By Debra Rose Wilson, PhD, MSN, RN, IBCLC, AHN-BC, and Dana Marie Dillard, MS, HSMI
Like many clinicians, you may experience stress frequently, both on and off the job. Chronic stress can alter your equilibrium (homeostasis), activating physiologic reactive pathways that cause your body to shift its priorities. Physiologic effects of stress may include:
slowed digestion
delay in reproductive and repair processes
priming of survival mechanisms (respiratory, cardiovascular, and muscular) for immediate use
Since its introduction almost 20 years ago, negative-pressure wound therapy (NPWT) has become a leading technology in the care and management of acute, chronic, dehisced, traumatic wounds; pressure ulcers; diabetic ulcers; orthopedic trauma; skin flaps; and grafts. NPWT applies controlled suction to a wound using a suction pump that delivers intermittent, continuous, or variable negative pressure evenly through a wound filler (foam or gauze). Drainage tubing adheres to an occlusive transparent dressing; drainage is removed through the tubing into a collection canister. NWPT increases local vascularity and oxygenation of the wound bed and reduces edema by removing wound fluid, exudate, and bacteria. (more…)
By Nancy Collins, PhD, RD, LD/N, FAPWCA, and Allison Schnitzer
Nutrition is a critical factor in the wound healing process, with adequate protein intake essential to the successful healing of a wound. Patients with both chronic and acute wounds, such as postsurgical wounds or pressure ulcers, require an increased amount of protein to ensure complete and timely healing of their wounds.
Elderly patients with wounds pose a special challenge because of their decreased lean body mass and the likelihood of chronic illnesses and insufficient dietary protein intake. To promote a full recovery, wound care clinicians must address the increased protein needs of wound patients, especially elderly patients. (more…)
Collagen, the protein that gives the skin its tensile strength, plays a key role
in each phase of wound healing. It attracts cells, such as fibroblasts and keratinocytes, to the wound, which encourages debridement, angiogenesis, and reepithelialization. In addition, collagen provides a natural scaffold or substrate for new tissue growth. (more…)
Achieving excellent wound care outcomes can be challenging, given the growing number of high-risk patients admitted to healthcare facilities today. Many of these patients have comorbidities, such as obesity, diabetes, renal disease, smoking, chronic obstructive pulmonary disease, and poor nutritional status. These conditions reduce wound-healing ability. (more…)
By Nancy Chatham, RN, MSN, ANP-BC, CCNS, CWOCN, CWS, and Lori Thomas, MS, OTR/L, CLT-LANA
An estimated 7 million people in the United States have venous disease, which can cause leg edema and ulcers. Approximately 2 to 3 million Americans suffer from secondary lymphedema. Marked by abnormal accumulation of protein-rich fluid in the interstitium, secondary lymphedema eventually can cause fibrosis and other tissue and skin changes. (more…)
The ability to understand or “read” lower-extremity redness in your patient is essential to determining its cause and providing effective treatment. Redness can occur in multiple conditions—hemosiderin staining, lipodermatosclerosis, venous dermatitis, chronic inflammation, cellulitis, and dependent rubor. This article provides clues to help you differentiate these conditions and identify the specific cause of your patient’s lower-extremity redness. (more…)
Assessing moisture and pressure risk in elderly patients continues to be a focus for clinicians in all settings, particularly long-term care. Ongoing research challenges our ideas about and practices for cleansing and protecting damaged skin. Until recently, most wound care clinicians have cleansed long-term care patients’ skin with mild soap and water. But several studies have shown pH-balanced cleansers are more efficient than soap and water for cleansing the skin of incontinent patients.
Various terms are used to describe skin breakdown related to moisture—incontinence-associated dermatitis, perineal dermatitis, diaper rash, intertriginal dermatitis, intertrigo, moisture-related skin damage, moisture-associated skin damage, and even periwound dermatitis. This article uses moisture-associated skin damage (MASD) because it encompasses many causes of skin breakdown related to moisture. Regardless of what we call the condition, we must do everything possible to prevent this painful and costly problem.
Skin assessment
Start with an overall assessment of the patient’s skin. Consider the texture and note dryness, flaking, redness, lesions, macerated areas, excoriation, denudement, and other color changes. (See Identifying pressure and moisture characteristics by clicking the PDF icon above.)
Assessing MASD risk
A patient’s risk of MASD can be assessed in several ways. Two of the most widely used pressure-ulcer risk scales, the Norton and Braden scales, address moisture risk. The Norton and Braden subscales should drive your plan for preventing skin breakdown related to moisture or pressure. The cause of breakdown (moisture, pressure, or shear/friction) must be identified, because treatment varies with the cause.
Both the Norton and Braden scales capture activity, mobility, and moisture scores. The Braden scale addresses sensory perception, whereas the Norton scale identifies mental condition. (See Subscales identifying pressure, shear, and moisture risk by clicking the PDF icon above.) Also, be aware that two scales have been published for perineal risk, but neither has been used widely.
You must differentiate pressure- and moisture-related conditions to determine correct treatment. Patients who are repositioned by caregivers are at risk for friction or shear. Also, know that agencies report pressure-ulcer prevalence. Care providers no longer classify mucous-membrane pressure areas in skin prevalence surveys; mucous membranes aren’t skin and don’t have the same tissue layers. Furthermore, don’t report skin denudement from moisture (unless pressure is present) in prevalence surveys.
When moisture causes skin breakdown
Skin has two major layers—epidermis and dermis. The epidermis itself has five layers: The outermost is the stratum corneum; it contains flattened, keratin protein–containing cells, which aid water absorption. These cells contain water-soluble compounds called natural moisturizing factor (NMF), which are surrounded by a lipid layer to keep NMF within the cell. When skin is exposed to moisture, its temperature decreases, the barrier function weakens, and skin is more susceptible to pressure and friction/shear injury. Also, when urea in urine breaks down into ammonia, an alkaline pH results, which may reactivate proteolytic and lipolytic enzymes in the stool. (See Picturing moisture and pressure effects by clicking the PDF icon above.)
Caring for moisture-related skin breakdown
The standard of care for moisture-related skin breakdown includes four major components: cleanse, moisturize, protect, and contain. Specific products used for each component vary with the facility’s product formulary.
Cleanse
Gently wash the area using a no-rinse cleanser with a pH below 7.0. Don’t rub the skin. Pat dry.
Moisturize
Use creams containing emollients or humectants. Humectants attract water to skin cells and help hold water in the cells; don’t use these products if the skin is overhydrated. Emollients slow water loss from skin and replace intracellular lipids.
Protect
Options for skin protectants include:
• liquid film-forming acrylate sprays or wipes
• ointments with a petroleum, zinc oxide, or dimethicone base
• skin pastes. Don’t remove these products totally at each cleansing, but do remove stool, urine, or drainage from the surface and apply additional paste afterward. Every other day, remove the paste down to the bare skin using a no-rinse cleanser or mineral oil.
Be sure to separate skinfolds and use products that wick moisture rather than trap it. These may include:
• commercial moisture-wicking products
• a light dusting with powder containing refined cornstarch or zinc oxide—not cornstarch from the kitchen or powder with talc as the only active ingredient
• abdominal pads.
Contain
To keep moisture away from skin, use absorbent underpads with wicking properties, condom catheters (for males), fecal incontinence collectors, fecal tubes (which require a healthcare provider order), or adult briefs with wicking or gel properties. Call a certified ostomy or wound care nurse for tips on applying and increasing wear time for fecal incontinence collectors.
If 4″ × 4″ gauze pads or ABD pads are saturated more frequently than every 2 hours, consider applying an ostomy or specially designed wound pouch to the area. Collecting drainage allows measurement and protects skin from the constant wetness of a saturated pad.
Don’t neglect the basics, for example, know that wet skin is more susceptible to breakdown. Turn the patient and change his or her position on schedule. Change linens and underpads when damp, and consider using a low-air-loss mattress or bed or mattress with microclimate technology.
Also, be aware that fungal rashes should be treated with appropriate medications. If the patient’s skin isn’t too moist, consider creams that absorb into the skin; a skin-protecting agent can be used as a barrier over the cream. Besides reviewing and using the standards of care, you may refer to the Incontinence-Associated Dermatitis Intervention Tool, which has categories related to skin damage. See the “Incontinence-Associated Dermatitis Intervention Tool” (IADIT).
Bottom line on skin breakdown
To help prevent skin breakdown related to moisture, assess patients’ skin appropriately, determine treatment using evidence-based guidelines, and implement an appropriate plan of care.
Selected references
Black JM, Gray M, Bliss DZ, et al. MASD part 2: incontinence-associated dermatitis and intertriginous dermatitis: a consensus. J Wound Ostomy Continence Nurs. 2011;38(4):359-70.
Borchert K, Bliss DZ, Savik K, Radosevich DM. The incontinence-associated dermatitis and its severity instrument: development and validation. J Wound Ostomy Continence Nurs. 2010;37(5):527-35.
Doughty D. Differential assessment of trunk wounds: pressure ulceration versus incontinence-associated dermatitis versus intertriginous dermatitis. Ostomy Wound Manage. 2012;58(4):20-2.
Doughty D, Junkin J, Kurz P, et al. Incontinence-associated dermatitis: consensus statements, evidence-based guidelines for prevention and treatment, and current challenges. J Wound Ostomy Continence Nurs. 2012;39(3):303-15.
Gray M, Beeckman D, Bliss DZ, et al. Incontinence-associated dermatitis: a comprehensive review and update. J Wound Ostomy Continence Nurs. 2012;
39(1):61-74.
Gray M, Black JM, Baharestani MM, et al. Moisture-associated skin damage: overview and pathophysiology. J Wound Ostomy Continence Nurs. 2011;38(3):233-41.
National Pressure Ulcer Advisory Panel and European Pressure Ulcer Advisory Panel. Prevention and treatment of pressure ulcers: clinical practice guideline.Washington, DC: National Pressure Ulcer Advisory Panel; 2009.
Wound, Ostomy and Continence Nurses Society. Guideline for Prevention and Management of Pressure Ulcers. Mt. Laurel, NJ: Wound, Ostomy and Continence Nurses Society; 2010.
Wound, Ostomy and Continence Nurses Society. Incontinence-Associated Dermatitis: Best Practice for Clinicians. Mt. Laurel, NJ: Wound, Ostomy and Continence Nurses Society; 2011.
Zulkowski K. Diagnosing and treating moisture-associated skin damage. Adv Skin Wound Care. 2012;25(5):231-6.
Patricia A. Slachta is an instructor at the Technical College of the Lowcountry in Beaufort, South Carolina.
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.
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-resistantS. 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.
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.
A research team led by UCLA biomolecular engineers and doctors has demonstrated a therapeutic material that could one day promote better tissue regeneration following a wound or a stroke. (more…)
