Basics of Chronic Wound Care
Basics of Chronic Wound Care
Authors: Travis Taylor, DO, Wright State University Boonshoft School of Medicine, Department of Emergency Medicine, Wound Healing and Hyperbaric Medicine Center, Kettering Medical Center, Dayton, OH; Louis Pilati, MD, FACEP, Medical Director, Wound Healing and Hyperbaric Medicine Center, Department of Emergency Medicine, Kettering Medical Center, Dayton, OH; and Scott Koncal, MD, Wright State University Boonshoft School of Medicine, Emergency Medicine Residency, Dayton, OH.
Peer Reviewer: Wendy B. Gelbard, MD, Faculty, Department of Emergency Medicine, University of Rochester School of Medicine, Rochester, NY.
Introduction
Chronic wounds represent a significant portion of the complaints seen by physicians, especially in the primary care setting. Visits for wound care account for just over 2% of all visits to office-based physicians in the United States.1 Venous stasis ulcers (VSU) alone affect 1% of the general population, with patients older than 65 being affected at much higher rates.2
The economic cost of treating these wounds is not insignificant, with the average lifetime cost of treating a single patient with VSU exceeding $40,000. The economic impact also extends to time lost from work, with an approximate 2 million workdays per calendar year lost due to chronic venous ulcers.2 Other estimates have placed the total annual cost of treating chronic wounds at $3.5 billion.3
The cost of chronic wounds is certainly not limited to mere economics. As with many other chronic conditions, it is impossible to quantify the emotional toll that this condition takes on its sufferers. A significant relationship between depression, anxiety, and impaired healing of chronic wounds has been proven.4 Diabetic patients, particularly, can experience significant long-term morbidity due to uncontrolled diabetic foot ulcers (DFU), with approximately 82,000 lower limb amputations being performed annually on diabetics.5 Furthermore, the management of chronic wounds very often is as frustrating a problem to the provider as it is to the patient. Providers can find themselves struggling to gain control over what initially is a seemingly insignificant problem that, despite weeks or even months of visits, testing, and repeated courses of antibiotics, simply fails to improve.
The keys to managing the patient with chronic wounds are to start with appropriate identification of the wound type, perform any additional needed testing, and make appropriate referrals in select cases. The physician must select the primary therapies and any adjunctive therapies. Once healed, measures must be taken to prevent recurrence.
Physiology of Normal Wound Healing
Not all wounds that patients sustain become chronic. In fact, the vast majority of patients who sustain a wound proceed to closure in a reasonable timeframe. Acute wound care is well known and should focus on established basics of cleansing, primary closure, if appropriate, infection prevention, and tetanus prophylaxis.
It is important to differentiate an acute wound from a chronic one. While definitions of what constitutes a chronic wound may vary subtly, a good working definition would be any wound that has failed to progress through the normal stages of healing in what would be considered a reasonable timeframe for a given patient.
To understand what makes a wound become refractory to healing, it is important to have a basic understanding of the normal phases of wound healing. The healing process can be divided into four sequential yet overlapping phases: hemostasis, inflammation, proliferation, and remodeling.6 These stages are summarized in Figure 1.
After the initial wound, hemostasis is achieved through platelet aggregation and clot formation. As platelets and other cells are deposited into the wound bed, they trigger the release of vasodilators and chemoattractants.7
These chemical signals trigger the inflammatory phase, drawing neutrophils into the injured tissue. These cells debride the area via phagocytosis and enzyme release. Later in this phase, macrophages begin to predominate.7
The proliferative phase occurs as fibroblasts begin to deposit new extracellular matrix. Clinically, this is seen as the formation of granulation tissue. Concurrent with the formation of new tissue, is the continuous breakdown of matrix by various enzymes including matrix metalloproteinases. The activity of this large family of proteolytic enzymes is regulated by inhibitors whose function is essential to preventing the process from tending excessively toward the degradative phase. Keratinocytes at the wound edges both clear the margins of debris and migrate across the wound bed re-epithelializing the surface of the wound.7
Over the following months, the wound is continually remodeled, eventually leading to an avascular scar.7
Pathophysiology of Chronic Wound Maintenance
A wound may stagnate in any of the four phases, but most often the arrest occurs in either the inflammatory or proliferative phase.6 As with many other processes in the body, such as clotting and lysis, the sympathetic and parasympathetic systems, the process of wound healing is a balance between degradative and regenerative processes. Although there are many contributory factors, a common feature of non-healing wounds is the imbalance toward the degradative phase. This leads to wounds in which either a stalemate exists or, worse yet, degradation prevails and the wound enlarges.
There are multiple reasons for this to occur. From a systemic standpoint, numerous factors contribute. (See Table 1.) Systemic factors as varied as advanced age, malnutrition, diabetes, anemia, renal disease, systemic steroid use, nicotine use, and even psychological factors may contribute.4 Certainly systemic and local infection plays a role. Although part of the intended wound care regimen would be to reduce the impact of these factors, it is not always possible to do so.7
From a cellular and biochemical standpoint, there can be a relative deficiency of growth factor expression. Commonly there is an imbalance between proteinases and their inhibitors. As described above, the matrix metalloproteinase enzymes particularly become overexpressed, resulting in abnormal degradation of the extracellular matrix. There is also a degree of inherent age-related decrease in proliferation potential of fibroblasts. This characteristic, referred to as senescence, results in a decreased responsiveness to growth hormone.7
Specific Wound Types
For practical purposes, the majority of wounds can be divided into the following types: pressure (decubitus), diabetic foot, venous stasis, and arterial insufficiency ulcers.
Pressure Ulcers. Whether due to paralysis, mental status decline, or severe medical illness leading to a bed-ridden state, pressure ulcers are almost exclusively seen in patients who are unable to reposition themselves spontaneously. As the weight of the body exerts pressure on skin and underlying tissues, capillary perfusion is compromised. Capillary perfusion pressure is around 20 mmHg (about 0.4 psi), as evidenced by the ability to blanch the nailbed with only light pressure on the nail. Body weight of a recumbent adult easily exceeds this value to the skin areas in direct contact with a firm or hard surface. In healthy individuals, this leads to inflammation, which is perceived as discomfort, and individuals reposition themselves. If a patient does not feel this stimulus or is unable to move, the pressure continues, leading to ischemia and necrosis. As little as two hours of uninterrupted pressure can result in permanent changes.
The process is complicated by many components. Shear forces and friction are significant aggravating factors. The affected skin can easily become macerated due to perspiration or incontinence. Patients who are most susceptible to decubitus ulcers are also frequently malnourished. As a result, they often lack any substantial subcutaneous fat and muscle tissue. This leaves skin overlying bony prominences very vulnerable to breakdown. Classic sites are the ischia, sacrum, and posterior heels.
A well recognized system of pressure ulcer staging has been set out by the National Pressure Ulcer Advisory Panel (www.npuap.org).
- Stage I: "Intact skin with non-blanchable redness of a localized area usually over a bony prominence."
- Stage II: "Partial thickness loss of dermis presenting as a shallow open ulcer, with a red pink wound bed without slough." Serum filled blisters, whether intact or ruptured, fall in this category.
- Stage III: "Full thickness tissue loss. Subcutaneous fat may be visible but bone, tendon, or muscle are not exposed. Slough may be present but does not obscure the depth of tissue loss. May include undermining or tunneling."
- Stage IV: "Full-thickness tissue loss with exposed bone, tendon, or muscle."8
Diabetic Foot Ulcers. Diabetic patients are at risk for ulcer formation for a number of reasons. They have a tendency to form heavy callus in load-bearing areas, especially when shear forces are involved, often due to wearing improperly fitted shoes. Blisters tend to form beneath these calluses, which can enlarge with surprising rapidity. Patients may present with a small "blood blister" beneath a large callus, which can have a deceptive appearance, leading to an underestimation of the extent of the problem. The pathophysiology behind this process is multifactorial. Due to the neuropathy that frequently results from diabetes, patients lack the sensation to warn them of injury or friction. These wounds are also at high risk for infection due to the hyperglycemic environment, impaired immunity, and poor blood flow often present.
Venous Stasis Ulcers. Increased pressure in the venous system of the lower extremities results from valvular dysfunction in the high-pressure deep veins, low-pressure superficial veins, or both. This results from initial dilation of the veins. As this occurs, the leaves of the valves are separated from each other, resulting in back flow of blood. When the patient is standing, blood pools in the legs, and when the patient is walking, the normal venous pumping action of the muscles becomes inefficient.
Furthermore, if the valves of the perforating veins become dysfunctional, blood from the high-pressure deep venous system flows toward the skin, leading to hypertension in the superficial veins and increased capillary permeability. This causes edema as fluid and protein leak into the surrounding tissues. Fibrinogen is converted into fibrin, which coats the capillaries and impairs the exchange of oxygen and nutrients. This, combined with the mechanical of stress of tissues taut with edema, leaves the skin extremely vulnerable to injury from even the most innocuous trauma. Patients often develop wounds spontaneously without being able to recall any specific injury.9
Arterial Insufficiency Ulcers. The majority of arterial ulcers are the result of chronic atherosclerosis. Over time, cholesterol is deposited along the lining of vessel walls. As this continues, blood flow is restricted, resulting in impaired delivery of oxygen and nutrients to distal tissues.
Arterial ulcers often have the typical "punched out" appearance. This is the result of the ulcer border having a clear demarcation from the adjacent tissue due to focal blood flow restriction. Pure arterial ulcers often have no edema and a pale, dry base with surrounding shiny skin. Frequently, in the setting of longstanding atherosclerosis, hair loss will be evident, however, the presence of hair does not rule out an arterial ulcer. These ulcers are often quite painful.
Other diseases account for a small percent of wounds considered to due to arterial insufficiency. These include vasospastic disease (Raynaud phenomenon) and vasculitis (rheumatoid diseases).
Arterial ischemia can also occur acutely. This often results from an embolic event, as part of a plaque is dislodged from the arterial wall and travels distally until it lodges in a peripheral artery. Distal tissues then become ischemic and subsequently necrotic.10
An Organized Approach to the Chronic Wound
History. The first step in treating a patient's wound is to determine the type of wound. Inquire as to the history of the wound. Inciting trauma, previous occurrences, and past therapies should be ascertained. Pain that is worse at night and is relieved by hanging the feet over the edge of the bed points toward a diagnosis of arterial insufficiency. On the other hand, discomfort and swelling that is worse at the end of the day may indicate venous insufficiency.
As with any other chronic or progressive disease process, a thorough past medical history is absolutely essential. Particularly important comorbidities that contribute to wound healing include diabetes, known atherosclerotic disease, chronic renal disease, and anemia. A thorough medication history, including inquiry about chronic steroid use, is necessary. Social history should also be included to screen for current and prior tobacco use as well as any illicit drug use. Also inquire as to the patient's support structure, as the care of these wounds can be overwhelming to individuals, particularly if they are elderly or physically impaired.
Physical Exam. The location of the wound will narrow the diagnosis. Pressure ulcers are usually self-evident given their location and the patient's history.
Diabetic foot ulcers will be present on weight-bearing plantar surfaces and sometimes on other portions of the foot if the patient's footwear is particularly ill-fitting. Diabetic foot wounds are characterized by heavy callous, which often needs to be filed or pared away. This not only allows for accurate determination of the extent of the wound, but it is essential to healing. Such patients frequently have diminished sensation, which may aid in surgical debridement, but requires the practitioner to be particularly careful.
For wounds higher on the leg, the diagnosis is most likely that of venous stasis or arterial insufficiency, or a mixture of the two. Assess the limb for edema, stasis dermatitis (red, rough scaling, often oozing skin), and hemosiderin depositssigns of venous insufficiency. Take note of shrunken musculature, hair loss, and shiny, tight skinevidence of arterial insufficiency. Patients with arterial insufficiency will also frequently have a deep-red colored limb when in the dependent position. Upon elevation, the limb blanches completely. Also known as Buerger's sign, this is an important test to distinguish cellulitis from the dependent erythema of arterial insufficiency.11
Next, evaluate arterial flow by palpating the central and peripheral pulses. If pulses are weak, capillary refill is poor, or there is any other suggestion of arterial insufficiency, an ankle-brachial index (ABI) should be performed. The ABI is calculated using a Doppler stethoscope and taking the ratio of the highest systolic blood pressure measured from one of the pedal pulses to the highest systolic blood pressure from one of the brachial arteries. Normal values for an ABI are considered to be 0.9 to 1.3; anything below 0.9 is considered a sign of vascular disease. ABIs are excellent screening tests because they are easy to perform, non-invasive, inexpensive, and have a sensitivity and specificity of 95% and 99%, respectively for obstructive atherosclerotic vascular disease.12
Next, assess the periwound area. Look for periwound erythema and signs of lymphangitis. Take note of any moisture, white blanching of the skin, and maceration, as these are indications of heavy exudate drainage. Next assess the wound itself. Evaluate for purulence and odor. Again, scrape away or trim devitalized tissue as tolerated by the patient. Assess for fluctuance, tunneling, undermining, and the presence of slough and debris in the wound bed. Check the depth of the wound, taking particular note of exposed muscle, tendon, or bone.
Clean the wound using gentle irrigation with saline or lactated Ringer's solution, avoiding high pressure irrigation as this may force bacteria and debris into the healthy underlying tissue. Use of a gentle cleanser designed for the purpose is appropriate. Avoid cytotoxic agents such as povidone iodine or hydrogen peroxide as they are indiscriminate in their activity. Measure the wound (length and width) so its progress can be tracked from visit to visit. For clinics or physicians who will follow these patients for a period of time, it is advisable to consider taking photographs of the wound to have a more accurate record of the progression.
Ancillary Testing and Referrals. If arterial insufficiency is suspected, it is recommended to image the affected area. Further characterization of the nature of the vascular obstruction can be made with arterial ultrasound, CT angiography or MR angiography. If this study confirms significant obstruction, or if initial clinical suspicion is high, it is appropriate to refer the patient to a vascular surgeon or interventional cardiologist to be evaluated for potential revascularization.
If osteomyelitis is suspected, image the area with plain radiographs, triple phase radionuclide bone scan, or MRI. Remember that plain films are often falsely negative early in the course of osteomyelitis, but often are used as a screening exam. If osteomyelitis is found, attempts can be made at salvage by combining systemic antibiotics with local wound care. Medication selection is best left to an infectious disease specialist as extended courses of intravenous antibiotics usually are required. If the osteomyelitis is limited to a small portion of the foot, such as a toe, the pragmatic approach would be to consider referring the patient to a surgeon for amputation.
When initially evaluating a patient with venous insufficiency, strongly consider ruling out a deep venous thrombosis (DVT). This is especially important for asymmetrical swelling, fairly new swelling, or swelling coupled with significant pain. Duplex Doppler ultrasound is the standard testing method. This has the added benefit of being able to evaluate for venous reflux, which, if present, may lend itself to correction by a vascular surgeon for prevention of wound recurrence.
If congestive heart failure (CHF) is suspected as the cause of the patient's lower extremity swelling, an echocardiogram also may be indicated. Diuresis and further cardiac workup may also be necessary.
Laboratory work also may be useful in the initial evaluation. An erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP) may be helpful if osteomyelitis is suspected. For bed-ridden patients, a serum albumin, pre-albumin, and hemogram will help in assessing overall nutrition and oxygen carrying capacity. A glycosylated hemoglobin level (HbA1c) will help in assessing a diabetic patient's overall glycemic control.
Superficial wound cultures are rarely of any use. Chronic wounds are essentially always colonized with bacteria.13 When considering the effect bacteria have on a wound, it is more accurate to think in terms of bioburden than infection. Signs of overt infection include fevers, periwound cellulitis, and grossly purulent drainage, and suggest the use of systemic antibiotics. Short of this, the bacteria in the wound bed usually can be dealt with using topical agents. This helps to lower the bacterial count in the wound bed, reducing competition for nutrients, and decreasing the inflammatory response that the bacteria help to perpetuate. If systemic antibiotics are desired, then biopsy from the ulcer base has been shown to be the most reliable method for determining the causative bacteria.14
Biopsy is also warranted to detect malignancy. In this instance, the biopsy should be taken from the wound margin. Biopsy is indicated in the patient with a history of skin malignancy or if the wound has an appearance that is worrisome for cancer. Consider biopsy in patients who are taking immunosuppressant medications, as they are at increased risk for developing malignant ulcers.15 Also, if a wound fails to show any signs of progress in a six-week timeframe, despite treatment, biopsy is recommended.
Furthermore, if a lesion does not seem to meet any of the criteria for the wounds described here, consider referral to a dermatologist. There are numerous skin diseases that, although relatively rare compared to venous or arterial insufficiency ulcers, do present occasionally with chronic skin wounds.
Selecting the Primary Therapy
For each of the main wound types described above, there is an optimal primary therapy. Once the wound has been properly identified, the primary therapy can be selected. Although there are numerous adjunctive therapies available, the likelihood of healing is significantly reduced if the mainstay treatment is neglected. In each instance, the treatment is directed toward the primary contributing factor that is maintaining the wound.
Pressure Ulcers. For patients with pressure ulcers, treatment should be directed toward reducing pressure on the affected area. Although these wounds are often preventable with good pressure relief measures, the effort involved in their prevention can be daunting, particularly for the patient without a significant social support structure. Once the wound has formed, good pressure relief is even more important. High quality mattresses and seat cushions are absolutely essential to wound healing. Diligent hygiene is also a must, as wound healing often is compromised by the presence of perspiration, stool, urine, and the significant exudate that often accompanies decubiti. Topical therapy and other systemic and adjunctive measures are particularly important for these patients.
Diabetic Foot Ulcers. Reducing pressure and shear forces in the area of the wound is the foundation of treatment for the diabetic foot ulcer. The goal is to distribute all the weight evenly across the intact plantar surface with an open area for the wound, and to firmly secure the foot into this device to eliminate any pressure or friction on the wound area. There are several commercially available footwear products that allow for this. Those easiest to fit to the patient have a segmented rubber or foam insole that can be plucked away in the area of the wound. Others require that a special impression of the bottom of the foot be made, which then is transferred to a casting from which a customized insole is produced. This can be placed in the patient's own footwear or in a special boot that locks the foot in tightly using straps or ski-boot style clamps. These insoles are also used for post-healing maintenance of the diabetic foot. There are some inherent drawbacks to treatment with these devices. The most important is patient compliance. Even a brief period of weight-bearing without the device can undo days of progress.
The ideal alternative is the use of total contact casting. With this technique, a short leg walking cast is placed on the leg. It incorporates a heavy felt "sole" that is trimmed to fit the foot and wound. The cast can be left in place for one to two weeks. Another benefit offered by this method is that the sole and cast can be adapted from week to week to accommodate the frequently changing anatomy of the foot and shrinking wound. This method can be suboptimal for very heavily draining wounds.
Venous Stasis Ulcers. The mainstay of treatment for venous stasis ulcers is the use of external compression.16 This effectively compensates for the impaired valvular function that leads to tissue edema. While compression stockings are effective at preventing recurrence of venous stasis ulcers, they are generally insufficient at healing an active ulcer. This is customarily accomplished using a multi-layered compression wrap system, which allows for an even, graded compression. Properly applied, this results in 40 mm Hg of pressure at the ankle, gradually reducing to ~20 mm Hg at the upper calf.17
There are numerous products available commercially. The benefit of these systems is that of exudate absorption and even, graded compression with a moisture-resistant outer layer. These wraps can usually be left on for one week at a time, although heavily exuding wounds require changes more frequently.
Certainly, care should be taken when applying external compression if there is concern for a mixed etiology of both venous and arterial insufficiency. Start with arterial studies if suspicion is high. If suspicion is low, a trial of a very light external compression wrap can be performed.
Arterial Insufficiency Ulcers. Unlike venous insufficiency, in which external compression can be an effective substitute for competent veins, there is no effective substitute for tissue perfusion. The ideal treatment for the patient with arterial insufficiency is reperfusion. This can be accomplished via percutaneous techniquesendovascular plaque excision or endoluminal angioplastyand open surgical bypass. The location and extent of the lesion, as well as the preference and experience of the treating physician will determine which technique is appropriate.
Not all patients are ideal interventional candidates. Advanced age and cumulative medical conditions may make the inherent risk of intervention and the requisite recovery period unacceptable to the patient or their medical decision maker. Presenting all the options will allow the patient to make an informed decision.
Topical Therapy
There are literally hundreds of specialized wound care products on the market today. They can be broadly divided into topical agents and dressings, although many products incorporate characteristics of both. For instance, an absorbent pad may be impregnated with an antimicrobial agent to suppress bacterial growth.18 There are several goals of topical agent/dressing use depending on what is felt to be the predominant problem in the wound at any point in time. If more than one problem is present, the use of a combination agent is warranted. Despite a logical method for selecting the topical therapy, there is a large degree of trial and error involved. If after 2-3 weeks no progress is seen, it may be time to try something else.
It is not possible to describe all the various ointments, gels, pads, foams, and films available. However, a general approach to the use of topical therapy is described. Physicians should try to become familiar with a handful of products and employ them on a case-by-case basis using these principles.
A good way to view the stages of chronic wound healing is as follows:
1. Remove necrotic tissue/slough (debridement phase);
2. Fill in depth with granulation tissue (granulation phase);
3. Cover over with epithelial tissue (epithelialization phase).
Each of the products should be directed at one of these particular phases, although, as with the healing of acute wounds, the various phases can overlap considerably.
Wound Cleansing. As already stated, the use of a gentle cleanser specifically designed for wound care is recommended. Generous irrigation with moderate pressure saline can clear a good amount of debris from the wound bed.
Peri-wound Protection. Whether the wound care will be done in the office or at home by the patient or caregiver, it is extremely important to protect the peri-wound area, particularly in heavily draining wounds. This can be done using a barrier cream or ointment. Over-the-counter petroleum jelly works well. Some also recommend diaper rash cream, although some preparations can harden to a concrete-like state that can be difficult to clear off later if left in place for extended periods of time.
Debridement and Slough Control. There are numerous methods of debridement of a wound. Debridement of slough and eschar (dried hardened skin and slough) is essential to wound healing. In the absence of the advanced wound care, dried slough (scab) serves a purpose in keeping a wound bed protected from further injury. With the products and care available today, however, dried slough or scab only serves as a substrate for bacterial growth, a physical barrier to re-epithelialization, and a retardant to wound closure.
Surgical Debridement. This is the act of cutting or scraping away debris. The ability to do so is often limited by the patient's sensation. Arterial and venous insufficiency ulcers are often rather painful. When tolerated, this is the preferred method as none of the following techniques can remove devitalized tissue as effectively. Also be cautious in attempting aggressive debridement in the patient who is on anticoagulant therapy.
Enzymatic Debridement. This is accomplished gradually with various ointments. Several products contain papain and urea (Accuzyme®, Panafil® – Healthpoint, Ltd.). Papain is a proteolytic substance derived from the papaya and has been used as a meat tenderizer for years. Coupled with urea, a denaturing agent, this compound is very effective at debriding away slough. Trypsin is also a useful debriding agent and is available in a formulation that also contains balsam peru, which improves capillary blood flow (Xenaderm®). Collagenase is another enzyme that can be very useful in dissolving away sloughy material (Santyl®).
Mechanical. This is essentially the use of wet-to-dry dressings. Sterile gauze is moistened with normal saline and placed into the wound bed. This moistened layer is then covered with dry layers of gauze. As the moistened gauze dries out, it then adheres to the wound surface. When the dressing is removed, these tissues are pulled away. Aside from the obvious discomfort that this technique may cause the patient, there is very little selectivity involved. Healthy granulation tissue is easily pulled away along with the fibrous slough material causing reinjury. For this reason, this technique, while still extensively used, is no longer recommended.19
Autolytic. This is the method of trapping the body's own exudative fluid against the wound bed so that the autolytic enzymes contained therein can debride slough. This can be done using occlusive dressings that create a seal around the edges of the wound (DuoDERM®). These dressings are typically left on for several days. This technique is very commonly used for decubitus ulcers. Criticisms of this method are that it does not allow for regular visualization of the wound and it essentially creates an artificial abscess by not allowing for drainage of fluid.
Biological. This involves the use of sterile maggots to debride the wound bed. Using the larvae of the green bottle fly, this method has been employed for decades to debride even the most necrotic wounds. While highly effective, the prospect of having maggots placed in their open wounds is objectionable to many patients.20
Moisture. Every physician is familiar with the oldest rule of dermatology, "If it's wet, dry it; if it's dry, wet it." There is wisdom in this adage when applied to the chronic wound. A good adaptation would be to "keep the wound moist, but not too moist." A moist wound environment contributes to healing speed and success, however too much fluid in the wound bed can become a breeding ground for microbes. Excess exudate can also spill over onto the peri-wound area causing maceration that can lead to expansion of the wound.
To achieve this goal, several products have been developed to absorb excess fluid. Many of them are alginate based. Alginates are seaweed derivatives that are highly absorbent. They are formed into sheets, pads, or ropes. As they are available in larger sizes, they can easily be packed into deeper wounds. They are particularly beneficial for the patient with a deep decubitus ulcer as exudate control is rather important in this setting.
Also available are products containing cadexomer iodine, which is a three-dimensional starch lattice containing 0.9% iodine (Iodosorb®). It is highly absorbent and has the added benefit of broad antimicrobial activity.21 This product is ideal for wounds with drainage that is felt to be due to heavy bioburden.
For wounds that are too dry or have minimal drainage, a simple wound gel (numerous manufacturers) can be used. These products keep the wound moist, minimizing eschar formation, and have the ability to actually take on excess fluid, keeping the moisture level at the wound surface at the right level.
Bioburden Control. As noted earlier, the term infection does not adequately describe a chronic wound, as they are essentially all colonized. Topical antimicrobial agents usually suffice. As already discussed, many of these products overlap substantially in their function, notably products that make use of iodine. Many products also benefit from the antimicrobial properties of silver. There are foam pads and absorbent sheets impregnated with silver.
Additionally, topical antibiotics can be used for chronic wounds. These are generally well known. Most commonly used are silver sulfadiazine, mupirocin, bacitracin, neomycin, and polymyxin. When used in the limited quantities typically needed for chronic wounds, systemic absorption is not a problem.
Wound Growth Stimulation. Perhaps the most exciting advances in wound care technology are in the area of growth factors and other advanced compounds. Numerous products are available, targeting different parts of the healing process where wounds tend to stall. Recombinant human-platelet derived growth factor (Becaplermin/Regranex®) has proven particularly effective in the treatment of diabetic foot ulcers.
More recently introduced are the matrix metalloproteinases inhibitors. These compounds are extremely effective at stimulating the formation of new granulation tissue (Promogran®).22 This compound is also available in a silver-containing preparation such that it not only stimulates healing but helps to control bacterial growth (Prisma®).
One of the debriding compounds also has growth stimulation properties. Papain urea chlorophyllin copper complex ointment not only serves to debride slough, but also stimulates the growth of granulation tissue (Panafil®).
Skin Products. Some other unique advances are the synthetic skin products in use today. Several such products are available. They are most often used by surgeons, dermatologists, and wound care specialists.23 One product is refined porcine small intestinal submucosa (Oasis®).24 Another is comprised of cultured cells derived from neonatal foreskin tissue (Apligraf®).25 These products are particularly effective at forming new granulation and epithelial tissue.
Secondary GoalsSystemic Therapy
There are a number of other systemic considerations that need to be taken to optimize a patient's healing. Obviously, anything that can be done to improve the patient's overall health will improve their chances of wound healing.
Smoking. Most importantly, smoking cessation is an absolute must. The impact of nicotine abuse on their wound needs to be emphasized strongly to the patient. It is interesting to note that patients who will not stop smoking despite being repeatedly warned about the risks of lung cancer will attempt smoking cessation when confronted with an unsightly and painful wound.
Nutrition. Bed-ridden patients with decubiti are very frequently under-nourished. Encouraging them to eat and supplement their diets apart from mealtime can be extremely important to their healing.
Glycemic Control. Diabetics need to be told frankly that their wound healing is directly proportional to their dietary compliance and blood sugar management. Despite optimization of diabetic treatment, however, they will still have impaired healing as compared to an otherwise similar non-diabetic patient.
CHF. Optimization of diuresis in the patient with congestive heart failure is the first step in managing their lower extremity edema and obviously has benefits farther reaching than venous stasis ulcers.
Medications. There are a number of adjunctive systemic medications that may aid in healing. Systemic antibiotics are indicated whenever spreading cellulitis is present, often with fever and chills to indicate systemic reaction. Strongly consider hospital admission for intravenous antibiotics for patients who present with significant cellulitis or those who have multiple other comorbidities. Prompt initiation of oral antibiotics and close follow-up are probably reasonable in most other patients. Also consider oral antibiotics for heavily exuding wounds with foul odor or purulent drainage. If systemic antibiotics are chosen, remember that wounds are often colonized by drug-resistant bacteria. (See Table 2 for common pathogens.) If local resistant patterns are known, or if cultures were previously taken, let these guide the selection of antibiotics. Otherwise, reasonable choices include trimethoprim-sulfamethoxazole, doxycycline, clindamycin, and a few others.
Pain management is also an important aspect of wound care. Despite concern for creating dependency on narcotic pain medications, they are often necessary for relief. With proper care and compliance, most patients should proceed to wound closure, and pain should gradually reduce while this process is ongoing, gradually reducing the need for analgesics in most patients.
There are medications available that have been successfully used to treat intermittent claudication, a problem of functional arterial insufficiency. Several studies have also shown that the medication pentoxifylline is effective in hastening the healing of venous insufficiency ulcers when used in combination with compression.26
Other Adjunctive Treatments. The use of negative pressure therapy or vacuum assisted closure is a very effective method used to treat a wide range of chronic wounds.27 This method is particularly beneficial for the patient with a deep cavitary wound. These devices use sponges or gauze placed into the wound bed covered by an occlusive dressing through which suction tubing runs to a vacuum device. The subatmospheric pressure generated by the device removes excess wound fluid from the extravascular space, leading to improved local oxygenation and blood flow. This in turn promotes angiogenesis and the formation of granulation tissue.15 While often used to treat decubitus ulcers, care must be taken not create a pressure point that will worsen the situation.
Hyperbaric oxygen is also a useful adjunctive therapy for the treatment diabetic foot ulcers. The patient is placed in a pressurized chamber and breathes 100% oxygen. This causes the free oxygen dissolved in the bloodstream, which is normally negligible, to increase by several times, making it physiologically significant. Among other effects, hyperbaric oxygen is felt to improve angiogenesis in healing tissues. Studies have demonstrated more rapid healing and reduced amputation rates in patients treated with hyperbaric oxygen than in control subjects.28 Unfortunately, many of the trials using hyperbaric oxygen have not been sufficiently randomized. More investigation is needed to accurately determine which patients benefit the most from hyperbaric oxygen therapy.29
Patients with extremely severe venous insufficiency or lymphedema benefit substantially from lymphedema pumps. These devices, now readily available for home use, are similar to the sequential compression devices used in the inpatient setting. They consist of a sleeve that wraps around the lower extremity and a pump that applies pressure, gradually pushing edema upward.2 This can be done over the patient's compression wrap and can then be used for maintenance once the wounds are healed. This ideally needs to be done for two hours at a time, making patient compliance problematic at times.
For some patients, particularly those with large defects secondary to pressure, reconstructive (e.g., flap) surgery may be particularly effective.30
Prevent Recurrence
Despite patients' commonly held misconception, scarred skin is not strong. In fact, it takes up to a year for the body to remodel a healed area completely, and even then the tensile strength may only reach 40% of that of intact, uninjured skin.8 For this reason, patients are very susceptible to recurrence of their wounds. Therefore, once healed, measures need to be taken to minimize reinjury and control the very factors that predisposed the wound to poor healing.
Pressure Ulcer. Once healed, these patients still require the constant use of pressure relief mattresses and seat cushions, regular repositioning, and vigilant observation for new ulceration. Nutritional status requires constant monitoring.
Diabetic Foot. Continued blood sugar control and medication and dietary compliance are essential. Once healed, pressure reduction should be continued by referring the patient for custom orthotics, which the patient should be instructed to wear at all times. Routine examination of the feet should be performed by the patient or a family member or caregiver. Instruct patients to perform gentle nightly filing of callous and to use moisturizing lotion judiciously on their feet.
Venous Stasis. External compression remains the key to treating patients with venous insufficiency. Once healed, patients with venous insufficiency should be fitted for compression stockings. These are available in both knee-high and thigh-high versions, with the former being adequate in most circumstances. Different strengths of compression are available, with those rated for 30-40 mm Hg usually being best. For some patients, however, lighter or heavier compression may be needed. If worn on a daily basis, a single stocking will maintain its strength for about six months, after which time it should be replaced. Note that prescription compression stockings differ from the anti-embolism stockings available over the counter, which supply significantly less compression.
For patients with superficial venous reflux, as determined by venous duplex ultrasonography, surgical correction is a very viable option.31 Several techniques are available, depending on whether the reflux occurs at the saphenofemoral junction, long saphenous vein, or short saphenous vein. Although such surgery has not been shown to speed healing times, one large study has clearly established a reduction in rates of recurrence of venous stasis ulcers in patients who underwent surgical correction.32
Arterial Insufficiency. Patients should maintain routine preventative healthcare with a focus on the vascular exam at each office visit. The importance of compliance with dietary directives, medications, and smoking cessation cannot be overstated
Summary
Despite being a frustrating problem for both patient and provider, the chronic wound is a very treatable disease. The ability to salvage a limb that might have eventually been amputated due to a non-healing ulcer is a very rewarding experience. With a good examination, a methodical approach to treatment, and a familiarity with a handful of basic wound care products, the vast majority of wounds can be dealt with in the office. For those particularly challenging wounds that yet fail to heal, consider referral to a specialty wound care clinic.
Disclaimer: The goal of this paper is not to endorse any particular product. As there are hundreds of wound care products on the market, it is impossible to be comprehensive here. The authors recommend that physicians familiarize themselves with examples of each of the main product types. Hospital or corporate supply chains may dictate availability.
References
1. Cherry DK, Woodwell DA, Rechtsteiner EA. National Ambulatory Medical Care Survey: 2005 Summary. Advance data from vital and health statistics; no 387. Hyattsville, MD: National Center for Health Statistics. 2007.
2. Rudolph DM. Pathophysiology and management of venous ulcers. J Wound Ostomy Continence Nurs 1998;27:248-255.
3. Onegnae K, Phillips T. Leg ulcer management. Emerg Med 1993;25:45-53.
4. Cole-King A, Harding KG. Psychological factors and delayed healing in chronic wounds. Psychosom Med 2001; 63:216-220.
5. American Diabetes Association. Economic costs of diabetes in the U.S. in 2007. Diabetes Care 2008;31:1-20.
6. Enoch S, Grey JE, Harding KG. Recent advances and emerging treatments. BMJ 2006;332:962-965.
7. Harding KG, Morris HL, Patel GK. Science, medicine, and the future: Healing chronic wounds. BMJ 2002;324:160-163.
8. Black J, Baharestani M, Cuddigan J, et al. National Pressure Ulcer Advisory Panel's updated pressure ulcer staging system. Urol Nurs 2007;27:144-150.
9. Beylin M. Continuing education: Treating venous stasis ulcers In the lower extremity. Podiatry Today 2004;17:68-74.
10. Sieggreen MY, Kline RA. Arterial insufficiency and ulceration: Diagnosis and treatment options. Adv Skin Wound Care 2004;17:242-251.
11. Mcgee SR, Boyko EJ. Physical examination and chronic lower-extremity ischemia. Arch Intern Med 1998;158:1357-1364.
12. Baxter GM, Polak JF. Lower limb colour flow imaging: A comparison with ankle: Brachial measurements and angiography. Clin Radiol 1993;47:91-95.
13. Grey JE, Enoch S, Harding KG. Wound assessment. BMJ 2006;332:285-288.
14. Bowler PG, Duerden BI, Armstrong DG. Wound microbiology and associated approaches to wound management. Clin Microbiol Rev 2001;14:244-269.
15. Enoch S, Grey JE, Harding KG. ABC of wound healing. Non-surgical and drug treatments. BMJ 2006;332:900-903.
16. Gaylarde PM, Sarkany I, Dodd HJ. The effect of compression on venous stasis. Br J Dermatol 1993;128:255-258.
17. Gohel MS, Barwell JR, Taylor M, et al. Long term results of compression therapy alone versus compression plus surgery in chronic venous ulceration (ESCHAR): Randomized controlled trial. BMJ 2007;335:83. Published online 1 June 2007. http://www.bmj.com/cgi/content/full/bmj.39216.542442.BEv1.
18. Palfreyman S, Nelson EA, Michaels JA. Dressings for venous leg ulcers: Systematic review and meta-analysis. BMJ Originally published online 13 Jul 2007; http://www.bmj.com/cgi/content/full/335/7613/244.
19. Jones V, Grey JE, Harding KG. Wound dressings. BMJ 2006;332:777-780.
20. Mumcuoglu KY. Clinical applications for maggots in wound care. Am J Clin Dermatol 2001;2:219-227.
21. Skog E, Arnesjö B, Troëng T, et al. A randomized trial comparing cadexomer iodine and standard treatment in the out-patient management of chronic venous ulcers. Br J Dermatol 1983;109:77-83.
22. Cullen B, Smith R, McCulloch E, et al. Mechanism of action of PROMOGRAN, a protease modulating matrix, for the treatment of diabetic foot ulcers. Wound Rep Regen 2002; 10:16-25.
23. Bello YM, Falabella AF. Use of skin substitutes in dermatology. Dermatologic Clinics 2001;19:555-561.
24. Brown-Etris M, Cutshall WD, Hiles MC. A new biomaterial derived from small intestine submucosa and developed into a wound matrix device. Wounds 2002;14:150-166.
25. Falanga V, Sabolinski M. A bilayered living skin construct (APLIGRAF®) accelerates complete closure of hard-to-heal venous ulcers. Wound Rep Regen 1999;7:201-207.
26. Jull AB, Waters J, Arroll B. Pentoxifylline for treating venous leg ulcers. Cochrane Database Syst Rev 2002;1:CD001733.
27. Argenta LC, Morykwas MJ. Vacuum-assisted closure: A new method for wound control and treatment: Clinical experience. Ann Plast Surg 2000;45:332-334; discussion 335-336.
28. Zamboni WA, Wong HP, Stephenson LL, et al. Evaluation of hyperbaric oxygen for diabetic wounds: A prospective study. Undersea Hyperb Med 1997;24:175-179.
29. Bowering, CK. Diabetic foot ulcers: Pathophysiology, assessment, and therapy. Canadian Family Physician 2001;47:1007-1016.
30. Grover R, Sanders R. Plastic surgery. BMJ 1998;317: 397-400.
31. Scriven JM, Hartshorne T, Thrush AJ, et al. Role of saphenous vein surgery in the treatment of venous ulceration. Br J Surgery 1998;85:781-784
32. Barwell JR, Davies CE, Deacon J, et al. Comparison of surgery and compression with compression alone in chronic venous ulceration (ESCHAR study): Randomised controlled trial. Lancet 2004;363:1854-1859.
Chronic wounds represent a significant portion of the complaints seen by physicians, especially in the primary care setting. Visits for wound care account for just over 2% of all visits to office-based physicians in the United States.Subscribe Now for Access
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