Вы находитесь на странице: 1из 43


Standards of Medical Care in Diabetes—2008


iabetes is a chronic illness that re- ing methods, was utilized to clarify and treatment of AIDS or after organ trans-
quires continuing medical care and codify the evidence that forms the basis plantation)
patient self-management education for the recommendations. The level of ev- ● Gestational diabetes mellitus (GDM)
to prevent acute complications and to re- idence that supports each recommenda- (diabetes diagnosed during pregnancy)
duce the risk of long-term complications. tion is listed after each recommendation
Diabetes care is complex and requires that using the letters A, B, C, or E. Some patients cannot be clearly classified
many issues, beyond glycemic control, be as type 1 or type 2 diabetes. Clinical pre-
addressed. A large body of evidence exists sentation and disease progression vary
that supports a range of interventions to considerably in both types of diabetes.
improve diabetes outcomes. I. CLASSIFICATION AND Occasionally, patients who otherwise
These standards of care are intended DIAGNOSIS have type 2 diabetes may present with ke-
to provide clinicians, patients, research- toacidosis. Similarly, patients with type 1
ers, payors, and other interested individ- A. Classification may have a late onset and slow (but re-
uals with the components of diabetes In 1997, ADA issued new diagnostic and lentless) progression of disease despite
care, treatment goals, and tools to evalu- classification criteria (4); in 2003, modi- having features of autoimmune disease.
ate the quality of care. While individual fications were made regarding the diagno- Such difficulties in diagnosis may occur in
preferences, comorbidities, and other pa- sis of impaired fasting glucose (5). The children, adolescents, and adults. The true
tient factors may require modification of classification of diabetes includes four diagnosis may become more obvious over
goals, targets that are desirable for most clinical classes: time.
patients with diabetes are provided.
These standards are not intended to pre- ● Type 1 diabetes (results from ␤-cell de- B. Diagnosis of diabetes
clude more extensive evaluation and struction, usually leading to absolute
management of the patient by other spe- insulin deficiency) Recommendations
cialists as needed. For more detailed in- ● Type 2 diabetes (results from a progres- ● The fasting plasma glucose (FPG) test is
formation, refer to refs. 1–3. sive insulin secretory defect on the the preferred test to diagnose diabetes
The recommendations included are background of insulin resistance) in children and nonpregnant adults. (E)
screening, diagnostic, and therapeutic ac- ● Other specific types of diabetes due to ● Use of the A1C for the diagnosis of di-
tions that are known or believed to favor- other causes, e.g., genetic defects in abetes is not recommended at this time.
ably affect health outcomes of patients ␤-cell function, genetic defects in insu- (E)
with diabetes. A grading system (Table 1), lin action, diseases of the exocrine pan-
developed by the American Diabetes As- creas (such as cystic fibrosis), and drug- Criteria for the diagnosis of diabetes in
sociation (ADA) and modeled after exist- or chemical-induced (such as in the nonpregnant adults are shown in Table 2.
● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ●
Three ways to diagnose diabetes are avail-
The recommendations in this article are based on the evidence reviewed in the following publication: able, and each must be confirmed on a
Standards of care for diabetes (Technical Review). Diabetes Care 17:1514 –1522, 1994.
Originally approved 1988. Most recent review/revision, October 2007.
subsequent day unless unequivocal
Abbreviations: ABI, ankle-brachial index; ACE, angiotensin-converting enzyme; ADAG, A1C-Derived symptoms of hyperglycemia are present.
Average Glucose; ARB, angiotensin receptor blocker; CAD, coronary artery disease; CBG, capillary blood Although the 75-g oral glucose tolerance
glucose; CHD, coronary heart disease; CHF, congestive heart failure; CKD, chronic kidney disease; CMS, test (OGTT) is more sensitive and mod-
Centers for Medicare and Medicaid Services; CSII, continuous subcutaneous insulin infusion; CVD, cardio- estly more specific than the FPG to diag-
vascular disease; DCCT, Diabetes Control and Complications Trial; DKA, diabetic ketoacidosis; DMMP,
diabetes medical management plan; DPN, distal symmetric polyneuropathy; DPP, Diabetes Prevention nose diabetes, it is poorly reproducible
Program; DRS, Diabetic Retinopathy Study; DSME, diabetes self-management education; DSMT, diabetes and difficult to perform in practice. Be-
self-management training; eAG, estimated average glucose; ECG, electrocardiogram; EDIC, Epidemiology of cause of ease of use, acceptability to pa-
Diabetes Interventions and Complications; ERP, education recognition program; ESRD, end-stage renal tients, and lower cost, the FPG is the
disease; ETDRS, Early Treatment Diabetic Retinopathy Study; FDA, Food and Drug Administration; FPG,
fasting plasma glucose; GDM, gestational diabetes mellitus; GFR, glomerular filtration rate; ICU, intensive
preferred diagnostic test. Although the
care unit; IFG, impaired fasting glucose; IGT, impaired glucose tolerance; MICU, medical ICU; MNT, FPG is less sensitive than the OGTT, the
medical nutrition therapy; NDEP, National Diabetes Education Program; NPDR, nonproliferative diabetic vast majority of people who do not meet
retinopathy; OGTT, oral glucose tolerance test; PAD, peripheral arterial disease; PDR, proliferative diabetic diagnostic criteria for diabetes by the FPG
retinopathy; PPG, postprandial plasma glucose; RAS, renin-angiotensin system; RDA, recommended dietary but would by the OGTT will have an A1C
allowance; SICU, surgical ICU; SMBG, self-monitoring of blood glucose; TSH, thyroid-stimulating hormone;
TZD, thiazolidinedione; UKPDS, U.K. Prospective Diabetes Study. value well below 7.0% (6).
DOI: 10.2337/dc08-S012 Although the OGTT is not recom-
© 2008 by the American Diabetes Association. mended for routine clinical use, it may be


Position Statement

Table 1—ADA evidence-grading system for clinical practice recommendations risk factors for diabetes (Table 3). In
those without these risk factors, testing
Level of should begin at age 45. (B)
● If tests are normal, repeat testing should
evidence Description
be carried out at least at 3-year inter-
A Clear evidence from well-conducted, generalizable, randomized controlled vals. (E)
trials that are adequately powered, including: ● To test for pre-diabetes or diabetes, ei-
● Evidence from a well-conducted multicenter trial ther an FPG test or a 2-h OGTT (75-g
● Evidence from a meta-analysis that incorporated quality ratings in the glucose load) or both are appropriate.
analysis (B)
Compelling nonexperimental evidence, i.e., “all or none” rule developed ● An OGTT may be considered in pa-
by the Centre for Evidence-Based Medicine at Oxford tients with IFG to better define the risk
Supportive evidence from well-conducted randomized controlled trials of diabetes. (E)
that are adequately powered, including: ● In those identified with pre-diabetes,
● Evidence from a well-conducted trial at one or more institutions identify and, if appropriate, treat other
● Evidence from a meta-analysis that incorporated quality ratings in the CVD risk factors. (B)
B Supportive evidence from well-conducted cohort studies, including:
For many illnesses, there is a major dis-
● Evidence from a well-conducted prospective cohort study or registry
tinction between screening and diagnos-
● Evidence from a well-conducted meta-analysis of cohort studies
tic testing. However, for diabetes, the
Supportive evidence from a well-conducted case-control study
same tests would be used for “screening”
C Supportive evidence from poorly controlled or uncontrolled studies,
as for diagnosis. Type 2 diabetes has a
long asymptomatic phase and significant
● Evidence from randomized clinical trials with one or more major or
three or more minor methodological flaws that could invalidate the clinical risk markers. Diabetes may be
results identified anywhere along a spectrum of
● Evidence from observational studies with high potential for bias (such clinical scenarios ranging from a seem-
as case series with comparison with historical controls) ingly low-risk individual who happens to
● Evidence from case series or case reports have glucose testing, to a higher-risk in-
Conflicting evidence with the weight of evidence supporting the dividual who the provider tests because of
recommendation high suspicion of diabetes, to the symp-
E Expert consensus or clinical experience tomatic patient. The discussion herein is
primarily framed as testing for diabetes in
those without symptoms. Testing for dia-
betes will also detect individuals with pre-
useful for further evaluation of patients in II. TESTING FOR PRE- diabetes.
whom diabetes is still strongly suspected DIABETES AND DIABETES
but who have normal FPG or impaired IN ASYMPTOMATIC
fasting glucose (IFG) (see Section 1.C). PATIENTS A. Testing for pre-diabetes and type
Due to lack of evidence on prognostic 2 diabetes in adults
significance and diagnostic thresholds, Recommendations Type 2 diabetes is frequently not diag-
the use of the A1C for the diagnosis of ● Testing to detect pre-diabetes and type nosed until complications appear, and
diabetes is not recommended at this time. 2 diabetes in asymptomatic people approximately one-third of all people
should be considered in adults who are with diabetes may be undiagnosed. Al-
overweight or obese (BMI ⱖ25 kg/m2) though the effectiveness of early identifi-
C. Diagnosis of pre-diabetes and who have one or more additional cation of pre-diabetes and diabetes
Hyperglycemia not sufficient to meet the
diagnostic criteria for diabetes is catego-
rized as either IFG or impaired glucose Table 2—Criteria for the diagnosis of diabetes
tolerance (IGT), depending on whether it
1. FPG ⱖ126 mg/dl (7.0 mmol/l). Fasting is defined as no caloric intake for at
is identified through the FPG or the
least 8 h.*
2. Symptoms of hyperglycemia and a casual plasma glucose ⱖ200 mg/dl (11.1
● IFG ⫽ FPG 100 mg/dl (5.6 mmol/l) to mmol/l). Casual is defined as any time of day without regard to time since last
125 mg/dl (6.9 mmol/l) meal. The classic symptoms of hyperglycemia include polyuria, polydipsia, and
● IGT ⫽ 2-h plasma glucose 140 mg/dl unexplained weight loss.
(7.8 mmol/l) to 199 mg/dl (11.0 OR
mmol/l) 3. 2-h plasma glucose ⱖ200 mg/dl (11.1 mmol/l) during an OGTT. The test
should be performed as described by the World Health Organization, using a
IFG and IGT have been officially termed glucose load containing the equivalent of 75 g anhydrous glucose dissolved in
“pre-diabetes.” Both categories of pre- water.*
diabetes are risk factors for future diabetes *In the absence of unequivocal hyperglycemia, these criteria should be confirmed by repeat testing on a
and for cardiovascular disease (CVD) (7). different day (5).


Standards of Medical Care

Table 3—Criteria for testing for pre-diabetes and diabetes in asymptomatic adult individuals rare in the general population (21). Con-
1. Testing should be considered in all adults who are overweight (BMI ⱖ25 kg/m *) and
2 sistent with recommendations for adults,
have additional risk factors:
children and youth at increased risk for
● physical inactivity
the presence or the development of type 2
● first-degree relative with diabetes
diabetes should be tested (22). The rec-
● members of a high-risk ethnic population (e.g., African American, Latino, Native
ommendations of the ADA consensus
American, Asian American, and Pacific Islander) statement on type 2 diabetes in children
● women who delivered a baby weighing ⬎9 lb or were diagnosed with GDM and youth are summarized in Table 4.
● hypertension (ⱖ140/90 mmHg or on therapy for hypertension)
● HDL cholesterol level ⬍35 mg/dl (0.90 mmol/l) and/or a triglyceride level ⬎250 C. Screening for type 1 diabetes
mg/dl (2.82 mmol/l) Generally, people with type 1 diabetes
● women with polycystic ovarian syndrome (PCOS) present with acute symptoms of diabetes
● IGT or IFG on previous testing and markedly elevated blood glucose lev-
● other clinical conditions associated with insulin resistance (e.g., severe obesity els, and most cases are diagnosed soon
and acanthosis nigricans) after the onset of hyperglycemia. Wide-
● history of CVD spread clinical testing of asymptomatic
2. In the absence of the above criteria, testing for pre-diabetes and diabetes should begin individuals for the presence of autoanti-
at age 45 years bodies related to type 1 diabetes cannot
3. If results are normal, testing should be repeated at least at 3-year intervals, with currently be recommended as a means to
consideration of more frequent testing depending on initial results and risk status. identify individuals at risk, for several rea-
*At-risk BMI may be lower in some ethnic groups. sons: 1) cutoff values for the immune
marker assays have not been completely
established or standardized for clinical
through mass testing of asymptomatic in- dividuals with IGT, not among individu- settings; 2) there is no consensus as to
dividuals has not been definitively proven als with IFG (who do not also have IGT). what follow-up testing should be under-
(and rigorous trials to provide such proof As noted in the diagnosis section (I.B), the taken when a positive autoantibody test
are unlikely to occur), pre-diabetes and FPG test is more convenient, more repro- result is obtained; and 3) because the in-
diabetes meet established criteria for con- ducible, less costly, and easier to admin- cidence of type 1 diabetes is low, testing of
ditions in which early detection is appro- ister than the 2-h OGTT (4,5). An OGTT healthy individuals will identify only a
priate. Both conditions are common, may be useful in patients with IFG to bet- very small number (⬍0.5%) who at that
increasing in prevalence, and impose sig- ter define the risk of diabetes. moment may be “prediabetic.” Finally,
nificant public health burdens. There is a The appropriate interval between though clinical studies are being con-
long presymptomatic phase before the di- tests is not known (17). The rationale for ducted to test various methods of pre-
agnosis of type 2 diabetes is usually made. the 3-year interval is that false negatives venting type 1 diabetes in high-risk
Relatively simple tests are available to de- will be repeated before substantial time individuals, no effective intervention has
tect preclinical disease (8). Additionally, elapses, and there is little likelihood that yet been identified. If studies uncover an
the duration of glycemic burden is a an individual will develop significant effective means of preventing type 1 dia-
strong predictor of adverse outcomes, complications of diabetes within 3 years betes, targeted screening (e.g., siblings of
and effective interventions exist to pre- of a negative test result. type 1 children) may be appropriate in the
vent progression of pre-diabetes to diabe- Because of the need for follow-up and future.
tes (see Section IV) and to reduce risk of discussion of abnormal results, testing
complications of diabetes (see Section VI). should be carried out within the health Table 4—Testing for type 2 diabetes in
Recommendations for testing for pre- care setting. Community screening out- asymptomatic children
diabetes and diabetes in asymptomatic, side a health care setting is not recom- Criteria
undiagnosed adults are listed in Table 3. mended because people with positive ● Overweight (BMI ⬎85th percentile for
Testing should be considered in all adults tests may not seek appropriate follow-up age and sex, weight for height ⬎85th
with BMI ⱖ25 kg/m2 and one or more testing and care, and, conversely, there percentile, or weight ⬎120% of ideal for
risk factors for diabetes. Because age is a may be failure to ensure appropriate re- height)
major risk factor for diabetes, testing of peat testing for individuals who test neg- Plus any two of the following risk factors:
those without other risk factors should ative. Community screening may also be ● Family history of type 2 diabetes in first-
begin no later than age 45. poorly targeted, i.e., it may fail to reach or second-degree relative
● Race/ethnicity (e.g., Native American,
Either FPG testing or the 2-h OGTT is the groups most at risk and inappropri- African American, Latino, Asian American,
appropriate for testing. The 2-h OGTT ately test those at low risk (the worried and Pacific Islander)
identifies people with either IFG or IGT well) or even those already diagnosed ● Signs of insulin resistance or conditions
and, thus, more prediabetic people at in- (18,19). associated with insulin resistance (e.g.,
creased risk for the development of dia- acanthosis nigricans, hypertension,
betes and CVD. It should be noted that B. Testing for type 2 diabetes in dyslipidemia, or PCOS)
the two tests do not necessarily detect the children ● Maternal history of diabetes or GDM

same prediabetic individuals (9). The ef- The incidence of type 2 diabetes in ado- Age of initiation: age 10 years or at onset of
ficacy of interventions for primary pre- lescents has increased dramatically in the puberty, if puberty occurs at a younger age
vention of type 2 diabetes (10 –16) has last decade, especially in minority popu- Frequency: every 2 years
primarily been demonstrated among in- lations (20), although the disease remains Test: FPG preferred


Position Statement

III. DETECTION AND Table 5—Screening for and diagnosis of GDM

DIAGNOSIS OF Carry out GDM risk assessment at the first prenatal visit.
GESTATIONAL DIABETES Women at very high risk for GDM should be screened for diabetes as soon as possible after
MELLITUS (GDM) the confirmation of pregnancy. Criteria for very high risk are:
● Severe obesity
Recommendations ● Prior history of GDM or delivery of large-for-gestational-age infant
● Screen for GDM using risk factor anal-
● Presence of glycosuria
ysis and, if appropriate, use of an ● Diagnosis of PCOS
OGTT. (C) ● Strong family history of type 2 diabetes
● Women with GDM should be screened
Screening/diagnosis at this stage of pregnancy should use standard diagnostic testing (Table 2)
for diabetes 6 –12 weeks postpartum All women of higher than low risk of GDM, including those above not found to have
and should be followed up with subse- diabetes early in pregnancy, should undergo GDM testing at 24–28 weeks of gestation.
quent screening for the development of Low risk status, which does not require GDM screening, is defined as women with all of
diabetes or pre-diabetes. (E) the following characteristics:
● Age ⬍25 years
Gestational diabetes mellitus is defined as ● Weight normal before pregnancy
any degree of glucose intolerance with on- ● Member of an ethnic group with a low prevalence of diabetes
set or first recognition during pregnancy ● No known diabetes in first-degree relatives
(4). Although most cases resolve with de- ● No history of abnormal glucose tolerance
livery, the definition applies whether or ● No history of poor obstetrical outcome
not the condition persists after pregnancy Two approaches may be followed for GDM screening at 24–28 weeks:
and does not exclude the possibility that 1. Two-step approach:
unrecognized glucose intolerance may A. Perform initial screening by measuring plasma or serum glucose 1 h after a 50-g oral
have antedated or begun concomitantly glucose load. A glucose threshold after 50-g load of ⱖ140 mg/dl identifies ⬃ 80% of
with the pregnancy. Approximately 7% of women with GDM, while the sensitivity is further increased to ⬃ 90% by a threshold of
all pregnancies (ranging from 1 to 14% ⱖ130 mg/dl.
depending on the population studied and B. Perform a diagnostic 100-g OGTT on a separate day in women who exceed the
the diagnostic tests used) are complicated chosen threshold on 50-g screening.
by GDM, resulting in more than 200,000 2. One-step approach (may be preferred in clinics with high prevalence of GDM): Perform
cases annually. a diagnostic 100-g OGTT in all women to be tested at 24–28 weeks.
Because of the risks of GDM to the The 100-g OGTT should be performed in the morning after an overnight fast of at least 8 h.
mother and neonate, screening and diag- A diagnosis of GDM requires at least two of the following plasma glucose values:
nosis are warranted. The screening and Fasting: ⱖ95 mg/dl (ⱖ5.3 mmol/l)
diagnostic strategies, based on the 2004 1 h: ⱖ180 mg/dl (ⱖ10.0 mmol/l)
ADA position statement on gestational di- 2 h: ⱖ155 mg/dl (ⱖ8.6 mmol/l)
abetes mellitus (23), are outlined in Table 5. 3 h: ⱖ140 mg/dl (ⱖ7.8 mmol/l)
Results of the Hyperglycemia and Ad-
verse Pregnancy Outcomes study were re-
ported at ADA’s 67th Annual Scientific
Sessions in June 2007. This large-scale GDM, go to www.ndep.nih.gov/diabetes/ IGT plus other risk factors) and who are
(⬃25,000 pregnant women), multi- pubs/NeverTooEarly_Tipsheet.pdf. obese and under 60 years of age. (E)
national, epidemiologic study demon- ● Monitoring for the development of di-
strated that risk of adverse maternal, fetal, abetes in those with pre-diabetes
and neonatal outcomes continuously in- IV. PREVENTION/DELAY should be performed every year. (E)
creased as a function of maternal glycemia OF TYPE 2 DIABETES
at 24 –28 weeks, even within ranges pre- Randomized controlled trials have shown
viously considered normal for pregnancy. Recommendations that individuals at high risk for develop-
For most complications, there was no ● Patients with IGT (A) or IFG (E) should ing diabetes (those with IFG, IGT, or
threshold for risk. These results may call be given counseling on weight loss of both) can be given interventions that sig-
for careful reconsideration of the diagnos- 5–10% of body weight, as well as on nificantly decrease the rate of onset of di-
tic criteria for GDM. increasing physical activity to at least abetes (10 –16). These interventions
Because women with a history of 150 min/week of moderate activity include an intensive lifestyle modification
GDM have a greatly increased subsequent such as walking. program that has been shown to be very
risk for diabetes (24), they should be ● Follow-up counseling appears to be im- effective (⬃58% reduction after 3 years),
screened for diabetes 6 –12 weeks post- portant for success. (B) and use of the pharmacologic agents met-
partum, using standard criteria, and ● Based on potential cost savings of dia- formin, acarbose, orlistat, and rosiglita-
should be followed up with subsequent betes prevention, such counseling zone, each of which has been shown to
screening for the development of diabetes should be covered by third-party pay- decrease incident diabetes to various de-
or pre-diabetes, as outlined in Section II. ors. (E) grees. A summary of major diabetes pre-
For information on the National Diabetes ● In addition to lifestyle counseling, met- vention trials is shown in Table 6.
Education Program (NDEP) campaign to formin may be considered in those who Based on the results of clinical trials
prevent type 2 diabetes in women with are at very high risk (combined IFG and and the known risks of progression of


Standards of Medical Care

Table 6—Therapies proven effective in diabetes prevention trials

Study Age Duration Follow Intervention subjects
(reference)‡ n Population (years) (years) up (daily dose) (%/year) Relative risk
Finnish DPS (15) 522 IGT, BMI ⱖ25 kg/m2 55 3.2 92 Individual 6 0.42 (0.30–070)
DPP (14) 2,161* IGT, BMI ⱖ24 kg/m2, 51 3 93 Individual 10 0.42 (0.34–0.52)
FPG ⬎5.3 (95) diet/exercise
Pan et al. (22) 259* IGT (randomized 45 6 92 Group diet/ 16 0.62 (0.44–0.86)
groups) exercise
Kosaka et al. (23) 458 IGT (men), BMI ⫽ 24 ⬃55 4 92 Individual 2 0.33 (0.10–1.0)†
kg/m2 diet/exercise
Indian DPP (24) 269* IGT 46 2.5 95 Individual 22 0.71 (0.63–0.79)
DPP (14) 2,155* IGT, BMI ⬎24 kg/m2, 51 2.8 93 Metformin 10 0.69 (0.57–0.83)
FPG ⬎5.3 (1,700 mg)
Indian DPP (24) 269* IGT 46 2.5 95 Metformin 22 0.74 (0.65–0.81)
(500 mg)
STOP NIDDM 1,419 IGT, FPG ⬎5.6 54 3.2 96 Acarbose 13 0.75 (0.63–0.90)
(16) (300 mg)
XENDOS (18) 3,277 BMI ⬎30 kg/m2 43 4 43 Orlistat 2 0.63 (0.46–0.86)
(360 mg)
DPP (25) 1,067* IGT, BMI ⬎24 kg/m2, 51 0.9 93 Troglitazone 12 0.25 (0.14–0.43)†
FPG ⬎5.3 (400 mg)
TRIPOD (26) 266 Previous GDM 35 2.5 67 Troglitazone 12 0.45 (0.25–0.83)
(400 mg)
DREAM (17) 5,269 IGT or IFG 55 3.0 94 Rosiglitazone 9 0.40 (0.35–0.46)
(8 mg)
Reprinted with permission (25). *Number of participants in the indicated comparisons and not the total randomized; †calculated from information in the article;
‡references are numbered as in original publication (25). DPP, Diabetes Prevention Program; DPS, Diabetes Prevention Study; GDM, gestational diabetes mellitus;
STOP, Study to Prevent Non-Insulin Dependent Diabetes; TRIPOD, Troglitazone in Prevention of Diabetes; XENDOS, Xenical in the prevention of Diabetes in Obese

pre-diabetes to diabetes, an ADA consen- V. DIABETES CARE interest in diabetes. It is essential in this
sus development panel in 2007 (7) con- collaborative and integrated team ap-
cluded that persons with pre-diabetes A. Initial evaluation proach that individuals with diabetes as-
(IGT and/or IFG) should be counseled on A complete medical evaluation should be sume an active role in their care.
lifestyle changes with goals similar to performed to classify the diabetes, detect The management plan should be for-
those of the Diabetes Prevention Program the presence of diabetes complications, mulated as an individualized therapeutic
(DPP) (5–10% weight loss and moderate review previous treatment and glycemic alliance among the patient and family, the
physical activity of ⬃30 min/day). Re- control in patients with established diabe- physician, and other members of the
garding the more difficult issue of drug tes, assist in formulating a management health care team. A variety of strategies
therapy for diabetes prevention, the con- plan, and provide a basis for continuing and techniques should be used to provide
care. Laboratory tests appropriate to the adequate education and development of
sensus panel felt that metformin should
evaluation of each patient’s medical con- problem-solving skills in the various as-
be the only drug considered for use in
dition should be performed. A focus on pects of diabetes management. Imple-
diabetes prevention. For other drugs, the the components of comprehensive care
issues of cost, side effects, and lack of per- mentation of the management plan
(Table 7) will assist the health care team to requires that each aspect is understood
sistence of effect in some studies led the ensure optimal management of the pa- and agreed on by the patient and the care
panel to not recommend their use for di- tient with diabetes. providers and that the goals and treat-
abetes prevention. Metformin use was
ment plan are reasonable. Any plan
recommended only for very high-risk in- should recognize diabetes self-manage-
B. Management
dividuals (combined IGT and IFG, and People with diabetes should receive med- ment education (DSME) as an integral
with at least one other risk factor). In ad- ical care from a physician-coordinated component of care. In developing the
dition, the panel highlighted the evidence team. Such teams may include, but are plan, consideration should be given to the
that in the DPP, treatment with met- not limited to, physicians, nurse practitio- patient’s age, school or work schedule
formin had the most relative effectiveness ners, physician’s assistants, nurses, dieti- and conditions, physical activity, eating
in those with BMI of at least 35 kg/m2 and tians, pharmacists, and mental health patterns, social situation and personality,
those under age 60. professionals with expertise and a special cultural factors, and presence of compli-


Position Statement

Table 7—Components of the comprehensive diabetes evaluation gets, postprandial SMBG may be appro-
Medical history
priate. (E)
● When prescribing SMBG, ensure that
● Age and characteristics of onset of diabetes (e.g., DKA, asymptomatic laboratory finding)
● Eating patterns, nutritional status, and weight history; growth and development in
patients receive initial instruction in,
children and adolescents and routine follow-up evaluation of,
● Diabetes education history SMBG technique and their ability to use
● Review of previous treatment regimens and response to therapy (A1C records) data to adjust therapy. (E)
● Continuous glucose monitoring may be
● Current treatment of diabetes, including medications, meal plan, physical activity
patterns, and results of glucose monitoring and patient’s use of data a supplemental tool to SMBG for se-
● DKA frequency, severity, and cause lected patients with type 1 diabetes, es-
● Hypoglycemic episodes pecially those with hypoglycemia
● Hypoglycemia awareness unawareness. (E)
● Any severe hypoglycemia: frequency and cause
● History of diabetes-related complications ADA’s consensus and position statements
● Microvascular: retinopathy, nephropathy, neuropathy (sensory, including history of on SMBG provide a comprehensive re-
foot lesions; autonomic, including sexual dysfunction and gastroparesis) view of the subject (26,27). Major clinical
● Macrovascular: CHD, cerebrovascular disease, PAD trials of insulin-treated patients that dem-
● Other: psychosocial problems,* dental disease* onstrated the benefits of intensive glyce-
Physical examination mic control on diabetes complications
● Height, weight, BMI have included SMBG as part of multifac-
● Blood pressure determination, including orthostatic measurements when indicated torial interventions, suggesting that
● Fundoscopic examination* SMBG is a component of effective ther-
● Thyroid palpation apy. SMBG allows patients to evaluate
● Skin examination (for acanthosis nigricans and insulin injection sites) their individual response to therapy and
● Comprehensive foot examination: assess whether glycemic targets are being
● Inspection achieved. Results of SMBG can be useful
● Palpation of dorsalis pedis and posterior tibial pulses in preventing hypoglycemia and adjust-
● Presence/absence of patellar and Achilles reflexes ing medications (particularly prandial in-
● Determination of proprioception, vibration, and monofilament sensation sulin doses), MNT, and physical activity.
Laboratory evaluation The frequency and timing of SMBG
● A1C, if results not available within past 2–3 months should be dictated by the particular needs
If not performed/available within past year: and goals of the patients. SMBG is espe-
● Fasting lipid profile, including total, LDL, and HDL cholesterol and triglycerides cially important for patients treated with
● Liver function tests insulin to monitor for and prevent asymp-
● Test for urine albumin excretion with spot urine albumin-to-creatinine ratio tomatic hypoglycemia and hyperglyce-
● Serum creatinine and calculated GFR mia. For most patients with type 1
● Thyroid-stimulating hormone in type 1 diabetes, dyslipidemia or women over age 50 diabetes and pregnant women taking in-
Referrals sulin, SMBG is recommended three or
● Annual dilated eye exam more times daily. For this population, it is
● Family planning for women of reproductive age often difficult to reach A1C targets safely
● Registered dietitian for MNT without hypoglycemia with the minimum
● Diabetes self-management education of three daily tests. The optimal frequency
● Dental examination and timing of SMBG for patients with type
● Mental health professional, if needed 2 diabetes on noninsulin therapy is not
*See appropriate referrals for these categories. known but should be sufficient to facili-
tate reaching glucose goals. A meta-
analysis of SMBG in non–insulin-treated
patients with type 2 diabetes concluded
cations of diabetes or other medical a. Self-monitoring of blood glucose that some regimen of SMBG was associ-
conditions. ated with a reduction in A1C of ⬃0.4%.
However, many of the studies in this anal-
C. Glycemic control Recommendations ysis also included patient education with
1. Assessment of glycemic control. ● SMBG should be carried out three or diet and exercise counseling and, in some
Two primary techniques are available for more times daily for patients using mul- cases, pharmacologic intervention, mak-
health providers and patients to assess the tiple insulin injections or insulin pump ing it difficult to assess the contribution of
effectiveness of the management plan on therapy. (A) SMBG alone to improved control (28).
glycemic control: patient self-monitoring ● For patients using less frequent insulin Because the accuracy of SMBG is in-
of blood glucose (SMBG) and A1C mea- injections, noninsulin therapies, or strument and user dependent (29), it is
surement. In addition, in recent years medical nutrition therapy (MNT) important to evaluate each patient’s mon-
technologies for continuous monitoring alone, SMBG may be useful in achiev- itoring technique, both initially and at
of interstitial glucose have entered the ing glycemic goals. (E) regular intervals thereafter. In addition,
market. ● To achieve postprandial glucose tar- optimal use of SMBG requires proper in-


Standards of Medical Care

Table 8—Summary of glycemic recommendations for adults with diabetes hemoglobin variants must be considered,
A1C ⬍7.0% * particularly when the A1C result does not
Preprandial capillary plasma glucose 70–130 mg/dl (3.9–7.2 correlate with the patient’s clinical situa-
mmol/l) tion (29). In addition, A1C does not pro-
Peak postprandial capillary plasma glucose† ⬍180 mg/dl (⬍10.0 mmol/l) vide a measure of glycemic variability or
Key concepts in setting glycemic goals: hypoglycemia. For patients prone to gly-
● A1C is the primary target for glycemic control cemic variability (especially type 1 dia-
● Goals should be individualized based on: betic patients, or type 2 diabetic patients
● duration of diabetes with severe insulin deficiency), glycemic
● pregnancy status control is best judged by the combination
● age of results of SMBG testing and the A1C.
● comorbid conditions The A1C may also serve as a check on the
● hypoglycemia unawareness accuracy of the patient’s meter (or the pa-
● individual patient considerations tient’s reported SMBG results) and the ad-
● More stringent glycemic goals (i.e., a normal A1C, equacy of the SMBG testing schedule.
⬍6%) may further reduce complications at the cost of
increased risk of hypoglycemia Table 9 contains the correlation be-
● Postprandial glucose may be targeted if A1C goals are
tween A1C levels and mean plasma glu-
not met despite reaching preprandial glucose goals cose levels based on data from the
*Referenced to a nondiabetic range of 4.0 – 6.0% using a DCCT-based assay. †Postprandial glucose mea- Diabetes Control and Complications Trial
surements should be made 1–2 h after the beginning of the meal, generally peak levels in patients with (DCCT) (34). The correlation is based on
diabetes. relatively sparse data from a primarily
Caucasian type 1 diabetic population.
Preliminary results of the multicenter
terpretation of the data. Patients should ment goals (and who have stable glyce- A1C-Derived Average Glucose (ADAG)
be taught how to use the data to adjust mic control). (E) Trial, presented at the European Associa-
food intake, exercise, or pharmacological ● Perform the A1C test quarterly in pa- tion for the Study of Diabetes meeting in
therapy to achieve specific glycemic goals, tients whose therapy has changed or September 2007, confirmed a close cor-
and these skills should be re-evaluated who are not meeting glycemic goals. (E) relation of A1C with mean glucose in pa-
periodically. ● Use of point-of-care testing for A1C al- tients with type 1, type 2, or no diabetes.
In recent years, methods to sample lows for timely decisions on therapy Final results of this study, not available at
interstitial fluid glucose (which correlates changes, when needed. (E)
the time this statement was completed,
highly with blood glucose) in a continu-
should allow more accurate reporting of
ous and minimally invasive way have Because A1C is thought to reflect average
the estimated average glucose (eAG) and
been developed. Most microdialysis sys- glycemia over several months (29), and
tems are inserted subcutaneously, while improve patients’ understanding of this
has strong predictive value for diabetes
an early system employed “reverse ionto- complications (10,31), A1C testing measure of glycemia. An updated version
phoresis” to move glucose across the skin. should be performed routinely in all pa- of Table 9, based on final results of the
The concentration of glucose is then mea- tients with diabetes, at initial assessment ADAG Trial, will be available at www.
sured by a glucose oxidase electrode de- and then as part of continuing care. Mea- diabetes.org after publication of the
tector. These systems require calibration surement approximately every 3 months study’s findings in 2008.
with SMBG readings, and the latter are determines whether a patient’s glycemic
still recommended for making treatment targets (Table 8) have been reached and
decisions. Continuous glucose sensors maintained. For any individual patient,
have alarms for hypo- and hyperglycemia. the frequency of A1C testing should be Table 9—Correlation between A1C level and
Small studies in selected patient popula- dependent on the clinical situation, the mean plasma glucose levels on multiple test-
tions have shown good correlation of treatment regimen used, and the judg- ing over 2–3 months
readings with SMBG and decreases in the ment of the clinician. Some patients with
mean time spent in hypo- and hypergly- stable glycemia well within target may do A1C (%) Mean plasma glucose
cemic ranges compared with blinded well with testing only twice per year,
sensor use (30). Although continuous while unstable or highly intensively man- mg/dl mmol/l
glucose sensors would seem to show aged patients (e.g., pregnant type 1 6 135 7.5
great promise in diabetes management, women) may be tested more frequently 7 170 9.5
as yet no rigorous controlled trials have than every 3 months. The availability of 8 205 11.5
demonstrated improvements in long- the A1C result at the time that the patient 9 240 13.5
term glycemia. is seen (point-of-care testing) has been re- 10 275 15.5
ported to result in increased intensifica- 11 310 17.5
b. A1C tion of therapy and improvement in 12 345 19.5
glycemic control (32,33).
These estimates are based on DCCT data (34). An
Recommendations The A1C test is subject to certain lim- updated version of this table, based on final results
● Perform the A1C test at least two times itations. Conditions that affect erythro- of the ADAG Trial, will be available at www.diabetes.
a year in patients who are meeting treat- cyte turnover (hemolysis, blood loss) and org after publication of the study’s findings in 2008.


Position Statement

2. Glycemic goals prospective clinical trials, treatment regi- The issue of pre- versus postprandial
mens that reduced average A1C to ⬃7% SMBG targets is complex (45). Elevated
Recommendations (⬃1% above the upper limits of normal) postchallenge (2-h OGTT) glucose values
● Lowering A1C to an average of ⬃7% were associated with fewer long-term mi- have been associated with increased car-
has clearly been shown to reduce mi- crovascular complications; however, in- diovascular risk independent of FPG in
crovascular and neuropathic complica- tensive control was found to increase the some epidemiological studies. In diabetic
tions of diabetes and, possibly, risk of severe hypoglycemia, most notably subjects, some surrogate measures of vas-
macrovascular disease. Therefore, the in the DCCT, and to lead to weight gain cular pathology, such as endothelial dys-
A1C goal for nonpregnant adults in (31,44). function, are negatively affected by
general is ⬍7%. (A) Epidemiological analyses of the postprandial hyperglycemia (46). It is
● Epidemiologic studies have suggested DCCT and UKPDS (31,35) demonstrate a clear that postprandial hyperglycemia,
an incremental (albeit, in absolute curvilinear relationship between A1C and like preprandial hyperglycemia, contrib-
terms, a small) benefit to lowering A1C microvascular complications. Such anal- utes to elevated A1C levels, with its rela-
from 7% into the normal range. There- yses suggest that, on a population level, tive contribution being higher at A1C
fore, the A1C goal for selected individ- the greatest number of complications will levels that are closer to 7%. However, out-
ual patients is as close to normal (⬍6%) be averted by taking patients from very come studies have clearly shown A1C to
as possible without significant hypogly- poor control to fair or good control. These be the primary predictor of complica-
cemia. (B) analyses also suggest that further lowering tions, and the glycemic control trials such
● Less stringent A1C goals may be appro- of A1C from 7 to 6% is associated with as the DCCT relied overwhelmingly on
priate for patients with a history of se- further reduction in the risk of complica- preprandial SMBG. Thus, a reasonable
vere hypoglycemia, patients with tions, albeit the absolute risk reductions recommendation is: In individuals who
limited life expectancies, children, in- become much smaller. Given the substan- have premeal glucose values within target
dividuals with comorbid conditions, tially increased risk of hypoglycemia (par- but have A1C values above target, moni-
and those with longstanding diabetes ticularly in those with type 1 diabetes) toring postprandial plasma glucose (PPG)
and minimal or stable microvascular and the relatively much greater effort re- 1–2 h after the start of the meal and treat-
complications. (E) quired to achieve near-normoglycemia, ment aimed at reducing PPG values to
the risks of lower targets may outweigh ⬍180 mg/dl will likely lower A1C and
Glycemic control is fundamental to the the potential benefits on a population may improve outcomes.
management of diabetes. The DCCT, a level. However, selected individual pa- In regard to glycemic control for
prospective, randomized, controlled trial tients, especially those with little comor- women with GDM, recommendations
of intensive versus standard glycemic bidity and long life expectancy (who may from the Fourth International Workshop-
control in type 1 diabetes, showed defin- reap the benefits of further lowering of Conference on Gestational Diabetes Mel-
itively that improved glycemic control is glycemia below 7%) may, at patient and litus (47) suggested lowering maternal
associated with sustained decreased rates provider judgment, have glycemic targets capillary whole-blood glucose concentra-
of microvascular (retinopathy and ne- as close to normal as possible without sig- tions to:
phropathy) as well as neuropathic com- nificant hypoglycemia becoming a barrier.
plications (35). Follow up of the DCCT Recommended glycemic goals for ● Preprandial: ⱕ95 mg/dl (5.3 mmol/l),
cohorts in the Epidemiology of Diabetes nonpregnant individuals are shown in Ta- and either:
Interventions and Complications (EDIC) ble 8. The recommendations are based on ● 1-h postmeal: ⱕ140 mg/dl (7.8
study has shown persistence of this effect data for A1C. The listed blood glucose mmol/l) or
in previously intensively treated subjects, goals are levels that appear to correlate ● 2-h postmeal: ⱕ120 mg/dl (6.7
even though their glycemic control has with achievement of an A1C of ⬍7%. Less mmol/l)
been equivalent to that of previous stan- stringent treatment goals may be appro-
dard arm subjects during follow-up priate for patients with limited life expect- Comparable plasma-referenced capillary
(36,37). In addition, EDIC has shown a ancies, in children, and in individuals blood glucose values suggested in the
significant reduction of the rate of cardio- with comorbid conditions. Severe or fre- ADA Position Statement on GDM (14)
vascular outcomes in the previous inten- quent hypoglycemia is an indication for are:
sive arm (38). the modification of treatment regimens,
In type 2 diabetes, the Kumamoto including setting higher glycemic goals. ● Preprandial: ⱕ105 mg/dl (5.8 mmol/l),
study (39) and the UK Prospective Diabe- Neither the DCCT nor the UKPDS ad- and either:
tes Study (UKPDS) (40,41) demonstrated dressed patient populations with long du- ● 1-h postmeal: ⱕ155 mg/dl (8.6
significant reductions in microvascular rations of diabetes. Clinical experience mmol/l) or
and neuropathic complications with in- suggests that it is uncommon for signifi- ● 2-h postmeal: ⱕ130 mg/dl (7.2
tensive therapy. The potential of intensive cant microvascular disease to begin after mmol/l)
glycemic control to reduce CVD in type 2 20 –30 years of diabetes. Furthermore,
diabetes is supported by epidemiological hypoglycemia unawareness becomes 3. Approach to treatment
studies (31,40 – 42) and a meta-analysis more prevalent with long duration of di-
(43), but has not yet been demonstrated abetes. Therefore, in patients with long- a. Therapy for type 1 diabetes. The
in a randomized clinical trial. Several standing diabetes (three or more decades) DCCT clearly showed that intensive insu-
large trials are currently under way to ad- and minimal or stable microvascular lin therapy (three or more injections per
dress this issue. complications, the risk-to-benefit ratio day of insulin or continuous subcutane-
In each of these large randomized for stringent A1C goals appears high. ous insulin infusion [CSII, or insulin


Standards of Medical Care

pump therapy]) was a key part of im- and pioglitazone. This new information loss (7% body weight) and regular
proved glycemia and better outcomes may prompt greater caution in using the physical activity (150 min/week), with
(35). At the time of the study, therapy was thiazolidinediones. Other medications dietary strategies including reduced
carried out with short- and intermediate- such as pramlintide, exenatide, ␣-gluco- calories and reduced intake of dietary
acting human insulins. Despite better mi- sidase inhibitors, the glinides, and dipep- fat, can reduce the risk for developing
crovascular outcomes, intensive insulin tidyl peptidase IV inhibitors were not diabetes and are therefore recom-
therapy was associated with a marked in- included in the consensus algorithm, ow- mended. (A)
crease in severe hypoglycemia (62 epi- ing to less glucose-lowering effectiveness, ● Individuals at high risk for type 2 dia-
sodes per 100 patient-years of therapy). limited clinical data, and/or relative ex- betes should be encouraged to achieve
Since the time of the DCCT, a number of pense. However, they may be appropriate the U.S. Department of Agriculture
rapid-acting and long-acting insulin ana- choices in individual patients to achieve (USDA) recommendation for dietary fi-
logs have been developed. These analogs glycemic goals. Initiation of insulin at ber (14 g fiber/1,000 kcal) and foods
were designed to be more “physiological” time of diagnosis is recommended for in- containing whole grains (one-half of
in their pharmacokinetics and pharmaco- dividuals presenting with weight loss or grain intake). (B)
dynamics, and are associated with less hy- other severe hyperglycemic symptoms or
poglycemia with equal A1C lowering in signs. For a list of currently approved Dietary fat intake in diabetes
type 1 diabetes (48,49). diabetes medications, see http://ndep. management
Therefore, recommended therapy for nih.gov/diabetes/pubs/Drug_tables_ ● Saturated fat intake should be ⬍7% of
type 1 diabetes consists of the following supplement.pdf. total calories. (A)
components: 1) use of multiple dose in- ● Intake of trans fat should be minimized.
sulin injections (3– 4 injections per day of D. MEDICAL NUTRITION (E)
basal and prandial insulin) or CSII ther- THERAPY (MNT)
apy; 2) matching of prandial insulin to Carbohydrate intake in diabetes
carbohydrate intake, premeal blood glu- General recommendations management
cose, and anticipated activity; and 3) for ● Individuals who have pre-diabetes or ● Monitoring carbohydrate intake,
many patients (especially if hypoglycemia diabetes should receive individualized whether by carbohydrate counting, ex-
is a problem), use of insulin analogs. MNT as needed to achieve treatment changes, or experience-based estima-
There are excellent reviews available that goals, preferably provided by a regis- tion, remains a key strategy in achieving
guide the initiation and management of tered dietitian familiar with the compo- glycemic control. (A)
insulin therapy to achieve desired glyce- nents of diabetes MNT. (B) ● For individuals with diabetes, the use of
mic goals (3,48,50). ● MNT should be covered by insurance the glycemic index and glycemic load
and other payors. (E) may provide a modest additional bene-
b. Therapy for type 2 diabetes. ADA and fit for glycemic control over that ob-
the European Association for the Study of Energy balance, overweight, and served when total carbohydrate is
Diabetes published a consensus state- obesity considered alone. (B)
ment on the approach to management of ● In overweight and obese insulin-
hyperglycemia in individuals with type 2 resistant individuals, modest weight Other nutrition recommendations
diabetes (51). Highlights of this approach loss has been shown to reduce insulin ● Sugar alcohols and nonnutritive sweet-
are 1) intervention at the time of diagnosis resistance. Thus, weight loss is recom- eners are safe when consumed within
with metformin in combination with life- mended for all overweight or obese in- the acceptable daily intake levels estab-
style changes (MNT and exercise) and 2) dividuals who have or are at risk for lished by the Food and Drug Adminis-
continuing timely augmentation of ther- diabetes. (A) tration (FDA). (A)
apy with additional agents (including ● For weight loss, either low-carbohy- ● If adults with diabetes choose to use
early initiation of insulin therapy) as a drate or low-fat calorie-restricted diets alcohol, daily intake should be limited
means of achieving and maintaining rec- may be effective in the short term (up to to a moderate amount (one drink per
ommended levels of glycemic control 1 year). (A) day or less for adult women and two
(i.e., A1C ⬍7% for most patients). The ● For patients on low-carbohydrate diets, drinks per day or less for adult men).
overall objective is to achieve and main- monitor lipid profiles, renal function, (E)
tain glycemic levels as close to the nondi- and protein intake (in those with ne- ● Routine supplementation with antioxi-
abetic range as possible and to change phropathy), and adjust hypoglycemic dants, such as vitamins E and C and
interventions at as rapid a pace as titration therapy as needed. (E) carotene, is not advised because of lack
of medications allows. ● Physical activity and behavior modifi- of evidence of efficacy and concern re-
The algorithm took into account the cation are important components of lated to long-term safety. (A)
evidence for A1C-lowering of the individ- weight loss programs and are most ● Benefit from chromium supplementa-
ual interventions, their synergies, and helpful in maintenance of weight loss. tion in people with diabetes or obesity
their expense. Of note, the consensus al- (B) has not been conclusively demon-
gorithm was developed before publica- strated and, therefore, cannot be rec-
tions that raised concerns about increased Primary prevention of diabetes ommended. (E)
risk of myocardial infarction with use of ● Among individuals at high risk for de-
rosiglitazone (52,53) and before addition veloping type 2 diabetes, structured MNT is an integral component of diabetes
of black box warnings about congestive programs that emphasize lifestyle prevention, management, and self-
heart failure (CHF) for both rosiglitazone changes that include moderate weight management education. ADA recognizes


Position Statement

that, in addition to its important role in the intensive lifestyle intervention in this viduals seeking guidance on macronutrient
preventing and controlling diabetes, nu- trial show an average 8.6% weight loss, distribution in healthy adults, the Dietary
trition is an essential component of an significant reduction of A1C, and reduc- Reference Intakes (DRIs) may be helpful
overall healthy lifestyle. A full review of tion in several CVD risk factors (64). (69). It must be clearly recognized that
the evidence regarding nutrition in pre- When completed, the Look AHEAD regardless of the macronutrient mix, total
venting and controlling diabetes and its study should provide insight into the ef- caloric intake must be appropriate to
complications and additional nutrition- fects of long-term weight loss on impor- weight management goal. Further, indi-
related recommendations can be found in tant clinical outcomes. vidualization of the macronutrient com-
the ADA position statement, “Nutrition The optimal macronutrient distribu- position will depend on the metabolic
Recommendations and Interventions for tion of weight loss diets has not been es- status of the patient (e.g., lipid profile,
Diabetes,” published in 2007 and up- tablished. Although low-fat diets have renal function).
dated for 2008 (54). Achieving nutrition- traditionally been promoted for weight The primary goal with respect to di-
related goals requires a coordinated team loss, several randomized controlled trials etary fat in individuals with diabetes is to
effort that includes the active involvement found that subjects on low-carbohydrate limit saturated fatty acids, trans fatty ac-
of the person with pre-diabetes or diabe- diets (⬍130 g/day of carbohydrate) lost ids, and cholesterol intake so as to reduce
tes. Because of the complexity of nutrition more weight at 6 months than subjects on risk for CVD. Saturated and trans fatty ac-
issues, it is recommended that a registered low-fat diets (65,66); however, at 1 year, ids are the principal dietary determinants
dietitian who is knowledgeable and the difference in weight loss between the of plasma LDL cholesterol. There is a lack
skilled in implementing nutrition therapy low-carbohydrate and low-fat diets was of evidence on the effects of specific fatty
into diabetes management and education not significant and weight loss was mod- acids on people with diabetes, so the rec-
be the team member who provides MNT. est with both diets. Another study of over- ommended goals are consistent with
Clinical trials/outcome studies of weight women randomized to one of four those for individuals with CVD (70).
MNT have reported decreases in A1C of diets showed significantly more weight The FDA has approved five nonnutri-
⬃1% in type 1 diabetes and 1–2% in type loss at 12 months with the Atkins low- tive sweeteners for use in the U.S.: acesul-
2 diabetes, depending on the duration of carbohydrate diet than with higher- fame potassium, aspartame, neotame,
diabetes (55,56). Meta-analyses of studies carbohydrate diets (67). Changes in saccharin, and sucralose. Before being al-
in nondiabetic, free-living subjects report serum triglyceride and HDL cholesterol lowed on the market, all underwent rig-
that MNT reduces LDL cholesterol by were more favorable with the low- orous scrutiny and were shown to be safe
15–25 mg/dl (57), while clinical trials carbohydrate diets. In one study, those when consumed by the public, including
support a role for lifestyle modification in subjects with type 2 diabetes demon- people with diabetes and women during
treating hypertension (58). strated a greater decrease in A1C with a pregnancy. Reduced-calorie sweeteners
Because of the effects of obesity on low-carbohydrate diet than with a low-fat approved by the FDA include sugar alco-
insulin resistance, weight loss is an im- diet (66). A recent meta-analysis showed hols (polyols) such as erythritol, isomalt,
portant therapeutic objective for over- that at 6 months, low-carbohydrate diets lactitol, maltitol, mannitol, sorbitol, xyli-
weight or obese individuals with pre- were associated with greater improve- tol, tagatose, and hydrogenated starch hy-
diabetes or diabetes (59). Short-term ments in triglyceride and HDL cholesterol drolysates. The use of sugar alcohols
studies have demonstrated that moderate concentrations than low-fat diets; how- appears to be safe; however, they may
weight loss (5% of body weight) in sub- ever, LDL cholesterol was significantly cause diarrhea, especially in children.
jects with type 2 diabetes is associated higher on the low-carbohydrate diets
with decreased insulin resistance, im- (68). Reimbursement for MNT
proved measures of glycemia and lipemia, The recommended dietary allowance MNT, when delivered by a registered di-
and reduced blood pressure (60); longer- (RDA) for digestible carbohydrate is 130 etitian according to nutrition practice
term studies (ⱖ52 weeks) showed mixed g/day and is based on providing adequate guidelines, is reimbursed as part of the
effects on A1C in adults with type 2 dia- glucose as the required fuel for the central Medicare program as overseen by the
betes (61– 63), and results were con- nervous system without reliance on glu- Centers for Medicare and Medicaid Ser-
founded by pharmacologic weight loss cose production from ingested protein or vices (CMS) (www.cms.hhs.gov/
therapy. Sustained weight loss is difficult fat. Although brain fuel needs can be met medicalnutritiontherapy).
for most people to accomplish. However, on lower-carbohydrate diets, long-term
the multifactorial intensive lifestyle inter- metabolic effects of very-low-carbohy-
vention employed in the DPP, which in- drate diets are unclear, and such diets E. DSME
cluded reduced intake of fat and calories, eliminate many foods that are important
led to weight loss averaging 7% at 6 sources of energy, fiber, vitamins, and Recommendations
months and maintenance of 5% weight minerals and are important in dietary pal- ● People with diabetes should receive
loss at 3 years, and these outcomes were atability (69). DSME according to national standards
associated with a 58% reduction in the Although numerous studies have at- when their diabetes is diagnosed and as
incidence of type 2 diabetes (10). The tempted to identify the optimal mix of needed thereafter. (B)
Look AHEAD (Action for Health in Dia- macronutrients for meal plans of people ● Self-management behavior change is
betes) study is a large clinical trial de- with diabetes, it is unlikely that one such the key outcome of DSME and should
signed to determine whether long-term combination of macronutrients exists. be measured and monitored as part of
weight loss will improve glycemia and The best mix of carbohydrate, protein, care. (E)
prevent cardiovascular events in subjects and fat appears to vary depending on in- ● DSME should address psychosocial is-
with type 2 diabetes. One-year results of dividual circumstances. For those indi- sues, since emotional well-being is


Standards of Medical Care

strongly associated with positive diabe- Reimbursement for DSME lowering value of resistance training in
tes outcomes. (C) DSME, when provided by a program that older adults with type 2 diabetes (90,91),
● DSME should be reimbursed by third- meets ADA ERP standards, is reimbursed and for an additive benefit of combined
party payors. (E) as part of the Medicare program as over- aerobic and resistance exercise in adults
seen by the Centers for Medicare and with type 2 diabetes (92).
DSME is an essential element of diabetes Medicaid Services (CMS) (www.cms.hhs.
care (71–77), and the National Standards gov/DiabetesSelfManagement).
for DSME (78) are based on evidence for Evaluation of the diabetic patient
its benefits. Education helps people with F. Physical activity before recommending an exercise
diabetes initiate effective self-care when program
they are first diagnosed. Ongoing DSME Recommendations Prior guidelines suggested that before rec-
also helps people with diabetes maintain ● People with diabetes should be advised ommending a program of physical activ-
effective self-management as their diabe- to perform at least 150 min/week of ity, the provider should assess patients
tes presents new challenges and as treat- moderate-intensity aerobic physical ac- with multiple cardiovascular risk factors
ment advances become available. DSME tivity (50 –70% of maximum heart for coronary artery disease (CAD). As dis-
helps patients optimize metabolic con- rate). (A) cussed more fully in Section VI.A.5, the
trol, prevent and manage complications, ● In the absence of contraindications, area of screening asymptomatic diabetic
and maximize quality of life, in a cost- people with type 2 diabetes should be patients for CAD remains unclear, and a
effective manner (79). encouraged to perform resistance train- recent ADA consensus statement on this
ing three times per week. (A) issue concluded that routine screening is
not recommended (93). Providers should
Evidence for the benefits of DSME ADA technical reviews on exercise in pa- use clinical judgment in this area. Cer-
Since the 1990s, there has been a shift tients with diabetes have summarized the tainly, high-risk patients should be en-
from a didactic approach, with DSME fo- value of exercise in the diabetes manage- couraged to start with short periods of
cusing on providing information, to a ment plan (84,85). Regular exercise has low-intensity exercise and increase the in-
skill-based approach that focuses on been shown to improve blood glucose tensity and duration slowly.
helping those with diabetes make in- control, reduce cardiovascular risk fac- Providers should assess patients for
formed self-management choices. Several tors, contribute to weight loss, and im- conditions that might contraindicate cer-
studies have found that DSME is associ- prove well-being. Furthermore, regular tain types of exercise or predispose to in-
ated with improved diabetes knowledge exercise may prevent type 2 diabetes in jury, such as uncontrolled hypertension,
and improved self-care behavior (72), im- high-risk individuals (10 –12). Struc- severe autonomic neuropathy, severe pe-
proved clinical outcomes such as lower tured exercise interventions of at least 8 ripheral neuropathy or history of foot le-
A1C (73,74,76,77,80), lower self- weeks’ duration have been shown to sions, and advanced retinopathy. The
reported weight (72), and improved qual- lower A1C by an average of 0.66% in peo- patient’s age and previous physical activ-
ity of life (75). Better outcomes were ple with type 2 diabetes, even with no ity level should be considered.
reported for DSME interventions that significant change in BMI (86). Higher
were longer and included follow-up sup- levels of exercise intensity are associated
port (72), that were tailored to individual with greater improvements in A1C and in Exercise in the presence of
needs and preferences (71), and that ad- fitness (87). nonoptimal glycemic control
dressed psychosocial issues (71,72,76). Hyperglycemia. When people with type
Both individual and group approaches 1 diabetes are deprived of insulin for
have been found effective (81,82). There Frequency and type of exercise 12– 48 h and are ketotic, exercise can
is increasing evidence for the role of a A U.S. Surgeon General’s report (88) rec- worsen hyperglycemia and ketosis (94);
community health worker in delivering ommended that most adults accumulate therefore, vigorous activity should be
diabetes education in addition to the core at least 30 min of moderate-intensity ac- avoided in the presence of ketosis. How-
team (83). tivity on most, ideally all, days of the ever, it is not necessary to postpone exer-
week. The studies included in the meta- cise based simply on hyperglycemia,
analysis of effects of exercise interventions provided the patient feels well and urine
The National Standards for DSME on glycemic control (86) had a mean and/or blood ketones are negative.
ADA-recognized DSME programs have number of sessions per week of 3.4, with Hypoglycemia. In individuals taking in-
staff who must be certified diabetes edu- a mean of 49 min per session. The DPP sulin and/or insulin secretagogues, phys-
cators or have recent experience in diabe- lifestyle intervention, which included 150 ical activity can cause hypoglycemia if
tes education and management. The min per week of moderate-intensity exer- medication dose or carbohydrate con-
curriculum of ADA-recognized DSME cise, had a beneficial effect on glycemia in sumption is not altered. For individuals
programs must cover all nine areas of di- those with pre-diabetes. Therefore, it on these therapies, added carbohydrate
abetes management, with the assessed seems reasonable to recommend ⬃150 should be ingested if pre-exercise glucose
needs of the individual determining min of exercise per week for people with levels are ⬍100 mg/dl (5.6 mmol/l)
which areas are addressed. The ADA Ed- diabetes. (95,96). Hypoglycemia is rare in diabetic
ucation Recognition Program (ERP) is a Resistance exercise improves insulin individuals who are not treated with in-
mechanism to ensure that diabetes educa- sensitivity to about the same extent as aer- sulin or insulin secretagogues, and no
tion programs meet the National Stan- obic exercise (89). Clinical trials have preventive measures for hypoglycemia
dards and provide quality diabetes care. provided strong evidence for the A1C- are usually advised in these cases.


Position Statement

Exercise in the presence of specific adherence to the medical regimen is do not achieve the desired goals of treat-
long-term complications of diabetes poor. (E) ment (Table 8). Intensification of the
Retinopathy. In the presence of prolifer- treatment regimen is suggested and may
ative diabetic retinopathy (PDR) or severe Psychological and social problems can include assessment of barriers to adher-
non-PDR (NPDR), vigorous aerobic or re- impair the individual’s (103–108) or fam- ence including income; educational at-
sistance exercise may be contraindicated ily’s (109) ability to carry out diabetes tainment; and competing demands,
because of the risk of triggering vitreous care tasks and can therefore compromise including those related to family respon-
hemorrhage or retinal detachment (97). health status. There are opportunities for sibilities and family dynamics; culturally
Peripheral neuropathy. Decreased pain the clinician to assess psychosocial status appropriate and enhanced DSME; co-
sensation in the extremities results in in- in a timely and efficient manner so that management with a diabetes team; refer-
creased risk of skin breakdown and infec- referral for appropriate services can be ac- ral to a medical social worker for
tion and of Charcot joint destruction. complished. assistance with insurance coverage;
Therefore, in the presence of severe pe- Key opportunities for screening of change in pharmacological therapy; initi-
ripheral neuropathy, it may be best to en- psychosocial status occur at diagnosis, ation of or increase in SMBG; more fre-
courage non–weight-bearing activities during regularly scheduled management quent contact with the patient; and
such as swimming, bicycling, or arm ex- visits, during hospitalizations, at discov- referral to an endocrinologist.
ercises (98,99). ery of complications, or when problems
Autonomic neuropathy. Autonomic with glucose control, quality of life, or ad- I. Intercurrent illness
neuropathy can increase the risk of exer- herence are identified (110). Patients are The stress of illness, trauma, and/or sur-
cise-induced injury or adverse event likely to exhibit psychological vulnerabil- gery frequently aggravates glycemic con-
through decreased cardiac responsive- ity at diagnosis and when their medical trol and may precipitate diabetic
ness to exercise, postural hypotension, status changes, i.e., the end of the honey- ketoacidosis (DKA) or nonketotic hyper-
impaired thermoregulation, impaired moon period, when the need for intensi- osmolar state, both of which are life-
night vision due to impaired papillary re- fied treatment is evident, and when threatening conditions that require
action, and unpredictable carbohydrate complications are discovered (105,107). immediate medical care to prevent com-
delivery from gastroparesis predisposing Issues known to impact self- plications and death (116). Any condition
to hypoglycemia (98). Autonomic neu- management and health outcomes in- leading to deterioration in glycemic con-
ropathy is also strongly associated with clude but are not limited to: attitudes trol necessitates more frequent monitor-
CVD in people with diabetes (100,101). about the illness, expectations for medical ing of blood glucose and (in ketosis-prone
People with diabetic autonomic neuropa- management and outcomes, affect/mood, patients) urine or blood ketones. Marked
thy should undergo cardiac investigation general and diabetes-related quality of hyperglycemia requires temporary ad-
before beginning physical activity more life, resources (financial, social, and emo- justment of the treatment program
intense than that to which they are accus- tional) (106), and psychiatric history and—if accompanied by ketosis, vomit-
tomed. (107,110,111). Screening tools are avail- ing, or alteration in the level of conscious-
Albuminuria and nephropathy. Physical able for a number of these areas (112). ness—immediate interaction with the
activity can acutely increase urinary pro- Indications for referral to a mental health diabetes care team. The patient treated
tein excretion. However, there is no evi- specialist familiar with diabetes manage- with noninsulin therapies or MNT alone
dence that vigorous exercise increases the ment may include gross noncompliance may temporarily require insulin. Ade-
rate of progression of diabetic kidney dis- with medical regimen (by self or others) quate fluid and caloric intake must be en-
ease; thus, there is likely no need for any (111), depression with the possibility of sured. Infection or dehydration is more
specific exercise restrictions for people self-harm (104,113), debilitating anxiety likely to necessitate hospitalization of the
with diabetic kidney disease (102). (alone or with depression), indications of person with diabetes than the person
an eating disorder (114), and cognitive without diabetes.
functioning that significantly impairs The hospitalized patient should be
G. Psychosocial assessment and care
judgment (113). It is preferable to incor- treated by a physician with expertise in
porate psychological assessment and the management of diabetes. For further
Recommendations treatment into routine care rather than information on management of patients
● Assessment of psychological and social wait for identification of a specific prob- with hyperglycemia in the hospital, see
situation should be included as an on- lem or deterioration in psychological sta- Section VIII.A. For further information on
going part of the medical management tus (115). Although the clinician may not management of DKA or nonketotic hy-
of diabetes. (E) feel qualified to treat psychological prob- perosmolar state, refer to the ADA posi-
● Psychosocial screening and follow-up lems, utilizing the patient-provider rela- tion statement on hyperglycemic crises
should include, but is not limited to, tionship as a foundation for further (116).
attitudes about the illness, expectations treatment can increase the likelihood that
for medical management and out- the patient will accept referral for other J. Hypoglycemia
comes, affect/mood, general and diabe- services. It is important to establish that
tes-related quality of life, resources emotional well-being is part of diabetes Recommendations
(financial, social, and emotional), and management (110). ● Glucose (15–20 g) is the preferred
psychiatric history. (E) treatment for the conscious individual
● Screen for psychosocial problems such H. When treatment goals are not met with hypoglycemia, although any form
as depression, anxiety, eating disor- For a variety of reasons, some people with of carbohydrate that contains glucose
ders, and cognitive impairment when diabetes and their health care providers may be used. If SMBG 15 min after


Standards of Medical Care

treatment shows continued hypoglyce- ical component of diabetes management. Safe and effective vaccines are avail-
mia, the treatment should be repeated. Teaching people with diabetes to balance able that can greatly reduce the risk of
Once SMBG glucose returns to normal, insulin use, carbohydrate intake, and ex- serious complications from these diseases
the individual should consume a meal ercise is a necessary but not always suffi- (122,123). In a case-control series, influ-
or snack to prevent recurrence of hypo- cient strategy. In type 1 diabetes and enza vaccine was shown to reduce diabe-
glycemia. (E) severely insulin-deficient type 2 diabetes, tes-related hospital admission by as much
● Glucagon should be prescribed for all the syndrome of hypoglycemia unaware- as 79% during flu epidemics (122). There
individuals at significant risk of severe ness, or hypoglycemia-associated auto- is sufficient evidence to support that peo-
hypoglycemia, and caregivers or family nomic failure, can severely compromise ple with diabetes have appropriate sero-
members of these individuals should be stringent diabetes control and quality of logic and clinical responses to these
instructed in its administration. Gluca- life. The deficient counter-regulatory hor- vaccinations. The Centers for Disease
gon administration is not limited to mone release and autonomic responses in Control and Prevention’s Advisory Com-
health care professionals. (E) this syndrome are both risk factors for, mittee on Immunization Practices recom-
● Individuals with hypoglycemia un- and caused by, hypoglycemia. A corollary mends influenza and pneumococcal
awareness or one or more episodes of to this “vicious cycle” is that several weeks vaccines for all individuals of any age with
severe hypoglycemia should be advised of avoidance of hypoglycemia has been diabetes (http://www.cdc.gov/vaccines/
to raise their glycemic targets to strictly demonstrated to improve counter- recs). For a complete discussion on the
avoid further hypoglycemia for at least regulation and awareness to some extent prevention of influenza and pneumococ-
several weeks in order to partially re- in many patients (117,119,120). Hence, cal disease in people with diabetes, con-
verse hypoglycemia unawareness and patients with one or more episodes of se- sult the technical review and position
reduce risk of future episodes. (B) vere hypoglycemia may benefit from at statement on this subject (121,124).
least short-term relaxation of glycemic
Hypoglycemia is the leading limiting fac- targets.
tor in the glycemic management of type 1 VI. PREVENTION AND
and insulin-treated type 2 diabetes (117). K. Immunization MANAGEMENT OF
Treatment of hypoglycemia (plasma glu- DIABETES COMPLICATIONS
cose ⬍70 mg/dl) requires ingestion of
glucose- or carbohydrate-containing Recommendations
● Annually provide an influenza vaccine A. CVD
foods. The acute glycemic response cor- CVD is the major cause of morbidity and
relates better with the glucose content to all diabetic patients ⱖ6 months of
age. (C) mortality for individuals with diabetes
than with the carbohydrate content of the and is the largest contributor to the direct
● Provide at least one lifetime pneumo-
food. Although pure glucose is the pre- and indirect costs of diabetes. The com-
ferred treatment, any form of carbohy- coccal vaccine for adults with diabetes.
A one-time revaccination is recom- mon conditions coexisting with type 2
drate that contains glucose will raise diabetes (e.g., hypertension and dyslipi-
blood glucose. Protein added to carbohy- mended for individuals ⱖ65 years of
age previously immunized when they demia) are clear risk factors for CVD, and
drate does not impair the glycemic re- diabetes itself confers independent risk.
sponse, but also has no benefit in were ⬍65 years of age if the vaccine was
administered ⬎5 years ago. Other indi- Numerous studies have shown the effi-
preventing subsequent hypoglycemia. cacy of controlling cardiovascular risk
Added fat may retard and then prolong cations for repeat vaccination include
nephrotic syndrome, chronic renal dis- factors in preventing or slowing CVD in
the acute glycemic response (118). Ongo- people with diabetes. Evidence is summa-
ing activity of insulin or insulin secreta- ease, and other immunocompromised
states, such as after transplantation. (C) rized in the following sections and re-
gogues may lead to recurrence of viewed in detail in the ADA technical
hypoglycemia unless further food is in- reviews on hypertension (125), dyslipide-
gested after recovery. Influenza and pneumonia are common, mia (126), aspirin therapy (127), and
Severe hypoglycemia (where the indi- preventable infectious diseases associated smoking cessation (128), and in the AHA/
vidual requires the assistance of another with high mortality and morbidity in the ADA scientific statement on prevention of
person and cannot be treated with oral elderly and in people with chronic dis- CVD in people with diabetes (129). Em-
carbohydrate due to confusion or uncon- eases. Though there are limited studies phasis should be placed on reducing car-
sciousness) should be treated using emer- reporting the morbidity and mortality of diovascular risk factors, and clinicians
gency glucagon kits, which require a influenza and pneumococcal pneumonia should be alert for signs and symptoms of
prescription. Those in close contact with, specifically in people with diabetes, ob- atherosclerosis.
or having custodial care of, people with servational studies of patients with a vari-
hypoglycemia-prone diabetes (family ety of chronic illnesses, including
1. Hypertension/blood pressure
members, roommates, school personnel, diabetes, show that these conditions are
child care providers, correctional institu- associated with an increase in hospitaliza-
tion staff, or coworkers) should be in- tions for influenza and its complications.
structed in use of such kits. An individual People with diabetes may be at increased Recommendations
does not need to be a health care profes- risk of the bacteremic form of pneumo-
sional to safely administer glucagon. Care coccal infection and have been reported Screening and diagnosis
should be taken to ensure that unexpired to have a high risk of nosocomial bactere- ● Blood pressure should be measured at
glucagon kits are available. mia, which has a mortality rate as high as every routine diabetes visit. Patients
Prevention of hypoglycemia is a crit- 50% (121). found to have systolic blood pressure


Position Statement

ⱖ130 mmHg or diastolic blood pres- Hypertension is a common comorbidity vascular protection than a systolic blood
sure ⱖ80 mmHg should have blood of diabetes, affecting the majority of pa- pressure level of ⬍140 mmHg in patients
pressure confirmed on a separate day. tients, with prevalence depending on type with type 2 diabetes (www.accord.org).
Repeat systolic blood pressure ⱖ130 of diabetes, age, obesity, and ethnicity.
mmHg or diastolic blood pressure ⱖ80 Hypertension is a major risk factor for
mmHg confirms a diagnosis of hyper- both CVD and microvascular complica- Treatment strategies
tension. (C) tions. In type 1 diabetes, hypertension is Although there are no well-controlled
often the result of underlying nephropa- studies of diet and exercise in the treat-
thy, while in type 2 diabetes it usually ment of hypertension in individuals with
Goals coexists with other cardiometabolic risk diabetes, studies in nondiabetic individu-
● Patients with diabetes should be treated factors. als have shown antihypertensive effects
to a systolic blood pressure ⬍130 similar to pharmacologic monotherapy of
mmHg. (C) reducing sodium intake and excess body
● Patients with diabetes should be treated Screening and diagnosis weight; increasing consumption of fruits,
to a diastolic blood pressure ⬍80 Measurement of blood pressure in the of- vegetables, and low-fat dairy products;
mmHg. (B) fice should follow the guidelines estab- avoiding excessive alcohol consumption;
lished for nondiabetic individuals: and increasing activity levels (130,138).
measurement in the seated position, with These nonpharmacological strategies may
Treatment feet on the floor and arm supported at also positively affect glycemia and lipid
● Patients with a systolic blood pressure heart level, and after 5 min of rest. Ele- control. Their effects on cardiovascular
of 130 –139 mmHg or a diastolic blood vated values should be confirmed on a events have not been established. An ini-
pressure of 80 – 89 mmHg may be given separate day. Because of the clear syner- tial trial of nonpharmacologic therapy
lifestyle therapy alone for a maximum gistic risks of hypertension and diabetes, may be reasonable in diabetic individuals
of 3 months and then, if targets are not the diagnostic cut-off for a diagnosis of with mild hypertension (systolic blood
achieved, be treated with addition of hypertension is lower in people with dia- pressure 130 –139 mmHg or diastolic
pharmacological agents. (E) betes (blood pressure ⱖ130/80) than blood pressure 80 – 89 mmHg). If the
● Patients with more severe hypertension those without diabetes (blood pressure blood pressure is ⱖ140 mmHg systolic
(systolic blood pressure ⱖ140 or dia- ⱖ140/90 mmHg) (130). and/or ⱖ90 mmHg diastolic at the time of
stolic blood pressure ⱖ90 mmHg) at Home blood pressure self-monitoring diagnosis, pharmacologic therapy should
diagnosis or follow-up should receive and 24-h ambulatory blood pressure be initiated along with nonpharmacologic
pharmacologic therapy in addition to monitoring may provide additional evi- therapy (130).
lifestyle therapy. (A) dence of “white coat” and masked hyper- Lowering of blood pressure with reg-
● Pharmacologic therapy for patients tension and other discrepancies between imens based on a variety of antihyperten-
with diabetes and hypertension should office and “true” blood pressure, and in sive drugs, including ACE inhibitors,
be with a regimen that includes either studies in nondiabetic populations, home ARBs, ␤-blockers, diuretics, and calcium
an ACE inhibitor or an angiotensin re- measurements may better correlate with channel blockers, has been shown to be
ceptor blocker (ARB). If one class is not CVD risk than office measurements effective in reducing cardiovascular
tolerated, the other should be substi- (131,132). However, the preponderance events. Several studies suggested that
tuted. If needed to achieve blood pres- of the clear evidence of benefits of treat- ACE inhibitors may be superior to dihy-
sure targets, a thiazide diuretic should ment of hypertension in people with dia- dropyridine calcium channel blockers in
be added to those with an estimated betes is based on office measurements. reducing cardiovascular events (139 –
glomerular filtration rate (GFR) (see be- 141). However, a variety of other studies
low) ⱖ50 ml/min per 1.73 m2 and a have shown no specific advantage to ACE
loop diuretic for those with an esti- Treatment goals inhibitors as initial treatment of hyper-
mated GFR ⬍50 ml/min per 1.73 m2. Randomized clinical trials have demon- tension in the general hypertensive pop-
(E) strated the benefit (reduction of coronary ulation, but rather an advantage on
● Multiple drug therapy (two or more heart disease [CHD] events, stroke, and cardiovascular outcomes of initial therapy
agents at maximal doses) is generally nephropathy) of lowering blood pressure with low-dose thiazide diuretics (130,
required to achieve blood pressure tar- to ⬍140 mmHg systolic and ⬍80 mmHg 142,143).
gets. (B) diastolic in individuals with diabetes In people with diabetes, inhibitors of
● If ACE inhibitors, ARBs, or diuretics are (130,133–135). Epidemiologic analyses the renin-angiotensin system (RAS) may
used, kidney function and serum potas- show that blood pressures ⬎115/75 have unique advantages for initial or early
sium levels should be closely moni- mmHg are associated with increased car- therapy of hypertension. In a nonhyper-
tored. (E) diovascular event rates and mortality in tension trial of high-risk individuals, in-
● In pregnant patients with diabetes and individuals with diabetes (130,136,137). cluding a large subset with diabetes, an
chronic hypertension, blood pressure Therefore, a target blood pressure goal of ACE inhibitor reduced CVD outcomes
target goals of 110 –129/65–79 mmHg ⬍130/80 mmHg is reasonable if it can be (144). In patients with CHF, including
are suggested in the interest of long- safely achieved. The ongoing Action to diabetic subgroups, ARBs have been
term maternal health and minimizing Control Cardiovascular Risk in Diabetes shown to reduce major CVD outcomes
impaired fetal growth. ACE inhibitors (ACCORD) trial is designed to determine (145–148), and in type 2 diabetic patients
and ARBs are contraindicated during whether lowering systolic blood pressure with significant nephropathy, ARBs were
pregnancy. (E) to ⬍120 mmHg provides greater cardio- superior to calcium channel blockers for


Standards of Medical Care

reducing heart failure (149 –151). Al- 2. Dyslipidemia/lipid management mmol/l), using a high dose of a statin, is
though evidence for distinct advantages an option. (E)
of RAS inhibitors on CVD outcomes in Recommendations ● If drug-treated patients do not reach the
diabetes remains conflicting (133,152), above targets on maximal tolerated sta-
the high CVD risks associated with Screening tin therapy, a reduction in LDL choles-
diabetes, and the high prevalence of un- ● In most adult patients, measure fasting terol of ⬃40% from baseline is an
diagnosed CVD, may still favor recom- lipid profile at least annually. In adults alternative therapeutic goal. (A)
mendations for their use as first-line with low-risk lipid values (LDL choles- ● Triglycerides levels ⬍150 mg/dl (1.7
hypertension therapy in people with dia- terol ⬍100 mg/dl, HDL cholesterol mmol/l) and HDL cholesterol ⬎40
betes (130). The compelling benefits of ⬎50 mg/dl, and triglycerides ⬍150 mg/dl (1.0 mmol/l) in men and ⬎50
RAS inhibitors in diabetic patients with mg/dl), lipid assessments may be re- mg/dl (1.3 mmol/l) in women are desir-
albuminuria or renal insufficiency pro- peated every 2 years. (E) able. However, LDL cholesterol–
vide additional rationale for use of these targeted statin therapy remains the
agents (see Section VI. B below). Treatment recommendations and preferred strategy. (C)
● Combination therapy using statins and
An important caveat is that most pa- goals
● Lifestyle modification focusing on the other lipid-lowering agents may be
tients with hypertension require multi-
reduction of saturated fat, trans fat, and considered to achieve lipid targets but
drug therapy to reach treatment goals,
cholesterol intake; weight loss (if indi- has not been evaluated in outcome
especially diabetic patients whose targets studies for either CVD outcomes or
are lower. Many patients will require cated); and increased physical activity
should be recommended to improve safety. (E)
three or more drugs to reach target goals ● Statin therapy is contraindicated in
(130). the lipid profile in patients with diabe-
tes. (A) pregnancy. (E)
During pregnancy in diabetic women
● Statin therapy should be added to life-
with chronic hypertension, target blood
style therapy, regardless of baseline Evidence for benefits of lipid-
pressure goals of systolic blood pressure
lipid levels, for diabetic patients: lowering therapy
110 –129 mmHg and diastolic blood ● with overt CVD (A) Patients with type 2 diabetes have an in-
pressure 65–79 mmHg are reasonable, as ● without CVD who are over the age of creased prevalence of lipid abnormalities,
they contribute to long-term maternal 40 and have one or more other CVD which contributes to their high risk of
health. Lower blood pressure levels may risk factors. (A) CVD. For the past decade or more, mul-
be associated with impaired fetal growth. ● For lower-risk patients than those spec- tiple clinical trials demonstrated signifi-
During pregnancy, treatment with ACE ified above (e.g., without overt CVD cant effects of pharmacologic (primarily
inhibitors and ARBs is contraindicated, and under the age of 40), statin therapy statin) therapy on CVD outcomes in sub-
since they are likely to cause fetal damage. should be considered in addition to jects with CHD and for primary CVD pre-
Antihypertensive drugs known to be ef- lifestyle therapy if LDL cholesterol re- vention (154). Sub-analyses of diabetic
fective and safe in pregnancy include mains ⬎100 mg/dl or in those with subgroups of larger trials (155–159) and
methyldopa, labetalol, diltiazem, multiple CVD risk factors (E) trials specifically in subjects with diabetes
clonidine, and prazosin. Chronic diuretic ● In individuals without overt CVD, the (160,161) showed significant primary
use during pregnancy has been associated primary goal is an LDL cholesterol and secondary prevention of CVD
with restricted maternal plasma volume, ⬍100 mg/dl (2.6 mmol/l). (A) events ⫾ CHD deaths in diabetic popula-
which might reduce uteroplacental perfu- ● In individuals with overt CVD, a lower tions. As shown in Table 10, and similar
sion (153). LDL cholesterol goal of ⬍70 mg/dl (1.8 to findings in nondiabetic subjects, re-

Table 10—Reduction in 10-year risk of major CVD end points (CHD death/nonfatal MI) in major statin trials, or substudies of major trials,
in diabetic subjects (n ⴝ 16,032)

CVD LDL cholesterol

Study (ref.) prevention Statin dose and comparator RRR ARR reduction
4S-DM (155) 20 Simvastatin 20–40 mg vs. placebo 85.7 to 43.2% (50%) 42.5% 186 to 119 mg/dl (36%)
ASPEN 20 (160) 20 Atorvastatin 10 mg vs. placebo 39.5 to 24.5% (34%) 12.7% 112 to 79 mg/dl (29%)
HPS-DM (156) 20 Simvastatin 40 mg vs. placebo 43.8 to 36.3% (17%) 7.5% 123 to 84 mg/dl (31%)
CARE-DM (157) 20 Pravastatin 40 mg vs. placebo 40.8 to 35.4% (13%) 5.4% 136 to 99 mg/dl (27%)
TNT-DM (158) 20 Atorvastatin 80 mg vs. 10 mg 26.3 to 21.6% (18%) 4.7% 99 to 77 mg/dl (22%)
HPS-DM (156) 10 Simvastatin 40 mg vs. placebo 17.5 to 11.5% (34%) 6.0% 124 to 86 mg/dl (31%)
CARDS (161) 10 Atorvastatin 10 mg vs. placebo 11.5 to 7.5% (35%) 4% 118 to 71 mg/dl (40%)
ASPEN 10 (160) 10 Atorvastatin 10 mg vs. placebo 11.0 to 7.9% (19%) 1.9% 114 to 80 mg/dl (30%)
ASCOT-DM (159) 10 Atorvastatin 10 mg vs. placebo 11.1 to 10.2% (8%) 0.9% 125 to 82 mg/dl (34%)
Studies were of differing lengths (3.3–5.4 years) and used somewhat different outcomes, but all reported rates of CVD death and nonfatal MI. In this tabulation,
results of the statin on 10-year risk of major CVD end points (CHD death/nonfatal MI) are listed for comparison between studies. Correlation between 10-year CVD
risk of the control group and the ARR with statin therapy is highly significant (P ⫽ 0.0007). Analyses provided by Craig Williams, Pharm.D., Oregon Health &
Science University, 2007. ARR, absolute risk reduction; RRR, relative risk reduction.


Position Statement

Table 11—Summary of recommendations for glycemic, blood pressure, and lipid control for ⬍70 mg/dl is an option in very-high-risk
adults with diabetes diabetic patients with overt CVD (172).
A1C ⬍7.0%* The addition of other drugs such as
Blood pressure ⬍130/80 mmHg ezetimibe to statins may achieve lower
Lipids LDL cholesterol goals, but no data are
LDL cholesterol ⬍100 mg/dl (⬍2.6 mmol/l)† available as to whether such combination
therapy is more effective than a statin alone
*Referenced to a nondiabetic range of 4.0 – 6.0% using a DCCT-based assay. †In individuals with overt CVD,
a lower LDL cholesterol goal of ⬍70 mg/dl (1.8 mmol/l), using a high dose of a statin, is an option. in preventing cardiovascular events.

Treatment of other lipoprotein

duction in “hard” CVD outcomes (CHD baseline lipid levels. Statins are the drugs fractions
death and nonfatal myocardial infarction) of choice for lowering LDL cholesterol. Severe hypertriglyceridemia may warrant
can be more clearly seen in diabetic sub- In patients other than those described immediate therapy of this abnormality
jects with high baseline CVD risk (known above, statin treatment should be consid- with lifestyle and usually pharmacologic
CVD and/or very high LDL cholesterol ered if there is an inadequate LDL choles- therapy (fibric acid derivative or niacin)
levels), but overall the benefits of statin terol response to lifestyle modifications to reduce the risk of acute pancreatitis. In
therapy in people with diabetes at mod- and improved glucose control, or if the the absence of severe hypertriglyceride-
erate or high risk for CVD are convincing. patient has increased cardiovascular risk mia, therapy targeting HDL cholesterol or
Low HDL cholesterol levels, which (e.g., multiple cardiovascular risk factors triglycerides has intuitive appeal but lacks
are often associated with elevated triglyc- or long duration of diabetes). Very little the evidence base of statin therapy (162).
eride levels, are the most prevalent pat- clinical trial evidence exists for type 2 di- If the HDL cholesterol is ⬍40 mg/dl and
tern of dyslipidemia in persons with type abetic patients under the age of 40 or for the LDL cholesterol between 100 and 129
2 diabetes. However, the evidence base type 1 diabetic patients of any age. In the mg/dl, gemfibrozil or niacin might be
for drugs that target these lipid fractions is Heart Protection Study (lower age limit used, especially if a patient is intolerant to
significantly less robust than that for sta- 40 years), the subgroup of ⬃600 patients statins. Niacin is the most effective drug
tin therapy (162). In a study conducted in with type 1 diabetes had a proportion- for raising HDL cholesterol. It can signif-
a nondiabetic cohort, nicotinic acid re- ately similar (though not statistically sig- icantly increase blood glucose at high
duced CVD outcomes (163). Gemfibrozil nificant) reduction in risk to patients with doses, but recent studies demonstrate that
has been shown to decrease rates of CVD type 2 diabetes (156). Although the data at modest doses (750 –2,000 mg/day),
events in subjects without diabetes are not definitive, consideration should significant improvements in LDL choles-
(164,165) and in the diabetic subgroup in be given to similar lipid-lowering goals in terol, HDL cholesterol, and triglyceride
one of the larger trials (164). However, in type 1 diabetic patients as in type 2 dia- levels are accompanied by only modest
a large trial specific to diabetic patients, betic patients, particularly if they have changes in glucose that are generally ame-
fenofibrate failed to reduce overall cardio- other cardiovascular risk factors. nable to adjustment of diabetes therapy
vascular outcomes (166). (173,174).
Combination therapy, with a statin
Dyslipidemia treatment and target Alternative LDL cholesterol goals and a fibrate or statin and niacin, may be
lipid levels Virtually all trials of statins and CVD out- efficacious for treatment for all three lipid
For most patients with diabetes, the first come tested specific doses of statins fractions, but this combination is associ-
priority of dyslipidemia therapy (unless against placebo, other doses of statin, or ated with an increased risk for abnormal
severe hypertriglyceridemia is the imme- other statins, rather than aiming for transaminase levels, myositis, or rhabdo-
diate issue) is to lower LDL cholesterol to specific LDL cholesterol goals (168). myolysis. The risk of rhabdomyolysis is
a target goal of ⬍100 mg/dl (2.60 mmol/l) As can be seen in Table 10, placebo- higher with higher doses of statins and
(167). Lifestyle intervention, including controlled trials generally achieved LDL with renal insufficiency, and seems to be
MNT, increased physical activity, weight cholesterol reductions of 30 – 40% from lower when statins are combined with fe-
loss, and smoking cessation, may allow baseline. Hence, LDL cholesterol lower- nofibrate than gemfibrozil (175). Several
some patients to reach lipid goals. Nutri- ing of this magnitude is an acceptable out- ongoing trials may provide much-needed
tion intervention should be tailored ac- come for patients who cannot reach LDL evidence for the effects of combination
cording to each patient’s age, type of cholesterol goals due to severe baseline therapy on cardiovascular outcomes.
diabetes, pharmacological treatment, elevations in LDL cholesterol and/or
lipid levels, and other medical conditions intolerance of maximal, or any, statin 3. Antiplatelet agents
and should focus on the reduction of sat- doses.
urated fat, cholesterol, and trans unsatur- Recent clinical trials in high-risk pa- Recommendations
ated fat intake. Glycemic control can also tients, such as those with acute coronary ● Use aspirin therapy (75–162 mg/day)
beneficially modify plasma lipid levels, syndromes or previous cardiovascular as a secondary prevention strategy in
particularly in patients with very high events (169 –171), have demonstrated those with diabetes with a history of
triglycerides and poor glycemic control. that more aggressive therapy with high CVD. (A)
In those with clinical CVD or over doses of statins to achieve an LDL choles- ● Use aspirin therapy (75–162 mg/day)
aged 40 with other CVD risk factors, terol of ⬍70 mg/dl led to a significant re- as a primary prevention strategy in
pharmacological treatment should be duction in further events. Therefore, a those with type 1 or 2 diabetes at in-
added to lifestyle therapy regardless of reduction in LDL cholesterol to a goal of creased cardiovascular risk, including


Standards of Medical Care

those who are ⬎40 years of age or who therapy in aspirin-intolerant patients reduce the risk of cardiovascular
have additional risk factors (family his- should be considered. events. (A)
tory of CVD, hypertension, smoking, ● In patients with a prior myocardial in-
dyslipidemia, or albuminuria). (A) 4. Smoking cessation farction, add ␤-blockers (if not contra-
● Aspirin therapy is not recommended in indicated) to reduce mortality. (A)
people under 30 years of age, due to Recommendations ● In patients ⬎40 years of age with an-
lack of evidence of benefit, and is con- ● Advise all patients not to smoke. (A) other cardiovascular risk factor (hyper-
traindicated in patients under the age of ● Include smoking cessation counseling tension, family history, dyslipidemia,
21 years because of the associated risk and other forms of treatment as a rou- microalbuminuria, cardiac autonomic
of Reye’s syndrome. (E) tine component of diabetes care. (B) neuropathy, or smoking), ACE inhibi-
● Combination therapy using other anti- tor, aspirin, and statin therapy (if not
platelet agents such as clopidrogel in Issues of smoking in diabetes are re- contraindicated) should be used to re-
addition to aspirin should be used in viewed in detail in the ADA technical re- duce the risk of cardiovascular events.
patients with severe and progressive view (128) and position statement (184) (B)
CVD. (C) on this topic. A large body of evidence ● In patients with treated CHF, met-
● Other antiplatelet agents may be a rea- from epidemiological, case-control, and formin and thiazolidinedione (TZD)
sonable alternative for high-risk pa- cohort studies provides convincing docu- use are contraindicated. (C)
tients with aspirin allergy, with mentation of the causal link between cig-
bleeding tendency, who are receiving arette smoking and health risks. Cigarette
anticoagulant therapy, with recent gas- smoking contributes to one of every five CHD screening and treatment are re-
trointestinal bleeding, and with clini- deaths in the U.S. and is the most impor- viewed in detail in the ADA consensus
cally active hepatic disease who are not tant modifiable cause of premature death. statement on CHD in people with diabe-
candidates for aspirin therapy. (E) Much of the prior work documenting the tes (187), and screening for CAD is re-
impact of smoking on health did not sep- viewed in a recently updated consensus
The use of aspirin in diabetes is reviewed arately discuss results on subsets of indi- statement (93). To identify the presence
in detail in the ADA technical review viduals with diabetes, suggesting that the of CAD in diabetic patients without clear
(127) and position statement (176) on identified risks are at least equivalent to or suggestive symptoms, a risk factor–
this topic. Aspirin has been recom- those found in the general population. based approach to the initial diagnostic
mended for primary (177,178) and sec- Other studies of individuals with diabetes evaluation and subsequent follow-up has
ondary (179,180) prevention of consistently found a heightened risk of intuitive appeal. However, recent studies
cardiovascular events in high-risk dia- CVD and premature death among smok- concluded that using this approach fails
betic and nondiabetic individuals. One ers. Smoking is also related to the prema- to identify which patients will have silent
large meta-analysis and several clinical ture development of microvascular ischemia on screening tests (100,188).
trials demonstrate the efficacy of using as- complications of diabetes and may have a Cardiovascular risk factors should be
pirin as a preventive measure for cardio- role in the development of type 2 diabetes. assessed at least once a year. These risk
vascular events, including stroke and A number of large randomized clini- factors include dyslipidemia, hyperten-
myocardial infarction. Many trials have cal trials have demonstrated the efficacy sion, smoking, a positive family history of
shown an ⬃30% decrease in myocardial and cost-effectiveness of smoking cessa- premature coronary disease, and the pres-
infarction and a 20% decrease in stroke in tion counseling in changing smoking be- ence of micro- or macroalbuminuria. Ab-
a wide range of patients, including young havior and reducing tobacco use. The
normal risk factors should be treated as
and middle-aged patients, patients with routine and thorough assessment of to-
described elsewhere in these guidelines.
and without a history of CVD, males and bacco use is important as a means of
Patients at increased CHD risk should re-
females, and patients with hypertension. preventing smoking or encouraging ces-
ceive aspirin, statin, and ACE inhibitor
Dosages used in most clinical trials sation. Special considerations should in-
ranged from 75 to 325 mg/day. There is clude assessment of level of nicotine therapy, unless there are contraindica-
little evidence to support any specific dependence, which is associated with dif- tions to a particular drug class.
dose, but using the lowest possible dosage ficulty in quitting and relapse (185,186). Candidates for a further cardiac test-
may help reduce side effects (181). Con- ing include those with 1) typical or atyp-
versely, a randomized trial of 100 mg of 5. CHD screening and treatment ical cardiac symptoms and 2) an
aspirin daily showed less of a primary pre- abnormal resting electrocardiogram
vention effect, without statistical signifi- Recommendations (ECG). The screening of asymptomatic
cance, in the large diabetic subgroup in patients remains controversial, especially
contrast to significant benefit in those Screening as intensive medical therapy, indicated in
without diabetes (182), raising the issue ● In asymptomatic patients, evaluate risk diabetic patients at high risk for CVD, has
of aspirin resistance in those with diabe- factors to stratify patients by 10-year an increasing evidence base for providing
tes. There is no evidence for a specific age risk, and treat risk factors accordingly. equal outcomes to invasive revasculariza-
at which to start aspirin, but at ages ⬍30 (B) tion, including in diabetic patients (189).
years, aspirin has not been studied. There is also recent preliminary evidence
Clopidogrel has been demonstrated Treatment that silent myocardial ischemia may re-
to reduce CVD events in diabetic individ- ● In patients with known CVD, ACE in- verse over time, adding to the controversy
uals (183). Adjunctive therapy in very- hibitor, aspirin, and statin therapy (if concerning aggressive screening strate-
high-risk patients or as alternative not contraindicated) should be used to gies (190).


Position Statement

B. Nephropathy screening and (e.g., urine albumin excretion rate and lay progression to microalbuminuria
treatment GFR) and is recommended (B) (198).
● When ACE inhibitors, ARBs, or diuret- In addition, ACE inhibitors have been
Recommendations ics are used, monitor serum creatinine shown to reduce major CVD outcomes
and potassium levels for the develop- (i.e., myocardial infarction, stroke, death)
ment of acute kidney disease and hy- in patients with diabetes (144), thus fur-
General recommendations ther supporting the use of these agents in
● To reduce the risk or slow the progres-
perkalemia. (E)
● Continued monitoring of urine albu- patients with microalbuminuria, a CVD
sion of nephropathy, optimize glucose risk factor. ARBs have also been shown to
min excretion to assess both response
control. (A) reduce the rate of progression from mi-
● To reduce the risk or slow the progres-
to therapy and progression of disease is
recommended. (E) cro- to macroalbuminuria as well as ESRD
sion of nephropathy, optimize blood ● in patients with type 2 diabetes (199 –
Consider referral to a physician experi-
pressure control. (A) 201). Some evidence suggests that ARBs
enced in the care of kidney disease
when there is uncertainty about the eti- have a smaller magnitude of rise in potas-
Screening ology of kidney disease (active urine sium compared with ACE inhibitors in
● Perform an annual test to assess urine sediment, absence of retinopathy, rapid people with nephropathy (202,203).
albumin excretion in type 1 diabetic pa- decline in GFR), difficult management Other drugs, such as diuretics, calcium
tients with diabetes duration of ⱖ5 issues, or advanced kidney disease. (B) channel blockers, and ␤-blockers, should
years and in all type 2 diabetic patients, be used as additional therapy to further
starting at diagnosis. (E) lower blood pressure in patients already
● Measure serum creatinine at least annu- Diabetic nephropathy occurs in 20 – 40% treated with ACE inhibitors or ARBs
ally in all adults with diabetes regard- of patients with diabetes and is the single (149), or as alternate therapy in the rare
less of the degree of urine albumin leading cause of end-stage renal disease individual unable to tolerate ACE inhibi-
excretion. The serum creatinine should (ESRD). Persistent albuminuria in the tors or ARBs.
be used to estimate GFR and stage the range of 30 –299 mg/24 h (microalbu- Studies in patients with varying stages
level of chronic kidney disease (CKD), minuria) has been shown to be the earliest of nephropathy have shown that protein
if present. (E) stage of diabetic nephropathy in type 1 restriction helps slow the progression of
diabetes and a marker for development of albuminuria, GFR decline, and occur-
Treatment nephropathy in type 2 diabetes. Mi- rence of ESRD (204 –207). Protein
● In the treatment of the nonpregnant pa- croalbuminuria is also a well-established restriction should be considered particu-
tient with micro- or macroalbuminuria, marker of increased CVD risk (191,192). larly in patients whose nephropathy
either ACE inhibitors or ARBs should Patients with microalbuminuria who seems to be progressing despite optimal
be used. (A) progress to macroalbuminuria (ⱖ300 glucose and blood pressure control and
● While there are no adequate head-to- mg/24 h) are likely to progress to ESRD use of ACE inhibitor and/or ARBs (207).
head comparisons of ACE inhibitors (193,194). However, a number of inter-
and ARBs, there is clinical trial support ventions have been demonstrated to re-
for each of the following statements: duce the risk and slow the progression of Assessment of albuminuria status
● In patients with type 1 diabetes, with renal disease. and renal function
hypertension and any degree of albu- Intensive diabetes management with Screening for microalbuminuria can be
minuria, ACE inhibitors have been the goal of achieving near-normoglyce- performed by measurement of the albu-
shown to delay the progression of ne- mia has been shown in large prospective min-to-creatinine ratio in a random spot
phropathy. (A) randomized studies to delay the onset of collection (preferred method); 24-h or
● In patients with type 2 diabetes, hy- microalbuminuria and the progression of timed collections are more burdensome
pertension, and microalbuminuria, micro- to macroalbuminuria in patients and add little to prediction or accuracy
both ACE inhibitors and ARBs have with type 1 (195,196) and type 2 (40,41) (208,209). Measurement of a spot urine
been shown to delay the progression diabetes. The UKPDS provided strong ev- for albumin only, whether by immunoas-
to macroalbuminuria. (A) idence that control of blood pressure can say or by using a dipstick test specific for
● In patients with type 2 diabetes, hy- reduce the development of nephropathy microalbumin, without simultaneously
pertension, macroalbuminuria, and (133). In addition, large prospective ran- measuring urine creatinine, is somewhat
renal insufficiency (serum creatinine domized studies in patients with type 1 less expensive but susceptible to false-
⬎1.5 mg/dl), ARBs have been shown diabetes have demonstrated that achieve- negative and -positive determinations as a
to delay the progression of nephrop- ment of lower levels of systolic blood result of variation in urine concentration
athy. (A) pressure (⬍140 mmHg) resulting from due to hydration and other factors.
● If one class is not tolerated, the other treatment using ACE inhibitors provides a Abnormalities of albumin excretion
should be substituted. (E) selective benefit over other antihyperten- are defined in Table 12. Because of vari-
sive drug classes in delaying the progres- ability in urinary albumin excretion, two
● Reduction of protein intake to 0.8 –1.0 sion from micro- to macroalbuminuria of three specimens collected within a 3- to
g 䡠 kg body wt⫺1 䡠 day⫺1 in individuals and can slow the decline in GFR in 6-month period should be abnormal be-
with diabetes and the earlier stages of patients with macroalbuminuria (150, fore considering a patient to have crossed
CKD and to 0.8 g 䡠 kg body wt⫺1 䡠 151,197). In type 2 diabetes with hyper- one of these diagnostic thresholds. Exer-
day⫺1 in the later stages of CKD may tension and normoalbuminuria, ACE cise within 24 h, infection, fever, CHF,
improve measures of renal function inhibition has been demonstrated to de- marked hyperglycemia, and marked hy-


Standards of Medical Care

Table 12—Definitions of abnormalities in albumin excretion Screening

● Adults and adolescents with type 1 di-
Category Spot collection (␮g/mg creatinine) abetes should have an initial dilated
and comprehensive eye examination by
Normal ⬍30 an ophthalmologist or optometrist
Microalbuminuria 30–299 within 5 years after the onset of diabe-
Macro (clinical)-albuminuria 300 tes. (B)
● Patients with type 2 diabetes should
have an initial dilated and comprehen-
sive eye examination by an ophthalmol-
pertension may elevate urinary albumin B is indicated in patients likely to progress ogist or optometrist shortly after the
excretion over baseline values. to end-stage kidney disease. diagnosis of diabetes. (B)
Information on presence of abnormal Consider referral to a physician expe- ● Subsequent examinations for type 1
urine albumin excretion in addition to rienced in the care of kidney disease when and type 2 diabetic patients should be
level of GFR may be used to stage CKD. there is uncertainty about the etiology of repeated annually by an ophthalmolo-
The National Kidney Foundation classifi- kidney disease (active urine sediment, ab- gist or optometrist. Less frequent exams
cation (Table 13) is primarily based on sence of retinopathy, rapid decline in (every 2–3 years) may be considered
GFR levels and therefore differs from GFR), difficult management issues, or ad- following one or more normal eye ex-
other systems in which staging is based vanced kidney disease. The threshold for ams. Examinations will be required
primarily on urinary albumin excretion referral may vary depending on the fre- more frequently if retinopathy is pro-
(210). Studies have found decreased GFR quency with which a provider encounters gressing. (B)
in the absence of increased urine albumin diabetic patients with significant kidney ● Women with pre-existing diabetes who
excretion in a substantial percentage of disease. Consultation with a nephrologist are planning pregnancy or who have
adults with diabetes (211,212). Epidemi- when stage 4 CKD develops has been become pregnant should have a com-
ologic evidence suggests that a substantial found to reduce cost, improve quality of prehensive eye examination and be
fraction of those with chronic kidney dis- care, and keep people off dialysis longer counseled on the risk of development
ease in the setting of diabetes have little or (214,215). However, nonrenal specialists and/or progression of diabetic retinop-
no detectable albuminuria (211). Serum should not delay educating their patients athy. Eye examination should occur in
creatinine should therefore be measured about the progressive nature of diabetic the first trimester with close follow-up
at least annually in all adults with diabe- kidney disease; the renal preservation throughout pregnancy and for 1 year
tes, regardless of the degree of urine albu- benefits of aggressive treatment of blood postpartum. (B)
min excretion. pressure, blood glucose, and hyperlipid-
Serum creatinine should be used to emia; and the potential need for renal re-
estimate GFR and to stage the level of placement therapy. Treatment
CKD, if present. GFR can be estimated ● Promptly refer patients with any level of
using formulae such as the Cockroft- macular edema, severe NPDR, or any
C. Retinopathy screening and
Gault equation or a prediction formula PDR to an ophthalmologist who is
using data from the Modification of Diet knowledgeable and experienced in the
and Renal Disease study (213). GFR cal- management and treatment of diabetic
culators are available at http://www. Recommendations retinopathy. (A)
nkdep.nih.gov. Many clinical laboratories ● Laser photocoagulation therapy is indi-
now report estimated GFR in addition to General recommendations cated to reduce the risk of vision loss in
serum creatinine. ● To reduce the risk or slow the progres- patients with high-risk PDR, clinically
The role of continued annual quanti- sion of retinopathy, optimize glycemic significant macular edema, and in some
tative assessment of albumin excretion af- control. (A) cases of severe NPDR. (A)
ter diagnosis of microalbuminuria and ● To reduce the risk or slow the progres- ● The presence of retinopathy is not a
institution of ACE inhibitor or ARB ther- sion of retinopathy, optimize blood contraindication to aspirin therapy for
apy and blood pressure control is unclear. pressure control. (A) cardioprotection, as this therapy does
Continued surveillance can assess both
response to therapy and progression of
disease. Some suggest that reducing ab- Table 13—Stages of CKD
normal albuminuria (⬎30 mg/g) to the
normal or near-normal range may im-
GFR (ml/min per 1.73
prove renal and cardiovascular prognosis,
Stage Description m2 body surface area)
but this approach has not been formally
evaluated in prospective trials. 1 Kidney damage* with normal or increased GFR 90
Complications of kidney disease cor- 2 Kidney damage* with mildly decreased GFR 60–89
relate with level of kidney function. When 3 Moderately decreased GFR 30–59
the estimated GFR is ⬍60 ml/min per 4 Severely decreased GFR 15–29
1.73 m2, screening for anemia, malnutri- 5 Kidney failure ⬍15 or dialysis
tion, and metabolic bone disease is indi- *Kidney damage defined as abnormalities on pathologic, urine, blood, or imaging tests. Adapted from ref.
cated. Early vaccination against hepatitis 209.


Position Statement

not increase the risk of retinal hemor- bling of the visual angle (e.g., 20/50 to discussion of diabetic retinopathy, see
rhage. (A) 20/100) from 20% in untreated eyes to ADA’s technical review and position state-
8% in treated eyes. The ETDRS also veri- ment on this subject (229,230).
fied the benefits of panretinal photocoag-
Diabetic retinopathy is a highly specific ulation for high-risk PDR, but not for
vascular complication of both type 1 and D. Neuropathy screening and
mild or moderate NPDR. In older-onset treatment
type 2 diabetes, with prevalence strongly patients with severe NPDR or less-than-
related to the duration of diabetes. Dia- high-risk PDR, the risk of severe visual
betic retinopathy is the most frequent loss or vitrectomy was reduced ⬃50% by Recommendations
cause of new cases of blindness among early laser photocoagulation surgery at ● All patients should be screened for dis-
adults aged 20 –74 years. Glaucoma, cat- these stages. tal symmetric polyneuropathy (DPN) at
aracts, and other disorders of the eye oc- Laser photocoagulation surgery in diagnosis and at least annually thereaf-
cur earlier and more frequently in people both trials was beneficial in reducing the ter, using simple clinical tests. (B)
with diabetes. risk of further visual loss, but generally ● Electrophysiological testing is rarely
In addition to duration of diabetes, not beneficial in reversing already dimin- needed, except in situations where the
other factors that increase the risk of, or ished acuity. This preventive effect and clinical features are atypical. (E)
are associated with, retinopathy include the fact that patients with PDR or macular ● Educate all patients about self-care of
chronic hyperglycemia (216), the pres- edema may be asymptomatic provide the feet. For those with DPN, facilitate
ence of nephropathy (217), and hyper- strong support for a screening program to enhanced foot care education and refer
tension (218). Intensive diabetes detect diabetic retinopathy. for special footware. (B)
management with the goal of achieving As retinopathy is estimated to take at ● Screening for signs and symptoms of
near normoglycemia has been shown in least 5 years to develop after the onset of autonomic neuropathy should be insti-
large prospective randomized studies to hyperglycemia (223), patients with type 1 tuted at diagnosis of type 2 diabetes and
prevent and/or delay the onset and pro- diabetes should have an initial dilated and 5 years after the diagnosis of type 1 di-
gression of diabetic retinopathy comprehensive eye examination within 5 abetes. Special testing is rarely needed
(35,40,41). Lowering blood pressure has years after the onset of diabetes. Patients and may not affect management or out-
been shown to decrease the progression with type 2 diabetes, who generally have comes. (E)
of retinopathy (133). Several case series had years of undiagnosed diabetes (224) ● Medications for the relief of specific
and a controlled prospective study sug- and who have a significant risk of preva- symptoms related to DPN and auto-
gest that pregnancy in type 1 diabetic pa- lent diabetic retinopathy at the time of nomic neuropathy are recommended,
tients may aggravate retinopathy diabetes diagnosis, should have an initial as they improve the quality of life of the
(219,220); laser photocoagulation sur- dilated and comprehensive eye examina- patient. (E)
gery can minimize this risk (220). tion soon after diagnosis. Examinations
One of the main motivations for should be performed by an ophthalmolo- The diabetic neuropathies are heteroge-
screening for diabetic retinopathy is the gist or optometrist who is knowledgeable neous with diverse clinical manifesta-
established efficacy of laser photocoagu- and experienced in diagnosing the pres- tions. They may be focal or diffuse. Most
lation surgery in preventing visual loss. ence of diabetic retinopathy and is aware common among the neuropathies are
Two large trials, the Diabetic Retinopathy of its management. Subsequent examina- chronic sensorimotor DPN and auto-
Study (DRS) and the Early Treatment Di- tions for type 1 and type 2 diabetic pa- nomic neuropathy. Although DPN is a
abetic Retinopathy Study (ETDRS), pro- tients are generally repeated annually. diagnosis of exclusion, complex investi-
vide the strongest support for the Less frequent exams (every 2–3 years) gations to exclude other conditions are
therapeutic benefits of photocoagulation may be cost-effective after one or more rarely needed (231).
surgery. normal eye exams (225–227), while ex- The early recognition and appropri-
The DRS (221) showed that panreti- aminations will be required more fre- ate management of neuropathy in the pa-
nal photocoagulation surgery reduced the quently if retinopathy is progressing. tient with diabetes is important for a
risk of severe vision loss from PDR from Examinations can also be done with number of reasons: 1) nondiabetic neu-
15.9% in untreated eyes to 6.4% in retinal photographs (with or without di- ropathies may be present in patients with
treated eyes. The benefit was greatest lation of the pupil) read by experienced diabetes and may be treatable; 2) a num-
among patients whose baseline evalua- experts. In-person exams are still neces- ber of treatment options exist for symp-
tion revealed high-risk characteristics sary when the photos are unacceptable tomatic diabetic neuropathy; 3) up to
(chiefly disc neovascularization or vitre- and for follow-up of abnormalities de- 50% of DPN may be asymptomatic and
ous hemorrhage). Given the risks of mod- tected. This technology has great poten- patients are at risk of insensate injury to
est loss of visual acuity and contraction of tial in areas where qualified eye care their feet; 4) autonomic neuropathy may
the visual field from panretinal laser sur- professionals are not available, and may involve every system in the body; and 5)
gery, such therapy is primarily recom- also enhance efficiency and reduce costs cardiovascular autonomic neuropathy
mended for eyes with PDR approaching when the expertise of ophthalmologists causes substantial morbidity and mortal-
or having high-risk characteristics. can be utilized for more complex exami- ity. Specific treatment for the underlying
The ETDRS (222) established the nations and for therapy (228). nerve damage is currently not available,
benefit of focal laser photocoagulation Results of eye examinations should be other than improved glycemic control,
surgery in eyes with macular edema, par- documented and transmitted to the refer- which may slow progression but not re-
ticularly those with clinically significant ring health care professional. For a de- verse neuronal loss. Effective symptom-
macular edema, with reduction of dou- tailed review of the evidence and further atic treatments are available for some


Standards of Medical Care

Table 14—Table of drugs to treat symptomatic DPN DPN. See Table 14 for examples of agents
to treat DPN pain.
Class Examples Typical doses*
Treatment of autonomic neuropathy
Tricyclic drugs Amitriptyline 10–75 mg at bedtime
Gastroparesis symptoms may improve
Nortriptyline 25–75 mg at bedtime
with dietary changes and prokinetic
Imipramine 25–75 mg at bedtime
agents such as metoclopramide or eryth-
Anticonvulsants Gabapentin 300–1,200 mg t.i.d.
romycin. Treatments for erectile dysfunc-
Carbamazepine 200–400 mg t.i.d.
tion may include phosphodiesterase type
Pregabalin† 100 mg t.i.d.
5 inhibitors, intracorporeal or intraure-
5-hydroxytryptamine and Duloxetine† 60–120 mg daily
thral prostaglandins, vacuum devices, or
norepinephrine uptake
penile prostheses. Interventions for other
manifestations of autonomic neuropathy
Substance P inhibitor Capsaicin cream 0.025–0.075% applied t.i.d. or q.i.d.
are described in the ADA statement on
*Dose response may vary; initial doses need to be low and titrated up; †has FDA indication for treatment of neuropathy (231). As with DPN treat-
painful diabetic neuropathy.
ments, these interventions do not change
the underlying pathology and natural his-
tory of the disease process, but may have a
positive impact on the quality of life of the
manifestations of DPN and autonomic Gastrointestinal neuropathies (e.g., patient.
neuropathy (231). esophageal enteropathy, gastroparesis,
constipation, diarrhea, fecal inconti-
Diagnosis of neuropathy nence) are common, and any section of E. Foot care
the gastrointestinal tract may be affected.
Distal symmetric polyneuropathy Gastroparesis should be suspected in in- Recommendations
Patients with diabetes should be screened dividuals with erratic glucose control or ● For all patients with diabetes, perform
annually for DPN using tests such as pin- with upper gastrointestinal symptoms an annual comprehensive foot exami-
prick sensation, vibration perception without other identified cause. Evalua- nation to identify risk factors predictive
(using a 128-Hz tuning fork), 10-g mono- tion of solid-phase gastric emptying using of ulcers and amputations. The foot ex-
filament pressure sensation at the distal double-isotope scintigraphy may be done amination can be accomplished in a
plantar aspect of both great toes and if symptoms are suggestive, but test re- primary care setting and should include
metatarsal joints, and assessment of ankle sults often correlate poorly with symp- the use of a monofilament, tuning fork,
reflexes. Combinations of more than one toms. Constipation is the most common palpation, and a visual examination. (B)
test have ⬎87% sensitivity in detecting lower gastrointestinal symptom but can ● Provide general foot self-care education
DPN. Loss of 10-g monofilament percep- alternate with episodes of diarrhea (232). to all patients with diabetes. (B)
tion and reduced vibration perception Diabetic autonomic neuropathy is ● A multidisciplinary approach is recom-
predict foot ulcers (231). also associated with genitourinary tract mended for individuals with foot ulcers
disturbances. In men, diabetic autonomic and high-risk feet, especially for those
Diabetic autonomic neuropathy neuropathy may cause erectile dysfunc- with a history of prior ulcer or amputa-
The symptoms and signs of autonomic tion and/or retrograde ejaculation. Evalu- tion. (B)
dysfunction should be elicited carefully ation of bladder dysfunction should be ● Refer patients who smoke, have loss of
during the history and physical examina- performed for individuals with diabetes protective sensation and structural ab-
tion. Major clinical manifestations of dia- who have recurrent urinary tract infec- normalities, or have history of prior
betic autonomic neuropathy include tions, pyelonephritis, incontinence, or a lower-extremity complications to foot
resting tachycardia, exercise intolerance, palpable bladder (232). care specialists for ongoing preventive
orthostatic hypotension, constipation, care and life-long surveillance. (C)
gastroparesis, erectile dysfunction, sudo- Symptomatic treatments ● Initial screening for peripheral arterial
motor dysfunction, impaired neurovas- DPN disease (PAD) should include a history
cular function, “brittle diabetes,” and The first step in management of patients for claudication and an assessment of
hypoglycemic autonomic failure (232). with DPN should be to aim for stable and the pedal pulses. Consider obtaining an
Cardiovascular autonomic neuropa- optimal glycemic control. Although con- ankle-brachial index (ABI), as many pa-
thy, a CVD risk factor (93), is the most trolled trial evidence is lacking, several tients with PAD are asymptomatic. (C)
studied and clinically important form of observational studies suggest that neuro- ● Refer patients with significant claudica-
diabetic autonomic neuropathy. Cardio- pathic symptoms improve not only with tion or a positive ABI for further vascu-
vascular autonomic neuropathy may be optimization of control, but also with the lar assessment, and consider exercise,
indicated by resting tachycardia (⬎100 avoidance of extreme blood glucose fluc- medications, and surgical options. (C)
bpm), orthostasis (a fall in systolic blood tuations. Patients with painful DPN may
pressure ⬎20 mmHg upon standing), or benefit from pharmacological treatment Amputation and foot ulceration, conse-
other disturbances in autonomic nervous of their symptoms: many agents have ef- quences of diabetic neuropathy and/or
system function involving the skin, pu- ficacy confirmed in published random- PAD, are common and major causes of
pils, or gastrointestinal and genitourinary ized controlled trials, with several FDA- morbidity and disability in people with
systems (232). approved for the management of painful diabetes. Early recognition and manage-


Position Statement

ment of risk factors can prevent or delay need extra-wide or -depth shoes. People VII. DIABETES CARE IN
adverse outcomes. with extreme bony deformities (e.g., SPECIFIC POPULATIONS
The risk of ulcers or amputations is Charcot foot) who cannot be accommo-
increased in people who have had diabe- dated with commercial therapeutic foot- A. Children and adolescents
tes ⬎10 years, are male, have poor glu- wear may need custom-molded shoes.
cose control, or have cardiovascular, Initial screening for PAD should in- 1. Type 1 diabetes
retinal, or renal complications. The fol- clude a history for claudication and an Three-quarters of all cases of type 1 dia-
lowing foot-related risk conditions are as- assessment of the pedal pulses. A diagnos- betes are diagnosed in individuals ⬍18
sociated with an increased risk of tic ABI should be performed in any pa- years of age. Because children are not sim-
amputation: tient with symptoms of PAD. Due to the ply “small adults,” it is appropriate to con-
● Peripheral neuropathy with loss of pro- high estimated prevalence of PAD in pa- sider the unique aspects of care and
tective sensation tients with diabetes and the fact that many management of children and adolescents
● Altered biomechanics (in the presence patients with PAD are asymptomatic, an with type 1 diabetes. Children with dia-
of neuropathy) ADA consensus statement on PAD (233) betes differ from adults in many respects,
● Evidence of increased pressure (ery- including insulin sensitivity related to
suggested that a screening ABI be per-
thema, hemorrhage under a callus) sexual maturity, physical growth, ability
formed in patients older than 50 years of
● Bony deformity to provide self-care, and unique neuro-
age and be considered in patients younger
● PAD (decreased or absent pedal pulses) logic vulnerability to hypoglycemia. At-
than 50 years who have other PAD risk tention to such issues as family dynamics,
● A history of ulcers or amputation
factors (e.g., smoking, hypertension, hy- developmental stages, and physiologic
● Severe nail pathology
perlipidemia, or duration of diabetes ⬎10 differences related to sexual maturity are
years). Refer patients with significant all essential in developing and imple-
All individuals with diabetes should re- symptoms or a positive ABI for further menting an optimal diabetes regimen. Al-
ceive an annual foot examination to iden- vascular assessment, and consider exer- though recommendations for children
tify high-risk foot conditions. This cise, medication, and surgical options and adolescents are less likely to be based
examination should include assessment (233). on clinical trial evidence, because of cur-
of protective sensation, foot structure and Patients with diabetes and high-risk rent and historical restraints placed on
biomechanics, vascular status, and skin foot conditions should be educated re- conducting research in children, expert
integrity. Evaluation of neurological sta- garding their risk factors and appropriate opinion and a review of available and rel-
tus in the low-risk foot should include a management. Patients at risk should un- evant experimental data are summarized
quantitative somatosensory threshold derstand the implications of the loss of in a recent ADA statement (237).
test, using the Semmes-Weinstein 5.07 protective sensation; the importance of Ideally, the care of a child or adoles-
(10-g) monofilament. The skin should be foot monitoring on a daily basis; the cent with type 1 diabetes should be pro-
assessed for integrity, especially between proper care of the foot, including nail and vided by a multidisciplinary team of
the toes and under the metatarsal heads. skin care; and the selection of appropriate specialists trained in the care of children
Patients at low risk may benefit from ed- footwear. Patients with loss of protective with pediatric diabetes. At the very least,
ucation on foot care and footwear. sensation should be educated on ways to education of the child and family should
The presence of erythema, warmth, substitute other sensory modalities (hand be provided by health care providers
or callus formation may indicate areas of palpation, visual inspection) for surveil- trained and experienced in childhood di-
tissue damage with impending break- lance of early foot problems. The patient’s abetes and sensitive to the challenges
down. Bony deformities, limitation in understanding of these issues and their posed by diabetes in this age-group. At
joint mobility, and problems with gait physical ability to conduct proper foot the time of initial diagnosis, it is essential
and balance should be assessed. People surveillance and care should be assessed. that diabetes education is provided in a
with one or more high-risk foot condi- Patients with visual difficulties, physical timely fashion, with the expectation that
tions should be evaluated more fre- the balance between adult supervision
constraints preventing movement, or cog-
quently for the development of additional and self-care should be defined by, and
nitive problems that impair their ability to
risk factors. People with neuropathy will evolve according to, physical, psy-
assess the condition of the foot and to in-
should have a visual inspection of their chological, and emotional maturity. MNT
feet at every visit with a health care stitute appropriate responses will need should be provided at diagnosis, and at
professional. other people, such as family members, to least annually thereafter, by an individual
People with neuropathy (e.g., ery- assist in their care. experienced with the nutritional needs of
thema, warmth, callus, or measured pres- For a detailed review of the evidence the growing child and the behavioral is-
sure) or evidence of increased plantar and further discussion, see ADA’s techni- sues that have an impact on adolescent
pressure may be adequately managed cal review and position statement on pre- diets.
with well-fitted walking shoes or athletic ventive foot care (234,235).
shoes that cushion the feet and redistrib- Foot ulcers and wound care may re- a. Glycemic control
ute pressure. Callus can be debrided with quire care by a podiatrist, orthopedic or
a scalpel by a foot care specialist or other vascular surgeon, or rehabilitation spe- Recommendations
health professional with experience and cialist experienced in the management of ● Consider age when setting glycemic
training in foot care. People with bony individuals with diabetes. For a complete goals in children and adolescents with
deformities (e.g., hammertoes, promi- discussion, see ADA’s consensus state- type 1 diabetes, with less stringent goals
nent metatarsal heads, bunions) may ment on diabetic foot wound care (236). for younger children. (E)


Standards of Medical Care

Table 15—Plasma blood glucose and A1C goals for type 1 diabetes by age-group

Plasma blood glucose

goal range (mg/dl)
Before Bedtime/
Values by age (years) meals overnight A1C Rationale
Toddlers and preschoolers (0–6) 100–180 110–200 ⬍8.5% (but ⬎7.5%) High risk and vulnerability to
School age (6–12) 90–180 100–180 ⬍8% Risks of hypoglycemia and relatively low
risk of complications prior to puberty
Adolescents and young adults (13–19) 90–130 90–150 ⬍7.5% ● Risk of severe hypoglycemia
● Developmental and psychological
● A lower goal (⬍7.0%) is reasonable if
it can be achieved without excessive
Key concepts in setting glycemic goals:
● Goals should be individualized and lower goals may be reasonable based on benefit-risk assessment.
● Blood glucose goals should be higher than those listed above in children with frequent hypoglycemia or hypoglycemia unawareness.
● Postprandial blood glucose values should be measured when there is a discrepancy between pre-prandial blood glucose values and A1C levels.

While current standards for diabetes fits on long-term health outcomes of reached with 3– 6 months of lifestyle
management reflect the need to maintain achieving a lower A1C must be weighed intervention, pharmacologic treatment
glucose control as near to normal as safely against the unique risks of hypoglycemia should be initiated. (E)
possible, special consideration must be and the difficulties achieving near- ● Pharmacologic treatment of hyperten-
given to the unique risks of hypoglycemia normoglycemia in children and youth. sion (systolic or diastolic blood pres-
in young children. Glycemic goals need to Age-specific glycemic and A1C goals are sure consistently above the 95th
be modified to take into account the fact presented in Table 15. percentile for age, sex, and height or
that most children ⬍6 or 7 years of age consistently ⬎130/80 mmHg, if 95%
have a form of “hypoglycemic unaware- b. Screening and management of chronic exceeds that value) should be initiated
ness.” Their counterregulatory mecha- complications in children and adoles- as soon as the diagnosis is confirmed.
nisms are immature, and they may lack cents with type 1 diabetes (E)
the cognitive capacity to recognize and ● ACE inhibitors should be considered
respond to hypoglycemic symptoms, i. Nephropathy for the initial treatment of hyperten-
placing them at greater risk for severe hy- sion. (E)
poglycemia and its sequelae. In addition, Recommendations
● Annual screening for microalbumin-
and unlike the case in adults, children Hypertension in childhood is defined as
younger than 5 years of age are at risk for uria, with a random spot urine sample an average systolic or diastolic blood pres-
permanent cognitive impairment after ep- for microalbumin-to-creatinine ratio, sure ⱖ95th percentile for age, sex, and
isodes of severe hypoglycemia (238 – should be initiated once the child is 10 height percentile measured on at least
240). Extensive evidence indicates that years of age and has had diabetes for 5 three separate days. “High-normal” blood
near normalization of blood glucose lev- years. (E) pressure is defined as an average systolic
● Confirmed, persistently elevated mi-
els is seldom attainable in children and or diastolic blood pressure ⱖ90th but
adolescents after the honeymoon (remis- croalbumin levels on two additional ⬍95th percentile for age, sex, and height
sion) period. The A1C level achieved in urine specimens should be treated with percentile measured on at least three sep-
the “intensive” adolescent cohort of the an ACE inhibitor titrated to normaliza- arate days. Normal blood pressure levels
DCCT group was ⬎1% higher than that tion of microalbumin excretion if pos- for age, sex, and height and appropriate
achieved by adult DCCT subjects and sible. (E) methods for determinations are available
above current ADA recommendations for online at www.nhlbi.nih.gov/health/prof/
patients in general. However, the in- ii. Hypertension heart/hbp/hbp_ped.pdf.
creased frequency of use of basal bolus
regimens (including insulin pumps) in Recommendations iii. Dyslipidemia
youth from infancy through adolescence ● Treatment of high-normal blood pres-
has been associated with more children sure (systolic or diastolic blood pres- Recommendations
reaching ADA blood glucose targets sure consistently above the 90th
(241,242) in those families in which both percentile for age, sex, and height)
parents and the child with diabetes are should include dietary intervention Screening
motivated to perform the required diabe- and exercise aimed at weight control ● If there is a family history of hypercho-
tes-related tasks. and increased physical activity, if ap- lesterolemia (total cholesterol ⬎240
In selecting glycemic goals, the bene- propriate. If target blood pressure is not mg/dl) or a cardiovascular event before


Position Statement

age 55 years, or if family history is un- equivalent to that seen in adults, as well as absorption and other gastrointestinal
known, then a fasting lipid profile efficacy in lowering LDL cholesterol lev- problems, and unexplained hypoglyce-
should be performed on children ⬎2 els, improving endothelial function, and mia or erratic blood glucose concentrations.
years of age soon after diagnosis (after causing regression of carotid intimal
glucose control has been established). thickening (250 –252). No statin is ap- vi. Hypothyroidism
If family history is not of concern, then proved for use under the age of 10, and
the first lipid screening should be per- statin treatment should generally not be Recommendations
formed at puberty (ⱖ10 years). All chil- used in type 1 children before this age. ● Patients with type 1 diabetes should be
dren diagnosed with diabetes at or after screened for thyroid peroxidase and
puberty should have a fasting lipid pro- iv. Retinopathy thyroglobulin antibodies at diagnosis.
file performed soon after diagnosis (E)
(after glucose control has been estab- Recommendations ● Thyroid-stimulating hormone (TSH)
lished). (E) ● The first ophthalmologic examination concentrations should be measured af-
● For both age groups, if lipids are abnor- should be obtained once the child is ter metabolic control has been estab-
mal, annual monitoring is recom- ⱖ10 years of age and has had diabetes lished. If normal, they should be
mended. If LDL cholesterol values are for 3–5 years. (E) rechecked every 1–2 years, or if the pa-
within the accepted risk levels (⬍100 ● After the initial examination, annual tient develops symptoms of thyroid
mg/dl [2.6 mmol/l]), a lipid profile routine follow-up is generally recom- dysfunction, thyromegaly, or an abnor-
should be repeated every 5 years. (E) mended. Less frequent examinations mal growth rate. Free T4 should be
may be acceptable on the advice of an measured if TSH is abnormal. (E)
Treatment eye care professional. (E)
● Initial therapy should consist of optimi- Auto-immune thyroid disease is the most
zation of glucose control and MNT Although retinopathy most commonly common autoimmune disorder associ-
using a Step 2 American Heart Associ- occurs after the onset of puberty and after ated with diabetes, occurring in 17–30%
ation diet aimed at a decrease in the 5–10 years of diabetes duration, it has of patients with type 1 diabetes (255). The
amount of saturated fat in the diet. (E) been reported in prepubertal children presence of thyroid auto-antibodies is
● After the age of 10, the addition of a and with diabetes duration of only 1–2 predictive of thyroid dysfunction (gener-
statin is recommended in patients who, years. Referrals should be made to eye ally hypothyroidism, but less commonly
after MNT and lifestyle changes, have care professionals with expertise in hyperthyroidism) (256). Subclinical hy-
LDL cholesterol ⬎160 mg/dl (4.1 diabetic retinopathy, an understanding of pothyroidism may be associated with
mmol/l) or have LDL cholesterol ⬎130 the risk for retinopathy in the pediatric increased risk of symptomatic hypoglyce-
mg/dl (3.4 mmol/l) and one or more population, and experience in counsel- mia (257) and with reduced linear growth
CVD risk factors. (E) ing the pediatric patient and family on (258). Hyperthyroidism alters glucose
● The goal of therapy is an LDL choles- the importance of early prevention/ metabolism, potentially resulting in dete-
terol value ⬍100 mg/dl (2.6 mmol/l). intervention. rioration of metabolic control.
v. Celiac disease c. “Adherence”
People diagnosed with type 1 diabetes in No matter how sound the medical regi-
childhood have a high risk of early sub- Recommendations men, it can only be as good as the ability of
clinical (243–245) and clinical (246) ● Patients with type 1 diabetes who be- the family and/or individual to implement
CVD. Although intervention data are come symptomatic for celiac disease it. Family involvement in diabetes re-
lacking, the American Heart Association should be tested by measuring tissue mains an important component of opti-
(AHA) categorizes type 1 children in the transglutaminase or anti-endomysial mal diabetes management throughout
highest tier for cardiovascular risk, and antibodies, with documentation of nor- childhood and into adolescence. Health
recommends both lifestyle and pharma- mal serum IgA levels. (E) care providers who care for children and
cologic treatment for those with elevated ● Children with positive antibodies adolescents, therefore, must be capable of
LDL cholesterol levels (247). Initial ther- should be referred to a gastroenterolo- evaluating the behavioral, emotional, and
apy should be with a Step 2 AHA diet, gist for evaluation. (E) psychosocial factors that interfere with
which restricts saturated fat to 7% of total ● Children with confirmed celiac disease implementation and then must work with
calories and restricts dietary cholesterol to should have consultation with a dieti- the individual and family to resolve prob-
200 mg/day. Data from randomized clin- tian and be placed on a gluten-free diet. lems that occur and/or to modify goals as
ical trials in children as young as 7 (E) appropriate.
months of age indicate that this diet is safe
and does not interfere with normal Celiac disease is an immune-mediated d. School and day care.
growth and development (248,249). disorder that occurs with increased fre- Since a sizable portion of a child’s day is
For children over the age of 10 with quency in patients with type 1 diabetes spent in school, close communication
persistent elevation of LDL cholesterol (1–16% of individuals compared with with school or day care personnel is es-
despite lifestyle therapy, statins should be 0.3–1% in the general population) sential for optimal diabetes management,
considered. Neither long-term safety nor (253,254). Symptoms of celiac disease in- safety, and maximal academic opportuni-
cardiovascular outcome efficacy has been clude diarrhea, weight loss or poor weight ties. See Section VIII.B, “Diabetes Care in
established for children. However, recent gain, growth failure, abdominal pain, the School and Day Care Setting,” for fur-
studies have shown short-term safety chronic fatigue, malnutrition due to mal- ther discussion.


Standards of Medical Care

2. Type 2 diabetes weeks of gestation, as defined by first- agement of diabetes before and during
The incidence of type 2 diabetes in ado- trimester A1C concentrations. There is no pregnancy. The goals of preconception
lescents is increasing, especially in ethnic threshold for A1C values below which care are to 1) involve and empower the
minority populations (20). Distinction risk disappears entirely. However, mal- patient in the management of her diabe-
between type 1 and type 2 diabetes in formation rates above the 1–2% back- tes, 2) achieve the lowest A1C test results
children can be difficult, since autoanti- ground rate of nondiabetic pregnancies possible without excessive hypoglycemia,
gens and ketosis may be present in a sub- appear to be limited to pregnancies in 3) ensure effective contraception until sta-
stantial number of patients with features which first-trimester A1C concentrations ble and acceptable glycemia is achieved,
of type 2 diabetes (including obesity and are ⬎1% above the normal range for a and 4) identify, evaluate, and treat long-
acanthosis nigricans). Such a distinction nondiabetic pregnant woman. term diabetic complications such as reti-
at the time of diagnosis is critical since Preconception care of diabetes ap- nopathy, nephropathy, neuropathy,
treatment regimens, educational ap- pears to reduce the risk of congenital mal- hypertension, and CHD.
proaches, and dietary counsel will differ formations. Five nonrandomized studies Among the drugs commonly used in
markedly between the two diagnoses. Be- compared rates of major malformations in the treatment of patients with diabetes, a
cause type 2 diabetes has a significant in- infants between women who participated number may be relatively or absolutely
cidence of hypertension, dyslipidemia, in preconception diabetes care programs contraindicated during pregnancy. St-
and microalbuminuria at diagnosis (259), and women who initiated intensive diabe- atins are category X (contraindicated for
it is recommended that screening for the tes management after they were already use in pregnancy) and should be discon-
comorbidities and complications of dia- pregnant. The preconception care pro- tinued before conception, as should ACE
betes, including fasting lipid profile, mi- grams were multidisciplinary and de- inhibitors (265). ARBs are category C
croalbuminuria assessment, and dilated signed to train patients in diabetes self- (risk cannot be ruled out) in the first tri-
eye examinations, begin at the time of di- management with diet, intensified insulin mester, but category D (positive evidence
agnosis. The ADA consensus statement therapy, and SMBG. Goals were set to of risk) in later pregnancy, and should
(22) provides guidance on the preven- achieve normal blood glucose concentra- generally be discontinued before preg-
tion, screening, and treatment of type 2 tions, and ⬎80% of subjects achieved nancy. Among the oral antidiabetic
diabetes and its comorbidities in young normal A1C concentrations before they agents, metformin and acarbose are clas-
people. became pregnant (260 –264). In all five sified as category B (no evidence of risk in
studies, the incidence of major congenital humans) and all others as category C. Po-
B. Preconception care malformations in women who partici- tential risks and benefits of oral antidia-
pated in preconception care (range 1.0 – betic agents in the preconception period
1.7% of infants) was much lower than the must be carefully weighed, recognizing
Recommendations incidence in women who did not partici- that data are insufficient to establish the
● A1C levels should be as close to normal
pate (range 1.4 –10.9% of infants). One safety of these agents in pregnancy.
as possible (⬍7%) in an individual pa- limitation of these studies is that partici- For further discussion of preconcep-
tient before conception is attempted. pation in preconception care was self- tion care, see ADA’s technical review
(B) selected rather than randomized. Thus, it (266) and position statement (267) on
● All women with diabetes and child-
is impossible to be certain that the lower this subject.
bearing potential should be educated malformation rates resulted fully from
about the need for good glucose control improved diabetes care. Nonetheless, the
before pregnancy and should partici- C. Older adults
evidence supports the concept that mal-
pate in family planning. (E) formations can be reduced or prevented
● Women with diabetes who are contem-
by careful management of diabetes before Recommendations
plating pregnancy should be evaluated pregnancy. ● Older adults who are functional, cogni-
and, if indicated, treated for diabetic Planned pregnancies greatly facilitate tively intact, and have significant life
retinopathy, nephropathy, neuropathy, preconception diabetes care. Unfortu- expectancy should receive diabetes
and CVD. (E) nately, nearly two-thirds of pregnancies treatment using goals developed for
● Medications used by such women
in women with diabetes are unplanned, younger adults. (E)
should be evaluated before conception, leading to a persistent excess of malfor- ● Glycemic goals for older adults who do
since drugs commonly used to treat di- mations in infants of diabetic mothers. To not meet the above criteria may be re-
abetes and its complications may be minimize the occurrence of these devas- laxed using individual criteria, but hy-
contraindicated or not recommended tating malformations, standard care for all perglycemia leading to symptoms or
in pregnancy, including statins, ACE women with diabetes who have child- risk of acute hyperglycemic complica-
inhibitors, ARBs, and most noninsulin bearing potential should include 1) edu- tions should be avoided in all patients.
therapies. (E) cation about the risk of malformations (E)
associated with unplanned pregnancies ● Other cardiovascular risk factors
Major congenital malformations remain and poor metabolic control and 2) use of should be treated in older adults with
the leading cause of mortality and serious effective contraception at all times, unless consideration of the timeframe of ben-
morbidity in infants of mothers with type the patient has good metabolic control efit and the individual patient. Treat-
1 and type 2 diabetes. Observational stud- and is actively trying to conceive. ment of hypertension is indicated in
ies indicate that the risk of malformations Women contemplating pregnancy virtually all older adults, and lipid and
increases continuously with increasing need to be seen frequently by a multidis- aspirin therapy may benefit those with
maternal glycemia during the first 6 – 8 ciplinary team experienced in the man- life expectancy at least equal to the


Position Statement

timeframe of primary or secondary pre- so and be treated using the goals for VIII. DIABETES CARE IN
vention trials. (E) younger adults with diabetes. SPECIFIC SETTINGS
● Screening for diabetic complications For patients with advanced diabetes
should be individualized in older complications, life-limiting comorbid ill- A. Diabetes care in the hospital
adults, but particular attention should ness, or substantial cognitive or func-
be paid to complications that would tional impairment, it is reasonable to set Recommendations
lead to functional impairment. (E) less intensive glycemic target goals. These ● All patients with diabetes admitted to

patients are less likely to benefit from re- the hospital should have their diabetes
ducing the risk of microvascular compli- clearly identified in the medical record.
Diabetes is an important health condition cations and more likely to suffer serious (E)
for the aging population. At least 20% of ● All patients with diabetes should have
adverse effects from hypoglycemia. How-
patients over the age of 65 years have di- ever, patients with poorly controlled dia- an order for blood glucose monitoring,
abetes, and this number can be expected betes may be subject to acute with results available to all members of
to grow rapidly in the coming decades. complications of diabetes, including de- the health care team. (E)
● Goals for blood glucose levels:
Older individuals with diabetes have hydration, poor wound healing, and hy- ● Critically ill patients: blood glucose
higher rates of premature death, func- perglycemic hyperosmolar coma.
tional disability, and coexisting illnesses levels should be kept as close to 110
Glycemic goals at a minimum should
such as hypertension, CHD, and stroke mg/dl (6.1 mmol/l) as possible and
avoid these consequences. generally ⬍140 mg/dl (7.8 mmol/l).
than those without diabetes. Older adults Although control of hyperglycemia
with diabetes are also at greater risk than (A) These patients require an intrave-
may be important in older individuals nous insulin protocol that has dem-
other older adults for several common ge- with diabetes, greater reductions in mor-
riatric syndromes, such as polypharmacy, onstrated efficacy and safety in
bidity and mortality may result from con- achieving the desired glucose range
depression, cognitive impairment, uri- trol of other cardiovascular risk factors
nary incontinence, injurious falls, and without increasing risk for severe hy-
than from tight glycemic control alone. poglycemia. (E)
persistent pain. There is strong evidence from clinical tri- ● Non– critically ill patients: there is no
The American Geriatric Society’s als of the value of treating hypertension in
guidelines for improving the care of the clear evidence for specific blood glu-
the elderly (269). There is less evidence cose goals. Since cohort data suggest
older person with diabetes mellitus (268)
for lipid-lowering and aspirin therapy, al- that outcomes are better in hospital-
have influenced the following discussion
though the benefits of these interventions ized patients with fasting glucose
and recommendations. The care of older
for primary and secondary prevention are ⬍126 mg/dl and all random glucoses
adults with diabetes is complicated by
likely to apply to older adults whose life ⬍180 –200, these goals are reason-
their clinical and functional heterogene-
expectancies equal or exceed the time- able if they can be safely achieved.
ity. Some older individuals developed di-
frames seen in clinical trials. Insulin is the preferred drug to treat
abetes years earlier and may have
Special care is required in prescribing hyperglycemia in most cases. (E)
significant complications; others who are ● Due to concerns regarding the risk of
newly diagnosed may have had years of and monitoring pharmacologic therapy in
older adults. Metformin is often contrain- hypoglycemia, some institutions may
undiagnosed diabetes with resultant com- consider these blood glucose levels to
plications or may have few complications dicated because of renal insufficiency or
significant heart failure. TZDs can cause be overly aggressive for initial targets.
from the disease. Some older adults with Through quality improvement, gly-
diabetes are frail and have other underly- fluid retention, which may exacerbate or
lead to heart failure. They are contraindi- cemic goals should systematically be
ing chronic conditions, substantial diabe- reduced to the recommended levels.
tes-related comorbidity, or limited cated in patients with CHF (New York
Heart Association class III and IV), and if (E)
physical or cognitive functioning. Other ● Scheduled prandial insulin doses
older individuals with diabetes have little used at all should be used very cautiously
should be appropriately timed in rela-
comorbidity and are active. Life expectan- in those with, or at risk for, milder degrees
tion to meals and should be adjusted
cies are highly variable for this popula- of CHF. Sulfonylureas, other insulin
according to point-of-care glucose lev-
tion, but often longer than clinicians secretagogues, and insulin can cause hy-
els. The traditional sliding-scale insulin
realize. Providers caring for older adults poglycemia. Insulin use requires that pa- regimens are ineffective as mono-
with diabetes must take this heterogeneity tients or caregivers have good visual and therapy and are generally not recom-
into consideration when setting and pri- motor skills and cognitive ability. Drugs mended. (C)
oritizing treatment goals. should be started at the lowest dose and ● Using correction dose or “supplemen-
There are few long-term studies in titrated up gradually until targets are tal” insulin to correct premeal hyper-
older adults demonstrating the benefits of reached or side effects develop. glycemia in addition to scheduled
intensive glycemic, blood pressure, and Screening for diabetic complications prandial and basal insulin is recom-
lipid control. Patients who can be ex- in older adults also should be individual- mended. (E)
pected to live long enough to reap the ized. Particular attention should be paid ● Glucose monitoring with orders for
benefits of long-term intensive diabetes to complications that can develop over correction insulin should be initiated in
management and who are active, have short periods of time and/or that would any patient not known to be diabetic
good cognitive function, and are willing significantly impair functional status, who receives therapy associated with
to undertake the responsibility of self- such as visual and lower-extremity com- high risk for hyperglycemia, including
management should be encouraged to do plications. high-dose glucocorticoids therapy, ini-


Standards of Medical Care

tiation of enteral or parenteral nutri- the year 2000, 12.4% of hospital dis- admission blood glucose averaged 109.8
tion, or other medications such as charges in the U.S. listed diabetes as a di- mg/dl (6.1 mmol/l), the relative risk for
octreotide or immunosuppressive agnosis, but this is likely an in-hospital mortality was increased signif-
medications. (B) If hyperglycemia is underestimate. The prevalence of diabe- icantly. When diabetes was present and
documented and persistent, initiation tes in hospitalized adults is conservatively admission glucose averaged 180 mg/dl
of basal/bolus insulin therapy may be estimated at 12–25%, depending on the (10 mmol/l), risk of death was moderately
necessary. Such patients should be thoroughness used in identifying pa- increased compared with patients who
treated to the same glycemic goals as tients. In the year 2003, there were 5.1 had diabetes but less hyperglycemia on
patients with known diabetes. (E) million hospitalizations with diabetes as a admission (277). Another study (278)
● A plan for treating hypoglycemia listed diagnosis, a 2.3-fold increase over demonstrated a strong independent rela-
should be established for each patient. 1980 rates (274). tionship between admission blood glu-
Episodes of hypoglycemia in the hospi- The management of hyperglycemia in cose values and both in-hospital and
tal should be tracked. (E) the hospital was traditionally considered 1-year mortality; rates were significantly
● All patients with diabetes admitted to secondary in importance to the condition lower in subjects with admission plasma
the hospital should have an A1C ob- that prompted admission (273). glucose ⬍100.8 mg/dl (5.6 mmol/l) than
tained if the result of testing in the pre- A rapidly growing body of literature in those with plasma glucose 199.8 mg/dl
vious 2–3 months is not available. (E) supports targeted glucose control in the (11 mmol/l).
● A diabetes education plan including hospital setting for potential improved These studies focused on admission
“survival skills education” and fol- mortality, morbidity, and health eco- blood glucose as a predictor of outcomes,
low-up should be developed for each nomic outcomes. Hyperglycemia in the rather than inpatient glycemic manage-
patient. (E) hospital may result from stress; decom- ment per se. Higher admission plasma
● Patients with hyperglycemia in the hos- pensation of type 1, type 2, or other forms glucose levels in patients with a prior his-
pital who do not have a diagnosis of of diabetes; and/or may be iatrogenic due tory of diabetes could reflect the degree of
diabetes should have appropriate plans to withholding of antihyperglycemic glycemic control in the outpatient setting,
for follow-up testing and care docu- medications or administration of hyper- thus linking outpatient glycemic control
mented at discharge. (E) glycemia-provoking agents such as glu- to outcomes in the inpatient population.
cocorticoids or vasopressors. In patients without a prior history of dia-
The management of diabetes in the hos- betes, admission hyperglycemia could
pital is extensively reviewed in an ADA represent case finding of patients with
technical review (270). This review, as 1. In-hospital hyperglycemia and previously undiagnosed diabetes, an un-
well as a consensus statement by the outcomes masking of risk in a population at high
American Association of Clinical Endocri- a. General medicine and surgery. Ob- risk for diabetes, or more severe illness at
nologists (AACE) with cosponsorship by servational studies suggest an association admission.
ADA (271,272) and a report of a joint between hyperglycemia and increased In the initial Diabetes and Insulin-
ADA-AACE task force on the topic (273), mortality. Surgical patients with at least Glucose Infusion in Acute Myocardial In-
forms the basis for the discussion and one blood glucose value ⬎220 mg/dl farction study (279,280), insulin-glucose
guidelines in this section. (12.2 mmol/l) on the first postoperative infusion followed by at least 3 months of
The literature on hospitalized pa- day have significantly higher infection subcutaneous insulin treatment in dia-
tients with hyperglycemia typically de- rates (275). betic patients with acute myocardial in-
scribes three categories: When admissions on general medi- farction improved long-term survival.
cine and surgery units were studied, pa- Mean blood glucose in the intensive insu-
● Medical history of diabetes: diabetes tients with new hyperglycemia had lin intervention arm was 172.8 mg/dl (9.6
has been previously diagnosed and ac- significantly increased in-hospital mortal- mmol/l), compared with 210.6 mg/dl
knowledged by the patient’s treating ity, as did patients with known diabetes. (11.7 mmol/l) in the “conventional”
physician. In addition, length of stay was higher for group. The broad range of blood glucose
● Unrecognized diabetes: hyperglycemia the new hyperglycemic group, and pa- levels within each arm limits the ability to
(fasting blood glucose 126 mg/dl or tients in either hyperglycemic group were define specific blood glucose target
random blood glucose 200 mg/dl) oc- more likely to require intensive care unit thresholds.
curring during hospitalization and con- (ICU) care and transitional or nursing Three more recent studies (281–283)
firmed as diabetes after hospitalization home care. Better outcomes were demon- using an insulin-glucose infusion did not
by standard diagnostic criteria but un- strated in patients with fasting and admis- show a reduction in mortality in the inter-
recognized as diabetes by the treating sion blood glucose ⬍126 mg/dl (7 vention groups. However, in each of these
physician during hospitalization. mmol/l) and all random blood glucose studies, blood glucose levels were posi-
● Hospital-related hyperglycemia: hyper- levels ⬍200 mg/dl (11.1 mmol/l) (276). tively correlated with mortality. In the
glycemia (fasting blood glucose 126 b. CVD and critical care. A significant Hyperglycemia: Intensive Insulin Infu-
mg/dl or random blood glucose ⱖ200 relationship exists between blood glucose sion In Infarction (HI-5) Study, a decrease
mg/dl) occurring during the hospital- levels and mortality in the setting of acute in both CHF and reinfarction was ob-
ization that reverts to normal after hos- myocardial infarction. A meta-analysis of served in the group receiving intensive in-
pital discharge. 15 studies compared in-hospital mortal- sulin therapy for at least 24 h.
ity in both hyper- and normoglycemic pa- c. Cardiac surgery. Attainment of tar-
The prevalence of diabetes in hospitalized tients with and without diabetes. In geted glucose control in patients with di-
adult patients is not precisely known. In subjects without known diabetes whose abetes undergoing cardiac surgery is


Position Statement

associated with reduced mortality and glycemic goals is less definitive. Epidemi- TZDs are not suitable for initiation in
risk of deep sternal wound infections ologic and physiologic data suggest that the hospital because of their delayed onset
(284,285) and supports the concept that lower blood glucose levels are associated of effect. In addition, they increase intra-
perioperative hyperglycemia is an inde- with improved outcomes. Glycemic tar- vascular volume, a particular problem in
pendent predictor of infection in patients gets similar to those of outpatients may be those predisposed to CHF and potentially
with diabetes (286), with the lowest mor- difficult to achieve in the hospital due to a problem for patients with hemody-
tality in patients with blood glucose ⬍150 the effects of stress hyperglycemia, altered namic changes related to admission diag-
mg/dl (8.3 mmol/l) (287). nutritional intake, and multiple interrup- noses (e.g., acute coronary ischemia) or
d. Critical care. A mixed group of pa- tions to medical care. Blood glucose levels interventions common in hospitalized pa-
tients with and without diabetes admitted shown to be associated with improved tients. Pramlintide and exenatide work
to a surgical ICU (SICU) were random- outcomes in these patients (fasting glu- mainly by reducing postprandial hyper-
ized to receive intensive insulin therapy cose ⬍126 mg/dl and all blood glucose glycemia, so they would not be appropri-
(target blood glucose 80 –110 mg/dl readings ⬍180 –200 mg/dl) would ap- ate for patients not eating (NPO) or with
[4.4 – 6.1 mmol/l]) or conventional ther- pear reasonable, if they can be safely reduced caloric consumption. Further-
apy. Intensive insulin therapy achieved a achieved. more, initiation of these drugs in the in-
mean blood glucose of 103 mg/dl (5.7 In both the critical care and non– patient setting would be problematic, due
mmol/l) and was associated with reduced critical care venue, glycemic goals must to alterations in normal food intake and
mortality during the ICU stay and de- take into account the individual patient’s their propensity to induce nausea ini-
creased overall in-hospital mortality situation as well as hospital system sup- tially. There is limited experience and no
(288). Hospital and ICU survival were lin- port for achieving these goals. A continu- published data on the DPP-IV inhibitors
early associated with ICU glucose levels, ous quality improvement strategy may in the hospital setting, but there are no
with the highest survival rates occurring facilitate gradual improvement in mean specific safety concerns. They are mainly
in patients achieving an average blood glycemia hospital-wide. effective on postprandial glucose and
glucose ⬍110 mg/dl (6.1 mmol/l) (289). therefore would have limited effect in pa-
A subsequent study of a similar inter- tients who are not eating.
vention in patients in a medical ICU 3. Treatment options in hospitalized In summary, each of the major classes
(MICU) (290) showed that the group re- patients of noninsulin glucose-lowering drugs has
ceiving intensive insulin therapy had re- a. Noninsulin glucose-lowering agents. significant limitations for inpatient use.
duced morbidity but no difference in No large studies have investigated the po- Additionally, they provide little flexibility
mortality overall. Death rates were signif- tential roles of various noninsulin glu- or opportunity for titration in a setting
icantly lower in those patients who were cose-lowering agents on outcomes of where acute changes often demand these
treated for ⬎3 days; these patients could hospitalized patients with diabetes. Use of characteristics. Therefore insulin, when
not be identified before therapy. A recent the various noninsulin classes in the inpa- used properly, is preferred for the major-
meta-analysis concluded that insulin tient setting presents some specific issues. ity of hyperglycemic patients in the hos-
therapy in critically ill patients had a ben- The long action of sulfonylureas and pital setting.
eficial effect on short-term mortality in their predisposition to hypoglycemia in b. Insulin
different clinical settings (291). patients not consuming their normal nu- i. Subcutaneous insulin therapy. Subcu-
trition serve as relative contraindications taneous insulin therapy may be used to
to routine use of these agents in the hos- attain glucose control in most hospital-
2. Glycemic targets in hospitalized pital (294). While the meglitinides, repa- ized patients with diabetes outside of the
patients glinide and neteglinide, theoretically critical care arena. The components of the
There is relatively strong evidence from would produce less hypoglycemia than daily insulin dose requirement can be met
randomized controlled trials for a glyce- sulfonylureas, lack of clinical trial data for by a variety of insulins, depending on the
mic target of blood glucose ⬍110 mg/dl these agents, and the fact that they are particular hospital situation. Subcutane-
(6.1 mmol/l) in patients in critical care primarily prandial in effect, would pre- ous insulin therapy should cover both
units (288 –290). However, the incidence clude their use. The major limitation to basal and nutritional needs, and is subdi-
of severe hyperglycemia (blood glucose metformin use in the hospital is a number vided into scheduled insulin and supple-
⬍40 mg/dl) in the MICU study was of specific contraindications to its use, re- mental, or correction-dose, insulin.
18.7%, much greater than the 5.1% ob- lated to risk of lactic acidosis, many of Correction-dose insulin therapy is an im-
served in the SICU population. The iden- which occur in the hospital. The most portant adjunct to scheduled insulin,
t i fi c a t i o n o f h y p o g l y c e m i a a s a n common risk factors for lactic acidosis in both as a dose-finding strategy and as a
independent risk factor for death in the metformin-treated patients are cardiac supplement when rapid changes in insu-
MICU population may merit caution in disease, including CHF, hypoperfusion, lin requirements lead to hyperglycemia. If
widely promoting the 80 –110 mg/dl tar- renal insufficiency, old age, and chronic correction doses are frequently required,
get range for all critically ill populations pulmonary disease (295). Lactic acidosis the appropriate scheduled insulin doses
(292). Two recent trials were discontin- is a rare complication in the outpatient should be increased to accommodate the
ued because of difficulty achieving de- setting (296), despite the relative fre- increased insulin needs. There are no
sired target ranges of blood glucose and quency of risk factors (297). However, in studies comparing human regular insulin
unacceptably high rates of hypoglycemia the hospital the risks of hypoxia, hypo- with rapid-acting analogs for use as cor-
(293,293a). perfusion, and renal insufficiency are rection-dose insulin.
For patients on general medical- much higher, and it is prudent to avoid The traditional “sliding-scale” insulin
surgical units, the evidence for specific the use of metformin in most patients. regimens, usually consisting of regular in-


Standards of Medical Care

sulin without any intermediate or long- Many institutions use insulin infusion conditions of hospitalization. For patients
acting insulins, have been shown to be algorithms that can be implemented by conducting self-management in the hos-
ineffective when used as monotherapy in nursing staff. Although numerous algo- pital, it is imperative that basal, prandial,
patients with an established insulin re- rithms have been published, there have and correction doses of insulin and results
quirement (298 –300). One problems been no head-to-head comparisons be- of bedside glucose monitoring are re-
with sliding-scale insulin regimens is that tween insulin infusion strategies. Algo- corded as part of the patient’s hospital
the sliding-scale regimen prescribed on rithms should incorporate the concepts medical record. While many institutions
admission is likely to be used throughout that maintenance requirements differ be- allow patients on insulin pumps to con-
the hospital stay without modification, tween patients and change over the tinue these devices in the hospital, others
even when control remains poor. Addi- course of treatment. Ideally, intravenous express concern regarding use of a device
tionally, sliding-scale insulin therapy insulin algorithms should consider both unfamiliar to staff, particularly in patients
treats hyperglycemia after it has already the current and previous glucose level, who are not able to manage their own
occurred, instead of preventing the occur- the rate of change of plasma glucose, and pump therapy. If a patient is too ill to
rence of hyperglycemia. This “reactive” the current intravenous insulin infusion self-manage either multiple daily injec-
approach can lead to rapid changes in rate. For all algorithms, frequent bedside tions or CSII, then appropriate subcuta-
blood glucose levels, exacerbating both glucose testing is required, but the ideal neous doses can be calculated on the basis
hyper- and hypoglycemia. frequency is not known. of their basal and bolus insulin needs dur-
A recent study demonstrated the iii. Transition from intravenous to sub- ing hospitalization, with adjustments for
safety and efficacy of using basal-bolus in- cutaneous insulin therapy. For those changes in nutritional or metabolic status.
sulin therapy utilizing weight-based dos- who will require subcutaneous insulin,
ing in insulin-naı̈ve hospitalized patients the very short half-life of intravenous in-
5. Preventing hypoglycemia
with type 2 diabetes (301). Glycemic con- sulin necessitates administering the first
Hypoglycemia, especially in insulin-
trol, defined as a mean blood glucose dose of subcutaneous insulin before dis-
treated patients, is the leading limiting
⬍140 mg/dl, was achieved in 68% of pa- continuation of the intravenous insulin
factor in the glycemic management of
tients receiving basal-bolus insulin versus infusion. If short- or rapid-acting insulin
type 1 and type 2 diabetes (117). In the
only 38% of those receiving sliding-scale is used, it should be injected 1–2 h before
hospital, multiple additional risk factors
insulin alone. There were no differences stopping the infusion. If intermediate- or
for hypoglycemia are present, even
in hypoglycemia between the two groups. long-acting insulin is used alone, it
among patients who are neither “brittle”
It is important to note that the patients in should be injected 2–3 h before. A com-
nor tightly controlled. Patients with or
this study were obese, and the doses used bination of short-/rapid- and intermedi-
without diabetes may experience hypo-
in this study (0.4 – 0.5 units 䡠 kg⫺1 䡠 ate-/long-acting insulin is usually
glycemia in the hospital in association
day⫺1) are higher that what may be re- preferred. Basal insulin therapy can be
with altered nutritional state, heart fail-
quired in patients who are more sensitive initiated at any time of the day, and
ure, renal or liver disease, malignancy, in-
to insulin, such as those who are lean or should not be withheld to await a specific
fection, or sepsis (303,304). Additional
who have type 1 diabetes. dosing time, such as bedtime. A recent
triggering events leading to iatrogenic hy-
ii. Intravenous insulin infusion. The only clinical trial demonstrated that a regimen
poglycemia include sudden reduction of
method of insulin delivery specifically de- using 80% of the intravenous insulin re-
corticosteroid dose, altered ability of the
veloped for use in the hospital is contin- quirement over the preceding 24 h, di-
patient to self-report symptoms, reduc-
uous intravenous infusion, using regular vided into basal and bolus insulin
tion of oral intake, emesis, new NPO sta-
crystalline insulin. There is no advantage components, was effective at achieving
tus, inappropriate timing of short- or
to using rapid-acting analogs, the struc- blood glucose levels between 80 and 150
rapid-acting insulin in relation to meals,
tural modifications of which increase the mg/dl following discontinuation of the in-
reduction of rate of administration of
rate of absorption from subcutaneous de- travenous insulin (302).
intravenous dextrose, and unexpected in-
pots, in an intravenous insulin infusion.
terruption of enteral feedings or paren-
The medical literature supports the use of
teral nutrition.
intravenous insulin infusion in preference 4. Self-management in the hospital
Despite the preventable nature of
to the subcutaneous route of insulin ad- Self-management of diabetes in the hos-
many inpatient episodes of hypoglyce-
ministration for several clinical indica- pital may be appropriate for competent
mia, institutions are more likely to have
tions among nonpregnant adults. These adult patients who have a stable level of
nursing protocols for the treatment of hy-
include DKA and nonketotic hyperosmo- consciousness, have reasonably stable
poglycemia than for its prevention.
lar state; general preoperative, intraoper- daily insulin requirements, successfully
Tracking such episodes and analyzing
ative, and postoperative care; the conduct self-management of diabetes at
their causes are important quality im-
postoperative period following heart sur- home, have physical skills needed to suc-
provement activities.
gery; following organ transplantation; cessfully self-administer insulin and per-
with cardiogenic shock; exacerbated hy- form SMBG, have adequate oral intake,
perglycemia during high-dose glucocorti- and are proficient in carbohydrate count- 6. Diabetes care providers in the
coid therapy; type 1 diabetic patients who ing, use of multiple daily insulin injec- hospital
are NPO; or in critical care illness in gen- tions or insulin pump therapy, and sick- Inpatient diabetes management may be
eral. It may be used as a dose-finding day management. The patient and effectively provided by primary care phy-
strategy in anticipation of initiation or physician, in consultation with nursing sicians, endocrinologists, or hospitalists,
reinitiation of subcutaneous insulin ther- staff, must agree that patient self- but involvement of appropriately trained
apy in type 1 or type 2 diabetes. management is appropriate under the specialists or specialty teams may reduce


Position Statement

length of stay, improve glycemic control, a realistic plan for nutrition therapy toring of blood glucose levels and ad-
and improve outcomes (305–308). In the (310,311). ministration of insulin and glucagon)
care of diabetes, implementation of stan- and in the appropriate response to high
dardized order sets for scheduled and cor- 9. Bedside blood glucose monitoring and low blood glucose levels. These
rection-dose insulin may reduce reliance Implementing intensive diabetes therapy school personnel need not be health
on sliding-scale management. A team ap- in the hospital setting requires frequent care professionals. (E)
proach is needed to establish hospital and accurate blood glucose data. This ● As specified in the DMMP and as devel-
pathways. To achieve glycemic targets measure is analogous to an additional “vi- opmentally appropriate, the student
associated with improved hospital out- tal sign” for hospitalized patients with di- with diabetes should have immediate
comes, hospitals will need multidisci- abetes. Bedside glucose monitoring using access to diabetes supplies at all times,
plinary support for using insulin infusion capillary blood has advantages over labo- should be permitted to monitor his or
therapy outside of critical care units or ratory venous glucose testing because the her blood glucose level, and should be
will need to develop protocols for subcu- results can be obtained rapidly at the able to take appropriate action to treat
taneous insulin therapy that effectively “point of care,” where therapeutic deci- hypoglycemia in the classroom or any-
and safely achieve glycemic targets (309). sions are made. where the student may be in conjunc-
Bedside blood glucose testing is usu- tion with a school activity. (E)
7. DSME in the hospital ally performed with portable meters that
are similar or identical to devices for There are ⬃206,000 individuals ⬍20
Teaching diabetes self-management to
home SMBG. Staff training and ongoing years of age with diabetes in the U.S.,
patients in hospitals is a challenging task.
quality control activities are important most of whom attend school and/or some
Patients are ill, under increased stress re-
components of ensuring accuracy of the type of day care and need knowledgeable
lated to their hospitalization and diagno-
results. Ability to track the occurrence of staff to provide a safe environment. De-
sis, and in an environment not conducive
hypo- and hyperglycemia is necessary. spite legal protections, including cover-
to learning. Ideally, people with diabetes
Results of bedside glucose tests should be age of children with diabetes under
should be taught at a time and place con-
readily available to all members of the Section 504 of the Individuals with Dis-
ducive to learning: as an outpatient in a
care team. abilities Education Act of 1991, children
recognized program of diabetes educa-
For patients who are eating, com- in the school and day care setting still face
monly recommended testing frequencies discrimination. The ADA position state-
For the hospitalized patient, diabetes
are premeal and at bedtime. For patients ment on diabetes care in the school and
“survival skills” education is generally a
not eating, testing every 4 – 6 h is usually day care setting (313) provides the legal
feasible approach. Patients receive suffi-
sufficient for determining correction in- and medical justifications for the recom-
cient information and training to enable
sulin doses. Patients on continuous intra- mendations provided herein.
them to go home safely. Those newly di-
venous insulin typically require hourly Appropriate diabetes care in the
agnosed with diabetes or who are new to
blood glucose testing until the blood glu- school and day care setting is necessary
insulin and/or blood glucose monitoring
cose levels are stable, then every 2 h. for the child’s immediate safety, long-
need to be instructed before discharge to
term well-being, and optimal academic
help ensure safe care upon returning
performance. Parents and the health care
home. Those patients hospitalized be- 10. Continuous blood glucose team should provide school systems and
cause of a crisis related to diabetes man- monitoring in the hospital day care providers with the information
agement or poor care at home need The introduction of real-time blood glu- necessary for children with diabetes to
education to prevent subsequent episodes cose monitoring as a tool for outpatient participate fully and safely in the school/
of hospitalization. diabetes management has potential bene- day care experience by developing an in-
fit for the inpatient population (312). dividualized DMMP.
8. MNT in the hospital However, at this time, data are lacking An adequate number of school per-
Hospital diets continue to be ordered by examining this new technology in the sonnel should be trained in the necessary
calorie levels based on the “ADA diet.” acutely ill patient population. Until more diabetes procedures (e.g., blood glucose
However, since 1994 the ADA has not en- studies are published, it is premature to monitoring and insulin and glucagon ad-
dorsed any single meal plan or specified use continuous blood glucose monitoring ministration) and in the appropriate re-
percentages of macronutrients, and the in the hospital except in a research setting. sponses to high and low blood glucose
term “ADA diet” should no longer be levels to ensure that at least one adult is
used. Current nutrition recommenda- B. Diabetes care in the school and present to perform these procedures in a
tions advise individualization based on day care setting timely manner while the student is at
treatment goals, physiologic parameters, school, on field trips, and participating in
and medication usage. Because of the Recommendations school-sponsored extracurricular activi-
complexity of nutrition issues in the hos- ● An individualized diabetes medical ties. These school personnel need not be
pital, a registered dietitian, knowledge- management plan (DMMP) should be health care professionals, although the
able and skilled in MNT, should serve as developed by the parent/guardian and school nurse may be instrumental in
an inpatient team member. The dietitian the student’s diabetes health care team. training nonmedical individuals.
is responsible for integrating information (E) The student with diabetes should
about the patient’s clinical condition, eat- ● An adequate number of school person- have immediate access to diabetes sup-
ing, and lifestyle habits and for establish- nel should be trained in the necessary plies at all times, with supervision as
ing treatment goals in order to determine diabetes procedures (including moni- needed. The student should be able to ob-


Standards of Medical Care

tain a blood glucose level and respond to should also have their basal rates speci- authority in a timely manner upon en-
the results as quickly and conveniently as fied. Because camp is often associated try. Insulin-treated patients should
possible, minimizing the need for missing with more physical activity than experi- have a capillary blood glucose (CBG)
instruction in the classroom and avoiding enced at home, the insulin dose may have determination within 1–2 h of arrival.
the risk of worsening hypoglycemia if the to be decreased during camp (316). Staff should identify patients with type
child must go somewhere else for treat- The diabetes camping experience is 1 diabetes who are at high risk for DKA
ment. The student’s desire for privacy short-term, with food and activity differ- with omission of insulin. (E)
during testing and insulin administration ent than the home environment. Thus, ● Medications and MNT should be con-
should also be accommodated. goals of glycemic control at camp are to tinued without interruption upon entry
ADA and partner organizations have avoid extremes in blood glucose levels into the correctional environment. (E)
developed tools for school personnel to rather than attempting optimization of in- ● In the correctional setting, policies and
provide a safe and nondiscriminatory ed- tensive glycemic control (316). procedures should enable CBG moni-
ucational environment for all students During camp, a daily record of the toring to occur at the frequency neces-
with diabetes (314,315). camper’s progress should be made, in- sitated by the patient’s glycemic control
cluding all blood glucose levels and insu- and diabetes regimen, and should re-
C. Diabetes care at diabetes camps lin dosages. To ensure safety and optimal quire staff to notify a physician of all
diabetes management, multiple blood CBG results outside of a specified
Recommendations glucose determinations should be made range, as determined by the treating
● Each camper should have a standard- throughout each 24-h period: before physician. (E)
ized medical form completed by his/her meals, at bedtime, after or during pro- ● For all inter-institutional transfers, a
family and the physician managing the longed and strenuous activity, and in the medical transfer summary should be
diabetes. (E) middle of the night when indicated for transferred with the patient, and diabe-
● Camp medical staff should be led by prior hypoglycemia. If major alterations tes supplies and medication should ac-
with a physician with expertise in man- of a camper’s regimen appear to be indi- company the patient. (E)
aging type 1 and type 2 diabetes, and cated, it is important to discuss this with ● Correctional staff should begin dis-
includes nurses (including diabetes ed- the camper and the family in addition to charge planning with adequate lead
ucators and diabetes clinical nurse spe- the child’s local physician. The record of time to ensure continuity of care and
cialists) and registered dietitians with what transpired during camp should be facilitate entry into community diabe-
expertise in diabetes. (E) discussed with the family at the end of the tes care. (E)
● All camp staff, including physicians, camp session and a copy sent to the
nurses, dietitians and volunteers, child’s physician (316).
should undergo background testing to Each camp should secure a formal re- At any given time, ⬎2 million people are
ensure appropriateness in working lationship with a nearby medical facility incarcerated in prisons and jails in the
with children. (E) so that camp medical staff can refer to this U.S., and it is estimated that nearly
facility for prompt treatment of medical 80,000 of these inmates have diabetes. In
The concept of specialized residential and emergencies. ADA requires that the camp addition, many more people with diabe-
day camps for children with diabetes has medical director be a physician with ex- tes pass through the corrections system in
become widespread throughout the U.S. pertise in managing type 1 and type 2 di- a given year (317).
and many other parts of the world. The abetes. Nursing staff should include People with diabetes in correctional
mission of diabetes camps is to provide a diabetes educators and diabetes clinical facilities should receive care that meets
camping experience in a safe environ- nurse specialists. Registered dietitians national standards. Correctional institu-
ment. An equally important goal is to en- with expertise in diabetes should have in- tions have unique circumstances that
able children with diabetes to meet and put into the design of the menu and the need to be considered so that all standards
share their experiences with one another education program. All camp staff, in- of care may be achieved. Correctional in-
while they learn to be more personally cluding medical, nursing, nutrition, and stitutions should have written policies
responsible for their disease. For this to volunteer staff, should undergo back- and procedures for the management of
occur, a skilled medical and camping staff ground testing to ensure appropriateness diabetes and for training of medical and
must be available to ensure optimal safety in working with children (316). correctional staff in diabetes care practices
and an integrated camping/educational (317).
experience (316). D. Diabetes management in Reception screening should empha-
Each camper should have a standard- correctional institutions size patient safety. In particular, rapid
ized medical form completed by his/her identification of all insulin-treated indi-
family and the physician managing the di- Recommendations viduals with diabetes is essential in order
abetes that details the camper’s past med- ● Correctional staff should be trained in to identify those at highest risk for hypo-
ical history, immunization record, and the recognition, treatment, and appro- and hyperglycemia and DKA. All insulin-
diabetes regimen. The home insulin dos- priate referral for hypo- and hypergly- treated patients should have a CBG deter-
age should be recorded for each camper, cemia, including serious metabolic mination within 1–2 h of arrival. Patients
including type(s) of insulin used, number decompensation. (E) with a diagnosis of diabetes should have a
and timing of injections and the correc- ● Patients with a diagnosis of diabetes complete medical history and physical ex-
tion factor and carbohydrate ratios used should have a complete medical history amination by a licensed health care pro-
for determining bolus dosages for basal- and physical examination by a licensed vider with prescriptive authority in a
bolus regimens. Campers using CSII health care provider with prescriptive timely manner. It is essential that medica-


Position Statement

tion and MNT be continued without region or just their household. Such pre- the same. People with diabetes should be
interruption upon entry into the correc- paredness will lessen the impact an emer- individually considered for employment
tional system, as a hiatus in either medi- gency may have on their condition. It is based on the requirements of the specific
cation or appropriate nutrition may lead recommended that people with diabetes job. Factors to be weighed in this decision
to either severe hyper- or hypoglycemia keep a waterproof and insulated disaster include the individual’s medical condi-
(317). kit ready with items critically important tion, treatment regimen (MNT, noninsu-
Patients must have access to prompt to their self-management. These may in- lin drugs, and/or insulin), and medical
treatment of hypo- and hyperglycemia. clude glucose testing strips, lancets, and a history, particularly in regard to the oc-
Correctional staff should be trained in the glucose-testing meter; medications in- currence of incapacitating hypoglycemic
recognition and treatment of these condi- cluding insulin in a cool bag; syringes; episodes (320).
tions, and appropriate staff should be glucose tabs or gels; antibiotic ointments/
trained to administer glucagon. Institu- creams for external use; glucagon emer-
tions should implement a policy requir- gency kits; and photocopies of relevant X. THIRD-PARTY
ing staff to notify a physician of all CBG medical information, particularly medi- REIMBURSEMENT FOR
results outside of a specified range, as de- cation lists and recent lab tests/ DIABETES CARE, SELF-
termined by the treating physician (317). procedures if available. If possible, MANAGEMENT
Correctional institutions should have prescription numbers should be noted, EDUCATION, AND
systems in place to ensure that insulin ad- since many chain pharmacies throughout SUPPLIES
ministration and meals are coordinated to the country will refill medications based
prevent hypo- and hyperglycemia, taking on the prescription number alone. In ad- Recommendations
into consideration the transport of resi- dition, it may be important to carry a list ● Patients and practitioners should have
dents off site and the possibility of emer- of contacts for national organizations, access to all classes of antidiabetic med-
gency schedule changes. The frequency of such as the American Red Cross and ADA. ications, equipment, and supplies with-
CBG monitoring will vary by patients’ This disaster kit should be reviewed and out undue controls. (E)
glycemic control and diabetes regimens. replenished at least twice yearly (319). ● MNT and DSME should be covered by
Policies and procedures should ensure insurance and other payors. (E)
that the health care staff has adequate
knowledge and skills to direct the man- To achieve optimal glucose control, the
agement and education of individuals IX. HYPOGLYCEMIA AND person with diabetes must have access to
with diabetes (317). EMPLOYMENT/LICENSURE health care providers who have expertise
Patients in jails may be housed for a in the field of diabetes. Treatments and
short period of time before being trans- Recommendations therapies that improve glycemic control
● People with diabetes should be individ-
ferred or released, and patients in prison and reduce the complications of diabetes
may be transferred within the system sev- ually considered for employment based will also significantly reduce health care
eral times during their incarceration. on the requirements of the specific job costs. Access to the integral components
Transferring a patient with diabetes from and the individual’s medical condition, of diabetes care, such as health care visits,
one correctional facility to another re- treatment regimen, and medical his- diabetes supplies and medications, and
quires a coordinated effort, as does plan- tory. (E) self-management education, is essential.
ning for discharge. The ADA Position All medications and supplies related to
Statement on Diabetes Management in Any person with diabetes, whether insu- the daily care of diabetes, such as sy-
Correctional Institutions (317) should be lin treated or non–insulin treated, should ringes, strips, and meters, must also be
consulted for more information on this be eligible for any employment for which reimbursed by third-party payors (321).
topic. he/she is otherwise qualified. Despite the It is recognized that the use of formu-
significant medical and technological ad- laries, prior authorization, and provisions
E. Emergency and disaster vances made in managing diabetes, dis- such as competitive bidding can manage
preparedness crimination in employment and licensure provider practices as well as costs to the
against people with diabetes still occurs. potential benefit of payors and patients.
This discrimination is often based on ap- However, any controls should ensure that
Recommendations prehension that the person with diabetes all classes of antidiabetic agents with
● People with diabetes should maintain a
may present a safety risk to the employer unique mechanisms of action and all
disaster kit that includes items impor- or the public, a fear sometimes based on classes of equipment and supplies de-
tant to their diabetes self-management misinformation or lack of up-to-date signed for use with such equipment are
and continuing medical care. (E) knowledge about diabetes. Perhaps the available to facilitate achieving glycemic
● The kit should be reviewed and replen-
greatest concern is that hypoglycemia will goals and to reduce the risk of complica-
ished at least twice yearly. (E) cause sudden unexpected incapacitation. tions. Without appropriate safeguards,
However, most people with diabetes can undue controls could constitute an ob-
The difficulties encountered by people manage their condition in such a manner struction of effective care (321).
with diabetes and their health care pro- that there is minimal risk of incapacita- Medicare and many other third-party
viders in the wake of Hurricane Katrina tion from hypoglycemia (320). payors cover DSME (the CMS term is di-
(318) highlight the need for people with Because the effects of diabetes are abetes self-management training
diabetes to be prepared for emergencies, unique to each individual, it is inappro- [DSMT]) and MNT. The qualified benefi-
whether natural or otherwise, affecting a priate to consider all people with diabetes ciary who meets the diagnostic criteria


Standards of Medical Care

and medical necessity can receive an ini- Web site should help users design and tronic medical record or patient regis-
tial benefit of 10 h of DSMT and 3 h of implement more effective health care de- try have been helpful at increasing
MNT, with a potential total of 13 h of livery systems for those with diabetes. adherence to standards of care by pro-
initial benefits. However, not all Medicare In recent years, numerous health care spectively identifying those requiring
beneficiaries with diabetes will qualify for organizations, ranging from large health assessments and/or treatment modifi-
both MNT and DSMT benefits. More in- care systems such as the U.S. Veteran’s cations. They likely could have greater
formation on Medicare policy, including Administration to small private practices, efficacy if they suggested specific ther-
follow-up benefits, is available at www. have implemented strategies to improve apeutic interventions to be considered
diabetes.org/for-health-professionals- diabetes care. Successful programs have for a particular patient at a particular
and-scientists/recognition.jsp or on the published results showing improvement point in time (331).
CMS Web sites: www.cms.hhs.gov/ in process measures such as measurement ● A variety of nonautomated systems,
DiabetesSelfManagement (DSME) and of A1C, lipids, and blood pressure. Effects such as mailing reminders to patients,
www.cms.hhs.gov/MedicalNutrition on in important intermediate outcomes, chart stickers, and flow sheets, have
Therapy (diabetes MNT) reimbursement. such as mean A1C for populations, have been useful to prompt both providers
been more difficult to demonstrate (323– and patients.
325) although examples do exist (326 – ● Availability of case or (preferably) care
XI. STRATEGIES FOR 330). Successful interventions have been management services, usually by a
IMPROVING DIABETES focused at the level of health care profes- nurse (332). Nurses, pharmacists, and
CARE sionals, delivery systems, and patients. other nonphysician health care profes-
The implementation of the standards of Features of successful programs reported sionals using detailed algorithms work-
care for diabetes has been suboptimal in in the literature include: ing under the supervision of physicians
most clinical settings. A recent report and/or nurse education calls have also
(322) indicated that only 37% of adults ● Improving health care professional ed- been helpful. Similarly, dietitians using
with diagnosed diabetes achieved an A1C ucation regarding the standards of care MNT guidelines have been demon-
of ⬍7%, only 36% had a blood pressure through formal and informal education strated to improve glycemic control.
⬍130/80 mmHg, and just 48% had a total programs. ● Availability and involvement of expert
cholesterol ⬍200 mg/dl. Most distressing ● Delivery of DSME, which has been consultants, such as endocrinologists
was that only 7.3% of people with diabe- shown to increase adherence to stan- and diabetes educators.
tes achieved all three treatment goals. dard of care.
While numerous interventions to im- ● Adoption of practice guidelines, with Evidence suggests that these individual ini-
prove adherence to the recommended participation of health care profession- tiatives work best when provided as com-
standards have been implemented, the als in the process. Guidelines should be ponents of a multifactorial intervention.
challenge of providing uniformly effective readily accessible at the point of service, Therefore, it is difficult to assess the con-
diabetes care has thus far defied a simple such as on patient charts, in examining tribution of each component; however, it
solution. A major contributor to subopti- rooms, in “wallet or pocket cards,” on is clear that optimal diabetes management
mal care is a delivery system that too often PDAs, or on office computer systems. requires an organized, systematic ap-
is fragmented, lacks clinical information Guidelines should begin with a sum- proach and involvement of a coordinated
capabilities, often duplicates services, and mary of their major recommendations team of health care professionals.
is poorly designed for the delivery of instructing health care professionals
chronic care. The Institute of Medicine what to do and how to do it.
has called for changes so that delivery sys- ● Use of checklists that mirror guidelines References
tems provide care that is evidence-based, have been successful at improving ad- 1. Medical Management of Type 1 Diabetes.
patient-centered, and systems-oriented, herence to standards of care. Alexandria, VA, American Diabetes As-
and takes advantage of information tech- ● Systems changes, such as provision of sociation, 2004
nologies that foster continuous quality automated reminders to health care 2. Medical Management of Type 2 Diabetes.
improvement. Collaborative, multidisci- professionals and patients, reporting of Alexandria, VA, American Diabetes As-
sociation, 2004
plinary teams should be best suited to process and outcome data to providers, 3. Intensive Diabetes Management. Alexan-
provide such care for people with chronic and especially identification of patients dria, VA, American Diabetes Associa-
conditions like diabetes and to empower at risk because of failure to achieve tar- tion, 2003
patients’ performance of appropriate self- get values or a lack of reported values. 4. Expert Committee on the Diagnosis and
management. Alterations in reimburse- ● Quality improvement programs com- Classification of Diabetes Mellitus: Re-
ment that reward the provision of quality bining continuous quality improve- port of the Expert Committee on the Di-
care, as defined by the attainment of qual- ment or other cycles of analysis and agnosis and Classification of Diabetes
ity measures developed by such programs intervention with provider perfor- Mellitus. Diabetes Care 20:1183–1197,
as the ADA/National Committee for Qual- mance data. 1997
ity Assurance Diabetes Provider Recogni- ● Practice changes, such as clustering of 5. Expert Committee on the Diagnosis and
Classification of Diabetes Mellitus: Fol-
tion Program, will also be required to dedicated diabetes visits into specific low-up report on the diagnosis of diabe-
achieve desired outcome goals. times within a primary care practice tes mellitus. Diabetes Care 26:3160 –
The NDEP recently launched a new schedule and/or visits with multiple 3167, 2003
online resource to help health care profes- health care professionals on a single day 6. Davidson MB, Schriger DL, Peters AL,
sionals better organize their diabetes care. and group visits. Lorber B: Relationship between fasting
The www.betterdiabetescare.nih.gov ● Tracking systems with either an elec- plasma glucose and glycosylated hemo-


Position Statement

globin: potential for false-positive diag- Hoogwerf B, Laakso M, Mohan V, Shaw 2005
noses of type 2 diabetes using new J, Zinman B, Holman RR: Effect of ros- 29. Sacks DB, Bruns DE, Goldstein DE,
diagnostic criteria. JAMA 281:1203– iglitazone on the frequency of diabetes in Maclaren NK, McDonald JM, Parrott M:
1210, 1999 patients with impaired glucose tolerance Guidelines and recommendations for
7. Nathan DM, Davidson MB, DeFronzo or impaired fasting glucose: a random- laboratory analysis in the diagnosis and
RA, Heine RJ, Henry RR, Pratley R, Zin- ised controlled trial. Lancet 368:1096 – management of diabetes mellitus. Clin
man B: Impaired fasting glucose and im- 1105, 2006 Chem 48:436 – 472, 2002
paired glucose tolerance: implications 17. Johnson SL, Tabaei BP, Herman WH: 30. Garg S, Zisser H, Schwartz S, Bailey T,
for care. Diabetes Care 30:753–759, The efficacy and cost of alternative strat- Kaplan R, Ellis S, Jovanovic L: Improve-
2007 egies for systematic screening for type 2 ment in glycemic excursions with a
8. Engelgau MM, Narayan KM, Herman diabetes in the U.S. population 45–74 transcutaneous, real-time continuous
WH: Screening for type 2 diabetes. Dia- years of age. Diabetes Care 28:307–311, glucose sensor: a randomized controlled
betes Care 23:1563–1580, 2000 2005 trial. Diabetes Care 29:44 –50, 2006
9. Gabir MM, Hanson RL, Dabelea D, Im- 18. Harris R, Donahue K, Rathore SS, Frame 31. Stratton IM, Adler AI, Neil HA, Mat-
peratore G, Roumain J, Bennett PH, P, Woolf SH, Lohr KN: Screening adults thews DR, Manley SE, Cull CA, Hadden
Knowler WC: The 1997 American Dia- for type 2 diabetes: a review of the evi- D, Turner RC, Holman RR: Association
betes Association and 1999 World dence for the U.S. Preventive Services of glycaemia with macrovascular and
Health Organization criteria for hyper- Task Force. Ann Intern Med 138:215– microvascular complications of type 2
glycemia in the diagnosis and prediction 229, 2003 diabetes (UKPDS 35): prospective ob-
of diabetes. Diabetes Care 23:1108 – 19. USPSTF: Screening for type 2 diabetes servational study. BMJ 321:405– 412,
1112, 2000 mellitus in adults: recommendations 2000
10. Knowler WC, Barrett-Connor E, Fowler and rationale. Ann Intern Med 138:212– 32. Cagliero E, Levina EV, Nathan DM: Im-
SE, Hamman RF, Lachin JM, Walker EA, 214, 2003 mediate feedback of HbA1c levels im-
Nathan DM: Reduction in the incidence 20. Dabelea D, Bell RA, D’Agostino RB, Jr, proves glycemic control in type 1 and
of type 2 diabetes with lifestyle interven- Imperatore G, Johansen JM, Linder B, insulin-treated type 2 diabetic patients.
tion or metformin. N Engl J Med 346: Liu LL, Loots B, Marcovina S, Mayer- Diabetes Care 22:1785–1789, 1999
393– 403, 2002 Davis EJ, Pettitt DJ, Waitzfelder B: Inci- 33. Miller CD, Barnes CS, Phillips LS, Zie-
11. Tuomilehto J, Lindstrom J, Eriksson JG, dence of diabetes in youth in the United mer DC, Gallina DL, Cook CB, Maryman
Valle TT, Hamalainen H, Ilanne-Parikka States. JAMA 297:2716 –2724, 2007 SD, El Kebbi IM: Rapid A1c availability
P, Keinanen-Kiukaanniemi S, Laakso M, 21. Liese AD, D’Agostino RB, Jr, Hamman improves clinical decision-making in an
Louheranta A, Rastas M, Salminen V, RF, Kilgo PD, Lawrence JM, Liu LL, urban primary care clinic. Diabetes Care
Uusitupa M: Prevention of type 2 dia- Loots B, Linder B, Marcovina S, Rodri- 26:1158 –1163, 2003
betes mellitus by changes in lifestyle guez B, Standiford D, Williams DE: The 34. Rohlfing CL, Wiedmeyer HM, Little RR,
among subjects with impaired glucose burden of diabetes mellitus among US England JD, Tennill A, Goldstein DE:
tolerance. N Engl J Med 344:1343–1350, youth: prevalence estimates from the Defining the relationship between
2001 SEARCH for Diabetes in Youth Study. plasma glucose and HbA(1c): analysis of
12. Pan XR, Li GW, Hu YH, Wang JX, Yang Pediatrics 118:1510 –1518, 2006 glucose profiles and HbA(1c) in the Di-
WY, An ZX, Hu ZX, Lin J, Xiao JZ, Cao 22. American Diabetes Association: Type 2 abetes Control and Complications Trial.
HB, Liu PA, Jiang XG, Jiang YY, Wang JP, diabetes in children and adolescents Diabetes Care 25:275–278, 2002
Zheng H, Zhang H, Bennett PH, Howard (Consensus Statement). Diabetes Care 35. DCCT: The effect of intensive treatment
BV: Effects of diet and exercise in pre- 23:381–389, 2000 of diabetes on the development and
venting NIDDM in people with impaired 23. American Diabetes Association: Gesta- progression of long-term complications
glucose tolerance. The Da Qing IGT and tional diabetes mellitus (Position State- in insulin-dependent diabetes mellitus.
Diabetes Study. Diabetes Care 20:537– ment). Diabetes Care 27 (Suppl. 1):S88 – The Diabetes Control and Complica-
544, 1997 S90, 2004 tions Trial Research Group. N Engl J Med
13. Buchanan TA, Xiang AH, Peters RK, Kjos 24. Kim C, Newton KM, Knopp RH: Gesta- 329:977–986, 1993
SL, Marroquin A, Goico J, Ochoa C, Tan tional diabetes and the incidence of type 36. DCCT-EDIC: Retinopathy and ne-
S, Berkowitz K, Hodis HN, Azen SP: 2 diabetes: a systematic review. Diabetes phropathy in patients with type 1 diabe-
Preservation of pancreatic beta-cell Care 25:1862–1868, 2002 tes four years after a trial of intensive
function and prevention of type 2 diabe- 25. Gerstein HC: Point: If it is important to therapy. The Diabetes Control and Com-
tes by pharmacological treatment of in- prevent type 2 diabetes, it is important to plications Trial/Epidemiology of Diabe-
sulin resistance in high-risk hispanic consider all proven therapies within a tes Interventions and Complications
women. Diabetes 51:2796 –2803, 2002 comprehensive approach. Diabetes Care Research Group. N Engl J Med 342:381–
14. Chiasson JL, Josse RG, Gomis R, 30:432– 434, 2007 389, 2000
Hanefeld M, Karasik A, Laakso M: Acar- 26. American Diabetes Association: Consen- 37. Martin CL, Albers J, Herman WH,
bose for prevention of type 2 diabetes sus statement on self-monitoring of Cleary P, Waberski B, Greene DA,
mellitus: the STOP-NIDDM randomised blood glucose. Diabetes Care 10:95–99, Stevens MJ, Feldman EL: Neuropathy
trial. Lancet 359:2072–2077, 2002 1987 among the diabetes control and compli-
15. Ramachandran A, Snehalatha C, Mary S, 27. American Diabetes Association: Self- cations trial cohort 8 years after trial
Mukesh B, Bhaskar AD, Vijay V: The In- monitoring of blood glucose. American completion. Diabetes Care 29:340 –344,
dian Diabetes Prevention Programme Diabetes Association. Diabetes Care 17: 2006
shows that lifestyle modification and 81– 86, 1994 38. Nathan DM, Cleary PA, Backlund JY,
metformin prevent type 2 diabetes in 28. Welschen LM, Bloemendal E, Nijpels G, Genuth SM, Lachin JM, Orchard TJ,
Asian Indian subjects with impaired glu- Dekker JM, Heine RJ, Stalman WA, Raskin P, Zinman B: Intensive diabetes
cose tolerance (IDPP-1). Diabetologia 49: Bouter LM: Self-monitoring of blood treatment and cardiovascular disease in
289 –297, 2006 glucose in patients with type 2 diabetes patients with type 1 diabetes. N Engl
16. Gerstein HC, Yusuf S, Bosch J, Pogue J, who are not using insulin: a systematic J Med 353:2643–2653, 2005
Sheridan P, Dinccag N, Hanefeld M, review. Diabetes Care 28:1510 –1517, 39. Ohkubo Y, Kishikawa H, Araki E, Miyata


Standards of Medical Care

T, Isami S, Motoyoshi S, Kojima Y, Fu- 50. Mooradian AD, Bernbaum M, Albert SG: 61. Norris SL, Zhang X, Avenell A, Gregg E,
ruyoshi N, Shichiri M: Intensive insulin Narrative review: a rational approach to Schmid CH, Kim C, Lau J: Efficacy of
therapy prevents the progression of dia- starting insulin therapy. Ann Intern Med pharmacotherapy for weight loss in
betic microvascular complications in 145:125–134, 2006 adults with type 2 diabetes mellitus: a
Japanese patients with non-insulin- 51. Nathan DM, Buse JB, Davidson MB, meta-analysis. Arch Intern Med 164:
dependent diabetes mellitus: a random- Heine RJ, Holman RR, Sherwin R, Zin- 1395–1404, 2004
ized prospective 6-year study. Diabetes man B: Management of hyperglycemia in 62. Wolf AM, Conaway MR, Crowther JQ,
Res Clin Pract 28:103–117, 1995 type 2 diabetes: a consensus algorithm Hazen KY, Nadler L, Oneida B, Bovbjerg
40. UKPDS: Effect of intensive blood-glu- for the initiation and adjustment of ther- VE: Translating lifestyle intervention to
cose control with metformin on compli- apy: a consensus statement from the practice in obese patients with type 2
cations in overweight patients with type American Diabetes Association and the diabetes: Improving Control with Activ-
2 diabetes (UKPDS 34). UK Prospective European Association for the Study of ity and Nutrition (ICAN) study. Diabetes
Diabetes Study (UKPDS) Group. Lancet Diabetes. Diabetes Care 29:1963–1972, Care 27:1570 –1576, 2004
352:854 – 865, 1998 2006 63. Manning RM, Jung RT, Leese GP, New-
41. UKPDS: Intensive blood-glucose control 52. Nissen SE, Wolski K: Effect of rosiglita- ton RW: The comparison of four weight
with sulphonylureas or insulin com- zone on the risk of myocardial infarction reduction strategies aimed at overweight
pared with conventional treatment and and death from cardiovascular causes. patients with diabetes mellitus: four-
risk of complications in patients with N Engl J Med 356:2457–2471, 2007 year follow-up. Diabet Med 15:497–502,
type 2 diabetes (UKPDS 33). UK Pro- 53. Singh S, Loke YK, Furberg CD: Long- 1998
spective Diabetes Study (UKPDS) term risk of cardiovascular events with 64. Pi-Sunyer X, Blackburn G, Brancati FL,
Group. Lancet 352:837– 853, 1998 rosiglitazone: a meta-analysis. JAMA Bray GA, Bright R, Clark JM, Curtis JM,
42. Kuusisto J, Mykkanen L, Pyorala K, 298:1189 –1195, 2007 Espeland MA, Foreyt JP, Graves K,
Laakso M: NIDDM and its metabolic 54. American Diabetes Association. Nutri- Haffner SM, Harrison B, Hill JO, Horton
control predict coronary heart disease in tion Recommendations and Interven- ES, Jakicic J, Jeffery RW, Johnson KC,
elderly subjects. Diabetes 43:960 –967, tions for Diabetes—2008. Diabetes Care Kahn S, Kelley DE, Kitabchi AE,
1994 31 (Suppl. 1):S61–S78, 2008 Knowler WC, Lewis CE, Maschak-Carey
43. Selvin E, Marinopoulos S, Berkenblit G, 55. Pastors JG, Warshaw H, Daly A, Franz BJ, Montgomery B, Nathan DM, Patricio
Rami T, Brancati FL, Powe NR, Golden M, Kulkarni K: The evidence for the ef- J, Peters A, Redmon JB, Reeves RS, Ryan
SH: Meta-analysis: glycosylated hemo- fectiveness of medical nutrition therapy DH, Safford M, Van Dorsten B, Wadden
globin and cardiovascular disease in in diabetes management. Diabetes Care TA, Wagenknecht L, Wesche-Thobaben
diabetes mellitus. Ann Intern Med 141: 25:608 – 613, 2002 J, Wing RR, Yanovski SZ: Reduction in
421– 431, 2004 56. Pastors JG, Franz MJ, Warshaw H, Daly weight and cardiovascular disease risk
44. Lawson ML, Gerstein HC, Tsui E, Zin- A, Arnold MS: How effective is medical factors in individuals with type 2 diabe-
man B: Effect of intensive therapy on nutrition therapy in diabetes care? J Am tes: one-year results of the Look AHEAD
early macrovascular disease in young in- Diet Assoc 103:827– 831, 2003 trial. Diabetes Care 30:1374 –1383,
dividuals with type 1 diabetes. A system- 57. Yu-Poth S, Zhao G, Etherton T, Naglak 2007
atic review and meta-analysis. Diabetes M, Jonnalagadda S, Kris-Etherton PM: 65. Foster GD, Wyatt HR, Hill JO,
Care 22 (Suppl. 2):B35–B39, 1999 Effects of the National Cholesterol McGuckin BG, Brill C, Mohammed BS,
45. American Diabetes Association: Post- Education Program’s Step I and Step II Szapary PO, Rader DJ, Edman JS, Klein
prandial blood glucose (Consensus dietary intervention programs on car- S: A randomized trial of a low-carbohy-
Statement). Diabetes Care 24:775–778, diovascular disease risk factors: a meta- drate diet for obesity. N Engl J Med 348:
2001 analysis. Am J Clin Nutr 69:632– 646, 2082–2090, 2003
46. Ceriello A, Taboga C, Tonutti L, Quagli- 1999 66. Stern L, Iqbal N, Seshadri P, Chicano
aro L, Piconi L, Bais B, Da Ros R, Motz E: 58. Appel LJ, Moore TJ, Obarzanek E, KL, Daily DA, McGrory J, Williams M,
Evidence for an independent and cumu- Vollmer WM, Svetkey LP, Sacks FM, Gracely EJ, Samaha FF: The effects of
lative effect of postprandial hypertri- Bray GA, Vogt TM, Cutler JA, Wind- low-carbohydrate versus conventional
glyceridemia and hyperglycemia on hauser MM, Lin PH, Karanja N: A clini- weight loss diets in severely obese
endothelial dysfunction and oxidative cal trial of the effects of dietary patterns adults: one-year follow-up of a random-
stress generation: effects of short- and on blood pressure. DASH Collaborative ized trial. Ann Intern Med 140:778 –785,
long-term simvastatin treatment. Circu- Research Group. N Engl J Med 2004
lation 106:1211–1218, 2002 336:1117–1124, 1997 67. Gardner C, Kiazand A, Alhassan S,
47. Metzger BE, Coustan DR: Summary and 59. Norris SL, Zhang X, Avenell A, Gregg E, Soowon K, Stafford R, Balise R, Kraemer
recommendations of the Fourth Interna- Bowman B, Schmid CH, Lau J: Long- H, and King A: Comparison of the At-
tional Workshop-Conference on Gesta- term effectiveness of weight-loss inter- kins, Zone, Ornish, and LEARN diets for
tional Diabetes Mellitus. The Organizing ventions in adults with pre-diabetes: a change in weight and related risk factors
Committee. Diabetes Care 21 (Suppl. 2): review. Am J Prev Med 28:126 –139, among overweight premenopausal
B161–B167, 1998 2005 women. JAMA 297:969 –977, 2007
48. DeWitt DE, Hirsch IB: Outpatient insu- 60. Klein S, Sheard NF, Pi-Sunyer X, Daly A, 68. Nordmann AJ, Nordmann A, Briel M,
lin therapy in type 1 and type 2 diabetes Wylie-Rosett J, Kulkarni K, Clark NG: Keller U, Yancy WS, Jr, Brehm BJ,
mellitus: scientific review. JAMA 289: Weight management through lifestyle Bucher HC: Effects of low-carbohydrate
2254 –2264, 2003 modification for the prevention and vs low-fat diets on weight loss and car-
49. Rosenstock J, Dailey G, Massi-Benedetti management of type 2 diabetes: ratio- diovascular risk factors: a meta-analysis
M, Fritsche A, Lin Z, Salzman A: Re- nale and strategies: a statement of the of randomized controlled trials. Arch In-
duced hypoglycemia risk with insulin American Diabetes Association, the tern Med 166:285–293, 2006
glargine: a meta-analysis comparing in- North American Association for the 69. Institute of Medicine: Dietary Reference
sulin glargine with human NPH insulin Study of Obesity, and the American So- Intakes: Energy, Carbohydrate, Fiber, Fat,
in type 2 diabetes. Diabetes Care 28: ciety for Clinical Nutrition. Diabetes Fatty Acids, Cholesterol, Protein, and
950 –955, 2005 Care 27:2067–2073, 2004 Amino Acids. National Academies Press,


Position Statement

Washington, DC, 2002 81. Rickheim PL, Weaver TW, Flader JL, sistance training, or both on glycemic
70. Franz MJ, Bantle JP, Beebe CA, Brunzell Kendall DM: Assessment of group versus control in type 2 diabetes: a randomized
JD, Chiasson JL, Garg A, Holzmeister individual diabetes education: a ran- trial. Ann Intern Med 147:357–369, 2007
LA, Hoogwerf B, Mayer-Davis E, Moora- domized study. Diabetes Care 25:269 – 93. Bax JJ, Young LH, Frye RL, Bonow RO,
dian AD, Purnell JQ, Wheeler M: Evi- 274, 2002 Steinberg HO, Barrett EJ: Screening for
dence-based nutrition principles and 82. Trento M, Passera P, Borgo E, Tomalino coronary artery disease in patients with
recommendations for the treatment and M, Bajardi M, Cavallo F, Porta M: A diabetes. Diabetes Care 30:2729 –2736,
prevention of diabetes and related com- 5-year randomized controlled study of 2007
plications. Diabetes Care 25:148 –198, learning, problem solving ability, and 94. Berger M, Berchtold P, Cuppers HJ,
2002 quality of life modifications in people Drost H, Kley HK, Muller WA, Wie-
71. Piette JD, Glasgow RE: Strategies for im- with type 2 diabetes managed by group gelmann W, Zimmerman-Telschow H,
proving behavioral and health outcomes care. Diabetes Care 27:670 – 675, 2004 Gries FA, Kruskemper HL, Zimmer-
among people with diabetes: self-man- 83. Norris SL, Chowdhury FM, Van Le K, mann H: Metabolic and hormonal effects
agement education. In Evidence-Based Horsley T, Brownstein JN, Zhang X, Jack of muscular exercise in juvenile type di-
Diabetes Care. Gerstein HC, Hayes RB, L, Jr, Satterfield DW: Effectiveness of abetics. Diabetologia 13:355–365, 1977
Eds. BC Decker, Ontario, Canada, 2000 community health workers in the care of 95. American Diabetes Association: Physical
72. Norris SL, Engelgau MM, Narayan KM: persons with diabetes. Diabet Med 23: activity/exercise and diabetes (Position
Effectiveness of self-management train- 544 –556, 2006 Statement). Diabetes Care 27 (Suppl. 1):
ing in type 2 diabetes: a systematic re- 84. Sigal RJ, Kenny GP, Wasserman DH, S58 –S62, 2004
view of randomized controlled trials. Castaneda-Sceppa C: Physical activity/ 96. Berger M: Adjustment of insulin and oral
Diabetes Care 24:561–587, 2001 exercise and type 2 diabetes. Diabetes agent therapy. In Handbook of Exercise in
73. Norris SL, Lau J, Smith SJ, Schmid CH, Care 27:2518 –2539, 2004 Diabetes. 2nd ed. Ruderman N, Devlin
Engelgau MM: Self-management educa- 85. Wasserman DH, Zinman B: Exercise in JT, Krisska A, Eds. Alexandria, VA,
tion for adults with type 2 diabetes: a individuals with IDDM. Diabetes Care American Diabetes Association, 2002, p.
meta-analysis of the effect on glycemic 17:924 –937, 1994 365–376
control. Diabetes Care 25:1159 –1171, 86. Boulé NG, Haddad E, Kenny GP, Wells 97. Aiello LP, Wong J, Cavallerano J, Bursell
2002 GA, Sigal RJ: Effects of exercise on gly- SE, Aiello LM: Retinopathy. In Hand-
74. Gary TL, Genkinger JM, Guallar E, Pey- cemic control and body mass in type 2 book of Exercise in Diabetes. 2nd ed.
rot M, Brancati FL: Meta-analysis of ran- diabetes mellitus: a meta-analysis of con- Ruderman N, Devlin JT, Kriska A, Eds.
domized educational and behavioral trolled clinical trials. JAMA 286:1218 – Alexandria, VA, American Diabetes As-
interventions in type 2 diabetes. Diabetes 1227, 2001 sociation, 2002, p. 401– 413
Educ 29:488 –501, 2003 87. Boulé NG, Kenny GP, Haddad E, Wells 98. Vinik A, Erbas T: Neuropathy. In Hand-
75. Steed L, Cooke D, Newman S: A system- GA, Sigal RJ: Meta-analysis of the effect book of Exercise in Diabetes. 2nd ed. Ru-
atic review of psychosocial outcomes fol- of structured exercise training on cardio- derman N, Devlin JT, Kriska A, Eds.
lowing education, self-management and respiratory fitness in type 2 diabetes Alexnadria, VA, American Diabetes As-
psychological interventions in diabetes mellitus. Diabetologia 46:1071–1081, sociation, 2002, p. 463– 496
mellitus. Patient Educ Couns 51:5–15, 2003 99. Levin ME: The diabetic foot. In Hand-
2003 88. US Department of Health and Human book of Exercise in Diabetes. Ruderman
76. Ellis SE, Speroff T, Dittus RS, Brown A, Services, Centers for Disease Control N, Devlin JT, Kriska A, Eds. Alexandria,
Pichert JW, Elasy TA: Diabetes patient and Prevention, National Center for VA, American Diabetes Association,
education: a meta-analysis and meta-re- Chronic Disease Prevention and Health 2002, p. 385–399
gression. Patient Educ Couns 52:97–105, Promotion: Physical Activity and Health: 100. Wackers FJ, Young LH, Inzucchi SE,
2004 A Report of the Surgeon General. Atlanta, Chyun DA, Davey JA, Barrett EJ,
77. Warsi A, Wang PS, LaValley MP, Avorn GA, Centers for Disease Control and Pre- Taillefer R, Wittlin SD, Heller GV, Filip-
J, Solomon DH: Self-management edu- vention, 1996 chuk N, Engel S, Ratner RE, Iskandrian
cation programs in chronic disease: a 89. Ivy JL: Role of exercise training in the AE: Detection of silent myocardial isch-
systematic review and methodological prevention and treatment of insulin re- emia in asymptomatic diabetic subjects:
critique of the literature. Arch Intern Med sistance and non-insulin-dependent di- the DIAD study. Diabetes Care 27:1954 –
164:1641–1649, 2004 abetes mellitus. Sports Med 24:321–336, 1961, 2004
78. Funnell MM, Brown TL, Childs BP, Haas 1997 101. Valensi P, Sachs RN, Harfouche B,
LB, Hosey GM, Jensen B, Maryniuk M, 90. Dunstan DW, Daly RM, Owen N, Jolley Lormeau B, Paries J, Cosson E, Paycha F,
Peyrot M, Piette JD, Reader D, Siminerio D, de Court, Shaw J, Zimmet P: High- Leutenegger M, Attali JR: Predictive
LM, Weinger K, Weiss MA: National intensity resistance training improves value of cardiac autonomic neuropathy
standards for diabetes self-management glycemic control in older patients with in diabetic patients with or without si-
education. Diabetes Care 30:1630 – type 2 diabetes. Diabetes Care 25:1729 – lent myocardial ischemia. Diabetes Care
1637, 2007 1736, 2002 24:339 –343, 2001
79. Mulcahy K, Maryniuk M, Peeples M, 91. Castaneda C, Layne JE, Munoz-Orians L, 102. Mogensen CE: Nephropathy. In Hand-
Peyrot M, Tomky D, Weaver T, Yarbor- Gordon PL, Walsmith J, Foldvari M, book of Exercise in Diabetes. 2nd ed. Ru-
ough P: Diabetes self-management edu- Roubenoff R, Tucker KL, Nelson ME: A derman N, Devlin JT, Kriska A, Eds.
cation core outcomes measures. Diabetes randomized controlled trial of resistance Alexandria, VA, American Diabetes As-
Educ 29: 768- 84:787, 2003 exercise training to improve glycemic sociation, 2002, p. 433– 449
80. Barker JM, Goehrig SH, Barriga K, Hoff- control in older adults with type 2 dia- 103. Anderson RJ, Grigsby AB, Freedland KE,
man M, Slover R, Eisenbarth GS, Norris betes. Diabetes Care 25:2335–2341, de Groot M, McGill JB, Clouse RE, Lust-
JM, Klingensmith GJ, Rewers M: Clinical 2002 man PJ: Anxiety and poor glycemic
characteristics of children diagnosed 92. Sigal RJ, Kenny GP, Boule NG, Wells control: a meta-analytic review of the lit-
with type 1 diabetes through intensive GA, Prud’homme D, Fortier M, Reid RD, erature. Int J Psychiatry Med 32:235–
screening and follow-up. Diabetes Care Tulloch H, Coyle D, Phillips P, Jennings 247, 2002
27:1399 –1404, 2004 A, Jaffey J: Effects of aerobic training, re- 104. Jacobson AM: Depression and diabetes.


Standards of Medical Care

Diabetes Care 16:1621–1623, 1993 glycemia in diabetes. Diabetes Care 26: 133. UKPDS: Tight blood pressure control
105. Rubin RR, Peyrot M: Psychosocial prob- 1902–1912, 2003 and risk of macrovascular and microvas-
lems and interventions in diabetes: a re- 121. Smith SA, Poland GA: Use of influenza cular complications in type 2 diabetes:
view of the literature. Diabetes Care 15: and pneumococcal vaccines in people UKPDS 38. UK Prospective Diabetes
1640 –1657, 1992 with diabetes. Diabetes Care 23:95–108, Study Group. BMJ 317:703–713, 1998
106. Surwit RS, Schneider MS, Feinglos MN: 2000 134. Hansson L, Zanchetti A, Carruthers SG,
Stress and diabetes mellitus. Diabetes 122. Colquhoun AJ, Nicholson KG, Botha JL, Dahlof B, Elmfeldt D, Julius S, Menard J,
Care 15:1413–1422, 1992 Raymond NT: Effectiveness of influenza Rahn KH, Wedel H, Westerling S: Ef-
107. Young-Hyman D: Psycosocial factors af- vaccine in reducing hospital admissions fects of intensive blood-pressure lower-
fecting adherence, quality of life, and in people with diabetes. Epidemiol Infect ing and low-dose aspirin in patients with
well-being: helping patients cope. In 119:335–341, 1997 hypertension: principal results of the
Medical Management of Type 1 Diabetes. 123. Bridges CB, Fukuda K, Uyeki TM, Cox Hypertension Optimal Treatment
4th ed. Bode B, Ed. Alexandria, VA, NJ, Singleton JA: Prevention and control (HOT) randomised trial. HOT Study
American Diabetes Association, 2004, p. of influenza. Recommendations of the Group. Lancet 351:1755–1762, 1998
162–182 Advisory Committee on Immunization 135. Adler AI, Stratton IM, Neil HA, Yudkin
108. Delahanty LM, Grant RW, Wittenberg E, Practices (ACIP). MMWR Recomm Rep JS, Matthews DR, Cull CA, Wright AD,
Bosch JL, Wexler DJ, Cagliero E, Meigs 51:1–31, 2002 Turner RC, Holman RR: Association of
JB: Association of diabetes-related emo- 124. American Diabetes Association: Influ- systolic blood pressure with macrovas-
tional distress with diabetes treatment in enza and pneumococcal immunization cular and microvascular complications
primary care patients with type 2 diabe- in diabetes (Position Statement). Diabe- of type 2 diabetes (UKPDS 36): prospec-
tes. Diabet Med 24:48 –54, 2007 tes Care 27 (Suppl. 1):S111–S113, 2004 tive observational study. BMJ 321:412–
109. Anderson BJ, Auslander WF, Jung KC, 125. Arauz-Pacheco C, Parrott MA, Raskin P: 419, 2000
Miller JP, Santiago JV: Assessing family The treatment of hypertension in adult 136. Lewington S, Clarke R, Qizilbash N,
sharing of diabetes responsibilities. J Pe- patients with diabetes. Diabetes Care 25: Peto R, Collins R: Age-specific relevance
diatr Psychol 15:477– 492, 1990 134 –147, 2002 of usual blood pressure to vascular mor-
110. McCulloch DK, Glasgow RE, Hampson 126. Haffner SM: Management of dyslipide- tality: a meta-analysis of individual data
SE, Wagner E: A systematic approach to mia in adults with diabetes. Diabetes for one million adults in 61 prospective
diabetes management in the post-DCCT Care 21:160 –178, 1998 studies. Lancet 360:1903–1913, 2002
era. Diabetes Care 17:765–769, 1994 127. Colwell JA: Aspirin therapy in diabetes. 137. Stamler J, Vaccaro O, Neaton JD, Went-
111. Rubin RR, Peyrot M: Psychological is- Diabetes Care 20:1767–1771, 1997 worth D: Diabetes, other risk factors,
sues and treatments for people with di- 128. Haire-Joshu D, Glasgow RE, Tibbs TL: and 12-yr cardiovascular mortality for
abetes. J Clin Psychol 57:457– 478, 2001 Smoking and diabetes. Diabetes Care 22: men screened in the Multiple Risk Fac-
112. Peyrot M, Rubin RR: Behavioral and psy- 1887–1898, 1999 tor Intervention Trial. Diabetes Care 16:
chosocial interventions in diabetes: a 129. Buse JB, Ginsberg HN, Barkis GL, Clark 434 – 444, 1993
conceptual review. Diabetes Care 30: NG, Costa F, Eckel R, Fonseca V, Ger- 138. Sacks FM, Svetkey LP, Vollmer WM, Ap-
2433–2440, 2007 stein HC, Grundy S, Nesto RW, Pignone pel LJ, Bray GA, Harsha D, Obarzanek E,
113. Lustman PJ, Griffith LS, Clouse RE, MP, Plutzky J, Porte D, Redberg R, Stit- Conlin PR, Miller ER, III, Simons-Mor-
Cryer PE: Psychiatric illness in diabetes zel KF, Stone N: J Primary prevention of ton DG, Karanja N, Lin PH: Effects on
mellitus: relationship to symptoms and cardiovascular diseases in people with blood pressure of reduced dietary so-
glucose control. J Nerv Ment Dis 174: diabetes mellitus: a scientific statement dium and the Dietary Approaches to
736 –742, 1986 from the American Heart Association Stop Hypertension (DASH) diet. DASH-
114. Marcus MD, Wing RR: Eating disorders and the American Diabetes Association. Sodium Collaborative Research Group.
and diabetes. In Neuropsychological and Diabetes Care 30:162–172, 2007 N Engl J Med 344:3–10, 2001
Behavioral Aspects of Diabetes. Holmes 130. Chobanian AV, Bakris GL, Black HR, 139. Tatti P, Pahor M, Byington RP, Di Mauro
CS, Ed. New York, Springer-Verlag, Cushman WC, Green LA, Izzo JL, Jr, P, Guarisco R, Strollo G, Strollo F: Out-
1990, p. 102–121 Jones DW, Materson BJ, Oparil S, come results of the Fosinopril versus
115. Peyrot M, Rubin RR: Behavioral and psy- Wright JT, Jr, Roccella EJ: The Seventh Amlodipine Cardiovascular Events ran-
chosocial interventions in diabetes: a Report of the Joint National Committee domized Trial (FACET) in patients with
conceptual review. Diabetes Care 30: on Prevention, Detection, Evaluation, hypertension and NIDDM. Diabetes
2433–2440, 2007 and Treatment of High Blood Pressure: Care 21:597– 603, 1998
116. American Diabetes Association: Hyper- the JNC 7 report. JAMA 289:2560 – 140. Estacio RO, Jeffers BW, Hiatt WR, Big-
glycemic crises in diabetes. Diabetes Care 2572, 2003 gerstaff SL, Gifford N, Schrier RW: The
27 (Suppl. 1):S94 –S102, 2004 131. Bobrie G, Chatellier G, Genes N, Clerson effect of nisoldipine as compared with
117. Cryer PE: Hypoglycaemia: the limiting P, Vaur L, Vaisse B, Menard J, Mallion enalapril on cardiovascular outcomes in
factor in the glycaemic management of JM: Cardiovascular prognosis of patients with non-insulin-dependent di-
type I and type II diabetes. Diabetologia “masked hypertension” detected by abetes and hypertension. N Engl J Med
45:937–948, 2002 blood pressure self-measurement in el- 338:645– 652, 1998
118. Gannon MC, Nuttall FQ: Protein and derly treated hypertensive patients. 141. Schrier RW, Estacio RO, Mehler PS, Hi-
Diabetes. In American Diabetes Associa- JAMA 291:1342–1349, 2004 att WR: Appropriate blood pressure
tion Guide to Medical Nutrition Therapy 132. Sega R, Facchetti R, Bombelli M, Cesana control in hypertensive and normoten-
for Diabetes. Franz MJ, Bantle JP, Eds. G, Corrao G, Grassi G, Mancia G: Prog- sive type 2 diabetes mellitus: a summary
Alexandria, VA, American Diabetes As- nostic value of ambulatory and home of the ABCD trial. Nat Clin Pract Nephrol
sociation, 1999, p. 107–125 blood pressures compared with office 3:428 – 438, 2007
119. Cryer PE: Diverse causes of hypoglyce- blood pressure in the general popula- 142. ALLHAT: Major outcomes in high-risk
mia-associated autonomic failure in dia- tion: follow-up results from the Pres- hypertensive patients randomized to an-
betes. N Engl J Med 350:2272–2279, sioni Arteriose Monitorate e Loro giotensin-converting enzyme inhibitor
2004 Associazioni (PAMELA) study. Circula- or calcium channel blocker vs diuretic:
120. Cryer PE, Davis SN, Shamoon H: Hypo- tion 111:1777–1783, 2005 the Antihypertensive and Lipid-Lower-


Position Statement

ing Treatment to Prevent Heart Attack North American Microalbuminuria tergren J: Reduction in cardiovascular
Trial (ALLHAT). JAMA 288:2981–2997, Study Group. Am J Med 99:497–504, events with atorvastatin in 2,532 pa-
2002 1995 tients with type 2 diabetes: Anglo-Scan-
143. Psaty BM, Lumley T, Furberg CD, Schel- 151. Bakris GL, Williams M, Dworkin L, El- dinavian Cardiac Outcomes Trial–lipid-
lenbaum G, Pahor M, Alderman MH, liott WJ, Epstein M, Toto R, Tuttle K, lowering arm (ASCOT-LLA). Diabetes
Weiss NS: Health outcomes associated Douglas J, Hsueh W, Sowers J: Preserv- Care 28:1151–1157, 2005
with various antihypertensive therapies ing renal function in adults with hyper- 160. Knopp RH, d’Emden M, Smilde JG, Po-
used as first-line agents: a network meta- tension and diabetes: a consensus cock SJ: Efficacy and safety of atorvasta-
analysis. JAMA 289:2534 –2544, 2003 approach. National Kidney Foundation tin in the prevention of cardiovascular
144. HOPE: Effects of ramipril on cardiovas- Hypertension and Diabetes Executive end points in subjects with type 2 diabe-
cular and microvascular outcomes in Committees Working Group. Am J Kid- tes: the Atorvastatin Study for Pre-
people with diabetes mellitus: results of ney Dis 36:646 – 661, 2000 vention of Coronary Heart Disease
the HOPE study and MICRO-HOPE 152. Psaty BM, Smith NL, Siscovick DS, Endpoints in non-insulin-dependent di-
substudy. Heart Outcomes Prevention Koepsell TD, Weiss NS, Heckbert SR, abetes mellitus (ASPEN). Diabetes Care
Evaluation Study Investigators. Lancet Lemaitre RN, Wagner EH, Furberg CD: 29:1478 –1485, 2006
355:253–259, 2000 Health outcomes associated with antihy- 161. Colhoun HM, Betteridge DJ, Durrington
145. Pfeffer MA, Swedberg K, Granger CB, pertensive therapies used as first-line PN, Hitman GA, Neil HA, Livingstone
Held P, McMurray JJ, Michelson EL, agents: a systematic review and meta- SJ, Thomason MJ, Mackness MI, Charl-
Olofsson B, Ostergren J, Yusuf S, Pocock analysis. JAMA 277:739 –745, 1997 ton-Menys V, Fuller JH: Primary preven-
S: Effects of candesartan on mortality 153. Sibai BM: Treatment of hypertension in tion of cardiovascular disease with
and morbidity in patients with chronic pregnant women. N Engl J Med 335:257– atorvastatin in type 2 diabetes in the Col-
heart failure: the CHARM-Overall pro- 265, 1996 laborative Atorvastatin Diabetes Study
gramme. Lancet 362:759 –766, 2003 154. Baigent C, Keech A, Kearney PM, Black- (CARDS): multicentre randomised pla-
146. Granger CB, McMurray JJ, Yusuf S, Held well L, Buck G, Pollicino C, Kirby A, cebo-controlled trial. Lancet 364:685–
P, Michelson EL, Olofsson B, Ostergren Sourjina T, Peto R, Collins R, Simes R: 696, 2004
J, Pfeffer MA, Swedberg K: Effects of can- Efficacy and safety of cholesterol-lower- 162. Singh IM, Shishehbor MH, Ansell BJ:
desartan in patients with chronic heart ing treatment: prospective meta-analysis High-density lipoprotein as a therapeu-
failure and reduced left-ventricular of data from 90,056 participants in 14 tic target: a systematic review. JAMA
systolic function intolerant to angio- randomised trials of statins. Lancet 366: 298:786 –798, 2007
tensin-converting-enzyme inhibitors: 1267–1278, 2005 163. Canner PL, Berge KG, Wenger NK,
the CHARM-Alternative trial. Lancet 155. Pyorala K, Pedersen TR, Kjekshus J, Stamler J, Friedman L, Prineas RJ,
362:772–776, 2003 Faergeman O, Olsson AG, Thorgeirsson Friedewald W: Fifteen year mortality in
147. McMurray JJ, Ostergren J, Swedberg K, G: Cholesterol lowering with simvasta- Coronary Drug Project patients: long-
Granger CB, Held P, Michelson EL, tin improves prognosis of diabetic pa- term benefit with niacin. J Am Coll Car-
Olofsson B, Yusuf S, Pfeffer MA: Effects tients with coronary heart disease: a diol 8:1245–1255, 1986
of candesartan in patients with chronic subgroup analysis of the Scandinavian 164. Rubins HB, Robins SJ, Collins D, Fye CL,
heart failure and reduced left-ventricular Simvastatin Survival Study (4S). Diabe- Anderson JW, Elam MB, Faas FH, Lin-
systolic function taking angiotensin- tes Care 20:614 – 620, 1997 ares E, Schaefer EJ, Schectman G, Wilt
converting-enzyme inhibitors: the 156. Heart Protection Study Collaborative TJ, Wittes J: Gemfibrozil for the second-
CHARM-Added trial. Lancet 362:767– Group: MRC/BHF Heart Protection ary prevention of coronary heart disease
771, 2003 Study of cholesterol-lowering with sim- in men with low levels of high-density
148. Lindholm LH, Ibsen H, Dahlof B, De- vastatin in 5963 people with diabetes: lipoprotein cholesterol. Veterans Affairs
vereux RB, Beevers G, de Faire U, a randomised placebo-controlled trial. High-Density Lipoprotein Cholesterol
Fyhrquist F, Julius S, Kjeldsen SE, Kris- Lancet 361:2005–2016, 2003 Intervention Trial Study Group. N Engl
tiansson K, Lederballe-Pedersen O, Ni- 157. Goldberg RB, Mellies MJ, Sacks FM, J Med 341:410 – 418, 1999
eminen MS, Omvik P, Oparil S, Wedel Moye LA, Howard BV, Howard WJ, 165. Frick MH, Elo O, Haapa K, Heinonen
H, Aurup P, Edelman J, Snapinn S: Car- Davis BR, Cole TG, Pfeffer MA, Braun- OP, Heinsalmi P, Helo P, Huttunen JK,
diovascular morbidity and mortality in wald E: Cardiovascular events and their Kaitaniemi P, Koskinen P, Manninen V,
patients with diabetes in the Losartan In- reduction with pravastatin in diabetic et al.: Helsinki Heart Study: primary-
tervention For Endpoint reduction in and glucose-intolerant myocardial in- prevention trial with gemfibrozil in mid-
hypertension study (LIFE): a random- farction survivors with average choles- dle-aged men with dyslipidemia: safety
ised trial against atenolol. Lancet 359: terol levels: subgroup analyses in the of treatment, changes in risk factors, and
1004 –1010, 2002 cholesterol and recurrent events (CARE) incidence of coronary heart disease.
149. Berl T, Hunsicker LG, Lewis JB, Pfeffer trial. The Care Investigators. Circulation N Engl J Med 317:1237–1245, 1987
MA, Porush JG, Rouleau JL, Drury PL, 98:2513–2519, 1998 166. Keech A, Simes RJ, Barter P, Best J, Scott
Esmatjes E, Hricik D, Parikh CR, Raz I, 158. Shepherd J, Barter P, Carmena R, Deed- R, Taskinen MR, Forder P, Pillai A, Davis
Vanhille P, Wiegmann TB, Wolfe BM, wania P, Fruchart JC, Haffner S, Hsia J, T, Glasziou P, Drury P, Kesaniemi YA,
Locatelli F, Goldhaber SZ, Lewis EJ: Car- Breazna A, LaRosa J, Grundy S, Waters Sullivan D, Hunt D, Colman P, d’Emden
diovascular outcomes in the Irbesartan D: Effect of lowering LDL cholesterol M, Whiting M, Ehnholm C, Laakso M:
Diabetic Nephropathy Trial of patients substantially below currently recom- Effects of long-term fenofibrate therapy
with type 2 diabetes and overt nephrop- mended levels in patients with coronary on cardiovascular events in 9795 people
athy. Ann Intern Med 138:542–549, heart disease and diabetes: the Treating with type 2 diabetes mellitus (the FIELD
2003 to New Targets (TNT) study. Diabetes study): randomised controlled trial. Lan-
150. Laffel LM, McGill JB, Gans DJ: The ben- Care 29:1220 –1226, 2006 cet 366:1849 –1861, 2005
eficial effect of angiotensin-converting 159. Sever PS, Poulter NR, Dahlof B, Wedel 167. NCEP: Executive Summary of the Third
enzyme inhibition with captopril on di- H, Collins R, Beevers G, Caulfield M, Report of the National Cholesterol Edu-
abetic nephropathy in normotensive Kjeldsen SE, Kristinsson A, McInnes GT, cation Program (NCEP) Expert Panel on
IDDM patients with microalbuminuria. Mehlsen J, Nieminen M, O’Brien E, Os- Detection, Evaluation, and Treatment of


Standards of Medical Care

High Blood Cholesterol in Adults (Adult row C: Aspirin for the primary preven- Coll Cardiol 47:65–71, 2006
Treatment Panel III). JAMA 285:2486 – tion of cardiovascular events: a summary 189. Boden WE, O’Rourke RA, Teo KK, Har-
2497, 2001 of the evidence for the U.S. Preventive tigan PM, Maron DJ, Kostuk WJ, Knudt-
168. Hayward RA, Hofer TP, Vijan S: Narra- Services Task Force. Ann Intern Med 136: son M, Dada M, Casperson P, Harris CL,
tive review: lack of evidence for recom- 161–172, 2002 Chaitman BR, Shaw L, Gosselin G,
mended low-density lipoprotein 178. USPSTF: Aspirin for the primary pre- Nawaz S, Title LM, Gau G, Blaustein AS,
treatment targets: a solvable problem. vention of cardiovascular events: recom- Booth DC, Bates ER, Spertus JA, Berman
Ann Intern Med 145:520 –530, 2006 mendation and rationale. Ann Intern Med DS, Mancini GB, Weintraub WS: Opti-
169. Cannon CP, Braunwald E, McCabe CH, 136:157–160, 2002 mal medical therapy with or without PCI
Rader DJ, Rouleau JL, Belder R, Joyal SV, 179. Antithrombotic Trialists Collaboration: for stable coronary disease. N Engl J Med
Hill KA, Pfeffer MA, Skene AM: Inten- Collaborative meta-analysis of random- 356:1503–1516, 2007
sive versus moderate lipid lowering with ised trials of antiplatelet therapy for pre- 190. Wackers FJ, Chyun DA, Young LH,
statins after acute coronary syndromes. vention of death, myocardial infarction, Heller GV, Iskandrian AE, Davey JA,
N Engl J Med 350:1495–1504, 2004 and stroke in high risk patients. BMJ Barrett EJ, Taillefer R, Wittlin SD, Filip-
170. de Lemos JA, Blazing MA, Wiviott SD, 324:71– 86, 2002 chuk N, Ratner RE, Inzucchi SE: Reso-
Lewis EF, Fox KA, White HD, Rouleau 180. Smith SC, Jr, Allen J, Blair SN, Bonow lution of asymptomatic myocardial
JL, Pedersen TR, Gardner LH, Mukher- RO, Brass LM, Fonarow GC, Grundy ischemia in patients with type 2 diabetes
jee R, Ramsey KE, Palmisano J, Bil- SM, Hiratzka L, Jones D, Krumholz HM, mellitus in the DIAD Study. Diabetes
heimer DW, Pfeffer MA, Califf RM, Mosca L, Pasternak RC, Pearson T, Pfef- Care 2007
Braunwald E: Early intensive vs a de- fer MA, Taubert KA: AHA/ACC guide- 191. Garg JP, Bakris GL: Microalbuminuria:
layed conservative simvastatin strategy lines for secondary prevention for marker of vascular dysfunction, risk fac-
in patients with acute coronary syn- patients with coronary and other athero- tor for cardiovascular disease. Vasc Med
dromes: phase Z of the A to Z trial. JAMA sclerotic vascular disease: 2006 update: 7:35– 43, 2002
292:1307–1316, 2004 endorsed by the National Heart, Lung, 192. Klausen K, Borch-Johnsen K, Feldt-Ras-
171. Nissen SE, Tuzcu EM, Schoenhagen P, and Blood Institute. Circulation 113: mussen B, Jensen G, Clausen P,
Brown BG, Ganz P, Vogel RA, Crowe T, 2363–2372, 2006 Scharling H, Appleyard M, Jensen JS:
Howard G, Cooper CJ, Brodie B, Grines 181. Campbell CL, Smyth S, Montalescot G, Very low levels of microalbuminuria are
CL, DeMaria AN: Effect of intensive Steinhubl SR: Aspirin dose for the pre- associated with increased risk of coro-
compared with moderate lipid-lowering vention of cardiovascular disease: a sys- nary heart disease and death indepen-
therapy on progression of coronary ath- tematic review. JAMA 297:2018 –2024, dently of renal function, hypertension,
erosclerosis: a randomized controlled 2007 and diabetes. Circulation 110:32–35,
trial. JAMA 291:1071–1080, 2004 182. Sacco M, Pellegrini F, Roncaglioni MC, 2004
172. Grundy SM, Cleeman JI, Merz CN, Avanzini F, Tognoni G, Nicolucci A: Pri- 193. Gall MA, Hougaard P, Borch-Johnsen K,
Brewer HB, Jr, Clark LT, Hunninghake mary Prevention of Cardiovascular Parving HH: Risk factors for develop-
DB, Pasternak RC, Smith SC, Jr, Stone Events With Low-Dose Aspirin and Vi- ment of incipient and overt diabetic ne-
NJ: Implications of recent clinical trials tamin E in Type 2 Diabetic Patients: Re- phropathy in patients with non-insulin
for the National Cholesterol Education sults of the Primary Prevention Project dependent diabetes mellitus: prospec-
Program Adult Treatment Panel III (PPP) trial. Diabetes Care 26:3264 – tive, observational study. BMJ 314:783–
guidelines. Circulation 110:227–239, 3272, 2003 788, 1997
2004 183. Bhatt DL, Marso SP, Hirsch AT, Ringleb 194. Ravid M, Lang R, Rachmani R, Lishner
173. Elam MB, Hunninghake DB, Davis KB, PA, Hacke W, Topol EJ: Amplified ben- M: Long-term renoprotective effect of
Garg R, Johnson C, Egan D, Kostis JB, efit of clopidogrel versus aspirin in pa- angiotensin-converting enzyme inhibi-
Sheps DS, Brinton EA: Effect of niacin on tients with diabetes mellitus. Am J tion in non-insulin-dependent diabetes
lipid and lipoprotein levels and glycemic Cardiol 90:625– 628, 2002 mellitus: a 7-year follow-up study. Arch
control in patients with diabetes and pe- 184. American Diabetes Asociation: Smoking Intern Med 156:286 –289, 1996
ripheral arterial disease: the ADMIT and diabetes (Position Statement). Dia- 195. Reichard P, Nilsson BY, Rosenqvist U:
study: a randomized trial. Arterial Dis- betes Care 27 (Suppl. 1):S74 –S75, 2004 The effect of long-term intensified insu-
ease Multiple Intervention Trial. JAMA 185. US Preventive Services Task Force: lin treatment on the development of mi-
284:1263–1270, 2000 Counseling to Prevent Tobacco Use and To- crovascular complications of diabetes
174. Grundy SM, Vega GL, McGovern ME, bacco-Related Diseases: Recommendation mellitus. N Engl J Med 329:304 –309,
Tulloch BR, Kendall DM, Fitz-Patrick D, Statement. Agency for Healthcare Re- 1993
Ganda OP, Rosenson RS, Buse JB, Rob- search and Quality, Rockville, MD, 2003 196. DCCT: Effect of intensive therapy on the
ertson DD, Sheehan JP: Efficacy, safety, 186. Ranney L, Melvin C, Lux L, McClain E, development and progression of dia-
and tolerability of once-daily niacin for Lohr KN: Systematic review: smoking betic nephropathy in the Diabetes Con-
the treatment of dyslipidemia associated cessation intervention strategies for trol and Complications Trial. The
with type 2 diabetes: results of the as- adults and adults in special populations. Diabetes Control and Complications
sessment of diabetes control and evalu- Ann Intern Med 145:845– 856, 2006 (DCCT) Research Group. Kidney Int 47:
ation of the efficacy of niaspan trial. Arch 187. American Diabetes Asociation: Consen- 1703–1720, 1995
Intern Med 162:1568 –1576, 2002 sus development conference on the di- 197. Lewis EJ, Hunsicker LG, Bain RP, Rohde
175. Jones PH, Davidson MH: Reporting rate agnosis of coronary heart disease in RD: The effect of angiotensin-convert-
of rhabdomyolysis with fenofibrate ⫹ people with diabetes: 10 –11 February ing-enzyme inhibition on diabetic ne-
statin versus gemfibrozil ⫹ any statin. 1998, Miami, Florida. American Diabe- phropathy. The Collaborative Study
Am J Cardiol 95:120 –122, 2005 tes Association. Diabetes Care 21:1551– Group. N Engl J Med 329:1456 –1462,
176. American Diabetes Association: Aspirin 1559, 1998 1993
therapy in diabetes (Position Statement). 188. Scognamiglio R, Negut C, Ramondo A, 198. Remuzzi G, Macia M, Ruggenenti P: Pre-
Diabetes Care 27 (Suppl. 1):S72–S73, Tiengo A, Avogaro A: Detection of coro- vention and treatment of diabetic renal
2004 nary artery disease in asymptomatic pa- disease in type 2 diabetes: the BENE-
177. Hayden M, Pignone M, Phillips C, Mul- tients with type 2 diabetes mellitus. J Am DICT study. J Am Soc Nephrol 17:S90 –


Position Statement

S97, 2006 617– 622, 2003 Study research group. Arch Ophthalmol
199. Lewis EJ, Hunsicker LG, Clarke WR, 209. Levey AS, Coresh J, Balk E, Kausz AT, 103:1796 –1806, 1985
Berl T, Pohl MA, Lewis JB, Ritz E, Atkins Levin A, Steffes MW, Hogg RJ, Perrone 223. Klein R, Klein BE, Moss SE, Davis MD,
RC, Rohde R, Raz I: Renoprotective ef- RD, Lau J, Eknoyan G: National Kidney DeMets DL: The Wisconsin epidemio-
fect of the angiotensin-receptor antago- Foundation practice guidelines for logic study of diabetic retinopathy. II.
nist irbesartan in patients with chronic kidney disease: evaluation, clas- Prevalence and risk of diabetic retinop-
nephropathy due to type 2 diabetes. sification, and stratification. Ann Intern athy when age at diagnosis is less than 30
N Engl J Med 345:851– 860, 2001 Med 139:137–147, 2003 years. Arch Ophthalmol 102:520 –526,
200. Brenner BM, Cooper ME, de Zeeuw D, 210. Kramer H, Molitch ME: Screening for 1984
Keane WF, Mitch WE, Parving HH, Re- kidney disease in adults with diabetes. 224. Harris MI, Klein R, Welborn TA,
muzzi G, Snapinn SM, Zhang Z, Shahin- Diabetes Care 28:1813–1816, 2005 Knuiman MW: Onset of NIDDM occurs
far S: Effects of losartan on renal and 211. Kramer HJ, Nguyen QD, Curhan G, Hsu at least 4 –7 yr before clinical diagnosis.
cardiovascular outcomes in patients CY: Renal insufficiency in the absence of Diabetes Care 15:815– 819, 1992
with type 2 diabetes and nephropathy. albuminuria and retinopathy among 225. Vijan S, Hofer TP, Hayward RA: Cost-
N Engl J Med 345:861– 869, 2001 adults with type 2 diabetes mellitus. utility analysis of screening intervals for
201. Parving HH, Lehnert H, Brochner- JAMA 289:3273–3277, 2003 diabetic retinopathy in patients with
Mortensen J, Gomis R, Andersen S, 212. Tsalamandris C, Allen TJ, Gilbert RE, type 2 diabetes mellitus. JAMA 283:
Arner P: The effect of irbesartan on the Sinha A, Panagiotopoulos S, Cooper ME, 889 – 896, 2000
development of diabetic nephropathy in Jerums G: Progressive decline in renal 226. Klein R: Screening interval for retinopa-
patients with type 2 diabetes. N Engl function in diabetic patients with and thy in type 2 diabetes. Lancet 361:190 –
J Med 345:870 – 878, 2001 without albuminuria. Diabetes 43:649 – 191, 2003
202. Pepine CJ, Handberg EM, Cooper-De- 655, 1994 227. Younis N, Broadbent DM, Vora JP, Har-
Hoff RM, Marks RG, Kowey P, Messerli 213. Levey AS, Bosch JP, Lewis JB, Greene T, ding SP: Incidence of sight-threatening
FH, Mancia G, Cangiano JL, Garcia-Bar- Rogers N, Roth D: A more accurate retinopathy in patients with type 2 dia-
reto D, Keltai M, Erdine S, Bristol HA, method to estimate glomerular filtration betes in the Liverpool Diabetic Eye
Kolb HR, Bakris GL, Cohen JD, Parmley rate from serum creatinine: a new pre- Study: a cohort study. Lancet 361:195–
WW: A calcium antagonist vs a non-cal- diction equation. Modification of Diet in 200, 2003
cium antagonist hypertension treatment Renal Disease Study Group. Ann Intern 228. Ahmed J, Ward TP, Bursell SE, Aiello
strategy for patients with coronary artery Med 130:461– 470, 1999 LM, Cavallerano JD, Vigersky RA: The
disease: the International Verapamil- 214. Levinsky NG: Specialist evaluation in sensitivity and specificity of nonmydri-
Trandolapril study (INVEST): a ran- chronic kidney disease: too little, too atic digital stereoscopic retinal imaging
domized controlled trial. JAMA 290: late. Ann Intern Med 137:542–543, 2002 in detecting diabetic retinopathy. Diabe-
2805–2816, 2003 215. American Diabetes Association: Ne- tes Care 29:2205–2209, 2006
203. Bakris GL, Siomos M, Richardson D, phropathy in diabetes (Position State- 229. American Diabetes Association: Reti-
Janssen I, Bolton WK, Hebert L, Agarwal ment). Diabetes Care 27 (Suppl. 1):S79 – nopathy in diabetes. Diabetes Care 27
R, Catanzaro D: ACE inhibition or an- S83, 2004 (Suppl. 1):S84 –S87, 2004
giotensin receptor blockade: impact on 216. Klein R: Hyperglycemia and microvas- 230. Ciulla TA, Amador AG, Zinman B: Dia-
potassium in renal failure. VAL-K Study cular and macrovascular disease in dia- betic Retinopathy and Diabetic Macular
Group. Kidney Int 58:2084 –2092, 2000 betes. Diabetes Care 18:258 –268, 1995 Edema: Pathophysiology, screening,
204. Pijls LT, de Vries H, Donker AJ, van Eijk 217. Estacio RO, McFarling E, Biggerstaff S, and novel therapies. Diabetes Care 26:
JT: The effect of protein restriction on Jeffers BW, Johnson D, Schrier RW: 2653–2664, 2003
albuminuria in patients with type 2 dia- Overt albuminuria predicts diabetic ret- 231. Boulton AJ, Vinik AI, Arezzo JC, Bril V,
betes mellitus: a randomized trial. Neph- inopathy in Hispanics with NIDDM. Am Feldman EL, Freeman R, Malik RA, Ma-
rol Dial Transplant 14:1445–1453, 1999 J Kidney Dis 31:947–953, 1998 ser RE, Sosenko JM, Ziegler D: Diabetic
205. Pedrini MT, Levey AS, Lau J, Chalmers 218. Leske MC, Wu SY, Hennis A, Hyman L, neuropathies: a statement by the Amer-
TC, Wang PH: The effect of dietary pro- Nemesure B, Yang L, Schachat AP: Hy- ican Diabetes Association. Diabetes Care
tein restriction on the progression of di- perglycemia, blood pressure, and the 28:956 –962, 2005
abetic and nondiabetic renal diseases: a 9-year incidence of diabetic retinopathy: 232. Vinik AI, Maser RE, Mitchell BD, Free-
meta-analysis. Ann Intern Med 124:627– the Barbados Eye Studies. Ophthalmology man R: Diabetic autonomic neuropathy.
632, 1996 112:799 – 805, 2005 Diabetes Care 26:1553–1579, 2003
206. Hansen HP, Tauber-Lassen E, Jensen 219. Fong DS, Aiello LP, Ferris FL, III, Klein 233. American Diabetes Association: Periph-
BR, Parving HH: Effect of dietary protein R: Diabetic retinopathy. Diabetes Care eral Arterial Disease in People With Di-
restriction on prognosis in patients with 27:2540 –2553, 2004 abetes (Consensus Statement). Diabetes
diabetic nephropathy. Kidney Int 62: 220. DCCT: Effect of pregnancy on microvas- Care 26:3333–3341, 2003
220 –228, 2002 cular complications in the diabetes 234. Mayfield JA, Reiber GE, Sanders LJ,
207. Kasiske BL, Lakatua JD, Ma JZ, Louis TA: control and complications trial. The Janisse D, Pogach LM: Preventive foot
A meta-analysis of the effects of dietary Diabetes Control and Complications care in people with diabetes. Diabetes
protein restriction on the rate of decline Trial Research Group. Diabetes Care 23: Care 21:2161–2177, 1998
in renal function. Am J Kidney Dis 31: 1084 –1091, 2000 235. American Diabetes Association: Preven-
954 –961, 1998 221. The Diabetic Retinopathy Study (DRS) tive foot care in diabetes (Position State-
208. Eknoyan G, Hostetter T, Bakris GL, He- Research Group. Preliminary report on ment). Diabetes Care 27 (Suppl. 1):S63–
bert L, Levey AS, Parving HH, Steffes the effects of photocoagulation therapy: S64, 2004
MW, Toto R: Proteinuria and other DRS Report #1. Am J Ophthalmol 81: 236. American Diabetes Association: Consen-
markers of chronic kidney disease: a po- 383–396, 1976 sus Development Conference on Dia-
sition statement of the national kidney 222. ETDRS: Photocoagulation for diabetic betic Foot Wound Care, 7– 8 April
foundation (NKF) and the national insti- macular edema. Early Treatment Dia- 1999, Boston, Massachusetts. American
tute of diabetes and digestive and kidney betic Retinopathy Study report number Diabetes Association. Diabetes Care 22:
diseases (NIDDK). Am J Kidney Dis 42: 1. Early Treatment Diabetic Retinopathy 1354 –1360, 1999


Standards of Medical Care

237. Silverstein J, Klingensmith G, Copeland and Metabolism, High Blood Pressure type 1 diabetes mellitus. Diabet Med 19:
KC, Plotnick L, Kaufman F, Laffel L, Research, Cardiovascular Nursing, and 70 –73, 2002
Deeb LC, Grey M, Anderson BJ, Hol- the Kidney in Heart Disease; and the In- 258. Chase HP, Garg SK, Cockerham RS,
zmeister LA, Clark N, American Diabe- terdisciplinary Working Group on Wilcox WD, Walravens PA: Thyroid
tes Association: Care of children and Quality of Care and Outcomes Research: hormone replacement and growth of
adolescents with type 1 diabetes melli- endorsed by the American Academy of children with subclinical hypothyroid-
tus: a statement of the American Diabe- Pediatrics. Circulation 114:2710 –2738, ism and diabetes. Diabet Med 7:299 –
tes Association. Diabetes Care 28:186 – 2006 303, 1990
212, 2005 248. Salo P, Viikari J, Hamalainen M, Lapin- 259. Eppens MC, Craig ME, Cusumano J,
238. Northam EA, Anderson PJ, Werther GA, leimu H, Routi T, Ronnemaa T, Sep- Hing S, Chan AK, Howard NJ, Silink M,
Warne GL, Adler RG, Andrewes D: Neu- panen R, Jokinen E, Valimaki I, Simell Donaghue KC: Prevalence of diabetes
ropsychological complications of IDDM O: Serum cholesterol ester fatty acids in complications in adolescents with type 2
in children 2 years after disease onset. 7- and 13-month-old children in a pro- compared with type 1 diabetes. Diabetes
Diabetes Care 21:379 –384, 1998 spective randomized trial of a low-satu- Care 29:1300 –1306, 2006
239. Rovet J, Alvarez M: Attentional function- rated fat, low-cholesterol diet: the STRIP 260. Kitzmiller JL, Gavin LA, Gin GD, Jo-
ing in children and adolescents with baby project. Special Turku coronary vanovic-Peterson L, Main EK, Zigrang
IDDM. Diabetes Care 20:803– 810, 1997 Risk factor Intervention Project for chil- WD: Preconception care of diabetes.
240. Bjorgaas M, Gimse R, Vik T, Sand T: dren. Acta Paediatr 88:505–512, 1999 Glycemic control prevents congenital
Cognitive function in type 1 diabetic 249. Efficacy and safety of lowering dietary anomalies. JAMA 265:731–736, 1991
children with and without episodes of intake of fat and cholesterol in children 261. Goldman JA, Dicker D, Feldberg D, Ye-
severe hypoglycaemia. Acta Paediatr 86: with elevated low-density lipoprotein shaya A, Samuel N, Karp M: Pregnancy
148 –153, 1997 cholesterol. The Dietary Intervention outcome in patients with insulin-depen-
241. Doyle EA, Weinzimer SA, Steffen AT, Study in Children (DISC). The Writing dent diabetes mellitus with preconcep-
Ahern JA, Vincent M, Tamborlane WV: Group for the DISC Collaborative Re- tional diabetic control: a comparative
A randomized, prospective trial compar- search Group. JAMA 273:1429 –1435, study. Am J Obstet Gynecol 155:293–
ing the efficacy of continuous subcuta- 1995 297, 1986
neous insulin infusion with multiple 250. McCrindle BW, Ose L, Marais AD: Effi- 262. Rosenn B, Miodovnik M, Combs CA,
daily injections using insulin glargine. cacy and safety of atorvastatin in chil- Khoury J, Siddiqi TA: Pre-conception
Diabetes Care 27:1554 –1558, 2004 dren and adolescents with familial management of insulin-dependent dia-
242. Nimri R, Weintrob N, Benzaquen H, hypercholesterolemia or severe hyper- betes: improvement of pregnancy out-
Ofan R, Fayman G, Phillip M: Insulin lipidemia: a multicenter, randomized, come. Obstet Gynecol 77:846 – 849,
pump therapy in youth with type 1 dia- placebo-controlled trial. J Pediatr 143: 1991
betes: a retrospective paired study. Pedi- 74 – 80, 2003 263. Tchobroutsky C, Vray MM, Altman JJ:
atrics 117:2126 –2131, 2006 251. de Jongh S, Lilien MR, op’t RJ, Stroes ES, Risk/benefit ratio of changing late ob-
243. Krantz JS, Mack WJ, Hodis HN, Liu CR, Bakker HD, Kastelein JJ: Early statin stetrical strategies in the management of
Liu CH, Kaufman FR: Early onset of sub- therapy restores endothelial function in insulin-dependent diabetic pregnancies.
clinical atherosclerosis in young persons children with familial hypercholesterol- A comparison between 1971–1977 and
with type 1 diabetes. J Pediatr 145:452– emia. J Am Coll Cardiol 40:2117–2121, 1978 –1985 periods in 389 pregnancies.
457, 2004 2002 Diabete Metab 17:287–294, 1991
244. Jarvisalo MJ, Putto-Laurila A, Jartti L, 252. Wiegman A, Hutten BA, de Groot E, Ro- 264. Willhoite MB, Bennert HW, Jr, Palomaki
Lehtimaki T, Solakivi T, Ronnemaa T, denburg J, Bakker HD, Buller HR, Si- GE, Zaremba MM, Herman WH, Wil-
Raitakari OT: Carotid artery intima-me- jbrands EJ, Kastelein JJ: Efficacy and liams JR, Spear NH: The impact of pre-
dia thickness in children with type 1 di- safety of statin therapy in children with conception counseling on pregnancy
abetes. Diabetes 51:493– 498, 2002 familial hypercholesterolemia: a ran- outcomes: the experience of the Maine
245. Haller MJ, Samyn M, Nichols WW, domized controlled trial. JAMA 292: Diabetes in Pregnancy Program. Diabetes
Brusko T, Wasserfall C, Schwartz RF, At- 331–337, 2004 Care 16:450 – 455, 1993
kinson M, Shuster JJ, Pierce GL, Silver- 253. Holmes GK: Screening for coeliac dis- 265. Cooper WO, Hernandez-Diaz S, Arbo-
stein JH: Radial artery tonometry ease in type 1 diabetes. Arch Dis Child gast PG, Dudley JA, Dyer S, Gideon PS,
demonstrates arterial stiffness in chil- 87:495– 498, 2002 Hall K, Ray WA: Major congenital mal-
dren with type 1 diabetes. Diabetes Care 254. Rewers M, Liu E, Simmons J, Redondo formations after first-trimester exposure
27:2911–2917, 2004 MJ, Hoffenberg EJ: Celiac disease asso- to ACE inhibitors. N Engl J Med 354:
246. Orchard TJ, Forrest KY, Kuller LH, ciated with type 1 diabetes mellitus. En- 2443–2451, 2006
Becker DJ: Lipid and blood pressure docrinol Metab Clin North Am 33: 266. Kitzmiller JL, Buchanan TA, Kjos S,
treatment goals for type 1 diabetes: 10- 197–214, xi, 2004 Combs CA, Ratner RE: Pre-conception
year incidence data from the Pittsburgh 255. Roldan MB, Alonso M, Barrio R: Thyroid care of diabetes, congenital malforma-
Epidemiology of Diabetes Complica- autoimmunity in children and adoles- tions, and spontaneous abortions. Dia-
tions Study. Diabetes Care 24:1053– cents with type 1 diabetes mellitus. Dia- betes Care 19:514 –541, 1996
1059, 2001 betes Nutr Metab 12:27–31, 1999 267. American Diabetes Association: Precon-
247. Kavey RE, Allada V, Daniels SR, Hayman 256. Kordonouri O, Deiss D, Danne T, ception care of women with diabetes
LL, McCrindle BW, Newburger JW, Dorow A, Bassir C, Gruters-Kieslich A: (Position Statement). Diabetes Care 27
Parekh RS, Steinberger J: Cardiovascular Predictivity of thyroid autoantibodies (Suppl. 1):S76 –S78, 2004
risk reduction in high-risk pediatric pa- for the development of thyroid disorders 268. Brown AF, Mangione CM, Saliba D,
tients: a scientific statement from the in children and adolescents with Type 1 Sarkisian CA: Guidelines for improving
American Heart Association Expert diabetes. Diabet Med 19:518 –521, 2002 the care of the older person with diabe-
Panel on Population and Prevention Sci- 257. Mohn A, Di Michele S, Di Luzio R, tes mellitus. J Am Geriatr Soc 51:S265–
ence; the Councils on Cardiovascular Tumini S, Chiarelli F: The effect of sub- S280, 2003
Disease in the Young, Epidemiology and clinical hypothyroidism on metabolic 269. Curb JD, Pressel SL, Cutler JA, Savage
Prevention, Nutrition, Physical Activity control in children and adolescents with PJ, Applegate WB, Black H, Camel G,


Position Statement

Davis BR, Frost PH, Gonzalez N, Guthrie Welin L: Randomized trial of insulin- 31:359 –366, 2003
G, Oberman A, Rutan GH, Stamler J: Ef- glucose infusion followed by subcutane- 290. van den Bergh G, Wilmer A, Hermans G,
fect of diuretic-based antihypertensive ous insulin treatment in diabetic Meersseman W, Wouters PJ, Milants I,
treatment on cardiovascular disease risk patients with acute myocardial infarc- Van Wijngaerden E, Bobbaers H, Bouil-
in older diabetic patients with isolated tion (DIGAMI study): effects on mortal- lon R: Intensive insulin therapy in the
systolic hypertension. Systolic Hyper- ity at 1 year. J Am Coll Cardiol 26:57– 65, medical ICU. N Engl J Med 354:449 –
tension in the Elderly Program Cooper- 1995 461, 2006
ative Research Group. JAMA 276:1886 – 281. Malmberg K, Ryden L, Wedel H, Birke- 291. Pittas AG, Siegel RD, Lau J: Insulin Ther-
1892, 1996 land K, Bootsma A, Dickstein K, Efendic apy for Critically Ill Hospitalized Pa-
270. Clement S, Braithwaite SS, Magee MF, S, Fisher M, Hamsten A, Herlitz J, Hilde- tients: A Meta-analysis of Randomized
Ahmann A, Smith EP, Schafer RG, Hirsh brandt P, MacLeod K, Laakso M, Torp- Controlled Trials. Arch Intern Med 164:
IB: Management of diabetes and hyper- Pedersen C, Waldenstrom A: Intense 2005–2011, 2004
glycemia in hospitals. Diabetes Care 27: metabolic control by means of insulin in 292. Krinsley J: Glycemic control in critically
553–591, 2004 patients with diabetes mellitus and acute ill patients: Leuven and beyond. Chest
271. American Association of Clinical Endo- myocardial infarction (DIGAMI 2): ef- 132:1–2, 2007
crinologists: Inpatient diabetes and met- fects on mortality and morbidity. Eur 293. Brunkhorst FM, Reinhart K: Intensive
abolic control: conference proceedings. Heart J 26:650 – 661, 2005 insulin therapy in the ICU: benefit ver-
Endocr Pract 10 (Suppl. 2):1–108, 2004 282. Mehta SR, Yusuf S, Diaz R, Zhu J, Pais P, sus harm? Intensive Care Med 33: 1302,
272. Garber AJ, Moghissi ES, Bransome ED, Xavier D, Paolasso E, Ahmed R, Xie C, 2007
Jr, Clark NG, Clement S, Cobin RH, Fur- Kazmi K, Tai J, Orlandini A, Pogue J, Liu 293a. Glucontrol Study. Available at www.
nary AP, Hirsch IB, Levy P, Roberts R, L: Effect of glucose-insulin-potassium glucontrol.org. Accessed 6 November
van den BG, Zamudio V: American Col- infusion on mortality in patients with 2007.
lege of Endocrinology position state- acute ST-segment elevation myocardial 294. Miller CD, Phillips LS, Ziemer DC,
ment on inpatient diabetes and infarction: the CREATE-ECLA random- Gallina DL, Cook CB, El Kebbi IM: Hy-
metabolic control. Endocr Pract 10 ized controlled trial. JAMA 293:437– poglycemia in patients with type 2 dia-
(Suppl. 2):4 –9, 2004 446, 2005 betes mellitus. Arch Intern Med 161:
273. ACE/ADA Task Force on Inpatient Dia- 283. Cheung NW, Wong VW, McLean M: 1653–1659, 2001
betes: American College of Endocrinol- The hyperglycemia: intensive insulin in- 295. Misbin RI, Green L, Stadel BV, Guerigu-
ogy and American Diabetes Association fusion in infarction (HI-5) study: a ran- ian JL, Gubbi A, Fleming GA: Lactic ac-
consensus statement on inpatient diabe- domized controlled trial of insulin idosis in patients with diabetes treated
tes and glycemic control: a call to action. infusion therapy for myocardial infarc- with metformin. N Engl J Med 338:265–
Diabetes Care 29:1955–1962, 2006 tion. Diabetes Care 29:765–770, 2006 266, 1998
274. Centers for Disease Control and Preven- 284. Furnary AP, Gao G, Grunkemeier GL, 296. Misbin RI: The phantom of lactic acido-
tion: Hospitalizations for Diabetes as Any- Wu Y, Zerr KJ, Bookin SO, Floten HS, sis due to metformin in patients with di-
Listed Diagnosis. Atlanta, GA, CDC, 2003 Starr A: Continuous insulin infusion re- abetes. Diabetes Care 27:1791–1793,
275. Pomposelli JJ, Baxter JK, III, Babineau duces mortality in patients with diabetes 2004
TJ, Pomfret EA, Driscoll DF, Forse RA, undergoing coronary artery bypass 297. Salpeter SR, Greyber E, Pasternak GA,
Bistrian BR: Early postoperative glucose grafting. J Thorac Cardiovasc Surg 125: Salpeter EE: Risk of fatal and nonfatal
control predicts nosocomial infection 1007–1021, 2003 lactic acidosis with metformin use in
rate in diabetic patients. J Parenter En- 285. Furnary AP, Zerr KJ, Grunkemeier GL, type 2 diabetes mellitus: systematic re-
teral Nutr 22:77– 81, 1998 Starr A: Continuous intravenous insulin view and meta-analysis. Arch Intern Med
276. Umpierrez GE, Isaacs SD, Bazargan N, infusion reduces the incidence of deep 163:2594 –2602, 2003
You X, Thaler LM, Kitabchi AE: Hyper- sternal wound infection in diabetic pa- 298. Queale WS, Seidler AJ, Brancati FL: Gly-
glycemia: an independent marker of in- tients after cardiac surgical procedures. cemic control and sliding scale insulin
hospital mortality in patients with Ann Thorac Surg 67:352–360, 1999 use in medical inpatients with diabetes
undiagnosed diabetes. J Clin Endocrinol 286. Golden SH, Peart-Vigilance C, Kao WH, mellitus. Arch Intern Med 157:545–552,
Metab 87:978 –982, 2002 Brancati FL: Perioperative glycemic con- 1997
277. Capes SE, Hunt D, Malmberg K, Ger- trol and the risk of infectious complica- 299. Gearhart JG, Duncan JL, III, Replogle
stein HC: Stress hyperglycaemia and in- tions in a cohort of adults with diabetes. WH, Forbes RC, Walley EJ: Efficacy of
creased risk of death after myocardial Diabetes Care 22:1408 –1414, 1999 sliding-scale insulin therapy: a compar-
infarction in patients with and without 287. Zerr KJ, Furnary AP, Grunkemeier GL, ison with prospective regimens. Fam
diabetes: a systematic overview. Lancet Bookin S, Kanhere V, Starr A: Glucose Pract Res J 14:313–322, 1994
355:773–778, 2000 control lowers the risk of wound infec- 300. Walts LF, Miller J, Davidson MB, Brown
278. Bolk J, van der PT, Cornel JH, Arnold tion in diabetics after open heart opera- J: Perioperative management of diabetes
AE, Sepers J, Umans VA: Impaired glu- tions. Ann Thorac Surg 63:356 –361, mellitus. Anesthesiology 55:104–109, 1981
cose metabolism predicts mortality after 1997 301. Umpierrez GE, Smiley D, Zisman A, Pri-
a myocardial infarction. Int J Cardiol 79: 288. van den Bergh G, Wouters P, Weekers F, eto LM, Palacio A, Ceron M, Puig A, Me-
207–214, 2001 Verwaest C, Bruyninckx F, Schetz M, jia R: Randomized study of basal-bolus
279. Malmberg K: Prospective randomised Vlasselaers D, Ferdinande P, Lauwers P, insulin therapy in the inpatient manage-
study of intensive insulin treatment on Bouillon R: Intensive insulin therapy in ment of patients with type 2 diabetes
long term survival after acute myocardial the critically ill patients. N Engl J Med (RABBIT 2 trial). Diabetes Care 30:
infarction in patients with diabetes 345:1359 –1367, 2001 2181–2186, 2007
mellitus. DIGAMI (Diabetes Mellitus, 289. van den Bergh G, Wouters PJ, Bouillon 302. Schmeltz LR, DeSantis AJ, Schmidt K,
Insulin Glucose Infusion in Acute Myo- R, Weekers F, Verwaest C, Schetz M, O’Shea-Mahler E, Rhee C, Brandt S,
cardial Infarction) Study Group. BMJ Vlasselaers D, Ferdinande P, Lauwers P: Peterson S, Molitch ME: Conversion of
314:1512–1515, 1997 Outcome benefit of intensive insulin intravenous insulin infusions to subcu-
280. Malmberg K, Ryden L, Efendic S, Herlitz therapy in the critically ill: Insulin dose taneously administered insulin glargine
J, Nicol P, Waldenstrom A, Wedel H, versus glycemic control. Crit Care Med in patients with hyperglycemia. Endocr


Standards of Medical Care

Pract 12:641– 650, 2006 tes care in the school and day care set- 1086, 2001
303. Shilo S, Berezovsky S, Friedlander Y, ting. Diabetes Care 31 (Suppl. 1):S79 – 324. Meigs JB, Cagliero E, Dubey A, Murphy-
Sonnenblick M: Hypoglycemia in hospi- S86, 2008 Sheehy P, Gildesgame C, Chueh H,
talized nondiabetic older patients. J Am 314. National Diabetes Education Program: Barry MJ, Singer DE, Nathan DM: A con-
Geriatr Soc 46:978 –982, 1998 Helping the Student with Diabetes Succeed: trolled trial of web-based diabetes dis-
304. Fischer KF, Lees JA, Newman JH: Hypo- A Guide for School Personnel. Available ease management: the MGH diabetes
glycemia in hospitalized patients. at http://www.ndep.nih.gov/diabetes/ primary care improvement project. Dia-
Causes and outcomes. N Engl J Med 315: youth/youth.htm. Accessed 6 November betes Care 26:750 –757, 2003
1245–1250, 1986 2007 325. O’Connor PJ, Desai J, Solberg LI, Reger
305. Markovitz LJ, Wiechmann RJ, Harris N, 315. American Diabetes Association. Diabetes LA, Crain AL, Asche SE, Pearson TL,
Hayden V, Cooper J, Johnson G, Harel- Care Tasks at School: What Key Personnel Clark CK, Rush WA, Cherney LM,
stad R, Calkins L, Braithwaite SS: De- Need to Know. Available at http://www. Sperl-Hillen JM, Bishop DB: Random-
scription and evaluation of a glycemic diabetes.org/advocacy-and-legalresources/ ized trial of quality improvement inter-
management protocol for patients with discrimination/school/schooltraining.jsp. vention to improve diabetes care in
diabetes undergoing heart surgery. En- Accessed 6 November 2007 primary care settings. Diabetes Care 28:
docr Pract 8:10 –18, 2002 316. American Diabetes Association: Diabe- 1890 –1897, 2005
306. Levetan CS, Salas JR, Wilets IF, Zumoff tes care at diabetes camps. Diabetes Care 326. Sperl-Hillen JM, O’Connor PJ: Factors
B: Impact of endocrine and diabetes 29 (Suppl. 1):S56 –S58, 2006 driving diabetes care improvement in a
team consultation on hospital length of 317. American Diabetes Association: Diabe- large medical group: ten years of
stay for patients with diabetes. Am J Med tes management in correctional institu- progress. Am J Manag Care 11:S177–
99:22–28, 1995 tions. Diabetes Care 31 (Suppl. 1):S87– S185, 2005
307. Levetan CS, Passaro MD, Jablonski KA, S94, 2008 327. Siminerio LM: Implementing diabetes
Ratner RE: Effect of physician specialty 318. Cefalu WT, Smith SR, Blonde L, Fonseca self-management training programs:
on outcomes in diabetic ketoacidosis. V: The Hurricane Katrina aftermath and
breaking through the barriers in primary
Diabetes Care 22:1790 –1795, 1999 its impact on diabetes care: observations
care. Endocr Pract 12 (Suppl. 1):124 –
308. Koproski J, Pretto Z, Poretsky L: Effects from “ground zero”: lessons in disaster
130, 2006
of an intervention by a diabetes team in preparedness of people with diabetes.
328. Mahoney JJ: Reducing patient drug ac-
hospitalized patients with diabetes. Dia- Diabetes Care 29:158 –160, 2006
betes Care 20:1553–1555, 1997 319. American Diabetes Association State- quisition costs can lower diabetes health
309. Furnary AP, Braithwaite SS: Effects of ment on Emergency and Disaster Pre- claims. Am J Manag Care 11:S170 –S176,
outcome on in-hospital transition from paredness: a report of the Disaster 2005
intravenous insulin infusion to subcuta- Response Task Force. Diabetes Care 30: 329. Maney M, Tseng CL, Safford MM, Miller
neous therapy. Am J Cardiol 98:557– 2395–2398, 2007 DR, Pogach LM: Impact of self-reported
564, 2006 320. American Diabetes Association: Hypo- patient characteristics upon assessment
310. American Diabetes Association: Diabe- glycemia and employment/licensure. of glycemic control in the Veterans
tes nutrition recommendations for Diabetes Care 31 (Suppl. 1):S95, 2008 Health Administration. Diabetes Care
health care institutions (Position State- 321. American Diabetes Association: Third- 30:245–251, 2007
ment). Diabetes Care 27 (Suppl. 1):S55– party reimbursement for diabetes care, 330. Bergenstal RM: Treatment models from
S57, 2004 self-management education, and sup- the International Diabetes Center: ad-
311. Boucher JL, Swift CS, Franz MJ, plies. Diabetes Care 31 (Suppl. 1):S96 – vancing from oral agents to insulin ther-
Kulkarni K, Schafer RG, Pritchett E, S97, 2008 apy in type 2 diabetes. Endocr Pract 12
Clark NG: Inpatient management of di- 322. Saydah SH, Fradkin J, Cowie CC: Poor (Suppl. 1):98 –104, 2006
abetes and hyperglycemia: implications control of risk factors for vascular dis- 331. O’Connor PJ: Electronic medical records
for nutrition practice and the food and ease among adults with previously diag- and diabetes care improvement: are we
nutrition professional. J Am Diet Assoc nosed diabetes. JAMA 291:335–342, waiting for Godot? Diabetes Care
107:105–111, 2007 2004 26:942–943, 2003
312. De Block C, Manuel YK, Van Gaal L, Ro- 323. Clark CM, Jr, Snyder JW, Meek RL, Stutz 332. Shojania KG, Ranji SR, McDonald KM,
giers P: Intensive insulin therapy in the LM, Parkin CG: A systematic approach Grimshaw JM, Sundaram V, Rushakoff
intensive care unit: assessment by con- to risk stratification and intervention RJ, Owens DK: Effects of quality im-
tinuous glucose monitoring. Diabetes within a managed care environment im- provement strategies for type 2 diabetes
Care 29:1750 –1756, 2006 proves diabetes outcomes and patient on glycemic control: a meta-regression
313. American Diabetes Association: Diabe- satisfaction. Diabetes Care 24:1079 – analysis. JAMA 296:427– 440, 2006