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SGA refers to a fetus that has failed to achieve

a specific biometric or estimated weight
threshold by a specific gestational age.
> 10 th centile

Abdominal circumference

Estimated fetal weight

severe SGA as an EFW or AC less than the 3rd

IntraUterine Growth Restriction(IUGR) is not
synonymous with SGA. Some, but not all, IUGR
fetuses/infants are SGA while 5070% of SGA
fetuses are constitutionally small, with fetal
growth appropriate for maternal size and
The likelihood of IUGR is higher in severe SGA
Growth restriction implies a pathological
As a result, growth restricted fetuses may
manifest evidence of fetal compromise (abnormal
Doppler studies, reduced liquor volume).
Normal Fetal Growth
Normal fetal growth is
characterized by
cellular hyperplasia followed
hyperplasia and hypertrophy
and lastly by
hypertrophy alone.

Weight gain
Symphysiofundal height
Abdominal girth

1. symmetrical or intrinsic IUGR

2. assymetric IUGR
3. Intermediate IUGR
symmetrical IUGR- (20-30%)
Occurs as a result of growth inhibition
early in pregnancy i.e. the
hyperplastic stage. Any pathological
insult at this phase leads to reduced no.
of cells in fetus and overall decreased
growth potential.
Causes include-
Intrauterine infections (TORCH )
Chromosomal disorders
Congenital malformations
All parameters(head and abdo
circumference, length and weight)
are below 10th percentile for
gestational age, hence normal
ponderal index (birth weight/ht3).
asymmetric IUGR (70-80%)

Occurs as a result of restriction of

nutrient supply in utero i.e.
uteroplacental insufficiency.
It is usually associated with
maternal diseases like:-
Chronic hypertension
Renal disease
The onset of growth restriction occurs
usually after 28 wks of gestation i.e. in the
stage of hypertrophy. The fetus has near
normal total no. of cells but cell size is
There is brain sparing effect so that the
head growth remains normal but the
abdominal girth slows down.
The Ponderal index is low.
This asymmetry results from redistribution
of fetal cardiac output with increased flow
to brain and heart at the expense of
reduced splanchnic circulation.
Liver size is reduced because
of diminished glycogen stores.
In case of severe placental
insufficiency the head growth
may also be affected.
This type of growth restriction
leads to decreased amniotic
fluid, chronic hypoxia and may
result in fetal death.
Intermediate IUGR

It is a combination of type 1 and

type 2.
Fetal growth restriction occurs
during intermediate phase of
growth affecting both hyperplasia
and hypertrophy, resulting in
decrease in cell no. as well as size.
Causes include
Chronic HT
Lupus nephritis
Complications of IUGR
Antepartum period- increased
incidence of-
-still births
IUGR is found in 52% of unexplained
During labour- higher incidence of-
-meconium aspiration
-fetal distress
-intrapartum fetal death
Neonatal period- increased incidence
-Hypoxic ischemic encephalopathy
-Persistent fetal circulation
They have difficulty in temperature
regulation because of absent brown fat
and small body mass relative to surface
Lack of glycogen stores may predispose to
Complications cont..
Childhood- increases mortality from-
-infectious diseases
-congenital anomalies
Incidence of cerebral palsy are 4-6 times
Subtle impairment of cognitive
performance and educational
Long term complications- increased risk
of coronary heart disease,
Diagnosis of IUGR
1. Clinically- Serial measurement of
fundal height and abdominal girth.
Symphysio-fundal height normally
increases by 1cm per wk b/w 14 and 32
A lag in fundal ht. of 4wks is
suggestive of moderate IUGR.
A lag of >6 wks is suggestive of
severe IUGR.
2. Sonographic evaluation-
Fetal biometry:
i. BPD(Biparietal Diameter)- determines
gestational age and type of IUGR.
ii. Head circumference- better than BPD in
predicting IUGR.
iii. Transeverse cerebellar diameter(TCD)- can
be used as a method to assess gestational
iv. Abdominal circumference(AC)- AC and fetal
wt are most accurate ultrasound parameters
for diagnosis of IUGR.
An increase in fetal AC of less than 10 mm in 14
days has sensitivity of 85% and specificity of
74% for identification of IUGR.
iv. Measurement ratios- there are some age
independent ratios to detect IUGR.
HC/AC: decreases linearly from 16 to 20 wks of
HC/AC >2 SD above mean is predictive of IUGR.
FL/AC: normal value ranges from 22 + 2% in the
second half of pregnancy. Ratio above 23.5% is
considered abnormal.
Placental Morphology: Acceleration of
placental maturation may occur with
Amniotic fluid volume: assymetrical
IUGR is usually associated with
3. Doppler Ultrasonography: doppler flow
studies are important adjuncts to fetal
biometry in identifying the IUGR fetuses at
risk of adverse outcome.
Most widely used arterial indices are :
Pulsatility index (PI): Systolic end diastolic
peak velocity / time averaged
maximum velocity , 1.2-0.9
Resistance Index(RI): Systolic end diastolic
peak velocity/ systolic peak velocity , 0.7-
Systolic to diastolic ratio(S/D): Systolic peak
Umblical Artery doppler- In IUGR there
is increased umblical artery resistance
(increased S/D ratio), absent end
diastolic flow and finally reversed end
diastolic flow.
Perinatal mortality rate increases
significantly in fetuses with absent end
diastolic flow (9-41%) and reversed end
diastolic flow (33-73%) in umblical
Middle cerebral artery doppler- in a
normal fetus has relatively little flow
during diastole. Increased resistance to
blood flow in placenta results in
redistribution of cardiac output to
favour cardiac and cerebral circulations
leading to increased flow in the
diastolic phase with decreased S/D
Cerebral/Placental ratio: ratio between
MCA PI and umblical artery PI is more
sensiive predictor than either MCA and
umblical artery velocimetry alone to
detect redistribution of blood flow.
Cut off values below 1.0 to 1.1 are
considered to be diagnostic of brain
spairing effect.
MCA peak systolic velocimetry: is good
indicator of fetal anaemia and is less
Ductus venosus doppler: Perinatal
mortality in growth restricted fetuses has
been found to be significantly worse
when abnormalities in fetal venous
circulation are detected.
In the normal fetus, flow in the ductus
venosus is forwards , moving towards the
heart during entire cardiac cycle.
When circulatory compensation of the fetus
fails, the ductus venosus waveform shows
absent or reverse blood flow during atrial
conraction. Perinatal mortality being 63-
Therefore it is recommended that fetus