Treating Venous Stasis Ulcers In The Lower Extremity

Author(s): 
By Mark Beylin, DPM

Chronic venous insufficiency is a significant disease that affects as much as 25 percent of the population in the United States. It is also a condition commonly treated by podiatric physicians. The condition results in blood pooling in the venous system of the lower extremities (see “A Guide To Normal Venous Anatomy And Physiology below). Venous stasis ulcers are the end stage of chronic venous insufficiency. In order to treat venous stasis ulceration, one must have a clear understanding of the pathophysiology of venous disease. Most of the vein problems that occur are due to increased pressure in the venous system. Venous insufficiency and subsequent hypertension are caused by valvular incompetence in the high-pressure deep venous system, low-pressure superficial venous system or both. Dilation of the veins is the primary problem. When the veins dilate, the valves are separated from each other. This causes a back flow of blood. When veins lose their functional capacity, gravity works against the flow of venous blood in the lower extremity. When one is walking, the blood flow is generally normal even through the incompetent veins and muscle contracture circulates blood out of the leg. On the contrary, when one stands, there is a reverse flow in the incompetent vein and a back flow occurs. This gets in the way of venous drainage and eventually results in an elevation of venous pressure. When valves of the perforating veins become incompetent, high-pressure blood from the deep venous system flows towards the skin, producing hypertension in the superficial veins.2 This process leads to the leaking of fluid from small veins makes into the surrounding tissues. This causes edema and characteristic discoloration. This is subsequently followed by an impaired exchange of nutrients and wastes between the arterial and venous systems. A Guide To Normal Venous Anatomy And Physiology Venous stasis disease has been a challenging problem to treat for centuries. Fabricius, an Italian surgeon, was the first to recognize the structure and function of the venous valve, which lead to the understanding of the pathophysiology of venous stasis ulcers. With this in mind, it is important to have a strong grasp of normal venous anatomy and physiology. The great saphenous vein is the main superficial vein in the leg. It begins just anterior to the medial malleolus and rises obliquely and posteriorly. The saphenous vein is joined by the posterior arch vein just below the knee. The superficial anterior vein in the lower leg and the anterolateral and posteromedial veins in the thigh join the saphenous vein near the inguinal ligament. The lesser saphenous vein is located posterior to the lateral malleolus advancing upward, lateral to the Achilles tendon. As it reaches the popliteal space, it is situated between the heads of the gastrocnemius muscle. The communicating veins are the connection between the superficial and deep veins. Blood flows through one-way valves from the superficial venous system to the deep venous system of the lower extremity. In the calf, the deep veins are paired and accompany their corresponding arteries with venous tributaries intertwining over the surface of the artery. At the knee, the veins usually join to form the popliteal vein. The function of the deep veins is to carry blood from the muscles of the extremity providing carrier function for the calf muscle pump. The calf muscle veins are covered with a tight fascia, similar to that of an elastic support stocking. This prevents dilation of the deep veins in contrast to the superficial veins, which are contained within loose non-supportive tissue. The popliteal vein becomes the superficial femoral vein. As far as physiology goes, the calf muscle pump cycle has two phases of blood pumping: systolic and diastolic. During the systolic phase, contraction of the calf muscles compresses the blood within the deep venous system, pumping it in the direction of the heart. Valves of the communicating veins act as the bridge between the deep and superficial systems. These valves are closed as they prevent the back flow of venous blood. At this time, the pressure within the deep venous system can reach 120 mm Hg.1 During the diastolic phase of the muscle pump, the muscle relaxation allows the deep venous system of the calf to refill. This facilitates blood flow from the superficial veins to the deep venous system through the perforating veins that now have open valves. At this point, the higher pressure in the superficial venous system favors flow to the deep venous system. Understanding The Etiology Of Venous Ulcers When venous insufficiency goes untreated, whether it is in the deep or superficial venous system, it can lead to leg pain, swelling, characteristic skin changes and eventual ulcer formation. Venous stasis ulcerations can result from sustained elevated pressure in the venous system of the lower extremities. Higher than normal pressures damage either the deep or superficial veins or both. A rise in the venous pressures and subsequent venous stasis leads to more permeability of capillaries. Protein leaks out of the vascular bed into the surrounding tissues. Subsequently, fibrinogen is converted into fibrin that coats the capillaries, thus interfering with the exchange of oxygen and nutrients.3 Tissue breakdown is almost inevitable and venous ulceration can occur. An early sign of longstanding venous insufficiency is edema in the ankles and legs that can lead to pain. Swelling results from the blood that has pooled in the veins due to abnormal valve function. This causes venous hypertension. As the edema and hypertension continue, the skin of the lower extremities may actually leak plasma. Eventually, the capillaries burst under the high pressure, releasing red blood cells and giving the area a typical reddish-brown discoloration. Hemosiderin and lipodermatosclerosis (indurated tissue) are common skin changes one would see in patients with venous disease.4 This skin is very vulnerable to even minor trauma as a scratch or bump can result in skin breakdown. Several theories have been proposed in reference to the exact mechanism of venous stasis ulcer formation. Some of these theories discuss white blood cell trapping, fibrin cuff hypothesis and local tissue hypoxia.5,6 Essential Diagnostic Keys Since many ulcers have certain characteristic and historic features, it is important to obtain a thorough patient history with a specific emphasis on detailing the duration and development of the ulcers. When asking the patient questions, one should determine the initial appearance of the ulcer, what possibly caused the ulcer, chronological steps in the ulcer’s development, and symptoms of the ulcer (if any). Clinicians should also ascertain whether the patient has attempted treatment, what medications he or she is currently taking, whether there is a history of any vascular diseases and if there is any pertinent family history. I go through a routine physical examination on every patient. A vascular component of the examination includes documenting the status of pedal pulses, capillary refill time, temperature gradient, edema, hair distribution, varicosities, skin color and appearance, and nail condition. I follow this exam with thorough neurological and orthopedic examinations. It is particularly important to perform a dermatological exam. One should accurately measure the ulceration, documenting its length, width and depth. Carefully examine the wound bed. Assess any present exudate for quantity and quality. Examine the borders of the wound to rule out the gross presence of an underlying skin cancer. It is important to note if the ulceration extends to deeper underlying tissues such as tendons, ligaments, capsules or bone. Carefully examine the surrounding skin. When it comes to ulcers resulting from venous insufficiency, one will often find them in the area of medial ankle or the gaiter area (in the area of the great saphenous vein). However, clinicians may find these ulcers laterally, anteriorly and posteriorly. They are usually more superficial than ulcers of other etiologies, with sharp or slanting borders and fibrotic material at the base. One will usually see moderate to high exudate due to venous hypertension. The patient may or may not have pain. One can relieve this pain by emphasizing leg elevation. When faced with a venous ulcer, it is crucial to determine the status of venous and arterial circulation in order to identify the primary cause of the wound. Non-invasive vascular studies such as Doppler flow studies, arteriography, venography and Doppler plethysmography offer good insight into diagnosing the ulceration. After determining the exact etiology, one can formulate an appropriate treatment plan. In the differential diagnosis of venous ulcers, one should exclude the presence of squamous cell, basal cell cancer or vasculitis. One can rule these out with a biopsy. One should have a stronger index of suspicion of a skin cancer if the ulceration is atypical in its presentation or has been present for a long time with no response to different treatment modalities. Pertinent Pearls On External Compression Venous stasis ulcers are typically persistent and sluggish to heal, making a comprehensive treatment protocol useful. Many approaches have been directed only with wound dressing systems, which are aimed at the wound healing process itself as opposed to addressing the underlying cause. Ulcers do not usually heal if edema, infection and eczematous inflammation are present. Hippocrates and Celsus recognized the benefit of leg elevation and compression therapy as important aspects of venous ulcer treatment. Indeed, compression is the hallmark of treatment for venous ulcers. Compression of the affected lower extremity assists in venous return, which facilitates decreasing edema. The theoretic advantage of external compression is that it blocks transcapillary fluid flow during the ambulatory venous pressure cycle. The pressure needed to reach this effect depends on the clinical presentation of the extremity. Additionally, researchers have shown that external compression not only increases the fibrinolytic activity of veins but also improves deep venous blood flow.7 When applying compression, it is important to exert more pressure distally with gradual decrease in the proximal direction. There are various forms of compression therapy, which range from simple Ace bandages, Unna boots, Profore wraps and elastic stockings to legging orthoses and pneumatic pumps. Selecting the type of compression depends on the physician’s familiarity with the available product and the patient’s need. Each of these products has its advantages as well as disadvantages. Compression bandages such as Ace wraps are the simplest and least costly form of external compression. Difficulty in consistently maintaining the correct pressure during the application and gradual loss of elasticity may result in poor patient compliance. Despite this disadvantage, the Ace wrap is very helpful for an older patient who may have difficulties putting on an elastic stocking. It is useful when there is a seeping wound that requires frequent dressing changes. An Unna boot is a variation of the compression bandage. It is an impregnated bandage, a mix of zinc oxide, sorbitol, gelatin, aluminum silicate, calamine and gelatin magnesium. The advantage of the Unna boot is that it provides both wound care and external compression. The drawbacks are sensitization of the paste, exudate formation underneath and personal hygiene problems.8 Elastic stockings, especially those that are custom-measured and fitted, are another example of external compression. Just like compression bandages, they should employ graduated pressure with the highest pressure distally and the lowest pressure proximally. These stockings can range from below-knee to thigh-high. The major disadvantage of the elastic stockings is the difficulty of putting them on and taking them off. Intermittent pneumatic compression is used more for preventing deep venous thrombosis and not as much for the actual ulcer treatment. This type of device comes as single-unit cell, two- or three-cell units or multi-cell sequential units. Two- or three-unit devices are more advantageous in treating venous insufficiency because they “milk” the fluid up the leg.9 Employing normal saline or silver nitrate wet-to-dry compresses help to control periwound inflammation. One may also use topical steroids twice a day with or without the compresses. What You Should Know About Wound Bed Preparation When assessing an ulcer, it is important to exclude the presence of infection. Topical and/or systemic antibiotics may enhance wound healing when heavy bacterial contamination is present. One must culture the ulceration to determine proper antibiotic coverage. Obtaining an appropriate consultation with an infectious disease specialist is always helpful. Once one has controlled edema, eczematous inflammation and infection, clinicians must prepare the wound bed for definitive treatment. One must debride all fibrous tissue, exudate and crust in order to stimulate granulation to produce new epithelium. You may perform surgical debridement or facilitate debridement with different dressings and compresses. Absorbent dressings are generally helpful when dealing with a draining ulcer. Such dressings absorb low-molecular weight substances. Calcium alginate dressings are very absorbent but need to be changed frequently. DuoDerm dressings work similarly but do not usually require such frequent changes. Other dressings include wet-to-dry normal saline, acetic acid or silver nitrate dressings. A gentle whirlpool may be helpful when dealing with an exudative wound. Synthetic occlusive dressings and proteolytic enzyme ointments (Panafil, Santyl, Travese) are helpful in facilitating the healing of venous ulcers. These modalities suppress crust formation and facilitate rapid migration of the epidermis over the moist granulation tissue. A Closer Look At Ancillary Treatments A physician may turn to ancillary modalities when treating venous stasis ulcers. One of these modalities is hyperbaric oxygen (HBO) treatment. The oxygen pressure is reduced to about 18 to 20 mm Hg to minimize obstruction of venous return. Patients receive 15 to 20 treatments during their course of HBO therapy.10 When dealing with chronic venous ulcers that are resistant to treatment, one may consider systemic therapy. Pentoxifylline increases fibrinolytic activity. The drug has a specific effect of promoting blood flow in ischemic areas. Researchers believe it is advantageous to use pentoxifylline in conjunction with topical treatments for a minimum of six to eight weeks.11 If the response to treatment remains insufficient, clinicians may consider surgical intervention. Split-thickness grafts, meshed grafts, partial-thickness and synthetic grafts have all been successful. Grafts “take” when one applies them to a wound that has granulation tissue free of infection and exudate, and when edema has been controlled. As noted earlier, if the ulceration has not responded to different treatment options or has been present for a long time, obtaining a biopsy is necessary as it may discover an underlying skin cancer. The Stages Of Chronic Venous Insufficiency The signs of chronic venous insufficiency may be divided into three general stages: Stage 1: Edema and skin pigmentation Stage 2: Edema, skin pigmentation and dermatitis Stage 3: Edema, skin pigmentation, dermatitis, varicosities and ulceration In Conclusion Venous stasis ulcerations are a very common condition affecting a large portion of the population in the United States and the world. Ensuring a timely diagnosis of the condition, differentiating venous stasis ulcers from those of arterial etiology, arriving at an appropriate treatment plan and emphasizing proper prevention are critical in treating such conditions. Dr. Beylin is an Associate of the American College of Foot and Ankle Surgeons. He is affiliated with the Foot and Ankle Surgical Group of South Florida in Hialeah, Fla., and is an Attending Physician at Palmetto General Hospital in Hialeah, Fla. Editor’s Note: For related articles, see “Vascular Intervention In Difficult Wounds” in the July 2002 issue or “Expert Tips On Wound Bed Preparation” in the July 2003 issue of Podiatry Today. CE Exam #124 Choose the single best response to each question listed below: 1. Untreated venous insufficiency can lead to … a) venous ulcer formation b) swelling c) leg pain d) all of the above e) a and b 2. What is an early sign of longstanding venous insufficiency? a) edema in ankles and legs b) hemosiderin c) local tissue hypoxia d) discoloration e) b and c 3. When obtaining information from a patient who presents with a venous ulcer, one should determine … a) whether there is a history of any vascular disease b) the initial appearance of the ulcer c) whether the patient has attempted treatment d) what possibly caused the ulcer e) all of the above 4. One will usually see lower extremity venous ulcers … a) on the plantar surface of the foot b) in the area of the medial ankle c) in the area of the greater saphenous vein d) a and b e) b and c 5. Which of the following answers is false? Venous ulcers usually do not heal if _______ is present. a) granulation tissue b) edema c) infection d) eczematous inflammation e) none of the above 6. Which of the following statements is false about external compression? a) It theoretically facilitates transcapillary fluid flow during the ambulatory venous pressure cycle. b) It increases the fibrinolytic activity of veins. c) It improves deep venous blood flow. d) All of the above e) None of the above 7. Which compression therapy is very helpful for older patients with venous ulcers? a) Unna boot b) Ace bandage c) elastic stockings d) pneumatic compression e) none of the above 8. Which external compression therapy is used more for preventing deep venous thrombosis than for treating venous ulcers? a) Unna boot b) Profore c) intermittent pneumatic compression d) Ace banadge e) none of the above 9. What is the leg’s main superficial vein? a) popliteal vein b) saphenous vein c) anterolateral vein d) posteromedial vein e) none of the above 10. The saphenous vein begins just anterior to the … a) posterior arch vein b) inguinal ligament c) medial malleolus d) lesser saphenous vein e) none of the above Instructions for Submitting Exams Fill out the enclosed card that appears on the following page or fax the form to the NACCME at (610) 560-0502. Within 60 days, you will be advised that you have passed or failed the exam. A score of 70 percent or above will comprise a passing grade. A certificate will be awarded to participants who successfully complete the exam. Responses will be accepted up to 12 months from the publication date.
 

 

References:

References 1. Darling RC, Kupinski AM: Preoperative evaluations of veins, Semin Vasc Surg 6:155, 1993. 2. Browse NL, Burnand KG, Lea TM: Diseases of the veins: pathology, diagnosis, and treatment. London, 1988, Edward Arnold. 3. Alguire P, Mathes B. Chronic venous insufficiency and venous ulceration. JGIM. 1997; 12:374-383. 4. Moschella, Hurley. Dermatology, 3rd edition. Boston: Harvard Medical School; 1992: 473-476. 5. Angle N, Bergan JJ. Chronic venous ulcer. Brit Med J, 1997; 314:1019-23. 6. Callam J et al: Chronic ulceration of the leg: extent of the problem and provision of care, Br Med J 290:1855, 1985. 7. Fletcher A, Cullum N, Sheldon TA. A systemic review of compression treatment for venous leg ulcers. Brit Med J, 1997; 315:576-80. 8. Hendricks WM, Swallow RT: Management of stasis leg ulcers with Unna boots versus elastic support stockings. J Am Acad Dermatol 12:90-8, 1985. 9. Kolari PJ, Pekanmaki P: Intermittent pneumatic compression in healing of venous ulcers, Lancet 2:1108, 1986. 10. Heng MCY, Pilgrim JP, Beck FWJ: A simplified hyperbaric oxygen technique for leg ulcers. Arch Dermatol, 120:640-45, 1984. 11. Weitgasser H: The use of pentoxifylline (Trental 400) in the treatment of leg ulcers: results of a double-blind trial. Pharmatherapeutica 3 (supl):143-51, 1983.

 

Add new comment