it explains about the IUGR

1. INTRA–UTERINE GROWTH RETARDATION
Presented by
Ms Mamatha
B.Sc Nursing

2. GENERAL OBJECTIVES
The group will be able to gain knowledge
regarding intra uterine growth retardation

3. SPECIFIC OBJECTIVES
The group will be able to
1. To Introduce the topic IUGR
2. To Define IUGR
3. To Explain about SGA
4. To Explain about IUGR and its types.
5. To Enumerate the etiology of IUGR and its
pathophysiology.
6. To enlist diagnostic evaluation and its
management along complication.

4. Introduction
Intra uterine growth retardation (IUGR) is
when a fetus in the womb does not grow as
expected.
The fetus as not as big would be expected for
the stage of the mother’s pregnancy due to
poor maternal nutrition or lack of adequate
oxygen supply to the fetus.
It can occur in preterm, term or post-term
babies.

5. Definition
Intra uterine growth restriction or retardation is defined
as to be present in those babies whose birth weight is
below the 10th percentiles of the average for the
gestational age.
Or
A condition where the fetus fails to achieve its genetic
growth potential and consequently is at risk of
increased perinatal morbidity and mortality.

6. Incidence
In developed countries its over all incidence is about 2 -
8%.
The incidence among the term babies is about 5% and
that among the post term babies is about 15%.
In India the incidence of IUGR has been found to be 6-
7%.
Nomenclature
Small for gestational age (SGA) and IUGR are too often
used synonymously although there is a degree of
overlap.

7. IUGR Vs SGA
Characteristics IUGR SGA
Definition Growth of a fetus is restricted or
retarded while in the uterus
Size of the fetus is small for
gestational age.
Appearance Babies always appear mal
nourished.
Babies appear small and do not
always appear to be mal
nourished
Diagnosis Ultra sound and Doppler of blood
flow, measurements of fundus to
the pubic bone.
Ultrasound and measurements of
the fundus to the pubic bone.
Measurement Measure is based on the change
in growth over time.
Measure is based on a one time
measurement that falls below a
statistical value.
Growth rate in utero Always slower than normal Can be normal or slower than
normal
Birth weight q Sometimes lower than normal but
not always
Always lower than normal
Pathological condition Always due to sort of problem or
disorder
Not always due to disorder or a
problem, sometimes the cause is
small- sized mother.

8. Small for Gestational
Age (SGA)
Intra Uterine Growth
Retardation (IUGR)

9. Normal fetal growth
1. Cellular hyperplasia- upto 16 weeks
2. Hyperplasia and hypertrophy- 16 to 32 weeks
3. Hypertrophy – after 32 weeks.
Most of fetal weight gain (23) occurs beyond 24th week of
pregnancy.

10. Types
Based on clinical evaluation and ultrasound
examination
Based on time of onset, relative size of their head,
abdomen and femur
1.symmetrical 2. asymmetrical

11. Based on clinical evaluation and ultrasound
examination
1. Fetuses who are small and healthy
The birth weight is less than 10th centiles 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(IUGR).

12. Based on time of onset, relative size of their head, abdomen and femur
Difference between symmetrical and asymmetrical
Symmetrical Asymmetrical
1. Affected from the noxious effect very
early in the phase of cellular
hyperplasia.- 20%
1. Affected in the later months during the
face of cellular hypertrophy about 80%
2. Total cell number is less but the size of
the cell is normal
2. Total cell number remains same but the
size of cell is smaller.
3. Often caused by structural, chromosomal
abnormalities or congenital
infection(TORCH) (intrinsic to fetus)
3. Pathological process that too often
results due to maternal diseases. (Extrinsic
fetus)
4. Neonatal course is complicated with
poor prognosis
4. Usually uncomplicated having good
prognosis
5. HC: AC and FL: AC- are normal 5. Elevated.

14. Maternal
Fetal
Placental
Unknown
Etiology

15. Maternal
1. Constitutional
2. Maternal nutrition
3. Social deprivation
4. Maternal disease
5. Toxins
6. Antiphospholipid antibody syndrome
7. Extra uterine pregnancy
1. Constitutional
• Small women, maternal genetic and racial
background
• Not at increased risk
• Pre-pregnancy weight less than 100 pounds
• Reduced intrauterine growth of the mother is a risk
factor .

16. 2. Maternal nutrition before and during pregnancy
-Glucose, amino acids and oxygen are deficient
during pregnancy
3. Social Deprivation
effects of associated lifestyle factors such as
smoking, alcohol or other substance abuse, and
poor nutrition.
4. Maternal diseases
Anemia(sickle cell disease, hereditary anemias),
hypertension, thrombotic diseases, heart diseases,
chronic renal disease, collagen vascular disease

17. 5. Toxins
Alcohol, smoking, cocaine, heroin, drugs
6. Antiphospholipid Antibody Syndrome
maternal platelet aggregation and placental
thrombosis.
7.Extrauterine Pregnancy

18. 2. Fetal abnormalities: There is enough substrate in the
maternal blood and also crosses the plecenta but it is
not utilized by the fetus
Fetal Substrate not utilized by fetus
1. Structural anomalies - cardiovascular, renal
2. Chromosomal abnormality - 8-12% growth retarded
infants - Triploidy, aneuploidy - Trisomies( 13, 18, 21),
Turner’s syndrome
3. Infection • TORCH and malaria
4. Multiple pregnancy Mechanical hindrance to growth
and excessive fetal demand

19. 3. Placental
• Poor uterine blood flow to placental site for a long
time
• This leads to chronic placental insufficiency with
inadequate substrate transfer
• Placenta praevia, Abruption, circumvallate, infarction,
mosaicism
4.Unknown- 40%

20. Pathophysiology
• Reduced availability of nutrients in mother
• Reduced transfer by placenta to fetus
• Reduced utilisation by fetus Brain size (asymmetric) as well as cell no
(symmetric) are reduced .
Liver glycogen content is reduced
Renal and pulmonary contribution to amniotic fluid are diminished due to
reduced blood flow to these organs
Oligohydramnios
SGA fetus is at risk of intrauterine hypoxia and acidosis if severe
Intra uterine fetal death.

21. Diagnosis
Clinical
• Palpation of uterus
Fundal height
Liqour volume
Fetal mass
• SFH
Closely correlates with gestational age after 24 weeks
Lag of 4 cm or more- IUGR
Fairly sensitive (30-80%)
Serial measurement is important
• Maternal weight gain
- stationary or falling during second half of pregnancy
• Abdominal girth
stationary or falling.
Investigations
Hemoglobin Blood group- ABO, Rh Urine- sugar, albumin, microscopy, culture and
sensitivity HIV, STS TSH HbSAg OGTT.

22. Biophysical
• First examination(16-20 weeks) should confirm gestational age,
anomalies
• USG
• 2-3 weekly •
2.diagnosis of IUGR
Sonographic predictive values that are
commonly used are
Head circumference (HC)
 Abdominal circumference(AC)
Femur length (FL)
Amniotic Fluid Volume

23. Head circumference/ Abdominal circumference
ratios
1-before 32 weeks Elevated-
asymmetrical IUGR
=1 - 32-34 weeks Normal –
asymmetrical IUGR
<1- after 34 weeks 85% IUGR fetuses
are detected AC-Single
most sensitive parameter
2-Femur length
Not affected in asymmetric IUGR
FL/AC =22 from 21 weeks to term
FL/AC> 23.5- IUGR.

24. 3-Amniotic fluid volume
Vertical pocket of amniotic fluid <1 cm suggests IUGR
Four quadrant technique –measuring vertical
diameter of largest pockets of fluid found in each of 4
quadrants of uterus. The sum of results is AFI AFI 5
to 25 cm- normal AFI< 5 cm- oligohydramnios.
4-Anatomical survey:
To exclude fetal abnormalities

25. Ultrasound Doppler parameters
1. Doppler velocimetry
Elevated systolic or diastolic ratio, the resistance index(RI) and the
pulsalioty (PI) indicate increased blood flow resistance and
decrease in end diastolic velocity. It is associated with IUGR and
Intra uterine fetal hypoxia.
2. Uterine Artery
The presence of diastolic notch suggests incomplete invasion of
placental trophoblasts to the uterine spinal arteries.
It predicts possible development of pre-eclampsia.
Normally the diastolic flow increases as pregnancy progress

26. 3. Umbilical artery
Decreased en diastolic velocity indicates increased
placental vascular resistance.
There is progressive decrease in the umbilical artery, end
diastolic velocity – reduced fetomaternal O2 and
nutrient exchange.
4. Umbilical artery Doppler study
It should be primary surveillance tool in the IUGR fetus.
It predicts, moderates acidosis and recommends delivery
when there presence of AREDV

27. 5. AREDV
It indicates fetal jeopardy and poor perinatal outcome.
6. Umbilical venous pulsations
Indicates inefficient cardiac output with rise in central venous pressure-
impending cardiac failure.
7. Middle cerebral Artery (MCA)
Method to assess the resistance to flow in the fetal brain circulation.
Increased diastolic velocity (Brain sparing effect) is observed in IUGR due to
cerebral vasodilatation in response to hypoxemia.
8. Biochemical markers
A low level of PAPP-A in maternal serum in the first trimester of pregnancy is
considered a marker of major risk factor for IGUR.

28. Complications
1. Fetal
• Antenatal
chronic fetal distress, fetal death, diminished amniotic fluid volume
increases the likelihood of cord compression
• Intranatal
hypoxia, acidosis • After birth- immediate –late
2.Immediate
• Asphyxia , bronchopulmonary dysplasia and RDS
• Hypoglycemia due to shortage of glycogen reserve in liver because
of chronic hypoxia
• Meconium aspiration syndrome
• Microcoagulation leading to DIC
• Hypothermia

29. Complications
• Pulmonary hemorrhage
• Polycythaemia, anemia, thrombocytopenia
• Electrolyte abnormalities ,
• Multiorgan failure
• Increased perinatal mortality and morbidity
3. Late
• Symmetrical growth retarded baby is likely to grow slowly after
birth
• Asymmetrical- catch up growth in early infancy

30. Long term complications:
• retarded neurologic and intellectual development in infancy
• Increased risk- metabolic syndrome in adult life: obesity, hypertension,
diabetes, coronary heart disease
• altered orexigenic mechanism that causes increased appetite and reduced
satiety 4. Reduced no of nephrons- renal vascular hypertension
• Maternal
• Per se IUGR does not cause any harm to mother
• Underlying disease process like pre-eclampsia, heart disease, malnutrition may
be life threatening

31. Immediate neonatal mortality
- 6 times more than normal newborn or even similar weight appropriate to
shorter gestational age Most babies
- die within 24 hours Morbidity rises to 50%.
Management
• Constitutionally small- no intervention
• symmetric IUGR
• investigated for anomalies, infections, genetic syndromes -No
effective therapy
• Placental disease or reduced placental blood flow
May be given some treatment

32. General
Antepatum
evaluation
Time of
delivery
Methods of
delivery
Care during
vaginal delivery
Immediate care
of the baby after
birth
It includes

33. 1.General
No proven therapy for reversing IUGR once it has established
• Adequate bed rest specially in left lateral position
• Correct malnutrition by balanced diet- 300 extra calories per day
• Appropriate therapy for complicating factors likely to produce IUGR
• Avoidance of smoking, alcohol
• Maternal hyperoxygenation at the rate of 2.5 mL/min by nasal prong ,for short
term prolongation of pregnancy
• Low dose aspirin (50 mg daily) in selected cases with history of thrombotic
disease, hypertension, pre- eclampsia or IUGR
2. Antepartum evaluation
Serial evaluations of fetal growth and assessment of well being should be done
1.USG: intervals of 3-4 weeks for assessment of BPD, HC/AC, fetal weight and AFI
2. Fetal well being
kick count, NST, biophysical profile, amniotic fluid volume and cordocentesis
for blood

34. 1.General
No proven therapy for reversing IUGR once it has established
• Adequate bed rest specially in left lateral position
• Correct malnutrition by balanced diet- 300 extra calories per day
• Appropriate therapy for complicating factors likely to produce IUGR
• Avoidance of smoking, alcohol
• Maternal hyperoxygenation at the rate of 2.5 mL/min by nasal prong ,for short
term prolongation of pregnancy
• Low dose aspirin (50 mg daily) in selected cases with history of thrombotic
disease, hypertension, pre- eclampsia or IUGR

35. 2. Antepartum evaluation
Serial evaluations of fetal growth and assessment of well being should be done
1.USG: intervals of 3-4 weeks for assessment of BPD, HC/AC, fetal weight and AFI
2. Fetal well being
kick count, NST, biophysical profile, amniotic fluid volume and cordocentesis
for blood gases
3 . Doppler ultrasound parameters

36. 3. Time of delivery Factors to be considered:
1. Presence of fetal abnormality
2. Duration of pregnancy
3. Degree of growth restriction
4. Associated complicating factor
5. Degree of fetal compromise
6. Previous obstetric history
7. Availability of NICU
Optimal time of delivery
1. Beyond 37 weeks Delivery should be done
2. Before 37 weeks
a) Uncomplicated mild IUGR:
General treatment
Placental function may improve
pregnancy is allowed to continue till at least 37 weeks

37. (b) Severe degree of IUGR
• If lung maturation is achieved:
Presence of phosphatidyl glycerol and L:S ratio at least 2 from amniotic fluid
study
termination
• Lung maturation not yet achieved
problems- prematurity, growth restriction Preterm IUGR requires highest level of
NICU.
Betamethasone therapy - <34 week
Corticosteroid reduce risk of neonatal HMD and IVH

38. Methods of delivery
Route and time decided considering:
1. Severity of IUGR
2. Maternal condition
3. Any other obstetric complication
Low rupture of membranes followed by oxytocin
• Beyond 34 weeks with favourable cervix and head is deep in pelvis
• PGE2 gel when cervix unfavourable
Intrapartum monitoring by clinical , continuous electronic and scalp blood
sampling is needed as risk of intrapartum asphyxia is high
Precautions
Caesarean section without a trial of labour- when risks of vaginal delivery are
more( fetal acidemia, absent or reversed diastolic flow in umbilical artery or
unfavourable cervix)

39. Care during vaginal delivery
• Equipped institution where intensive intranatal monitoring (clinical and electronic) is
possible and having facilities for NICU.
First stage
• Ensure adequate fetal oxygenation by giving oxygen to mother by mask
• Epidural analgesia is of choice
• Labour carefully monitored preferably with continuous EFM
Second stage
• Birth should be gentle and slow to avoid rapid compression and decompression of head
• Episiotomy may be done to minimise head compression
• Tendency to delay is curtailed by low forceps • Cord is to be clamped immediately at birth
Immediate care of the baby
A pediatrician should be available at the time delivery
The baby should be placed preferably in the neonatal intensive care unit.

40. Management protocol of IUGR
•To confirm IUGR and type
•To exclude cong malformation
•To treat specific cause if found
•Fetal surveillance
• Daily fetal movement count
• Cardiotocography, NST
• Biophysical profile
• Doppler USG parameters, umbilical vein

41. Management protocol of IUGR
Pregnancy< 37 weeks Delivery Pregnancy >= 37 weeks
Severe IUGR Mild IUGR
•Increased rest
•Folic acid
•Increased fliud intake
•General management
•Fetal monitoring till 37 weeks
Delivery
Equipped centre Centre with
limited facilities In utero
transfer to a referral centre
Fetal surveillance
Reassuring Non reassuring
fetal status fetal status
Doppler after 1 week assess lung maturity
Delivery

42. Assess lung maturity
•L:S ratio
•Phosphatidyl
glycerol level
Not mature
Delivery
Betamethasone therapy
Delivery
Mature

43. Presented by
Ms Mamatha
B.Sc Nursing