Venous and lymphatic circulation is an essential component of the vascular system. When one considers disorders of extremity circulation, arterial insufficiently usually comes to mind. However, an adequate peripheral vascular circulation must also include a healthy venous and lymphatic system, which is extremely important to complete the cycle. A healthy heart with normal cardiac pump ejection fraction is also, of course, an essential component of healthy circulation. Congestive heart failure, other organ system failures, and many other conditions may contribute to limb swelling in patients with venous hypertension or lymphatic obstruction.

This chapter is dedicated to the types of direct treatment available for problem wounds related to abnormalities of the venous and lymphatic systems. Care of wounds as well as management of all of the factors contributing to venous and lymphatic diseases, as discussed previous chapters, is critical in the long-term care and prevention of venous and lymphatic wounds. This requires communication and professional interaction among all of the patients’ physicians.

Clinicians in practice have recently realized that management of recurrent venous ulcerations is difficult and is a long-term challenge. More than 40% of patients present with their first ulcer before 50 years of age, and recurrence rates are reported to be as high as 72% within 1 year of treatment.¹ Other associated illnesses that have affected wound healing of venous and lymphatic ulcers are also discussed.

Most patients with wounds initially seek care from a primary care physician or nurse. In the early phase of lymphatic or venous skin ulcerations, simple treatment with Unna’s boot, elevation, topical antiseptics, systemic antibiotics, and patient compliance may result in rapid healing. This is particularly true in younger patients and patients who have not had previous wounds. If the wound does not improve after 30 days of care or if the wound is unusual, it is appropriate for the initial treating physician or nurse to refer the patient to a wound treatment center or appropriate specialist for a more detailed evaluation and specialized wound care.

The venous system begins at the postcapillary level where venules join to form small veins, which coalesce to larger veins that travel from the skin and subcutaneous tissue to the more central location of the deep venous system. Deep veins are generally paired, having numerous anastomoses, and are located parallel with the respective artery in the calf, joining to the popliteal vein, which proceeds upward in the thigh as the femoral vein, where it joins the deep femoral vein and the greater saphenous vein to form the common femoral vein. The greater saphenous vein (GSV) is found anterior to the medial malleolus and may be bifurcated along its course. The saphenous vein in the calf is connected to the deep veins through numerous perforator veins. The majority of patients with venous hypertension have valve dysfunction in the greater saphenous and frequently also in the perforating veins. For that reason, initial venous ulcers are generally in the distal calf above the medial malleolus (the “Gaitor zone”). The lesser saphenous vein drains the posterior lateral calf and lateral ankle and is less frequently involved in venous hypertension.

Veins in the lower extremity have bileaflet valves that passively close to prevent retrograde flow of blood. Incompetent valves at any level contribute to venous stasis. Incompetent venous valves may be related to congenital valve absence, dilatation of veins related to prolonged standing, pressure on pelvic veins, pregnancy, “frozen valves” after deep venous thrombosis (DVT), or superficial phlebitis. Exogenous obesity and inheritance may be factors in vein dysfunction.

Patients who initially present to their primary care physician often have symptoms of venous hypertension presenting as lower extremity heaviness and swelling and visible varicosities attributable to dilated veins and valvular incompetence. Initial venous ulcers may be initiated by trauma or swelling and blisters. These initial wounds or ulcers frequently heal rather rapidly with cleansing of the wound, traditional Unna’s boot application, elevation, and oral antibiotics (if cellulitis is present).

The patient is then advised to wear compression stockings and take other measures to alleviate venous hypertension. These patients may be referred to a vascular specialist for consideration of minimally invasive ablation of varicosities or other appropriate surgical procedures.

Patients referred to a wound specialist with problem wounds are generally older patients who have had venous hypertension for many years. These wounds may have deep, irregular edges with congested, purple, friable tissue; severe edema; hemosiderin stain; and dermatitis of much of the calf. Ulcers related to lymphedema and chronic venous ulcers may have associated pale scar tissue and a mixed fibrous and granular base. If the pain is severe, arterial insufficiency may be a major factor.

Chronic, recurrent wounds are difficult to treat in an office setting. Recurrent problem wounds, repeatedly presenting in the midst of a busy office day, can be very inconvenient and frustrating.² Practicing in a dedicated wound treatment center allows physicians to give their full attention to disabling, complicated problem wounds.

At the time of initial evaluation of a patient with serious venous or lymphatic wounds, a complete history and physical examination are obtained. This includes obtaining records from the referring physician, who may also be treating other medical problems contributing to the patient’s inability to heal. Venous hypertension and lymphedema are both chronic circulation diseases of increased hydrostatic pressure in the lower extremities, with secondary tissue damage.

Venous stasis results in extravasation of red blood cells (RBCs), and both conditions have extravasation of fibrinogen into the intracellular fluid of the subcutaneous tissue. It has been proposed that the RBCs and protein molecules break down and release chemoattractants, causing leukocyte clumping. The activated leukocytes release inflammatory substances and growth factors that result in tissue inflammation and fibrosis with occlusion of capillaries, venules, and lymphatic ductules. These tissue changes could result in very fragile skin and lead to ulceration with minor trauma.² There is still much to be discovered about this complex process.

If the patient complains of severe pain, one should also consider possible associated arterial insufficiency, which additionally inhibits healing because of hypoxia.

Ulcers secondary to severe, advanced lymphedema are often more difficult to treat than venous ulcers. Lymphedema is most often caused by progressive damage to the lymphatic system with serious reduction in the capacity for lymph transport. Progressive fibrosis of the lymphatic ducts may be partly caused by chronic accumulation of protein-rich fluid. As the limb enlarges, fibrosis with brawny (nonpitting) edema may progress to hyperkeratosis and papillomatosis and to the final stage of elephantiasis. At this stage, the skin loses its elastic component, and ulcerations become irreversible. Surgery to debulk the limb or to establish veno–lymphatic anastomoses may be considered when all other measures fail.

The treatment of patients with ulcers caused by lymphedema is initially similar to that of venous ulcers. (The care and dressing of these wounds is discussed in more detail under Venous Ulcers.) Both types of ulcer therapy initially include frequent debridement of slough and biofilm, antibiotics as needed, calcium alginate, foam, and four-layered compression. The compression dressings applied for lymphatic ulcers require more skill because of greater limb deformity. In addition to massage and compression dressings, one must also be alert to frequent recurrent cellulitis and lymphangitis leading to more severe obstruction. Patients should be given standing prescriptions for antibiotics to be filled at the first sign of infection.

Long-term prevention of recurrent wounds secondary to lymphedema includes extensive patient education and a lifetime treatment plan that addresses the individual co-factors for each patient and may include physiotherapy, massage, sequential compression, 40-to 60-mm Hg compression bandaging, exercises, and skin care.

A 53-year-old overweight woman with history of hypertension, sleep apnea, and diabetes mellitus type II, presented with ulcer of the anterior right leg and bilateral lower extremity swelling of about 1 year’s duration (Figure 44-1A). She was hospitalized 3 months earlier for cellulitis and increased bilateral edema. She had no DVT or abscess formation. She was diagnosed with progressive lymphedema with secondary ulceration. Ankle brachial indices (ABIs) could not be obtained because of edema. Toe brachial indices (TBIs) were above 0.65 with normal Doppler waveforms in tibial and peroneal arteries at the ankle indicating adequate arterial perfusion. She was treated with 10 days of oral antibiotics, leg elevation, protein supplements, probiotics, multivitamins, and strict diabetic control. Calcium alginate, foam, and Profore compression dressings were applied weekly at the wound center after light sharp debridement of necrotic tissue. The wound healed in 4 weeks.

The patient was then referred to the lymphedema center. The circumference of the leg 20 cm above the ankle was 61.5 cm on the right and 55 cm on the left (Figure 44-1B). She was started on complete decongestive therapy (CDT) with compression bandaging to both lower extremities along with manual lymph drainage. The patient came to therapy four times per week. After 4 weeks, the measurements were 44.6 cm and 49.6 cm, respectively (Figure 44-1C). She was subsequently referred to be measured and fitted with compression stockings.

The examining physician must remember that although venous valve incompetence is the most frequent cause of venous hypertension, other comorbidities may also lead to lower extremity edema, swelling, and poor venous return. These conditions may include but are not limited to peripheral edema from congestive heart disease, chronic liver disease, chronic renal insufficiency, malnutrition, anemia, hypoalbuminemia, and lifestyles or work requiring standing with the legs in a dependent position. Factors contributing to lack of “calf muscle pump” may include strokes, arthritis, muscle and fascial injuries, or general debilitation with the extremity in a chronic dependent position. Patients may have lymphedema related to surgical procedures involving groin or pelvic node excisions, radiation therapy, or reoccurring bouts of lymphangitis and secondary fibrosis associated with cellulitis.

Clinicians skilled in differential assessment will be especially aware of the general appearance of the limb, including arterial profusion, sensory function, pain, and range of motion as well as peripheral pulses either palpated or documented by a handheld Doppler ultrasound examination.

Patients with long-term or recurrent venous ulcerations commonly have varicosities, a history of vein surgery, edema, hemosiderin skin staining in the lower medial calf (Gaitor zone), dermatitis, and inflammation. A history of DVT has been shown to be associated with 37% of venous ulcers.³

Venous Stasis Ulcers

A 57-year-old woman presented with a history of recurrent venous stasis ulcers of the right leg over the past 10 years. Her history included a DVT of the right popliteal and tibial veins in the remote past, diabetes, cirrhosis, hypertension, hypothyroidism, hyperlipidemia, anemia, and depression. Treatment had included compression hose, right GSV ligation, and extensive microphlebectomies and skin grafts. Examination revealed a large medial ulcer and smaller lateral ulcers of the right calf with extensive scarring and hyperpigmentation but no cellulitis (Figure 44-2A). Venous studies revealed incompetent valves of the right popliteal vein and an incompetent perforating vein in the medial distal calf. Her ABI was 0.85 on the right leg. She was treated with topical vitamin A, calcium alginate with silver, foam, and Profore compression dressings changed weekly. We worked closely with her primary care physician on diabetic control in addition to multivitamins TID, protein supplements and leg elevation with intermittent walking for calf pump activity. She healed completely in 5 weeks (Figure 44-2B) and was discharged with 30 to 40 TOOR support hose and an appointment made with a vascular surgeon for consideration of treatment of the incompetent perforating vein.