Venous ulcers affect approximately 1% of the U.S. population, and when managed conservatively, demonstrate a protracted course of healing with a high recurrence rate. Venous ulceration costs the healthcare system over $3 billion annually in the United States alone. Two million workdays are lost each year due to venous leg ulcers.

Chronic venous hypertension resulting from superficial and deep valvular incompetence leads to sustained pressure at specific sites on the leg, especially where incompetent perforating veins are present. The typical location of a venous ulcer is just above the medial malleolus overlying a Cockett perforator. Local intravenous pressures as high as 90 mmHg have been demonstrated in patients with venous ulcers. While the exact pathophysiology has not been elucidated, it is clear that decreased O2 diffusion is the final common pathway leading to ischemic necrosis of skin and subcutaneous tissue. Transcutaneous oxygen tension of the skin surrounding a venous ulcer is decreased. In addition, hyperbaric O2  has been shown to improve healing of venous ulcers. Associated factors predisposing to the formation of venous ulcers are history of deep venous thrombosis and poor lymphatic drainage.