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

Hypoxic events FMC associated with a 73% reduction in

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

 Congenital anomalies In suboptimally oxygenated fetus:
(eg.neuromuscular disorders, -the resultant intermittent worsening in
fetal akinesia syndrome) oxygenation will lead to the FHR pattern of late
 Duration of fetal movements decelerations
Sustained decelerations uteroplacental
o Uterine insufficiency
 Placental location
 Amniotic fluid volume
How to Perform FMC How to Perform CST
-patient lies on her left side and count distinct -lying in a lateral recumbent position, the
fetal movements patient has an external fetal monitor recording
-counting 10 movements in a period of up to both the FHR and uterine contractions
2hours is felt to be reassuring: 10count:2hrs simulatenously for 20-30min interval
-if the count is nonreassuring or decreased,
further assessment is recommended no uterine stimulation is required if:
-patient is spontaneously contracting
Dangers of Decrease Fetal Movement - ≥ 3 contractions/10mins
-35% risk of stillbirths -duration of each contraction is ≥45sec
-poor neonatal condition at birth: (1:45sec)
1. abnormal labor FHR patterns Methods
2. Caesarean for fetal distress - nipple stimulation
3. 5-min APGAR scores ≤ 6 -exogenous oxytocin

II. Contraction Stress Test (CST) Contraindications of CST

Rationale: based on the response of the FHR to -prior myomectomy
uterine contractions on the premise that fetal -classical Cesarean section scar
oxygenation will be transiently worsened by -placenta previa or abruption placenta
contractions -premature rupture of membranes
- Each time the uterus contracts, (PROM)lead to premature labor
there is a concomitant change in -current preterm labor
fetal heart rate (FHR) -multiple gestations
- Contraction is a transient hypoxic -incompetent cervix
event for the fetus Negative CST (good result)
- Adequate fetal oxygenation in the
Transient decrease in FHR presence of contractions
- Incidence of antepartum fetal death
“Bawi”, increase in FHR (within 1 week of negative CST) =
0.2-0.7 %
If there is no “bawi” after an Positive CST
intrauterine contraction, there will - Uteroplacental insufficiency
be fetal distress/fetal complication - Adverse perinatal outcome
(uteroplacental insufficiency) - Increased incidence of intrauterine
Objective: to detect uteroplacental insufficiency Management: terminate pregnancy or
before fetal compromise do other tests

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
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

-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

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
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

Persistently minimal or absent FHR variability – -maternal seizure
most significant intrapartum sign of fetal
compromise VIII. Alfa-Fetoprotein (AFP) Testing
Good FHR variability – may not always be AFP – protein synthesized first by the yolk sac
predicitive of good outcome and then primarily by the fetal liver
Causes of Decreased Variability -increases until about 20weeks and then
-fetal metabolic acidosis declines to term
-CNS depressants Normal AFP levels in maternal serum –
-fetal sleep cycles continues to rise until around 32 weeks
-congenital anomalies Increase in maternal serum AFP – neutral tube
-prematurity defect eg. Spina bifida, meningocele,
-fetal tachycardia nasofrontal meningocele
-preexisting neurologic abnormality
-normal variant IX. Multiple Marker Screening
-betamethasone -mostly commonly consists of:
Accelerations -MSAFP (maternal serum AFP)
-abrupt increase in FHR above baseline with -hCG (human chorionic gonadotropin)
onset to peak of the acceleration <30seconds -unconjugated estriol
and < 2mins duration Trisomy 21(Down’s Syndrome) – high hCG, low
Duration of acceleration – time from initial estriol and AFP
change in FHR from the baseline to the time of Trisomy 18 (Edward’s syndrome) – all three
return to the FHR to baseline values are low
<32 weeks ≥ 10BPM above baseline for ≥ 10 sec
>32 weeks ≥ 15BPM above baseline for ≥ 15 sec Indications for Fetal Monitoring
1. Diabetes
Prolonged acceleration – increase in FHR lasts -poorly controlled maternal diabetes is
for 2-10mins associated with increased perinatal
Absence of accelerations for more than 80 mins mortality (congenital anomalies),
–correlates with increased neonatal moribidity preterm deliveries, sudden unexplained
Reactivity fetal death
-NST is considered reactive when 2 or more FHR -no evidence supporting routine
accelerations peak at least 15 BPM above the antepartum fetal assessment in diet-
baseline controlled gestational diabetes
-last 15 seconds from baseline to baseline within
a 20min period with or without fetal movement 2. Hypertensive disorders
-discernible by the mother -maternal HPN in pregnancy, whether
Prolonged Decelerations chronic, pregnancy induced, or a
-decrease in FHR of ≥ 15 BPM measured from combination, is a risk factor for perinatal
the most recently determined baseline rate death
-last ≥ 2mins but less than 10 mins -mild to moderate chronic HPN in the
Causes of Prolonged Decelerations absence of growth restriction or
-maternal hypotension superimposed preeclampsia is NOT an
-uterine hyperactivity indication for routine fetal surveillance
-cord prolapsed
-cord compression
-rapid descent of fetal head
-artifact (maternal heart rate)

-National High Blood Pressure -polyhdramnios frequently coexist with
Education Program Working Group on other maternal or fetal problems such
High Blood Pressure in as congenital anomalies, diabetes,
Pregnancyrecommended: hypertension, postterm pregnancy, and
-daily fetal movement assessment fetal growth restriction
-weekly nonstress tests and/or -few data on which to base
biophysical profiles for patients recommendations for antenatal testing
with mild preeclampsia before in pregnancies with abnormalities in AFV
-if with IUGR, or decreased AFV, 6. Preterm premature rupture of
test twice weekly membranes (PPROM)
-Daily fetal cardiographic or -associated with oligohydramnios and
ultrasound surveillance – subclinical intrauterine infection
conservative management of -goal of antenatal testing: early
severe preterm preeclampsia recognition of chorioamnionitis
necessitating delivery
3. Fetal growth restriction -most experts recommend daily
-no data from randomized trials antenatal testing in patients with
indicating the optimal mode and PPROM, either with the NST or the BPP
frequency of antenatal testing of the -roughly 40% of third-trimester
fetus with growth restriction polyhydramnios cases diagnosed by
-risks of fetal loss must be balanced ultrasound have normal or near-normal
against the risks of iatrogenic AFV on subsequent assessments,
prematurity outcomes in these cases are generally
4. Multiple Pregnancy -persistent polyhydramnios - associated
-greater prevalence of maternal risk with poorer pregnancy outcomes,
factors (eg. Advance maternal age of >, including fetal anomalies, maternal
preterm labor, preeclampsia) and fetal diabetes and perinatal death
risk factors (eg. Abnormal growth,
abnormal placentation, congenital 7. Postterm Pregnancy
anomalies) contribute to higher -associated with increased fetal
perinatal mortality rates in multiple mortality and neonatal seizures,
gestations especially if growth restriction is present
-lowest risk for intrauterine death in -ACOG (American College of Obstetrics
multiple gestations at 37-38 weeks and Gynecology) guidelines support
initiating antenatal assessment after
Chorionicity: adverse outcomes among 40weeks
monochorionic twins
-limited data specific to twin pregnancy 8. History of Prior Stillbirth
suggest that weekly simultaneous NSTs, -two to ten tenfold increased risk of
BPPs, mBPPS, and UAD, alone or in fetal death in subsequent pregnancy,
combination may be of benefit in depending in part on the etiology of the
predicting outcomes in twin pregnancies previous loss
-previous stillbirth has long been
5. Amniotic fluid abnormalities considered an indication for antepartum
-have long been viewed as risk factors testing
for poor perinatal outcome

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
-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
-advanced maternal age
-grand multiparity (>5 pregnancies)
-conception with assisted reproductive
-hereditary and acquired
thrombophilieass.a. factor V Leiden
-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

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
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