Necrosis evolution during high-temperature hyperthermia through implanted heat sources

Abstract

A nonstationary model for high-temperature hyperthermic treatments is developed. The aim of this model is to describe the thermal propagation within a living tissue and to quantify its clinical effects as it regards the physiological status (necrosis) of a neoplastic body. Particular attention is turned to the description of the necrotic transition induced by heating. This leads to the introduction of a necrosis field and to an effective-medium approximation for the corresponding physiological status (vascularization, necrosis, etc.) of the exposed tissue. The resulting nonlinear, nonstationary model is applied to a multilayered spherical structure with a temperature-regulated implant, and to a clinical case of a solid liver tumor. Clinical data on the spatial extent of the necrotized region are in good agreement with model predictions.

Ex Vivo Characterization of Canine Liver Tissue Viscoelasticity after High-Intensity Focused Ultrasound Ablation

“…Within a low temperature range, i.e. 42-46 ° C , only apoptosis has been shown to occur (Badini et al 2003), however, much higher temperature increase have shown to replace natural apoptosis by forced necrosis where severely damaged cells permeate into the tissue extracellular matrix (Samali et al 1999; Kiss et al 2009). Shear elasticity imaging of porcine liver during histotripsy ex vivo has shown the Young's modulus to linearly correlate with the number of structurally-intact cell nuclei (Wang et al 2012).…”

Elasticity and safety of alkoxyethyl cyanoacrylate tissue adhesives

“…This may be related to the faster rate of polymerization of the shorter CA monomers [45,46]. The heat generated by polymerization can be a determinant of biocompatibility [47]. Thus, for example, a new acrylic surgical glue, Glubran 2 (GEM Srl, Viareggio, Italy), incorporates metacryloxysulpholane to slow polymerization, thus decreasing the peak polymerization temperature to ~45 °C.…”

Investigation of temperature-dependent viscoelastic properties of thermal lesions in ex vivo animal liver tissue

“…Apoptosis is a highly regulated process of programmed cell death that occurs from 42–46 °C (Badini et al, 2003), essentially cell suicide, in which the cell initially releases heat shock proteins intended to protect from thermal stress injury. In the case of exposure to sustained thermal stresses or high temperatures, excess production of these proteins eventually leads to cell death (Badini et al, 2003; Samali et al, 1999). Necrosis occurs when the damage to a cell is so severe that it cannot repair itself or provide adequate defensive measures.…”