Recovery of liver perfusion after focal outflow obstruction and liver resection

Live liver donation requires extended liver resection in the donor with transection of the middle hepatic vein. This leads to focal outflow obstruction in the remnant liver or the partial graft. This study was designed to characterize the pathophysiological correlate of focal outflow obstruction in a small-for-size liver and its course of recovery in a rat model.

Ligation of the right median hepatic vein was combined with 50% hepatectomy. Microcirculation was visualized by orthogonal polarization spectroscopy after each operative step and before killing on days 1, 2, and 7. Histologic evaluation included morphological assessment, immunohistochemical determination of proliferation using BrdU, and laminin and von Willebrand factor expression, which both indicate vascularization of sinusoids.

After ligation of the right median hepatic vein, congestion was visible and no sinusoidal blood flow was detected in the obstruction zone. By day 1 confluent centrilobular necrosis developed. Sinusoidal perfusion in the obstruction zone recovered partially. Many dilated vascularized sinusoidal canals connecting the obstruction zone with the normal zone were visible. Proliferative activity in the obstruction zone was markedly reduced compared with the normal zone. By day 7, liver parenchyma in the obstruction zone looked normal as did sinusoidal perfusion. In the border zone, few dilated vascular canals were apparent.

Confluent centrilobular necrosis in the early postoperative phase, resulting from focal outflow obstruction, may be crucial for the development of a small-for-size syndrome. The exclusion of the outflow-obstructed zone from the functional liver mass during preoperative radiological risk assessment seems to be the logical consequence. Recovery of focal outflow obstruction occurs spontaneously by means of dilated sinusoids in the border zone, forming vascularized sinusoidal canals, which could serve as intrahepatic anastomosis.