PHYSIOLOGIC OB REVIEW CLINICAL SIGNIFICANCE:CAN BE ENTRAPPED IN A PFANNENSTEIL

INCISION AND CAUSE LOSS OF SENSATION IN THE AREA

Skin
LANGER LINES
orientation of dermal fibers
vertical skin incisions
more tension, wider scars
low transverse incisions (Pfannenstiel)
follow Langer lines; superior cosmetic
results
Subcutaneous Layer
Campers fascia
Superficial
predominantly fatty layer
Scarpas fascia
Deeper
more membranous layer

Arcuate Line
Cephalad- aponeuroses invest the rectus abdominis bellies
above and below
Caudal- all aponeuroses lie anterior to the rectus abdominis
muscle, and only the thin transversalis fascia and peritoneum
lie beneath.

EXTERNAL GENERATIVE ORGANS

Blood Supply
A. Femoral Artery Branches:
skin , subcutaneous layers , mons pubis
superficial epigastric
superficial circumflex iliac
external pudendal
B. External Iliac Artery : PUDENDA or VULVA
- muscles , fascia all structures visible externally from the pubis to the perineum:
inferior "deep" epigastric vessels
deep circumflex iliac vessels-. MONS PUBIS
mons veneris
Hesselbach triangle fat-filled
CLINICAL SIGNIFICANCE: covered by curly hair ( escutcheon )in a triangular area
Direct hernias- Hesselbach triangle LABIA MAJORA
Indirect hernias- deep inguinal ring Male homologue: scrotum
WHERE round ligaments terminate
Outer surface with hair while inner surface without hairs
Merge posteriorly ( posterior commissure.)
LABIA MINORA
Lacks hair follicles,eccrine and apocrine glands
MALE HOMOLOGUE-VENTRAL SHAFT OF PENIS
many nerve endings
2 lamellae superiorly
lower pair: frenulum of the clitoris
upper pair: prepuce
Inferiorly fourchette.

Anterior Abdominal Wall Innervation

ILIOHYPOGASTRIC NERVES- suprapubic area
ILIOINGUINAL NERVES (L1)-
lower abdominal wall
upper portion of the labia majora
medial portion of the thigh

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CLITORIS VAGINAL OPENING AND HYMEN
Male homologue: penis
PARTS: glans, a corpus, and two crura HYMEN
richly supplied with nerve ending Elastic collagenous connective tissue
principal female erogenous Stratified squamous epithelium
organ Hymenal caruncles-remnants after delivery

Imperforate hymen
CLINICALLY:
Primary amenorrhea,cyclic pelvic pain,bulging mass at the
introitus
Management:cruciate incision or excision

VESTIBULE
almond-shaped
BOUNDARIES:
Lateral- Hart line
Medial hymen
Anterior- frenulum
Posterior-fourchette
6 openings:
urethra
vagina VAGINA
ducts of the Bartholin glands (2) Embryology
ducts of the paraurethral glands/skene glands (2) upper portion - mllerian ducts
lower portion - urogenital sinus
Vestibular Glands NO GLANDS WITH ABUNDANT VESSELS
vesicovaginal septum-(VAGINA AND BLADDER)
rectovaginal septum (VAGINA AND RECTUM)
CLINICAL IMPORTANCE)
Posterior fornix-(POUCH OF DOUGLAS)surgical access of the
peritoneal cavity
LATERAL FORNICES-BI MANUAL EXAMINATION TO PALPATE THE
ADNEXA

1. BARTHOLINS GLANDS
greater vestibular glands
Open distal to the hymenal ring at 5 & 7 o'clock
INFECTION of ducts:BARTHOLINS CYST/ABSCESS

2. PARAURETHRAL GLANDS
Skene glands
Minor vestibular glands
INFECTION:URETHRAL DIVERTICULUM

Vestibular Bulbs
Male homologue: corpus spongiosum of the penis
aggregations of veins beneath the bulbocavernosus muscle
CLINICAL SIGNIFICANCE:
CAUSES VULVAR HEMATOMA DURING DELIVERY

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VAGINA
BLOOD SUPPLY LYMPHATIC DRAINAGE

cervicovaginal branches
External, internal and
Upper Third of uterine artery and
common iliac nodes
vaginal artery

Middle third inferior vesical arteries Internal iliac nodes

middle rectal and

Lower third Inguinal nodes
internal pudendal arteries

PERINEUM Perineal body

Blood supply:
Internal pudendal artery (inferior rectal artery and posterior labial
artery)
NERVE SUPPLY-PUDENDAL NERVE LOCATED IN PUDENDAL CANAL ALSO
CALLED AS
ALCOCKS CANAL

ANTERIOR TRIANGLE
Urogenital Triangle
1.Superficial space closed compartment
2.Deep space continuous superiorly with the pelvic
cavity
CLINICAL SIGNIFICANCE:
o INFECTION OR HEMATOMA IN DEEP SPACE CAN
SPREAD TO ABDOMINAL CAVITY
MUSCLES CUT IN EPISIOTOMY
Levator ani
Central tendon of the perineum
Bulbocavernosus m.
Superficial transverse perineal m.
External anal sphincter

Development of the internal generative organs

POSTERIOR TRIANGLE
Contains:
Ischiorectal fossa
Anal canal
Anal sphincter complex
Branches of the internal pudendal vessels
Pudendal nerve

Embryological development

PUDENDAL NERVE
Formed by the anterior rami of S2-S4
Lies posteromedial to the ischial spines

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Two mllerian (paramesonephric) - MALE HOMOLOGUE: gubernaculum testis
DEVELOPS INTO:
oviducts uterus,upper vagina

INTERNAL GENERATIVE ORGANS

Cervix

Majority-collagen, elastin and proteoglycan
10% smooth muscle
IF WITH MORE MUSCLE CONTENTINCOMPETENT CERVIX
Ectocervix nonkeratinized squamous epithelium
BROAD LIGAMENTS
Endocervix columnar epithelium
Drapes over structures :
(FALLOPIAN TUBES)Mesosalpinx, (ROUND
Uterus
LIGAMENT)mesoteres, (OVARIES)mesovarium,
Nulliparous: fundus= cervix
(UTERUS)mesometrium
Multiparous:cervix is 1/3 of the total length
2.SUSPENSORY LIGAMENT OR INFUNDIBULOPELVIC LIGAMENT
Posterior wall completely covered by serosa
fimbriated end of the fallopian tube to the pelvic
Blood supply:
wall, where OVARIAN vessels traverse
uterine artery(from internal iliac OR HYPOGASTRIC)
CARDINAL LIGAMENTS
ovarian artery(direct branch of aorta)
Transverse cervical or Mackendrodt ligament
Thick base of the broad ligament
ISTHMUS-FORMS THE LOWER UTERINE SEGMENT OF UTERUS
UTEROSACRAL LIGAMENTS
posterior supravaginal portion of the cervix to the fascia over
Uterus: Myometrium
the sacrum
More muscles in the inner wall than the outer wall, anterior and
posterior walls than in the lateral walls
LYMPHATICS
CLINICALLY:
Cervix
Interlacing myometrial fibers - control of bleeding during the
hypogastric nodes
third stage of labor
Body of the uterus
Uterus: Endometrium
internal iliac and periaortic lymph nodes
Uterine and ovarian arteries arcuate radial
spiral/coiled and basal/straight
CLINICALLY:
SPIRAL ARTERIES RESPONSIVE TO HORMONES

FALLOPIAN TUBES
PARTS
interstitial portion
isthmus
ampulla
infundibulum or fimbriated (fimbria ovarica)

Ovaries
Childbearing years- 2.5 to 5 cm
ROUND LIGAMENTS Rest in a slight depression OVARIAN FOSSA OF WALDEYER
Terminate in labium majus. Ligaments:
BLOOD SUPPLY:Sampson artery Broad ligament,uterovarian,infundibulopelvic ligaments

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 Blood supply:ovarian granulosa cell capacity to convert androstenedione to estradiol is
Oocytes are located in the CORTEX controlled by
follicle-stimulating hormone (FSH). After ovulation (right panel), the corpus
FOLLICULAR (PREOVULATORY) OVARIAN PHASE luteum forms and both theca-lutein and granulosa-lutein cells respond to
LH. The theca-lutein cells continue to produce androstenedione, whereas
Birth 2 million oocytes granulosa-lutein cells greatly increase their capacity to produce
progesterone and to convert androstenedione to estradiol. LH and hCG
Puberty 400,000 follicles bind to the same LH-hCG receptor. If pregnancy occurs (right panel),
human chorionic gonadotropin (hCG) rescues the corpus luteum through
Rate of depletion of follicle per month until 35 1000 follicles/month their shared LH-hCG receptor. Low-density lipoprotein (LDL) is an
years old important source of cholesterol for steroidogenesis. cAMP = cyclic
adenosine monophosphate.
# of follicles ovulated during 400 follicles
the entire reproductive age STAGES OF HUMAN FOLLICULAR DEVELOPMENT
EARLY FOLLICULAR PHASE:
percentage of follicles which underwent 99.9 % Inhibin B( granulosa cells) inhibit FSH only 1 follicle to reach
atresia during lifetime maturity

Estrogen Surge 34 36 hours before ovulation

precise predictor of ovulation
LH Surge 10 12 hours before ovulation

o Gonadotropin control of the ovarian and endometrial cycles.

The ovarian-endometrial cycle has been structured as a 28-
day cycle. The follicular phase (days 1 to 14) is characterized
by rising estrogen levels, endometrial thickening, and selection
of the dominant ovulatory follicle.
o During the luteal phase (days 14 to 21), the corpus luteum (CL)
produces estrogen and progesterone, which prepare the
endometrium for implantation. If implantation occurs, the
developing blastocyst begins to produce human chorionic
gonadotropin (hCG) and rescues the corpus luteum, thus
maintaining progesterone production. FSH = follicle-stimulating
hormone; LH = luteinizing hormone.

FOLLICULAR PHASE

Luteal (Postovulatory) Phase

Corpus luteum maintained by LH
Estrogensecondary RISE at midluteal phase
Progesterone peaks in the midluteal phase

The two-cell, two-gonadotropin principle of ovarian steroid hormone

production. During
the follicular phase (left panel), luteinizing hormone (LH) controls theca
cell production of androstenedione, which diffuses into the adjacent
granulosa cells and acts as precursor for estradiol biosynthesis. The

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 21 to 24 Stroma becomes edematous.
Human Corpus Luteum 22 to 25 predecidual transformation of
Regresses 9 11 days after ovulationDECREASED estradiol and extensive coiling and secretions of glands
progesterone MENSTRUATION
WHAT WILL MAINTAIN THE CORPUS LUTEUMHCG IN CASE OF PREGNANCY
PREMENSTRUAL PHASE
PROLIFERATIVE PHASE PREMENSTRUAL PHASE
EARLY PROLIFERATIVE PHASE: Infiltration of the stroma by polymorphonuclear leukocytes
THIN ENDOMETRIUM pseudoinflammatory appearance to the tissue
Narrow and tubular glands,with
Mitotic figures MENSTRUAL PHASE
NO extravascular blood or leukocyte infiltration SEVERE coiling of the spiral arteries hypoxia of the
endometriumstasis/ischemia
VASOCONSTRICTION most constant and striking event
MENSTRUAL BLOOD MORE OF ARTERIAL BLOOD

ACTION OF PROSTAGLANDINS DURING MENSES:

Prostaglandin F2 (PGF2) vasoconstrictor

myometrial contractions and uterine ischemia-
DYSMENORRHEA

DECIDUAL STRUCTURES
Decidua beneath blastocyst implantation
Basalis

LATE PROLIFERATIVE PHASE: Decidua Overlying the enlarging blastocyst

Endometrium thickens, Capsularis CHORION LAEVE- Internally, avascular
glandular hyperplasia extraembryonic fetal membrane
increase in stromal ground substance (edema and
proteinaceous material). Decidua Remainder of uterus
Parietalis Fused with capsularis(14-16
weeks)DECIDUA VERA

3 LAYERS OF DECIDUA PARIETALIS AND BASALIS

3 layers

1. zona compacta zona functionalis

2. zona spongiosa

3. zona basalis gives rise to new endometrium

after delivery

DECIDUAL HISTOLOGY
NITABUCH LAYER-zone of fibroid degeneration
if defective Placenta accreta

Role & Relationship of the Placenta

The blood of the mother and baby DOES NOT mix in a
HEMOCHORIAL placenta
SECRETORY PHASE
MATERNAL BLOOD IN THE INTERVILLOUS SPACE BATHE THE
EARLY SECRETORY PHASE:
SYNCITIOTROPHOBLAST BEFORE IT ENTERS THE
ENDOTHELIAL WALL OF THE FETAL CAPILLARIES
DATING OF endometrium POSSIBLE histology of the
glandular epithelium
Blastocyst Implantation
6 7 days after fertilization
DAY 17 FIRST SIGN OF OVULATION
Glycogen accumulates SUBNUCLEAR VACUOLES
STAGE AT THE TIME OF IMPLANTATION

Trophoblast Differentiation
Villous trophoblast
Extravillous trophoblast
intervillous trophoblast
endovascular trophoblast
Penetrates the spiral artery lumen .IMPORTANT
CLINICALLY IN PRE ECLAMPSIA PREVENTION
Other Structures Formed
Umbilical cord
Originates from the body stalk

The Amnion
Innermost avascular fetal membrane
Provides the tensile strength
IN CASE OF INFECTION MAY WEAKENED
PROM preterm delivery

Amniotic Fluid
AF INCREASE UP TO 34 WEEKS then it declines
1,000 ml. at term

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 STEROIDOGENESIS
Syncitiotrophoblast major site of steroid production Amniotic fluid estrogen Ferning pattern

STEROIDOGENESIS IN PREGNANCY
Fetal adrenal secretion of C-19 steroids, precursor of estrogen
synthesis
LDL-cholesterol from maternal plasma for progesterone OVARIES
biosynthesis CORPUS LUTEUM
HUMAN CHORIONIC GONADOTROPIN (hCG) functions maximally 6-7 weeks
Alpha sub unit is similar to FSH,LH,TSH CLINICAL SIGNIFICANCE:DONT REMOVE
Detected in blood and urine either in pregnancy or in ASYMPTOMATIC OVARIAN TUMORS AT THIS
neoplastic disease TIMEABORTION
Early pregnancy produced by syncitiotrophoblast and
cytotrophoblast THECA-LUTEIN CYST
DUE TO HIGH HCG (hyperreactio luteinalis)
Concentration of hCG in Serum and Urine BILATERAL
Detectable in plasma 7 to 9 days after the midcycle LH surge ASSOCIATED WITH
Doubling TIME every 2 days 1. Gestational trophoblastic diseases
Maximal levels 8 to 10 weeks gestation 2. DM,
60th and 80th days after the last menses - peak levels 100,000 3. D-isoimmunization,
mIU/mL 4. multiple fetuses
5. chronic renal failure
Significance of Abnormally High or Low hCG levels 6. hyperthyroidism
HIGH hCG LEVELS Maternal virilization-30%
Multifetal pregnancy Diagnosis: Ultrasound of enlarged ovaries with multiple cysts
Erythroblastosis fetalis Management: self limited; Asymptomatic - resolves after
(Fetal hemolytic anemia) delivery
Gestational Trophoblastic Disease Some hemorrhage into cysts causing abdominal pain
Fetus w/ Down Syndrome
LOW hCG LEVELS PREGNANCY LUTEOMA
Early pregnancy wastage solid ovarian tumor
Ectopic Pregnancy maternal virilization, but usually female fetus is NOT affected!!!
WHY?BECAUSE OF THE CAPACITY OF THE PLACENTA TO
Human Placental Lactogen (hPL) CONVERT ANDROGEN TO ESTROGEN
Also called human chorionic somatomammotropin or chorionic Trophoblasts has the capacity to convert androgen and
growth hormone androgen-like factors to estrogen
potent lactogenic and growth hormone-like
bioactivity CARBOHYDRATE METABOLISM
Metabolic Actions of hPL NORMAL PREGNANCY:
1. Maternal lipolysis and increase in the levels of circulating free Mild fasting hypoglycemia
fatty acids Postprandial hyperglycemia
2. Anti-insulin or "diabetogenic" action Hyperinsulinemia
3. Potent angiogenic hormone
POST-PRANDIAL HYPERGLYCEMIA IS DUE TO INCREASED PERIPHERAL
Relaxin INSULIN RESISTANCE TO ENSURE SUSTAINED POST-PRANDIAL GLUCOSE
myometrial smooth muscle to promote uterine relaxation and SUPPLY TO THE FETUS
the quiescence observed in early pregnancy
Leptin
secreted by adipocytes INSULIN SENSITIVITY is LOWER in pregnancy to about 45-70%
an anti-obesity hormone - food intake Mediated by:
regulates bone growth and immune function Estrogen and Progesterone
correlated positively with fetal birthweight Human Placental Lactogen
fetal development and growth
FAT METABOLISM
PREGNANT UTERUS MATERNAL HYPERLIPIDEMIA
UTERINE ENLARGEMENT: Increase: lipids, lipoproteins, apolipoproteins
Stretching and hypertrophy of muscle cells *Fat is deposited mostly in the central rather than peripheral
not hyperplasia sites.
INCREASE Fibrous tissue AND elastic tissue
HEMATOLOGICAL CHANGES IN PREGNANCY
CONTRACTILITY HYPERVOLEMIA
Braxton Hicks metabolic demands
irregular, painlesss contractions support the growing placenta & fetus
Unpredictable, sporadic, non-rhythmic, and intensity 5-25 protect FROM blood loss
mmHg HYPERVOLEMIA after 32-34 week

CERVIX
SOFTENING OF CERVIX(GOODELS SIGN)
ISTHMUS(HEGARS SIGN)
CYANOSIS
Cervical Eversion

HGB: will average 12.5 at term

Mucus plug Iron requuirement is not available from Marernal storage in most women
Beading pattern progesterone OPTIMAL INCREASE in maternal erythrocyte VOLUME WILL NOT DEVELOP
(Normal)
WITHOUT IRON SUPPLEMENTATION
WITH MATERNAL ANEMIA, FETAL RBC PRODUCTION IS NOT INHIBITED

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 ACID BASE EQUILIBRIUM
Hyperventilationdecreased maternal PCO2 transport of carbon DEFINITIONS
dioxide from the fetus to the mother and facilitates release of oxygen
from maternal blood to the fetus.

URINALYSIS in PREGNANCY
Glucosuria may not be abnormal, and is common.

Proteinuria is abnormal.

Hematuria is usually a result of contamination.

URETERAL DILATATION which is greater on the Right side; likely

Progesterone effect
NORMAL PREGNANCY DURATION
GASTROINTESTINAL TRACT
Prolonged gastric emptying timeconstipation
Pyrosis (heartburn)

SIGNS AND SYMPTOMS

SUBSEQUENT PRENATAL VISITS

MONTHLY UP TO 28 WEEKS
EVERY 2 WEEKS 28 WEEKS TILL 36 WEEKS
WEEKLY THEREAFTER

ASSESSMENT OF GESTATIONAL AGE

RDA

SOUNDS PERCEIVED BY THE EXAMINER OTHER THAN THE FHT

Funic (umbilical cord) souffle

Rush of blood in the umbilical arteries
Sharp, whistling sound synchronous with fetal pulse

Uterine souffle
Rush of blood through dilated uterine vessels
Soft blowing sound that is synchronous with maternal pulse

Sounds resulting from fetal movement

Maternal pulse

Sounds from maternal intestinal peristalsis

ULTRASONIC RECOGNITION OF PREGNANCY

PHYSIO OB REVIEW FEU-NRMF Page 8

COMMON CONCERNS

This is just a diagram showing you the weeks of development and wPre-
implantation period: 2 weeks from implantation to fertlization
Embryonic Period
Fetal Period

Food and Drug Administration Categories for Drugs and Medications

Category A:
Studies in pregnant women have not shown an
increased risk for fetal abnormalities.
Examples :Levothyroxine, Potassium
supplementation, and Prenatal multivitamins , when
taken at recommended doses.
Category B:
Animal studies have shown an adverse effect, but
adequate and well controlled studies in pregnant
women have failed to demonstrate a risk to the fetus
Examples include many antibiotics, such as
penicillins, macrolides, and most cephalosporins
Category C:
Animal reproduction studies have shown that this
medication is teratogenic (Or embryocidal or has
other adverse effect), and there are no adequate
and well controlled studies in pregnant women.
TERATOGEN Approximately two thirds of all medications are in this
category.
Teratogen: may be defined as any agent that acts during embryonic or Category D:
fetal development to produce a permanent alteration of form or function. This medication can cause fetal harm when
form and function, acts during embryonic and fetal development administered to a pregnant woman.
most major structural anomalies are easily recognized at birth, and an systemic cortocosteroids, azathioprine, Phenytoin,
association with a specific prenatal exposure is likely to be suspected Carbamazepine, Valproic acid, and Lithium.
Many congenital abnormalities, however, do not become apparent until Category X:
later This medication is contraindicated in women who
are or may become pregnant.
STRUCTURAL abnormalities May cause fetal harm.
EXAMPLE: rubella vaccine.
HADEGEN
AFFECTS THE FUNCTION of an organ Features of Fetal Alcohol Syndrome
TROPHOGEN Minimum amount of alcohol to produce adverse fetal
an agent that alters GROWTH consequences is UNKNOWN.
BINGE drinking- high risk for birth defects and increased risk for
Hadegens and trophogens generally affect processes occurring after stillbirth
organogenesis or even after birth Dose Effect
Chemical or physical exposures that act as hadegens or trophogens are Fetal vulnerability to alcohol is modified by genetic factors,
much harder to document nutritional status, environmental factors, coexisting maternal
For simplification, most use the word teratogen to refer to all three types of disease, and maternal age (Abel, 1995). The minimum amount
agents of alcohol required to produce adverse fetal consequences is
unknown. Binge drinking, however, is believed to pose
particularly high risk for alcohol-related birth defects and has
also been linked to an increased risk for stillbirth (Centers for
Disease Control, 2012; Maier, 2001; Strandberg-Larsen, 2008).

ACE Inhibitors and ARBs

Enalapril, captopril, lisinopril
prolonged fetal hypotension and hypoperfusionrenal
ischemia, renal tubular dysgenesis, anuria oligohydramnios
lungs & limbs
Disrupt the Fetal Renin-Angiotensin system that is essentail in
normal Renal development

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 Study in 2006: major congenital anomalies: cardiovascular &
CNS
Angiotensin-converting enzyme (ACE) inhibitors are considered
fetotoxic and result in ACE-inhibitor fetopathy. Normal renal
development depends on the fetal renal-angiotensin system.
ACE-inhibitor medication causes fetal hypotension and renal
hypoperfusion, with subsequent ischemia and anuria
Reduced perfusion may cause fetal-growth restriction and
calvarium maldevelopment, whereas oligohydramnios may
result in pulmonary hypoplasia and limb contractures
Because angiotensin-receptor blockers have a similar
mechanism of action, concerns regarding fetotoxicity have
been generalized to include this entire medication class.
The possible embryotoxicity of these two drug classes is less
certain. First-trimester ACE-inhibitor exposure was associated
with a two- to threefold increased risk for cardiac and central
nervous system abnormalities, but these observations have not
been corroborated. It is reasonable to offer specialized
sonography for pregnancies with firsttrimester exposure. Given
the many therapeutic options for treating hypertension during
pregnancy, it is recommended that ACE inhibitors and
angiotensin receptorblocking drugs be avoided.
ANTIFUNGALS
Fluconazole
Antley Bixler syndrome
oral clefts, abnormal facies, and cardiac, skull, long-
bone, and joint abnormalities
3 fold increase for tetralogy of Fallot
Category D
Anti-inflammatory Agents (NSAIDS)
Indomethacin and other PG inhibitors
1. Constriction of fetal ductus arteriosus
2. persistent fetal circulation
3. pulmonary hypertension in the neonate
Complications morelikely if the drug is taken >72 hours
Importantly, NSAIDs may cause adverse fetal effects when
taken in late pregnancy
Indomethacin may cause constriction of the fetal ductus
arteriosus, resulting in pulmonary hypertension. The drug may
also decrease fetal urine production and thereby reduce
amnionic fluid volume. This is presumed due to an increase in
vasopressin levels and vasopressin responsiveness
Fetal ductal constriction is more likely when the drug is taken in
the third trimester for longer than 72 hours duration.
Fortunately, ductal flow velocity returned to normal in all
fetuses following discontinuation of therapy. Other NSAIDs are
assumed to confer similar risks.
ANTIMICROBIALS
Aminoglycosides
gentamicin or streptomycin nephrotoxicity and ototoxicity
Medications used to treat infections are among those most
commonly administered during pregnancy.
Over the years, experience has accrued regarding their
general safety. With a few exceptions cited below, most of the
commonly used antimicrobial agents are considered safe for
the embryo/fetus.
Aminoglycosides
Preterm infants treated with gentamicin or streptomycin have
developed nephrotoxicity and ototoxicity. Despite theoretical
concern for potential fetal toxicity, no adverse effects have
been demonstrated, and no congenital defects resulting from
prenatal exposure have been identified.
Chloramphenicol
Gray baby syndrome in preterm neonates
abdominal distention,
respiratory abnormalities,
an ashen-gray color
vascular collapse
Nitrofurantoin
Hyperbilirubinemi a in G6PD deficiency
Sulfonamides
- Hyperbilirubinemia of a preterm infant
Tetracyclines
yellowish brown discoloration of deciduous teeth
PHYSIO OB REVIEW FEU-NRMF
Sex Hormones
Testosterone and Anabolic Steroids
virilization and may result in ambiguous genitalia
Diethylstilbestrol
vaginal and cervical intraepithelial neoplasia
Genital tract abnormalities
earlier menopause and breast cancer
Danazol
virilization
MERCURY
not a drug, but is a known teratogen
developmental delay and mild neurological abnormalities to
microcephaly and severe brain damage
May be concentrated in large fishes
Tuna
King mackerel
Tile fish
FDA recommendation: DO NOT EAT: shark, swordfish, king mackerel &
tilefish and more than 6 oz of tuna
RETINOIDS
Vitamin A
vitamin A supplements may be safe during pregnancy
Doses higher than the recommended daily
allowance of 5000 IU should be avoided
Isotretinoin
anti-acne medication
ONE OF THE MOST POTENT TERATOGEN IN COMMON USE
SIMILAR TO THALIDOMIDE
THALIDOMIDE
Limb-reduction defects (es.upper limbs)
Days 27 to 30: upper limb phocomelia
Days 30 to 33: lower limb phocomelia
GESTATIONAL AGE OR MENSTRUAL AGE
time elapsed since the first day of the last menstrual period
280 days or 40 weeks or 9 1/3 calendar months duration
12 Gestational Weeks
centers of ossification
external genitalia are
beginning to show definitive signs of male or female gender
16 Gestational Weeks
gender can be correctly
determined by experienced observers by inspection of the external
genitalia
20 Gestational Weeks
Cochlear function - 22 and 25WEEKS
28 Gestatational weeks
90% chance of survival without physical or neurological impairment.
FETAL HEAD
Frontal - between the two frontal bones
Sagittal - between the two parietal bones
Coronal - between the frontal and parietal bones
Lambdoid - between the posterior margins of the parietal
bones and upper margin of the occipital bone
Page 10
Diameters of the head
Occipitofrontal (11.5 cm)- root of the nose to the most
prominent portion of the occipital bone.
Biparietal (9.5 cm) - from one parietal boss to the other.
Bitemporal (8.0 cm)- the greatest distance between the two
temporal sutures
Occipitomental (12.5 cm)- from the chin to the most prominent
portion of the occiput.
Suboccipitobregmatic (9.5 cm) - from the middle of the large
fontanel to the undersurface of the occipital bone
Circumferences of the head
Greatest circumference of the head- corresponds to the plane
of the occipitofrontal diameter , averages 34.5 cm
Smallest circumference - corresponding to the plane of the
suboccipitobregmatic diameter is 32 cm.
Glucose, Insulin, and Fetal Macrosomia
fetal hyperinsulinemia
insulin-like growth factor and fibroblast growth factor
FETAL PHYSIOLOGY
Amnionic Fluid
early pregnancy ultrafiltrate of maternal plasma.
second trimester extracellular fluid that diffuses through the
fetal skin(fetal plasma)
After 20 weeks amnionic fluid fetal urine.
Function of the amniotic fluid
1. Cushions the fetus
- allows musculoskeletal development
- protection from trauma
2. Maintains temperature
3. Minimal Nutritive function
4. Presence of growth factors
5. Growth and differentiation of tissues: lungs, GIT
Fetal Circulation
Umbilical veins oxygenated blood
Umbilical arteriesunoxygenated blood
CRISTA DIVIDENS preferentially shunts the well-oxygenated
blood through the foramen ovale
Circulatory changes at birth
hypogastric arteries umbilical ligaments
umbilical vein ligamentum teres.
ductus venosus ligamentum venosum
Fetal Blood Hemopoiesis
yolk sac-first trimester
liver-mid pregnancy
bone marrow-third trimester
Fetal Hemoglobin
fetal erythrocytes( hemoglobin F) bind to
oxygen more than hemoglobin A because hemoglobin A
binds 2,3-diphosphoglycerate (2,3-DPG) which
lowers the affinity of hemoglobin A for oxygen .
Fetal Coagulation Factors
Factors II, VII, IX, X, XI, prekallikrein, protein S, protein C,
antithrombin and plasminogen- 50 % of adult levels
CLINICAL APPLICATION:
Vit. K is routinely given to newborn after delivery
Immunoglobulin G
Transfer of IgG from the motherPREVENT INFECTION IN
NEONATES BUT CAN BE HARMFUL IN CASE OF:
Ex. Hemolytic Disease of the Newborn (resulting from D-antigen
alloimmunization)
Immunoglobulin M
IgM is increased in newborns with congenital infection such as
rubella, cytomegalovirus, or toxoplasmosis
PHYSIO OB REVIEW FEU-NRMF
Meconium
dark greenish-black ( biliverdin)
1. normal bowel peristalsis in the mature fetus
2. vagal stimulation.
3. Hypoxia stimulates arginine vasopressin (AVP)
CONTRACTION OF smooth muscle of the colon defecation
Surfactant Composition
Formed by type II Pneumocytes
90% - lipid
50% dipalmitoylphosphatidylcholine (DPPC)
principal active component(lecithin)
8-15% phosphatidylglycerol (PG)- capable of
reducing surface tension in the alveolus
5% phosphatidyl ethanolamine
4% phosphatidyl inositol
10% - protein
Corticosteroids and Fetal Lung Maturation
Fetal cortisol is the natural stimulus for lung maturation
Glucocorticosteroids (24-34 weeks)
( betamethasone & dexamethasone )
accelerate fetal lung maturity
Sexual Differentiation of the Embryo-Fetus
Genetic genderXX or XYis established at the time of
fertilization.
Gonadal Gender
If Y chromosome is present(6 weeks )after conception TESTES
Phenotypic Gender
WITH TESTES male phenotypic sexual differentiation
WITHOUT TESTES female differentiation ensues irrespective of
the genetic gender.
Fetal Testicular Contributions to Male Sexual Differentiation
Mllerian-inhibiting substance
prevents the development of uterus, fallopian tube, and upper
vagina
Testosterone
virilization of the external and internal genital anlagen.
Genital Ambiguity of the Newborn
Excessive androgen action in female fetus , or inadequate
androgen in one destined to be male.
Rarely, genital ambiguity indicates true hermaphroditism.
Category 1. Female Pseudohermaphroditism
1. Mllerian-inhibiting substance is NOT produced.
2. Androgen exposure of the embryo-fetus is excessive
3. The karyotype is 46,XX.
4. Ovaries are present.
MOST COMMON CAUSE :congenital adrenal hyperplasia
Category 2. Male Pseudohermaphroditism
Production of mllerian-inhibiting substance.
Incomplete but variable androgenic representation for a fetus
predestined to be male.
A 46,XY karyotype.
The presence of testes or no gonads.
MOST COMMON CAUSE:ANDROGEN INSENSITIVITY SYNDROME
OR REINFENSTEIN SYNDROME
Category 3: Dysgenetic Gonads
Mllerian-inhibiting substance is NOT produced.
Page 11
 Fetal androgen exposure is variable.
The karyotype varies among subjects and is commonly Non Stress Test (NST)
abnormal. Test of fetal condition
Neither normal ovaries nor testes are present INTERPRETATION:
MOST COMMON CAUSE :TURNERS SYNDROME(46X) Reactive NST-at least 2 accelerations of 15 beats per min
PHENOTYPICALLY FEMALE WITH SEXUAL INFANTILISM lasting for 15 secs in a 20 min observation
INTERVAL OF TESTING:7 DAYS UNLESS HIGH RISK
Category 4: True Hermaphroditism
both ovarian and testicular tissues, PRINCIPLE OF NONSTRESS TESTING
NON REACTIVE NST:
Sleep Awake Cycles 1. hypoxia
Independent of the maternal sleep-awake state 2. neurologic depression
Sleep cyclicity - 20 minutes -75 minutes 3. fetal sleep
4. medications (magnesium sulfate)
Fetal movement counting 5. maternal cigarette smoking)
Best practice recommendations
ACOG (2002): Daily fetal movement count after 28 DECELERATIONS DURING NON STRESS TESTING
weeks' gestation. Repetitive variable decelerations do an ultrasound to check
Perception of 10 distinct movements in 2 hours is for the amount of amniotic fluid volume
considered reassuring.
ACOUSTIC STIMULATION TESTS
Loud external sounds used to startle the fetus acceleration of
the heart rate
Positive response fetal heart accelerations following acoustic
stimulation

Contraction stress test

EFM Definition of Terms: Test of uteroplacental function
Baseline fetal heart rate Fetal heart rate characteristics in response to uterine
Heart rate during a 10min segment rounded to the nearest 5bpm contractions
increment
Early deceleration
EARLY DECELERATION
Visually apparent usually symmetrical gradual decrease and return of the
FHR to baseline associated with a uterine contraction. The nadir of the
deceleration occurs at the same time as the peak of the contraction.
Significance: HEAD COMPRESSION

Baseline variability
Fluctuations in the baseline FHR, visually quantitated as the
amplitude of the peak-to-trough in beats per minute (bpm)
Examine a 1min segment and determine the highest peak and
lowest trough.

Acceleration
Late deceleration
symmetrical gradual decrease and return of the FHR to the
baseline associated with a uterine contraction. The nadir of
the deceleration occurs after the peak of the contraction.
Significance: UTEROPLACENTAL INSUFFICIENCY

PHYSIO OB REVIEW FEU-NRMF Page 12

Interpretation of CST

SIGNIFICANCE OF AMNIONIC FLUID VOLUME

NORMAL VALUE
AFI ( 5 24 cm)
deepest vertical pocket ( 2- 8 cm)

Significance of AFI < 5 cm:

- increased risk of fetal distress
- low 5 minute apgar score
- increased perinatal morbidity and mortality

DOPPLER VELOCIMETRY
a non-invasive technique to assess fetal and maternal blood
flow
BEST TEST FOR IUGR
Goal: TO OPTIMIZE TIME OF DELIVERY
Sonographic assessment
FETAL VESSELS: to determine fetal health and for timely delivery of growth
FETAL BIOMETRY monitor lag of growth or absence of growth
restricted fetuses
BIOPHYSICAL SCORE monitor amniotic fluid and fetal
MATERNA VESSELS: to predict placental dysfunction
behavior
DOPPLER VELOCIMETRY assess the adequacy of blood flow in
CURRENT ANTENATAL TESTING RECOMMENDATIONS
maternal and fetal vessels
There is no "best test" to evaluate fetal well-being (ACOG,1999)
Three testing systemscontraction stress test, nonstress test,
THE BIOPHYSICAL PROFILE
and biophysical profile
The combined use of 5 fetal biophysical variables is a more accurate
means of assessing fetal health than a single element.
Definitions of the FHR patterns
5 biophysical components BASELINE NORMAL: 110-160 bpm
(1) fetal heart rate acceleration (NST) Bradycardia <110bpm
(2) fetal breathing Tachycardia >160bpm
(3) fetal movements
(4) fetal tone A BALANCE between sympathetic & paraS (vagal ) stimulation
(5) amnionic fluid volume Under the influence of ARTERIAL CHEMORECEPTORS- hypoxia &
hypercapnia modulate rate
o 2-5: ULTRASOUND
Causes of Fetal Bradycardia
Head Compression
Congenital Heart Block
Fetal Compromise
Maternal HypoThermia

Causes of Fetal Tachycardia

Maternal fever*MOST COMMON
Fetal compromise
Cardiac arrhythmias
Medications:
Parasympathomimetic medications ( Atropine )
Sympathomimetic ( terbutaline)

Baseline FHR variability

ABSENT Amplitude range undetectable
MINIMAL Amplitude range 5bpm or fewer
MODERATE Amplitude range of 6-25bpm
MARKED Amplitude range >25bpm

NST may be omitted if the 4 ultrasound parameters are all normal

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Significance of a normal FHR variability
Excellent indicator of good fetal well being
INCREASED VARIABILITY WITH fetal breathing, movement, AOG

Causes of Decreased or Absent Variability

Fetal acidemia, Maternal acidemia
Fetal sleep
Prematurity
Drugs (MgSO4, diazepam, meperidine
Vagal blockade (atropine)
Defective cardiac conduction system

Reduced baseline heart rate variability is the SINGLE MOST

RELIABLE SIGN OF FETAL COMPROMISE
Definitions of the FHR patterns
SINUSOIDAL FETAL HEART RATE
PATTERN
Observed in fetal anemia: Rh
isoimmunization, fetomaternal
hemorrhage, twin-twin transfusion,
vasa previa bleeding
ACCELERATIONS
Accelerations are always
reassuring and always confirm that
the fetus is not acidemic at that
time
Smooth, sine wave like undulating
Frequency 2-5/minute for 20 mins
Usually assoc with FETAL ANEMIA
Fetal asphxia; chorioamnionitis,
fetal distress, cord occlusions
Insignificant sinusoidal patterns:
meperidine, morphine, butophanol
Visually apparent increase in FHR
15bpm above baseline lasting
15 seconds
Absence of acceleration is not
necessarily an unfavorable sign
PROLONGED deceleration Isolated decrease in FHR
15 bpm, 2 minutes but < 10 mins
in duration from onset to return to
baseline
Causes of Prolonged Deceleration
Common causes
Cervical examination
Uterine hyperactivity
Cord entanglement
Maternal supine hypotension
Other causes:
Conduction analgesia
Maternal hypothermia
Abruption
Umbilical cord prolapse
Maternal seizure
Valsalva maneuver
FETAL SCALP BLOOD SAMPLING
PROTOCOL TO CONFIRM FETAL DISTRESS:
pH > 7.25, observe
pH 7.20 - 7.25, repeat within 30 minutes.
pH is < 7.20, another scalp blood sample is collected if < 7.20
DELIVER

FHR TRACINGS FALL INTO ONE OF THREE CATEGORIES

Category Clearly abnormal requiring

immediate action
III
Category Indeterminate requiring careful
evaluation and possible corrective
II measures

EARLY Decelerations Nadir of the deceleration occurs at

HEAD COMPRESSION
the same time as the peak of
contraction.
Category Clearly normal requiring no change
in management
I
Category I Normal
Baseline rate: 110-160bpm
Baseline FHR variability: moderate
Late or variable decelarations: absent
Early decelerations: present or absent
Accelerations: present or absent

Category II Indeterminate
Baseline rate:
o Bradycardia not accompanied by absent baseline
variability
o Tachycardia
LATE decelerations Onset, nadir and recovery of the
Baseline FHR variability
UTEROPLACENTAL deceleration occur after the
o Absent baseline variability not accompanied by
INSUFFICIENCY beginning, peak and end of the
recurrent decelerations
contraction, respectively.
o Minimal baseline variability
o Marked baseline variability
VARIABLE decelerations An ABRUPT decrease in the FHR Accelerations
UMBILICAL below the baseline o Absence of induced accelerations after fetal
COMPRESSION Less than 30 seconds from onset to stimulation
nadir Periodic or episodic decelerations
o Recurrent variable decelerations accompanied by
minimal or moderate baseline variability
o Prolonged deceleration 2 minutes but < 10 minutes
o Recurrent late decelerations with moderate baseline
variability

PHYSIO OB REVIEW FEU-NRMF Page 14

 o Variable decelerations with other characteristics,
such as slow return to baseline, "overshoots," or
"shoulders"
Not predictive of abnormal fetal acid-base status
Requires continued surveillance and re-evaluation
Do resusitative measures or do ancillary tests to ensure fetal
well-being

Category III - Abnormal

Absent FHR variability along with any of the following:
o Recurrent late decelerations
o Recurrent variable decelerations
o Bradycardia
o Sinusoidal pattern
Associated with abnormal fetal acid-base saturation at the time
of observation
Maternal O2 RISK FACTORS for NTDs
Discontinue of labor stimulation 1. Family history
Treatment of maternal hypotension 2. environmental agents
Change of maternal position 3. genetic syndrome or anatomical anomalies associated with
Treatment of tachysystole NTDs
DELIVER 4. high-risk racial or ethnic group
5. anti-folate receptor antibodies

AMNIOINFUSION 95% of NTD occur in the absence of risk factors

INDICATIONS: Recurrence risk is approximately 4% if a couple previously has a child with
prolonged variable decelerations. NTD one etiology is a mutation in the MTHFR gene
oligohydramnios and with PROM Environmental exposure: hyperthermia, medications that disturb folic acid
dilute or wash out thick meconium. metabolism, hyperglycemia from IDDM
Many women at increased risk for NTD benefit from taking 4mg of FA daily
PATTERNS OF UTERINE ACTIVITY: before conception and through the first trimester.
Montevideo units to define uterine activity
Total uterine pressure per contractions in a 10 minute Maternal Serum AFP Screening
observation The American College of Obstetricians and Gynecologists
(2003) recommends that ALL PREGNANT WOMEN BE OFFERED
New Terminology for Uterine Contractions: SECOND-TRIMESTER MATERNAL SERUM AFP SCREENING
Normal Uterine Activity: five or less uterine contractions in 10 15 - 20 weeks
minutes Normal Value: =/< 2-2.5 MoM
Tachysystole: more than 5 contractions in 10 minutes Abnormal screening test - Genetic Counseling
consideration for a Diagnostic test(ULTRASOUND)
ETIOLOGY OF BIRTH DEFECTS
1. MALFORMATION - an intrinsic abnormality "programmed" in Some Conditions Associated with LOW Maternal Serum AFP
development 1. obesity
a. Example: Spina bifida 2. DM
2. DEFORMATION - genetically normal fetus develops abnormally 3. Chromosomal trisomies
because of mechanical forces imposed by the uterine 4. GTD
environment. 5. Fetal death
a. Ex: prolonged oligohydramnios->contractures 6. Overestimated gestational age
3. DISRUPTION
a more severe change in form or function DOWN SYNDROME
a. Ex: amnionic band causing a cephalocele or limb- low maternal serum AFP levels at 15 to 20 weeks
reduction abnormality.
FIRST TRIMESTER DOWN SYNDROME SCREENING
MULTIPLE STRUCTURAL OR DEVELOPMENTAL ABNORMALITIES between 11 and 13 6/7 weeks
SYNDROME - a cluster of several anomalies or defects that have 1. Maternal serum screening
the same cause free beta hCG
Example: Trisomy 18 Pregnancy-associated plasma protein A (PAPP-A)
SEQUENCE - anomalies that all develop sequentially as result of 2. Sonographic evaluation: Nuchal translucency (NT)
one initial insult
Example: Oligohydramnios leading to pulmonary The American College of Obstetricians and Gynecologists
hypoplasia, limb contractures, and facial (2007b) recommends that when the NUCHAL TRANSLUCENCY
deformities. MEASUREMENT IS 3.5 MM OR GREATER with a normal fetal
ASSOCIATION - particular anomalies occur together frequently karyotype, targeted sonographic examination, fetal
but do not seem to be linked etiologically echocardiography, or both should be considered.

Example: VACTERL association: includes three or more of the following
vertebral defects, anal atresia, cardiac defects, tracheoesophageal
fistula, renal anomalies, limb abnormalities
PRENATAL DIAGNOSIS OF NEURAL-TUBE DEFECTS
NEURAL TUBE DEFECTS (NTDS)
second most common class of birth defect
Open neural-tube defects include:
Anencephaly
Spina bifida
Cephalocele
Other rare spinal fusion (schisis)
abnormalities
95% occur without risk factor or family history
SECOND TRIMESTER DOWN SYNDROME SCREENING
Multiple Maternal Serum Markers could reliably differentiate
pregnancies affected by trisomy 18 and 21 from unaffected
pregnancies
Serum markers: Triple Test &Quad Test*
AFP
Human chorionic gonadotropin (hCG)
Unconjugated estriol concentration
Dimeric inhibin alpha*
Ultrasonographic screening for MINOR ABNORMALITIES
Nuchal Translucency (NT) 1st trimester finding
Thickened Nuchal Fold 2nd trimester finding
Absent nasal bone
Space between the 1st and 2nd toes Sandal gap

AMNIOCENTESIS

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 15 and 20 weeks
Complications: transient vaginal spotting or amnionic fluid
leakage and chorioamnionitis

Femur length (FL) - variation of 7 to 11 days in the second

trimester
Abdominal circumference (AC) - fetal growth

EARLY AMNIOCENTESIS
Between 11 and 14 weeks
Same technique
Many centers no longer perform amniocentesis before 14
weeks

CHORIONIC VILLUS SAMPLING

10 to 13 weeks
transcervically or transabdominally,
Complications are similar to those of amniocentesis

First Trimester ULTRASOUND

1. viability
2. anembryonic gestation / embryonic demise
3.Multifetal gestation - OPTIMAL TIME to determine chorionicity
4.BEST TIME to evaluate the uterus, adnexal structures, and cul-
de-sac
Transabdominal scanning
Gestational sac 6 weeks
Fetal echoes & cardiac activity 7 weeks
Transvaginal examination
Cardiac motion embryo is 5 mm in length
Abdominal Wall Defects
Gastroschisis
full-thickness defect right of the umbilical cord insertion
bowel herniates into the amnionic cavity
survival rate 90 percent
Cause: early vascular occlusionabdominal wall ischemia.
Omphalocele
abdominal contents covered only by a two-layered sac of
amnion and peritoneum.
The umbilical cord inserts into the apex of the sac
part of a genetic syndrome, such as BeckwithWiedemann or
pentalogy of Cantrell
(CRL= 6wks)
Renal Agenesis
compressed face, and death from cord compression or
pulmonary hypoplasia.
renal agenesis Potter syndrome,
oligohydramnios sequence.

DOPPLER VELOCIMETRY
Diminished blood flow may be reflected such as
the following:
1. Diastolic notch
2. Increased SD ratio (Stuart Index)
3. Pulsatility index; Resistance index
4. Absence or reversed end diastolic (ARED) blood flow

PELVIC ANATOMY

Fetal Measurements LINEA TERMINALIS separates the true and false pelvis
Gestational sac (GS) - 4 6 weeks
Crown-Rump Length(CRL) - 8-10 weeks
Biparietal Diameter (BPD) - 14- 26 weeks most accurate
parameter

PHYSIO OB REVIEW FEU-NRMF Page 16

ISCHIAL SPINES
distance between them usually represents the shortest
diameter of the pelvic cavity
valuable landmarks for fetal head descent

PLANES AND DIAMETERS OF THE PELVIS

Four Imaginary Planes
Plane of the Pelvic Inletthe Superior strait
Plane of the Pelvic Outletthe Inferior strait
Plane of the Midpelvisthe LEAST pelvic dimensions
Plane of Greatest Pelvic dimensionof no obstetrical
significance

PELVIC INLET
Boundaries:
Posterior: Sacrum -promontory and alae
Lateral: Linea terminalis
Anterior: horizontal pubic rami and the symphysis pubis
Shape: round or gynecoid in 50 % of white women

MIDPELVIS (Plane of least pelvic dimension)

Boundaries:
Anterior - inferior portion of symphysis pubis
Lateral - Ischial spines
Posterior tip of sacrum
A, Anteroposterior Diameter (1) AnteroPosterior diameter (APM) = 11.5 cm
1. Obstetrical conjugate (OC) from symphysis pubis to tip of sacrum(4 to 5th sacral
midposition of the symphysis pubis to promontory of vertebrae)
the sacrum (2) Interspinous diameter (IS)= 10 cm
between 2 ischial spines
shortest anteroposterior diameter of the inlet Smallest pelvic diameter
Measures >/=10 cm (3) Posterior sagittal diameter of the midplane (PSM)
OC= Diagonal conjugate 1.5-2 cm = 4.5 cm
between sacrum and the line created by the interspinous
diameter

PELVIC OUTLET

2. Diagonal conjugate (DC)

lower margin of the symphysis to the promontory of
the sacrum
N.V. = 12 cm
3. True conjugate (TC) Boundaries:
Superior portion of symphysis pubis to promontory of Anterior: undersurface of Pubic Arch
the sacrum Posterior - tip of the Sacrum
N.V. = 11 cm Lateral: Sacrosciatic ligaments & the Ischial tuberosities
TC= Diagonal conjugate-1.2cm Anteroposterior diameter of the outlet (APO) undersurface of
pubic arch to tip of the sacrum
B. Transverse diameter AP: 9.5-11.5 cm
greatest transverse diameter (GTI) - distance between the Intertuberous diameter (IT) - between 2 ischial tuberosities
linea terminalis IT 11 cm
= 13.5 cm Posterior sagittal diameter of the outlet* (PSO) between the tip
of the sacrum and the line created by the intertuberous
diameter
PS: =/> 7.5 cm

PELVIC SHAPES
Caldwell and Moloy classification
Posterior segment determines the type of pelvis
Anterior segment determines the tendency
Many pelvis are not pure but are mixed

PHYSIO OB REVIEW FEU-NRMF Page 17

 Ex: a Gynecoid pelvis with an android tendency
PHASES OF PARTURITION
Gynecoid
suited for delivery of most fetuses
found in almost 50 percent of women

Anthropoid
oval anteroposteriorly
> AP diameter than Transverse diameter

Android
poor prognosis for vaginal delivery

Phase 1 of Parturition: Uterine Quiescence and Cervical Softening

Uterine Quiescence
Platypelloid Braxton Hicks contractions or False labor
Short AP and wide Transverse diameters Low-intensity myometrial contractions felt
by the mother but DO NOT cause
cervical dilatation

Phase 2 of Parturition: Preparation for Labor

LIGTHENING
Abdomen undergoes a shape change, described
by women as THE BABY DROPPED.

Phase 3 of Parturition: Labor

Stages of Labor
First stage
Stage of cervical effacement and
dilatation
Ends when the cervix is fully dilated( 10
Engagement cm)
Descent of the biparietal plane of the fetal head to a level The Second stage
below that of the pelvic inlet Stage of fetal expulsion
IF HEAD is engaged the INLET is adequate Begins when cervical dilatation is
ascertained by vaginal exam and by abdominal palpation complete(10cms) and ends with delivery
When the lowermost portion of the fetal head is at or below the Third stage of labor
ischial spines, it is usually engaged EXCEPT if there is molding or Stage of placental separation and
caput formation expulsion
Begins after delivery of the fetus and ends
PELVIC OUTLET MEASUREMENTS with the delivery of the placenta
Intertuberous diameter (IT) = >8cm 2 Phases of cervical dilatation:
Distance between two ischial tuberosities Latent phase
Place a closed fist against the perineum between two ischial variable and sensitive to extraneous
tuberosities factors , sedation and myometrial
stimulation
Midpelvis Estimation Active phase
Suspicious findings for MIDPELVIC CONTRACTION Acceleration phase
Prominent ischial spines predictive of the outcome of a
sidewalls are convergent particular labor
shallow concavity of the sacrum

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 Phase of maximum slope
good measure of over all
efficiency of the uterus
Deceleration phase
reflective of feto-pelvic
relationship

First Stage of Labor: Clinical Onset of Labor

Show or bloody show.
Causes of labor pains: As labor progresses, sinciput and brow presentations almost always
(1) hypoxia of the contracted convert into vertex or face presentations by neck flexion or extension,
myometrium respectively.
(2) compression of nerve
ganglia
(3) cervical stretching
(4) stretching of the peritoneum
Ferguson reflex
Manipulation of the cervix and stripping the fetal
membranes cause the release of prostaglandin F2
metabolite (PGFM)

Distinct Lower and Upper Uterine Segments

UPPER SEGMENT:
firm during contractions
contracts,retracts and expels fetus
BREECH PRESENTATION
Frank Breech thighs are flexed and the legs extended
LOWER SEGMENT:
Complete Breech thighs AND legs are flexed
Softer ,distended and more passive
Incomplete, or Footling Breech - if one or both feet, or one or
both knees, are lowermost or extended
Uterine Changes during Labor
physiological retraction ring-junction between the
lower and upper segment
In obstructed labor--> the ring is prominent-->
pathological retraction ring or Bandl ring

Stages of Labor
1st Stage of Labor: Clinical Onset of Labor
2nd Stage of Labor: Fetal Descent
3rd Stage of Labor: Delivery of Placenta and
Membranes

MECHANISM OF PLACENTAL SEPARATION: FETAL POSITION

SCHULTZE relationship of the chosen portion of the fetal presenting part to
Central separation, the right or left side of the birth canal.
blood does not escape externally
Fetal membranes appears first at the vulva
DUNCAN
Separates at periphery
blood escapes from the vagina
placenta descends sideways
(cotyledons)appears first

Phase 4 of Parturition: The Puerperium

lactogenesis and milk let-down
Reinstitution of ovulation
Within 4 to 6 weeks after birth, but dependent on
lactation-induced amenorrhea(LAM)

FETAL LIE
Relation of the long axis of the fetus to that of the mother
TYPES:
Longitudinal
99% of labors at term
Transverse lie
Predisposing factors: multiparity, placenta previa,
hydramnios, and uterine anomalies
Oblique Lie
45-degree angle
unstable
Varieties of Presentations and Positions
Shoulder presentations( acromion (scapula) is the portion of the
FETAL ATTITUDE
fetus
UNIVERSAL FLEXION Another term used is transverse lie, with back up or back down.
the arms are usually crossed over the thorax or
become parallel to the sides.
The umbilical cord lies in the space between them
DIAGNOSIS OF FETAL PRESENTATION AND POSITION
and the lower extremities.
LEOPOLDS MANEUVER
L1, L2 and L3 examiner stands at the side of the bed and faces
FETAL PRESENTATION
the patient
portion of the fetal body foremost within the birth canal
L4 examiner faces patients feet

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First Maneuver Fundal Grip Extension
Breech sensation of a large, nodular body Head presses upon the pelvic floor
Cephalic hard and round movable and balottable Two forces :
1. exerted by the uterus
Second Maneuver Lumbar Grip 2. resistant pelvic floor
Back hard, resistant
Extremities numerous small, irregular and mobile parts External Rotation
bisacromial diameter into relation with the anteroposterior
Third Maneuver Pawliks grip diameter of the pelvic outlet
The lower portion of the abdomen is grasped just above the
symphysis pubis Expulsion
Engaged or not engaged anterior shoulder appears under the symphysis pubis.
After delivery of the shoulders, the rest of the body quickly
Fourth Maneuver Pelvic grip passes.
DETERMINE THE CEPHALIC PROMINENCE
Vertex Presentation the prominence is on the same side as ASYNCLITISM
the small parts It is the lateral deflection of the head to a more anterior or
Face Presentations the prominence is on the same side as the posterior position in the pelvis
back
2 TYPES OF ASYNCLITISM
CARDINAL MOVEMENTS OF LABOR 1. ANTERIOR ASYNCLITISM
1. Engagement 2. POSTERIOR ASYNCLITISM
2. Descent
3. Flexion ANTERIOR ASYNCLITISM
4. Internal Rotation o Sagittal suture approaches the sacral promontory
5. Extension o More of the ANTERIOR parietal bone presents
6. External Rotation
7. Expulsion
POSTERIOR ASYNCLITISM
o Sagittal suture lies close to the symphysis
o POSTERIOR parietal bone will present

Changes in Shape of the Fetal Head

CAPUT SUCCEDANEUM
The portion of the fetal scalp becomes edematous

MOLDING
The change in fetal head shape from external compressive
forces

Latent Phase
Mother perceives regular contractions.
The latent phase for most women ends at between 3 and 5 cm
of dilatation.

Prolonged Latent Phase

> 20 hours in nullipara
CARDINAL MOVEMENTS OF LABOR >14 hours in multipara
Descent
first requisite for birth of the newborn Active Labor
Nulliparas= engagement before labor, and further descent cervical dilatation of 3 to 5 cm or more, in the presence of
follow until the onset of the second stage uterine contractions
Multiparous= descent begins with engagement

Four forces FOR DESCENT

1. pressure of the amnionic fluid
2. direct pressure of the fundus upon the breechs
3. bearing down efforts
4. extension and straightening of the fetal body

Flexion
suboccipitobregmatic diameter is substituted for the longer
occipitofrontal diameter

Internal Rotation
occiput gradually moves toward the symphysis pubis anteriorly
from its original position

PHYSIO OB REVIEW FEU-NRMF Page 20

 THIRD STAGE 15-30 mins 15-30 mins
ABNORMAL LABOR PATTERNS, DIAGNOSTIC CRITERIA, AND METHODS OF
TREATMENT

MANAGEMENT OF FIRST STAGE OF LABOR

FETAL HEART RATE MONITORING

First stage of labor:
every 30 minutes (LOW RISK) 15 MINS (HIGH RISK)
Second stage:
every 15 mins(LOW RISK) 5 MINS (HIGH RISK)

Maternal monitoring and management during labor

BENEFITS FROM AMNIOTOMY
1. Rapid Labor
2. Early detection of meconium staining
3. Opportunity to apply electrode

RITGEN MANUEVER OR MODIFIED RITGEN MANUEVER

Pressure on the chin of the fetus through the perineum , the
other hand exerts pressure superiorly against the occiput

Factors contributing to both protraction and arrest disorders

excessive sedation
epidural analgesia
fetal malposition

Signs of placental separation

1. Calkins Sign the uterus becomes globular The earliest SIGN to appear.
2. Sudden gush of blood
3. Uterus rises in the abdomen
4. Lengthening of the umbilical cord

Delivery of the Placenta

Traction on the umbilical cord must not be used to pull the
placenta out of the uterus--->
UTERINE INVERSION

Active management of the 3rd stage

UTERINE MASSAGE
OXYTOCIN, ERGONOVINE, AND METHYLERGONOVINE
DETECTION OF RUPTURED MEMBRANES
SIGNIFICANCE OXYTOCIC AGENTS
1. prolapse of the umbilical cord Oxytocin (pitocin, syntocinon)
2. labor is likely to occur Not effective by mouth
3. increased incidence of intrauterine infection SIDE EFFECTS: ANTIDIURETIC/HYPOTENSION
NOT GIVEN AS IV BOLUS
DIAGNOSIS
1. amniotic fluid pooling Ergonovine and Methylergonovine
2. Testing the pH of the vaginal fluid : From ergot
pH above 6.5 is consistent with ruptured membranes Powerful stimulants of myometrial contraction
3. the use of the indicator Nitrazine SIDE EFFECTS: transient severe hypertension
yellow-->blue NOT USED IN PATIENTS WITH BRONCHIAL ASTHMA
4. Other Tests :
Arborization or ferning pattern Prostaglandins
alpha-fetoprotein positive Not used routinely
injection of various dyes into amniotic sac management of postpartum hemorrhage due to uterine atony
PG F2-NOT USED IN B. ASTHMA
STATION PG E2-SAFE FOR BRONCHIAL ASTHMA
When lowermost portion of presenting part is at level of ischial
spines designated as zero LACERATIONS OF THE BIRTH CANAL
Divisions represent cms above and below the spines into fifths First Degree Laceration
fourchette, perineal skin and vaginal mucous membrane
DURATION OF STAGES OF LABOR Second Degree Laceration
skin and mucous membrane, the fascia and muscles
Nullipara Multipara
Third Degree Laceration
skin, mucous membrane, perineal body and sphincter
FIRST STAGE Fourth Degree Laceration
Extends through the rectal mucosa to expose the lumen of the
Latent Phase <20 hours <14 hours rectum

Active Phase 1.2cm/hr 1.5cm/hr

SECOND STAGE 50 mins 20 mins

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MIDLINE versus MEDIOLATERAL EPISIOTOMY LACTATION
COLOSTRUM
Characteristic Midline Mediolateral
deep lemon-yellow-colored liquid
2nd postpartum day
Surgical repair Easy More difficult rich in immunological components(Ig A), minerals, amino
acid,protein
but less sugar and fat
Faulty hearing Rare More common
HUMAN MILK
Postoperative Minimal Common All vitamins EXCEPT VIT K are found in human milk
pain Vitamin K after delivery is required to prevent hemorrhagic
disease of the newborn
Anatomical Excellent Occasionally
results faulty IMMUNOLOGICAL CONSEQUENCES OF BREASTFEEDING

Blood loss Less More SECRETORY IgA

less prone to enteric infection against rotavirus
infections,Escherichia coli infections
contains both T and B lymphocyte
Dyspareunia Rare Occasional
LACTATION INHIBITION
Milk leakage, engorgement, and breast pain ( 3 to 5 days)
Extensions Common Uncommon TREATMENT:
Ice packs
analgesics
PUERPERIUM Bromocriptine , for lactation inhibition is associated with
considered to be between 4 and 6 weeks strokes, myocardial infarctions, seizures, and psychiatric
disturbances.
INVOLUTION OF THE REPRODUCTIVE TRACT
UTERINE INVOLUTION CONTRACEPTION FOR BREASTFEEDING WOMEN
4 weeks after delivery Recommendations for Hormonal Contraception if Used by Breast Feeding
uterus regains its previous nonpregnant size Women
1.Progestin-only oral contraceptives --> started 23 weeks postpartum
LOCHIA 2.Depot medroxyprogesterone acetate --> 6 weeks postpartum.a
LOCHIA RUBRA- first few days after delivery, RED color i 3.Hormonal implants -->inserted at 6 weeks postpartum.
LOCHIA SEROSA- After 3 or 4 days, PALE in color
LOCHIA ALBA- After about the 10th day, WHITE or YELLOWISH WHITE color CONTRAINDICATIONS TO BREASTFEEDING
Breastfeeding is not contraindicated if hepatitis B immune
DECIDUA AND ENDOMETRIAL REGENERATION globulin is given to infants of seropositive mothers.
Superficial layer Hepatitis C infection is not a contraindication to breast feeding
BECOMES NECROTIC--> sloughed in the lochia Herpes simplex virus if there are no breast lesions is NOT a
Basal layer contraindication to breast feeding
adjacent to the myometrium--> the source of new
endometrium BREAST FEVER
breasts -->distended, firm, and nodular
SUBINVOLUTION elevation of temperature (ranged from 37.8 to 39)
arrest or retardation of involution
Causes: Treatment: binder or brassiere, ice bag, analgesic, pumping of the breast
Infection
retained placental fragments MASTITIS
incompletely remodeled uteroplacental arteries unilateral, marked engorgement, inflammation.
SIGNS AND SYMPTOMS chills, fever and tachycardia.
irregular or excessive uterine bleeding ETIOLOGY: Staphylococcus aureus 40 %; c
uterus is larger and softer Immediate source of organisms --> infant's nose and throat

Management of Subinvolution TREATMENT: MASTITIS

Ergonovine or methylergonovine culture of the expressed milk
Antibiotic therapy for infection antimicrobial therapy:
Chlamydia trachomatis Dicloxacillin 500 mg orally four times daily,
MOST COMMON CAUSE Erythromycin if penicillin sensitive
MANAGEMENT: Azithromycin or Vancomycin is effective against MRSA
Doxycycline treatment for 10 to 14 days

PLACENTAL SITE INVOLUTION
6 weeks
Complete extrusion of the placental site
LATE POSTPARTUM HEMORRHAGE
American College of Obstetricians and Gynecologists (2013b)
bleeding 24 hours to 12 weeks after delivery
Causes:
MOST COMMON CAUSE:
retention of a placental fragments
Treatment
oxytocin, ergonovine, methylergonovine, or
prostaglandins
Antimicrobial with infection
Suction curettage large clots
Curettage- NON RESPONSIVE TO medical
management
Postpartum blues- degree of depressed mood a few days after delivery
Excitement and fears during pregnancy and delivery
Discomforts of the early puerperium
Fatigue from loss of sleep during labor and postpartum
anxiety over the ability to provide appropriate infant care, and
body image concerns
TREATMENT
anticipation, recognition, and reassurance
Mild and self-limited to 2 to 3 days, although it sometimes lasts
for up to 10 days
CONTRACEPTION
Not breastfeeding, menses usually return within 6 to 8 weeks
HOME CARE
COITUS - no definite time after delivery when coitus should be resumed
-coitus may be resumed based on the patient's desire and comfort

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 Lidocaine or Chloroprocaine at 3 and 9 oclock
Complication: fetal bradycardia
ANESTHESIA AND ANALGESIA
MATERNAL RISK FACTORS THAT SHOULD PROMPT ANESTHESIA CONSULTATION: SPINAL (SUBARACHNOID) BLOCK
Vaginal Delivery
forceps or vacuum delivery
1. Marked Obesity
T10 dermatome
2. Severe edema or anatomical abnormalities of face, neck, or spine, Lidocaine or Bupivacaine
including trauma or surgery Cesarean Delivery
T4 dermatome
3. Abnormal dentition, small mandible, or difficulty opening mouth
COMPLICATIONS OF SPINAL (SUBARACHNOID) BLOCK
4. Extremely short stature , short neck, or arthritis of the neck Hypotension
High spinal blockade
5. Goiter Spinal (Postural puncture) headache
Convulsions
6. Serious maternal medical problems, such as cardiac, pulmonary or
Bladder dysfunction
neurological disease
Oxytocics and hypertension
Arachnoiditis and meningitis
7. Bleeding disorders
Contraindications to Spinal Anesthesia
8. Severe preeclampsia ABSOLUTE CONTRAINDICATIONS
9. Previous history of anesthetic complications hypotension
coagulopathy
bacteremia
10. Obstetrical complications likely lead to operative delivery Skin infection
e.g., placenta previa or higher-order multiple gestation Increased intracranial pressure

EPIDURAL ANESTHESIA
Goals for Optimizing Obstetrical Anesthesia Services
Continuous Lumbar Epidural Block
Nonpharmacological Methods of Pain Control
VAGINAL DELIVERY - T10 to S5
1. LAMAZE
CESAREAN DELIVERY - T4 to S1
teaching pregnant women relaxed breathing and their labor
partners psychological support techniques.
COMPLICATIONS OF EPIDURAL ANESTHESIA
2. CLINICAL HYPNOSIS power of the mind to heal the body;
Total spinal blockade
increases of beta endorphins in the peripheral blood
Ineffective analgesia
3. ACUPUNCTURE
Hypotension
Central nervous stimulation
EFFICACY AND SAFETY OF PARENTERAL AGENTS
Maternal pyrexia
1. Meperidine is the most common opioid used worldwide for pain
Back pain
relief in labor.
Meperidine or other narcotics cause newborn respiratory
Effects on Labor
depression
Prolongs active phase of labor by 1 hour
Increases the need for instrumental delivery LIKE FORCEPS AND
NARCOTIC ANTAGONISTS
VACUUM due to prolonged second-stage labor
Naloxone
Reverses respiratory depression induced by opioid narcotics
Contraindications
NITROUS OXIDE
Hemorrhage
50% nitrous oxide and oxygen provides satisfactory analgesia

during labor
Infection at or near the sites of puncture

REGIONAL ANALGESIA
Suspicion of neurological disease
SENSORY INNERVATION OF THE GENITAL TRACT
Anticoagulation
Uterine Innervation
Early in labor SENSORY T11 and T12 nerves
Severe Preeclampsia-Eclampsia
Motor pathways T7 and T8 vertebrae
BEST ANESTHESIA: EPIDURAL ANESTHESIA
Lower Genital Tract Innervation
GENERAL ANESTHESIA
Pudendal nerve sensory nerve fibers from S2 through S4
PATIENT PREPARATION
nerves
ANTACIDS
Passes beneath the posterior surface of the
UTERINE DISPLACEMENT
sacrospinous ligament just as the ligament attaches
Lateral uterine displacement
to the ischial spine
Preoxygenation
ANESTHETIC AGENTS
Thiopental
(Table 19-3. Some Local Anesthetic Agents used in Obstetrics)
Ease and rapid/ minimal risk of vomiting
Poor analgesic agents
Central Nervous System Toxicity
May cause newborn depression
Bizarre behavior, slurred speech, muscle fasciculation and
Ketamine
excitation, generalized convulsions, loss of consciousness
causes a rise in blood pressure
Unpleasant delirium and hallucination.
Cardiovascular Toxicity
Hypertension , tachycardia, hypotension and cardiac
INTUBATION
arrhythmias
Sellick maneuver Cricoid pressure is used to occlude the
esophagus from induction until intubation
PUDENDAL BLOCK
Relatively safe and simple
Failed Intubation
Complications: serious systemic toxicity, hematoma formation
Morbid obesity is also a major risk factor for failed or difficult
from perforation of a blood vessel
intubation.
PARACERVICAL BLOCK
Pain relief during the first stage of labor

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 GAS ANESTHETICS
Volatile Anesthetics
Most commonly used is isoflurane.
produce remarkable uterine relaxation
USES:
Internal podalic version of the second twin
Breech decomposition
Replacement of acutely inverted uterus
.
ASPIRATION
Aspiration pneumonitis has been the most common cause of
anesthetic deaths in obstetrics.

.
ASPIRATION
Aspiration pneumonitis has been the most common cause of
anesthetic deaths in obstetrics.
A fasting period of 8 hours or more is preferable for
uncomplicated parturients undergoing elective cesarean
delivery.

FASTING
A fasting period of 8 hours or more is preferable for
uncomplicated parturients undergoing elective cesarean
delivery.

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