Continuing Medical EducationChronic venous insufficiency and venous leg ulceration☆
Section snippets
Epidemiology
Venous leg ulcers are responsible for more than half of lower extremity ulcerations, with an overall prevalence ranging from 0.06% to 2%.6, 8 This variance may be due to contributory factors including the use of overall versus point prevalence; the inclusion or exclusion of foot ulcers; the age and sex distribution of the patient series; the methodology used to identify patients6, 18; the patients' often inaccurate assessment of ulcer duration, healing, and recurrence; and the lack of a uniform
Normal anatomy and physiology
Venous blood flow of the lower extremity is divided into 3 components: the superficial, communicating, and deep veins. The superficial system comprises both the long and short saphenous veins and their tributaries. The long saphenous vein originates from the medial end of the dorsal venous arch of the foot and ascends the leg and thigh medially. It joins the femoral vein just below the inguinal ligament. The lesser or short saphenous vein originates from the lateral aspect of the dorsal venous
Patient history
The clinical history of patients with venous ulceration is characterized by the lack of specific symptoms. There is variable discomfort associated with venous ulcers, the severity of which varies unpredictably between patients and their particular ulcers. The surface area of the ulcer does not correlate well with the presence of pain. Deep ulcers, particularly around the malleoli, or small venous ulcers surrounded by atrophie blanche are the most painful. Patients with venous ulcers commonly
Risk factors for venous leg ulceration
Most epidemiologic studies on chronic venous insufficiency are cross-sectional surveys that suggest potential risk factors by describing their study population. However, these relationships could be due to the older age of the population with chronic venous insufficiency. Scott et al76 conducted a prospective dual case-control study to address this issue. They found that in addition to being older, patients with chronic venous insufficiency tend to be obese. They also commonly report a history
Clinical presentation
One of the first obvious clinical signs of chronic venous insufficiency is varicose veins, although the recently described acute lipodermatosclerosis (see below) may precede the presence of varicosities.85 The size of varicose veins may range from a submalleolar venous flare to various degrees of vessel dilation (Figs 2 and 3).
Differential diagnosis
Although most leg ulcers in large series are venous, the pathogenesis is not venous in all patients.1 Other common causes are arterial and neuropathic; however, the cause of an ulcer is often multifactorial.100
Arterial ulcers typically appear round or punched out with a sharply demarcated border.7, 9, 86 A fibrous yellow base or a true necrotic eschar with scant or absent granulation tissue is commonly seen. Necrotic tissue or the exposure of tendons and deep tissues also suggests an arterial
Assessment for venous insufficiency
In up to 76% of the cases, the diagnosis of venous ulceration may be made by clinical criteria alone.109, 110 Noninvasive methods are helpful for accurate diagnosis and anatomic and functional evaluation, but do not exclude overlapping causes for the ulceration.9, 110
Measurement of the ABI by Doppler ultrasonography, as described earlier, is useful to exclude concomitant arterial disease because compression therapy in patients with undiagnosed arterial insufficiency can lead to ulcer worsening,
Treatment
Treatment goals for patients with chronic venous insufficiency include reduction of edema, alleviation of pain, improvement of lipodermatosclerosis, healing of ulcers, and prevention of recurrence.29 Better understanding of the pathophysiology of venous disease and leg ulceration has in turn suggested new approaches to the management of ulcer disease with new types of wound dressings, compression bandages, topical and systemic therapeutic agents, and surgical modalities.8
The primary role of
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Reprint requests: William H. Eaglstein, MD, Chairman and Harvey Blank Professor, Department of Dermatology and Cutaneous Surgery, University of Miami, School of Medicine, Room 2023, RMSB (R-250), 1600 NW 10th Ave, Miami, FL 33136.