Disclosure
Problem: Vascular ulcers are a common cause of surgical consultation. For vascular surgeons, only painful extremities and swollen legs are more likely to trigger a consultation. The great majority of vascular ulcers are chronic and/or recurrent. They cause a considerable amount of morbidity among patients with peripheral vascular disease, including work incapacity. The burden placed on the patient and the health care system due to the care of chronic vascular ulcers is significant. Additionally, these nonhealing ulcers place the patient at much higher risk for lower extremity amputation. Frequency: In the United States, the prevalence of vascular ulcers in the general population is not known. In Missouri, venous ulcers are seen in 2.5% of patients admitted to long-term care facilities. This rate is believed to be much higher than the overall population prevalence. Internationally, studies performed in Ireland and Australia estimate the prevalence of current chronic leg ulcers at approximately 1%. Of these, most (approximately 80%) are thought to be caused by venous disease rather than arterial disease. A telephone survey performed in Sweden estimated the prevalence over time to be 9.8% for both healed and nonhealed ulcers in persons older than 70 years. Etiology: Ulceration due to vascular causes is often multifactorial and can be caused by both arterial and venous disease. Hypertension and atherosclerosis of the peripheral vessels lead to arterial disease associated with ischemic ulcers. Chronic venous insufficiency and the resulting venous hypertension cause venous ulcers. Vasculitides such as Buerger disease (thromboangiitis obliterans) or Takayasu disease can also be associated with ulceration. The former tends to manifest with arterial or ischemic-type ulcers, while the latter manifests with cutaneous disease such as pyoderma gangrenosum or erythema nodosum. Pathophysiology: Arterial (or ischemic) ulceration can be caused by either progressive atherosclerosis or arterial embolization. Both lead to ischemia of the skin and ulceration. Venous (or stasis) ulceration is initiated by venous hypertension that develops because of inadequate calf muscle pump action and after the onset of either primary (with no obvious underlying etiology) or secondary (as seen after deep venous thrombosis) valvular incompetence. Two hypotheses have been proposed to explain venous ulceration once venous hypertension develops. The first states that distension of the capillary beds occurs because of increased stasis. This leads to leakage of fibrinogen into the surrounding dermis. Over time, a fibrinous pericapillary cuff is formed, impeding the delivery of oxygen and other nutrients or growth factors to the affected tissue. The resulting hypoxic injury leads to fibrosis and then ulceration. The other hypothesis suggests that the endothelium is damaged by increased venous pressure and leukocyte activation. Proteolytic enzymes and free radicals are released, escape through the leaky vessel walls, and damage the surrounding tissue, leading to injury and ulceration. Clinical: Chronic leg or vascular ulcers typically manifest as arterial, neurotrophic, or venous ulcers. They are distinct with regard to their location, appearance, bleeding, and associated pain and findings. Arterial ulcers Arterial ulcers are often located distally and on the dorsum of the foot or toes. Initially they have irregular edges, but they may progress to have a better-defined appearance. The ulcer base contains grayish, unhealthy-appearing granulation tissue. With manipulation, such as debriding, these ulcers bleed very little or not at all. The patient may report characteristic pain, especially at night when supine, which is relieved by dependency of the extremity. Upon examination, characteristic findings of chronic ischemia, such as hairlessness, pale skin, and absent pulses, are noted. Neurotrophic ulcers Neurotrophic ulcers are characterized by a punched-out appearance with a deep sinus. These are often seen underlying calluses or over pressure points (eg, plantar aspect of the first or fifth metatarsophalangeal joint). They are commonly surrounded by chronic inflammatory tissue. Probing or debriding may lead to brisk bleeding. Because these patients usually have a neuropathy leading to hypesthesia and diminished positional sense or 2-point discrimination, these ulcers are frequently painless. Venous ulcers Venous ulceration is commonly noted in the “gaiter” region of the legs. This region is located circumferentially around the lower leg from approximately mid calf to just below the medial and lateral malleoli. Larger but shallower than other ulcers, stasis ulcers have a moist granulating base and an irregular border. This base oozes venous blood when manipulated. The tissue surrounding these ulcers may exhibit signs of stasis dermatitis. Patients often report mild pain that is relieved by elevation.
Surgical therapy is an integral part of the treatment of nonhealing wounds. Wounds with necrosis or infection usually require debridement or incision of the affected tissue. The goal is to achieve a clean, granulating bed upon which a split-thickness skin graft (STSG) may be placed for closure. In other circumstances, the wound bed may be unable to support a skin graft or debridement or disease may have resulted in the exposure of a structure such as a joint or bone. Under these conditions, local or free flaps of tissue may be used to provide coverage of the wound. These flaps may be performed in concert with or independent of arterial revascularization or venous repair procedures. Revascularization often causes even moderately sized ulcers to heal primarily.
Contraindications: Surgical therapy of vascular ulcers may be accomplished by a number of methods; tailor the choice to fit both the patient's and surgeon's expectations. Primary coverage and/or revascularization may be most appropriate in one patient and amputation with rehabilitation most suitable in another. Evaluate contraindications to treating an ulcer with either an STSG or pedicled or free flap based on the likelihood of survival of the coverage tissue versus the risks of undergoing the procedure, each of which is associated with varying degrees of morbidity. Factors to consider when evaluating an ulcer to determine the likelihood of successful coverage include existing infection or the likelihood of developing infection at the surgical site; the perfusion of the surgical site; the condition of the surrounding tissue, such as edema or ischemia; the rehabilitation potential of the patient; any existing comorbid conditions; or habits of the patient that preclude survival of the graft or flap. |
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Imaging Studies:
Other Tests:
Medical therapy: The latest research on wound care has resulted in increased use of interactive and active dressings rather than passive dressings that cover and absorb. Interactive hydrocolloid dressings provide a controlled microenvironment for wound healing. Active dressings deliver substances such as growth factors, which are important in the healing cascade. Interactive dressings are typically occlusive dressings. They provide important moisture and supply a favorable microenvironment for the growth of new tissue. The advantages of moist occlusive dressings are numerous. Exudate is controlled, while epithelial cell migration is encouraged. Eschar is liquefied and fibrin is lysed to allow convenient debridement. Infection is managed through wound fluid rich in leukocytes. These dressings are also believed to provide symptomatic relief, such as decreased pain and pruritus. Dressings that deliver substances active in the healing process, such as growth factors, have been the subject of much recent investigation. While normal wounds heal because of epidermal division and migration within a neovascularized mesh of granulation tissue, resulting in a cover of new skin, chronic wounds typically show inadequate repair due to insufficient perfusion or wound infection. Topically applied growth factors are meant to assist the chronic wound with establishing healthy granulation tissue or epidermal cell function for improved healing. Several growth factors have been studied to this end. Platelet-derived growth factor has been shown to reduce the size of chronic ulcers by up to 70%, as compared to 17% for placebo, probably via acceleration of provisional wound matrix deposition. Epidermal growth factor supplementation was associated with healing of 8 of 9 wounds in which therapy had previously failed. Fibroblast growth factor has also been studied, but positive results have not yet been achieved. Chronic wounds may be associated with active infection, such as cellulitis. Additionally, an occasional chronic wound may be the nidus for bacteremia and sepsis. In these cases, administer systemic antibiotics. Alternatively, the wound itself may be infected, without systemic effects. Take steps to lower the bacterial count of these wounds, including topical methods to encourage wound healing. Edlich et al have shown that dressing changes alone usually lower the bacterial load, regardless of the type. Silver sulfadiazine has been shown to almost universally reduce the bacterial load to levels acceptable for wound closure. It is a broad-spectrum antibiotic and does not cause pain, as has been noted with mafenide acetate (Sulfamylon). However, penetration of eschar is questionable with this antibiotic. Saline-dampened gauze dressing changes also reduce the bacterial load in the large majority of wounds, but not as effectively as silver sulfadiazine. Povidone-iodine solution (Betadine) has also been used as a topical antibiotic and is largely successful at reducing bacterial counts. However, a widely held belief is that this solution also kills granulation tissue, which significantly impairs healing of these wounds. Surgical therapy: When considering surgical therapy for chronic vascular ulcers, consider which is more appropriate for the patient: (1) revascularization and/or coverage of the wound or (2) primary amputation and rehabilitation. The plastic surgeon has several options when choosing operative coverage of an ulcer. Revision of the wound followed by STSG long has been an option for chronic wound management. Once a clean granulating wound bed has been established through debridement, placement of a skin graft is usually all that is required to attain closure. Skin grafting can be effective for coverage of venous ulcers, but attention must be paid to extremity elevation during healing. Ischemic wounds located in areas that are difficult to treat also may be closed with skin grafting; studies have reported closure rates of 40% for diabetic foot wounds. Often, the wound bed is not suitable for grafting or a structure such as a bone or tendon is exposed. Under these circumstances, consider pedicled or free flaps. These flaps are desirable for several reasons. Healing is promoted even in a suboptimal bed. All diseased tissue, including bone, may be debrided or excised. Neovascularization of the ischemic bed from the flap may occur, and vascular graft patency may be improved by the vascular runoff provided by free tissue transfer. Microvascular flap coverage of chronic ulcers has met with much success in the treatment of arterial ulcers. Colen performed 10 such transfers in patients with peripheral vascular disease, 7 of whom had revascularization prior to the procedure. All anastomoses were successful, although 1 patient underwent amputation after sepsis and its cardiovascular sequelae. Ciresi and coworkers reported successful salvage of limb length and function in 5 of 7 patients who underwent free tissue transfer for ischemic ulcers. Recently, plastic surgeons have begun treating venous ulcers with free tissue transfer, with mixed results. Steffe and Caffee report a 43% complication rate after tissue transfer to venous wounds and the development of new ulcers in all patients at approximately 17 months. Alternatively, Kumins et al and Weinzweig and Schuler reported good success using free muscle flaps and skin grafting to cover venous ulcers. In the first study, all ulcers were healed, and the second study reports a 90% success rate. Both studies were notable for a low recurrence of ulceration and an acceptable complication rate. Preoperative details: Familiarity with the perfusion and vascular supply to the lower extremity is critical to the surgeon for operative planning. Studies estimating perfusion can help predict healing of the wound or flap. Specific knowledge of the arterial supply is invaluable when performing either pedicled or free tissue transfer. Angiography yields detailed visualization of the vessels. Colen and Musson advocate using duplex imaging to select both the recipient vessel and the region of the vessel most suitable for vascular anastomosis. Intraoperative details: Normally, vascular ulcers are treated conservatively with nonoperative techniques. When treated surgically, STSG to the affected areas is the usual procedure. Applying a skin graft to a vascular ulcer requires the same techniques as grafting to other wounds or burns. Varying degrees of ulcer debridement may be required prior to grafting. Harvest a graft from an area of healthy tissue; it may be left in its contracted state or meshed for greater surface-area coverage. Then, apply the graft to the clean, granulating ulcer. It may be secured in place using sutures or skin staples. Grafts also adhere without suturing or stapling if protected well from disruptive forces. Pedicled and free flaps also may be used for coverage of a vascular ulcer. A wide array of choices may be used, based on the location of the ulcer and the status of the vessels perfusing the various pedicled flaps. The patency of the vessel providing inflow for a free flap is also a consideration. The details for performing flap coverage of a chronic ulcer are best studied in a text dedicated to tissue flaps (eg, Flaps, Random Skin Flaps ).
The greatest risk of complications in surgical coverage of vascular ulcers lies with tissue transfer. An obvious source of postoperative concern with regard to successful free tissue transfer is the vascular supply to the flap. The rate of vascular complications in flaps transferred to vascularly compromised tissue is not known, but Rieck et al report a 16% rate of vascular complications out of 631 cases of free tissue transfers. Yajima et al experienced 39 complications in 250 similar cases. The complication rate in patients with ischemic ulcers is expected to be higher than these rates because of the patients' primary diseases. Indeed, Lepantalo and Tukiainen observed vascular patency rates of 68% in their study. Ciresi et al report minor wound complications in 4 of 7 patients studied. Complication rates among cases of tissue transfer for venous ulceration are less well defined. Weinzweig and Schuler report a loss of 2 of 20 flaps, both due to vasospasm, although one occurred in a patient with a history of cocaine abuse. They also noted 3 cases of infection with partial flap and/or graft loss and 2 cases of partial graft loss. Steffe and Caffee experienced a loss of 2 of 14 flaps, caused by venous thrombosis. Two patients had partial flap necrosis in their study, while another 2 had partial graft loss.
Care of chronic ulcers can be accomplished by an array of medical and surgical modalities. Regardless of the method of choice, the primary goal of treating vascular ulcers is preservation of limb length and function. The etiology of the patient's disease and the choice of treatment both play an important role in reaching a successful outcome. The patient's goals and expectations should be taken into account, and the approach should be multidisciplinary in nature.
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