Geralyn Spollett, MSN, C-ANP, CDE1
1Spollett is an adult nurse practitioner at Yale Diabetes Center, New Haven, CT.
Just as diabetes interferes with the physiology of the microvasculature of the eye and kidney, it similarly affects the small vessels of the skin, which may lead to skin changes.1 Although there are theories concerning the pathophysiology of certain cutaneous disorders associated with diabetes, many causes are unknown.2 In a clinical analysis of 750 patients with diabetes, a skin disorder was present in 594 patients, with the most common being cutaneous infection (47.5%), xerosis (26.4%), and inflammatory skin diseases (20.7%).3
Dyslipidemia and other metabolic changes associated with diabetes also can create dermatological changes. Autoimmune skin diseases such as vitiligo can occur in autoimmune type 1 diabetes (T1D). In rare cases, medications that are used to treat diabetes can cause adverse skin reactions. In general, how the disruption of normal insulin and glucose metabolism affects the skin is not completely understood.1
Necrobiosis Lipoidica Diabeticorum
Necrobiosis lipoidica diabeticorum, one of the least common diabetic lesions, has no known etiology (Figure 15.1). The lesions may be related to trauma, microangiopathy, immunoglobulins, and fibrin deposition. In general, this type of lesion is seen in individuals with diabetes of long duration, but its progression seems to have little to do with glucose control.1 NLD occurs in 0.3–1.6% of individuals with diabetes and is three times more common in women than in men.4 It most commonly appears during the third or fourth decade of life.2
Figure 15.1—Necrobiosis lipoidica diabeticorum. Lighter tinge at the center of the lesion is caused by a lack of collagen.
When the lesion occurs in people who do not have diabetes, many of these patients (~90%) go on to develop impaired glucose tolerance or are found to have a family history of diabetes.3 Therefore, screening for diabetes in these individuals is highly recommended.
The NLD lesion progresses through a series of changes, beginning as a shiny, demarcated dusky pink plaque that is slightly elevated. Size varies from 1–3 cm to ~25 cm, and over time, it becomes redder and can take on a brownish tinge. As the weeks and months progress, it becomes atrophic, with a thin, shiny, slightly pigmented appearance. The center may have a yellowish tinge, indicating a loss of collagen or severe thinning of the skin, making the subcutaneous fat visible. The lesion initially may present as a series of closely grouped small plaques that coalesce into a larger plaque over time. Usually, the lesions are asymptomatic, but they may be pruritic or tender, or cause hypohidrosis of the affected skin.5 With thinning, the plaque becomes susceptible to spontaneous ulceration, and the most minor trauma can cause a rupture. The resulting ulcers are painful and difficult to heal. Approximately 20% of NLD lesions will resolve spontaneously after 6–12 years.6
Classically, NLD occurs bilaterally on the pretibial or medial malleolar areas. Lesions can also present on the hands, forearms, abdomen, face, and scalp, but these locations are less often associated with diabetes. Spontaneous remission occurs in 13–19% of patients.5
No standard guidelines or well-established treatment exist for NLD. Middle- to high-potency topical steroids with or without occlusion, intralesional injections of steroids at the active border, and, in some rare instances, systemic steroids have been used to treat NLD.7 Steroids can help control the initial erthyema of the lesion, but once it has progressed to the atrophic phase, the steroids are no longer effective and in fact can worsen the atrophy.8 Other treatments such as cyclosporine, psoralen and ultraviolet A (PUVA) light, high-dose nicotinamide, clofazimine, pentoxifylline, aspirin, and dipyridamole have been tried with varying rates of success.4 Laser treatment may help reduce bleeding and improve the appearance of the lesion.9 Specialized wound care clinics are best equipped to treat the ulcerated lesions.
The association of diabetes with granuloma annulare (GA) is debatable. The lesion presentation is so similar to NLD that a connection between GA and diabetes has been sought. Several studies indicate that generalized GA, especially in older patients, is associated with diabetes, whereas others suggest that recurrent localized GA may precede diabetes.
The initial presentation is small, flesh-colored papules that progress to one larger plaque. The papules may arrange in an annular fashion. The dermal plaques have a ring border and a depressed center. The lesions may be pruritic or create a burning sensation but are not painful. Histological testing shows collagen degeneration, chronic inflammation, and fibrosis.7 Commonly, lesions appear over the extensor joint areas in children and young adults and may be distributed more generally in middle-age to older adults. In its more generalized form, plaques are smaller, and hundreds of small lesions may be present. In patients with recurring lesions, screening for diabetes is recommended.
Treatment for GA is similar to that for NLD: topical, intralesional, and general steroid use. Other forms of treatment include cryosurgery, ultraviolet-light therapy, and CO2 laser.10 Localized GA remits spontaneously without scarring, but the more generalized version has a longer course with rare spontaneous resolution.4 The duration is variable. It is generally self-limited, and 50% of patients are without lesions within 2 years; however, 40% can experience reoccurrence at the same site.7
Generalized granuloma annulare (GGA) has been associated not only with diabetes but also with other serious diseases such as HIV, hepatitis C, Epstein-Barr virus infection, and sarcoidosis.11
Diabetic dermopathy (DD), a condition that presents as small (<1 cm) demarcated, pigmented pretibial papules, is by far the most common cutaneous manifestation of diabetes (Figure 15.2). Although it can be present in individuals without diabetes, it is found in as many as 40% of people with diabetes. It occurs more frequently in men >50 years old.4
Figure 15.2—Diabetic dermopathy. The most common dermatologic lesion, usually seen in the lower extremities.
The pigmented shin spots, usually seen on the extensor surfaces of the lower legs, begin as circumscribed round or oval red papules that progress to atrophic hyperpigmented macules. A fine scale over the surface of the macule sometimes is seen. The lesions are usually bilateral but have an asymmetric distribution. They may appear on the forearms, thighs, and lateral malleoli.4 Histological findings indicate edema of the papillary dermis, thickened superficial blood vessels, extravasation of erythrocytes, and a mild lymphocytic infiltrate.12 DD differs from NLD in that the collagen change is much less marked and necrobiosis is absent.13 DD lesions are asymptomatic but may become painful if they ulcerate. Usually the lesions spontaneously heal and disappear within 1–2 years without treatment, leaving an atrophic, hypopigmented area.8
Patients may comment that the lesions occurred after a trauma. Research findings indicate that the blood flow values at dermopathy sites are similar to those found at scar sites. It is possible that the skin scarring seen in dermopathy relates to poor skin perfusion associated with diabetes. Blood flow studies, however, also indicate that DD lesions do not represent local ischemia.14
Although some studies link DD to the microvascular complications of diabetes, such as nephropathy and retinopathy, other studies have been unable to substantiate these findings. Capillary changes may predispose to shin spots but are not the only cause of this condition.4 Blood glucose control is unrelated to the occurrence or progression of the problem, and there is no effective treatment for these lesions. Patients should prevent skin breakdown and infection by using moisturizers and avoiding trauma to the area.15
Diabetic bullae, also known as bullosis diabeticorum, are a clinically distinct marker for diabetes often reported in adults with diabetes of long duration and peripheral neuropathy (Figure 15.3). Usually confined to the feet and only occasionally seen on the hands, the blisters occur spontaneously and can be a few millimeters to several centimeters in size. It is seen more frequently in men and in those with T1D. It also can occur, however, as one of the first signs of diabetes. The pathology is unknown.
Figure 15.3—Diabetic bullae. Large fluid-filled sacs usually found on the feet or hands are a marker for diabetes.
The three types of diabetic bullae are 1) sterile and fluid filled (the most common form), 2) hemorrhagic, and 3) multiple, nonscarring bullae on tanned skin. Of these, only the hemorrhagic type leaves scarring. The bullae resolve spontaneously without treatment in 2–3 weeks but may reoccur in the same or a different anatomical place.
There is no treatment and preventing infection is a major focus in caring for these lesions. Thorough cleaning, topical antibiotics, and protective dressings on a daily basis will reduce the occurrence of infection. Usually steroidal creams or systemic antibiotic therapy is not necessary. The bullae fluid can be aspirated, but the blister roof should be preserved and used as a physiological cover for the wound.
Acanthosis nigricans (AN) is characterized by velvety, light brown to black hyperpigmented plaques that appear in the folds of the skin (Figure 15.4). The thickened skin is most commonly seen around the neck and axillae. Other affected areas include the groin, umbilicus, submammary regions, and hands. It initially presents with hyperpigmentation, which then is followed by a hypertrophy of the epidermis.12 In addition to its velvety appearance, it can be hyperkeratotic or include skin tags. It is among the most recognizable of dermatologic lesions associated with diabetes.
Figure 15.4—Acanthosis nigricans. The dark, velvety appearance of this condition is usually seen in the skinfolds of the neck and axillae.
Although there are eight different forms of AN, the one most commonly seen in diabetes is associated with insulin resistance and obesity. When it occurs in those without diabetes, it may be a prognostic indicator for the disease. The pathogenesis may be related to insulin-like growth factor receptors on the keratinocytes and dermal fibroblasts, stimulating growth.4 The dark color of these plaques is related to the thickness of the keratin-containing superficial epithelium. AN has been linked to impaired glucose tolerance in younger patients and, as a marker, can serve to alert providers to screen the patient for diabetes. A possible genetic predisposition or increased sensitivity of the skin to hyperinsulinemia may be present in African Americans and people of Hispanic or Latin American origins.8
Certain forms of AN are associated with carcinoma (stomach adenocarcinoma) and various endocrinopathies. The sudden appearance of AN after 40 years of age is an ominous sign. When malignancy is present, the lesion develops suddenly and progresses rapidly. Despite a strong association with diabetes, all AN lesions warrant a workup to rule out underlying causes, the most common of which are pineal tumors, occult malignancies, stomach adenocarcinoma, and drug use (nicotinic acid, estrogen, corticosteroids).7
AN lesions are usually asymptomatic. Although there is no specific treatment for those related to diabetes, a lowering of insulin resistance through weight loss, and improved glucose control can improve the condition. Retinoic and salicylic acid may help cosmetic appearance.
DIABETIC THICK SKIN
Diabetic thick skin has been reported in as many as 33% of individuals with diabetes.1 The three categories are 1) scleroderma-like changes of the hand associated with stiff joints and limited mobility—known as diabetic cheiroarthropathy, 2) measurable skin thickness, and 3) scleredema diabeticorum. The etiology of diabetic thick skin is not fully known. The skin has abnormal collagen accumulation that may be related to hyperglycemic accelerated nonenzymatic glycosylation. A second theory identifies insulin, acting as a growth factor, as causing an overproduction and buildup of collagen.
Tiny pebble-like papules that become confluent appear on the back of the hand, the knuckles, and along the fingernails. A third of these patients will have thick, tight waxy skin on the dorsal surface of their hands. There is limited mobility of the large and small joints of the hands but no pain. Patients may report difficulty completely extending fingers, as seen in tabletop (or prayer sign) and a slight contractures of the palmar surface (Dupuytren’s contracture) may be seen (Figure 15.5).
Figure 15.5—Failure of the palmar surfaces of interphalageal joints to approximate in a patient with stiff joints and waxy skin (prayer sign).
Diabetic scleredema (Figure 15.6) is characterized by diffuse nonpitting induration of the skin with loss of skin markings over the upper back, neck, and shoulders.2 It can extend to the face, arms, chest, and abdomen. The condition is usually asymptomatic, and because of its location, the patient may not even be aware of it. The lack of skin flexibility may cause decreased range of motion with neck and back discomfort. Scleredema occurs in 2.5–14% of individuals with type 2 diabetes (T2D).
Figure 15.6—Diabetic scleredema. The thickened, nonpitting skin of this condition can affect the flexibility of the upper back, shoulders, and neck.
The thickening of the skin is due to the deposition of glycosaminoglycans within the dermis. When the follicular openings are depressed, the skin will take on a peau d’orange appearance.
Improved glucose control and use of potent topical and intralesional steroids, penicillamine, intralesional insulin, low-dose methotrexate, prostaglandin E1, and pentoxifylline have had limited therapeutic success in the treatment of scleredema.4 In symptomatic patients a 12-week course of PUVA light may help. In extreme cases, electron beam therapy has been used.
Xanthoma or eruptive xanthoma usually appears as a consequence of hyperlipidemia, particularly hypertriglyceridemia associated with diabetes (Figure 15.7). Triglyceride levels are often >800 mg/dL and may exceed 1,500 or 2,000 mg/dL.1 Cutaneous xanthomas are a result of an extracellular deposition of lipid in the form of cholesterol or triglycerides in the dermis or subcutaneous fat.16 Biopsy of the xanthomas will show lipid-laden macrophages in the mid-dermis. The eruptive lesions develop suddenly over the extensor surfaces of the arms, legs, and buttocks, originally as red papules, but they subsequently change to yellow papules on an erythematous base. The lesion may remain as scattered individual papules or may cluster and form a rosette. They occur more often in patients with uncontrolled T2D.
Figure 15.7—Xanthomas. This condition can result from elevated cholesterol, particularly hypertriglyceridemia. Note the pearly color of the lesions.
Diabetes and lipid control play key roles in the resolution of the lesions. If the patient is insulin depleted, as in diabetic ketoacidosis, a rapid correction of glucose levels will lead to a faster resolution of the lesions. If the problem is based on chronically elevated triglycerides, lipid chemistry should be corrected, and once achieved, it may take several weeks before the lesions fully respond.
In a patient presenting with xanthoma, a fasting lipid profile is necessary to assess for hypertriglyceridemia, which increases the risk for coronary artery disease. In addition, hypertriglyceridemia with levels >400 mg/dL can result in pancreatitis. Dietary modifications and lipid- and triglyeride-lowering medications aimed at correcting the abnormal lipid profile will reduce cardiac risk as well as help to treat the xanthoma.
Xerosis or dry skin is one of the most common skin conditions in diabetes and is seen in ~50% of patients. Anhidosis, associated with autonomic neuropathy, and renal disease produce dry skin. Skin lacking in moisture is at increased risk for breakdown and subsequent infection or trauma. Fissuring of the hands and fingertips can lead to infection or pain in patients who practice self-monitoring of blood glucose (SMBG) using the fingertips. Using moisturizing creams or oils on the hands helps to reduce this fissuring. Cleansing hands with mild soap and water before SMBG is preferable to using alcohol wipes as alcohol promotes dry skin. Educating the patient on the importance of skin hygiene is essential in preventing skin lesions.
Vitiligo, an absence of melanocytes that causes hypopigmentation of the skin, can be seen in patients with autoimmune diseases, such as T1D, Addison’s disease, Hashimoto’s thyroiditis, Grave’s disease, rheumatoid arthritis, psoriasis, systemic lupus erythematosus, and pernicious anemia (Figure 15.8). It is seen in men and women alike.
Figure 15.8—Vitiligo. Usually associated with autoimmune T1D. The loss of skin pigment accounts for the white color of this lesion.
The lymphocytes attack the melanocytes, resulting in chalk-white lesions on the skin that commonly are found over extensor joints, such as the elbow and knuckles, and around orifices, such as the mouth and eye. Although vitiligo can occur in children as well as adults and is found in 0.2–1.0% of the general population, it appears in ~5% of individuals with diabetes.1
The treatment for vitiligo focuses on an attempt to reduce T-cell response and cause melanocytes to return and regenerate at the site. First-line treatment includes systemic PUVA light or corticosteroids with ultraviolet B. Moderate sun exposure also can be helpful.
Most patients continue to see new patches of vitiligo throughout their lives. It is not symptomatic but can be disfiguring causing high psychosocial stress.
Skin infections in patients with well-controlled diabetes occur at the same rate and severity as in the general population. Those with suboptimal glycemic control have more frequent infections that are more severe and difficult to resolve. Approximately 20–50% of those with T2D experience a skin infection.17 Elevated glucose levels cause numerous immunological dysfunctions that make the patient more vulnerable to infection and impede the healing process. With hyperglycemia, leukocytes are not able to move through the thickened capillary wall as effectively, phagocytic action is reduced, and chemotaxis is delayed, allowing an infection to worsen. Neuropathy and peripheral vascular disease can mask the symptoms of the infection, permitting it to advance unchecked. The presence of the infection further elevates glucose levels, contributing to the cycle of hyperglycemia and lengthening the recovery process.
Staphylococcal and fungal infections, particularly of the lower extremities, develop more often in patients with diabetes and are more resistant to therapy. For some patients, the skin infections become chronic problems, promoting skin breakdown and placing them at risk for more severe secondary infections.
Candida infections of the vagina, anogenital area, submammary regions, and axillae tend to be recurrent and occur most frequently in obese patients with T2D. In men, the folds of the foreskin and coronal rim of the penis are sites for balanitis and phimosis. Difficult to keep clean and dry, these skinfold areas provide the ideal warm, moist environment for dermatophyte growth. The location of the infection makes applying topical antibacterial or antifungal creams an arduous task, and patients may not complete the full course of therapy, allowing some of the infective agent to persist.
Candidiasis can affect the interdigital web spaces of the hands with eroded patches and inflammatory papules. Frequent hand washing or jobs in which the hands are continually moist predispose individuals to the infection. This condition is called interdigitalis blastomycetia.15
If the patient suspects an infection, the health-care provider should be notified immediately, so that treatment can begin as soon as possible. In the individual with inadequately controlled diabetes, the course of therapy may be longer than in the general population, and the patient must understand that to eradicate the infection, the treatment must be used consistently and the course of medication or topical treatment must be completed.
Prevention of skin infections begins with good personal hygiene (i.e., inspecting and washing areas at highest risk for bacterial or fungal growth). Avoid hot showers and baths, which may promote skin dryness. Use moisturizing soaps and apply a body lotion after bathing. Preventing dry skin improves skin elasticity making it more resistant to breakdown. The patient may need assistance from a family member or may need to find creative solutions for accessing hard-to-reach areas, such as using a long-handled sponge to wash and a handheld hair dryer (set to low) to dry the area, or a squirt bottle with warm water to help cleanse the anogenital area.
Skin infections that involve the lower extremities can have severe consequences. Foot ulcers are a leading causative factor in amputations.12 The podiatric emergency and preventive foot care guidelines are discussed in Chapter 17, Evaluation and Management of the Diabetic Foot. The importance of these guidelines in preventing foot infection or injuries that lead to infection cannot be overemphasized.
Skin lesions as a result of trauma or other causes such as surgery are at risk for infection. Factors that can delay wound healing in patients with diabetes are related to alterations in glucose metabolism and neovascular complications. The basic principle in the treatment of wounds is to promote healing and avoid complications. Maintaining glucose levels <180 mg/dL is critical in the healing process. Hyperglycemia can have negative effects on wound healing through the formation of advanced glycation end products (AGEs), which cause the production of inflammatory molecules.
Management of wounds that are expected to heal is based on the use of dressings to maintain a moist wound bed, application of a topical antimicrobial, and debridement as necessary to remove dead tissue that impedes the growth of healthy tissue. No clinical findings support the use of one topical antimicrobial preparation over another. More aggressive or deeper wounds usually require advanced wound care, off-loading to improve circulation, and systemic antimicrobials. Although most infections are caused by gram-positive cocci, a common practice is to select an antimicrobial with broad-spectrum coverage.18
The treatment for ulcers, particularly those of long duration, such as foot ulcers, is more complicated and includes adjuvant care, such as hyperbaric oxygen, topical biological therapy, autologous skin transplantation, or vacuum-assisted closure-negative pressure. These treatments are discussed in more detail in Chapter 17, Evaluation and Management of the Diabetic Foot. The structure of the wound care process—that is, the frequency of assessment, the use of a multidisciplinary team, and patient support so that off-loading can be carried out—are far more significant determinants of outcome than the type of product or wound dressing used in the treatment.19
Because many patients with neuropathy have impaired sensation, education regarding skin care must emphasize the need to assess the area for changes in color or temperature or the presence of swelling or discharge. Any cut or wound should be washed immediately with a mild soap and water. Cleansing with harsh chemical antiseptics causes inflammation and can further damage the skin. The wound must be kept clean and covered. If the area shows signs of infection or becomes worse in a 24-h period, the patient should notify the health-care provider.
When caring for a patient with diabetes, it is important to remember that in areas of reduced blood flow, such as the feet, systemic antibiotics used to treat skin infections have difficulty permeating the tissue and their effectiveness is reduced, necessitating a longer time frame for treatment.
INSULIN ALLERGIES AND SKIN MANIFESTATIONS
Although rare, cutaneous reactions to insulin have been reported, usually as raised, warm, itchy nodules forming at the injection site that appear 15 min to 2 h after injection. With the production of purified and recombinant insulins, the incidence of insulin allergy has been reduced. Since the marketing of recombinant insulins, the estimated prevalence of allergic reactions to insulin is <1%. Of the reported reactions, however, a true allergy to insulin is rare. In some instances, the skin reacted to the latex of the vial stopper, the alcohol or cleanser used to prepare the injection site, a preservative used in the insulin such as phenol, an additive such as protamine, or an intradermal rather than a subcutaneous injection.20
True insulin allergy with systemic response such as urticaria or anaphylaxis is extremely rare. More common is a delayed hypersensitivity response. In the case of a true insulin allergy, treatment involves a desensitization program that generally is carried out under medical observation. For hypersensitivity, antihistamines or the use of a steroid added to the insulin is effective.21
Patients also may report skin changes that are benign and are intrinsic to he insulin or injected medication’s formulation. With the long-acting insulin, glargine having a pH level of 4, some patients report a stinging or slight burning at the injection site that disappears within 10–15 min after injection.
The weekly formulation of glucagon-like peptide-1 agonist, exenatide, may leave a pea-size lump at the injection site. This swelling should disintegrate over time as the drug is released into the system. For some patients, the small swelling at the area of injection persists and may last 7–14 days.
Use of purified and recombinant insulin has reduced the occurrence of lipoatrophy, a hollowing of the skin at the injection site. More common is the problem of lipohypertrophy in areas of repeated insulin injections (Figure 15.9). These large fatty-like deposits in the subcutaneous tissue can be disfiguring but are not physically painful. In fact, patients may continue to inject into the same area because the sensation of administering the insulin is blunted. The continued use of a hypertrophied area, however, may reduce insulin absorption and could interfere with glucose control. Ceasing insulin injections at the hypertrophied site allows the skin to return to its normal state. Hypertrophy is avoided by rotating injection sites within anatomical areas and carefully observing the skin’s reaction to injections.
Figure 15.9—Lipohypertrophy. Usually appears in an area of repeated insulin injections.
SKIN MANIFESTATIONS FROM ORAL TREATMENTS
Of the oral agents currently on the market, sulfonylureas are most likely to cause dermatological side effects. The sulfa component of the drug can produce an allergic reaction that usually presents as an uncomfortable “measles-like” maculopapular rash. The most common offenders are the first-generation sulfonylureas, such as tolbutamide and chlorpropamide, medications that rarely are used. Occasionally, glyburide and glimepiride, second-generation drugs, have caused urticaria, photosensitivity, erythema, and pruritus; these symptoms disappear with drug discontinuation.21 Sensitivity to a sulfonylurea may indicate that the patient will react adversely to other sulfa medications. Caution should be used in prescribing any sulfa-containing medication.
The remaining oral medications used in the treatment of diabetes typically are not associated with cutaneous side effects. Metformin, a biguanide, has been associated with rare occurrences of psoriasiform drug eruptions, erythema multiforme, leukocytoclastic vasculitis, photosensitivity, urticaria, and exanthema.21 The thiazolidinediones (pioglitazone and rosiglitazone) are linked with edema, particularly in patients also using insulin. Dipeptidyl peptidase 4 inhibitors have an anecdotal report of painful skin followed by a reddish or purple rash. Sodium glucose co-transporter 2 inhibitors have been associated with the occurrence of vulvo-vaginal candida infection. The mechanism of action in this drug causes the disposal of a higher concentration of glucose in the urine, providing a medium for the increase in candida.
Preventive skin care education that centers on improved hygiene and early assessment and intervention for any suspected skin condition is a key component of nursing care. Many of the lesions associated with diabetes, such as NLD and diabetic bullae, have no prescribed protocol for treatment. The various trials of different forms of treatment, the consistent daily attention that the care of these lesions requires, and the long duration of the self-care process can be a heavy burden for the patient. Supportive nursing care and education enable the patient to understand the condition and be alert for any signs or symptoms of secondary infection.
In other skin conditions, such as xanthomas and injection-site hypertrophy, addressing and treating the underlying cause is an essential component of care. For xanthomas, improved glucose control and lipid management must be achieved for resolution of the lesions to occur. In hypertrophy, patient education regarding insulin injection site rotation and its importance in both skin care and glucose control is central to the plan of care.
In AN, the nurse must realize that not all cases are related to diabetes and that sudden appearance and rapid progression of the lesion may indicate a life-threatening medical condition. Noting changes in size and texture of AN lesions and documenting them, provides vital information for future assessment and analysis.
Patients with diabetes are just as susceptible to skin cancer as the general population. Sunburns not only increase the risk of carcinoma but also cause the breakdown of fragile skin, leading to infection, hyperglycemia, and disruption of glucose control. The patient must be educated in sun protection guidelines to avoid these negative consequences.
With the introduction of any new drug treatment, the nurse has the responsibility to monitor for adverse events or side effects. Nurses should be aware of possible cutaneous manifestations associated with diabetes medications, intervene, and report these changes before they further affect the treatment program and threaten the well-being of the patient.
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