Symptoms of CVI are variable and include leg tiredness, cramping, itching, burning, and swelling. Physical findings may include prominent dilated superficial veins, edema, skin changes, and ulceration.

The typical presentation of a patient with CVI is one of edematous lower extremities (unilateral or bilateral) with hyperpigmentation, eczema, and/or lipodermatosclerosis (scarring of the skin and fat). Accompanying varicose veins or skin ulceration may also be present. Edema is the initial finding and most commonly occurs at and above the ankle, without involvement of the forefoot or toes. It usually responds to leg elevation and is typically worse in the evening. When ulcers occur, they are most often large, irregular, and associated with a shallow moist granulation base (Fig. 22.1). They are often very painful and occur on the medial or lateral surface of the leg in the supramalleolar position. Because of the significant variability in the manifestations and severity of CVI, several classification schemes have been designed to help categorize patients. Two such schemes will be briefly reviewed later in this chapter.

The symptoms of CVI (pain, edema, skin changes, and ulcerations) must be distinguished from other etiologies of these symptoms. Likewise, venous ulcers can be mistaken for other lesions such as squamous cell carcinoma (Marjolin’s ulcers).

The pathophysiology of CVI can be broken down into changes occurring at the level of the large venous vessels, the microvasculature, and the tissue. CVI occurs as a result of valvular dysfunction within the large veins of the leg. The resulting standing column of blood leads to venous hypertension. Venous hypertension is defined as end-exercise venous pressure at the ankle greater than 30 mm Hg (normal is 15 mm Hg). This, in turn, leads to capillary dysfunction and tissue injury. Common causes of valvular dysfunction include primary valvular incompetence and secondary valvular incompetence after DVT. In patients with no history or evidence of DVT, primary valve abnormalities such as valvular agenesis or aplasia are most likely, although vein wall abnormalities can also lead to valvular insufficiency. Contemporary data in DVT patients suggest that the incidence of severe CVI after 8 years follow-up is approximately 30% and may be even higher if associated with ipsilateral recurrent DVT. It has also been shown that valvular dysfunction occurs more commonly if there is delayed DVT resolution and if the more proximal veins are involved in the initial venous thrombosis. Skin ulceration is also more common in patients with recurrent DVT. Risk factors for DVT formation can be inherited, acquired, or multifactorial (Table 22.1). Once valvular dysfunction occurs, the ensuing chronic venous hypertension has profound effects at the microvascular level. Capillaries become dilated and
tortuous, allowing extravasation of fluid, red blood cells, and macromolecules. There is an increase in white blood cell adhesion to the endothelium as well as leukocyte activation. Increased microvascular blood flow is seen initially, but there can be late findings of capillary thrombosis leading to tissue hypoxia. Within the tissues, the extravasated red blood cells break down to produce a dark pigment called hemosiderin. The perivascular space becomes surrounded by intracellular matrix proteins. Chronic accompanying inflammation leads to scarring and fibrosis of the subcutaneous tissues. Macrophages, mast cells, and T lymphocytes are the cell types most commonly involved in tissue destruction. As skin perfusion decreases, the resulting ischemia can lead to skin breakdown and ulceration.

As illustrated in the previous section, there are many manifestations of venous hypertension. Due to the variety of presentations, it is important to standardize the classification of degree of CVI. The most commonly used classification is the CEAP system illustrated in Table 22.2. In addition, the Villalta

scoring system and Venous Clinical Severity Score (VCSS) system have been described in order to objectively describe the clinical response. The Villalta scale gives 0 (none) to 3 (severe) points for five patient-given symptoms and six physician-observed signs. A score greater than 5 is consistent with the postthrombotic syndrome and has been shown to correlate with quality of life. The VCSS also awards 0 (none) to 3 (severe) for ten different complaints (see Table 22.3). These systems are recommended by various organizations including the American Venous Forum in order to standardize reporting and allow more objective observation of clinical benefit and improved research.

Several diagnostic studies may be employed in the evaluation of CVI, and they can be divided into invasive and noninvasive tests. A careful history and physical examination including arterial evaluation form the cornerstone of diagnostic evaluation. Within the last 10 years, duplex ultrasound has become the primary noninvasive diagnostic modality due to high sensitivity and specificity rates greater than 95%. Duplex ultrasound is safe during pregnancy and may also elucidate other causes of the patients’ symptoms. Additional noninvasive tests may be performed selectively and include air plethysmography (APG). Magnetic resonance venography or invasive testing such as phlebography is usually reserved for the evaluation of proximal venous structures in patients in whom surgical treatment is being considered. Historically, the Brodie-Trendelenburg test has been performed as an in-office evaluation for patients with prominent varicose veins. This tourniquet-based test, which helps discriminate saphenofemoral junction (SFJ) incompetence from deep-to-superficial communication via incompetent perforators, has been supplanted by the use of ultrasoundbased testing and is not usually performed in modern practice. The duplex evaluation helps localize specific perforators that may be contributing to the varicosities along with other points of reflux and may discriminate obstruction from valvular incompetence and reflux.