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How I Do it? - Quantifying Placental function and Identifying Placental Reserve By Dr. K. K. Das (Bokaro)

NATURAL HISTORY OF FETAL DETERIORATION
 
How Can We Quantify Placental function and Identify Placental Reserve?
 
Dr. K.K.Das
drkkdas@rediffmail.com

Introduction

With the use of Doppler in the clinical practice our focus on the subject of IUGR has currently been shifted from fetal growth assessment to   the study of deep rooted functional obstruction in the tertiary placental villous complex. Increasing obstruction progressively increases the circulatory resistance in the umbilical artery and decreases pO2 level in umbilical vein. Both these events set into motion, a phenomenon of a circulatory re-distribution, principally characterized by reopening of ductus venosus sphincter and centralization of blood flow modulated by chemoreceptors. The better oxygenated blood goes towards the most vital organs brain, heart & adrenal; while vasoconstriction limits the blood arrival at the organs considered less indispensable like liver, kidney, lower extremities, muscle and skin.

 Recent studies in clinical and animal experiment

The redistribution of blood flow   was extensively studied in fetal sheep and primates by injecting radioactively labeled micro-spheres. Hypoxemia and acidosis was induced by different procedures,   such as maternal breathing of a mixture low in oxygen, hypotension, partial umbilical compression using clamps and by micro-embolisation of umbilical arteries.

In all cases, the pattern of redistribution of blood flow was confirmed and two  types of fetal deterioration were identified.

1.    When fetal hypoxia was caused  by maternal internal medium without placental lesion like   cardio-respiratory pathology, acute deficit of specific nutrients,  severe anemia, altered maternal hemodynamic due to hypertensive crisis of  renal or endocrinal origin not only was there an increase in cardiac and cerebral perfusion but there was no change in  umbilical blood flow.

2.     But this was not the case when the fetal hypoxia originated from microembolisation of the umbilical arteries thus creating conditions similar to those of a human fetus with a placental lesion. A progressive decrease in the umbilical blood flow was evident with the increasing  obstruction in terminal villous arterioles.

Fetal hypoxemia in IUGR is thus a result of functional obstruction of terminal villous complex and not the cause of altered hemodynamic in umbilical artery. So centralization of blood flow may develop independently of umbilical wave form.

Using Color Doppler since 1997 in more than 7500 cases (nearly 30% high risk pregnancies) we now can confidently quantify placental deficit better, and identify different stages of fetal ill health, as below:

A.  Stage I sub-clinical or silent phase: From animal experiment, we know there is no clinical reflection in the Doppler analysis of the feto-placental circulation up to 50% of placental obstruction. Fetal growth, BPP, Liquor volume remains normal. Clinician can not detect this theoretical placental deficit which is made up by the remaining 50% placental function. This is called ‘Placental Reserve’

B.  Stage II or Pre centralization: Beyond 50% placental obstruction, the umbilical artery displayed progressive loss of end diastolic flow (EDF) with intermittent opening up of Ductus venous floodgate and delay the onset of centralization of blood flow.  AFI, BPP score and NST tracings still remain  normal.  The Increasing number of SGA babies  are delivered in  stage II with nearly 25-30% increase in C-Section rate, due to display of early fetal distress in CST. This is the clinical significance of Stage II.

C.  Stage III or Centralization of blood flow

a.    Stage III A or initial phase:  Umbilical artery  EDF continues to decrease but still showing forward flow during the whole cardiac cycle. When compared to Middle cerebral artery , Cerebro-placental ratio (CPR) becomes equal or less than one. Most of the clinician believes that This is the best fluxo-metric index for early diagnosis of IUGR to warn the clinician well in advance about the prospective risk from chronic vascular changes. BPP and AFI often found normal or equivocal having normal NST tracing.

b.      Stage III B or advanced phase: When 80 % blockage reaches in villous circulation advance phase starts, displaying absent end diastolic flow (AEDF) in umbilical artery and aorta. BPP and NST may still   show normal tracing.

c.     Stage III C or terminal phase: In addition to AEDF umbilical artery (and aorta) may now show REDF.   Ductus Venosus shows reversed blood flow at atrial contractions suggest central venous stasis due to right heart failure with possible display of umbilical venous pulsations. IVC also shows increasing reversed blood flow during atrial contraction, reaches up to 30% (normal up to 10 %). Ventricular Ejection Force (VEF) reduced to 5th percentile. The CST now registers late deceleration and loss of reactivity due to loss of cardiac automatism. Fetus is very critical but still the fetus can be salvaged, if delivered promptly with good NICU support.

d.    Stage IV decentralization of B/F or irreversible hemodynamic changes:  Lastly if the fetus is not rescued from the  extreme hostile intra-uterine environment; in a day or two, an irreversible state of generalized vascular paralysis sets in with 95% blockage. Brain edema and rise of intracranial pressure hinder cerebral blood perfusion -> alter cell membrane permeability -> increased intra-cellular osmotic pressure -> tissue necrosis.  CTG display flat heart rate tracing even with good uterine contractions. Such neonates often  die due to brain death in spite of best neonatal care.

KEY POINTS TO CLINICIAN : CTG AND DOPPLER

1.    Doppler sonogram is an outstanding “early warning device“ for a slowly developing threat to fetal well-being  from chronically impaired nutritional supply and offers advance warning  several days before the CTG. It can lead to a significant reduction in the incidence of acidosis if the Doppler findings are analyzed correctly for the optimum time and type of delivery.  A normal  Doppler finding reflects normal circulation in the vascular region where as abnormal Doppler in umbilical artery, reflects deep rooted placental pathology, thus a chronic parameter but can not indicate acute hypoxic changes that commonly supervene at term or during labour.

2.    A normal CTG  reflects only  normal cerebral function of fetus; where as a highly abnormal CTG  expresses depression in cerebral function

3.    However we wish to point out again, the threat to the fetus arising acutely, such as acute placental insufficiency in a previously normal pregnancy can not be detected by Doppler examination especially after 38 weeks gestation. In such situation CTG is clearly superior.

When comparing the validity of these two methods the differences between them must be borne in mind. Seeing is believing.  We documented two IUGR case reports managed more than eight years back during our initial learning phase.  

Conclusion: Study of feto placental hemodynamic using Color Doppler and CTG is considered indispensable in the hands of a modern clinician  managing high risk pregnancies. However, it is essential to understand the natural history of fetal deterioration to obtain significant fetal outcome.  

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