Wounds on the Web: Accessing the best online resources

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

Knowledge is exploding online, making it essential that you’re comfortable using the Internet. You can also go online to save time and find a job, among other tasks. (See Online value.)

However, you also need to keep in mind that anyone can put information on the Internet. As the caption of a cartoon by Peter Steiner, published in The New Yorker says, “On the Internet, nobody knows you’re a dog.”

Be sure to evaluate the information, including such criteria as validity, authorship, integrity, and timeliness (be wary of undated information). Here are specifics to check.


Who is the intended audience for the website? Children, teenagers, adults? General audience, professionals, students, researchers? Members of a certain group or proponents of a certain viewpoint? Content varies according to audience.


Why was the website created? To sell, advertise, inform, persuade? The purpose of a website may not be stated clearly, so review content to discern its purpose.


Here are some questions to ask about the website:
• Has the website been created by a layperson or a well-known organization?
• Who sponsors the website? What is the sponsor’s reputation?
• Is contact information provided?

You can often find this information under headings such as “About us” or “Our Philosophy.”


Consider these questions for authors of online content:
• What credentials does the author have? If you don’t know what a credential means, search for it online.
• What are the author’s experience and expertise? Consider looking up the author’s name in a search engine, using three forms:
• without quotes: Firstname Lastname
• enclosed in quotes as a phrase: “Firstname Lastname”
• enclosed in quotes with * between the first and last name: “Firstname * Lastname” (The * can stand for any middle initial or name in Google only.)
• What is the end of the main URL address (called the domain extension)? This tells you the type of organization associated with the URL.

Domain extension/Organization type

.com Commercial company, usually for-profit
.edu Educational institutions, usually colleges and
.gov Government agency
.mil Limited to use by the U.S. military
.net Network, sometimes an internet service provider
.org Organizations, usually nonprofit


The following questions help you determine objectivity:
• Is any bias evident? Does the author present the information objectively from various points of view, or from one particular point of view?
• Does the author or sponsor have a known affiliation that would indicate a specific agenda or bias?
• To what extent does the information attempt to persuade or sway the audience?
• Does the information include vague statements, generalizations, stereotypes, or emotional appeals?


Ask the following:
• Where did the author get the information? As in printed journals and books, you should expect support for the information, such as references or links.
• If there are links to other pages as sources, are they to reliable sources?
Do the links work? Do links to references work and are the references from reputable sources? Keep in mind that it’s possible to create fake references.
• Is permission to reproduce copyright information provided? If so, this
typically means the website values its content.
• If the site has health information, does it display the Health on the Net Foundation Code of Conduct (HONcode) symbol? This means HON has evaluated the website and has deemed it meets HON’s ethical principles. Absence of the symbol doesn’t mean there is a problem with the site, but its presence is another point in the site’s favor.

By asking questions like these, you can ensure you access accurate information for you and your patients.

Donna Sardina is Editor-in-Chief of Wound Care Advisor and cofounder of the Wound Care Education Institute in Plainfield, Illinois.

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

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

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

Hemosiderin staining and lipodermatosclerosis

Hemosiderin staining is dark purple or rusty discoloration of the lower legs caused by chronic venous disease. A 2010 study found hemosiderin staining in all subjects with lipodermatosclerosis and venous ulcers. When vein valves fail, regurgitated blood forces red blood cells (RBCs) out of capillaries. Dead RBCs release iron, which is stored in tissues as hemosiderin, staining the skin.

Hemosiderin staining and active lipodermatosclerosis may be misdiagnosed as cellulitis. Active lipodermatosclerosis causes painful, sharply demarcated red patches on medial aspects of the lower leg. Unlike in cellulitis, redness in lipodermatosclerosis is localized to areas of hemosiderin staining and induration. Also, the skin isn’t hot and the patient is afebrile and unresponsive to antibiotics. Lipodermatosclerosis progresses to fibrosis and constriction, causing an inverted champagne-bottle appearance of the legs.

Treat active lipodermatosclerosis with compression therapy and topical corticosteroids, if needed. Control chronic venous hypertension with compression, and hemosiderin staining will fade. Refer the patient for potential corrective venous surgical procedures.

Venous dermatitis

Defined as inflammation of the epidermis and dermis, venous (stasis) dermatitis is common in patients with lower-extremity venous disease. Signs and symptoms include scaling, crusting, weeping, erythema, erosions, and intense itching. This disorder increases the risk of contact sensitivity. Advise the patient to avoid such products as lanolin, balsam of Peru, rubber, adhesives, fragrances, dyes, preservatives, skin sealants, silver sulfadiazine, neomycin, and bacitracin—all known to exacerbate venous dermatitis.

Venous dermatitis commonly is confused with cellulitis. A 2011 study found that 28% of 145 patients hospitalized for cellulitis had been misdiagnosed. The most common mistaken diagnosis was venous dermatitis. Unlike cellulitis, venous dermatitis causes itching and crusting; also, the skin isn’t acutely painful or hot and the patient is afebrile.

Treat acute venous dermatitis with compression therapy and mild-potency topical corticosteroids. Apply corticosteroids sparingly to affected areas once or twice daily for 2 weeks; be aware that premature discontinuation can lead to recurrence, while prolonged use can cause skin thinning and reduced efficacy. Domeboro soaks also decrease weeping, irritation, and itching. Paste bandages impregnated with calamine or zinc oxide are soothing and drying. However, some patients may react to the preservatives in paste bandages, so a patch test is prudent.

Chronic inflammation

Lymphedema causes chronic inflammation. About 50% of plasma proteins leak into the interstitial space daily and are recycled through the lymphatics. Lymphatic failure traps proteins in the tissues; the proteins act like sponges, attracting and binding fluid. The proteins then denature, triggering a chronic inflammatory response. This response sometimes is misdiagnosed and treated as chronic cellulitis.

Compared to cellulitis, high-protein chronic inflammation is diffuse and nontender, with light redness and mildly increased warmth. Local skin changes may include thickening or papillomatosis (a lumpy, bumpy appearance). A positive Stemmer’s sign confirms lymphedema. Complete decongestive physiotherapy promotes protein reabsorption and resolves chronic inflammation.


Cellulitis is a rapidly spreading infection of the dermis and subcutaneous tissue. In adults, it most commonly stems from Staphylococcus aureus infection of the legs. Erysipelas, a superficial form of cellulitis, involves the lymphatic system and is differentiated by “streaking” toward a regional lymph node.

Cellulitic skin is hot, acutely painful, edematous, and indurated. Redness spreads and the borders usually are irregular, sharply defined, and slightly elevated. Blisters, hemorrhagic bullae, abscesses, erosions, and necrosis may develop. About 30% to 80% of patients with lower limb cellulitis are afebrile. The white blood cell count, erythrocyte sedimentation rate, and C-reactive protein levels commonly are elevated, but normal values don’t rule out cellulitis.

Treat cellulitis with oral antibiotics effective against staphylococcus and streptococcus. Adding a brief course of oral corticosteroids significantly shortens cellulitis duration. Severe cases may necessitate hospitalization and I.V. antibiotics, plus abscess incision and drainage. Control edema with bed rest and leg elevation.

Recurrent cellulitis is common in patients with lymphedema. With compromised skin immunity, bacteria invade and spread with little resistance. If lymphedema is present, refer the patient for treatment after acute cellulitis resolves. If the patient already is being treated for lymphedema, suspend manual lymphatic drainage and compression until acute cellulitis resolves.

The most common disorders mistaken for lower-limb cellulitis are venous dermatitis, lipodermatosclerosis, irritant dermatitis, and lymphedema. It also may be mistaken for deep vein thrombosis (DVT) or dependent rubor. Rule out DVT using venous duplex ultrasound. Dependent rubor disappears with leg elevation, whereas cellulitic redness doesn’t.

Click here to view image of cellulitis.

Dependent rubor

Dependent rubor is a fiery to dusky-red coloration visible when the leg is in a dependent position but not when it’s elevated above the heart. The underlying cause is peripheral arterial disease (PAD), so the extremity is cool to the touch. To test for dependent rubor, position the patient supine and elevate the legs 60 degrees for 1 minute; then examine sole color. PAD causes the soles to change from pink to pale in fair-skinned people and to gray or ashen in dark-skinned people. The faster the pallor appears, the worse the PAD. Pallor within 25 seconds of leg elevation indicates severe occlusive disease, which warrants further evaluation for potential revascularization.

Next, observe skin color changes with the patient in a sitting position. Normally, the foot and leg should remain pink with elevation and dependency. In PAD, the color changes from pale to pink and then progresses to purple-red or bright red. The longer dependent rubor takes to reappear, the worse the PAD. Rubor that appears in 25 to 40 seconds indicates severe ischemia. If rubor disappears quickly with elevation and returns in less than 25 seconds, consider the possibility that the patient has venous reflux, not PAD. In this case, pooled blood causing the rubor drains rapidly from the veins when the leg is elevated and regurgitates back into the tissues when the leg is dependent.

If you detect dependent rubor, obtain the ankle-brachial index (ABI) to confirm PAD. For moderate PAD (ABI of 0.5 to 0.79), refer the patient for a routine vascular specialist consultation. For severe PAD (ABI below 0.5), maintain dry, stable wound eschar and urgently refer the patient to a vascular specialist for potential revascularization.

Click here to view images and read a case study on dependent rubor.

Knowledge summary

“Reading” the common causes of leg redness helps you determine what’s causing your patient’s redness so you can provide effective treatment. Remember—chronic venous disease causes hemosiderin staining, lipodermatosclerosis, and venous dermatitis. Dermatitis is itchy and crusty; lipodermatosclerosis causes sclerosis and an inverted champagne-bottle appearance of the legs. Relieve inflammation and itching with topical corticosteroids and treat venous disease with compression and corrective surgery. Lymphedema causes chronic inflammation; treat with complete decongestive physiotherapy. Cellulitis is a spreading skin infection that’s acutely painful and hot; treat with antibiotics. PAD causes dependent rubor, which disappears with leg elevation.

Selected references
Abbade LP, Lastória S, Rollo Hde A. Venous ulcer: clinical characteristics and risk factors. Int J Dermatol. 2011;50(4):405-11.

Bailey E, Kroshinsky D. Cellulitis: diagnosis and management. Dermatol Ther. 2011;24(2):229-39.

Beasley A. Management of patients with cellulitis of the lower limb. Nurs Stand. 2011;26(11):50-5.

Bryant R, Nix D. Acute and Chronic Wounds:
Current Management Concepts. 4th ed. St. Louis, MO: Mosby; 2011.

Buttaro TM, Trybulski J, Polgar P, Sandberg-Cook, J. Primary Care: A Collaborative Practice. 4th ed. St. Louis, MO: Mosby; 2012.

Caggiati A, Rosi C, Casini A, et al. Skin iron deposition characterises lipodermatosclerosis and leg ulcer. Eur J Vasc Endovasc Surg. 2010;40(6):777-82.

David CV, Chira S, Eells SJ, et al. Diagnostic accuracy in patients admitted to hospitals with cellulitis. Dermatol Online J. 2011;17(3):1.

Dieter R, Dieter RA Jr, Dieter RA III. Venous and Lymphatic Diseases. New York, NY: McGraw-Hill; 2011.

Foeldi M. Földi’s Textbook of Lymphology: For Physicians and Lymphedema Therapists. 3rd ed. Mosby, Urban & Fischer; 2012.

Hirschmann JV, Raugi GJ. Lower limb cellulitis and its mimics: part I. Lower limb cellulitis. J Am Acad Dermatol. 2012;67(2):163.e1-12.

Hirschmann JV, Raugi GJ. Lower limb cellulitis and its mimics: part II. Conditions that simulate lower limb cellulitis. J Am Acad Dermatol. 2012;67(2):177.e1-9

Keller EC, Tomecki KJ, Alraies MC. Distinguishing cellulitis from its mimics. Cleve Clin J Med. 2012;79(8):547-52.

Krasner, DL, et al. Chronic Wound Care 5: A Clinical Source Book for Healthcare Professionals. (Kindle ed.). Malvern, PA: HMP Communications; 2012.

Nazarko L. Diagnosis and treatment of venous eczema. Br J Community Nurs. 2009;14(5):188-94.

O’Connell DG, O’Connell JK, Hinman MR. Special Tests of the Cardiopulmonary, Vascular, and Gastrointestinal Systems. Thorofare, NJ: Slack Incorporated; 2011.

Sussman C, Bates-Jensen B. Wound Care: A Collaborative Practice Manual for Health Professionals. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2012.

Uzun G, Mutluoglu M. Images in clinical medicine. Dependent rubor. N Engl J Med. 2011;364(26):e56.

Robyn Bjork is a physical therapist, a certified wound specialist, and a certified lymphedema therapist. She is also chief executive officer of the International Lymphedema and Wound Care Training Institute, a clinical instructor, and an international podoconiosis specialist.

Is your wound-cleansing practice up to date?

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

With so much focus on dressing choices, it’s easy to forget the importance of wound cleansing. Cleaning a wound removes loose debris and planktonic (free-floating) bacteria, provides protection to promote an optimal environment for healing, and facilitates wound assessment by optimizing visualization of the wound. You should clean a wound every time you change a dressing, unless it’s contraindicated.

Here’s a review of how to choose and use a wound cleanser so you can see if your practice is up to date.

Choosing a wound cleanser

The ideal wound cleanser is hypoallergenic, nontoxic to viable tissue, readily available, cost effective, and stable. The wound cleanser should also:

• be effective in the presence of organic material, such as blood, slough, or necrotic tissue
• reduce the number of microorganisms that form on the surface of the wound
• have a delivery force less than 15 pounds per square inch.

Common wound cleansers

Below are common types of wound cleansers:

Normal saline solution. Normal saline solution is the preferred cleansing agent because as an isotonic solution, it doesn’t interfere with the normal healing process. It’s also cost effective and available in many different formats, including unit dose, half liters, liters, and spray bottles.
Commercial cleansers. Ingredients in commercial cleansers may include surfactants, wetting agents, moisturizers, and/or antimicrobials.

  • Surfactants are agents that facilitate removal of wound contaminants. Each surfactant molecule has a hydrophilic (water-loving) head that is attracted to water molecules and a hydrophobic (water-hating) tail that repels water and simultaneously attaches itself to wound contaminants, oils, or grease.

These opposing forces loosen the particles and suspend them in the water.

Skin cleansers. Skin cleansers are
formulated to remove fecal matter, so they should never be used on open wounds, as they tend to be stronger than a wound cleanser and toxic to wound tissues.
Lactated Ringer’s solution. Lactated Ringer’s solution provides sodium, potassium, and calcium chloride to the wound, while safely cleaning it and avoiding damage to viable cells. Be careful when the solution is used for continuous irrigation or allowed to dwell inside body cavities; otherwise the solution could be absorbed into the bloodstream, leading to circulatory overload.
Potable (drinkable) tap water. Potable tap water can be used if there is no other alternative. Check the quality of the water source. Advantages of tap water for wound cleansing are efficiency, cost effectiveness, and accessibility. However, use normal saline solution instead of water for wounds with exposed bone or tendon.

Click here to see examples of wound cleansers.

How to clean a wound

Before you start, make sure the cleansing solution is at room temperature or slighter warmer. It can take up to 40 minutes after cleaning for a wound to regain its original temperature, and up to 3 hours for miotic cell division and leukocytic activity to return to normal.

Once the solution is warm, wash your hands and put on gloves.

View a video on wound cleaning

Manual cleansing technique
For a linear wound or incision:
1. Pour irrigation solution into the irrigation tray. Moisten clean 4″×4″ gauze pads in the solution; squeeze out excess.
2. Gently wipe the wound from top to bottom in one motion, starting directly over the wound.
3. Discard the used gauze pad.
4. Using a new moistened 4″×4″ gauze pad, repeat cleaning, using a gentle downward stroke parallel to the incision.
5. Repeat steps, working outward from the incision in lines parallel to the incision.
6. Remember to use a new 4″×4″ gauze pad for each downward stroke.
7. If needed, dry the wound, following the same procedure as for cleaning, using dry gauze pads.

For an open wound:
1. Pour the irrigation solution into the irrigation tray. Moisten 4″×4″ gauze pads in the solution; squeeze out excess.
2. Gently clean the wound in a full or half circle, beginning in the center and working toward the outside.
3. Use a new 4″×4″ gauze pad for each circle.
4. Clean at least 1 inch beyond the end of the new dressing or 2 inches beyond the wound margins if you aren’t applying a dressing.
5. If needed, dry the wound, using the same procedure as for cleaning. Gently pat the wound dry, using dry gauze pads.

Spray cleansers
1. Spray cleansers may be applied directly to the wound or sprayed onto clean 4″×4″ gauze pads and then applied to the wound.
2. Check your organization’s policy for required personal protective equipment (PPE). Generally, wound irrigation
that involves squirting, spraying, or pressure release of fluid will require the use of PPE (such as gloves, gown, and mask with eye shield) to prevent exposure to debris and airborne microorganisms.
3. Protect the environment, equipment, and other supplies from contamination from spray aerosolization by covering or removing the supplies.
4. Hold the spray bottle approximately
1 inch from the wound bed. Aim the nozzle at the wound and squeeze the bottle, directing the stream of cleanser along the base and sides of the wound.
5. Blot up excess moisture with a clean gauze pad.
6. Dry the surrounding skin.

Cleaning with a saline bullet
1. Position the patient so that the cleansing solution will flow by gravity from the upper end of the wound to the lower end.
2. Twist off the top.
3. Position the container at any angle required to access the area to be moistened or cleaned.
4. Apply firm pressure to the container to obtain the desired flow rate.
5. Blot up excess moisture with a clean gauze pad.
6. Dry the surrounding skin.

After you have finished cleaning the wound, dispose of the waste in a trash bag; then remove and discard your gloves and any other PPE you used.

Selected references

European Pressure Ulcer Advisory Panel and National Pressure Ulcer Advisory Panel. Treatment of pressure ulcers: Quick reference guide. Washington, DC: National Pressure Ulcer Advisory Panel; 2009.

Hess CT (ed.). Clinical Guide to Wound Care. 7th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2012.

Kosier B. Fundamentals of Nursing: Concepts, Process, and Practice. 6th ed. Upper Saddle River, NJ: Prentice-Hall, Inc; 2000.

Ovington LG. Hanging wet-to-dry dressings out to dry. Adv Skin Wound Care. 2002;15(2):79-84.

Wound Source. Wound cleansers. http://www.woundsource.com/product-category/wound-cleansers/wound-cleansers. Accessed April 1, 2013.

Donna Sardina is Editor-in-Chief of Wound Care Advisor and cofounder of the Wound Care Education Institute in Plainfield, Illinois.

When you can’t rely on ABIs

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

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.

This article explains why ABIs can be deceptive when considering the safety of compression and wound-healing potential in diabetic patients. As a wound care clinician, you need to stay alert for both falsely elevated and false-normal ABIs—and when these occur, suspect underlying peripheral artery disease (PAD).

Falsely elevated ABIs

Most wound care clinicians are familiar with a falsely elevated ABI. But do you understand what it means? ABI compares blood pressure measured at the ankle with blood pressure measured at the arm. Traditionally, an ABI of 1.3 or more has been deemed falsely elevated. But a 2011 guideline from the American College of Cardiology and the American Heart Association raised the false-elevation threshold to 1.4.
Falsely elevated ABI stems from calcification of the arterial wall and is common in patients with diabetes. Yet such calcification doesn’t automatically indicate plaque in the lumen of that artery; nor does a normal ABI indicate absence of plaque. A 2008 study of 1,762 patients found atherosclerotic plaque in 62% of those with falsely elevated ABIs, whereas the other subjects had normal blood flow. PAD was significantly more prevalent in patients with the clinical indicators of resting pain, ulcers, or gangrene. Also, PAD risk was 10 times higher in patients with chronic renal failure, three times higher in those with coronary artery disease, and five times higher in those with a history of smoking. Therefore, these concurrent diagnoses and clinical indicators can serve as distinguishing factors when arterial calcification obscures underlying PAD.

Download Ankle-brachial index tool

False-normal ABIs

False-normal ABIs are more problematic than falsely elevated ABIs. An otherwise diseased and occluded artery may calcify just enough to raise the ABI to a normal range before reaching falsely elevated levels. Therefore, a normal ABI (from 1.0 to 1.3) isn’t sufficient to rule out PAD, according to a 2011 study.

In calculating ABI, the higher measurment of the dorsalis pedis and posterior tibial arteries is used. This in itself can lead to false-normal ABIs in diabetic patients. Diabetes commonly causes segmental arterial disease, in which one artery may be occluded while the other isn’t. Therefore, blood supply to one area of the foot may be ischemic while blood supply to another is patent. If the more patent artery is used to calculate ABI, blood flow to the limb could appear normal even if significant occlusion and ischemia are present.

In a 2012 study, 8 of 30 legs with diabetic gangrene were found to have PAD, even though the patients’ ABIs were normal. In one shocking case, a 69-year-old man had a normal ABI of 0.99, yet his angiogram showed complete occlusion of the distal peroneal and distal posterior tibial arteries and near-total occlusion of the anterior tibial artery.

Alternative tests for patients with falsely elevated ABI

Because the smaller arteries of the toes are less likely to become calcified, a toe brachial index (TBI) typically is used to detect PAD in patients with falsely elevated ABIs.

• TBI above 0.7 is normal.
• TBI below 0.64 indicates PAD.
• TBI of 0.64 to 0.7 is borderline.

However, a normal TBI doesn’t necessarily mean blood flow is sufficient to promote healing of diabetic foot ulcers. TBI and total blood perfusion can be normal in the diabetic foot even if the skin has chronic ischemia. This condition (possibly caused by abnormal autonomic innervation of the vessels) occurs when blood is routed through arteriovenous shunts, bypassing capillaries. Because blood fails to deliver oxygen and nutrients via capillaries, the skin becomes chronically ischemic and wounds fail to heal. Keep this in mind when interpreting ABI and TBI results, because it may help reconcile discrepancies between what we see in wound healing and what seems like good blood flow in patients with diabetes.

View: TBI exam with PPG pressure

Transcutaneous oxygen pressure measurements

Unlike TBI, transcutaneous oxygen pressure measurements (TcPo2) indicate the wound-healing potential of diabetic foot ulcers. (However, TcPo2 testing is less readily available than TBI.) Sensors are placed on the skin around the wound to determine actual capillary perfusion via oxygen delivery to the skin.
• TcPo2 above 40 mm Hg indicates wound-healing potential.
• TcPo2 of 20 to 30 mm Hg predicts chronic wound-healing complications.
• TcPo2 below 20 mm Hg signals critical limb ischemia and the possible need for amputation.

TcPo2 is used widely in hyperbaric oxygen therapy for patients with wounds and is gaining wider use in predicting potential candidates for this therapy.

View: hyperbaric oxygen therapy

When you must measure TcPo2

When a patient’s ABI is falsely elevated, standard practice is to obtain a TBI. But a normal TBI isn’t definitive proof of adequate blood flow through the capillaries. When wound healing doesn’t correspond with apparently sufficient blood flow in the diabetic foot, the patient may have arteriovenous shunting and chronic capillary ischemia. In this case, TcPo2 measurements can help determine actual capillary perfusion and wound-healing potential.

Selected references

Aboyans V, Ho E, Denenberg JO, Ho LA, Natarajan L, Criqui MH. The association between elevated ankle systolic pressures and peripheral occlusive arterial disease in diabetic and nondiabetic subjects. J Vasc Surg. 2008;48(5):1197-203.

Aerden D, Massaad D, von Kemp K, et al. The ankle–brachial index and the diabetic foot: a troublesome marriage. Ann Vasc Surg. 2011;25(6):770-7.

Arsenault KA, McDonald J, Devereaux PJ, Thorlund K, Tittley JG, Whitlock RP. The use of transcutaneous oximetry to predict complications of chronic wound healing: a systematic review and meta-analysis. Wound Repair Regen. 2011 Nov;19(6):657-63. PubMed PMID: 22092835.

Bjork R. Bedside ankle-brachial index testing: time-saving tips. Wound Care Advisor. 2013;2(1):22-6.

Jörneskog G. Why critical limb ischemia criteria are not applicable to diabetic foot and what the consequences are. Scand J Surg. 2012;101(2):114-8.

Potier L, Abi Khalil C, Mohammedi K, Roussel R. Use and utility of ankle brachial index in patients with diabetes. Eur J Vasc Endovasc Surg. 2011; 41(1);110-6.

Park SC, Choi CY, Ha YI, Yang HE. Utility of toe-brachial index for diagnosis of peripheral artery disease. Arch Plast Surg. 2012;39(3):227-31.

Rooke TW, Hirsch AT, Misra S, et al; American College of Cardiology Foundation; American Heart Association Task Force; 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). Vasc Med. 2011; 16(6):452-76.

Singh PP, Abbott JD, Lombardero MS, et al; Bypass Angioplasty Revascularization Investigation 2 Diabetes Study Group. The prevalence and predictors of an abnormal ankle-brachial index in the Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI 2D) trial. Diabetes Care. 2011;34(2): 464-7

Suominen V, Rantanen T, Venermo M, Saarinen J, Salenius J. Prevalence and risk factors of PAD among patients with elevated ABI. Eur J Vasc Endovasc Surg. 2008;35(6):709-14.

Robyn Bjork is a physical therapist, certified wound specialist, and certified lymphedema therapist. She is also chief executive officer of the International Lymphedema and Wound Care Training Institute, a clinical instructor, and an international podoconiosis specialist.

Debridement options: BEAMS made easy


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.

The normal healing process is complex and can contribute to wound chronicity, which causes delayed healing. Local and systemic factors that can impede wound healing include lack of growth factors, a prolonged inflammatory response, abnormal matrix metalloproteinases, desiccation or decreased perfusion of the wound bed, wound hypoxia, infection or increased bacteria, aged cells, necrotic tissue, excessive or sustained pressure at the wound site, poor nutritional status, and certain medical conditions.

Autolysis, a natural process that occurs during wound healing, requires a moist vascular environment and a functioning immune system. During the inflammatory stage, neutrophils and macrophages digest and remove devitalized tissue debris. In chronic wounds, the autolysis process becomes overwhelmed by high levels of endotoxins released from damaged tissue and use of other debriedement methods are necessary.

Managing chronic wounds requires a holistic and comprehensive approach that considers all factors that can affect wound healing. Debridement remains a standard of care. Fundamental to proper wound healing, it can be done by surgical or nonsurgical methods. Debridement is integral to transforming the hostile environment of a chronic wound to a receptive environment that promotes healing. This article gives an overview of debridement techniques.

Why debridement is crucial to healing

Debridement refers to removal of dead, devitalized, or contaminated tissue or foreign material from a wound to reduce the number of microbes, toxins, and other substances that inhibit healing. Wound care clinicians must strive to achieve a stable, well-vascularized wound bed with minimal exudates. Presence of necrotic or compromised tissue is common in chronic nonhealing wounds. Devitalized tissue provides a growth medium for bacteria, increasing the infection risk. Also, it exudes endotoxins that inhibit migration of fibroblasts and keratinocytes to the wound. Necrotic tissue prevents formation of granulation tissue, wound contraction, and epithelialization.

While all components of wound bed preparation are crucial to an optimal wound-healing environment, both historical and current research indicates that removing exudates and devitalized tissue is essential. Many wounds with underlying pathologies that are untreatable or hard to treat require repeated debridement. (See Wound bed preparation by clicking the PDF icon above.)

Debridement methods can be selective or nonselective. Selective methods remove only devitalized tissue. Nonselective methods don’t differentiate between viable and nonviable tissue.

Debridement methods

Five major debridement methods exist, collectively known as BEAMS—an acronym made up of the first letters of each method. Selective methods include Biological/Biosurgical, Enzymatic, and Autolytic debridement. Nonselective methods include Mechanical and Sharp debridement. (See Choosing the right debridement method by clicking the PDF icon above.)

In some cases, more than one debridement method may be appropriate. In others, no method may be appropriate. For instance, stable eschar (eschar that’s dry, adherent, and intact with no erythema or fluctuance) on the heels serves as a natural covering and shouldn’t be removed. Another example is when healing isn’t an option, as when decreased blood flow from arterial insufficiency delays or impedes wound healing.

Biological/biosurgical debridement

Also known as maggot debridement, larval therapy, or larvae therapy, this method uses medicinal maggots to remove nonviable tissue. Sterile maggots are applied to the wound and covered by a dressing, which remains in place 1 to 3 days. Maggots have three actions:

View: a video for teaching patients about how maggot therapy works

  • They debride the wound by liquefying and digesting necrotic tissue.
  • They disinfect by killing and consuming bacteria.
  • They stimulate wound healing by promoting fibroblast growth.

Rapid and selective, biological debridement has proven effective in debriding chronic wounds and aiding limb salvage.

Enzymatic debridement

Enzymatic debridement involves application of collagenase ointment, which doesn’t harm healthy tissue. Fast acting and highly selective, it involves once-daily application of Santyl, a prescription product with no generic equivalent. This collagenase ointment works from the bottom up by selectively degrading (dissolving) collagen anchored to the wound. It breaks down only denatured collagen, leaving other proteins unaffected. Also, it doesn’t harm the collagen needed to form a scaffold, which is crucial for healing during the second phase of the wound healing cascade.

Enzymatic debridement is faster than autolytic debridement but more conservative than sharps surgical debridement. While Santyl is the only enzymatic debriding ointment available, other topical agents, such as Iodosorb, Oakin, and Mesalt, can promote debridement in the wound bed as well.

View: enzymatic debridement

Autolytic debridement

A natural physiologic process, autolytic debridement uses the body’s own enzymes to soften and break down necrotic tissue. White blood cells and enzymes enter the wound site during the inflammatory phase of healing, liquefying necrotic tissue. All wounds go through autolytic debridement to some extent. Products that support a moist wound environment can enhance this type of debridement.

Autolytic debridement is slow, selective, painless, and noninvasive. However, it’s not used for infected wounds and isn’t the best choice for wounds with a large amount of necrotic tissue.

Mechanical debridement

Mechanical debridement uses an external force great enough to separate or break the adhesive forces of necrotic tissue. This nonselective method, which can be painful, may involve a whirlpool, wet-to-dry dressings, scrubbing, and irrigation. Contraindications include epithelializing wounds and granulating wounds.

View: a video of administering low-pressure irrigation, a type of mechanical debridement

Sharp debridement

Sharp debridement refers to removal of necrotic devitalized tissue by sharp instruments, such as scalpels, scissors, lasers, curettes, or forceps. Nonselective, this method is the fastest debridement method. It can be either surgical or conservative.

  • Surgical debridement is a major procedure performed by a surgeon, another physician, or a podiatrist. It involves complete debridement and transforms a chronic wound to an acute wound. It produces rapid results but sacrifices some viable tissue. Pain control during and after the procedure is important and can be accomplished with analgesics. (See Sharp debridement by clicking the PDF icon above.)
  • Conservative debridement is done at the bedside by a trained clinical practitioner (such as a therapist or nurse, if the state practice act allows) or a physician. This minor procedure, which involves use of scalpels, scissors, or curettes, removes only devitalized tissue. It may require several sessions.

One type doesn’t fit all

Not all patients with necrotic wounds are candidates for every debridement method. To choose the most appropriate method, clinicians must understand the need for debridement and the available options. Keep in mind that in many cases, debridement isn’t a one-time intervention but must be repeated until healthy granulation tissue appears. Be sure to reassess the patient and wound regularly to ensure the best care.

Selected references
Benbow M. Available options for debridement. Independent Nurse. June 6, 2011. www.independentnurse.co.uk/cgi-bin/go.pl/library/articlehtml.cgi?
. Accessed February 27, 2013.

European Wound Management Association. Wound Bed Preparation in Practice: Position Document. 2004. www.smith-nephew.com/global/assets/en/documents/
. Accessed February 27, 2013.

Harris RJ. The nursing practice of conservative sharp wound debridement: promotion, education and proficiency. Wound Care Canada. 2009;7(1):22-30. http://cawc.net/images/uploads/wcc/harris.pdf. Accessed February 27, 2013.

Hess CT. Checklist for factors affecting wound healing. Adv Skin Wound Care. 2011;24(4):192.

Hess CT. Clinical Guide to Skin and Wound Care. 7th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2012.

Moore M, Jensen P. Assessing the role and impact of enzymatic debridement. Podiatry Today. 2004;17(7). www.podiatrytoday.com/article/2785?page=1. Accessed February 27, 2013.

Payne WG, Salas RE, Ko F, Naidu DK, Donate G, et al. Enzymatic debriding agents are safe in wounds with high bacterial bioburdens and stimulate healing. Eplasty. 2008;7;8:e17.

Sardina D. Wound bed preparation. In: Skin and wound management course workbook. Lake Geneva, WI: Wound Care Education Institute; August 2010;5:42-58.

Sen CK, Gordillo GM, Roy S, Kirsner R, Lambert L, et al. Human skin wounds: a major and snowballing threat to public health and the economy. Wound Repair Regen. 2009;17(6):763-71.

Singhal A, Reis ED, Kerstein MD. Options for nonsurgical debridement of necrotic wounds. Adv Skin Wound Care. 2001;14(2):96-100.

Cindy Broadus is a clinical instructor at the Wound Care Education Institute in Plainfield, Illinois.

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

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

In a busy wound clinic, quick and accurate differential diagnosis of edema is essential to appropriate treatment or referral for comprehensive care. According to a 2010 article in American Family Physician, 80% of lower extremity ulcers result from chronic venous insufficiency (CVI). In 2007, the German Bonn Vein Study found 100% of participants with active venous ulcers also had a positive Stemmer’s sign, indicating lymphedema.

Lymphedema secondary to CVI is called phlebolymphedema (“phlebo” means veins). Whereas CVI warrants compression therapy alone, phlebolymph-edema may require complete decongestive physiotherapy. To provide optimal care, a wound care clinician must differentiate between CVI and phlebolymphedema. Fortunately, differential diagnosis can be made in 10 seconds or less by performing Stemmer’s test.

How to perform Stemmer’s test

Stemmer’s test results in either a positive or negative sign for lymphedema. To perform it, try to pinch and lift a skinfold at the base of the second toe or middle finger. If you can pinch and lift the skin, Stemmer’s sign is negative. If you can’t, the sign is positive. False positives never occur. On the other hand, a negative test doesn’t rule out lymphedema.

Stemmer’s test is diagnostic for phlebolymphedema or any other form of lymphedema. Not all wound-care clinicians need to determine the type or underlying causes of lymphedema. A positive Stemmer’s sign means the patient has lymphedema and should be referred for further evaluation and treatment by a lymphedema specialist.

Understanding the pathophysiology behind the test

A 10-second test might seem too good to be true. Also, how can Stemmer’s sign never be falsely positive? The answers lie in understanding the pathophysiology behind the test.

The primary function of the lymphatic system is to recycle blood proteins. Half of plasma proteins leak into the interstitial space and are recovered by the lymphatic system each day. Think of them as delivery men carrying nutrients to cells. They deliver their packages and go back into the bloodstream via the lymphatics to make more deliveries. But when the lymphatic system is blocked or damaged, proteins accumulate in the tissues. This causes the pathologic changes that lead to a positive Stemmer’s sign.

Like butter turning rancid, proteins accumulating in the tissues become denatured; macrophages migrate to the area to digest them. In what resembles the wound-healing process, macrophages release interleukin 1, which activates fibroblasts to produce collagen. This normal cascade becomes pathologic as excessive collagen is produced and denatured proteins trigger chronic inflammation. This process causes thickened, dense, fibrotic skin.

Typically, chronic lymphedema progresses from the toes or fingers proximally. The thin skin of the dorsum of the foot or hand is the first area to show signs of thickening, which leads to a positive Stemmer’s sign. (See Positive Stemmer’s sign by clicking the PDF icon above.)

Clinical considerations and test modifications

Unlike protein-rich lymphedema, edema in a patient with CVI or congestive heart failure (CHF) is watery. Proteins continue to circulate through the lymphatic system and don’t accumulate in tissues. If your patient has only CVI, no swelling occurs in the toes, and Stemmer’s sign is negative. Hemosiderin staining, the classic sign of CVI, likely will occur in the lower legs. (See Negative Stemmer’s sign in a patient with CVI by clicking the PDF icon above.)

In contrast, a patient with CHF has swelling of the toes and dorsum of the foot. In this case, when performing the Stemmer’s test, allow sufficient time for pitting edema to displace. Then note skin texture and try to pinch a skinfold. Edema solely from CHF displaces slowly, and Stemmer’s sign is negative. If the sign is positive, it means the patient has both CHF and lymphedema.

What happens in phlebolymphedema

Phlebolymphedema refers to lymphedema caused by CVI—a disorder that leads to valvular failure of the veins and increased tissue edema. Normally, as skin stretches from edema, elastic fibers pull open the lymphatic capillaries via their attachments by anchoring filaments. However, extreme distention causes rupture of these filaments and shredding of lymphatic capillary walls. What’s more, lymphatic overloading to compensate for venous insufficiency can lead to valvular failure of lymphatic vessels. As lymphedema progresses, the skin thickens and becomes lumpy, and wartlike knobs or projections may develop. Called papillomatosis, this condition indicates advanced lymphedema. (See Phlebolymphedema.)

Sometimes localized lymphatic damage occurs, with skin changes arising only in affected areas such as periwound tissues. In this case, you can modify Stemmer’s test by assessing skin texture in affected areas.

Understanding localized periwound lymphedema and its treatment aids healing of chronic wounds. White blood cells use lymphatics to drag bacteria and toxins to lymph nodes, in turn triggering an immune response. As wound care clinicians, we are acutely aware of bacterial bioburden and its negative effect on wound healing. Without a continuous flow of lymph, the body’s natural ability to fight bacteria is compromised. Further, debris, dead cells, and other byproducts of wound healing—normally removed via the lymphatics—cause stagnation of the wound environment and slow wound healing.

What a negative sign may mean

As mentioned, a negative Stemmer’s sign doesn’t rule out lymphedema. For example, a malignant tumor may cause lymphedema proximally in a limb; because lymphedema onset is acute and swelling is worse proximally, Stemmer’s sign may be negative.

Useful screening tool

Stemmer’s sign is a useful tool for screening patients in the wound clinic and promotes recognition of many lymphedema cases that otherwise might go undiagnosed and untreated. (See Clinical wisdom: Stemmer’s sign by clicking the PDF icon above.) Remember that patients with CVI and chronic venous ulcers have a high prevalence of secondary lymphedema. Also keep in mind that while a positive Stemmer’s sign always indicates lymphedema, a negative test doesn’t exclude lymphedema. Refer lymphedema patients to a lymphedema specialist for further assessment and treatment.

Click here www.lympho.org/resources.php to download International Consensus: Best Practice for the Management of Lymphoedema.

Selected references
Brenner E, Putz D, Moriggl B. Stemmer’s (Kaposi-Stemmer-) sign—30 years later: case report and literature review. Phlebologie. 2007;36(6):320-324.

Collins L, Seraj S. Diagnosis and treatment of venous ulcers. Am Fam Physician. 2010;81(8): 989-996.

Farrow W. Phlebolymphedema–a common underdiagnosed and undertreated problem in the wound care clinic. J Am Col Certif Wound Spec. 2010;2(1):14-23.

Föeldi M. Földi’s Textbook of Lymphology: For Physicians and Lymphedema Therapists. 3rd ed. Urban & Fischer; 2012.

Lymphoedema Framework. Best Practice for the Management of Lymphoedema. International consensus. London: MEP Ltd; 2006.

Macdonald JM, Ryan TJ, eds. Lymphoedema and the chronic wound: the role of compression and other interventions. In: World Health Organization. Wound and Lymphoedema Management. 2010:63-84.

Nelzén O. Prevalence of venous leg ulcer: the importance of the data collecting method. Phlebolymphology. 2008;15(4):143-150.

O’Connell DG, O’Connell JK, Hinman MR. Special Tests of the Cardiopulmonary, Vascular, and Gastrointestinal Systems. Thorofare, NJ: Slack; 2010.

Pannier F, Hoffmann B, Stang A, Jöckel KH, Rabe E. Prevalence of Stemmer’s sign in the general population. Phlebologie. 2007;36(6):287-342.

Piller N. Phlebolymphoedema/chronic venous lymphatic insufficiency: an introduction to strategies for detection, differentiation and treatment. Phlebology. 2009;24(2):51-55.

Simonian SJ, Morgan CL, Tretbar LL, Blondeau B. Differential diagnosis of lymphedema. In: Tretbar LL, Morgan CL Lee BB, Simonian SJ, Blondeau B. Lymphedema: Diagnosis and Treatment. London: Springer-Verlag; 2008;12-20.

Photos used with permission from the International Lymphoedema Framework. The author provided the remaining photos.

Robyn Bjork is a physical therapist, certified wound specialist, and certified lymphedema therapist. She is also chief executive officer of the International Lymphedema and Wound Care Training Institute, a clinical instructor, and an international podoconiosis specialist.

How to choose a digital camera for wound documentation

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

Digital cameras have many helpful features, but the most important considerations for choosing a camera are hardware features. Focus on the following when choosing a camera:

Resolution. The resolution determines picture quality. The National Pressure Ulcer Advisory Panel recommends using a digital camera with a minimum of 3 megapixels
for wound photography. A megapixel is 1 million pixels. The more pixels used to produce a photo, the less grainy it will appear and the clearer any enlargements made from it will be. In essence, the more megapixels a camera produces, the clearer and more detailed the photograph will be.

Lens. The type of lens affects quality and versatility. Lenses made from glass give you sharper images and are less likely than plastic to get scratched. Be sure the camera has an optical zoom lens. Optical zoom lenses vary from 2X to 10X: The greater the zoom range, the greater its versatility, and the greater the cost. A camera with 3X optical zoom is sufficient for wound photos. Digital zoom shouldn’t be an important factor in choosing a camera: In effect, it crops the picture as you take it, reducing resolution of the picture and the size you can print it.

Automatic features. Automatic features make it easier for you to use the camera. Look for a camera with auto focus, auto exposure, auto white balance, auto advance, and auto flash. Auto exposure calculates the correct light exposure for the scene. Automatic white balance adjusts the colors in the image to match the source of light. Auto advance prepares the camera for the next photo. An automatic flash is a must as it illuminates a subject when there is not enough available light.

Additional features. These features are common in point-and-shoot digital cameras, which produce high-quality pictures with a minimum of effort. Point-and-shoot cameras take the guesswork out of taking photos.

  • Memory card. This determines how many photos you can take without deleting some to make room in the camera’s memory. The digital equivalent of film, removable memory cards are what digital cameras use to store the images they have taken. The size of commonly used memory cards is measured in megabytes (MB). Purchase a memory card that can store at least 100 images in the highest-quality Joint Photographic Experts Group (JPEG) format—usually 512 MB. Although memory cards are reusable, they don’t have a limitless capacity, and it’s always good to have more memory than you need.
  • Interface connection. This is what you use to transfer photos to the computer. To make your life easier, look for a camera and a computer with a 2.0 USB connection. A USB connection is a cable that connects the camera to the computer or printer to transfer your photos.
  • Digital photo printer. The quickest and easiest way to print your photos is using a compact photo printer. These printers can be connected to your computer or even print the photos directly from the camera. The size of the printed photos is 4 × 6 inches.

Here’s a summary of recommended digital camera specifications:

  • Lens type: Glass with optical zoom 3X or greater
  • Auto features: Auto focus, auto exposure, auto white balance, auto advance, and auto flash
  • Memory card: 512 MB
  • Photo file format: JPEG
  • Interface: USB 2.0

Tips for photographing wounds

Now that you’ve chosen your camera, follow these tips to obtain the best possible photos:

  • Position the camera at a standard distance from the wound (usually about 4 feet) each time you take a photo.
  • Take the photographs at a consistent angle; even a slight deviation in the angle can change perspective, depth, and shadow.
  • The most difficult variable to control is the patient’s position. A good starting point is for the patient to be comfortably positioned in the anatomically correct position, placing the wound as far from the sleep surface as possible. For example, if the wound is on the left hip, position the patient with the right hip resting on the mattress.
  • In every photograph include a measurement grid adjacent to the wound, preferably one labeled in centimeters and millimeters.
  • Do not use a white background for photos. Drape the patient with colored sheets, towels, or blue-backed disposable underpads. The color contrast will give you higher-quality results.
  • If the hands of the person holding the patient while you take the photograph will be visible, have the person wear gloves. That way you have evidence gloves were worn, and the person will be protected against any wound drainage.

Donna Sardina is Editor-in-Chief of Wound Care Advisor and cofounder of the Wound Care Education Institute in Plainfield, Illinois.

Bedside ankle-brachial index testing: Time-saving tips

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

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.

If you can relate to this story, you’re not alone. Although a 2009 study found an ABI test can be done in 5 to 10 minutes on healthy individuals, it can be more time-consuming in older patients with limited mobility, significant edema or lymphe-dema, obesity, tissuefibrosis, or diminished pulses. In 2005, Lorraine French found that 74% of 50 trained home health nurses took 51 to 90 minutes to complete an ABI procedure and 20% took 30 to 50 minutes.

ABI is the ratio of systolic blood pressure (BP) in the ankle to systolic BP in the arm. An ABI of 0.90 or lower indicates peripheral arterial disease (PAD) and is linked to an increased risk of heart attack or stroke. For wound care clinicians, ABI testing helps determine how much compression is safe to apply and reflects the wound’s healing potential. (See Interpreting ABI results by clicking the PDF icon above.)
However, finding the time to obtain ABIs in a busy clinic can be challenging. This article offers time-saving tips you can use when performing a bedside ABI test.

Tip #1: Request ABI testing before referrals.

Save time by acquiring ABI results from a diagnostic service instead of performing bedside ABIs. Initially, this may take some proactive education, especially if your referral sources don’t routinely order ABIs. According to 2011 guidelines from the American College of Cardiology and American Heart Association, an ABI should be done if a patient has leg pain with exertion, has a nonhealing wound, is age 65 or older, or is age 50 or older with a history of smoking or diabetes. Many patients fall into these categories, so it’s reasonable to ask referral sources to order ABIs before referrals.
Click to view and print patient educational flyers about PAD and ABI.

Tip #2: Multitask ABIs into the initial assessment.

Before your initial assessment, instruct the patient to take all medications as prescribed and avoid tobacco, caffeine, alcohol, and heavy exercise for an hour before the appointment. (These factors can affect ABI results.) Also, have the patient rest supine for at least 10 minutes before the ABI procedure. During this rest period, perform a lower-extremity vascular and skin assessment. If an ABI is indicated, you can then perform the test immediately. (If you suspect severe PAD, increase the rest period to 20 minutes. You can use this time to take wound or edema measurements.)
Assess the patient for PAD risk factors. Pain on rest is associated with severe PAD and an ABI below 0.5. Observe and feel the patient’s skin. Signs of PAD include dry, brittle skin and nails, lack of toe hair, cool skin, rubor on dependency, pallor on elevation, and bluish or dusky purplish discoloration. Assess for arterial ulcers or necrotic areas on the tips of toes, lateral malleolus, and metatarsal heads. These ulcers are associated with an ABI below 0.20 and severe PAD.

Tip #3: Use Doppler sounds to avoid unnecessary ABIs.

A triphasic Doppler signal is distinctive and indicates normal blood flow, whereas biphasic or monophasic signals indicate PAD. By learning to identify triphasic sounds, you can eliminate unnecessary ABIs. Some portable Doppler units include printable waveforms or reversing arrows, which give visual confirmation of Doppler sounds and are useful when learning to distinguish normal and abnormal signals.
Research during the 1990s showed pulse palpation alone is unreliable in detecting PAD. However, most pulses were nonpalpable when ABI was less than 0.82; the lowest ABI with a palpable pulse was 0.5. Doppler auscultation and ABIs were used to validate pulse palpation. The combination of a normal palpable pulse, low PAD risk factors, and a triphasic Doppler signal indicates adequate lower-extremity blood flow for the purpose of compression therapy and wound healing. When these findings are present, an ABI test isn’t necessary.
Even if a clinician misses underlying mild or moderate PAD using pulse palpation and Doppler auscultation alone, compression therapy is safe when inelastic or short-stretch bandaging systems are used. A new study found these bandaging systems are safe up to 30 or 40 mm Hg in patients with ABIs as low as 0.5, as long as ankle systolic pressure exceeds 60 mm Hg. Also, these systems improve venous return to near-normal levels and increase arterial blood flow by up to 33% in mixed venous-arterial disease.

View: Doppler sounds

Tip #4: Reverse the test sequence to avoid inconclusive ABIs.

The standard procedure for ABI testing is to obtain systolic pressures in bilateral brachial arteries first. But you can save time by first obtaining systolic pressure for the leg(s) that will be treated. This allows you to avoid procedures that would end up being inconclusive.
First, palpate for pulses to locate the dorsalis pedis and posterior tibial arteries. With soft edema, let your fingertips gently sink into the tissue closer to the artery. Next, place the Doppler probe at an angle of 45 to 60 degrees toward arterial blood flow until you hear the strongest signal.
If you can’t auscultate either artery, you won’t be able to calculate ABI; abandon the test as inconclusive and refer the patient to a vascular lab or mobile diagnostic service. If you can find only one artery, use that for the test and continue the procedure. Ultimately, you’ll throw out the lower of the two ankle pressures (don’t use it to calculate ABI). Record systolic pressure; a result above 60 mm Hg correlates better with leg viability and safe compression levels than the ABI does.
Typically, atherosclerosis advances symmetrically in both arteries, but patients with diabetes commonly have segmental arterial disease, causing perfusion levels to vary in different parts of the foot. One artery may be occluded while the other isn’t. So if your patient has diabetes, assess systolic pressure in both arteries, and use the lower reading for your calculation. If you’re unable to auscultate pressure in one of the arteries, consider possible occlusion and refer the patient to a vascular lab for further testing.
In patients with diabetes, falsely elevated ABIs are common because of arterial-wall calcification. If you inflate the ankle BP cuff to 200 mm Hg and still hear arterial sounds, stop. Inflating the cuff beyond 200 mm Hg can cause plaques to dislodge from the arterial wall. Also, such inflation isn’t needed because it yields falsely elevated ABI results. Document the test as “inconclusive due to noncompressible vessels” and refer the patient to a vascular lab for further testing.
Note: Be sure to choose the right cuff size for each patient. (See Choosing the right cuff size by clicking the PDF icon above.)

View: ABI video

Tip #5: Save time by obtaining ABI correctly.

Using incorrect technique when obtaining ABI can result in inaccurate findings. (See Standard vs. incorrect ABI procedure by clicking the PDF icon above.)
Click to download an ABI policy and procedure. Scroll down to “Procedure Ankle Brachial Index (ABI) updated May 2012 (2.07 MB).”


Allison MA, Aboyans V, Granston T, McDermott MM, Kamineni A, et al. The relevance of different methods of calculating the ankle-brachial index: the multi-ethnic study of atherosclerosis. Am J Epidemiol. 2010;171(3):368-76.

American College of Cardiology Foundation; American Heart Association Task Force; Society for Cardiovascular Angiography and Interventions; Society of Interventional Radiology, Society for Vascular Medicine; Society for Vascular Surgery; Rooke TW, Hirsch AT, Misra S, Sidawy AN, Beckman JA, et al. 2011 ACCF/AHA focused update of the guideline for the management of patients with peripheral artery disease (updating the 2005 guideline). Vasc Med. 2011;16(6):452-76.

Caruana MF, Bradbury AW, Adam DJ. The validity, reliability, reproducibility and extended utility of ankle to brachial pressure index in current vascular surgical practice. Eur J Vasc Endovasc Surg. 2005;29(5):443-51.

Clemens MW, Attinger CE. Angiosomes and wound care in the diabetic foot. Foot Ankle Clin. 2010; 15(3):439-64.

French L. Community nurse use of Doppler ultrasound in leg ulcer assessment. Br J Community Nurs. 2005;10(9):S6, S8, S10, passim.

Johansson K, Behre CJ, Bergström G, Schmidt C. Ankle-brachial index should be measured in both the posterior and the anterior tibial arteries in studies of peripheral arterial disease. Angiology. 2010;61(8):780-3.

Kazmers A, Koski ME, Groehn H, Oust G, Meeker C, Bickford-Laub T, et al. Assessment of noninvasive lower extremity arterial testing versus pulse exam. Am Surg. 1996;62 (4):315-9.

Khan NA, Rahim SA, Anand SS, Simel DL, Panju A. Does the clinical examination predict lower extremity peripheral arterial disease? JAMA. 2006; 295(5):536-46.

Khan TH, Farooqui FA, Niazi K. Critical review of the ankle brachial index. Curr Cardiol Rev. 2008;4(2):101-6.

Kravos A, Bubnic-Sotosek K. Ankle-brachial index screening for peripheral artery disease in asymptomatic patients between 50 and 70 years of age. J Int Med Res. 2009;37(5):1611-9.

Mosti G, Iabichella ML, Partsch H. Compression therapy in mixed ulcers increases venous output and arterial perfusion. J Vasc Surg. 2012;55(1):122-8.

Mourad JJ, Cacoub P, Collet JP, Becker F, Pinel JF, et al; ELLIPSE scientific committee and study investigators. Screening of unrecognized peripheral arterial disease (PAD) using ankle-brachial index in high cardiovascular risk patients free from symptomatic PAD. J Vasc Surg. 2009;50(3):572-80.

Nicolaï SP, Kruidenier LM, Rouwet EV, Wetzels-Gulpers L, Rozeman CA, et al. Pocket Doppler and vascular laboratory equipment yield comparable results for ankle brachial index measurement. BMC Cardiovasc Disord. 2008;8:26.

Pearson T, Kukulka G, Ur Rahman Z. Ankle brachial index measurement in primary care setting: how long does it take? South Med J. 2009;102(11):1106-10.

Sihlangu D, Bliss J. Resting Doppler ankle brachial pressure index measurement: a literature review. Br J Community Nurs. 2012;17(7):318-20, 322-4.

WOCN Clinical Practice Wound Subcommittee, 2005. Ankle brachial index: quick reference guide for clinicians. J Wound Ostomy Continence Nurs. 2012;39
(2 Suppl):S21-9.

Robyn Bjork is a physical therapist, a certified wound specialist, and a certified lymphedema therapist. She is also chief executive officer of the International Lymphedema and Wound Care Training Institute, a clinical instructor, and an international podoconiosis specialist.

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