Diabetic Foot Ulcers: Assessment and Management

Introduction

The World Health Organization (WHO) Global Report on Diabetes (2016) estimates that globally 422 million adults are living with diabetes mellitus (DM)which is thesixth leading cause of death in the United States. Of those in the U.S. with this life-long condition twenty-five percent will develop diabetic foot ulcers (DFU). These wounds increase the risk of amputation and increase mortality rates (Alavi, Sibbald, Mayer, Goodman, Botros, Armstrong, Woo, Boeni, Ayello, & Kirsner, 2014). A study by Hick, Selvarajah,  Mathioudakis, Sherman, Hines, Black, & Abularrage (2016)  showed the direct medical cost associated with treating patients with diabetes is 2.3 times higher than those related to the care and treatment of patients with other conditions and was estimated at $176 billion in 2012.

The study also showed that 33% of these costs are directly linked to the treatment of DFU and this cost is rising exponentially year after year. Individuals with DM have as high as a 25% chance of developing a DFU and recurrence can be as high as 70% within five years of the first ulceration (Alavi, Sibbald, Mayer, Goodman, Botros, Armstrong, Woo, Boeni, Ayello, & Kirsner, 2014). Over half of all DFU become infected and 20% of those result in amputation. The mortality rate for those with DFU is 2.5 times as high as it is for those with diabetes but without a DFU. For those with amputation as a result of DFU amputation of the remaining limb commonly occurs within five years of the first amputation. The mortality rate is 70% for post amputation diabetes patients within five years of amputation and is 74% at two years for those receiving renal dialysis (Armstrong & Boulton, 2017). The purpose of this paper is to discuss the pathophysiology, assessment, and management of diabetic foot ulcers.

Pathophysiology of Diabetic Foot Ulcers

Numerous biochemical factors accelerate the development of neuropathy and vascular foot changes in individual with diabetes mellitus. Hyperglycemia inhibits the activation of endothelial nitric oxide synthesis and proteins reacting with sugars triggers additional complications and aging (Alavi, Sibbald, Mayer, Goodman, Botros, Armstrong, Woo, Boeni, Ayello, & Kirsner, 2014). The pathophysiology of diabetic foot ulcers can be described as the perfect storm between neuropathy, ischemia from peripheral vascular disease, and infection. Each of these can severely impact any individual, but for those with diabetes the combination of these issues simultaneously can lead to ulceration, amputation, and death (WHO, 2016). Understanding each of these causes independently allows for a better understanding of how devastating the results can be when they are combined.

Neuropathy

Diabetes leads to neuropathy in many individuals and is manifested by the impact on the motor, autonomic, and sensory components of the nervous system. Neuropathy plays a key role in the risk and development of DFU. Motor neuropathy refers to physical or structural changes that occur and symptoms may include muscle weakness, loss of control of coordination, muscle twitching, and muscle paralysis. Damage to nerves in the feet leads to improper flexion and extension functions of foot muscles. This in turn leads to altered foot anatomy and alterations in the individual’s gait. As deformities progress so does the creation of abnormal bony prominences and pressure points gradually causing skin breakdown and ulceration (Alavi, Sibbald, Mayer, Goodman, Botros, Armstrong, Woo, Boeni, Ayello, & Kirsner, 2014). Common physical findings due to motor neuropathy include (Mayo Clinic, 2017):

• Charcot Foot – results from weakening of the bones of the foot and ankle leading to fracture. Due to loss of pain sensation the person continues to walk on the foot and it gradually changes shape altering its weight bearing pressure points.
• Hammer Toes – results from an imbalance in the muscles, tendons, and ligaments that normally hold the toe straight. It occurs when the middle joint of the toes becomes permanently in a bent position and usually only impacts one or two toes.
• Claw toes – results from the the two distal toe joints bend and curl under while the joint at the ball of the foot bends slightly upward. This results in the toes having a claw like appearance and usually impacts all the toes of the involved foot at once
• Prominent metatarsal heads – when the plantar heads of the metatarsals are physically palpable.
• Pes cavus – occurs when there is an abnormally high medial longitudinal arch, which extends between the first metatarsal head and the calcaneus
• Excessive callous formation over bony pressure points – excessive hyperkeratotic tissue formation as a result of shear stresses over or near bony prominences. With loss of protective sensation and continued pressure callosities thicken, hemorrhage underneath, and ulcerate.

The autonomic nervous system works without our will controlling many organ functions and aids the body in adapting to changes in the internal and external environment. Diabetic autonomic neuropathy (DAN) increases morbidity and mortality in patients with both Type 1 and Type 2 diabetes mellitus and impacts every organ system of the body. DAN is almost always asymptomatic in the early stages so it is easy to miss opportunities for early diagnosis and treatment. Clinical manifestations may occur in the cardiovascular, gastrointestinal, genitourinary, pupillomotor, thermoregulatory, and other organs. In individuals with prediabetes, hypoglycemia, and diabetes who develop DFU it significantly impacts the integumentary system or the skin. With DAN there is a change in the sympathetic nervous system, rendering changes to involuntary functions such as the ability to perspire and sweat. As the skin becomes dryer cracks and fissures form allowing further skin deterioration, the entry of bacteria, and finally infection (Jin, Baek, & Park, 2015, Freeman, 2014).

Sensory neuropathy alters tactile sensation, especially pain perception. This is called loss of protective sensation or LOPS. The loss of sensation also increases the risk of injury due to trauma since the individual is unable to feel the insult or injury to the skin. There may be numbness, impaired temperature perception, weakness, a variety of paresthesia’s and unusual pain such as tingling, stabbing pain, burning and other abnormal sensations (Vinik, 2016). Approximately 10-26% of patients with diabetes develop painful neuropathy severe enough to impact quality of life and results from small-fiber dysfunction. This discomfort occurs in those patients with poor long-term glycemic control. Other contributing factors to the increase in pain include age, obesity, smoking, hypertension, dyslipidemia, and peripheral artery disease (Yazdanpanah, Nasiri, & Adarvishi, 2015). Loss of vibration and position sensation may also occur. The inability to accurately perceive pain and tactile stimulus puts the patient at risk for trauma, friction injury, and wound development. If they do not realize it has occurred it either goes completely unnoticed or if it is realized since there is no pain the individual feels it is of little consequence until it becomes painful and infected. Weight-bearing, shearing, and repetitive pressure on damaged tissue results in further deterioration of the area. Bone demineralization and impaired vascular smooth muscle also result from autonomic denervation (Alavi, Sibbald, Mayer, Goodman, Botros, Armstrong, Woo, Boeni, Ayello, & Kirsner, 2014).

Peripheral vascular disease, ischemia, and diabetic foot ulcers

Both individuals with and without diabetes can develop atherosclerosis. However, in those with diabetes it occurs prematurely and progresses more rapidly. Manifestations may be coronary artery (CAD), cerebrovascular (CVD), or peripheral vascular disease (PVD). Those with PVD typically have CAD but those with a primary diagnosis of CAD are less likely to have PVD. Occurring at all levels of the vascular tree, PVD of the lower extremities is either macrovascular or microvascular. When sufficient blood flow in these vessels is impaired it can result in ischemia, which leads to increased risk of infection and tissue death. Only 10% of DFU are purely ischemic and the remaining 90% are due to neuropathy or neuropathy and ischemia combined (Yazdanpanah, Nasiri, & Adarvishi, 2015).

Macrovascular PVD results in atheromas commonly found at the bends and bifurcations of blood vessels such as the aortoiliac segment, the superficial femoral artery, and more distal vessels below the trifurcations at the peroneal, anterior, and posterior tibials. However, the dorsalis pedis is frequently spared (Alavi, Sibbald, Mayer, Goodman, Botros, Armstrong, Woo, Boeni, Ayello, & Kirsner, 2014). Microvascular PVD combined with neuropathy predisposes those with diabetes to an increased risk of foot infections which can range from simple superficial cellulitis to chronic osteomyelitis.   It also makes these infections harder to treat since poor microvascular circulation inhibits access of phagocytic cells to the area or the delivery of antibiotics to infected tissues (Chandrashekar & Muralidhar, 2017).

Infection

Infection associated with diabetic foot ulcer are not only difficult to treat or heal but also can become limb and life threatening. The anatomy of the lower limb, especially the foot, makes these infections more disastrous than infections in other parts of the body.  Because of the compartmental structure of the foot infection can spread rapidly from one to the other. This can be especially exacerbated due to the loss of sensation and individuals ability to feel pain which in turn makes it possible for the individual to remain ambulatory facilitating the further spread of infection. Soft tissues of the foot such as the plantar aponeurosis, tendons, muscle and fascia are more susceptible to the spread of infections. The infection along with neuropathy, ischemia, and hyperglycemia further compromises the body’s natural defenses (Alavi, et al., 2014).

Most deep long duration foot infections are associated with osteomyelitis which develops when the infection spreads through the deep soft tissue to the bone cortex and into the bone marrow (van Asten, La Fontaine, Peters, Bhavan, Kim, & Lavery, 2016). It is estimated that 44-68% of patients with DFU will develop osteomyelitis and is the leading cause of amputation among these patients. Gram-positive organisms such as Staphylococcus aureus and beta hemolytic streptococci are the primary responsible organisms. Most DFU cultures reveal that the infections are monomicrobial. Only 3-14% of DFU infections are caused by anaerobic organisms (Michno, Nowak, & Krolicki, 2018).

Diagnosing osteomyelitis is difficult since it is hard to differentiate soft tissue infection from bone infection. Focal osteopenia, cortical erosion or periosteal reactions are typically what is seen in these films. The simplest clinical test for osteomyelitis is to use a sterile metal probe and insert into the ulcer. If it penetrates to the bone it almost always confirms osteomyelitis. Other clinical indicators are chronic draining sinuses and sausage-like appearance of the toe. Computerized tomography or CT scans, positive emission tomography or PET scans, and magnetic resonance imaging or MRI can be used but definitive diagnosis should be made by obtaining a bone biopsy (van Asten, et al., 2016).

Assessment of the Diabetic Foot Ulcer

Assessment should always be of the whole patient not just the hole in the patient and this is especially true for those with diabetic foot ulcers. A complete social and medical history should be obtained including previous ulcerations, surgery, trauma, or amputations. Remember that the individual who has had a previous amputation is at a higher risk for loss of the other limb.

Physical examination of the feet

Physical examination of the fee of the patient with diabetes should be an integral part of routine exams and skin care. Observations should include neuropathic changes such as dry skin, cracks and fissures, deformities, callus formations, hemorrhagic callus formation, abnormal foot shape or deformity, condition of the nails, and prominent veins. Special attention should be paid to the interdigital spaces. The metatarsal heads should be examined on the plantar surface of the foot to determine if they have become prominent or have developed callus over them (Chadwick, Edmonds, McCardle, & Armstrong, 2013).

Peripheral neuropathy characteristics include loss of vibratory and position sense, loss of deep tendon reflexes (especially ankle jerk), trophic ulceration, foot drop, muscle atrophy, and excessive callus formation especially over bony prominences such as metatarsal heads and calcaneus. Sensory perception should be evaluated using a 5.07 monofilament.  In the event these are not available cotton swabs, a pinprick, or a tuning fork may be used to detect the level of sensation. This will help in determining if the individual has lost protective sensation posing a higher risk of DFU formation (Rowe, 2018).

Characteristics of ischemia will include decreased temperature in affected extremity, dependent rubor, pallor with elevation, loss of hair on the dorsal foot, faint or absent dosalis pedis and posterior tibial pulses. The femoral artery should be palpated as well as auscultated for the presence of bruit (Armstrong & Boulton, 2017). To confirm the presence or absence of pulses and validate adequate blood supply a hand-held Doppler may be used. Utilizing the Doppler and a sphygmomanometer an Ankle Brachial Index (ABI) may be obtained. This is accomplished by taking the ankle systolic pressure and dividing it by the brachial systolic pressure. According the Wound Ostomy Continence Nurses Society (2018) ABI are interpreted as the following:

• > 1.4 Indicates noncompressible vessels
• > 1.0 Normal
• ≤ 0.9 Lower extremity peripheral vascular disease
• < 0.6 to 0.8 Borderline
• < 0.5 Severe ischemia

Additionally, toe pressures and transcutaneous oxygen pressure (TCPO₂) measurements can be helpful in measuring tissue perfusion. Claudication, which is pain in the legs with walking or other exercise and temperature difference between the feet are also signs of ischemia. When it is determined that a limb has critical ischemia the individual should be urgently referred to a vascular surgeon. Critical ischemia is characterized with the six “P’s” including pulselessness, pain, pallor, perishing cold, paresthesia, and paralysis and poses a limb threatening clinical emergency (Chadwick, et al., 2013).

Diabetic foot ulcers are classified into two categories. Neuropathic Foot in which neuropathy is the dominant issue and neuroischemic where neuropathy is present but ischemia is the primary issue. As discussed previously neuropathy leads to drying and fissure development in the skin of the feet, as well as Charcot joints and digital necrosis. Friction leads to bullae formation and breaks in the skin as well. Poor blood flow or ischemia of the foot leads to pain at rest, ulcerations on the plantar surface and other pressure bearing points on the foot, digital necrosis and the development of gangrene. Treatment strategies for each differ because the complications vary so being able to differentiate is important (Pendsey, 2010). There are also classification systems for describing the severity and condition of DFU’s.

Classification systems

There are no universally accepted classification scales for diabetic foot ulcers. The two most widely accepted are The Wagner Diabetic Foot Ulcer Grade Classification System and the University of Texas Diabetic Foot Ulcer Classification System. The Wagner is an older classification scale for foot ulcers and takes into account the depth, appearance, presence of osteomyelitis or gangrene, and is described by Grades 0 through 5 (Fsg, Vaithiyanathan, & Vijayaragavan, 2017).

• Grade 0 – intact skin
• Grade 1 – superficial ulcer of skin or subcutaneous tissue
• Grade 2 – ulcer extends into tendon, bone, or joint capsule
• Grade 3 – deep ulcer with osteomyelitis or abscess
• Grade 4 – partial foot gangrene
• Grade 5 – whole foot gangrene

The newer scale or system is the University of Texas Diabetic Foot Ulcer Classification System which grades DFU’s by depth then stages based on the presence or absence of infection and ischemia as follows:

• Grade 0 – pre ulcerative site or poste ulcerative site that has healed
• Grade 1 – superficial wound not involving tendon, joint capsule, or bone
• Grade 2 – wound penetrating to tendon or joint capsule
• Grade 3 – wound penetrating the bone or joint

The grades within each wound include:

• Stage A – clean wounds
• Stage B – non-ischemic infected wounds
• Stage C – ischemic non-infected wounds
• Stage D – ischemic infected wounds

Neuropathy leads to fissures, bullae, neuropathic (Charcot) joint, neuropathic edema, and digital necrosis. Ischemia leads to pain at rest, ulceration on foot margins, digital necrosis, and gangrene. Differentiating between these entities is essential because their complications are different and they require different therapeutic strategies

Assessment of Ulcer Characteristics

The initial assessment and documentation of the DFU establishes a baseline for clinical diagnosis, development of the plan of care, initiation of treatment, and monitoring the response to treatment. The size (Length x Width x Depth), appearance and location should be documented. The color and status of the wound bed (which should be healthy beefy red) and, if present, the amount and characteristics of necrotic nonviable tissue should be recorded. The presents of exposed bone, necrosis, or gangrene may indicate osteomyelitis or worsening infection. What is the type, color, amount, presence of purulence, and odor associated with wound drainage? The condition of the periwound skin should also be documented since maceration and spreading erythema may indicate excessive exudate and worsening of the wound. Also the presence of callus, edema, and undermining should be documented. Photographs are especially important at onset of treatment and periodically thereafter to monitor and document the progress toward or lack of healing (Chadwick, et al., 2013).

Other Assessment Parameters

Hemoglobin A1c (Hgb A1c) should be obtained to see how well the individual is managing their blood glucose levels.  A study by Zubair, Malik, & Ahmad (2015) discussed that higher prolonged Hgb A1c levels place the individual at higher risk of developing complications, especially DFU. Higher Hgb A1c rates were also found to delay healing in these patients. The American Diabetes Association recommends Hgb A1c levels being maintained at around or below 7% to reduce microvascular and neuropathic complications (ADA, 2018).

Smoking habits should also be documented. Individuals who smoke are at high risk of developing other comorbid conditions such as coronary artery disease, peripheral vascular disease, and chronic obstructive pulmonary disease, all which have a detrimental effect on healing (AHA, 2018). It should also be determined how motivated the individual is to stopping smoking. Individuals with diabetes are already at high risk of vascular disease and stroke which smoking only compounds.

Management of Diabetic Foot Ulcers

The primary focus of DFU management is achieving wound healing. Management should consist of treating the underlying disease process, achieving and maintaining adequate perfusion, wound care and infections control, and offloading.  Identifying the underlying cause, correcting and eliminating it, is essential to effective management of DFU (Chadwick, et al., 2013). Interventions for ischemia are the most essential to achieving wound healing and limb preservation. Patients with critical ischemia should have emergent consultation for interventions which will reestablish and maintain blood supply. In addition to glycemic control managing other risk factors such as hypertension, high cholesterol, smoking and malnutrition are essential to keep DFU’s on a healing trajectory.  Identifying the cause of trauma or potential for repetitive trauma is important as well. This would also include assessing the patient’s footwear for proper fit, wear and tear, possible foreign bodies such as rocks, pieces of glass, pins, needles, or pet dander which have the potential to induce trauma. Also it is important to keep in mind that footwear should accommodate the dressing or other foot protection should be chosen (Alavi, et al., 2014).

Optimal wound care is also essential and should include a focus on initial and serial debridement to keep the wound in an acute state free of debris and non-viable necrotic tissue, frequent assessment, and dressing interventions that aid in bacterial control and maintain a moist healing environment without the risk of maceration. Additionally, offloading of at risk and ulcerated areas of the foot aids in maximizing pressure redistribution across the plantar surface of the foot, thus helping maintain perfusion and aid healing (Armstrong, McCulloch, & de Asia, 2018). Although there are multiple devices available to provide offloading, total contact casting is the gold standard for offloading DFU. This is a padded foot and lower leg cast with an opening over the DFU. The cast provides the offloading and the opening in the cast provides access to the wound for dressing changes. It also provides a method of ensuring patient compliance since it is very difficult to remove. Total contact casting has also been found to reduce healing time by as much as six weeks (Yazdanpanah, et al., 2015). Contraindications for total contact cast include infected DFU’s and osteomyelitis, due to difficult observation, and those with critical ischemia due to the risk of increasing ischemia.

Patient Education for Diabetic Foot Ulcers

Successful prevention of DFU’s is a result of partnerships between care givers and patients. Studies have shown that with effective patient education DFU’s can be prevented by up to 50% reinforcing the fact that self-management should be the foundation of DFU prevention (Yazdanpanah, Nasiri, & Adarvishi,  2015). Emphasis on positive health practices especially for those with diabetes will help prevent foot ulcers and possible amputation.  Effective programs include and array of methods from brief education to comprehensive education which includes hands on teaching and teach back methods. Priority topics should be on management of risk factors, proper foot care with visual self-inspection, monitoring of skin temperature and hair growth, proper foot hygiene and footwear choices, and glycemic control. This comprehensive approach not only reduces the frequency but also decreases the rate of amputations and mortality associated with DFU’s (Rowe, 2018).

Patients need information simplified into laymen’s terms so that it is easy to comprehend. Ascertaining their comprehension level is imperative to developing an effective personalized education program. If patients do not understand what is being done or the rationale and purpose it is very hard to promote compliance with the plan of care. For example patients must understand how reduction of pressure on the wound and proper offloading can stop the repetitive trauma and callus formation that inhibits wound healing. Many times it takes repetitive education to drive the point home and ensure that understanding is achieved. As outcomes improve patients appreciate their role in preventing and caring for DFU’s, which also drives and promotes adherence to the plan of care (Mayer, 2014).

Conclusion

Unfortunately diabetic foot ulcers are a dreaded and common malady for patients with diabetes which often leads to frequent hospitalizations, lower limb amputation, and in some cases death. Targeted management strategies can lead to successful healing outcomes and include education, glycemic control, wound debridement, infection control, offloading, surgical interventions and advanced therapies. Screening for DFU should be completed in all care settings and self-assessment taught as part of the patient’s self-management plan. Utilization of an interprofessional approach can support patients in the prevention and management of DFU.

References

ADA (2017). 2018 Standards of medical care in diabetes. American Diabetes Association. Retrieved from http://www.diabetes.org/newsroom/press-releases/2017/american-diabetes-association-2018-release-standards-of-medical-care-in-diabetes.html

AHA (2018). Cardiovascular disease and diabetes. American Heart Association.  Retrieved from http://www.heart.org/HEARTORG/Conditions/More/Diabetes/WhyDiabetesMatters/Cardiovascular-Disease-Diabetes_UCM_313865_Article.jsp#.Wz5Bz2eWz2Q

Alavi, A.,  Sibbald, R.G., Mayer, D., Goodman, L., Botros, M., Armstrong, D.G., Woo, K., Boeni, T., Ayello, E.A., & Kirsner, R.S. (2014). Diabetic foot ulcers: Part I. Pathophysiology and prevention. Journal American Academy of Dermatology, 70(1), e1-18. Retrieved from http://scholar.google.com/scholar_url?url=https3A2F2Fwww.sciencedirect.com/science2Farticle%2Fpii%2FS0190962213008207&hl=en&sa=T&ct=res&cd=0&d=3339579570344298433&ei=vy45W_ihG4_-yQTF6rbgDA&scisig=AAGBfm0fc1d-6UoWT8iF5Rb2spFObKIbrg&nossl=1&ws=1600×767

Armstrong, D.G. & Boulton, A.J.M. (2017). Diabetic foot ulcers and their recurrence. New England Journal of Medicine, 376(24), 2367-2375. doi: 10.1056/NEJMra1615439. Retrieved from http://dickyricky.com/Medicine/Papers/2017_06_15%20NEJM%20and%20%Their%20Recurrence.pdf

Armstrong, D.G., McCulloch, D.K., & de Asia, R.J. (2018). Management of diabetic foot ulcers. UptoDate. Retrieved from https://www.uptodate.com/contents/management-of-diabetic-foot-ulcers

Chadwick, P., Edmonds, M., McCardle, J., & Armstrong, D. (2013).  International Best Practice Guidelines: Wound management of diabetic foot ulcers. Wounds International. Retrieved from http://www.woundsinternational.com

Chandrashekar, S., & Muralidhar, S. (2017). A study on the prevalence of risk factors and presence of diabetic foot ulcers in T2DM patients in K. R. Hospital, Mysuru. International Surgery Journal, 4(9), 2983-2986. doi: http://dx.doi.org/10.18203/2349-2902.isj20173611. Retrieved from https://ijsurgery.com/index.php/isj/article/viewFile/1730/1412

Freeman, R. (2014). Chapter 6 Diabetic autonomic neuropathy. In Handbook of Clinical Neurology, 126 ( Zochodne & Malik, Ed., pages 63-79). Elsevier, Cambridge, MA. Retrieved from https://www.sciencedirect.com/science/article/pii/B9780444534804000060

Fsg, A.J. M., Vaithiyanathan, R., & Vijayaragavan, R. (2017). Effectiveness of conventional and herbal treatment on diabetic foot ulcer using Texas and Wagner wound scales. International Journal of Nursing Education, 9(14), 1-5. Retrieved from https://web.b.ebscohost.com/abstract?direct=true&profile=ehost&scope=site&authtype=crawler&jrnl=09749349&AN=127723866&h=RD8fkmqwaB77mAjv66z%2bh%2b%2bY%2f%2fJcihSL6iWXUlo1xwi5Xd%2fLTDpFw5FbBU3CEAz77QsY9ULi3T7BO2U%2bpL%2bvEg%3d%3d&crl=c&resultNs=AdminWebAuth&resultLocal=ErrCrlNotAuth&crlhashurl=login.aspx%3fdirect%3dtrue%26profile%3dehost%26scope%3dsite%26authtype%3dcrawler%26jrnl%3d09749349%26AN%3d127723866

Hicks, C.W., Selvarajah, S., Mathioudakis, N., Sherman, R.E., Hines, K., Black, J.H., & Abularrage, C.J. (2016). Burden of infected diabetic foot ulcers on hospital admissions and costs. Annal of Vascular Surgery, 33, 149-158. doi: 10. 1016/j.avsg.2015.11.025. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/26907372

Jin, H.Y., Baek, H.S., & Park, T.S. (2015). Morphologic changes in autonomic nerves in diabetic autonomic neuropathy. Diabetes & Metabolic Journal, 39(6), 461-467. doi: 10.4093/dmj.2015.39.6.461. Retrieved from https://www.synapse.koreamed.org/search.php?where=aview&id=10.4093/dmj.2015.39.6.461&code=2004DMJ&vmode=FULL

Mayer, P. (2014). Emphasizing the fundamentals and patient education in diabetic foot care. Podiatry Today, 27(9), 20-24. Retrieved from https://www.podiatrytoday.com/emphasizing-fundamentals-and-patient-education-diabetic-footcare

Mayo Clinic (2017). Common foot deformities related to diabetes. Mayo Clinic, Rochester, MN. Retrieved from https://www.mayoclinic.org/diseases-conditions/hammertoe-and-mallet-toe/symptoms-causes/syc-20350839

Michno, A., Nowak, A., & Krolicki, L. (2018). Review of contemporary knowledge of osteomyelitis diagnosis. World Scientific News, 92(2), 272-282. Retrieved from http://psjd.icm.edu.pl/psjd/element/bwmeta1.element.psjd-d25c555d-b435-46b8-9ba7-b5c4dc85d075

Pendsey, S.P. (2010). Understanding diabetic  foot. International Journal of Diabetes in Developing Countries, 30(2), 75-70. doi: : 10.4103/0973-3930.62596 Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2878694/?report=printable

Rowe, V.L. (2018). Diabetic ulcers. Medscape. Retrieved from https://emedicine.medscape.com/article/460282-print

van Asten, S.A.A., La Fontaine, J., Peters, E.J.G., Bhavan, K., Kim, P.J., & Lavery, L.A. (2016). The microbiome of diabetic foot osteomyelitis. European Journal of Clinical Microbiology & Infectious Diseases, 35(2), 293-298. Retrieved from https://link.springer.com/article/10.1007/s10096-015-2544-1

Vinik, A.I. (2016). Diabetic sensory and motor neuropathy. New England Journal of Medicine, 374(15), 1455-1464. Retrieved from https://www.nejm.org/doi/full/10.1056/NEJMcp1503948

WHO (2016). Global report on diabetes. World Health Organization, Geneva Switzerland. Retrieved from http://apps.who.int/iris/bitstream/handle/10665/204871/9789241565257_eng.pdf;jsessionid=E6D20EEF1AF98289F09365A4847B4C01?sequence=1

WOCN (2014). Guideline for Management of Wounds in Patients with Lower Extremity Arterial Disease. Wound Ostomy Continence Nurses Society, Mt. Laurel, NJ

Yazdanpanah, L., Nasiri, M., & Adarvishi, S. (2015). Literature review on the management of diabetic foot ulcer. World Journal of Diabetes, 6(1), 37-53. doi: 10.4239/wjd.v6.i1.37

Zubair M, Malik A, Ahmad J (2015) Glycosylated hemoglobin in diabetic foot and its correlation with clinical variables in a North Indian tertiary care hospital. Journal of Diabetes & Metabolism, 6:571. doi:10.4172/2155-6156.1000571. Retrieved from https://www.omicsonline.org/open-access/glycosylated-hemoglobin-in-diabetic-foot-and-its-correlation-with-clinical-variables-in-a-north-indian-tertiary-care-hospital-2155-6156-1000571.php?aid=54493

BLOG #18

Our clients with wounds and lymphedema incur many expenses in dealing with their recovery or disease process. When the ACA was passed, it afforded coverage for care that was denied, paid out of pocket and just didn’t happen in the past. Most Lymphedema garments were still not covered due to the lack of definition as a covered DME by Medicare. The individual mandates’ repeal would take billions of dollars off the US deficit but leave millions of folks without health insurance and therefore likely, poor to no healthcare. Eliminating preexisting conditions coverage would mean much sicker people making do and making difficult choices between food, rent, schooling, gas, etc …….and healthcare.

Working in wound care, be it a clinic, hospital, home care, or wherever, we have all seen the difference that access and affordability can mean. As an example, Diabetics with poorly managed glucose control are subject to increased trauma to their vascular system, can have poorly fitting shoes and poor foot care. Preventive care doesn’t happen and when the resultant Diabetic emergency sends them reluctantly to the ED, many more problems are often found. The feet can have infection, overgrown nails that can’t be trimmed at home and callus hiding infection. The brain is subject to these glucose peaks and valleys, and so is less able to direct self-care. In the past I have seen more expensive absorbent or water proof dressings substituted with cheaper but also absorbent baby diapers and feminine hygiene pads. They cover the wound but don’t come with the care a wound professional can provide. I’m sure many of us recall trying to find patients charitable care or donated bandage supplies. Other wound related diagnoses such as trauma, venous disease, cancer, surgical sites, skin diseases will leave people subject to less than adequate home remedies and result often in a visit to the ED.

Any time someone appears in an ED, law mandates that they cannot be turned down for care due to inability to pay. Someone will pay. Either the patient themselves will pay the burdensome payments to the health system, or you and I will through higher care costs passed on by the hospital as they absorb costs from nonpayment. This is how it had been done for decades before ACA and before Medicare.

I encourage you to have insurance coverage. Anyone can end up in the ED, even healthy people after an accident or an unexpected health emergency such as cancer, infectious disease, stroke or heart attack. I strongly encourage you to let your elected officials know that you value healthcare for all and every diagnosis. I implore you to investigate each candidate’s stance on healthcare reform before you vote. (Kindly register if you  aren’t already!) The care we can provide our patients and ourselves receive depends on it. All the pretty bandages and medications aren’t worth anything if insurance doesn’t cover it and the patient can’t afford it.

www.cbo.gov/system/files/115th-congress-2017-2018/reports/53300-individualmandate.pdf

Is it pressure?

Holly Hovan MSN, APRN.ACNS-BC, CWOCN-AP

As WOC nurse specialists, we are forever in a role of wearing many hats.  We are educators to patients, staff, and providers… we are patient advocates and supporters of our bedside nurses… we are liaisons in many aspects of care and help to coordinate care and services for our patient population.  We are often referred to as the specialist and are called upon when there is a patient with a wound, skin, ostomy, or continence concern.  Our peers trust us and it is important that we possess the knowledge and skills to share with others when determining etiology and treatment for wounds and skin issues.

An issue we are often faced with as skin specialists is determining the etiology of wounds and skin concerns.  When determining the etiology of wounds, it is important to look at the entire picture… and, when doing so, understand that many variables can and do make wounds better or worse, but there is usually an isolated variable that caused the wound.

Some things to keep in mind… pressure injuries are usually round, can appear punched out, may be partial or full thickness, may have slough/necrotic tissue, and are usually over a bony prominence.  In terms of shape, pressure injuries related to devices usually take the shape of that device (think of a linear, fluid-filled blister from foley catheter tubing on the thigh… a stage 2 device related pressure injury, or a purple/discolored, non-blanchable area on the lip from an endotracheal tube… a mucosal pressure injury (MPI)).  Other devices that may be responsible for pressure injuries are: prosthetics devices (prosthetic limbs, shrinkers, hearing aids), tubes (foley catheters, endotracheal tubes, feeding tubes, nephrostomy tubes, fecal management system tubes) – always be sure that your tube is secured with an appropriate tube securement device to prevent pressure injuries!  Other devices sometimes responsible for pressure injuries are foot pedals on chairs, bed pans, external catheters, shoes and glasses.  One of my mentors always said… if your patient was not born with it, and they have it now, you need to check under/around it!  Device related rounds are also helpful in areas that have a high incidence of device related pressure injuries… this helps to bring awareness to the different types of devices we should be checking for and helps nurses to understand pressure injuries vs. wounds/skin issues not related to pressure.

So, to reinforce… always look back at what caused the wound, not what contributed to the wound happening.  Things such as diabetes, peripheral vascular disease, incontinence, immobility, poor nutrition, and impaired sensory perception are all contributing factors to pressure injuries.

Always remember to look at the big picture, the main culprit of the skin injury, and consult your skin specialist with any questions!  Take an interdisciplinary approach for prevention and healing, and be sure that everyone is on the same page.  Frequent communication between the interdisciplinary team and involving the patient/family in the plan of care definitely helps with prevention.

One more thing to briefly mention… skin failure.  Skin failure occurs at the end of life (hours to days) and while it can be related to pressure, the real cause of it is just that… skin failure.  When all prevention measures are in place and our patient still develops a wound at the end of life (hours to days), it is usually related to skin failure.  The skin is our largest organ and much like other organs, it can fail us, especially when near death.  I will discuss this topic more in future blogs!

Military – Combat Wound Care Management

As a veteran of the U.S. Army, and having a Grandfather who was a U.S. Army combat medic, I have always had an interest in combat wound care.

Wound care has evolved immensely throughout the years in the military arena.  The treatments used as far back as the 5^th Century B.C. were inconceivable.  Ex: Keeping wounds dry, wound irrigation with water and wine, burning oil into infected wounds, and topicals such as egg yolks, rose oil, and turpentine to the wound bed. [2] Odor was controlled with bags of lavender at the soldier’s bedside. [2]

Now days, the military is using the latest technologies, such as digital imaging and telemedicine. This allows them to send combat wound images from the battlefield, or to prepare the hospital site for their injured soldier.

Common Combat Wound Types [2]

Combat wounds are much more complex due to higher contamination.  This is due mostly to the environment where the wound occurred.  Faster wound healing times or surgical closure, is indicated due to painful dressing changes and risk of infection. [1]

Most common combat wounds:

1. Blast wounds – landmines, grenades, IED’s (explosive devices), suicide bombings.  Amputation rates high.
2. Gunshot and shrapnel
3. Head injuries and fractured bones

Dressings [1]

The challenge and complexity of combat wounds are the large wound size and heavy amount of drainage.

a] Impregnated polyhexamethylene biguanide gauze dressings

b] Silver dressings – antimicrobial properties

c] Negative Pressure Wound Therapy – less frequent dressing changes, and controls high amounts of exudate.

d] Moisture sensors- allows dressing decisions without disturbing the dressing.

Debridement in Combat Wounds [1]

Combat wounds must be debrided aggressively, both bony and soft tissues. Debridement must be performed as soon as possible, and under magnification using surgical operating loupes. High pressure water jets and surgical instruments are used in combination to clean bone and soft tissues.

Nutritional Challenges [1]

Soldiers that have been deployed for a longer duration, are more likely to be malnourished at the time of traumatic injury. Enteral feeding is implemented for soldiers with complex injuries.

Conclusion

Combat wound care has improved immensely throughout the years.  Utilizing a combination of technologies may be necessary in developing a most effective treatment plan.    Using a holistic approach in managing combat wounds has been shown to be most beneficial. The quality of life of a soldier is paramount.

References:

1. Advances in Wound Care: The Management of Combat Wounds: The British Military Experience Steven L.A. Jeffery^1,,2,*  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5067872/
2. Management of Miltary Wounds in the Modern Era: Chris Taylor and Steve Jeffery http://www.woundsinternational.com/media/issues/280/files/content_8827.pdf

Nutrition Management of Individuals with Pressure Injury and Diabetes Mellitus

by Dr. Nancy Munoz, DCN, MHA, RDN, FAND

OVERVIEW OF DIABETES MELLITUS

Diabetes is an illness in which the individual’s blood glucose level is above the established range. Glucose is present in the foods we eat. Most foods contain a blend of carbohydrates, proteins, and fats. The amount of each of these nutrients in the foods we consume determines how quickly the body transforms food into glucose. For instance, consuming carbohydrates affects blood glucose levels one to two hours after the meal. Ingesting protein has very little influence on blood glucose levels, and the glucose from the fat in foods is slowly absorbed and does not contribute to increase glucose levels.¹

Insulin is a hormone that helps glucose enter the cells to release energy. In individuals with type 1 diabetes, the body does not produce insulin. Type 2 diabetes is the most common type of diabetes. In type 2 diabetes the body either does not make or does not use the insulin produced by the body in an efficient manner. With reduced insulin production or use, the glucose released by food stays in the bloodstream (reflected as increased glucose levels). Prediabetes is a condition in which individuals have increased blood glucose levels, but not sufficiently high levels to meet diagnostic criteria for diabetes. The presence of prediabetes increases the risk of developing type 2 diabetes.¹

In 2015, 30.3 million Americans had diabetes. Of these, only 23.1 million had a formal diagnosis. The remainder were undiagnosed. Twenty-five percent of older Americans have diabetes. Of the 7.2 million hospital discharges related to diabetes, 1.5 million were of patients who also had cardiovascular disease, five of each 1,000 had a lower extremity amputation, and 7.7 of 1,000 individuals had diabetic ketoacidosis. It is also estimated that in 2011 to 2012, 36.5% of individuals with diabetes also had chronic kidney disease. Diabetes is the seventh leading cause of death in the United States.²

PRESSURE INJURY OVERVIEW

Pressure injury is defined as follows: “A pressure injury is localized damage to the skin and underlying soft tissue usually over a bony prominence or related to a medical or other device. The injury can present as intact skin or an open ulcer and may be painful. The injury occurs as a result of intense and/or prolonged pressure or pressure in combination with shear. The tolerance of soft tissue for pressure and shear may also be affected by microclimate, nutrition, perfusion, co-morbidities and condition of the soft tissue.”³

Pressure injuries normally develop over bony prominences. These include the elbows, heels ankles, buttocks, shoulder blades, spine, greater trochanters, among others. Individuals with decreased sensation, impaired blood flow, and limited mobility (bedridden or in wheelchairs) are at increased risk for developing pressure injuries. The neuropathy and poor circulation seen in patients with diabetes make the presence of this condition a risk factor for developing pressure injuries. As a rule, individuals with reduced sensation may not be aware of the constant pressure on their tissues, thus reducing their attentiveness to shifting positions. The constant pressure reduces blood flow (circulation) to the tissue and results in decreased tissue perfusion and atrophy. Impaired blood flow also contributes to decreased nutrient delivery to the site. This change increases the risk for tissue injury. Individuals unable to x turn and position themselves independently are especially vulnerable to develop pressure injuries.³

PRESSURE INJURIES AND DIABETES MELLITUS

The presence of diabetes can contribute to a decreased wound healing rate. Increased glucose levels can stiffen the arteries and contribute to narrowing of the blood vessels. This can contribute to pressure injury development and is a risk factor for impaired wound healing.

As previously mentioned, narrowing of the blood vessels contributes to decreased flow of blood and oxygen to a wound. High glucose levels can impair the function of red blood cells that carry nutrients to the tissue. Without adequate nutrients and oxygen, a wound heals slowly.⁴

NUTRITION CARE OF DIABETIC PATIENTS WITH PRESSURE INJURIES

Managing the nutritional status of individuals with diabetes and pressure injuries to promote adequate nutrient consumption and stable blood glucose levels is important in promoting wound healing. Encouraging individuals to consume a healthy diet and maintaining a balanced nutritional status can help to modulate blood glucose levels and provide sufficient vitamins and minerals to support the healing process.⁵

The consumption of adequate protein, carbohydrates, fluids, vitamins, and minerals is a vital aspect of promoting wound healing. The National Pressure Ulcer Advisory Panel (NPUAP) pressure injury prevention and treatment guidelines encourage the provision of individualized energy intake based on underlying medical condition and level of activity for individuals at risk for or with actual pressure injures. The NPUAP guidelines support providing sufficient calories (30–35 calories per kilogram of body weight), protein (1.25–1.5 g protein per kilogram of body weight), and fluids (30 mL per kilogram of body weight), as well as good sources of vitamins and minerals.⁶

Determining what to eat can be the most challenging part of daily self-management for people with diabetes. The American Diabetes Association (ADA) has long held that there is no “one size fits all” approach to nutrition therapy for individuals with diabetes. The ADA goals for providing nutrition therapy for individuals with diabetes include promoting adhering to healthful eating patterns and emphasizing a variety of nutrient-dense foods in appropriate portion sizes to improve overall health and specifically to⁵:

• Achieve and maintain body weight goals
• Attain individualized glycemic, blood pressure, and lipid goals
• Delay or prevent complications of diabetes

There is no single ideal dietary distribution of calories among carbohydrates, protein, and fats for individuals with diabetes. Therefore, macronutrient distribution should be individualized while maintaining total calorie and metabolic goals in mind. As appropriate, individuals with pressure injuries and diabetes should be referred to the registered dietitian or nutritionist to provide medical nutrition therapy.⁵

IMPLICATIONS FOR PRACTICE

Providing nutrition therapy to individuals with pressure injuries in the presence of other comorbidities can be a challenge. Not only can the presence of diabetes be a risk factor for developing pressure injuries, but also uncontrolled blood glucose levels can interfere with wound healing. The good news is that the nutrition care guidelines for these medical conditions seem to complement each other, thus making the development of a patient-centered healthful eating pattern less complex. With appropriate nutritional interventions, it is possible to obtain metabolic homeostasis that promotes wound healing. A meal pattern high in protein with an adequate amount of calories can be a good starting point. A consistent meal pattern with similar nutritional composition can be healthful by controlling blood glucose levels and promoting wound healing. Meal patterns should be customized to meet the individual’s regular eating pattern.

References

1. National Institute of Diabetes and Digestive and Kidney Diseases. Managing Diabetes. 2016. https://www.niddk.nih.gov/health-information/diabetes/overview/managing-diabetes. . Accessed June 27, 2018.

2. Centers for Disease Control and Prevention, US Department of Health and Human Services. Centers for Disease Control and Prevention. National Diabetes Statistics Report, 2017. 2017. https://www.cdc.gov/diabetes/pdfs/data/statistics/national-diabetes-statistics-report.pdf. Accessed June 27, 2018.

3. National Pressure Ulcer Advisory Panel. NPUAP Pressure Injury Stages. National Pressure Ulcer Advisory Panel website. 2014. http://www.npuap.org/resources/educational-and-clinical-resources/npuap-pressure-injury-stages/. Accessed June 27, 2018.

4. Chauhan VS GS, Kumar P, Srivastava S, Shukla VK. . The prevalence of pressure ulcers in hospitalised patients in a university hospital in India. J Wound Care. Wound Cre. 2005;14(1):36-37. https://www.magonlinelibrary.com/doi/abs/10.12968/jowc.2005.14.1.26724. Accessed June 27, 2018.

5. American Diabetes Association. Standards of Medical Care in Diabetes-2018 Abridged for Primary Care Providers. Clin Diabetes 2018. 2018;36(1):14-37. http://clinical.diabetesjournals.org/content/36/1/14. Accessed June27, 2019.

6. European Pressure Ulcer Advisory Panel, National Pressure Ulcer Advisory Panel, Pan Pacific Pressure Injury Alliance. Pressure Ulcer Treatment: Quick Reference Guide. 2014. https://www.npuap.org/wp-content/uploads/2014/08/Updated-10-16-14-Quick-Reference-Guide-DIGITAL-NPUAP-EPUAP-PPPIA-16Oct2014.pdf. Accessed June 27, 2018.