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MRSA: What wound care professionals need to know

Wound Care Advisor

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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From the Editor

Wound Care Advisor

The pros and cons of formularies

In health care, we frequently use the terms formulary and protocol interchangeably even though they have different meanings. A formulary is an official list of available dressings, products, and medications. A protocol is a roadmap or guideline on how to use the formulary.

Formularies became popular several years ago when reimbursement changed to bundling and wound-product costs were included in the routine cost of care rather than separately billable. In an effort to control costs, hospitals, home health agencies, and long-term care facilities began exclusive partner agreements with supply and buying groups. (“You use our products exclusively and we’ll give you a huge discount on cost.”)

A good formulary not only can help save money. It can also assist in streamlining care delivery, reducing waste, and directing treatment decisions. But on the flip side, using formularies can have disastrous results. I realized this last week while speaking on the phone with a wound clinician who’d called to ask for wound treatment ideas for a hospice patient. As she described the situation, it became apparent that the patient’s symptoms definitely pointed to high levels of bacteria in the wound. As I began sharing recommendations for treatment ideas, she kept responding: “Nope. Can’t use that, not on our formulary.” “Nope, not on formulary.” The only options available on her hospice formulary were hydrocolloid, hydrogel, or foam dressings, none of which had antibacterial properties.

Providing an appropriate standard of care shouldn’t be dictated by a formulary, and choosing substandard care just because the patient is in hospice isn’t acceptable or appropriate. Evidence-based guidelines, wound characteristics, underlying complications, and patient care goals should dictate management and treatment.

To ensure your formulary is adequate, determine if it includes a variety of product categories, and negotiate the ability to go off formulary if needed. Although cost control is essential, clinicians need access to products and therapies that yield positive outcomes. One size doesn’t fit all in wound care.

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

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How to write effective wound care orders

Wound Care Advisor

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

Writing effective orders for wound care is vital to ensure patients receive the right care at the right time, to protect yourself from possible litigation, and to facilitate appropriate reimbursement for clinicians and organizations.
Below are some overall strategies you can use:

  • Avoid “blanket” orders, for example, “continue previous treatment” or “resume treatment at home.” These types of general orders lack the specificity clinicians require to deliver care the patient needs and can be easily misinterpreted. For instance, treatments can change multiple times, and someone could pick a treatment from an incorrect date. (more…)
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Network effectively

Wound Care Advisor

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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Clinician Resources

Wound Care Advisor

Here are a variety of resources related to quality that wound care clinicians may find valuable.

Home Health Quality Improvement National Campaign

If you are interested in home care, you’ll want to visit The Home Health Quality Improvement (HHQI) National Campaign’s website. HHQI is a grassroots project of the Centers for Medicare & Medicaid Services designed “to unite home health stakeholders and multiple health care settings under the shared vision of reducing avoidable hospitalizations and improving medication management.”
The many available free resources on the campaign’s website include:
•    webinars; for example, “Hospital Readmissions and the Role of Home Care”
•    best practice innovation packages, including ones on medication management and fall prevention.

You must register to obtain some of the resources.

◊   http://www.homehealthquality.org/hh/default.aspx

Reducing Avoidable Readmissions Effectively

Reducing Avoidable Readmissions Effectively (RARE) is a campaign in Minnesota that is working with hospitals and care providers to prevent hospital readmissions within 30 days of discharge.
Even if you aren’t in Minnesota, you can access resources such as a webinars. Past webinars include “Involving Patients and Families in Reducing Avoidable Readmissions” and “Home Care and Reducing Hospital Readmissions.”
You can also download “Recommended Actions for Improved Transitions,” which covers five key areas: patient and family engagement and activation, medication management, comprehensive transition planning, care transition support, and transition communication.

◊   http://rarereadmissions.org/resources/RARE_Report_2012_06.html

TeamSTEPPS®

Effective communication is essential for any quality initiative to be successful. TeamSTEPPS is a teamwork system that improves communication through train-ing and tools. The Agency for Healthcare Research and Quality and the Defense Department have teamed up to provide
resources for implementing Team STEPPS.
Tools include:
•    Core TeamSTEPPS Training Curriculum Materials
•    TeamSTEPPS Rapid Response Systems (RRS) Training Module
•    TeamSTEPPS Teamwork Perception Questionnaire
•    Pocket Guide that summarizes TeamSTEPPS principles in a portable, easy-
to-use format.

The educational materials contain information that clinicians can integrate into their practice. Video vignettes illustrate how failures in teamwork and communication can place patients in jeopardy and how successful teams can work to improve patient outcomes.
You can order free TeamSTEPPS materials, which are available online.

◊   http://teamstepps.ahrq.gov

Institute for Healthcare Improvement

The Institute for Healthcare Improvement is an independent, not-for-profit organization that focuses on testing new models of care, disseminating best practices, and building the will to change to improve health care.
Among the many resources on the website:
•    tools such as “Self-Management Toolkit for People with Chronic Conditions and Their Families”
•    useful publications
•    white papers such as “Using Care
Bundles to Improve Health Care
Quality”
•    case studies of successful strategies
•    audio and video broadcasts
•    links to other helpful websites.

Registration is free.

◊   http://www.ihi.org/Pages/default.aspx   

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Lymphedema 101 – Part 1: Understanding the pathology and diagnosis

Wound Care Advisor

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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Teaching ostomy patients to regain their independence

Wound Care Advisor

By Goranka Paula Bak, BSN, RN, ET, CWOCN

Every year, thousands of people of all ages have ostomy surgery in the United States. That means no matter where you work, you’re likely to care for patients with new ostomies and teach them to care for themselves. (See Why patients need ostomy surgery by clicking the PDF icon above.)
These patients present two challenges: staying up-to-date on ostomy equipment and procedures and having only 3 to 5 days after surgery to teach basic ostomy care to patients who are unlikely to be physically or emotionally ready to learn. This review and update of ostomy care should help you meet both challenges. Let’s start with the common types of stomas and ostomies.

Reviewing stoma types

The three common types of stomas are the end stoma, loop stoma, and double-barrel stoma. The patient’s surgeon decides on the most appropriate type based on the disease or injury, the amount of intestine available, and the patient’s health status.
To create an end stoma, the most common type, a surgeon creates a small opening in the abdominal wall, then resects the intestine and pulls it through the opening. Next, the surgeon turns the end of the intestine onto itself—somewhat like cuffing a sock—and sutures the stoma to the skin. Next to the stoma, the surgeon may create a mucous fistula, which secretes mucus from the nonfunctioning portion of the intestine.
A loop stoma is usually created for a temporary ostomy. The surgeon creates a small opening in the abdominal wall and pulls a loop of intestine through it. With an external rod or bridge placed under the loop to keep it from slipping back into the peritoneal cavity, the surgeon cuts the top of the loop to form the apex of the stoma. Next, the surgeon everts the intestine around the opening and sutures the stoma edges to the skin. After a few days, the rod is removed, and the stoma stays above skin level on its own.
Double-barrel stomas aren’t common in adults, but they are used frequently in neonates. For this type, a surgeon cuts through the bowel to create two separate end stomas, one to evacuate stool and the other to evacuate mucus. The two stomas can be placed next to each other, so one pouching system can be used for both. If the stomas are further apart, the patient may need two pouches. If mucus secretions are slight, you may be able to apply a nonadherent dressing after gently cleaning the stoma and peristomal skin, instead of using a pouch.
An ideal stoma protrudes above the skin surface and has a flat peristomal skin surface that allows the ostomy barrier to adhere to it. (See Characteristics of an ideal stoma by clicking the PDF icon above.) A healthy stoma is red and moist and looks like gum tissue. In fact, the entire alimentary canal from mouth to anus has the same type of tissue. Keep in mind that while cleaning a stoma, you’ll commonly see a small amount of bleeding, just as your gums may bleed when you brush your teeth too vigorously. If you note excessive bleeding, report it immediately.

Reviewing types of ostomies

The three most common types of ostomies you’ll see are a colostomy, an ileostomy, and a urostomy.
A surgeon creates a colostomy by making an opening in the large intestine and connecting it to the stoma. The location of the surgical opening will affect the consistency of the stool exiting the body through the stoma: The lower the opening, the firmer the consistency. A colostomy produces flatus because of the high bacterial content in the large intestine. A colostomy can be temporary or permanent, depending on the diagnosis and the patient’s ability to heal.
To create an ileostomy, a surgeon makes an opening in the small intestine and forms a stoma. Patients with ileostomies are prone to dehydration because a large amount of enzymatic fluid is discharged through the ileostomy instead of being absorbed in the disconnected large intestine. Teach your patient to be alert for the signs and symptoms
of dehydration—thirst; decreased urination; darker, concentrated urine; warm, flushed skin; fever; and malaise. Also, warn the patient to keep enzymatic effluent off the skin because it can quickly cause skin breakdown. As with a colostomy, an ileostomy may be temporary or permanent.
To create a urostomy, a surgeon removes the diseased bladder and uses a portion of resected small intestine to create a conduit. The ureters, which were connected to the bladder, are sutured into the resected small intestine so urine can exit the body through the stoma. Uros­tomies are permanent.

Choosing the right pouching system

An ostomy pouching system has two parts: an adhesive barrier that attaches to the skin around the stoma and a pouch connected to the barrier that collects effluent. Determining the right ostomy pouching system for your patients will depend on their needs and preferences. Let’s look at some of the important choices.
A pouching system may come in one or two pieces. With one-piece systems, the barrier (also called the wafer, flange, or baseplate) and pouch come as a single unit. (See One- and two-piece ostomy pouching systems by clicking the PDF icon above.) One-piece systems are easier to apply and more flexible. Plus, they’re flatter and thus more discreet.
With two-piece systems, the barrier and pouch are separate components that must be attached. Depending on the product, the patient may need to press the pouch onto the barrier or use a locking ring mechanism or an adhesive coupling system. Two-piece systems allow the patient to remove the pouch without removing the barrier. Also, a patient can apply a smaller pouch, such as a stoma cap or close-ended pouch, before exercise or intimate relations.
Today, ostomy pouching systems offer many options that weren’t available just a few years ago—options such as built-in, varying levels of convexity and integrated closures. Skin-friendly barriers now eliminate the need for accessory products, such as skin prep, ostomy powder, and stoma paste. By knowing the new options, you can help simplify the pouch application process for your patient and increase patient satisfaction.

Selecting barriers

Barriers may be cut-to-fit or precut. Cut-to-fit barriers are used during the postoperative period while the stoma size is changing and for oval or irregularly shaped stomas. Precut sizes are convenient for round stomas after they stabilize.
The choice of a barrier also depends on abdominal contours and the effluent consistency. A standard-wear barrier is appropriate for thicker output. An extended-wear barrier is better for loose or watery output and for problematic ostomies.
Convex barriers can be used to push down the peristomal skin and help the stoma project into the pouch. These barriers help ensure that the effluent goes into the pouch and not between the skin and the barrier, causing leakage.
For ostomies that are difficult to manage and frequently leak, you may select an ostomy belt. This device helps secure a convex pouching system by increasing its pressure. The plastic hooks at the end of the belt attach to the belt loops of the pouching system. Depending on the manufacturer, the belt loops may be on the barrier or the pouch.

Selecting pouches

Pouches can be transparent or opaque. Transparent pouches allow you to see the stoma postoperatively and allow patients to watch as they place the pouch over the stoma. Opaque pouches, of course, have the advantage of concealing the effluent.
Some pouches have filters. Colostomy patients usually prefer filtered pouches because they eliminate the need to burp the pouch to remove gas. Ileostomy output is usually watery, so the charcoal filters may get wet and quit working.
The appropriate type of pouch closure also varies, depending on the type of output and the patient’s needs and preferences. A patient with a colostomy or ileostomy needs a drainable pouch. Newer clamps and integrated closures can make closing the pouch easier for the patient.
Close-ended pouches are available for patients who empty their pouch once or twice a day. Reimbursement guidelines for Medicare, which most insurance companies follow, allow 60 close-ended pouches a month. Thus, someone who empties once or twice a day will have enough pouches.
Patients with urostomies use pouches with spigots on the end to allow for urine drainage.
Urostomy pouches can be connected to a continuous urinary drainage bag at bedtime or to a leg bag during the day for those in a wheelchair.

Dealing with complications

Report the following postoperative complications to the surgeon and the ostomy clinician caring for the patient:
• allergic reaction
• candidiasis
• contact dermatitis
• folliculitis
• ischemic or necrotic stoma
• mechanical irritation
• mucocutaneous separation
• parastomal hernia
• prolapse.

Many complications result from surgical technique or the patient’s disease status, but complications also result from an incorrect fit or an ostomy that frequently leaks. To determine why and where leakage occurred, examine the back of the barrier. If leakage results from a flush or recessed stoma or an irregular surface around the stoma, the patient may need a convex barrier. Or the patient may need a convex barrier and an ostomy belt.
Remember that a firm abdomen requires a soft, flexible barrier that conforms to the abdominal contours. A soft belly, on the other hand, may need the rigidity of a convex barrier to help the stoma empty into the pouch.
For weepy, extremely denuded skin, apply ostomy powder, brush off the excess, and dab an alcohol-free skin seal­ant, such as No-Sting by 3M, on the area. Allow the area to air-dry before applying the barrier.

Discharge planning and patient teaching

Because the postoperative length of stay is short, start preparing for discharge and teaching the pouch-change procedure at your first hospital encounter with the patient. Teaching the patient at each encounter creates a continuum of care throughout hospitalization and recovery. If possible, include the caregiver. (See Teaching your patient to change an ostomy pouch by clicking the PDF icon above.) Before discharge, give the patient two or three ostomy pouches to take home, step-by-step printed instructions on applying pouches, a list of supplies the patient will need, and a list of ostomy product suppliers in the area.
Also, teach the patient about complications, activity, diet, and drug therapy and provide the names of local support groups. (See Finding support by clicking the PDF icon above.)

Complications at home

Tell the patient to call the physician if any of the following occurs: fever, increased pain or discomfort, diarrhea, dehydration, or signs and symptoms of infection at the surgical site. The patient should also call the physician if there’s no output from the stoma for more than 24 hours.
Patients with urostomies who develop the following signs and symptoms may have a urinary tract infection: fever, chills, abdominal or retroperitoneal pain, and bloody, cloudy, or foul-smelling urine. Clear urine with mucus shreds is normal.

Increasing activity

Explain that after surgery the patient should feel a little bit stronger every day. Teach the patient to alternate rest and activity periods and to increase the activity period a little each day while building endurance. Refer the patient to the physician for clearance to resume exercise and sexual relations.

Dietary considerations

After ostomy surgery, your patient will start on a clear liquid diet and progress to a normal, preoperative diet. The patient should reintroduce one food at a time to help determine if it’s well tolerated. High-fiber foods should be introduced slowly.
Tell your patient to expect his or her body to tolerate the food as it did before surgery: if onions caused gas before surgery, they will do so after surgery, too, but the stoma will expel the gas. Make the patient aware of other gas-forming foods, such as hard-boiled eggs, spicy foods, fish, dried beans, carbonated beverages, and beer.
Tell the patient to chew food well and to drink plenty of liquids, which will prevent blockage. Explain the importance of hydration to avoid constipation, dehydration, and urinary tract infection. To prevent dehydration, ileostomy patients who are not on fluid restriction should drink 64 ounces of fluid a day. Teach these patients to replace fluids by drinking a glass of water every time they empty their pouches.

Drug therapy

Tell the patient to adhere to the prescribed regimen and to call the physician before using any new drugs. Instruct patients with ileostomies not to take laxatives because they may become dehydrated. These patients should tell their pharmacist that they have an ileostomy, so the proper form of prescription drugs can be ordered. Extended-release tablets will not break down in time and may be found in the pouch.

Rewarding work

Keeping up with the changes in ostomy equipment and care and teaching new ostomy patients the skills they need can be challenging. But helping these patients regain the confidence and learn the skills they need to improve their quality of life makes the rewards much greater than the challenges.

Selected references
Colwell J. Principles in stoma management. In: Colwell JC, Goldberg MT, Carmel JE, eds. Fecal and Urinary Diversions Management Principles. St. Louis, MO: Mosby; 2004:240-262.

Discharge Planning for a Patient with a New Ostomy: Best Practice for Clinicians. Glenview, IL: Wound, Ostomy and Continence Nurses Society; 2004.

Hampton BG, Bryant RA. Ostomies and Continent Diversions: Nursing Management. St. Louis, MO: Mosby; 1992.

McCann E. Common ostomy problems. In: Milne C, Corbett L, Dubuc D. Wound, Ostomy, and Continence Nursing Secrets: Questions and Answers Reveal the Secrets to Successful WOC Care. Philadelphia, PA: Hanley & Belfus, Inc; 2004.

The Sarah Cole Hirsh Institute for Best Nursing Practices Based on Evidence. State of the evidence review hospital to home: Planning the transitions. 2000; Cleveland, OH.

Goranka Paula Bak is an Ostomy Sales Territory Manager for Coloplast Corporation.

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

Wound Care Advisor

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

Wound Care Advisor

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

Wound Care Advisor

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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