A thorough understanding of underlying pathological problems and the roles of compression and ambulation are integral components in the management of venous leg ulcers.

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enous leg ulcers have often gone unrecognized, misdiagnosed, and ineffectively treated. In the past 10 years, however, significant strides have been made in understanding and managing this medical “step child.” Chronic venous disease is most likely the underlying cause in 80–95% of lower leg

Table 1

ulcers.^1,2 Venous leg ulcers are a chronic and debilitating medical condition. These ulcerations have been commonly known as venous stasis ulcers, since their occurrence was thought to be due to a blood pooling in the venous system of the lower extremity.³ Today, however, this is known to be untrue; they are most likely the result of venous hypertension.² Venous leg ulcers are usually located over the inner aspect of the ankle or gaiter area (see Figure 1), and recurrence at the same location is common.⁴

Figure 1

       Risk factors for development of venous disease (eg, ulcers) include aging, being female, a history of leg injury, obesity, phlebitis, a family history of varicose veins, smoking, a sedentary lifestyle (ie, prolonged standing or sitting), deep-venous thrombosis (DVT), and previous varicose vein surgery (see Table 1).

Blood Return to the Heart

       Blood return from the legs to the heart is accomplished by the venous system.

Figure 2

This system is comprised of the superficial veins (ie, those just below the skin) and the deep veins in the leg muscles. The superficial and deep-vein systems are joined by perforator or communicating veins (see Figure 2).These veins are thin, low-pressure blood vessels that have unidirectional bicuspid valves (see Figure 3). The valves in the perforator veins ensure that blood flows from the superficial system into the deeper system. The unidirectional valves in the perforator veins are crucial in preventing backflow or regurgitation that increase pressure within the superficial system.

Figure 3

       Normal pressure in a supine person is approximately 10 mmHg. When a person stands, a hydrostatic pressure in the ankle area increases to around 80 mmHg. During ambulation (ie, walking, running, or biking, as the foot is dorsiflexed and a person pushes off on the ball of the foot), the calf muscles compress the deep-venous system, increasing the pressure to 150–250 mmHg. This increase in pressure snaps the valves in the deep system open and propels the blood toward the heart. When the foot is in flexion, the valves in the deep veins close, and the system refills by allowing blood to pass through the perforator system from the superficial veins.⁵ This compression action of the calf muscle pump causes the hydrostatic venous pressure in the ankle region to gradually fall until it reaches a near-steady state (ie, 30 mmHg in the deep veins and 40 mmHg in the superficial veins). If the patient is standing still, the pressure in both systems will return to a stable level of about 90 mmHg in 20–30 seconds. This may place a sedentary or nonambulatory individual at greater risk for developing venous disease.

What Causes a Venous Leg Ulcer?

       In most ulcer occurrences, the valves connecting the superficial and deep veins are not functioning properly, resulting in a stretching and weakening of the vein wall. The valve leaflets fail to co-apt, and the system is unable to pump blood back to the heart against the force of gravity (ie, venous insufficiency). The failure of these valves allows blood flow from the deep veins back out to the superficial veins (ie, venous regurgitation), resulting in venous distention/tortuosity, which are recognizable as varicose veins and, more importantly, venous hypertension (the hallmark of venous disease).
       While the exact pathogenesis of venous ulcer formation is unknown, venous hypertension plays a major role in venous disease and ulceration. Pericapillary fibrin cuff formation and the trapping of white blood cells and growth factors both result in venous hypertension and have been proposed as probable mechanisms of ulcerations. Both culminate in an increased hydrostatic pressure, which extends to the most distal veins, including the perforating veins. Hypertension is transmitted to the capillaries, resulting in skin and subcutaneous tissue changes.
       The first proposed mechanism is fibrin cuffing.⁶ Venous blood pooling leads to dilatation and subsequent venous tortuosity. Pore-widening causes an increase in capillary permeability and edema formation. This results in a “leakage” of fibrinogen (polymerized to fibrin) accumulating in the dermis, forming a cuff around blood vessels. The fibrin cuff impedes the diffusion of oxygen and nutrients from the capillaries to the tissue, resulting in anoxia/ischemia, tissue death, and ulcer formation.
       The second mechanism is related to leukocyte cell trapping.⁷ The accumulation of fluid in the vein results in leukocytes activation, occlusion, and damage to the capillaries. These leukocytes may activate and release proteolytic enzymes, which lead to the formation of free radicals that ultimately may cause tissue damage.⁸ Activated leukocytes also can release cytokines, such as tumor necrosis factor (TNF), interleukin-1 (IL-1), and transforming growth factor (TGF b-1), an important mediator of dermal fibrosis. In addition to leukocyte activation, margination of white cells leads to oxygen deprivation of nearby tissues.

Diagnosing a Venous Leg Ulcer

       Diagnosis is usually made on the basis of the appearance, location, signs, and symptoms of the ulcer (see Table 2). Patients with suspected venous disease experience changes in the skin of the legs due to the hypertension in the venous system of the legs.

Table 2

Hemoglobin leaks out into the skin secondary to pooling of the venous blood and stains the skin a characteristic brown color (hemosiderin staining). Patients often complain of a dull, aching sensation in the legs on prolonged standing that is relieved with leg elevation. Assessment and clinical investigation should be undertaken by healthcare professionals trained and experienced in the management of leg ulcers. A comprehensive clinical history and physical examination, including blood pressure measurement, weight, urinalysis, and blood glucose level to rule out diabetes, should be recorded for a person presenting with his or her first or recurrent leg ulcer and should continue thereafter.
       The ankle brachial pressure index (ABPI) is the first line of defense in diagnosing venous disease. This is used to screen and rule out arterial disease.⁹ Indexing is accomplished by hand-held Doppler pressure measurement of the upper and lower extremities. The patient is placed in a supine position, and systolic brachial pressure measurements are taken in both arms. The higher of the 2 values is used as the brachial arterial measurement. Normally, there is less than a 10 mmHg difference between the 2 sides. An ankle pressure measurement is then taken from both lower extremities, using the anterior and posterior tibial arteries. The higher of these 2 measurements should be used as the ankle measurement. The selected ankle value is divided by the brachial value.
       A value of 0.9–1.2 is considered normal (see Table 3). A value of 0.75–0.90 indicates a mixed arterial venous disease and that compression is possible. An ABPI value of 0.50–0.75 indicates severe arterial disease and precludes compression.^3,10 It is possible that further tissue damage may occur at a value less that 0.75, and a vascular surgical consult is warranted if compression is to be done.
       Venography, an invasive examination, has historically been used for diagnosis of venous disease like a thrombus. During a venogram, contrast dye is injected directly into the veins to visualize flow and valve damage. This method is not without complications, including reaction to the contrast dye or infection, so it has given way to noninvasive forms of testing.

Table 3

       Doppler bidirectional-flow and Duplex color-flow ultrasonography studies are noninvasive tests used to assess venous flow velocity, its direction, venous valve function, and the possible presence of a thrombus. Duplex color-flow is now considered as the gold standard when evaluating the venous system.⁴ Light photoplethysmography uses infrared light/transducer to assess vascular competence (ie, capillary filling) during exercise. Increased capillary filling is indicative of venous reflux and, consequently, incompetent veins. Normal refill is greater than 18–20 seconds. A refill of 10–15 seconds is indicative of venous disease and less than 10 seconds is the heralding of a possible venous ulcer.

Ulcer Presentation

       Venous ulcers vary in size from very small to circumferential (ie, around the entire leg) and are usually located in the malleolar (gaiter area). Depending on severity of the ulcer, however, the associated signs of venous disease may extend up the lower leg. Clinically, the ulcer borders are irregular and often not well defined. The ulcer typically presents with moderate to heavy drainage, and the surrounding tissue may be edematous. A fibrous coating may cover the surface of the ulcer. The scar tissue often present is evidence of previous ulceration.
       In long-standing venous disease, scar tissue and the subcutaneous fibrosis/inflammatory process (lipodermatosclerosis) cause the tissue to become inflexible and have a woody appearance and texture. This tissue has lost its elasticity and will not stretch in the presence of edema. Further ulceration may develop at the site of old scars. Scar tissue does not have blood vessels, compromising local ulcer healing.
       Edema and hyperpigmented skin with induration in the gaiter area are the clinical characteristics of long-standing chronic venous insufficiency. Edema, with or without ulceration, may create a leaking of fluid through the skin, causing chronic itching. Frequently, pruritus and subsequent scratching by the patient cause a break in the skin that leads to a new ulcer and possible infection.

Complications

       Venous ulcers tend to be heavily contaminated and polymicrobial, with anaerobes reported in 30% of clinical noninfected wounds and Staphylococcus aureus, a facultative anaerobe, most prevalently isolated.¹¹ These ulcers are most often heavily colonized but rarely reach clinical infection. Bacterial overload can result in increased inflammatory cytokines and matrix metalloprotease (MMP) levels. This chronic increase is associated with decreased growth factor levels at the ulcer bed.
       Safe, broad-spectrum antimicrobials that inactivate microorganisms and wound dressing products containing these agents have been developed to address the needs of chronic wounds with the intent to minimize colonization and prevent local infection, thereby enhancing healing. A good example of this is the use of ionic silver. It is effective against both gram-negative and positive bacteria, including most methycillin-resistant Staphylococcus aureus (MRSA) and vancomycin-resistant enterococcus (VRE), viruses, fungi, and yeast. The amount of wound drainage can be considerable with venous ulcers. Therefore, an ionic silver impregnate, such as a calcium alginate, performs a dual role of absorption and delivery of the antimicrobial silver to the wound bed.
       Another resourceful antimicrobial is polyhexamethylene biguanide (PHMB). This agent has recently been added to wound dressings as both barriers and active antimicrobials capable of impairing or preventing the growth and tissue penetration of most pathogens, including MRSA and VRE.
       Cellulitis is a significant problem to patients with venous insufficiency and venous disease. The reason is that the edema provides an ideal microenvironment for the rapid growth of bacterial organisms, the most common being Staphylococcus aureus and group-A streptococcus. Mild cases of cellulitis may be treated on a outpatient basis with oral antibiotics, broad-spectrum topical antimicrobials, and leg elevation. Patients with a severe case of cellulitis are usually admitted to the hospital and administered parenteral antibiotic therapy.
       Deep-venous thrombosis occurs when a blood clot (thrombus) blocks blood from flowing out of a deep or perforating vein. Blocked veins can increase vein blood pressure, which overloads a person’s valves. Vein valves that do not work properly are called incompetent, and incompetent valves contribute to chronic venous insufficiency. A potentially serious condition, DVT causes leg swelling. It requires immediate medical attention because sometimes the blood clots in the veins can break off and travel to the lungs, resulting in pulmonary embolism. Phlebitis occurs when a superficial vein becomes swollen and inflamed. This causes a blood clot to form, which can also cause DVT.

Nutrition

       Nutritional support plays an important role in wound healing, maintaining immune competence, and decreasing the risk of infections. Patients with suspected malnutrition should be assessed by a dietitian or nutritionist. Calorie, protein, vitamin, and mineral deficiencies are not uncommon, especially in the elderly population. Management of these deficiencies is essential to ulcer management and to prevent the ulcer from recurring. In cases where malnutrition is suspected, a qualified nutritionist or dietitian may be required.

Skin Care

       Venous hypertension and disease is often associated with skin issues, such as severe xerosis, thickened sclerotic skin changes, and venous dermatitis. The epidermis becomes thickened, hardened, dehydrated, flaky, and compromised, leading to microscopic breaks in the skin where bacteria can thrive and ulcers begin. A good skin management routine should be undertaken by patients with a tendency for venous hypertension. A 4-pronged approach that has been shown to decrease excessive transepidermal water loss (e-TEWL) and skin tears¹² and restore the skin’s health¹³ includes gentle, soap-free cleansing with one of the newer phospholipids cleansers; moisturizing with a quality moisturizer with antioxidants and nutritional oils; protecting vulnerable areas with high-tech barriers that contain dimethicone, sophisticated silicones, or zinc oxide to provide extra protection; and nourishing with vitamins and amino acids.
       Barriers are especially important under compression hosiery and 4-layer compression bandages. Itching can be managed by treating the cause. Products with methylsulfonylmethane (MSM) can help with any stinging or itching sensations by slowing the conduction of pain fibers without causing a thinning of the skin.¹⁵

Treatment

       Treatment and care is based on normalizing the patient’s life. This can only be achieved with the patient’s compliance, participation, and understanding of the problem. Leg elevation results in a lowering of the venous pressures and ameliorating the edema. While sitting, the legs should be above the thighs. Supine, the legs should be above the level of the heart. Treatment of the underlying medical condition and venous hypertension are paramount to ulcer closure and recidivism.
       Sclerotherapy at the level of valvular incompetence in the superficial vein can have beneficial results. A sclerosant is introduced into the vein, which irritates the intimal lining. Pressure is applied over the area by bandage, and the area is sealed as the irritated lining heals. This method has been used for the treatment of varicosities. Results vary from person to person, and the patient is advised to seek medical consultation before undergoing this procedure.
       The nonsurgical treatment of choice for uncomplicated venous ulceration is compression and ambulation.¹⁶ One of the first forms of compression used were Unna boots. This moist wrap contains zinc oxide, calamine lotion, and glycerine. As the wrap dries, it becomes inelastic and rigid. Major disadvantages to Unna boot use include difficultly in application and removal, the inability to absorb wound drainage, and the fact that this wrap does not constrict to accommodate for a decrease in edema. The result is a frequent change schedule to maintain compression.
       Elastic wraps with adequate padding of the short, stretch variety will sustain compression, as there is a decrease in edema in the lower extremity. They conform to the leg, allowing for sustained compression, and are easy to use. Their application can be managed either by the patient or a caregiver with adequate training. Multilayer wrapping incorporates a 2-, 3-, or 4-layer system and allows for greater wear time with a less frequent change schedule (about once per week).
       Compression hosiery-graded pressures to decrease edema, minimize venous hypertension, and prevent possible clot formation are the first line of defense. Diagnostic testing is imperative to rule out arterial disease, and care must be taken in their use. Hosiery is designed to provide a gradient of pressure (ie, raising in the toe area and decreasing below the knee). The exact amount of pressure required depends on the type of venous disease and its severity (see Table 4).

Table 4

       Proper fit is important. Hose should be measured (ie, fitted by a certified fitter and applied according to manufacturer’s recommendations) and replaced approximately every 6 months. Great care must be exercised, particularly if there is suspected arterial insufficiency. Multilayered compression wraps with a sustained compression of 35–40 mm Hg achieved with a multilayer bandage often result in rapid healing of chronic venous ulcers that have failed to heal in many months of compression at lower pressures with more conventional bandages.¹⁷ After venous ulcers heal, compression must continue for life in order to prevent future ulcers.
       Intermittent pneumatic compression may be indicated for patients with chronic venous insufficiency and cellulitis as well as for the prevention of DVT.¹⁸ It uses an air pump to inflate and deflate an air-tight bag that encompasses the leg. This form of therapy should be used with caution, particularly for patients with a history of cardiac problems like congestive heart failure or possible embolism formation. If possible, a prescribed regular vascular exercise, such as controlled walking and exercise to improve the function of the upper ankle and calf muscle, should be instituted. A physical therapist may need to be consulted. Any patient who follows the prescribed treatment and fails to make progress toward healing in 2 or 3 weeks should have a biopsy of the ulcer to determine possible malignancy.¹⁹

How to Prevent Venous Leg Ulcers

       Patient education and compliance with compression and ambulation are paramount to successful ulcer management. Education regarding venous leg ulcers should include a routine walking or exercise program that activates the calf muscles regularly. Patients should start slow and build up endurance. They should stop smoking. If a patient is overweight, losing weight will help prevent ulcers. He or she should reduce the amount of fat in the diet and/or discuss a nutritional plan with a certified nutritionist or dietitian. Patients should sit with the legs raised whenever there is an opportunity, above the heart level if possible, and avoid sitting with the legs crossed as this impairs blood circulation.
       Those in occupations that require a lot of standing or sitting should vary their stance as much as possible and walk around from time to time. On long trips or when seated for a prolonged period of time, patients should flex and extend the legs, feet, and ankles about 10 times every 30 minutes to keep the blood flowing in the leg veins. Support stockings may be useful, but their use should be discussed with the attending physician first. Daily inspection of the patient’s feet and leg, looking for sores or changes in color, are important. Prevention includes good skin care with the 4-pronged approach. But, as always, a physician consultation is the best preventive medicine.