By Jeri Lundgren, BSN, RN, PHN, CWS, CWCN

Every year, all long-term care (LTC) facilities funded by Medicare or Medicaid are inspected to ensure they are in compliance with federal and state regulations. The regulations are broken down into so-called F-Tags to help track data. The F-Tag designated for review of the facility’s pressure-ulcer prevention and management program is F314. If a resident develops a pressure ulcer in the facility or if a pressure ulcer worsens while the resident is in the facility (even

if the resident was admitted with the pressure ulcer), the facility could face a citation under F314. Such a citation, if not remedied, could lead to financial penalties, Medicare and Medicaid fund stoppages, or even closing of the facility.
When preparing for this annual survey, many providers focus on the charts of residents with wounds. However, many citations are triggered from residents without wounds. For example, a surveyor may observe a resident lying in a position longer than the plan of care indicates. So when preparing for a survey, staff should always look at the big picture—wound prevention and management.
The following items should be audited to help ensure your documentation is compliant with the F314 tag:

1. The risk assessment (such as with the Braden risk assessment tool) should be current and accurate. In LTC facilities, the risk assessment should be done:

• on admission or readmission
• weekly for the first 4 weeks after
admission
• with a change in the resident’s condition
• quarterly or annually with the minimum data set (MDS).

2. The plan of care should be audited to ensure that:
• all risk factors identified from the risk assessment, MDS, care area assessment, resident history, physical examination, and overall chart review are pulled forward and listed on the skin integrity plan of care
• the plan of care identifies correlating interventions to help stabilize or modify individual risk factors
• staff have been interviewed and have physically observed the resident to ensure all risk factors and interventions provided are reflected accurately on the plan of care.

3. Nursing-assistant assignment sheets should match the information on the plan of care.

4. Head-to-toe skin checks are performed weekly on all residents by licensed staff.

5. Wound assessments are done at least every 7 days, are complete and accurate, and include evaluation of wound progress.

6. Documentation reflects that the physician or nurse practitioner, family, and interdisciplinary team are notified when a wound is discovered, when no progress has occurred in 2 weeks, when the resident declines, and when the wound heals.

7. The treatment sheet order is transcribed accurately and treatment is being provided as prescribed.

Other items to audit

Also audit these items to prepare for the survey:

• resident turning and repositioning
• incontinence care
• use of supplies, equipment, and devices (such as heel lift boots, wheelchair cushions, and powered mattresses) to ensure these are functioning properly and are in good condition
• dressing-change technique
• storage of wound care supplies to ensure they meet infection-control guidelines and haven’t expired.

Ideally, the wound care nurse or nurse manager should set aside a designated number of hours every month to audit charts and observe hands-on care. This person also can use weekly wound rounds to monitor dressing changes, nurses’ ability to assess wounds, and equipment and dressing supplies.

Jeri Lundgren is director of clinical services at Pathway Health in Minnesota. She has been specializing in wound prevention and management since 1990.

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.

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.

By Joseph G. Garner, MD, FIDSA, FSHEA

Staphylococcus aureus is one of the most feared human pathogens, causing a wide range of infections. Most wound care professionals can expect to frequently encounter patients with S. aureus infections. Soft-tissue infections caused by S. aureus include impetigo, cellulitis, and cutaneous abscesses, as well as such life-threatening processes as necrotizing fasciitis and pyomyositis (a hematogenous intramuscular abscess). Serious non-soft-tissue infections include septic arthritis, osteomyelitis, pneumonia, endocarditis, and sepsis.

Why is S. aureus such a nasty bug?

S. aureus produces various cellular and extracellular factors involved in the pathogenesis of infection. S. aureus protein A, an important surface protein, helps the organism resist phagocytosis. Also, S. aureus produces several cytotoxins and enzymes that contribute to infection spread and severity. In addition, some strains produce toxins (including toxic shock syndrome toxin-1) that function as superantigens—molecules that nonspecifically trigger release of large amounts of cytokines, leading to a sepsislike condition. Taken together, such factors combine to make S. aureus a dangerous pathogen.

MRSA emergence

When penicillin was introduced in the 1940s, virtually all S. aureus isolates were sensitive to that drug. But soon thereafter, S. aureus strains that produced a β-lactamase enzyme capable of inactivating penicillin became widespread. During the 1950s, outbreaks of penicillin-resistant S. aureus occurred in many U.S. hospitals. Introduction of penicillinase-resistant antibiotics, such as methicillin and oxacillin, temporarily restored the ability to treat all strains of this pathogen using penicillin antibiotics. The first strain of methicillin-resistant S. aureus (MRSA) was described in 1961 shortly after introduction of penicillinase-resistant antibiotics.
The mechanism of methicillin resistance involves a mutation in one of the bacterial cell-wall proteins to which penicillins must bind to kill the bacterium. This mutation renders the organism resistant to all penicillins and penems and almost all cephalosporins.
MRSA incidence has increased steadily to the point where it currently constitutes up to 60% of S. aureus isolates in many U.S. hospitals. These organisms commonly carry genetic material that makes them resistant to various non-β lactam antibiotics as well, leading some to suggest that the term MRSA should stand for multiply resistant S. aureus.
S. aureus has continued to mutate in the face of persistent antibiotic pressure. Vancomycin-intermediate S. aureus (VISA) was described in 1997; vancomycin-resistant S. aureus (VRSA), in 2003. Fortunately, these two strains remain rare and haven’t become established pathogens. (See Strains of antibiotic-resistant S. aureus by clicking the PDF icon above.)

Healthcare- versus community-acquired MRSA

Although MRSA initially arose and spread within healthcare settings (chiefly acute-care hospitals), a community-based variant was described in 1998. Called community-
acquired MRSA (CA-MRSA), this variant differs from healthcare-associated MRSA (HCA-MRSA) in more ways than the acquisition site. CA-MRSA occurs predominately in otherwise healthy children and young adults.
It most commonly presents as recurrent cutaneous abscesses, although life-threatening infections (such as necrotizing fasciitis and pneumonia) also have occurred. The pro­pensity to cause cutaneous abscesses isn’t fully understood but may relate partly to production of the Panton-Valentine toxin by many CA-MRSA isolates.
In contrast, HCA-MRSA afflicts mainly older patients, particularly those with chronic illnesses, including chronic wounds. It typically causes wound infections, urinary tract infections, pneumonia, and bacteremia.
Besides these epidemiologic and clinical differences, many CA-MRSA isolates derive from a single clone, known as clone USA 300, whereas HCA-MRSA is composed of multiple non-USA 300 clones. Finally, many CA-MRSA isolates are sensitive to non-β
lactam antibiotics, whereas most HCA-MRSA isolates resist multiple antibiotics. More recently, the distinction between CA-MRSA and HCA-MRSA has been blurred as evidence emerges that CA-MRSA now is being transmitted in healthcare settings as well as in the community.

S. aureus carrier state

Staphylococci are frequent colonizers of humans. Common colonization sites include the skin, anterior nares, axillae, and inguinal regions. Individuals can be colonized continuously or transiently, with nasal carriage rates varying from 20% to 40%. Most S. aureus infections result from the strain carried by the infected patient.
Three patterns of S. aureus carriage exist in humans:
• 20% of individuals are continuously colonized.
• 30% of individuals are intermittently colonized.
• 50% of individuals are never colonized.

The highest carriage rates occur in patients receiving frequent injections (such as insulin-dependent diabetics, hemodialysis patients, and I.V. drug users) and those with chronic skin conditions (for instance, psoriasis or eczema). In the general population, MRSA carriage rates have increased to 1% or 2%, with clinical consequences hinging on the colonizing strain (CA-MRSA versus HCA-MRSA) and host characteristics. The most consistent carriage site is the anterior nares, but many other sites may carry this pathogen, including the axillae, inguinal regions, and perirectal area.

MRSA treatment

Therapy for MRSA infection depends on the infection location and antibiotic sensitivity of the infecting strain.
• Cutaneous abscesses are treated by incision and drainage; antibiotics play a secondary role to adequate drainage.
• Therapy for necrotizing fasciitis caused by MRSA involves aggressive debridement with removal of all necrotic tissue, plus adequate antibiotic therapy. Typically, patients require serial debridement followed by subsequent careful wound care, often with eventual skin grafting.
• Pyomyositis  treatment entails drainage of the muscle abscess (which sometimes can be done with percutaneous tube placement instead of open drain­age), plus appropriate antibiotic therapy.

Vancomycin has been the mainstay of I.V. therapy for MRSA for decades, but some clinicians are concerned that its effectiveness may be declining due to slowly increasing minimum inhibitory concentrations (the minimum concentration of an
antibiotic needed to inhibit pathogen growth). Other parenteral options have emerged in the last few years. (See I.V. drugs used to treat MRSA by clicking the PDF icon above.) Several oral antibiotics also are available for MRSA treatment. (See Oral agents used to treat MRSA by clicking the PDF icon above.)
Knowing the antibiotic sensitivity pattern of the infecting MRSA strain is crucial to ensuring that the patient receives an appropriate antibiotic. Treatment duration for soft-
tissue infections usually ranges from 7 to 14 days, but bacteremia and bone or joint infections call for more prolonged therapy.

Efforts to eradicate MRSA carriage

Because the carrier state increases the risk of subsequent S. aureus infection, efforts have been made to eradicate carriage. Unfortunately, this has proven to be difficult. A commonly used regimen involves 5 days of twice-daily mupirocin nasal ointment with either chlorhexidine gluconate showers or immersion up to the neck in a dilute bleach solution. However, success in eliminating carriage is limited, although the bleach bath seems to improve eradication rates better than other modalities.

Controlling MRSA in hospitals

How best to control MRSA spread within hospitals is controversial. Some experts advocate an aggressive, “search and destroy” approach involving screening all patients for nasal carriage on admission and initiating contact precautions with subsequent decolonization efforts. Others focus on improving the overall level of hand hygiene and other general infection-control measures, arguing that nasal screening misses at least 20% of MRSA-colonized patients and thus gives an unwarranted sense of security.
Many hospitals use a mixed approach, screening patients suspected to be at high risk for MRSA carriage (such as those admitted from extended-care facilities or to the intensive care unit), while simultaneously trying to improve hand hygiene and general infection-control measures. Recent data suggest MRSA colonization and infection rates have stopped increasing and are beginning to decline.
MRSA is one of the most problematic pathogens encountered on a regular basis, and among the most dangerous pathogens we face. While some MRSA infections are relatively mild, many are serious or life-threatening. Severe soft-tissue infections, such as necrotizing fasciitis and pyomyositis, require surgical debridement or drainage, appropriate antibiotic therapy, and assistance from a wound-care professional to achieve optimal outcomes. n

Selected references
Calfee DP. The epidemiology, treatment and prevention of transmission of methicillin-resistant Staphylococcus aureus. J Infus Nurs. 2011 Nov-Dec;34(6):359-64.

DeLeo FR, Otto M, Kreiswirth BN, Chambers HF. Community-associated meticillin-resistant Staphylococcus aureus. Lancet. 2010 May 1;375(9725): 1557-68.

Dryden MS. Complicated skin and soft tissue infection. J Antimicrob Chemother. 2010 Nov;65 Suppl 3:iii35-44.

Ippolito G, Leone S, Lauria FN, et al. Methicillin-resistant Staphylococcus aureus: the superbug. Int J Infect Dis. 2010 Oct;14 Suppl 4:S7-11.

Landrum ML, Neumann C, Cook C, et al. Epidemiology of Staphylococcus aureus blood and skin and soft tissue infections in the US military health system, 2005-2010. JAMA. July 4;308:50-9.

Lee AS, Huttner B, Harbarth S. Control of methicillin-resistant Staphylococcus aureus. Infect Dis Clin North Am. 2011 Mar;25(1):155-79.

Moellering RC Jr. MRSA: the first half century. J Antimicrob Chemother. 2012 Jan;67(1):4-11.

Otter JA, French GL. Community-associated meticillin-resistant Staphylococcus aureus strains as a cause of healthcare-associated infection. J Hosp Infect. 2011 Nov:79(3):189-93.

Rivera AM, Boucher HW. Current concepts in antimicrobial therapy against select gram-positive organisms: methicillin-resistant Staphylococcus aureus, penicillin-resistant pneumococci, and vancomycin-resistant enterococci. Mayo Clin Proc. 2011 Dec;86(12):1230-43.

Simor AE. Staphylococcal decolonization: an effective strategy for prevention of infection? Lancet Infect Dis. 2011 Dec;11(12):952-62.

Joseph G. Garner is director of the infectious disease division and hospital epidemiologist at the Hospital of Central Connecticut and a professor of medicine at the University of Connecticut.

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.