american diabetes association (ada) guidelines

Standards of Medical Care in Diabetes—2008AMERICAN DIABETES ASSOCIATION

D iabetes is a chronic illness that re-quires continuing medical care andpatient self-management education

to prevent acute complications and to re-duce the risk of long-term complications.Diabetes care is complex and requires thatmany issues, beyond glycemic control, beaddressed. A large body of evidence existsthat supports a range of interventions toimprove diabetes outcomes.

These standards of care are intendedto provide clinicians, patients, research-ers, payors, and other interested individ-uals with the components of diabetescare, treatment goals, and tools to evalu-ate the quality of care. While individualpreferences, comorbidities, and other pa-tient factors may require modification ofgoals, targets that are desirable for mostpatients with diabetes are provided.These standards are not intended to pre-clude more extensive evaluation andmanagement of the patient by other spe-cialists as needed. For more detailed in-formation, refer to refs. 1–3.

The recommendations included arescreening, diagnostic, and therapeutic ac-tions that are known or believed to favor-ably affect health outcomes of patientswith diabetes. A grading system (Table 1),developed by the American Diabetes As-sociation (ADA) and modeled after exist-

ing methods, was utilized to clarify andcodify the evidence that forms the basisfor the recommendations. The level of ev-idence that supports each recommenda-tion is listed after each recommendationusing the letters A, B, C, or E.

I. CLASSIFICATION ANDDIAGNOSIS

A. ClassificationIn 1997, ADA issued new diagnostic andclassification criteria (4); in 2003, modi-fications were made regarding the diagno-sis of impaired fasting glucose (5). Theclassification of diabetes includes fourclinical classes:

● Type 1 diabetes (results from �-cell de-struction, usually leading to absoluteinsulin deficiency)

● Type 2 diabetes (results from a progres-sive insulin secretory defect on thebackground of insulin resistance)

● Other specific types of diabetes due toother causes, e.g., genetic defects in�-cell function, genetic defects in insu-lin action, diseases of the exocrine pan-creas (such as cystic fibrosis), and drug-or chemical-induced (such as in the

treatment of AIDS or after organ trans-plantation)

● Gestational diabetes mellitus (GDM)(diabetes diagnosed during pregnancy)

Some patients cannot be clearly classifiedas type 1 or type 2 diabetes. Clinical pre-sentation and disease progression varyconsiderably in both types of diabetes.Occasionally, patients who otherwisehave type 2 diabetes may present with ke-toacidosis. Similarly, patients with type 1may have a late onset and slow (but re-lentless) progression of disease despitehaving features of autoimmune disease.Such difficulties in diagnosis may occur inchildren, adolescents, and adults. The truediagnosis may become more obvious overtime.

B. Diagnosis of diabetes

Recommendations● The fasting plasma glucose (FPG) test is

the preferred test to diagnose diabetesin children and nonpregnant adults. (E)

● Use of the A1C for the diagnosis of di-abetes is not recommended at this time.(E)

Criteria for the diagnosis of diabetes innonpregnant adults are shown in Table 2.Three ways to diagnose diabetes are avail-able, and each must be confirmed on asubsequent day unless unequivocalsymptoms of hyperglycemia are present.Although the 75-g oral glucose tolerancetest (OGTT) is more sensitive and mod-estly more specific than the FPG to diag-nose diabetes, it is poorly reproducibleand difficult to perform in practice. Be-cause of ease of use, acceptability to pa-tients, and lower cost, the FPG is thepreferred diagnostic test. Although theFPG is less sensitive than the OGTT, thevast majority of people who do not meetdiagnostic criteria for diabetes by the FPGbut would by the OGTT will have an A1Cvalue well below 7.0% (6).

Although the OGTT is not recom-mended for routine clinical use, it may be

● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ●

The recommendations in this article are based on the evidence reviewed in the following publication:Standards of care for diabetes (Technical Review). Diabetes Care 17:1514–1522, 1994.

Originally approved 1988. Most recent review/revision, October 2007.Abbreviations: ABI, ankle-brachial index; ACE, angiotensin-converting enzyme; ADAG, A1C-Derived

Average Glucose; ARB, angiotensin receptor blocker; CAD, coronary artery disease; CBG, capillary bloodglucose; CHD, coronary heart disease; CHF, congestive heart failure; CKD, chronic kidney disease; CMS,Centers for Medicare and Medicaid Services; CSII, continuous subcutaneous insulin infusion; CVD, cardio-vascular disease; DCCT, Diabetes Control and Complications Trial; DKA, diabetic ketoacidosis; DMMP,diabetes medical management plan; DPN, distal symmetric polyneuropathy; DPP, Diabetes PreventionProgram; DRS, Diabetic Retinopathy Study; DSME, diabetes self-management education; DSMT, diabetesself-management training; eAG, estimated average glucose; ECG, electrocardiogram; EDIC, Epidemiology ofDiabetes Interventions and Complications; ERP, education recognition program; ESRD, end-stage renaldisease; ETDRS, Early Treatment Diabetic Retinopathy Study; FDA, Food and Drug Administration; FPG,fasting plasma glucose; GDM, gestational diabetes mellitus; GFR, glomerular filtration rate; ICU, intensivecare unit; IFG, impaired fasting glucose; IGT, impaired glucose tolerance; MICU, medical ICU; MNT,medical nutrition therapy; NDEP, National Diabetes Education Program; NPDR, nonproliferative diabeticretinopathy; OGTT, oral glucose tolerance test; PAD, peripheral arterial disease; PDR, proliferative diabeticretinopathy; PPG, postprandial plasma glucose; RAS, renin-angiotensin system; RDA, recommended dietaryallowance; SICU, surgical ICU; SMBG, self-monitoring of blood glucose; TSH, thyroid-stimulating hormone;TZD, thiazolidinedione; UKPDS, U.K. Prospective Diabetes Study.

DOI: 10.2337/dc08-S012© 2008 by the American Diabetes Association.

P O S I T I O N S T A T E M E N T

S12 DIABETES CARE, VOLUME 31, SUPPLEMENT 1, JANUARY 2008

useful for further evaluation of patients inwhom diabetes is still strongly suspectedbut who have normal FPG or impairedfasting glucose (IFG) (see Section 1.C).

Due to lack of evidence on prognosticsignificance and diagnostic thresholds,the use of the A1C for the diagnosis ofdiabetes is not recommended at this time.

C. Diagnosis of pre-diabetesHyperglycemia not sufficient to meet thediagnostic criteria for diabetes is catego-rized as either IFG or impaired glucosetolerance (IGT), depending on whether itis identified through the FPG or theOGTT:

● IFG � FPG 100 mg/dl (5.6 mmol/l) to125 mg/dl (6.9 mmol/l)

● IGT � 2-h plasma glucose 140 mg/dl(7.8 mmol/l) to 199 mg/dl (11.0mmol/l)

IFG and IGT have been officially termed“pre-diabetes.” Both categories of pre-diabetes are risk factors for future diabetesand for cardiovascular disease (CVD) (7).

II. TESTING FOR PRE-DIABETES AND DIABETESIN ASYMPTOMATICPATIENTS

Recommendations● Testing to detect pre-diabetes and type

2 diabetes in asymptomatic peopleshould be considered in adults who areoverweight or obese (BMI �25 kg/m2)and who have one or more additional

risk factors for diabetes (Table 3). Inthose without these risk factors, testingshould begin at age 45. (B)

● If tests are normal, repeat testing shouldbe carried out at least at 3-year inter-vals. (E)

● To test for pre-diabetes or diabetes, ei-ther an FPG test or a 2-h OGTT (75-gglucose load) or both are appropriate.(B)

● An OGTT may be considered in pa-tients with IFG to better define the riskof diabetes. (E)

● In those identified with pre-diabetes,identify and, if appropriate, treat otherCVD risk factors. (B)

For many illnesses, there is a major dis-tinction between screening and diagnos-tic testing. However, for diabetes, thesame tests would be used for “screening”as for diagnosis. Type 2 diabetes has along asymptomatic phase and significantclinical risk markers. Diabetes may beidentified anywhere along a spectrum ofclinical scenarios ranging from a seem-ingly low-risk individual who happens tohave glucose testing, to a higher-risk in-dividual who the provider tests because ofhigh suspicion of diabetes, to the symp-tomatic patient. The discussion herein isprimarily framed as testing for diabetes inthose without symptoms. Testing for dia-betes will also detect individuals with pre-diabetes.

A. Testing for pre-diabetes and type2 diabetes in adultsType 2 diabetes is frequently not diag-nosed until complications appear, andapproximately one-third of all peoplewith diabetes may be undiagnosed. Al-though the effectiveness of early identifi-cation of pre-diabetes and diabetes

Table 1—ADA evidence-grading system for clinical practice recommendations

Level ofevidence Description

A Clear evidence from well-conducted, generalizable, randomized controlledtrials that are adequately powered, including:● Evidence from a well-conducted multicenter trial● Evidence from a meta-analysis that incorporated quality ratings in the

analysisCompelling nonexperimental evidence, i.e., “all or none” rule developed

by the Centre for Evidence-Based Medicine at OxfordSupportive evidence from well-conducted randomized controlled trials

that are adequately powered, including:● Evidence from a well-conducted trial at one or more institutions● Evidence from a meta-analysis that incorporated quality ratings in the

analysisB Supportive evidence from well-conducted cohort studies, including:

● Evidence from a well-conducted prospective cohort study or registry● Evidence from a well-conducted meta-analysis of cohort studies

Supportive evidence from a well-conducted case-control studyC Supportive evidence from poorly controlled or uncontrolled studies,

including:● Evidence from randomized clinical trials with one or more major or

three or more minor methodological flaws that could invalidate theresults

● Evidence from observational studies with high potential for bias (suchas case series with comparison with historical controls)

● Evidence from case series or case reportsConflicting evidence with the weight of evidence supporting the

recommendationE Expert consensus or clinical experience

Table 2—Criteria for the diagnosis of diabetes

1. FPG �126 mg/dl (7.0 mmol/l). Fasting is defined as no caloric intake for atleast 8 h.*

OR2. Symptoms of hyperglycemia and a casual plasma glucose �200 mg/dl (11.1

mmol/l). Casual is defined as any time of day without regard to time since lastmeal. The classic symptoms of hyperglycemia include polyuria, polydipsia, andunexplained weight loss.

OR3. 2-h plasma glucose �200 mg/dl (11.1 mmol/l) during an OGTT. The test

should be performed as described by the World Health Organization, using aglucose load containing the equivalent of 75 g anhydrous glucose dissolved inwater.*

*In the absence of unequivocal hyperglycemia, these criteria should be confirmed by repeat testing on adifferent day (5).

Position Statement

DIABETES CARE, VOLUME 31, SUPPLEMENT 1, JANUARY 2008 S13

through mass testing of asymptomatic in-dividuals has not been definitively proven(and rigorous trials to provide such proofare unlikely to occur), pre-diabetes anddiabetes meet established criteria for con-ditions in which early detection is appro-priate. Both conditions are common,increasing in prevalence, and impose sig-nificant public health burdens. There is along presymptomatic phase before the di-agnosis of type 2 diabetes is usually made.Relatively simple tests are available to de-tect preclinical disease (8). Additionally,the duration of glycemic burden is astrong predictor of adverse outcomes,and effective interventions exist to pre-vent progression of pre-diabetes to diabe-tes (see Section IV) and to reduce risk ofcomplications of diabetes (see Section VI).

Recommendations for testing for pre-diabetes and diabetes in asymptomatic,undiagnosed adults are listed in Table 3.Testing should be considered in all adultswith BMI �25 kg/m2 and one or morerisk factors for diabetes. Because age is amajor risk factor for diabetes, testing ofthose without other risk factors shouldbegin no later than age 45.

Either FPG testing or the 2-h OGTT isappropriate for testing. The 2-h OGTTidentifies people with either IFG or IGTand, thus, more prediabetic people at in-creased risk for the development of dia-betes and CVD. It should be noted thatthe two tests do not necessarily detect thesame prediabetic individuals (9). The ef-ficacy of interventions for primary pre-vention of type 2 diabetes (10–16) hasprimarily been demonstrated among in-

dividuals with IGT, not among individu-als with IFG (who do not also have IGT).As noted in the diagnosis section (I.B), theFPG test is more convenient, more repro-ducible, less costly, and easier to admin-ister than the 2-h OGTT (4,5). An OGTTmay be useful in patients with IFG to bet-ter define the risk of diabetes.

The appropriate interval betweentests is not known (17). The rationale forthe 3-year interval is that false negativeswill be repeated before substantial timeelapses, and there is little likelihood thatan individual will develop significantcomplications of diabetes within 3 yearsof a negative test result.

Because of the need for follow-up anddiscussion of abnormal results, testingshould be carried out within the healthcare setting. Community screening out-side a health care setting is not recom-mended because people with positivetests may not seek appropriate follow-uptesting and care, and, conversely, theremay be failure to ensure appropriate re-peat testing for individuals who test neg-ative. Community screening may also bepoorly targeted, i.e., it may fail to reachthe groups most at risk and inappropri-ately test those at low risk (the worriedwell) or even those already diagnosed(18,19).

B. Testing for type 2 diabetes inchildrenThe incidence of type 2 diabetes in ado-lescents has increased dramatically in thelast decade, especially in minority popu-lations (20), although the disease remains

rare in the general population (21). Con-sistent with recommendations for adults,children and youth at increased risk forthe presence or the development of type 2diabetes should be tested (22). The rec-ommendations of the ADA consensusstatement on type 2 diabetes in childrenand youth are summarized in Table 4.

C. Screening for type 1 diabetesGenerally, people with type 1 diabetespresent with acute symptoms of diabetesand markedly elevated blood glucose lev-els, and most cases are diagnosed soonafter the onset of hyperglycemia. Wide-spread clinical testing of asymptomaticindividuals for the presence of autoanti-bodies related to type 1 diabetes cannotcurrently be recommended as a means toidentify individuals at risk, for several rea-sons: 1) cutoff values for the immunemarker assays have not been completelyestablished or standardized for clinicalsettings; 2) there is no consensus as towhat follow-up testing should be under-taken when a positive autoantibody testresult is obtained; and 3) because the in-cidence of type 1 diabetes is low, testing ofhealthy individuals will identify only avery small number (�0.5%) who at thatmoment may be “prediabetic.” Finally,though clinical studies are being con-ducted to test various methods of pre-venting type 1 diabetes in high-riskindividuals, no effective intervention hasyet been identified. If studies uncover aneffective means of preventing type 1 dia-betes, targeted screening (e.g., siblings oftype 1 children) may be appropriate in thefuture.

Table 3—Criteria for testing for pre-diabetes and diabetes in asymptomatic adult individuals

1. Testing should be considered in all adults who are overweight (BMI �25 kg/m2*) andhave additional risk factors:● physical inactivity● first-degree relative with diabetes● members of a high-risk ethnic population (e.g., African American, Latino, NativeAmerican, Asian American, and Pacific Islander)● women who delivered a baby weighing �9 lb or were diagnosed with GDM● hypertension (�140/90 mmHg or on therapy for hypertension)● HDL cholesterol level �35 mg/dl (0.90 mmol/l) and/or a triglyceride level �250mg/dl (2.82 mmol/l)● women with polycystic ovarian syndrome (PCOS)● IGT or IFG on previous testing● other clinical conditions associated with insulin resistance (e.g., severe obesityand acanthosis nigricans)● history of CVD

2. In the absence of the above criteria, testing for pre-diabetes and diabetes should beginat age 45 years

3. If results are normal, testing should be repeated at least at 3-year intervals, withconsideration of more frequent testing depending on initial results and risk status.

*At-risk BMI may be lower in some ethnic groups.

Table 4—Testing for type 2 diabetes inasymptomatic children

Criteria● Overweight (BMI �85th percentile for

age and sex, weight for height �85thpercentile, or weight �120% of ideal forheight)

Plus any two of the following risk factors:● Family history of type 2 diabetes in first-

or second-degree relative● Race/ethnicity (e.g., Native American,

African American, Latino, Asian American,and Pacific Islander)

● Signs of insulin resistance or conditionsassociated with insulin resistance (e.g.,acanthosis nigricans, hypertension,dyslipidemia, or PCOS)

● Maternal history of diabetes or GDMAge of initiation: age 10 years or at onset of

puberty, if puberty occurs at a younger ageFrequency: every 2 yearsTest: FPG preferred

Standards of Medical Care


III. DETECTION ANDDIAGNOSIS OFGESTATIONAL DIABETESMELLITUS (GDM)

Recommendations● Screen for GDM using risk factor anal-

ysis and, if appropriate, use of anOGTT. (C)

● Women with GDM should be screenedfor diabetes 6–12 weeks postpartumand should be followed up with subse-quent screening for the development ofdiabetes or pre-diabetes. (E)

Gestational diabetes mellitus is defined asany degree of glucose intolerance with on-set or first recognition during pregnancy(4). Although most cases resolve with de-livery, the definition applies whether ornot the condition persists after pregnancyand does not exclude the possibility thatunrecognized glucose intolerance mayhave antedated or begun concomitantlywith the pregnancy. Approximately 7% ofall pregnancies (ranging from 1 to 14%depending on the population studied andthe diagnostic tests used) are complicatedby GDM, resulting in more than 200,000cases annually.

Because of the risks of GDM to themother and neonate, screening and diag-nosis are warranted. The screening anddiagnostic strategies, based on the 2004ADA position statement on gestational di-abetes mellitus (23), are outlined in Table 5.

Results of the Hyperglycemia and Ad-verse Pregnancy Outcomes study were re-ported at ADA’s 67th Annual ScientificSessions in June 2007. This large-scale(�25,000 pregnant women), multi-national, epidemiologic study demon-strated that risk of adverse maternal, fetal,and neonatal outcomes continuously in-creased as a function of maternal glycemiaat 24–28 weeks, even within ranges pre-viously considered normal for pregnancy.For most complications, there was nothreshold for risk. These results may callfor careful reconsideration of the diagnos-tic criteria for GDM.

Because women with a history ofGDM have a greatly increased subsequentrisk for diabetes (24), they should bescreened for diabetes 6–12 weeks post-partum, using standard criteria, andshould be followed up with subsequentscreening for the development of diabetesor pre-diabetes, as outlined in Section II.For information on the National DiabetesEducation Program (NDEP) campaign toprevent type 2 diabetes in women with

GDM, go to www.ndep.nih.gov/diabetes/pubs/NeverTooEarly_Tipsheet.pdf.

IV. PREVENTION/DELAYOF TYPE 2 DIABETES

Recommendations● Patients with IGT (A) or IFG (E) should

be given counseling on weight loss of5–10% of body weight, as well as onincreasing physical activity to at least150 min/week of moderate activitysuch as walking.

● Follow-up counseling appears to be im-portant for success. (B)

● Based on potential cost savings of dia-betes prevention, such counselingshould be covered by third-party pay-ors. (E)

● In addition to lifestyle counseling, met-formin may be considered in those whoare at very high risk (combined IFG and

IGT plus other risk factors) and who areobese and under 60 years of age. (E)

● Monitoring for the development of di-abetes in those with pre-diabetesshould be performed every year. (E)

Randomized controlled trials have shownthat individuals at high risk for develop-ing diabetes (those with IFG, IGT, orboth) can be given interventions that sig-nificantly decrease the rate of onset of di-abetes (10 –16). These interventionsinclude an intensive lifestyle modificationprogram that has been shown to be veryeffective (�58% reduction after 3 years),and use of the pharmacologic agents met-formin, acarbose, orlistat, and rosiglita-zone, each of which has been shown todecrease incident diabetes to various de-grees. A summary of major diabetes pre-vention trials is shown in Table 6.

Based on the results of clinical trialsand the known risks of progression of

Table 5—Screening for and diagnosis of GDM

Carry out GDM risk assessment at the first prenatal visit.Women at very high risk for GDM should be screened for diabetes as soon as possible after

the confirmation of pregnancy. Criteria for very high risk are:● Severe obesity● Prior history of GDM or delivery of large-for-gestational-age infant● Presence of glycosuria● Diagnosis of PCOS● Strong family history of type 2 diabetes

Screening/diagnosis at this stage of pregnancy should use standard diagnostic testing (Table 2)All women of higher than low risk of GDM, including those above not found to have

diabetes early in pregnancy, should undergo GDM testing at 24–28 weeks of gestation.Low risk status, which does not require GDM screening, is defined as women with all ofthe following characteristics:● Age �25 years● Weight normal before pregnancy● Member of an ethnic group with a low prevalence of diabetes● No known diabetes in first-degree relatives● No history of abnormal glucose tolerance● No history of poor obstetrical outcome

Two approaches may be followed for GDM screening at 24–28 weeks:1. Two-step approach:

A. Perform initial screening by measuring plasma or serum glucose 1 h after a 50-g oralglucose load. A glucose threshold after 50-g load of �140 mg/dl identifies � 80% ofwomen with GDM, while the sensitivity is further increased to � 90% by a threshold of�130 mg/dl.B. Perform a diagnostic 100-g OGTT on a separate day in women who exceed thechosen threshold on 50-g screening.

2. One-step approach (may be preferred in clinics with high prevalence of GDM): Performa diagnostic 100-g OGTT in all women to be tested at 24–28 weeks.

The 100-g OGTT should be performed in the morning after an overnight fast of at least 8 h.A diagnosis of GDM requires at least two of the following plasma glucose values:

Fasting: �95 mg/dl (�5.3 mmol/l)1 h: �180 mg/dl (�10.0 mmol/l)2 h: �155 mg/dl (�8.6 mmol/l)3 h: �140 mg/dl (�7.8 mmol/l)

Position Statement


pre-diabetes to diabetes, an ADA consen-sus development panel in 2007 (7) con-cluded that persons with pre-diabetes(IGT and/or IFG) should be counseled onlifestyle changes with goals similar tothose of the Diabetes Prevention Program(DPP) (5–10% weight loss and moderatephysical activity of �30 min/day). Re-garding the more difficult issue of drugtherapy for diabetes prevention, the con-sensus panel felt that metformin shouldbe the only drug considered for use indiabetes prevention. For other drugs, theissues of cost, side effects, and lack of per-sistence of effect in some studies led thepanel to not recommend their use for di-abetes prevention. Metformin use wasrecommended only for very high-risk in-dividuals (combined IGT and IFG, andwith at least one other risk factor). In ad-dition, the panel highlighted the evidencethat in the DPP, treatment with met-formin had the most relative effectivenessin those with BMI of at least 35 kg/m2 andthose under age 60.

V. DIABETES CARE

A. Initial evaluationA complete medical evaluation should beperformed to classify the diabetes, detectthe presence of diabetes complications,review previous treatment and glycemiccontrol in patients with established diabe-tes, assist in formulating a managementplan, and provide a basis for continuingcare. Laboratory tests appropriate to theevaluation of each patient’s medical con-dition should be performed. A focus onthe components of comprehensive care(Table 7) will assist the health care team toensure optimal management of the pa-tient with diabetes.

B. ManagementPeople with diabetes should receive med-ical care from a physician-coordinatedteam. Such teams may include, but arenot limited to, physicians, nurse practitio-ners, physician’s assistants, nurses, dieti-tians, pharmacists, and mental healthprofessionals with expertise and a special

interest in diabetes. It is essential in thiscollaborative and integrated team ap-proach that individuals with diabetes as-sume an active role in their care.

The management plan should be for-mulated as an individualized therapeuticalliance among the patient and family, thephysician, and other members of thehealth care team. A variety of strategiesand techniques should be used to provideadequate education and development ofproblem-solving skills in the various as-pects of diabetes management. Imple-mentation of the management planrequires that each aspect is understoodand agreed on by the patient and the careproviders and that the goals and treat-ment plan are reasonable. Any planshould recognize diabetes self-manage-ment education (DSME) as an integralcomponent of care. In developing theplan, consideration should be given to thepatient’s age, school or work scheduleand conditions, physical activity, eatingpatterns, social situation and personality,cultural factors, and presence of compli-

Table 6—Therapies proven effective in diabetes prevention trials

Study(reference)‡ n Population

Age(years)

Duration(years)

Followup

Intervention(daily dose)

Controlsubjects(%/year) Relative risk

Finnish DPS (15) 522 IGT, BMI �25 kg/m2 55 3.2 92 Individualdiet/exercise

6 0.42 (0.30–070)

DPP (14) 2,161* IGT, BMI �24 kg/m2,FPG �5.3 (95)

51 3 93 Individualdiet/exercise

10 0.42 (0.34–0.52)

Pan et al. (22) 259* IGT (randomizedgroups)

45 6 92 Group diet/exercise

16 0.62 (0.44–0.86)

Kosaka et al. (23) 458 IGT (men), BMI � 24kg/m2

�55 4 92 Individualdiet/exercise

2 0.33 (0.10–1.0)†

Indian DPP (24) 269* IGT 46 2.5 95 Individualdiet/exercise

22 0.71 (0.63–0.79)

DPP (14) 2,155* IGT, BMI �24 kg/m2,FPG �5.3

51 2.8 93 Metformin(1,700 mg)

10 0.69 (0.57–0.83)

Indian DPP (24) 269* IGT 46 2.5 95 Metformin(500 mg)

22 0.74 (0.65–0.81)

STOP NIDDM(16)

1,419 IGT, FPG �5.6 54 3.2 96 Acarbose(300 mg)

13 0.75 (0.63–0.90)

XENDOS (18) 3,277 BMI �30 kg/m2 43 4 43 Orlistat(360 mg)

2 0.63 (0.46–0.86)

DPP (25) 1,067* IGT, BMI �24 kg/m2,FPG �5.3

51 0.9 93 Troglitazone(400 mg)

12 0.25 (0.14–0.43)†

TRIPOD (26) 266 Previous GDM 35 2.5 67 Troglitazone(400 mg)

12 0.45 (0.25–0.83)

DREAM (17) 5,269 IGT or IFG 55 3.0 94 Rosiglitazone(8 mg)

9 0.40 (0.35–0.46)

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 ObeseSubjects.



cations of diabetes or other medicalconditions.

C. Glycemic control1. Assessment of glycemic control.Two primary techniques are available forhealth providers and patients to assess theeffectiveness of the management plan onglycemic control: patient self-monitoringof blood glucose (SMBG) and A1C mea-surement. In addition, in recent yearstechnologies for continuous monitoringof interstitial glucose have entered themarket.

a. Self-monitoring of blood glucose

Recommendations● SMBG should be carried out three or

more times daily for patients using mul-tiple insulin injections or insulin pumptherapy. (A)

● For patients using less frequent insulininjections, noninsulin therapies, ormedical nutrition therapy (MNT)alone, SMBG may be useful in achiev-ing glycemic goals. (E)

● To achieve postprandial glucose tar-

gets, postprandial SMBG may be appro-priate. (E)

● When prescribing SMBG, ensure thatpatients receive initial instruction in,and routine follow-up evaluation of,SMBG technique and their ability to usedata to adjust therapy. (E)

● Continuous glucose monitoring may bea supplemental tool to SMBG for se-lected patients with type 1 diabetes, es-pecially those with hypoglycemiaunawareness. (E)

ADA’s consensus and position statementson SMBG provide a comprehensive re-view of the subject (26,27). Major clinicaltrials of insulin-treated patients that dem-onstrated the benefits of intensive glyce-mic control on diabetes complicationshave included SMBG as part of multifac-torial interventions, suggesting thatSMBG is a component of effective ther-apy. SMBG allows patients to evaluatetheir individual response to therapy andassess whether glycemic targets are beingachieved. Results of SMBG can be usefulin preventing hypoglycemia and adjust-ing medications (particularly prandial in-sulin doses), MNT, and physical activity.

The frequency and timing of SMBGshould be dictated by the particular needsand goals of the patients. SMBG is espe-cially important for patients treated withinsulin to monitor for and prevent asymp-tomatic hypoglycemia and hyperglyce-mia. For most patients with type 1diabetes and pregnant women taking in-sulin, SMBG is recommended three ormore times daily. For this population, it isoften difficult to reach A1C targets safelywithout hypoglycemia with the minimumof three daily tests. The optimal frequencyand timing of SMBG for patients with type2 diabetes on noninsulin therapy is notknown but should be sufficient to facili-tate reaching glucose goals. A meta-analysis of SMBG in non–insulin-treatedpatients with type 2 diabetes concludedthat some regimen of SMBG was associ-ated with a reduction in A1C of �0.4%.However, many of the studies in this anal-ysis also included patient education withdiet and exercise counseling and, in somecases, pharmacologic intervention, mak-ing it difficult to assess the contribution ofSMBG alone to improved control (28).

Because the accuracy of SMBG is in-strument and user dependent (29), it isimportant to evaluate each patient’s mon-itoring technique, both initially and atregular intervals thereafter. In addition,optimal use of SMBG requires proper in-

Table 7—Components of the comprehensive diabetes evaluation

Medical history● Age and characteristics of onset of diabetes (e.g., DKA, asymptomatic laboratory finding)● Eating patterns, nutritional status, and weight history; growth and development inchildren and adolescents● Diabetes education history● Review of previous treatment regimens and response to therapy (A1C records)● Current treatment of diabetes, including medications, meal plan, physical activitypatterns, and results of glucose monitoring and patient’s use of data● DKA frequency, severity, and cause● Hypoglycemic episodes

● Hypoglycemia awareness● Any severe hypoglycemia: frequency and cause

● History of diabetes-related complications● Microvascular: retinopathy, nephropathy, neuropathy (sensory, including history offoot lesions; autonomic, including sexual dysfunction and gastroparesis)● Macrovascular: CHD, cerebrovascular disease, PAD● Other: psychosocial problems,* dental disease*

Physical examination● Height, weight, BMI● Blood pressure determination, including orthostatic measurements when indicated● Fundoscopic examination*● Thyroid palpation● Skin examination (for acanthosis nigricans and insulin injection sites)● Comprehensive foot examination:

● Inspection● Palpation of dorsalis pedis and posterior tibial pulses● Presence/absence of patellar and Achilles reflexes● Determination of proprioception, vibration, and monofilament sensation

Laboratory evaluation● A1C, if results not available within past 2–3 months

If not performed/available within past year:● Fasting lipid profile, including total, LDL, and HDL cholesterol and triglycerides● Liver function tests● Test for urine albumin excretion with spot urine albumin-to-creatinine ratio● Serum creatinine and calculated GFR● Thyroid-stimulating hormone in type 1 diabetes, dyslipidemia or women over age 50

Referrals● Annual dilated eye exam● Family planning for women of reproductive age● Registered dietitian for MNT● Diabetes self-management education● Dental examination● Mental health professional, if needed

*See appropriate referrals for these categories.

Position Statement


terpretation of the data. Patients shouldbe taught how to use the data to adjustfood intake, exercise, or pharmacologicaltherapy to achieve specific glycemic goals,and these skills should be re-evaluatedperiodically.

In recent years, methods to sampleinterstitial fluid glucose (which correlateshighly with blood glucose) in a continu-ous and minimally invasive way havebeen developed. Most microdialysis sys-tems are inserted subcutaneously, whilean early system employed “reverse ionto-phoresis” to move glucose across the skin.The concentration of glucose is then mea-sured by a glucose oxidase electrode de-tector. These systems require calibrationwith SMBG readings, and the latter arestill recommended for making treatmentdecisions. Continuous glucose sensorshave alarms for hypo- and hyperglycemia.Small studies in selected patient popula-tions have shown good correlation ofreadings with SMBG and decreases in themean time spent in hypo- and hypergly-cemic ranges compared with blindedsensor use (30). Although continuousglucose sensors would seem to showgreat promise in diabetes management,as yet no rigorous controlled trials havedemonstrated improvements in long-term glycemia.

b. A1C

Recommendations● Perform the A1C test at least two times

a year in patients who are meeting treat-

ment goals (and who have stable glyce-mic control). (E)

● Perform the A1C test quarterly in pa-tients whose therapy has changed orwho are not meeting glycemic goals. (E)

● Use of point-of-care testing for A1C al-lows for timely decisions on therapychanges, when needed. (E)

Because A1C is thought to reflect averageglycemia over several months (29), andhas strong predictive value for diabetescomplications (10,31), A1C testingshould be performed routinely in all pa-tients with diabetes, at initial assessmentand then as part of continuing care. Mea-surement approximately every 3 monthsdetermines whether a patient’s glycemictargets (Table 8) have been reached andmaintained. For any individual patient,the frequency of A1C testing should bedependent on the clinical situation, thetreatment regimen used, and the judg-ment of the clinician. Some patients withstable glycemia well within target may dowell with testing only twice per year,while unstable or highly intensively man-aged patients (e.g., pregnant type 1women) may be tested more frequentlythan every 3 months. The availability ofthe A1C result at the time that the patientis seen (point-of-care testing) has been re-ported to result in increased intensifica-tion of therapy and improvement inglycemic control (32,33).

The A1C test is subject to certain lim-itations. Conditions that affect erythro-cyte turnover (hemolysis, blood loss) and

hemoglobin variants must be considered,particularly when the A1C result does notcorrelate with the patient’s clinical situa-tion (29). In addition, A1C does not pro-vide a measure of glycemic variability orhypoglycemia. For patients prone to gly-cemic variability (especially type 1 dia-betic patients, or type 2 diabetic patientswith severe insulin deficiency), glycemiccontrol is best judged by the combinationof results of SMBG testing and the A1C.The A1C may also serve as a check on theaccuracy of the patient’s meter (or the pa-tient’s reported SMBG results) and the ad-equacy of the SMBG testing schedule.

Table 9 contains the correlation be-tween A1C levels and mean plasma glu-cose levels based on data from theDiabetes Control and Complications Trial(DCCT) (34). The correlation is based onrelatively sparse data from a primarilyCaucasian type 1 diabetic population.Preliminary results of the multicenterA1C-Derived Average Glucose (ADAG)Trial, presented at the European Associa-tion for the Study of Diabetes meeting inSeptember 2007, confirmed a close cor-relation of A1C with mean glucose in pa-tients with type 1, type 2, or no diabetes.Final results of this study, not available atthe time this statement was completed,should allow more accurate reporting ofthe estimated average glucose (eAG) andimprove patients’ understanding of thismeasure of glycemia. An updated versionof Table 9, based on final results of theADAG Trial, will be available at www.diabetes.org after publication of thestudy’s findings in 2008.

Table 8—Summary of glycemic recommendations for adults with diabetes

A1C �7.0%*

Preprandial capillary plasma glucose 70–130 mg/dl (3.9–7.2mmol/l)

Peak postprandial capillary plasma glucose† �180 mg/dl (�10.0 mmol/l)Key concepts in setting glycemic goals:

● A1C is the primary target for glycemic control● Goals should be individualized based on:

● duration of diabetes● pregnancy status● age● comorbid conditions● hypoglycemia unawareness● individual patient considerations

● More stringent glycemic goals (i.e., a normal A1C,�6%) may further reduce complications at the cost ofincreased risk of hypoglycemia

● Postprandial glucose may be targeted if A1C goals arenot met despite reaching preprandial glucose goals

*Referenced to a nondiabetic range of 4.0–6.0% using a DCCT-based assay. †Postprandial glucose mea-surements should be made 1–2 h after the beginning of the meal, generally peak levels in patients withdiabetes.

Table 9—Correlation between A1C level andmean plasma glucose levels on multiple test-ing over 2–3 months

A1C (%) Mean plasma glucose

mg/dl mmol/l

6 135 7.57 170 9.58 205 11.59 240 13.510 275 15.511 310 17.512 345 19.5

These estimates are based on DCCT data (34). Anupdated version of this table, based on final resultsof the ADAG Trial, will be available at www.diabetes.org after publication of the study’s findings in 2008.



2. Glycemic goals

Recommendations● Lowering A1C to an average of �7%

has clearly been shown to reduce mi-crovascular and neuropathic complica-tions of diabetes and, possibly,macrovascular disease. Therefore, theA1C goal for nonpregnant adults ingeneral is �7%. (A)

● Epidemiologic studies have suggestedan incremental (albeit, in absoluteterms, a small) benefit to lowering A1Cfrom 7% into the normal range. There-fore, the A1C goal for selected individ-ual patients is as close to normal (�6%)as possible without significant hypogly-cemia. (B)

● Less stringent A1C goals may be appro-priate for patients with a history of se-vere hypoglycemia, patients withlimited life expectancies, children, in-dividuals with comorbid conditions,and those with longstanding diabetesand minimal or stable microvascularcomplications. (E)

Glycemic control is fundamental to themanagement of diabetes. The DCCT, aprospective, randomized, controlled trialof intensive versus standard glycemiccontrol in type 1 diabetes, showed defin-itively that improved glycemic control isassociated with sustained decreased ratesof microvascular (retinopathy and ne-phropathy) as well as neuropathic com-plications (35). Follow up of the DCCTcohorts in the Epidemiology of DiabetesInterventions and Complications (EDIC)study has shown persistence of this effectin previously intensively treated subjects,even though their glycemic control hasbeen equivalent to that of previous stan-dard arm subjects during follow-up(36,37). In addition, EDIC has shown asignificant reduction of the rate of cardio-vascular outcomes in the previous inten-sive arm (38).

In type 2 diabetes, the Kumamotostudy (39) and the UK Prospective Diabe-tes Study (UKPDS) (40,41) demonstratedsignificant reductions in microvascularand neuropathic complications with in-tensive therapy. The potential of intensiveglycemic control to reduce CVD in type 2diabetes is supported by epidemiologicalstudies (31,40–42) and a meta-analysis(43), but has not yet been demonstratedin a randomized clinical trial. Severallarge trials are currently under way to ad-dress this issue.

In each of these large randomized

prospective clinical trials, treatment regi-mens that reduced average A1C to �7%(�1% above the upper limits of normal)were associated with fewer long-term mi-crovascular complications; however, in-tensive control was found to increase therisk of severe hypoglycemia, most notablyin the DCCT, and to lead to weight gain(31,44).

Epidemiological analyses of theDCCT and UKPDS (31,35) demonstrate acurvilinear relationship between A1C andmicrovascular complications. Such anal-yses suggest that, on a population level,the greatest number of complications willbe averted by taking patients from verypoor control to fair or good control. Theseanalyses also suggest that further loweringof A1C from 7 to 6% is associated withfurther reduction in the risk of complica-tions, albeit the absolute risk reductionsbecome much smaller. Given the substan-tially increased risk of hypoglycemia (par-ticularly in those with type 1 diabetes)and the relatively much greater effort re-quired to achieve near-normoglycemia,the risks of lower targets may outweighthe potential benefits on a populationlevel. However, selected individual pa-tients, especially those with little comor-bidity and long life expectancy (who mayreap the benefits of further lowering ofglycemia below 7%) may, at patient andprovider judgment, have glycemic targetsas close to normal as possible without sig-nificant hypoglycemia becoming a barrier.

Recommended glycemic goals fornonpregnant individuals are shown in Ta-ble 8. The recommendations are based ondata for A1C. The listed blood glucosegoals are levels that appear to correlatewith achievement of an A1C of �7%. Lessstringent treatment goals may be appro-priate for patients with limited life expect-ancies, in children, and in individualswith comorbid conditions. Severe or fre-quent hypoglycemia is an indication forthe modification of treatment regimens,including setting higher glycemic goals.

Neither the DCCT nor the UKPDS ad-dressed patient populations with long du-rations of diabetes. Clinical experiencesuggests that it is uncommon for signifi-cant microvascular disease to begin after20–30 years of diabetes. Furthermore,hypoglycemia unawareness becomesmore prevalent with long duration of di-abetes. Therefore, in patients with long-standing diabetes (three or more decades)and minimal or stable microvascularcomplications, the risk-to-benefit ratiofor stringent A1C goals appears high.

The issue of pre- versus postprandialSMBG targets is complex (45). Elevatedpostchallenge (2-h OGTT) glucose valueshave been associated with increased car-diovascular risk independent of FPG insome epidemiological studies. In diabeticsubjects, some surrogate measures of vas-cular pathology, such as endothelial dys-function, are negatively affected bypostprandial hyperglycemia (46). It isclear that postprandial hyperglycemia,like preprandial hyperglycemia, contrib-utes to elevated A1C levels, with its rela-tive contribution being higher at A1Clevels that are closer to 7%. However, out-come studies have clearly shown A1C tobe the primary predictor of complica-tions, and the glycemic control trials suchas the DCCT relied overwhelmingly onpreprandial SMBG. Thus, a reasonablerecommendation is: In individuals whohave premeal glucose values within targetbut have A1C values above target, moni-toring postprandial plasma glucose (PPG)1–2 h after the start of the meal and treat-ment aimed at reducing PPG values to�180 mg/dl will likely lower A1C andmay improve outcomes.

In regard to glycemic control forwomen with GDM, recommendationsfrom the Fourth International Workshop-Conference on Gestational Diabetes Mel-litus (47) suggested lowering maternalcapillary whole-blood glucose concentra-tions to:

● Preprandial: �95 mg/dl (5.3 mmol/l),and either:● 1-h postmeal: �140 mg/dl (7.8

mmol/l) or● 2-h postmeal: �120 mg/dl (6.7

mmol/l)

Comparable plasma-referenced capillaryblood glucose values suggested in theADA Position Statement on GDM (14)are:

● Preprandial: �105 mg/dl (5.8 mmol/l),and either:● 1-h postmeal: �155 mg/dl (8.6

mmol/l) or● 2-h postmeal: �130 mg/dl (7.2

mmol/l)

3. Approach to treatment

a. Therapy for type 1 diabetes. TheDCCT clearly showed that intensive insu-lin therapy (three or more injections perday of insulin or continuous subcutane-ous insulin infusion [CSII, or insulin

Position Statement


pump therapy]) was a key part of im-proved glycemia and better outcomes(35). At the time of the study, therapy wascarried out with short- and intermediate-acting human insulins. Despite better mi-crovascular outcomes, intensive insulintherapy was associated with a marked in-crease in severe hypoglycemia (62 epi-sodes per 100 patient-years of therapy).Since the time of the DCCT, a number ofrapid-acting and long-acting insulin ana-logs have been developed. These analogswere designed to be more “physiological”in their pharmacokinetics and pharmaco-dynamics, and are associated with less hy-poglycemia with equal A1C lowering intype 1 diabetes (48,49).

Therefore, recommended therapy fortype 1 diabetes consists of the followingcomponents: 1) use of multiple dose in-sulin injections (3–4 injections per day ofbasal and prandial insulin) or CSII ther-apy; 2) matching of prandial insulin tocarbohydrate intake, premeal blood glu-cose, and anticipated activity; and 3) formany patients (especially if hypoglycemiais a problem), use of insulin analogs.There are excellent reviews available thatguide the initiation and management ofinsulin therapy to achieve desired glyce-mic goals (3,48,50).

b. Therapy for type 2 diabetes. ADA andthe European Association for the Study ofDiabetes published a consensus state-ment on the approach to management ofhyperglycemia in individuals with type 2diabetes (51). Highlights of this approachare 1) intervention at the time of diagnosiswith metformin in combination with life-style changes (MNT and exercise) and 2)continuing timely augmentation of ther-apy with additional agents (includingearly initiation of insulin therapy) as ameans of achieving and maintaining rec-ommended levels of glycemic control(i.e., A1C �7% for most patients). Theoverall objective is to achieve and main-tain glycemic levels as close to the nondi-abetic range as possible and to changeinterventions at as rapid a pace as titrationof medications allows.

The algorithm took into account theevidence for A1C-lowering of the individ-ual interventions, their synergies, andtheir expense. Of note, the consensus al-gorithm was developed before publica-tions that raised concerns about increasedrisk of myocardial infarction with use ofrosiglitazone (52,53) and before additionof black box warnings about congestiveheart failure (CHF) for both rosiglitazone

and pioglitazone. This new informationmay prompt greater caution in using thethiazolidinediones. Other medicationssuch as pramlintide, exenatide, �-gluco-sidase inhibitors, the glinides, and dipep-tidyl peptidase IV inhibitors were notincluded in the consensus algorithm, ow-ing to less glucose-lowering effectiveness,limited clinical data, and/or relative ex-pense. However, they may be appropriatechoices in individual patients to achieveglycemic goals. Initiation of insulin attime of diagnosis is recommended for in-dividuals presenting with weight loss orother severe hyperglycemic symptoms orsigns. For a list of currently approveddiabetes medications, see http://ndep.nih.gov/diabetes/pubs/Drug_tables_supplement.pdf.

D. MEDICAL NUTRITIONTHERAPY (MNT)

General recommendations● Individuals who have pre-diabetes or

diabetes should receive individualizedMNT as needed to achieve treatmentgoals, preferably provided by a regis-tered dietitian familiar with the compo-nents of diabetes MNT. (B)

● MNT should be covered by insuranceand other payors. (E)

Energy balance, overweight, andobesity● In overweight and obese insulin-

resistant individuals, modest weightloss has been shown to reduce insulinresistance. Thus, weight loss is recom-mended for all overweight or obese in-dividuals who have or are at risk fordiabetes. (A)

● For weight loss, either low-carbohy-drate or low-fat calorie-restricted dietsmay be effective in the short term (up to1 year). (A)

● For patients on low-carbohydrate diets,monitor lipid profiles, renal function,and protein intake (in those with ne-phropathy), and adjust hypoglycemictherapy as needed. (E)

● Physical activity and behavior modifi-cation are important components ofweight loss programs and are mosthelpful in maintenance of weight loss.(B)

Primary prevention of diabetes● Among individuals at high risk for de-

veloping type 2 diabetes, structuredprograms that emphasize lifestylechanges that include moderate weight

loss (7% body weight) and regularphysical activity (150 min/week), withdietary strategies including reducedcalories and reduced intake of dietaryfat, can reduce the risk for developingdiabetes and are therefore recom-mended. (A)

● Individuals at high risk for type 2 dia-betes should be encouraged to achievethe U.S. Department of Agriculture(USDA) recommendation for dietary fi-ber (14 g fiber/1,000 kcal) and foodscontaining whole grains (one-half ofgrain intake). (B)

Dietary fat intake in diabetesmanagement● Saturated fat intake should be �7% of

total calories. (A)● Intake of trans fat should be minimized.

(E)

Carbohydrate intake in diabetesmanagement● Monitoring carbohydrate intake,

whether by carbohydrate counting, ex-changes, or experience-based estima-tion, remains a key strategy in achievingglycemic control. (A)

● For individuals with diabetes, the use ofthe glycemic index and glycemic loadmay provide a modest additional bene-fit for glycemic control over that ob-served when total carbohydrate isconsidered alone. (B)

Other nutrition recommendations● Sugar alcohols and nonnutritive sweet-

eners are safe when consumed withinthe acceptable daily intake levels estab-lished by the Food and Drug Adminis-tration (FDA). (A)

● If adults with diabetes choose to usealcohol, daily intake should be limitedto a moderate amount (one drink perday or less for adult women and twodrinks per day or less for adult men).(E)

● Routine supplementation with antioxi-dants, such as vitamins E and C andcarotene, is not advised because of lackof evidence of efficacy and concern re-lated to long-term safety. (A)

● Benefit from chromium supplementa-tion in people with diabetes or obesityhas not been conclusively demon-strated and, therefore, cannot be rec-ommended. (E)

MNT is an integral component of diabetesprevention, management, and self-management education. ADA recognizes



that, in addition to its important role inpreventing and controlling diabetes, nu-trition is an essential component of anoverall healthy lifestyle. A full review ofthe evidence regarding nutrition in pre-venting and controlling diabetes and itscomplications and additional nutrition-related recommendations can be found inthe ADA position statement, “NutritionRecommendations and Interventions forDiabetes,” published in 2007 and up-dated for 2008 (54). Achieving nutrition-related goals requires a coordinated teameffort that includes the active involvementof the person with pre-diabetes or diabe-tes. Because of the complexity of nutritionissues, it is recommended that a registereddietitian who is knowledgeable andskilled in implementing nutrition therapyinto diabetes management and educationbe the team member who provides MNT.

Clinical trials/outcome studies ofMNT have reported decreases in A1C of�1% in type 1 diabetes and 1–2% in type2 diabetes, depending on the duration ofdiabetes (55,56). Meta-analyses of studiesin nondiabetic, free-living subjects reportthat MNT reduces LDL cholesterol by15–25 mg/dl (57), while clinical trialssupport a role for lifestyle modification intreating hypertension (58).

Because of the effects of obesity oninsulin resistance, weight loss is an im-portant therapeutic objective for over-weight or obese individuals with pre-diabetes or diabetes (59). Short-termstudies have demonstrated that moderateweight loss (5% of body weight) in sub-jects with type 2 diabetes is associatedwith decreased insulin resistance, im-proved measures of glycemia and lipemia,and reduced blood pressure (60); longer-term studies (�52 weeks) showed mixedeffects on A1C in adults with type 2 dia-betes (61– 63), and results were con-founded by pharmacologic weight losstherapy. Sustained weight loss is difficultfor most people to accomplish. However,the multifactorial intensive lifestyle inter-vention employed in the DPP, which in-cluded reduced intake of fat and calories,led to weight loss averaging 7% at 6months and maintenance of 5% weightloss at 3 years, and these outcomes wereassociated with a 58% reduction in theincidence of type 2 diabetes (10). TheLook AHEAD (Action for Health in Dia-betes) study is a large clinical trial de-signed to determine whether long-termweight loss will improve glycemia andprevent cardiovascular events in subjectswith type 2 diabetes. One-year results of

the intensive lifestyle intervention in thistrial show an average 8.6% weight loss,significant reduction of A1C, and reduc-tion in several CVD risk factors (64).When completed, the Look AHEADstudy should provide insight into the ef-fects of long-term weight loss on impor-tant clinical outcomes.

The optimal macronutrient distribu-tion of weight loss diets has not been es-tablished. Although low-fat diets havetraditionally been promoted for weightloss, several randomized controlled trialsfound that subjects on low-carbohydratediets (�130 g/day of carbohydrate) lostmore weight at 6 months than subjects onlow-fat diets (65,66); however, at 1 year,the difference in weight loss between thelow-carbohydrate and low-fat diets wasnot significant and weight loss was mod-est with both diets. Another study of over-weight women randomized to one of fourdiets showed significantly more weightloss at 12 months with the Atkins low-carbohydrate diet than with higher-carbohydrate diets (67). Changes inserum triglyceride and HDL cholesterolwere more favorable with the low-carbohydrate diets. In one study, thosesubjects with type 2 diabetes demon-strated a greater decrease in A1C with alow-carbohydrate diet than with a low-fatdiet (66). A recent meta-analysis showedthat at 6 months, low-carbohydrate dietswere associated with greater improve-ments in triglyceride and HDL cholesterolconcentrations than low-fat diets; how-ever, LDL cholesterol was significantlyhigher on the low-carbohydrate diets(68).

The recommended dietary allowance(RDA) for digestible carbohydrate is 130g/day and is based on providing adequateglucose as the required fuel for the centralnervous system without reliance on glu-cose production from ingested protein orfat. Although brain fuel needs can be meton lower-carbohydrate diets, long-termmetabolic effects of very-low-carbohy-drate diets are unclear, and such dietseliminate many foods that are importantsources of energy, fiber, vitamins, andminerals and are important in dietary pal-atability (69).

Although numerous studies have at-tempted to identify the optimal mix ofmacronutrients for meal plans of peoplewith diabetes, it is unlikely that one suchcombination of macronutrients exists.The best mix of carbohydrate, protein,and fat appears to vary depending on in-dividual circumstances. For those indi-

viduals seeking guidance on macronutrientdistribution in healthy adults, the DietaryReference Intakes (DRIs) may be helpful(69). It must be clearly recognized thatregardless of the macronutrient mix, totalcaloric intake must be appropriate toweight management goal. Further, indi-vidualization of the macronutrient com-position will depend on the metabolicstatus of the patient (e.g., lipid profile,renal function).

The primary goal with respect to di-etary fat in individuals with diabetes is tolimit saturated fatty acids, trans fatty ac-ids, and cholesterol intake so as to reducerisk for CVD. Saturated and trans fatty ac-ids are the principal dietary determinantsof plasma LDL cholesterol. There is a lackof evidence on the effects of specific fattyacids on people with diabetes, so the rec-ommended goals are consistent withthose for individuals with CVD (70).

The FDA has approved five nonnutri-tive sweeteners for use in the U.S.: acesul-fame potassium, aspartame, neotame,saccharin, and sucralose. Before being al-lowed on the market, all underwent rig-orous scrutiny and were shown to be safewhen consumed by the public, includingpeople with diabetes and women duringpregnancy. Reduced-calorie sweetenersapproved by the FDA include sugar alco-hols (polyols) such as erythritol, isomalt,lactitol, maltitol, mannitol, sorbitol, xyli-tol, tagatose, and hydrogenated starch hy-drolysates. The use of sugar alcoholsappears to be safe; however, they maycause diarrhea, especially in children.

Reimbursement for MNTMNT, when delivered by a registered di-etitian according to nutrition practiceguidelines, is reimbursed as part of theMedicare program as overseen by theCenters for Medicare and Medicaid Ser-v ices (CMS) (www.cms.hhs .gov/medicalnutritiontherapy).

E. DSME

Recommendations● People with diabetes should receive

DSME according to national standardswhen their diabetes is diagnosed and asneeded thereafter. (B)

● Self-management behavior change isthe key outcome of DSME and shouldbe measured and monitored as part ofcare. (E)

● DSME should address psychosocial is-sues, since emotional well-being is

Position Statement


strongly associated with positive diabe-tes outcomes. (C)

● DSME should be reimbursed by third-party payors. (E)

DSME is an essential element of diabetescare (71–77), and the National Standardsfor DSME (78) are based on evidence forits benefits. Education helps people withdiabetes initiate effective self-care whenthey are first diagnosed. Ongoing DSMEalso helps people with diabetes maintaineffective self-management as their diabe-tes presents new challenges and as treat-ment advances become available. DSMEhelps patients optimize metabolic con-trol, prevent and manage complications,and maximize quality of life, in a cost-effective manner (79).

Evidence for the benefits of DSMESince the 1990s, there has been a shiftfrom a didactic approach, with DSME fo-cusing on providing information, to askill-based approach that focuses onhelping those with diabetes make in-formed self-management choices. Severalstudies have found that DSME is associ-ated with improved diabetes knowledgeand improved self-care behavior (72), im-proved clinical outcomes such as lowerA1C (73,74,76,77,80), lower self-reported weight (72), and improved qual-ity of life (75). Better outcomes werereported for DSME interventions thatwere longer and included follow-up sup-port (72), that were tailored to individualneeds and preferences (71), and that ad-dressed psychosocial issues (71,72,76).Both individual and group approacheshave been found effective (81,82). Thereis increasing evidence for the role of acommunity health worker in deliveringdiabetes education in addition to the coreteam (83).

The National Standards for DSMEADA-recognized DSME programs havestaff who must be certified diabetes edu-cators or have recent experience in diabe-tes education and management. Thecurriculum of ADA-recognized DSMEprograms must cover all nine areas of di-abetes management, with the assessedneeds of the individual determiningwhich areas are addressed. The ADA Ed-ucation Recognition Program (ERP) is amechanism to ensure that diabetes educa-tion programs meet the National Stan-dards and provide quality diabetes care.

Reimbursement for DSMEDSME, when provided by a program thatmeets ADA ERP standards, is reimbursedas part of the Medicare program as over-seen by the Centers for Medicare andMedicaid Services (CMS) (www.cms.hhs.gov/DiabetesSelfManagement).

F. Physical activity

Recommendations● People with diabetes should be advised

to perform at least 150 min/week ofmoderate-intensity aerobic physical ac-tivity (50 –70% of maximum heartrate). (A)

● In the absence of contraindications,people with type 2 diabetes should beencouraged to perform resistance train-ing three times per week. (A)

ADA technical reviews on exercise in pa-tients with diabetes have summarized thevalue of exercise in the diabetes manage-ment plan (84,85). Regular exercise hasbeen shown to improve blood glucosecontrol, reduce cardiovascular risk fac-tors, contribute to weight loss, and im-prove well-being. Furthermore, regularexercise may prevent type 2 diabetes inhigh-risk individuals (10 –12). Struc-tured exercise interventions of at least 8weeks’ duration have been shown tolower A1C by an average of 0.66% in peo-ple with type 2 diabetes, even with nosignificant change in BMI (86). Higherlevels of exercise intensity are associatedwith greater improvements in A1C and infitness (87).

Frequency and type of exerciseA U.S. Surgeon General’s report (88) rec-ommended that most adults accumulateat least 30 min of moderate-intensity ac-tivity on most, ideally all, days of theweek. The studies included in the meta-analysis of effects of exercise interventionson glycemic control (86) had a meannumber of sessions per week of 3.4, witha mean of 49 min per session. The DPPlifestyle intervention, which included 150min per week of moderate-intensity exer-cise, had a beneficial effect on glycemia inthose with pre-diabetes. Therefore, itseems reasonable to recommend �150min of exercise per week for people withdiabetes.

Resistance exercise improves insulinsensitivity to about the same extent as aer-obic exercise (89). Clinical trials haveprovided strong evidence for the A1C-

lowering value of resistance training inolder adults with type 2 diabetes (90,91),and for an additive benefit of combinedaerobic and resistance exercise in adultswith type 2 diabetes (92).

Evaluation of the diabetic patientbefore recommending an exerciseprogramPrior guidelines suggested that before rec-ommending a program of physical activ-ity, the provider should assess patientswith multiple cardiovascular risk factorsfor coronary artery disease (CAD). As dis-cussed more fully in Section VI.A.5, thearea of screening asymptomatic diabeticpatients for CAD remains unclear, and arecent ADA consensus statement on thisissue concluded that routine screening isnot recommended (93). Providers shoulduse clinical judgment in this area. Cer-tainly, high-risk patients should be en-couraged to start with short periods oflow-intensity exercise and increase the in-tensity and duration slowly.

Providers should assess patients forconditions that might contraindicate cer-tain types of exercise or predispose to in-jury, such as uncontrolled hypertension,severe autonomic neuropathy, severe pe-ripheral neuropathy or history of foot le-sions, and advanced retinopathy. Thepatient’s age and previous physical activ-ity level should be considered.

Exercise in the presence ofnonoptimal glycemic controlHyperglycemia. When people with type1 diabetes are deprived of insulin for12–48 h and are ketotic, exercise canworsen hyperglycemia and ketosis (94);therefore, vigorous activity should beavoided in the presence of ketosis. How-ever, it is not necessary to postpone exer-cise based simply on hyperglycemia,provided the patient feels well and urineand/or blood ketones are negative.Hypoglycemia. In individuals taking in-sulin and/or insulin secretagogues, phys-ical activity can cause hypoglycemia ifmedication dose or carbohydrate con-sumption is not altered. For individualson these therapies, added carbohydrateshould be ingested if pre-exercise glucoselevels are �100 mg/dl (5.6 mmol/l)(95,96). Hypoglycemia is rare in diabeticindividuals who are not treated with in-sulin or insulin secretagogues, and nopreventive measures for hypoglycemiaare usually advised in these cases.



Exercise in the presence of specificlong-term complications of diabetesRetinopathy. In the presence of prolifer-ative diabetic retinopathy (PDR) or severenon-PDR (NPDR), vigorous aerobic or re-sistance exercise may be contraindicatedbecause of the risk of triggering vitreoushemorrhage or retinal detachment (97).Peripheral neuropathy. Decreased painsensation in the extremities results in in-creased risk of skin breakdown and infec-tion and of Charcot joint destruction.Therefore, in the presence of severe pe-ripheral neuropathy, it may be best to en-courage non–weight-bearing activitiessuch as swimming, bicycling, or arm ex-ercises (98,99).Autonomic neuropathy. Autonomicneuropathy can increase the risk of exer-cise-induced injury or adverse eventthrough decreased cardiac responsive-ness to exercise, postural hypotension,impaired thermoregulation, impairednight vision due to impaired papillary re-action, and unpredictable carbohydratedelivery from gastroparesis predisposingto hypoglycemia (98). Autonomic neu-ropathy is also strongly associated withCVD in people with diabetes (100,101).People with diabetic autonomic neuropa-thy should undergo cardiac investigationbefore beginning physical activity moreintense than that to which they are accus-tomed.Albuminuria and nephropathy. Physicalactivity can acutely increase urinary pro-tein excretion. However, there is no evi-dence that vigorous exercise increases therate of progression of diabetic kidney dis-ease; thus, there is likely no need for anyspecific exercise restrictions for peoplewith diabetic kidney disease (102).

G. Psychosocial assessment and care

Recommendations● Assessment of psychological and social

situation should be included as an on-going part of the medical managementof diabetes. (E)

● Psychosocial screening and follow-upshould include, but is not limited to,attitudes about the illness, expectationsfor medical management and out-comes, affect/mood, general and diabe-tes-related quality of life, resources(financial, social, and emotional), andpsychiatric history. (E)

● Screen for psychosocial problems suchas depression, anxiety, eating disor-ders, and cognitive impairment when

adherence to the medical regimen ispoor. (E)

Psychological and social problems canimpair the individual’s (103–108) or fam-ily’s (109) ability to carry out diabetescare tasks and can therefore compromisehealth status. There are opportunities forthe clinician to assess psychosocial statusin a timely and efficient manner so thatreferral for appropriate services can be ac-complished.

Key opportunities for screening ofpsychosocial status occur at diagnosis,during regularly scheduled managementvisits, during hospitalizations, at discov-ery of complications, or when problemswith glucose control, quality of life, or ad-herence are identified (110). Patients arelikely to exhibit psychological vulnerabil-ity at diagnosis and when their medicalstatus changes, i.e., the end of the honey-moon period, when the need for intensi-fied treatment is evident, and whencomplications are discovered (105,107).

Issues known to impact se l f -management and health outcomes in-clude but are not limited to: attitudesabout the illness, expectations for medicalmanagement and outcomes, affect/mood,general and diabetes-related quality oflife, resources (financial, social, and emo-tional) (106), and psychiatric history(107,110,111). Screening tools are avail-able for a number of these areas (112).Indications for referral to a mental healthspecialist familiar with diabetes manage-ment may include gross noncompliancewith medical regimen (by self or others)(111), depression with the possibility ofself-harm (104,113), debilitating anxiety(alone or with depression), indications ofan eating disorder (114), and cognitivefunctioning that significantly impairsjudgment (113). It is preferable to incor-porate psychological assessment andtreatment into routine care rather thanwait for identification of a specific prob-lem or deterioration in psychological sta-tus (115). Although the clinician may notfeel qualified to treat psychological prob-lems, utilizing the patient-provider rela-tionship as a foundation for furthertreatment can increase the likelihood thatthe patient will accept referral for otherservices. It is important to establish thatemotional well-being is part of diabetesmanagement (110).

H. When treatment goals are not metFor a variety of reasons, some people withdiabetes and their health care providers

do not achieve the desired goals of treat-ment (Table 8). Intensification of thetreatment regimen is suggested and mayinclude assessment of barriers to adher-ence including income; educational at-tainment; and competing demands,including those related to family respon-sibilities and family dynamics; culturallyappropriate and enhanced DSME; co-management with a diabetes team; refer-ral to a medical social worker forassistance with insurance coverage;change in pharmacological therapy; initi-ation of or increase in SMBG; more fre-quent contact with the patient; andreferral to an endocrinologist.

I. Intercurrent illnessThe stress of illness, trauma, and/or sur-gery frequently aggravates glycemic con-trol and may precipitate diabeticketoacidosis (DKA) or nonketotic hyper-osmolar state, both of which are life-threatening conditions that requireimmediate medical care to prevent com-plications and death (116). Any conditionleading to deterioration in glycemic con-trol necessitates more frequent monitor-ing of blood glucose and (in ketosis-pronepatients) urine or blood ketones. Markedhyperglycemia requires temporary ad-justment of the treatment programand—if accompanied by ketosis, vomit-ing, or alteration in the level of conscious-ness—immediate interaction with thediabetes care team. The patient treatedwith noninsulin therapies or MNT alonemay temporarily require insulin. Ade-quate fluid and caloric intake must be en-sured. Infection or dehydration is morelikely to necessitate hospitalization of theperson with diabetes than the personwithout diabetes.

The hospitalized patient should betreated by a physician with expertise inthe management of diabetes. For furtherinformation on management of patientswith hyperglycemia in the hospital, seeSection VIII.A. For further information onmanagement of DKA or nonketotic hy-perosmolar state, refer to the ADA posi-tion statement on hyperglycemic crises(116).

J. Hypoglycemia

Recommendations● Glucose (15–20 g) is the preferred

treatment for the conscious individualwith hypoglycemia, although any formof carbohydrate that contains glucosemay be used. If SMBG 15 min after

Position Statement


treatment shows continued hypoglyce-mia, the treatment should be repeated.Once SMBG glucose returns to normal,the individual should consume a mealor snack to prevent recurrence of hypo-glycemia. (E)

● Glucagon should be prescribed for allindividuals at significant risk of severehypoglycemia, and caregivers or familymembers of these individuals should beinstructed in its administration. Gluca-gon administration is not limited tohealth care professionals. (E)

● Individuals with hypoglycemia un-awareness or one or more episodes ofsevere hypoglycemia should be advisedto raise their glycemic targets to strictlyavoid further hypoglycemia for at leastseveral weeks in order to partially re-verse hypoglycemia unawareness andreduce risk of future episodes. (B)

Hypoglycemia is the leading limiting fac-tor in the glycemic management of type 1and insulin-treated type 2 diabetes (117).Treatment of hypoglycemia (plasma glu-cose �70 mg/dl) requires ingestion ofglucose- or carbohydrate-containingfoods. The acute glycemic response cor-relates better with the glucose contentthan with the carbohydrate content of thefood. Although pure glucose is the pre-ferred treatment, any form of carbohy-drate that contains glucose will raiseblood glucose. Protein added to carbohy-drate does not impair the glycemic re-sponse, but also has no benefit inpreventing subsequent hypoglycemia.Added fat may retard and then prolongthe acute glycemic response (118). Ongo-ing activity of insulin or insulin secreta-gogues may lead to recurrence ofhypoglycemia unless further food is in-gested after recovery.

Severe hypoglycemia (where the indi-vidual requires the assistance of anotherperson and cannot be treated with oralcarbohydrate due to confusion or uncon-sciousness) should be treated using emer-gency glucagon kits, which require aprescription. Those in close contact with,or having custodial care of, people withhypoglycemia-prone diabetes (familymembers, roommates, school personnel,child care providers, correctional institu-tion staff, or coworkers) should be in-structed in use of such kits. An individualdoes not need to be a health care profes-sional to safely administer glucagon. Careshould be taken to ensure that unexpiredglucagon kits are available.

Prevention of hypoglycemia is a crit-

ical component of diabetes management.Teaching people with diabetes to balanceinsulin use, carbohydrate intake, and ex-ercise is a necessary but not always suffi-cient strategy. In type 1 diabetes andseverely insulin-deficient type 2 diabetes,the syndrome of hypoglycemia unaware-ness, or hypoglycemia-associated auto-nomic failure, can severely compromisestringent diabetes control and quality oflife. The deficient counter-regulatory hor-mone release and autonomic responses inthis syndrome are both risk factors for,and caused by, hypoglycemia. A corollaryto this “vicious cycle” is that several weeksof avoidance of hypoglycemia has beendemonstrated to improve counter-regulation and awareness to some extentin many patients (117,119,120). Hence,patients with one or more episodes of se-vere hypoglycemia may benefit from atleast short-term relaxation of glycemictargets.

K. Immunization

Recommendations● Annually provide an influenza vaccine

to all diabetic patients �6 months ofage. (C)

● Provide at least one lifetime pneumo-coccal vaccine for adults with diabetes.A one-time revaccination is recom-mended for individuals �65 years ofage previously immunized when theywere �65 years of age if the vaccine wasadministered �5 years ago. Other indi-cations for repeat vaccination includenephrotic syndrome, chronic renal dis-ease, and other immunocompromisedstates, such as after transplantation. (C)

Influenza and pneumonia are common,preventable infectious diseases associatedwith high mortality and morbidity in theelderly and in people with chronic dis-eases. Though there are limited studiesreporting the morbidity and mortality ofinfluenza and pneumococcal pneumoniaspecifically in people with diabetes, ob-servational studies of patients with a vari-ety of chronic illnesses, includingdiabetes, show that these conditions areassociated with an increase in hospitaliza-tions for influenza and its complications.People with diabetes may be at increasedrisk of the bacteremic form of pneumo-coccal infection and have been reportedto have a high risk of nosocomial bactere-mia, which has a mortality rate as high as50% (121).

Safe and effective vaccines are avail-able that can greatly reduce the risk ofserious complications from these diseases(122,123). In a case-control series, influ-enza vaccine was shown to reduce diabe-tes-related hospital admission by as muchas 79% during flu epidemics (122). Thereis sufficient evidence to support that peo-ple with diabetes have appropriate sero-logic and clinical responses to thesevaccinations. The Centers for DiseaseControl and Prevention’s Advisory Com-mittee on Immunization Practices recom-mends influenza and pneumococcalvaccines for all individuals of any age withdiabetes (http://www.cdc.gov/vaccines/recs). For a complete discussion on theprevention of influenza and pneumococ-cal disease in people with diabetes, con-sult the technical review and positionstatement on this subject (121,124).

VI. PREVENTION ANDMANAGEMENT OFDIABETES COMPLICATIONS

A. CVDCVD is the major cause of morbidity andmortality for individuals with diabetesand is the largest contributor to the directand indirect costs of diabetes. The com-mon conditions coexisting with type 2diabetes (e.g., hypertension and dyslipi-demia) are clear risk factors for CVD, anddiabetes itself confers independent risk.Numerous studies have shown the effi-cacy of controlling cardiovascular riskfactors in preventing or slowing CVD inpeople with diabetes. Evidence is summa-rized in the following sections and re-viewed in detail in the ADA technicalreviews on hypertension (125), dyslipide-mia (126), aspirin therapy (127), andsmoking cessation (128), and in the AHA/ADA scientific statement on prevention ofCVD in people with diabetes (129). Em-phasis should be placed on reducing car-diovascular risk factors, and cliniciansshould be alert for signs and symptoms ofatherosclerosis.

1. Hypertension/blood pressurecontrol

Recommendations

Screening and diagnosis● Blood pressure should be measured at

every routine diabetes visit. Patientsfound to have systolic blood pressure



�130 mmHg or diastolic blood pres-sure �80 mmHg should have bloodpressure confirmed on a separate day.Repeat systolic blood pressure �130mmHg or diastolic blood pressure �80mmHg confirms a diagnosis of hyper-tension. (C)

Goals● Patients with diabetes should be treated

to a systolic blood pressure �130mmHg. (C)

● Patients with diabetes should be treatedto a diastolic blood pressure �80mmHg. (B)

Treatment● Patients with a systolic blood pressure

of 130–139 mmHg or a diastolic bloodpressure of 80–89 mmHg may be givenlifestyle therapy alone for a maximumof 3 months and then, if targets are notachieved, be treated with addition ofpharmacological agents. (E)

● Patients with more severe hypertension(systolic blood pressure �140 or dia-stolic blood pressure �90 mmHg) atdiagnosis or follow-up should receivepharmacologic therapy in addition tolifestyle therapy. (A)

● Pharmacologic therapy for patientswith diabetes and hypertension shouldbe with a regimen that includes eitheran ACE inhibitor or an angiotensin re-ceptor blocker (ARB). If one class is nottolerated, the other should be substi-tuted. If needed to achieve blood pres-sure targets, a thiazide diuretic shouldbe added to those with an estimatedglomerular filtration rate (GFR) (see be-low) �50 ml/min per 1.73 m2 and aloop diuretic for those with an esti-mated GFR �50 ml/min per 1.73 m2.(E)

● Multiple drug therapy (two or moreagents at maximal doses) is generallyrequired to achieve blood pressure tar-gets. (B)

● If ACE inhibitors, ARBs, or diuretics areused, kidney function and serum potas-sium levels should be closely moni-tored. (E)

● In pregnant patients with diabetes andchronic hypertension, blood pressuretarget goals of 110–129/65–79 mmHgare suggested in the interest of long-term maternal health and minimizingimpaired fetal growth. ACE inhibitorsand ARBs are contraindicated duringpregnancy. (E)

Hypertension is a common comorbidityof diabetes, affecting the majority of pa-tients, with prevalence depending on typeof diabetes, age, obesity, and ethnicity.Hypertension is a major risk factor forboth CVD and microvascular complica-tions. In type 1 diabetes, hypertension isoften the result of underlying nephropa-thy, while in type 2 diabetes it usuallycoexists with other cardiometabolic riskfactors.

Screening and diagnosisMeasurement of blood pressure in the of-fice should follow the guidelines estab-lished for nondiabetic individuals:measurement in the seated position, withfeet on the floor and arm supported atheart level, and after 5 min of rest. Ele-vated values should be confirmed on aseparate day. Because of the clear syner-gistic risks of hypertension and diabetes,the diagnostic cut-off for a diagnosis ofhypertension is lower in people with dia-betes (blood pressure �130/80) thanthose without diabetes (blood pressure�140/90 mmHg) (130).

Home blood pressure self-monitoringand 24-h ambulatory blood pressuremonitoring may provide additional evi-dence of “white coat” and masked hyper-tension and other discrepancies betweenoffice and “true” blood pressure, and instudies in nondiabetic populations, homemeasurements may better correlate withCVD risk than office measurements(131,132). However, the preponderanceof the clear evidence of benefits of treat-ment of hypertension in people with dia-betes is based on office measurements.

Treatment goalsRandomized clinical trials have demon-strated the benefit (reduction of coronaryheart disease [CHD] events, stroke, andnephropathy) of lowering blood pressureto �140 mmHg systolic and �80 mmHgdiastolic in individuals with diabetes(130,133–135). Epidemiologic analysesshow that blood pressures �115/75mmHg are associated with increased car-diovascular event rates and mortality inindividuals with diabetes (130,136,137).Therefore, a target blood pressure goal of�130/80 mmHg is reasonable if it can besafely achieved. The ongoing Action toControl Cardiovascular Risk in Diabetes(ACCORD) trial is designed to determinewhether lowering systolic blood pressureto �120 mmHg provides greater cardio-

vascular protection than a systolic bloodpressure level of �140 mmHg in patientswith type 2 diabetes (www.accord.org).

Treatment strategiesAlthough there are no well-controlledstudies of diet and exercise in the treat-ment of hypertension in individuals withdiabetes, studies in nondiabetic individu-als have shown antihypertensive effectssimilar to pharmacologic monotherapy ofreducing sodium intake and excess bodyweight; increasing consumption of fruits,vegetables, and low-fat dairy products;avoiding excessive alcohol consumption;and increasing activity levels (130,138).These nonpharmacological strategies mayalso positively affect glycemia and lipidcontrol. Their effects on cardiovascularevents have not been established. An ini-tial trial of nonpharmacologic therapymay be reasonable in diabetic individualswith mild hypertension (systolic bloodpressure 130 –139 mmHg or diastolicblood pressure 80 – 89 mmHg). If theblood pressure is �140 mmHg systolicand/or �90 mmHg diastolic at the time ofdiagnosis, pharmacologic therapy shouldbe initiated along with nonpharmacologictherapy (130).

Lowering of blood pressure with reg-imens based on a variety of antihyperten-sive drugs, including ACE inhibitors,ARBs, �-blockers, diuretics, and calciumchannel blockers, has been shown to beeffective in reducing cardiovascularevents. Several studies suggested thatACE inhibitors may be superior to dihy-dropyridine calcium channel blockers inreducing cardiovascular events (139 –141). However, a variety of other studieshave shown no specific advantage to ACEinhibitors as initial treatment of hyper-tension in the general hypertensive pop-ulation, but rather an advantage oncardiovascular outcomes of initial therapywith low-dose thiazide diuretics (130,142,143).

In people with diabetes, inhibitors ofthe renin-angiotensin system (RAS) mayhave unique advantages for initial or earlytherapy of hypertension. In a nonhyper-tension trial of high-risk individuals, in-cluding a large subset with diabetes, anACE inhibitor reduced CVD outcomes(144). In patients with CHF, includingdiabetic subgroups, ARBs have beenshown to reduce major CVD outcomes(145–148), and in type 2 diabetic patientswith significant nephropathy, ARBs weresuperior to calcium channel blockers for

Position Statement


reducing heart failure (149 –151). Al-though evidence for distinct advantagesof RAS inhibitors on CVD outcomes indiabetes remains conflicting (133,152),the high CVD risks associated withdiabetes, and the high prevalence of un-diagnosed CVD, may still favor recom-mendations for their use as first-linehypertension therapy in people with dia-betes (130). The compelling benefits ofRAS inhibitors in diabetic patients withalbuminuria or renal insufficiency pro-vide additional rationale for use of theseagents (see Section VI. B below).

An important caveat is that most pa-tients with hypertension require multi-drug therapy to reach treatment goals,especially diabetic patients whose targetsare lower. Many patients will requirethree or more drugs to reach target goals(130).

During pregnancy in diabetic womenwith chronic hypertension, target bloodpressure goals of systolic blood pressure110 –129 mmHg and diastolic bloodpressure 65–79 mmHg are reasonable, asthey contribute to long-term maternalhealth. Lower blood pressure levels maybe associated with impaired fetal growth.During pregnancy, treatment with ACEinhibitors and ARBs is contraindicated,since they are likely to cause fetal damage.Antihypertensive drugs known to be ef-fective and safe in pregnancy includemethyldopa, labetalol , di l t iazem,clonidine, and prazosin. Chronic diureticuse during pregnancy has been associatedwith restricted maternal plasma volume,which might reduce uteroplacental perfu-sion (153).

2. Dyslipidemia/lipid management

Recommendations

Screening● In most adult patients, measure fasting

lipid profile at least annually. In adultswith low-risk lipid values (LDL choles-terol �100 mg/dl, HDL cholesterol�50 mg/dl, and triglycerides �150mg/dl), lipid assessments may be re-peated every 2 years. (E)

Treatment recommendations andgoals● Lifestyle modification focusing on the

reduction of saturated fat, trans fat, andcholesterol intake; weight loss (if indi-cated); and increased physical activityshould be recommended to improvethe lipid profile in patients with diabe-tes. (A)

● Statin therapy should be added to life-style therapy, regardless of baselinelipid levels, for diabetic patients:● with overt CVD (A)● without CVD who are over the age of

40 and have one or more other CVDrisk factors. (A)

● For lower-risk patients than those spec-ified above (e.g., without overt CVDand under the age of 40), statin therapyshould be considered in addition tolifestyle therapy if LDL cholesterol re-mains �100 mg/dl or in those withmultiple CVD risk factors (E)

● In individuals without overt CVD, theprimary goal is an LDL cholesterol�100 mg/dl (2.6 mmol/l). (A)

● In individuals with overt CVD, a lowerLDL cholesterol goal of �70 mg/dl (1.8

mmol/l), using a high dose of a statin, isan option. (E)

● If drug-treated patients do not reach theabove targets on maximal tolerated sta-tin therapy, a reduction in LDL choles-terol of �40% from baseline is analternative therapeutic goal. (A)

● Triglycerides levels �150 mg/dl (1.7mmol/l) and HDL cholesterol �40mg/dl (1.0 mmol/l) in men and �50mg/dl (1.3 mmol/l) in women are desir-able. However, LDL cholesterol–targeted statin therapy remains thepreferred strategy. (C)

● Combination therapy using statins andother lipid-lowering agents may beconsidered to achieve lipid targets buthas not been evaluated in outcomestudies for either CVD outcomes orsafety. (E)

● Statin therapy is contraindicated inpregnancy. (E)

Evidence for benefits of lipid-lowering therapyPatients with type 2 diabetes have an in-creased prevalence of lipid abnormalities,which contributes to their high risk ofCVD. For the past decade or more, mul-tiple clinical trials demonstrated signifi-cant effects of pharmacologic (primarilystatin) therapy on CVD outcomes in sub-jects with CHD and for primary CVD pre-vention (154). Sub-analyses of diabeticsubgroups of larger trials (155–159) andtrials specifically in subjects with diabetes(160,161) showed significant primaryand secondary prevention of CVDevents � CHD deaths in diabetic popula-tions. As shown in Table 10, and similarto 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 � 16,032)

Study (ref.)CVD

prevention Statin dose and comparator RRR ARRLDL cholesterol

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 CVDrisk 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.



duction in “hard” CVD outcomes (CHDdeath and nonfatal myocardial infarction)can be more clearly seen in diabetic sub-jects with high baseline CVD risk (knownCVD and/or very high LDL cholesterollevels), but overall the benefits of statintherapy in people with diabetes at mod-erate or high risk for CVD are convincing.

Low HDL cholesterol levels, whichare often associated with elevated triglyc-eride levels, are the most prevalent pat-tern of dyslipidemia in persons with type2 diabetes. However, the evidence basefor drugs that target these lipid fractions issignificantly less robust than that for sta-tin therapy (162). In a study conducted ina nondiabetic cohort, nicotinic acid re-duced CVD outcomes (163). Gemfibrozilhas been shown to decrease rates of CVDevents in subjects without diabetes(164,165) and in the diabetic subgroup inone of the larger trials (164). However, ina large trial specific to diabetic patients,fenofibrate failed to reduce overall cardio-vascular outcomes (166).

Dyslipidemia treatment and targetlipid levelsFor most patients with diabetes, the firstpriority of dyslipidemia therapy (unlesssevere hypertriglyceridemia is the imme-diate issue) is to lower LDL cholesterol toa target goal of �100 mg/dl (2.60 mmol/l)(167). Lifestyle intervention, includingMNT, increased physical activity, weightloss, and smoking cessation, may allowsome patients to reach lipid goals. Nutri-tion intervention should be tailored ac-cording to each patient’s age, type ofdiabetes, pharmacological treatment,lipid levels, and other medical conditionsand should focus on the reduction of sat-urated fat, cholesterol, and trans unsatur-ated fat intake. Glycemic control can alsobeneficially modify plasma lipid levels,particularly in patients with very hightriglycerides and poor glycemic control.

In those with clinical CVD or overaged 40 with other CVD risk factors,pharmacological treatment should beadded to lifestyle therapy regardless of

baseline lipid levels. Statins are the drugsof choice for lowering LDL cholesterol.

In patients other than those describedabove, statin treatment should be consid-ered if there is an inadequate LDL choles-terol response to lifestyle modificationsand improved glucose control, or if thepatient has increased cardiovascular risk(e.g., multiple cardiovascular risk factorsor long duration of diabetes). Very littleclinical trial evidence exists for type 2 di-abetic patients under the age of 40 or fortype 1 diabetic patients of any age. In theHeart Protection Study (lower age limit40 years), the subgroup of �600 patientswith type 1 diabetes had a proportion-ately similar (though not statistically sig-nificant) reduction in risk to patients withtype 2 diabetes (156). Although the dataare not definitive, consideration shouldbe given to similar lipid-lowering goals intype 1 diabetic patients as in type 2 dia-betic patients, particularly if they haveother cardiovascular risk factors.

Alternative LDL cholesterol goalsVirtually all trials of statins and CVD out-come tested specific doses of statinsagainst placebo, other doses of statin, orother statins, rather than aiming forspecific LDL cholesterol goals (168).As can be seen in Table 10, placebo-controlled trials generally achieved LDLcholesterol reductions of 30–40% frombaseline. Hence, LDL cholesterol lower-ing of this magnitude is an acceptable out-come for patients who cannot reach LDLcholesterol goals due to severe baselineelevations in LDL cholesterol and/orintolerance of maximal, or any, statindoses.

Recent clinical trials in high-risk pa-tients, such as those with acute coronarysyndromes or previous cardiovascularevents (169 –171), have demonstratedthat more aggressive therapy with highdoses of statins to achieve an LDL choles-terol of �70 mg/dl led to a significant re-duction in further events. Therefore, areduction in LDL cholesterol to a goal of

�70 mg/dl is an option in very-high-riskdiabetic patients with overt CVD (172).

The addition of other drugs such asezetimibe to statins may achieve lowerLDL cholesterol goals, but no data areavailable as to whether such combinationtherapy is more effective than a statin alonein preventing cardiovascular events.

Treatment of other lipoproteinfractionsSevere hypertriglyceridemia may warrantimmediate therapy of this abnormalitywith lifestyle and usually pharmacologictherapy (fibric acid derivative or niacin)to reduce the risk of acute pancreatitis. Inthe absence of severe hypertriglyceride-mia, therapy targeting HDL cholesterol ortriglycerides has intuitive appeal but lacksthe evidence base of statin therapy (162).If the HDL cholesterol is �40 mg/dl andthe LDL cholesterol between 100 and 129mg/dl, gemfibrozil or niacin might beused, especially if a patient is intolerant tostatins. Niacin is the most effective drugfor raising HDL cholesterol. It can signif-icantly increase blood glucose at highdoses, but recent studies demonstrate thatat modest doses (750 –2,000 mg/day),significant improvements in LDL choles-terol, HDL cholesterol, and triglyceridelevels are accompanied by only modestchanges in glucose that are generally ame-nable to adjustment of diabetes therapy(173,174).

Combination therapy, with a statinand a fibrate or statin and niacin, may beefficacious for treatment for all three lipidfractions, but this combination is associ-ated with an increased risk for abnormaltransaminase levels, myositis, or rhabdo-myolysis. The risk of rhabdomyolysis ishigher with higher doses of statins andwith renal insufficiency, and seems to belower when statins are combined with fe-nofibrate than gemfibrozil (175). Severalongoing trials may provide much-neededevidence for the effects of combinationtherapy on cardiovascular outcomes.

3. Antiplatelet agents

Recommendations● Use aspirin therapy (75–162 mg/day)

as a secondary prevention strategy inthose with diabetes with a history ofCVD. (A)

● Use aspirin therapy (75–162 mg/day)as a primary prevention strategy inthose with type 1 or 2 diabetes at in-creased cardiovascular risk, including

Table 11—Summary of recommendations for glycemic, blood pressure, and lipid control foradults with diabetes

A1C �7.0%*Blood pressure �130/80 mmHgLipids

LDL cholesterol �100 mg/dl (�2.6 mmol/l)†

*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.

Position Statement


those who are �40 years of age or whohave additional risk factors (family his-tory of CVD, hypertension, smoking,dyslipidemia, or albuminuria). (A)

● Aspirin therapy is not recommended inpeople under 30 years of age, due tolack of evidence of benefit, and is con-traindicated in patients under the age of21 years because of the associated riskof Reye’s syndrome. (E)

● Combination therapy using other anti-platelet agents such as clopidrogel inaddition to aspirin should be used inpatients with severe and progressiveCVD. (C)

● Other antiplatelet agents may be a rea-sonable alternative for high-risk pa-tients with aspirin allergy, withbleeding tendency, who are receivinganticoagulant therapy, with recent gas-trointestinal bleeding, and with clini-cally active hepatic disease who are notcandidates for aspirin therapy. (E)

The use of aspirin in diabetes is reviewedin detail in the ADA technical review(127) and position statement (176) onthis topic. Aspirin has been recom-mended for primary (177,178) and sec-ondary (179,180) prevent ion ofcardiovascular events in high-risk dia-betic and nondiabetic individuals. Onelarge meta-analysis and several clinicaltrials demonstrate the efficacy of using as-pirin as a preventive measure for cardio-vascular events, including stroke andmyocardial infarction. Many trials haveshown an �30% decrease in myocardialinfarction and a 20% decrease in stroke ina wide range of patients, including youngand middle-aged patients, patients withand without a history of CVD, males andfemales, and patients with hypertension.

Dosages used in most clinical trialsranged from 75 to 325 mg/day. There islittle evidence to support any specificdose, but using the lowest possible dosagemay help reduce side effects (181). Con-versely, a randomized trial of 100 mg ofaspirin daily showed less of a primary pre-vention effect, without statistical signifi-cance, in the large diabetic subgroup incontrast to significant benefit in thosewithout diabetes (182), raising the issueof aspirin resistance in those with diabe-tes. There is no evidence for a specific ageat which to start aspirin, but at ages �30years, aspirin has not been studied.

Clopidogrel has been demonstratedto reduce CVD events in diabetic individ-uals (183). Adjunctive therapy in very-high-risk patients or as alternative

therapy in aspirin-intolerant patientsshould be considered.

4. Smoking cessation

Recommendations● Advise all patients not to smoke. (A)● Include smoking cessation counseling

and other forms of treatment as a rou-tine component of diabetes care. (B)

Issues of smoking in diabetes are re-viewed in detail in the ADA technical re-view (128) and position statement (184)on this topic. A large body of evidencefrom epidemiological, case-control, andcohort studies provides convincing docu-mentation of the causal link between cig-arette smoking and health risks. Cigarettesmoking contributes to one of every fivedeaths in the U.S. and is the most impor-tant modifiable cause of premature death.Much of the prior work documenting theimpact of smoking on health did not sep-arately discuss results on subsets of indi-viduals with diabetes, suggesting that theidentified risks are at least equivalent tothose found in the general population.Other studies of individuals with diabetesconsistently found a heightened risk ofCVD and premature death among smok-ers. Smoking is also related to the prema-ture development of microvascularcomplications of diabetes and may have arole in the development of type 2 diabetes.

A number of large randomized clini-cal trials have demonstrated the efficacyand cost-effectiveness of smoking cessa-tion counseling in changing smoking be-havior and reducing tobacco use. Theroutine and thorough assessment of to-bacco use is important as a means ofpreventing smoking or encouraging ces-sation. Special considerations should in-clude assessment of level of nicotinedependence, which is associated with dif-ficulty in quitting and relapse (185,186).

5. CHD screening and treatment

Recommendations

Screening● In asymptomatic patients, evaluate risk

factors to stratify patients by 10-yearrisk, and treat risk factors accordingly.(B)

Treatment● In patients with known CVD, ACE in-

hibitor, aspirin, and statin therapy (ifnot contraindicated) should be used to

reduce the risk of cardiovascularevents. (A)

● In patients with a prior myocardial in-farction, add �-blockers (if not contra-indicated) to reduce mortality. (A)

● In patients �40 years of age with an-other cardiovascular risk factor (hyper-tension, family history, dyslipidemia,microalbuminuria, cardiac autonomicneuropathy, or smoking), ACE inhibi-tor, aspirin, and statin therapy (if notcontraindicated) should be used to re-duce the risk of cardiovascular events.(B)

● In patients with treated CHF, met-formin and thiazolidinedione (TZD)use are contraindicated. (C)

CHD screening and treatment are re-viewed in detail in the ADA consensusstatement on CHD in people with diabe-tes (187), and screening for CAD is re-viewed in a recently updated consensusstatement (93). To identify the presenceof CAD in diabetic patients without clearor suggestive symptoms, a risk factor–based approach to the initial diagnosticevaluation and subsequent follow-up hasintuitive appeal. However, recent studiesconcluded that using this approach failsto identify which patients will have silentischemia on screening tests (100,188).

Cardiovascular risk factors should beassessed at least once a year. These riskfactors include dyslipidemia, hyperten-sion, smoking, a positive family history ofpremature coronary disease, and the pres-ence of micro- or macroalbuminuria. Ab-normal risk factors should be treated asdescribed elsewhere in these guidelines.Patients at increased CHD risk should re-ceive aspirin, statin, and ACE inhibitortherapy, unless there are contraindica-tions to a particular drug class.

Candidates for a further cardiac test-ing include those with 1) typical or atyp-ical cardiac symptoms and 2) anabnormal resting electrocardiogram(ECG). The screening of asymptomaticpatients remains controversial, especiallyas intensive medical therapy, indicated indiabetic patients at high risk for CVD, hasan increasing evidence base for providingequal outcomes to invasive revasculariza-tion, including in diabetic patients (189).There is also recent preliminary evidencethat silent myocardial ischemia may re-verse over time, adding to the controversyconcerning aggressive screening strate-gies (190).



B. Nephropathy screening andtreatment

Recommendations

General recommendations● To reduce the risk or slow the progres-

sion of nephropathy, optimize glucosecontrol. (A)

● To reduce the risk or slow the progres-sion of nephropathy, optimize bloodpressure control. (A)

Screening● Perform an annual test to assess urine

albumin excretion in type 1 diabetic pa-tients with diabetes duration of �5years and in all type 2 diabetic patients,starting at diagnosis. (E)

● Measure serum creatinine at least annu-ally in all adults with diabetes regard-less of the degree of urine albuminexcretion. The serum creatinine shouldbe used to estimate GFR and stage thelevel of chronic kidney disease (CKD),if present. (E)

Treatment● In the treatment of the nonpregnant pa-

tient with micro- or macroalbuminuria,either ACE inhibitors or ARBs shouldbe used. (A)

● While there are no adequate head-to-head comparisons of ACE inhibitorsand ARBs, there is clinical trial supportfor each of the following statements:● In patients with type 1 diabetes, with

hypertension and any degree of albu-minuria, ACE inhibitors have beenshown to delay the progression of ne-phropathy. (A)

● In patients with type 2 diabetes, hy-pertension, and microalbuminuria,both ACE inhibitors and ARBs havebeen shown to delay the progressionto macroalbuminuria. (A)

● In patients with type 2 diabetes, hy-pertension, macroalbuminuria, andrenal insufficiency (serum creatinine�1.5 mg/dl), ARBs have been shownto delay the progression of nephrop-athy. (A)

● If one class is not tolerated, the othershould be substituted. (E)

● Reduction of protein intake to 0.8–1.0g � kg body wt�1 � day�1 in individualswith diabetes and the earlier stages ofCKD and to 0.8 g � kg body wt�1 �day�1 in the later stages of CKD mayimprove measures of renal function

(e.g., urine albumin excretion rate andGFR) and is recommended (B)

● When ACE inhibitors, ARBs, or diuret-ics are used, monitor serum creatinineand potassium levels for the develop-ment of acute kidney disease and hy-perkalemia. (E)

● Continued monitoring of urine albu-min excretion to assess both responseto therapy and progression of disease isrecommended. (E)

● Consider referral to a physician experi-enced in the care of kidney diseasewhen there is uncertainty about the eti-ology of kidney disease (active urinesediment, absence of retinopathy, rapiddecline in GFR), difficult managementissues, or advanced kidney disease. (B)

Diabetic nephropathy occurs in 20–40%of patients with diabetes and is the singleleading cause of end-stage renal disease(ESRD). Persistent albuminuria in therange of 30–299 mg/24 h (microalbu-minuria) has been shown to be the earlieststage of diabetic nephropathy in type 1diabetes and a marker for development ofnephropathy in type 2 diabetes. Mi-croalbuminuria is also a well-establishedmarker of increased CVD risk (191,192).Patients with microalbuminuria whoprogress to macroalbuminuria (�300mg/24 h) are likely to progress to ESRD(193,194). However, a number of inter-ventions have been demonstrated to re-duce the risk and slow the progression ofrenal disease.

Intensive diabetes management withthe goal of achieving near-normoglyce-mia has been shown in large prospectiverandomized studies to delay the onset ofmicroalbuminuria and the progression ofmicro- to macroalbuminuria in patientswith type 1 (195,196) and type 2 (40,41)diabetes. The UKPDS provided strong ev-idence that control of blood pressure canreduce the development of nephropathy(133). In addition, large prospective ran-domized studies in patients with type 1diabetes have demonstrated that achieve-ment of lower levels of systolic bloodpressure (�140 mmHg) resulting fromtreatment using ACE inhibitors provides aselective benefit over other antihyperten-sive drug classes in delaying the progres-sion from micro- to macroalbuminuriaand can slow the decline in GFR inpatients with macroalbuminuria (150,151,197). In type 2 diabetes with hyper-tension and normoalbuminuria, ACEinhibition has been demonstrated to de-

lay progression to microalbuminuria(198).

In addition, ACE inhibitors have beenshown to reduce major CVD outcomes(i.e., myocardial infarction, stroke, death)in patients with diabetes (144), thus fur-ther supporting the use of these agents inpatients with microalbuminuria, a CVDrisk factor. ARBs have also been shown toreduce the rate of progression from mi-cro- to macroalbuminuria as well as ESRDin patients with type 2 diabetes (199–201). Some evidence suggests that ARBshave a smaller magnitude of rise in potas-sium compared with ACE inhibitors inpeople with nephropathy (202,203).Other drugs, such as diuretics, calciumchannel blockers, and �-blockers, shouldbe used as additional therapy to furtherlower blood pressure in patients alreadytreated with ACE inhibitors or ARBs(149), or as alternate therapy in the rareindividual unable to tolerate ACE inhibi-tors or ARBs.

Studies in patients with varying stagesof nephropathy have shown that proteinrestriction helps slow the progression ofalbuminuria, GFR decline, and occur-rence of ESRD (204 –207). Proteinrestriction should be considered particu-larly in patients whose nephropathyseems to be progressing despite optimalglucose and blood pressure control anduse of ACE inhibitor and/or ARBs (207).

Assessment of albuminuria statusand renal functionScreening for microalbuminuria can beperformed by measurement of the albu-min-to-creatinine ratio in a random spotcollection (preferred method); 24-h ortimed collections are more burdensomeand add little to prediction or accuracy(208,209). Measurement of a spot urinefor albumin only, whether by immunoas-say or by using a dipstick test specific formicroalbumin, without simultaneouslymeasuring urine creatinine, is somewhatless expensive but susceptible to false-negative and -positive determinations as aresult of variation in urine concentrationdue to hydration and other factors.

Abnormalities of albumin excretionare defined in Table 12. Because of vari-ability in urinary albumin excretion, twoof three specimens collected within a 3- to6-month period should be abnormal be-fore considering a patient to have crossedone of these diagnostic thresholds. Exer-cise within 24 h, infection, fever, CHF,marked hyperglycemia, and marked hy-

Position Statement


pertension may elevate urinary albuminexcretion over baseline values.

Information on presence of abnormalurine albumin excretion in addition tolevel of GFR may be used to stage CKD.The National Kidney Foundation classifi-cation (Table 13) is primarily based onGFR levels and therefore differs fromother systems in which staging is basedprimarily on urinary albumin excretion(210). Studies have found decreased GFRin the absence of increased urine albuminexcretion in a substantial percentage ofadults with diabetes (211,212). Epidemi-ologic evidence suggests that a substantialfraction of those with chronic kidney dis-ease in the setting of diabetes have little orno detectable albuminuria (211). Serumcreatinine should therefore be measuredat least annually in all adults with diabe-tes, regardless of the degree of urine albu-min excretion.

Serum creatinine should be used toestimate GFR and to stage the level ofCKD, if present. GFR can be estimatedusing formulae such as the Cockroft-Gault equation or a prediction formulausing data from the Modification of Dietand Renal Disease study (213). GFR cal-culators are available at http://www.nkdep.nih.gov. Many clinical laboratoriesnow report estimated GFR in addition toserum creatinine.

The role of continued annual quanti-tative assessment of albumin excretion af-ter diagnosis of microalbuminuria andinstitution of ACE inhibitor or ARB ther-apy and blood pressure control is unclear.Continued surveillance can assess bothresponse to therapy and progression ofdisease. Some suggest that reducing ab-normal albuminuria (�30 mg/g) to thenormal or near-normal range may im-prove renal and cardiovascular prognosis,but this approach has not been formallyevaluated in prospective trials.

Complications of kidney disease cor-relate with level of kidney function. Whenthe estimated GFR is �60 ml/min per1.73 m2, screening for anemia, malnutri-tion, and metabolic bone disease is indi-cated. Early vaccination against hepatitis

B is indicated in patients likely to progressto end-stage kidney disease.

Consider referral to a physician expe-rienced in the care of kidney disease whenthere is uncertainty about the etiology ofkidney disease (active urine sediment, ab-sence of retinopathy, rapid decline inGFR), difficult management issues, or ad-vanced kidney disease. The threshold forreferral may vary depending on the fre-quency with which a provider encountersdiabetic patients with significant kidneydisease. Consultation with a nephrologistwhen stage 4 CKD develops has beenfound to reduce cost, improve quality ofcare, and keep people off dialysis longer(214,215). However, nonrenal specialistsshould not delay educating their patientsabout the progressive nature of diabetickidney disease; the renal preservationbenefits of aggressive treatment of bloodpressure, blood glucose, and hyperlipid-emia; and the potential need for renal re-placement therapy.

C. Retinopathy screening andtreatment

Recommendations

General recommendations● To reduce the risk or slow the progres-

sion of retinopathy, optimize glycemiccontrol. (A)

● To reduce the risk or slow the progres-sion of retinopathy, optimize bloodpressure control. (A)

Screening● Adults and adolescents with type 1 di-

abetes should have an initial dilatedand comprehensive eye examination byan ophthalmologist or optometristwithin 5 years after the onset of diabe-tes. (B)

● Patients with type 2 diabetes shouldhave an initial dilated and comprehen-sive eye examination by an ophthalmol-ogist or optometrist shortly after thediagnosis of diabetes. (B)

● Subsequent examinations for type 1and type 2 diabetic patients should berepeated annually by an ophthalmolo-gist or optometrist. Less frequent exams(every 2–3 years) may be consideredfollowing one or more normal eye ex-ams. Examinations will be requiredmore frequently if retinopathy is pro-gressing. (B)

● Women with pre-existing diabetes whoare planning pregnancy or who havebecome pregnant should have a com-prehensive eye examination and becounseled on the risk of developmentand/or progression of diabetic retinop-athy. Eye examination should occur inthe first trimester with close follow-upthroughout pregnancy and for 1 yearpostpartum. (B)

Treatment● Promptly refer patients with any level of

macular edema, severe NPDR, or anyPDR to an ophthalmologist who isknowledgeable and experienced in themanagement and treatment of diabeticretinopathy. (A)

● Laser photocoagulation therapy is indi-cated to reduce the risk of vision loss inpatients with high-risk PDR, clinicallysignificant macular edema, and in somecases of severe NPDR. (A)

● The presence of retinopathy is not acontraindication to aspirin therapy forcardioprotection, as this therapy does

Table 12—Definitions of abnormalities in albumin excretion

Category Spot collection (g/mg creatinine)

Normal �30Microalbuminuria 30–299Macro (clinical)-albuminuria 300

Table 13—Stages of CKD

Stage DescriptionGFR (ml/min per 1.73m2 body surface area)

1 Kidney damage* with normal or increased GFR 902 Kidney damage* with mildly decreased GFR 60–893 Moderately decreased GFR 30–594 Severely decreased GFR 15–295 Kidney failure �15 or dialysis

*Kidney damage defined as abnormalities on pathologic, urine, blood, or imaging tests. Adapted from ref.209.



not increase the risk of retinal hemor-rhage. (A)

Diabetic retinopathy is a highly specificvascular complication of both type 1 andtype 2 diabetes, with prevalence stronglyrelated to the duration of diabetes. Dia-betic retinopathy is the most frequentcause of new cases of blindness amongadults aged 20–74 years. Glaucoma, cat-aracts, and other disorders of the eye oc-cur earlier and more frequently in peoplewith diabetes.

In addition to duration of diabetes,other factors that increase the risk of, orare associated with, retinopathy includechronic hyperglycemia (216), the pres-ence of nephropathy (217), and hyper-tension (218). Intensive diabetesmanagement with the goal of achievingnear normoglycemia has been shown inlarge prospective randomized studies toprevent and/or delay the onset and pro-gress ion of diabet ic re t inopathy(35,40,41). Lowering blood pressure hasbeen shown to decrease the progressionof retinopathy (133). Several case seriesand a controlled prospective study sug-gest that pregnancy in type 1 diabetic pa-t ients may aggravate ret inopathy(219,220); laser photocoagulation sur-gery can minimize this risk (220).

One of the main motivations forscreening for diabetic retinopathy is theestablished efficacy of laser photocoagu-lation surgery in preventing visual loss.Two large trials, the Diabetic RetinopathyStudy (DRS) and the Early Treatment Di-abetic Retinopathy Study (ETDRS), pro-vide the strongest support for thetherapeutic benefits of photocoagulationsurgery.

The DRS (221) showed that panreti-nal photocoagulation surgery reduced therisk of severe vision loss from PDR from15.9% in untreated eyes to 6.4% intreated eyes. The benefit was greatestamong patients whose baseline evalua-tion revealed high-risk characteristics(chiefly disc neovascularization or vitre-ous hemorrhage). Given the risks of mod-est loss of visual acuity and contraction ofthe visual field from panretinal laser sur-gery, such therapy is primarily recom-mended for eyes with PDR approachingor having high-risk characteristics.

The ETDRS (222) established thebenefit of focal laser photocoagulationsurgery in eyes with macular edema, par-ticularly those with clinically significantmacular edema, with reduction of dou-

bling of the visual angle (e.g., 20/50 to20/100) from 20% in untreated eyes to8% in treated eyes. The ETDRS also veri-fied the benefits of panretinal photocoag-ulation for high-risk PDR, but not formild or moderate NPDR. In older-onsetpatients with severe NPDR or less-than-high-risk PDR, the risk of severe visualloss or vitrectomy was reduced �50% byearly laser photocoagulation surgery atthese stages.

Laser photocoagulation surgery inboth trials was beneficial in reducing therisk of further visual loss, but generallynot beneficial in reversing already dimin-ished acuity. This preventive effect andthe fact that patients with PDR or macularedema may be asymptomatic providestrong support for a screening program todetect diabetic retinopathy.

As retinopathy is estimated to take atleast 5 years to develop after the onset ofhyperglycemia (223), patients with type 1diabetes should have an initial dilated andcomprehensive eye examination within 5years after the onset of diabetes. Patientswith type 2 diabetes, who generally havehad years of undiagnosed diabetes (224)and who have a significant risk of preva-lent diabetic retinopathy at the time ofdiabetes diagnosis, should have an initialdilated and comprehensive eye examina-tion soon after diagnosis. Examinationsshould be performed by an ophthalmolo-gist or optometrist who is knowledgeableand experienced in diagnosing the pres-ence of diabetic retinopathy and is awareof its management. Subsequent examina-tions for type 1 and type 2 diabetic pa-tients are generally repeated annually.Less frequent exams (every 2–3 years)may be cost-effective after one or morenormal eye exams (225–227), while ex-aminations will be required more fre-quently if retinopathy is progressing.

Examinations can also be done withretinal photographs (with or without di-lation of the pupil) read by experiencedexperts. In-person exams are still neces-sary when the photos are unacceptableand for follow-up of abnormalities de-tected. This technology has great poten-tial in areas where qualified eye careprofessionals are not available, and mayalso enhance efficiency and reduce costswhen the expertise of ophthalmologistscan be utilized for more complex exami-nations and for therapy (228).

Results of eye examinations should bedocumented and transmitted to the refer-ring health care professional. For a de-tailed review of the evidence and further

discussion of diabetic retinopathy, seeADA’s technical review and position state-ment on this subject (229,230).

D. Neuropathy screening andtreatment

Recommendations● All patients should be screened for dis-

tal symmetric polyneuropathy (DPN) atdiagnosis and at least annually thereaf-ter, using simple clinical tests. (B)

● Electrophysiological testing is rarelyneeded, except in situations where theclinical features are atypical. (E)

● Educate all patients about self-care ofthe feet. For those with DPN, facilitateenhanced foot care education and referfor special footware. (B)

● Screening for signs and symptoms ofautonomic neuropathy should be insti-tuted at diagnosis of type 2 diabetes and5 years after the diagnosis of type 1 di-abetes. Special testing is rarely neededand may not affect management or out-comes. (E)

● Medications for the relief of specificsymptoms related to DPN and auto-nomic neuropathy are recommended,as they improve the quality of life of thepatient. (E)

The diabetic neuropathies are heteroge-neous with diverse clinical manifesta-tions. They may be focal or diffuse. Mostcommon among the neuropathies arechronic sensorimotor DPN and auto-nomic neuropathy. Although DPN is adiagnosis of exclusion, complex investi-gations to exclude other conditions arerarely needed (231).

The early recognition and appropri-ate management of neuropathy in the pa-tient with diabetes is important for anumber of reasons: 1) nondiabetic neu-ropathies may be present in patients withdiabetes and may be treatable; 2) a num-ber of treatment options exist for symp-tomatic diabetic neuropathy; 3) up to50% of DPN may be asymptomatic andpatients are at risk of insensate injury totheir feet; 4) autonomic neuropathy mayinvolve every system in the body; and 5)cardiovascular autonomic neuropathycauses substantial morbidity and mortal-ity. Specific treatment for the underlyingnerve damage is currently not available,other than improved glycemic control,which may slow progression but not re-verse neuronal loss. Effective symptom-atic treatments are available for some

Position Statement


manifestations of DPN and autonomicneuropathy (231).

Diagnosis of neuropathy

Distal symmetric polyneuropathyPatients with diabetes should be screenedannually for DPN using tests such as pin-prick sensation, vibration perception(using a 128-Hz tuning fork), 10-g mono-filament pressure sensation at the distalplantar aspect of both great toes andmetatarsal joints, and assessment of anklereflexes. Combinations of more than onetest have �87% sensitivity in detectingDPN. Loss of 10-g monofilament percep-tion and reduced vibration perceptionpredict foot ulcers (231).

Diabetic autonomic neuropathyThe symptoms and signs of autonomicdysfunction should be elicited carefullyduring the history and physical examina-tion. Major clinical manifestations of dia-betic autonomic neuropathy includeresting tachycardia, exercise intolerance,orthostatic hypotension, constipation,gastroparesis, erectile dysfunction, sudo-motor dysfunction, impaired neurovas-cular function, “brittle diabetes,” andhypoglycemic autonomic failure (232).

Cardiovascular autonomic neuropa-thy, a CVD risk factor (93), is the moststudied and clinically important form ofdiabetic autonomic neuropathy. Cardio-vascular autonomic neuropathy may beindicated by resting tachycardia (�100bpm), orthostasis (a fall in systolic bloodpressure �20 mmHg upon standing), orother disturbances in autonomic nervoussystem function involving the skin, pu-pils, or gastrointestinal and genitourinarysystems (232).

Gastrointestinal neuropathies (e.g.,esophageal enteropathy, gastroparesis,constipation, diarrhea, fecal inconti-nence) are common, and any section ofthe gastrointestinal tract may be affected.Gastroparesis should be suspected in in-dividuals with erratic glucose control orwith upper gastrointestinal symptomswithout other identified cause. Evalua-tion of solid-phase gastric emptying usingdouble-isotope scintigraphy may be doneif symptoms are suggestive, but test re-sults often correlate poorly with symp-toms. Constipation is the most commonlower gastrointestinal symptom but canalternate with episodes of diarrhea (232).

Diabetic autonomic neuropathy isalso associated with genitourinary tractdisturbances. In men, diabetic autonomicneuropathy may cause erectile dysfunc-tion and/or retrograde ejaculation. Evalu-ation of bladder dysfunction should beperformed for individuals with diabeteswho have recurrent urinary tract infec-tions, pyelonephritis, incontinence, or apalpable bladder (232).

Symptomatic treatmentsDPNThe first step in management of patientswith DPN should be to aim for stable andoptimal glycemic control. Although con-trolled trial evidence is lacking, severalobservational studies suggest that neuro-pathic symptoms improve not only withoptimization of control, but also with theavoidance of extreme blood glucose fluc-tuations. Patients with painful DPN maybenefit from pharmacological treatmentof their symptoms: many agents have ef-ficacy confirmed in published random-ized controlled trials, with several FDA-approved for the management of painful

DPN. See Table 14 for examples of agentsto treat DPN pain.

Treatment of autonomic neuropathyGastroparesis symptoms may improvewith dietary changes and prokineticagents such as metoclopramide or eryth-romycin. Treatments for erectile dysfunc-tion may include phosphodiesterase type5 inhibitors, intracorporeal or intraure-thral prostaglandins, vacuum devices, orpenile prostheses. Interventions for othermanifestations of autonomic neuropathyare described in the ADA statement onneuropathy (231). As with DPN treat-ments, these interventions do not changethe underlying pathology and natural his-tory of the disease process, but may have apositive impact on the quality of life of thepatient.

E. Foot care

Recommendations● For all patients with diabetes, perform

an annual comprehensive foot exami-nation to identify risk factors predictiveof ulcers and amputations. The foot ex-amination can be accomplished in aprimary care setting and should includethe use of a monofilament, tuning fork,palpation, and a visual examination. (B)

● Provide general foot self-care educationto all patients with diabetes. (B)

● A multidisciplinary approach is recom-mended for individuals with foot ulcersand high-risk feet, especially for thosewith a history of prior ulcer or amputa-tion. (B)

● Refer patients who smoke, have loss ofprotective sensation and structural ab-normalities, or have history of priorlower-extremity complications to footcare specialists for ongoing preventivecare and life-long surveillance. (C)

● Initial screening for peripheral arterialdisease (PAD) should include a historyfor claudication and an assessment ofthe pedal pulses. Consider obtaining anankle-brachial index (ABI), as many pa-tients with PAD are asymptomatic. (C)

● Refer patients with significant claudica-tion or a positive ABI for further vascu-lar assessment, and consider exercise,medications, and surgical options. (C)

Amputation and foot ulceration, conse-quences of diabetic neuropathy and/orPAD, are common and major causes ofmorbidity and disability in people withdiabetes. Early recognition and manage-

Table 14—Table of drugs to treat symptomatic DPN

Class Examples Typical doses*

Tricyclic drugs Amitriptyline 10–75 mg at bedtimeNortriptyline 25–75 mg at bedtimeImipramine 25–75 mg at bedtime

Anticonvulsants Gabapentin 300–1,200 mg t.i.d.Carbamazepine 200–400 mg t.i.d.Pregabalin† 100 mg t.i.d.

5-hydroxytryptamine andnorepinephrine uptakeinhibitor

Duloxetine† 60–120 mg daily

Substance P inhibitor Capsaicin cream 0.025–0.075% applied t.i.d. or q.i.d.

*Dose response may vary; initial doses need to be low and titrated up; †has FDA indication for treatment ofpainful diabetic neuropathy.



ment of risk factors can prevent or delayadverse outcomes.

The risk of ulcers or amputations isincreased in people who have had diabe-tes �10 years, are male, have poor glu-cose control, or have cardiovascular,retinal, or renal complications. The fol-lowing foot-related risk conditions are as-sociated with an increased risk ofamputation:

● Peripheral neuropathy with loss of pro-tective sensation

● Altered biomechanics (in the presenceof neuropathy)

● Evidence of increased pressure (ery-thema, hemorrhage under a callus)

● Bony deformity● PAD (decreased or absent pedal pulses)● A history of ulcers or amputation● Severe nail pathology

All individuals with diabetes should re-ceive an annual foot examination to iden-tify high-risk foot conditions. Thisexamination should include assessmentof protective sensation, foot structure andbiomechanics, vascular status, and skinintegrity. Evaluation of neurological sta-tus in the low-risk foot should include aquantitative somatosensory thresholdtest, using the Semmes-Weinstein 5.07(10-g) monofilament. The skin should beassessed for integrity, especially betweenthe toes and under the metatarsal heads.Patients at low risk may benefit from ed-ucation on foot care and footwear.

The presence of erythema, warmth,or callus formation may indicate areas oftissue damage with impending break-down. Bony deformities, limitation injoint mobility, and problems with gaitand balance should be assessed. Peoplewith one or more high-risk foot condi-tions should be evaluated more fre-quently for the development of additionalrisk factors. People with neuropathyshould have a visual inspection of theirfeet at every visit with a health careprofessional.

People with neuropathy (e.g., ery-thema, warmth, callus, or measured pres-sure) or evidence of increased plantarpressure may be adequately managedwith well-fitted walking shoes or athleticshoes that cushion the feet and redistrib-ute pressure. Callus can be debrided witha scalpel by a foot care specialist or otherhealth professional with experience andtraining in foot care. People with bonydeformities (e.g., hammertoes, promi-nent metatarsal heads, bunions) may

need extra-wide or -depth shoes. Peoplewith extreme bony deformities (e.g.,Charcot foot) who cannot be accommo-dated with commercial therapeutic foot-wear may need custom-molded shoes.

Initial screening for PAD should in-clude a history for claudication and anassessment of the pedal pulses. A diagnos-tic ABI should be performed in any pa-tient with symptoms of PAD. Due to thehigh estimated prevalence of PAD in pa-tients with diabetes and the fact that manypatients with PAD are asymptomatic, anADA consensus statement on PAD (233)suggested that a screening ABI be per-formed in patients older than 50 years ofage and be considered in patients youngerthan 50 years who have other PAD riskfactors (e.g., smoking, hypertension, hy-perlipidemia, or duration of diabetes �10years). Refer patients with significantsymptoms or a positive ABI for furthervascular assessment, and consider exer-cise, medication, and surgical options(233).

Patients with diabetes and high-riskfoot conditions should be educated re-garding their risk factors and appropriatemanagement. Patients at risk should un-derstand the implications of the loss ofprotective sensation; the importance offoot monitoring on a daily basis; theproper care of the foot, including nail andskin care; and the selection of appropriatefootwear. Patients with loss of protectivesensation should be educated on ways tosubstitute other sensory modalities (handpalpation, visual inspection) for surveil-lance of early foot problems. The patient’sunderstanding of these issues and theirphysical ability to conduct proper footsurveillance and care should be assessed.Patients with visual difficulties, physicalconstraints preventing movement, or cog-nitive problems that impair their ability toassess the condition of the foot and to in-stitute appropriate responses will needother people, such as family members, toassist in their care.

For a detailed review of the evidenceand further discussion, see ADA’s techni-cal review and position statement on pre-ventive foot care (234,235).

Foot ulcers and wound care may re-quire care by a podiatrist, orthopedic orvascular surgeon, or rehabilitation spe-cialist experienced in the management ofindividuals with diabetes. For a completediscussion, see ADA’s consensus state-ment on diabetic foot wound care (236).

VII. DIABETES CARE INSPECIFIC POPULATIONS

A. Children and adolescents

1. Type 1 diabetesThree-quarters of all cases of type 1 dia-betes are diagnosed in individuals �18years of age. Because children are not sim-ply “small adults,” it is appropriate to con-sider the unique aspects of care andmanagement of children and adolescentswith type 1 diabetes. Children with dia-betes differ from adults in many respects,including insulin sensitivity related tosexual maturity, physical growth, abilityto provide self-care, and unique neuro-logic vulnerability to hypoglycemia. At-tention to such issues as family dynamics,developmental stages, and physiologicdifferences related to sexual maturity areall essential in developing and imple-menting an optimal diabetes regimen. Al-though recommendations for childrenand adolescents are less likely to be basedon clinical trial evidence, because of cur-rent and historical restraints placed onconducting research in children, expertopinion and a review of available and rel-evant experimental data are summarizedin a recent ADA statement (237).

Ideally, the care of a child or adoles-cent with type 1 diabetes should be pro-vided by a multidisciplinary team ofspecialists trained in the care of childrenwith pediatric diabetes. At the very least,education of the child and family shouldbe provided by health care providerstrained and experienced in childhood di-abetes and sensitive to the challengesposed by diabetes in this age-group. Atthe time of initial diagnosis, it is essentialthat diabetes education is provided in atimely fashion, with the expectation thatthe balance between adult supervisionand self-care should be defined by, andwill evolve according to, physical, psy-chological, and emotional maturity. MNTshould be provided at diagnosis, and atleast annually thereafter, by an individualexperienced with the nutritional needs ofthe growing child and the behavioral is-sues that have an impact on adolescentdiets.

a. Glycemic control

Recommendations● Consider age when setting glycemic

goals in children and adolescents withtype 1 diabetes, with less stringent goalsfor younger children. (E)

Position Statement


While current standards for diabetesmanagement reflect the need to maintainglucose control as near to normal as safelypossible, special consideration must begiven to the unique risks of hypoglycemiain young children. Glycemic goals need tobe modified to take into account the factthat most children �6 or 7 years of agehave a form of “hypoglycemic unaware-ness.” Their counterregulatory mecha-nisms are immature, and they may lackthe cognitive capacity to recognize andrespond to hypoglycemic symptoms,placing them at greater risk for severe hy-poglycemia and its sequelae. In addition,and unlike the case in adults, childrenyounger than 5 years of age are at risk forpermanent cognitive impairment after ep-isodes of severe hypoglycemia (238 –240). Extensive evidence indicates thatnear normalization of blood glucose lev-els is seldom attainable in children andadolescents after the honeymoon (remis-sion) period. The A1C level achieved inthe “intensive” adolescent cohort of theDCCT group was �1% higher than thatachieved by adult DCCT subjects andabove current ADA recommendations forpatients in general. However, the in-creased frequency of use of basal bolusregimens (including insulin pumps) inyouth from infancy through adolescencehas been associated with more childrenreaching ADA blood glucose targets(241,242) in those families in which bothparents and the child with diabetes aremotivated to perform the required diabe-tes-related tasks.

In selecting glycemic goals, the bene-

fits on long-term health outcomes ofachieving a lower A1C must be weighedagainst the unique risks of hypoglycemiaand the difficulties achieving near-normoglycemia in children and youth.Age-specific glycemic and A1C goals arepresented in Table 15.

b. Screening and management of chroniccomplications in children and adoles-cents with type 1 diabetes

i. Nephropathy

Recommendations● Annual screening for microalbumin-

uria, with a random spot urine samplefor microalbumin-to-creatinine ratio,should be initiated once the child is 10years of age and has had diabetes for 5years. (E)

● Confirmed, persistently elevated mi-croalbumin levels on two additionalurine specimens should be treated withan ACE inhibitor titrated to normaliza-tion of microalbumin excretion if pos-sible. (E)

ii. Hypertension

Recommendations● Treatment of high-normal blood pres-

sure (systolic or diastolic blood pres-sure consistently above the 90thpercentile for age, sex, and height)should include dietary interventionand exercise aimed at weight controland increased physical activity, if ap-propriate. If target blood pressure is not

reached with 3–6 months of lifestyleintervention, pharmacologic treatmentshould be initiated. (E)

● Pharmacologic treatment of hyperten-sion (systolic or diastolic blood pres-sure consistently above the 95thpercentile for age, sex, and height orconsistently �130/80 mmHg, if 95%exceeds that value) should be initiatedas soon as the diagnosis is confirmed.(E)

● ACE inhibitors should be consideredfor the initial treatment of hyperten-sion. (E)

Hypertension in childhood is defined asan average systolic or diastolic blood pres-sure �95th percentile for age, sex, andheight percentile measured on at leastthree separate days. “High-normal” bloodpressure is defined as an average systolicor diastolic blood pressure �90th but�95th percentile for age, sex, and heightpercentile measured on at least three sep-arate days. Normal blood pressure levelsfor age, sex, and height and appropriatemethods for determinations are availableonline at www.nhlbi.nih.gov/health/prof/heart/hbp/hbp_ped.pdf.

iii. Dyslipidemia

Recommendations

Screening● If there is a family history of hypercho-

lesterolemia (total cholesterol �240mg/dl) or a cardiovascular event before

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

Values by age (years)

Plasma blood glucosegoal range (mg/dl)

A1C RationaleBeforemeals

Bedtime/overnight

Toddlers and preschoolers (0–6) 100–180 110–200 �8.5% (but �7.5%) High risk and vulnerability tohypoglycemia

School age (6–12) 90–180 100–180 �8% Risks of hypoglycemia and relatively lowrisk of complications prior to puberty

Adolescents and young adults (13–19) 90–130 90–150 �7.5% ● Risk of severe hypoglycemia● Developmental and psychological

issues● A lower goal (�7.0%) is reasonable if

it can be achieved without excessivehypoglycemia

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.



age 55 years, or if family history is un-known, then a fasting lipid profileshould be performed on children �2years of age soon after diagnosis (afterglucose control has been established).If family history is not of concern, thenthe first lipid screening should be per-formed at puberty (�10 years). All chil-dren diagnosed with diabetes at or afterpuberty should have a fasting lipid pro-file performed soon after diagnosis(after glucose control has been estab-lished). (E)

● For both age groups, if lipids are abnor-mal, annual monitoring is recom-mended. If LDL cholesterol values arewithin the accepted risk levels (�100mg/dl [2.6 mmol/l]), a lipid profileshould be repeated every 5 years. (E)

Treatment● Initial therapy should consist of optimi-

zation of glucose control and MNTusing a Step 2 American Heart Associ-ation diet aimed at a decrease in theamount of saturated fat in the diet. (E)

● After the age of 10, the addition of astatin is recommended in patients who,after MNT and lifestyle changes, haveLDL cholesterol �160 mg/dl (4.1mmol/l) or have LDL cholesterol �130mg/dl (3.4 mmol/l) and one or moreCVD risk factors. (E)

● The goal of therapy is an LDL choles-terol value �100 mg/dl (2.6 mmol/l).(E)

People diagnosed with type 1 diabetes inchildhood have a high risk of early sub-clinical (243–245) and clinical (246)CVD. Although intervention data arelacking, the American Heart Association(AHA) categorizes type 1 children in thehighest tier for cardiovascular risk, andrecommends both lifestyle and pharma-cologic treatment for those with elevatedLDL cholesterol levels (247). Initial ther-apy should be with a Step 2 AHA diet,which restricts saturated fat to 7% of totalcalories and restricts dietary cholesterol to200 mg/day. Data from randomized clin-ical trials in children as young as 7months of age indicate that this diet is safeand does not interfere with normalgrowth and development (248,249).

For children over the age of 10 withpersistent elevation of LDL cholesteroldespite lifestyle therapy, statins should beconsidered. Neither long-term safety norcardiovascular outcome efficacy has beenestablished for children. However, recentstudies have shown short-term safety

equivalent to that seen in adults, as well asefficacy in lowering LDL cholesterol lev-els, improving endothelial function, andcausing regression of carotid intimalthickening (250–252). No statin is ap-proved for use under the age of 10, andstatin treatment should generally not beused in type 1 children before this age.

iv. Retinopathy

Recommendations● The first ophthalmologic examination

should be obtained once the child is�10 years of age and has had diabetesfor 3–5 years. (E)

● After the initial examination, annualroutine follow-up is generally recom-mended. Less frequent examinationsmay be acceptable on the advice of aneye care professional. (E)

Although retinopathy most commonlyoccurs after the onset of puberty and after5–10 years of diabetes duration, it hasbeen reported in prepubertal childrenand with diabetes duration of only 1–2years. Referrals should be made to eyecare professionals with expertise indiabetic retinopathy, an understanding ofthe risk for retinopathy in the pediatricpopulation, and experience in counsel-ing the pediatric patient and family onthe importance of early prevention/intervention.

v. Celiac disease

Recommendations● Patients with type 1 diabetes who be-

come symptomatic for celiac diseaseshould be tested by measuring tissuetransglutaminase or anti-endomysialantibodies, with documentation of nor-mal serum IgA levels. (E)

● Children with positive antibodiesshould be referred to a gastroenterolo-gist for evaluation. (E)

● Children with confirmed celiac diseaseshould have consultation with a dieti-tian and be placed on a gluten-free diet.(E)

Celiac disease is an immune-mediateddisorder that occurs with increased fre-quency in patients with type 1 diabetes(1–16% of individuals compared with0.3–1% in the general population)(253,254). Symptoms of celiac disease in-clude diarrhea, weight loss or poor weightgain, growth failure, abdominal pain,chronic fatigue, malnutrition due to mal-

absorption and other gastrointestinalproblems, and unexplained hypoglyce-mia or erratic blood glucose concentrations.

vi. Hypothyroidism

Recommendations● Patients with type 1 diabetes should be

screened for thyroid peroxidase andthyroglobulin antibodies at diagnosis.(E)

● Thyroid-stimulating hormone (TSH)concentrations should be measured af-ter metabolic control has been estab-lished. If normal, they should berechecked every 1–2 years, or if the pa-tient develops symptoms of thyroiddysfunction, thyromegaly, or an abnor-mal growth rate. Free T4 should bemeasured if TSH is abnormal. (E)

Auto-immune thyroid disease is the mostcommon autoimmune disorder associ-ated with diabetes, occurring in 17–30%of patients with type 1 diabetes (255). Thepresence of thyroid auto-antibodies ispredictive of thyroid dysfunction (gener-ally hypothyroidism, but less commonlyhyperthyroidism) (256). Subclinical hy-pothyroidism may be associated withincreased risk of symptomatic hypoglyce-mia (257) and with reduced linear growth(258). Hyperthyroidism alters glucosemetabolism, potentially resulting in dete-rioration of metabolic control.

c. “Adherence”No matter how sound the medical regi-men, it can only be as good as the ability ofthe family and/or individual to implementit. Family involvement in diabetes re-mains an important component of opti-mal diabetes management throughoutchildhood and into adolescence. Healthcare providers who care for children andadolescents, therefore, must be capable ofevaluating the behavioral, emotional, andpsychosocial factors that interfere withimplementation and then must work withthe individual and family to resolve prob-lems that occur and/or to modify goals asappropriate.

d. School and day care.Since a sizable portion of a child’s day isspent in school, close communicationwith school or day care personnel is es-sential for optimal diabetes management,safety, and maximal academic opportuni-ties. See Section VIII.B, “Diabetes Care inthe School and Day Care Setting,” for fur-ther discussion.

Position Statement


2. Type 2 diabetesThe incidence of type 2 diabetes in ado-lescents is increasing, especially in ethnicminority populations (20). Distinctionbetween type 1 and type 2 diabetes inchildren can be difficult, since autoanti-gens and ketosis may be present in a sub-stantial number of patients with featuresof type 2 diabetes (including obesity andacanthosis nigricans). Such a distinctionat the time of diagnosis is critical sincetreatment regimens, educational ap-proaches, and dietary counsel will differmarkedly between the two diagnoses. Be-cause type 2 diabetes has a significant in-cidence of hypertension, dyslipidemia,and microalbuminuria at diagnosis (259),it is recommended that screening for thecomorbidities and complications of dia-betes, including fasting lipid profile, mi-croalbuminuria assessment, and dilatedeye examinations, begin at the time of di-agnosis. The ADA consensus statement(22) provides guidance on the preven-tion, screening, and treatment of type 2diabetes and its comorbidities in youngpeople.

B. Preconception care

Recommendations● A1C levels should be as close to normal

as possible (�7%) in an individual pa-tient before conception is attempted.(B)

● All women with diabetes and child-bearing potential should be educatedabout the need for good glucose controlbefore pregnancy and should partici-pate in family planning. (E)

● Women with diabetes who are contem-plating pregnancy should be evaluatedand, if indicated, treated for diabeticretinopathy, nephropathy, neuropathy,and CVD. (E)

● Medications used by such womenshould be evaluated before conception,since drugs commonly used to treat di-abetes and its complications may becontraindicated or not recommendedin pregnancy, including statins, ACEinhibitors, ARBs, and most noninsulintherapies. (E)

Major congenital malformations remainthe leading cause of mortality and seriousmorbidity in infants of mothers with type1 and type 2 diabetes. Observational stud-ies indicate that the risk of malformationsincreases continuously with increasingmaternal glycemia during the first 6–8

weeks of gestation, as defined by first-trimester A1C concentrations. There is nothreshold for A1C values below whichrisk disappears entirely. However, mal-formation rates above the 1–2% back-ground rate of nondiabetic pregnanciesappear to be limited to pregnancies inwhich first-trimester A1C concentrationsare �1% above the normal range for anondiabetic pregnant woman.

Preconception care of diabetes ap-pears to reduce the risk of congenital mal-formations. Five nonrandomized studiescompared rates of major malformations ininfants between women who participatedin preconception diabetes care programsand women who initiated intensive diabe-tes management after they were alreadypregnant. The preconception care pro-grams were multidisciplinary and de-signed to train patients in diabetes self-management with diet, intensified insulintherapy, and SMBG. Goals were set toachieve normal blood glucose concentra-tions, and �80% of subjects achievednormal A1C concentrations before theybecame pregnant (260–264). In all fivestudies, the incidence of major congenitalmalformations in women who partici-pated in preconception care (range 1.0–1.7% of infants) was much lower than theincidence in women who did not partici-pate (range 1.4–10.9% of infants). Onelimitation of these studies is that partici-pation in preconception care was self-selected rather than randomized. Thus, itis impossible to be certain that the lowermalformation rates resulted fully fromimproved diabetes care. Nonetheless, theevidence supports the concept that mal-formations can be reduced or preventedby careful management of diabetes beforepregnancy.

Planned pregnancies greatly facilitatepreconception diabetes care. Unfortu-nately, nearly two-thirds of pregnanciesin women with diabetes are unplanned,leading to a persistent excess of malfor-mations in infants of diabetic mothers. Tominimize the occurrence of these devas-tating malformations, standard care for allwomen with diabetes who have child-bearing potential should include 1) edu-cation about the risk of malformationsassociated with unplanned pregnanciesand poor metabolic control and 2) use ofeffective contraception at all times, unlessthe patient has good metabolic controland is actively trying to conceive.

Women contemplating pregnancyneed to be seen frequently by a multidis-ciplinary team experienced in the man-

agement of diabetes before and duringpregnancy. The goals of preconceptioncare are to 1) involve and empower thepatient in the management of her diabe-tes, 2) achieve the lowest A1C test resultspossible without excessive hypoglycemia,3) ensure effective contraception until sta-ble and acceptable glycemia is achieved,and 4) identify, evaluate, and treat long-term diabetic complications such as reti-nopathy, nephropathy, neuropathy,hypertension, and CHD.

Among the drugs commonly used inthe treatment of patients with diabetes, anumber may be relatively or absolutelycontraindicated during pregnancy. St-atins are category X (contraindicated foruse in pregnancy) and should be discon-tinued before conception, as should ACEinhibitors (265). ARBs are category C(risk cannot be ruled out) in the first tri-mester, but category D (positive evidenceof risk) in later pregnancy, and shouldgenerally be discontinued before preg-nancy. Among the oral antidiabeticagents, metformin and acarbose are clas-sified as category B (no evidence of risk inhumans) and all others as category C. Po-tential risks and benefits of oral antidia-betic agents in the preconception periodmust be carefully weighed, recognizingthat data are insufficient to establish thesafety of these agents in pregnancy.

For further discussion of preconcep-tion care, see ADA’s technical review(266) and position statement (267) onthis subject.

C. Older adults

Recommendations● Older adults who are functional, cogni-

tively intact, and have significant lifeexpectancy should receive diabetestreatment using goals developed foryounger adults. (E)

● Glycemic goals for older adults who donot meet the above criteria may be re-laxed using individual criteria, but hy-perglycemia leading to symptoms orrisk of acute hyperglycemic complica-tions should be avoided in all patients.(E)

● Other cardiovascular risk factorsshould be treated in older adults withconsideration of the timeframe of ben-efit and the individual patient. Treat-ment of hypertension is indicated invirtually all older adults, and lipid andaspirin therapy may benefit those withlife expectancy at least equal to the



timeframe of primary or secondary pre-vention trials. (E)

● Screening for diabetic complicationsshould be individualized in olderadults, but particular attention shouldbe paid to complications that wouldlead to functional impairment. (E)

Diabetes is an important health conditionfor the aging population. At least 20% ofpatients over the age of 65 years have di-abetes, and this number can be expectedto grow rapidly in the coming decades.Older individuals with diabetes havehigher rates of premature death, func-tional disability, and coexisting illnessessuch as hypertension, CHD, and strokethan those without diabetes. Older adultswith diabetes are also at greater risk thanother older adults for several common ge-riatric syndromes, such as polypharmacy,depression, cognitive impairment, uri-nary incontinence, injurious falls, andpersistent pain.

The American Geriatric Society’sguidelines for improving the care of theolder person with diabetes mellitus (268)have influenced the following discussionand recommendations. The care of olderadults with diabetes is complicated bytheir clinical and functional heterogene-ity. Some older individuals developed di-abetes years earlier and may havesignificant complications; others who arenewly diagnosed may have had years ofundiagnosed diabetes with resultant com-plications or may have few complicationsfrom the disease. Some older adults withdiabetes are frail and have other underly-ing chronic conditions, substantial diabe-tes-related comorbidity, or limitedphysical or cognitive functioning. Otherolder individuals with diabetes have littlecomorbidity and are active. Life expectan-cies are highly variable for this popula-tion, but often longer than cliniciansrealize. Providers caring for older adultswith diabetes must take this heterogeneityinto consideration when setting and pri-oritizing treatment goals.

There are few long-term studies inolder adults demonstrating the benefits ofintensive glycemic, blood pressure, andlipid control. Patients who can be ex-pected to live long enough to reap thebenefits of long-term intensive diabetesmanagement and who are active, havegood cognitive function, and are willingto undertake the responsibility of self-management should be encouraged to do

so and be treated using the goals foryounger adults with diabetes.

For patients with advanced diabetescomplications, life-limiting comorbid ill-ness, or substantial cognitive or func-tional impairment, it is reasonable to setless intensive glycemic target goals. Thesepatients are less likely to benefit from re-ducing the risk of microvascular compli-cations and more likely to suffer seriousadverse effects from hypoglycemia. How-ever, patients with poorly controlled dia-be tes may be subjec t to acutecomplications of diabetes, including de-hydration, poor wound healing, and hy-perglycemic hyperosmolar coma.Glycemic goals at a minimum shouldavoid these consequences.

Although control of hyperglycemiamay be important in older individualswith diabetes, greater reductions in mor-bidity and mortality may result from con-trol of other cardiovascular risk factorsthan from tight glycemic control alone.There is strong evidence from clinical tri-als of the value of treating hypertension inthe elderly (269). There is less evidencefor lipid-lowering and aspirin therapy, al-though the benefits of these interventionsfor primary and secondary prevention arelikely to apply to older adults whose lifeexpectancies equal or exceed the time-frames seen in clinical trials.

Special care is required in prescribingand monitoring pharmacologic therapy inolder adults. Metformin is often contrain-dicated because of renal insufficiency orsignificant heart failure. TZDs can causefluid retention, which may exacerbate orlead to heart failure. They are contraindi-cated in patients with CHF (New YorkHeart Association class III and IV), and ifused at all should be used very cautiouslyin those with, or at risk for, milder degreesof CHF. Sulfonylureas, other insulinsecretagogues, and insulin can cause hy-poglycemia. Insulin use requires that pa-tients or caregivers have good visual andmotor skills and cognitive ability. Drugsshould be started at the lowest dose andtitrated up gradually until targets arereached or side effects develop.

Screening for diabetic complicationsin older adults also should be individual-ized. Particular attention should be paidto complications that can develop overshort periods of time and/or that wouldsignificantly impair functional status,such as visual and lower-extremity com-plications.

VIII. DIABETES CARE INSPECIFIC SETTINGS

A. Diabetes care in the hospital

Recommendations● All patients with diabetes admitted to

the hospital should have their diabetesclearly identified in the medical record.(E)

● All patients with diabetes should havean order for blood glucose monitoring,with results available to all members ofthe health care team. (E)

● Goals for blood glucose levels:● Critically ill patients: blood glucose

levels should be kept as close to 110mg/dl (6.1 mmol/l) as possible andgenerally �140 mg/dl (7.8 mmol/l).(A) These patients require an intrave-nous insulin protocol that has dem-onstrated efficacy and safety inachieving the desired glucose rangewithout increasing risk for severe hy-poglycemia. (E)

● Non–critically ill patients: there is noclear evidence for specific blood glu-cose goals. Since cohort data suggestthat outcomes are better in hospital-ized patients with fasting glucose�126 mg/dl and all random glucoses�180–200, these goals are reason-able if they can be safely achieved.Insulin is the preferred drug to treathyperglycemia in most cases. (E)

● Due to concerns regarding the risk ofhypoglycemia, some institutions mayconsider these blood glucose levels tobe overly aggressive for initial targets.Through quality improvement, gly-cemic goals should systematically bereduced to the recommended levels.(E)

● Scheduled prandial insulin dosesshould be appropriately timed in rela-tion to meals and should be adjustedaccording to point-of-care glucose lev-els. The traditional sliding-scale insulinregimens are ineffective as mono-therapy and are generally not recom-mended. (C)

● Using correction dose or “supplemen-tal” insulin to correct premeal hyper-glycemia in addition to scheduledprandial and basal insulin is recom-mended. (E)

● Glucose monitoring with orders forcorrection insulin should be initiated inany patient not known to be diabeticwho receives therapy associated withhigh risk for hyperglycemia, includinghigh-dose glucocorticoids therapy, ini-

Position Statement


tiation of enteral or parenteral nutri-tion, or other medications such asoctreotide or immunosuppressivemedications. (B) If hyperglycemia isdocumented and persistent, initiationof basal/bolus insulin therapy may benecessary. Such patients should betreated to the same glycemic goals aspatients with known diabetes. (E)

● A plan for treating hypoglycemiashould be established for each patient.Episodes of hypoglycemia in the hospi-tal should be tracked. (E)

● All patients with diabetes admitted tothe hospital should have an A1C ob-tained if the result of testing in the pre-vious 2–3 months is not available. (E)

● A diabetes education plan including“survival skills education” and fol-low-up should be developed for eachpatient. (E)

● Patients with hyperglycemia in the hos-pital who do not have a diagnosis ofdiabetes should have appropriate plansfor follow-up testing and care docu-mented at discharge. (E)

The management of diabetes in the hos-pital is extensively reviewed in an ADAtechnical review (270). This review, aswell as a consensus statement by theAmerican Association of Clinical Endocri-nologists (AACE) with cosponsorship byADA (271,272) and a report of a jointADA-AACE task force on the topic (273),forms the basis for the discussion andguidelines in this section.

The literature on hospitalized pa-tients with hyperglycemia typically de-scribes three categories:

● Medical history of diabetes: diabeteshas been previously diagnosed and ac-knowledged by the patient’s treatingphysician.

● Unrecognized diabetes: hyperglycemia(fasting blood glucose 126 mg/dl orrandom blood glucose 200 mg/dl) oc-curring during hospitalization and con-firmed as diabetes after hospitalizationby standard diagnostic criteria but un-recognized as diabetes by the treatingphysician during hospitalization.

● Hospital-related hyperglycemia: hyper-glycemia (fasting blood glucose 126mg/dl or random blood glucose �200mg/dl) occurring during the hospital-ization that reverts to normal after hos-pital discharge.

The prevalence of diabetes in hospitalizedadult patients is not precisely known. In

the year 2000, 12.4% of hospital dis-charges in the U.S. listed diabetes as a di-agnos i s , but th i s i s l ike ly anunderestimate. The prevalence of diabe-tes in hospitalized adults is conservativelyestimated at 12–25%, depending on thethoroughness used in identifying pa-tients. In the year 2003, there were 5.1million hospitalizations with diabetes as alisted diagnosis, a 2.3-fold increase over1980 rates (274).

The management of hyperglycemia inthe hospital was traditionally consideredsecondary in importance to the conditionthat prompted admission (273).

A rapidly growing body of literaturesupports targeted glucose control in thehospital setting for potential improvedmortality, morbidity, and health eco-nomic outcomes. Hyperglycemia in thehospital may result from stress; decom-pensation of type 1, type 2, or other formsof diabetes; and/or may be iatrogenic dueto withholding of antihyperglycemicmedications or administration of hyper-glycemia-provoking agents such as glu-cocorticoids or vasopressors.

1. In-hospital hyperglycemia andoutcomesa. General medicine and surgery. Ob-servational studies suggest an associationbetween hyperglycemia and increasedmortality. Surgical patients with at leastone blood glucose value �220 mg/dl(12.2 mmol/l) on the first postoperativeday have significantly higher infectionrates (275).

When admissions on general medi-cine and surgery units were studied, pa-tients with new hyperglycemia hadsignificantly increased in-hospital mortal-ity, as did patients with known diabetes.In addition, length of stay was higher forthe new hyperglycemic group, and pa-tients in either hyperglycemic group weremore likely to require intensive care unit(ICU) care and transitional or nursinghome care. Better outcomes were demon-strated in patients with fasting and admis-sion blood glucose �126 mg/dl (7mmol/l) and all random blood glucoselevels �200 mg/dl (11.1 mmol/l) (276).b. CVD and critical care. A significantrelationship exists between blood glucoselevels and mortality in the setting of acutemyocardial infarction. A meta-analysis of15 studies compared in-hospital mortal-ity in both hyper- and normoglycemic pa-tients with and without diabetes. Insubjects without known diabetes whose

admission blood glucose averaged 109.8mg/dl (6.1 mmol/l), the relative risk forin-hospital mortality was increased signif-icantly. When diabetes was present andadmission glucose averaged 180 mg/dl(10 mmol/l), risk of death was moderatelyincreased compared with patients whohad diabetes but less hyperglycemia onadmission (277). Another study (278)demonstrated a strong independent rela-tionship between admission blood glu-cose values and both in-hospital and1-year mortality; rates were significantlylower in subjects with admission plasmaglucose �100.8 mg/dl (5.6 mmol/l) thanin those with plasma glucose 199.8 mg/dl(11 mmol/l).

These studies focused on admissionblood glucose as a predictor of outcomes,rather than inpatient glycemic manage-ment per se. Higher admission plasmaglucose levels in patients with a prior his-tory of diabetes could reflect the degree ofglycemic control in the outpatient setting,thus linking outpatient glycemic controlto outcomes in the inpatient population.In patients without a prior history of dia-betes, admission hyperglycemia couldrepresent case finding of patients withpreviously undiagnosed diabetes, an un-masking of risk in a population at highrisk for diabetes, or more severe illness atadmission.

In the initial Diabetes and Insulin-Glucose Infusion in Acute Myocardial In-farction study (279,280), insulin-glucoseinfusion followed by at least 3 months ofsubcutaneous insulin treatment in dia-betic patients with acute myocardial in-farction improved long-term survival.Mean blood glucose in the intensive insu-lin intervention arm was 172.8 mg/dl (9.6mmol/l), compared with 210.6 mg/dl(11.7 mmol/l) in the “conventional”group. The broad range of blood glucoselevels within each arm limits the ability todefine specific blood glucose targetthresholds.

Three more recent studies (281–283)using an insulin-glucose infusion did notshow a reduction in mortality in the inter-vention groups. However, in each of thesestudies, blood glucose levels were posi-tively correlated with mortality. In theHyperglycemia: Intensive Insulin Infu-sion In Infarction (HI-5) Study, a decreasein both CHF and reinfarction was ob-served in the group receiving intensive in-sulin therapy for at least 24 h.c. Cardiac surgery. Attainment of tar-geted glucose control in patients with di-abetes undergoing cardiac surgery is



associated with reduced mortality andrisk of deep sternal wound infections(284,285) and supports the concept thatperioperative hyperglycemia is an inde-pendent predictor of infection in patientswith diabetes (286), with the lowest mor-tality in patients with blood glucose �150mg/dl (8.3 mmol/l) (287).d. Critical care. A mixed group of pa-tients with and without diabetes admittedto a surgical ICU (SICU) were random-ized to receive intensive insulin therapy(target blood glucose 80 –110 mg/dl[4.4–6.1 mmol/l]) or conventional ther-apy. Intensive insulin therapy achieved amean blood glucose of 103 mg/dl (5.7mmol/l) and was associated with reducedmortality during the ICU stay and de-creased overall in-hospital mortality(288). Hospital and ICU survival were lin-early associated with ICU glucose levels,with the highest survival rates occurringin patients achieving an average bloodglucose �110 mg/dl (6.1 mmol/l) (289).

A subsequent study of a similar inter-vention in patients in a medical ICU(MICU) (290) showed that the group re-ceiving intensive insulin therapy had re-duced morbidity but no difference inmortality overall. Death rates were signif-icantly lower in those patients who weretreated for �3 days; these patients couldnot be identified before therapy. A recentmeta-analysis concluded that insulintherapy in critically ill patients had a ben-eficial effect on short-term mortality indifferent clinical settings (291).

2. Glycemic targets in hospitalizedpatientsThere is relatively strong evidence fromrandomized controlled trials for a glyce-mic target of blood glucose �110 mg/dl(6.1 mmol/l) in patients in critical careunits (288–290). However, the incidenceof severe hyperglycemia (blood glucose�40 mg/dl) in the MICU study was18.7%, much greater than the 5.1% ob-served in the SICU population. The iden-t ificat ion of hypoglycemia as anindependent risk factor for death in theMICU population may merit caution inwidely promoting the 80–110 mg/dl tar-get range for all critically ill populations(292). Two recent trials were discontin-ued because of difficulty achieving de-sired target ranges of blood glucose andunacceptably high rates of hypoglycemia(293,293a).

For patients on general medical-surgical units, the evidence for specific

glycemic goals is less definitive. Epidemi-ologic and physiologic data suggest thatlower blood glucose levels are associatedwith improved outcomes. Glycemic tar-gets similar to those of outpatients may bedifficult to achieve in the hospital due tothe effects of stress hyperglycemia, alterednutritional intake, and multiple interrup-tions to medical care. Blood glucose levelsshown to be associated with improvedoutcomes in these patients (fasting glu-cose �126 mg/dl and all blood glucosereadings �180–200 mg/dl) would ap-pear reasonable, if they can be safelyachieved.

In both the critical care and non–critical care venue, glycemic goals musttake into account the individual patient’ssituation as well as hospital system sup-port for achieving these goals. A continu-ous quality improvement strategy mayfacilitate gradual improvement in meanglycemia hospital-wide.

3. Treatment options in hospitalizedpatientsa. Noninsulin glucose-lowering agents.No large studies have investigated the po-tential roles of various noninsulin glu-cose-lowering agents on outcomes ofhospitalized patients with diabetes. Use ofthe various noninsulin classes in the inpa-tient setting presents some specific issues.

The long action of sulfonylureas andtheir predisposition to hypoglycemia inpatients not consuming their normal nu-trition serve as relative contraindicationsto routine use of these agents in the hos-pital (294). While the meglitinides, repa-glinide and neteglinide, theoreticallywould produce less hypoglycemia thansulfonylureas, lack of clinical trial data forthese agents, and the fact that they areprimarily prandial in effect, would pre-clude their use. The major limitation tometformin use in the hospital is a numberof specific contraindications to its use, re-lated to risk of lactic acidosis, many ofwhich occur in the hospital. The mostcommon risk factors for lactic acidosis inmetformin-treated patients are cardiacdisease, including CHF, hypoperfusion,renal insufficiency, old age, and chronicpulmonary disease (295). Lactic acidosisis a rare complication in the outpatientsetting (296), despite the relative fre-quency of risk factors (297). However, inthe hospital the risks of hypoxia, hypo-perfusion, and renal insufficiency aremuch higher, and it is prudent to avoidthe use of metformin in most patients.

TZDs are not suitable for initiation inthe hospital because of their delayed onsetof effect. In addition, they increase intra-vascular volume, a particular problem inthose predisposed to CHF and potentiallya problem for patients with hemody-namic changes related to admission diag-noses (e.g., acute coronary ischemia) orinterventions common in hospitalized pa-tients. Pramlintide and exenatide workmainly by reducing postprandial hyper-glycemia, so they would not be appropri-ate for patients not eating (NPO) or withreduced caloric consumption. Further-more, initiation of these drugs in the in-patient setting would be problematic, dueto alterations in normal food intake andtheir propensity to induce nausea ini-tially. There is limited experience and nopublished data on the DPP-IV inhibitorsin the hospital setting, but there are nospecific safety concerns. They are mainlyeffective on postprandial glucose andtherefore would have limited effect in pa-tients who are not eating.

In summary, each of the major classesof noninsulin glucose-lowering drugs hassignificant limitations for inpatient use.Additionally, they provide little flexibilityor opportunity for titration in a settingwhere acute changes often demand thesecharacteristics. Therefore insulin, whenused properly, is preferred for the major-ity of hyperglycemic patients in the hos-pital setting.b. Insulini. Subcutaneous insulin therapy. Subcu-taneous insulin therapy may be used toattain glucose control in most hospital-ized patients with diabetes outside of thecritical care arena. The components of thedaily insulin dose requirement can be metby a variety of insulins, depending on theparticular hospital situation. Subcutane-ous insulin therapy should cover bothbasal and nutritional needs, and is subdi-vided into scheduled insulin and supple-mental, or correction-dose, insulin.Correction-dose insulin therapy is an im-portant adjunct to scheduled insulin,both as a dose-finding strategy and as asupplement when rapid changes in insu-lin requirements lead to hyperglycemia. Ifcorrection doses are frequently required,the appropriate scheduled insulin dosesshould be increased to accommodate theincreased insulin needs. There are nostudies comparing human regular insulinwith rapid-acting analogs for use as cor-rection-dose insulin.

The traditional “sliding-scale” insulinregimens, usually consisting of regular in-

Position Statement


sulin without any intermediate or long-acting insulins, have been shown to beineffective when used as monotherapy inpatients with an established insulin re-quirement (298 –300). One problemswith sliding-scale insulin regimens is thatthe sliding-scale regimen prescribed onadmission is likely to be used throughoutthe hospital stay without modification,even when control remains poor. Addi-tionally, sliding-scale insulin therapytreats hyperglycemia after it has alreadyoccurred, instead of preventing the occur-rence of hyperglycemia. This “reactive”approach can lead to rapid changes inblood glucose levels, exacerbating bothhyper- and hypoglycemia.

A recent study demonstrated thesafety and efficacy of using basal-bolus in-sulin therapy utilizing weight-based dos-ing in insulin-naıve hospitalized patientswith type 2 diabetes (301). Glycemic con-trol, defined as a mean blood glucose�140 mg/dl, was achieved in 68% of pa-tients receiving basal-bolus insulin versusonly 38% of those receiving sliding-scaleinsulin alone. There were no differencesin hypoglycemia between the two groups.It is important to note that the patients inthis study were obese, and the doses usedin this study (0.4 – 0.5 units � kg�1 �day�1) are higher that what may be re-quired in patients who are more sensitiveto insulin, such as those who are lean orwho have type 1 diabetes.ii. Intravenous insulin infusion. The onlymethod of insulin delivery specifically de-veloped for use in the hospital is contin-uous intravenous infusion, using regularcrystalline insulin. There is no advantageto using rapid-acting analogs, the struc-tural modifications of which increase therate of absorption from subcutaneous de-pots, in an intravenous insulin infusion.The medical literature supports the use ofintravenous insulin infusion in preferenceto the subcutaneous route of insulin ad-ministration for several clinical indica-tions among nonpregnant adults. Theseinclude DKA and nonketotic hyperosmo-lar state; general preoperative, intraoper-ative, and postoperative care; thepostoperative period following heart sur-gery; following organ transplantation;with cardiogenic shock; exacerbated hy-perglycemia during high-dose glucocorti-coid therapy; type 1 diabetic patients whoare NPO; or in critical care illness in gen-eral. It may be used as a dose-findingstrategy in anticipation of initiation orreinitiation of subcutaneous insulin ther-apy in type 1 or type 2 diabetes.

Many institutions use insulin infusionalgorithms that can be implemented bynursing staff. Although numerous algo-rithms have been published, there havebeen no head-to-head comparisons be-tween insulin infusion strategies. Algo-rithms should incorporate the conceptsthat maintenance requirements differ be-tween patients and change over thecourse of treatment. Ideally, intravenousinsulin algorithms should consider boththe current and previous glucose level,the rate of change of plasma glucose, andthe current intravenous insulin infusionrate. For all algorithms, frequent bedsideglucose testing is required, but the idealfrequency is not known.iii. Transition from intravenous to sub-cutaneous insulin therapy. For thosewho will require subcutaneous insulin,the very short half-life of intravenous in-sulin necessitates administering the firstdose of subcutaneous insulin before dis-continuation of the intravenous insulininfusion. If short- or rapid-acting insulinis used, it should be injected 1–2 h beforestopping the infusion. If intermediate- orlong-acting insulin is used alone, itshould be injected 2–3 h before. A com-bination of short-/rapid- and intermedi-ate-/long-acting insulin is usuallypreferred. Basal insulin therapy can beinitiated at any time of the day, andshould not be withheld to await a specificdosing time, such as bedtime. A recentclinical trial demonstrated that a regimenusing 80% of the intravenous insulin re-quirement over the preceding 24 h, di-vided into basal and bolus insulincomponents, was effective at achievingblood glucose levels between 80 and 150mg/dl following discontinuation of the in-travenous insulin (302).

4. Self-management in the hospitalSelf-management of diabetes in the hos-pital may be appropriate for competentadult patients who have a stable level ofconsciousness, have reasonably stabledaily insulin requirements, successfullyconduct self-management of diabetes athome, have physical skills needed to suc-cessfully self-administer insulin and per-form SMBG, have adequate oral intake,and are proficient in carbohydrate count-ing, use of multiple daily insulin injec-tions or insulin pump therapy, and sick-day management. The patient andphysician, in consultation with nursingstaff, must agree that patient self-management is appropriate under the

conditions of hospitalization. For patientsconducting self-management in the hos-pital, it is imperative that basal, prandial,and correction doses of insulin and resultsof bedside glucose monitoring are re-corded as part of the patient’s hospitalmedical record. While many institutionsallow patients on insulin pumps to con-tinue these devices in the hospital, othersexpress concern regarding use of a deviceunfamiliar to staff, particularly in patientswho are not able to manage their ownpump therapy. If a patient is too ill toself-manage either multiple daily injec-tions or CSII, then appropriate subcuta-neous doses can be calculated on the basisof their basal and bolus insulin needs dur-ing hospitalization, with adjustments forchanges in nutritional or metabolic status.

5. Preventing hypoglycemiaHypoglycemia, especially in insulin-treated patients, is the leading limitingfactor in the glycemic management oftype 1 and type 2 diabetes (117). In thehospital, multiple additional risk factorsfor hypoglycemia are present, evenamong patients who are neither “brittle”nor tightly controlled. Patients with orwithout diabetes may experience hypo-glycemia in the hospital in associationwith altered nutritional state, heart fail-ure, renal or liver disease, malignancy, in-fection, or sepsis (303,304). Additionaltriggering events leading to iatrogenic hy-poglycemia include sudden reduction ofcorticosteroid dose, altered ability of thepatient to self-report symptoms, reduc-tion of oral intake, emesis, new NPO sta-tus, inappropriate timing of short- orrapid-acting insulin in relation to meals,reduction of rate of administration ofintravenous dextrose, and unexpected in-terruption of enteral feedings or paren-teral nutrition.

Despite the preventable nature ofmany inpatient episodes of hypoglyce-mia, institutions are more likely to havenursing protocols for the treatment of hy-poglycemia than for its prevention.Tracking such episodes and analyzingtheir causes are important quality im-provement activities.

6. Diabetes care providers in thehospitalInpatient diabetes management may beeffectively provided by primary care phy-sicians, endocrinologists, or hospitalists,but involvement of appropriately trainedspecialists or specialty teams may reduce



length of stay, improve glycemic control,and improve outcomes (305–308). In thecare of diabetes, implementation of stan-dardized order sets for scheduled and cor-rection-dose insulin may reduce relianceon sliding-scale management. A team ap-proach is needed to establish hospitalpathways. To achieve glycemic targetsassociated with improved hospital out-comes, hospitals will need multidisci-plinary support for using insulin infusiontherapy outside of critical care units orwill need to develop protocols for subcu-taneous insulin therapy that effectivelyand safely achieve glycemic targets (309).

7. DSME in the hospitalTeaching diabetes self-management topatients in hospitals is a challenging task.Patients are ill, under increased stress re-lated to their hospitalization and diagno-sis, and in an environment not conduciveto learning. Ideally, people with diabetesshould be taught at a time and place con-ducive to learning: as an outpatient in arecognized program of diabetes educa-tion.

For the hospitalized patient, diabetes“survival skills” education is generally afeasible approach. Patients receive suffi-cient information and training to enablethem to go home safely. Those newly di-agnosed with diabetes or who are new toinsulin and/or blood glucose monitoringneed to be instructed before discharge tohelp ensure safe care upon returninghome. Those patients hospitalized be-cause of a crisis related to diabetes man-agement or poor care at home neededucation to prevent subsequent episodesof hospitalization.

8. MNT in the hospitalHospital diets continue to be ordered bycalorie levels based on the “ADA diet.”However, since 1994 the ADA has not en-dorsed any single meal plan or specifiedpercentages of macronutrients, and theterm “ADA diet” should no longer beused. Current nutrition recommenda-tions advise individualization based ontreatment goals, physiologic parameters,and medication usage. Because of thecomplexity of nutrition issues in the hos-pital, a registered dietitian, knowledge-able and skilled in MNT, should serve asan inpatient team member. The dietitianis responsible for integrating informationabout the patient’s clinical condition, eat-ing, and lifestyle habits and for establish-ing treatment goals in order to determine

a realistic plan for nutrition therapy(310,311).

9. Bedside blood glucose monitoringImplementing intensive diabetes therapyin the hospital setting requires frequentand accurate blood glucose data. Thismeasure is analogous to an additional “vi-tal sign” for hospitalized patients with di-abetes. Bedside glucose monitoring usingcapillary blood has advantages over labo-ratory venous glucose testing because theresults can be obtained rapidly at the“point of care,” where therapeutic deci-sions are made.

Bedside blood glucose testing is usu-ally performed with portable meters thatare similar or identical to devices forhome SMBG. Staff training and ongoingquality control activities are importantcomponents of ensuring accuracy of theresults. Ability to track the occurrence ofhypo- and hyperglycemia is necessary.Results of bedside glucose tests should bereadily available to all members of thecare team.

For patients who are eating, com-monly recommended testing frequenciesare premeal and at bedtime. For patientsnot eating, testing every 4–6 h is usuallysufficient for determining correction in-sulin doses. Patients on continuous intra-venous insulin typically require hourlyblood glucose testing until the blood glu-cose levels are stable, then every 2 h.

10. Continuous blood glucosemonitoring in the hospitalThe introduction of real-time blood glu-cose monitoring as a tool for outpatientdiabetes management has potential bene-fit for the inpatient population (312).However, at this time, data are lackingexamining this new technology in theacutely ill patient population. Until morestudies are published, it is premature touse continuous blood glucose monitoringin the hospital except in a research setting.

B. Diabetes care in the school andday care setting

Recommendations● An individualized diabetes medical

management plan (DMMP) should bedeveloped by the parent/guardian andthe student’s diabetes health care team.(E)

● An adequate number of school person-nel should be trained in the necessarydiabetes procedures (including moni-

toring of blood glucose levels and ad-ministration of insulin and glucagon)and in the appropriate response to highand low blood glucose levels. Theseschool personnel need not be healthcare professionals. (E)

● As specified in the DMMP and as devel-opmentally appropriate, the studentwith diabetes should have immediateaccess to diabetes supplies at all times,should be permitted to monitor his orher blood glucose level, and should beable to take appropriate action to treathypoglycemia in the classroom or any-where the student may be in conjunc-tion with a school activity. (E)

There are �206,000 individuals �20years of age with diabetes in the U.S.,most of whom attend school and/or sometype of day care and need knowledgeablestaff to provide a safe environment. De-spite legal protections, including cover-age of children with diabetes underSection 504 of the Individuals with Dis-abilities Education Act of 1991, childrenin the school and day care setting still facediscrimination. The ADA position state-ment on diabetes care in the school andday care setting (313) provides the legaland medical justifications for the recom-mendations provided herein.

Appropriate diabetes care in theschool and day care setting is necessaryfor the child’s immediate safety, long-term well-being, and optimal academicperformance. Parents and the health careteam should provide school systems andday care providers with the informationnecessary for children with diabetes toparticipate fully and safely in the school/day care experience by developing an in-dividualized DMMP.

An adequate number of school per-sonnel should be trained in the necessarydiabetes procedures (e.g., blood glucosemonitoring and insulin and glucagon ad-ministration) and in the appropriate re-sponses to high and low blood glucoselevels to ensure that at least one adult ispresent to perform these procedures in atimely manner while the student is atschool, on field trips, and participating inschool-sponsored extracurricular activi-ties. These school personnel need not behealth care professionals, although theschool nurse may be instrumental intraining nonmedical individuals.

The student with diabetes shouldhave immediate access to diabetes sup-plies at all times, with supervision asneeded. The student should be able to ob-

Position Statement


tain a blood glucose level and respond tothe results as quickly and conveniently aspossible, minimizing the need for missinginstruction in the classroom and avoidingthe risk of worsening hypoglycemia if thechild must go somewhere else for treat-ment. The student’s desire for privacyduring testing and insulin administrationshould also be accommodated.

ADA and partner organizations havedeveloped tools for school personnel toprovide a safe and nondiscriminatory ed-ucational environment for all studentswith diabetes (314,315).

C. Diabetes care at diabetes camps

Recommendations● Each camper should have a standard-

ized medical form completed by his/herfamily and the physician managing thediabetes. (E)

● Camp medical staff should be led bywith a physician with expertise in man-aging type 1 and type 2 diabetes, andincludes nurses (including diabetes ed-ucators and diabetes clinical nurse spe-cialists) and registered dietitians withexpertise in diabetes. (E)

● All camp staff, including physicians,nurses, dietitians and volunteers,should undergo background testing toensure appropriateness in workingwith children. (E)

The concept of specialized residential andday camps for children with diabetes hasbecome widespread throughout the U.S.and many other parts of the world. Themission of diabetes camps is to provide acamping experience in a safe environ-ment. An equally important goal is to en-able children with diabetes to meet andshare their experiences with one anotherwhile they learn to be more personallyresponsible for their disease. For this tooccur, a skilled medical and camping staffmust be available to ensure optimal safetyand an integrated camping/educationalexperience (316).

Each camper should have a standard-ized medical form completed by his/herfamily and the physician managing the di-abetes that details the camper’s past med-ical history, immunization record, anddiabetes regimen. The home insulin dos-age should be recorded for each camper,including type(s) of insulin used, numberand timing of injections and the correc-tion factor and carbohydrate ratios usedfor determining bolus dosages for basal-bolus regimens. Campers using CSII

should also have their basal rates speci-fied. Because camp is often associatedwith more physical activity than experi-enced at home, the insulin dose may haveto be decreased during camp (316).

The diabetes camping experience isshort-term, with food and activity differ-ent than the home environment. Thus,goals of glycemic control at camp are toavoid extremes in blood glucose levelsrather than attempting optimization of in-tensive glycemic control (316).

During camp, a daily record of thecamper’s progress should be made, in-cluding all blood glucose levels and insu-lin dosages. To ensure safety and optimaldiabetes management, multiple bloodglucose determinations should be madethroughout each 24-h period: beforemeals, at bedtime, after or during pro-longed and strenuous activity, and in themiddle of the night when indicated forprior hypoglycemia. If major alterationsof a camper’s regimen appear to be indi-cated, it is important to discuss this withthe camper and the family in addition tothe child’s local physician. The record ofwhat transpired during camp should bediscussed with the family at the end of thecamp session and a copy sent to thechild’s physician (316).

Each camp should secure a formal re-lationship with a nearby medical facilityso that camp medical staff can refer to thisfacility for prompt treatment of medicalemergencies. ADA requires that the campmedical director be a physician with ex-pertise in managing type 1 and type 2 di-abetes. Nursing staff should includediabetes educators and diabetes clinicalnurse specialists. Registered dietitianswith expertise in diabetes should have in-put into the design of the menu and theeducation program. All camp staff, in-cluding medical, nursing, nutrition, andvolunteer staff, should undergo back-ground testing to ensure appropriatenessin working with children (316).

D. Diabetes management incorrectional institutions

Recommendations● Correctional staff should be trained in

the recognition, treatment, and appro-priate referral for hypo- and hypergly-cemia, including serious metabolicdecompensation. (E)

● Patients with a diagnosis of diabetesshould have a complete medical historyand physical examination by a licensedhealth care provider with prescriptive

authority in a timely manner upon en-try. Insulin-treated patients shouldhave a capillary blood glucose (CBG)determination within 1–2 h of arrival.Staff should identify patients with type1 diabetes who are at high risk for DKAwith omission of insulin. (E)

● Medications and MNT should be con-tinued without interruption upon entryinto the correctional environment. (E)

● In the correctional setting, policies andprocedures should enable CBG moni-toring to occur at the frequency neces-sitated by the patient’s glycemic controland diabetes regimen, and should re-quire staff to notify a physician of allCBG results outside of a specifiedrange, as determined by the treatingphysician. (E)

● For all inter-institutional transfers, amedical transfer summary should betransferred with the patient, and diabe-tes supplies and medication should ac-company the patient. (E)

● Correctional staff should begin dis-charge planning with adequate leadtime to ensure continuity of care andfacilitate entry into community diabe-tes care. (E)

At any given time, �2 million people areincarcerated in prisons and jails in theU.S., and it is estimated that nearly80,000 of these inmates have diabetes. Inaddition, many more people with diabe-tes pass through the corrections system ina given year (317).

People with diabetes in correctionalfacilities should receive care that meetsnational standards. Correctional institu-tions have unique circumstances thatneed to be considered so that all standardsof care may be achieved. Correctional in-stitutions should have written policiesand procedures for the management ofdiabetes and for training of medical andcorrectional staff in diabetes care practices(317).

Reception screening should empha-size patient safety. In particular, rapididentification of all insulin-treated indi-viduals with diabetes is essential in orderto identify those at highest risk for hypo-and hyperglycemia and DKA. All insulin-treated patients should have a CBG deter-mination within 1–2 h of arrival. Patientswith a diagnosis of diabetes should have acomplete medical history and physical ex-amination by a licensed health care pro-vider with prescriptive authority in atimely manner. It is essential that medica-



tion and MNT be continued withoutinterruption upon entry into the correc-tional system, as a hiatus in either medi-cation or appropriate nutrition may leadto either severe hyper- or hypoglycemia(317).

Patients must have access to prompttreatment of hypo- and hyperglycemia.Correctional staff should be trained in therecognition and treatment of these condi-tions, and appropriate staff should betrained to administer glucagon. Institu-tions should implement a policy requir-ing staff to notify a physician of all CBGresults outside of a specified range, as de-termined by the treating physician (317).

Correctional institutions should havesystems in place to ensure that insulin ad-ministration and meals are coordinated toprevent hypo- and hyperglycemia, takinginto consideration the transport of resi-dents off site and the possibility of emer-gency schedule changes. The frequency ofCBG monitoring will vary by patients’glycemic control and diabetes regimens.Policies and procedures should ensurethat the health care staff has adequateknowledge and skills to direct the man-agement and education of individualswith diabetes (317).

Patients in jails may be housed for ashort period of time before being trans-ferred or released, and patients in prisonmay be transferred within the system sev-eral times during their incarceration.Transferring a patient with diabetes fromone correctional facility to another re-quires a coordinated effort, as does plan-ning for discharge. The ADA PositionStatement on Diabetes Management inCorrectional Institutions (317) should beconsulted for more information on thistopic.

E. Emergency and disasterpreparedness

Recommendations● People with diabetes should maintain a

disaster kit that includes items impor-tant to their diabetes self-managementand continuing medical care. (E)

● The kit should be reviewed and replen-ished at least twice yearly. (E)

The difficulties encountered by peoplewith diabetes and their health care pro-viders in the wake of Hurricane Katrina(318) highlight the need for people withdiabetes to be prepared for emergencies,whether natural or otherwise, affecting a

region or just their household. Such pre-paredness will lessen the impact an emer-gency may have on their condition. It isrecommended that people with diabeteskeep a waterproof and insulated disasterkit ready with items critically importantto their self-management. These may in-clude glucose testing strips, lancets, and aglucose-testing meter; medications in-cluding insulin in a cool bag; syringes;glucose tabs or gels; antibiotic ointments/creams for external use; glucagon emer-gency kits; and photocopies of relevantmedical information, particularly medi-cat ion lists and recent lab tests/procedures if available. If possible,prescription numbers should be noted,since many chain pharmacies throughoutthe country will refill medications basedon the prescription number alone. In ad-dition, it may be important to carry a listof contacts for national organizations,such as the American Red Cross and ADA.This disaster kit should be reviewed andreplenished at least twice yearly (319).

IX. HYPOGLYCEMIA ANDEMPLOYMENT/LICENSURE

Recommendations● People with diabetes should be individ-

ually considered for employment basedon the requirements of the specific joband the individual’s medical condition,treatment regimen, and medical his-tory. (E)

Any person with diabetes, whether insu-lin treated or non–insulin treated, shouldbe eligible for any employment for whichhe/she is otherwise qualified. Despite thesignificant medical and technological ad-vances made in managing diabetes, dis-crimination in employment and licensureagainst people with diabetes still occurs.This discrimination is often based on ap-prehension that the person with diabetesmay present a safety risk to the employeror the public, a fear sometimes based onmisinformation or lack of up-to-dateknowledge about diabetes. Perhaps thegreatest concern is that hypoglycemia willcause sudden unexpected incapacitation.However, most people with diabetes canmanage their condition in such a mannerthat there is minimal risk of incapacita-tion from hypoglycemia (320).

Because the effects of diabetes areunique to each individual, it is inappro-priate to consider all people with diabetes

the same. People with diabetes should beindividually considered for employmentbased on the requirements of the specificjob. Factors to be weighed in this decisioninclude the individual’s medical condi-tion, treatment regimen (MNT, noninsu-lin drugs, and/or insulin), and medicalhistory, particularly in regard to the oc-currence of incapacitating hypoglycemicepisodes (320).

X. THIRD-PARTYREIMBURSEMENT FORDIABETES CARE, SELF-MANAGEMENTEDUCATION, ANDSUPPLIES

Recommendations● Patients and practitioners should have

access to all classes of antidiabetic med-ications, equipment, and supplies with-out undue controls. (E)

● MNT and DSME should be covered byinsurance and other payors. (E)

To achieve optimal glucose control, theperson with diabetes must have access tohealth care providers who have expertisein the field of diabetes. Treatments andtherapies that improve glycemic controland reduce the complications of diabeteswill also significantly reduce health carecosts. Access to the integral componentsof diabetes care, such as health care visits,diabetes supplies and medications, andself-management education, is essential.All medications and supplies related tothe daily care of diabetes, such as sy-ringes, strips, and meters, must also bereimbursed by third-party payors (321).

It is recognized that the use of formu-laries, prior authorization, and provisionssuch as competitive bidding can manageprovider practices as well as costs to thepotential benefit of payors and patients.However, any controls should ensure thatall classes of antidiabetic agents withunique mechanisms of action and allclasses of equipment and supplies de-signed for use with such equipment areavailable to facilitate achieving glycemicgoals and to reduce the risk of complica-tions. Without appropriate safeguards,undue controls could constitute an ob-struction of effective care (321).

Medicare and many other third-partypayors cover DSME (the CMS term is di-abetes se l f -management tra in ing[DSMT]) and MNT. The qualified benefi-ciary who meets the diagnostic criteria

Position Statement


and medical necessity can receive an ini-tial benefit of 10 h of DSMT and 3 h ofMNT, with a potential total of 13 h ofinitial benefits. However, not all Medicarebeneficiaries with diabetes will qualify forboth MNT and DSMT benefits. More in-formation on Medicare policy, includingfollow-up benefits, is available at www.diabetes.org/for-health-professionals-and-scientists/recognition.jsp or on theCMS Web sites: www.cms.hhs.gov/DiabetesSelfManagement (DSME) andwww.cms.hhs.gov/MedicalNutritionTherapy (diabetes MNT) reimbursement.

XI. STRATEGIES FORIMPROVING DIABETESCAREThe implementation of the standards ofcare for diabetes has been suboptimal inmost clinical settings. A recent report(322) indicated that only 37% of adultswith diagnosed diabetes achieved an A1Cof �7%, only 36% had a blood pressure�130/80 mmHg, and just 48% had a totalcholesterol �200 mg/dl. Most distressingwas that only 7.3% of people with diabe-tes achieved all three treatment goals.

While numerous interventions to im-prove adherence to the recommendedstandards have been implemented, thechallenge of providing uniformly effectivediabetes care has thus far defied a simplesolution. A major contributor to subopti-mal care is a delivery system that too oftenis fragmented, lacks clinical informationcapabilities, often duplicates services, andis poorly designed for the delivery ofchronic care. The Institute of Medicinehas called for changes so that delivery sys-tems provide care that is evidence-based,patient-centered, and systems-oriented,and takes advantage of information tech-nologies that foster continuous qualityimprovement. Collaborative, multidisci-plinary teams should be best suited toprovide such care for people with chronicconditions like diabetes and to empowerpatients’ performance of appropriate self-management. Alterations in reimburse-ment that reward the provision of qualitycare, as defined by the attainment of qual-ity measures developed by such programsas the ADA/National Committee for Qual-ity Assurance Diabetes Provider Recogni-tion Program, will also be required toachieve desired outcome goals.

The NDEP recently launched a newonline resource to help health care profes-sionals better organize their diabetes care.The www.betterdiabetescare.nih.gov

Web site should help users design andimplement more effective health care de-livery systems for those with diabetes.

In recent years, numerous health careorganizations, ranging from large healthcare systems such as the U.S. Veteran’sAdministration to small private practices,have implemented strategies to improvediabetes care. Successful programs havepublished results showing improvementin process measures such as measurementof A1C, lipids, and blood pressure. Effectson in important intermediate outcomes,such as mean A1C for populations, havebeen more difficult to demonstrate (323–325) although examples do exist (326–330). Successful interventions have beenfocused at the level of health care profes-sionals, delivery systems, and patients.Features of successful programs reportedin the literature include:

● Improving health care professional ed-ucation regarding the standards of carethrough formal and informal educationprograms.

● Delivery of DSME, which has beenshown to increase adherence to stan-dard of care.

● Adoption of practice guidelines, withparticipation of health care profession-als in the process. Guidelines should bereadily accessible at the point of service,such as on patient charts, in examiningrooms, in “wallet or pocket cards,” onPDAs, or on office computer systems.Guidelines should begin with a sum-mary of their major recommendationsinstructing health care professionalswhat to do and how to do it.

● Use of checklists that mirror guidelineshave been successful at improving ad-herence to standards of care.

● Systems changes, such as provision ofautomated reminders to health careprofessionals and patients, reporting ofprocess and outcome data to providers,and especially identification of patientsat risk because of failure to achieve tar-get values or a lack of reported values.

● Quality improvement programs com-bining continuous quality improve-ment or other cycles of analysis andintervention with provider perfor-mance data.

● Practice changes, such as clustering ofdedicated diabetes visits into specifictimes within a primary care practiceschedule and/or visits with multiplehealth care professionals on a single dayand group visits.

● Tracking systems with either an elec-

tronic medical record or patient regis-try have been helpful at increasingadherence to standards of care by pro-spectively identifying those requiringassessments and/or treatment modifi-cations. They likely could have greaterefficacy if they suggested specific ther-apeutic interventions to be consideredfor a particular patient at a particularpoint in time (331).

● A variety of nonautomated systems,such as mailing reminders to patients,chart stickers, and flow sheets, havebeen useful to prompt both providersand patients.

● Availability of case or (preferably) caremanagement services, usually by anurse (332). Nurses, pharmacists, andother nonphysician health care profes-sionals using detailed algorithms work-ing under the supervision of physiciansand/or nurse education calls have alsobeen helpful. Similarly, dietitians usingMNT guidelines have been demon-strated to improve glycemic control.

● Availability and involvement of expertconsultants, such as endocrinologistsand diabetes educators.

Evidence suggests that these individual ini-tiatives work best when provided as com-ponents of a multifactorial intervention.Therefore, it is difficult to assess the con-tribution of each component; however, itis clear that optimal diabetes managementrequires an organized, systematic ap-proach and involvement of a coordinatedteam of health care professionals.

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4. Expert Committee on the Diagnosis andClassification of Diabetes Mellitus: Re-port of the Expert Committee on the Di-agnosis and Classification of DiabetesMellitus. Diabetes Care 20:1183–1197,1997

5. Expert Committee on the Diagnosis andClassification of Diabetes Mellitus: Fol-low-up report on the diagnosis of diabe-tes mellitus. Diabetes Care 26:3160–3167, 2003

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