
If bleeding subsides,
the catheter is
typically removed after
12 to 24 hours
Similar devices that have been used for tamponade
include Segstaken-Blakemore and Rusch
balloons and condom catheters
Alternatively, the uterus or pelvis may be packed
directly with gauze
Enthusiasm has developed for specially
constructed intrauterine balloons to treat
hemorrhage from uterine atony and other causes
A Bakri Postpartum Balloon (Cook Medical) or BT-
Cath (Utah Medical Products)
o may be inserted and inflated to
tamponade the endometrial cavity and
stop bleeding
o Insertion requires two or three team
members
The first performs abdominal
sonography during the
procedure.
The second places the deflated
balloon into the uterus and
stabilizes it.
The third member instills fluid
to inflate the balloon
rapidly infusing at
least 150mL -> further
instillation over a few
minutes (for a total of
300 to 500 mL) to
arrest hemorrhage.

balloon tamponade + uterine compression = Good

Prognosis
Failures for all of these require various surgical
methods (hysterectomy)

Well-designed studies are needed before instituting

intrauterine balloon tamponade as a second-line treatment
for atony.

Surgical Procedures

Several invasive procedures can be used to control

8
Mentioned by lecturer: this magandang shade of
BLUE
Summary of LABOR:
Definition: Uterine contractions that bring about
demonstrable effacement and dilatation of the
cervix
Onset:
- commences with the time of admission
- Painful contractions become regular
intact membranes, then a cervical dilatation of 3
to 4 cm or greater is presumed to be a
reasonably reliable threshold for the diagnosis of
labor
Cervical dilatation in the absence of uterine
contractions = incompetent cervix
Uterine contractions without cervical changes =
NOT true labor
Admission criteria:
Uterine contractions plus any of the ff:
1. Ruptured membranes
2. Bloody show
3. Complete cervical effacement and dilatation
The ideal management of labor and delivery
requires two potentially opposing viewpoints on the
part of clinicians.
1. Birthing should be recognized as a normal
physiological process that most women experience
without complications
2. Intrapartum complications should be anticipated.
- clinicians must simultaneously make every
woman and her supporters feel comfortable and safe
- Call o Ac ion - provide detailed information
on the appropriate content of intrapartum care,
including both personnel and facility requirements
Admission Procedures
Early admittance to the labor and delivery unit is
important, especially if during antepartum care the
woman, her fetus, or both have been identified as
being at risk.
Identification of Labor
Differentiation between false and true labor -
can be clarified by contraction frequency
and intensity and by cervical dilatation.
o instances when a diagnosis of labor
cannot be established with certainty,
observation for a longer period is
often wise
In the absence of ruptured membranes or
bleeding, uterine contractions 5 minutes
apart for 1 hour ha i , 12 con rac ion in
1 hour may signify labor onset
Active labor defined a cer ical dila a ion
4 cm i h 12 con rac ion per ho r.
Women admitted during latent-phase labor
had more active-phase arrest, more frequent
need for oxytocin labor stimulation, and
higher rates of chorioamnionitis
Stage of cervical effacement and dilatation
Involves widely spaced uterine contractions
(intervals diminishes from 10 mins at onset
of stage 1 to 1 min or less in stage 2)
Period of relaxation in between is important
for fetal welfare
o Unremitting contractions may result
to fetal hypoxemia
3 parameters to assess in uterine
contractions:
1. Interval
2. Duration
3. Intensity
Has 2 phases: latent phase & active phase
1. Latent phase: period between the
onset of labor and when rate of
cervical dilatation changes most
rapidly (0-4cm dilatation)
Contractions are still not too
close to each other (8-10
mins interval)
Normal duration:
o 8 ½ hrs in
nulliparas
o 5 hrs in multiparas
Abnormal:
o > 20 hrs in
nulliparas
o > 12 hrs in
multiparas
2. Active phase: period of increased
rapidity of cervical dilatation
Contractions with 2-3mins interval (ideal), lasting
40-60 secs
Ends with full cervical dilatation at 10cm (also marks
the end of the first stage of labor)
Also coincides with descent of presenting
part into pelvis
Normal duration and rate of
dilatation:
o 5-7 hrs in nulliparas (1- 2cm/hr)
o 2-4 hrs in multiparas
(1.5cm/hr)
o Pelvic exams done every
o 2-3 hrs to evaluate labor progress
(lack of progress in
dilatation/descent may indicate
dystocia)
o *Crowning encirclement of the
largest head diameter by the vulvar
ring
Emergency Medical Treatment and Labor Act
EMTALA
Ensure public access to emergency services
regardless of the ability to pay
Must provide an appropriate screening
examination for any pregnant woman
experiencing contractions and presenting to
the emergency department for evaluation
Labor i defined a he proce of childbir h
beginning with the latent phase of labor
continuing through delivery of the placenta.
A woman experiencing contractions is in true
labor unless a physician certifies that after a
reasonable time of observation the woman is
in false labor.
A woman in true labor is considered
n able for in erho pi al ran fer p rpo e
until the newborn and placenta are delivered.
Electronic Fetal Heart Rate Monitoring
- routinely used for high-risk pregnancies
commencing at admission
- some recommend monitoring women with
low-risk pregnancies upon admission as a test of
fetal well being the so-called
Fetal admission test/ Labor Admission Test.
20 min EFM strip done on
admission
1
 Get heartbeat, acceleration and
deceleration in relation
to uterine contractions
Purpose: to find out whether
the fetus in utero can
undergo the stress of labor
If you have decelerations
while baby is in utero, you
expect that it will be worse
during labor
Allows you to detect high
risk/compromised fetuses
and allows for early
intervention
Studies show greater
benefit in using LAT for high
risk patients only
If no fetal heart rate abnormalities are
detected, continuous electronic monitoring is
replaced by intermittent assessment for the
remainder of labor.
Home Births
most studies suggest increased risks with
home deliveries
Initial Evaluation (lahat naman ito sinabi plus the
opinion of the all knowing ever researching
Williams MALIBAN NA LANG KAPAG
NAKASULAT na hindi)
1. Get px history (Gen data)
Chief complaint
o Vaginal bleeding
o Watery vaginal discharge
o Hypogastric pain
Ask how many hours,
intervals, if accompanied
by watery/bloody
discharge
Note the no. of hours she
has been experiencing them
because the longer the
bag of water has ruptured,
the higher the risk for
infection =
chorioamnionitis
increased maternal and
infant mortality and
morbidity
Menstrual hx (important for
determining AOG)
Obstetrical hx
o Ask for the ff: manner of
delivery in past pregnancies,
complications, duration of
labor, hx of difficult labor,
weight of babies (may indicate
a problem in descent or an
arrest in cervical dilatation)
2. Physical Exam
Get vital signs
o Temperature, pulse, and blood
pressure are evaluated at least
every 4 hours.
o If membranes have been
ruptured for many hours before
labor onset or if there is a
borderline temperature
elevation, the temperature is
checked hourly.
o With prolonged membrane
rupture, defined as greater than
18 hours, antimicrobial
administration for prevention of
group B streptococcal infections
is recommended
o Temperature: important in
chorioamnionitis
o BP is taken more frequently
during active phase (usually
timed after contraction) a
rise in BP is usually seen
during contraction
Abdominal exam
o Fundic height: important for
estimating fetal weight and
lightening (if FH is 35-36: this
may be a big baby)
o Leopold maneuver: LM3 allows
determination of presentation
o Uterine contractions (normal must
be alternating contract and relax)
o Uterine tenderness
o Tenderness over scar may
indicate dehiscence or possible
uterine rupture (abruption
placenta)
o Check for fetal heart tones
Pelvic exam
o Cervical dilatation, effacement,
station, presentation, position,
consistency of cervix
Cervical Assessment
usually is expressed in terms of the length of the
cervical canal compared with that of an
uneffaced cervix.
When the cervix becomes as thin as the
adjacent lower uterine segment, it is completely,
or 100-percent, effaced.
Cervical dilatation is determined by estimating
the average diameter of the cervical opening by
sweeping the examining finger from the margin
of the cervical opening on one side to that on the
opposite side.
The diameter traversed is estimated in
centimeters.
The position of the cervix is determined by the
relationship of the cervical os to the fetal head
and is categorized as posterior, mid-position, or
anterior
Consistency of cervix is determined to be soft,
firm, or intermediate between these two.
The level or station of the presenting fetal
part in the birth canal is described in relationship
to the ischial spines, which are halfway between
the pelvic inlet and the pelvic outlet.
When the lowermost portion of the presenting
fetal part is at the level of the spines, it is
designated as being at zero (0) station.
Classification of station that divides the pelvis
above and below the spines into fifths. Each fifth
represents 1 cm above or below the spines.
Thus, as the presenting fetal part descends from
the inlet toward the ischial spines
Station +5 cm corresponds to the fetal head
being visible at the introitus
If the leading part of the fetal head is at 0 station
or below, most often the fetal head has
engaged thus, the biparietal plane has passed
through the pelvic inlet. If the head is unusually
molded or if there is an extensive caput
formation or both, engagement might not have
taken place although the head appears to be at
0 station.
2
Clinical pelvimetry for primigravidas
- Check for intact bag of water and ruptured
Membranes
Significant for three reasons.
1. First, if the presenting part is not fixed in the
pelvis, the possibility of umbilical cord prolapse
and compression is greatly increased
2. Second, labor is likely to begin soon if the
pregnancy is at or near term.
3. Third, if delivery is delayed after membrane
rupture, intrauterine infection is more likely as the
time interval increases
Upon sterile speculum examination, ruptured
membranes are diagnosed if amnionic fluid
pools in the posterior fornix or clear fluid flows
from the cervical canal. *none is completely
reliable
pH determination of vaginal fluid. The pH of
vaginal secretions normally ranges from 4.5 to
5.5, whereas that of amnionic fluid is usually
7.0 to 7.5.
Nitrazine - Test papers are impregnated with
the dye, and the color of the reaction between
these paper strips and vaginal fluids is
interpreted by comparison with a standard color
chart. A pH above 6.5 is consistent with
ruptured membranes. False-positive test results
may occur with coexistent blood, semen, or
bacterial vaginosis, whereas false-negative
tests may result with scant fluid.
Arborization or ferning of vaginal fluid, which
suggests amnionic rather than cervical fluid.
Amnionic fluid crystallizes to form a fernlike
pattern due to its relative concentrations of
sodium chloride, proteins, and carbohydrates
(Fig. 4-2, p. 49).
Detection of alpha-fetoprotein in the vaginal
vault
Rarely required, identification may also follow
injection of indigo carmine into the amnionic
sac via abdominal amniocentesis.
*There are 2 indications for a
speculum exam: Watery vaginal discharge and
bleeding
Laboratory Studies (hindi nabanggit)
When admitted in labor, most often the
hematocrit or hemoglobin concentration
should be rechecked
o Hematocrit
o Blood type and antibody screen,
if needed
o Syphilis and human
immunodeficiency virus (HIV)
serology.
o Urine specimen for protein
determination in hypertensive
women only
Women who have had no prenatal care
should be considered to be at risk for
syphilis, hepatitis B, and HIV
Management of the First Stage of Labor
- Rational plan for monitoring labor can then be
established based on the needs of the fetus and the
mother
- marked individual variations in labor lengths,
precise statements as to its anticipated duration are
unwise
Intrapartum Fetal Monitoring
Recommend that during first-stage labor, in
the absence of any abnormalities
Fetal heart rate should be checked
immediately after a contraction at least
every 30 minutes and then every 15 minutes
during the second stage.
If continuous electronic monitoring is used,
the tracing is evaluated at least every 30
minutes during the first stage and at least
every 15 minutes during second-stage labor.
For women with pregnancies at risk, fetal
heart auscultation is performed at least
every 15 minutes during first-stage labor and
every 5 minutes during the second stage
Uterine Contractions
With the palm of the hand resting lightly on
the uterus, the time of contraction onset is
determined
Intensity is gauged from the degree of
firmness the uterus achieves.
At the acme of effective contractions, the
finger or thumb cannot readily indent the
er d ring a firm con rac ion. The ime
at which the contraction disappears is noted
next. This sequence is repeated to evaluate
the frequency, duration, and intensity of
uterine contractions
* See Labor Admission Test above
Subsequent Cervical Examinations
During the first stage of labor, the need for
subsequent vaginal examinations to monitor
cervical change and presenting part position
will vary considerably
When the membranes rupture, an
examination to exclude cord prolapse should
be performed expeditiously if the fetal head
was not definitely engaged at the previous
examination
The fetal heart rate should also be checked
immediately and during the next uterine
contraction to help detect occult umbilical
cord compression
Periodic pelvic examinations are typically
performed at 2- to 3-hour intervals to
evaluate labor progress.
Oral Intake
Food should be withheld during active labor
and delivery (NPO 8 hours)
Gastric emptying time is remarkably
prolonged once labor is established and
analgesics are administered (note:
Progesterone effect of delayed gastric
emptying)
As a consequence, ingested food and most
medications remain in the stomach and are
not absorbed. Instead, they may be vomited
and aspirated
Sips of clear liquids, occasional ice chips,
and lip moisturizers are permitted
In the new protocol, it has been studied that
intake and presence of IV line does not
contribute to the increased effectiveness of
labor. BUT, these are still done due to the
physician beneficial belief
3
Intravenous Fluids
Although it has become customary in many
hospitals to establish an intravenous
infusion system routinely early in labor, there
is seldom any real need for this in the
normal pregnant woman, at least until
analgesia is administered.
An intravenous infusion system is
advantageous during the immediate
puerperium to administer oxytocin
prophylactically and at times therapeutically
when uterine atony persists.
With longer labors, the administration of
glucose, sodium, and water to the otherwise
fasting woman at the rate of 60 to 120 mL/hr
prevents dehydration and acidosis
IV fluids are given when px has nothing per
orem for 6-8 hrs to prevent dehydration
(provide glucose and water)
Ph ician di cre ion a o ha ing an IV
line open for emergencies
However caution must also be exercised
because full NPO may cause
hypoglycaemia, shock, seizures
Maternal Position
The normal laboring woman need not be
confined to bed early in labor
In bed, the laboring woman should be
allowed to assume the position she finds
most comfortable this will be lateral
recumbency most of the time
She must not be restricted to lying supine
because of resultant aortocaval
compression and its potential to lower
uterine perfusion
o aortocaval system reduce blood
flow to fetus fetal compromise
o May also reduce intensity of
contractions interferes with
progress of labor
Upright position: speed contractions in early
labor
Exceptions to allowing pregnant woman to
take desired/comfortable positions:
a) Membranes have ruptured in the
presence of a NON- engaged fetal head
b) Sedated patients
- In these cases, ask patient to assume left
lateral decubitus as it increases blood flow
to fetus
Analgesia
In general, pain relief should depend on the
needs and desires of the woman.
Give only during active phase
o Non-medicated measures
Natural childbirth
Support person/doula
provide coaching during delivery
Soaking tubs (temp kept at 98-
100oF to prevent fever in mother
and baby)
Analgesics you can give:
o Benzodiazepine
o Nalbuphine Hcl
o Meperedine Hcl (give in smallest
possible dose to prevent adverse
effects in fetus)
Anesthesia: pudendal, epidural, spinal,
general (*epidural is still the best)
Amniotomy
If the membranes are intact, there is a great
temptation, even during normal labor, to
perform amniotomy.
The presumed benefits are:
o more rapid labor,
o earlier detection of meconium-
stained amnionic fluid, and the
o opportunity to apply an electrode to
the fetus or insert a pressure
catheter into the uterine cavity for
monitoring.
Importantly, the fetal head must be well
applied to the cervix and not be dislodged
from the pelvis during the procedure to avert
umbilical cord prolapse.
The advantages and disadvantages of
amniotomy were NOT DISCUSSED so you
may skip this part if you want:
A common indication for artificial rupture of
which
the membranes
require immediate
surgical
infusion
amniotomy
of medication
includes the need for direct monitoring of the
fetal heart rate or uterine contractions or
both.
During amniotomy, to minimize cord
prolapse risk, dislodgement of the fetal head
is avoided
Fundal or suprapubic pressure or both may
be helpful.
Some clinicians prefer to rupture
membranes during a contraction
If the vertex is not well applied to the lower
uterine segment, a gradual egress of
amnionic fluid can sometimes be
accomplished by several membrane
punctures with a 26-gauge needle held with
a ring forceps and with direct visualization
using a vaginal speculum.
In many of these, however, membranes tear
and fluid is lost rapidly. Because of the risk
of cord prolapse or rarely abruption, the fetal
heart rate is assessed before and
immediately after amniotomy.
Elective Amniotomy
o Membrane rupture with the intention
of accelerating labor is often
performed.
o In the investigations presented,
amniotomy at approximately 5-cm
dilation accelerated spontaneous
labor by 1 to 1½ hours.
o Neither the need for oxytocin
stimulation nor the overall cesarean
delivery rate was increased.
o Although mild and moderate cord
compression patterns were
increased following amniotomy,
cesarean delivery rates for fetal
distress were not increased.
o Most importantly, there were no
adverse perinatal effects.
Amniotomy Induction
o Artificial rupture of the
membranes sometimes called
surgical induction can be used to
induce labor, and it always implies a
commitment to delivery.
o The main disadvantage of
amniotomy used alone for labor
induction is the unpredictable and
occasionally long interval until labor
onset
4
 o Found that amniotomy alone or
combined with oxytocin was
superior to oxytocin alone
o Oxytocin induction to either early
amniotomy at 1 to 2 cm or late
amniotomy at 5 cm.
o Early amniotomy was associated
with a significant 4-hour reduction in
labor duration.
o With early amniotomy, however,
there was an increased incidence of
chorioamnionitis.
Amniotomy Augmentation
o It is common practice to perform
amniotomy when labor is abnormally
slow
o Amniotomy with oxytocin
augmentation for arrested active-
phase labor shortened the time to
delivery by 44 minutes compared
with that of oxytocin alone.
o Although amniotomy did not alter
the delivery route, one drawback
was that it significantly increased
the incidence of chorioamnionitis.
o Use of amniotomy to enhance
progress in active labor, but
cautions that this may increase the
risks of infection and maternal fever
**OPPABELLS STOP SKIPPING AND READ hi
part again.
Urinary Bladder Function
Distention of the bladder should be avoided
because it can hinder descent of the fetal
presenting part and lead to subsequent
bladder hypotonia and infection
During each abdominal examination, the
suprapubic region should be inspected and
palpated to detect distention.
If the bladder is readily seen or palpated
above the symphysis, the woman should be
encouraged to void.
If the bladder is distended and voiding is not
possible, catheterization is indicated.
Most women resumed normal voiding before
discharge from the hospital.
Labor epidural analgesia
o Risk factors for retention were
primiparity, oxytocin-induced or -
augmented labor, perineal
lacerations, operative vaginal
delivery, catheterization during
labor, and labor duration > 10 hours.
Enema and Vulvar & Perineal Preparation (with
the new protocol this is no longer recommended but
again..this varies wi h he ph ician di cre ion)
Prevent contamination of newborn with feces
Cleanse GI tract
Minimizes infection in episiotomy wound
Fleet enema
o Do early because if you do it at 7
o cm dilatation, the baby might
come out before she empties the
GI tract
Woman in lithotomy position w/ cleansing
of vulva and perineal scrubbing downward
and away from introitus
C/I: ruptured membranes, sedated
Fetal Monitoring
o Main parameters: FHR and FHR
variability
o Usually based on recordings while
o px is hooked to
electronic fetal
monitor
o Normal baseline HR: 110-160bpm
o (varies by 6-25
o Accelerates appropriately for gest age
o Does not decelerate during
contractions
o Fetoscope/stethoscope for
auscultation OR
o If manual ausculatation, follow one px to one
attendant ratio
o Normal pregnancies: get FHR after each
contraction every 30 mins during 1st stage
of labor and every 15 mins during 2nd stage
o High risk pregnancies: get FHR every 15
mins during 1st stage and 3-5 mins during
2nd stage
o Always listen for heart tones AFTER
contractions because contractions may
cause a slowing of HR
o EFM: standard of care for high risk
pregnancies and is now used for ALL
pregnancies
o Abnormal EFM findings are confirmed via
fetal pulse oximetry (help det if C/S is
needed)
Monitoring Progress of Labor (not discussed but
uhmm..ang ikli lang naman wag ka na mag-skip..You
are not a hiphopper so do not hop.)
Check for cervical dilatation - most
accurate measure of labor progress
Partograph (sigmoid curve) used to
assess progress of labor and identify when
intervention is needed
o Graphical record of cervical
dilatation in cm against duration
of labor in hrs
o Highly effective in reducing
complications from prolonged
labor (postpartum hemorrhage,
sepsis, uterine rupture)
o Plotting begins in the active
phase when cervix is 4cm
dilated
3 components of partograph:
1. Fetal condition
2. Progress of labor
3. Maternal condition

Content of the partograph:
o Px info
o Fetal HR (every half hour)
o Amniotic fluid record color
every 
vaginal exam

I: membranes intact

C: membranes
ruptured; clear fluid
M: meconium-stained

B: blood-stained
o Moulding

1: sutures apposed 

2: sutures overlap but
reducible 

3: sutures overlap but not
reducible
o Cervical dilatation (begin plot at
4cm)
o Alert line: line starts at 4cm to
the point 
of expected full
dilatation at a rate of 1cm/hr) 

You go beyond this IF
dilatation is less than
1cm/hr
o Action line: parallel and 4 hrs to
the right of alert line
You go beyond this if
5
 there is delay in progress
(>4hrs)
o Descent assessed by
abdominal palpation
Refers to part of head
palpable above symphysis
pubis

At zero, sinciput is at the
level of symphysis pubis
o Hours time since onset of
labor
o Time Actual time
o Contractions chart every ahlf
an hour
Palpate number of
contractions in 10
minutes and their
duration
o Oxytocin reconrd the
amount of oxy given per
voulume IC fluids
o Drugs given
o Pulse (every 30 minutes)
o Temp. (every 2 hours)
o Protein, acetion and voume
(record each time urine is
passed)
Check for uterine contractions every 30
minutes
o IF high risk, do it every 15
minutes
IE or vaginal exam is done as needed
o Done every 4 hours in latent
phase and after rupture of
membranes
o IF with ruptured membranes,
limit IE (possible infection)

6
INTRAPARTUM ASSESSMENT
Sources: Lecture slides, Dra. Coloma lec re,
th
William 24 Ed, previous notes from
upperclassmen
Conduct of Labor and Delivery
Monitoring
─ Maternal
Vital signs
Uterine contractions
General condition
─ Fetal
FHR
FHT
─ Progress of labor
dilatation and descent (done by
partograph)
Monitoring the fetus
─ Clinical (signs and symptoms)
Auscultation of fetal heart tones
Character of the amniotic fluid
─ Electronic FHR monitoring (EFM)/
Cardiotocograph ( CTG)
** LOOK OUT FOR FETAL DISTRESS to
recognize when it will happen and then apply
appropriate action so that we can have a healthy
fetus at the end of the delivery
If the delivery went on and we have
a baby that is not well, it will reflect
on the way labor and delivery is
conducted
Distress is no longer the
acceptable term, instead
compromi e i ed when we are
describing the reason for doing
actions such as cesarean section.
** LOOK OUT FOR FETAL COMPROMISE
AMNIOTIC FLUID
─ Also used as a gauge
If the fetus becomes hypoxic, it will incite
the pituitary to release arginine
vasopressin. Arginine vassopresin is a
substance that will increase peristalsis
and with the movement of the bowels, it
is possible that meconium wil be passed
so that the amniotic fluid, which is
naturally colorless or white, becomes
stained green We can say that there is
fetal compromise based on this
mechanism
Meconium staining of amniotic fluid is
always considered as fetal compromise,
unless proven otherwise
Fetal hypoxia Pituitary release of
arginine vasopressin
Auscultation
─ Stethoscope or Doppler devices
Doppler devices small gadgets
that use the principle of transmitting
sounds towards the blood vessels
and then the impulses are bounced
back to it
Although directing the
sound of the Doppler device
towards the blood vessel,
the frequency of red cells
passing under the monitor is
based on heart action so if
the heart pumps, more
blood cells are passing
through and when the heart
relaxes, lesser blood
vessels pass through
Blood vessel reflects the
action of the heart
─ The maternal pulse must be counted as the
FHR is counted to make sure that it is the
FHR is counted and not the maternal heart
rate
Tachycardia of the mother may
sometimes be misinterpreted as
FHR. (Example is in cases of
h a idiform mole here mo her
heart rate is increased)
─ The fetal heart must be auscultated
IMMEDIATELY AFTER CONTRACTION
because if there will be changes in the heart
rate, they will be most likely detectable
immediately after the uterine contraction
** Changes in the fetal heart rate that are most likely
to be ominous almost always are detectable
immediately after a uterine contraction
Recommendations:
In the absence of any abnormalities
─ First stage every 30 min
─ Second stage every 15 minutes
High-risk pregnancies there are more
complications therefore FHR is auscultated more
frequently
─ First stage every 15 minutes
─ Second stage every 5 minutes
Suspect compromise if:
─ FHT repeatedly below 110 bpm, even
though there is recovery to 110-160 bpm
** Further labor if allowed should be should be
monitored electronically
Electronic FHR monitoring
ADMISSION TEST (baseline trace)
─ Hooking the mother to a electronic monitor
and we obtain a baseline trace
If normal, we can shift to intermittent
auscultation then check again the
trace every 2 hrs (no continuous
trace)
If abnormal trace or high-risk case,
then it has to be continuous trace
If at any point that we get an
abnormal trace, from that
point on it will be continuous
trace/ continuous electronic
Increased intestinal Passage of meconium
peristalsis
1
 Chemo- and baro-receptors
Chemoreceptors senses in
changes in oxygen and
carbon dioxide in the blood
Baroreceptors sensitive to
blood pressure changes
BASELINE RATE
─ Approximate mean rate rounded to
increments of 5 bpm during a 10-minute
segment, minimum interpretable duration of
2 min
The average fetal heart rate is
considered the result of tonic
balance between accelerator and
decelerator influences on the
pacemaker cells
Sympathetic system accelerator
influence
Parasympathetic system
decelerator factor mediated via
vagal slowing of heart rate
─ Normal: 110-150 bpm
─ Bradycardia : < 110 bpm, for at least 3 min.
(more than 2 mins)
moderate 80-100
severe less than 80
A rate between 100 and 119
bpm, in the absence of
other changes, usually is
not considered to represent
fetal compromise may be
attributed to head
compression from occiput
posterior or transverse
positions particularly during
nd
the 2 stage of labor
Bradycardia within the
range pf 80-120bpm with
good variability may be
considered reassuring
<180 bpm nonreassuring
and generally considered
nonreassuring
Congenital fetal heart block
and serious fetal
compromise may cause
bradycardia
─ Tachycardia: > 160 bpm
mild 161-180 bpm
severe > 180 bpm
Maternal fever from
chorioamnionitis most
common explanation of fetal
tachycardia
Other causes: fetal
compromise, arrhythmias
and maternal administration
of parasympathetic
Reading EFM trace
(atropine) or
─ Baseline heart rate
sympathomimetic
─ Baseline variability (terbutaline) drugs
─ Accelerations Wandering baseline baseline rate is
─ Decelerations unsteady and wanders between 120-
Of all the 4, variability has 160; a rare finding associated with
the greatest import neurologically abnormal fetus and may
occur in preterminal event
FHR regulation
─ Under this various systems:
Central nervous system
Autonomic nervous system
- Sympathetic
- Parasympathetic
2

Cardiotocograph
- Cardio heart
- Toco uterine contractions
How to read uterine contractions (Toco part):
─ anything around 50 mild
─ 75 moderate
─ If at the top point strong contractions
200 units adequate contractions
- Shows moderate contractions
- Frequency: contractions every3-
4mins
For the FHR (Cardio part):
- Read portions of the trace
where there are no contractions
Example:
- For the most part, the rate is
along 140 to 150 so FHR= 140-
150 normal
Usually, it should be expressed only
as 1 number. So FHR= 145bpm
But 140, 145 or 150bpm all are
acceptable
BASELINE VARIABILITY
─ Oscillations at the baseline or jiggliness
─ Ano her erm i a oo hedne (parang
bagong lagare, hindi yung pudpud na
lagare)
─ Is an important index of cardiovascular
function and appears to be regulated by the
autonomic nervous system
A sympathetic and parasympathetic
p h and p ll media ed ia he SA
node produces moment-to-moment
or beat-to-beat oscillation of the
baseline heart rate
Variability may be further divided into
short term and long term
Short-term variability
reflects instantaneous
change in FHR from one
beat or R wave to the
next
measures the time interval
between cardiac systoles
Long-term variability
used to describe the
oscillatory changes during 1
minute and result in the
waviness of the baseline
normal frequency: 3-5
cycles per minute
Grades of baseline variability
─ Absent variability only a straight line
─ Minimal (poor) +/< 5 bpm
─ Moderate = NORMAL 6-25 bpm
─ Marked > 25 bpm
How do we know if it is 5-25?
─ 1 row 10bpm
Example:
- Shows moderate variability
good/ normal variability
If it shows a sawtooth appearance
good variability
3
If straight bad Up t o 30 weeks baseline
variability is similar during both fetal
rest and activity
>30 weeks fetal inactivity was
associated with diminished baseline
variability and conversely, variability
was increased during fetal activity
Decreased variability
Can be an ominous sign indicating
seriously compromised fetus
Fetal acidemia loss of
variability in combination
with decelerations
Common cause is administration of
analgesic drugs during labor
CNS depressants can
cause transient diminished
beat-to-beat variability
Fetal Hypoxia decreased
variability in the absence of
decelerations
A persistently flat FHR
baseline/ absent variability
within normal baseline rate
range and without
decelerations may reflect
previous insult to the fetus
that has resulted to
neurological damage
** It is generally believed that reduced
baseline heart rate variability is considered the
single most reliable sign of fetal compromise

Sinusoidal heart rate

May be observed in fetal intracranial
hemorrhage, with severe fetal
asphyxia and with severe fetal
anemia from Rh alloimmunization,
fetomaternal hemorrhage, twin-twin
transfusion syndrome or vasa previa
with bleeding
may be attributed to administration
of meperidine, morphine,
alpharodine and butorphanol
shows a sine frequency of 6 cycles
per minute when due to narcotics
has also been described with
chorioamnionitis, fetal distress and
umbilical cord occlusion
not generally associated with fetal
compromise

Increased Variability
Seen during fetal beathing
May be affected by fetal body
movements

4
 column is equal to 10
seconds.
─ The heart rate is
considered to have
accelerations if from
baseline, it will
increase to 15bpm
and sustained for 15
seconds (increase in
1 ½ column and 1 ½
row)
─ If it is not sustained
for 15secs only
considered as a
variability, not an
acceleration
From Williams:
- >32 weeks acceleration has a
peak of 15bpm with a duration
of 15 seconds or more but
<2min
- <32 weeks peak of 10bpm for
15 seconds to 2 minutes is
considered normal
- Prolonged accelerations 2
minutes or more but less than
10 minutes

─ DECELERATION
ADVANCING GESTATION - may be correlated with different
─ Parasympathetic dominance (vagus nerve) conditions
As the baby grows older, the - pagbaba from the baseline
parasympathetic become dominate Early Decelerations
Results to: in time with the contractions
- Decreasing rate (pag taas ng contraction,
- Increasing variability bababa yung heart rate, pag
nd
Ex. First and 2 trimester baba ng contraction, babalik
babies HR= 180 OR 160, but yung heart rate sa baseline)
as it grows older like at 30 gradual decrease and return
weeks, HR decreases to baseline associated with
The normal gradual contraction
slowing of the fetal heart rate drop with
heart rate is thought to contractions
correspond to the associated with head
maturation of the compression
parasympathetic (vagal) Head compression may
heart control occur during the pelvic
nd
stage of labor/ 2 stage of
PERIODIC PATTERNS labor (as the baby goes
The baby reacts with the through the passage)
environment, therefore there are Fitting the head through the
accelerations and decelerations. bony passage head
(but mostly accelerations) compression reflected in
─ ACCELERATION the heart rate
Visually abrupt increase above FHR It can be milder compared
baseline defined as onset of to late and variable
acceleration to peak in less than 30 decelerations since it can be
nd
seconds physiologic during the 2
Intact neurohormonal cardiovascular stage of labor (however,
control mechanisms may be abnormal if not in
nd
Favorable sign of fetal well-being the 2 stage of labor or if
baby is still above the
pelvis)

How do we know if there is

acceleration? (According to
Dra. Coloma)
─ There are 6 columns
between 2 dark lines.
So if 6 columns are
equal to 1 min, then 1

5
 Variable Decelerations
Late Decelerations
pagbaba ng contraction,
tsaka pa lang bababa yung
heart rate
smooth, gradual,
symmetrical decrease in
FHR beginning at or after
the contraction peak and
returning to baseline only
after the contraction has
ended
Gradual decrease
defined as 30 seconds
or more from the onset
of deceleration to the
nadir
associated with placental
insufficiency
Placenta ages there is
degeneration with age
In some cases of
pregnancy, placental
degeneration occurs early
placenta is insufficient
function-wise reflected in
the heart rate
The only solution for this is
to deliver the baby
Anytime, anywhere; abrupt
(kahit saan niya gusto
pumwesto)
Defined as an abrupt
decrease in FHR beginning
with the onset of the
contraction and reaching
nadir in less than 30
seconds
The decrease must last
between >15 seconds
and 2 minutes and must
be >15bpm in amplitude
Associated with cord
compression
If the cord is compressed
(cord is compressed by the
head or if hinahawakan ng
bata yung cord kasi bored
na bored na siya sa loob
kasi 9 months na siyaa
loob) FHR changes
Cord compression depends
on how badly it is
compressed sometimes it
can be relieved by changing
the position of the mother
6
 <10mins from onset to
return to baseline
common causes: cervical
examination, uterine
hyperactivity, cord
entanglement and maternal
supine hypotension
may be due to epidural,
spinal, or paracervical
analgesia

FETAL DISTRESS
too broad and vague to be applied with any
precision to clinical situations
Uncertainty regarding the diagnosis
based on interpretation of FHR
patterns has given rise to
descriptions such as reassuring or
nonreassuring.
Reassuring suggests
a restoration of
Usually, decelerations are associated with confidence by a
some deviations from the normal, which can particular pattern
be excessive to produce compromise Nonreassuring
Whereas accelerations means that baby is inability to remove
reactive and can indicate well being doubt
Late and early decelerations are usually These patterns during
symmetrical appearance (just like Mt. Fuji or labor are dynamic
Mt. Mayon), while variable decelerations are they can rapidly change
abrupt from reassuring to
nonreassuring and vice
Electronic monitoring can be used before versa
and during labor ** These assessments are subjective clinical
No contraction and not in labor non-stress judgments that are inevitably subject to imperfection
test using electronic monitor and must be recognized as such
If with contractions and patient is in labor
Intrapartum INTERPRETATION
FIGO classification
Shouldering ─ Normal
─ There an o er hoo ─ Suspicious
─ Shows that there is compensation ─ Abnormal
If there is no overshoot fetal NICHD
compromise ─ Reassuring = FIGO normal
─ Non-reassuring = FIGO suspicious
─ Ominous = FIGO abnormal

NORMAL TRACE or REASSURING PATTERN

Prolonged decelerations
defined as an isolated
deceleration >15bpm lasting
2mins or longer but
(memorize this!)
─ Baseline rate 110-160 bpm
─ Baseline variability 6-25 bpm good
variability
─ Accelerations present
─ Decelerations absent
SUSPICIOUS or NON-REASSURING
─ One of the 4 features falls into non-
reassuring category and the remainder are
reassuring
7
 If one of the reassuring pattern
is abnormal considered
suspicious or non-reassuring
─ If rate or variability is abnormal
─ Outside of the normal
ABNORMAL or OMINOUS
─ 2 or more features fall in non-reassuring OR
1 or more fall in abnormal
Abnormal (memorize this!)
─ Baseline rate
<100, >180 for more than 10 min*
Sinusoidal pattern
There is no variability in
sinusoidal
─ Baseline variability
<5 for 90min
Atypical Variable
─ >60 sec duration, >60 beat drop
─ Late component late in relation to UC or
slow return to baseline
─ Associated with poor variability
─ No shouldering
** Take note of these categories since these will
be used in the exams
CATEGORY I TRACINGS
─ Baseline rate: 110 to 160 beats per minutes
─ Moderate baseline fetal heart rate variability
(amplitude 6 to 25bpm)
─ No late or variable decelerations
─ Early decelerations may be present or
absent
─ Accelerations may be present or absent
** Category I electronic fetal monitoring (EFM)
racing are con idered normal beca e die
have demonstrated that these findings are
associated with the absence of fetal metabolic
academia at the time of observation
** No intervention is indicated
CATEGORY II TRACINGS: DEFINITION AND
MANAGEMENT
─ Category II fetal heart rate (FHR) tracings
include all FHR patterns that are not
classified as category I (normal) or category
III (abnormal)
CATEGORY III TRACINGS: DEFINITION AND
MANAGEMENT
A category III tracing is defined by either of the
following criteria:
─ Absent baseline fetal heart rate (FHR)
variability and (any of the following):
─ Recurrent late decelerations and
─ Recurrent variable decelerations
─ Bradycardia
─ A sinusoidal pattern
** Category 3 tracings are considered abnormal
and require prompt evaluation, according to
ACOG.
In category II, it is in between so we need to
verify.
How do we verify?
- For example, loss of variability
may be hypoxia or may be baby
is just sleeping
- If asleep can be awakened
using vibroacoustic stimulation
(VAS)
General approach Patients with category
II tracings should be evaluated for factors
that may reduce fetal oxygenation, taking
into account associated clinical
circumstances
Resuscitative measures can be initiated with
frequent reassessment to determine
whether to perform an operative intervention
and the urgency of the intervention
Continued surveillance and frequent
reassessment are indicated until the pattern
resolves of progresses to category III
Fetus hypoxic or asleep?
─ Vibroacoustic stimulation (VAS) special
gadget that emits sounds that can evoke
response or stimulate
─ Digital scalp stimulation scratch, pinch or
rub the scalp of the baby
─ Allis scalp stimulation allis is a clamp with
small teethlike edge which can elicit pain or
response from the baby if baby is asleep
─ Fetal scalp blood sampling gadget used to
ake blood from bab calp o de ermine
blood gasses
Management approach to non-reassuring FHR
pattern
INTRAUTERINE RESUSCITATION
1. Administer oxygen to mother given if baby
is presumed to be hypoxic
2. Reposition patient not specified what
position but most likely left lateral (reposition
the uterus out of the aorta or vena cava to
improve the circulation)
3. Discontinue uterine stimulants oxytocin is
used to improve the contractions but if we
see a nonreassuring pattern, immediately
stop oxytocin drop
4. Hydrate patient IVF
8
 These 4 are the basic
management approach

5. Vaginal examination
6. Alert anesthesia, nursing and neonatal care
staff
7. Possible abdominal delivery done if there
is no improvement in the tracing even
though the basic management approaches
were done

Examples:

3. Baseline FHR: 130-140

Variability: poor
Acceleration: (-)
Deceleration: (+) Late deceleration
CATEGORY III

1. Intrapartum? Yes --? Kasi may

contractions
Baseline FHR: 130-140
Variability: moderate
Acceleration: (+)
Deceleration: (-)
CATEGORY I

4. Baseline FHR: 130-140

Variability: none
Acceleration: (-)
Deceleration: (-)
CATEGORY III kasi sinusoidal pattern

2. Baseline FHR: 170-180 tachycardia

Variability: moderate
Acceleration: (-)
Deceleration: (-)
CATEGORY II

9
 7. Baseline FHR: 150-160
Variability: moderate
Acceleration: (-)
Deceleration: (+) Variable decelerations
CATEGORY II kasi may variable
decelerations with shouldering/
overshoots

5. Baseline FHR: 140

Variability: none
Acceleration: (-)
Deceleration: (+) late deceleration
CATEGORY III

6. Baseline FHR: 130-140

Variability: morderate
Acceleration: (-)
Deceleration: (+) Early deceleration
CATEGORY I

10
 OB Anesthesia
nd
Dr. Irma A. Lee, MD, FPOGS, MHPed Somatic Pain (pain during 2 stage of labor)

BLACK PPT BLUE SuperSubsec ORANGE - LECTURE From distention (due to the stretching) of
pelvic floor, vagina, perineum
Goals of Childbirth Preparation Via somatic nerve fibers transmitted from
pudendal nerve to S2-S4
Patient education concerning pregnancy,
labor and delivery
Relaxation training Analgesia during Labor
Instruction in breathing techniques
Husband (support person) participation A) Regional Analgesia/Anesthesia
Early prenatal bonding
Ideal Anesthetic for Labor & Delivery Epidural Analgesia/Anesthesia
o Most effective method of intrapartum
Safe for mother and baby pain relief
Parturient is conscious, cooperative, o Doe n need o ai for a 4-5cm
comfortable and in control cervical dilatation to be implemented
Will promote EINC (Essential Intrapartum o Catheter can be inserted as early as
Newborn Care) in the latent phase
o Early Parental Bonding core of Placed on the epidural
EINC space
There are no perfec ane he ic or analge ia for Do not puncture the dura
Labor and Delivery, only near ideal and that is
epid ral analge ia. (Dra. Lee, 2014) o (+) regular contractions = give
anesthetics/analgesics
Agent of choice o takes a longer time to take effect as
o based on what is safe for the Mother compared with spinal blockade
and the Baby o Patient still has (+) motor function
o almost all anesthetics especially IV o Uses local anesthetics
and gas INH Bupivacaine, lidocaine,
crosses the placenta ropivacaine, 2-
induces a sedative effect to chloroprocaine, epinephrine
the mother that could lead
to fetal respiratory
depression Epidural Analgesia for Labor and Vaginal Delivery
narcotic analgesics
(opioids) Stage of Pain Pathway Local
To be able to implement the EINC Labor Anesthetics
o < 0.25%
comfortable bupivacaine or
First Stage T10-L1
o ✖ parturient in labor when the baby < 0.20%
Lidocaine
is sleeping
Obstetric Pain Pathways S2-S4
Second Stage Same as above
T10-L1
Visceral Pain

From uterine contractions and cervical
dilatation
o Main problem that an applicant
comes for labor
Via visceral afferent fibers entering spinal
cord at T11-T12 and fibers entering T10 and
L1
Pain Pathway during the First Stage
Pain of uterine contractions
Uterine plexus
Pelvic ganglia and plexus
Hypogastric nerve
Concentration of Local Anesthetics Agent for
Epidural
- For Maintenance of Epidural Anesthesia
Intermittent Bolus Injection
Administer initially 7cc of 0.125%
bupivacaine or 0.1% lidocaine after a 3cc
test dose
st
Same amount is injected once 1 dose
wears off at 5-10cc
Gradually increase but not to exceed 0.25
for bupivacaine or 0.20% lidocaine to avoid
motor block
Supplemental doses of local anesthetics
given for the duration of labor
Results in blockade of sacral segments,
intense motor blockade or both

Superficial hypogastric plexus

Infusion pump (patient-controlled epidural
Lumbar and lower sympathetic chain and white rami anesthesia)
of T11-T12
1
 - preferred to be used than a single shot of
anesthetics
o Single shot used for short term
procedures, one time use
- Wait for the progress in labor
o (+) Full cervical dilatation, in need
for episiotomy, assisted vaginal
delivery with the use of forceps or
vacuum, or end up with CS delivery
- Used even as postoperative analgesia
- More popular for maintaining epidural
anesthesia
- Benefits
o Easy to maintain level of analgesia
o More stable maternal VS
o Decrease risk of systemic
anesthesia toxicity
Bupivacaine
Oftenly used local anesthetic for epidural
analgesia
Drug of choice
o Provides essential sensory blockade
with minimal motor blockade
8-10mL of 0.25% to 0.5% for 2hrs
Peak effect achieved in 20 mins
Provide excellent sensory blockade with
minimal motor blockade
Complications can still manifest even after 6mos
postpartum
Alternative Regional Anesthetics Techniques
Spinal Analgesia / Anesthesia
o Low Spinal Block or Saddle Block
o For vaginal delivery requiring
perineal anesthesia
o Total motor inhibition = (-)
movement
o Other indications:
delivery of preterm fetuses
low forceps delivery
cerclage procedure to
manage cervical
insufficiency/incompentency
due to recurrent pregnancy
completion curettage
o All local anesthetics can be used
o Lidocaine short duration
o Tetracaine & Bupivacaine
Intermediate to long
duration
nd
Saddle Block (Subarachnoid) for 2 Stage of Labor

DO NOT MEMORIZE THE VOLUME OR o Loss of sensory input from the perineum and
THE # OF CC inner thigh
o Hindi pa raw sila gagawa ng mga o Blocks S2-S4 segments
nd
future Anes sa 2 year OB1 o Intended for outlet forceps and vacuum
delivery
o (+) hyperbaric solution = mixture of
anesthetic agent with dextrose
o ask the patient to lie down after
administration
o
Epidural Analgesia

Complicati Contraindications Other Alternative Regional Anesthetic Techniques

ons Indications
Hypotens Patient refusal or Vaginal Paracervical block
ion inability to delivery of
st
spinal or cooperate twins Used during 1 stage of labor
regional (due to Vaginal Introduced intravaginally at about 3 or 9
Inadequa meningitis) delivery of o clock
nd
te infection at the site preterm infants If full cervical dilatation (2 stage
analgesia of needle puncture Pre-eclampsia
High or (psoriasis/leprosy/ Patient with
total eczema) medical No sensory or motor blockade
spinal coagulopathy (ITP) complications Blocks transmission of impulse thru the
respirator uncorrected (mitral paracer ical ganglion (Frankenha en
y arrest maternal stenosis/regurg ganglion)
Urinary hypovolemia itation, SC Unpopular due to Fetal Bradycardia
retention (hemorrhage 2° to injuries, Maternal complications: hematoma,
Headach placenta previa) intracranial systemic local anesthetic toxicity, vasovagal
e inadequate neurovascular syncope)
Postdural training or disease, Agent of choice: 2-chloroprocaine
puncture experience in the asthma) Blocks uterine pain pathway at the pelvic
seizures technique inferior hypogastric ganglia and plexus in the
Meningiti (anesthesiologist) uterosacral ligament 1-1.5cm on the lateral
s vaginal fornices
Back Use of 5-10cc 1% lidocaine or 0.25%
pain bupivacaine

2
 nd
Pudendal Nerve Block must know procedure Hindi ka o p ede makapa a ng 2 year if hindi
kayo
Pudendal nerve provides:
maka-iden if a q i ni o.
Sensory innervation for the lower vagina,
vulva and perineum Meperidine HCl (Demerol)
o Mostly used during fetal o Most widely used opioid for labor
delivery/episiotomy analgesia
Motor innervation to perineal muscles and o Given at 25-50mg IV or 50-100mg
external anal sphincter IM q2-4hrs
Transperineal administration not advisable o Can be given even during the latent
o Instead do transvaginal phase
administration o Onset of analgesia 5min after IV
o Pudendal nerve anatomical and 45min after IM
landmark Anticipate that upon
Need to aspirate after delivery, baby will not cry
due to depressive side
Analgesia for spontaneous vaginal delivery effect
and outlet forceps delivery o Often used with phenothiazines
Complications (systemic local anesthetic (Promethazine) to
toxicity, hematoma) vomiting
75mg Meperidine + 25mg

Pudendal Block 50mg Meperidine + 25mg

nd
Safe and effective for the 2 stage of labor, o Treatment of choice for hypertonic
episiotomy, and episiorrhaphy uterine contractions (at latent phase
Uses 10cc 1-2% lidocaine or 0.25% of labor)
bupivacaine o To prevent neonatal respiratory
depression
delivery should be within the
st
Perineal Infiltration 1 hr or more than 4hrs
after IV administration
Most common local anesthetic technique for o Decrease FHR variability 25 min
vaginal delivery after IV or 40min after IM
administration but recovers within
Anesthetics for episiotomy and repair
60mins
infiltrate perineum on the side (along the
area) where you are going to cut
Nalbuphine (Nubain) synthetic form
o Demonstrate ceiling effect for
B) Systemic Analgesia respiratory depression at 30mg
dose
o 10-20mg q4-6hrs
Used when conditions contraindicated the
o onset within 2-3 mins after IV and
use of regional (hemorrhage,
within 15min after IM
coagulopathies)
o Advantages - less maternal nausea
Epidural anesthesia is not available
and vomiting
o Risks for episdural anesthesia when
o Disadvantage - more maternal
there are no anesthesiologist
sedation and dizziness
around (Meningitis,

systemic! Naloxone (Narcan)

o Opioid antagonist to reverse
neonatal respiratory depression
Opioids o Given at 0.1mg/kg of a 1mg/mL IV
o Lipid soluble with low MW easily or IM at thighs of the baby
crosses the placenta
o Causes neonatal respiratory
depression Inhalational Analgesics
o Result in -to-beat variability of Nitrous Oxide
FHR (intrauterine) o Gas Anesthetics
o Do not give to parturients who o Given intermittently as 50%nitrous
oxide in 50% oxygen (Nitronox; 1:1)
by mask or mouthpiece
o For forceps delivery and generalized
NEED TO KNOW FOR THE QUIZ: endotracheal anesthesia
o Part of balanced general anesthesia
o Baseline heartbeat
o Presence or absence of acceleration
o Type of variability present Halogenated Agents
o Deceleration late, variable or early o Volatile anesthetics

3
 o Causes dose related uterine SM
relaxation
halothane, enflurane,
isoflurane
o For internal podalic version of the
nd
2 twin, breech decomposition and
replacement of acute uterine
inversion put 2 IV line, one for
blood one is for halothane or
isoflurane
o With cardio-depressant and
hypotensive effects
o Hepatotoxic
Problems Regarding Use of Inhalational Anesthetics
Need for specialized vaporizers
Concern regarding pollution of labor and
delivery room
Incomplete analgesia
Potential for maternal amnesia
Potential for loss of protective airway
reflexes and pulmonary aspiration of gastric
contents
Ob er e hen a he pa ien la
meal or oral intake
Intravenous Drugs during Anesthesia
Ketamine (Ketalar)
Sedative, good analgesia prior to delivery
Avoid in HPN patients
IMPORTANT SIDE EFFECT (remain patient
asleep, do not wake her up)
Propofol (Diprivan)
Sedation for short surgical procedures
Thiopental (Pentothal)
Short-acting barbiturate
Used with a muscle relaxant
(succinylcholine) prior to tracheal intubation
Induces sleep, poor analgesic
Causes neonatal respiratory depression
nd
Used during 2 stage of labor, short minor
gynecologic procedures (for excisional
biopsy)
Anesthesia for Cesarean Section
1. Spinal Block
o for elective CS
o level of sensory block up to T4
dermatome (below the xyphoid
process)
o first stage labor block up
to T10 (Level of the
umbilicus)
o larger dose of anesthetic agent +
de ro e = h perbaric ol n
o Tetracaine: 8-10mg
o Bupivacaine: 12mg
o Lidocaine: 50-75mg
Spinal (Subarachnoid Block) for CS
15mg 0.5% heavy bupivacaine 3cc or 10mg
tetracaine 2cc + epinephrine 1:200000
(0.0005%)
L3-L4 or L2-L3 using G26 spinal needle
Complications (same as epidural)
Hypotension due to vasodilatation from
sympathetic blockade and veno-caval
compression
To al pinal blockade d e o do e of
analgesic
Spinal headache due to CSF leakage
Use smaller spinal gauge needle
Convulsions
Bladder dysfunction
Contraindications
Hypotension (ruptured ectopic pregnancy)
Coagulopathies
Neurologic disorders
Infection on sites of skin puncture
Management of Spinal Block Complications
Hypotension
Uterine displacement to the left
Hydration with 0.5 to 1L of NSS
Ephedrine 5-10mg/IV
Total spinal block
Treat associated hypotension
Tracheal intubation
Ventilator support
2. Continuous lumbar epidural block
block is from T8-S5 dermatomes
opiates are added to avoid motor block
3. Combines Spinal Epidural Techniques
Provide effective analgesia for labor and
cesarean delivery
4. Balanced General Anesthesia
Uses nitrous oxide, thiopental and
succinylcholine
o Thiopental put patient to sleep
o Succinylcholine SM relaxation
for endotracheal tube insertion
Used fo
within 5mins
o
Causes maternal and fetal CNS
depression
Major hazard is aspiration pneumonitis
Prophylaxis for Aspiration during General
Anesthesia
o Fasting for 8hrs
4
 o Histamine H2 antagonists to reduce
gastric activity (Cimetidine)
o Sellick maneuver skillful tracheal
intubation with pressure on cricoid
cartilage to occlude esophagus
o NGT
o Awake extubation

5. Local Anesthetic Block for CS

Emergency CS in the absence of
anesthesiologist
To augment patchy regional block given
in an emergency
Requires a lot of LA agents

Non-Pharmacologic Analgesic Techniques

Minimal Training Specialized Training

Emotional support Lamaze/Biofeedback
Touch & massage TENS
Therapeutic use of Acupuncture
heat & cold Hypnosis
Hydrotherapy
Vertical position

5
Partograph

2 Phases of Labor:
1. Latent Phase
- Not much of the contraction that would effect good cervical dilatation
Hypertonic contractions strong contractions yet not effective in dilating the cervix
Allow the patient to rest energy is needed later on
Sedation may be given
- Period of waiting
- Primigravid may take as long as 14- 20 hours
- Multigravid 8 hours
Going beyond this time would mean that the patient may not be going into labor yet
In cases of rupture of membranes needs immediate intervention because it may lead to
infection in the uterine cavity causing amnionitis causing further the non-contractile function of the
uterus
2. Active Phase
- Enough powers/ contractions that would make the cervix dilate in order to have effective delivery of fetus
- 4cm dilatation represents that patient has already entered active phase of labor
- Primigravid cervical dilatation of 1cm/ hour
- Multigravid cervical dilatation of 1.5cm per hour
No progress of cervical dilation in 2 hours arrest in cervical dilatation
Protracted disorder not conforming to the 1cm/hour dilatation; not necessarily warrant cesarean/
abdominal delivery, reassess first the patient in terms of the passenger, passages and the power
(may be given oxytocin, stimulants)
At the time the patient has entered 8cm dilatation, there must be descent, if descent does not
happen, there may be inadequate pelvic diameter
Partograph
- Does not tell us when to do cesarean section
- It cautions us that if there is a problem is the passenger, passages and the power in order to have a more
effective vaginal deliver

Acceleration phase
- Expect cervical dilatation to be happening
1
Phase of Maximum Slope
- More rapid cervical dilatation
The phase of maximum slope tells us that we anticipate a rapid cervical rate of cervical dilatation
compared to the deceleration phase
Deceleration phase
- Descent of the presenting part
- Pelvic division of labor
- Corresponds more to the descent than the cervical dilatation
- There will be a slowing in the cervical dilatation
TRUE LABOR FALSE LABOR
- Regular contractions - Irregular contractions
- Increased intensity of contractions - No change in intensity of contractions
- Increased/ long duration of contractions - Short duration of contractions
- Decreased interval between contractions - No change in interval between
3 regular contractions in a 10 minute period contractions
- Pain/ discomfort starts from the fundus going to - Pain/discomfort is on the lower abdomen
the hypogastric area then to the lumbosacral - Relieved by sedation
area/ lower back
- Not relieved by sedation

Examples:
Case 1: JS, 25 year old primigravid 38-39 weeks
Hypogastric pains radiating to the lumbosacral area
VS: BP= 100/60, PR= 80/min, RR= 20/min
Abdomen: FH= 32cm, FHT= 140bpm; LM 1- breech, LM 2- FBL, LM3- Cephalic
Uterine contractions: 5-6min, 40-50 sec moderate
IE: Cervix 3cm, 80% effaced, LOT, (+) BOW, Station -2

3 hours after, UC every 3-4min, 50secs moderate

IE: Cervix 4cm, 80% effaced, LOT, (+) BOW, Station -2

2 hours after, complained of watery vaginal discharge

UC: 3-4 min, 50-60sec, moderate
Speculum exam: pooling of clear amniotic fluid
IE: Cervix 5cm, 90% effaced, LOA, (-)BOW, station -2

2 hours after, IE: Cervix 8cm dilated, fully effaced, LOA, (-)BOW, station 0
One and a half hour later, she complained of having urge to defecate
IE: Cervix fully dilated, fully effaced, OA, (-)BOW, station +2

Case 2: GS, 20 years old, primi 39-40 weeks

Painful uterine contractions since 4 hours ago with bloody mucoid discharge
PPE: BP= 110/70, FH: 34CM, LM1- breech, LM2- FBR, LM3- cephalic, FHT- 140bpm
IE: Cervix 3 cm dilated, 70% effaced, (+) BOW, cephalic, station 0
After 4 hours, Cervic 5cm, 80%effaced, station 0, ROA
After 4 hours, cervix fully dilated, OA, station +1
2
Case 3: AM, 28 years old, G3P2 (2002) 38-39weeks
Watery vaginal discharge with painful uterine contractions since 3 hours ago
PPE: BP= 120/70, FH= 33cm, LM1- breech, LM2-FBL, LM3- cephalic, FHT= 155bpm
Speculum: (+) pooling of clear amniotic fluid
IE: Cervix 2cm dilated, 70% effaced, (-)BOW, cephalic, station -2
After 5 hours, Cervix 6cm, 80% effaced, station -1, LOA
After 2 hours, cervix 6cm, OA, Station -1
3 hours later, cervix 9cm, fully effaced, station 0
1 hour later, cervix fully dilated, fully effaced, station +1