Venous Insufficiency

Article Author:
Shivik Patel
Article Editor:
Scott Surowiec
Updated:
11/18/2018 8:58:00 PM
PubMed Link:
Venous Insufficiency

Introduction

Chronic venous insufficiency (CVI) typically refers to lower extremity edema, skin trophic changes, and discomfort secondary to venous hypertension. Chronic venous insufficiency is a prevalent disease process. Disability-related to chronic venous insufficiency attributes to diminished quality of life and loss of work productivity. In most cases, the cause is incompetent valves. Each year approximately 150,000 new patients are diagnosed with chronic venous insufficiency, and nearly $500 million is used in the care of these patients. The CEAP classification (clinical, etiology, anatomy, and pathophysiology) has been developed to guide decision-making in chronic venous insufficiency evaluation and treatment. The system has shown to predict the patient quality of life and severity of their symptoms.[1][2][3]

Etiology

The etiology of chronic venous insufficiency can also be classified as either primary or secondary to deep venous thrombosis (DVT). Primary chronic venous insufficiency refers to the symptomatic presentation without a precipitating event and is due to congenital defects or changes in venous wall biochemistry. Recent studies suggest that approximately 70% of patients have primary chronic venous insufficiency and 30% have the secondary disease. Studies into primary chronic venous insufficiency have identified reduced elastin content, increased extra-cellular matrix remodeling and inflammatory infiltrate. The culmination of which alters the integrity of the vein promoting dilation and valvular incompetence. Secondary chronic venous insufficiency occurs in response to a DVT which triggers an inflammatory response subsequently injuring the vein wall. Irrespective of the specific etiology, chronic venous insufficiency promotes venous hypertension. The most common non-modifiable risk factors are female gender and non-thrombotic iliac vein obstruction (May-Thurner syndrome). Several studies have also suggested a genetic component contributing to vein wall laxity. Modifiable risk factors include smoking, obesity, pregnancy, prolonged standing, DVT, and venous injury.[4][5]

Epidemiology

An estimated six to seven million people within the United States have an existing diagnosis of advanced venous disease and meet diagnostic criteria for chronic venous insufficiency. Results across studies suggest that in the general population between 1% to 17% of men and 1% to 40% of women may experience chronic venous insufficiency. Despite this wide range, non-western countries appear to have a lower overall prevalence. Among all chronic venous insufficiency patients, approximately 1% to 2.7% will develop a venous stasis ulcer. Formation of an ulcer carries a poor prognosis, with 40% of patients developing recurrence despite standard treatment. Management of chronic venous insufficiency accounts for approximately 2% of the United States total healthcare.[6][7]

Pathophysiology

Chronic venous insufficiency pathophysiology is either due to reflux (backward flow) or obstruction of venous blood flow. Chronic venous insufficiency can develop from the protracted valvular incompetence of superficial veins, deep veins or perforating veins which connect them. In all cases, the result is venous hypertension of the lower extremities. Superficial incompetence is usually due to weakened or abnormally shaped valves or widened venous diameter which prevents normal valve congruence. Deep vein dysfunction is usually owing to the previous DVT which results in inflammation, valve scarring and adhesion, and luminal narrowing. Perforating vein valvular failure allows a higher pressure to enter the superficial venous system. The subsequent dilation prevents the proper closure of the valve cusps in the superficial veins. Most patients will also have the disease in the superficial veins. The resting venous pressure is a summation of the outflow obstruction, capillary inflow, valve function, and muscle pump function. Regardless of the cause, the persistently elevated venous hydrostatic pressure may result in lower extremity pain, edema, and venous microangiopathy. Some patients develop permanent skin hyperpigmentation from hemosiderin deposition as red blood cells extravasate into the surrounding tissue. Many of these patients will also have lipodermatosclerosis, which is skin thickening from fibrosis of subcutaneous fat. As the disease progresses, the perturbed microcirculation and dermal weakening can result in ulcer formation.[8]

History and Physical

Patients with chronic venous insufficiency commonly present initially with a combination of dependent pitting edema, leg discomfort, and fatigue, and itching. Although there can be variation in presentation among patients, certain features are more prevalent: pain, cramping, itching, prickling, and throbbing sensation. Patients may describe symptoms that improve with rest and leg elevation, and with no association for exercise. This latter feature can be used to distinguish venous from arterial claudication. As their disease progresses, the presence of varicose veins and tenderness can be noted along with refractory edema and skin changes. Patients with advanced disease will present with a severe blanched skin lesion, dermal atrophy, hyperpigmentation, dilated venous capillaries, and ulcer formation most commonly overlying the medial malleolus. The physical exam must involve a detailed assessment of any ulcers, distal pulses, and neuropathy. A thorough history should note any hypercoagulable condition, oral contraceptive use, previous DVT or intervention, the level of physical activity, and occupation. The patient’s presentation should carefully be distinguished from other pathologies with similar symptoms: diabetic ulcers, ischemic ulcers, and dermatologic conditions including cancer.

Evaluation

In addition to a full history and physical exam, initial evaluation should include objective stratification. Venous reflux testing can identify regions affected and give some indication of the etiology and pathophysiology. Duplex ultrasonography, particularly B-mode imaging, can be helpful for identifying the regions of the affected anatomy. Insufficiency within a venous segment is defined as reflux of more than 0.5 seconds with distal compression. Invasive venography can be used in patients who may require surgery or have suspicion for venous stenosis. Other modalities which may be employed are: ankle-brachial index to exclude arterial pathology, air or photoplethysmography, intravascular ultrasound, and ambulatory venous pressures, which provides a global assessment of venous competence.[9][10]

Treatment / Management

Patients with chronic venous insufficiency should be treated based on their severity and nature of the disease. The treatment goals include reducing discomfort and edema, stabilizing skin appearance, removing painful varicose veins and healing ulcers. Most patients should initially be treated conservatively with leg elevation, exercise (which improves calf muscle pump), weight management, and compression therapy. Ulcers are treated best with compression bandaging systems. Chronic venous ulcerations entail a risk of infection and cancerous transformation (Marjolin ulcer). Compression therapy should be used with caution in patients with the coexisting peripheral arterial disease. Significant arterial insufficiency should be treated before instituting a compression regimen. Patients whose ulcers fail to respond to compression may ultimately need surgical intervention. Superficial vein reflux can be managed with foam sclerotherapy, endovenous thermal ablation, or stripping. Deep vein reflux may be treated with valve reconstruction or valve transplant. Perforator reflux can either be managed with sclerotherapy, endovenous thermal ablation, or with subfascial endoscopic perforator surgery (SEPS). It should be noted, however, that compression therapy regimens that are adhered to are highly effective in treating all forms of venous pathophysiology.[3][11][12]

Differential Diagnosis

  • Lymphedema
  • Cellulitis
  • Stasis dermatitis
  • Varicose veins

Complications

  • Venous ulcer
  • Leg discoloration
  • Thrombophlebitis
  • DVT
  • Pulmonary embolism
  • Bleeding

Enhancing Healthcare Team Outcomes

CVI is best managed by a team of healthcare professionals that include a wound care nurse, vascular surgeon, general surgeon, bariatric nurse, and physical therapist. Most cases of CVI can be treated, but the key is compliance. Patients should be encouraged to wear compression stockings, unless there is a contraindication. Just the use of stockings alone can markedly improve the symptoms and appearance. In addition, the patient should be encouraged to lose weight and avoid standing in one position for prolonged times. [13][14](Level V)

Outcomes

CVI if left untreated leads to very high morbidity and disability. Without treatment, the condition is progressive, ultimately leading to skin breakdown and ulcer formation. And these ulcers are difficult to heal leading to significant pain and increased costs of healthcare. Many patients end up in wound clinics where they are treated for months and years, without any significant benefit. These patients are also at an increased risk for deep vein thrombus and pulmonary embolism. In addition, any minor trauma is associated with torrential bleeding that can sometimes be fatal. [15][16](Level V)


References

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