Key Clinical Questions
Introduction/Epidemiology
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.
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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.
Pathophysiology
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.
Does the Patient Have a Venous Ulcer?
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 greater in individuals with higher CEAP (clinical, etiologic, anatomical, and pathophysiological) classifications (Table 146-2). It is not unusual for venous ulcers to persist for years. Venous ulcers often recur at the same site.
Class | Definition |
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C0 | No visible or palpable signs of venous disease |
C1 | Telangiectases (dilated venules, <1 mm diameter), reticular veins (dilated, nonpalpable, veins, ≤3 mm diameter), malleolar venous flare (arrays of small veins about the ankles) |
C2 | Varicose veins (dilated, palpable veins, >3 mm diameter) |
C3 | Edema without skin changes |
C4 | Skin changes* |
C5 | Skin changes* with healed ulceration |
C6 | Skin changes* with active ulceration |
Although venous ulcers are often less painful than other ulcer types, up to 75% of venous ulcer patients complain of pain. Deep ulcers around the ankles and ulcers with surrounding atrophie blanche (stellate white scars) can be particularly painful. Patients with venous ulcers may also have problems with physical function, mobility, depression, and social isolation that significantly impact their quality of life.
Clinical signs of venous disease are listed in Table 146-3. Up to 76% of venous ulcers may be diagnosed by clinical evaluation. Venous ulcers are typically ill-defined with irregular borders, a shallow wound bed, and may have a yellowish fibrinous exudate or pink granulation tissue. Around the ulcer, there can be skin dyspigmentation (darkening or lightening), purpura, and thickening of the skin. Venous ulcers tend to be located over the medial malleolus or within the “gaiter area” (the distal third of the leg, from the mid-calf to the ankle). Ulcers outside this area should raise the possibility of another cause.
Sign | Description |
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Pitting edema | Swelling of lower legs that retain an indentation after applying firm pressure |
Venous eczema/stasis dermatitis | Redness, scaling, itch, +/– exudates |
Dyspigmentation | Reddish-brown discoloration, especially around the ankle |
Purpura | Nonblanching red to purple spots |
Hemosiderosis | Cayenne pepper-appearing specks on shins |
Varicosities
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Atrophie blanche | Stellate white scars |
Induration/dermatosclerosis | Hardening of the skin |
Lipodermatosclerosis
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When pain is particularly severe, the ulcer is of long duration, or fails to improve with treatment, one should consider the possibility of concomitant infection, allergic contact dermatitis (to topical wound treatments), malignancy, or other ulcer etiologies.
All nonhealing ulcers should be evaluated with tissue cultures (not surface cultures) for bacterial, fungal, viral, mycobacterial, and atypical mycobacterial infection.
Patients with chronic nonhealing ulcers should have a skin biopsy to evaluate for malignancy.
Arterial ulcers can present with claudication or rest pain, and are often exquisitely painful. They present as sharply demarcated, punched-out ulcers with a fibrinous yellow base or black necrotic eschar, sometimes with exposure of deep tissues, such as tendons. They often occur distally, especially on the foot, or over bony prominences. Associated clinical findings include absent dorsalis pedis pulse, prolonged capillary refill time (>4–5 seconds), pallor with limb elevation and reactive hyperemia on dependency (dependent rubor), loss of hair, shiny skin, cool feet, abnormal toenails, and a low ankle/brachial pressure index (ABI) ≤0.5.
Neuropathic ulcers are common in diabetic patients. They are often associated with numbness, burning, and tingling, but can also be asymptomatic. They tend to occur over pressure-bearing areas, such as the soles of the feet. These ulcers are often deep, and associated infections of soft tissue and bone are common.
Inflammatory conditions commonly associated with ulceration include pyoderma gangrenosum and vasculitis. Pyoderma gangrenosum often begins as a small pustule that rapidly enlarges. It develops violaceous, undermined borders with a cribriform (perforated, sieve-like) base and tends to worsen with trauma, including debridement. Two-thirds are associated with inflammatory bowel disease, rheumatoid arthritis, or hematologic malignancies. Vasculitis can be associated with palpable purpura (nonblanching red to blue papules), livedo reticularis (netlike, red-purple erythema, especially on the legs), and necrosis. Rheumatoid arthritis, systemic lupus erythematosus, scleroderma, and other connective tissue diseases may also be associated with lower extremity ulcers in the absence of overt vasculitis.
Sickle cell anemia, anticardiolipin antibodies, and other procoagulant disorders can result in chronic wounds similar to venous ulcers.
What Is the Approach to a Patient with a Suspected Venous Ulcer?
Table 146-4 outlines key components of ulcer evaluation. A thorough history may support the diagnosis of venous stasis or suggest alternative diagnoses. Patients should be questioned about risk factors for venous ulcers (Table 146-1), associated symptoms and modifying factors, and response to prior treatments. Patients with venous leg ulcers often experience worsening symptoms in the dependent position and symptom relief with elevation. Claudication (calf pain or cramping with ambulation) is more consistent with arterial disease. Decreased or altered sensation in distal extremities suggests a neuropathic ulcer. Patients with pyoderma gangrenosum ulcers may note ulcer enlargement after trauma, such as mechanical debridement. Ulcers can be multifactorial and may have secondary complications, such as infection.