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…)
By Rosalyn Jordan, RN, BSN, MSc, CWOCN, WCC, and Marci Christian, BBE
Any patient with a fecal or urinary ostomy may experience complications on the skin surface around the stoma. These complications may occur lifelong, although they’re more common during the first 5 years after the initial ostomy surgery. Causative factors include infection, trauma, certain diseases, and chemical irritation; most of these problems stem from the pouching system or pouch leakage.
Peristomal skin complications can cause a wide range of signs and symptoms, from skin discoloration to polyp-like growths, from erythema to full-thickness wounds. They can lead to discomfort, pain, poor self-image, social isolation, and impaired quality of life, not to mention additional care costs.
Incidence and types of these complications are hard to compare or contrast across multiple patients. Until recently, no standardized assessment or documentation tools were available to characterize or define complications. For this reason, reported rates ranged widely, from 10% to 70%. And because no designated common language or categories related to peristomal skin complications existed, documentation was inconsistent.
In the late 2000s, a group of nurses experienced in caring for ostomy patients worked with the World Council of Enterostomal Therapists to develop a resource called the Ostomy Skin Tool, which clinicians can use to categorize and describe peristomal skin complications in a consistent, objective manner. The tool also provides a common language for documentation.
The Ostomy Skin Tool has three major assessment domains—discoloration (D), erosion/ulceration (E), and tissue overgrowth (T), known collectively as DET. The DET combined rating ranges from normal, rated 0, to the worst condition possible, rated 15. Mild DET complications are documented as less than 4, moderate as less than 7, and severe as 8 or higher. (See Using the Ostomy Skin Tool by clicking the PDF icon above.)
The tool describes four categories of peristomal complications:
• chemical irritation
• mechanical trauma
• disease-related complications
• infection-related complications.
Chemical irritation
Chemical irritation can stem from irritants (as in contact dermatitis) or allergic reactions (allergic dermatitis). The most likely cause of chemical dermatitis is effluent leakage (feces or urine) from the colostomy, ileostomy, or urostomy, in which effluent comes in contact with peristomal skin. Other potential causes include contact with soap, certain adhesives, and adhesive removers.
The major treatment of chemical irritation is identification and removal of the offending agent, followed by patient and caregiver education on the new pouching procedure the patient must use. Follow-up assessment also is recommended. In a 2010 study that followed 89 patients for 1 year after ostomy surgery, about 50% of subjects experienced peristomal skin complications, most of them from pouch leakage. Another investigator estimated that 85% of ostomy patients experience pouch leakage at some time during their lives. Pouch leakage usually occurs when stool is extremely liquid (for instance, ileostomy effluent). Other causes of pouch leakage include wearing a pouch more than half full of effluent and abdominal contours that aren’t level. Besides changes in the pouching system, treatment may entail adding products to the pouching system or removing certain agents.
Some patients experience allergic dermatitis in reaction to products used in the pouching system (such as skin barriers, belts, pouch closures, or adhesives). However, allergic dermatitis is rare. One 2010 study suggested allergic reactions to these products occur in only about 0.6% of patients with peristomal skin irritation. Most major ostomy product manufacturers provide a patch test on request to help identify allergic conditions. Once the offending product is discontinued, allergic dermatitis should resolve rapidly.
Mechanical trauma
Mechanical trauma usually results from either the pouching system itself or its removal. It also may result from harsh or multiple skin-barrier removals, pressure from convex rings or pouches, and abrasive cleansing techniques. Some researchers believe the stronger the adhesive barrier and the more often a pouch is changed, the greater the risk of epidermal damage.
Mechanical trauma may present as a partial-thickness ulcer caused by pressure, shear, friction, tearing, or skin stripping. Patients with fragile skin are susceptible to mechanical trauma, so less aggressive pouching systems may be preferred for them. Of course, if the pouching system is changed, the patient or caregiver needs to learn about the new system.
Disease-related complications
Disease-related peristomal complications may be linked to preexisting skin conditions, such as psoriasis, eczema (atopic dermatitis), or seborrheic dermatitis. Hyperplasia also may occur. This overgrowth of cells, which may appear as gray or reddish brown pseudoverrucous lesions, usually is linked to urinary ostomies, although it can occur with fecal ostomies as well. Vinegar soaks are the recommended treatment, in addition to a change in the pouching system and corresponding patient education.
Occasionally, other disease-related complications occur, including primary adenocarcinoma of the peristomal skin and peristomal pyoderma gangrenosum, a painful and problematic condition that presents as peristomal ulcers. Ulcer borders are well-defined with a bluish purple coloration at the edges. Infection must be ruled out, as this condition usually is linked to an autoimmune condition. Treatment includes pain management and, in most cases, a topical corticosteroid. Crohn’s disease also may manifest as a peristomal skin ulcer.
Infection-related complications
Infection-related complications may be bacterial or fungal. Two common peristomal skin infections are folliculitis and Candida fungal infections. An infection of the hair follicle that causes pustules, folliculitis usually stems from traumatic hair pulling in the peristomal area during pouch removal. It may warrant a prescribed antibiotic, along with patient teaching regarding proper hair removal using an electric razor.
Candida infections may arise because peristomal skin provides a warm, dark, moist environment that promotes fungal growth. These infections appear as erythema with pustules or papules and satellite lesions. Treatment usually involves antifungal powder and use of the crusting technique to secure the pouching system. (See Using the crusting technique by clicking the PDF icon above.)
Management
Many complications are well advanced by the time patients seek assistance, perhaps because they don’t understand the significance of their symptoms and think they can manage the problem themselves. In some cases, they don’t know where to turn for assistance. Commonly, the complication progresses to the point where the patient goes to the emergency department or (particularly during the immediate postoperative period) needs to be readmitted for treatment. The best way to manage peristomal skin complications is to prevent them in the first place. (See Preventing peristomal skin complications by clicking the PDF icon above.)
Patient education
Over the past 20 years, hospital stays for ostomy surgery patients have decreased from about 2 weeks to less than 5 days. Reduced stays decrease the time available for caregivers to teach patients and family members how to empty and change the pouch. They need alternative education covering (among other topics) how to recognize peristomal skin complications and when to seek help. Not only do these complications require vigilant self-observation, but many patients don’t understand their implications or how rapidly they can worsen. In some cases, the first symptoms are itching and redness under the skin barrier. Fortunately, some patients may know or remember that itching, burning, stinging, reddened, or weeping peristomal skin requires professional attention. They can avoid serious complications by seeking assistance early, such as right after noticing pouch leakage.
Early treatment can reduce the cost of treatment. In a 2012 study, researchers estimated care costs related to peristomal skin complications for a 7-week treatment period, using the Ostomy Skin Tool as a reference. Severe complications (those with a DET score above 8) cost six times more to treat than mild cases (those with a DET score below 4) and 4.5 times more than moderate cases.
Along with early intervention by a trained ostomy care specialist, self-assessment by ostomy patients promotes a better quality of life, reduces pain, and may decrease care costs. Clinicians’ use of the Ostomy Skin Tool to assess and document peristomal skin complications promotes more reliable, objective, comparable assessment data for reporting.
Selected references
Al-Niaimi F, Lyon CC. Primary adenocarcinoma in peristomal skin: a case study. Ostomy Wound Manage. 2010;56(1):45-7.
Burch J. Management of stoma complications. Nurs Times. 2011;107(45):17-8, 20.
Jemec GB, Martins L, Claessens I, et al. Assessing peristomal skin changes in ostomy patients: validation of the Ostomy Skin Tool. Br J Dermatol. 2011; 164;330-5.
Jones T, Springfield T, Brudwick M, Ladd A. Fecal ostomies: practical management for the home health clinician. Home Healthc Nurse. 2011;29(5):306-17.
Martins L, Samai O, Fernandez A, et al. Maintaining healthy skin around an ostomy: peristomal skin disorders and self-assessment. Gastrointest Nurs. 2011;
9(2):9-13.
Martins L, Tavernelli K, Serrano JLC. Introducing a peristomal skin assessment tool: The Ostomy Skin Tool. World Council Enterostomal Therapists J. 2008;28(2):3-13.
Meisner S, Lehur P, Moran B, et al. Peristomal skin complications are common, expensive, and difficult to manage: a population based cost modeling study. PLoS One. 2012;7(5):e37813.
Omura Y, Yamabe M, Anazawa S. Peristomal skin disorders in patients with intestinal and urinary ostomies: influence of adhesive forces of various hydrocolloid wafer skin barriers. J Wound Ostomy Continence Nurs. 2010;37(3):289-98.
Ratliff CR. Early peristomal skin complications reported by WOC nurses. J Wound Ostomy Continence Nurs. 2010;37(5):505-10.
Shabbir J, Britton DC. Stomal complications: a literature overview. Colorectal Dis. 2010;12(10):958- 64.
Wound, Ostomy, Continence Clinical Practice Ostomy Subcommittee. Peristomal skin complications: Best practice for clinicians. Mt. Laurel, NJ; 2007.
The authors work for RecoverCare, LLC, in Louisville, Kentucky. Rosalyn Jordan is director of clinical education and Marci Christian is a clinical associate product specialist.
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.
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.
Every year, thousands of people of all ages have ostomy surgery in the United States. That means no matter where you work, you’re likely to care for patients with new ostomies and teach them to care for themselves. (See Why patients need ostomy surgery by clicking the PDF icon above.)
These patients present two challenges: staying up-to-date on ostomy equipment and procedures and having only 3 to 5 days after surgery to teach basic ostomy care to patients who are unlikely to be physically or emotionally ready to learn. This review and update of ostomy care should help you meet both challenges. Let’s start with the common types of stomas and ostomies.
Reviewing stoma types
The three common types of stomas are the end stoma, loop stoma, and double-barrel stoma. The patient’s surgeon decides on the most appropriate type based on the disease or injury, the amount of intestine available, and the patient’s health status.
To create an end stoma, the most common type, a surgeon creates a small opening in the abdominal wall, then resects the intestine and pulls it through the opening. Next, the surgeon turns the end of the intestine onto itself—somewhat like cuffing a sock—and sutures the stoma to the skin. Next to the stoma, the surgeon may create a mucous fistula, which secretes mucus from the nonfunctioning portion of the intestine.
A loop stoma is usually created for a temporary ostomy. The surgeon creates a small opening in the abdominal wall and pulls a loop of intestine through it. With an external rod or bridge placed under the loop to keep it from slipping back into the peritoneal cavity, the surgeon cuts the top of the loop to form the apex of the stoma. Next, the surgeon everts the intestine around the opening and sutures the stoma edges to the skin. After a few days, the rod is removed, and the stoma stays above skin level on its own. Double-barrel stomas aren’t common in adults, but they are used frequently in neonates. For this type, a surgeon cuts through the bowel to create two separate end stomas, one to evacuate stool and the other to evacuate mucus. The two stomas can be placed next to each other, so one pouching system can be used for both. If the stomas are further apart, the patient may need two pouches. If mucus secretions are slight, you may be able to apply a nonadherent dressing after gently cleaning the stoma and peristomal skin, instead of using a pouch.
An ideal stoma protrudes above the skin surface and has a flat peristomal skin surface that allows the ostomy barrier to adhere to it. (See Characteristics of an ideal stoma by clicking the PDF icon above.) A healthy stoma is red and moist and looks like gum tissue. In fact, the entire alimentary canal from mouth to anus has the same type of tissue. Keep in mind that while cleaning a stoma, you’ll commonly see a small amount of bleeding, just as your gums may bleed when you brush your teeth too vigorously. If you note excessive bleeding, report it immediately.
Reviewing types of ostomies
The three most common types of ostomies you’ll see are a colostomy, an ileostomy, and a urostomy.
A surgeon creates a colostomy by making an opening in the large intestine and connecting it to the stoma. The location of the surgical opening will affect the consistency of the stool exiting the body through the stoma: The lower the opening, the firmer the consistency. A colostomy produces flatus because of the high bacterial content in the large intestine. A colostomy can be temporary or permanent, depending on the diagnosis and the patient’s ability to heal.
To create an ileostomy, a surgeon makes an opening in the small intestine and forms a stoma. Patients with ileostomies are prone to dehydration because a large amount of enzymatic fluid is discharged through the ileostomy instead of being absorbed in the disconnected large intestine. Teach your patient to be alert for the signs and symptoms
of dehydration—thirst; decreased urination; darker, concentrated urine; warm, flushed skin; fever; and malaise. Also, warn the patient to keep enzymatic effluent off the skin because it can quickly cause skin breakdown. As with a colostomy, an ileostomy may be temporary or permanent.
To create a urostomy, a surgeon removes the diseased bladder and uses a portion of resected small intestine to create a conduit. The ureters, which were connected to the bladder, are sutured into the resected small intestine so urine can exit the body through the stoma. Urostomies are permanent.
Choosing the right pouching system
An ostomy pouching system has two parts: an adhesive barrier that attaches to the skin around the stoma and a pouch connected to the barrier that collects effluent. Determining the right ostomy pouching system for your patients will depend on their needs and preferences. Let’s look at some of the important choices.
A pouching system may come in one or two pieces. With one-piece systems, the barrier (also called the wafer, flange, or baseplate) and pouch come as a single unit. (See One- and two-piece ostomy pouching systems by clicking the PDF icon above.) One-piece systems are easier to apply and more flexible. Plus, they’re flatter and thus more discreet.
With two-piece systems, the barrier and pouch are separate components that must be attached. Depending on the product, the patient may need to press the pouch onto the barrier or use a locking ring mechanism or an adhesive coupling system. Two-piece systems allow the patient to remove the pouch without removing the barrier. Also, a patient can apply a smaller pouch, such as a stoma cap or close-ended pouch, before exercise or intimate relations.
Today, ostomy pouching systems offer many options that weren’t available just a few years ago—options such as built-in, varying levels of convexity and integrated closures. Skin-friendly barriers now eliminate the need for accessory products, such as skin prep, ostomy powder, and stoma paste. By knowing the new options, you can help simplify the pouch application process for your patient and increase patient satisfaction.
Selecting barriers
Barriers may be cut-to-fit or precut. Cut-to-fit barriers are used during the postoperative period while the stoma size is changing and for oval or irregularly shaped stomas. Precut sizes are convenient for round stomas after they stabilize.
The choice of a barrier also depends on abdominal contours and the effluent consistency. A standard-wear barrier is appropriate for thicker output. An extended-wear barrier is better for loose or watery output and for problematic ostomies.
Convex barriers can be used to push down the peristomal skin and help the stoma project into the pouch. These barriers help ensure that the effluent goes into the pouch and not between the skin and the barrier, causing leakage.
For ostomies that are difficult to manage and frequently leak, you may select an ostomy belt. This device helps secure a convex pouching system by increasing its pressure. The plastic hooks at the end of the belt attach to the belt loops of the pouching system. Depending on the manufacturer, the belt loops may be on the barrier or the pouch.
Selecting pouches
Pouches can be transparent or opaque. Transparent pouches allow you to see the stoma postoperatively and allow patients to watch as they place the pouch over the stoma. Opaque pouches, of course, have the advantage of concealing the effluent.
Some pouches have filters. Colostomy patients usually prefer filtered pouches because they eliminate the need to burp the pouch to remove gas. Ileostomy output is usually watery, so the charcoal filters may get wet and quit working.
The appropriate type of pouch closure also varies, depending on the type of output and the patient’s needs and preferences. A patient with a colostomy or ileostomy needs a drainable pouch. Newer clamps and integrated closures can make closing the pouch easier for the patient.
Close-ended pouches are available for patients who empty their pouch once or twice a day. Reimbursement guidelines for Medicare, which most insurance companies follow, allow 60 close-ended pouches a month. Thus, someone who empties once or twice a day will have enough pouches.
Patients with urostomies use pouches with spigots on the end to allow for urine drainage.
Urostomy pouches can be connected to a continuous urinary drainage bag at bedtime or to a leg bag during the day for those in a wheelchair.
Dealing with complications
Report the following postoperative complications to the surgeon and the ostomy clinician caring for the patient:
• allergic reaction
• candidiasis
• contact dermatitis
• folliculitis
• ischemic or necrotic stoma
• mechanical irritation
• mucocutaneous separation
• parastomal hernia
• prolapse.
Many complications result from surgical technique or the patient’s disease status, but complications also result from an incorrect fit or an ostomy that frequently leaks. To determine why and where leakage occurred, examine the back of the barrier. If leakage results from a flush or recessed stoma or an irregular surface around the stoma, the patient may need a convex barrier. Or the patient may need a convex barrier and an ostomy belt.
Remember that a firm abdomen requires a soft, flexible barrier that conforms to the abdominal contours. A soft belly, on the other hand, may need the rigidity of a convex barrier to help the stoma empty into the pouch.
For weepy, extremely denuded skin, apply ostomy powder, brush off the excess, and dab an alcohol-free skin sealant, such as No-Sting by 3M, on the area. Allow the area to air-dry before applying the barrier.
Discharge planning and patient teaching
Because the postoperative length of stay is short, start preparing for discharge and teaching the pouch-change procedure at your first hospital encounter with the patient. Teaching the patient at each encounter creates a continuum of care throughout hospitalization and recovery. If possible, include the caregiver. (See Teaching your patient to change an ostomy pouch by clicking the PDF icon above.) Before discharge, give the patient two or three ostomy pouches to take home, step-by-step printed instructions on applying pouches, a list of supplies the patient will need, and a list of ostomy product suppliers in the area.
Also, teach the patient about complications, activity, diet, and drug therapy and provide the names of local support groups. (See Finding support by clicking the PDF icon above.)
Complications at home
Tell the patient to call the physician if any of the following occurs: fever, increased pain or discomfort, diarrhea, dehydration, or signs and symptoms of infection at the surgical site. The patient should also call the physician if there’s no output from the stoma for more than 24 hours.
Patients with urostomies who develop the following signs and symptoms may have a urinary tract infection: fever, chills, abdominal or retroperitoneal pain, and bloody, cloudy, or foul-smelling urine. Clear urine with mucus shreds is normal.
Increasing activity
Explain that after surgery the patient should feel a little bit stronger every day. Teach the patient to alternate rest and activity periods and to increase the activity period a little each day while building endurance. Refer the patient to the physician for clearance to resume exercise and sexual relations.
Dietary considerations
After ostomy surgery, your patient will start on a clear liquid diet and progress to a normal, preoperative diet. The patient should reintroduce one food at a time to help determine if it’s well tolerated. High-fiber foods should be introduced slowly.
Tell your patient to expect his or her body to tolerate the food as it did before surgery: if onions caused gas before surgery, they will do so after surgery, too, but the stoma will expel the gas. Make the patient aware of other gas-forming foods, such as hard-boiled eggs, spicy foods, fish, dried beans, carbonated beverages, and beer.
Tell the patient to chew food well and to drink plenty of liquids, which will prevent blockage. Explain the importance of hydration to avoid constipation, dehydration, and urinary tract infection. To prevent dehydration, ileostomy patients who are not on fluid restriction should drink 64 ounces of fluid a day. Teach these patients to replace fluids by drinking a glass of water every time they empty their pouches.
Drug therapy
Tell the patient to adhere to the prescribed regimen and to call the physician before using any new drugs. Instruct patients with ileostomies not to take laxatives because they may become dehydrated. These patients should tell their pharmacist that they have an ileostomy, so the proper form of prescription drugs can be ordered. Extended-release tablets will not break down in time and may be found in the pouch.
Rewarding work
Keeping up with the changes in ostomy equipment and care and teaching new ostomy patients the skills they need can be challenging. But helping these patients regain the confidence and learn the skills they need to improve their quality of life makes the rewards much greater than the challenges.
Selected references
Colwell J. Principles in stoma management. In: Colwell JC, Goldberg MT, Carmel JE, eds. Fecal and Urinary Diversions Management Principles. St. Louis, MO: Mosby; 2004:240-262.
Discharge Planning for a Patient with a New Ostomy: Best Practice for Clinicians. Glenview, IL: Wound, Ostomy and Continence Nurses Society; 2004.
Hampton BG, Bryant RA. Ostomies and Continent Diversions: Nursing Management. St. Louis, MO: Mosby; 1992.
McCann E. Common ostomy problems. In: Milne C, Corbett L, Dubuc D. Wound, Ostomy, and Continence Nursing Secrets: Questions and Answers Reveal the Secrets to Successful WOC Care. Philadelphia, PA: Hanley & Belfus, Inc; 2004.
The Sarah Cole Hirsh Institute for Best Nursing Practices Based on Evidence. State of the evidence review hospital to home: Planning the transitions. 2000; Cleveland, OH.
Goranka Paula Bak is an Ostomy Sales Territory Manager for Coloplast Corporation.
Necrotizing fasciitis (NF) results from an infection that attacks the fascia and subcutaneous tissues. The primary bacterial etiology is group A streptococcus, a facultative anaerobic bacterium. However, other bacteria may contribute. Sometimes called the “flesh-eating” disease because of the potentially devastating effect on the afflicted patient, NF can be monomicrobial or polymicrobial.
The four typical settings for NF are:
surgical bowel or abdominal trauma surgery
pressure ulcer and perianal abscess
injection sites (especially in drug users)
Bartholin abscess or minor vulvovaginal infection.
Because of the rapid course and ravaging nature of acute NF, clinicians must maintain a high index of suspicion if the patient has suggestive signs and symptoms. In 1990, puppeteer Jim Henson (best known for creating the Muppets) died from NF. At that time, little was known about the progression of group A streptococcal infection.
The disease can quickly cause death, so starting immediate treatment is even more crucial than confirming the diagnosis. Once the disease is suspected, antibiotics must be given immediately and the patient must be prepared for surgery at once. NF spreads rapidly, capable of progressing from a small lesion to death in days to weeks. Thus, delayed diagnosis increases the risk of death. Lack of knowledge about the disease and inability to recognize it promptly are the main reasons many victims die. This article can improve your knowledge base.
Overview
NF was discovered in 1871 by Joseph Jones, a Confederate Army surgeon. At that time, it was called hemolytic streptococcal gangrene, nonclostridial gas gangrene, nonclostridial crepitant cellulitis, necrotizing or gangrenous erysipelas, necrotizing cellulitis, bacterial synergistic gangrene, or synergistic necrotizing cellulitis.
NF involves the fascia, muscle compartments, or both. It can affect not only the muscle fascia but the superficial fascia. NF and cellulitis differ in the amount of tissue involved and extent of tissue involvement.
The most common areas of infection are the abdominal wall, perineum, and extremities. When NF affects the perineum and scrotum, it’s called Fournier gangrene, after the French dermatologist and virologist Alfred Jean Fournier.
The most common causes are trauma, surgery, and insect bites. The disease can affect persons of any age. Such comorbidities as diabetes, chronic renal failure, immunosuppressive therapy, hypertension, obesity, and malnutrition increase susceptibility.
Pathophysiology
NF falls into four classifications based on wound microbiology. Type 1, the most common, involves polymicrobial bacteria. Type 2 results from trauma and is associated with comorbidities. Type 3, rare in this country, stems from gram-negative marine bacteria. Type 4 is a fungal infection occurring mostly in immunocompromised persons. (See Comparing types of necrotizing fasciitis by clicking the PDF icon above.)
Disease progression
The four types of NF progress in a similar way. Bacteria secrete pyrogenic exotoxin A, which stimulates cytokines. These cytokines damage the endothelial lining; fluid then leaks into the extravascular space.
M proteins in streptococci and β-hemolytic streptococci exacerbate the immune reaction by inhibiting phagocytosis of polymorphonuclear leukocytes and normal neutrophil chemotaxis. As the immune reaction increases, blood vessels dilate, allowing toxins to leak through vessel walls, which in turn decreases blood flow. As the cascade continues, hypoxic conditions cause facultative aerobic organisms to grow and become anaerobic. These bacteria exacerbate destruction of surrounding cells and lead to release of carbon dioxide, water, hydrogen, nitrogen, hydrogen sulfide, and methane. As the infection continues to progress, toxins spread throughout the bloodstream and the patient becomes septic.
Assessment
Obtain the patient’s medical history and description of the wound. Determine when the changes first appeared and whether the affected area seemed to get worse recently.
In all NF types, patients commonly present with a small, painful area (possibly with entry marks) but no other signs or symptoms. The wound may appear as a bulla, cellulitis, or dermatitis, representing an infection developing in underlying tissues. The skin may have a wooden-hard feel as the infection progresses to the subcutaneous space and causes necrosis. The wound becomes discolored and necrotic; drainage is rare until surgical debridement begins. The patient quickly develops fever, chills, nausea, and vomiting. As NF progresses, bullae become dark purple with darkened edges; the patient grows disoriented and lethargic, and organ failure and respiratory failure
ensue. Without treatment, the patient dies.
Diagnosis
Diagnostic tests usually include magnetic resonance imaging, complete blood count with differential, comprehensive metabolic panel, and cultures. (See Diagnostic findings in necrotizing fasciitis by clicking the PDF icon above.)
Treatment
Immediate surgical debridement and broad-spectrum antibiotics are needed to stop the immune response to infection. Clindamycin, gentamicin, penicillin, or metronidazole may be given alone or in combination until culture results are available. Supportive care includes total parenteral nutrition for nutritional support, I.V. fluids, and oxygen. Limb amputation should be done only as a last resort.
Surgical debridement involves penetrating deep into the fascia and removing all necrotic tissue. After the first debridement, release of “dishwater fluid” may occur.
Administering hyperbaric oxygen therapy (HBOT) after the first debridement increases tissue oxygenation, thus reducing tissue destruction by anaerobic bacteria. During HBOT (usually given as a 90-minute treatment), the patient breathes 100% oxygen in an environment of increasing atmospheric pressure.
HBOT should be given in conjunction with surgical debridement (usually after each debridement) and should continue until necrotic tissue ceases and cell destruction stops. HBOT also promotes collagen synthesis and neoangiogenesis (new blood vessel growth), which boosts blood supply and oxygen to tissues.
Adverse effects of HBOT include ear pain, oxygen toxicity, and seizures. Ear pain can be minimized by swallowing or yawning. If the patient continues to have ear pain, ear tubes may be inserted by an otolaryngologist. During HBOT, air breaks (intervals of breathing room air) are important in controlling oxygen toxicity (the main cause of seizures).
Throughout the HBOT treatment period, wound dressings must be simple. Well-moistened gauze dressings and an abdominal pad provide good support. Once necrotic destruction occurs, dressings depend on wound size and the need to fill cavities. The patient may require a diverting colostomy, depending on wound
location and the amount of uncontrolled diarrhea. Blood glucose levels must be monitored before and after HBOT, as this treatment affects blood glucose.
Supportive care and follow-up treatment
During initial treatment, patients need supportive care and monitoring. Once they’re out of danger, begin teaching them how to prevent NF recurrences. Advise them to control blood glucose levels, keeping the glycated hemoglobin (HbA1c) level to 7% or less. Caution patients to keep needles capped until use and not to reuse needles. Instruct them to clean the skin thoroughly before blood glucose testing or insulin injection, and to use alcohol pads to clean the area afterward.
Before discharge, help arrange the patient’s aftercare, including home health care for wound management and teaching, social services to promote adjustment to lifestyle changes and financial concerns, and physical therapy to help rebuild strength and promote the return to optimal physical health. One helpful patient resource is the National Necrotizing Fasciitis Foundation. The Centers for Disease Control and Prevention section on necrotizing fasciitis includes “Common sense and great wound care are the best ways to prevent a bacterial skin infection.”
The life-threatening nature of NF, scarring caused by the disease, and in some cases the need for limb amputation can alter the patient’s attitude and viewpoint, so be sure to take a holistic approach when dealing with the patient and family. Today, NF has a much better survival rate than 2 decades ago when Jim Henson died. In my practice, I’ve seen four NF cases. Thanks to early identification, good wound care, and HBOT, these patients suffered only minimal damage.
Selected references
Boyer A, Vargas F, Coste F, et al. Influence of surgical treatment timing on mortality from necrotizing soft tissue infections requiring intensive care management. Intensive Care Med. 2009;35(5):847-853. doi:10.1007/s00134-008-1373-4.
Cain S. Necrotizing fasciitis: recognition and care. Practice Nurs. 2010;21(6):297-302.
Centers for Disease Control and Prevention. Notes from the field: fatal fungal soft-tissue infections after a tornado—Joplin, Missouri, 2011. MMWR. 2011;60(29):992.
Chamber AC, Leaper DJ. Role of oxygen in wound healing: a review of evidence. J Wound Care. 2011; 20(4):160-164.
Christophoros K, Achilleas K, Vasilia D, et al. Postraumatic zygomycotic necrotizing abdominal wall fasciitis with intraabdominal invasion in a non immunosuppressed patient. Internet J Surg. 2007;11(1). doi:10.5580/17a8.
Ecker K-W, Baars A, Topfer J, Frank J. Necrotizing fasciitis of the perineum and the abdominal wall-surgical approach. Europ J Trauma Emerg Surg. 2008;
34(3):219-228. doi:10.1007/s00068-008-8072-2.
Hunter J, Quarterman C, Waseem M, Wills A. Diagnosis and management of necrotizing fasciitis. Br J Hosp Med. 2011;72(7):391-395.
Magel DC. The nurse’s role in managing necrotizing fasciitis. AORN J. 2008;88(6):977-982.
Phanzu MD, Bafende AE, Imposo BB, Meyers WM, Portaels F. Under treated necrotizing fasciitis masquerading as ulcerated edematous Mycobacterium ulcerans infection (Buruli ulcer). Am J Trop Med Hyg. 2012;82(3):478-481.
Ruth-Sahd LA, Gonzales M. Multiple dimensions of caring for a patient with acute necrotizing fasciitis. Dimens Crit Care Nurs. 2006;25(1):15-21.
Stevens DL, Bisno AL, Chambers HF, et al; Infectious Diseases Society of America. Practice guidelines for the diagnosis and management of skin and soft-tissue infections. Clin Infect Dis. 2005;41(10):1373-1406.
Su YC, Chen HW, Hong YC, Chen CT, et al. Laboratory risk indicator for necrotizing fasciitis score and the outcomes. ANZ J Surg. 2008;78(11):968-972.
Taviloglu K, Yanar H. Necrotizing fasciitis: strategies for diagnosis and management. World J Emerg Surg. 2007;2:19.
Lydia Meyers is a medical reviewer for National Government Services in Castleton, Indiana, and a clinical liaison at CTI Nutrition in Indianapolis. She has 11 years of wound care experience in nursing homes, wound clinics, and home health.
Venous leg ulcers are the most common cause of lower extremity ulcers, affecting 1% of the U.S. population (approximately 3 million people). Annual treatment costs for venous disease in this country range from $1.9 to $3.5 billion.
The gold standard for venous ulcer treatment includes moist wound healing and compression therapy. But before compression wraps are applied, we must determine if adequate arterial blood flow exists—or consequences could be life-threatening.
Raise your hand if you know what ABI is. Now raise your hand if you routinely obtain ABIs for patients. I’ve been asking these questions at wound care seminars around the country for the last 10 years, and the answers are always the same:
Between 50% and 95% of the audience know what an ABI is, but only 1% to 2% say they perform the ABI test. My next question is “Why not?”
The ABI (ankle brachial index) is a noninvasive screening test performed with a handheld vascular Doppler and a blood pressure cuff. This simple test helps determine if you can safely apply compression therapy, aids diagnosis of peripheral arterial disease, and even helps monitor the efficacy of therapeutic interventions.
Numerous standard practice guidelines from various organizations recommend obtaining ABIs to determine arterial blood flow. These organizations include the American College of Cardiology, American Heart Association, American Diabetes Association, Society for Vascular Nursing, Wound Ostomy Continence Nurses, Society for Vascular Medicine, U.S. Preventive Services Task Force, and World Union of Wound Healing Societies.
Instructions for most compression therapy products include indications for Doppler ABI readings above 0.8. So if you don’t get an ABI reading, how can you safely apply these products? A report by Allie and colleagues found that more than 50% of lower extremity amputations occur without previous vascular testing of any type, including ABI.
So why aren’t more practitioners obtaining ABIs? The leading answer: “We don’t have a Doppler.” I understand the dilemma of not having equipment or the funds to get the equipment. But do we want to tell a patient who has just lost her leg, “Oh, sorry. We didn’t have a Doppler”?
It’s our responsibility and duty as WCCs, wound care experts, and health care clinicians to ensure we provide the highest standard of care for patients with venous leg ulcers. So communicate with management, explaining what you need and why you need it. Work with your medical supply company for an extended payment plan. Hold a fundraiser. Consider using the alternative Lanarkshire Oximetry Index procedure. Or send the patient to a wound clinic or other healthcare provider who can perform the test.
It’s time to step it up and take greater accountability—and to no longer use the excuse “We don’t have a Doppler.”
Donna Sardina, RN, MHA, WCC, CWCMS, DWC Editor-in-Chief Wound Care Advisor
Cofounder, Wound Care Education Institute
Plainfield, Illinois
Selected references
Allie DE, Hebert CJ, Lirtzman MD, et al. Critical limb ischemia: a global epidemic. A critical analysis of current treatment unmasks the clinical and economic costs of CLI. EuroIntervention. 2005; 1(1):75-84. http://www.ncbi.nlm.nih.gov/pubmed/
19758881. Accessed June 4, 2012.
Lazarus GS, Cooper DM, Knighton DR, et al. Definitions and guidelines for assessment of wounds and evaluation of healing. Arch Dermatol. 1994; 130(4):489-493. http://www.ncbi.nlm.nih.gov/pubmed/8166487. Accessed June 4, 2012.
Olin JW, Allie DE, Belkin M, et al. ACCF/AHA/ACR/SCAI/SIR/SVM/SVN/SVS 2010 performance measures for adults with peripheral artery disease: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Performance Measures, the American College of Radiology, the Society for Cardiac Angiography and Interventions, the Society for Interventional Radiology, the Society for Vascular Medicine, the Society for Vascular Nursing, and the Society for Vascular Surgery (Writing Committee to Develop Performance Measures for Peripheral Artery Disease). J Am Coll Cardiol. 2010;56(25):2147-2181. http://content.onlinejacc
.org/cgi/content/full/j.jacc.2010.08.606. Accessed June 4, 2012.
O’Meara S, Al-Kurdi D, Ologun Y, Ovington LG. Antibiotics and antiseptics for venous leg ulcers. Cochrane Database Syst Rev. 2010;(1):CD003557. http://www.ncbi.nlm.nih.gov/pubmed/20091548. Accessed June 4, 2012.
Rooke TW, Hirsch AT, Misra S, et al; Society for Cardiovascular Angiography and Interventions; Society of Interventional Radiology; Society for Vascular Medicine; Society for Vascular Surgery. 2011 ACCF/AHA focused update of the guideline for the management of patients with peripheral artery disease (updating the 2005 guideline): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2011;58(19):2020-2045. http://
content.onlinejacc.org/cgi/content/full/j.jacc.2011.08.023v1. Accessed June 4, 2012.
Valencia IC, Falabella A, Kirsner RS, Eaglstein WH. Chronic venous insufficiency and venous leg ulceration. J Am Acad Dermatol. 2001;44(3):401-421. http://www.ncbi.nlm.nih.gov/pubmed/11209109. Accessed June 4, 2012.
World Union of Wound Healing Societies. Principles of best practice:. Compression in venous leg ulcers: a consensus document. London: MEP Ltd; 2008. www.woundsinternational.com/pdf/content_25.pdf. Accessed June 4, 2012.
