New insights in_pih_pune_new

NEW IN PIH

DR SAMEER DIKSHITMD.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

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 > 3Absent End Diastolic Velocity

MCAS/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

• Tertiary villi float in the venous lake

• Exchange of gases takes place

http://upload.wikimedia.org/wikipedia/commons/7/79/Gray35.png

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

http://upload.wikimedia.org/wikipedia/commons/7/79/Gray35.png

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 LimbsKidneys

Descending Aorta

AortaCarotid Arteries

DV

Terminal IVC

IVC

RALV

Effect of PIH on fetus- Fetal centralisation

1) Normoxemic centralisation

2) Hypoxemic centralisation

3) Decompensation

1) Stage of Normoxemic centralisation

The trans- villus gas exchange is affected

1. Spiral arterioles stenosis2. Sluggish flow in

Placental Lakes3. 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

Placental Bed

Umbilical Artery

Umbilical Vein

Lower LimbsKidneys

Descending Aorta


DV

Terminal IVC

IVC

RALV

Cerebral circulation is maintained

• 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

Por

tal

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 LimbsKidneys

Descending Aorta


DV

Terminal IVC

IVC

RALV

• 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 O2 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 LimbsKidneys

Descending Aorta


DV

Terminal IVC

IVC

RALV

• 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

http://static.howstuffworks.com/gif/tornado-2.jpg

http://en.wikipedia.org/wiki/File:Aerosol.png

Placental Bed

Umbilical Artery

Umbilical Vein

Lower LimbsKidneys

Descending Aorta


DV

Terminal IVC

IVC

RALV

• 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 pO2 of blood

reaching cerebral vasculature

• Drastic fall in O2 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 PO2

• 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 3rd May,2010; GA 32 weeks

• G2 P1, 32 years old

• Previous LSCS

• BP 140/90, on T Labetolol

• Good Kick count

• Good Liquor

• Doppler ………


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 ……….


DV PSV=31.67 cm/s IVC PSV=10.40 cm/s


Decision taken to conserve the pregnancy

Date 31st May,2010; GA 36 weeks

• BP 140/90, on T Labetolol

• Decreased FM

• Reduced Liquor

• Doppler ………


MCA S/D=2.64 UA=AEDV


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 PO2

• 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 3rd 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

New insights in_pih_pune_new

Health & Medicine

Transcript of New insights in_pih_pune_new