ICD-9 : 459.81 ° ICD-10 : I87.2
Epidemiology and Etiology
Varicose veins: peak incidence of onset 30–40 years. Varicose veins are three times more common in women than in men.
CVI is most commonly associated with varicose veins and the postphlebitic syndrome. Varicose veins are an inherited characteristic.
Pregnancy, increased blood volume, increased cardiac output, increased venocaval pressure, progesterone.
The damaged valves of the deep veins of the calf are incompetent at restricting backflow of blood. Damaged communicating veins connecting deep and superficial calf veins also cause CVI in that blood flows from deep veins to superficial venous plexus. Fibrin is deposited in the extravascular space and undergoes organization, resulting in sclerosis and obliteration of lymphatics and microvasculature. Perivascular fibrosis results in diminished nutrition of the epidermis, which breaks down with ulcer formation.
This cycle repeats itself: initial event → aggravation of venous stasis and varicose vein dilatation → lipodermatosclerosis → thrombosis → stasis dermatitis → ulceration.
Prior episode(s) of superficial phlebitis and DVT. Risk factors are listed in Table 16-1.
CVI commonly associated with heaviness or aching of leg, which is aggravated by standing (dependency) and relieved by walking. Lipodermatosclerosis may limit movement of ankle and cause pain and limitation of movement, which in turn increases stasis. Leg edema aggravated by dependency (end of the day, standing), summer season. Shoes feel tight in the evening. Night cramps.
A simple staging system for CVI is shown in Table 16-2.
Table 16-2 Staging of CVI (CEAP Classification) |Favorite Table|Download (.pdf)
Table 16-2 Staging of CVI (CEAP Classification)
Clinical Picture (C)
C0 no clinical signs
C1 small varicose veins
C2 large varicose veins
C4 skin changes
C5 healed ulcer
C6 active ulcer
Ap perforans (communicating vein)
Pr,0 reflux +obstruction
Superficial leg veins are enlarged, tortuous, with incompetent valves; best evaluated with the patient standing (Fig. 16-7A). “Blow-out” at sites of incompetent communicating veins. Tourniquet test: A tourniquet is applied to the leg that has been elevated to empty the veins; when the patient stands up and the tourniquet is released, there is instant filling of a varicose vein due to absent or ill-functioning valves. Varicose veins may or may not be associated with starburst phlebectasia usually overlying the area of an incompetent communicating vein (Fig. 16-7B). These small venectasias per se have no pathogenic significance but are of cosmetic concern to the patient. Superficial venectasias (spider phlebectasia) without a starburst pattern occur also and far more commonly without CVI, usually on the thighs and lateral lower legs in women.
Varicose veins A. There are meandering and convoluted irregular varicose veins on the thigh of a 70-year-old man who also had lipodermatosclerosis and stasis dermatitis on the lower legs. B.Starburst venectasias on the calf. This is an area overlying an insufficient communicating vein.
Dependent; improved or resolved in the morning after a night in the horizontal position. Dorsa of feet, ankles, lower legs.
Eczematous (Stasis) Dermatitis
Occurs in setting of CVI about the lower legs and ankles (Fig. 16-8). It is a classic eczematous dermatitis with inflammatory papules, scaly and crusted erosions; in addition, there is pigmentation, stippled with recent and old hemorrhages (Fig. 16-9); dermal sclerosis; and excoriations due to scratching. It must be distinguished from contact dermatitis secondary to topical agents, with which it is often combined. In addition, there may be concomitant irritant dermatitis due to secretion from stasis ulcer (see below) and bacterial colonization. If extensive, may be associated with generalized eczematous dermatitis, i.e., “id” reaction or autosensitization (see Section 2).
Stasis dermatitis in CVI A patch of eczematous dermatitis overlying venous varicosities on the medial ankle in a 59-year-old woman. The lesion is papular, scaly, and itching.
Chronic venous insufficiency. Atrophie blanche An area of diffuse and mottled pigmentation due to hemosiderin and ivorywhite patches of atrophie blanche. Such lesions are both itchy and painful.
Small ivory-white depressed plaques (Fig. 16-9) on the ankle and/or foot; stellate and irregular, coalescing; stippled pigmentation; hemosiderin-pigmented border, usually within stasis dermatitis. Often following trauma.
Inflammation, induration, pigmentation of lower third of leg creating “champagne bottle” or “piano leg” appearance with edema above and below the sclerotic region (Fig. 16-10). “Groove sign” created by varicose veins meandering through sclerotic tissue. A verrucous epidermal change can occur overlying the sclerosis; if combined with chronic lymphedema, it is referred to as elephantiasis nostras verrucosa. In long-standing sclerosis, calcification can occur.
Chronic venous insufficiency and lipodermatosclerosis The ankle is relatively thin and the upper calf edematous, creating a “champagne bottle” or “piano leg” appearance. A. Varicose veins are embedded in pigmented, sclerotic tissue. There are also areas of atrophie blanche. B. Varicose veins are less visible here but can be easily palpated in the sclerotic plaque encasing the entire calf (“groove” sign). There is also pigmentation and minor papular stasis dermatitis.
Occurs in 30% of cases; very painful “hyperalgesic microulcer” in area of atrophie blanche; larger superficial or deep ulcers, sharply defined with deep margin, necrotic base surrounded by atrophie blanche, stasis dermatitis, and lipodermatosclerosis (Fig. 16-11). Venous ulcers usually occur medially and above ankles (Fig. 16-11). Venous ulcers and their differential diagnosis are discussed in more detail below (Most Common Leg/Foot Ulcers).
Venous insufficiency A. Two coalescing ulcers with a necrotic base in an area of atrophie blanche, lipodermatosclerosis, and stasis dermatitis. Scratch marks indicate itchiness of surrounding skin, while the ulcers are painful. B. A giant ulcer, well-defined with scalloped borders and a beefy red base in a leg with lipodermatosclerosis.
Doppler and Color-Coded Duplex Sonography
These detect incompetent veins, venous occlusion due to thrombus.
Contrast medium is injected into veins to detect incompetent veins and venous occlusion.
X-ray may show subcutaneous calcification (10% of chronic cases), i.e., postphlebitic subcutaneous calcinosis. Bony changes include periostitis underlying ulceration, osteoporosis as a result of disuse, fibrous ankylosis of ankle. Osteomyelitis.
Early: small venules and lymphatic spaces appear dilated; edema of extracellular space with swelling and separation of collagen bundles. Later: capillaries dilated, congested with tuft formation and tortuousity of venules; deposition of fibrin. Endothelial cell hypertrophy: may be associated with venous thrombosis; angioendotheliomatous proliferation mimicking Kaposi sarcoma. In all stages, extravasation of red blood cells that break down forming hemosiderin, which is taken up by macrophages. Lymphatic vessels become encased in a fibrotic stroma, i.e., lipodermatosclerosis. Calcification of fat and fibrous tissue may occur.
Usually made on history, clinical findings, Doppler and color-coded Duplex sonography, phlebography.
Compression dressings or stockings; Unna boot.
Avoid trauma to area involved. Intralesional triamcinolone into painful lesions. Compression.
Topical gluscocorticoids (short term). Topical antibiotic treatments (e.g., mupirocin) when secondarily infected. Culture for methicillin-resistant Staphylococcus aureus (MRSA).
A sclerosing agent such as tetradecyl sulfate is injected into varicosities, followed by prolonged compression. Used mainly to treat minor branch varicosities not associated with saphenous incompetence and new branch vein varicosities developing after surgery. Recurrence is common within 5 years.
Incompetent perforating veins are identified, ligated, and cut, followed by stripping long and/or short saphenous veins out of the main trunk. Residual perforating veins are the main cause of recurrences after surgery. In patients with combined arterial and CVI, bypass or angioplasty may prove beneficial.
These new technologies encompass endoscopic subfascial dissection of perforating veins (employed primarily in the elimination of insufficient perforating veins in CVI); and endoscopic endovenous diode laser or radiofrequency thermal heating, which leads to occlusion of varicose vein.