Early Intervention for Wound Care

  1. Chronic conditions usually exist long before a lower extremity ulcer develops.

    For approximately 2.5 million people in the United States who experience lower extremity ulcers, life-long deficiencies loom if the problem isn't treated.

    Most leg ulcers are caused by chronic venous insufficiency, peripheral arterial disease or diabetes.1 However, patients with these chronic conditions usually present with vascular, neurological or skin changes in the lower extremities long before an ulcer develops. By recognizing these changes early, clinicians can take preventive measures to avoid ulceration.

    As part of this process, therapists should identify the following underlying disease processes.

    Ischemic Ulcers
    Ischemic ulcers can't heal due to impaired blood flow into the wound. This may be caused by disrupted microvascular blood flow, which occurs with disorders such as vasculitis, microthrombosis, Raynaud's phenomenon and sickle cell anemia.

    In addition, atherosclerosis can disrupt macrovascular flow. Atherosclerosis, which is caused by deposits of cholesterol, lipids and calcium in the lumen of vessels, may affect arteries and lead to impaired arterial flow.2,3 Peripheral arterial disease (PAD) is atherosclerosis of large and medium-sized vessels of the lower extremities.4 A patient with PAD may present with a history of coronary artery disease, cerebrovascular disease, hyperlipidemia, diabetes, hypertension or smoking.5

    Ischemic ulcers from PAD are often the result of trauma. In these cases, a chronic wound occurs when blood flow can't meet the metabolic demands of tissue repair. A patient with PAD may complain of intermittent claudication or pain while resting.1

    Claudication-ischemic pain in leg muscles (calves, thighs, buttocks)-occurs during exercise and abates with rest. Resting pain affects the feet and usually occurs at night.

    A patient with an ischemic ulcer secondary to PAD also may complain of severe tenderness at the wound site, and may not tolerate aggressive cleansing. These ischemic ulcers occur on the distal extremities and have a deep, punched-out appearance with regular wound edges.4,6 The wound bed appears pale and may include necrotic tissue.

    If you suspect PAD as the etiologic factor of a leg ulcer, obtain further data through noninvasive vascular testing (NIVT), segmental pressures, toe pressures, Doppler waveform analysis and duplex scanning.7,8 Lipid panels can rule out hyperlipidemia, and radiographic films can determine osteomyelitis. This provides baselines for future comparisons.

    To treat ischemic ulcers secondary to PAD, you must restore blood flow. A vascular surgeon may need to perform a revascularization procedure, which can include bypass surgery, angioplasty or placing an intravascular stent.5,9 Bypass surgery (in smaller vessels between the knees and ankles) is the best treatment for diabetic patients with PAD.10

    Topical therapy for an ischemic ulcer depends on vascular supply. If NIVT indicates adequate blood flow to support healing, or if the patient has been successfully revascularized, you should debride and provide a moist wound-healing environment to promote tissue repair.

    When NIVT suggests severe ischemia and the patient isn't a candidate for revascularization, leave dry eschars intact. Debriding intact eschar exposes underlying tissues to possible contamination and infection. Debriding viable tissue can cause additional tissue damage and, in the presence of severe ischemia, may lead to necrosis extension. Simply keep the eschar dry and protected.

    Venous Ulcers
    Chronic venous insufficiency (CVI) is the etiologic factor in a majority of leg ulcers.11 CVI is the result of damaged leg vein valves, which causes impaired venous return and abnormally high venous pressure. In turn, this leads to edema and altered microcirculation in the skin, which impairs healing.11,12

    Risk factors for CVI include a history of deep-vein thrombosis, obesity, lower leg trauma (crush injury, fracture or surgery), congenital venous abnormality, limited mobility with impaired calf muscle pump (arthritis, paralysis, muscular disorders) and pregnancy.13

    Venous ulcers are frequently precipitated by trauma. A patient may have traumatized the leg weeks earlier, and the wound never healed. He may also report a previous pruritic rash and determine that the ulcer started after scratching the skin.

    Venous ulcers usually occur on the lower calves, above the malleoli.14 These superficial ulcers have irregular wound edges and ruddy granulation tissue. Necrotic tissue isn't present unless there's coexisting PAD or severe infection.

    Venous ulcers have high amounts of exudates, due to edema in surrounding tissues. Patients complain of low to moderate pain, especially with leg dependence. Leg elevation relieves the pain. Associated manifestations include normal pulses, edema, hyperpigmentation of the skin, stasis dermatitis and dilated superficial veins. In late CVI, you may see lipodermatosclerosis-fibrosis of the skin and subcutaneous tissue in the lower leg.

    Compression therapy is the treatment mainstay for venous ulcers. Options for sustained pressure include elastic wraps, stockings, multilayer wraps, paste bandages (gauze impregnated with substances) and custom-legging orthoses.

    In addition, topical therapy provides a moist wound healing environment. Use caution when introducing any topical treatment, since patients with venous ulcers tend to have multiple contact allergies. Apply a 48-hour patch test with the product to prevent widespread contact dermatitis.

    Diabetic Foot Ulcers
    An estimated 15 percent of people with diabetes develop foot ulcers, and up to 24 percent eventually require amputation.15 You must understand the primary cause of diabetic foot ulcers, because early intervention can prevent amputations.

    Many providers mistakenly believe that peripheral arterial disease is the primary etiologic factor in developing diabetic foot ulcers. While 20 percent of diabetic foot ulcers are due to PAD, at least 60 percent are secondary to peripheral neuropathy. Another 20 percent of diabetic patients with foot ulcers have both PAD and neuropathy.16

    Diabetic foot ulcers due to peripheral neuropathy occur as a result of repetitive trauma from pressure and shear.17-19 Sensory neuropathy creates an insensate foot that prevents patients from feeling trauma. Motor neuropathy causes atrophy of foot muscles that support the joints, which leads to foot deformities and abnormal bony prominences that are subjected to repeated mechanical stress during ambulation.

    During this repetitive trauma, a thick, hard callus forms over the bony prominence. The patient lacks sensation, isn't aware of the callus and continues to walk on it. This puts pressure on underlying tissues, which are compressed between the callus and bony prominence. A blister or hematoma forms under the callus and it eventually ruptures. Unfortunately, many patients present with foot infection as the first sign of a problem.

    A diabetic foot ulcer that's secondary to neuropathy has a characteristic appearance. It occurs over a bony prominence, typically on the plantar surface of the foot. It's punched out, with a clean, pink wound bed (in the absence of infection or PAD) and surrounding callus. Loss of sympathetic tone from autonomic neuropathy impairs sweating and results in dry skin with possible fissures.

    Before initiating treatment for diabetic foot ulcers, perform a complete neurovascular exam.15,18 Patients with neuropathic diabetic foot ulcers have lower protective and vibratory sensations, proprioception and deep tendon reflexes. You must also assess the unaffected foot for deformities, calluses and unrecognized trauma.

    Infection is a leading cause of amputation and must be addressed promptly.19 Nonthreatening limb infections include conditions without systemic symptoms, absence of abscess, osteomyelitis and gangrene, and peri-wound cellulitis less than 2 cm.15 Oral antibiotics can usually treat these wounds.

    Limb-threatening infections are associated with advancing cellulitis, a deep abscess or osteomyelitis. Gangrene may be present, especially with coexisting PAD. Nonviable tissue in the wound increases the risk of infection. The peri-wound callus--a source of ongoing pressure--impairs epithelialization from wound margins and creates a ledge that can trap bacteria. Patients with limb-threatening infections may need to be hospitalized, and undergo intravenous antibiotics and surgical debridement.15,19

    Goals of wound management include identifying and treating infection, administering callus debridement, providing a moist wound environment and making sure the patient doesn't bear weight on the foot.15,18

    Local wound care involves sharp debridement of nonviable tissue and peri-wound callus. Aggressive debridement is essential, as long as the patient doesn't have severe PAD. A care plan should include a moist wound-healing environment with gels or creams for low draining wounds, and absorptive fillers for high draining wounds.20

    Off-weighting is another key to treating these ulcers.15 Because diabetic foot ulcers occur secondary to repetitive trauma, you must remove the trauma. The patient must not bear weight on the foot.

    Once the wound heals, an orthotist can fit the patient for appropriate long-term shoe gear. Edmonds et al. reported only a 26 percent recurrence rate of foot ulceration in patients with healed diabetic foot ulcers who used special shoes.21 On the other hand, patients who wore regular shoes had an 83 percent recurrence rate.

    By Susie Seaman, NP
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    About betts

    Joined: Oct '01; Posts: 1,024; Likes: 20
    Nursing Mgmt.


  3. by   maureeno
    'venous ulcers have high amounts of exudates'; wow, this brought back memories. six years ago this month our family helped with the hospice home care of a beloved neighbor. fluid poured from her legs.
  4. by   jenac
    Thank you betts.
  5. by   Shirdent
    I learned recently that periodontal infections are very much like chronic wounds. They are closer than I thought just five years ago.
    What I learned recently may sound like a commercial but I'm not selling anything so I hope this doesn't get booted. I'd like to think aloud and would really appreciate other's comments.

    Xylitol is used quite a bit in dentistry. Not only does it not promote dental decay, it establishes a healthy flora with effects that last for outwards of five years after using a specified amount for one year.

    This five carbon sugar is also effective against sinus infections. A saline solution with xylitol can work wonders! xylitol interferes with all strep. It also has a negative affect on h. influenza and other caustic bacteria. The mechanism of xylitol has been studied quite a bit with respect to strep because strep mutans is the current causative agent in dental decay.

    I was invited to speak at a xylitol conference a couple of years ago and had an opportunity to listen to another speaker from the Bozeman Biofilm Engineering dept. on a very interesting study using xylitol on chronic wounds. A wound clinic in Texas is using xylitol to break apart the oozy mass associated with chronic wounds, a biofilm.
    This biofilm is the complicating factor in chronic wounds. Part of the way xylitol works is that it decreases the ability of the bacteria to pump out that sticky mucopolysaccharide that blocks the antibiotics, and oxygen from getting down there to heal the wound. Along with the xylitol they're using lactoferrin, no kidding.

    Anyway, you can find their research at PubMed using the search string: xylitol wound.
    What I'd hoped to get from this group is a little insight into how you're dealing with biofilm in the context of a chronic wound treatment. I'd like to glean some knowledge from chronic wound nurses.
    The link I'm sharing is to a video on biofilm illnesses. If you click the link above the video you'll see some interviews of the best minds in biofilm research. http://www.youtube.com/watch?v=bukQbvbU2Jc

    Shirley Gutkowski, RDH, BSDH, FACE:spin: