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1. Definition :
• Intra uterine growth restriction is said to be
present in those babies whose birth weight is
below the tenth percentile of the average for
the gestational age.
• Growth restriction can occur in preterm, term
or post-term babies.

2. Nomenclature :
• SGA and IUGR are too often used synonymously
although there is a degree of overlap.
• SGA fetus is not necessarily growth retarded.
• The baby may be constitutionally small.
• Similarly late onset of pathological cessation of
growth may produce a baby with typical features of
IUGR but may not be small for gestation (ie.
Appropriate for gestational age).
• However, both attempt to identify fetuses or
neonates that are small for reasons other than being
preterm.

3. Normal fetal growth
• Is characterized by cellular
hyperplasia followed by
hyperplasia and hypertrophy and
lastly by hypertrophy alone.

4. Types: Based on the clinical evaluation and ultrasound
examination the small fetuses are divided into:
1. Fetuses that are small and healthy. The birth weight is
less than 10th percentile for their gestational age. They
have normal ponderal index, normal subcutaneous fat
and usually have 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:
(a) Symmetrical or Type I
(b) Asymmetrical or Type II.

5. Symmetrical (20%) –
• The fetus is affected from the noxious effect
very early in the phase of cellular hyperpllasia.
• The total cell number is less. This form of
growth retardation is most often caused by
structural or chromosomal abnormalities or
congenital infection (TORCH).
• The pathologic process is intrinsic to the fetus
and involves all the organs including the head.

6. Asymmetrical (80%) –
• The fetus is affected in later months during the
phase of cellular hypertrophy.
• The total cell number remains the same but size
is smaller than normal.
• The pathologic processes that too often result in
asymmetric growth retardation are maternal
diseases extrinsic to the fetus.
• These diseases alter the fetal size by reducing
utero-placental blood flow or by restricting the
oxygen and nutrient transfer or by reducing the
placental size.

7. Etiology: The causes of fetal growth retardation can be
divided into four types.
Maternal –
• Maternal nutrition before and during pregnancy –
Critical substrate requirement for the fetus such as
glucose, aminoacids and oxygen are lacking during
pregnancy.
• This is an important cause of small weight of the
babies in the developing countries.
• As most of the fetal weight gain (two-third) occurs
beyond 24th week of pregnancy, malnutrition,
anaemia, hypertension, antiphospholipid syndrome
in the second half of pregnancy play significant role
in the reduction of the birth weight.

8. Fetal –
There is enough substrate in the maternal blood and
also crosses the placenta but is not utilized by the
fetus. The failure of non utilization may be due to
(1) Congenital anomalies either cardio vascular, renal or
others
(2) Chromosomal abnormality is associated with 8-12%
of growth retarded infants. The common
abnormalities are trisomy 21, trisomy 18 (Edward’s
Syndrome), trisomy 16, trisomy 13 and Turner’s
syndrome
(3) Accelerated fetal metabolism due to TORCH agents
(toxoplasmosis, rubella, cytomegalovirus and herpes
simplex) and parvo virus B19
(4) Multiple pregnancy – There is mechanical hindrance
to growth and excessive fetal demand.

9. Placental –
• The causes include cases of poor uterine blood flow to
the placental site for a long time.
• This leads to chronic placental insufficiency with
inadequate substrate transfer.
• This occurs in conditions such as preeclampsia,
essential hypertension, chronic nephritis, organic heart
disease, placental and cord abnormalities such as
chronic placental abruption, infarction, small placenta,
circumvallate placenta, vellamentous insertion of cord
etc.
Unknown –
The cause remains unknown in about 40%

10. • Measurement of the abdominal girth showing
stationary or falling values.
• Serial clinical examination by abdominal
palpation to measure the relative growth of the
uterus and its contents is the commonly used
method. The diminishing amniotic fluid
volume can also be assessed with fair degree of
accuracy.

11. Physical features at birth
• Physical features show dry and wrinkled skin
because of less subcutaneous fat, scaphoid
abdomen, thin meconium stained vernix
caseosa and thin umbilical cord. All these give
the baby an ‘old man look’. Pinna of ear has
cartilaginous ridges. Plantar creases are well
defined.
• The baby is alert and having normal cry. Eyes
are open.
• Reflexes are normal including Moro-reflex.

12. Complications
Fetal:
(A) Antenatal – Chronic fetal distress, fetal death,
(B) Intranatal – Hypoxia and acidosis
(C) After birth:
Immediate:
(1) Asphyxia (intrauterine and neonatal),
(2) Hypoglycemia due to shortage of glycogen reserve in the
liver as a result of chronic hypoxia
(3) Meconium aspiration pneumonia
(4) Microcoagulation leading to DIC during first day of life.
(5) Hypothermia
(6) Pulmonary hemorrhage
(7) Polycythaemia
(8) Hyperviscosity syndrome
(9) Necrotizing enterocolitis due to reduced intestinal blood flow.

13. Late:
• Symmetrical growth retarded baby is likely to
grow slowly after birth.
• Whereas the asymmetrical one is more likely to
grow faster after birth.
• The fetuses have retardation of growth
evidenced before third trimester are likely to
have retarded neurologic and intellectual
development in infancy.
• The worst prognosis is for IUGR caused by
congenital infection, congenital abnormalities
and chromosomal defects.