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    New insights in_pih_pune_new New insights in_pih_pune_new Presentation Transcript

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