Each month, Apple Bites brings you a tool you can apply in your daily practice.
Description
A hydrocolloid dressing is a wafer type of dressing that contains gel-forming agents in an adhesive compound laminated onto a flexible, water-resistant outer layer. Some formulations contain an alginate to increase absorption capabilities. The wafers are self-adhering and available with or without an adhesive border and in various thicknesses and precut shapes for such body areas as the sacrum, elbows, and heels. Click here to see examples of
hydrocolloid dressings.
At some point, most of us have encountered a bully—most commonly when we were kids. You might think that as we get older, bullying wouldn’t be a problem we have to deal with. Unfortunately, that’s not the case. In the healthcare field, bullying can be even worse than it was when we were children.
Bullying in health care takes many different forms, including fighting among different types of clinicians, managers bullying subordinates, peer-to-peer bullying and, most commonly, specialists bullying other specialists. Years ago when I realized my dream of becoming a wound care specialist, I thought other specialists would be relieved I was on board to help with the overwhelming task of spreading wound care knowledge and healing wounds. But I found out quickly that I was pretty much alone with those thoughts, and my first encounter with wound care bullies occurred.
I began to ask myself: What did I do wrong? Why are they slamming me? What did I do to them? They don’t even know me; they’ve never even talked to me. This may sound familiar to many of you, whether you’re a wound care specialist, an ostomy specialist, or a diabetes or lymphedema specialist.
Workplace bullying is defined as repeated, unreasonable actions by individuals (or a group) directed toward an employee (or group of employees) that are intended to intimidate, degrade, humiliate, or undermine. Bullying occurs for many reasons; these reasons almost always include insecurity, competition, and the desire to feel more powerful and be in control.
So how do we deal with the bullies?
• Follow the Golden Rule: Treat others as you’d like others to treat you. Don’t stoop to the bully’s level.
• Stay calm and rational. Don’t get emotional. Bullies take pleasure in manipulating people emotionally.
• Don’t lose your confidence or blame yourself. Recognize that this isn’t about you; it’s about the bully. Be proud and confident in your certification credential.
• Focus on your purpose—to provide safe, competent, high-quality care to every patient.
• Document the bullying incident. Start a diary detailing the nature of the bullying, including dates, times, places, what was said or done, and who was present. Start a file with copies of anything in print that shows harassment and bullying; hold onto copies of documents that contradict the bully’s accusations against you.
• If the bullying behavior compromises patient safety and care, report the bully.
Stopping all bullying in health care may seem like an insurmountable goal, but I believe that together we can try to stop the bullying cycle in our specialty. By setting the example and supporting each other, we can turn the focus back to healing and caring for our patients as a team, not as one practitioner against the world.
Actions speak louder than words. As Ralph Waldo Emerson said, “What you do speaks so loudly that I cannot hear what you say.”
Donna Sardina, RN, MHA, WCC, CWCMS, DWC, OMS
Editor-in-Chief Wound Care Advisor
Cofounder, Wound Care Education Institute
Plainfield, Illinois
To begin appropriate treatment for chronic venous insufficiency (CVI), clinicians must be able to make the correct diagnosis. Part 1 (published in the March-April edition) described CVI and its presentation. This article provides details of the CVI diagnosis (including the differential diagnosis from other diseases), disease classification to help assess the extent of CVI, diagnostic studies used to diagnose CVI, and various treatment options to “rescue” the patient from CVI. (more…)
Assessing moisture and pressure risk in elderly patients continues to be a focus for clinicians in all settings, particularly long-term care. Ongoing research challenges our ideas about and practices for cleansing and protecting damaged skin. Until recently, most wound care clinicians have cleansed long-term care patients’ skin with mild soap and water. But several studies have shown pH-balanced cleansers are more efficient than soap and water for cleansing the skin of incontinent patients.
Various terms are used to describe skin breakdown related to moisture—incontinence-associated dermatitis, perineal dermatitis, diaper rash, intertriginal dermatitis, intertrigo, moisture-related skin damage, moisture-associated skin damage, and even periwound dermatitis. This article uses moisture-associated skin damage (MASD) because it encompasses many causes of skin breakdown related to moisture. Regardless of what we call the condition, we must do everything possible to prevent this painful and costly problem.
Skin assessment
Start with an overall assessment of the patient’s skin. Consider the texture and note dryness, flaking, redness, lesions, macerated areas, excoriation, denudement, and other color changes. (See Identifying pressure and moisture characteristics by clicking the PDF icon above.)
Assessing MASD risk
A patient’s risk of MASD can be assessed in several ways. Two of the most widely used pressure-ulcer risk scales, the Norton and Braden scales, address moisture risk. The Norton and Braden subscales should drive your plan for preventing skin breakdown related to moisture or pressure. The cause of breakdown (moisture, pressure, or shear/friction) must be identified, because treatment varies with the cause.
Both the Norton and Braden scales capture activity, mobility, and moisture scores. The Braden scale addresses sensory perception, whereas the Norton scale identifies mental condition. (See Subscales identifying pressure, shear, and moisture risk by clicking the PDF icon above.) Also, be aware that two scales have been published for perineal risk, but neither has been used widely.
You must differentiate pressure- and moisture-related conditions to determine correct treatment. Patients who are repositioned by caregivers are at risk for friction or shear. Also, know that agencies report pressure-ulcer prevalence. Care providers no longer classify mucous-membrane pressure areas in skin prevalence surveys; mucous membranes aren’t skin and don’t have the same tissue layers. Furthermore, don’t report skin denudement from moisture (unless pressure is present) in prevalence surveys.
When moisture causes skin breakdown
Skin has two major layers—epidermis and dermis. The epidermis itself has five layers: The outermost is the stratum corneum; it contains flattened, keratin protein–containing cells, which aid water absorption. These cells contain water-soluble compounds called natural moisturizing factor (NMF), which are surrounded by a lipid layer to keep NMF within the cell. When skin is exposed to moisture, its temperature decreases, the barrier function weakens, and skin is more susceptible to pressure and friction/shear injury. Also, when urea in urine breaks down into ammonia, an alkaline pH results, which may reactivate proteolytic and lipolytic enzymes in the stool. (See Picturing moisture and pressure effects by clicking the PDF icon above.)
Caring for moisture-related skin breakdown
The standard of care for moisture-related skin breakdown includes four major components: cleanse, moisturize, protect, and contain. Specific products used for each component vary with the facility’s product formulary.
Cleanse
Gently wash the area using a no-rinse cleanser with a pH below 7.0. Don’t rub the skin. Pat dry.
Moisturize
Use creams containing emollients or humectants. Humectants attract water to skin cells and help hold water in the cells; don’t use these products if the skin is overhydrated. Emollients slow water loss from skin and replace intracellular lipids.
Protect
Options for skin protectants include:
• liquid film-forming acrylate sprays or wipes
• ointments with a petroleum, zinc oxide, or dimethicone base
• skin pastes. Don’t remove these products totally at each cleansing, but do remove stool, urine, or drainage from the surface and apply additional paste afterward. Every other day, remove the paste down to the bare skin using a no-rinse cleanser or mineral oil.
Be sure to separate skinfolds and use products that wick moisture rather than trap it. These may include:
• commercial moisture-wicking products
• a light dusting with powder containing refined cornstarch or zinc oxide—not cornstarch from the kitchen or powder with talc as the only active ingredient
• abdominal pads.
Contain
To keep moisture away from skin, use absorbent underpads with wicking properties, condom catheters (for males), fecal incontinence collectors, fecal tubes (which require a healthcare provider order), or adult briefs with wicking or gel properties. Call a certified ostomy or wound care nurse for tips on applying and increasing wear time for fecal incontinence collectors.
If 4″ × 4″ gauze pads or ABD pads are saturated more frequently than every 2 hours, consider applying an ostomy or specially designed wound pouch to the area. Collecting drainage allows measurement and protects skin from the constant wetness of a saturated pad.
Don’t neglect the basics, for example, know that wet skin is more susceptible to breakdown. Turn the patient and change his or her position on schedule. Change linens and underpads when damp, and consider using a low-air-loss mattress or bed or mattress with microclimate technology.
Also, be aware that fungal rashes should be treated with appropriate medications. If the patient’s skin isn’t too moist, consider creams that absorb into the skin; a skin-protecting agent can be used as a barrier over the cream. Besides reviewing and using the standards of care, you may refer to the Incontinence-Associated Dermatitis Intervention Tool, which has categories related to skin damage. See the “Incontinence-Associated Dermatitis Intervention Tool” (IADIT).
Bottom line on skin breakdown
To help prevent skin breakdown related to moisture, assess patients’ skin appropriately, determine treatment using evidence-based guidelines, and implement an appropriate plan of care.
Selected references
Black JM, Gray M, Bliss DZ, et al. MASD part 2: incontinence-associated dermatitis and intertriginous dermatitis: a consensus. J Wound Ostomy Continence Nurs. 2011;38(4):359-70.
Borchert K, Bliss DZ, Savik K, Radosevich DM. The incontinence-associated dermatitis and its severity instrument: development and validation. J Wound Ostomy Continence Nurs. 2010;37(5):527-35.
Doughty D. Differential assessment of trunk wounds: pressure ulceration versus incontinence-associated dermatitis versus intertriginous dermatitis. Ostomy Wound Manage. 2012;58(4):20-2.
Doughty D, Junkin J, Kurz P, et al. Incontinence-associated dermatitis: consensus statements, evidence-based guidelines for prevention and treatment, and current challenges. J Wound Ostomy Continence Nurs. 2012;39(3):303-15.
Gray M, Beeckman D, Bliss DZ, et al. Incontinence-associated dermatitis: a comprehensive review and update. J Wound Ostomy Continence Nurs. 2012;
39(1):61-74.
Gray M, Black JM, Baharestani MM, et al. Moisture-associated skin damage: overview and pathophysiology. J Wound Ostomy Continence Nurs. 2011;38(3):233-41.
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.
Wound, Ostomy and Continence Nurses Society. Guideline for Prevention and Management of Pressure Ulcers. Mt. Laurel, NJ: Wound, Ostomy and Continence Nurses Society; 2010.
Wound, Ostomy and Continence Nurses Society. Incontinence-Associated Dermatitis: Best Practice for Clinicians. Mt. Laurel, NJ: Wound, Ostomy and Continence Nurses Society; 2011.
Zulkowski K. Diagnosing and treating moisture-associated skin damage. Adv Skin Wound Care. 2012;25(5):231-6.
Patricia A. Slachta is an instructor at the Technical College of the Lowcountry in Beaufort, South Carolina.
One of the worst fears of a wound care clinician is inadvertently compressing a leg with critical limb ischemia—a condition marked by barely enough blood flow to sustain tissue life. Compression (as well as infection or injury) could lead to necrosis, the need for amputation, or even death. The gold standard of practice is to obtain an ankle-brachial index (ABI) before applying compression. However, recent research and expert opinion indicate an elevated or normal ABI is deceptive in patients with advanced diabetes. What’s worse, in the diabetic foot, skin may die from chronic capillary ischemia even when total blood perfusion is normal. For information on how to perform an ABI and interpret results, click on this link. (more…)
Here are resources that can help you in your busy clinical practice by giving you information quickly.
Pressure ulcer resources
Instead of searching through Google or another search engine for pressure ulcer resources, start with this comprehensive list on the Centers for Medicare & Medicaid Services website.
Examples of resources included are:
“Preventing pressure ulcers in hospitals: A toolkit for improving quality of care.” This toolkit from the Agency for Healthcare Research and Quality (AHRQ) is designed to help hospitals in implementing pressure ulcer prevention strategies.
“On-time pressure ulcer healing project.” Another AHRQ initiative, this resource is designed for those working in long-term care facilities.
“Pressure ulcer prevention.” This table from the Institute for Healthcare Improvement lists possible mentors you can work with in the area of ulcer prevention.
“Shawnee Medical Center wound care quick reference guide.” This is a handy one-page reference guide that includes photographs and recommendations.
“How-to guide: Prevent pressure ulcers—pediatric supplement.” This guide, tailored for pediatrics, describes key evidence-based care components for preventing pressure ulcers and describes how to implement these interventions.
You can also access case studies from a variety of facilities around the United States.
The National Lymphedema Network is a nonprofit organization founded in 1988 to provide education and other information to healthcare professionals and patients with lymphedema, as well as the general public. The site includes an explanation of lymphedema that may be helpful for you to use in teaching your patients. It also includes access to some of the articles from the newsletter LymphLink.
Many patients with chronic wounds have diabetes. To ensure those patients receive the best possible care, you can refer to the 2013 Standards of Medical Care in Diabetes from the American Diabetes Association, which were published in the January issue of Diabetes Care.
The journal provides a summary of the revisions and an executive summary of the standards related to each area, including diagnosis, testing, prevention, monitoring, and pharmacologic and nonpharmacologic management.
The guidelines include valuable information related to neuropathy screening and treatment and foot care. Recommendations for foot care include performing an annual comprehensive foot examination to identify risk factors predictive of ulcers and amputations. The foot examination should include inspection, assessment of foot pulses, and testing for loss of protective sensation.
Most of us have had days when we jump from meeting to meeting and at the end of the day wonder, “Did I get anything accomplished or am I more behind than ever?”
Many clinicians tell me that although their wound team meets regularly, the meetings aren’t meaningful enough, leaving the team still facing issues with their wound care program. As a consultant, when I review the wound team agenda, it’s typically missing one or more of four key ingredients:
appropriate member representation
proactive approach that highlights prevention
review of the plan of care and update of the medical record
review of supplies and products. Here’s a closer look at each of these ingredients.
Build a top team
Having the appropriate members on the wound care team is the first ingredient for success. A comprehensive, interdisciplinary team approach is the key to preventing skin breakdown and ensuring good clinical outcomes for residents with skin breakdown. Teams should include representation from nursing, dietary, and physical and occupational therapy, as well as a nurse practitioner or physician.
Nursing representation should include nurses from all three shifts and nursing assistants, who are too often missing from the team. Keep in mind that when it comes to preventing pressure ulcers, nursing assistants carry out most of interventions (for example, turning, incontinence management, heel lift). Even when a patient has a wound, the only intervention carried out by the nurses is the topical treatment; nursing assistants perform all other interventions necessary to ensure healing. Clinicians who empower nursing assistants to have a strong influence with the wound care team—and the program—tend to have very successful prevention programs and good clinical outcomes.
Think prevention
The second key ingredient is prevention. Most wound team meetings only discuss the patients with wounds, missing the bigger goal of preventing wounds in the first place. Once the patients with wounds are discussed, the team should review all high-risk patients to ensure proper preventative measures are in place and care planned. All patients should be quickly reviewed for evidence of:
decline or change in mobility and activity
new onset or change in continence status
decline in nutritional status
decline or change in cognition.
Any triggers in these areas should prompt a review of the plan of care to ensure they are being effectively addressed.
Review and update the plan
The third key ingredient for success is to use meeting time to review and update the plan of care. I’ve observed highly productive meetings and great discussions of the care the facility is providing. Then I review the medical record and discover that none of the interventions discussed are on the plan of care. Always review the patient’s plan of care to ensure it’s accurate, reflects all interventions, and is up to date. This will give you peace of mind that the medical record reflects all the good work you’re doing and helps make the team meetings feel productive.
Discuss products and supplies
The fourth key ingredient is to take the time to quickly discuss current wound care supplies and products with the team. Ask the team if the current supplies are user-friendly, are adequate, provide good outcomes, and are in good working condition.
Many times staff will not say how they’re struggling with, modifying, or not using something until they’re asked. Remember that the most expensive product is the one that doesn’t work or doesn’t get used.
A recipe for success
Using these four key ingredients will lead you to a successful wound team meeting—and a successful program. The mix may not solve your too-many-meetings days, but will give you peace of mind that at least one meeting is productive.
Jeri Lundgren is director of clinical services at Pathway Health in Minnesota. She has been specializing in wound prevention and management since 1990.
An Unna boot is a special dressing of inelastic gauze impregnated with zinc, glycerin, or calamine that becomes rigid when it dries. It is used for managing venous leg ulcers and lymphedema in patients who are ambulatory. When the patient walks, the rigid dressing restricts outward movement of the calf muscle, which directs the contraction force inward and improves the calf-muscle pumping action, thereby improving venous flow. An Unna boot does not provide compression and is contraindicated for arterial insufficiency. (more…)
Chronic 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.
Understanding normal anatomy and physiology
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.
Pathophysiology
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.
CVI and the “broken rung” analogy
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:
leg swelling
tissue anoxia, inflammation, or necrosis
subcutaneous fibrosis
Compromised flow of venous blood or lymphatic fluid from the extremity.
“Water balloon” analogy
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.
Effects of elevated venous pressure or hypertension
Increased pressure in the venous system causes:
abnormally high pressure in the superficial veins—60 to 90 mm Hg, compared to the normal pressure of 20 to 30 mm Hg
dilation and distortion of leg veins, because blood refluxes abnormally away from the heart and toward the lower leg and may move from the deep venous system into the superficial veins.
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.
Patient history
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:
Do you have pain?
Is your pain worse toward the end of the day?
Is the pain relieved with leg elevation at night?
Is it relieved with leg elevation during the day?
Do you have leg pain that awakens you at night?
How would you describe the pain?
Does the skin on your leg feel tight or irritated?
Have you noticed visible changes of your leg?
Do you have a leg ulcer?
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 .)
Common CVI symptoms
Approximately 20% of CVI patients have symptoms of the disease without physical findings. These symptoms may include:
tired, “heavy” legs that feel worse toward the end of the day
discomfort that worsens on standing
legs that feel best in the morning after sleeping or after the legs have been
elevated during the day.
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:
leg swelling (seen in 25% to 75% of patients)
skin changes (such as hemosiderin staining or dermatitis)
telangiectasia, reticular veins, or both; while these are the most common signs, they represent an overall less severe finding
varicose veins with or without bleeding, occurring in one-third of patients with CVI.
Venous ulcers
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.
CVI: From a heavy sensation to visible changes
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.
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.
At one time or another, all wound care professionals encounter a chronic wound, defined as a wound that fails to heal in an orderly and timely manner. Globally, about 67 million people (1% to 5% of the world’s population) suffer chronic wounds. In the United States, chronic wounds affect 6.5 million people and cost more than $25 billion annually to treat. (more…)
In a busy wound clinic, quick and accurate differential diagnosis of edema is essential to appropriate treatment or referral for comprehensive care. According to a 2010 article in American Family Physician, 80% of lower extremity ulcers result from chronic venous insufficiency (CVI). In 2007, the German Bonn Vein Study found 100% of participants with active venous ulcers also had a positive Stemmer’s sign, indicating lymphedema. (more…)
A hot flush of embarrassment creates a bead of sweat on my forehead. “I’ve got to get this measurement,” I plead to myself. One glance at the clock tells me this bedside ankle-brachial index (ABI) procedure has already taken more than 30 minutes. My stomach sinks as I realize I’ll have to abandon the test as inconclusive. (more…)
