Gravidity

: the total number of pregnancies of any gestation

o includes abortions, ectopic pregnancies, and hydatidiform moles

o twins count as one pregnancy

Parity : the number of pregnancies that have been carried to > 20 weeks

o twins count as one

o grand multiparity is parity of 4 or more

four digit number (T P A L)

o 1st digit: number of term infants delivered (> 37 weeks)

o 2nd digit: number of premature infants delivered (20 to 37 weeks)

o 3rd digit: number of abortions (< 20 weeks)

o 4th digit: number of living children

Trimesters

o T1: 0 to 12 weeks
o T2: 12 to 28 weeks

o T3: 28 to 40 weeks

o normal pregnancy term: 37 to 42 weeks

Abortion : loss of intrauterine pregnancy prior to viability of fetus

o < 20 weeks and/or < 500 g fetal weight

o ncludes induced (therapeutic) and spontaneous (miscarriage)

Stillbirth : loss of intrauterine pregnancy after 20 weeks and/or > 500 g fetal weight

Stillbirth Rate : the annual number of stillbirths per 1000 total births

Perinatal Mortality Rate : the annual number of stillbirths and early neonatal deaths (in the
first seven days of life) per 1000 total births

causes
prematurity
congenital anomalies
Neonatal Mortality Rate : the annual number of deaths of liveborn infants within 28 days per
1000 live births

Infant Mortality Rate the annual number of deaths of liveborn infants in the first year of life
per 1000 live births (includes neonatal mortality)

Maternal Mortality Rate the annual number of deaths of women while pregnant or within 90
days of pregnancy per 100 000 live births

direct: from obstetrical causes such as ectopic, PIH, PPH, infection, PE

indirect: from pre-existing illness or by accident

Birth Rate : the annual number of live births per 1000 population

Fertility Rate : the annual number of live births per 1000 women aged 15-44 years

DIAGNOSIS OF PREGNANCY

Symptoms

1. amenorrhea
2. nausea and/or vomiting
3. breast tenderness
4. urinary frequency fatigue

Signs

1. softening of the cervix (Goodell sign): 4-6 weeks

2. bluish discoloration of the cervix and vagina due to engorgement of pelvic vasculature
(Chadwick sign): 6 weeks
3. uterine enlargement
4. softening of the isthmus (Hegar sign): 6-8 weeks

Investigations

1. Beta hCG

o positive in the serum at 9 days post-conception

o positive in the urine 28 days after LMP

2. Transvaginal ultrasound
 o 5 weeks: gestational sac visible (Beta hCG = 1200 -1500 mIU/mL)
o 6 weeks: fetal pole seen

o 7-8 weeks: fetal heart tones visible

3. Transabdominal U/S
intrauterine pregnancy visible at Beta hCG = 5000 mIU/mL

A very early, 3-mm mean diameter intrauterine gestational

sac at 5 weeks postmenstruation ( arrow ).

A. An eccentrically-placed intrauterine gestational sac 6 weeks postmenstruation (arrow).

B. In contrast, a pseudosac (arrow) in a patient with ectopic pregnancy representing a collection
of blood or fluid collected within the endometrial cavity.

MATERNAL PHYSIOLOG CHANGES (Part 01)

General Principles

progesterone induces relaxation of smooth muscle, among other effects

physiologic changes are more pronounced in multiple gestations

Cardiovascular System

1. increased cardiac output, heart rate, and blood volume (hyperdynamic circulation)
2. decreased blood pressure (especially diastolic, maximal in T2) due to decreased
peripheral vascular resistance
 3. blood flow to the uterus, kidneys, breasts, and skin increases with
gestational age
4. enlarging uterus compresses IVC and pelvic veins leading to risk of hypotension (by
decreasing venous return) as well as varicose veins, hemorrhoids and leg edema (because
of increased venous pressure)

Hematologic System

1. apparent decrease in hemoglobin and hematocrit due to hemodilution

: plasma volume increases more than RBC mass
2. increased risk of DVT and PE secondary to hypercoagulable state

increase in factors I, VII, VIII, IX, X, XII

decrease in factors XI, XIII and antithrombin III activity
venous stasis from uterine compression of veins

3. increased leukocyte count but impaired function

o 5000 to 12 000/uL in pregnancy

o up to 25 000/uL in labour/postpartum

o depressed immunity but often have improvement in autoimmune conditions

*** Placenta and the foetus are made up of different genetic components, the immune
tolerance that is necessary for the non-rejection of the foetus

Respiratory System

1. increased oxygen consumption by 20%

2. increased sensitivity to carbon dioxide (progesterone effect on respiratory centre)
results in hyperventilation and respiratory alkalosis compensated by increased renal
excretion of serum bicarbonate
3. 50% increase in minute ventilation
4. decreased total lung capacity, FRC and residual volume
5. vital capacity unchanged
6. increased tidal volume by 35-50%
7. increased alveolar ventilation by 65%

** This maintain higher concentration gradient of CO2 between mother and Foetus

Gastrointestinal System
 1. increased gastroesophageal reflux ,due to

o decreased sphincter tone

o delayed gastric emptying

o increased intra-abdominal pressure

2. increased stasis in gallbladder

3. decreased GI motility----> increase water absorption ---->constipation

4. upward displacement of appendix

(appendicitis may have atypical presentation in pregnancy )

5. hemorrhoids caused by constipation and elevated venous pressure

Neurologic System

carpal tunnel syndrome and Bell's palsy more common

Integumentary System

1. pigmentation changes (fade after delivery)

o increased pigmentation of perineum and areola

o chloasma (pigmentation changes under eyes and bridge of nose)

o linea nigra (midline abdominal pigmentation)

o spider angiomas

o palmar erythema

2. striae gravidarum (fade but seldom disappear)

chloasma
linea nigra

spider angiomas

striae gravidarum

MATERNAL PHYSIOLOG CHANGES (Part 02)

Genitourinary System
 1. increased GFR 50% (therefore decreased BUN and serum creatinine) but no change in
urine output because of increased reabsorption in tubules glycosuria can be physiologic;
with increase in GFR the threshold for glucose reabsorption can be surpassed
2. increased urinary frequency
3. physiologic dilatation of ureters and renal pelvis (R > L) due to progesterone-induced
smooth muscle relaxation and uterine enlargement
4. increased incidence of UTI and pyelonephritis due to stasis

asymptomatic bacteriuria more likely to become a clinically significant infection (i.e.

pyelonephritis) in pregnancy and therefore should be treated

Endocrine System

1. estrogen

1. main estrogen is estradiol (E2)

2. production involves an intricate pathway, requiring maternal, placental and fetal
contributions
3. sudden decline may indicate fetal compromise

2. progesterone

1. produced by corpus luteum during first 7 weeks, thereafter synthesized by the

placenta
2. maintains the endometrium
3. absolutely necessary for continuation of pregnancy

3. Human chorionic gonadotropin (hCG)

1. produced by placental trophoblastic cells peptide hormone composed of two subunits:

alpha (common to all glycoproteins) and beta (specific to hCG)
2. has LH-like actions: maintains the corpus luteum
3. serum -hCG positive 8-9 days after ovulation
4. plasma levels double every 1-2 days, peak (8-10 weeks) and then fall to a plateau until
delivery
5. rule of 10's
 10 IU at time of missed menses
100 000 IU at 10 weeks (peak)
10 000 IU at term

6. levels below expected by dates suggest an ectopic pregnancy, abortion or wrong dates
7. levels higher than expected suggest multiple gestation, molar pregnancy, trisomy 21, or
wrong dates

4. thyroid

1. moderate enlargement and increased basal metabolic rate

2. increased total thyroxine and thyroxine binding globulin (TBG)
3. free thyroxine index and TSH levels are normal

5. adrenal : maternal cortisol rises throughout pregnancy (total and free)

6. prolactin

produced by maternal pituitary in response to increasing estrogen in pregnancy

stimulates lactation

7. relaxin

produced by the corpus luteum/ovary

relaxes symphysis pubis and other pelvic joints
helps soften and dilate the cervix
inhibits uterine contraction

Ca++ metabolism

1. total maternal Ca decreased due to decreased albumin

2. free ionized (i.e. active) proportion remains the same due to increased PTH which results
in increased bone resorption and gut absorption bone turnover increased but no loss of
bone density because estrogen counteracts the PTH effect by inhibiting resorption

PRENATAL CARE : INITIAL VISIT

PRECONCEPTION COUNSELLING

1. folic acid to prevent NTD s (0.4 to 1 mg daily in all women, 4 mg if past NTD)
2. genetic history and risk factors
3. modify medications, alcohol, smoking
4. rubella immunity
5. proper nutrition
6. use of prenatal vitamin and iron supplementation
7. impact on family and occupation (maternity/paternity leave)
8. domestic violence (50% of domestic violence begins in
pregnancy) depression / mental health

INITIAL VISIT

generally after 12 weeks

History

1. determine GA by dates from the first day of the LMP (if regular periods and sure dates)
2. if LMP unsure, get a dating ultrasound
3. determine EDC using the Naegele Rule

first day of LMP + 7 days - 3 months

e.g. LMP = 1 Apr. 1999, EDC = 8 Jan. 2000

modify appropriately for longer or shorter cycles

4. obtain obstetric history of all previous pregnancies (GTPAL)

5. obtain relevant medical, social, and family history

6. counselling
drug use, alcohol consumption, smoking
breastfeeding

Physical
1. complete physical exam
2. baseline BP (very important for relating subsequent changes)
3. baseline weight
4. pelvic exam
 Investigations

1. blood work

CBC, blood group and type, Rh antibodies

rubella titre, VDRL, HBsAg routine; HIV serology should be
offered to all

2. urine
R&M (Routine and Microscopy), C&S (Urine culture and sensitivity)
asymptomatic bacteriuria in 5% of pregnant women
if untreated 25-30% will get a UTI in pregnancy (increased risk of preterm labour)

3. pelvic exam
Pap smear (if none within 6 months), culture for GC and Chlamydia

PRENATAL CARE : SUBSEQUENT VISITS Part 01

for low-risk, uncomplicated pregnancy

o Visit monthly until 28 weeks

o Visit 2 weeks from 28 to 36 weeks

o Visit weekly from 36 weeks until delivery

With Every Visit

1. estimate GA
2. urine dip for glucose and protein
3. weight gain

o expect gain of roughly 1 lb/month in first half of pregnancy, 1 lb/week in second

half of pregnancy
o average weight gain 25-35 lbs with only 40% of weight gain products of
conception

4. blood pressure
5. symphyseal-fundal height measurement:

SFH should be within 2 cm of gestational age in weeks between 20 and 37 weeks,

i.e. SFH = 20 cm @ 20 weeks
12 weeks fundus @ pubic symphysis
 20 weeks @ umbilicus
37 weeks @ sternum

6. differential diagnosis of uterus incorrect size for dates (accurate dates essential)

maternal--> DM
maternal-fetal--> polyoligo-hydramnios, multiple gestation
fetal--> abnormal karyotype, IUGR, fetal anomaly

7. examination of abdomen for lie, position and presentation (Leopold maneuvers) in T3

8. fetal heart tones starting at ~ 12 weeks if using doppler U/S

Gestation-Dependent Management

PRENATAL CARE : SUBSEQUENT VISITS Part 02

Maternal Serum Screen (MSS or Triple Screen)

1. offers a risk estimate of whether the fetus may be affected with Downs
syndrome, trisomy 18, or a NTD
2. to make accurate diagnosis, positive MSS should be followed up with U/S and/or
amniocentesis
3. three markers

MSAFP (Maternal Serum Alpha-Fetoprotein Screening)

Beta hCG,
uE3 (Maternal estriol)
 Trisomy 21: high Beta hCG, low MSAFP, low uE3
Trisomy 18: low Beta hCG,low MSAFP, low uE3

4. differential diagnosis of high MSAFP

wrong gestational age
> 1 fetus (e.g. twins)

fetal demise (death of the baby in utero)

NTD
abdominal wall defects (e.g. omphalocele)

5. differential diagnosis of low MSAFP

GTN
incorrect GA

missed abortion
chromosomal anomalies (e.g. Trisomy 18, 21)

6. 80% of Downs babies born to women under 35 years, so MSS is a valuable screening tool

7. MSS has a 6-7% false positive rate

8. detection rate of Trisomy 21 with the 3 markers is 2-3 times higher than with MSAFP alone,
however will still miss 20-30% of Trisomy 21 pregnancies in older women and will not reliably
detect other chromosomal anomalies that occur more frequently in older women so
amniocentesis should still be offered to high risk women

Group B Streptococcus

1. danger of vertical transmission (neonatal sepsis, meningitis or pneumonia)

2. indications for antibiotic prophylaxis (intrapartum ampicillin or clindamycin in pen-
allergic - guidelines controversial)

positive GBS screen based on vaginal cultures taken at 36-38 weeks or

GBS status unknown and one of the following risk factors

o previous GBS bacteriuria even if treated

o previous infant with GBS infection

o preterm labour
 o PROM > 12 hours

o maternal intrapartum temperature > 37.7C

o fetal tachycardia

PRENATAL DIAGNOSIS

Indications

1. Maternal age > 35 (increased risk of some chromosomal anomalies)

2. abnormal MSS or ultrasound
3. past history of pregnancy with chromosomal anomaly or genetic disease
4. either parent a known carrier of a genetic disorder or balanced translocation
5. three or more miscarriages
6. family history of chromosomal anomaly, genetic disorder, birth defect,
or undiagnosed mental retardation
7. consanguinity

Amniocentesis

ultrasound-guided transabdominal extraction of amniotic fluid at

15-16 weeks gestation to identify genetic problems such as trisomies
during 3rd trimester for assessment of fetal lung maturity

L/S ratio: if > 2:1, fetal lungs are mature enough that RDS less likely to occur
used to quantitate amniotic fluid bilirubin concentration in Rh-isoimmunized pregnancies
advantages

1. screen for NTD (acetyl cholinesterase and amniotic AFP)

2. more accurate genetic testing

disadvantages

1. 0.5% risk of spontaneous abortion

2. results take 10-14 days,FISH (Fluorescent In Situ Hybridisation)available in 72
hours
 in women over 35 years, the risk of chromosomal anomaly (1/180) is greater than the
increased risk of miscarriage from the procedure, so it
is offered routinely

Chorionic Villus Sampling (CVS)

needle through abdomen or catheter through cervix at 10-12 weeks

advantages
1. enables pregnancy to be terminated earlier
2. more rapid karyotyping, DNA tests, chromosome status, biochemical assay
(results in 48 hours; do not have to wait for culture)
3. increasing availability of probes to allow diagnosis of genetic abnormalities (i.e.
FISH)

disadvantages

1. 1-2% risk of spontaneous abortion

2. does not screen for neural tube defects (NTD)
3. risk of limb injury
4. poor test because of genetic mosaicism

ANTENATAL MONITORING

Fetal Movements

Assessed by

1. maternal perception (quickening-after 4 to 5 month)

2. choose a time when baby is normally active to count movements
3. if < 6 movements in 2 hours, notify MD
4. 10 movements in 12 hour period is lower limit of normal (32 weeks and over)
5. palpation
6. U/S

Ultrasound
 routinely done at 4-5 month to assess fetal growth and anatomy
earlier or subsequent U/S only when medically indicated

1. confirm intrauterine pregnancy

2. identify multiple pregnancy
3. past history of early fetal losses
4. bleeding or other complications
5. measure fetal growth and identify IUGR
6. placental localization
7. determine gestational age (most accurately determined through measurement of
crown-rump length prior to 11-12 weeks gestational age)

Non-Stress Test (NST)

constant fetal heart rate (FHR) tracing using an external doppler to assess fetal heart rate
and its relationship to fetal movement (see Intrapartum Fetal Cardiotocography)
indicated when there is any suggestion of uteroplacental insufficiency or suspected fetal
distress
reactive NST (normal)

observation of two accelerations of FHR > 15 bpm from the baseline lasting >15 seconds in 20
minutes
nonreactive NST (abnormal)

one or no FHR acceleration of at least 15 bpm and 15 seconds duration associated

with fetal movement in 40 minutes
if no observed accelerations or fetal movement in the first 20 minutes, stimulate
fetus (fundal pressure, acoustic/vibratory stimulation) and continue monitoring for
30 minutes
if NST nonreactive then perform BPP
.

Biophysical Profile (BPP)

consists of NST and 30 minute ultrasound assessment of the fetus five scored parameters
of BPP (see Table 2)

scores

8-10 perinatal mortality rate 1: 1000 repeat BPP as clinically indicated

6 perinatal mortality 31:1000 repeat BPP in 24 hours
0-4 perinatal mortality rate 200:1000 deliver fetus if mature
AFV (Amniotic Fluid Volume) a marker of chronic hypoxia, all other parameters
indicative of acute hypoxia

INTRA-PARTUM MONITORING

Vaginal Exam

1. membrane status
2. cervical effacement (thinning), dilatation, consistency, position, application
3. fetal presenting part, position, and station
4. bony pelvis size and shape

Intrapartum Fetal Cardiotocography (CTG)

external (doppler) vs. internal (scalp electrode) monitoring

describe in terms of baseline FHR, variability (short term, long term) and
periodicity(accelerations, decelerations)
 baseline FHR

normal range is 120-160 bpm

a parameter of fetal well-being vs. distress
variability

1. short term - beat to beat (requires scalp monitor)

2. long term - described with respect to frequency and amplitude of change in
baseline
3. frequency is defined as number of times in a 1 minute period with an increase or
decrease of at least 5 bpm lasting 5 seconds (average frequency is 3)
4. amplitude is based on difference between highest and lowest FHR within a 1
minute period (11-25 bpm is average)

periodicity

accelerations

excursion of 15 bpm or more lasting for at least 15 seconds, in response to fetal movement or
uterine contraction

decelerations

describe in terms of shape, onset, depth, duration, recovery, occurrence, and impact on baseline
FHR and variability
early decelerations
1. uniform shape with onset early in contraction, returns to baseline by end of contraction;
slow gradual deceleration
2. often repetitive, no effect on baseline FHR or variability
3. due to vagal response to head compression
4. benign, usually seen with cervical dilatation of 4-7cm

variable decelerations

1. most common type of periodicity seen during labour

2. variable in shape, onset and duration
3. may or may not be repetitive
4. often with abrupt rapid drop in FHR, usually no effect on baseline FHR or variability
5. due to cord compression or, in second stage, forceful pushing with contractions
6. benign unless repetitive, with slow recovery, or when associated with other abnormalities
of FHR

late decelerations
 1. uniform (symmetric) in shape, with onset late in contraction, lowest depth after peak of
contraction, and returns to baseline after end of contraction
2. may cause decreased variability and change in baseline FHR
3. must see 3 in a row, all with the same shape to define as late deceleration
4. due to fetal hypoxia and acidemia, maternal hypotension, or uterine hypertonus
5. usually a sign of uteroplacental insufficiency (ominous)
6. manage with position change to left lateral decubitus,oxygen, stopping oxytocin, C/S

Approach to Abnormal FHR

1. if external monitor, ensure fetal tracing and not maternal

2. change position of mother
3. give 100% oxygen by mask and discontinue oxytocin
4. rule out cord prolapse consider fetal scalp electrode to assess beat-to-beat variability and
fetal scalp blood sampling if abnormality persists
5. immediate delivery if recurrent prolonged bradycardia

Fetal Scalp Blood Sampling

1. indicator of fetal distress

2. > 7.25 pH is normal
3. < 7.25 indicates that test should be repeated in 30 minutes
4. < 7.20 indicates fetal acidosis severe enough to warrant immediate delivery

Meconium in the Amniotic Fluid

1. usually not present early in labour

2. may occur prior to ROM or after rupture has occurred with passage of clear fluid
3. classified as thick or thin
4. thin meconium appears as a lightly stained yellowish or greenish fluid
 5. thick meconium appears dark green or black and may have pea-soup

consistency

o associated with lower APGARS and increased risk of meconium aspiration

o call pediatrics to delivery

o may indicate undiagnosed breech

6. increasing amount during labour may be a sign of fetal distress

MULTIPLE GESTATION

1. incidence of twins is 1/80 and triplets 1/6400

2. 2/3 of twins are dizygotic (i.e. fraternal)
3. hereditary factors (on maternal side only) and fertility drugs/procedures affect the
dizygotic twins rate only
4. monozygous twinning occurs at a constant rate worldwide (1/250)
5. determination of zygosity by number of placentas, thickness of membranes, sex, blood
type

Classification of Twin Pregnancies

Monoamnionic Monochorionic (forked Cord)

Monoamnionic Diamnionic Monochorionic

Diamnionic Monochorionic

Diamnionic Dichorionic (fused)

Diamnionic Monochorionic Dichorionic (separated)

Monoamnionic Monochorionic (Double Monster, one cord)

Complications Associated with Multiple Gestation

Maternal Maternal-Fetal Fetal

1. hyperemesis 1. increased 1. prematurity*
gravidarum PROM / PTL 2. IUGR
2. DM 2. polyhydramnios 3. mal presentation
3. preeclampsia / PIH 3. umbilical cord 4. congenital
4. PPH (uterine atony) prolapse anomalies
5. placental abruption 4. placenta previa 5. twin-twin
6. anemia (increased transfusion (DA/MC)
iron and folate needs)
increased physiological 6. increased perinatal
stress on all systems morbidity and
7. increased mortality
compressive symptoms 7. twin interlocking
(win A breech, win B
8. C-section vertex)
8. single fetal demise
Management

1. rest in T3
2. increased antenatal surveillance
3. close monitoring for growth (serial ultrasounds)
4. vaginal examinations in third trimester to check for cervical dilatation
5. may attempt vaginal delivery if twin A presents as vertex, otherwise C-section
6. twin B should be delivered within 15-20 minutes after twin A (may be longer if FHR
tracing adequate)

MEDICAL CONDITIONS IN PREGNANCY

URINARY TRACT INFECTION

1. occurs more frequently in pregnancy and puerperium (time immediately after the delivery
of a baby)
2. most common medical complication of pregnancy due to increased urinary stasis from
mechanical and hormonal (progesterone) factors
3. organisms : same as non-pregnant woman, also GBS
4. may be symptomatic or asymptomatic; treat all
5. risk of acute cystitis, pyelonephritis, and possible PPROM (Preterm Premature Rupture
of Membranes)
6. recurrence common treatment of pyelonephritis during pregnancy requires
hospitalization and IV antibiotics
7. treatment of asymptomatic bacteruria or acute cystitis

o amoxicillin first line

o alternatives are TMP-SMX (Septra) or nitrofurantoin (avoid during last 6 weeks
of pregnancy)
o follow with monthly urine cultures
 IRON DEFICIENCY ANEMIA

ron requirements increase during pregnancy (mother needs 1000 mg of elemental iron per fetus;
this amount exceeds normal stores)

o fetus (500 mg)

o RBC mass (500 mg)

o losses (200 mg)

Etiology

1. inadequate iron intake

2. iron malabsorption
3. bleeding, vaginal or other source
4. multiple gestation
5. concurrent antacid use (may prevent iron absorption)

Complications

1. maternal: angina, CHF, infection, slower recuperation, preterm labour

2. fetal: decreased oxygen carrying capacity leading to fetal distress, IUGR, low birth
weight and hydrops

Diagnosis

1. CBC, blood film, serum ferritin (changes in ferritin stores first sign of anemia)
2. microcytic, hypochromic anemia with decreased ferritin
3. morphology not good indicator because of RBC half life
4. TIBC not reliable because increased during pregnancy

Treatment
1. Prevention :

o dietary iron and iron mobilized from stores insufficient to meet demands
o adequate iron intake (30 mg elemental iron/day) for all women
 2. oral supplement of 200 mg/day of elemental iron if anemic
3. monitor

FOLATE DEFICIENCY ANEMIA

1. most often associated with iron deficiency anemia

2. necessary for closure of neural tube during early fetal development
3. minimum daily requirement is 0.5 mg
4. takes approximately 18 weeks of folate deficient diet to produce anemia
5. leafy green vegetables good source of dietary folate

Etiology
1. malnutrition
2. malabsorption (e.g. sprue) c
3. hronic hemolytic anemia (e.g. SCD)
4. multiple gestation medications (i.e. phenytoin, trimethoprim-sulfamethoxazole, oral
contraceptives)

Complications

1. maternal: smaller blood volume, nausea, vomiting, anorexia

2. fetal: NTD in T1, low birth weight, prematurity

Diagnosis

1. suspect if iron deficiency anemia fails to respond to treatment

2. CBC, blood film, red blood cell folate levels
3. megaloblastic anemia and hypersegmented neutrophils on smear
4. glossitis and skin roughness
5. NO neurologic symptoms (unlike B12 deficiency)
6. elevated serum iron and transferrin saturation

Treatment
1. 1 mg folic acid PO daily
2. 4 mg folic acid per day with past history of neural tube defect
 DIABETES MELLITUS IN PREGANACY

Incidence

2-3% of pregnancies are complicated by diabetes mellitus

Normal Physiology in Pregnancy

1. in early pregnancy (T1) insulin secretion is increased and its anabolic

actions are potentiated, decreasing fasting maternal glucose levels and
promoting maternal energy storage
2. in later pregnancy (T2,T3) insulin resistance develops due to anti-insulin factors: human
placental lactogen (increased secretion with
growth of the placenta) and cortisol
3. result: higher fasting glucose and enhanced lipolysis (increased FFA,TG, lipids, ketones)
to supply energy for fetal growth

Classification of Diabetes Mellitus (DM)

1. Insulin Dependent DM (Type I)

2. Non-Insulin Dependent DM (Type II)
3. Gestational Diabetes: DM diagnosed during pregnancy

Complications of Pregnancy in the Diabetic

 Maternal

1. hypertension/PET, polyhydramnios, pyelonephritis/UTI

2. ketoacidosis, diabetic coma, worsening retinopathy in Type I or Type II, NOT in GDM

Fetal

1. maternal hyperglycemia leads to fetal hyperinsulinism : accelerated anabolism and

macrosomia result
2. increased congenital anomalies and miscarriage from preconception or T1 hyperglycemia
3. cardiac (VSD), neural tube, genitourinary, gastrointestinal and MSK (sacral agenesis)
defects
4. IUGR if mother has end-organ damage
5. delayed fetal lung maturity
6. preterm labour/prematurity
7. increased incidence of stillbirth

pregnancies complicated by GESTATIONAL diabetes do not manifest an

increased risk of congenital anomalies because it develops later (i.e. after T1)

Neonatal

macrosomia and associated birth trauma, hypoglycemia, hyperbilirubinemia and

jaundice, hypocalcemia, polycythemia, and RDS

Treatment of DM in Pregnancy

T1

1. see prior to pregnancy to optimize glycemic control (will reduce risk of congenital
anomalies)
2. since oral hypoglycemics are contraindicated, Type IIs must be switched to insulin
3. counsel : potential complications and risks
 4. advise preconception folic acid
5. see early and date pregnancy
6. consult internist and dietitian to manage insulin and diet
7. measure hemoglobin A 1C early in T1 or preconception if possible; this gives an
indication of glycemic control during embryogenesis and can be used to estimate risk of
birth defects
8. initial evaluations: 24 hour urine (protein and creatinine clearance), retinal exam, ECG,
urine C&S, hemoglobin A 1C
9. throughout pregnancy monitor BP, urine dip (protein/glucose/ketones), weight gain,
blood glucose (self-monitor) every visit and occasional urine C&S and hemoglobin A1 C
10. in early pregnancy transfer of glucose and amino acids to the fetus results in a tendency
toward maternal hypoglycemia
11. nausea and vomiting may reduce food intake, therefore may need to decrease insulin dose

T2

1. clinic visits 2 weekly

2. MSAFP (at 16 weeks) and 3 detailed U/S examinations
3. consider fetal echocardiography to exclude congenital heart defect
4. admit for blood sugar control if needed
5. in the second half of pregnancy, the diabetogenic action of placental hormones outweigh
the continuous siphoning of glucose by the fetus
6. demand for insulin is increased, hence insulin dosages need to be increased

T3

1. clinic visits weekly

2. fetal surveillance (BPP, NST); frequency depends on risk
o < 36 weeks = weekly

o > 36 weeks = weekly or biweekly

3. timing of delivery dependent upon fetal and maternal risk factors

4. can wait for spontaneous labour if glucose well-controlled and BPP normal
 5. induce by 40 weeks

Labor

1. increased risk of CPD (Cephalopelvic Disproportion), shoulder dystocia with babies

weighing over 4000 g
2. elective C-section for predicted birth weights of greater than 4500 g (controversial)
3. during labour monitor sugars 1h with patient on insulin and dextrose drip and aim for
blood sugar of 3.5 to 6.5 to reduce the risk of neonatal hypoglycemia

Postpartum

1. increased risk of hypoglycemia

2. once eating a regular diet, resume insulin at two-thirds of prepregnancy dose and monitor
6 hourly

GESTATIONAL DIABETES

1. glucose intolerance that is present only during pregnancy

2. genetic predisposition to the development of glucose intolerance exists in this population
of women
3. 50% risk of developing Type II DM in next 20 years

Risk Factors

1. age > 30
2. previous history of high blood glucose, GDM, or macrosomic infant (> 4.5 kg) p
3. ositive family history (GDM, Type II DM, macrosomic infant)
4. excessive weight gain in pregnancy, prepregnancy obesity
5. baby > 4.5 kg or large for GA
6. previous unexplained stillbirth
7. previous congenital anomaly
8. early preeclampsia or polyhydramnios
 9. repeated vaginal candidiasis
10. member of high risk ethnic group
11. multiple gestation

Diagnosis

1. screen at 26 weeks (or earlier) with 50 g oral glucose challenge test if risk factors or
glycosuria are present
2. > 7.8 mmol/L at 1 hour is abnormal
3. confirm with 3 hour 100 g oral glucose tolerance test (OGTT)
4. need 2 out of 4 values to be abnormal to diagnose GDM
o fasting: > 5.8 mmol/L

o 1 hour: > 10.6 mmol/L

o 2 hour: > 9.2 mmol/L

o 3 hour: > 8.1 mmol/L

Management of Gestational Diabetes

1. controversial
2. aim to achieve normal blood sugars post-prandial (i.e. < 6.7 mmol/L)
3. start with diabetic diet
4. if blood sugars 2 hours post-prandial are > 6.7, add insulin
5. oral hypoglycemic agents contraindicated in pregnancy
6. fetal monitoring and timing of delivery same as for DM above
7. insulin and diabetic diet should be stopped post-partum
8. follow-up testing recommended postpartum because of increased risk of overt diabetes
(i.e. OGTT at 6 weeks postpartum)

HYPERTENSIVE DISORDERS OF PREGNANCY Part 01

Classification
 1. preeclampsia/eclampsia
2. chronic hypertension
3. chronic hypertension with superimposed preeclampsia/eclampsia
4. transient or gestational hypertension

Preeclampsia/Preeclamptic Toxemia/Eclampsia (PET)

1. hypertension accompanied by proteinuria and/or non-dependent edema with onset

> 20 weeks
2. BP > 140/90 mmHg or an increment of 30 mmHg systolic and 15 mmHg diastolic over a
nonpregnant or T1 BP
3. non-dependent edema (e.g. face, hands) is generalized and usually associated with
excessive weight gain (> 2 kg/week)
4. proteinuria is defined as > 1+ protein on random dipstick analysis or > 300 mg in a 24
hour urine collection
5. 50% of all hypertension in pregnancy
6. due to an imbalance of thromboxane (vasoconstrictor) and prostaglandin (vasodilator),
causing generalized arteriolar constriction
7. resultant vasospasm damages capillaries, leading to protein extravasation and hemorrhage

Conditions Associated with Preeclampsia/Eclampsia

Maternal factors

1. 80-90% of cases in primagravidas

2. past history or family history of preeclampsia/eclampsia
3. diabetes, chronic hypertension, or renal disease
4. extremes of maternal age

Fetal factors
 1. IUGR
2. hydatidiform mole
3. > 1 fetus
4. fetal hydrops

Fetal Complications

mainly due to placental insufficiency

1. fetal loss
2. IUGR
3. prematurity
4. abruptio placentae

Maternal Complications

1. cerebral hemorrhage (50% of deaths)

2. left ventricular failure/pulmonary edema
3. liver and renal dysfunction
4. abruption
5. seizures
6. DIC : release of placental thromboplastin, leading to a consumptive coagulopathy
7. HELLP
o hemolysis,

o elevated liver enzymes

o low platelets

may only respond to fresh frozen plasma with plasma exchange

HYPERTENSIVE DISORDERS OF PREGNANCY Part 02

Mild Preeclampsia

PET uncomplicated by neurologic symptoms or criteria for a diagnosis of severe PET

Management of Mild Preeclampsia

1. maternal evaluation
2. history and physical examination
3. laboratory
o CBC and electrolytes

o renal function tests ----> BUN, creatinine, uric acid

o liver enzymes and coagulation studies ----> PT, PTT, FDP

o urinalysis for protein and casts

o 24 hour urine for protein and creatinine clearance

4. fetal evaluation of FHR, NST,BPP

5. management with bed rest in left lateral decubitus position (reduces abdominal vessel
compression) normal dietary salt and protein intake
6. no use of diuretics/antihypertensives

Severe Preeclampsia

PET complicated by at least two of the following

1. BP > 160/110
2. congestive heart failure
3. pulmonary edema or cyanosis
4. proteinuria > 5 g/24 hours or > 2+ on dipstick
5. elevated serum creatinine
6. oliguria (< 400 mL/24 hours)
7. thrombocytopenia (< 100 000 - 150 000/mL)
8. ascites
9. RUQ or epigastric pain (subcapsular hemorrhage)
10. elevated liver enzymes
 11. hyperbilirubinemia
12. headache (cerebral artery vasospasm)
13. visual disturbances (i.e. scotomas, loss of peripheral vision)
14. hyperreflexia, clonus
15. IUGR

.
Management of Severe Preeclampsia

1. stabilize and deliver; the only "cure" is delivery

2. admit and complete maternal evaluation (same as for mild) --->keep NPO
3. start IV, cross and type
4. Foley catheter to monitor urine output

Maternal monitoring
1. hourly input and output, check urine 12 hours for protein
2. vitals and DTR 1 hour

Fetal evaluation
1. NST followed by continuous electronic fetal monitoring until delivery

Anticonvulsant therapy
1. given to increase seizure threshold
2. baseline magnesium blood level
3. magnesium sulphate (4g IV push) followed by maintenance of 2-4 g/hour
4. excretion of magnesium sulfate is via kidney therefore patients with oliguria require a
lower infusion rate

Signs of magnesium toxicity (> 13 mg % serum level)

1. depression of DTR (deep tendon reflex)
2. depression of RR < 10/minute
3. decreased muscle tonicity
4. CNS or cardiac depression
5. antagonist to magnesium sulphate is calcium gluconate (10%) 10 mL IV if respiratory
arrest occurs

Antihypertensive therapy
 1. decreasing the BP decreases the risk of stroke (indicated only if BP > 140-170/90-110)
2. first line: hydralazine 5 - 10 mg IV push over 5 minutes q 15 - 30 minutes until desired
effect (an arteriolar vasodilator with minimal venous effect)
3. controls BP for hours not days (deliver as soon as possible)
4. next dose is given ~6 hours later with BP readings 15 minutes duration
5. also used in postpartum state if BP remains elevated and urinary output < 25 mL/hour
6. second line: labetalol 20 - 50 mg IV q 10 minutes
7. third line: nifedipine 10 -20 mg po q 20 - 60 minutes (puncture capsule and swallow
liquid)

Postpartum management
1. all antepartum therapy and monitoring continued until stable
2. risk of seizure highest in first 24 hours postpartum
3. continue magnesium sulfate for 12-24 hours after delivery
4. the patient who continues to remain in serious condition may have HELLP
5. most women return to a normotensive BP within 2 weeks but BP may worsen transiently
in that time

HYPERTENSIVE DISORDERS OF PREGNANCY Part 03

Eclampsia

Grand mal seizures in a woman with preeclampsia

Management of Eclampsia

1. airway, breathing, circulation seizure control and prevention

2. do not attempt to shorten or abolish the initial convulsion
3. prevent maternal injury and maintain adequate oxygenation
4. minimize risk of aspiration, auscultate lungs after every seizure
5. give adequate magnesium sulphate as soon as convulsion has ended
6. correct maternal acidemia (obtain post-ictal blood gases)
 7. some use diazepam for seizure control

Chronic Hypertension

Features

1. history of hypertension (> 140/90) before gestation

2. detection of hypertension prior to 20 weeks gestation (unless there is a GTN)
3. persistence of hypertension postpartum
4. strong family history of hypertension
5. most gravidas have essential hypertension, associated with an increased risk of
preeclampsia or eclampsia, abruptio placenta, IUGR and IUD

Management

1. methyldopa and/or labetalol

2. no ACE inhibitors, diuretics, propranolol

Chronic Hypertension with Superimposed Preeclampsia/ Eclampsia

1. 2-7 fold increased likelihood of developing preeclampsia/ eclampsia if pre-existing

maternal hypertension
2. tends to recur
3. occurs early in pregnancy, tends to be severe, often with IUGR

Transient or Gestational Hypertension

1. hypertension alone that develops during the latter half of pregnancy or during the first 24
hours after delivery and disappears within 10 days following parturition
2. monitor for signs of preeclampsia/eclampsia

HYPEREMESIS GRAVIDARUM

Definition
 1. intractable nausea and vomiting to extent of weight loss, dehydration and electrolyte
imbalance, acid-base disturbance and if severe, hepatic and renal damage
2. usually present in T1 then diminishes or persists throughout pregnancy
in a minority

Etiology

1. presently thought to be multifactorial with hormonal, immunologic and psychologic

components
2. high or rapidly rising beta-hCG or estrogen levels are implicated

Maternal Complications

1. Mallory Weiss tears

2. Wernicke's encephalopathy, if protracted course
3. death

Fetal Complications

1. usually none
2. IUGR is 15x more common in women losing > 5% of prepregnant weight

Differential Diagnosis of Nausea and Vomiting

1. hyperemesis is a diagnosis of exclusion

2. GI inflammation/infection
o appendicitis

o cholecystitis

o hepatitis

o gastroenteritis

o pancreatitis
 o PUD

o fatty liver of pregnancy

3. pyelonephritis
4. thyrotoxicosis
5. multiple gestation
6. GTN
7. HELLP syndrome

Investigations

1. labs (CBC, lytes, BUN and creatinine, urinalysis, LFTs)

2. ultrasound (to R/O molar pregnancy, multiple pregnancy and to assess liver, pancreas,
gallbladder, etc...)

Treatment

General

1. early recognition is important

2. if severe, admit to hospital
3. NPO initially, then small frequent meals of appealing foods
4. correct hypovolemia, electrolyte imbalance and ketosis
5. thiamine, if indicated
6. TPN if severe to reverse catabolic state
7. consider emotional support, dietary and psychologic counselling

Pharmacological options

1. dimenhydrinate (Gravol)
2. vitamin B6 and doxylamine succinate (Diclectin)
Non-pharmacological options

1. accupressure at inner aspect of the wrists, just proximal to the flexor crease has been
shown to significantly reduce symptoms of nausea and vomiting
2. avoid triggers (i.e. certain smells)

Rh ISOIMMUNIZATION

1. antibodies produced against a specific RBC antigen as a result of antigenic stimulation

with RBC of another individual
2. most common is anti-Rh Ab produced by a sensitized Rh-negative mother
3. other antibodies can lead to fetal red blood cell hemolysis --->much less common and no
prophylaxis is available

Pathogenesis

1. maternal-fetal circulation normally separated by placental barrier

2. upon first exposure, initially IgM and then IgG antibodies are produced;IgG antibodies
cross the placental barrier
3. sensitization routes
o incompatible blood transfusion

o previous fetal-maternal transplacental hemorrhage

o invasive procedure while pregnant

o therapeutic abortion, D&C, amniocentesis

4. complications
o anti-Rh Ab can cross the placenta and cause fetal hemolysis resulting in fetal
anemia, CHF, edema, and ascites
o severe cases can lead to fetal hydrops (total body edema), or erythroblastosis
fetalis

Diagnosis
 1. routine screening at first visit for blood group, Rh status, antibodies
2. Ab titres < 1:16 considered benign
3. Ab titres > 1:16 necessitates amniocentesis (correlation exists between amount of biliary
pigment in amniotic fluid and severity of fetal anemia) from 24 weeks onwards
4. Liley curve is used to determine bilirubin level and appropriate
management
5. Kleihauer-Betke test can be used to determine extent of feto-maternal
hemorrhage
o fetal red blood cells are identified on a slide treated with citrate phosphate buffer

o adult hemoglobin is more readily eluted through cell membrane in presence of

acid

Prophylaxis

1. Rhogam binds to Rh Ag of fetus and prevents it from contacting maternal immune

system
2. Rhogam must be given to all Rh negative women
o at 28 weeks

o within 48 hours of the birth of an Rh positive fetus

o positive Kleihauer-Betke test

o with any invasive procedure in pregnancy

o in the case of ectopic pregnancy

o with miscarriage, therapeutic abortion

o antepartum hemorrhage

3. if Rh neg and Ab screen positive, follow mother with serial monthly Ab titres throughout
pregnancy +/- serial amniocentesis as needed (Rhogam of no benefit)

Treatment

1. falling biliary pigment warrants no intervention (usually indicative of fetus which is

unaffected or mildly affected)
 2. rising or stable biliary pigment on serial amniocentesis must be compared to a standard
table which is divided into 3 zones based on severity of hemolysis (Liley Curve)
3. intrauterine transfusion of O-negative packed red blood cells may be required for
severely affected fetus or early delivery of the fetus for exchange transfusion

TORCH INFECTIONS DURING PREGNANCY Part 01

TORCH is an acronym that is used to describe the more common fetal infections :

T oxoplasmosis
O ther, which refers to syphilis and HIV infection principally, but may also refer to
gonorrhoea and varicella
R ubella
C ytomegalovirus
H erpes, and also hepatitis

Toxoplasmosis

1. protozoal infection (Toxoplasma gondii)

2. incidence: 1/1000 pregnancies
3. source: raw meat, unpasteurized goats milk, cat urine/feces
4. greatest risk of transmission in T3
5. severity of fetal infection greatest in T1
6. 75% asymptomatic at birth, but may later develop sequelae
7. risk of congenital toxoplasmosis (chorioretinitis, hydrocephaly,intracranial calcifications,
MR, microcephaly) if primary maternal infection during pregnancy
8. diagnosis based on serologic testing for both IgM and IgG
9. confirmation of diagnosis based on presence of IgM antibodies in cord blood
10. self-limiting infection, spiramycin (macrolide) decreases fetal morbidity

Rubella
 1. RNA togavirus with transmission by respiratory droplets (highly contagious)
2. maternal infection during pregnancy (greatest in T1) may cause spontaneous abortion or
Congenital Rubella Syndrome: hearing loss, cataracts, cardiovascular lesions, MR,
symmetric IUGR, hepatitis, CNS defects and osseous changes
3. diagnosis best made by serologic testing
4. all pregnant women screened for rubella immunity (rubella titer > 1:16 = immune)
5. non-immune
o should be offered vaccination following pregnancy (not a contraindication for
breast feeding)
o rubella vaccine should be avoided before (3 months) or during pregnancy
since it is an attenuated live vaccine

Cytomegalovirus

1. DNA virus (herpes family)

2. transmission:
o blood transfusion

o organ transplant

o sexual contact

o breast milk

o transplacental

o direct contact during delivery

3. congenital infection can occur from primary or re-infection of the mother

4. increased fetal morbidity with primary infection
5. risk of transmission constant across trimesters
6. 5-10% of fetuses infected in utero will develop neurologic involvement (MR, cerebral
calcification, hydrocephalus or microcephaly, deafness, chorioretinitis)
7. diagnosis:
o isolation of virus in urine culture (or culture of other secretions)

o serologic screening for antibodies

TORCH INFECTIONS DURING PREGNANCY Part 02

Herpes

1. DNA herpes virus

2. transmission: intimate mucocutaneous contact
3. primary infection during pregnancy increases risk of neonatal complications
4. 50% transmission if primary infection, 4% transmission if secondary
recurrence
5. infection to fetus may occur in utero but more commonly occurs
during delivery
6. C-section if active genital lesions present within 4-6 hours of ROM, even if lesions
remote from vulvar area

Syphilis

1. Treponema pallidum
2. may have transplacental transmission
3. serological tests
o VDRL screening done at first prenatal visit (non-specific)

4. to confirm a positive VDRL

o TPHA (Treponema Pallidum Hemagglutinating Ab)

o FTA-ABS (Fluorescent Treponema Antibody Absorption) Test

5. risk of preterm labour, fetal death

6. treatment: Penicillin G 2.4 million units IM, monthly VDRL during pregnancy to ensure
treatment is adequate

Hepatitis B

1. transmitted via blood, saliva, vaginal secretions, semen, breast milk,

transplacental
2. fetal infection most likely with T3 maternal infection
 3. risk of vertical transmission 10% if asymptomatic HBsAg +ve
4. risk of vertical transmission 85-90% if HBsAg +ve and HBcAg +ve
5. chronic active hepatitis increases risk of prematurity, low birth weight,neonatal death
6. treatment of neonate with Hep B immune globulin (HBIG) and vaccine (at birth, one and
six months) is 90% effective
7. vaccine safe during pregnancy

Erythema Infectiosum (Fifth Disease)

1. parvovirus B19
2. febrile illness with bilateral erythema of cheeks (slapped cheek rash) followed by
maculopapular rash of trunk and extremities
3. fetus of infected woman may develop hydrops in utero
o follow fetus with weekly U/S (if hydrops occurs, consider fetal transfusion)

4. risk of intrauterine death 1-12 weeks after infection

HIV

1. offer screening to all women

2. risk of vertical transmission 12 to 28%; more likely if maternal CD4 count < 300
3. risks to infected mom include decreased CD4 count, cancer, increased opportunistic
infection (PCP, TB, CMV, toxoplasmosis, mycoplasma)
4. care of HIV positive patient
o PCP(Pneumocyctis Pneumonia) prophylaxis with Bactrim if CD4 < 200

o AZT (azidothymidine) shown to decrease transmission to fetus from 25% to 8%

risk
o exclude cervical dysplasia

o toxoplasmosis and CMV antibodies

Group B Streptococccus (see Prenatal Care Section)

SURGICAL CONDITIONS IN PREGNANCY

ACUTE SURGICAL CONDITIONS

1. incidence is approximately 1 in 500

2. pregnancies generally manage acute surgical condition regardless of pregnancy
pregnancy
3. substantially increases complications associated with surgery
4. EX:
o acute appendicitis

o acute cholecystitis

o acute pancreatitis

o abdominal trauma

o torsion of the uterine adnexa

o pelvic abcess

o peptic ulcer disease

o bowel obstruction

o intracranial hemorrhage

o thromboembolic disease

NON-EMERGENCY SURGICAL CONDITIONS

1. surgery in first trimester has highest risk of teratogenicity and spontaneous abortion
2. surgery for nonemergent conditions usually delayed until the more stable second
trimester
3. EX :
o adnexal tumours

o cervical cancer

o breast cancer
 o gastrointestinal trauma

o melanoma, osteosarcoma

ANTENATAL HEMORRHAGE : 1st 2nd and 3rd TRIMESTER

BLEEDING

FIRST AND SECOND TRIMESTER BLEEDING

Differential Diagnosis

1. abortion (threatened, inevitable, incomplete, complete)

2. < 5% of threatened abortions go on to abort
3. abnormal pregnancy (ectopic, molar)
4. trauma (post-coital)
5. physiologic bleeding (due to placental development)
6. genital lesion (e.g. cervical polyp, neoplasms)

THIRD TRIMESTER BLEEDING

Differential Diagnosis

1. placenta previa
2. abruptio placentae
3. vasa previa
4. bloody show (shedding of cervical mucous plug)
5. marginal sinus bleeding
6. cervical lesion (cervicitis, polyp, ectropion, cervical cancer)
7. uterine rupture
 8. other: bleeding from bowel or bladder, placenta accreta, abnormal
coagulation
9. NB - do NOT perform a vaginal exam until placenta previa has been ruled out by U/S

VASA PREVIA

1. incidence 1 in 5000
2. occurs with velamentous insertion of cord into membranes of placenta; unprotected fetal
vessels pass over the cervical os
3. since bleeding is from fetus a small amount of blood loss can have catastrophic
consequences
4. presents with painless vaginal bleeding and fetal distress (tachy- to bradyarrhythmia)
5. Apt test (NaOH mixed with the blood) can be done immediately to determine if the
source of the bleeding is fetal (supernatant turns pink) or maternal (supernatant turns
yellow)
6. Wright stain on blood smear and look for nucleated red blood
cells (in cord not maternal blood)
7. management is STAT C-section
8. 50% perinatal mortality, increasing to 75% if membranes rupture (most infants die of
exsanguination)

Types of Abortions
THERAPEUTIC ABORTIONS

Medical management
< 9 weeks use methotrexate plus misoprostol (experimental)
> 12 weeks use prostaglandins intra- or extra-amniotically, or IM

Surgical management
< 12-16 weeks use dilatation and curettage
> 16 weeks use dilatation and evacuation

Complications
1. perforation of uterus
2. hemorrhage
3. laceration of cervix
4. risk of sterility
5. infection - usually due to retained products, occasionally endometritis
6. Asherman's syndrome (fibrosis of the uterus)

ABRUPTIO PLACENTAE

premature separation of a normally implanted placenta after 20 weeks OF gestation

incidence = 0.5-1.5%


Classification

1. total (fetal death inevitable) vs. partial

2. external/revealed/apparent; blood dissects downward toward cervix
3. Internal/concealed (20%); blood dissects upward toward fetus
4. most are mixed

Etiology

unknown, but associated with

1. maternal hypertension (chronic or PIH) in 50% of abruptions

2. multiparity
3. previous abruption (recurrence rate 10%)
4. PROM
5. maternal age > 35 (felt to reflect parity)
6. maternal vascular disease
7. cigarette smoking
8. alcohol consumption
9. uterine distension (polyhydramnios, multiple gestation)
10. short cord
11. trauma
12. Sudden decompression of the uterus (twins)
13. uterine anomaly, fibroids

Fetal Complications
 1. perinatal mortality 25-60%
2. prematurity
3. intrauterine hypoxia

Maternal Complications

1. < 1% maternal mortality

2. DIC (in 20% of abruptions)
3. acute renal failure
4. anemia hemorrhagic shock
5. pituitary necrosis (Sheehan syndrome)
6. amniotic fluid embolus

Clinical Features

1. PAINFUL vaginal bleeding; blood may be bright red or dark or clotted

2. uterine tenderness and increased tone
3. degree of anemia may not correlate with degree of observed blood loss
4. fetal distress; loss of variability, late decelerations
5. 15% present with fetal demise

Diagnosis

clinical
U/S NOT helpful except to rule out placenta previa

Management

Initial management

1. maternal stabilization, IV hydration

2. fetal monitoring
 3. monitor maternal vitals, urine output
4. blood for hemoglobin, platelets, PT/PTT, fibrinogen, FDP, cross and type
5. blood products on hand (red cells, platelets, cryoprecipitate) because of DIC risk
6. Rhogam if Rh negative

Mild abruption and GA < 36 weeks

1. close observation of fetal well-being and amount of bleeding

2. limited physical activity
3. serial Hct to assess concealed bleeding
4. delivery when fetus is mature or when hemorrhage dictates

Mild abruption and GA > 36 weeks

1. stabilization and delivery

Moderate to severe abruption

1. hydrate and restore blood loss and correct coagulation defect if present
2. vaginal delivery if no evidence of fetal or maternal distress and if cephalic presentation
OR with dead fetus
3. labour must progress actively

Severe abruption and live fetus

1. C-section if fetal or maternal distress develops with fluid/blood replacement, labour fails
to progress or non-cephalic fetal presentation

PLACENTA PREVIA

1. abnormal location of the placenta at or near the internal cervical os

2. 1/200 at time of delivery
3. many are low lying in early pregnancy but due to development of lower uterine segment
appear to "move upward" as pregnancy nears term
 4. 95% of previas diagnosed in T2 resolve by T3; repeat U/S at 30-32 weeks GA

Classification

Total : placenta completely covers the internal os

Partial : placenta partially covers the internal os
Marginal : placenta reaches margin but does not cover any part of the intemal os
Low lying (NOT a previa) : placenta in lower segment but clear of os,can also bleed,
usually later (i.e. in labour)

Etiology

unknown but many associated conditions and risk factors

1. multiparity
2. multiple pregnancy
3. increased maternal ageterine scar due to previous abortion, C-section, D&C,
myomectomy
4. uterine tumour (e.g. fibroids) or other uterine anomalies
5. history of placenta previa (4-8% recurrence risk)

Fetal Complications

1. perinatal mortality low but still higher than with a normal pregnancy
2. prematurity (bleeding often dictates early C/S)
3. intrauterine hypoxia (acute or IUGR)
4. fetal malpresentation
5. PPROM
6. risk of fetal blood loss from placenta, especially if incised during C/S

Maternal Complications
 1. < 1% maternal mortality
2. hemorrhage and hypovolemic shock
3. anemia
4. acute renal failure
5. pituitary necrosis (Sheehan syndrome)
6. PPH (because lower uterine segment is atonic)
7. hysterectomy
8. placenta accreta

Clinical Features

1. recurrent, PAINLESS bright red vaginal bleeding

o onset of bleeding depends on degree of previa (i.e. complete bleed earlier)

o mean GA is 30 weeks; one third present before

o initially, bleeding may be minimal and cease spontaneously but can be

catastrophic later
o bleeding at onset of labour can occur with marginal placenta previa

2. uterus soft and non-tender

3. presenting part high or displaced
4. diagnosed by U/S (95% accuracy with transabdominal)

Management

1. maternal stabilization; large bore IV with hydration

2. electronic fetal monitoring
3. maternal monitoring
o vitals, urine output, blood loss
 o bloodwork including hematocrit, CBC, PTT/PT, platelets,fibrinogen, FDP, type
and cross match
4. when fetal and maternal condition permit, perform careful U/S examination to determine
fetal viability, gestational age and placental status/position
5. Rhogam given if mother is Rh negative
6. management decision depends on
o previa characteristics (amount of bleeding, degree of previa)

o fetal condition (GA, level of distress, presentation)

o uterine activity

7. expectant management and observation of mother and fetus if the initial bleeding episode
is slight and GA < 37 weeks
o admit to hospital

o limited physical activity

o no douches, enemas, or sexual intercourse

o consider corticosteriods for fetal lung maturity

o delivery when fetus is mature or hemorrhage dictates

8. delivery if bleeding is profuse, GA > 36 weeks, or L/S ratio is 2:1 or greater

9. usually C-section (incision site dictated by location of previa)

INTRA-UTERINE GROWTH RESTRICTION

Definition

1. infants whose weight is < 10th %ile for a particular GA

2. weight not associated with any constitutional or familial cause
3. prone to problems such as meconium aspiration, asphyxia, polycythemia, hypoglycemia,
and mental retardation
4. greater risk of perinatal morbidity and mortality
Etiology

Maternal causes

1. poor nutrition,
2. cigarette smoking,
3. drug abuse, alcoholism,
4. cyanotic heart disease,
5. severe DM,
6. SLE,
7. pulmonary insufficiency

Maternal-fetal

1. any disease which causes placental insufficiency leading to inadequate transfer of

substrate across the placenta
2. includes PIH, chronic HTN, chronic renal disease, gross placental morphological
abnormalities (infarction, hemangiomas)

Fetal causes

1. TORCH infections,
2. multiple gestation,
3. congenital anomalies

Clinical Features

Symmetric/Type I (20%)

1. occurs early in pregnancy

2. inadequate growth of head and body although the head:abdomen ratio may be normal
 3. usually associated with congenital anomalies or TORCH

Asymmetric/Type II (80%)

1. occurs late in pregnancy

2. brain is spared therefore the head:abdomen ratio is increased
3. usually associated with placental insufficiency
4. more favorable prognosis than Type I

Diagnosis

1. clinical suspicion
2. SFH measurements at every antepartum visit
3. more thorough assessment if mother is in high risk category or if SFH lags > 2 cm behind
GA
4. U/S exam should include assessment of BPD, head and abdomen circumference,
head:body ratio, femur length and fetal weight
5. doppler analysis of umbilical cord blood flow

Management

1. prevention via risk modification prior to pregnancy ideal

2. most important consideration is accurate menstrual history and GA in which to assess the
above data
3. modify controllable factors: smoking, alcohol, nutrition
4. bed rest (in LLD position)
5. serial BPP (monitor fetal growth)
6. delivery when extrauterine existence is less dangerous than continued intrauterine
existence or if GA > 34 weeks with significant oligohydramnios
7. liberal use of C-section since IUGR fetus withstands labour poorly

OLIGOHYDRAMNIOS
Definition

Amniotic fluid index of 5 cm or less

Etiology of Early Onset Oligohydramnios

1. decreased production
o renal agenesis or dysplasia,

o urinary obstruction,

o posterior urethral valves (male)

2. increased loss
o prolonged amniotic fluid leak (although most often labour ensues)

3. 15-25% of cases have fetal anomalies

Fetal Complications

1. cord compression
2. T1 onset
o Potters facies

o limb deformities

o abdominal wall defects

3. onset at > 20 weeks

o pulmonary hypoplasia

Late Pregnancy Onset Oligohydramnios

1. amniotic fluid normally decreases after 35 weeks

2. common in post-term pregnancies
3. may be a marker for infants who may not tolerate labour well
Management

oligohydramnios is an important sign of chronic placental insufficiency and always warrants

admission and investigation

rule out ROM

fetal monitoring (NST, CTG, BPP)
consider delivery if at term

PRETERM LABOUR

Definition

1. labour occurring between 20 and 37 weeks gestation

2. complicates about 10% of pregnancies
3. prematurity is the leading cause of perinatal morbidity and mortality
4. at 30 weeks or 1500 g = 90% survival
5. at 33 weeks or 2000 g = 99% survival
6. major causes of morbidity = asphyxia, sepsis, RDS
7. intrapartum asphyxia may lead to cerebral hemorrhage

Etiology

idiopathic (most common)

Maternal

1. preeclampsia/hypertension
2. placenta previa or abruption
3. uncontrolled diabetes
4. recurrent pyelonephritis and untreated bacteriuria
 5. maternal genital tract infection
6. chorioamnionitis
7. other medical illness (heart disease, renal disease, severe anemia, systemic infection,
chronic vascular disease)
8. maternal age < 18 years or > 40 years
9. fibroids or other uterine anomalies
10. incompetent cervix
11. history of abortions or stillbirths
12. surgical (intra-abdominal surgery, cholecystitis, peritonitis)
13. previous incision into uterus or cervix (C/S, conization)
14. low socioeconomic class
15. lack of prenatal care
16. poor nutrition
17. low prepregnancy weight
18. smoking
19. drug addiction (alcohol, cocaine)
20. stress/anxiety/fatigue
21. prior history of premature delivery (recurrence risk of 17-40%)

Maternal-fetal

1. PPROM (a common cause)

2. polyhydramnios

Fetal

1. multiple gestation
2. congenital abnormalities of fetus

Requirements for Consideration of Labour Suppression(Tocolysis)

 1. live fetus
2. fetal immaturity
3. intact membranes
4. cervical dilatation of 4 cm or less
5. absence of maternal or fetal contraindications (see below)
6. availability of necessary personnel and equipment to assess mother and fetus during
labour and care for baby of the predicted GA if therapy fails

Maternal Contraindications to Tocolysis

1. bleeding (placenta previa or abruption)

2. maternal disease (hypertension, diabetes, heart disease)
3. preeclampsia or eclampsia
4. chorioamnionitis

Fetal Contraindications to Tocolysis

1. erythroblastosis fetalis
2. severe congenital anomalies
3. fetal distress/demise IUGR,
4. multiple gestation (relative)

Diagnosis

1. regular contractions (2 in 10 minutes)

2. cervix > 2 cm dilated or 80% effaced OR documented change in cervix

Prevention
 1. good prenatal care
2. identify pregnancies at risk
3. treat silent vaginal infection or UTI
4. patient education
5. the following may help but evidence for their effectiveness is lacking
6. rest, time off work, stress reduction
7. improved nutrition
8. U/S measurement of cervical length or frequent vaginal exams to assess cervix; this
would catch PTL earlier so tocolysis would be more effective

Management

Initial

1. transfer to appropriate facility

2. hydration (NS @ 150 mL/hour)
3. bed rest in left lateral decubitus position
4. sedation (morphine)
5. avoid repeated pelvic exams (increased infection risk)
6. U/S examination of fetus (for GA, BPP, position)
7. prophylactic antibiotics; controversial but may help delay delivery

aggressiveness depends on the GA

Tocolytic agents - if no contraindications present

1. have no impact on neonatal morbidity or mortality but may buy time to allow celestone
use or to transfer to appropriate centre
2. beta-mimetics: ritodrine, terbutaline
3. magnesium sulphate (if diabetes or cardiovascular disease present)
 4. calcium channel blockers: nifedipine
5. PG synthesis inhibitors (2nd line agent): indomethacin

Enhancement of Pulmonary Maturity

1. most effective between 28 and 34 weeks gestation

2. treatment: betamethasone valerate 12 mg IM q12h times 2
3. wait 24 hours for delivery
4. specific maternal contraindications
o active TB

o viral keratosis

o maternal DM

RUPTURE OF MEMBRANES

Premature ROM

rupture of membranes prior to the onset of labour at any GA

Prolonged ROM

if 24 hours elapse between rupture of membranes and onset of labour

Preterm ROM

ROM occurring before 37 weeks gestation (associated with PTL)

PPROM
 preterm premature rupture of membranes (not in labour)

Associated Conditions

congenital anomaly
infection

Causes

idiopathic (most common)

frequently associated with
1. multiparity
2. cervical incompetence
3. infection: cervicitis, vaginitis, STD, UTI
4. multiple gestation
5. family history of PROM
6. low socioeconomic class/poor nutrition
7. and other risk factors associated with PTL (see above)

Complications

1. cord prolapse
2. intrauterine infection (chorioamnionitis)
3. premature delivery

Diagnosis

1. history of fluid gush or continued leakage

2. avoid introducing infection with examinations (do not do a digital pelvic exam)
3. sterile speculum exam
 4. pooling of fluid in the posterior fornix
5. may observe fluid leaking out of cervix on valsalva
6. amniotic fluid turns nitrazine paper blue (low specificity as can be blood, urine or semen)
7. ferning (high salt content of amniotic fluid evaporates and looks like ferns under
microscope)
8. U/S

Management

1. cultures (cervix for GC, lower vagina for GBS)

2. dependent upon gestational age; must weigh degree of prematurity vs risk of amnionitis
and sepsis by remaining in utero
o < 24 weeks consider termination (poor outlook due to pulmonary hypoplasia)

o 26-34 weeks: expectant management as prematurity complications significant

o 34-36 weeks: grey zone" where risk of death from RDS and neonatal sepsis is the
same
o > 36 weeks: induction of labour since the risk of death from sepsis is greater than
RDS
3. assess fetal lung maturity by L/S ratio of amniotic fluid
4. consider administration of betamethasone to accelerate maturity
5. if not in labour or labour not indicated, consider antibiotics (controversial)
6. admit and monitor vitals q4h, daily BPP and WBC count

ANTENATAL COMPLICATIONS

1. UMBILICAL CORD PROLAPSE

2. CHORIOAMNIONITIS
3. PRETERM LABOUR
4. RUPTURE OF MEMBRANES
5. POST-DATE PREGNANCY
6. INTRAUTERINE FETAL DEATH
UMBILICAL CORD PROLAPSE

1. descent of the cord to a level adjacent to or below the presenting part causing cord
compression between presenting part and pelvis
2. visible or palpable cord FHR changes (variable decelerations, bradycardia or both)
3. increased incidence with prematurity/PROM, fetal malpresentations,low-lying placenta,
polyhydramnios, multiple gestation, CPD

Management

1. STAT C-section
2. adjunctive measures
3. alleviate pressure of the presenting part on the cord
4. keep cord warm and moist by replacing it into the vagina and/or applying warm saline
soaks

CHORIOAMNIONITIS

Definition: infection of the chorion, amnion and amniotic fluid

Risk factors:

1. prolonged ROM,
2. long labour,
3. multiple vaginal examsduring labour,
4. internal monitoring,
5. bacterial vaginosis and other vaginal infections
Clinical features:

1. maternal fever,
2. maternal or fetal tachycardia,
3. uterine tenderness,
4. foul cervical discharge,
5. leukocytosis,
6. presence of leukocytes or bacteria in amniotic fluid

Management:

1. blood and amniotic fluid cultures,

2. IV antibiotics (ampicillin and gentamycin)
3. expedient delivery regardless of gestational age

POST-DATE PREGNANCY

Definition and Clinical Features

1. pregnancy beyond 42 weeks (10% of pregnancies)

2. accurate dating essential
3. etiology unknown
4. morbidity increased with hypertension/PET, DM, abruption, IUGR and multiple gestation

Complications

1. perinatal mortality 2-3 x higher

2. oligohydramnios
 3. meconium passage; risk of meconium aspiration
4. asphyxia
5. macrosomia placental insufficiency; infarction of aging placenta
6. postmaturity syndrome: 10-20% of post-term pregnancies (fetal weight loss, reduction in
subcutaneous fat, scaling, dry skin from placental insufficiency)

Management

1. fetal movement count by the mother

2. BPP twice weekly from 40 weeks
3. delivery after 41 weeks if not already in labour since perinatal mortality is higher
secondary to progressive uteroplacental insufficiency
4. if BPP < 10/10 at any time, deliver
5. decreased tolerance for asphyxia during intrapartum

INTRAUTERINE FETAL DEATH

incidence = 1% of pregnancies

Etiology

1. unknown in 50%
2. hypertension,
3. DM
4. erythroblastosis fetalis
5. congenital anomalies
6. umbilical cord or placental complications
7. intrauterine infection
8. antiphospholipid Abs

Clinical Features history

 1. decreased perception of fetal movement by mother examination
2. SFH and maternal weight not increasing
3. absent fetal heart tones (not diagnostic) investigations
4. absent cardiac activity and fetal movement on U/S required for diagnosis
5. high MSAFP

Management

1. labour induction
2. must monitor for maternal coagulopathy (10% risk of DIC)
3. psychologic aspects of fetal loss
4. investigations to determine cause
5. subsequent pregnancies high risk

NORMAL LABOUR AND DELIVERY Part 01

THE FETUS

Fetal Lie

1. refers to the orientation of the long axis of the fetus with respect to the long axis of the
uterus
o longitudinal

o transverse

o oblique

2. transverse/oblique often due to uterine anomalies (C-section if they dont convert)

Fetal Presentation

1. refers to the fetal part presenting at pelvic outlet

o breech (complete, frank, footling)
 o cephalic

1. vertex
2. brow
3. face
4. sinciput ( Forehead and above it )
o shoulder

2. compound (fetal extremity prolapses along with presenting part)

3. all except vertex considered malpresentations

Fetal Position

1. refers to position of fetal occiput in relation to maternal pelvis

o occiput anterior (OA): commonest presentation (normal")

o occiput posterior (OP): most rotate spontaneously to OA : may cause prolonged

second stage of labour
o occiput transverse (OT): leads to arrest of dilatation

2. normally, fetal head enters maternal pelvis and engages in OT position subsequently
rotates to OA position or OP (in a small percentage of cases)

Attitude

refers to flexion/extension of fetal head relative to shoulders

1. brow presentation : head partially extended (requires C-section)

2. face presentation: head fully extended (mentum posterior always requires C-
section, mentum anterior will deliver vaginally)

Station

defined by position of presenting part relative to ischial spines

@ ischial spines = station 0 = engaged

THE CERVIX
1. Dilatation
o latent phase: 0-3 cm

o active phase: 4-10 cm

2. Effacement : thinning of the cervix (25%-50%-100%)

3. Consistency
o soft vs. hard position

o posterior vs. anterior

4. Application : contact between the cervix and presenting part