Diabetes mellitus is a group of physiological
dysfunctions characterized by hyperglycemia resulting directly from insulin resistance, inadequate insulin secretion, or excessive glucagon secretion. Type 1 diabetes (T1D) is an autoimmune disorder leading to the destruction of pancreatic beta-cells. Type 2 diabetes (T2D), which is much more common, is primarily a problem of progressively impaired glucose regulation due to a combination of dysfunctional pancreatic beta cells and insulin resistance. The purpose of this article is to review the basic science of type 2 diabetes and its complications, and to discuss the most recent treatment guidelines.
Key Words: Diabetes mellitus, insulin, hyperglycemia, glucose regulation.
Diabetes mellitus is a group of physiological dysfunctions characterized by hyperglycemia resulting directly from insulin resistance, inadequate insulin secretion, or excessive glucagon secretion (Ignatavicius & Workman, 2016; Lewis, Dirksen, Heitkemper, & Butcher, 2014). There are two main types of diabetes. Type 1 diabetes (T1D) is an autoimmune disorder leading to the destruction of pancreatic beta-cells. Type 2 diabetes (T2D), which is much more common, is primarily a problem of progressively impaired glucose regulation due to a combination of dysfunctional pancreatic beta cells and insulin resistance (Ignatavicius & Workman, 2016; Lewis et al., 2014). T2D is specifically defined by the American Diabetes Association (ADA) (2014a) as “a condition characterized by hyperglycemia resulting from the body’s inability to use blood glucose for energy…either the pancreas does not make enough insulin or the body is unable to use insulin correctly.” Currently, there are approximately 26 million people in the United States (U.S.) diagnosed with diabetes and another 79 million people with prediabetes, resulting in nearly one-third of the population being affected by the disease (Ignatavicius & Workman, 2016; Lewis et al., 2014). The purpose of this article is to review the basic science of type 2 diabetes and its complications, and to discuss the most recent treatment guidelines.
Pathophysiology, Etiology, And Manifestations
T2D generally develops in people with known risk factors and genetic predisposition, and may be related to environmental causes, such as viruses (Ignatavicius & Workman, 2016; Lewis et al., 2014; McCance, Huether, Brashers, & Rote, 2014; Seggelke & Everhart, 2012). The major risk factor for T2D is obesity, with abdominal obesity conferring the highest risk. Obesity is often associated with the consumption of high fat/carbohydrate diets and lack of physical activity. Obesity can also lead to insulin resistance. Other predisposing risk factors include low levels of HDL (“good cholesterol”), sedentary lifestyle, and polycystic ovary disease. There is also some data in the literature suggesting that people with depression have higher rates of diabetes and should be screened. A worrisome development is the increase in T2D in children, most likely related to obesity. Age, ethnicity, and heredity are non-modifiable risk factors (Ignatavicius & Workman, 2016; Lewis et al., 2014; McCance et al., 2014; Seggelke & Everhart, 2012).
While the person with T2D may have the classic signs related to hyperglycemia more often seen in T1D (polyuria, polydipsia, and polyphagia), signs and symptoms of T2D are often more vague and may include fatigue, possible weight gain, frequent infections, sores that heal slowly, and frequent vaginal yeast infections in women. Visual changes and alterations in sensation represent later signs and symptoms that occasionally drive people to seek health care (Ignatavicius & Workman, 2016; Lewis et al., 2014; McCance et al., 2014; Seggelke & Everhart, 2012).
Diagnostic studies for T2D usually include measures of both short-term and long-term glucose levels. Short-term measurements include a fasting blood glucose or a two-hour blood glucose drawn during an oral glucose tolerance test (OGGT). A random blood glucose can be useful in a patient with the classic symptoms of hyperglycemia. Long-term glucose measurement is combined with the hemoglobin A1C. (see Table 1). A diagnostic value obtained via fasting blood glucose, OGGT, or random blood glucose must be confirmed by a second test, preferably with the same test (ADA, 2013 2014b; Ignatavicius & Workman, 2016; Lewis et al., 2014; Pagana & Pagana, 2014).
The hemoglobin A1C measures the amount of glycosylated hemoglobin as a percent of the patient’s total hemoglobin over a period of two to three months, so it is particularly valuable for determining long-term control of disease in individuals with diabetes (Ignatavicius & Workman, 2016; Lewis et al., 2014; Pagana & Pagana, 2014). The hemoglobin A1C is a tiny part of normal hemoglobin. As red blood cells circulate through the body, some of the glucose that is also present in the bloodstream attaches to the A1C portion. The more glucose that is present, the more often this happens. Because the average lifespan of a red blood cell is 90 to 120 days, the measured A1C reflects the amount of glucose in the blood over the last approximately 120 days (ADA, 2014b; Pagana & Pagana, 2014).
Readings are expressed as a percentage. The higher the percent, the higher the glucose level over time. A hemoglobin A1C of 5% means that 5% of the hemoglobin is saturated with glucose. For the person without diabetes, a normal reading is 4% to 5.9%. Good diabetic control is indicat- ed when readings are less than 7%. Fair control is considered to be 8% to 9%, and poor control is anything over 9%. There is a discrepancy between recommended readings by the ADA (good control: A1C less than 7%) and the American College of Endocrinologists (good control less than 6.5%). The reading is not affected by fasting and can be taken at any time (ADA, 2013; Pagana & Pagana, 2014).
For those with known diabetes, other screening and diagnostic testing should be performed. These include annual fundoscopic eye examination, annual urine screen for creatinine (indicative for microalbuminuria and possible kidney involvement), visual examination of the feet at every visit to a health care provider, annual comprehensive foot examination (including microfilament testing for sensation), and at least annual assessments for cardiovascular risks. Routine monitoring can prevent complications related to diabetes or at least catch them in time for early treatment (Ignatavicius & Workman, 2016; Lewis et al., 2014).
Diabetes complications can be separated into two categories: microvascular and macrovscular (World Health Organization, 2013). Microvascular complications are due to damage of small blood vessels. Macrovascular complications are due to damage to larger blood vessels. Microvascular complications involve damage to the kidneys (nephropathy), leading to renal failure; eyes (retinopathy), leading to blindness; and the nerves (neuropathy), causing impotence and diabetic foot disorders that can result in infections and amputations. Macrovascular complications include cardiovascular diseases, such as strokes, heart attacks, and blood flow insufficiency to the legs. According to the literature, lower limb amputations are approximately 10 times greater in people with diabetes than in individuals without diabetes in developed countries (Ignatavicius & Workman, 2016; Lewis et al., 2014).
There are more macrovascular complications among individuals with diabetes that present at an earlier age (ADA, 2014a, c, 2015a; Ignatavicius & Workman, 2016; Lewis et al., 2014). Controlling blood pressure (target less than 130/80 mmHg) is vital to prevent or slow the onset of these conditions. The ADA recently revised its diastolic blood pressure standard to less than or equal to 90 mmHg. Managing lipid abnormalities is also vital to preventing and/or managing complications. The ADA targets are total cholesterol less than 200 mg/dL, lowdensity lipoproteins (LDL) less than 100 mg/dL, triglycerides less than 150 mg/dL, and high-density lipoproteins (HDL) cholesterol greater than 40 mg/dL in men and 50 mg/dL in women (ADA, 2014a, c, 2015a; Ignatavicius & Workman, 2016; Lewis et al., 2014).
Microvascular complications are unique and common to diabetics (micro = small; seen in the smaller population of diabetics as compared with the larger general [non-diabetic] population). They result from exposure to high glucose that causes thickening of blood vessels. The end-target organs are affected by these complications, which include diabetic retinopathy, neuropathy, and nephropathy. Dermopathies also exist, but typically cause only mild discomfort and cosmetic dysfunction, and are not discussed here (Ignatavicius & Workman, 2016; Lewis et al., 2014).
Diabetes is the leading cause of blindness in adults (Ignatavicius, & Workman, 2016; Lewis et al., 2014; Shotliff & Balasanthiran, 2009). The types of retinopathy include nonproliferative (most common) and proliferative. Nonproliferative retinopathy occurs when small blood vessels become partly occluded, leading to microaneurysms and leaking of capillary fluid. Vision is affected if the macula is involved. Proliferative retinopathy occurs when retinal capillaries become occluded and the body forms new capillaries in response. These new vessels are abnormal and fragile, which leads to hemorrhage. The new vessels can pull the retina out of place, leading to tears. Blindness results if the macula is involved. Individuals with diabetes tend to develop glaucoma and cataracts more frequently and at an earlier age than the general population (Ignatavicius, & Workman, 2016; Lewis et al., 2014; Shotliff & Balasanthiran, 2009). Dilated eye examinations are recommended annually to detect these conditions. Prevention is best obtained through tight control of blood glucose and blood pressure. Current treatments include photocoagulation and vitrectomy (Ignatavicius & Workman, 2016; Lewis et al., 2014; Shotliff & Balasanthiran, 2009). In photocoagulation, lasers seal the leaking blood vessels in the eye with heat (“Laser Photocoagulation for Diabetic Retinopathy,” 2015). Vitrectomy removes the vitreous gel from the eye (“Diabetic Retinopathy – Surgery,” 2014).
Diabetic neuropathy affects nearly two-thirds of all individuals with diabetes, and is probably the result of chronic high blood glucose that damages the nerves and blood vessels. Other risk factors include increasing age, obesity, and having concurrent peripheral vascular disease (Benbow, 2012; Sharp & Clark, 2011; Turns, 2011; Woo, Santos, & Gamba, 2013; Ziegler & Fonesca, 2015). Peripheral neuropathy involves altered sensations and ischemia, which usually occurs in the bilateral extremities starting first in the lower extremities and gradually moving upward. Individuals with diabetes can have a total lack of sensation, paresthesias, numbness, and loss of temperature sensation. This leads to complications, such as ulcers, amputations, atrophy of muscles, and loss of fine movements. The most common presentation is the “dia- betic foot,” where an infected ulcer started with an injury the patient was unaware of due to loss of sensation (Benbow, 2012; Turns, 2011; Sharp & Clark, 2011; Woo et al., 2013; Ziegler & Fonesca, 2015).
Prevention is the best method of management; tight glycemic control and daily foot inspections are crucial. Unfortunately, this works best in patients with T1D. The paresthesias can be managed with medications, such as topical creams, tricyclic antidepressants, antiseizure medications, selective serotonin reuptake inhibitors, or selective norepinephrine reuptake inhibitors (Benbow, 2012; Turns, 2011; Sharp & Clark, 2011; Woo et al., 2013; Ziegler & Fonesca, 2015). The FDA has only approved two drugs for the treatment of diabetic neuropathy: pregabalin ([Lyrica®], an anticonvulsant; and duloxetine [Cymbalta®], a serotonin-norepinephrine reuptake inhibitor) (Ziegler & Fonesca, 2015).
Although peripheral neuropathy is best known, autonomic neuropathy also affects many individuals with diabetes. This group of disorders includes diabetic gastroparesis, urinary retention, sexual dysfunction in men and women, bowel incontinence and/or diarrhea, postural hypotension, tachycardia at rest, angina-free myocardial infarction, and hypoglycemic unawareness (Ignatavicius, & Workman, 2016; Lewis et al., 2014.
Diabetic nephropathy is due to damage to small vessels in the glomeruli of the kidneys and affects up to 40% of individuals with diabetes (Thomas & Kodack, 2011). Diabetic nephropathy is commonly defined by abnormally high albumin levels in urine in a patient without known renal disease. The earliest indicator is microalbuminuria, defined as albumin excretion of less than 30 mg/day or a urinary albumin/creatinine ratio of greater than 3.0 mg/mmol (Bennett & Aditya, 2015). It is the leading cause of end stage renal disease and is more common among individuals with diabetes who smoke, and who have uncontrolled hypertension and chronically high blood glucose (Bakris & Weir, 2002; Bennett & Aditya, 2015; Thomas, & Kodack, 2011; Williams, Manias, Walker, & Gorelik, 2012). Despite the use of therapy to protect the kidneys of individuals with diabetes, end stage renal disease is increasing in the diabetic population at the rate of about 9% a year (Joint Committee on Diabetic Nephropathy, 2015; Kazawa & Moriyama, 2013; Krolewski, 2015).
The treatment of choice for diabetic nephropathy is either an angiotensin-converting enzyme inhibitor (ACEI) such as lisinopril [Zestril®] or an angiotensin receptor blocker (ARB) such as losartan [Cozaar®]. These drugs have a dual effect of controlling hypertension and slowing the progression of kidney damage and dysfunction. For patients with normal blood pressure and normal kidney function, this form of treatment may not be necessary. Patients who spill albumin in their urine should be treated with one of the described drugs. Providers should monitor these patients’ creatinine, potassium, and urine albumin excretion routinely. These laboratory values help assess the patient’s therapeutic response and monitor disease progression. However, relying on creatinine alone may lead to renal impairment being missed. If the glomerular filtration rate (GFR) meets the criteria for chronic kidney disease (< 60 mL/min/1.73 m2 for three months or more), the patient should be referred to a specialist for further management. Albumin concentration is a strong independent predictor of renal prognosis, but the severity of the albumin concentration does not always correlate closely with renal function. Renal impairment also increases the risk of hypoglycemia in the patient with diabetes. This is often multifactorial in etiology but is often the result of impaired gluconeogenesis seen in kidney disease (Andresdottir et al., 2014; Bakris & Weir, 2002; Bennett & Aditya, 2015; Thomas & Kodack, 2011; Williams et al., 2012).
A recent Cochrane review of 26 studies showed that the use of an ACEI decreased the number of diabetics who went on to develop chronic kidney disease (CKD) compared to other types of antihypertensive medications (Jicheng et al., 2013). The ACEIs significantly reduced the risk of new onset for both micro- and macroalbuminuria. ARBs did not show the same benefit; however, a subgroup analysis showed benefits in using ARBs in high-risk patients. There were only two published studies regarding the combination of ACEI and ARB (Jicheng et al, 2013). Of these two studies, only one demonstrated a benefit of using combined drugs. The current recommendation remains that ACEIs are the drug of choice to prevent CKD in patients with diabetes (Fried et al., 2015; Jicheng et al., 2013).
ACE inhibitors and ARBs inhibit the renin-angiotensin system, which leads to lowered blood pressure. This, in turn, reduces both cardiovascular and renal risk, both of which are significant contributors to morbidity in the diabetic population, particularly in the older adult subset. However, research has shown that ACEIs and ARBs are vastly under-utilized in this population due mainly to concerns of providers about potential side effects. The ADA (2014a) recommends them as first-line treatment for patients with hypertension with or without albuminuria or other signs of renal insufficiency, no matter what age. Diuretics can also be considered in conjunction with this therapy. Appropriate labs (serum creatinine, potassium) should be monitored when using these drugs (Bennett & Aditya, 2015; Fried et al., 2015; Pagana & Pagana, 2015; Pappoe, & Winkelmayer, 2010).
Krolewski (2015) has proposed a “new paradigm” for diabetic nephropathy that does not use albuminuria as the marker of impaired renal function. After 25 years of research, Krolewski proposes monitoring the decline of GFR as a more accurate indicator of renal involvement in diabetics. Specifically in this model, the loss of greater than 3.5 mL/min/year of GFR indicates progressive renal decline. The decline in GFR precedes the onset of albuminuria, and unchecked, this process can lead to end stage kidney disease. Although the exact mechanism of this process is unclear, Krolewski claims that by using this model, one can separate patients into groups with rapid, moderate, or minimal rates of progression which can lead to better targeted therapies (Krolewski, 2015).
Lower urinary tract complications can also occur in patients with diabetes. Dysfunction can occur at the level of the bladder and the sphincter leading to problems of both storage and emptying. Bladder contractility is especially affected in patients with diabetes, often leading to hypocontractility, which worsens the longer the disease lasts. Urinary incontinence is a frequent finding that may not be related to age. Urinary retention, nocturia, weak urine stream, urinary tract infections (UTIs), and frequency are other complications. Erectile dysfunction (ED) can also occur. These seem to be related to increased responsiveness to parasympathetic input and decreased responsiveness to adrenergic input (autonomic neuropathy) (Kempler et al., 2011; Lee et al., 2015; Lemack, 2007; Pop-Busui et al., 2015; Vinik, Maser, Mitchell, & Freeman, 2003; Yilmaz et al,, 2014).
Bladder dysfunction occurs in 25% of patients with T2D. There is a high correlation between bladder disturbances and peripheral neuropathy. Patients often complain of symptoms, such as frequency and urgency, often leading to incontinence, nocturia, and the sensation of incomplete bladder emptying. Men may complain of symptoms confused with benign prostatic hyperplasia (BPH): weak urinary stream, dribbling, and interrupted urinary stream. The pathophysiology of this dysfunction appears to be a combination of alteration in detrusor smooth muscle, dysfunction of neurons, and urothelial dysfunction, all related to chronically high blood glucose (Kempler et al., 2011; Pop-Busui et al., 2015; Yilmaz et al., 2014).
Providers should screen patients complaining of these symptoms with a validated tool assessing incontinence and lower urinary tract symptoms (LUTS). A urinalysis with culture should be obtained to rule out UTI because patients with diabetes are so prone to infection and because UTI can lead to these symptoms. Urodynamic testing may be valuable for bladder dysfunction assessment. Post-void residual should be assessed. For patients who have severe bladder dysfunction, intermittent catheterization is the treatment of choice. Bladder training, including timed voiding and doublevoiding, is used for incontinence. (Kempler et al., 2011; Nazarko, 2015; Pop-Busui et al., 2015). Many medications used to treat bladder dysfunction (cholinergic and anti-cholinergic drugs) are inappropriate for older adults. Sacral neuromodulation, a surgical procedure, has good success with patients with diabetes (66.7%); however, infected devices had to be removed in 37.5% of diabetic recipients, limiting their practical usefulness (Nazarko, 2015).
ED is estimated to affect up to 90% of men with diabetes. Although many providers and patients are embarrassed to broach this topic, it is important to recognize and assess for it. ED is a well-established risk factor and independent predictor of serious cardiovascular events and coronary artery disease in men with diabetes. The pathophysiology relates mainly to decreased ability of the smooth muscle of the corpus cavernosum to relax and to impaired nitric oxide function. Neuropathy may also be implicated leading to decreased sensation in the glans penis, further compounding the ED. Providers should use validated tools to assess for the presence and impact of ED (Kempler et al., 2011; Moussa, Hill, Claydon, & Klufio, 2015; Pop-Busui et al., 2015). Women can also suffer from diabetes-induced impairment of sexual function, such as decreased desire, diminished lubrication, and decreased ability to achieve an orgasm (Yilmaz et al., 2014).
Management of ED includes sexual counseling (including the patient’s partner), good glycemic control, and medications, such as sildenafil (Viagra®), vardenafil (Levitra®), and tadalafil (Cialis®). Other treatments can include intracavernous injections, intraurethral alprostadil (Caverject®), constriction devices, or prosthetic implants (Kempler et al., 2011). A challenge in treating these patients is the relationship to coronary artery disease. Many of these men are on nitrate preparations, which preclude the use of phosphodiesterase inhibitors, such as sildenafil. Patients should be encouraged to discuss this matter with their cardiologists; a “nitrate holiday” may make limited use of these types of drugs possible (Ignatavicius & Workman, 2016; Lewis et al., 2014).
Individuals with diabetes present special challenges during the perioperative period. The hospital stay of the post-operative patient with diabetes is longer, with the patient experiencing more complications, including a 50% higher risk of mortality than patients without diabetes. Specific complications include wound infection (2 to 3 times higher), poor wound healing, hyperglycemia (including diabetic ketoacidosis), hypoglycemia, joint infection, and thrombotic events. Complications from other co-morbid conditions are also a possible problem (Dhinsa, Khan, & Puri, 2010; Levasque, 2013; Munoz, Lowry, & Smith, 2012; Sharp, & Clark, 2011; Wallace, 2012).
Good glycemic control is vital in the perioperative patient with diabetes, although there is disagreement on specific protocols. Tight control may decrease the incidence of wound infection. In fact, for elective surgery, reducing the A1C to 7% or less is ideal because patients in this range have an overall lower rate of wound infection. Control is complicated by the body’s response to surgery; stress increases the release of catabolic hormones and pro-inflammatory mediators, while at the same time decreases the release of insulin. This tends to lead to hyperglycemia. Overly aggressive glucose control, combined with hypoglycemic unawareness (common in older patients) can lead to hypoglycemia. Patients are best managed with a specific and detailed protocol using insulin during the operative and immediate post-operative period while the patient is still not eating. Typically, oral medications can be started once the patient is eating well. See the discussion on medications below for more detail (Dhinsa et al., 2010; Levasque, 2013; Munoz et al., 2012; Wallace, 2012).
Medications to treat T2D include insulins and several different classes of oral medications. Insulin replaces the patient’s own endogenous insulin and is required in patients with T1D. Patients with T2D may need exogenous insulin to manage blood glucose levels during periods of acute stress (i.e., surgery or serious illness) or may use insulin to supplement their oral medications for tighter control (Ignatavicius & Workman, 2016; Lewis et al., 2014).
Insulins come in rapid-acting, short-acting, intermediateacting, long-acting, and combination formulas (see Table 2). Regimes can include taking injections once, twice, or three times a day, or can involve a basal-bolus routine in which the patient takes a long-acting insulin once a day and supplements with rapid acting insulin at mealtimes. This allows greater flexibility in working with food intake (Cleary, 2013; Vallerand, & Sanoski, 2013).
Oral and Non-Insulin Injectable Medications
Several classifications of oral medications are available, with new drugs being developed at a rapid pace. Patients may be on mono- or dual therapy. When desired results are not achieved on single drug therapy, it is more beneficial to add a medication from a different class instead of switching drugs altogether (ADA, 2015c). Hospitalized patients, unless very stable, should have oral medications discontinued and their blood glucose values managed with insulin. See Table 3 for a discussion of oral and noninsulin injectable medications (ADA, 2015b; D’Arrigo, 2015; Ignatavicious & Workman, 2016; Vallerand & Sanoski, 2013).
Medication Use in the Hospitalized Patient With Diabetes Mellitus
The hospitalized patient (unless quite stable) should be taken off oral medications and switched to insulin. Most hospital policy calls for fasting and preprandial testing with sliding scale insulin based on the patient’s blood glucose readings. However, this does not take into account the upcoming meal with its carbohydrate load. The 2009 consensus statement from the ADA and the American Association of Clinical Endocrinologists discourages the use of this standard protocol. There is no scientific evidence to support this approach, and its use can be dangerous to patients. Rather, the consensus statement recommends scheduled subcutaneous insulin (for non-critical patients) using “basal, nutritional, and correctional components” (Kubacker, 2014, p. 33). The correctional component factors in the patient’s sensitivity to insulin and is calculated using available formulas (DeYoung, Bauer, Brady, & Eley, 2011). Poor glycemic control in the hospitalized patient can lead to several adverse outcomes, including increased morbidity and mortality, length of stay, number of admissions, and cost (Crawford, 2013; DeYoung et al., 2011; Kubacka, 2014; Seggelke & Everhart, 2012).
Other Care Measures
It is important that diabetics have an in-depth knowledge of certain self-care measures. They need to have a good understanding about appropriate nutrition, physical activity, sick day management, and self-monitoring of blood glucose (SMBG). It is the role of the health care provider to provide this education. To efficiently accomplish this, health care providers must remain current in these topics.
Nutrition is a cornerstone of care for all patients with diabetes. Nutritional modifications can be challenging for many patients, and the ADA recommends a registered dietician with knowledge and expertise in diabetes as part of the care team. A healthy diet for a diabetic can incorporate the same foods typically eaten by non-diabetics. The dietary goal is to eat in a way that promotes tight glycemic control and helps limit complications (i.e., cardiovascular). For the majority of individuals with diabetes, this includes eating 45 grams of carbohydrates at each of three meals and 15 grams of carbohydrates each of two to three daily snacks. As part of the total carbohydrate intake, 25 to 30 grams should be fiber. Protein should be 20% to 30% of total intake, with the rest being composed of healthy fats. Alcohol is allowed but should be used in moderation and with food to avoid hypoglycemia accompanied by unawareness because the effects of alcohol blunt the body’s response to hypoglycemia (Ignatavicious & Workman, 2016; Lewis et al., 2014).
The ADA (2014a) recommends that individuals with diabetes get at least 150 minutes of exercise a week, which is an average of 30 minutes five days a week. Exercise has many benefits, both for glycemic control and reducing risk factors and co-morbidities, such as cardiovascular disease. The decrease in insulin resistance seen with exercise can last up to 48 hours. The ADA also recommends that diabetics not be sedentary for more than 90 minutes at a time (ADA, 2014a; Ignatavicious & Workman, 2016; Lewis et al., 2014).
Blood Glucose Monitoring
Blood glucose is considered a fifth vital sign for patients with diabetes. However, timing of testing is somewhat controversial. There are multiple potential times during the day to test: fasting, before each of three meals, after each of three meals, before and/or after exercising, and at bedtime (Ignatavicious, & Workman, 2016; Lewis et al., 2014; Schrott, 2004). Patients with type 2 diabetes tend towards fasting and 2-hour postprandial testing, which evaluates the effect of a carbohydrate load on blood glucose (Ignatavicious, & Workman, 2016; Lewis et al., 2014; Schrott, 2004). This allows the patient with diabetes to make decisions regarding meal composition and the timing of exercise toward fasting and 2-hour postprandial testing, which evaluates the effect of a carbohydrate load based on their individual responses. Even with normal fasting levels and “controlled” A1C readings, a large percentage of patients with diabetes will have higher than desired postprandial levels less than or equal to 140 mg/dL (Ignatavicious & Workman, 2016; Lewis et al., 2014; Schrott, 2004). Over the years, some studies have demonstrated better glycemic control in specific patient popula- tions who test after meals versus before (de Vegiana et al., 1995; Muhamad, Kadir, & Mohamed, 2012). However, a testing plan should ideally be developed in conjunction with the patient’s goals and willingness to participate in active care. Postprandial testing appears to be more highly correlated to reducing cardiovascular risk, which is an added benefit (Schrott, 2004) and is better correlated to tighter long-term control. Patients with T1D often test fasting and before meals; however, this is also controversial, especially in hospitalized patients (Ignatavicious & Workman, 2016; Lewis et al., 2014).
Sick Day Management
Sick day management should be planned in advance. The patient and provider should discuss and agree on a plan for when the patient is ill and not eating. The patient should be advised to check blood sugars more frequently, have food and beverage on hand that can be tolerated and that provide some carbohydrates, and continue at least a partial dose of his or her medication. Diabetic ketoacidosis is often caused by individuals with diabetes who discontinue their medications not realizing that their blood glucose continues to rise even though they may not be eating. Patients with diabetes should also know when to seek health care (Ignatavicious & Workman, 2016; Lewis et al., 2014).
Diabetes mellitus is a growing health care problem with ramifications affecting individuals’ health, the health care system, and the economy of the United States and the world (Ignatavicious & Workman, 2016; Lewis et al., 2014). Nurses in every setting will encounter patients/clients with diabetes. It is the role of all nurses to be properly educated about diabetes and the most current recommended treatments. It is also important to involve patients in the active management of their condition. These important roles could have a great impact on the prevention and management of this disease that has such high morbidity and mortality rates.
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