FETAL GROWTH RETARDATION In Modern Practice –Made Simple

FETAL GROWTH RETARDATION In Modern Practice –Made Simple

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  FETAL GROWTH RETARDATION In ModernPractice –Made Simple DR. SHARDA JAIN DR JYOTI AGARWAL
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  SHARING KNOWLEDGE &SKILL IS OUR BIGGEST MOTTO
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  Elephants come indifferent sizes!
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  Babies come indifferent sizes!
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  PLACENTA do comein DIFFERENT SIZES
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  FETAL GROWTH RETARDATION •Is defined as FAILURE OF A FETUS TO REACH TO ITS FULL GENETIC GROWTH POTENTIAL IN-UTERO,PUTTING IT AT RISK OF PERINATAL MORTALITY & MORBIDITY. I.U.G.R...X / S.G.A. / L.B.W. (<2.5 kg ) • WHO • ACOG S.G.A.< 10 th percentile for gestational age SGA <3rd centile
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  THE STEPS ..
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  3-10 % SINGLETON 12-40 % TWINS True FGR INCIDENCE MORTALITY 6-8 TIMES MORE & majority we loose in ist 24 hrs only bcz Hypoxia /academia
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  MAJOR CONCERN INFGR • Cause of concern is not the size ,but the possibility of life threatening fetal compromise Hypoxia /Acedemia which we fail to detect. • Timely identification of fetal compromise is difficult but crucial for proper management & a favourable neonatal outcome as it is 2nd leading cause of Perinatal mortality after prematurity. No treatment ,diagnosis difficult
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  FGR Babies poseBig Challenge ! • 50% of still births • 75% of unexplained fetal deaths • 8-10 times Increased Perinatal morbidity and mortality Bcz of considerable advances , to detect fetal compromise in FGR fetus still remains COFUSING!
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  WHY GYNAECOLOGISTS ARE CONCERNED? ABNORMAL LONG TERM • NEURODEVELOPMENTAL OUTCOME. • LONGTERM CARDIOVASCULAR DYSFUNCTION • METABOLIC SYNDROME
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  WHY WE AREUNABLE TO PICK UP THE BABY AT RISK ?
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  FUNCTIONAL CLASSIFICATION of SMALLFETUS • Contitutional Small FETUS ( normal ) 70% • ABNORMAL SMALL FETUS – symmetrical (10%) • FROWTH RESTRICTED FETUS-Asymmertrical (20%)
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  10% 70% CONSTITUTIONALLY SMALL Uteroplacental Insuffiency :asymmetrical Chrosomal , structural abn, infection : symmetrical
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  NORMAL SMALL FETUS •No Structural abnormality. Normal umbilical Doppler. Normal AFI. • Less than 10th percentile • Good prognosis. • No increased risk. • No special care Needed. 70% INDIA -2.6 KG USA 3.6 KG
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  ABNORMAL SMALL FETUS •Chromosomal abnormality or structural defect or infection with small size. • Poor prognosis 10%
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  GROWTH RESTRICTED FETUS •Small due to placental dysfunction. • Variable prognosis. ( late -80% sail through) (early 20% -bad prognosis) • Appropriate and timely treatment can improve outcome. 20%
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  CLASSIFICATION of SGA HEALTHYSGA (70% ) HEALTHY SMALL TYPE- 1 • SYMMETRICAL FGR ( 10 %) TYPE -2 ASYMMETRICAL FGR (20 % ) TRUE FGR
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  PATHOPHYSIOLOGY MADE SIMPLE SUPPLY PLACENTA MATERNAL FETUS SUPPLYPLACENTA FETUS HYPOXIA ACIDOSIS SUPPLY PLACENTA FETUS All well70% 20% 80-20% 10% 20/80%
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  TRUE FGR SYMMETRICAL FGR •Less common, 20% cases. • Both head & abdomen are small • HC/AC RATIO IS NORMAL • FL: AC ratio is normal • Etiology : Chromosomal, fetal infection ?chemical exposure • POOR PROGNOSIS ASYMMETRICAL FGR • More common & 80% cases of FGR • Abdomen is smaller than head • HC/AC ratio increases • FL: AC ratio increases • Placental insufficiency (e.g pre-eclampsia) • FAIR to GOOD PROGNOSIS
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  In SEVERE symmetricalFGR karyotyping , malformation & infection screen (Very Bad Prognosis) Symmetrical FGR Asymmetrical FGR 10 – 12 % Poor prognosis Fair prognosis
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  22 Early Onset Late Onset IncreasedPerinatalrisk LesserPerinatalRisk
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  Early – OnsetFGR Problem # 1: Mortality
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  FETAL HYPOXIA-ACIDOSIS FETAL HYPOXIA-ACIDOSIS
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  Sequence of eventsin growth restricted fetus Increased impedance to flow in umbilical artery Arterial redistribution in fetal circulation Failure of compensatory mechanism Abnormal venous flow emergency Abnormal fetal heart rate patterns
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  ARTERIAL REDISTRIBUTION INCREASED FLOW •BRAIN • HEART • ADRENALS DECREASED FLOW • KIDNEYS • LUNGS • GUT • LIVER • MUSCLE • BODY FAT/ GLYCOGEN STORAGE BRAIN & VITAL ORGAN SPARING EFFECT
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  FIRST 16 WKS:HYPERPLASIA 16-32WKS:HYPERPLASIA + HYPERTROPHY > 32 WKS :MOSTLY HYPERTROPHY PHASES OF FETAL GROWTH EARLY insult : affect CELLS ,LATER one affects SIZE
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  BRAIN WEIGHT NORMAL 3 TIMES MORE THANLIVER ASYMMETRICAL FGR 5 TO 6 TIMES MORE THAN LIVER
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  IDENTIFYING ETIOLOGY IS NECESSARY?
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  FETAL • CHROMOSOMAL • MALFORMATIONS •INFECTION • MULTIPLE GESTATIONS
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  MALFORMATION CONDITION CHANCE OFBEING SEEN (%) Anencephaly 98 Open spina bifida 90 Cleft 75 Diaphragmatic hernia 60 Gestroschisis 98 Exomphalos 80 Serious cardiac abnormalities 50 Bilateral renal agenesis 84 Lethal skeletal dysplasia 60 Edward’s syndrome (trisomy 18) 95 Patau’s syndrome (trisomy 13) 95 Available at: <http://www.fetalanomaly.screening.nhs.uk/getdata.
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  FACTORS AFFECTING FETALFROWTH Fetus
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  ABNORMAL PLACENTAL FACTORS (RETROSPECTIVEVALUE) • ABNORMAL TROPHOBLASTIC INVASION • CHRONIC ABRUPTION • VELAMENTOUS CORD • CIRCUMVALLATE PLACENTA • CHORIOANGIOMA
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  FGR & MATERNALFACTORS • PREGNANCY COMPLICATIONS PET/ APH RENAL APLA SYNDROME • ENVIRONMENT / DRUGS • INFECTIONS PIH /HDP
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  COMPLICATIONS MOTHER • NIL • LIFE-THREATENINGIN Severe PET / Eclampsia • 2 FOLD > Of FGR in next pregnancy BABY-6 to 8 fold Increase in Intra partum & Postpartum Deaths ANTEPARTUM – CHRONIC HYPOXIA /DEATH INTRAPARTUM HYPOXIA & ACIDOSIS POSTPARTUM MORBIDITY RATE IS > 50 %
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  DIAGNOSIS OF FGR Accuratedating /Risk factors Accurate measuring: Clinical examination/Close Monitoring Imaging : Biometry and Doppler
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  SCREENING SCORE ??? PREDICTIONS
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  CLINICAL EXAMINATION • 4OR MORE DISCREPANCY • SYMPHYSEO-FUNDAL HEIGHT 18 to 30 wks if 2-3 cm less - FGR suspected. • ACOG –SPECIFICITY- 96 % ,SENSITIVETY – 70 to 85 % • Maternal wt –stationary or decrease • ABDOMINAL GIRTH –Stationary or decrease
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  ULTRASOUND • Estimated FETALWT < 10 TH OR 3 rd CENTILE ON GROWTH CHARTS • NO INCREASE IN HEAD OR ABDOMEN SIZE ON TWO SCANS 2 WKS APART.
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  UNTIL DELIVERY CLOSE SURVEILLANCE
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  + DOPPLER B.P.P DFMC +NST+ AFI
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  Timeline for fetalhypoxemia Doppler ultrasound can predict fetal distress sooner than BPP &CTG DOPPLER IS EARLIEST& ABNORMAL CTG IS LATE
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  PANDORA BOX DR JYOTIAGARWAL
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  Ultrasound helps to…. •Assign fetal age • Assess fetal size • Estimate fetal weight • Exclude Anomalies • Amniotic fluid assessment • Placental ultrasound • Color Doppler • Biophysical profile
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  Ultrasound has revolutionizedthe practice of obstetrics • It has high negative predictive value to r/o FGR • Cochrane database (2000) reveals that there is 40 % improvement in perinatal mortality by judicious use of doppler
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  Dating is importanti trimester Compare USG GA with LMP GA Assign LMP EDD < 1wk > 1wk Re assign EDD VARIBILITY +/- 5-7 days
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  GOOD TO DATEAT N.T. SCAN
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  Abdominal cirumference hasthe highest sensitivity and greatest negative predictive value for diagnosing FGR
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  Growth – datesuncorrected Routine Foetal Biometry Based on customised Growth Curve “VISUAL EFFECT”
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  DOPPLER STUDY :GOLD STANDARD To identify hypoxia & fetal adaptation To plan timing of delivery
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  Highest accuracy isrequired in assessment of the Degree of Fetal Deterioration Degree of fetal Hypoxia - Fetal arterial doppler Degree of fetal Acidemia –Fetal Venous doppler Each additional day gained in utero can significantly increase neonatal survival
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  First sign ofhypoxia is picked up by Umbilical Artery forward wave flow 1º trimester Absent Diastolic Flow early 2ºtrimester Low Diastolic Flow late 2º and 3º trimester Resistance further reduces more diastolic flow
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  DECREASED EDF ABSENTEDF REVERSED EDF Abnormal Umb. A doppler appears when at least 60 % of the placental vascular bed is obliterated PositiveDiastolic Flow 10 - 12% Hypoxic 00% Acidemic Absent/ Reverse Diastolic Flow 80% Hypoxic 40 – 45 % Acidemic
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  UMBILICAL ARTERY DOPPLERSHOULD BE THE PRIMARY SURVEILLANCE TOOL • If umbilical artery flow is normal repeat every 15 days • If abnormal repeat it twice weekly if end diastolic velocity is present • Should be done daily with absent or reversed end diastolic velocity • In low risk , no conclusive evidence that routine umbilical artery doppler benefits either mother or baby
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  Overstressed fetus canlose the “brain sparing effect” Disappearance of brain sparing effect very critical event Precedes Fetal Death MCA has tremendous implication for determining the proper timing of delivery
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  CEREBRO-PLACENTAL RATIO Although S/Dratio, RI, and PI have been reported when computing CPR, more recently PI is the computation of choice Greggory R et al. American Journal of Obstetrics & Gynecology, July 2015 Cerebroplacental ration (CPR) = middle cerebral artery Pl Umbilical artery Pi
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  SIMPLE FUNDA • MCA>1.5 PI • UMBLICAL ART < 1 PI
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  DUCTUS VENOSUS DOPPLER Withworsening placental vascular insufficiency • “a” wave velocity in DV doppler reduces & finally reverses b’cos of increased afterload & preload • Has excellent predictive value for acidemia • In preterm fetus it is used to time delivery
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  A retrograde “a- wave” and pulsatile flow in umbilical vein signifies the onset of overt fetal cardiac compromise Double pulsatile patternEND POINT Cardiac Failure : Impending Death
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  Good correlation BetweenDoppler & Hypoxia Umbilical artery 50% placenta is not functioning Mild Hypoxia MCA > 70% placenta not functioning Compensatory redistribution Moderate Hypoxia DV > 90% placenta not functioning Failure of Compensatory redistribution Severe Hypoxia & acidemia IMPENDING DEATH
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  What does DOPPLER tellIn FGR ? UMBLICAL ART DOPPLER , MCA DOPPLER,DUVTUS VENOSUS DOPPLER
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  1To identify etiologyof IUGR • Placental / non placental • To identify hypoxia & fetal adaptation • To plan timing of delivery? • To identify fetuses at risk of perinatal complications DOPPLER IN FGR
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  Management Medical therapy Antepartum surveillance Timingof delivery Stage based approach
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  IS THERE ANY ANTENATAL TREATMENT??
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  Antenatal Treatment *Amino acids? *Oxygen? *Rest ? *Monitoring *Steroids *Mag sulf ( < 32 wks ) 3 WAYS TO GIVE( 4 GM + 24 hrs ) Drugs • Aspirine ? • Progesterone (Inj/tablet) ? • Heparin ? • Sildinafil ? • L- arginine ? • Micronutrients GIVING STEROID & DELIVERY WITHIN 48 HOURS. DELAYING DOES NOT IMPROVE OUTCOME |(GRIT TRIAL LEVEL I EVIDANCE)
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  STEROID TREATMENT REPEAT ORNOT, DEXA √ OR BETAMETHASONE LETS REVISE
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  Early – OnsetFGR Problem #2 (Neurological) Morbidity 67 Role of Magsulf (<32 weeks) To decrease Neurological morbidity 24 hours
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  IN FGR :AIM OF DELIVERY A live fetus That Grows & survives ! Riskof intrauterine compromisehas tobe weighed against the potential risksfrom iatrogenic prematuredelivery Best Time Is When Fetal Redistribution Mechanism Starts Failing
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  Intervene Timely
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  When to deliver? There is a better outcome with timely intervention & delivery for fetus who shows sign significant compromise
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  Time to Deliver Factorsto decide time to deliver • Degree of Prematurity • NICU facility • Degree of Hypoxia, acidemia, hepatic metabolic derangement (mother) Challenge to weigh the risks and benefits of interventions
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  Gestational age atdecompensation is the primary determinant of perinatal survival Ft < 32 weeks • Every day gained is Bonus • Every week gained improves outcome by 40% • Here venous Doppler's help delay delivery 32 – 34 wks • Deliver once Umb A ABSENT / REDV At term • Prompt delivery at 37 wks of gestation • Even when Umb.AD is normal Steroid cover
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  24 – 28weeks Monitor Abn doppler / BPP Discuss with family 28 – 32 weeks Monitor Arrested fetal growth A / R EDV UA Abn. DV Abn BPP Steroids- Deliver magsulph Neonatal care 32 – 34 weeks Monitor Deliver Arrested growth Oligo hyd Abn CTG A /R EDV
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  74 1. Identify Small Fetus 2.Distinguish SGA vs FGR 3. Timing delivery (and Follow Up)
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  How to Deliver?
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  MODE OF DELIVERY dependson Mode of Delivery • Parity • Cervical score • Degree of growth restriction Vaginal Delivery • In well compensated babies with reassuring fetal well being tests and diastolic flow-- LSCS • IF HYPOXIC FETUS - AVOID TRIAL OF LABOUR • – RISK OF DECOMPENSATION IN LABOUR IS VERY HIGH AS RESERVE IS POOR • THERE IS ROLE OF LSCL IN THE PRESENCE OF SIGNIFICANT ABNORMALITIES OF UADW
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  BABIES OUTCOME
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  is 5-20 timesgreater than for AGA, mainly due to • intrauterine death, • perinatal asphyxia, • Congenital anomalies. Perinatal mortality for FGR infants
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  Is 5-10 timeshigher than for AGA infants, especially for infants with ↓ head circumference at birth. Intellectual and motor function (excluding those with congenital infections, chromosomal abnormalities) depends on adverse perinatal events and on the specific cause of growth restriction. Early identification and treatment of hypoglycemia and polycythemia improves outcome. Neurologic abnormalities are usual with genetic and infectious causes of IUGR. NEUROLOGIC MORBIDITY
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  Catch-up growth occursfast after birth but these patients usually remain smaller than expected. FGR: With placental causes of IUGR
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  Recent studies implicateFGR with adult onset of • Hypertension, • Coronary heart disease, • Hypercholesterolemia, • Diabetes. These studies suggest that Fetal growth retardation has long term affects on endocrine development and homeostasis. Fetal “Programming” of cardiovascular disease:
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  TAKE HOME MESSAGE •Timing of delivery in FGR: • Before 32-34 weeks, base delivery on ductus venosus • After 34 weeks, absent/reversed EDF indication to deliver • If umbilical artery normal but MCA at or below 5th centile – sign of cerebral redistribution – offer delivery at 37 weeks (RCOG, 2013) • No role of aortic isthmus as yet