Background and Objective: Although cryogen spray cooling (CSC) is used to minimize the risk of epidermal damage during laser dermatologic surgery, concern has been expressed that CSC may induce cryo-injury. The objective of this study is to measure temperature variations at the epidermal-dermal junction in ex vivo human skin during three clinically relevant multiple cryogen spurt-laser pulse sequences (MCS-LPS). Study Design/Materials and Methods: The epidermis of ex vivo human skin was separated from the dermis and a thin-foil thermocouple (13 mm thickness) was inserted between the two layers. Thermocouple depth and epider-mal thickness were measured using optical coherence tomography (OCT). Skin specimens were preheated to 308C before the MCS-LPS were initiated. Three MCS-LPS patterns, with total cryogen spray times of 38, 30, and 25 milliseconds respectively, were applied to the specimens in combination with laser fluences of 10 and 14 J/cm 2 , while the thermocouple recorded the temperature changes at the epidermal-dermal junction. Results: The thermocouple effectively recorded fast temperature changes during three MCS-LPS patterns. The lowest temperatures measured corresponded to the sequences with longer pre-cooling cryogen spurts. No sub-zero temperatures were measured for any of the MCS-LPS patterns under study. Conclusions: The three clinically relevant MCS-LPS patterns evaluated in this study do not cause sub-zero temperatures in ex vivo human skin at the epidermal-dermal junction and, therefore, are unlikely to cause significant cryogen induced epidermal injury.
Cartilage laser thermoforming (CLT) is a new surgical procedure that allows in situ treatment of deformities in the head and neck with less morbidity than traditional approaches. While some animal and human studies have shown promising results, the clinical feasibility of CLT depends on preservation of chondrocyte viability, which has not been extensively studied. The present paper characterizes cellular damage due to heat in rabbit nasal cartilage. Damage was modelled as a first orderrate process for which two experimentally derived coefficients, A = 1.2 x 10(70) s(-1) and Ea = 4.5 x 10(5) J mole(-1), were determined by quantifying the decrease in concentration of healthy chondrocytes in tissue samples as a function of exposure time to constant-temperature water baths. After immersion, chondrocytes were enzymatically isolated from the matrix and stained with a two-component fluorescent dye. The dye binds nuclear DNA differentially depending upon chondrocyte viability. A flow cytometer was used to detect differential cell fluorescence to determine the percentage of live and dead cells in each sample. As a result, a damage kinetic model was obtained that can be used to predict the onset, extent and severity of cellular injury to thermal exposure.
During laser irradiation of biological tissue, a number of physical processes take place that determine temperature elevation and thermal damage rates. Some of those important to laser-tissue interaction are: 1) propagation of light in scattering media; 2) transformation of laser light into photochemical, acoustic, or thermal energy; 3) tissue-tissue and tissue-environment heat and mass transfer; 4) and the occurrence of low-energy phase transformations responsible for structural alterations. The aim of this study was to formulate a finite-element model (FEM) able to predict the temperature distribution in a slab of porcine nasal cartilage during laser irradiation. The FEM incorporates heat diffusion, light propagation in tissue, and water evaporation from the surfaces of the slab. Numerical results were compared to experimental temperature distributions where surface and internal temperatures were measured while heating cartilage using a pulsed Nd : YAG laser (= 1 32 m). Rectangular specimens, 1-4-mm thick, were secured perpendicular to the laser beam and irradiated for 1-15 s using different laser-beam powers (1-10 W).
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