This course presents assessment and diagnosis of common chronic wounds of the lower extremity and differentiates common wound etiologies (includes simple wound documentation and assessment case examples).
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 (Majno, 1975). Scientific advances have provided modern man with a plethora of evidence-based wound treatment methodologies. It is interesting to note science has demonstrated effective employment 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 (Schultz et al., 2003; Leaper et al., 2012; Sibbald et al., 2014). However, throughout history and unfortunately in modern day healthcare, far too many approaches to wound care are also steeped in tradition rather than scientific evidence (Ayello, Baronoski & Salati, 2005; Cowan, 2009; Gillespie et al., 2014). This educational program is the first in a series on wound care, intended to provide the health care clinician a general overview of evidence-based wound care. We will start this series with a basic review of acute wound healing versus chronic wound healing and present a simple initial approach for differentiating and diagnosing common chronic wounds of the lower extremity.
Wounds are classified as either being partial thickness in nature (depth of injury only extends to 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). Most partial thickness wounds heal without scar tissue formation because they heal by re-epithelialization (Bryant & Nix 2012). 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) (Schultz et al., 2003; Bryant & Nix, 2012; Sussman & Bates-Jensen, 2012).
Full thickness wound healing takes place by one of three main mechanisms:
Wounds healing by primary intention tend to heal faster than wounds left open. 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 the 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 (McNichol & Doughty, 2016 –pg.31).
In an acute wound (such as when a teenager falls while skateboarding and causing 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 other describe four or more phases or steps, but the mechanisms are the same. Initially, after a full thickness injury, there is Hemostasis and the Inflammatory phase is initiated. Bleeding occurs and the coagulation pathway commences (aggregation of platelets, release of clotting factors, neutrophils, macrophages, and a host of chemical messengers to alert the body to stop the bleeding and begin the repair processes). Hemostasis is typically achieved within several minutes. The inflammatory phase typically lasts a few days. Next, 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 (Schultz et al., 2003; Bryant & Nix, 2012; Sussman & Bates-Jensen, 2012) to fill in the open defect of any full thickness wound. Enzymes such as 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. Finally, there is the Maturation phase (scar maturation), which occurs after the wound is actually closed (epithelialized), but the protein-rich extra cellular 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 80% of the tensile strength of the surrounding tissue (Baraonoski & Ayello, 2016). Therefore, once a full thickness scar has formed, it may always be considered a ‘weak link’ or vulnerable area in the body needing protection (Bryant & Nix, 2012), particularly from sun and pressure related damage. Scar tissue contains no melanocytes, thus requiring 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 (Bryant & Nix, 2012; Sussman & Bates-Jensen, 2012; McNichol & Doughty, 2016).
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 at 4 weeks, we would consider it a chronic wound. Likewise, a large surgical wound may take 6 weeks or more 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. The latter surgical wound 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 (Schultz et al., 2003; Leaper et al., 2012; Bryant & Nix, 2012; Sussman & Bates-Jensen, 2012; McNichol & Doughty, 2016). Current research demonstrates most chronic wounds tend to get “stuck” in the Inflammatory Phase of wound healing. High levels of MMPs (enzymes) and inflammatory cytokines and the presence of bacterial biofilms are common characteristics of chronic wounds (James et al., 2008; Phillips et al., 2010; Zhou et al., 2013; McNichol & Doughty, 2016). 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. Biofilms are typically polymicrobial colonies of bacterial organisms which produce their own polymeric (plastic-like) coating to protect the community of organisms. Biofilm colonies 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 are present in more than 60% of all chronic wounds (James et al., 2008; Phillips et al., 2010; Zhou et al., 2013). 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 (Dowd et al., 2008; James, et al, 2008; Phillips et al., 2010). In addition, research suggests topical wound products as well as systemic antibiotics may not be able to penetrate mature biofilm growth (James et al., 2008; Zhao et al., 2013). One of the most effective ways to eliminate biofilm is to physically remove it (sharp debridement for example). However, biofilm is not visible to the naked eye, making it difficult to detect or determine when it has been completely removed (Schultz, et al., 2003; Leaper et al., 2012; Wolcott et al, 2010; Wolcott & Dowd, 2011; Zhao et al., 2013).
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 treatment within 2 weeks, or the wound worsens, and the suspected wound etiology is being addressed, consider further evaluation of these factors that are strongly associated with impaired wound healing (Schultz et al., 2003; Bryant & Nix, 2012; Sussman and Bates-Jensen, 2012; Baranoski & Ayello, 2016).
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 2-4 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 and 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 address treatment, but even during assessment, the clinician’s mind should always consider these factors.
Reminder: This course will not delve into wound treatments, but rather will focus on tips for diagnosing common chronic wounds of the lower extremities and identifying common impediments to wound healing. Future courses will 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 of 6 weeks duration.|
Would you know where to start?
|Evaluate the patient’s chief complaint (wound on leg that is not healing). 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 longest axis length x widest width x straight depth at deepest point (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 pointing towards the head of the body and 6 o’clock pointing at the foot of the body - as a way to document exact location of particular features of the wound such as tunneling, undermining, etc. The wound bed characteristics should be noted with a description of the amount of healthy appearing as well as unhealthy appearing tissue (100% pale pink and rather dry). Drainage is documented as amount, color and odor (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. Note the duration/date of onset (6 weeks duration), and any reported known trauma (type of injury) and comorbid conditions (diabetes, hypertension, etc.). 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 lawn mower 2 months ago, but can’t really remember how the wound started. It is also important to remember to ask the patient about any pain related to the wound, and 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.). Also, document any allergies the patient has (McNichol & Doughty, 2016).|
|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). Certain animal bites may also warrant rabies vaccines and rabies immune globulin. See the Centers for Disease Control (CDC) website for more information.|
Assess and document all pertinent information including social and current dietary/nutritional information. Review important past medical history: any diabetes, hypertension, high cholesterol, or cardiac diagnoses? Peripheral arterial disease (PAD) is expected 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 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. 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.
Rheumatoid arthritis, Crohn’s disease, ulcerative colitis and other auto immune 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). 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 which may impair wound healing (Sussman & Bates-Jensen, 2012; McNichol & Doughty, 2016). 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). This is often overlooked despite the fact that adequate nutrition (especially protein and essential micronutrients and amino acids) is imperative for wound healing (Stechmiller & Cowan, 2007; Sussman & Bates-Jensen, 2012; Baranoski & Ayello, 2016; McNichol & Doughty, 2016).
Pertinent social information (literacy level, health insurance, smoker, place of residence, electricity, running water, 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. Other information to ascertain about the patient includes what treatments he/she has tried so far, their pain level in the wound, exacerbating or alleviating factors and any changes in the wound since wounding. Also, assess sensation and pain in the affected extremity, especially if the patient is a diabetic (Frykberg, 2002; Frykberg et al., 2006; McNichol & Doughty, 2016).
Physically assess the wound as described above as well as the surrounding skin and the extremity. 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 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. 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. Note any wound drainage color, amount and odor. ALWAYS assess pulses for any wound involving the extremities!! If there are no palpable pulses in the effected lower extremity, perform an Ankle Brachial Index (ABI) of both lower extremities. This is a quick screening assessment for arterial insufficiency (Bryant & Nix, 20012; McNichol & Doughty, 2016).
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.
Wounds that occur due to arterial insufficiency tend to be seen on the lower extremities over toes and ankle joints. 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). Please 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 an 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 less than 0.7 is strongly associated with lower extremity arterial disease (McNichol & Doughty, 2016, p.434). 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 (McNichols & Doughty, 2016).
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 includes: smoking, hypertension, obesity, diabetes mellitus, high blood cholesterol, physical inactivity, age over 50, African American ethnicity, history of stroke, heart disease or other vascular disease. Common symptoms of PAD include: A “crampy” type of leg/foot pain in the muscles (not joints) that is worse with walking (early symptom), rest pain when feet are elevated and improves when foot is in a dependent position (late effects of PAD disease), cooler skin temperature of lower extremities compared to the rest of the body, toe or foot wounds that do not heal, or gangrene of the toes/foot (Bryant & Nix, 2012; Sussman & Bates-Jensen, 2012; McNichol & Doughty, 2016).
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 which 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 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.
In 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 (Hogan, 2007; Bryant & Nix, 2012; Sussman & Bates-Jensen, 2012; McNichol & Doughty, 2016).
Venous insufficiency is caused by valvular incompetence (or blockages) of the lower extremity deep veins, decreasing the efficacy of the venous return portion of the circulatory system and allowing a pooling of fluid in the dependent lower extremities. Risk factors for venous insufficiency includes 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 (Bryant & Nix, 2012; Sussman & Bates-Jensen, 2012; Baraonoski & Ayello, 2016; McNichol & Doughty, 2016).
|Clinical Tip: Scientific literature suggests mixed venous and arterial disease occurs in at least 20% of all venous insufficiency cases (Bryant & Nix, 2012). 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).|
Data from the 2011 National Diabetes Fact Sheet indicate that 25.8 million individuals in the United States have diabetes (8.3% of the population). It is estimated that 7 million of this 25.8 million people are currently 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.
Diabetes is a group of diseases characterized by high levels glucose in the blood caused by abnormalities in insulin production and/or insulin action (2011 National Diabetes Fact Sheet). 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 poorer the diabetes control (blood sugars above normal) the more likely nerve damage will occur and cause some symptom (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. Approximately 20% of diabetics will develop a foot ulcer at some time during the course of their disease. The most common causes of foot ulcerations in diabetics are: peripheral neuropathy, minor trauma and foot deformities (Frykberg, 2002). More than 60% of non-traumatic amputations in the US occur in diabetics, which accounted for over 65,700 of the non-traumatic amputations in 2006 (2011 National Diabetes Fact Sheet). 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%.”
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. 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 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 (Smieja et al., 1999). Smieja 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. 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 (McNichols & Doughty, 2016; Sussman & Bates-Jensen, 2012).
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 (Clinical Practice Guidelines for the Prevention and Management of Diabetes Foot Complications, Saskatchewan Ministry of Health, February 6, 2008).
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 hammer toes (contracture of the 2nd, 3rd, 4th, or 5th toes). Because diabetics often have co morbid micro-vascular changes, arterial insufficiency may also occur in conjunction with peripheral neuropathy. Adequate blood flow is necessary for optimal wound healing, therefore, assessing tissue perfusion as well as sensation of the feet is imperative to determine most significant wound etiology and develop appropriate treatment plans.
|Tips to help you differentiate the probable etiology of lower extremity wounds are available on the WOCN website (Fact Sheets on arterial insufficiency, venous insufficiency, and peripheral neuropathic wounds).|
The history and physical assessment of Mr. Jones reveals he has a history of diabetes, hypertension, and high cholesterol. He is on standard medication for all of these conditions. He denies taking over the counter medications recently (such as NSAIDS). He reports having a good appetite and eating 3 meals per day plus 2 small snacks. He states he has a high school education, his wife is his caregiver, but he drives himself to his health care visits. His most recent glycosylated hemoglobin (hemoglobin A1c) was 6.5% two weeks 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.
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 (plantar aspect of the big toe, 3rd metatarsal, and 5th metatarsal) in 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 touch points, 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 (McNichol and Doughty, 2016).
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 rather dry. Drainage is scant amount of clear yellow fluid with no remarkable odor. The surrounding skin is clear and intact. 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. 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 an arterial insufficiency etiology. However, it is likely complicated by his diabetes. 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. (Percival et al., 2012; Gardner et al., 2013; Scales, 2013; Zhao et al., 2013; McNichols & Doughty, 2016).
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.
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. She is overweight with a BMI of 35 and a history of hypertension and hypothyroidism (taking a thyroid replacement medication). Other than hypertension (well controlled), she has no known history of cardiovascular disease or congestive heart failure (CHF). 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. Bilateral pulses of her lower extremities are all 3+ and equal. Capillary refill is < 3 seconds in all toes. 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. 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 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. She denied fever, chills or severe pain (she reports her pain level is a dull “aching pain” about a “2” on a scale of 1 to 10), but feels better when her legs are elevated.
Given the above clinical information, Mrs. Smith’s wound is likely a venous leg ulcer due to venous insufficiency.
This concludes a basic 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 unusual etiologies may be discussed in future wound modules.
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