Influences of sodium and glycosaminoglycans on skin oedema and the potential for ulceration: a finite-element approach

Venous ulcers are chronic transcutaneous wounds common inthe lower legs. They are resistant to healing and have a 78%chance of recurrence within 2 years. It is commonly acceptedthat venous ulcers are caused by the insufficiency of the calfmuscle pump, leading to blood pooling in the lower legs,resulting in inflammation, skin oedema, tissue necrosis andeventually skin ulceration. However, the detailed physiologicalevents by which inflammation contributes to woundformation are poorly understood. We therefore sought todevelop a model that simulated the inflammation, using it todetermine the internal stresses and pressure on the skin thatcontribute to venous ulcer formation. A three-layer finite-element skin model (epidermis, dermis and hypodermis) wasdeveloped to explore the roles in wound formation of twoinflammation identifiers: glycosaminoglycans (GAG) andsodium. A series of parametric studies showed that increasedGAG and sodium content led to oedema and increased tissuestresses of 1.5 MPa, which was within the reported range ofskin tissue ultimate tensile stress (0.1–40 MPa). These resultssuggested that both the oedema and increased fluid pressurecould reach a threshold for tissue damage and eventual ulcerformation. The models presented here provide insights to thepathological events associated with venous insufficiency,including inflammation, oedema and skin ulceration.