Intrauterine growth restriction

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<ul><li> 1. Intrauterine Growth Restriction (IUGR) Prof. M.C.Bansal MBBS,MS,MICOG,FICOG Professor OBGY Ex-Principal &amp; ControllerJhalawar Medical College &amp; Hospital Mahatma Gandhi Medical College,Jaipur.</li></ul><p> 2. Definition Foetuses of birth weight less than 10th percentileof those born at same gestational ageortwo standard deviations below the populationmean are considered growth restricted. small for gestational age (SGA) fetuses, all ofwhich may not necessarily growth restricted as many ofthese may be just constitutionally small and not atrisk of any adverse outcome.) 3. Therefore the term IUGR shouldmore strictly refer to foetusesthat are small for gestational ageand display other signs of chronichypoxia or failure to thrive. 4. Incidence Approximately 3-5% of allpregnancies. 5. Normal Ftal Growth Ftal growth depends on two components: Genetic Potential Substrate supplyThe genetic potential is derived from both parentsand is mediated through growth factors such asinsulin-like growth factor.Adequate substrate supply is essential to achievegenetic potential. This is derived from placentawhich is dependent upon the uterine andplacental vascularity 6. A comparision between normal andIUGR babies. 7. Normal and IUGR placenta 8. Normal Fetal Growth Normal fetal growth is characterizedbycellular hyperplasia followed byhyperplasia and hypertrophy andlastly byhypertrophy alone. 9. Foetal Growth indices Weight gain Foetal growth accelerates from about5g per day at 14 -15 wks of gestation to 10g per day at 20 wks Peaks at 30 -35g per day at 32-34wks After which growth rate decreases. 10. Symphysiofundal height increases byabout 1cm per wk between 14 and32 wks. Abdominal girth increases by 1 inchper wk after 30 wks. It is about 30inches at 30wks in an average builtwoman. 11. Classification of Inrauterine GrowthRestriction 1. Type 1 or symmetrical or intrinsicIUGR 2. Type 2 or assymetric IUGR 3. Intermediate IUGR 12. Classification of IUGR Type 1 or symmetrical IUGR- (20-30%)Occurs as a result of growth inhibition early inpregnancy i.e. the hyperplastic stage. Anypathological insult at this phase leads to reducedno. of cells in fetus and overall decreased growthpotential.Causes include- Intrauterine infections (TORCH )Chromosomal disordersCongenital malformations 13. All parameters(head and abdo circumference,length and weight) are below 10th percentilefor gestational age, hence normal ponderalindex (birth weight/ht3). 14. Type 2 or asymmetric IUGR (70-80%)Occurs as a result of restriction of nutrientsupply in utero i.e. uteroplacentalinsufficiency.It is usually associated with maternaldiseases like:- Chronic hypertension Renal disease Vasculopathies 15. The onset of growth restriction occurs usuallyafter 28 wks of gestation i.e. in the stage ofhypertrophy. The fetus has near normal totalno. of cells but cell size is reduced. There is brain sparing effect so that the headgrowth remains normal but the abdominal girthslows down. The Ponderal index is low. This asymmetry results from redistribution offetal cardiac output with increased flow to brainand heart at the expense of reduced splanchniccirculation. 16. Liver size is reduced because ofdiminished glycogen stores. In case of severe placentalinsufficiency the head growth may alsobe affected.This type of growth restriction leads todecreased amniotic fluid, chronichypoxia and may result in fetal death. 17. Intermediate IUGR (5-10% of all growthrestricted fetuses) It is a combination of type 1 and type 2. Fetal growth restriction occurs duringintermediate phase of growth affectingboth hyperplasia and hypertrophy,resulting in decrease in cell no. as well assize. Causes include Chronic HT Lupus nephritis Maternal vascular diseases that are severe and 18. IUGR may also be classified simplyas Early onset (onset before 32 weeks) Late onset (onset after 32 weeks) 19. Aetiology IUGR is a manifestation of fetal, maternal andplacental disorders that affect fetal growth.A.Fetal Causes1. Chromosomal Disorders- usually result in early onset IUGR. Trisomies 13, 18, 21 contribute to 5% of IUGR cases Autosomal deletions Ring chromosomes Sex chromosome disorders are frequently lethal, fetuses that survive may have growth restriction (Turner Syndrome) 20. Fetal causes contd..2. Congenital Infections: The growth potential of fetus may be severelyimpaired by intrauterine infections. The timing of infection is crucial as the resultanteffects depends on the phase of organogenesis. Viruses- rubella, CMV, varicella and HIV rubella is the most embryotoxic virus, it cause capillaryendothelial damage during organogenesis and impairs fetalgrowth. CMV causes cytolysis and localized necrosis in fetus. Protozoa- like malaria, toxoplasma, trypanosomahave also been associated with growth restriction. 21. Fetal causes contd..3. Structural Anomalies-All major structural defects involvingCNS,CVS,GIT, Genitourinary and musculoskeletalsystem are associated with increased risk of fetalgrowth restriction.If growth restriction is associated withpolyhydramnios, the incidence of structuralanomaly is substantially increased. 22. Fetal causes contd..4. Genetic Causes- Maternal genes have greater influence on fetal growth.Inborn errors of metabolism like agenesis of pancreas, congenital lipodystrophy, galactosemia, phenylketonuria also result in growth restriction of fetus. 23. B. Placental causes Placenta is the sole channel for nutrition andoxygen supply to the fetus.Single umblical arteryabnormal placental implantationvelamentous umblical cord insertionbilobed placentaplacental haemangiomas have all been associated with fetal growth restriction 24. C. Maternal Causes1. Maternal Characteristics:those contributing to IUGR are- Extremes of maternal age Grandmultiparity History of IUGR in previous pregnancy Low maternal weight gain in pregnancy 25. 2. Maternal diseases: Uteroplacental insufficiency resulting from medical complications like Hypertension Renal disease Autoimmune disease Hyperthyroidism Long term insulin dependent diabetes 26. Maternal causes contd.. Smoking- active or passive, especially duringthird trimester is important cause of IUGR.Nicotine has vasoconstrctive effect on thematernal circulation and leads to formaton oftoxic metabolites in fetus. Alchohol and Drugs- Alchohol crosses theplacenta freely. It acts as a cellular poisonreducing fetal growth potential. Cocaine and opiates are potent vasoconstrictors. Warfarin, anticonvulsants and antineoplasticagents are also implicated in growth restriction 27. Thrombophilias- antiphospholipid antibodysyndrome and other thrombophilias leading toplacental thrombosis and impaired trophoblasticfunction. Nutritional Deficiency- poor intake-inflammatory bowel disease 28. Complications of IUGRPerinatal mortality and morbidity of IUGR infantsis 3-20 times greater than normal infants. Antepartum period- increased incidence of--still births-oligohydramniosIUGR is found in 52% of unexplained stillbirths. During labour- higher incidence of--meconium aspiration-fetal distress-intrapartum fetal death 29. Complications of IUGR contd.. Neonatal period- increased incidence of--Hypoxic ischemic encephalopathy-Persistent fetal circulation insufficiencyThey have difficulty in temperature regulation becauseof absent brown fat and small body mass relative tosurface area.Lack of glycogen stores may predispose tohypoglycemiaChronic intrauterine hypoxia may lead topolycythemia, necrotizing enterocolitis, othermetabolic abnormalities. 30. Complications cont.. Childhood- increases mortality from- -infectious diseases -congenital anomaliesIncidence of cerebral palsy are 4-6 times higher.Subtle impairment of cognitive performance and educational underachievement. Long term complications- increased risk ofcoronary heart disease, hypertension, type IIdiabetes mellitus, dyslipidaemia and stroke. 31. Diagnosis of IUGRIdentifying mothers at risk:Poor maternal nutritionPoor BMI at conceptionPre-eclampsiaRenal disordersDiseases causes vascular insufficiencyInfections (TORCH)Poor maternal wt. gain during pregnancy 32. Determination of gestational age is of utmostimportance- Can be calculated from the date of LMP- notreliable Ultrasound dating before 21 wks of pregnancyprovides more accurate estimate. 33. Diagnosis of IUGR1. Clinically- Serial measurement of fundal height and abdominal girth. Symphysio-fundal height normally increases by1cm per wk b/w 14 and 32 wks. A lag in fundal ht. of 4wks is suggestive ofmoderate IUGR. A lag of &gt;6 wks is suggestive of severe IUGR. 34. 2. Sonographic evaluation- most useful tool for diagnosis of IUGR To differentiate between symmetrical andasymmetrical IUGR To monitor the fetal condition.Fetal biometry:i. BPD(Biparietal Diameter)- determines gestational age and type of IUGR. When growth rate of BPD is below 5th percentile, 82% of births are below 10th percentile(i.e. IUGR). 35. ii. Head circumference- better than BPD in predicting IUGR.iii. Transeverse cerebellar diameter(TCD)- can be used as a method to assess gestational age.iv. Abdominal circumference(AC)- AC and fetal wt are most accurate ultrasound parameters for diagnosis of IUGR. AC has highest sensitivity and greatest negative predictive value for sonographic diagnosis of IUGR 36. An increase in fetal AC of less than 10 mm in 14 days has sensitivity of 85% and specificity of 74% for identification of IUGR.iv. Measurement ratios- there are some ageindependent ratios to detect IUGR.HC/AC: decreases linearly from 16 to 20 wks of gestation. HC/AC &gt;2 SD above mean is predictive of IUGR.FL/AC: normal value ranges from 22 + 2% in the second half of pregnancy. Ratio above 23.5% is considered abnormal. 37. Placental Morphology: Acceleration ofplacental maturation may occur with IUGRand PIH.(Placenta is graded from grade 0 to grade III) Amniotic fluid volume: type 2 IUGR is usuallyassociated with oligohydramnios.Amniotic fluid index(AFI) between 8 and 25 is normal. 38. 3. Doppler Ultrasonography: doppler flow studies are important adjuncts to fetal biometry in identifying the IUGR fetuses at risk of adverse outcome.Most widely used arterial indices are :Pulsatility index (PI): Systolic end diastolic peakvelocity / time averaged maximum velocityResistance Index(RI): Systolic end diastolic peak velocity/ systolic peak velocitySystolic to diastolic ratio(S/D): Systolic peak velocity / diastolic peak velocity 39. Umblical Artery doppler- In IUGR there isincreased umblical artery resistance (increasedS/D ratio), absent end diastolic flow and finallyreversed end diastolic flow.Perinatal mortality rate increases significantly infetuses with absent end diastolic flow (9-41%)and reversed end diastolic flow (33-73%) inumblical artery. 40. Middle cerebral artery doppler- in a normal fetushas relatively little flow during diastole.Increased resistance to blood flow in placentaresults in redistribution of cardiac output tofavour cardiac and cerebral circulations leadingto increased flow in the diastolic phase withdecreased S/D ratio. 41. Normal Flow velocity waveforms of middle Cerebral ArteryDoppler 42. Cerebral artery doppler 43. Cerebral/Placental ratio: ratio between MCA PI and umblical artery PI is more sensiive predictor than either MCA and umblical artery velocimetry alone to detect redistribution of blood flow.Cut off values below 1.0 to 1.1 are considered to be diagnostic of brain spairing effect. MCA peak systolic velocimetry: is good indicatorof fetal anaemia and is less useful in IUGR. 44. Ductus venosus doppler: Perinatal mortality in growth restricted fetuses has been found to be significantly worse when abnormalities in fetal venous circulation are detected.In the normal fetus, flow in the ductus venosus is forwards , moving towards the heart during entire cardiac cycle.When circulatory compensation of the fetus fails, the ductus venosus waveform shows absent or reverse blood flow during atrial conraction. Perinatal mortality being 63-100%.Therefore it is recommended that fetus should be delivered before the development of absent of reversed blood flow of DV. 45. : Representation of fetal umbilical and hepaticvenous system. The arrows indicate the directionof flow.FO, foramen ovale; RA, right atrium; DV, ductusvenous; UV, umbilical vein; HV, hepatic veins; IVC, inferior venacava; PS, portal sinus; LPV, left portal vein; RPV, right portalvein; EPV, extrahepatic portal vein; GB, gallbladder 46. MANAGEMENT Principles:1. Identify the cause of growth restriction.2. Treat the cause if found.3. General management 47. MANAGEMENT First step is to identify the aetiology of IUGR:- Maternal history pertaining to the risk factors ofIUGR. Clinical examination- maternal habitus, height,weight, BP etc. Laboratory investigations- Hb, blood sugar, renalfunction tests, serology for TORCHSpecific investigations for thrombophilias in pts withhistory suggestive of early onset growth restriction. Fetal evaluation: thorough ultrasound for growthrestriction, amniotic fluid, congenital anomalies anddoppler evaluation 48. Management cont.. Treatment of underlying cause: such ashypertension, cessation of smoking, proteinenergy supplementation in poorly nourished andunderweight women. 49. General Management: Bed rest in left lateral position to increaseuteroplacental blood flow Maternal nutritional supplementation with highcaloric and protein diets, antioxidents,haematinics and omega 3 fatty acids, arginine . Maternal oxygen therapy: Adminitration of 55%oxygen at a rate of 8L/min round the clock hasshown decreased perinatal mortality rate. 50. Effect of bed rest on various parameters of fetalgrowth 51. Management cont.. Pharmacological therapy:Aspirin in low doses(1-2 mg/kg body wt.),betamimetics etc have been tried but all havefailed to show any significant difference inincidence of IUGR.Thus there is no form of therapy currently availablewhich can reverse IUGR, the only interventionpossible in most cases is delivery. 52. Delivery: Since IUGR fetus is at increased risk ofintrauterine hypoxia and intrauterine demise, thedecision needs to delicately balance the risk to thefetus in utero with continuation of pregnancy andthat of prematurity if delivered before term. Judge Optimum Time Of DeliveryRISK OF PREMATURITYRISK OF IUDDIFFICULT EXTRA HOSTILE INTRA UTERINE UTERINE EXISTENCE ENVIRONMENT 53. The optimum timing of delivery is determinedby gestational age, underlying aetiology,possibility of extrauterine survival and fetalcondition. Strict fetal surveillance is needed to monitorfetal well being and to detect signs of fetalcompromise 54. Fetal Surveillance1. Daily fetal movement score2. Non stress test(NST)3. Biophysical profile(BPP)4. Amniotic fluid index(AFI)5. Growth parameters6. Doppler studiesSonography is usually repeated every 2 wks. 55. Management cont.. Role of steroids: Antenatal glucocorticoid administration red...</p>


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