Intra uterine growth retardation

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IUGR
Intra Uterine Growth Retardation
Razieh M.Jaafari,MD Ahwaz.u.m.s Dept of ObGyn
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Small for Gestational Age

• SGA infants are those with weights below the 10
  percentile for their gestational age

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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
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Incidence

• 3 -10 of infants are growth restricted

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25 -60 of infants conventionally diagnosed to
be SGA were in fact AGA when
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Determinant of birth weight such as maternal

• Ethnic group
• Parity
• Weight
• Height

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MORTALITY MORBIDITY

• Hypothermia
• Abnormal neurological development

• Fetal demise
• Birth asphyxia
• Meconium aspiration
• Neonatal hypoglycemia

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• ACCELERATED MATURATION

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Accelerated maturation

• The fetus resoponses to stressed envirorment by
  adrenal glucocorticoid

Earlier or accelerated maturation
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SYMMETRICAL VERSUS ASYMMETRICAL GR..
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Fetal growth has been divided into three phases.

• cell size
• fat deposition
• fetal weight as much as 200 G.r. per week.

• 1-cellular hyperplasia
• 2- hyperplasy hypertrophy
• 3- hypertrophy

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symmetrical

• An early insult
• due to
• chemical
• viral
• aneuploidy

• Cell size
• Cell num.

Proportionate reduction in head body
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Asymmetrical
A late pregnancy insult such as placental
insufficiency would affect cell size.
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The ratio of brain weight to liver weight over in
the last 12 wk of pregnancy is increased to 5/1
or more
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Growth pattern may potentially reveal the cause
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• In practice accurate identification of
  symmetrical versus asymmetrical fetus has proved
  difficult.

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Risk factors for FGR

• Maternal
• fetal
• placental and cord abn.

FGR - fetal growth retardation
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Maternal causes

• Constitutionally small mother
• Poor maternal weight gain nutrition
• Social deprivation

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• vascular disease
• maternal anemia
• anti phospholipid Ab syn.
• Extra uterine pregnancy
• chronic renal disease

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FETAL CAUSES

• fetal infections
• congenital malformations
• chromosomal abnormalities
• trisomy 16
• multiple fetus

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Placental and cord abnormalities

• chromic partial placental sep.
• extensive infarct.
• Chorioangioma
• placenta previa

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ADDITIONAL INSIGHT OF FGR
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These fetus also had

• Hypoglycemia
• hypoinsulinemia
• glycin/valin
• hypertriglycemia
• thrombocytemia

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Screening and identification of F.G.R

• Early establishment of G.A
• Attention to maternal weight gain
• Measurement of uterine height throughout pregnancy

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Identification of risk factors

• A previously GR fetus in women with
• significant risk factors

Serial sonography
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Definitive diagnosis usually can not be made
until delivery.
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MANAGEMENT

• Once a SGA is suspected , intensive effort should
  be made to determine if GR is present and if so,
  its type and etiology.

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In the presence of sonographically detectable
anomalies, cordocentesis may be performed for
kariotyping.
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Prompt delivery is likely to afford the best
outcome for the GR fetus
GR. NEAR TERM
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In the presence of significant oligohydraminos
most fetus will be delivered if G.A has
reachedgt34 wk.
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Such often tolerate labor less than AGA and C/S
is indicated for intrapartum fetal compromise.
Unfortunately
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Importantly
Uncertainly about the diagnosis of GR should
preclude intervention until fetal lung maturity
is assured.
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GR. REMOTE FROM TERM
before 34 wk Normal Amniotic
volume Normal fetal surveillance
Observation
Sono is repeated at interval 2-3 wk
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Pregnancy is allowed to continue until fetal
maturity is achieved.
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At times amniocentesis for assessment of
pulmonary maturity may be helpful in clinical
decision making.
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There is no specific treatment that will
ameliorate the condition
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Many clinicians advised a program of modified
rest in the lateral recumbent position in which
c.o.p and placental perfusion is maximized.
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Optimal management of the preterm GR fetus remain
undefined.
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Mortality and morbidity in GR fetuses were
determined by GA and birth weight and not by
abnormal fetal testing.
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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

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LABOR AND DELIVERY

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FHR MONITORING

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• GR is the result of insufficient
• placental function

• c/s

• A.f cord
• compression
• breech presentation

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Expert assistance

• In making a successful transition to air
  breathing
• clear the airway below the vocal cord
• ventilate the infant as needed

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The severely GR newborn is susceptible to

• Hypothermia
• serious hypoglycemia
• polycytemia
• hyper viscosity

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Prolonged symmetrical FGR is likely to be
followed by slow growth after birth.
Subsequent development of the GR
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The asymmetrically GR is more likely to catch up
after birth.
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• NEUROLOGICAL AND INTELLECTUAL CAPABILITY

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A LONG TERM FABORABLE OUT COME MAY BE EXPECTED.

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In a 9-11 year follow up study learning deficit
in almost half of GRF
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A significant association between fetal growth
restriction and cerebral palsy.
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The risk of recurrent FGR is increased in women

• Who have previously had this complication
• With Hx of FGR
• A continuing medical complication

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In the name of Allah, the beneficent. the
merciful