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COLOR DOPPLER STUDIES ESTABLISHED FACTS IDENTIFY THE FETUS AT RISK FOR DAMAGE OR DEATH IN UTERO ARE AN ESTABLISHED TOOL TO ASSESS MODE AND TIMING OF DELIVERY PREDICT REASONABLY WELL THE FETUS AT RISK FOR A GROWTH DISORDER IMPROVE PREGNANCY OUTCOMES
COLOR DOPPLER STUDIES ESTABLISHED UTILITY HIGH RISK PREGNANCY FETAL WELL-BEING RISK OF CONTINUED INTRAUTERINE EXISTENCE LOW RISK PREGNANCY IDENTIFYING A SUB-GROUP OF FETUSES THAT NEED INCREASED SURVEILLANCE
COLOR DOPPER IN IUGRMETHODOLOGYNORMAL FETAL CICULATIONHYPOXIA-REDISTRIBUTION MECHANISM IN IUGRMANAGEMENT STATEGIES
PART I :METHODOLOGY 3.5- or 5-MHz curved-array transducer Spatial peak temporal average intensities <100 mW/cm2. High-pass filter - 125 Hz. Size of the sample volume adapted to the vessel diameter to cover it entirely. Recordings for measurements were obtained in the absence of fetal breathing movements and fetal heart R between 120 -160 bpm The angle between the ultrasound beam and the direction of blood flow was always less than 50°.
Principles of Color DopplerColor Doppler Power Doppler
Principles of Color Doppler
Quantitative analysis Doppler indices
The Supply Line to the Human Fetus PlacentaCuningham FG, MacDonald PC, Leveno K, Gant NF, Gilstrap LC II Williams Obstetrics 1993
Small for Gestational Age Environmental Infection/ Inflammation Genetic Endocrine MaternalNutritionalPlacental Unknown
FETAL HYPOXIA-ACIDOSIS AORTIC BODY CHEMORECEPTOR STIMULATIONREFLEX REDISTRIBUTION OF FETAL CARDIAC OUTPUT
REFLEX REDISTRIBUTION OF FETAL CARDIAC OUTPUT DECREASED FLOW INCREASED FLOW KIDNEYS (OLIGURIA) BRAIN (OLIGOAMNIOS) LUNGS (RDS) HEART GUT (NEC) LIVER/MUSCLE (IUGR) BODY FAT/ ADRENALS GLYCOGEN STORES
Organ-sparing effects Heart and brain sparing act synergistically with venous and arterial redistribution. Both of these organs derive their blood supply from the left ventricle. Vasodilatation at the organ level acts synergistically to increase organ blood flow.
Doppler vessels to be studied MATERNAL SIDEUterine artery PLACENTAL SIDEUmbilical a FETAL SIDEArterial:mca,fetal a,renal and othersVenous:ductus,hepatic,umbilicalFetal echocardiography
UTERINE ARTERIESREFLECTS : TROPHOBLASTIC INVASIONEND POINTS : ELEVATED RESISTIVE INDICES (>2SD) PERSISTENT DIASTOLIC NOTCHING PRESENCE OF SYSTOLIC NOTCHING MAJOR LEFT TO RIGHT VARIATION
Utero placental circulationConversion of spiral artery into uteroplacental vessel Brosens et al
Utero placental circulation Uterine Artery Normal impedance to flow the uterine arteries in 1º trimester Normal impedance to flow the uterine arteries in early 2ºtrimester Normal impedance to flow the uterine arteries in late 2º and 3º trimester
Uterine artery At 24 weeks No Dichrotic Notch PI < 1.2 Routine Screening Pre eclampsia & it’s severity can be predicted Monitoring of fetus
Uteroplacental circulation Normal Uterine Artery Abnormal
UMBILICAL ARTERIESREFLECTS : PLACENTAL OBLITERATIONEND POINTS : ABSENT END DIASTOLIC FLOW REVERSED END DIASTOLIC FLOW
NORMAL & ABNORMAL WAVEFORM IN ADVANCED PREGNANCY
UMBILICAL ARTERYAdvancing gestation Progressive rise in the end- diastolic velocity Decrease in the pulsatility index.
Umbilical artery Flow S/D ratio 2-3 in 2nd & 3rdtrimester PI1.5 – 2.0 in 2nd trimester1.0 –1.5 in 3rd trimester RI decreases with gest. In late Whether at fetal end, 2nd and 3rd it is around 0.5 placental end or in between – no difference
Umbilical Artery flow What does it tell us ?? First sign of hypoxia & growth retardation
Utero-placental circulation Umbilical artery progressive maturation of the placenta and increase in the number of tertiary stem villi.
Umbilical Artery Changes in umbilical artery waveform are evident only when 60% of Placental blood flow is obliterated
Normal Umbilical Artery 1º trimester Absent Diastolic Flow early 2ºtrimester Low Diastolic Flow late 2º and 3º trimester Resistance further reduce, more diastolic flow
Umbilical Artery - Abnormal Umbilical arteries - normal Umbilical arteries - high pulsatility index Umbilical arteries - Absent end diastolic velocity - very high pulsatility index. - pulsation in the umbilical vein Umbilical arteries reversal of end diastolic
Utero placental circulation Normal Abnormal Umbilical Artery
Umbilical Artery Cordocentesis was carried out in 39 IUGR fetuses Positive Diastolic Flow 12% Hypoxic 00% Acidemic Absent / Reverse Diastolic 80% Hypoxic Flow 46% Acidemic Nicolaides
N = 459 Umbilical ArteryFlow in Umbilical No of Relative Risk Artery fetus of Mortality Positive End 214 1 Diastolic Flow Absent End 178 4 Diastolic Flow Reverse End 67 10.6 Diastolic flow Clinical significance of absent or reversed end diastolic velocity waveforms in umbilical artery. Lancet 1994;344:1664–8
Absent / Reverse End Diastolic Flow Risk to Neonate More admissions to NICU Increase ICH Increase Anemia Increase Hypoglycemia Increase long term permanent neurological damage High Resistance Reversal of Diastole
Umbilical artery & CTG Umbilical artery 90% more sensitive to CTG Interval between absence of end diastolic flow & onset of late deceleration was 3-12 days High Resistance Bekedam DJ et al. Early Hum Dev 1990;24:79–89
MIDDLE CEREBRAL ARTERIES REFLECTS : CEREBRAL FLOWEND POINTS : RISING PI AFTER A NADIR
NORMAL & ABNORMAL WAVEFORM
Middle cerebral arteryThe blood velocity increases, PI decreases with advancinggestation
Middle cerebral artery DecompensationBrain sparing effect may be transientOverstressed fetus can lose the brain sparing effect.Disappearance of brain sparing effect - very criticalevent for the fetus- precedes fetal death.MCA may have tremendous implication for determiningthe proper timing of delivery.
DESCENDING ABDOMINAL AORTAREFLECTS : FLOW TO THE ABDOMINAL VISCERA AND LOWER LIMBSEND POINTS : PULSATILITY INDEX>6
FETAL AORTA Reflects cardiac output& per. Resistance. Diastolic velocities present during 2nd &3rd trimesters , PI remains constant. Summation of blood flows to flow in kidneys, abdominal organs, lower limbs and placenta. Approximately 50% of flow >>umb.artery.
Cardiac Function ? RV LV
Pulmonary Right Valve Coronary ArteryRight PulmonaryVentricle artery Aorta Left Atrium Left Coronary Artery Gembruch & Baschat. Ultrasound Obstet Gynecol 1996;7:10-15
3 D STIC AND INVERSION MODE ANALYSIS
Can a fetus have a heart attack ?
FETAL ILLNESS AND USG PATHOLOGICAL DECREASE IN RATE OF GROWTH (ULTRASOUND B MODE) SOONER OR LATER GROWTH RESTRICTED FETUSES BECOME HYPOXEMIC,HYPOXIC AND ACIDOTIC (THIS CAN BE DIAGNOSED BY DOPPLER) FETAL ILLNESS IS RELATED TO FETAL,MATERNAL AND PLACENTAL CAUSES MOST FREQUENT ETIOLOGY OF A SICK FETUS IS MILD TO MODERATE UTEROPLACENTAL INSUFF DUE TO P.I.H.
Markers For Fetal illness AFI Chronic Marker NST FT Acute Markers FM FBM
Manning’s Biophysical Profile NST FBM FM FT AFI Maximum score 10 Minimum 0 Oligohydramnios indicates abnormal BPP regardless of the total score of others
Oligohydramnios IndicatesAbnormal BPP independent of other variables because of a risk of cord complications and fetal death.
Modified Biophysical Profile (MBPP) VAST with NST for index of acute hypoxia ® AF Volume – index for chronic fetal problems ® Excellent negative & positive predictive values (Vintzielos) ® Can be performed in 20 mins.
FETAL BPP VS DOPPLER AMNIOTIC FLUID IS DUE TO PLACENTAL FUNCTION ,FETAL URINATION,FETAL SKIN,UMBILICAL CORD AND THE BLOOD VOLUME. AT EARLY PLACENTAL HYPOFUNCTION THE AFI REMAINS NORMAL,NOR IS THE AFI REDUCED IN ACUTE HYPOXIA THIS PHASE OF F.G.R IS DECEPTIVE TO BPP AND IT IS THIS WHICH IS PICKED UP BY DOPPLER B’COS BY THIS TIME DOPPLER WILL SHOW AEDF OR REDF AND ABNORMAL VENOUS FLOW HENCE WAITING FOR LESS LIQ WILL DELAY THE
Hypoxia & MarkersUmb. pH at which abnormal Test7.20 Abnormal NST<7.20 FBM7.10 - 7.20 Movements< 7.10 ToneThis should be kept in mind for interpretation of Hypoxia andacidosis
Time to deliverFactors to decide time to deliver Degree of Prematurity NICU facility Degree of Hypoxia, acidemia, hepatic metabolic derangement Challenge to weigh the risks and benefits of interventions
Time to deliverWhen you want to deliver? ? Mild to moderate Hypoxia ? Moderate Hypoxia with early acidemia ?? Severe hypoxia with moderate to severe acidemia & hepatic metabolic derangements Best time when fetal redistribution mechanism start failing
Take Home Message Doppler is very sensitive to detect fetal hypoxia & acedimia Serial doppler study is required to decide time of delivery to reduce the perinatal morbidity & mortality
Low-RiskSuggestions If Doppler is available It may identify a fetus with IUGR who registers later and you are uncertain of the gestational age Doppler French Study Group Br J Obstet Gynecol 1997, 104:419
CARDIAC FAILURE -VENOUS BLOOD FLOW Retrograde flow in IVC , DV with atrial contraction UV pulsations
Staging of growth restricted fetus:Intrauterine growth restriction was defined as the presence of an estimated fetal weight below the 10th percentile. Intrauterine growth-restricted fetuses were staged according to the following parameters, with the presence of any 1 parameter in a stage placing the fetus in that stage
stage I an abnormal umbilical artery or middle cerebral artery pulsatility index;
stage IIan abnormal MCA PSV,absent/reversed diastolic velocityin the UA,UV pulsation and an abnormal DV PI(an absent DV A wave is consideredpart of thisstage)
stage III reversed flow at the ductus venosus or reversed flow at the umbilical vein, an abnormal tricuspid E wave (early ventricular filling)/A wave (late ventricular filling) ratio, and tricuspid regurgitation.
Each stage divided in A & B A is AMNIOTIC FLUID INDEX <5 B is AMNIOTIC FLUID INDEX OF >5
The rationale for the division of IUGR fetuses into 3 stages was based on the results of previous studies in which we serially determined the changes of 15 Doppler parameters occurring in IUGR fetuses from the time the diagnosis was made up to delivery.On the basis of results of those studies, we should have divided the set of IUGR fetuses into 15 stages, but to keep the staging as a practical diagnostic tool, we limited it to 3 stages.
MANAGEMENT STRATEGIES Mild utero-placental insufficiency No effect is seen on Doppler and growth until 26-32 weeks gestation. The umbilical artery and the middle cerebral artery waveforms may be abnormal However process is not severe enough to stop fetal growth completely or to deteriorate These cases may be followed with outpatient monitoring and they often deliver at term.
Assessment of IUGR Fetus Biometry Fetal assessment for malformation AF Fetal Activity (Biophysical Profile) Color Doppler
IUGR Fetal surveillance Fetal heart rate monitoring Biophysical profile NST CST VAST Fetal blood sampling Color Doppler Study
What Kind of Information on CD ? Utero placental circulation – Predictive Uterine Artery & Umbilical Artery Fetal Arterial Circulation – Cut Off Line Redistribution of Blood & brain Sparing Effect Fetal Venous Circulation - Decision Timing of Delivery Degree of acidemia & Hypoxia
Changes due to Hypoxia When > 50% placenta is not functioning Mild Hypoxia – Umbilical artery When > 70% placenta not functioning Moderate Hypoxia -> Compensatory redistribution in MCA When > 90% placenta not functioning Severe Hypoxia -> Failure of Compensatory redistribution - DV
How to Judge Degree of Hypoxia? Fetal arterial doppler Cut off Line
Fetal arterial circulation Fetal Arterial Circulation – Cut Off Line Redistribution of Blood & brain Sparing EffectCompensatory RedistributionMore flow of oxygenated blood Less flow of oxygenated bloodBrain KidneysMyocardium GITFetal adrenal Limbs, LungsMCA – Nadir reached 2 weeks before fetal jeopardy
Pulsatile Umbilical vein Flow
MCA flowPI More than 1.45 before term Fall down to 1 If less than 1 peak of redistribution
How to Judge degree of Acidemia? Fetal Venous doppler
Fetal Venous Doppler The PI of the middle cerebral was the best predictors of hypoxemia, DV flow was the best predictor of Acidemia and hyper capnia. Fetal Venous Doppler IVC Rizzo et al. Ductus Venosus Br J Ob Gyn 1995; 102:963-69 Umbilical Vein SVC
RA RV HV DV RA RV HV DVGrowth Retardation
Umbilical Veinstudy of 37 fetuses ~~ absent end-diastolic frequenciesin the umbilical arteryNeonatal mortality• in group with pulsatile venous flow was 63%,• In group without pulsation was 19% Arduini D, Rizzo G et al Am J Obstet Gynecol 1993;168: 43–50