Chronic venous insufficiency affects up to 5% of people in the US. Postphlebitic syndrome may affect 20 to 50% of patients with deep venous thrombosis (DVT), usually within 1 to 2 years after acute DVT.
Venous return from the lower extremities relies on contraction of 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, 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.
The most common risk factor for chronic venous insufficiency is
Other risk factors include
Idiopathic cases are often attributed to a history of occult DVT.
Postphlebitic syndrome is symptomatic chronic venous insufficiency that follows DVT. Risk factors for postphlebitic 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 but are probably nonspecific. Use of compression stockings after DVT decreases risk.
Clinically evident chronic venous insufficiency may not cause any symptoms but always causes signs; postphlebitic 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.
Clinical Classification of Chronic Venous Insufficiency
Venous stasis dermatitis consists of reddish brown hyperpigmentation, induration, venous ectasia, lipodermatosclerosis (fibrosing subcutaneous panniculitis), and venous stasis ulcers.
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 arterial disease eventually expose tendons or bone.
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 drugs (eg, calcium channel blockers).
In general, unless the lower extremities are adequately cared for, patients with any manifestation of chronic venous insufficiency or postphlebitic syndrome are at risk of progression to more advanced forms.
Diagnosis is usually based on history and physical examination. 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 increasingly recognized as a standard diagnostic tool of disease severity. 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 ultrasonography reliably excludes or confirms DVT. Absence of edema and a reduced ankle-brachial index suggest peripheral arterial disease rather than chronic venous insufficiency and postphlebitic syndrome.
Treatment depends on the disorder's severity and involves
Some experts also believe that weight loss, regular exercise, and reduction of dietary sodium may benefit patients with bilateral chronic venous insufficiency. However, all interventions may be difficult to implement.
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/day for ≥ 30 minutes. However, most patients cannot adhere to this schedule during the day.
Compression is effective for treatment and prevention of the effects of chronic venous insufficiency and postphlebitic syndrome and is indicated for all patients. 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 disease; and 40 to > 60 mm Hg is indicated for severe disease. 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 younger or more active patients consider stockings irritating, restricting, or cosmetically undesirable; elderly patients may 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 postphlebitic syndrome and venous stasis ulcers but may be no more effective than compression stockings alone and is much less practical for patients to adhere to on an ongoing basis.
Topical wound care is important in venous stasis ulcer management. When an Unna boot (zinc oxide–impregnated bandages) is properly applied, covered by compression bandages, and changed weekly, almost all ulcers heal. Occlusive interactive 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 and are expensive. Dry passive dressings are absorptive, making them most appropriate for heavier exudate.
Drugs have no role in routine treatment of chronic venous insufficiency, although many patients are given aspirin, topical corticosteroids, diuretics for edema, or antibiotics.
Surgery (eg, venous ligation, stripping, valve reconstruction) is also typically ineffective. Grafting autologous skin or skin created from epidermal keratinocytes or dermal fibroblasts may be an option for patients with stasis ulcers when all other measures are ineffective, but the graft will reulcerate unless underlying venous hypertension is managed.
Primary prevention involves adequate anticoagulation after DVT and use of compression stockings for up to 2 years after DVT or lower extremity venous trauma. However, a recent study using sham-compression stockings failed to show any decrease in postphlebitic syndrome. Lifestyle changes (eg, weight loss, regular exercise, reduction of dietary sodium) can decrease risk by decreasing lower extremity venous pressure.
Skin changes range on a continuum from normal skin or mildly ectatic veins to severe stasis dermatitis and ulceration.
Symptoms are more common with postphlebitic syndrome and include heaviness, aching, and paresthesias.
Diagnosis is based on inspection, but patients should have ultrasonography to rule out deep venous thrombosis.
Treatment is with elevation and compression; drugs and surgery are typically ineffective.
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