Cvi Khurana Rathbun

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1 The online version of this article, along with access to discussion threads on NATF’s eForum, is available at: www.NATFonline.org/ethrombosis.php (March, 2010) Chronic Venous Insufficiency Authored by, Aman Khurana, MD, Vascular Medicine Fellow and Suman Rathburn MD, MS, Associate Professor of Medicine and Director of Vascular Medicine Program from the University of Oklahoma Health Sciences Center Abstract: Chronic Venous Insufficiency (CVI) is a common medical condition but often overlooked by the medical community. Manifestations of CVI are a result of longstanding venous hypertension due to chronic venous obstruction or venous valvular reflux. Most patients present with symptoms of leg heaviness, aching, cramps, itching, tingling, restless leg, swelling, fatigue, pruritus and skin changes. Skin changes in the extremities range from dilated veins (small reticular veins, teleangiectases and varicose veins) to edema, hyperpigmentation, fibrosis and ulceration. Complications include cellulitis and venous ulcers. Treatment is aimed at reducing venous pooling, either with conservative measures initially, or with endovascular interventions if disabling symptoms persist. Compression therapy using short-stretch bandages and then graded compression garments are the mainstay of therapy. Skin and wound care is of paramount importance in preventing more serious complications.

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Transcript of Cvi Khurana Rathbun

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    The online version of this article, along with access to discussion threads on NATFs eForum, is available at: www.NATFonline.org/ethrombosis.php (March, 2010) Chronic Venous Insufficiency Authored by, Aman Khurana, MD, Vascular Medicine Fellow and Suman Rathburn MD, MS, Associate Professor of Medicine and Director of Vascular Medicine Program from the University of Oklahoma Health Sciences Center

    Abstract:

    Chronic Venous Insufficiency (CVI) is a common medical condition but often

    overlooked by the medical community. Manifestations of CVI are a result of

    longstanding venous hypertension due to chronic venous obstruction or venous

    valvular reflux. Most patients present with symptoms of leg heaviness, aching,

    cramps, itching, tingling, restless leg, swelling, fatigue, pruritus and skin changes.

    Skin changes in the extremities range from dilated veins (small reticular veins,

    teleangiectases and varicose veins) to edema, hyperpigmentation, fibrosis and

    ulceration. Complications include cellulitis and venous ulcers. Treatment is aimed

    at reducing venous pooling, either with conservative measures initially, or with

    endovascular interventions if disabling symptoms persist. Compression therapy

    using short-stretch bandages and then graded compression garments are the

    mainstay of therapy. Skin and wound care is of paramount importance in

    preventing more serious complications.

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    eDiscussion Points:

    1. What is the role of sclerotherapy in the treatment of chronic venous

    insufficiency?

    2. What is the role of iliac vein angioplasty and stenting in the treatment of

    chronic venous insufficiency?

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    Chronic Venous Insufficiency (CVI) is an extremely common disease of the

    veins of lower extremities affecting 80% of men and 85% of women (1). It is

    often underreported and overlooked by patients and doctors. It is estimated

    that more than 2.5 million people in United States have CVI and of those,

    roughly 20% develop the most troublesome and costly complication, venous

    ulceration (2). Risk factors for CVI include age, obesity, pregnancy, phlebitis,

    female sex, obesity, pregnancy, prolonged standing, leg trauma and history of

    phlebitis or deep venous thrombosis (3).

    The veins of lower extremity are divided into the deep and superficial system

    connected by perforator veins (4). These veins have series of bicuspid valves

    that ensures that blood moves in antegrade direction towards the head.

    Incompetent venous valves, venous outflow obstruction and/or muscle pump

    dysfunction lead to increased venous pressure resulting in vein dilatation and

    turtuosity (5). Longstanding untreated venous hypertension results in dermal

    changes associated with CVI.

    CVI may be asymptomatic with cosmetically bothersome teleangiectasias and

    reticular veins of the lower extremities or patients may complain of leg heaviness,

    aching, cramps, itching, tingling, restless legs, swelling, fatigue, pruritus and skin

    changes to the lower extremity due to inflammation (6). Patients with

    longstanding edema often develop cellulitis, requiring hospitalization if not

    recognized and treated early.

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    The most common clinical manifestations of CVI are dilated cutaneous veins

    such as teleangiectases also know as spider veins, bluish reticular veins and

    larger varicose veins. Physical examination may also reveal edema, eczema,

    hyperpigmentation of the skin and subcutaneous fibrosis known as

    lipodermatosclerosis. Advanced disease may be present as venous ulceration,

    commonly seen in the perimalleolar medial ankle (7). The prognosis of venous

    ulcers is poor, requiring prolonged intensive wound care in some cases. Despite

    aggressive treatment, delayed healing and recurrent ulcers are often seen (7).

    The diagnosis of CVI is based upon the clinical history, physical examination for

    signs of CVI and use of noninvasive testing to document venous obstruction or

    valvular reflux. In 2004, the American Venous Forum updated the diagnostic

    classification of chronic venous disease allowing comparison of the clinical

    severity of disease (8). This classification is given in Figure 1.

    Venous duplex imaging is used to test for reflux in the lower extremity veins and

    exclude thrombotic obstruction (9). Plethysmography assesses the effectiveness

    of venous emptying in the presence of residual thrombosis and can quantify the

    severity of venous reflux (10). Although rarely performed today for diagnostic

    purposes, venography may be used to confirm valvular reflux or document iliac

    vein obstruction in advance of an endovascular treatment (11).

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    The treatment goals for patients with CVI include improvement of symptoms,

    reduction in edema and prevention of complications such as cellulitis,

    lipodermatosclerosis and venous ulceration. The initial treatment of CVI involves

    conservative measures that aim to reduce venous hypertension.

    Patients should be encouraged to avoid prolonged standing or sitting that may

    exacerbate venous insufficiency. Patients should elevate the feet above their

    thighs while sitting and above their heart when supine for 30 min at least three to

    four times daily if possible (12). Leg elevation alone is sometimes effective in

    relieving symptoms in patients with mild venous disease, but usually does not

    provide adequate relief in more advanced disease. Structured exercise to

    strengthen calf musculature can have beneficial effects on calf muscle pump

    function (13). This can be achieved by a walking regimen or even ankle flexion

    exercises while seated.

    The use of compressive therapy is an essential component of conservative

    treatment of CVI. The objective is to provide external compression to the leg

    thereby reducing venous volume, preventing venous distension and reducing

    venous wall tension with improvement of calf muscle pump function (14). While

    short stretch bandages may be used acutely to reduce edema, graded

    compression garments donned daily are used for prevention of swelling long-

    term (15).

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    Short stretch bandages resist changes in leg circumference, thereby, reinforcing

    calf pump function during ambulation, but not during rest. These are used for

    moderate to severe edema in CVI patients to reduce swelling prior to fitting

    graded compression stockings. Multi-layered bandages may be used for patients

    with weeping edema or ulceration. Intermittent pneumatic compression therapy

    may be indicated for patients with massive edema, morbid obesity and/or

    lipodermatosclerosis to reduce swelling until more durable compression

    garments can be fitted. Intermittent pneumatic compression therapy is most

    effective when used several hours per day (16).

    Elastic graded compressive stockings are available in a variety of lengths and

    compression grades. These should be fitted based on limb length and diameter.

    The level of tension of the stocking is based on the clinical stage of CVI and

    patient tolerance. Class I (20-30 mmHg) is appropriate for patients with CEAP

    classes 2-3, Class II (30-40 mmHg) for CEAP classes 4-6 and Class III (40-50

    mm Hg) is appropriate for patients with recurrent ulcers (16). Ulcer healing rates

    are as high as 93% in patients who undergo structured regimen of compression

    therapy (17). Acute infection, severe peripheral arterial disease (ABI

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    Cellulitis can develop and progress quickly and requires systemic antibiotics,

    often necessitating hospitalization. Statis dermatitis can be treated initially with a

    topical steroid such as 0.1% triamcinolone cream; however compression therapy

    is required to prevent recurrence (18). With venous ulcers, aggressive wound

    care including debridement, local skin care and silver impregnanted dressings

    may decrease infectious complications.

    The routine use of diuretics to reduce swelling is not recommended. Small doses

    may be prescribed for a short duration to reduce massive edema. Patients

    should be followed carefully for signs of volume depletion and electrolyte

    imbalance (19).

    Although not regulated by the FDA in the U.S., the use of over-the-counter herbal

    supplements may be effective adjunct treatment in refractory patients.

    Saponosides containing horse chestnut extract and flavonoids have been used to

    promote vein health, reduce swelling, and promote venous ulcer healing (20, 21).

    Further study is needed to document the effectiveness and safety of these

    products.

    If these conservative measures are not effective, more invasive endovascular

    procedures including incompetent perforator ligation, or iliac vein angioplasty and

    stenting for relief of venous outflow obstruction, may be helpful in patients with

    unrelenting pain or recurrent venous ulcers (22,23).

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    References:

    1. Evans CJ, Fowkes FG, Ruckley CV, Lee AJ. Prevalence of varicose veins and chronic venous insufficiency in men and women in the general population: Edinburgh Vein Study.J Epidemiol Community Health. 1999;53:149-53.

    2. Rhodes JM, Gloviczki P, Canton LG, Rooke T, Lewis BD, Lindsey JR. Factors

    affecting clinical outcome following endoscopic perforator vein ablation. Am J Surg 1998;176:162-167

    3. Criqui MH, Denenberg JO, Bergan J, Langer RD, Fronek A. Risk factors for

    chronic venous disease: the San Diego Population Study. J Vasc Surg. 2007; 46:331-7

    4. Mozes G, Carmichael SW, Gloviczki P. Development and anatomy of the

    venous system. Handbook of Venous Disorders. 2nd ed. New York, NY: Arnold; 2001:25-35

    5. Burnand KG. The physiology and hemodynamics of chronic venous

    insufficiency of the lower limb. In Gloviczki P, Yao JS, eds. Handbook of Venous Disorders. 2nd ed. New York, NY: Arnold; 2001:58-67

    6. Bergan J, Schmid-Schonbein G, Smith P et al.: Chronic Venous Disease. N

    Engl J Med 2006, 355:488-498 7. Callam MJ, Harper DR, Dale JJ, Ruckley CV. Chronic ulcer of the leg: clinical

    history. Br Med J. 1987;294:1389-91. 8. Eklf B, Rutherford RB, Bergan JJ et al. Revision of the CEAP classification

    for chronic venous disorders: consensus statement. J Vasc Surg Dec;40:1248-52.

    9. Mattos MA, Sumner DS. Direct noninvasive tests (duplex scan) for the

    evaluation of chronic venous obstructin and valvular incompetence. In Gloviczki P, Yao JS, eds. Handbook of Venous Disorders. 2nd ed. New York, NY: Arnold; 2001:120-131

    10. Nicolaides AN, Miles C. Photoplethysmography in the assessment of venous

    insufficiency. J Vasc Surg. 1987;5:405-412

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    11. Kamida CB, Kistner RL, Eklof B, Masuda EM. Lower extremity ascending and descending venography. In Gloviczki P, Yao JS, eds. Handbook of Venous Disorders. 2nd ed. New York, NY: Arnold; 2001:132-139

    12. Xia, ZD, Hu D, Wilson JM et al. How echographic image analysis of venous

    edema reveals the benefits of leg elevation. J Wound Care 2004, 13:125-128 13. Padbrg FT, Johnston MV, Sisto SA. Structured exercise improves calf muscle

    function in chronic venous insufficiency: a randomized trial. J Vasc Surg 2004, 39:79-87

    14. Zajkowski PJ, Proctor MC, Wakefield TW et al : Compression stockings and

    venous function. Arch Surg 2002 137:1064-1068. 15. Berliner E, Ozbilgin B, Zarin DA. A systematic review of pneumatic

    compression for treatment of chronic venous insufficiency and venous ulcers. J Vasc Surg 2003, 37:539-544.

    16. Eberhardt RT, Raffetto JD: Chronic venous insufficiency. Circulation 2005,

    111:2398-2409. 17. Mayberry JC, Moneta Gl, Taylor LM, Porter JM. Fifteen year results of

    ambulatory compression therapy for chronic venous ulcers. Surgery. 1991;109:575-581

    18. Hess CT. Identifying and managing venous dermatitis. Adv Skin Wound Care

    2005, 18:242-243 19. Rathbun SW, Kirkpatrick AC. Treatment of Chronic Venous Insufficiency.

    Curr Treat Options Cardiovasc Med. 2007 Apr;9(2):115-26 20. Pittler MH, Ernst E. Horse chestnut seed extract for chronic venous

    insufficiency. Cochrane Database Syst Rev 2006, 1:CD003230. 21. Martinez MJ, Bonfill X, Moreno RM, et al.: Phlebotonics for venous

    insufficiency. Cochrane Database Syst Rev 2005, 3:CD003229. 22. Tenbrook JA Jr, Iafrati MD, O Donnell T, et al.: Systematic review of

    outcomes after surgical management of venous disease incorporating subfascial endoscopic perforator surgery.J Vasc Surg. 2004 Mar;39(3):583-589

    23. Neglen P, Thrasher T, Raju S. Venous outflow obstruction: an

    underestimated contributor to chronic venous disease. J Vasc Surg 2003, 38:879-885

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    Figure 1 Clinical , Etiologic, Anatomic, Pathophysiologic (CEAP)

    Classification of Chronic Venous Insufficiency