Defusing lateral violence and abuse

By Julie Donley, MBA, BSN, RN

Renee asks her mentor, Susan, a question. Susan puts her hand near Renee’s face, gesturing for her to “Stop,” and says in a loud voice, “I told you the answer to that this morning. Why are you bothering me again?”

You’re working your shift with Amy, who’s in charge of the unit. She refuses to have a meaningful conversation with you, and ignores you or sighs impatiently when you try to share patient information with her.

These examples reflect lateral (horizontal) violence or abuse in the workplace, defined as violence or abuse occurring between workers. It includes both overt and covert acts of verbal and nonverbal aggression.
Chances are you’ve experienced or witnessed disruptive or inappropriate behavior by a peer or colleague. Intimidation, bullying, insults, humiliation, gossip, constant criticism, and angry outbursts are a few examples. More subtle examples include favoritism, unfair work assignments, inappropriate or unfair evaluations, sarcasm, snide comments, withholding information, holding a grudge, and belittling gestures.
Lateral violence in any form feels bad. It creates fear—and fear causes you to shrink and hold back from being your best. You can’t be productive in a fearful environment. Instead, you may feel violated, anxious, stressed, disrespected, and angry. A response of silence or ignoring the offender is common, but not ideal. Here are some better strategies.

Acknowledge your feelings

Admit to yourself that you’re hurting and something is wrong. Many victims dismiss or minimize the event, or even blame themselves. Resist that temptation. If it feels bad, it is bad. And if you allow the behavior, that person is sure to repeat it—not because she’s a bad person, but because she doesn’t realize her behavior is wrong. If you respond by acting surprised and assuming she doesn’t know what she’s doing and has no idea how her actions affect you, it will be easier to respond professionally and quickly.
If abuse or violence of any form is tolerated, it will continue. And the negative workplace culture will significantly affect the health and well-being of both staff and patients.

Respond appropriately

Here are the four keys to responding appropriately to lateral violence in the workplace—or anywhere else, for that matter.

Manage your emotions

Take a deep breath and pause. Don’t react right away. Self-awareness is crucial to managing your emotions and your responses. Take a time-out if you’ve become emotional. Use calming techniques, such as deep breathing, guided imagery, humor, or prayer. If you try to deal with the perpetrator while upset, you’re more likely to behave unprofessionally. Restrain yourself until you feel able to assert yourself in a professional manner.

Use empathy

Try to find out where the person’s coming from to help understand what’s going on with her that might have triggered her behavior. For example, a person may engage in negative behavior because she’s going through a divorce. (See It’s not about you by clicking the PDF icon above.)
Keep in mind that bad behavior reflects poor self-esteem and serves as a wall to keep people out. It’s also learned behavior. Someone who behaves badly has learned this behavior brings some kind of reward; otherwise, she wouldn’t do it. Perhaps the reward is attention or power. Whatever it is, she gains something from the behavior at others’ expense. Most likely, she’s unaware of this dynamic.
By using empathy, you not only learn more about the offender; that person learns more about herself. Show an interest in why she behaved that way by asking questions; for instance: “I’ve noticed you’ve been more impatient lately. Are you okay? Is there something going on I should know about?” When you’ve gained a clearer understanding of the person, you can set clear expectations and boundaries.

Assert your boundaries

Asserting your boundaries tells others what behaviors are unacceptable. When you assert your boundaries, you honor yourself. When something doesn’t feel right, tell the person directly that her behavior is inappropriate and ask her to stop it. If you say nothing, your silence implies the behavior is acceptable.
Tell the person directly that her behavior is inappropriate. Keep it simple and clear. Use such language as “This doesn’t work for me.” That way, you’re accepting responsibility for your feelings and you’re not making her wrong.
Asserting a boundary might sound like this: “Please lower your voice.” But be careful of the tone you use when making the request. You might ask, “Did you realize you were yelling?” She might not be aware of how angry or loud she is at that moment.

Make direct requests

Tell the person directly how you’d like to be treated or how you want the two of you to work together. Identify what you want instead of what you’re getting—and then ask for it. Don’t assume she knows how to treat you. Determine what your goals are and what you need from her to accomplish what’s expected. If you can, try to establish a mutual goal for you both to work on, such as a more productive relationship so there’s less tension. Clearly communicating your requests informs others of the behavior you expect.

A case of respect

You might not want to befriend people at work, and you don’t have to like them. But each of us deserves to be treated with respect. To get respect, you must give it. If it’s not reciprocated, ask for it. Treat everyone with respect.
If you experience lateral hostility or violence on the job, deal with it directly and immediately. If it happens again, deal with it directly again and report it to your supervisor.
No matter how professional and respectful you are or how assertively you express your boundaries and needs, if your work environment remains abusive and leadership doesn’t address it or do enough to change it, you may need to leave your job. Stop wasting time and energy trying to fix a problem no one else wants to fix. Life is too short, and you deserve better.

Selected references

American Nurses Association. Workplace violence. http://nursingworld.org/workplaceviolence. Accessed July 9, 2012.

Behaviors that undermine a culture of safety. The Joint Commission Sentinel Event Alert, Issue 40, July 9, 2008. www.jointcommission.org/assets/1/18/
SEA_40.PDF
. Accessed July 9, 2012.

Julie Donley is nurse manager for Devereux Children’s Behavioral Health Services in Pennsylvania. She has published hundreds of articles and just released her new book, Does Change Have to Be So H.A.R.D.? Visit www.JulieDonley.com to learn more.

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Clinician Resources

There’s an app for that! Here are a variety of medical apps that you might want to try. You can download them in the iTunes store, and the basic service is free.

Medscape

More than 1.4 million healthcare professionals use this app from WebMD, which includes:
• medical news
• clinical reference information, such as drugs and diseases
• medical calculators (not available for iPad).
The app is available for Android, iPad, and iPhone/iPod touch devices.

http://medscape.com

Pressure Wound Analyzer

Use this app to take a photo of a wound. The app segments the image into red, yellow, and black to help with ulcer classification. You can also use the app to track changes in the wound over time. The app is available for iPad and iPhone/iPod touch devices. Note: This is free for a limited time.

http://woundanalyzer.blogspot.com

AHRQ ePSS

The ePSS (Electronic Preventive Services Selector) app allows you to search and browse the U.S. Preventive Services Task Force recommendations on the Web or a mobile device. The app is from the U.S. Department of Health & Human Services and is available for Android, iPad, and iPhone/iPod touch devices.

http://epss.ahrq.gov

UMSkinCheck

This app from the University of Michigan Health System allows users to complete and store photographs of the skin. Features include:
• guidance on performing a skin cancer self-exam and full-body photographic survey
• tracking of detected skin lesions and moles for changes over time
• notifications/reminders to perform self-exams on a routine basis
• storage of photos for baseline comparisons during routine follow-up self-
exams
• informational videos and literature on skin cancer prevention and healthy skin as well as a skin cancer risk calculator function.
The app is available for iPad and iPhone/iPod touch devices.

http://uofmhealth.org/patient%20and%20visitor%20guide/my-skin-check-app

Glucose Buddy—Diabetes Logbook Manager w/syncing, blood pressure, weight tracking

This data storage utility app is perfect for your patients with diabetes who want all their information in one place. Users can manually enter their glucose results, carbohydrate consumption, insulin dosages, and activities, and then view the data in a free glucosebuddy.com online account. Another option is the ability to set reminders for when it’s time to check blood glucose.
The app is available for Android, iPad, and iPhone/iPod touch devices.

http://www.glucosebuddy.com

3M Health Care Pressure Ulcer Staging

Use this app to learn more about pressure ulcer staging. It includes information about 3M pressure ulcer products.
The app is available for iPad and iPhone/iPod touch devices.

https://itunes.apple.com/us/app/3m-health-care-pressure-ulcer/id454537520?mt=8

SACS™ Instrument

This evidence-based tool is helpful for assessing and classifying peristomal skin lesions. Click here for more information about the SACS Instrument.
The app is available for iPad and iPhone/iPod touch devices.

http://www.convatec.com/en/cvtus-homeus/cvt-home/0/home/0/393/0/default.html?
hwcr=flex

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Clinical Notes

NPUAP releases new position statement on exposed cartilage as Stage IV ulcer

The National Pressure Ulcer Advisory Panel (NPUAP) has released a new position statement, “Pressure ulcers with exposed cartilage are Stage IV pressure ulcers,” which states that pressure ulcers with exposed cartilage should be classified as Stage IV.
NPUAP notes that although the presence of “visible or palpable cartilage at the base of a pressure ulcer” wasn’t included in Stage IV terminology, cartilage “serves the same anatomical function as bone,” so it fits into the current Stage IV definition, “Full thickness tissue loss with exposed bone, tendon or muscle. Slough or eschar may be present on some parts of the wound bed. Often including undermining and tunneling.”

Medicare expenditures for diabetic foot care varies significantly by region

Medicare spending on patients with diabetes who have foot ulcers and lower extremity amputations varies significantly by region, according to a study in Journal of Diabetes and Its Complications, but more spending doesn’t significantly reduce 1-year mortality.
Geographic variation in Medicare spending and mortality for diabetic patients with foot ulcers and amputations” examined data from 682,887 patients with foot ulcers and 151,752 patients with lower extremity amputations.
Macrovascular complications in patients with foot ulcers were associated with higher spending, and these complications in patients with amputations were more common in regions with higher mortality rates.
Rates of hospital admission were associated with higher spending and increased mortality rates for patients with foot ulcers and amputations.
“Geographic variation in Medicare spending and mortality rates for diabetic patients with foot ulcers and amputations is associated with regional differences in the utilization of inpatient services and the prevalence of macrovascular complications,” the study concludes.

Patients who develop pressure ulcers in hospital more likely to die

Medicare patients who develop pressure ulcers in the hospital are more likely to die during the hospital stay, have longer lengths of stay, and to be readmitted within 30 days after discharge, according to a study of 51,842 patients in the Journal of the American Geriatrics Society.
Hospital-acquired pressure ulcers: results from the National Medicare Patient Safety Monitoring System Study” found that 4.5% of patients developed at least one new pressure ulcer during their hospitalization. Length of stay averaged 4.8 days for patients who didn’t develop a pressure ulcer, compared to 11.2 days for those with a new pressure ulcer.

Patients with diabetic foot ulcers may have higher risk of death

Patients with diabetes who have foot ulcers have a higher risk of cardiovascular disease and mortality, according to a meta-analysis in Diabetologia.
The association of ulceration of the foot with cardiovascular and all-cause mortality in patients with diabetes: a meta-analysis” notes that the more frequent occurrence of cardiovascular disease only partly explains the increased mortality rate. Other explanations may include the more advanced stage of diabetes associated with those who had foot ulcers.
A Drugs.com article about the study reported that “analysis of data from more than 17,000 diabetes patients in eight studies found that the more than 3,000 patients with a history of foot ulcers had an extra 58 deaths per 1,000 people each year than those without foot ulcers.”
The study authors emphasize the importance of screening patients with diabetes for foot ulcers so intervention can begin early, as well as lowering cardiovascular risk factors.
Access patient information on foot care from the American Diabetes Association.

Nurse’s innovation for ostomy patients could improve quality of life

An oncology nurse in Australia has developed StomaLife, an alternative to ostomy bags.
StomaLife is a ceramic appliance that eliminates the need for an ostomy bag. According to the StomaLife website, the appliance uses a magnetic implant technology that provides a “pushing force” from within the body outward in order to keep the site intact, while a second part is placed on the stoma site. A cotton gauze pad is used between the skin and the appliance to keep the site separated and to provide air circulation to the surrounding skin.
“The benefits of StomaLife to ostomy patients are continence all day, reduced skin irritation and infection, odour and sound control, leak prevention, waste material flow control and on-demand gas release,” says Saied Sabeti.
StomaLife still needs to be tested and is not yet being produced.

View: StomaLife video

New laser-activated bio-adhesive polymer aims to replace sutures

The Journal of Visualized Experiments, a peer-reviewed video journal, has published “A chitosan based, laser activated thin film surgical adhesive, ‘SurgiLux’: preparation and demonstration.”
SurgiLux is a laser-activated, bio-adhesive polymer that is chitosan-based. Chitosan is a polymer derived from chitin, which is found in fungal cell walls or in exoskeletons of crustaceans and insects. This molecular component allows SurgiLux to form low-energy bonds between the polymer and the desired tissue when it absorbs light.
The technology may be able to replace traditional sutures in the clinical setting. SurgiLux polymer can achieve a uniform seal when activated by a laser and has antimicrobial properties, which help prevent a wound from becoming infected. It also maintains a barrier between the tissue and its surroundings.
SurgiLux has been tested both in vitro and in vivo on a variety of tissues, including nerve, intestine, dura mater, and cornea.

Palliative care raises patient satisfaction and reduces costs

Kaiser Permanente’s home-based palliative care program increased patient satisfaction and decreased emergency department visits, inpatient admissions, and costs, according to an innovation profile in the Agency for Healthcare Research and Quality’s Innovations Exchange.
In-home palliative care allows more patients to die at home, leading to higher satisfaction and lower acute care utilization and costs” notes that the program uses an interdisciplinary team of providers to manage symptoms and pain, provide emotional and spiritual support, and educate patients and family members on an ongoing basis about changes in the patient’s condition.
Other components of the program include a 24-hour nurse call center, biweekly team meetings, and bereavement services to the family after the patient dies.

More research needed to determine efficacy of maggot debridement therapy

The efficacy of maggot debridement therapy (MDT)—a review of comparative clinical trials” concludes that “poor quality of the data used for evaluating the efficacy of MDT highlights the need for more and better designed investigations.”
The authors of the article in International Wound Journal reviewed three randomized clinical trials and five nonrandomized clinical trials evaluating the efficacy of sterile Lucilia sericata applied on ulcers.
The studies found that MDT was “significantly more effective than hydrogel or a mixture of conventional therapy modalities, including hydrocolloid, hydrogel and saline moistened gauze,” but the designs of the study were “suboptimal.”

Use tool to select correct antimicrobial dressing

Ensuring that the correct antimicrobial dressing is selected,” in Wounds International, emphasizes that dressing selection should be based on assessment of the microbial burden in the wound, the wound type, and the location and condition of the wound.
The article includes a checklist that may be helpful for deciding on the level of bacterial burden in a wound. The checklist is used to determine four levels of risk—colonized: at risk; localized infection; spreading infection; and systemic infection. Each level has a corresponding definition.
A table of antimicrobial dressings reviews the antimicrobial agent and dressing form, and the article ends with a case study.

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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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MRSA: What wound care professionals need to know

By Joseph G. Garner, MD, FIDSA, FSHEA

Staphylococcus aureus is one of the most feared human pathogens, causing a wide range of infections. Most wound care professionals can expect to frequently encounter patients with S. aureus infections. Soft-tissue infections caused by S. aureus include impetigo, cellulitis, and cutaneous abscesses, as well as such life-threatening processes as necrotizing fasciitis and pyomyositis (a hematogenous intramuscular abscess). Serious non-soft-tissue infections include septic arthritis, osteomyelitis, pneumonia, endocarditis, and sepsis.

Why is S. aureus such a nasty bug?

S. aureus produces various cellular and extracellular factors involved in the pathogenesis of infection. S. aureus protein A, an important surface protein, helps the organism resist phagocytosis. Also, S. aureus produces several cytotoxins and enzymes that contribute to infection spread and severity. In addition, some strains produce toxins (including toxic shock syndrome toxin-1) that function as superantigens—molecules that nonspecifically trigger release of large amounts of cytokines, leading to a sepsislike condition. Taken together, such factors combine to make S. aureus a dangerous pathogen.

MRSA emergence

When penicillin was introduced in the 1940s, virtually all S. aureus isolates were sensitive to that drug. But soon thereafter, S. aureus strains that produced a β-lactamase enzyme capable of inactivating penicillin became widespread. During the 1950s, outbreaks of penicillin-resistant S. aureus occurred in many U.S. hospitals. Introduction of penicillinase-resistant antibiotics, such as methicillin and oxacillin, temporarily restored the ability to treat all strains of this pathogen using penicillin antibiotics. The first strain of methicillin-resistant S. aureus (MRSA) was described in 1961 shortly after introduction of penicillinase-resistant antibiotics.
The mechanism of methicillin resistance involves a mutation in one of the bacterial cell-wall proteins to which penicillins must bind to kill the bacterium. This mutation renders the organism resistant to all penicillins and penems and almost all cephalosporins.
MRSA incidence has increased steadily to the point where it currently constitutes up to 60% of S. aureus isolates in many U.S. hospitals. These organisms commonly carry genetic material that makes them resistant to various non-β lactam antibiotics as well, leading some to suggest that the term MRSA should stand for multiply resistant S. aureus.
S. aureus has continued to mutate in the face of persistent antibiotic pressure. Vancomycin-intermediate S. aureus (VISA) was described in 1997; vancomycin-resistant S. aureus (VRSA), in 2003. Fortunately, these two strains remain rare and haven’t become established pathogens. (See Strains of antibiotic-resistant S. aureus by clicking the PDF icon above.)

Healthcare- versus community-acquired MRSA

Although MRSA initially arose and spread within healthcare settings (chiefly acute-care hospitals), a community-based variant was described in 1998. Called community-
acquired MRSA (CA-MRSA), this variant differs from healthcare-associated MRSA (HCA-MRSA) in more ways than the acquisition site. CA-MRSA occurs predominately in otherwise healthy children and young adults.
It most commonly presents as recurrent cutaneous abscesses, although life-threatening infections (such as necrotizing fasciitis and pneumonia) also have occurred. The pro­pensity to cause cutaneous abscesses isn’t fully understood but may relate partly to production of the Panton-Valentine toxin by many CA-MRSA isolates.
In contrast, HCA-MRSA afflicts mainly older patients, particularly those with chronic illnesses, including chronic wounds. It typically causes wound infections, urinary tract infections, pneumonia, and bacteremia.
Besides these epidemiologic and clinical differences, many CA-MRSA isolates derive from a single clone, known as clone USA 300, whereas HCA-MRSA is composed of multiple non-USA 300 clones. Finally, many CA-MRSA isolates are sensitive to non-β
lactam antibiotics, whereas most HCA-MRSA isolates resist multiple antibiotics. More recently, the distinction between CA-MRSA and HCA-MRSA has been blurred as evidence emerges that CA-MRSA now is being transmitted in healthcare settings as well as in the community.

S. aureus carrier state

Staphylococci are frequent colonizers of humans. Common colonization sites include the skin, anterior nares, axillae, and inguinal regions. Individuals can be colonized continuously or transiently, with nasal carriage rates varying from 20% to 40%. Most S. aureus infections result from the strain carried by the infected patient.
Three patterns of S. aureus carriage exist in humans:
• 20% of individuals are continuously colonized.
• 30% of individuals are intermittently colonized.
• 50% of individuals are never colonized.

The highest carriage rates occur in patients receiving frequent injections (such as insulin-dependent diabetics, hemodialysis patients, and I.V. drug users) and those with chronic skin conditions (for instance, psoriasis or eczema). In the general population, MRSA carriage rates have increased to 1% or 2%, with clinical consequences hinging on the colonizing strain (CA-MRSA versus HCA-MRSA) and host characteristics. The most consistent carriage site is the anterior nares, but many other sites may carry this pathogen, including the axillae, inguinal regions, and perirectal area.

MRSA treatment

Therapy for MRSA infection depends on the infection location and antibiotic sensitivity of the infecting strain.
Cutaneous abscesses are treated by incision and drainage; antibiotics play a secondary role to adequate drainage.
• Therapy for necrotizing fasciitis caused by MRSA involves aggressive debridement with removal of all necrotic tissue, plus adequate antibiotic therapy. Typically, patients require serial debridement followed by subsequent careful wound care, often with eventual skin grafting.
Pyomyositis  treatment entails drainage of the muscle abscess (which sometimes can be done with percutaneous tube placement instead of open drain­age), plus appropriate antibiotic therapy.

Vancomycin has been the mainstay of I.V. therapy for MRSA for decades, but some clinicians are concerned that its effectiveness may be declining due to slowly increasing minimum inhibitory concentrations (the minimum concentration of an
antibiotic needed to inhibit pathogen growth). Other parenteral options have emerged in the last few years. (See I.V. drugs used to treat MRSA by clicking the PDF icon above.) Several oral antibiotics also are available for MRSA treatment. (See Oral agents used to treat MRSA by clicking the PDF icon above.)
Knowing the antibiotic sensitivity pattern of the infecting MRSA strain is crucial to ensuring that the patient receives an appropriate antibiotic. Treatment duration for soft-
tissue infections usually ranges from 7 to 14 days, but bacteremia and bone or joint infections call for more prolonged therapy.

Efforts to eradicate MRSA carriage

Because the carrier state increases the risk of subsequent S. aureus infection, efforts have been made to eradicate carriage. Unfortunately, this has proven to be difficult. A commonly used regimen involves 5 days of twice-daily mupirocin nasal ointment with either chlorhexidine gluconate showers or immersion up to the neck in a dilute bleach solution. However, success in eliminating carriage is limited, although the bleach bath seems to improve eradication rates better than other modalities.

Controlling MRSA in hospitals

How best to control MRSA spread within hospitals is controversial. Some experts advocate an aggressive, “search and destroy” approach involving screening all patients for nasal carriage on admission and initiating contact precautions with subsequent decolonization efforts. Others focus on improving the overall level of hand hygiene and other general infection-control measures, arguing that nasal screening misses at least 20% of MRSA-colonized patients and thus gives an unwarranted sense of security.
Many hospitals use a mixed approach, screening patients suspected to be at high risk for MRSA carriage (such as those admitted from extended-care facilities or to the intensive care unit), while simultaneously trying to improve hand hygiene and general infection-control measures. Recent data suggest MRSA colonization and infection rates have stopped increasing and are beginning to decline.
MRSA is one of the most problematic pathogens encountered on a regular basis, and among the most dangerous pathogens we face. While some MRSA infections are relatively mild, many are serious or life-threatening. Severe soft-tissue infections, such as necrotizing fasciitis and pyomyositis, require surgical debridement or drainage, appropriate antibiotic therapy, and assistance from a wound-care professional to achieve optimal outcomes. n

Selected references
Calfee DP. The epidemiology, treatment and prevention of transmission of methicillin-resistant Staphylococcus aureus. J Infus Nurs. 2011 Nov-Dec;34(6):359-64.

DeLeo FR, Otto M, Kreiswirth BN, Chambers HF. Community-associated meticillin-resistant Staphylococcus aureus. Lancet. 2010 May 1;375(9725): 1557-68.

Dryden MS. Complicated skin and soft tissue infection. J Antimicrob Chemother. 2010 Nov;65 Suppl 3:iii35-44.

Ippolito G, Leone S, Lauria FN, et al. Methicillin-resistant Staphylococcus aureus: the superbug. Int J Infect Dis. 2010 Oct;14 Suppl 4:S7-11.

Landrum ML, Neumann C, Cook C, et al. Epidemiology of Staphylococcus aureus blood and skin and soft tissue infections in the US military health system, 2005-2010. JAMA. July 4;308:50-9.

Lee AS, Huttner B, Harbarth S. Control of methicillin-resistant Staphylococcus aureus. Infect Dis Clin North Am. 2011 Mar;25(1):155-79.

Moellering RC Jr. MRSA: the first half century. J Antimicrob Chemother. 2012 Jan;67(1):4-11.

Otter JA, French GL. Community-associated meticillin-resistant Staphylococcus aureus strains as a cause of healthcare-associated infection. J Hosp Infect. 2011 Nov:79(3):189-93.

Rivera AM, Boucher HW. Current concepts in antimicrobial therapy against select gram-positive organisms: methicillin-resistant Staphylococcus aureus, penicillin-resistant pneumococci, and vancomycin-resistant enterococci. Mayo Clin Proc. 2011 Dec;86(12):1230-43.

Simor AE. Staphylococcal decolonization: an effective strategy for prevention of infection? Lancet Infect Dis. 2011 Dec;11(12):952-62.

Joseph G. Garner is director of the infectious disease division and hospital epidemiologist at the Hospital of Central Connecticut and a professor of medicine at the University of Connecticut.

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Why not call it a pressure ulcer?

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

The most basic principle of healing a wound is to determine the cause—and then remove it. This is easier said than done, as many wounds have similar characteristics and we don’t always know all the facts leading up to the wound.
The process has been unnecessarily complicated by the recent pressure (no pun intended) to avoid at all costs calling a pressure ulcer a pressure ulcer. I use the term “unnecessarily” because it doesn’t matter what it’s called—a pressure ulcer, decubitus, “de-cube,” or bedsore—because in the end, the general idea is it’s bad news.
So what’s behind the desire to avoid calling it a pressure ulcer? First, a pressure ulcer has traditionally been equated to poor nursing care. As Florence Night­in­gale, the “Mother of Nursing,” wrote:
If he has a bedsore, it’s generally not the fault of the disease, but of the nursing.”
No one likes to feel that he or she gave poor care, and as more hospital complications data are available to the public, reports of complications such as pressure ulcers affect people’s perceptions—right or wrong—about the care a hospital delivers.
The second reason gets at the “at all costs” part of the desire. The recent attention given to Medicare’s “present on admission” rule and “never” events has
elevated pressure ulcers high up the chain of “no-no’s” and put the hospital at risk for nonreimbursement. And many private insurers have followed Medicare’s lead in denying coverage for pressure ulcers that occur in the hospital. Unfortunately, all the focus on reimbursement is beginning to challenge even the best wound care experts, who simply want to get the patient’s wound healed.
Pressure from upper management has resulted in experts trying to bargain and rationalize their way out of calling it what it is (a pressure ulcer), instead calling it a bruise, not a deep-tissue injury. Or saying, “This is a shearing ulcer, not a pressure ulcer.” Or, my favorite: “It’s not an ischial pressure ulcer but a diabetic ulcer because the patient is a diabetic.” Wound care experts are being forced to question and doubt themselves because money, quality assurance, and reputation are on the line when an in-house wound is labeled a pressure ulcer.
Like crime scene investigation, determining wound etiology requires us to gather all the facts. Once the facts are in, systematically comparing and contrasting the clinical findings aids differential identification to pin down the type of wound present. It’s important that we assess and investigate all the following when searching for the cause:
•    patient’s medical history
•    recent activities (such as surgery, extensive X-rays, or long emergency-
department waits)
•    comorbidities
•    specific wound characteristics, such as location, distribution, shape, wound bed, and surrounding skin.

Naming the wound is an important first step in intervening. If the wound is caused by pressure, call it a pressure ulcer and jump into action. Remove the cause, heal the wound, and prevent further breakdown. Don’t let yourself be influenced by those who aren’t experts in wound care.

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

Selected reference
Nightingale F. Notes on Nursing: What It Is, And What It Is Not. London: Harrison and Sons; 1859. http://ia600204.us.archive.org/17/items/notes
nursingnigh00nigh/notesnursingnigh00nigh.pdf.

Accessed August 30, 2012.

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Network effectively

By Joan C. Borgatti, MEd, RN

Sherry stands nervously in the doorway, watching several dozen people chat each other up. The sound of her heartbeat threatens to drown out the conversational din. For the people on the other side of the door, this is a networking event. But for Sherry, it seems like a swap meet of business cards.
If Sherry sounds like you, know that you’re not alone. For many people, networking means an awkward evening spent cradling a wine glass in one hand, thrusting a business card at someone with the other hand, and exchanging small talk.

“Hello. My name is…”

Networking is one of the most overused, misunderstood, and underestimated terms in the business world (and yes, that includes health care). Actually, networking is just a newish term for an activity that has been around for millennia. Savvy people have always seen the wisdom of seeking out others who can help them get ahead.
Simply put, networking is an information exchange, a forum for communicating your needs or agenda and, in return, listening and responding to others’ needs or agendas. Good networking requires emotional reciprocity, which means caring about the needs and agendas of the people you network with. Caring about others’ needs is what nurses do, so networking really shouldn’t be that difficult for a nurse.
Think of networking as a great opportunity to make yourself known, gather critical information, and meet people who can help you now and in the future. Through networking, you can make contacts that further your agenda—whether it’s to find
a mentor, get information on a program you’re interested in, change jobs, or advance from your current position.
Networking isn’t just who you know, but who knows you. If you listen to other networkers and give them the resources they seek (as by introducing them to key people or sharing valuable information), they’ll become grateful—and indebted—networking colleagues.

Set a networking goal

At a networking event, the idea isn’t to meet the greatest number of people possible in one evening. It’s to meet the “right” people—those who can help you realize your goal.
When approaching a networking situation, ask yourself, “What do I want this experience to lead to?” You’ll be much more effective if you have a laser-focused goal. The most successful networker isn’t the one who walks away with the most business cards. It’s the one who leaves with the contacts and information he or she had been seeking.

A tale of two networkers

To demonstrate this point, let’s take the case of two wound care specialists, Myrna and Doris—colleagues who’ve carpooled together to a meeting of their professional organization.
Myrna arrives with an agenda and a plan for the evening: She wants to develop a wound care speakers bureau to boost the community profile of staff at her facility. She seeks out several speakers, who give her valuable tips on how to market her expertise. She also shares her vision of a speakers bureau with attendees from other facilities—and is surprised by the support and tips they offer. She leaves the meeting with valuable information that can further her vision. On the way home, she jots down a reminder to send one of the people she met an article he might find helpful. She also makes notes about what she learned tonight, so she can follow up that week. Clearly, Myrna’s networking has been effective.
Doris, on the other hand, goes to the meeting unfocused. She meanders about the room speaking with a lot of attendees, and exchanges a few business cards. But the “Where-do-you-work?” conversations that ensue provide little insight. Although she enjoys the meeting somewhat, she has accomplished little. That’s understandable, as she set out with no goals. She might have been better off spending the night watching television.

Networking etiquette

To succeed at networking, learn networking etiquette. Rule #1: Turn off your cell phone—or at least put the ringer on vibrate. If you absolutely must take a phone call, discreetly leave the room.
More etiquette advice:
• Wear your name tag on your left lapel so you don’t block your name when shaking hands. If you fill out the name tag yourself, print clearly so your name and title are visible from about 5 feet away. That way, others won’t need to squint at your chest to read your name.
• Keep your handshake firm and friendly. Don’t hang on, and don’t pump! Remember to make eye contact, and smile.
• Keep breath mints handy. Networking usually takes place around drinks and food, and the first thing that greets a new contact shouldn’t be the garlic and onion dip.
• Keep your business cards handy (a business card holder is best), but don’t throw them at everyone you meet. Hand your business card to a contact so it’s right side up and facing that person. When someone hands you a business card, take a moment to look at it; then say thank you and carefully put it away. It’s disrespectful to deface a business card, so don’t write on the back of it.

What happens next?

Okay—you’ve set an agenda, attended the networking event without violating etiquette, and made some good contacts. Now what? This is where many people drop the ball. They fail to follow through on the contacts they make and the information they gain. They simply shove the contacts’ business cards into a Rolodex, where they will sit forgotten.
Instead of letting business cards collect dust, develop a system that helps you follow through with your contacts—whether it’s an electronic tool, a simple calendar notation, or a color-coded filing system. Jot down contact information on each
person you met, along with a summary
of your conversations, when you need to follow up, and so forth. Make the system work for you.
Next, follow through with appropriate communication. Send handwritten thank-you notes to the contacts who gave you valuable information or resources—for instance, those who introduced you to a key player or offered to make a phone call on your behalf. If possible, your note should mention how that information worked out for you. (See Seven steps to effective networking by clicking the PDf icon above.)
In the coming weeks, months, or years, keep these relationships alive and thriving by sending tips or information to each contact. If you see a newspaper article or Internet story about a topic a particular contact was interested in, send it to him or her. This shows you’re thinking about that person, and conveys your generosity and willingness to continue a reciprocal relationship.

Make it happen

Networking opportunities can happen anywhere. Don’t wait for them—create them. Pinpoint your goal, identify the key people who can help make it happen—and then network! It’s as simple as picking up the phone, sending an e-mail, or meeting over lunch. With a little effort, networking can be an enjoyable and valuable career resource.

Selected references
Ames G. Follow-up after the networking meeting and job interview. www.garyames.net/5-followupaftermeet.htm. Accessed August 15, 2012.

Wiklund P. Follow up: key to networking success. Approved Articles Website. www.approvedarticles.com/Article/Follow-up—Key-to-Networking-Success/5022. Accessed August 15, 2012.

Joan C. Borgatti, MEd, RN, is the owner of Borgatti Communications in Wellesley Hills, Mass., which provides writing, editing, and coaching services. You may e-mail her at [email protected].

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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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Mission possible: Getting Medicare reimbursement for wound care in acute-care settings

By Susan Reinach-Lannan, BSOM

In the current healthcare environment, wound care practitioners need to capitalize on all available reimbursement avenues for care delivery and wound care supplies and dressings. And when it comes to reimbursement, there’s one constant: The rules change constantly. Whether these changes always benefit the patient is questionable. Nowhere is this more evident than in acute-care settings. Clinicians constantly are challenged to make sure their patient-care decisions comply with current Medicare reimbursement guidelines. (And if you’re not sure about today’s guidelines, be prepared for the guidelines to change tomorrow.) (more…)

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Necrotizing fasciitis: Frightening disease, potentially grim prognosis

By Lydia Meyers, BSN, RN, CWCN

Necrotizing fasciitis (NF) results from an infection that attacks the fascia and subcutaneous tissues. The primary bacterial etiology is group A streptococcus, a facultative anaerobic bacterium. However, other bacteria may contribute. Sometimes called the “flesh-eating” disease because of the potentially devastating effect on the afflicted patient, NF can be monomicrobial or polymicrobial.

The four typical settings for NF are:

  • surgical bowel or abdominal trauma surgery
  • pressure ulcer and perianal abscess
  • injection sites (especially in drug users)
  • Bartholin abscess or minor vulvovaginal infection.

Because of the rapid course and ravaging nature of acute NF, clinicians must maintain a high index of suspicion if the patient has suggestive signs and symptoms. In 1990, puppeteer Jim Henson (best known for creating the Muppets) died from NF. At that time, little was known about the progression of group A streptococcal infection.
The disease can quickly cause death, so starting immediate treatment is even more crucial than confirming the diagnosis. Once the disease is suspected, antibiotics must be given immediately and the patient must be prepared for surgery at once. NF spreads rapidly, capable of progressing from a small lesion to death in days to weeks. Thus, delayed diagnosis increases the risk of death. Lack of knowledge about the disease and inability to recognize it promptly are the main reasons many victims die. This article can improve your knowledge base.

Overview

NF was discovered in 1871 by Joseph Jones, a Confederate Army surgeon. At that time, it was called hemolytic streptococcal gangrene, nonclostridial gas gangrene, nonclostridial crepitant cellulitis, necrotizing or gangrenous erysipelas, necrotizing cellulitis, bacterial synergistic gangrene, or synergistic necrotizing cellulitis.
NF involves the fascia, muscle compartments, or both. It can affect not only the muscle fascia but the superficial fascia. NF and cellulitis differ in the amount of tissue involved and extent of tissue involvement.
The most common areas of infection are the abdominal wall, perineum, and extremities. When NF affects the perineum and scrotum, it’s called Fournier gangrene, after the French dermatologist and virologist Alfred Jean Fournier.
The most common causes are trauma, surgery, and insect bites. The disease can affect persons of any age. Such comorbidities as diabetes, chronic renal failure, immunosuppressive therapy, hypertension, obesity, and malnutrition increase susceptibility.

Pathophysiology

NF falls into four classifications based on wound microbiology. Type 1, the most common, involves polymicrobial bacteria. Type 2 results from trauma and is associated with comorbidities. Type 3, rare in this country, stems from gram-negative marine bacteria. Type 4 is a fungal infection occurring mostly in immunocompromised persons. (See Comparing types of necrotizing fasciitis by clicking the PDF icon above.)

Disease progression

The four types of NF progress in a similar way. Bacteria secrete pyrogenic exotoxin A, which stimulates cytokines. These cyto­kines damage the endothelial lining; fluid then leaks into the extravascular space.
M proteins in streptococci and β-hemolytic streptococci exacerbate the immune reaction by inhibiting phagocytosis of polymorphonuclear leukocytes and normal neutrophil chemotaxis. As the immune reaction increases, blood vessels dilate, allowing toxins to leak through vessel walls, which in turn decreases blood flow. As the cascade continues, hypoxic conditions cause facultative aerobic organisms to grow and become anaerobic. These bacteria exacerbate destruction of surrounding cells and lead to release of carbon dioxide, water, hydrogen, nitrogen, hydrogen sulfide, and methane. As the infection continues to progress, toxins spread throughout the bloodstream and the patient becomes septic.

Assessment

Obtain the patient’s medical history and description of the wound. Determine when the changes first appeared and whether the affected area seemed to get worse recently.
In all NF types, patients commonly present with a small, painful area (possibly with entry marks) but no other signs or symptoms. The wound may appear as a bulla, cellulitis, or dermatitis, representing an infection developing in underlying tissues. The skin may have a wooden-hard feel as the infection progresses to the subcutaneous space and causes necrosis. The wound becomes discolored and necrotic; drainage is rare until surgical debridement begins. The patient quickly develops fever, chills, nausea, and vomiting. As NF progresses, bullae become dark purple with darkened edges; the patient grows disoriented and lethargic, and organ failure and respiratory failure
ensue. Without treatment, the patient dies.

Diagnosis

Diagnostic tests usually include magnetic resonance imaging, complete blood count with differential, comprehensive metabolic panel, and cultures. (See Diagnostic findings in necrotizing fasciitis by clicking the PDF icon above.)

Treatment

Immediate surgical debridement and broad-spectrum antibiotics are needed to stop the immune response to infection. Clindamycin, gentamicin, penicillin, or metronidazole may be given alone or in combination until culture results are available. Supportive care includes total parenteral nutrition for nutritional support, I.V. fluids, and oxygen. Limb amputation should be done only as a last resort.
Surgical debridement involves penetrating deep into the fascia and removing all necrotic tissue. After the first debridement, release of “dishwater fluid” may occur.
Administering hyperbaric oxygen therapy (HBOT) after the first debridement increases tissue oxygenation, thus reducing tissue destruction by anaerobic bacteria. During HBOT (usually given as a 90-minute treatment), the patient breathes 100% oxygen in an environment of increasing atmospheric pressure.
HBOT should be given in conjunction with surgical debridement (usually after each debridement) and should continue until necrotic tissue ceases and cell destruction stops. HBOT also promotes collagen synthesis and neoangiogenesis (new blood vessel growth), which boosts blood supply and oxygen to tissues.
Adverse effects of HBOT include ear pain, oxygen toxicity, and seizures. Ear pain can be minimized by swallowing or yawning. If the patient continues to have ear pain, ear tubes may be inserted by an otolaryngologist. During HBOT, air breaks (intervals of breathing room air) are important in controlling oxygen toxicity (the main cause of seizures).
Throughout the HBOT treatment period, wound dressings must be simple. Well-moistened gauze dressings and an abdominal pad provide good support. Once necrotic destruction occurs, dressings depend on wound size and the need to fill cavities. The patient may require a diverting colostomy, depending on wound
location and the amount of uncontrolled diarrhea. Blood glucose levels must be monitored before and after HBOT, as this treatment affects blood glucose.

Supportive care and follow-up treatment

During initial treatment, patients need supportive care and monitoring. Once they’re out of danger, begin teaching them how to prevent NF recurrences. Advise them to control blood glucose levels, keeping the glycated hemoglobin (HbA1c) level to 7% or less. Caution patients to keep needles capped until use and not to reuse needles. Instruct them to clean the skin thoroughly before blood glucose testing or insulin injection, and to use alcohol pads to clean the area afterward.
Before discharge, help arrange the patient’s aftercare, including home health care for wound management and teaching, social services to promote adjustment to lifestyle changes and financial concerns, and physical therapy to help rebuild strength and promote the return to optimal physical health. One helpful patient resource is the National Necrotizing Fasciitis Foundation. The Centers for Disease Control and Prevention section on necrotizing fasciitis includes “Common sense and great wound care are the best ways to prevent a bacterial skin infection.”
The life-threatening nature of NF, scarring caused by the disease, and in some cases the need for limb amputation can alter the patient’s attitude and viewpoint, so be sure to take a holistic approach when dealing with the patient and family. Today, NF has a much better survival rate than 2 decades ago when Jim Henson died. In my practice, I’ve seen four NF cases. Thanks to early identification, good wound care, and HBOT, these patients suffered only minimal damage.

Selected references

Boyer A, Vargas F, Coste F, et al. Influence of surgical treatment timing on mortality from necrotizing soft tissue infections requiring intensive care management. Intensive Care Med. 2009;35(5):847-853. doi:10.1007/s00134-008-1373-4.

Cain S. Necrotizing fasciitis: recognition and care. Practice Nurs. 2010;21(6):297-302.

Centers for Disease Control and Prevention. Notes from the field: fatal fungal soft-tissue infections after a tornado—Joplin, Missouri, 2011. MMWR. 2011;60(29):992.

Chamber AC, Leaper DJ. Role of oxygen in wound healing: a review of evidence. J Wound Care. 2011; 20(4):160-164.

Christophoros K, Achilleas K, Vasilia D, et al. Postraumatic zygomycotic necrotizing abdominal wall fasciitis with intraabdominal invasion in a non immunosuppressed patient. Internet J Surg. 2007;11(1). doi:10.5580/17a8.

Ecker K-W, Baars A, Topfer J, Frank J. Necrotizing fasciitis of the perineum and the abdominal wall-surgical approach. Europ J Trauma Emerg Surg. 2008;
34(3):219-228. doi:10.1007/s00068-008-8072-2.

Hunter J, Quarterman C, Waseem M, Wills A. Diagnosis and management of necrotizing fasciitis. Br J Hosp Med. 2011;72(7):391-395.

Magel DC. The nurse’s role in managing necrotizing fasciitis. AORN J. 2008;88(6):977-982.

Phanzu MD, Bafende AE, Imposo BB, Meyers WM, Portaels F. Under treated necrotizing fasciitis masquerading as ulcerated edematous Mycobacterium ulcerans infection (Buruli ulcer). Am J Trop Med Hyg. 2012;82(3):478-481.

Ruth-Sahd LA, Gonzales M. Multiple dimensions of caring for a patient with acute necrotizing fasciitis. Dimens Crit Care Nurs. 2006;25(1):15-21.

Stevens DL, Bisno AL, Chambers HF, et al; Infectious Diseases Society of America. Practice guidelines for the diagnosis and management of skin and soft-tissue infections. Clin Infect Dis. 2005;41(10):1373-1406.

Su YC, Chen HW, Hong YC, Chen CT, et al. Laboratory risk indicator for necrotizing fasciitis score and the outcomes. ANZ J Surg. 2008;78(11):968-972.

Taviloglu K, Yanar H. Necrotizing fasciitis: strategies for diagnosis and management. World J Emerg Surg. 2007;2:19.

Lydia Meyers is a medical reviewer for National Government Services in Castleton, Indiana, and a clinical liaison at CTI Nutrition in Indianapolis. She has 11 years of wound care experience in nursing homes, wound clinics, and home health.

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Get positive results with negative-pressure wound therapy

By Ronald Rock, MSN, RN, ACNS-BC

Complex wound failures are costly and time-consuming. They increase length of stay and contribute to morbidity and mortality in surgical patients. Negative-pressure wound therapy (NPWT)—a common adjunct to wound-care therapy—is used to accelerate wound healing in all fields of surgery. Using a vacuum device and wound-packing material, it applies subatmospheric pressure to complex wounds.
But NPWT alone doesn’t ensure adequate wound healing. Many physiologic factors—including infection, excessive moisture, nutrition, and medications—influence wound-healing success. Failure to account for these factors or improper application of NPWT can limit patient outcomes and cause debilitating complications.
For clinicians, applying and establishing an airtight seal on a complex wound is among the most dreaded, time-consuming, and challenging NPWT-related tasks. Simply applying NPWT material under layers of transparent drape may delay wound healing or exacerbate the wound. This article provides tips on safe application of NPWT to enhance the outcomes of patients with complex wounds.

 Consider wound location

Wounds on the body’s anterior surfaces are less susceptible to the forces of pressure, friction, and shear than those on posterior and lateral surfaces. Posterior and lateral wounds commonly require posterior off­loading or repositioning the patient in bed to reduce or eliminate direct pressure. This can be done with judicious and frequent patient turning using a specialty bed or support surface.
Bridge a posterior or lateral wound to an anterior surface by placing the drainage collection tubing to a nonpressure-bearing surface away from the wound. Bridging keeps the tubing from exerting pressure on intact skin and decreases the risk of a pressure ulcer. To create the bridge, cut foam into a single spiral of 0.5 to 1 cm, or if using gauze, fold gauze into 8 single layers.
Place the spiraled foam or gauze layers onto the drape, ensure the bridge is wider than the collection tubing disc, and secure it with an additional drape. Next, apply the NPWT collection tubing on the end of the bridge away from the wound. A wide bridge under the collection tubing disc will minimize the potential for periwound breakdown when negative pressure is initiated. You may modify this spiraling technique by varying the width of the foam to fill undermining and wounds of irregular configuration and depth.

 Protect the periwound

An intact periwound may break down from exposure to moisture, injury from repetitive removal of a transparent drape, or NPWT material coming in contact with skin. Skin protection is critical in preventing additional breakdown stemming from contact with potentially damaging material.
Transparent drapes are designed to permit transmission of moisture vapor and oxygen. Avoid using multiple layers of transparent drapes to secure dressings over intact skin, as this can decrease the transmission of moisture vapor and oxygen, which in turn may increase the risk of fungal infection, maceration, and loss of an intact seal.
Periwound maceration also may indicate increased wound exudate, requiring an increase in negative pressure. Conversely, an ecchymotic periwound may indicate excessively high negative pressures. If either occurs, assess the need to adjust negative pressure and intervene accordingly. Reassess NPWT effectiveness with subsequent dressing changes.
Apply a protective liquid skin barrier to the periwound and adjacent healthy tissue to help protect the skin surface from body fluids. The skin barrier also helps prevent stripping of fragile skin by minimizing shear forces from repetitive or forceful removal of transparent drapes. Excessive moisture can be absorbed by using a light dusting of ostomy powder sealed with a skin barrier. A “window pane” of transparent drape or hydrocolloid dressing around the wound also can protect surface tissue from contactwith NPWT material and prevent maceration.

 Avoid creating rolled wound edges

In the best-case scenario, epithelial tissue at the wound edge is attached to the wound bed and migrates across healthy granulation tissue, causing the wound to contract and finally close. With deep wound environments that lack moisture or healthy granulation tissue, the wound edges may roll downward and epibole may develop. Epibole is premature closure of the wound edges, which prevents epi­thelialization and wound closure when it comes in contact with a deeper wound bed. (See Picturing epibole by clicking the PDF icon above.)
Materials used in NPWT are primarily air-filled. Applying negative pressure causes air removal, leading to wound contraction by pulling on the wound edges—an action called macrostrain. Without sufficient NPWT material in the wound, macrostrain can cause the wound to contract downward and the wound edges to roll.
Ensure that enough NPWT material has been applied into the wound to enhance wound-edge approximation and avoid creating a potential defect as the wound heals. Before NPWT begins, material should be raised 1 to 2 cm above the intact skin. Additional material may be needed with subsequent changes if the NPWT material compresses below the periwound. The amount of NPWT material needed to remain above the periwound once NPWT starts varies with the amount of material compressed and the wound depth.

 Reduce the infection risk

To some degree, all wounds are contaminated. Usually, the body’s immunologic response is able to clear bacterial organisms and wound healing isn’t delayed. But a patient who has an infection of a complex wound needs additional support.
Systemic antibiotics alone aren’t enough because they’re selective for specific organisms and don’t reach therapeutic levels in the wound bed. In contrast, topical anti­microbial adjuncts, such as controlled-release ionic silver, provide broad-spectrum antimicrobial coverage against fungi, viruses, yeasts, and gram-negative and gram-positive bacteria, including methicillin-resistant Staphylococcus aureus and vancomycin-resistant enterococci.
Consider using controlled-release ionic silver for a wound known to be infected or at risk for infection due to its location or potential urine or fecal contamination. To be bactericidal, ionic silver must be in concentrations of at least 20 parts per million; also, it must be kept moist and must come in direct contact with infected wound bed. At lower concentrations, organisms may develop resistance. Ionic silver has no known resistance or contraindications. Dressings using it come in several forms, including a hydrogel sheet, perforated sheet, cavity version, and semiliquid hydrogel. Be sure the form you choose doesn’t occlude the NPWT material and compromise therapy. (See NPWT for a patient with necrotizing fasciitis by clicking the PDF icon above.)

View: NPWT

Obtain a negative-pressure environment

One of the most daunting aspects of NPWT is obtaining and maintaining a good seal—in other words, avoiding the dreaded leak. Preventive skin measures may contribute to a poor seal; skin-care products containing glycerin, surfactant, or dimethicone may prevent adequate adhesion of NPWT drapes. Body oil, sweat, and hair may need to be minimized or removed.
To avoid leaks, don’t overlook the obvious—loose connections, a loose drainage collection canister, exposed NPWT material, and skinfolds extending beyond the transparent drape. Tincture of benzoin (with or without a thin hydrocolloid dressing) increases tackiness to enhance the adhesive property of a transparent drape on the diaphoretic patient and on hard-to-drape areas, such as the perineum. But be sure to use tincture of benzoin with discretion, as it may remove fragile periwound tissue when the dressing is removed.
Ostomy paste products can serve as effective filler. These pliable products can be spread into position to obtain a secure seal under the transparent drape in hard-to-seal areas, such as the perineum. Pastes remain flexible and can be removed without resi­due. Temporarily increasing NPWT pressure to a higher setting may help locate a subtle leak or provide enough negative pressure to self-seal the leak. Once the leak resolves, remember to return the pressure to the ordered setting.

 Knowledge optimizes healing

It’s important to be aware of potential complications of NPWT (See Take care with NPWT by clicking on the PDF icon above). However, when applied correctly, NPWT is an effective option for managing complex wounds. Recognizing and managing potential complications at the wound site, ensuring periwound protection, minimizing epibole formation, and preventing wound infection can result in a better-prepared wound bed and promote optimal healing.

View: NPWT case study

Selected references
Baranoski S, Ayello EA. (2012). Wound Care Essentials: Practice Principles. 3rd ed. Springhouse, PA; Lippincott Williams & Wilkins.

Bovill E, Banwell PE, Teot L, et al. Topical negative pressure wound therapy: a review of its role and guidelines for its use in the management of acute wounds. Int Wound J. 2008;5:511-529.

Sussman C, Bates-Jensen B. Wound Care: A Collaborative Practice Manual for Health Professionals. 4th ed. Baltimore, MD; Lippincott Williams & Wilkins; 2011.

Ronald Rock is an Adult Health Clinical Nurse Specialist in the Digestive Disease Institute at the Cleveland Clinic in Cleveland, Ohio.

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