Fetal growth restriction:Evidence based management 2018

Fetal growth restriction:Evidence based management 2018

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  D.G.F. CME ON Fetalgrowth restriction: Evidence based management 29TH JANUARY 2018 at WOOD APPLE DELHI Contributors Dr. Kiran Aggarwal Dr. Sharda Jain Dr. Jyoti Agarwal PART ONE
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  DR KIRAN AGGARWAL DIRECTORPROFESSOR LADY HARDINGE MEDICAL COLLEGE AND ASSOCIATED HOSPITALS Part 1
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  Fetal Growth Restriction •Definition: Less than 10th percentile weight for gestational age on a singleton growth curve defined as small for gestational age.(SGA) a. Constitutionally small fetus who has achieved its normal growth potential b. Small fetus with growth restriction with increased risk of perinatal morbidity and mortality c. Fetus who is not small but has not achieved its genetic potential
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  Constitutionaly small fetus Modestsmallness 5th till 10th percentiles. Normal growth velocity across gestation. Normal physiology i.e. normal amniotic fluid volume and umbilical artery Doppler. abdominal circumference growth velocity above lowest decile and appropriate size in terms of maternal characteristics( height weight race and ethnicity). Lower threshold (< 3rd percentile) may help distinguish small fetus at increased risk of adverse outcome from the small fetus at low risk. (PORTO Trial AJOG, 2013)
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  Diagnosis of FGR •Sonographic estimation of fetal weight is the single best morphometric test to screen for and diagnose fetuses with weight less than 10th centile. • Other test like AC HC and ratios may overlook symmetrical FGR. • AC is the most sensitive single morphometric indicator of FGR. Sens, spec, positive and negative predictive values of 61, 95, 86, 83 %. • Measurement of AC was more predictive of asymmetric FGR than head circumference or BPD or combination of AC with either of these. The optimal time to screen for FGR was 34 wks app. • Biochemical markers of hypoxia and acidemia are more common when the AC is below the 5th percentile.
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  Fetal weight estimations •WHO charts for fetal growth and common ultrasound biometric measurements based on longitudinal data derived from 10 countries. • Equations that use AC, BPD, FL seem to provide the most accurate estimates of fetal weight. • EFW performed within one to two weeks of delivery is more predictive than when performed earlier in gestation. • The sensitivity of EFW for predicting FGR and adverse outcome is highest for infants with birth weight <3rd centile. • Customised charts take care of maternal variables like parity ethnicity height, weight , age and fetal gender.
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  USG parameters • Growthvelocity use of any parameter requires exact dating. If unavailable serial sonographic examinations at two week intervals should be done. • HC/AC ratio for asymmetric FGR decreases linearly through out pregnancy and a ratio greater than 2 SD above the mean for GA is considered abnormal. • FL/AC ratio is independent of GA in normally grown fetuses in last half of pregnancy however not good for symmetric FGR. • Ponderal index poor correlation between fetal and neonatal PI.
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  Transverse cerebellar diameter •Transverse cerebellar diameter not affected in FGR may serve as and independent indicator of GA against which other potential deviations of growth may be compared. • TCD /AC ratio exceeding 2SD above the mean is predictive of asymmetrical growth restriction. • The status of the TCD/AC ratio as a predictor of FGR remains controversial due to limited data from large and controlled studies.
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  Amniotic fluid volume •Amniotic fluid volume; decreased urine production due to hypoxia induced redistribution of blood flow to vital organs at the expense of less vital organs such as kidney. • r/o ruptured membranes, congenital genitourinary anomalies or prolonged pregnancy • Oligohydramnios with EFW <3rd percentile is predictive of adverse outcome.
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  Assessment Maternal, placental orfetal proceses. Complete history, physical examination to assess for maternal disorders. Obstetrical imaging and laboratory evaluations for fetal and placental aetiologies. Detailed fetal anatomic survey for congenital anomalies and 20-60% of malformed infants are SGA. Anomalies ass with FGR include omphalocele diaphragmatic hernia skeletal dysplasia and some congenital heart defects. Fetal echocardiogram is indicated if level II USG suggest any cardiac abnormality.
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  Risk assessment atfirst trimester Minor risk factors Maternal age >35 yrs, IVF ,singleton pregnancy, nulliparity, BMI<20,.25- 34.9,smoking 1-10 cig /day, previous preeclampsia, pregnancy interval <6 months,>60 months Major risk factors , previous still birth, chronic hypertension, renal disease, diabetes with vasMaternal age>40yrs,Paternal SGA, Smoking >11cig /day, previous SGA babycular disease,heavy bleeding , papp A < 0.4 moM, Cocaine, dailly vigorous excrcise Antiphospholipid syndrome 3 or more one Uterine artery doppler at 20- 24wks Serial assessment of fetal growth and umbilical artery doppler from 26-28 wks norm al Fetal assemem ent and umbilical artery doppler in third trimester abno rmal Aspirin from <16 wks if risk facrtors preeclampsia
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  Pregnancy assessment • Accurateassessment of gestational age. • Assessment of risk factors • Symphysial fundal height measurement: • fundal height in cms that is at least three cm below the GA in weeks ( 13-86% sensitivity). • Serial measurement of symphysis fundal height (SFH) is recommended at each antenatal appointment from 24 weeks of pregnancy as this improves prediction of a SGA neonate • Abdominal palpation: clinical assessment of fetal size by abdominal palpation does not perform well as a test for detecting FGR ( 30-50% sensitivity).(rcog 2013) • Serial ultrasound measurement of fetal size and assessment of wellbeing with umbilical artery Doppler should be offered in cases of fetal echogenic bowel..
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  Fetal genetic studies Offer referral for a detailed fetal anatomical survey and uterine artery Doppler by a fetal medicine specialist if severe SGA is identified at the 18–20 week scan.  Cell free DNA followed by fetal karyotype/microarray should be offered in severely SGA fetuses with structural anomalies and in those detected before 23 weeks of gestation, especially if uterine artery Doppler is normal.  No structural abnormalities but presence of soft ultrasound markers associated with an increased risk of aneuploidy such as thickened nuchal fold, choroid plexus cyst and abnormal hand positioning.  If FGR after 24 wks, asymmetric, and anatomy is normal no need for screening for genetic abnormalities.
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  Work up forinfection If infection is suspected clinically because of maternal history, examination or fetal USG findings maternal serum should be examined for seroconversion. Cytomegalovirus, toxoplasmosis. rubella and varicella. Amniotic fluid DNA testing if indicated Sonographic markers for fetal infection are often nonspecific but include echogenicity and calcification of brain and or liver and hydrops Malaria can also cause FGR Serological screening for congenital cytomegalovirus (CMV) and toxoplasmosis infection should be offered in severely SGA fetuses. Testing for syphilis and malaria should be considered in high risk populations.(RCOG 2014)
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  Thrombophilia Inherited thrombophilic disordersscreening is not recommended as association with FGR is weak. Antiphospholipid syndrome acquired thrombophilia is clearly associated with FGR.
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  Sequence of dopplerand biophysical changes in FGR Reduction in umbilical venous flow is initial hemodynamic change. Venous flow is redistributed away from fetal liver and towards the heart. Liver size decreases and abdominal circumference lags which is the first biometric sign of fetal growth restriction. Umbilical artery doppler index increases and diminished diastolic flow due to increased resistance in the placental vasculature.
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  Brain sparing effect Middlecerebral artery doppler index decreased, increased end diastolic flow preferential perfusion of the brain Increasing placental resistance absent and then reversed end diastolic flow in the umbilical artery. MCA doppler index normalizes or abnormal increases as diastolic flow falls due to loss of brain sparing hemodynamic changes
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  Cardiac decompensation MCA dopplerindex normalizes or abnormal increases as diastolic flow falls due to loss of brain sparing hemodynamic changes. Cardiac performance deteriorates due to chronic hypoxia and nutritional deprivation absent or reversed end diastolic flow in the ductus venousus and pulsatile umbilical venous flow may develop. These may be the preterminal events. NST becomes nonreactive BPP score falls and late decelerations accompany contractions.
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  MANAGEMENT For structurally andchromosomally normal fetuses. Mostly by uteroplacental insufficiency. Serial ultrasound evaluation of fetal growth, fetal behaviour (BPP) impedance to blood flow doppler velocimetry Identify those fetuses at highest risk inutero and will benefit from preterm delivery.
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  management Hospitalisations: on caseto case to basis where intensive monitoring is needed. Provides monitoring as in REDF interventions promptly but no evidence that bed rest improves fetal growth or outcome. Growth velocity use of any parameter requires exact dating. If unavailable serial sonographic examinations at two-four week intervals should be done. For mild FGR longer interval and for moderate or severe shorter interval.
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  Nonstress test andbiophysical profile BPP evaluates both acute and chronic fetal physiologic parameters, is easy and fetal death within one week of a normal test score is rare. If NST is used amniotic fluid volume assessment should also be performed weekly. chronic placental insufficiency results in both FGR and oligohydramnios. If doppler indices are normal normally NST and BPP are not needed. In other FGR weekly, if with oligohydramnios, preeclampsia .decelerating fetal growth, severe FGR increased doppler index twice per week. For absent or reversed diastolic flow daily.
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  Umbilical artery Doppler Notfor screening and diagnosis of FGR. It is for evaluation and management of suspected FGR.. abnormal doppler is:pulsatility index >95th centile or AREDF Combination of EFW less than 10th percentile and abnormal umbilical artery doppler is highly predictive of FGR and is best tool available for identifying the growth restricted fetus at risk of adverse outcome. Weekly doppler of umbilical artery if FGR. If follow up normal then two weekly doppler esp if weight >5 th centile,and normal growth and amniotic fluid. If PI > 95 th percenile then weekly If absent or reversed it is a sign of impendiing fetal CVS and metabolic derangements.
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  Doppler studies Fetal cerebralarteries in normal pregnancies has a high resistance flow, with FGR increased flow causes increased end diastolic velocities and decreased s/d ratio. High placental impedance precedes the onset of the redistribution reflex.( brain sparing). Cerebroplacental ratio: it is the MCA PI divided by the umbilical artery PI. Low CPR indicates fetal blood flow distribution and is predictive of adverse neonatal outcome. Low CPR with abnormal UA doppler values predicts adverse neonatal outcome, cesarean delivery for fetal distress.( PORTO TRIAL).
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  Venous doppler assessment It is for monitoring of fetal well being and is used for prediction of stillbirth and acidemia over use of umbilical artery doppler alone.  In normal pregnancies flow is forward and uniform.  Absent or reversed a wave or pulsatile umilical venous flow are late findings occurring two weeks after arterial changes.  Its abnormalities constitute a late circulatory finding and impending acidemia and death.  Fetal survival of more than a week is difficult. TRUFFLE trial showed no immediate neonatal benefit from delaying till DV abnormalities and only a marginal two year neurodev benefit.(LANCET 2015)
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  DOPPLER STUDIES AND3D USG  Fetal descending aorta. Normal flow is pulsatile with a minimal end diastolic component. Elevated pulsatility index is associated with both FGR and adverse outcomes. Absent EDF in descending aorta for prediction of FGR with FHR abnormalities sensitivity and specificity is 85 and 80 %. These pregnancies are with higher rates of CS, right ventricular failure and perinatal mortality  Three dimensional ultrasound measurement of thigh femur or humerus volume measurement: simple more accurate than two dimensional techniques but is not widely assessed and available.
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  MANAGEMENT  When umbilicalartery Doppler flow indices are normal it is reasonable to repeat surveillance every 14 days.  More frequent Doppler surveillance may be appropriate in a severely SGA fetus. When umbilical artery Doppler flow indices are abnormal (pulsatility or resistance index > +2 SDs above mean for gestational age) and delivery is not indicated repeat surveillance twice weekly in fetuses with end–diastolic velocities present and daily in fetuses with absent/reversed end–diastolic frequencies.  CTG should not be used as the only form of surveillance in SGA fetuses. Interpretation of the CTG should be based on short term fetal heart rate variation from computerised analysis.
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  MANAGEMENT  Ultrasound assessmentof amniotic fluid volume should not be used as the only form of surveillance in SGA fetuses. Interpretation of amniotic fluid volume should be based on single deepest vertical pocket.  Biophysical profile should not be used for fetal surveillance in preterm SGA fetuses  In the preterm SGA fetus, middle cerebral artery (MCA) Doppler has limited accuracy to predict acidaemia and adverse outcome and should not be used to time delivery.  In the term SGA fetus with normal umbilical artery Doppler, an abnormal middle cerebral artery Doppler (PI < 5th centile) has moderate predictive value for acidosis at birth and should be used to time delivery.  Ductus venosus Doppler has moderate predictive value for acidaemia and adverse outcome. Ductus venosus Doppler should be used for surveillance in the preterm SGA fetus with abnormal umbilical artery Doppler and used to time delivery
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  ANTENATAL STEROIDS One coursebetween 24-34 weeks of gestation in the week before delivery is expected. The steroids in babies with absent end DF often show slight improvement in blood flow and very sick ones don’t.
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  Maternal interventions Any interventionin healthy women doesn’t help growth of FGR fetuses. Maternal nutritiional supplements, oxygen therapy plasma volume expansion low dose aspirin bed rest and anticoagulation doesn’t help. Use of phosphodiesterase 5 enzyme inhibitor like sildenafil or a statin may be promising but under investigation. Antihypertensives doesn’t help Cessation of smoking is of value
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  Timing of delivery Growth restriction intervention trial (GRIT)  Disproportionate intrauterine growth intervention trial at term (DIGITAT)  Trial of randomized umbilical and fetal flow in europe(TRUFFLE)  DECISION: gestational age, doppler of umbilical artery , biophysical score, ductus venosus doppler, and other high risk factors.  Greatest risk before 32 weeks and between 26-29 weeks of gestation each day in utero improves suvival 1-2%.  Abnormal ductus venosus doppler deliver immediately  REDF > or equal to 32 weeks deliver  AEDF > or equal to 34 deliver  REDF <32 OR AEDF<34 weeks regardless of presence or absence of oligohydramnios , daily BPP delay till 32 weeks ( REDF) and 34 wks (AEDF), till BPP is normal, if ductus venosus abnormal or BPP abnormal then deliver.  Decreased diastolic flow , BPS twice a week deliver at 37 weeks if with oligoamnios preeclampsia or weight <5th centile.  Normal umbilical artery doppler if in absence of risk factors deliver at 39-40 weeks
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  Method of delivery Unfavourable cervix is not a reason to avoid induction.  In the SGA fetus with umbilical artery AREDV delivery by caesarean section is recommended  if NST and BPP is normal antenatally trial of labor with continuous intrapartum monitoing is reasonable.  In the SGA fetus with normal umbilical artery Doppler or with abnormal umbilical artery PI but end–diastolic velocities present, induction of labour can be offered but rates of emergency caesarean section are increased and continuous fetal heart rate monitoring is recommended from the onset of uterine contractions.  Early admission is recommended in women in spontaneous labour with a SGA fetus in order to instigate continuous fetal heart rate monitoring
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  consequences Mother with SGAmay develop IHD Babies may have obesity, metabolic dysfunction hypertension and CAD. RECURERENCE RISK: risk of nonanomalous SGA <5th centile in second pregnancy is 23% Prevention in subsequent pregnancies: treat cause, address smoking, alcohol, malaria, nutritional, low dose aspirin in women with high risk of preeclampsia
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  Single measurement <10th customised centile &/or serial measurements indicative of FGR High risk of SGA fetus/neonate Based on history, biochemistry or uterine artery Doppler Fetal biometry Single AC or EFW < 10th customised centile Serial measurements indicative of FGR UA Doppler Normal PI or RI > 2 SDs, EDV present AREDV Repeat USG fortnightly AC &EFW UA DOPPLER MCA after 32 wks Delivery Offer delivery by 37 weeks with the involvement of a senior clinician Recommend delivery by 37 weeks if MCA Doppler PI < 5th centile Consider delivery > 34 weeks if static growth over 3weeks Recommend steroids if delivery is by CS Repeat ultrasound Weekly AC & EFW1,2 Twice weekly UA Doppler Delivery Recommend delivery by 37 weeks Consider steroids if delivery by CS Consider delivery > 34 weeks if static growth over 3 weeks Recommend steroids if delivery is by CS Repeat ultrasound Weekly AC & EFW1,2 Daily UA Doppler DV Doppler [cCTG]3 Recommend delivery before 32 weeks after steroids if: – abnormal DV Doppler and/or cCTG provided ≥ 24 weeks & EFW > 500 g Recommend delivery by 32 weeks after steroids Consider delivery at 30–32 weeks even when DV
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