UPDATE OF FETAL

GROWTH
RESTRICTION
I Nyoman Suetri Tapayana
 INTRODUCTION
Fetal growth restriction (FGR) is defined as a failure to
achieve the endorsed growth potential

Estimated fetal weight (EFW) below 10th centile

Associated with poorer perinatal outcome

Opportunities for preventing cases of intrauterine fetal

death, perinatal brain injury, and severe intrapartum
fetal distress
Normal Intrauterine Growth
 FETAL
CIRCULATION
FETAL GROWTH RESTRICTION vs
SMALL FOR GESTATIONAL AGE
FGR  Small fetuses with higher risk for fetal in utero
deteriotation, stillbirth, and overall poorer perinatal
outcome  Fetal adaptation to an abnormal
environment and with perinatal outcomes

SGA  Subgroup of small fetuses that do not present

the changes of FGR
Umbilical artery (UA) as a standalone standard is not
valid anymore
Usually Doppler UA can differentiated FGR vs SGA
UA identifies severe placental disease, but it fails to pick
up instances of mild placental disease
We should improving the definition of Fetal Growth
Restriction
IDENTIFING THE SMALL FETUS WITH
POOR OUTCOME
Doppler cerebroplacental ratio (CPR)
• Dividing the MCA PI /UA PI
• Reflect increases in placental resistance with mild
reductions in fetal brain vascular resistance

Uterine artery Doppler PI

Very small EFW (<p3)
PATOPHYSIOLOGICAL AND CLINICAL
DIFFERENCE IN EARLY- vs LATE-
ONSET FGR
Differentiating between early- and late-Onset FGR
Early Onset FGR
• Under 32 weeks
• 20-30% of all FGRs
• 50% association with early PE
• Highly associated with severe placental insufficiency and
chronic fetal hypoxia
• Abnormal of UA Doppler
• Early severe placental insufficiency  Fetal hypoxia and
acidosis  UA Doppler abnormal  Increased Ductus
Venosus (DV) PI
• Early Onset FGR  Severe injury and/or fetal death before
term
Late-Onset FGR
• GA > 32 weeks
• 70-80% of FGR
• Association with PE is low (10%)
• Degree of placental disease is mild
• Abnormal CPR
• Advance brain vasodilation  Chronic hypoxia 
MCA PI <p5 (25% of late FGR)
• Late-Onset FGR  Acute fetal deterioration before
labor (intrapartum fetal distress, neonatal acidosis) 
very low tolerance of term fetuses to hypoxia
Early- and Late-Onset FGR
• Both associated with poor long-term outcome from
neurodevelopmental, cardiovascular and metabolic
condition
• Both caused by placental disease, but it is unknown
whether they are associated with the same type of
disease
 DOPPLER VELOCIMETRY
• Analysis of doppler wave forms is done as follows

MEASURING (1) Peaksystolic (s)

(2) end diastolic velocity(D)

Three indices are calculated for knowing vascular resistance.

SD ratio(systolic/ diastolic ratio).
Resistance Index(RI)= systolic velocity – diastolic velocity
_______________________________
Diastolic Velocity

Pulsatile Index ( P I )= Systolic Velocity – Diastolic Velocity

_________________________________
. Mean Velocity
Uterine circulation
• as the feto- placental compartment develops
• Doppler study at this time shows appearance of a
diastolic component in uterine artery flow velocity wave
form, during early 2nd trimester i.e. 14 weeks’
gestation and progressively increases Up to 24 weeks. in
normal pregnancy it continued to show increased
diastolic flow velocity and loss of diastolic notches by
22weeks .
• Pregnancies associated with high persistent resistance
wave forms and early diastolic notches, are at risk of
preterm delivery due to IUGR, Hypertension on
pregnancy, abruptio placenta and overall higher
morbidity and mortality.
Uterine artery
UTERINE ARTERY DOPPLER WAVE
FORMS
• Umbilical Artery 
– It is direct reflection of placental flow.
– Is assessed at three sites
• the placental origin ,
• fetal abdominal insertion site and
• in the middle of free floating vessel.
– Resistance at abdominal insertion site is higher and
progressively decreases towards placental site.
– In normal fetus ,pulsatile index (PI) decreases with
advancing gestational period. This indicates
progressive decrease in vascular resistance in
placental bed.
 Normal Umbilical Artery Doppler indices
PI {2nd trimester = 2 to 1.5}

PI{ 3rd trimester=1.5 to1}

S/D RATIO = Decrease as

pregnancy advance

Before 28 week <5

28 to 34 week <4

From 34 week to term <3to3.5

UMBILICAL ARTERY Normal doppler wave form
 UMBILICAL ARTERY DOPPLER : (a) NORMAL (b)
LOSS END-DIASTOLIC FLOW (c) REVERSED END-
DIASTOLIC FLOW
• Fetal Cerebral Circulation 
– Middle cerebral artery is the vessel of choice to assess
the cerebral circulation, as it is easy to identify and has
high reproducibility.
– During normal pregnancy the MCA shows high
resistance and low diastolic flow pattern with
continuous fore ward flow through out the cardiac
cycle.
– If there is continued and progressive hypoxia, a
phenomenon known as “ BRAIN SPARING EFFECT
”is noted.
• There is dilatation of cerebral vessels to increase blood flow to
brain at the expenses of other organs of abdomen.
• Doppler study depicts it as increase in diastolic flow with
decreased PI
Normal MCA waveforms

Circle of willis

Normal impedance to flow in first trimester

Normal impedance to flow in second trimester

 Middle cerebral artery

The blood velocity increases with advancing gestation, and

this increase is significantly associated with the decrease in PI
MCA Doppler : High systolic wave in anemic fetus
 NORMAL VALUES
VESSELS PI RI

Umbilical artery Early 2nd trimester (1.5-2) <0.7

Term = 1 (1-1.5)

Middle cerebral artery At 28-32 wks (>1.45) 0.7-0.9

Term =1

Uterine artery 18-22 wks(<1.2) 0.33-0.55

If PI >1.45 with b/l
notching then it indicates
severe ischaemia.
CLINICAL ASSESSMENT
FOR FGR
Umbilical Artery Doppler (UA)
• Provides diagnostic and prognostic information
• Progression of UA Doppler patterns to absent or
reversed end-diastolic flow correlates with risks of injury
or death
• Absent or reversed end-diastolic velocities  + 1 week
before acute deterioration  Sensitivity and Specificity
about 60%
Middle Cerebral Artery (MCA) Doppler
• Abnormal MCA PI informs about the existence of brain
vasodilation  Fetal hypoxia
• Late manifestation with acceptable specificity but low
sensitivity  But can be improved by the use of CPR
• Fetus with abnormal MCA PI had sixfold risk of
emergency CS
 Cerebroplacental Ratio (CPR)
• Abnormal CPR present before delivery in 20-25% of cases and
associated with a higher risk of adverse outcome at induction

Ductus Venosus (DV) Doppler

• DV is the strongest single Doppler parameter to predict the
short-term risk of fetal death in early-onset FGR
• Absent or reversed velocities during atrial contraction are
associated with perinatal mortality  40-100% in early-onset
FGR
• 50% abnormal DV precedes loss of short-term variability in
CTG and about 90% cases abnormal DV at 48-72 h before
BPP (Biophysical Profile)
Fetal deterioration and monitoring in early-severe FGR
Fetal deterioration and monitoring in late-mild FGR
FHR analysis by CTG
• CTG has 50% false positive
• Silent FHR pattern or spontaneous decelerations
represent a very late event preceding fetal demise
• Provide a value similar to DV reverse atrial flow for the
short-term prediction of fetal death

Biophysical Profile (BPP)

• BPP is calculated by combining USG assessment of fetal
tone, respiratory and body movement, with amniotic
fluid index and a conventional CTG
• High false positive rate (50%)
Reduced variability
 Late Deceleration
no variability

Late deceleration with loss of variability. This is an ominous pattern, and

immediate delivery is indicated.
Amniotic Fluid Index (AFI)
• Chronic parameter
• Reduced AFI is associated with an abnormal 5-min
APGAR score but no association with acidosis or
perinatal death
• One week before acute deterioration  20-30% of cases
have oligohydramnion
CLINICAL ASSESSMENT
FOR FGR
Firstly to distinguish FGR from SGA
• Once the EFW < 10th centile identified  measure UtA
PI, UA PI, MCA PI, and CPR to classify FGR vs SGA
• FGR  Analysis change in UA, DV, AoI (Aortic Itsmus)
Doppler and CTG to define stage of deterioration

Secondly to ascertain whether there is risk of in utero

fetal injury or death
 STAGING FOR FGR
Stage I
• Severe smallness or mild placental insufficiency
• Either UtA, UA, MCA Doppler or CPR are abnormal
• Suggests a low risk of fetal deterioration before term
• Labor induction beyond 37 weeks is acceptable, but risk of
intrapartum fetal distress is increased

Stage II
• Severe placental insufficiency
• UA absent-end diastolic velocity or reverse AoI
• Delivery should be recommended after 34 weeks
• Risk of emergent CS at labor induction exceeds 50%
Stage III
• Advanced fetal deterioration, low-suspicion signs of fetal acidosis
• Reverse absent-end diastolic velocity or DV PI >95 centile
• Higher risk of stillbirth and poorer neurological outcome
• Reasonable to delay elective delivery to reduce as possible the effects of
severe prematurity
• Delivery should recommended after 30 weeks
• Monitoring every 24-48 h

Stage IV
• High suspicion of fetal acidosis and high risk of fetal death
• Spontaneous FHR decelerations, reduced variability (<3ms) or
reversed atrial flow in DV doppler
• High risk of stillbirth within next 3-7 days
• Delivery after 26 weeks by CS at tertiary care center under steroid
treatment for long maturity
• Survival rate exceeds 50% only after 26-28 weeks
• Monitoring every 12-24 h
THANK YOU
Figueras F, Gratacos E. 2013. Update on the diagnosis
and classification of fetal growth restriction and
proposal of a stage-based management protocol. Fetal
Diagnosis Therapy.