Iugr 11july

Iugr 11july

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  IUGR-ETIOLOGY & DIAGNOSIS Dr.SumanKumari MS OBGY TATA MAIN HOSPITAL
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  Introduction IUGR/FGR A fetus thathas not reached its growth potential because of genetic or envoirnmental factors. Results in  BW < 10%tile as per the customised growth curve.  Inhibition of normal growth potential  implies pathology SGA:  BW less than population norms < 10th %-tile  usually physiological or constitutional
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  Cause of concern •Leading contributor - Perinatal mortality rate(50%) at preterm and 20% at term. • 40% of all stillbirths are IUGR. • Perinatal morbidity as well as delayed effects including cerebral palsy(CP) .
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  Effect of birthweight on Perinatal morbidity and mortality.
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  The developmental originsof adult disease — Barker’s hypothesis Growth retardation in utero can Cause hypertension, diabetes , Cardiac problems in adult life.
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  Why antenatal diagnosis •Early detection of IUGR categorised the women into high risk group. • Early identification, further investigation and intervention leads to significantly improved outcome. • Depending upon the severity optimal timing of delivery could be decided. • Antenatal detection of IUGR has better outcome.(Molin J.2005). • Identification and management lowers this perinatal mortality and morbidity.
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  Normal Intrauterine Growth
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  IUGR - Types •Symmetric Stage I growth inhibition Fewer cells but normal size weight, head, length all < 10th percentile • Asymmetric Stage II/III growth inhibition Decrease in cell size, less effect on total cell number weight below 10th percentile,head and length preserved
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  Physiology
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  Pathophysiology • Gas exchangeand nutrient delivery to the fetus are not sufficient - IUGR maternal disease  diabetes with vascular disease, hypertension, autoimmune disease affecting the vessels-- dysfunctional oxygen delivery system  cyanotic heart disease, smoking, hemoglobinopathy--- causing decreased oxygen-carrying capacity  smoking, thrombophilia, various autoimmune diseases-- placental damage
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  Pre-eclampsia/ HELLP
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  Diabetes • Diabetes-usually macrosomic. •IUGR-15-20% when preeclampsia associated with diabetes without nephropathy . • IUGR-50% when preeclampsia associated diabetic nephropathy.
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  Etiology- Overlapping Maternal factor •Chronic hypertension • Pregnancy associated hypertension. • Cyanotic heart disease • Class F or higher diabetes • Hemoglobinopathies • Autoimmune disease • Protein-calorie malnutrition • Smoking • Substance abuse
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  Placenta • Placental insufficiency –PIH,Preeclampsia,diabetes mellitus. – Chronic hypertension • Anatomic – abnormal insertion – hemangiomas – infarcts – Abruption – Twin to twin transfusion syndrome.
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  Fetal factors • Genetic •Congenital malformations • Genetic/ chromosomal (trisomies, syndromes) • Cardiovascular disease • Congenital infection • Inborn errors of metabolism
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  Discordant twins • Growthstandards for multiple pregnancies are there but singleton nomograms are more used commonly with good accuracy. Discordance >20-25% is significant.
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  Trisomy 13 Turner syndrome
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  Toxoplasmosis Rubella
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  Uterine factors • Morphologicalabnormalities • Fibromyoma
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  Diagnosis • History • Physicalexamination • Biochemical screening in ANC • Ultrasound and Fetal biometry • USG doppler
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  HISTORY • Risk factorassessment by history. • Previous h/o still birth baby have a 50% increase risk of severe growth restriction in current pregnancy. (Villar J,AJOG 2006) • h/o dysmorphic feature or chromosomal anomaly .
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  TORCH” Stigmata – hepatoslpenomegaly –petechiae/ ecchymoses – blueberry muffin rash – vesicles/ mucocutaneous lesions – chorioretinitis/ cataracts/ salt-pepper retinopathy – PDA – microcephaly/ hydrocephaly • Intracranial calcifications
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  Physical exam. • Abdominalexam-detection rate-30 to 50%. • Symphysio fundal height(SFH)-sensitivity is 50%.  Uterine fundal height corresponds to week of gestation between 18 to 36 week.  Serial SFH supplemented with anatomic USG- increases the accuracy of diagnosis.  Lag of 3 cm-- prompt USG indicated.  Unsuitable in case of fibroid uterus,obesity.
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  Clinical examination • SFH
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  Customised growth curve(CGC) Customised growth curve (CGC)-design to identify fetus <10%tile of their genetic growth potential
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  Biochemical test inANC • Biochemical screening –for at risk pregnancy. • First trimester-low pregnancy associated plasma protein –A(PAPP-A) . • Decrease PAPP-A with increase AFP,inhibin and hCG suggest IUGR.(Dugoff L,AJOG 2004)
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  Ultrasound diagnosis • USGassessment requires three basic steps 1. Accurate dating 2. Biometric evaluation and 3. Assessment of growth.
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  USG 1. Accurate assessmentof the gestational age is most important before diagnosing IUGR. • 1ST trimester USG can confirm the date with margin of 1 wk. • TCD-most effective ,for dating in second and third trimester and being normal in 75% of 73 previously dated IUGR fetuses. • serial measurement are nessessary to depict actual growth lag. • Interval between growth scan should be atleast 2 wk.
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  Parameters 2.Parameters to assessbiometric growth are-  Biparietal diameter(BPD)  Head circumference(HC)  Abdominal circumference(AC)  Femur length.(FL) To estimate fetal weight(EFW)-sensitivity 89%,specificity-91%  HC/AC ratio,FL/AC ratio
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  Abdominal circumference(AC)  Mostaccurate measurement to predict IUGR.  Cut off-below the 10TH %tile.  Sensitivity 74-94% ,specificity-50%  Should increase by atleast 10mm / 2 week.  So SFH measurment and biometry scan are basically surveillance test,require serial monitoring.
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  USG • For fetalanatomy (anomaly scan)  At 18 -20 wk gestation.  Risk factors are-  Asymmetry of parameters  Short femur  Bowel echogenisity  Oligohydraminous • Placental mlorphology • Amniotic fluid volume.(AFI)-when oligohydraminous AFI<5cm at 37 wk-suspected IUGR. • Polyhydraminous with suspected IUGR s/o fetal cause.
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  Doppler velocimetry. • Purposeto dectect IUGR fetus at risk of hypoxia • Not to be used as routine screening method. • Used only when USG picks up IUGR.
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  Umbilical artery doppler •Umblical artey doppler is the standard test ,to detect Placental insufficiency(m.c cause of IUGR) • Diffrentiate between SGA and IUGR. • Progression is from normal end-diastolic velocity (EDV)---- to decreased,---- to absent to ------reverse EDV. • Absent or reversed end-diastolic velocities are mostly S/O early-onset IUGR. • These patterns seen to be present approx. 1 week before the acute deterioration.(Ferrazzi E,2002)
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  • The normalumbilical artery flow --marked positive end-diastolic velocity (A). • Moderate abnormalities in the villous vascular structure raise the blood flow resistance and are associated with a decline in end-diastolic velocities (B). • When a significant proportion of the villous vascular tree is abnormal (50-70%), end-diastolic velocities may be absent (C) or even reversed (D). • Depending on the magnitude of placental blood flow resistance and the fetal cardiac function, reversal of end-diastolic velocities may be minimal (D), moderate (E), or severe (F).
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  Uterine artery doppler •By 20 weeks, low-impedance waveform and no diastolic notch. • If still high impedance and diastolic notch, high risk of IUGR and/or preeclampsia. • As screening test, 82% sensitivity, 38% specificity (Bewley, 1991) • Value in high-risk patients only
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  Flow velocity waveforms obtainedfrom the uterine artery • (A) high-volume diastolic flow –normal • placental vascular resistance is associated with a decline in diastolic velocities and a subsequent rise in the Dopplerindex (B). • Persistence of an early diastolic notch is evidence of increased spiral artery blood flow resistance. (C) “notching” (D).
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  Ductus venosus doppler •Normal is forward flow during atrial contraction. • IUGR causes  peripheral resistance and eventually heart failure with no forward flow. • When back pressure reaches umbilical vein, normally minimally pulsatile waveform becomes pulsatile as sign of imminent demise.
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  In the ductusvenosus blood flow is always antegrade throughout the cardiac cycle under normal circumstances. Pulsatility is less pronounced in waveform patterns obtained at the inlet (A) versus the outlet (B). With impaired cardiac forward function there is a decline in forward flow during atrial systole (C). If progressive atrial forward flow may be lost (D) or reversed (E, F).
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  Middle cerebral arterydoppler • In normal fetus –increase in middle cerebral artery resistance as shown by resistance indices. • When there is hypoxia,or stress,fetus show redistribution of blood flow preferentially to brain and heart(brain sparing). • doppler showing decrease in middle cerebral artery resistance.
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  MCA doppler cont.... •Up to 20% of SGA fetuses have reduced resistance in the middle cerebral artery (MCA), • This sign is associated with poorer perinatal outcome • suboptimal neurodevelopmental development at 2 years of age.
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  A, Color Dopplerassessment of the MCA at the level of the circle of Willis. B, Normal and abnormal(high diastolic velocities and decreased pulsatility index) C,
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  Diagnostic algorythm History s/o–IUGR Usg for dating Biochemical markers serial SFH and biometric assessment Umblical artery doppler Ut. artery doppler MCA/DV doppler