Cell-level temperature distributions in skeletal muscle post spinal cord injury as related to deep tissue injury.

Deep tissue injury (DTI) is a severe pressure ulcer, which initiates in skeletal muscle tissue under intact skin. Patients with spinal cord injury (SCI) are especially vulnerable to DTI, due to their impaired motosensory capacities. The underlying mechanisms that lead to DTI are, however, still poorly understood. This study focuses on cell-level temperature distributions in muscles of patients with SCI, which typically contain thinner muscle fibers and fewer capillaries. It has been shown previously by our group that ischemic muscles of rat models of DTI cool down mildly and locally, which is very likely to slow the diffusivity of metabolites in the ischemic regions. However, it is unclear how these temperature decreases affect diffusivity at the scale of individual muscle cells in the microanatomy of SCI patients. We hypothesize that a 2 degrees C drop in the temperature of inflowing capillary blood, as shown in our animal studies, has a substantial effect on lowering the diffusivity of metabolites in skeletal muscle, but the pathological microanatomy in the chronic phase of SCI is less dominant in affecting the local temperatures in and around muscle cells. In order to test this hypothesis, two-dimensional finite element (FE) models of cross sections through the microanatomy of muscle tissue were developed using COMSOL Multiphysics software for normal and SCI muscles. The models included muscle cells, extracellular matrix (ECM), and capillaries, each with its own geometrical, thermal, and heat production properties. The SCI model configuration specifically included reduced cross section of myofibrils in favor of more ECM, less capillaries, and decreased blood inflow rate. After a 20-s heat transfer simulation, it was found that temperatures around the cells of the SCI muscle were approximately 2 degrees C lower than that in the normal muscle, that is, heat production from the muscle cell metabolism did not compensate for the lower inflowing blood temperature in the SCI model. We conclude that the temperature and rate of inflowing capillary blood are the dominant factors determining the localized temperatures in the microarchitecture of an ischemic SCI muscle tissue. The altered SCI microanatomy was shown to be less influential. Taken together with the Stokes-Einstein theory, our results indicate that diffusivity of metabolites would be approximately 50% less around the cells of SCI muscle due to local cooling, which is yet another factor compromising tissue viability in the patients with SCI.