Venous Disorders of the Lower Limbs (PDF)

Chronic venous disorders of the lower limbs rank among the most common conditions affecting individuals. There is a wide spectrum of disease that varies from asymptomatic, minor varicose veins to disabling deep venous thromboembolism. In contrast to many other chronic conditions, patients often acce...

Chronic venous disorders of the lower limbs rank among the most common conditions affecting individuals. There is a wide spectrum of disease that varies from asymptomatic, minor varicose veins to disabling deep venous thromboembolism. In contrast to many other chronic conditions, patients often accept venous disease as a slowly progressive condition related to aging and do not seek health care for these disorders. Although venous disease is most common in adults older than age 50 years, immobility at any age increases susceptibility to deep venous thromboembolism (DVT)—a potentially fatal disease. Epidemiology There are mainly three different types of venous disease: venous insufficiency, DVT, and varicose veins. Venous disease is a common disorder that is more prevalent in females, increases in severity with age, and is a major cause of illness. Between 6% and 30% of all medical expenditures for cardiovascular disease are for venous disease. Chronic venous disease of the legs commonly occurs in the general population and is underreported. Studies estimate that the prevalence of varicose veins, the most common venous disorder, is as high as 56% in males and 60% in females. Venous ulcers are less common, affecting approximately 0.3% of the adult population. Deep venous thrombosis is one of the most underdiagnosed diseases, but studies estimate it affects 80 persons per 100,000 annually. Basic Concepts of Venous Structure and Function Veins are thin-walled, flexible blood vessels that return blood to the heart. Their walls are composed of three layers: tunica intima, which is an endothelial cell lining; tunica media, a thin layer of smooth muscle; and tunica adventitia, an exterior layer of connective tissue (see Fig. 19-1). There are two systems of veins: (1) superficial, small-diameter veins and (2) deep, large-diameter veins. Perforating veins connect the two systems. Blood from the skin and subcutaneous tissue collects in the superficial veins, which empty into the perforating veins. From the perforating veins, blood travels into the deep veins, which empty into the body’s major venous vessels, the inferior and superior vena cava, which empty into the right atrium. The venous system and right side of the heart are low-pressure regions. Veins do not pump blood as do arteries; instead, they direct blood toward the heart. In the extremities, veins rely on the supportive action of skeletal muscles that help pump the blood toward the heart. When an individual is walking, the gastrocnemius muscle in the calf provides pumping action for venous blood to return to the heart. Also, within the lumen of the veins are valves that prevent retrograde flow of venous blood (see Fig. 19-2). Veins carry deoxygenated blood back to the right side of the heart and into the pulmonary artery, moving to the lungs for oxygenation. The exception to this rule occurs in the pulmonary veins and pulmonary artery. Pulmonary veins carry oxygenated blood from the lungs to the left atrium. The pulmonary artery carries the deoxygenated blood into the lungs from the right ventricle. The deoxygenated blood within the veins is a dark red color, which appears blue because of the light dispersion on the skin. Veins are large-capacity vessels that carry almost two-thirds of the body’s blood volume. Their walls can expand to hold a large volume of blood, which renders the system susceptible to stasis of blood. The number of valves and anatomy and structural strength of veins differ among people. The hardiness of the veins is an inheritable quality, which explains familial predisposition to the development of venous insufficiency. FIGURE 19-1. Anatomy of a vein. A vein is a collapsible, thin-walled vessel. Different from arteries, veins contain a thin wall of smooth muscle and valvular structures. FIGURE 19-2. Valves of a deep vein. Valves keep the flow of venous blood up toward the heart. Basic Pathophysiological Concepts of Venous Dysfunction The return of venous blood to the heart constantly opposes the downward pull of gravity. The unidirectional blood flow up to the heart is dependent on valvular competence and skeletal muscle contraction against the vessel walls. Prolonged standing or any obstruction to upward blood flow from the lower extremities places excess pressure on the valves of the veins. Obesity and pregnancy are the two main conditions that cause weakness of the valve leaflets with resultant retrograde flow of venous blood. Retrograde blood flow leads to stasis of venous blood and susceptibility to thrombus formation, the conditions known as venous insufficiency. Venous insufficiency occurs in the superficial or deep venous system. Superficial venous incompetence is the most common form of venous disease. In superficial venous insufficiency, the deep veins are normal, but venous blood flows backward through distended superficial veins in which the valves have failed. The superficial veins that become distended and distorted under the high pressure are termed varicose veins. Venous insufficiency in the deep veins can also occur as in the superficial veins because of valvular dysfunction. In deep venous insufficiency, after prolonged standing, the veins are completely filled, and all the venous valves are open. Venous congestion and high hydrostatic capillary pressure develop in the lower extremities, which causes edema in the interstitial tissues. Within the tissue there is poor clearance of waste products, cellular debris, carbon dioxide, and lactic acid. Wounds in this area are difficult to heal. Unlike superficial vein insufficiency, deep venous insufficiency can lead to deep venous thrombosis, a potentially fatal condition. Thrombus formation can occur in a deep vein in the leg and then travel within the bloodstream, at which point it is called DVT. Pathophysiology of Selected Venous Disorders The major venous disorders include chronic venous insufficiency, DVT, varicose veins, and venous ulcers. Deep Venous Thromboembolism Venous thromboembolism (VTE) is a term that is used to encompass both DVT and pulmonary embolism (PE). DVT occurs when a thrombus develops in a deep leg vein accompanied by inflammation. The thrombus can travel as an embolism within the venous system and then enter the lungs where it becomes a PE, a potentially fatal consequence. Epidemiology The exact incidence of DVT is unknown because many episodes go undiagnosed; however, data indicate that DVT occurs in 80 patients per 100,000 annually. It is estimated that approximately 1 person in 20 will develop DVT over the course of their lifetime. Hospital admissions for DVT have more than doubled over the past decade, mainly due to the greater sensitivity of new technology that can detect small, insignificant emboli, and approximately 900,000 new cases of DVT occur annually in the United States. According to the CDC (2022), 60,000 to 100,000 persons in the United States die of venous thromboembolism annually. Etiology The predisposing factors to DVT are venous stasis, vascular damage, and hypercoagulability, a trio of risk factors that together are known as Virchow’s triad (see Fig. 19-3). Venous stasis occurs because of poor venous return associated with sedentary behavior, immobility, or valve dysfunction in the leg veins. Venous blood tends to pool in the lower extremities, and stagnant blood forms clots. Conditions that cause vascular damage such as surgery or trauma can also lead to DVT. Vein injury often leads to endothelial injury, inflammation, platelet aggregation, and stimulus of the coagulation cascade, which in turn causes formation of a clot. Any condition that causes hypercoagulability of blood can also lead to DVT. Cancers, which commonly secrete coagulation factors, and high estrogen states—which increase blood coagulability—increase risk of DVT as well. Other conditions that can contribute to formation of DVT are obesity and smoking, as both increase the risk of clot formation. Orthopedic surgery in particular causes a high risk of DVT because of vein injury during surgery and venous stasis, commonly associated with postoperative conditions. Some genetic conditions can increase predisposition to DVT and PE such as factor V Leiden, antithrombin, and protein S or protein C deficiency. In addition, some inflammatory-linked conditions can trigger DVT and PE such as inflammatory bowel disease, type 2 diabetes, obesity and metabolic syndrome, antiphospholipid syndrome, hyperlipidemia, rheumatoid arthritis, acute coronary syndrome, and acute stroke. FIGURE 19-3. Virchow’s triad. Virchow’s triad describes the three risk factors that contribute to formation of a venous clot: hypercoagulability, venous stasis, and vascular damage. CLINICAL CONCEPT DVT occurs in 30% to 80% of postoperative orthopedic surgery patients. Many of these DVTs are asymptomatic, and it is unknown what percentage become PEs. For this reason, prophylactic anticoagulant treatment is used after orthopedic surgery. Pathophysiology DVT occurs when a thrombus develops in a deep vein in the lower extremity. The thrombus forms at an area of inflammation in the vein. The sequela to DVT is pulmonary embolism (PE). A venous thrombus can travel from the leg vein into the inferior vena cava (IVC) and then continue upward into the right side of the heart and into the pulmonary arterial circulation. When the thrombus enters the pulmonary circulation, it becomes a PE, which can cause pulmonary infarction and can be fatal (see Fig. 19-4). Venous thrombi often form silently and increase in size without producing manifestations. Deep venous thrombi can develop in the hips, knee, calf, or pelvic veins. Any condition that increases coagulation of the venous blood can cause DVT. Clinical Presentation The most common symptom of DVT is a cramp or “charley horse” in the lower calf that persists and intensifies. A large DVT can cause thigh swelling, tenderness, ropiness, and erythema along the course of a vein. The patient who develops DVT will commonly have a condition that causes venous stasis, venous injury, or hypercoagulability. A patient may have venous stasis caused by immobility or sedentary behavior. The patient may have a history of venous injury, such as trauma or recent surgery. The patient should be questioned about recent history of cancer, recent surgery, use of estrogen, and smoking, as these conditions increase the risk of DVT. CLINICAL CONCEPT Patients who undergo orthopedic surgery are at high risk for DVT and PE. FIGURE 19-4. Formation of a PE from a DVT. A clot (called a DVT) forms in the deep vein of a lower extremity and travels into the IVC. From the IVC, the clot travels into the right atrium of the heart, then right ventricle, and finally lodges in a pulmonary artery or arteriole. At the pulmonary arteriole, the PE can obstruct the diffusion of oxygen into the bloodstream. CLINICAL CONCEPT The incidence of DVT in the lower extremity is 10 times the rate of DVT occurrence in the upper extremity. However, as peripherally inserted central catheter (PICC) use has increased, so has the rate of upper-extremity DVT. The physical examination findings associated with DVT include unilateral leg pain, redness, ropiness, tenderness, and/or warmth over a vein; edema; and some may exhibit a positive Homan’s sign, which is calf pain with dorsiflexion of the foot. Although Homan’s sign can occur in DVT, 50% of persons can have the sign without DVT. PE presents with dyspnea, chest pain, tachycardia, hemoptysis, hypotension, and syncope, but both DVT and PE often can be silent without overt clinical symptoms. CLINICAL CONCEPT Silent PE is very common in hospitalized patients. Preventive treatment of DVT and PE with anticoagulants is based on the patient’s risk factors. Diagnosis DVT and PE cannot be diagnosed based on clinical symptoms because their symptoms often are not present, are subtle, or resemble other clinical disorders. DVT is frequently suspected but only diagnosed in 20% of cases. It is not ideal to perform imaging studies in every patient suspected of having DVT. DVT is most commonly diagnosed through clinical criteria in conjunction with the D-dimer test, which is a blood test that detects the presence of fibrin clot degradation products in the blood. A positive D-dimer test is greater than 500 ng/mL. The sensitivity of the D-dimer test is greater than 80% for DVT and greater than 95% for PE. A normal D-dimer test is useful to rule out PE; however, D-dimer is not specific. D-dimer levels may be elevated in any medical condition where clots form, so the level is only used to rule out DVT, not to confirm diagnosis of DVT. D-dimer levels remain elevated in DVT and PE for about 7 days. The Wells criteria are used to evaluate clinical signs of DVT, such as leg swelling and tenderness along a vein. The criteria summarize the risk of DVT with a score between 0 and 3 (see Table 19-1). A negative D-dimer assay in combination with a Wells criteria score of fewer than 2 rules out the possibility of DVT. All patients with a positive D-dimer assay and a Wells criteria score of greater than or equal to 2 require venous duplex ultrasonography, which combines ultrasound images with Doppler blood flow studies. Venous duplex ultrasonography is the principal diagnostic test for suspected DVT. The absence of normal phasic Doppler signals arising from changes to venous flow in an extremity provides indirect evidence of venous occlusion. Computed tomography (CT) of the chest with intravenous contrast is the principal imaging test for the diagnosis of PE. Lung scanning (ventilation-perfusion scan) is a second-line diagnostic test for PE, used mostly for patients who cannot tolerate intravenous contrast. When ultrasound is equivocal, magnetic resonance venography (MRV) with gadolinium contrast is an excellent imaging modality for diagnosis of DVT. TABLE 19-1. Wells Criteria Pretest – One point is given for each positive finding in the pretest, and 2 points are subtracted if an alternative diagnosis is likely as DVT is identified. Finding​ Point Value Active cancer (treatment within last 6 months or palliative) 1 Calf swelling greater than 3 cm compared with other calf measured 10 cm below tibial tuberosity 1 Collateral superficial veins (nonvaricose) 1 Pitting edema (confined to symptomatic leg) 1 Previously documented DVT 1 Swelling of entire leg 1 Localized pain along distribution of deep venous system 1 Paralysis, paresis, or recent cast immobilization of lower extremities 1 Recently bedridden longer than 3 days, or major surgery requiring regional or general anesthetic in past 4 weeks 1 Alternative diagnosis at least as likely 2 DVT RISK CLASSIFICATION High probability 3 points Moderate probability 2 points Low probability 0 points CLINICAL CONCEPT Venous duplex ultrasonography is the principal diagnostic test for DVT, and CT of the chest with intravenous contrast is the principal imaging test for diagnosing PE. Treatment Preventive strategies should be employed in all patients at increased risk for DVT. While a patient is immobile, sequential venous compression devices may be used to promote venous return. These devices are usually used with antiembolism stockings. They alternate inflation and deflation of chambers to provide sequential pressure over the lower extremity and promote venous return. When the patient is out of bed in a chair, their feet should be elevated to promote venous return. The patient should be taught not to stand for prolonged periods, to avoid constricting garments, to elevate legs periodically during the day, and to ambulate or do leg exercises that will promote blood flow and reduce venous stasis. Patients are also treated prophylactically with drugs that interfere with clotting. Factor Xa inhibitors, direct thrombin inhibitors, low molecular weight heparin, unfractionated heparin, and warfarin are the medications used for DVT. To monitor the therapeutic effects of heparin and warfarin, prothrombin time (PT) and activated partial thromboplastin time (aPTT) laboratory tests have been used. Each of these tests measures the time it takes for the blood to clot; PT measures the extrinsic coagulation system, and aPTT measures the intrinsic coagulation system. The actual blood clotting time is given in seconds, and the normal blood clotting time is given for comparison. The goal is to prolong clotting time in DVT, so a clotting time that is 1.5 to 2.5 times normal is achieved. For example, if normal clotting time is 30 seconds, a therapeutic level of anticoagulant would prolong clotting time to 45 to 75 seconds. While the patient is on anticoagulants, the PT and aPTT have to be measured often. CLINICAL CONCEPT When using warfarin, an effective INR is 2 to 3 for prophylaxis of DVT in most patients. Low molecular weight heparin, factor Xa inhibitors, and direct thrombin inhibitors do not require PT/aPTT or INR monitoring. A simpler blood test called an international normalized ratio (INR) can also be used to monitor anticoagulant therapy. The INR indicates clotting time, which has to be kept in a specific range to avoid excessive anticoagulation. An INR result between 2 and 3 is commonly required for adequate anticoagulation. Primary therapy for an existing DVT or PE consists of clot dissolution and pharmaco-mechanical therapy using catheter-directed thrombolytic agents. Catheter-directed treatment pulverizes the clot mechanically and pharmacologically dissolves the clot using tissue plasminogen activator (tPA). Ultrasound is used to facilitate catheter-directed surgery. Only patients with no risk of bleeding are eligible for this treatment. A Greenfield filter, also known as an IVC filter, is often inserted to block clots from traveling up from the lower extremity to the pulmonary circulation (see Fig. 19-5). The IVC filter is used in persons with absolute contraindication to anticoagulant medication or those who have recurrent VTE despite anticoagulant treatment. These filters are inserted with the use of abdominal ultrasonography. The filter should be removed when the patient no longer requires it. Surgical removal of a thrombus, also called thrombectomy, may be used if other treatments prove ineffective or if risk of hemorrhage with anticoagulant is too great. Pulmonary embolectomy or pulmonary thromboendarterectomy are surgical procedures to remove PE. FIGURE 19-5. Greenfield filter. A Greenfield filter is an apparatus placed in the IVC that can trap a clot as it moves upward with venous flow. It can prevent a DVT from becoming a PE. Chronic Venous Insufficiency Chronic venous insufficiency occurs as a result of damage to valves in the deep veins of the legs. Valves may become incompetent as a result of impaired venous return caused by trauma, central obesity, pregnancy, or prolonged standing. Genetic disorders can increase predisposition to venous insufficiency. Also, the left iliac vein can become occluded by extrinsic pressure from the overlapping right iliac artery in May-Thurner syndrome. Chronic venous insufficiency affects 7.5% of males and 5% of females in the United States. Valve damage leads to impaired venous return and abnormally high venous pressure in the venous system, which in turn leads to pooling and stasis of blood in the lower extremities. Venous congestion will affect capillary filtration by inhibiting movement of fluid and waste products out of the interstitial spaces. This usually causes edema in the lower extremities. Approximately 20% of patients with chronic venous insufficiency develop venous ulcers, which are shallow wounds near the medial and lateral malleoli of the ankle. Clinical Presentation Clinical presentation of venous insufficiency includes thin, shiny skin; dusky discoloration; edema; poor healing; and reduced or absent hair distribution. The patient often endures dull ache or heaviness in the legs with swelling typically after prolonged standing. These symptoms may be relieved by elevation of the leg. Other signs and symptoms include cramping, pruritus, telangiectasias, corona phlebectatica, and skin irritation that can lead to venous ulceration. Telangiectasias (commonly known as “spider veins”) are dilated or broken blood vessels located near the surface of the skin or mucous membranes. Corona phlebectatica is a fan-shaped pattern of dilated veins near the ankle or foot. A circumferential dusky discoloration called stasis dermatitis is often noted around the ankle, instep, and lower leg (see Fig. 19-6). The discoloration is caused by the buildup of hemosiderin in the tissues. Hemosiderin is the iron-containing pigment found in hemoglobin that is liberated from disintegration of red blood cells. Chronic venous congestion will lead to edema, waste product accumulation, and impaired healing. Edema occurs because stasis of blood increases hydrostatic pressure, resulting in fluid movement out of the vascular compartment into the interstitial spaces. A condition called lipodermatosclerosis can occur in severe venous insufficiency. Lipodermatosclerosis is the combination of inflammation, hemosiderin accumulation, and induration in the lower part of the leg just above the ankle. FIGURE 19-6. Stasis dermatitis. (From Dr. P. Marazzi/Science Source.) Diagnosis Key diagnostic tests for peripheral venous disorders include venous Doppler ultrasonography, photoplethysmography (PPG), and venography. Ultrasonography and PPG determine venous blood flow. PPG involves a noninvasive device that emits light that is applied to the skin. The device analyzes the light absorption in the region to determine the volume of blood in circulation. Venography, which requires injection of a radiopaque dye, can also be used to identify occlusions and patterns of collateral blood flow. The severity of chronic venous disorders is classified according to the CEAP (clinical, etiological, anatomic, pathophysiologic) system. It broadly categorizes the patient’s disease according to characteristics that allow more precise communication about the clinical status of the disease. Treatment Graduated compression is the main treatment of venous insufficiency. Gradient compression stockings are supportive hosiery that provide higher compression at the ankle than proximally up the leg. Pneumatic compression devices are also available that use inflatable compression sleeves on the legs to enhance venous blood flow. Graduated compression in combination with anticoagulant or antiplatelet medications is a common medical treatment. Catheter-delivered thrombolytic agents may also be used. Surgical therapy can be used to improve venous circulation by removing the major reflux pathways through venoablation methods. Sclerotherapy, radio frequency ablation (RFA), and endovenous laser therapy are some venoablation procedures that aim to destroy the refluxing superficial veins by either injection of a sclerosing substance, passing a laser over the vein, or using thermal injury. Surgical therapy may also involve ligation and stripping of the great and small saphenous veins. Endovascular interventions, surgical bypass, and reconstruction of the valves of the deep veins can be performed in patients with severe venous insufficiency. Catheter-based stent placement may be considered to treat patients with chronic occlusion of the iliac vein. Valvuloplasty or valve transfer procedures may be performed in patients with severe venous ulcerations that do not heal. Valvuloplasty involves tightening of the valve leaflets surgically. Valve transfer involves taking another vein with competent valves and inserting into the segment of vein with incompetent valves. Varicose Veins A varicose vein, also called a varicosity, is an abnormally dilated superficial vein (see Fig. 19-7). Superficial leg veins are most commonly affected because they hold a large amount of blood. In the absence of disease, the action of muscles on the deep veins helps to promote venous return. The superficial veins have less supporting tissue than do deep veins; thus, varicosities are more likely in superficial veins. FIGURE 19-7. Varicose veins. Epidemiology Studies show that the incidence of superficial varicose veins is twice as high in females compared with males. The hormone progesterone enhances relaxation of the walls of veins in the lower extremities, which increases susceptibility to varicose veins in females. CLINICAL CONCEPT The prevalence of varicose veins increases with age. In one study, 40-year-old individuals had a prevalence of 22%, 50-year-olds a prevalence of 35%, and 60-year-olds a prevalence of 41%. Etiology The cause of varicose veins is high pressure within the superficial veins that weaken venous valves. High pressure is known to occur in prolonged standing, sitting, pregnancy, and obesity. The Framingham Heart Study found that females with varicose veins generally are obese, have lower levels of physical activity, and have higher systolic blood pressure. Females who reported spending 8 or more hours in an average day in sedentary activities (sitting or standing) also had a significantly higher incidence of varicose veins than those who spent 4 or fewer hours a day in such activities. Pregnancy is a particular risk factor for varicose veins, as venous return is obstructed by the enlarged uterus. For males, varicose veins were associated with lower levels of physical activity and higher smoking rates. These results suggest that increased physical activity, smoking cessation, and weight control may help prevent varicose veins among adults at high risk. Pathophysiology Varicose veins occur because of valvular incompetence in the legs. Valve incompetence occurs as a result of pressure on the valves over time. Gravitational pull and prolonged standing promote blood stagnation and pooling in the lower extremities. Valves are damaged from chronic pressure and become less competent at preventing backflow from one section of the vein into another. Venous valves are particularly stressed during pregnancy due to the venous pressure created by the gravid uterus. Also, the hormone progesterone in females causes blood vessel walls to relax. When these walls relax, the tiny valves within the vessels also relax and the pressure exerted by blood further weakens the vessels. Diagnosis Clinical examination of the legs in the standing position reveals the regions of varicose veins. The duplex ultrasound, which highlights the major superficial vein in the leg, the great saphenous vein, has become the most useful tool for diagnosing varicose veins. Treatment Treatment for varicose veins aims to remove the superficial veins either through surgery, endovenous ablation, or sclerotherapy ablation. Sclerotherapy is the most commonly used treatment. Under ultrasound guidance, a sclerosing substance is injected into the collapsed varicose veins, destroys the vessel’s endothelial layer, and causes fibrosis of the remainder of the vessel. The body eventually reabsorbs all dead vascular tissue layers. Elastic supportive stockings, which compress the superficial veins, are also recommended. Venous Ulcers Venous ulcers, also called venous stasis ulcers, occur in lower extremities affected by venous insufficiency. They are wounds caused by trauma or pressure on the lower limbs. Skin breakdown, tissue damage, and necrosis occur because of lack of venous circulation. Venous ulcers are the most common type of chronic lower extremity ulcers, affecting 1% to 3% of the U.S. population. In the United States, 10% to 35% of adults have chronic venous insufficiency, and 4% of adults 65 years or older have venous ulcers. Risk factors for venous ulcers include age 55 years or older, family history of chronic venous insufficiency, obesity, history of PE or superficial/deep venous thrombosis, lower extremity skeletal or joint disease, multiple pregnancies, parental history of ankle ulcers, physical inactivity, and venous reflux in deep veins. Pathophysiology Sluggish circulation, poor tissue oxygenation, deprivation of cellular nutrition, and impaired waste product removal are the pathophysiological changes found in venous stasis ulcers. Venous hypertension is defined as increased venous pressure resulting from venous reflux or obstruction. This process is thought to be the primary underlying mechanism for venous ulcer formation. Valve dysfunction, outflow obstruction, arteriovenous malformation, and calf muscle pump failure contribute to the pathogenesis of venous hypertension. Once skin breakdown occurs, tissue that is attempting to heal has high metabolic demands that cannot be met because of venous insufficiency. Clinical Presentation A venous ulcer is dark red in color, has an uneven margin, is usually painful, and is accompanied by a large amount of edema and drainage (see Fig. 19-8). Most ulcers are located medially over the ankle just above the medial malleolus of the lower leg. Pulses are usually present, and capillary refill time is normal. Other findings in the leg with venous ulceration include telangiectasias (spider veins), corona phlebectatica (fan-shaped dilated veins around the ankle and foot), atrophie blanche (atrophic, white scarring of skin), and lipodermatosclerosis (indurated, hemosiderin-stained skin). FIGURE 19-8. Venous ulcer. (From Roberto A. Penne-Casanova/Science Source.) Diagnosis Noninvasive imaging with venous duplex ultrasonography, arterial pulse examination, and measurement of ankle-brachial index is recommended for all patients with suspected venous ulcers. Ultrasonography should be used to assess for deep and superficial venous reflux and obstruction. Treatment Lifestyle modifications will reduce the pressure on the valves and may reduce edema. These modifications include avoidance of prolonged standing, institution of a regular exercise program, avoidance of constrictive clothing, and wearing elasticized compression gradient stockings. Measures are aimed at promoting venous return and decreasing venous pooling. Susceptibility to infection is high with venous ulcers because poor circulation impairs the immune and inflammatory response. Specialized wound care measures are usually necessary, such as antibiotic-impregnated semipermeable or occlusive dressings. Topical medications that contain epidermal, fibroblastic, and platelet-derived growth factors are used to assist chronic wounds with establishing healthy granulation tissue. Intermittent pneumatic compression has been shown to increase healing compared with no compression. Pentoxifylline, a vasoactive agent that improves blood flow by decreasing blood viscosity, is effective in some patients. An oral antibiotic is necessary if infection is suspected. Removal of necrotic tissue by débridement can facilitate healing. Early venous ablation and surgical intervention to correct superficial venous reflux can improve healing and decrease recurrence rates. Skin grafting may be required with large ulcerations.