Does this patient have a venous ulcer?
What is the diagnostic approach to a patient with a suspected venous ulcer?
What are appropriate treatments for venous ulcers?
How might patients prevent venous ulcers?
Up to 80% of all leg ulcers are venous ulcers. Approximately 1–2% of the U.S. adult population has a history of a venous ulcer. Several risk factors (Table 146-1) are associated with venous ulcers. Coexisting diseases are not uncommon; 5–12% of venous ulcer patients have diabetes mellitus, and 10–15% have rheumatologic disease.
Table 146-1 Risk Factors ||Download (.pdf)
Table 146-1 Risk Factors
- Age (peak prevalence between 60–80 years)
- Female sex (1.6 female: 1 male)
- History of
- Leg injury
- Varicose vein surgery
- Deep vein thrombosis
- Congenital absence of valves
- Venous valve or wall degeneration
- Arteriovenous shunts
- Prolonged standing
- Taller height
- Inadequate treatment of chronic venous Insufficiency or edema
Because of their unpredictable and often chronic course, venous ulcers impose a significant economic burden, accounting for 1–3% of the total health care budgets in developed countries, and approximately $3 billion per year in the United States. Venous ulcers also result in substantial indirect costs, including an estimated loss of 2 million working days per year in the United States, as well as decreased work productivity, premature disability, and other impacts on quality of life.
The lower extremity venous system is made up of superficial veins, communicating (perforating) veins, and deep veins. These veins have one-way valves that, under normal conditions, prevent reflux and promote cephalad blood flow with leg muscle contraction.
Venous ulcers typically occur in the setting of chronic venous insufficiency, due to reflux through incompetent valves, venous outflow obstruction, as in venous thrombosis, or failure of the calf-muscle pump. Valvular incompetence may occur in the superficial (45%) or deep (12%) venous systems, or both (43%). Obesity, leg immobility, inflammatory conditions of muscles or joints, fibrosis, and neuropathies can result in calf-muscle pump failure.
Several mechanisms may contribute to the development of venous ulcers. Elevated venous pressures may lead to capillary distention and leakage of fibrin, resulting in fibrin cuff formation around dermal capillaries and decreased oxygen diffusion to tissues. Abnormalities in fibrinolysis may contribute to this process. Fibrinogen and other macromolecules that have leaked into tissues may trap growth factors, making them unavailable for tissue maintenance and repair. Trapping of white cells may cause enzyme release and inflammation that further increases vessel permeability and damages tissues.
Patients should be assessed for risk factors (Table 146-1), symptoms, prior treatments, and ulcer course. Patients with venous ulcers have variable symptoms that tend to be worse at the end of the day, and improve with leg elevation. These include aching, cramping, swelling, heaviness, tingling, itching, burning, copious, sometimes malodorous drainage, and restless legs. Symptoms are ...