Sores, cuts, scrapes, and other skin breaks come in various shapes and sizes, but the management of persistent cases is based on a few basic tenets.
Call them ulcers. Call them wounds. Call them open sores. Whatever you call a particular break in the skin, your role is more than just filling the hole. As a wound-care specialist, I’ve developed a few time-tested tips that can help you avoid common errors in diagnosis and treatment and allow you to minimize liability while maximizing outcomes.
Begin by determining whether the wound is acute or chronic. The difference is simple. Acute wounds (scratches, insect bites, skin tears, etc.) go through the usual phases of healing (inflammation, proliferation, and maturation), and in a fairly short time there is some form of epithelium where once there was a wound.
Chronic wounds, the focus of this article, fail to heal. They do not progress through the aforementioned phases but, for various reasons, remain open. Unfortunately, there really is no time frame that defines a wound as chronic, although there are clues that suggest failure to heal. Among the most common: persistence of periwound redness, little or no evidence of healing after a reasonable amount of time, granulation tissue that appears pale rather than a robust reddish color, and granulation tissue that forms initially but fails to increase in amount.
Establish the diagnosis
The three major types of chronic wounds are diabetic, venous, and pressure (decubiti). In treating any chronic wound, one of the most common errors is to concentrate solely on the wound, start an oral antibiotic and/or apply antibiotic creams, and expect rapid healing. When the wound fails to heal or does so minimally, the usual response is to change antibiotics, lengthen the course, or admit the patient to the hospital, where more and stronger antibiotics are used.
Sometimes the wound will surrender and heal a bit, allowing the patient to go home, but complete healing remains elusive. Of course, the literature is replete with evidence of superinfections, sensitivities, and other misadventures from knee-jerk antibiotic use, so the first tip I offer is that if the wound fails to respond to a reasonable course of antibiotic therapy, the likelihood is high that infection is not the culprit.
Keep the wound moist
One of the basic tenets of modern wound care is to keep the skin dry and the wound moist. When your grandmother told you to “let the air get to it,” she was misinformed. Moisture is necessary for capillary and matrix development, continued tissue health and viability, and elastic skin edges that allow for wound contraction. Wounds that are allowed to dry form a rock of desiccated fibrin, cells, and bacteria that prevents the wound from healing. So the second tip is to keep the wound covered at all times.
Dressing changes for most wounds should be done on an every-other-day basis. Twice- or thrice-daily changes are cost-ineffective and labor-intensive. A wound needs the opportunity to establish a microenvironment of healing. Changing the dressing too frequently risks damaging the healing wound or the adjacent skin.
For wounds that are draining heavily, make sure there is enough absorbent material to wick away excess moisture because too much moisture allows for skin maceration. This reduces healing and increases the risk of injury to the skin near the wound. Wounds that are on the dry side should have a dressing that promotes adequate wound moisture.
Check the circulation
In a wound of the lower extremities, be sure to ascertain the status of the arterial circulation. Regardless of etiology, circulatory compromise minimizes your chances of healing the wound. Before you pull out your prescription pad, pull out your Doppler device (every primary-care office should have one). Evaluate the signal generated by the dorsalis pedis artery and the posterior tibial artery of the involved foot or leg.
With minimal training, clinicians should also be able to measure systolic pressures in the ankle and brachial arteries to calculate the ankle-brachial index (ABI). The ABI is very sensitive and very specific for arterial disease of the lower extremity. An ABI 1.3 suggests peripheral arterial disease. Patients with nonhealing ulcers or other similar complaints (intermittent claudication, gangrenous changes, leg or foot pain at rest, etc.) whose ABI meets these criteria should be seen by a vascular specialist.
Since the problem in diabetic patients is likely related to the microcirculation rather than the larger vessels, a more complex test called the transcutaneous oxygen measurement will provide greater accuracy for assessing circulatory status. Whatever technique you use, it is paramount to assure blood flow to the wound area before attempting treatment.
Wounds associated with diabetesDiabetics do not heal more slowly than the general population. Moreover, not all open nonhealing sores in a diabetic patient can be attributed to her disease. In simplest terms, a wound above the ankle of a diabetic patient is likely not due to her diabetes.
Neuropathic mechanisms play a significant role in diabetic foot ulcers. Alteration of skin moisture and blood supply (autonomic neuropathy) promotes more significant skin injury through loss of tensile strength and turgor of the skin. Lack of sensation (sensory neuropathy) allows the patient to walk on a pin or a pebble or to tolerate ill-fitting shoes without pain, often resulting in an open sore on the bottom, sides, or top of the foot (Figure 1). Thus, a wound below the ankle of a diabetic patient has a high likelihood of being related to her diabetes in some way.
Once the circulatory status has been found adequate for healing, eliminating the cause of the problem is key. Since diabetic ulcers are caused by pressure, removing the pressure (offloading) is the immediate goal. For plantar ulcers, putting the patient on non-weight-bearing status or using special offloading boots or shoes is mandatory.
A wound located between the ankle and the knee has a high probability of being venous-based. Predisposing factors include obesity, pregnancy, and trauma to the leg (e.g., saphenous vein removal for vascular surgeries, etc.). The legs usually have a shiny, hairless appearance and may be edematous up to the knees with a brownish discoloration (hemosiderin deposition) or whitish scars that indicate old healed wounds (atrophie blanche).
One of the most common misdiagnoses involves venous disease, more commonly known as chronic venous insufficiency (CVI). In patients with this condition, the venous valves that promote flow from distal to proximal (or superficial to deep) areas become compromised, allowing for retrograde flow either through the perforators or the deep/superficial venous system.
As venous hypertension develops, leakage of fluids compromises the surrounding tissues, including the supporting fascia. With progression, the venous return worsens, allowing for a number of sequelae, including stasis dermatitis and venous insufficiency ulcers, also known as venous leg ulcers (VLUs). (“Venous stasis ulcers” is no longer an accepted term.) Unfortunately, when edema develops (even if only in one leg) the knee-jerk treatment is diuretics, which do not address the underlying etiology but can wreak havoc on the patient’s electrolytes. More important, the edema rarely responds.
Stasis dermatitis is an inflammatory condition of the leg caused by an exacerbation of CVI and is not infection-based. In this disorder, the patient’s legs may suddenly become swollen and inflamed with no obvious cause (Figure 2). Too many clinicians see the red, swollen legs and race to prescribe antibiotics.
A simple key to the diagnosis is to evaluate the patient for fever and elevated WBC count and use any of your favorite tests for infection. Odds are they will be negative, especially in a patient who has had several similar previous episodes that were negative. Of course, obtaining a venous Doppler to assess for deep venous thrombosis (DVT) is acceptable if the patient has sudden onset of pain or any associated signs of DVT.
Once you have determined that the patient has CVI or venous insufficiency ulcers, treatment is fairly simple. You need to provide a “stiff” outer layer against which the calf muscle can compress the veins (Figure 3), while compressing the leg to promote venous valvular competence and one-way flow of blood out of the leg. Since stockings do not provide any stiffness to support the fascia, they cannot be used to treat the disease but are best used instead for prevention of recurrence after treatment has been successful.
I prefer not to use zinc oxide Unna’s boots because they do not shrink as the edema resolves, essentially leaving the leg untreated once it has shrunk within this wrap. The wound-care literature supports a system involving inner wraps of padding and/or inelastic support over which are placed elastic wraps. This allows for the wraps to perform their individual functions even as the swelling resolves and the leg shrinks. The wraps are usually replaced once a week unless significant drainage from the leg mandates more frequent changes.
These wounds, known also as bedsores or decubitus ulcers, occur over bony prominences, with the most common locations being the heels, coccyx, sacrum, or ischial tuberosities. The etiology is plain. Pressure on the tissues overlying a bony prominence compromises capillary blood flow with subsequent tissue injury and then necrosis.
Since the skin is better suited to take the pressure than the deeper tissues (fat, muscle, and tendons), reddish skin will mask deeper necrotic tissues. Worsening of the reddish area despite care indicates a deep tissue injury (DTI). It is important to recognize a DTI when it occurs. Otherwise the injury will appear to progress when in fact it was pre-existing but not evident.
Pressure ulcers are staged (not graded) according to specific criteria regarding their depth. (Since a DTI is not an open wound, it does not have a stage but rather must be recognized as an injury to the deeper supporting tissue structures. If the overlying skin either sloughs off or is removed as part of a debridement, the depth of this area will determine the stage.)
Stage 1 is nonblanchable redness of the skin (Figure 4). A stage 2 injury is partial-thickness skin loss involving epidermis, dermis, or both. The ulcer is superficial and presents clinically as an abrasion, blister, or shallow crater. Stage 3 ulcers (Figure 5) are full-thickness skin loss involving damage to or necrosis of subcutaneous tissue that may extend down to, but not through, underlying fascia. The ulcer presents clinically as a deep crater with or without undermining of adjacent tissue. Stage 4 pressure ulcers (see opening photo, page 57) involve full-thickness skin loss with extensive destruction, tissue necrosis, or damage to muscle, bone, or supporting structures (e.g., tendon, joint capsule). Undermining and sinus tracts also may be associated.
The use of a staging system is a means to assess the amount of risk a patient has for ongoing morbidity and mortality.
For example, an elderly patient with a stage 1 or 2 lesion should respond well and rapidly to aggressive, thorough treatment. The presence of a stage 3 or 4 lesion signals more significant system problems and may indicate that the external care being provided to the patient is not sufficient. Other interventions (nutrition, hygiene, pressure reduction, activity, etc.) may need to be more aggressively addressed.
Regardless of what treatment is instituted, the primary goal is to relieve pressure on the involved area. The key is frequent position changes to reduce pressure on the injured area while minimizing the same pressures to other areas. The specific wound treatments selected depend on numerous factors, including location of the wound, amount of drainage, depth, amount of adjacent healthy tissue, patient mobility, and, of course, financial constraints.
There has been a significant push by the federal government regarding these types of wounds such that failure to identify them and provide correct treatment now carries significant penalties. I recommend that you read the federal guidelines regarding pressure sores in nursing home patients (www.cms.hhs.gov/transmittals. Accessed August 9, 2007). These guidelines will likely be used as the model for those who provide acute and home health care.
The keys to successful wound healing are familiar to every primary-care clinician. Take the time to make an accurate diagnosis, and treat based on your diagnosis. If unsuccessful, review your diagnosis and institute a different treatment. Address all factors relating to the wound, and remember that wound care is more than filling holes.