Venous Insufficiency Ulcers

Basics

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.

Incidence

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.

Prevalence

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.

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.

Genetics

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

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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