Transcript Intra uterine growth retardation

Intra Uterine
Growth Retardation
What is the definition of IUGR?
•< 10th centile for age  include normal fetuses
at the lower ends of the growth curve +
fetuses with IUGR
This definition is not helpful clinically
• < 5th centile for age 
•< 3rd centile for age the most appropriate
definition but associated with adverse
perinatal outcome
What is the deference between IUGR & SGA?
SGA  < 10th centile for
the population, which
means it is at the lower
end of the normal
distribution ie.
Constitutionally small but
have reached their full
growth potential
• IUGR Failure of the
fetus to chieve the expected
weight for a given gestation
Small for Gestational Age
SGA infants
are those with weights
below the 10 percentile
for their gestational age
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
• Birth asphyxia
• Meconium
aspiration
• Neonatal
hypoglycemia
• Hypothermia
• Abnormal
neurological
development
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
hyperplasia
• 2- hyperplasy
& hypertrophy
• 3- hypertrophy
cell size
fat deposition
fetal weight as
much as 200
G.r. per week.
symmetrical
An early insult
due to :
chemical
viral
aneuploidy
Cell size
Cell num.
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 retardation
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
glycin/valin
hypertriglycemia
thrombocytemia
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
Normal
fetal surveillance
Observation
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 c.o.p and 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 Hx of recurrent sever GR
LABOR AND
DELIVERY
FHR
MONITORING
GR is the result of insufficient
placental function
A.f
cord
compression
breech presentation
c/s
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
A LONG TERM
FABORABLE OUT COME
MAY BE EXPECTED.
In a 9-11 year follow up
study learning deficit in
almost half of GRF
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 Hx of FGR
&A continuing medical
complication
In the name of Allah, the
beneficent. the merciful