New insights in_pih_pune_new

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New insights in_pih_pune_new

  1. 1. NEW IN PIH
  2. 2. DR SAMEER DIKSHIT MD.DGO.FCPS.FICOG <ul><ul><li>Hon Sonologist, Nowrosjee Wadia Maternity Home,Parel,Mumbai </li></ul></ul><ul><ul><li>Hon Fetal Medicine Consultant, BSES MG Hospital, Andheri,Mumbai </li></ul></ul><ul><ul><li>Irla Nursing Home,Irla,Mumbai </li></ul></ul><ul><ul><li>Sanket Sonography, Borivali, Mumbai </li></ul></ul><ul><ul><li>Boisar Fetal Medicine Consultant,Boisar </li></ul></ul>
  3. 3. <ul><li>Pathophysiology of PIH </li></ul><ul><li>Use of Doppler in PIH </li></ul><ul><li>Evolution of Doppler changes </li></ul><ul><li>“ Point of action” </li></ul><ul><li>Arterial v/s Venous Dopplers </li></ul><ul><li>Special conditions </li></ul>
  4. 4. Pathophysiology of PIH <ul><li>It’s a disorder of placental function </li></ul><ul><li>Syndrome of endothelial dysfunction with associated vasospasm </li></ul>
  5. 8. Placental Circulation <ul><li>Spiral Arterioles  Placental Lake  Uterine Vein </li></ul><ul><li>Umbilical Arteries  Placental Lake  Umbilical Vein </li></ul>
  6. 9. Placental Circulation
  7. 10. Application of Doppler in PIH <ul><li>(1) Prediction of PIH </li></ul><ul><li>(2) Monitoring the fetus </li></ul>
  8. 11. Vessels studied <ul><li>Arteries </li></ul><ul><li>Uterine Artery </li></ul><ul><li>Umbilical Artery </li></ul><ul><li>Middle Cerebral Artery </li></ul><ul><li>Thoracic Aorta </li></ul><ul><li>Renal Artery </li></ul><ul><li>Veins </li></ul><ul><li>Umbilical Vein </li></ul><ul><li>Ductus Venosus </li></ul><ul><li>IVC </li></ul>
  9. 12. Monitoring of the Fetus
  10. 13. Doppler Parameters Umbilical Artery S/D > 3 Absent End Diastolic Velocity
  11. 14. MCA S/D > 4
  12. 15. Why should increased spiral arteriole resistance lead to increased UA resistance??? <ul><li>PIH is Maternal Vasculitis </li></ul><ul><li>There is no direct connection between Spiral Arteriole & UA </li></ul><ul><li>Spiral A  Venous lake  circulates  Uterine Vein </li></ul>
  13. 16. The answer lies in the anatomy of placental villi
  14. 17. Placental Circulation
  15. 18. <ul><li>Tertiary villi float in the venous lake </li></ul><ul><li>Exchange of gases takes place </li></ul>
  16. 19. Placental circulation in case of normal spiral vessels
  17. 20. Increased resistance of the spiral arterioles
  18. 21. Effect of stenosis of spiral arterioles <ul><li>Normal-Lamellar flow </li></ul><ul><li>Effects of Stenosis </li></ul>Increased Velocity Turbulent flow and dampened velocity
  19. 22. The circulation in placental lakes becomes sluggish
  20. 23. This affects the gas exchange at the level of tertiary Villus <ul><li>Sluggish spiral arterioles to placental circulation </li></ul><ul><li>Trans-Villus gas exchange is affected </li></ul>
  21. 24. The Fetal vascular adjustments overcome this situation
  22. 25. Decision to deliver...... <ul><li>Primi </li></ul><ul><li>35 weeks A </li></ul><ul><li>BP 140/90 </li></ul><ul><li>Came for routine check up </li></ul><ul><li>On enquiry…..slightly reduced movements </li></ul><ul><li>Umb Artery S/D 3.4 ? </li></ul><ul><li>MCA S/D 3.6 ? </li></ul><ul><li>USG-AFI=8.3 </li></ul><ul><li>Non reactive NST </li></ul>
  23. 26. Umbilical Artery Doppler Indices in Small for Gestational age fetuses J Ultrasound Med 2009 <ul><li>When UA S/D & UA PI are adjusted for gestational age, their prediction of risk of complications is insignificant </li></ul>
  24. 27. Comparison of NST with the evaluation of centralisation of blood flow for prediction of neonatal compromise Journal of Ultrasound in Obstetrics and Gynaecology 1999;14; 38-41
  25. 28. Perinatal Morbidity Reactive NST + Normal Doppler 11.3% Reactive NST + Abnormal Doppler 37.5% Non reactive NST + Normal Doppler 52.4% Non reactive NST + Abnormal Doppler 60%
  26. 29. Odds ratio Non reactive NST Abnormal Doppler Significant neonatal complications 5.71 3.44 LSCS for fetal distress 4.73 2.84
  27. 30. International Society of Ultrasound in Obstetrics and Gynaecology Workshop on Second and Third Trimester Doppler 4-7 October,2001, Zagreb, Croatia
  28. 31. <ul><li>Normal UA S/D ratio </li></ul><ul><li>Abnormal UA S/D ratio </li></ul><ul><li>Absent Diastolic flow </li></ul><ul><li>Reversed Diastolic flow </li></ul>
  29. 32. <ul><li>Normal UA S/D ratio - 0% perinatal mortality </li></ul><ul><li>Abnormal UA S/D ratio- 7%perinatal mortality </li></ul><ul><li>Absent Diastolic flow- 10% perinatal mortality </li></ul><ul><li>Reversed Diastolic flow- 27% perinatal mortality </li></ul>
  30. 33. Use of Doppler for “point of action” <ul><li>Abnormal indices can not be taken as indicators for “point of action” i.e. early delivery </li></ul><ul><li>At the most, they indicate an ongoing process </li></ul><ul><li>Indicate that, the fetus is at risk of complications </li></ul>
  31. 35. IN PIH… <ul><li>Same information can be obtained by </li></ul><ul><ul><li>Clinical Examination (BP, Edema) </li></ul></ul><ul><ul><li>Urine Albumin </li></ul></ul><ul><ul><li>Gross USG features (IUGR, Oligohydramnios) </li></ul></ul>
  32. 36. Why does the Doppler examination not have “cutting edge” And…..can we give it the edge ???
  33. 38. Placental Bed Umbilical Artery Umbilical Vein Lower Limbs Kidneys Descending Aorta Aorta Carotid Arteries DV Terminal IVC IVC RA LV
  34. 39. Effect of PIH on fetus- Fetal centralisation <ul><li>Normoxemic centralisation </li></ul><ul><li>2) Hypoxemic centralisation </li></ul><ul><li>3) Decompensation </li></ul>
  35. 40. 1) Stage of Normoxemic centralisation
  36. 41. The trans- villus gas exchange is affected <ul><li>Spiral arterioles stenosis </li></ul><ul><li>Sluggish flow in Placental Lakes </li></ul><ul><li>Trans Villus gas exchange affected </li></ul>
  37. 42. <ul><li>The fetus adjusts to the milieu of privation </li></ul><ul><li>Maintains oxygen supply to the fetal brain </li></ul><ul><li>Decreased cerebral resistance  Increased cerebral perfusion </li></ul>
  38. 43. Cerebral circulation is maintained Placental Bed Umbilical Artery Umbilical Vein Lower Limbs Kidneys Descending Aorta Aorta Carotid Arteries DV Terminal IVC IVC RA LV
  39. 44. <ul><li>Decreased cerebral resistance  Increasing Diastolic velocities  Decreasing MCA S/D ratio & PI ratio </li></ul>
  40. 45. <ul><li>More oxygenated blood from UV shunted through DV at the expense of the blood to the portal circulation </li></ul>Fetal Liver also chips in….
  41. 46. Umbilical Vein (LUV) Intra hepatic portion of UV Portal Sinus Right Portal vein Ductus Venosus IVC Left Portal vein Left Hepatic vein Right Hepatic vein Superior mesenteric vein & splenic vein Left Liver Lobe Right Liver Lobe
  42. 47. <ul><li>Decreased blood to the portal circulation </li></ul><ul><li>Shrinking liver size  Shrinking AC </li></ul><ul><li>IUGR </li></ul>
  43. 48. The Fetal vascular adjustments overcome this situation Faster fetal circulation turnover maintains the fetal vascular PO2 in the face of sluggish placental circulation
  44. 49. The fetal heart improves its inotropic force and helps to circulate the blood faster
  45. 50. <ul><li>Increased peripheral resistance  Emptying of the peripheral venous compartment  Increased venous return </li></ul>
  46. 52. <ul><li>But there is also concurrent increased tone of the Umbilical Arteries  Decreased diastolic velocities </li></ul>
  47. 53. <ul><li>Increased UA resistance  Decreasing Diastolic velocities  Increasing UA S/D ratio & PI ratio </li></ul>
  48. 54. Placental Bed Umbilical Artery Umbilical Vein Lower Limbs Kidneys Descending Aorta Aorta Carotid Arteries DV Terminal IVC IVC RA LV
  49. 55. <ul><li>Increased UA PI with decreased MCA PI </li></ul><ul><li>Altered CPR </li></ul>
  50. 56. (2)Stage of Hypoxemic centralisation
  51. 57. <ul><li>The compensatory mechanisms are no longer sufficient </li></ul><ul><li>The fetal brain starts experiencing hypoxia </li></ul><ul><li>The renal arteries have increased resistance </li></ul>
  52. 58. <ul><li>Decreasing blood supply to the kidneys  Oliguria  </li></ul><ul><li>Cerebral hypoxia  The brain stem autonomic reflexes get sluggish </li></ul>
  53. 59. Most of the clinical tests pick up at this point <ul><li>NST is non reactive </li></ul><ul><li>Beat to beat variability is affected </li></ul><ul><li>Liquor is reduced </li></ul><ul><li>Fetal movements reduced </li></ul><ul><li>Fetal breathing pattern reduced </li></ul>
  54. 60. (3) Decompensation
  55. 61. <ul><li>Further hypoxia </li></ul><ul><li>Build up of tissue lactic acid </li></ul><ul><li>Rapid shifting of O 2 dissociation curve to right </li></ul><ul><li>Acidosis </li></ul>
  56. 62. <ul><li>Further brain hypoxia  Loss of fetal tone </li></ul><ul><li>Failing heart  “A” wave reversal of DV  Pulsations of Umbilical Vein </li></ul><ul><li>IUFD </li></ul>
  57. 63. What shifts the fetus from Stage of compensated hypoxia to Stage of decompensation
  58. 64. Is it because of worsening of utero-placental resistance?? <ul><li>That should lead to cardiac failure </li></ul><ul><li>Hydrops should be seen in PIH patients </li></ul>
  59. 65. Is it because of increasing blood flow in the cerebral circulation?? <ul><li>Aneurysm of vein of Galen </li></ul><ul><li>Rh incompatibility </li></ul><ul><ul><li>Babies die of Hydrops and cardiac failure </li></ul></ul><ul><ul><li>No evidence of hypoxia in these cases </li></ul></ul>
  60. 66. The answer lies in venous flow
  61. 68. <ul><li>“ S” wave  Depends on “Venous Return” (Determined by After Load) </li></ul>
  62. 69. <ul><li>“ D” wave  How much the forward flow occurs immediately after the ventricular systole (Forward flow across AV valves) </li></ul>
  63. 70. <ul><li>“ A” wave  How much blood is remaining in RA after ventricular systole(Determined by Pre-load) </li></ul>
  64. 71. Placental Bed Umbilical Artery Umbilical Vein Lower Limbs Kidneys Descending Aorta Aorta Carotid Arteries DV Terminal IVC IVC RA LV
  65. 73. 1) Stage of Normoxemic centralisation
  66. 74. <ul><li>IVC bringing deoxygenated blood gets oxygenated blood from DV (D) </li></ul><ul><li>Both these flows travel together in terminal portion of IVC (T) </li></ul><ul><li>The two flows remain separate because of pressure gradient between the two flows </li></ul>
  67. 75. What keeps the two flows separate in the terminal IVC?? <ul><li>There is no mechanical cordoning off…… </li></ul><ul><li>It is a principle of fluid dynamics that keeps the flows separate </li></ul>
  68. 76. <ul><li>“ Boundary layer phenomenon” </li></ul><ul><li>Simply put, the two currents in a tube remain separate, if the pressure difference between them is high </li></ul>
  69. 78. Venturi Effect
  70. 81. Placental Bed Umbilical Artery Umbilical Vein Lower Limbs Kidneys Descending Aorta Aorta Carotid Arteries DV Terminal IVC IVC RA LV
  71. 83. <ul><li>IVC PSV approaches DV PSV </li></ul><ul><li>Loss of separation </li></ul><ul><li>Mixing of de-oxygenated & oxygenated blood flow </li></ul>
  72. 84. <ul><li>Altered DV & IVC Pr Gradient </li></ul><ul><li>Normal DV & IVC Pr Gradient </li></ul>
  73. 85. Mount Everest in Utero <ul><li>Drop in pO 2 of blood reaching cerebral vasculature </li></ul><ul><li>Drastic fall in O 2 bound to the fetal hemoglobin </li></ul><ul><li>Fetal Hypoxia </li></ul>
  74. 86. (2)Stage of Hypoxemic centralisation
  75. 87. <ul><li>Fetal Hypoxia  More vasoconstriction  Increasing VR  Loss of pressure gradient  More mixing of blood  Decrease of PO 2 </li></ul><ul><li>Cerebral hypoxia  Vascular endothelium affected  Cerebral hemorrhage </li></ul><ul><li>Cerebral hypoxia  Ischemic injury </li></ul>
  76. 89. <ul><li>Increasing VR  Heart is not able to cope up with it  More blood left over in the RA  Increased “Pre-load” </li></ul><ul><li>Loss of forward “A” wave </li></ul>
  77. 91. Fetal Demise…..
  78. 92. Date 3 rd May,2010; GA 32 weeks <ul><li>G2 P1, 32 years old </li></ul><ul><li>Previous LSCS </li></ul><ul><li>BP 140/90, on T Labetolol </li></ul><ul><li>Good Kick count </li></ul><ul><li>Good Liquor </li></ul><ul><li>Doppler ……… </li></ul>
  79. 93. Date 3 rd May,2010; GA 32 weeks <ul><li>MCA S/D= 4.1 </li></ul><ul><li>Umb Art= AEDV </li></ul>
  80. 94. <ul><li>UA AEDV  deliver or conserve?? </li></ul><ul><li>Good kick count/ adequate liquor </li></ul><ul><li>BP 140/90 </li></ul><ul><li>GA 32 weeks </li></ul><ul><li>Dilemma ………. </li></ul>
  81. 95. Date 3 rd May,2010; GA 32 weeks <ul><li>DV PSV=31.67 cm/s </li></ul><ul><li>IVC PSV=10.40 cm/s </li></ul>
  82. 96. 1) Stage of Normoxemic centralisation Decision taken to conserve the pregnancy
  83. 97. Date 31 st May,2010; GA 36 weeks <ul><li>BP 140/90, on T Labetolol </li></ul><ul><li>Decreased FM </li></ul><ul><li>Reduced Liquor </li></ul><ul><li>Doppler ……… </li></ul>
  84. 98. Date 31 st May,2010; GA 36 weeks <ul><li>MCA S/D=2.64 </li></ul><ul><li>UA=AEDV </li></ul>
  85. 99. Date 31 st May,2010; GA 36 weeks <ul><li>DV PSV=43.27 cm/s </li></ul><ul><li>IVC PSV=45.06 cm/s </li></ul>
  86. 100. 2) Stage of Hypoxemic centralisation Decision taken to deliver
  87. 101. Other things to consider <ul><li>Fetal vascular adjustments through increasing VR, occur in chronic situations </li></ul><ul><li>In acute conditions  Tachycardia </li></ul><ul><li>Tachycardia has very limited time frame </li></ul>
  88. 102. <ul><li>The fetal oxygenation can be affected by worsening of placental conditions  Oxygenation of blood in placenta affected  The blood arriving via DV itself is of low PO 2 </li></ul><ul><li>Worsening of Toxemia, Maternal fever </li></ul>
  89. 103. <ul><li>Doppler values reflect adjustment of the fetus </li></ul><ul><li>When fetus does not have time for adjustments, doppler values are of no value </li></ul><ul><li>Abruptio Placenta </li></ul>
  90. 104. Summary
  91. 105. Uterine Artery Doppler <ul><li>An artery which feeds arterioles, has tri- phasic spectral flow </li></ul><ul><li>Phase of reversal represents high resistance downstream </li></ul><ul><li>Blood vessels which feed organs have bi- phasic spectral flow </li></ul>
  92. 106. <ul><li>This ensures continuous flow for the organ </li></ul><ul><li>High resistance of spiral arterioles is symbolised by occurrence of diastolic notch </li></ul><ul><li>Diastolic notch/ Uterine Artery RI are used to predict development of PIH </li></ul>
  93. 107. Doppler for assessing fetal health <ul><li>Doppler values reflect fetal adjustment </li></ul><ul><li>Arterial Dopplers only identify the subset of fetuses who are at risk of complications </li></ul><ul><li>They do not tell you when to deliver </li></ul>
  94. 108. <ul><li>In 3 rd Trimester, in the face of adverse utero-placental resistance, the UA may be minimally affected </li></ul><ul><li>Abnormal UA/ MCA  stage of Normoxaemic centralisation or beyond </li></ul>
  95. 109. <ul><li>Cerebro Placental Ratio (CPR)- MCA/UA PI </li></ul><ul><li>Better predictor of the stage of hypoxemic centralisation </li></ul><ul><li>Cut off 1.07 </li></ul>
  96. 110. <ul><li>Venous dopplers reflect fetal oxygenation </li></ul><ul><li>Increasing PSV of IVC suggests worsening of oxygen status </li></ul><ul><li>Usually indicate timing of delivery </li></ul>
  97. 111. Thank you

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