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Antenatal & Intrapartum Fetal

Objectives of Evaluation

• Location • Morphology
• Viability • Biophysical profile
• Number • Adaptation to stress
• Biometry(size, growth) • Lung Maturity
• Placental exam • Prediction of hypoxic-
• Amniotic fluid volume acidotic insults
Tools of Evaluation
1. History.
2. Physical Exam.
3. Pregnancy test.
4. Ultrasound.
5. Doppler: Auscultation; Blood flow studies.
6. Biochemical screening tests.
Tools of Evaluation

7. Invasive procedures: Amniocentesis,

cordocentesis, Chorionic villous sampling
and other sampling.
8. Electronic fetal heart rate (FHR)
9. Tests of acid-base balance.

• Amenorrhea
• Pain & bleeding in first trimester
• Pregnancy symptoms
• Significant past obstetrical and general history
• Fetal movement first felt at 16-20 weeks “Quickening”.
– Fetal sleep cycle.
• Pain, bleeding, leaking in 2nd and 3rd trimester.
Physical exam

• General: BP, Temp, edema, anemia

• Size of uterus
• Signs of abortion
• Abdominal obstetrical examination
– Uterine fundal growth
• 12 weeks: just above pubis
• 20-24 weeks at umbilicus (variable)
• 24-34 weeks: SFH (cm) = gestational age (wks)
Physical exam

• FHR auscultation starting at 11-12 weeks by daptone

– FHR in early gestation may reach 160-170 bpm,
– Subsequently become less (120-160) due to autonomic
– Do not confuse other sounds e.g. fetal movement,
maternal uterine pulse
Laboratory Investigations
• Pregnancy test
– Urine β HCG
– Serum β HCG: level normally doubles every 48 hrs.
• Routine Investigations
– Blood group and Rh type
– Rh antibodies
– VDRL, Rubella, Hepatitis
– Urine r/m and c/s
– Other tests according to case e.g. APL in recurrent abortions, RFT in renal disease …etc.

Ultrasound in First Trimester
• Location of gestational sac
• Number of fetuses
• Viability of fetus
• Nuchal translucency: chromosomal
Ultrasound in First Trimester
Vaginal Abdominal
Ultrasound Ultrasound

5 weeks 6 weeks
Interauterine Sac β HCG > 1200 IU/L β HCG > 5000 IU/L

Cardiac Pulsation 6 weeks 7 weeks

Ultrasound in 2nd & 3rd Trimesters
• 16-20 weeks (≈ 18 weeks)
– Number of fetuses
– Presentation
– Viability
– Amniotic fluid volume
– Placental localization
– Fetal biometry
– Basic morphological surveillance
– Detailed morphological exam, if required
• Fetal echocardiography if high risk congenital heart disease.
Prenatal screening tests
• 3 biochemical tests: α -fetoprotein, β -HCG & S. estriol
• Tests risk of chromosomal abnormalties, mainly trisomy 21, but
not diagnsotic.
• Diagnosis confirmed by ultrasound and/or amniocentesis.
• Done where abortion laws are permissive. Not practiced in
Invasive Procedures
Chorionic villous sampling

• Not practiced in Kuwait on routine basis for religious

• Reserved for diagnosis if anomalies present on ultrasound.
• Amniocentesis and cordocentesis are used for diagnosis
and management of other diseases e.g. Rh
Isoimmunization, hydrops, suspected infection.
• Complications of procedure:
– Fetal loss: CVS 1%, Amnio 0.5%, Cordo 2-3%
– Bleeding
– Infection
– Membrane rupture
Doppler Study
In cases of utero-placental insufficiency, fetal
blood flow redistribution occur more to (less
resistance) fetal brain, heart and adrenals and
less to (less resistance) abdominal viscera and
lower limbs.

Therefore, measurements of fetal umbilical

artery blood flow (represents lower body flow)
and cerebral artery flow may show this
asymmetrical changes.
Doppler Study
• Systolic:diastolic ratio indicates the
resistance index
• Decreased diastolic flow, becoming absent
or even reversed correlates with the severity
of impaired blood flow.
Degrees of Placental

Normal Flow

Decreased diastolic flow (Mild)

Absent diastolic flow (Moderate)

Reversed diastole (Severe)

Tests of Fetal Lung Maturity

Lecithin-to-Sphingomyelin (LS) Ratio

• L & S are phospholipids components of
• Lung maturity is related to surfactant maturity.
• Before 34 weeks, L & S are present in
amniotic fluid in similar concentrations.
• After 34 weeks, L begins to rise relative to S.
• Increased Respiratory distress if LS ratio is < 2
• LS ratio sample is obtained by amniocentesis
Tests of Fetal Lung Maturity
Phosphatidylglycerol (PG)
• PG enhances surfactant function.
• Identification of PG in amniotic fluid assures, but not
absolutely, against respiratory distress.
• PG is not present in (so not contaminated by) blood,
meconium, or vaginal secretions so can be sampled by
amniocentesis or directly from AF in the vagina.
Biophysical profile (BPP)
No Yes
Fetal movement ≥ 3 times 0 2
Breathing movement ≥ 30 0 2
Tone: ≥ 1 limb flexion-extension 0 2

Amniotic fluid ≥ 2 cm 0 2
Reactive Non-stress test 0 2
Total 10
Biophysical profile (BPP)

• Total score of 8 or 10 is normal

• Total score of 6 is equivocal and

should be repeated in 12-24 hours
• Total score of 4 or less is
abnormal, consider delivery soon.
Electronic Fetal Heart Rate Monitoring

A. Contraction stress test (CST)

B. Non-Stress Test
Contraction stress test (CST)

• Marginally adequate fetal oxygenation with the uterus at

rest will be transiently worsened by uterine contractions
resulting in fetal hypoxemia and late deceleration.

• Contractions may be induced by I.V. oxytocin or nipple


• Most used in USA but not very popular elsewhere because

of its risk.
Antenatal Assessment
Reactive Pattern

Baseline FHR 120-160 bpm

∀ ≥ 2 accelerations in 20 minutes
• Acceleration amplitude > 15 beats lasting > 15 seconds
• Variability 15 beats (5-10 beats in premature fetuses)
• No periodic or significant decelerations (>30 beats)
Non-Reactive Pattern

• Lack of reactive criteria over 40 minutes.

• Always of concern ante-partum & delivery
is generally indicated.
Intrapartum (During Labour) Fetal
Fetal Hypoxemia and Hypoxia

• Transient and repetitive even at the level of CNS

• Extremely common during normal labor.
• Generally well tolerated by the fetus.
• Levels that are ominous to an infant or adult are
commonly seen in normal newborns.
• Only when hypoxia and resultant metabolic
acidemia reach extreme levels is the fetus at risk
for long-term neurologic impairment.
• Fetal oxygen extraction from the maternal
circulation is well adapted even with the
additional stress of normal labor and delivery.

• Insufficient fetoplacental unit resulting from labor

or intrapartum complications may compromise
fetal oxygenation.

• Oxygen delivery is critically dependent on uterine

blood flow.
Factors that decrease placental blood
• Uterine contractions
• Maternal position
• Conduction anesthesia
• Pathologic situations: Preeclampsia, abruptio placentae,
chorioamnionitis, and others.
• Cord compression by entanglement, oligohydramnios, knots,
or prolapse.
• Susceptible fetuses
Fetal CNS, Hypoxia and FHR
H y p o x ia


S y m p a t h P e a t ir c a s y m p

F H R A lt e r a t io n
Methods of Intrapartum Monitoring
Oxygen Saturation Scalp pH or Lactic Umbilical Blood
Acid Gases

H y p o x ia

Biophysical C N S
Profile S y m p a t h P e a t i rc a s y m p
a t h e t ic

F H R A lt e r a t io n s

Fetal ECG
Monitoring of FHR &
Uterine Contractions
Auscultation Amnioinfusion
Monitoring of FHR & Uterine Contractions
Patterns of The FHR
• Normal Pattern
• Baseline Tachycardia/Bradycardia
• Reduced Variability
• Early Decelerations
• Late Decelerations
• Variable Decelerations
• Other Patterns e.g Sinusoidal
FHR Accelerations

• Are common periodic changes in labor and are nearly

always associated with fetal movement.

• Virtually always reassuring and almost always confirm

that the fetus is not acidotic at that time.

• A useful indicator of fetal CNS integrity.

• May serve as a barometer of the fetal

response to hypoxia.

• In most situations, decelerations of the FHR

will precede the loss of variability, indicating
the cause of neurologic depression.
• Factors such as a fetal sleep cycle or medications may decrease

the activity of the CNS and the variability of the FHR.

• Decreased variability in the absence of decelerations is

unlikely to be due to hypoxia.

Early Decelerations
• Benign changes caused by fetal head compression.

• Seen in the active phase of labor.

• They are usually shallow and symmetrical.

• Reach their nadir at the same time as the peak of

the contraction.
Baseline Tachycardia

• Tachycardia may be associated with:

– Severe and prolonged fetal hypoxia
– maternal fever
– Fetal anemia
– Intraamniotic infection i.e. chorioamnionitis
– congenital heart disease
– Hyperthyroidism
Prolonged Deceleration
• An isolated, abrupt decrease in the FHR to levels below the baseline that
lasts at least 60-90 seconds.

• Always of concern and may be caused by virtually any mechanism that

can lead to fetal hypoxia.
Variable Decelerations

• Umbilical cord compression or, occasionally, head


• Abrupt onset and return

• Vary in depth, duration, and shape.

Variable Decelerations

• Frequently preceded and followed by small accelerations of

the FHR.

• Coincide in timing and duration with the compression

which coincides with the timing of the uterine contractions.
Variable Decelerations

• Generally associated with a favorable outcome.

• Non-reassuring if:
– Persistent.
– Progressively deeper to less than 70 bpm
lasting greater than 60 seconds.
– Persistently slow return to baseline .
Late Decelerations

• U-shaped, gradual onset and return, usually

shallow 10-30 beats per minute.

• Reach their deepest point after the peak of the


• A result of CNS hypoxia; in more severe cases, it

may be the result of direct myocardial depression.
Sinusoidal Heart Rate Pattern
• Regular oscillation of the baseline long-term variability resembling a sine
wave, lasting at least 10 minutes.

• Rare and associated with:

– Severe chronic fetal anemia

– Medications: e.g. pethidine

– Severe hypoxia and acidosis.

CTG prediction of neonatal outcome

• Highly sensitive but non-specific resulting in many unnecessary


• Cesarean section rates had risen after introduction of CTG without major
impact on neonatal outcome.
Intermittent Auscultations

• Fetal monitoring by intermittent

auscultation has been shown to be equally
effective to electronic FHR monitoring in
predicting fetal outcome with less need for
cesarean sections.
Fetal Scalp pH Testing
• Gold standard test of acid-base status.
• Management:
• pH > 7.25 Reassuring
• pH < 7.2 Immediate delivery
• pH 7.2-7.25 Repeat after 20-30 minutes
• Used in only 10% of obstetric centers.
• Invasive, labour-intensive, requires repetitions.
Other tests: Limited evidence & use
• Amnioinfusion
• Vibroacoustic Stimulation
• Oxygen Saturation
• Scalp Lactic Acid
• Fetal ECG Monitoring
Management of abnormal FHR
1. Turn patient onto side to alleviate vena
cava compression.
2. Discontinue intravenous oxytocin.
3. Apply 100% oxygen to mother by face
4. Correct maternal hypertension.

5. Vaginal examination to rule out prolapsed cord.

6. Consider fetal scalp blood sampling for pH

7. Search for the cause
– Late decelerations: excessive uterine contractions,
maternal hypotension, or maternal hypoxemia.

– Severe variable or prolonged decelerations:

• Umbilical cord prolapse
• Rapid descent of the fetal head
• Cord compression
8. With decreased variability, consider fetal scalp stimulation.

9. With prolonged bradycardia unresponsive to other

maneuvers or late decelerations with worsening fetal acidosis
(pH <7.20), consider immediate delivery.
10.The decision to intervene depends on:

– Assessment of the likelihood of severe hypoxia

and the possibility of metabolic acidosis

– The estimated time to spontaneous delivery.