Dr. Mariam Al-Bloushi Consultant Fetomaternal Women s ... · 1. In case of maternal clinical...
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Dr. Mariam Al-Bloushi
Consultant FetomaternalWomen’s Hospital Hamad Medical Corporation
DR. MARIAM ALBLOUSHI
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I have no financial interests or relationship to disclose
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Fetal Growth Restriction
Definition and prevalence
Aetiology – risk factors
Screening
Diagnosis
Monitoring
Timing of Delivery
Outline of Presentation
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Is IUGR = SGA
Is SGA a pathological condition ?
? ? ? ?DR. MARIAM ALBLOUSHI
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Is a major problem
in perinatal medicine
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Fetal growth restriction remains a major cause of perinatal morbidity and mortality in modern obstetric practice.
Placental insufficiency is the most common association, but is often a diagnosis of exclusion.
Currently, no treatment can ameliorate or reverse established growth restriction.
However the potentially exciting use of maternal gene therapy is being investigated (USOG March 2016)
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The clinical significance of FGR relates to the dramatically increased perinatal mortality:
with mortality being eight times higher when weight is below the 10th percentile .
nearly 20 times higher when weight is below the 3rd centile.
When associated with prematurity, outcomes are even worse with
survival figures of less than 50% for gestations less than 28 weeks.
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Perinatal Mortality and Birthweight
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increased mortality, both short- and long-term morbidity are increased in the growth-restricted fetus,
Short term neonatal complications :
birth hypoxia.
when combined with prematurity, increased risks of respiratory distress syndrome.
necrotising enterocolitis.
retinopathy of prematurity.
infection .
hypoglycaemia.
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long-term metabolic consequences growth restriction:
increased risks of insulin resistance. cardiovascular complications. psychiatric disorders.
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As a result of these effects on perinatal morbidity and mortality, accurate diagnosis and management of the
growth-restricted fetus remains one of the most important
goals of antenatal care
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Fetal “overgrowth”
Fetal growth restriction
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Most commonly used Birth weight below a defined centile for gestation, gender and race3rd or 5th or 10th
Fetal growth restriction (FGR, also called intrauterine growth restriction [IUGR]) is the term used to designate a fetus that has not reached its growth potential because of genetic or environmental factors.
Definition
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Failure of the baby to achieve its predetermined genetic growth potential
Small for Gestational age (SGA) – bwt<10th centile
Fetal growth restriction [FGR] is not synonymous
with SGA SOME, but not all [FGR] are SGA while 50-70% of SGA fetuses are constitutionally small .
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It may be caused by fetal, placental, or maternal factors, with significant overlap among these entities.
This term should not be used to describe a constitutionally small, but otherwise healthy fetus.
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Normal Growth Patters of Fetuses
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Constitutional – 50-70% of casesPathological – FGR
Non-placental mediated Structural Chromosomal In-born errors of metabolism Fetal infections
Placental mediated Essential hypertension Pre-eclampsia Autoimmune disease Thrombophilia Renal disease Diabetes
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Causes of FGR
Complex interaction
Fetal Growth
Restriction
Fetal•Chromosomal (T13,18,21 etc)
•Mendelian single gene disorders
•Congenital malformations
•Other syndromes (e.g. Cornelia de Lange)
•Inborn errors of metabolism
Extrinsic•Cigarette smoking
•Alcohol
•Substance abuse (e.g.cocaine, marijuana)
•Viral infections
Maternal•Hypertensive disorders
•Antiphospholipid syndrome
•Thrombophilias
•Hypermomocysteinema
•Low weight, severe anaemia,
Placental factors•Confined placental mosaicism
•Abnormal placentation
•Uterine abnormality
•Chronic placental abruption
Idiopathic
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Chromosomal abnormalities are present in
8% of those morphologically normal
30 - 40% of those with associated malformations
Common abnormalities – T13, 18 & 21
Others – Triplody and other trisomies
Monosomies (45XO)
Confined placental mosaicism – most (mitosis or somatic errors) arise from non-disjunction post fertilisation.
Non-chromosomal cases may be syndromes and other genetic abnormalities
Prevalence of Genetic abnormalities associated with FGR
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Risk factors for Small for Gestational Age
RCOG Green-Top Guideline No 31, 2013
Risk factor Odds Ratio
Maternal Risk FactorsAge >40 years 3.2Smoker > 11 cigarettes/day 2.21Cocaine use 3.23Daily vigorous exercise 3.23
Previous HistoryPrevious SGA 3.9Previous SB (unexplained) 6.4
Past Medical HistoryMaternal SGA 2.64Chronic hypertension 2.5Diabetes and vascular disease 6.0Renal Disease 5.3Antiphospholipid syndrome 6.22
Paternal Medical HistoryPaternal SGA 3.47
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Risk factors for Small for Gestational AgeRCOG Green-Top Guideline No 31, 2013
Risk factor Odds Ratio
Current Pregnancy
Heavy bleeding similar to menses 2.6
Echogenic bowel 2.3
Pre-eclampsia 2.26
PIH – severe 2.5
Unexplained APH 5.6
Low maternal weight gain 4.9
Low PAPP-A (<0.4MoM) 2.6
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Screening for FGR
Identification of risk factors
History
Physical examination – identifies maternal disease/complex pregnancies
Ultrasound Doppler velocimetry
Uterine artery
Biochemistry
αFP (AFP) (>2.5MoM) – not now considered important??
βhCG (>3.0 MoM) ? relevance
PAPP-A (<0.4MoM)
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Radiological Screening
Uterine Artery – only clinical useful screening tool available today
Why?
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UA Doppler at 20-24 week has a moderate predictive value for severly SGA fetus.
Abnormal uterine artery Doppler PI>95TH
centile or notching.
Serial ultrasound measurement of fetal size
& assessment of wellbeing with UA Doppler
at 26-28 week of pregnancy.
Normal uterine artery Doppler
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Specific pregnancy complications:
1- APH
2- Hypertension
However they should be offered a scan for fetal size & UmA Doppler during 3rd trimester.
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Diagnosis of FGR
Clinical Examination – SFH at each visit from 24 weeks, plotted on customised population-based charts –as this may improve prediction (not diagnosis).
□ Will identify ~30% of cases.
□ Inaccurate in women with BMI >35, fibroids,
polyhydramnios.
Serial USS biometry (AC & HC) every 2-3 wks combined with SFH – 67% of cases
Routine AC measurement in the 3rd trimester does not reduce risk of neonate with FGR
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AFI/SDVP/Dopplers – not used for diagnosis
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IUGR MANAGEMENT
A three step approach:
1. Recognition of IUGR.
2. Identification of etiology.
3. Monitoring and timing of delivery
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After the introduction of fetal ultrasonic biometry it became possible to move to a
prenatal recognition.
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WHICH BIOMETRIC PARAMETER?
1. Estimated fetal weight.
2. Abdominal circumference.
They should be at least 2-3 week apart to
minimise false –positive rates for diagnosing
FGR.
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Fetal Biometry
Biparietal Diameter and Head Circumference
T
T
CSP
AntPost
BPD
OFD
Atria
Frontal Horn
Frontal Horn
Insula
*
* 3° Ventricle
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Fetal Biometry
Abdominal Circumference
Stomach
Spine
Umbilical
Vein
Aorta
IVC
Left portal vein
Left
Right
Ant Post
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Fetal Biometry
Femur Length
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CRITERIA FOR IUGR RECOGNTION BY US BIOMETRY
To know exactly the GA.
To compare the biometry with growth charts (customized)
To repeat the scan at >2 weeks distance.
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Clinically suspected FGR
Ultrasound scan to confirm diagnosis?
Yes - diagnosis confirmed
Questions
What is the type of FGR?
Any associated aneuploidy or infection?
Is delivery warranted?
When is delivery recommended or appropriate?
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What is the type of FGR?
Symmetrical/asymmetrical
Based on Ratio of HC to AC
Reduced AFI/SDVP
Any fetal abnormalities?
Fetal vascular studies – umbilical and middle cerebral
Maternal vascular – uterine artery Dopplers
Co-existing pathology e.g pre-eclampsia
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Any associated infection or thrombophilia?
Infection screen – maternal blood and fetal specimens
CMV, Toxoplasmosis
Syphilis in high risk populations
Malaria in high risk populations
Thrombophilia – changes with pregnancy
Undertake these only if indicated
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Any associated karyotypicabnormality?
When is karyotyping necessary?
Symmetric FGR (especially <24 wks.) with
Normal AFI
Polyhydramnios
Normal umbilical artery Doppler
Normal uterine artery Doppler
FGR and Structural abnormalities
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Monitoring of FGR
Fetal biometry.
Doppler of the fetal arterial circulation.
Doppler of the fetal venous circulation.
Biophysical profilometry.
Fetal kick chart.
Cardiotocography.
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Any Interventions to prevent FGR?
Antiplatelet agents – effect size is small though
In women at risk of PE
Started at or before, 16 weeks (maybe started after)
Smoking cessation promotion
No evidence that dietary modification ,progesterone and calcium make improve outcome
Anti-thrombotic therapy – promising but no sufficient evidence yet
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Management of IUGR is dependent on the primary etiology of IUGR
1. In case of maternal clinical conditions like preeclampsia it is mainly dependent on the characteristics of the maternal disease.
2. when the etiology is fetal {infection, chromosomal abnormalities & malformations} no management can significantly improve the outcome & sometime it can be considered as a contraindication for aggressive management.
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4. Affected by CFH the fetus undergoes changes of many vital function ,so the close monitoring of these changes is the basis of the management .
3. Placental obliterative vasculopathy, the out come can be improved & the management should be based on its careful monitoring.
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As the only therapy for CFH is the delivery it is crucial to choose the best timing.
The most commonly used methods are represented by:
- Doppler studies.- CTG.- Amniotic fluid evaluation.- Fetal biophysical profile.
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UmA Doppler is the primary surveillance tool in the SGA fetus.
When UmA Doppler flow indices are normal
………… 2 week
UmA Doppler flow indices are abnormal
– P or RI ≥2 SD & delivery is not indicated repeat Doppler twice weekly (i.e. every 2-3 days)
– A&REDF – Repeat Doppler Daily.
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Management of FGR
Delivery Timing – when fetal maturity is maximum
Balancing the risks of a hostile intrauterine environment and those of early delivery
Prematurity
Intrauterine asphyxia and death
Neonatal complications
Operative maternal delivery
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Timing of delivery
When risk of intrauterine existence exceeds that of extra-uterine existence
This is achieved through monitoring
Timing difficult for FGR between 24-28 weeks
GRIT Trial – (Hornbuckle et al BJOG 2003 2003) no answer
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Interventions at the time of delivery
Corticosteroids if:
Delivery contemplated between 24+0 and 35+6 weeks
Magnesium sulphate if <30 weeks may be neuroprotective (Cochrane Review 2016)
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Factors influencing the timing of delivery
Gestational age
Neonatal facilities and survival rates for unit
Growth profile
Health of the mother
Indices of fetal health/well being - MONITORING
CTGs
Dopplers – UmA, MCA, Ductus venosus other vessels
Amniotic fluid index/SDVP
Fetal blood gases
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Thank you
DR. MARIAM ALBLOUSHI