Antepartum Fetal Monitoring

Dr. Cristina Woo

Group I – N1nja StONEs
June 17, 2013

Ultimate goal: improve perinatal outcome, Loss of fetal movement – ongoing CNS hypoxia
specifically by decreasing stillbirth and long term and injury
neurologic impairments such as injury to the
fetal central nervous system Fetal Monitoring

Causes of 3.1M neonatal deaths in 193 I. Fetal Movement Counting(FMC)

countries in 2010 (WHO, 2012)
 Intrapartum related – 720,000
 Neonatal infections – 830,000
 Congenital anomalies – 270,000
 Preterm birth complications – 1.08M
 Other neonatal conditions – 181,000
Antenal testing
 Can prevent stillbirth
 Prevent delivery of babies who are alive
but with CNS abnormalities
 Prevent delivery of babies with cerebral
palsy
 Detect early on fetal hypoxia, fetal
abnormalities  early prevention
 Results to:
- Poor fetal outcome
- Baby born alive but with
CNS abnormalities
-Maternal assessment of fetal movements;
potentially simple method of monitoring fetal
oxygenation and well being
- done by mother
- start at 2nd trimester  early part of 3rd
term  38 weeks labor
- decreased fetal movement fetal
compromise (most common cause: fetal
hypoxia)
 Normal Fetus
- first perceptible at 17-20weeks
-peak frequency at 28-32 weeks up to 38
weeks
 Decrease fetal movement
- Hypoxemia
- Maternal assessment of fetal
movements – a potentially simple
method of monitoring fetal
oxygenation and well being

Hypoxic events FMC associated with a 73% reduction in

fetus attempts to Chemoreceptor
conserve energy response
decreasefetal Vagally-mediated
movement reflex slowing down
of the heart
Appear clinically as
late decelerations
associated with
uterine contractions
avoidable stillbirths [RR(risk) -0.27, 95%
CI(confidence interval), 0.08-0.93]
Factors affecting maternally perceived fetal
movements:
o Maternal
 Activity
 Obesity
 Drugs that depress
(eg.methadone) or increase
(eg.cocaine) fetal movements
o Fetal
 Behavioural states
 Gestational age

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  Congenital anomalies
(eg.neuromuscular disorders,
fetal akinesia syndrome)
 Duration of fetal movements
o Uterine
 Placental location
 Amniotic fluid volume
How to Perform FMC
-patient lies on her left side and count distinct
fetal movements
-counting 10 movements in a period of up to
2hours is felt to be reassuring: 10count:2hrs
-if the count is nonreassuring or decreased,
further assessment is recommended
Dangers of Decrease Fetal Movement
-35% risk of stillbirths
-poor neonatal condition at birth:
1. abnormal labor FHR patterns
2. Caesarean for fetal distress
3. 5-min APGAR scores ≤ 6
II. Contraction Stress Test (CST)
Rationale: based on the response of the FHR to
uterine contractions on the premise that fetal
oxygenation will be transiently worsened by
contractions
- Each time the uterus contracts,
there is a concomitant change in
fetal heart rate (FHR)
- Contraction is a transient hypoxic
event for the fetus
Transient decrease in FHR
“Bawi”, increase in FHR
If there is no “bawi” after an
intrauterine contraction, there will
be fetal distress/fetal complication
(uteroplacental insufficiency)
Objective: to detect uteroplacental insufficiency
before fetal compromise
In suboptimally oxygenated fetus:
-the resultant intermittent worsening in
oxygenation will lead to the FHR pattern of late
decelerations
Sustained decelerations uteroplacental
insufficiency
How to Perform CST
-lying in a lateral recumbent position, the
patient has an external fetal monitor recording
both the FHR and uterine contractions
simulatenously for 20-30min interval
no uterine stimulation is required if:
-patient is spontaneously contracting
- ≥ 3 contractions/10mins
-duration of each contraction is ≥45sec
(1:45sec)
Methods
- nipple stimulation
-exogenous oxytocin
Contraindications of CST
-prior myomectomy
-classical Cesarean section scar
-placenta previa or abruption placenta
-premature rupture of membranes
(PROM)lead to premature labor
-current preterm labor
-multiple gestations
-incompetent cervix
Negative CST (good result)
- Adequate fetal oxygenation in the
presence of contractions
- Incidence of antepartum fetal death
(within 1 week of negative CST) =
0.2-0.7 %
Positive CST
- Uteroplacental insufficiency
- Adverse perinatal outcome
- Increased incidence of intrauterine
demise
Management: terminate pregnancy or
do other tests
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 III. Nonstress Test (NST) Lowest score for every parameter =0
Rationale: based on the premise that the heart *the perinatal mortality is 0.8/1000 for
rate of the fetus that is not academic or
neurologically depressed will temporarily Perinatal Mortality and BPP Score
accelerate with fetal movement Score interpretation Perinatal
Objective: identify both normal fetuses and mortality/1000
those with asphyxia/hypoxia 8-10 Normal 1.86*
 Asphyxia (suffocation) –most common 6 Equivocal 9.76
cause of hypoxia 4 Abnormal 26.3
FHR Reactivity 2 Abnormal 94.0
-good indicator of normal fetal autonomic 0 Abnormal 285.7
function and well-being, depends on normal structurally normal foetuses with a normal
neurological development and normal test within 7 days
integration of CNS control of FHR *Normal = 8/10 – 10/10 or 8/8 excluding NST
How to Perform NST
-ascultation of FHR using an electronic monitor V. Amniotic Fluid Volume (AFV) Assessment
Reactive NST (good result) Amniotic fluid
-good outcomes -essential to pregnancy, providing a
Non-reactive NST compartment for normal development,
-requires biophysical profile to be done growth and movement of the fetus
- for fetus to swim around
IV.Biophysical Profile (BPP) - no factors will impede growth and
Rationale: the fetus will respond to central development
hypoxemia/acidemia by altering its movement, AFV -chronic marker for fetal well-being
tone, breathing and heart rate pattern Normal AFV – protects the fetus from cord
 Combines the ultrasonographic estimation compression during fetal activity or uterine
- Amniotic fluid volume (AFV) contractions
- Fetal breathing, body and Average AFV by gestational age
reflex/tone/flexion-extension Weeks AOG Ave AFV (mL)
movements with NST 22 630
Objectives: 28 770
1. Assess indicators of acute hypoxia 29 - 37 800
-NST, breathing, body movement >39 AFV decreases, 515ml at
2. Assess indicators of chronic hypoxia 41weeks
-amniotic fluid volume (AFV)
42 33% decline in AFV per
Week
Modified Biophysical Profile (mBPP)
-relies on NST as measure of acute oxygenation
Postterm infants have dry skin because of
and AFI (amniotic fluid index) as a measure of
decreased AF
longer term oxygenation
AFI –checked by ultrasound
How to Perform AFV Assessment
Parameters in Biophysical Profile
-linea nigra is used to divide the uterus into
1. Fetal breathing patterns
right and left halves
2. Gross body movements
-umbilicus serves as the dividing point for
3. Fetal tone
the upper and lower halves
4. Reactive fetal heart rate
5. Qualitative amniotic fluid volume
Highest score for every parameter = 2

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 -transducer is kept parallel to patient’s -significant because of its known association
longitudinal axis and perpendicular to the with adverse pregnancy outcome:
floor -umbilical cord occlusion
-fetal distress in labor
Interpretation of the AFI -meconium aspiration
10.1 - 24.0cm Normal Relaxed fetal anal sphincter
5.1 - 10.0cm Borderline passage of meconium  may
≤ 5.0 cm Abnormal be aspirated  airway
> 24 cm Abnormal obstruction
-operative deliveries
Abnormalities in AFV -stillbirth
1. Polyhydramnios If with oligohydramnios, think of renal
-pathologic accumulation of AF problems
- AFI >25cm
-occurs in 0.2-1.6% of general population Causes of Oligohydramnios
-associated with increase maternal and -intrauterine growth restriction (IUGR)
perinatal morbidity and mortality -urinary tract malformations
In polyhydramnios, fetus can’t swallow, -postdate pregnancies
AF is retained. Suspect for GI or CNS -ruptured membranes
problems -placental insufficiency

Causes of Polyhydramnios Risk of Oligohydrmanios after “Low-Normal

-fetal malformations such as AFI”
gastroschisis or duodenal atresia Gestational AFI Risk of
Gastroschis –open skin defect in age (weeks) Oligohydrmnios
abdomen with extrusion of after 4 days
abdominal contents >41 5-8 23.3%
Duodenal atresia – small 37-40 5-8 17.8%
opening in the duodenum >41 >8 7.4%
-anencephaly 37-40 >8 3.7%
-genetic disorders
-diabetes VI. Doppler Velocimetry
-Rh (Rhesus) sensitization
-congenital infections Rationale: measurement of blood flow velocities
-fetal swallowing impairment in the maternal and fetal vessels gives
information about uteroplacental blood flow
Potential Complications with Polyhydramnios and fetal responses to physiologic changes
-premature labor
-placental abruption (premature Vessel Clinical Information
detachment of a normally situated Examined
placenta) Uterine artery Maternal (flow resistance to
-Puerperal hemorrhage uterus)
-perinatal mortality Umbilical artery Placental (flow resistant to
-maternal respiratory difficulties placenta)
Arterial Fetal (fetal adaptation to
2. Oligohydramnios circulation flow resistance change)
-reduced AFV (MCA)
-occurs in 5.5-37.8% of pregnancies

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Venous Fetal (fetal cardiac function) -baseline rate
circulation -baseline FHR variability
(umbilical vein, -presence of accelerations
IVC, -periodic or episodic decelerations
ductusvenosus) -changes or trends of FHR patterns over time
Umbilical artery –most commonly used -frequency and intensity of uterine
contractions
A. Umbilical Artery
-failure of adequate trophoblast invasion and Bradycardia
remodeling of maternal spiral arteries is -mean FHR <110 bpm
characterized by persistent high-pressure -a rate of 100-119 bpm in the absence of other
uterine circulation and increased impedance to non-reassuring patterns is not usually a sign of
uterine artery blood flow compromise
-Elevated resistance indices and/or persistent Causes of Bradycardia:
UtA waveform notching at 22-24weeks -heart block (little or no variability)
-reduced blood flow in the maternal -occiput posterior or transverse position
compartment of the placenta: -serious fetal compromise
-future preeclampsia maternal SLE – common cause of heart block
-fetal growth restriction (FGR) Heart block –common cause of bradycardia
-perinatal death
- in IUGR, absent or reversed end diastolic flow Tachycardia
is associated with fetal hypoxia and increased -mean FHR >160bpm
perinatal mortality and morbidity -in the presence of good variability, tachycardia
-ACOG Guidelines – use of Doppler assessment is NOT a sign of distress
only in IUGR Causes of Tachycardia
-maternal fever
B.Middle Cerebral Artery -fetal hypoxia
-compromised fetus, systemic blood flow is -fetalanemia
redistributed from the periphery to the brain -amnionitis
-doppler flow velocity in the fetal MCA detects -normal variant
this “brain-sparing effect” -fetal tachyarrhythmia (usu. >200bpm with
IUGR but no decrease MCA blood flow no abrupt onset little to no variability)
 brain-sparing effect  good prognosis -SVT (200-240bpm)
C.Fetal veins (umbilical vein, inferior vena cava, -fetal heart failure
ductusvenosus) -drugs (beta sympathomimetics, vistaril,
-blood flow in the umbilical vein is continuous in phenothiazines)
normal pregnancies after 15 weeks gestation -rebound transient tachycardia following a
Fetal Growth Retardation deceleration accompanied by decreased
-pulsatile flow in the umbilical vein that reflects variability
cardiac dysfunction against increased afterload
DuctusVenosus FHR Variability
-regulates oxygenated blood in the fetus and is Absent variability Amplitude range
resistant to alterations in flow except in the undetectable
most severely growth restricted foetuses Minimal <bpm
Moderate 6-25bpm
VII. Fetal Heart Rate Monitoring Tracing Marked >25bpm
Full qualitative and quantitative description of
the following: Moderate FHR variability – reassuring

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Persistently minimal or absent FHR variability –
most significant intrapartum sign of fetal
compromise
Good FHR variability – may not always be
predicitive of good outcome
Causes of Decreased Variability
-fetal metabolic acidosis
-CNS depressants
-fetal sleep cycles
-congenital anomalies
-prematurity
-fetal tachycardia
-preexisting neurologic abnormality
-normal variant
-betamethasone
Accelerations
-abrupt increase in FHR above baseline with
onset to peak of the acceleration <30seconds
and < 2mins duration
Duration of acceleration – time from initial
change in FHR from the baseline to the time of
return to the FHR to baseline
<32 weeks ≥ 10BPM above baseline for ≥ 10 sec
>32 weeks ≥ 15BPM above baseline for ≥ 15 sec
Prolonged acceleration – increase in FHR lasts
for 2-10mins
Absence of accelerations for more than 80 mins
–correlates with increased neonatal moribidity
Reactivity
-NST is considered reactive when 2 or more FHR
accelerations peak at least 15 BPM above the
baseline
-last 15 seconds from baseline to baseline within
a 20min period with or without fetal movement
-discernible by the mother
Prolonged Decelerations
-decrease in FHR of ≥ 15 BPM measured from
the most recently determined baseline rate
-last ≥ 2mins but less than 10 mins
Causes of Prolonged Decelerations
-maternal hypotension
-uterine hyperactivity
-cord prolapsed
-cord compression
-rapid descent of fetal head
-abruption
-artifact (maternal heart rate)
-maternal seizure
VIII. Alfa-Fetoprotein (AFP) Testing
AFP – protein synthesized first by the yolk sac
and then primarily by the fetal liver
-increases until about 20weeks and then
declines to term
Normal AFP levels in maternal serum –
continues to rise until around 32 weeks
Increase in maternal serum AFP – neutral tube
defect eg. Spina bifida, meningocele,
nasofrontal meningocele
IX. Multiple Marker Screening
-mostly commonly consists of:
-MSAFP (maternal serum AFP)
-hCG (human chorionic gonadotropin)
-unconjugated estriol
Trisomy 21(Down’s Syndrome) – high hCG, low
estriol and AFP
Trisomy 18 (Edward’s syndrome) – all three
values are low
Indications for Fetal Monitoring
1. Diabetes
-poorly controlled maternal diabetes is
associated with increased perinatal
mortality (congenital anomalies),
preterm deliveries, sudden unexplained
fetal death
-no evidence supporting routine
antepartum fetal assessment in diet-
controlled gestational diabetes
2. Hypertensive disorders
-maternal HPN in pregnancy, whether
chronic, pregnancy induced, or a
combination, is a risk factor for perinatal
death
-mild to moderate chronic HPN in the
absence of growth restriction or
superimposed preeclampsia is NOT an
indication for routine fetal surveillance
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 -National High Blood Pressure
Education Program Working Group on
High Blood Pressure in
Pregnancyrecommended:
-daily fetal movement assessment
-weekly nonstress tests and/or
biophysical profiles for patients
with mild preeclampsia before
term
-if with IUGR, or decreased AFV,
test twice weekly
-Daily fetal cardiographic or
ultrasound surveillance – subclinical intrauterine infection
conservative management of
severe preterm preeclampsia
3. Fetal growth restriction
-no data from randomized trials
indicating the optimal mode and
frequency of antenatal testing of the
fetus with growth restriction
-risks of fetal loss must be balanced
against the risks of iatrogenic
prematurity
4. Multiple Pregnancy
-greater prevalence of maternal risk
factors (eg. Advance maternal age of >,
preterm labor, preeclampsia) and fetal
risk factors (eg. Abnormal growth,
abnormal placentation, congenital
anomalies) contribute to higher
perinatal mortality rates in multiple
gestations
-lowest risk for intrauterine death in
multiple gestations at 37-38 weeks
Chorionicity: adverse outcomes among
monochorionic twins
-limited data specific to twin pregnancy
suggest that weekly simultaneous NSTs,
BPPs, mBPPS, and UAD, alone or in
combination may be of benefit in
predicting outcomes in twin pregnancies
5. Amniotic fluid abnormalities
-have long been viewed as risk factors
for poor perinatal outcome
-polyhdramnios frequently coexist with
other maternal or fetal problems such
as congenital anomalies, diabetes,
hypertension, postterm pregnancy, and
fetal growth restriction
-few data on which to base
recommendations for antenatal testing
in pregnancies with abnormalities in AFV
6. Preterm premature rupture of
membranes (PPROM)
-associated with oligohydramnios and
-goal of antenatal testing: early
recognition of chorioamnionitis
necessitating delivery
-most experts recommend daily
antenatal testing in patients with
PPROM, either with the NST or the BPP
-roughly 40% of third-trimester
polyhydramnios cases diagnosed by
ultrasound have normal or near-normal
AFV on subsequent assessments,
outcomes in these cases are generally
good
-persistent polyhydramnios - associated
with poorer pregnancy outcomes,
including fetal anomalies, maternal
diabetes and perinatal death
7. Postterm Pregnancy
-associated with increased fetal
mortality and neonatal seizures,
especially if growth restriction is present
-ACOG (American College of Obstetrics
and Gynecology) guidelines support
initiating antenatal assessment after
40weeks
8. History of Prior Stillbirth
-two to ten tenfold increased risk of
fetal death in subsequent pregnancy,
depending in part on the etiology of the
previous loss
-previous stillbirth has long been
considered an indication for antepartum
testing
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 9. Decreased fetal movement -impaired or maturational delay of the fetal
-associated with adverse pregnancy ANS
outcomes s.a. congenital malformations,
FGR, preterm delivery, and perinatal
death
-requires evaluation
-ACOG/AAP guidelines for perinatal care
recommend an NST and AFI for
evaluation of DFM

Newer Indications for Antenatal Testing

ACOG practice bulletin on antepartum fetal
surveillance – suggest that antepartum testing
may be appropriate for any “pregnancies in
which the risk of anterpartumfetal demise is
increased”
-advanced maternal age
-nulliparity
-grand multiparity (>5 pregnancies)
-obesity
-conception with assisted reproductive
technologies
-hereditary and acquired
thrombophilieass.a. factor V Leiden
mutation
-abnormalities in 1st and 2nd trimester
-serum screening results
Emerging Methods of Fetal Assessment
1. Fetal Physiology Assessment
-as fetal CNS matures, there are distinctive
alterations in fetal physiological behavioural
parameters, such as heart rate patterns, motor
activity and sleep-wake cycles
-coupling between fetal movements (FM) and
FHR that normally occurs with advancing
gestational age  reflects maturation of the
parasympathetic and sympathetic components
of the fetal autonomic nervous system

2. FetalAutocardiography
-electronically records FHR and FM
-novel analytical techniques allow computation
of time-dependent cross-correlation coefficients
between FHR and FM
- Alterations in FM/FHR coupling:
-maternal stress, preterm birth, pregnancy
complications

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 Name Component Results/Scoring
Contraction -Continuous FHR Negative- no late or significant variable decelerations
Stress Test monitoring Postive –late decelerations following ≥ 50% of
(oxytocin -at least 3 contractionscontractions
challenge test) of ≥ 40s duration Equivocal –suspcious – intermittent late
FN: 0.04% within 10min decelerations or significant variable decelerations
FP: 36-65% Equivocal-hyperstimulatory – deceleratons with
contractions occurring more frequently than every
2min or lasting > 90sec
Unsatisfactory - < 3 contractions in 10 min or
uninterpretable FHR tracing
Nonstress Test -continuous FHR Reactive: ≥ 2 accelerations within 20 min (may be
FN: 0.2 – 06.65% monitoring extended to 40min)
FP: 55- 90% -FHR accelerations: Nonreactive: < 2 accelerations in 40 min
≥32 weeks: reaching
15 BPM above
baseline and lasting
≥15 sec
Biophysical -presence or absence Each component present is assigned score is 2 points
Profile of 3 components Maximum score: 10/10
FN: 0.07- 0.08% within 30 min Normal: ≥ 8/10 or 8/8 excluding NST
FP: 40-50% Reactive NST: Equivocal: 6/10
- ≥1 episode of fetal Abnormal: 4/10
breathing movements
≥ 30sec
- ≥ 3 discrete body or
limb movements
- ≥ 1 episode of
extremity extension
with return to flexion
or opening or closing
of a hand
-maximal vertical AF
pocket > 2 com or AFI
> 5cm
Modified -NST Normal: reactive; NST and AFI > 5cm
Biophysical -AFI Abnormal: non reactive; NST and/or AFI ≤ 5cm
Profile
FN: 0.08%

References: Shriver National Institute of Child Health

1.) Antenatal Testing – A Reevaluation: and Human Development Workshop
Executive Summary of a Eunice Kennedy 2.) Lecturer Slides
3.) Audio