Leg Ulcer Management

Venous ulcers

While chronic venous insufficiency is often the cause of venous ulceration, the exact mechanism by which ulcers result is not known; a connection between deep vein damage and ulceration is suspected. Normally, the calf muscles pump blood back up to the heart. Without adequate use of calf muscles, blood collects in the saphenous venous system and its tributaries, and is transmitted instead to the cutaneous vasculature, leading to chronic venous hypertension. Microcirculatory changes associated with chronic ulcers, diabetes, and repeated bouts of previous vessel damage lead to fibrin cuffs, resulting in impaired cutaneous nutrition, and ultimately ulceration. Neutrophils adhere to tissue damaged by ambulatory venous hypertension and release substances, which generate free radicals, causing further tissue injury. Up to 50% of patients with chronic venous insufficiency have a history of leg injury.

Venous ulcers exude copious drainage. A greenish–yellowish fibrinopurulent, irregularly-shaped adherent exudate may be seen at the base of the ulcer. Superinfection, pain, and malodorous drainage may ensue ( Fig. 46.1A ). A pruritic rash often appears, leading to excoriations. Topical agents used to try to keep it under control often aggravate venous dermatitis. Further acute inflammation produces a panniculitis, which becomes more sclerotic with time, leading to lipodermatosclerosis ( Fig. 46.2 ), which probably results from the sequelae of high venous pressure. Sometimes dystrophic calcium deposits develop.

Arterial ulcers

Arterial disease results from the narrowing of the vessel lumen by the accumulation of cholesterol plaques and other tissue debris. The resulting obstruction leads to the development of collateral circulation. Risk factors for arteriosclerotic occlusion are diabetes, smoking, hyperlipidemia, hypertension, obesity, and age.

Arteriosclerotic occlusion usually affects the entire femoropopliteal trajectory, including important distal branches (anterior peroneal, anterior tibial, and posterior tibial), and may lead to significant distal damage. Involvement of only small-sized branches may lead to limited skin and subcutaneous tissue infarction. On physical examination, there may be hair loss, atrophy, cold surrounding skin, and thickened toenails. Peripheral pulses may range from palpable to absent. Capillary refill time is usually prolonged. Typically, arterial ulcers are located over pressure points, such as the toes and ankles, and are sharply demarcated with little granulation tissue and tend to have a punched-out appearance ( Fig. 46.1B ). The wound bed often has a necrotic-appearing base. Large occlusions require revascularization by means of bypasses, either using the patient's own veins or artificial vein grafts or by means of intravascular procedures such as balloon dilatation (percutaneous transluminal angioplasty), sometimes combined with thrombolysis and the placement of stents.

Diabetic ulcers

Diabetes mellitus affects 5–10% of the US population at some point in their lives and patients have a 1–4% incidence of foot ulcers; the incidence of lower extremity amputation ranges from 2.1 to 13.7 per 1000.

Approximately 85% of all diabetes-related lower extremity amputations are preceded by foot ulcers. Ulcers from diabetes occur as neuropathic or ischemic. While a mixture of each can occur, most patients will exhibit a preponderance of one type. Patients may display other cutaneous markings of diabetes, such as necrobiosis lipoidica diabeticorum, diabetic dermopathy, or diabetic bullae. The most characteristic lesion of the diabetic foot is a mal perforans ulceration ( Fig. 46.1C ). The neuropathic ulcer is essentially a pressure ulcer resulting from the individual's loss of sensation. It is indistinguishable from the neurotrophic ulcers seen in leprosy, tabes dorsalis, and other neurological syndromes. The ulcer is most characteristically over the pressure points of the first and fifth metatarsal heads, and the great toes. Classically well circumscribed, with a surrounding halo of hard callus-like material, the foot involved may have a normal color and even strong arterial pulses. Touch, pressure, and proprioception are diminished or lost. Motor and autonomic nerves may also be involved. Weakening muscles may also lead to toe and foot deformities. Loss of sweating may lead to fissuring and a Charcot foot can develop.

Pressure ulcers

Pressure ulcers have an incidence in acute-care facilities that has varied from 2.7% to 29.5%, and a prevalence that has ranged between 3.5% and 29.5%. There is a study that reported that 17–35% of the patients have pressure ulcer at the time of admission to a nursing home, and the prevalence among the nursing home residents ranges from 7% to 23%. Immobility is a necessary condition for pressure ulcer development, and therefore the most significant risk factor. Impaired nutritional states, along with hypoalbuminemia and immobility, can lead to epidermal moisture vapor loss, which causes maceration and then a breakdown of the stratum corneum barrier, rendering the skin more permeable to noxious agents and trauma. Fecal incontinence, and even slight pressure over skin overlying bony prominences, such as the heel or the malleoli of the ankles, can cause enough injury under these conditions to start the process that leads eventually to a pressure ulcer ( Fig. 46.1D ). Other causes of ulcers need to be excluded, such as venous stasis, arterial insufficiency, diabetes, neuropathy, vasculitis, systemic lupus erythematosus, drug allergies, neoplasm, sickle cell disease and other hematological abnormalities, polycythemia, pyoderma gangrenosum, bacterial and fungal infections, and trauma.

Inflammatory ulcers

Many diseases can lead to leg ulcers. A broad category that excludes venous, arterial, pressure, and diabetic ulcers, as well as the ulcers resulting from neoplasms is the inflammatory ulcer. Kerdel and Paquette and Falanga offer excellent reviews on the subject. One major subcategory is the vasculitis ulcer resulting from small vessel thrombi or emboli. Lesions beginning as palpable purpura can lead to vesicles and pustules. The process involving immune complexes, much like an Arthus reaction, sets off the inflammatory cascade, eventuating in the release of vasoactive amines and other mediators. These mediators serve to amplify the process with the deposition of more immune complexes, leading to an ischemic area, cutaneous necrosis, and ultimately, an ulcer.

A group of conditions involve dermal thrombi in the absence of vasculitis. They include thrombotic thrombocytopenic purpura, disseminated intravascular coagulation, cryoglobulinemia, cryofibrinogenemia, purpura fulminans, coumadin necrosis, and the antiphospholipid syndrome (also known as the lupus anticoagulant syndrome). Individuals with this syndrome may or may not have lupus erythematosus. These patients possess antibodies (IgG or IgM) that interfere with the conversion of prothrombin to thrombin. In the laboratory, they have a prolonged activated partial thromboplastin time. Some may have a prolongation of the prothrombin time. (The Russell viper venom time and Exner's test may also be helpful.) The lesions are purpuric, leading to ischemia and ulceration. Livedo reticularis may be seen. There is no frank vasculitis. Lesions are often painful and heal with atrophic scars (atrophie blanche).

Another condition, pyoderma gangrenosum, is a non-infectious neutrophilic dermatosis that produces recurrent painful inflammatory ulcerations, associated with underlying systemic disease such as inflammatory bowel disease, rheumatoid arthritis, or malignancy in up to 70% of cases. The specific cause is poorly understood and diagnosis is clinically based on appearance – sharply circumscribed ulcers with violaceous, undermined borders ( Fig. 46.3 ).

Phase 1: inflammation

The first phase of normal wound healing begins immediately after an acute injury, and can last for 24–48 h. This phase is characterized by the disruption of blood vessels, which leads to a local release of blood cells and blood-borne elements. The main cellular constituent of the inflammatory phase of tissue repair is the platelet, which initiates clotting of the acute wound by both intrinsic and extrinsic pathways. Platelets release a number of chemoattractant factors, which recruit other platelets, leukocytes, endothelial cells, and fibroblasts to the wound area. The inflammatory phase progresses with the addition of neutrophils and macrophages, which acutely debride the wound by scavenging cellular debris and killing bacteria, leading to the second phase of healing ( Table 46.3 , Fig. 46.4 ).

Phase 2: proliferation and tissue formation

The second phase of wound healing is characterized by proliferation and tissue formation and begins approximately 72 h after injury. This phase can last up to several weeks. In this phase, the keratinocyte plays the primary role in the tissue repair process and undergoes significant changes in morphology and function, allowing for its migration over the wound bed to provide coverage. Additionally, the keratinocyte releases a number of chemokines, which stimulate cellular migration and other key cellular functions, leading to eventual reconstitution of the epidermis and the basement membrane.

The latter segment of the second phase of wound healing is characterized by the formation of granulation tissue. Fibroblasts are instrumental in the reconstitution of the dermal matrix, termed fibroplasia, while endothelial cells play an integral role in the development of new blood vessels, known as angiogenesis. Additionally, the extracellular matrix, with its collection of proteins, growth factors, and enzymes, plays an active role in influencing the keratinocytes, fibroblasts, and endothelial cells.

Phase 3: tissue remodeling

The final phase of wound healing, tissue remodeling, begins at the same time as the onset of cellular proliferation and tissue formation. This phase can last several months after the acute injury. This phase is one of gradual physiologic evolution and is characterized by heterogeneous stages of healing throughout the wound; hence, the macromolecular physical composition of the wound margin can vary greatly, both quantitatively and qualitatively, from that of the central wound bed. Over the course of this phase, granulation tissue becomes mature scar tissue. Several enzymes are involved in breaking down matrix components, whereas the fibroblasts produce substances such as fibronectin, hyaluronic acid, proteoglycans, and collagen, to ultimately restore the functional barrier of the skin and increase the tensile strength of the scar. Each of these components plays an important role in the wound healing process. Fibronectin acts as a matrix for cellular migration, as scaffolding for collagen deposition, and as a linkage for myofibroblasts to aid in wound contraction. Hyaluronic acid stimulates wound maturation by promoting cell migration and division. Proteoglycans increase tissue strength, modify collagen deposition, and help to modulate cellular function. Last, collagen is essential for providing structural support and tensile strength, while also playing an important role in the regulation of cellular function.

In summary, the tissue-remodeling phase of wound healing is an evolving series of cellular events characterized by extracellular matrix formation, which should result in complete wound maturation and scar formation.