Abstract

Juxtahepatic vein injuries present a high mortality rate. Our objectives were to develop an experimental model of endovascular lethal injury of the juxtahepatic inferior vena cava (JHIVC) and to evaluate its hemodynamic alterations; to treat the lesion with volume replacement, and a stent graft (SG); and to follow the animals after treatment. Twenty dogs were anesthetized and monitored [heart rate (HR), mean arterial pressure (MAP), vesical and peritoneal pressures], and submitted to a JHIVC endovascular injury. After volume replacement the dogs were divided into two groups: control (GI) and experimental (GII). GI was observed until death. GII was treated with SG and followed by Doppler ultrasound (DUS) and cavography for 4 (GIIA), and 8 weeks (GIIB), and then sacrificed and IVC and SG were analyzed. GI presented increased abdominal pressures, arterial hypotension, and death after 80 minutes. GII had a 100% survival rate till sacrifice, without clinical repercussions. At DUS and cavography all SG were patent, with monophasic pulsatile flow. On US, SG diameters after 2, 4, and 8 weeks did not show differences. On cavography IVC diameters presented no difference between groups GIIA and GIIB throughout the experiment. These data analyzed for the GII as a whole, showed statistically significant differences. Average lumen diameter reduction of SG was 27.43+/-20,00%. Pressure values in the IVC cranially, caudally to the SG, and inside the SG, did not show differences. In the IVC with the SG we observed a thicker neointima layer, and the injury in the media layer was covered with fibroconnective tissue. We developed an experimental dog model of endovascular lethal injury of the JHIVC with significant increase in abdominal pressures, and a mortality rate of 100%. The treatment of this lesion with SG resulted in a thickened neointima layer, and a 27% reduction in the JHIVC lumen diameter, without clinical repercussion, and with a 100% survival rate.

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