Essentials of Diagnosis
- History of phlebitis or leg injury.
- Ankle edema is the earliest sign.
- Late signs are stasis pigmentation, dermatitis, subcutaneous induration, varicosities, and ulceration.
Chronic venous insufficiency is most often secondary to DVT, although a history of phlebitis is not obtainable in about 25% of patients. Other possible causes are leg trauma, varicose veins, neoplastic obstruction of the pelvic veins, or congenital or acquired arteriovenous fistula.
The basic physiologic abnormality in patients with chronic venous insufficiency is chronic elevation in venous pressure. The normal venous capacitance can accommodate large-volume changes that occur during exercise with only minimal changes in venous pressure. However, when valves in the deep or perforating veins are destroyed by thrombophlebitis, valvular reflux and bidirectional blood flow result in abnormally high ambulatory venous pressures. Proximal venous obstruction also results in venous hypertension. High ambulatory venous pressure transmitted through perforating veins of the calf and ankle results in superficial varicosities, edema and fibrosis of the subcutaneous tissue and skin, hyperpigmentation, and, later, dermatitis and ulceration.
Chronic venous insufficiency is characterized by progressive edema of the leg that begins at the ankle and calf and is accompanied by a dull aching discomfort. Typically, the edema is worst at the end of the day and improves with leg elevation. Varicosities are often present. Stasis dermatitis, brownish pigmentation, brawny induration, and ulceration develop with long-standing disease. The skin is usually thin, shiny, atrophic, and cyanotic. Cellulitis may appear in scaly, dry, itchy regions with skin breakdown; in other areas, a weeping dermatitis may develop. Venous stasis ulcers are large, painless, and irregular in outline. They have a shallow, moist granulation bed and occur in the gaiter area on the medial or lateral aspects of the ankle. Healing of these ulcers results in a thin scar on a fibrotic base that often breaks down with minor trauma.
Congestive heart failure and chronic renal disease may result in bilateral edema of the lower extremities. Lymphedema is associated with a brawny thickening in the subcutaneous tissue that does not respond readily to elevation; edema is particularly prominent on the dorsum of the feet and in the toes; varicosities are absent, and there is often a history of recurrent cellulitis.
Primary varicose veins or acute DVT may be difficult to differentiate from chronic venous insufficiency without diagnostic tests.
Other conditions associated with chronic ulcers of the leg include autoimmune diseases (eg, Felty’s syndrome), arterial insufficiency (often painful, well circumscribed, and located over pressure points), sickle cell anemia, erythema induratum (bilateral and usually on the posterior aspect of the lower part of the leg), and fungal infections (cultures specific; no chronic swelling or varicosities).
The irreversible tissue changes that accompany chronic venous stasis disease can be minimized by early and aggressive management of conditions associated with deep venous reflux such as acute DVT and varicose veins.
A. General Measures
The key to successful management of chronic venous stasis disease is the realization that it is an incurable but manageable problem. Most patients respond to a conservative treatment program. The causes of complications of chronic venous insufficiency are largely mechanical, and so the solutions are mechanical. Bed rest with leg elevation is fundamental in the treatment of the acute complications. Similarly, chronic care of the leg includes (1) intermittent elevation of the legs during the day and elevation of the legs at night (kept above the level of the heart with pillows under the mattress), (2) avoidance of long periods of sitting or standing, (3) the daily use of fitted knee-high or thigh-high graduated compression stockings (20-30 mm Hg), and (4) regular exercise.
B. Management of Stasis Dermatitis
Eczematous eruption may be acute or chronic; treatment varies accordingly. The simplest treatment for acute weeping dermatitis is strict bed rest, leg elevation, and wet saline compresses. Antiseptic solutions containing peroxide, boric acid, or buffered aluminum acetate (Burow’s solution) are not recommended because they impede wound healing. Cadexomer iodine is an iodine-containing starch powder dressing that has been shown to speed healing of weepy ulcers. Alginate dressings are also effective in this setting. In general, however, no definitive advantage has emerged of occlusive over semiocclusive dressings or of topical antibiotics, growth factors, or free radical scavengers over simple inert dressings.
Systemic antibiotics and topical antifungal agents (1% clotrimazole or 2% miconazole cream) are indicated only if active infection is suspected. With reduction of the acute edema, 0.5% hydrocortisone cream is applied to the area for 1-2 weeks or until no further improvement is noted. Cordran tape, a plastic tape impregnated with flurandrenolide, is a convenient way to apply both medication and dressing. Zinc oxide ointment with ichthammol, 3%, applied once or twice daily, is an alternative treatment for chronic dermatitis.
Venous ulcerations can be treated by wet-to-dry normal saline dressings and Ace wrap compression, or with an Unna boot. The Unna boot is a layered dressing composed of a medicated bandage (such as the original Dome paste composed of calamine, zinc oxide, glycerin, sorbitol, gelatin, and magnesium aluminum silicate), followed by a gauze dressing, followed by an elastic wrap. It must be kept dry and is usually changed weekly. Occasionally, the ulcer is so large and chronic that wide debridement and skin grafting are the best approach. This can be combined with open or endoscopic ligation of incompetent perforating veins contributing to elevated venous pressure in the ulcer bed. Venous reconstructive surgery is performed in some centers for intractable chronic venous stasis disease. The goal of the surgery is to increase venous outflow and decrease venous hypertension in the limb by repairing or replacing incompetent valves in the deep system. Valvuloplasty, venous segment transposition, and valvular transplantation have been performed with variable reported success rates.
Recurrent venous stasis ulcers and progressive venous stasis changes of the skin are not uncommon, particularly if patients do not adhere to a lifelong routine of intermittent leg elevation, regular exercise, and use of graduated compression stockings.
Berliner E et al: A systematic review of pneumatic compression for treatment of chronic venous insufficiency and venous ulcers. J Vasc Surg 2003;37:539.
Mohr DN et al: The venous stasis syndrome after deep venous thrombosis or pulmonary embolism: a population-based study. Mayo Clin Proc 2000;75:1249.
Tawes RL et al: Optimal therapy for advanced chronic venous insufficiency. J Vasc Surg 2003;37:545.
Revision date: June 20, 2011
Last revised: by Dave R. Roger, M.D.