Concomitant peripheral arterial disease in patients with venous leg ulcers has been reported to be between 15 and 25% [8, 9]. The identification of arterial occlusive disease prior to starting treatment of venous ulcers remains paramount to obtaining healing. All patients should have a thorough evaluation of their lower extremity arterial circulation. Knowing the risk factors for peripheral arterial disease, such as hypertension, diabetes mellitus, obesity, and tobacco use, will help to identify those at risk. While a pulse examination is important, it can be misleading due to signs of edema and lipodermatosclerosis. In addition, a palpable pulse does not equate to presumed normal circulation. Therefore, all patients should have a lower extremity ankle-brachial index (ABI) [9]. If ulcers on the ankle prevent cuff placement or the arteries in the lower extremity are non-compressible , then toe pressures are necessary. Patients who have a chronic venous ulcer and an ABI in the range of 0.80–1.20 (or toe pressure greater than 50 mmHg) do not need revascularization and may proceed with the next stage of therapy. Patients with an ABI <0.50 (or a toe pressure of <30 mmHg) should undergo further evaluation for peripheral artery disease and, if possible, will require some form of revascularization prior to the next stage of therapy. For those patients with ABI between 0.50 and 0.80 (or toe pressures between 30 and 50 mmHg), selective revascularization may be necessary depending on such factors as initial ulcer size (i.e., greater than 25 cm²), chronicity of the ulcer (present greater than 1 year), whether the ulcer is recurrent, and whether an ulcer fails to show 50% healing with the next phases of therapy over 4–6 weeks [9]. The reason that revascularization must occur in those selected patients is for fear that compression therapy will worsen the ulcer due to decreasing the capillary perfusion pressure and worsening ischemia.

Compression therapy is the cornerstone for the prevention and treatment of venous hypertension, a crucial step to healing venous ulcers [6]. The external pressure provided by compression therapy reduces venous hypertension and improves calf muscle pump performance [10]. Compression on the superficial venous system also allows for a larger volume of blood to return to the deep venous system, furthering the action of the calf muscle pump [11].

Narrowing of the venous lumen begins at a median pressure of 30–40 mmHg when the patient is sitting or standing [12]. Strength of compression is grouped into three main categories: low, or class 1, comprised of pressures less than 20 mmHg; medium, or class 2, comprised of pressures 20–30 mmHg; high, or class 3, comprised of pressures greater than 30 mmHg [13].

Compression therapy of any kind has been shown to reduce the time of venous ulcer healing compared to no compression therapy; however, compression therapy varies in type and effectiveness. Compression wrap therapy uses layers of fabric to create increased pressure. The number of layers can range from two to four and has some degree of stretch—elastic bandages are referred to as long stretch, and inelastic bandages are referred to as short stretch. In a Cochrane analysis, multicomponent compression systems with elastic were found to be more effective than those comprised of inelastic components. The number of layers does not seem to coincide with higher pressures in that two-layer wraps have been shown to be just as effective as four-component wraps [14].

Compression stockings (considered long stretch) have been used since the 1950s to prevent and treat venous ulcers [15]. They have been shown to be more effective in healing ulcers than inelastic wraps [14]; however, no data is available on the effectiveness of compression stockings versus multicomponent compression wrap therapy with elastic. One small cohort study demonstrated, when combined with debridement and dressing changes, compression stocking therapy achieved a 97% ulcer healing rate with a median healing time of 5 months [11]. Generally, when a new active venous ulcer appears, a multilayer compression wrap is used for the first line of therapy. When the ulcer gets close to healing, the transition to compression stockings is made. For obese patients or patients who do not have the strength or means to put on a compression stocking, a short-stretch compression device, such as a CircAid (Fig. 34.1), may work well to prevent recurrence.

The usage of compression therapy by both providers and patients can vary. One German study showed that among patients with venous ulcers, compression therapy was used in only 40% [16]. Compliance, once prescribed, is also variable, with some estimated 26–41% of patients adhering to therapy [17]. Increasing use of compression therapy includes education at the provider level as well as increasing patient awareness to the importance to compliance. Patient adherence may be increased by aiding patients in donning compression therapy independently, either by education or through assist devices [18].

Infection in chronic venous ulcers leads to an inability in wound healing which may cause enlargement of the ulcer and/or lead to systemic illness. Increased risk of infection also stems from the presence of lower extremity edema, hemosiderin deposits, and a weakened skin barrier secondary to chronic dermatitis [19]. Patient-related risk factors for infection include obesity, diabetes mellitus, immunosuppression, tobacco use, and PAD [19–21]. Infection should be suspected in the presence of frank purulence, increasing pain, erythema, foul smell, and/or an increasingly wet or weeping wound [9, 19]. Ulcer debridement to remove necrotic tissue and excessive bioburden should be performed [1]. When clinical signs of infection are present, a swab or tissue culture should be performed. If no clinical signs of infection are present, routine culture and antibiotic therapy are not warranted [9, 21]. If performing a swab or tissue culture, it should be done after the debridement of the ulcer. Identification of colonized bacteria by routine culture has been shown to be unhelpful in guiding treatment [22–24]. Systemic antibiotic choice, which may be given intravenously or orally, should be guided by patient presentation and local antimicrobial susceptibility patterns. A large Cochrane review in 2013 found limited evidence to support both systemic and local antibiotic therapy [25]. Additionally, there was limited evidence to support the use of povidone-iodine, peroxide-based preparations, and other tropical antibiotics and antiseptics in the treatment of venous ulcers [25]. There was no evidence supporting the use of honey- or silver-based preparations in treating chronic venous ulcers. There was evidence to support the use of cadexomer iodine compared with standard therapy (compression) in terms of improved healing time [25]. Nherera et al. recently examined the use of cadexomer iodine with and without standard care, defined as multilayer compression bandaging and debridement. The results found the addition of cadexomer iodine resulted in more wounds healed at decreased cost [26]. However, when compared to silver-based preparations, hydrocolloid or paraffin dressings, there were no differences.

One of the main causes of venous hypertension is venous valvular incompetence. Valvular incompetence can be primary or secondary. Primary valvular incompetence has been associated with factors such as obesity, female gender, prolonged standing, and family history [27]. Secondary valvular incompetence can be from postthrombotic syndrome or proximal venous obstruction such as May-Thurner syndrome. Secondary valve incompetence, or postthrombotic syndrome (PTS), occurs in about one-third of patients after acute deep venous thrombosis [28].

Venous reflux is objectively diagnosed using a duplex ultrasound. Lower extremity axial veins (superficial and deep) are examined with the patient in the standing position. A cuff is placed distal to the venous segment that is undergoing duplex insonation. With rapid deflation of the cuff, venous valves should close quickly, and reversal of flow should be less than 500 ms. If reversal of flow is greater than 500 ms, then valvular incompetence is present in that segment [28].

Initial treatment of chronic venous ulcers from venous insufficiency consists of compression therapy. If there is failure of the venous ulcer to heal approximately 50% within 4–6 weeks, then venous reflux testing should be performed. Other relative indications to perform venous reflux testing include a large ulcer (>25 cm²), a recurrent ulcer, or an ulcer that has been present for more than 1 year. When these clinical scenarios exist and superficial axial valvular reflux is present (in great saphenous vein, accessory saphenous vein, and/or small saphenous vein), operative stripping or thermal ablation in combination with phlebectomy or sclerotherapy (for branch varicosities) should be performed [6]. In a prospective randomized controlled trial comparing compression alone to high ligation and stripping plus compression, venous ulcer recurrence was found to be significantly lower in patients who underwent surgery at 1 year (12% versus 28%) [29].

Catheter-based percutaneous ablation of superficial axial venous reflux has gradually replaced open surgery as the procedure of choice. Endovenous laser ablation uses laser light that causes either water or hemoglobin absorption which then results in heat energy damage to the endothelium and closure of the vein [30]. Radiofrequency ablation uses an electrical current that, when in contact with the venous wall, causes thermal energy and resultant endothelial destruction and closure [31]. Compared to open surgery, hematoma and infection rates are significantly lower, and recovery time is shorter [32]. In a meta-analysis of randomized controlled trials, endovenous ablation has been shown to be as effective as open surgery in treatment of great saphenous varicose veins [33]. In several small cohort studies [34–36], endovenous ablation has been shown to prevent ulcer recurrence. There have been no randomized controlled trials comparing endovenous thermal ablation to open surgery or compression therapy on ulcer healing or recurrence [37]. Treatment with either endovenous laser or radiofrequency ablation appears to be nearly equivalent. Endovenous ablation by radiofrequency was shown in one small randomized controlled trial to have lower post-procedure pain and bruising, but there were no significant differences in patient satisfaction, adverse effects, or recurrence at 1 year [38].

Proximal venous obstruction impeding venous return from the lower extremities can also cause venous hypertension in the deep and superficial axial veins. As with venous valvular incompetency, this can result in distension of the capillary walls, inflammation, and leakage of macromolecules into the subcutaneous tissues and dermis leading to ulcer formation [9, 20]. The most common cause of venous obstruction is postthrombotic syndrome which can arise after a past history of deep vein thrombosis (DVT) [39]. Early treatment of DVT is recommended to improve functional outcomes and decrease sequelae of postthrombotic syndrome [40]. A recent review found that catheter-directed thrombolysis plus anticoagulation improved venous patency, decreased venous obstruction, and decreased incidence of postthrombotic syndrome [41]. Interestingly, there was no benefit in reducing mortality, pulmonary embolism, or recurrent DVT [42]. The ATTRACT trial represents a large multicenter prospective randomized trial that is currently in progress and addresses the question of postthrombotic severity in patients with DVT above and below the inguinal ligament [43].

May-Thurner syndrome represents another form of venous obstruction, whereby the right common iliac artery compresses the left common iliac vein. The true incidence of May-Thurner syndrome is not known; however, approximately 50–60% of left-sided iliofemoral DVTs are secondary to right iliac artery compression of the left common iliac vein [39]. Not all people with May-Thurner syndrome will develop a DVT; however, the stenosis can cause venous hypertension. Duplex ultrasound can be useful in diagnosing the presence of May-Thurner syndrome if there is lack of respiratory phasicity in the ipsilateral common femoral vein. When considering stenting of a left common iliac vein stenosis due to May-Thurner syndrome, intravascular ultrasound is necessary to make the diagnosis because venography may be falsely negative due to compression causing “pancaking” of the vein. Patients with venous ulcers who fail to show healing of approximately 50% with compression after 4–6 weeks should have computed tomographic or magnetic resonant venography to evaluate for May-Thurner syndrome [44]. If demonstrated and then confirmed with intravascular ultrasound, venous stenting is indicated [45, 46]. Other indications in making the diagnosis for May-Thurner include presenting initially with large ulcer (>25 cm²), having an ulcer for greater than 1 year, and having a recurrent ulcer.

Risk factors for development of venous ulcers include age, female gender, family history [47], pregnancy, and prior lower extremity trauma. Modifiable risk factors that can improve healing and prevent recurrence include treatment of postthrombotic syndrome, obesity, calf muscle pump dysfunction, smoking, prolonged standing, and nutrition [48].