Data from: Influences of sodium and glycosaminoglycans on skin edema and the potential for ulceration: a finite element approach

Venous ulcers are chronic transcutaneous wounds common in the lower legs.
They are resistant to healing and have a 78% chance of recurrence within
two years. It is commonly accepted that venous ulcers are caused by the
insufficiency of the calf muscle pump, leading to blood pooling in the
lower legs, resulting in inflammation, skin edema, tissue necrosis and
eventually skin ulceration. However, the detailed physiological events by
which inflammation contributes to wound formation are poorly understood.
We therefore sought to develop a model that simulated the inflammation,
using it to determine the internal stresses and pressure on the skin that
contribute to venous ulcer formation. A three-layer Finite Element skin
model (epidermis, dermis and hypodermis) was developed to explore the
roles in wound formation of two inflammation identifiers:
Glycosaminoglycans (GAGs) and sodium. A series of parametric studies
showed that increased GAGs and sodium content lead to edema and increased
tissue stresses of 1.5 MPa, which was within the reported range of skin
tissue Ultimate Tensile Stress (0.1-40 MPa). These results suggested that
both the edema and increased fluid pressure could reach a threshold for
tissue damage and eventual ulcer formation. The models presented here
provide insights to the pathological events associated with venous
insufficiency including inflammation, edema, and skin ulceration.