Chronic Venous Insufficiency and Post-Thrombotic Syndrome

Venous return from the lower extremities relies on contraction of the calf muscles to push blood from intramuscular (soleal) sinusoids and gastrocnemius veins into and through deep veins. Venous valves direct blood proximally to the heart. Chronic venous insufficiency occurs when venous obstruction (eg, in DVT), venous valvular insufficiency, lymphatic dysfunction, or decreased contraction of muscles surrounding the veins (eg, due to immobility) decrease forward venous flow and increase venous pressure (venous hypertension).

Fluid accumulation in the lower extremities (eg, in right heart failure) can also contribute by causing venous hypertension. Prolonged venous hypertension causes tissue edema, inflammation, and hypoxia, leading to symptoms. Pressure may be transmitted to superficial veins if valves in perforator veins, which connect deep and superficial veins, are ineffective.

Common risk factors for chronic venous insufficiency include (1):

• Deep venous thrombosis

• Older age

• Obesity

• Trauma

• Occupations requiring prolonged standing or carrying heavy loads

• Pregnancy

Idiopathic cases are often attributed to a history of occult DVT.

Post-thrombotic syndrome is symptomatic chronic venous insufficiency that follows DVT. Risk factors for post-thrombotic syndrome in patients with DVT include proximal thrombosis, recurrent ipsilateral DVT, and body mass index (BMI) ≥ 22 kg/m². Age, female sex, and estrogen therapy are also associated with the syndrome.

Clinically evident chronic venous insufficiency may not cause any symptoms but always causes signs; post-thrombotic syndrome always causes symptoms. Both disorders are a concern because their symptoms can mimic those of acute DVT and both can lead to substantial reductions in physical activity and quality of life.

Symptoms include a sense of fullness, heaviness, aching, cramps, pain, tiredness, and paresthesias in the legs; these symptoms worsen with standing or walking and are relieved by rest and elevation. Pruritus may accompany skin changes. Signs occur along a continuum: no changes to varicose veins (rare) to edema to stasis dermatitis on the lower legs and at the ankles, with or without ulceration (see table Clinical Classification of Chronic Venous Insufficiency). The calf may be painful when compressed.

Venous stasis dermatitis consists of erythema, hyperpigmentation, induration, venous ectasia, lipodermatosclerosis (fibrosing subcutaneous panniculitis), lichenification, and venous stasis ulcers. Erythema may be difficult to appreciate in dark skin.

Stasis Dermatitis (Chronic Changes)

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Chronic stasis dermatitis may appear as fibrotic skin thickening and hyperpigmentation. The changes are characteristic in both lightly pigmented skin (top) and darkly pigmented skin (bottom), here appearing more pronounced in the bottom photo.

Images provided by Thomas Habif, MD.

Atrophie Blanche

Image

BELMONTE/VABRES/SCIENCE PHOTO LIBRARY

Venous stasis ulcers may develop spontaneously or after affected skin is scratched or injured. They typically occur around the medial malleolus, tend to be shallow and moist, and may be malodorous (especially when poorly cared for) or painful. They do not penetrate the deep fascia. In contrast, ulcers due to peripheral artery disease eventually expose tendons or bone.

Venous Stasis Ulcer Manifestations

Early Venous Stasis Ulcer

Venous stasis includes lichenification and hyperpigmentation. A shallow ulcer is developing superior to the medial malleolus.

Venous stasis includes lichenification and hyperpigmentation. A shallow ulcer is developing superior to the medial mall

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© Springer Science+Business Media

Large Venous Stasis Ulcer

This large venous stasis ulcer is surrounded by brawny induration.

This large venous stasis ulcer is surrounded by brawny induration.

© Springer Science+Business Media

Stasis Dermatitis (Ulcer)

Venous stasis ulcers develop as a result of inadequately treated stasis dermatitis; they may quickly follow the first signs of stasis dermatitis.

Venous stasis ulcers develop as a result of inadequately treated stasis dermatitis; they may quickly follow the first s

... read more

Image provided by Thomas Habif, MD.

Healed Venous Stasis Ulcer

Roberto A. Penne-Casanova/SCIENCE PHOTO LIBRARY

Early Venous Stasis Ulcer

Venous stasis includes lichenification and hyperpigmentation. A shallow ulcer is developing superior to the medial malleolus.

Venous stasis includes lichenification and hyperpigmentation. A shallow ulcer is developing superior to the medial mall

... read more

© Springer Science+Business Media

Large Venous Stasis Ulcer

This large venous stasis ulcer is surrounded by brawny induration.

This large venous stasis ulcer is surrounded by brawny induration.

© Springer Science+Business Media

Stasis Dermatitis (Ulcer)

Venous stasis ulcers develop as a result of inadequately treated stasis dermatitis; they may quickly follow the first signs of stasis dermatitis.

Venous stasis ulcers develop as a result of inadequately treated stasis dermatitis; they may quickly follow the first s

... read more

Image provided by Thomas Habif, MD.

Healed Venous Stasis Ulcer

Roberto A. Penne-Casanova/SCIENCE PHOTO LIBRARY

Leg edema tends to be unilateral or asymmetric; bilateral symmetric edema is more likely to result from a systemic disorder (eg, heart failure, hypoalbuminemia) or certain medications (eg, calcium channel blockers).

In general, unless the lower extremities are adequately cared for, patients with any manifestation of chronic venous insufficiency or post-thrombotic syndrome are at risk of progression to more advanced disease.

• History and Physical Examination

• Ultrasound to exclude DVT

Diagnosis is usually based on history and physical examination. The Villalta score, a clinical scoring system that ranks 5 symptoms (pain, cramps, heaviness, pruritus, paresthesia) and 6 signs (edema, hyperpigmentation, induration, venous ectasia, blanching hyperemia, pain with calf compression) on a scale of 0 (absent or minimal) to 3 (severe) is an effective diagnostic tool of disease severity (1, 2, 3, 4). Scores of 5 to 14 on 2 visits separated by ≥ 6 months indicate mild-to-moderate disease, and scores of ≥ 15 indicate severe disease.

Lower-extremity duplex ultrasound reliably excludes or confirms DVT. Absence of edema and a reduced ankle-brachial index suggest peripheral artery disease rather than chronic venous insufficiency or post-thrombotic syndrome.

• Elevation

• Compression using bandages, stockings, and/or pneumatic devices

• Exercise training

• Topical treatments

• Treatment of secondary infection, when present

• Sometimes surgical and endovascular approaches

Weight loss, regular exercise, and reduction of dietary sodium may benefit patients with bilateral chronic venous insufficiency (1). Weight loss can also improve venous hypertension by reducing concomitant sleep apnea and right heart failure. Leg-strengthening exercises and aerobic exercise, preferably in a supervised program, may also benefit patients with post-thrombotic syndrome (2).

Elevating the leg above the level of the right atrium decreases venous hypertension and edema, is appropriate for all patients, and should be done a minimum of 3 times a day for ≥ 30 minutes. However, many patients cannot reliably adhere to this schedule during the day.

Compression is recommended for treatment and prevention of the effects of chronic venous insufficiency (ie, edema, venous ulcers) and can be used for all patients (1, 2). Although the data are mixed as to whether compression stockings prevent post-thrombotic syndrome, they are useful to reduce symptoms of swelling, pain, and tightness that may occur after deep vein thrombosis (2).

Elastic bandages are used initially until edema and ulcers resolve and leg size stabilizes; commercial compression stockings are then used. Stockings that provide 20 to 30 mm Hg of distal circumferential pressure are indicated for smaller varicose veins and mild chronic venous insufficiency; 30 to 40 mm Hg is indicated for larger varicose veins and moderate to severe disease. Infrequently, higher compression pressures (eg, > 40 mm Hg) can be used but may not be tolerated for long-term use. Stockings should be put on when patients awaken, before leg edema worsens with activity, and should exert maximal pressure at the ankles and gradually less pressure proximally. Adherence to this treatment varies; many patients consider stockings irritating, restricting, or cosmetically undesirable, and many patients have difficulty putting them on.

Intermittent pneumatic compression (IPC) uses a pump to cyclically inflate and deflate hollow plastic leggings. IPC provides external compression, squeezing blood and fluid out of the lower legs. It effectively treats severe post-thrombotic syndrome (2) and venous stasis ulcers but is less practical than compression stockings for patients to adhere to on an ongoing basis.

Options for venous ulcer management include compression, oral pentoxifylline, and topical treatments (include compression, oral pentoxifylline, and topical treatments (2). There is no strong evidence that one approach is superior, and management should be individualized. Involvement of a wound care specialist may be helpful to guide management. An Unna boot (zinc oxide–impregnated bandages) properly applied, covered by compression bandages, and changed weekly is associated with ulcer healing in some patients (). There is no strong evidence that one approach is superior, and management should be individualized. Involvement of a wound care specialist may be helpful to guide management. An Unna boot (zinc oxide–impregnated bandages) properly applied, covered by compression bandages, and changed weekly is associated with ulcer healing in some patients (3, 4). Occlusive dressings (eg, hydrocolloids such as aluminum chloride) provide a moist environment for wound healing and promote growth of new tissue; they may be used for ulcers with light to moderate exudate, but they probably add little to simple Unna bandaging. Dry dressings are absorptive, making them most appropriate for heavier exudate.). Occlusive dressings (eg, hydrocolloids such as aluminum chloride) provide a moist environment for wound healing and promote growth of new tissue; they may be used for ulcers with light to moderate exudate, but they probably add little to simple Unna bandaging. Dry dressings are absorptive, making them most appropriate for heavier exudate.

Other medications have little to no role in routine treatment of chronic venous insufficiency (2), although many patients are given aspirin, topical glucocorticoids, or antibiotics. Diuretics should be reserved for treating volume overload rather than local edema. If used, thiazides and mineralocorticoid receptor antagonists are preferred over loop diuretics because they can increase venous compliance (1).

Surgery (eg, venous ligation, stripping, valve reconstruction) has limited effectiveness (1). Grafting autologous skin or skin created from epidermal keratinocytes or dermal fibroblasts may be an option for patients with stasis ulcers refractory to all other measures (5); however, there is a risk that the graft may reulcerate, especially if there is ongoing venous hypertension. For patients with refractory venous ulcers, venous valve reconstruction may be considered (2). Surgical venovenous bypass procedures as well as endovascular stent venoplasty are options for patients with severe symptoms.

Primary prevention of chronic venous insufficiency involves DVT prophylaxis for those at risk, adequate anticoagulation after DVT and use of compression stockings for up to 2 years after DVT or lower extremity venous trauma. However, a meta-analysis of randomized trials comparing compression stockings with placebo (ie, either none or sham-compression stockings) failed to show a significant reduction in post-thrombotic syndrome (1).

Lifestyle changes (eg, weight loss, regular exercise) can decrease risk of chronic venous insufficiency by decreasing lower extremity venous pressure (2).