It has been recognized for over 2000 years that ulceration of the leg may be associated with visible varices of the lower limb. More recent physiological investigation has shown that the pressure in the veins of the lower limb remains raised in patients with venous ulceration during ambulation, whereas in normal subjects the pressure in superficial veins falls to a low level. This elevated pressure appears to cause damage to the superficial capillaries in the skin culminating in the production of venous ulceration. Events in the dermal capillaries which result in skin destruction have yet to be fully defined. Pericapillary fibrin cuffs have been demonstrated histologically and suggested as a cause of diminished nutrition to the skin. White blood cells have been shown to accumulate in the lower limb of patients with venous disease and these accumulations are particularly located around the dermal capillaries. Activated white blood cells releasing free radicals and destructive enzymes may precipitate skin destruction. An understanding of these mechanisms may help to explain the efficacy of compression hosiery and bandaging as well as some of the new pharmacological agents which have been shown to influence venous ulcer healing.