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
- 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
- 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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