iugr

1. IUGR Intra Uterine Growth
Retardation
Chandni Thampi
Assistant Professor
Travancore College Of Nursing

2. 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.

3. 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.

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

5. 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.

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

7. 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.

9. Etiology

10. 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.
• Maternal diseases- anaemia, hypertension,
antiphospholipid syndrome in the second half of
pregnancy play significant role in the reduction
of the birth weight.
• Toxins- alcohol, smoking ,cocaine,heroine drugs

11. 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 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.

12. 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

13. Diagnosis

14. • Maternal weight gain remains stationary or at
times falling (less than 2 kg/month during
second half of pregnancy).
• If there is reduction of symphysis fundal height
by 2 cm before 36 weeks or 3 cm thereafter or
the measurement falls below the 10th
percentile.

15. • Measurement of the abdominal girth showing
stationary or falling values.
• 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.

16. Fetal ultrasound: BPD and AC measured.
- BPD (biparietal diam) 43-100% accurate
but inaccuracy due to head-sparing in
asymmetric IUGR.
- AC (Abdominal circumference better
sensitivity than that of cephalometry for
IUGR detection.
- HC/AC (Head circumference/abdominal
circumference ratio) is an important
measurement for detection of asymmetric
IUGR infants.

17. - Ratio of femoral length to abdominal
circumference (FL/AC) provides also an
accurate prediction of IUGR.

18. Amniotic fluid volume: oligohydramnios
due to decreased renal blood flow and
urine output.
Blood flow measurements: by Doppler
flow studies, fetal and uterine blood flow
can be measured and therefore
uteroplacental circulation dysfunctions
can be assessed.

19. Biochemical markers
Elevated levels of MSAFP and hcg in
second trimester are markers of
abnormal placentation and risk of IUGR

20. Physical features at birth
• Weight deficit at birth is about 600 gm
below the minimum in percentile
standard.
• Length is unaffected.
• Head circumference is relatively larger
than the body.

21. Physical features at birth
• Physical features show dry and wrinkled skin
because of less subcutaneous fat,
abdomen, thin meconium stained
scaphoid
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.

22. Physical features

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

24. 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.

25. Mortality
• The immediate neonatal mortality is about 6
times more than the normal newborn or even
similar weight appropriate to the shorter
gestational age.
• Most of the babies die within 24 hours.
• The morbidity rate rises to about 50%.

26. Management during pregnancy
1. Adequate bed rest specially in left lateral position
(2 hours following lunch and 8 hours at night).
2. To correct malnutrition by adequately balanced
diet, 300 extra calories per day are to be taken.
3. Maternal hyper oxygenation 2.5 l/mt
4. Avoidance of smoking and alcohol.
5. Low dose aspirin (50 mg daily) for hypertention,
pre eclampsia may be helpful.
6. Detect fetal anomalies.

27. At delivery:
- IUGR infants are more prone to
hypoxemia during labor and delivery
because of uteroplacental insufficiency,
and more prone to cord compression due
to lack of amniotic fluid and a thin cord.

28. - A neonatal team capable of managing
asphyxia and meconium aspiration
syndrome should be available at the time
of delivery.
- Special attention should be addressed to
prevention of hypothermia and
hypoglycemia.

29. Management after birth:
1. Respiratory care – esp. with meconium
2. Hypoglycaemia due to low sugar
reserves and higher energy consumption – esp.
with cold stress.

30. 3. Hypothermia due to lack of
subcutaneous fat
4. infection – at risk as immature immune
system of babies is common

31. 5. Polycythaemia – due to in-utero hypoxia.
Can cause venous thrombo-emboli and
can also worsen cerebral ischaemia and
perpetuate hypoglycaemia.
6. Haemorrhage – can develop due to lack
of liver coagulation factor production, and
also may have low platelets if TORCH
7. Management of asphyxia

32. Investigations of SGA baby:
Initially, babies need to be examined in a
warm environment.
True blood glucose should be assessed at ½
to 1 hour of age, and pre-feeds for at least
the next 2 feeds. Feeds should be frequent
(2-3 hourly initially).

33. If baby jittery, then glucose and calcium
and magnesium must be checked.
Full blood count -
- polycythaemia
- platelet count
- white cells

34. Other investigations
- chromosomes
- TORCH screen
- CXR if respiratory distress
- Sepsis workup if possibility of infection -
- Urine drug screen, etc., if suspect
maternal substance abuse

35. Nutrition:
- Important to establish nutrition as early as
possible
- If delay in establishing enteral feeds, must
use TPN.
- Weight gain monitoring needed to ensure
sufficiency of caloric intake.

36. - It is common that caloric intake in IUGR
infants will exceed the usual intake of 100-
120 Kcal/kg/day, and daily weight gain will
exceed 25 g/day.
- Neurologic prognosis may relate directly to
restoring good nutrition