KR, Jayakumar RV, et al. Foot care practice - the key to prevent diabetic foot ulcers in India. Foot (Edinb). 2012 Dec;22(4):298â302. 66. Takehara K, Amemiya A, ...
Diabetic Foot Ulcers and Peripheral Arterial Disease Clinical Education
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Table of Contents 1. Background........................................................................................................................Page 1 2. How Diabetic Foot Ulcers Develop.............................................................................Page 3 3. Managing & Assessing Neuropathy...........................................................................Page 4 4. Managing & Assessing Peripheral Artery Disease (PAD)..........................................Page 6 5. Preventing Diabetic Foot Ulcers.................................................................................Page 8
A. Lifestyle & Medications........................................................................................Page 8
B. Footcare..................................................................................................................Page 8
C. Education................................................................................................................Page 9
6. Assessing Diabetic Foot Ulcers.................................................................................Page 10
A. Wound Assessment........................................................................................Page 10
B. Staging............................................................................................................Page 11
C. Infections........................................................................................................Page 12
7. Managing Diabetic Foot Ulcers.................................................................................Page 14
A. Surgical Treatment Options...........................................................................Page 14
B. Debridement & Wound Cleansing.................................................................Page 14
C. Address any Infection.....................................................................................Page 15
D. Local Wound Management............................................................................Page 16
8. Re-evaluation............................................................................................................Page 19
A. Revascularization............................................................................................Page 20
B. Advanced Therapies........................................................................................Page 20
9. Tools for Clinicians.....................................................................................................Page 22
A. Diabetic Foot Ulcer Treatment Protocol Summary..........................................Page 22
B. Decision Tree Diabetic Foot Ulcers.....................................................................Page 26
C. Diabetic Foot Ulcer Treatment Procedure.........................................................Page 27
D. Diabetic Foot Ulcer Dressing Selection Guide..................................................Page 28
E. Printable Tools, Brochures, & Educational Websites........................................Page 30
10. References................................................................................................................Page 31
BACKGROUND Worldwide, 415 million people had diabetes in 2015; 75% of these live in low- and middleincome countries.1 Persons with diabetes tend to be of working age: 320.5 million people between the ages of 20 and 64, worldwide, have diabetes.1 Between 1980 and 2012 the number of adults in the USA diagnosed with diabetes increased from 5.5 million to 21 million, and it is estimated that another 8 million remained undiagnosed.1,2 Among adults in the USA, the lifetime risk of developing diabetes has increased to 40% as of 2014, and the risk is over 50% for Hispanics, Native Americans, and black women. 3 The prevalence of type 1 diabetes in young people has increased slowly over the years, and the prevalence of type 2 diabetes is increasing at an alarming rate, particularly among youth from minority groups.3 Common serious complications include kidney damage, blindness, heart disease, stroke, lower extremity amputations, and gum disease.3 By 2012, the estimated costs from diabetes-related loss of ability, premature death, and medical expenses in the USA was estimated at $245 billion per year.2
(David Adam Kess / Wikimedia Commons / Public Domain)
diabetes.4 Increased awareness, improved care, and control of risk factors led to a decrease in diabetes complication rates as well; in particular, between 1990 to 2010 amputations resulting from diabetic foot ulcers decreased by over 50%. 3 Diabetic foot ulcers (DFUs) are among the most debilitating complications of diabetes, and are the leading cause of hospitalizations for persons with diabetes.5 The International Working Group on the Diabetic Foot (IWGDF) defines a DFU as any full-thickness wound in a person with diabetes that is located below the level of the ankle. 5 Infected DFUs account for fully 20% of all diabetes-related hospital admissions in the USA.6 Each year about 5% of people with diabetes will develop a new foot ulcer, and over the course of their lifetimes, 15% of people with diabetes will suffer from a DFU.7–9 Two out of every three people with diabetic neuropathy whose foot ulcers close will suffer a recurrence.8 Studies consistently show that diabetic patients with foot ulcers are much more likely to die within 3 years than are those without foot ulcers.10
Intensive efforts to reverse this epidemic are succeeding. After decades of steadily increasing rates of newly diagnosed diabetes among adults in the USA, in 2009 the rate peaked at 1.7 million.4 Since then, the number of new cases has dropped annually; in 2014 only 1.4 million additional adults were diagnosed with GLOSSARY ABI = Ankle Brachial Index CBC = Complete Blood Count CHF = Congestive Heart Failure DFU = Diabetic Foot Ulcer DPP = Diabetes Prevention Program ESR or Sed Rate = Erythrocyte Sedimentation Rate HgbA1c = Hemoglobin A1c test, also called Glycated Hemoglobin NPWT = Negative Pressure Wound Therapy PAD = Peripheral Artery Disease SPEP = Serum Protein Electrophoresis TSH = Thyroid Stimulating Hormone WBC = White Blood Cells NOTE This integrated educational package summarizes the information and recommendations pertaining to the prevention and management of foot ulcers related to neuropathy and/or PAD, even in patients whose diagnoses do not include diabetes.
People with diabetes carry a 25 times greater risk of amputation than those without diabetes. 1 As many as 20% of DFU patients will require an amputation.11 If a DFU patient has one foot 1
amputated, the odds are 50:50 that the other foot will require amputation within 5 years.8 In 2010, 73,000 nontraumatic lower-limb amputations were performed in adults with diabetes in the USA; diabetes remains the leading cause of nontraumatic lower-limb amputations.2 The amputation was preceded by a DFU at least 85% of the time.12 The mortality rate of persons with diabetes five years after a major amputation has improved over the years, but it is still a sobering 50%.13
Not all lower extremity wounds in persons with diabetes are DFUs. If the wound is above the ankle, consult the WOCN’s Quick Reference Guide for Lower-Extremity Wounds: Venous, Arterial and Neuropathic to determine the appropriate diagnosis.18 Ferris® Mfg. Corp. offers Clinical Education materials similar to this one on topics such as Venous Ulcers, Pressure Ulcers, and Skin Tears.
Although diabetes is the primary cause of neuropathy (nerve damage) of the foot, other less common diseases which cause peripheral neuropathy lead to foot wounds with challenges similar to those of diabetes. Prevention and treatment of neuropathic foot ulcers is largely the same whether the neuropathy is caused by Hansen’s disease (leprosy) or diabetes.5,11,14
Patients and families are care plan team members
A multidisciplinary team approach to managing the whole patient with the DFU, rather than treating only the ulcer itself, improves outcomes.19,20 The most basic team consists of a general practitioner, a podiatrist, and a diabetic nurse, acting with mutual respect and understanding, with at least one member available to the patient at all times.20 Additional disciplines should be added as possible.20 One group found that relying upon a nurse to guide patients in consulting with the specialist doctors on the team based upon an intensive diabetic foot protocol can save money, decrease amputations, and improve patient quality of life.21 In 2012, the IWGDF observed, “Comprehensive foot care programs, i.e., 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%.”15 This educational information, protocol, procedure, and decision tree are all designed to facilitate preparation of educational materials for communities that include families, patients and staff in order to increase the implementation of evidence-based recommendations.
Peripheral arterial disease (PAD) is an increasingly common factor in DFUs.5 PAD can lead to ischemic ulcers from decreased blood supply, and it will make any DFU far more difficult to heal.5,15–17 It is estimated that 35% of DFUs are neuropathic, 15% are ischemic, and 50% are a combination of the two.5 This integrated educational package summarizes the information and recommendations pertaining to the prevention and management of foot ulcers related to neuropathy and/or PAD, even in patients who have not been diagnosed with diabetes. 2
HOW DIABETIC FOOT ULCERS DEVELOP DFUs are caused by direct injury, pressure gradually leading to tissue ischemia, or inflammation caused by repeated stress, any of which can allow infection to enter the foot.11 The microcirculatory system damage caused by high blood sugar in persons with diabetes damages the peripheral nerves, causing sensory, motor, and autonomic neuropathy.11,16 Autonomic neuropathy (damage to the Cracks and nerves that regulate the moisture and fissures temperature of the skin) may be the most important type of neuropathy, because it decreases sweating and causes severe dryness, increasing the vulnerability of the skin and leading to cracks and fissures.11 Autonomic neuropathy also impairs vascular flow and thermal regulation.16
can occur and develop into serious ulcers because the patient with neuropathy cannot feel the pain of injury or the pressure of overly tight shoes.12,15 Patients with neuropathy but no deformity are 1.7 times as likely as patients without neuropathy to develop a DFU.25 Patients with both neuropathy and deformity have a 12.1 times increased risk.25 Patients with Charcot deformity or a history of a previous DFU or amputation have a 36.1 times increased risk of developing a new DFU.25 Microcirculatory system damage from high blood sugar also causes PAD.11,16 PAD weakens the skin, making it more susceptible to breakdown.5 PAD can lead to a purely ischemic DFU.16 More frequently, PAD causes patients with neuropathy to be at higher risk for developing ulcers, and PAD causes DFUs to heal very poorly.12,16,26 Ultimately, skin breakdown occurs due to either acute trauma (usually punctures or shoe related damage) or inflammation.12,23
Patients may not notice the gradual onset of sensory neuropathy, which leads to a vulnerable insensate foot.11 Just as subtly, motor neuropathy gradually leads to deformity and an altered gait due to muscle changes and tightening of the ligaments and tendons in the lower extremities.15,16,20 Foot rigidity leads to increased pressure on areas of the foot that are not sufficiently padded.12 Rigid toe contractures, such as hammer toe, mallet toe, and claw toe can be caused by a combination of tightened muscles and poorly fitting shoes.12 These deformities can cause the toes to rub against shoes or the floor, resulting in a DFU. Motor neuropathy from diabetes is also the most common cause of a group of deformities Charcot foot called Charcot foot, the most serious of which is midfoot collapse, or “rockerbottom” foot.11 Foot deformities contribute to thinning of the fat pad under the metatarsal heads.22
Over half (56.3%) of all DFUs are located under the metatarsal heads.12 The dorsal (16.5%) and plantar (15.6%) aspects of the toes and between the toes (3.9%) are also common DFU sites.12 The plantar (2.9%) and dorsal (1.0%) aspects of a transmetatarsal amputation stump, the heel (1.9%), and the lateral or medial aspects of the foot (1.9%) are the remaining DFU locations.12 Toe ulcers tend to heal more quickly than midfoot ulcers, with heel ulcers taking the longest to close.27
The inflammation which accompanies these structural changes can cause ulceration.23 Ulcers can also form as a result of inflammation from pressure under ever-expanding callus, which forms at the site of abnormal mechanical loading of the foot from any deformities.12,15,16,20 Regular callus debridement can decrease pressure significantly.12,16 Offloading pressure areas can also decrease callus.24 Small traumatic injuries
Common locations of DFUs
3
MANAGING AND ASSESSING NEUROPATHY Surgeon Paul Brand, reflecting upon the many health challenges patients with neuropathy must confront, concluded, “Pain is God’s greatest gift to mankind” because pain is usually protective.11,14 Dr. Brand noted that any plantar ulcer patient who walks into the clinic without a limp has neuropathy, and he advocated for assessment of the shoes and socks, as well as the feet, of all persons with diabetes.14
glucose levels, 2 hour glucose tolerance tests, serum B12 levels, and SPEP are the preferred tests to determine the cause of peripheral neuropathy in a previously undiagnosed patient.33 Patients with impaired glucose tolerance may experience a reversal of their neuropathy and avoid developing diabetes if they adhere to a program of diet and exercise.33 The use of fibrates, even in patients without abnormal cholesterol levels, can also help prevent or even reduce symptoms of neuropathy.19,35,36 Long-term statin use (>2 years) significantly increases the risk of developing atypical peripheral neuropathy, which is sometimes reversible when statin use is discontinued.37,38 Prolonged metformin use often depletes vitamin B12 levels.39 Targeted correction of any deficiency in vitamin D or B12 can help prevent neuropathy.40 If the cause of the neuropathy is a low vitamin level, restoring B12 to normal may reverse some of the neuropathy and can arrest its progression.33,39
Although neuropathy causes patients to lose their ability to feel pressure, vibration, or an object that will cause a penetrating injury if stepped upon, it can also cause spontaneous burning, shock-like, or stabbing pain.14,28,29 Neuropathic pain can prevent patients from walking or even sleeping well, leading to weight gain and decreased control over blood sugar levels.29 Lowering blood sugar, blood pressure, and blood lipids can decrease this pain.28 Oral medications and topical treatments should be used to bring relief to patients with neuropathic pain, but they do not alter the underlying neuropathy.28–30 Antiseizure or antidepressant medications can be more effective than opioids for relieving neuropathic pain.31,32
At least once a year, two tests should be used to rule out peripheral neuropathy in all persons with diabetes.40 The 10-gram (5.07 gauge) Semmes-
Although diabetes (including prediabetes) is the most common cause of distal symmetric neuropathy, Hansen’s disease and Vitamin B12 deficiency are other causes which should be ruled out early on when uncertainty exists.33 Patients who present with neuropathy should undergo the inexpensive tests that are the most likely to yield a diagnosis first.33 Hansen’s Disease, which is found primarily in California, Florida, Hawaii, Louisiana, Massachusetts, New York and Texas, but is more often imported from developing countries, is easily diagnosed because it leads to characteristic skin lesions.34 An MRI or EMG is unwarranted until diabetes, prediabetes, and low vitamin B12 are excluded.33 Because prediabetes can cause reversible neuropathy, relying upon a HgbA1c within the normal range is unwise.33 Fasting glucose levels and glucose tolerance tests are more sensitive.33 Serum protein electrophoresis (SPEP) is mildly elevated early in diabetic neuropathy.33 Fasting 4
Weinstein monofilament test, which is the most widely accepted method of screening for diabetic peripheral neuropathy, should be one of these two tests.40 Research to determine the best method of performing this test resulted in the following guidelines:
least some peripheral neuropathy and aggressive measures to prevent foot ulcers should be implemented.17,20 The Ipswich Touch Test replaces the monofilament with lightly touching or resting an index finger on the tips of the first, third, and fifth toes for 1 – 2 seconds.45 This simple test has been adopted as an alternative to the Semmes-Weinstein monofilament test in the 2015 IWGDF guidelines.20 Studies show the Ipswich Touch Test is as effective in assessing for loss of sensation and it has the advantage of using only materials which are always readily available.20,45,46
1) The monofilament testing devices can be purchased for about $0.50 each,17 or can even be home-made from a 4 cm segment of Nylon 6 (homopolymer) or inexpensive 25# test monofilament fishing line with one cm held between the fingers.41,42 2) When screening large populations, use a new monofilament on each patient for infection control and to avoid filament fatigue, which occurs after about 100 consecutive compressions.43 Monofilaments regain their accuracy with rest, so the patient can keep their monofilament to test themselves.43
In addition to the monofilament or Ipswich Touch Test, measure vibratory sensation with a 128-Hz tuning fork or a biothesiometer, or test ankle reflexes with a percussion hammer.20,40 Apply the still tuning
3) Apply the monofilament to the patient’s arm or hand until it bends so that they can see what you will be doing and will understand that it will not hurt.15,17,20 4) With the patient’s head turned so that they cannot see, the monofilament is applied to each test site on the foot perpendicularly until it bends, and is left in place until the patient says “yes” (they sense the pressure).15,17,20 Up to a full second should be allowed for the patient to feel the monofilament.17,20 The monofilament should be applied at irregular time intervals with at least two “mock” tests in which no pressure is applied.17,20
fork to the patient’s wrist, then hit it and apply it again so that the patient knows that he is expected to sense the vibration.15,20 Then, with the patient’s eyes averted, apply the tuning fork perpendicular to the bony area on the top of the patient’s great toe with constant pressure.15,20 Repeat twice for each great toe, with at least one “mock” application in which the tuning fork is not vibrating.15,20 If the patient cannot reliably recognize when the tuning fork is vibrating, they have at least some level of neuropathy.15,20
5) Although ten sites on the foot have been identified for monofilament testing, because the more distal areas of the foot tend to lose sensation first, studies show that time can be saved without significantly decreasing accuracy by testing only three sites on each foot: The plantar aspect of the great toes, and the first or third and fifth metatarsal heads.15,17,20,44 Apply the monofilament beside, rather than on, any areas of callus, scar or ulceration.15,17,20
Patients who learn from these tests that they have peripheral neuropathy should be educated to understand that just as they were unable to feel the monofilament or tuning fork, they will also be unable to accurately feel objects in their environment which could harm them.
6) If the patient is unable to feel the monofilament at any one of the test sites, the patient has at 5
Summary of tests for patients who have or are at risk for neuropathy Test
Implication
fasting glucose or 2 hr glucose tolerance
Abnormally high value indicates diabetes or prediabetes. Neuropathy may be reversible and diabetes may be avoided if patients improve glucose tolerance through adherence to a diet and exercise program.
Serum B12 SPEP (Serum protein electrophoresis) 10 gram monofilament or Ipswich Touch Test Vibratory test OR ankle reflex testing with a percussion hammer
Abnormally low levels can cause neuropathy. The neuropathy may be at least partially reversible with supplemental oral B12. Mild elevation could indicate early diabetic neuropathy. If the patient is unable to feel the monofilament or finger at any one of three sites tested, at least some neuropathy is present. If the patient is unable to distinguish between a vibrating and a still instrument, at least some neuropathy is present. Diminished ankle reflexes indicate possible neuropathy.
MANAGING AND ASSESSING PERIPHERAL ARTERY DISEASE (PAD) Diabetes dramatically increases the risk of developing PAD.47 Every 1% increase in HgbA1c is associated with a 25% increased risk of PAD.16 PAD impairs the healing of DFUs.11,20,26 High blood sugar levels lead to vascular inflammation, which accelerates the process of plaque formation.47 High blood sugar also makes the platelets aggregate (clump) more easily and can cause plaque to become unstable, thus greatly increasing the risk of thrombi occluding blood vessels.47 Medial arterial calcification was found in 30% of patients with DFUs.26 As many as 41% of people with diabetes over 50 years old have PAD, but the classic symptoms of claudication (calf pain with exercise which is relieved by 10 minutes of rest) are rarely present.47,48 Absence of peripheral pulses is also an unreliable way to detect PAD in persons with diabetes.16,47,49 A tendency to walk slowly (less than 2 mph) is another sign of PAD.47 Dependent rubor (the lower leg blanches when elevated), hair loss on the legs/feet, and relatively cool feet are all physical signs of PAD.49 Purely ischemic ulcers tend to form on the tips of the toes and sides of the foot, rather than at the sites of callus or boney prominences.18,20
level.50 These patients are more likely to have nonhealing infected DFUs.50 In fact, renal failure is a major precursor of amputation.50 High blood sugars can also damage the microcirculatory system which feeds the retina, resulting in vision loss, which makes patients less able to assess their feet for the early signs of injury.3 Microvascular changes in persons with diabetes directly cause decreased skin elasticity so that the skin ulcerates more easily when exposed to normal wear and tear.5
Diabetes was the primary cause of renal failure in 44% of new cases in the USA in 2011.3 Patients with damage to the microcirculatory system in the kidneys will have a high serum creatinine
Prompt diagnoses of PAD can help decrease the prevalence of chronic DFUs and limb-threatening ischemia because patients can become more proactive in protecting their feet, improve
Recent studies show that persons with diabetes who do not have PAD already are less likely to develop it and are far less likely to have an amputation in the future if they control their blood sugars using insulinsensitizing medications such as metformin or a thiazolidinedione, rather than using insulinproviding medications such as sulfonylureas, repaglinide, nateglinide, or insulin itself.51
6
management of their diabetes, take appropriate medications regularly, and seek surgical remedies to improve circulation.47,48 Intermittent treadmill walking is highly recommended to control the progression of PAD.47 Supervised exercise 3 to 5 days a week outperforms surgical procedures for PAD, perhaps because it decreases inflammation.52
device.47,48 The patient should lie supine for 5 minutes prior to obtaining the ankle pressure readings.47 Place the cuff just above the ankle and listen for a pulse at the dorsalis pedis and posterior tibial arteries.47 Divide the pressures from each ankle by the higher of the two brachial systolic blood pressure readings.48 Up to a third of DFU patients may have calcified leg arteries.58 An ABI of > 1.30 suggests that arterial calcification is interfering with the test.20,47 These patients should be referred to a vascular lab for further evaluation.47 In patients with calcifications, a drop in ABI assessed one minute after 5 minutes of exercise such as treadmill walking at 2 mph indicates PAD.58 In contrast, the ABI of a normal individual will not change or may even rise slightly.58
In addition to an exercise regimen, patients with PAD and DFU should be encouraged to not smoke and should receive cholesterol-lowering medications, aspirin or another antiplatelet medication, and hypertension treatment as needed to keep their blood pressure less than 130/80.47,52 Fibrates and statins both reduce the risk of heart attacks for patients with diabetes and PAD and reduce the progression of existing PAD.10
PAD can also be detected by other noninvasive tests: toe pressure < 40 mm Hg and TcPO2 < 30 mm Hg are associated with poor wound healing.47 However, edema and infection can lower TcPO2 values in the absence of PAD.49 A monophasic Doppler signal indicates severe PAD, while a triphasic signal with an ABI between 0.90 and 1.30 rules out PAD.20,49 Arterial duplex ultrasonography will yield a triphasic waveform in normal patients, but not in patients with PAD.58 Angiography is appropriate only for planning surgery to correct PAD.58
A fibrate has also been found to dramatically reduce the incidence of diabetic retinopathy.53–55 Fibrates appear to be more effective for individuals over the age of 50, while statins are more effective for younger patients.56 Fibrates and statins are both recommended even for DFU patients with normal lipid levels because they increase tissue perfusion, promote ulcer healing, and lower amputation rates.10 Fibrates and statins appear to both improve PAD and have neuroprotective attributes. However, statin use leads to a 46% increase in the risk of developing diabetes, increased fasting blood sugar, and decreased insulin secretion and sensitivity.51 Fibrates, in contrast, lower both fasting glucose levels and insulin resistance while decreasing triglycerides and increasing HDL.56,57
If the ABI is 0.90 or less for either leg, the patient has significant obstruction from PAD.26,47,48,58 Refer patients with an ABI of less than 0.50 for possible revascularization surgery.20 An ABI of less than 0.40 indicates severe obstruction – the patient requires an immediate vascular consultation.47,58 Physical signs of critical limb ischemia (rest pain, tissue loss, gangrene) are also an indication of limb-threatening PAD, which should prompt an emergency vascular consult regardless of the ABI values because arterial calcification can lead to false-normal ABIs.47
At least every five years, vital signs for all persons with diabetes or prediabetes who are over 50 years of age should include an ABI, which is obtained using a Doppler (hand-held ultrasound) 7
PREVENTING DIABETIC FOOT ULCERS Amputation occurs as a result of multiple factors which build upon one another.5 DFUs can be prevented by preventing diabetes, preventing or correcting diabetic complications such as neuropathy and PAD, preventing injury to the foot, protecting feet that have boney changes as a result of neuropathy, and aggressively treating any infection.5 Regular podiatric visits for preventative care can help protect persons with diabetes from developing DFUs.11 Education and appropriate self-care can help people with diabetes stay healthy.2 Early response to hotspots (small areas of warmer skin), which are a measurable sign of inflammation, can often prevent significant DFUs as well.14,40,59,60
years) patients and in adults with a body mass index ≥35.61 The lifestyle interventions consisted of losing 7% of weight through healthy eating and engaging in exercise such as brisk walking 150 minutes each week.61 These diabetes prevention and delay methods (lifestyle or metformin intervention) are effective across racial and ethnic lines and can persist for at least 10 years.61 Controlled progressive increased number of daily steps does not lead to an increase in plantar DFUs.64 Therapeutic exercises can increase plantar range of motion, decrease peak pressures, and improve gait biomechanics in patients with neuropathy.64
Lifestyle and Medications
Persons with diabetes should be advised against walking barefoot, even indoors, because their diminished ability to feel objects as soon as their feet start to touch them makes them twice as likely as persons without diabetes to develop puncture injuries.12,20 Frequency of barefoot walking is correlated with DFU depth.65 41% of serious puncture wounds in persons with diabetes occur while the patient is not wearing shoes.12 Walking barefoot with insensate feet and wearing poorly-fitting shoes are the leading causes of DFUs.20
Foot Care
Improved glycemic control benefits people with either type 1 or type 2 diabetes. Nutritional therapy targets a HgbA1c < 7 to minimize complications from diabetes.40 In general, every percentage point drop in HgbA1c blood test results (e.g., from 8.0% to 7.0%)
Foot washing to prevent skin infections is a skill which must be taught, just as handwashing is taught.66 Feet should be washed regularly in warm water (body temperature) and carefully dried, paying particular attention to drying between the toes to prevent maceration.15,20 Toe spacers may help keep this area from staying too moist.40 Lubricating oils or lotions should be applied to dry skin, avoiding the areas between the toes.15,20 Urea-containing creams are proven to reduce the formation of callus and remove existing callus in persons with diabetes.67 Corns and calluses should be addressed by the trained health care provider rather than the patient.15 Toenails should be cut straight across to avoid ingrown nails.15 A health care professional should demonstrate how toenails should be cut.20 Many methods for warming the feet are unsafe for persons with neuropathy.15,20
can reduce the risk of microvascular complications (eye, kidney, and nerve diseases) by 40%.61 High blood glucose levels alter WBC function, leading to inflammation, which can cause DFUs, and infection, which become limb or life threatening.62 Elevated HgbA1c is associated with poor wound healing.62 Lifestyle interventions for diabetes are more costeffective than medications.3,63 The Diabetes Prevention Program (DPP) showed that a lifestyle intervention to lose weight and increase physical activity can reduce the development of type 2 diabetes by 58% during a 3-year period.61 The reduction was even greater (71%) among adults aged 60 years or older.61 Treatment with metformin reduced the risk of developing type 2 diabetes by 31% overall and was most effective in younger (aged 25–44 8
It is important for health care providers to thoroughly inspect the shoes and socks as well as the feet of persons with diabetes.12,15,20 Footwear which is damaged or ill-fitting can cause DFUs.12 Although most patients do not require expensive therapeutic shoes, if they have toe deformities, they need shoes with a large toebox.12 The inside of the shoe should be 1 – 2 cm longer than the foot.20 Some discount retailers are aware of this need and have committed to including inexpensive shoes with large toeboxes on their shelves. Patients with neuropathy must be taught how to fit themselves for shoes: shoes which fit well may feel uncomfortably lose to them because the shoes do not provide enough pressure to stimulate the nerve endings.12,68 Over-the-counter shoes can reduce pressure as well as some prescription shoes, but insoles (stock or prescription) may be a beneficial addition.12 Patients with significant foot deformities may require specially fitted footwear.15,20 The IWGDF 2015 recommends that foot deformities be managed with an orthosis, rather than surgery, whenever possible.20
or a temperature monitoring step-on pad. Temperature differences of greater than 4°F or 2°C are significant.23 Studies suggest that patients who respond to this information with rest and consultation with a health care provider are one-third as likely to develop a DFU as patients who do not check skin temperatures.14,40,59,60 All individuals with diabetes should have a thorough foot screening by a health care provider at least annually, even if they have not noticed symptoms.20 Patients with neuropathy should be screened every 6 months; those who also have PAD and/or a foot deformity should be screened every 3 – 6 months, and those with a history of a foot ulcer or amputation should be screened every 1 – 3 months.20 Screening should include questioning regarding any symptoms of neuropathy and PAD, previous education, barefoot walking, support systems, and medical history, as well as a physical examination including assessment of the skin, bones, and joint mobility of both feet, a thorough assessment for neuropathy and PAD (see previous discussion), and inspection of socks (inside and out) and all frequently worn shoes.20 Abundant callous, fungal infections, blisters, and ingrown or thickened nails warrant immediate intervention to prevent ulceration.20
Socks or stockings should be changed daily.15,20 Socks or stockings should not be constrictive and should not have seams.15,20 The cushioning provided by ordinary sports socks can decrease risk of ulceration.65 High-risk patients should inspect their feet daily, including between the toes, with the assistance of a mirror or another person as necessary.15 Interdigital fungal infections should be treated aggressively with antifungal powder.40 Any blister or break in the skin should be reported to the healthcare provider at once.15 Footwear and socks should be inspected for rough areas daily as well.15 Charcot foot presents with local redness, edema, bounding pulse, and significant 22 warmth. To prevent ulceration from acute Charcot foot, compression bandages are applied until the edema subsides, then the foot is immobilized with a non-weight-bearing cast for 3 – 4 months.22 Patients should compare the skin temperature on symmetrical sites of the soles of each foot to identify early signs of inflammation, or “hotspots.”14,40,59,60,69 Foot temperatures can be monitored with a thermometer
Education Structured, repeated education for patients and close family members by a member of the health care team helps prevent DFUs.20 Studies consistently show that brief one-on-one educational programs may improve specific behaviors, such as foot care, but do not influence DFU recurrence.70,71 Rather, motivation seems to be the key to improving health outcomes.65,72,73 Group education seems to provide increased motivation to change habits, particularly if some members of the group have previous experience with a DFU and discussion is encouraged.15,72,74 High-risk patients should receive ongoing group education and individualized podiatric care every 1 – 6 months.15,72 Primary care providers’ assessment of poor patient motivation and effort helps predict DFUs and amputations.73 Evidence is accumulating for the 9
use of formal Motivational Interviewing strategies to improve adherence in diabetes management.75
cessation education and counseling is imperative for DFU patients who smoke.40
Because PAD and neuropathy can result in impaired postural balance, patients with these two common complications of diabetes should receive balance training to slow the progression of disability.76 Smoking one cigarette decreases the local circulation 30% for an hour.77 Smoking places patients with neuropathy at such high risk of DFUs and amputation that smoking
Evaluation is an important component of an educational program, and should include knowledge of content, skills, and motivation.20 The team member who provides patient/family education should receive periodic continuing education to improve their skills.20 See appendix A for patient education materials, including methods of increasing patient motivation.
ASSESSING DIABETIC FOOT ULCERS Diagnosing diabetes, neuropathy, and PAD promptly • Type of tissue in the wound base as a percentage of the whole. helps prevent DFUs because these conditions are Note: Evaluating a tissue type by color alone treatable, and even when they cannot be eliminated, is overly simplistic: not all red wound tissue is precautions can be taken to prevent foot damage as a healthy granulation; structures such as tendons, result of these disabilities. joint capsule, and bone may appear yellow; etc. Wound Assessment
• Structures that are either visible or palpable (the
ability to probe to bone suggests osteomyelitis).
DFUs should be monitored by care providers with training in signs of improvement and deterioration at • Exudate (drainage) amount, consistency and type. Autolytic debridement should result in thin yellow each dressing change. At least weekly, DFUs should or tan exudate. be fully reassessed by a qualified health professional. The anatomic location of the ulcer will not change over • Odor strength and character (see Guide, Page 11). Note: all wounds have an odor, which is influenced time, but should be included as a reference point on by the type of dressing used, patient hygiene and every weekly assessment report. The weekly assessment presence of nonviable tissue. includes: • Anatomic location of the wound using the name
• Wound edges, or margins: presence of epibole
(closed or rolled edges) vs. attached to the wound bed, callus.
of the relevant boney prominence.
• Periwound (surrounding skin) condition – texture,
color, temperature, any rash.
• Wound pain assessed with a pain scale. Scales
with 0 – 10 should not be used to compare patients with one another, but are very useful in noting improvement or worsening of pain for a given patients.
No Pain
0
2
Analog Pain Scale
4
6
8
10 Worst Possible Pain
• Stage or Grade of the ulcer using Wagner or UT
System.
• Size, with the dimensions of the wound
in cm (length is longest initial dimension,width is perpendicular to length, depth at deepest point; tunneling (sinus tracts) and undermining length with position using a clock face as a reference.80 10
From: Hicks CL, von Baeyer CL, Spafford P, van Korlaar I, Goodenough B. Faces Pain Scale-Revised: Toward a Common Metric in Pediatric Pain Measurement. PAIN 2001; 93:173-183. With the instructions and translations as found on the website: www.iasp-pain.org/FPSR. This Faces Pain Scale-Revised has been reproduced with permission of the International Association for the Study of Pain® (IASP). The figure may NOT be reproduced for any other purpose without permission.
WOUND ASSESSMENT GUIDE Parameter
Definitions and Descriptors Pick-List
Location*
R or L – patient’s right or left foot + dorsal, plantar, or lateral surface + when applicable, boney prominence over which the ulcer formed (heel, malleolus, or specific metatarsal head or toe, numbered 1 - 5)
Grade/Stage*
Use UT Grading/Staging System 0 – III/Stage A - D (or Wagner Grading System 0 - 5)
Size
Length is the longest initial dimension and width is its longest perpendicular. Depth is the deepest point – measure with a cotton-tipped applicator, pinched at the depth of the skin. Using towards the head as 12 o’clock, record the position and depth of any undermining and tunneling. Measure depth using two side-by-side applicators: one inside and one outside
0
cm
1
(measure wounds in cm)
Tissue Type (as a percentage of the whole)
Necrotic (nonviable, devitalized tissue): is it loosely or firmly adherent? Eschar: Black, brown, tan; Hard, soft, boggy
Slough: White, yellow, tan, green; Soft, moist, stringy (fibrin), pulpy,mucoid
Clean avascular or nongranulating: pink or red, smooth without new growth
Blister (bullae)
Granulation: pink, red or dusky. May be friable (bleeds easily) or have pocketing (weak areas) Epithelialized: closed new skin where the wound once was: pink or white
Structures
Note any structures such as bone, muscle fascia, tendon, or joint capsule as visible or palpable
Exudate (Drainage)
Amount: none, scant, minimal, moderate, large,copious - How long was the dressing in place? Consistency: thick (common in infection), thin (typical of autolytic debridement), sticky, watery Type: serous (clear), serosanguineous (pink), bloody, purulent (yellow, tan, green)
Odor
Absent, faint, moderate, strong, sweet, foul – dressings, diet, and hygiene also influence odor
Edges
Margins attached and sloped (healthy), unattached (undermined), fibrotic (hard, hyperkeratotic), epibole (rolled – scar has closed off edge, which will prevent cell migration), scarred, callus
Periwound
Texture: moist, dry, scaled, boggy, crepitus, indurated (hard), macerated (swollen and wet), denuded (weepy), edematous (swollen: is it pitting?), intact (normal), good turgor, tenting Color: erythema (reddened), pale Temperature: (warm, cool, hot). If there is a rash, describe it
(Surrounding skin)
Pain
0 – 10: Use the pain scales provided. Try to record pain at rest (persistent pain), pain with activity, and pain during dressing changes (procedural pain)
* Location and Grade/Stage are the same throughout the treatment and are repeated to identify the ulcer. Wound assessments to include all parameters in red.
Staging
The IWGDF also advises against the use of the Wagner System.84 However, because some regulatory agencies require DFUs to be assessed using the Wagner staging system, both are included here.
A study in 2001 showed that the UT system of staging DFUs, which adds the dimension of grading the ulcers for ischemia or presence of infection, is a better predictor of wound healing than is the classic Wagner system, which simply stages the ulcer with respect to depth and severity.81 Unlike the Wagner system, the UT system has been validated in populations with diabetes.82 The UT grading system does not necessarily reflect the severity of the infection.83 A 2010 Consensus Panel recommends staging DFUs using the UT system, rather than the Wagner system.79
As the chart (on the next page) illustrates, the Wagner and UT Systems are comparable for Grades 0 and 1, with the UT System adding information about infection and ischemia. The UT System has only two additional Grades (II and III) based upon the structures penetrated. The Stage indicates the presence of ischemia and/or infection. The Wagner System defines four more Grades (2 – 5) based upon the depth, 11
University of Texas Diabetic Foot Classification Systemn System Stage
Grade 0
Grade 1
Grade II
Grade III
A
Intact skin: High risk for DFU, such as pre- or post-ulcer, deformity, inflamed pressure areas
Superficial wound
Wound penetrates to tendon Wound penetrates to or capsule bone or joint
B
+ Infection
+ Infection
+ Infection
+ Infection
C
+ Ischemia
+ Ischemia
+ Ischemia
+ Ischemia
D
+ Infection & Ischemia + Infection & Ischemia Wagner Grade 0: Same Wagner Grade criteria as UT System 1: Same criteria as UT System. May be uninfected or superficially infected
+ Infection & Ischemia
+ Infection & Ischemia Wagner Grade 2: ulcer extends through fat to structures, no osteomyelitis or abscess Wagner Grade 3: Deep ulcer with osteomyelitis, abscess, or joint sepsis, no gangrene Wagner Grade 4: Toe or forefoot gangrene only Wagner Grade 5: Add midfoot or hindfoot gangrene
Wagner Grading System for Diabetic Foot Infections location, and infection of the ulcer, but because infection and ischemia are not indicated individually, it does not make a distinction between life-threatening gas gangrene and relatively benign dry gangrene. For example, shallow dry stable eschar on the heel, which is usually a sign of ischemia, would be classified as Grade/Stage IC using the UT system, but under Wagner’s classification system it would be a Grade 5 ulcer. Ideally, neuropathy should be included in grading systems for DFUs, because neuropathy significantly impacts poor healing.85 An improved predictive model for DFU healing (The Wound Healing Index) is currently being refined.86
pain, or swelling), or secondary signs of infection such as foul odor, discolored or friable granulation tissue, or wound breakdown are present, the DFU is probably infected.16,20,78,79 Severe tissue infections and even osteomyelitis can be difficult to diagnose in persons with diabetes because neuropathy may mask the usual signs of inflammation.84 Suspect a severe infection if the patient presents with nausea, vomiting, chills, and/ or anorexia.83 Demetriou, et al. (2013), found that higher microbial load in DFUs correlated with higher platelet count and WBCs.88 Patients with severe diabetic foot infections can be identified as those having two or more of the following objective signs of metabolic instability or systemic signs of toxicity at initial assessment: temperature >38ºC or 90, respirations >20, systolic BP 12,000 or 200, serum urea nitrogen/creatinine ratio >20, or metabolic acidosis.83,89 Increased ESR (>70mm/h) and increased platelets with decreased serum albumin are also signs of severe infection or osteomyelitis.82,89,90 ESR > 90 is a predictor of amputation.90 Patients with low serum albumin levels are more likely to require a below-knee amputation.83,90 Obtaining an MRI is appropriate if an abscess or pockets of gas are suspected.78
Infections DFU patients with PAD and infection should be seen by a foot care specialist team within 24 hours because diabetic foot infections can be a medical emergency in the presence of ischemia.6,49 The most common diabetes-related reason for hospitalization and amputation is an infected DFU.87 However, one should not assume that all DFUs are infected.20,79 Risk factors for diabetic foot infection include a history of recurrent DFUs, DFU caused by trauma, previous lower limb amputation, renal insufficiency, peripheral vascular disease in the affected limb, walking barefoot, ulceration present for > 30 days, and a positive probeto-bone test.78 If purulent drainage, at least two principle signs of inflammation (redness, warmth,
Newer shallower DFUs tend to be colonized primarily with Staphylococci, while deeper, older wounds have 12
more bacterial diversity and usually include anaerobes and gram negative Proteobacteria.20,91,92 Patients with higher HgbA1c levels are more likely to have both Staphylococci and Streptococci in their wounds.91 A study in India, where more people with diabetes are found than in any other country, found that 75% of ulcers over one month old contained biofilms.92 This study also found that gram negative bacteria (E. coli and Pseudomonas) were common in chronic DFUs.92 Anaerobic organisms and organisms in biofilms are easier to detect now that molecular testing is becoming more widespread.91,92 Use molecular testing or obtain a culture using the Levine technique to confirm which pathogens are present in infected DFUs.16,40,79
does not improve despite 6 weeks of appropriate treatment.94 All infected DFUs should be assessed with the probe-to-bone test and if it is positive (bone feels gritty when touched with a sterile blunt metal probe), osteomyelitis is assumed to be present.16,78,94,95 An ESR > 70 provides additional support for the diagnosis.96 Osteomyelitis diagnosed with a positive probe-to-bone test need not be confirmed with a bone biopsy.97 However, a negative probe-to-bone test does not rule out osteomyelitis.96 The probe-to-bone test is less reliable on the lesser toes because tendons often cover bone.94 Radiographic findings are often inconclusive and are therefore not recommended, but an MRI can be very helpful for diagnosing osteomyelitis.16,78,89,93,96 When uncertainty persists, a bone biopsy can definitively diagnose osteomyelitis.96 The patient should be free of antibiotics for at least a few days and preferably two weeks prior to a bone biopsy being performed.89,93
Osteomyelitis is present in 10% of mildly infected DFUs and up to 60% of severely infected DFUs.89,93 Clinicians should be suspicious of osteomyelitis if a DFU has two signs of inflammation (redness, heat, pain, swelling, malodor, crepitus, loss of function) plus purulent exudate, bone fragments, a swollen toe with loss of contours (“sausage toe”), or if an exudating wound
Summary: Initial Visit with a Patient with Suspected DFU • Obtain a full medical and social history, medication review, dietary questionnaire, record of past diabetes management (if any), allergies, patient goals
• Assess for biomechanical and autonomic complications (foot deformities, callus, dry or cracked pedal skin, muscle wasting, altered gait, abnormal sweat function)78,79
• Vital signs should include height and weight, BMI
• Assess for venous insufficiency, CHF, or other sources of edema
• Complete head-to-toe physical assessment
• Ask the patient about how this DFU occurred and any previous DFU events, as well as previous DFU treatments and response. How has the wound affected activity and quality of life?
• Blood tests to assess glucose control, nutritional status, infection, kidney function, and risk of circulatory system complications (HgbA1c, CBC, Creatinine/BUN, prealbumin, 2 hour glucose tolerance test, serum B12 levels, SPEP, ESR, TSH, and lipid profile)78,79
• Describe the location, shape, edges, wound bed, wound base, periwound skin, exudate
• If infection is suspected, a wound culture (Levine technique or tissue biopsy) should be considered
• Measure size, sinus tracts, perform a probe to bone test on every ulcer
• Assess for arterial insufficiency (palpate pulses, evaluate ABI, check for a triphasic pulse via Doppler, check for dependent rubor, hair loss, capillary refill, foot temperature)
• Assess all patient pain (wound and other) – location, duration, quality, quantity (0 – 10 scale), antecedents, medications, coping mechanisms • Assist patients who smoke to enroll in a smoking cessation plan79
• Assess for neuropathy (three site 10-g monofilament test or Ipswich Touch Test and vibration perception with 128-Hz tuning fork or biothesiometer or reflexes)
13
MANAGING DIABETIC FOOT ULCERS The IWGDF recommends that DFU treatment include addressing any infection, revascularization as appropriate, offloading, and promoting healing through effective wound and wound bed management.20,98
mobility.101 Pain should be assessed and medication offered to patients with neuropathic pain or persistent wound pain.28,77,101 Surgical Treatment Options
Patients should be informed about the advantages and disadvantages of their treatment options so that they can be participants in planning their own care, in keeping with the ethos, “No decision about me without me.”99 Patient nonadherence is not patient failure, but rather, it is an indication that the patient did not adequately “buy in” to the plan of care.100 Therefore, the solution to non-adherence is more thorough teaching or a change in the plan.100 Quality of life decreases dramatically when the DFU patient is unable to stand or walk without assistance.101 This problem can be mitigated by limiting periods of immobility, offloading with the lowest possible negative effect on mobility, and obtaining physical therapy to improve
Revascularization surgery should be considered for DFU patients with toe pressure20, systolic BP 12,000 or 200, serum urea nitrogen/creatinine ratio >20, or metabolic acidosis. • Increased ESR (>70mm/h) and increased platelets with decreased serum albumin are also signs of severe infection or osteomyelitis. • When clinical signs of infection do not respond to treatment, osteomyelitis and joint infection should be ruled out. An MRI may be needed to visualize a deep abscess, gas pocket, or osteomyelitis. • If the probe-to-bone test is positive, osteomyelitis can be assumed. • DFU infections can usually be treated with 6 weeks of oral systemic antibiotics • Topical antimicrobials are not recommended for infected DFUs • Silver or iodine impregnated dressings may be useful for preventing, or even treating, mild DFU infections. Unlike most antimicrobial dressings, PolyMem Silver® is designed to kill microorganisms when pulled into contact with the silver locked in the dressings. V. Dressings: • Dressings should absorb excess exudate, fill dead space, maintain a moist wound environment, allow gaseous exchange, provide thermal insulation, protect the wound from contamination, and relieve pain. • PolyMem meets all of the ideal dressing criteria. • Dressings can be chosen using the accompanying Diabetic Foot Ulcer Dressing Selection Guide. • PolyMem dressings should be changed, at minimum, when the exudate visible through the clear semipermeable outer membrane reaches the approximate wound edge (this can be drawn on the top of the dressing). • PolyMem can enhance autolytic debridement. Changing the dressings more often is advisable while removing large quantities of slough. When PolyMem is used, dressing changes do not usually require additional wound bed cleansing or rinsing. 24
• Dry stable eschar (“dry gangrene”) in a patient whose PAD cannot be corrected should be kept clean, dry, and intact. Moisture-retentive dressings should not be used on these wounds. VI. Offloading • DFUs must be offloaded to prevent further injury to the wound area • If the patient is not ambulatory, float the ulcer area so that it does not come in contact with bedding • If the wound is on the lateral or dorsal foot or on a toe (other than the plantar aspect) offloading consists of providing soft PolyMem® dressings, cushioning socks, and appropriately-fitted shoes. • For plantar ulcers, apply a total contact cast or modify a removable cast walker so that it cannot be removed • A modified sandal may be substituted for a cast walker if the latter is unavailable • Offloading devices must be removed at least weekly for wound evaluation and dressing changes • Offloading devices should allow the patient to stand and walk without assistance; physical therapists should be a part of the patient treatment team to facilitate achieving this goal. VII. Pain Management: Wound pain usually includes persistent (background) pain, activity pain, and incident-related pain (from dressing changes or debridement). Patients with neuropathy can still have significant wound pain. New pain may indicate a developing infection. • Manage pain by eliminating the source (keep the wound moist, ensure that shoes fit well, etc.). • PolyMem dressings often reduce persistent wound pain dramatically because they can moderate the nociceptor response, which in turn reduces excess wound inflammation and edema. • Incident-related pain is reduced through the use of a non-adherent dressing, such as PolyMem. • Autolytic debridement is usually pain-free. PolyMem’s built-in wound cleansing system works with the body to support brisk autolytic debridement. • When local measures are not able to eliminate or control the source of pain, analgesics should be provided as needed. If opioids are used, patients should be given stool softeners as well. • Neuropathic pain often responds to antiseizure and antidepressant medications rather than opioids. VIII. Re-evaluation: • Evaluate changes in diabetic foot ulcer size, tissue type, exudate, odor, and pain weekly. • If the goal of care is healing and no progress has been made after 4 – 6 weeks of appropriate care, reassess the overall plan and look for subtle complications, such as a deep tissue infection, osteomyelitis, or elevated homocysteine. Use non-invasive imaging to assess for PAD. • Check to ensure that the patient is adhering to an effective method for offloading the wound • The evidence base for the use of advanced therapies for diabetic foot ulcers is poor. IX. Surgical Treatment Options: • Revascularization should be considered for patients who are ambulatory and are expected to survive for a year or more post-procedure • High risk patients may require endovascular procedures • Surgical interventions for foot deformities can sometimes facilitate DFU healing • A minor amputation should include correction of biomechanical abnormalities to avoid a new DFU • Major amputations should be reserved for medical emergencies and patients whose quality of life is likely to be improved with a prosthesis.
25
Decision Tree for Diabetic Foot Ulcers Incorporating PolyMem Dressings Initial Assessment •
Perform a complete health history and physical, following up on correctible deficits, such as (pre)diabetes and vitamin D or B12 deficiency, as outlined on page 22.
•
Provide guidance to patient to enroll in exercise, diet, and smoking cessation programs if indicated on pages 22 & 23.
•
Perform an initial wound assessment as outlined on pages 10 & 11.
•
Perform a complete pain assessment as outlined on pages 10 & 11. If peripheral arterial disease (PAD) is present: Consider statins to slow the progression of PAD
If neuropathy is present: Aggressively treat any (pre)diabetes Teach measures to prevent further foot trauma (page 8) Guide patient in the purchase of appropriate footwear Inspect shoes and socks at each visit
Assess if surgical interventions to improve circulation are suitable for this patient (pages 14 & 20)
Wound Management Are cellulitis, sepsis, abscesses, or gas pockets present?
This could be life threatening! Immediate thorough surgical debridement is indicated.
YES
NO Is the wound covered with dry stable eschar?
YES
NO
Leave dry stable eschar intact unless PAD is reversed. Try to keep the area dry. (If the eschar becomes moist and unstable, treat as an infected wound.)
Use appropriate PolyMem® dressings for autolytic debridement of wound bed. (See page 15). Initial cleansing should include irrigating at 4 – 15 psi with a surfactant-containing wound cleanser, saline, or clean water. Sharply debride callus if possible, otherwise, offload to remove callus. PolyMem’s continuous wound cleansing system usually meets all subsequent wound cleansing needs. Obvious loose wound bed debris can be removed at dressing changes. If cloth-backed or unbordered dressings are used, change PolyMem immediately after showering so that the dressings can protect the wound bed from soap and spray. Otherwise change dressings when exudate, visible through the outer backing, reaches the approximate wound edge. At least weekly, assess the wound at a dressing change. Is the wound infected (see pages 12-13)?
Provide 6 weeks of oral antibiotics (see pages 15-16) Use PolyMem Silver® Dressings
YES
NO
YES
Does the wound bed contain large quantities of slough?
Change PolyMem dressings frequently to clean wound bed more quickly
NO Is the wound on the plantar surface of the foot?
YES
Provide an appropriate offloading device (page 19)
NO Re-evaluate treatment 4-6 weeks. If no improvement, assess for homocysteine elevation (blood), osteomyelitits, and PAD (non-invasive imaging). Also assess for adherence and effectiveness of offloading device. If these measures do not result in improvement, surgical options must be considered (page 14).
26
27
Yes
28
Configurations of PolyMem Most Often Used on DFUs and Arterial Ulcers Products especially well suited for diabetic foot ulcer care: 5733
1814
1333
7203
Cavity, Undermining, Tunneling Rope Dressing 1814
0.4” x 14” (1cm x 35cm)
1022 1044 1077
3”x 3” (8cm x 8cm) 8” x 8” (20cm x 20cm) 1” x 3” (2.5cm x 7.6cm) 3”x 3” (8cm x 8cm) 8” x 8” (20cm x 20cm)
7203 7405 7606 7042 1766
5022 5033 5044
1”x 3”adhesive (2.5cm x 8cm) 1”x 1” pad (2.5cm x 2.5cm) 2”x 2” adhesive (5cm x 5cm) 1”x 1” pad (2.5cm x 2.5cm)
5035 5045 5088 1045 1088
4”x 5” adhesive (10cm x 13cm) 2”x 3” pad (5cm x 8cm) 6”x 6” adhesive (15cm x 15cm) 3.5”x 3.5” pad (9cm x 9cm) 2”x 4” adhesive (5cm x 10cm) 2”x 1.5” pad (5cm x 4cm) 6”x 6” adhesive (15cm x 15cm) 3.5”x 3.5” pad (9cm x 9cm)
2”x 2” adhesive (5cm x 5cm) 1”x 1” pad (2.5cm x 2.5cm) 405 4”x 5” adhesive (10cm x 13cm) 2”x 3” pad (5cm x 8cm) 0230 2.75” x 3” Adhesive (7cm x 7.6cm) 1.25” x 1.5” MAX pad (3.1cm x 3.8cm) 606 6”x 6” adhesive (15cm x 15cm) 3.5”x 3.5” MAX pad (9cm x 9cm)
(measured in circumference) 4401 4402 4403 4404 4405
Adhesive Oval-Shaped and Oval-Shaped Silver Film-Backed Dressings
1823 1853
3” x 3” (7.6cm x 7.6cm) 4.5”x 4.5” (11cm x 11cm) 8”x 8” (20cm x 20cm) 4”x 4” (10cm x 10cm) 8”x 8”(20cm x 20cm)
Finger/Toe Dressings
203
8053
1.8” x 1.8” (4.7cm x 4.7cm) 3”x 3” (8cm x 8cm) 4”x 4” (10cm x 10cm)
Non-Adhesive MAX and MAX Silver Pad Dressing
Adhesive Film-Backed Standard and MAX Dressings
8023
1.8”x 1.8” (4.7cm x 4.7cm) 4.25”x 4.25” (10.8cm x 10.8cm) 6.5”x 7.5” (17cm x 19cm)
Non-Adhesive Pad Dressing
Adhesive Cloth-Backed and Cloth-Backed Silver Dressings 7031
1404-1405
Non-Adhesive Silver Pad Dressing
WIC and WIC Silver Cavity Filler 5733 5788 1331 1333 1788
4401-4405
7405
1823
#1 small: 1.8”-2.2” (46.7mm - 57mm) #2 medium: 2.2” - 2.6” (57mm - 67.2mm) #3 large: 2.6” - 3” (67.2mm - 77.4mm) #4 Xlarge: 3” - 3.4” (77.4mm - 87.6mm) #5 XXL: 3.4” - 3.8” (87.6mm - 97.8mm) (measured in circumference)
2”x 3” 1”x 2” 5”x 3.5” 3”x 2”
adhesive (5cm x 7.6cm) pad (2.5cm x 5cm) adhesive (12.7cm x 8.8cm) pad (7.6cm x 5cm)
2”x 3” 1”x 2” 5”x 3.5” 3”x 2”
adhesive (5cm x 7.6cm) pad (2.5cm x 5cm) adhesive (12.7cm x 8.8cm) pad (7.6cm x 5cm)
29
1401 1402 1403 1404 1405
#1 small: 1.8”-2.2” (46.7mm - 57mm) #2 medium: 2.2” - 2.6” (57mm - 67.2mm) #3 large: 2.6” - 3” (67.2mm - 77.4mm) #4 Xlarge: 3” - 3.4” (77.4mm - 87.6mm) #5 XXL: 3.4” - 3.8” (87.6mm - 97.8mm)
Printable Tools, Brochures, and Educational Websites: For clinicians: 1) Wagner and University of Texas Wound Classification Systems of Diabetic Foot Ulcers http://www.medicalcriteria.com/site/en/criteria/49-diabetes/114-dbtfoot.html 2) Appropriate pain assessment http://www.iasp-pain.org/Education/Content.aspx?ItemNumber=1519 3) New on the horizon? http://jdfc.org/2012/volume-4-issue-1/a-new-classification-of-diabetic-foot-complications-a-simple-and-effectiveteaching-tool/ For patient teaching: 1) National Diabetes Education Program (NIH, USA) Downloadable PDF of Brochure Take Care of Your Feet for a Lifetime https://www.niddk.nih.gov/health-information/health-topics/Diabetes/take-care-feet/Pages/publicationdetail.aspx • Publications lists: http://ndep.nih.gov/resources/ResourceDetail.aspx?ResId=171 • Videos: http://ndep.nih.gov/resources/diabetes-healthsense/ 2) UpToDate website (Wolters Kluwer publishing) http://www.uptodate.com/contents/foot-care-in-diabetes-mellitus-beyond-the-basics 3) Johns Hopkins Patient Education http://www.hopkinsmedicine.org/gim/core_resources/Patient%20Handouts/ 4) ECare-Diabetes http://www.ecarediabetes.org/Tools/DiabetesEducation.cfm 5) Academy of Nutrition and Diabeties: Diabetics Care and Education Handouts https://www.dce.org/publications/education-handouts/#ed 6) Meta-analysis of studies about Brief Motivational Interviewing, with links to references http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1463134/ 7) More on Brief Motivational Interviewing http://spectrum.diabetesjournals.org/content/19/1/5.full http://www.ecarediabetes.org/Tools/MotivationalInterviewing.cfm (more links in Power Point Presentation) http://her.oxfordjournals.org/content/14/3/399.full
30
REFERENCES
14. Boulton AJM. Diabetic foot--what can we learn from leprosy? Legacy of Dr Paul W. Brand. Diabetes Metab Res Rev. 2012 Feb;28 Suppl 1:3–7.
1. The International Diabetes Federation. IDF Diabetes Atlas 7th Edition [Internet]. The International Diabetes Federation; 2015 [cited 2016 Feb 19]. Available from: http://www.diabetesatlas.org/
15. Bakker K, Apelqvist J, Schaper NC, International Working Group on Diabetic Foot Editorial Board. Practical guidelines on the management and prevention of the diabetic foot 2011. Diabetes Metab Res Rev. 2012 Feb;28 Suppl 1:225–31.
2. Centers for Disease Control and Prevention. National Diabetes Statistics Report: Estimates of Diabetes and Its Burden in the United States, 2014 [Internet]. Atlanta, GA: United States Department of Health and Human Services; 2014.
16. Thomas DR. Clinical management of diabetic ulcers. Clin Geriatr Med. 2013 May;29(2):433–41.
3. Centers for Disease Control and Prevention. Diabetes Report Card 2014 [Internet]. Atlanta, GA: Centers for Disease Control and Prevention, United States Department of Health and Human Services; 2015 [cited 2016 Feb 19]. 18 p. Available from: www.cdc.gov/diabetes/library/ reports/congress.html
17. Feng Y, Schlösser FJ, Sumpio BE. The Semmes Weinstein monofilament examination as a screening tool for diabetic peripheral neuropathy. Journal of Vascular Surgery. 2009 Sep;50(3):675–82.e1. 18. WOCN Wound Committee. A Quick Reference Guide for LowerExtremity Wounds: Venous, Arterial, and Neuropathic [Internet]. Wound, Ostomy and Continence Nurses Society; 2013.
4. Centers for Disease Control and Prevention. CDC - Number of New Cases - Incidence of Diabetes - Data & Trends - Diabetes DDT [Internet]. Annual Number (in Thousands) of New Cases of Diagnosed Diabetes Among Adults Aged 18-79 Years, United States, 1980-2014. [cited 2016 Feb 20]. Available from: http://www.cdc.gov/diabetes/statistics/ incidence/fig1.htm
19. Game F. The advantages and disadvantages of non-surgical management of the diabetic foot. Diabetes Metab Res Rev. 2008 Jun;24 Suppl 1:S72–5. 20. Schaper NC, Van Netten JJ, Apelqvist J, Lipsky BA, Bakker K, on behalf of the International Working Group on the Diabetic Foot (IWGDF). Prevention and management of foot problems in diabetes: a Summary guidance for daily practice 2015, based on the IWGDF Guidance Documents. Diabetes Metab Res Rev. 2016 Jan 1;32:7–15.
5. Armstrong DG, Cohen K, Courric S, Bharara M, Marston W. Diabetic foot ulcers and vascular insufficiency: our population has changed, but our methods have not. J Diabetes Sci Technol. 2011 Nov;5(6):1591–5. 6. Edmonds M. Body of knowledge around the diabetic foot and limb salvage. J Cardiovasc Surg (Torino). 2012 Oct;53(5):605–16.
21. Rerkasem K, Kosachunhanun N, Tongprasert S, Guntawongwan K. A multidisciplinary diabetic foot protocol at Chiang Mai University Hospital: cost and quality of life. Int J Low Extrem Wounds. 2009 Sep;8(3):153–6.
7. Margolis DJ, Malay DS, Hoffstad OJ, Leonard CE, MaCurdy T, de Nava KL, et al. Incidence of Diabetic Foot Ulcer and Lower Extremity Amputation Among Medicare Beneficiaries, 2006 to 2008: Data Points #2. In: Data Points Publication Series [Internet]. Rockville, MD: Agency for Healthcare Research and Quality (US); 2011 [cited 2013 Nov 11]. Available from: http://www.ncbi.nlm.nih.gov/books/NBK65149/
22. Driver VR, Landowski MA, Madsen JL. Neuropathic Wounds: The Diabetic Wound. In: Acute & Chronic Wounds: Current Management Concepts. 3rd ed. Elsevier Health Sciences; 2007. p. 307–36.
8. Rowe VL, Kaufman JL. Diabetic Ulcers. Medscape Reference [Internet]. 2013 May 17 [cited 2013 Nov 27]; Available from: http:// emedicine.medscape.com/article/460282-overview
23. Bharara M, Schoess J, Armstrong DG. Coming events cast their shadows before: detecting inflammation in the acute diabetic foot and the foot in remission. Diabetes Metab Res Rev. 2012 Feb;28 Suppl 1:15–20.
9. Edwards J, Stapley S. Debridement of diabetic foot ulcers. In: Cochrane Database of Systematic Reviews [Internet]. John Wiley & Sons, Ltd; 2010 [cited 2016 Feb 20]. Available from: http://onlinelibrary.wiley. com/doi/10.1002/14651858.CD003556.pub2/abstract
24. Melo M, McCullough J, Bernecker T, Hong J, Trumbauer J. A Pilot Study Investigating the Utilization of Crest Pads for Treatment of Toe Callus and Ulceration. Patient Care Services / Nursing [Internet]. 2015 Oct 30; Available from: http://scholarlyworks.lvhn.org/patient-careservices-nursing/529
10. Antonoglou C, Papanas N, Maltezos E. Lipid-lowering therapy in the diabetic foot: seeing the whole iceberg and not just the tip. Curr Vasc Pharmacol. 2012 Sep 24;
25. Maderal AD, Vivas AC, Zwick TG, Kirsner RS. Diabetic foot ulcers: evaluation and management. Hosp Pract (1995). 2012 Aug;40(3):102–15.
11. Malhotra S, Bello E, Kominsky S. Diabetic foot ulcerations: biomechanics, charcot foot, and total contact cast. Semin Vasc Surg. 2012 Jun;25(2):66–9.
26. Brechow A, Slesaczeck T, Münch D, Nanning T, Paetzold H, Schwanebeck U, et al. Improving major amputation rates in the multicomplex diabetic foot patient: focus on the severity of peripheral arterial disease. Ther Adv Endocrinol Metab. 2013 Jun;4(3):83–94.
12. Lavery LA, Peters EJG, Armstrong DG. What are the most effective interventions in preventing diabetic foot ulcers? Int Wound J. 2008 Jun;5(3):425–33.
27. Pickwell KM, Siersma VD, Kars M, Holstein PE, Schaper NC, Eurodiale consortium. Diabetic foot disease: impact of ulcer location on ulcer healing. Diabetes Metab Res Rev. 2013 Jul;29(5):377–83.
13. Icks A, Scheer M, Morbach S, Genz J, Haastert B, Giani G, et al. Time-Dependent Impact of Diabetes on Mortality in Patients After Major Lower Extremity Amputation Survival in a population-based 5-year cohort in Germany. Dia Care. 2011 Jun 1;34(6):1350–4.
28. Ko S-H, Cha B-Y. Diabetic peripheral neuropathy in type 2 diabetes mellitus in Korea. Diabetes Metab J. 2012 Feb;36(1):6–12. 29. Tesfaye S, Boulton AJM, Dickenson AH. Mechanisms and
31
management of diabetic painful distal symmetrical polyneuropathy. Diabetes Care. 2013 Sep;36(9):2456–65. 30. Campbell CM, Kipnes MS, Stouch BC, Brady KL, Kelly M, Schmidt WK, et al. Randomized control trial of topical clonidine for treatment of painful diabetic neuropathy. Pain. 2012 Sep;153(9):1815–23. 31. Fleck C. Wound Pain: Assessment and Management. Wound Care Canada. 2007;5(1):10–6,51. 32. Woo KY, Abbott LK, Librach L. Evidence-based approach to manage persistent wound-related pain. Curr Opin Support Palliat Care. 2013 Mar;7(1):86–94. 33. Callaghan B, McCammon R, Kerber K, Xu X, Langa KM, Feldman E. Tests and expenditures in the initial evaluation of peripheral neuropathy. Arch Intern Med. 2012 Jan 23;172(2):127–32. 34. Health Resources and Services Administration. Hansen’s Disease: Frquently Asked Questions [Internet]. United States Department of Health and Human Services; [cited 2016 Feb 20]. Available from: http://www. hrsa.gov/hansensdisease/pdfs/faq.pdf 35. Antonoglou C, Papanas N, Maltezos E. Lipid-lowering therapy in the diabetic foot: seeing the whole iceberg and not just the tip. Curr Vasc Pharmacol. 2014;12(5):745–50. 36. Othman A, Benghozi R, Alecu I, Wei Y, Niesor E, von Eckardstein A, et al. Fenofibrate lowers atypical sphingolipids in plasma of dyslipidemic patients: A novel approach for treating diabetic neuropathy? J Clin Lipidol. 2015 Aug;9(4):568–75. 37. Lei Q, Peng WN, You H, Hu ZP, Lu W. Statins in nervous systemassociated diseases: angels or devils? Pharmazie. 2014 Jun;69(6):448– 54. 38. Grover HS, Luthra S, Maroo S. Are statins really wonder drugs? Journal of the Formosan Medical Association. 2014 Dec 1;113(12):892–8.
diabetic foot. Wound Healing Southern Africa. 2015 Jun;8(1):17–30. 47. American Diabetes Association. Peripheral Arterial Disease in People With Diabetes. Dia Care. 2003 Dec 1;26(12):3333–41. 48. Hirsch AT, Criqui MH, Treat-Jacobson D, et al. Peripheral arterial disease detection, awareness, and treatment in primary care. JAMA. 2001 Sep 19;286(11):1317–24. 49. Schaper NC, Andros G, Apelqvist J, Bakker K, Lammer J, Lepantalo M, et al. Specific guidelines for the diagnosis and treatment of peripheral arterial disease in a patient with diabetes and ulceration of the foot 2011. Diabetes Metab Res Rev. 2012 Feb;28 Suppl 1:236–7. 50. Lee KM, Kim WH, Lee JH, Choi MSS. Risk factors of treatment failure in diabetic foot ulcer patients. Arch Plast Surg. 2013 Mar;40(2):123–8. 51. Cederberg H, Stančáková A, Yaluri N, Modi S, Kuusisto J, Laakso M. Increased risk of diabetes with statin treatment is associated with impaired insulin sensitivity and insulin secretion: a 6 year follow-up study of the METSIM cohort. Diabetologia. 2015 May;58(5):1109–17. 52. Hamburg NM, Balady GJ. Exercise rehabilitation in peripheral artery disease: functional impact and mechanisms of benefits. Circulation. 2011 Jan 4;123(1):87–97. 53. Sharma N, Ooi J-L, Ong J, Newman D. The use of fenofibrate in the management of patients with diabetic retinopathy: an evidence-based review. Aust Fam Physician. 2015 Jun;44(6):367–70. 54. Simó R, Ballarini S, Cunha-Vaz J, Ji L, Haller H, Zimmet P, et al. Non-traditional systemic treatments for diabetic retinopathy: an evidencebased review. Curr Med Chem. 2015;22(21):2580–9. 55. Frank RN. Diabetic Retinopathy and Systemic Factors. Middle East Afr J Ophthalmol. 2015;22(2):151–6.
39. Bell DSH. Metformin-induced vitamin B12 deficiency presenting as a peripheral neuropathy. South Med J. 2010 Mar;103(3):265–7.
56. Krysiak R, Gdula-Dymek A, Marek B, Okopień B. The effect of hypolipidemic treatment on monocyte cytokine release in different age groups of patients with type 2 diabetes and atherogenic dyslipidemia. Endokrynol Pol. 2016 Feb 17;
40. Crawford PE, Fields-Varnado M. Guideline for the management of wounds in patients with lower-extremity neuropathic disease: an executive summary. J Wound Ostomy Continence Nurs. 2013 Feb;40(1):34–45.
57. Feng X, Gao X, Jia Y, Zhang H, Pan Q, Yao Z, et al. PPAR; Agonist Fenofibrate Decreased Serum Irisin Levels in Type 2 Diabetes Patients with Hypertriglyceridemia, PPAR Research. 2015 Nov 26;2015, 2015:e924131.
41. Bourcier ME, Ullal J, Parson HK, Dublin CB, Witherspoon CAG, Ward SA, et al. Diabetic peripheral neuropathy: how reliable is a homemade 1-g monofilament for screening? J Fam Pract. 2006 Jun;55(6):505–8.
58. Begelman SM, Jaff MR. Noninvasive diagnostic strategies for peripheral arterial disease. Cleveland Clinic Journal of Medicine. 2006 Oct 1;73(Suppl 4):S22.
42. Parisi MCR, Giannella D, Fernandes TD, Rezende KF, Nery M. Diabetic foot screening: study of a 3000 times cheaper instrument. Clinics (Sao Paulo). 2011 Jun;66(6):1105–7.
59. Armstrong DG, Holtz-Neiderer K, Wendel C, Mohler MJ, Kimbriel HR, Lavery LA. Skin temperature monitoring reduces the risk for diabetic foot ulceration in high-risk patients. Am J Med. 2007 Dec;120(12):1042–6.
43. Spruce MC, Bowling FL. Diabetic foot screening: new technology versus 10g monofilament. Int J Low Extrem Wounds. 2012 Mar;11(1):43–8.
60. Lavery LA, Higgins KR, Lanctot DR, Constantinides GP, Zamorano RG, Athanasiou KA, et al. Preventing diabetic foot ulcer recurrence in high-risk patients: use of temperature monitoring as a self-assessment tool. Diabetes Care. 2007 Jan;30(1):14–20.
44. Lee S, Kim H, Choi S, Park Y, Kim Y, Cho B. Clinical usefulness of the two-site Semmes-Weinstein monofilament test for detecting diabetic peripheral neuropathy. J Korean Med Sci. 2003 Feb;18(1):103–7. 45. Rayman G, Vas PR, Baker N, Taylor, CG, Gooday C, Alder AI, et al. The Ipswich Touch Test. Diabetes Care. 2011 Jul;34(7):1517–8. 46. Naude L, Smart H, Tudhope L, van Rensburg GJ, Alexander H, AbdoolCarrim T, et al. WHASA consensus document on the management of the
61. Diabetes Prevention Program Research Group. Reduction in the incidence of Type 2 diabetes with lifestyle intervention or metformin. N Engl J Med. 2002 Feb 7;346(6):393–403. 62. Friedrich L, Collins N. Nutrition 411: the diabetic foot ulcer - can diet make a difference? Ostomy Wound Manage. 2013 Nov;59(11):10–2.
32
63. Centers for Disease Control and Prevention. National diabetes fact sheet: national estimates and general information on diabetes and prediabetes in the United States, 2011 [Internet]. Atlanta, GA: United States Department of Health and Human Services, Centers for Disease Control and Prevention; 2011 [cited 2016 Feb 20]. Available from: www. cdc.gov/diabetes/pubs/pdf/ndfs_2011.pdf
guideline for the diagnosis and treatment of diabetic foot infections. J Am Podiatr Med Assoc. 2013 Feb;103(1):2–7. 79. Snyder RJ, Kirsner RS, Warriner RA 3rd, Lavery LA, Hanft JR, Sheehan P. Consensus recommendations on advancing the standard of care for treating neuropathic foot ulcers in patients with diabetes. Ostomy Wound Manage. 2010 Apr;56(4 Suppl):S1–24.
64. Sacco ICN, Sartor CD. From treatment to preventive actions: improving function in patients with diabetic polyneuropathy. Diabetes Metab Res Rev. 2016 Jan;32 Suppl 1:206–12.
80. Baranoski S, Ayello EA. Wound care essentials: practice principles. 2nd ed. Philadelphia: Lippincott Williams & Wilkins; 2008.
65. Chellan G, Srikumar S, Varma AK, Mangalanandan TS, Sundaram KR, Jayakumar RV, et al. Foot care practice - the key to prevent diabetic foot ulcers in India. Foot (Edinb). 2012 Dec;22(4):298–302.
81. Oyibo SO, Jude EB, Tarawneh I, Nguyen HC, Harkless LB, Boulton AJ. A comparison of two diabetic foot ulcer classification systems: the Wagner and the University of Texas wound classification systems. Diabetes Care. 2001 Jan;24(1):84–8.
66. Takehara K, Amemiya A, Mugita Y, Tsunemi Y, Seko Y, Ohashi Y, et al. Association between Washing Residue on the Feet and Tinea Pedis in Diabetic Patients. Nursing Research & Practice. 2015 Feb 22;2015:1–7.
82. Karthikesalingam A, Holt PJE, Moxey P, Jones KG, Thompson MM, Hinchliffe RJ. A systematic review of scoring systems for diabetic foot ulcers. Diabet Med. 2010 May;27(5):544–9.
67. Locke J, Baird S, Hendry G. The use of urea-based creams in the prevention of diabetic ulceration. Journal of Dermatological Nursing. 2012;11(2):26–32.
83. Wukich DK, Hobizal KB, Brooks MM. Severity of diabetic foot infection and rate of limb salvage. Foot Ankle Int. 2013 Mar;34(3):351–8. 84. Game FL, Hinchliffe RJ, Apelqvist J, Armstrong DG, Bakker K, Hartemann A, et al. A systematic review of interventions to enhance the healing of chronic ulcers of the foot in diabetes. Diabetes Metab Res Rev. 2012 Feb;28 Suppl 1:119–41.
68. Boulton AJM. What you can’t feel can hurt you. J Am Podiatr Med Assoc. 2010 Oct;100(5):349–52. 69. van Netten JJ, Price PE, Lavery LA, Monteiro-Soares M, Rasmussen A, Jubiz Y, et al. Prevention of foot ulcers in the at-risk patient with diabetes: a systematic review. Diabetes Metab Res Rev. 2016 Jan;32 Suppl 1:84–98.
85. Game F. Classification of diabetic foot ulcers. Diabetes Metab Res Rev. 2016 Jan 1;32:186–94. 86. Fife CE, Horn SD, Smout RJ, Barrett RS, Thomson B. A Predictive Model for Diabetic Foot Ulcer Outcome: The Wound Healing Index. Advances in Wound Care [Internet]. 2015 Nov 17 [cited 2016 Feb 22]; Available from: http://online.liebertpub.com/doi/abs/10.1089/ wound.2015.0668
70. Dorresteijn JAN, Kriegsman DM, Assendelft WJJ, Valk GD. Patient education for preventing diabetic foot ulceration. Cochrane Database Syst Rev. 2012;10:CD001488. 71. Lincoln NB, Radford KA, Game FL, Jeffcoate WJ. Education for secondary prevention of foot ulcers in people with diabetes: a randomised controlled trial. Diabetologia. 2008 Nov;51(11):1954–61.
87. Uçkay I, Gariani K, Dubois-Ferrière V, Suvà D, Lipsky BA. Diabetic foot infections: recent literature and cornerstones of management. Curr Opin Infect Dis. 2016 Jan 15;
72. Bruun C, Guassora AD, Nielsen ABS, Siersma V, Holstein PE, de Fine Olivarius N. Motivation, effort and life circumstances as predictors of foot ulcers and amputations in people with Type 2 diabetes mellitus. Diabetic Medicine. 2014 Nov;31(11):1468–76.
88. Demetriou M, Papanas N, Panopoulou M, Papatheodorou K, Maltezos E. Determinants of microbial load in infected diabetic foot ulcers: a pilot study. Int J Endocrinol. 2013;2013:858206.
73. Nemcová J, Hlinková E. The efficacy of diabetic foot care education. J Clin Nurs. 2013 Jul 22;
89. Lipsky BA, Peters EJG, Senneville E, Berendt AR, Embil JM, Lavery LA, et al. Expert opinion on the management of infections in the diabetic foot. Diabetes Metab Res Rev. 2012 Feb;28 Suppl 1:163–78.
74. van der Does AMB, Mash R. Evaluation of the “Take Five School”: An education programme for people with Type 2 Diabetes in the Western Cape, South Africa. Prim Care Diabetes. 2013 Dec;7(4):289-95
90. Yesil S, Akinci B, Yener S, Bayraktar F, Karabay O, Havitcioglu H, et al. Predictors of amputation in diabetics with foot ulcer: single center experience in a large Turkish cohort. Hormones (Athens). 2009 Dec;8(4):286–95.
75. Hall K, Gibbie T, Lubman DI. Motivational interviewing techniques - facilitating behaviour change in the general practice setting. Aust Fam Physician. 2012 Sep;41(9):660–7.
91. Gardner SE, Hillis SL, Heilmann K, Segre JA, Grice EA. The neuropathic diabetic foot ulcer microbiome is associated with clinical factors. Diabetes. 2013 Mar;62(3):923–30.
76. Suominen V, Salenius J, Sainio P, Reunanen A, Rantanen T. Peripheral arterial disease, diabetes and postural balance among elderly Finns: a population-based study. Aging Clin Exp Res. 2008 Dec;20(6):540–6.
92. Malik A, Mohammad Z, Ahmad J. The diabetic foot infections: biofilms and antimicrobial resistance. Diabetes Metab Syndr. 2013 Jun;7(2):101–7.
77. Woo KY, Botros M, Kuhnke J, Evans R, Alavi A. Best practices for the management of foot ulcers in people with diabetes. Adv Skin Wound Care. 2013 Nov;26(11):512–24; quiz 225–6.
93. Lipsky BA. Diabetic foot infections: Current treatment and delaying the “post-antibiotic era.” Diabetes Metab Res Rev. 2016 Jan;32 Suppl 1:246–53.
78. Lipsky BA, Berendt AR, Cornia PB, Pile JC, Peters EJG, Armstrong DG, et al. 2012 Infectious Diseases Society of America clinical practice
33
94. Alvaro-Afonso FJ, Lázaro-Martínez JL, Aragón-Sánchez FJ, GarcíaMorales E, Carabantes-Alarcón D, Molines-Barroso RJ. Does the location of the ulcer affect the interpretation of the probe-to-bone test in the diagnosis of osteomyelitis in diabetic foot ulcers? Diabet Med. 2014 Jan;31(1):112-13
108. Ramundo J. Wound debridement. In: Acute & Chronic Wounds: Current Management Concepts. 3rd ed. St. Louis, MO: Mosby Elsevier; 2007. p. 176–92. 109. Game FL, Apelqvist J, Attinger C, Hartemann A, Hinchliffe RJ, Löndahl M, et al. Effectiveness of interventions to enhance healing of chronic ulcers of the foot in diabetes: a systematic review. Diabetes Metab Res Rev. 2016 Jan;32 Suppl 1:154–68.
95. Pittet D, Wyssa B, Herter-Clavel C, Kursteiner K, Vaucher J, Lew P. Outcome of diabetic foot infections treated conservatively: A retrospective cohort study with long-term follow-up. Arch Intern Med. 1999 Apr 26;159(8):851–6.
110. Bolton LL. Quality Randomized Clinical Trials of Topical Diabetic Foot Ulcer Healing Agents. Advances in Wound Care. 2014 Sep 12;5(3):137–47.
96. Mutluoglu M, Uzun G, Sildiroglu O, Turhan V, Mutlu H, Yildiz S. Performance of the probe-to-bone test in a population suspected of having osteomyelitis of the foot in diabetes. J Am Podiatr Med Assoc. 2012 Oct;102(5):369–73.
111. Agathangelou C. Painless Autolytic Debridement on 250 Chronic Wounds by Using Polymeric Membrane Dressings. Poster #241 presented at: 4th Congress of the World Union of Wound Healing Societies (WUWHS); 2012 Sep 2; Pacifico Yokohama, Yokohama, Japan.
97. Acharya S, Soliman M, Egun A, Rajbhandari SM. Conservative management of diabetic foot osteomyelitis. Diabetes Res Clin Pract. 2013 Sep;101(3):e18–20.
112. Dabiri G, Damstetter E, Phillips T. Choosing a Wound Dressing Based on Common Wound Characteristics. Advances in Wound Care [Internet]. 2014 [cited 2014 Dec 12]; 2016 Jan;5(1):32-41
98. Game FL, Hinchliffe RJ, Apelqvist J, Armstrong DG, Bakker K, Hartemann A, et al. Specific guidelines on wound and wound-bed management 2011. Diabetes Metab Res Rev. 2012 Feb;28 Suppl 1:232–3.
113. Benskin L. Letter to the Editor. Wounds. 2015 Jul;27(7):1 p following 198.
99. Ousey K, Cook L, Milne J. Negative Pressure Wound Therapy — Does It Affect Quality of Life? Wounds UK. 2012 Nov;8(4):18–28.
114. Cahn A, Y K. A novel approach to the treatment of diabetic foot abscesses - a case series. J Wound Care. 2014 Aug;23(8):394, 396–9.
100. Jeffcoate WJ. Wound healing--a practical algorithm. Diabetes Metab Res Rev. 2012 Feb;28 Suppl 1:85–8.
115. Benskin LLL. PolyMem Wic Silver Rope: A Multifunctional Dressing for Decreasing Pain, Swelling, and Inflammation. Advances in Wound Care. 2012 Feb;1(1):44–7.
101. Siersma V, Thorsen H, Holstein PE, Kars M, Apelqvist J, Jude EB, et al. Importance of factors determining the low health-related quality of life in people presenting with a diabetic foot ulcer: the Eurodiale study. Diabet Med. 2013 Nov;30(11):1382-7;
116. Weissman O, Hundeshagen G, Harats M, Farber N, Millet E, Winkler E, et al. Custom-fit polymeric membrane dressing masks in the treatment of second degree facial burns. Burns. 2013 Sep;39(6):1316–20.
102. Attinger CE, Brown BJ. Amputation and ambulation in diabetic patients: function is the goal. Diabetes Metab Res Rev. 2012 Feb;28 Suppl 1:93–6.
117. Cutting KF, Vowden P, Wiegand C. Wound inflammation and the role of a multifunctional polymeric dressing. Wounds International Journal [Internet]. 2015 [cited 2016 Feb 25];6(2). Available from: http:// www.wintjournal.com/journal-content/view/wound-inflammation-andthe-role-of-a-multifunctional-polymeric-dressing
103. Fiorito J, Trinidad-Hernadez M, Leykum B, Smith D, Mills JL, Armstrong DG. A tale of two soles: sociomechanical and biomechanical considerations in diabetic limb salvage and amputation decision-making in the worst of times. Diabet Foot Ankle. 2012;3.
118. Wilson JR, Mills JG, Prather ID, Dimitrijevich SD. A toxicity index of skin and wound cleansers used on in vitro fibroblasts and keratinocytes. Adv Skin Wound Care. 2005 Sep;18(7):373–8.
104. Ogden J. A “New Approach” to Healing Chronic Wounds Accompanied by Dramatically Lower Cost of Wound Management. Poster #1 presented at: WOW Wild On Wounds Conference; 2011 Sep 7; Las Vegas, Nevada USA.
119. Lipsky BA, Peters EJG, Berendt AR, Senneville E, Bakker K, Embil JM, et al. Specific guidelines for the treatment of diabetic foot infections 2011. Diabetes Metab Res Rev. 2012 Feb;28 Suppl 1:234–5.
105. Rahman S, Shokri A. Total Knee Arthroplasty (TKA) Infections Eliminated and Rehabilitation Improved Using Polymeric Membrane Dressing Circumferential Wrap Technique: 120 Patients at 12-month Follow-up. Poster #398 presented at: European Wound Management Association (EWMA); 2013 May 15; Copenhagen, Denmark.
120. Margolis DJ, Gupta J, Hoffstad O, Papdopoulos M, Glick HA, Thom SR, et al. Lack of effectiveness of hyperbaric oxygen therapy for the treatment of diabetic foot ulcer and the prevention of amputation: a cohort study. Diabetes Care. 2013 Jul;36(7):1961–6. 121. Peters EJG, Lipsky BA, Berendt AR, Embil JM, Lavery LA, Senneville E, et al. A systematic review of the effectiveness of interventions in the management of infection in the diabetic foot. Diabetes Metab Res Rev. 2012 Feb;28 Suppl 1:142–62.
106. Man D, Aleksinko P. Intra-Operative Use Followed with PostOp Application of Polymeric Membrane Dressings Reduces Post-Op Pain, Edema and Bruising After Full Face Lift Surgery. Poster #CS-071 presented at: Symposium on Advanced Wound Care (SAWC) SPRING; 2010 Apr 17; Orlando, FL USA.
122. Vig S, Dowsett C, Berg L, Caravaggi C, Rome P, Birke-Sorensen H, et al. Evidence-based recommendations for the use of negative pressure wound therapy in chronic wounds: steps towards an international consensus. J Tissue Viability. 2011 Dec;20 Suppl 1:S1–18.
107. Bell DP Jr. Diabetic foot ulcers: current treatment options and new developments. Surg Technol Int. 2010 Oct;20:97–105.
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123. Jones V, Grey J, Harding K. Wound dressings. BMJ. 2006 Apr 1;332(7544):777–80.
Feb;23(2):59–72. 138. Denyer J. Polymeric membrane dressings in the management of infants with epidermolysis bullosa (EB). Poster presented at: 19th Conference of the European Wound Management Association; 2009 May 20; Helsinki, Finland.
124. Scales JT. Wound Healing and the Dressing*. Br J Ind Med. 1963 Apr;20(2):82–94. 125. Thomas S. Surgical Dressings and Wound Management. 2nd ed. Hinesburg VT: Kestrel Health Information; 2012. 708 p.
139. Selekof J, Shutt D, Roney A. Diabetic foot ulcers: multicenter case studies using silver polymeric membrane dressings to promote wound healing. Poster presented at: Symposium on Advanced Wound Care FALL; 2009 Sep 16; Washington, D.C. USA.
126. Agathangelou A. Deep ulcer on charcot foot closed after treatment with polymeric membrane silver cavity dressing. Poster presented at: 3rd Congress of the World Union of Wound Healing Societies; 2008 Jun 4; Ontario Canada.
140. Nair H, Har M. Utilisation of Multifunctional Dressing on Stagnate, Draining Neuropathic Wound Using Polymeric Membrane Silver Dressing. Poster presented at: Australian Wound Management Association conference; 2012 Mar 18; Sydney, Australia.
127. Benskin L. Chronic Wounds Close Using Various Configurations of Polymeric Membrane Dressings Despite Fear-Generated Non-Compliance. Poster presented at: 3rd Congress of the World Union of Wound Healing Societies; 2008 Jun 4; Toronto, Ontario Canada.
141. Tamir J. Mesh reinforced silver rope dressing for acute infected cavity wounds. Poster presented at: Symposium on Advanced Wound Care (SAWC) SPRING; 2010 Apr 17; Orlando, FL USA.
128. Benskin L. Deep Ulceration Treated with Polymeric Membrane Dressings Until Complete Wound Closure. Poster presented at: 3rd Congress of the World Union of Wound Healing Societies; 2008 Jun 4; Toronto, Ontario Canada.
142. Reaves K. Silver polymeric membrane dressings:* An economical choice for resolving diabetic wounds. Poster presented at: 21st annual (SAWC) Symposium on Advanced Wound Care & WHS meeting; 2008 Apr 24; San Diego, CA.
129. Hess CT. Clinical Guide to Skin and Wound Care (Clinical Guide: Skin & Wound Care). 7 edition. Lippincott Williams & Wilkins; 2012. 624 p. 130. Seemann P. Stalled infected diabetic foot wounds respond rapidly to various polymeric membrane dressing* types. Poster presented at: 22nd annual (SAWC) Symposium on Advanced Wound Care & WHS meeting; 2009 Apr 26; Dallas, TX.
143. Benskin L. Diabetic foot salvaged, wounds closed in only two months using polymeric membrane cavity filler* and polymeric membrane dressings. Poster presented at: 39th annual meeting of the Wound Ostomy Continence Nurses Society (WOCN); 2007 Jun 10; Salt Lake City, UT.
131. Curtin C. The new diabetic foot ulcer standard of care: Instant total contact cast plus polymeric membrane dressings. Poster presented at: 9th annual Desert Foot: High Risk Diabetic Foot Conference; 2012 Nov 14; Phoenix, AZ.
144. Agathangelou C. Huge sacral pressure ulcer closed in four months using silver polymeric membrane cavity filler and dressings. Poster #40 presented at: NPUAP 11th Biennial Conference; 2009 Feb 27; Arlington, VA USA.
132. Hjalmarsson M. Diabetic foot saved from amputation with Polymeric membrane dressings. Poster #228 presented at: 19th Conference of the European Wound Management Association; 2009 May 20; Helsinki, Finland.
145. Agathangelou C. Patients with Chronic Wound Pain Stop Hurting, Why? Poster #348 presented at: European Wound Management Association (EWMA); 2011 May 25; Brussels, Belgium. 146. Benskin L. Excellent healing of pediatric wounds using polymeric membrane dressings. Poster #3228 presented at: 41st Annual WOCN Conference; 2009 Jun 6; St. Louis, MO USA.
133. Yip W, Wong M, Yu O, Choi Y, Tang S, Hui, et al. Extensive, Amputation threatening, diabetic foot ulcer closed rapidly with multifunctional silver polymeric membrane dressings. Poster #59 presented at: Australian Wound Management Association; 2010 Mar 22; Perth, Western Australia.
147. Benskin L. Extensive tunneling lower leg wounds with exposed tendons closed quickly using various polymeric membrane dressing configurations. Poster #41 presented at: 23rd Annual Clinical Symposium on Advances in Skin & Wound Care; 2008 Oct 26; Las Vegas, NV USA.
134. Benskin L. Combining Email Wound Consulting and Polymeric Membrane Dressings to Dramatically Improve Quality of Life. Poster #R003 presented at: 22nd Annual (SAWC) Symposium on Advanced Wound Care & WHS Meeting; 2009 Apr 26; Dallas, TX USA.
148. Lee B. The diabetic foot: a comprehensive approach. In: The wound management manual. New York: McGraw-Hill; 2005. p. 360–1.
135. Smith D, Houle H, Searls L. Hypergranulation Tissue, A Challenging Problem with an Easy Solution. Poster #21 presented at: WOW Wild On Wounds Conference; 2012 Sep 11; Las Vegas, Nevada.
149. Davies SL, White RJ. Defining a holistic pain-relieving approach to wound care via a drug free polymeric membrane dressing. J Wound Care. 2011 May;20(5):250, 252, 254 passim.
136. Burd A, Kwok CH, Hung SC, Chan HS, Gu H, Lam WK, et al. A comparative study of the cytotoxicity of silver-based dressings in monolayer cell, tissue explant, and animal models. Wound Repair Regen. 2007 Feb;15(1):94–104.
150. Vanwallghem G. Rapid closure of infected diabetic foot through the use of polymeric membrane cavity filler. Poster presented at: 19th conference of the European wound management association; 2009 May 20; Helsinki, Finland.
137. Langemo DK, Black J, National Pressure Ulcer Advisory Panel. Pressure ulcers in individuals receiving palliative care: a National Pressure Ulcer Advisory Panel white paper. Adv Skin Wound Care. 2010
151. Wilson D. Stalled diabetic ulcer closed in six weeks using PolyMem Silver dressings. Poster presented at: 39th annual meeting of the Wound
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Ostomy Continence Nurses Society (WOCN); 2007 Jun 10; Salt Lake City, UT.
166. Phillips P. Postoperative endonasal dressing with polymeric membrane material. Poster presented at: American Rhinologic Society; 2003 Sep; Orlando, FL.
152. Schwindling R. Schon wieder eine neue wundauglage? V.A.C. therapy und Polymem - ein ester erfahurgsbericht. KCI Times. 2013;
167. Phillips PP. Polymeric membrane dressing role in epistaxis control [Internet]. Poster presented at: American Academy of Otolaryngology Head and Neck Surgery Foundation, Inc.; 2003 Sep [cited 2015 Feb 2]; Orlando, FL.
153. Agathangelou C. Injured finger salvaged using PolyMem Silver dressings to keep the wound bed clean and warm. Poster #PF430 presented at: 3rd Congress of the World Union of Wound Healing Societies; 2008 Jun 4; Toronto, Ontario Canada. 154. Yastrub DJ. Relationship between type of treatment and degree of wound healing among institutionalized geriatric patients with stage II pressure ulcers. Care Manag J. 2004;5(4):213–8.
168. Yastrub D. Heel Ulcer in Hospice Patient Closed Quickly Using Polymeric Membrane Dressings. Poster presented at: 40th annual meeting of the Wound Ostomy Continence Nurses Society (WOCN); 2008 Jun 21; Orlando, FL.
155. Hayden JK, Cole BJ. The effectiveness of a pain wrap compared to a standard dressing on the reduction of postoperative morbidity following routine knee arthroscopy: a prospective randomized single-blind study. Orthopedics. 2003 Jan;26(1):59–63; discussion 63.
169. Agathangelou C. Unique dressing provides nutrients for wound closure in a profoundly malnourished patient. Poster#36 presented at: NPUAP 11th Biennial Conference; 2009 Feb 27; Arlington, VA USA. 170. Wilson D. Application of Polymeric Membrane Dressings to Stage I Pressure Ulcers Speeds Resolution, Reduces Ulcer Site Discomfort and Reduces Staff Time Devoted to Management of Ulcers. Poster # CS-128 presented at: Symposium on Advanced Wound Care (SAWC)SPRING; 2010 Apr 17; Orlando, FL USA.
156. Beitz AJ, Newman A, Kahn AR, Ruggles T, Eikmeier L. A polymeric membrane dressing with antinociceptive properties: analysis with a rodent model of stab wound secondary hyperalgesia. The Journal of Pain. 2004 Feb;5(1):38–47.
171. Harrison J. Polymeric membrane dressings bring brisk healing to bilateral pressure ulcers. Poster #32 presented at: NPUAP 11th Biennial Conference; 2009 Feb 27; Arlington, VA USA.
157. Man D, Aleksinko P. Use of Polymeric Membrane Dressings Immediately After Fractionated Facial Laser Resurfacing Procedures Improves Outcomes. Poster #CS-069 presented at: Symposium on Advanced Wound Care(SAWC) SPRING; 2010 Apr 17; Orlando, FL USA.
172. Winblad R, Harvey R. A new wound care approach yields significant clinical, economic, logistical and training satisfaction. Poster #P121 presented at: European Wound Management Association (EWMA) meeting; 2010 May 26; Geneva Switzerland.
158. Agathangelou C. Three years experience of treating 46 painful diabetic foot ulcers with polymeric membrane dressings. Poster #47 presented at: European Wound Management Association (EWMA); 2012 May 23; Vienna, Austria. 159. Agathangelou C. Closing stalled heel pressure ulcers: two problem patients, one easy solution. Poster #33 presented at: NPUAP 11th Biennial Conference; 2009 Feb 27; Arlington, VA USA.
173. Meltzer AJ, Graham A, Connolly PH, Meltzer EC, Karwowski JK, Bush HL, et al. The Comprehensive Risk Assessment for Bypass (CRAB) facilitates efficient perioperative risk assessment for patients with critical limb ischemia. J Vasc Surg. 2013 May;57(5):1186–95.
160. Rodeheaver GT, Kurtz L, Kircher BJ, Edlich RF. Pluronic F-68: a promising new skin wound cleanser. Ann Emerg Med. 1980 Nov;9(11):572–6.
174. Ince P, Game FL, Jeffcoate WJ. Rate of Healing of Neuropathic Ulcers of the Foot in Diabetes and Its Relationship to Ulcer Duration and Ulcer Area. Dia Care. 2007 Mar 1;30(3):660–3.
161. Wilson D. Skin tear healing improved through the use of polymeric membrane dressings. Poster #PW725 presented at: 3rd Congress of the World Union of Wound Healing Societies; 2008 Jun 4; Toronto, Ontario Canada.
175. Snyder RJ, Cardinal M, Dauphinée DM, Stavosky J. A post-hoc analysis of reduction in diabetic foot ulcer size at 4 weeks as a predictor of healing by 12 weeks. Ostomy Wound Manage. 2010 Mar 1;56(3):44– 50.
162. Benskin L. Crush injury treated with extra-thick polymeric membrane dressings until complete wound closure. Poster #PW368 presented at: 3rd Congress of the World Union of Wound Healing Societies; 2008 Jun 4; Toronto, Ontario Canada.
176. Brantley JN, Verla TD. Use of Placental Membranes for the Treatment of Chronic Diabetic Foot Ulcers. Adv Wound Care (New Rochelle). 2015 Sep 1;4(9):545–59. 177. Hinchliffe RJ, Andros G, Apelqvist J, Bakker K, Fiedrichs S, Lammer J, et al. A systematic review of the effectiveness of revascularization of the ulcerated foot in patients with diabetes and peripheral arterial disease. Diabetes/Metabolism Research and Reviews. 2012;28:179–217.
163. Hoglin G, Melin A. Improving clinical outcome while reducing cost of treatment. Poster#108 presented at: European Wound Management Association (EWMA); 2012 May 23; Veinna, Austria.
178. Goodney PP, Nolan BW, Schanzer A, Eldrup-Jorgensen J, Stanley AC, Stone DH, et al. Factors associated with death 1 year after lower extremity bypass in Northern New England. J Vasc Surg. 2010 Jan;51(1):71–8.
164. Pacheco M. Best clinical practices, based on single dressing type, improves wound healing while reducing health care costs. Poster#9 presented at: Wild on Wounds Conference (WOW); 2013 Sep 11; Las Vegas, Nevada.
179. Diegelmann RF, Evans MC. Wound healing: an overview of acute, fibrotic and delayed healing. Front Biosci. 2004 Jan 1;9:283–9.
165. Bolhuis J, Benskin L. Evidence-based skin tear protocol yields phenomenal results. Poster #2403 presented at: 40th Annual WOCN Conference; June 21-28; Orlando, FL.
180. Fedorko L, Bowen JM, Jones W, Oreopoulos G, Goeree R, Hopkins RB, et al. Hyperbaric Oxygen Therapy Does Not Reduce Indications for
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Amputation in Patients With Diabetes With Nonhealing Ulcers of the Lower Limb: A Prospective, Double-Blind, Randomized Controlled Clinical Trial. Dia Care. 2016 Jan 6;dc152001.
for diabetic foot ulcers. J Vasc Surg. 2016 Feb;63(2 Suppl):59S – 68S.e2. 185. Buchberger B, Follmann M, Freyer D, Huppertz H, Ehm A, Wasem J. The importance of growth factors for the treatment of chronic wounds in the case of diabetic foot ulcers. GMS Health Technol Assess. 2010;6:Doc12.
181. Löndahl M, Landin-Olsson M, Katzman P. Hyperbaric oxygen therapy improves health-related quality of life in patients with diabetes and chronic foot ulcer. Diabet Med. 2011 Feb;28(2):186–90.
186. Shaw J, Hughes CM, Lagan KM, Stevenson MR, Irwin CR, Bell PM. The effect of topical phenytoin on healing in diabetic foot ulcers: a randomized controlled trial. Diabet Med. 2011 Oct;28(10):1154–7.
182. Ma L, Li P, Shi Z, Hou T, Chen X, Du J. A prospective, randomized, controlled study of hyperbaric oxygen therapy: effects on healing and oxidative stress of ulcer tissue in patients with a diabetic foot ulcer. Ostomy Wound Manage. 2013 Mar;59(3):18–24.
187. Papanas N, Eleftheriadou I, Tentolouris N, Maltezos E. Advances in the topical treatment of diabetic foot ulcers. Curr Diabetes Rev. 2012 May;8(3):209–18.
183. Kranke P, Bennett MH, Martyn-St James M, Schnabel A, Debus SE, Weibel S. Hyperbaric oxygen therapy for chronic wounds. Cochrane Database Syst Rev. 2015;6:CD004123. 184. Elraiyah T, Prutsky G, Domecq JP, Tsapas A, Nabhan M, Frykberg RG, et al. A systematic review and meta-analysis of off-loading methods
37
Index
B
common locations of DFUs 3
bacterial diversity 13
complication rates 1
bacterial load 21
complications 1, 8, 10, 13, 22, 23, 25
barefoot 8, 9, 12, 22
congestive heart failure 20
bioburden 19
cool feet 6
A
bio-engineered tissue 16
cooling 17
ABI (Ankle Brachial Index) 7, 13, 22, 23
biofilms 13, 33
coping mechanisms 13, 23
abscess 12, 14, 24, 26
biomechanical 13, 14, 23, 25
corns 8, 22
adherence (to plan) 6, 10, 14, 23, 26
biopsy 13, 23
cost effective 18, 19
adjunct (See advanced therapies)
biothesiometer 5, 13, 23
costs 1, 21
advanced therapies 16, 20
blister 9, 11, 22
cracks 3
age 1, 7, 20
blood pressure 4, 7
creatinine 6, 12, 24
albumin 12, 24
blood sugar 3, 4, 6, 7, 22
crepitus 11, 13
alginates 15
body mass index (BMI) 8
crest pads 14, 15
amino acid-containing gels 21
bone biopsy 13
critical limb ischemia 7, 20
amnion 21
bones 9, 16
cushioning 9, 17, 25
amputation 1, 2, 3, 6, 7, 9, 10, 12, 14, 20, 21, 25
boney changes 8, 22
cytotoxic 15, 17, 18
boney prominence 6, 10, 11
D
Symbols 2010 Consensus Panel 11
anaerobes 13 Analog (See also, Pain Scale) 10 anatomic location 10, 23 Ankle Brachial Index (See ABI)
brisk walking 8
daily steps 8
bruising 16
dead space 18, 24
bypass surgery 20
debridement 3, 10, 11, 14, 15, 17, 24, 25, 26
ankle pressure (See ABI)
C
ankle reflexes 5, 6
calcified arteries 6, 7
anorexia 12, 24
callus 3, 5, 6, 7, 8, 10, 11, 13, 14, 15, 22, 23, 26
antibiotics 13, 16, 24, 26 antidepressant medications 4, 25 antifungal powder 9, 22 antiseizure 4 arterial insufficiency (See PAD) artery 14, 20 arthroplasties 14 aspirin 7 assessment 2, 4, 9, 10 (major topic), 12, 13, 20, 23, 26
deformity 3, 9, 12 denuded 11 devitalized tissue 11, 14, 15, 24
capillary refill 13, 23
diabetic retinopathy 7
Charcot foot 3, 9
diet 4, 6, 11, 19, 22, 26
chills 12, 24
dimension 10, 11
chorion 21
Doppler 7, 13, 23
chronic wound 16, 17, 20
DPP (Diabeties Prevention Program) 8
claudication 6
drainage 10, 12, 14, 16, 24
cleanse 15, 16
dry 8, 11, 12, 13, 15, 16, 17, 22, 23, 24, 25, 26
cleansing system 17, 24, 25, 26 clinically effective 19
autolysis, autolytic debridement 10, 15, 25
Cochrane Review 15, 21
autonomic neuropathy 3, 8, 9
collagen 16
avascular 11
Collagenase 15 colonized 12
38
dryness 3 dry stable eschar 25
E
gangrene 7, 12, 15, 25
intermittent treadmill walking 7, 22
edematous 11
gas 12, 14, 15, 17, 24, 26
iodine 24
education 2, 9, 10
glossary 1
Ipswich Touch Test 5, 6, 13, 23
electrical stimulation 21
glucose tolerance tests 4
irremovable (“instant” total contact cast) 19
electromagnetic 21
granulate, granulation 11, 17
emergency 7, 12
gritty 13
ischemia, ischemic 2, 3, 6, 7, 11, 12, 16, 20, 21
EMG 4
group education 9
endovascular 20, 25
growth factors 15, 16, 21
enzymes 15
H
epibole 10, 11, 23 eschar 11, 12, 14, 15, 24, 25, 26 ESR (Sed Rate) 12, 13, 23, 24 evaluation 10, 33 exercise 4, 6, 7, 8, 22, 26 exudate 10, 13, 16, 17, 18, 23, 24, 25, 26
F Faces Pain Scale-Revised 10 fasting glucose 4 fat pad 3 feet 4, 6, 8, 9, 15, 22 felted foam 19 fibrates 4, 7, 22 fibroblast 15 fishing line 5
ischemic ulcers 2, 6
K keratinocyte 15
hair loss 6, 13, 23
L
Hansen’s disease 2, 4
larval 16
HBOT (See hyperbaric oxygen therapy)
lasers 21
HDL 7
latex 17
healing 6, 7, 8, 11, 12, 14, 15, 16, 17, 18, 19, 20, 21, 24, 25
Levine technique 13, 23, 24
healthy body weight 19 HgbA1c 1, 4, 6, 8, 13, 22, 23 homocysteine 20, 25, 26 hotspots 8, 9, 22
lifestyle 2, 8 lifetime risk 1 limb salvage 20 lipid levels 7 lipids 4
hydrate 17
lotions 8
hydrophilic 17
lubricating oils 8
hydrotherapy 15 hyperbaric oxygen therapy (HBOT) 16, 20, 21
M macerated 11
I
maceration 8, 15, 17, 23 malnutrition 19
flexible 17
IASP (International Association for the Study of Pain) 10
float 25
Ideal Dressing 16
management 1, 2, 7, 10, 13, 14 (major topic), 15, 19, 23
fluid pressure 15
imaging 20, 25, 26
mask 12
folic acid 20
indurated 11
measure 11, 13, 23
foot care 2, 8, 9, 12
infection 3, 5, 7, 8, 11, 12, 13, 14, 15, 16, 19, 20, 23, 24, 25
medications 4, 6, 7, 8, 13, 22, 23, 25
foot washing 8
inflammation 3, 6, 7, 8, 9, 12, 13, 14, 16, 19, 20, 25
metabolic instability 12, 24
footwear (See shoes) 9
ingrown nails 8
friable 11, 12, 24
insensate 3, 8
fungal infections 9, 22
insoles 9, 22
G
inspect 9, 22
gait 3, 8, 13, 23
insulin 6, 7
fissures 3
foot screening 9
metabolic acidosis 12, 24
metformin 4, 6, 8 microcirculatory system damage 3 minority groups 1 mirror 9 moist 8, 11, 14, 15, 16, 17, 20, 24, 25, 26 moisture-retentive dressings 15, 25
39
molecular testing 13
P
pulsatile flow 20
monofilament (test) 4, 5, 6, 13, 23
PAD (peripheral artery disease) 1, 2, 3, 6, 7, 8, 9, 10, 12, 13, 19, 20, 22, 23, 25, 26
puncture 3, 8
Motivational Interviewing 10
pain 3, 4, 6, 7, 10, 11, 12, 13, 14, 16, 17, 18, 23, 24, 25, 26
Q
motor neuropathy 3
pain scale 10, 11, 23
MRI 4, 12, 13, 24
participants 14
multifunctional dressings 16
patient independence 19
R
peak pressures 8
radiographic 13
percussion hammer 5, 6
reactive oxygen species 21
perfusion 7, 20
rebalancing tendons 14
peripheral arterial disease (See PAD)
recurrence 1, 9, 17
peripheral neuropathy 2, 4, 5
redistributing pressure 19
peripheral pulses 6
re-evaluation 19 (major topic), 25
periwound 10, 11, 23
referred 7
phenytoin 21
reinjured 19
neuroprotective 7
physical activity 8
remodeling phase 16
neutrophils 15
physical examination 9
removable cast walker 19, 25
nitric oxide 20
physical therapy 14
renal failure 6
nociceptor 16, 17, 25
placental 21
repaglinide 6
non-adherence 14
plaque 6
restenosis 20
nonviable (tissue) 10, 11
platelets 6, 12, 21, 24
rest pain 7
non-weight-bearing cast 9
pocketing 11
revascularization 7, 14, 15, 20
NPWT (negative wound pressure therapy) 1, 16, 21
podiatrist 2
reversal 4
PolyMem 15, 16, 17, 18, 19, 24, 25, 26
reversible 4, 6, 22
postural balance 10
rigidity 3
prediabetes 4, 6, 7, 22
risk 1, 2, 3, 4, 6, 7, 8, 9, 10, 12, 13, 15, 20, 22, 23, 25
mortality rate 2 motivation 9, 10
N nateglinide 6 nausea 12 necrotic 11 negative pressure (See NPWT) neuropathic pain 4, 14, 25 neuropathy 1, 2, 3, 4, 5, 6, 8, 9, 10, 12, 13, 14, 22, 23, 25, 26
nurse 2, 15 nutrition 16, 19, 30, 32 nutritional supplements 19 nutritional therapy 8
O
predictor 11, 12 pressure 3, 4, 5, 7, 9, 12, 14, 15, 16, 19, 20, 21
purulent 11, 12, 13, 14, 24
quality of life 2, 13, 14, 19, 21, 23, 25 quantitative swab culture 24
risk of amputation 1 rockerbottom 3
prevalence 1, 6
rubor 6, 13, 23
odor control 17
prevent 4, 5, 8 (major topic), 9, 10, 11, 14, 15, 17, 18, 19, 22, 25, 26
S
offloading 3, 14, 15, 17, 19, 23, 25, 26
proactive 6
opioids 4, 25
probe-to-bone test 10, 12, 13, 23, 24
oral antibiotics 16, 26
progress 19, 20, 25
orthosis 9
prosthesis 14, 25
osteomyelitis 10, 12, 13, 16, 24, 25
protective 4, 15
ozone 16
psi 15, 24, 26
odor 10
saline 15, 17, 26 sandal 19, 25 sausage toe 13 scar 5, 11, 16 screening 9 seams 9
40
Semmes-Weinstein (See monofilament test) sensory neuropathy (See neuropathy) serial sharp debridement 15 serum protein electrophoresis (See SPEP) sharp debridement 14, 15 shockwaves 21 shoes 3, 4, 8, 9, 22, 25, 26 showering 24, 26 silver 16, 17, 18, 19, 24 sinus tracts 10, 13, 23 skin barriers 15 skin elasticity 6 skin substitutes 21 sleeping 4 slough 11 small vessel disease 20 smoke 7, 10, 13, 23 smoking cessation 10, 13, 23, 26 soaking 15 social interaction 21 socks 4, 9, 25, 26 SPEP 1, 4, 6, 13, 22, 23 Stage or Grade 10 statin 4, 7, 26, 32 stem cell therapy 21 sterile 13, 18 stool softeners 25
T
vascular lab 7
team 2, 9, 10, 12, 19, 25
venous insufficiency 13, 23
temperature monitoring 9
vibration 4, 5, 13, 23
tendon lengthening 14
vital signs 7, 13, 23
tendons 3, 10, 13, 14, 16
vitamin B6 20
tests 4, 5, 6, 7, 13, 22, 23
vitamin B12 4, 6, 13, 20, 22, 23, 26
The Diabetes Prevention Program 8
vitamin D 4, 26
thermal regulation 3
vomiting 12, 24
The Wound Healing Index 12
W
thiazolidinedione 6 thrombi 6
Wagner scale 10, 11, 12, 23 walking 4, 7, 8, 9, 12, 19, 22
tissue type 10, 25
water 8, 17, 18, 26
toebox 9
weekly assessment 10
toenails 8
weight 4, 8, 9, 13, 19, 23
toe pressure 7, 14 toe spacers 8
white blood cells 15 WOUND ASSESSMENT GUIDE 11
topical negative pressure (See NPWT) topical oxygen 16
wound breakdown 12, 24 wound cleanser 15, 24, 26
topical treatments 4 total contact casting 19 toxicity 12, 17, 24 trajectory 20 treatments 4, 13, 23 triglycerides 7 tuning fork 5, 13, 23 tunnel 10, 11, 17, 18, 23 turgor 11
structural changes 3
U
sulfonylureas 6
ulceration 3, 5, 9, 12
Summary of tests 6
ultrasonography 7
super-absorbent 17
ultrasound 7, 21
surfactant 15, 17, 24, 26
undermining 10, 11, 18
surgery 7, 9, 14, 16, 18, 20
urea-containing creams 8
surgical mesh 18
UT system 11, 12
symmetrical sites 9
V
symptoms 4, 6, 9, 22
validated 11 vascular inflammation 6
41
wound cleansing system 17, 24, 25, 26 wound edges 10, 23 wound pain 10
