Lecture 4 - IUGR, Dr. Dr. Diah Rumekti H SP - OG (K) (2021)

Intra Uterine Growth
Restriction
Diah Rumekti Hadiati

Consultant Maternal Fetal Medicine,
Departement ofObstetrics & Gynaecology
RSUP DR Sardjito/Faculty of Medicine UGM
Thin
Pale
Loose,
dry skin
Malnouris
hed
Wizened
•Intrauterine growth
retardation (iugr)
•Fetal growth
restriction (fgr)
Manning, 1995
SGA vs. FGR
SGA
SGA vs. FGR
SGAFGR
SGA vs. FGR
SGAFGR
Failed to
Constitutio
achieve full
nally small
growth
potential
SGA vs. FGR
SGAFGR
Failed to achieve
full INDIVIDUAL
growth potential
SGA vs. FGR
SGA:NO SGA
80-90:10-20
SGAFGR
FGR:NO FGR
50:50 Failed to achieve
full INDIVIDUAL
growth potential
The neonatal mortality
rate of a SGA infant born
at 38 weeks 1%
compared 0.2% in those
with AGA
* AGA -appropriate for gestational age
Incidence
3 -10% of infants are
growth restricted
25 -60 % of infants
conventionally diagnosed
to be SGA were in fact
AGA when
Determinant of birth weight
such as maternal
* Ethnic group
* Parity
* Weight
* Height
MORTALITY & MORBIDITY
• Fetal demise • Hypothermia

• Birth asphyxia • Abnormal
• Meconium neurological
aspiration development
• Neonatal
hypoglycemia
ACCELERATED
MATURATION
Accelerated maturation
The fetus resoponses to
stressed envirorment by
adrenal glucocorticoid
Earlier or accelerated maturation

SYMMETRICAL VERSUS
ASYMMETRICAL GR..
Fetal growth has been
divided into three phases.
• 1-cellular cell size
hyperplasia fat deposition
• 2- hyperplasy
& hypertrophy fetal weight as
• 3- hypertrophy much as 200
G.r. per week.
symmetrical
An early insult
due to : Cell size
chemical Cell num.
viral
aneuploidy
Proportionate reduction in head & body

Asymmetrical
A late pregnancy insult

such as placental
insufficiency would
affect cell size.
The ratio of brain weight
to liver weight over in the
last 12 wk of pregnancy is
increased to 5/1 or more
Growth pattern
may potentially
reveal the cause
In practice accurate
identification of symmetrical
versus asymmetrical fetus has
proved difficult.
Risk factors for FGR
*Maternal
*fetal
*placental and cord abn.
* FGR - fetal growth restriction
Maternal causes
*Constitutionally small mother
*Poor maternal weight gain &
nutrition
*Social deprivation
*vascular disease
*maternal anemia
*anti phospholipid Ab syn.
*Extra uterine pregnancy
*chronic renal disease
FETAL CAUSES
*fetal infections
*congenital malformations
*chromosomal abnormalities
*trisomy 16
*multiple fetus
Placental and cord
abnormalities
• chromic partial placental sep.
• extensive infarct.
• Chorioangioma
• placenta previa
ADDITIONAL
INSIGHT OF FGR
These fetus also had
•Hypoglycemia
•Hypoinsulinemia
•hypertriglycemia
•thrombocytopenia
Screening and identification
of F.G.R
• Early establishment of G.A
• Attention to maternal weight
gain
• Measurement of uterine height
throughout pregnancy
Identification of risk factors
A previously GR fetus in women with

significant risk factors
Serial sonography
Definitive diagnosis
usually can not be
made until delivery.
MANAGEMENT
Once a SGA is suspected , intensive
effort should be made to determine
if GR is present and if so, its type
and etiology.
In the presence of
sonographically detectable
anomalies, cordocentesis
may be performed for
kariotyping.
GR. NEAR TERM
Prompt delivery is likely to
afford the best outcome for
the GR fetus
In the presence of significant
oligohydraminos most fetus
will be delivered if G.A has
reached>34 wk.
Unfortunately
Such often tolerate labor less than

AGA and C/S is indicated for
intrapartum fetal compromise.
Importantly
Uncertainly about the diagnosis

of GR should preclude
intervention until fetal lung
maturity is assured.
GR. REMOTE FROM TERM
before 34 wk
Normal
Amniotic volume
Observation
Normal
fetal surveillance
Sono is repeated at interval 2-3 wk

Pregnancy is allowed
to continue until fetal
maturity is achieved.
At times amniocentesis for
assessment of pulmonary
maturity may be helpful in
clinical decision making.
There is no specific
treatment that will
ameliorate the
condition
Many clinicians advised a
program of modified rest in the
lateral recumbent position in
which placental perfusion is
maximized.
Optimal management of the
preterm GR fetus remain
undefined.
Mortality and morbidity in GR
fetuses were determined by GA
and birth weight and not by
abnormal fetal testing.
Early anti platelet therapy with
low dose aspirin may prevent
• uretroplacental thrombosis
• placental infarction
• idiopathic GR in women with
a history of recurrent severe
GR
LABOR AND
DELIVERY
FHR
MONITORING
GR is the result of insufficient
placental function
A.F cord
compression c/s
breech presentation
Expert assistance
• In making a successful
transition to air breathing
• clear the airway below the
vocal cord
• ventilate the infant as needed
The severely GR newborn is
susceptible to
• Hypothermia
• serious hypoglycemia
• polycytemia
• hyper viscosity
Subsequent
development of the GR
Prolonged symmetrical FGR

is likely to be followed by
slow growth after birth.
The asymmetrically
GR is more likely to
catch up after birth.

NEUROLOGICAL AND
INTELLECTUAL
CAPABILITY
In a 9-11 year follow up
study learning deficit in
almost half of FGR
A significant association
between fetal growth
restriction and cerebral
palsy.
The risk of recurrent FGR
is increased in women
• Who have previously had
this complication
• With History of FGR
• A continuing medical
complication

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Intra Uterine Growth

Diah Rumekti Hadiati

• Fetal demise • Hypothermia

Earlier or accelerated maturation

Proportionate reduction in head & body

A late pregnancy insult

A previously GR fetus in women with

Such often tolerate labor less than

Uncertainly about the diagnosis

Sono is repeated at interval 2-3 wk

Prolonged symmetrical FGR

catch up after birth.

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