• Venous hypertension and insufficiency represent the most common causes of chronic leg ulcers.

• Prevalence increases with age, and risk factors include female sex, obesity, pregnancy, prolonged standing, and family history of venous insufficiency; hypercoagulability can be a contributing factor, especially in patients with a history of deep vein thrombosis or livedoid vasculopathy (Fig. 86.3; see Chapter 18).

• Ulcers tend to have irregular borders and a yellow fibrinous base, with a predilection for the area above the medial malleolus

(Fig. 86.4); the ulcers can become large but are often fairly shallow, with granulation tissue evident upon debridement.

• Surrounding skin has signs of venous hypertension such as yellow-brown discoloration due to hemosiderin deposits, pinpoint petechiae, stasis dermatitis, lipodermatosclerosis, and, occasionally, acroangiodermatitis (Fig. 86.5).

• Other findings include varicosities and edema > lymphedema of the lower extremities (Fig. 86.6); swelling and aching of the legs is worsened by dependency (e.g. prolonged standing) and improved by leg elevation and the use of compression therapy; other dependent sites, such as a large pannus, can develop similar clinical changes (Fig. 86.7).

• DDx: see Fig. 86.1; coexistent arterial insufficiency (see below) or uncompensated congestive heart failure should be excluded before initiating compression therapy.

• Evaluation and Rx: an approach to the patient with a chronic venous ulcer is presented in Fig. 86.8.

• Compression represents a mainstay of therapy.

– Graduated compression stockings: pressures of 30–40 mmHg at the ankle are required for moderate edema and to promote healing of venous ulcers, although lower pressures (20–30 mmHg) can be used for mild edema and as an initial step; stockings should be applied immediately upon arising from bed in the morning, and lifelong use is recommended.

– Compression bandages: the Unna boot, a zinc oxide-impregnated bandage that is covered by a self-adherent elastic wrap such as Coban™, provides semi-rigid compression and is usually changed weekly; four-layer bandages represent another option for highly exudative wounds.

• Peripheral arterial disease (PAD), a manifestation of atherosclerosis, is present in up to 25% of patients with leg ulcers; risk factors include cigarette smoking, diabetes mellitus, dyslipidemia, and hypertension; ulceration is often precipitated by trauma.

• Well-demarcated, round, ‘punched out’ ulcers with a dry necrotic base; occur primarily on the distal lower extremities, favoring the toes and sites of pressure.

• Surrounding skin is typically hairless, shiny, and atrophic (Fig. 86.9).

• Other findings include cool feet, weak or absent peripheral pulses, prolonged capillary refill time (>3–4 seconds), pallor ± pain upon leg elevation (45° for 1 minute), and dependent rubor; patients may report pain induced by ambulation and relieved by rest.

• DDx: other causes of ulcers in patients with PAD include cholesterol emboli (Fig. 86.10), diffuse dermal angiomatosis (painful violaceous plaques with central ulceration), and Buerger’s disease (thrombangiitis obliterans; inflammatory and vaso-occlusive disorder in smokers affecting upper and lower extremities); patients with co-existing diabetes mellitus may have overlapping features (see below).

• Evaluation: the ankle–brachial index (ABI) is used to screen for PAD (Table 86.2); additional assessment may include duplex ultrasonography, CT angiography, and magnetic resonance angiography.

• Rx: surgical or endovascular restoration of blood flow; wound care (see below), but with avoidance of sharp debridement.

• Diabetes mellitus confers a 15–25% lifetime risk of foot ulcers, ~15% of which eventuate in an amputation; diabetic neuropathy is the major cause of these ulcers, although ischemia, venous hypertension, and infection often contribute to pathogenesis.

• Sensory neuropathy leads to unrecognized foot trauma, motor neuropathy leads to altered biomechanics and structural deformities that increase mechanical stress, and autonomic neuropathy leads to both arteriovenous shunting that decreases perfusion and reduced sweating that predisposes to dryness and fissuring.

• Neuropathic ulcers are typically ‘punched out’ with a hyperkeratotic rim, arising in a background of callused skin; they are usually located on pressure points and over bony prominences (e.g. metatarsal heads, heels, great toes) (Fig. 86.11).

• Other findings include decreased sensation due to peripheral neuropathy and sometimes foot deformities (e.g. hammer toes, Charcot foot).

• Evaluation: neurologic examination using nylon monofilament to test sensation ± nerve conduction studies/electromyography and determination of the ABI (see Table 86.2); assessment for infection utilizing laboratory studies (e.g. CBC, ESR/C-reactive protein), wound cultures (tissue from biopsy is higher yield than swabs), and imaging to exclude osteomyelitis (e.g. radiographs [low sensitivity], MRI) as indicated by clinical suspicion.

• Rx: wound care with debridement of necrotic material and the hyperkeratotic rim, eradication of infection, and mechanical offloading (e.g. bed rest, wheelchair, crutches, total contact casting, felted foam, orthotic shoes); additional options include hyperbaric oxygen and becaplermin gel (recombinant platelet-derived growth factor [PDGF]); patient instructions are provided in Table 86.3.

• Occur as a consequence of prolonged immobility, affecting ~10% of hospitalized patients and ~25% of nursing home residents; other risk factors include sensory deficits, older age, and poor nutrition.

• Soft tissues are compressed between a bony prominence (e.g. sacrum, ischial tuberosity; Figs. 86.12 and 86.13) and an external surface; pathogenic factors include continuous pressure, shearing forces/friction, and moisture (e.g. perspiration, urine, feces).

• Classified according to a four-stage system (Fig. 86.14); ulcers do not necessarily progress sequentially through these stages, and extensive deep tissue damage may initially have few superficial manifestations.

• Prevention: frequent position changes together with use of softer surfaces (e.g. containing foam, air, or liquid) and devices (e.g. pillows, foam wedges) to relieve pressure; optimize nutrition.

• Rx: relief of pressure and wound care – for example, utilizing an occlusive dressing (see below); stage IV ulcers may require surgical intervention.

• Lymphedema is the interstitial accumulation of lymphatic fluid due to reduced drainage by lymphatic vessels.

• Divided into primary forms due to abnormal lymphatic development (see Chapter 85) and secondary forms due to lymphatic damage or obstruction (Table 86.4).

• Usually presents as chronic, painless swelling and heaviness of an extremity (leg > arm), typically beginning distally (e.g. on the dorsal foot) and progressing proximally (Fig. 86.15); initially pitting, but becomes indurated and nonpitting as fibrosis develops; prone to ulceration and often worsens following secondary infections.

• Elephantiasis nostras verrucosa is a complication of severe lymphedema characterized by massive enlargement of the affected area, marked fibrosis, and verrucous epidermal changes with a mossy, cobblestoned appearance (Fig. 86.16).

• DDx: edema secondary to venous insufficiency, lipedema (bilateral lower extremity swelling that spares the feet, almost exclusively affecting women; Fig. 86.17), obesity-associated lymphedematous mucinosis.

• Rx: difficult; compression (e.g. garments, wrapping), pneumatic pumps and massage to decrease accumulation of lymph; treatment of secondary infections.

• In a patient with an ulcer, modifiable local and systemic factors that may impair wound healing should be addressed, including deleterious mechanical forces, inadequate perfusion, and poor nutritional or immune status.

• A moist wound environment such as that provided by a semipermeable ‘occlusive’ dressing enhances healing by stimulating collagen synthesis, promoting angiogenesis, encouraging re-epithelialization, and providing autolytic debridement.

• The choice of dressing depends on the wound type and amount of exudate (Table 86.5), and it may be helpful to protect the skin around the wound with a thin coat of ointment to prevent maceration; the frequency of dressing changes is based on their absorbency as well as the amount of exudate.

• Debridement of nonviable tissue from the wound bed also promotes healing.

– Autolytic debridement utilizing the body’s own proteolytic enzymes is provided by moist retentive dressings; it is best suited for non-infected wounds with minimal debris.

– Mechanical debridement (e.g. ‘sharp’ with surgical instruments, wet-to-dry [can disrupt viable tissue]) may be helpful for wounds with large amounts of necrotic and/or infected tissue.

– Enzymatic debridement utilizes topical proteolytic enzyme preparations such as collagenase and papain-urea.

– Maggot debridement can be considered for recalcitrant ulcers with excessive necrotic tissue.

• Bacterial colonization occurs in all chronic wounds and must be distinguished from true soft tissue infection; wounds with clinical evidence of infection (e.g. purulent discharge, surrounding cellulitis) should be cultured and treated with systemic antibiotics (initially broad-spectrum and then adjusted based on sensitivities); topical antimicrobial agents (e.g. dressings containing silver or cadexomer-iodine) can be considered for nonhealing wounds with ‘critical colonization’ (>10⁶ colony-forming units of bacteria per gram of tissue).

• In addition to wound care, treatment of ulcers should be directed at the underlying cause (see above).

• Other adjuncts to wound care may include topical growth factors (e.g. PDGF), topical negative pressure therapy, and tissue-engineered skin equivalents.