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Venous ulcers are chronic transcutaneous wounds common in the lower legs. They are resistant to healing and have a 78% chance of recurrence within 2 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 oedema, 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 (GAG) and sodium. A series of parametric studies showed that increased GAG and sodium content led to oedema 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 oedema 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, oedema and skin ulceration.