Modeling interstitial transport and fluid flow induced by actuation-enabled implantable medical devices

An important obstacle to the long-term operation of implantable medical devices is the foreign body response (FBR), which is typified by rapid neutrophil infiltration and the subsequent development of fibrous capsules that ultimately isolate the device from surrounding tissue. Recent research has shown that dynamic mechanical actuation can improve the efficacy of implantable devices by actively regulating the immune microenvironment. We aim to develop a numerical model to examine how the dynamics of chemokine and neutrophil species are affected in the early phases of FBR by the interstitial fluid flow induced by actuation. We model the tissue microenvironment as a poroelastic medium and we solve Biot's equation coupled with Darcy's law to model the solid deformation and fluid flow induced by the actuator displacement. We then implement a coupled reaction-advection-diffusion system capturing the spatiotemporal evolution of neutrophil and chemokine concentrations. The model incorporates chemotaxis, chemokine degradation and uptake, and neutrophil apoptosis, parameterized from available experimental data. Our simulations reveal that periodic actuation alters interstitial fluid flow, chemokine transport and redistributes neutrophil infiltration profiles compared to static controls. We also identify actuation parameter regimes that optimizes interstitial transport and fluid flow.