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Dilemmas in Diagnosis and Management of FGR Dr NNC 06082022.pptx
1. DILEMMAS IN DIAGNOSIS
AND MANAGEMENT OF FGR
Dr. Niranjan Chavan
National FOGSI Conference – Obstetric Dilemmas
06th August 2022
2. Professor and Unit Chief, L.T.M.M.C & L.T.M.G.H, Sion Hospital
Joint Treasurer, FOGSI (2021-2024)
President, MOGS (2022-2023)
Member Oncology Committee, SAFOG (2021-2023)
Joint Secretary, AFG(2022-2023)
Dean AGOG & Chief Content Director, HIGHGRAD & FEMAS Courses
Editor-in-Chief, FEMAS, JGOG & TOA Journal
60 publications in International and National Journals with 109 Citations
National Coordinator, FOGSI Medical Disorders in Pregnancy Committee (2019-2022)
Chair & Convener, FOGSI Cell Violence Against Doctors (2015-16)
Member, Oncology Committee AOFOG (2013-2015)
Coordinator of 11 batches of MUHS recognized Certificate Course of B.I.M.I.E at L.T.M.G.H (2010-16)
Member, Managing Committee IAGE (2013-17), (2018-20), (2022-2023)
Editorial Board, European Journal of Gynaec. Oncology (Italy)
Course Coordinator of 3 batches of Advanced Minimal Access Gynaec Surgery (AMAS) at LTMGH
(2018-19)
DR. NIRANJAN CHAVAN
MD, FCPS, DGO, MICOG, DICOG, FICOG, DFP,
DIPLOMA IN ENDOSCOPY (USA)
3. “
”
EVERY CHILD COMES WITH THE MESSAGE THAT GOD
IS NOT YET DISCOURAGED OF MAN
Rabindranath Tagore
4. FETAL GROWTH RESTRICTION
• Fetal growth restriction (FGR) is a pathological condition in
which a fetus fails to achieve its genetic growth potential
• It comes under a much broader concept of small for
gestational age (SGA) fetuses
• SGA also carries under it babies that are constitutionally small
but have achieved their growth potential and hence are not
associated with adverse perinatal outcomes, much unlike FGR
fetuses
• FGR can be classified grossly as ones beginning before 32 of
gestation (early FGR) vs the ones after (late FGR)
5. • 3 - 5% of all pregnancies
• 20 % of still borns are growth restricted
• 1/3 of infants with BW < 2750 gms are growth
restricted and not premature
• Only 20-30% of growth restricted fetuses are small
due to pathological restriction of growth
• Perinatal mortality is 8 - 10 times higher for these
fetuses
INCIDENCE
6. AETIOLOGY
• General-
• Racial / Ethnic origin, Small maternal / paternal height
/weight, Fetal sex
• Maternal causes
• Fetal causes
• Placental causes
• Idiopathic - In a majority of cases (40%) the cause is
unknown– probably due to placental insufficiency
7. • Previous baby who suffered from
IUGR
• Extremes of age
• Is small in size (Ht & Wt)
• Has poor weight gain and
malnutrition during pregnancy
• Is socially deprived
• Has a low total blood volume
during early pregnancy
MATERNAL RISK FACTORS
8. • Uses substances (like tobacco,
narcotics, alcohol) that can cause
abnormal development or birth
defects
• Multiple Gestation
• High altitude
• Has a cardio-vascular disease-
preeclampsia, hypertension,
cyanotic heart disease, cardiac
disease Grade III & IV, diabetic
vascular lesions
9. • Chronic kidney disease
• Chronic infection- UTI, Malaria, TB, genital
infections
• Has an antibody problem that can make
successful pregnancy difficult (antiphospholipid
antibody syndrome, SLE)
MATERNAL RISK FACTORS
10. • Intrauterine infections - German measles (rubella), cytomegalovirus, herpes
simplex, tuberculosis, syphilis, or toxoplasmosis, TB, Malaria, Parvo virus
B19
• A birth defect (cardiovascular, renal, anencephaly, limb defect, etc)
• A chromosome defect - Trisomy-18 (Edwards’ syndrome), 21(Down’s
syndrome), 16, 13, XO (Turner’s syndrome)
• Primary disorder of bone or cartilage
• Chronic lack of oxygen during development (hypoxia)
• Placenta or umbilical cord defects
• Exposure to Teratogens/Drugs(Anti-convulsant, Anticoagulants, Alcohol,
Narcotics)
FETAL RISK FACTORS
11. • Uteroplacental insufficiency resulting from -
• Improper / inadequate trophoblastic invasion
and placentation in the first trimester
• Lateral insertion of placenta
• Reduced maternal blood flow to the placental
bed
• Fetoplacetal insufficiency due to -
• Vascular anomalies of placenta and cord
• Decreased placental functioning mass
• Small placenta, abruptio placenta, placenta
previa, post term pregnancy
PLACENTAL FACTORS
12. 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
95% of fetal weight gain occurs during last 20 weeks of gestations
13. • The optimal definition of growth restriction, in particular the differentiation between physiological (SGA) and
pathological (IUGR) small fetal size, is one of the most common, controversial, and complex problems in modern
obstetrics
• There is greement internationally that an EFW <10th centile for gestation should alert clinicians to potential small
fetal size
• All fetuses with an EFW <3rd centile, or those fetuses with a combination of EFW <10th centile and abnormal
UA Doppler, are at increased risk of either adverse perinatal outcome or NICU admission when compared to
those with EFW or AC <10th or <5th centiles or normal UA Doppler indices
14. DEFINING FGR USING USG
For less than 32 weeks:
1. AC/EFW < 3rd centile or,
2. AEDF in the Umbilical Artery (UA) or,
3. AC/EFW < 10th centile + Uterine Artery (UtA) and/or UA PI > 95th centile
For more than 32 weeks:
1. AC/EFW < 3rd centile or,
2. AC/EFW < 10th centile + UA PI > 95th centile or CPR < 5th centile
15.
16. INDIVIDUAL DOPPLER INDICES AND FGR
Placental Development Indicators:
• Uterine Artery Doppler: Carries a moderate
degree of predictive value for adverse perinatal
outcome when performed between 20-24
weeks of gestation. Persistence of these
changes carries higher risk.
• Umbilical Artery Doppler: With increasing
gestation, a gradual decrease in PI is normally
seen. Whereas in patients with poor
trophoblastic invasion, this is reversed
17. Fetal Indices:
• Middle Cerebral Artery Doppler: Normally the PI increases with
course of gestation, but as a result of chronic hypoxemia, there is
cerebral vasodilation and decreased PI and CPR, leading to brain
sparing effect.
• Develops before 32 weeks when there was already impaired
placentation or after 32 weeks when fetal metabolic demands
exceed normal placental limits
• Ductus Venosus Doppler: Increased PI and retrograde a wave
reflects onset of overt cardiac compromise
18. AFI AND FGR
• Amniotic fluid index is an indicator of fetal renal
perfusion, which lower values reflecting
shunting of blood from kidneys to the brain
• Deepest vertical pocket is a better indicator
than AFI as a predictor of fetal well being over
last 2-3 weeks
19. Early-Onset FGR Minimum Surveillance
Frequency
UA Doppler PI >95th centile, no other
testing abnormalities
Every 2 weeks Doppler, weekly
BPS or cCTG
Low MCA PI or CPR Weekly Doppler with BPS or cCTG
UA absent end-diastolic flow
(AEDF)
Consider admission, twice weekly
Doppler with BPS or cCTG
UA reversed end-diastolic flow,
increased DV or oligoamnios
(deepest pool <2 cm)
Admission, 3 times per week Doppler
with BPS, daily CTG or cCTG
Absent or reversed DV
a-wave
Daily Doppler with BPS or cCTG
in preparation to delivery
Late-Onset FGR Minimum Surveillance
Frequency
UA Doppler PI >95th centile, no other
testing abnormalities
Weekly Doppler with BPS
Low MCA PI or CPR 2-3 times/week Doppler with BPS
Minimum Surveillance Frequency Prior to the
Delivery Threshold
23. ROLE OF DOPPLER IN SELECTIVE FGR
• sFGR, conventionally, is defined as a condition in which
one fetus has EFW < 10th centile and the intertwin EFW
discordance is > 25%
• According to the NICE guidance (year), EFW
discordance should be calculated and documented at
every scan from 20 weeks onwards.
• If this discordance reaches 25% or more, increased fetal
surveillance, including fetal Doppler, and planning of
delivery when appropriate , is warranted
24. CLASSIFICATION OF MONOCHORIONIC TWIN
PREGNANCY COMPLICATED BY SFGR
Classification of sFGR in monochorionic twins
depends on the pattern of end-diastolic velocity
at umbilical artery Doppler -
In Type I, the umbilical artery Doppler waveform
has positive end-diastolic flow. The survival rate
in Type-I sFGR is greater than 90% (in-utero
mortality rates of up to 4%).
25. • In Type II, there is absent or reversed
end-diastolic flow (AREDF).
• Type-II, sFGR is associated with
• A high risk of IUD of the growth-
restricted twin a and/or
• Very preterm delivery with associated risk
of neurodevelopmental delay if the other
twin survives (IUD of either twin in up to
29% and
• Risk of neurological sequelae in up to
15% of cases born prior to 30 weeks)
26. • In Type III, there is a cyclical/intermittent
pattern of AREDF.
• Type-III sFGR is associated with a 10–20%
risk of sudden death of the growth-
restricted fetus, which is unpredictable
(even in cases in which ultrasound features
have been stable).
• There is also a high (up to 20%) associated
rate of neurological morbidity in the
surviving larger twin
27. MONITORING CASES WITH SFGR
• In monochorionic twin pregnancy complicated by sFGR, fetal growth
should be assessed at least every 2 weeks, and fetal Doppler (umbilical
artery and MCA) at least weekly
• If the umbilical artery Doppler is abnormal, an assessment of the DV blood
flow should be undertaken
• The aim in managing these pregnancies is to prolong the pregnancy at
least until viability is achieved, while at the same time avoiding a single IUD
with its associated severe consequences for the surviving cotwin
28. • 8.8% neonates delivered had birth weight of<2.5 kg out of which 20% had intrauterine growth restriction and
22.4% were preterm
29. • 40% babies delivered had birth weight of <2.5 kg out of which 13.33% had IUGR and 26.66% were preterm
30. CASE 1
• 32 year G2P1L1 k/c/o GDM on
PI 8-8-8 came at 38 weeks by
scan
• On examination BP was
160/100 mm Hg
• P/A –
• Ut 34 weeks, Cephal, FHS
regular 150-160 bpm, relaxed
• Doppler Findings –
• Raised PI of Umbilical Artery
• Absent End Diastolic flow (AEDF)
at fetal site
• Raised PI of Left uterine artery
with Early Diastolic notch
• Pathological CPR with Reduced
PI of MCA s/o brain sparing
effect
• What is the next step in Management?
31. • Features are suggestive of Late onset IUGR
• Immediate delivery by caesarean section after steroid cover if CTG facility available
32. CASE 2
• 26 year old primigravida 32
weeks B/S came with BP-
160/110 with premonitory
symptoms
• P/A- Ut 24-26 weeks,
Cephal, fhs regular 140-150
bpm, relaxed
USG Findings –
• Single live intrauterine gestation of
approximate gestational age of 29-
30 weeks
• Scanty liquor – AFI 1-2
• Relatively smaller abdominal
parameter
• EFW – 1137+/- 166gms
• Above findings suggest IUGR
• Fetoplacental insufficiency with
absent diastolic flow on Colour
Doppler
• No evidence of utero-placental
insufficiency on Colour Doppler
What is the next step in management?
34. CASE 3
• 24 year primigravida with 32.3
weeks BS came with raised BP of
140/90 mm Hg for the first time,
UA trace, knee jerks normal, no
PMS
• P/A- Ut 30 week size, cephal, FHS
regular at 130-140 bpm, relaxed
• USG Obs doppler done
Doppler Findings –
• Raised PI of Umbilical Artery
• B/L Uterine artery shows Early
Diastolic Notch
What will be your plan of action?
35. • Late Onset IUGR with only Raised PI of Umbilical Artery
• Weekly Doppler with Biophysical Score
36. TAKE HOME MESSAGES
• Fetal growth restriction (FGR) is a pathological condition in which a fetus
fails to achieve its genetic growth potential
• FGR can be Early or Late Onset depending upon gestational age at occurrence
• Abnormal Umbilical Artery Doppler and EFW < 3rd centile were strongly and most
consistently associated with adverse perinatal outcome
• All fetuses with an EFW < 3rd centile, or those fetuses with a combination of EFW
< 10th centile and abnormal UA Doppler, are at increased risk of either adverse
perinatal outcome or NICU admission when compared to those with EFW or AC <
10th or < 5th centiles or normal UA Doppler indices
37. REFERENCES
1. Badawi N, Kurinczuk JJ, Keogh JM, et al. Antepartum risk factors for newborn encephalopathy: the
Western Australian case-control study. BMJ 1998;317:1549-53.
2. Barker DJ. Adult consequences of fetal growth restriction. Clin Obstet Gynecol 2006; 49:270-83.
3. American College of Obstetricians and Gynecologists. Intrauterine growth restriction. Wash- ington, DC:
American College of Obstetricians and Gynecologists; 2000.
4. Royal College of Obstetricians and Gynecologists. The investigation and management of the small-for-
gestational-age fetus (guideline no. 31). London: Royal College of Obstetricians and Gynecologists;
2002.
5. Lausman A, McCarthy FP, Walker M, Kingdom J. Screening, diagnosis, and management of intrauterine
growth restriction. J Obstet Gynaecol Can 2012;34:17-28.
6. Gardosi J, Chang A, Kalyan B, Sahota D, Symonds EM. Customized antenatal growth charts. Lancet
1992;339:283-7
7. Unterscheider J, Daly S, Geary MP, et al. Optimizing the definition of intrauterine growth restriction: the
multicenter prospective PORTO Study. Am J Obstet Gynecol 2013;208:290.e1-6.