Ulcers and Wound Healing of Venous Stasis Ulcers
by Robert C. Kiser, DO, MSPH
Human skin is messy. Epidermis, from microscopic cells to macroscopic flakes are constantly being shed and replenished from lower layers. Furthermore, if epidermis is injured by trauma it must replenish itself to provide the protective, semi-permeable barrier against the environment that it maintains. This process requires a dynamic balance between building up of skin and shedding or breaking down skin. If the building up of skin is too exuberant, conditions such as psoriasis and Ichthyosis occur in which the skin becomes thick and scaly. When skin does not replenish and heal fast enough, or when conditions favor break- down of skin more than growth of new skin, ulcers develop.
Types of Ulcers: Mechanical Pressure
Ulcers may be caused by many different factors, or several factors acting in concert. Pressure ulcers, decubitus ulcers, or “bed sores” occur when constant pressure and/or sheer forces are exerted on tissue, usually overlying a bony prominence, over a prolonged period of time. Curiously, although decubitus ulcers have been known of for thousands of years, the exact pathophysiology has not been elucidated. It is believed that the mechanical forces change interstitial pressures and pressure gradients, reduce capillary exchange, and create an environment in which tissue necrosis is favored over tissue healing.
Malignancy
Skin cancer can manifest as erosive non- healing ulcers
Systemic Diseases
Numerous systemic diseases are associated with cutaneous ulcers, including diabetes, renal disease, lupus and inflammatory bowel diseases.
Ulcers of Venous Insufficiency or Venous Stasis Ulcers
Venous stasis ulcers will be the topic of the rest of this article. Ulcers are the end- stage of venous insufficiency. The region most commonly affected is the “gaiter region” – the area just above the ankle, most commonly the medial, but sometimes the lateral malleolus. Venous insufficiency occurs when the valves within the veins no longer function properly. Valves within veins assist venous blood to go up the leg against gravity. When these valves no longer function properly, blood flows back down the lower extremity and creates a gravity-dependent, gradient pressure within the venous system. This leads to elevated pressures within the veins, all the way back to the capillary networks where oxygen from arterial blood is exchanged with tissues, and deoxygenated venous blood full of metabolic byproducts of cellular respiration is collected. These “dammed-back” capillaries undergo changes such as fibrin cuffing, which further diminish nutrient exchange. The befouled environment leads to changes in the surrounding tissues including the deposition of collagen in the skin and adipose tissue.
Epidemiology
The point prevalence of venous stasis ulceration western nations is estimated to be from 0.02 to 1 percent.1 Risk factors include age, obesity, history of leg injury and history of venous thromboembolism (VTE). Venous stasis ulcers were responsible for 2 million work days lost in 2002.
Symptoms and Presentation
Venous stasis ulcers present with areas of poorly healing skin wounds, generally of the medial malleolus, red-based or exudative, with local skin necrosis and irregular borders. Frequently the surrounding tissue has other signs of venous insufficiency, such as hyperpigmentation, pitting or woody edema, excess collagen deposition and fibrosis. The patient will frequently complain of factors that limit quality of life, including pain, odor, exudation, spontaneous bleeding and alteration of lifestyle (such as no longer being able to swim or wear shorts). Without proper treatment, venous stasis ulcers can take many months to heal. Patients may suffer with their ulcers for months or even many years without bringing the condition to the attention of their physician. Often there is some provoking trauma such as a scrape or bump, and barring such trauma patients will often complain that that they have been bitten by a “spider.” Frequently the patient self-diagnoses the ulcer as a “brown-recluse bite,” even in areas that brown recluse spiders are extremely uncommon. Like proteolytic spider bites, ulcers take a long time to heal and heal with scarring. Unlike such bites, ulcers tend to recur after healing if appropriate measures are not taken to treat the underlying venous insufficiency causing the ulcer.
Conservative Treatment
The mainstay of treatment for venous stasis ulcers is compression. Compression can be provided by dressings, single or multilayered bandaging, graduated compression stockings, or Velcro-strap devices. Compression may be elastic or inelastic. The most common form of single-layer bandage is the zinc-paste bandage created by Paul Gerson Unna (1850-1929). Unna’s boots have numerous formulations, but the principle components are a cotton bandage impregnated with zinc paste, glycerin and sometimes calamine. Gelatin and other chemicals sometimes are used to emulsify and spread the zinc paste. The application of the boot requires hands- on training to perform effectively. Principles include starting at the metatarsal bases and wrapping to the tibial tubercle and applying with sufficient firmness in an even, contour-forming pressure to avoid gauging the skin. The boot is left in place for 7-10 days and then changed – although earlier changes can be necessary for very exudative wounds or if there is sufficient edema that the bandage becomes loose. Unna’s boot has many advantages, including being an inelastic compression that provides compression during ambulation, but is non-compressive when the patient is recumbent and not ambulating.
Multilayer bandages may include layers of sponge-foam, cotton- wool, crepe, elastic-stretch bandages, and Coban-type self-adherent bandages. The advantages of the multilayer bandages include the ability to absorb moisture and exudate, the increased circumference the wadding or foam layer provides allows for decreased point pressure while maintaining adequate circumferential pressure to the limb, the ability to apply granulation favoring or antimicrobial dressings directly to the wound. The disadvantages of the multi- layer dressings include cost and the bulk of the dressing.
Debridement
Another aspect of wound care that is important is debridement. Debridement of necrotic debris should be provided to encourage growth of granulation tissue. Debridement can be mechanical (sharp or blunt) or chemical. Several products are available for chemical debridement, including balsam of Peru-castor oil mixes (such as Granulex) and collagenase (Santyl). One of the most effective and safe chemical debridement creams, in the author’s opinion and experience, was papain-urea cream (Accuzyme). Unfortunately, the Food and Drug Administration took Accuzyme off the market several years ago.3
Antimicrobials
Antibiotics are seldom useful in the treatment of venous stasis ulcers unless signs of infection are present. These signs include increase in pain beyond the baseline, increasing erythema of the skin surrounding the ulcer, and lymphangitis, a rapid increase in the size of the ulcer.4 Antibiotics are frequently overprescribed for venous stasis ulcers on the basis of necrosis and exudate. Unfortunately, the necrosis of ulcerating skin is generally not due to bacteria, but due to autolysis of the skin cells, and therefore antimicrobials do not improve the situation, and may increase the potential for super- infection with resistant organisms.5
Phlebological Treatment
The underlying cause of venous stasis ulceration is venous stasis. Using modern techniques such as radiofrequency ablation, endovenous laser ablation, and ultrasound-guided sclerotherapy the root cause of the imbalance in healing and breaking down skin tissue can be corrected, and balance restored. By addressing and correcting the increased pressure in the superficial system, but ablating refluxing axial veins or perforating veins, the phlebologist not only can help to heal the venous stasis ulcer, but can prevent chronic recurrence. Older techniques such as vein stripping and ligation and the Linton procedure for perforator closure were sometimes avoided while the ulcer was open, as these techniques utilized incisions through or near already compromised skin. With more modern, minimally invasive techniques, the points of high superficial venous pressure can be addressed with 2mm or smaller incisions, and the balance of healing versus lysis of skin restored. By addressing the underlying cause of the ulcer, the phlebologist, working with the primary physician and/or wound healing center, can help to provide long-term wound healing for the venous stasis ulcer.