Tissue temperature estimation in-vivo with pulse-echo

Part of Proceedings of the IEEE Ultrasonics Symposium, Volume 2Time-shifts between echoes from volumes of tissue heated with focused ultrasound has been shown to track temperature changes accurately in-vitro. In this study we report the application of this method in-vivo where motion and perfusion have an additional effect on the measured shifts. Motion was characterized by the time-shifts detected on an echo segment from a proximal non-heated tissue site and a correction was applied to minimize their effect. The delay vs. temperature relationship (δ(T)) was similar to that previously described in-vitro but parameter variations were larger. Unlike in-vitro, the mean dδ/dT during temperature increases differs some from that during the cooling phases. It is suggested that this behavior can be predicted from the characteristics of the irradiating transducer and the acoustic parameters of the tissue and incorporated to the delay detection procedure

Noninvasive temperature estimation in tissue via ultrasound echo- shifts. Part II. In vitro study

Time shifts in echo signals returning from a heated volume of tissue correlate well with the temperature changes. In this study the relationship between these time shifts (or delays) and the tissue temperature was investigated in excised muscle tissue (turkey breast) as a possible dosimetric method. Heat was induced by the repeated activation of a sharply focused high-intensity ultrasound beam. Pulse echoes were sent and received with a confocal diagnostic transducer during the brief periods when the high- intensity ultrasonic beam was inactive. The change in transit time between echoes collected at different temperatures was estimated using cross- correlation techniques. With spatial-peak temporal-peak intensities (I(SPTP)) of less than 950 W/cm2, the delay versus temperature relationship was fit to a linear equation with highly reproducible coefficients. The results confirmed that for spatial-peak temperature increases of ~10 °C, temperature-dependent changes in velocity were the single most important factor determining the observed delay, and a linear approximation could produce accurate temperature estimations. Nonlinear phenomena that occurred during the high-intensity irradiation had no significant effect on the measured delay. At I(SPTP) of 1115-2698 W/cm2, the delay-temperature relationship showed a similar monotonically decreasing pattern, but as the temperature peaked its slope gradually increased. This may reflect the curvilinear nature of the velocity-temperature relationship, but it may also be related to irreversible tissue modifications and to the use of the spatial-peak temperature to experimentally characterize the temperature changes. Overall, the results were consistent with theoretical predictions and encourage further experimental work to validate other aspects of the technique

Ultrasonic attenuation of dog tissues as a function of temperature

Proceedings of the IEEE Ultrasonics Symposium, Volume 2The effect of temperature and thermal dose referenced at 43 °C on the attenuation and absorption was studied in dog muscle, liver and kidney in vitro. It was found that the attenuation and absorption increased for temperatures higher than 50 °C, and eventually reached a maximum at 65 °C. The change in attenuation or absorption when necrosis is produced was to about twice the value at 37 °C. The change in attenuation or absorption occurred at thermal doses of 100-1000 min which corresponds to the range of threshold of necrosis. The maximum attenuation or absorption was reached at thermal dosages in the order of 107 min

Dependence of ultrasonic attenuation and absorption in dog soft tissues on temperature and thermal dose

The effect of temperature and thermal dose (equivalent minutes at 43 °C) on ultrasonic attenuation in fresh dog muscle, liver, and kidney in vitro, was studied over a temperature range from room temperature to 70 °C. The effect of temperature on ultrasonic absorption in muscle was also studied. The attenuation experiments were performed at 4.32 MHz, and the absorption experiments at 4 MHz. Attenuation and absorption increased at temperatures higher than 50 °C, and eventually reached a maximum at 65 °C. The rate of change of tissue attenuation as a function of temperature was between 0.239 and 0.291 Np m-1 MHz-1 °C-1 over the temperature range 50-65 °C. A change in attenuation and absorption was observed at thermal doses of 100-1000 min, where a doubling of these loss coefficients was observed over that measured at 37 °C, presumably the result of changes in tissue composition. The maximum attenuation or absorption was reached at thermal dosages on the order of 107 min. It was found that the rate at which the thermal dose was applied (i.e., thermal dose per min) plays a very important role in the total attenuation absorption. Lower thermal dose rates resulted in larger attenuation coefficients. Estimations of temperature- dependent absorption using a bioheat equation based thermal model predicted the experimental temperature within 2 °C