Thomas M. Fiedler1, Mark E. Ladd1,2, and Andreas K. Bitz1
1Medical Physics in Radiology, German Cancer Research Center (DKFZ), Heidelberg, Germany, 2Erwin L. Hahn Institute for Magnetic Resonance Imaging, University Duisburg-Essen, Essen, Germany
Synopsis
RF safety of Tx coils can
be assessed based on SAR or temperature limits; however, temperature is
directly correlated to tissue damage and enables a more precise RF exposure
assessment. Both safety assessments were compared for a 7T breast coil.
Temperature depends on the individual thermoregulation system and was taken
into account using three different temperature-dependent blood perfusions. Results
for a subject with impaired thermoregulation showed that temperature limits are
exceeded by up to 6.17 °C even when SAR limits are complied with. For a healthy
subject, up to 40% higher input power is allowed if temperature limits are
applied instead of SAR. Target audience
Researchers involved in RF safety and/or
high-field MRI
Introduction
Due to dielectric losses in body tissue,
radio-frequency (RF) energy is absorbed and converted into heat. Heat can
increase tissue temperature, and high temperatures subsequently result in
tissue damage. The IEC safety standard1 for medical equipment
defines limits for local tissue temperature and specific absorption rate (SAR) for
the safe use of an MR scanner. According to the IEC standard, compliance with temperature
limits may be achieved by limiting the SAR. In the majority of cases, RF safety
assessment of transmit coils is based on SAR, whose determination is well
defined in the standard.
SAR depends on the body physique (tissue distribution)
and on the Tx coil design and MR environment (geometry).
As temperature is directly correlated with tissue
damage whereas SAR is not, the evaluation of tissue temperature allows a more
precise safety assessment of RF coils. Tissue temperature, however, depends on
the thermal tissue properties (conductivity, specific heat), ambient
temperature, heat convection on body surface (ventilation and clothing),
metabolism, and blood perfusion. The SAR influences the temperate as an
RF-induced heat source.
Individual health status affects the thermoregulatory
system and can be taken into account by different temperature-dependent
blood perfusion models proposed in the literature but which are not specified
in safety standards.
In this study, the safety of an RF coil was assessed based
on both SAR and temperature limits by numerical simulations. The correlation
between SAR and temperature were analyzed with respect to spatial distribution
and maximum permissible input power.
Methods
Numerical calculations were
performed for a coil model of a 4-ch Tx/Rx bilateral breast coil for 7 T2 (Fig. 1a). A new body
model conforming to the coil housing was generated from 3 Tesla data (1.2 mm tissue resolution,
17 different tissues). The maximum permissible input power was determined for
the normal (NM) and first-level (FLM) controlled operating modes (10g-averaged SAR
limits of 10 W/kg and 20 W/kg, respectively). Subsequently, temperature
simulations were performed with the Pennes bio heat equation3 (Fig. 2).
Different health states were considered via temperature-dependent blood
perfusion models: A constant blood perfusion was assumed for an impaired thermoregulation
system, e.g. due to diabetes, whereas a linear increase4 and an exponential
increase5 in blood perfusion were assumed as possible models for a
healthy thermoregulatory system, Fig. 3. An ambient temperature of 25 °C, a blood
temperature of 37 °C, and a heat convection coefficient of 2 W/(m²K) were used.
Thermal simulations were performed based on the two power levels, and resulting
tissue temperature distributions were analyzed. In addition, the maximum
permissible input power was determined for temperature limits in NM (39 °C) and
FLM (40 °C). Simulations were performed with CST Studio Suite 2015 (CST AG,
Darmstadt, Germany).
Results/Discussion
Maximum 10g-averaged SAR was located inside the left
mamma, where the prevailing tissue is fat, Fig. 1b2. Maximum
permissible time-averaged input power was 36.5 W (NM) and 73 W (FLM). For the
constant perfusion model, the corresponding temperature limits were exceeded by
2.28 °C (NM) and 6.17 °C (FLM), Table 1. To satisfy the SAR and the temperature
limit, the input power would have to be decreased by 46% (NM) and 62% (FLM).
For the linear perfusion model, the maximum tissue temperatures were lower
compared to the constant model but also exceeded the temperature limits in NM
and FLM. For the exponential perfusion model, the tissue temperature stays
below the limits in both operating modes. Consequently, for a healthy subject, the
input power level can be increased by 37% (NM) or 40% (FLM) when applying
temperature limits rather than SAR limits. For all simulations, the SAR and
temperature distributions correlated well for the configuration considered
here, Fig. 4, which is a consequence of the low perfusion in fat tissue. This
finding is not expected for tissues with higher blood perfusion6.
The
proposed perfusion models yield a large variation in tissue temperature. So
far, there is no general agreement on which perfusion models yield realistic
tissue temperature for impaired or healthy subjects. The results indicate that
a validation of the thermal models is needed and that different thermal models
for different health status may be required.
Conclusion
The results indicate that
it is possible to exceed the IEC local temperature limit while satisfying the
IEC limits for local SAR when a patient with impaired thermoregulatory system
is examined. As a consequence, the maximum permitted input power needs to be
decreased if temperature is considered to be the fundamental limit most closely
related to possible tissue damage.
Acknowledgements
The research leading to these results has received
funding from the European Research Council under the European Union's Seventh
Framework Programme (FP/2007-2013) / ERC Grant Agreement n. 291903 MRexcite.References
1. IEC 60601-2-33 Medical electrical equipment, Ed. 3
(2010).
2. Fiedler et al. Proc. ISMRM 23 (2015) #283.
3. Pennes, H. H. Journal of Applied Physiology Volume
1 (2) (1948).
4. Hirata et al. Bioelectromagnetics 27, 602-612
(2006).
5. Laakso et al. Phys Med Biol 56, 7449-7471 (2011).
6. Collins et al. J. Magn. Reson. Imaging 19 (5)
650-656 (2004).