Spontaneous pneumothorax, a prevalent medical challenge in most trauma cases, is a formof sudden lung collapse closely associated\r\nwith risk factors such as lung cancer and emphysema. Our work seeks to explore and quantify the currently unknown pathological\r\nfactors underlying lesion rupture in pneumothorax through biomechanical modeling. We hypothesized that lesion instability is\r\nclosely associated with elastodynamic strain of the pleural membrane from pulsatile air flow and collagen-elastin dynamics. Based\r\non the principles of continuummechanics and fluid-structure interaction, our proposedmodel coupled isotropic tissue deformation\r\nwith pressure from pulsatile air motion and the pleural fluid. Next, we derived mathematical instability criteria for our ordinary\r\ndifferential equation system and then translated these mathematical instabilities to physically relevant structural instabilities via\r\nthe incorporation of a finite energy limiter. The introduction of novel biomechanical descriptions for collagen-elastin dynamics\r\nallowed us to demonstrate that changes in the protein structure can lead to a transition from stable to unstable domains in the\r\nmaterial parameter space for a general lesion. This result allowed us to create a novel streamlined algorithm for detecting material\r\ninstabilities in transient lung CT scan data via analyzing deformations in a local tissue boundary.
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