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Defining disorders of growth requires relating a
given achieved growth to an expected growth.
Actual fetal growth judged by Fetal weight is
determined by the
- genetic growth potential

- the health of the fetus with good fetal circulation,

- maternal ability to supply adequate quality and

quantities of substrates

- placental ability to transport substrates

 GROWTH – The process whereby the body
mass of the living being increases in size as a
result of increase in number and or size of its

 DEVELOPMENT – the process by which the

organs acquire their particular anatomic and
their specific functions in the living being , and
consequently ,

 the progressive anatomical and functional

3 PHASE of all of=them
GROWTH as well its
physiological regulation.
• LOW BIRTH WEIGHT – fetal weight <
2500gms irrespective of gestational age.
• SGA (small of gestational age ) - It is a
statistical definition , which includes all
newborn infants found below the lower range
limits of normal weight by gestational age.
• IUGR – Any process that is capable of limiting
intrinsic fetal growth potential “ in utero”
But , IUGR & SGA are frequently used
 IUGR can complicate 10% to 15% of all
pregnancies .

 Only 20–30% of these fetuses are

small due to pathological reasons rest are
normal(constitutionally small) SGA ??

 Second most common cause of perinatal

mortality, after prematurity. ~50% preterm
SB & 1/4 term SB are growth restricted.
 30% to 60% of the IUGR perinatal deaths
have undetected minor /major congenital
anomalies (50% of stillbirths and 20% of
neonatal deaths).
 The incidence of intrapartum fetal distress
with IUGR approximates 25% to 50%.
Increased risk of perinatal complication
such as Fetal demise, birth asphyxia,
meconium aspiration, and neonatal
hypoglycemia and hypothermia.
 Cardiovascular, metabolic, or endocrine
disorders in later life . The Barker
Endocrine regulation of fetal growth –
IGF -1 IGF -2

Placental regulation of fetal growth –

Implantation and early placentation play
crucial role

Genomic imprinting and fetal growth

Alterations in the uteroplacental and fetal–
placental circulations
• Abnormal trophoblast invasion:
Harper et al AJOG 2010

• pre-eclampsia
• placenta accreta.
• Infarction ,villitis , hemorragic endovasculitis,
• Abruption

• Placental location: ??placenta previa , ( lateral)

• Tumours: chorioangiomas ,placental


• Abnormal umbilical cord or cord insertion: two-

1. Associated with placental vascular
- Preeclampsia - Chronic hypertension
- Chronic renal dis - Connective tissue
-Diabetes with vascular lesions - Sickle cell
-Cardiac disease class III/IV -Multiple
-Autoimmune diseases, including: APS
-Genetic disorders, including: phenylketonuria.

2. Not associated with placental insufficiency

-Severe malnutrition
•Lack of substrate and inability to reach genetic
A) Genetic abnormalities, including:
• trisomy 13, 18, or 21
• turner’s syndrome
• triploidy.
B) Congenital abnormalities, including:
• cardiac, e.g. TOF, transposition of the great vessels
• gastroschisis.
C) Congenital infection, including:
• rubella
• toxoplasmosis.
• Multiple pregnancy
-Placental insufficiency 75–80%

-Maternal conditions not associated with

placental insufficiency 5%

-Fetal chromosome abnormalities 5%

-Multifactorial fetal abnormalities 2–3%

-Fetal infections 1%
-Type I or symmetric FGR corresponds to fetuses
that are symmetrically small and have normal H/A
and F/A ratios.

- Type II or asymmetric FGR corresponds to fetuses

that have an AC that is smaller than the HC and the
FL resulting in abnormally high H/A and F/A ratios.

-Type III or intermediate FGR corresponds to fetuses

that are initially symmetric but become asymmetric
later in the pregnancy.
“Intrinsic”- FGR occurs when the fetuses are
small due to fetal conditions such as viral
infections or chromosomal abnormalities.

“Extrinsic” -FGR occurs when the growth failure

is due to an element outside of the fetus such as a
placental condition or a maternal disease.

“Combined”- FGR occurs when there are extrinsic

and intrinsic factors causing the growth failure

“Idiopathic” -FGR when the cause of the fetal


1) Small for gestational age (SGA) refers to those

small fetuses with no discernible pathology and
with normal umbilical artery and middle cerebral
artery Doppler results;

2) Growth-restriction refers to small fetuses with

recognizable pathology and abnormal Doppler
studies; and

3) Idiopathic growth restriction applies to small

fetuses with no discernable pathology and have
abnormal Doppler studies.
20-30 % 70-80%
severe mild

Associated with Weaker

association with
and/or hypertensive
preeclampsia disorders(10%)
1) Maternal socio-economic condition and nutritional
2) Maternal smoking , alcohol intake , teratogen intake or
substance abuse in past and present
3) Previous history of growth restriction or still birth
- 50% increased risk of severe growth restriction
- Stillbirths before 32 weeks’ gestation have a
particularly strong association with IUGR.
4) Medical disorders
5) Diabetes -Preeclampsia is observed in 15-20% of
pregnancies complicated by type 1 diabetes mellitus
without nephropathy and approximately 50% in the
presence of nephropathy.
6) Low PAPP-A , two vessel cord and multiple pregnancy
7) IVF pregnancy
•Biochemical markers. Low PAPP A and ß HCG are
associated with an increased risk of placental-
related diseases such as IUGR or preeclampsia. (
PAPP A < 0.35 )

•Early growth restriction. Low first-trimester

measurement of crown-rump length in
pregnancies dated by the last menstrual period is
also linked with FGR.

•Slow growth between the first and second

trimester is able to identify a subgroup of slow-
growing babies that are at increased risk of
Biochemical markers - an unexplained elevation of
serum alpha-fetoprotein, hCG, or inhibin-A is also
Different strategies
associated with thesecombining maternal risk
adverse outcomes.
factors, mean blood pressure, and
Uterine arterymarkers
Dopplers have been
-. Uterine published
with in therates
detection second (22-24than
greater WKS)90%or first
trimester haspreeclampsia and associated
been proposed
IUGR ( very highas negative
a screening tool for early-onset
IUGR,with detection rates of about 75% and 25%,
respectively, for a false-positive rate of 5-10%.
These sensitivities are higher for predicting early
IUGR associated with preeclampsia and lower for
late IUGR.
•Serial fundal height assessment : ( 25- 60%DR)

•Routine/intermittent third-trimester ultrasound


•Serial ultrasound biometry. For pregnancies at

risk due to past or current situation , serial
assessment of estimated fetal weight or
abdominal circumference is the best predictor of.
Therefore, serial biometry is the recommended
gold standard

First, the standard is customized for sex as well as
maternal characteristics such as height, weight,
parity, and ethnic origin based on-one size does not
fit all theory.
Second, pathological factors such as smoking,
hypertension, diabetes, and preterm delivery are
excluded to predict the optimum weight that a baby
can reach at the end of a normal pregnancy.
Third, the term optimal weight and associated
normal range is projected backward for all
gestational age points, using an ultrasound growth
based proportionality curve
It is calculated by computer software
•1 . Identify small fetus !

•2. FGR vs. SGA !

•3. Early vs. Late !

•4 Appropriate survelliance tool and FU


•5. Stage-based management protocol &

optimising timing of delivery
inbuilt charts)
A total of 223 infants (112 SGA and 111 AGA) were
included. The groups differed significantly with respect to
socioeconomic status and gestational age at delivery. All
studied neurodevelopmental domains were poorer in the
SGA group, reaching significance for the cognitive
language. motor and adaptive scores. 
Compared with normal-sized babies, full-term SGA infants,
without placental have lower 2-year neurodevelopmental
scores. These data challenge the concept that SGA fetuses
with normal umbilical artery Doppler are ‘constitutionally

OXYGEN – No role
BETA MIMETICS - Larger, well-designed studies are needed
to evaluate the effects of betamimetics on fetal growth.
Since there is potential for adverse effects due to the
pharmacological characteristics of this group of drugs
BED REST IN HOSPITAL- There is not enough evidence to
evaluate the use of a bed rest in hospital policy for women
with suspected impaired fetal growth.
AMNIOINFUSION - Amnioinfusion with saline solution
should be one of the initial steps in the intrapartum
management of the PFGR fetus with decreased amniotic
fluid volume or early MSL.
SILDENAFIL ( NO promoter ) – Phosphodiesterase
inhibitors. The enzyme phosphodiesterase breaks down
cGMP, an enzyme critical to the effect of NO. But sildenafil
incidence of stillbirth, oligohydramnios, and
antepartum fetal distress.


hypoxia, acidosis, and high rate of cesarean


include hypoglycemia, hyperbilirubinemia,
meconium aspiration, persistent fetal circulation,
hypoxic-ischemic encephalopathy, hypocalcemia,
- Always determine the correct gestational age

- In the majority of cases the clinical findings and

ultrasound measurements allow only the diagnosis
of “small fetus.” The majority of small fetuses are
healthy. Only a modest proportion of small fetuses
are truly undernourished or PFGR.

- To distinguish between fetuses that are small and

healthy and PFGR it is necessary to use serial
growth charts and Doppler assessment of the
uterine, umbilical, and mid cerebral artery
resistance. Dopplers are not only diagnostic but
-Uterine artery, UA, and MCA Doppler do not
identify all PFGR fetuses. Doppler technology is
exclusively for the identification of PFGR because
of placental insufficiency. Small fetal size in the
presence of normal uterine, umbilical, and
midcerebral Doppler rules out placental
insufficiency .

- The most important surveillance tests to follow

the PFGR fetus are the FHR monitoring by CTG
and the umbilical and cerebral Doppler. As long
as the FHR monitoring is normal and the Doppler
does not show fetal decompensation (ADF or
RDF) expectant management is adequate.
- The placentas of all PFGR babies should be
examined by a competent placental pathologist.
In many cases the placenta will provide evidence
regarding the etiology of the problem.

-The earlier in gestation IUGR is detected, the

greater the possibility of developmental
problems later in life. The worst prognosis is for
IUGR secondary to congenital infections,
congenital abnormalities, and chromosomal
Staging system and management
· Stage 0 SGA fetuses have a good prognosis. They are managed as outpatient with Doppler assessment every
2 weeks. If the Doppler remains normal, delivery is recommended at term. If the Doppler becomes abnormal, these
fetuses are managed as Stage I IUGR fetuses.
· Stage I IUGR fetuses are considered to have mild growth restriction, and affected mothers who are without
preeclampsia are usually managed as outpatients. Antenatal corticosteroids should be given at time of diagnosis. In
these fetuses, twice-weekly antenatal testing is recommended. If the non-stress testing (NST) remains reactive and
the AFI remains >5.0 cm, delivery is recommended at 37 weeks’ gestation. If the umbilical artery Doppler becomes
absent, these fetuses should be managed as Stage II IUGR.
· Stage II IUGR fetuses should be managed as inpatients. During hospital admission, the fetuses should undergo
daily antenatal testing with twice-daily NST and daily biophysical profile (BPP). If the NST remains reassuring and
the BPP score remains between 6 and 8 of 8, continuation of expectant management is recommended. In addition,
antenatal corticosteroids should be given at time of diagnosis. Delivery is recommended at 34 weeks. If any of the
aforementioned NSTs become non-reassuring or if the BPP score is 4 of 8 on 2 occasions at least 4 hours apart,
immediate delivery is recommended. Delivery should occur via cesarean delivery because fetuses with an
absent/reversed flow of the umbilical artery will not tolerate labor induction.
· Stage III IUGR fetuses are managed the same as Stage II except for delivery at 32 weeks’ gestation, regardless
of gestational age at time of diagnosis. As with Stage I and II, antenatal corticosteroids should be given at time of
The advantage of the above scoring system is its simplicity. Only fetal biometry, sonographic interrogation of three
fetal vessels, and the amniotic fluid index are needed. It also allows classification of all small fetuses. Of note is that
if the umbilical artery and middle cerebral artery Doppler is normal, it is determination of flow velocity waveforms of
the ductus venosus is unnecessary because it will be normal as well. The presence of IUGR in the setting of
preeclampsia should not deter standard management of preeclampsia.

It is important to note the rate of mortality in the staging system.29 No deaths occurred in Stage 0 or Stage I fetuses,
whereas the mortality for stage III fetuses is high (50% if there was reversal of flow in the ductus venosus; 85%
mortality was observed when reversal of flow in the ductus venosus was present in combination with one of the other
parameters that characterize stage III), whereas the mortality in stage II IUGR fetuses was intermediate between
stages I and III (Figure 4). Also, studies have shown that fetuses can survive for days or weeks with reversal of flow
in the ductus venosus.29 A recent preliminary study reported that fetuses with reversal of flow in the ductus venosus
will not necessarily be acidemic at birth.30 In addition, the majority of affected pregnancies have an AFI <5 cm before
Lin and Santolaya-Forgas (1998) have divided cell growth
into three consecutive phases. The initial phase of hyperplasia occurs in the first
16 weeks and is characterized by a rapid
increase in cell number. The second phase, which extends up
to 32 weeks, includes both cellular hyperplasia and hypertrophy. After 32 weeks,
fetal growth is by cellular hypertrophy, and it is during this phase that most fetal
fat and glycogen deposition takes place. The corresponding fetal-growth
rates during these three phases are 5 g/day at 15 weeks, 15 to
20 g/day at 24 weeks, and 30 to 35 g/day at 34 weeks
(Williams and co-workers, 1982). As shown in Figure 38-1,
there is considerable biological variation in the velocity of
fetal growth.
Although many factors have been implicated, the precise cellular and molecular
mechanisms by which normal fetal growth
occurs are not well understood. In early fetal life, the major determinant is the
fetal genome, but later in pregnancy, environmental, nutritional, and hormonal
influences become increasingly important (Holmes and colleagues, 1998). For
there is considerable evidence that insulin and insulin-like
growth factor-I (IGF-I) and II (IGF-II) have a role in the regulation of fetal growth
and weight gain (Chiesa and associates,
2008; Forbes and Westwood, 2008). These growth factors are
produced by virtually all fetal organs beginning early in development. They are
Applications of Doppler Ultrasound in Fetal
Growth Assessment Summary • Uterine
artery Doppler – screening examination •
Umbilical artery Doppler – assessment of
SGA fetuses • MCA Doppler – to detect
brain sparing on fetuses with abnormal UA
Dopplers • Ductus venosus Dopplers – to
detect impaired cardiac function on SGA
fetuses and to time delivery