Improving outcomes with noncontact low-frequency ultrasound

By Ronnel Alumia, BSN, RN, WCC, CWCN, OMS

Achieving excellent wound care outcomes can be challenging, given the growing number of high-risk patients admitted to healthcare facilities today. Many of these patients have comorbidities, such as obesity, diabetes, renal disease, smoking, chronic obstructive pulmonary disease, and poor nutritional status. These conditions reduce wound-healing ability.

At the same time patient acuity has been rising, reimbursement for some types of care has been declining. For certain hospital-acquired conditions, such as stage III or IV pressure ulcers and certain surgical-site infections, reimbursement has been eliminated. Thus, clinicians can’t choose products based solely on their proven ability to obtain a good clinical outcome; they also must consider economic factors. Noncontact low-frequency ultrasound (NLFU) can help improve clinical outcomes and provide cost savings.

Ultrasound: Simple but effective

NLFU delivers sound waves to tissues through a saline mist. Unlike most wound care treatments, whose effects are limited to the surface, NLFU penetrates into and below the wound bed to reach previously inaccessible tissues. (See A glimpse of NLFU in action by clicking the PDF icon above.)

View: See how NLFU works

Ultrasound energy produces biophysical effects from mechanical stimulation of cells, promoting wound healing. A mechanical vibration, ultrasound is transmitted at a frequency above the upper limit of human hearing—20 kHz. The most common form of therapeutic ultrasound uses devices that operate in the 1- to 3-MHz range to treat various musculoskeletal disorders with a thermal effect. Diagnostic ultrasound, in contrast, operates in a high-frequency (20 to 40 MHz) range. It has a wide number of uses, from fetal monitoring to echocardiography.

In contrast, NLFU delivers low-frequency (40 kHz), low-intensity (0.2 to 0.6 W/cm2) ultrasound energy to the wound bed with no thermal effect. With most ultrasound therapy, a gel serves as a conduit to deliver sound waves to tissues. However, NLFU uses a saline mist, which eliminates contact with tissue and thus is painless.

NLFU can be performed by nurses with special training. The patient usually undergoes the procedure at the bedside three to five times per week, with the machine preset to a certain number of minutes based on wound measurement (length × width). Typically, the course of therapy ends when the desired outcome is achieved or the patient is discharged or transferred out of the facility.

The science of NLFU

The micromechanical forces produced by ultrasound energy at a cellular and molecular level have a wide range of effects on the wound-healing process, including reduction of bacteria within and below the wound bed. Unlike other body cells, bacteria have a rigid cell membrane; repeated pressing of sound waves can disrupt the bacterial membrane, causing cell death. (See NLFU: The science behind the solution by clicking the PDF icon above.)

Laboratory tests show NLFU reduces a wide range of bacteria, including some of the hardest to treat, such as methicillin- resistant Staphylococcus aureus (MRSA), vancomycin-resistant enterococci (VRE), and Acinetobacter baumannii. In a clinical study of patients who had stage III pressure ulcers with high levels of bacteria, punch biopsies were used to determine baseline and posttreatment bacterial counts. Results showed significant reduction in S. aureus (93.9%), A. baumannii (94%), and Escherichia coli (100%) after six NLFU treatments over a 2-week period. In live animal studies, NLFU disrupted the bacterial biofilm after just three treatments. (See NLFU and the healing process by clicking the PDF icon above.)

Sustained inflammation is a common barrier to healing. NLFU reduced pro- inflammatory cytokines in two studies—one involving patients with chronic diabetic foot ulcers and the other involving patients with nonhealing venous leg ulcers. This reduction correlated to reduced wound areas in these previously nonhealing wounds. In one of these studies, researchers reported a decrease in MMP-9, a matrix metalloproteinase that breaks down new granulation tissue and delays healing.

Studies also show NLFU increases vasodilation, stimulates vascular endothelial growth factor and angiogenesis, promotes early release of growth factors, and provides greater amounts of high-quality collagen. The overall result of these cellular effects is accelerated healing.

Clinical outcomes

Use of NLFU is supported by clinical data, including a meta-analysis, three randomized-control trials, 11 peer-reviewed studies, and multiple case series. A 2011 meta-analysis compiled data from eight published studies reporting the effect of NLFU on wound size and healing rates in 444 patients with various chronic wounds. It found 85% wound-area reduction in a mean of 7 weeks, wound-volume reduction of 80% at a mean of 12 weeks, and 42% complete wound closure at 12 weeks. By comparison, a meta-analysis of standard-of-care treatment found only 24% complete wound closure at 12 weeks. Thus, NLFU achieves almost twice the healing of the standard treatment.

Besides consistently speeding healing of open wounds, NLFU is an effective early treatment for suspected deep-tissue injuries (sDTI). In a study of 127 sDTIs treated with standard of care alone (63) or standard of care with NLFU (64), only 22% of standard-of-care-alone sDTIs resolved without opening or progressed only to a stage II pressure ulcer, compared to 80% in the NLFU arm. At my hospital, we found similar results in our patient population using NLFU to resolve sDTIs before they became full-thickness wounds. (See Clinical outcomes and cost savings from NLFU by clicking the PDF icon above.)

NLFU has been used in wound care settings across the country for several years. Increasingly, it’s being used in acute-care settings as clinicians are grasping its substantial clinical and economic benefits. This technology can help healthcare providers meet both clinical and economic outcome goals. NLFU is rapidly becoming the new standard for early sDTI intervention.

Selected references

Centers for Medicare & Medicaid Services. Hospital-acquired conditions in acute inpatient prospective payment system hospitals. October 2012. Medicare/Medicare-Fee-for-Service-Payment/Hospital AcqCond/downloads/hacfactsheet.pdf. Accessed July 13, 2013.

Driver VR, Yao M, Miller CJ. Noncontact low- frequency ultrasound therapy in the treatment of chronic wounds: a meta-analysis. Wound Rep Reg. 2011;19(4):475-80.

Escandon J, VIvas AC, Perez R, Kirsner R, Davis S. A prospective pilot study of MIST therapy’s effectiveness on bacterial bioburden reduction and wound progression in refractory venous leg ulcers. Poster presented at Symposium on Advanced Wound Care; Orlando, FL. April 17-20, 2010.

Honaker JS, Forston MR, Davis EA, Wiesner MM, Morgan JA. Effects of noncontact low-frequency ultrasound on healing of suspected deep tissue injury: a retrospective analysis. Int Wound J. 2013;10(1):65-72.

Kavros SJ, Miller JL, Hanna SW. Treatment of ischemic wounds with noncontact, low-frequency ultrasound: the Mayo Clinic experience, 2004-2006. Adv Skin Wound Care. 2007;20(4):221-6.

Kavros SJ, Schenck EC. Use of noncontact low-frequency ultrasound in the treatment of chronic foot and leg ulcerations: a 51-patienr analysis. J Am Podiatr Med Assoc. 2007;97(2):95-101.

Lai J, Pittelkow MR. Physiological effect of ultrasound mist on fibroblasts. Int J Dermatol. 2007;46(6):587-93.

Liedl DA, Kavros SJ. The effect of MIST ultra-sound transport technology on cutaneous microcirculatory blood flow. Abstract presented at Symposium on Advanced Wound Care, 2001.

Margolis DJ, Kantor J, Berlin JA. Healing of diabetic neuropathic foot ulcers receiving standard treatment. A meta-analysis. Diabetes Care. 1999;22(5):692-5.

Serena T, Lee SK, Lam K, Attar P, Meneses P, Ennis W. The impact of noncontact, nonthermal, low-frequency ultrasound on bacterial counts in experimental and chronic wounds. Ostomy Wound Manage. 2009;55(1):22-30.

Seth AK, Nguyen KT, Geringer MR, et al. Noncontact, low-frequency ultrasound as an effective therapy against Pseudomonas aeruginosa–infected biofilm wounds. Wound Repair Regen. 2013;21(2):266-74.

Thawer HA, Houghton PE. Effects of ultrasound delivered through a mist of saline to wounds in mice with diabetes mellitus. J Wound Care. 2004;13(5):171-6.

Yao M, Hasturk H, Kantarci A, et al. A pilot study evaluating noncontact low frequency ultrasound and underlying molecular mechanism on diabetic foot ulcers. Int Wound J. 2012 Nov 19. doi:10.1111/iwj.12005.

Ronnel Alumia is a wound care and ostomy nurse at Acuity Specialty Hospital of New Jersey in Atlantic City.

Preventing pressure ulcers starts on admission

By Jeri Lundgren, BSN, RN, PHN, CWS, CWCN

The first 24 hours after a patient’s admission are critical in preventing pressure ulcer development or preventing an existing ulcer from worsening. A skin inspection, risk assessment, and temporary care plan should all be implemented during this time frame. Essentially, it’s the burden of the care setting to prove to insurers, regulators, and attorneys the pressure ulcer was present on admission and interventions were put into place to avoid worsening of the condition. Of course, patients also benefit from having their condition identified and treated promptly.

Taking a close look

Newly admitted patients must undergo a thorough skin inspection within 24 hours of admission. Many times, a wound care nurse is designated to perform this task. Although wound care nurses bring great expertise, their lack of availability can sometimes delay assessment. To avoid delay, all nurses must be capable of completing a skin inspection and accurately documenting their findings. A wound care nurse can educate nurses in skin inspection and documenting skin concerns.

Assessing risk and planning care

Performing a risk assessment within the first 24 hours ensures interventions are put in place to prevent skin breakdown and promote healing. That’s done as part of developing a temporary care plan. The care plan should contain interventions designed to minimize, stabilize, or remove identified risk factors. The interventions need to be put in place as soon after admission as possible.

Whenever possible, try to identify risk factors and/or wounds before the patient’s admission to ensure interventions are in place before the patient arrives.

Even if the care setting allows several days to complete a care plan, a temporary care plan for prevention of skin breakdown is strongly recommended within the first 24 hours. At a minimum, the temporary care plan should address the following:

• support surface for the bed and the wheelchair/sitting surface
• individualized turning and repositioning schedules for patients and helping patients to be as mobile and active as possible
• incontinence management, if needed
• keeping the skin clean and dry
• keeping the heels elevated off the bed
• addressing nutritional/hydration concerns for wound healing, dietary referral
• referrals to therapy, as appropriate
• daily inspection of the skin by nonlicensed staff and weekly skin inspections by licensed staff
• risk assessment per policy.
If the patient has a wound, the temporary care plan should also include:
• applying topical treatment, as ordered
• monitoring the patient for signs and symptoms of infection
• reporting any decline or changes to the primary care provider and family designee
• completing a comprehensive assessment of the wound at least weekly.

If nurses are uncomfortable with developing a care plan based on the risk assessment, it might be helpful for a manager or wound care expert to develop a “cheat sheet” with potential interventions that correlate with the individual risk factors identified. Once the temporary care plan is developed, it should be communicated to the nurses, nursing assistants, and and others on the interdisciplinary team.

Meeting your goal

Your goal as a clinician is to prevent the development of a pressure ulcer and ensure proper interventions are in place to promote healing in pressure ulcers present on admission. If you complete a skin assessment and risk inspection and then develop and communicate a care plan within the first 24 hours of admission, you should be successful in achieving that goal.

Jeri Lundgren is director of clinical services at Pathway Health in Minnesota. She has been specializing in wound prevention and management since 1990.

Power up your patient education with analogies and metaphors

By Janice M. Beitz, PhD, RN, CS, CNOR, CWOCN, CRNP

Quality patient education is essential for comprehensive health care and will become reimbursable under healthcare reform in 2014. However, it’s difficult to provide effective education when time for patient interactions is limited. You can enhance your instruction time—and make your teaching more memorable—by using the techniques of analogy and metaphor.

Powerful tools

Analogy and metaphor are figures of speech that have been used since the time of Aristotle and Plato. (See Comparing analogy and metaphor by clicking the PDF icon above.) Why are they so powerful for patient education? Because analogy and metaphor can make abstract concepts real, helping patients understand why they are ill and how suggested changes will help correct underlying causes.

Analogy and metaphor create a form of cognitive “scaffolding” on which patients can hook new material to information they already understand. Educational theorist David Ausubel suggests that learners (such as patients) require frameworks into which new information can be assimilated. An analogy or metaphor can act as an anchoring concept or an organizer for providing such a framework.

Research supports that analogies and metaphors can improve communication with seriously ill patients, such as those with advanced cancer. Casarett and colleagues conducted a cross-sectional study of audio-recorded conversations between patients and physicians. The results demonstrated that analogies and metaphors improved patient understanding and communication.

Using analogy and metaphor effectively

How can analogy and metaphor be used in patient education? The uses are limited only by the clinician’s creativity.

A primary care practitioner uses analogy to discuss good self-care practices. She tells patients that persons with quality self-care drive their bodies like Cadillacs while self-
neglecters drive their bodies like jalopies.

Even bad life circumstances can be used educationally. A psychiatric colleague uses the metaphor of a toaster: Acute illness is like a toaster. You put something in (the patient) and it comes out better than it was before (in terms of resilience). An oncology specialist colleague discusses the role of heredity (genetic predisposition) and environment in cancer development: Genes load the gun; environment pulls the trigger.

A metaphor for chronic wound healing is the light switch: The prolonged inflammatory process of delayed healing is similar to a light switch stuck in the “on” position. Interventions, such as debridement and other advanced modalities, aim at switching the light (inflammation) off. Another colleague specializing in GI disorders likens constipation to “not taking the garbage out enough.”

In a relatively recent systematic review of effective teaching strategies and methods of delivery for patient education, the analysis of published research studies found that the best patient education strategies were culturally appropriate, patient specific, and structured. Analogy and metaphor can address all three characteristics if well planned.

The literature also suggests that Humor (used appropriately) can augment the use of Analogy and Metaphor and allow teachers to HAM it up for better learning. Humorous analogies or metaphors that are relevant to patients’ interests offer maximum effectiveness. The vividness and active engagement that typify funny meta­phors and analogies have the capability to instruct in ways beyond words alone. Laughter and humor may allow the patient to experience a “refreshing pause” cognitively and help “ha-ha” become “aha!”

Metaphors and analogies can describe the education or learning process itself. The clinical educator helps the patient “plant seeds,” “peel away the layers,” or “switch on a light bulb.” The educator can capture boring, lifeless lecture material and “bring it to life.” This outcome is particularly helpful in more abstract areas, such as mental health issues and science concepts.

Optimal outcomes

Understanding quality patient education is important for optimal patient outcomes. Techniques such as analogy and metaphor can help patients learn more effectively and create a positive, relaxed learning environment. More importantly, metaphor and analogy appeal to multiple learning senses and can instruct in ways eclipsing the limits of words.

Selected references

Ausubel DP. Educational Psychology: A Cognitive View. New York, NY: Holt, Rinehart, and Winston; 1968.

Casarett D, Pickard A, Fishman J, Alexander S, Arnold RM, Pollak K, Tulsky J. Can metaphors and analogies improve communication with seriously ill patients? J Palliat Med. 2010;13(3):255-60.

Clark AM. Getting street wise: a metaphor for empowering nurses for evidence-based practice [editorial]. Nurse Educ Today. 2013;33:3-4.

Friedman AJ, Cosby R, Boyko S, Hatton-Bauer J, Turnbull G. Effective teaching strategies and methods of delivery for patient education: a systematic review and practice guideline recommendations. J Cancer Educ. 2011;26:12-21.

Garner R. Humor, analogy, and metaphor: H.A.M. it up in teaching. Radical Pedagogy. 2005;6:2.*qzYyjGFuedV09FP4crWmZ/
. Accessed April 7, 2013.

Hume K. Unexpected connections: teaching through metaphor and analogy. Teach Magazine. May 3, 2011. Accessed April 7, 2013.

Hydo SK, Marcyjanik DL, Zorn CR, Hooper NM. Art as a scaffolding teaching strategy in baccalaureate nursing education. Int J Nurs Educ Scholarsh. 2007;4(1):1-13.

Neibert K, Marsch S, Treagust DF. Understanding needs embodiment: a theory-guided re-analysis of the role of metaphors and analogies in understanding science. Sci Educ. 2012;96(5):849-77.

Sutherland JA. Teaching abstract concepts by metaphor. J Nurs Educ. 2001;40(9):417-19.

Janice M. Beitz is professor of nursing at Rutgers University School of Nursing in Camden, New Jersey.

Forging a communication bond with prescribers

By T. Michael Britton, RN, NHA, WCC, DWC

As wound care professionals, we’ve all experienced a time when we felt that our patient didn’t have the appropriate wound treatment orders. However, the physician, nurse practitioner, or other prescriber wouldn’t follow your recommendation. This situation is not only frustrating but can delay the healing process. This article explores why a prescriber might not follow your recommendation and offers solutions. It focuses on physicians, because I’ve had the most experience with them.

Know the physician’s “type”

For 5 years, I was vice president of a company that managed physicians. I started asking them, “What makes you follow or not follow the wound clinician specialist’s orders?” Responses varied, but one response gave me an important insight. The physician told me there are three types of physicians: those who know, those who think they know, and those who don’t know.

With this in mind, the first thing you need to do is identify which of the three physician types you’re dealing with. Ask mutual coworkers who’ve worked with the physician, as well as the physician’s peers, for input so you get a feel for his or her personality. Then tailor your interaction based on your findings. For example, if a physician is the “think they know” type, prepare ahead of time what your response will be in case the physician disagrees with your recommendation. If a physician falls into the “don’t know” category, you’ll need to provide more detailed information about the nature of your recommendation.

Start off on the right foot

Your first interaction with the physician is crucial because it sets the stage for your ongoing relationship. When you introduce yourself, include all your credentials and don’t be embarrassed to talk about your training and experience. If possible, you already should have assessed the patient and reviewed the chart. It may be helpful to have someone familiar to the physician and who knows your expertise provide the introduction.

Make your case

Physicians say that clinicians who make a recommendation commonly aren’t prepared to provide the information the physician needs to make an informed decision. Having your information organized and readily available increases the chance that the physician will accept your recommendation. Many tools can help you get organized. One of the most user-friendly is SBAR—Situation, Background, Assessment, Recommendation. (See SBAR communication tool.)

Before you call or see the physician, be sure you can answer “yes” to the following questions:
• Have I seen and assessed the patient myself (instead of relying on someone else’s report)?
• Am I calling the right physician to address this situation? For example, can the patient’s primary care physician address the problem or do I need to call one of the consulting specialists?
• Do I know the admitting diagnosis and admission date?
• Have I read the most recent progress and nurses’ notes?
• Do I have the patient’s chart available so I can easily access information, such as age, current medication, wound treat­ments, allergies, laboratory results, and most recent vital signs?
• Do I know the patient’s resuscitation status?

Know what to do in the case of inappropriate treatment

If you believe the physician’s prior treatment orders were inappropriate, calmly express your concerns, and give rationales for your opinion. Be ready to cite a reputable source, such as protocols or research studies, to validate your position. Use correct medical terminology but don’t overcomplicate your language. Share your ideas for alternatives and try to get permission for a trial period.

Also tap into other resources, such as pharmacists, other physicians, and even product representatives, for information or support to make your case. For instance, a pharmacist may be able to bolster your argument for making a switch from one antibiotic to another.

If all else fails, report the problem to the appropriate supervisor.

Know when to suggest and when to recommend

It’s important to understand the difference between a suggestion and a recommendation. A suggestion implies a possibility or proposal. A recommendation is something presented as worthy of acceptance or trial. The difference is in the direction of the flow. A recommendation flows from upper level to lower level and between equals; a suggestion flows from lower level to upper level. Making a recommendation when the situation calls for a suggestion can lead to someone in a higher position than you being offended or feeling that you have overstepped your boundaries. On the other hand, using a suggestion when a recommendation is needed can result in the other party taking it as an option, something they don’t have to do; therefore, they don’t follow through.

An example of a suggestion from lower level to upper level is when a unit nurse says to the physician, “Dr. Jones, we are currently changing Ms. Johnson’s dressing three times a day. Studies have shown that dressings should be removed as infrequently as possible to prevent excess wound cooling.”

Here’s an example of a recommendation between equals is this interaction between a unit nurse and a wound care nurse: “We should change Ms. Johnson’s dressing change from three times a day to every day. Her drainage has decreased and we can reduce the wound’s exposure time.” Note that the unit nurse provided a rationale for her recommendation.

Here’s another example of a recommendation: As the wound care expert, you’re consulted to evaluate a patient in a long-term care facility who continues to have skin breakdown. After reviewing the medical record, you realize the patient is being turned only once every 3 to 4 hours. When you meet with staff on the floor, you state,
“Ms. Johnson has had two pressure ulcers in the past 6 months, and has a history of diabetes, which can affect healing. She’s at high risk for skin breakdown, so she needs to be turned every hour.” Again, note that support is provided for the recommendation.

Pick your battles

It’s not important to win every battle. Instead, remember that you want to win the war. There will always be some physicians and other prescribers who aren’t willing to follow your suggestions. As professionals, we have to accept that. Of course, if a physician’s unwillingness to follow your suggestion puts the patient at risk for harm, you’ll need to take your case to the next level.

Download SBAR tool

T. Michael Britton is president and CEO of Consult Us, LLC, in Montgomery, Alabama.

Wounds on the Web: Accessing the best online resources

By Donna Sardina, RN, MHA, WCC, CWCMS, DWC, OMS

Knowledge is exploding online, making it essential that you’re comfortable using the Internet. You can also go online to save time and find a job, among other tasks. (See Online value.)

However, you also need to keep in mind that anyone can put information on the Internet. As the caption of a cartoon by Peter Steiner, published in The New Yorker says, “On the Internet, nobody knows you’re a dog.”

Be sure to evaluate the information, including such criteria as validity, authorship, integrity, and timeliness (be wary of undated information). Here are specifics to check.


Who is the intended audience for the website? Children, teenagers, adults? General audience, professionals, students, researchers? Members of a certain group or proponents of a certain viewpoint? Content varies according to audience.


Why was the website created? To sell, advertise, inform, persuade? The purpose of a website may not be stated clearly, so review content to discern its purpose.


Here are some questions to ask about the website:
• Has the website been created by a layperson or a well-known organization?
• Who sponsors the website? What is the sponsor’s reputation?
• Is contact information provided?

You can often find this information under headings such as “About us” or “Our Philosophy.”


Consider these questions for authors of online content:
• What credentials does the author have? If you don’t know what a credential means, search for it online.
• What are the author’s experience and expertise? Consider looking up the author’s name in a search engine, using three forms:
• without quotes: Firstname Lastname
• enclosed in quotes as a phrase: “Firstname Lastname”
• enclosed in quotes with * between the first and last name: “Firstname * Lastname” (The * can stand for any middle initial or name in Google only.)
• What is the end of the main URL address (called the domain extension)? This tells you the type of organization associated with the URL.

Domain extension/Organization type

.com Commercial company, usually for-profit
.edu Educational institutions, usually colleges and
.gov Government agency
.mil Limited to use by the U.S. military
.net Network, sometimes an internet service provider
.org Organizations, usually nonprofit


The following questions help you determine objectivity:
• Is any bias evident? Does the author present the information objectively from various points of view, or from one particular point of view?
• Does the author or sponsor have a known affiliation that would indicate a specific agenda or bias?
• To what extent does the information attempt to persuade or sway the audience?
• Does the information include vague statements, generalizations, stereotypes, or emotional appeals?


Ask the following:
• Where did the author get the information? As in printed journals and books, you should expect support for the information, such as references or links.
• If there are links to other pages as sources, are they to reliable sources?
Do the links work? Do links to references work and are the references from reputable sources? Keep in mind that it’s possible to create fake references.
• Is permission to reproduce copyright information provided? If so, this
typically means the website values its content.
• If the site has health information, does it display the Health on the Net Foundation Code of Conduct (HONcode) symbol? This means HON has evaluated the website and has deemed it meets HON’s ethical principles. Absence of the symbol doesn’t mean there is a problem with the site, but its presence is another point in the site’s favor.

By asking questions like these, you can ensure you access accurate information for you and your patients.

Donna Sardina is Editor-in-Chief of Wound Care Advisor and cofounder of the Wound Care Education Institute in Plainfield, Illinois.

What’s causing your patient’s lower-extremity redness?

By Robyn Bjork, MPT, CWS, WCC, CLT-LANA

The ability to understand or “read” lower-extremity redness in your patient is essential to determining its cause and providing effective treatment. Redness can occur in multiple conditions—hemosiderin staining, lipodermatosclerosis, venous dermatitis, chronic inflammation, cellulitis, and dependent rubor. This article provides clues to help you differentiate these conditions and identify the specific cause of your patient’s lower-extremity redness.

Hemosiderin staining and lipodermatosclerosis

Hemosiderin staining is dark purple or rusty discoloration of the lower legs caused by chronic venous disease. A 2010 study found hemosiderin staining in all subjects with lipodermatosclerosis and venous ulcers. When vein valves fail, regurgitated blood forces red blood cells (RBCs) out of capillaries. Dead RBCs release iron, which is stored in tissues as hemosiderin, staining the skin.

Hemosiderin staining and active lipodermatosclerosis may be misdiagnosed as cellulitis. Active lipodermatosclerosis causes painful, sharply demarcated red patches on medial aspects of the lower leg. Unlike in cellulitis, redness in lipodermatosclerosis is localized to areas of hemosiderin staining and induration. Also, the skin isn’t hot and the patient is afebrile and unresponsive to antibiotics. Lipodermatosclerosis progresses to fibrosis and constriction, causing an inverted champagne-bottle appearance of the legs.

Treat active lipodermatosclerosis with compression therapy and topical corticosteroids, if needed. Control chronic venous hypertension with compression, and hemosiderin staining will fade. Refer the patient for potential corrective venous surgical procedures.

Venous dermatitis

Defined as inflammation of the epidermis and dermis, venous (stasis) dermatitis is common in patients with lower-extremity venous disease. Signs and symptoms include scaling, crusting, weeping, erythema, erosions, and intense itching. This disorder increases the risk of contact sensitivity. Advise the patient to avoid such products as lanolin, balsam of Peru, rubber, adhesives, fragrances, dyes, preservatives, skin sealants, silver sulfadiazine, neomycin, and bacitracin—all known to exacerbate venous dermatitis.

Venous dermatitis commonly is confused with cellulitis. A 2011 study found that 28% of 145 patients hospitalized for cellulitis had been misdiagnosed. The most common mistaken diagnosis was venous dermatitis. Unlike cellulitis, venous dermatitis causes itching and crusting; also, the skin isn’t acutely painful or hot and the patient is afebrile.

Treat acute venous dermatitis with compression therapy and mild-potency topical corticosteroids. Apply corticosteroids sparingly to affected areas once or twice daily for 2 weeks; be aware that premature discontinuation can lead to recurrence, while prolonged use can cause skin thinning and reduced efficacy. Domeboro soaks also decrease weeping, irritation, and itching. Paste bandages impregnated with calamine or zinc oxide are soothing and drying. However, some patients may react to the preservatives in paste bandages, so a patch test is prudent.

Chronic inflammation

Lymphedema causes chronic inflammation. About 50% of plasma proteins leak into the interstitial space daily and are recycled through the lymphatics. Lymphatic failure traps proteins in the tissues; the proteins act like sponges, attracting and binding fluid. The proteins then denature, triggering a chronic inflammatory response. This response sometimes is misdiagnosed and treated as chronic cellulitis.

Compared to cellulitis, high-protein chronic inflammation is diffuse and nontender, with light redness and mildly increased warmth. Local skin changes may include thickening or papillomatosis (a lumpy, bumpy appearance). A positive Stemmer’s sign confirms lymphedema. Complete decongestive physiotherapy promotes protein reabsorption and resolves chronic inflammation.


Cellulitis is a rapidly spreading infection of the dermis and subcutaneous tissue. In adults, it most commonly stems from Staphylococcus aureus infection of the legs. Erysipelas, a superficial form of cellulitis, involves the lymphatic system and is differentiated by “streaking” toward a regional lymph node.

Cellulitic skin is hot, acutely painful, edematous, and indurated. Redness spreads and the borders usually are irregular, sharply defined, and slightly elevated. Blisters, hemorrhagic bullae, abscesses, erosions, and necrosis may develop. About 30% to 80% of patients with lower limb cellulitis are afebrile. The white blood cell count, erythrocyte sedimentation rate, and C-reactive protein levels commonly are elevated, but normal values don’t rule out cellulitis.

Treat cellulitis with oral antibiotics effective against staphylococcus and streptococcus. Adding a brief course of oral corticosteroids significantly shortens cellulitis duration. Severe cases may necessitate hospitalization and I.V. antibiotics, plus abscess incision and drainage. Control edema with bed rest and leg elevation.

Recurrent cellulitis is common in patients with lymphedema. With compromised skin immunity, bacteria invade and spread with little resistance. If lymphedema is present, refer the patient for treatment after acute cellulitis resolves. If the patient already is being treated for lymphedema, suspend manual lymphatic drainage and compression until acute cellulitis resolves.

The most common disorders mistaken for lower-limb cellulitis are venous dermatitis, lipodermatosclerosis, irritant dermatitis, and lymphedema. It also may be mistaken for deep vein thrombosis (DVT) or dependent rubor. Rule out DVT using venous duplex ultrasound. Dependent rubor disappears with leg elevation, whereas cellulitic redness doesn’t.

Click here to view image of cellulitis.

Dependent rubor

Dependent rubor is a fiery to dusky-red coloration visible when the leg is in a dependent position but not when it’s elevated above the heart. The underlying cause is peripheral arterial disease (PAD), so the extremity is cool to the touch. To test for dependent rubor, position the patient supine and elevate the legs 60 degrees for 1 minute; then examine sole color. PAD causes the soles to change from pink to pale in fair-skinned people and to gray or ashen in dark-skinned people. The faster the pallor appears, the worse the PAD. Pallor within 25 seconds of leg elevation indicates severe occlusive disease, which warrants further evaluation for potential revascularization.

Next, observe skin color changes with the patient in a sitting position. Normally, the foot and leg should remain pink with elevation and dependency. In PAD, the color changes from pale to pink and then progresses to purple-red or bright red. The longer dependent rubor takes to reappear, the worse the PAD. Rubor that appears in 25 to 40 seconds indicates severe ischemia. If rubor disappears quickly with elevation and returns in less than 25 seconds, consider the possibility that the patient has venous reflux, not PAD. In this case, pooled blood causing the rubor drains rapidly from the veins when the leg is elevated and regurgitates back into the tissues when the leg is dependent.

If you detect dependent rubor, obtain the ankle-brachial index (ABI) to confirm PAD. For moderate PAD (ABI of 0.5 to 0.79), refer the patient for a routine vascular specialist consultation. For severe PAD (ABI below 0.5), maintain dry, stable wound eschar and urgently refer the patient to a vascular specialist for potential revascularization.

Click here to view images and read a case study on dependent rubor.

Knowledge summary

“Reading” the common causes of leg redness helps you determine what’s causing your patient’s redness so you can provide effective treatment. Remember—chronic venous disease causes hemosiderin staining, lipodermatosclerosis, and venous dermatitis. Dermatitis is itchy and crusty; lipodermatosclerosis causes sclerosis and an inverted champagne-bottle appearance of the legs. Relieve inflammation and itching with topical corticosteroids and treat venous disease with compression and corrective surgery. Lymphedema causes chronic inflammation; treat with complete decongestive physiotherapy. Cellulitis is a spreading skin infection that’s acutely painful and hot; treat with antibiotics. PAD causes dependent rubor, which disappears with leg elevation.

Selected references
Abbade LP, Lastória S, Rollo Hde A. Venous ulcer: clinical characteristics and risk factors. Int J Dermatol. 2011;50(4):405-11.

Bailey E, Kroshinsky D. Cellulitis: diagnosis and management. Dermatol Ther. 2011;24(2):229-39.

Beasley A. Management of patients with cellulitis of the lower limb. Nurs Stand. 2011;26(11):50-5.

Bryant R, Nix D. Acute and Chronic Wounds:
Current Management Concepts. 4th ed. St. Louis, MO: Mosby; 2011.

Buttaro TM, Trybulski J, Polgar P, Sandberg-Cook, J. Primary Care: A Collaborative Practice. 4th ed. St. Louis, MO: Mosby; 2012.

Caggiati A, Rosi C, Casini A, et al. Skin iron deposition characterises lipodermatosclerosis and leg ulcer. Eur J Vasc Endovasc Surg. 2010;40(6):777-82.

David CV, Chira S, Eells SJ, et al. Diagnostic accuracy in patients admitted to hospitals with cellulitis. Dermatol Online J. 2011;17(3):1.

Dieter R, Dieter RA Jr, Dieter RA III. Venous and Lymphatic Diseases. New York, NY: McGraw-Hill; 2011.

Foeldi M. Földi’s Textbook of Lymphology: For Physicians and Lymphedema Therapists. 3rd ed. Mosby, Urban & Fischer; 2012.

Hirschmann JV, Raugi GJ. Lower limb cellulitis and its mimics: part I. Lower limb cellulitis. J Am Acad Dermatol. 2012;67(2):163.e1-12.

Hirschmann JV, Raugi GJ. Lower limb cellulitis and its mimics: part II. Conditions that simulate lower limb cellulitis. J Am Acad Dermatol. 2012;67(2):177.e1-9

Keller EC, Tomecki KJ, Alraies MC. Distinguishing cellulitis from its mimics. Cleve Clin J Med. 2012;79(8):547-52.

Krasner, DL, et al. Chronic Wound Care 5: A Clinical Source Book for Healthcare Professionals. (Kindle ed.). Malvern, PA: HMP Communications; 2012.

Nazarko L. Diagnosis and treatment of venous eczema. Br J Community Nurs. 2009;14(5):188-94.

O’Connell DG, O’Connell JK, Hinman MR. Special Tests of the Cardiopulmonary, Vascular, and Gastrointestinal Systems. Thorofare, NJ: Slack Incorporated; 2011.

Sussman C, Bates-Jensen B. Wound Care: A Collaborative Practice Manual for Health Professionals. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2012.

Uzun G, Mutluoglu M. Images in clinical medicine. Dependent rubor. N Engl J Med. 2011;364(26):e56.

Robyn Bjork is a physical therapist, a certified wound specialist, and a certified lymphedema therapist. She is also chief executive officer of the International Lymphedema and Wound Care Training Institute, a clinical instructor, and an international podoconiosis specialist.

Is your wound-cleansing practice up to date?

By Donna Sardina, RN, MHA, WCC, CWCMS, DWC, OMS

With so much focus on dressing choices, it’s easy to forget the importance of wound cleansing. Cleaning a wound removes loose debris and planktonic (free-floating) bacteria, provides protection to promote an optimal environment for healing, and facilitates wound assessment by optimizing visualization of the wound. You should clean a wound every time you change a dressing, unless it’s contraindicated.

Here’s a review of how to choose and use a wound cleanser so you can see if your practice is up to date.

Choosing a wound cleanser

The ideal wound cleanser is hypoallergenic, nontoxic to viable tissue, readily available, cost effective, and stable. The wound cleanser should also:

• be effective in the presence of organic material, such as blood, slough, or necrotic tissue
• reduce the number of microorganisms that form on the surface of the wound
• have a delivery force less than 15 pounds per square inch.

Common wound cleansers

Below are common types of wound cleansers:

Normal saline solution. Normal saline solution is the preferred cleansing agent because as an isotonic solution, it doesn’t interfere with the normal healing process. It’s also cost effective and available in many different formats, including unit dose, half liters, liters, and spray bottles.
Commercial cleansers. Ingredients in commercial cleansers may include surfactants, wetting agents, moisturizers, and/or antimicrobials.

  • Surfactants are agents that facilitate removal of wound contaminants. Each surfactant molecule has a hydrophilic (water-loving) head that is attracted to water molecules and a hydrophobic (water-hating) tail that repels water and simultaneously attaches itself to wound contaminants, oils, or grease.

These opposing forces loosen the particles and suspend them in the water.

Skin cleansers. Skin cleansers are
formulated to remove fecal matter, so they should never be used on open wounds, as they tend to be stronger than a wound cleanser and toxic to wound tissues.
Lactated Ringer’s solution. Lactated Ringer’s solution provides sodium, potassium, and calcium chloride to the wound, while safely cleaning it and avoiding damage to viable cells. Be careful when the solution is used for continuous irrigation or allowed to dwell inside body cavities; otherwise the solution could be absorbed into the bloodstream, leading to circulatory overload.
Potable (drinkable) tap water. Potable tap water can be used if there is no other alternative. Check the quality of the water source. Advantages of tap water for wound cleansing are efficiency, cost effectiveness, and accessibility. However, use normal saline solution instead of water for wounds with exposed bone or tendon.

Click here to see examples of wound cleansers.

How to clean a wound

Before you start, make sure the cleansing solution is at room temperature or slighter warmer. It can take up to 40 minutes after cleaning for a wound to regain its original temperature, and up to 3 hours for miotic cell division and leukocytic activity to return to normal.

Once the solution is warm, wash your hands and put on gloves.

View a video on wound cleaning

Manual cleansing technique
For a linear wound or incision:
1. Pour irrigation solution into the irrigation tray. Moisten clean 4″×4″ gauze pads in the solution; squeeze out excess.
2. Gently wipe the wound from top to bottom in one motion, starting directly over the wound.
3. Discard the used gauze pad.
4. Using a new moistened 4″×4″ gauze pad, repeat cleaning, using a gentle downward stroke parallel to the incision.
5. Repeat steps, working outward from the incision in lines parallel to the incision.
6. Remember to use a new 4″×4″ gauze pad for each downward stroke.
7. If needed, dry the wound, following the same procedure as for cleaning, using dry gauze pads.

For an open wound:
1. Pour the irrigation solution into the irrigation tray. Moisten 4″×4″ gauze pads in the solution; squeeze out excess.
2. Gently clean the wound in a full or half circle, beginning in the center and working toward the outside.
3. Use a new 4″×4″ gauze pad for each circle.
4. Clean at least 1 inch beyond the end of the new dressing or 2 inches beyond the wound margins if you aren’t applying a dressing.
5. If needed, dry the wound, using the same procedure as for cleaning. Gently pat the wound dry, using dry gauze pads.

Spray cleansers
1. Spray cleansers may be applied directly to the wound or sprayed onto clean 4″×4″ gauze pads and then applied to the wound.
2. Check your organization’s policy for required personal protective equipment (PPE). Generally, wound irrigation
that involves squirting, spraying, or pressure release of fluid will require the use of PPE (such as gloves, gown, and mask with eye shield) to prevent exposure to debris and airborne microorganisms.
3. Protect the environment, equipment, and other supplies from contamination from spray aerosolization by covering or removing the supplies.
4. Hold the spray bottle approximately
1 inch from the wound bed. Aim the nozzle at the wound and squeeze the bottle, directing the stream of cleanser along the base and sides of the wound.
5. Blot up excess moisture with a clean gauze pad.
6. Dry the surrounding skin.

Cleaning with a saline bullet
1. Position the patient so that the cleansing solution will flow by gravity from the upper end of the wound to the lower end.
2. Twist off the top.
3. Position the container at any angle required to access the area to be moistened or cleaned.
4. Apply firm pressure to the container to obtain the desired flow rate.
5. Blot up excess moisture with a clean gauze pad.
6. Dry the surrounding skin.

After you have finished cleaning the wound, dispose of the waste in a trash bag; then remove and discard your gloves and any other PPE you used.

Selected references

European Pressure Ulcer Advisory Panel and National Pressure Ulcer Advisory Panel. Treatment of pressure ulcers: Quick reference guide. Washington, DC: National Pressure Ulcer Advisory Panel; 2009.

Hess CT (ed.). Clinical Guide to Wound Care. 7th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2012.

Kosier B. Fundamentals of Nursing: Concepts, Process, and Practice. 6th ed. Upper Saddle River, NJ: Prentice-Hall, Inc; 2000.

Ovington LG. Hanging wet-to-dry dressings out to dry. Adv Skin Wound Care. 2002;15(2):79-84.

Wound Source. Wound cleansers. Accessed April 1, 2013.

Donna Sardina is Editor-in-Chief of Wound Care Advisor and cofounder of the Wound Care Education Institute in Plainfield, Illinois.

When you can’t rely on ABIs

By Robyn Bjork, MPT, CWS, WCC, CLT-LANA

One of the worst fears of a wound care clinician is inadvertently compressing a leg with critical limb ischemia—a condition marked by barely enough blood flow to sustain tissue life. Compression (as well as infection or injury) could lead to necrosis, the need for amputation, or even death. The gold standard of practice is to obtain an ankle-brachial index (ABI) before applying compression. However, recent research and expert opinion indicate an elevated or normal ABI is deceptive in patients with advanced diabetes. What’s worse, in the diabetic foot, skin may die from chronic capillary ischemia even when total blood perfusion is normal. For information on how to perform an ABI and interpret results, click on this link.

This article explains why ABIs can be deceptive when considering the safety of compression and wound-healing potential in diabetic patients. As a wound care clinician, you need to stay alert for both falsely elevated and false-normal ABIs—and when these occur, suspect underlying peripheral artery disease (PAD).

Falsely elevated ABIs

Most wound care clinicians are familiar with a falsely elevated ABI. But do you understand what it means? ABI compares blood pressure measured at the ankle with blood pressure measured at the arm. Traditionally, an ABI of 1.3 or more has been deemed falsely elevated. But a 2011 guideline from the American College of Cardiology and the American Heart Association raised the false-elevation threshold to 1.4.
Falsely elevated ABI stems from calcification of the arterial wall and is common in patients with diabetes. Yet such calcification doesn’t automatically indicate plaque in the lumen of that artery; nor does a normal ABI indicate absence of plaque. A 2008 study of 1,762 patients found atherosclerotic plaque in 62% of those with falsely elevated ABIs, whereas the other subjects had normal blood flow. PAD was significantly more prevalent in patients with the clinical indicators of resting pain, ulcers, or gangrene. Also, PAD risk was 10 times higher in patients with chronic renal failure, three times higher in those with coronary artery disease, and five times higher in those with a history of smoking. Therefore, these concurrent diagnoses and clinical indicators can serve as distinguishing factors when arterial calcification obscures underlying PAD.

Download Ankle-brachial index tool

False-normal ABIs

False-normal ABIs are more problematic than falsely elevated ABIs. An otherwise diseased and occluded artery may calcify just enough to raise the ABI to a normal range before reaching falsely elevated levels. Therefore, a normal ABI (from 1.0 to 1.3) isn’t sufficient to rule out PAD, according to a 2011 study.

In calculating ABI, the higher measurment of the dorsalis pedis and posterior tibial arteries is used. This in itself can lead to false-normal ABIs in diabetic patients. Diabetes commonly causes segmental arterial disease, in which one artery may be occluded while the other isn’t. Therefore, blood supply to one area of the foot may be ischemic while blood supply to another is patent. If the more patent artery is used to calculate ABI, blood flow to the limb could appear normal even if significant occlusion and ischemia are present.

In a 2012 study, 8 of 30 legs with diabetic gangrene were found to have PAD, even though the patients’ ABIs were normal. In one shocking case, a 69-year-old man had a normal ABI of 0.99, yet his angiogram showed complete occlusion of the distal peroneal and distal posterior tibial arteries and near-total occlusion of the anterior tibial artery.

Alternative tests for patients with falsely elevated ABI

Because the smaller arteries of the toes are less likely to become calcified, a toe brachial index (TBI) typically is used to detect PAD in patients with falsely elevated ABIs.

• TBI above 0.7 is normal.
• TBI below 0.64 indicates PAD.
• TBI of 0.64 to 0.7 is borderline.

However, a normal TBI doesn’t necessarily mean blood flow is sufficient to promote healing of diabetic foot ulcers. TBI and total blood perfusion can be normal in the diabetic foot even if the skin has chronic ischemia. This condition (possibly caused by abnormal autonomic innervation of the vessels) occurs when blood is routed through arteriovenous shunts, bypassing capillaries. Because blood fails to deliver oxygen and nutrients via capillaries, the skin becomes chronically ischemic and wounds fail to heal. Keep this in mind when interpreting ABI and TBI results, because it may help reconcile discrepancies between what we see in wound healing and what seems like good blood flow in patients with diabetes.

View: TBI exam with PPG pressure

Transcutaneous oxygen pressure measurements

Unlike TBI, transcutaneous oxygen pressure measurements (TcPo2) indicate the wound-healing potential of diabetic foot ulcers. (However, TcPo2 testing is less readily available than TBI.) Sensors are placed on the skin around the wound to determine actual capillary perfusion via oxygen delivery to the skin.
• TcPo2 above 40 mm Hg indicates wound-healing potential.
• TcPo2 of 20 to 30 mm Hg predicts chronic wound-healing complications.
• TcPo2 below 20 mm Hg signals critical limb ischemia and the possible need for amputation.

TcPo2 is used widely in hyperbaric oxygen therapy for patients with wounds and is gaining wider use in predicting potential candidates for this therapy.

View: hyperbaric oxygen therapy

When you must measure TcPo2

When a patient’s ABI is falsely elevated, standard practice is to obtain a TBI. But a normal TBI isn’t definitive proof of adequate blood flow through the capillaries. When wound healing doesn’t correspond with apparently sufficient blood flow in the diabetic foot, the patient may have arteriovenous shunting and chronic capillary ischemia. In this case, TcPo2 measurements can help determine actual capillary perfusion and wound-healing potential.

Selected references

Aboyans V, Ho E, Denenberg JO, Ho LA, Natarajan L, Criqui MH. The association between elevated ankle systolic pressures and peripheral occlusive arterial disease in diabetic and nondiabetic subjects. J Vasc Surg. 2008;48(5):1197-203.

Aerden D, Massaad D, von Kemp K, et al. The ankle–brachial index and the diabetic foot: a troublesome marriage. Ann Vasc Surg. 2011;25(6):770-7.

Arsenault KA, McDonald J, Devereaux PJ, Thorlund K, Tittley JG, Whitlock RP. The use of transcutaneous oximetry to predict complications of chronic wound healing: a systematic review and meta-analysis. Wound Repair Regen. 2011 Nov;19(6):657-63. PubMed PMID: 22092835.

Bjork R. Bedside ankle-brachial index testing: time-saving tips. Wound Care Advisor. 2013;2(1):22-6.

Jörneskog G. Why critical limb ischemia criteria are not applicable to diabetic foot and what the consequences are. Scand J Surg. 2012;101(2):114-8.

Potier L, Abi Khalil C, Mohammedi K, Roussel R. Use and utility of ankle brachial index in patients with diabetes. Eur J Vasc Endovasc Surg. 2011; 41(1);110-6.

Park SC, Choi CY, Ha YI, Yang HE. Utility of toe-brachial index for diagnosis of peripheral artery disease. Arch Plast Surg. 2012;39(3):227-31.

Rooke TW, Hirsch AT, Misra S, et al; American College of Cardiology Foundation; American Heart Association Task Force; Society for Cardiovascular
Angiography and Interventions; Society of Interventional Radiology; Society for Vascular Medicine; Society for Vascular Surgery. 2011 ACCF/
AHA focused update of the guideline for the management of patients with peripheral artery disease (updating the 2005 guideline). Vasc Med. 2011; 16(6):452-76.

Singh PP, Abbott JD, Lombardero MS, et al; Bypass Angioplasty Revascularization Investigation 2 Diabetes Study Group. The prevalence and predictors of an abnormal ankle-brachial index in the Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI 2D) trial. Diabetes Care. 2011;34(2): 464-7

Suominen V, Rantanen T, Venermo M, Saarinen J, Salenius J. Prevalence and risk factors of PAD among patients with elevated ABI. Eur J Vasc Endovasc Surg. 2008;35(6):709-14.

Robyn Bjork is a physical therapist, certified wound specialist, and certified lymphedema therapist. She is also chief executive officer of the International Lymphedema and Wound Care Training Institute, a clinical instructor, and an international podoconiosis specialist.

Debridement options: BEAMS made easy


At one time or another, all wound care professionals encounter a chronic wound, defined as a wound that fails to heal in an orderly and timely manner. Globally, about 67 million people (1% to 5% of the world’s population) suffer chronic wounds. In the United States, chronic wounds affect 6.5 million people and cost more than $25 billion annually to treat.

The normal healing process is complex and can contribute to wound chronicity, which causes delayed healing. Local and systemic factors that can impede wound healing include lack of growth factors, a prolonged inflammatory response, abnormal matrix metalloproteinases, desiccation or decreased perfusion of the wound bed, wound hypoxia, infection or increased bacteria, aged cells, necrotic tissue, excessive or sustained pressure at the wound site, poor nutritional status, and certain medical conditions.

Autolysis, a natural process that occurs during wound healing, requires a moist vascular environment and a functioning immune system. During the inflammatory stage, neutrophils and macrophages digest and remove devitalized tissue debris. In chronic wounds, the autolysis process becomes overwhelmed by high levels of endotoxins released from damaged tissue and use of other debriedement methods are necessary.

Managing chronic wounds requires a holistic and comprehensive approach that considers all factors that can affect wound healing. Debridement remains a standard of care. Fundamental to proper wound healing, it can be done by surgical or nonsurgical methods. Debridement is integral to transforming the hostile environment of a chronic wound to a receptive environment that promotes healing. This article gives an overview of debridement techniques.

Why debridement is crucial to healing

Debridement refers to removal of dead, devitalized, or contaminated tissue or foreign material from a wound to reduce the number of microbes, toxins, and other substances that inhibit healing. Wound care clinicians must strive to achieve a stable, well-vascularized wound bed with minimal exudates. Presence of necrotic or compromised tissue is common in chronic nonhealing wounds. Devitalized tissue provides a growth medium for bacteria, increasing the infection risk. Also, it exudes endotoxins that inhibit migration of fibroblasts and keratinocytes to the wound. Necrotic tissue prevents formation of granulation tissue, wound contraction, and epithelialization.

While all components of wound bed preparation are crucial to an optimal wound-healing environment, both historical and current research indicates that removing exudates and devitalized tissue is essential. Many wounds with underlying pathologies that are untreatable or hard to treat require repeated debridement. (See Wound bed preparation by clicking the PDF icon above.)

Debridement methods can be selective or nonselective. Selective methods remove only devitalized tissue. Nonselective methods don’t differentiate between viable and nonviable tissue.

Debridement methods

Five major debridement methods exist, collectively known as BEAMS—an acronym made up of the first letters of each method. Selective methods include Biological/Biosurgical, Enzymatic, and Autolytic debridement. Nonselective methods include Mechanical and Sharp debridement. (See Choosing the right debridement method by clicking the PDF icon above.)

In some cases, more than one debridement method may be appropriate. In others, no method may be appropriate. For instance, stable eschar (eschar that’s dry, adherent, and intact with no erythema or fluctuance) on the heels serves as a natural covering and shouldn’t be removed. Another example is when healing isn’t an option, as when decreased blood flow from arterial insufficiency delays or impedes wound healing.

Biological/biosurgical debridement

Also known as maggot debridement, larval therapy, or larvae therapy, this method uses medicinal maggots to remove nonviable tissue. Sterile maggots are applied to the wound and covered by a dressing, which remains in place 1 to 3 days. Maggots have three actions:

View: a video for teaching patients about how maggot therapy works

  • They debride the wound by liquefying and digesting necrotic tissue.
  • They disinfect by killing and consuming bacteria.
  • They stimulate wound healing by promoting fibroblast growth.

Rapid and selective, biological debridement has proven effective in debriding chronic wounds and aiding limb salvage.

Enzymatic debridement

Enzymatic debridement involves application of collagenase ointment, which doesn’t harm healthy tissue. Fast acting and highly selective, it involves once-daily application of Santyl, a prescription product with no generic equivalent. This collagenase ointment works from the bottom up by selectively degrading (dissolving) collagen anchored to the wound. It breaks down only denatured collagen, leaving other proteins unaffected. Also, it doesn’t harm the collagen needed to form a scaffold, which is crucial for healing during the second phase of the wound healing cascade.

Enzymatic debridement is faster than autolytic debridement but more conservative than sharps surgical debridement. While Santyl is the only enzymatic debriding ointment available, other topical agents, such as Iodosorb, Oakin, and Mesalt, can promote debridement in the wound bed as well.

View: enzymatic debridement

Autolytic debridement

A natural physiologic process, autolytic debridement uses the body’s own enzymes to soften and break down necrotic tissue. White blood cells and enzymes enter the wound site during the inflammatory phase of healing, liquefying necrotic tissue. All wounds go through autolytic debridement to some extent. Products that support a moist wound environment can enhance this type of debridement.

Autolytic debridement is slow, selective, painless, and noninvasive. However, it’s not used for infected wounds and isn’t the best choice for wounds with a large amount of necrotic tissue.

Mechanical debridement

Mechanical debridement uses an external force great enough to separate or break the adhesive forces of necrotic tissue. This nonselective method, which can be painful, may involve a whirlpool, wet-to-dry dressings, scrubbing, and irrigation. Contraindications include epithelializing wounds and granulating wounds.

View: a video of administering low-pressure irrigation, a type of mechanical debridement

Sharp debridement

Sharp debridement refers to removal of necrotic devitalized tissue by sharp instruments, such as scalpels, scissors, lasers, curettes, or forceps. Nonselective, this method is the fastest debridement method. It can be either surgical or conservative.

  • Surgical debridement is a major procedure performed by a surgeon, another physician, or a podiatrist. It involves complete debridement and transforms a chronic wound to an acute wound. It produces rapid results but sacrifices some viable tissue. Pain control during and after the procedure is important and can be accomplished with analgesics. (See Sharp debridement by clicking the PDF icon above.)
  • Conservative debridement is done at the bedside by a trained clinical practitioner (such as a therapist or nurse, if the state practice act allows) or a physician. This minor procedure, which involves use of scalpels, scissors, or curettes, removes only devitalized tissue. It may require several sessions.

One type doesn’t fit all

Not all patients with necrotic wounds are candidates for every debridement method. To choose the most appropriate method, clinicians must understand the need for debridement and the available options. Keep in mind that in many cases, debridement isn’t a one-time intervention but must be repeated until healthy granulation tissue appears. Be sure to reassess the patient and wound regularly to ensure the best care.

Selected references
Benbow M. Available options for debridement. Independent Nurse. June 6, 2011.
. Accessed February 27, 2013.

European Wound Management Association. Wound Bed Preparation in Practice: Position Document. 2004.
. Accessed February 27, 2013.

Harris RJ. The nursing practice of conservative sharp wound debridement: promotion, education and proficiency. Wound Care Canada. 2009;7(1):22-30. Accessed February 27, 2013.

Hess CT. Checklist for factors affecting wound healing. Adv Skin Wound Care. 2011;24(4):192.

Hess CT. Clinical Guide to Skin and Wound Care. 7th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2012.

Moore M, Jensen P. Assessing the role and impact of enzymatic debridement. Podiatry Today. 2004;17(7). Accessed February 27, 2013.

Payne WG, Salas RE, Ko F, Naidu DK, Donate G, et al. Enzymatic debriding agents are safe in wounds with high bacterial bioburdens and stimulate healing. Eplasty. 2008;7;8:e17.

Sardina D. Wound bed preparation. In: Skin and wound management course workbook. Lake Geneva, WI: Wound Care Education Institute; August 2010;5:42-58.

Sen CK, Gordillo GM, Roy S, Kirsner R, Lambert L, et al. Human skin wounds: a major and snowballing threat to public health and the economy. Wound Repair Regen. 2009;17(6):763-71.

Singhal A, Reis ED, Kerstein MD. Options for nonsurgical debridement of necrotic wounds. Adv Skin Wound Care. 2001;14(2):96-100.

Cindy Broadus is a clinical instructor at the Wound Care Education Institute in Plainfield, Illinois.

Positive Stemmer’s sign yields a definitive lymphedema diagnosis in 10 seconds or less

By Robyn Bjork, MPT, CWS, WCC, CLT-LANA

In a busy wound clinic, quick and accurate differential diagnosis of edema is essential to appropriate treatment or referral for comprehensive care. According to a 2010 article in American Family Physician, 80% of lower extremity ulcers result from chronic venous insufficiency (CVI). In 2007, the German Bonn Vein Study found 100% of participants with active venous ulcers also had a positive Stemmer’s sign, indicating lymphedema.

Lymphedema secondary to CVI is called phlebolymphedema (“phlebo” means veins). Whereas CVI warrants compression therapy alone, phlebolymph-edema may require complete decongestive physiotherapy. To provide optimal care, a wound care clinician must differentiate between CVI and phlebolymphedema. Fortunately, differential diagnosis can be made in 10 seconds or less by performing Stemmer’s test.

How to perform Stemmer’s test

Stemmer’s test results in either a positive or negative sign for lymphedema. To perform it, try to pinch and lift a skinfold at the base of the second toe or middle finger. If you can pinch and lift the skin, Stemmer’s sign is negative. If you can’t, the sign is positive. False positives never occur. On the other hand, a negative test doesn’t rule out lymphedema.

Stemmer’s test is diagnostic for phlebolymphedema or any other form of lymphedema. Not all wound-care clinicians need to determine the type or underlying causes of lymphedema. A positive Stemmer’s sign means the patient has lymphedema and should be referred for further evaluation and treatment by a lymphedema specialist.

Understanding the pathophysiology behind the test

A 10-second test might seem too good to be true. Also, how can Stemmer’s sign never be falsely positive? The answers lie in understanding the pathophysiology behind the test.

The primary function of the lymphatic system is to recycle blood proteins. Half of plasma proteins leak into the interstitial space and are recovered by the lymphatic system each day. Think of them as delivery men carrying nutrients to cells. They deliver their packages and go back into the bloodstream via the lymphatics to make more deliveries. But when the lymphatic system is blocked or damaged, proteins accumulate in the tissues. This causes the pathologic changes that lead to a positive Stemmer’s sign.

Like butter turning rancid, proteins accumulating in the tissues become denatured; macrophages migrate to the area to digest them. In what resembles the wound-healing process, macrophages release interleukin 1, which activates fibroblasts to produce collagen. This normal cascade becomes pathologic as excessive collagen is produced and denatured proteins trigger chronic inflammation. This process causes thickened, dense, fibrotic skin.

Typically, chronic lymphedema progresses from the toes or fingers proximally. The thin skin of the dorsum of the foot or hand is the first area to show signs of thickening, which leads to a positive Stemmer’s sign. (See Positive Stemmer’s sign by clicking the PDF icon above.)

Clinical considerations and test modifications

Unlike protein-rich lymphedema, edema in a patient with CVI or congestive heart failure (CHF) is watery. Proteins continue to circulate through the lymphatic system and don’t accumulate in tissues. If your patient has only CVI, no swelling occurs in the toes, and Stemmer’s sign is negative. Hemosiderin staining, the classic sign of CVI, likely will occur in the lower legs. (See Negative Stemmer’s sign in a patient with CVI by clicking the PDF icon above.)

In contrast, a patient with CHF has swelling of the toes and dorsum of the foot. In this case, when performing the Stemmer’s test, allow sufficient time for pitting edema to displace. Then note skin texture and try to pinch a skinfold. Edema solely from CHF displaces slowly, and Stemmer’s sign is negative. If the sign is positive, it means the patient has both CHF and lymphedema.

What happens in phlebolymphedema

Phlebolymphedema refers to lymphedema caused by CVI—a disorder that leads to valvular failure of the veins and increased tissue edema. Normally, as skin stretches from edema, elastic fibers pull open the lymphatic capillaries via their attachments by anchoring filaments. However, extreme distention causes rupture of these filaments and shredding of lymphatic capillary walls. What’s more, lymphatic overloading to compensate for venous insufficiency can lead to valvular failure of lymphatic vessels. As lymphedema progresses, the skin thickens and becomes lumpy, and wartlike knobs or projections may develop. Called papillomatosis, this condition indicates advanced lymphedema. (See Phlebolymphedema.)

Sometimes localized lymphatic damage occurs, with skin changes arising only in affected areas such as periwound tissues. In this case, you can modify Stemmer’s test by assessing skin texture in affected areas.

Understanding localized periwound lymphedema and its treatment aids healing of chronic wounds. White blood cells use lymphatics to drag bacteria and toxins to lymph nodes, in turn triggering an immune response. As wound care clinicians, we are acutely aware of bacterial bioburden and its negative effect on wound healing. Without a continuous flow of lymph, the body’s natural ability to fight bacteria is compromised. Further, debris, dead cells, and other byproducts of wound healing—normally removed via the lymphatics—cause stagnation of the wound environment and slow wound healing.

What a negative sign may mean

As mentioned, a negative Stemmer’s sign doesn’t rule out lymphedema. For example, a malignant tumor may cause lymphedema proximally in a limb; because lymphedema onset is acute and swelling is worse proximally, Stemmer’s sign may be negative.

Useful screening tool

Stemmer’s sign is a useful tool for screening patients in the wound clinic and promotes recognition of many lymphedema cases that otherwise might go undiagnosed and untreated. (See Clinical wisdom: Stemmer’s sign by clicking the PDF icon above.) Remember that patients with CVI and chronic venous ulcers have a high prevalence of secondary lymphedema. Also keep in mind that while a positive Stemmer’s sign always indicates lymphedema, a negative test doesn’t exclude lymphedema. Refer lymphedema patients to a lymphedema specialist for further assessment and treatment.

Click here to download International Consensus: Best Practice for the Management of Lymphoedema.

Selected references
Brenner E, Putz D, Moriggl B. Stemmer’s (Kaposi-Stemmer-) sign—30 years later: case report and literature review. Phlebologie. 2007;36(6):320-324.

Collins L, Seraj S. Diagnosis and treatment of venous ulcers. Am Fam Physician. 2010;81(8): 989-996.

Farrow W. Phlebolymphedema–a common underdiagnosed and undertreated problem in the wound care clinic. J Am Col Certif Wound Spec. 2010;2(1):14-23.

Föeldi M. Földi’s Textbook of Lymphology: For Physicians and Lymphedema Therapists. 3rd ed. Urban & Fischer; 2012.

Lymphoedema Framework. Best Practice for the Management of Lymphoedema. International consensus. London: MEP Ltd; 2006.

Macdonald JM, Ryan TJ, eds. Lymphoedema and the chronic wound: the role of compression and other interventions. In: World Health Organization. Wound and Lymphoedema Management. 2010:63-84.

Nelzén O. Prevalence of venous leg ulcer: the importance of the data collecting method. Phlebolymphology. 2008;15(4):143-150.

O’Connell DG, O’Connell JK, Hinman MR. Special Tests of the Cardiopulmonary, Vascular, and Gastrointestinal Systems. Thorofare, NJ: Slack; 2010.

Pannier F, Hoffmann B, Stang A, Jöckel KH, Rabe E. Prevalence of Stemmer’s sign in the general population. Phlebologie. 2007;36(6):287-342.

Piller N. Phlebolymphoedema/chronic venous lymphatic insufficiency: an introduction to strategies for detection, differentiation and treatment. Phlebology. 2009;24(2):51-55.

Simonian SJ, Morgan CL, Tretbar LL, Blondeau B. Differential diagnosis of lymphedema. In: Tretbar LL, Morgan CL Lee BB, Simonian SJ, Blondeau B. Lymphedema: Diagnosis and Treatment. London: Springer-Verlag; 2008;12-20.

Photos used with permission from the International Lymphoedema Framework. The author provided the remaining photos.

Robyn Bjork is a physical therapist, certified wound specialist, and certified lymphedema therapist. She is also chief executive officer of the International Lymphedema and Wound Care Training Institute, a clinical instructor, and an international podoconiosis specialist.

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