The primary pathophysiology involves incompetent one-way venous valves or dysfunctional calf muscle pumping, leading to insufficient venous blood return to the heart and chronic leg venous hypertension. This venous hypertension leads to aberrant tissue perfusion and subsequent decreased delivery of oxygen and nutrients, failure to remove metabolic byproducts, and tissue ischemia.
Additional clinical features commonly associated include leg and ankle edema, varicose veins, yellow-brown pigmentation secondary to hemosiderin deposition and extravasated red blood cells, eczematous changes with scaling and crusting (stasis dermatitis), and lymphedema. Lipodermatosclerosis is also seen and corresponds to fibrotic changes in subcutaneous tissue leading to a hard and indurated feel to the skin. An "inverted champagne bottle" leg indicates end stage lipodermatosclerosis and is caused by severe fibrotic changes in the distal leg and leg edema of the proximal leg. Atrophie blanche are smooth, ivory-colored atrophic plaques secondary to sclerosis seen in approximately 40% of patients with venous insufficiency.
Additional key points are that stasis ulcers usually begin on the medial malleolus but may become circumferential over time. They may be painful, are difficult to treat, and frequently recur. They may become secondarily infected.
I83.009 – Varicose veins of unspecified lower extremity with ulcer of unspecified site
41915009 – Stasis ulcer
Differential Diagnosis & Pitfalls