In contrast to other groups, who administered up to 150mg of doxorubicin per intervention, we did not charge the maximum dose possible to the beads (i.e. epirubicin 75mg per 2ml vial) because we were afraid of possible toxic local or systemic side effects. Furthermore, as mentioned above, we appreciated a standard-dose (i.e. epirubicin 50mg per embolisation) strategy. This strategy was based on one case we experienced when treating a patient with a large diffuse HCC predominantly affecting the right liver lobe (see ‘Illustrated Case Study One’). In this patient, we followed a double-dose strategy and embolised a tumour mass, replacing more than two-thirds of the right liver lobe. The embolisation was successful and the patient was discharged from hospital two days later. However, the patient returned within a fortnight with right upper quadrant pain, fever and elevated liver enzymes. He recovered after 14 days in hospital; however, from then on he was treated with the standard dose of 50mg.

Figure 2b: Intra-arterial Angiography Confirmed the Hypervascular Nature of the Liver Lesion and Depicted the Presence of a Main Feeder Vessel

The standard particle sizes we used were 100–300 and 300–500µ, as we believed that it would be useful to deliver as many of the beads to the tumour tissue as possible. This could have been hampered by using large beads that occluded the tumour vessels at a more proximal level. In all cases, a contrast-enhanced computed tomography (CT) or magnetic resonance (MR) scan was obtained prior to the intervention. In cases where a CT scan was obtained, the pelvic vessels were also examined, thus giving the interventional radiologist an idea as to which material (sheath, etc.) to use. After catheterising the coeliac trunc or the superior mesenteric artery (SMA) (in case of a hepatomesenteric artery) with the help of a guiding catheter, an overview was obtained. A microcatheter was then used for superselective embolisation in order to treat as much of the tumour as possible while sparing the ‘healthy’ parts of the liver (see ‘Illustrated Case Study Two’). One day after intervention, a contrast-enhanced CT was obtained in order to document the areas of the tumour that were embolised properly, as well as documenting possible side effects related to the intervention. Overall, the procedure was tolerated well by most of the patients, even though we gave neither antiemetics nor antibiotics in advance.

The six- and 12-month survival rates achieved for the patients suffering from HCC were 93 and 90%, respectively, which are in line with the results published by Varela et al. but below the survival rates achieved by Malagari et al. One reason for this might be that when we began using DC Beads we exclusively used the 300–500µ Beads, which probably resulted in lower intratumoral drug doses. Furthermore, we treated nearly every patient, which means that even patients with large tumours replacing more than 50% of the liver were treated, as well as patients with partial portal vein thrombosis, extrahepatic tumour manifestations and other life-limiting conditions. On the other hand, although the patient population was not well selected, we observed very few complications, and most of these were related to the intervention. We observed two cases of cholecystitis when using the small beads (100–300µ); in one patient a cholecystectomy had to be performed. Additionally, we documented a total of three abscesses (see ‘Illustrated Case Study Three’). In the case of the patient with the large, diffuse growing HCC mentioned above (see ‘Illustrated Case Study One’), we were lucky not to lose the patient after the first ‘double-dose’ intervention, as the laboratory findings temporarily suggested nearby liver failure.