Case Reference No. CC-0498-08 The patient is a 73-year-old man with a history of cirrhosis secondary to chronic hepatitis C and a remote history of ethanol abuse. By palpation, the left lobe was diffusely enlarged and a bruit was audible. A liver-spleen scan showed a large defect involving almost the entire left lobe of the liver. CT and ultrasound imaging could not define a discrete mass in the left lobe. At least three masses were detected in the right lobe, one measuring up to 4 cm. The patient was Childs-Pugh class B. The alpha-fetoprotein (AFP) level was 177. Biopsy of the left lobe revealed hepatocellular carcinoma. The patient desired treatment and was referred for chemoembolization (CE). Arteriography revealed normal hepatic arterial anatomy. The SMA portogram revealed a patent main portal vein with hepatopetal flow, as well as hepatopetal flow within right lobe portal branches. The left portal vein was totally occluded. A lobular filling defect was noted at the origin of the left portal vein from the main portal vein, consistent with a tumor nodule projecting into the main portal vein, that resulted in approximately 50% luminal narrowing. Hepatic arteriography revealed a diffuse increase in opacity of the left lobe on the parenchymal phase. This was interpreted as representing hypervascular tumor and/or increased arterial flow due to the left portal vein occlusion. Hypervascular lesions were also identified in the right lobe. A CE mixture consisting of 50 mg of Adriamycin in 10 mL of nonionic contrast material and emulsified with 10 mL of Ethiodol was prepared and injected in its entirety into the left hepatic artery. The left hepatic artery was then embolized to near stasis with a slurry of Gelfoam pledgets. On the first postprocedure day the patient had mild nausea and mild epigastric discomfort and was discharged home at his request. The patient returned for clinic follow-up on the sixth postprocedure day. He was somewhat lethargic and was judged to be slightly encephalopathic. He had persistent mild nausea and mild pain. A small amount of ascites was detected on physical examination. The epigastric bruit was no longer present. The effects of CE on the patient's liver functions are detailed in Table 1.		Fig. 1 Celiac arteriogram shows enlarged left hepatic arteries and diffuse blush in the left lobe. Fig. 2. Parenchymal phase of the celiac arteriogram shows two hypervascular nodules visible in the right lobe (arrows). Arterioportal shunting is seen in the left lobe (arrowhead).   Fig. 3. Superior mesenteric arteriogram, portal phase shows a lobular filling defect in the main portal vein and absent portal flow to the left lobe.
Twenty days after the procedure, his liver functions had improved (Table 1). His appetite was still poor, but his nausea had resolved, ascites was no longer detectable, and he was no longer encephalopathic. In view of his marked response to embolization of the left lobe, we planned CE of the anterior and posterior segments for different times. At 28 days postprocedure, the patient returned for CE of the posterior segment of the right lobe. The filling defect in the main portal vein was slightly larger than noted previously, but hepatopetal flow was maintained. There were visible oil deposits in this tumor thrombus. The posterior segment was embolized with the same CE mixture. Ten mL of the mixture was injected until there was considerable stasis of flow. An additional 3 mL mixed with one third of a vial of Ivalon particles (250­355 µm) was injected, producing near-complete stasis of flow. The second procedure produced minimal symptomatology, minimal alteration in liver function, and no encephalopathy. At 43 days postprocedure, the anterior segment of the right lobe was chemoembolized in the same fashion as in the second procedure, with a total of 10 mL of the chemoembolizate. The artery to the posterior segment, injected at the second procedure, remained occluded. There was very dense oil retention within a 4-cm lesion of the posterior segment. The third procedure produced minimal symptomatology, minimal alteration in liver function, and no encephalopathy. The AFP after the three treatments (55 days after begining treatment) is 238. Questions: 1) Would anyone have withheld treatment because of the left portal vein occlusion or have treated the patient differently? 2) Should the patient be treated further and if so, what agents should be used? How often? 3) Should percutaneous ethanol injection be added to the treatment plan as a substitute for CE or as an adjunct to it?