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Practical Issues in Wound, Skin and Ostomy Management
In a busy wound clinic, quick and accurate differential diagnosis of edema is essential to appropriate treatment or referral for comprehensive care. According to a 2010 article in American Family Physician, 80% of lower extremity ulcers result from chronic venous insufficiency (CVI). In 2007, the German Bonn Vein Study found 100% of participants with active venous ulcers also had a positive Stemmer’s sign, indicating lymphedema. (more…)
Read MoreBy Carrie Carls, BSN, RN, CWOCN, CHRN; Michael Molyneaux, MD; and William Ryan, CHT
Every year, 1.9% of patients with diabetes develop foot ulcers. Of those, 15% to 20% undergo an amputation within 5 years of ulcer onset. During their lifetimes, an estimated 25% of diabetic patients develop a foot ulcer. This article discusses use of hyperbaric oxygen therapy (HBOT) in treating diabetic foot ulcers, presenting several case studies.
HBOT involves intermittent administration of 100% oxygen inhaled at a pressure greater than sea level. It may be given in a:
• multi-place chamber (used to treat multiple patients at the same time), compressed to depth by air as the patient breathes 100% oxygen through a face mask or hood (more…)
Writing effective orders for wound care is vital to ensure patients receive the right care at the right time, to protect yourself from possible litigation, and to facilitate appropriate reimbursement for clinicians and organizations.
Below are some overall strategies you can use:
Here are a variety of resources related to quality that wound care clinicians may find valuable.
If you are interested in home care, you’ll want to visit The Home Health Quality Improvement (HHQI) National Campaign’s website. HHQI is a grassroots project of the Centers for Medicare & Medicaid Services designed “to unite home health stakeholders and multiple health care settings under the shared vision of reducing avoidable hospitalizations and improving medication management.”
The many available free resources on the campaign’s website include:
• webinars; for example, “Hospital Readmissions and the Role of Home Care”
• best practice innovation packages, including ones on medication management and fall prevention.
You must register to obtain some of the resources.
◊ http://www.homehealthquality.org/hh/default.aspx
Reducing Avoidable Readmissions Effectively (RARE) is a campaign in Minnesota that is working with hospitals and care providers to prevent hospital readmissions within 30 days of discharge.
Even if you aren’t in Minnesota, you can access resources such as a webinars. Past webinars include “Involving Patients and Families in Reducing Avoidable Readmissions” and “Home Care and Reducing Hospital Readmissions.”
You can also download “Recommended Actions for Improved Transitions,” which covers five key areas: patient and family engagement and activation, medication management, comprehensive transition planning, care transition support, and transition communication.
◊ http://rarereadmissions.org/resources/RARE_Report_2012_06.html
Effective communication is essential for any quality initiative to be successful. TeamSTEPPS is a teamwork system that improves communication through train-ing and tools. The Agency for Healthcare Research and Quality and the Defense Department have teamed up to provide
resources for implementing Team STEPPS.
Tools include:
• Core TeamSTEPPS Training Curriculum Materials
• TeamSTEPPS Rapid Response Systems (RRS) Training Module
• TeamSTEPPS Teamwork Perception Questionnaire
• Pocket Guide that summarizes TeamSTEPPS principles in a portable, easy-
to-use format.
The educational materials contain information that clinicians can integrate into their practice. Video vignettes illustrate how failures in teamwork and communication can place patients in jeopardy and how successful teams can work to improve patient outcomes.
You can order free TeamSTEPPS materials, which are available online.
The Institute for Healthcare Improvement is an independent, not-for-profit organization that focuses on testing new models of care, disseminating best practices, and building the will to change to improve health care.
Among the many resources on the website:
• tools such as “Self-Management Toolkit for People with Chronic Conditions and Their Families”
• useful publications
• white papers such as “Using Care
Bundles to Improve Health Care
Quality”
• case studies of successful strategies
• audio and video broadcasts
• links to other helpful websites.
Registration is free.
◊ http://www.ihi.org/Pages/default.aspx
Read MoreThe new Essen Rotary swabbing technique takes a few seconds longer to perform than traditional techniques, but improves bacterial count accuracy in patients with chronic leg ulcers, according to a study published by Wounds International.
“Evaluation of the Essen Rotary as a new technique for bacterial swabs: Results of a prospective controlled clinical investigation in 50 patients with chronic leg ulcers” reports that Essen Rotary detected significantly more bacteria compared to standard techniques and was the only one to identify five patients with methicillin-resistant Staphylococcus aureus (MRSA), compared to three detected by other techniques.
The Essen Rotary technique samples a larger surface area of the wound, which is beneficial for detecting MRSA.
“The Essen Rotary may become the new gold standard in routinely taken bacteriological swabs especially for MRSA screenings in patients with chronic leg ulcers,” the study authors write.
A study presented at the American Diabetes Association 72nd Scientific Sessions found lowering HbA1c an average of 0.8% (from a mean of 7.8% to 7.0%, the treatment target) reduced the risk of cardiovascular death by 45% in patients with type
2 diabetes.
The absolute risk of mortality from a cardiovascular event was 9.9 events per 1,000 person-years in patients with decreasing HbA1c compared to 17.8 events in patients with stable or increasing HbA1c.
“HbA1c reduction and risk of cardiovascular diseases in type 2 diabetes: An observational study from the Swedish NDR” examined data from 18,035 patients in the Swedish National Diabetes Register.
The Centers for Medicare & Medicaid Services (CMS) has enhanced two websites designed to help the public make informed choices about their health care.
Hospital Compare and Nursing Home Compare now have better navigation and new comparison tools. The two sites include data on quality measures, such as frequency of hospital-acquired infections, and allow the user to compare hospitals on these measures.
Improvements include easy-to-use maps for locating hospitals, a new search function that enables the user to input the name of a hospital, and glossaries that are easier to understand. It’s now also possible to access the data on the sites through mobile applications.
CMS maintains the websites, which are helpful for anyone who wants to compare facilities, not just patients on Medicare or Medicaid.
For more information, read the article in Healthcare IT News.
The Institute of Medicine (IOM) released “Accelerating the development of new drugs and diagnostics: Maximizing the impact of the Cures Acceleration Network—Workshop Summary.” The report is a summary of a forum that brought together members of federal government agencies, the private sector, academia, and advocacy groups to explore options and opportunities in the implementation of Cures Acceleration Network (CAN). The newly developed CAN has the potential to stimulate widespread changes in the National Institutes of Health and drug development in general.
As a result of two extensive literature reviews, a researcher at the University of Missouri found that emphasizing quality of life—not just reducing swelling—is important for patients with lymphedema. Many providers and insurance companies base treatment on the degree of edema, but the volume of fluid doesn’t always correspond with the patients’ discomfort. Instead, an individualized plan of care should be developed.
The researchers found that Complete Decongestive Therapy (CDT), a comprehensive approach for treating lymphedema that includes skin and nail care, exercise, manual lymphatic drainage, and compression, may be the best form of specialized lymphedema management. For more information about CDT, watch for the November/December issue of Wound Care Advisor.
An article about a case of the plague in Oregon has appeared on Huffington Post. A welder contracted the disease as a result of unsuccessfully removing a mouse from a stray cat’s mouth. Part of his hands have, in the words of the article, “darkened to the color of charcoal.” Later tests confirmed the cat had the plague.
Plague cases are rare in the United States. According to the Centers for Disease Control and Prevention, an average of 7 human cases are reported each year, with a range of 1 to 17 cases. Antibiotics have significantly reduced morality. About half of cases occur in people ages 12 to 45.
“Optimal use of negative pressure wound therapy for skin grafts,” published by International Wound Journal, reviews expert opinion and scientific evidence related to the use of negative pressure wound therapy with reticulated open-cell foam for securing split-thickness skin grafts.
The article covers wound preparation, treatment criteria and goals, economic value, and case studies. The authors conclude that the therapy has many benefits, but note that future studies are needed “to better measure the expanding treatment goals associated with graft care, including increased patient satisfaction, increased patience compliance and improved clinical outcomes.”
Researchers have identified that aberrantly expressed microRNAs inhibit healing of chronic venous ulcers, according to a study in The Journal of Biological Chemistry.
Six microRNAs were plentiful in 10 patients with chronic venous ulcers. The microRNAs target genes important in healing the ulcers. In an article about the study, one of the researchers said, “The more we know about the molecular mechanisms that contribute to [the development of venous ulcers], the more we can rationally develop both diagnostic tools and new therapies.”
Both patients with diabetes and those without are at risk for hemodialysis-related foot ulcers, according to a study published by International Wound Journal.
Researchers assessed 57 patients for ulcer risk factors (peripheral neuropathy, peripheral arterial disease, and foot pathology, such as claw toes, hallux valgus, prominent metatarsal heads, corns, callosities, and nail pathologies) at baseline, and noted mortality 3 years later.
In all, 79% of patients had foot pathology at baseline, and 18% of patients without diabetes had peripheral neuropathy. Peripheral arterial disease was present in 45% of diabetic and 30% of nondiabetic patients. Nearly half (49%) of patients had two or more risk factors. Only 12% of patients had no risk factors. The presence of peripheral arterial disease and peripheral neuropathy increased risk of mortality.
The authors of “Prevalence of risk factors for foot ulceration in a general haemodialysis population” state that the high prevalence of risk factors in nondiabetic patients indicates that they are at risk for developing foot ulcers.
A study in Emerging Infectious Diseases found that older age, living in a nursing home, severe bacteremia, and organ impairment increase the risk of death from methicillin-resistant Staphylococcus aureus (MRSA) bacteremia.
Consultation with a specialist in infectious disease lowers the risk of death, and MRSA strain types weren’t associated with mortality.
“Predicting risk for death from MRSA bacteremia” studied 699 incidents of blood infection from 603 patients who had MRSA bacteremia.
Lymphedema is characterized by regional immune dysfunction, distorted limb contours, and such skin changes as papillomas, hyperkeratosis, and increased girth. The condition may involve the limbs, face, neck, trunk, and external genitals; its effects may include psychological distress. For optimal patient management, clinicians must understand what causes lymphedema and how it’s diagnosed and treated.
This two-part series provides an overview of lymphedema. Part 1 covers etiology, pathology, and diagnosis. Part 2, which will appear in the November-
December issue, will focus on treatment.
Lymphedema occurs when protein-rich fluid accumulates in the interstitium due to impaired lymphatic function. Proteins, other macromolecular wastes, and water constitute lymphatic loads. These wastes rely on specially structured absorptive and transport structures in peripheral regions for their return to central circulation.
When lymph stasis prevails, inflammatory processes and lymphostatic fibrosis trigger tissue-density changes, further entrapping superficial vessels and accelerating mechanical insufficiency. (See Physiologic changes caused by lymphatic disruption by clicking the PDF icon above.)
Lymphedema can be primary or secondary. Primary lymphedema either is congenital (present at birth) or arises around puberty. In the vast majority of cases, it is associated with structural changes in the lymphatic system and isn’t associated with another disease or condition. Most structural changes (87%) manifest before age 35 and cause hypoplasia of vessels and nodes. Syndromes involving hyperplasia, node fibrosis, or aplasia also may occur, although they’re much less common. Dysplasia (either hypoplasia, hyperplasia, or aplasia) predisposes drainage regions to inadequate lymph collection, resulting in edema and secondary tissue changes, such as chronic inflammation and reactive fibrosis. Genetic variability in lymphatic constitution may explain why seemingly similar patients receiving the same surgical protocol have different lymphedema risks over time.
Secondary lymphedema stems from a significant insult to lymphatic tissues, as from lymphadenectomy, radiation therapy, trauma, infection, or cancer. It commonly results from direct trauma to regional nodes or vessel structures. Slow degradation of lymphatic function also occurs when adjacent tissues (such as superficial and deep veins) become diseased, when cellulitis occurs, or when accumulations
of adipose or radiation fibrosis mechanical-ly disrupt drainage of skin lymphatics.
Lymphedema progresses in stages, which involve secondary connective-tissue disease combined with disturbed fluid update and transport. These conditions cause a universal and classic clinical picture.
• Stage 0 (latency stage) is marked by reduced transport capacity and functional reserve. The patient has no visible or palpable edema, but has such subjective complaints as heaviness, tightness, and waterlogged sensations.
• In Stage 1 edema (reversible lymphedema), edema decreases with elevation. Pitting edema is present, but fibrosis is absent.
• During Stage 2 (spontaneously irreversible lymphedema), lymphedema doesn’t resolve entirely, although it may fluctuate. Pitting is more pronounced and fibrosis is present.
• Stage 3 (lymphostatic elephantiasis) is marked by dermal hardening, nonpitting edema, papillomas, hyperkeratosis, and in some cases, extreme girth.
Diagnosing lymphedema can be challenging because edema may be associated with other diseases and disorders. For a summary of signs and symptoms, see Clinical findings in lymphedema by clicking the PDF icon above.
Lymphedema rarely causes pain because the skin accommodates gradual, insidious fluid accumulation. However, secondary orthopedic discomfort may result from increased weight of the affected limb due to deconditioning or decreased range of motion.
Because lymphedema usually progresses slowly, gravity and centrifugal forces pull fluids toward distal limb areas, causing an entrenched, stubborn pitting edema. Later, further valvular incompetence contributes to worsening distal edema in the fingers, toes, and dorsal regions of the hand and foot. Prominent lower-extremity structures, such as the malleolus, patella, tibia, anterior tibialis tendon, and Achilles tendon, become progressively less distinct. This creates a columnar limb appearance; the swollen limb has the same girth from distal to proximal aspects, unlike the natural cone shape of a normal limb.
Lymphatic failure doesn’t tax the venous system, so skin color remains normal. Blood supply remains patent, helping to prevent secondary ulcers.
Lymphedema severity correlates directly with such factors as onset of the condition and extent of cancer therapy, if given (number of nodes resected, number of positive nodes, and use of radiotherapy). Lymphedema may worsen with a greater number of infection episodes, weight gain, injury, diuretics, limb disuse, pneumatic compression therapy (when used for pure lymphedema), and ill-fitting compression garments. The single most important contributor to increasing lymphedema severity is lack of patient education, which can result in improper treatment or none at all.
Lymphedema causes regional immune suppression and leads to an increase in opportunistic infections such as cellulitis. As skin integrity suffers, scaling and dryness allow resident skin pathogens (such as streptococci and staphylococci) to gain access through the defective skin barrier into protein-rich interstitial fluid, creating a medium favorable to bacterial colonization. Lymphocyte migration decreases, and dissected or irradiated nodal sites are slow to detect invaders. Furthermore, stagnant lymph promotes further delays in the immune response. Patients with opportunistic infections may exhibit high fever, local erythema, regional hypersensitivity or acute pain, flulike symptoms, and rapidly advancing “map-like” borders in the skin.
Several methods can aid differential diagnosis.
Clinical findings. Lymphedema can be diagnosed from patient history, physical examination, palpation, and inspection. Trauma to lymph nodes (each of which governs a distinct body region) decreases the transport capacity of lymph formed in that region, in turn causing local swelling (lymphedema). Trauma to the axillary or inguinal lymph nodes, which exist on both the left and right of the body and in both the upper and lower regions, predisposes these quadrants to swelling. Therefore, if lymph nodes on only one side are damaged, lymphedema occurs only on that side of the body. Using the universal characteristics cited above as a guide, while ruling out cancer recurrence, acute deep vein thrombosis, or plasma protein abnormalities, yields sufficient data to form a diagnosis.
Imaging. Lymphography involves subcutaneous injection of a lymph vessel–
specific dye (Patent Blue V), followed by X-ray. Although it provides high-resolution images of lymphatic structures, this technique is invasive, painful, damaging to lymphatics, and potentially lethal—and therefore is no longer recommended.
Lymphangioscintigraphy (LAS) uses interdigital subcutaneous injection of protein-labeled radioisotopes, followed by
imaging at specific intervals to gather information about uptake and transport time. Images are hazy and false-negatives are common, so well-trained radiotherapists familiar with lymphology and lymphedema should administer and interpret the test. Also, experts don’t agree on standard criteria for LAS administration, so measures may not be similarly conclusive.
Limb-measuring instruments and methods. Serial measurement of affected limb circumference using a standard garment tape measure is the most widely accessible approach. Intra-rater reliability is comparable to that of currently used tools; however, these methods can’t be used for early detection, for screening, or when various raters are used to assess the same patient. Circumferences are measured at four points and are considered positive if a distance of 2 cm or more separates the involved from uninvolved extremity in comparison. Water displacement techniques for limb-volume calculation, although accurate, are impractical in most clinical settings and rarely used.
Various devices have been used to obtain measurements. For instance, the Perometer® uses optoelectronic volumetry. By scanning the limb with infrared beams circumferentially, the device accurately records girth at 4-mm intervals along the limb length and transmits these measurements to a computer. The Perometer is used mainly in the research setting. Preoperative and postoperative measurements at intervals can detect lymphedema early.
Impedimed XCA® uses bioelectrical
impedance to calculate ratios of intracellular to extracellular fluid. A weak electrical current is passed through affected and unaffected limbs, allowing comparison of results. Impedance is lower in edematous tissue, supporting an accurate diagnosis.
Once a diagnosis is made, the next step is treatment. Part 2 of this series covers lymphedema treatment.
Selected references
Foeldi M. Foeldi’s Textbook of Lymphology: For Physicians and Lymphedema Therapists. 3rd ed. St. Louis, MO: Mosby; 2012.
Kubik S, Manestar M. Anatomy of the lymph capillaries and precollectors of the skin. In: Bollinger A, Partsch H, Wolfe JHN, eds. The Initial Lymphatics. Stuttgart: Thieme-Verlag; 1985:66-74.
Lee B, Andrade M, Bergan J, et al. Diagnosis and treatment of primary lymphedema. Consensus document of the International Union of Phlebology (IUP)—2009. Int Angiol. 2010 Oct;29(5):454-70.
Lerner R. Chronic lymphedema. In: Prasad H, Olsen ER, Sumpio BE, Chang JB, eds. Textbook of Angiology. Springer; 2000.
Mayrovitz HN. Assessing lymphedema by tissue indentation force and local tissue water. Lymphology. 2009 June;42(2):88-98
National Cancer Institute. Lymphedema (PDQ®): Health Professional Version. Updated June 30, 2011. www.cancer.gov/cancertopics/pdq/supportivecare/
lymphedema/healthprofessional. Accessed September 5, 2012.
Northrup KA, Witte MH, Witte CL. Syndromic classification of hereditary lymphedema. Lymphology. 2003 Dec:36(4):162-89.
Olszewski WL. Lymph Stasis: Pathophysiology, Diagnosis and Treatment. CRC Press; 1991.
Pecking AP, Alberini JL, Wartski M, et al. Relationship between lymphoscintigraphy and clinical findings in lower limb lymphedema (LO): toward a comprehensive staging. Lymphology. 2008 Mar;41(1):1-10.
Stanton AW, Northfield JW, Holroyd, B, et al. Validation of an optoelectronic volumeter (Perometer). Lymphology. 1997 June;30(2):77-97
Weissleder H, Schuchhardt C. Lymphedema: Diagnosis and Therapy. 4th ed. Viavital Verlag GmbH; 2007.
Steve Norton is cofounder of Lymphedema & Wound Care Education and executive director of the Norton School of Lymphatic Therapy in Matawan, New Jersey.
Read MoreNecrotizing 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:
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.
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.
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.)
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.
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.
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.)
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.
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 Donna Sardina, RN, MHA, WCC, CWCMS, DWC
Starting your own consulting business is an exciting and rewarding experience: You’re the boss; you’re in charge. The question is, do you have what it takes? Along with the excitement of being the boss comes the responsibility of decisions and commitment. Your decisions will affect whether the business is a failure or a success.
To succeed in consulting, you must be an expert at recognizing problems and shaping solutions to those problems, and you must possess excellent time-management and networking skills. If you think you have what it takes to be a consultant, read on. This article gives an overview of the process.
Businesses hire consultants for their expertise to help them identify problems, supplement staff, institute change, provide an objective viewpoint, or teach.
Examples of specific services you can offer include single patient reviews, serving as a member of the wound care team, making wound rounds on all patients, providing education, patient teaching, protocol development, and troubleshooting. These services are provided in many settings—long-term care, home care, long-term acute care, rehabilitation hospitals, acute-care hospitals, insurance companies, and primary-care provider groups. (more…)
Moisture-related skin breakdown has been called many things-perineal dermatitis, irritant dermatitis, contact dermatitis, heat rash, and anything else caregivers could think of to describe the damage occurring when moisture from urine or stool is left on the skin. At a 2005 consensus conference, attendees chose the term incontinence-associated dermatitis (IAD).
IAD can be painful, hard to properly identify, complicated to treat, and costly. It’s part of a larger group of moisture-associated skin damage that also includes intertrigo and periwound maceration. IAD prevalence and incidence vary widely with the care setting and study design. Appropriate diagnosis, prompt treatment, and management of the irritant source are crucial to long-term treatment.
IAD stems from the effects of urine, stool, and containment devices on the skin. The skin’s pH contributes to its barrier functions and defenses against bacteria and fungus; ideal pH is 5.0 to 5.9. Urine pH ranges from 4.5 to 8.0; the higher range is alkaline and contributes to skin damage.
Skin moisture isn’t necessarily damaging. But when moisture that contains irritating substances, such as alkaline urine, contacts the skin for a prolonged period, damage can occur. Urine on the skin alters the normal skin flora and increases permeability of the stratum corneum, weakening the skin and making it more susceptible to friction and erosion. Fecal incontinence leads to active fecal enzymes on the skin, which contribute to skin damage. Fecal bacteria can penetrate the skin, increasing the risk of secondary infection. Wet skin has a lower temperature than dry skin; wet skin under a pressure load has less blood flow than dry skin.
Containment devices, otherwise known as adult diapers or briefs, are multilayer disposable garments containing a superabsorbent polymer. The polymer is designed to wick and trap moisture in the containment device. This ultimately affects the skin by trapping heat and moisture, which may cause redness and inflammation that can progress to skin erosion. This trapping can lead to increased pressure against the skin, especially if the device has absorbed liquid and remains in contact with the skin.
IAD is categorized as mild, moderate, or severe. (See Picturing IAD by clicking the PDF icon above.)
Screen the patient’s skin for persistent redness, inflammation, rash, pain, and itching at least daily. To differentiate IAD from pressure ulcers, keep in mind that:
The three essentials of IAD prevention are to cleanse, moisturize, and protect.
If the treatment protocol fails, the patient should be referred to an appropriate skin care specialist promptly.
To help prevent urine or stool from contacting the patient’s skin, consider using a male external catheter, a female urinary pouch, a fecal pouch, or a bowel management system. Avoid containment devices. If the patient has a containment pad, make sure it’s highly absorbent and not layered, to decrease pressure under the patient.
A comprehensive multidisciplinary approach to IAD is essential to the success of any skin care protocol. Identify skin care champions within your facility and educate them on IAD. Incorporating administrators, physicians, nursing staff, therapists, and care assistants makes implementation of protocols and algorithms within an institution seamless.
Administrators support the skin care program in the facility, including authorizing a budget so product purchases can be made. The certified wound clinician is the team expert regarding skin care, incontinence, prevention, and product recommendation. The physician oversees protocol development and evaluates and prescribes additional treatment when a patients fails to respond to treatment algorithms. Nursing staff identify patients at risk, incorporate the algorithm into the patient’s plan of care, and direct care
assistants. Therapists address function, strength, and endurance issues to improve the patient’s self-care abilities in activities of daily living to manage or prevent episodes of incontinence.
In severe inflammation, topical dressings, such as alginates and foam dressings, may be used along with topical corticosteroids. In complex IAD, antifungals or antibiotics may be required if a secondary fungal or bacterial infection is suspected.
Additional diagnostic tests may be done to identify and treat secondary infections. These tests may include skin scraping, potassium hydroxide test or Gram’s stain for fungal components, or a swab culture and sensitivity for bacterial infections. If your patient has a suspected secondary fungal or bacterial infection, use appropriate treatments for the full course of recommended therapy. In severe secondary fungal infection, an oral agent may be added to topical therapy. If cost is a concern, consider using a pharmacy knowledgeable about compounding for topical combination therapies.
For assessment and treatment of under-lying incontinence, refer the patient to a continence specialist if appropriate. Teach the patient strategies for managing incontinence through dietary measures, toileting programs, pelvic-floor muscle training, clothing modification, and mobility aids.
Selected references
Beguin A, Malaquin-Pavan E, Guihaire C, et al., Improving diaper design to address incontinence associated dermatitis. BMC Geriatrics. 2010;10:86. http://www.biomedcentral.com/1471-2318/10/86. Accessed March 15, 2012.
Black JM, Gray M, Bliss DZ, et al. MASD part 2: incontinence-associated dermatitis and intertriginous dermatitis. J Wound Ostomy Continence Nurs. 2011; 38(4):359-370.
Bliss DZ, Zehrer C, Savik K, et al. An economic evaluation of four skin damage prevention regimens in nursing home residents with incontinence: economics of skin damage prevention. J Wound Ostomy Continence Nurs. 2007;34(2):143-152.
Denat Y, Khorshid L. The effect of 2 different care products on incontinence-associated dermatitis in patients with fecal incontinence. J Wound Ostomy Continence Nurs. 2011;38(2):171-176.
Doughty DB. Urinary and Fecal Incontinence: Current Management Concepts. 3rd ed. St. Louis, MO: Mosby Elsevier; 2006.
Gray, M. Optimal management of incontinence-associated dermatitis in the elderly. Am J Clin Dermatol. 2010;11(3):201-210.
Gray M, Beeckman D, Bliss DZ, et al. Incontinence-associated dermatitis: a comprehensive review and update. J Wound Ostomy Continence Nurs. 2012;39(1):61-74
Gray M, Bliss DZ, Doughty DB, et al. Incontinence-associated dermatitis: a consensus. J Wound Ostomy Continence Nurs. 2007;34(1):45-54.
Gray M, Bohacek L, Weir D, et al. Moisture vs pressure: making sense out of perineal wounds. J Wound Ostomy Continence Nurs. 2007;34(2):134-42.
Institute for Clinical Systems Improvement. Health care protocol: Pressure ulcer prevention and treatment. Bloomington, MN: Institute for Clinical Systems Improvement. January 2012. http://www.icsi.org/pressure_ulcer_treatment_protocol__review_and_comment_/pressure_ulcer_treatment__protocol__.html. Accessed March 15, 2012.
Junkin J, Lerner-Selekof JL. Prevalence of incontinence and associated skin injury in the acute care inpatient. J Wound Ostomy Continence Nurs. 2007;34(3):260-269.
Landefeld CS, Bowers BJ, Feld AD, et al. National Institutes of Health state-of-the-science conference statement: prevention of fecal and urinary incontinence in adults. Ann Intern Med. 2008;148(6):449-458.
Langemo D, Hanson D, Hunter S, et al. Incontinence and incontinence-associated dermatitis. Adv Skin Wound Care. 2011;24(3):126-142.
Scheinfeld NS. Cutaneous candidiasis workup. 2011 update. http://emedicine.medscape.com/article/1090632-workup. Accessed March 15, 2012.
U.S. Census Bureau. The older population 2010. November 2011. www.census.gov/prod/cen2010/briefs/c2010br-09.pdf. Accessed March 15, 2012.
Nancy Chatham is an advanced practice nurse at Passavant Physician Associates in Jacksonville, Illinois. Carrie Carls is the nursing director of advanced wound healing and hyperbaric medicine at Passavant Area Hospital in Jacksonville, Illinois.
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