This document discusses color Doppler ultrasound in the evaluation of intrauterine growth restriction (IUGR). It provides details on: 1. Changes seen in the fetal circulation in IUGR, including increased placental resistance seen on umbilical artery Doppler leading to absent or reversed end diastolic flow in severe cases. 2. Brain sparing effect seen on middle cerebral artery Doppler in IUGR fetuses, shown as increased diastolic flow. 3. Changes in the ductus venosus Doppler waveform seen in IUGR, from decreased forward flow to eventual reversal, indicating worsening fetal hypoxia and myocardial dysfunction.

1. Color Doppler In IUGR
Prof. M.C Bansal
MBBS.,M.S. FICOG, MICOG

2. IUGR
• Definition Intra Uterine Growth Retardation
is a term used to describe the fetus with a
birth weight at or below the 10th percentile for
gestational age and sex. Such fetus does not
reach its growth potential.
(a) birth weight < 10th percentile
(b) inadequate interval growth in sequential
screening.

3. FETAL GROWTH CURVE

5. Fetal Growth
• Placenta is life line of fetus and when challenged ,it has
a remarkable ability to adapt.
• Developmental problems can occur from the maternal
side, fetal side , or both .Development of a good utero-
placental circulation is essential nfor achievement of a
normal pregnancy.
• To facilitate it remarkable changes occur in maternal ,
placental and fetal vasculatures.
• When this mechanism fails , abnormal vascular
resistance develops which leads to compromised fetal
oxygenation and nutrition resulting into IUGR—IUFD–
6-10 times increased perinatal mortality.

6. • Mal development of villous tree in pregnancy is
complicated by fetal growth restriction.
• FGR is associated with abnormal uterine artery wave
form ,indicating sub normal feto placental blood
flow.
• In pregnancies complicated by absent end diastolic
umbilical blood flow have , elongated placental villi
and sparse , uncoiled capillary loops.
• These findings are well correlated with an increase in
fetal placental vascular impedance and impaired
exchange of nutrients and oxygen to fetus.
• An enhanced ranching angiogenesis represent
adaptive response to impaired feto placental blood
flow.

7. IMPLANTATION OF BLASTOCYST EARLY TROPHOBLAST
NO VASCULARITY

8. VILLOUS DEVELOPMENT

9. BLASTOCYST – PRIMIARY VILLI DEVELOPMENT

10. BLASTOCYST – VILLI DEVELOPMENT

11. TROPHOBLAST CELL COLUMN : INTERSTITIAL TROPHOBLAST :
INTRAMURAL ENDOVASCULAR TROPHOBLAST

12. EARLY IMPLANTATION

13. Normal Fetal Circulation
• Blood with highest O2 concentration and
nutrients enters the fetus via umbilical vein and
reaches the liver the 1st major organ.
• Umbilical vein carrying Oxygenated blood from
placenta ---distributed to right atrium (18-
25%),55% to dominant left lobe of liver and 20%
to right lobe.
• Ductus venosus is the 1st shunt that determines
the proportional distribution of nutrients between
liver and central circulation.
• Depleted portal blood from splanchnic circulation
mixes with umbilical blood at this point.

14. Fetal circulation------------
1. The heart is the next organ receiving
blood with a range of nutrients from
different sources----Right atrial
tributaries ,ductus venosus, left
hepatic vein, inferior and superior
vena cava, right and middle hepatic
veins ., coronary sinus.
1. Right atrial tributaries, dutus venosus and left hepatic vein bring blood with
higher O2 and nutrients.
2. Pulmonary veins to left atrium of heart bring depleted blood from
nonfunctioning lungs.
3. Foramen ovale is another shunt partitioning these incoming blood streams.
4. It is possible due to the different direction and velocities of these blood
streams as wellas position of crist divdens of valve of foramen ovale.
5. Saturated blood from ductus venosus reaches left ventricle through foramen
ovale—left atrium –left ventricle.
6. Relatively depleted blood coming from other strems reches right ventricle.

15. Fetal Circulation -----------
• Pre-ductal aorta delivers oxygenated blood to
Myocardium and brain.
• Less oxygenated blood from right ventircle enters ductus
arteriosus and lungs.
• Ductus arteriosus serves as link between these two
streams through its position (insertion) in aorta distal to
the left subclavian artery.
• Aortic isthmus is another point of shunting between two
streams originating from left and right ventricles.
• Down stream of ductus arteriosus ,the descending aorta
supplies mixed blood to rest of fetal body.
• umbilical arteries provide the 4th shunt where depleted
blood is carried to placenta for oxygenation and

16. FETAL
CIRCULATION

18. • Introdction of color doppler has provide 1st
opportunity for repetitive non invasive to
monitor fetal haemodynamics.
• Doppler indices of blood flow can reliably
predict adverse outcome in cases of IUGR.
• Doppler reveals changes of hypoxia at least a
week before the non stress test or biophysical
profile.
• It has become gold standard in the
management of IUGR

19. FETOPLACENTAL CIRCULATION ON 3-D POWER DOPPLER SCANNING

22. Technique of color Doppler
• Pt is 1st screened in the routine fashion using B mode using
3.5 or 5 MHz curved array transducer.
• The vessel of interest is located by color doppler.
• The spectral doppler wave form is then obtained by placing
the doppler gate directly over the vessel of interest.
• These recordings should be done in the absence of fetal
breathing movement and fetal heart between 120-160.No
fetal movements
• The best wave form is obtained when angle of insonation is
between 30-60 degree. Difficulty is faced when fetus is
moving or vessels are not linear i.e. umbilical artery.
• The pulse repetition frequency and wall filter is kept minimum
in order to not obscure minimal end diastolic flow when
present.

26. Fetal Haemodynamics In IUGR
• IUGR in majority of cases is secondary to Utero placental insufficiency.
• Doppler gives us vital information on the utero-p lacental vascular resistance and
indirectly quantity of blood flow carrying o2 and nutrients to fetus.
• Analysis of doppler wave forms is done as follows----
MEASURING (1) Peaksystolic (s)
(2) end diastolic velocity(D)
Three indices are calculated for knowing vascular resistance.
SD ratio(systolic/ diastolic ratio).
Resistance Index(RI)=systolic velocity – diastolic velocity
_______________________________
Diastolic Velocity
Pulsatile Index ( P I )=Systolic Velocity – Diastolic Velocity
_________________________________
. Mean Velocity
flow changes can be observed in both arterial and venous blood flowin fetus and
uterine arter

28. .
(1)Changes in the arterial circulation 
(a) Uterine circulation----as the feto- placental
compartment develops and gestational age advances ,
there is an increase in number of tertiary stem villi and
arterial channels to meet the need of developing fetus.
hence the Doppler study at this time shows
appearance of a diastolic component in uterine artery
flow velocity wave form,. during early 2nd trimester
i.e.. 14 weeks’ gestation and progressively increases
Up to 24 weeks. in normal
pregnancy it continued to show increased diastolic
flow velocity and loss of diastolic notches by 22weeks .
Pregnancies associated with high persistent resistance
wave forms and early diastolic notches, are at risk of
preterm delivery due to IUGR, PIH, abruptio placenta
and overall higher morbidity and mortality.

29. Abnormal flow velocity wave form in the uter
ine arteries demonstrating a persistent diastolic
notch and low diastolic blood flow beyond 24
weeks of gestation reflects abnormal to blood
flow down stream to utero placental vascular
bed., there by increase in uterine artery PI and
bilateral notching. Combined Doppler and
hormonal profile of placental function may be
a valuable tool to screen pregnancies that are at
risk of PIH, IUGR, IUFD and abruptio placenta.

30. UTERINE ARTERY DOPPLER WAVE FORMS

31. UTERINE ARTERY DOPPLER WAVE FORMS –Journal of Obstetrics & Gynaecology India

32. • (b)Umbilical Artery-It is direct reflection of
placental flow. umbilical artery is assessed at
three sites--- the placental origin ,fetal
abdominal insertion site and in the middle of
free floating vessel.
Resistance at abdominal insertion site
is higher and progressively decreases towards
placental site.(figure 5)
In normal fetus ,pulsatile index (PI)
decreases with advancing gestational period.This
indicates progressive decrease in vascular
resistance in placental bed.(figure 6)

33. • in Cases of IUGR there is increase in PI index secondary to
decrease, absence or reversal of end diastolic blood flow.
These changes in wave form indicate increased
placental resistance.
The absent or reversed end diastolic flow strongly
associated with worst fetal outcome(40%.Perinatal deaths).
In milder form of placental insufficiency, diastolic flow is
decreased, but absent or reversal of end diastolic flow may
not develop and fetus is thriving well in utero.
In some IUGR cases fetus maintains the normal diastolic flow
velocity in umbilical artery by altering Cardiac out put in order
to maintain Oxygenation. This suggests that umbilical artery
works as a shunt .
Hence umbilical artery is not a KEY vessel to have a
conclusive evidence of fetal Oxygenation status.

34. UMBILICAL ARTERY Normal doppler wave form

35. REVERSAL OF BLOOD FLOW IN UMBILICAL ARTERY

36. UMBILICAL ARTERY DOPPLER : (a) NORMAL (b) LOSS END-
DIASTOLIC FLOW (c) REVERSED END-DIASTOLIC FLOW

38. • (c)Fetal Cerebral Circulation-Middle cerebral artery
is the vessel of choice to assess the cerebral
circulation., as it is easy to identify and has high
reproducibility.
Middle cerebral artery wave forms are best
obtained with the cranium in a transverse position as
angle of insonation will be close to 0 degree.
During normal pregnancy the MCA shows high
resistance and low diastolic flow pattern with continuous
fore ward flow through out the cardiac cycle.
In mild fetal hypoxia when resistance of umbilical
artery increased ,no changes in MCA blood flow pattern
may be noted(Adoptive phase) .An increased MCA PSV
may only be the finding.

39. • If there is continued and progressive hypoxia, a
phenomenon known as “ BRAIN SPARING EFFECT ”is
noted.
There is dilatation of cerebral vessels to
increase blood flow to brain at the expenses of other
organs of abdomen.
Doppler study depicts it as increase in diastolic
flow with decreased PI. The presence of such
compensation indicates compromised fetus in utero.
In pregnancies with chronic fetal hypoxia , blood
volume is redistributed in favor of vital organs like brain,
heart and kidneys.
When hypoxia is continuous , brain edema ,increased
intra cranial pressure and reversal of diastolic flow
suggest grave and irreversible neurological outcome.

40. • To describe the evaluation of placental
resistance and cerebral adaptation Arbeille et
al described the cerebral placental ratio .
• C:p is constant during pregnancy particularly
after 30 weeks and all value < 1 are abnormal.
• It has higher sensitivity(100%)predictive value
when compared to PI of MCA alone(50%)

42. MCA Doppler : High systolic wave in
anemic fetus

43. • (d) Fetal Aorta It reflects the cardiac out put and the
peripheral resistance of systemic circulation, it gives
the summation of blood flow information to kidneys,
abdominal organs lower limbs and placenta.
• Normal blood flow in fetal descending aorta is highly
pulsatile with minimal diastolic component.
• Diastolic velocities start to present in 2nd and 3rd
trimester. Pi remains constant(1.7-1.8)
• In hypoxic fetus due to redistribution of blood flow ,
there is increased vasoconstriction and peripheral
resistance i.e. rise in RI and PI values.
• In presence of severe hypoxia , diastolic flow reverses.
• It is well co-related to acidemia and development of
necrotising enterocolitis.

45. (2) Changes in venous circulation
Doppler wave from obtained from central venous
system of the fetus reflects the physiological status of
right ventricle. It gives information about—1.
ventricular preload,2. myocardial compliance and3.
right ventricular end diastolic pressure. Following veins
give us invaluable information-----
(a) Inferior vena Cava.
(b) Ductus venosus.
( c) Umblilical vein.

46. Ductus Venosus
• It can be identified in sagittal section / oblique section
through fetal upper abdomen.
• It is seen as a continuation of intra abdominal umbilical vein
with narrow inlet and wider outlet connected to inferior vena
cava of fetus.
• Turbulent flow through its narrow end and resulting aliasing
of color signals seen with in it makes it identifiable on color
doppler.
• Spectral wave form seen in this vessel can be described as a
classic “ M” pattern characterized by 1st and 2nd peaks.
• 1st peak coinciding with ventricular systole and early diastole.
• Following this there is 2nd peak coinciding with nadir before
the onset of the next systole .this nadir of diminished
foreward flow coincide with atrial contraction during late
diastole.

47. • In IUGR when there is progressive hypoxia and
worsening contractility of myocardium , dutus
venosus shows a progressive decrease in forward
flow. It is due to increase pressure gradient in the
right atrium.
• Tricuspid regurgitation at this stage leads to
reversal of flw in inferior vena cava and ductus
arteiosus.
• This reversal flow of is have been associated with
worsening fetal hypoxia, acidemia,precede with
fetal heart rate andrhythm.

48. ASSESSMENT OF DUCTUS VENOSUS
NORMAL WAVE FORM  s, d, a

49. ASSESSMENT OF DUCTUS VENOSUS

50. Umbilical Vein
• The umbilical vein carries oxygenated blood from placenta to fetus.
• This blood is reaching to right side of fetal heart through ductus
venosus.
• It can be assessed at 3 points---(1) its entering point in abdomen i.e.
point of its insertion (2) in free floating loop of umbilicus and
(3)umbilical attachment at placenta .
• Normal doppler wave form reveals monophasic wave form with
continuous forwardflow through out cardiac cycle.
• this continuous diastolic flow gradually increases from 20weeks to
38 weeks of gestation.
• It is the last vessel to be affected when hypoxia develope.
• In severe degree of hypoxia when reversal of flow develops in
inferior vana cava,apulsatile flow pattern begins to develop in
umbilica vein due to right heart failure (myocardial hypoxia) -----
there is high resistance to forward flow.
• Presence of pulsatile wave form in umbilical vein is associated with
very high perinatal mortality.

51. Changes in fetal heart in IUGR
• Basics of fetal heart function 
. Both ventricles pump blood to systemic circulation in a parallel
fashion ,right ventricular volume is more than that of left sided.
. 85-95% right ventricular output is supplied to sub diaphragm
organs(Descending aorta via ductus arteriosus ).10-15% goes to
pulmonary area.
. Dormant pulmonary system puts increased resistance ()almost
equalto systemic resistance) to blood flow to it.Hence there is left to
right shunt across foramen ovale.
. As gestational period increases flow to pulmonary system also
increases and by end of 34-36 weeks R> L shunt decreases by 45%
Cephalic part of fetus and heart gets blood supply from left ventricular
out put.
Aortic isthmus establishes communication between the 2 arterial
outlets.that perfuse upper and lower body of fetus.

52. • Changes seen in adapting IUGR fetus involve
preload ,after load ventricular complience, and
myocardial contractility.
• Umbilical artery and MCA wave forms are 1st to
become abnormal.
• These are followed by right cardiac diastole
indices ---right cardiac systolic indices.
• Finally by both left cardiac diastolic and systolic
indices.
• A significant correlation between severity of
fetal acidosis and decreased ventricular ejection
force values validates the association of this
index and severity of fetal compromise.

53. Changes in Right Heart
• Increase in after load is seen at the level of right
ventricle due to increased placental impedance.
• This in turn causes increased systemic venous pressure
and increased venous shunting through ductus venosus .
This result in decreased blood flow to live.
• there is also increased shunting from left heart to right
heart through foramen ovale . Further deterioration is
associated with Tricuspid Regurgitation.
• Now reversal of flow develops in inferior vena cava and
ductus venosus.
• Doppler wave forms abnormalities are strong predictor
of myocardial cell damage(anoxic).

54. Changes in Left Heart
• A decreased after load is noted at the level of
left ventricle due to decreased cerebral
impedance indicating brain spairing reflex.
• Decrease after load result in redistribution of
cardiac out put from right to left. In order to
have adequate blood supply to brain.this is
known as “ Arteralization of the circulation “
•

55. Changes in both sides.
• Preload is reduced at both atrio- ventriular
valves., secondary to hypovolemia and decreased
filling in IUGR cases.
• Decreased myocardial contractility ---hypoxia and
acidemea.
• both sided Ventricle ejection force decreased.
• Association of decreased ventricular ejection
force, severity of fetal acidosis and cordocentesis
values validates fetal compromise.

56. Mmode with superimposed doppler
ATRIAL & VENTRICULAR activity

57. Doppler based Management of IUGR
(A) Cause for development of utero placental
insufficiency ( IUGR) may be operating at the
time of implantation.
However effect is not recognized until 22-24
weeks of gestation.
These fetuses do not show any significant
doppler abnormality at this period of gessation.

58. • (B). At 22-24 weeks fetus measurements indicate small
fetus for the gestational period.
1. Umbilical artery may have normal PI,RI and S/D.
MCA has normal PI.
2.if Umbilical artery abnormal indices ,MCA may have
normal or abnormal value of PI.
3.Umblilica as well as MCA both have abnormal values
of PI.
Fetus needs weekly monitoring, Maternal bed rest in
left latral position,O2 and nutritional therapy .
If both vessels are developing abnormal indices , fetal
condition is likely to deteriorate and term delivery with
healthy fetus is remote.
.

59. (C). The PI of umbilical artery may increase while
that of MCA may decrease , other fetal vessels may
have normal flow pattern and indices . Although
fetus has IUGR and biophysical profile study is also
normal.
At this time IUGR progresses , PIH or eclampsia
may supervene or a persistent abnormal bio physical
profile may need immediate delivery . Such fetus is at
lower risk of developing RDS and intracranial
hemorrhage as compare to the premature fetus .
Distress may produce endogenous corticosteroids to
bring early maturity in IUGR fetus.
If the fetus is not delivered the IUGR pathology
continues to progress.

60. • (D).At this time tricuspid regurgitation may
appear ductus venosus reverse flow and
umbilical vein pulsation may be present
intermitently. Biophysical profile may be
normal.
• (E ). Ductus venosus reversal and umbilica vein
pulsatios now become continuous, fetus starts
losing brain sparing effect. Biophysical profile
become abnormal.
• (F) . sudden fetal demise with in 6-12 hrs to 2
weeks. Oligo hydraminos may be present at
any stage of these events.

61. Changing Trends in Doppler study in
IUGR
• Aim Of doppler study in IUGR-
1.Identify those pregnancy at risk of IUGR,
before the fetus is actually become growth
restricted.
2.To prevent fetal decompensation if IUGR
is all ready developed.
3.To decide the appropriate point of time
of delivery of IUGR fetus with the aim to avoid
prematurity and sudden fetal death in utero.

62. Plan of Doppler Study in IUGR
• 1. First trimester uterine artery screening--- maternal
adaption starts with trophoblastic invasion in
decidua(maternal spiral arterioles).
The invaded arterioles are rendered maximally dilated and
minimal response to sympathetic/ parasympathetic stimuli .
This adaptation is to ensure sustained and increasing blood
supply to placenta  fetus. Serial doppler study of uterine
artery in women who carry H/O predisposing factors for
develop IUGR at later date will help in identifying the future
culprits.
Persistence of pre diastolic notch and gradually increasing
impedance indices suggest an abnormal uterine artery
circulation. These women need active treatment in 2nd
trimester by bed rest antihypertnsives,O2, nutritional
suplimentation .

63. • 2.New vessels giving new hope The Aortic
isthmus is only arterial shunt between right and
left ventricular out put , it is located between left
subclavian artery and insertion of ductus
arteriosus to aorta . It is a physiological shunt in
fetal life.
• Aortic isthmus is i the link between the parallel
vascular systems perfused by right and left
ventricles , blood flow velocity patterns in it
reflect the balance between 2 ventricular out
puts . the velocity indices in this (aortic isthmus)
are influenced by differences in the impedance to
flowin the placnta and cerebral vascular system.

64. • When net peripheral resistance is low (seen in normal fetus
with normal S/D in umbilical artery) flow in aortic isthmus is
forward directed through out the cardiac cycle.
• In the event of fetal hypoxia, placental resistance become high
causing decreased blood flow in umbilical vessels by 50%.
There is diastolic reversal is seen . the diastolic flow in the
umbilical artery may remain forward., with increasing hypoxia
resistance in placental flow increases by 70% corresponding
to further decreased umbilical blood flow. Now blood flow in
aortic isthmus becomes retrograde.
• Retrograde flow in aortic isthmus represent abnormal right
ventricular ejection and o2 ,nutrients supply to brain is very
poor ,fetal neurological deveolpment is going to be
compromised. These changes are noted well before changes
in ductus venosus

65. • Isthmus Flow Index (IFI) reflects both amount
and direction of flow through fetal aortic isthmhs
.It is sensitive to change in direction of diastolic
flow.
• IFI = Systolic Velocity + diastolic velocity
-----------------------------------------------
Systolic Velocity
Greater the reverse isthmic flow , lower is I F I .,
and higher risk of cerebral damage.
Reversal of flow in isthmus ( IFI <1 ) indicates
significant fall in left ventricular output. Upper body
is now perfused by right ventircular output.

66. Conclusion
• Uterine artery doppler plays an important role in
predicting PIH and IUGR at earlier stage of fetal growth
i.e. in early 2nd trimester.
• Now preventing role of uterine artery doppler has
shifted to 1st trimester – the time when development
of feto- placental can be circulation.
• Sequential studies enable us to determine the
condition of these fetuses by observing the doppler
changes in different vascular territories.
• The delivery of sick fetus can be appropriately timed to
prevent sequelies.
• Role of doppler has shifted from preventive to curative.
• Advent of aortic isthmus as new vessel of hope in
analyzing early disruption in the cerebral perfusion.