Arterial buffer response capacity - an important factor for future liver remnant hypertrophy in patients undergoing portal vein embolization

Introduction The liver is unique in that it is supplied by dual blood inflow. Changes in portal flow, by portal vein embolization (PVE) or ligation are known to induce atrophy of downstream liver lobes and hypertrophy of contralateral lobes. In case of decreased hepatic portal flow the livers’ arterial buffer response is called into action facilitating increased arterial blood flow to affected segments. In this context we investigated the mechanisms of PVE mediated liver hypertrophy, using a novel intraoperative hyperspectral camera system.

Material and methods Patients with PVE scheduled for trisectorectomy were analyzed. Liver function and size was assessed by LiMAX and CT volumetry. Intraoperative perfusion and oxygenation measurements were performed using the TIVITA hyperspectral camera. Images for tissue oxygenation (StO₂) and near infrared (NIR) perfusion were analyzed using specialized computer software.

Results Ten patients operated for cholangiocellular carcinoma (n=8) or hepatocellular carcinoma (n=2). PVE was effective in n=9 patients. One patient was subsequently subject to the associated liver partition and portal vein ligation (ALPPS) strategy. Mortality was 10%. R0 resection rate was 90%. StO₂ and NIR was significantly increased in liver segments subject to PVE when compared to unaffected hypertrophied segments (p <  0.001). Ineffectively embolized segments did not display arterial hyper-perfusion on TIVITA hyperspectral images.

Conclusion More than one mechanism has been proposed for liver parenchyma hypertrophy induction after PVE. Our hyperspectral data for the first time clearly demonstrates that hyperoxygenation due to arterial hyper-perfusion in PVE segments is the key element in a sequence of events leading to liver parenchyma hypertrophy in the human liver.

Publication History

Article published online:
08 September 2020