This document discusses intrauterine growth restriction (IUGR) and small for gestational age (SGA) infants. It defines IUGR as impaired fetal growth and SGA as weight below the 10th percentile. IUGR incidence in India is 3-10% of pregnancies and is associated with higher stillbirth and infant mortality rates. IUGR can be symmetric, asymmetric, or combined based on effects on weight, length, and head circumference. Etiologies include placental insufficiency, genetic factors, infections, and maternal health conditions. Complications include hypoglycemia, hypothermia, and immune dysfunction. Proper management involves antenatal diagnosis, skilled delivery and resuscitation, glucose monitoring, screening for

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.