Greater than or equal to 90% of participants will identify key differences between acute and chronic wound healing, discuss common impediments to normal wound healing, and describe a T-I-M-E-S evidence-based approach to manage chronic wounds of the lower extremity.
After completing this course, the participant will be able to:
Wounds have been occurring for thousands of years. The ancient Babylonians, Sumatrans, Egyptians and Chinese (from 2600 b.c. to 1500 b.c.) described several types of wounds and common treatments that included “lint” (some kind of plant fiber), oil, grease, animal fat, honey, resins, and/or wine.1 Scientific advances have provided modern man with a plethora of evidence-based wound treatment methodologies. While technology has vastly improved medical treatment, science has also demonstrated the effectiveness of similar wound care principles as were used over 2000 years ago: keep the wound clean, keep the wound bed moist, and protect the wound from infection.2-4 However, throughout history and unfortunately in modern-day healthcare, far too many approaches to wound care are steeped in tradition rather than scientific evidence.5-7 This educational course is intended to provide the health care clinician a general overview of evidence-based wound care utilizing a focus on lower extremity wounds. This course is a basic review of acute wound healing versus chronic wound healing and a simple initial approach for differentiating and diagnosing common chronic wounds of the lower extremity.
Wounds are classified by the depth of the wound as either partial thickness in nature (depth of injury only involves the epidermis and sometimes the dermis but not beyond the subcutaneous tissue) or full thickness in nature (damaged tissue which extends down thru the epidermis, dermis, and involves at least some subcutaneous tissue, muscle, tendon or bone.8 Most partial thickness wounds heal without scar tissue formation because they heal by re-epithelialization.9,10 A superficial epidermal tissue loss is experienced and this epidermal skin is regenerated by cells readily available at the surface of the skin or within hair follicles (mainly keratinocytes). These partial thickness wounds heal faster than full thickness wounds, which involve greater tissue loss and more extensive cellular damage (requiring more complex mechanisms of repair, with many more cell types and chemical messengers involved in the process to coordinate the healing efforts within the wound bed).2, 9-12
Full thickness wound healing takes place by one of three main mechanisms9, 11-15:
Wounds healing by primary intention tend to heal faster than wounds left open to heal by secondary intention. They may heal as fast as partial thickness wounds because the wound edges have been approximated, and the body does not have to build or produce as much new tissue or extracellular matrix (scaffolding) or granulation tissue, necessary for scar tissue formation. Since the body is basically repairing a defect similar to sewing together a torn garment, it takes less resources than having to manufacture a patch and fill in the hole and hold it all together.15-17
In an acute wound (such as when a teenager falls while skateboarding, causing a small amount of full thickness tissue loss), the pathway to healing is expected to follow progressive phases of wound healing. Some scientists have described three phases or steps, and others describe four or more overlapping phases or steps, but the mechanisms are the same.
Initially, after a full thickness injury, there is hemostasis and the inflammatory phase is initiated. Immediately after injury, bleeding occurs and the coagulation pathway commences (aggregation of platelets, the release of clotting factors, neutrophils, macrophages, and a host of chemical messengers to alert the body to stop the bleeding). Hemostasis is typically achieved within several minutes. At the same time the body completing hemostasis, it is also sending immune cells such as neutrophils, monocytes which may convert to macrophages, other cells (fibroblasts), proteinases (enzymes), and chemical messengers, to the area to clear invading pathogens and debris and begin the repair processes. The inflammatory phase typically lasts a few days.
The next overlapping phase is the proliferative phase. As the expected pathways to healing occur, cytokines (chemical messengers) alert fibroblasts and other cells to produce growth factors and build new capillaries (neoangiogenesis) and connective or “granulation” tissue largely made of collagen to fill in the open defect of any full thickness wound.2, 9-11, 16, 18 Enzymes such as more than 15 types of matrix metalloproteinases (MMPs), secreted by fibroblasts, epithelial cells, neutrophils and macrophages play a major role during the inflammatory and proliferative phases, breaking down damaged proteins (such as collagen) and debris. Epithelial cells (particularly keratinocytes) are very active during the proliferative phase, helping to make the wound smaller and smaller (“contracting” the wound edges). The proliferative phase typically lasts a few weeks.10
Finally, there is the maturation phase (scar maturation), which occurs after the wound is actually closed (epithelialized), but the protein-rich extracellular matrix (ECM) or new tissue “scaffolding” within the scar tissue is continuously being broken down and replaced with stronger scar tissue. This ‘scar tissue’ is comprised of various types of collagen (our bodies produce more than 10 types of collagen for this purpose), elastin, laminin, etc. This phase can take up to 18 months or longer. It is important to remember that even after the scar maturation phase has concluded, the maximum tensile strength of the scar tissue of full thickness wounds only reaches 70-80% of the tensile strength of the surrounding tissue.10, 19, 20 Therefore, once a full thickness scar has formed, it may always be considered a ‘weak link’ or vulnerable area in the body, needing protection, particularly from sun and pressure-related damage.9 Scar tissue contains no melanocytes, so the scar will require sunblock for protection against the sun’s rays on any exposed body part. Likewise, scars over boney prominences will require additional protection against pressure-related injury for the rest of the individual’s life. These two realities are often overlooked by health care providers, caregivers, and patients, but should be incorporated into lifelong health promotion education for all applicable individuals.
In the past, clinicians have attempted to assign a specific timeframe for classifying an acute wound versus a chronic wound. Many clinicians have mistakenly thought that any wound which heals within 6 weeks is an acute wound, and any wound that takes 6 weeks or more to close is a chronic wound. That classification of acute versus chronic wound is no longer supported by the scientific literature.9-11, 17, 20
An acute wound that follows the expected pathway to healing may close within 2 weeks (such as the 16-year-old skateboarder’s knee abrasion). However, if this wound was not improved in a few weeks after wounding, we would consider it a chronic wound. Likewise, a large surgical wound may take more than 6 weeks to heal (example: a 15cm long by 10cm wide by 3 cm deep abdominal surgical wound that was left open to heal by secondary intention). As long as it continues to improve (get smaller) as expected without any signs of infection or complication, it would be considered an acute healing wound. This surgical wound described in the example could certainly be considered a complex wound because of its size and nature, but if it progresses through the phases of healing as expected, it could also be considered an ‘acute’ wound.
A chronic wound, on the other hand, is a wound that does NOT follow the expected pathway to healing.2, 3, 9-11, 16, 17, 20 Current research demonstrates most chronic wounds tend to get “stuck” in the Inflammatory Phase of wound healing.12, 20 High levels of MMPs (enzymes) and inflammatory cytokines and the presence of bacterial biofilms are common characteristics of chronic wounds.12, 17, 20-22 High levels of enzymes and pro-inflammatory cytokines in wounds are detrimental because they continue to break down new tissue and healthy cells before the wound bed has a chance to be repaired or “rebuild.” Bacterial biofilm also impairs wound healing.3, 20, 24 Biofilms are typically polymicrobial colonies of bacterial organisms that produce their own polymeric (plastic-like) coating to protect the community of organisms. Biofilms are felt to be responsible for 60-80% of infections in the human body.21,24 Biofilm colonies in wounds establish tightly adherent “footers” into the wound bed, which extend 2 to 3 mm beneath the surface of the wound bed and help secure the biofilm in place. Scientific literature demonstrates biofilm is present in more than 60% of all chronic wounds.21-23 Bacterial swab cultures may identify planktonic (free-floating) bacteria but may be unable to accurately identify the many types of bacterial (and fungal) organisms which symbiotically exist in a biofilm.21, 22, 24, 25 In addition, research suggests topical wound products, as well as systemic antibiotics, may not be able to penetrate mature biofilm growth.21, 23, 24, 26 One of the most effective ways to eliminate biofilm is to remove it physically (sharp debridement for example).26, 27 However, biofilm is not visible to the naked eye, making it difficult to detect or determine when it has been completely removed.2, 3, 23, 24, 27, 28
Other common impediments to wound healing include: inadequate nutrition (especially inadequate protein intake and vitamin/mineral deficiencies), smoking, decreased immune function, advanced age, diabetes, poor oxygenation or perfusion of tissues, lymphedema, infection, certain medications (chemotherapy agents, NSAIDS, immune modulators) and continued or repeated mechanical trauma (especially pressure/friction/shearing forces). If wounds do not respond well to evidence-based treatment within 2 weeks, or if the wound worsens, and the suspected wound etiology is being addressed, healthcare providers should consider further evaluation of:
In our previous example, the 16-year-old skateboarder’s knee is expected to heal in 2 to 3 weeks (if there are no confounding reasons why his/her wound healing should take longer). However, if the wound is not improved (or it worsens) within several weeks, it could be considered a chronic, complex, or recalcitrant wound, even though it may be rather small and is less than six weeks old. Another point to consider with all wounds, especially this skateboarder’s knee, is the depth and location of the wound. A simple abrasion may seem rather shallow, but if it occurs over joints or where the dermis and epidermis is very thin (shin), there may be joint capsule or bone involvement, which may severely complicate healing. Being mindful of these facts will help you to address wound healing more effectively. This course does not specifically address different forms of treatment or dressings for chronic wounds, but even during an assessment, the clinician’s mind should always consider these factors.
|Reminder: This course will not delve deeply into specific wound treatments, but rather will focus on tips for diagnosing common chronic wounds over the lower extremities and identifying common impediments to wound healing. Other CEUfast, Inc. courses review wound treatments and dressings as well as less common wounds.|
Mr. Jones is a 70-year-old male who is seen in the primary care clinic with a non-healing wound on his left lower leg that he reports having for about 2 months.
Would you know where to start?
Below is an example of one possible approach:
Evaluate the patient’s chief complaint (wound on the lower leg that is not healing). Note the duration/date of onset (2 months duration).
How did the patient say he got the wound (trauma, stepped on a dirty nail, animal or human bite, maybe the patient doesn’t know)? Mr. Jones says he thinks he must have hit the outer part of his leg on his lawnmower 2 months ago, but can’t really remember how the wound started. When considering possible etiologies, asking the patient how he thinks he got the wound as well as why he believes the wound is not healing is important (but realize the patient is not always correct about this). Other information to ascertain about the patient includes what treatments he/she has tried so far, and any changes in the wound since wounding.
Describe Past Medical History/Co-morbid Conditions and Physical Limitations
Review important past medical history: Co-morbid conditions can lead you to suspect certain etiological factors. Diabetes, hypertension, high cholesterol, or cardiac diagnoses? Peripheral arterial disease (PAD) is likely in patients with an existing diagnosis of coronary artery disease (CAD) or related risk factors (diabetes, smoking, high cholesterol, and hypertension). The distal blood vessels are the smallest, so it is logical that atherosclerotic arterial disease would first affect distal blood vessels before the involvement of the larger coronary arteries is obvious. Respiratory problems or pneumonia (as well as cardiovascular problems and anemia) are associated with potential wound oxygenation/perfusion issues. Rheumatoid arthritis, Crohn's disease, ulcerative colitis and other autoimmune diseases are associated with impaired wound healing and a higher incidence of pyoderma gangrenosum (an autoimmune disease typically causing chronic wounds especially of the lower extremities).
Physical limitations are important to note because neuropathies and arthritis in the hands could make dexterity an issue in the patient’s self-care of wounds.
Allergies may lead you to consider why treatment may not have been very successful so far, as well as what treatments to avoid in the future.
It is important to ask about (and document) the patient’s last tetanus shot, especially if it has been 10 years or more since the last tetanus vaccine or the wound was traumatic/dirty (stepped on a nail, hit lower leg on the lawnmower). Tetanus is a bacterial infection that is now rare (thanks to vaccination), but still very dangerous and there is no cure. Two out of every 10 people who get it will die. In the United States deaths attributed to tetanus have dropped by 99% since 1947, largely due to current CDC vaccination guidelines.
Clinical Tip: Be aware that certain injuries (especially outdoor puncture wounds) and animal bites have much higher incidence of serious infections. Particular types of bacteria are associated with particular animals or humans and cultures are recommended, but treatment may be started presumptively based on type of bite/injury. Individuals should be offered a Tetanus vaccine as soon as possible after injury, especially puncture wounds, but this also includes animal or insect bites (spider bites). In addition, certain animal bites may also warrant rabies vaccines and rabies immune globulin. See the Centers for Disease Control (CDC) website for more information.
Social and Dietary History
Assess and document all pertinent information, including social and current dietary/nutritional information. Pertinent social information (literacy level, health insurance, smoker, place of residence, electricity, running water, a caregiver at home, heavy alcohol or illegal drug use) are important to note and can influence the clinician’s diagnosis as well as treatment options and management approaches available to the clinician and the patient. Assess the current nutritional intake and dietary habits of the patient (3 meals per day versus 1 meal per day, portion size, types of food). Poor nutritional intake is often overlooked despite the fact that adequate nutrition (especially protein and essential micronutrients and amino acids) is imperative for wound healing.11, 17, 19, 29
Any medications the patient is taking (even over the counter medications) are also important to document. Corticosteroids and non-steroidal anti-inflammatory drugs (NSAIDs) are common medications that may impair wound healing.11, 17, 19
General Exam and Vital Signs
While a focused exam of the wound is reasonable if that is the main purpose for the patient’s visit, it is good to document general findings (especially general appearance, hygiene , skin lesions or rashes, edema) and vital signs (blood pressure, pulse, respiration, and temperature), height and weight (useful to calculate body mass index or BMI).
Assess the Wound
Document the location, size and characteristics of the wound (left lateral lower leg – you inspect it and note it is just above the malleolus/ankle). The wound size and characteristics should be noted as length x width x depth at deepest point in centimeters (cm) (for our case example: 2.0cm Length x 2.0cm Width x 0.4cm Depth at 6 o’clock). The clock face is visualized over the wound with 12 o’clock always pointing towards the head of the body and 6 o’clock pointing at the foot of the body - as a way to document the exact location of particular features of the wound such as tunneling, undermining, etc. When the wound is measured (Length in cm x Width in cm x Depth in cm), take care to note any tunneling or tracking in the wound bed (and where it tracks to if possible, for instance, if wound #1 tracks to/communicates via tunneling to wound #2) or any undermining present (a “lip” or “shelf” under unattached wound edges). Note the wound bed appearance for the presence of non-viable tissue and describe the color (white, grey, yellow, or black non-living tissue) versus healthy pink or red “granulating” tissue. List the amounts of these tissues in estimates of percentages covering the wound bed. Note any exposed bone, muscle, tendons or ligaments in the wound bed. Be careful not to confuse any exposed tendons or ligaments, which have a linear flat white or yellow appearance, as non-living tissue Drainage is documented as the amount, color and odor (for our case example: scant amount of clear yellow fluid with no remarkable odor). The location and appearance of the wound provides the clinician with important clues about the etiology or contributing factors to the wound. Physically assess the wound as described above as well as the surrounding skin and the whole extremity (for example, are there any rashes, lesions or other remarkable findings?).
Pain and Sensation
It is also important to remember to ask the patient about any pain related to the wound, and document their answers. What are relieving or aggravating factors (pain worse at night or when leg is elevated, or worse after all day on feet and better when elevated at night?) What is their pain level on a scale of 1 to 10, and what is the character of the pain (constant, intermittent, throbbing, etc.)?17 Also assess sensation and pain in the affected extremity, especially if the patient is a diabetic.17, 30, 31
Pulses: Check Dorsalis Pedis and Posterior Tibial Pulses
Always assess dorsalis pedis (DP) and posterior tibialis (PT) pulses for any wound involving the lower extremities! Check Popliteal pulses if warranted. In general, if there are strong DP and PT pulses (and capillary refill of the distal affected extremity appears normal/no other circulatory warning signs of arterial, venous or lymphatic insufficiency), they probably do not need further vascular evaluation by a specialist. However, if there are no palpable pulses in the affected lower extremity below the level of the wound, perform an Ankle Brachial Index (ABI) of both lower extremities. This is a quick screening assessment for arterial insufficiency.9,17, 32, 33 If this is difficult to obtain, consider referral for further vascular studies such as doppler arterial blood flow studies and/or transcutaneous oxygen tension (TcPO2) testing to the peri-wound skin (> 40 mmHg is desired) to determine adequate arterial blood supply and/or perfusion to the affected extremity/wound area.17, 32, 33
Clinical Tip: There is a very nice quick reference guide for clinicians on how to perform ABI assessment on the Wound, Ostomy, Continence Nurses (WOCN) Society website.
Peripheral arterial disease (PAD) affects more than 10 million people in the United States. Evidence-based clinical care guidelines strongly recommend all patients with lower extremity wounds be assessed for arterial disease (Level 1A evidence based on meta-analyses of multiple randomized controlled trials). Studies indicate that less than half of patients with PAD (7.5% to 33%) experience classic claudication symptoms (increasing pain in the affected lower extremity with walking exercise).34 Therefore, a diagnosis should not rest on this symptom alone. While venous insufficiency is the most common cause of lower extremity ulcers, mixed disease (both venous and arterial insufficiency) have been reported in up to 25% of patients with lower extremity ulcers.33-35
Wounds that occur due to arterial insufficiency tend to be seen on the lower extremities over toes and ankle joints (malleolus). The wound appearance for these arterial ulcers tends to be round with a “punched out” appearance. Wound beds for arterial ulcers tend to be pale and rather dry. The skin of the lower extremities in persons with arterial insufficiency is commonly rather thin with a shiny appearance and sparse hair growth. The patient may or may not demonstrate longer capillary refill times in the toe beds (over 3 seconds). The patient may demonstrate weaker pulses in the distal lower extremities (pedal and posterior tibial pulses).33-35Please Note: All patients with a wound on a lower extremity should have pulses evaluated in the most distal part of that extremity; any patient with absent or difficult to palpate pulses in the lower extremities, should have a doppler-derived ABI screening. ABI of less than 0.9 indicates some measure of arterial insufficiency. ABI over 1.2 is likely due to incompressible (atherosclerotic) vessels of the lower extremity (more common with diabetics and patients with existing CAD). If ABI results are suspected to be falsely elevated, toe pressures may be obtained instead (and calculate a toe brachial index or TBI). A TBI of less than 0.7 is strongly associated with lower extremity arterial disease.17 If the clinician does not have the equipment or expertise to perform an ABI or TBI, the patient should be referred to a vascular diagnostic laboratory. If ABI/TBI cannot be obtained, other non-invasive diagnostic studies which may be useful for determining arterial blood flow, tissue perfusion or severity of stenosis and occlusion include (but is not limited to) the following:
Other diagnostic procedures include Skin Perfusion Pressure, Pulse Volume Recordings, Magnetic Resonance Angiography, Computed Tomographic Angiography, Multidetector and Computed Tomographic Angiography.17
The primary cause of arterial insufficiency is atherosclerosis or arteriosclerotic vascular disease (“hardening of the arteries”) due to plaque buildup and damage to arterial walls. Risk factors associated with PAD include:
Common symptoms of PAD include9, 11, 17:
Chronic venous insufficiency (CVI) remains the most etiology of chronic wounds of the lower extremities, accounting for up to 80% of all leg ulcers. Although more commonly associated with older individuals, over 20% of VLU occur in those under 40 years old and almost 13% of venous leg ulcers (VLU) develop in people under 30 years old.36, 37 Leg ulcers due to CVI tend to be shallow, irregularly shaped, and indurated or erythematous and often have macerated wound edges and/or periwound skin surrounding the ulcer. These wounds tend to be on the lower extremities over the fleshy parts of the legs, usually in the area just above the ankle to about ¾ of the way to the level of the knee. This area of the lower leg is called the “gaiter” area because gaiters are protective clothing that covers the shoe and lower pants leg. In the early 19th century, someone who could not afford regular riding boots for riding horses used leather ‘gaiters’ to protect the ankles and the lower leg below the knee. The area of the lower leg about one handbreadth below the knee to just above the ankles may display darkly discolored skin pigmentation. This darkening of the gaiter area of the leg is called hemosiderin staining. This is due to the leaking of fluid from the blood vessels into the interstitial spaces of lower extremity tissues. Red blood cells die in the interstitial spaces and release hemoglobin (iron carrying component), which is engulfed by macrophages (white blood cells responsible for “clean up” in the body). The macrophages break down the hemoglobin and leave behind hemosiderin in the tissue spaces, which discolors the tissues. Other skin changes frequently associated with venous leg ulcers include eczematous changes, lipodermatosclerosis (thickening and hardening of the tissue), purpura (small purple spots usually 4 to 10 mm in diameter just beneath the skin or in the mucous membranes due to small blood vessels bursting), and atrophie blanche (white to ivory colored scarring of tissue typically due to healed ulcers or vascular inflammation associated with livedoid vasculopathy).35-37
In chronic venous insufficiency, one or both legs will typically demonstrate edema, usually “pitting” edema. Pitting edema indicates an increase of interstitial fluid trapped in tissues of the dependent extremities. With pitting edema, the skin will retain an indentation when pressure is applied by pressing down with your thumb (usually over the tibia). Pitting edema is usually documented with a ‘plus’ system, 1+ demonstrates an indentation of 2mm which rebounds quickly, 2+ demonstrates an indentation of 4mm which does not immediately rebound, 3+ demonstrates an indentation of 6mm which takes at least 10 seconds to rebound, and 4+ demonstrates an indentation of 8mm or more which takes more than 20 seconds to rebound.9, 11, 17, 19, 36, 37
Venous insufficiency is caused by valvular incompetencies (or blockages) of the lower extremity deep veins, decreasing the efficacy of the venous return portion of the circulatory system and allowing the pooling of fluid in the dependent lower extremities. Risk factors for venous insufficiency include obesity, pregnancy, previous pelvic or leg surgery, frequent and prolonged periods of standing or sitting, inactivity, older age, history of deep vein thrombosis (clot), and genetics. Typical symptoms of venous insufficiency include: swelling in the lower extremities below the knees, itching of the skin, dull aching or “heavy” feeling in the lower legs, and pain that gets worse when standing for long periods. In advanced cases, the skin of the lower extremities in the gaiter area may demonstrate hemosiderin staining and thickening and hardening of the tissue (lipodermatosclerosis). Edema and pain in the lower legs associated with venous insufficiency are usually improved when the legs are raised to heart level or higher for a period of time, or compression garments are utilized.9, 11, 17, 19, 37
Clinical Tips and Resources:
Scientific literature suggests mixed venous and arterial disease occurs in up to 25% of all venous insufficiency cases.9, 35 Arterial blood flow to lower extremities should be evaluated in all venous insufficiency cases (check pulses of both lower extremities, obtaining at least a screening ABI, toe pressures or Doppler studies if necessary).
Studies indicate lymphedema is often a contributing factor to lower extremity edema and lower extremity wounds and is often overlooked in venous insufficiency cases – this course will not specifically address lymphedema, please see the CEUfast, Inc. course on lymphedema.
Over 25.8 million individuals in the United States were reported to have diabetes in 2011 (8.3% of the population), and it was estimated that 7 million of these 25.8 million people were undiagnosed. An additional 79 million people may be classified as having “pre-diabetes” (blood sugars or HemaglobinA1c levels are elevated but not high enough to be diagnosed with diabetes), which increases their risk of developing type II diabetes, stroke and heart disease. It is estimated that almost 30% of individuals over the age of 65 years old have diabetes.38 More recently, it was estimated that 25% of all diabetics would develop a diabetic foot ulcer (DFU) in their lifetime. About 85% of all lower-extremity amputations in diabetics occur due to DFUs that become infected, and up to 70% of diabetic patients who have an amputation related to a DFU die within 5 years after the amputation.33
Diabetes is a group of diseases characterized by high levels of glucose in the blood caused by abnormalities in insulin production and/or insulin action. This abnormally elevated blood sugar causes many changes in the human body, particularly to the microvasculature and nerve damage. Over time, it is estimated that 60-70% of people with diabetes will develop some degree of nerve damage. This nerve damage can occur in almost every organ of the body. Often, this damage causes few noticeable symptoms, but if a person does develop symptoms, one of the most frequently seen is peripheral neuropathy. Symptoms of diabetic peripheral neuropathy (DPN) may be noticed as numbness or tingling in feet, legs, arms and/or hands. It may also cause burning or pain in the extremities. The longer an individual has the disease and the more inadequate the diabetes control (blood sugars above normal), the more likely nerve damage will occur and cause some symptoms (National Diabetes Information Clearinghouse, Publication #09-3185, February 2009). Impaired sensation to the feet occurs in 30% of diabetics who are 40 years old or older. This decreased sensation is the leading cause of foot ulcerations in diabetics which leads to non-traumatic amputations of the lower extremity. The most common causes of foot ulcerations in diabetics are peripheral neuropathy, ischemia, and minor trauma and foot deformities.30, 33
Prevention activities are paramount for all health care providers. The Centers for Disease Control and Prevention (2011) states, “Comprehensive foot care programs such as those that include risk assessment, foot-care education and preventive therapy, treatment of foot problems, and referral to specialists, can reduce amputation rates by 45% to 85%.” Preventive approaches include foot visual inspection (with socks removed, including the plantar aspect of both feet), assessment of lower extremity pulses, and screening for sensory changes of the lower extremities should be conducted at least annually but is recommended at every primary care and diabetes care visit.
The gold standard screening examination for diabetic peripheral neuropathy (DPN) is the Semmes Weinstein 5.07 gauge 10-gram monofilament examination.32, 39 This exam is performed by holding the monofilament against the skin of the foot (for one second) at a perpendicular angle and with only enough pressure to cause a slight bowing of the monofilament. Care must be taken not to apply the monofilament over callused skin, as callus areas do not have the sensation of normal skin. The patient keeps their eyes closed during the exam and tells the examiner when they feel the monofilament touching their skin. Originally, monofilament testing was intended to be done by touching 8 to 10 points on each foot. However, studies revealed a 4-touch-point-per-foot process (two toes and the first and third metatarsal heads) had 90% to 93% sensitivity and takes less than one minute to complete.39 Smeija et al. (1999) suggests, “Foot care providers with the time to perform a more complete examination may reasonably choose to do so.” Any failure to sense the monofilament indicates the patient is at risk of foot ulceration and amputation. Neurological examination for DPN may also include vibratory sensation with a 128-Hz tuning fork and cold-warm discrimination assessment. Preventive education and special protective footwear is critical for all diabetics, and especially for those who exhibit altered sensation to one or more areas of either foot.11, 17, 32, 33
When sensation in the feet changes over time, it may not be perceived by the diabetic, and they may obtain tighter fitting shoes because their old shoes do not feel snug anymore. They may not be able to sense areas of rubbing or mechanical irritation. If special protective footwear is not initiated for these individuals, they may experience blisters or alterations in skin integrity. Any alteration in skin integrity in a diabetic is dangerous, even small cracks in the heel from dry skin. In addition, diabetics with peripheral neuropathy are likely to experience multiple small fractures of the bones of the feet (many times without severe symptoms) and eventually develop a Charcot Foot deformity, where the foot significantly changes shape and is at great risk of eventual amputation. Any diabetic with sudden redness, swelling, warmth or pain and soreness in the foot should have an x-ray and prompt treatment of any fracture.32
To differentiate diabetic foot ulcers from venous or arterial ulcers, clinicians need to ascertain if there are any sensory changes to the foot/feet. Ulcers in diabetics tend to develop in areas of trauma or repeated mechanical irritation, cracks in the heels and callus formation, especially on the plantar aspect of the foot, large toe, 2nd and 5th metatarsal heads, bunion areas (hallux valgus of the 1st metatarsal head at the base of the big toe) and over any foot or toe deformity such as hammertoes (contracture of the 2nd, 3rd, 4th, or 5th toes). Because diabetics often have comorbid micro-vascular changes, arterial insufficiency may also occur in conjunction with peripheral neuropathy. Adequate blood flow is necessary for optimal wound healing; therefore, vascular assessment and evaluating tissue perfusion as well as sensation of the feet is imperative to determine the most significant wound etiology and develop appropriate treatment plans.33 Tissue perfusion in a foot with a DFU can be measured by toe pressure, Doppler ultrasound or transcutaneous oxygen tension (as mentioned above in the arterial insufficiency section). A toe pressure of < 50 mmHg in the foot with a DFU ulceration indicates severe limb ischemia. Similarly, in a foot with warm, pink skin, a capillary refill time of > 5 seconds or delayed discoloration may indicate poor arterial perfusion. Any diabetic patient with a DFU and any symptoms of limb ischemia should be referred immediately to vascular services since limb ischemia in a diabetic is limb-threatening and possibly life-threatening.32-33
Additional Clinical Resources:
The Wound, Ostomy, Continence Nurses’ Society (WOCN) published a nice “Venous, Arterial,and Neuropathic Lower-ExtremityWounds: Clinical Resource Guide” in 2017 to help differentiate between these potential etiologies of lower extremity wounds. It is available here.
Dr. Karen Zulkowski has published a quick guide to Wound Terms and Definitions which may also be helpful.
Venous (common characteristics may include):
Arterial (common characteristics may include):
Diabetic Neuropathic (common characteristics may include):
Atypical etiologies for non-healing lower extremity wounds are not discussed in this brief course but may include Pyoderma Gangrenosum, Vasculopathies, Allergic Dermatitis, Previous injury with retained foreign body, Insect bite, Parasitic involvement, or even Cancer (to name a few).
Chief Complaint: Wound on the lower leg that is not healing for 2 months duration.
Possible Etiologies and Current Treatments: He thinks he originally injured the area by accidentally hitting the edge of the lawnmower. He reports the wound at the time was dirty with grass clippings and the lawnmower is rusted at the edges. He reports he cleaned the wound immediately with lots of soap and water and then applied hydrogen peroxide. He does not think he had any retained foreign bodies from the lawnmower because he could not see any part of the lawnmower edge that may be missing. He reports washing it with tap water daily for the past 8 weeks and applying an over-the-counter non-stick pad, securing it with paper tape. He has not used anything else in the wound. He states it seemed better for 1-2 weeks but since then seems the same, “maybe with a little redness at the edges.”
Describe Past Medical History/Co-morbid Conditions and Physical Limitations
A review of the history and physical assessment of Mr. Jones reveals he has a history of diabetes, hypertension, and high cholesterol. His most recent labs (a basic metabolic panel and complete blood count 2 months ago) were all within normal limits, including his last glycosylated hemoglobin (hemoglobin A1c) which was 6.5% 2 months ago, indicating adequate glycemic control. The American Diabetes Association recommends diabetics maintain a hemoglobin A1c level of 6.5% to 7% to minimize complications of diabetes.
Allergies: Mr. Jones reports no known allergies.
Vaccination history: Mr. Jones's medical record indicates he is up to date on his immunizations including a Tetanus vaccination 5 years ago.
Social and dietary history: He states he has a high school education, his wife is his caregiver, but he drives himself to his health care visits. He reports both he and his wife have been changing his wound dressings daily. He reports having a good appetite and eating 3 meals per day with a hand-sized portion of protein at each of these meals plus 2 small snacks (usually a handful of almonds or 3 to 4 peanut butter crackers or wheat crackers and cheese).
Medications: He is on standard medication for his hypertension (an ACE inhibitor) and a statin for his high cholesterol and oral diabetes medication (a biguanide). He denies taking any over the counter medications recently (such as NSAIDs). He reports having taken these medications as ordered for over 2 years with no recent dosage changes.
General exam and vital signs: General impression is a 70-year-old male that appears his stated age. He is neatly dressed and his appearance suggests good daily hygiene. His skin is thin and somewhat dry, with leathery appearance to sun-exposed surfaces. His vital signs today are: Oral temperature 98.8 Fahrenheit, blood pressure (BP) is 128/70, radial pulse is 72 beats per minute, and respirations are 18 per minute and appear unlabored. His weight is 175 lbs and he is 5 foot 10 inches tall.
Wounds Assessment: Mr. Jones has a full thickness wound on his left lateral lower extremity just above the ankle, which measures 2.0cm Length x 2.0cm Width x 0.4cm Depth. The wound bed is 100% pale pink and slightly dry. Drainage is scant amount of clear yellow fluid with no remarkable odor. The surrounding skin is clear and intact, with slight erythema noted where the tape was securing the dressing to the surrounding skin. Furthermore, the wound is noted to have a “punched out” appearance. There is sparse hair growth noted on both lower legs and the general appearance of the skin on the lower extremities is taught and somewhat shiny. There is no noticeable edema. The skin of his feet and toes feels slightly cooler to touch than the rest of his body. Mr. Jones is also noted to have a hard callus over the plantar aspect of the 2nd metatarsal head on his left foot, but there is no open wound or drainage noted in this area.
Pain and Sensation: Mr. Jones also demonstrates decreased sensation in the plantar aspect of both feet. A 10 g Semmes Weinstein monofilament examination (SWME) of at least 3 points (the plantar aspect of the big toe, 3rd metatarsal, and 5th metatarsal) is used in diagnosing diabetic peripheral neuropathy (DPN). Some texts recommend 4 to 10 sites for this test on each foot (1st, 3rd, and 5th toes and metatarsal heads, medial and lateral foot, and dorsal surface between 2nd toe and great toe). This test has a positive predictive value of 87% to 100% (95%CI of 74% to 100%). Mr. Jones demonstrated decreased sensation in 2 out of four touchpoints, indicating he is at risk for diabetic foot ulcer and amputation and a need for protective footwear. Most diabetic foot ulcers occur on the plantar aspect of the feet, particularly over the metatarsal heads and heels. These are frequently (but not always) preceded by callus formation.17, 33 Mr. Jones reports wearing “work boots” at home most of the time and is wearing sneakers today.
Pulses: Capillary refill of his toes seems to be around 3 seconds or perhaps slightly more sluggish in the toes of the left foot. Both left and right pedal pulses and posterior tibial pulses are very weak and difficult to palpate (right is slightly stronger than left), and an ABI is performed which reveals ABI on left of 0.70 and ABI on right of 0.80. An ABI of <0.9 is indicative of mild arterial insufficiency; ABI of less than 0.8 is indicative of moderate arterial insufficiency, and an ABI of < 0.6 is indicative of severe arterial insufficiency (ischemia). If ABI results were over 1.2, one would expect it was a false high due to decreased elasticity of the blood vessels, which may occur in diabetics and with atherosclerotic changes. In that case, we would have considered transcutaneous oxygen tissue perfusion (TCPO2) tests (requiring expensive equipment) or simple toe pressures as the screening test of choice (toe systolic blood pressure of at least 40mm/hg would indicate adequate arterial blood flow to the lower extremity).
Given the above clinical information, Mr. Jones’ open full-thickness wound on his left lower leg just above the ankle is most likely a non-healing ulcer with some arterial insufficiency. However, it is also likely complicated by his diabetes and his wound care (see another CEUfast, Inc. wound course for evidence-based wound dressing selection tips). Diabetes affects sensory, motor and autonomic factors in the human body, which may impair wound healing. Sensory factors include hyperglycemia disrupting myelin sheaths (which protect nerves). This demyelination can slow down nerve conduction and impair sensory perception. Motor factors: Diabetes is also known to increase atrophy of the muscles of the foot and may cause contractures of the Achilles tendon and subluxation of metatarsophalangeal joints as well as results in foot deformities and gait abnormalities. With regards to Autonomic factors: Diabetes is associated with loss of some vasomotor control, impaired skin microvascular perfusion, bone flow hyperemia, and arterial-venous shunting which all may lead to anhidrosis, skin fissure formation, fungal skin and toenails, peripheral edema, callus formation, and Charcot formation. Other factors identified which may impair wound healing in diabetic foot ulcers may be related to the microbiome or bacterial load in the diabetic foot chronic wound.21-28,40 The fact that he has kept the wound bed mostly dry and just covered it with a non-stick pad daily may also have impaired wound healing (moist wound beds tend to improve faster than dry wound beds).2
Mr. Jones’ plantar callus indicates a diabetic neuropathic etiology and requires immediate preventive attention (off-loading shoes) before there is additional ulcer development in this area. If the open wound was on the plantar aspect of his foot, especially over a callused or insensate area such as a metatarsal head, the etiology would most likely be diabetic peripheral neuropathy. If the wound was over a toe in a diabetic, it could likely be a mixed etiology (both peripheral neuropathy and arterial insufficiency), unless a clear mode of injury could be established in a foot with strong pulses or good toe pressures but sensory impairment. Recommendations for Mr. Jones could include referral to a wound specialist, podiatrist, and/or vascular specialist. In the mean-time, reinforcing Mr. Jones has been doing very well at his medication and diet compliance, compliment him and his wife for trying to walk a mile 2-3 times per week. Studies indicate that progressive walking exercise may actually improve peripheral arterial circulation and claudication symptoms.41-42 Key components for any treatment plan for Mr. Jones should include addressing his arterial insufficiency and evaluating it further, addressing wound care principles and wound care education with the patient and his wife, asking him to record his fasting blood sugars daily for 2 weeks (diabetics may see a rise in their blood sugars as one of the first indicators of infection). Recommendations may also include repeating labs that will check his CBC (looking for anemia and any elevation of White Blood Cells), zinc and vitamin D levels (deficiencies may impair wound healing), and pre-albumin (pre-albumin is a serum biomarker of nutritional status) of < 20 may indicate higher risk of impaired healing and/or infection. 43
Chief Complaint: Mrs. Smith is a 68-year-old non-smoking female seen in urgent care for worsening edema of both legs and a large open wound on her right leg of 6 months duration.
Possible Etiologies and Current Treatments: Mrs. Smith reports she does not know what caused the wound. She denied any injury, and she reports it showed up on her right leg one day as about a quarter-sized sore but has gotten bigger. Her edema has gotten worse too. She states she has been wrapping gauze around her legs a few times a day and trying to stay off of her feet. She says she sits a lot at home with her legs under a desk, sewing.
Describe Past Medical History/Co-morbid Conditions and Physical Limitations: Mrs. Smith is overweight with a BMI of 35 and a history of hypertension and hypothyroidism. Other than hypertension (well controlled), she has no known history of cardiovascular disease or congestive heart failure (CHF). Mrs. Smith reports she has had “problems with swelling in my legs for a few years.” She says the swelling grows worse as the day progresses but is better when she first wakes up or keeps her legs elevated for several hours. She reports she has not been wearing her compression stockings, which her primary care health care provider ordered for her last year because she was not able to pull them on by herself any longer. She denied any recent fever, chills or severe pain.
Allergies: Allergic to bananas and possible latex allergy (gets a rash).
Vaccination History: Current vaccinations up to date except there is no record of recent tetanus vaccine within the past 10 years.
Social and Dietary History: Non-smoker, widow, lives alone with 2 cats. Reports eating 2 meals per day (tends to be heavy carbohydrates and low on protein) and frequent snacks (more carbohydrates like cookies and chips with occasional fruit).
Medications: Beta-blockers for hypertension, levothyroxine for hypothyroidism. Patient reports rarely missing any doses.
General Exam and Vital Signs: Overweight appearing female who looks slightly older than the stated age of 68 years. Walking with unsteady gait and slightly disheveled appearance with musty odor noted. Vital signs: Temperature is 98.6 degrees Fahrenheit, radial pulse is 88 beats per minute, blood pressure is 138/84, and respirations are 22 per minute. Height is 5 foot and 3 inches, Weight is 200 lbs.
Wound Assessment: The exam reveals a 5cm L x 4cm W x 0.2 cm D wound on the anterior-lateral aspect of her right lower leg above the ankle but below the knee in the gaiter area of the leg). The wound bed is 80% red/viable tissue and 20% scattered yellow, loose slough/non-viable tissue (resembles chicken fat). The skin around the wound is macerated (white edges from excessive moisture), and a moderate amount of clear/serous wound drainage is noted to have saturated the gauze wrap and dressing that was removed from the wound, which Mrs. Smith says has only been on the wound for a few hours. In addition, Mrs. Smith has 2+ pitting edema bilaterally, and the skin on her legs appears tight with a brownish discoloration noted (hemosiderin staining) to the skin just above the ankles to about one handbreadth below the knees bilaterally. The skin temperature of her feet and toes is warm but not warmer than the skin of the rest of her body, and no unusual erythema is noted in either lower extremity. She also reports that the wound on her lower right leg has been “weeping an awful lot,” so that she must change the bandages frequently/several times per day.
Pain and sensation: Mrs. Jones reports her pain level is a dull “aching pain” that worsens as the day progresses (currently about a “2” or “3” on a scale of 1 to 10), but she reports it feels better when her legs are elevated.
Pulses: Bilateral pulses of her lower extremities are all 3+ and equal. Capillary refill is <3 seconds in all toes.
Given the above clinical information, Mrs. Smith’s wound is likely a venous leg ulcer due to venous insufficiency. The gold standard treatment includes compression therapy, which the patient states have been ordered for her in the past. She may need to be re-measured for the correct size compression stockings (2 pair every 6 months is typical), and consideration for zippered stockings or some sort of device which may help her apply them herself could be helpful. A wound specialist consult could address these issues. Recommendations to be considered for Mrs. Smith also include (but are not limited to):
This concludes a fundamental overview of the 3 most common etiologies for lower extremity ulcers (diabetic neuropathy, venous insufficiency and arterial insufficiency). Other etiological considerations such as lymphedema, vasculitis, or atypical/unusual etiologies may be discussed in future wound modules.