The mechanobiology theory of the development of medical device-related pressure ulcers revealed through a cell-scale computational modeling framework.

Pressure ulcers are localized sites of tissue damage which form due to the continuous exposure of skin and underlying soft tissues to sustained mechanical loading, by bodyweight forces or because a body site is in prolonged contact with an interfacing object. The latter is the common cause for the specific sub-class of pressure ulcers termed 'medical device-related pressure ulcers', where the injury is known to have been caused by a medical device applied for a diagnostic or therapeutic purpose. Etiological research has established three key contributors to pressure ulcer formation, namely direct cell and tissue deformation, inflammatory edema and ischemic damage which are typically activated sequentially to fuel the injury spiral. Here, we visualize and analyze the above etiological mechanism using a new cell-scale modeling framework. Specifically, we consider here the deformation-inflicted and inflammatory contributors to the damage progression in a medical device-related pressure ulcer scenario, forming under a continuous positive airway pressure ventilation mask at the microarchitecture of the nasal bridge. We demonstrate the detrimental effects of exposure to high-level continuous external strains, which causes deformation-inflicted cell damage almost immediately. This in turn induces localized edema, which exacerbates the cell-scale mechanical loading state and thereby progresses cell damage further in a nonlinear, escalating pattern. The cell-scale quantitative description of the damage cascade provided here is important not only from a basic science perspective, but also for creating awareness among clinicians as well as industry and regulators with regards to the need for improving the design of skin-contacting medical devices.