Venous DOPLLER for fetal assessment

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Venous DOPLLER for fetal assessment

• AKRAM ABDEL GHANy
• M.D., OBS.GYN.
• CONSULTANT OBS.GYN.
• PORTSAID ,EGYPT

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• Evaluation of cardiovascular status by arterial
  doppler alone is inadequate in fetal disorders
  with impaired cardiac function.
• cardiac function is not accounted for in
  arterial waveform analysis.
• Extending doppler ultrasound assessment to the
  fetal venous circulation overcomes this
  limitation.

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• Examination of venous Doppler waveforms was first
  reported in the early 1980s 4-6.
• in the 1990s Clinical utilization of this
  technique has began.
• the primary means of assessing forward function
  of the fetal heart in many fetal disease.

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venous Doppler

• Abnormal venous Doppler parameters are the
• strongest peripheral Doppler predictors of
  stillbirth.
• Even among fetuses with severe arterial
• Doppler abnormalities (e.g. absent/reversed
  umbilical artery end-diastolic velocity).
• the risk of stillbirth is largely confined to
  those fetuses that have abnormal venous Doppler
  BASCHAT2004.

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VENOUS DOPPLER

• OMINOUS Venous Doppler
• absence, or reversal of the ductus venous a-wave.
• biphasic/triphasic umbilical vein pulsations.
• these Doppler findings have
• 65 sensitivity
• 95 specificity
• 
  BASCHAT2004.

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• abnormal venous Dopplers are associated with
  severe fetal acidemia.
• pulsations in the umbilical vein occurs just
  prior to abnormal fetal heart rate patterns.In
  growth restricted fetuses, neonatal mortality is
  at least 60 compared to 20 in the absence of
  venous pulsations.

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FETAL CIRCULATION 

• Allow differential distribution of oxygen and
  nutrient rich blood to vital organs and
  recirculation of oxygen and nutrient poor blood
  back to the placenta.

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Venous anatomy 

•  Oxygen and nutrient rich blood from the placenta
  enters the fetal circulation through the
  umbilical vein. The intraabdominal portion of the
  umbilical vein ascends in the falciform ligament
  and then enters the fetal liver where it turns
  right and joins the transverse portion of the
  left portal vein.

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• The ductus venosus originates from the umbilical
  vein just before its turn to the right and
  courses upward to join the IVC in a funnel-like
  venous confluence just below the level of the
  right atrium.
• This subdiaphragmatic venous vestibulum is formed
  by the confluence of the three hepatic veins, the
  ductus venous, and the IVC 8. The right atrium
  receives venous return from the upper part of the
  body through the superior vena cava (SVC) and
  from the myocardium via the coronary sinus.

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ductus venosus

• develops at approximately 7 weeks of
  gestation and shows little increase in size
  subsequently, in contrast to the other precordial
  veins which grow proportionally with the embryo
  9. The diameter of the ductus measures
  approximately one-third of the umbilical vein
  diameter from midgestation onwards. blood from
  the umbilical vein undergoes significant
  acceleration upon entering the ductus venosus
  10. This accelerated blood stream enters the
  IVC together with left hepatic venous return and
  the combined flow is directed through the foramen
  ovale into the left atrium

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• By comparison, the venous return from the right
  and middle hepatic veins and IVC have slower
  blood flow velocities and are directed towards
  the right atrium. There is little mixing of the
  venous returns from the ductus venosus/left
  hepatic vein and the right-middle hepatic
  veins/IVC because of the differences in velocity
  and direction of the incoming blood streams

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• As a result, oxygen rich blood reaches the left
  ventricle through the foramen ovale while
  oxygen-poor blood enters the right ventricle
  through the tricuspid valve.

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Distribution of cardiac output

• Left ventricular output is distributed to the
  myocardium via the coronary vessels and to the
  brain and upper body via the brachiocephalic
  vessels.
• Right ventricular output bypasses the lungs and
  reaches the aorta through the ductus arteriosus.
• The admixture of blood originating from the
  individual ventricles eventually reaches the
  placenta via the umbilical arteries.
• From 18 to 41 weeks of pregnancy one-third of
  fetal cardiac output is directed to the placenta
  the proportion drops to one fifth after 32 weeks
  11.

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ductus venosus

• The ductus venosus has two central regulatory
  roles.
• control the proportions of oxygen/nutrient
  rich umbilical venous blood that are distributed
  to the liver and heart.
• maintain intra-atrial separation of blood
  streams by accelerating the velocity of blood
  from the umbilical vein.
•  

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• Under physiologic conditions, 60 to 70 percent of
  umbilical venous blood in the human fetus is
  distributed to the liver and the remainder to the
  heart.
• With chronic hypoxemia, this proportion may be
  modulated so that a larger proportion of
  umbilical venous blood can bypass the liver to
  reach the heart

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Ductus Venosus Doppler

• The ductus venosus can best be identified in a
  sagittal section or an oblique section through
  the upper fetal abdomen. It is seen as a
  continuation of the intraabdominal umbilical vein
  with a narrow inlet and a wider outlet and
  connects to the IVC. Once it is identified, color
  Doppler imaging can confirm it. The blood flow
  velocity recording can be made with the gate
  placed above the inlet of the ductus venosus.

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Ductus Venosus Doppler

• A transverse view of the fetal abdomen is
  obtained at the level of the intrahepatic portion
  of the umbilical vein. Rotate the probe slightly
  to image the entire length of the umbilical vein,
  from the umbilicus to its anastomosis with the
  portal sinus. The large right portal vein can be
  seen as a continuation of the portal sinus, which
  also gives rise to a smaller left portal vein.
  The probe is then moved to an oblique transverse
  position to image this intrahepatic vessel
  complex.Using color flow imaging, the ductus
  venosus can be idendified.

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• as a small vessel running from the portal sinus
  to the junction of the inferior vena cava and
  right atrium. This is often best visualized by
  imaging the full length of the umbilical vein
  with color Doppler. The ductus can then be
  identified arising from the intrahepatic vessel
  complex at the end of the umbilical vein by its
  higher velocities.
• The high velocity of blood flow in the ductus
  venosus is characteristically triphasic and
  typically produces an aliasing effect on color
  flow Doppler. The pulsed Doppler sample gate
  should be placed at the inlet of the ductus
  venosus from the portal sinus.

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RA
DV
RPV
LPV
UV
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The Ductus Venosus
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Oblique transverse view of the fetalabdomen
demonstrating the ductus venosus. Note
therelative positions of the umbilical vein,
portal sinus, rightand left portal veins and
ductus venosus.
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Doppler gate placed on ductus venosus in a 30
week fetus. Waveform obtained from the normal
ductus venosus. Note the triphasic appearance of
the normal waveform.
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DV
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Doppler examination of the ductus venosus with
normal flow velocity waveforms Abnormal
waveform with reversal of flow during atrial
contraction in a growth-restricted fetus.
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Abnormal ductus venosus Doppler and trisomy
.retrograde flow during atrial contractions.
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Doppler examination of the ductus venosus with
normal flow velocity waveforms (top). Abnormal
waveform with reversal of flow during atrial
contraction in a growth-restricted fetus (bottom).
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UMBILICAL VEIN

• Of interest is the abrupt change of a
  nonpulsatile
• flow pattern in the umbilical vein into a
• clearly pulsatile flow pattern in the ductus
  venosus
• and inferior vena cava. During ventricular
• systole, the right atrium unfolds after its
  contraction,
• which, in turn, will lead to a passive suction
• in compliant afferent vessels. Pulsations in the
• umbilical vein in physiological conditions have
  been reported in fetuses in the first trimester
• as well as in later gestation at more proximal
• levels in the fetal abdomen.

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UMBILICAL VEIN

• Pathological pulsations a result from the
  decompensation of the fetal right heart in
  (nonimmune) hydrops, severe growth-retardation,
  and arrythmias.in these conditions, it is
• a sign that the fetal heart function
  deteriorates and right atrial filling patterns
  are disturbed. The pooling of blood and the
  increase of obstructed venous inflow causes
  reversed flow at the level of the vessels
  responsible for the venous return, including the
  umbilical vein.

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UMBILICAL VEIN

• Umbilical venous frequency shift was recorded at
  the placental origin of the umbilical vein
  Registration of the frequency spread was
  performed using a pulsed 2-MHz Doppler scanner
  with a constant 50 angle between the Doppler
  beam and the axis of the vessel.
• The frequency of pulse repetition was between 2.5
  and 5 kHz, depending on the distance of the
  Doppler probe from the vessel.
• The Doppler gate was positioned to completely
  cover the diameter of the vessel, with a probe
  volume of 5-11 mm.
• filter (100 Hz) was used to eliminate jamming
  signals from the wall of the umbilical vein.

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UMBILICAL VEIN

• The physiological pulsations in the first
  trimester and the pathological pulsations in
  growth retardation in the
• umbilical vein probably reflect
• a high placental
• vascular resistance.

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U V DOPPLER
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U V PULSATION
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IVC

• Flow velocities in the inferior vena cava are
• similar to those obtained at the superior vena
• cava, so that the same interpretations can be
• performed on both vessels.
• They show a gestational age dependent increase
  without a change in the typical three-component
  waveform.
• The retrograde flow component represents
• the performance of the right atrium.

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IVC
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IVC
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IVC
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Atrial pressure changes

•  Umbilical vein blood flow is constant towards
  the fetus. With this notable exception,
• all venous vessels have a complex waveform
  pattern that is related to the pressure changes
  in the atria throughout the cardiac cycle.
• The events of the cardiac cycle that are of
  importance in this context are ventricular
  systole, the early phase of ventricular diastole
  (before atrial systole), and atrial systole

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Ventricular systole

• shortens the myocardial muscle mass, which makes
  the closed atrioventricular (AV) valves descend
  and results in
• pressure drop in both atria

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Early ventricular diastole 

• the myocardium relaxes, the AV valves move back
  up toward their resting position, and
• intraatrial pressures increase.

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Atrial systole 

• The discharge of the sinoatrial node at the end
  of diastole initiates an atrial contraction that
  produces a
• rapid rise in intraatrial pressure. When atrial
  pressure exceeds intraventricular pressure, the
  AV valves open leading to a
• rapid pressure drop in the atria.

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• Forward flow in the venous system is
  determined by the pressure difference to the
  right atrium. Forward flow is greatest during
  ventricular systole, with the next greatest flow
  during early ventricular diastole. This results
  in a larger systolic and a smaller diastolic peak
  in the venous flow velocity profile
• (S- and D- waves respectively).

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• The ductus venosus has the highest forward
  velocities in the venous system, therefore blood
  flow is antegrade throughout the cardiac cycle
  13.
• The hepatic veins have lower antegrade velocities
  so the pressure difference to the right atrium
  may result in a temporary reversal of blood flow
  during atrial systole.
• The same can be observed in the IVC and SVC,
  which have the most direct connection to the
  right atrium 15,16.

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• The clinical utility of venous Doppler
  velocimetry is greatest in fetal conditions with
  cardiac manifestations and/or marked placental
  insufficiency. These conditions include
• fetal growth restriction due to placental
• insufficiency,
• twin-twin transfusion,
• fetal hydrops, and fetal arrhythmia.

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Fetal growth restriction 

• Abnormal vascular tone, as well as obliterative
  loss of fetal villous vessels, raises umbilical
  artery Doppler resistance. A decrease in
  end-diastolic velocity becomes apparent when some
  30 percent of placenta is affected and progresses
  to
• absent or reversed end-diastolic velocity when
• the damage extends to 60 to 70 percent 26.

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Early Doppler changes

• Elevation of right ventricular afterload
  (placental resistance) forces redistribution of
  cardiac output towards the left ventricle and
  left ventricular output rises.
• A decrease in the ratio between cerebral and
  umbilical artery Doppler indices
  (cerebroplacental Doppler ratio) is an early and
  sensitive marker of redistribution of cardiac
  output, often preceding overt growth delay by up
  to two weeks 30.

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Late Doppler changes 

•   accompany metabolic deterioration and are a
  result of declining forward cardiac function and
  abnormal organ autoregulation. Increasing venous
  Doppler indices are the hallmark of advancing
  circulatory deterioration since they document the
  decreasing ability of the heart to accommodate
  venous return 32,33. Elevations of placental
  blood flow resistance and venous Doppler indices
  frequently progress in parallel.

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• Reversed umbilical artery end-diastolic
  velocity, abnormal venous Doppler indices, and
  the development of oligohydramnios are
  characteristic manifestations of ineffective
  downstream delivery of cardiac output.

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• Persistent excessive shunting across the ductus
  venosus compromises hepatic perfusion and may
  cause organ dysfunction and trigger hepatic
  artery vasodilatation as an alternative source of
  hepatic blood supply 34.
• Liver damage with elevated transaminases is an
  important contributor to metabolic deterioration
  under these circumstances.
• Coronary vasodilatation also becomes exaggerated
  in an attempt to recruit all the available
  coronary blood flow reserve 35.

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• Cardiac dilatation with holosystolic tricuspid
  regurgitation and loss of cerebral autoregulation
  (normalizing cerebral Doppler indices) are
  observed at this level of compromise and indicate
  loss of cardiovascular homeostasis 31.
• If the fetus remains undelivered spontaneous
  late decelerations of the fetal heart rate and
  stillbirth ensue.

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• Daily biophysical profile scoring in fetuses with
  absent or reversed umbilical artery end-diastolic
  velocity with strict delivery criteria has been
  associated with good outcome, suggesting that
  safe prolongation of these pregnancies is indeed
  possible 39.

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• Preterm growth restricted fetuses with elevated
  umbilical artery Doppler resistance have an
  overall perinatal mortality rate of 5.6 percent
  41. This rate increases to 11.5 percent when
  end-diastolic velocity is absent or reversed,
• and rises to 38.8 percent when venous Doppler
  indices become abnormal (predominantly due to an
  increase in the rate of stillbirth).

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 Twin to twin transfusion syndrome (TTTS)

• is a complication of monochorionic multiple
  gestation that results from unequal sharing of
  intravascular volume through communicating
  placental blood vessels. Differential blood flow
  across the placenta results in fetal size and
  amniotic fluid volume discordancies. This
  syndrome complicates approximately 10 to 15
  percent of monochorionic pregnancies and often
  results in death of one or both fetuses 43.

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• the Quintero staging of this disorder is based
  upon assessment of bladder filling as a marker of
  volume status, umbilical artery Doppler as a
  marker of placental blood flow resistance, and
  ductus venosus and/or umbilical venous Doppler as
  a marker of cardiac forward function .44

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• Stage 1 is defined by polyhydramnios (maximum
  pocket gt8 cm) and oligohydramnios (maximum pocket
  lt3 cm).
• Stage 2 is reached when bladder filling in the
  donor is no longer observed.
• stage 3 absent umbilical artery end-diastolic
  velocity, absent forward flow during atrial
  systole in the ductus venosus or umbilical venous
  pulsations.
• stage 4 Fetal hydrops .
• stage 5 fetal death .

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Nonimmune hydrops 

• Fetuses with nonimmune hydrops may have abnormal
  ventricular function,is reflected in abnormal
  venous flow velocity waveforms. With marked
  elevations in central venous pressure, abnormal
  flow in the precordial veins may progress to the
  development of umbilical venous pulsations in a
  similar fashion to that described for FGR.

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• The development of umbilical venous pulsations in
  hydropic fetuses is an ominous finding associated
  with demise in over 70 percent of patients 46.
• venous Doppler should form part of the
  diagnostic assessment of nonimmune fetal hydrops.

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Fetal arrhythmia

• the Doppler technique obtain simultaneous
  waveform recordings from an arterial and a venous
  vessel.
• This is possible at anatomic sites where arterial
  and venous vessels run in close proximity to each
  other such that the sample volume encompasses
  both vessels (eg, the aorta and inferior vena
  cava in the abdomen 47.
• the relationship between the a-wave of the
  venous waveform and systolic pulse of the
  arterial waveform indicate the timing of the
  electrical events that correspond to the p wave
  and qrs complex of the ECG.

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supraventricular tachycardia

• The normal triphasic venous waveform pattern is
  lost at heart rates in excess of 210 beats per
  minute and is replaced by a monophasic forward
  flow with reversal during atrial contraction.
• Above this critical heart rate, there is a 75
  percent increase in central venous pressure that
  predisposes to the rapid progression of fetal
  hydrops 48,49