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Defusing lateral violence and abuse

Wound Care Advisor

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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Legal Matters

Wound Care Advisor

What caused Mr. M’s pressure ulcer?

A court case answers the question as to whether a pressure ulcer was preventable

By Nancy J. Brent, MS, RN, JD

Pressure ulcers are a major health risk for every adult patient. Risk factors include sepsis, hypotension, and age 70 or older. These risk factors became all too real when Mr. M developed pressure ulcers after being admitted to a Texas hospital.

Background

Mr. M, age 81, presented at a medical center’s emergency department on January 2 complaining of abdominal pain. After undergoing an assessment, he was diagnosed with gallstones and admitted to the hospital. The next day, he had gallbladder surgery. He subsequently developed a bowel obstruction and had to undergo two more surgeries for this condition over the next 10 days.
On January 13, he was transferred to the intensive care unit (ICU) because of multiple serious medical conditions, including respiratory distress syndrome (necessitating ventilatory support), septic shock, a “blood infection” that caused his blood pressure to drop, and multiorgan failure. His primary physician discontinued tube feedings out of concern they might exacerbate his renal failure; he wrote a do-not-resuscitate order and ordered sedation.
Mr. M was unable to turn or position himself in any way. While in the ICU, he developed a “skin tear” on the tailbone (coccyx) that progressed to a serious pressure ulcer. On February 6, his condition improved enough to allow his transfer to a rehabilitation hospital, where he developed pressure ulcers on his heels. He was transferred to another hospital; the ulcer on his coccyx healed by August. He remained in that hospital for 1 year before being discharged home.
Despite healing of the pressure ulcer on his coccyx, the wound area remained hard and painful, and Mr. M experienced “daily discomfort” there. Also, he was unable to do many of the things he’d been able to do before his hospitalization.

Mr. M files a medical malpractice suit

Mr. M sued the medical center, alleging the hospital was negligent by failing to prevent the pressure ulcer from forming through the use of known “pressure relief” methods, and that the hospital failed to provide proper care and treatment of the wound once it was discovered.
At trial, the medical center lawyers argued that Mr. M’s grave condition caused the pressure ulcer to develop. The jury returned a verdict for Mr. M, finding that the medical center’s negligence proximately caused the injuries he sustained. It awarded him $35,000 for medical expenses; $135,000 for past physical pain and mental anguish; $25,000 for future physical pain and mental anguish; $25,000 for past physical impairment; and $25,000 for future physical impairment. The medical center appealed the decision.

Medical center appeals the verdict

Several issues were raised by the medical center on appeal. Of particular interest to nurses and wound care practitioners was the “cause in fact” or the “proximate cause” of Mr. M’s pressure ulcer on the coccyx. Because an expert witness must establish proximate cause based on a reasonable degree of medical certainty, Mr. M’s case became a battle of the experts regarding the care he received, or lack of care, relative to development of the pressure ulcer.

Expert witness testimony for Mr. M

The first nurse expert to testify was Mr. M’s highly qualified expert. She testified about the various acceptable ways to provide pressure relief, including turning the patient or, if the patient can’t be turned, repositioning. The latter requires use of foam wedges or pillows to elevate a particular body part. The nurse expert testified that if a patient can’t be turned or repositioned, that fact must be documented along with the reason for inability to carry out this nursing care.
Proper assessment of the pressure ulcer is required so that other team members can “see” the wound; the clinician who assesses the wound should draw a picture of exactly what he or she saw when documenting the note in the patient’s chart. The nurse expert testified that the assessment should include the color, duration, and depth of the pressure ulcer; presence or absence of infection; and whether the tissue was dead or perfused.
After reviewing the medical center’s policies and protocols on pressure relief, which required nurses to provide pressure relief every 2 hours, and the depositions of the nurses who’d cared for Mr. M, the nurse expert testified there was no documentation showing Mr. M received any pressure relief from January 13 to January 16. She said she could only conclude that the nurses failed to turn or reposition him during those days. The only notation made about his skin condition was when nurses discovered the “skin tear” on January 14. After this discovery, the physician wasn’t notified of it until January 19. On that date, the physician ordered a wound care consult, but the actual consultation didn’t occur until 3 days later. Even with the wound consultant’s specific, written orders to care for the wound, only one notation existed showing that the orders were followed. Also, the wound care orders weren’t entered into Mr. M’s care plan until January 28. Additionally, in their depositions, the nurses caring for Mr. M couldn’t recall changing the dressing as ordered.
Therefore, in the nurse expert’s opinion, the pressure ulcer on Mr. M’s coccyx was caused directly by failure of the ICU nurses to provide pressure relief from January 14 to January 16 and that providing the wound care that was ordered would have prevented the ulcer from getting worse and would have healed the ulcer.
Although a physician serving as a second expert for Mr. M also testified that pressure relief should have been provided, he couldn’t say that development of the pressure ulcer was unpreventable.

Expert witness testimony for the medical center

Not surprisingly, the medical center’s expert witnesses, two of whom were physicians, testified that because of Mr. M’s general medical condition, he would have developed the pressure ulcer even if hospital policies and protocols had been followed. The hospital’s nurse expert witness stated that Mr. M’s pressure ulcer was not preventable because of his medical condition, regardless of whether or not he was turned. In her opinion, the active range of motion his nurses put him through was enough to reperfuse the area.

Appellate court’s decision

The appellate court upheld the trial court jury’s verdict, stating that evidence presented at the trial was legally and factually sufficient to support that verdict.

Take-away points

Mr. M’s case undoubtedly was complicated by his age and general medical condition, as well as disagreement among expert witnesses as to the cause of the pressure ulcer on his coccyx. Even so, the appellate court held that the evidence at trial (specifically that presented by Mr. M’s nurse expert witness) was sufficient legally and factually to support the verdict in favor of Mr. M.
This case illustrates many areas of importance for nurses in terms of formation and care of pressure ulcers. They include the following:
• Risk factors supporting potential formation of pressure ulcers can’t be overlooked or underestimated by nursing staff.
• A plan to prevent pressure ulcers should be initiated on admission for every patient who is immobile or has other risk factors for pressure ulcers.
• Documentation of every aspect of nursing care that’s initiated and continued to prevent pressure ulcers from forming must be carried out as ordered and pursuant to hospital policy and protocol.
• Care plans, communications with other health team members, and carrying out of orders must be done as soon as possible.
• Assessment and documentation of pressure ulcers should include enough detail so other health team members can visualize what the nurse entering the documentation has seen.
• The nurse should assess and stage the pressure ulcer at each dressing change.
• One’s expert witness must be credentialed, educated, and experienced in would care prevention and treatment, because his or her testimony can win or lose a case.

Nursing remains at the forefront of protecting and safeguarding patients from pressure ulcers. Although not every ulcer can be prevented, the goal is to prevent as many ulcers as possible. If a pressure ulcer does occur, caregivers’ essential focus must be on healing or preventing further deterioration and infection.

Selected references
Columbia Medical Center Subsidiary, L.P., d/b/a/
North Central Medical Center, Appellant, v. John Meier, Appellee. 198 S.W. 3d 408 (Ct. Appeals 2006).

Lyder CH, Ayello EA. Pressure ulcers: A Patient Safety Issue. In: Hughes RG, ed. Patient Safety and Quality: An Evidence-Based Handbook For Nurses. Rockville, MD: Agency For Healthcare Research and Quality. April 2008. www.ncbi.nlm.nih.gov/books/
NBK2650/. Accessed November 1, 2012.

Nancy J. Brent is an attorney in Wilmette, Illinois. The information in this article is for educational purposes only and doesn’t constitute legal advice.

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Business Consult

Wound Care Advisor

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Feel more relaxed with restorative yoga

By Lisa Marie Bernardo, PhD, MPH, RN, HFI, RYT

Do you experience chronic stress? Is your body stiff and inflexible? Does your mind seem dull and sluggish, your spirit exhausted?
Restorative yoga may help “open” your joints, ease your mind, and revive your spirit. It’s based on the concept that we’re overstimulated and don’t get enough rest. Constant stimulation activates the sympathetic nervous system, overtaxing the fight-or-flight response. The body responds by increasing cortisol and glucose production, which (along with additional unhealthy responses) raises the risk of metabolic syndrome.
Restorative yoga promotes active relaxation, helping to halt the overstimulation cycle. It promotes balance by alternately stimulating and relaxing the body, which is supported in yoga poses with such props as blankets, pillows, yoga mat, and eye covers. Research suggests restorative yoga may ease hot flashes in postmenopausal women and may promote a calm, positive mood in women with ovarian or breast cancer.

Five facets of restorative yoga

Restorative yoga takes a five-faceted approach to relieve the effects of stress. Over time, you’re likely to notice a new awareness of and appreciation for your body, mind, and spirit.
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.
1. Using props, restorative yoga supports the body in yoga poses, helping muscles and joints release tension and achieve muscular balance.
2. The restorative poses move the spine in all directions—flexion, extension, rotation, and lateral flexion. This enhances spinal flex­-ibility, lubricates vertebrae, and strengthens the deep muscles that stabilize the spine.
3. Inverted poses, in which the feet and legs are elevated, counter the effects of gravity and promote lymph and fluid drainage to the heart.
4. The poses compress and release internal organs, cleansing them while aiding removal of cellular waste and renewing oxygen and nutrients.
5. Finally, the poses balance the body’s male (prana) and female (apana) energies.

Learning the poses

To learn the poses, consider taking a restorative yoga class. (See Finding an instructor.) Beforehand, make sure to tell the instructor about any special health concerns you have, so the instructor can modify the poses for you. Expect to bring your own blankets, pillows, eye covers, and yoga mat. The class will last from 60 to 90 minutes.
Restorative yoga typically doesn’t involve active (hatha) yoga poses, although it may include stretching poses to warm muscles and joints before the restorative poses begin. The instructor will help you use your props to make the poses right for you, and will direct you into a pose using them. Expect to stay in the pose for 5 to 10 minutes. The instructor will guide you by helping you focus on your breath and turn your attention inward. If your mind wanders and your body stays active, accept this reaction and don’t judge yourself. Over time, you’ll learn to use your breath to release tension and to focus and calm your mind.
After you hold the pose for the required duration, the instructor will help you into the next one. Generally, the class is near-silent, with minimal talking; the lights are low and music may play.
W­hen the class ends, you may feel more relaxed and in touch with yourself. If you feel restless and jittery instead, accept your reaction. Don’t judge yourself. Try again. Give yourself the opportunity to experience something different.
Restorative yoga is just one method to renew and reconnect with your inner being. Only you can know if it’s right for you. n

Selected references
Cohen B, Kanaya A, Macer J, Shen H, Chang A, Grady D. Feasibility and acceptability of restorative yoga for treatment of hot flushes: a pilot trial. Maturitas. 2007;56(2):198-204.
Danhauer SC, Tooze JA, Farmer DF, Campbell CR, McQuellon RP, Barrett R, Miller BE. Restorative yoga for women with ovarian or breast cancer: findings from a pilot study. J Soc Integr Oncol. 2008;6(2):47-58.

Lisa Marie Bernardo is the managing member of The PIlates Centre, LLC, in Hampton Township, Pennsylvania, and adjunct faculty at Carlow University School of Nursing in Pittsburgh, Pennsylvania.

To find a certified yoga instructor in your area, check the Yoga Alliance website at www.yogaalliance.com.  Restorative Yoga Teachers (www.restorativeyogateachers.com) focuses exclusively on restorative yoga. This site is operated by Judith Hansen Lasater, PhD, the leader in restorative yoga practice.

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Sample procedure for nonsterile dressing change

Wound Care Advisor

By Nancy Morgan, RN, BSN, MBA, WOC, WCC, DWC, OMS

Each month, Apple Bites brings you a tool you can apply in your daily practice.

Description

• Nonsterile dressings protect open wounds from contamination and absorb drainage.
• Clean aseptic technique should be used to change nonsterile dressings.
• In the event of multiple wounds, each wound is considered a separate treatment. (more…)

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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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“Ouch! That hurts!”

Wound Care Advisor

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

Wound pain can have a profound effect on a person’s life and is one of the most devastating aspects of living with a wound. In addition to pharmaceutical options, wound care clinicians should consider other key aspects of care that can alleviate pain. Here is a checklist to ensure you are thorough in your assessment. (more…)

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Clinical Notes

Wound Care Advisor

New wound-swabbing technique detects more bacteria

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

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

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

CMS revises hospital, nursing home comparison websites

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

IOM releases report on accelerating new drug and diagnostics development

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

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

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

Plague case in Oregon draws national attention

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

Use of negative pressure wound therapy with skin grafts

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

Mechanism for halting healing of venous ulcers identified

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

Hemodialysis-related foot ulcers not limited to patients with diabetes

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

Study identifies risk factors for mortality from MRSA bacteremia

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

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Lymphedema 101 – Part 1: Understanding the pathology and diagnosis

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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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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