Venous Insufficiency Ulcers


  • Venous insufficiency is a condition that occurs when the venous wall and/or valves in the leg veins are not working effectively, making it difficult for blood to return to the heart and causing stasis.
  • Signs of chronic venous insufficiency include edema, bulging veins, hyperpigmentation, dermatitis, woody fibrosis, lipodermatosclerosis, and ulcers.
  • Venous stasis ulcers are the most serious consequence of chronic venous insufficiency.
  • Venous stasis ulcers affect up to 3% of adults in developed countries at some point during their lives.
  • The annual estimated treatment cost of chronic venous ulcers is 2.5 to 3.5 billion dollars per year.


  • Irregular and shallow skin defect with surrounding hyperpigmentation and well-defined borders
  • Most frequently located in the lower leg or ankle over the bony prominences
  • Present for >30 days and fails to heal spontaneously
  • May only have mild pain unless infected


80% of leg ulcers are caused by venous disease versus 10–25% arterial disease.


  • The overall incidence of venous ulcers is 18/100,000 persons; more common in women than men (20.4 vs. 14.6/100,000); incidence increases with age in both men and women.
  • >20,000 patients are newly diagnosed with venous ulcers in the United States yearly.


  • Venous ulcers are seen in ~1% of the adult population and up to 4% in adults ≥80 years old in industrialized countries.
  • 70% of ulcers recur within 5 years of closure.

Etiology and Pathophysiology

  • In a diseased venous system, venous pressure in the deep system fails to fall with ambulation, causing venous hypertension.
  • Venous hypertension comes from the following:
    • Venous obstruction
    • Incompetent venous valves in the deep or superficial system
    • Inadequate muscle contraction (e.g., arthritis, myopathies, neuropathies)
  • Venous pressure transmitted to capillaries leads to venous hypertensive microangiopathy and extravasation of RBCs and proteins (especially fibrinogen).
  • Increased RBC aggregation leads to reduced oxygen transport, slowed arteriolar circulation, and ischemia at the skin level, contributing to ulcers.
  • Leukocytes aggregate to the hypoxic areas and increase local inflammation.
  • Prolonged chronic inflammation and bacterial infection promote the persistence of ulcers.


  • Autosomal dominant trait with variable penetrance with no specific gene or gene set identified
  • Forkhead box protein C2 identified as possible marker in patients with varicose veins

Risk Factors

  • History of leg injury, age >55 years, high BMI
  • Congestive heart failure (CHF)
  • History of deep venous thrombosis (DVT)
  • Failure of the calf muscle pump (e.g., ankle fusion, inactivity)
  • Previous varicose vein surgery or ulcers
  • Smoking, prolonged standing, pregnancy

General Prevention

  • After DVT: compression hose for at least 2 years (≥20 to 30 mm Hg compression)
  • For recurrent ulceration: compression, treat underlying problem, exercise.
  • Avoid triple antibiotic ointment, including anything containing neomycin sulfate.

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