Venous ulcers affect approximately 1% of the world's population, increasing healthcare expenditures and decreasing quality of life. Several hypotheses may help explain their origin. Incompetent veins or valves or impaired muscle function may lead to abnormal calf muscle pump function that can elevate ambulatory venous pressure (venous hypertension). This hypertension subsequently results in local venous dilatation and pooling, concomitantly trapping leukocytes that may release proteolytic enzymes that destroy tissues. Venous pooling also induces interendothelial pore widening and deposition of fibrin and other macromolecules that "trap" growth factors within them, rendering them unavailable for wound repair. Compression therapy, the mainstay treatment, reduces edema, reverses venous hypertension, and improves calf muscle pump function. Several treatment options can be employed as adjuvants to compression--eg, systemic therapy with pentoxifylline or aspirin, autologous grafts, tissue-engineered skin, growth factor therapy, and/or vein surgery. The epidemiology, pathophysiology, diagnosis, and management options regarding venous ulcers are reviewed.