Complete Nurse's Guide to Diabetes Care, 3rd Edition

Chapter 2:

Diagnosis and Classification

Marjorie Cypress, PhD, MSN, RN, C-ANP, CDE,1 and Donna Tomky, MSN, RN, ANP-BC, CDE1

1Adult nurse practitioners and certified diabetes educators in Albuquerque, NM.

The prevalence of diabetes and prediabetes continues to increase at alarming rates. From 1980 to 2014, the number of individuals with diagnosed diabetes has increased fourfold to 22 million with continued estimates of 8.1 million people with undiagnosed diabetes.1 Prediabetes rates also are increasing, and it is estimated that 86 million Americans ages 20 years or older have prediabetes.2 These problems are not limited to the U.S.

In 2014, the World Health Organization estimated that more than 422 million people worldwide had diabetes, and that number is expected to double by the year 2030.3 Almost 40% of the population over the age of 65 years suffers from diabetes.4 Diabetes is listed as the seventh leading cause of death and is linked with heart disease, hypertension, blindness, kidney disease, nervous system disease, amputations, and dental disease.2 Although historically type 2 diabetes (T2D) has been an adult disease, more children are being diagnosed with T2D and risk earlier and more serious complications. As the U.S. and the world continue to see rising rates of diabetes, it stands as one of the most common diseases that nurses will encounter in their professional lives. It is essential that nurses appreciate the tremendous growth of diabetes in the population and be knowledgeable about the classification and diagnostic criteria for diabetes and prediabetes so that early and appropriate interventions can be instituted. Diagnosing diabetes or prediabetes early decreases the risks for complications and improves outcomes to lessen the burden on individuals, families, communities, and society.

Diabetes is a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both. The chronic hyperglycemia of diabetes is associated with long-term damage, dysfunction, and failure of different organs, especially the eyes, kidneys, nerves, heart, and blood vessels. Importantly, patients with diabetes are at much higher risk for cardiovascular events, including myocardial infarctions and cerebrovascular accidents.

Diabetes is classified into four distinct categories: type 1 diabetes (T1D), T2D, other specific types of diabetes that may be due to other causes, and gestational diabetes mellitus (GDM). T1D accounts for 5–10% of people with diabetes, while T2D accounts for ~90% of all people with diagnosed diabetes. Another classification category is “increased risk of diabetes,” also known as prediabetes. Many of the people who meet the criteria for prediabetes are obese and have abnormal glucose levels but do not meet the criteria for a diagnosis of diabetes.

DIAGNOSING DIABETES

The clinical presentation and disease progression vary in T1D and T2D.5 Although the categories appear straightforward, it may be difficult to correctly diagnose some children, teens, and adults, and the true diagnosis may become evident over time.

Classic symptoms of diabetes, all caused by elevated blood glucose, include polyuria, polydipsia, weight loss, fatigue, blurred vision, and dry mouth. Many people, usually those with milder elevations in blood glucose, have no symptoms at all or may not recognize them as problems. The diagnosis therefore first may be suspected on routine measurement of blood glucose or on an incidental finding of glucose in the urine. Sometimes, diagnosis occurs when evidence already exists of chronic diabetes complications, such as retinopathy, other vascular disease, or neuropathy. The onset of diabetes is generally insidious. Many patients with T2D are often free of classic symptoms and, thereby, may remain undiagnosed for a prolonged period.

The diagnosis of diabetes can be made based on one or more plasma glucose criteria: hemoglobin A1c (A1C), or fasting blood glucose (FBG), or a 2-h plasma glucose during an oral glucose tolerance test (OGTT), or in a patient with classic symptoms of hyperglycemia or hyperglycemic crisis and random plasma glucose ≥200 mg/dL (see Table 2.1).5

Table 2.1—Criteria for the Diagnosis of Diabetes

Table 2.1—Criteria for the Diagnosis of Diabetes

FPG, fasting plasma glucose; PG, plasma glucose.

Source: From American Diabetes Association.5

The A1C test should be performed using a method that is certified by the National Glycohemoglobin Standardization Program. Interpreting A1C levels in patients with certain anemias and hemoglobinopathies may be problematic. For those with abnormal hemoglobin such as sickle cell trait, an A1C assay without interference from certain abnormal hemoglobins should be used. In those with increased red blood cell turnover such as in pregnancy, hemodialysis, recent blood cell losss or transfusion, or erythropoietin therapy, only blood glucose criteria should be used to diagnose diabetes.

Diagnosing GDM

GDM is defined as diabetes diagnosed in the second or third trimester of pregnancy that was not clearly overt diabetes prior to gestation. GDM carries risks for the mother and neonate. With the ongoing epidemic of overweight and obesity and higher rates of T2D among women of childbearing age, the number of pregnant women with undiagnosed T2D has increased. If possible, a patient’s risk for GDM should be determined before conception to detect undiagnosed T2D in high-risk women, but certainly, if not before, at the onset of the diagnosis of pregnancy. It is reasonable to screen women with risk factors for T2D at the initial prenatal visit using standard diagnostic criteria (Table 2.2). The Hyperglycemia and Adverse Pregnancy Outcomes Study of ~25,000 pregnant women demonstrated that risk of adverse maternal, fetal, and neonatal outcomes continuously increases as a function of maternal glycemia at ~24–28 weeks’ gestation, even within ranges previously considered normal for pregnancy.6 As a result of this study, two groups met to establish the most appropriate criteria for diagnosing GDM, but they developed different criteria. The International Association of Diabetes and Pregnancy Study recommends GDM screening as a two-step method,7 and the National Institutes of Health (NIH) consensus statement recommends a one-step method for GDM screening.8 GDM screening can be accomplished with either of these two strategies: 1) the one-step 2-h 75 g OGTT, or 2) the two-step approach with a 1-h 50 g (nonfasting) screen followed by a 3-h 100 g OGTT for those who screen positive (see Table 2.3). Abnormal blood glucose levels in the first trimester of pregnancy suggest a diagnosis of T2D or prediabetes as opposed to typical GDM. Regardless of the diagnosis, because GDM is a risk factor for the development of T2D, women with abnormal blood glucose levels should be screened for diabetes 4–12 weeks postpartum, using OGTT diagnostic criteria for individuals who are not pregnant.5 Women with a history of GDM should have lifelong screening for the development of T2D or prediabetes at least every 3 years. Women with a history of GDM found to have prediabetes should receive intensive lifestyle interventions or metformin to prevent diabetes.5

Table 2.2—Criteria for Testing for Diabetes or Prediabetes in Asymptomatic Adults and Children

1. Testing should be considered in overweight or obese (BMI ≥25 kg/m2 or ≥23 kg/m2 in Asian Americans) adults who have one or more of the following risk factors:

• A1C ≥5.7% (39 mmol/mol), IGT, or IFG on previous testing

• first-degree relative with diabetes

• high-risk race/ethnicity (e.g., African American, Latino, Native American, Asian American, Pacific Islander)

• women who were diagnosed with GDM

• history of CVD

• hypertension (≥140/90 mmHg or on therapy for hypertension)

• HDL cholesterol level <35 mg/dL (0.90 mmol/L) and/or a triglyceride level >250 mg/dL (2.82 mmol/L)

• women with polycystic ovary syndrome

• physical inactivity

• other clinical conditions associated with insulin resistance (e.g., severe obesity, acanthosis nigricans).

2. For all patients, testing should begin at age 45 years.

3. If results are normal, testing should be repeated at a minimum of 3-year intervals, with consideration of more frequent testing depending on initial results (e.g., those with prediabetes should be tested yearly) and risk status.

Source: From American Diabetes Association.5

Table 2.3—Screening for and Diagnosis of GDM

Table 2.3—Screening for and Diagnosis of GDM

NDDG, National Diabetes Data Group.

*The ACOG recommends either 135 mg/dL (7.5 mmol/L) or 140 mg/dL (7.8 mmol/L). A systematic review determined that a cutoff of 130 mg/dL (7.2 mmol/L) was more sensitive but less specific than 140 mg/dL (7.8 mmol/L).

Source: From the American Diabetes Association.5

Categories of Increased Risk for Diabetes (Prediabetes)

This section reviews recommendations for individuals at increased risk for diabetes and prediabetes.5 Testing to assess risk for future diabetes in asymptomatic people should be considered in adults of any age who are overweight or obese (BMI ≥25 kg/m2 or ≥23 kg/m2 in Asian Americans) and who have one or more additional risk factors for diabetes. The American Diabetes Association T2D risk test is helpful as a general screen and to refer those with high risk to have diagnostic tests (Figure 2.1).

Figure 2.1—American Diabetes Association Risk Test for T2D

Figure 2.1—American Diabetes Association Risk Test for T2D.

Source: From the American Diabetes Association.5

Table 2.2 outlines the criteria for testing for diabetes and prediabetes in asymptomatic adults and children. For all patients, particularly those who are overweight or obese, testing should begin at age 45 years.

To test for prediabetes, A1C, fasting plasma glucose (FPG), and 2-h plasma glucose (PG) after 75 g OGTT are appropriate. In patients with prediabetes, identify and, if appropriate, treat other cardiovascular risk factors.

Testing to detect prediabetes should be considered in children and adolescents who are overweight or obese and who have two or more additional risk factors (see Table 2.2).

PATHOGENESIS OF DIABETES

Several pathogenic processes are involved in the development of diabetes. These range from autoimmune destruction of the pancreatic β-cells with consequent insulin deficiency to abnormalities that result in resistance to insulin action. Both type 1 and type 2 diabetes may result from various genetic and environmental factors that result in progressive loss of β-cell mass and/or function that manifests as hyperglycemia. The basis of the abnormalities in carbohydrate, fat, and protein metabolism in diabetes is deficient insulin action on target tissues. Deficient insulin action results from inadequate insulin secretion or diminished tissue responses to insulin at one or more points along the complex pathways of hormone action. Impairment of insulin secretion and deficient insulin action frequently coexist in the same patient, and it often is unclear which abnormality, if either alone, is the primary cause of the hyperglycemia.

Type 1 Diabetes

TID is due to β-cell destruction leading to absolute deficiency of insulin secretion resulting from an autoimmune destruction of the β-cells of the pancreas (see Figure 2.2). Diabetic ketoacidosis can be present at diagnosis or may develop if insulin replacement therapy is not started immediately upon diagnosis or later, into the course of the disease, if insulin delivery is halted or inadequate for some reason (i.e., insulin pump failure, infusion site problems, poor absorption, damaged or expired insulin, omission by the patient, etc.).

Figure 2.2—Natural History of T1DM

Figure 2.2—Natural History of T1DM.

Source: Reprinted with permission from Lancet. 2014;383:69–82.

The pathogenesis of T1D is divided into autoimmune-mediated diabetes and idiopathic diabetes. In autoimmune-mediated diabetes, insulin-producing β-cells are destroyed by an autoimmune-mediated process. Typically, β-cells are totally destroyed, but in some patients, destruction is incomplete, resulting in residual insulin production. The rate of β-cell destruction is variable, can be very rapid in infants and children and slower in adults. Some will present with ketoacidosis and others will have increasing hyperglycemia but this can occur at any age, even adults in their 80s and 90s. Antibody markers usually are seen. Autoimmune markers include islet cell antibodies and autoantibodies to glutamic acid decarboxylase (GAD65), insulin, the tyrosine phosphates IA-2 and 1A2β and ZnT8.5 T1D is defined by the presence of one or more of these markers. There are well-recognized associations with several genes in the human leukocyte antigen (HLA) loci, including both predisposing and protective genes (DQA and DQB). Patients with T1D have increased incidences of other autoimmune diseases, including Hashimoto’s thyroiditis, Graves’ disease, pernicious anemia, vitiligo, celiac disease, and Addison’s disease.

Three distinct stages of T1D can be identified (see Table 2.4) dependent upon presence and number of autoantibodies and are a predictor of hyperglycemia and diabetes. Increasing glucose and A1c levels often rise before clinical symptoms, and staging is useful to make a diagnosis of T1D before the onset of DKA.

Table 2.4—Staging of Type 1 Diabetes

Table 2.4—Staging of Type 1 Diabetes

A less common form of T1D, known as idiopathic diabetes, reveals no evidence of autoimmune disease and immune markers are absent. This form of T1D appears to be inherited, but the cause is unknown. They do not have any evidence of β-cell autoimmunity but do have permanent insulinopenia. Idiopathic diabetes is more common in those of African or Asian ethnic origin and is characterized by episodic ketoacidosis and varying degrees of insulin deficiency. The need for insulin replacement is intermittent—and may change over time.

Type 2 Diabetes

T2D accounts for ~90–95% of those with diabetes (previously referred to as noninsulin-dependent diabetes or adult-onset diabetes). T2D is due to a progressive loss of insulin secretion, frequently with a background of insulin resistance. Most people with T2D (or prediabetes) are obese, with obesity itself causing some degree of insulin resistance. Ketoacidosis is rare (although not unheard of ) and usually seen in association with the stress of another illness, infection, or trauma. T2D may remain undiagnosed for many years because the hyperglycemia develops gradually and, at earlier stages, often is not severe enough for the patient to notice any of the classic symptoms of diabetes.

The pathogenesis of T2D is complex (see Figure 2.3). T2D develops progressively, with the pathogenic abnormalities already present in the prediabetes phase. Virtually all individuals with T2D have peripheral insulin resistance combined with a relative, not absolute, insulin deficiency and throughout their lifetime they may not need insulin treatment to survive.

Figure 2.3—Pathophysiology of Type 2 Diabetes

Figure 2.3—Pathophysiology of Type 2 Diabetes.

Source: Reprinted with permission from DeFronzo.9

The progressive decline in β-cell function over several years, regardless of type of therapy, was demonstrated in the U.K. Prospective Diabetes Study (UKPDS),10 wherein the ability to maintain A1C levels continued to decrease markedly throughout the 9 years of follow-up, even when the researchers controlled for lifestyle issues, such as diet, physical activity, and medication. Notably, in the UKPDS, insulin resistance did not change, suggesting that decreasing β-cell function is responsible for diabetes progression. This progression of insulin deficiency is reflected in the treatment required by those with T2D. Many individuals with T2D require multiple anti-hyperglycemic medications and later will require insulin therapy either in combination with anti-hyperglycemic agents or as monotherapy. T2D is associated with insulin secretory defects related to inflammation and metabolic stress including genetic factors. Other defects in T2D include increased hepatic glucose production, decreased peripheral muscle uptake, defects in the gut or incretin hormones (g>lucagon-like peptide-1 [GLP1] and gastric inhibitory polypeptide [GIP]),11,12increased kidney reabsorption of glucose, and increased lipolysis of adipose tissue (See Figure 2.3).

Obesity and sedentary lifestyle are risk factors for the development of T2D. Obesity, particularly abdominal or visceral obesity, increases insulin resistance and the risk for T2D. Genetic factors (i.e., those unrelated to obesity) also contribute to insulin resistance. Clearly, however, many obese individuals do not develop T2D. These individuals presumably have adequate β-cell function to produce sufficient insulin to overcome the insulin resistance. Even with insulin resistance, diabetes usually will not develop unless a concomitant defect in β-cell function results in a deficiency of insulin secretion. Weight loss in overweight individuals with diabetes improves insulin resistance but usually does not fully restore insulin sensitivity.

Socioecological and other environmental issues also contribute to diabetes and prediabetes. These include the prevalent rates of obesity in adults and youth, increased consumption of high-caloric fast food and soft drinks, larger portion sizes, and a sedentary population (only 19% of adults are meeting physical activity guidelines). In addition, low socioeconomic status, decreased access to health care, communities that do not have safe areas conducive to walking or exercising, and food deserts where access to fresh produce is limited all can increase risk for diabetes and prediabetes.13 Food insecurity also has been associated with higher rates of diabetes.14

GDM

GDM is initially diagnosed during the second or third trimester of pregnancy. The diagnosis can be made in either of two strategies, a one step 75-g OGTT, or a two-step with a 50-g (nonfasting) screen followed by a 100-g OGTT for those who screen positive (Table 2.3). The one-step strategy has been anticipated to increase the incidence of GDM (from 5–6% to 15–20%) in order to optimize gestational outcomes. However, either of these strategies can be used. GDM occurs more frequently in African American, Hispanic/Latino, and Native American populations. Although GDM is glucose intolerance during pregnancy, 5–10% of women with GDM are discovered to have T2D, and women with a history of GDM have a 40–60% chance of developing diabetes over the next 5–10 years.

GDM shares pathogenic features in common with T2D. The insulin resistance experienced during pregnancy leads to hyperglycemia in susceptible women, which often resolves after delivery but may recur in subsequent pregnancies. Screening on the first prenatal visit should include assessment for high-risk ethnic group, personal history of impaired glucose tolerance or fasting glucose, family history of diabetes, previous history of GDM, and obesity.5 Consistent with this pathogenesis, women who have had GDM are at increased risk of developing diabetes later in life and should be screened at least every 3 years for the subsequent development of diabetes or prediabetes throughout their lives.

Other Causes of Diabetes

Other specific types of diabetes may be caused by genetic abnormalities causing defects in β-cell function, abnormalities in insulin action, injury to or surgical excision of the pancreas, and excess secretion of hormones that work against insulin or may result from taking a drug toxic to the pancreas or β-cells.

Diabetes may be seen in diseases of the exocrine pancreas, such as cystic fibrosis. Various endocrine diseases, such as Cushing’s syndrome, acromegaly, and pheochromocytoma, can cause diabetes. Drug-induced diabetes is an important clinical problem. Corticosteroid drugs are the most frequent cause of hyperglycemia in clinical practice, but numerous other drugs can impair insulin action and precipitate diabetes. Most likely, these drugs are not the sole cause of diabetes but unmask hyperglycemia in individuals already at risk.5

Monogenic Diabetes Syndromes

Monogenic defects that cause β-cell dysfunction, such as neonatal diabetes and maturity-onset diabetes of the young (MODY), represent a small fraction of patients with diabetes (<5%). Neonatal diabetes is diagnosed in the first 6 months of life, whereas MODY may be diagnosed up until early adulthood. These monogenic defects cause impaired insulin secretion without insulin resistance. Monogenic diabetes, however, should not be applied to T2D, which, unfortunately, is being diagnosed more frequently in children and adolescents and should be diagnosed in appropriate individuals with genetic testing.

EPIDEMIOLOGY

Type 1 Diabetes

The incidence of T1D has been increasing 2–5% worldwide and prevalence is estimated to be 1 in 300 people in the U.S. under age 18 years.15 The Search for Diabetes in Youth, a Centers for Disease Control and Prevention (CDC) and National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)–supported study, found a general increase in T1D and T2D among those <20 years of age but noted that it primarily was driven by an increase in T1D and was among all race and ethnic groups.16 This increase was most significant among non-Hispanic white youth from 2002 to 2009 in the U.S. and was 2.72% per year (2.84% among males and 2.57% among females).17

Clinical Features of Type 1 Diabetes

Most often, T1D occurs in children and young adults, but it may occur in individuals of any age. The rate of β-cell destruction varies; it is typically more rapid in younger individuals, who present frequently with severe symptomatic hyperglycemia and sometimes with DKA. This suggests severe insulin deficiency. Insulin therapy is required for survival. Those with a slower progression of β-cell destruction may retain some insulin secretion for many years and may present with only modest asymptomatic hyperglycemia. As the disease progresses, they require insulin for survival and are at risk for ketoacidosis. Patients with T1D are not typically obese at diagnosis; however, obesity at the time of diagnosis does not exclude a diagnosis of T1D and sometimes confuses the diagnosis.

Type 2 Diabetes

It is estimated that 29.1 million people in the U.S. have diabetes (9.3%), with 8.1 million of them undiagnosed, and 86 million (37%) Americans >20 years old with prediabetes. 1.4 million Americans aged 20 years or older are newly diagnosed with diabetes each year. For those aged 65 years or older, 11.2 million, or 25.9% of all people in this age group, have T2D. This prevalence is believed to be related to the increasing rates of obesity and higher frequency of sedentary lifestyle among Americans and the rapidly growing high-risk populations of Native Americans, Hispanics/Latinos, African Americans, Asians, and Pacific Islanders. In those under 20 years of age, 1 in 400 has diabetes. Although, historically, diagnoses of diabetes in children have been almost exclusively of T1D, the incidence of the development of T2D in children has increased significantly as a result of increasing obesity. Worldwide there is a significant increase in the prevalence of T2D in children and adolescents, particularly among those ethnic groups with high susceptibility to T2D.

In the U.S., T2D is more common in minority populations. From an international perspective, however, an increased risk for T2D is seen in many diverse ethnic groups. Typically, T2D increases when susceptible populations adopt an industrialized lifestyle with increased caloric intake and reduced physical activity.

Clinical Features of Type 2 Diabetes

The clinical presentation of T2D is even more variable than that of T1D. Because the insulin deficiency is only relative, many of these patients can be treated without insulin, at least initially. Most patients with T2D are obese or overweight with increased abdominal adiposity. Adiposity is seen most commonly in adults, but also increasingly is being seen in adolescents and children, usually in association with obesity. The development of T2D in children and adolescents is a rapidly increasing clinical problem. These individuals are usually obese and most often belong to ethnic groups with a high incidence of T2D. No longer is age of onset a reliable indicator of the type of diabetes present.

Symptoms may be mild or nonexistent in many patients with T2D. Although DKA characteristically is associated with T1D, it may be seen in some cases in which patients with T2D are under severe physical stress, such as major infection, pneumonia, or even cardiac event. It is more likely that those with T2D under severe stress may develop hyperglycemic hyperosmolar syndrome (HHS). HHS is a syndrome characterized by severe hyperglycemia, hyperosmolality, and dehydration in the absence of ketoacidosis. Typically patients are elderly and most present with stupor or coma.18 This is different from the situation in T1D, in which patients are ketosis prone and may develop ketoacidosis rapidly by simply omitting insulin.

Although it may be easy to distinguish the classic presentation of T1D seen in a lean child with weight loss and ketoacidosis and that of T2D seen in an obese older adult with no symptoms and mildly elevated glucose levels, other individuals may be difficult to classify in the initial stages of the disease process. Overlap between the two common forms of diabetes does exist. It may not be clear whether a middle-age adult with onset of fasting hyperglycemia has T2D or a slowly evolving form of T1D. In addition, an individual with a clear history of T1D subsequently may become obese and develop additional features associated with insulin resistance that are common in patients with T2D. Some patients who develop diabetes in adulthood and who initially may appear to have T2D may have a form of autoimmune diabetes. These individuals are usually leaner than the typical patient with T2D. Insulin deficiency may develop more rapidly than in a typical T2D patient but more slowly than in a child with T1D.

Practical Point

Assess clinical characteristics in new-onset hyperglycemia to help determine the safest and most effective treatment.

High-Risk Ethnicities and Type 2 Diabetes

The following ethnicities are at the highest risk for developing diabetes:

• Non-Hispanic blacks/African Americans. A total of 13.3% of all non-Hispanic blacks ≥20 years of age have diabetes. The risk of T2D is 1.8 times that for non-Hispanic whites.3

• Hispanic/Latino Americans. An estimated 12.8% of Hispanics ≥20 years of age have T2D. Hispanic/Latino Americans are 1.7 times more likely to have diabetes than non-Hispanic whites. Mexican Americans and Puerto Ricans have a risk for diabetes more than twice that of non-Hispanics whites.1

• Native Americans/Alaska Natives. Native Americans/Alaska Natives have the highest risk of developing T2D (2.3 times that of non-Hispanic whites), and it is estimated that 15.9% of this population ≥20 years of age has T2D. Among all Native Americans, Alaska Natives have the least risk (6.0%), whereas Native Americans in the southeastern U.S. (24.1%) and in southern Arizona (27.8%) have the highest risk of developing diabetes.4

• Asians/Native Hawaiians/Pacific Islanders. An estimated 9.0% of Asian Americans ≥20 years of age have T2D, with highest risk among Filipinos at 11.3% and Asian Indians at 13.0%.4

Clues to Determining Type of Diabetes

Type 1 Diabetes

Type 2 Diabetes

Usually lean-(recent reviews indicate overweight T1D youth prevalence of 12.5-33.3%)19

Usually overweight or obese (BMI >25 kg/m2 or BMI ≥23 kg/m2 in Asians)

May not have a family history

Almost always has a family history

May not be a member of a high-risk ethnic group

Often a member of a high-risk ethnic group

Ketone prone

Generally not ketosis prone*

Onset slow to rapid (3–4 weeks)

Onset usually slow and progressive

Usually young but can be any age

Usually >30 years old, but can occur in youth May have history of GDM

May have associated complications, such as hypertension, atherogenic dyslipidemia, cardiovascular disease, or risk factors

Markers for insulin resistance (e.g., acanthosis nigricans, characteristic dyslipidemia of high triglycerides, and low HDL cholesterol)

*Idiopathic diabetes with features of T2D may present with ketosis20

SUMMARY

The diagnosis of diabetes is made strictly by FPG, A1C, random blood glucose with symptomatology, or 75-g OGTT. Therapy is initiated based on the level of blood glucose and the type of diabetes diagnosed. Nurses in all settings have the opportunity to identify patients who are at risk for diabetes, have prediabetes, or have diabetes. Studies indicate that early diagnosis and aggressive therapy will delay and possibly prevent the complications of diabetes. Nurses have the opportunity to counsel, refer, and promote healthy behaviors among individuals with diabetes and prediabetes and those who are at high risk for diabetes. Identifying high-risk individuals and providing education about preventive strategies is of utmost importance to slow the seemingly epidemic increase in diabetes.

REFERENCES

1. American Diabetes Association. Fast facts: data and statistics about diabetes, revised 12/2015. Available from http://professional.diabetes.org/sites/professional.diabetes.org/files/media/fast_facts_12-2015a.pdf. Accessed 3 February 20

2. Centers for Disease Control and Prevention. National Diabetes Statistics Report: Estimates of Diabetes and Its Burden in the United States, 2014. Atlanta, GA, U.S. Department of Health and Human Services, 2014

3. World Health Organization. Global report on diabetes, 2016. Available from http://www.who.int/diabetes/global-report. Accessed 21 June 2016

4. Selvin E, Parrinello M, Sacks DB, Coresh J. Trends in prevalence and control of diabetes in the United States 1988–1994 and 1999–2010. Ann Intern Med 2014;160:517–525

5. American Diabetes Association. Diagnosis and classification of diabetes. Sec 2. Standards of medical care in diabetes—2017. Diabetes Care 2017; 40(Suppl. 1):S11–S24

6. Metzger BE, Lowe LP, Dyer AR, et al. HAPO Study Cooperative Research Group. Hyperglycemia and adverse pregnancy outcomes. Diabetes Care 2008;31:899–904

7. International Association of Diabetes and Pregnancy Study Groups Consensus Panel. IADPSG recommendations on the diagnosis and classification of hyperglycemia in pregnancy. Diabetes Care 2010;33:676–682

8. Vandorsten JP, Dodson WC, Espeland MA, et al. NIH consensus development conference: diagnosing gestational diabetes mellitus. NIH Consens State Sci Statements 2013;29:1–31

9. DeFronzo, R. Banting Lecture. From the triumvirate to the ominous octet: a new paradigm for the treatment of type 2 diabetes mellitus. Diabetes 2009;58:773–795

10. U.K. Prospective Diabetes Study Group. Overview of 6 years’ therapy of type II diabetes: a progressive disease. Diabetes 1995;44:1249–1258

11. Maranthe CS, Rayner CK, Jones KL, Horowitz M. Relationships between gastric emptying, post prandial glycemia and incretin hormones. Diabetes Care 2013;36:1396–1405

12. Schwartz SS, Epstein S, Corkey B, et al. The time is right for a new classification system for diabetes: rationale and implications of the B-C-Centric classification schema. Diabetes Care 2016;39:179–186

13. Hill JO, Galloway JM, Goley A, et al. Scientific statement: socioecological determinants of type 2 diabetes and prediabetes. Diabetes Care 2013;36:2430–2439

14. Seligman HK, Schillinger D. Hunger and socioeconomic disparities in chronic disease. N Engl J Med 2010;363:6–9

15. Maahs, DM, et al. Chapter 1: Epidemiology of type 1 diabetes. Endocrinol Metabol Clin North Am 2010;39:481–497

16. Pettitt DJ, Talton J, Dabelea D, et al. Prevalence of diabetes in U.S. youth in 2009: the SEARCH for Diabetes in Youth study. Diabetes Care 2014;37: 402–408

17. Lawrence JM, Imperatore G, Dabelea D, et al. Trends in incidence of type 1 diabetes among non-hispanic white youth in the U.S., 2002–2009Diabetes 2014;63:3938–3945. https://doi.org/10.2337/db13-1891

18. Pasquel FJ, Umpierrez GE. Hyperosmolar hyperglycemic state: a historic review of the clinical presentation, diagnosis, and treatment. Diabetes Care 2014;37:3124–3131. doi: 10.2337/dc14-0984

19. Minges KE, Whitteore R, Grey M. Overweight and obesity in youth with type 1 diabetes. Annu Rev Nurs Res 2013;31:47–69. doi: 10.1891/ 0739-6686.31.47

20. Umpierrez GE. Ketosis prone type 2 diabetes. Diabetes Care 2006;29: 2755–2757. https://doi.org/ 10.2337/dc06-1870