Angiology
http://ang.sagepub.com/
Contemporary Treatment of Venous Lower Limb Ulcers William R. Hiatt ANGIOLOGY 1992 43: 852 DOI: 10.1177/000331979204301008 The online version of this article can be found at: http://ang.sagepub.com/content/43/10/852
Published by: http://www.sagepublications.com
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Contemporary
Treatment of Venous Lower Limb Ulcers
William R. Hiatt, M.D.
DENVER,COLORADO
Abstract
postphlebitic syndrome is a significant management problem that aflarge number of patients. Primary prophylaxis of deep-vein thrombophlebitis would reduce the risk of developing the postphlebitic syndrome and should be considered in high-risk patients. Patients who have had a phlebitis should be monitored with noninvasive tests of the deep venous circulation for the development of venous valve incompetence. Patients with venous hypertension should be placed in compression stockings to prevent the postphlebitic syndrome. In patients who progress to venous ulceration, several aggressive measures must be undertaken. Systemic treatment includes management of obesity, edema, immobility, poor nutrition, and comorbid illnesses. Some patients may require a short hospitalization of bed rest, lower limb elevation, and daily dressings and wound care. Outpatient therapy requires sustained compression of 35 to 40 mmHg at the ankle for many months to allow the ulcer to heal. The standard bandage material is Unna’s boots, which is applied every one to two weeks by a trained nurse. Cadexomer iodide is an effective local treatment that helps debride the ulcer and accelerate healing. Finally, pentoxifylline therapy has also been shown to significantly improve the healing of venous ulThe fects a
cers.
Prevalence
250,000 new cases of deep vein thrombophlebitis occur each year resulting in approximately 500,000 patients presenting for the treatment of venous stasis ulcers.’ The More than
between phlebitis and subsequent ulceration is well established. For example, when followed for five to ten years after a venographically documented thrombophlebitis, 80 % of patients will have some symptoms of venous hypertension in association with valvular incompetence.2 In particular, 49% had varicosities, 62 % edema, 34% pigmentation, and 4%
relationship
From the Section of Vascular Medicine, University of Colorado School of Medicine, Denver, Colorado Presented at the 38th Annual Meeting, American College of Angiology, Maui, Hawaii, October, 1991
852
Downloaded from ang.sagepub.com at UNIV TORONTO on June 2, 2014
853 ulceration. The location of the clot influenced the probability of subsequent complications: 100% of iliac thromboses had symptoms, 94 % of femoral clots were symptomatic, and even 47 % of calf clots resulted in symptoms.2 Thus, the postphlebitic syndrome represents a tremendous management problem, the most difficult cases being those with venous ulceration. An important consideration in the development of the postphlebitic syndrome is the primary prevention of thrombophlebitis. There are well-established protocols of prophylaxis against thrombophlebitis in high-risk patients such as those undergoing surgery. The widespread application of these strategies may result in a decrease in the incidence of some, but not all, of the new cases of the postphlebitic syndrome. Therefore, management of patients with lower limb edema and ulceration following an episode of phlebitis will remain a problem.
Pathophysiology The primary initiating event of the postphlebitic syndrome is venous valve destruction from a phlebitis. This leads to venous valve incompetence2 and venous hypertension, particularly during standing and with exercise.3 Over time the increase in venous pressure leads to varicose veins and limb swelling. More chronic forms of the disease are associated with pigmentation changes, induration, and venous ulceration. The causes of venous ulceration are multifactorial and not simply related to the increase in venous pressure. It has been noted that the capillary supply and tissue oxygen tension are normal in areas of venous varicosities, decreased in areas of hyperpigmentation and induration, and absent in avascular skin.4 Therefore, loss of capillary supply and tissue hypoxia may play a crucial role in the development of a venous ulcer.5 White cell activation and plugging of capillaries may further exacerbate the tissue ischemia. Finally, secondary infection with Staphylococcus aureus, Pseudomonas aeruginosa, Streptococcus, Proteus, enterobacteria, and Klebsiella significantly delay healing.
Management General Measures The diagnosis of venous insufficiency should be well established by appropriate noninvasive tests. Particularly useful is the Doppler venous survey to document valvular incompetence of the deep veins. Venous outflow obstruction from extensive, proximal clots leads to a more severe venous hypertension. This condition is diagnosed by an abnormal impedance plethysmographic tracing. In patients with known venous insufficiency or chronic venous obstruction, use of calf-length compression stockings and frequent lower limb elevation are cornerstones of therapy. In compliant patients, these measures may prevent the development of the postphlebitic syndrome and venous ulceration. Patients who present with venous ulcers need attention to their general medical condition. In particular management of obesity, if present, is critical to facilitate healing of the ulcer. On the other hand, patients who are poorly nourished also do not heal well. The mobility of the patient may play a role, particularly in those who are confined to a wheelchair and are unable to elevate their lower limbs. Finally, other medical diseases such as diabetes, or conditions associated with fluid retention, need to be managed with appropriate therapy. The acute management of the venous ulcer may require an initial week of bed rest in the hospital with lower limb elevation.’ During this time patients need to be treated daily with a
Downloaded from ang.sagepub.com at UNIV TORONTO on June 2, 2014
854 of measures. These include soaking the ulcer in potassium permanganate for twenty minutes twice a day or cleaning the wound with hydrogen peroxide to debride the ulcer and treat any fungal infection. If there is evidence of cellulitis, a course of a broad-spectrum antibiotic may be necessary. Acute stasis dermatitis is treated with topical corticosteroids. Finally, if there is pitting edema (in association with congestive heart failure or liver or kidney disease), then a diuretic is helpful.
variety
Sustained
Compression initiating event of venous ulceration is venous hypertension, and thus external compression is critical to reverse this process. Compression is initially achieved by elastic bandages. Once the ulcer is healed, external compression is maintained by custom-made elastic stockings. In the acute case, external pressures of 35 to 40 mmHg at the ankle are necessary for healing.6 The usual bandage systems achieve pressures of only 20 to 30 mmHg at the ankle that rapidly decrease with use over the ensuring week . More extensive, multilayer bandages maintain the necessary pressures over an extended time, and higher pressures are associated with better healing rates. In fact, one system utilizes a balloon that is placed over the ulcer and is intermittently inflated to pressures of 50 to 70 mmHg.7 Although cumbersome, this treatment has been claimed to heal refractory ulcers . Bandage Material In addition to external compression, an occlusive bandage is also employed in the management of the venous ulcer. Historically, Unna’s boots have been used, which consist of gauze impregnated with gelatin, zinc oxide, and caladryl. The bandage is applied moist, wrapped in dry gauze, and followed by an elastic wrap to maintain external pressure. Once applied, the bandage protects the ulcer from the environment, as well as from the patient’s attempts to scratch the area. Initial therapy requires changing the boot weekly. Once healing is established, the boot may be changed less often, but excellent nursing care is essential for best results. Some studies have evaluated newer dressings such as hydroactive material. Initial results suggested that the hydroactive dressing was as effective as the Unna’s boot but better tolerated by the patient. However, in a subsequent study, healing rates were significantly worse with the hydroactive material. With a randomized design, Unna’s boots healed 70% of patients as compared with 38 % with the hydroactive dressings at six months.9 In addition, several complications occurred in the hydroactive dressing, including worsening cellulitis and exudate. Finally, while Unna’s boots and the hydroactive dressings had similar material costs, the hydroactive dressing was less effective, and therefore, the cost per healed ulcer was greater for the hydroactive dressing. The
7
Cadexomer Iodide Cadexomer iodine is a starch polymer bead impregnated with iodide that absorbs large amounts of fluid and is bactericidal. Wound healing is promoted by removal of fluid and bacteria. In an early randomized trial of 74 patients, the ulcer healing rates were significantly greater with cadexomer iodide than with standard therapy.’° The cadexomer iodide also debrided the ulcer, relieved pain, and reduced bacterial counts as compared with standard therapy. More recent controlled trials have confirmed better ulcer healing rates with cadexomer iodide than with standard therapy but have not substantiated the claim that the compound reduces the rate of bacterial infection. 11,12
Downloaded from ang.sagepub.com at UNIV TORONTO on June 2, 2014
855
Systemic Therapy As previously discussed,
activation of white cells in the area of the venous ulcer may exacerbate the local ischemia by the plugging of capillaries. Pentoxifylline is a medication that lowers blood fibrinogen levels, improves red cell deformability, and alters white cell function. It has, therefore, been hypothesized that pentoxifylline may lessen tissue hypoxia and improve the healing of venous ulcers. Recently, a randomized trial has been completed in 80 patients comparing the effects of oxpentifylline with those of placebo in the healing of venous ulcers.’3 All patients had refractory venous ulcers that had not healed on standard therapy. In addition, the patients were all treated with standard two-layer compression dressings. At six months, 64% had healed with oxpentifylline and 34% with placebo (significantly different), but side effects were similar between groups. Thus, oxpentifylline resulted in significantly better healing rates than standard therapy, but these results should be confirmed in larger trials. William R. Hiatt, M. D. Section of Vascular Medicine 4200 E. Ninth Ave. , Box B-180 Denver, Colorado 80262
References 1. Coon
2.
3.
4.
5.
6.
7.
8.
9.
10.
WW, Willis PW, Keller JB: Venous thromboem-
bolism and other venous disease in the Tecumseh Community Health Study. Circulation 48:839-847, 1973. Lindner DJ, Edwards JM, Phinney ES, et al: Longterm hemodynamic and clinical sequelae of lower extremity deep vein thrombosis. J Vasc Surg 4:436-442, 1986. Rutherford RB, Johnson G: Nonoperative management of chronic venous insufficiency. In: Vascular Surgery, ed. by Rutherford RB. Philadelphia: WB Saunders Co, 1984, pp 1394-1399. Franzeck UK, Bollinger A, Huch R, et al: Transcutaneous oxygen tension and capillary morphologic characteristics and density in patients with chronic venous incompetence. Circulation 70:806-811, 1984. Coleridge-Smith PD, Thomas P, Scurr JH, et al: Causes of venous ulceration: A new hypothesis. Br MedJ 296:1726-1727, 1988. Blair SD, Wright DDI, Blackhouse CM, et al: Sustained compression and healing of chronic venous ulcers. Br Med J 297:1159-1161, 1988. Dillon RS: Treatment of resistant venous stasis ulcers and dermatitis with the end-diastolic pneumatic compression boot. Angiology 37:47-56, 1986. Eriksson G: Comparison of two occlusive bandages in the treatment of venous leg ulcers. Br J Dermatol 114:227-230, 1986. Kikta MJ, Schuler JJ, Meyer JP, et al: A prospective, randomized trial of Unna’s boots versus hydroactive dressing in the treatment of venous stasis ulcers. J Vasc Surg 7:478-486, 1988. Skog E, Arnesjo B, Troeng T, et al: A randomized trial comparing cadexomer iodine and standard treatment in the out-patient management of chronic venous ulcers. Br Med J 109:77-83, 1983.
11.
Holloway GA, Johansen KH,
Barnes RW, et al: Multicenter trial of cadexomer iodine to teat venous stasis
ulcer. West J Med 151:35-38, 1989. 12. Ormiston MC, Seymour MTJ, Venn GE, et al: Controlled trial of iodosorb in chronic venous ulcers. Br Med J 291:308-310, 1985. 13. Colgan MP, Dormandy JA, Jones PW, et al: Oxpentifylline treatment of venous ulcers of the leg. Br Med J 300:972-975, 1990.
Contemporary
Treatment
of Venous Lower Limb Ulcers
Objectives
develop an understanding of the prevalence and pathophysiology of venous lower leg ulcers. To understand the major treatment modalities for venous ulcers, in particular: a. The importance of external compression in the pre-
1. To
2.
vention and treatment of venous ulcers b. The value of bandage material and specific local therapies such as cadexomer iodide c. The role of pentoxifylline in healing venous ulcers.
Test Questions 1. What is the recommended pressure at the ankle to promote optimal healing of a venous ulcer? Answer: 35 to 40 mmHg. 2. Local wound care with Unna’s boots and compression bandages are standard therapy. List additional specific local and systemic therapies that also are effective in promoting the healing of venous ulcers. Answer: Cadexomer iodide and pentoxifylline.
Downloaded from ang.sagepub.com at UNIV TORONTO on June 2, 2014
http://ang.sagepub.com/
Contemporary Treatment of Venous Lower Limb Ulcers William R. Hiatt ANGIOLOGY 1992 43: 852 DOI: 10.1177/000331979204301008 The online version of this article can be found at: http://ang.sagepub.com/content/43/10/852
Published by: http://www.sagepublications.com
Additional services and information for Angiology can be found at: Email Alerts: http://ang.sagepub.com/cgi/alerts Subscriptions: http://ang.sagepub.com/subscriptions Reprints: http://www.sagepub.com/journalsReprints.nav Permissions: http://www.sagepub.com/journalsPermissions.nav Citations: http://ang.sagepub.com/content/43/10/852.refs.html
>> Version of Record - Oct 1, 1992 What is This?
Downloaded from ang.sagepub.com at UNIV TORONTO on June 2, 2014
Contemporary
Treatment of Venous Lower Limb Ulcers
William R. Hiatt, M.D.
DENVER,COLORADO
Abstract
postphlebitic syndrome is a significant management problem that aflarge number of patients. Primary prophylaxis of deep-vein thrombophlebitis would reduce the risk of developing the postphlebitic syndrome and should be considered in high-risk patients. Patients who have had a phlebitis should be monitored with noninvasive tests of the deep venous circulation for the development of venous valve incompetence. Patients with venous hypertension should be placed in compression stockings to prevent the postphlebitic syndrome. In patients who progress to venous ulceration, several aggressive measures must be undertaken. Systemic treatment includes management of obesity, edema, immobility, poor nutrition, and comorbid illnesses. Some patients may require a short hospitalization of bed rest, lower limb elevation, and daily dressings and wound care. Outpatient therapy requires sustained compression of 35 to 40 mmHg at the ankle for many months to allow the ulcer to heal. The standard bandage material is Unna’s boots, which is applied every one to two weeks by a trained nurse. Cadexomer iodide is an effective local treatment that helps debride the ulcer and accelerate healing. Finally, pentoxifylline therapy has also been shown to significantly improve the healing of venous ulThe fects a
cers.
Prevalence
250,000 new cases of deep vein thrombophlebitis occur each year resulting in approximately 500,000 patients presenting for the treatment of venous stasis ulcers.’ The More than
between phlebitis and subsequent ulceration is well established. For example, when followed for five to ten years after a venographically documented thrombophlebitis, 80 % of patients will have some symptoms of venous hypertension in association with valvular incompetence.2 In particular, 49% had varicosities, 62 % edema, 34% pigmentation, and 4%
relationship
From the Section of Vascular Medicine, University of Colorado School of Medicine, Denver, Colorado Presented at the 38th Annual Meeting, American College of Angiology, Maui, Hawaii, October, 1991
852
Downloaded from ang.sagepub.com at UNIV TORONTO on June 2, 2014
853 ulceration. The location of the clot influenced the probability of subsequent complications: 100% of iliac thromboses had symptoms, 94 % of femoral clots were symptomatic, and even 47 % of calf clots resulted in symptoms.2 Thus, the postphlebitic syndrome represents a tremendous management problem, the most difficult cases being those with venous ulceration. An important consideration in the development of the postphlebitic syndrome is the primary prevention of thrombophlebitis. There are well-established protocols of prophylaxis against thrombophlebitis in high-risk patients such as those undergoing surgery. The widespread application of these strategies may result in a decrease in the incidence of some, but not all, of the new cases of the postphlebitic syndrome. Therefore, management of patients with lower limb edema and ulceration following an episode of phlebitis will remain a problem.
Pathophysiology The primary initiating event of the postphlebitic syndrome is venous valve destruction from a phlebitis. This leads to venous valve incompetence2 and venous hypertension, particularly during standing and with exercise.3 Over time the increase in venous pressure leads to varicose veins and limb swelling. More chronic forms of the disease are associated with pigmentation changes, induration, and venous ulceration. The causes of venous ulceration are multifactorial and not simply related to the increase in venous pressure. It has been noted that the capillary supply and tissue oxygen tension are normal in areas of venous varicosities, decreased in areas of hyperpigmentation and induration, and absent in avascular skin.4 Therefore, loss of capillary supply and tissue hypoxia may play a crucial role in the development of a venous ulcer.5 White cell activation and plugging of capillaries may further exacerbate the tissue ischemia. Finally, secondary infection with Staphylococcus aureus, Pseudomonas aeruginosa, Streptococcus, Proteus, enterobacteria, and Klebsiella significantly delay healing.
Management General Measures The diagnosis of venous insufficiency should be well established by appropriate noninvasive tests. Particularly useful is the Doppler venous survey to document valvular incompetence of the deep veins. Venous outflow obstruction from extensive, proximal clots leads to a more severe venous hypertension. This condition is diagnosed by an abnormal impedance plethysmographic tracing. In patients with known venous insufficiency or chronic venous obstruction, use of calf-length compression stockings and frequent lower limb elevation are cornerstones of therapy. In compliant patients, these measures may prevent the development of the postphlebitic syndrome and venous ulceration. Patients who present with venous ulcers need attention to their general medical condition. In particular management of obesity, if present, is critical to facilitate healing of the ulcer. On the other hand, patients who are poorly nourished also do not heal well. The mobility of the patient may play a role, particularly in those who are confined to a wheelchair and are unable to elevate their lower limbs. Finally, other medical diseases such as diabetes, or conditions associated with fluid retention, need to be managed with appropriate therapy. The acute management of the venous ulcer may require an initial week of bed rest in the hospital with lower limb elevation.’ During this time patients need to be treated daily with a
Downloaded from ang.sagepub.com at UNIV TORONTO on June 2, 2014
854 of measures. These include soaking the ulcer in potassium permanganate for twenty minutes twice a day or cleaning the wound with hydrogen peroxide to debride the ulcer and treat any fungal infection. If there is evidence of cellulitis, a course of a broad-spectrum antibiotic may be necessary. Acute stasis dermatitis is treated with topical corticosteroids. Finally, if there is pitting edema (in association with congestive heart failure or liver or kidney disease), then a diuretic is helpful.
variety
Sustained
Compression initiating event of venous ulceration is venous hypertension, and thus external compression is critical to reverse this process. Compression is initially achieved by elastic bandages. Once the ulcer is healed, external compression is maintained by custom-made elastic stockings. In the acute case, external pressures of 35 to 40 mmHg at the ankle are necessary for healing.6 The usual bandage systems achieve pressures of only 20 to 30 mmHg at the ankle that rapidly decrease with use over the ensuring week . More extensive, multilayer bandages maintain the necessary pressures over an extended time, and higher pressures are associated with better healing rates. In fact, one system utilizes a balloon that is placed over the ulcer and is intermittently inflated to pressures of 50 to 70 mmHg.7 Although cumbersome, this treatment has been claimed to heal refractory ulcers . Bandage Material In addition to external compression, an occlusive bandage is also employed in the management of the venous ulcer. Historically, Unna’s boots have been used, which consist of gauze impregnated with gelatin, zinc oxide, and caladryl. The bandage is applied moist, wrapped in dry gauze, and followed by an elastic wrap to maintain external pressure. Once applied, the bandage protects the ulcer from the environment, as well as from the patient’s attempts to scratch the area. Initial therapy requires changing the boot weekly. Once healing is established, the boot may be changed less often, but excellent nursing care is essential for best results. Some studies have evaluated newer dressings such as hydroactive material. Initial results suggested that the hydroactive dressing was as effective as the Unna’s boot but better tolerated by the patient. However, in a subsequent study, healing rates were significantly worse with the hydroactive material. With a randomized design, Unna’s boots healed 70% of patients as compared with 38 % with the hydroactive dressings at six months.9 In addition, several complications occurred in the hydroactive dressing, including worsening cellulitis and exudate. Finally, while Unna’s boots and the hydroactive dressings had similar material costs, the hydroactive dressing was less effective, and therefore, the cost per healed ulcer was greater for the hydroactive dressing. The
7
Cadexomer Iodide Cadexomer iodine is a starch polymer bead impregnated with iodide that absorbs large amounts of fluid and is bactericidal. Wound healing is promoted by removal of fluid and bacteria. In an early randomized trial of 74 patients, the ulcer healing rates were significantly greater with cadexomer iodide than with standard therapy.’° The cadexomer iodide also debrided the ulcer, relieved pain, and reduced bacterial counts as compared with standard therapy. More recent controlled trials have confirmed better ulcer healing rates with cadexomer iodide than with standard therapy but have not substantiated the claim that the compound reduces the rate of bacterial infection. 11,12
Downloaded from ang.sagepub.com at UNIV TORONTO on June 2, 2014
855
Systemic Therapy As previously discussed,
activation of white cells in the area of the venous ulcer may exacerbate the local ischemia by the plugging of capillaries. Pentoxifylline is a medication that lowers blood fibrinogen levels, improves red cell deformability, and alters white cell function. It has, therefore, been hypothesized that pentoxifylline may lessen tissue hypoxia and improve the healing of venous ulcers. Recently, a randomized trial has been completed in 80 patients comparing the effects of oxpentifylline with those of placebo in the healing of venous ulcers.’3 All patients had refractory venous ulcers that had not healed on standard therapy. In addition, the patients were all treated with standard two-layer compression dressings. At six months, 64% had healed with oxpentifylline and 34% with placebo (significantly different), but side effects were similar between groups. Thus, oxpentifylline resulted in significantly better healing rates than standard therapy, but these results should be confirmed in larger trials. William R. Hiatt, M. D. Section of Vascular Medicine 4200 E. Ninth Ave. , Box B-180 Denver, Colorado 80262
References 1. Coon
2.
3.
4.
5.
6.
7.
8.
9.
10.
WW, Willis PW, Keller JB: Venous thromboem-
bolism and other venous disease in the Tecumseh Community Health Study. Circulation 48:839-847, 1973. Lindner DJ, Edwards JM, Phinney ES, et al: Longterm hemodynamic and clinical sequelae of lower extremity deep vein thrombosis. J Vasc Surg 4:436-442, 1986. Rutherford RB, Johnson G: Nonoperative management of chronic venous insufficiency. In: Vascular Surgery, ed. by Rutherford RB. Philadelphia: WB Saunders Co, 1984, pp 1394-1399. Franzeck UK, Bollinger A, Huch R, et al: Transcutaneous oxygen tension and capillary morphologic characteristics and density in patients with chronic venous incompetence. Circulation 70:806-811, 1984. Coleridge-Smith PD, Thomas P, Scurr JH, et al: Causes of venous ulceration: A new hypothesis. Br MedJ 296:1726-1727, 1988. Blair SD, Wright DDI, Blackhouse CM, et al: Sustained compression and healing of chronic venous ulcers. Br Med J 297:1159-1161, 1988. Dillon RS: Treatment of resistant venous stasis ulcers and dermatitis with the end-diastolic pneumatic compression boot. Angiology 37:47-56, 1986. Eriksson G: Comparison of two occlusive bandages in the treatment of venous leg ulcers. Br J Dermatol 114:227-230, 1986. Kikta MJ, Schuler JJ, Meyer JP, et al: A prospective, randomized trial of Unna’s boots versus hydroactive dressing in the treatment of venous stasis ulcers. J Vasc Surg 7:478-486, 1988. Skog E, Arnesjo B, Troeng T, et al: A randomized trial comparing cadexomer iodine and standard treatment in the out-patient management of chronic venous ulcers. Br Med J 109:77-83, 1983.
11.
Holloway GA, Johansen KH,
Barnes RW, et al: Multicenter trial of cadexomer iodine to teat venous stasis
ulcer. West J Med 151:35-38, 1989. 12. Ormiston MC, Seymour MTJ, Venn GE, et al: Controlled trial of iodosorb in chronic venous ulcers. Br Med J 291:308-310, 1985. 13. Colgan MP, Dormandy JA, Jones PW, et al: Oxpentifylline treatment of venous ulcers of the leg. Br Med J 300:972-975, 1990.
Contemporary
Treatment
of Venous Lower Limb Ulcers
Objectives
develop an understanding of the prevalence and pathophysiology of venous lower leg ulcers. To understand the major treatment modalities for venous ulcers, in particular: a. The importance of external compression in the pre-
1. To
2.
vention and treatment of venous ulcers b. The value of bandage material and specific local therapies such as cadexomer iodide c. The role of pentoxifylline in healing venous ulcers.
Test Questions 1. What is the recommended pressure at the ankle to promote optimal healing of a venous ulcer? Answer: 35 to 40 mmHg. 2. Local wound care with Unna’s boots and compression bandages are standard therapy. List additional specific local and systemic therapies that also are effective in promoting the healing of venous ulcers. Answer: Cadexomer iodide and pentoxifylline.
Downloaded from ang.sagepub.com at UNIV TORONTO on June 2, 2014
