Leg Ulcers
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[edit] Leg Ulcers
Carolyn I. Hale
[edit] EPIDEMIOLOGY/ETIOLOGY
There are many causes of leg ulcers (Box 93-1). Venous insufficiency accounts for 80% to 90%, arterial insufficiency for 5%, and a mixture of arterial and venous accounts for another 5%. Approximately 2% of ulcers are caused by diabetes and only 1% of ulcers will be caused by one of the many diseases listed in Box 93-1. Ulcers are costly to treat, cause loss of work time, and tend to be chronic and recurrent. Median duration of ulceration was 9 months, and 20% had not healed in over 2 years. The great majority of patients have recurrence.
| Box 93-1 - Differential Diagnosis of Leg Ulcers |
Vascular
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[edit] PATHOPHYSIOLOGY
Venous ulcers, also known as varicose ulcers, venous hypertension ulcers, venous stasis ulcers, or postphlebitic ulcers are caused by the common mechanism of too much hydrostatic pressure in the superficial venous system of the leg. At least 80% of the time this is caused by incompetent valves in deep veins. In the leg, venous blood is returned to the heart via the deep venous system and the superficial venous system. The superficial system, consisting of the short and greater saphenous veins and their tributaries, is emptied into the deep system via perforating veins. Directional flow is maintained by a series of one-way valves. Flow is maintained by the pump action of the calf muscle or elevation of the leg above the level of the heart. Alteration in this system by a previous deep venous thrombosis is the most common predecessor of leg ulcers, although frequently there is no clinical history of thrombosis. Incompetent superficial veins leading to varicose veins account for less than 20% of leg ulcers. This group can be surgically cured and should be identified. Trauma to the leg and rare congenital fistulas cancause arteriovenous fistulas, which also result in venous hypertension.
Basically, an increased venous pressure results in increased pressure in the capillary bed, transudation of fluid and protein into the interstitial space, and altered delivery of oxygen and nutrients to the skin and subcutaneous tissues resulting in ulceration of the overlying tissue. Current theories of the pathophysiology are more complex than this. In 1982, Browse and Burnand suggested that increased back pressure into the capillaries distended endothelial gaps, allowing for leaky capillaries. Fibrin then forms around the capillaries and impedes oxygen diffusion. These findings of pericapillary fibrin cuffs have been confirmed with immunologic staining. It is also known that fibrinolysis is abnormal in this group of patients, but the clinical importance of this is unknown. More recent evidence supports a trapped leukocyte theory. With decreased perfusion pressure, white cells become trapped in the capillaries and release proteolytic enzymes and superoxide radicals that cause endothelial damage. This damage may result in leaky capillaries and fibrin deposition, as well as blockage of local capillary filling and resultant ischemia.
Arterial ulcers are primarily a result of arteriosclerosis obliterans of the lower extremity as previously described. Although this accounts for only 5% to 10% of all leg ulcers, by the age of 80, over 90% of patients have an arterial component. In other words, a venous ulcer at age 50 will become a mixed venous and arterial ulcer by the time the patient reaches 80 and treatment will need to be changed to address the arterial component. Risk factors are diabetes mellitus, smoking, hyperlipidemia, hypertension, and early menopause in women.
Diabetes mellitus results in ulceration from atherosclerosis, peripheral neuropathy, and less commonly necrobiosis lipoidica, diabetic dermopathy, and bacterial and fungal infections. Hyperemia and capillary hypertension, loss ofautoregulation and neurogenic regulation, disturbed endothelial function, and abnormal rheology also play a part in the abnormal microcirculation of diabetic patients.
The pathophysiology of other leg ulcers varies with the disease. A few of these are mentioned briefly. Rheumatoid arthritis is associated with ulcers both from vasculitis and from immobility of the leg with resultant inadequate venous return. In sickle cell anemia there is an incidence of ulcers of 25% to 75%, probably from the abnormal rheologic properties of the red blood cells resulting in an ulcer that resembles venous ulcers. Recurrent hemorrhages and infections also play a role. Other hematologic diseases also share common factors with venous ulcers. Polycythemia vera results in increased viscosity, as do various dysproteinemias.
Pyoderma gangrenosum most likely represents a small vessel vasculitis, although not all cases show vasculitis. It may be associated with ulcerative colitis, rheumatoid arthritis, leukemias, regional enteritis, or may occur without any underlying disease.
Drugs may cause ulcers by a number of mechanisms. Hydroxyurea may cause ulcerative lichen planus or a livedo vasculitis-like picture. Some drugs, such as corticosteroids, alter wound healing, although low antiinflammatory products (e.g., cortisone acetate and prednisone in oral doses under 10 mg daily) have no appreciable effect on wound healing. Coumarin necrosis is a rare disease caused by an imbalance in the anticoagulant and procoagulant factors. Inhibition of production of protein C and protein S in hereditary deficiency states or rarely acquired deficiencies associated with disseminated intravascular coagulation, multiple myeloma, and the lupus anticoagulant may disproportionately balance the coagulation system toward thrombosis in early coumarin treatment (see Chapter 115 ).
Antibodies to phospholipids cause recurrent thrombosis with a vasculitic-appearing ulcer. These antibodies are manifested by false positive VDRL, a lupus anticoagulant, or anticardiolipin antibodies, and may be associated with lupus and lupus-like diseases and livedo vasculitis and may cause their effects through interactions with protein C or protein S. It has been proposed that they may promote thrombosis by binding to endothelial cells and impairing prostacyclin release or damaging platelet adhesiveness.
The clinical features of leg ulcers are frequently nonspecific, although several characteristics can help identify the most common types of ulcers (Table 93-1).
Table 93-1 Physical Examination
| Â | Venous | Arterial | Diabetic | Vasculitic |
|---|---|---|---|---|
| Location | Medial malleolus, gaitor area. | Toes, heels, bony prominences of foot, lateral malleolus, rarely over medial malleolus. | Same as arterial trophic ulcers on pressure points on the plantar foot, especially metatarsal heads. | Pretibial and dorsum of foot but may be any-where and frequently is also on other areas. |
| Appearance | Irregularly shaped, surrounded by brown pigmentation with edema or sometimes fibrotic, hard skin (lipo-dermatosclerosis). Ulcer base has granulation tissue and exudate, and the borders may be hyperkeratotic. | Punched out ulcer with round well-demarcated borders and pale or white ulcer bed. Sometimes covered with dry eschar. Surrounding skin cool atrophic and hairless. | Punched out, often surrounded by hyper-keratotic borders; purulent drainage may indicate osteomyelitis. | Palpable purpura, hemorrhagic vesicle, typically small and multiple, with black, gray, or yellow base and minimal or no granulation tissue; may have thin undermined border; surrounding skin shows reticulated vascular pattern. |
| Pain | Increases with leg dependency, decreases with elevation. | Frequently very painful. Decreases with leg dependency, increases with exercise and leg elevation. | Painless but associated with paresthesia, anesthesia, inconstant, mostly at night. | Extremely painful. |
| Vascular examination | Ankle/brachial index greater than 0.9. Pulses present. Plethysmography or Doppler studies show abnormal venous system. | Ankle/brachial index less than 0.9. Pulses decreased. Abnormal pallor of leg with elevation, and subsequent rubor with dependency. Delayed venous filling. | Mixed, usually associated with arterial disease. | Normal. |
| History | Edema, trauma, rapid onset. Thrombophlebitis 20% varicosities. | Arteriosclerosis, claudication. Usually >45 yr. Slow progression. | Diabetes mellitus; peripheral neuropathy. | Association with other systemic disease; rapid onset. |
| Treatment | Leg elevation, compression by elastic bandages or stockings, 30 mm Hg, moist wound dressings. Grafts. | Vascular surgical consultation. No compression. Moist wound dressings. Pentoxyphylline? | Control diabetes; careful wound care, early intervention for infections; vascular surgical consult. | Control underlying disease; nonadherent dressings; oral steroids, ASA, bed rest. |
Extensive laboratory testing is not necessary except in unusual ulcers. Generally a complete blood count, glucose, sedimentation rate, albumin, protein, and thyroid screen are sufficient. If a vasculitis is suspected an antinuclear antibody, rheumatoid factor, syphilis serology, cold agglutinins, cryoglobulins, serum protein electrophoresis, protein C and S levels, and anticardiolipin antibodies may be evaluated.
Bacteriologic cultures of the wound are not necessary and are frequently misleading as most wounds are colonized. If there is clinical evidence of cellulitis, a culture should be taken to direct antibiotic therapy. A tissue biopsy is the most accurate method and is necessary if deep fungal or acid-fast organisms are suspected by the clinician.
Biopsies of a leg ulcer should be undertaken with caution. Frequently the biopsy site will not heal, and the patient is left with another ulcer. However, if an ulcer does not heal for 4 months on adequate therapy, a biopsy from the ulcer edge should be taken.
Vascular studies are needed when pulses are nonpalpable. An ankle/brachial pressure index should be measured in all patients. Venous studies are indicated if needed to confirm the diagnosis of venous ulcers or in the case that superficial varicose veins are the cause. In this case, surgical intervention can prevent recurrent disease and compression stockings will not be needed.
[edit] MANAGEMENT
Although there are a number of causes of leg ulcers, the most common cause is venous insufficiency. Compression therapy is the most important treatment for these ulcers. Moist wound dressings, growth factors, and grafting, although beneficial in treatment of venous ulcers, pale in comparison to the use of adequate compression of the leg. Arterial ulcers, however, should not be compressed for fear of further arterial compromise. Treatment of this condition is discussed in Chapter 70 . Once an ulcer is healed continued care will be needed to prevent recurrences (Fig. 93-1).
[edit] ADDITIONAL READINGS
- KG Burnand,et al.: Pericapillary fibrin deposition in the ulcer bearing skin of the lower limb, the cause of lipodermatosclerosis and venous ulceration. Br Med J 1982; 285:1071.
- MJ Callam, DR Harper, JJ Dale,et al.: Chronic ulcer of the leg: clinical history. Br Med J 1987; 294:1389.
- PD Coleridge-Smith,et al.: Causes of venous ulceration: a new hypothesis. Br Med J 1988; 296:1726.
- MD Flynn, JE Tooke: Aetiology of diabetic foot ulceration: a role for the microcirculation?. Diabet Med 1992; 8:320.
- M Harahap,et al.: Leg ulcers. Clin Dermatol 1990; 8:3 - 4.
- TJ Phillips,et al.: Leg ulcers. J Am Acad Dermatol 1991; 25:965.
- L Renfro, J Moy, M Sanchez: Cutaneous ulcers caused by drugs. Wound 1990; 2 (6):236 - 246.
- TJ Ryan: Current management of leg ulcers. Drugs 1985; 30:461.
- JR Young: Differential diagnosis of leg ulcers. Cardiovascular Clin 1983; 13:171.
