2014 Journal: May – June Vol. 3 No. 3

Wound Care Advisor Journal 2014 Vol3 No3

Understanding therapeutic support surfaces

Pressure-ulcer prevention and management guidelines recommend support-surface therapy to help prevent and treat pressure ulcers. Support surfaces include pads, mattresses, and cushions that redistribute pressure. Full cushions and cushion pads are considered therapeutic support surfaces if used to redistribute a patient’s pressure in a chair or wheelchair.

The National Pressure Ulcer Advisory Panel (NPUAP) defines support surfaces as “specialized devices for pressure redistribution designed for the management of tissue loads, microclimate, and/or other therapeutic functions.” These surfaces address the mechanical forces associated with skin and tissue injury, such as pressure, shear, friction, and excess moisture and heat. (See Clearing up the confusion.)

Read more

Clinical Notes: Pressure Injury Prevention, Diabetes, LIV

Incidence density best measure of pressure-ulcer prevention program According to the National Pressure Ulcer Advisory Panel (NPUAP), incidence density is the best quality measure of pressure-ulcer prevention programs. Pressure-ulcer incidence density is calculated by dividing the number of inpatients who develop a new pressure ulcer by 1,000 patient days. Using the larger denominator of patient days allows fair comparisons between institutions…

Clinician Resources: Patient Safety, Ostomy, Wound Management

This issue’s resources include patient tools and new guidelines. Improving patient safety Research suggests that adverse events affect patients with limited English proficiency (LEP) more frequently, are commonly caused by communication problems, and are more likely to result in serious harm compared to adverse events affecting English-speaking patients. Your hospital can take steps to reduce risks of adverse events for…

Eating better to help manage chronic stress

By Debra Rose Wilson, PhD, MSN, RN, IBCLC, AHN-BC, and Dana Marie Dillard, MS, HSMI Like many clinicians, you may experience stress frequently, both on and off the job. Chronic stress can alter your equilibrium (homeostasis), activating physiologic reactive pathways that cause your body to shift its priorities. Physiologic effects of stress may include: slowed digestion delay in reproductive and…

Hidden complications: A case study in peripheral arterial disease

By Pamela Anderson, MS, RN, APN-BC, CCRN, and Terri Townsend, MA, RN, CCRN-CMC, CVRN-BC Jan Smith, age 59, is admitted to the coronary intensive care unit with an acute inferior myocardial infarction (MI). Recently diagnosed with hypertension and hyperlipidemia, she smokes a pack and a half of cigarettes daily. She reports she has always been healthy and can’t believe she…

I’m going to conference!

By: Donna Sardina, RN, MHA, WCC, CWCMS, DWC, OMS Years ago, when I first started out in the wound care specialty, the only way to learn about new products and what was going on in the field was to “go to conference” (wound care conference). All year long, planning and excitement continued to build for our big trip. Not going…

Successful documentation of wound care

By Cheryl Ericson, MS, RN, CCDS, CDIP Providers are often surprised at how pages upon pages of documentation in a patient’s health record can result in few reportable diagnosis and/or procedure codes, which often fail to capture the complexity of the patient’s condition. However, providers need to be aware of the implications of coding. As healthcare data become increasingly digital…

The DIME approach to peristomal skin care

By Catherine R. Ratliff, PhD, APRN-BC, CWOCN, CFCN It’s estimated that about 70% of the 1 million ostomates in the United States and Canada will experience or have experienced stomal or peristomal complications. Peristomal complications are more common, although stomal complications (for example, retraction, stenosis, and mucocutaneous separation) can often contribute to peristomal problems by making it difficult to obtain…

Understanding the crusting procedure

By Nancy Morgan, RN, BSN, MBA, WOC, WCC, DWC, OMS Each issue, Apple Bites brings you a tool you can apply in your daily practice. The crusting procedure produces a dry surface and absorbs moisture from broken skin through an artificial scab that’s created by using skin barrier powder (stoma powder) and liquid polymer skin barrier. The crusting procedure is…

Understanding therapeutic support surfaces

By Rosalyn S. Jordan, BSN, RN, MSc, CWOCN, WCC, and Sandra Phipps, BSN, RN, MBA, WCC Pressure-ulcer prevention and management guidelines recommend support-surface therapy to help prevent and treat pressure ulcers. Support surfaces include pads, mattresses, and cushions that redistribute pressure. Full cushions and cushion pads are considered therapeutic support surfaces if used to redistribute a patient’s pressure in a…

What is a comprehensive risk assessment?

By Jeri Lundgren, BSN, RN, PHN, CWS, CWCN Prevention of pressure ulcers and skin breakdown begins with a comprehensive risk assessment. Most providers use a skin risk assessment tool, such as the Braden or Norton scale. While these tools have been validated to predict pressure ulcer development, their use alone isn’t considered a comprehensive assessment, and frequently the individual risk…

Wound Care Advisor Journal 2014 may-june-vol3_no3

Click here to access the digital edition

Read More

A Saudi rehabilitation facility fights pressure ulcers

Sultan Bin Abdulaziz Humanitarian City

By Joanne Aspiras Jovero, BSEd, BSN, RN; Hussam Al-Nusair, MSc Critical Care, ANP, RN; and Marilou Manarang, BSN, RN

A common problem in long-term care facilities, pressure ulcers are linked to prolonged hospitalization, pain, social isolation, sepsis, and death. This article explains how a Middle East rehabilitation facility battles pressure ulcers with the latest evidence-based practices, continual staff education, and policy and procedure updates. Sultan Bin Abdulaziz Humanitarian City (SBAHC) in Riyadh, Saudi Arabia, uses an interdisciplinary approach to address pressure-ulcer prevention and management. This article describes the programs, strategies, and preventive measures that have reduced pressure-ulcer incidence. (more…)

Read More

Guidelines for safe negative-pressure wound therapy

safe negative-pressure wound therapy

By Ron Rock MSN, RN, ACNS-BC

Since its introduction almost 20 years ago, negative-pressure wound therapy (NPWT) has become a leading technology in the care and management of acute, chronic, dehisced, traumatic wounds; pressure ulcers; diabetic ulcers; orthopedic trauma; skin flaps; and grafts. NPWT applies controlled suction to a wound using a suction pump that delivers intermittent, continuous, or variable negative pressure evenly through a wound filler (foam or gauze). Drainage tubing adheres to an occlusive transparent dressing; drainage is removed through the tubing into a collection canister. NWPT increases local vascularity and oxygenation of the wound bed and reduces edema by removing wound fluid, exudate, and bacteria. (more…)

Read More

How do you prove a wound was unavoidable?

unavoidable pressure ulcers

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

A pressure ulcer that a patient acquires in your facility or a patient’s existing pressure ulcer that worsens puts your organization at risk for regulatory citations as well as litigation. Unless you can prove the pressure ulcer was unavoidable, you could find yourself burdened with citations or fines, or could even end up in court. (more…)

Read More

The long and short of it: Understanding compression bandaging

By Robyn Bjork, MPT, WCC, CWS, CLT-LANA

Margery Smith, age 82, arrives at your wound clinic for treatment of a shallow, painful ulcer on the lateral aspect of her right lower leg. On examination, you notice weeping and redness of both lower legs, 3+ pitting edema, several blisters, and considerable denude­ment of the periwound skin. She is wearing tennis shoes and her feet have relatively little edema, but her ankles are bulging over the edges of her shoes; both socks are wet. Stemmer’s sign is negative. The wound on the right leg is draining copious amounts of clear fluid; it’s dressed with an alginate, which is secured with conforming roll gauze. No signs or symptoms of infection are present. (more…)

Read More

Preventing pressure ulcers starts on admission

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

The first 24 hours after a patient’s admission are critical in preventing pressure ulcer development or preventing an existing ulcer from worsening. A skin inspection, risk assessment, and temporary care plan should all be implemented during this time frame. Essentially, it’s the burden of the care setting to prove to insurers, regulators, and attorneys the pressure ulcer was present on admission and interventions were put into place to avoid worsening of the condition. Of course, patients also benefit from having their condition identified and treated promptly. (more…)

Read More

2013 Journal: September – October Vol. 2 No. 5

Wound Care Advisor Journal 2013 Vol2 No5

Developing a cost-effective pressure-ulcer prevention program in an acute-care setting

Pressure ulcers take a hefty toll in both human and economic terms. They can lengthen patient stays, cause pain and suffering, and increase care costs. The average estimated cost of treating a pressure ulcer is $50,000; this amount may include specialty beds, wound care supplies, nutritional support, and increased staff time to care for wounds. What’s more, national patient safety organizations and insurance payers have deemed pressure ulcers avoidable medical errors and no longer reimburse the cost of caring for pressure ulcers that develop during hospitalization.

Read more

Clinical Notes: Debridement, Optimal Wound Healing, Diabetes, Sacral Wounds

Frequent debridement improves wound healing A study in JAMA Dermatology reports that fre­quent debridements speed wound healing. “The more frequent the debridement, the better the healing outcome,” concludes “Frequency of debridements and time to heal: A retrospective cohort study of 312 744 wounds.” The median number of debridements was two. Most of the wounds in the 154,644 patients were diabetic foot…

Clinician Resources: Guideline Clearinghouse, Patient Safety, Diabetic Foot-Ulcers

Here are some resources of value to your practice. National Guideline Clearinghouse The National Guideline Clearinghouse, supported by the Agency for Healthcare Research and Quality, summarizes many guidelines of interest to wound care, ostomy, and lymph­edema clinicians. Here are some examples: Guideline for management of wounds in patients with lower-extremity neuropathic disease Pressure ulcer prevention and treatment protocol Lower limb…

Compassionate care

Compassionate care: The crucial difference for ostomy patients

By Gail Hebert, RN, MS, CWCN, WCC, DWC, LNHA, OMS; and Rosalyn Jordan, BSN, RN, MSc, CWOCN, WCC, OMS Imagine your physician has just told you that your rectal pain and bleeding are caused by invasive colon cancer and you need prompt surgery. She then informs you that surgery will reroute your feces to an opening on your abdominal wall.…

Dealing with difficult people

By Rose O. Sherman, EdD, RN, NEA-BC, FAAN Unfortunately, most clinicians can’t avoid having to work with difficult people. However we can learn how to be more effective in these situations, keeping in mind that learning to work with difficult people is both an art and a science. How difficult people differ from the rest of us We can all…

Developing a cost-effective pressure-ulcer prevention program in an acute-care setting

By Tamera L. Brown, MS, RN, ACNS-BC, CWON, and Jessica Kitterman, BSN, RN, CWOCN Pressure ulcers take a hefty toll in both human and economic terms. They can lengthen patient stays, cause pain and suffering, and increase care costs. The average estimated cost of treating a pressure ulcer is $50,000; this amount may include specialty beds, wound care supplies, nutritional…

How to fit in fast at your new job

By Gregory S. Kopp, RN, MN, MHA A new job can be stimulating, but it can also be stressful. Not only will you have new responsibilities, but you’ll also have a new setting, new leaders, and new colleagues. And the quicker you can figure out who’s who and what’s what—without stepping on anyone’s toes—the better off you’ll be. But establishing…

Improving outcomes with noncontact low-frequency ultrasound

By Ronnel Alumia, BSN, RN, WCC, CWCN, OMS Achieving excellent wound care outcomes can be challenging, given the growing number of high-risk patients admitted to healthcare facilities today. Many of these patients have comorbidities, such as obesity, diabetes, renal disease, smoking, chronic obstructive pulmonary disease, and poor nutritional status. These conditions reduce wound-healing ability.

Power up your patient education with analogies and metaphors

By Janice M. Beitz, PhD, RN, CS, CNOR, CWOCN, CRNP Quality patient education is essential for comprehensive health care and will become reimbursable under healthcare reform in 2014. However, it’s difficult to provide effective education when time for patient interactions is limited. You can enhance your instruction time—and make your teaching more memorable—by using the techniques of analogy and metaphor.

Preventing pressure ulcers starts on admission

By Jeri Lundgren, BSN, RN, PHN, CWS, CWCN The first 24 hours after a patient’s admission are critical in preventing pressure ulcer development or preventing an existing ulcer from worsening. A skin inspection, risk assessment, and temporary care plan should all be implemented during this time frame. Essentially, it’s the burden of the care setting to prove to insurers, regulators,…

Taking care of the caregiver—you

By: Donna Sardina, RN, MHA, WCC, CWCMS, DWC, OMS Why is it that the people who are the most caring toward others neglect their own needs? Have you noticed this? I’ve seen it time and time again. The healthcare worker who’s always the last to leave work, who always volunteers to work those extra shifts so patient care won’t be…

2013 Journal: September – October Vol. 2 No. 5
Read More

From the Editor – Wound care superhero

by Donna Sardina, RN, MHA, WCC, CWCMS, DWC, OMS

What an honor it is to be the wound care “superhero”—the guru, the healer, the go-to person. Unfortunately, this honor may be accompanied by wound care overload—too much to do in too little time.

Once someone is crowned the superhero specialist, others may try to transfer every aspect of wound and skin care to that person—all treatment plans, assessments, documentation, prevention, education, and accountability. Superheroes don’t cry, so they don’t complain about the workload. Yet, the overload must be controlled. (more…)

Read More

Assessing risk of pressure and moisture-related problems in long-term care patients

By Patricia A. Slachta, PhD, RN, ACNS-BC, CWOCN

Assessing moisture and pressure risk in elderly patients continues to be a focus for clinicians in all settings, particularly long-term care. Ongoing research challenges our ideas about and practices for cleansing and protecting damaged skin. Until recently, most wound care clinicians have cleansed long-term care patients’ skin with mild soap and water. But several studies have shown pH-balanced cleansers are more efficient than soap and water for cleansing the skin of incontinent patients.

Various terms are used to describe skin breakdown related to moisture—incontinence-associated dermatitis, perineal dermatitis, diaper rash, intertriginal dermatitis, intertrigo, moisture-related skin damage, moisture-associated skin damage, and even periwound dermatitis. This article uses moisture-associated skin damage (MASD) because it encompasses many causes of skin breakdown related to moisture. Regardless of what we call the condition, we must do everything possible to prevent this painful and costly problem.

Skin assessment

Start with an overall assessment of the patient’s skin. Consider the texture and note dryness, flaking, redness, lesions, macerated areas, excoriation, denudement, and other color changes. (See Identifying pressure and moisture characteristics by clicking the PDF icon above.)

Assessing MASD risk

A patient’s risk of MASD can be assessed in several ways. Two of the most widely used pressure-ulcer risk scales, the Norton and Braden scales, address moisture risk. The Norton and Braden subscales should drive your plan for preventing skin breakdown related to moisture or pressure. The cause of breakdown (moisture, pressure, or shear/friction) must be identified, because treatment varies with the cause.

Both the Norton and Braden scales capture activity, mobility, and moisture scores. The Braden scale addresses sensory perception, whereas the Norton scale identifies mental condition. (See Subscales identifying pressure, shear, and moisture risk by clicking the PDF icon above.) Also, be aware that two scales have been published for perineal risk, but neither has been used widely.

You must differentiate pressure- and moisture-related conditions to determine correct treatment. Patients who are repositioned by caregivers are at risk for friction or shear. Also, know that agencies report pressure-ulcer prevalence. Care providers no longer classify mucous-membrane pressure areas in skin prevalence surveys; mucous membranes aren’t skin and don’t have the same tissue layers. Furthermore, don’t report skin denudement from moisture (unless pressure is present) in prevalence surveys.

When moisture causes skin breakdown

Skin has two major layers—epidermis and dermis. The epidermis itself has five layers: The outermost is the stratum corneum; it contains flattened, keratin protein–containing cells, which aid water absorption. These cells contain water-soluble compounds called natural moisturizing factor (NMF), which are surrounded by a lipid layer to keep NMF within the cell. When skin is exposed to moisture, its temperature decreases, the barrier function weakens, and skin is more susceptible to pressure and friction/shear injury. Also, when urea in urine breaks down into ammonia, an alkaline pH results, which may reactivate proteolytic and lipolytic enzymes in the stool. (See Picturing moisture and pressure effects by clicking the PDF icon above.)

Caring for moisture-related skin breakdown

The standard of care for moisture-related skin breakdown includes four major components: cleanse, moisturize, protect, and contain. Specific products used for each component vary with the facility’s product formulary.

Cleanse

Gently wash the area using a no-rinse cleanser with a pH below 7.0. Don’t rub the skin. Pat dry.

Moisturize

Use creams containing emollients or humectants. Humectants attract water to skin cells and help hold water in the cells; don’t use these products if the skin is overhydrated. Emollients slow water loss from skin and replace intracellular lipids.

Protect

Options for skin protectants include:
• liquid film-forming acrylate sprays or wipes
• ointments with a petroleum, zinc oxide, or dimethicone base
• skin pastes. Don’t remove these products totally at each cleansing, but do remove stool, urine, or drainage from the surface and apply additional paste afterward. Every other day, remove the paste down to the bare skin using a no-rinse cleanser or mineral oil.

Be sure to separate skinfolds and use products that wick moisture rather than trap it. These may include:
• commercial moisture-wicking products
• a light dusting with powder containing refined cornstarch or zinc oxide—not cornstarch from the kitchen or powder with talc as the only active ingredient
• abdominal pads.

Contain

To keep moisture away from skin, use absorbent underpads with wicking properties, condom catheters (for males), fecal incontinence collectors, fecal tubes (which require a healthcare provider order), or adult briefs with wicking or gel properties. Call a certified ostomy or wound care nurse for tips on applying and increasing wear time for fecal incontinence collectors.

If 4″ × 4″ gauze pads or ABD pads are saturated more frequently than every 2 hours, consider applying an ostomy or specially designed wound pouch to the area. Collecting drainage allows measurement and protects skin from the constant wetness of a saturated pad.

Don’t neglect the basics, for example, know that wet skin is more susceptible to breakdown. Turn the patient and change his or her position on schedule. Change linens and underpads when damp, and consider using a low-air-loss mattress or bed or mattress with microclimate technology.

Also, be aware that fungal rashes should be treated with appropriate medications. If the patient’s skin isn’t too moist, consider creams that absorb into the skin; a skin-protecting agent can be used as a barrier over the cream. Besides reviewing and using the standards of care, you may refer to the Incontinence-Associated Dermatitis Intervention Tool, which has categories related to skin damage. See the “Incontinence-Associated Dermatitis Intervention Tool” (IADIT).

Bottom line on skin breakdown

To help prevent skin breakdown related to moisture, assess patients’ skin appropriately, determine treatment using evidence-based guidelines, and implement an appropriate plan of care.

Selected references
Black JM, Gray M, Bliss DZ, et al. MASD part 2: incontinence-associated dermatitis and intertriginous dermatitis: a consensus. J Wound Ostomy Continence Nurs. 2011;38(4):359-70.

Borchert K, Bliss DZ, Savik K, Radosevich DM. The incontinence-associated dermatitis and its severity instrument: development and validation. J Wound Ostomy Continence Nurs. 2010;37(5):527-35.

Doughty D. Differential assessment of trunk wounds: pressure ulceration versus incontinence-associated dermatitis versus intertriginous dermatitis. Ostomy Wound Manage. 2012;58(4):20-2.

Doughty D, Junkin J, Kurz P, et al. Incontinence-associated dermatitis: consensus statements, evidence-based guidelines for prevention and treatment, and current challenges. J Wound Ostomy Continence Nurs. 2012;39(3):303-15.

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, Black JM, Baharestani MM, et al. Moisture-associated skin damage: overview and pathophysiology. J Wound Ostomy Continence Nurs. 2011;38(3):233-41.

Langemo D, Hanson D, Hunter S, Thompson P, Oh IE. Incontinence and incontinence-associated dermatitis. Adv Skin Wound Care. 2011;24(3):126-40.

National Pressure Ulcer Advisory Panel and European Pressure Ulcer Advisory Panel. Prevention and treatment of pressure ulcers: clinical practice guideline.Washington, DC: National Pressure Ulcer Advisory Panel; 2009.

Sibbald RG, Krasner DL, Woo KY. Pressure ulcer staging revisited: superficial skin changes & Deep Pressure Ulcer Framework©. Adv Skin Wound Care. 2011;24(12):571-80.

Wound, Ostomy and Continence Nurses Society. Guideline for Prevention and Management of Pressure Ulcers. Mt. Laurel, NJ: Wound, Ostomy and Continence Nurses Society; 2010.

Wound, Ostomy and Continence Nurses Society. Incontinence-Associated Dermatitis: Best Practice for Clinicians. Mt. Laurel, NJ: Wound, Ostomy and Continence Nurses Society; 2011.

Zulkowski K. Diagnosing and treating moisture-associated skin damage. Adv Skin Wound Care. 2012;25(5):231-6.

Patricia A. Slachta is an instructor at the Technical College of the Lowcountry in Beaufort, South Carolina.

Read More

Positive Stemmer’s sign yields a definitive lymphedema diagnosis in 10 seconds or less

By Robyn Bjork, MPT, CWS, WCC, CLT-LANA

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 More

Lymphedema 101 – Part 1: Understanding the pathology and diagnosis

By Steve Norton, CDT, CLT-LANA

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.

Causes of lymphedema

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.)

Classifying lymphedema

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 stages

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.

Assessment and diagnosis

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.

Discomfort and skin appearance

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.

Severity

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.

Opportunistic infections

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.

Differential diagnosis

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.

Next step: Treatment

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 More

Necrotizing fasciitis: Frightening disease, potentially grim prognosis

By Lydia Meyers, BSN, RN, CWCN

Necrotizing fasciitis (NF) results from an infection that attacks the fascia and subcutaneous tissues. The primary bacterial etiology is group A streptococcus, a facultative anaerobic bacterium. However, other bacteria may contribute. Sometimes called the “flesh-eating” disease because of the potentially devastating effect on the afflicted patient, NF can be monomicrobial or polymicrobial.

The four typical settings for NF are:

  • surgical bowel or abdominal trauma surgery
  • pressure ulcer and perianal abscess
  • injection sites (especially in drug users)
  • Bartholin abscess or minor vulvovaginal infection.

Because of the rapid course and ravaging nature of acute NF, clinicians must maintain a high index of suspicion if the patient has suggestive signs and symptoms. In 1990, puppeteer Jim Henson (best known for creating the Muppets) died from NF. At that time, little was known about the progression of group A streptococcal infection.
The disease can quickly cause death, so starting immediate treatment is even more crucial than confirming the diagnosis. Once the disease is suspected, antibiotics must be given immediately and the patient must be prepared for surgery at once. NF spreads rapidly, capable of progressing from a small lesion to death in days to weeks. Thus, delayed diagnosis increases the risk of death. Lack of knowledge about the disease and inability to recognize it promptly are the main reasons many victims die. This article can improve your knowledge base.

Overview

NF was discovered in 1871 by Joseph Jones, a Confederate Army surgeon. At that time, it was called hemolytic streptococcal gangrene, nonclostridial gas gangrene, nonclostridial crepitant cellulitis, necrotizing or gangrenous erysipelas, necrotizing cellulitis, bacterial synergistic gangrene, or synergistic necrotizing cellulitis.
NF involves the fascia, muscle compartments, or both. It can affect not only the muscle fascia but the superficial fascia. NF and cellulitis differ in the amount of tissue involved and extent of tissue involvement.
The most common areas of infection are the abdominal wall, perineum, and extremities. When NF affects the perineum and scrotum, it’s called Fournier gangrene, after the French dermatologist and virologist Alfred Jean Fournier.
The most common causes are trauma, surgery, and insect bites. The disease can affect persons of any age. Such comorbidities as diabetes, chronic renal failure, immunosuppressive therapy, hypertension, obesity, and malnutrition increase susceptibility.

Pathophysiology

NF falls into four classifications based on wound microbiology. Type 1, the most common, involves polymicrobial bacteria. Type 2 results from trauma and is associated with comorbidities. Type 3, rare in this country, stems from gram-negative marine bacteria. Type 4 is a fungal infection occurring mostly in immunocompromised persons. (See Comparing types of necrotizing fasciitis by clicking the PDF icon above.)

Disease progression

The four types of NF progress in a similar way. Bacteria secrete pyrogenic exotoxin A, which stimulates cytokines. These cyto­kines damage the endothelial lining; fluid then leaks into the extravascular space.
M proteins in streptococci and β-hemolytic streptococci exacerbate the immune reaction by inhibiting phagocytosis of polymorphonuclear leukocytes and normal neutrophil chemotaxis. As the immune reaction increases, blood vessels dilate, allowing toxins to leak through vessel walls, which in turn decreases blood flow. As the cascade continues, hypoxic conditions cause facultative aerobic organisms to grow and become anaerobic. These bacteria exacerbate destruction of surrounding cells and lead to release of carbon dioxide, water, hydrogen, nitrogen, hydrogen sulfide, and methane. As the infection continues to progress, toxins spread throughout the bloodstream and the patient becomes septic.

Assessment

Obtain the patient’s medical history and description of the wound. Determine when the changes first appeared and whether the affected area seemed to get worse recently.
In all NF types, patients commonly present with a small, painful area (possibly with entry marks) but no other signs or symptoms. The wound may appear as a bulla, cellulitis, or dermatitis, representing an infection developing in underlying tissues. The skin may have a wooden-hard feel as the infection progresses to the subcutaneous space and causes necrosis. The wound becomes discolored and necrotic; drainage is rare until surgical debridement begins. The patient quickly develops fever, chills, nausea, and vomiting. As NF progresses, bullae become dark purple with darkened edges; the patient grows disoriented and lethargic, and organ failure and respiratory failure
ensue. Without treatment, the patient dies.

Diagnosis

Diagnostic tests usually include magnetic resonance imaging, complete blood count with differential, comprehensive metabolic panel, and cultures. (See Diagnostic findings in necrotizing fasciitis by clicking the PDF icon above.)

Treatment

Immediate surgical debridement and broad-spectrum antibiotics are needed to stop the immune response to infection. Clindamycin, gentamicin, penicillin, or metronidazole may be given alone or in combination until culture results are available. Supportive care includes total parenteral nutrition for nutritional support, I.V. fluids, and oxygen. Limb amputation should be done only as a last resort.
Surgical debridement involves penetrating deep into the fascia and removing all necrotic tissue. After the first debridement, release of “dishwater fluid” may occur.
Administering hyperbaric oxygen therapy (HBOT) after the first debridement increases tissue oxygenation, thus reducing tissue destruction by anaerobic bacteria. During HBOT (usually given as a 90-minute treatment), the patient breathes 100% oxygen in an environment of increasing atmospheric pressure.
HBOT should be given in conjunction with surgical debridement (usually after each debridement) and should continue until necrotic tissue ceases and cell destruction stops. HBOT also promotes collagen synthesis and neoangiogenesis (new blood vessel growth), which boosts blood supply and oxygen to tissues.
Adverse effects of HBOT include ear pain, oxygen toxicity, and seizures. Ear pain can be minimized by swallowing or yawning. If the patient continues to have ear pain, ear tubes may be inserted by an otolaryngologist. During HBOT, air breaks (intervals of breathing room air) are important in controlling oxygen toxicity (the main cause of seizures).
Throughout the HBOT treatment period, wound dressings must be simple. Well-moistened gauze dressings and an abdominal pad provide good support. Once necrotic destruction occurs, dressings depend on wound size and the need to fill cavities. The patient may require a diverting colostomy, depending on wound
location and the amount of uncontrolled diarrhea. Blood glucose levels must be monitored before and after HBOT, as this treatment affects blood glucose.

Supportive care and follow-up treatment

During initial treatment, patients need supportive care and monitoring. Once they’re out of danger, begin teaching them how to prevent NF recurrences. Advise them to control blood glucose levels, keeping the glycated hemoglobin (HbA1c) level to 7% or less. Caution patients to keep needles capped until use and not to reuse needles. Instruct them to clean the skin thoroughly before blood glucose testing or insulin injection, and to use alcohol pads to clean the area afterward.
Before discharge, help arrange the patient’s aftercare, including home health care for wound management and teaching, social services to promote adjustment to lifestyle changes and financial concerns, and physical therapy to help rebuild strength and promote the return to optimal physical health. One helpful patient resource is the National Necrotizing Fasciitis Foundation. The Centers for Disease Control and Prevention section on necrotizing fasciitis includes “Common sense and great wound care are the best ways to prevent a bacterial skin infection.”
The life-threatening nature of NF, scarring caused by the disease, and in some cases the need for limb amputation can alter the patient’s attitude and viewpoint, so be sure to take a holistic approach when dealing with the patient and family. Today, NF has a much better survival rate than 2 decades ago when Jim Henson died. In my practice, I’ve seen four NF cases. Thanks to early identification, good wound care, and HBOT, these patients suffered only minimal damage.

Selected references

Boyer A, Vargas F, Coste F, et al. Influence of surgical treatment timing on mortality from necrotizing soft tissue infections requiring intensive care management. Intensive Care Med. 2009;35(5):847-853. doi:10.1007/s00134-008-1373-4.

Cain S. Necrotizing fasciitis: recognition and care. Practice Nurs. 2010;21(6):297-302.

Centers for Disease Control and Prevention. Notes from the field: fatal fungal soft-tissue infections after a tornado—Joplin, Missouri, 2011. MMWR. 2011;60(29):992.

Chamber AC, Leaper DJ. Role of oxygen in wound healing: a review of evidence. J Wound Care. 2011; 20(4):160-164.

Christophoros K, Achilleas K, Vasilia D, et al. Postraumatic zygomycotic necrotizing abdominal wall fasciitis with intraabdominal invasion in a non immunosuppressed patient. Internet J Surg. 2007;11(1). doi:10.5580/17a8.

Ecker K-W, Baars A, Topfer J, Frank J. Necrotizing fasciitis of the perineum and the abdominal wall-surgical approach. Europ J Trauma Emerg Surg. 2008;
34(3):219-228. doi:10.1007/s00068-008-8072-2.

Hunter J, Quarterman C, Waseem M, Wills A. Diagnosis and management of necrotizing fasciitis. Br J Hosp Med. 2011;72(7):391-395.

Magel DC. The nurse’s role in managing necrotizing fasciitis. AORN J. 2008;88(6):977-982.

Phanzu MD, Bafende AE, Imposo BB, Meyers WM, Portaels F. Under treated necrotizing fasciitis masquerading as ulcerated edematous Mycobacterium ulcerans infection (Buruli ulcer). Am J Trop Med Hyg. 2012;82(3):478-481.

Ruth-Sahd LA, Gonzales M. Multiple dimensions of caring for a patient with acute necrotizing fasciitis. Dimens Crit Care Nurs. 2006;25(1):15-21.

Stevens DL, Bisno AL, Chambers HF, et al; Infectious Diseases Society of America. Practice guidelines for the diagnosis and management of skin and soft-tissue infections. Clin Infect Dis. 2005;41(10):1373-1406.

Su YC, Chen HW, Hong YC, Chen CT, et al. Laboratory risk indicator for necrotizing fasciitis score and the outcomes. ANZ J Surg. 2008;78(11):968-972.

Taviloglu K, Yanar H. Necrotizing fasciitis: strategies for diagnosis and management. World J Emerg Surg. 2007;2:19.

Lydia Meyers is a medical reviewer for National Government Services in Castleton, Indiana, and a clinical liaison at CTI Nutrition in Indianapolis. She has 11 years of wound care experience in nursing homes, wound clinics, and home health.

Read More
1 2 3