Robert J. Spence
Glen S. Roseborough
Lower Extremity Ulcers
Ulceration of the lower extremity, most often caused by either macrovascular or microvascular disease, is a common and important problem in ambulatory medical practice.
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As a result of the aging population, the incidence of leg ulcers is rising (1). The ambulatory setting frequently is the best place to treat lower extremity ulcerations to maintain mobility and avoid the complications of hospital bedrest (2).
Accurate diagnosis is based mainly on history and physical examination and is essential for appropriate treatment. Inappropriate therapy can lead to the loss of a toe or even a limb. Generally, it is necessary to give detailed instructions to the patient and to have a great deal of patience. Patient compliance with treatment has been shown to be critical in the success of therapy and the prevention of recurrent ulceration (3).
History
The medical history is important. Illnesses such as arteriosclerotic vascular disease or hypertension, diabetes mellitus, renal failure and dialysis, sickle cell disease, and collagen-vascular disease may be associated with ulcers of the lower extremities. A history of corticosteroid therapy may explain failure of ulcers to heal. Drug abuse or a psychiatric history may be pertinent in the explanation of factitious ulcers. Furthermore, aspects of the patient's lifestyle, particularly mobility and lower extremity dependency, are important.
Specific attention should be paid to duration of ulceration and previous attempts at therapy; symptoms of peripheral arterial vascular disease, such as intermittent calf claudication, intermittent thigh or gluteal claudication, impotence, calf pain at rest, and feelings of coldness and tingling in the legs; a history of deep vein thrombosis, ulceration, or injury to the lower extremities; and a history of discomfort associated with footwear or of chronic swelling, and, if swelling has occurred, whether it has been alleviated by lying down.
Ischemic pain in the calf at rest is usually a symptom of advanced peripheral arterial disease (PAD), and it is characteristically alleviated if the patient dangles his or her feet over the edge of the bed or sits in a chair when awakened at night by ischemic pain. These symptoms must be differentiated from nocturnal leg cramps that occur in many people who have no evidence of peripheral vascular disease. Leg cramps are usually accompanied by palpable hardening of the calf muscles and involuntary muscle contraction of the flexor muscles of the toes. The cramps usually are relieved if the patient gets out of bed and walks around. Examination of the extremities in these patients (see below) is usually normal.
Physical Examination
A general physical examination of the patient is undertaken in conjunction with the examination of the lower extremities. The general examination should include a documentation of weight and, ideally, body mass index (BMI). Abdominal aortic aneurysm and other intra-abdominal masses, lymphatic masses in the groin, and signs of long-standing hypertension and cardiac disease should be sought. Needle tracks and brawny indurated hands may indicate a history of drug abuse, as may skin ulcers in areas other than the lower extremities.
Examination of the Lower Extremities
Both lower extremities should be bared. Initial examination is performed while the patient is supine. Both legs are examined and compared. Particular points to be noted include the following:
After inspection of the feet and legs, a vascular examination of the lower extremities is conducted. Femoral, popliteal, dorsalis pedis, and posterior tibial pulses are palpated and graded. Ideally, an ankle-brachial index (ABI) is obtained, particularly if compression dressings are contemplated as therapy. The capillary refill time is observed after placing pressure on the toes with the legs elevated 45 degrees (normally less than 5 seconds). Auscultation from the mid-abdomen down to the popliteal regions is performed to detect bruits that are produced by narrowed atherosclerotic arteries. The temperature of the legs is felt with the dorsum of the hand, both descending from the thigh to the foot and comparing one side with the other. The patient is asked to sit up and to dangle his or her legs so that venous filling time and dependent rubor can be assessed. Evidence of varicose veins is best sought with the patient standing.
Inspection and Palpation of Ulcer or Ulcers
Ulcerated areas on the legs are often very tender; palpation, although necessary, should be done gently, with the gloved hand.
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Site
An accurate description of the site of the ulcer, preferably with reference to an anatomic landmark (e.g., the medial or the lateral malleolus), should be recorded.
Size
The size of the ulcer must be documented. A personal or institutional convention should be established to measure the size in millimeters. Only by measuring in millimeters can the often subtle changes be appreciated in future evaluations. For example, the horizontal and vertical dimensions, or the longest axis and the longest width perpendicular to that axis can be reproducibly measured. Digital photographic imaging with a scale present, which is then converted to area using planimetry, is the best measurement mode currently available, but clearly not accessible to all health care professionals. This measurement is particularly important for future reference when the progress of healing and the efficacy of treatment are assessed.
General Character
It should be noted whether the ulcer is regular or irregular in outline. The edges should be examined to determine whether they are raised, heaped, everted, or flat, and whether they are undermined. Any evidence of healing manifested by epithelial ingrowth from the edge of the ulcer toward the center should be noted. The base should be examined to see whether it is clean or covered with exudate and to see the type of tissue of which it is constituted (e.g., clean fascia, granulation tissue, dirty exudate, debris). The vascularity of the base is the most critical characteristic to be noted when considering the potential of the ulcer for healing.
Tenderness
If the ulcer is tender, it should be determined whether it is very tender, such as in acute inflammation or ischemia, or only mildly tender, as in a neuropathy with loss of superficial sensation.
Changes in Adjoining Skin
It should be noted whether there are fluctuant areas or purulence near the ulcer, particularly on the sole of the foot; any callosities surrounding the ulcer; heavy deposition of pigment near the ulcer; or local edema.
When the examination of the ulcer is completed, the patient should stand, preferably on a standing stool, and face the examiner. Edema should now be looked for, as should the presence of varicose veins along the course of the short and long saphenous veins on the front and back of the legs (Fig. 95.1). In particular, the appearance of perforator varicosities (see Physical Examination, under Varicose Veins, below) should be noted, usually above the medial malleolus, and the relationship of these perforators to ulcerated areas should be sought.
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FIGURE 95.1. Venous circulation of the lower extremity. 1, Hunter canal perforator; 2, anterior communicating vein of the leg; 3, ankle perforators. |
Types and Characteristics of Leg Ulcers
Most lower extremity ulcers are caused by venous insufficiency, arterial insufficiency, diabetes, or a combination of these conditions. An exhaustive list of these and other rare causes may be found in a recent review (4). Table 95.1 shows the principal characteristics of common ulcers.
Ulceration Associated with Venous Insufficiency
Venous ulcerations are caused by increased pressure because of insufficiency of the valves of the deep venous system and of the lower perforator veins. The valvular
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disorder most commonly follows deep venous thrombosis (DVT) with destruction of valves in the deep venous system and reversal of normal superficial-to-deep flow of blood in the perforating veins. Congenital weakness of the valves is hypothesized for those with no history of DVT. The muscular action of the calf becomes ineffective, and blood flows to the superficial veins instead of in the usual centripetal direction through the deep venous system. Valves in the superficial (saphenous) system become incompetent, thereby raising the hydrostatic venous pressure at the ankle. Alternatively, immobilization and dependency with absent muscle contraction can result in edema and ulceration even with intact venous valves. This condition is known as the dependency syndrome.
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TABLE 95.1 Characteristics of Common Leg Ulcers |
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On a microcirculatory level, the old theory that stasis of venous blood was the cause of tissue hypoxia and necrosis has long been disproved; therefore, the term stasis ulcer is technically a misnomer. However, the exact pathophysiologic cascade from valve insufficiency to ulcer is still not certain. Browse and Burnand (5) proposed the fibrin cuff theory, popular until recently, in which venous hypertension was postulated to distend the local capillary bed and widen the endothelial pores, allowing large molecules to escape. The most important of these molecules was assumed to be fibrinogen, which was believed to clot and form a fibrin cuff around the capillary. This cuff would be a barrier to the passage of oxygen and other nutrients, leading to cell death and ulceration (5). More recent research suggests that venous hypertension leading to attachment and inappropriate activation of leukocytes in the cutaneous microcirculation with resultant endothelial injury is the more likely cause of ulceration associated with venous insufficiency. Although increased plasma fibrinogen and decreased fibrinolytic activity are present, there is also evidence for local release of leukocyte-derived free radicals, proteolytic enzymes, cytokines, and other noxious mediators (6,7). Increased venous pressure increases transendothelial and interendothelial capillary passage of protein rich fluid resulting in edema. Edema itself may contribute to tissue hypoxia simply by increasing the diffusion distance of oxygen around the nourishing capillaries (8).
An important additional cause of recalcitrant venous ulcer is coexisting arterial disease seen in as many as 15% to 20% of patients (6). Often, minor trauma at the site is the initiating event in the process that culminates in an ulcer in a susceptible patient (see Ulceration Associated with Arterial Insufficiency).
The physical examination reveals edema, hemosiderin deposition, and ulceration, usually in line with the long saphenous vein, the short saphenous vein, or over a medial ankle perforator (Fig. 95.1). Arterial circulation in the leg may be entirely normal. Varicosities may or may not be present. The ulcer is usually fairly superficial and involves the skin, with irregular margins and with exudate covering the floor of the ulcer. The ulcer is usually movable with the skin and is tender. In grossly neglected cases, the ulceration may be massive and may involve most of the circumference of the leg. Occasionally, cellulitis may be evident, with erythema, tenderness, and fever secondary to superimposed invasive bacterial infection (see Chapter 32).
Ulceration Associated with Arterial Insufficiency
Arterial insufficiency (see also Chapter 94) is the second most common cause of leg ulcers and, along with venous insufficiency, accounts for most leg ulcers. Ulcers associated with peripheral arterial occlusive disease usually begin with trauma and therefore appear at sites that are most subject to trauma (e.g., on toes, over the lateral or medial malleolus, at the base of the fifth metatarsal, at the head of the first metatarsal, on the heel or the ball of the foot, and in the distal pretibial region).
Ulcers secondary to occlusive arterial disease are characteristically painful, probably related to local inflammation and to ischemia. The foot may appear atrophic with shiny, fragile, transparent, hairless skin; the nails are often hypertrophied and deformed. Other hallmarks of arterial insufficiency (e.g., pulselessness and coolness) may be present. Because some patients are relieved of pain when they dangle the ulcerated leg, dependent edema may be present.
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Dystrophic Ulcers
A neuropathic or dystrophic ulcer is usually associated with somatic or sympathetic neurologic dysfunction. The precise pathogenesis of these ulcers is unknown. Perhaps sympathetic dysfunction causes a reduction of arterial blood flow to local areas of skin that result in ulceration. Furthermore, hypesthesia or anesthesia renders the patient more susceptible to trauma. Dystrophic ulcers are most commonly associated with peripheral neuropathies (see Chapter 92) and the neuropathies of congenital or acquired disease of the spinal cord, such as Friedreich ataxia, syringomyelia, or multiple sclerosis. Peripheral neuropathies caused by vitamin deficiency or injuries may also result in ulcers. Ulceration almost always occurs in areas of pressure. The patient may complain of pain in the ulcer, but the ulcer is usually insensitive to light touch. There may be deformity in the foot associated with the neuropathy (talipes calcaneovalgus or equinus, deformities in which the anterior part of the foot is elevated and the heel is turned outward or in which the foot is plantar-flexed, respectively) or there may be a back deformity or surgical scar, as might occur in a patient with a meningomyelocele. Usually, neurologic examination of the lower extremity is abnormal, revealing decreased proprioception, decreased cutaneous sensation, and perhaps impaired movement. The ulcer may be undermined, and there may be subcutaneous tracking of infected material into adjacent tissues that, on pressure, exude loculated pus from the undermined border of the ulcer. If the neuropathy is severe, the patient may be ambulating without pain, yet show advanced ulceration of the sole of the foot.
Diabetic Ulcers
Diabetic ulcers have features of dystrophic, traumatic, and arterial ulcers because all three factors contribute to their development. The characteristic location of such an ulcer is in an area of pressure, such as a corn or a callosity (see Chapter 73). The ulcer is fairly insensitive, often heavily infected, with undermined edges and tracks under the plantar fascia or proximally on the dorsum of the foot. Although usually patients are aware that they are diabetic, some are not, and a thorough evaluation upon suspicion of diabetes is mandatory because control of the ulcer depends to a large extent on control of the diabetes. Radiologic examination is important because the bone underlying the ulcer may be the site of chronic osteomyelitis that may necessitate surgical intervention (see Chapter 40).
Posttraumatic Ulcers
Posttraumatic ulcers are common and usually are associated with impairment in nerve or vascular supply of the leg. Minor injury to the toe of a patient with arteriosclerotic occlusive vascular disease or a leg injury in a patient with chronic venous insufficiency may lead to ulceration. However, such ulcers may develop in the legs of otherwise healthy people, particularly after major injuries such as fractures that involve areas where vascular supply is normally marginal. The most susceptible site is the junction of the middle and lower third of the subcutaneous surface of the tibia. In this situation, most traumatic ulcers, even in healthy youngsters, heal with some difficulty, and in older patients and in those with even minimal arterial insufficiency, injury at this site resolves with great difficulty. Posttraumatic ulcers may be accompanied by problems of chronic infection and present with tenderness and local cellulitis.
Factitious Ulcers
Factitious ulcers are self-inflicted or self-maintained ulcers. Because they develop in the absence of any other local or systemic cause, diagnosis of factitious ulcers requires a high degree of suspicion. They most commonly occur in the legs of addicts who inject drugs into slightly varicose leg veins. The distribution of these ulcers is usually bizarre. They may be multiple and bilateral; if the history can be obtained, the diagnosis is easily made.
Factitious ulcers may also occur in patients with poor hygiene, psychiatric disorders, or disorders associated with pruritus, such as scabies, which has led to excoriation. The diagnosis should be suspected if the patient appears to derive some real or imaginary gain from having the ulcer. An ulcer without a definite cause that fails to heal in an apparently healthy environment should lead to the suspicion that it is factitious.
Neoplastic Ulcers
Neoplastic ulcers of the leg are rare, but when they do occur, they are usually either basal cell or squamous cell carcinomas and have the usual characteristics of these tumors (see Chapter 114). They have elevated or rolled edges, are anesthetic, and are usually attached to deeper tissue.
Marjolin ulcer, a rare form of squamous cell carcinoma that occurs in burn wounds of long duration and other chronic wounds, may also be seen on the legs. Because of the improved ability to close burn and other chronic wounds, Marjolin ulcers are seen exceedingly rarely in present day practice. However, a high level of suspicion must be maintained in the setting of a chronic wound to prevent failure to diagnose this malignant condition.
Hypertensive Ulcers
Another rare type of ulcer is associated with uncontrolled systemic arterial hypertension. It is thought that there
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is a progressive increase in the thickness of the arteriolar wall, decrease in the diameter of its lumen, progressive ischemia, and infarction of the skin (9). These ulcers are extremely painful and occur most often in women on the posterolateral aspect of the leg and ankle. Ordinarily there is no evidence of peripheral arterial or venous disease.
Ulcerating Skin Diseases
Pyoderma gangrenosum presents with ulceration as the first symptom. The etiology is unknown, but it is associated with inflammatory bowel disease (IBD) and other diseases such as lymphoma, myeloma, and other malignancies. It presents with deep, necrotic ulcers with elevated violaceous borders. It is progressive if left untreated. It is treated using immunosuppressive drugs including prednisone, cyclosporine, and other immunomodifiers (10). Ulceration is also a common but not defining feature in diseases such as vasculitis, scleroderma, calciphylaxis, lichen planus, and necrobiosis lipoidica (4).
Miscellaneous
Ulceration of the legs may occur in sickle cell disease, polyarteritis nodosa, collagen-vascular diseases, and other systemic conditions (e.g., ulcerative colitis). In these instances, the diagnosis depends on accurate diagnosis of the systemic disorder.
Corticosteroid therapy, particularly if it is long-standing, can lead to atrophy of the skin, increasing its fragility and susceptibility to injury. Furthermore, the impairment by corticosteroids of wound healing may prevent some ulcers from healing.
A toxic cause of skin ulceration is the brown recluse spider bite, common in the southeastern United States. The poison of the brown recluse spider contains a necrotizing enzyme that causes a rounded sloughing ulcer of approximately 3 to 4 cm with an indurated edge. The patient may not be aware of having been bitten by a spider. These ulcers are refractory to healing by use of conservative measures and should be surgically excised and closed.
Cutaneous cytomegalovirus (CMV) infection has become more common in association with the increased incidence of acquired immune deficiency from human immunodeficiency virus (HIV) infection. CMV infection can cause lower extremity ulceration. Even syphilis, ulcerating tuberculosis, and histoplasmosis must be considered in the differential diagnosis of skin ulceration in HIV-positive individuals.
In the tropics, ulceration of the foot and leg may occur from local mycoses such as maduromycosis and cutaneous leishmaniasis; these conditions should be kept in mind when a patient has returned from a tropical climate.
Laboratory Aids in Diagnosis
Bacteriology
Leg ulcers are often infected and almost invariably contaminated, usually with enteric organisms. Infections are particularly hazardous in diabetic patients and those with chronic arterial insufficiency. Biopsy cultures of the ulcer bed may be useful, and cultures of obviously purulent ulcers are mandatory because antibiotic therapy is an important part of management, particularly when invasive infection is apparent (see Chapter 32). Viral culture of a small biopsy may be necessary to diagnose CMV-induced cutaneous ulceration. When there is an unusual degree of scaling and excoriation, fungal infection should be suspected. Unless the clinician is experienced in the scraping of lesions and the microscopic identification of fungi, dermatologic consultation is indicated.
Biopsy
Biopsy by a surgeon or a dermatologist is indicated if neoplastic, vasculitic, or obscure fungal disease is suspected. Biopsy may be performed in the office under local anesthesia and should include a wedge-shaped section of the edge and floor of the ulcer. Any chronic ulcer that exists in a long-standing scar of any type should be biopsied to rule out squamous cell carcinoma. Sometimes only a biopsy of bone makes a definitive diagnosis of osteomyelitis that underlies a chronic ulcer.
Laboratory Tests for Systemic Disease
These tests are performed as dictated by the clinical diagnosis when the ulcer is suspected to be part of a systemic disorder (e.g., diabetes, systemic vasculitis, or sickle cell disease).
Noninvasive Vascular Testing
Diagnosis of arterial disease is made by physical examination and calculation of the ABI. An ABI greater than 0.8 is considered within normal limits and is safe for the application of compression therapy. An ABI less than 0.5 indicates arterial insufficiency. When high systolic pressures are measured one must consider that calcification of the arteries has reduced their compressibility making the ABI unreliable.
Noninvasive vascular testing such as venous Doppler examination can define the anatomy and function of the venous system of the lower extremities. Particularly in the case of persistent lower extremity ulceration, noninvasive testing may be helpful in determining the cause and determining whether surgery might correct a venous or arterial problem, and help heal the ulcer. When ulceration is noted in a patient with occlusive arterial disease, the
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patient should be referred to a vascular laboratory for noninvasive arterial testing. Noninvasive vascular testing is discussed more fully later in this chapter.
Natural History and Management
Generally, chronic ulcers develop initially from skin trauma, which may be exceedingly minor. However, the insult may occur in a milieu of macrocirculatory or microcirculatory disease or other unfavorable local or systemic factors. Once the wound becomes inflamed, the local metabolic rate increases the demand for oxygen and nutrients, which leads to compromise and death of tissue when the demands are not met. The tissue then may become infected, resulting in more inflammation, propagating the cycle, making the ulcer enlarge and then become chronic. Treatment of the ulcer requires breaking this cycle.
Edema is commonly associated with lower extremity ulcers, particularly those related to chronic venous disease. When present, it retards healing and reduces the skin resistance to trauma and subsequent infection (8). This makes the treatment of edema a very important component of ulcer therapy and prevention.
Chronic open wounds are all colonized by microorganisms to a greater or lesser extent. As long as an ulcer is an open wound, invasion by organisms is rare, and the threat of invasive infection and systemic toxicity is minimal. Furthermore, because the bacteria are on the surface of the wound rather than in the tissue, and the tissue in the base of the ulcer is often poorly vascularized, systemic antibiotics do not affect the surface flora significantly. Topical antibiotics are generally more appropriate for open wounds, and systemic antibiotics are reserved for evidence of invasive infections.
An abscess greatly increases the risk of invasive infection. When a collection of loculated pus exists, it must be adequately drained. Eschars that overlie ulcers may hide such loculated pus and should generally be débrided. Wet eschars can simply be lifted with a tweezer and snipped. Dry eschars must be cut with a scissors or a scalpel along the plane of necrosis to avoid incising healthy tissue.
Most ulcers of the lower extremities can be treated on an ambulatory basis. Generally outpatient care maintains mobility and thus the muscle pumping action that enhances venous and fluid return from the legs. Furthermore, it reduces the cost of hospitalization and the complications of bed rest (2). However, the presence of one or both of the following may be an indication for hospitalization:
Ensuring adequate nutrition is an important aspect of managing the patient with a leg ulcer. Identification and correction of nutritional deficiencies improves management: however, there is no evidence that supplementation in the absence of a specific deficiency accelerates healing (11).
Ulceration Associated with Venous Insufficiency
Probably no other form of ulcer taxes the patient or the practitioner as much as that associated with chronic venous insufficiency. The mainstays of therapy are elimination of necrotic tissue and infection, cleansing of the ulcer bed to facilitate healthy tissue growth, reduction of edema by elevation and compression, and ensuring adequate arterial perfusion. Most of these ulcers heal by the use of nonoperative therapy.
The first step in managing these ulcers is to create an optimal environment. In the absence of other systemic factors, this step is primarily an attack on necrotic tissue, edema, and the bacterial colonization of the wound. Initial outpatient treatment consists of débridement of necrotic tissue and determination of the adequacy of arterial supply to the lower extremity in the office. Débridement can be performed safely using sharp scissors and forceps. Cutting within the necrotic tissue, leaving a thin layer above vascularized tissue, allows débridement without pain and bleeding. The residual necrotic layer resolves with further local débridement as performed during appropriate changes of dressings and through wound and bacterial autolysis.
The traditional and still most common effective way to minimize exudates and débride residual necrotic tissue has been the wet-to-dry dressing. A sterile gauze pad moistened in normal saline (not soaking wet, because this can cause maceration) is secured over the ulcer (with a rolled bandage, not with an adhesive tape, which can damage the skin adjacent to an ulcer) and left to dry. Necrotic tissue and other debris are removed when the dried dressing is removed, gently, at the end of each dressing interval. This procedure is appropriate early in ulcer management when there is substantial exudate and debris to remove and when there has been little healing. For a tender wound in which pain prevents the use of wet-to-dry dressings, the dressing can be moistened with saline before removal making it a wet-to-wet dressing. This is a less aggressive way of débriding, but is gentler to the healing wound tissues.
Enzymatic débriding agents may also be helpful when only a thin layer of necrotic tissue remains on the ulcer. These agents are not effective when there is more than minimal necrotic tissue left on the wound. A newly reported ultrasonic mist device to clean the wound and stimulate wound healing also seems to show some promise (12).
If arterial flow is adequate, compression dressings can be used to reduce the edema and should be worn
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whenever the extremity is dependent. The external compression counteracts the internal venous hypertension, reduces and prevents further edema and allows the patient to be somewhat ambulatory. Arterial inflow is adequate if bounding foot pulses are present or the patient's ABI is greater than 0.8 (most accurately measured by a vascular laboratory). Patients at home should be placed at rest with the extremity elevated.
Wounds will not heal with contamination greater than 105 organisms per gram of tissue. After adequate bacteriologic cultures, a suitable topical antibacterial preparation such as silver sulfadiazine cream (e.g., Silvadene Cream 1%) or sodium oxychlorosene solution (Clorpactin 0.4% in water or isotonic saline) should be applied. Recently, multiple products containing silver have been advanced to reduce the bacterial contamination of wounds. Silver is a heavy metal with innate antiseptic action with a long history of preventing and treating burn wound infections. The recent products include silver impregnated fabrics, hydrocolloid, and calcium alginate dressings. They promise to combine bacteria killing effectiveness with the provision of an environment that supports wound healing, although there is yet little published evidence about to the effectiveness of these types of dressings and comparisons among them (2).
Invasive infection in the tissue surrounding the ulcer is uncommon, but should be suspected in ulcers in which an eschar traps pus under pressure before débridement and in those that exhibit evidence of cellulitis, such as erythema, tenderness, and swelling locally. The wound should be cultured and the infection should be treated with an appropriate systemic antibiotic.
Recent studies suggest that systemic medical treatment with pentoxifylline (400 mg three times a day) may be given as adjunctive therapy. The drug is thought to reduce leukocyte activation and enhance fibrinolysis along with its well-recognized rheologic effects on blood and blood flow (6,13). Use of other systemic medications is less well established.
With intensive therapy, edema and bacterial overgrowth can be controlled in 48 to 72 hours. Thereafter, these optimal conditions must be maintained, healing encouraged, and edema kept to a minimum by the use of compression dressings and leg elevation.
The lower extremity may be wrapped with a zinc oxide–gelatin dressing (Unna boot, Dome paste boot) that has long been used successfully in the treatment of leg ulcers. If used, it is imperative that it is not wrapped tightly and that it is placed smoothly from the metacarpal–phalangeal joints to just below the tibial tuberosity, including the heel. This can be done best by keeping the bandage roll on the surface of the leg as the leg is wrapped. Wrinkles, failure to wrap the heel, and compression that is either too tight or too loose result in treatment failure and can result in further ulcerations. The Unna boot is then covered with an elastic wrap for gentle compression. When first applied it should be removed within 48 hours to ascertain that the compression is adequate and that further problems are not being created. The bandage may then be reapplied and changed weekly, and healing usually results. An Unna boot should not be applied if there is a suspicion of PAD because it could cause more ischemia.
A similar type of dressing that has gained popularity is the four-layer compression dressing. This dressing works on a similar principle but has an absorptive layer that may be useful, particularly for more exudative wounds.
When the ulcer is clean, or if it is quite shallow, a good alternative is a hydrocolloid dressing (e.g., DuoDERM) under an elastic bandage. This dressing does not disrupt the growth of healing tissue and allows healing in a moist environment (14). Small amounts of residual necrotic debris in the ulcer are removed by fibrinolytic action of the fluid that builds up under the dressing. The ulcer usually requires a change of dressing every 48 to 72 hours. However, it requires changing more frequently if the fluid that develops leaks out the side of the dressing.
Many new dressings are currently being evaluated in the treatment of lower extremity ulcers. These include calcium alginate, hydrogels, and new types of débriding gauzes. Serial compression pumps to reduce edema are now available for home use. No conclusions can be drawn at this time regarding the efficacy of any of these new treatments due to the dearth of well-controlled comparative trials.
Similarly, dressings that apply subatmospheric pressure to various types of wounds have become very popular (15). Reports seem to indicate that wounds get smaller in volume, may be more easily débrided, and may develop better beds for skin grafting with this technique. However, evidence-based recommendations for this technique in the management of lower extremity ulcers are not possible currently.
Occasionally, diuretics may be helpful in managing edema even when no element of cardiac or renal failure exists. Elastic compression should always be used first to avoid the danger of volume depletion. Ultimately, if edema and bacterial colonization can be controlled, the ulcer will usually heal, although several weeks to months may be required. After the healing, the patient must be advised to keep the leg elevated, if possible, when sitting down and to wear some form of elastic compression permanently, preferably a made-to-measure elastic support garment. If the ulcer still fails to heal, skin grafting may be required along with venous ligation and stripping. This requires surgical consultation and hospitalization.
Ulceration Associated with Arterial Insufficiency
Arterial ulcers are very difficult to heal unless blood flow to the area can be improved. Therefore, if there is any
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suspicion of arterial insufficiency, the patient should be referred for noninvasive vascular testing and, possibly, surgical evaluation. If the patient's lesion is unsuitable for surgical correction, or if the patient has already had an operation but ulceration persists, the ulcer can sometimes be healed with painstaking débridements every 2 or 3 days. The addition of pentoxifylline may also be of benefit (13). However, this treatment requires expertise; if doubt exists, surgical referral should be made.
A pair of sharp scissors or a scalpel is used to remove the dry eschar that covers the ulcer and to remove the necrotic edges of the ulcer carefully without causing bleeding, similar to the approach to venous insufficiency ulcers (see Ulceration Associated with Venous Insufficiency). Wet-to-wet dressings are then applied, using a topical antibiotic solution such as sodium oxychlorosene or polymyxin–bacitracin 5% aqueous suspension. The patient is instructed to apply the bandage wet in the morning and to remove it in the evening after wetting it again. This has the effect of debriding the ulcer and promoting wound healing, consisting of wound contraction and re-epithelialization.
Very tenacious residual necrotic debris after sharp débridement may be removed with a short course of a proteolytic enzyme applied three to four times a day followed by the application of a wet-to-wet dressing or by hydrocolloid dressings. In conjunction with these measures, meticulously compulsive foot protection, soft footwear, elevation of the extremity, and avoidance of weight bearing are mandatory.
Dystrophic Ulcers
Dystrophic ulcers are a real threat to the limb because infection often advances unnoticed by the patient until there is considerable spread of pus under the eschar or in the tissue around the ulcer. Treatment consists of bed rest, relieving pressure on bony prominences frequently, appropriate antibiotic therapy as indicated after culture (see Chapter 32), débridement of necrotic skin edges (which can be done without anesthesia in the office; see above), and wet-to-wet dressings as described above.
Once the ulcer has been rendered clean by débridement and dressings, slow healing may progress, often over several months. In patients with dystrophic foot ulcers, total contact casting (see Diabetic Ulcers, below) has been successful in relieving pressure on the ulcer and providing an environment conducive to healing. This technique has provided a new means of treating these patients while they remain ambulatory and has considerably reduced hospitalization rates for this condition.
Diabetic Ulcers
Patients with uninfected diabetic ulcers may be treated as outpatients. However, infected diabetic ulcers impose such a serious risk of limb loss that serious consideration should be given to hospitalizing these patients. The very important regulation of blood glucose levels can best be effected in the hospital (16,17). Furthermore, any pockets of suppuration can be drained, proper débridement can be carried out, and bone biopsy can be done if osteomyelitis is suspected (18).
Once the ulcers are clean and uninfected, leg elevation and avoidance of pressure and shearing forces on the area of ulceration will allow healing. In patients with foot ulcers, total contact casting has been successful in alleviating these forces and in providing an optimal environment for healing while the patient remains ambulatory (19). The procedure involves the application of a plaster cast directly to the foot (without first wrapping the foot in gauze, as would be done for a fracture). The patient's weight is thereby distributed evenly over the entire foot, reducing pressure on the ulcer. Ordinarily, the cast is left in place for approximately a week. This technique is best provided by specialists experienced in its use because improper cast application can result in development of other skin problems or of worsening of the ulcer.
Subatmospheric pressure dressings may hold promise in diabetic foot ulcers. They may débride the ulcer, reduce the volume of the ulcer defect, and prepare the wound for secondary healing more quickly than tradition dressings (15).
Traumatic Ulcers
Traumatic ulcers usually heal by avoidance of weight bearing, elevation, topical antibiotic therapy when the ulcer is infected, and protection of the ulcer by dressings. If no progress is made within 2 to 3 weeks, the patient should be seen by a surgeon for possible operative débridement and surgical closure of the wound.
Factitious Ulcers
The key to the management of factitious ulcers is making the diagnosis. The diagnosis is made by maintaining a high degree of suspicion, particularly in ulcers that have no clear cause and occur in what appears to be an otherwise healthy environment. These ulcers usually heal if the cause can be found and controlled. Psychiatric consultation may be indicated if there is evidence of anxiety, depression, or other serious mental health concerns (see Chapter 19). An ulcer suspected of being a factitious ulcer can often be diagnosed and treated simultaneously by placing an occlusive dressing that prevents the patient from manipulating the ulcer. These patients must be carefully followed to monitor progress and to avoid the development of problems under the occlusive dressing.
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Hypertensive Ulcers
Control of the patient's chronic hypertension and education regarding the importance of long-term control are the two keystones in the management of hypertensive ulcers. Some antihypertensive drugs, particularly β-blockers, can interfere with wound healing due to peripheral vasoconstriction, so they should be avoided (20). Otherwise, the management follows the general principles applied to venous stasis ulcers.
Chronic Ulcers Associated with Corticosteroid Treatment
Systemic corticosteroids have an inhibitory effect on wound healing that can be partially reversed by vitamin A. Ulcers that fail to heal in patients being treated with corticosteroids may be treated with vitamin A 25,000 units per day orally; ointments containing vitamin A (e.g., A and D Ointment) may be used alone or in combination (e.g., with silver sulfadiazine cream) directly on the ulcer.
Neoplastic and Other Ulcers
Neoplastic and other unusual ulcers, such as that from the previously mentioned brown recluse spider bite, are a surgical problem; these patients should be referred promptly for surgical consultation.
Growth Factor Therapy
Certain growth factors may be capable of reversing some or all the adverse effects caused by underlying local and systemic factors that contribute to the formation of ulcers in the lower extremities. Platelet-derived growth factor and epidermal growth factor and recombinant platelet-derived growth factor-BB (becaplermin) have shown some promise for the topical treatment of diabetic neuropathic ulcers. The use of cultured (Apligraf) or banked allograft skin as a biologic dressing in an effort to enhance local wound growth factors has been established (21). Further research should identify other growth factors or clarify the sequencing of actions of known growth factors to improve our ability to use them in wound healing. However, topical growth factor therapy should not be considered a substitute for proper wound care.
Prevention and General Foot Care in Susceptible Patients
With the exception of varicose veins, factitious ulcers, and surgically corrected occlusive arterial disease, foot and leg ulcers often recur after healing because the underlying disease is difficult to reverse (22). It is therefore mandatory to be familiar with the principles of foot care, and patients must understand and carry out instructions aimed at minimizing exposure to trauma.
Patients with PAD or diabetes should wear very comfortable footwear, even if it is not fashionable (see Chapter 73). The front of the shoe should be broad so that the toes can spread. Areas of pressure caused by foot deformities should be corrected by orthopedic shoes with appropriate fittings (e.g., insoles or metatarsal bars); patients with these problems should be referred to an orthopedic surgeon or podiatrist.
Patient with ulcers from venous insufficiency that have healed should wear lower extremity compression garments when their legs are dependent.
Patients should be instructed to keep their feet very clean with at least once-daily showers or footbaths in tepid water. Patients with impaired cutaneous sensation should use a mirror to examine the undersurface of their feet daily. Nails should be carefully trimmed, preferably with clippers; under no circumstances should sharp scissors be used to trim the sides of nails because they may injure the delicate nail fold and become a portal of entry for infection. Patients can protect their toes during walking by inserting small fluffy pieces of cotton wool between them. Lanolin or other emollient creams are useful in preventing cracking of hardened areas of skin and keeping the skin soft and supple. Patients should avoid extremes of temperature and should reduce exposure to trauma (e.g., a night-light in the bedroom to avoid stubbing a toe). With attention to these small details, recurring trouble can often be prevented.
Varicose Veins
Causes
Varicose (swollen) veins of the lower extremities are common; they affect women more often than men and usually become symptomatic between the ages of 20 and 40 years. The prevalence of varicose veins varies widely, ranging from a low among women of lowland New Guinea of 0.1% to a high among the women of South Wales of 50%. In the United States, varicose veins affect 19% of men and 36% of women.
The venous system of the lower extremity consists of three distinct systems: the deep venous system, the superficial venous system (of which the greater and lesser saphenous veins are the predominant veins), and perforator veins that run horizontally between the deep and superficial systems. Varicose veins result primarily from incompetence of valves in the superficial veins, or secondarily from perforator vein or deep vein incompetence (23). When a valve becomes incompetent, the next valve distal to this valve becomes exposed to a higher column of blood and therefore higher venous pressure, which in turn makes that valve weak and more prone to incompetence. The process repeats itself, causing the patient to develop
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more extensive disease and become more symptomatic (23).
The disorder is aggravated, and indeed may be caused, by conditions that elevate intra-abdominal pressure (pregnancy, large intra-abdominal tumors) or chronic straining (prostatic obstruction, carcinoma of the sigmoid colon), and occasionally by mechanical interference with venous return in the venous system itself (thrombosis of the pelvic veins).
Symptoms
The symptoms of uncomplicated varicose veins usually consist of heaviness and aching in the area of the veins or in the calves. The patient may complain of mild edema at the end of the day. Occasionally, patients complain of varicose veins for cosmetic reasons and desire treatment. Patients with uncomplicated varicose veins do not complain of intermittent claudication or severe pain; these symptoms suggest coexistent arterial disease or significant outflow obstruction to the venous system (“venous claudication”). Varicose veins can be complicated by superficial thrombophlebitis, bleeding, and venous stasis ulcers, although these complications occur in only a small minority of patients. Superficial thrombophlebitis is usually associated with an intense inflammatory reaction around a tender palpable subcutaneous cord, and is often mistaken for an infectious process. However, antibiotics usually have no role in the treatment of this problem. After rest, elevation, application of local heat, and appropriate anti-inflammatory therapy (e.g., aspirin), the varix in the thrombosed vein disappears. Bleeding varicose veins may require direct suturing. and the treatment of venous stasis ulcers is discussed earlier in this chapter.
Physical Examination
It is useful to have some idea of the anatomy of the venous system of the leg (Fig. 95.1). This makes it possible to judge the patient's symptoms on the basis of an anatomic abnormality detected by physical examination. There are several types of varicose veins, which conform to the underlying anatomic arrangement of these veins. It is important to classify varicose veins on the basis of the anatomic involvement, since appropriate treatment depends on this information.
Telangiectasia (Sunburst Varices)
These are not, in the true sense of the word, varicose veins but rather dilations of subcutaneous venous plexuses that have a spider-like arrangement and an unsightly purple color. These veins are generally less than a millimeter in diameter and are often the object of cosmetic complaints by patients. Otherwise, they are essentially asymptomatic.
Superficial Varicosities
All varicosities result from dilated subcutaneous veins. Simple (primary) superficial varicosities develop in the absence of involvement of more extensive venous structures. Often, however, superficial varicosities develop secondarily as a consequence of reflux in the saphenous, perforator, or in the deep venous systems. It is important to determine whether varicosities are primary or secondary, since this will influence treatment.
Varicosities of Long Saphenous System
Incompetence of the long saphenous system is the most common cause of varicose veins. The long saphenous vein begins anterior to the medial malleolus at the ankle, courses superficially to the medial side of the knee posterior to the medial femoral condyle, and then passes up the medial side of the thigh to the groin where it joins the common femoral vein just below the inguinal ligament. The vein has several tributaries in the calf and in the thigh that are superficial, and it is also joined by several perforating veins from the deep venous system; the valves at these junctions can become incompetent and lead to focal varicosities (Fig. 95.1). There are several consistent perforators: Dodd vein, located just above the knee, Boyd vein, located just below the tibial plateau, and a group of three veins above the medial malleolus at a distance separated by approximately 3 cm, known as Cockett veins. Incompetence of the long saphenous vein is often clearly visible with the patient standing but may not be evident on visual inspection alone. In these instances it may be evident on palpation or diagnosed with additional noninvasive testing (see Noninvasive Vascular Testing).
Varicosities of Short Saphenous System
The short saphenous vein arises behind the lateral malleolus and courses upward behind the calf to join the popliteal vein in the popliteal space (Fig. 95.1). Varicosities of this system are best seen with the patient standing with his or her back to the examiner.
Perforator Varicosities
Perforator incompetence is usually noticed in the long saphenous vein where the ankle perforators and the perigeniculate perforators join the vein; however, perforators join other superficial veins that, in turn, join the long and short saphenous system. Examination may reveal that there is no incompetence of the short or long saphenous veins, only of the perforators. The location of an incompetent perforator vein may often be determined clinically by palpating a divot in the patient's leg, where the muscular fascia has dilated around a dilated perforator vein. There
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may not always be a superficial varicose vein visible overlying this area so the examiner must perform a thorough physical examination of the lower leg. Incompetent perforator veins may cause varicose veins in regions other than the saphenous system.
Clinical Testing to Determine Level of Incompetence
One or two easy clinical tests can be performed in the office that will aid in determination of the severity of the problem and selection of appropriate treatment.
Trendelenburg Test
The patient lies supine and raises the affected leg to empty the veins. A venous tourniquet is applied just below the saphenous opening about 3 inches (7 to 8 cm) below the inguinal ligament. The patient then stands up, and constriction is released. If the saphenofemoral valve is incompetent, the veins will fill immediately from above; if not, the veins fill slowly from below. If the veins fill rapidly before the release of the tourniquet, this indicates the presence of incompetent perforator veins allowing reflux from the deep system. This test is then repeated at successively lower levels in the leg so the location of incompetence may be mapped.
Perthes Test
The Perthes test is a test for DVT in association with varicose veins. A tourniquet is lightly applied below the inguinal ligament, as in the Trendelenburg test, and the patient is instructed to walk in place. If varicose veins are accompanied by a thrombosed deep femoral system, the varicose veins become prominent after this exercise.
Noninvasive Vascular Testing
The advent of the modern vascular laboratory has revolutionized the evaluation of varicose veins. Any patient who, by physical examination, is suspected of having venous incompetence at the saphenous femoral junction should be referred to a noninvasive vascular laboratory for evaluation before treatment is planned.
Effective treatment of lower extremity venous insufficiency is predicated on accurate localization of the problem. Various noninvasive vascular examinations and radiologic studies can be successfully used to define the anatomic extent of venous reflux (24). The utility and limitations of these modalities are based on the concept of systolic and diastolic closure of lower extremity venous valves. Venous valves close in response to two distinct physiologic actions. Coaptation of valve cusps occurs during muscular contraction and subsequent forward (toward the heart) flow of blood (systolic closure). These valves include side branches and perforator veins. Diastolic closure occurs immediately after relaxation of muscular contraction when valves proximal to that contraction close to prevent reflux of blood.
The simplest noninvasive test for lower extremity venous reflux is continuous wave Doppler. The examiner insolates the venous system with a Doppler probe and listens for venous reflux after provocative maneuvers, such as Valsalva maneuver or manual compression proximal to the transducer. The Valsalva maneuver and proximal compression normally result in the cessation of venous flow. The presence of venous signals during these maneuvers is indicative of venous reflux. Continuous wave Doppler samples any structure in the path of the emitted ultrasound and does not allow for discrimination of the vein being tested. Similarly, anatomic variations such as bifid veins will be unrecognized. Analysis with continuous wave Doppler is qualitative, and may be used at the bedside as an initial test. For the definitive assessment of venous anatomy and abnormalities in the vascular laboratory, plethysmography (photoplethysmography or air plethysmography) has been superseded by duplex ultrasound.
Vascular duplex scanning combines high-resolution ultrasonic imaging with pulsed-wave Doppler. This allows real-time visualization of vascular structures and analysis of physiologic and pathologic flow through valves and vessels. The spectral waveforms and color coding obtained by Doppler depicts the velocity of the blood flow as defined by the Doppler equation. The Doppler-derived velocity is a vector that processes both magnitude and direction. Analysis of the Doppler data can therefore demonstrate the direction of blood flow relative to the transducer (26). The saphenofemoral and saphenopopliteal junctions can be imaged in the groin and popliteal space, respectively, and venous flow recorded by spectral analysis or color Doppler. Venous reflux in response to Valsalva maneuver or proximal limb compression can be observed as either waveforms that are inverted to the normal antegrade flow or with color coding indicating retrograde flow. Duplex ultrasonography offers selective sampling of venous structures and precise localization of disease. Valves can be observed directly and valve incompetence is defined by a prolonged valve closure time. The time to valve closure can be measured after a Valsalva maneuver with the patient in 10 degrees reversed Trendelenburg position, or after a cuff on the thigh is released when the patient is standing. Normal valve closure time is less than 2 seconds with the former method and less than 1 second with the latter method. The entire length of the deep and superficial systems can be evaluated. Careful duplex examination of the medial calf and thigh can demonstrate incompetent perforator veins. Not only is this diagnostic, but it can also be used to localize and mark perforators for surgical ligation. DVT can also be readily identified by this modality.
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Venous duplex scanning must be performed by a skilled operator and requires expensive ultrasound equipment (26). However, its noninvasive nature makes it acceptable to patients. Duplex scanning can be used to quantitate the volume of reflux, which correlates with the degree of venous stasis skin changes (24).
Ambulatory venous pressure (AVP) measurement is an invasive technique performed by cannulating a vein on the dorsum of the foot with a small gauge butterfly needle connected to a pressure transducer, amplifier, and recorder. With the use of a pneumatic cuff or elastic tourniquet, it can differentiate between superficial and deep vein or perforator vein incompetence. Elevated AVP correlates with the presence of venous stasis ulcers. AVP measurement is highly sensitive in the detection of venous reflux and is a direct measure of venous pressure. Limitations of this test include inconsistent reproducibility, patient discomfort from its invasive nature, and lack of efficacy as a screening test. It is rarely performed in most vascular labs today.
Descending phlebography is sometimes performed in patients with advanced venous insufficiency who are being considered for repair or autotransplantation of damaged deep venous valves. A catheter is placed in the ipsilateral external iliac vein and the patient is tilted 60 degrees on a fluoroscopy table. As contrast is injected it falls in the leg due to its relative density compared to blood, documenting the extent of reflux. This study defines valvular anatomy well, can identify specific refluxing valves, and can differentiate between primarily insufficient valves that may be repaired and postphlebitic valves that must be replaced.
Treatment
The goals of treatment are to control symptoms and prevent complications. When an intervention is performed, it should be done with full knowledge of the extent of the patient's reflux so that treatment can be aimed at the highest point of reflux. Several options are available.
Observation
Observation is an acceptable option in patients with mild to moderate asymptomatic subcutaneous varices with no history of postural edema, superficial phlebitis, stasis dermatitis, or pain. If the offending telangiectatic venous plexus is large enough to accommodate a 25-gauge needle, a sclerosing solution may be injected. The technique is described below in the section Sclerotherapy. Other treatments such as freezing with carbon dioxide snow, cautery under local anesthesia, and even laser therapy have been advocated, but their use requires a great deal of skill, and unnecessary skin scarring may result that is, in the end, more unsightly than the original vein. Probably the safest treatment of this kind of vein is the use of masking cosmetic creams, together with reassurance.
Support Hose
Support hose maintain compression of subcutaneous varicose veins and prevent edema. Graduated compression hose in the 30- to 40-mm Hg range are available in most pharmacies in various ready-to-fit sizes, including knee, thigh, and panty hose configurations. The patient should be measured and fitted early in the morning before any edema has developed to obtain maximal therapeutic benefit from the compression hose. They should be worn continuously, removed at bedtime, and reapplied immediately upon arising in the morning.
Transcutaneous Laser Ablation
Spider telangiectasias and small varicosities less than 1 to 1.5 mm may be treated with transcutaneous laser ablation. Several lasers have been used for this purpose, including the Nd-to-YAG laser, tunable pulsed-dye laser, copper bromide laser, and the alexandrite laser (27). The procedure is completely noninvasive and is therefore the preferred approach to treating small lesions of this kind. Complications include temporary ulceration and permanent hyperpigmentation or hypopigmentation. Multiple treatments and adjunctive sclerotherapy may be required for optimal results. The lasers are expensive and treatments are typically performed by dermatologists and cosmetic surgeons who use lasers for multiple purposes. Patients are often charged directly for a cosmetic procedure and are not reimbursed by medical insurers, decreasing patient satisfaction with this procedure.
Sclerotherapy
Sclerotherapy is efficacious for segmental subcutaneous varicose veins up to 5 mm in diameter that are not associated with significant greater or lesser saphenous valvular incompetence, and for cosmetically unacceptable telangiectasia (28). The procedure is performed in the office; however, the patient should be told that several treatments may be required for complete elimination of the veins.
The patient stands with a tight tourniquet around the thigh, just enough to make the vein prominent. The area of the vein is lightly prepared with a suitable antiseptic, and 0.5 mL of sclerosing solution is injected by use of a 2-mL syringe, after initial aspiration to make sure the needle is in the vein. Immediately after the end of the injection, the needle is withdrawn and the vein is gently compressed with a 2 × 2-inch gauze for 3 minutes, after which the tourniquet is released and compression is continued for 2 minutes more. The patient wears an elastic bandage on the area for approximately 4 hours. The sclerosant produces an inflammatory reaction in the intima, which obliterates the vein. Failure to use a tourniquet may release an unnecessarily large amount of sclerosant into the major veins of the leg and cause undesirable thrombosis at distant sites. The patient should be warned that extravasation of the
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sclerosant is a possibility and may cause skin necrosis. Several commercially available sclerosant solutions, including sodium morrhuate, sodium tetradecylsulfate (STS), ethanolamine, polidocanol, and hypertonic saline are suitable for injection. Larger varicose veins, up to 10 mm or more, including the saphenous vein and perforator veins, are being treated with a new technique in which a foam is created by mixing the sclerosant (usually STS or polidocanol) with air and then injecting it (29,30). Perforator and saphenous vein sclerotherapy should be done under ultrasound guidance, whereas superficial varicosities are injected blindly.
Surgical Therapy
Surgical therapy for varicose veins depends on the degree of involvement of perforator veins, the saphenous system, and the deep system. The goal is to control the highest point of reflux. Simple superficial varicosities that are too large for sclerotherapy can be treated with stab phlebectomy. This can be done under local anesthesia in an outpatient setting. Incisions are generally 2 to 3 mm long and phlebectomy is facilitated by specialized hooked instruments. General anesthesia may be required if multiple incisions are anticipated.
Direct ligation of incompetent perforator veins can result in ablation of large clusters of varicose veins, and prevent recurrence of stasis ulcers. It is also performed under local anesthesia but incisions are larger, usually 1 to 2 cm. Multiple incompetent perforator veins were previously controlled by the Linton procedure, a radical operation where the medial leg is opened longitudinally and all perforators are ligated through one continuous incision. This procedure has significant morbidity and has now been abandoned. It has been replaced by subfascial endoscopic perforator vein surgery (SEPS). An operating port and an observation port are placed through two incisions in the medial lower leg and perforators are identified and ligated with clips in the subfascial plane. This procedure requires general anesthesia and can be complicated by significant degloving of the medial skin of the lower leg. Clinical trials have confirmed its effectiveness at healing and preventing stasis ulcers (31,32).
If varicosities are associated with incompetent greater or lessor saphenous systems, these systems should be ablated. Until recently therapy consisted of surgical stripping. The greater saphenous vein is stripped between the groin and just below the knee—stripping more distally may result in injury to the saphenous nerve. The saphenofemoral junction is divided and all branches is this area are ligated. The lesser saphenous vein is stripped from the popliteal fossa from where it inserts on the popliteal vein. Stripping requires general anesthesia and is typically associated with significant postoperative pain and swelling. It can be complicated by significant wound hematomas and infections.
Percutaneous endovenous ablation of the saphenous vein has recently been introduced and has been shown to effectively ablate both the greater and lesser saphenous veins. The vein is cannulated with a wire, a sheath is advanced over the wire and then a probe is advanced through the sheath. The tissues surrounding the saphenous vein are infused with a dilute solution of local anesthetic using tumescent technique, to compress the vein around the probe for more effective ablation and to create a heat sink that protects adjacent tissues from thermal injury. Laser or radiofrequency energy is delivered to the endothelium as the probe is withdrawn from the vein (33,34). The procedure is performed under ultrasound guidance and requires intravenous sedation only.
For varicosities accompanied by valvular incompetence in the iliac, femoral, and popliteal deep veins, reconstructive approaches may include various methods of direct and indirect valvuloplasty (35, 36, 37). Postphlebitic valves can be replaced by autotransplanting a valve from the axillary vein. These operations are not practiced widely and results are mixed. They should be performed only after reflux in the perforator and saphenous systems has been addressed, and are usually performed only to control recurrent ulceration.
Varicose veins should not be treated in patients who have an underlying cause associated with increased intra-abdominal pressure until the primary cause has been removed. However, the wearing of elastic stockings may give comfort during this time. Such stockings may be advisable for support in any patient with varicose veins in whom other treatment is undesirable or contraindicated. A further consideration in the selection of therapy is whether the patient has coronary artery disease; although veins that are severely varicose are not suitable for use in coronary bypass surgery, if patients have minimal varicose veins and may become candidates for a coronary artery bypass, these veins should be preserved, if possible, for potential future use (38). Weight reduction in overweight patients is advisable for anyone with varicose veins, regardless of other modes of treatment.
Specific References
For annotated General References and resources related to this chapter, visit http://www.hopkinsbayview.org/PAMreferences.
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