Unna Boot

An Unna boot is a special dressing of inelastic gauze impregnated with zinc, glycerin, or calamine that becomes rigid when it dries. It is used for managing venous leg ulcers and lymphedema in patients who are ambulatory. When the patient walks, the rigid dressing restricts outward movement of the calf muscle, which directs the contraction force inward and improves the calf-muscle pumping action, thereby improving venous flow. An Unna boot does not provide compression and is contraindicated for arterial insufficiency.
(more…)

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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. (more…)

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Bedside ankle-brachial index testing: Time-saving tips

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

A hot flush of embarrassment creates a bead of sweat on my forehead. “I’ve got to get this measurement,” I plead to myself. One glance at the clock tells me this bedside ankle-brachial index (ABI) procedure has already taken more than 30 minutes. My stomach sinks as I realize I’ll have to abandon the test as inconclusive. (more…)

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Lymphedema 101 – Part 2: Treatment

By Steve Norton, CDT, CLT-LANA

Editor’s note: Part 1 of this series, published in the September-October issue, discussed lymphedema pathology and diagnosis. This article, Part 2, covers treatment.

Traditional treatment approaches

Traditionally, lymphedema treatment has been approached without a clear understanding of the underlying structure and function of lymphatic tissues. Ineffective traditional treatments include elevation, elastic garments, pneumatic pumps, surgery, diuretics, and benzopyrones (such as warfarin). Because many traditional treatments are still overused and some may be appropriate for limited use, it’s important for clinicians to understand these approaches.

Elevation

As a sole therapy for lymphedema, elevation of the affected part provides only short-lived results. Ever-increasing macromolecular wastes retain water against the effects of gravity. Increased interstitial colloid osmotic pressure must be addressed by interventions targeted at improving lymphatic function—not just a position change. Otherwise, lymphedema will progress. Furthermore, elevation alone is impractical, promotes deconditioning, and alters lifestyle for prolonged periods.

Elastic garments

Elastic garments prove inadequate because they attempt to treat lymphedema with compression alone. Medically correct garments are engineered with thoughtful attention to high-quality textiles and offer gradient support, which promotes proximal flow. However, without precise tissue stimulation leading to improved lymphangioactivity (lymph-vessel pulsation), macromolecular wastes can’t be removed.
Interstitial pressure increases caused by compression garments impede further fluid accumulation. When these garments are removed, the spontaneous girth increase causes an imprecise fit, and the garment rapidly leads to a countertherapeutic effect. Furthermore, compression garments don’t combat the osmotic forces generated by ever-increasing interstitial wastes. Except in patients diagnosed with stage 0 or stage 1 lymphedema, disease progression involving metaplasia ensues. Although elastic compression garments are a cornerstone of long-term management, they shouldn’t be used as a stand-alone treatment.

Pneumatic compression pump

Formerly, the pneumatic compression pump (PCP) was considered the standard of care for lymphedema. However, when inflated, the pump doesn’t increase the frequency of lymph-vessel contraction or enhance lymph capillary absorption. What’s more, accelerated fibrosis development and rapid tissue refilling occur when a PCP is removed. Also, PCP use disregards the ipsilateral territory of the excised regional nodes, effectively dumping fluid from the leg into the trunk. A PCP is appropriate only when nothing else is available, as it may worsen the patient’s condition.

Surgery

Surgical approaches to treating lymphedema involve either excisional (debulking) or microsurgical techniques. The most extensive surgical technique, the radical Charles procedure, completely debulks all involved tissue down to the muscle fascia. Split-thickness grafts are then harvested from excised skin and donor sites, and applied to the fascia to achieve so-called limb reduction.
Most debulking procedures have been applied to lower-extremity lymphedema and offer poor cosmetic results. Less radical surgeries favor long incisions, preserving the skin but excising subcutaneous edematous portions to reduce girth. Although less cosmetically alarming, these procedures effectively amputate the subcutaneous space where lymph vessels reside. Other surgical approaches are beyond the scope of this article.
Generally, surgery isn’t a good approach for any patient, as it’s linked to significant morbidity, such as skin necrosis, infection, and sensory changes. In the future, less invasive procedures may be available that yield significant improvement without these adverse effects.

Diuretics

Although diuretics are prescribed appropriately to address water-rich edemas of venous origin, they disregard the fact that lymphedema is a protein-rich edema. Long-term, high-dose diuretic therapy leads to treatment-resistant limbs, similar to those that have received intensive pneumatic compression.

Benzopyrones

Benzopyrones such as warfarin decrease swelling by combating protein accumulation in fluid. Such drugs have undergone clinical trials abroad. Their mechanism is to promote macrophage migration into interstitial fluid, as well as subsequent proteolysis. Due to significant risk of liver damage or failure, benzopyrones haven’t been approved for treating lymphedema.

Complete decongestive therapy: The current treatment approach

Currently, the gold standard for lymphedema treatment is complete decongestive therapy (CDT). Michael Foeldi and Etelka Foeldi, who originated this method, discovered a unique symbiotic relationship among five distinct modalities that addresses the challenges of lymphedema treatment. In 1989, CDT was brought to the United States by Robert Lerner and has become the mainstay of lymphedema treatment here.
CDT is a two-phase approach involving an intensive clinical effort followed by a semi-intensive home-care program geared toward autonomous management, stabilization, and continual improvement. It involves manual lymph drainage (MLD), compression bandaging, exercise, skin and nail hygiene, and self-care education. (See Phases of complete decongestive therapy by clicking the PDF icon above.)

Manual lymph drainage

A type of soft-tissue mobilization, MLD provides skin traction, stimulating superficial lymph vessels and nodes. Lymph capillaries contain large inter-endothelial inlets called swinging tips, akin to overlapping shingles. Each overlapping cell is tethered to the interstitial matrix by anchoring filaments, so that fluid increases cause immediate distention and lymph inflow. Manual skin traction using MLD promotes greater lymph fluid uptake by stretching these filamentous structures, opening the swinging tips.
MLD also provides extrinsic stimulation of the lymphangion (the segment of a lymph vessel between a distal and proximal valve), drawing fluid into the system at the capillary level and promoting flow at the vessel level toward regional lymph nodes. Usually, these segments contract and relax in a rhythmic fashion six times per minute. MLD triples this output to 18 or 20 times per minute, greatly enhancing systemic transport.
MLD requires intensive daily treatment sessions to strengthen collateral flow as a pathway to circumventing surgical or developmental lymphatic disruption. Treatment strategies further recruit more deeply situated lymphatics such as the thoracic duct, as well as lumbar trunks that empty at the juncture of the internal jugular and subclavian veins to improve global uptake. MLD thus stimulates deeper vessel angioactivity to help drain the superficial vessels that drain toward them.

Compression bandaging

Compression bandaging provides tissue support after MLD to prevent reflux, slow new fluid formation, and mechanically soften fibrotic areas. Bandaging techniques provide a high working pressure to harness the muscle and joint pumps as a propellant for lymph while resisting retrograde flow created by gravity and centrifugal forces during movement. Pure cotton materials coupled with specialized padding create a soft, castlike environment, which confines swollen tissues without constriction. By relying on high working pressure and low resting pressures to decrease limb swelling, this strategy achieves greater control over intensity (level of compression/pressure exerted), with little to no soft-tissue injury or discomfort.
The patient wears this bulky inelastic complex after each MLD treatment until the next day’s session to ensure limb-volume reduction in a stable, linear fashion. Once a plateau is reached, tissue stabilization and self-care education are the goals of additional sessions.

Exercise

Exercise always must be done with adequate support to counteract fluid formation. During the intensive CDT phase, limbs are bandaged to provide complete around-the-clock containment. Gentle exercises encourage blood flow into the muscle; during muscle contraction, this creates a favorable internal pressure that effectively squeezes the subcutaneous space between the bandage wall and muscle. Because every bandage strives to provide a gradient of support, fluid tends to drain proximally to the bandage—in most cases, to the trunk.

Skin and nail hygiene

Without intact, well-hydrated skin, cellulitic infections occur in many lymphedema patients whose immune response has been diminished by regional lymphadenectomy or inherited deficiencies. To prevent infection caused by avoidable external events, patients receive clear guidelines to reinforce appropriate behavior. As most cellulitis results from resident skin pathogens (streptococci and staphylococci), maintaining a low skin pH helps control colonization. Ways to avoid recurrent infections include maintaining an acid mantle on the skin using low-pH-formulated lotions and avoiding injury from daily tasks that may scratch, puncture, burn, or abrade the skin. Patients should receive lists of self-care precautions at the time of treatment.

Self-care education

Because lymphedema is a chronic condition, patients must receive self-care education for daily management to avoid lymphedema destabilization, which can lead to tissue saturation and subsequent skin changes. Therapists must provide patients with appropriate self-care tools and knowledge to maintain adequate treatment results. Teaching topics include how to apply and remove compression garments and bandages and how to exercise safely, preserve skin integrity, monitor for infection, and respond appropriately to infection and significant changes in limb mobility.

An underrecognized and mistreated problem

Lymphedema remains an underrecognized and mistreated condition, even though CDT yields safe, reliable results. Early detection, accurate staging, proper diagnosis, and appropriate treatment can slow the inevitable progression of lymphedema. Wound care specialists should adapt wound therapy to address not just the wound but the edematous environment responsible for delayed wound resolution.

Selected references
Al-Niaimi F, Cox N. Cellulitis and lymphedema: a vicious cycle. J Lymphoedema. 2009;4:38-42.

Browse N, Burnand KG, Mortimer PS. Diseases of the Lymphatics. London: Hodder Arnold; 2003.

Casley-Smith JR, Casley-Smith JR. Modern Treatment for Lymphoedema. 5th ed. The Lymphoedema Association of Australia; 1997.

Cooper R, White R. Cutaneous infections in lymphoedema. J Lymphoedema. 2009:4:44-8.

Foeldi M. Foeldi’s Textbook of Lymphology: For Physicians and Lymphedema Therapists. 3rd ed. St. Louis, MO: Mosby; 2012.

International Society of Lymphology. The diagnosis and treatment of peripheral lymphedema. Consensus Document of the International Society of Lymphology. Lymphology. 2009 Jun;42(2):51-60.

Leduc A, Bastin R, Bourgeois P. Lymphatic reabsorption of proteins and pressotherapies. Progress in Lymphology XI. 1988:591-2.

National Lymphedema Network Medical Advisory Committee. Position Statement: Lymphedema Risk Reduction Practices. Revised May 2012. http://www.lymphnet.org/pdfDocs/nlnriskreduction.pdf. Accessed September 5, 2012.

Pappas CJ, O’Donnell TF Jr. Long-term results of compression treatment for lymphedema. J Vasc Surg. 1992 Oct;16(4):555-62.

Whittlinger H. Textbook of Dr. Vodder’s Manual Lymphatic Drainage. Vol 1. 7th ed. New York, NY: Thieme; 2003.

Steve Norton is cofounder of Lymphedema & Wound Care Education and executive director of the Norton School of Lymphatic Therapy in Matawan, New Jersey.

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Clinical Notes

New wound-swabbing technique detects more bacteria

The new Essen Rotary swabbing technique takes a few seconds longer to perform than traditional techniques, but improves bacterial count accuracy in patients with chronic leg ulcers, according to a study published by Wounds International.
Evaluation of the Essen Rotary as a new technique for bacterial swabs: Results of a prospective controlled clinical investigation in 50 patients with chronic leg ulcers” reports that Essen Rotary detected significantly more bacteria compared to standard techniques and was the only one to identify five patients with methicillin-resistant Staphylococcus aureus (MRSA), compared to three detected by other techniques.
The Essen Rotary technique samples a larger surface area of the wound, which is beneficial for detecting MRSA.
“The Essen Rotary may become the new gold standard in routinely taken bacteriological swabs especially for MRSA screenings in patients with chronic leg ulcers,” the study authors write.

Reducing HbA1c by less than 1% cuts cardiovascular risk by 45% in patients with type 2 diabetes

A study presented at the American Diabetes Association 72nd Scientific Sessions found lowering HbA1c an average of 0.8% (from a mean of 7.8% to 7.0%, the treatment target) reduced the risk of cardiovascular death by 45% in patients with type
2 diabetes.
The absolute risk of mortality from a cardiovascular event was 9.9 events per 1,000 person-years in patients with decreasing HbA1c compared to 17.8 events in patients with stable or increasing HbA1c.
HbA1c reduction and risk of cardiovascular diseases in type 2 diabetes: An observational study from the Swedish NDR” examined data from 18,035 patients in the Swedish National Diabetes Register.

CMS revises hospital, nursing home comparison websites

The Centers for Medicare & Medicaid Services (CMS) has enhanced two websites designed to help the public make informed choices about their health care.
Hospital Compare and Nursing Home Compare now have better navigation and new comparison tools. The two sites include data on quality measures, such as frequency of hospital-acquired infections, and allow the user to compare hospitals on these measures.
Improvements include easy-to-use maps for locating hospitals, a new search function that enables the user to input the name of a hospital, and glossaries that are easier to understand. It’s now also possible to access the data on the sites through mobile applications.
CMS maintains the websites, which are helpful for anyone who wants to compare facilities, not just patients on Medicare or Medicaid.
For more information, read the article in Healthcare IT News.

IOM releases report on accelerating new drug and diagnostics development

The Institute of Medicine (IOM) released “Accelerating the development of new drugs and diagnostics: Maximizing the impact of the Cures Acceleration Network—Workshop Summary.” The report is a summary of a forum that brought together members of federal government agencies, the private sector, academia, and advocacy groups to explore options and opportunities in the implementation of Cures Acceleration Network (CAN). The newly developed CAN has the potential to stimulate widespread changes in the National Institutes of Health and drug development in general.

Focus on individualized care—not just reducing swelling—in lymphedema patients

As a result of two extensive literature reviews, a researcher at the University of Missouri found that emphasizing quality of life—not just reducing swelling—is important for patients with lymphedema. Many providers and insurance companies base treatment on the degree of edema, but the volume of fluid doesn’t always correspond with the patients’ discomfort. Instead, an individualized plan of care should be developed.
The researchers found that Complete Decongestive Therapy (CDT), a comprehensive approach for treating lymphedema that includes skin and nail care, exercise, manual lymphatic drainage, and compression, may be the best form of specialized lymphedema management. For more information about CDT, watch for the November/December issue of Wound Care Advisor.

Plague case in Oregon draws national attention

An article about a case of the plague in Oregon has appeared on Huffington Post. A welder contracted the disease as a result of unsuccessfully removing a mouse from a stray cat’s mouth. Part of his hands have, in the words of the article, “darkened to the color of charcoal.” Later tests confirmed the cat had the plague.
Plague cases are rare in the United States. According to the Centers for Disease Control and Prevention, an average of 7 human cases are reported each year, with a range of 1 to 17 cases. Antibiotics have significantly reduced morality. About half of cases occur in people ages 12 to 45.

Use of negative pressure wound therapy with skin grafts

Optimal use of negative pressure wound therapy for skin grafts,” published by International Wound Journal, reviews expert opinion and scientific evidence related to the use of negative pressure wound therapy with reticulated open-cell foam for securing split-thickness skin grafts.
The article covers wound preparation, treatment criteria and goals, economic value, and case studies. The authors conclude that the therapy has many benefits, but note that future studies are needed “to better measure the expanding treatment goals associated with graft care, including increased patient satisfaction, increased patience compliance and improved clinical outcomes.”

Mechanism for halting healing of venous ulcers identified

Researchers have identified that aberrantly expressed microRNAs inhibit healing of chronic venous ulcers, according to a study in The Journal of Biological Chemistry.
Six microRNAs were plentiful in 10 patients with chronic venous ulcers. The microRNAs target genes important in healing the ulcers. In an article about the study, one of the researchers said, “The more we know about the molecular mechanisms that contribute to [the development of venous ulcers], the more we can rationally develop both diagnostic tools and new therapies.”

Hemodialysis-related foot ulcers not limited to patients with diabetes

Both patients with diabetes and those without are at risk for hemodialysis-related foot ulcers, according to a study published by International Wound Journal.
Researchers assessed 57 patients for ulcer risk factors (peripheral neuropathy, peripheral arterial disease, and foot pathology, such as claw toes, hallux valgus, promi­nent metatarsal heads, corns, callosities, and nail pathologies) at baseline, and noted mortality 3 years later.
In all, 79% of patients had foot pathology at baseline, and 18% of patients without diabetes had peripheral neuropathy. Peripheral arterial disease was present in 45% of diabetic and 30% of nondiabetic patients. Nearly half (49%) of patients had two or more risk factors. Only 12% of patients had no risk factors. The presence of peripheral arterial disease and peripheral neuropathy increased risk of mortality.
The authors of “Prevalence of risk factors for foot ulceration in a general haemodialysis population” state that the high prevalence of risk factors in nondiabetic patients indicates that they are at risk for developing foot ulcers.

Study identifies risk factors for mortality from MRSA bacteremia

A study in Emerging Infectious Diseases found that older age, living in a nursing home, severe bacteremia, and organ impairment increase the risk of death from methicillin-resistant Staphylococcus aureus (MRSA) bacteremia.
Consultation with a specialist in infectious disease lowers the risk of death, and MRSA strain types weren’t associated with mortality.
Predicting risk for death from MRSA bacteremia” studied 699 incidents of blood infection from 603 patients who had MRSA bacteremia.

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Lymphedema 101 – Part 1: Understanding the pathology and diagnosis

By Steve Norton, CDT, CLT-LANA

Lymphedema is characterized by regional immune dysfunction, distorted limb contours, and such skin changes as papillomas, hyperkeratosis, and increased girth. The condition may involve the limbs, face, neck, trunk, and external genitals; its effects may include psychological distress. For optimal patient management, clinicians must understand what causes lymphedema and how it’s diagnosed and treated.
This two-part series provides an over­view of lymphedema. Part 1 covers etiology, pathology, and diagnosis. Part 2, which will appear in the November-
December issue, will focus on treatment.

Causes of lymphedema

Lymphedema occurs when protein-rich fluid accumulates in the interstitium due to impaired lymphatic function. Proteins, other macromolecular wastes, and water constitute lymphatic loads. These wastes rely on specially structured absorptive and transport structures in peripheral regions for their return to central circulation.
When lymph stasis prevails, inflammatory processes and lymphostatic fibrosis trigger tissue-density changes, further entrapping superficial vessels and accelerating mechanical insufficiency. (See Physiologic changes caused by lymphatic disruption by clicking the PDF icon above.)

Classifying lymphedema

Lymphedema can be primary or secondary. Primary lymphedema either is congenital (present at birth) or arises around puberty. In the vast majority of cases, it is associated with structural changes in the lymphatic system and isn’t associated with another disease or condition. Most structural changes (87%) manifest before age 35 and cause hypoplasia of vessels and nodes. Syndromes involving hyperplasia, node fibrosis, or aplasia also may occur, although they’re much less common. Dysplasia (either hypoplasia, hyperplasia, or aplasia) predisposes drainage regions to inadequate lymph collection, resulting in edema and secondary tissue changes, such as chronic inflammation and reactive fibrosis. Genetic variability in lymphatic constitution may explain why seemingly similar patients receiving the same surgical protocol have different lymphedema risks over time.
Secondary lymphedema stems from a significant insult to lymphatic tissues, as from lymphadenectomy, radiation therapy, trauma, infection, or cancer. It commonly results from direct trauma to regional nodes or vessel structures. Slow degradation of lymphatic function also occurs when adjacent tissues (such as superficial and deep veins) become diseased, when cellulitis occurs, or when accumulations
of adipose or radiation fibrosis mechanical-ly disrupt drainage of skin lymphatics.

Lymphedema stages

Lymphedema progresses in stages, which involve secondary connective-tissue disease combined with disturbed fluid update and transport. These conditions cause a universal and classic clinical picture.
•    Stage 0 (latency stage) is marked by reduced transport capacity and functional re­serve. The patient has no visible or palpable edema, but has such subjective complaints as heaviness, tightness, and waterlogged sensations.
•    In Stage 1 edema (reversible lymphedema), edema decreases with elevation. Pitting edema is present, but fibrosis is absent.
•    During Stage 2 (spontaneously irreversible lymphedema), lymphedema doesn’t resolve entirely, although it may fluctuate. Pitting is more pronounced and fibrosis is present.
•    Stage 3 (lymphostatic elephantiasis) is marked by dermal hardening, nonpitting edema, papillomas, hyperkeratosis, and in some cases, extreme girth.

Assessment and diagnosis

Diagnosing lymphedema can be challenging because edema may be associated with other diseases and disorders. For a summary of signs and symptoms, see Clinical findings in lymphedema by clicking the PDF icon above.

Discomfort and skin appearance

Lymphedema rarely causes pain because the skin accommodates gradual, insidious fluid accumulation. However, secondary orthopedic discomfort may result from increased weight of the affected limb due to deconditioning or decreased range of motion.
Because lymphedema usually progresses slowly, gravity and centrifugal forces pull fluids toward distal limb areas, causing an entrenched, stubborn pitting edema. Later, further valvular incompetence contributes to worsening distal edema in the fingers, toes, and dorsal regions of the hand and foot. Prominent lower-extremity structures, such as the malleolus, patella, tibia, anterior tibialis tendon, and Achilles tendon, become progressively less distinct. This creates a columnar limb appearance; the swollen limb has the same girth from distal to proximal aspects, unlike the natural cone shape of a normal limb.
Lymphatic failure doesn’t tax the venous system, so skin color remains normal. Blood supply remains patent, helping to prevent secondary ulcers.

Severity

Lymphedema severity correlates directly with such factors as onset of the condition and extent of cancer therapy, if given (number of nodes resected, number of positive nodes, and use of radiotherapy). Lymphedema may worsen with a greater number of infection episodes, weight gain, injury, diuretics, limb disuse, pneumatic compression therapy (when used for pure lymphedema), and ill-fitting compression garments. The single most important contributor to increasing lymphedema severity is lack of patient education, which can result in improper treatment or none at all.

Opportunistic infections

Lymphedema causes regional immune suppression and leads to an increase in opportunistic infections such as cellulitis. As skin integrity suffers, scaling and dryness allow resident skin pathogens (such as streptococci and staphylococci) to gain access through the defective skin barrier into protein-rich interstitial fluid, creating a medium favorable to bacterial colonization. Lymphocyte migration decreases, and dissected or irradiated nodal sites are slow to detect invaders. Furthermore, stagnant lymph promotes further delays in the immune response. Patients with opportunistic infections may exhibit high fever, local erythema, regional hypersensitivity or acute pain, flulike symptoms, and rapidly advancing “map-like” borders in the skin.

Differential diagnosis

Several methods can aid differential diagnosis.
Clinical findings. Lymphedema can be diagnosed from patient history, physical examination, palpation, and inspection. Trauma to lymph nodes (each of which governs a distinct body region) decreases the transport capacity of lymph formed in that region, in turn causing local swelling (lymphedema). Trauma to the axillary or inguinal lymph nodes, which exist on both the left and right of the body and in both the upper and lower regions, predisposes these quadrants to swelling. Therefore, if lymph nodes on only one side are damaged, lymphedema occurs only on that side of the body. Using the universal characteristics cited above as a guide, while ruling out cancer recurrence, acute deep vein thrombosis, or plasma protein abnormalities, yields sufficient data to form a diagnosis.
Imaging. Lymphography involves sub­cutaneous injection of a lymph vessel–
specific dye (Patent Blue V), followed by X-ray. Although it provides high-resolution images of lymphatic structures, this technique is invasive, painful, damaging to lymphatics, and potentially lethal—and therefore is no longer recommended.
Lymphangioscintigraphy (LAS) uses interdigital subcutaneous injection of protein-labeled radioisotopes, followed by
imaging at specific intervals to gather information about uptake and transport time. Images are hazy and false-negatives are common, so well-trained radiotherapists familiar with lymphology and lymphedema should administer and interpret the test. Also, experts don’t agree on standard criteria for LAS administration, so measures may not be similarly conclusive.
Limb-measuring instruments and methods. Serial measurement of affected limb circumference using a standard garment tape measure is the most widely accessible approach. Intra-rater reliability is comparable to that of currently used tools; however, these methods can’t be used for early detection, for screening, or when various raters are used to assess the same patient. Circumferences are measured at four points and are considered positive if a distance of 2 cm or more separates the involved from uninvolved extremity in comparison. Water displacement techniques for limb-volume calculation, although accurate, are impractical in most clinical settings and rarely used.
Various devices have been used to obtain measurements. For instance, the Perometer® uses optoelectronic volumetry. By scanning the limb with infrared beams circumferentially, the device accurately records girth at 4-mm intervals along the limb length and transmits these measurements to a computer. The Perometer is used mainly in the research setting. Preoperative and postoperative measurements at intervals can detect lymphedema early.
Impedimed XCA® uses bioelectrical
impedance to calculate ratios of intracellular to extracellular fluid. A weak electrical current is passed through affected and unaffected limbs, allowing comparison of results. Impedance is lower in edematous tissue, supporting an accurate diagnosis.

Next step: Treatment

Once a diagnosis is made, the next step is treatment. Part 2 of this series covers lymphedema treatment.

Selected references
Foeldi M. Foeldi’s Textbook of Lymphology: For Physicians and Lymphedema Therapists. 3rd ed. St. Louis, MO: Mosby; 2012.

Kubik S, Manestar M. Anatomy of the lymph capillaries and precollectors of the skin. In: Bollinger A, Partsch H, Wolfe JHN, eds. The Initial Lymphatics. Stuttgart: Thieme-Verlag; 1985:66-74.

Lee B, Andrade M, Bergan J, et al. Diagnosis and treatment of primary lymphedema. Consensus document of the International Union of Phlebology (IUP)—2009. Int Angiol. 2010 Oct;29(5):454-70.

Lerner R. Chronic lymphedema. In: Prasad H, Olsen ER, Sumpio BE, Chang JB, eds. Textbook of Angiology. Springer; 2000.

Mayrovitz HN. Assessing lymphedema by tissue indentation force and local tissue water. Lymphology. 2009 June;42(2):88-98

National Cancer Institute. Lymphedema (PDQ®): Health Professional Version. Updated June 30, 2011. www.cancer.gov/cancertopics/pdq/supportivecare/
lymphedema/healthprofessional
. Accessed September 5, 2012.

Northrup KA, Witte MH, Witte CL. Syndromic classification of hereditary lymphedema. Lymphology. 2003 Dec:36(4):162-89.

Olszewski WL. Lymph Stasis: Pathophysiology, Diagnosis and Treatment. CRC Press; 1991.

Pecking AP, Alberini JL, Wartski M, et al. Relationship between lymphoscintigraphy and clinical findings in lower limb lymphedema (LO): toward a comprehensive staging. Lymphology. 2008 Mar;41(1):1-10.

Stanton AW, Northfield JW, Holroyd, B, et al. Validation of an optoelectronic volumeter (Perometer). Lymphology. 1997 June;30(2):77-97

Weissleder H, Schuchhardt C. Lymphedema: Diagnosis and Therapy. 4th ed. Viavital Verlag GmbH; 2007.

Steve Norton is cofounder of Lymphedema & Wound Care Education and executive director of the Norton School of Lymphatic Therapy in Matawan, New Jersey.

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“We don’t have a Doppler”

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

Venous leg ulcers are the most common cause of lower extremity ulcers, affecting 1% of the U.S. population (approximately 3 million people). Annual treatment costs for venous disease in this country range from $1.9 to $3.5 billion.

The gold standard for venous ulcer treatment includes moist wound healing and compression therapy. But before compression wraps are applied, we must determine if adequate arterial blood flow exists—or consequences could be life-threatening.

Raise your hand if you know what ABI is. Now raise your hand if you routinely obtain ABIs for patients. I’ve been asking these questions at wound care seminars around the country for the last 10 years, and the answers are always the same:
Between 50% and 95% of the audience know what an ABI is, but only 1% to 2% say they perform the ABI test. My next question is “Why not?”

The ABI (ankle brachial index) is a non­invasive screening test performed with a handheld vascular Doppler and a blood pressure cuff. This simple test helps determine if you can safely apply compression therapy, aids diagnosis of peripheral arterial disease, and even helps monitor the efficacy of therapeutic interventions.

Numerous standard practice guidelines from various organizations recommend obtaining ABIs to determine arterial blood flow. These organizations include the American College of Cardiology, American Heart Association, American Diabetes Association, Society for Vascular Nursing, Wound Ostomy Continence Nurses, Society for Vascular Medicine, U.S. Preventive Services Task Force, and World Union of Wound Healing Societies.

Instructions for most compression therapy products include indications for Doppler ABI readings above 0.8. So if you don’t get an ABI reading, how can you safely apply these products? A report by Allie and colleagues found that more than 50% of lower extremity amputations occur without previous vascular testing of any type, including ABI.

So why aren’t more practitioners obtaining ABIs? The leading answer: “We don’t have a Doppler.” I understand the dilemma of not having equipment or the funds to get the equipment. But do we want to tell a patient who has just lost her leg, “Oh, sorry. We didn’t have a Doppler”?

It’s our responsibility and duty as WCCs, wound care experts, and health care clinicians to ensure we provide the highest standard of care for patients with venous leg ulcers. So communicate with management, explaining what you need and why you need it. Work with your medical supply company for an extended payment plan. Hold a fundraiser. Consider using the alternative Lanarkshire Oximetry Index procedure. Or send the patient to a wound clinic or other healthcare provider who can perform the test.

It’s time to step it up and take greater accountability—and to no longer use the excuse “We don’t have a Doppler.”

Donna Sardina, RN, MHA, WCC, CWCMS, DWC
Editor-in-Chief
Wound Care Advisor
Cofounder, Wound Care Education Institute
Plainfield, Illinois

Selected references
Allie DE, Hebert CJ, Lirtzman MD, et al. Critical limb ischemia: a global epidemic. A critical analysis of current treatment unmasks the clinical and economic costs of CLI. EuroIntervention. 2005; 1(1):75-84. http://www.ncbi.nlm.nih.gov/pubmed/
19758881
. Accessed June 4, 2012.

Lazarus GS, Cooper DM, Knighton DR, et al. Definitions and guidelines for assessment of wounds and evaluation of healing. Arch Dermatol. 1994; 130(4):489-493. http://www.ncbi.nlm.nih.gov/pubmed/8166487. Accessed June 4, 2012.

Mayfield JA, Reiber GE, Sanders LJ, Janisse D, Pogach LM. Preventive foot care in diabetes. Diabetes Care. 2004;27(suppl 1):S63-S64. doi:10.2337/diacare.27.2007.S63.
McGuckin M, Kerstein MD. Venous ulcers and the family physician. Adv Skin Wound Care. 1998;11(7): 344-346. http://journals.lww.com/aswcjournal/Abstract/1998/11000/Venous_Leg_Ulcers_and_the_Family_Physician.13.aspx. Accessed June 4, 2012.

Olin JW, Allie DE, Belkin M, et al. ACCF/AHA/ACR/SCAI/SIR/SVM/SVN/SVS 2010 performance measures for adults with peripheral artery disease: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Performance Measures, the American College of Radiology, the Society for Cardiac Angiography and Interventions, the Society for Interventional Radiology, the Society for Vascular Medicine, the Society for Vascular Nursing, and the Society for Vascular Surgery (Writing Committee to Develop Performance Measures for Peripheral Artery Disease). J Am Coll Cardiol. 2010;56(25):2147-2181. http://content.onlinejacc
.org/cgi/content/full/j.jacc.2010.08.606
. Accessed June 4, 2012.

O’Meara S, Al-Kurdi D, Ologun Y, Ovington LG. Antibiotics and antiseptics for venous leg ulcers. Cochrane Database Syst Rev. 2010;(1):CD003557. http://www.ncbi.nlm.nih.gov/pubmed/20091548. Accessed June 4, 2012.

Rooke TW, Hirsch AT, Misra S, et al; 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): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2011;58(19):2020-2045. http://
content.onlinejacc.org/cgi/content/full/j.jacc.2011.08.023v1
. Accessed June 4, 2012.

U.S. Preventive Services Task Force. Screening for peripheral arterial disease: brief evidence update. 2005. http://www.uspreventiveservicestaskforce.org/uspstf05/pad/padup.htm. Accessed June 4, 2012.

Valencia IC, Falabella A, Kirsner RS, Eaglstein WH. Chronic venous insufficiency and venous leg ulceration. J Am Acad Dermatol. 2001;44(3):401-421. http://www.ncbi.nlm.nih.gov/pubmed/11209109. Accessed June 4, 2012.

World Union of Wound Healing Societies. Principles of best practice:. Compression in venous leg ulcers: a consensus document. London: MEP Ltd; 2008. www.woundsinternational.com/pdf/content_25.pdf. Accessed June 4, 2012.

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Clinical Notes

Study finds ultrasound therapy improves venous ulcer healing

In a study of 10 venous ulcers not responding to treatment, the use of noncontact ultrasound significantly reduced the wound area over 4 weeks of treatment.

It has been unclear exactly how ultrasound achieves its positive results. The
authors of “A prospective pilot study of ultrasound therapy effectiveness in refractory venous leg ulcers,” an article published online on February 1 by the International Wound Journal, found that patients treated with ultrasound and compression therapy had reduced inflammatory cytokines and bacterial counts, but the reduction wasn’t statistically significant.

The study found another important benefit for patients-reduced pain.

Serum albumin is not a goodindicator of nutritional status

Traditionally the standard of practice for wound care patients has been to review albumin blood levels as a measure of nutritional status and the effect of nutritional interventions. But as noted in The Role of Nutrition in Pressure Ulcer Prevention and Treatment: National Pressure Ulcer Advisory Panel White Paper, recent studies show that hepatic proteins (albumin, trans­thyretin, and transferrin) correlate with the severity of an underlying disease, not nutritional status. Moreover, many factors can alter albumin levels even when protein intake is adequate, including infection, acute stress, surgery, cortisone excess, and hydration status.

For these reasons, the National Pressure Ulcer Advisory Panel (NPUAP) and the Academy of Nutrition and Dietetics (previously known as The American Dietetic Association) recommend against using serum proteins as a nutritional assessment tool. Evaluation of lab values is just one part of the nutritional assessment process and should be considered along with other factors such as ensuring that the patient receives what is prescribed; daily food/fluid intake; changes in weight status, diagnosis, and medications; and clinical improvement in the wound.

For more information read “Serum proteins as markers of malnutrition: What are we treating?” and “Albumin as an indicator of nutritional status: Professional refresher.”

A profile of outpatients with wounds

Wound care outcomes and associated cost among patients treated in US outpatient wound centers: Data from the US Wound Registry” a study using data from the US Wound Registry to determine outcomes and costs for outpatient wound care, found the mean patient age was 61.7 years, slightly more than half (52.3%) were male, most (71.3%) were white, and more than half (52.6%) were Medicare beneficiaries.

Other interesting findings:

  • The mean number of serious comorbid conditions was 1.8.
  • The most common comorbid conditions were obesity/overweight (71.3%), cardiovascular or peripheral vascular disease (51.3%), and diabetes (46.8%).
  • Nearly two-thirds (65.8%) of wounds healed, with an average healing time
    of 15 weeks.
  • In half of the wounds that healed, patients received only moist wound care and no advanced therapeutics.
  • The mean cost for wound healing was $3,927.

The authors of the article, published in March’s Wounds, analyzed 5,240 patients with 7,099 wounds in 59 hospital-based outpatient wound centers in 18 states over 5 years.

LOI index comparable to ABI for assessing PAD in patients with type 2 diabetes

The pilot study “Lanarkshire Oximetry Index as a diagnostic tool for peripheral arterial disease in type 2 diabetes,” published in Angiology, compared the gold standard ankle bra­chial index (ABI) to the Lanarkshire Oximetry Index (LOI) in 161 patients with type 2 diabetes. Researchers assessed the patients for peripheral artery disease (PAD, defined as ABI < 0.9) using both ABI and LOI.

Using a LOI cut-off value of 0.9., the sensitivity and specificity for PAD were 93.3% and 89.1%, respectively. The study concluded that LOI is a “potentially useful alternative diagnostic test for PAD” in patients with type 2 diabetes.

LOI is a noninvasive procedure similar to ABI; both indices indicate whether it’s safe to apply compression to the limb of a patient who has lower leg ulceration or venous hypertension. With LOI, a pulse oximeter is used in place of a hand-held Doppler to determine the index.

Start planning for World Diabetes Day

It’s not too early to begin planning for World Diabetes Day, November 14. Started by the World Health Organization (WHO) and the International Diabetes Federation (IDF), the day is designed to raise global awareness of diabetes.

Access materials, including posters, a campaign book, and the Word Diabetes Day Logo, from IDF’s website, which also has activity ideas.

WHO estimates that more than 346 million people worldwide have diabetes, and the number is expected to double by 2030. World Diabetes Day is celebrated on November 14 to mark the birthday of Frederick Banting who, along with Charles Best, was instrumental in the discovery of insulin in 1922.

Guidelines for PAD in patients with diabetes and foot ulceration published

February’s issue of Diabetes/Metabolism Research and Reviews includes “Specific guidelines for the diagnosis and treatment of peripheral arterial disease in a patient with diabetes and ulceration of the foot 2011,” which is based on two companion International Working Group on the Diabetic foot papers. The guidelines state that if a patient’s PAD is impairing wound healing, revascularization through bypass or endovascular technique must be considered except in a few cases such as severely frail patients. Limb salvage rates after revascularization procedures are about 80-85%, and there is ulcer healing in > 60% at 12 months.

Other points of particular interest to wound care professionals:

  • Patients with PAD and a foot infection are at high risk for major limb amputation, so should be treated as a “medical emergency”, preferably within 24 hours.
  • Half of patients with diabetes, a foot ulcer, and PAD die within 5 years because of higher cardiovascular morbidity and mortality. Cardiovascular risk management should include “support for cessation of smoking, treatment of hypertension, and prescription of a statin as well as low-dose aspirin or clopidrogel.

AHA statement focuses on PAD in women

A call to action: Women and peripheral artery disease: A scientific statement from the American Heart Association” summarizes evidence in this area and addresses risk-management issues. The statement notes that women (particularly black females) are more likely than men to experience graft failure of limb loss and calls for more research related to PAD and gender.

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Caring for chronic wounds: A knowledge update

By: Patricia A. Slachta, PhD, RN, ACNS-BC, CWOCN

Wound care has come a long way in just a few decades. With our expanded knowledge of wound healing and recent advances in treatment, we’re now able to assess wounds more accurately, recognize wound-related problems sooner, provide better interventions, and reduce morbidity.

To bring you up to date on current evidence-based wound management, this article focuses on assessing patients with chronic wounds, optimizing wound healing with effective wound-bed preparation, and selecting an appropriate dressing.

Wound chronicity and cause

Developing an appropriate plan of care hinges on conducting a thorough, accurate evaluation of both the patient and the wound. The first step is to determine whether the wound is acute or chronic.
•    A chronic wound is one that fails to heal within a reasonable time—usually
3 months.
•    An acute wound heals more quickly, causing minimal functional loss in the part of the body with the wound.
Identifying the cause of the wound also is essential. If the wound etiology is unknown, explore the patient’s medical history (including medication history) for clues to possible causes. Also review the patient’s history for conditions that could impede wound healing. (See What factors hamper healing? by clicking the PDF icon above)
Other important aspects of assessment include evaluating the patient’s nutritional status, quantifying the level of pain (if present), and gauging the patient’s self-care abilities.

General physical appearance

Conduct a general head-to-toe physical examination, focusing on the patient’s height, weight, and skin characteristics.

Height, weight, and weight trend

On admission, the patient’s height and weight should be measured to ensure appropriate nutritional and pharmacologic management. After a weight gain or loss, various factors may complicate wound healing. For instance, involuntary weight loss and protein-energy malnutrition may occur in both acute-care and long-term-care patients.

Especially note trends in your patient’s weight. For a long-term-care patient, a 5% weight loss over 30 days or a 10% loss over 180 days is considered involuntary. Arrange for a nutritional consult for any patient with an involuntary weight loss, as adequate nutrition is essential for general well-being and wound healing. (See A wound on the mend by clicking the PDF icon above.)

Skin color

Evaluate the patient’s skin color in light of ethnic background. If you note erythema—especially on a pressure point over a bony prominence—examine this area carefully for nonblanching erythema. Keep in mind that darkly pigmented skin doesn’t show such erythema and subsequent blanching, yet the patient may still be in jeopardy. So in dark-skinned patients, check for differences in skin color, temperature, or firmness compared to adjacent tissue; these differences may signify skin compromise.

Skin texture and turgor

Generally, healthy skin feels smooth and firm and has an even surface and good turgor (elasticity). To test turgor, gently grasp and pull up a fold of skin on a site such as the anterior chest below the clavicle. Does the skin return to place almost immediately after you release it, or does it stand up (“tent”)? Tenting indicates dehydration. But keep in mind that skin loses elasticity with age, so elderly patients normally have decreased turgor.

Skin temperature

With normal circulatory status, the skin is warm and its temperature is similar bilaterally. Areas of increased warmth or coolness suggest infection or compromised circulation. Be sure to check the temperature of skin surrounding the wound.

Wound assessment

Proper wound assessment can significantly influence patient outcome. Measure the wound carefully and document the condition of the wound bed. Remember that accurate descriptions are essential for guiding ongoing wound care. Repeat wound measurement and wound-bed assessment at least weekly, after the wound bed has been cleaned and debrided.

Keep in mind that assessing a chronic wound can be challenging. Wounds commonly have irregular shapes that can change quickly. Also, the multiple clinicians caring for the same patient may each describe the wound a bit differently.

Wound location

Note the precise anatomic location of the wound, as this can influence the wound care plan. A venous ulcer on the lower leg, for instance, requires different care than an arterial ulcer in the same site or a pressure ulcer on the ischium.

Circumference and depth

Use a paper or plastic measuring device to measure wound circumference and depth in centimeters (cm) or millimeters (mm). To promote accurate assessment of healing, be sure to use the same reference points each time you measure the wound.

You can use several methods to measure circumference. The most commonly used method of measurement is done in the head to toe direction. Measure the wound at its greatest length in that direction & measure the width at a 90 degree angle, at the widest point of the wound. Then multiply these two measurements (greatest length x greatest width) to obtain the total wound area. Although such linear measurements are imprecise, they yield gross information relative to wound healing when repeated over time.

Classify wound depth as partial thickness or full thickness.
•    Partial-thickness wounds are limited to the skin layers and don’t penetrate the dermis. They usually heal by reepithelialization, in which epidermal cells regenerate and cover the wound. Abrasions, lacerations, and blisters are examples of partial-thickness wounds.
•    Full-thickness wounds involve tissue loss below the dermis.
(Note: Pressure ulcers usually are classified by a four-stage system and diabetic foot ulcers by a grading system. Both systems are beyond this article’s scope.)
Measure and record wound depth based on the deepest area of tissue loss. To measure depth, gently place an appropriate device (such as a foam-tipped applicator) vertically in the deepest part of the wound, and mark the applicator at the patient’s skin level. Then measure from the end of the applicator to the mark to obtain depth.

Surrounding skin and tissue

Inspect for and document any erythema, edema, or ecchymosis within 4 cm of the wound edges, and reevaluate for these signs frequently. Because compromised skin near the wound is at risk for breakdown, preventive measures may be necessary.

Appearance of wound-bed tissue

Document viable tissue in the wound bed as granulation, epithelial, muscle, or subcutaneous tissue. Granulation tissue is connective tissue containing multiple small blood vessels, which aid rapid healing of the wound bed; appearing red or pink, it commonly looks shiny and granular. Epithelial tissue consists of regenerated epidermal cells across the wound bed; it may be shiny and silvery.

Check for nonviable tissue (also called necrotic, slough, or fibrin slough tissue), which may impede wound healing. It may vary in color from black or tan to yellow, and may adhere firmly or loosely to the wound bed. (See Picturing a necrotic wound by clicking the PDF icon above.)

Be sure to document the range of colors visible throughout the wound. Identify the color that covers the largest percentage of the wound bed. This color—and its significance—guide dressing selection.

Wound exudate

Document the amount, color, and odor of exudate (drainage) in the wound. Exudate with high protease levels and low growth factor levels may impede healing.

If the wound is covered by an occlusive dressing, assess exudate after the wound has been cleaned. Describe the amount of exudate as none, minimal, moderate, or heavy.

Describe exudate color as serous, serosanguineous, sanguineous, or purulent. Serous exudate is clear and watery, with no debris or blood present. Serosanguineous exudate is clear, watery, and tinged pink or pale red, denoting presence of blood. Sanguineous exudate is bloody, indicating active bleeding. Purulent exudate may range from yellow to green to brown or tan.

Describe wound odor as absent, faint, moderate, or strong. Note whether the odor is present only during dressing removal, if it disappears after the dressing is discarded, or if it permeates the room.

Wound edges

Wound edges indicate the epithelialization trend and suggest the possible cause and chronicity of the wound. The edges should attach to the wound bed. Edges that are rolled (a condition called epibole) indicate a chronic wound, in which epithelial cells are unable to adhere to a moist, healthy wound bed and can’t migrate across and resurface the wound.

Undermining and tracts

Gently probe around the wound edges and in the wound bed to check for undermining and tracts. Undermining, which may occur around the edges, presents as a space between the intact skin and wound bed (resembling a roof over part of the wound). It commonly results from shear forces in conjunction with sustained pressure. A tract, or tunnel, is a channel extending from one part of the wound through subcutaneous tissue or muscle to another part.

Measure the depth of a tract or undermining by inserting an appropriate device into the wound as far as it will go without forcing it. Then mark the skin on the outside where you can see or feel the applicator tip. Document your findings based on a clock face, with 12 o’clock representing the patient’s head and 6 o’clock denoting the feet. For instance, you might note “2.0-cm undermining from 7:00 to 9:00 position.”

Pain level

Ask the patient to quantify the level of pain caused by the wound, using the pain scale designated by your facility. Find out which pain-management techniques have relieved your patient’s pain in the past; as appropriate, incorporate these into a pain-management plan. Reevaluate the patient’s pain level regularly.

Wound-bed preparation

An evolving science, wound-bed preparation is crucial for minimizing or removing barriers to healing. The goal is to minimize factors that impair healing and maximize the effects of wound care. The key elements of wound-bed preparation are controlling bioburden and maintaining moisture balance. (For online resources on wound-bed preparation and other wound-care topics, see Where to get more information by clicking the PDF icon above.)

Controlling bioburden

Necrotic tissue and exudate harbor bacteria. A wound’s bioburden—the number of contaminating microbes—contributes to poor healing. All chronic wounds are considered contaminated or colonized, but not necessarily infected. In a colonized wound, healing is impeded as bacteria compete for nutrients; also, bacteria have harmful byproducts. To control bioburden, the wound must be cleaned and necrotic tissue must be debrided.

Cleaning the wound. Clean the wound before assessing it and applying a dressing. Use a noncytotoxic agent (typically, potable water, normal saline irrigating solution, or an appropriate wound-cleaning agent). Anti­septic solutions generally aren’t recommended for wound irrigation or dressings because they’re toxic to fibroblasts and other wound-repairing cells. If you must use such a solution, make sure it’s well diluted.

To ensure gentle cleaning or irrigation, pour solution over the wound bed or gently flush the wound with solution (using a 60-mL catheter-tip syringe) until the drainage clears. Know that pressurized irrigation techniques and whirlpool therapy aren’t recommended for wound cleaning because they disturb cell proliferation in the wound bed.

Debriding the wound. Debridement removes slough and necrotic tissue. Nonselective debridement techniques remove any type of tissue within the wound bed, whereas selective methods remove only necrotic tissue. (See Wound debridement techniques by clicking the PDF icon below.)

Maintaining moisture balance

To maintain moisture balance in the wound bed, you must manage exudate and keep the wound bed moist. The proper dressing (which may stay in place for days or longer) supports moist wound healing and exudate management. To minimize fluid pooling, a drain may be inserted into the wound. Negative-pressure wound therapy also may aid removal of excess exudate.

Choosing an appropriate dressing

The wound dressing plays a major role in maintaining moisture balance. Dressing selection is challenging because of the large number and variety of dressings available. Each product has specific actions, benefits, and drawbacks, so determining which dressing best suits the patient’s needs is a multifaceted process.

Dressing choice depends on such factors as wound type and appearance, exudate, presence or absence of pain, and required dressing change frequency. (See Dressings Options by clicking the PDF icon above.)

In a traditional dressing, gauze is applied in layers. The initial (contact) layer in the wound bed absorbs drainage and wicks it to the next layer; most often, this layer consists of woven cotton gauze or synthetic gauze. Remove the gauze gently, because it may be stuck to the wound or incision (especially if the gauze is cotton). For easier removal, moisten the dressing with normal saline solution to loosen it.

With a traditional dressing, the cover layer or secondary dressing is an abdominal pad with a “no-strike-through” layer next to the outside of the dressing. Be aware that wet-to-dry dressings are highly discouraged for their nonselective debriding effect and inability to provide a moist wound bed.

Reassess the patient’s wound at least weekly (after preparing the wound bed and dressing the wound) to determine healing progress. Keep in mind that wound-care management is a collaborative effort. Once you’ve assessed the patient, discuss your findings and subsequent wound management with other members of the team.

Wound care wisdom

Getting wiser about wound care will help your patients achieve good outcomes. Poor wound healing can be frustrating to patients, family members, and healthcare providers alike. Chronic wounds may necessitate lifestyle changes and lead to severe physical consequences ranging from infection to loss of function and even death. By performing careful assessment, tailoring patients’ wound care to wound etiology, and using evidence-based protocols to manage wounds, you can promote speedier wound healing, help lower morbidity, and improve quality of life.

Selected references
Bryant RA, Nix DP. Acute and Chronic Wounds: Current Management Concepts. 4th ed. St. Louis, MO: Mosby; 2011.

Gardener SE, Frantz R, Hillis SL, Park H, Scherubel M. Diagnostic validity of semiquantitative swab cultures. Wounds. 2007;(19)2:31-38.

Krasner DL, Rodeheaver GT, Sibbald RG. Chronic Wound Care: A Clinical Source Book for Healthcare Professionals. 4th ed. Wayne, PA: HMP Communications; 2007.
Langemo DK, Brown G. Skin fails too: acute, chronic, and end-stage skin failure. Adv Skin Wound Care. 2006;19(4):206-211.

Langemo DK, Anderson J, Hanson D, Hunter S, Thompson P. Measuring wound length, width, and area: which technique? Adv Skin Wound Care. 2008;21:42-45.

Milne C, Armand OC, Lassie M. A comparison of collagenase to hydrogel dressings in wound debridement. Wounds. 2010:22(11):270-274.

National Pressure Ulcer Advisory Panel and European Pressure Ulcer Advisory Panel. Prevention and Treatment of Pressure Ulcers: Clinical Practice Guideline. Washington, DC: National Pressure Ulcer Advisory Panel; 2009.

Ovington LG. Hanging wet-to-dry dressings out to dry. Adv Skin Wound Care. 2002;15(2):79-86.

Sibbald RG, Coutts P, Woo KY. Reduction of bacterial burden and pain in chronic wounds using a new polyhexamethylene biguanide antimicrobial foam dressing—clinical trial results. Adv Skin Wound Care. 2011;24(2):78-84.

Solway DR, Consalter M, Levinson DJ. Microbial cellulose wound dressing in the treatment of skin tears in the frail elderly. Wounds. 2010:22(1):17-19.

Wound Ostomy and Continence Nurses Society. Guideline for Prevention and Management of Pressure Ulcers. Mt. Laurel, NJ: Author; 2010

Patricia A. Slachta is a Clinical Nurse Specialist at The Queens Medical Center in Honolulu, Hawaii and an adjunct nursing instructor at the Technical College of the Lowcountry in Beaufort, South Carolina.

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Wound Healing Improves With New Bioactive Peptide Combo

bioactive peptide

By combining bioactive peptides, researchers have successfully stimulated wound healing in an in vitro and in vivo study. The studies, published in PLoS ONE, show that the combination of two peptides stimulates growth of blood vessels and promotes tissue re-growth of tissue. Further research into these peptides could potentially lead to new therapies for chronic and acute wounds.

The researchers evaluated a newly-created peptide, UN3, in pre-clinical models with the goal of simulating impaired wound healing as in patients suffering from peripheral vascular diseases or uncontrolled diabetes. They discovered that the peptide increased the development of blood vessel walls by 50%, with an 250% increase in blood vessel growth, and a 300% increase in cell migration in response to the injury. (more…)

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