“ I AM A FETUS IN THE WOMB I FEAR IT MAY BECOME MY TOMB IF ONLY I COULD GIVE A SHOUT

1. Current role of ultrasound in detection and management ofpregnancies complicated by fetal growth restriction

2. FGR : Magnitude of the problem* Perinatal mortality 120/1000* 2nd leading contributor to perinatal mortality rate* 40% of all stillbirths are IUGR

3. What is in a name ?Intrauterine growth retardation (IUGR)Intrauterine growth restriction (IUGR)Fetal growth restriction (FGR)Small for gestational age (SGA)

4. Definition : Fetal growth restriction* Ultrasound estimated fetal weight or abdominal circumference suboptimal for gestational age * FGR = FETAL diagnosis ( not neonatal ) * Defining threshold : < 10th centile for gestational age < 5th centile for gestational age (worse outcome)

5. Definition : Small for gestational age (SGA)* Birth weight suboptimal for gestational age* SGA = NEONATAL diagnosis (not fetal)* Defining threshold : < 10th centile for gestational ageBirth ratio : Actual birth weight / Expected birth weight

9. “ I AM A FETUS IN THE WOMB I FEAR IT MAY BECOME MY TOMB IF ONLY I COULD GIVE A SHOUT TO MAKE MY DOCTOR GET ME OUT!” UNKNOWN MEDICAL STUDENT DUBLIN, UK 1982

10. Dilemmas in FGRHow to monitor When to deliver?cCTGArterial DopplersVenous Dopplers Biophysical profile

11. Dilemmas in management of FGR * Severe FGR due to placenta dysfunction - Progressive - No treatment to reverse the process * Timing of delivery - Risks : prematurity vs continued intrauterine life* Objective - Buy time to reduce prematurity risks, but deliver prior to organ damage * Question : Can this be accomplished ?* Answer : DOPPLER

12. Hecher K et al : Monitoring of fetuses with IUGR : a longitudinal study. UOG 2001; 18:564-570 Baschat AA et al: The sequence of changes in Doppler and BPP as severe FGR worsens.UOG 2001; 18: 571-577 Ferrazzi E et al : Temporal sequence of abnormal Doppler changes in severe IUGR.UOG 2002; 19: 140-146

13. Phases of placental dysfunction causing FGR

14. Patterns of clinical progression in early FGR

15. STV and metabolic acidosis in IUGRSTV (msec ) <2.6 2.6-3.0 > 3.0-----------------------------------------------------------------------------------Gestation (wks ) 25-38 26 – 38 27 – 37Metabolic acidosis * 10.3% 4.3% 2.7%IUFD 24.1% 4.3% 0.0%-----------------------------------------------------------------------------------* pH< 7.12 ; base deficit >12 mmol/l PardeyJ et al AJOG 2002; 186:1095-1103

16. IUGR : DV , STV and perinatal mortality n alive IUFD NND-----------------------------------------------------------------------------------Both abnormal 33 20 6 7 13/33 (39%) Both normal/orone abnormal 60 56 0 4 4/60 (7%)-----------------------------------------------------------------------------------Total 93 76 6 11 HecherK et al, UOG 2001

17. Derks JB et al: The effects of maternal betamethasone administration on the fetus. BJOG 1995; 102:40-46 within 48 hours after initial betamethasone administration :* Reduction of fetal movements* Reduction of fetal breathing movements* Reduction of STV on NSTAll changes disappeared after 4 days following treatment

18. Thuring A et al: Effect of maternal betamethasone on fetal and uteroplacental blood flow .UOG 2011; 37: 668-672within 48 hours after initial betamethasone administration :* decreased UMA diastolic flow* decreased DV flow at time of atrial contraction* no changes of MCA and UTA flowsAll changes disappeared after 4 days following treatment

19. Patterns of clinical progression in late FGR

20. LATE-ONSET FGR AND NEURODEVELOPMENTAL DELAY Late-onset FGR > 34 wks Normal or UMAPI MCAPI Intracerebral Redistribution of Blood Flow Frontal Lobes Basal ganglia Neurodevelopmental delay Neonatal period Early childhood Impaired -Performance attention -Communication -Problem solving -Emotions -Social function Social-interactive attention Cruz-Martinez R et al, AJOG 2009

21. Review of determinants of fetal neurodevelopment.

22. FGR monitoring – key points* UMA flow is useful parameter for assessment of high-risk population not a screening test* UMA flow unless it is severely abnormal does not tell us anything about fetalcondition* MCA flow reflects the extent of fetal “brain sparing”=sign of arterial redistribution as fetal response to hypoxemia* One of drawbacks of existing fetal arterial redistribution is subsequent development of oligohydramnios*Computerized CTG is currently the best parameter to detect fetalacidosis by decreased STV ( < 3 msec)* Ductusvenosus flow indirectly reflects the efficiency of the fetal heart and seems to correlate with the presence or absence of metabolic acidosis* Longitudinal monitoring ( at least 3 detailed studies) facilitates definition of trends of evaluated parameters in FGR. Different fetusesare showing different responses to impaired placental function i.e. all fetuses should be used as their own control

23. FGR delivery timing – key points* As IUGR fetus decompensates there are progressive Doppler velocimetry changes* These Doppler changes usually tend to follow a consistent pattern and largely occur prior to abnormalities in BPP.* Abnormal DVPI and STV values are important indicators for the optimal timing of delivery before 32wks of gestation* Metabolic acidosis, not necessarily hypoxia, correlates with neurological outcome in the infant* Gestational age overrides the effect of fetalcardiovascular condition until 32-34 weeks* Neurodevelopment is affected by severely abnormal UMA and DV flows in early-onset FGR and by abnormal MCA flow in late-onset FGR

24. FGR MANAGEMENT PROTOCOL 26-34 weeks NST & Doppler studies 34-36 weeks NST & Doppler studies NST Reactive NST Non-Reactive Either Test Non-Reassuring Both Tests Reassuring UMA Doppler Reassuring UMA Doppler Non-Reassuring Deliver Repeat in 1W Repeat in 1W Venous Doppler BPP < 4 Deliver Non-reassuring Reassuring Repeat in 6-24 hours BPP 6 Repeat in 1W Deliver Callen 2010

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