Sample procedure for nonsterile dressing change

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

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

Description

• Nonsterile dressings protect open wounds from contamination and absorb drainage.
• Clean aseptic technique should be used to change nonsterile dressings.
• In the event of multiple wounds, each wound is considered a separate treatment. (more…)

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Clinical Notes

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

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

Medicare expenditures for diabetic foot care varies significantly by region

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

Patients who develop pressure ulcers in hospital more likely to die

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

Patients with diabetic foot ulcers may have higher risk of death

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

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

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

View: StomaLife video

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

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

Palliative care raises patient satisfaction and reduces costs

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

More research needed to determine efficacy of maggot debridement therapy

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

Use tool to select correct antimicrobial dressing

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

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Why not call it a pressure ulcer?

By: Donna Sardina, RN, MHA, WCC, CWCMS, DWC, OMS

The most basic principle of healing a wound is to determine the cause—and then remove it. This is easier said than done, as many wounds have similar characteristics and we don’t always know all the facts leading up to the wound.
The process has been unnecessarily complicated by the recent pressure (no pun intended) to avoid at all costs calling a pressure ulcer a pressure ulcer. I use the term “unnecessarily” because it doesn’t matter what it’s called—a pressure ulcer, decubitus, “de-cube,” or bedsore—because in the end, the general idea is it’s bad news.
So what’s behind the desire to avoid calling it a pressure ulcer? First, a pressure ulcer has traditionally been equated to poor nursing care. As Florence Night­in­gale, the “Mother of Nursing,” wrote:
If he has a bedsore, it’s generally not the fault of the disease, but of the nursing.”
No one likes to feel that he or she gave poor care, and as more hospital complications data are available to the public, reports of complications such as pressure ulcers affect people’s perceptions—right or wrong—about the care a hospital delivers.
The second reason gets at the “at all costs” part of the desire. The recent attention given to Medicare’s “present on admission” rule and “never” events has
elevated pressure ulcers high up the chain of “no-no’s” and put the hospital at risk for nonreimbursement. And many private insurers have followed Medicare’s lead in denying coverage for pressure ulcers that occur in the hospital. Unfortunately, all the focus on reimbursement is beginning to challenge even the best wound care experts, who simply want to get the patient’s wound healed.
Pressure from upper management has resulted in experts trying to bargain and rationalize their way out of calling it what it is (a pressure ulcer), instead calling it a bruise, not a deep-tissue injury. Or saying, “This is a shearing ulcer, not a pressure ulcer.” Or, my favorite: “It’s not an ischial pressure ulcer but a diabetic ulcer because the patient is a diabetic.” Wound care experts are being forced to question and doubt themselves because money, quality assurance, and reputation are on the line when an in-house wound is labeled a pressure ulcer.
Like crime scene investigation, determining wound etiology requires us to gather all the facts. Once the facts are in, systematically comparing and contrasting the clinical findings aids differential identification to pin down the type of wound present. It’s important that we assess and investigate all the following when searching for the cause:
•    patient’s medical history
•    recent activities (such as surgery, extensive X-rays, or long emergency-
department waits)
•    comorbidities
•    specific wound characteristics, such as location, distribution, shape, wound bed, and surrounding skin.

Naming the wound is an important first step in intervening. If the wound is caused by pressure, call it a pressure ulcer and jump into action. Remove the cause, heal the wound, and prevent further breakdown. Don’t let yourself be influenced by those who aren’t experts in wound care.

Donna Sardina, RN, MHA, WCC, CWCMS, DWC, OMS
Editor-in-Chief
Wound Care Advisor
Cofounder, Wound Care Education Institute
Plainfield, Illinois

Selected reference
Nightingale F. Notes on Nursing: What It Is, And What It Is Not. London: Harrison and Sons; 1859. http://ia600204.us.archive.org/17/items/notes
nursingnigh00nigh/notesnursingnigh00nigh.pdf.

Accessed August 30, 2012.

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Necrotizing fasciitis: Frightening disease, potentially grim prognosis

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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