Permanent Hepatic Artery Ligation Versus Temporary Dearterialization in the Treatment of Hepatic Tumors

Abstract

The rationale for treating liver tumors by occlusion therapy is based on the derivation of the nutrition of liver tumors from the hepatic artery. Vascularity of malignant neoplasms in the liver has been investigated by many authors. Breedis and Young [10] studied the tumor circulation of experimental liver neoplasms and autopsy specimens of patients, using various dyes, gelatin, and vinyl acetate for injections into hepatic arteries and veins. Dye was demonstrated within the tumors after hepatic artery injections, but only in the periphery after the portal injection. The authors estimated that 80%–100% of the human liver tumor circulation was derived from the hepatic artery. Blanchard et al. [9] used isotope-labeled microspheres injected into the hepatic artery and portal vein in rabbits with implanted liver tumors. They found a tumor/liver ratio of 4.2 after hepatic artery injection, but only 0.3 after injection into the portal vein. Nilsson and Zettergren [22] investigated primary hepatic carcinoma induced in rats by injecting barium sulfate and formalin into hepatic vessels and used an X-ray technique to visualize vascular penetration of the tumors. In some neoplasms the contrast material from the portal vein filled vessels resembling sinusoids, although the main filling occurred from the hepatic artery. Around the periphery of the tumor a zone of vessels was filled with contrast material from the portal vein. In a series of studies, Ackerman [1] examined the blood supply of experimental liver metastases. Using isotope-labeled microspheres, he found that smaller tumors, less than 30 mg in weight, were fed by both the hepatic artery and the portal vein, while larger tumors had a predominant arterial blood supply. In an investigation of 117 patients with primary and secondary carcinoma of the liver, Suzuki et al.