Nonoperative Treatment of Venous Ulcers Joseph D. Raffetto Chronic venous ulcers reflect a complex interplay that involves sustained venous hypertension, leukocyte activation and inflammation, changes in the microcirculation, cytokine and matrix metalloproteinase (MMP) expression, and altered cellular function. The fundamental of nonoperative therapy in venous ulcer pathology is correction of the chronic venous insufficiency (CVI) with compression therapy. Understanding the science involved in the pathophysiology of venous ulcer formation has led to the development of adjunctive treatment directed at the dysregulated inflammatory, cytokine, and MMP expression and molecular pathways that depend on growth factors. Randomized clinical trials are critical to determine the most effective evidence-based treatments for venous ulcer. Compression Therapy and Chronic Venous Ulcer Wound Therapy The successful treatment of patients with venous ulcers requires consistent compression of the limb to eliminate edema, counteracting the venous hypertension underlying existing inflammatory mechanisms. Based on multicenter prospective randomized trials, it appears that high-strength compression (>30 mm Hg) and multilayered compression methods are more effective than lower-strength or single-layered compression. The Cochrane database has unequivocally established that compression therapy heals venous ulcers and prevents recurrences. After ulcer healing, compression must be maintained to prevent recent ulceration. Ulcers healed in 97% of patients who wore elastic compression stockings. Ulcers healed in only 55% of noncompliant patients. Importantly, only 16% of compliant patients wearing compression stockings after healing had recurrences, but in noncompliant patients the recurrence was 100% at 36 months. The dysregulation of cytokines has been proposed as a mechanism for inflammatory response and ulcer formation. The importance of compression therapy received support from a clinical study showing that after 4 weeks of compression therapy, the levels of proinflammatory cytokines decreased significantly and the ulcers began to heal. In addition, levels of transforming growth factor β1 (TGF-β1) increased significantly as the ulcers improved. It was also found that those with higher levels of proinflammatory cytokines including interleukin-1 (IL-1) and IFN-γ healed significantly better than those who had lower levels of these cytokines before compression. The importance of this study was that it showed compression therapy is able to modulate the expression of inflammatory and antiinflammatory cytokines in these ulcers. Future study is required to assess if novel therapies such as cytokine stimulation affects venous ulcer healing. In 15% to 20% of patients with venous ulcerations the limb is also affected by arterial insufficiency. Patients who do not have palpable pedal pulses should be tested with Doppler ultrasound to determine their ankle-to-brachial index (ABI). If the ABI is above 0.8, the arterial supply is likely adequate for high-strength compression. For patients with significant arterial insufficiency (ABI < 0.8) consultation with a vascular specialist is recommended before applying compression therapy because of risk of additional tissue damage with excessive compression. It is important that other standard aspects of venous leg ulcer care are combined with compression to obtain optimal results. Necrotic tissue should be débrided whenever necessary. If infection or bacterial overgrowth is present, appropriate antibiotic therapy is essential. A primary wound dressing is selected based on the amount of exudate expected and the duration of the dressing before the next application. Most venous leg ulcers have heavy exudate, especially at initial treatment. Therefore, foams, alginates, or other highly absorptive primary dressings are appropriate selections. Cadexomer iodine and silver sulfadiazine have been shown in randomized trials to reduce the venous ulcer area. There is little evidence to suggest that one dressing is optimal for the treatment of venous ulcers. The Cochrane database in 2006 concluded that the type of dressing applied to the wound under compression had not been found to affect ulcer healing. Similarly, although silver-containing dressings have become popular choices in the treatment of venous ulcers, there is little evidence that they reduce the incidence of ulcer infection or accelerate wound healing. A randomized, controlled study (VULCAN trial) compared the healing rate for venous ulcers treated with silver-donating dressings or standard dressing in 213 patients. No significant difference in wound closure between the two groups was noted. In numerous studies using various methods of compression, ulcer healing rates have consistently averaged 60% to 70% at 12 to 24 weeks of treatment. Pharmacologic Treatment Modulation of the inflammatory leukocyte response in venous ulcers might have therapeutic benefits in controlling tissue edema and promote healing. Flavonoids are γ-benzopyrones derived from plants and have venotonic properties. Flavonoids act on leukocytes and endothelium, resulting in decreased inflammation and permeability, thus reducing edema. A micronized purified flavonoid fraction (MPFF, Daflon 500), reduces edema and related symptoms as either primary therapy or in conjunction with surgery. A trial of 231 patients with chronic venous disease found that a combination of coumarin and troxerutin (a flavonoid), with compression therapy, for 12 weeks reduced edema and pain compared with placebo. In addition, a meta-analysis of randomized prospective studies using MPFF as adjunctive therapy found that venous leg ulcers healed more rapidly. Pentoxifylline has also been demonstrated to have significant benefit in chronic venous ulcer healing. There have been several randomized, double-blind, placebo-controlled trials. In one study, at 6 months, treatment of venous ulcers with pentoxifylline (400 mg three times a day) demonstrated 67% healed, versus only 31% with placebo (p < .02). At 12 months of treatment, the pentoxifylline treated group demonstrated 88% healed ulcer versus 44% in the placebo group (p < .02). General treatments to reduce inflammation, such as doxycycline and nonsteroidal antiinflammatory drugs (NSAIDs), have been studied in animal models and considered for clinical use. However, no substantial clinical data are available to suggest that these agents are beneficial for accelerating the healing of chronic wounds. Only gold members can continue reading. 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Nonoperative Treatment of Venous Ulcers Joseph D. Raffetto Chronic venous ulcers reflect a complex interplay that involves sustained venous hypertension, leukocyte activation and inflammation, changes in the microcirculation, cytokine and matrix metalloproteinase (MMP) expression, and altered cellular function. The fundamental of nonoperative therapy in venous ulcer pathology is correction of the chronic venous insufficiency (CVI) with compression therapy. Understanding the science involved in the pathophysiology of venous ulcer formation has led to the development of adjunctive treatment directed at the dysregulated inflammatory, cytokine, and MMP expression and molecular pathways that depend on growth factors. Randomized clinical trials are critical to determine the most effective evidence-based treatments for venous ulcer. Compression Therapy and Chronic Venous Ulcer Wound Therapy The successful treatment of patients with venous ulcers requires consistent compression of the limb to eliminate edema, counteracting the venous hypertension underlying existing inflammatory mechanisms. Based on multicenter prospective randomized trials, it appears that high-strength compression (>30 mm Hg) and multilayered compression methods are more effective than lower-strength or single-layered compression. The Cochrane database has unequivocally established that compression therapy heals venous ulcers and prevents recurrences. After ulcer healing, compression must be maintained to prevent recent ulceration. Ulcers healed in 97% of patients who wore elastic compression stockings. Ulcers healed in only 55% of noncompliant patients. Importantly, only 16% of compliant patients wearing compression stockings after healing had recurrences, but in noncompliant patients the recurrence was 100% at 36 months. The dysregulation of cytokines has been proposed as a mechanism for inflammatory response and ulcer formation. The importance of compression therapy received support from a clinical study showing that after 4 weeks of compression therapy, the levels of proinflammatory cytokines decreased significantly and the ulcers began to heal. In addition, levels of transforming growth factor β1 (TGF-β1) increased significantly as the ulcers improved. It was also found that those with higher levels of proinflammatory cytokines including interleukin-1 (IL-1) and IFN-γ healed significantly better than those who had lower levels of these cytokines before compression. The importance of this study was that it showed compression therapy is able to modulate the expression of inflammatory and antiinflammatory cytokines in these ulcers. Future study is required to assess if novel therapies such as cytokine stimulation affects venous ulcer healing. In 15% to 20% of patients with venous ulcerations the limb is also affected by arterial insufficiency. Patients who do not have palpable pedal pulses should be tested with Doppler ultrasound to determine their ankle-to-brachial index (ABI). If the ABI is above 0.8, the arterial supply is likely adequate for high-strength compression. For patients with significant arterial insufficiency (ABI < 0.8) consultation with a vascular specialist is recommended before applying compression therapy because of risk of additional tissue damage with excessive compression. It is important that other standard aspects of venous leg ulcer care are combined with compression to obtain optimal results. Necrotic tissue should be débrided whenever necessary. If infection or bacterial overgrowth is present, appropriate antibiotic therapy is essential. A primary wound dressing is selected based on the amount of exudate expected and the duration of the dressing before the next application. Most venous leg ulcers have heavy exudate, especially at initial treatment. Therefore, foams, alginates, or other highly absorptive primary dressings are appropriate selections. Cadexomer iodine and silver sulfadiazine have been shown in randomized trials to reduce the venous ulcer area. There is little evidence to suggest that one dressing is optimal for the treatment of venous ulcers. The Cochrane database in 2006 concluded that the type of dressing applied to the wound under compression had not been found to affect ulcer healing. Similarly, although silver-containing dressings have become popular choices in the treatment of venous ulcers, there is little evidence that they reduce the incidence of ulcer infection or accelerate wound healing. A randomized, controlled study (VULCAN trial) compared the healing rate for venous ulcers treated with silver-donating dressings or standard dressing in 213 patients. No significant difference in wound closure between the two groups was noted. In numerous studies using various methods of compression, ulcer healing rates have consistently averaged 60% to 70% at 12 to 24 weeks of treatment. Pharmacologic Treatment Modulation of the inflammatory leukocyte response in venous ulcers might have therapeutic benefits in controlling tissue edema and promote healing. Flavonoids are γ-benzopyrones derived from plants and have venotonic properties. Flavonoids act on leukocytes and endothelium, resulting in decreased inflammation and permeability, thus reducing edema. A micronized purified flavonoid fraction (MPFF, Daflon 500), reduces edema and related symptoms as either primary therapy or in conjunction with surgery. A trial of 231 patients with chronic venous disease found that a combination of coumarin and troxerutin (a flavonoid), with compression therapy, for 12 weeks reduced edema and pain compared with placebo. In addition, a meta-analysis of randomized prospective studies using MPFF as adjunctive therapy found that venous leg ulcers healed more rapidly. Pentoxifylline has also been demonstrated to have significant benefit in chronic venous ulcer healing. There have been several randomized, double-blind, placebo-controlled trials. In one study, at 6 months, treatment of venous ulcers with pentoxifylline (400 mg three times a day) demonstrated 67% healed, versus only 31% with placebo (p < .02). At 12 months of treatment, the pentoxifylline treated group demonstrated 88% healed ulcer versus 44% in the placebo group (p < .02). General treatments to reduce inflammation, such as doxycycline and nonsteroidal antiinflammatory drugs (NSAIDs), have been studied in animal models and considered for clinical use. However, no substantial clinical data are available to suggest that these agents are beneficial for accelerating the healing of chronic wounds. Only gold members can continue reading. Log In or Register to continue Share this:Click to share on Twitter (Opens in new window)Click to share on Facebook (Opens in new window) Related Related posts: Technical Aspects of Percutaneous Carotid Angioplasty and Stenting for Arteriosclerotic Disease In-Situ Treatment of Aortic Graft Infection with Prosthetic Grafts and Allografts Treatment of Acute Upper Extremity Venous Occlusion Intraoperative Assessment of the Technical Adequacy of Carotid Endarterectomy Stay updated, free articles. Join our Telegram channel Join
