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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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 Connie Johnson, RN, BSN, WCC, LLE, DAPWCA

Jim, a 52-year-old patient with colon cancer, received a new ostomy. He needed a custom fit for his appliance, which took 10 days. During this time, trying to obtain a good seal and treat the peristomal area wasn’t easy. Despite my best efforts, Jim’s skin was denuded from contact with stool. Although he was in great discomfort, he wanted to wait until my next visit to tell me about the problem. Fortunately, his wife was worried and contacted me directly.

Jim lives in a neighborhood with a low crime rate, so I’m able to see him within
a few hours of his wife’s call, even though it’s late at night. As it turns out, I make
extra visits to help him manage his stoma until the customized appliance is ready.  As with any home care situation, I’m ready to do my best for my patient.

Many home-care patients like Jim benefit from the interventions of a wound care clinician (WCC). More than one-third of all home-care admissions are wound related, and home wound care has become one of the fastest growing needs and skills in home-care services. So if you’re a WCC, you may want to consider home care as a practice option.

Delivering wound care in the home differs dramatically from delivering it in the hospital. Given the complexity of wound care and the multiple factors that affect healing, home wound care is a challenge. Some patients have chronic conditions, such as diabetes or wounds or open sores that don’t heal easily. In other cases, the patient or caregiver is unable to change dressings. That’s where the WCC comes in.

Special needs of home-care patients

Like other patients across the continuum of care, home-care wound patients require accurate and thorough wound assessment, as well as documentation that provides information about wound status and aids development of a plan that supports healing.
Of course, the plan of care must address the whole patient, not just the “hole” in the patient. The WCC must take into account comorbidities, individual wound-care requirements, assistance the patient may need due to physical or mental deficits, and nutritional support. Additional factors that affect wound-care strategies include wound characteristics, family support, and insurance guidelines and reimbursement.

Role of the WCC

The WCC’s role in home care includes providing clinical expertise, working with other healthcare team members, and providing education.

• The WCC provides clinical expertise regarding wound and ostomy care to ensure delivery of the highest quality of care. This expertise helps reduce the need for readmissions to the emergency department (ED) for wound-related complications. The WCC also plays a vital role in product awareness, formu-lary development, and maintenance of cost-effective, evidence-based practice in the agency.
• Working with other healthcare team members, the WCC serves as patient advocate, strengthening the relationship between patient and healthcare team members while promoting care coordination to help the patient achieve goals. Effective communication with the patient’s primary care pro­vider is essential to delivering the best-quality, research-based wound care. A tool for strengthening such communication is the SBAR (Situation-Background-Assessment-Recommendation) technique. SBAR structures conversations so all parties provide complete yet concise information. (See SBAR wound and skin provider communication record by clicking the PDF icon above).
• The WCC educates patients and family members about wound healing, dressing applications, and other interventions. Teaching families allows them to be involved in the patient’s care and start to take ownership of it. The WCC also educates home health aides, who can play a vital role in preventing such problems as pressure ulcers and may be responsible for ensuring staff members are aware of the products, procedures, and dressings available.

Challenges of home care

If you’re a WCC and considering home care as a career option, know that practicing in the home can be a real eye opener. For starters, consider geography. Shortly after I started as a wound care nurse/consultant in home care, I was visiting patients all over New Jersey, some days driving 200 miles. As I quickly discovered, once you enter the home, don’t assume you’ll simply change a dressing and then be on your way. Instead, you may find you are, in essence, the family case manager who’s expected to “fix everything.” This role requires equal doses of planning and creativity.

What’s more, expect to do some improvising. In acute-care settings, all the supplies you may need to prevent infection—gowns, gloves, masks—usually are within arm’s reach. But in home care, these supplies may be absent, meaning you’ll need to set up the cleanest environment you can under the circumstances. That might mean using disposable drapes and dressings. Be sure to carry large amounts of hand sanitizer.

Dressing selection is perhaps the biggest challenge in home wound care because
it involves not just wound-specific issues but financial and practical considerations. The ideal dressing in the home is one that needs to be changed only every other day, at most. Evidence shows it’s not practical to try to change dressings two or three times daily at home unless the family is providing care.

Develop a checklist

Because the home environment may lack all the resources you need, remembering every­thing you need to do before you leave the patient’s home may be challenging. To help keep things on track, develop a checklist of reminders that covers these points:

• Have necessary medical appointments been arranged? Does the patient have transportation to appointments?
• Are there sufficient supplies in the home?
• Is there enough medicine? If not, who will pick up the medicine?
• Are consults needed, such as social worker or physical therapist?
• Who will help with any activities of daily living that the patient is unable to do?
• Does the patient with diabetes have a glucometer?

Hours and safety concerns

Typical home wound-care hours are 8:30 a.m. to 4:30 p.m. But realistically, expect variations. For instance, as you’re about to leave, the patient might say, “My wife isn’t feeling well. Could you take her blood pressure?” This means you’ll stay a little longer.

When planning home visits, be aware of safety concerns. If visiting after hours could put you in danger, it’s safer to instruct the patient to call an ambulance and go to the local ED.

Reimbursement

Reimbursement is an important factor in wound care in the home. To be eligible for home care through Medicare, patients must be homebound—meaning they don’t routinely travel to run errands or visit or they’re not able to obtain or receive needed medical services. (With private insurance and workers’ compensation, eligibility requirements may be less restrictive.)

Know that a Medicare patient receives home care as an “episode.” Episodes are 60-day periods; within each 60-day episode, a $592 cap is allotted should a patient require supplies for wound or ostomy care needs. Except for negative-pressure wound therapy, a home care agency can’t bill Medicare for products used; instead, the home-care agency is responsible for the cost of all topical wound-care products and dressings. Agencies may keep patients on service even if they exceed the allowed amount, although patients reaching maximum benefits commonly are discharged from service. Home-care agencies have no choice but to discharge Medicare patients they find aren’t truly homebound.

Also, be aware that Medicare views home health service as an interim service. When a patient is no longer making progress, Medicare expects that the family will provide the patient’s care or the patient will enter a skilled care facility. So it’s important to work hard to obtain good outcomes—not just for the patient but to maintain Medicare reimbursement. Like many private insurance companies, Medicare reimbursement is based on pay for performance; if an agency doesn’t deliver optimal outcomes, it receives lower reimbursement, increasing its financial burden.

A worthwhile option

WCCs use their knowledge and clinical expertise to improve patient outcomes and teach patients, families, and other healthcare team members. They also give the agency recommendations for care and supplies that are evidence based and reflect current best practices in wound care. Accomplishing these goals in a timely fashion under various constraints can be challenging. But if you choose to work in the home, try to keep a smile on your face and joy in your voice for each patient and family. If you like challenges and want a job where you can apply your creativity and function independently, becoming a home-care WCC might be the right choice for you.

Connie Johnson provides wound care in the home and in acute-care settings.

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By Nancy J. Brent, MS, RN, JD

Often nurses get named in a lawsuit when they are involved in clearly negligent conduct that causes an injury to or the death of a patient. Examples include administering the wrong medication to the wrong patient or not positioning a patient correctly in the operative suite prior to surgery. Sometimes, however, the negligent behavior of a nurse is not as clear to the nurse involved in the care of the patient.
That was apparently the circumstance in the reported case, Olsten Health Services, Inc v. Cody.¹ In September 2000, Mr. Cody was the victim of a crime that resulted in paraplegia. He was admitted to a rehabilitation center and discharged on November 15, 2000. His physician ordered daily home health care services in order to monitor his “almost healed” Stage 2 pressure ulcer.² The home health care agency assigned a registered nurse (RN) to Mr. Cody and, after Mr. Cody’s healthcare insurance company would not approve daily visits, a reduced visit plan was approved by Mr. Cody’s physician.

A progressive problem

On November 16, 2000, the nurse visited Mr. Cody for the first time. During that visit, she did an admission assessment and noted that the pressure ulcer, located at the area
of the tailbone, measured 5 cm by 0.4 cm wide and 0.2 cm deep. She believed the pressure ulcer could be completely healed within 3 weeks. The nurse called Mr. Cody’s physician and left him a voice message concerning her visit and her findings.
On November 19, a second visit took place and the nurse observed and documented that Mr. Cody’s pressure ulcer was “100%” pink and no odor was detected.
On November 20, she attempted another visit but did not see Mr. Cody because the front gate surrounding his home was locked. The nurse buzzed the gate doorbell several times to no avail. She left a note on the front gate for the Cody family and left a voice message for Mr. Cody’s physician.

The next visit took place on November 21. The pressure ulcer was now only “90% pink” and had a “fetid” odor; this condition did not improve over the next 24 hours. The nurse documented this fact in her nurses’ notes. Again, she left a voice mail message for the physician concerning these findings.

The nurse could not get into the house on November 23, the next scheduled visit, so she again left a note on the house gate and left a voice mail message for the physician.
On November 24, the home health care nurse saw Mr. Cody and observed the pressure ulcer to be “90% pink” but the “fetid” odor was still present. In addition, Mr. Cody’s right lower extremity was swollen. She was concerned that the wound care that was to be done by the family or the health aide was not being done. Even so, she did not contact Mr. Cody’s physician or the patient again until November 27.

Mr. Cody’s pressure ulcer on November 27 had no odor but the home health aide who was also caring for Mr. Cody told the nurse that he was “very cold and having chills.” The nurse did not document this reported observation in her nurses’ notes.
Attempts to visit Mr. Cody on November 28 and 29 were again unsuccessful because of the locked gate at the front of the house. No one answered the buzzer, either. The nurse left another note on the house gate and left a voice mail message for the physician.

When the nurse saw Mr. Cody on November 30, she observed that the ulcer had “serious changes”: an increase in the serous drainage from the wound; the wound had a “fetid” odor; 80% of the wound was necrotic; the necrotic tissue was “undermined”; and the wound was significantly larger—9 cm by 8 cm wide and 1 cm deep.³ She left a voice mail message for Mr. Cody’s physician, but did not alter her visits to Mr. Cody’s home or attempt to see him over the next 2 days.

Admission to hospital

When the nurse did visit Mr. Cody on December 1, the pressure ulcer consisted of 40% necrotic tissue. She then told the family to take Mr. Cody to the physician’s office. Later that same day he was admitted to the hospital with a Stage 4 pressure ulcer that reached his tailbone. After 3 weeks of treatment, the ulcer measured 20 cm by 30 cm.

Mr. Cody endured many procedures during the following years to treat his
ulcer, but it never really healed. A “flap” enclosure was done to try to cover the wound.

Lawsuit

Mr. Cody sued the home health care company, alleging that the employees breached the standard of care by failing to appropriately diagnose and treat/or to prevent the formation or aggravation of pressure ulcers, resulting in severe and significant injury to him.

Verdict

The Florida Court of Appeals affirmed the trial court’s verdict in favor of Mr. Cody—a $3,050,000 verdict in economic damages⁴—on several legal bases, the most important for the purposes of this article being that the home health care agency and its employees were negligent in the care of Mr. Cody.

Key testimony

Key testimony in reaching this verdict came from the expert testimony of an RN and certified wound care expert. The nurse expert testified unequivocally that the home health care nurse breached the standard of nursing care. She said that not contacting the physician personally about Mr. Cody’s condition and the family being overwhelmed about his condition, but instead leaving voice mail messages on an answering machine, did not meet the standard of nursing care in this situation.
Additionally, the nurse expert testified that the nurse caring for Mr. Cody failed to recognize the symptoms of his deteriorating condition and did not intervene when necessary to avoid the infection he suffered from the deteriorating wound, and that her failure to do so resulted in the development of the Stage 4 ulcer that never healed.

Take-away points

So, what does this case tell you as a wound care professional caring for someone who has a pressure ulcer?

• Meet the standard of care. You must always meet the standard of care when caring for a patient. That means your care must be what other ordinary, reasonable, and prudent nurses caring for a patient with a decubitus ulcer would do in the same or similar circumstances in the same or similar community. Clearly, the nurse did not meet this standard in her care of Mr. Cody.
• Document accurately and completely. Remember that the nurse did not document Mr. Cody’s condition when the home health aide reported it to her. This omission may not only have compromised Mr. Cody’s care. If the communication during the trial became an “I told her”/”I don’t remember being told” debate when each party testified about the communication, it surely caused a rift between the aide and the nurse during the trial proceedings. Such a disagreement between defendant employees always helps a plaintiff’s case.
• Know that photographs can be used in court. This case used a specific form of evidence, demonstrative evidence: photographs taken of the pressure ulcer, which were admitted into evidence during the trial. The photographs were testified to by the wound care expert. In addition to her testimony, this evidence further showed the “natural and continual progression” of the ulcer as it existed on December 1, 2000.
• Understand the importance of expert testimony. In professional negligence cases, expert testimony is essential to establish the standard of care and to provide an opinion as to whether the standard of care was met or breached, the breach of which led to the injury to the patient. Typically, the attorney of a nurse cited in this type of case would want to use a certified wound care expert to support the care given. Apparently, the home care agency’s expert witness was not as convincing as the expert witness’s testimony for Mr. Cody.

Indeed, in this case, the expert witness’s testimony was invaluable and essentially secured a verdict for the plaintiff. Not only was the expert witness board certified but her testimony was credible, based on the evidence presented, and given after a careful review of Mr. Cody’s medical records, admission and discharge summaries from hospitals and health centers that provided care to Mr. Cody, the depositions of several doctors and nurses, and Mr. Cody’s deposition.

• Know your limits. The nurse’s conduct also stresses the importance of another legal principle—knowing the limits of your abilities and capabilities. Nowhere in the reported opinion are the RN’s qualifications listed or a reason given as to why she was selected to care for Mr. Cody. It is assumed she was not certified. Even basic nursing guidelines for wound care and communication to the physician were not followed. Why, then, did she agree to take this assignment? She did so not only at her own folly but to the detriment of Mr. Cody.
• Protect your patient. Last, and by no means least, this case stands for the principle that if you simply document something in the patient’s record that
  is important regarding the patient’s well-being and you just leave voice mail messages for a physician about that “something,” such conduct is not adequate. By simply leaving messages and notes, this RN violated an age-old principle in the law of professional negligence.⁵

Your duty in any situation in which the patient is at risk for a foreseeable and unreasonable risk of harm is to prevent that harm from happening insofar as humanly possible. What those specific steps might be will depend on the circumstances and your patient’s condition. Remember, liability is always fact-specific. Although legal principles exist, how each applies to a particular situation may vary.

Mr. Cody was clearly at risk for a foreseeable and unreasonable risk of harm—the further deterioration of his pressure ulcer. The nurse would only have had to intervene sooner by, for example (and as testified to by the expert witness), personally talking with his physician, visiting the patient more frequently when the deterioration began, contacting social services to help the family with its “overwhelmed” feelings, and following up with the home health aide’s observations of Mr. Cody.

Think about this, too: Nowhere in the court of appeals’ record was it indicated that Mr. Cody’s family or the physician ever received the notes or voice mail messages left by the nurse.⁶ At a minimum, wouldn’t you as the nurse want to follow up and check if those communications had been received?

References
1. Olsten Health Services, Inc. v. Cody, 979 So. 2d 1221 (FL District Ct of Appeals) 2008. (pages 1-8). http://caselaw.findlaw.com/fl-district-court-of-appeal/1160380.html. Accessed June 22, 2012.

2. Id. at 1.

3. Id. at 4.

4. Id. at 2. The doctrine of comparative negligence was used in this case. This doctrine, adopted by most states, reduces a plaintiff’s recovery of money proportionally to the plaintiff’s degree of fault in causing the injury that is the basis of the suit (Blacks Law Dictionary, Second Pocket Edition, Bryan Garner, ed. St. Paul, MN: West; 2001). In this case, the home health care agency’s fault was attributed to be 70%. Mr. Cody’s degree of fault was assessed by the jury at 30%, most probably due to the inability of the home care nurse to be given access into the house on the days she visited and the family not providing the wound care required by Mr. Cody’s decubitus ulcer.

5. This age-old principle was established in a 1965 Illinois case, Darling v. Charleston Community Hospital, 211 N.E. 2d 353 (IL Supreme CT) 1965.

6. Tammelleo D. Treatment of decubitus ulcers botched: verdict for $3,050,000. Nurs Law Regan Rep. 2008;49(1):1.

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

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