PMC8336983_01
Portal phase axial tomographic images during preoperative preparation for the first endovascular intervention (A) and before the second endovascular intervention (B) (2 years and 8 months later), demonstrating development of the stenoses in the outflows of the hepatic veins (long arrows) and the change in the proportion of perfusional disorder in the hepatic parenchyma (arrowheads). Non-opacification of the middle hepatic vein is also observed.
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Visibility of the middle HV was poor, suggesting thrombosis (Figure 1A). After puerperium, CT demonstrated a reduction in the outlet diameter (7 mm) compared to the previous scan (12 mm) and ascites was detected by CT, despite no clinical evidence (Figure 1B).
Images from intraoperative phlebography of the suprahepatic vein followed by balloon angioplasty in the first intervention. In (A), phlebography demonstrating hepatic vein stasis, caused by stenosis of the suprahepatic vein outflow. In (B), pre-dilation with an 8 mm balloon. Observe the stenosis induced in the balloon. In (C), dilation with a 12 mm balloon. Observe the reduced stenosis induced in the balloon. In (D), control phlebography demonstrating considerable improvement in outflow.
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Flow was reestablished by angioplasty of the stenosis using high pressure balloons, initially an 8 mm balloon and then a 12 mm balloon, (Figure 2).
Intraoperative phlebography images of the suprahepatic vein followed by balloon angioplasty in the second intervention. In (A), phlebography demonstrating hepatic vein stasis, caused by stenosis of the suprahepatic vein outflow. In (B), pre-dilation with a 10 mm balloon. Observe the stenosis induced in the balloon. In (C), dilation with a 14mm balloon. In (D), control phlebography demonstrating considerable improvement in outflow.
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The result was satisfactory on venography and the patient was discharged from hospital the day after the procedure (Figure 3).