  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.
