1. Intrauterine Growth
Restriction
Prof. M.C.Bansal
MBBS,MS,MICOG,FICOG
Professor OBGY
Ex-Principal & Controller
Jhalawar Medical College & Hospital
Mahatma Gandhi Medical College, Jaipur.

2. Definitions
 IUGR: A condition where the fetus fails
to achieve its genetic growth potential
and cosequently is at risk of increased
perinatal morbidity & mortality.
 SGA: Infant with weight < 10th
percentile of those born at the same
gestational age or > 2 SDs below
mean for Gestational Age.

3. Easiest way to think about these
terms are
 IUGR: is a term used by Obstetrician to
describe a pattern of growth over a
period of time.
 SGA: is a term used by Pediatrician to
describe a single point on a growth
curve.

4. Incidence
 3 - 5% of all pregnancies.
 20 % of stillborns are growth retarded.
 1/3 of infants with BW < 2750 gms are
growth retarded and not premature.
 Only 20-30% of growth restricted
fetuses are small due to pathological
restriction of growth.
 Perinatal mortality is 8 - 10 times higher
for these fetuses.

5. Normal Intrauterine Growth pattern
 Stage I (Hyperplasia)
- 4 to 20 weeks
- Rapid mitosis
- Increase of DNA content
 Stage II (Hyperplasia & Hypertrophy)
- 20 to 28 weeks
- Declining mitosis.
- Increase in cell size.

6. Normal Intrauterine Growth pattern
 Stage III ( Hypertrophy)
- 28 to 40 weeks
- Rapid increase in cell size.
- Rapid accumulation of fat, muscle
and connective tissue.
 95% of fetal weight gain occurs during
last 20 weeks of gestations.

7. Classification
 Based on evaluation & USG examination small
fetuses are divided into two categaries
Healthy SGA or True IUGR
or
Constitutionally small Pathologically growth
restricted
Type –I Type –II
Symmetrical IUGR Asymmetrical

8. Symmetrical IUGR(20-30%)


9. Symmetrical IUGR
 Etiology- Structural
 Congenital malformation
Chromosomal
 Intrauterine Infection
-
Toxoplasma,Rubella,Cytomegalovirus,Herpes
simplex
 Toxins & Drugs
Neonatal course-
Complicated with poor prognosis

10. Asymmetrical IUGR(70-80%)


11. Asymmetrical IUGR
 Etiology-
 Maternal Diseases - Chronic hypertention
Renal diseases
Vasculopathy
 Placental Insufficiency
 Neonatal course-
Uncomplicated and good prognosis

12. Comparison between PFGR and
Normal SGA
Normal, Small for gestation Pathological Growth
Age Restriction
Birth weight <10% Birth weight usaully <10% but
may be <25%
Birth weight <2500gms Birth weight usaully <2500gms
but may be larger
Normal Ponderal Index
Low Ponderal Index
Normal subcutaneous fat Decreased subcutaneous fat
Normal nucleated blood red Elevated nucleated blood red
cells & thrombocytopenia cells & thrombocytopenia
Uneventful neonatal period Complicated neonatal period
usually

13. Etiology
1) Fetal factors:
 Genetic Factors:
- Race, ethnicity, nationality
- sex ( male weigh 150 -200 gm more
than female )
-genetic disorders ( Achondroplasia,
Russell - silver syn.)
 Chromosomal anomalies:
- Chromosomal deletions
- Trisomies 13,18 & 21

14. Etiology
 Congenital malformations:
Anencephaly, GI atresia, potter’s syndrome,
and pancreatic agenesis.
 Fetal Cardiovascular anomalies
 Congenital Infections:
mainly TORCH infections.
 Inborn error of metabolism:
- Transient neonatal diabetes
- Galactosemia
- PKU

15. Etiology
2) Maternal Factors:
 Decrease Uteroplacental blood flow:
- Pre eclampsia / eclampsia
- chronic renovascular disease
- Chronic hypertension
 Maternal malnutrition
 Multiple pregnancy
 Drugs
- Cigarettes, alcohol, heroin, cocaine
- Teratogens, antimetabolites and
therapeutic agents such as trimethadione,
warfarin, phenytoin

16. Etiology
 Maternal hypoxemia
- Hemoglobinopathies
- High altitudes
• Others
- Short stature
- Younger or older age (<15 and >45)
- Low socioeconomic class
- Primiparity
- Grand multiparity
- Low pregnancy weight
- Previous h/o preterm IUGR baby
- Chronic illness ( DM, renal failure, cyanotic
heart

17. Etiology
3) Placental Factors:
 Placental insufficiency ( most imp in 3rd
trimester)
 Anatomic problems:
– Multiple infarcts
– Aberrant cord insertions
– Umbilical vascular thrombosis &
hemangiomas
– Premature placental separation
– Small Placenta

18. Diagnosis
Clinical Biophysical Biochemical
Ultrasonography MSAFP & hCG in
2nd trimester
Erythropoietin
level in cord blood
is high in IUGR

19. Diagnosis- Clinically
 Maternal weight gain-
 Stationary or falling during second half of
pregnancy
 Palpation of uterus-
 Symphysio Fundal Height-Normally
increases by 1 cm per week between 14 –
32 wks
- A lag in fundal height of 4 wks s/o
moderate
IUGR and over 6 wks s/o severe IUGR

21. Complications
FETAL
 Antepartum-
 Oligohydroamnios
 Fetal distress
 Fetal death
 Intrapartum-
 Fetal Acidosis
 Fetal Hypoxia

22.  MATERNAL-
Per se fetal growth restriction does not cause
any harm to mother.
 But underlying disease progress like pre-
eclampsia, heart diseases, malnutrition may
be life threatening.
 A woman with a growth restricted infant , risk
of having another is two fold.

23. Prevention
 Strategies include
– prenatal care modalities for high risk
screening
– protein/energy supplementation
– vitamin/mineral supplementation
– fish oil supplementation
– prevention and treatment of
 Hypertensive disorders
 Infection
 Anemia

24. Prevention
 Strong evidence of benefit only for the
following interventions:
– balanced protein/energy supplementation
& maternal volume expansion
– strategies to reduce maternal smoking
– antibiotic administration to prevent urinary
tract infections and
– antimalarial prophylaxis.
 Few statistically significant reductions in
the risk of IUGR have been
demonstrated with other interventions.

25. Antenatal Fetal Surveillance
 The purpose is to identify further progression of
the disease process that would jeopardize the
foetus to a point that it would be better to be
delivered than to remain in utero.
 There are four testing modalities which are
helpful –Daily fetal movement count,Non-
Stress Test, Amniotic Fluid Index, Doppler
of the Umbilical Artery & Biophysical
Profile, each of which addresses different
aspects of surveillance.
 Combination of tests are better than an
isolated test.

26.  Some more complex protocols have been
also proposed like—
 Kramer & Weiner suggested that UmA
doppler is more reliable because severely
abnormal doppler findings can precede an
abnormal FHR by several weeks.
 Harman & Baschat suggested a
different strategy which includes multiple
venous & arterial doppler and Biophycal
profile

27. MANAGEMENT
Suspect IUGR clinically
Confirm IUGR & Type of IUGR
Symmetrical Asymmetrical
-Screening for TORCH Management depends
upon
-USG to r/o cong.malformation -Complicating
factor
-Fetal blood sampling to r/o -Previous obs
history-
Chromosomal abnormality -Gestational Age

28. Treatment
IUGR has many causes, therefore, there
is not one treatment that always works.

29. Treatment
 Although there are many causes of IUGR, the
treatment consists of either delivery or
remaining in utero and improving blood flow to
the uterus.
 When blood flow is improved, the delivery of
oxygen and other nutrients to the foetus occurs.
If the foetus is lacking in these substances, their
increased availability may result in improved
growth and development.

30. Treatment
1.Maternal Bed Rest
This is the initial approach for the
treatment of IUGR.
Adequate bed rest in left lateral position
results in increased blood flow to the
uterus & placenta.

31. Treatment

32. Treatment
2. Aspirin Therapy(1- 2mg/kg/day)
 The use of aspirin to treat fetuses with
IUGR is still controversial.
 If aspirin is used, it may be advantageous if
given to patients before 20 weeks of
gestation. It is minimal to limited benefit if
given at the time of diagnosis (third
trimester).
 The Maternal-Fetal Medicine Network randomized
3135 women to receive 60mg/d aspirin or placebo

33. Aspirin Therapy(1-
2mg/kg/day)
 However it is benificial in cases
with history of thrombotic disease,
hypertension, pre-eclampsia.

34. Treatment
3.Hyperoxygenation
 Fetal oxygenation is crucial for fetal growth .
 A positive response to maternal oxygen
therapy found by decreased resistance in
placental circulation is marker of good
prognosis and lack of response is an
indication of poor outcome.
(Bilardo et al 1991)

35. Treatment
 Other forms of treatment that have been
studied are maternal hyperalimantation by
aminoacids,nutritional supplementation, zinc
supplementation, fish oil and hormones.
 Maternal volume expansion may be helpful
in improving placental perfusion.
 Limited studies are available regarding the
use of these modalities in the treatment of
IUGR.

36. Judge Optimum Time Of Delivery
RISK OF PREMATURITY RISK OF IUD
Difficult extra uterine Hostile intra uterine
existence environment

37. Management according to
Gestational Age
Less than 24 weeks of gestational age
 Antenatal surveillance with Umbilical & Ductus
venosus doppler study is reliable.
If UmA diastolic flow +nt If UmA –RDF
DV – Uninterrupted DV– Interrupted
forward flow forward flow
Fetal Acidosis& Hypoxia
Expectant Management Imminent Fetal Death
Termination

38. Less than 24 weeks of gestational age
 There is no evidence that
corticosteroids accelerate the fetal
pulmonary maturity or prevent the
development of Intraventricular
haemorrhage.
 On the other hand, there is evidence
that the use of steroids in severe IUGR
may cause hemodynamic
decompensation
(Simchen et al 2004).

39. 26 to 34 weeks Gestational Age
 Antenatal surveillance with NST and Umbilical
A, Middle cerebral A, Ductus venosus doppler.
1. NST-Reactive
UmA Doppler-Reassuring Repeat in 1wk
UmA Doppler-Non reassuring
Ductus venosus Doppler Reassuring--Repeat in
1wk
Non reassuring—Deliver

40. 2. NST-Non reactive
UmA Doppler—follow as above
Or Biophysical profile
≥8 UmA doppler
≤4 Deliver 6 Repeat in 6-24hrs
wait till ≥36wks
Deliver

41. 34 to 37 weeks Gestational Age
Antenatal surveillance with FHR monitoring by
 NST and Color doppler velocimery.
1. Both the tests reassuring Repeat in 1
wk
Test for lung maturity
Immature Mature
Repeat in 1 wk Deliver
2.Either test non reassuring Deliver

42. Delivery of Pathological Growth
Restricted Fetus
 The full term fetus has a large capacity to
tolerate the hypoxic stress of labour which is
substantially reduced in PGRF due to
marked depletion of energy stores in liver &
subcutaneous tissue.
 Thus, intrapartum asphyxia is the major
cause of perinatal morbidity & mortality in

43.  Therefore, when umbilical doppler
shows Absent flow or Reverse flow
 Fetal aciosis & hypoxia is more
common
 Delivery by cesarean section is
indicated

44.  Now ,the question is how to deliver the
PGRF with lesser degrees of doppler or
FHR abnormalities.
Skinner et al (1998) and Li et al (2003)
Conclusion- Vaginal delivery is not
contraindicated in patients with resistance in
UmA velocimetry but cesarean delivery should
be anticipated in a large number of them.
Indications for LSCS in IUGR pregnancies
1. Established fetal acidosis
2. Absent or Reverse flow in UmA doppler
3. Unfavourable cervix

45. Precautions to be taken during delivery
 Delivery should be in an equipped institution with
Intensive intranatal monitoring & neonatal
intensive care facilities.
 Continous FHR monitoring
 Amnioinfusion in early stage of labour if amniotic
fluid volume is decreased.
 Second stage of labour requires special attention.
 Second stage should not be prolonged > 2 hrs in
nulliparous and 1 hr in multiparous .
 Placenta needs careful examination as in many
cases it will provide evidence about the etiology of
the problem (Rayburn et al 1989).

46. Amnioinfusion
 Amnioinfusion refers to the instillation of fluid
into the amniotic cavity.
 This procedure is typically performed during
labor through an intrauterine pressure
catheter introduced transcervically after
rupture of the fetal membranes.
 Alternatively, fluid can be infused through a
needle transabdominally, the reverse process
of amniocentesis.

47. Randomised trial of amnioinfusion during
labour with meconium stained amniotic
fluid
(BJOG Jan 2002)
 Conclusion- Amnioinfusion in an under
resourced labour ward decreases
caesarean section rates and fetal
morbidity

48. T
H Y
A O
N U
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