By Rosalyn Jordan, RN, BSN, MSc, CWOCN, WCC, and Marci Christian, BBE

Any patient with a fecal or urinary ostomy may experience complications on the skin surface around the stoma. These complications may occur lifelong, although they’re more common during the first 5 years after the initial ostomy surgery. Causative factors include infection, trauma, certain diseases, and chemical irritation; most of these problems stem from the pouching system or pouch leakage.

Peristomal skin complications can cause a wide range of signs and symptoms, from skin discoloration to polyp-like growths, from erythema to full-thickness wounds. They can lead to discomfort, pain, poor self-image, social isolation, and impaired quality of life, not to mention additional care costs.

Incidence and types of these complications are hard to compare or contrast across multiple patients. Until recently, no standardized assessment or documentation tools were available to characterize or define complications. For this reason, reported rates ranged widely, from 10% to 70%. And because no designated common language or categories related to peristomal skin complications existed, documentation was inconsistent.

Download “How to Use” education program for the Ostomy Skin Tool

Ostomy Skin Tool

In the late 2000s, a group of nurses experienced in caring for ostomy patients worked with the World Council of Enterostomal Therapists to develop a resource called the Ostomy Skin Tool, which clinicians can use to categorize and describe peristomal skin complications in a consistent, objective manner. The tool also provides a common language for documentation.

The Ostomy Skin Tool has three major assessment domains—discoloration (D), erosion/ulceration (E), and tissue overgrowth (T), known collectively as DET. The DET combined rating ranges from normal, rated 0, to the worst condition possible, rated 15. Mild DET complications are documented as less than 4, moderate as less than 7, and severe as 8 or higher. (See Using the Ostomy Skin Tool by clicking the PDF icon above.)

The tool describes four categories of peristomal complications:
• chemical irritation
• mechanical trauma
• disease-related complications
• infection-related complications.

Chemical irritation

Chemical irritation can stem from irritants (as in contact dermatitis) or allergic reactions (allergic dermatitis). The most likely cause of chemical dermatitis is effluent leakage (feces or urine) from the colostomy, ileostomy, or urostomy, in which effluent comes in contact with peristomal skin. Other potential causes include contact with soap, certain adhesives, and adhesive removers.

The major treatment of chemical irritation is identification and removal of the offending agent, followed by patient and caregiver education on the new pouching procedure the patient must use. Follow-up assessment also is recommended. In a 2010 study that followed 89 patients for 1 year after ostomy surgery, about 50% of subjects experienced peristomal skin complications, most of them from pouch leakage. Another investigator estimated that 85% of ostomy patients experience pouch leakage at some time during their lives. Pouch leakage usually occurs when stool is extremely liquid (for instance, ileostomy effluent). Other causes of pouch leakage include wearing a pouch more than half full of effluent and abdominal contours that aren’t level. Besides changes in the pouching system, treatment may entail adding products to the pouching system or removing certain agents.

Some patients experience allergic dermatitis in reaction to products used in the pouching system (such as skin barriers, belts, pouch closures, or adhesives). However, allergic dermatitis is rare. One 2010 study suggested allergic reactions to these products occur in only about 0.6% of patients with peristomal skin irritation. Most major ostomy product manufacturers provide a patch test on request to help identify allergic conditions. Once the offending product is discontinued, allergic dermatitis should resolve rapidly.

Mechanical trauma

Mechanical trauma usually results from either the pouching system itself or its removal. It also may result from harsh or multiple skin-barrier removals, pressure from convex rings or pouches, and abrasive cleansing techniques. Some researchers believe the stronger the adhesive barrier and the more often a pouch is changed, the greater the risk of epidermal damage.

Mechanical trauma may present as a partial-thickness ulcer caused by pressure, shear, friction, tearing, or skin stripping. Patients with fragile skin are susceptible to mechanical trauma, so less aggressive pouching systems may be preferred for them. Of course, if the pouching system is changed, the patient or caregiver needs to learn about the new system.

Disease-related complications

Disease-related peristomal complications may be linked to preexisting skin conditions, such as psoriasis, eczema (atopic dermatitis), or seborrheic dermatitis. Hyperplasia also may occur. This overgrowth of cells, which may appear as gray or reddish brown pseudoverrucous lesions, usually is linked to urinary ostomies, although it can occur with fecal ostomies as well. Vinegar soaks are the recommended treatment, in addition to a change in the pouching system and corresponding patient education.

Occasionally, other disease-related complications occur, including primary adenocarcinoma of the peristomal skin and peristomal pyoderma gangrenosum, a painful and problematic condition that presents as peristomal ulcers. Ulcer borders are well-defined with a bluish purple coloration at the edges. Infection must be ruled out, as this condition usually is linked to an autoimmune condition. Treatment includes pain management and, in most cases, a topical corticosteroid. Crohn’s disease also may manifest as a peristomal skin ulcer.

Infection-related complications

Infection-related complications may be bacterial or fungal. Two common peristomal skin infections are folliculitis and Candida fungal infections. An infection of the hair follicle that causes pustules, folliculitis usually stems from traumatic hair pulling in the peristomal area during pouch removal. It may warrant a prescribed antibiotic, along with patient teaching regarding proper hair removal using an electric razor.

Candida infections may arise because peristomal skin provides a warm, dark, moist environment that promotes fungal growth. These infections appear as erythema with pustules or papules and satellite lesions. Treatment usually involves antifungal powder and use of the crusting technique to secure the pouching system. (See Using the crusting technique by clicking the PDF icon above.)

Management

Many complications are well advanced by the time patients seek assistance, perhaps because they don’t understand the significance of their symptoms and think they can manage the problem themselves. In some cases, they don’t know where to turn for assistance. Commonly, the complication progresses to the point where the patient goes to the emergency department or (particularly during the immediate postoperative period) needs to be readmitted for treatment. The best way to manage peristomal skin complications is to prevent them in the first place. (See Preventing peristomal skin complications by clicking the PDF icon above.)

Patient education

Over the past 20 years, hospital stays for ostomy surgery patients have decreased from about 2 weeks to less than 5 days. Reduced stays decrease the time available for caregivers to teach patients and family members how to empty and change the pouch. They need alternative education covering (among other topics) how to recognize peristomal skin complications and when to seek help. Not only do these complications require vigilant self-observation, but many patients don’t understand their implications or how rapidly they can worsen. In some cases, the first symptoms are itching and redness under the skin barrier. Fortunately, some patients may know or remember that itching, burning, stinging, reddened, or weeping peristomal skin requires professional attention. They can avoid serious complications by seeking assistance early, such as right after noticing pouch leakage.

Early treatment can reduce the cost of treatment. In a 2012 study, researchers estimated care costs related to peristomal skin complications for a 7-week treatment period, using the Ostomy Skin Tool as a reference. Severe complications (those with a DET score above 8) cost six times more to treat than mild cases (those with a DET score below 4) and 4.5 times more than moderate cases.

Along with early intervention by a trained ostomy care specialist, self-assessment by ostomy patients promotes a better quality of life, reduces pain, and may decrease care costs. Clinicians’ use of the Ostomy Skin Tool to assess and document peristomal skin complications promotes more reliable, objective, comparable assessment data for reporting.

Selected references
Al-Niaimi F, Lyon CC. Primary adenocarcinoma in peristomal skin: a case study. Ostomy Wound Manage. 2010;56(1):45-7.

Burch J. Management of stoma complications. Nurs Times. 2011;107(45):17-8, 20.

Jemec GB, Martins L, Claessens I, et al. Assessing peristomal skin changes in ostomy patients: validation of the Ostomy Skin Tool. Br J Dermatol. 2011; 164;330-5.

Jones T, Springfield T, Brudwick M, Ladd A. Fecal ostomies: practical management for the home health clinician. Home Healthc Nurse. 2011;29(5):306-17.

Martins L, Samai O, Fernandez A, et al. Maintaining healthy skin around an ostomy: peristomal skin disorders and self-assessment. Gastrointest Nurs. 2011;
9(2):9-13.

Martins L, Tavernelli K, Serrano JLC. Introducing a peristomal skin assessment tool: The Ostomy Skin Tool. World Council Enterostomal Therapists J. 2008;28(2):3-13.

Meisner S, Lehur P, Moran B, et al. Peristomal skin complications are common, expensive, and difficult to manage: a population based cost modeling study. PLoS One. 2012;7(5):e37813.

Nybaek H, Jemec GB. Skin problems in stoma patients. J Eur Acad Dermatol Venereol. 2010;24(3):249-57.

Omura Y, Yamabe M, Anazawa S. Peristomal skin disorders in patients with intestinal and urinary ostomies: influence of adhesive forces of various hydrocolloid wafer skin barriers. J Wound Ostomy Continence Nurs. 2010;37(3):289-98.

Ratliff CR. Early peristomal skin complications reported by WOC nurses. J Wound Ostomy Continence Nurs. 2010;37(5):505-10.

Shabbir J, Britton DC. Stomal complications: a literature overview. Colorectal Dis. 2010;12(10):958- 64.

Wound, Ostomy, Continence Clinical Practice Ostomy Subcommittee. Peristomal skin complications: Best practice for clinicians. Mt. Laurel, NJ; 2007.

The authors work for RecoverCare, LLC, in Louisville, Kentucky. Rosalyn Jordan is director of clinical education and Marci Christian is a clinical associate product specialist.

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Here are resources that can help you in your busy clinical practice by giving you information quickly.

New guidelines for managing diabetic foot ulcers

The International Affairs & Best Practice Guidelines has released “Assessment and Management of Foot Ulcers for People with Diabetes, Second Edition,” published by the Registered Nurses’ Association of Ontario.

The guidelines include recommendations for practice, education, policy, and future resource. Strategies for implementation are given, as well as several useful appendices, such as:

• Debridement Decision-Making Algorithm
• A Guide to Dressing Foot Wounds
• PEDIS: Diabetes Foot Ulcer Classification System
• Offloading Devices
• Optimal Treatment Modalities.

The guidelines also recommend that clinicians refer to “Toolkit: Implementation of Best Practice Guidelines, Second Edition.”

PREPARE for complex medical decisions

PREPARE is a useful and patient-friendly website designed to help prepare people to make complex medical decisions. The website was developed by clinical researchers from the San Francisco VA Medical Center; the University of California, San Francisco; and NCIRE—The Veterans Health Research Institute.

PREPARE uses videos to provide concrete examples of how to identify what is most important in life; how to communicate that with family, friends, and doctors; and how to make informed medical decisions when the time comes. Users can also download a PDF of a PREPARE pamphlet.

Free guides for infection prevention from APIC

Download two free implementation guides for infection prevention from the Association for Professionals in Infection Control and Epidemiology (APIC):

2013 Guide to Preventing Clostridium difficile Infections

This revised guide contains strategies for prevention, considerations for specific patient populations, evolving practices, and how to incorporate current regulations.

Topics include:

• C. difficile in pediatrics and skilled nursing facilities
• pathogenesis and changing epidemiology of C. difficile infection diagnosis
• environmental control
• new and emerging technologies
• tools and examples to help apply preventative measures, such as hand hygiene monitoring, environmental cleaning, and isolation compliance.

2013 Guide to Infection Prevention in Emergency Medical Services

This guide includes infection-prevention standards, regulations, and best practices, as well as instructions, examples, and tools to conduct surveillance and risk assessments.

Making health care safer

“Making Health Care Safer II: An Updated Critical Analysis of the Evidence for Patient Safety Practices,” from the Agency for Healthcare Research and Quality, covers several topics of interest, such as preventing in-facility pressure ulcers, promoting a culture of safety, and human factors and ergonomics. The report lists 22 patient-safety strategies that are ready for adoption. You can access more information about these strategies, read a related special supplement from the Annals of Internal Medicine, and read a thoughtful commentary about the report, “Treat the system, not the error: Patient safety in 2013.”

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Guidelines for managing prosthetic joint infections released

The Infectious Diseases Society of America has released guidelines for diagnosing and managing prosthetic joint infections.
“Diagnosis and management of prosthetic joint infection: Clinical practice guidelines by the Infectious Diseases Society of America,” published in Clinical Infectious Diseases, notes that of the 1 million people each year who have their hips or knees replaced, as many as 20,000 will get an infection in the new joint.
The guidelines describe the best methods for diagnosing these infections, which are not easy to identify. Specifically, infection should be suspected in a patient who has any of the following: persistent wound drainage in the skin over the joint replacement, sudden onset of a painful prosthesis, or ongoing pain after the prosthesis has been implanted, especially if there had been no pain for several years or if there is a history of prior wound healing problems or infections.
Guidelines for treating infections are included and note that 4 to 6 weeks of I.V. or highly bioavailable oral antibiotic therapy is almost always necessary to treat prosthetic joint infections.

A decade of TIME

The TIME acronym (tissue, infection/inflammation, moisture balance, and edge of wound) was first developed more than 10 years ago to provide a framework for a structured approach to wound bed preparation and a basis for optimizing the management of open chronic wounds healing by secondary intention. To mark the event, the International Wound Journal has published “Extending the TIME concept: What have we learned in the past 10 years?”
The review points out four key developments:
• recognition of the importance of biofilms (and the need for a simple diagnostic)
• use of negative-pressure wound therapy
• evolution of topical antiseptic therapy as dressings and for wound lavage (notably, silver and polyhexamethylene biguanide)
• expanded insight into the role of molecular biological processes in chronic wounds (with emerging diagnostics).
The authors conclude, “The TIME principle remains relevant 10 years on, with continuing important developments that incorporate new evidence for wound care.”

Bed alarms fail to reduce patient falls

A study in Annals of Internal Medicine found that the use of bed alarms had no statistical or clinical effect on falls in an urban community hospital.
The 18-month trial included 16 nursing units and 27,672 inpatients. There was no difference in fall rates per 1,000 patient-days, the number of patients who fell, or the number of patients physically restrained on units using bed alarms, compared with control units.
Authors of “Effects of an intervention to increase bed alarm use to prevent falls in hospitalized patients: A cluster randomized trial” speculate the lack of response may be related to “alarm fatigue.”

Drug for HIV might help in Staph infections

A study in Nature reports that the drug maraviroc, used to treat HIV, might be useful for treating Staphylococcus aureus infections.
“CCR5 is a receptor for Staphylococcus aureus leukotoxin ED” found that the CCR5 receptor, which dots the surface of immune T cells, macrophages, and dendritic cells, is critical to the ability of certain strains of Staph to specifically target and kill cells with CCR5, which orchestrate an immune response against the bacteria. One of the toxins the bacterium releases, called LukED, latches on to CCR5 and subsequently punches holes through the membrane of immune cells, causing them to rapidly die.
When researchers treated cells with CCR5 with maraviroc and exposed the cells to the Staph toxin, they found maraviroc blocked toxic effects.

Dog able to sniff out C. difficile

A 2-year-old beagle trained to identify the smell of Clostridium difficile was 100% successful in identifying the bacteria in stool samples, and correctly identified 25 of 30 cases of patients with C. difficile, according to a study in BMJ.
“Using a dog’s superior olfactory sensitivity to identify Clostridium difficile in stools and patients: Proof of principle study” discusses how the dog was trained to detect C. difficile and concludes that although more research is needed, dogs have the potential for screening for C. difficile infection.

After-hours access to providers reduces ED use

Patients who have access to their primary healthcare providers after hours use emergency departments (EDs) less frequently, according to a study in Health Affairs.
“After-hours access to primary care practices linked with lower emergency department use and less unmet medical need” found that 30.4% of patients with after-hours access to their primary care providers reported ED use, compared with 37.7% of those without this access. In addition, those with after-hours access had lower rates of unmet needs (6.1% compared to 12.7%).
The findings come from the 2010 Health Tracking Household Survey of the Center for Studying Health System Change. The total sample included 9,577 respondents.

Neuropathic pain in patients with DPN might contribute to risk of falling

The presence of neuropathic pain in patients with diabetic peripheral neuropathy (DPN) contributes to gait variability, which could in turn contribute to the risk of falling, according to “Increased gait variability in diabetes mellitus patients with neuropathic pain.”
The study, published in the Journal of Diabetes and Its Complications, compared patients with at least moderate neuropathic pain with those who had no pain. Researchers used a portable device to measure gait parameters, such as step length and step velocity.

Amputation rates decrease significantly in patients with PAD

“Temporal trends and geographic variation of lower-extremity amputation in patients with peripheral artery disease (PAD): Results from U.S. Medicare 2000–2008” found that amputation rates have decreased significantly, but that significant patient and geographic variations remain.
The study, published in the Journal of the American College of Cardiology, found that among 2,730,742 older patients with identified PAD, the overall rate of lower extremity amputation decreased from 7,258 per 100,000 patients to 5,790 per 100,000. Predictors of lower-extremity amputation included male sex, black race, diabetes mellitus, and renal disease.

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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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By Lydia Meyers, BSN, RN, CWCN

Necrotizing fasciitis (NF) results from an infection that attacks the fascia and subcutaneous tissues. The primary bacterial etiology is group A streptococcus, a facultative anaerobic bacterium. However, other bacteria may contribute. Sometimes called the “flesh-eating” disease because of the potentially devastating effect on the afflicted patient, NF can be monomicrobial or polymicrobial.

The four typical settings for NF are:

• surgical bowel or abdominal trauma surgery
• pressure ulcer and perianal abscess
• injection sites (especially in drug users)
• Bartholin abscess or minor vulvovaginal infection.

Because of the rapid course and ravaging nature of acute NF, clinicians must maintain a high index of suspicion if the patient has suggestive signs and symptoms. In 1990, puppeteer Jim Henson (best known for creating the Muppets) died from NF. At that time, little was known about the progression of group A streptococcal infection.
The disease can quickly cause death, so starting immediate treatment is even more crucial than confirming the diagnosis. Once the disease is suspected, antibiotics must be given immediately and the patient must be prepared for surgery at once. NF spreads rapidly, capable of progressing from a small lesion to death in days to weeks. Thus, delayed diagnosis increases the risk of death. Lack of knowledge about the disease and inability to recognize it promptly are the main reasons many victims die. This article can improve your knowledge base.

Overview

NF was discovered in 1871 by Joseph Jones, a Confederate Army surgeon. At that time, it was called hemolytic streptococcal gangrene, nonclostridial gas gangrene, nonclostridial crepitant cellulitis, necrotizing or gangrenous erysipelas, necrotizing cellulitis, bacterial synergistic gangrene, or synergistic necrotizing cellulitis.
NF involves the fascia, muscle compartments, or both. It can affect not only the muscle fascia but the superficial fascia. NF and cellulitis differ in the amount of tissue involved and extent of tissue involvement.
The most common areas of infection are the abdominal wall, perineum, and extremities. When NF affects the perineum and scrotum, it’s called Fournier gangrene, after the French dermatologist and virologist Alfred Jean Fournier.
The most common causes are trauma, surgery, and insect bites. The disease can affect persons of any age. Such comorbidities as diabetes, chronic renal failure, immunosuppressive therapy, hypertension, obesity, and malnutrition increase susceptibility.

Pathophysiology

NF falls into four classifications based on wound microbiology. Type 1, the most common, involves polymicrobial bacteria. Type 2 results from trauma and is associated with comorbidities. Type 3, rare in this country, stems from gram-negative marine bacteria. Type 4 is a fungal infection occurring mostly in immunocompromised persons. (See Comparing types of necrotizing fasciitis by clicking the PDF icon above.)

Disease progression

The four types of NF progress in a similar way. Bacteria secrete pyrogenic exotoxin A, which stimulates cytokines. These cyto­kines damage the endothelial lining; fluid then leaks into the extravascular space.
M proteins in streptococci and β-hemolytic streptococci exacerbate the immune reaction by inhibiting phagocytosis of polymorphonuclear leukocytes and normal neutrophil chemotaxis. As the immune reaction increases, blood vessels dilate, allowing toxins to leak through vessel walls, which in turn decreases blood flow. As the cascade continues, hypoxic conditions cause facultative aerobic organisms to grow and become anaerobic. These bacteria exacerbate destruction of surrounding cells and lead to release of carbon dioxide, water, hydrogen, nitrogen, hydrogen sulfide, and methane. As the infection continues to progress, toxins spread throughout the bloodstream and the patient becomes septic.

Assessment

Obtain the patient’s medical history and description of the wound. Determine when the changes first appeared and whether the affected area seemed to get worse recently.
In all NF types, patients commonly present with a small, painful area (possibly with entry marks) but no other signs or symptoms. The wound may appear as a bulla, cellulitis, or dermatitis, representing an infection developing in underlying tissues. The skin may have a wooden-hard feel as the infection progresses to the subcutaneous space and causes necrosis. The wound becomes discolored and necrotic; drainage is rare until surgical debridement begins. The patient quickly develops fever, chills, nausea, and vomiting. As NF progresses, bullae become dark purple with darkened edges; the patient grows disoriented and lethargic, and organ failure and respiratory failure
ensue. Without treatment, the patient dies.

Diagnosis

Diagnostic tests usually include magnetic resonance imaging, complete blood count with differential, comprehensive metabolic panel, and cultures. (See Diagnostic findings in necrotizing fasciitis by clicking the PDF icon above.)

Treatment

Immediate surgical debridement and broad-spectrum antibiotics are needed to stop the immune response to infection. Clindamycin, gentamicin, penicillin, or metronidazole may be given alone or in combination until culture results are available. Supportive care includes total parenteral nutrition for nutritional support, I.V. fluids, and oxygen. Limb amputation should be done only as a last resort.
Surgical debridement involves penetrating deep into the fascia and removing all necrotic tissue. After the first debridement, release of “dishwater fluid” may occur.
Administering hyperbaric oxygen therapy (HBOT) after the first debridement increases tissue oxygenation, thus reducing tissue destruction by anaerobic bacteria. During HBOT (usually given as a 90-minute treatment), the patient breathes 100% oxygen in an environment of increasing atmospheric pressure.
HBOT should be given in conjunction with surgical debridement (usually after each debridement) and should continue until necrotic tissue ceases and cell destruction stops. HBOT also promotes collagen synthesis and neoangiogenesis (new blood vessel growth), which boosts blood supply and oxygen to tissues.
Adverse effects of HBOT include ear pain, oxygen toxicity, and seizures. Ear pain can be minimized by swallowing or yawning. If the patient continues to have ear pain, ear tubes may be inserted by an otolaryngologist. During HBOT, air breaks (intervals of breathing room air) are important in controlling oxygen toxicity (the main cause of seizures).
Throughout the HBOT treatment period, wound dressings must be simple. Well-moistened gauze dressings and an abdominal pad provide good support. Once necrotic destruction occurs, dressings depend on wound size and the need to fill cavities. The patient may require a diverting colostomy, depending on wound
location and the amount of uncontrolled diarrhea. Blood glucose levels must be monitored before and after HBOT, as this treatment affects blood glucose.

Supportive care and follow-up treatment

During initial treatment, patients need supportive care and monitoring. Once they’re out of danger, begin teaching them how to prevent NF recurrences. Advise them to control blood glucose levels, keeping the glycated hemoglobin (HbA1c) level to 7% or less. Caution patients to keep needles capped until use and not to reuse needles. Instruct them to clean the skin thoroughly before blood glucose testing or insulin injection, and to use alcohol pads to clean the area afterward.
Before discharge, help arrange the patient’s aftercare, including home health care for wound management and teaching, social services to promote adjustment to lifestyle changes and financial concerns, and physical therapy to help rebuild strength and promote the return to optimal physical health. One helpful patient resource is the National Necrotizing Fasciitis Foundation. The Centers for Disease Control and Prevention section on necrotizing fasciitis includes “Common sense and great wound care are the best ways to prevent a bacterial skin infection.”
The life-threatening nature of NF, scarring caused by the disease, and in some cases the need for limb amputation can alter the patient’s attitude and viewpoint, so be sure to take a holistic approach when dealing with the patient and family. Today, NF has a much better survival rate than 2 decades ago when Jim Henson died. In my practice, I’ve seen four NF cases. Thanks to early identification, good wound care, and HBOT, these patients suffered only minimal damage.

Selected references

Boyer A, Vargas F, Coste F, et al. Influence of surgical treatment timing on mortality from necrotizing soft tissue infections requiring intensive care management. Intensive Care Med. 2009;35(5):847-853. doi:10.1007/s00134-008-1373-4.

Cain S. Necrotizing fasciitis: recognition and care. Practice Nurs. 2010;21(6):297-302.

Centers for Disease Control and Prevention. Notes from the field: fatal fungal soft-tissue infections after a tornado—Joplin, Missouri, 2011. MMWR. 2011;60(29):992.

Chamber AC, Leaper DJ. Role of oxygen in wound healing: a review of evidence. J Wound Care. 2011; 20(4):160-164.

Christophoros K, Achilleas K, Vasilia D, et al. Postraumatic zygomycotic necrotizing abdominal wall fasciitis with intraabdominal invasion in a non immunosuppressed patient. Internet J Surg. 2007;11(1). doi:10.5580/17a8.

Ecker K-W, Baars A, Topfer J, Frank J. Necrotizing fasciitis of the perineum and the abdominal wall-surgical approach. Europ J Trauma Emerg Surg. 2008;
34(3):219-228. doi:10.1007/s00068-008-8072-2.

Hunter J, Quarterman C, Waseem M, Wills A. Diagnosis and management of necrotizing fasciitis. Br J Hosp Med. 2011;72(7):391-395.

Magel DC. The nurse’s role in managing necrotizing fasciitis. AORN J. 2008;88(6):977-982.

Phanzu MD, Bafende AE, Imposo BB, Meyers WM, Portaels F. Under treated necrotizing fasciitis masquerading as ulcerated edematous Mycobacterium ulcerans infection (Buruli ulcer). Am J Trop Med Hyg. 2012;82(3):478-481.

Ruth-Sahd LA, Gonzales M. Multiple dimensions of caring for a patient with acute necrotizing fasciitis. Dimens Crit Care Nurs. 2006;25(1):15-21.

Stevens DL, Bisno AL, Chambers HF, et al; Infectious Diseases Society of America. Practice guidelines for the diagnosis and management of skin and soft-tissue infections. Clin Infect Dis. 2005;41(10):1373-1406.

Su YC, Chen HW, Hong YC, Chen CT, et al. Laboratory risk indicator for necrotizing fasciitis score and the outcomes. ANZ J Surg. 2008;78(11):968-972.

Taviloglu K, Yanar H. Necrotizing fasciitis: strategies for diagnosis and management. World J Emerg Surg. 2007;2:19.

Lydia Meyers is a medical reviewer for National Government Services in Castleton, Indiana, and a clinical liaison at CTI Nutrition in Indianapolis. She has 11 years of wound care experience in nursing homes, wound clinics, and home health.

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By Nancy Chatham, MSN, RN, ANP-BC, CWOCN, CWS, and Carrie Carls, BSN, RN, CWOCN, CHRN

Moisture-related skin breakdown has been called many things-perineal dermatitis, irritant dermatitis, contact dermatitis, heat rash, and anything else caregivers could think of to describe the damage occurring when moisture from urine or stool is left on the skin. At a 2005 consensus conference, attendees chose the term incontinence-associated dermatitis (IAD).

IAD can be painful, hard to properly identify, complicated to treat, and costly. It’s part of a larger group of moisture-associated skin damage that also includes intertrigo and periwound maceration. IAD prevalence and incidence vary widely with the care setting and study design. Appropriate diagnosis, prompt treatment, and management of the irritant source are crucial to long-term treatment.

Causes

IAD stems from the effects of urine, stool, and containment devices on the skin. The skin’s pH contributes to its barrier functions and defenses against bacteria and fungus; ideal pH is 5.0 to 5.9. Urine pH ranges from 4.5 to 8.0; the higher range is alkaline and contributes to skin damage.

Skin moisture isn’t necessarily damaging. But when moisture that contains irritating substances, such as alkaline urine, contacts the skin for a prolonged period, damage can occur. Urine on the skin alters the normal skin flora and increases permeability of the stratum corneum, weakening the skin and making it more susceptible to friction and erosion. Fecal incontinence leads to active fecal enzymes on the skin, which contribute to skin damage. Fecal bacteria can penetrate the skin, increasing the risk of secondary infection. Wet skin has a lower temperature than dry skin; wet skin under a pressure load has less blood flow than dry skin.

Containment devices, otherwise known as adult diapers or briefs, are multilayer disposable garments containing a superabsorbent polymer. The polymer is designed to wick and trap moisture in the containment device. This ultimately affects the skin by trapping heat and moisture, which may cause redness and inflammation that can progress to skin erosion. This trapping can lead to increased pressure against the skin, especially if the device has absorbed liquid and remains in contact with the skin.

Categorizing IAD

IAD is categorized as mild, moderate, or severe. (See Picturing IAD by clicking the PDF icon above.)

Screening for IAD

Screen the patient’s skin for persistent redness, inflammation, rash, pain, and itching at least daily. To differentiate IAD from pressure ulcers, keep in mind that:

• IAD can occur wherever urine or stool contacts the skin. In contrast, pressure ulcers arise over bony prominences in the absence of moisture.
• With IAD, affected skin is red or bright red. With a pressure ulcer, skin may take on a bluish purple, red, yellow, or black discoloration.
• The skin-damage pattern in IAD usually is diffuse. With a pressure ulcer, edges are well defined.
• The depth of IAD-related skin damage usually is partial-thickness without necrotic tissue. With a pressure ulcer, skin damage depth may vary.

Preventing IAD

The three essentials of IAD prevention are to cleanse, moisturize, and protect.

• Cleanse the skin with a mild soap that’s balanced to skin pH and contains surfactants that lift stool and urine from the skin. Clean the skin routinely and at the time of soiling. Use warm (not hot) water, and avoid excess force and friction to avoid further skin damage.
• Moisturize the skin daily and as needed. Moisturizers may be applied alone or
  incorporated into a cleanser. Typically, they contain an emollient such as lanolin to replace lost lipids in the stratum corneum.
• To protect the skin, apply a moisture-barrier cream or spray if the patent has significant urinary or fecal incontinence (or both). The barrier may be zinc-based, petrolatum-based, dimethicone-based, an acrylic polymer, or another type. Consider using an algorithm developed by wound and skin care specialists that’s customized for skin care products your facility uses. (See Skin care algorithm by clicking the PDF icon above.)

If the treatment protocol fails, the patient should be referred to an appropriate skin care specialist promptly.

To help prevent urine or stool from contacting the patient’s skin, consider using a male external catheter, a female urinary pouch, a fecal pouch, or a bowel management system. Avoid containment devices. If the patient has a containment pad, make sure it’s highly absorbent and not layered, to decrease pressure under the patient.

Managing IAD

A comprehensive multidisciplinary approach to IAD is essential to the success of any skin care protocol. Identify skin care champions within your facility and educate them on IAD. Incorporating administrators, physicians, nursing staff, therapists, and care assistants makes implementation of protocols and algorithms within an institution seamless.

Administrators support the skin care program in the facility, including authorizing a budget so product purchases can be made. The certified wound clinician is the team expert regarding skin care, incontinence, prevention, and product recommendation. The physician oversees protocol development and evaluates and prescribes additional treatment when a patients fails to respond to treatment algorithms. Nursing staff identify patients at risk, incorporate the algorithm into the patient’s plan of care, and direct care
assistants. Therapists address function, strength, and endurance issues to improve the patient’s self-care abilities in activities of daily living to manage or prevent episodes of incontinence.

In severe inflammation, topical dressings, such as alginates and foam dressings, may be used along with topical corticosteroids. In complex IAD, antifungals or antibiotics may be required if a secondary fungal or bacterial infection is suspected.

Additional diagnostic tests may be done to identify and treat secondary infections. These tests may include skin scraping, potassium hydroxide test or Gram’s stain for fungal components, or a swab culture and sensitivity for bacterial infections. If your patient has a suspected secondary fungal or bacterial infection, use appropriate treatments for the full course of recommended therapy. In severe secondary fungal infection, an oral agent may be added to topical therapy. If cost is a concern, consider using a pharmacy knowledgeable about compounding for topical combination therapies.

Referrals and education

For assessment and treatment of under-lying incontinence, refer the patient to a continence specialist if appropriate. Teach the patient strategies for managing incontinence through dietary measures, toileting programs, pelvic-floor muscle training, clothing modification, and mobility aids.

Selected references

Beguin A, Malaquin-Pavan E, Guihaire C, et al., Improving diaper design to address incontinence associated dermatitis. BMC Geriatrics. 2010;10:86. http://www.biomedcentral.com/1471-2318/10/86. Accessed March 15, 2012.

Black JM, Gray M, Bliss DZ, et al. MASD part 2: incontinence-associated dermatitis and intertriginous dermatitis. J Wound Ostomy Continence Nurs. 2011; 38(4):359-370.

Bliss DZ, Zehrer C, Savik K, et al. An economic evaluation of four skin damage prevention regimens in nursing home residents with incontinence: economics of skin damage prevention. J Wound Ostomy Continence Nurs. 2007;34(2):143-152.

Denat Y, Khorshid L. The effect of 2 different care products on incontinence-associated dermatitis in patients with fecal incontinence. J Wound Ostomy Continence Nurs. 2011;38(2):171-176.

Doughty DB. Urinary and Fecal Incontinence: Current Management Concepts. 3rd ed. St. Louis, MO: Mosby Elsevier; 2006.

Gray, M. Optimal management of incontinence-associated dermatitis in the elderly. Am J Clin Dermatol. 2010;11(3):201-210.

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, Bliss DZ, Doughty DB, et al. Incontinence-associated dermatitis: a consensus. J Wound Ostomy Continence Nurs. 2007;34(1):45-54.

Gray M, Bohacek L, Weir D, et al. Moisture vs pressure: making sense out of perineal wounds. J Wound Ostomy Continence Nurs. 2007;34(2):134-42.

Institute for Clinical Systems Improvement. Health care protocol: Pressure ulcer prevention and treatment. Bloomington, MN: Institute for Clinical Systems Improvement. January 2012. http://www.icsi.org/pressure_ulcer_treatment_protocol__review_and_comment_/pressure_ulcer_treatment__protocol__.html. Accessed March 15, 2012.

Junkin J, Lerner-Selekof JL. Prevalence of incontinence and associated skin injury in the acute care inpatient. J Wound Ostomy Continence Nurs. 2007;34(3):260-269.

Landefeld CS, Bowers BJ, Feld AD, et al. National Institutes of Health state-of-the-science conference statement: prevention of fecal and urinary incontinence in adults. Ann Intern Med. 2008;148(6):449-458.

Langemo D, Hanson D, Hunter S, et al. Incontinence and incontinence-associated dermatitis. Adv Skin Wound Care. 2011;24(3):126-142.

Scheinfeld NS. Cutaneous candidiasis workup. 2011 update. http://emedicine.medscape.com/article/1090632-workup. Accessed March 15, 2012.

U.S. Census Bureau. The older population 2010. November 2011. www.census.gov/prod/cen2010/briefs/c2010br-09.pdf. Accessed March 15, 2012.

Nancy Chatham is an advanced practice nurse at Passavant Physician Associates in Jacksonville, Illinois. Carrie Carls is the nursing director of advanced wound healing and hyperbaric medicine at Passavant Area Hospital in Jacksonville, Illinois.

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