POSTGRADUATE SEMINAR PRESENTATION SEPTEMBER 2016

1. Diagnosis and Management of
Intrauterine Growth Restriction
Dr Okechukwu Ugwu
Lagos University Teaching Hospital.
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2. OUTLINE
INTRODUCTION
DEFINITIONS
PATHOPHYSIOLOGY
CLASSIFICATION OF IUGR
RISK FACTORS
DIAGNOSIS
MANAGEMENT
COMPLICATIONS
PREVENTION
CONCLUSION
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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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8. PATHOPHYSIO-3 Physiology of Growth Factors
Glucose
IGF-1
IGF-2
Thyroxine- cerebral and skeletal
Leptin
Angiogenic factors
Cortisol
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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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13. RISK
Maternal
Placental
Foetal
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14. RISK FACTORS- MATERNAL
Maternal malnutrition
low socioeconomic status
Substance abuse/Alcohol
Maternal BMI
Previous hx of IUGR baby
Smoking
Drugs- warfarin, anticonvulsants, antineoplastic agents, and folic
acid antagonists
 Maternal Chronic anaemia
Caffeine
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15. RISK FACTORS-2 MATERNAL
Hemoglobinopathies
High altitudes
short inter pregnancy interval
ART
maternal disease conditions- HTN, DM, Renal dx, PE.
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16. RISK FACTORS-3 PLACENTA
Placental abruption,
Placental infarction
Foetal villous obliteration
Diffuse chronic villitis
Placental haemangioma
Single umbilical artery
Velamentous cord insertion
Placenta praevia
Chorioangioma
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17. RISK FACTORS-4 Foetal
Congenital malformations
Inborn errors of metabolism
Congenital Infections
Chromosomal anomalies
Multiple pregnancies
sex ( male 150 -200g >female )
Single gene disorders such as Cornelia de Lange syndrome, Russell
Silver syndrome, Fanconi’s anemia, Bloom syndrome
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18. Diagnosis- 1
Establish accurate dating
Identification of risk factors by obtaining medical history
 BP, Urinalysis
SFH/ Abdominal girth
Infectious workup/MP/FBC
Ultrasound- Biometry
HC/AC ratio, FL/AC ratio, BPD
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19. Diagnosis-2
 Ponderal index (PI),
Amniocentesis
serum analytes screening
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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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22. Doppler Studies
Recent advances in foetal surveillance technique
Umbilical artery
MCA
Ductus Venosus
Descending aorta
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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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31. COMPLICATIONS- Neonate
Prematurity
Perinatal asphyxia
Meconium aspiration
Sepsis
NEC
Stillbirth
SIDS
Increased PN morbidity and mortality
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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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