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Glucose, 1-5 Anhydroglucitol, and Fructosamine Core Lab Study

Synonym/Acronym

Blood sugar, fasting blood sugar (FBS), postprandial glucose, 2-hr PC (post cibum).

Rationale

To assist in the diagnosis, treatment, and management of diabetes.

A small group of studies in this manual have been identified as Core Lab Studies. The designation is meant to assist the reader in sorting the basic “always need to know” laboratory studies from the hundreds of other valuable studies found in the manual—a way to begin putting it all together.

Normal, abnormal, or various combinations of core lab study results can indicate that all is well, reveal a problem that requires further investigation with additional testing, signal a positive response to treatment, or suggest that the health status is as expected for the associated situation and time frame.

Glucose is mainly used to screen and assess for diabetes. Glucose is included in the basic metabolic panel (BMP), comprehensive metabolic panel (CMP), diabetes profile, obstetric panel, pancreatic profile, and renal function panel. Panels are used as general health and targeted screens to identify or monitor conditions such as bone disease, diabetes, hypertension, kidney disease, liver disease, or malnutrition.

Patient Preparation

There are no activity or medication restrictions unless by medical direction. There are no restrictions for the random glucose test. Instruct the patient to fast for at least 8 hr before specimen collection for the fasting glucose test and not to consume any caffeinated products or chew any type of gum before specimen collection; these factors are known to elevate glucose levels. Instruct the patient to follow the instructions given for 2-hr postprandial glucose test. Some health-care providers (HCPs) may order administration of a standard glucose solution, whereas others may instruct the patient to eat a meal with a known carbohydrate composition.

Normal Findings

Method: Spectrophotometry for Glucose, 1-5 Anhydroglucitol, and Fructosamine.

AgeConventional UnitsSI Units (Conventional Units × 0.0555)
Nondiabetic, fasting
Cord blood45–96 mg/dL2.5–5.3 mmol/L
Premature infant20–80 mg/dL1.1–4.4 mmol/L
Newborn 2 days–2 yr30–100 mg/dL1.7–5.6 mmol/L
Child60–100 mg/dL3.3–5.6 mmol/L
Adult–older adultLess than 100 mg/dLLess than 5.6 mmol/L
Nondiabetic, 2-hr postprandial65–139 mg/dL3.6–7.7 mmol/L
Nondiabetic, randomLess than 200 mg/dLLess than 11.1 mmol/L
Prediabetic, fasting100–125 mg/dL5.6–6.9 mmol/L
Prediabetic, 2-hr postprandial140–199 mg/dL7.8–11 mmol/L

Fasting means no caloric intake for 8 hr or longer. Values tend to increase in older adults.

1-5, Anhydroglucitol (Short-term indicator of good glycemic management)
Male10.7–32 mcg/mL
Female6.8–29.3 mcg/mL
Fructosamine (Glycated albumin)
Conventional UnitsSI Units (Conventional Units × 0.01)Status
205–286 micromol/L3.05–2.86 mmol/LNondiabetic
210–563 micromol/L2.10–5.63 mmol/LDiabetic (values vary with degree of management)

Critical Findings and Potential Interventions

Glucose

Adults & children

Newborns

Consideration may be given to verification of critical findings before action is taken. Policies vary among facilities and may include requesting immediate recollection and retesting by the laboratory or retesting using a rapid point-of-care testing instrument at the bedside, if available.

Glucose monitoring is an important measure in achieving tight glycemic management. Glucose meters that use the enzymatic GDH-PQQ test strips may produce falsely elevated results in patients who are receiving products that contain other sugars (e.g., oral xylose, parenterals containing maltose or galactose, and peritoneal dialysis solutions that contain icodextrin, a metabolite of maltose). Glucometers that use GDH-NAD, GDH-FAD, and glucose oxidase test strips are specific for glucose and do not detect other sugars. Clinical laboratories do not use the GDH-PQQ method or reagents to determine glucose levels.

Symptoms of decreased glucose levels include headache, confusion, polyphagia, irritability, nervousness, restlessness, diaphoresis, and weakness. Possible interventions include oral or IV administration of glucose, IV or intramuscular injection of glucagon, and continuous glucose monitoring.

Symptoms of elevated glucose levels include abdominal pain, fatigue, muscle cramps, nausea, vomiting, polyuria, polyphagia, and polydipsia. Possible interventions include fluid replacement in addition to subcutaneous or IV injection of insulin with continuous glucose monitoring.

Overview

Study type: Plasma collected in a gray- [sodium fluoride] or green-top [heparin] tube, plasma is recommended for diagnosis of diabetes. Serum collected in a gold-, red-, or red/gray-top tube is also acceptable. It is important to use the same type of collection container if serial samples are to be collected; blood in a lavender-top [EDTA], red-, gold-, red/gray-top tube for 1,5 anhydroglucitol; blood collected in a gold-, red-, or red/gray-top tube for fructosamine; related body system: Endocrine system.

Glucose, a simple six-carbon sugar (monosaccharide), enters the diet as part of the sugars sucrose, lactose, and maltose and from the complex polysaccharide, dietary starch. The body acquires most of its energy from the oxidative metabolism of glucose. Excess glucose is stored in the liver or in muscle tissue as glycogen. Glucose levels in plasma (one of the components of blood) are generally 10% to 15% higher than glucose measurements in whole blood (and even more after eating). This is important because home blood glucose meters measure the glucose in whole blood, whereas most laboratory tests measure the glucose in either plasma or serum.

There are two other notable indicators of glucose management discussed later in this study: 1,5-anhydroglucitol and fructosamine.

Diabetes is a group of diseases characterized by hyperglycemia, or elevated glucose levels. Hyperglycemia can result from a defect in insulin secretion due to destruction of the beta cells of the pancreas (type 1 diabetes and latent autoimmune diabetes, sometimes referred to as type 1.5 diabetes), a defect in insulin action, or a combination of defects in secretion and action (type 2 diabetes), or from a specific cause such as gestational diabetes, neonatal hyperglycemia, cystic fibrosis related diabetes, or hyperglycemia induced by drugs used to treat other medical conditions (e.g., corticosteroids, HIV treatment, or post–organ transplantation). The chronic hyperglycemia of diabetes over time may lead to damage, dysfunction, and eventually failure of the eyes (retinopathy), kidneys (nephropathy), nerves (neuropathy), heart (cardiovascular disease), and blood vessels (micro- and macrovascular conditions).

The American Diabetes Association (ADA) and National Institute of Diabetes and Digestive and Kidney Disease (NIDDK) have established criteria for diagnosing diabetes. For additional information tests for diagnosing diabetes related to other conditions, refer to the study titled “Glucose Tolerance Tests.”

CF related diabetes (CFRD) is a co-morbidity that occurs in about 20% of children and almost half of adults. CF is more common in Caucasians. Annual screening with an oral glucose tolerance test should begin by age 10 in CF patients who have not been previously diagnosed with CFRD. The hemoglobin A1c test is not recommended to screen for CFRD. Annual monitoring for complications of CFRD should begin 5 yr after diagnosis.

Screening for hyperglycemia should also be done after organ transplantation when the patient has achieved stable levels of immunosuppressant therapy and is free of an acute infection. The oral glucose tolerance test is the preferred method to diagnose posttransplantation diabetes (PTDM). The hemoglobin A1c test is not recommended to screen for PTDM.

The ACOG and ADA recommend screening for all pregnant women at 24 to 28 wk of gestation using patient history, clinical risk factors, and carbohydrate challenge testing. Protocol recommendations may vary among requesting HCPs.

The Centers for Medicare and Medicaid Services (CMS) developed a screening tool in 2017 to assess areas unrelated to health that affect health outcomes, which include access to housing, food, transportation, utilities, and interpersonal safety. The 2019 American College of Cardiology (ACC) and American Heart Association (AHA) guidelines for the prevention of cardiovascular disease and the 2022 American Diabetes Association (ADA) recommendations regarding diabetes self-management education and support suggest these topics be included in the patient-HCP conversation along with assessment of evidence-based risk factors in order to better and more realistically improve diabetes and cardiovascular disease health outcomes. Especially important are patient concerns that result in cost-related medication nonadherence to treatment.

Diagnostic Criteria for Diabetes in the Absence of Classic Symptoms of Hyperglycemia*: Any Two of the Following Three Findings from the Same or Separate Samples:
GlucoseConventional UnitsSI Units (Conventional Units × 0.0555)
1.Fasting plasma glucoseEqual to or greater than 126 mg/dLEqual to or greater than 7 mmol/L
2.2-hr post-challenge plasma glucose with standardized 75-mg load Note: The ADA recommends a diet with sufficient carbohydrate content (mixed diet of at least 150 gm carbohydrates/day) be consumed for at least 3 days before the test.Greater than 200 mg/dLGreater than 11.1 mmol/L
3.A1c6.5% or greater6.5% or greater
OR
Random plasma glucose in the presence of classic symptoms of hyperglycemia or a hyperglycemic crisisGreater than 200 mg/dLGreater than 11.1 mmol/L
*Note:The combination of a fasting glucose and 2 hr post-challenge is especially helpful if evaluating inconsistent A1c values. Disagreement or lack of correlation between A1c and glucose values indicates the possibility of an interference with the method used to determine the A1c value.

Glucose measurements have been used for many years as an indicator of short-term glycemic management to identify diabetes and assist in management of the disease. Glycated hemoglobin, or hemoglobin A1c, is used to indicate long-term glycemic management over a period of 3 to 4 mo and is used as a diagnostic tool in the diagnosis of type 2 diabetes. The estimated average glucose (eAG) is a mathematical relationship between hemoglobin A1c and glucose levels expressed by the formula eAG = (mg/dL) = [(A1c × 28.7) – 46.7]For example, eAG for a patient with an A1c of 6% would be calculated as: [(6 × 28.7) – 46.7] = 125.5 mg/dL.

1,5 anhydroglucitol: A Marker for Short-Term Glycemic Management

Studies have documented the need for markers that reflect intermediate glycemic management, or the period of time between 2 to 4 wk as opposed to hours or months. Many patients who appear to be well managed according to glucose and A1c values actually have significant postprandial hyperglycemia. Management of postprandial hyperglycemia is considered to be extremely important in preventing or delaying the development of diabetes-related complications. The GlycoMark assay measures serum 1,5-anhydroglucitol, a validated marker of short-term glycemic management, and can be used in combination with glucose and hemoglobin A1c measurements to provide a more complete picture of glucose levels over time. Serum 1,5-anhydroglucitol is a naturally occurring monosaccharide found in most foods. It is not normally metabolized by the body and is excreted by the kidneys. During periods of normal glucose levels, there is an equilibrium between glucose and 1,5-anhydroglucitol concentrations. When blood glucose concentration rises above 180 mg/dL (SI = 10 mmol/L), the renal threshold for glucose, levels of circulating serum 1,5-anhydroglucitol decrease due to competitive inhibition of renal tubular absorption favoring glucose over serum 1,5-anhydroglucitol. As glucose is retained in the circulating blood and levels of glucose increase, correspondingly higher amounts of 1,5-anhydroglucitol are excreted in the urine, resulting in lower serum concentrations. The change in serum 1,5-anhydroglucitol levels is directly proportional to the severity and frequency of hyperglycemic episodes. Serum 1,5-anhydroglucitol concentration returns to normal after 2 wk with no recurrence of hyperglycemia.

Fructosamine: A Marker for Long-Term Glycemic Management

Fructosamine is the result of a covalent linkage between glucose and albumin or other proteins. Similar to glycated hemoglobin, fructosamine can be used to monitor long-term management of glucose in patients with diabetes. It has a shorter half-life than glycated hemoglobin and is thought to be more sensitive to short-term fluctuations in glucose concentrations. Some glycated hemoglobin methods are affected by hemoglobin variants. Fructosamine is not subject to this interference.

Hemoglobin A1c: A Marker for Long-Term Glycemic Management

Hemoglobin A1c measures the mean plasma glucose levels over the previous 3 to 4 months; blood glucose levels in the month prior to measurement have a more significant effect on the A1c value obtained than the blood glucose levels that occurred 3 to 4 months prior to measurement. A number of conditions are known to produce discordant results between plasma glucose and A1c. For additional information refer to the study titled “Hemoglobin A1c.”

The Centers for Disease Control and Prevention releases a National Diabetes Statistics Report about every other year (www.cdc.gov/diabetes/data/index.html). The report provides up-to-date statistical information on diabetes and prediabetes in the United States. The combined use of available markers of glycemic management will greatly improve the ability to achieve tighter, more timely glycemic management.

Continuous Glucose Monitoring and the Ambulatory Glucose Profile

Continuous glucose monitoring (CGM) has become a technology more frequently used to monitor and successfully manage diabetes. The Ambulatory Glucose Profile (AGP) was developed by the International Diabetes Center. It is a one-page report of in-vivo glucose data that can be generated by most CGM monitors and is recognized as the standard of care for reporting CGM data by the ADA. The program converts glucose readings into simple, easy to understand, color-coded graphs that cover seven or more days of data showing:

The AGP report is identical in how it looks and presents the data regardless of the type of CGM system being used. However, the report generated by some systems may vary in the total number of glucose data points used to generate the statistics (e.g., the International Diabetes Center report includes 90% of glucose values; a different system might use 80% of the glucose data points).

Comparison of Markers of Glycemic Management to Approximate Blood Glucose Concentration

1,5-Anhydroglucitol Measured Using the GlycoMark AssayHemoglobin A1cEstimated Blood Glucose (mg/dL)Degree of Glycemic Management
14 mcg/mL or greater4%–5%68–97 mg/dLNormal/nondiabetic
10–12 mcg/mL4%–6%68–126 mg/dLWell managed
5–10 mcg/mL6%–8%126–183 mg/dLModerately well managed
2–5 mcg/mL8%–10%183–240 mg/dLPoorly managed
Less than 2 mcg/mLGreater than 10% (11%–14%)269–355 mg/dLVery poorly managed

Assessment of medications used to manage diabetes is an important facet of managing the disease and its health-related complications. Drug response is an active area of study to ensure that the medications prescribed are meeting the needs of the patients who are taking them.

Examples of Medications Used to Lower Blood GlucoseDrug Class/(Route of Administration)Mechanism for Lowering Blood Glucose
Acarbose, MiglitolAlpha-glucosidase inhibitors (PO)Delays digestion of carbohydrates and decreases absorption of glucose in the GI tract.
MetforminBiguanides (PO)Decreases glucose production by the liver, decreases absorption of glucose in the intestines, and increases insulin sensitivity.
ColesevelamBile acid sequestrants (PO)Exact mechanism unknown. Colesevelam binds to bile acids in the intestines and prevents their reabsorption. The decrease in bile acids causes a feedback process whereby cholesterol is converted to bile acids. An increase in the number of LDLC receptors also occurs. The result is that LDLC and glucose levels decrease.
Bromocriptine mesylate quick-release (Cycloset)Dopamine-2 agonists (PO)Exact mechanism unknown. Formulations of bromocriptine work in different ways, based on the type of condition being treated (e.g., acromegaly related to excessive production of growth hormone; amenorrhea, galactorrhea, or infertility related to hyperprolactemia; hypogonadism related to decreased testosterone levels; Parkinson disease; type 2 diabetes). Cycloset is not interchangeable with other formulations of bromocriptine.
Alogliptin, Linagliptin, Saxagliptin, SitagliptinDipeptidyl peptidase–4 inhibitors (DPP-4 Inhibitors) (PO)Incretins are hormones that stimulate release of insulin from the pancreas. GLP-1 (glucagon-like peptide-1) is one of two main incretin hormones secreted by endocrine cells in the small intestine in response to the presence of glucose in the GI tract.
Glucose levels are decreased when the action of DPP-4 enzymes is inhibited and the inactivation of incretins is slowed down.
Albiglutide, Dulaglutide, Liraglutide, SemaglutideGlucagon-like peptide-1 (GLP-1) receptor agonists (Subcut)Agonists act like other similar substances, in this case GLP-1. GLP-1 receptor agonists inhibit glucagon secretion, and thereby reduce glucose production by the liver; delay stomach emptying and glucose absorption; stimulate release of insulin. These actions decrease blood glucose.
ExenatideIncretin mimetic agents (Subcut)Agonists that mimic the effect of incretins decrease blood glucose by stimulating secretion of insulin and by increasing insulin sensitivity at insulin receptor sites. Exenatideis is resistant to natural degradation by DPP-4 enzymes.
Nateglinide, RepaglinideMeglitinides (PO)Decreases blood glucose by stimulating secretion of insulin and increasing insulin sensitivity at receptor sites.
Canagliflozin, Dapagliflozin, EmpagliflozinSodium-glucose transporter 2 inhibitors (SGLT2 Inhibitors) (PO)Decreases blood glucose by inhibiting the enzyme (SLGT2) that promotes reabsorption of glucose in the proximal tubules of the kidneys, lowering the renal threshold and increasing excretion of glucose in the urine.
Chlorpropamide, Glimepiride, Gliclazide, Glipizide, GlyburideSulfonylureas (PO)Decreases blood glucose by stimulating secretion of insulin and increasing insulin sensitivity at receptor sites.
Rosiglitazone, PioglitazoneThiazolidinediones (TZDs) (PO)Decreases blood glucose by increasing insulin sensitivity. TZDs bind to fat cell receptors to promote adipocyte maturation. Mature fat cells leave circulation and are deposited in peripheral tissues. The net effect is decreased insulin resistance in the liver, adipose, and muscle tissue.
Insulins (For additional information refer to the studies titled “Insulin” and “Insulin Antibodies.”)Note: Antidiabetic drugs are sometimes used together.Hormones (injection or infusion)Note: Combination therapy is sometimes used for oral medications.Decreases blood glucose by promoting glucose storage as glycogen and production of proteins in skeletal muscle; increases production of lipids such as triglycerides. Also decreases glucose production by the liver and inhibits the release of free fatty acids.

Indications

Interfering Factors

Factors That May Alter the Results of the Study

Glucose

  • Drugs and other substances that may increase glucose levels include albuterol, anesthetics, anticonvulsants, antidepressants (tricyclic), antifungals, antipsychotics, antiretrovirals, beta blockers, calcium channel blockers, corticosteroids (corticotropin, cortisone, dexamethazone, prednisone), cyclosporins, diuretics (loop, thiazides, triamterene), epinephrine, ethacrynic acid, glucagon, immunosuppressants, isoniazid, IV solutions containing dextrose, octreotide, oral contraceptives, niacin, somatotropin, TB medications, and thyroid hormone.
  • Drugs and other substances that may decrease glucose levels include ACE inhibitors (captopril, enalapril), acetylsalicylic acid, alcohol, antidiabetic medications (refer to table above), calcium channel blockers (verapamil), fibrates (clofibrate, gemfibrozil), and theophylline.
  • Elevated urea levels and uremia can lead to falsely elevated glucose levels related to reduced kidney function.
  • Administration of insulin or oral hypoglycemic drugs within 8 hr of a fasting blood glucose can lead to falsely decreased values.
  • Specimens should never be collected above an IV line because of the potential for dilution when the specimen and the IV solution combine in the collection container, falsely decreasing the result. There is also the potential of contaminating the sample with the substance of interest, if it is present in the IV solution, falsely increasing the result.
  • Failure to follow dietary restrictions 8 hr before the fasting test can lead to falsely elevated glucose values.
  • Failure to ingest a diet with sufficient carbohydrate content (mixed diet of at least 150 gm carbohydrates/day) for at least 3 days before the test; fasting and carbohydrate restriction can falsely increase oral glucose challenge levels.

Fructosamine

  • Drugs and other substances that may increase fructosamine levels include bendroflumethiazide and captopril.
  • Drugs and other substances that may decrease fructosamine levels include ascorbic acid, pyridoxine, and terazosin.
  • Decreased albumin levels may result in falsely decreased fructosamine levels.

Potential Medical Diagnosis: Clinical Significance of Results

Increased In

  • Acromegaly, gigantism (growth hormone [GH] stimulates the release of glucagon, which in turn increases glucose levels)
  • Acute stress reaction (hyperglycemia is stimulated by the release of catecholamines and glucagon)
  • Cerebrovascular accident (possibly related to stress)
  • Chronic kidney disease (glucagon is degraded by the kidneys; when damaged kidneys cannot metabolize glucagon, glucagon levels in blood rise and result in hyperglycemia)
  • Cushing syndrome (related to elevated cortisol)
  • Diabetes (glucose intolerance and elevated glucose levels define diabetes)
  • Glucagonoma (glucagon releases stored glucose; glucagon-secreting tumors will increase glucose levels)
  • Hemochromatosis (related to iron deposition in the pancreas; subsequent damage to pancreatic tissue releases cell contents, including glucagon, resulting in hyperglycemia)
  • Liver disease (severe) (damaged liver tissue releases cell contents, including stored glucose, into circulation)
  • Metabolic syndrome (related to the development of diabetes)
  • Myocardial infarction (related to stress and/or preexisting diabetes)
  • Pancreatic adenoma (damage to pancreatic tissue releases cell contents, including glucagon, resulting in hyperglycemia)
  • Pancreatitis (acute and chronic) (damage to pancreatic tissue releases cell contents, including glucagon, resulting in hyperglycemia)
  • Pancreatitis due to mumps (damage to pancreatic tissue releases cell contents, including glucagon, resulting in hyperglycemia)
  • Pheochromocytoma (related to increased catecholamines, which increase glucagon; glucagon increases glucose levels)
  • Shock, trauma (hyperglycemia is stimulated by the release of catecholamines and glucagon)
  • Somatostatinoma (somatostatin-producing tumor of pancreatic delta cells, associated with diabetes)
  • Strenuous exercise (hyperglycemia is stimulated by the release of catecholamines and glucagon)
  • Thyrotoxicosis (related to loss of kidney function)
  • Vitamin B1 deficiency (thiamine is involved in the metabolism of glucose; deficiency results in accumulation of glucose)

Decreased In

  • Acute alcohol ingestion(most glucose metabolism occurs in the liver; alcohol inhibits the liver from making glucose)
  • Addison disease (cortisol affects glucose levels; insufficient levels of cortisol result in diminished glucose levels)
  • Ectopic insulin production from tumors (adrenal cancer, cancer of the stomach, fibrosarcoma)
  • Excess insulin by injection
  • Galactosemia (inherited enzyme disorder that results in accumulation of galactose in excessive proportion to glucose levels)
  • Glucagon deficiency (glucagon controls glucose levels; hypoglycemia occurs in the absence of glucagon)
  • Glycogen storage diseases (deficiencies in enzymes involved in conversion of glycogen to glucose)
  • Hereditary fructose intolerance (inherited disorder of fructose metabolism; phosphates needed for intermediate steps in gluconeogenesis are trapped from further action by the enzyme deficiency responsible for fructose metabolism)
  • Hypopituitarism (decreased levels of hormones such as adrenocorticotropic hormone [ACTH] and GH result in decreased glucose levels)
  • Hypoproteinemia (severe) will cause a decrease in fructosamine (decreased levels of hormones such as adrenocorticotropic hormone [ACTH] and GH result in decreased glucose levels)
  • Hypothyroidism (thyroid hormones affect glucose levels; decreased thyroid hormone levels result in decreased glucose levels)
  • Insulinoma (the function of insulin is to decrease glucose levels)
  • Malabsorption syndromes (insufficient absorption of carbohydrates)
  • Maple syrup urine disease (inborn error of amino acid metabolism; accumulation of leucine is believed to inhibit the rate of gluconeogenesis, independently of insulin, and thereby diminish release of hepatic glucose stores)
  • Poisoning resulting in severe liver disease (decreased liver function correlates with decreased glucose metabolism)
  • Postgastrectomy (insufficient intake of carbohydrates)
  • Starvation (insufficient intake of carbohydrates)
  • von Gierke disease (most common glycogen storage disease; G6PD deficiency)

Nursing Implications, Nursing Process, Clinical Judgement

Potential Nursing Problems: Assessment & Nursing Diagnosis

ProblemsSigns and Symptoms
Glucose (related to sedentary lifestyle, circulating insulin deficiency secondary to pancreatic insufficiency, excessive dietary intake, insulin resistance)Excess: Fatigue, mild dehydration, elevated blood glucose, weight loss, weakness, polyuria, polydipsia, polyphagia, blurred vision, headache, paresthesia, poor skin turgor, dry mouth, nausea, vomiting, abdominal pain, Kussmaul respirations
Deficit: Tremor, diaphoresis, decreased concentration, elevated blood pressure; palpitations; headache, polyphagia; restlessness, lethargy, altered mental status, combativeness, altered speech, altered coordination
Nutrition (excess—related to excessive dietary intake more than body requirements, insulin deficiency, stress, anxiety, depression, cultural lifestyle, unhealthy food sources, financial restrictions)Polydipsia, polyuria, weight loss, fatigue, elevated blood glucose levels, inadequate glucose management, polyphagia

Before the Study: Planning and Implementation

Teaching the Patient What to Expect

  • Discuss how this test can assist in evaluating blood sugar levels.
  • Explain that a blood sample is needed for the test.

Potential Nursing Actions

  • Verify adherence to dietary restrictions for the specified study prior to specimen collection.

After the Study: Implementation & Evaluation Potential Nursing Actions

Treatment Considerations

  • Resume the usual diet, as directed by the HCP, once the specimen collection is completed.
  • Comparative studies demonstrate that certain populations are disproportionately affected by type 2 diabetes and complications of type 2 diabetes as compared to the general population.
  • Nonmodifiable risk factors include age, ethnicity, and family history of diabetes or metabolic syndrome.
  • The risk of developing type 2 diabetes increases with age. In the United States, affected populations include African Americans, Asian Americans, Hispanics, native Hawaiians and Pacific Islanders, American Indians, and Alaska natives.
  • Modifiable risk factors include lifestyle choices related to making healthy dietary choices, maintaining a healthy body weight, and meeting recommended levels of physical activity.
  • Prevention and medical management strategies for patients with type 2 diabetes should be provided through the coordinated efforts of multidisciplinary partners using strategies that are culturally appropriate.

Glucose

  • Instruct in the use of continuous glucose monitoring systems; home testing strips or meters approved for glucose, ketones, or A1c by the U.S. Food and Drug Administration, if prescribed.
  • Discuss the value of blood glucose checks before meals and at bedtime.
  • Monitor blood glucose results and administer ordered insulin or oral and injectable antihyperglycemic drugs.
  • Verify accurate self-administration of prescribed insulin or oral and injectable antihyperglycemic drugs.
  • Explain that long-term use of metformin can lead to deficiencies in folate and/or vitamin B12 especially in the presence of anemia and peripheral neuropathy, which can also affect memory. Encourage collaboration with the HCP regarding frequency of vitamin B12 monitoring.
  • Assess the cultural aspects of diet selection.
  • Correlate dietary intake with blood glucose.
  • Monitor laboratory studies that may be impacted by altered glucose and trend results (Hemoglobin A1c, BUN, Cr, electrolytes, arterial pH, magnesium, urine ketones, urine albumin, WBC count, amylase, Hgb/Hct, CRP, liver enzymes).
  • Correlate blood glucose with other laboratory values and medical conditions, address the psychosocial aspects of the disease, and monitor serum insulin levels.
  • Advise reporting signs and symptoms of hypoglycemia (weakness, confusion, diaphoresis, rapid pulse) or hyperglycemia (thirst, polyuria, hunger, lethargy).
  • Collaborate with the HCP regarding type and frequency of glucose monitoring.
  • Collaborate with the HCP to develop a plan of exercise commensurate with the patient’s physical abilities and discuss lifestyle alterations necessary to support positive health management.
  • Individuals with poor glycemic management have a greater infection risk.
  • Discuss the value of vigilant hand hygiene and the correlation between poor hygiene and infection risk.
  • Discuss how adequate rest and avoiding exposure to opportunistic hosts can minimize infection risk.
  • Explain that nonadherence to medication, diet, and activity therapeutic goals can make glycemic management problematic.
  • Assess the patient’s ability and prior efforts to manage the disease process, including blood glucose self-checks, dietary management, exercise, and medication self-administration.
  • Evaluate for personal factors that may limit the patient’s ability to self-perform, such as visual, cognitive, or hearing deficits or lack of financial resources.
  • Discuss how good glycemic management delays the onset and slows the progression of diabetic retinopathy, nephropathy, and neuropathy.
  • Discuss the implications of abnormal test results on the patient’s lifestyle.

Nutritional Considerations

  • Increased glucose levels may be associated with diabetes.
  • Discuss the nutritional management of diabetes.
  • There is no “diabetic diet”; however, many meal-planning approaches with nutritional goals are endorsed by the ADA.
  • Patients who adhere to dietary recommendations report a better general feeling of health, better weight management, better management of glucose and lipid values, and improved use of insulin.
  • Variety of dietary patterns are beneficial for people with diabetes.
  • Encourage consultation with a registered dietitian who is a certified diabetes educator.
  • Ensure the patient understands the relationship between caloric intake, ordered medication, and glucose results.
  • Monitor blood glucose results, and evaluate the effectiveness of administered insulin or oral and injectable antihyperglycemic drugs.
  • The Centers for Disease Control and Prevention (CDC) defines obesity as body mass index (BMI) at or above the 95th percentile for CDC gender specific BMI by age growth charts.

Clinical Judgement

  • Consider how to overcome cultural and socioeconomic barriers related to glucose management.

Follow-Up and Desired Outcomes

  • Acknowledges contact information provided for the ADA (www.diabetes.org), American Heart Association (www.heart.org/HEARTORG), National Heart, Lung, and Blood Institute (www.nhlbi.nih.gov), NIDDK (www.niddk.nih.gov), and U.S. Department of Agriculture’s resource for nutrition (www.choosemy plate.gov).
  • Understands that the ADA recommends A1c testing four times a year for insulin-dependent type 1 or type 2 diabetes when glycemic targets are not being met or when therapy has changed and twice a year when treatment goals are being met for non–insulin-dependent type 2 diabetes. The ADA also recommends that testing for diabetes commence at age 35 for asymptomatic individuals, be considered for adults of any age who are overweight and have additional risk factors, and continue every 3 yr in the absence of symptoms; be performed on patients with HIV, in relation to the timing of therapeutic interventions; Annual screening with an oral glucose tolerance test should begin by age 10 in CF patients who have not been previously diagnosed with CF related diabetes (CFRD) and annual monitoring for complications of CFRD should begin 5 yr after diagnosis; be performed annually on patients with prediabetes; be performed every three years (lifelong) for patients diagnosed with gestational diabetes.