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Clinical Notes

Wound Care Advisor

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

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

Medicare expenditures for diabetic foot care varies significantly by region

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

Patients who develop pressure ulcers in hospital more likely to die

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

Patients with diabetic foot ulcers may have higher risk of death

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

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

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

View: StomaLife video

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

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

Palliative care raises patient satisfaction and reduces costs

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

More research needed to determine efficacy of maggot debridement therapy

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

Use tool to select correct antimicrobial dressing

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

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Lymphedema 101 – Part 2: Treatment

Wound Care Advisor

By Steve Norton, CDT, CLT-LANA

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

Traditional treatment approaches

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

Elevation

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

Elastic garments

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

Pneumatic compression pump

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

Surgery

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

Diuretics

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

Benzopyrones

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

Complete decongestive therapy: The current treatment approach

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

Manual lymph drainage

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

Compression bandaging

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

Exercise

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

Skin and nail hygiene

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

Self-care education

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

An underrecognized and mistreated problem

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

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

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

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

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

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

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

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

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

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

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

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

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MRSA: What wound care professionals need to know

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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Network effectively

Wound Care Advisor

By Joan C. Borgatti, MEd, RN

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

“Hello. My name is…”

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

Set a networking goal

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

A tale of two networkers

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

Networking etiquette

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

What happens next?

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

Make it happen

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

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

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

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

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Foam dressing

Wound Care Advisor

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

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

Description

•    Semipermeable polyurethane foam dressing
•    Nonadherent and nonlinting
•    Hydrophobic or waterproof outer layer
•    Provides moist wound environment
•    Permeable to water vapor but blocks entry of bacteria and contaminants
•    Available in various thicknesses with or without adhesive borders
•    Available in pads, sheets, and cavity dressings (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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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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In the current healthcare environment, wound care practitioners need to capitalize on all available reimbursement avenues for care delivery and wound care supplies and dressings. And when it comes to reimbursement, there’s one constant: The rules change constantly. Whether these changes always benefit the patient is questionable. Nowhere is this more evident than in acute-care settings. Clinicians constantly are challenged to make sure their patient-care decisions comply with current Medicare reimbursement guidelines. (And if you’re not sure about today’s guidelines, be prepared for the guidelines to change tomorrow.) (more…)

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