Guidelines for the prevention of venous ulcers

Abstract

The Wound Healing Society (WHS) is a professional society of physicians, nurses, physical therapists, podiatrists, and other wound care specialists, basic scientists, clinical researchers, and industrial researchers dedicated to assuring that every patient receives optimal wound care. Its mission is to advance the science and practice of wound healing. To that end, the following comprehensive, evidence- and consensus-based guidelines were developed to address the Prevention of Venous Ulcers. The guidelines are presented in generic terms; the details of specific tests, therapies, and procedures are at the discretion of an interdisciplinary team of health care professionals who establish, implement, and evaluate policies and procedures directed at prevention of venous ulcers. Evidence references for each standard are listed and coded. The code abbreviations for the evidence citations were as follows: The strength of evidence supporting a guideline is listed as Level I, Level II, or Level III, using the following definitions: Level I: Meta-analysis of multiple RCTs or at least two RCTs supporting the intervention in the guideline or multiple laboratory or animal experiments with at least two clinical series supporting the laboratory results. Level II: Less evidence than Level I, but at least one RCT and at least two significant clinical series or expert opinion papers with literature reviews supporting the intervention. Experimental evidence that is quite convincing but without support by adequate human experience. Level III: Suggestive data of proof-of-principle, but lacking sufficient data such as meta-analysis, RCT, or multiple clinical series. Capeheart JK. Chronic venous insufficiency: a focus on prevention of ulceration. Wound Ostomy Contin Nurs 1996; 23: 227–34 [LIT REV]. Miller WL. Chronic venous insufficiency. Curr Opin Cardiol 1995; 10: 543–8 [LIT REV]. MacKenzie RK, Brown DA, Allan PL, Bradbury AW, Ruckley CV. A comparison of patients who developed venous leg ulceration before and after their 50th birthday. Eur J Vasc Endovasc Surg 2003; 26: 176–8 [RETRO S]. Beebe HG, Bergan JJ, Bergqvist D, Eklof B, Eriksson I, Goldman MP, Greenfield LJ, Hobson RW 2nd, Juhan C, Kistner RL, Labropoulos N, Malouf GM, Menzoian JO, Moneta GL, Myers KA, Neglen P, Nicolaides AN, O'Donnell TF, Partsch H, Perrin M, Porter JM, Raju S, Rich NM, Richardson G, Sumner DS. Classification and grading of chronic venous disease in the lower limbs: a consensus statement. Eur J Vasc Endovasc Surg 1996; 12: 487–92 [STAT]. Porter JM, Moneta GL. International Consensus Committee on Chronic Venous Disease. J Vasc Surg 1996; 21: 635–45 [STAT]. Preamble: There are several conditions that render a patient susceptible to development of a venous ulcer. Among these are deep vein thrombosis, incompetence of the direct calf and ankle perforating veins, elevation of ambulatory venous pressure (venous hypertension), calf pump dysfunction, edema, cellulitis, and lipodermatosclerosis. Lower extremity edema can be due to a variety of conditions, including congestive heart failure, lymphedema, pregnancy, obesity, trauma, and constriction proximal to the area of edema. Minimizing or controlling these conditions should theoretically prevent the development of a venous ulcer. Literature-based evidence for prevention of recurrence of venous ulcers has been reviewed and summarized in “Guidelines for the treatment of venous ulcers” (Wound Repair Regen 2006; 14: 649–62). The evidence for prevention of the first venous ulcer or primary ulcer is less voluminous. Fewer randomized clinical trials (RCTs) have been performed in patients with predisposing conditions before their first venous ulcer. Guideline #1: Patients with signs of increased ambulatory venous pressure (venous hypertension) and/or postphlebitic syndrome should use compression stockings constantly and forever. Level of Evidence: I. Principle: A degree of compression is necessary in the long term to minimize the preexisting conditions conducive to venous ulcer formation. Because of this, attempts need to be made to aid patient compliance, including teaching the patient techniques to help them don the compression stockings. Evidence: Kakkos SK, Daskalopoulou SS, Daskalopoulos ME, Nicolaides AN, Geroulakos G. Review of the value of graduated elastic compression stockings after deep vein thrombosis. Thromb Haemost 2006; 96: 441–5 [STAT]. Prandoni P, Lensing AW, Prins MH, Frulla M, Marchiori A, Bernardi E, Tormene D, Mosena L, Pagnan A, Girolami A. Below-knee elastic compression stockings to prevent post-thrombotic syndrome: a randomized, controlled trial. Ann Int Med 2004; 141: 249–56 [RCT]. Ginsberg JS, Hirsh J, Julian J, Vander LaandeVries M, Magier D, MacKinnon B, Gent M. Prevention and treatment of post-phlebitic syndrome: results of a 3-part study. Arch Intern Med 2001; 161: 2105–9 [RCT]. Gniadecka N, Karlsmark T, Bertram A. Removal of dermal edema with class I and II compression stockings in patients with lipodermatosclerosis. J Am Acad Dermatol 1998; 39: 966–70 [RCT]. Lippmann HI, Fishman LM, Farrar RH, Bernstein RK, Zybert PA. Edema control in the management of disabling chronic venous insufficiency. Arch Phys Med Rehabil 1994; 75: 436–41 [RETRO S]. Kurz X, Kahn SR, Abenhaim L, Clement D, Norgren L, Baccaglini U, Berard A, Cooke JP, Cornu-Thenard A, Depairon M, Dormandy JA, Durand-Zaleski I, Fowkes GR, Lamping DL, Partsch H, Scurr JH, Zuccarelli F. Epidemiology, outcomes, diagnosis, and management. Summary of an evidence-based report of the VEINES task force venous insufficiency, epidemiologic, and economic studies. Int Angiol 1999; 18: 83–102 [STAT]. Vogeley LL, Coeling H. Prevention of venous ulceration by use of compression after deep vein thrombosis. J Vasc Nurs 2000; 18: 123–7 [LIT REV]. Bernardi E, Prandoni P. The post-phlebitic syndrome. Curr Opin Pulm Med 2000; 6: 335–42 [LIT REV]. Franks PJ, Oldroyd MI, Dickson D, Sharp EJ, Moffatt CJ. Risk factors for leg ulcer recurrence: a randomized trial of two types of compression stocking. Age Ageing 1995; 24: 490–4 [RCT]. Guideline #2: Exercises to increase calf muscle pump function have been demonstrated to be helpful in long-term maintenance and venous ulcer prevention. Level of Evidence: II. Principle: Calf muscle pump function has been shown to be improved with exercise. Evidence: Padberg FT, Johnston MV, Sisto SA. Structured exercise improves calf muscle pump function in chronic venous insufficiency: a randomized trial. J Vasc Surg 2004; 39: 79–87 [RCT]. Kan YM, Delis KT. Hemodynamic effects of supervised calf muscle exercise in patients with venous leg ulceration: a prospective controlled study. Arch Surg 2001; 136: 1364–9 [RCT]. Yang D, Vandongen YK, Stacey MC. Effect of exercise on calf muscle pump function in patients with chronic venous disease. Brit J Surg 1999; 86: 338–44 [CLIN S]. Guideline #3: Venous thromboembolism prophylaxis after deep vein thrombosis decreases recurrent deep vein thrombosis and the postphlebitic syndrome and their complications such as venous ulceration. Level of Evidence: II. Principle: Recurrent venous thromboembolic events can lead to the complication of postphlebitic or postthrombotic syndrome. This can be minimized with thromboembolism prophylactic therapy. Evidence: Ferretti G, Bria E, Giannarelli D, Carlini P, Felici A, Mandalà M, Papaldo P, Fabi A, Ciccarese M, Cuppone F, Cecere FL, Nuzzo C, Terzoli E, Cognetti F. Is recurrent venous thrombo-embolism after therapy reduced by low-molecular-weight heparin compared to oral anticoagulants? Chest 2006; 130: 1808–16 [STAT]. Valiukiene L, Naudziunas A, Unikauskas A. Treatment and prophylaxis of deep vein thrombosis with low molecular weight heparins (meta-analysis of clinical trials). Medicina (Kaunas) 2003; 39: 352–8 [STAT]. Huisman MV, Bounameaux H. Treating patients with venous thrombo-embolism: initial strategies and long-term secondary prevention. Seminars Vasc Med 2005; 5: 276–84 [STAT]. Kahn SR. The post-phlebitic syndrome: progress and pitfalls. Brit J Haemotol 2006; 134: 357–65 [LIT REV]. Messmore HL, Coyne E, Wehrmacher WH, Demir AM, Fareed J. Studies comparing low molecular weight heparin with heparin for the treatment of thrombo-embolism: a literature review. Curr Pharm Des 2004; 10: 1001–10 [LIT REV]. Guideline #4: Subfascial endoscopic perforator surgery (SEPS) is the procedure of choice when it is desirable to address the underlying venous pathologic etiology of venous ulceration by preventing backflow from the deep to the superficial venous system. To achieve the greatest effectiveness when using this procedure, care must be taken to divide all visible perforators. The procedure is not effective if the patient has severe deep venous disease with either deep reflux or obstruction. Level of Evidence: III. Principle: Interruption of incompetent perforating vessels will aid in decreasing ambulatory venous pressure in the leg. Evidence: Gloviczki P, Bergan JJ, Rhodes JM, Canton LG, Harmsen S, Ilstrup DM. Mid-term results of endoscopic perforator vein interruption for chronic venous insufficiency: lessons learned from the North American subfascial endoscopic perforator surgery registry. The North American Study Group. J Vasc Surg 1999; 29: 489–502 [STAT]. Baron HC, Wayne MG, Santiago CA, Grossi R. Endoscopic subfascial perforator vein surgery for patients with severe, chronic venous insufficiency. Vasc Endovasc Surg 2004; 38: 439–42 [CLIN S]. Mendes RR, Marston WA, Farner MA, Keagy BA. Treatment of superficial and perforator venous incompetence without deep vein insufficiency: is routine perforator ligation necessary? J Vasc Surg 2003; 38: 891–5 [CLIN S]. Guideline #5: Less extensive surgery on the venous system such as superficial venous ablation, endovenous laser ablation, or valvuloplasty, especially when combined with compression therapy, can help decrease venous hypertension. Level of Evidence: II. Principle: Procedures that are less extensive than deep ligation of multiple perforating veins can help decrease venous hypertension when combined with an adequate compression system. Although surgery can help prevent venous ulceration, ulcers that do occur following surgery may be more difficult to treat. Evidence: Perrin M, Hiltbrand B, Bayon JM. Results of valvuloplasty in patients presenting with deep vein insufficiency and recurring ulceration. Ann Vasc Surg 1999; 13: 524–32 [CLIN S]. Masuda EM, Kistner RL. Long-term results of venous valve reconstruction: a four- to-twenty-one year follow-up. J Vasc Surg 1994; 19: 391–403 [STAT]. Gohel MS, Barwell JR, Earnshaw JJ, Heather BP, Mitchell DC, Whyman MR, Poskitt KR. Randomized clinical trial of compression plus surgery versus compression alone in chronic venous ulceration. (ESCHAR study)—hemodynamic and anatomical changes. Brit J Surg 2005; 92: 291–7 [RCT]. Barwell JR, Davies CE, Deacon J, Harvey K, Minor J, Sassano A, Taylor M, Usher J, Wakely C, Earnshaw JJ, Heather BP, Mitchell DC, Whyman MR, Poskitt KR. Comparison of surgery and compression with compression alone in chronic venous ulceration (ESCHAR study): randomized controlled trial. Lancet 2004; 363: 1854–9 [RCT]. Zamboni P, Cisno C, Marchetti F, Mazza P, Fogato L, Carandina S, De Palma M, Liboni A. Minimally invasive surgical management of primary venous ulcers vs. compression treatment: a randomized trial. Eur J Vasc Endovasc Surg 2003; 25: 313–8 [RCT]. Ahmad I, Ahmad W, Dinqui M. Prevention or reversal of deep venous insufficiency by aggressive treatment of superficial venous disease. Am J Surg 2006; 191: 33–8 [CLIN S]. Margolis DJ, Berlin JA, Strom BL. Risk factors associated with the failure of a venous leg ulcer to heal. Arch Dermatol 1999; 135: 920–6 [RETRO S]. Guideline #6: Cellulitis (inflammation and infection of the skin and subcutaneous tissue most commonly due to streptococci or staphylococci) in the edematous lower extremity should be treated with systemic antibiotics appropriate for those organisms. Level of Evidence: II. Principle: Edema fluid (plasma) neutralizes the fatty acids of sebum and inactivates the normal bactericidal properties of skin. This renders the skin and subcutaneous tissue susceptible to infection by streptococci and staphylococci. Evidence: Ricketts LR, Squire JR, Topley E, et al. Human skin lipids with particular reference to the self-sterilizing power of the skin. Clin Sci Mol Med 1951; 10: 89–93 [EXP]. Baddour LM. Cellulitis syndromes: an update. Int J Antimicrob Agents 2000; 14: 113–6 [LIT REV]. Chiller K, Selkin BA, Murakawa GJ. Skin microflora and bacterial infections of the skin. J Invest Dermatol Symp Proc 2001; 6: 170–4 [LIT REV]. Guay DR. Treatment of bacterial skin and skin structure infection. Expert Opin Pharmacother 2003; 4: 1259–75 [LIT REV]. Edlich RF, Winters KL, Britt LD, Long WB 3rd. Bacterial diseases of the skin. J Long Term Eff Med Implants 2005; 15: 499–510 [LIT REV]. Dall L, Peterson S, Simmons T, Dall A. Rapid resolution of cellulitis in patients managed with combination antibiotic and anti-inflammatory therapy. Cutis 2005; 75: 177–80 [RCT]. Guideline #7: Fibrinolytic enhancement with an anabolic steroid such as stanozolol in conjunction with compression therapy may be useful in treating lipodermatosclerosis of the lower extremity; however, one must be aware of the side effects. Level of Evidence: III. Principle: A fibrinolytic agent capable of decreasing extravascular fibrin should be able to decrease induration and inflammation in cases of lipodermatosclerosis. Evidence: Burnand K, Clemenson G, Morland M, Jarrett PE, Browse NL. Venous lipodermatosclerosis: treatment with fibrinolytic enhancement and elastic compression. Brit Med J 1980; 280: 7–11 [RCT]. Kirsner RS, Pardes JB, Eaglstein WHF, Alanga V. The clinical spectrum of lipodermatosclerosis. J Am Acad Dermatol 1993; 28: 623–7 [LIT REV]. Helfman T, Falanga V. Stanozolol as a novel therapeutic agent in dermatology. J Am Acad Dermatol 1995; 33: 254–8 [LIT REV]. Segal S, Cooper J, Bolognia J. Treatment of lipodermatosclerosis with oxandrolone in a patient with stanozolol-induced hepatotoxicity. J Am Acad Dermatol 2000; 13: 588–9 [RETRO S]. Guideline #8: Oral treatment with micronized purified flavonoid fraction (MPFF) may be a useful adjunct to conventional compression therapy in managing chronic venous insufficiency. Level of Evidence: III. Principle: Agents that inhibit synthesis of prostaglandins and free oxygen radicals, decrease microvascular leakage, and inhibit leukocyte trapping and activation should theoretically improve chronic venous insufficiency and prevent venous ulceration. Evidence: Bergan JJ, Schmid-Schonbein GW, Takase S. Therapeutic approach to chronic venous insufficiency and its complications. Place of Daflon 500 mg. Angiology 2001; 52 (Suppl. 1): S43–7 [LIT REV]. Ramelet AA. Clinical benefits of Daflon 500 mg in the most severe stages of chronic venous insufficiency. Angiology 2001; 52 (Suppl. 1): s49–56 [LIT REV]. Coleridge-Smith P, Lok C, Ramelet AA. Venous leg ulcer: a meta-analysis of adjunctive therapy with micronized purified flavonoid fraction. Eur J Vasc Endovasc Surg 2005; 30: 198–208 [STAT].