USG AND DOPPLER IN DIAGNOSIS AND MANAGEMENT OF IUGR

USG AND DOPPLER IN DIAGNOSIS AND MANAGEMENT OF IUGR

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  USG & DOPPLERIN DIAGNOSIS & MANAGEMENT OF IUGR Dr. Shivshankar Lasune (MS Obstetrics and Gynaecology)
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  SGA(small for gestationalage) • Def: a fetus that has not attained or achieved a particular biometric parameter threshold for given gestational age. • Most universally accepted parameter is EFW 10th centile. • Other parameters AC, HC, BPD -5th centile.
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  • Appropriate sensitivityfor fetal risks • Lower the centile - greater the risk of IUD • Perinatal mortality & morbidity increases when birth weight is less than 3rd & 5th centile for gestational age. Why 10th centile ? FGR SGA LGA SGA 70% LGP 30% FGR
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  MATERNAL RISK FACTORS •PIH • Hypertension • Diabetic vasculopathy • APLA • Renal disease • Heart disease • Asthma • Hbpathy • PKU • Severe malnutrion • Smoking • Substance abuse
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  FETAL FACTORS • Multiplegestation • Infection • Malformation • Syndromes
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  PLACENTAL FACTORS • Confinedplacental mosaicism • Placenta previa • Abruption • Infarction • Circumvallate placenta • Morbid adherence • Velamentous insertion
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  HYPERPLASIA • First 16wks • Rapid mitosis • Inc. in DNA content HYPERPLASIA & HYPERTROPHY • 17-32 wks • Dec. mitosis • Inc. in cell size HYPERTROPHY • After 32 wks • Inc. in cell size, fat deposition, muscle mass & connective tissue WILLIAMS OBSTETRICS -24rd EDITION 34 wks - 30- 35g/day 24 wks - 10- 20g/day 15 wks - 5g/day
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  GENETIC POTENTIAL • Derivedfrom both parents • Mediated through factors like insulin like growth factor  SUBSTRATE SUPPLY • Derived from placenta • Depend upon Uterine & Placental vascularity
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  GLUCOSE AMINO ACIDS OXYGEN FETAL GROWTH
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  Small for gestationalage Low growth profile • Constitutionally small • Serial monitoring • Curve to nomograms or parallel • Anatomy normal • BPP/AF normal • Doppler normal • No treatment • Smallness is not equal to sickness Fetal growth restriction (fetal cause) • Syndrome/anomoly / aneuploidy • Serial monitoring • Curve drops off • Anatomy normal/abnormal • AF normal/ abnormal • Doppler normal/ abnormal • Karyotype, inf., markers of aneuploidy.
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  Small for GA •Fetal growth restriction – classical placental cause • Failure to attain genetic potential • Serial monitoring • Curves drops off (cuts across percentile) • Body disproportion • Anatomy normal • BPP Normal / Abnormal • Amniotic fluid Normal/ Abnormal • Doppler Normal // Abnormal • Surveillance for fetal growth and well being • Optimisation of the time of delivery • Decreases perinatal morbidity and mortality
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  SGA = EFW< 10th percentile Constitutionally small 70% • EFW 4 to 10th percentile • UAD –N • CPR – N • Ut AD – N • Placental histology – normal • Maternal biochemical parameter – Normal • Good outcome Intra uterine growth restriction 30% • EFW < 3rd percentile or • UAD – Abnormal or • CPR - < 5th percentile or • Ut AD - Abnormal • Placental morphology – Abnormal. • Maternal biochemical parameter - Abnormal • Poorer outcome
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  Distribution of caseswhen IUGR = abnormal UA Doppler
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  Distribution of caseswhen IUGR = abnormal CPR or UtA or EFW<p3
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  Prognostic criteria of“poor outcome”-SGA! CS for distress and/or neonatal acidosis
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  FGR classification • Earlyvs Late • Symmetric vs Asymmetric • Early onset FGR – Diagnosed before 34 weeks of GA • Cellular hyperplasia is stunted • Proportionally small fetus (EFW < 10th pct) • Late onset FGR – Diagnosed after 34 weeks • Cellular hypertrophy stunted • Disproportionally small fetus (EFW< 10th pct) • HC/AC and FL/AC ratios (assymetric) • Substrate inadequacy • Associated with maternal disease
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  Importance of earlyvs late Cause – Severity – Counselling - Management
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  Summary of themain difference between early and late onset forms of FGR Early onset FGR 1- 2% • Problem : management • Placental disease : severe ( UA Doppler abnormal, high association with preeclampsia) • Hypoxia ++ :systemic cardiovascular adaptation • Immature fetus = higher tolerance to hypoxia = natural history • High mortality & morbidity • Lower prevalence • 20 – 30% of FGR Late onset FGR 3 – 5% • Problem : diagnosis • Placental disease : mild ( UA Doppler normal, low association with preeclampsia) • Hypoxia +/- : central cardiovascular adaptation • Mature fetus = lower tolerance to hypoxia = no or very short natural history • Lower mortality but common cause of late stillbirth, affects large fraction of pregnancy • 70 – 80 % of FGR.
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  EARLY ONSET FGR
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  LATE ONSET FGR
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  Nomogram concept • Portraysrelation between two variables • In the context of fetal growth (Fetal size – cms or kg vs Time – weeks ) • Biological diversity / variability • Continuous foetal growth • Graph or chart forms • Gives mean & confidence limits of a parameter for a given gestational age • Standard deviation / percentile
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  Biological variability offoetal size Ethical Altitude Social - Economical Racial Birth order • The variability of range in size for a given gestation increases with advancing gestational age.
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  Percentile HC 95 1 2 34 5 6 7 8 9 10 .............................................................50..................................................................................95...................
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  Percentiles • Arrange 100items in order of magnitude • The 50th item has 49 items below & 50 above – 50th percentile • The 95th item has 94 items below & 5 above – 95th percentile • The 5th item has 4 items below & 95 above – 5th percentile • +2SD = 97.72nd percentile -2SD = 2.28th percentile
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  SIZE TIME A lot ofdolls rolled out from a factory
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  Foetal population isheterogeneous Much like the adult population size TIME Ethnic, Racial, Social & Economic influences y x
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  TIME SIZE SIZE TIME Differencebetween the two graphs x x y y
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  • Y Y TIMESIZE SIZE TIME DATING GROWTH X – axis known parameter Y – axis derived information x x y y
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  Foetal size GestationalAge cms weeks Dating Growth
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  US determination ofGA – Dating scan Good in the 1st trimister & 1st half of 2nd trimister. First trimister - CRL up to 13wks + 6 days Second trimister – BPD, HC, AC and FL Dating is poor in the 3rd trimister Reassignment is done if there is more than one week difference from menstrual age. If not the Menstrual age is validated. Once reassigned the GA is not changed during the rest of the gestation.
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  RELIABILITY OF USDATING • +/- 8% of actual gestational age • 10weeks +/- 6 days • 24 weeks +/- 14 days • 34 weeks +/- 20 days
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  Essence Of DiagnosisOf Fetal Growth • Growth Normal / Abnormal • Date – Determination of Gestational age • Plot – Determination of growth • Date – only once (earliest) • Plot – more than once (growth) • No diagnosis of fetal growth or disorders without plotting growth curve.
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  Case study • LMP– 14- 3- 16 ; Dating scan – 11- 5- 16 ; MA = 9 weeks. • CRL = 2.7 cms = 9 weeks • Hence US GA correlates with MA • 2nd Scan 2- 8- 16 • GA = 8-9 weeks + interval = 9 wks + 11 wks = 20 wks. • The biometry is then done and the results are : • Parameter cms • BPD 4.8 • HC 17.3 • AC 15.2 • FL 3.0
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  CASE STUDY • Thedating scan could be from another centre in your town / city / country • 2nd scan – 2 – 8- 16 • GA = 8-9 weeks + interval = 9 wks + 11 wks = 20 wks. • The biometry is then done and the results are : • Parameter cms • BPD 4.8 • HC 17.3 • AC 15.2 • FL 3.0
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  Case study • Hence2nd scan parameters fall within the confidence limits for 20weeks and therefore the interval growth is normal. • 3rd scan 12 – 11 – 2016 • GA = 9wks + interval = 9 wks + 26 weeks = 35 weeks • The biometry is • Parameters cms • BPD 7.6 • HC 29.3 • AC 25.5 • FL 6.0
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  DOPPLER
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  Doppler effect: • Changein the apparent frequency due to relative motion between the source & the observer. (Doppler probe & RBCs) • When the sound wave strikes a moving target, the frequency of sound waves reflected back is proportionate to the velocity & direction of moving object. • Used to determine the volume & rate of blood flow through vessels.
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  Types: 1) CONTINUOUS WAVEDOPPLER: Two crystals are used, one transmits & other receives wave Used in M-mode echocardiography 1) PULSE WAVE DOPPLER: Only one crystal that Transmits-wait-Receives-wait-Transmits Allows precise targeting & visualization of the vessel of interest Have software that displays blood flow- Towards transducer as RED Away from transducer as BLUE
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  • Angle ofInsonation: Between Doppler beam & direction of flow • Higher the angle lesser the frequency & more the error.
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  Frequency change relativeto angle of insonation
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  To minimize errorwe use RATIOS, to cancel off the cosϴ Arterial Doppler indices  S/D Ratio: Peak systolic flow(S) End diastolic flow(D)
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   PULSATILITY INDEX: S-D ----------- Mean  RESISTANCE INDEX : S-D ---------- S Venous Doppler indices:
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  Quantitative analysis Doppler indices
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  • MATERNAL SIDE Uterineartery • PLACENTAL SIDE Umbilical artery • FETAL SIDE Arterial: MCA, Aortic Isthmus Venous: Ductus venosus, Hepatic vein, Umbilical vein Fetal echocardiography Doppler vessels to be studied
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  PLACENTAL RESISTANCE CARDIC FAILURE UMBILICAL. V DUCTUS VENOSUS DESCENDING AORTA
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  Uterine artery Doppler •Its main use is in screening. • Early diastolic notch in the uterine artery @ 12-14 wks. suggest delayed trophoblastic invasion . • Persistence of B/L notch beyond 24 wks confirms & indicates an increased risk of Pre-eclampsia, Placental abruption & Early onset IUGR. • Increase impedence of flow in Uterine artery @ 16-20 wks was predictive of superimposed pre-eclampsia developing in women with chronic hypertension.
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  Utero placental circulation Conversionof spiral artery into utero placental vessel Brosens et al
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  NORMAL ABNORMAL
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  Uterine artery Doppler: •As gestation increases diastolic flow velocities •High diastolic flow velocities
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  • UMBILICAL ARTERY •UA Doppler is the only measure that provides both diagnostic and prognostic information for the management of FGR. • On the one hand, increased UA Doppler PI has a great clinical value for the identification of FGR, alone or combined in the CPR ratio. • On the other hand, the progression of UA Doppler patterns to absent or reverse end-diastolic flow correlates with the risks of injury or death. • When Umbilical artery Doppler are incorporated into management algorithm of growth restricted fetus, perinatal death is reduced as much as 29%. • Umbilical artery Doppler becomes abnormal when at least 30% of the fetal villous structure is abnormal. • In extreme cases of growth restriction, end-diastolic flow may become absent or even reversed (AREDF).
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  • AREDF occurswhen 60-70% of the fetal villous structure is abnormal. • About ½ of the cases of AREDF are associated with aneuploidy or a major anomaly • Absent or reversed end-diastolic velocities, the end of the spectrum of the abnormalities of the UA Doppler, have been reported to be present on average 1 week before the acute deterioration. • There is an association between reversed end-diastolic flow in the UA and adverse perinatal outcome (with a sensitivity and specificity of about 60%), which seems to be independent of prematurity. • After 30 weeks the risk of stillbirth of a fetus with isolated reversed end-diastolic velocities in the UA Doppler overcomes the risks of premaurity.
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  UMBILICAL ARTERY DOPPLER •The amount of flow during diastole increases as gestation advances • Thus the S/D ratio and PI decreases.
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  ABNORMALUmbilicalARTERYWAVEFORM • Resistance index,S/D ratio and PI is increasing
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  ABNORMAL Umbilical ARTERYWAVEFORM Perinatal mortality rate in AEDF- 9-41%.
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  ABNORMAL Umbilical ARTERYWAVEFORM • Reversal of the End Diastolic Flow. • Perinatal mortality rate of REDF- 33-73%.
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  UMBILICAL ARTERY DOPPLER Umbilicalarteries NORMAL HIGH RESISTANCE ABSENT REVERSAL
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  MIDDLE CEREBRAL ARTERYDOPPLER • Middle cerebral artery pulsatility index < 5th percentile is considered early stage change of IUGR. • The nadir of MCA PI is reached 14 days or more before fetal compromise. • Normalisation of MCA PI  The reversal of adaptation in growth restricted fetus is considered a poor prognostic sign.  Due to cerebral edema. • MCA informs about the existence of brain vasodilatation, a surrogate marker of hypoxia. • Abnormal MCA PI had a six fold risk of emergency caesarean section for fetal distress when compared with SGA fetuses with normal MCA PI. • Abnormal MCA PI is associated with poor perinatal outcome and @ 2 years neurological outcome.
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  • REFLEX REDISTRIBUTIONOF FETAL CARDIAC OUTPUT  KIDNEYS (OLIGURIA) (OLIGOAMNIOS)  LUNGS (RDS)  GUT (NEC)  LIVER/MUSCLE (IUGR) BODY FAT/ GLYCOGEN STORES INCREASED FLOWDECREASED FLOW  BRAIN HEART ADRENAL
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  Normal MCA WAVEFORM
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  MCA WAVEFORM INIUGR • INCREASED FLOW DURING DIASTOLE
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  CEREBRO-PLACENTAL RATIO(CPR): MCA PulsatilityIndex Umbilical A. Pulsatility Index • The CPR is essentially a diagnostic index. • It is more sensitive index for detecting poor perinatal outcome than UA or MCA Doppler alone, the CPR is already decreased when its individual components suffer mild changes but are still within normal ranges. • Abnormal CPR predicts neurobehavioral problems at 18 months of age.
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  AORTIC ISTHMUS DOPPLER This vessel reflects the balance between the impedance of the brain and systemic vascular systems.  Strong association with both adverse perinatal and neurological outcome.  AoI precedes Ductus Venosus abnormalities by 1 week.
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  DUCTUS VENOSUS • Itis strongest single Doppler parameter to predict the short-term risk of fetal death in early-onset FGR. • DV flow waveforms become abnormal only in advanced stages of fetal compromise. • There is a good correlation of abnormal DV waveform with late- stage acidemia at cordocentesis. • Absent or reversed velocities during atrial contraction are associated with perinatal mortality independently of the gestational age at delivery, with a risk ranging from 40 to 100% in early-onset FGR. • In about 50% of cases, abnormal DV precedes the loss of short-term variability (STV) in computerized cardiotocography (cCTG), and in about 90% of cases it is abnormal 48–72 h before the biophysical profile (BPP).
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  Protocol IUGR Firststep: UtA + CPR + EFW = SGA or IUGR
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  STEROID PROPHYLAXIS • RCOG •Single course of antenatal corticosteroids to women between 24+0 to 34+6 weeks of gestation who are at risk of preterm delivery. • Antenatal corticosteroids can be considered for women between 23+0 to 23+6 weeks gestation who are at risk of preterm delivery, decision should made at senior level. • IUGR Single course of antenatal corticosteroid should receive between 24+0 to 35+6 weeks of gestation who are at risk of preterm delivery. • Antenatal corticosteroids should be given to all women for whom elective LSCS planned before 39 weeks.
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  continue • Single rescuecourse may be considered where initial course was given at less than 26+0 weeks. • In multifetal gestation single course of antenatal corticosteroids should be given between 24+0 to 34+6 weeks gestation at risk of preterm delivery. • Regularly scheduled repeat courses or serial courses of antenatal corticosteroids are not recommended.
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  ACOG • Single courseof antenatal corticosteroids should given to women between 24+0 to 33+6 weeks of gestation at risk of preterm delivery. (PPROM, MULTIPLE GESTATION, FGR) • Also consider for 23 0/7 weeks if risk of preterm delivery within 7 days, based on family decision regarding resuscitation. • Single course of corticosteroid should given between 34 0/7 to 36 6/7weeks at risk of preterm delivery within 7 days, who have not received a previous course of corticosteroid. • Single rescue course of antenatal corticosteroid should be considered in women less than 34 0/7 weeks of gestation at risk of preterm delivery within 7 days & prior course given more than 14days.
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  continue • Rescue courseshould be provided as early as 7 days from the prior dose, if clinically indicated. • Regularly scheduled repeat courses or serial courses of antenatal corticosteroids are not recommended.
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  • DOSAGE • Inj.Betamethasone 12mg i.m 2 doses 24 hrs apart. • Inj. Dexamethasone 6mg i.m 4 doses 12 hrs apart. • Betamethasone most preferred to Dexamethasone • Most effective 24 hrs after and up to 7 days after administration second dose of antenatal corticosteroids.
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  ADVERSE EFFECT OFMULTIPLE DOSES OF STEROIDS • Fetal growth restriction • Reduced birth weight • Reduced HC • Delayed myelination of CNS • Altered blood pressure soon after birth • Increased insulin response to glucose challenge in early childhood. • Behavioural disorders at 3 years of age. • Placental infarction • Adrenal gland insufficiency
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  • Perinatal morbidity& mortality of IUGR infants is 3-20 times greater than normal infants.(IanDonalds) • Risk is increased 3 times at 26 weeks compared with only a 1.13-fold increased risk at 40 weeks.(Williams 24rd edition)
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  Antenatal Period: • Oligohydraminos •Fetal Distress • IUD During labour: • Meconium aspiration • Fetal distress • Acidosis • Still birth
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  Neonatal period: • HypoxicIschemic Encephalopathy • Persistent Fetal circulation • Difficulty in temperature regulation • Hypoglycemia • Polycythemia • Necrotising Enterocolitis
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  Childhood: • Infectious Diseases •Cerebral Palsy(4-6 times higher) • Subtle impairment in cognitive improvement • Educational underachievement
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  Long term: Increase riskof  • Coronary Heart Disease • Hypertension • Type II Diabetes Mellitus • Dyslipidaemia • Stroke
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  BARKERS HYPOTHESIS David JP Barker British epidemiologist
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  • Management algorithmdepends heavily on  Gestational age  Doppler changes Difficult extrauterine environment Hostile intrauterine environment
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