PMC4166603_01
Doppler parameters at the time of hospital admission (20 weeks and 5 days) when fetal growth restriction and preeclampsia were diagnosed.
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F1
There was reversal of flow during diastole in the aortic isthmus, bilateral uterine notching, and increased uterine artery PI (Figure 1).
Doppler parameters before fetal demise (21 weeks and 3 days).
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F2
The last Doppler examination prior to the diagnosis of fetal death at 21 weeks and 3 days showed signs of severe fetal-placental hemodynamic deterioration such as: reverse diastolic velocities in the umbilical artery, biphasic umbilical vein pulsations, bilateral uterine notching and increased uterine artery PI, reduced middle cerebral artery PI, abnormal ductus venosus waveform with reverse atrial flow, and reduced intermediate flow between the systolic and diastolic components of the waveform, reversed diastolic flow in the aortic isthmus, and coronary artery vasodilatation (Figure 2).
Changes in the pulsatility index of the umbilical artery (UA), middle cerebral artery (MCA), uterine arteries (Ut Art) and ductus venosus (DV) during hospitalization.
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F3
Representative images of Doppler interrogation of the different vessels are shown in Figure 3.
Progressive changes in the echogenicity of the placental lesion in relation to gestational age (a-c). The area inside the cyst became more echogenic as gestation progressed (arrows). Additional small cystic areas are shown in Figure 4d.
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F4
The placental cyst measured 16 x 14 mm with central areas of mixed echodensity (Figures 4a-c); additional small cystic lesions were observed in the placenta (Figure 4d).
Pathological examination of the placenta: a) the maternal surface shows an ill-defined yellow area (arrows) which coincided with the infarction hematoma; b) cut sections of the placenta show a large round hemorrhagic lesion surrounded by yellow infarcted placental tissues. Two additional small infarcts (arrows) are also present; c) basal decidual vessels with thick muscularized walls (arrows) and absent physiologic remodeling (persistent muscularization), d) fibrinoid deposition (arrow) in the arterial walls (atherosis), and e) decreased number of distal villi with increased syncytial knots and prominent stem villi.
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F5
Sections of the placenta showed pale surfaces (Figures 5a and 5b). Microscopic evaluation of the placenta also showed persistent muscularization (Figure 5c), atherosis (Figure 5d), persistent endovascular trophoblast, mural hypertrophy and thrombi in decidual vessels, as well as abnormal villous morphology including distal villous hypoplasia (Figure 5e) and foci of villous dysmaturity.