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Introduction

Intrauterine growth restriction (IUGR) is a term usedto describe the fetus with a birth weight at or below the10th percentile for gestational age and sex. The IUGRfetus is a fetus that does not reach its growth potential.

The two components that are necessary to define an

IUGR fetus are:

a) birth weight < 10th percentile; b) Inadequate intervalgrowth in sequential screening

The placenta is the lifeline of the fetus and, when chal-lenged, it has a remarkable ability to adapt. Develop-mental problems can occur from the maternal side, thefetal side, or both 1.

The development of a good utero-placental circulationis essential for the achievement of a normal pregnancy.To facilitate this, remarkable changes occur in the ma-ternal, placental and fetal vasculatures 2. When thismechanism fails, abnormal vascular resistance patternsdevelop which lead to compromise of fetal well-beingwith a 6 to 10 times higher risk of perinatal mortality,

J Obstet Gynecol India Vol. 60, No. 4 : July / August 2010 pg 301 - 311

Review Article

Colour Doppler in IUGR- Where are we and where do we go?

Lulla Chander 1 & Garg Sonal2

1Sonologist 2 Senior ResidentDept. of Ultrasonography, Jaslok Hospital and Research Centre, Mumbai

Paper received on 05/08/2010: accepted on 15/08/2010

Correspondence:Dr. Garg Sonal(Radiodiagnosis) (2012)Senior Ultrasound Resident,Jaslok Hospital and Research Centre, Mumbai.Email: [email protected]

Abstract

Intra-uterine growth restriction (IUGR) is an important perinatal problem giving rise to increased morbidity and mortality in thegrowth restricted fetus. The aim of fetal medicine today, is to prevent the mere occurrence of IUGR in high risk pregnancies andto deliver the fetuses already afflicted with growth restriction, before they have suffered from the effects of hypoxia. The useof Doppler provides this information, which is not readily obtained from the other conventional tests of fetal well being. TheDoppler patterns follow a longitudinal trend in the arterial and venous circulation of the fetus as well as the placental vasculatureguiding management decisions regarding the appropriate time of delivery. Progressive knowledge of the fetal circulation andits adaptation when the fetus is subjected to hypoxia, has helped us recognize the early signs of IUGR thereby improving theprognosis of these complicated pregnancies. It has therefore become the gold standard in the management of the growth-restrictedfetus.

Key words: Intra uterine growth restriction, Fetal circulatory changes in IUGR, Doppler based management in IUGRAortic Isthmus

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morbidity, and impaired neurodevelopment 3, 34.

Kingdom et al demonstrated that maldevelopment ofthe villous tree in pregnancies complicated by fetalgrowth restriction is associated with abnormal uterineartery waveforms, indicating abnormal uteroplacentalblood flow. In pregnancies also complicated by absentend-diastolic umbilical flow, the placental villi are elon-gated, and the capillary loops are uncoiled and sparse.These findings are correlated with an increase in fetal-placental vascular impedance and impaired gas and nu-trient exchange. An enhanced branching angiogenesisrepresents an adaptive response to impaired uteropla-cental blood flow 4.

The introduction of color Doppler technology has pro-vided the first opportunity for repetitive noninvasivehaemodynamic monitoring in pregnancy. There isample evidence that Doppler indices from the fetal cir-culation can reliably predict adverse perinatal outcomein an intrauterine growth restricted (IUGR) pregnancy.Compared to other methods of fetal monitoring,Doppler has proved to be more sensitive in detectingfetal compromise early and aids in the guiding andmaking of decisions regarding the appropriate timingof delivery 5. The Doppler patterns follow a longitudi-nal trend with early changes in the middle cerebral ar-tery and umbilical artery followed by other peripheralarteries. These indicate the occurrence of redistributionof blood flow in growth restricted fetuses and thereforecaution us to closely monitor the fetus and intervenebefore the situation becomes unsalvageable. If adequatemeasures are not taken at this point, venous changesappear in the severely compromised fetus. These arestrong predictors of poor perinatal outcome and indi-cate impending irreversible damage.

Doppler reveals changes of hypoxia at least a week be-fore the non-stress test or the biophysical profile. It hastherefore become the gold standard in the managementof the growth-restricted fetus 6, 7.

Technique of Color Doppler ultrasound

The patients are first scanned in the routine fashionusing B-mode with a 3.5- or 5-MHz curved-array trans-ducer. The vessel of interest is located by color Doppler.The spectral Doppler waveform is then obtained byplacing the Doppler gate directly over the vessel of in-terest. The spectral recordings should ideally be ob-tained in the absence of fetal breathing movements and

fetal heart rate between 120 and 160 bpm. . The bestwaveform will be obtained when the angle of in-sonation is between 30 to 60 degrees. Difficulty maybeencountered when studying fetal vessels that move withfetal movements and that are non-linear, e.g. the um-bilical artery. The pulse repetition frequency and wallfilter is kept to a minimum in order to not obscure min-imal end-diastolic flow when present. However, itshould not be set inappropriately low to avoid eliminat-ing valuable high frequency information in a high ve-locity circulation such as that in the fetal aorta 8.

Normal Fetal circulation

Blood with the highest concentration of oxygen andsubstrates enters the fetus via the umbilical vein andreaches the liver as the first major organ. The umbilicalvein delivering oxygenated blood from the maternalplacenta to the fetus distributes 18-25% of its supply tothe right atrium, 55% to the dominant left hepatic lobeand 20% to the right hepatic lobe. The ductus venosusis the first shunt that determines the proportional distri-bution of these nutrients between the liver and the cen-tral circulation 2. The watershed area associated withthe ductal shunt is the left portal vein, where umbilicalvenous blood that continues to the liver comes in con-tact with depleted portal blood that drains the splanch-nic circulation.

The heart is the next major organ receiving blood witha range of nutritional content from different sources.Among the right atrial tributaries, the ductus venosusand the left hepatic vein carry blood with higher nutri-tional content than do the other venous tributaries viz.inferior and superior vena cavae, right and the middlehepatic veins and the coronary sinus. On the left side,the pulmonary veins return depleted blood to the leftatrium. The foramen ovale is the second shunt parti-tioning these incoming bloodstreams. Due to their dif-ferent directionality and velocities, the position of thecrista dividens and valve of the foramen ovale, satu-rated blood from the ductus venosus reaches the leftventricle preferentially, while the relatively depletedblood enters the right ventricle.

The preductal aorta delivers nutrient rich blood to themyocardium and brain (via the brachiocephalic circu-lation), while less saturated blood from the right ventri-cle enters the lungs and ductus arteriosus. The ductusarteriosus serves as a conduit that unites these twobloodstreams through its insertion in to the aorta distal


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to the left subclavian artery. The aortic isthmus is theassociated watershed area where the shunting betweenthe bloodstreams originating from the left and the rightventricle occurs. Downstream of the ductus arteriosus,the descending aorta carries the blood with the nutri-tional content that results from the mixture of these twobloodstreams.

The umbilical artery provides the fourth shunt wheredepleted blood is channeled to the placenta for gas, nu-trient and food exchange.

Fetal Haemodynamics in IUGR

IUGR in a majority of the cases is secondary to utero-placental insufficiency.

Doppler ultrasound gives us information on the utero-placental vascular resistance and, indirectly on theblood flow. Analyses of the Doppler waveforms aremade by measuring the peak systolic (S) and end dias-tolic (D) velocities. Three indices are considered relatedto the vascular resistance: S/D ratio (systolic/diastolicratio), resistive index (RI = systolic velocity - diastolicvelocity/systolic velocity), and pulsatility index (sys-tolic velocity - diastolic velocity/mean velocity). Ges-tational age based normative data have been establishedfor all measurements. Flow changes can be observed inboth the arterial and venous system of the fetus and inthe uterine arteries.

Changes in the Arterial Circulation

Uterine circulation

The uterine artery Doppler waveform is best obtainedby first identifying the maternal internal iliac artery.The transducer is then moved slightly cephalad and me-dial until a vessel is noted running perpendicular to theinternal iliac artery, going into the myometrium. TheDoppler gate is then placed over the artery to obtain theDoppler waveform, which is easily recognized by itsshape and the slower rate consistent with maternalpulse (Figure 1).

Uterine Artery Doppler correlates well with hemody-namic changes in the placental circulation. As the feto-placental compartment develops and gestational ageadvances, there is an increase in the number of tertiarystem villi and arterial channels, and hence the imped-ance in the uterine artery decreases.A diastolic compo-

nent in the uterine artery flow velocity waveform ap-pears during the early second trimester, i.e., at 14weeks' gestation, and progressively increases up to 20to 24 weeks (Figure 2).

Pregnancies that are destined to result in normal termdeliveries show increased diastolic blood flow velocityand loss of the early diastolic notch by 22 weeks of ges-tation, whereas pregnancies that show persistent high-resistance waveforms with early diastolic notches areat risk of preterm delivery from pre-eclampsia, abrup-tion, intrauterine growth restriction and overall highermorbidity as well as mortality 9.

An abnormal flow velocity waveform in the uterine ar-teries demonstrating a persistent diastolic notch andlow diastolic flow beyond 24 weeks gestation reflectsabnormal resistance downstream in the uteroplacentalvascular bed (Figure 3). Fleischer and Schulman havefound that in IUGR complicated by pregnancy-inducedhypertension, there is inadequate trophoblastic invasionof the spiral arteries, leading to increased resistance inthe spiral arteries (Figure 4) and decreased blood flowin the placental vascular bed and in the uterine artery,thereby resulting in an increase in the uterine artery PIand bilateral notching 10. This is described as uteropla-cental insufficiency and leads to the delivery ofneonates who are small for gestational age 9.

A combined Doppler and hormonal profile of placentalfunction may be of value to screen for pregnancies thatare at increased risk of pre-eclampsia, fetal death, andIUGR even as early as the first trimester 11, 12.

Umbilical artery

The umbilical artery is the signature vessel in theDoppler study of the fetus as it is a direct reflection ofthe flow within the placenta. It is usually the first vesselto be studied when suspecting an IUGR fetus.

The umbilical artery is assessed at three sites, the pla-cental origin, fetal abdominal insertion site and in themid free floating loop. Resistances at the abdominalcord insertion tend to be higher and those at the placen-tal insertion tend to be lower than those at themidcord 13 (Figure 5).

In the normal fetus, the pulsatility index decreases withadvancing gestation. This reflects a decrease of the pla-cental vascular resistance (Figure 6). In fetuses with


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Figure 2: Increased resistance wave pattern in theuterine arteries seen in uteroplacental insufficiency

Figure 1: Abnormal uterine artery waveform seen inpre-eclampsia showing persistent pre-diastolic notch.

Figure 4: Absent end diastolic flowFigure 3: Reversal of diastolic flow

Figure 5 : Brain- sparing effect seen in MCA- Increasedend diastolic flow and decreased P.I.

Figure 6: Reversal of diastolic flow in the aorta sug-gestive of severe hypoxia, predictor of academia andneonatal necrotizing enterocolitis.


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IUGR there is an increase of the pulsatility index sec-ondary to the decrease, absence or reversal of end- di-astolic flow. The changes of these waveforms arethought to be indicative of increased placental resist-ance. The absent or reversed end-diastolic flows arestrongly associated with ,an abnormal course of preg-nancy and a higher incidence of perinatal complica-tions, when compared to fetuses with IUGRcharacterized by the presence of end-diastolic flow 14.

The prevalence of perinatal death in fetuses with absentor reversed end diastolic flow velocity is reported to beover 40%. Yoon et al demonstrated in their study thatAEDF is a strong and independent predictor of ad-verse perinatal outcome 15.

Some fetuses have decreased diastolic flow that re-mains constant with advancing gestation and never be-comes absent or reversed which may be due to a milderform of placental insufficiency.

In some IUGR fetuses, the fetus maintains a normal di-astolic flow velocity in the umbilical artery by alteringthe fetal cardiac output in an attempt to conserve pla-cental oxygenation and hence function. This suggeststhat the umbilical artery functions as a shunt to maintainplacental oxygenation.

Although the umbilical artery waveform is a good re-flector of placental resistance it has lost its status asthe key vessel as it does not give any information as tohow the fetus is coping with the compromised bloodsupply and hence does not help to determine optimumtime of delivery.

Fetal cerebral circulation

The middle cerebral artery is the vessel of choice to as-sess the fetal cerebral circulation because it is easy toidentify and has a high reproducibility. Fetal middlecerebral artery waveforms are best obtained with thecranium in a transverse position as the angle of in-sonation would be as close to 0 degrees as possible ,and therefore, information on the true velocity of theblood flow may be obtained. During normal pregnancy,the MCA shows high resistance and low diastolic flowpattern with continuous forward flow throughout thecardiac cycle.

In mild cases of fetal hypoxia when the resistance ofthe umbilical artery is increased, no change maybe

demonstrated in the flow pattern of the MCAdue to theadaptation of the fetal circulation in maintaining theafter load of the left ventricle 16. An increase in theMCA PSV maybe the only perceivable finding at thisearly stage 17. However, if there is continued and pro-gressive fetal hypoxia, a phenomenon known as "brainsparing effect" is seen with dilation of the fetal intracra-nial vessels, which provides increased blood flow to thebrain at the expense of other organs. The Dopplerwaveform depicts this as increase in diastolic flow withdecreased pulsatility index . The presence of such com-pensation suggests a compromised fetus 18. In pregnan-cies with chronic fetal hypoxia, the blood volume in thefetal circulation is redistributed in favor of vitally im-portant organs, i.e., the heart, kidneys and brain (2). Withcontinuing hypoxia, the overstressed fetus loses thebrain sparing effect and the diastolic flow returns to thenormal level. Presumably, this reflects a terminal de-compensation in the setting of acidemia or brain edema.When brain edema becomes severe, reversal of dias-tolic flow maybe seen due to the raised intracranialtension, which suggests grave and irreversible fetalneurological outcome 16.

To describe the correlation of placental resistance andcerebral adaptationArbeille et al described the cerebralplacental ratio .This is constant during pregnancy es-pecially after 30 weeks and suggested 1 as the cut offvalue; all values less than 1 is considered abnormal (19).This ratio is shown to have higher sensitivity (100%) inpredicting adverse perinatal outcome and fetal hypoxiawhen compared to pulsatility index of MCA or umbil-ical artery alone (50%) according to study by T. Ozcanet al 17.

Fetal Aorta

The fetal aorta provides a direct reflection of the cardiacoutput and the peripheral resistance of the systemic cir-culation. It gives the summation of blood flow infor-mation to the kidneys, abdominal organs, lower limbsand placenta.

Normal blood flow in the fetal descending aorta ishighly pulsatile with a minimal end diastolic compo-nent. The diastolic velocities start to present during thesecond and third trimesters, however the PI remainsconstant 24. Wladimiroff et al in their study got a normalpulsatility index of 1.7-1.8 in the descending aorta 20. Inthe hypoxic fetus, due to redistribution of flow to thebrain, there is peripheral vasoconstrictions, which is re-


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flected in the rising RI and PI values. In presence of se-vere hypoxia, the diastolic flow reverses and thisstrongly correlates with gross acidemia and impendingneonatal necrotizing enterocolitis due to severe mesen-teric ischemia 21.

Changes in the Venous Circulation

Doppler waveforms obtained from the central venoussystem of the fetus reflect the physiologic status of theright ventricle giving specific information regarding theventricular preload, myocardial compliance and rightventricular end-diastolic pressure. The vessels that giveus invaluable Doppler information regarding the adap-tation to fetal hypoxia are the inferior vena cava, theductus venosus and the umbilical vein.

Ductus venosus

The ductus venosus can best be identified in a sagittalsection or an oblique section through the upper fetal ab-domen. It is seen as a continuation of the intraabdomi-nal umbilical vein with a narrow inlet and a wider outletand connects to the IVC. On colour Doppler, it usuallystands out due to the turbulent flow seen through itsnarrow lumen and resultant aliasing of colour signalsseen within it.

The spectral waveform seen in this vessel can be de-scribed as a classic M pattern characterized by a firstand second peak coinciding with ventricular systole andearly diastole when there is passive filling of the ven-tricles. Following this second peak is the nadir beforethe onset of the next systole. This nadir of brief dimin-ished forward flow coincides with atrial contractionsduring late diastole.

In IUGR when there is progressive hypoxia and wors-ening contractility of the ventricles and atria secondaryto myocardial ischemia, the ductus venosus shows aprogressive decrease in forward flow due to an increas-ing pressure gradient in the right atrium. In such cases,tricuspid regurgitation causes a reversal of flow in theinferior vena cava, which eventually leads to reversal offlow in the ductus venosus.Abnormalities in this wave-form have been associated with worsening fetal hypox-emia and acidemia, which may precede abnormalitiesin the fetal heart rate 17. Gonzalez et al observed 5 fe-tuses with reverse flow velocity waveforms at the duc-tus venosus and all the fetuses died in utero. In 18 otherfetuses with abnormal umbilical and middle cerebral

artery waveforms, but without reverse flow in the duc-tus venosus, no deaths occurred (6).

Umbilical Vein

The umbilical vein carries oxygenated blood from thematernal side of the placenta to the fetus. This blood isthen carried via the ductus venosus into the right side ofthe heart. It can be assessed either within its entranceinto the fetal abdomen at the site of umbilical cord in-sertion, further up near the liver or in the free floatingloops in the amniotic fluid.

The normal Doppler waveform reveals a monophasicwaveform with continuous forward flow throughout thecardiac cycle. This continuous diastolic flow, graduallyincreases from the 20th wk of gestation up to the 38thweek. The umbilical vein is probably one of the lastvessels to change its flow pattern in the setting of fetalhypoxia. In severe cases, when there is reversal of flowin the IVC and ductus venosus due to right heart failure,a pulsatile flow pattern begins to appear due to the highresistance to forward flow. The presence of umbilicalvein pulsations is associated with an increased risk ofadverse perinatal outcome.

Changes in the Fetal Heart in IUGR

IUGR is associated with several changes at the level ofthe fetal heart as it plays a central role in the adaptivemechanisms for hypoxemia and fetal insufficiency. Inorder to understand these changes, it is imperative toknow the basics of the fetal circulation

Two ventricular pumps perfuse the same systemiccirculation in a parallel fashion with the right ven-tricular output being greater than the left 22.

85 to 90 % of the Right ventricular output suppliesthe sub diaphragmatic organs and carcass via theblood going into the descending aorta from the pul-monary artery via the ductus arteriosus, and1015%goes into the pulmonary circulation.

The dormant pulmonary circulation (due to physio-logic non-functioning of the lungs) maintains a highpulmonary vascular resistance, which is almostequal to the systemic side. Hence there is small leftto right shunt across the foramen ovale. The flow tothe pulmonary vascular bed gradually increases to-wards the end of gestationWith advancing gestationthe R>L shunting across the foramen ovale de-creases by 45% due to corresponding increase in the


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pulmonary blood flow. Cephalic part of the fetus gets perfused by the left

ventricular output 2. Aortic Isthmus establishes communication between

the two arterial outlets that perfuse in parallel theupper and lower body of the fetus namely the rightand left ventricular output 2.

The changes seen in an adapting IUGR fetal heart in-volve preload, after load, ventricular compliance, andmyocardial contractility. Longitudinal data on thehaemodynamic sequence of the natural history of fetalgrowth restriction show that the umbilical artery andthe MCA are the first variables to become abnormal.These arterial Doppler abnormalities are followed byabnormalities in the right cardiac diastolic indices, fol-lowed by right cardiac systolic indices, and finally, byboth left diastolic and systolic cardiac indices. Preserv-ing the left systolic function as the last variable to be-come abnormal ensures an adequate left ventricularoutput, which supplies the left cerebral and coronarycirculation.

Changes in the right heart: An increase in after load isseen at the level of the right ventricle owing to in-creased placental impedance. This in turn causes in-creased systemic venous pressure and increase invenous shunting through the ductus which leads to aconcomitant reduction in umbilical flow to the liver 2.There is also increased shunting from the left to theright heart through the foramen ovale. With further de-terioration, these adaptive mechanisms are over-whelmed, and there is a high incidence of tricuspidregurgitation followed by reversal of flow in the IVCand ductus venosus. These Doppler abnormalities arestrong predictors of myocardial cell damage 23.

Changes in the left heart: A decrease in the after load isnoted at the level of the left ventricle owing to de-creased cerebral impedance associated with the brainsparing reflex. These changes in the after load resultin a redistribution of the cardiac output from the rightto left ventricle in order to maintain an adequate supplyto the brain, heart and the adrenals 24. This is known asarterialization of the circulation.

Changes on both sides: Preload is reduced at both atri-oventricular valves owing to hypovolemia and de-creased filling associated with IUGR. Evidence ofreduced myocardial contractility has also been reportedin the presence of IUGR. Ventricular ejection force, an

index of ventricular systolic function that is independ-ent of preload and afterload is decreased at the level ofthe right and left ventricle in fetal growth restriction.IUGR fetuses with reduced ventricular ejection forcehave a shorter time to delivery, a higher incidence ofnon- reassuring fetal heart tracing and a lower pH atbirth. A significant correlation between the severity ofthe fetal acidosis and cordocentesis and ventricularejection force values validates the association of thisindex and severity of fetal compromise.

Doppler based management in IUGRSevere Uteropla cental insufficiency

A) The cause for the development of uteroplacental in-sufficiency may begin as early as the time of the im-plantation. However, no effect is seen on growth orDoppler until 20-24 weeks gestation. These fetusesdo not have signs of growth restriction or abnormalDoppler ultrasound prior to this period

B) At 22-24 weeks gestation if the fetus is measurablysmall by ultrasound, several Doppler patterns mayoccur. 1) The umbilical artery may still have a nor-mal pulsatility index (resistance index or S/D ratio);the middle cerebral artery may have either a normalor abnormal pulsatility index. 2) The umbilical ar-tery has an abnormal pulsatility index; the middlecerebral artery has either a normal or abnormalvalue of pulsatility index. 3) The umbilical arteryand the middle cerebral artery have both an abnor-mal value of pulsatility index. The fetus needs to bemonitored very closely. Bed rest and oxygen ther-apy may be useful; however, if both vessels have anabnormal value at this early gestational age, it isvery likely that the fetus will continue to deteriorateand the chance of a delivery at term is remote.

C) The pulsatility index of the umbilical artery may in-crease while that of the middle cerebral artery maydecrease. The other fetal vessels may still appearnormal and the only Doppler abnormalities are theumbilical artery and middle cerebral artery. Thefetus starts to show signs of IUGR. The biophysicalprofile is normal. At this time the lack of fetalgrowth, and/or the development of pre-eclampsia/eclampsia, or a persistent abnormal biophysical pro-file may interrupt the process with delivery of thefetus. These fetuses are at lower risk for the devel-opment of respiratory distress syndrome and intra-ventricular hemorrhage. The reason is not


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completely understood. However, production ofsteroids with stress may play an important role inthis process. If the fetus is not delivered, the processcontinues.

D)At this time tricuspid regurgitation may appear, duc-tus venosus reverse flow and umbilical vein pulsa-tions may be present intermittently. The biophysicalprofile may still appear normal 36.

E) Ductus venosus reverse flow and umbilical vein pul-sations are present continuously. The fetus starts tolose the brain sparing effect. The biophysical profilebecomes abnormal 38.

F) Fetal demise. The time interval between E and F isvariable (from 6-12 hours to 2 weeks). Oligohy-dramnios may be present at any stage of the aboveprocess.

Muld uteroplacental insufficiency

In mild Uteroplacental insufficiency no effect may beseen on Doppler and growth until 26-32 weeks gesta-tion. The umbilical artery and the middle cerebral arterywaveforms may be abnormal. However, the process isnot severe enough to stop fetal growth completely or todeteriorate as above. These cases may be followed withoutpatient monitoring and they often deliver at term (39).

Changing trends in Doppler assessment of IUGR fe-tuses

There has been a dramatic shift in the role and goals ofthe Doppler study from its advent in the early 80swhen it was used to recognize the presence of IUGRby assaying the umbilical artery and MCA, which inturn led to the understanding of management protocolsin the 90s by diagnosing adverse fetal outcome inutero. However, there remained a large gap as we con-tinued to produce fetuses afflicted with different man-ifestations of hypoxia in the postnatal period. We havesurely come a long way since then and now in thetwenty-first century, the main focus has been to devisetechniques to predict the likelihood of fetal morbidityin the setting of IUGR and avert the occurrence of fetalcompromise. The aim is to identify those pregnanciesat risk of IUGR before the fetus has actually becomegrowth restricted and to prevent the occurrence of fetaldecompensation if growth restriction has already oc-curred. Hence the role of Doppler is shifting from cur-

ative to preventive medicine.

1. First trimester uterine artery screening: The mater-nal adaptation to pregnancy is thought to result fromthe trophoblastic invasion of the maternal spiral ar-terioles in the first half of pregnancy. The invadedarterioles are rendered maximally dilated and min-imally responsive to the sympathetic and parasym-pathetic systems. This adaptation is intended toensure a sustained increase in the blood flow to theuterus during the pregnancy 2. Numerous studieshave shown that late first trimester screening of theuterine artery in high-risk women can accuratelyidentify a subset of women who are destined formajor complications that will be attributable to pla-cental disease. Serial Doppler assessment of theuterine artery is performed from the 16th wk on-wards in these high risk women who may have his-tory of factors known to cause IUGR 25, 26. Thepersistence of the pre-diastolic notch and graduallyincreasing impedance indices suggest an abnormaluterine circulation and hence is an indicator to treatthese women with bed rest, antihypertensives andoxygen therapy right from the onset of the pathol-ogy. This has helped in completely averting seriouspregnancy complications including IUGR itself,pre-eclampsia, preterm delivery and poor postnatalfetal outcome 27.

2. New vessels giving new hope- The Aortic IsthmusThe Aortic Isthmus (AoI) is the only arterial shuntbetween the right and left ventricular output (Figure26,27). It is located between the Left Subclavian ar-tery and aortic insertion of the ductus arteriosus (28).The ductus arteriosus is a physiologic shunt andhence blood flow through it is considered physio-logical in fetal life and not as a pathologic diversionfrom the right circulation to the left. The aortic isth-mus, on the other hand is the link between the par-allel vascular systems perfused by the left and rightventricle 29. As a consequence, AoI blood flow ve-locity patterns reflect the balance between left andright ventricular outputs and are influenced by dif-ferences in the impedance to flow in the placentaland cerebral vascular systems 30.

When the net peripheral resistance is low (as is seen ina normal fetus with normal S/D ratio in the umbilicalartery) blood flow in the aortic isthmus is forward di-rected throughout the cardiac cycle. In the advent offetal hypoxia, when the placental resistance becomeshigh causing a fall in umbilical blood flow of approxi-


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mately 50%, there is diastolic reversal of flow seen eventhough the diastolic flow in the umbilical artery remainsforward. However, because of the systolic predomi-nance, the net flow in the isthmus is forward. Whenthere is more severe increase in placental resistance cor-responding to a decrease of 75% in umbilical bloodflow, the net flow through the isthmus becomes retro-grade. Retrograde blood flow in the aortic isthmus rep-resents abnormal flow ejected by RV into a vascularterritory usually perfused by the left ventricle.When thenet flow in the aortic isthmus becomes retrograde, nu-trient and O2 content of the left ventricle drops andthere is markedly increased risk for adverse childhoodneurodevelopment in fetuses. The study ofAoI velocitywaveform is a promising tool allowing a comprehensivestudy of the fetal circulation when peripheral resistancesto ventricular output are changed. Studies have conclu-sively proved that Aortic Isthmus velocity waveformsbecome abnormal at an earlier stage of fetal compro-mise than Ductus Venosus 31.

In order to objectively gauge the flow through the aorticisthmus, the Isthmic Flow Index (IFI) was proposed.The circulatory indices that are clinically used thus farare useful for indirect assessment of the impedance ofvascular networks. They however, do not give any in-formation about the direction of flow. Hence, for clini-cal purposes, the IFI is used which reflects both theamount and the direction of blood flow through the fetalisthmus and is particularly sensitive to the change in di-rection of the diastolic flow. IFI is equal to the Systolicvelocity + Diastolic velocity / Systolic velocity 28. Pos-itive and negative signs are assigned to antegrade andretrograde velocity values, respectively.

To summarize, greater the reverse isthmic flow, lower isthe IFI and higher risk of cerebral damage. This indexhas implications in understanding and grading the leftventricular dysfunction in a hypoxemic fetus. Reversalof flow in the isthmus (IFI < 1) indicates a significantfall in left ventricular output causing compensatory per-fusion of the upper body circulation by the right ventri-cle. This suggests that the left ventricle will not be ableto take charge of the postnatal systemic circulationwhich will continue to be ductus dependent.

Conclusion

Placental insufficiency is the most common cause of in-trauterine growth restriction (IUGR) and Pregnancy in-duced Hypertension (PIH). It is an important obstetric

problem on account of the high associated perinatalmortality and morbidity. Uterine artery Doppler has im-portant role to play in predicting the onset of PIH andIUGR at 20-24 weeks There seems to be a need to rec-ognize placental insufficiency early so that its hazardscan be reduced, if not averted. The preventive role ofuterine artery Doppler is hence shifting to the firsttrimester 32.

Fetuses with IUGR show evident modifications ofDoppler parameters in the uteroplacental and fetal cir-culation. Sequential studies enable us to determine thecondition of these fetuses by observing the Dopplerchanges in different vascular territories. The delivery ofthe sick fetus can hence be appropriately timed to pre-vent the associated complications 33, 34.

In the past the focus has been to reduce near term mor-tality and morbidity, but recent studies have docu-mented adverse long term neurological sequelae evenin those fetuses subjected to hypoxia for a shortduration 37. Hence the role of Doppler has shifted froma curative to a preventive one with truly informed andmeaningful brain-oriented fetal care becoming a clinicalreality .The advent of the aortic isthmus as the new ves-sel of hope in analyzing early disruption in the cerebralperfusion, is in this direction 35.

There are, however, still many uncertainties concerningthe relationships between the Doppler changes and themetabolic situation of the fetus and therefore, on the op-timal timing of delivery in order to completely preventthe occurrence of any intrauterine injury.

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