3. INTRODUCTION
IUGR is a common and complex obstetric problem
3 - 10% of all pregnancies
50 % of preterm stillbirths/ 25% of term stillbirths.
Perinatal mortality is 8 - 10 times higher for these fetuses: 6- 30% in developing
countries
IUGR is the second leading cause of perinatal mortality
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4. DEFINITIONS
IUGR is failure of a foetus to reach its full growth potential.
EFW ≤ 10th percentile for GA- (ACOG and RCOG)
EFW < 2 SDs below mean weight for GA
AC < 10% for GA
EFW ≤ 5th percentile for GA
Ponderal Index < 10th percentile
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5. Normal & IUGR Newborn babies
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6. PATHOPHYSIO -1 (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
Stage III ( Hypertrophy)
- 28 to 40 weeks
- Rapid increase in cell size.
- Rapid accumulation of fat, muscle
and connective tissue.
80% of fetal weight gain occurs during
last 20 weeks of gestations.
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7. PATHOPHYSIO-2 DETERMINANTS OF FETAL GROWTH
Maternal nutrition and health status- weight and height
Uteroplacental blood flow
Uteroplacental substrate uptake
Placental transfer function
Umbilical blood flow
Fetal endocrine status
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9. CLASSIFICATION
Based on onset in pregnancy, cause and prognosis
Symmetric: early onset, proportionate decrease in all organs, ≈ 20%
Assymetric : late onset ,disproportionate decrease in all organs- AC
affected > HC- 80%
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10. Classification
• Based on USS examination small fetuses are divided
into two categories
Healthy SGA or True IUGR
or
Constitutionally small Pathologically growth
restricted
Type –I Type –II
Symmetrical IUGR Asymmetrical IUGR
Intrinsic IUGR Extrinsic IUGR01/10/2016 Okechukwu Ugwu 10
11. Symmetrical IUGR(20%)
Growth inhibition in stage I (hyperplastic stage):
- Reduced number of cells in fetus.
- Normal cell size.
Features-
Uniformly small
Ponderal Index(Birth wt /𝐿𝑒𝑛𝑔ℎ𝑡3) −Normal
HC/AC-Normal
FL/AC-Normal
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12. Asymmetrical IUGR(80%)
Pathophysiology
Growth Inhibition in Stage II/III (Hyperplasia &
Hypertrophy)
-Decrease in cell size and fetal weight
-Less effect on total cell numeric, fetal length,
head circumference.
Features
Head > Abdomen(Due to brain sparing effect)
Ponderal Index(Birth wt /𝑙𝑒𝑛𝑔ℎ𝑡3) -Low
HC/AC- Increased
FL/AC- Increased
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20. MANAGEMENT-1
Gestational age at diagnosis, confirmed aetiology, Risk of IUD versus
preterm delivery, level of expertise- Paradox
Parental counselling extremely important
Each case must be individualized
Investigating for underlying causes and instituting appropriate
treatment
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21. MANAGEMENT -2
Fetal movement count (FMC)
Biophysical profile (BPP)/modified BPP
Serial USS for growth
Doppler studies
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23. Timing of Delivery
At present there is no effective intervention to alter the course of FGR except delivery-
GRIT
Risk of fetal hypoxaemia and acidaemia versus complications of prematurity must be
weighed
Evidence of fetal Lung maturity
Delivery should be considered at or near term
Must be in a center with facilities for CS and Neonatal care
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24. GROWTH RESTRICTION NEAR TERM
Prompt delivery is likely best for the foetus
Most obstetricians recommend delivery from 34 weeks and beyond
With reassuring foetal surveillance, Vaginal delivery may be attempted
Expectant management can be guided using Antepartum foetal surveillance
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25. GROWTH RESTRICTION REMOTE FROM TERM
Observation is recommended while doing foetal surveillance
Screen for likely aetiology
Managements decision depends on relative risk of foetal death versus preterm
delivery
No specific treatment measure ameliorates the condition.
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26. TREATMENT MEASURES
Admission, Bed rest- Left lateral position
Improving diet
Cessation of alcohol, smoking, illicit drugs
Corticosteroids
Frequent antenatal visits
3-4 Weekly USS for EFW
Aspirin, nitric oxide donors
MgSO4
Phosphodiesterase inhibitors Sildenafil
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27. Mode of Delivery
Every case must be individualized
Determinants: underlying aetiology, GA, severity of IUGR, fetal surveillance
Parameters, Facilities available
Obstetric factors e.g. malpresentation
Vaginal delivery
Low threshold for CS
CS better with severe growth restriction
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28. Mode of Delivery
• Fetuses with significant IUGR should be preferably delivered in well equiped
centres which can provide intrapartum continuous fetal heart monitoring , fetal
blood sampling and expert neonatal care.
• Vaginal delivery: can be allowed as long as there is no obstetric indication for
caesarian section and fetal heart rate is normal.
• Fetuses with major anomaly incompatible with life should also be delivered
vaginally.
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29. Labour and Delivery
Intense surveillance in labour
High risk of fetal distress, cord compression
Use of Pantograph
Continuous electronic fetal monitoring
Left lateral position
O2 administration (if indicated)
Low threshold for CS
Neonatologist or personnel skilled in NN resuscitation present
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30. Caesarian section
These include:
Repetitive late decelerations
poor biophysical profile
reversal of end diastolic flow in umbilical artery
abnormal venous doppler
blood gas analysis showing acidic pH on cordocentesis.
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32. COMPLICATIONS- Long term
Risk of IHD, stroke ,HTN, DM , Metabolic syndrome
Low IQ
Short stature in adult life
Poor neurologic and cognitive function
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33. Prevention
• Improvement in nutritional status
• Preconception counseling and care
• Malarial antiprophylaxis
• Cessation of smoking, alcohol and illicit drug use
• Low dose aspirin
• Correction of anaemia, iron supplememtation
• Care with use of medications
• Immunization with rubella vaccine in susceptible females
• protein/energy supplementation
• vitamin/mineral supplementation
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34. Conclusion
IUGR is associated with high perinatal morbidity and
mortality. It is important for obstetricians to recognize the
foetus(es) at risk of IUGR. The foremost priority is to
establish the dating criteria and further identify the
modifiable risk factors and optimize the maternal systemic
disease.
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35. REFERENCES
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Obstet Gynecol Rep. 2013;2:102–11
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diagnosis, and management. Am J Obstet Gynecol (AJOG) 2011;204:288–300
3. Juncao C, Xiaoyuan G, Pingyang C. Effect of L-arginine and sildenafil citrate on intrauterine
growth restriction fetuses: a meta-analysis. BMC Pregnancy Childbirth. 2016; 16: 225.
4. Nassar AH, Masrouha KZ, Itani H, Nader KA, Usta IM. Effects of sildenafil in Nω-nitro-L-
arginine methyl ester-induced intrauterine growth restriction in a rat model. Am J
Perinatol. 2012 Jun;29(6):429-34
5. Radoń-Pokracka M, Huras H, Jach R. Intrauterine growth restriction--diagnosis and
treatment. Przegl Lek. 2015;72(7):376-82.
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Ultrasounds for Fetal Growth Restriction: A Pilot Randomized Clinical Trial. AJP Rep. 2016
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7. Ohkawa N, Shoji H, Ikeda N, Suganuma H, Shimizu T. Relationship between insulin-like
growth factor 1, leptin and ghrelin levels and catch-up growth in small for gestational age
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Notas del editor
In IUGR, challenge is to identify – Small but healthy and small but unhealthy.
Multifactorial- both the foetal genome and environment.
Cortisol- surfactant, deposition of glycogen in the liver via beta adrenoceptor receptors.
Villus proliferation and induction of digestive enzymes
Symmetric- Decrease cellular immunity- decrease size of thymus, small brains due decrease number of brain cells.
maternal caffeine consumption ≥ 300 mg per day in the third trimester40
Reversed umbilical artery Doppler EDF after 32weeks, Absent EDF after 34weeks, Reduced MCA PI/umbilical artery PI (cerebroplacental ratio) is therefore an early sign of fetal hypoxia
Maternally administered magnesium sulphate has a neuroprotective effect and reduces the incidence of cerebral palsy amongst preterm infants. Australian guidelines recommend the administration of magnesium sulphate when delivery is before 30 weeks of gestation.