## 3 Imaging in the Follow-Up of Treated HCC
### Expected Post-Treatment Imaging Features in the Absence of Viable Tumor Tissue  
Coagulative necrosis is defined as the type of cell death secondary to the decrease or complete stop of blood flow. In consequence, contrast-enhanced MRI will show no uptake. The size of the necrosis should be similar to or larger than the tumor nodule when compared to the pre-therapeutic scans. Within the ablated area, MRI depicts heterogeneous T1-WI hyperintense or isointense areas and a relatively low signal intensity on T2-WI [33]. A target appearance may be seen after thermal ablation, where a central area of T2 hyperintensity corresponding to tissue loss is surrounded by a lower T2-WI intensity and higher T1-WI hyperintense concentric area represented by the coagulation necrosis; the latter may itself be surrounded by a third area of T2-WI hyperintensity with T1-WI isointensity [30]. These target areas evolve with a signal drop in T1-WI in the coagulative necrosis area, while the third concentric area might develop contrast enhancement due to the infiltration by inflammatory cells and may grow thicker over time, while the coagulative necrosis decreases in size [30]. It is commonly accepted that these MRI features of the necrosis are similar in RFA and MWA. After HIFU-treated HCC, it was reported that a discrepancy between the predicted ablation area and the area identified by MRI may occur, the latter being almost half of the expected size [127]. There is a paucity of studies regarding the MRI features after HIFU due to the limited application of this method. MRI imaging features after CA are similar to findings after RFA or MWA. Generally, in the days after the procedure, the ablation zone appears hypointense in T1-WI and hyperintense in T2-WI, with heterogeneous areas represented by focal hemorrhage [128]. If large vessels are not punctured, the bleeding is small and evolves in the weeks after the procedure; it can be identified as iso- to hyperintense T1-WI foci and is usually hypointense in T2-WI [129]. The coagulation necrosis appears similar to other thermal ablative procedures; however, a significantly intense T2-WI signal could suggest fluid accumulation within the nodule [129]. A peripheral area of inflammatory response is seen after CA, evolving into fibrosis within the following months. Vascular changes may be identified around the nodule in the form of wedge-shaped areas of increased contrast uptake, which are produced by the arterial hyperperfusion secondary to portal venous flow reduction [130]. If imaging follow-up is performed at 24 h after the procedure, persistent tumor enhancement may be seen; the contrast uptake is gradual and is thought to be caused by reperfusion through injured vessels within the ablation area [131]. This is specific to cryoablation due to the mechanism of inducing the coagulative necrosis. Contrast enhancement after cryoablation within the tumor nodule may be a normal finding if the uptake is less intense and slower than in the adjacent unablated areas, and this usually resolves within the following months [132]. HCC nodules successfully treated with PEI will show iso- or hyperintensity on T1-WI and uniform hypointensity on T2-WI [71]. However, PEI-treated nodules are associated with persistent fan-shaped T2-hyperintense areas in the vicinity caused by perfusion abnormalities; this was found to be secondary to ethanol infiltration in the peritumoral normal tissues, which caused arterioportal shunts that lasted several months [133]. Additionally, ethanol-related direct toxic effects on healthy liver cells around the treated nodule were identified, causing coagulative necrosis and secondary fibrosis [134]. These T2-hyperintense areas might partly obscure the presence of viable tumor tissue, so careful analysis of these areas is recommended [135]. Imaging follow-up after successful HCC treatment with IRE may show features distinctive to those after thermal ablations.