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Care of patients with leg ulcers: A nursing perspective
Care of Patients with Leg Ulcers: A Nursing Perspective Nursing care of leg ulcers in geriatric patients requires knowledge of pathology leading to ulcers, ulcer assessment, and optimal treatment. BY
NANCY
A.
STOTTS
AND
CAROLE
Care of patients with leg ulcers is challenging as well as rewarding. Recent advances in scientific knowledge about healing should be incorporated in the nursing care of leg ulcer patients. This article provides an update on the state of the science in the care of leg ulcers in geriatric patients, and focuses on assessment and local care of such ulcers. Ulcer assessment provides the basis for selecting therapies to maximize healing. Wound cleansing and appropriate dressings are essential to good patient outcomes. Furthermore, healing is enhanced when these interventions are combined with strategies that maximize oxygen to the ulcer, promote appropriate levels of activity, optimize perfusion through physiological positioning, and reduce mechanical shear through selection of proper footwear. Care of patients with leg ulcers provides the nurse an opportunity to apply pathophysiology, utilize scientific dam, and function as an integral player on the wound care team. (Geriatr Nurs 1997;18:255-9.) he majority of leg ulcers (85%) are found in the T elderly. 1 They cause discomfort, interfere with a c t i v i t i e s and m o b i l i t y , require a d j u s t m e n t s in lifestyle to a c c o m m o d a t e treatment, and often significantly decrease individuals' quality of life. 2 The goals of rapid healing and prevention of infection are paramount. Conscientious, skilled nursing care is critical to achieve these goals. The purpose of this article is to provide an update on the scientific knowledge of leg ulcer assessment and the methods used to support optimal healing. Pathology of the major types of leg u l c e r s - - arterial, venous, and neuropathic--is discussed, along with their assessment and local care. NANCY A. STOTTS, RN, EdD, is a professor and CAROLE E. DEITRICH, RN, GNR MS, is a clinical professor in the Department of Physiological Nursing at the University of California, San Francisco. Copyright © 1997 by Mosby-Year Book, Inc. 0197-4572/97/$5.00 + 0 34/1185623
GERIATRICNURSING Volume18, Number 6
E.
DEITRICH
Pathology of Leg Ulcers Fundamental to understanding the nursing care of leg ulcers is knowledge of the underlying pathophysiology leading to their occurrence. Venous ulcers. Venous ulcers are caused by stasis of blood in the veins that results in increased venous pressure and failure of valves in the venous system to stop regurgitant (backward) flow. Vein walls are thinner and more distensible than artery walls and so expand more easily. When blood pools in the veins, there is a buildup of waste products, and minor trauma to the area results in tissue breakdown (Table 1). Because venous disease is a chronic condition, changes occur slowly in the vasculature. However, when pathology progresses to the stage where valves are incompetent, the changes are permanent and require ongoing treatment that continues even after the ulcer heals. The fibrin cuff theory suggests that slowed healing in venous ulcers is due to a buildup of fibrin that forms a mechanical barrier to nutrients and oxygen and reduces the ability of cells to adhere to new tissue) Fibrin also is thought to trap growth factors, reducing their availability for use in healing. 4 At the same time, white blood cells (WBCs) mechanically occlude the capillaries, leading to slowed flow 5 and continue to damage tissue because of their chemical activation and release of proteolytic enzymes. 6 Rising pressure in the venous system causes increased venular hypertension, which blocks reabsorption of fluid from the capillaries and results in edema. In most patients, the edema is made worse when legs are dependent and is relieved when legs are at the level of the heart. Trapping of hemosiderin, the byproduct of red blood cell metabolism, in the tissues results in permanent reddishbrown discoloration of the skin in the ankle area. Venous ulcers are usually located in the medial malleolar area (the inner aspect of the ankle). Their distribution is due to the configuration of the vasculature in the leg. Venous ulcers classically are inflamed, beefy-red, irStotts and Deitrich 2 5 5
regular, often exudative, and usually quite painful. 6,7 Ulcer depth varies. Arterial ulcers. Arterial ulcers result from inadequate blood flow, usually to the ankle and foot. They most commonly are due to arteriosclerotic disease that eventually results in ischemia and necrosis) Arteriosclerotic disease is a progressive condition that manifests early as fatigue or discomfort in the calves of the legs when walking and later as intermittent claudication (pain on walking). The pain occurs after walking a specific distance and abates when the person stops walking. With progression of the disease, pain occurs even without activity--a phenomenon known as rest pain. Rest pain is due to ischemia; when it is present, even minor leg, foot, or ankle trauma can result in an ulcer. With mild and moderate disease, pulses are present. It is only with severe disease that pedal and/or posterior tibial pulses are diminished or absent.
Rest pain is due to ischemia; when it is present, even minor leg, foot, or ankle trauma can result in an ulcer. Arterial ulcers usually are small, with regular edges and a weak inflammatory response around the border. The base of the wound is pale. They usually occur below the ankle, on the lateral malleolus (outer aspect of the ankle), and often are found on the toes (Table 1). Neuropathic ulcers. Neuropathic ulcers are due to impaired innervation to the lower extremities, most often caused by diabetes. Although the exact mechanism is not known, both vascular and metabolic factors are thought to contribute to the problem (Table 1). The mechanical stress exerted by walking probably is pivotal in ulcer formarion. 9 The neuropathy parallels the duration and severity of hyperglycemia and all nerves are affected (autonomic, motor, and sensory). 5 This problem is compounded with muscle atrophy, where changes in foot architecture result 256
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in foot deformity and new pressure points are created. Areas of highest pressure are on the plantar surface of the foot just below the second metatarsal. With neuropathic ulcers, minor trauma causes tissue damage that progresses to ulceration. Where persons with normal sensation would stop trauma that results in pain, those with neuropathology lack this protective sensation. Ulcers also occur with a buildup of callus at pressure points; subsequent shearing of the callus results in an ulcer.
Ulcer Assessment Although knowledge in the area of wound assessment has accumulated over the years, there is no agreement on a definitive method to measure healing. 1° Some nursing research suggests that characteristics such as exudate or granulation tissue are not valid measures of healing. 11 Still, it is the skilled observation of such characteristics that is most commonly used in clinical practice to evaluate healing. Meaningful observation and accurate evaluation of healing depends on consistency among team members. Such consistency requires, at a minimum, common definitions of terms and agreement among evaluators concerning wound characteristics such as granulation tissue, slough, and fibrin. Wound characteristics. There is consensus that the nature of the wound bed is an important factor in wound assessment. ~2,13 In a healing ulcer, there is a clean granulation bed that progresses from pale to beefy red. Venous ulcers often present with a beefy-red base, while arterial ulcers often have a very pale base because they lack sufficient blood flow. Neuropathic ulcers tend to have a pale base. Open ulcers should be moist; however, venous ulcers tend to be wet while arterial ulcers are more likely dry. The edges are flat and attached closely to the sides of the wound, and the epithelial edge is intact. The surrounding tissue is intact, healthy, warm, and dry, but not to the point of scaling or itching. The shape of the wound varies depending on its etiology. Venous ulcers have irregular borders, arterial ulcers are more regular, and neuropathic ulcers have a "punched out" appearance. Because the shape of the November/December1997GERIATRICNURSING
to clean the area using a solution such as normal s a l i n e or hydrogen peroxide that does not contain bacteriostatic substances. Wound fluid should be obtained by aggressively swabbing a small area (1 cm 2) where the ulcer tissue is healthy. A culture is performed to determine which organisms are present in the ulcer tissue; thus the culture is taken from healthy tissue rather than exudate or pus in the ulcer.
There is c o n s e n s u s
t h a t the
n a t u r e o f the w o u n d b e d is an i m p o r t a n t factor in wound assessmenL wound changes as it heals, documentation of wound healing can be difficult. In addition, neuropathic ulcers usually form excess epithelial tissue that presents as a callus surrounding the ulcer. Sharp debridement by a physician, or in some settings by a nurse or physical therapist who is specially trained in the technique, should occur regularly. If the callus that forms with these ulcers is not regularly debrided, it can cause increased shear during walking and result in enlargement of the ulcer. Only after sharp debridement can ulcer size be accurately evaluated. One of the issues in wound assessment is how to measure wound size. Some authorities support measuring surface area; others believe the volume should be measured. 13 An accepted approach for measurement in clinical practice is to make a tracing on a clear plastic sheet or to measure length, width, and depth. 12 Regardless of the approach used, there should be a standard method for measuring in your institution and it should be used by all members of the team. In a wound that is not healing, there may be excessive wound drainage, increased/excess fibrin, and an excessive or insufficient inflammatory response. On the other hand, in some situations the only indication that healing is delayed is that wound size does not decrease. Table 2 lists the characteristics of normal and delayed healing in leg ulcers. Infection. Infection is one factor that often delays healing in patients with leg ulcers. At times the signs are overt, but often infection can be difficult to diagnose. Common signs of infection are an increased and often purulent exudate, foul odor, increased inflammation around the wound that extends out more than 0.5 cm, and pain at the site. Cellulitis may develop where the skin tissue is inflamed and increased interstitial fluid is present. Occasionally there may be fever. At times there is no sign that the wound is infected but the wound size has not changed and the patient has received optimal therapy. Infection should be suspected and a culture taken to determine that the organisms are sensitive to the antibiotic selected empirically. I4 The culture is p e r f o r m e d before the antibiotics are started. When a swab culture is used, it is important GERIATRIC NURSING Volume 18, Number 6
Because legs and feet have little subcutaneous tissue, ulcers increase the possibility of osteomyelitis, or bone infection. Whenever bone is visible or can be probed through the ulcer, the possibility of osteomyelitis should be considered, immediately reported to the physician, and treated. Osteomyelitis is a serious threat to life and limb and is most successfully treated in its earliest stages.
Local Care Leg ulcer care should be based on scientific knowledge of factors in the local environment that support healing (see Table 3). The major advances that have been made in knowledge of healing should be incorporated in local care. Moist environment. First, the wound bed needs to be moist to support cell division and migration. This recommendation is based on the classic work of Winter, 15 who showed that epithelialization occurs faster in a moist environment than in a semimoist or dry environment. There was initial fear that a moist wound bed would support growth of microorganisms and result in infection. Data show, however, that the moist environment does not result in infection, even in the elderly, who have slower responding immune systems than younger persons.12 A moist environment is accomplished most commonly through dressings applied to the wound. Keeping the wound covered maintains wound moisture to keep cells hydrated and prevents additional contamination and trauma. Wound cleansing. Data show that all wounds are contaminated and that chronic wounds heal better with fewer organisms present. 14 Research has focused on cleansing the wound bed as a means of reducing the bacterial burden. The current recommendation is that high-pressure irrigation (such as that produced with a 35 cc syringe and #18 angiocatheter) with a nontoxic agent such as sterile normal saline be used for cleansing. 16 The recommendation to use nontoxic solutions rather than antiseptics is based on data pertaining to acute wounds over a short period; the use of such solutions has not been evaluated in chronic wounds over a prolonged period. When simple cleansing is the goal, normal saline continues to make sense. However, in an infected wound, topical chemical Stotts and Deitrich 2 5 7
agents often have a role. Here it is essential to understand the particular needs of the wound and the specific actions of available chemical agents. The recommendation for more than 10 years has been to avoid the iodine-based antiseptics because of their tissue toxicity. More recently, however, researchers have questioned this recommendation, noting problems in the original study design. 17 Pure iodine, long used as an antiseptic in the preantibiotic era, is toxic and should not be used. It is now understood, however, that it is the formulation of iodine that needs to be considered, not merely the presence of iodine in a topical compound. Povidone-iodine mixed with surfactant delays healing when used on open tissue but is effective in reducing bacteria on intact skin. Although povidone-iodine solution without surfactant is effective in initially lowering bacteria counts, its sustained effect is quickly depleted by wound debris. A new formulation of iodine, cadexomer-iodine, is recommended for treatment of infected chronic wounds. 17,18 Clinicians must understand the goal of therapy and select agents that are consistent with it, rather than simply banning all antiseptics from wound care. G r o w t h factors. Growth factors are another area of scientific development in wound healing. Although there is increasing knowledge about the various growth factors and how they signal a cascade of systemic elements to enhance healing, the exact quantity of growth factors, which ones are needed, and in what sequence are not entirely understood. Some growth factors that are commercially available to aid healing are effective in certain patients with chronic wounds. 19 Blood flow. The role of blood flow in local healing has long been a focus of research. Recent work in the area has 258
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supported the importance of strategies to enhance blood flow by reducing sympathetic nervous system outflow to overcome vasoconstriction. These strategies include maintaining warmth (even in the presence of arterial disease), reducing pain, avoiding factors that cause vasoconstriction (for example, smoking), and maintaining an adequate blood volume. 2°21 Warmth causes vasodilation and brings oxygen to the tissues. Adequate intravascular volume is needed to bring the oxygen to the tissue. Simple interventions such as ensuring that leg ulcer patients keep their legs covered and wear heavy socks will maximize perfusion and healing. If off-loading pressure on a neuropathic ulcer is needed, special foot equipment may be used. Also, smoking causes vasoconstriction and inhibits healing. 2a Smoking even a few cigarettes per day can produce vasoconstriction that persists throughout the entire day. Smoking in most cases should be stopped completely. Pain control. Pain control is essential. Because sympathetic outflow associated with pain causes subcutaneous vasoconstriction and shunts blood flow away from the ulcer, untreated pain slows healing. It may be necessary to obtain a consult from a pain specialist or refer the patient to the pain team. 21 Neuropathic pain is a special case in which, in addition to the usual analgesics (such as Tylenol or opiates), low-dose antidepressant medication may be helpful. Dosages are much lower than those used to treat depression, greatly reducing the possibility of side effects. Amitriptyline (Elavil) is sometimes used in these circumstances. However, for older adults, Norpramin (desipramine) is usually better tolerated because it has fewer anticholinergic effects. 23 November/December1997GERIATRICNURSING
Pathology-specific Considerations
Conclusion
Compression. Compression is important for patients with venous ulcer disease. It should not be used with pure arterial disease or in patients with neuropathic ulcers who do not have concomitant venous disease. In venous disease, c o m p r e s s i o n is used to aid venous return and reduce the distance that nutrients and oxygen must diffuse to support healing. 3 Frequently used strategies for c o m p r e s s i o n include Unna's boot, m u l t i p l e - l a y e r bandages, and elastic stockings. It is critical that patients apply c o m p r e s s i o n prior to getting out of bed in the morning, or if they do arise, return to bed for 20-30 minutes to reduce edema before applying compression. Activity. Activity is important for patients with leg ulcers to help prevent the complications of immobility. However, for healing to occur, relative immobility may be used for a period of time to reduce metabolic needs and support maximal perfusion to the ulcer. This may mean periods of lying down for the patient, with the feet positioned to maximize blood flow. 3,7,s Positioning. Positioning needs to be planned on an individual basis. For most patients with pure venous disease, this means feet at heart level to enhance venous return. For patients with arterial disease, the optimal position may be with feet dependent to allow gravity to enhance perfusion. Patients with neuropathic ulcers often have degrees of arterial disease present; however, the position of their feet usually is not as important for them as is removing weight from their ulcer. 3,7,8
The nursing care needed for healing in patients with leg ulcers is continually changing as new knowledge develops through research. Clinicians must continue to read and examine the evolving body of literature on leg ulcer care so patients can benefit from the optimal blend of therapies. Current thinking is that healing is maximized when local care is combined with strategies that enhance oxygen to the ulcer, promote appropriate levels of activity, optimize perfusion through physiological positioning, and reduce mechanical shear through selection of proper footwear. The nurse is pivotal to providing and coordinating this care in the geriatric patient with leg ulcers. •
Neuropathic pain is a special case in which, in addition to the usual analgesics, low-dose antidepressant medication may be helpful Footwear. Special footwear may be needed for patients with all types of foot ulcers. For persons with venous disease, the c o m p r e s s i o n often makes their legs and feet so large that they do not fit in their usual shoes. For those with arterial ulcers, the ulcer dressings create the same problem. Patients with neuropathic ulcers often require special f o o t w e a r that is designed to remove all pressure f r o m the ulcer area and protect the insensate foot from trauma. For patients with neuropathic ulcers, referral to an orthotist or a brace shop for special footwear may be needed. 9 Regardless of the fact that patients have ulcers, they need sturdy shoes for walking. The nurse must take the initiative to inspect their f o o t w e a r to ensure that it is safe to prevent unstable gait and falls.
GERIATRIC NURSING Volume 18, Number 6
REFERENCES i. Nelzen O, Bergqvist B, Lindhagen A, Hallbrook T. Chronic leg ulcers: an underestimated problem in primary health care among elderly patients. J Epidemiol Comanunity Health 1991 ;5:184-7. 2. Price PE, Harding KG. The reliability of a new disease specific measure of quality-of-life for patients with chronic wounds. Wound Repair and Regeneration 1997;5:A102. 3. Black SB. Venous stasis ulcers: a review. Ostomy/Wound Management, 1995;41:20-32. 4. Falanga V, Eaglstein WH. The trap hypothesis of venous ulceration. Lancet 1993;341:1006-8. 5. Ziegler D, Cicmir I, Mayer R Wiefeks K, Gries FA. Peripheral and autonomic nerve function in newly diagnosed insulin dependent diabetics. Diabetes Res 1987;4:9-14. 6. Wipke-Tevis DD, Stotts N. Leukocytes, ischemia, and wound healing: a critical interaction. Wounds: A Compendium of Clinical Research and Practice 1991;3:227-38. 7. Ennis WJ, Meneses R Leg ulcers: a practical approach to the leg ulcer patient. Ostomy/Wound Management 1995;41(7A Suppl):52S-62S. 8. Holloway GA. Arterial ulcers: assessment and diagnosis. Ostomy/Wound Management 1996;42:46-51. 9. Armstrong DG, Lavery LL, Harkless LB. Treatment-base classification system for assessment and care of diabetic feet. Ostomy/Wound Management 1996;4:50-61. 10. Lazarus GS, Cooper DM, Knighton DR, Margolis DJ, Pecoraro RE, Rodeheaver GS, et ai. Definitions and guidelines for assessment of wounds and evaluation of healing. Arch Dermatol 1994; 130:489-93. 11. Johnson M; Miller R. Measuring healing in leg ulcers: practice considerations. Appl Nurs Res 1996;9:204-8. 12. Stotts NA. Impaired healing. In: Pathophysiological phenomena in nursing. Carrieri VK, Lindsey AM, West C, editors. Philadelphia: WB Sannders; 1993. 13. Van Rijswijk L. The fundamentals of wound assessment. Ostomy/Wound Management 1996;42:40-52. 14. Stotts NA. Determination of bacterial burden in wounds. Adv Wound Care 1995;8:28-52. 15. Winter GD, Scales JT. Effect of air drying and dressings on the surface of the wound. Nature 1963;197:91-2. 16. Bergstrom N, Bennett MA, Carlson CE, et al. Treatment of pressure ulcers. Clinical practice guideline no. 15. Rockville (MD): U.S. Dept. of Health and Human Services, Public Health Service, Agency for Health Care Policy Research; 1994 Dec. AHCPR publication no. 95-0652. 17. Eaglstein WH, Falanga V. Chronic wounds, Surg Clin North Am 1997;77:689700. 18. Mertz PM, Davis SC, Oliveira-Gandia M, Eaglstein WH. The wound environment: implications from research studies for healing and infection. Wounds 1996;8:1-8. 19. Robson MC. The role of growth factors in the healing of chronic wounds. Wound Repair and Regeneration 1997;5:12-7. 20. Stotts NA, Hunt TK. Managing bacterial colonization and infection. Clin Gefiatr Med. In press. 21. Hunt TK, Hopf H. Wound healing and infection: what surgeons and anesthesiologists can do. Surg Clin North Am 1997;77:587-606. 22. Silverstein P. Smoking and wound healing. Am J Med t992;93(suppl 1A):lA22S. 23. Lipman AG. Analgesic drugs for neuropathic and sympathetically maintained pain. Clin Geriatr Med 1996;12:501-15.
Stotts a n d D e i t r i c h
259
NANCY
A.
STOTTS
AND
CAROLE
Care of patients with leg ulcers is challenging as well as rewarding. Recent advances in scientific knowledge about healing should be incorporated in the nursing care of leg ulcer patients. This article provides an update on the state of the science in the care of leg ulcers in geriatric patients, and focuses on assessment and local care of such ulcers. Ulcer assessment provides the basis for selecting therapies to maximize healing. Wound cleansing and appropriate dressings are essential to good patient outcomes. Furthermore, healing is enhanced when these interventions are combined with strategies that maximize oxygen to the ulcer, promote appropriate levels of activity, optimize perfusion through physiological positioning, and reduce mechanical shear through selection of proper footwear. Care of patients with leg ulcers provides the nurse an opportunity to apply pathophysiology, utilize scientific dam, and function as an integral player on the wound care team. (Geriatr Nurs 1997;18:255-9.) he majority of leg ulcers (85%) are found in the T elderly. 1 They cause discomfort, interfere with a c t i v i t i e s and m o b i l i t y , require a d j u s t m e n t s in lifestyle to a c c o m m o d a t e treatment, and often significantly decrease individuals' quality of life. 2 The goals of rapid healing and prevention of infection are paramount. Conscientious, skilled nursing care is critical to achieve these goals. The purpose of this article is to provide an update on the scientific knowledge of leg ulcer assessment and the methods used to support optimal healing. Pathology of the major types of leg u l c e r s - - arterial, venous, and neuropathic--is discussed, along with their assessment and local care. NANCY A. STOTTS, RN, EdD, is a professor and CAROLE E. DEITRICH, RN, GNR MS, is a clinical professor in the Department of Physiological Nursing at the University of California, San Francisco. Copyright © 1997 by Mosby-Year Book, Inc. 0197-4572/97/$5.00 + 0 34/1185623
GERIATRICNURSING Volume18, Number 6
E.
DEITRICH
Pathology of Leg Ulcers Fundamental to understanding the nursing care of leg ulcers is knowledge of the underlying pathophysiology leading to their occurrence. Venous ulcers. Venous ulcers are caused by stasis of blood in the veins that results in increased venous pressure and failure of valves in the venous system to stop regurgitant (backward) flow. Vein walls are thinner and more distensible than artery walls and so expand more easily. When blood pools in the veins, there is a buildup of waste products, and minor trauma to the area results in tissue breakdown (Table 1). Because venous disease is a chronic condition, changes occur slowly in the vasculature. However, when pathology progresses to the stage where valves are incompetent, the changes are permanent and require ongoing treatment that continues even after the ulcer heals. The fibrin cuff theory suggests that slowed healing in venous ulcers is due to a buildup of fibrin that forms a mechanical barrier to nutrients and oxygen and reduces the ability of cells to adhere to new tissue) Fibrin also is thought to trap growth factors, reducing their availability for use in healing. 4 At the same time, white blood cells (WBCs) mechanically occlude the capillaries, leading to slowed flow 5 and continue to damage tissue because of their chemical activation and release of proteolytic enzymes. 6 Rising pressure in the venous system causes increased venular hypertension, which blocks reabsorption of fluid from the capillaries and results in edema. In most patients, the edema is made worse when legs are dependent and is relieved when legs are at the level of the heart. Trapping of hemosiderin, the byproduct of red blood cell metabolism, in the tissues results in permanent reddishbrown discoloration of the skin in the ankle area. Venous ulcers are usually located in the medial malleolar area (the inner aspect of the ankle). Their distribution is due to the configuration of the vasculature in the leg. Venous ulcers classically are inflamed, beefy-red, irStotts and Deitrich 2 5 5
regular, often exudative, and usually quite painful. 6,7 Ulcer depth varies. Arterial ulcers. Arterial ulcers result from inadequate blood flow, usually to the ankle and foot. They most commonly are due to arteriosclerotic disease that eventually results in ischemia and necrosis) Arteriosclerotic disease is a progressive condition that manifests early as fatigue or discomfort in the calves of the legs when walking and later as intermittent claudication (pain on walking). The pain occurs after walking a specific distance and abates when the person stops walking. With progression of the disease, pain occurs even without activity--a phenomenon known as rest pain. Rest pain is due to ischemia; when it is present, even minor leg, foot, or ankle trauma can result in an ulcer. With mild and moderate disease, pulses are present. It is only with severe disease that pedal and/or posterior tibial pulses are diminished or absent.
Rest pain is due to ischemia; when it is present, even minor leg, foot, or ankle trauma can result in an ulcer. Arterial ulcers usually are small, with regular edges and a weak inflammatory response around the border. The base of the wound is pale. They usually occur below the ankle, on the lateral malleolus (outer aspect of the ankle), and often are found on the toes (Table 1). Neuropathic ulcers. Neuropathic ulcers are due to impaired innervation to the lower extremities, most often caused by diabetes. Although the exact mechanism is not known, both vascular and metabolic factors are thought to contribute to the problem (Table 1). The mechanical stress exerted by walking probably is pivotal in ulcer formarion. 9 The neuropathy parallels the duration and severity of hyperglycemia and all nerves are affected (autonomic, motor, and sensory). 5 This problem is compounded with muscle atrophy, where changes in foot architecture result 256
Stottsand Deitrich
in foot deformity and new pressure points are created. Areas of highest pressure are on the plantar surface of the foot just below the second metatarsal. With neuropathic ulcers, minor trauma causes tissue damage that progresses to ulceration. Where persons with normal sensation would stop trauma that results in pain, those with neuropathology lack this protective sensation. Ulcers also occur with a buildup of callus at pressure points; subsequent shearing of the callus results in an ulcer.
Ulcer Assessment Although knowledge in the area of wound assessment has accumulated over the years, there is no agreement on a definitive method to measure healing. 1° Some nursing research suggests that characteristics such as exudate or granulation tissue are not valid measures of healing. 11 Still, it is the skilled observation of such characteristics that is most commonly used in clinical practice to evaluate healing. Meaningful observation and accurate evaluation of healing depends on consistency among team members. Such consistency requires, at a minimum, common definitions of terms and agreement among evaluators concerning wound characteristics such as granulation tissue, slough, and fibrin. Wound characteristics. There is consensus that the nature of the wound bed is an important factor in wound assessment. ~2,13 In a healing ulcer, there is a clean granulation bed that progresses from pale to beefy red. Venous ulcers often present with a beefy-red base, while arterial ulcers often have a very pale base because they lack sufficient blood flow. Neuropathic ulcers tend to have a pale base. Open ulcers should be moist; however, venous ulcers tend to be wet while arterial ulcers are more likely dry. The edges are flat and attached closely to the sides of the wound, and the epithelial edge is intact. The surrounding tissue is intact, healthy, warm, and dry, but not to the point of scaling or itching. The shape of the wound varies depending on its etiology. Venous ulcers have irregular borders, arterial ulcers are more regular, and neuropathic ulcers have a "punched out" appearance. Because the shape of the November/December1997GERIATRICNURSING
to clean the area using a solution such as normal s a l i n e or hydrogen peroxide that does not contain bacteriostatic substances. Wound fluid should be obtained by aggressively swabbing a small area (1 cm 2) where the ulcer tissue is healthy. A culture is performed to determine which organisms are present in the ulcer tissue; thus the culture is taken from healthy tissue rather than exudate or pus in the ulcer.
There is c o n s e n s u s
t h a t the
n a t u r e o f the w o u n d b e d is an i m p o r t a n t factor in wound assessmenL wound changes as it heals, documentation of wound healing can be difficult. In addition, neuropathic ulcers usually form excess epithelial tissue that presents as a callus surrounding the ulcer. Sharp debridement by a physician, or in some settings by a nurse or physical therapist who is specially trained in the technique, should occur regularly. If the callus that forms with these ulcers is not regularly debrided, it can cause increased shear during walking and result in enlargement of the ulcer. Only after sharp debridement can ulcer size be accurately evaluated. One of the issues in wound assessment is how to measure wound size. Some authorities support measuring surface area; others believe the volume should be measured. 13 An accepted approach for measurement in clinical practice is to make a tracing on a clear plastic sheet or to measure length, width, and depth. 12 Regardless of the approach used, there should be a standard method for measuring in your institution and it should be used by all members of the team. In a wound that is not healing, there may be excessive wound drainage, increased/excess fibrin, and an excessive or insufficient inflammatory response. On the other hand, in some situations the only indication that healing is delayed is that wound size does not decrease. Table 2 lists the characteristics of normal and delayed healing in leg ulcers. Infection. Infection is one factor that often delays healing in patients with leg ulcers. At times the signs are overt, but often infection can be difficult to diagnose. Common signs of infection are an increased and often purulent exudate, foul odor, increased inflammation around the wound that extends out more than 0.5 cm, and pain at the site. Cellulitis may develop where the skin tissue is inflamed and increased interstitial fluid is present. Occasionally there may be fever. At times there is no sign that the wound is infected but the wound size has not changed and the patient has received optimal therapy. Infection should be suspected and a culture taken to determine that the organisms are sensitive to the antibiotic selected empirically. I4 The culture is p e r f o r m e d before the antibiotics are started. When a swab culture is used, it is important GERIATRIC NURSING Volume 18, Number 6
Because legs and feet have little subcutaneous tissue, ulcers increase the possibility of osteomyelitis, or bone infection. Whenever bone is visible or can be probed through the ulcer, the possibility of osteomyelitis should be considered, immediately reported to the physician, and treated. Osteomyelitis is a serious threat to life and limb and is most successfully treated in its earliest stages.
Local Care Leg ulcer care should be based on scientific knowledge of factors in the local environment that support healing (see Table 3). The major advances that have been made in knowledge of healing should be incorporated in local care. Moist environment. First, the wound bed needs to be moist to support cell division and migration. This recommendation is based on the classic work of Winter, 15 who showed that epithelialization occurs faster in a moist environment than in a semimoist or dry environment. There was initial fear that a moist wound bed would support growth of microorganisms and result in infection. Data show, however, that the moist environment does not result in infection, even in the elderly, who have slower responding immune systems than younger persons.12 A moist environment is accomplished most commonly through dressings applied to the wound. Keeping the wound covered maintains wound moisture to keep cells hydrated and prevents additional contamination and trauma. Wound cleansing. Data show that all wounds are contaminated and that chronic wounds heal better with fewer organisms present. 14 Research has focused on cleansing the wound bed as a means of reducing the bacterial burden. The current recommendation is that high-pressure irrigation (such as that produced with a 35 cc syringe and #18 angiocatheter) with a nontoxic agent such as sterile normal saline be used for cleansing. 16 The recommendation to use nontoxic solutions rather than antiseptics is based on data pertaining to acute wounds over a short period; the use of such solutions has not been evaluated in chronic wounds over a prolonged period. When simple cleansing is the goal, normal saline continues to make sense. However, in an infected wound, topical chemical Stotts and Deitrich 2 5 7
agents often have a role. Here it is essential to understand the particular needs of the wound and the specific actions of available chemical agents. The recommendation for more than 10 years has been to avoid the iodine-based antiseptics because of their tissue toxicity. More recently, however, researchers have questioned this recommendation, noting problems in the original study design. 17 Pure iodine, long used as an antiseptic in the preantibiotic era, is toxic and should not be used. It is now understood, however, that it is the formulation of iodine that needs to be considered, not merely the presence of iodine in a topical compound. Povidone-iodine mixed with surfactant delays healing when used on open tissue but is effective in reducing bacteria on intact skin. Although povidone-iodine solution without surfactant is effective in initially lowering bacteria counts, its sustained effect is quickly depleted by wound debris. A new formulation of iodine, cadexomer-iodine, is recommended for treatment of infected chronic wounds. 17,18 Clinicians must understand the goal of therapy and select agents that are consistent with it, rather than simply banning all antiseptics from wound care. G r o w t h factors. Growth factors are another area of scientific development in wound healing. Although there is increasing knowledge about the various growth factors and how they signal a cascade of systemic elements to enhance healing, the exact quantity of growth factors, which ones are needed, and in what sequence are not entirely understood. Some growth factors that are commercially available to aid healing are effective in certain patients with chronic wounds. 19 Blood flow. The role of blood flow in local healing has long been a focus of research. Recent work in the area has 258
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supported the importance of strategies to enhance blood flow by reducing sympathetic nervous system outflow to overcome vasoconstriction. These strategies include maintaining warmth (even in the presence of arterial disease), reducing pain, avoiding factors that cause vasoconstriction (for example, smoking), and maintaining an adequate blood volume. 2°21 Warmth causes vasodilation and brings oxygen to the tissues. Adequate intravascular volume is needed to bring the oxygen to the tissue. Simple interventions such as ensuring that leg ulcer patients keep their legs covered and wear heavy socks will maximize perfusion and healing. If off-loading pressure on a neuropathic ulcer is needed, special foot equipment may be used. Also, smoking causes vasoconstriction and inhibits healing. 2a Smoking even a few cigarettes per day can produce vasoconstriction that persists throughout the entire day. Smoking in most cases should be stopped completely. Pain control. Pain control is essential. Because sympathetic outflow associated with pain causes subcutaneous vasoconstriction and shunts blood flow away from the ulcer, untreated pain slows healing. It may be necessary to obtain a consult from a pain specialist or refer the patient to the pain team. 21 Neuropathic pain is a special case in which, in addition to the usual analgesics (such as Tylenol or opiates), low-dose antidepressant medication may be helpful. Dosages are much lower than those used to treat depression, greatly reducing the possibility of side effects. Amitriptyline (Elavil) is sometimes used in these circumstances. However, for older adults, Norpramin (desipramine) is usually better tolerated because it has fewer anticholinergic effects. 23 November/December1997GERIATRICNURSING
Pathology-specific Considerations
Conclusion
Compression. Compression is important for patients with venous ulcer disease. It should not be used with pure arterial disease or in patients with neuropathic ulcers who do not have concomitant venous disease. In venous disease, c o m p r e s s i o n is used to aid venous return and reduce the distance that nutrients and oxygen must diffuse to support healing. 3 Frequently used strategies for c o m p r e s s i o n include Unna's boot, m u l t i p l e - l a y e r bandages, and elastic stockings. It is critical that patients apply c o m p r e s s i o n prior to getting out of bed in the morning, or if they do arise, return to bed for 20-30 minutes to reduce edema before applying compression. Activity. Activity is important for patients with leg ulcers to help prevent the complications of immobility. However, for healing to occur, relative immobility may be used for a period of time to reduce metabolic needs and support maximal perfusion to the ulcer. This may mean periods of lying down for the patient, with the feet positioned to maximize blood flow. 3,7,s Positioning. Positioning needs to be planned on an individual basis. For most patients with pure venous disease, this means feet at heart level to enhance venous return. For patients with arterial disease, the optimal position may be with feet dependent to allow gravity to enhance perfusion. Patients with neuropathic ulcers often have degrees of arterial disease present; however, the position of their feet usually is not as important for them as is removing weight from their ulcer. 3,7,8
The nursing care needed for healing in patients with leg ulcers is continually changing as new knowledge develops through research. Clinicians must continue to read and examine the evolving body of literature on leg ulcer care so patients can benefit from the optimal blend of therapies. Current thinking is that healing is maximized when local care is combined with strategies that enhance oxygen to the ulcer, promote appropriate levels of activity, optimize perfusion through physiological positioning, and reduce mechanical shear through selection of proper footwear. The nurse is pivotal to providing and coordinating this care in the geriatric patient with leg ulcers. •
Neuropathic pain is a special case in which, in addition to the usual analgesics, low-dose antidepressant medication may be helpful Footwear. Special footwear may be needed for patients with all types of foot ulcers. For persons with venous disease, the c o m p r e s s i o n often makes their legs and feet so large that they do not fit in their usual shoes. For those with arterial ulcers, the ulcer dressings create the same problem. Patients with neuropathic ulcers often require special f o o t w e a r that is designed to remove all pressure f r o m the ulcer area and protect the insensate foot from trauma. For patients with neuropathic ulcers, referral to an orthotist or a brace shop for special footwear may be needed. 9 Regardless of the fact that patients have ulcers, they need sturdy shoes for walking. The nurse must take the initiative to inspect their f o o t w e a r to ensure that it is safe to prevent unstable gait and falls.
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REFERENCES i. Nelzen O, Bergqvist B, Lindhagen A, Hallbrook T. Chronic leg ulcers: an underestimated problem in primary health care among elderly patients. J Epidemiol Comanunity Health 1991 ;5:184-7. 2. Price PE, Harding KG. The reliability of a new disease specific measure of quality-of-life for patients with chronic wounds. Wound Repair and Regeneration 1997;5:A102. 3. Black SB. Venous stasis ulcers: a review. Ostomy/Wound Management, 1995;41:20-32. 4. Falanga V, Eaglstein WH. The trap hypothesis of venous ulceration. Lancet 1993;341:1006-8. 5. Ziegler D, Cicmir I, Mayer R Wiefeks K, Gries FA. Peripheral and autonomic nerve function in newly diagnosed insulin dependent diabetics. Diabetes Res 1987;4:9-14. 6. Wipke-Tevis DD, Stotts N. Leukocytes, ischemia, and wound healing: a critical interaction. Wounds: A Compendium of Clinical Research and Practice 1991;3:227-38. 7. Ennis WJ, Meneses R Leg ulcers: a practical approach to the leg ulcer patient. Ostomy/Wound Management 1995;41(7A Suppl):52S-62S. 8. Holloway GA. Arterial ulcers: assessment and diagnosis. Ostomy/Wound Management 1996;42:46-51. 9. Armstrong DG, Lavery LL, Harkless LB. Treatment-base classification system for assessment and care of diabetic feet. Ostomy/Wound Management 1996;4:50-61. 10. Lazarus GS, Cooper DM, Knighton DR, Margolis DJ, Pecoraro RE, Rodeheaver GS, et ai. Definitions and guidelines for assessment of wounds and evaluation of healing. Arch Dermatol 1994; 130:489-93. 11. Johnson M; Miller R. Measuring healing in leg ulcers: practice considerations. Appl Nurs Res 1996;9:204-8. 12. Stotts NA. Impaired healing. In: Pathophysiological phenomena in nursing. Carrieri VK, Lindsey AM, West C, editors. Philadelphia: WB Sannders; 1993. 13. Van Rijswijk L. The fundamentals of wound assessment. Ostomy/Wound Management 1996;42:40-52. 14. Stotts NA. Determination of bacterial burden in wounds. Adv Wound Care 1995;8:28-52. 15. Winter GD, Scales JT. Effect of air drying and dressings on the surface of the wound. Nature 1963;197:91-2. 16. Bergstrom N, Bennett MA, Carlson CE, et al. Treatment of pressure ulcers. Clinical practice guideline no. 15. Rockville (MD): U.S. Dept. of Health and Human Services, Public Health Service, Agency for Health Care Policy Research; 1994 Dec. AHCPR publication no. 95-0652. 17. Eaglstein WH, Falanga V. Chronic wounds, Surg Clin North Am 1997;77:689700. 18. Mertz PM, Davis SC, Oliveira-Gandia M, Eaglstein WH. The wound environment: implications from research studies for healing and infection. Wounds 1996;8:1-8. 19. Robson MC. The role of growth factors in the healing of chronic wounds. Wound Repair and Regeneration 1997;5:12-7. 20. Stotts NA, Hunt TK. Managing bacterial colonization and infection. Clin Gefiatr Med. In press. 21. Hunt TK, Hopf H. Wound healing and infection: what surgeons and anesthesiologists can do. Surg Clin North Am 1997;77:587-606. 22. Silverstein P. Smoking and wound healing. Am J Med t992;93(suppl 1A):lA22S. 23. Lipman AG. Analgesic drugs for neuropathic and sympathetically maintained pain. Clin Geriatr Med 1996;12:501-15.
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