Portal Vein Embolisation PVE

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In patients with normal liver function, safe hepatic resection should preserve at least 25% of total hepatic volume; in patients submitted to per-operative chemotherapy with chronic liver disease at least 40% of total liver volume should be preserved due to a higher risk of post-operative liver failure [50, 51]. When planned resection exceeds these values, peroperative PVE may be utilised to reduce the risk of post-operative liver failure. PVE was described for the first time in 1990 by Makuuchi et al. [52].

The scope of PVE is to induce compensatory hypertrophy of remnant liver and atrophy of the lobe with tumour induced by closure of one of more of the portal branches in the part of the liver to be resected

[53]. The procedure is performed with percutaneous approach under fluoroscopic control. After percutaneous portography, the portal vein branches are embolised by the use of various types of substances associated to contrast agents (Lipiodol® or Urografin®): cyano-acrylate, Gelfoan®, Tissucol®. Among these embolising materials some Authors prefer cyanoacrylate because other substances (Tissucol, Gelfoam) may be reabsorbed a few weeks after the procedure, leading to re-establishment of blood flow

Induced compensatory hypertrophy, is assessed after 5 or 6 weeks by CT (Fig. 3).

Portal embolisation induces modifications in hepatic haemodynamics with a considerable increase of portal pressure; similar disturbances are observed after a major hepatic resection. In the embolised part of the liver, absence of portal flow leads to cellular apoptosis, which leads to atrophy of the embolised lobe and to hyperplasia and hypertrophy of the contralateral lobe, determined by active cell proliferation, which increases 2 weeks after PVE. Hepatic hypertrophy is mediated by intra- and extra-hepatic growth factors; the extra-hepatic ones are transported through the portal vein system (insulin, noradren-alin, portal hormones). This response seems to be mediated by the same factors that are responsible for hepatic regeneration after hepatectomy (hepatocyte growth factor, TGF-a, TNF-a and IL-6). The time for maximal hypertrophy after PVE is not clear yet, but it is clear that patients with diabetes or with chronic liver disease need a longer period to obtain hypertrophy, at least 6-8 weeks [55, 56].

PVE is usually well tolerated and determines only a low inflammation of the periportal space. Patients usually suffer mild side effects: fever, nausea, slight abdominal pain and mild temporary alteration of total bilirubin levels [52]. Abdalla et al. [57] reported side effects in less than 15% of patients, including haemobilia, sepsis and the need to repeat PVE, whereas mortality following the procedure was almost zero.

In the literature, the time elapsed between PVE and hepatic resection is variable and ranges from 3 to 9 weeks [57].

PVE has proved to be a safe method to increase resectability and reduces the risk of major liver resection (Table 7) [58]. Some Authors suggest that this procedure may favour oncogenesis. Jaeck et al. [59] suggest that hepatic hypertrophy processes after PVE would increase growth of metastases located in the residual hepatic lobe. It was observed that, after PVE, 4-37% of patients are ineligible for liver resection due to neoplastic progression. In order to decrease the risk of progression of the tumour after PVE, it would be useful to treat patients with chemotherapy until surgery [60].

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