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.

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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 Joseph G. Garner, MD, FIDSA, FSHEA

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

Why is S. aureus such a nasty bug?

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

MRSA emergence

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

Healthcare- versus community-acquired MRSA

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

S. aureus carrier state

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

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

MRSA treatment

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

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

Efforts to eradicate MRSA carriage

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

Controlling MRSA in hospitals

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

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

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

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

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

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

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

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

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

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

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

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

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