Study Points

Hyperglycemia and Wound Management

Course #34373 - $25 • 5 Hours/Credits

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  • Participation Instructions
    • Review the course material online or in print.
    • Complete the course evaluation.
    • Review your Transcript to view and print your Certificate of Completion. Your date of completion will be the date (Pacific Time) the course was electronically submitted for credit, with no exceptions. Partial credit is not available.
  1. Which of the following is NOT a main cause of hyperglycemia?

    CAUSES OF HYPERGLYCEMIA

    There are three main causes of hyperglycemia: diabetes, certain medications, and physiologic or psychologic stress. Diabetes is by far the most common cause of chronic hyperglycemia and is associated with many adverse effects on a patient's health, including impaired wound healing and increased risk for lower extremity ulcers and amputation. However, medication use and physiologic/psychologic stresses are also important contributors to hyperglycemia, particularly among hospitalized patients. When all of these factors are combined, a patient can be at significantly heightened risk for wound complications and poor outcomes.

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  2. As of 2018, how many Americans were estimated to have diabetes?

    CAUSES OF HYPERGLYCEMIA

    Diabetes, known clinically as diabetes mellitus, is a progressive disease process affecting the fuel metabolism functioning within the body [1]. According to the Centers for Disease Control and Prevention (CDC), the prevalence of diabetes has increased 900% since 1958, when 0.93% of Americans had diabetes, with the sharpest increase occurring in the 2000s [2]. As of 2018, 13% of the United States population, or 34.1 million Americans, had diabetes [3]. Unfortunately, 7.3 million of these individuals are unaware of their diabetes diagnosis. Diabetes has been considered epidemic since the 1970s, and the number of Americans expected to have diagnosed or undiagnosed diabetes is estimated to be 84 million by the year 2060 [4].

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  3. Which of the following is an established risk factor for the development of type 2 diabetes?

    CAUSES OF HYPERGLYCEMIA

    All adults older than 45 years of age should be screened for diabetes every three years or every two years if they have any risk factors for type 2 diabetes [15,17]. In addition, individuals of any age who are at risk for or are suspect of having diabetes should be screened. Established risk factors for type 2 diabetes include:

    • Age older than 45 years

    • Body mass index (BMI) greater than or equal to 25 kg/m2

    • Family history of type 2 diabetes

    • Habitual physical inactivity

    • Race/ethnicity (e.g., African American, Hispanic American, American Indian, Alaska Native, Pacific Islander)

    • IGT or elevated fasting glucose

    • Previous history of gestational diabetes or giving birth to a child weighing more than 9 pounds

    • Hypertension (i.e., blood pressure greater than 140/90 mm Hg in adults)

    • Abnormal lipid levels (i.e., high-density lipoprotein [HDL] level <35 mg/dL and/or triglyceride level >250 mg/dL)

    • Polycystic ovarian syndrome

    • History of vascular disease

    • Acanthosis nigricans (most common among individuals of African descent)

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  4. A fasting plasma glucose level of 117 mg/dL would fit the diagnostic criteria for

    CAUSES OF HYPERGLYCEMIA

    DIAGNOSTIC CRITERIA FOR TYPE 2 DIABETES

    StageFasting Plasma Glucose LevelsTwo-Hour Postprandial Plasma Glucose Levels
    Euglycemia<100 mg/dL<140 mg/dL
    Prediabetes>100 mg/dL but <126 mg/dL>140 mg/dL but <200 mg/dL
    Diabetes≥126 mg/dL≥200 mg/dL
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  5. Which of the following physiologic changes is triggered by acute illness and can lead to hyperglycemia?

    CAUSES OF HYPERGLYCEMIA

    THE RELATIONSHIP BETWEEN ACUTE ILLNESS AND HYPERGLYCEMIA

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  6. What is the first phase of acute wound healing?

    AN OVERVIEW OF WOUND HEALING

    The pathophysiology of acute wound healing has been characterized as a hierarchical progression through four distinct phases. The first phase is coagulation and occurs immediately at the time of tissue injury [29]. The key cell activated in this phase is the platelet, which aggregates at the area of injury and binds with thrombin to form a plug. Vasoconstriction occurs, and cytokines and growth factors, including platelet-driven growth factors and fibroblast growth factors, are released [29]. These reactions initiate healing and act as chemoattractants for circulating polymorphonuclear cells and macrophage [30].

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  7. The time necessary for an acute wound to be considered healed is typically

    AN OVERVIEW OF WOUND HEALING

    Simultaneously, scar tissue formation and collagen shortening occur, and fibroblasts are transformed into myofibroblasts, causing the wound to react and contract [30]. When the wound is completely covered with epithelium and not draining, it is considered healed. The entire process typically takes 10 to 14 days to complete in an acute wound [31]. This is followed closely by the remodeling phase, during which collagen fibrils in scar tissue are remodeled in a turnover process resulting from the interplay of degradation of the matrix metalloproteases and the production of matrix components from the fibroblasts. This final phase may continue for the next 6 to 12 months [30].

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  8. Unlike the orderly healing process associated with most acute wounds, chronic wounds

    AN OVERVIEW OF WOUND HEALING

    Unlike the orderly healing process described for acute wounds, chronic wounds are stuck in a disorderly mix of inflammation and failed eruptions of proliferation [30]. Dysfunctional wound healing may occur during any phase of the healing process and may involve insufficient repair, excessive repair, or infection. The causes can be related to a predisposing disorder, such as diabetes, an acquired condition, such as hypoxia, or one of many potential medication interactions or alterations in nutrition [24].

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  9. Which of the following delays wound healing in chronic wounds?

    AN OVERVIEW OF WOUND HEALING

    Hypovolemia also inhibits inflammation, as the physiologic response is vasoconstriction rather than the dilatation required to deliver inflammatory cells to the site of injury. Anti-inflammatory steroids prevent macrophages from migrating to the site of injury and inhibit the release of collagenase and plasminogen activator. Anti-inflammatory steroids also inhibit fibroblast migration into the wound during the reconstructive phase [24].

    Optimal nutrition is important during all phases of healing because metabolic needs are increased. The substances most vital to healing include glucose, oxygen, and protein [31]. Because leukocytes require a glucose-rich environment to produce the adenosine-5 triphosphate (ATP) needed for chemotaxis, phagocytosis, and intracellular killing, individuals with poorly controlled diabetes heal poorly, mainly because of infection [33]. Individuals with diabetes are also at an increased risk for ischemic wounds, because they are likely to have both microvascular diseases that impair the microcirculation and altered glycosylated hemoglobin affinity for oxygen, with oxygen not readily released into the tissue. Oxygen delivery is also compromised by the hypoxemia state. Ischemic tissue is susceptible to infection, which in turn prolongs the inflammatory process.

    Along with hypoxemia, hypoproteinemia lengthens inflammation by impairing fibroblast proliferation [24]. Most of the factors that interfere with the production of collagen in healing tissues are nutritional [24]. Scurvy, for example, is caused by a lack of ascorbic acid (vitamin C), which is one of the cofactors required for collagen formation by fibroblasts. As a result, patients with scurvy have poorly formed connective tissue and greatly impaired healing. Protein and other nutrients, including iron, oxygen, β-ketoglutarate, manganese, copper, and calcium, are required for collagen synthesis [34]. However, minute amounts of these substances are usually required as cofactors, so deficiencies are not generally clinically significant. Dysfunctional collagen overwhelming the surface of a wound is manifested by a keloid or hypertrophic scar, both of which are related to increased collagen synthesis and decreased collagen lysis [35].

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  10. What percentage of patients with diabetes will develop diabetic ulcers?

    DIABETES AND WOUND DEVELOPMENT AND HEALING

    The public health impact of wounds is immense. An estimated 2.5 million inpatients develop pressure injuries each year, particularly older and malnourished individuals [37]. Furthermore, as many as 34% of the 34.1 million individuals with diabetes in the United States will develop diabetic ulcers; many more will have venous ulcers or wounds that result from vascular disease [38]. The annual cost of treating wounds of this nature is estimated to be more than $15 billion, which has led to specific guidelines based on specialist organization consensus [37,39,40,41,75]. In patients with diabetes, neuropathy and microvascular disease are the greatest contributors to impaired wound healing, both of which can be improved with optimal management of blood glucose levels.

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  11. Which of the following is the most common type of neuropathy among patients with diabetes?

    DIABETES AND WOUND DEVELOPMENT AND HEALING

    Neuropathy refers to the impaired effectiveness of the nerves in conducting pain, pressure, or movement sensations. In many patients with diabetes, the development of neuropathy in the lower extremities leads to loss of protective sensation, resulting in undetected trauma and infection. The most common type of neuropathy in patients with diabetes is peripheral neuropathy, which affects the ends of the longest nerves first; the toes and feet are the most severely affected. Other types or neuropathy include autonomic neuropathy, mononeuropathy, and diabetic amyotrophy (also referred to as radiculoplexus neuropathy). In patients with peripheral neuropathy, the development of foot ulcers and even foot deformities is common, and the healing of these ulcers can be complicated by the presence of hyperglycemia [42].

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  12. The most common triad leading to breakdown of the diabetic foot is

    DIABETES AND WOUND DEVELOPMENT AND HEALING

    Foot deformities, such as claw toes or prominent metatarsal heads, are a proven risk factor for ulceration [26,42]. One cross-sectional study demonstrated that plantar callus accumulation was associated with an 11-fold increase in formation of diabetic foot ulceration [30]. In follow-up with these individuals, plantar ulceration occurred only at sites of callus in neuropathic feet. Other risk factors include a past history of foot ulcers or amputation, the presence of other microvascular complications, long duration of poorly controlled diabetes, increase in plantar foot pressures, and peripheral edema [30,43]. The most common triad leading to breakdown of the diabetic foot is peripheral neuropathy (insensitivity), deformity (claw toe), and trauma (from ill-fitting footwear, repetitive stress, or thermal damage) [30,42,44].

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  13. Venous ulcers are caused by

    VASCULAR ULCERS

    Vascular ulcers may develop in the arterial, venous, or lymphatic systems from a variety of causes [33]. Patients with diabetes are at an increased risk for both arterial and venous ulcers. The pathophysiology of venous (or stasis) ulcers is related to venous hypertension that develops as the result of inadequate calf muscle pump action and either primary or secondary valvular incompetence [46]. Arterial ulcers, on the other hand, are wounds that will not heal due to compromised or inadequate arterial blood flow [33]. Arterial calcification is commonly detected in radiographs of diabetic feet and hands. This is related to calcification of the media on muscular arteries [43]. Differentiating between arterial and venous ulcers involves careful patient history and evaluating the appearance of the ulcer and surrounding skin (Table 2) [32].

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  14. The surrounding skin of arterial ulcers

    VASCULAR ULCERS

    CHARACTERISTICS OF ARTERIAL AND VENOUS ULCERS

    AspectsVenous UlcersArterial Ulcers
    Location
    Superior to medial malleolus
    Medial aspect of the leg and ankle
    "Gaiter" region of the legs
    Areas exposed to excessive pressure or repetitive trauma
    Lateral malleolus
    Mid-tibial
    Phalangeal heads
    Toe tips or web spaces
    Surrounding skin
    Erythemic
    Scaling
    Crusting
    Brown staining
    Lipodermatosclerosis
    Normal skin temperature (warm to touch)
    Pitting or nonpitting edema, with possible induration and cellulitis
    Scarring from previous ulcers
    Ankle flare
    Dependent rubor
    Shiny
    Taut
    Dry, thin, hairless
    Atypical edema
    Decreased skin temperature (cool to touch)
    Atrophy of subcutaneous tissue
    General appearance
    Ruddy red base
    Yellow adherent or loose slough
    Granulation tissue present
    Vary in size (small to full circumference of the leg)
    Pale, sloughy base
    Granulation rarely present
    Necrosis, eschar, gangrene (wet or dry)
    Smaller, but deep
    Tendon or bone may be visible
    DepthUsually shallowDeep
    Margins
    Irregular
    Undermining or tunneling uncommon
    Edges rolled
    Punched out
    Smooth and undermining
    ExudateModerate to heavyMinimal
    InfectionLess commonFrequent, but signs may be subtle
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  15. Which of the following is NOT a treatment approach recommended for vascular ulcers?

    VASCULAR ULCERS

    Treatment and management of vascular ulceration include the following approaches [30,31,47]:

    • Pressure off-loading, utilizing crutches, wheelchairs, therapeutic footwear, half shoes, and removable cast walkers to relieve pressure on the affected area.

    • Debridement of necrotic tissue from the ulceration to allow for healing. This can be accomplished by surgical or nonsurgical means and allows for viable skin to be produced and adhere to the surface of the ulcer. This therapy is commonly utilized in the mid- or chronic stages of ulceration.

    • Adjunctive wound therapy, including low-adherent dressings, interactive (occlusive) hydrocolloid dressings, semi-permeable films, hydrogels, and alginate dressings. Synthetic foams work as healing agents, and antimi-crobial barriers are commonly utilized in all stages of acute and chronic ulceration.

    • Growth factor, in combination with a platelet releasate or delivered through recombinant platelet-derived growth factor technology, is utilized in early and involved diabetic ulcerations.

    • Hyperbaric oxygen therapy. Intermittent inhalation of pure oxygen at a pressure greater than one atmosphere absolute (15 pounds pressure/in2) increases the percentage of oxygen available to produce adequate wound healing. This therapy is utilized in the chronic stages of diabetic ulcerations when other therapies have lost their efficacy. Authors of a 2012 Cochrane review concluded that hyperbaric oxygen therapy is significantly beneficial in the short term but not in the long term.

    • Electrical stimulation to increase the blood flow. Utilizing asymmetric biphasic stimulation is associated with increased healing of nearly 60%. This form of therapy can be utilized in early or involved stages of diabetic ulceration therapy.

    • Low-intensity ultrasonic stimulation improves the rate of wound healing.

    • Topical radiant heat. This therapy optimizes the enzymatic processes involved in wound healing and can be utilized in early or involved stages of diabetic ulceration therapy.

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  16. Loss of sensation caused by sensory neuropathy typically begins with

    SENSORY-NEUROPATHIC ULCERS

    Sensory neuropathy contributes to an inability to perceive injury to the foot due to the loss of protective sensation [33]. Individuals with sensory loss are seven times more likely to develop foot ulcers compared to those without neuropathic disorders [30]. Loss of sensation is the result of demyelination of the peripheral nerves (particularly the distal nerve endings) [27]. Presentation of this loss of sensory sensation typically begins with numbness or paresthesia of the toes and progresses upward to create a "stocking" effect to the extremity [48].

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  17. Which of the following is a risk factor for the development of pressure injuries?

    PRESSURE INJURIES

    In addition to diabetes and hyperglycemia, there are many risk factors for the development of pressure injuries, including [24]:

    • Older age

    • Neurologic disorders, such as spinal cord injuries, dementia, or cerebrovascular disease, resulting in decreased sensation and/or mobility

    • Immobilization

    • Incontinence

    • Fractures (e.g., hip or femur)

    • Coarse bed sheets

    • Reduced tissue perfusion (e.g., as from edema or hypotension)

    • Obesity

    • Skin dehydration

    • Stress

    • Depression

    • Low body weight and impaired nutrition

    • Smoking

    • Certain medications

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  18. A partial thickness pressure ulcer with partial loss of dermis, without slough visible, is categorized as

    PRESSURE INJURIES

    Stage 2 pressure injury presents as shallow, open wounds with partial loss of the dermis. The wound bed is pink/red and without slough. A stage 2 pressure ulcer may also present as a serous fluid-filled blister [55]. Fat and deeper tissues are not visible, and slough and eschar are not present. These injuries are most commonly seen on the sacrum due to moisture and shear, and on the heel due to shear [55]. Skin tears, tape burns, incontinence-associated dermatitis, maceration, or excoriation of the skin should not be classified as stage 2 pressure ulcers [33].

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  19. Patients with diabetes have been shown to have increased carriage rates for

    SURGICAL WOUNDS

    In addition to hyperglycemia, obese patients with or without diabetes have a significantly increased risk of impaired wound healing than those of normal weight [60]. Severe obesity is associated with venous stasis disease, pitting pretibial edema, bronze edema (a result of extravasation of red blood cells into the skin), cellulitis, and obesity hypoventilation [65]. Furthermore, obesity is a known risk factor for surgical-site infection. Patients with diabetes have been shown to have increased carriage rates for Staphylococcus aureus colonization, a leading cause of surgical-site infection [61]. These conditions impact the body's ability to heal an incision, potentially leading to wound dehiscence, rhabdomyolysis, and complications of the skin and underlying tissue [60].

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  20. When documenting wounds and ulcers, what is the optimum time interval between measurements?

    WOUND DOCUMENTATION

    The optimal time interval between wound measurements is approximately seven days. More frequent measurement is unlikely to demonstrate clinically relevant differences in wound dimension [24]. Weekly documentation should minimally include a reassessment of wound appearance. The NPIAP recommends the use of digital photography in documenting changes in dimension and base of wounds over time. These photographs may be used to supplement written documentation, but they should never be used as a replacement for clearly written documentation [69,70]. As noted, the face of a clock can be used to provide additional accuracy to the description of wound characteristics [71]. The terms used in documentation should represent objective data rather than subjective findings [24]. When documenting wounds, descriptive words such as "huge" or "deep" and diagnostic terms such as "infected" should be avoided. Instead, the objective descriptors such as "perierythema" or "induration" should be used [68].

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  • Back to Course Home
  • Participation Instructions
    • Review the course material online or in print.
    • Complete the course evaluation.
    • Review your Transcript to view and print your Certificate of Completion. Your date of completion will be the date (Pacific Time) the course was electronically submitted for credit, with no exceptions. Partial credit is not available.