Colour doppler in iugr
Upcoming SlideShare
Loading in...5
×
 

Like this? Share it with your network

Share

Colour doppler in iugr

on

  • 9,043 views

 

Statistics

Views

Total Views
9,043
Views on SlideShare
8,914
Embed Views
129

Actions

Likes
9
Downloads
488
Comments
1

4 Embeds 129

http://drmcbansal.blogspot.in 95
http://drmcbansal.blogspot.com 25
http://drmcbansal.blogspot.ca 8
http://drmcbansal.blogspot.com.au 1

Accessibility

Categories

Upload Details

Uploaded via as Microsoft PowerPoint

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Processing…
Post Comment
Edit your comment

Colour doppler in iugr Presentation Transcript

  • 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
  • 4. 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.
  • 5. • 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.
  • 6. IMPLANTATION OF BLASTOCYST EARLY TROPHOBLAST NO VASCULARITY
  • 7. VILLOUS DEVELOPMENT
  • 8. BLASTOCYST – PRIMIARY VILLI DEVELOPMENT
  • 9. BLASTOCYST – VILLI DEVELOPMENT
  • 10. TROPHOBLAST CELL COLUMN : INTERSTITIAL TROPHOBLAST : INTRAMURAL ENDOVASCULAR TROPHOBLAST
  • 11. EARLY IMPLANTATION
  • 12. 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.
  • 13. 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.
  • 14. 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
  • 15. FETALCIRCULATION
  • 16. • 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
  • 17. FETOPLACENTAL CIRCULATION ON 3-D POWER DOPPLER SCANNING
  • 18. 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.
  • 19. 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 anduterine arter
  • 20. .(1)Changes in the arterial circulation  (a) Uterine circulation----as the feto- placentalcompartment develops and gestational age advances ,there is an increase in number of tertiary stem villi andarterial channels to meet the need of developing fetus.hence the Doppler study at this time showsappearance of a diastolic component in uterine arteryflow velocity wave form,. during early 2nd trimesteri.e.. 14 weeks’ gestation and progressively increasesUp to 24 weeks. in normalpregnancy it continued to show increased diastolicflow velocity and loss of diastolic notches by 22weeks .Pregnancies associated with high persistent resistancewave forms and early diastolic notches, are at risk ofpreterm delivery due to IUGR, PIH, abruptio placentaand overall higher morbidity and mortality.
  • 21. Abnormal flow velocity wave form in the uter ine arteries demonstrating a persistent diastolicnotch and low diastolic blood flow beyond 24weeks of gestation reflects abnormal to bloodflow down stream to utero placental vascularbed., there by increase in uterine artery PI andbilateral notching. Combined Doppler andhormonal profile of placental function may bea valuable tool to screen pregnancies that are atrisk of PIH, IUGR, IUFD and abruptio placenta.
  • 22. UTERINE ARTERY DOPPLER WAVE FORMS
  • 23. UTERINE ARTERY DOPPLER WAVE FORMS –Journal of Obstetrics & Gynaecology India
  • 24. • (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 siteis higher and progressively decreases towardsplacental site.(figure 5) In normal fetus ,pulsatile index (PI)decreases with advancing gestational period.Thisindicates progressive decrease in vascularresistance in placental bed.(figure 6)
  • 25. • 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 increasedplacental resistance. The absent or reversed end diastolic flow stronglyassociated with worst fetal outcome(40%.Perinatal deaths). In milder form of placental insufficiency, diastolic flow isdecreased, but absent or reversal of end diastolic flow maynot develop and fetus is thriving well in utero.In some IUGR cases fetus maintains the normal diastolic flowvelocity in umbilical artery by altering Cardiac out put in orderto maintain Oxygenation. This suggests that umbilical arteryworks as a shunt . Hence umbilical artery is not a KEY vessel to have aconclusive evidence of fetal Oxygenation status.
  • 26. UMBILICAL ARTERY Normal doppler wave form
  • 27. REVERSAL OF BLOOD FLOW IN UMBILICAL ARTERY
  • 28. UMBILICAL ARTERY DOPPLER : (a) NORMAL (b) LOSS END- DIASTOLIC FLOW (c) REVERSED END-DIASTOLIC FLOW
  • 29. • (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 bestobtained with the cranium in a transverse position asangle of insonation will be close to 0 degree. During normal pregnancy the MCA shows highresistance and low diastolic flow pattern with continuousfore ward flow through out the cardiac cycle. In mild fetal hypoxia when resistance of umbilicalartery increased ,no changes in MCA blood flow patternmay be noted(Adoptive phase) .An increased MCA PSVmay only be the finding.
  • 30. • If there is continued and progressive hypoxia, a phenomenon known as “ BRAIN SPARING EFFECT ”is noted. There is dilatation of cerebral vessels toincrease blood flow to brain at the expenses of otherorgans of abdomen. Doppler study depicts it as increase in diastolicflow with decreased PI. The presence of suchcompensation indicates compromised fetus in utero. In pregnancies with chronic fetal hypoxia , bloodvolume is redistributed in favor of vital organs like brain,heart and kidneys.When hypoxia is continuous , brain edema ,increasedintra cranial pressure and reversal of diastolic flowsuggest grave and irreversible neurological outcome.
  • 31. • 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%)
  • 32. MCA Doppler : High systolic wave in anemic fetus
  • 33. • (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.
  • 34. (2) Changes in venous circulation Doppler wave from obtained from central venoussystem of the fetus reflects the physiological status ofright ventricle. It gives information about—1.ventricular preload,2. myocardial compliance and3.right ventricular end diastolic pressure. Following veinsgive us invaluable information----- (a) Inferior vena Cava. (b) Ductus venosus. ( c) Umblilical vein.
  • 35. 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.
  • 36. • 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.
  • 37. ASSESSMENT OF DUCTUS VENOSUS NORMAL WAVE FORM  s, d, a
  • 38. ASSESSMENT OF DUCTUS VENOSUS
  • 39. 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.
  • 40. Changes in fetal heart in IUGR• Basics of fetal heart function  . Both ventricles pump blood to systemic circulation in a parallelfashion ,right ventricular volume is more than that of left sided. . 85-95% right ventricular output is supplied to sub diaphragmorgans(Descending aorta via ductus arteriosus ).10-15% goes topulmonary area. . Dormant pulmonary system puts increased resistance ()almostequalto systemic resistance) to blood flow to it.Hence there is left toright shunt across foramen ovale. . As gestational period increases flow to pulmonary system alsoincreases and by end of 34-36 weeks R> L shunt decreases by 45%Cephalic part of fetus and heart gets blood supply from left ventricularout put.Aortic isthmus establishes communication between the 2 arterialoutlets.that perfuse upper and lower body of fetus.
  • 41. • 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.
  • 42. 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).
  • 43. 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 “•
  • 44. 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.
  • 45. Mmode with superimposed doppler ATRIAL & VENTRICULAR activity
  • 46. Doppler based Management of IUGR (A) Cause for development of utero placentalinsufficiency ( IUGR) may be operating at thetime of implantation. However effect is not recognized until 22-24weeks of gestation. These fetuses do not show any significantdoppler abnormality at this period of gessation.
  • 47. • (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 havenormal or abnormal value of PI. 3.Umblilica as well as MCA both have abnormal valuesof PI. Fetus needs weekly monitoring, Maternal bed rest inleft latral position,O2 and nutritional therapy . If both vessels are developing abnormal indices , fetalcondition is likely to deteriorate and term delivery withhealthy fetus is remote..
  • 48. (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 eclampsiamay supervene or a persistent abnormal bio physicalprofile may need immediate delivery . Such fetus is atlower risk of developing RDS and intracranialhemorrhage as compare to the premature fetus .Distress may produce endogenous corticosteroids tobring early maturity in IUGR fetus.If the fetus is not delivered the IUGR pathologycontinues to progress.
  • 49. • (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.
  • 50. 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 growthrestricted. 2.To prevent fetal decompensation if IUGRis all ready developed. 3.To decide the appropriate point of timeof delivery of IUGR fetus with the aim to avoidprematurity and sudden fetal death in utero.
  • 51. 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 andminimal response to sympathetic/ parasympathetic stimuli .This adaptation is to ensure sustained and increasing bloodsupply to placenta  fetus. Serial doppler study of uterineartery in women who carry H/O predisposing factors fordevelop IUGR at later date will help in identifying the futureculprits. Persistence of pre diastolic notch and gradually increasingimpedance indices suggest an abnormal uterine arterycirculation. These women need active treatment in 2ndtrimester by bed rest antihypertnsives,O2, nutritionalsuplimentation .
  • 52. • 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.
  • 53. • 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
  • 54. • 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 ) indicatessignificant fall in left ventricular output. Upper bodyis now perfused by right ventircular output.
  • 55. 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.