1. DR Laxman Singh Charan
Neonatal division
Department of Pediatrics
Safdarjang Hospital

2. Definitions
IUGR: Failure of normal fetal growth caused by
multiple adverse effects on the fetus.
SGA: Infant with wt < 10% ile for GA, or > 2
SDs below mean for GA.

3. Easiest way to think about these terms are
IUGR: is a term used by Obstetricians 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
In india.
3 - 10 % of all pregnancies.
20 % of stillborns are growth retarded.
30 % of infants with SIDS were IUGR.
1/3 of infants with BW < 2800 grams are growth
retarded and not premature.
9 - 27 % have anatomic and/or genetic abnormalities.
Perinatal mortality is 8 - 10 times higher for these
fetuses.

5. Types of IUGR
Symmetric IUGR: weight,length and head
circumference are all below the 10th percentile.
(33 % of IUGR Infants)
Asymmetric IUGR: weight is below the 10 th
percentile and head circumference and length are
preserved. (55 % of IUGR)
Combined type IUGR: Infant may have skeletal
shortening, some reduction of soft tissue mass.
(12% of IUGR)

6. Ponderal Index
Way of characterizing the relationship of height to
mass for an individual.
PI = 100 x
Mass (gm)
Height (cm)3
Typical values are 2.0 to 2.5
PI is normal in symmetric IUGR.
PI is low in asymmetric IUGR.

7. 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.

8. 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.

9. Etiology
Growth inhibition in stage I:
- Undersized fetus with fewer cells.
- Normal cell size.
Result in symmetric IUGR.
Associated conditions:
- Genetic
- Congenital anomalies
- Intrauterine infections
- Substance abuse
- Cigarette smoking
- Therapeutic irradiation

10. Etiology
Growth Inhibition in Stage II/III
-Decrease in cell size and fetal weight
- Less effect on total cell numeric, fetal length,
head circumferance.
Result in asymmetric IUGR.
Associated Conditions:
- Uteroplacental insufficiency.
• Combination above associated mixed type IUGR.

11. Pathophysiology
(1) Fetal factors:
Genetic Factors:
- Race, ethnicity, nationality
- sex ( male weight 150 -200 gm more than
female )
- parity ( primiparous, weight less than
subsequent siblings)
-genetic disorders ( Achondroplasia,
Russell-silver syndrome.)
Chromosomal anomalies:
- Chromosomal deletions
- trisomies 13,18 & 21

12. Pathophysiology
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

13. Pathophysiology
(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

14. Pathophysiology

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 heartdisease etc.)

15. Pathophysiology
(3) Placental Factors:
Placental insufficiency (most importent in 3rd
trimester)
Anatomic problems:
Multiple infarcts
Aberrant cord insertions
Umbilical vascular thrombosis & hemangiomas
Premature placental separation
Small Placenta

16. Postnatal Assessment
Growth parameters- weight, height, HC
Assess GA-with Ballard score.
Growth chart -Plotted growth parameters in growth chart.

19. Physical appearance:
• Heads are disproportionately large for their trunks and
extremities
• Facial appearance has been likened to that of a
“wizened old man”.
• Long nails.
• Scaphoid abdomen

20. • Signs of recent wasting-
- soft tissue wasting
- diminished skin fold thickness
- decrease breast tissue
- reduced thigh circumference
• Signs of long term growth failure-
- Widened skull sutures, large fontanelles
- shortened crown – heel length
- delayed development of epiphyses
• Comparison to premature infants,IUGR has brain
and heart larger in proportion to the body weight,
in contrast the liver, spleen, adrenals and thymus
are smaller.

21. Complication
Hypoxia
- Perinatal asphyxia
- Persistent pulmonary hypertension
- meconium aspiration
Thermoregulation
- Hypothermia due to diminished subcutaneous fat and
elevated surface/volume ratio.

22. Complications
Metabolic
- Hypoglycemia
- result from inadequate glycogen stores.
- diminished gluconeogenesis.
- increased BMR
- Hypocalcemia
- due to high serum glucagon level, which
stimulate calcitonin excretion.

23. Complications
Hematologic
- Hyperviscosity and polycythemia due to increase
erythropoietin level secondary to hypoxia
Immunologic
- IUGR have increased protein catabolism and
decreased in protein, prealbumin and
immunoglobulins, which decreased humoral and
cellular immunity.

24. Management
Antenatal diagnosis and management is the key to proper
management of IUGR
Delivery and Resuscitation
- appropriate timing of delivery
- skilled resuscitation should be available
- prevention of heat loss
Hypoglycemia
- close monitoring of blood glucose
- early treatment ( IV dextrose,early feeding)

25. Management
Hematological Disorder
- Hematocrit to detect polycythemia
- CBC with differential to rule out leukopenia or
thrombocytopenia
Congenital infection
- Infant should be examined for signs of congenital
infection (eg.rash, microcephaly hepatosplenomegaly,
lymphadenopathy, cardiac anomalies etc….)
- TORCH titer screening
- Examination of urine, nasopharynx
- Head CT to rule out calcification

26. Management
Genetic anomalies
- screening as indicated by physical exam
- chromosomal analysis (infant with
dysmorphic features)
Others
- serum calcium to r/o hypocalcemia
- fractionated bilirubin secondary to polycythmia.
congenital infection
- urine,meconium for substance abuse

27. Management
Early feeding and caloric intake should be 100-120
kcal/kg/d
Developmental and growth f/u in all IUGR infants

28. Outcome
Symmetric vs. Asymmetric IUGR
- symmetric has poor outcome compare to asymmetric
Preterm IUGR has high incidence of abnormalities
IUGR with chromosomal disease has 100% incidence
of handicap
Congenital infection has poor outcome - handicap
rate > 50%
IUGR has higher rate of learning disability.

29. FOLLOW-UP
IUGR babies are risk for poor growth and neuro-
developmental outcome.
Routinely follow IUGR babies with birth weight below 3rd
centile and those with birth weight 3-10th centile if they
develop significant morbidities (e.g. hypoglycemia,
polycythemia,birth asphyxia) during hospital stay.