Interpretation
Early onset preeclampsia and placenta-related FGR are associated with
incomplete transformation of the spiral arteries, which result in
hypoperfusion of the placenta and induced placental infarction5, 6. SMI is good for visualizing minute blood flow;
therefore, it can easily help identify lesions of placental infarction
as lack of vascularity surrounding normal placental blood flow. In
contrast, in tissues with avascular villi, only capillaries are absent
in the villous tissue 7, which is not distinguishable
from normal placenta using B-mode ultrasound. Even with conventional
color Doppler, it is difficult to visualize the minute blood flow of the
capillaries in the terminal villi. If the flow velocity range is lowered
to detect such minute flow, motion artifacts would disturb the
expression of real blood flow. However, SMI enables the expression of
such thin and sharp terminal villous blood vessels. Therefore,
ultrasound diagnosis of avascular villi can be established by
identifying the presence of slow congested maternal blood flow in the
intervillous space with absent peripheral villous blood vessels. We
believe that this is a breakthrough outcome of the current study.
Maternal vascular malperfusion, such as pre-eclampsia and FGR, cause
utero-placental hypoxic disorder due to incomplete remodeling of the
spiral arteries in the first trimester, thus, resulting in placental
infarction 8. Isolated small infarcts can be found
pathologically in uncomplicated pregnancies; however, multiple central
infarcts often associated with intervillous fibrin deposition are found
in severe preeclampsia and FGR 7. Although
conventional ultrasound can detect these large lesions as complex
echogenic intra-placental masses close to the basal plate9, SMI enables the detection of these small lesions
even in tertiary villous tissues. However, the diagnostic accuracy for
predicting infarction and avascular villi using SMI was higher in cases
with FGR than that in cases with pre-eclampsia. Cases more adversely
affected by maternal malperfusion, such as those with FGR and
preeclampsia, are likely to have many and/or large pathologic findings
in the placenta, which we believe might be the reason that much larger
lesions could be easily detected. Diffuse small infarctions might be
difficult to distinguish from avascular villi expressed as scatter
without villous trees (Figure 5, Appendix S6) .
Contrary to maternal vascular malperfusion, occlusion or compression of
the umbilical cord, such as hyper-coiled cord, can cause a dilation of
stem villi 7. Consequently, fetal vascular
malperfusion, which is characterized by thrombosis and ischemic villi
due to umbilical cord blood flow stasis result in FGR10. Therefore, in cases of FGR, we hypothesized that
various placental causes of FGR, both maternal and fetal vascular
malperfusion, could be distinguished using SMI. We focused on the
dilatation of stem villi as one of the findings of fetal vascular
malperfusion; however, the accuracy of ultrasound diagnosis was low.
Since SMI is an ultrasound Doppler method, SMI blood flow image can be
easily enhanced. Furthermore, in histological evaluation, the slice of
the tissue does not always include the cross section of the blood vessel
in the center. Therefore, we believe the discrepancy between the
ultrasound findings and sliced histological findings to be large. The
findings of congestion in stem villi are relatively large compared to
the other findings in the present study. In such a large vascular
evaluation, comparison between the B-mode ultrasound and macroscopic
placental findings might be superior to the comparison between SMI and
histological findings.
Placental histological findings of chorangiosis are often investigated
in the placenta in cases of preeclampsia. Chorangiosis is believed to
form due to an adaptive response to placental hypoxia11. In the present study, we defined chorangiosis as
an ultrasonographic finding when the Doppler strength of SMI was higher
than that of the surrounding villi. However, it was difficult to
distinguish the exact chorangiosis from normal placental tissue. We
believe that this is because of the relative comparison of echogenicity
with the standard villous findings. Originally, the diagnosis of
chorangiosis should be pathologically made when hyperbranching is
confirmed 12. Radically, we noticed that the
definition of ultrasound findings of chorangiosis should be
reconsidered.