Cryotherapy

Cryosurgery is defined as local tumor destruction in situ caused by the rapid freezing of tumor cells. Cryosurgery was introduced as an ablative technique mainly in patients with prostatic malignancies and, in some centers, also for the treatment of patients with liver metastases and primary liver tumors such as hepatocellular carcinoma (HCC).

Since cryotherapy does not destroy the walls of large vessels such as the inferior caval vein or large liver veins and portal branches, this approach is particularly well-suited to the treatment of unre-sectable lesions located near these vessels.

Frequently, resection and cryotherapy are combined during a single invasive procedure. Moreover, cryosurgery is appropriate as an adjunct to liver surgery (so-called "edge cryotherapy") in cases in which a very close or histological-positive resection margin is anticipated. During this procedure, flat cryoprobes are positioned at the resection edge of the remaining liver and adequate freezing is performed to a depth of at least 1.5 cm into the liver tissue.

The mechanism of tumor cell destruction in cryotherapy depends on the location of the tumor tissue in relation to the cryoprobe. In areas close to the cryoprobe temperatures rapidly fall to -190 °C, causing ice crystals to form within and around the cells. Subsequent thawing and re-hydration results in rupture of the cell membrane and hence tissue death. At distances slightly further from the cryoprobe, the temperature drops more slowly and ice forms within the small vessels. Since cell membranes impede intracellular ice crystal formation in this case, the parenchy-mal cells dehydrate to equilibrate the resulting chemical gradient. This results in cellular disintegration and expansion of the blood vessels, which rupture upon thawing, resulting in tissue hypox-ia. Thus, cell death in cryotherapy is a combination of intra- and extracellular ice crystal formation, cellular dehydration, rupture of small vessels and hypoxia from small vessel destruction [10, 20]. Cellular damage can be increased by re peated application of consecutive freeze-thaw cycles [28].

Cryotherapy within the liver has experienced a renaissance with the availability of intraoperative ultrasound (US) as a real-time control for the ablative procedure. Nevertheless, the expansion of the forming ice ball cannot be detected opposite the ultrasound transducer, since the ice front orientated towards the transducer builds a reflection wall with a "shadow zone" behind it [26]. MR imaging can overcome this disadvantage, showing excellent contrast between ice formation and unaffected perfused liver tissue on the basis of decreased T2 relaxation time of the frozen tissue [27].

As a result of the histopathologic changes, lesions after cryotherapy may show signs of hemorrhage on unenhanced T1-weighted and T1-weight-ed fat-suppressed images and appear hyper- or rarely isointense on T2-weighted images. On contrast-enhanced T1-weighted images, the destroyed tissue is seen as a hypovascular region. In cases of complete tumor destruction, contrast-enhanced T1-weighted images acquired during the equilibrium phase reveal a hypointense lesion typically surrounded by a closed hyperintense rim, most likely formed by fibrovascular granulation tissue (Figs. 7, 8). If this rim is interrupted, the site of the interruption should be considered as indicating residual or recurrent tumor, since typically neither a homogeneous rim nor evidence of edema is seen in unaffected tumor tissue. Often the size of the resulting cryo-lesions remains relatively stable for three to six months. Thereafter lesions begin to shrink until they are either no longer visible or can be identified only by the presence of a small scar (Fig. 9) [2,26].

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