A (quasi)evidence-based approach to the management of early-onset IUGR

Transcription

1 A (quasi)evidence-based approach to the management of early-onset IUGR Eduard Gratacós Barcelona Center for Maternal-Fetal and Neonatal Medicine Hospital Clínic and Hospital Sant Joan de Deu, University of Barcelona

2 What is early-onset IUGR Predictors of poor outcome Stage-based management Long term consequences

3 What is early-onset IUGR Predictors of poor outcome Stage-based management Long term consequences

4 EARLY-ONSET LATE-ONSET PREECLAMPSIA 2-8 % % PREECLAMPSIA + IUGR 2 % IUGR 4-8 %

5 Savchev 2013 EARLY IUGR (1/3) LATE IUGR (2/3) PROBLEM: MANAGEMENT Placental disease: high (UA+, PE high) Hypoxia ++: systemic CV adaptation Tolerance to hypoxia. Natural history High mortality and morbidity PROBLEM: DIAGNOSIS Placental disease: low (UA-, PE low) Hypoxia +/-: central CV adaptation Low tolerance: no natural history Low mortality but poor long outcome.

6 What is early-onset IUGR Predictors of poor outcome Stage-based management Long term consequences

7 FETAL DETERIORATION IN PLACENTAL INSUFFICIENCY PLACENTAL DISEASE COMPENSATED HYPOXIA DECOMPENSATED HYPOXIA SERIOUS INJURY DEATH Increment placental impedance UTERINE A. CPR / UMBILICAL A. Centralization MIDDLE CEREBRAL A. growth Ao ISTHMUS cardiac ischemia Diastolic failure DUCTUS VENOSUS cctg: reduced shortterm variability CTG ABNORMAL Systolic cardiac failure

8 Early-onset IUGR PROBLEM #1: MORTALITY cctg- STV<3 ms Pathological CGT BPP 60% DVa (rev) IUFD 23% in BPP=6 and 11% in BPP=8 Poor correlation with DVa(rev) Cochrane: poor contribution to prediction 19% Baschat 2007, Kafur 2008, Lalor 2010, Crispi 2009 Yes <26 Perinatal Mortality >90% No % >28 <10% Baschat 2003 Hecher 2003 Grivell 2010 Cruz- Lemini 2012

9 Early-onset IUGR PROBLEM #2: (NEUROLOGICAL) MORBIDITY Brain US anomalies in 30w IUGR Controls IUGR antegrade AoI IUGR retrograde AoI * Controls IUGR DV<5 z-score IUGR DV>5 z-score * (%) < >32.0 Neurologic >90% 30-40% <10% Morbidity Fouron 2004 Del Rio 2008 Cruz- MarQnez 2012

10 What is early-onset IUGR Predictors of poor outcome Stage-based management Long term consequences

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12 Protocol IUGR First step: UtA + CPR + EFW = SGA or IUGR I low EFW (<p3) or mild placental resistance / redistribution CPR <p5 Ut A >p95 MCA <p5 III Severe placental resistance / redistribution AEDV AoI >p95 III Severe hemodynamic adaptation - Low suspicion acidosis DV >p95 REDV UVpuls IV High suspicion of acidosis - High risk of death DV (a rev) CGT decelerations of reduced short-term variability

13 RATIONALE FOR A STAGE-BASED APPROACH TO THE MANAGEMENT OF FGR PLACENTAL DISEASE HYPOXIA ACIDOSIS SERIOUS INJURY DEATH Diagnostic/chronic markers Early and Late IUGR Increment placental impedance Prognostic/Acute markers Early IUGR Centralization cardiac Diastoli cctg: reduced STV Stage fetal deterioration I II III IV Systolic cardiac failure Risks of prematurity LOW MODERATE HIGH Red Line LATE IUGR Red Line EARLY IUGR

14 IUGR Management protocol according to severity stages Stage IV III II I Follow- up Hours/Daily 1-2 d 2/w 1/w Delivery DV(a- ) cctg abn. CTG dec. DV>p95 UV puls REDV (a) AEDV (b) AoI>95 Mode CS CS CS or LI LI EFW<p3 CPR>p95 UtA>p95 MCA<p5 <26w Mort. >90% 50% <10% Morb. >90% 50%

15 EARLY-ONSET IUGR Key points for clinical management 1 - <28 w : PROBLEM IS MORTALITY First determinant: GA Second (most useful) determinant 26-28w: DV 2 - >28 PROBLEM IS NEUROLOGICAL MORBIDITY 3 - NATURAL HISTORY: USE A PROTOCOL 4 - (IF PREECLAMPSIA NATURAL HISTORY ALTERED) 5 - LONG TERM SEQUELAE: EARLY POSTNATAL INTERVENTION

16 umbilical artery normal and anormal hemodynamics S D Placental status Cardiac pump normal function >30% placenta + cardiac ischemia Cardiac pump abnormal function

17 middle cerebral artery normal and abnormal hrmodynamics Normal oxygenation [normal waveform] [mild vasodilation] [marked vasodilation] hypoxia

18 30 % venous return REFLECTS DIASTOLIC PRESSURE IN RIGHT (AND LEFT) HEART

19 ductus venosus Normal and abnormal flow patterns cardiac compliance: effect on right return P S D A P no myocardial ischemia P compliance P

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22 Z-scores MPI AoI DV Remaining percentageof normality (%) MPI AoI DV Days before delivery or fetal death Days before delivery or fetal death MPI, AoI, and DV >95 th centile at 26, 12 and 5 d before delivery or fetal death One week before delivery, proportion of normal MPI, AoI, and DV was 60%, 80%, and 90%, respectively. Cruz

23 Fetal deterioration and monitoring in early-severe IUGR. Placental disease affects a large proportion of the surface, and this is reflected in changes in the UA Doppler in a high proportion of cases. The figure depicts in a schematic and simplified fashion the pathophysiologic progression with the main adaptation/consequence in placental-fetal physiology, and the accompanying cascade of changes in Doppler parameters. The sequence illustrates the average temporal relation among changes in parameters, but the actual duration of deterioration is influenced by severity. Regardless of the velocity of progression, In the absence of accompanying PE this sequence is relatively constant, particularly as regards end-stage signs and the likelihood of serious injury/death. However, severe PE may distort the natural history and fetal deterioration may occur unexpectedly at any time. PLACENTAL DISEASE Increased impedance HYPOXIA Centralization ADVANCED HYPOXIA / ACIDOSIS Reduced cardiac compliance SERIOUS INJURY DEATH Chronic / Diagnostic markers Weeks Acute / Prognostic markers 7-10 days UtA PI >p95 CPR <p5 UA PI >p95 UA AEDV UA REDV MCA PI <p5 AoI PI >p95 DV PI >p95 DV rev. atrial cctg STV<3ms BPP <4 CTG decelerations Growth Restric-on Abbreviations: UtA: Uterine artery Doppler. PI: pulsatility index. CPR: cerebro-placental ratio. UA: umbilical artery Doppler. AEDV: absent-end distolic velocity. REDF. Reverse absent-end distolic velocity. MCA: middle cerebral artery Doppler. AoI: aortic isthmus Doppler. DV: ductus venosus Doppler. ccgt: computerized cardiotocography. STV: short term variability. BPP: biophysical profile.cgt: cardiotocography.

24 Fetal deterioration and monitoring in late-mild IUGR. Placental disease is mild and UA Doppler values are not elevated above the 95th centile. effects of fetal adaptation are best detected by the CPR, which detects mild changes int he AU and MCA Doppler. A large fraction of cases do progress to baseline hypoxia so that they remain with abnormal CPR. Once baseline hypoxia is established, placental reserve is minimal progression to fetal deterioration may occur quickly, as suggested by the high risk of severe deterioration or IUFD after 37 weeks in these cas possibly due to a combination of a higher susceptibility to hypoxia of the term-mature fetus and the more common presence of contractions at term. PLACENTAL DISEASE Reduced placental reserve HYPOXIA Centralization ACIDOSIS INJURY / DEATH UtA PI >p95 Diagnostic markers Weeks Acute deterioration Hours CPR <p5 MCA PI <p5 AoI PI >p95 AoI reverse CTG decelerations!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! Growth!Restric-on! Abbreviations: UtA: Uterine artery Doppler. PI: pulsatility index. CPR: cerebro-placental ratio. MCA: middle cerebral artery Doppler. AoI: aortic isthmus Doppler. DV: ductus venosus Doppler. CGT: cardiotocography. 24

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