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COMPLICATION
S
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
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?
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
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
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
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
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
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
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
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
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
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
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