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OBSTETRIC

COMPLICATION
S

Ma. Bernadette O. Cruz, MD, MSc, FPOGS


OBSTETRIC
COMPLICATIONS
 Selected maternal and fetal conditions that make
the pregnancy at risk for maternal and fetal
morbidity and mortality.
 Multifetal pregnancy
 Preterm labor
 Postterm pregnancy
 Inappropriate fetal growth
 Premature rupture of membranes
 Congenital malformations and inherited diseases
 Diseases and injuries of the fetus and the newborn
infant
VARIATIONS IN THE
DURATION OF PREGNANCY
 Average duration of normal
pregnancy
 260 days from conception
 280+14 days from LMP
 Incidence of preterm birth - 5% of
pregnancies (<36 weeks)
 10% of cases, the pregnancy is
prolonged.
 birth >41 weeks
Preterm Labor and Delivery
Preterm Delivery

 Preterm – infants delivered before


completion of 37 weeks (259th day)
 Low birthweight – <2500 grams
 Very low birthweight – <1500 grams
 Extremely-low birthweight – <1000
grams
Etiology of preterm labor
1. Medical and 2. Lifestyle factors
obstetric a. low prepregnancy weight
complications b. smoking
c. alcohol abuse
a. Preeclampsia d. Young gravida
e. Poverty
b. fetal distress
f. short stature
c. fetal growth
g. occupational factors
restriction
h. psychological stress
d. abruptio placentae
e. fetal death
f. spontaneous
preterm labor
Etiology of preterm labor

3. Genetic factors
4. Amnionic fluid and chorioamnionic
infection
 initiated by secretory products
(interleukin-1, tumor necrosis factor,
interleukin-6) resulting from monocyte
activation in response to infection
 Phospholipase A  cleaves arachidonic
acid  prostaglandin synthesis
Etiology of preterm labor

5. Epidemiologic studies: Low SES,


nonwhite race, maternal age <18
years or >40 years, low
prepregnancy weight.
6. Multiple gestation – although
incidence is only 1.1%, MP accounts
for 10% of all preterm births
Etiology of preterm labor

7. History of preterm birth


 Recurrence risk: of 17-37%
 Risk increases with number of preterm births
and decreases with number of term
deliveries.
7. Risk of preterm birth increases with
women who had spontaneous second-
trimester abortion(s).
8. No PNC regardless of SES
Etiology of preterm labor

10. Coitus and orgasm (?); sexual


abstinence in the prevention of
preterm labor (?).
11. PROM
12. Uterine malformations – unicornuate
and bicornuate uteri
13. Uterine myoma – submucosal or
subplacental
Etiology of preterm labor
14. Cervical incompetence
 0.1-2% of all pregnancies
 due to trauma from prior obstetric or
gynecologic procedure,
diethylstilbestrolexposure in utero
14. Infectious causes
 STDs
 Chorioamnionitis
 Group B streptococci, N. gonorrhoeae, C.
trachomatis, U. urealyticum, T. pallidum, T.
vaginalis or G vaginalis.
Signs and symptoms
 Painful or painless uterine contractions,
pelvic pressure
 Watery or bloody vaginal discharge
 Menstrual-like cramps and low back pain
 Asymptomatic cervical dilatation after
midpregnancy
 mean cervical length (UTZ) at 24 weeks = 35 mm
 women with progressively shorter cervices
experienced increased rates of preterm birth
Diagnostics: 1. Fetal fibronectin
 A glycoprotein produced by fetal amnion,
hepatocytes, malignant cells, fibroblasts,
endothelial cells
 Plays a role in intercellular adhesion:
implantation, adhesion of placenta to
decidua
 Detection of fetal fibronectin in
cervicovaginal secretions prior to
membrane rupture may be a marker for
impending preterm labor
Diagnostics

2. Ambulatory uterine contraction


testing – use of home monitoring of
uterine contractions for prevention
of preterm labor controversial
3. maternal salivary estriol
associated with preterm delivery
CRITERIA FOR DIAGNOSIS
(American Academy of Pediatrics and the American
College of Obstetricians and Gynecologists, 1997)

1. Contractions occurring at a
frequency of four in 20 minutes or
eight in 60 minutes + progressive
change in the cervix
2. Cervical dilatation > 1 cm
3. Cervical effacement of > 80%
Management

1. Gestational age?
2. Condition of membranes?

 Successful treatment achieved


when initiated early, before
advanced cervical dilatation and
rupture of membranes
1. Premature labor with intact
membranes
A. Glucocorticoid therapy
 Corticosteroids accelerate lung maturation
 lower incidence of RDS, mortality from
hyaline membrane disease
 Induction of proteins that regulate
biochemical systems within type II cells in
the fetal lung to produce surfactant
A. Cervical cerclage – in recurrent
midtrimester losses
Premature labor with intact
membranes
C. Treat bacterial vaginosis linked to increased
preterm birth at <32 weeks or less
 treatment of asymptomatic BV did not improve
pregnancy outcomes
 Other vaginal infections: trichomoniasis, chlamydial
C. Bed rest
 most often used treatment regimen
 no conclusive evidence that bed rest is effective
C. Hydration and sedation
Premature labor with intact
membranes
F. Tocolysis
1. Beta-adrenergic receptor agonists
2. Magnesium sulfate
3. Prostaglandin inhibitors
4. Calcium channel blockers
Tocolytic Agents
DRUGS Mechanism Side Example
Effects
β -adrenergic Combines w/ Pulmo edema, Ritodrine,
receptor receptor to inc. capillary terbutaline
agonist activate adenyl permeability,
cyclase w/c arrhythmia,
converts ATP to myocardial
cAMP; decreases ischemia
intracellular CA+ 
prevents
contraction
Magnesium blocks calcium influx Hyporeflexia at
sulfate at membrane, 6-12
activates adenylate mEq/L, Loss of
cyclase, increases DTRs at 10
cAMP which reduces mEqs,
intracellular calcium Respiratory
paralysis at 15
mEqs
Tocolytic Agents
DRUGS Mechanism Side Example
Effects
Prostaglandin inhibits synthesis closure of Indomethacin,
inhibitor of PGs, blocks ductus sulindac
action of PGs on arteriosus,
target organs; necrotizing
PGs are involved enterocolitis,
in myometrial intracranial
contractions of hemorrhage
normal labor

Calcium inhibit entry of maternal Nifedipine


channel CA+ thru cell hypotension
blockers membrane and decreased
channels  uteroplacental
reduction in CA+ perfusion,
concentration tachycardia
inhibits
Tocolytic Agents
DRUGS Mechanism Side Example
Effects
Atosiban oxytocin analog;
competitive
oxytocin-
vasopressin
antagonist
Nitric oxide potent
endogenous
smooth-
muscle
relaxant
Management

2. Preterm labor + preterm premature


rupture of membranes (PPROM)
 Expectant management or
nonintervention – spontaneous labor is
simply awaited
 Corticosteroids + tocolytic agents to
allow corticosteroids to work (induce
fetal lung maturation)
Premature rupture of
membranes (PROM)
Premature rupture of
membranes
 Rupture of membranes before onset of labor
 Incidence: 8-10%
 25% of cases the fetus is preterm.
 Preterm premature rupture of membranes –
rpture of membranes before onset of labor
at gestational age <37 weeks.
 Prolonged rupture of membranes – PROM
>24 hours before delivery.
 Latency period – time between PROM and
onset of labor.
 Amniotic fluid is necessary for normal
fetal lung development.
 It also protects the fetus from trauma
and umbilical cord from compression.

RUPTURE OF MEMBRANES

OLIGOHYDRAMNIOS
Premature rupture of
membranes
 May lead to onset of preterm labor
 In most cases, the baby is born
within 7 days of the prelabor rupture.
 Prolonged PROM increases risk for
chorioamnionitis.
Risk factors for PROM
1. Local infection – weakening of
membranes
 N. gonorrhoeae, C. trachomatis, Group B
strep, T. vaginalis, G. vaginalis
1. Polyhydramnios
2. Incompetent cervix
3. Cervical cerclage
4. Previous cervical laceration or
operation
5. Smoking
Clinical presentation
 Gush of fluid from the vagina
followed by persistent leakage of
fluid (90%)
 Differentiate from urine, excessive vaginal
discharge or mucus, bloody show
associated with labor
 Chorioamnionitis
 Preterm labor
Diagnostics
1. Tests to document rupture of
membranes
 Nitrazine test for pH of vagina
 Normal vaginal pH: 4.5 – 6
 AF pH: 7.1 – 7.3
 Nitrazine paper: yellow  blue pH >6.0
 Microscopic slide test for ferning of
vaginal fluid
 (+) ferning with AF
Diagnostics
2. Ultrasound examination
 Establish AOG
 Fetal presentation
 Low AF index
2. Cervical cultures
Diagnostics
4. Tests to rule out chorioamnionitis
a. CBC with differential
b. Serum C-reactive protein >0.8 mg/dl
c. Amniocentesis and AF culture
d. Biophysical profile
a. Fetal breathing movements
b. Gross body movement
c. Fetal tone
d. Reactive FHR
e. Qualitattive AFV
Diagnostics
5. Tests for fetal lung maturity
a. Fetal lung maturity – impt factor in PROM
b. Lecithin-sphingomyelin (L/S) ratio >2
c. (+) Phosphatidylglycerol
d. Foam stability test – shake test
a. AF with sufficient surfactant forms stable stable
foam at air-surface interface for 15 min
a. High false-negatives: LS ratio 4-6
Complications from PROM
Threats to the fetus

1. Prematurity
 Responsible for 30% of all preterm births
(>low SES, STD)
 PROM at term: 90% of patients will go into
labor <24 hours
 PPROM 28-34 weeks AOG: 50% in labor
within 24 hours; 80-90% within 1 week
 PPROM <26 weeks: 50% in labor within 1
week
Complications from PROM
Threats to the fetus

2. Infection
 Serous infection: 5% of preterm PROM
15-20% with chorioamnionitis
 Fetal pneumonia, sepsis, UTI,
conjunctivitis
2. Fetal distress
 Incidence: 8.5% (6-fold increase in
risk)
 Umbilical cord compression or
prolapse
Complications from PROM
Threats to the fetus

 Fetal deformations
 Early preterm PROM: impaired feltal
lung development  pulmonary
hypoplasia
 IUGR
 Compression malformations of face
and limbs (3.5%)
 esp <26 weeks AOG
Complications from PROM
Threats to the Mother
 Sepsis secondary to
chorioamnionitis Overall: 0.5-1%.
 Prolonged PROM chorioamnionitis:
3-15%.
 Preterm PROM: 15-25%
Management of PROM

1. PROM + advanced labor,


chorioamnionitis, fetal distress
regardless of gestation
 Vaginal delivery
 CS for obstetric reasons
 Antibiotic treatment
 Ampicillin
 Cephalosporins
 Gentamycin
Management of PROM

2. PROM at term
 Goal: deliver before chorioamnionitis

a. Expectant management
b. Induction of labor immediately
Management of Term PROM
 Expectant management
a. Await spontaneous labor
b. Avoid digital cervical examination until
patient in labor
c. Electronic fetal heart monitoring
d. Serial monitoring for chorioamnionitis
e. Deliver ASAP if (+) chorioamnionitis
Management of Term PROM
 Labor induction immediately
a. Induce labor with oxytocin infusion
 Intracervical prostaglandin E2 gel for
preinduction cervical ripening
 Bishop’s score
a. Continuous electronic fetal heart
monitoring
Management of PRETERM PROM
 Prematurity  if not in labor, prolong
pregnancy for as long as no
chorioamnionitis

 2 Options
1. Expectant management
2. Tocolysis + corticosteroids followed by
delivery
Management of PRETERM PROM:
Expectant management
1. Prophylactic antibiotics
 Decreases maternal and fetal infections
 Increases latency period by 5-7 days
1. Bed rest
2. Avoid digital cervical exam until labor
3. Fetal well-being studies
4. Serial monitoring for chorioamnionitis
5. Test for fetal lung maturity if >32
weeks
Management of PRETERM PROM:
Tocolysis + corticosteroids followed by
delivery

1. Corticosteroid therapy
 Maximum effect 24 hours after
administration
1. Tocolysis
 Continued for 48 hrs after steroids
1. Expectant management or induce
labor
Management of PREVIABLE PROM

 PROM <25 weeks


 25-40% chance of achieving viable
fetus
 Risk of chorioamnionitis: 40%
 Fetal deformities
 Counseling for couple
 2 Options
1. Expectant management
2. Termination of pregnancy
MULTIFETAL
PREGNANCY
ETIOLOGY
 Monozygotic twins arise from a single
fertilized ovum that subsequently divides
into two similar structures, each with
potential for developing into a separate
individual (single-ovum, monozygotic or
identical twins).
 Dizygotic twins result from fertilization of
two separate ova (double-ovum, dizygotic
or fraternal twins).
1. Monozygotic 2. Dizygotic
twins twins
3. Chimerism -
in an
individual
whose cells
originated
from more
than one
fertilized
ovum.
ETIOLOGY
 Superfetation when an interval as
long as or longer than an ovulatory
cycle intervenes between
fertilizations.
 Superfecundation refers to the
fertilization of two ova within a short
period of time but not at the same
coitus, nor necessarily by sperm from
the same male.
ETIOLOGY OF MULTIFETAL PREGNANCY
RISK FACTORS FOR
TWINNNG
1. Race

2. Heredity – maternal family history >


paternal

3. Maternal age – peak at age 37, when


maximum hormonal stimulation
increases rate of double ovulation

4. Parity – fertility and multiparity (~7)


RISK FACTORS FOR
TWINNNG
5. Nutritional factors
6. Pituitary gonadotropin – common
factor linking race, age, weight, and
fertility to multiple gestation.

7. Infertility therapy – induction of


ovulation by use of gonadotropins
(FSH plus HCG) or clomiphene.
DIAGNOSIS: History and
PE
1. History
 identification of risk factors
1. Physical examination
 Fundic height larger than expected for
gestational age
 Multiplicity of fetal parts by palpation
 Two distinct fetal heart tones
DIAGNOSIS: 3. Ultrasound

 Presence of 2
separate placental
sites and a thick
dividing membrane
that generally is 2
mm or greater
supports
dichorionicity.
DIAGNOSIS: Ultrasound
 “Twin peak” sign –
triangular projection of
placental tissue extending
beyond the chorionic
surface between the
layers of the dividing
membrane seen in fused
placenta
DIAGNOSIS

4. Biochemical test: Human chorionic


gonadotropin in plasma and urine
are higher than those in singleton
pregnancies
5. Radiograph of the maternal abdomen
demonstrates multiple fetuses,
helpful in rare circumstances
Maternal Adaptations to Multifetal
Pregnancy

1. Nausea and vomiting - > in


singleton pregnancy
2. Blood volume expansion
 50-60% with twins vs 40-50% with
singletons  more pronounced
“physiologic anemia”
Maternal Adaptations to Multifetal
Pregnancy

3. Cardiac output – increased due to


increased heart rate and stroke
volume
4. Uterus – larger size (volume of 10L,
weight of 20 lbs)
OUTCOMES OF MULTIFETAL
PREGNANCY

1. Spontaneous abortion more


common in monozygotic twins.
2. Malformations
 Defects from twinning itself
 Defects from vascular interchange
 Defects due to crowding
Defect from twinning: Conjoined
twins
Defect from
twinning:
SIRENOMELIA

 Persistence of
vitelline artery 
abnormal aortic
development  blood
flow to lower
extremities curtailed
Defect from twinning:
Holoprosencephaly
 Failure of brain to
divide into
hemispheres.
 Always accompanied
by midline defects
e.g. cleft lip and
palate, fused eye
sockets, deformities
of limb, heart, GIT,
internal organs
Defect from twinning: Neural tube
defect
Defect from twinning: Neural tube
defect
Exencephaly
Folic acid in the prevention of
NTDs
b. Defects from vascular interchange:
ACARDIA
Defects from vascular interchange:
Microcephaly
Defects from vascular
interchange:

INTESTINAL
ATRESIA
Defects from vascular interchange:

APLASIA CUTIS
c. Defect from crowding: Talipes
OUTCOMES OF MULTIFETAL
PREGNANCY
3. Low birthweight
 From restricted fetal growth and preterm delivery
 Degree of growth restriction related to monozygosity
and number of twins
 Monozygotic twins more likely to be discordant in
size.
OUTCOMES OF MULTIFETAL
PREGNANCY

4. Preterm birth
 Duration of
gestation decreases
as the number of
fetuses increases.
 Major reason for the
increased risk of
neonatal death and
morbidity in twins.
OUTCOMES OF MULTIFETAL
PREGNANCY
5. Prolonged pregnancy
 fetal growth restriction and associated
morbidity increases significantly in twins
delivered at 39-41 weeks compared with
delivery at 38 weeks or less.
5. Long-term postnatal development
 twinning may result to delayed
developmental milestones.
 in discordant twins, pattern of
development appears to be better in the
twin who weighed more at birth.
OUTCOMES OF MULTIFETAL
PREGNANCY
7. Conjoined twins
 twinning initiated after the embryonic
disc and rudimentary amnionic sac
have formed and if the division of the
embryonic disc is incomplete
 commonly shared body site:
 anterior (thoracopagus)
 posterior (pyopagus)
 cephalic (craniopagus)
 caudal (ischiopagus)
PYGOPAGUS 

Conjoined twins

THORACOPAGUS CRANIOPAGUS
OUTCOMES OF MULTIFETAL
PREGNANCY
8. Monoamnionic twins – intertwining of
umbilical cords
9. Vascular communication between
fetuses
 most vascular communications are
hemodynamically balanced and of little
fetal consequence
 ie. artery-to-artery, vein-to-vein, or
artery-to-vein
OUTCOMES OF MULTIFETAL
PREGNANCY
a) Acardiac twin – TRAP (Twin reversed-
arterial-perfusion) sequence
 complication of monochorionic,
monozygotic multiple gestation
 normally formed donor twin with
features of heart failure
 Recipient twin recipient twin without a
normal heart (acardius) and missing
other structures, ie. acephalus
B. Defects from
vascular
interchange:
ACARDIA
OUTCOMES OF MULTIFETAL
PREGNANCY
b) Twin-to-twin
transfusion
syndrome
 Blood from donor
twin to recipient twin
 donor develops
anemia and IUGR
 recipient has
polycythemia with
circulatory overload 
hydrops
 donor twin is pale,
recipient is plethoric
Twin-to-twin transfusion
syndrome
ANTENATAL
 Same sex fetuses POSTNATAL
 Monochorionicity with  Diagnosed
placental vascular
connections
postnatally:
 weight
 Intertwin weight
difference >20% discordance of
 Hydramnios in the large 15 or 20%
twin, oligohydramnios or
 Hgb difference >
stuck twin (in donor sac)
 Hemoglobin difference >5 5 g/dL with the
g/dL smaller twin
being anemic
OUTCOMES OF MULTIFETAL
PREGNANCY
10. Discordant twin
 unequal size of twin
fetuses  sign of
pathological growth
restriction in one
fetus
 defined using larger
twin as the index
 direct proportional
increase in perinatal
mortality as weight
difference within
twin increases
OUTCOMES OF MULTIFETAL
PREGNANCY
13. Death of one (or two) twin(s)
 maternal risk and prognosis for the surviving twin
depend on the gestational age the time of the
demise, the chorionicity, and time interval between
demise and delivery of surviving twin

FETUS
PAPYRACEOUS
OUTCOMES OF MULTIFETAL
PREGNANCY
14. Complete hydatidiform
mole and coexisting
fetus
 Two separate
conceptuses: a normal
placenta in one twin and
a complete molar
gestation in the other
 Management is
uncertain
MANAGEMENT OF MULTIFETAL
PREGNANCY
1. Antenatal
 Dietary requirements for calories,
proteins, minerals, vitamins and
essential fatty acids are increased.
 Hypertension
 Prevention of preterm labor and
delivery:
 bed rest
 tocolytic therapy
 prophylactic cervical cerclage.
MANAGEMENT OF MULTIFETAL
PREGNANCY
2. Labor and delivery
 Fetal presentation and position
 cephalic-cephalic, cephalic-breech, and
cephalic-transverse
 Conduct of labor and delivery:
 preterm labor,
 uterine dysfunction,
 abnormal presentations
 prolapse of the umbilical cord
 premature separation of the placenta
 immediate postpartum hemorrhage
MANAGEMENT OF MULTIFETAL
PREGNANCY
2. Labor and delivery
 Route of delivery by fetal presentation:
 Cephalic-cephalic – vaginal
 Cephalic-noncephalic – controversial
 Breech or transverse first of twin – abdominal

 Anesthesia: epidural
 provides pain relief
 skeletal muscle relaxation required for
internal podalic version
 rapidly extended cephalad if CS required
Postterm Pregnancy
Postterm Pregnancy

 Postterm pregnancy – >42


completed weeks (294 days) from
LMP
 Postmaturity – infant clinical features
indicating a pathologically prolonged
pregnancy
Pathophysiology

 Postmaturity syndrome – postmature


infant with characteristic
appearance:
 wrinkled, patchy peeling skin,
 long, thin body suggesting wasting
 advanced maturity: open-eyed,
unusually alert, old and worried-looking
 attributed to placental senescence
Pathophysiology
 Oligohydramnios
 due to decreased amniotic fluid volume
 Fetal distress
 consequence of cord compression associated
with oligohydramnios
 Fetal release of meconium in reduced
amniotic fluid thick, viscous meconium
 thick, viscous meconium
 Fetal growth restriction in 1/3 of cases
Management
 Antenatal surveillance
 Nonstress tests, amniotic fluid
determinations
 Cervical ripening
 Prostaglandin gels
 Induction of labor
 Use of oxytocin
Inappropriate fetal growth

 Baby too small


 Baby too big
3 PHASES OF FETAL
GROWTH
1. 1st 16 weeks gestation 
hyperplasia
 5 gram/day
1. 16-32 weeks hyperplasia and
hypertrophy
 15-20 g/day
1. >32 weeks  hypertrophy with
fetal fat and glycogen deposition
 30-35 g/day
Factors that influence fetal growth
1. Genetics
2. Hormones
 Insulin – somatic growth and adiposity
 Insulin-like growth factors (IGF-I, IGF-II) –
cell division and differentiation
 Leptin – correlates with birthweight,
synthesized in adipose tissue
1. Nutrition
 Maternal glucose: excessive glycemia
causes macrosomia; decreased glycemia
causes growth restriction
FETAL GROWTH
RESTRICTION
 Small for gestational age
 Birthweight <10th percentile for
gestational age
 At risk for fetal death
 0.2% for normal 38 weekers vs 2% for SGAs
 Uteroplacental isufficiency
Complications of SGA
babies
 Fetal demise
 Asphyxia
 Meconium aspiration
 Neonatal hypoglycemia
 Hypothermia
 Abnormal neurological development
Symmetrical FGR
 Head to abdomen circumference ratio (HC/AC)
 Ratio >95% percentile
 Asymmetric fetus had bigger brain, protected from full
effects of growth retarding stimulus.
 Preferential shunting of oxygen and nutrients to brain
 Early insult from viral infection, chemical
exposure, aneuploidy affecting cellular number
an size
 Severe preeclampsia, fetal distress, operative
intervention, low apgar score
Asymmetrical FGR

 Late insult: uteroplacental


insufficiency affecting cell size
 Hypertension
Risk factors
1. Constitutionally small mothers
 Mother <100 lbs with two-fold increase
in risk for SGA
1. Poor maternal weight gain and
nutrition
 Weight gain during pregnancy
1. Social deprivation
 Lifestyle and use of illicit substances,
alcohol, smoking, nutrition
Risk factors
4. Fetal infections
a. Cytomegalovirus – direct cytolysis and loss of
functional cells
b. Rubella – vascular insufficiency endothelial
cell damage, decreased rate of cell division
c. Hepatitis A and B
d. Listeriosis
e. Tuberculosis
f. Syphilis –megaplacenta due to edema and
perivascular inflammation
g. Toxoplasmosis
h. Congenital malaria
Risk factors
5. Chromosomal abnormalities
 Autosomal trisomies (21, 18, 13, 16) –
reduced number of small arteries in tertiary
villi  uteroplacental insufficiency and
abnormal cell growth and differentiation
5. Congenital malformations
6. Primary disorders of bone and cartilage
Risk factors

8. Chemical teratogens
 Anticonvulsants: phenytoin and
trimethadione
 Narcotics
 Smoking
 Alcohol
 Cocaine
Risk factors
9. Vascular disease
10. Chronic renal disease
11. Chronic hypoxia
12. Maternal anemia
13. Placental and cord abnormalities
 Chronic placental separation
 Infarction
 Chorioangioma
Risk factors
14. Multiple gestation
15. APAS – vascular thrombosis;
maternal platelet aggregation and
placental thrombosis
 Anticardiolipin antibody
 Lupus anticoagulant
14. Extrauterine pregnancy
SCREENING AND DIAGNOSIS

1. Establish gestational age


2. Maternal weight gain
3. Uterine fundal growth
 Normal: 18-30 weeks, fundic height in cm =
gestation in weeks +1 cm
4. Identify risk factors
 history of growth retarded fetus
SCREENING AND DIAGNOSIS

5. Serial sonographic measurements of


head, abdominal, femoral
 Abdominal circumference is most reliable
5. Doppler velocimetry
 Umbilical artery – absent or reversed flow
 increased impedance  IUGR
 Adjunct to NST and BPP
Management of Growth Restricted
Fetus
 Look for congenital malformations
 Determine if fetus is in poor
condition
 Cordocentesis for karyotyping
 Lethal aneupliody
 Weigh risk of fetal death vs preterm
delivery
FGR near TERM

1. Prompt delivery: >34 weeks


 Reassuring FHR pattern: vaginal
delivery
 Fetal distress: CS

2. Expectant management
 Fetal well being studies
FGR remote from TERM
1. <34 weeks + normohydramnios +
normal fetal surveillance
 Observation
 Fetal surveillance every 2-3 weeks
 Amniocentesis for fetal lung maturity
1. With fetal growth  allow
pregnancy to continue
2. Fetal compromise  Deliver
FGR remote from TERM
 Bed rest, LLD position
 Nutritional supplementation
 Hydration
 Oxygen therapy
 Medications
 Antihypertensive drugs
 Aspirin
 Heparin
 Dipyridamole
 Nitrol patch
Labor and Delivery of Growth-
restricted Fetus
 Continuous fetal heart rate pattern
surveillance
 Uteroplacental insufficiency
 Oligohydramnios  cord compression
 Meconium aspiration
 Hypothermia
 Polycythemia and hyperviscosity
 Hypoglycemia
DISEASES and INJURIES of
the FETUS and the
NEWBORN
HYALINE MEMBRANE DISEASE

 Etiology: inadequate surfactant


production by type II pneumonocytes
 Signs and symptoms
 tachypnea and chest wall retraction
 expiration is accompanied by a whimper
and grunt (combination of “grunting and
flaring
HYALINE MEMBRANE DISEASE

 chest x-ray:
diffuse
reticulogranula
r infiltrate with
an air-filled
tracheobronchi
al tree (air
bronchogram)
HYALINE MEMBRANE DISEASE

 Complications
 bronchopulmonary dysplasia
 pulmonary hypertension
 retinopathy of prematurity
HYALINE MEMBRANE DISEASE
 Continuous positive
airway pressure
(CPAP) prevents
collapse of
unstable alveoli
 Surfactant
 prophylaxis of
preterm infants at
risk for RDS
 Rescue for those
with established
disease
RETINOPATHY OF PREMATURITY

 Retinal vessels
damaged by
excessive oxygen
 Oxygen induces
severe
vasoconstriction,
endothelial
damage and
vessel obliteration
MECONIUM ASPIRATION
 Peripartum inhalation of meconium-stained
amniotic fluid  inflammation of
pulmonary tissues and hypoxia
 May progress to persistent pulmonary
hypertension, morbidity and death
 Pregnancies at risk for meconium
aspiration
 Oligohydramnios
 Cord compression
 Uteroplacental insufficiency
MECONIUM ASPIRATION

 Chest X ray
MECONIUM ASPIRATION
 Prevention
 Suction infant’s
mouth and nares
before shoulders are
delivered
 Suction under direct
visualization as soon
as infant who has
passed thick,
particulate meconium
is placed on radiant
warmer
INTRAVENTRICULAR
HEMORRHAGE
 Etiology
 Subdural hematoma – trauma
 Subarachnoid and intracerebellar
hemorrhage – trauma in term infants,
hypoxia in preterm infants
 Periventricular-intraventricular hemorrhage
 Unknown cause in 25% of cases
INTRAVENTRICULAR
HEMORRHAGE
INTRAVENTRICULAR
HEMORRHAGE
 Patholophysiology: damage to the germinal
matrix capillary network  extravasation of
blood into the surrounding tissues
 capillary network is fragile in preterm infants
 Long term sequelae
 Periventricular leukomalacia
 Neurodevelopmental handicaps
 Treatment: corticosteroids before delivery
appears to prevent intraventricular
hemorrhage in preterm infants
CEREBRAL PALSY
 Nonprogressive motor
disorder of early infancy
involving > 1 limbs 
resulting from muscular
spasticity or paralysis
 Types
 Spastic quadriplegia

 Diplegia

 Hemiplegia

 Choreoathetoid type

 Mixed varieties
CEREBRAL PALSY
 Risk factors
1. Genetic abnormalities such
as maternal mental
retardation, microcephaly,
congenital malformations
2. Birthweight l< 2000 grams
3. Gestational age <32 weeks
4. Infection
 Correlation with
intrapartum asphyxia
controversial
NEONATAL ENCEPHALOPATHY

 Syndrome of disturbed neurological


function in the earliest days of life in term
infant
 Consists of difficulty in initiating and
maintaining respiration, depressed tone
and reflexes, subnormal level of
consciousness and frequently seizures
 Believed to be a consequence of an
hypoxic-ischemic insult
ANEMIA
 Cord hemoglobin < 14 g/dl (>35 weeks, mean
cord hemoglobin concentration = 17 g/dL)
 Hemoglobin due to delayed cord clamping 
appreciable volume of blood being expressed from
the placenta through the cord of the infant
 Hemoglobin if placenta is cut or torn, a fetal
vessel is perforated or lacerated, or the infant is
held well above the level of the placenta before
cord clamping
ABO INCOMPATIBILITY

 Incompatibility for the major blood


group antigens A and B is the most
common cause of hemolytic disease
of the newborn
 Invariably causes mild disease, such
as neonatal jaundice or anemia but
not erythroblastosis fetalis
 Treatment: Phototherapy
IMMUNE HYDROPS
 Subcutaneous edema
 Effusion into the
serous cavities -
presence of abnormal
fluid in > 2 sites such
as thorax, abdomen
or skin;
 Edematous placenta,
enlarged and boggy
IMMUNE HYDROPS
 Pathophysiology: obscure
 Theories
 Heart failure and capillary leakage from profound anemia,
 Portal and umbilical venous hypertension from hepatic parenchymal
disruption by extramedullary hematopoiesis
 Decreased colloid oncotic pressure from hypoproteinemia caused by liver
dysfunction
IMMUNE HYDROPS
 Treatment: identify woman at risk at first
prenatal appointment
 After identification of isoimmunization and the
fetus at risk for optimal outcome, subsequent
management is individualized
 Prevention:
 anti-D immunoglobulin to Rh(-) women at 28
weeks, and after delivery if the infant is D-
positive
 Immunoglobulin given to Rh(-) women after
miscarriage, abortion, or evacuation of a molar
or ectopic pregnancy
NONIMMUNE HYDROPS
 Etiology
 cardiac abnormalities
 fetal heart failure
 chromosomal abnormalities
 twin-to-twin transfusion syndrome
 severe anemia
 inborn errors of metabolism
 anomalous lymph system
 Treatment depends on the cause
HEMORRHAGIC DISEASE of the
NEWBORN
 Spontaneous internal or external bleeding
accompanied by hypoprothrombinemia &
very low levels of other vitamin K-
dependent coagulation factors (V, VII, IX
and X)
 Etiology
 dietary vitamin K deficiency – main cause
 Hemophilia
 congenital syphilis
 Sepsis
 thrombocytopenia purpura
 erythroblastosis
 intracranial hemorrhage
 Prevention: Vit K 1 mg IM at delivery
NECROTIZING ENTEROCOLITIS

 Clinical findings:
abdominal
distention, ileus
and bloody stools
 Seen in low
birthweight infants
NECROTIZING ENTEROCOLITIS

 Radiologic
evidence:
pneumatosis
intestinalis caused
by intestinal wall
gas from invasion
by gas-forming
bacteria and bowel
perforation
FETAL DEATH
 Fetal causes (25-40%)  Uterine rupture
 chromosomal  Postterm pregnancy
anomalies  Drugs
 nonchromosomal birth  Placental causes (25-
defects 35%)
 nonimmune hydrops  Abruption, previa
 infections  fetal-maternal
 Maternal (5-10%) hemorrhage
 APAS  cord accident

 DM  placental insufficiency,
 Hypertension intrapartum asphyxia
 Trauma  twin-to-twin transfusion
 Abnormal labor  chorioamnionitis
 Sepsis  Unexplained (25-35%)
 Acidosis, hypoxia
INJURIES of the FETUS and
NEWBORN
Intracranial hemorrhage
 Sites: subdural, subarachnoid, cortical, white
matter, cerebellar, intraventricular, and
periventricular
 Most common type: IC bleed in the germinal
matrix
 Severe molding & overlapping of parietal
bones, bridging veins from the cerebral
cortex to the sagittal sinus may tear
 Causes
 Birth trauma during difficult labor and delivery
 Prenatal factors: genetic and environmental
CEPHALHEMATOMA

 Injury to periosteum
of the skull during
labor and delivery
 Periosteal limitations,
definite palpable
edges
 May not appear for
hours after delivery,
often growing larger
and disappearing
only after weeks or
even months
CAPUT SUCCEDANEUM
 Focal swelling of the
scalp from edema that
overlies the periosteum
 Maximal at birth, then
grows smaller
 Usually disappears
within a few hours if
small, and within a few
days if very large
CAPUT SUCCEDANEUM vs
CEPHALHEMATOMA

CAPUT SUCCEDANEUM CEPHALHEMATOMA


NERVE INJURIES

 Spinal injury –
overstretching the
spinal cord and
associated
hemorrhage
following excessive
traction during a
breech delivery
NERVE INJURIES

 Brachial plexus
injury – Duchenne
paralysis results
from stretching or
tearing of the upper
roots of the brachial
plexus
NERVE INJURIES

 Facial paralysis –
seen with delivery
of an infant in
which head has
been seized
obliquely with
forceps
FRACTURES

 Fractures
 Clavicular
 Humeral
 Femoral
 Skull fractures
CONGENITAL MALFORMATIONS
AND INHERITED DISEASES
Women at risk for fetal aneuploidy
1. Women with singleton pregnancy at least
age 35 at delivery
2. Women with dizygotic twin pregnancy at
least age 31 at delivery
 Risk for fetal Down syndrome – 1:190
1. Previous pregnancy with autosomal trisomy
 1% occurrence, until age-related risk >1.
1. Previous pregnancy with triple XXX (47XXX)
or Klinefelter syndrome 47 XXY
 Extra X may be maternal or paternal
 47 XYY and 45 X not at high risk for recurrence
Women at risk for fetal aneuploidy

5. Woman or partner who is a translocation


carrier.
 5 – 30% risk
5. Woman or partner who is a chromosomal
inversion carrier.
 5 – 10% risk
5. History of triploidy
 Recurrence risk is 1 – 1.5% if fetus survives 1st
trimester
Women at risk for fetal aneuploidy

8. Repetitive spontaneous 1st trimester


losses
 Karyotype on the parents most useful
9. Parental aneuploidy
 Trisomy 21, 47,XXX and 47,XYY have 30%
risk of having trisomic offspring
 Detect it through maternal and paternal
karyotyping
9. Fetus with major structural defect
identified by ultrasound
Congenital Heart Disease
 Most common birth defect, 7:1000 births
 Etiology
 Genetic
 Environmental – DM, viral infections, poor OB history,
smoking, drug use
 Recurrence risk for CHD:
 Mother > 2 siblings > 1 sibling > father
 Prenatal diagnosis: fetal 2D echocardiogram at
20 – 22 weeks gestation
Congenital Heart Disease

ASD
PDA
Congenital Heart Disease

TETRALOGY OF
FALLOT

TRICUSPID ATRESIA
Neural Tube Defects
 Family history of neural tube defects
 most important risk factor
 Risk to 10 relative 2-3%, related to degree of
relations, # of relatives affected
 Exposure to environmental agents
 Period of risky exposure: 1st 28 days gestation
 Hyperglycemia
 Hyperthermia
 Drugs: carbamazepine, valproic acid,
aminopterin, isotretinoin
Neural Tube Defects

 NTDs as part of a genetic syndrome


with known recurrence risk
 Inherited syndromes: Meckel-Gruber,
Roberts-SC phocomelia
 Known high-risk racial, ethnic groups
or living in high-risk geographic areas
 UK – highest incidence
 Sikhs in India > Sikhs in Canada
Screening for NTDs
 Maternal serum α -fetoprotein
 At 15-22 weeks gestation, >2.0-2.5 MOM
 Targeted ultrasound
 Major cranial, spinal defects can be detected
 Lemon sign, banana sign
 Risk of NTD reduced by 95% if none found by
UTZ
 Amniocentesis for AF α FP
 NTD suspect with elevated α FP but (-) UTZ
 Elevated serum and AF α FP, do karyotyping
Ultrasound-guided AMNIOCENTESIS
Neural Tube Defects
ANENCEPHALY

INIENCEPHAL
Y
Neural Tube Defects
DOWN’S SYNDROME
 Majority of Down syndrome pregnancies
are de novo and in women age <35.
 Maternal age – most important risk factor
 Multiple marker screening
 Low α −fetoprotein
 Elevated β −human chorionic gonadotrophin
 Decreased unconjugated estriol
FRAGILE X SYNDROME
 Most common
cause of familial
mental retardation
 Affected female
carriers are normal.
 Long face,
elongated ears,
testes larger than
normal.
CYSTIC FIBROSIS
 Autosomal Recessive
1:25 Euro Caucasians
 Abnormal sweat
chloride level, chr
pulmonary disease,
pancreatic
insufficiency, liver
disease, obstructive
azoospermia
 Pregnancy
termination
CONGENITAL DIAPHRAGMATIC HERNIA

 1:3700
 Fetal surgical
correction to
restore normal
intrathoracic
anatomy and allow
pulmo dev’t 
prevent pulmo
hypoplasia
Management of fetuses with
congenital anomalies
 Team approach

 Route of delivery
 CS if malformation will cause dystocia
 e.g. conjoined twins, hydrocephalus

 Intrauterine fetal therapy


 Pulmonary immaturity – transplacental glucocorticoids
 Intrauterine growth restriction – protein-calores
Management of fetuses with
congenital anomalies
 Malformations needing  Malformations best
early correction ex corrected in term infant
utero  GIT atresias
 Meconium ileus
 Obstructive
hydrocephalus,  Small meningocoele, spina
hydronephrosis bifida
 Smal sacrococcygeal
 Hydrops
teratoma
 IUGR  Craniofacial, chest wall and
 Intestinal ischemia extremity deformities
 Volvulus
 Meconium ileus
OBSTETRIC
COMPLICATIONS
 Maternal and fetal  Premature rupture of
membranes
conditions that  Congenital
make the malformations and
pregnancy at risk inherited diseases
Diseases and injuries of
for morbidity and

the fetus and the
mortality: newborn infant

 Multifetal pregnancy  Definition


Preterm labor Risk factors


 Postterm pregnancy
 Inappropriate fetal
 Pathophysiology
growth  Management
hydranencephaly