INTRA UTERINE GROWTH RESTRICTION (IUGR)

INTRODUCTION

Intrauterine growth restriction (IUGR) is a common diagnosis in obstetrics and carries an increased risk of
perinatal mortality and morbidity.
DEFINITION: Intrauterine growth restriction refers to a fetus whose weight is below the 10th percentile of the
average for its gestational age.
IUGR is defined as failure of the fetus to achieve its genetic growth potential.
INCIDENCE: It comprises of 1/3rd of low birth weight babies. Among term babies it is 5% and preterm babies
15%.
ETIOLOGY:

Maternal:
 Constitutional: Small women, maternal genetic and racial background are associated with small
babies.
 Poor maternal nutrition before and during the pregnancy
 Maternal diseases: Heart disease, preeclampsia or eclampsia, anemia, chronic renal disease etc.
 Toxins: Alcohol abuse, drug addiction, smoking

Fetal: there is enough substrate in maternal blood and also crosses the placenta but is not utilized by the fetus.
The failure of non utilization may be due to:
 Structural anomalies: cardiovascular, renal or others
 Chromosomal abnormality: Turner’s syndrome ,trisomies (13.18,21)
 Infection: TORCH agents, malaria
 Multiple pregnancies: there is mechanical hindrance to growth and excessive fetal demand.

Placental:
 Poor uterine blood flow to the placenta for a long time.
 Placental pathology: Placenta praevia , Abruption, Infarction, Circumvallete and Mosaichism.

TYPES: based on the clinical evaluation and ultrasound examination the small fetuses are divided into:

1. Fetuses that are small and healthy, normal pondrel index and subcutaneous fat and usually have an
uneventful neonatal course.
2. Fetuses where growth is restricted by pathological process (true IUGR). Depending upon the relative
size of their head, abdomen and femur, the fetuses are subdivided into:
Symmetrical (20%): The fetus is affected from the noxious effect very early in the phase of cellular
hyperplasia. The pathologic process is intrinsic to the fetus and involves all the organs including the
head.
Asymmetrical (80%): the fetus is affected in the later months during the phase of cellular hypertrophy.
The total cell number remains the same but size is smaller than normal.

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 Features of symmetrical and asymmetrical IUGR

Symmetrical Asymmetrical

Uniformally small Head larger than abdomen

Pondrel index (birth weight/crown-heel3) low

HC:AC and FL:AC ratios normal elevated

Total cell number- less, cell size normal Normal cell size smaller

Neonatal course complicated with poor Usually un complicated with good prognosis.
prognosis

PATHOPHYSIOLOGY

Due to reduced availability of the nutrients in the mother or its reduced transfer by the placenta to the fetus and
also due to reduced utilization by the fetus brain cell size (asymmetric) as well as cell numbers (symmetric) are
reduced. Liver glycogen is reduced. There is oligohydramnios as the renal and pulmonary contributions to
amniotic fluid are diminished due to reduced blood flow to these organs. The fetus is at risk for intrauterine
hypoxia and acidosis leading to intrauterine death.
DIAGNOSIS

Clinical
 Symphysis fundal height less than expected for gestational age after 24 weeks. A lag of 4 cm or more
suggest growth restriction.
 Maternal weight gain remains stationary or at times falling during the second half of pregnancy.
Ultrasound Biometry

 Ultrasound biometry of the fetus is now the gold standard for assessing fetal growth. The measurements
most commonly used are the biparietal diameter, head circumference, abdominal circumference
and femur length. Percentiles have been established for each of these parameters, and fetal weight can
be calculated. The most sensitive indicator of symmetric and asymmetric IUGR is the abdominal
circumference, which has a sensitivity of over 95 percent if the measurement is below the 2.5th
percentile. Accurate dating of the pregnancy is essential in the use of any parameter. In the absence of
reliable dating, serial scans at two- or three-week intervals must be performed to identify IUGR. It
should always be remembered that each parameter measured has an error potential of about one week
up to 20 gestational weeks, about two weeks from 20 to 36 weeks of gestation, and about three weeks
thereafter.
 Head circumference to the abdominal circumference (HC/AC) ratio. Between 20 and 36 weeks of
gestation, the HC/AC ratio normally drops almost linearly from 1.2 to 1.0. The ratio is normal in the
fetus with symmetric growth restriction and elevated in the infant with asymmetric growth restriction.
 Amniotic fluid volume: a vertical pocket of amniotic fluid <2cm suggest IUGR
 Femur length(FL): it is not affected in asymmetric IUGR. The FL/AC ratio is 22 at all gestational
ages from 21 weeks to term. FL/AC ratio > 23.5 suggest IUGR.
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Doppler velocimetry: elevated uterine artery systolic/ diastolic(S/D) ratio(>2.6) and or presence of diastolic
notch are associated with IUGR. The presence of diastolic notch in uterine artery suggests incomplete invasion
of placental trophoblasts to the uterine spiral arteries.
Three-dimensional Ultrasonography

Pondrel index PI: it is determined by dividing the estimated fetal weight by the third power of crown- heel
length( weight/length3. PI below 10th percentile is taken as IUGR
Middle cerebral artery Doppler

Biochemical markers: erythropoietin level in cord blood is high in fetuses with IUGR.

PHYSICAL FEATURES of IUGR BABY AT BIRTH

 Weight deficit at birth is about 600gm below the minimum in percentile standard. Length is unaffected.
 HC is relatively larger than body in asymmetric variety.
 Physical features show dry and wrinkled skin because of less subcutaneous fat, scaphoid abdomen, thin
meconium stained vernix caseosa and thin umbilical cord. Old Man Look for the baby.
 Baby is alert active and has normal cry. Reflexes are normal.

COMPLICATIONS

Fetal

a. Antenatal : chronic fetal distress, fetal death

b. Intranatal : hypoxia and acidosis
c. After birth
Immediate: asphyxia and RDS
Hypoglycemia , Meconium Aspiration Syndrome, Hyperviscosity Syndrome, Necrotizing Enterocolitis
Microcoagulation leading to DIC during 1st day of life.
Hypothermia, Pulmonary Hemorrhage, Polycythemia, Intraventricular Hemorrhage.

Late: symmetrical IUGR baby is likely to grow slowly after birth. Asymmetrical IUGR baby tend to catch up
growth in early infancy. The fetuses having retardation of growth evidenced before third trimester are likely to
have retarded neurological and intellectual development in infancy.

MANAGEMENT

IUGR increases the risk for intrauterine death. If this condition is suspected, the pregnant woman will be
closely monitored with several pregnancy ultrasounds to measure the baby's growth, movements, blood flow,
and fluid around the baby. Non-stress testing will also be done. Depending on the results of these tests,
delivery may be necessary.

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 Management protocol of IUGR
 To confirm IUGR and the type
 To exclude congenital malformation
and genetic disorder
 To treat the specific cause if found
 Fetal surveillance
 DFMC
 NST, Cardiotopography
 Biophysical profile
 Umbilical artery Doppler
Flow velocimetry

Pregnancy < 37 weeks Pregnancy equalling or more than 37 weeks

Termination

Severe IUGR Mild IUGR

Dual problem
Prematurity & Dysmaturity Increased rest
Folic acid
Fetal monitoring till 37 weeks

Equipped centre Centre with limited facilities Termination

Assess lung maturity transfer inutero to referral centre or
L:S ratio manage according to available resources
Phosphatidyl glycerol level Hospitalization
Bed rest
Not Mature Mature Folic acid
termination Maternal hperoxygenation
Dexamethasone Low dose aspirin

therapy pregnancy continued to 34 weeks if possible

Termination Termination

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Methods of termination
 Low rupture of membranes followed by oxytocin if pregnancy beyond 34 weeks with favourable cervix
and head deep in the pelvis.PGE2 gel can be used if cervix is unfavourable.
 Intrapartum monitoring by clinical, continuos electronic and scalp blood sampling may be needed as
risk for intrapartum asphyxia is high.
 Caesarean section
CONCLUSION

IUGR remains a challenging problem for clinicians. Most cases of IUGR occur in pregnancies in which no risk
factors are present; therefore, the clinician must be alert to the possibility of a growth disturbance in all
pregnancies. No single measurement helps secure the diagnosis; thus, a complex strategy for diagnosis and
assessment is necessary. The ability to diagnose the disorder and understand its pathophysiology still outpaces
the ability to prevent or treat its complications. The current therapeutic goals are to optimize the timing of
delivery to minimize hypoxemia and maximize gestational age and maternal outcome.

REFERENCE

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 Dutta DC. Textbook of obstetrics. 6th edition. Kolkata: New Central Book Agency; 2004
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 Evans AT. Manual of Obstetrics. 7th edition. New Delhi: Wolter Kluwer Pvt Ltd; 2007
 Pilliteri A. Maternal and child health nursing. Philadelphia: Lippincott Williams and Wilkins; 2007
 Ladewig PW, London ML, Olds SB. Maternal newborn nursing. California: Addison Wesley nursing;
2007
 Neerhof MG. Causes of intrauterine growth restriction. Clin Perinatol 1995;22:375-85.
 Leitich H, Egarter C, Husslein P, Kaider AK, Schemper M. A meta-analysis of low dose aspirin for the
prevention of intra uterine growth retardation. Br J Obstet Gynaecol 1997;104:450-9
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