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VENOUS DISEASE

Varicose veins

The venous system is lined with one-way valves that direct blood back to the heart. With age, or as a result of inherited poor or absent valves, these valves may become progressively incompetent. Dilated or varicose veins result.

    Large varicose veins (Fig.15.47) and smaller telangiectases (spider veins) occur on the legs. One of the first signs of venous insufficiency is the ankle flare (Fig.15.48), which appears as a crown of dilated venules about the medial ankle. Occasionally, a superficial varicosity may ulcerate through the skin, with significant bleeding.

    Investigation to define the origin and extent of the varicose veins and the competence of the deeper venous system can involve physical examination, blood pressure measurement, Doppler ultrasound, and phlebography. Sclerotherapy may be helpful for smaller vessels, surgery for larger lesions. An intense pulsed light source is effective for leg veins of 0.1–3mm in diameter, with most cases showing better than 50% clearance.

Acroangiodermatitis

This disease is a vascular lesion of the extremities, clinically resembling Kaposi sarcoma. It may occur in the setting of venous insufficiency or it may arise over either a congenital vascular malformation or an acquired arteriovenous fistula (Fig. 15.49).

Figure 15.47 Varicose veins.

Figure 15.48 Ankle flare. A crown of dilated venules about the medial ankle is a sure sign of underlying chronic venous insufficiency. No treatment is needed, but appropriate work-up and therapy for chronic venous insufficiency may be needed at some point. (Sclerotherapy may be used in appropriate cases.)

Stasis dermatitis and venous ulceration

Etiology and pathogenesis

Stasis dermatitis is an eczematous condition of the leg that results from edema. If the stasis is severe, ulceration may result. The calf pump mechanism ensures adequate blood flow through the lower leg. When the calf muscle contracts, the blood is forced out and back to the heart. When the muscle relaxes, reflux of blood is prevented by venous valves. If either the superficial or deep venous valves are incompetent, venous hypertension occurs. If the muscle does not contract adequately in the first place, musculoskeletal calf pump dysfunction may occur. Osteoarthritis, stroke, rheumatoid arthritis, or obesity are common causative factors.

Clinical

The patient will present with swollen legs and a red, scaly rash over the medial part of the ankle (Figs 15.50 and 15.51). The entire lower leg may be involved. In later stages, the skin may develop a red-brown hue secondary to hemosiderin deposition. Allergic contact dermatitis to topical medication may complicate the clinical picture. Lipodermatosclerosis may also be present.

Figure 15.49 Acroangiodermatitis in the setting of venous insufficiency.

    In severe cases, ulceration may develop. A venous ulcer is most common just above the medial malleolus. This is where venous hypertension is the highest. The ulcer is usually moist. The edges may be raised up or relatively level with the base of the ulcer. The surrounding skin may be eczematous. An odor may result from infection or simple colonization (Fig. 15.52).

Differential diagnosis

The differential diagnosis of leg ulceration is given in Table 15.4.

    Venous eczema is usually apparent by its distribution, but asteatotic eczema, eczema due to sudden development of leg edema, and contact dermatitis (either primary or as a complication of treating venous eczema or ulcers) need to be excluded.

    Bacterial colonization of ulcers may need to be distinguished from local cellulitis.

Treatment

Leg edema must be controlled or prevented. Prolonged standing should be avoided. Walking is allowed. Elevate the legs, ankle above the heart, for 20min every 2–3 h. Elevate the foot of the bed 2–3 inches. Compression stockings or bandages from the mid-foot (including the heel) to just below the knee are essential. A three- or four-layer compression bandage (multilayer elastic compression) is very helpful in treating both stasis dermatitis and stasis ulcer. However, an ankle:brachial systolic pressure ratio should be calculated. If significantly lower than 0.8, then arterial compromise is present and compression therapy should not be used; compression should be used with caution if the ratio is between 0.8 and 1.0.

    Salt restriction may be needed to control swelling. Diuretics may be appropriate for some patients with cardiac disease causing edema. Medium-potency topical steroid ointments twice daily are useful for eczematous changes. Soaks twice a day are helpful if the skin is exudative. Scratching should not be allowed.

    If ulceration has developed, wound care must be carried out, including daily wound cleansing followed by application of an occlusive dressing. Stop all topical salves except those absolutely necessary, as allergic contact dermatitis is common. Once the ulcer is clean, a four-layer bandage can be applied for a week at a time.

    Both superficial and deep venous incompetence occur, and sclerotherapy or surgery may speed healing and/or reduce recurrences. The lesion should be monitored for secondary infection by both bacteria and Candida . Any putrid smell may be combated with metronidazole gel. If the ulcer is uninfected, a plaster boot (e.g. Unna boot) may be applied and changed every 1–2 weeks.

    Pentoxifylline 400–800mg t.i.d. when combined with compression does seem to improve healing rates.

Atrophie blanche

A stellate white scar is seen on the ankle. Many consider atrophie blanche to be the scarred end point of various diseases (Fig. 15.53).

Figure 15.50 Stasis ulcer. Any ulcer in this location with surrounding edema, redness, and scale is typical of a stasis ulcer.

Figure 15.51 Stasis dermatitis. (a) Red, scaly changes over the medial ankle have developed in this older man with impaired venous circulation. (b) A leg that served as the donor site of a vein graft is at increased risk for stasis dermatitis. (c) Stasis dermatitis associated with varicose veins. In this patient, eczematous changes occurred over varicose veins. (d) The leg on the left shows active disease, whereas the one on the right shows chronic changes.

Figure 15.52 Basal cell carcinoma. This chronic ulcer of the shin was treated for 2 years as a venous ulcer. A biopsy should be performed on any non-healing leg ulcer.

Figure 15.53 Atrophie blanche.

Lipodermatosclerosis

Lipodermatosclerosis, also known as sclerosing panniculitis, represents deep stasis; that is, the dermis and fat develop inflammation and sclerosis in the setting of venous insufficiency. In the acute phase, the skin of the medial lower leg, just above the ankle, is tender, warm, and erythematous. Ulceration is uncommon. As the condition becomes chronic, the skin becomes indurated and adherent. Other signs of chronic venous insufficiency may be noted (Fig.15.54). A biopsy should be avoided if possible, as healing will invariably be difficult. Large series associate lipodermatosclerosis with female gender, high body mass index, venous disease, and middle age.

    The usual measures to diagnose and treat chronic venous insufficiency should be followed, with emphasis on the faithful use of compression stockings. Stanozolol (2mg twice a day) has been recommended for the acute phase, although it may cause significant side effects and should be used only by those familiar with it. It is also helpful to reduce the chronic signs of lipodermatosclerosis, but not to heal any ulcers that have developed. Pentoxifylline (400mg three times a day) has been suggested.

PRACTICE POINTS

White/Cox: Diseases of the Skin, 2ed.(c) 2006, Elsevier Inc. All rights reserved.