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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What caused Mr. M’s pressure ulcer?

A court case answers the question as to whether a pressure ulcer was preventable

By Nancy J. Brent, MS, RN, JD

Pressure ulcers are a major health risk for every adult patient. Risk factors include sepsis, hypotension, and age 70 or older. These risk factors became all too real when Mr. M developed pressure ulcers after being admitted to a Texas hospital.

Background

Mr. M, age 81, presented at a medical center’s emergency department on January 2 complaining of abdominal pain. After undergoing an assessment, he was diagnosed with gallstones and admitted to the hospital. The next day, he had gallbladder surgery. He subsequently developed a bowel obstruction and had to undergo two more surgeries for this condition over the next 10 days.
On January 13, he was transferred to the intensive care unit (ICU) because of multiple serious medical conditions, including respiratory distress syndrome (necessitating ventilatory support), septic shock, a “blood infection” that caused his blood pressure to drop, and multiorgan failure. His primary physician discontinued tube feedings out of concern they might exacerbate his renal failure; he wrote a do-not-resuscitate order and ordered sedation.
Mr. M was unable to turn or position himself in any way. While in the ICU, he developed a “skin tear” on the tailbone (coccyx) that progressed to a serious pressure ulcer. On February 6, his condition improved enough to allow his transfer to a rehabilitation hospital, where he developed pressure ulcers on his heels. He was transferred to another hospital; the ulcer on his coccyx healed by August. He remained in that hospital for 1 year before being discharged home.
Despite healing of the pressure ulcer on his coccyx, the wound area remained hard and painful, and Mr. M experienced “daily discomfort” there. Also, he was unable to do many of the things he’d been able to do before his hospitalization.

Mr. M files a medical malpractice suit

Mr. M sued the medical center, alleging the hospital was negligent by failing to prevent the pressure ulcer from forming through the use of known “pressure relief” methods, and that the hospital failed to provide proper care and treatment of the wound once it was discovered.
At trial, the medical center lawyers argued that Mr. M’s grave condition caused the pressure ulcer to develop. The jury returned a verdict for Mr. M, finding that the medical center’s negligence proximately caused the injuries he sustained. It awarded him $35,000 for medical expenses; $135,000 for past physical pain and mental anguish; $25,000 for future physical pain and mental anguish; $25,000 for past physical impairment; and $25,000 for future physical impairment. The medical center appealed the decision.

Medical center appeals the verdict

Several issues were raised by the medical center on appeal. Of particular interest to nurses and wound care practitioners was the “cause in fact” or the “proximate cause” of Mr. M’s pressure ulcer on the coccyx. Because an expert witness must establish proximate cause based on a reasonable degree of medical certainty, Mr. M’s case became a battle of the experts regarding the care he received, or lack of care, relative to development of the pressure ulcer.

Expert witness testimony for Mr. M

The first nurse expert to testify was Mr. M’s highly qualified expert. She testified about the various acceptable ways to provide pressure relief, including turning the patient or, if the patient can’t be turned, repositioning. The latter requires use of foam wedges or pillows to elevate a particular body part. The nurse expert testified that if a patient can’t be turned or repositioned, that fact must be documented along with the reason for inability to carry out this nursing care.
Proper assessment of the pressure ulcer is required so that other team members can “see” the wound; the clinician who assesses the wound should draw a picture of exactly what he or she saw when documenting the note in the patient’s chart. The nurse expert testified that the assessment should include the color, duration, and depth of the pressure ulcer; presence or absence of infection; and whether the tissue was dead or perfused.
After reviewing the medical center’s policies and protocols on pressure relief, which required nurses to provide pressure relief every 2 hours, and the depositions of the nurses who’d cared for Mr. M, the nurse expert testified there was no documentation showing Mr. M received any pressure relief from January 13 to January 16. She said she could only conclude that the nurses failed to turn or reposition him during those days. The only notation made about his skin condition was when nurses discovered the “skin tear” on January 14. After this discovery, the physician wasn’t notified of it until January 19. On that date, the physician ordered a wound care consult, but the actual consultation didn’t occur until 3 days later. Even with the wound consultant’s specific, written orders to care for the wound, only one notation existed showing that the orders were followed. Also, the wound care orders weren’t entered into Mr. M’s care plan until January 28. Additionally, in their depositions, the nurses caring for Mr. M couldn’t recall changing the dressing as ordered.
Therefore, in the nurse expert’s opinion, the pressure ulcer on Mr. M’s coccyx was caused directly by failure of the ICU nurses to provide pressure relief from January 14 to January 16 and that providing the wound care that was ordered would have prevented the ulcer from getting worse and would have healed the ulcer.
Although a physician serving as a second expert for Mr. M also testified that pressure relief should have been provided, he couldn’t say that development of the pressure ulcer was unpreventable.

Expert witness testimony for the medical center

Not surprisingly, the medical center’s expert witnesses, two of whom were physicians, testified that because of Mr. M’s general medical condition, he would have developed the pressure ulcer even if hospital policies and protocols had been followed. The hospital’s nurse expert witness stated that Mr. M’s pressure ulcer was not preventable because of his medical condition, regardless of whether or not he was turned. In her opinion, the active range of motion his nurses put him through was enough to reperfuse the area.

Appellate court’s decision

The appellate court upheld the trial court jury’s verdict, stating that evidence presented at the trial was legally and factually sufficient to support that verdict.

Take-away points

Mr. M’s case undoubtedly was complicated by his age and general medical condition, as well as disagreement among expert witnesses as to the cause of the pressure ulcer on his coccyx. Even so, the appellate court held that the evidence at trial (specifically that presented by Mr. M’s nurse expert witness) was sufficient legally and factually to support the verdict in favor of Mr. M.
This case illustrates many areas of importance for nurses in terms of formation and care of pressure ulcers. They include the following:
• Risk factors supporting potential formation of pressure ulcers can’t be overlooked or underestimated by nursing staff.
• A plan to prevent pressure ulcers should be initiated on admission for every patient who is immobile or has other risk factors for pressure ulcers.
• Documentation of every aspect of nursing care that’s initiated and continued to prevent pressure ulcers from forming must be carried out as ordered and pursuant to hospital policy and protocol.
• Care plans, communications with other health team members, and carrying out of orders must be done as soon as possible.
• Assessment and documentation of pressure ulcers should include enough detail so other health team members can visualize what the nurse entering the documentation has seen.
• The nurse should assess and stage the pressure ulcer at each dressing change.
• One’s expert witness must be credentialed, educated, and experienced in would care prevention and treatment, because his or her testimony can win or lose a case.

Nursing remains at the forefront of protecting and safeguarding patients from pressure ulcers. Although not every ulcer can be prevented, the goal is to prevent as many ulcers as possible. If a pressure ulcer does occur, caregivers’ essential focus must be on healing or preventing further deterioration and infection.

Selected references
Columbia Medical Center Subsidiary, L.P., d/b/a/
North Central Medical Center, Appellant, v. John Meier, Appellee. 198 S.W. 3d 408 (Ct. Appeals 2006).

Lyder CH, Ayello EA. Pressure ulcers: A Patient Safety Issue. In: Hughes RG, ed. Patient Safety and Quality: An Evidence-Based Handbook For Nurses. Rockville, MD: Agency For Healthcare Research and Quality. April 2008. www.ncbi.nlm.nih.gov/books/
NBK2650/. Accessed November 1, 2012.

Nancy J. Brent is an attorney in Wilmette, Illinois. The information in this article is for educational purposes only and doesn’t constitute legal advice.

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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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