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Understanding stoma complications

By Rosalyn S. Jordan, RN, BSN, MSc, CWOCN, WCC, OMS; and Judith LaDonna Burns, LPN, WCC, DFC

About 1 million people in the United States have either temporary or permanent stomas. A stoma is created surgically to divert fecal material or urine in patients with GI or urinary tract diseases or disorders.

A stoma has no sensory nerve endings and is insensitive to pain. Yet several complications can affect it, making accurate assessment crucial. These complications may occur during the immediate postoperative period, within 30 days after surgery, or later. Lifelong assessment by a healthcare provider with knowledge of ostomy surgeries and complications is important. (more…)

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What’s causing your patient’s lower-extremity redness?

patient lower extremity redness

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

The ability to understand or “read” lower-extremity redness in your patient is essential to determining its cause and providing effective treatment. Redness can occur in multiple conditions—hemosiderin staining, lipodermatosclerosis, venous dermatitis, chronic inflammation, cellulitis, and dependent rubor. This article provides clues to help you differentiate these conditions and identify the specific cause of your patient’s lower-extremity redness. (more…)

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MRSA: What wound care professionals need to know

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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Staying out of sticky situations: How to choose the right tape for your patient

By Ann-Marie Taroc, MSN, RN, CPN

Are you using the wrong kind of medical tape on your patients? Although we strive to provide the safest care possible, some nurses may not realize that medical tape used to secure tubes and dressings can cause harm. The harm may stem from using the wrong product or using a product incorrectly, which can cause adhesive failure or skin injury. (more…)

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Helping patients overcome ostomy challenges

By Beth Hoffmire Heideman, MSN, RN

No one wants an ostomy, but sometimes it’s required to save a patient’s life. As ostomy specialists, our role is to assess and intervene for patients with a stoma or an ostomy to enhance their quality of life. We play an active role in helping patients perform self-care for their ostomy and adjust to it psychologically, starting even before surgery. (more…)

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Providing evidence-based care for patients with lower-extremity cellulitis

By Darlene Hanson, PhD, RN; Diane Langemo, PhD, RN, FAAN; Patricia Thompson, MS, RN; Julie Anderson, PhD, RN; and Keith Swanson, MD

Cellulitis is an acute, painful, and potentially serious spreading bacterial skin infection that affects mainly the subcutaneous and dermal layers. Usually of an acute onset, it’s marked by redness, warmth, swelling, and tenderness. Borders of the affected skin are characteristically irregular. Although cellulitis may occur in many body areas, this article discusses the most common location—the lower limb. (more…)

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Hyperbaric oxygen therapy for treatment of diabetic foot ulcers

By 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…)

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Lymphedema 101 – Part 2: Treatment

By Steve Norton, CDT, CLT-LANA

Editor’s note: Part 1 of this series, published in the September-October issue, discussed lymphedema pathology and diagnosis. This article, Part 2, covers treatment.

Traditional treatment approaches

Traditionally, lymphedema treatment has been approached without a clear understanding of the underlying structure and function of lymphatic tissues. Ineffective traditional treatments include elevation, elastic garments, pneumatic pumps, surgery, diuretics, and benzopyrones (such as warfarin). Because many traditional treatments are still overused and some may be appropriate for limited use, it’s important for clinicians to understand these approaches.

Elevation

As a sole therapy for lymphedema, elevation of the affected part provides only short-lived results. Ever-increasing macromolecular wastes retain water against the effects of gravity. Increased interstitial colloid osmotic pressure must be addressed by interventions targeted at improving lymphatic function—not just a position change. Otherwise, lymphedema will progress. Furthermore, elevation alone is impractical, promotes deconditioning, and alters lifestyle for prolonged periods.

Elastic garments

Elastic garments prove inadequate because they attempt to treat lymphedema with compression alone. Medically correct garments are engineered with thoughtful attention to high-quality textiles and offer gradient support, which promotes proximal flow. However, without precise tissue stimulation leading to improved lymphangioactivity (lymph-vessel pulsation), macromolecular wastes can’t be removed.
Interstitial pressure increases caused by compression garments impede further fluid accumulation. When these garments are removed, the spontaneous girth increase causes an imprecise fit, and the garment rapidly leads to a countertherapeutic effect. Furthermore, compression garments don’t combat the osmotic forces generated by ever-increasing interstitial wastes. Except in patients diagnosed with stage 0 or stage 1 lymphedema, disease progression involving metaplasia ensues. Although elastic compression garments are a cornerstone of long-term management, they shouldn’t be used as a stand-alone treatment.

Pneumatic compression pump

Formerly, the pneumatic compression pump (PCP) was considered the standard of care for lymphedema. However, when inflated, the pump doesn’t increase the frequency of lymph-vessel contraction or enhance lymph capillary absorption. What’s more, accelerated fibrosis development and rapid tissue refilling occur when a PCP is removed. Also, PCP use disregards the ipsilateral territory of the excised regional nodes, effectively dumping fluid from the leg into the trunk. A PCP is appropriate only when nothing else is available, as it may worsen the patient’s condition.

Surgery

Surgical approaches to treating lymphedema involve either excisional (debulking) or microsurgical techniques. The most extensive surgical technique, the radical Charles procedure, completely debulks all involved tissue down to the muscle fascia. Split-thickness grafts are then harvested from excised skin and donor sites, and applied to the fascia to achieve so-called limb reduction.
Most debulking procedures have been applied to lower-extremity lymphedema and offer poor cosmetic results. Less radical surgeries favor long incisions, preserving the skin but excising subcutaneous edematous portions to reduce girth. Although less cosmetically alarming, these procedures effectively amputate the subcutaneous space where lymph vessels reside. Other surgical approaches are beyond the scope of this article.
Generally, surgery isn’t a good approach for any patient, as it’s linked to significant morbidity, such as skin necrosis, infection, and sensory changes. In the future, less invasive procedures may be available that yield significant improvement without these adverse effects.

Diuretics

Although diuretics are prescribed appropriately to address water-rich edemas of venous origin, they disregard the fact that lymphedema is a protein-rich edema. Long-term, high-dose diuretic therapy leads to treatment-resistant limbs, similar to those that have received intensive pneumatic compression.

Benzopyrones

Benzopyrones such as warfarin decrease swelling by combating protein accumulation in fluid. Such drugs have undergone clinical trials abroad. Their mechanism is to promote macrophage migration into interstitial fluid, as well as subsequent proteolysis. Due to significant risk of liver damage or failure, benzopyrones haven’t been approved for treating lymphedema.

Complete decongestive therapy: The current treatment approach

Currently, the gold standard for lymphedema treatment is complete decongestive therapy (CDT). Michael Foeldi and Etelka Foeldi, who originated this method, discovered a unique symbiotic relationship among five distinct modalities that addresses the challenges of lymphedema treatment. In 1989, CDT was brought to the United States by Robert Lerner and has become the mainstay of lymphedema treatment here.
CDT is a two-phase approach involving an intensive clinical effort followed by a semi-intensive home-care program geared toward autonomous management, stabilization, and continual improvement. It involves manual lymph drainage (MLD), compression bandaging, exercise, skin and nail hygiene, and self-care education. (See Phases of complete decongestive therapy by clicking the PDF icon above.)

Manual lymph drainage

A type of soft-tissue mobilization, MLD provides skin traction, stimulating superficial lymph vessels and nodes. Lymph capillaries contain large inter-endothelial inlets called swinging tips, akin to overlapping shingles. Each overlapping cell is tethered to the interstitial matrix by anchoring filaments, so that fluid increases cause immediate distention and lymph inflow. Manual skin traction using MLD promotes greater lymph fluid uptake by stretching these filamentous structures, opening the swinging tips.
MLD also provides extrinsic stimulation of the lymphangion (the segment of a lymph vessel between a distal and proximal valve), drawing fluid into the system at the capillary level and promoting flow at the vessel level toward regional lymph nodes. Usually, these segments contract and relax in a rhythmic fashion six times per minute. MLD triples this output to 18 or 20 times per minute, greatly enhancing systemic transport.
MLD requires intensive daily treatment sessions to strengthen collateral flow as a pathway to circumventing surgical or developmental lymphatic disruption. Treatment strategies further recruit more deeply situated lymphatics such as the thoracic duct, as well as lumbar trunks that empty at the juncture of the internal jugular and subclavian veins to improve global uptake. MLD thus stimulates deeper vessel angioactivity to help drain the superficial vessels that drain toward them.

Compression bandaging

Compression bandaging provides tissue support after MLD to prevent reflux, slow new fluid formation, and mechanically soften fibrotic areas. Bandaging techniques provide a high working pressure to harness the muscle and joint pumps as a propellant for lymph while resisting retrograde flow created by gravity and centrifugal forces during movement. Pure cotton materials coupled with specialized padding create a soft, castlike environment, which confines swollen tissues without constriction. By relying on high working pressure and low resting pressures to decrease limb swelling, this strategy achieves greater control over intensity (level of compression/pressure exerted), with little to no soft-tissue injury or discomfort.
The patient wears this bulky inelastic complex after each MLD treatment until the next day’s session to ensure limb-volume reduction in a stable, linear fashion. Once a plateau is reached, tissue stabilization and self-care education are the goals of additional sessions.

Exercise

Exercise always must be done with adequate support to counteract fluid formation. During the intensive CDT phase, limbs are bandaged to provide complete around-the-clock containment. Gentle exercises encourage blood flow into the muscle; during muscle contraction, this creates a favorable internal pressure that effectively squeezes the subcutaneous space between the bandage wall and muscle. Because every bandage strives to provide a gradient of support, fluid tends to drain proximally to the bandage—in most cases, to the trunk.

Skin and nail hygiene

Without intact, well-hydrated skin, cellulitic infections occur in many lymphedema patients whose immune response has been diminished by regional lymphadenectomy or inherited deficiencies. To prevent infection caused by avoidable external events, patients receive clear guidelines to reinforce appropriate behavior. As most cellulitis results from resident skin pathogens (streptococci and staphylococci), maintaining a low skin pH helps control colonization. Ways to avoid recurrent infections include maintaining an acid mantle on the skin using low-pH-formulated lotions and avoiding injury from daily tasks that may scratch, puncture, burn, or abrade the skin. Patients should receive lists of self-care precautions at the time of treatment.

Self-care education

Because lymphedema is a chronic condition, patients must receive self-care education for daily management to avoid lymphedema destabilization, which can lead to tissue saturation and subsequent skin changes. Therapists must provide patients with appropriate self-care tools and knowledge to maintain adequate treatment results. Teaching topics include how to apply and remove compression garments and bandages and how to exercise safely, preserve skin integrity, monitor for infection, and respond appropriately to infection and significant changes in limb mobility.

An underrecognized and mistreated problem

Lymphedema remains an underrecognized and mistreated condition, even though CDT yields safe, reliable results. Early detection, accurate staging, proper diagnosis, and appropriate treatment can slow the inevitable progression of lymphedema. Wound care specialists should adapt wound therapy to address not just the wound but the edematous environment responsible for delayed wound resolution.

Selected references
Al-Niaimi F, Cox N. Cellulitis and lymphedema: a vicious cycle. J Lymphoedema. 2009;4:38-42.

Browse N, Burnand KG, Mortimer PS. Diseases of the Lymphatics. London: Hodder Arnold; 2003.

Casley-Smith JR, Casley-Smith JR. Modern Treatment for Lymphoedema. 5th ed. The Lymphoedema Association of Australia; 1997.

Cooper R, White R. Cutaneous infections in lymphoedema. J Lymphoedema. 2009:4:44-8.

Foeldi M. Foeldi’s Textbook of Lymphology: For Physicians and Lymphedema Therapists. 3rd ed. St. Louis, MO: Mosby; 2012.

International Society of Lymphology. The diagnosis and treatment of peripheral lymphedema. Consensus Document of the International Society of Lymphology. Lymphology. 2009 Jun;42(2):51-60.

Leduc A, Bastin R, Bourgeois P. Lymphatic reabsorption of proteins and pressotherapies. Progress in Lymphology XI. 1988:591-2.

National Lymphedema Network Medical Advisory Committee. Position Statement: Lymphedema Risk Reduction Practices. Revised May 2012. http://www.lymphnet.org/pdfDocs/nlnriskreduction.pdf. Accessed September 5, 2012.

Pappas CJ, O’Donnell TF Jr. Long-term results of compression treatment for lymphedema. J Vasc Surg. 1992 Oct;16(4):555-62.

Whittlinger H. Textbook of Dr. Vodder’s Manual Lymphatic Drainage. Vol 1. 7th ed. New York, NY: Thieme; 2003.

Steve Norton is cofounder of Lymphedema & Wound Care Education and executive director of the Norton School of Lymphatic Therapy in Matawan, New Jersey.

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Caring for chronic wounds: A knowledge update

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

Wound care has come a long way in just a few decades. With our expanded knowledge of wound healing and recent advances in treatment, we’re now able to assess wounds more accurately, recognize wound-related problems sooner, provide better interventions, and reduce morbidity.

To bring you up to date on current evidence-based wound management, this article focuses on assessing patients with chronic wounds, optimizing wound healing with effective wound-bed preparation, and selecting an appropriate dressing.

Wound chronicity and cause

Developing an appropriate plan of care hinges on conducting a thorough, accurate evaluation of both the patient and the wound. The first step is to determine whether the wound is acute or chronic.
•    A chronic wound is one that fails to heal within a reasonable time—usually
3 months.
•    An acute wound heals more quickly, causing minimal functional loss in the part of the body with the wound.
Identifying the cause of the wound also is essential. If the wound etiology is unknown, explore the patient’s medical history (including medication history) for clues to possible causes. Also review the patient’s history for conditions that could impede wound healing. (See What factors hamper healing? by clicking the PDF icon above)
Other important aspects of assessment include evaluating the patient’s nutritional status, quantifying the level of pain (if present), and gauging the patient’s self-care abilities.

General physical appearance

Conduct a general head-to-toe physical examination, focusing on the patient’s height, weight, and skin characteristics.

Height, weight, and weight trend

On admission, the patient’s height and weight should be measured to ensure appropriate nutritional and pharmacologic management. After a weight gain or loss, various factors may complicate wound healing. For instance, involuntary weight loss and protein-energy malnutrition may occur in both acute-care and long-term-care patients.

Especially note trends in your patient’s weight. For a long-term-care patient, a 5% weight loss over 30 days or a 10% loss over 180 days is considered involuntary. Arrange for a nutritional consult for any patient with an involuntary weight loss, as adequate nutrition is essential for general well-being and wound healing. (See A wound on the mend by clicking the PDF icon above.)

Skin color

Evaluate the patient’s skin color in light of ethnic background. If you note erythema—especially on a pressure point over a bony prominence—examine this area carefully for nonblanching erythema. Keep in mind that darkly pigmented skin doesn’t show such erythema and subsequent blanching, yet the patient may still be in jeopardy. So in dark-skinned patients, check for differences in skin color, temperature, or firmness compared to adjacent tissue; these differences may signify skin compromise.

Skin texture and turgor

Generally, healthy skin feels smooth and firm and has an even surface and good turgor (elasticity). To test turgor, gently grasp and pull up a fold of skin on a site such as the anterior chest below the clavicle. Does the skin return to place almost immediately after you release it, or does it stand up (“tent”)? Tenting indicates dehydration. But keep in mind that skin loses elasticity with age, so elderly patients normally have decreased turgor.

Skin temperature

With normal circulatory status, the skin is warm and its temperature is similar bilaterally. Areas of increased warmth or coolness suggest infection or compromised circulation. Be sure to check the temperature of skin surrounding the wound.

Wound assessment

Proper wound assessment can significantly influence patient outcome. Measure the wound carefully and document the condition of the wound bed. Remember that accurate descriptions are essential for guiding ongoing wound care. Repeat wound measurement and wound-bed assessment at least weekly, after the wound bed has been cleaned and debrided.

Keep in mind that assessing a chronic wound can be challenging. Wounds commonly have irregular shapes that can change quickly. Also, the multiple clinicians caring for the same patient may each describe the wound a bit differently.

Wound location

Note the precise anatomic location of the wound, as this can influence the wound care plan. A venous ulcer on the lower leg, for instance, requires different care than an arterial ulcer in the same site or a pressure ulcer on the ischium.

Circumference and depth

Use a paper or plastic measuring device to measure wound circumference and depth in centimeters (cm) or millimeters (mm). To promote accurate assessment of healing, be sure to use the same reference points each time you measure the wound.

You can use several methods to measure circumference. The most commonly used method of measurement is done in the head to toe direction. Measure the wound at its greatest length in that direction & measure the width at a 90 degree angle, at the widest point of the wound. Then multiply these two measurements (greatest length x greatest width) to obtain the total wound area. Although such linear measurements are imprecise, they yield gross information relative to wound healing when repeated over time.

Classify wound depth as partial thickness or full thickness.
•    Partial-thickness wounds are limited to the skin layers and don’t penetrate the dermis. They usually heal by reepithelialization, in which epidermal cells regenerate and cover the wound. Abrasions, lacerations, and blisters are examples of partial-thickness wounds.
•    Full-thickness wounds involve tissue loss below the dermis.
(Note: Pressure ulcers usually are classified by a four-stage system and diabetic foot ulcers by a grading system. Both systems are beyond this article’s scope.)
Measure and record wound depth based on the deepest area of tissue loss. To measure depth, gently place an appropriate device (such as a foam-tipped applicator) vertically in the deepest part of the wound, and mark the applicator at the patient’s skin level. Then measure from the end of the applicator to the mark to obtain depth.

Surrounding skin and tissue

Inspect for and document any erythema, edema, or ecchymosis within 4 cm of the wound edges, and reevaluate for these signs frequently. Because compromised skin near the wound is at risk for breakdown, preventive measures may be necessary.

Appearance of wound-bed tissue

Document viable tissue in the wound bed as granulation, epithelial, muscle, or subcutaneous tissue. Granulation tissue is connective tissue containing multiple small blood vessels, which aid rapid healing of the wound bed; appearing red or pink, it commonly looks shiny and granular. Epithelial tissue consists of regenerated epidermal cells across the wound bed; it may be shiny and silvery.

Check for nonviable tissue (also called necrotic, slough, or fibrin slough tissue), which may impede wound healing. It may vary in color from black or tan to yellow, and may adhere firmly or loosely to the wound bed. (See Picturing a necrotic wound by clicking the PDF icon above.)

Be sure to document the range of colors visible throughout the wound. Identify the color that covers the largest percentage of the wound bed. This color—and its significance—guide dressing selection.

Wound exudate

Document the amount, color, and odor of exudate (drainage) in the wound. Exudate with high protease levels and low growth factor levels may impede healing.

If the wound is covered by an occlusive dressing, assess exudate after the wound has been cleaned. Describe the amount of exudate as none, minimal, moderate, or heavy.

Describe exudate color as serous, serosanguineous, sanguineous, or purulent. Serous exudate is clear and watery, with no debris or blood present. Serosanguineous exudate is clear, watery, and tinged pink or pale red, denoting presence of blood. Sanguineous exudate is bloody, indicating active bleeding. Purulent exudate may range from yellow to green to brown or tan.

Describe wound odor as absent, faint, moderate, or strong. Note whether the odor is present only during dressing removal, if it disappears after the dressing is discarded, or if it permeates the room.

Wound edges

Wound edges indicate the epithelialization trend and suggest the possible cause and chronicity of the wound. The edges should attach to the wound bed. Edges that are rolled (a condition called epibole) indicate a chronic wound, in which epithelial cells are unable to adhere to a moist, healthy wound bed and can’t migrate across and resurface the wound.

Undermining and tracts

Gently probe around the wound edges and in the wound bed to check for undermining and tracts. Undermining, which may occur around the edges, presents as a space between the intact skin and wound bed (resembling a roof over part of the wound). It commonly results from shear forces in conjunction with sustained pressure. A tract, or tunnel, is a channel extending from one part of the wound through subcutaneous tissue or muscle to another part.

Measure the depth of a tract or undermining by inserting an appropriate device into the wound as far as it will go without forcing it. Then mark the skin on the outside where you can see or feel the applicator tip. Document your findings based on a clock face, with 12 o’clock representing the patient’s head and 6 o’clock denoting the feet. For instance, you might note “2.0-cm undermining from 7:00 to 9:00 position.”

Pain level

Ask the patient to quantify the level of pain caused by the wound, using the pain scale designated by your facility. Find out which pain-management techniques have relieved your patient’s pain in the past; as appropriate, incorporate these into a pain-management plan. Reevaluate the patient’s pain level regularly.

Wound-bed preparation

An evolving science, wound-bed preparation is crucial for minimizing or removing barriers to healing. The goal is to minimize factors that impair healing and maximize the effects of wound care. The key elements of wound-bed preparation are controlling bioburden and maintaining moisture balance. (For online resources on wound-bed preparation and other wound-care topics, see Where to get more information by clicking the PDF icon above.)

Controlling bioburden

Necrotic tissue and exudate harbor bacteria. A wound’s bioburden—the number of contaminating microbes—contributes to poor healing. All chronic wounds are considered contaminated or colonized, but not necessarily infected. In a colonized wound, healing is impeded as bacteria compete for nutrients; also, bacteria have harmful byproducts. To control bioburden, the wound must be cleaned and necrotic tissue must be debrided.

Cleaning the wound. Clean the wound before assessing it and applying a dressing. Use a noncytotoxic agent (typically, potable water, normal saline irrigating solution, or an appropriate wound-cleaning agent). Anti­septic solutions generally aren’t recommended for wound irrigation or dressings because they’re toxic to fibroblasts and other wound-repairing cells. If you must use such a solution, make sure it’s well diluted.

To ensure gentle cleaning or irrigation, pour solution over the wound bed or gently flush the wound with solution (using a 60-mL catheter-tip syringe) until the drainage clears. Know that pressurized irrigation techniques and whirlpool therapy aren’t recommended for wound cleaning because they disturb cell proliferation in the wound bed.

Debriding the wound. Debridement removes slough and necrotic tissue. Nonselective debridement techniques remove any type of tissue within the wound bed, whereas selective methods remove only necrotic tissue. (See Wound debridement techniques by clicking the PDF icon below.)

Maintaining moisture balance

To maintain moisture balance in the wound bed, you must manage exudate and keep the wound bed moist. The proper dressing (which may stay in place for days or longer) supports moist wound healing and exudate management. To minimize fluid pooling, a drain may be inserted into the wound. Negative-pressure wound therapy also may aid removal of excess exudate.

Choosing an appropriate dressing

The wound dressing plays a major role in maintaining moisture balance. Dressing selection is challenging because of the large number and variety of dressings available. Each product has specific actions, benefits, and drawbacks, so determining which dressing best suits the patient’s needs is a multifaceted process.

Dressing choice depends on such factors as wound type and appearance, exudate, presence or absence of pain, and required dressing change frequency. (See Dressings Options by clicking the PDF icon above.)

In a traditional dressing, gauze is applied in layers. The initial (contact) layer in the wound bed absorbs drainage and wicks it to the next layer; most often, this layer consists of woven cotton gauze or synthetic gauze. Remove the gauze gently, because it may be stuck to the wound or incision (especially if the gauze is cotton). For easier removal, moisten the dressing with normal saline solution to loosen it.

With a traditional dressing, the cover layer or secondary dressing is an abdominal pad with a “no-strike-through” layer next to the outside of the dressing. Be aware that wet-to-dry dressings are highly discouraged for their nonselective debriding effect and inability to provide a moist wound bed.

Reassess the patient’s wound at least weekly (after preparing the wound bed and dressing the wound) to determine healing progress. Keep in mind that wound-care management is a collaborative effort. Once you’ve assessed the patient, discuss your findings and subsequent wound management with other members of the team.

Wound care wisdom

Getting wiser about wound care will help your patients achieve good outcomes. Poor wound healing can be frustrating to patients, family members, and healthcare providers alike. Chronic wounds may necessitate lifestyle changes and lead to severe physical consequences ranging from infection to loss of function and even death. By performing careful assessment, tailoring patients’ wound care to wound etiology, and using evidence-based protocols to manage wounds, you can promote speedier wound healing, help lower morbidity, and improve quality of life.

Selected references
Bryant RA, Nix DP. Acute and Chronic Wounds: Current Management Concepts. 4th ed. St. Louis, MO: Mosby; 2011.

Gardener SE, Frantz R, Hillis SL, Park H, Scherubel M. Diagnostic validity of semiquantitative swab cultures. Wounds. 2007;(19)2:31-38.

Krasner DL, Rodeheaver GT, Sibbald RG. Chronic Wound Care: A Clinical Source Book for Healthcare Professionals. 4th ed. Wayne, PA: HMP Communications; 2007.
Langemo DK, Brown G. Skin fails too: acute, chronic, and end-stage skin failure. Adv Skin Wound Care. 2006;19(4):206-211.

Langemo DK, Anderson J, Hanson D, Hunter S, Thompson P. Measuring wound length, width, and area: which technique? Adv Skin Wound Care. 2008;21:42-45.

Milne C, Armand OC, Lassie M. A comparison of collagenase to hydrogel dressings in wound debridement. Wounds. 2010:22(11):270-274.

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.

Ovington LG. Hanging wet-to-dry dressings out to dry. Adv Skin Wound Care. 2002;15(2):79-86.

Sibbald RG, Coutts P, Woo KY. Reduction of bacterial burden and pain in chronic wounds using a new polyhexamethylene biguanide antimicrobial foam dressing—clinical trial results. Adv Skin Wound Care. 2011;24(2):78-84.

Solway DR, Consalter M, Levinson DJ. Microbial cellulose wound dressing in the treatment of skin tears in the frail elderly. Wounds. 2010:22(1):17-19.

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

Patricia A. Slachta is a Clinical Nurse Specialist at The Queens Medical Center in Honolulu, Hawaii and an adjunct nursing instructor at the Technical College of the Lowcountry in Beaufort, South Carolina.

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