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Key Clinical Questions

  • image Does this patient have a venous ulcer?

  • image What is the diagnostic approach to a patient with a suspected venous ulcer?

  • image What are appropriate treatments for venous ulcers?

  • image How might patients prevent venous ulcers?

The prevalence of leg ulcers is rising. Up to 1% of adults in developed countries have leg ulcers, with venous disease as the cause in up to 80% of cases. Because of their often chronic course, venous ulcers impose a significant economic burden, accounting for 1% to 3% of the total health care budgets in developed countries. 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 diminished quality of life.

Risk factors associated with venous leg ulcers are listed in Table 148-1. Up to 60% of patients with venous ulcers have a prior history of deep venous thrombosis. Annual recurrence rates of venous ulcers are high, ranging from 6% to 27%, perhaps reflecting the high prevalence of underlying venous insufficiency.

TABLE 148-1Risk Factors


The lower-extremity venous system is made up of superficial, communicating, perforating, and deep veins. The deep system lies beneath the muscle fascia. The superficial system is located between the muscle fascia and skin, and includes the saphenous veins. The perforating system connects the superficial system to the deep system, and communicating veins connect veins within the same system. Veins have one-way valves that 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 or deep venous systems, or both. Obesity, leg immobility, inflammatory conditions of muscles or joints, fibrosis, and neuropathies can result in calf-muscle pump failure.

Several mechanisms contribute to the development of venous ulcers. Gravity plays a key role, as most venous ulcers are located on the lower extremities. Venous hypertension increases shear stress on vessel walls, leading to endothelial dysfunction and cytokine release. Inflammation stimulates the release of matrix metalloproteinases and other enzymes, with further damage to veins and soft tissue. Wound healing is handicapped by decreased oxygen diffusion to tissues in the setting of venous congestion, setting up a vicious cycle of endothelial activation, unchecked inflammation, soft tissue ...

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