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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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Why not call it a pressure ulcer?

Wound Care Advisor

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

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

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

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

Selected reference
Nightingale F. Notes on Nursing: What It Is, And What It Is Not. London: Harrison and Sons; 1859. http://ia600204.us.archive.org/17/items/notes
nursingnigh00nigh/notesnursingnigh00nigh.pdf.
Accessed August 30, 2012.

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“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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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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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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Providing wound care in the home: An option to explore

Wound Care Advisor

By Connie Johnson, RN, BSN, WCC, LLE, DAPWCA

Jim, a 52-year-old patient with colon cancer, received a new ostomy. He needed a custom fit for his appliance, which took 10 days. During this time, trying to obtain a good seal and treat the peristomal area wasn’t easy. Despite my best efforts, Jim’s skin was denuded from contact with stool. Although he was in great discomfort, he wanted to wait until my next visit to tell me about the problem. Fortunately, his wife was worried and contacted me directly.

Jim lives in a neighborhood with a low crime rate, so I’m able to see him within
a few hours of his wife’s call, even though it’s late at night. As it turns out, I make
extra visits to help him manage his stoma until the customized appliance is ready.  As with any home care situation, I’m ready to do my best for my patient.

Many home-care patients like Jim benefit from the interventions of a wound care clinician (WCC). More than one-third of all home-care admissions are wound related, and home wound care has become one of the fastest growing needs and skills in home-care services. So if you’re a WCC, you may want to consider home care as a practice option.

Delivering wound care in the home differs dramatically from delivering it in the hospital. Given the complexity of wound care and the multiple factors that affect healing, home wound care is a challenge. Some patients have chronic conditions, such as diabetes or wounds or open sores that don’t heal easily. In other cases, the patient or caregiver is unable to change dressings. That’s where the WCC comes in.

Special needs of home-care patients

Like other patients across the continuum of care, home-care wound patients require accurate and thorough wound assessment, as well as documentation that provides information about wound status and aids development of a plan that supports healing.
Of course, the plan of care must address the whole patient, not just the “hole” in the patient. The WCC must take into account comorbidities, individual wound-care requirements, assistance the patient may need due to physical or mental deficits, and nutritional support. Additional factors that affect wound-care strategies include wound characteristics, family support, and insurance guidelines and reimbursement.

Role of the WCC

The WCC’s role in home care includes providing clinical expertise, working with other healthcare team members, and providing education.

  • The WCC provides clinical expertise regarding wound and ostomy care to ensure delivery of the highest quality of care. This expertise helps reduce the need for readmissions to the emergency department (ED) for wound-related complications. The WCC also plays a vital role in product awareness, formu-lary development, and maintenance of cost-effective, evidence-based practice in the agency.
  • Working with other healthcare team members, the WCC serves as patient advocate, strengthening the relationship between patient and healthcare team members while promoting care coordination to help the patient achieve goals. Effective communication with the patient’s primary care pro­vider is essential to delivering the best-quality, research-based wound care. A tool for strengthening such communication is the SBAR (Situation-Background-Assessment-Recommendation) technique. SBAR structures conversations so all parties provide complete yet concise information. (See SBAR wound and skin provider communication record by clicking the PDF icon above).
  • The WCC educates patients and family members about wound healing, dressing applications, and other interventions. Teaching families allows them to be involved in the patient’s care and start to take ownership of it. The WCC also educates home health aides, who can play a vital role in preventing such problems as pressure ulcers and may be responsible for ensuring staff members are aware of the products, procedures, and dressings available.

Challenges of home care

If you’re a WCC and considering home care as a career option, know that practicing in the home can be a real eye opener. For starters, consider geography. Shortly after I started as a wound care nurse/consultant in home care, I was visiting patients all over New Jersey, some days driving 200 miles. As I quickly discovered, once you enter the home, don’t assume you’ll simply change a dressing and then be on your way. Instead, you may find you are, in essence, the family case manager who’s expected to “fix everything.” This role requires equal doses of planning and creativity.

What’s more, expect to do some improvising. In acute-care settings, all the supplies you may need to prevent infection—gowns, gloves, masks—usually are within arm’s reach. But in home care, these supplies may be absent, meaning you’ll need to set up the cleanest environment you can under the circumstances. That might mean using disposable drapes and dressings. Be sure to carry large amounts of hand sanitizer.

Dressing selection is perhaps the biggest challenge in home wound care because
it involves not just wound-specific issues but financial and practical considerations. The ideal dressing in the home is one that needs to be changed only every other day, at most. Evidence shows it’s not practical to try to change dressings two or three times daily at home unless the family is providing care.

Develop a checklist

Because the home environment may lack all the resources you need, remembering every­thing you need to do before you leave the patient’s home may be challenging. To help keep things on track, develop a checklist of reminders that covers these points:

  • Have necessary medical appointments been arranged? Does the patient have transportation to appointments?
  • Are there sufficient supplies in the home?
  • Is there enough medicine? If not, who will pick up the medicine?
  • Are consults needed, such as social worker or physical therapist?
  • Who will help with any activities of daily living that the patient is unable to do?
  • Does the patient with diabetes have a glucometer?

Hours and safety concerns

Typical home wound-care hours are 8:30 a.m. to 4:30 p.m. But realistically, expect variations. For instance, as you’re about to leave, the patient might say, “My wife isn’t feeling well. Could you take her blood pressure?” This means you’ll stay a little longer.

When planning home visits, be aware of safety concerns. If visiting after hours could put you in danger, it’s safer to instruct the patient to call an ambulance and go to the local ED.

Reimbursement

Reimbursement is an important factor in wound care in the home. To be eligible for home care through Medicare, patients must be homebound—meaning they don’t routinely travel to run errands or visit or they’re not able to obtain or receive needed medical services. (With private insurance and workers’ compensation, eligibility requirements may be less restrictive.)

Know that a Medicare patient receives home care as an “episode.” Episodes are 60-day periods; within each 60-day episode, a $592 cap is allotted should a patient require supplies for wound or ostomy care needs. Except for negative-pressure wound therapy, a home care agency can’t bill Medicare for products used; instead, the home-care agency is responsible for the cost of all topical wound-care products and dressings. Agencies may keep patients on service even if they exceed the allowed amount, although patients reaching maximum benefits commonly are discharged from service. Home-care agencies have no choice but to discharge Medicare patients they find aren’t truly homebound.

Also, be aware that Medicare views home health service as an interim service. When a patient is no longer making progress, Medicare expects that the family will provide the patient’s care or the patient will enter a skilled care facility. So it’s important to work hard to obtain good outcomes—not just for the patient but to maintain Medicare reimbursement. Like many private insurance companies, Medicare reimbursement is based on pay for performance; if an agency doesn’t deliver optimal outcomes, it receives lower reimbursement, increasing its financial burden.

A worthwhile option

WCCs use their knowledge and clinical expertise to improve patient outcomes and teach patients, families, and other healthcare team members. They also give the agency recommendations for care and supplies that are evidence based and reflect current best practices in wound care. Accomplishing these goals in a timely fashion under various constraints can be challenging. But if you choose to work in the home, try to keep a smile on your face and joy in your voice for each patient and family. If you like challenges and want a job where you can apply your creativity and function independently, becoming a home-care WCC might be the right choice for you.

Connie Johnson provides wound care in the home and in acute-care settings.

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“We don’t have a Doppler”

Wound Care Advisor

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Rooke TW, Hirsch AT, Misra S, et al; Society for Cardiovascular Angiography and Interventions; Society of Interventional Radiology; Society for Vascular Medicine; Society for Vascular Surgery. 2011 ACCF/AHA focused update of the guideline for the management of patients with peripheral artery disease (updating the 2005 guideline): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2011;58(19):2020-2045. http://
content.onlinejacc.org/cgi/content/full/j.jacc.2011.08.023v1. Accessed June 4, 2012.

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

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

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

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