Abstract

Cryoablation refers to all methods of destroying tissue by freezing [ 1 ]. Cryoablation can be performed via surgical (open or laparoscopic) or percutaneous approaches. Percutaneous cryoablation begins with the insertion of a specialized needle (cryoprobe) into malignant tissue under imaging guidance; the needle is then rapidlycooled to subzero temperatures, causing removal of heat from the tissue via conduction. Rapid extracellular cooling results in the formation of extracellular ice crystals, which sequesters free water, increasing the tonicity of the extracellular space. Osmotic tension draws free intracellular water from cells, resulting in dehydration [ 2 ]. The concomitant increase in intracellular solute concentration results in damage to cytoplasmic enzymes and the destabilization of the cell membrane. Rapid intracellular cooling results in intracellular ice crystal formation, a harbinger of lethal cellular injury and subsequent cell [ 3 ]. Although the exact mechanism of cellular damage from intracellular ice formation is unknown, injury is thought to be mediated by physical damage to intracellular membranes of organelles and the plasma membrane. During thawing, melting ice within the extracellular space results in its hypotonicity with respect to the intracellular compartment. This osmotic gradient can trigger a fl uid shift, leading to cell swelling and/or bursting. In addition, an in flux of free water into the intracellular space provides substrate for the growth of intracellular ice crystals, exacerbating their biocidal effects Cellular injury is maximized by optimizing four factors: increasing cooling rate, lowering target temperature, increasing time at target temperature, and decreasing thawing rate [ 5 ] (Fig. 3.1 ).

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