A theoretical framework for multi-physics modeling of poro-visco-hyperelasticity-induced time-dependent fracture of blood clots

Fracture resistance of blood clots plays a crucial role in physiological hemostasis and pathological thromboembolism. Although recent experimental and computational studies uncovered the poro-viscoelastic property of blood clots and its connection to the time-dependent deformation behavior, the effect of these time-dependent processes on clot fracture and the underlying time-dependent fracture mechanisms are not well understood. This work aims to formulate a thermodynamically consistent, multi-physics theoretical framework for describing the time-dependent deformation and fracture of blood clots. This theory concurrently couples fluid transport through porous fibrin networks, non-linear visco-hyperelastic deformation of the solid skeleton, solid/fluid interactions, mechanical degradation of tissues, gradient enhancement of energy, and protein unfolding of fibrin molecules. The constitutive relations of tissue constituents and the governing equation of fluid transport are derived within the framework of porous media theory by extending non-linear continuum thermodynamics at large strains. A physics-based, compressible network model is developed for the fibrin network of blood clots to describe its mechanical response. An energy-based damage model is developed to predict the damage and fracture of blood clots, and a transient non-local characterization length function is proposed to limit the damage zone bandwidth. The proposed model is experimentally validated using single-edge cracked clot specimens with different constituents. The fracture of blood clots subject to different loading conditions is simulated, and the mechanisms of clot fracture are systematically analyzed. Computational results show that the viscoelasticity and fluid transport play essential roles in the fracture of blood clots under physiological loading.