Recent Published Articles

Recognizing and Managing Venous Leg Ulcers

Advances in Skin & Wound Care, Jul/Aug 2004 by Sieggreen, Mary Y, Kline, Ronald A

PURPOSE
To provide physicians and nurses with an overview of the pathophysiology, assessment, diagnosis, and treatment of venous insufficiency and ulceration.

TARGET AUDIENCE

This continuing education activity is intended for physicians and nurses with an interest in managing patients with venous insufficiency and ulceration.

OBJECTIVES

After reading the article and taking the test, the participant will be able to:

1. Describe the anatomy, physiology, and pathophysiology of the lower extremity venous system.
2. Describe the assessment and diagnosis of venous insufficiency and ulceration.
3. Identify treatment options and teaching considerations for patients with venous insufficiency and ulceration.

ADV SKIN WOUND CARE 2004;17:302-11; quiz 312-3.

Venous leg ulcers are a painful problem for those who have them and for the health care providers who manage them. Between 10% and 35% of the population has some type of venous disease,1 and lower extremity skin ulcers are reported in 1% to 22% of individuals over age 60.2 Chronic venous disease is most likely the underlying cause in 80% to 95% of leg ulcers.1,3 Even with these high numbers, the problem may be underestimated: In one study, subjects were found to be caring for their leg ulcers at home, without the knowledge of a health care provider.4 Lifetime costs for a patient with recurrent ulcers are estimated at about $40,000.5

ANATOMY AND PHYSIOLOGY OF THE VENOUS SYSTEM

The venous system of the legs consists of superficial and deep systems joined together by perforator veins that cross the deep fascia (Figure 1). The veins in the deep system drain the gastrocnemius and soleus muscles of the calf. The long and short saphenous veins are part of the superficial system. Beginning at the medial malleolus, the long saphenous vein extends along the medial leg and enters the common femoral vein in the groin. Above the knee, 2 long veins-the anterolateral and posteromedial veins-join the long saphenous vein as it enters the common femoral vein.

The deep veins below the knee run parallel to the corresponding arteries-anterior tibial, posterior tibial, and peroneal. Cockett perforator veins empty into the posterior tibial veins. Considerable variation exists in the deep vein anatomy.

More than 100 perforator veins are found in the leg; only a few are significant. Connections of the long saphenous vein to the deep system are from Cockett perforator veins, just behind the medial malleolus and approximately 6, 13.5, and 18.5 cm above the tip of the medial malleolus. Boyd's perforating vein connects the long saphenous vein with the posterior tibial veins, and Dodd's perforator veins in the thigh connect the long saphenous vein with the femoral vein.6 Perforator vein incompetence is responsible for the failure of some venous ulcers to heal.

The calf muscle pump is the primary mechanism to return blood from the periphery to the heart. The calf muscles, the deep venous compartment, the superficial veins, and the perforator veins are all part of the venous conduit that moves blood against gravity toward the heart. During diastole, blood fills the veins and moves cephalad with each heartbeat. No backflow occurs if the valves are functioning. During active muscle contraction, compartmental pressure increases, pushing against the veins and propelling the blood upward.

Venous valves are a significant part of the venous system, maintaining the blood's upward flow. More valves are located below the knee than above. They are present between the superficial and deep systems at the saphenofemoral and saphenopopliteal junctions. Venous valves have 2 cusps, with sinuses on the base of each cusp. A venogram of a normal vein with a functioning valve shows dilation at the sinuses (Figure 2). During retrograde flow, the sinuses fill with blood and the pressure forces the valve leaflets toward each other. Normal veins withstand a retrograde pressure over 300 mm Hg,6 and dilation does not cause reflux. Loss of valve function causes venous insufficiency.

PATHOPHYSIOLOGY OF THE VENOUS SYSTEM

Varicose veins

Varicose veins are generally caused by an incompetent deep and superficial venous system. One case study reported that incompetent perforators contribute to varicose veins and that sclerosing the perforator can essentially remove the varicose vein.7

Varicose veins are a frequent problem seen in primary care and vascular offices. Patients may experience no symptoms, or they may present with aching and swelling. Noninvasive vascular testing is necessary to distinguish superficial varicose veins as a separate problem from deep venous disease. Many patients and their primary care providers mistakenly assume that varicose veins are a natural consequence of aging.

Deep vein thrombosis

Venous thrombosis is probably the most common acute problem that occurs in the veins. An estimated 600,000 patients in the United States are treated annually for deep vein thrombosis (DVT).8 Classic symptoms are swelling, calf tenderness or pain, and erythema; many patients, however, are asymptomatic. Romans sign (calf pain with ankle dorsiflexion) had once been considered a sign of DVT. However, because Homans sign is found in only one-third of DVT cases, it is an unreliable way to indicate or rule out DVT. Venous duplex imaging is commonly used to diagnose DVT.

To recognize DVT and prevent its long-term sequelae, clinicians must understand risk factors for DVT, take appropriate prophylactic measures, and test patients when a high degree of suspicion exists.

The swollen leg

Legs swell for many reasons. Systemic disorders that cause edema include chronic heart failure, renal failure, cirrhosis, hypoprotcincmia, and paralysis. Edema caused by vascular problems is usually classified as venous or lymphatic. Lymphcdema can be primary (congenital or early and late onset) or secondary (filariasis, infection, surgical, compression, radiation, or paralysis). Swelling from venous disease may be caused by acute or chronic venous insufficiency, direct compression, arterial-venous malformations or fistulas, surgery, or traumatic injury. A noninvasive ultrasound test can identify whether swelling is from a longstanding chronic problem or from one that requires urgent attention. Pressure from longstanding venous edema can lead to lymphedema.

Chronic venous insufficiency and ulcers

Chronic venous insufficiency occurs when venous hypertension is present in the deep and superficial venous systems, with incompetent venous valves causing reflux. This problem leads to significant morbidity, affecting 0.5% of the population in the United States and the United Kingdom.9 Valve dysfunction is usually the result of DVT; primary vein valvular incompetence is another possible culprit.10

One or more problems may cause a venous leg ulcer. Examining the possibilities and identifying factors contributing to the ulcer will direct the plan of care. The most common problems that lead to leg ulcers include venous disease, arterial disease, diabetes, or a combination of these diagnoses. An important part of the assessment is to determine if there is an arterial component to the problem. Arterial insufficiency will prevent healing of any ulcer and must be addressed first if it is present. Any other systemic comorbid medical conditions must be normalized simultaneously with treatment of the ulcer.

Venous ulcers are sometimes called venous stasis ulcers because they were previously attributed to blood pooling in the veins. However, researchers now believe they are the result of underlying venous hypertension caused by venous valve incompetence.3 This process often begins with a venous thrombosis, possibly occurring years before the ulcer presents.11 Although the vein recanalizcs, valves lose their function after the thrombosis. Wves in the distal vein are subjected to increased venous hypertension and the loss of more proximal valve function. This increase in hydrostatic pressure extends until the most distal veins, including the perforating veins, are involved. Hypertension is transmitted to the capillaries, resulting in skin and subcutaneous tissue changes. Pressure causes the capillaries to dilate and elongate, and it increases capillary filtration. With increasing intravascular hydrostatic pressure, fluid reabsorption from the interstitial space decreases and causes ankle edema.

Initially, ankles swell by the end of the day; swelling is reduced at night with the legs elevated. Over time, edema increases and destruction of subcutaneous tissues occurs, with fibrotic tissue replacing normal tissue. Loss of red cells into the subcutaneous tissue, followed by their disintegration, causes the brown color change in the skin (nemosidcrin deposits).

Venous ulcers vary in size from very small to circumferential ulcers that may extend nearly up to the knee (Table 1). The borders are irregular and often not well defined, and a soft yellow fibrous film may cover the surface of the ulcer (Figure 3). The ulcer is moist with moderate to heavy drainage; surrounding tissue may be edematous. Scar tissue may be present from previous ulcers. In longstanding venous disease, scar tissue and subcutaneous fibrosis cause the tissue to be inflexible and to 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, which further compromises local ulcer healing.

Edema and hyperpigmented skin with induration in the gaiter area are the clinical characteristics of longstanding chronic venous insufficiency, also called postphlebitic syndrome. Longstanding edema, with or without ulceration, may create an oozing of fluid through the skin, causing itching. Topical products placed over sensitive skin further exacerbate the condition. Frequently, pruritus and subsequent scratching by the patient causes a break in the skin that leads to a new ulcer.

The incidence of allergic contact dermatitis in venous ulcer patients varies from 51% to 85%.12 Two types of exogenous eczema, or contact dermatitis, can occur in patients with leg ulcers: irritant contact dermatitis and allergic contact dermatitis.13 In these patients, irritant contact dermatitis is caused by chemical irritation of the skin or from mechanical irritations such as bandages. Allergic contact dermatitis develops after a patient has been sensitized with an allergen. On subsequent exposure to the allergen, dermatitis will develop. Many patients with chronic leg ulcers have used numerous products on their wounds. Common allergens include topical antibiotics, lanolin in topical moisturizers, chemicals in dressings, preservatives, and fragrances.

When a patient presents with eczema or contact dermatitis, the skin and ulcer must be managed with dressings and preparations that are not likely to exacerbate dermatitis. If dermatitis continues, the patient should see a dermatologist for patch testing to identify the allergen.13

Some patients with venous hypertension may not experience pain; others report aching or tired leg muscles after standing for long periods or if considerable swelling is present. Patients may also report pain directly over a visible varicose vein. Unlike arterial ulcers, venous ulcers were not considered to be painful. However, research has shown that patients with venous ulcers may have considerable pain.14 Pain with venous ulcers has been described as sharp, achy, burning, or a feeling of pressure.

Venous hypertension also causes muscle irritability that is manifested by nocturnal leg cramps. Fluid causes the muscular cells to distend and depolarize.This results in tetanic-like contractions of muscle groups.

PATHOGENESIS OF VENOUS ULCERS

Wounds caused by venous insufficiency heal slowly and often recur. Two hypotheses attempt to explain why venous ulcers form. One is the fibrin cuff theory, which suggests that sustained venous hypertension causes distention of capillary beds, allowing fibrin to escape through the capillary wall and leading to a pericapillary fibrin cuff.15 This cuff prevents oxygen and nutrients from reaching the tissue and metabolic wastes from being carried away.

Another study identified the fibrin around the capillaries but suggested that it does not interfere with healing.16 Instead, the white cell trapping theory states that neutrophils aggregate in the capillaries, causing lipodermatosclerosis. This theory suggests that reduced capillary flow rate stimulates leukocyte adherence, which releases byproducts of the white cell and endothelial cell interaction (proteolytic enzymes, oxygen free radicals, and lipids). The white cells damage the cell wall, increasing its permeability, and larger molecules are released from the capillaries.17

Falanga and Eaglstein18 proposed a trap theory that suggests macromolecules, such as fibrin, leak out and trap substances needed for normal tissue function and healing.

DIAGNOSIS

Venous ulcers have a typical presentation; diagnosis is often made on clinical examination. However, this does not rule out the possibility that another problem coexists with chronic venous insufficiency. If pulses cannot be palpated due to edema, noninvasive arterial studies should be performed to assess the arterial system. A careful history will also identify a patient with diabetes that is not being well managed. 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 if it is malignant.19

Vascular laboratory tests provide objective information to diagnose venous insufficiency and to help determine a treatment plan. Lower extremity studies, including arterial segmentai pressures and waveforms and the ankle-brachial index, can confirm the presence of an arterial component. This will help determine if the patient has sufficient arterial inflow to heal an ulcer.

Venous tests performed in the vascular laboratory are first done to determine if reflux or obstruction is causing hypertension, then to identify the location of the reflux or obstruction. Doppler ultrasound and color duplex scanners are among the instruments that are used to obtain information about the venous system. Doppler ultrasound reproduces a signal identifying presence of flow in the arteries or veins. The Duplex scanner combines B-mode ultrasound imaging with the Doppler6; it identifies specific veins where reflux occurs. When venous ulcers are present, a duplex scan can identify perforator veins contributing to venous hypertension.

Some laboratories also use a photoplethysmograph (PPG) or an air plethysmograph (APG). With PPG, an infrared light or photo detector assesses whether venous incompetence is in the superficial or the deep system. An APG provides quantitative information, including variation in leg volume produced over a defined time in a standing position, the venous volume, the volume ejected with ambulation, and the residual volume after exercise. The residual volume and the ambulatory venous pressure can be correlated. A positive association exists between the increase in ambulatory venous pressure and the incidence in leg ulcers.

Invasive venous tests can be performed as well, including ascending and descending venous phlebography. These angiographie tests are ordered if the patient is to undergo deep venous reconstruction or deep valve replacement.

TREATMENT STRATEGIES

When a patient is diagnosed with venous insufficiency or venous valve incompetence, treatment to prevent further venous destruction leading to ulcers should begin immediately. Typically, treatment is external compression to counteract the internal pressure of venous hypertension. Many topical treatments have been evaluated for venous ulcers; however, treatment of underlying venous hypertension is necessary to realize a positive outcome. Edema is also controlled with external compression.

Patients must understand that compression is part of a lifelong management plan. Therapeutic compression stockings with compression of 30 to 40 mm Hg will counteract the capillary pressure in the tissues. Because the damage to the skin and subcutaneous tissue occurs at the ankle, knee-high compression stockings are sufficient. Some patients prefer the panty-length stocking, which may provide more comfort for varicose veins. Thigh-high stockings are also available. Caution patients to avoid allowing the stocking to roll down the leg; this could create a tourniquet effect and increase distal venous pressure. Stockings must be replaced every 4 to 6 months to ensure they provide the intended compression.

Elastic compression is worn during waking hours, when the patient is upright. During sleep or if the patient is on bed rest for another reason, compression is not needed because the legs are elevated. Gravity works in favor of venous return in this position rather than against it, creating an increase in venous flow toward the heart. Using elastic compression while at rest may provide too much pressure.

For more information on compression therapy, see Compression: Cornerstone of Therapy.

Dressings used to treat venous ulcers vary depending on the condition of the ulcer and the goals of treatment. They are chosen for their ability to absorb moisture if the wound is draining or for their ability to stimulate autolytic debridement if the wound has necrotic tissue. Enzymatic debriding agents can also be used for effective debridement.

Graftskin (Apligraf; Organogenesis, Canton, MA), a bioengineered human skin equivalent, has been approved by the Food and Drug Administration to treat venous ulcers that have failed to heal after 4 weeks of conventional therapy. The product is used in conjunction with standard compression therapy. It should not be applied over infected or deteriorating wounds until the underlying condition has been resolved.

Antibiotics should be administered only if the patient has a documented infection. Extensive cellulitis may require hospitalization with systemic antibiotics and leg elevation.

Surgical management

Surgical procedures for venous ulcers include skin grafts and tissue transfer for topical treatment and venous vein operative procedures to manage the underlying problem contributing to the ulcer.

Surgical intervention for venous disease is limited. Interventions to correct venous valvular insufficiency include insertion of artificial vein valves, vein valve transplantation, or direct valvuloplasty. Patients with recurrent leg ulcers and incompetent perforators may benefit from a procedure called a Linton flap, endoscopie perforator ligation, or sclerotherapy.

In the 1940s, incompetent perforator veins were recognized as significant contributors to venous ulcers. The Linton procedure was designed to remove the perforators; however, the operation involved making an incision along the entire length of the leg to identify and ligate the incompetent perforators.21 Wound healing was a problem, increasing the risks of this procedure.

Current endoscopie techniques have been applied to venous surgery. Subfascial endoscopie perforator surgery (SEPS) is one procedure proven to benefit patients with known perforator incompetence.21 The SEPS procedure, which has replaced the Linton procedure, assumes that incompetent perforator veins have a significant responsibility in the development of venous ulcers. Incompetent perforator veins identified near or under venous ulcers are suspect and, if they can be ligated, the ulcer should heal with the usual conservative treatment. Incisions are made in the leg to insert endoscopie surgical instruments proximal to the ulcer and perforator veins. The incisions are made in healthy tissue and are less likely to cause problems with healing than if they were made in the fibrotic and lipodermatosclerotic tissue of the lower leg.21

Telangiectasias and small reticular veins are suitable for sclerotherapy and may be used to complement other procedures. However, sclerotherapy is not a primary treatment for venous ulcers.

PATIENT EDUCATION

Patient education is the most effective intervention for chronic venous insufficiency (Table 3). Because of the chronic and progressive nature of the disease, the patient must take ownership of its management. If the patient with early venous insufficiency manages edema and controls venous hypertension, the long-term characteristics of postphlebetic syndrome-skin discoloration, tissue fibrosis, and leg ulcers-can be prevented. Unfortunately, many health care providers do not realize the importance of diagnosing venous disease early and treating it with long-term prevention in mind.

Patients should be taught the physiology of venous disease and the potential outcomes of their decisions in an understandable manner. The patient should be given responsibility for managing the disease and the ulcer, which requires daily vigilance. Emphasize that this is not a passive process-progression or maintenance of the disease depends on strictly following individualized recommendations. A videotape available from Family Health Media (http://www.familyhealthmedia.com) provides information about the problem of venous ulcers and outlines appropriate care, with emphasis on the patient's responsibility for self-care.

SUMMARY

Venous ulcers are a difficult problem to manage. They frequently recur, with tissue destruction becoming more progressive. Prevention is always the best treatment. Underlying venous hypertension must be managed concurrently with ulcer treatment.

Many modalities for treatment have been used in an effort to find the most effective treatment for venous leg ulcers; however, the use of moist wound healing for the ulcer and compression for the underlying venous disease are still the guiding principles for this problem.

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PURPOSE To provide physicians and nurses with an overview of the pathophysiology, assessment, diagnosis, and treatment of venous insufficiency and ulceration.

TARGET AUDIENCE This continuing education activity is intended for physicians and nurses with an interest in managing patients with venous insufficiency and ulceration.

OBJECTIVES After reading the article and taking the test, the participant will be able to:

1. Describe the anatomy, physiology, and pathophysiology of the lower extremity venous system.
2. Describe the assessment and diagnosis of venous insufficiency and ulceration.
3. Identify treatment options and teaching considerations for patients with venous insufficiency and ulceration.

1. Which vein extends along the medial leg and enters the common femoral vein in the groin?
a. anterior tibial vein
b. Boyd's perforating vein
c. long saphenous vein
d. peroneal vein

2. How many perforator veins are found in the leg?
a. more than 100
b. more than 200
c. more than 300
d. more than 400

3. The long saphenous vein connects to the posterior tibial vein via the
a. Cockett's perforator veins,
b. Boyd's perforating vein,
c. anterior tibial vein,
d. short saphenous vein.

4. Venous valves
a. maintain upward venous blood flow.
b. are more prevalent above the knee than below.
c. do not bridge the superficial and deep systems,
d. have 4 cusps.

5. Varicose veins
a. are a natural consequence of aging,
b. are the most common acute problem that occurs in the vein.
c. can be treated by sclerosing the incompetent perforator contributing to the problem.
d. always cause aching and swelling.

6. Although many patients are asymptomatic, a classic symptom of DVT is
a. pale skin.
b. skin that is cool to the touch,
c. a woody texture to the skin,
d. erythema.

7. Venous valve dysfunction is usually the result of
a. edema,
b. DVT.
c. prior ulceration,
d. traumatic injury.

8. Venous ulcers
a. have well-defined, regular borders,
b. are generally dry, with little to no drainage,
c. may be covered with a soft yellow fibrous film.
d. are not associated with edematous surrounding skin.

9. In patients with venous ulcers, allergic contact dermatitis
a. rarely occurs.
b. is only associated with chemical irritation,
c. is commonly associated with lanolin in topical moisturizers.
d. is only associated with mechanical irritation.

10. The white cell trapping theory suggests that
a. distended capillary beds allow fibrin to escape through the capillary walls and lead to a pericapillary fibrin cuff,
b. venous ulcers begin to form when neutrophils aggregate in the capillaries, causing lipodermatosclerosis.
c. macromolecules leak out and trap substances needed for normal tissue function and healing.
d. a fibrin cuff prevents oxygen and nutrients from reaching the tissue and metabolic wastes from being carried way.

11. A biopsy should be performed to rule out malignancy if a venous ulcer has failed to make progress toward healing in
a. 5 to 7 days.
b. 7 to 10 days.
c. 2 to 4 weeks
d. 4 to 6 weeks.

12. Which vascular test identifies perforator veins contributing to venous hypertension?
a. air plethysmograph
b. photoplethysmograph
c. duplex scan
d. Doppler ultrasound

13. Which vascular test provides quantitative information, such as venous volume?
a. air plethysmograph
b. photoplethysmograph
c. duplex scan
d. Doppler ultrasound

14. To counteract capillary pressure in the tissues, therapeutic compression stockings should be
a. 10 to 20 mm Hg.
b. 20 to 30 mm Hg.
c. 30 to 40 mm Hg.
d. 40 to 50 mm Hg.

15. Which length is sufficient for therapeutic compression stockings?
a. ankle-high
b. knee-high
c. thigh-high
d. waist-high

16. Therapeutic compression stockings should be replaced every
a. 4 to 6 weeks,
b. 1 to 2 months,
c. 3 to 4 months,
d. 4 to 6 months.

17. Which surgical procedure might be performed on a patient with incompetent perforator veins?
a. insertion of artificial vein valves
b. vein valve transplant
c. SEPS
d. direct valvuloplasty

18. A compression bandage would be categorized as
a. rigid.
b. class 1.
c. class 2.
d. class 3.

19. Elastic multilayer compression bandaging systems typically provide sustained, graduated compression for at least
a. 7 days,
b. 10 days,
c. 2 weeks,
d. 3 weeks.

20. A patient with venous disease should be told
a. not to moisturize the skin.
b. that it is okay to continue smoking.
c. to avoid extremes of hot and cold next to the skin.
d. that walking barefoot is okay.

REFERENCES

1. Young JR. Differential diagnosis of leg ulcers. Cardiovasc Clin 1983;13:171-93.
2. Callam MJ, Harper DR, Dale JJ, Ruckley CV. Chronic ulcer of the leg: clinical history. Br Med J (Clin Res Ed) 1987: 294:1389-91.
3. Rutherford RB. The vascular consultation. In: Rutherford RB, editor. Vascular Surgery, 4th ed. Philadelphia: WB Saunders Co; 1995.
4. Nelzen O, Bergqvist D, Lindhagen A. The prevalence of chronic lower limb ulc[iota]ration has been underestimated: results of a validated population questionnaire. Br J Surg 1996;83:255-8.
5. Cikrit DF, Nichols WK1 Silver D. Surgical management of refractory venous stasis ulc[iota]ration. J Vase Surg 1988;7:473-8.:
6. Belcaro G, Labropoulos N, Christopoulos D, et al. Noninvasive tests in venous insufficiency. J Cardiovasc Surg 1993;34:3-11.
7. Van Neer PA. Perforans varicosis: treatment of the incompetent perforating vein is important. Dermatol Surg 2004;30:754-5.
8. Deep vein thrombosis: advancing awareness to protect patient lives. White Paper: Public Health Leadership Conference on Deep Vein Thrombosis. Washington, DC: American Public Health Association; February 26, 2003.
9. Goldstone J. Veins and lymphatics. In: Way LW, editor. Current Surgical Diagnosis and Treatment, 10th ed. New York: McGraw-Hill (Lange); 1994.
10. Ferris EB, Kistner RL. Femoral vein reconstruction in the management of chronic venous insufficiency. A 14 -year experience. Arch Surg 1982;11:1571-9.
11. The postthrombotic syndrome and venous ulceration in the pathology and surgery of the veins of the lower iimbs. In: Dodd H, Cockett F, editors. The Pathophysiology and Surgery of the Veins of the Lower Limbs. New York: Churchill Livingstone; 1976. p 246-68.
12. Bucalo BD, Eaglestein WH, Streilein JW, Taylor JR, Nemeth AJ. Ability of venous ulcer patients to develop allergic contact sensitivity. J Geriatr Dermatol 1993;1:157-60.
13. Powell S. Contact dermatitis in patients with chronic leg ulcers. J Tissue Viability 1966;6:103-6.
14. Krasner D. Painful venous ulcers: themes and stories about their impact on quality of life. Ostomy Wound Manage 1988:44:38-42, 44, 46 passim.
15. Burnand KG, Whimster I, Naidoo A, Browse NL. Pericapillary fibrin in the ulcer-bearing skin of the leg: the cause of lipodermatosclerosis sand venous ulceration. Br Med J (Clin Res Ed)1982;285:1071-2.
16. FalangaV, Kirsner R, Katz MH, Gould E, Eaglstein WH, McFaIIs S. Pericapillary fibrin cuffs in venous ulceration. Persistence with treatment and during ulcer healing. J Dermatol SurgOncol 1992;18:409-14.
17. Coleridge-Smith PD, Thomas P, Scurr JH1 Dormandy A. The aetiology of venous ulceration-a new hypothesis. Br Med J 1988;296:1726-7.
18. Falanga V Eaglstein WH. The "trap" hypothesis of venous ulceration. Lancet 1993;341:1006-8.
19. Snyder RJ, Stillman RM, Weiss SD. Epidermoid cancers that masquerade as venous ulcer disease. Ostomy Wound Manage 2003;49:63-6.
20. Gloviczki P, Bergan JJ, Menawat SS, et al. Safety, feasibility, and early efficacy of subfascial endoscopie perforator surgery: a preliminary report from the North American registry. J Vase Surg 1997;2:94-105.

Mary Y. Sieggreen, APRN, CVN * Nurse Practitioner, Vascular Surgery * Clinical Nurse Specialist, Wound Care * Harper University Hospital * Detroit Medical Center * Assistant Clinical Professor * Wayne State University * Detroit, MI

Ronald A. Kline, MD, FACS, FAHA * Vascular Surgeon * Arizona EndoVascular Center * Tucson, AZ

The authors have disclosed that they have no significant relationships or financial interests in any commercial companies that pertain to this education activity.

Copyright Springhouse Corporation Jul/Aug 2004

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