Antenatal & Intrapartum Fetal

Monitoring

Objectives of Evaluation

Location
Viability
Number
Biometry(size,
growth)
Placental exam
Amniotic fluid
volume assessment

Morphology
Biophysical profile
Adaptation to stress
Lung Maturity
Prediction of hypoxicacidotic insults

Tools of Evaluation
1.
2.
3.
4.
5.

History.
Physical Exam.
Pregnancy test.
Ultrasound.
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)
monitoring.
9. Tests of acid-base balance.
4

History

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.
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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
maturation.
Do not confuse other sounds e.g. fetal movement,
maternal uterine pulse

Laboratory Investigations
Pregnancy test
Urine HCG
Serum HCG: level normally doubles every 48 hrs.
Routine Investigations
CBC
Blood group and Rh type
Rh antibodies
VDRL, Rubella, Hepatitis
FBS
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
abnormalities.

Ultrasound in First Trimester

Vaginal
Ultrasound
(TVS)

Abdominal
Ultrasound
(TAS)

Interauterine Sac

5 weeks
HCG > 1200
IU/L

6 weeks
HCG > 5000
IU/L

Cardiac Pulsation

6 weeks

7 weeks
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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.

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Prenatal screening tests

3 biochemical tests: -fetoprotein, -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 Kuwait.
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Invasive Procedures
Chorionic villous sampling
Amniocentesis
Cordocentesis
Not practiced in Kuwait on routine basis for religious
issues.
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.
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14

 Complications of procedure:
Fetal loss: CVS 1%, Amnio 0.5%, Cordo 2-3%
Bleeding
Infection
Membrane rupture

15

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.
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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.

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Degrees of Placental
Insufficiency
Normal Flow

Decreased diastolic flow (Mild)

Absent diastolic flow (Moderate)

Reversed diastole (Severe)

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Tests of Fetal Lung Maturity

Lecithin-to-Sphingomyelin (LS) Ratio
L & S are phospholipids components of
surfactants.
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
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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.
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Biophysical profile (BPP)

Fetal movement 3 times

No
0
30
0

Breathing movement
seconds
Tone: 1 limb flexion-extension
Amniotic
fluid

2
perpendicular
Reactive Non-stress test

cm

Yes
2
2

0
Total

2
1021

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

or

less

is

abnormal, consider delivery soon.

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Electronic Fetal Heart Rate Monitoring

A. Contraction stress test (CST)

B. Non-Stress Test

23

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
stimulation
Most used in USA but not very popular elsewhere because
of its risk.
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Antenatal Assessment

25

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)
26

Non-Reactive Pattern
Lack of reactive criteria over 40 minutes.
Always of concern ante-partum & delivery
is generally indicated.

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28

Intrapartum (During Labour) Fetal

Monitoring

29

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.
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 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.
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Factors that decrease placental blood

flow
Uterine contractions
Maternal position
Conduction anesthesia
Pathologic
situations:
Preeclampsia,
placentae, chorioamnionitis, and others.

abruptio

Cord compression by entanglement, oligohydramnios,

knots, or prolapse.
Susceptible fetuses
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Fetal CNS, Hypoxia and FHR

H y p o x ia
C N S
S y m p a t h e t ic

P a r a s y m p a t h e t ic

F H R A lt e r a t io n s
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Methods of Intrapartum Monitoring

Oxygen Saturation

Umbilical Blood
Gases

Scalp pH or Lactic
Acid
H y p o x ia

Biophysical
Profile

C N S
S y m p a t h e t ic

P a r a s y m p a t h e t ic

Vibroacoustic
Stimulation

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

Monitoring of FHR &

Uterine Contractions
(Cardiotocography)

Fetal ECG
Monitoring
Intermittent
Auscultation

Amnioinfusion
34

Monitoring of FHR & Uterine Contractions

(Cardio-toco-graphy)

35

Patterns of The FHR

Normal Pattern
Baseline Tachycardia/Bradycardia
Reduced Variability
Early Decelerations
Late Decelerations
Variable Decelerations
Other Patterns e.g Sinusoidal
36

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.

37

Variability
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.
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Variability
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.

39

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.

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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
41

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.

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43

Variable Decelerations
Umbilical cord compression or, occasionally, head
compression.
Abrupt onset and return
Vary in depth, duration, and shape.
44

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.
45

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 .
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Late Decelerations
U-shaped, gradual onset and return, usually
shallow 10-30 beats per minute.
Reach their deepest point after the peak of the
contraction.
A result of CNS hypoxia; in more severe cases, it
may be the result of direct myocardial depression.
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49

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.
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CTG prediction of neonatal outcome

Highly sensitive but non-specific resulting in many
unnecessary interventions.
Cesarean section rates had risen after introduction of
CTG without major impact on neonatal outcome.

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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.
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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.
53

Other tests: Limited evidence & use

Amnioinfusion
Vibroacoustic Stimulation
Oxygen Saturation
Scalp Lactic Acid
Fetal ECG Monitoring

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Management of abnormal FHR

pattern
1. Turn patient onto side to alleviate vena
cava compression.
2. Discontinue intravenous oxytocin.
3. Apply 100% oxygen to mother by face
mask.
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4. Correct maternal hypertension.

5. Vaginal examination to rule out prolapsed cord.
6. Consider fetal scalp blood sampling for pH
determination.

56

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

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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.

58

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.

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