Chronic venous insufficiency (CVI) affects 10% to 35% of adults in the United States, and represents the more advanced and clinically significant phase in the progression of chronic venous disease (CVD).1-3 Although initial clinical findings associated with CVD may appear innocuous (varicose veins and spider veins), progression of the disease to CVI can ultimately result in chronic nonhealing skin ulceration.1,2

Once patients have had an ulceration, the likelihood of recurrence is high and the effect on morbidity, quality of life, and cost of care is substantial. Early identification of venous disease, therefore, is vital. With up-to-date knowledge regarding the etiology and evidence-based management strategies for CVD/CVI, providers can improve their ability to identify venous disease early and intervene effectively in a timelier manner.2

Etiology

The lower extremity venous system is composed of 3 major components: the superficial system (saphenous veins), the deep system, and the perforator veins that connect the two, which normally prevent backflow from the high-pressure deep system to the low-pressure superficial system. The 2 elements most critical to the normal function of the lower extremity venous system include valvular competence and a functional calf muscle “pump.” When both factors are working, the lower leg has high resting (filling) pressures and low walking (emptying) pressures.


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When there is venous insufficiency, ambulatory venous hypertension (ie, a chronic high-pressure system) develops. Ambulatory venous hypertension is most common in the superficial system and is the hallmark of CVI, as well as the cause of all skin changes found with CVI.1,3

From a clinical standpoint, CVD can present with a variety of symptoms that progress in severity over time (Table 1).3,4 Vascular experts consider CVI to be more advanced than CVD, with increased resting venous pressures resulting in skin changes, edema, ulceration, or a combination of all 3 findings.3,4

Table 1. Clinical Findings of Chronic Venous Disease

  • Varicose veins and spider veins
  • Phlebitis
  • Thrombosis
  • Vascular malformation
  • Leg pain*
  • Valvular incompetence with reflux*
  • Leg edema*
  • Lower extremity skin changes (hemosiderosis, atrophie blanche, lipodermatosclerosis)*
  • Lower leg ulcerations*

*Findings associated with disease progression to CVI

CVI, chronic venous insufficiency

Because the anatomic changes and clinical findings associated with CVI exist on a spectrum of severity, it may be helpful to use a standardized classification tool to maintain uniformity when discussing the condition and treatment. The CEAP (Clinical-Etiology-Anatomy-Pathophysiology) Classification is the most common severity classification system for lower extremity venous disease. Although the CEAP score is commonly used in a vascular clinic, it is helpful to be familiar with the scoring system to recognize how venous disease is described in terms of skin changes, etiology, anatomic location (which venous system), and underlying pathophysiology.4

The significance of risk factors varies throughout the literature, with the strongest risk correlating to genetically related CVI or a history of deep vein thrombosis. Other risk factors for the development of CVI include3,5,6

  • Older age
  • Female sex
  • Obesity
  • Standing occupation
  • Pregnancy (or history of)

Additional risk factors with varying significance in the literature include constipation/low fiber intake, low activity level, trauma to the area, smoking, and oral contraceptive or hormonal therapy use.

Conditions Resulting From CVI

Poorly managed CVI can result in conditions that range from those that minimally affect health (hemosiderin staining) to stasis dermatitis to limb-threatening (full-thickness ulcerations). Initial clinical findings usually include dependent edema that improves with elevation. Hemosiderin staining (hemosiderosis) is also frequently seen early in the disease course and results from heme deposits and breakdown in the soft tissues, which cause the brawny discoloration that can usually be seen over the anterior portion of the lower leg between the ankle and the knee. Occasionally, the appearance of hemosiderosis improves slightly with consistent use of compression, but typically it will persist even once the patient’s venous disease is appropriately managed.

Later in the course of the disease, patients may develop lipodermatosclerosis, or a woody appearance and texture to the leg. This is a result of fibrosis and sclerosing of the dermis and subcutaneous tissue, thought to occur from fibrinogen leaking out of the dermal capillaries because of long-term venous hypertension. The patient may also have an upside-down champagne bottle appearance to the leg as the lipodermatosclerosis progresses; this is a result of skin tightening around the ankle as the tissue fibroses.7 Atrophie blanche, a condition in which there are pearly white, sclerotic skin changes with a scar-like appearance in places where patients have never had previous scarring, may also develop. Atrophie blanche is a result of small-vessel thrombosis of the subpapillary vascular plexus and should be regarded as a significant red flag, as patients who exhibit this skin change frequently go on to develop ulceration in that area if their CVI isn’t managed.8

Late in the disease, patients are at high risk of developing ulcerations and stasis dermatitis. Ulcerations may be a result of the spontaneous breakdown of the skin, but often develop when the patient sustains minor trauma that results in a nonhealing ulceration.1 Stasis dermatitis is an inflammatory skin condition that can be multifactorial. It is most frequently associated with active ulcerations, as the drainage from the wound irritates the surrounding skin. However, it also occurs in generally intact skin.

The pathogenesis of stasis dermatitis is not fully understood, but current findings indicate that inflammatory cells, such as macrophages, produce enzymes that play a role in skin tissue irritation and damage. Stasis dermatitis is characterized by poorly defined erythematous and scaly patches, as well as plaques on the lower legs, most commonly starting on the medial malleolus. The condition frequently causes itching, which helps differentiate it from other dermatologic processes, such as cellulitis.6

Evaluation

Evaluating patients for CVI begins with taking a history focused on predisposing factors and symptoms that would suggest the presence of venous problems. Symptomatology may include leg pain, leg heaviness or fatigue, lower extremity swelling (especially after standing), and burning pain over known varicosities. Patients may comment that they have varicose veins, or that they have noticed brown spots or discoloration over their lower legs that do not wash off.2

The clinician should inquire as to the patient’s occupation, as well as medical history, focusing on a history of deep vein thrombosis, phlebitis, varicose veins, injection drug use, trauma, lower extremity surgery, and any family medical history of varicosities or venous disease.2