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Practical Issues in Wound, Skin and Ostomy Management
Factors associated with better adherence to antidiabetic medications taken by patients with diabetes include older age, male sex, higher education, higher income, use of mail-order vs. retail pharmacies, primary care vs. nonendocrinology specialist prescribers, higher daily total pill burden, and lower out-of-pocket costs. (more…)
Read MoreBy 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…)
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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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Researchers have found that using hybrid 67Ga single-photon emission computed tomography and X-ray computed tomography (SPECT/CT) imaging combined with a bedside percutaneous bone puncture in patients with a positive scan is “accurate and safe” for diagnosing osteomyelitis in patients with diabetes who have a foot ulcer without signs of soft-tissue infection.
The new method, which avoids an invasive bone biopsy, has a sensitivity of 88% and a specificity of 93.6%. In the study of 55 patients, antibiotic treatment was avoided in 55% of suspected cases.
“Diagnosing diabetic foot osteomyelitis in patients without signs of soft tissue infection by coupling hybrid 67Ga SPECT/CT with bedside percutaneous bone puncture,” published by Diabetes Care, followed patients for at least a year.
The strains of methicillin-resistant Staphylococcus aureus (MRSA) differ in the hospital and community settings, and both are likely to coexist in the future, according to a study in PLOS Pathogens.
“Hospital-community interactions foster coexistence between methicillin-resistant strains of Staphylococcus aureus” notes that previously it was thought that the more invasive community strains would become more prevalent (and even eliminate) hospital strains. This new information could have significant consequences for public health because of the differences in the resistance of the two strains.
Despite increasing activities to prevent the spread of Clostridium difficile, infection from C. difficile remains a problem in healthcare facilities, according to a survey of infection preventionists by the Association for Professionals in Infection Control and Epidemiology (APIC).
The survey found that 70% of preventionists have adopted additional interventions in their healthcare facilities since March 2010, but only 42% have seen a decline in C. difficile infection rates; 43% saw no decline.
A total of 1,087 APIC members completed the survey in January 2013. The survey also found that more than 92% of respondents have increased emphasis on environmental cleaning and equipment decontamination practices, but 64% said they rely on observation, rather than more accurate and reliable monitoring technologies, to assess cleaning effectiveness.
In addition, 60% of respondents have antimicrobial stewardship programs at their facilities, compared with 52% in 2010. Such programs promote the appropriate use of antibiotics, which can help reduce the risk of C. difficile infection.
According to the Centers for Disease Control and Prevention, diarrhea caused by C. difficile is linked to 14,000 American deaths each year.
Mast cells may not play significant role in wound healing
“Evidence that mast cells are not required for healing of splinted cutaneous excisional wounds in mice,” published in PLOS One, analyzed wound healing in three types of genetically mast-deficient mice and found they reepithelialized their wounds at rates similar to control mice. At the time of closure, the researchers found that scars in all the mice groups were similar in both “quality of collagen deposition and maturity of collagen fibers.” The findings fail to support the previously held belief that mast cells are important in wound healing.
Nonremovable casts that relieve pressure are more effective than removable casts or dressings alone for the treatment of plantar foot ulcers caused by diabetes, according to an analysis of clinical trials.
The authors of “Pressure-relieving interventions for treating diabetic foot ulcers,” published by The Cochrane Library, reviewed 14 randomized clinical trials that included 709 participants. Nonremovable pressure-relieving casts were compared to dressings alone, temporary therapeutic shoes, removable pressure-relieving devices, and surgical lengthening of the Achilles tendon.
The study also notes that when combined with Achilles tendon lengthening, nonremovable devices were more successful in one forefoot ulcer study than the use of a nonremovable cast alone.
Most studies were from the United States (five) and Italy (five), with Germany, the Netherlands, Australia, and India each contributing one study.
“Prolonged antibiotic treatment in long-term care: Role of the prescriber,” published by JAMA Internal Medicine, found that the preferences of prescribers, rather than patient characteristics, drive antibiotic treatment.
The study of 66,901 patients from 630 long-term care facilities found that 77.8%
received a course of antibiotics. The most common length (41%) was 7 days, but the length exceeded 7 days in 44.9% of patients. Patient characteristics were similar among short-, average-, and long-duration prescribers.
The study authors conclude: “Future trials should evaluate antibiotic stewardship interventions targeting prescriber preferences to systematically shorten average treatment durations to reduce the complications, costs, and resistance associated with antibiotic overuse.”
“Electrophysical therapy for managing diabetic foot ulcers: A systematic review” concludes that electrophysical therapy is potentially beneficial because in each randomized clinical trial it outperformed the control or sham electrical stimulation.
The authors of the study in International Wound Journal reviewed eight trials with a combined total of 325 patients. Five studies were on electrical stimulation, two on phototherapy, and one on ultrasound. Because of the small number of trials, the possibility of harmful effects can’t be ruled out, and the authors recommend “high-quality trials with larger sample sizes.”
“Geographic variation in Medicare spending and mortality for diabetic patients with foot ulcers and amputations” reports healthcare spending and mortality rates vary “considerably” across the United States.
The study in Journal of Diabetes and Its Complications found that higher spending wasn’t associated with a significant reduction in 1-year patient mortality. In addition, rates of hospital admission were associated with higher per capita spending and higher mortality rates for patients.
An individualized, home-based progressive resistance exercise program improves upper-limb volume and circumference and quality of life in postmastectomy patients with lymphedema, according to a study published in the Journal of Rehabilitation Research and Development.
“Effect of home-based exercise program on lymphedema and quality of life in female postmastectomy patients: Pre-post intervention study” included 32 women who participated in an 8-week program. The women received education about the program and an initial training session from a physiotherapist. They practiced the exercise sequence and received a program and logbook once their performance was satisfactory. Patients were told to increase weight only when two sets of 15 repetitions became easy to perform.
Read MoreChronic venous insufficiency (CVI) is the most common cause of lower extremity wounds. The venous tree is defective, incapable of moving all the blood from the lower extremity back to the heart. This causes pooling of blood and intravascular fluid at the lowest gravitational point of the body—the ankle.
This article has two parts. Part 1 enhances your understanding of the disease and its clinical presentation. Part 2, which will appear in a later issue, explores the differential diagnosis of similar common diseases, the role that coexisting peripheral artery disease (PAD) may play, disease classification of venous insufficiency, and a general approach to therapy.
The most common form of lower extremity vascular disease, CVI affects 6 to 7 million people in the United States. Incidence increases with age and other risk factors. One study of 600 patients with CVI ulcers revealed that 50% had these ulcers for 7 to 9 months, 8% to 34% had them for more than 5 years, and 75% had recurrent ulcers.
Thrombotic complications of CVI include thrombophlebitis, which may range from superficial to extensive. If the thrombophlebitis extends up toward the common femoral vein leaving the leg, proximal ligation may be needed to prevent clot extension or embolization.
Lower extremity veins flow horizontally from the superficial veins to the perforating veins and then into the deep veins. Normally, overall venous blood flows vertically against gravity from the foot and ankle upward toward the inferior vena cava (IVC). This antigravity flow toward the IVC results from muscular contraction around nonobstructed veins and one-way valves that close as blood passes them. These valves prevent abnormal backward blood flow toward the foot and ankle region.
The lower extremities have four types of veins. Superficial veins are located within the subcutaneous tissue between the dermis and muscular fascia. Examples are the greater and lesser (smaller) saphenous veins. Perforating veins connect the superficial veins to the deep veins of the leg. The deep veins are located below the muscular fascia. The communicating veins connect veins within the same system.
The greater saphenous vein is on the leg’s medial (inner) side. It originates from the dorsal veins on top of the foot and eventually drains into the common femoral vein in the groin region. By way of perforating veins, the greater saphenous vein drains into the deep venous system of both the calf and thigh.
The lesser saphenous vein is situated on the lateral (outer) side of the leg and originates from the lateral foot veins. As it ascends, it drains into the deep system at the popliteal vein behind the knee. Communicating veins connect the greater saphenous vein medially and the lesser saphenous vein laterally.
Intramuscular veins are the deep veins within the muscle itself, while the intermuscular veins are located between the muscle groups. The intermuscular veins are more important than other veins in development of chronic venous disease. Below the knee, the intermuscular veins are paired and take on the name of the artery they accompany—for example, paired anterior tibial, paired posterior tibial, and paired peroneal veins. Eventually, these veins form the popliteal vein behind the knee, which ultimately drains into the femoral vein of the groin.
As the common femoral vein travels below the inguinal ligament of the groin, it’s called the external iliac vein. Eventually, it becomes the common iliac vein, which drains directly into the IVC.
Abnormally elevated venous pressure stems from the leg’s inability to adequately drain blood from the leg toward the heart. Blood drainage from the leg requires the muscular pumping action of the leg onto the veins, which pump blood from the leg toward the heart as well as from the superficial veins toward the deep veins. Functioning one-way valves within the veins close when blood passes them, preventing blood from flowing backward toward the ankle. This process resembles what happens when you climb a ladder with intact rungs: As you step up from one rung to the next, you’re able to ascend.
If the one-way valves are damaged or incompetent, the “broken rung” situation occurs. Think how hard it would be to climb a ladder with broken rungs: You might be able to ascend the ladder, but probably you would fall downward off the ladder due to the defective, broken rungs.
Normally, one-way valves ensure that blood flows from the lower leg toward the IVC and that the superficial venous system flows toward the deep venous system. The venous system must be patent (open) so blood flowing from the leg can flow upward toward the IVC. Blockage of a vein may result from an acute thrombosis (clot) in the superficial or deep systems. With time, blood may be rerouted around an obstructed vein. If the acute thrombosis involves one or more of the one-way valves, as the obstructing thrombosis opens up within the vein’s lumen, permanent valvular damage may occur, leading to post-thrombotic syndrome—a form of CVI.
CVI may result from an abnormality of any or all of the processes needed to drain blood from the leg—poor pumping action of the leg muscles, damage to the one-way valves, and blockage in the venous system. CVI commonly causes venous hypertension due to reversal of blood flow in the leg. Such abnormal flow may cause one or more of the following local effects:
The effect of elevated venous pressure or hypertension is worst at the lowest gravitational point (around the ankle). Pooling of blood and intravascular fluid around the ankle causes a “water balloon” effect. A balloon inflated with water has a thin, easily traumatized wall. When it bursts, a large volume of fluid drains out. Due to its thicker wall, a collapsed balloon that contains less fluid is more difficult to break than one distended with water.
In a leg with CVI, subcutaneous fluid that builds up requires a weaker force to break the skin and ulcerate than does a nondistended leg with less fluid. This principle is the basis for compression therapy in treating and preventing CVI ulcers.
Increased pressure in the venous system causes:
Abnormal vein swelling from elevated pressure in itself may impair an already abnormally functioning one-way valve. For instance, the valve may become more displaced due to the increase in intraluminal fluid, which may in turn worsen hypertension and cause an increase in leg swelling. Increased pressure from swollen veins also may dilate the capillary beds that drain into the veins; this may cause leakage of fluid and red blood cells from capillaries into the interstitial space, exacerbating leg swelling. Also, increased venous pressure may cause fibrinogen to leak from the intravascular plasma into the interstitial space. This leakage may create a fibrin cuff around the capillary bed, which may decrease the amount of oxygen entering the epidermis, increase tissue hypoxia, trigger leukocyte activation, increase capillary permeability, and cause local inflammation. These changes may lead to ulceration, lipodermatosclerosis, or both.
Visible changes may include dilated superficial veins, hemosiderin staining due to blood leakage from the venous tree, atrophie blanche, and lipodermatosclerosis. (See CVI glossary by clicking the PDF icon above.) Both atrophie blanche and lipodermatosclerosis result from local tissue scarring secondary to an inflammatory reaction of the leg distended with fluid.
Lipodermatosclerosis refers to scarring of subcutaneous tissue in severe venous insufficiency. Induration is associated with inflammation, which can cause the skin to bind to the subcutaneous tissue, causing narrowing of leg circumference. Lymphatic flow from the leg also may become compromised and inhibited in severe venous hypertension, causing additional leg swelling.
In a patient with known or suspected CVI, a thorough history may lead to a working diagnosis. Be sure to ask the patient these questions:
Also determine if the patient has comorbidities that may exacerbate CVI, including PAD, renal failure, venous thrombosis, lymphedema, diabetes mellitus, heart failure, or malnutrition. (See CVI risk factors by clicking the PDF icon above .)
Approximately 20% of CVI patients have symptoms of the disease without physical findings. These symptoms may include:
Although patients may report leg discomfort, the history indicates that it doesn’t awaken them at night. Be aware that discomfort from CVI differs from that caused by PAD. With PAD, patients may report pain on exercise (claudication), pain with elevation (nocturnal pain), or constant pain (resting pain).
Signs of CVI (with or without ulcers) include:
Venous ulcers are the most common type of lower extremity ulcer. They’re commonly found on the medial aspect of the lower extremity, from the ankle to the more proximal calf area. Usually, they arise along the course of the greater saphenous vein, but also may be lateral and may occur at multiple locations. They aren’t found above the knee or on the forefoot. Venous ulcers are shallower than arterial ulcers and have considerable exudate consistent with drainage from a ruptured water balloon. They may extend completely around the leg.
In patients with CVI, blood flows within a lower extremity in an abnormal, reverse direction, causing build-up of blood and intravascular fluid around the ankle. Initially, this may cause only a sensation of heavy legs toward the end of the day, with no visible changes. Eventually, it may lead to venous ulcers or other visible changes. This abnormal blood flow results from dysfunction of the normal mechanisms that drain blood from the leg against gravity into the IVC.
Selected references
Alguire PC, Mathes BM. Clinical evaluation of lower extremity chronic venous disease. UpToDate. Last updated April 18, 2012. http://www.uptodate.com/contents/clinical-evaluation-of-lower-extremity-chronic-venous-disease?source=search_result&
search=Clinical+evaluation+of+lower+extremity+chronic+venous+disease&selectedTitle=1%7E150. Accessed March 3, 2013.
Alguire PC, Mathes BM. Diagnostic evaluation of chronic venous insufficiency. UpToDate. Last updated May 7, 2012. www.uptodate.com/contents/diagnostic-evaluation-of-chronic-venous-insufficiency?source=search_result&search=Diagnostic+evaluation
+of+chronic+venous+insufficiency&selectedTitle=1%7E127. Accessed March 3, 2013.
Alguire PC, Mathes BM. Pathophysiology of chronic venous disease. UpToDate. Last updated April 12, 2012. www.uptodate.com/contents/pathophysiology-of-chronic-venous-disease?source=search_result&search=Pathophysiology+of+chronic+venous+disease
&selectedTitle=1%7E127. Accessed March 3, 2013.
Alguire PC, Scovell S. Overview and management of lower extremity chronic venous disease. UpToDate. Last updated June 27, 2012. www.uptodate.com/contents/overview-and-management-of-lower-extremity-chronic-venous-disease?source=search_
result&search=Overview+and+management+of+lower+extremity+chronic+venous+disease&selectedTitle=1%7E150. Accessed March 3, 2013.
Moneta G. Classification of lower extremity chronic venous disorders. UpToDate. Last updated October 22, 2011. www.uptodate.com/contents/classification-of-lower-extremity-chronic-venous-disorders. Accessed March 3, 2013.
Sardina D. Skin and Wound Management Course; Seminar Workbook. Wound Care Education Institute; 2011:92-112.
Donald A. Wollheim is a practicing wound care physician in southeastern Wisconsin. He also is an instructor for Wound Care Education Institute and Madison College. He serves on the Editorial Board for Wound Care Advisor.
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Clinical practice guidelines help ensure we are applying the latest knowledge and expertise when we’re caring for patients. Here are a few recent guidelines that you may find useful.
An American Heart Association scientific statement, “Measurement and interpretation of the ankle-brachial index (ABI),” published in Circulation, outlines the use of ABI, terminology, how to calculate the value, training, standards, and suggestions for future research.
Recommendations for obtaining an ABI measurement include:
• Use the Doppler method to determine the systolic blood pressure in each arm and each ankle.
• Use the appropriate cuff size, with a width of at least 40% of the limb circumference.
• Place the ankle cuff just above the malleoli with the straight wrapping method.
• Cover open lesions with the potential for contamination with an impermeable dressing.
• Avoid using a cuff over a distal bypass.
The article also recommends measurement and interpretation of ABI be part of the standard curriculum for nursing and medical students. For more information about ABI, read “Bedside ankle-brachial index testing: Time-saving tips” in this issue of Wound Care Advisor.
http://circ.ahajournals.org/content/126/24/2890
Childhood obesity continues to be a significant problem in the United States, requiring innovative approaches for prevention and management. Those who are obese run the risk of poorer wound healing.
“Approaches to the prevention and management of childhood obesity: The role of social networks and the use of social media and related electronic technologies: A scientific statement from the American Heart Association,” published in Circulation, evaluates the role of social networks and social media in relation to childhood obesity and presents five steps for using social networks:
1 Define the goal of the intervention.
2 Identify the social network.
3 Develop and pilot test the intervention.
4 Implement the intervention.
5 Spread the intervention.
The guidelines conclude that social media holds promise as a tool, but more research is needed.
http://circ.ahajournals.org/content/early/2012/12/03/CIR.0b013e3182756d8e
Many patients with wound or ostomy needs have comorbid heart disease. Be sure you are aware of the most current information for managing these patients by accessing “2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS guideline for the diagnosis and management of patients with stable ischemic heart disease,” published in Circulation.
The guidelines acknowledge the vital importance of shared decision making between the healthcare provider and the patient. The information is divided into four sections with supporting algorithms:
• approaches to diagnosis
• risk assessment
• treatment
• follow-up.
Access the top 10 things to know and the executive summary.
http://circ.ahajournals.org/content/126/25/e354
The Agency for Healthcare Research and Quality (AHRQ) has made it easier to compare guidelines for managing pressure ulcers by publishing two guideline syntheses:
• Management of pressure ulcers
• Prevention of pressure ulcers
In each case, the synthesis includes information in the following categories:
• areas of agreement and difference
• comparison of recommendations
• strength of evidence and recommendation grading schemes
• methodology
• source(s) of funding
• benefits and harms
• abbreviations
• status.
Access these and other guideline syntheses from AHRQ.
Free, one-time registration is required to view the entire video and all other
content on the Medscape website.
Patients have a right to make their own decisions, but what happens when a decision is so painful for staff that it affects morale? Arthur Caplan, PhD, Division of Medical Ethics at the NYU Langone Medical Center in New York, discusses such a case: “Patients have the right to choose death from bedsores.”
Read MoreLymphedema 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.
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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.
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.
Conduct a general head-to-toe physical examination, focusing on the patient’s height, weight, and skin characteristics.
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.)
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.
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.
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.
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.
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.
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.
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.
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.
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 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.
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.”
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.
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.)
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.)
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.
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.
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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