More results...
Practical Issues in Wound, Skin and Ostomy Management
By Jennifer Zinn, MSN, RN, CNS-BC, CNOR, and Vangela Swofford, BSN, RN, ASQ-CSSBB
For surgical patients, operative wound classification is crucial in predicting postoperative surgical site infections (SSIs) and associated risks. Information about a patient’s wound typically is collected by circulating registered nurses (RNs) and documented at the end of every surgical procedure. (more…)
Read More
By Marcia Spear, DNP, ACNP-BC, CWS, CPSN
Chronic wound infections are a significant healthcare burden, contributing to increased morbidity and mortality, prolonged hospitalization, limb loss, and higher medical costs. What’s more, they pose a potential sepsis risk for patients. For wound care providers, the goal is to eliminate the infection before these consequences arise.
Most chronic wounds are colonized by polymicrobial aerobic-anaerobic microflora. However, practitioners continue to debate whether wound cultures are relevant. Typically, chronic wounds aren’t cultured unless the patient has signs and symptoms of infection, which vary depending on whether the wound is acute or chronic. (See Differentiating acute and chronic wounds.) (more…)
Read MoreBy Lydia A. Meyers RN, MSN, CWCN
Missed care, a relatively new concept in the medical community, refers to any part ofrequired patient care that is omitted of delayed. It’s not the same as a mistake or error, but like them, missed care can negatively affect patient outcomes.
I want to share the case of a patient admitted into home health care for wound care. The case includes several areas of missed care from many different different sources. (more…)
Read MorePerformance scores for rates of hospital-acquired pressure ulcers might not be appropriate for comparing hospitals, according to a study in the Annals of Internal Medicine.
“Hospital report cards for hospital-acquired pressure ulcers: How good are the grades?,” funded by the Agency for Healthcare Research and Quality, analyzed 2 million all-payer administrative records from 448 California hospitals and quarterly hospital surveillance data from 213 hospitals from the Collaborative Alliance for Nursing Outcomes. (more…)
Read Moreby Donna Sardina, RN, MHA, WCC, CWCMS, DWC, OMS
With uncertainty over how the Affordable Care Act (ACA) ultimately will affect operations, hospitals and other healthcare facilities are tightening up. In many areas, they’re laying off staff. In May, the healthcare industry lost 9,000 jobs—the worst month for the industry in a decade—and another 4,000 jobs were lost in July.
Medicare, Medicaid, and private insurance companies are reducing reimbursements to care providers, meaning less money is coming in and healthcare facilities have less money to pay out. In my experience, when job cuts are needed, the specialty and subspecialty positions go first. Wound and ostomy care is a subspecialty, so we need to be prepared to protect our jobs—not only for ourselves but for our patients. (more…)
Read MoreBy 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…)
Read More
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.
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 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 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 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 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.)
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.)
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.
Read MoreChronic venous insufficiency (CVI) is the most common cause of lower extremity wounds. The venous tree is defective, incapable of moving all the blood from the lower extremity back to the heart. This causes pooling of blood and intravascular fluid at the lowest gravitational point of the body—the ankle.
This article has two parts. Part 1 enhances your understanding of the disease and its clinical presentation. Part 2, which will appear in a later issue, explores the differential diagnosis of similar common diseases, the role that coexisting peripheral artery disease (PAD) may play, disease classification of venous insufficiency, and a general approach to therapy.
The most common form of lower extremity vascular disease, CVI affects 6 to 7 million people in the United States. Incidence increases with age and other risk factors. One study of 600 patients with CVI ulcers revealed that 50% had these ulcers for 7 to 9 months, 8% to 34% had them for more than 5 years, and 75% had recurrent ulcers.
Thrombotic complications of CVI include thrombophlebitis, which may range from superficial to extensive. If the thrombophlebitis extends up toward the common femoral vein leaving the leg, proximal ligation may be needed to prevent clot extension or embolization.
Lower extremity veins flow horizontally from the superficial veins to the perforating veins and then into the deep veins. Normally, overall venous blood flows vertically against gravity from the foot and ankle upward toward the inferior vena cava (IVC). This antigravity flow toward the IVC results from muscular contraction around nonobstructed veins and one-way valves that close as blood passes them. These valves prevent abnormal backward blood flow toward the foot and ankle region.
The lower extremities have four types of veins. Superficial veins are located within the subcutaneous tissue between the dermis and muscular fascia. Examples are the greater and lesser (smaller) saphenous veins. Perforating veins connect the superficial veins to the deep veins of the leg. The deep veins are located below the muscular fascia. The communicating veins connect veins within the same system.
The greater saphenous vein is on the leg’s medial (inner) side. It originates from the dorsal veins on top of the foot and eventually drains into the common femoral vein in the groin region. By way of perforating veins, the greater saphenous vein drains into the deep venous system of both the calf and thigh.
The lesser saphenous vein is situated on the lateral (outer) side of the leg and originates from the lateral foot veins. As it ascends, it drains into the deep system at the popliteal vein behind the knee. Communicating veins connect the greater saphenous vein medially and the lesser saphenous vein laterally.
Intramuscular veins are the deep veins within the muscle itself, while the intermuscular veins are located between the muscle groups. The intermuscular veins are more important than other veins in development of chronic venous disease. Below the knee, the intermuscular veins are paired and take on the name of the artery they accompany—for example, paired anterior tibial, paired posterior tibial, and paired peroneal veins. Eventually, these veins form the popliteal vein behind the knee, which ultimately drains into the femoral vein of the groin.
As the common femoral vein travels below the inguinal ligament of the groin, it’s called the external iliac vein. Eventually, it becomes the common iliac vein, which drains directly into the IVC.
Abnormally elevated venous pressure stems from the leg’s inability to adequately drain blood from the leg toward the heart. Blood drainage from the leg requires the muscular pumping action of the leg onto the veins, which pump blood from the leg toward the heart as well as from the superficial veins toward the deep veins. Functioning one-way valves within the veins close when blood passes them, preventing blood from flowing backward toward the ankle. This process resembles what happens when you climb a ladder with intact rungs: As you step up from one rung to the next, you’re able to ascend.
If the one-way valves are damaged or incompetent, the “broken rung” situation occurs. Think how hard it would be to climb a ladder with broken rungs: You might be able to ascend the ladder, but probably you would fall downward off the ladder due to the defective, broken rungs.
Normally, one-way valves ensure that blood flows from the lower leg toward the IVC and that the superficial venous system flows toward the deep venous system. The venous system must be patent (open) so blood flowing from the leg can flow upward toward the IVC. Blockage of a vein may result from an acute thrombosis (clot) in the superficial or deep systems. With time, blood may be rerouted around an obstructed vein. If the acute thrombosis involves one or more of the one-way valves, as the obstructing thrombosis opens up within the vein’s lumen, permanent valvular damage may occur, leading to post-thrombotic syndrome—a form of CVI.
CVI may result from an abnormality of any or all of the processes needed to drain blood from the leg—poor pumping action of the leg muscles, damage to the one-way valves, and blockage in the venous system. CVI commonly causes venous hypertension due to reversal of blood flow in the leg. Such abnormal flow may cause one or more of the following local effects:
The effect of elevated venous pressure or hypertension is worst at the lowest gravitational point (around the ankle). Pooling of blood and intravascular fluid around the ankle causes a “water balloon” effect. A balloon inflated with water has a thin, easily traumatized wall. When it bursts, a large volume of fluid drains out. Due to its thicker wall, a collapsed balloon that contains less fluid is more difficult to break than one distended with water.
In a leg with CVI, subcutaneous fluid that builds up requires a weaker force to break the skin and ulcerate than does a nondistended leg with less fluid. This principle is the basis for compression therapy in treating and preventing CVI ulcers.
Increased pressure in the venous system causes:
Abnormal vein swelling from elevated pressure in itself may impair an already abnormally functioning one-way valve. For instance, the valve may become more displaced due to the increase in intraluminal fluid, which may in turn worsen hypertension and cause an increase in leg swelling. Increased pressure from swollen veins also may dilate the capillary beds that drain into the veins; this may cause leakage of fluid and red blood cells from capillaries into the interstitial space, exacerbating leg swelling. Also, increased venous pressure may cause fibrinogen to leak from the intravascular plasma into the interstitial space. This leakage may create a fibrin cuff around the capillary bed, which may decrease the amount of oxygen entering the epidermis, increase tissue hypoxia, trigger leukocyte activation, increase capillary permeability, and cause local inflammation. These changes may lead to ulceration, lipodermatosclerosis, or both.
Visible changes may include dilated superficial veins, hemosiderin staining due to blood leakage from the venous tree, atrophie blanche, and lipodermatosclerosis. (See CVI glossary by clicking the PDF icon above.) Both atrophie blanche and lipodermatosclerosis result from local tissue scarring secondary to an inflammatory reaction of the leg distended with fluid.
Lipodermatosclerosis refers to scarring of subcutaneous tissue in severe venous insufficiency. Induration is associated with inflammation, which can cause the skin to bind to the subcutaneous tissue, causing narrowing of leg circumference. Lymphatic flow from the leg also may become compromised and inhibited in severe venous hypertension, causing additional leg swelling.
In a patient with known or suspected CVI, a thorough history may lead to a working diagnosis. Be sure to ask the patient these questions:
Also determine if the patient has comorbidities that may exacerbate CVI, including PAD, renal failure, venous thrombosis, lymphedema, diabetes mellitus, heart failure, or malnutrition. (See CVI risk factors by clicking the PDF icon above .)
Approximately 20% of CVI patients have symptoms of the disease without physical findings. These symptoms may include:
Although patients may report leg discomfort, the history indicates that it doesn’t awaken them at night. Be aware that discomfort from CVI differs from that caused by PAD. With PAD, patients may report pain on exercise (claudication), pain with elevation (nocturnal pain), or constant pain (resting pain).
Signs of CVI (with or without ulcers) include:
Venous ulcers are the most common type of lower extremity ulcer. They’re commonly found on the medial aspect of the lower extremity, from the ankle to the more proximal calf area. Usually, they arise along the course of the greater saphenous vein, but also may be lateral and may occur at multiple locations. They aren’t found above the knee or on the forefoot. Venous ulcers are shallower than arterial ulcers and have considerable exudate consistent with drainage from a ruptured water balloon. They may extend completely around the leg.
In patients with CVI, blood flows within a lower extremity in an abnormal, reverse direction, causing build-up of blood and intravascular fluid around the ankle. Initially, this may cause only a sensation of heavy legs toward the end of the day, with no visible changes. Eventually, it may lead to venous ulcers or other visible changes. This abnormal blood flow results from dysfunction of the normal mechanisms that drain blood from the leg against gravity into the IVC.
Selected references
Alguire PC, Mathes BM. Clinical evaluation of lower extremity chronic venous disease. UpToDate. Last updated April 18, 2012. http://www.uptodate.com/contents/clinical-evaluation-of-lower-extremity-chronic-venous-disease?source=search_result&
search=Clinical+evaluation+of+lower+extremity+chronic+venous+disease&selectedTitle=1%7E150. Accessed March 3, 2013.
Alguire PC, Mathes BM. Diagnostic evaluation of chronic venous insufficiency. UpToDate. Last updated May 7, 2012. www.uptodate.com/contents/diagnostic-evaluation-of-chronic-venous-insufficiency?source=search_result&search=Diagnostic+evaluation
+of+chronic+venous+insufficiency&selectedTitle=1%7E127. Accessed March 3, 2013.
Alguire PC, Mathes BM. Pathophysiology of chronic venous disease. UpToDate. Last updated April 12, 2012. www.uptodate.com/contents/pathophysiology-of-chronic-venous-disease?source=search_result&search=Pathophysiology+of+chronic+venous+disease
&selectedTitle=1%7E127. Accessed March 3, 2013.
Alguire PC, Scovell S. Overview and management of lower extremity chronic venous disease. UpToDate. Last updated June 27, 2012. www.uptodate.com/contents/overview-and-management-of-lower-extremity-chronic-venous-disease?source=search_
result&search=Overview+and+management+of+lower+extremity+chronic+venous+disease&selectedTitle=1%7E150. Accessed March 3, 2013.
Moneta G. Classification of lower extremity chronic venous disorders. UpToDate. Last updated October 22, 2011. www.uptodate.com/contents/classification-of-lower-extremity-chronic-venous-disorders. Accessed March 3, 2013.
Sardina D. Skin and Wound Management Course; Seminar Workbook. Wound Care Education Institute; 2011:92-112.
Donald A. Wollheim is a practicing wound care physician in southeastern Wisconsin. He also is an instructor for Wound Care Education Institute and Madison College. He serves on the Editorial Board for Wound Care Advisor.
Read MoreBy Carrie Carls, BSN, RN, CWOCN, CHRN; Michael Molyneaux, MD; and William Ryan, CHT
Every year, 1.9% of patients with diabetes develop foot ulcers. Of those, 15% to 20% undergo an amputation within 5 years of ulcer onset. During their lifetimes, an estimated 25% of diabetic patients develop a foot ulcer. This article discusses use of hyperbaric oxygen therapy (HBOT) in treating diabetic foot ulcers, presenting several case studies.
HBOT involves intermittent administration of 100% oxygen inhaled at a pressure greater than sea level. It may be given in a:
• multi-place chamber (used to treat multiple patients at the same time), compressed to depth by air as the patient breathes 100% oxygen through a face mask or hood (more…)
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.
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.
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.)
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.
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.
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.
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.
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.
Read More
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.
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.
IAD is categorized as mild, moderate, or severe. (See Picturing IAD by clicking the PDF icon above.)
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:
The three essentials of IAD prevention are to cleanse, moisturize, and protect.
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.
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.
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.
Read More