Diabetic Ulcers
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Diabetic foot ulcers, as shown in the images below, occur as a result of various factors, such as mechanical changes in conformation of the bony architecture of the foot, peripheral neuropathy, and atherosclerotic peripheral arterial disease, all of which occur with higher frequency and intensity in the diabetic population. [1, 2]
Nonenzymatic glycation predisposes ligaments to stiffness. Neuropathy causes loss of protective sensation and loss of coordination of muscle groups in the foot and leg, both of which increase mechanical stresses during ambulation.
Diabetic foot lesions are responsible for more hospitalizations than any other complication of diabetes. [3] Diabetes is the leading cause of nontraumatic lower extremity amputations in the United States, with approximately 5% of diabetics developing foot ulcers each year and 1% requiring amputation.
Physical examination of the extremity having a diabetic ulcer can be divided into examination of the ulcer and the general condition of the extremity, assessment of the possibility of vascular insufficiency, [4] and assessment for the possibility of peripheral neuropathy.
The staging of diabetic foot wounds is based on the depth of soft tissue and osseous involvement. [5, 6, 7] A complete blood cell count should be done, along with assessment of serum glucose, glycohemoglobin, and creatinine levels.
The management of diabetic foot ulcers requires offloading the wound by using appropriate therapeutic footwear, [8, 9] daily saline or similar dressings to provide a moist wound environment, [10] debridement when necessary, antibiotic therapy if osteomyelitis or cellulitis is present, [11, 12] optimal control of blood glucose, and evaluation and correction of peripheral arterial insufficiency.
A vascular surgeon and/or podiatric surgeon should evaluate all patients with diabetic foot ulcers so as to determine the need for debridement, revisional surgery on bony architecture, vascular reconstruction, or soft tissue coverage.
The hemorrheologic agent cilostazol is contraindicated in patients with congestive heart failure. See Medication regarding the product’s black box warning.
For more information, see Diabetes Mellitus, Type 1 and Diabetes Mellitus, Type 2.
Atherosclerosis and peripheral neuropathy occur with increased frequency in persons with diabetes mellitus (DM).
Overall, people with diabetes mellitus (DM) have a higher incidence of atherosclerosis, thickening of capillary basement membranes, arteriolar hyalinosis, and endothelial proliferation. Calcification and thickening of the arterial media (Mönckeberg sclerosis) are also noted with higher frequency in the diabetic population, although whether these factors have any impact on the circulatory status is unclear.
Diabetic persons, like people who are not diabetic, may develop atherosclerotic disease of large-sized and medium-sized arteries, such as aortoiliac and femoropopliteal atherosclerosis. However, significant atherosclerotic disease of the infrapopliteal segments is particularly common in the diabetic population. Underlying digital artery disease, when compounded by an infected ulcer in close proximity, may result in complete loss of digital collaterals and precipitate gangrene.
The reason for the prevalence of this form of arterial disease in diabetic persons is thought to result from a number of metabolic abnormalities, including high low-density lipoprotein (LDL) and very-low-density lipoprotein (VLDL) levels, elevated plasma von Willebrand factor, inhibition of prostacyclin synthesis, elevated plasma fibrinogen levels, and increased platelet adhesiveness.
The pathophysiology of diabetic peripheral neuropathy is multifactorial and is thought to result from vascular disease occluding the vasa nervorum; endothelial dysfunction; deficiency of myoinositol-altering myelin synthesis and diminishing sodium-potassium adenine triphosphatase (ATPase) activity; chronic hyperosmolarity, causing edema of nerve trunks; and effects of increased sorbitol and fructose. [13]
The result of loss of sensation in the foot is repetitive stress; unnoticed injuries and fractures; structural foot deformity, such as hammertoes, bunions, metatarsal deformities, or Charcot foot (see the image below); further stress; and eventual tissue breakdown. Unnoticed excessive heat or cold, pressure from a poorly fitting shoe, or damage from a blunt or sharp object inadvertently left in the shoe may cause blistering and ulceration. These factors, combined with poor arterial inflow, confer a high risk of limb loss on the patient with diabetes.
See Diabetic Neuropathy for more information.
The etiologies of diabetic ulceration include neuropathy, [14] arterial disease, [15] pressure, [8] and foot deformity. [16] Diabetic peripheral neuropathy, present in 60% of diabetic persons and 80% of diabetic persons with foot ulcers, confers the greatest risk of foot ulceration; microvascular disease and suboptimal glycemic control contribute.
A study by Naemi et al indicated that tissue mechanics may be associated with foot ulceration in patients with diabetic neuropathy, with an evaluation of 39 patients finding that the heel pad in nonulcerated feet tended to be stiffer than in ulcerated feet. [17] . These results were further elucidated in another study by Naemi et al, which reported that the risk of diabetic foot ulcer is higher in diabetic neuropathy patients who have greater plantar soft tissue thickness and lower stiffness in the area of the first metatarsal head. The investigators found that adding the mechanical properties of plantar soft tissue (stiffness and thickness) to commonly evaluated clinical parameters improved specificity, sensitivity, prediction accuracy, and prognosis strength by 3%, 14%, 5%, and 1%, respectively. [18]
The anatomy of the foot must be considered in risk calculation. A person with flatfoot is more likely to have disproportionate stress across the foot and may have an increased risk for tissue inflammation in high-stress regions.
Sensory neuropathy involving the feet may lead to unrecognized episodes of trauma due to ill-fitting shoes. Motor neuropathy, causing intrinsic muscle weakness and splaying of the foot on weight bearing, compounds this trauma. The result is a convex foot with a rocker-bottom appearance. Multiple fractures are unnoticed until bone and joint deformities become marked. This is termed a Charcot foot (neuropathic osteoarthropathy) and most commonly is observed in diabetes mellitus, affecting about 2% of diabetic persons.
If a Charcot foot is neglected, ulceration may occur at pressure points, particularly the medial aspect of the navicular bone and the inferior aspect of the cuboid bone. Sinus tracts progress from the ulcerations into the deeper planes of the foot and into the bone. Charcot change can also affect the ankle, causing displacement of the ankle mortise and ulceration, which can lead to the need for amputation.
According to the National Institute of Diabetes and Digestive and Kidney Diseases, an estimated 16 million Americans are known to have diabetes, and millions more are considered to be at risk for developing the disease. Diabetic foot lesions are responsible for more hospitalizations than any other complication of diabetes. [3] Among patients with diabetes, 15% develop a foot ulcer, and 12-24% of individuals with a foot ulcer require amputation. Indeed, diabetes is the leading cause of nontraumatic lower extremity amputations in the United States. In fact, every year approximately 5% of diabetics develop foot ulcers and 1% require amputation.
Diabetes occurs in 3-6% of Americans. Of these, 10% have type 1 diabetes and are usually diagnosed when they are younger than 40 years. Among Medicare-aged adults, the prevalence of diabetes is about 10% (of these, 90% have type 2 diabetes). Diabetic neuropathy tends to occur about 10 years after the onset of diabetes, and, therefore, diabetic foot deformity and ulceration occur sometime thereafter.
The issue of diabetic foot disease is of particular concern in the Latino communities of the Eastern United States, in African Americans, [19] and in Native Americans, who tend to have the highest prevalence of diabetes in the world.
See Diabetic Foot Infections for more information.
Mortality in people with diabetes and foot ulcers is often the result of associated large vessel arteriosclerotic disease involving the coronary or renal arteries.
In assessing the health-related quality of life (HRQOL) in adults with diabetic foot ulcers, a literature review by Khunkaew et al found that such patients scored poorly on four of eight scales on the 36-Item Short Form Health Survey (SF-36), specifically, physical functioning, role physical, general health, and vitality. Risk factors for a lower HRQOL included the existence of pain, a C-reactive protein level above 10 mg/L, an ulcer size of over 5 cm2, an ankle-brachial index value of less than 0.9, a high glycosylated hemoglobin level, and a body mass index of over 25 kg/m2. [20]
Limb loss is a significant risk in patients with diabetic foot ulcers, particularly if treatment has been delayed. [21] Diabetes is the predominant etiology for nontraumatic lower extremity amputations in the United States. Half of all nontraumatic amputations are a result of diabetic foot complications, and the 5-year risk of needing a contralateral amputation is 50%. [22]
In diabetic people with neuropathy, [23] even if successful management results in healing of the foot ulcer, the recurrence rate is 66% and the amputation rate rises to 12%.
A study by Chammas et al indicated that ischemic heart disease is the primary cause of premature death in patients with diabetic foot ulcer, finding it to be the major source of mortality on postmortem examination in 62.5% of 243 diabetic foot ulcer patients. The study also found that in patients with diabetic foot ulcer, the mean age of death from ischemic heart disease, as derived from postmortem examination, was 5 years below that of controls. Patients with neuropathic foot ulcers were determined to have the highest risk of premature death from ischemic heart disease. [24]
A study by Chen et al indicated that following hospital treatment for diabetic foot ulcer, invasive systemic infection associated with the ulcer (DFU-ISI) is an important late complication that increases mortality risk. In the study’s patients, methicillin-resistant Staphylococcus aureus (MRSA) gave rise to 57% of the ISIs. Using Cox regression modeling, the investigators found that complicated ulcer healing and the presence of MRSA in the initial ulcer culture predicted the development of DFU-ISIs (hazard ratios of 3.812 and 2.030, respectively), with the hazard ratio for mortality risk in association with DFU-ISIs being 1.987. [25]
The risk of foot ulceration and limb amputation in people with diabetes is lessened by patient education stressing the importance of routine preventive podiatric care, appropriate shoes, avoidance of cigarette smoking, control of hyperlipidemia, and adequate glycemic control. For excellent patient education resources, visit eMedicineHealth’s Diabetes Center. Also, see eMedicineHealth’s patient education article Diabetic Foot Care.
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Category
Examples
Description
Applications
Alginate
AlgiSite
Comfeel
Curasorb
Kaltogel
Kaltostat
Sorbsan
Tegagel
This seaweed extract contains guluronic and mannuronic acids that provide tensile strength and calcium and sodium alginates, which confer an absorptive capacity. Some of these can leave fibers in the wound if they are not thoroughly irrigated. These are secured with secondary coverage.
These are highly absorbent and useful for wounds having copious exudate. Alginate rope is particularly useful to pack exudative wound cavities or sinus tracts.
Hydrofiber
Aquacel
Aquacel-Ag
Versiva
An absorptive textile fiber pad, also available as a ribbon for packing of deep wounds. This material is covered with a secondary dressing. The hydrofiber combines with wound exudate to produce a hydrophilic gel. Aquacel-Ag contains 1.2% ionic silver that has strong antimicrobial properties against many organisms, including methicillin-resistant Staphylococcus aureus and vancomycin-resistant Enterococcus.
These are absorbent dressings used for exudative wounds.
Debriding agents
Hypergel (hypertonic saline gel)
Santyl (collagenase)
Accuzyme (papain urea)
Various products provide some degree of chemical or enzymatic debridement.
These are useful for necrotic wounds as an adjunct to surgical debridement.
Foam
LYOfoam
Spyrosorb
Allevyn
Polyurethane foam has some absorptive capacity.
These are useful for cleaning granulating wounds having minimal exudate.
Hydrocolloid
Aquacel
CombiDERM
Comfeel
Duoderm CGF Extra Thin
Granuflex
Tegasorb
These are made of microgranular suspension of natural or synthetic polymers, such as gelatin or pectin, in an adhesive matrix. The granules change from a semihydrated state to a gel as the wound exudate is absorbed.
They are useful for dry necrotic wounds, wounds having minimal exudate, and clean granulating wounds.
Hydrogel
Aquasorb
Duoderm
IntraSite Gel
Granugel
Normlgel
Nu-Gel
Purilon Gel
(KY jelly)
These are water-based or glycerin-based semipermeable hydrophilic polymers; cooling properties may decrease wound pain. These gels can lose or absorb water depending upon the state of hydration of the wound. They are secured with secondary covering.
These are useful for dry, sloughy, necrotic wounds (eschar).
Low-adherence dressing
Mepore
Skintact
Release
These are various materials designed to remove easily without damaging underlying skin.
These are useful for acute minor wounds, such as skin tears, or as a final dressing for chronic wounds that have nearly healed.
Transparent film
OpSite
Skintact
Release
Tegaderm
Bioclusive
These are highly conformable acrylic adhesive film having no absorptive capacity and little hydrating ability, and they may be vapor permeable or perforated.
These are useful for clean dry wounds having minimal exudate, and they also are used to secure an underlying absorptive material. They are used for protection of high-friction areas and areas that are difficult to bandage such as heels (also used to secure IV catheters).
Vincent Lopez Rowe, MD Professor of Surgery, Program Director, Vascular Surgery Residency, Department of Surgery, Division of Vascular Surgery, Keck School of Medicine of the University of Southern California
Vincent Lopez Rowe, MD is a member of the following medical societies: American College of Surgeons, American Surgical Association, Pacific Coast Surgical Association, Society for Clinical Vascular Surgery, Society for Vascular Surgery, Western Vascular Society
Disclosure: Nothing to disclose.
Romesh Khardori, MD, PhD, FACP Professor of Endocrinology, Director of Training Program, Division of Endocrinology, Diabetes and Metabolism, Strelitz Diabetes and Endocrine Disorders Institute, Department of Internal Medicine, Eastern Virginia Medical School
Romesh Khardori, MD, PhD, FACP is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians, American Diabetes Association, Endocrine Society
Disclosure: Nothing to disclose.
Jeffrey Lawrence Kaufman, MD Associate Professor, Department of Surgery, Division of Vascular Surgery, Tufts University School of Medicine
Jeffrey Lawrence Kaufman, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Surgeons, American Society for Artificial Internal Organs, Association for Academic Surgery, Association for Surgical Education, Massachusetts Medical Society, Phi Beta Kappa, and Society for Vascular Surgery
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment
Diabetic Ulcers
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