OBSTETRICS2 HIGH YIELD FINALS REVIEWER

RISK FACTORS
I.

PRE-TERM LABOR

II.

III.

Presence of contraction of
sufficient strength and
frequency
to
effect
progressive dilatation and
effacement of the cervix
between 20 weeks and 37
weeks of gestation
Contractions of 4 in 20
minutes OR 8 in 60 minutes
PLUS: progressive change
in the cervix, cervical
dilatation greater than 2cm,
cervical effacement of 80%
or greater

Intrauterine infection
Bacterial vaginosis
Multiple pregnancy
Previous pre-term delivery
Cigarette smoking
Cervical incompetencies
Uterine abnormalities
Younger age of the mother
Lower socioeconomic class
Anti-phospholipid syndrome
OB complications

Passage of cervical mucus

Low back pain
Pelvic pressure
Menstrual-like cramps, intestinal cramps
with or without diarrhea

DIAGNOSIS
Vaginal examination: traditional method
UTZ: 30mm cut-off; look for decreased
cervical length, measurement, funneling,
positive stress test
Fibronectin test: positive at 50ng/mL

POST-TERM LABOR
Prolonged or extended
pregnancy (>42 weeks)
Significance of
deceleration:
compression

MANAGEMENT

<37 weeks AOG

variable
cord

Significance
of
late
deceleration: uteroplacental
insufficiency
INAPPROPRIATE FETAL
GROWTH

CLINICAL MANIFESTATIONS

Small fetus: <10th percentile

Large fetus: >90th percentile
Symmetrical
Growth
Restriction: fetal growth is
impaired during the 1st and
2nd trimesters; impairment
of fetal cellular hyperplasia
due to intrinsic factors
Asymmetrical
Growth
Restriction:
decreased
fetal growth velocity in the
3rd trimester; most common
type of IUGR; adaptation to
extrinsic
insult;
head
sparring phenomenon
Uteroplacental insufficiency:
defining feature of IUGR

Maternal risks and complications:

o Operative delivery
o Infection and hemorrhage
o Considerable psychological morbidity
Fetal/ neonatal risks and complications:
o Macrosomia and possible fetal trauma
o Fetal hypoxia
o Oligohydramnios and associated cord accidents
o Meconium aspiration syndrome and neonatal
pneumothorax
o IUGR
o Post-maturity syndrome (old-man facies)
Placental tumors
Hypoxic mothers (high altitude places)
Family history
Nutrition
Multiple pregnancies
Infections
Environmental factors (smoking, drugs, alcohol)
Endocrine disorders
o Screening for risk factors:
Screening sonography UTZ in 2nd
trimester to verify gestational age and
identify anomalies; 18-22 weeks is a good
time to do anatomic survey of fetus
(chromosomal abnormalities); repeated at
32-34 weeks to evaluate fetal growth
(growth abonormalities)
Sonographic
measurement
of
abdominal circumference and EFW:
best predictors of BW below 10th
percentile in high risk pregnancies

Settle the AOG

Assess fetal condition
UTZ evaluation
Pelvic exam

Clinical diagnosis: early dating is the MOST

IMPORTANT factor in the diagnosis of
IUGR
Sonographic
Surveillance:
o Serial fetal biometry: for size of fetus
(growth)
o Amniotic fluid volume: for hypoxia
o Doppler velocimetry: for blood flow
o Biophysical scoring: for hypoxia

Calcium Channel Blockers: first line tocolytics

(mainstay of treatment)
o Nicardipine drip
o Nifedipine oral
Corticosteroids at 24-34 weeks
o Betamethasone
o Dexamethasone
Antibiotics
17-alpha hydroxyprogesterone carpoate
Non-pharmacologic:
o Bed rest
o Cervical cerclage
Prevention
o Progesterone
o MgSO4: preventing convulsions/ cerebral
palsy in pre-eclampsia (neuroprotector)
Side effects of betamimetics: tachycardia,
pulmonary edema, palpitations
Conservative management
o Intensive fetal monitoring (NST and AFI)
o Non-delivery until cervix is favorable for
induction (BISHOP score 5)
o Presence of any problem related to postterm pregnancy
Active induction of labor
o Done in pregnancies at least 41 weeks
o Deliver vaginally

Steroids
IV hydration
Nutritional supplementation
Hyperbaric oxygen
Bed rest

regardless of origin; use

Doppler velocimetry
HYPERTENSIVE
DISORDERS
IN
PREGNANCY

IV.

V.

Gestational HPN: SBP

140 or DBP 90mmHg for
the first time after 20 weeks
AOG
Pre-eclampsia: BP 140/90
mmHg after 20 weeks and
proteinuria 300 mg/24 hrs
or 1 + dipstick

Risk factors for Pre-eclampsia:

o Chronic hypertension
o Previous history of pre-eclampsia
o Young and nulliparous
o Maternal age > 35 y/o
o Genetic predisposition
o Obesity
o Medical complications
o Multifetal gestation
o Primipaternity
o Low socioeconomic status

Blood
volume
and
coagulation:
hemoconcentration (hallmark of preeclampsia)
HELLP syndrome: hemolysis, elevated liver
enzymes, low platelets
Cardiovascular, kidney, liver and brain
problems
Visual changes and blindness

Roll-Over Test: NOT used anymore

MAP
Fibronectin
Coagulation activation
Oxidative stress
Presence of fetal DNA
Uric acid
Uterine artery Doppler velocimetry
Angiogenic factors
Detection of pre-eclampsia: BP monitoring
and 24 hour urine proteins

Severe Pre-eclampsia: BP
160/110 mmHg; elevated
LDH, ALT or AST
Eclampsia: seizures that
cannot be attributed to other
causes in women with
preeclampsia; with sever
headache,
visual
disturbances and epigastric
pain

Chronic HPN: BP140/90

mmHg before pregnancy or
diagnosed before 20 weeks
AOG; HPN first diagnosed
after 20 weeks AOG and
persistent after 20 weeks
post partum; no proteinuria
Superimposed
Preeclampsia: new onset
proteinuria 300 mg/24 hrs.
in HPN women but no
proteinuria before 20 weeks
AOG; preeclmapsia on preexsisting HPN
MULTIPLE PREGNANCY
Monozygotic: result from
fertilization of 1 sperm and
1 egg; same genetic makeup
Dichorionic,
diamniotic:
division during the first 72
hours after fertilization; 2
placentas
Monochorionic, diamniotic:
division during the 4th-8th
day; only 1 placenta
Monochorionic,
monoamniotic: division after
8th day but before 12th day;

Heredity
Race
Maternal age and parity
Periconception intake of vitamins
Infertility treatment

Uterine size larger than expected based on

given AOG
Nausea and vomiting: 1st trimester
Identification of excess fetal parts: 3rd
trimester
Maternal complications:
o Abortion
o Pre-term labor
o Placenta previa
o Pregnancy-induced HPN
o Gestational DM
Fetal complications:
o Twin-Twin Transfusion Syndrome
o Congenital anomalies: 2nd trimester
o Low birthweight
o Discordant growth

Ultrasound
o Lambda sign: 1st trimester
o Twin peak sign: sign of dichorionicity
o Twin intervening membrane: sign of
monochronicity
History and PEfindings

Laboratory findings:
o Elevated alpha-fetoprotein and hCG are
not diagnostic
o No reliable biochemical marker

Mild Pre-eclampsia:
o Home health care
o Antepartum surveillance
o Delivery (40 weeks deliver the baby)
Severe Pre-eclampsia:
o Aggressive management: high neonatal
mortality and morbidity; prolonged NICU
stay; long-term disability
o Expectant management: fetal death;
asphyxia damage, increased maternal
morbidity
Hospitalization
(Tertiary
hospital)
MgSO4
Anti-hypertensives:
ACE
inhibitors are contraindicated
during pregnancy due to fetal
side effects such as defective
skull,
ossifications,
oligohydramnios,
neonatal
anuria
Corticosteroids
Prevention of Pre-eclampsia:
o Bed rest effective in the prevention of
pre-eclampsia; 3rd trimester
o Calcium supplementation significant
reduction in pre-eclampsia
o Low-dose aspirin only one that has
proven to be beneficial in preventing
pre-eclampsia in high risk patients;
decrease pre-term birth, SGA and
deaths; 16 weeks AOG
Management of Eclampsia:
o Control of convulsions: MgSO4
o IV anti-HPN drugs
o Delivery

Antepartum Management:
o Nutrition and weight gain
o Pre-natal diagnosis
o Fetal surveillance
o Prevention and treatment of pre-term
labor and delivery
o Timing of delivery: labor and delivery
Fetal presentation: most important
factor determining mode of delivery
Mode of delivery determined by:
fetal presentation/lie, estimated
fetal weight of twin B relative to
twin A, skill of OB, fetal status
o Management of TTTS:
Serial therapeutic amniocentesis
Septostomy

VI.

VII.

enlargement of the cord

Conjoined twins: division
after the 12th day
Dizygotic:
result
from
fertilization of 2 ova by 2
sperms; different genetic
make-up
DIABETES MELLITUS IN
PREGNANCY
Pre-gestational Diabetes
Type I (Insulin Deficient):
due to an autoimmune
process that targets the
pancreas
!
insulin
production stops; mostly
associated with congenital
anomalies and ketoacidosis
Type II (Insulin Resistant):
associated with obesity and
sedentary living ! insulin
resistance
Gestational
Diabetes:
glucose tolerance that
begins or is first recognized
during pregnancy

THYROID DISORDERS IN
PREGNANCY
Second most common
cause endocrine disease
affecting
women
of
reproductive age
BOTH hyperthyroidism and
hypothyroidism may initially
manifest during pregnancy
Obstetric conditions may
affect thyroid gland function:
gestational
trophoblastic
disease and hyperemesis
gravidarum

o Pre-term birth (MAJOR REASON for

increased neonatal morbidity and
mortality in twins)
o Cerebral palsy
o Perinatal mortality
o Vanishing twin

Maternal age > 25years

Previous macrosomic infant
Previous unexplained fetal demise
Previous pregnancy with GDM
Member of ethnic/racial group
Family history of DM
Obesity
Glucosuria
PCOS
Current use of corticosteroids
Essential HPN or pregnancy
Previous birth of malformed child

Adverse effects of GDM (Fetal):

o Abortion
o Congenital anomalies: heart defects
and neural tube defects (MOST
COMMON
congenital
anomalies
associated with DM)
o Macrosomia
o Birth inury
o IUGR
o Polyhydramnios
o Pre-term labor and delivery
o Unexplained fetal demise
Adverse effects of GDM (Maternal):
o Diabetic nephropathy
o Diabetic retinopathy
o Diabetic neuropathy
o Pre-eclampsia
o Ketoacidosis
o Infections
Adverse effects of GDM (Neonatal):
o RDS
o Hypoglycemia
o Hypocalcemia
o Hyperbilirubinemia
o Cardiac hypertrophy
o Childhood obesity
o Childhood impaired glucose tolerance

Summary of changes during pregnancy:

o Moderate enlargement of glandular
hyperplasia and increased vascularity
o Sharp rise in T4 and T3
o Increase in serum TBG
o High serum concentration of hCG
activates TSH receptor
o No alteration in TRH secretion
Congenital hypothyroidism: maternal
thyroid hormone crosses the placenta
Hyperthyroidism
o 95% of cases are due to Graves
disease (MOST COMMON)
o Ophthalmopathy
o Dermopathy
o Serum TFTs differentiate thyroid
disease from non-thyroid disease
o High FT4 or FTI + suppressed TSH
o Heat intolerance, diarrhea, hair loss,
weight loss, palpitations, fatigue,
diaphoresis

Screening and detection:

o High risk: screen at first pre-natal visit
(Filipinos)
o GDM: If FBS is between 92mg/dL and <
126mg/dL
o Low risk: screen at 24-28 weeks AOG;
use 2 hour 75g OGTT
o Results:
Abnormal 1 hour plasma glucose =
GDM (only 1 abnormal value to
diagnose GDM)
If OGTT is normal, repeat at 32 weeks
or earlier
mg/dL
Fasting
> 92
1 hour
180
2 hour
153
o Overt DM
RBS >200mg/dL
Fbs 126mg/dL
2 hour plasma glucose > 200mg/dL
during a 75g OGTT
HbA1C 6.5%

TSH: initial test for screening and evaluation

of symptomatic disease
Free TSH: biologically active portion
In pregnant patient, suspected of being
hyper or hypothyroid, TSH, FT4 or FTI must
be measured
Free thyroxine
FTI: if FT4 is not available
FT3: in patients with thyrotoxicosis with
suppressed TSH but normal FT4
measurements
TRH stimulation test: evaluates the
secretory ability of the pituitary
Antibody test

Diet: mainstay treatment in GDM; 6 meals

distribution
Exercise: mainstay treatment in GDM
Self-monitoring of blood glucose: 7 point blood
glucose monitoring
Insulin: higher incidence of maternal
hypoglycemia
Oral Hypoglycemic Agents (OHA): ACOG
does not recommend these agents during
pregnancy
o
Glyburide: first-line therapy for diet
failure with GDM; same outcome
compared with insulin; does not
readily cross the placenta
o
Metformin: increased incidence of preterm birth
Fetal Surveillance

Treatment guidelines for hyperthyroidism:

o
Lowest dose of Thioamide (PTU) to
maintain maternal T4 within high normal
range
o
Monitor maternal T4 every 2-4 weeks
and titrate Thioamide as necessary
o
Measure TSH receptor antibodies at 2628 weeks
o
Fetal UTZ at 26-28 weeks
o
Consider thyroidectomy if persistently
high doses of Thioamide are required
o
Peri-operative use of beta-blockers and
iodide
o
Check fetal cord blood at delivery for
TSH and T4
Treatment guidelines for hypothyroidism:
o Check serum TSH once pregnancy is
confirmed
o For
newly
diagnosed:
initiate
Levothyroxine
o For previously diagnosed: monitor serum
TSH every 3-4 weeks during 1st half of

 Hypothyroidism
o Subclinical hypothyroidism: High TSH +
normal FTI
o Untreated hypothyroidism is associated
with an increased risk of pre-eclampsia
o High incidence of LBW in neonates
associated with inadequately treated
hypothyroidism
o Cold
intolerance,
constipation,
slowness, lethrgy

VIII.
-

PULMONARY DISEASES
IN PREGNANCY
Pulmonary changes in
pregnancy:

Decrease in RV

Decrease in functional
residual capacity
Expiratory reserve volume
Total lung capacity

Increase in respiratory
capacity
Unchanged vital capacity or FEV1
and unchanged RR

Predisposing factors to Bacterial Pneumonia:

o
Anatomical changes in the
chest
o
Changes in the immune status
Predisposing factors to Aspiration Pneumonia:
o
Increased iatrogenic pressure
o
Relaxed GE sphincter
o
Delayed gastric emptying
o
Sedation and analgesia
o
Vigorous abdominal palpation
Pregnant patients with TB at risk for:
o
Pre-eclampsia
o
Vaginal bleeding
o
Early fetal death
o
Pre-term delivery
o
LBW and low APGAR scores
Risk factors for Pulmonary Embolism:
o
Maternal age > 35 y/o
o
Parity of 3
o
> 165lbs (obesity)
o
Personal/ family history
o
Prolonged immobilization
o
Assisted or surgical delivery
o
Hemorrhage
Sepsis

Asthma
o

Chronic
inflammatory
disorder associated with
airway
hyperresponsiveness and
bronchospasm
o
Airflow obstruction
o
Rule of thirds in
pregnancy:
1/3
will
worsen, 1/3 will get
better, 1/3 will remain
unchanged
Bacterial Pneumonia
o
Major
complications
associated
with
pneumonia:
pre-term
labor
o
Etiology of uncomplicated
CAP: Pneumococcus, H.
influenzae,
atypical
agents (MOST COMMON
pathogens)
o
Most common cause of
pneumonia
during
pregnancy: S. pneumonia
o
Etiology of superinfection:

pregnancy and every 6 weeks thereafter

Adjust Levothyroxine to maintain serum
TSH of 2.5mU/L
o Monitor serum TSH and total T4 levels 34 weeks after every dosage adjustment
o Separate Levothyroxine intake from
prenatal vitamins by at least 4 hours to
ensure adequate absorption
o After delivery, reduce levothyroxine to
pre-pregnancy dosage and check serum
TSH in 6 weeks
Thioamides (PTU and Methimazole): PTU
preferred in pregnancy: crossed the
placenta less well than Methimazole
o MOA of PTU: reduces the peripheral
conversion of T4 to T3
o AE: Fetal goiter, fetal thyrotoxicosis,
neonatal
thyroid
dysfunction,
agranulocytosis
o PTU and Methimazole: safe during
breastfeeding
Beta-blockers:
Propranolol
(MOST
COMMON beta-blocker used)
Thyroidectomy
Iodine 131: contraindicated in pregnant
women due to risk of fetal thyroid ablation;
avoid pregnancy for 4 months after
treatment; inhibits thyroidal release of T3
and T4 in thyroid storm
Levothyroxine: TSH levels increased while
FTI decreased during pregnancy
Treatment of Asthma:
o
Goal: sufficient oxygenation of
fetus
o
Salmeterol: initial treatment for
all
o
Salbutamol: rescue medication
o
ICS (Budesonide): for persistent
asthma
o
Inhaled beta-agonist: mild
intermittent asthma
o
Antibiotics: for fever
o
Obtain PEFR upon admission to
delivery
o
Management during labor in
asthmatic
patients:
Hydrocortisone
o
Avoid narcotic analgesics that
release histamine during labor
o
Ergotamine
maleate:
contraindicated
due
to
bronchospasm
Treatment of Bacterial Pneumonia:
o
Penicillins, Cephalosporins and
Macrolides = SAFE
o
Macrolides: to cover for atypical
organisms
o

Spirometry: standard test

ABG: indicates decompensation
Diagnosis of Asthma:
o
Spirometry + subjective
evaluation: preferred method
of pulmonary function testing;
women with mild or wellcontrolled asthma
o
UTZ + antenatal testing:
women with moderate to
severe
asthma
during
pregnancy

Diagnosis of Bacterial Pneumonia:

o
CXR: increased isk for
developmental anomalies
and growth retardation
o
Shield patient with lead
apron

Diagnosis of Tuberculosis:
o
Sputum microscopy: test of
choice for initial work-up for
TB-symptomatic patients
o
3 early morning samples
o
At least 2 positive
o
If unable to bring up
sputum: give hypertonic

S. aureus
Etiology of aspiration
pneumonia: gram (-)
organisms
o
Triad of fever, cough and
dyspnea
o
Pneumonia during midpregnancy carries this
risk: IUGR

Aspiration Pneumonia
o
Aspiration
includes
bacteria in the oropharynx
and liquid or solid gastric
contents
o
Pneumonia
due
to
aspiration occurs 24
hours after solid particles
and gastric fluid

Tuberculosis
o
Chronic cough >2 weeks,
weight loss, sweat and
chills, body malaise, fever
o
Clinical clue: failure to
gain weight

Pulmonary Embolism
o
Venous thromboembolic
disease: leading cause of
morbidity and mortality
during pregnancy
o
Risk of DVT: highest in
the antepartum period
o
But the highest possibility
of pulmonary embolism is
immediately after delivery
o
Pregnancy:
hypercoagulable state
Clinical presentation: leg swelling, dyspnea,
tachypnea, tachycardia, palpitations

saline solution
For smear negative patient:
do culture and CXR
o
In high risk population and
with evidence of CXR the
cut-off value is 5mm
o
Latent infection diagnosis:
Quantiferon-TB Gold

Diagnosis of DVT:
o
Compressive UTZ and
Impedance Pletysmography
o
Do not use D-dimer test

Diagnosis of Pulmonary Embolism:

o
VQ scan or helical CT
Safe during pregnancy

Classic Triad:
o Chorioamnionitis
o Intracrainial calcification
o Hydrocephalus with seizure
Congenital Toxoplasmosis
o At birth maculopapular rash,
hepatosplenomegaly,
seizures,
convulsions
o Blindness,
deafness,
mental
retardation

Maternal SSx
o Non-tender
posterior
cervical
lymphadenopathy
o Flu-like symptoms
Serologic Test for IgG or IgM
o IgG: appears 1-2 weeks of infection;
peaks between 6-8 weeks
o IgM: appears within 1st week of infection
then declines over several months
PCR testing of amniotic fluid most accurate
test for fetal infection (2nd trimester)

Tetracycline AE: staining and

deformation of fetal teeth
o
Chloramphenicol AE: aplastic
anemia, gray baby syndrome
o
Sulfonamides
AE:
fetal
kernicterus
o
Aminoglycosides AE: ototoxicity
and nephrotoxicity
o
Supportive therapy: hydration,
antipyretics, supplemental O2
Management of Aspiration Pneumonia:
o
Supportive
therapy:
supplemental
O2,
bronchodilators,
ventilator
support
o
If with signs of infection:
antibiotics
o
Prevention: major thrust of
management
o
Regional anesthesia is preferred
over general anesthesia
Treatment of Tuberculosis:
o
HRZE: safe to give in pregnancy
o
Do not give streptomycin:
ototoxic (vestibular or auditory
damage)
o
Isoniazid: crosses placenta but
no adverse effects to fetus: add
pyridoxine to prevent peripheral
neuropathy and optic neuritis;
induced hepatitis risk
o
Do not discontinue treatment if
pregnancy
occurs
after
treatment initiation
Treatment of Pulmonary Embolism:
o
Heparin: mainstay of treatment
for acute VTE
o
Supportive
therapy:
fluid
resuscitation, lateral decubitus
position to displace gravid
uterus
Warfarin/ Coumadin: relatively contraindicated in
pregnancy; safe during first 6 weeks of gestation
o

IX. INFECTIONS
Toxoplasmosis
Rare

Acquired through ingestion of encysted organism in

raw or uncooked meat or contact with cat feces

Spiramycin given once maternal infection

is confirmed
Pyrimethamine and Sulfadiazine and Folinic
acid given once fetal infection is
confirmed; can cross placenta and
penetrate fetal brain

Rubella

Transmission: airborne

Cytomegalovirus
Most common cause of viral
intrauterine infection
Infection can oocur in-utero,
intrapartum and through
breastmilk

Transmission: contact with body fluid or sexual

contact

Herpes Simplex Virus

Recurrent STD caused by
HSV-1 (oral) or HSV-2
(genital)

Risk of fetal transmission:

o Contact with infected genital secretions
o If delivery occurs during primary infection (4050%)
o If delivery occurs during recurrent infection (03%)
o Sites of intrapartum entry: fetal eyes
nasopharynx, break in the skin

30% of mothers asymptomatic

or with mild 3-day rash with
potential auricular adenopathy
Classic Triad for Congenital
Rubella:
Cataract
Heart Disease
Sensorineural Deafness

o
o
o
o
CMV infection:
o 4-8 week incubation period
o viremia: 3-12 months
o viral transmission via primary or
recurrent maternal infection
o Rate of transmission increases with
gestational age highest at 3rd
trimester
Recurrent CMV infection:
o Occur with immunosuppression and
during pregnancy
o Reactivation of endogenous virus
o Infected neonates with <8% chance
of hearing loss and chorioretinitis
o IgG confers good protection
Neonatal CMV infection:
o UTZ findings: ventriculomegaly,
oligohydramnios, echogenic bowel,
choroid plexus cyst, pleural effusion,
brain/liver calcifications
Congenital CMV:
o Blueberry muffin baby
o Jaundice,
thrombocytopenia,
hepatosplenomegaly, chorioretinitis,
deafness, microcephaly, etc.
Ulceration in genitalia with
severe local pain, dysuria,
sacral paresthesia, tender
inguinal lymph nodes, fever,
malaise
Primary First episode:
o HSV without prior HSV-1 or HSV-2
antibodies
o No fetal consequences unless
convert shortly before labor and
delivery
Non-primary First episode:
o HSV-2 confirmed with prior findings
of HSV-1 antibodies or vice-versa
o Symptoms milder
Recurrent Genital Herpes:
o Reactivation of HSV usually HSV-2
o Virons travel from skin or mucosa to
sensory dorsal root ganglion where
latency is established

Serologic Testing of IgG and IgM antibody

titer which becomes (+) 4 weeks after
exposure

CMV screening not routinely recommended

IgM and IgG screening at 8-12 weeks
AFI PCR for CMV to detect infection
Neonatal CMV infection: CMV virus in AF by
PCR at 21 weeks at 6 weeks interval

HSV culture -48-72 hrs at appearance of

lesions
Serologic testing
PCR assay
Tzank smear (multinucleated giant cells and
viral inclusions)

Prevention: MMR vaccine

o Given to children 12-15 months of age
and at school age
o Non-pregnant women and women at
reproductive age
No treatment

Prevention:
o Hygiene

Prevention:
o Avoid sexual contact
o Condoms
o Suppression decreases recurrent genital
lesions
Primary HSV:
o Analgesia
o Hygiene
o Acyclovir 7-14 days or Valcyclovir
o Suppression: Acyclovir or Valcyclovir at 36
weeks to delivery
First episode within 6-12 weeks of delivery
o IV acyclovir intrapartum to both mother and
neonate
o Daily acyclovir or valcyclovir from 36 weeks
until delivery
Complicated CMV infection
o IV acyclovir
Recurrent HSV
o Analgesia
o Hygiene
o Acyclovir
o Suppression therapy


Varicella Zoster
Double-stranded
DNA
acquired in childhood
Reactivation
of
latent
varicella: Herpes Zoster

Transmission:
droplets

direct

contact

and

respiratory

Parvovirus
Human parvovirus B19
causes Fifth disease or
erythema infectiosum
Most common cause of
nonimmune hydrops
Hepatitis A
RNA virus transmitted via
fecal-oral route

Hepatitis B
Most common form of viral
hepatitis in pregnancy

HIV
-

Infects T lymphocytes that

express DC4 antigen !
opportunistic infection

Group B Streptococcus Infection

(S. agalactiae or Lancefield group B
streptococcus)
Major cause of postpartum
infection
Most common cause of
neonatal sepsis
X. HEMATOLOGIC DISORDERS
Iron Deficiency Anemia

Congenital Parvovirus infection known to cause:

o
Abortion
o
Hydrops fetalis (between 13-16 weeks)
o
Severe anemia
o
CHF
o
Generalized edema
o
Fetal death
Travel to prevalent country
Homosexual
IV drug users
Working with non-human primates
Chronic liver disease
Perinatal transmission
Sexual contact
IV drug users
STDs
Multiple sex partners
Mental institutions/prisons
Acupuncture
HBV infected patients at high risk HIV and HCV
infections
Closely related to viral load at time of delivery
Low CD4 ad T-lymphocytes count
Lack of antiretroviral therapy
Biological phenotype of the virus
Substance abuse
Rupture of membranes >4 hours
Vertical transmission in utero from maternal genital
tract or at delivery
Risk factors:
o Prolonged ROM >18 hours
o Preterm delivery
o Temp: 38 C
o Maternal chorioamnionitis
o Young maternal age

Varicella
o Maculopapular vesicular purpuritic
lesions
Herpes Zoster
o Painful lesions over sensory nerve
root distributions
Maternal Primary Varicella
o Pneumonitis
o Bacterial superinfection (cellulitis,
abscess formation)
Congenital Varicella Syndrome
Neonatal VZV infection
o Fetal exposure just before or during
delivery
20-30% asymptomatic
Slapped check appearance
Rash spread to trunk and
extremities
Polyarthralgia

VZV IgG titer

Serologic testing for IgG and IgM

Modes of Delivery:
o With active lesion ! CS
o PPROM ! expectant

Supportive care

Acyclovir for complicated varicella or

immunocompromised

Varicella Zoster Immunoglobulin up to 96

hours post exposure

Anti-HAV IgM

Treatment of hydrops fetalis: intrauterine

transfusion and digoxin
Serial sonography every 2 weeks
MCA Doppler evaluation (elevated peak
systolic velocity predict fetal anemia)

Supportive
No perinatal transmission

HBV vaccine 3 IM injections over 6 months

Engerix B within 12 hours of deliver

Screening with ELIS (Western blot)

Azidothymidine
Zidovudine
Continue monitoring CD4 count and HIVRNA levels

Early onset: illness in the newborn within

24 hours of life
Late onset: 3-4 weeks of age or between 7
days to 3 months of age

Anovaginal swab at 35-37 weeks ! culture

PCR

Penicillin
Ampicillin
For penicillin allergic:
o Clindamycin
o Erythromycin

Maternal need for iron: 1000 mg

Serum ferritin

Ferrous sulfate, fumarate or gluconate

Vertical transmission is high when HBsAg

(+) and (+)HBeAg
Higher transmission during 3rd trimester

Hepatitis B panel
Screen for HBV by HBsAg
HBV DNA quantitative PCR
Liver biopsy

2 most common causes of

anemia during pregnancy:
IDA and acute blood loss

IDA is often manifested by an appreciable

drop in Hgb especially during 2nd trimester
3rd trimester: additional iron needs
newborn infant of a severely anemic
mother does not suffer from IDA

Anemia from Acute Blood Loss

In early pregnancy, common in instances of

abortion, ectopic pregnancy and H.mole

Megaloblastic Anemia
Blood and bone-marrow
abnormalities form impaired
DNA synthesis
-thalassemia

FAD: women who do not consume fresh green leafy

vegetables, legumes or animal protein
Vitamin B12 Deficiency: after partial or total gastric
restriction

-thalassemia

Immune Thrombocytopenia Purpura

cluster of IgG antibodies
directed against one or
more platelet glycoproteins
XI. CONNECTIVE TISSUE DISORDERS
SLE
-

Overly
active
B
lymphocytes
that
are
responsible
for
autoantibody production

APS

Inheritance of autoimmunity gene or ch.16

Anticardiolipin against 2-glycoprotein I

XII.

RENAL AND UTI IN

PREGNANCY
Structural changes during
pregnancy:
Increase by 1-1.5cm in
length and 30% in volume
Collecting system expands
> 80%

Predisposing factors to UTI:

o
Stasis associated with hydroureter
and hydronephrosis
o
Bladder trauma
o
Vesicoureteral reflux
o
Increased glucosuria
Most common causes of Chronic Renal Disease:
o
DM
o
HPN
o
Glomerulonephritis

provides approximately 200 mg daily

elemental iron
o Continued for 3 months after anemia has
been corrected

Hgb: <10 to 15 mg/L confirm diagnosis of

IDA

Folic acid requirement during pregnancy:

400g/day

Deletion of all 4 genes: hydrops fetalis

Deletion of 3 out of 4 genes: hemolytic
anemia
Deletion 2 out of 4 genes: alphathalassemia minor (minimal or moderate
hypochromic microcytic anemia)
Deletion of 1 out of 4 genes: silent carrier
-thalassemia major
o hallmark: elevated hemoglobin A2
levels
-thalassemia minor: mild hypochromic
microcytic anemia
In adults, ITP is primarily a chronic
disease of young women and rarely
resolves spontaneously

Hydrops fetalis detected by fetal Doppler

flow measurement of MCA

Malaise
Fever
Arthritis
Rash
Pleuropericarditis
Photosensitivity
Anemia
Cognitive dysfunction
Recurrent arterial or venous thrombosis
Thrombocytopenia
Fetal losses especially during 2nd half of
pregnancy
CNS involvement

UTI

Progesterone
makes
muscle of the bladder less
motile
o
Common in pregnancy
Asymptomatic Bacteriuria
o
Presence of bacteria within
the urinary tract, excluding
urethra without symptoms
of infection
o

If pregnant woman has moderate anemia

defined by 7 g/dl, hemodynamically stable
and able to ambulate without AE ! no
need to transfuse blood
o Give iron therapy for 3 months
Folic acid and Vitamin B12 supplementation

-thalassemia minor: prophylactic iron and

folic acid are given

Platelet count: 10,000-100,000/L

If platelet count is <30,000/L ! treat

Prednisone + IVIg
Splenectomy
Azathioprine,
cyclophosphamide,cyclosporine

ANA best screening test

Anti-dsDNA and anti-Sm; C3 and C4
activity of disease
Anti SS-A and anti SS-B marker for
affectation of heart
Diagnosis: 4 out of 11 from crieria

NSAIDs and aspirin

Prednisone severe disease
Azathioprine,
cyclophosphamide,
cyclosporine
Hydroxychloroquine skin rash

Clinical Criteria:
o Thrombosis
o Pregnancy (recurrent fetal losses)
Laboratory Criteria:
o Anticardiolipin antibodies
o Lupus anticoagulant
Routine assessment of renal function:
o
Proteinuria
should
be
assessed every pre-natal visit
o
Urine dipstick value > 1+ =
clean catch urine sample for
culture and microscopy
o
Persistent proteinuria: 24
hour urine culture needed
o
Proteinuria
>
300mg:
abnormal

Low dose aspirin + Heparin

Treatment of choice for Urethritis:

Azithromycin 1g single oral dose
Treatment of Pyelonephritis:
o
Hospitalization
o
IV hydration, anti-pyretics,
broad-spectrum antibiotics
o
Antibiotics of choice: Cefazolin,
Penicillin,
Ampicillin
+
Gentamycin
Treatment of Nephrolithiasis:

Glucosuria
pregnancy

Hydroureter
hydronephrosis

and

Increase renal plasma flow

by 50-80% ! increase
GFR
creatinine

Decreased mean serum

BUN and serum creatinine
Renal Tubular Function
Decreased
reabsorption

PKD

o
o

Short urethra predisposes

women to infection
Renal Filtration

Increased
clearance

tubular

Calcium
clearance
is
balanced
by
GUT
absorption
Physiologic hyponatremia
Urinary excretion of glucose
increases by 10 to 100 fold
is common in normal

Associated with LBW,

IUGR and pre-term delivery
Screen patient on the
FIRST visit
E.coli: most common cause
of infection

Acute Cystitis
o
Honeymoon cystitis
o
Urinary frequency, urgency,
dysuria, hematuria and
suprapubic discomfort
Urethritis
o
Frequency:
common
complaint
o
C. trachomatis: common
causative organism
o
Patients with symptoms of
acute cystitis and (-) culture
o
Mucopurulent cervicitis may
be present
Pyelonephritis
o
Leading cause of septic
shock in pregnancy
o
High grade fever (spiking
appearance), chills, flank
pain, nausea and vomiting,
frequency, urgency, dysuria
Nephrolithiasis
o
Suspected UTI and (-) urine
culture
o
Patient with persistent/
recurrent UTI
Chronic Renal Disease
Degree of renal impairment: major
determinant of pregnancy outcome

Serum creatinine persistently

>0.9mg/dL: investigate for
intrinsic renal disease
Confirmatory test for Asymptomatic
Bacteriuria: 24 hour urine collection for
culture (clean catch urine 100, 000
colonies/mL OR catheterized urine culture
100 colonies warrants treatment)
Diagnosis of Pyelonephritis:
o
Clinical findings of + CVA
tenderness
o
Blood culture and urine
culture
o
CBC, serum creatinine and
electrolytes
Diagnosis of Nephrolithiasis:
o
Primary clinical: colicky
abdominal
pain
and
hematuria
UTZ: for any obstruction
o

o
IV hydration and analgesics
30% of symptomatic cases require surgical
intervention